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■S'* •it -*• v- ■*• ■-.... v- *•* A BIBLIOGRAPHICAL SOURCEBOOK 
OF 
COMPRESSED AIR, DIVING 
AND SUBMARINE MEDICINE 
VOLUME II 
By 
Ebbe Curtis Hoff, Ph. D., M. D. 
I** 
Professor of Neurological Science 
Medical College of Virginia 
Richmond, Virginia 
and 
Leon Jack Greenbaum, Jr. 
Lieutenant, MSC, U. S. Naval Reserve 
NOVEMBER 1954 
OFFICE OF NAVAL RESEARCH 
AND 
BUREAU OF MEDICINE AND SURGERY 
DEPARTMENT OF THE NAVY 
WASHINGTON, D. C. TO 
THE SUBMARINERS, DIVERS, AND UNDERWATER SWIMMERS 
OF THE 
UNITED STATES NAVY 
THIS VOLUME IS INSCRIBED 
IN RECOGNITION OF 
THEIR DISTINGUISHED SERVICE PREFACE 
THE publication of A Bibliographical Source- 
book of Compressed Air, Diving and Sub- 
marine Medicine in February 1948 provided 
a source of reference to the literature in medical 
problems of diving, compressed-air work, and sub- 
marine operations. Coverage in that volume ex- 
tended to 1 January 1946. Since the appearance of 
the Sourcebook, the subject has rapidly advanced 
and hopes have been expressed that a second volume 
of the Sourcebook would be prepared. The en- 
couragement of members of the Panel on Shipboard 
and Submarine Medicine of the Committee on 
Medical Sciences, Research and Development 
Board, Department of Defense, served as an im- 
portant impetus to our undertaking the heavy task 
of bringing out this second volume. To facilitate 
the work, a contract (Nonr-199(00)NR 112-063) 
was negotiated and set up between the Office of 
Naval Research, Department of the Navy, and the 
Medical College of Virginia. This contract was 
effective between 1 November 1950 and 31 July 
1953. 
The literature cited in the present volume com- 
prises pertinent unclassified reports and documents 
as well as published books, monographs, and papers 
appearing between 1 January 1946 and 31 Decem- 
ber 1951. Because of the exigencies of war, it was 
impossible to obtain many items that should have 
been included in the first volume. These have sub- 
sequently become available and although they were 
published before the beginning of 1946, they have 
been included in the present volume for the sake 
of completeness. We have also added to the present 
volume all pertinent unpublished reports which 
appeared before 1 January 1946 and which have 
now been declassified. Some of these were open 
unpublished reports at the time of appearance. The 
reader will observe a number of new sections in 
the present volume which are not found in the first 
volume. In preparing these new sections, we have 
gone back and picked up contributory unpublished 
reports and published articles appearing before 1 
January 1946. 
The contents of the present volume have been 
handled according to the same policies that pre- 
vailed in assembling the first volume. In the text 
the observations and opinions of the investigators 
have been reported briefly and accurately, and all 
aspects of controversial issues have been considered. 
In our arrangement of the material and in our tex- 
tual discussions, we have attempted to indicate re- 
search trends where these can be discerned. 
As in the first volume, we have assigned a code 
symbol at the end of each entry in the bibliographi- 
cal lists. C refers to classical or very early reports. 
D refers to discussion papers of a general character. 
P indicates articles reporting experimental investiga- 
tions which have contributed to progress in the sub- 
ject in question. M denotes recent papers presenting 
modern or current points of view. R designates re- 
view articles with comprehensive coverage. We have 
indicated with a B those reports with particularly 
useful bibliographies, and have designated with Ch 
those items which contain case histories. 
ARRANGEMENT AND 
STYLE 
The classification, arrangement, and style in the 
present volume follow the conventions observed in 
the first volume of this Sourcebook. We have as- 
sembled the references according to the scheme of 
subject-matter classification given below in the table 
of contents. As in the first volume, wherever un- 
signed articles are quoted, they are listed under 
“Anonymous” at the end of each subject group. A 
serial number has been assigned to each entry, and 
the reference is cited by this number in the index of 
authors and the text. We have followed the policy 
of spelling the surnames of authors as they appear 
in the original source in citing entries in the text 
and reference lists. In books and theses, the authors’ 
names are given exactly as printed on the original 
title page. In citing papers in the journal literature 
and unpublished agency reports, only the initials of given names are used. No attempt has been made 
to distinguish between male and female authors 
in citing papers and reports. In some cases, par- 
ticularly in the French literature, an author’s sur- 
name appears without given names or initials. In 
citing such items in the lists of references, the 
omission of the initials is indicated by square 
brackets following or preceding the surname. 
The citation of published papers and books and 
other separate publications follows the style used 
in the first volume. Wherever possible, the title is 
given in the original language. Title translations of 
the romance languages are not provided. In all 
titles, the original language is used except in those 
languages requiring special alphabets. In such cases, 
if a translation into one of the commoner languages 
was supplied in the original article, this is quoted 
in the citation in parentheses. Wherever a new 
translation was made, this has been indicated by 
inclosing the translated title in square brackets. 
Whenever articles contain summaries in a second 
or third language, this information is given at the 
end of the citation. 
In preparing citations of unpublished reports, we 
have followed insofar as possible the style for 
citation of published papers by placing the authors’ 
names at the beginning of the citation if authors’ 
names are given. In the citation of unpublished 
reports, the abbreviated name of the agency follows 
the subject title. In the case of those reports in 
which authors’ names are not given, an abbreviated 
name of the agency is given at the beginning of the 
citation. 
All journals and handbooks from which refer- 
ences have been taken are cited in a separate list 
at the end of this volume. These items are arranged 
in alphabetical order of their abbreviations, fol- 
lowed in each case by the full name of the publi- 
cation. The system of abbreviations used conforms 
to A World List of Scientific Periodicals published 
in the years 1900-1950, 3d edition. New York and 
London. For journals not included in the World 
List, abbreviations have been created which con- 
form to World List conventions and these abbre- 
viations are followed by an asterisk in the journal 
list but not in the lists of references. In the Index 
of Authors, the names are listed in alphabetical 
order without distinction as to sole or joint author- 
ship. In cases where variations of spelling of names 
are found, serial numbers are indexed under the 
commonest form of the name. 
Following the Index of Authors, there is an In- 
dex of Sources for Unpublished Reports. Opposite 
each agency name are given the serial number or 
serial numbers of the reports by the agency in ques- 
tion. Following the Index of Sources for Unpub- 
lished Reports, a Key to Agency Abbreviations is 
included for the convenience of the reader. 
ACKNOWLEDGMENTS 
We desire to acknowledge with thanks our in- 
debtedness for help, encouragement, and criticism 
to members of the staffs of the Bureau of Medicine 
and Surgery; the Office of Naval Research; the 
Medical Research Laboratory, U. S. Submarine 
Base, New London, Conn.; the Naval Medical Re- 
search Institute, National Naval Medical Center, 
Bethesda, Md.; the Experimental Diving Unit, 
U. S. Naval Gun Factory, Washington, D. G.; and 
the Naval Research Laboratory, Washington, D. C. 
Among the staff members of these naval activities, 
we particularly wish to thank Gapt. O. E. Van Der 
Aue, (MG) U. S. Navy, Gapt. Walter Welham, 
(MG) U. S, Navy, and Comdr. G. J. Duffner, 
(MG) U. S. Navy. 
We were stimulated and encouraged to under- 
take the preparation of this volume through the 
initiative of Gapt. C. W. Shilling, (MG) U. S. Navy. 
In all phases of the planning and execution of the 
work, Captain Shilling gave liberally of his time 
and shared freely with us his broad experience. His 
helpfulness in providing facilities and expediting 
plans have proved invaluable. His own deep con- 
cern for the advancement of naval research has been 
an inspiration to us and we wish to take this oppor- 
tunity of expressing to him our grateful thanks. 
We are especially grateful to Dr. Freeman H. 
Quimby, Head, Physiology Branch, Biological 
Sciences Division, Office of Naval Research, for 
his encouragement, understanding advice, and sup- 
port. It is our privilege to express our appreciation 
to Dr. W. T. Sanger, president of the Medical Col- 
lege of Virginia, and to the staff of the College. We 
wish to record our gratitude to Maj. Gen. W. F. 
Tompkins, comptroller of the Medical College of 
Virginia, and his staff. To all of these, we would 
offer sincere thanks for continuing help and encour- 
agement given us throughout the course of this 
project. 
Lt. Edward H. Lanphier, (MG) U. S. Naval 
Reserve, Assistant Medical Officer, Experimental 
Diving Unit, U. S. Naval Gun Factory, Washing- 
ton, D. G., gave generously of his time and energy 
in working with us in the planning and preparation 
of the section on special problems of swim-diving. 
We offer our grateful thanks to him. 
We are deeply grateful to Prof. C. P. Yaglou, 
Harvard School of Public Health, for his helpful 
review and criticism of the sections on heat. We also 
desire to thank Dr. C. R. Spealman, Medical Divi- sion, Civil Aeronautics Administration, for his kind- 
ness in reviewing the sections dealing with cold. 
It is a pleasure to record our appreciation to Sur- 
geon Commander Eric James, Royal Navy, for lists 
of names and copies of reports very kindly supplied 
by the British Admiralty. We also desire to thank 
Lt. Comdr. John Sebelien, Medical Corps, Nor- 
wegian Navy, for valuable advice on several over- 
seas reference sources. 
Most of the labor of assembling the literature 
included in this volume of the Sourcebook was con- 
ducted at the Armed Forces Medical Library, Wash- 
ington, D. C. We desire to express our appreciation 
to Lt. Col. Frank B. Rogers, Director of the Library, 
for so generously placing at our disposal the facili- 
ties of the library during a period of over two years. 
Among the many members of the library staff who 
have helped us, we wish, in particular, to thank 
Mr. Kanardy L, Taylor, Dr. Estelle Broadman, Mr. 
Joseph G. Tucker, Mr. Robert B. Austin, Mr. 
Charles A. Roos, Mr. Edward A. Miller, Mr. Harold 
F. Koehler, Mr. H. Lynn Womack, Mr. Robert L. 
Carey, Mr. Joseph Bauer, and Dr. Anne Caldwell. 
Dr. Leon H. Warren and Mrs. Faith Ferguson 
of the Division of Medical Sciences, National Re- 
search Council, Washington, D. C., were most co- 
operative and helpful in making available to us re- 
ports from their files. We wish to acknowledge our 
indebtedness to them. Our thanks are due also to 
Mr. W. A. Hahn, Committee on Amphibious 
Operations, National Research Council, Washing- 
ton, D. C., for help in obtaining source material on 
swim-diving. 
We desire to express our grateful thanks to Mr. 
J. Heston Heald, head, Reference Section, Techni- 
cal Information Division, Library of Congress. Mr. 
Heald and his staff provided us with a large volume 
of unpublished report literature. The generous aid 
offered by Miss Margaret McCluer, librarian of 
the Tompkins-McCaw Library, Medical College of 
Virginia, and the staff of the library is deeply 
appreciated. 
The text of the present volume has been pre- 
pared using as source material special abstracts and 
translations prepared for this purpose. We have 
been assisted in this heavy task of preparing abstracts 
by Mrs. G. W. Shilling, Miss Betty Sugarman, Dr. 
Madeleine Wiener, Mr. Tiber W. Marton, Mr. 
Stanley Jablonsky, and Mr. Nils H. Randers-Pehr- 
son. Our grateful thanks are extended to all of them 
for their willing cooperation. 
It is a special pleasure to accord thanks to Miss 
Marjorie D. Kratz who handled the many details in- 
volved in the office management of the contract 
under which this project was carried out. We also 
wish to thank Mrs. Anne F. Black and Mrs. Mayme 
P. Wright of the staff of the Office of Naval Re- 
search for many courtesies. 
We desire to express our thanks to Mrs. Phebe 
M. Hoff for technical advice and assistance in 
developing the style for citation of unpublished 
references. 
The work of making ready the manuscript for 
the press has involved many hours of diligent effort 
and close attention to detail. For devoted work on 
the manuscript, we wish to offer our sincere thanks 
to Miss Hagalyn H. Seay, Mrs. Delight Mathilda 
Hamilton, Miss Marguita B. Karson, and Mrs. 
Minna L. Hamner. We also wish to thank Chief 
Yeoman Jack Hamner, U. S. Navy, for his valuable 
assistance. 
In a work of this magnitude, it is inevitable that 
errors and omissions will be found, although we 
have given minute attention to accuracy and com- 
pleteness. The authors must assume entire responsi- 
bility for any deficiencies of the volume and will be 
grateful to readers who use it if they will draw our 
attention to mistakes that they may find. The opin- 
ions or assertions recorded herein are not to be 
construed as official or reflecting the views of the 
Department of the Navy or the naval service at 
large. 
E. C. H., 
L. J. G., Jr. 
Medical College of Virginia, 
Richmond, Va. 
Office of Naval Research, 
Washington, D. C. Table of Contents 
Page 
PREFACE ui 
GENERAL STUDIES OF SUBMARINE MEDICAL PROBLEMS 2 
TECHNICAL PROCEDURES AND RESEARCH APPARATUS IN COMPRESSED AIR, 
DIVING, AND SUBMARINE MEDICINE 2 
I. General studies 2 
II. Gas analysis in air and in blood 2 
HI. Respiratory apparatus 4 
IV. Apparatus for testing visual functions 5 
V. Chambers 5 
VI. Air compressors 6 
VII. Pressure gages 6 
VIII. Temperature measurement 6 
IX. Other technical procedures and apparatus 6 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY OF COMPRESSED AIR, 
DIVING, AND SUBMARINE MEDICINE 7 
I. Physiological effects of raised atmospheric pressures 7 
A. Central nervous system 7 
B. Heart and circulation 7 
C. Respiration 8 
II. Physiological effects of decompression from pressures higher than one atmosphere ... 9 
A. General studies of the effects of decompression 9 
B. Physiology of bubble formation 9 
C. Saturation and desaturation of gases in the body 15 
D. Fat and water content 16 
HI. Physiological effects of low oxygen tensions of environmental air 17 
A. Low oxygen percentages without decompression 17 
1. Special senses 17 
2. Nervous system 18 
3. Muscular activity 23 
4. Heart and circulation 23 
5. Blood 28 
6. Lymphatics 29 
7. Respiration 29 
8. Alimentary tract 31 
9. Metabolism 31 
10. Temperature 33 
11. Kidney 34 
12. Effect of carbon dioxide on hypoxia 35 
13. Tolerance 35 SPECIAL ANATOMY, PHYSIOLOGY, ETC .—Continued 
III. Physiological effects of low oxygen tensions of environmental air—Continued page 
B. Low oxygen tensions due to decompression 36 
1. General studies 36 
2. Special senses 37 
3. Nervous system 38 
4. Heart and circulation 41 
5. Blood 43 
6. Respiration 45 
7. Alimentary tract 46 
8. Metabolism 47 
9. Kidney 50 
10. Reproduction 50 
11. Effects of carbon dioxide on hypoxia 51 
12. Tolerance 51 
13. Acclimatization 53 
IV. Physiological effects of high carbon dioxide content on environmental air 54 
A. General studies 54 
B. Nervous system 55 
C. Heart and circulation 59 
D. Blood 63 
E. Cerebrospinal fluid 63 
F. Respiration 64 
G. Alimentary tract 66 
H. Metabolism 66 
I. Endocrine glands 68 
J. Acclimatization 69 
K. Pathological changes 70 
V. Heat and humidity problems 71 
A. General considerations of temperature, humidity, and climate 71 
B. Temperature and humidity problems on shipboard and in submarines 73 
C. Physiological effects of raised temperatures 73 
D. Tolerance and acclimatization to heat and humidity 82 
E. Effect of heat on efficiency 87 
F. Heat disease 89 
G. Skin diseases associated with heat and humidity 92 
VI. Cold exposure problems 95 
A. General considerations of cold 95 
B. Physiological effects of cold 96 
C. Chilblains 107 
D. Acclimatization and tolerance to cold 107 
E. Effect of cold on efficiency 112 
F. Immersion in cold water 112 
G. Rewarming after cold exposure 114 
H. Pathological effects of cold 117 
VII. Visual problems 119 
A. General considerations 119 
B. Acuity 119 
C. Color vision 121 
D. Visual performance 122 
E. Accommodation 123 SPECIAL ANATOMY, PHYSIOLOGY, ETC.—Continued 
VII. Visual problems—Continued page 
F. Phoria 123 
G. Night vision and dark adaptation 123 
H. Underwater vision 128 
VIII. Auditory problems 128 
IX, Noise and vibration 129 
A, Noise 129 
1. General studies 129 
2. Physiological and pathological effects of noise 130 
3. Hearing defects from exposure to noise 132 
4. Ear damage 136 
5. Effects of noise on efficiency 138 
6. Sound communication and noise 139 
7. Protection against noise 142 
B. Vibration 144 
1. Physiological effects on vibration 144 
2. Effects of vibration on performance 147 
BIOLOGY OF VERY HIGH HYDROSTATIC PRESSURES 148 
DISEASES AND ACCIDENTS IN SUBMARINE PERSONNEL, DIVERS, AND COM- 
PRESSED AIR WORKERS 149 
I. Diseases and accidents in naval personnel: morbidity 149 
II. Ear, nose, and throat disturbances 151 
A. General studies of otorhinolaryngological disturbances 151 
B. Otological effects of compression and decompression 152 
C. Aerotitis media and aerosinusitis 153 
D. Otitis media therapy 155 
1. General considerations 155 
2. Use of vasoconstrictor and analgesic drugs 155 
3. Chemotherapy 156 
4. Irradiation therapy 157 
5. Dental therapy 157 
6. Surgical and physical procedures 158 
E. Otitis externa 158 
F. Otitis externa therapy 159 
HI. Decompression sickness 159 
A. General considerations 159 
B. Clinical picture of decompression sickness 161 
C. Case reports 161 
D. Incidence, diagnosis, and prognosis of decompression sickness 163 
E. Etiology of decompression sickness 164 
F. Pathological lesions 165 
G. Prevention and treatment of decompression sickness, including preselection tests . 167 
1. General studies 167 
2. Decompression procedures 167 
3. Helium-oxygen administration 170 
4. Hydrogen-oxygen administration 171 
5. Oxygen administration 171 
6. Recompression treatment and procedures 172 
7. Drugs in prevention and treatment of decompression sickness 174 
8. Preselection tests 174 
291222—54 2 DISEASES AND ACCIDENTS, ETC.—Continued page 
IV, Explosive decompression 175 
A. General studies 175 
B. Effects of explosive decompression upon heart and circulation 176 
C. Effects of explosive decompression on cerebrospinal fluid pressure 178 
D. Effects of explosive decompression on the respiratory system 178 
E. Effects of explosive decompression on occurrence of intravascular bubbles .... 180 
F. Lethal factors in explosive decompression injury 180 
G. Tolerance of explosive decompression 181 
V. Oxygen intoxication 182 
A. Effects of increased oxygen tension not in excess of one atmosphere 182 
1. General studies 182 
2. Effects on the central nervous system 183 
3. Effects on the cardiovascular system 183 
4. Effects on the blood 184 
5. Effects on the respiratory system 185 
6. Effects on metabolism 186 
B. Effects of oxygen tension in excess of one atmosphere 187 
1. General studies 187 
2. Convulsions and other disturbances of the central nervous system 189 
3. Effects on respiration 192 
4. Effects on metabolism 192 
C. Mechanisms of intoxication 194 
1. Role of carbon dioxide and other factors in oxygen intoxication 194 
2. Disturbances of cellular metabolism in the production of oxygen intoxication. 196 
D. Effects of high oxygen tensions on micro-organisms 197 
E. Oxygen paradox 197 
VI. Noxious agents 198 
A. General studies of noxious agents 198 
B. Noxious gases, dusts, and vapors 199 
1. Carbon monoxide 199 
(a) General studies of carbon monoxide poisoning 199 
(b) Carbon monoxide in submarines and other naval vessels 200 
(c) Clinical picture, functional changes, and pathological effects of carbon 
monoxide poisoning 201 
(d) Mechanisms of carbon monoxide poisoning 206 
(e) Carbon monoxide uptake, absorption, and elimination 207 
(f) Tolerance and acclimatization to carbon monoxide 210 
(g) Treatment of carbon monoxide poisoning 211 
(h) Carbon monoxide detection in air and blood 216 
2. Arsine 216 
3. Beryllium 218 
4. Cadmium 223 
5. Chlorine 224 
6. Lead 226 
7. Mercury 229 
8. Stibine 231 
9. Tobacco smoke 233 
10. Organic solvents 235 
(a) Benzene 235 
(b) Carbon tetrachloride 235 
11. Other noxious agents 236 DISEASES AND ACCIDENTS, ETC.—Continued page 
VII. Motion sickness 236 
A. General studies on motion sickness 236 
B. Signs and symptoms of motion sickness (physiological and pathological changes) . 237 
C. Susceptibility to motion sickness 239 
D. Mechanisms of motion sickness 242 
E. Effect of motion sickness on performance 246 
F. Prevention and treatment of motion sickness 246 
VIII. Submarine escape problems 250 
A. Breath holding 250 
B. Escape procedures 251 
C. Escape accidents from submarines or escape training tanks 254 
D. Gas embolism 255 
IX. Special diving accidents 257 
X. Blast injuries 258 
XI, Drowning 261 
XII. Special problems of snorkel operations 261 
XIII. Dental problems 263 
XIV. Effects of radioactivity on personnel 264 
PROTECTION AND PRESERVATION OF PERSONNEL 268 
I. General studies 268 
II. Habitability 268 
A. Lighting 268 
B. Ventilation and air conditioning 270 
1. General studies 270 
2. Air flow and volume 270 
3. Humidity control 271 
4. Temperature control 272 
5. Disinfection of air 273 
6. Elimination of dust, gases, fumes, and odors from air 276 
7. Carbon dioxide absorbents, carbon dioxide absorption, and tolerable concen- 
trations of carbon dioxide and oxygen 277 
8. Oxygen generators 278 
C. Bunking facilities 279 
HI. Food and water supply 280 
IV. Diet and physical fitness 282 
V. Clothing 284 
A. General studies 284 
B. Physical properties, testing, and standards 284 
C. Effect of clothing on physiological responses to environmental changes 286 
D. Clothing for cold and dry conditions 287 
E. Protective clothing for immersion and rain 287 
F. Clothing for conditions of heat and humidity 288 
VI. Deep-sea-diving equipment and procedures 289 
VII. Resuscitation and respiratory devices 290 
VIII. Diffusion respiration 293 
IX. Pressure breathing 294 
SELECTION AND TRAINING OF SUBMARINE PERSONNEL, DIVERS, AND COM- 
PRESSED-AIR WORKERS 299 
I. Selection 299 
II. Training 304 
HI. Performance—submarine operations 305 
IV. Special sonar problems 306 Page 
SPECIAL PSYCHOLOGICAL AND PSYCHIATRIC PROBLEMS 309 
I. General studies 309 
II. Human factors and engineering design 309 
III. Psychomotor responses 314 
IV. Psychological factors in performance 315 
V. Stress 315 
VI. Fatigue 318 
VII. Morale 320 
VIII. Sleep-wakefulness 321 
IX. Duty and rest periods 325 
X. Psychiatric breakdown 327 
SPECIAL PROBLEMS OF SWIM-DIVING 329 
I. General studies 329 
II. Special physiological problems of swimming and swim-diving 330 
III. Diseases prevalent in swimmers 332 
IV. Hazards from dangerous fish and other marine organisms 334 
V. Underwater breathing apparatus and related gear 335 
KEY TO ABBREVIATIONS OF JOURNALS AND HANDBOOKS CITED 338 
KEY TO AGENCY ABBREVIATIONS 343 
INDEX OF AUTHORS 345 
INDEX OF SOURCES FOR UNPUBLISHED REPORTS 362 
INDEX OF SUBJECTS 365 General Studies of Submarine Medical 
Problems 
THE references included in this section offer a 
comprehensive survey of the field. Papers by 
Behnke (7 and 2) 1947 and (3) 1951, and 
Benson and Behnke (4) 1951, give highlights of 
physiological research in service laboratories and 
also summarize the physiological and medical as- 
pects of deep-sea diving. Willmon (72) 1949, (73) 
1950, and (74) 1951, has discussed the relationships 
between medicine and engineering in submarines 
and has considered the effects of future submarine 
engineering developments upon the health of the 
crew. Medical problems of future submarines have 
also been considered by Yarbrough (75) 1948. 
1. Behnke, A. R. Physiologic and medical aspects of 
aviation and deep sea diving. Advances Intern. Med., 1947, 
2: 262-307. [R] 
2. Behnke, A. R. Highlights of physiological research in 
military laboratories, pp. 57-66 in: Symposium on military 
physiology. Digest series no. 4, GE 61/1, 4-6 December 
1947. 
3. Behnke, A. R. Physical agents and trauma; trauma 
due to stress and physical agents. Annu. Rev. med., 1951, 
2: 243-272.[R] 
4. Benson, 0. 0., Jr., and A. R, Behnke. Problemes 
medicaux poses par la navigation aerienne et sous-marine. 
Pr. med., 1951,59: 1098-1099. 
5. Dolatkowski, A. Fizjo-patologiczne zagadnienia w 
pracy nurkow. [Physiopathological aspects of deep sea div- 
ing.] Lek. wojsk., 1949, 25: 89-100. [R] 
6. Gemmill, C. L. Aviation physiology. Annu. Rev. 
Physiol., 1946, 8: 499-514. [R] 
7. Gt. Brit., Ministry of labour and national service. 
Part VII. Work in compressed air. pp. 30-35 in: Factories 
acts, 1937 and 1948, Work of engineering construction. 
London, His Majesty’s Stationery Office, 1951. 55 pp. 
8. Klimenko, N. A., K. A. Pavlovskii, and V. P. Mak- 
simenko. Divers’ illness and first aid. pp. 78-91 in: Man- 
ual for divers of the navy. Moskow, Military Printing 
Office, 1948, 172 pp. (Russian text.) 
9. Rozanow, L. S. Badanie zagadnienia choroby keso- 
nowej w zwiazku radzieckim. Polsk. Tygod. lek., 1949, 4: 
182. 
10. Sebelien, J. Undervannsbaattjenestens Medisinske 
problemer. [Submarine service medical problems.] Nor- 
wegian naval officers association, Oslo, Norway, 1951, 
26 pp. 
11. Stelzner, H. Tauchertechnik. Handbuch fiir Tau- 
cher iiber den Bau und die Anwendung von Tauchergerd- 
ten aller Art. Lubeck, Charles Coleman, 1943, 403 pp. 
12. Willmon, T. L. Medicine and engineering in sub- 
marines. Mech. Engr., 1949, 71: 583-596. 
13. Willmon, T. L. The marriage of medicine and engi- 
neering in submarines. Marine News, 1950, 36: 14—19. 
14. Willmon, T. L. Man and the submarine. /. Amer. 
med. Assn., 1951,147: 1028-1030. 
15. Yarbrough, 0. D. Medical problems of future sub- 
marines. Milit. Surg., 1948,102: 342-346. 
1 Technical Procedures and Research 
Apparatus in Compressed Air, Diving 
and Submarine Medicine 
THE literature included under this title repre- 
sents a selection of reference material and is 
admittedly not complete. The reports chosen 
are for the most part selected because they have been 
referred to in papers dealing with problems of com- 
pressed air, diving, and submarine medicine. The 
technical procedures and research apparatus de- 
scribed in these reports are therefore particularly 
relevant to the subject matter of this volume. 
I. GENERAL STUDIES 
Shilling and Kohl’s chapter on submarine medi- 
cal facilities and equipment {16) 1947 has been in- 
cluded and is suggested for readers who desire a 
complete list of medical equipment provided in the 
submarine. 
16. Shilling, C. W. and J. W. Kohl. Submarine medical 
facilities and equipment, pp. 77-93 in: History of sub- 
marine medicine in World War II. U. S. Navy. Subma- 
rine base, New London, Conn. Medical research laboratory. 
25 May 1947,328 pp. 
II. GAS ANALYSIS IN AIR AND BLOOD 
The references given below constitute the prin- 
cipal reports encountered in the compressed air, 
diving, and submarine medicine literature dealing 
with gas analysis in air and blood. These and other 
technical procedures are also referred to throughout 
this volume in other appropriate sections. 
17. Bardeen, A. and 0, S. Orth. A rapid and simple 
method for carbon dioxide analysis in anesthetic atmos- 
pheres. Fed. Proc. Amer. Soc. exp. Biol., 1950, 9: 255. 
18. Barger, A. C., G. S. Richardson, and E. II. Landis. 
A Gciger-Miiller counter system for tracer studies of gas 
exchanges in man. Fed. Proc. Amer. Soc. exp. Biol., 1948, 
7; 5. 
19. Behrmann, V. G. and F. W. Hartman. Rapid 
COa determination with the Pauling Oa analyzer. Fed. 
Proc. Amer. Soc. exp. Biol., 1951, 10: 12. 
20. Beischer, D. E. Accuracy and limits of the Lilly- 
Anderson nitrogen meter. U. S. Navy. NATB, Pen- 
sacola, Fla. School of aviation medicine. Project NM 
001 036 Kept. no. 1, 27 December 1948, 4 pp. 
21. Beischer, D. E. A spectrophotometric method for 
the continuous quantitative analysis of nitrogen in gas 
mixtures. U. S. Navy. NATC, Pensacola, Fla. School of 
aviation medicine and research. Project NM 001 036, 
Rept no. 1, 27 December 1948, 4 pp. 
22. Benzinger, T. H. and C. Kitzinger. A method for 
continuous recording of gas composition by means of an 
interferometer. U. S. Navy. NMRI. NM 001-011, Rept. 
no. 1, 4 May 1948, 5 pp. 
23. Berg, W. E. Rapid and simultaneous analyses of 
oxygen and carbon dioxide in respired air by the thermal 
conductivity method. U. S. NRG-CAM. OEMcmr—196, 
C. A. M. rept. no. 451, June 1945, 14 pp. 
24. Blockwick, T. N. Report of determination of 02 
percentage change due to stratification or diffusion 
through the cylinder walls of He-02 mixtures. U. S. Navy. 
Naval gun factory, EDU. Project NS 186-042 (g) (7), 
Rept. no. 4-49, 3 February 1949, 5 pp. 
25 Boyer, M. H. and F. S. Thomas. A study of the 
Dwyer zero to 5% carbon dioxide indicator to determine 
its suitability for naval use. U. S. Navy. NRL. N. R. L. 
rept. no. P—1877—A, 6 July 1942, 20 pp. 
26. Brinkman, R. Haemoxymetry. Acta Physiol. Phar- 
macol. need., 1950, 1: 173. Excerpta Medica. Section II. 
(Physiology, Biochemistry, and Pharmacology.) 1950, 3: 
1233. 
27. BuBois, E. F. Apparatus for testing the air in sub- 
marines. pp. 19-23 in: Review of recent work on air 
purification in submarines. U, S. Navy. BuMed. Sub- 
marine ventilation, Bulletin no. 4 {126632), 15 March 
1919,47 pp. [R] GAS ANALYSIS IN AIR AND BLOOD 
28-61 
28. Elliott, M. A. A positive filter type of infrared gas 
analyzer. U. S. Navy. NRL. N. R. L. rept. C-3449, 15 
April 1949, 11 pp. 
29. Flemister, S. C. Estimation of carbon dioxide and 
oxygen in a 12 cubic millimeter blood sample. Fed. Proc. 
Amer. Soc. exp. Biol., 1947,6: 104. [P] 
30. Frey, F. E. J. A simple gas analyzer. Canad. J. Res., 
1949, 27E: 188-190. 
31. Geraci, J. E., G. E. Montgomery, Jr., and E. H. 
Wood. Studies of arterial oxygen saturation in patients 
with suspected arterial hypoxemia, with use of a modified 
oximeter. Fed. Proc. Amer. Soc. exp. Biol., 1948, 7: 41. 
32. Goldman, D. E. and J. A. Mathis. A continuous 
sampling device for gases in ambient air. U. S. Navy. 
NMRI. Project X-417, Rept. no. 4, 15 February 1945, 
6 pp. [M] 
33. Goldman, D. E. and J. A. Mathis. A sampling device 
for average gas concentrations in air. J. industr. Hyg., 
1948, 30: 129-132. [P] 
34. Goodman, I. and R. G. Gustavson. An improved 
oxygen absorption bulb for the Carpenter-Haldane gas 
analysis apparatus. Science, 1947,105: 264. [P] 
35. Grant, W. C. Determination of oxygen capacity on 
39.3 cubic millimeters of blood. Proc. Soc. exp. Biol, N. Y., 
1947,66: 60-62. [M] 
36. Gullickson, G. and A. Hemingway. Oximetry in 
physical medicine. Arch. phys. Med., 1948. 29: 632-636. 
37. Habisch, H. Eine unblutige Methode zur Bestim- 
mung der Ch-Konzentration des venosen Mischblutes. 
Pfliig. Arch. ges. Physiol, 1949, 251: 785-787. Excerpta 
Medica. (Section II. Physiology, Biochemistry and 
Pharmacology), 1951,4; 177. Abstr. 
38. Hickam, J. B. and R. Frayser, Spectrophotometric 
determination of blood oxygen. /. biol. Chem., 1949, 180: 
457-465. [P] 
39. Holmes, F. E. Modifications of Scholander’s appa- 
ratus for the determination of carbon dioxide in blood 
plasma. /. Lab. din. Med., 1950, 36: 148-153. Excerpta 
Medica. (Section II. Physiology, Biochemistry and 
Pharmacology) 1951,4: 411. Abstr. 
40. Hull, W. E. Circular slide-rule computer for respira- 
tory gas problems. USAF. Wright-Patterson air force base, 
Dayton, Ohio. Air materiel command, Aero medical 
laboratory. Serial no. TSEAA-696-107, 17 pp. [M] [P] 
41. Hunter, J. A., R. W. Stacy, and F. A. Hitchcock. 
A mass spectrometer for continuous gas analysis. Rev. sci. 
Instrum., 1949, 20: 333—336. 
42. Kaplan, H. The atmosphere in a submarine. U. S. 
Navy. ONR. Res. Rev., July 1949, 20-21 [P] 
43. Lash, J. J. A simply constructed micro-extractor for 
blood analysis. Amer. J. din. Path., 1948, 18: 584-586. 
[M] [P]. Excerpta Medica. (Section II. Physiology, Bio- 
chemistry, and Pharmacology), 1949, 2: 627. Abstr. 
44. Lazarow, L. A simple apparatus for quantitative 
microcolorimetric analysis in final volumes of 0.15 cc. 
/. Lab. din. Med., 1947,32: 215-219. 
45. Lilly, J. C. and I. F. Anderson. The nitrogen meter: 
an instrument for continuously recording the concentra- 
tion of nitrogen in gas mixtures. U. S. NRG-CAM. 
OEMcmr-28, Report no. 299, 28 February 1944, 1 pp. 
Abstr, 
46. Lindgren, I. Kontinuerlig oblodig bestamning av 
relativa syremattnaden i blod med en kliniskt anvandbar 
svensk oximeter. [Continuous bloodless measurement of 
the relative oxygen saturation in the blood by a Swedish 
oxymeter for clinical use]. Svenska Lakartidn., 1947, 44: 
401-411. Abstr. Excerpta Medica. (Section II. Physi- 
ology, Biochemistry and Pharmacology), 1948, 1: 291. 
Abstr. 
47. Loomis, T. A. and R. E. Beyer. An apparatus for 
the continuous and simultaneous measurement of carbon 
dioxide and nitrous oxide in respired air. Anesthesiol., 
1951,12: 173-180. [M] 
48. MacArthur, J. J. Evaluation of Beckman model “G” 
gas analyzer. U. S. Navy. Submarine base, New London, 
Conn, Medical research laboratory. Project NM 002 
014.03.03, Kept. no. 176, 10 August 1951, 11 pp. 
49. Maegraith, B. G., E. S. Jones, and H. H. Sculthorpe. 
Pathological processes in disease. I. Adaptation of the 
Warburg respirometer for the determination of blood 
gases. Abstr. World Med., 1950, 8: 370. Ann. trop. Med. 
Parasit., 1950, 44: 101-106. 
50. Maier-Leibnitz, H. and E. 0. Richey. A special am- 
plifier for photo-electric analysis of oxygen saturation of 
blood. USAF. Randolph Field, Texas. School of aviation 
medicine. Project 21-02-080, Kept. no. I, July 1948, 
6 pp. 
51. Malm, E. and 0. Vuorelainen. Apparatus for con- 
tinuous determination of the oxygen percentage in air. 
Scand. J. Clin. lab. Invest., 1950, 2: 139-142. 
52. Miller, F. A., A. Hemingway, A. 0. Nier, R. T. 
Knight, E. B. Brown, Jr., and R. L. Varco. The develop- 
ment of, and certain clinical applications for, a portable 
mass spectrometer. /. thorac. Surg., 1950, 20: 714-728. 
[PJ 
53. Minter, C. C. and L. M. J. Burdy. A new instrument 
for determining hydrogen in submarines. U. S. Navy. NRL. 
N. R. L. rept. no. 3669, 1 June 1950, 10 pp. 
54. Olson, R. A., F. S. Brackett, and R. G. Crickard. 
Oxygen tension measurement by a method of time selection 
using the static platinum electrode with alternating poten- 
tial. /. gen. Physiol, 1949, 32: 681-702. [P] 
65. Paul, W. Contribution to oximeter design using 
modulated light. Fed. Proc. Amer. Soc. exp. Biol, 1950, 
9: 99. 
56. Pauling, L., R. E. Wood, and J. H. Sturdivant. An 
instrument for determining the partial pressure of oxygen 
in a gas. Science, 1946,103: 338. 
57. Pecora, L. J. and W. V. Consolazio. Appraisal of 
the method of determining arterial oxygen saturation by 
using arterialized ear blood. U. S. Navy. NMRI. Project 
X-373, 13 December 1944, 3 pp. [P] 
58. Prentiss, S. S. Instruments for testing oxygen, pp. 
309-329 in; Improved equipment for oxygen production. 
Summary technical report of Division 11, U. S. OSRD- 
NDRG. Washington, D. G., 1946, 428 pp. 
59. Rahn, H., J. Mohney, A. B. Otis, and W. 0. Fenn. 
A method for the continuous analysis of alveolar air. U. S. 
NRC-CAM. OEMcmr—147, C. A. M. rept. no. 476, 20 
October 1945, 10 pp. 
60. Riley, R. L. A direct method for determination of 
oxygen and carbon dioxide tensions in blood. U. S. Navy. 
NATB, Pensacola, Fla. School of aviation medicine. Proj- 
ect X-450 (Av-236-f), Rept. no. 1, 9 January 1945, 25 
PP- [P] 
61. Riley, R. L. A direct method for determination of 
oxygen and carbon dioxide tensions in blood. U. S. Navy. 62-91 
TECHNICAL PROCEDURES 
NATB, Pensacola, Fla. School of aviation medicine. Proj- 
ect X-450 (Av-236-f), Rept. no. 2, 16 July 1945, 10 pp. 
62. Riley, R. L. and J. L. Lilienthal, Jr. On the deter- 
mination of the physiologically effective pressures of oxy- 
gen and carbon dioxide in alveolar air. U. S. Navy. NATO, 
Pensacola, Fla. School of aviation medicine. Project X- 
484 (Av-258-f), Rept. no. 2, 22 January 1946, 12 pp. 
63. Riley, R. L., J. L. Lilienthal, Jr., D. D. Proemmel, 
and R. E. Franke. On the determination of the physiologi- 
cally effective pressures of oxygen and carbon dioxide in 
alveolar air. Amer. J. Physiol., 1946, 147: 191—198. [M] 
[P] 
64. Roos, A. and H. Black. Direct determination of 
partial and total tensions of respiratory gases in blood. 
Amer. J. Physiol., 1950, 160: 163-176. [P] 
65. Schmidt-Nielsen, B. Accurate analysis of 0.4-0.1 
cubic millimeter of gas. Fed. Proc. Amer. Soc. exp. Biol., 
1947, 6: 197. [P] 
66. Scholander, P. F. Analyzer for accurate estimation 
of respiratory gases in one-half cubic centimeter samples. 
/. biol. Chem., 1947, 167: 235-250. U. S. NRC-CAM. 
C. A. M. Rept. no. 57, July 1942, 4 pp. [M] 
67. Scholander, P. F. and H. J. Evans. Microanalysis 
of fractions of a cubic millimeter of gas. /. biol. Chem., 
1947, 169: 551-560. [P] 
68. Scholander, P. F., S. C, Flemister, and L. Irving. 
Microgasometric estimation of the blood gases. V. Com- 
bined carbon dioxide and oxygen. /. biol. Chem., 1947, 
169: 173-181. [P] 
69. Scholander, P. F. and L. Irving. Micro blood gas 
analysis in fractions of a cubic millimeter of blood. J. biol. 
Chem., 1947, 169: 561-569. [P] 
70. Scholander, P. F., H. Niemeyer, and C. L. Claff. 
Simple calibrator for Warburg respirometers. Science, 
1950* 112: 437-438. 
71. Scott, C. C., and H. M. Worth. An apparatus for 
continuous recording of the volume of expired air. J. Lab. 
din. Med., 1947, 32: 1496-1499. Excerpta Medico. 
(Section II. Physiology, Biochemistry and Pharmacology), 
1949, 2: 74. 
72. Siri, W. A mass spectroscope for analysis in the low 
mass range. Rev. sci. Instrum., 1947, 18: 540-545. 
73. Sjostrand, T. A method for the determination of 
carboxyhaemoglobin concentrations by analysis of the 
alveolar air. Acta physiol, scand., 1948, 16: 201-210. 
74. Smith, J. H. G. An apparatus for measuring exceed- 
ingly small quantities of oxygen. XVIII Intern, physiol. 
Congr., 1950, 455-456. 
75. Specter, N. A. and B. F. Dodge. Colorimetric 
method for determination of traces of carbon dioxide in 
air. Analyst, 1947, 72: 418. Abstr. 
76. Stacy, R. W., J. A. Hunter, and F. A. Hitchcock. 
A mass spectrometer for the rapid, continuous analysis of 
respiratory gases. Fed. Proc. Amer. Soc. exp. Biol., 1948, 
7: 120. 
77. Tobias, J. M. Syringe oxygen cathode for measure- 
ment of oxygen tension in solution and in respiratory 
gases. Rev. sci. Instrum., 1949, 20: 519—523. 
78. TJ. S. OSRD-NDRC. A summary report. Infra-red 
detector and gas analyzer. O. S. R. D. Rept. no. 1642, 
1 January 1944, 20 pp. 
79. Vacca, C. II fotometro Coleman (Modello 17-A) 
per le misure continue della capacita de ossigeno del 
sangue. Riv. Med. aero., Roma, 1949, 12: 400-410. 
Excerpta Medico. (Section II. Physiology, Biochemistry, 
and Pharmacology), 1950, 3: 1222. 
80. Watkins, E., Jr. Rapid measurement of the oxygen 
saturation of whole blood samples with the Millikan 
oximeter. Proc. Soc. exp. Biol., N. Y., 1949, 72: 180-184. 
81. Whiteley, A. H, A microvolumetric Van Slyke blood 
gas apparatus. J. biol. Chem., 1948, 174: 947-960. 
Excerpta Medico.. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1949,2: 754. Abstr. 
82. Young, A. C., L. D. Carlson, W. F. Quinton and H. I. 
Burns. Electronic polyneumograph. Electronic recording of 
tidal instananeous flow, respiratory rate, and minute 
volume with a gas sampling device for oxygen and carbon 
dioxide analysis in expired air. University of Washington, 
Contract No. AF 33{038)-422, E. O. No. 211-01-021, 
USAF. Wright-Patterson air force base, Dayton, Ohio. 
Air materiel command. AF technical rept. No. 6243, 
March 1951, 17 pp. 
III. RESPIRATORY APPARATUS 
A limited number of respiratory devices are re- 
ferred to in the reports which follow. For further 
details on respirators and other breathing appli- 
ances, the reader should consult the sections on deep- 
sea diving equipment and procedures (p. 289), re- 
suscitation and respiratory devices (p. 290), and 
underwater breathing apparatus and related gear 
(p. 335). 
83. Blockwick, T. FT. Tests and evaluation of the Bendix 
and MSA 02 breathing appliances for use in the recom- 
pression chamber. U. S. Navy. Naval gun factory, EDU. 
Project NS-186-017, Rept. no. 12-49, 21 October 1949, 
16 pp. 
84. Blockwick, T. N. Evaluation of the Scott type “A” 
oxygen demand inhalator. U. S. Navy. Naval gun factory, 
EDU. Project NS—186-201, sub task no. 1, test no. C. 
rept. no. 5-51, 14 March 1951, 5 pp. 
85. Duncan, J. E. An improved helmet for breathing 
oxygen or other gases. Science, 1946, 104: 395-396. 
86. Forssander, C. A. A suction tube for the collection 
of respiratory gases under diverse conditions. J. Lab. din. 
Med., 1950, 35: 324-327. Excerpta Medico. Section II. 
(Physiology, Biochemistry, and Pharmacology), 1951, 4: 
60-61. Abstr. 
87. Grove, G. W. and E. E. Quenon. Approval of newly 
developed self-contained breathing apparatus, instructions 
in its care and use and training procedure. U. S. Bureau 
of Mines. Information Circular 7413. July 1947, 18 pp. 
[R] 
88. Hayter, R. Design and test of oxygen breathing 
equipment for use in the recompression chamber. U. S. 
Navy. NMRI. Project X-540, Rept. no. 1, 10 March 1947, 
8 pp- 
89. Kvacek, J. Otevren y okruh ve spirometrii. [The 
open circuit in spirometry.] Cas. Lek. ces., 1950, 89: 
1030-1032. Excerpta Medico. Section II. (Physiology, 
Biochemistry, and Pharmacology), 1951, 4: 647. Abstr. 
90. Miller, F., A. Hemingway, R. L, Varco, and A. 0. C. 
Hier. Alveolar ventilation studies using the mass spectrom- 
eter. Proc. Soc. exp. Biol., N. Y., 1950, 74: 13—16. Ex- 
cerpta Medico. Section II (Physiology, Biochemistry, and 
Pharmacology), 1951, 4: 301. 
91. Pearce, S. J. and L. B. Berger. List of respiratory 
protective devices approved by the Bureau of Mines. U. S. 
Bureau of Mines. Information Circular 7570. June 1950, 
15 pp. CHAMBERS 
92-120 
92. Van Der Aue, 0. E. and M. K. Holler. Tests and 
evaluation of various types of oxygen breathing equip- 
ment for use in the recompression chamber. U. S. Navy. 
Naval gun factory, EDU. Project SRD 1162/47, Kept. no. 
I, September 1948, 15 pp. 
93. Van der Valk, J. M, A simple method for the record- 
ing of human respiration. Acta Physiol., Pharmacol., 
Need., 1950, 1: 323-326. Excerpta Medica. Section II. 
(Physiology, Biochemistry, and Pharmacology), 1951, 4: 
410. 
IV. APPARATUS E0R TESTING VISUAL 
FUNCTIONS 
For reports describing the uses of the apparatus 
and devices considered below, the reader should 
consult the section on visual problems (p. 119). 
94. Draeger, R. H., R. H. Lee, and M. B. Fisher. Design, 
construction and preliminary evaluation of a portable 
multiple brightness radium plaque adaptometer. U. S. 
Navy. NMRI. Project X-311, Kept. no. 1, 11 August 
1945, 16 pp. 
95. Farnsworth, D. Abridgment and administration of 
the A. O. 1st edition pseudo-isochromatic plates. U. S. 
Navy. Submarine base. New London, Conn. Medical re- 
search department. Project X—749 (Av—384-k), Color 
Vision Rept. no. 14, 9 December 1946, 21 pp. [P] 
96. Farnsworth, D. Standards for sunglasses. U. S. Navy. 
Submarine base, New London, Conn. Medical research 
laboratory. Project NM 003 041.18, Rept. no. 4, 6 pp. 
Summer, 1950, 20: 81-87. 
97. Farnsworth, D. Inspection goggle for checking visi- 
ble spectral quality of lighting for dark adaption. U. S. 
Navy. Submarine base, New London, Conn. Medical re- 
search laboratory. Project NM 003 041.40, Rept. no. 1, 
15 March 1951, 17 pp. 
98. Grether, W. F., S. C. Connell, and J. M. Bjornstad. 
Experimental evaluation of the New London Navy Lantern 
for testing color perception. USAF. Wright-Patterson air 
force base, Dayton, Ohio. Aero Medical laboratory. Tech, 
rept. no. MCREXD-694-21B, 1 March 1949, 11 pp. [P] 
99. Hill, J. M. and F. T. Ralph. A penlight projector 
for the Lancaster red-green muscle test. Amer. J. Ophthal., 
1949, 32: 1407. 
100. Inins, H. A. Comparison of ortho-rater with clinical 
ophthalmic examinations. U. S. Navy. NATB, Pensacola, 
Fla. School of aviation medicine, Project 499, Rept. no. 2, 
1 March 1946, 7 pp. 
101. Koch, W. An improved dark-adaptometer. Brit. J. 
Ophthal, 1947, 31: 235-237. [P] 
102. Krimsky, E. A new hand-slitlamp. Amer. J. 
Ophthal, 1949, 32: 1591-1592. 
103. Lehensohn, J. E. A simplified astignometer. Amer. 
J. Ophthal, 1949, 32: 1128-1130. 
104. Lee, R. H., and R. H. Draeger. Design of a semi- 
automatic night vision scotometer. U. S. Navy. NMRI. 
Project X—467, Rept. no. 1, 2 July 1947, 4 pp. [P] 
105. Lee, R. H. and M. B. Fischer. Evaluation of the 
modified Rostenberg adaptometer. U. S. Navy. NMRI. 
Project X-466, Rept. no. 1, 8 May 1945, 8 pp. 
106. Littmann, H. A new slitlamp apparatus. Amer. J. 
Ophthal, 1950, 33: 1863-1870. 
107. Pinson, E. A. and A. Chapanis. AML portable 
radium plaque night vision tester. Air Surg. Bull., 1945, 2: 
285. 
108. Raiford, M. B. Magnetic perimetry set. Amer. J. 
Ophthal, 1950, 33: 120. 
109. Schmidt, I. A color signal apparatus for testing 
color vision in aviation. U. S. AAF. Heidelberg, Germany. 
Aero medical center. Kept. P3-46-19, Translated 26 May 
1946, 10 pp. 
110. Schober, H. Ein neues Adaptometer. Klin. Mbl. 
Augenheilk., 1950, 117: 51-58. Excerpta Medica. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1951, 
4: 1295. 
111. Von Schelling, H. and D. Farnsworth. Trichro- 
matic specifications of the Munsell 100 hues at 5/5 for 
illuminant A. U. S. Navy. Submarine base. New London, 
Conn. Medical research laboratory. Project NM Oil 019, 
Kept. no. 3, 15 April 1949, 8 pp. 
112. Wolpaw, B. J. and H. A, Inins. Comparison of 
ortho-rater with clinical ophthalmic examinations. U. S. 
Navy. NATB, Pensacola, Fla. School of aviation medicine. 
Project X—499, Final Kept., 29 September 1945, 26 pp. 
[P] 
V. CHAMBERS 
Literature that follows represents a selection from 
a large number of reports on pressure chambers. 
For applications of such equipment in compressed 
air, diving, and submarine medicine, the reader is 
referred especially to the section on decompression 
sickness (p. 159). 
113. Blockwick, T. N. Test and evaluation of a portable 
recompression tank. U. S. Navy. Naval gun factory, EDU. 
Project NS-186-024, Kept. no. 11-49, 25 July 1949, 
6 pp. 
114. Brice, R. and P. Gaspa. Les nouveaux caissons 
a depression mobiles du service de sante de Fair. Med. 
aeronaut., 1950, 5: 377-382. 
115. Clarke, R. W. Yale refrigerated decompression 
chamber performance tests. Yale aeromedical research 
unit. Kept. no. 10A, 11 October 1942, 2 pp. 
116. Davis, R. H. Deep diving with the Davis submerged 
decompression chamber. Oxy-helium diving by the Royal 
Navy. The Siebe, Gorman & Go. decompression tables, 
pp. 136—179 in: Deep diving and submarine operations. 
A manual for deep sea divers and compressed air workers. 
London, The Saint Catherine Press Ltd., Fifth edition, 
1951, 670 pp. [D] 
117. Davis, R. H. Diving bells, pp. 197-203 in: Deep 
diving and submarine operations. A manual for deep sea 
divers and compressed air workers. London, The Saint 
Catherine Press Ltd., Fifth edition, 1951, 670 pp. [D] 
118. Gt. Brit., Ministry of labour and national service. 
Part V. Cofferdams and caissons, pp. 28-29 in: Factories 
acts, 1937 and 1948. Work of engineering construction. 
London, His Majesty’s Stationery Office, 1951, 55 pp. 
119. Siebe, Gorman and Company, Ltd. Recompression 
chamber for deep sea divers. Descriptive information cir- 
cular. Siebe, Gorman and Company, Ltd., London, 2 pp. 
120. IT. S. Navy, BuShips. Preliminary instruction book. 
Submarine rescue chamber modified for deep submergence. 
Navships No. 394-0051, December 1949, 37 pp. 121-139 
TECHNICAL PROCEDURES 
VI. AIR COMPRESSORS 
The following reports on air compressors are in- 
cluded because of their particular pertinence in 
diving. 
121. Davis, R. H. Standard diving apparatus and equip- 
ment with instructions for care, maintenance and testing, 
pp. 41-85 in: Deep diving and submarine operations. A 
manual for deep sea divers and compressed air workers. 
London, The Saint Catherine Press Ltd., Fifth edition, 
1951, 670 pp. [D] 
122. Klimenko, N. A., K. A. Pavlovskii, and V. P. 
Maksimenko. Equipment of the diver, pp. 25-64 in; Man- 
ual for divers of the navy. Moskow, Military Printing 
Office, 1948, 172 pp. (Russian text.) 
123. Molumphy, C. 6. Preliminary volumetric test of 
lightweight diver’s model no. SK 375 Dapco Air Com- 
pressor, test 2, priority “B.” U. S. Navy. Naval gun fac- 
tory, EDU. Project SRD 805/47, 26 January 1948, 6 pp. 
124. Siehe, Gorman and Company, ltd. Portable air 
compressing set for diving (two divers). Descriptive infor- 
mation circular. Siebe, Gorman and Company, Ltd., Lon- 
don, 2 pp. 
125. U. S. Navy, Bureau of ships. Lightweight air com- 
pressor pp. 44-45 in: Chapter 94, Salvage section II. Div- 
ing. 25 January 1951, Washington, D. C., Government 
printing office, 1951. 
VII. PRESSURE GAGES 
The following references have been included since 
they have been mentioned in other reports pub- 
lished in this volume. 
126. Bruhach, H. F, and H. Specht. Barostat for high- 
altitude chamber. Science, 1951, 114: 362-363. 
127. Grundfest, H. A strain gage recorder for physiolog- 
ical volume, pressure and deformation measurements. 
Science, 1945, 101: 255-256. [P] 
128. Higgs, P. M. A recording mechanical pressure 
gauge of high range. Rev. sci. Instrum., 1949, 20: 23—26. 
[P] 
VIII. TEMPERATURE MEASUREMENT 
Most of the references that follow describe equip- 
ment discussed under the section on heat and hu- 
midity problems (p. 71) and the section on ventilat- 
ing and air conditioning (p. 270). 
129. Benzinger, T. H. and C. Kitzinger. Black body 
radiometer, a 4 pie receiver for measurement of total 
radiated heat output. U. S. NMRI. Project NM 
004.006.01 (02), 6 October 1949, 17 pp. 
130. Challoner, A. R. and E. Griffiths. Experiments 
with the globe thermometer. Gt. Brit. MRG-RNPRC, 
HS. R. N. P. 45/254, H. S. 99, December 1945, 3 pp. [P] 
131. Hardy, J. D. and C. H. Richards. A new instru- 
ment for measuring the thermal radiation of the environ- 
ment. ]. industr. Hgy., 1949, 31: abstract section; 14. [P] 
132. Jehn, K. H. Wet bulb temperatures without a 
wick. Electrical engineering research laboratory. Univer- 
sity of Texas, Contract N6onr-266, Task Order II, NR 
082 005,1 September 1948, pp. 30. 
133. Macradyen, A. A simple device for recording mean 
temperatures in confined spaces. Nature, 1949, 164: 965- 
966. Excerpta Medica. Section II. (Physiology, Biochem- 
istry, and Pharmacology), 1950, 3: 1153. 
134. Zahl, H. A. and M. J. E. Golay. Pneumatic heat 
detector. Rev. sci. Instrum., 1946, 17: 511-515. 
IX. OTHER TECHNICAL PROCEDURES AND 
APPARATUS 
A number of reports not classified elsewhere have 
been included in the list that follows. 
135. Fisher, R. L. and W. A, White, Jr. The design of 
a circular slide rule for selecting decompression tables 
following compressed air dives. U. S. Navy. NMRI. NH6- 
1/A11 /NMRI-86, 26 September 1944, 3 pp. 
136. Houghton, F. C., W. A. White, Jr., and F. H. 
Davis. A study of the accuracy and reliability of the mine 
safety appliances carbon monoxide alarm. U. S. Navy. 
NMRI. Project X-160, Rept. no. 3, 8 July 1943, 6 pp. 
137. Kramer, K. and D. E. Timmons. A photoelectric 
hypoxia warning device. J. Aviat. Med., 1951, 22: 70—74. 
138. Van Slyke, D. D., J. R. Weisiger, and K. K. Van 
Slyke. Photometric measurement of plasma pH. /. biol. 
Chem., 1949, 179: 743-756. [P] 
139. Wing, K. G. Suggestions for working with celloidin 
with special reference to the inner ear. U. S. Navy. Sub- 
marine base, New London, Conn. Medical research labora- 
tory. Project NM 003 041.27.01, Rept. no. 151, 2 Novem- 
ber 1949, 50 pp. Special Anatomy, Physiology and 
Biochemistry of Compressed Air, 
Diving and Submarine Medicine 
I. PHYSIOLOGICAL EPPECTS OF RAISED 
ATMOSPHERIC PRESSURES 
A. CENTRAL NERVOUS SYSTEM 
Generally speaking, personnel are capable of 
withstanding the effects of raised atmospheric pres- 
sures, per se, under conditions ordinarily encoun- 
tered in compressed-air work and in diving. But 
the effects of pressure itself are not all that must 
be considered for it must be borne in mind that the 
caisson environment, for example, not only imposes 
raised atmospheric pressure upon the organism but 
also may involve factors such as increased humidity, 
extremes of temperature, inadequate ventilation, 
toxic gases, and heavy work in mud and cold water. 
Therefore, the physiological adjustments to be con- 
sidered are, strictly speaking, not to be attributed 
to raised pressure alone. In deep-sea diving, pres- 
sures are reached at which oxygen intoxication be- 
comes a severe and limiting factor. This problem is 
considered in an appropriate section (p. 182). At 
great depths there is a slowing of mental function 
and reduction of motor responsiveness attributed 
to the narcotic action of nitrogen under pressure. 
In both oxygen intoxication and nitrogen narcosis 
the effects upon the body are not to be ascribed 
to the influence of pressure itself, so that if nitrogen 
is replaced by helium, divers are capable of descend- 
ing to much greater depths without adverse effects. 
It should also be remembered that at very high 
hydrostatic pressures, physiological processes are 
brought to a standstill and living protoplasm tends 
to become coagulated. A discussion of the biology 
of very high hydrostatic pressures is given on page 
148. It is clear, however, that such pressures do not 
come within the range of possible effects on human 
beings. Within the pressure ranges at present en- 
countered or likely to be encountered in diving or 
other underwater operations, increased pressure 
may be supported by living tissues without harm. 
Studies on dogs carried out by Rikkl and Krivo- 
sheenko {140) 1948 suggest that raised atmospheric 
pressure above two atmospheres gage pressure may 
exert inhibitory action upon the functions of the 
cerebral cortex. There appears to be an inhibition 
of condition reflexes. 
140. Rikkl’, A. V. and N. K. Krivosheenko. Vliianie 
povyshennogo atmosfernogo davleniia na vysshuiu nerv- 
nuiu deiatel’nost’sobaki. [The effect of increased atmos- 
pheric pressure on the higher nervous function of the 
dog.] pp. 62—69 in: Trudy Nauchnoi Sessii, Posviashchen- 
noi Tridtsatiletiiu Velikoi Oktiabr’skoi Sotsialisticheskoi 
Revolutsii. Edited by A. V. Triumfov. Leningrad, Voenno- 
Morskoi Meditsinskoi Akademii, 1948, 310 pp. 
B. HEART AND CIRCULATION 
It may be concluded from earlier studies that 
raised atmospheric pressures do not produce very 
marked changes in cardiovascular action. On ex- 
posure to pressure, there tends to be a slight fall in 
pulse rate and blood pressure, although some reports 
have indicated a blood-pressure rise and sometimes 
an increase in pulse rate. Generally speaking, per- 
sons subjected to compressed-air work for long 
periods show no permanent change in blood pres- 
sure or cardiac function. Young and Cook {142) 
1946, have investigated the effect of increased 
atmospheric pressure on blood pressure. Prelimi- 
nary uncontrolled observations on 30 students at 
the School for Second-Class Divers, U. S. Subma- 
rine Base, New London, Conn., revealed an 
apparent drop in blood pressure during the 4 weeks’ 
course. On the basis of these observations, an at- 
tempt was made to demonstrate, under controlled 
conditions, the effects on blood pressure of increased 
atmospheric pressure. A total of 60 subjects were 
exposed to raised atmospheric pressure. No ap- 141-145 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
preciable, lasting effect was demonstrated. The 
blood pressure was recorded on each subject before 
he got up in the morning and again at 1300. Sub- 
jects were seated 15 minutes before the reading 
and not permitted to smoke. The arm was placed 
at the heart level. Group A was exposed to a simu- 
lated pressure of 50 feet depth (reached in 4 min- 
utes) and remained at this pressure for 3 minutes; 
subjects were then decompressed to 10 feet for 5 
minutes and then surfaced. This was done for 13 
days. Group B went through the same routine ex- 
cept that members of group B were not exposed to 
pressure. As stated, no appreciable effect of pres- 
sure on the arterial blood pressure was demon- 
strated. According to Farr, White, and Hay ter 
{141) 1945, the specific gravity of whole blood or 
plasma of a group of 11 subjects did not change 
significantly following exposure to pressures as high 
as 10 atmospheres. In two subjects who developed 
symptoms of decompression sickness, significant 
changes were not observed in blood specific gravity 
before, during or after treatment for this disorder. 
141. Farr, L, E., W. A. White, Jr., and K. Hayter. 
The effects of increased atmospheric pressure, posture and 
exercise on the blood specific gravity of normal men. U. S. 
Navy. NMRI. Project X—443, Rept. no. 2, 27 November 
1945, 11 pp. [P] 
142. Young, M. H. and W. E. Cook. The effect of 
increased atmospheric pressure on blood pressure. U. S. 
Navy. Submarine base. New London, Conn. Medical re- 
search department. Project X-595, 1 March 1946, 6 pp. 
[P] 
C. RESPIRATION 
Early investigations of the effects of raised atmos- 
pheric pressures on respiration have shown that 
daily exposure to increased atmospheric pressure 
produces a permanent increase in vital capacity. 
This claim was made by nearly all of the investi- 
gators interested in the use of raised atmospheric 
pressures for therapeutic purposes. However, more 
recent studies have thrown some doubt on this 
claim. Increase in vital capacity has been found 
but tends to be of low magnitude. Under raised 
atmospheric pressure, respiratory rate may be 
slowed and there may be an increase in breath- 
holding time. 
Changes in alveolar carbon dioxide tension re- 
sulting from compression have been reported by 
Bean {143) 1945. Samples of air were drawn at 
the end of expiration from the lungs of anesthetized 
dogs by means of an implanted catheter. The first 
samples were taken at atmospheric pressure and 
compression of air was then carried to slightly over 
5.5 atmospheres within 1.5 to 3.5 minutes. The 
second sample was taken just after maximum com- 
pression, the third a few minutes later. The pres- 
sure was then lowered to atmospheric level and a 
fourth sample taken. In 21 out of 22 compressions 
carried out on 4 animals, the carbon dioxide tension 
in the lung just after maximum compression was 
10 to 85 percent higher than that obtaining before 
compression was begun. This increase in carbon 
dioxide tension was explained by the author as due 
to the compressional inflow of air into the lung 
preventing exhalation of alveolar air during the 
compression. Compressional inflow, according to 
the author, also tends to compress the alveolar air, 
thus temporarily elevating the carbon dioxide ten- 
sion in immediate contact with the alveolar wall. 
It was concluded that the carbon dioxide thus 
dammed back in the blood and tissues constitutes 
an important etiological factor in those reactions 
which occur in highly compressed air, especially 
in the early stages and which have been attributed 
by some authors solely to a narcotic action of nitro- 
gen. In 1950, Bean {145) also reported that rapid 
compression to 4.5 or 9 atmospheres resulted in a 
pronounced increase in alveolar carbon dioxide 
tension. These changes temporarily diminish and in 
some cases reverse the normal alveolar carbon 
dioxide diffusion gradient and dam up or drive 
back carbon dioxide into the blood. Although Bean 
did not categorically deny the possibility , of nitrogen 
narcosis, he considered that his data showed that 
until the narcotic action of carbon dioxide is ruled 
out, substantial and conclusive evidence that nitro- 
gen acts as a narcotic in the usual sense of the term 
is wanting. Bean {144) 1947 compressed anes- 
thetized, heparinized dogs in air to about 90 
pounds pressure in 3 or 4 minutes. During com- 
pression there was a shift of the arterial pH in the 
acid direction. Rapid decompression produced the 
reverse effect. The compressional shift was ex- 
plained by the author as due to interference with 
carbon dioxide removal. The decompressional pH 
changes were held by the author to have important 
implications relative to explosive decompression, 
rapid ascent to high altitudes, and rapid decom- 
pression from high pressures. 
143. Bean, J. W, Changes in alveolar carbon dioxide 
tension resulting from compression. Fed. Proc. Amer. Soc. 
exp. Biol., 1945, 4: 6. 
144. Bean, J. W. Changes in arterial pH induced by 
compression and decompression. Fed. Proc. Amer. Soc. 
exp. Biol., 1947, 6: 76-77. 
145. Bean, J. W. Tensional changes of alveolar gas in 
reactions to rapid compression and decompression and 
question of nitrogen narcosis. Amer. J. Physiol., 1950, 161: 
417-425. [P] DECOMPRESSION PHYSIOLOGY OF BUBBLE FORMATION 
146-147 
II. PHYSIOLOGICAL EFFECTS OF DECOMPRES- 
SION FROM PRESSURES HIGHER THAN 
ONE ATMOSPHERE 
A. GENERAL STUDIES OF THE EFFECTS OF 
DECOMPRESSION 
Eggleton, Elsden, Fegler, and Hebb {146) 1945 
and Specht {147) 1948 provide a general intro- 
duction to the problem of the effects of decompres- 
sion from pressures higher than one atmosphere. 
The source material given in this section makes 
available information applicable to the study of the 
etiology of decompression sickness and its preven- 
tion and treatment. 
146. Eggleton, P., S. R. Elsden, J. Fegler, and C. 0. 
Hebb. A study of the effects of rapid “decompression” in 
certain animals. /. Physiol., 1945, 104: 129-150. [P] [D] 
147. Specht, H. Physiological effects of abnormal atmos- 
pheric pressure, pp. 135—174 in: Industrial Hygiene and 
Toxicology. Edited by F. A. Patty. New York, Interscience 
Publishers, Inc., 1948. [R] 
B. PHYSIOLOGY OF BUBBLE FORMATION 
For a comprehensive discussion of the genesis of 
the tissue bubble, Fulton’s chapter {159) 1948 
should be consulted by the reader. Reference should 
also be made to a report by Catchpole and Gersh 
{157) 1946 on the physical factors in the patho- 
genesis of aeroembolism. These inclusive and well- 
prepared reviews will serve as a guide to orient the 
reader to the vast literature on the subject of bubble 
formation. 
For experimental observations on the actual for- 
mation of gas bubbles in blood vessels and tissues 
following decompression from high-pressure atmos- 
pheres, papers by the following should be consulted; 
Gersh {161) 1945, Gersh and Hawkinson {165) 
1944, Gersh, Hawkinson, and Jenney {166) 1944, 
Gersh, Hawkinson, Rathbun, and Behnke {167) 
1944, and Wagner {192) 1944. In Wagner’s experi- 
ments gas bubbles were observed directly in pial 
blood vessels following rapid decompression of 
anesthetized cats from air compressed to 75 lbs. per 
sq. in. (gage pressure). When gas bubbles were visi- 
ble in the pial vessels, they always appeared first in 
the arteries and later in the veins. Gas bubbles were 
also present in other blood vessels of the body as 
well as in the right auricle and ventricle. Some ani- 
mals died although no bubbles appeared in the pial 
vessels of the microscopic field under observation. 
Since in all animals the distribution of gas bubbles 
elsewhere in the body was the same, it was assumed 
that in those instances in which gas bubbles were 
not seen under the field, they were actually present 
in arteries supplying portions of the central nervous 
system other than the field under observation. 
Since gas bubbles appear in pial arteries before they 
appear in the veins and since distribution occurs in 
other vessels irrespective of their appearance in pial 
vessels, it was concluded by the author that pial 
gas bubbles are borne to their site of lodgment as 
gas emboli. Secondarily, as the blood flow through 
the region decreases, gas bubbles appear in the veins. 
The object of the experiments of Gersh and 
Hawkinson was to describe the origin, occurrence, 
and appearance of tissue and vascular bubbles in 
fat tissue, adrenal glands, nerve, liver, skeletal 
muscle, and tendon after decompression from high 
atmospheric pressures. Adult guinea pigs in good nu- 
tritional state were used in these studies. The ani- 
mals were kept for 60 minutes in a small pressure 
tank at 30, 45, 60, 75, 90, or 105 lbs. per sq. in, 
(gage pressure) and decompressed in 4 seconds. 
Extravascular gas bubbles were observed in tissues 
rich in fat, adrenal cortex, and nerve fibers, but were 
not seen in liver, skeletal muscle, or tendon. Intra- 
vascular bubbles were observed in all these tissues 
and organs, but were far more numerous in those 
rich in fat. The number, size, and location of extra- 
vascular bubbles appeared related to the total fat 
content of the fat tissue. Although tissue bubbles 
showed the same distribution in the tissues and 
organs of fat and lean guinea pigs, it was found 
that they occurred much more readily and were far 
more extensive in the fat animals than in the lean 
ones. Gersh, Hawkinson, Rathbun, and Behnke 
found a significant fall in the specific gravity of 
guinea pigs after decompression from high pres- 
sures. This fall was greater in fat animals than in 
lean animals and was attributed to the presence of 
gas bubbles. Gersh, Hawkinson, and Jenney com- 
pared the occurrence of bubbles following decom- 
pression from high-pressure atmospheres of oxygen, 
helium-oxygen, argon-oxygen, and air. In fat tissue, 
extra-vascular gas bubbles occurred in the order of 
decreasing frequency following decompression from 
high-pressure atmospheres of argon-oxygen, air, 
oxygen, and helium-oxygen. Intracellular gas 
bubbles were observed after decompression from 
argon-oxygen, air, and helium-oxygen, but not from 
oxygen alone. Intravascular bubbles were present 
with all gas mixtures. In the adrenal cortex, gas 
bubbles occurred in the order of decreasing severity 
following decompression from high-pressure at- 
mospheres of argon-oxygen, air, and helium-oxygen 
atmospheres. After decompression in oxygen only 
occasional bubbles were seen. In the myelin sheath 
of nerve fibers, minute bubbles were more numerous 
following decompression from argon-oxygen than 
from compressed air and less numerous after decom- SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
pression from helium-oxygen and oxygen. In the 
liver, intravascular gas bubbles were common after 
decompression from argon-oxygen, rare after air 
and helium-oxygen, and absent when oxygen was 
used. In the hepatic cells, cytoplasmic watery vacu- 
oles were present following decompression from all 
gas mixtures. Gas bubbles were not found in muscle 
fibers or tissue fluid spaces of skeletal muscles after 
decompression in any of the gas mixtures. Bubbles 
were present intravascularly after argon-oxygen, air 
and helium-oxygen, air and helium-oxygen mix- 
tures, though not after oxygen. Survival of guinea 
pigs decompressed from high-pressure atmospheres 
was favored with gas mixtures in the following 
order; oxygen, helium-oxygen, air, and argon- 
oxygen. The relative effects of decompression from 
various gas mixtures may be explained by differ- 
ences in solubility in oil and in water, in the oil- 
water solubility ratios and in the diffusibility of the 
gases and permeability of the tissues. 
Gersh {161) 1945 reported studies on gas bubbles 
in bone and associated structures as well as in the 
lung and spleen of guinea pigs decompressed 
rapidly from high pressure atmospheres. In bone, 
small numbers of gas bubbles were found and these 
only in the veins and the sinusoids of bone marrow 
of the tibia after exposure of guinea pigs to com- 
pressed air for one hour. After exposure for 3 hours 
both intravascular (artery, vein, and sinusoid) and 
extravascular disruptive gas bubbles were visible. 
In some animals the Haversian systems of bone 
were occluded by gas columns. Periostial blood 
vessels were only occasionally distended with gas. 
Gas bubbles were also found in the blood vessels 
of the tendon sheaths near the ankle and knee joint, 
but were more numerous in the former. These find- 
ings are related by the author to aseptic bone 
necrosis of caisson workers and to theories of the 
origin of the pain of bends. In the lungs gas bubbles 
were found only in the pulmonary artery and its 
branches, stretching the walls of the medium-sized 
and small vessels. These findings are related to 
theories as to the origin of the pain of chokes. 
Gas bubbles were found in decreasing order of fre- 
quency in the sinusoids, arteries, and veins of the 
spleen of guinea pigs decompressed after exposure 
to compressed air. Their origin is related to the 
peculiarities of the vascular system of the spleen 
and to the occurrence of vascular emboli. 
Gersh {160) 1945 and {162) 1946 carried out 
investigations designed to correlate X-ray and gross 
observations on gas bubbles in guinea pigs decom- 
pressed from high atmospheric pressures. The ani- 
mals were compressed at 75, 90, and 105 lbs. per 
sq. in. (gage pressure) for 1 to I/2 hours and 
decompressed in 4 seconds. Medium-fat and fat 
animals were used. X-rays of the extended left 
hind leg were made of each animal before and 
after decompression. Following the second X-ray 
the animals were autopsied and the distribution of 
gas bubbles in the body observed grossly. In animals 
that died following decompression, X-rays of the 
leg revealed radio-translucent lines corresponding 
to the larger veins. The regions occupied by fat 
between the hamstring muscles or in the inguinal 
regions became somewhat radio-translucent with a 
clear outlining of lymph nodes present in the fat 
depots. Except in one instance, no evidence was 
found of patterns suggesting bubbles. Yet such 
bubbles ranging from 0.05 to 0.7 mm. in diameter 
were seen in large numbers in these areas on gross 
examination at autopsy. In the X-ray plates there 
was no evidence of the bubbles which were found 
on gross examination to be present along the course 
of, but outside of, the larger blood vessels. Many 
bubbles were found in the inguinal fat. It was con- 
cluded that bubbles in blood vessels are recognizable 
in X-rays, while bubbles in fat or other forms of 
connective tissue are usually recognizable only as a 
general X-ray shadow. Tissue bubbles or extra- 
vascular bubbles are rarely identifiable as such, 
probably because of a combination of the following 
factors: the small size of the bubble, poor resolution, 
and overlay. Failure to recognize bubbles in the 
X-rays of men suffering from bends may, according 
to the author, result from limitations of the X-ray 
method and cannot be interpreted as indicating the 
absence of gas bubbles intravascularly or extra- 
vascularly. 
X-ray examination of animals following decom- 
pression from high pressures has also been carried 
out by Colonna and Jones (158) 1948. These 
authors commented that X-rays provide a crude 
means for early detection of manifestations of cais- 
son disease in bones. Autopsy of animals that died 
following decompression showed numerous air 
bubbles in the venous circulation, in fat and sub- 
cutaneous tissues, the mesentery, fascial planes, and 
mediastinum. The lungs were congested and the 
heart dilated. Cavities were consistently found in 
the bone marrow, both grossly and microscopically, 
presumably formed by large bubbles collecting in 
the soft marrow of the long bones. Early evidence of 
a permanent defect in bony tissue was present fol- 
lowing repeated decompression. The author inter- 
preted the changes in the bones of the rabbits used 
in these experiments as an early stage in the produc- 
tion of asceptic necrosis of bone. 
A series of reports has been given by Gersh and 
Catchpole on bubble formation in rabbits decom- DECOMPRESSION PHYSIOLOGY OF BUBBLE FORMATION 
pressed to altitudes. These authors {163) 1945 and 
{164) 1946 made gross observations on rabbits de- 
compressed after a 10-second period of preoxygena- 
tion to a simulated altitude of 45,000 feet. The ani- 
mals were prepared for histological studies at 30,- 
000 feet, the tissues being frozen in situ with isopen- 
tane chilled to — 150° C., or removed with all blood 
vessels clamped and then frozen by immersion into 
the chilled fluid. When animals died as a result of 
decompression, bubbles were found only in the 
blood vessels. No extravascular bubbles were seen. 
Bubbles were seen with equal frequency in the 
arteries and veins in all tissues and organs studied. 
They occurred chiefly in the relatively large vessels, 
and the only capillaries containing gas were those 
in the fat tissues. Gas bubbles in the kidney were 
never seen in vessels smaller than the interlobular 
vessels. The largest vessels occluded with gas were 
those in the fatty tissue. Little gas was found in the 
fascial planes of skeletal muscle. Gas bubbles were 
present in the sinusoids of the spleen and some in 
the bone marrow. They were absent in the sinusoids 
of the liver and adrenal cortex. Very few bubbles 
were seen in the pulmonary vessels. Only one 
bronchiolar vessel contained gas. Epineural and 
intraneural vessels were occluded by gas bubbles. 
Catchpole and Gersh {154) 1945, {156) 1946, 
carried out an investigation to determine the effect 
of preoxygenation, electrical stimulation, anesthe- 
sia, carbon dioxide, sodium bicarbonate, lactic acid, 
and ammonium chloride on bubble formation in 
rabbits decompressed to reduced atmospheric pres- 
sures. It was found that 30 minutes of preoxygena- 
tion before decompression to a simulated altitude of 
45,000 feet permitted rabbits to survive while the 
controls died. Respiratory gas mixtures containing 
5 and 10 percent carbon dioxide failed to affect 
survival. The beneficial effects ascribed to carbon 
dioxide at altitude do not extend to the prevention 
of aeroembolism. Intraperitoneal injections of so- 
dium bicarbonate were likewise ineffective. Intra- 
peritoneal administration of ammonium chloride 
and of lactic acid prevented death from aeroembo- 
lism. Electrical stimulation of a hind limb with re- 
sulting muscular contractions at altitude caused the 
death of animals decompressed to a simulated alti- 
tude and at a decompression rate at which unstimu- 
lated controls survived. Conversely, muscular immo- 
bilization by nembutal anesthesia tended to favor 
survival. 
In a further study on the physiological factors 
affecting the production of gas bubbles in rabbits 
decompressed to altitudes, Catchpole and Gersh 
{153) 1945 and {155) 1946 found that decompres- 
sion time had an important influence on bubble 
formation at altitude. Rapid decompression led to 
a high incidence of bubbles and early death, while 
slow decompression gave low bubble incidence and 
late death or survival. At the critical decompression 
time of 10 minutes to reach a simulated altitude of 
45,000 feet, 80 percent of the animals survived for 
30 minutes after reaching altitude, while with de- 
compression times of less than 10 minutes, 80 per- 
cent of the animals died with vascular bubbles in 30 
minutes or less after reaching altitude. Bubble inci- 
dence and time of death were unrelated to body fat- 
ness, previous activity, spontaneous activity at alti- 
tude, body weight, and the sex of adult animals. 
Very few bubbles were found in the coronary ar- 
teries or pulmonary system. The authors considered 
that the probable cause of death was embolism of 
the central nervous system. 
As to other physiological factors affecting experi- 
mental bubble formation, Wedral and Ivy {191) 
1941 have examined the relation of circulatory rate 
to aeroembolism and aeroemphysema. The relation 
of temperature and exercise to bubble formation in 
rats and in torniqueted legs of rabbits and goats has 
been reported by Reed and Blinks {186, 188) 1944 
and Reed, Blinks, and Pease {189) 1944. In dead 
animals or in tourniqueted legs, low temperature 
protects against bubble formation and is the con- 
trolling factor in preventing bubbles in decom- 
pressed animals. Low temperature over a period of 
several hours protected against bubbling regard- 
less of motion, and high temperatures facilitated 
bubbling even in the absence of motion. In living 
animals, however, exercise is the important factor 
over the tolerated temperature range, the latter 
having little effect. The main temperature effect 
seems to be upon the rate of carbon dioxide produc- 
tion in anaerobic glycolyses. Both carbon dioxide 
and nitrogen are significant in bubble formation and 
resistance, the former acting as a facilitator. If nitro- 
gen is previously removed by preoxygenation, few or 
no bubbles occur. According to Reed and Blinks 
{187) 1944, vasoconstriction does not enhance 
bubbling in the blood. Vasodilatation apparently 
protects somewhat against bubble formation but 
only if the animal is taken very slowly to altitude 
allowing time for nitrogen to be flushed out. 
For a further study on various physiological fac- 
tors affecting bubble formation in animals, a paper 
by McElroy, Whiteley, Cooper, Pease, Warren, and 
Harvey {183) 1944 should be consulted. 
A large number of studies have been carried out 
on the physical conditions for the formation and 
growth of gas bubbles. For such studies, reports by 
Bateman {148 and 149) 1942 should be consulted. SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
A long series of reports by Harvey and coworkers 
likewise provide essential and definitive source ma- 
terial on this subject. In 1942, Harvey, Cooper, 
Pease, McElroy, and Whiteley [174) showed that 
pure water or aqueous solutions, including blood, 
supersaturated under 8 atmospheres with air or 
carbon dioxide, can remain so without bubble 
formation indefinitely, provided they are fr.ee of a 
preformed gas phase in the form of small gas masses 
or gas nuclei. Any kind of gas or even water vapor 
itself may serve as a nucleus for visible bubble 
formation from any other kind of gas, but without 
these minute gas nuclei, no visible bubbles are 
formed. These small gas nuclei stick to any dirty, 
especially greasy surfaces in vitro and by growth are 
converted into bubbles or series of bubbles which 
detach themselves. In 1943, Harvey, Cooper, Pease, 
McElroy, and Whiteley [175) described a device 
for detecting bubble-forming nuclei in the blood of 
mammals. No nuclei were found in the carotid blood 
of nembutalized cats and dogs at ground level, at 
altitude or under decompression. This indicates 
that nuclei do not enter through the lung membrane 
or form in lung capillaries. Possible turbulence near 
the heart is not a factor in bubble formation of the 
quiet animal. Bubbles can form in water free of gas 
nuclei as a result of movement by pressure pulses, 
shock waves, sound waves, turbulence, Reynolds’ 
cavitation effects, and tearing of a liquid. Gas nu- 
clei greatly favor bubble formation under these 
conditions, as does dissolved gas and low initial pres- 
sure on the liquid. In still, supersaturated water, 
gas nuclei seem to be the only source of bubbles. 
According to Harvey, Barnes, McElroy, Whiteley, 
and Pease [173) 1944, the conventional method of 
removing gas nuclei by prolonged boiling or evacu- 
ation has the disadvantage of removing dissolved 
gas in addition to the gas nuclei. It was found that 
strong centrifuging of the liquid and the container 
will remove gas macro nuclei so that no bubbles 
form when the liquid is evacuated to the vapor pres- 
sure of water. Also, previous exposure of liquid and 
container to high hydrostatic pressures (10,000 to 
16,000 lbs. per sq. in.) will remove all gas nuclei 
from a liquid by forcing them into solution. 
For other studies on bubble formation, papers by 
Harvey [169) 1945, [170) 1950, [171) 1951, and 
[172) 1951; Harvey, Cooper, Pease, McElroy, 
Whiteley, and Warren [176) 1943; and Harvey, 
McElroy, Pease, Whiteley, Warren, Barnes, and 
Kleinberg [177) 1943 should be consulted. Of spe- 
cial interest is a report by Harvey, Whiteley, 
Cooper, Pease, and McElroy [178) 1946 on the 
effect of mechanical disturbance on bubble forma- 
tion in single cells and tissue after saturation with 
very high gas pressures. In these studies cells and 
tissues were placed in small glass dishes in a shallow 
layer of liquid and exposed to pressures of 152, 80, 
and 76.5 atmospheres in a steel chamber with glass 
windows so that observation of the material could 
be made through a microscope. Amebae were sub- 
jected to 75 atmospheres for 2 hours, paramecia 
were exposed to 78 atmospheres for 2 hours. Vari- 
ous other cells were also used. In those studies in 
which precautions were taken to remove external 
gas nuclei by preliminary high hydrostatic pressure 
treatment (16,000 lbs. per sq. in. for 2 hours), no 
bubbles appeared in the water or on the outside or 
inside of the cells on decompression, although the 
cells themselves died. Cells without prepressure 
treatment formed many bubbles on the outside, 
demonstrating that bubble formation is dependent 
on gas nuclei which are found on the outside of the 
cell. The formation of gas in single living cells is 
considered unusual even after decompression from 
high nitrogen pressures or decompression to high 
vacuums. 
Fresh rat tissues subjected to 16,000 lbs. per sq. in. 
for an hour to remove all gas nuclei were subse- 
quently compressed to 40 to 80 atmospheres for 
15 to 30 hours and afterwards decompressed to 
atmospheric pressure. Bubbles arose in the fat, in 
skeletal muscle, and in fragments of clotted blood. 
Copious extracellular bubbles were observed deep 
within the fat tissue. A very few intracellular 
bubbles were seen only when the pressure difference 
was greater than 50 atmospheres. Decompression 
of fat tissue after saturation with 20 atmospheres of 
nitrogen was not enough to elicit intracellular 
bubbles although large intercellular bubbles did 
appear. Stretching the connective tissue with glass 
needles after decompression resulted in more 
abundant bubble formation. This burst of bubbles 
was believed to be due to the separation of the 
surfaces previously in contact. At the moment of 
separation a “dry” spot is left into which a few 
dissolved molecules diffuse before water can again 
cover the region. The gas molecules act as gas 
nuclei which quickly grow under the conditions of 
high supersaturation. The tearing of one surface 
from another must result in formation of a small 
cavity into which gas molecules diffuse before col- 
lapse can occur. This small group of gas molecules 
constitutes a gas nucleus. Such a mechanism is con- 
sidered to be involved in formation of bubbles in 
animals and man in decompression sickness. 
A definitive article on bubble formation in liquid 
is that of Harvey published in 1950 [170). Physical 
factors in bubble formation are also considered by 
Harvey in a chapter published in 1951 [171). In DECOMPRESSION PHYSIOLOGY OF BUBBLE FORMATION 
148-154 
summarizing the problem, Harvey states that pres- 
sure differences are regarded as the driving force 
for bubble formation, while the size of the bubbles 
and rate of formation are largely determined by 
gas diffusion which depends not only on pressure 
difference, but also on surface area, diffusion con- 
stants, and particularly on gas solubility. Gas nuclei 
or rough surfaces may act as generators for new 
bubbles. Bubbles can easily form in blood vessels 
because the endothelium is hydrophilic. The author 
refers to all nuclei which grow at or above vapor 
pressure of water as gas macronuclei and those 
requiring a greater pressure difference for growth 
as gas micronuclei. For de novo formation of 
bubbles in a homogeneous liquid at rest containing 
dissolved gas, it is necessary that the pressure dif- 
ference be of the order of 100 to 1,000 atmospheres. 
Techniques for demonstration of gas bubbles in- 
volving the freezing of decompressed tissues for 
histological study are questioned by the author on 
the grounds that bubbles may arise from surfaces 
of rapidly formed ice crystals. If a nitrogen bubble 
is surrounded by a solution of carbon dioxide at 
the same tension, the bubble will grow because 
carbon dioxide diffuses in much more rapidly than 
nitrogen can diffuse out. Possibly respiratory move- 
ments, heart beat, circulation, or peristalsis are re- 
sponsible for local tensions than cause bubble 
formation. It appears that bubbles can arise from 
tissues in the complete absence of gas micronuclei 
and that gas micronuclei are unnecessary for bubble 
formation under conditions that might be impor- 
tant in the body. In a chapter on bubble formation 
in cats, Harvey {172) 1951 states that an altitude 
of 45,000 feet seems to be the critical altitude in 
cats for bubble formation. Muscle contraction intro- 
duces two factors, both of which favor the early 
formation of bubbles under all conditions: Excess 
carbon dioxide production and decreased hydro- 
static pressure resulting from the mechanical ten- 
sion developed. One of these factors, the decreased 
hydrostatic pressure, becomes particularly impor- 
tant at altitude because the animal is already near 
the vapor pressure of water. 
Regarding the role of carbon dioxide as a facili- 
tating agent in the initiation and growth of bubbles 
in animals, papers by Blinks, Twitty, and Whitaker 
{152) 1951 and Harris, Berg, Whitaker, Twitty, 
and Blinks {168) 1945 should be consulted. These 
authors believe that carbon dioxide greatly increases 
the ease with which bubbles may be initiated and 
may be responsible for their rapid growth in early 
stages of development. At later stages nitrogen is 
more directly concerned with their further growth 
and development. Dead rabbits and frogs were 
found to bubble profusely on decompression to sim- 
ulated high altitudes. This was attributed primarily 
to accumulation of carbon dioxide derived from 
residual cellular respiration after death and from 
anaerobic glycolysis with attendant decomposition 
of bicarbonates in blood and tissue fluids. If anaero- 
bic glycolysis was inhibited by using sodium iodo- 
acetate as the lethal agent, bubble formation was 
greatly reduced or lacking on subsequent decom- 
pression. Administration of carbon dioxide in high 
concentrations to living frogs lowered the minimum 
altitude at which bubble formation occurred with 
exercise. Pretreatment with carbon dioxide also re- 
duced the degree of muscular activity necessary for 
bubbles to form in frogs at high altitudes. Bubbles 
from decompressed rats were found to contain as 
much as 60 to 80 percent carbon dioxide. It is be- 
lieved that as bubbles move out into larger vessels, 
there is loss of carbon dioxide and increase in nitro- 
gen which is responsible for the further growth and 
maintenance of the bubbles. 
For further studies on bubble formation, papers 
by the following may be consulted: Berg {150) 
1945-46; Berg, Harris, Whitaker, and Twitty (151) 
1944; Hill {179) 1951; Horiuti {180) 1946; Le- 
maire {181) 1947; McElroy and Whiteley {182) 
1946; Pease, Blinks, and Reed {184) 1944; Piccard 
{185) 1944; and Rodbard {190) 1946. 
148. Bateman, J. Bubble formation in vitro and the 
problem of decompression sickness. Canada. University of 
Toronto, Banting & Best department of medical research. 
16 May 1942, 4 pp. [R] 
149. Bateman, J. B. Formation and growth of bubbles 
in aqueous solutions. Canada. University of Toronto, Bant- 
ing & Best department of medical research. Canadian 
Aviation, Kept. no. 113, 16 May 1942, 14 pp. 
150. Berg, W. E. Intravascular bubble formation in 
animals at simulated high altitudes. Stanford University, 
California. Abstracts of Dissertations. 1945-46, 21: 3-5. 
IP] 
151. Berg, W,, M. Harris, D. M, Whitaker, and V. C. 
Twitty. Additional mechanisms for the origin of bubbles 
in animals decompressed to simulated altitudes. J. gen. 
Physiol., 1944, 28: 253-258. 
152. Blinks, L. A., V. C. Twitty, and D. M. Whitaker. 
Bubble formation in frogs and rats, pp. 145-164 in: De- 
compression sickness. Caisson sickness, diver’s and flier’s 
bends and related syndromes. Edited by J. F. Fulton for 
the Subcommittee on decompression sickness, National 
Research Council, Philadelphia. W. B. Saunders, Com- 
pany. 1951, 437 pp. [D] 
153. Catchpole, H. R. and I. Gersh. Physiological 
factors affecting the production of gas bubbles in rabbits 
decompressed to altitude. U. S. Navy. NMRI. Project 
X-284, Kept. no. 6, 27 April 1945, 7 pp. [P] 
154. Catchpole, H. R. and I. Gersh. Bubble formation 
in rabbits decompressed to altitude; effect of preoxygena- 
tion, electrical stimulation, and some pharmacological 
factors. U. S. Navy. NMRI. Project X—284, Kept. no. 7, 
5 May 1945, 5 pp. [P] 155-184 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
155. Catchpole, H. R. and I. Gersh. Physiological 
factors affecting the production of gas bubbles in rabbits 
decompressed to altitude. J. cell. comp. Physiol, 1946, 
27: 15-26. [P] 
156. Catchpole, H. R. and I. Gersh. Bubble formation 
in rabbits decompressed to altitude: effect of preoxygena- 
tion, electrical stimulation, and some pharmacological 
factors. J. cell. comp. Physiol, 1946, 27: 27-34. [P] 
157. Catchpole, H. R. and I. Gersh. Physical factors in 
the pathogenesis of aeroembolism—a review. U. S. Navy. 
NMRI. Project X-284, Rept. no. 11, 26 April 1946, 12 pp. 
158. Colonna, P. C. and E. D. Jones. Aeroembolism of 
bone marrow. Arch. Surg., Chicago, 1948, 56: 161-171. 
159. Fulton, J. F. Decompression sickness. The genesis 
of the tissue bubble, pp. 51-90 in: Aviation medicine in 
its preventive aspects. An historical survey. London, Ox- 
ford University Press, 1948, 174 pp. [R] 
160. Gersh, I. Correlation of X-ray and gross observa- 
tions on gas bubbles in guinea pigs decompressed from 
high pressure atmospheres. U. S. Navy. NMRI. Project 
X-284, Rept. no. 9, 9 May 1945, 4 pp. [P] 
161. Gersh, I. Gas bubbles in bone and associated struc- 
tures, lung and spleen of guinea pigs decompressed rapidly 
from high pressure atmospheres. U. S. Navy. NMRI. 
Project X-284, Rept. no. 10, 10 May 1945, 12 pp. [P] 
162. Gersh, I. Correlation of X-ray and gross observa- 
tions on gas bubbles in guinea pigs decompressed from 
high pressure atmospheres. /. cell. comp. Physiol, 1946, 
28: 271-276.[P] 
163. Gersh, I. and H. R. Catchpole. Appearance and 
distribution of gas bubbles in rabbits decompressed to 
altitude. U. S. Navy. NMRI. Project X-284, Rept. no. 8, 
7 May 1945,8 pp. [P] 
164. Gersh, I. and H. R. Catchpole. Appearance and 
distribution of gas bubbles in rabbits decompressed to 
altitude. /. cell. comp. Physiol, 1946, 28: 253-270 [P] 
165. Gersh, I. and G. E. Hawkinson. The formation 
and appearance of tissue and vascular gas bubbles after 
rapid decompression of guinea pigs from high pressure 
atmospheres. U. S. Navy. NMRI. Project X-284, Rept. 
no. 1, 7 March 1944, 15 pp. C. A. M. rept. no. 290, 
7 March 1944, 21 pp. [P] 
166. Gersh, I., G. E. Hawkinson, and E. H. Jenney. 
Comparison of vascular and extra-vascular bubbles follow- 
ing decompression from high pressure atmospheres of 
oxygen, helium-oxygen, argon-oxygen and air. U. S. Navy. 
NMRI. Project X—284, Rept. no. 5, 8 November 1944, 
9 pp. [P] 
167. Gersh, I., G. E. Hawkinson, E. H. Rathhun, and 
A. R. Behnke. Changes in specific gravity of tissues, organs, 
and the animal as a whole resulting from rapid decom- 
pression of guinea pigs from high pressure atmospheres. 
U. S. Navy. NMRI. Project X-284, Rept. no. 2, 8 March 
1944, 6 pp. [P] 
168. Harris, M., W. E. Berg, D. M. Whitaker, V. C. 
Twitty, and L. R. Blinks. Carbon dioxide as a facilitating 
agent in the initiation and growth of bubbles in animals 
decompressed to simulated altitudes. J. gen. Physiol, 1945, 
28: 225-240. [P] 
169. Harvey, E. N. Bubble formation in animals. U. S. 
NRC—CAM. Division of medical sciences. OEMcmr—166, 
C. A. M. rept. no. 469, October 1945, 16 pp. [R] 
170. Harvey, E. N. Bubble formation in liquids, pp. 
137—150 in: Medical physics. Volume II. Edited by Otto 
Glasser. Chicago, The Year Book Publishers, Inc., 1950, 
1227 pp. 
171. Harvey, E. N. Physical factors in bubble forma- 
tion. pp. 90-114 in: Decompression sickness. Caisson 
sickness, diver’s and flier’s bends and related syndromes. 
Edited by J. F. Fulton for the Subcommittee on decom- 
pression sickness, National Research Council. Phila- 
delphia, W. B. Saunders Company, 1951, 437 pp. 
172. Harvey, E. H. Bubble formation in cats. pp. 115- 
144 in: Decompression sickness. Caisson sickness, diver’s 
and flier’s bends and related syndromes. Edited by J. F. 
Fulton for the Subcommittee on decompression sickness, 
National Research Council. Philadelphia, W. B. Saunders 
Company, 1951, 437 pp. 
173. Harvey, E. H., D. K. Barnes, W. D. McElroy, A. H. 
Whiteley, and D. C. Pease. Removal of gas nuclei from 
liquids and surfaces. U. S. NRG-CAM. OEMcmr-166, 
C. A. M. rept. no. 407, November 1944, 1 pp. 
174. Harvey, E. N., K. W. Cooper, D. C. Pease, W. D. 
McElroy, and A. H. Whiteley. The formation of gas 
bubbles in supersaturated water. U. S. NRC—CAM. 
C. A. M. rept. no. 77, October 1942, 18 pp. [P] 
175. Harvey, E. N., K. W. Cooper, D. C. Pease, W. D. 
McElroy, and A. H. Whiteley. A pompholygometer for 
detecting bubble forming nuclei in the blood of living 
mammals, and observations on bubble formation in liquids 
free of such nuclei. U. S. NRG-CAM. C. A. M. rept. no. 
105, 7 January 1943, 9 pp. [P] 
176. Harvey, E. N., K. W. Cooper, D. C. Pease, W. D. 
McElroy, A. H. Whiteley, and G. H. Warren. Conditions 
for gas bubble formation at altitude in cats and dogs. 
U. S. NRC-CAM. C. A. M. rept. no. 106, 8 January 1943, 
8 pp. [PI 
177. Harvey, E. N., W. D. McElroy, D. C. Pease, A. H. 
Whiteley, G. Warren, D. K. Barnes, and W. Kleinherg. 
The mechanism of bubble formation in the blood of 
mammals in relation to decompression sickness. U. S. 
NRC-CAM. C. A. M. rept. no. 229, 25 October 1943, 
5 pp. [P] 
178. Harvey, E. N., A. H. Whiteley, K. W. Cooper, 3). C. 
Pease, and W. D. McElroy. The effect of mechanical dis- 
turbance on bubble formation in single cells and tissues 
after saturation with extra high gas pressures. /. cell, 
comp. Physiol, 1946, 28: 325-337. [P] 
179. Hill, T. L. Concerning the dependence of the sur- 
face tension of spherical drops and bubbles on radius. 
U. S. Navy. NMRI. Project NM 000 018.06.05, 14 March 
1951, 5 pp. 
180. Horiuti, K. [The conditions under which reducing 
air bubbles are produced in the living body.] Igaku & 
Seibutugaku, 1946, 9: 258-259. (English pagination) 
(Japanese text). 
181. Lemaire, R. Une theorie nouvelle concernant le 
mechanisme de formation des bulles au sein des tissus 
et des liquides biologiques. Med. areonaut., 1947, 2: 
524-528. [M] 
182. McElroy, W. D. and A. H. Whiteley. Relation of 
gas tension and hydrostatic pressure to intravascular 
bubble formation. Amer. J. Physiol, 1946, 147: 19-27. 
[P] 
183. McElroy, W. D., A. H. Whiteley, K. W. Cooper, 
D. C. Pease, G. H. Warren, and E. H. Harvey. Bubble 
formation in animals. VI. Physiological factors; the role 
of circulation and respiration. U. S. NRC-CAM. C. A. M. 
rept. no. 380, November 1944, 1 p. 
184. Pease, D. C., L. R. Blinks, and E. A. Reed. Physical 
factors in bubble formation. U. S. NRC-CAM. C. A. M. 
rept. no. 378, 15 October 1944, 1 p. [P] DECOMPRESSION—GAS SATURATION 
185-204 
185. Piccard, J. Aero-emphysema and caisson disease, a 
problem of colloid chemistry, pp. 1082-1093 in: Colloid 
chemistry, theoretical and applied. Volume V. Theory and 
Methods. Biology and Medicine. Edited by Jerome Alex- 
ander. New York, Reinhold Publishing Corp., 1944, 1256 
pp. 
186. Reed, E. and L. R. Blinks. The relation of tem- 
perature and exercise to bubble formation in rats, and in 
tourniquetted legs of rabbits and goats. U. S. NRG—GAM. 
C. A. M. rept. no. 365, 15 October 1944, 1 p. [P] 
187. Reed, E. and L. R. Blinks. Vasoconstriction and 
the relation of the vascular bed to bubble formation in 
frogs. U. S. NRG-CAM. C. A. M. rept. no. 377, 15 Octo- 
ber 1944, 1 p. 
188. Reed, E. A. and L. R. Blinks. The relation of 
temperature and exercise to bubble formation in rats, and 
in tourniquetted legs of rabbits and goats. Resume. U. S. 
NRG-CAM. C. A. M. rept. no. 379, 15 October 1944, 1 p. 
[P] 
189. Reed, E., L. R. Blinks, and D. C. Pease. Bubble 
formation in decompressed animals. U. S. NRG-CAM. 
C. A. M. rept. no. 365, OSRD Contract no. OEMcmr— 
193, 15 October 1944, 1 p. Abstr. 
190. Rodbard, S, Factors affecting bubble volume in the 
tissues at various altitudes. Fed. Proc. Amer. Soc. exp. 
Biol, 1946, 5: 88. 
191. Wedral, J. W. and A. C. Ivy. The relation of 
circulatory rate to aeroembolism and aeroemphysema. /. 
Aviat. Med., 1941, 22: 13-21. Excerpta Medica. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1951, 
4: 1420. 
192. Wagner, C. E. Observations of gas bubbles in pial 
vessels of cats following rapid decompression from high 
pressure atmospheres. U. S. Navy. NMRI. Project X-284, 
Rept. no. 4, 4 October 1944, 4 pp. 
C. SATURATION AND DESATURATION OF GASES 
IN THE BODY 
The elimination of nitrogen from tissues and 
fluids of the body is of particular significance as a 
factor in bubble formation. The references included 
in this section have been chosen because of their 
value as source material in connection with the 
section on decompression sickness (p. 159). For 
studies of nitrogen elimination, the following 
references may be consulted: 193, 194, 195, 196, 
197,198,200, 203, and 209. The reader should con- 
sult a review by Kety {199) 1951. This article dis- 
cusses the theories and formulas which have been 
offered to explain and calculate exchange of inert 
gases in the lungs and tissues. 
For theoretical papers on blood-tissue exchange 
of inert gases, reports by the following should be 
consulted: Morales and Smith {204) 1944, {205 
and 206) 1945, and {207) 1948; Morales, Smith, 
and Behnke {208) 1945; and Smith and Morales 
{213) 1944. For studies on neon, argon, krypton, 
xenon, and radon, papers by the following should 
be consulted: Lawrence, Loomis, Tobias, and 
Turpin {201) 1946; Smith and Labaw {212) 1948; 
Tobias, Jones, Lawrence, and Hamilton {215) 
1949; and Turpin, Loomis, Lawrence, Jones, and 
Tobias {216) 1945. Carbon dioxide elimination and 
the effect of carbon dioxide on the rate of denitro- 
genation have been investigated by Margaria and 
Sendroy {202) 1950, Schaefer and Scheer {210) 
1951, and Sendroy and Margaria {211) 1950. For 
a study of denitrogenation of muscle and fat tissues, 
a paper by Whiteley and McElroy {217) 1946 may 
be consulted. The rate of nitrogen elimination from 
the body through the lungs has been investigated 
by Stevens, Ryder, Ferris, and Inatome {214) 1947. 
193. Behnke, A. R. The absorption and elimination of 
gases of the body in relation to its fat and water content. 
Medicine, Baltimore, 1945,24: 359-379. [R] 
194. Boothby, W. M., TJ. C. Luft, and 0. 0. Benson, Jr. 
Gaseous nitrogen elimination. Experiments when breath- 
ing oxygen at rest and at work, with comments on dysbar- 
ism. USAF. Randolph Field, Tex. School of aviation 
medicine. Project 21-53-003, Kept. no. 1, August 1951, 
33 pp. 
195. Boothby, W. M., G. Lnndin, and H. F. Helmholz, 
Jr. A gaseous nitrogen elimination test to determine pul- 
monary efficiency. Proc. Soc. exp. Biol., N. Y., 1948, 67: 
558—561. Acta physiol, scand. 1948, Supplementum 53: 
9. [P] 
196. Jones, H. B. Respiratory system: nitrogen elimina- 
tion, pp. 855-871 in: Medical physics. Volume II. Edited 
by Otto Glasser. Chicago, The Year Book Publishers, Inc., 
1950, 1227 pp. [R] 
197. Jones, H. B. Gas exchange and blood-tissue per- 
fusion factors in various body tissues, pp. 278—321 in: 
Decompression sickness. Caisson sickness, diver’s and flier’s 
bends and related syndromes. Edited by J. F. Fulton for 
the Subcommittee on decompression sickness. National 
Research Council. Philadelphia, W. B. Saunders Co., 
1951,437 pp. [R] [D] 
198. Jones, H. B., E. Myers, and W. E. Berg. Gas ex- 
change, circulation and diffusion. U. S. NRG-CAM. 
OEMcmr-196, C. A. M. rept. no. 429, 10 April 1945, 
25 pp. 
199. Kety, S. S. The theory and applications of the 
exchange of inert gas in the lungs and tissues. Pharmacol. 
Rev., 1951,5; 1-41. [R] 
200. Lawrence, J. H., H. B. Jones, W. E. Berg, F. M. 
Henry, and B. C. Ivy. Studies on gas exchange. USAF. 
Wright-Patterson air force base, Dayton, Ohio. Air ma- 
teriel command, ENG, Aero medical laboratory. Serial no. 
MCREXD-696-114, 3 March 1948, 224 pp. [M] [R] 
201. Lawrence, J. H., W. F. Loomis, C. A. Tobias, and 
F. H, Turpin. Preliminary observations on the narcotic 
effect of xenon with a review of values for solubilities of 
gases in water and oils. /. Physiol., 1946, 105: 197-204. 
202. Margaria, R. and J. Sendroy, Jr. Effect of carbon 
dioxide on rate of denitrogenation in human subjects. 
J. appl. Physiol, 1950, 3: 295-308. U. S. Navy. NMRI. 
Project NM 004 005.04.05, 8 August 1950, 18 pp. 
203. Marshall, J. M. Nitrogen narcosis in frogs and 
mice. Amer. J. Physiol, 1951, 166: 699-711. [P] 
204. Morales, M. F, and B. E. Smith. On the theory 
of blood tissue exchanges. III. Circulation and inert gas 
exchanges at the lung with special reference to saturation. 
U. S. Navy. NMRI. Project X-43, Rept. no. 2, 29 July 
1944. 12 pp. 205-231 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
205. Morales, M. F. and R. E. Smith. A note on the 
physiological arrangement of tissues. Bull math. Biohpys., 
1945, 7: 47-50. 
206. Morales, M. F. and R. E. Smith. U. S. Navy. 
NMRI. On the possible determination of gross human 
body composition by the use of radioactive inert gases. 
U. S. Navy. NMRI. Project X-43, Rept. no. 4, 1 August 
1945, 5 pp. [M] 
207. Marales, M. F. and R. E. Smith. On the theory of 
blood-tissue exchange of inert gases: VI. Validity of ap- 
proximate uptake expressions. Bull. math. Biophys., 1948, 
10: 191-200. 
208. Morales, M. F., R. E. Smith, and A. R. Behnke. The 
quantitative physiological basis of inert gas exchange: 
applications to decompression sickness. U. S. Navy. NMRI. 
Project X—43, Rept. no. 3, 18 July 1945, 9 pp. 
209. Robertson, J. S., W. E. Siri, and H. B. Jones. 
Lung ventilation patterns determined by analysis of nitro- 
gen elimination rates; use of the mass spectrometer as a 
continuous gas analyzer. /. din. Invest., 1950, 29: 577- 
590. [P] 
210. Schaefer, K. E. and K. Scheer. Regional differ- 
ences in carbon dioxide elimination through the skin. Fed. 
Proc. Amer. Soc. exp. Biol, 1951, 10: 119. Exp. Med. 
Surg., 1951, 9: 449-457. 
211. Sendroy, J,, Jr. and R. Margaria. Effect of carbon 
dioxide on rate of denitrogenation in human subjects. 
Fed. Proc. Amer. Soc. exp. Biol, 1950, 9: 226. 
212. Smith, F. and L. W. Lahaw. The development of 
a tracer method for determining the rate of diffusion of 
inert gas through living tissue. /. cell. comp. Physiol, 
1948, 32: 407-419. 
213. Smith, R. E. and M. F. Morales. On the theory 
of blood tissue exchanges. I. Fundamental equations. 
U. S. Navy. NMRI. Project X—43, Rept. no. I, 8 May 
1944, 7 pp. 
214. Stevens, C. D., H. W. Ryder, E. B. Ferris, and 
M. Inatome. The rate of nitrogen elimination from the 
body through the lungs. J. Aviat. Med., 1947, 18: 111— 
132. [P] 
215. Tobias, C. A., H. B. Jones, J. H. Lawrence, and 
J. G. Hamilton, The uptake and elimination of krypton 
and other inert gases by the human body. /. din. Invest., 
1949, 28: 1375-1385. [P] 
216. Turpin, F. H., W. F. Loomis, J. H. Lawrence, 
H. B. Jones, and C. A. Tobias. Solubilities of gases in 
water and oils. U. S. NRG-CAM. Acting for OSRD- 
CMR. OEMcmr-196, Rept. no. 455, 1945, 4 pp. [R] [P] 
217. Whiteley, A. H. and W. D. McElroy. Denitro- 
genation of muscle and fat tissues of the anesthetized cat. 
Amer. J. Physiol, 1946, 146: 229-240. [P] 
D. FAT AND WATER CONTENT 
Fats and water are so distributed in the body that 
during saturation a large part of the nitrogen ab- 
sorbed by fat diffuses from the body fluid. During 
decompression following partial saturation, the dif- 
fusion of nitrogen from the rapidly saturating body 
fluids into slowly saturating lipoids and fats tends 
to equalize the partial pressure of nitrogen in the 
different tissues of the body. After short exposures 
to high pressures, the fat acts as a nitrogen ab- 
sorbent during decompression and serves as a buffer 
against bubble formation in the bloodstream. Ac- 
cording to Behnke (193) 1945, fat men with ade- 
quate blood supply and circulation should be better 
suited for short exposures in compressed air than 
lean men. In view of these facts and the differential 
solubility of nitrogen and other inert gases in fats 
as distinct from fluids, importance has been at- 
tached to studies of the fat and water content of the 
body. The references given in this section constitute 
the principal reports on this subject. 
218. Berger, E, Y., M. F. Dunning, J. M. Steele, R. 
Jackenthal and B. B. Brodie. Estimation of intracellular 
water in man. Amer. J. Physiol., 1950, 162: 318-325. [P] 
219. Brooks, M. C. and D. N. Marine. A study of oxygen 
consumption in obesity. Fed. Proc. Amer. Soc. exp. Biol., 
1946, 5: 12. 
220. Brozek, J., A. Henschel, and A. Keys. Effect of 
submersion in water on the volume of residual air in man. 
/. appl. Physiol, 1949, 2: 240-246. [P] 
221. Dupertius, C. W., G. C. Fitts, E. F, Osserman, 
W, C. Welham, and A. B. Behnke. The relation of spe- 
cific gravity to body build in a group of healthy men. 
U. S. Navy. NMRI. Project NM 004 006.03.06, 19 June 
1950, 11 pp. 
222. Dupertius, C, W., G. C. Pitts, E. F. Osserman, 
W. C. Welham, and A. R. Behnke. The relation of body 
water content to body build in a group of healthy men. 
U. S. Navy. NMRI. Project NM 004 006.03.07, 28 July 
1951, 7 pp. [P] 
223. Galvao, P. E. Human heat production in relation 
to body weight and body surface. III. Inapplicability of 
surface law on fat men of the tropical zone. IV. General 
interpretation of climatic influence on metabolism. J. appl. 
Physiol, 1950, 3: 21-28. 
224. Gersh, I., and M. A. Still. Relations of capillaries 
to fat cells. U. S. Navy. NMRI. Project X-284, Kept, 
no. 3, 12 September 1944, 10 pp. [P] 
225. McCance, R. A. and E. M. Widdowson. Composi- 
tion of the body. Brit. med. Bull, 1951, 7: 297-306. [R] 
226. Moore, F. D. Determination of total body water 
and solids with isotopes. Science, 1946, 104: 157—160. 
227. Morales, M. F., E. N. Rathhun, R. E. Smith, and 
N. Pace. Studies on body composition. II. Theoretical 
considerations regarding the major body tissue compo- 
nents, with suggestions for application to man. U. S. Navy. 
NMRI. Project X-191, Rept. no. 2, 7 August 1944, 8 pp. 
[P] 
228. Newlin, H. E. and C. M, McCay. Bone marrow for 
fat storage in rabbits. Arch. Biochem., 1948, 17: 125-128. 
[P] 
229. Osserman, E. F., G. C. Pitts, W. C. Welham, and 
A. R. Behnke. In vivo measurement of body fat and body 
water in a group of normal men. J. appl. Physiol, 1950, 
2: 633-639. Excerpta Medica. Section II. (Physiology, 
Biochemistry, and Pharmacology), 1951, 4: 841. 
230. Pace, N. Equations for the estimation of total body 
fat and total body water from the solubility of inert gases 
in the body. U. S. Navy. NMRI. Project X—191, Rept. 
no. 4, 25 September 1945, 7 pp. [M] 
231. Pace, N., L. Kline, H. K. Schachman, and M. 
Harfenist. Studies on body composition. IV. Use of radio- 
active hydrogen for measurement in vivo of total body 
water. J. biol. Chem., 1947, 168: 459-469. [P] LOW OXYGEN PERCENTAGES—SPECIAL SENSES 
232-238 
232. Rathbun, E. N. and N. Pace. Studies on body 
composition. The determination of total body fat by 
means of the body specific gravity. U. S. Navy. NMRI. 
Project X—191, Kept. no. 1, 7 August 1944, 8 pp. [P] 
233. Pace, N. and E. N. Rathbun. Studies on body com- 
position. III. The body water and nitrogen content in re- 
lation to fat content. U. S. Navy. NMRI. Project X—191, 
Kept. no. 3, 7 August 1944, 5 pp. [P] 
234. Sarkisian, S. S. The specific gravity of healthy 
men. A report of 835 cases. Nav. Med. Bull., Wash., 1946, 
46: 1207-1210.[P] 
235. Schloerb, P. R., B. J. Friis-Hansen, I. S. Edelman, 
A. K. Soloman, and F. D. Moore. The measurement of 
total body water in the human subject by deuterium oxide 
dilution. With a consideration of the dynamics of deu- 
terium distribution. /. din. Invest., 1950, 29: 1296-1310. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1951, 4: 1135. 
236. Steele, J. M., E. Y. Berger, M. F, Dunning, and 
B. B. Brodie. Total body water in man. Amer. J. Physiol., 
1950, 162: 313-317. [P] 
237. Steffensen, K. A. Some determinations of the total 
body water in man by means of intra-venous injections of 
urea. Acta physiol, scand., 1947,13: 282-290. 
238. Wertheimer, E. and B, Shapiro. The physiology 
of adipose tissue. Physiol. Rev., 1948, 28: 451-464. [R] 
III. PHYSIOLOGICAL EFFECTS OF LOW OXY- 
GEN TENSIONS OF ENVIRONMENTAL AIR 
A. LOW OXYGEN PERCENTAGES WITHOUT 
DECOMPRESSION 
1. SPECIAL SENSES 
Experimental and clinical findings as well as 
results of operational experience reveal a deteriora- 
tion of acuity of function of special senses under 
conditions of hypoxia. Continued submergence may 
lead to a reduction in oxygen percentage in the 
submarine air that may cause sensory loss. Only a 
few reports in this field are included here. 
Of interest experimentally are the lenticular opac- 
ities produced in rats and rabbits by hypoxia. These 
so-called hypoxic cataracts have been discussed by 
Morone and Citroni {246) 1950. These authors 
call attention to disturbances of anaerobic glycolysis 
of the crystalline lens both during and at the end of 
the opacification phase and even when no opacifica- 
tion occurs. Pretreatment did not alter the frequency 
of occurrence or severity of hypoxic cataracts. 
Scano, Bietti, and Schupfer {248) 1947, have 
studied the modifications of the retinal resolving 
power under conditions of hypoxia produced by the 
rebreathing method. There was a reduction of 6 
percent in the retinal resolving power until an oxy- 
gen percentage corresponding to an altitude of 
5,000 meters had been reached. At lower oxygen 
percentages a diminution of about 12 percent was 
observed. For a report on reduction of fusional am- 
plitude in human subjects breathing low oxygen 
mixtures (8.5 to 10 percent), a paper by Bietti and 
Giardini {239) 1949, may be consulted. Bietti and 
Scano {240) 1948, subjected normal subjects to 
hypoxia by breathing an air mixture containing 8.3 
percent oxygen. In these subjects there was an in- 
crease in the contraction speed of the pupil as well 
as the dilatation speed. Aniseikonia appeared as an 
inconstant finding. In some subjects the mydriatic 
pupil could not be excited. Changes in the visual 
field during oxygen deficiency have been reported 
by Ikui, Nakano, and Hosio {245) 1947, and Smith, 
Seitz, and Clark {249) 1946, have discussed varia- 
tions in the angioscotoma in response to prolonged 
mild anoxia. In these experiments subjects were 
exposed for I/2 hours in a low oxygen mixture cor- 
responding to an altitude of 10,000 feet. There was 
a progressive and significant increase in the size of 
scotoma observed. It became more marked at the 
end of I/2 hours. The time course of failure of the 
visual pathway in rabbits during nitrogen breathing 
has been reported by Noell and Chinn {247) 1949. 
In these studies the potentials resulting from illu- 
mination of the eye and from electrical stimulation 
of the optic nerve were recorded from different 
parts of the visual pathway. The curves for decline 
in responsiveness revealed complete unresponsive- 
ness at the surface of the striate area of the occipital 
cortex following either photic or electrical stimuli 
after 88 seconds of nitrogen breathing. For further 
studies of the effect of hypoxia upon the visual 
mechanism, papers by Giulio {243 and 244) 1948, 
may be consulted. 
Wever, Lawrence, Hemphill, and Straut {250) 
1949 have examined the effects of oxygen depriva- 
tion upon the cochlear potentials. They measured 
electrical potentials generated in the cochlea during 
stimulation with sound (1,000 cycles) under normal 
conditions and in the course of oxygen deprivation. 
Cats under Dial anesthesia were curarized to the 
point where reflexes were absent and spontaneous 
respiration ceased. They were maintained by artifi- 
cial respiration. Cochlear potentials were picked up 
from the membrane of the round window and meas- 
ured by a selective voltmeter. Low oxygen mixtures 
produced a progressive deterioration of the poten- 
tials, and there was a delay in recovery of such 
potentials after air breathing was reestablished. 
Bornschein and Krejci {241) 1950 in experiments 
on guinea pigs also showed a depression of the 
cochlear potentials during hypoxia. They found 
that this depression is independent of the frequency 
of the auditory stimuli. The sensitivity of the corti- 
cal auditory projection area to hypoxia has been 
investigated by Gellhorn {242) 1951. In these ex- 
periments cats were subjected to an air mixture 
containing 7.5 percent oxygen. The auditory and 239-250 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
visual cortical potentials were found to be about 
equally sensitive to hypoxia. Breathing oxygen- 
nitrogen mixtures containing 7.5 percent oxygen 
led to a distinct and nevertheless reversible diminu- 
tion of the visual and auditory responses due 
apparently to a reduction in the number of respond- 
ing neurons. 
239. Bietti, G. B. and A. Giardini. Influenza dell’ anos- 
sia sui movimenti oculari. III. Azione della anossia acuta 
sul potere di fusione delle immagini retiniche. Riv. Med. 
aero., Roma, 1949,12: 339-349. [P] 
240. Bietti, G. and A. Scano. Ricerche di pupillografia 
in anossia. Riv. med. aero., Roma, 1948, II: 177—209. 
(English, French, Spanish, and German summaries.) [P] 
241. Bornschein, H. and F. Krejci. Uber die Frequen- 
zabhangigkeit reversibler Anderungen der Cochlearpoten- 
tiale bei temporarer Anoxie. Experientia, 1949, 5: 359- 
360. Excerpta Medica. Section II. (Physiology, Biochem- 
istry, and Pharmacology), 1950,3: 944. 
242. Gellhorn, E. Sensitivity of the auditory projection 
area to anoxia. Amer. J. Physiol., 1951, 164: 748-751. [P] 
243. Giulio, L, La verticale ottica apparente durante 
la respirazione con miscele al 10 e al 7% di 02. Boll. Soc. 
ital. Biol, sper., 1948, 24: 789-790. Riv. Med. aero., Roma, 
1949, 12: 16-27. Excerpta Medica. Section II. (Physi- 
ology, Biochemistry, and Pharmacology), 1949, 2: 793. 
Abstr. 
244. Giulio, L. Modification! nella capacita di fissozione 
al limiti estremi del campo di squardo, curante le 
respirazione con miscele al 7-8% di 02. Boll. Soc. ital. 
Biol, sper., 1948, 24: 791—792. Excerpta Medica. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1949, 
2: 793. Abstr. [P] 
245. Ikui, H., K. Nakano, and S. Ohsio. [The effect of 
oxygen deficiency on the visual function and changes in 
the visual field during the oxygen deficiency.] Rinsyo & 
Kenkyo, 1947,24: 250. (English pagination.) [P] 
246. Morone, G. and M. Citroni. Indagini sugli intor- 
bidamenti lenticolari da anossia. Riv. Med. aero., Roma, 
1950, 13: 655-672. (English, French, Spanish, and 
German summaries.) 
247. Noell, W. K. and H. I. Chinn. Time course of 
failure of the visual pathway in rabbits during anoxia. 
Fed. Proc. Amer. Soc. exp. Biol., 1949, 8: 119. 
248. Scano, A., G. B. Bietti, and F. Schupfer. Influenza 
dell’anossia sul potere risolutivo retinico. Rev. Med. aero., 
Roma, 1947, 10: 490-498. (Italian, English, French, 
Spanish, and German summaries.) 
249. Smith, G. M., C. P. Seitz, and K. B. Clark. Varia- 
tions in the angioscotoma in response to prolonged mild 
anoxia. /. Aviat. Med., 1946, 17: 590-595. [P] 
250. Wever, E. G., M. Lawrence, R. W. Hemphill, and 
C. B. Straut. Effects of oxygen deprivation upon the 
cochlear potentials. Amer. ]. Physiol, 1949, 159: 199-208. 
[P] 
2. NERVOUS SYSTEM 
Effects of hypoxia on peripheral nerve activity 
have been reported by the following: Aykut and 
Winterstein {251) 1950; Beyne, Chauchard, and 
Chau chard (252) 1948; Fenn and Gerschman 
(269) 1950; and Laget, Lavigne, and Gaillard 
(279) 1951. 
The effect of asphyxia on the monosynaptic path- 
way through the spinal cord has been investigated 
by Brooks and Eccles {255) 1947. Changes were 
observed in the monosynaptic pathway obtained by 
means of a needle electrode in the quadriceps nu- 
cleus at the rostral end of the sixth lumbar segment 
of the cord. Orthodromic volleys were excited by 
way of the sixth dorsal root or the nerve to the quad- 
riceps after severance of motor fibers. Antidromic 
excitation was produced by stimulation of the deaf- 
ferented quadriceps nerve of the sixth ventral root. 
Asphyxia produced by stopping the artificial respi- 
ration, causing the heart to fail, or clamping the 
thoracic aorta gave brief depression followed by a 
period of hyperexcitability attributable to depolari- 
zation of the membranes of the afferent nerve fibers 
and the motoneurone somas. Continued asphyxia- 
tion caused progressive depolarization with final 
failure of impulse propagation. The effect of anoxia 
and hypoxia as well as carbon dioxide upon the 
monosynaptic and multisynaptic reflex discharges 
in spinal and decerebrate cats was investigated by 
Kirstein {278) 1950. Monosynaptic and multisynap- 
tic reflex volleys in the ventral roots at the seventh 
lumbar and first sacral levels elicited by stimulation 
of the afferent fibers from the gastrocnemius and 
anterior tibial muscles and the sural nerve were 
examined. Both in anoxia produced by administra- 
tion of pure nitrogen, and in ischemia produced by 
clamping the abdominal or thoracic aorta, the mon- 
osynaptic reflex showed an initial depression fol- 
lowed by a period of augmentation. In long-stand- 
ing anoxia and ischemia the reflex was eventually 
depressed. In some experiments the initial decrease 
was preceded by a transient facilitation. Interrup- 
tion of anoxia or ischemia during the period of 
maximal facilitation brought about an immediate 
depression of the reflex. The multisynaptic response 
behaved differently, showing a gradual depression 
sometimes preceded by a transient augmentation. 
The depression of the multisynaptic reflex always 
occurred later than the initial depression of the 
monosynaptic reflex. Both anoxia and ischemia 
gave the same results, indicating that the effects 
observed were due to oxygen deficit and not to 
carbon dioxide excess. A mixture of 7.9 percent 
oxygen in nitrogen produced only depression in 
nearly all cases. A mixture of 8.9 percent carbon 
dioxide in oxygen caused pure depression in all 
cases. With both mixtures, the depressant effect was 
more pronounced in the monosynaptic than in the 
multisynaptic reflex system. In the studies of Brooks 
and Eccles {255), oxygen lack (7 to 10 percent 
oxygen) had the same effect as asphyxia except for IOW OXYGEN PERCENTAGES—NERVOUS SYSTEM 
absence of early transient depression of activity 
which precedes the phase of hyperexcitability. Sud- 
den readmission of oxygen during the period of 
asphyxial or anoxic hyperexcitability resulted in 
depression. Carbon dioxide excess (11 to 14 per- 
cent) produced pure depression of the monosynap- 
tic pathway in Brooks and Eccles’ experiments. 
Accumulation of carbon dioxide was seen to explain 
early depression in asphyxia. 
Gellhorn (27/) 1943 has pointed out that when 
animals are subjected to progressive degrees of 
hypoxia, there is first a respiratory reaction (in- 
crease in ventilation) and that only with more 
severe degrees of hypoxia does the blood pressure 
rise. Experiments indicated that the chemoreceptors 
act more efficiently on the respiratory than on the 
vasomotor center. If the carotid sinus is removed, 
the animal shows respiratory failure which is ac- 
companied by a striking fall in blood pressure. If 
the respiratory failure is prevented by artificial 
respiration in an animal with pneumothorax, the 
blood pressure rises in hypoxia. Chemoreceptors 
from the sinoaortic area excite both vasomotor and 
respiratory centers. The two centers are different 
inasmuch as the removal of the carotid sinuses alone 
produces respiratory failure in hypoxia whereas, in 
order to obtain a similar failure of the vasomotor 
apparatus (fall of blood pressure in anoxia), all 
four buffer nerves must be removed. In spite of the 
depression of the vasomotor center in hypoxia it 
still reacts with a slight rise in blood pressure to 
stimulation from higher parts of the central nervous 
system. The depressor reflexes are weakened in 
hypoxia. Hypoxia may produce a syndrome similar 
to that observed in orthostatic hypotension. The 
blood flow through the extremities in hypoxia is the 
resultant of the centrally controlled vasoconstriction 
and the local dilating effect. The former predomi- 
nates particularly under more severe degrees of 
hypoxia. The tissues incur an oxygen debt which is 
paid off after readmission of air. The significance 
of the excitation of the sympathetic system lies in 
the rise in blood pressure which provides a more 
adequate circulation to the brain and heart at the 
expense of the extremities and of the visceral organs. 
This action on the brain is supplemented by the 
dilating effect of hypoxia on the brain vessels. The 
sympathetic effects are intensified by the secretion 
of adrenalin. 
Hypoxia leads to a lowering of the temperature 
of the body. This reaction greatly increases resist- 
ance to hypoxia, since hypoxia more rapidly be- 
comes fatal when the lowering of the body tem- 
perature is prevented. In a further report on the 
medulla oblongata in hypoxia, Gellhorn (272) 
1948, concluded from the physiological literature 
that in chronic hypoxia respiration and possibly 
blood pressure are regulated through the medullary 
centers alone. These data were adduced to explain 
how even mild degrees of chronic hypoxia may 
have fatal effects if they act on diseased medullary 
neurons. In experiments of Malmejac and Chardon 
{284) 1946, dogs breathed an air mixture contain- 
ing 6 to 10 percent oxygen in nitrogen with the 
carotid sinuses denervated. In some experiments 
crossed circulation was established with a donor 
dog. These studies of the resistance to hypoxia of 
the respiratory center, the vasomotor center, and 
adrenal secretions showed that the latter is most 
resistant to hypoxia. In the terminal phase the 
respiratory center was most vulnerable; cessation 
of respiratory movements preceded the beginning 
of severe terminal cardiovascular effects. In a fur- 
ther series of experiments, Malmejac, Chardon, Ne- 
verre, and Fontanille (289) 1948, found that, in 
dogs inhaling air containing only 4 percent oxygen, 
there was a diminution of carotid sinus excitability 
during the first stage, but in the second stage syncope 
of the respiratory center predominated. According 
to Gordier and Cordier (258) 1950, there was no 
alteration of the sensitivity of the respiratory center 
during hypoxia (oxygen concentrations of 4.26 to 
8.60 percent) in animals deprived of the chemo- 
receptors and the stellate ganglia and inferior 
cervical ganglia. 
Effects of hypoxia on the vasomotor center have 
also been reported by Malmejac, Chardon, and 
Gross (285, 286, 287, and 288) 1948. The carotid 
sinus in hypoxia is considered to play a double role, 
mechanical and chemical, the latter being much 
more important and more durable (285). The 
vasoconstrictor reactions are nervous in origin. The 
chemical action of the carotid bodies causes a 
peripheral vasodilatation and a central vasocon- 
striction. Sudden hypoxia may cause a transient 
excitation of the vasomotor centers. To demonstrate 
this central action, Malmejac, Chardon, and Gross 
(285) used a dog in which one of the hind legs was 
perfused by a donor. The dog was curarized and its 
vasodepressor nerves cut and artificial respiration in- 
duced. At a given moment a mixture of nitrogen 
and oxygen was substituted for the air in the respi- 
rator. Under these conditions it was seen that 1 to 3 
minutes after respiration of a mixture with 2 to 3 
percent oxygen, the perfused hind limb showed a 
vasoconstriction. Respiration of mixtures with more 
than 5 to 6 percent oxygen did not cause this effect. 
The same authors (287) pointed out that oxygen SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
lack ultimately produces a progressive breakdown 
of the vasomotor centers. In the terminal stages of 
hypoxia the vasocontrictor tone of central origin is, 
however, sometimes reestablished. 
In a discussion of the brain and the symptoma- 
tology of hypoxia, Himwich (275) 1949, gives evi- 
dence of the high sensitivity of the upper cortical 
centers to oxygen lack. If one accepts the concept 
of a metabolic gradient in the central nervous sys- 
tem, it follows that not all parts of the brain will be 
equally affected by hypoxia, but that those regions 
with the highest metabolic rates will succumb first 
and those with the lowest will be last. Gradual pro- 
gression down the phyletic centers reveals the release 
of control of cortical areas giving unhampered ex- 
pression to lower centers. During a slow, progressive 
hypoxia, contact with the environment is first lost. 
There is then aimless motor restlessness followed by 
torsional spasms and then tonic spasms with flexion 
of the arms and extension of the legs as the mid- 
brain is released. Finally opisthotonus is seen. Cold, 
clammy skin follows, with a feeble heart, depressed 
respiration, and finally muscular flaccidity. 
For further study of differential effects of hypoxia 
upon the nervous system, reports by Noell and Chinn 
{291) 1950 and (292) 1951, maybe consulted. In 
rabbits, potentials were recorded from different 
parts of the visual pathway in response to flashes of 
light into the eye and to electrical stimulation at 
various levels during suddenly induced anoxia. In- 
excitability involved first the cortex, next the 
geniculate bodies, then the retinal ganglian cells, 
then the bipolar cells, and finally the photorecep- 
tors. The propagation of excitation towards the 
bipolar cell level induced by a light stimulus sur- 
vived anoxia for about 20 minutes as indicated by 
the appearance of an electronegative retinogram. 
The measured survival time of the retinal ganglian 
cells was about 5 minutes; that of the geniculate 
cells and the most resistant cortical neurons about 2 
minutes. When strong light stimulus was applied, 
conduction across the retinal ganglian cell layer 
was nearly as resistant to anoxia as optic nerve con- 
duction. Similarly, conduction across the geniculate 
synapses failed only slightly earlier than conduction 
of the geniculocortical fibres. Summation, facilita- 
tion, or inhibition were in many instances early 
affected by anoxia. The authors suggested that the 
rapidity with which a central mechanism involving 
numerous neuronal chains is impaired by anoxia 
depends largely upon properties of its functional 
organization rather than on the true anoxic resist- 
ance of its neuronal members as measured by 
inexcitability or blockage of impulse conduction. 
The effect of anoxia upon electrically induced 
convulsions has been investigated in rabbits by 
Dahlberg-Parrow (265) 1951. It was found that 
hypercapnia produced by pretreatment for 5 min- 
utes with 12 percent carbon dioxide in oxygen pro- 
longed the flexion stage of the gastrocnemius muscle 
in electrically induced convulsions and shortened 
the subsequent extensor phase. The total tonic phase 
was shortened. Conversely, the succeeding clonic 
phase was prolonged and a clonic phase produced 
in animals normally having none. Under anoxia 
(pretreatment for 10 seconds with 100 percent 
nitrogen) the tonic phase was shorter and in most 
animals the clonic phase was absent. The duration 
of seizure was shortened markedly by anoxia in 
animals normally having no clonic phase or only a 
short one. The author concluded that in such ani- 
mals central anoxia may be the factor for discontin- 
uation of convulsive activity. Gellhorn and Hey- 
mans (273) 1948, found in cats and dogs that in- 
halation of 4 percent oxygen in nitrogen abolished 
convulsive potentials from the cortex at a time when 
normal potentials were practically unchanged. On 
readmission of air, normal potentials were found to 
appear in previously convulsive areas before con- 
vulsive spikes reappeared. Asphyxia induced by 
cessation of artificial respiration likewise abolished 
spikes before normal potentials and lead to earlier 
reappearance of the latter on readmission of air. 
The data indicated to the authors that hypoxia and 
asphyxia induce progressive decruitment of cortical 
cells and reoxygenation a progressive recruitment. 
The limiting factor which determines the number 
of discharging neurons and degree of their activity, 
whether convulsive or nonconvulsive, seems to be 
the supply of oxygen. Restitution of normal oxygen 
supply after hypoxia or asphyxia is often accom- 
panied by a rebound phenomenon with convulsive 
potentials appearing which were absent under con- 
trol conditions. Regarding the effects of low oxygen 
on the cortical potentials as recorded in the electro- 
encephalogram or the electrocorticogram, Brazier 
(254) 1946, found in human subjects that lowering 
the oxygen concentration of the inspired air slowed 
the rate of cortical potentials. The slowing was 
greater the lower the oxygen level. The greatest 
slowing occurred when both the oxygen and carbon 
dioxide content were low. The electroencephalo- 
grams of psychoneurotic patients showed a greater 
degree of slowing than did those of normal adults, 
suggesting a more labile metabolic process in the 
cortical cells of psychoneurotic patients than in nor- 
mal persons. Iwama (277) 1950-51, also reported 
changes in the electroencephalogram in human LOW OXYGEN PERCENTAGES—NERVOUS SYSTEM 
subjects breathing low oxygen mixtures. In these 
studies the subjects breathed 6 or 7 percent oxygen 
for 5 minutes. Within a minute after the start of the 
hypoxic period, small, rapid waves appeared. Two 
to three minutes later, there were slow, large delta 
waves appearing in groups. The mean amplitude 
increased rapidly. The final stage contained almost 
all delta waves. In oxygen lack of slight degree, the 
potentials were markedly suppressed at an early 
stage. In rabbits exposed to a 12-percent oxygen 
mixture, the electrocorticogram showed an in- 
creased amplitude of the predominant rhythm with 
a frequency of about 5 cycles per second from studies 
reported by Crossland and Richter (264) 1950. 
Hypoxia in these experiments produced a fall in 
brain acetylcholine. 
For studies of the effect of hypoxia upon psycho- 
logical functions, papers by the following may be 
consulted: Fabre and Rougier (267) 1946, Fletcher 
(270) 1945, Lovett-Doust (281) 1951, Smith (298) 
1946, Smith and Seitz (299), 1946, and Waldfogel, 
Finesinger, and Verzeano (302) 1950. A report on 
the effect of low oxygen on psychological perform- 
ance tests in psychoneurotic patients and normal 
control subjects has been given by Waldfovel, Fine- 
singer, and Verzeano (302) 1950. Psychoneurotic 
patients and control subjects were given psycho- 
motor tests while breathing 21 percent oxygen and 
while breathing 10 percent oxygen, the total period 
of exposure to low oxygen tension being about 20 
minutes. The average performance in both the pa- 
tients and the control groups dropped in almost 
every instance despite the counteracting effects of 
practice. This general downward trend is consistent 
with other studies of the effects of hypoxia upon 
performance. The control subjects dropped more 
on the reaction time tests while the patients showed 
a greater drop on the tapping speed and stylus tests. 
However, when the two groups were compared di- 
rectly with one another in regard to the amount of 
change produced by hypoxia, it was found that 
there was no statistically significant difference be- 
tween them. The two groups were compared also 
as to the appearance of physical symptoms. It was 
found that they were very much alike in type, fre- 
quency, and severity of symptoms reported. The 
only difference was that the controls seemed to ex- 
perience headaches and giddiness more frequently, 
while the patients experienced more difficulty in 
breathing and more tremor and unsteadiness. Smith 
and Seitz (299) 1946 and Smith (298) 1946 have 
shown that hypoxia produced by breathing low 
oxygen mixtures results in deterioration in speech 
intelligibility. In subjects exposed to oxygen mix- 
tures simulating an altitude of 10,000 feet for an 8- 
hour period, the decrement in speech intelligibility 
was slight and unreliable at the 45-minute period. 
There were more marked effects at the 2*4- and 
4%-hour periods and considerable lessening of the 
altitude effect hours after entering the chamber. 
The tests indicated that the loss of efficiency under 
the conditions of the experiments was primarily 
due to subjective factors such as wandering atten- 
tion and boredom. The subjects reported that there 
was an increase in somnolence and greater boredom 
in the altitude runs than in the control runs. It 
thus seems apparent that even relatively mild de- 
grees of hypoxia may result in significant losses of 
speech intelligibility which may affect performance. 
For studies of the pathological effects of hypoxia 
upon the nervous system, papers by the following 
should be consulted: Courville (259, 260 and 261) 
1947, Courville (262 and 263) 1950, Douglas (266) 
1949, Morrison (290) 1946, Petrov (294) 1949, 
and Plambeck (295) 1950. In a series of contri- 
butions to the study of cerebral hypoxia, Courville 
(259-263) has described pyknotic changes, lique- 
faction, vacuolation, and lipoid degeneration in 
nerve cells. Interstitial cells are less affected. In 
acute cases, small, perivascular hemorrhages are 
often found. The cortex and basal ganglia and the 
choroid plexus and pia mater are filled with blood. 
Courville has pointed out (263) that the effect of 
hypoxia on the nervous system is not generalized, 
but that certain areas are more susceptible than 
others. These susceptible areas include the globus 
pallidus and other nuclei of the basal ganglia. The 
pathological changes in the basal ganglia may be 
designated as the key lesion of hypoxia. Some 
transitory and reversible effects of hypoxia may be 
evidenced by Parkinsonian manifestations and 
emotional flattening. This may disappear after 
weeks or months. Chronic exposures result in 
changes in the myelin sheaths, the demyelinization 
being patchy and the sheaths swollen. It appears 
that the hypoxic state provokes a vascular spasm 
of sufficient duration to result in physical changes 
in the myelin sheaths. In reporting histopathologi- 
cal changes in the brain of a man deprived of 
oxygen for a period of 5 to 10 minutes, Douglas 
(266) 1949 described severe degenerative changes 
in the cerebral cortex (particularly in the motor 
and visual areas), in the putamen, and in the cere- 
bellum. In both the precentral and visual cortex 
there was considerable softening. In dogs and 
monkeys exposed to hypoxia for considerable 
periods, Morrison (290) 1946 found that the de- 
gree and duration of hypoxia is correlated with 
progressive necrosis and cellular exhaustion. The 
first histological changes occur in the granular cells 
291222—54 3 251-278 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
of the supragranular layer of the cortex at a level of 
about 12 or 13 volumes percent of oxygen in the 
blood. At 10 volumes percent and down to 4.5, 
there was progressive chromato lysis, swelling, 
vacuolation, and massive laminar necrosis in the 
gray matter, and at this point the white matter 
showed signs of blanching, demyelinization, gitter 
cell formation, and microglial hyperplasia. There 
was a certain amount of reversibility upon restora- 
tion of normal oxygen tension. The order of effect 
in decreasing severity was found to be: the frontal 
lobe, the parietal lobe, the occipital lobe, the tem- 
poral lobe, the basal ganglia, and the cerebellum. 
No injury to the cord was observed at oxygen 
tensions compatible with life. 
For further studies on the physiological and 
pathological effects of low oxygen pressures on the 
nervous system, papers by the following may be con- 
sulted: Binet and Strumza (255) 1950, Callebaut, 
Rodbard, and Katz (256) 1950; Cerletti and Kal- 
lenberger (257) 1948; Fender, Neff, and Binger 
(265) 1946; Grenell and Rabat {274) 1947; lan- 
dolo (276) 1947; Loeschcke (256) 1948-49; 
Lowenback (252) 1951; Lucas (255) 1946; Petrov 
(265) 1949; Royer and Thiebaux (266) 1951; 
Sloan (267) 1950; Steegmann (566) 1951; and 
Volochov and Obraszova {301) 1950. 
251. Aykut, R. and H. Winterstein. Anoxybiose des 
Froschnerven in sauerstoffreien Losungen. Arch. int. 
Pharmacodyn., 1950, 81: 222—229. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1950, 3: 1085. 
252. Beyne, J., B. Chauchard, and P. Chanchard. In- 
fluence sur 1’excitabilite nerveuse de 1’homme des varia- 
tions de tension des gaz dans 1’air respire. Application a 
1’etude des troubles nerveux en depression atmospherique. 
Med. aeronaut., 1949, 3: 3-25. [P] 
253. Binet, L. and M. V. Strumza. Variations du taux 
du C02 total du plasma arteriel et resistance des centres 
respiratoires a 1’anoxie. /. Physiol., Paris, 1950, 42: 249- 
258. 
254. Brazier, M. A. B. Studies related to the physiology 
of flight: The effect of anoxia on the electroencephalo- 
gram in psychoneurotic and normal adults. /. nerv. ment. 
Dis., 1946, 104: 688-694. 
255. Brooks, C. M. and J. C. Eccles. A study of the 
effects of anaesthesia and asphyxia on the mono-synaptic 
pathway through the spinal cord. /. N euro physiol., 1947, 
10: 349-360. [P] 
256. Callebaut, C., S. Rodbard, and I. N. Katz. Sensi- 
tivity of the supraventricular pacemakers to acetylcholine 
in acute hypoxemia. Circulation, 1950, 1: 712-716. [P] 
257. Cerletti, A. and A. Kallenberger. fiber die 
Bereinflussung der Hypoxie-probe am Menschen durch 
pharmakodynamische Sympathicdyse. Helv. physiol, acta, 
1948, 6: 795-806. [P] 
258. Cordier, D, and G. Cordier. Influence de la 
stellectomie sur la resistance a 1’anoxie progressive des 
chiens prives de leurs chimiorecepteurs reflexogenes. C. R. 
Soc. Biol., Paris, 1950, 144: 1375-1376. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1951, 4: 1129. [P] 
259. Courville, C. B. Cerebral anoxia and its residuals. 
I. Historical introduction. Med. Arts Sci., 1947, I: 16-27. 
260. Courville, C. B. Cerebral anoxia and its residuals. 
II. Respiration, normal and pathological. Med. Arts Sci., 
1947, 1: 35-44. 
261. Courville, C. B. Cerebral anoxia and its residuals. 
III. The structural changes. Med. Arts Sci., 1947, 1: 
67-78.[D] 
262. Courville, C. B. Contributions to the study of 
cerebral anoxia. I. Asphyxia in legend, folklore and his- 
tory. Bull. Los Angeles neural. Soc., 1950, 15: 99-128. [C] 
263. Courville, O. B. Contributions to the study of 
cerebral anoxia. II. The mechanism and nature of conse- 
quent structural alterations. Bull. Los Angeles neural. Soc., 
1950,15: 129-154. [R] 
264. Crossland, J, and D. Richter. Relation of func- 
tional activity of the brain to its acetylcholine content in 
anoxia. XVIII Intern, physiol. Congr., 1950, 170-171. 
265. Dahlberg-Parrow, R. The effect of hypercapnia 
and hypoxia on electrically induced convulsions in rabbits. 
Acta physiol, scand., 1951,23: 55-63. 
266. Douglas, A. S. Cerebral changes related to anoxia, 
with report of a case, Canad. med. Ass. J., 1949, 61: 123- 
129. [CH] 
267. Fabre, R. and G. Rougier. Les perturbations de 
1’activite volontaire et de la conscience provoquee par une 
anoxemie subtotale et rapide. Arch. int. Physiol., 1946, 
54: 156-160. [D] 
268. Fender, F. A., W. B. Neff, and G. Binger. Con- 
vulsions produced by fetal anoxia; experimental study. 
Anesthesiol., 1946, 7: 10-13. 
269. Fenn, W, 0. and R. Gerschman. The loss of 
potassium from frog nerves in anoxia and other conditions. 
/. gen. Physiol., 1950, 33: 195-204. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharma- 
cology), 1950,5; 1084. 
270. Fletcher, D. E. Personality disintegration incident 
to anoxia; observations with nitrous oxide anesthesia. 
/. nerv. ment. Dis., 1945, 102: 392-403. 
271. Gellhorn, E. Adjustment reactions to anoxia, pp. 
37-53 in: Autonomic regulations. Their significance for 
physiology, psychology and neuropsychiatry. New York, 
Interscience Publishers, Inc., 1943, 308 pp. 
272. Gellhorn, E. The medulla oblongata in anoxia. 
Arch. phys. Med., 1948, 29: 88-91. [R] 
273. Gellhorn, E. and C. Heymans. Differential action 
of anoxia, asphyxia and carbon dioxide on normal and con- 
vulsive potentials. /. Neurophysiol., 1948, 11: 261-273. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1950, 3: 87. 
274. Grenell, R. G. and H. Rabat. Central nervous 
system resistance. II. Lack of correlation between vascu- 
larity and resistance to circulatory arrest in hypothalmic 
nuclei. /. Neuropath, 1947, 6: 35-43. 
275. Himwich, H. E. The brain and the symptomatology 
of the anoxias. Anesthesiology, 1949, 10: 663-672. [D] 
276. landolo. G. Sul concetto de “anossia aglicidica.” 
Boll. Soc. ital. Biol, sper., 1947, 23: 1197-1199. 
277. Iwama, K. The influence of oxygen lack on brain 
waves in man. Tohoku J. exp. Med., 1950/51, 52-53: 
63-68. [P] 
278. Kirstein, L. The effect of anoxia, hypoxia and 
carbon dioxide on the monosynaptic and multisynaptic 
reflex discharges in spinal and decerebrate cats. XVIII 
Intern, physiol. Congr., 1950, 304. LOW OXYGEN PERCENTAGES—HEART AND CIRCULATION 
279-302 
279. Laget, P., S. Lavigne, and R. Gaillard. Contri- 
bution a 1’etude electrophysiologique de Panoxie du nerf 
de mammifere. C. R. Soc. Biol., Paris, 1950, 144: 1602- 
1604. 
280. Loeschcke, H. H. Plotzlicher Tod durch Sauers- 
toffmangel. Dtsch. Z. ges. gerichtl. Med., 1948/49, 
39: 480-486. [P] 
281. Lovett-Doust, J. W. Studies in the physiology of 
awareness: oximetric evidence of the role of anoxia in 
certain psychiatric states. Proc. R. Soc. Med., 1951, 
44: 347-352. [CH] [P] 
282. Lowenbach, H. Hypoxemia and the temperature 
of the hypothalamus of the cat. J. Neuropath, exp. Neurol., 
1951, 10: 67—76. Excerpta Medica. Section II. (Physiol- 
ogy, Biochemistry, and Pharmacology), 1951, 4: 1439. 
283. Lucas, G. B. Anoxia and the central nervous 
system: an experimental and clinical study. Thorax, 1946, 
1: 128-142. 
284. Malmejac, J. and G. Chardon. Resistance des 
centres respiratoires vasomoteurs et adrenalino-secreteurs 
a Panoxie. Med. aeronaut., 1946, 1: 344-350. [P] 
285. Malmejac, J., G. Chardon, and A. Gross. Role des 
sinus carotidiens dans le declenchement des reactions vas- 
culaires en anoxie. Algerie med., 1948, 51: 36-38. [D] 
286. Malmejac, J,, G. Chardon, and A. Gross. Sur 
Paction vaso-motrice d’origine centrale du deficit en oxy- 
gene. C. R. Soc. Biol., Paris, 1948, 142: 682-684. Excerpta 
Medica. Section II. (Physiology, Biochemistry and Phar- 
macology), 1949, 2: 493. [P] 
287. Malmejac, J., G. Chardon, and A. Gross. Sur le 
determinisme complexe des reactions vasomotrices d’ori- 
gine centrale dans la periode terminale de Panoxie. C. R. 
Soc. Biol., Paris, 1948, 142: 678—680. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1949,2:492. [P] 
288. Malmejac, J., G. Chardon, and A. Gross. Ex- 
citation des centres vasomoteurs medullaires par le deficit 
en oxygene. C. R. Soc. Biol., Paris, 1948, 142: 1102-1104. 
[P] 
289. Malmejac, J., 6. Chardon, G. Neverre, and P. 
Fontanille. Roles respectifs des fatigues sinusienne et 
nerveuse centrale dans la production de la defaillance 
respiratoire en anoxie. C. R. Soc. Biol., Paris, 1948, 142: 
1525-1528. [P] 
290. Morrison, L. R. Histopathologic effect of anoxia 
on the central nervous system. J. industr. Hyg., 1946, 28: 
abstract section: 83. Arch. Neurol., Psychiat., Chicago, 
1946,55: 1-34. [P] 
291. Noell, W. and H. I. Chinn. Failure of visual path- 
way during anoxia. Amer. J. Physiol., 1950, 161: 573- 
590. [P] 
292. Noell, W. K. and H. I. Chinn. The effect of anoxia 
on excitatory mechanisms of the retina and the visual 
pathway. USAF. Randolph Field, Texas. School of avia- 
tion medicine. Project 21-23-012, Final Rept. (formerly 
Project 21-02-111), January 1951,43 pp. [P] 
293. Petrov, I. P. Anemiia golovnogo mozga; zakliu- 
chenie. [Anemia of the cerebrum: conclusion.] pp. 85-98 
in: Kislorodnoe golodanie golovnogo mozga; eksperimen- 
tal’nye materialy. [Oxygen deficiency of the cerebrum; 
experimental material.] Leningrad, Medgiz, 1949, 204 pp. 
294. Petrov, I. P. Sravnitel’nye morfologichesie i funkt- 
sional’nye izmeneniia golovnogo mozga u ozhivlennikh 
zhivotnykh. [Comparative morphologic and functional 
changes in the brain of revived animals.] pp. 127-129 in; 
Kislorodnoe golodanie golovnogo mozga; eksperimentaV- 
nye materialy. [Oxygen deficiency of the cerebrum; experi- 
mental material.] Leningrad, Medgiz, 1949, 204 pp. 
295. Plambeck, H. Veranderungen des menschlichen 
Gehirms bei chronischem und akutem allgemeinem Sauer- 
stoffmangel. Beitr. path. Anat., 1950, 111: 77-94. [CH] 
296. Royer, P. and R. Thiehaux. L’anoxie cerebrale 
provoquee en therapeutique psychiatrique. Rev. med., 
Nancy, 1951, 76: 372-378. 
297. Sloan, H. E. The vagus nerve in cardiac arrest; 
the effect of hypercapnia, hypoxia, and asphyxia on reflex 
inhibition of the heart. Surg. Gynec. Obstet., 1950, 91: 
257-264. [P] 
298. Smith, G. M, The effect of prolonged mild anoxia 
on speech intelligibility. /. appl. Psychol., 1946, 30: 
255-264. [P] 
299. Smith, G. M. and C. P. Seitz. Speech intelligibility 
under various degrees of anoxia. /. appl. Psychol., 1946, 
30: 182-191. [P] 
300. Steegmann, A. T. Clinical aspects of cerebral 
anoxia in man. Neurology, 1951, 1: 261—274. [D] 
301. Volochov, A. A. and G. A. Obraszova. [Influence of 
anoxia on the nervous system; change of respiratory func- 
tions in anoxia.] Fiziol. Zh. S. S. S. R., 1951, 36: 545-551. 
(Russian text). 
302. Waldfogel, S., J. E. Finesinger, and M. Verzeano. 
The effect of low oxygen on psychologic performance tests 
in psychoneurotic patients and normal controls. Psy- 
chosom. Med., 1950, 12: 244-249. 
3. MUSCULAR ACTIVITY 
Daoud and Wilson {303) 1950, have shown that 
subjects breathing air containing 12 percent oxygen 
suffer a definite loss in muscular strength, as meas- 
ured by the pressure of a squeezed ball held in the 
hand. There is loss both of the strength of an initial 
maximal effort and a muscular effort sustained for 
1 minute. This decrement becomes very striking 
at oxygen percentages below 9 percent, and with 
8 percent there is 100 percent loss. For studies on 
the effect of complete anoxia on contractility and 
metabolism of intestinal smooth muscle, two papers 
by Furchgott and Shorr {304, 305) 1950 and 1948 
may be consulted. 
303. Daoud, F. and W. H. Wilson. The capacity to 
maintain a sustained effort under normal and anoxic 
conditions. /. Egypt, med. Ass., 1950, 33: 181-193. [P] 
304. Furchgott, R. F. and E. Shorr. Effect of anoxia 
on contractility and metabolism of intestinal smooth 
muscle. Amer. J. Physiol., 1950, 162: 88-98. [P] 
305. Furchgott, R. F. and E. Shorr, Effect of anoxia 
on contractility and metabolism of intestinal smooth 
muscle. Fed. Proc. Amer. Soc. exp. Biol., 1948, 7: 38-39. 
[P] 
4. HEART AND CIRCULATION 
Early cardiovascular responses to hypoxia involve 
changes which tend to compensate for reduced oxy- 
gen tension and enhance circulatory efficiency. 
There may be acceleration of the pulse, increased 
cardiac output, elevation of systemic arterial blood 
pressure, and vasoconstriction in certain viscera. SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
When the degree of hypoxia exceeds the limits of 
toleration, cardiovascular collapse supervenes. 
The effects of hypoxia upon the electrocardio- 
gram have been widely investigated. A few selected 
reports are included here {316, 326, 338, 351 and 
356). Of interest is a report by Hoyos {338) 1949 in 
which rabbits wei’e exposed to sudden anoxia by 
various drastic methods. There was first a sinus 
tachycardia with a normal or shortened P-R inter- 
val. This was succeeded by sinus brady-cardia with 
prolonged P-R interval and deviation of the S-T 
segment. In the final agonal stages, the QRS com- 
plexes become monophasic, large and wide. Some- 
times a partial A-V block was found. The first 
phase of sinus tachycardia is probably a compensa- 
tory effect and nervous origin. The third or agonal 
phase is due to the direct action of anoxia upon the 
myocardium. The second phase is probably due to 
the combined effects of anoxia of the myocardium 
and of secondary vagotonia. 
In studies of cardiac output in acute anoxia 
Feldman, Rodbard, and Katz {327) 1949 demon- 
strated that after the onset of nitrogen breathing in 
anesthetized dogs, the blood flow nearly doubles in 
the superior vena cava, with a lesser increase in the 
inferior vena cava. Within 70 seconds there is a 
rise of blood pressure of 10 to 40 mm. Hg. After the 
blood pressure began to fall from its peak value and 
when it had almost returned to its control value 
(after 100 seconds), the flow in the inferior vena 
cava suddenly fell to nearly zero, although the flow 
in the superior vena cava was almost undiminished. 
With the resumption of air breathing, there was a 
rapid return of flow in the superior and inferior 
venae cavae with a striking rise in blood pressure. 
Continuous exposure to simulated altitude may 
result in cardiac dilatation, according to Grand- 
pierre and Franck {334) 1947. This paper contains 
69 references to dilatation and hypertrophy of the 
heart due to hypoxia. The extreme sensitivity of 
cardiac muscle to hypoxia is well established. In 
experiments by Lemley and Meneely {341) 1951, 
the oxygen uptake was measured in homogenized 
myocardial tissue from rats exposed to acute 
hypoxia produced in a decompression chamber. The 
animals were subjected to an atmosphere equiva- 
lent to 7 percent oxygen for 1 hour and killed by 
exposure to an equivalent of 3 percent oxygen. At 
the moment of respiratory arrest the hearts were 
removed, homogenized in buffered saline solution, 
and the oxygen uptake measured. It was found that 
homogenized myocardial tissue from rats exposed 
to hypoxia used only one-half as much oxygen as 
homogenates from normal animals. The oxygen 
consumption of homogenates from hypoxic hearts 
was increased threefold by addition of an extract 
of boiled myocardial tissue. Boiled-heart extract 
from both normal and hypoxic animals produced 
this increase, but the former was slightly more ef- 
fective than the latter. Grundmann (337) 1950 
exposed cats to air mixtures containing 6 to 8 per- 
cent oxygen until death. There was acute edematous 
swelling of the myocardium with infiltration of the 
wall of the cardiac arteries. Blood-pressure changes 
in the right and left ventricles associated with a 
reduction of oxygen tension in the inspired air in 
dogs have been investigated by Gauer and Kramer 
{330) 1948. As the tension in the inspiratory air 
decreased from 200 mm. Hg. to 48 mm. Hg, the 
systolic pressure in the ventricles and carotid 
arteries increased. 
Pulse-rate changes in response to hypoxia have 
been reported by the following: Chardon, Gross, 
and Fourrier {318) 1947; Chardon, Gross, and 
Fourrier {319) 1947;Dahlene {321) 1948; Dripps 
and Comroe {322) 1946; Efimov {325) 1942; 
Georg and Sonne {331) 1947; and Steinmann and 
Konig {359) 1951. Cardiac acceleration resulting 
from hypoxia is mediated partly by augmentation 
of cardioaccelerator nerve activity, partly by dimi- 
nution of moderator tone, and partly by adrenalin 
secretion {318, 319). According to Dripps and 
Comroe {322) 1946, there are no measureable cir- 
culatory responses in human subjects to 18 percent 
oxygen. Some subjects show a slight but definite 
response to 16 percent oxygen, and this is noticeable 
in pulse-rate changes. Acceleration of the pulse is 
thus one of the earliest physiological responses to 
hypoxia. Other studies {325, 331 and 359) indicate 
that pulse-rate increase is a constant finding in 
hypoxia of sufficient intensity to evoke any com- 
pensatory responses. 
It is well known that an early compensatory 
physiological response to hypoxia is provided in the 
contraction of the spleen. In recent studies of Luft 
and Kramer {342) 1950, changes in spleen weight 
and in the hemoglobin content of systemic blood 
were recorded during acute hypoxia in nembutal- 
ized dogs. Contraction of the spleen occurred regu- 
larly in these authors’ experiments; however, the 
response did not appear early but was a terminal 
event immediately preceding respiratory failure. 
Loss in spleen weight during its contraction coin- 
cided with an increase in systemic hemoglobin con- 
tent. During the refilling phase of the spleen after 
hypoxia, the same inverse relationship was evident 
when systemic hemoglobin returned to the initial 
level. An estimate of the hemoglobin concentration 
in the stored blood in the spleen based on the LOW OXYGEN PERCENTAGES—HEART AND CIRCULATION 
amount of blood released by the spleen and the 
subsequent increase in total circulating hemoglobin 
gave a figure of approximately 40 grams percent. 
This implies that the splenic stores consist almost 
entirely of packed red cells. Continuous records of 
the hemoglobin content in the splenic vein showed 
very rapid changes in the final stages of hypoxia 
with peak values twice as high as in the arterial 
blood. During recovery, the hemoglobin level in 
the splenic vein was slightly lower than in the artery. 
Spontaneous rhythmic fluctuations in the hemoglo- 
bin content of the splenic vein were frequently ob- 
served in the control periods. The oxygen satura- 
tion remained consistently higher in the splenic 
vein during hypoxia than in the arterial blood, and 
even improved when splenic contraction reached its 
peak. In the critical phase of hypoxia, the spleen 
of the dog releases a large number of red cells with 
a relatively high oxygen content into the portal 
venous system. 
Alella (306 and 307) 1950 and 1951 studied in 
human subjects the effect of hypoxia on the velocity 
of the pulse wave. Hypoxia did not affect the 
velocity of the pulse wave in the aorta, but, in gen- 
eral, the velocity in the femoral and tibial arteries is 
increased. This is presumed to be due to variation in 
muscular tone of these latter arteries and not to 
blood-pressure changes accompanying hypoxia. 
Alteration in the lesser circulation as a result of 
hypoxia has been investigated by the following: 
Atwell, Hickam, Pryor, and Page {309) 1951; 
Beard, Alexander, Howell, and Reissmann {310) 
1951; Bierman {315) 1951; Duke {323) 1951; 
Duke and Killick {324) 1950; Motley, Cournand, 
Werko, Himmelstein, and Dresdal {352) 1947; 
Nahas, Mather, Hemingway, and Visscher {353) 
1951; Nisell {355) 1951; and Wescott, Fowler, 
Scott, Hauenstein, and McGuire {368) 1951. 
The influence of short periods of acute hypoxia 
upon pulmonary artery pressures in man has been 
reported by Motley, Cournand, Werko, Himmel- 
stein, and Dresdal {352) 1947. Pulmonary hyper- 
tension was rapidly induced in subjects with normal 
blood pressure by breathing 10 percent oxygen for 
short periods of time with only a very slight rise in 
systemic blood pressure. The pulmonary pressures 
rapidly returned to normal when low oxygen breath- 
ing was discontinued. Cardiac output was decreased 
slightly during hypoxia and the stroke volume mar- 
kedly reduced. Pulmonary vascular resistance was 
almost doubled during hypoxia while the systemic 
peripheral resistance increased only slightly. West- 
cott, Fowler, Scott, Hauenstein, and McGuire 
{368) 1951 have examined the effects of hypoxia on 
the human pulmonary circulation by means of car- 
diac catheterization. Breathing 13 percent oxygen 
caused an average rise in mean pulmonary artery 
pressure of 24.6 percent above control levels. No 
significant change in the mean pulmonary capillary 
pressure was observed in subjects who breathed 13 
percent oxygen. No statistically significant change 
in cardiac output could be attributed to hypoxia 
in subjects in whom multiple Frick determinations 
were made. Simultaneous determinations of mean 
pulmonary artery and pulmonary capillary pres- 
sures and cardiac output were made before, during, 
and after 13 percent oxygen breathing. The pul- 
monary arteriolar resistances calculated therefrom 
showed an average increase of 48.5 percent during 
the low oxygen breathing, a difference which was 
shown to be highly significant statistically. Duke and 
Killick [324) 1950 and Duke [323) 1951 have ex- 
amined pulmonary vasomotor responses to hypoxia, 
hypercapnia, and other conditions in a study of 
perfused isolated cat lungs [323). It was found that 
pulmonary vasoconstriction was produced by in- 
haling gas mixtures containing 5 to 10 percent car- 
bon dioxide or gas mixtures containing less than 15 
percent oxygen. Pressor responses in the pulmonary 
arterial system were found under both conditions. 
Ventilation of the lungs with pure oxygen had no 
effect in these experiments. Ventilation of the lungs 
with pure neon or hydrogen produced effects simi- 
lar to those produced by pure nitrogen. Pulmonary 
vasomotor responses to carbon dioxide and oxygen 
lack were not abolished by dihydro-ergotamine or 
atropine. Since dihydro-ergotamine and atropine 
did not affect the pulmonary vasomotor responses to 
carbon dioxide or hypoxia, it seemed unlikely that 
adrenergic or cholinergic nervous elements were 
involved. The available evidence seemed in favor 
of the change in alveolar air composition exerting 
a direct effect upon some part of the pulmonary 
vascular bed. Nisell [355) 1951 reported reduction 
in pulmonary vascular resistance during perfusion 
of hypoxic or hypercapnic blood through the cat 
lungs. This effect was concluded to be due to a 
dilatation of the pulmonary arteries or arterioles. 
The constriction of the pulmonary vessels follow- 
ing inhalation of gas deficient in oxygen or con- 
taining carbon dioxide presumably occurred in the 
venules or veins. A reduction in blood flow through 
the hypoxic lung has been reported by Atwell, 
Hickam, Pryor, and Page [309) 1951. Studies were 
made of individual lung blood flows in the dog 
when both lungs breathed air and when one lung 
breathed air while the other was in equilibrium 
with the pulmonary arterial blood by rebreathing 
while the other lung continued to breathe air, half 
the animals showed a shift of pulmonary blood flow 306-310 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
through the air breathing lung and away from the 
rebreathing lung. 
The influence of short periods of acute hypoxia 
upon pulmonary artery and left atrial pressures in 
dogs has been investigated by Nahas, Mather, Hem- 
ingway, and Visscher {353) 1951. Pressures in the 
left atrium and pulmonary artery of the conscious 
animals were recorded by means of strain gage 
manometers when the animals breathed room air 
and after breathing a mixture of 8 percent oxygen 
in nitrogen for 10 minutes. On room air the average 
mean integrated pressure in the left atrium was 5.8 
mm. Hg (range 1 to 11.2 mm. Hg). The pressure 
in the pulmonary artery was 18.2 mm. Hg (range 
13 to 22.5 mm. Hg). The average cardiac output 
was 3.3 liters per minute. After the dogs had 
breathed 8 percent oxygen in nitrogen for 10 min- 
utes, the mean integrated pressure of the pulmonary 
artery rose in all cases. The average rise was 5.2 
mm. Hg (range 2 to 8 mm. Hg). The pressures in 
the left atrium remained the same or fell slightly. 
During the same period the average cardiac output 
fell from 3.3 down to 2.3 liters per minute, a 30 
percent drop. The average oxygen consumption fell 
from 171 cu. cm. per minute to 109 cu. cm. per 
minute, a 36 percent fall. The average carbon diox- 
ide production rose from 121 cu. cm. per minute 
to 176 cu. cm. per minute, a 31 percent increase. 
The average respiratory quotient rose from 0.72 
up to 2.6. These results, confirming previous inter- 
pretations, indicated to the authors that the increase 
in pulmonary pressure occurring during short 
periods of acute hypoxia truly results from a vascu- 
lar change taking place in the pulmonary vascular 
bed. In contrast, Beard, Alexander, Howell, and 
Reissmann {310) 1951 found no significant change 
in pulmonary arterial pressure in dogs after 15 min- 
utes of exposure to a mixture containing 8.5 percent 
oxygen. 
Reduction of oxygen percentage in the respired 
air results in disturbances of visceral circulation 
and in particular in the circulation through the 
kidneys. Franklin, McGee, and Ullmann {328) 
1950 have reported that, in rabbits and other ani- 
mals, acute anoxia produced a marked diversion of 
the renal cortical blood flow in the innervated, but 
not in the denervated kidney. Direct observation of 
the kidney during anoxia showed a generalized 
paling, diminution in size of the organ, and 
wrinkling of the capsule. Brull and Divry {317) 
1950 have shown that when anoxemia combines 
with poor venous output so that the amount of avail- 
able oxygen in the kidneys drops from normal levels 
above 0.25 down to below 0.10 ml. per gram of 
kidney per minute, urinary secretion practically 
stops. Kreienberg, Prokop, and Schiffer {340) 
1949 found that decrease in the oxygen supply 
resulted in a striking decrease in renal blood flow 
correlated with a degree of hypoxemia. The renal 
blood flow was found to be dependent on systemic 
blood pressure. When normal air breathing was 
resumed, there was an additional renal blood-flow 
decrement and then the flow rate began to rise 
slowly, taking a long time to return to normal. 
Addition of 1.2 to 3 percent carbon dioxide to the 
air mixture intensified and hastened the decrement 
of renal blood flow during hypoxemia. 
For further studies of the effects of hypoxia upon 
heart and circulation, papers by the following should 
be consulted: Anderson, Allen, Barcroft, Edholm, 
and Manning {308) 1946; Bernthal {311) 1947; 
Bernthal, Greene, and Reufin {312) 1951; Bernthal 
and Woodcock {313) 1951; Betourne {314) 1950; 
Comroe and Dripps {320) 1950; Feldman, Rod- 
bard, and Katz {327) 1949; Frey {329) 1948; 
Gordon and Turner {332) 1951; Grandpierre and 
Franck {333) 1947; Grandpierre, Franck, and Le- 
maire {335) 1949; Grandpierre, Franck, and Le- 
maire {336) 1950; Huerkamp and Rittinghaux 
{339) 1950; Malmejac and Chardon {343) 1947; 
Malmejac and Chardon {344) 1949; Malmejac 
and Chardon {345) 1951; Malmejac, Chardon, 
and Gross {346) 1949; Malmejac, Chardon, and 
Neverre {347) 1949; Malmejac, Chardon, and 
Neverre {348) 1949; Malmejac, Chardon, and Ne- 
verre {349) 1949; McMichael and Snyder {350) 
1943; Nairn {354) 1951; Scano {357) 1947; Scar- 
digli {358) 1949; Surtshin, Rodbard, and Katz 
{360) 1947; Surtshin, Rodbard, and Katz {361) 
1948; Swann and Brucer {362) 1949; Swann and 
Brucer {363) 1949; Swann and Brucer {364) 1949; 
Swann and Brucer {365) 1949; Van Loo, Surtshin, 
and Katz {366) 1948; Vannotti {367) 1946; and 
Woodcock {369) 1945. 
306. Alella, A. La velocita dell’onda sfigmica aortica 
nell’uomo durante la respirazione normale ed in condi- 
zioni di ipossia; (studio statistico). Riv. Med. aero., Roma, 
1950, 13: 30-49. (English, French, Spanish, and German 
summaries.) 
307. Alella, A. Effetti dell’ipossia sulla velocita dell’- 
onda sfigmica in arterie di tipo muscolare. Riv. Med. 
aeronaut., 1950, 13: 432-440. Excerpta Medica. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1951, 
4: 1243. 
308. Anderson, D. P., W. J. Allen, J. Barcroft, 0. G. 
Edholm, and G. W. Manning. Circulatory changes during 
fainting and coma caused by oxygen lack. /. Physiol., 
1946, 104: 426-434. [P] 
309. Atwell, R. J., J. B. Hickam, W. W. Pryor, and 
E. B. Page. Reduction of blood flow through the hypoxic 
lung. Amer. J. Physiol., 1951, 166: 37-44 [P] 
310. Beard, E. F., J. D. Alexander, T. W. Howell, and 
K. R. Reissmann. Dynamics of blood flow under abnormal LOW OXYGEN PERCENTAGES—HEART AND CIRCULATION 
311-346 
pressure. 1. Alterations in respiration, systemic circulation, 
and pulmonary circulation during moderate hypoxia in 
the dog. USAF. Randolph Field, Texas. School of aviation 
medicine. Project 21-26-003, Rept. no. 1, December 1951, 
7 pp. 
311. Bernthal, T. G. Direct action of hypoxia upon the 
vasomotor center. Amer. J. Med., 1947, 3: 506. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and 
Pharmacology), 1948, 1: 627. Abstr. [P] 
312. Bernthal, T. G., W. Greene, Jr. and A. Reufin. 
Role of carotid chemoreceptors in hypoxic cardiac ac- 
celeration. Proc. Soc. exp. Biol, N. Y., 1951, 76: 121—124. 
313. Bernthal, T. G. and C. C. Woodcock, Jr. Responses 
of the vasomotor center to hypoxia after denervation of 
carotid and aortic bodies. Amer. J. Physiol, 1951, 166: 
45-53. [P] 
314. Betourne, C. Mise au point de physiologic. Anoxie. 
Sem. Hop., Paris, 1950, 26: 1925-1930. [D] 
315. Bierman, H. R. Pulmonary circulation times with 
particular relationship to acute hypoxia. Amer. J. med. 
Sci., 1951,222: 162-173. 
316. Binet, L., M. V. Strumza, and P. Vernant. Deriva- 
tions precordiales dans 1’etude electrocardiographique de 
I’anoxemie experimentale. C. R. Soc. Biol, Paris, 1951, 
145: 196-197. [P] 
317. Brull, L. and A. Divry. Renal anoxemia. XVIII 
Intern. Physiol. Congr., 1950, 132. 
318. Chardon, G., A. Gross, and A. Founder. Meca- 
nismes de production de 1’acceleration cardiaque en anoxie. 
C. R. Soc. Biol, Paris, 1947, 141: 1049-1050. [R] 
319. Chardon, G., A. Gross and A. Fourrier. Sur le de- 
clenchment de 1’acceleration cardiaque en anoxie. C. R. 
Soc. Biol, Paris, 1947, 141: 1050-1051. [R] 
320. Comroe, J. H. and R. D. Dripps. Anoxia: etiology, 
diagnosis and treatment, pp. 19-52 in: The physiological 
basis for oxygen therapy. Springfield, Illinois, Charles C. 
Thomas. First edition. 1950, 85 pp. [D] 
321. Dahlene, 0., Jr. The effects of anoxia on pulse rate 
and blood pressure. Quart. Phi Beta Pi med. Frat., 1948, 
44: 255-264. 
322. Dripps, R. D. and J. H. Comroe, Jr. The respira- 
tory and circulatory response of normal man to 100, 18, 
16, 14, 12, 10, and 8% O2. Fed. Proc. Amer. Soc. exp. 
Biol, 1946,5: 24. [P] 
323. Duke, H. IT. Pulmonary vasomotor responses of 
isolated perfused cat lungs to anoxia and hypercapnia. 
Quart. J. exp. Physiol, 1951, 36: 75-88. 
324. Duke, H. and E. M. Killick. The effects of the 
inhalation of various gas mixtures on the pulmonary blood 
vessels. XVIII Intern, physiol. Congr., 1950, 182. 
325. Efimov, V. V. [Physiological action of oxygen defi- 
ciency on man. I. Effect of inhalation of gaseous mixtures 
of nitrogen and oxygen.] Byull. eksp. Biol. Med., 1942, 
14: 23-27. 
326. Fabre, R., G. Rougier, and Y. Hibert. A propos 
des modifications electrocardiographiques consecutives au 
travail musculaire en anoxemie. Med. aeronaut., 1946, 
1: 554-570. [P] 
327. Feldman, M., S. Rodbard, and L. N. Katz. Cardiac 
output in acute hypoxemia. Amer. Heart J., 1949, 37: 
631-632. Abstr. [P] 
328. Franklin, K. J., L. E. McGee, and E. Ullmann. 
Anoxic diversion of the renal cortical blood flow. Proc. 
Soc. exp. Biol, N. Y., 1949, 71: 339-341. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and 
Pharmacology), 1950, 3: 916. 
329. Frey, J. Experimenteller Beitrag zur Wirkung der 
Hypoxamie auf die Gefassweite. Klin. Wschr., 1948, 26: 
42-43. [P] 
330. Gauer, 0. and K. Kramer. Druckmessungen im 
rechten und linken Herzventrikel am intakten Tier bei 
Sauerstoffmangel. Pfliig. Arch. ges. Physiol., 1948, 250: 
26-34. [P] 
331. Georg, J. and L. M. Sonne. Undersogelser over 
puls og respiration ved faldende ilttension I inspirations- 
luften. [Investigation of pulse and respiration by decreas- 
ing oxygen tension in the inspired air.] Bibl. Laeger., 1947, 
139: 1-30. 
332. Gordon, I. and R. Turner. Deaths from rapid 
anoxia. Arch. Path., Chicago, 1951, 52: 160—167. 
333. Grandpierre, R. and C. Franck. Les principales 
reactions du coeur a 1’anoxemie. Med. aeronaut., 1947, 2: 
265-278.[R] 
334. Grandpierre, R. and C. Franck. La dilatation et 
1’hypertrophie cardiaques dues a 1’anoxemie. Med. aero- 
naut., 1947,2: 279-294. [R] 
335. Grandpierre, R., C. Franck, and R. Lemaire. 
L’action de 1’anoxemie hypocapnique sur les mecanismes 
vaso-moteurs mis en jeu par 1’injection d’adrenaline. 
C. R. Soc. Biol., Paris, 1949, 143: 1103-1105. [P] 
336. Grandpierre, R., C. Franck, and R. Lemaire. 
Mecanisme des modifications de 1’activite vaso-motrice de 
1’adrenaline au cours de 1’anoxemie hypocapnique. /. 
Physiol., Paris, 1949, 41: 189-190-A. Excerpta Medica. 
Section II. Physiology, Biochemistry, and Pharmacology), 
1950, 3: 1211. 
337. Grundmann, E. Histologische Untersuchungen 
fiber die Wirkungen experimentellen Sauerstoffmangels 
auf das Katzenherz. Beitr. path. Anat., 1950, 111: 35—76. 
[R] [P] 
338. Hoyos, J. M. El electrocardiograma de la anoxia 
experimental. Sanid. mil., 1949, 2: 243—251. [P] 
339. Huerkamp, B. and F. W. Rittinghans. Uber die 
Blutversorgung der menschlichen Retina unter der Ein- 
wirkung veranderter Sauerstoffspannung, von Kohlen- 
saure. Hyperventilation und Adrenalin. Pfliig. Arch. ges. 
Physiol., 1950, 252: 312-330. [P] 
340. Kreienberg. W., L. Prokop, and T. Schiffer. Die 
Nierendurchblutung bei Hypoxamie. Pfliig. Arch. ges. 
Physiol, 1949, 251: 675-688. [P] 
341. Lemley, J. M. and G. R. Meneely. Effect of anoxia 
on metabolism of myocardial tissue. Fed. Proc. Amer. Soc. 
exp. Biol, 1951,10: 214. 
342. Luft, U. C. and K. Kramer. The function of the 
spleen as a blood and oxygen reservoir in severe hypoxia. 
XVIII Intern, physiol. Congr., 1950, 344. 
343. Malmejac, J. and G. Chardon. Etude analytique 
des reactions vasomotrices declenchees par 1’anoxia. Med. 
aeronaut., 1947, 2: 449—471. [R] 
344. Malmejac, J. and G. Chardon. Sur le role des 
presso-recepteurs sino-carotidiens dans la lutte contre 
1’hypotension declenchee par I’anoxie apres exclusion des 
glomus. C. R. Soc. Biol., Paris, 1949, 143: 852—854. [P] 
345. Malmejac, J. and G. Chardon. Action vaso-motrice 
centrale du deficit en oxygene. Med. aeronaut., 1949, 4: 
99-110. Excerpta Medica. Section II. (Physiology, Bio- 
chemistry, and Pharmacology), 1951, 4: 540. Abstr. 
346. Malmejac, J., G. Chardon, and A. Gross. Action ex- 
citante directe de I’anoxie sur les centres vaso-moteurs: 
influence sur la circulation splanchnique. Limites de son 
efficacite. /. Physiol., Paris, 1949, 41: 220—223A. C. R. 
Soc. Biol, Paris, 1949, 143: 846-849. [P] 347-369 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
347. Malmejac, J., G. Chardon, and G. Neverre. Influ- 
ence de 1’adrenaline sur les reactions adrenalino-secre- 
trices declenchees par 1’anoxie. C. R. Soc. Biol., Paris, 1949, 
143: 1526-1527. [P] 
348. Malmejac, J,, G. Chardon, and G. Neverre. Influence 
de 1’adrenaline sur les reactions vaso-motrices d’origine 
centrale a 1’anoxie. C. R. Soc. Biol., Paris, 1949, 143: 
849-852. [P] 
349. Malmejac, J., G. Chardon, and G. Neverre. Action 
vaso-motrice centrale de 1’adrenaline: influence sur les 
reactions a 1’anoxie. /. Physiol., Paris, 1949, 41: 226-228A. 
[P] 
350. McMichael, M. and C. H. Snyder. The effect of 
ascent to 16,000 and 18,000 feet upon arm blood flow. 
U. S. NRG-CAM. C. A. M. rept. no. 185, 30 August 1943, 
3 PP- [P] 
351. Master, A. M. Anoxic effects on the electrocardio- 
gram produced by the 2-step test. Bull. N. Y. Acad. Med., 
1950, 26: 361-370. [P] 
352. Motley, H. L., A. Cournand, L. Werko, A. Himmel- 
stein, and D. Dresdal, The influence of short periods of 
induced acute anoxia upon pulmonary artery pressures in 
man. Amer. J. Physiol., 1947, 150: 315-320. [P] 
353. Nahas, G. G., G. C. Mather, A. Hemingway, and 
M. B. Visscher. Influence of short periods of acute anoxia 
upon pulmonary artery and left atrial pressures in un- 
anesthetized dogs. Amer. J. Physiol., 1951, 167: 812-813. 
Abstr. 
354. Nairn, R. C. Oedema and capillary anoxia. /. Path. 
Bact., 1951, 63: 213-234. 
355. Nisell, 0. The influence of blood gases on the 
pulmonary vessels of the cat. Acta physiol. Scand., 1951, 
23: 85-90. [P] 
356. Penneys R., and C. B. Thomas. The relationship 
between the arterial oxygen saturation and the cardio- 
vascular response to induced anoxemia in normal young 
adults. Circulation, 1950, 1: 415-425. [P] 
357. Scano, A. Sul comportamento della pressione del 
liquido cefalo-rachidiano in anossia. Riv. Med. aero., 
Roma, 1947, 70; 144-170. (Italian, English, French, Span- 
ish, and German summaries.) 
358. Scardigli, G. La via intracardiaca nelle anossie 
acute. Settimana med., 1949, 37: 23. 
359. Steinmann, B. and H. Konig. Uber die Wirkung 
sauerstoffarmer Luftgemische auf den Kreislauf des Ge- 
sunden und Herzkranken. Helvet. med. Acta, 1950, 17: 
179—194. Excerpt a Medica. Section II. (Physiology, Bio- 
chemistry, and Pharmacology), 1951, 4: 1420. 
360. Surtshin, A., S. Rodbard, and L. N. Katz. Inhibi- 
tion of the pressor response to epinephrine injection in 
complete anoxia. Proc. cent. Soc. din. Res., 1947, 20: 23. 
[P] 
361. Surtshin, A., S. Rodbard, and L. N. Katz. Inhibi- 
tion of epinephrine action in severe hypoxemia. Amer. J. 
Physiol, 1948, 152: 623-632. [P] 
362. Swann, H. G. and M. Brucer, The cardiorespira- 
tory and biochemical events during rapid anoxic death. 
I. Fulminating anoxia. Texas Rep. Biol. Med., 1949, 
7: 511-538. [P] 
363. Swann H. G., and M. Brucer. The cardiorespira- 
tory and biochemical events during rapid anoxic death. 
II. Acute anoxia. Texas Rep. Biol. Med., 1949, 7: 539- 
552. [P] 
364. Swann, H. G. and M. Brucer. The cardiorespira- 
tory and biochemical events during rapid anoxic death. 
III. Progressive anoxia. Texas Rep. Biol. Med., 1949, 
7: 553-568. Abstr. World Med., 1950, 8: 230. [P] 
365. Swann, H. G. and M. Brucer. The cardiorespira- 
tory and biochemical events during rapid anoxic death. 
V. Obstructive asphyxia. Texas Rep. Biol. Med., 1949, 
7: 593-603. 
366. Van Loo, A., A. Surtshin, and L. N. Katz. The role 
of the adrenal in the arterial pressure responses to severe 
hypoxemia. Fed. Proc. Amer. Soc. exp. Biol., 1948, 
7: 127. [P] 
367. Vannotti, A. L’adaptation de la cellule a 1’effort, 
a altitude et a 1’insuffisance pathologique de 1’oxygene. 
Med. et Hyg., Anvers, 1946, 4 {84): 2-3. [D] 
368. Westcott, R. N., N. 0. Fowler, R. C. Scott, V. D. 
Hauenstein, and J. McGuire. Anoxia and human pulmo- 
nary vascular resistance. /. din. Invest., 1951, 30: 957—970. 
Trans. Ass. Amer. Phys., 1951, 64: 404-419. [P] 
369. Woodcock, C. C., Jr. The response of the vasomotor 
center to the direct action of hypoxia. Fed. Proc. Amer. 
Soc. exp. Biol., 1945, 4: 7. 
5. BLOOD 
For studies on the effects of hypoxia on the blood, 
papers by the following may be consulted: Berk, 
Burchenal, Wood, and Castle {370) 1948; Cordier 
and Coudier {371, 372) 1950; Germanov {373) 
1949; Magnussen {374) 1949; Malmejac, Cruck, 
and Neverre {375) 1948; Penneys, Thomas, and 
Lewis {376) 1950; Reissmann {377) 1950; Riska 
{378) 1950; Rosin and Rachmilewitz {379) 1948. 
Studies on the production of erythrocytes in vitro 
(374 and 379) have indicated that the maximum 
production occurs at oxygen percentages from 10 to 
30 percent. Rosin and Rachmilewitz found that gas 
mixtures containing 1, 3, 5, 10, and 12 percent oxy- 
gen have an injurious effect on hemic cells in the 
bone marrow of rabbits in vitro. The bone marrow 
showed various degrees of degeneration, more pro- 
nounced at the lower oxygen percentages. Bone 
marrow cultures in 15 percent oxygen did not show 
any appreciable changes and were similar to con- 
trols in normal air. Berk, Burchenal, Wood, and 
Castle {370) 1948 measured the oxygen saturation 
of sternal marrow blood in human subjects. In gen- 
eral, no significant differences were demonstrated 
between normal subjects, convalescent control sub- 
jects, anemic patients, and patients with polycythe- 
mia vera. In some patients with leukemia and with 
myeloid metaplasia and in some patients with poly- 
cythemia vera with evidence of excessive myeloid 
activity, the data suggested an increased local oxy- 
gen utilization relative to the blood flow in the bone 
marrow. However, it was concluded that the tech- 
niques used were not adequate to demonstrate a 
hypoxic stimulus to increased erythropoiesis, even in 
the marrow of patients with chronic anemia, prob- 
ably because of the difficulty of obtaining blood 
samples satisfactorily representative of the undis- 
turbed environment of the erythropoietic tissue. 
Reissmann {377) 1950 has reported studies on the LOW OXYGEN PERCENTAGES—BLOOD 
370-381 
mechanism of erythropoietic stimulation in para- 
biotic rats during hypoxia. Chronic hypoxemia was 
induced in one partner of a pair of parabiotic rats 
by exposure to defined gas mixtures with low oxygen 
content. The other partner of the pair was kept in 
normal atmosphere throughout the experiment and 
showed normal values of the oxygen saturation of 
the blood. Erythropoiesis, estimated by the percent- 
age of nucleated red cells in the bone marrow, 
showed a statistically significant stimulation in both 
animals. It was concluded, therefore, by the author 
that under these experimental conditions, the stimu- 
lus to erythropoiesis was not the partial pressure of 
oxygen in the bone marrow directly but a humoral 
factor elicited by hypoxemia in the one partner and 
transferred to the other one. 
According to Tagliamonte {380) 1947, there is 
a reduction in corpuscular resistance in normal 
human subjects undergoing hypoxia by the re- 
breathing method. According to Penneys, Thomas, 
and Lewis {376) 1950, exposure of normal human 
subjects to low oxygen concentrations producing 
arterial oxygen saturations of 70 to 80 percent led 
to a significant drop in the eosinophil count. This 
effect was believed by the authors to indicate an 
increase of adrenal cortical activity following 
anoxemia. In one case the addition of carbon 
dioxide to the breathing mixture caused a slight rise 
in arterial oxygen saturation with a corresponding 
fall in the eosinophils while no change was observed 
in other subjects. In these experiments the total 
period of anoxemia ranged from 17 to 24 minutes. 
In experimental animals, hypoxia may produce 
changes in plasma protein {371, 372, 375). Gordier 
and Coudier {372) found that dogs subjected to 7 
percent oxygen showed an increase in plasma 
protein. 
370. Berk, L., J. H. Burchenal, T, Wood, and W. B. 
Castle. Oxygen saturation of sternal marrow blood with 
special reference to pathogenesis of polycythemia vera. 
Proc. Soc. exp. Biol, N. Y., 1948, 69: 316-320. [P] 
371. Cordier, D. and R. Coudier. Etude spectrale du 
sang au cours de 1’anoxie progressive. Spectres d’absorp- 
tion de I’hemoglobine dans les hematics et en solution 
apres hemolyse. C. R. Soc. Biol, Paris, 1950, 144: 844- 
847. Excerpta Medica. Section II. (Physiology, Biochem- 
istry, and Pharmacology), 1951, 4: 656. Abstr. 
372. Cordier, D. and R. Coudier. Etude spectrale du 
sang au cours de 1’anoxie progressive. Spectres d’absorp- 
tion du plasma dans 1’ultra-violet. C. R. Soc. Biol, Paris, 
1950, 144: 1053-1055. [P] 
373. Germanov, V. A. O krovotverenii pri tsirkuliarnoi 
gipoksii. [Hematopoiesis in circulatory hypoxia.] pp. 
234—236 in: Gipoksiia, Kiev, Akad. Nauk. Ukr., 1949, 
415 pp. 
374. Magnussen, J. D. The influence of oxygen tension 
on the production of erythrocytes in vitro. Acta pharm., 
toxical, Kbh., 1949,5: 153-163. 
375. Malmejac, J., S. Cruck, and G. Neverre. Influence 
du deficit en ozygene sur 1’equilibre protidique sanguin. 
Bull. Acad. nat. Med., Paris, 1948, 132: 92-96. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and 
Pharmacology), 1949, 2: 211. Abstr. [P] 
376. Penneys, R., C. B. Thomas, and R. A. Lewis. 
Reduction in the number of circulating eosinophils fol- 
lowing induced anoxemia. Johns Hopk. Hasp. Bull., 1950, 
86: 102-106. [P] 
377. Reissmann, K. R. Studies on the mechanism of 
erythropoietic stimulation in parabiotic rats during 
hypoxia. Blood, 1950, 5: 372—380. [P] 
378. Riska, N. Veranderungen der Retikulozytenzahl 
in unmittelbarem Anschluss an experimentell erzeugten 
Sauerstoffmangel. Experientia, 1950, 6: 345-348. [P] 
379. Rosin, A. and M. Rachmilewitz. Studies on bone 
marrow in vitro. III. The effect of anoxia and hyperoxia 
on explanted bone marrow. Blood, 1948, 3: 165—174. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1949, 2: 223, Abstr. [P] 
380. Tagliamonte, B. Comportamento del numero degli 
eritrociti e della resistenza globulare in soggetti sottoposti 
ad anossia con il metodo della ri-respirazione. Riv. Med. 
aero., Roma, 1947, 10: 302-315. (Italian, English, French, 
Spanish, and German summaries.) 
6. LYMPHATICS 
Malmejac, Ghardon, and Gross {381) 1948 have 
reported modifications in the production of lymph 
in the course of hypoxia in chloralosed dogs sub- 
jected to oxygen-nitrogen mixtures with an oxygen 
percentage from 4 to 10 percent. When the 
respiratory movements diminished after an initial 
rise, the lymphatic flow was found to be rapidly 
reduced. During hypoxic hyperventilation there was 
an immediate augmentation and discharge of lymph 
from the thoracic canal, but when this was inter- 
rupted the discharge of lymph was reduced. The 
authors considered that the influence of vasomotor 
reactions initiated by hypoxia, especially in the 
splanchnic area, are the principal cause of the re- 
duction of the lymphatic flow. This action was con- 
sidered to be produced by vasoconstriction or by 
the local action of epinephrine. 
381. Malmejac, J., G. Chardon, and A, Gross. Modifi- 
cations dans la production de la lymphe au cours de 
1’anoxic. Analyse des mecanismes efficients. C. R. Soc. 
Biol, Paris, 1948,142: 509-510. [P] 
7. RESPIRATION 
The effects of hypoxia upon respiration have 
been investigated by a large number of investigators. 
Some of these studies are reported in the references 
given in the following list. For recent descriptions of 
the actual respiratory responses to hypoxia, papers 
by the following should be consulted: Chambers, 
Brewer, Davenport, and Goldschmidt {386) 1947; 
Davenport, Brewer, Chambers, and Goldschmidt 
{387) 1947; Dripps and Gomroe {388) 1948; 
Georges and Sonne {394) 1947; Gollwitzer-Meier 
{395) 1947; Houston {401) 1946; Korkes, Chinn, 
291222—54 4 382-409 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
and Marriott {403) 1948; Peyser, Sass-Kortsak, 
and Verzar {406) 1951; Sillani {407) 1947; and 
Smith {408) 1948. 
Papers by the following may be consulted for 
investigations on the physiology of the respiratory 
center as affected by hypoxia; Bjurstedt {384) 
1946; Ferro-Milone {392) 1951; Georg and Sonne 
{393) 1948-49; Grandpierre and Franck {396) 
1950; Jaggi {402) 1950; and Weterings {409) 
1948. 
For papers offering hypotheses to explain the 
mechanisms of the effects of hypoxia on respiration, 
reports by the following authors may be consulted: 
Binet and Strumza {382) 1946; Fabinyi and Szebe- 
hely {390) 1949 and {391) 1950; Grandpierre, 
Franck, and Lemaire {397) 1949; Gray {398) 
1946; and Lenggenhager {404) 1947. 
382. Binet, L. and M. II. Strumza, Mecanisme de la 
persistance de 1’activite nerveuse respiratoire dans 1’anoxe- 
mie. Med. aeronaut., 1946,1: 338-340. [P] 
383. Binet, L. and M. V. Strumza. Le taux de 1’oxygene 
dans le sang arteriel au debut de 1’apnee anoxique. C. R. 
Soc. Biol, Paris, 1949,143: 44. [P] 
384. Bjurstedt, A. G. H. Interaction of centrogenic and 
chemoreflex control of breathing during oxygen deficiency 
at rest. Acta physiol, scand., 1946, Supplementum. 38: 
88 pp. [R] [P] 
385. Brucer, M., G. L. Herman, and H. G. Swann. 
Interrelationship of cardiorespiratory events in anoxia. 
Amer. J. Physiol, 1950, 160: 138-148. [M] [R] 
386. Chambers, A. H., G. Brewer, H. W. Davenport, 
and S. Goldschmidt, The respiratory responses to anoxe- 
mia of the normal unanesthetized dog and their causes. 
Amer. J. Physiol, 1947,148: 392-405. [P] 
387. Davenport, H. W., G. Brewer, A. H. Chambers, 
and S. Goldschmidt. The respiratory responses to anoxe- 
mia of unanesthetized dogs with chronically denervated 
aortic and carotid chemoreceptors and their causes. Amer. 
J. Physiol, 1947,148: 406-416. [P] 
388. Dripps, R. D. and J. H. Comroe, Jr. The effect 
of inhalation of high and of low oxygen concentration upon 
human respiration and circulation. Amer. J. med. Sci., 
1947, 213/2: 248-294. Excerpta Medica. Section II. 
(Physiology, Biochemistry, and Pharmacology), 1948, 1: 
174. 
389. Euler, IT. S. and G. Liljestrand. Observations on 
the pulmonary arterial blood pressure in the cat. Acta 
physiol, scand., 1946, 12: 301-320. [P] 
390. Fabinyi, M., and J. Szebehely. Further investiga- 
tions about the histamine hypothesis of the oxygen de- 
ficiency. Arch. int. Pharmacodyn., 1949, 78: 354-361. 
Abstr. World Med., 1949, 6: 264. 
391. Fabinyi, M. and J. Szebehely. On the role of hista- 
mine in hyperpnoea caused by oxygen lack. XVIII Intern. 
Physiol Congr., 1950, 191-192. 
392. Ferro-milone, F. Riglessi da impossia nella dimi- 
nuita eccitabilita del centra respiratorio bulbare. Boll. Soc. 
ital Biol, sper., 1951,27: 34-36. [P] 
393. Georg, J. and 1. M. Sonne. The relation of the 
oxygen tension of the inspiratory air to the chemoreceptor 
response during work. Acta physiol, scand., 1948-49, 16: 
52—62. Excerpta Medica. Section II. (Physiology, Bio- 
chemistry, and Pharmacology), 1949, 2: 778. Abstr. [P] 
394. Georg, J and L. M. Sonne. Unders0gelser over 
puls og respiration ved faldende ilttension i inspirations- 
luften. [An investigation of the effect of falling oxygen 
tension in the inspired air on pulse and respiration.] 
Bibl. Laeger., 1947,139: 41-50. Excerpta Medica. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1948, 
I: 142. Abstr. 
395. Gollwitzer-Meier, K. Uber die Nachdauer der At- 
mungsveranderungen des Sauerstoffmangels. Pfliig. Arch, 
ges Physiol., 1947, 249: 17—31. Excerpta Medica. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1948, 
1: 628. Abstr. [P] 
396. Grandpierre, R. and C. Franck. Notions actuelles 
sur 1’organisation et le fonctionnement des centres nerveux 
respiratoires. II. La regulation de la respiration. Med. 
aeronaut., 1950, 5: 297-353. [P] [R] 
397. Grandpierre, R., C. Franck, and R. Lemaire. 
Action de 1’adrenaline sur le rythme respiratoire au cours 
de 1’anoxemie hypocapnique. C. R. Soc. Biol., Paris, 1949, 
143: 1105-1107. [P] 
398. Gray, J. S. The multiple factor theory of the con- 
trol of respiratory ventilation. Science, 1946, 103: 739— 
744. 
399. Harris, A. S. Inspiratory tonus in anoxia. Amer. 
J. Physiol, 1945,143: 140-147. 
400. Hesse, R., E. Opitz, and F. Palme. Darstellung der 
Hohenanpassung im Gebirge durch Sauerstoffmangel. 
I. Atmung und Alveolarluft bei Riickatmungsversuchen 
berschiedener Dauer. Pfliig. Arch, ges Physiol, 1944, 248: 
283-297. [P] 
401. Houston, C. S. The effect of pulmonary ventilation 
on anoxemia. Amer. J. Physiol, 1946, 146: 613-621. [P] 
402. Jaggi, F. tlber die Sensibilisierung des Atemzen- 
trums durch den Sauerstoffmangel in der Hohe. Med. 
aeronaut., 1950, 5: 97. (French abstract.) These (Med.) 
Berne, Langnau, Vogeli et Moser, Editeur. 1948. [P] 
403. Korkes, S., H. I. Chinn, and W. Marriott. Oxygen 
consumption at low oxygen tensions. USAF. Randolph 
Field, Texas. School of aviation medicine, Project 21-02— 
101, Kept. no. 1, November 1948,4 pp. 
404. Lenggenhager, K. Worauf beruhen die Storungen 
bei Hyperventilation? Kritische Einwande gegen die 
herrschende theorie des Gasaustausches. Helv. med. acta., 
1947, 14: 137-173. [P] 
405. Melik-Megrabov, A. M. lavleniia gipoksii naru- 
sheniiakh krovoobrashcheniia i dykhaniia razlichnoi etio- 
logii. [The phenomenon of hypoxia in blood circulation 
and respiratory disorders of various etiology.] pp. 162—167 
in: Gipoksiia, Kiev, Akad. Nauk. Ukr., 1949, 415 pp. 
406. Peyser, E., A. Saas-Kortsak, and F. Verzar. In- 
fluence of 02 content of inspired air on total lung volume. 
Amer. J. Physiol, 1950, 163: 111-117. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1951, 4: 760. Abstr. 
407. Sillani, L. S. Comportamento della ventilazione 
polmonare in anossia. Riv. med. aero., Roma, 1947, 10: 
499-508. [P] 
408. Smith, R. E. Physiological responses to hypoxia 
induced in man by inspiration of a low O2—N2 mixture. 
U. S. Navy. NMRI. Project NM 001 003 X-313, Rept. 
no. 2, 3 May 1948, 5 pp. 
409. Weterings, P. A. A. The inhibitory effect of the 
oxygen pressure in blood on respiration through the inter- 
mediacy of chemo-receptors. Acta med. scand., 1948, 
130: 232-258. I0W OXYGEN PERCENTAGES—ALIMENTARY TRACT 
410-413 
8. ALIMENTARY TRACT 
The name of Van Liere has come to be associated 
with research upon the effects of low oxygen on the 
functions of the alimentary tract. In a recent paper, 
Van Liere, Stickney, and Northup {412) 1951 have 
examined the effects of anoxia on intestinal motility 
and on blood sugar in pups. Anoxic anoxia produced 
a signficant decrease in propulsive motility, but 
anemic anoxia had no significant effect. This is in 
direct contrast to the findings in adult dogs. The 
hyperglycemic response of pups to hypoxia was dis- 
tinctly less than that of adult dogs. These findings 
are in conformity with those of Lemaire and 
Bouverot {411) 1949, who found in dogs a fall in 
intestinal tonus during anoxemia and adrenalin in- 
jection. The drop in tone was accompanied by a 
striking diminution of the amplitude of intestinal 
movements. In these experiments, the splanchnic 
nerves were sectioned and the movements of the 
intestine were noted during inhalation, for 2 min- 
utes and 45 seconds, to a mixture containing 7 per- 
cent oxygen. Cordier and Chanel {410) 1949 sub- 
jected rats to oxygen percentages as low as 1 per- 
cent. Just before exposure there was introduced into 
the stomach 2 cu. cm. of glucose solution (5.4 per- 
cent to 50 percent). At oxygen concentrations of 
12 to 21 percent, 99 percent of the glucose had 
passed into the intestine within an hour’s time. In 
those rats breathing 5 percent oxygen, only 35 per- 
cent of the glucose passed into the intestine at the 
end of an hour. Cordier and Chanel {419) 1949 
also pointed out that prolonged and severe hypoxia 
diminishes intestinal absorption of glucose in the 
rat. For a study of the effects of exposure of iso- 
lated rabbit’s intestine to a mixture containing no 
oxygen, a paper by West, Hadden, and Farsh {413) 
1951 may be consulted. Complete anoxia resulted 
in total mechanical inactivity in 3 to 5 minutes. 
410. Cordier, D. and J. Chanel. Influence de la tension 
d’oxygene dans 1’air inspire sur la vitesse du transit gas- 
trique chez le rat. C. R. Soc. Biol., Paris, 1949, 143: 
493-495. [P] 
411. Lemaire, R. and P. Bouverot. Action de 1’adrena- 
line sur 1’intestin au cours de 1’anoxemie hypocapnique. 
C. R. Soc. Biol, Paris, 1949, 143: 1113-1115. [P] 
412. Van Liere, E. J., J. C. Stickney, and D. W. 
Northup. Effect of anoxia on intestinal motility and on 
blood sugar in pups. Amer. J. Physiol, 1951, 167: 103- 
107. [P] 
413. West, T, C., G. Hadden, and A. Farah. Effect of 
anoxia on response of the isolated intestine to various 
drugs and enzyme inhibitors. Amer. J. Physiol, 1951, 
164: 565-572. [P] 
9. METABOLISM 
The effect of decrease of oxygen tension in the 
inspired air upon the rate of oxygen consumption 
has been investigated experimentally by Beyne, Boy, 
and Polonovski {414) 1946. These investigators 
concluded that with a decrease of oxygen tension 
there was also a decrease in oxygen consumption. 
The suppression of oxidation was accompanied by a 
decrease in body temperature and an accumulation 
in the body of products of incomplete oxidation. 
Other investigations reported in the physiological 
literature indicate a considerable variation in the 
oxygen consumption rate of man and animals dur- 
ing hypoxia. Both increases and decreases have been 
found. Hemingway and Nahas {427) 1951 carried 
out a series of observations using normal unanesthe- 
tized dogs breathing an 8 percent oxygen mixture. 
The oxygen consumption rate was first found to 
decrease and then to increase to a value exceeding 
the control value of air breathing. In a study of the 
effects of altered arterial tensions of carbon dioxide 
and oxygen on cerebral blood flow and cerebral 
oxygen consumption of normal young men, Kety 
and Schmidt {430) 1948 found that inhalation of 
a 10-percent oxygen mixture resulted in an increase 
of cerebral blood flow, but no significant change in 
cerebral oxygen consumption. 
Hypoxia results in a mobilization of blood sugar 
with a drainage on glycogen stores. For experimen- 
tal studies on this phenomenon, papers by the fol- 
lowing may be consulted: Cordier and Dessaux 
{420) 1949 and {421) 1951; Cordier and Touze 
{422) 1949; Leonardi {432) 1947; Leonard! {433) 
1947; and Smith and Oster {444) 1946. The results 
of decrease in partial pressure of oxygen of the in- 
spired air upon lactic-acid metabolism have been 
reported by Loeschicke and Loeschicke {434) 1947 
and Lundin and Strom {435) 1947. 
According to Sillani {443) 1948, exposure of 
human subjects to short-lasting periods of hypoxia 
results in a slight decrease of ketone bodies and 
total fats as well as lipoid phosphorus. In control 
tests under normal air conditions, these variations 
did not occur. 
Regarding the effects of anoxic anoxia on bile 
secretion in the rat, MacLachlan, Sleeth, and Cover 
{436) 1947 found no significant difference in the 
amount of bile salts excreted by a bile fistula rat 
when exposed for 4-hour periods to decreased oxy- 
gen tension (63 mm. Hg and 53 mm. Hg). Char- 
don, Neverre, and Jeannoel {418) 1948 measured 
the bile flow in the cystic canal in chloralosed dogs 
subjected to 3 percent oxygen in nitrogen. At first 
there was an acceleration of bile flow. This was 
followed by a decrease of bile secretion. For studies 
on the metabolism of the liver and spleen under con- 
ditions of hypoxia, papers by Brin {416) 1949 and 
Rein {442) 1950 should be consulted. SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
Regarding the influence of hypoxia on pancreatic 
secretion, Chardon and Gross {417) 1946 found 
in dogs under chloralose anesthesia exposed to 2 to 
5 percent oxygen that there was at first a consider- 
able decrease in pancreatic secretion with return to 
normal values after the first 30 minutes. 
Ivy, Farmer, Krasno, Freeman, Burrill, Bouth- 
well, Gilley, Scow, and Friedemann {429) 1945 re- 
ported a detailed study on the metabolic effects of 
mild hypoxia on human subjects. Eleven young sub- 
jects were exposed to a simulated altitude of 18,000 
feet for 1 hour each day, 3 times a week for 9 weeks. 
The subjects were maintained on a complete diet 
containing 91 mg. of ascorbic acid daily. The ex- 
posure period was preceded by 5 weeks on the diet 
and followed by a post-exposure period of 3 weeks 
during which control determinations were made. 
Repeated exposure to altitude caused a decrease in 
the daily urinary excretion of viamin C from an 
average of 33.6 mg. to 0.12 mg. The plasma level 
of ascorbic acid decreased from an average control 
level from 0.73 mg. percent to 0.58 mg. percent 
during the last 3 weeks of exposure. Repeated ex- 
posure to a simulated altitude of 18,000 feet without 
supplementary oxygen did not affect the urinary 
output of thiamin, riboflavin, and alpha-ketoglutaric 
acid, pyruvic acid, and acetone bodies. There was 
no clearly significant change in the sedimentation 
rate of the erythrocytes or in the hematocrit deter- 
minations. Glucose tolerance was not decidely 
changed. Depletion of ascorbic acid was considered 
to be due to increased utilization. Exposure to a 
simulated altitude of 18,000 feet without added oxy- 
gen caused a temporary increase in the excretion of 
sodium, potassium, and chloride. The excretion of 
17-ketosteroids decreased for the first 6 weeks, but 
during the last 3 weeks tended to return to the 
control level but did not quite reach it. The excre- 
tion of ascorbic acid, amino nitrogen, and 17-keto- 
steroids tended to be parallel when subjects were 
repeatedly exposed to 18,000 feet without supple- 
mentary oxygen. Exposure of subjects to a simu- 
lated altitude of 35,000 feet with oxygen inhalation 
resulted in hypersecretion of these substances. 
Crossed circulation studies on dogs reported by 
Malmejac and Chardon {437) 1946, {438) 1947, 
and {439) 1950 indicate that hypoxia produced by 
inhalation of gas mixtures containing 6 to 10 per- 
cent oxygen results in increased secretion of 
epinephrine. According to Grandpierre, Franck, and 
Lemaire {426) 1948, exposure to a 14-percent oxy- 
gen mixture causes a diminution of the efficacy of 
epinephrine in producing hypertensive and hyper- 
glycemic reactions. Van Loo, Surtshin, and Katz 
{445) 1948 have investigated the role of the adrenal 
glands in hypoxia. In unilaterally adrenalectomized 
animals they found that diversion into a syringe of 
the venous blood draining from the remaining 
adrenal gland resulted in no significant change in 
the hypoxemic pressor response, but diminished 
considerably the posthypoxemic pressor response. 
Blood collected from the phase of falling blood 
pressure during nitrogen breathing had more pressor 
activity than that collected during the earlier phases 
of hypoxemia. Reinjection of such collected blood 
immediately after the peak of the posthypoxemia 
response caused the pressure to rise to a level similar 
to that attained in the controls. The authors con- 
cluded that the adrenal gland plays only a small 
part in the production of the arterial pressor re- 
sponse after reaeration. Pressor substances liberated 
from the adrenal gland during severe hypoxemia 
do not exert pressor effects until the tissues are 
reoxygenated. 
For a study of the metabolic changes in muscle 
produced by oxygen lack, a paper by Endo {423) 
1944 may be consulted. This paper contains a num- 
ber of references. Kottke, Phalen, Taylor, Visscher, 
and Evans {431) 1948 have studied the effect of 
hypoxia upon temperature regulation of mice, dogs, 
and man. Hypoxia was found under the conditions 
of these experiments to decrease the capacity of 
both the animals and human subjects to control 
body temperature during exposure to cold. Loss of 
temperature control and fall in body temperature 
was most striking in the mouse and least marked in 
man. Hypoxia was found to inhibit shivering in all 
three species studied. Hypoxia in man was also 
shown to result in a greater dissipation of heat from 
the skin in the cold environment. Decreased en- 
vironmental and body temperature favored the 
survival of mice exposed to progressive hypoxia. 
Between 20° to 37° C. the survival was increased 
by approximately 1,000 feet per 1° C. drop in tem- 
perature. This striking protection against death at 
altitude afforded by drop in body in temperature of 
mice would seem to be due to decreased oxygen 
demand at lower body temperatures and parallels 
the increased altitude tolerance of thyroidectomized 
animals. Goebel, Fukas, Klante, and Imdahl {425) 
1951 subjected rats to 20-hour sessions in an atmos- 
phere containing 7 percent oxygen in nitrogen. 
Oxygen consumption fell soon after exposure, and 
after 20 hours was only 50 percent of the normal 
value. The body temperature was observed to de- 
crease quickly after exposure. At the end of the ex- 
periment the temperature rapidly climbed to nor- 
mal. Oxygen consumption and body temperature 
reached control valves, at the same time, in about 
6 hours. LOW OXYGEN PEECENTAGES—METABOLISM 
414-445 
For further studies on the effects of hypoxia upon 
metabolism, papers by the following authors may 
be consulted: Bollman, Fazio, and Faulconer {415) 
1951; Fabinyi and Szebehelyi {424) 1948; Herber 
{428) 1948; Moon {440) 1950; and Parkes {441) 
1951. 
414. Beyne, J., G. Boy, and M. Polonovski. Le metab- 
olism de Foxygene au cours de 1’anoxie. Med. aeronaut., 
1946, 1: 131-145. [D] [R] 
415. Bollman, J. L., A. N. Fazio, and A. Faulconer, Jr. 
Some factors influencing the effects of anoxic anoxia. 
Anesthesiol, 1951, 12: 420-430 and 441. 
416. Brin, B. M. Izmenenie intensivnosti okisleniia pri 
gipoksii pecheny (fistula Ekka). [Changes in oxidation 
intensivity in liver hypoxia.] [Eck fistula.] pp. 205-209 in: 
Gipoksiia, Kiev, Akad. Nauk. Ukr. SSR., 1949, 415 pp. 
417. Chardon, G. and A. Gross. Influence de 1’anoxie 
sur la secretion pancreatique externe. C. R. Soc. Biol, 
Paris, 1946,140: 1004. [P] 
418. Chardon, 6., G. Neverre, and G. Jeannoel. Modifi- 
cations de la secretion biliaire sous 1’influence du deficit 
en oxygene. C. R. Soc. Biol, Paris, 1948,143: 697-698. [P] 
419. Cordier, D. and J. Chanel. Influence de la tension 
d’oxygene dans Fair inspire sur la vitesse de 1’absorption 
intestinale des solutions de glucose chez le rat. J. Physiol, 
Paris, 1949,41: 151-154A. [P] 
420. Cordier, D. and G. Dessaux. Modifications du taux 
du glycogene cardiaque chez le rat sous Finfluence de 
Fanoxie et du choc traumatique. /. Physiol, Paris, 1949, 
41: 159A-161A. [P] 
421. Cordier, D. and 6. Dessaux, Modifications du 
taux du glycogene cardiaque sous Finfluence de Fanoxie, 
de Fasphyxie et de Fintoxication carbonique rapides. 
C. R. Soc. Biol, Paris, 1951, 145: 727-729. 
422. Cordier, D. and M. Touze. Modifications reversi- 
bles de la phosphorolyse hepatique du glycogene sous 
Finfluence de Fanoxie anoxique chez le rat. C. R. Soc. 
Biol., Paris, 1949, 143: 1060-1063. [P] 
423. Endo, K. Uber die Veranderungen der Stoffumsatze 
des Muskels in der Ruhe und bei der Arbeit im O2—Man- 
gel. Tohoku J. exp. Med., 1944, 47: 195-222. [P] 
424. Fahinyi, M. and J. Szebehelyi. The role of hista- 
mine in the symptoms caused by decreased partial pressure 
of oxygen. Arch. int. Pharmacodyn., 1948, 76: 397—416. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1949, 2: 254. Abstr. [P] 
425. Goebel, A., H. K. Fukas, W. Klante, and H. 
Imdahl. Sauerstoffverbrauch und Korpertemperatur von 
Ratten im Sauerstoffmangel. Z. ges. exp. Med., 1951, 
117: 384-392. 
426. Grandpierre, R., C. Franck, and R. Lemaire. In- 
fluence des variations du taux des gaz respiratoires sur 
Fefficacite de Fadrenaline. Med. aeronaut., 1948, 3: 227— 
229. [P] 
427. Hemingway, A. and G. 6. Mahas. Oxygen con- 
sumption rate during hypoxia. Amer. J. Physiol, 1951, 
167: 794. Abstr. 
428. Herber, F, J. Metabolic changes of blood and 
tissue gases during asphyxia. Amer. J. Physiol, 1948, 152: 
687-695. [P] 
429. Ivy, A, C., C. J. Farmer, L. R. Krasno, S. Freeman, 
M. W. Burrill, J. H. Boutwell, J. H. Cilley, J. Scow, and 
T. E. Friedemann. The effect on human subjects of the 
degree of ascorbic acid deficiency induced and of the 
disturbance of the metabolism of the vitamin by mild 
anoxia and its correlation with acid-base disturbances and 
17-ketosteroid excretion. U. S. NRC-CAM. OEMcmr— 
236, C. A. M. rept. no. 457, 30 June 1945, 4 pp. [P] 
430. Kety, S. S. and C. F. Schmidt. The effects of 
altered arterial tensions of carbon dioxide and oxygen on 
cerebral blood flow and cerebral oxygen consumption of 
normal young men. /. din. Invest., 1948, 27: 484—492. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1949, 2: 488—489. [P] 
431. Kottke, F. J., J. S. Phalen, C. B. Taylor, M. B. 
Visscher, and G. T. Evans. Effect of hypoxia upon tem- 
perature regulation of mice, dogs, and man. Amer. J. 
Physiol, 1948, 153: 10-15. [P] 
432. Leonard!, G. Iperalcolemia endogena in condizioni 
di anossia. Boll. Soc. ital. Biol, sper., 1947, 23: 477-480. 
[P] 
433. Leonard!, G. Iperalcolemia endogena nell’uomo in 
condizioni di ipossia sperimentale. Boll. Soc. ital. Biol, 
sper., 1947, 23: 703-705. 
434. Loeschicke, G. and H. H. Loeschicke. Uber den 
Milchsaureaustausch zwischen arteriellem Blut und Ge- 
hirngewebe und seine Veranderungen im Sauerstoffmangel. 
Pfliig. Arch. ges. Physiol, 1947, 249: 521—538. [P] 
435. Lundin, G. and G. Strom. The concentration of 
blood lactic acid in man during muscular work in relation 
to the partial pressure of oxygen of the inspired air. Acta 
physiol, scand., 1947, 13: 253-266. 
436. MacLachlan, P. L., D. K. Sleeth, and J. Gover. 
Effect of anoxic anoxia on bile secretion in the rat. Proc. 
Soc. exp. Biol, N. Y., 1947, 66: 275-276 [P] 
437. Malmejac, J. and G. Chardon. Sur la resistance 
du systeme adrenalino-secreteur a 1’anoxie. C. R. Soc. 
Biol, Paris, 1946, 140: 1005-1006. [P] 
438. Malmejac, J. and G. Chardon. Mecanisme de 
declenchement et d’entretien de la secretion surrenale 
d’arenaline en anoxie. C. R. Soc. Biol, Paris, 1947, 
141: 395-396. [P] 
439. Malmejac, J. and G. Chardon. Influence du deficit 
en oxygene sur Fadrenalino-secretion. Med. aeronaut., 
1950,5; 19-30. 
440. Moon, V. H. Symposium on inhalational therapy. 
The origins and effects of anoxia. Bull. N. Y. Acad. Med., 
1950, 26: 361-370. 
441. Parkes, A. S. Some factors affecting resistance to 
anoxia in mice. /. Endocrin., October 1951, 7: LXII. [P] 
442. Rein, F. H. Die Funktion von Milz und Leber zur 
Ertragung von lokalem und allgemeinem Sauerstoff- 
Mangel. XVIII Intern, physiol, Congr., 1950, 409. [D] 
443. Sillani, L. S, Comportamento dei grassi totali, del 
fostoro lipoideo, e dei corpi chetonici nel sangue dell 
organismo umano sottoposto all azione di prolungata 
anossia. Riv. Med. aero., Roma, 1948, 11: 15-24. (Eng- 
lish, French, Spanish, and German summaries.) [P] 
444. Smith, D, C. and R. H. Oster. Influence of blood 
sugar levels on resistance to low oxygen tension in the 
cat. Amer. J. Physiol, 1946, 146: 26-32. [P] 
445. Van Loo, A., A. Snrtshin, and L. N. Katz. Nature 
of the two pressor responses to acute hypoxemia with 
some observations on the role of the adrenals in hypoxia. 
Amer. J. Physiol, 1948, 154: 397-404. [P] 
10. TEMPERATURE 
Tolerance to reduced oxygen tensions is known 
to be greater in new-born animals. Adolph (446) 
1948 found that rats between 1 and 4 days of age 
showed a greater tolerance to complete anoxia than 446-447 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
those 11 days old or older. As indicated by a report 
of Miller, Miller, and Farrar {447) 1951, guinea 
pigs showed an increased resistance to asphyxia if 
moderately cooled. The time of death of 202 
asphyxiated, neonatal animals was recorded at 
colonic temperatures between 45.2° C. and 10.9° C. 
Death from temperature occurred at colonic levels 
above 44°C. and below 19° C. A linear increase 
in survival of approximately 50 percent per 10° C. 
decrease in temperature was recorded for the entire 
nonlethal temperature range. The shortest anoxic 
survival was 81 seconds at 44.2° G., the longest was 
at 617 seconds at 14° C. One hundred and three 
young adults similarly tested showed a linear in- 
crease of 35 percent per each 10° C. decrease in 
temperature. In the adult animals, deaths occurred 
above 44° G. and below 16° C. 
446. Adolph, E. E. Loss of tolerances to cold and to 
anoxia in infant rats. Anat. Rec., 1948, 101: 737, Abstr. 
[P] 
447. Miller, J. A., Jr., F. S, Miller, and C. B. Farrar. 
Effects of temperature upon resistance of guinea pigs to 
anoxia. Fed. Proc. Amer. Soc. exp. Biol., 1951, 10: 92. 
11. KIDNEY 
Franklin, McGee, and Ullman {451) 1951 in 
observations on rabbits reported a diversion of the 
renal cortical blood flow following intense anoxia 
and hypercapnia. Urine flow was also inhibited. 
These renal and urinary changes were not seen 
after denervation of the renal pedicle. The blood- 
flow changes in the kidney were independent of the 
blood pressure and may have depended, according 
to the authors, upon chemosensitive centers in the 
spinal cord. Malmejac, Chardon, and Gross {453) 
1946 observed intense vasoconstriction at the be- 
ginning of 8 percent oxygen inhalation, but second- 
arily the hypoxia was not sufficient to evoke a 
change in urinary output. Similar findings have 
been reported by Brull and Divry {449) 1951. 
With Brull’s mechanical heart technique, the kid- 
neys of dogs were perfused alternately with arterial 
and venous blood under varying pressures. It was 
found that under normal conditions of flow the 
oxygen requirements of the kidney could be com- 
pletely covered by an oxygen content of only 30 
percent of normal. A decrease of the inflow pres- 
sure to 50 mm. Hg or lower caused a decrease in 
venous outflow, a cessation of secretion, and a de- 
crease of oxygen consumption to 70 percent of 
normal. It was concluded by the authors that a 
decrease of blood flow through the kidney is prac- 
tically the only mechanism capable of stopping 
secretion. Hypoxia itself was considered to be with- 
out effect. 
Berger, Galdston, and Horwitz {448, 452) 1949 
have investigated the effect of hypoxia upon human 
renal function. In these experiments, human sub- 
jects with normal cardiovascular and respiratory 
systems inhaled air mixtures containing 14 percent 
oxygen. This degree of hypoxia in the normal sub- 
jects resulted in barely perceptible changes in cir- 
culatory and respiratory dynamics. Similar studies 
were conducted on two emphysematous subjects 
with arterial blood oxygen tensions of approxi- 
mately 50 mm. Hg while breathing room air and, 
again, while breathing 100 percent oxygen. For the 
emphysematous subjects the periods of breathing 
room air were considered as the hypoxic periods. 
In both the normal and emphysematous subjects, 
studies were made of glomerular filtration rate, 
inulin clearance, renal plasma flow, and para-amino- 
hippurate clearance. The urine was collected in 15- 
to 30-minute periods by catheter. Urine pH was 
measured. Blood was drawn from the femoral 
artery. The average pulse rate did not change sig- 
nificantly in 4 subjects, while in 5 others it rose 8 
to 14 beats per minute during the anoxic periods. 
Only in 1 instance did the blood pressure rise as 
much as 13 mm. Hg. Renal plasma flow remained 
the same or tended to increase during hypoxia in all 
normal subjects. In the two subjects with pulmonary 
emphysema, the administration of 100 percent 
oxygen induced a fall in renal plasma flow. In these 
subjects the period of breathing room air was asso- 
ciated with an increase in renal plasma flow of 29 
percent. The filtration rate did not change during 
hypoxia in four cases. There was an increase of 9 
to 23 percent in 4 cases, and a decrease of 19 percent 
in 1. The most pronounced effect of hypoxia on 
renal function was an invariable and frequently 
marked increase in the rate of excretion of sodium, 
chloride, and water. Urine flow tended to increase 
during the hypoxic periods. Urinary pH shifted to 
higher values in all subjects except one. Ammonia 
production decreased in all but one observation. 
Potassium was increased. Proteinuria did not de- 
velop. The authors drew the conclusion that 
hypoxia alone does not appear to result in reduc- 
tion of renal plasma flow or retention of salt and 
water. In similar studies on two normal young male 
subjects carried out by Caldwell, Rolf, and White 
{450) in 1949, it was determined that breathing 
low oxygen mixtures at atmospheric pressure, the 
oxygen percentage being 9.3 percent, for periods of 
a few minutes produced no effect on para-aminohip- 
purate or inulin clearance. In these normal subjects 
there was no effect on renal vascular resistance or 
plasma glucose levels. LOW OXYGEN PERCENTAGES—CARBON DIOXIDE EFFECTS 
448—460 
448. Berger, E. Y., M. Galdston, and S. A. Horwitz. 
The effect of anoxic anoxia on the human kidney. /. din. 
Invest., 1949,28: 648-651. [P] 
449. Brull, L. and A, Divry. Metabolic and secretory 
activity of the kidney under anoxemia. Arch. int. Physiol., 
1951, 58: 415-423. 
450. Caldwell, F. T., D. Rolf, and H. L. White. Effects 
of acute hypoxia on renal circulation in man. /. appl. 
Physiol, 1949,1: 597-600. [P] 
451. Franklin, K. J., L. E. McGee, and E. ITllman. 
Effects of severe asphyxia on the kidney and urine flow. 
J. Physiol, 1951,112: 43-53. [P] 
452. Galdston, M., E. Y. Berger, and S. A. Horwitz. 
The effect of anoxic anoxia on the human kidney. /. din. 
Invest., 1949, 28: 648-652. 
453. Malmejac, J., G. Shardon, and A. Gross. Influence 
de 1’anoxie sur la secretion urinaire. C. R. Soc. Biol, Paris, 
1946, 140: 1000-1002. [P] 
12. EFFECTS OF CARBON DIOXIDE ON HYPOXIA 
For studies on the effects of carbon dioxide ad- 
ministration in oxygen mixtures on the hypoxic sub- 
ject and the effect of adding carbon dioxide to 
inspired oxygen on tolerance to hypoxia, papers by 
the following should be consulted: Adler {454) 
1947; Binet and Strumza {455) 1950; Ivy, Grodins, 
Adler, and Snapp {456,457) 1947; Otis, Rahn, and 
Chadwick {458) 1949; Smith {459) 1950; and 
Stone, Webster, Kopala, and Gurdjian {460) 1946. 
Studies on the effects of carbon dioxide inhala- 
tion on the hypoxic animal carried out by Ivy, 
Grodins, Adler, and Snapp {456, 457) 1947 con- 
sisted of tests of the respiratory and circulatory 
responses to carbon dioxide (5 percent, 6 percent, 
and 15 percent) in dogs during the course of acute, 
severe hypoxia produced by the inhalation of 4 per- 
cent oxygen. Under these conditions the stimulatory 
effects of carbon dioxide progressively decreased, 
soon disappeared, and were finally reversed. Fifteen 
percent carbon dioxide produced more frequent and 
more profound respiratory and circulatory depres- 
sion than did 5 percent carbon dioxide. Five percent 
carbon dioxide given at the beginning of collapse 
had no demonstrable effect on blood pressure or 
respiration. Adler {454) 1947 has concluded that 
under conditions of severe hypoxia in dogs, carbon 
dioxide is not indicated as an inhalant in gas mix- 
tures used for resuscitation since it not only fails to 
stimulate the respiratory center and the peripheral 
chemoreceptors but also in the presence of severe 
hypoxia a 5 percent carbon dioxide concentration 
may act as a respiratory and circulatory depressant. 
The depressing effects of a 15-percent concentration 
are even more striking. In confirmation of experi- 
mental findings, the recent literature emphasizes the 
potential hazard of use of carbon dioxide in oxygen 
for purposes of resuscitation. 
Although there is evidence in the literature that 
carbon dioxide may under certain circumstances 
increase tolerance to hypoxia (see, for example, 
459 and 460), nevertheless it does not appear that 
addition of carbon dioxide to respiratory mixtures 
is a practicable or effective means of improving 
efficiency under conditions of hypoxia. For an addi- 
tional report on this subject, a paper by Otis, Rahn, 
and Chadwick {458) 1949 may be consulted. 
454. Adler, H. F. Effect of carbon dioxide on an anoxic 
animal. USAF. Randolph Field, Texas. School of avia- 
tion medicine. Project 474, Kept. no. 2, 31 March 1947, 
1 p. [P] 
455. Binet, L. and M. V. Strumza. Variations du taux 
du C02 total du plasma arterial et resistance des centres 
respiratoires a 1’anoxie. /. Physiol., Paris, 1950, 42: 249- 
258.[P] 
456. Ivy, J. H., F. S. Grodins, H. F. Adler, and F. E. 
Snapp, Studies on asphyxia. II. Effects of carbon dioxide 
inhalation on an anoxic animal. /. Aviat. Med., 1947, 18: 
577-589.[P] 
457. Ivy, J. H., F. S. Grodins, H. F. Adler, and F. E. 
Snapp. Studies on asphyxia. II. Effects of carbon dioxide 
inhalation on an anoxic animal. U. S. AAF. Randolph 
Field, Texas, School of aviation medicine. Project 474, 
Kept. no. 2, 17 July 1947, 5 pp. [P] 
458. Otis, A. B., H. Hahn, and L. E. Chadwick. Effects 
of adding carbon dioxide to inspired oxygen on tolerance 
to high altitudes. Proc. Soc. exp. Biol., N. Y., 1949, 70: 
487-490. 
459. Smith, R. E. Effects of carbon dioxide inhalation 
upon the hypoxia response of normal men. XVIII Intern, 
physiol. Congr., 1950, 457. 
460. Stone, W. E., J. E. Webster, J. Kopala, and E. S. 
Gurdjian. Effects of carbon dioxide administration on 
cerebral metabolism in hypoxia. Fed. Proc. Amer. Soc. 
exp. Biol., 1946,5; 101. 
13. TOLERANCE 
For studies on the effects of various factors on 
sensitivity to hypoxia, papers by the following 
should be consulted: Dustin {461) 1949; Miller, 
Miller, and Farrar {462) 1951; Smith and Smith 
{463) 1951; and Snapp, Adler, and Kramer {464) 
1948. According to Dustin {461) 1949, adrenolytic 
drugs were ineffective in increasing the suscepti- 
bility of anesthetized dogs to hypoxia. According 
to Snapp, Adler, and Kramer {464) 1948, alpha- 
lobeline and coramine were not effective in stimu- 
lating lightly nembutalized dogs rendered apneic by 
breathing pure nitrogen. Metrazol caused spon- 
taneous respiration in 2 out of 9 dogs injected. 
Amphetamine sulfate caused spontaneous respira- 
tion in 10 out of 18 dogs. Intravenous injection of 
glucose before hypoxia did not increase the resist- 
ance of the animal to oxygen lack. Artificial respira- 
tion with 100 percent oxygen was more effective 
in resuscitation than any of the drugs used. Miller, 
Miller, and Farrar {462) 1951 have shown experi- 
mentally in guinea pigs that each degree of tem- 461-481 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
perature reduction increases resistance to asphyxia 
until cold itself become lethal. In contrast, it is 
well known that increasing basal metabolic rate 
enhances the sensitivity of both man and animals 
to hypoxia. For example, Smith and Smith {463) 
1951 have reported increased sensitivity to pro- 
gressive hypoxia in thyroid-treated mice showing in- 
creased basal oxygen consumption. There was also 
decreased tolerance to exercise in these same ani- 
mals. Thyroid administration superimposed upon 
radiation resulted in no increase in basal oxygen 
consumption beyond that caused by thyroid alone. 
However, resistance to progressive hypoxia was 
greater than with thyroid alone in these cases. 
461. Dustin, E. H. Effects of hypoxia on respiration after 
adrenolytic drugs. USAF. Wright-Patterson air force base, 
Dayton, Ohio. Air materiel command, Aero medical lab- 
oratory. Memo. rept. serial no. MCREXD—696—79H, 10 
February 949, 66 pp. [P] 
462. Miller, J. A., Jr., F. S. Miller, and C. B. Farrar. 
Effects of temperature upon resistance of guinea pigs to 
anoxia. Fed. Proc. Amer. Soc. exp. Biol., 1951, 10: 92. 
463. Smith, W. W. and F. Smith, Effects of thyroid 
and irradiation on sensitivity to hypoxia, basal rate of 
oxygen consumption and tolerance to exercise. Amer. J. 
Physiol, 1951, 165: 651-661. 
464. Snapp, F. E., H. F. Adler, and K. Kramer. The 
effect of various respiratory stimulants on dogs depressed 
by anoxia. UASF. Randolph Field, Texas. School of avia- 
tion medicine. Project 21-02-034, Rept. no. 1, Novem- 
ber 1948, 6 pp. [P] 
B. LOW OXYGEN TENSIONS DUE TO DECOMPRESSION 
1. GENERAL STUDIES 
The references cited in this section provide access 
to the general subject of hypoxia due to decom- 
pression in aircraft or in decompression chambers 
or in mountain climbing. This subject is included in 
this Sourcebook because problems of hypoxia are 
encountered in submarine operations and will be- 
come more and more significant under conditions 
of submarine operations involving prolonged sub- 
mergence. For discussions of the literature on hy- 
poxia, reference may be made to annual review 
articles by Hoff and Fulton {473) 1947 and Hoff 
{474) 1948, {475) 1949, and {476) 1950. These 
reviews contain comprehensive bibliographies. Ex- 
cellent reviews on hypoxia in man and animals by 
Fulton and Nims {471) 1941-46 and Nims {480) 
1948 should be read. These serve as a useful guide 
to studies on the physiology of low oxygen tensions. 
A good review article coming from Italy is that of 
Vacca {482) 1949. This article covers research on 
hypoxia carried out between 1945 and 1948 and 
contains approximately 200 references on the sub- 
ject as it applies to respiration, heart and circula- 
tion, nervous system, and metabolism. 
465. Balanina, N. V. K voprosu o reaktivnosti organ- 
izma i o sostoianii aktivino soedinitel’noi tkani pri gipok- 
semii. [Reactivity of the organism and the condition of 
active connective tissue in hypoxemia.] Arkhiv patol., 
Moskva, 1947, 4: 86-90. 
466. Barach, A. L, Additional studies on anoxia and its 
treatment, pp. 43—85 in: Physiologic therapy in respiratory 
diseases. Second edition. Philadelphia, J. B. Lippincott 
Company, 1948, 408 pp. 
467. Bartley, S. H. and E. Chute. Anoxia and related 
living conditions, pp. 71-90 in: Fatigue and impairment 
in man. New York, McGraw-Hill Book Co., Inc. 1947, 
429 pp. [R] [P] 
468. Binet, L. and M. V. Strumza. Effets de 1’apnee 
anoxique prolongee et repetee. C. R. Acad. Sci., Paris, 
1949, 229: 688—690. Excerpta Medica. Section II. (Physi- 
ology, Biochemistry, and Pharmacology), 1950, 3: 1494. 
469. Castaigne, P. Les anoxies. Pr. med., 1950, 
58: 120—123. Excerpta Medica. Section II. (Physiology, 
Biochemistry, and Pharmacology), 1950, 3: 1050. 
470. Evrard, E. Observations experimentales relatives 
aux effets des vitesses ascensionnelles rapides sur 1’organ- 
isme de Paviateur. (A suivre.) Brux. med., 1949, 29: 
3639-3657. Excerpta Medica. Section II. (Physiology, 
Biochemistry, and Pharmacology), 1950, 5; 1003. 
471. Fulton, J. F. and L. F. Nims. Decompression sick- 
ness. Anoxia in man and animals. Anoxia in man. pp. 11— 
14 in Final Rept. in: Studies in Aviation Medicine. Yale 
University School of Medicine, New Haven, Conn., Yale 
aero-medical research unit. 1941-1946. [P] 
472. Gray, J. S. and F. S. Grodins. Respiration. Respira- 
tory disturbances. Annu. Rev. Physiol., 1951, 13: 227- 
229. [R] 
473. Hoff, E. C. and J. F. Fulton. Aviation medicine, 
pp. 261-285 in: The cyclopedia of medicine, surgery, and 
specialties. Edited by G. M. Piersol and E. L. Bortz. 
Philadelphia, F. A. Davis Co., 1947, pp. 1153. [R] 
474. Hoff, E. C. Aviation medicine, pp. 229-252 in: 
The cyclopedia of medicine, surgery, and specialties. 
Edited by G. M. Piersol and E. L. Bortz. Philadelphia, 
F. A. Davis Co., 1948, 953 pp. [R] 
475. Hoff, E. C. Aviation medicine, pp. 227-249 in: 
The cyclopedia of medicine, surgery, and specialties. 
Edited by G. M. Piersol and E. L. Bortz. Philadelphia, 
F. A. Davis Co., 1949, 989 pp. [R] 
476. Hoff, E. C. Aviation medicine, pp. 229-256 in: 
The cyclopedia of medicine, surgery, and specialties. 
Edited by G. M. Piersol and E. L. Bortz. Philadelphia, 
F. A. Davis Co., 1950, 1021 pp. [R] 
477. Ivy, A. C. High altitude problems in aviation. 
Fed. Proc. Amer. Soc. exp. Biol., 1946, 5: 319-327. 
478. Lund, D, W. Altitude sickness, acute and chronic, 
pp. 4—378—4-384 in; Treatment in general medicine. 
Volume 4. Edited by Hobart A. Reimann. Fourth edition. 
Philadelphia, F. A. Davis Co., 1948, 776 pp. 
479. Muralt, A. V. Klimaphysiologische Untersuchungen 
in der Schweiz. Helvet. physiol, pharm. Acta., {suppi.), 
1944, 3: 7-14. [D] 
480. Nims, L. F, Anoxia in aviation. Annu. Rev. Physiol., 
1948, 10: 305-314. [R] 
481. Tufts College. Altitude. 15 pp. in: Handbook of 
human engineering data for design engineers. Tufts Col- 
lege, Institute for applied experimental psychology. SDC 
Human Engineering Project 20-G-l, Project Designation 
NR-783-001, Technical Report 199-1—1, 1 December 
1949,410 pp. LOW OXYGEN TENSIONS—SPECIAL SENSES 
482-484 
482. Vacca, C. Risultati di moderne ricerche sugli effetti 
provocati dall’anossia neU’organismo umano. Riv. Med. 
aero., Roma, 1949, 12: 59-92. Excerpta Medica. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1950, 
3: 762. [R] 
483. Von Tavel, F. The influence of oxygen-lack on the 
human organism on brief exposure to high altitudes. A 
contribution to the question of functional capacity during 
flight at high altitude. Helvet. physiol, pharm. Acta, 
(Supplementum) 1943, 1: 1-128. [P] 
484. White, M. S. Prolonged hypoxia in aircraft passen- 
gers. The effects of a flight around the world in 6% days. 
/. Aviat. Med., 1947, 18: 244-251 and 288. [P] 
2. SPECIAL SENSES 
The use of flicker frequency, dotting, and writing 
tests in untrained subjects as a measure of response 
to hypoxia, has been critically tested by Murray 
{498) 1943. Results suggest that none of the tests 
are to be confidently recommended for selection 
of the individual with respect to response to hy- 
poxia. However, the flicker test might prove useful 
in preliminary testing of a group. In experiments 
of Birren, Fisher, Vollmer, and King {485) 1946, 
critical flicker frequency and perimetry were used 
to determine changes in performance of small 
groups of subjects under hypoxic conditions, simu- 
lating altitudes of 10,000 feet and above. Body 
sway was used to demonstrate differences in per- 
formance at simulated altitudes of 14,000 feet and 
above. The magnitude of most changes were such 
that individual scores were within normal distribu- 
tion of values at sea level and so could not be used 
as criteria, in a clinical sense, of extent of hypoxia 
in the individual. Perimetry and critical flicker fre- 
quency were not significantly altered. Apparently 
visual functions do not reflect factors determining 
imminent collapse of a subject to hypoxia. Accord- 
ing to the authors, lack of correlation between per- 
formance decrements and these tests suggests con- 
siderable variation in the underlying physiological 
adjustments to hypoxia. 
According to Motokawa and Iwama {497) 1949, 
the electric excitability of the human eye is a sensi- 
tive and accurate measure for oxygen deficiency 
and more suitable as an index of oxygen deficiency 
than light sensitivity. 
Visual contrast discrimination has been used as 
a method of demonstrating the effect of hypoxia on 
sensory performance. Hecht, Hendley, and Frank 
{494) 1943 have studied visual-contrast discrimi- 
nation in oxygen concentrations corresponding to 
altitudes up to 17,000 feet at 3 brightness levels 
corresponding to visual conditions between dawn 
and sunrise, between sunset and dark, and day- 
time conditions only. At these brightnesses, con- 
trast discrimination was found to deteriorate at 
fairly low altitudes. The deterioration was obvious 
at 8,000 feet simulated altitude and became striking 
at a simulated altitude of 15,000 feet where, at low 
brightness, it was found that the contrast must be 
increased 100 percent over sea level before it can be 
recognized. The impairment of contrast recogni- 
tion with increase in altitude was found to be 
greater at higher altitudes than lower. The impair- 
ment of contrast discrimination was found to vary 
inversely with brightness. It was found to be most 
evident under the lowest light intensities studied, 
but it was observed in all light intensities examined. 
The thresholds for night vision and day vision were 
equally affected by hypoxia. The authors recom- 
mended that even at moderate altitudes, say 8,000 
feet, extra oxygen be taken at all illuminations ex- 
cept during full daylight. For further studies on con- 
trast sensitivity, papers by Chapanis {486) 1946 
and Peckham {499) 1943 may be consulted. 
Regarding other effects of hypoxia upon visual 
function, Duquet {487) 1947 found that stereo- 
scopic vision is quite resistant to hypoxia. In sub- 
jects exposed to 6,000 meters altitude, there was no 
appreciable difference between the values of stereo- 
scopic parallax at altitude and sea level. In contrast, 
fatigue rate of accommodation and convergence 
are stated by Giardini {491) 1949 to be adversely 
affected at an altitude of 3,900 meters. 
For studies on the effects of hypoxia on visual 
field, papers by the following may be consulted: 
Duguet and Bailliart {488) 1947, Halstead {493) 
1945, Livingston {495) undated, and Posternak 
{501) 1948. For effects on night vision, papers by 
Maynard {496) 1945 and Posternak {500) 1948 
should be read. According to Grandjean and Zwah- 
len {492) 1948, there was a rise in retinal arterial 
pressure in human subjects during a stay at the 
Jungfraujoch (3,450 meters). This elevation of 
pressure was considered by the authors to reflect a 
circulatory modification parallel to the level of the 
cerebral vessels. In a study by Duguet, Dumont, and 
Bailliard {489) 1947, young male subjects were 
submitted to simulated altitudes in a decompres- 
sion chamber while changes in retinal vessels were 
continually studied by photographing the retina, 
first at ground level and then at 4,000, 5,000, and 
6.000 meters. Experiments were first carried out 
without additional oxygen and then during admin- 
istration of oxygen. Dilatation of the retinal vessels 
became noticeable and could be measured in photo- 
graphs beginning at 4,000 meters. The dilatation 
increased with altitude, reaching its maximum at 
6.000 meters, but did not increase after the subject 
had been at that level for 15 minutes. The magni- 485-505 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
tude of the dilatation varied from one subject to 
another, ranging from 10 to 39 percent of the 
diameter as measured at sea level. The average 
change was 21 percent. There was also venous dila- 
tation ranging from 10 to 34 percent (average 18 
percent) of the sea-level values. The retinal vessels 
were found to return to their original size imme- 
diately on return to sea level or while breathing 
oxygen at high altitudes. Hypoxic dilation of the 
retinal vessels was seen to be a test of circulatory 
efficiency. 
For other studies on the effects of hypoxia upon 
visual function, papers by Ferrata {490) 1950, 
Scobee {502) 1944, and Tschirren and Wiesinger 
{504) 1948 should be consulted. 
According to studies of Seitz and Smith {503) 
1942, exposure of human subjects to a simulated 
altitude of 18,500 feet resulted in a decrement of 
auditory sensitivity as measured by speech intelli- 
gibility. As to tactile sensitivity, this was found to be 
increased by Awahlen and Grandjean {505) 1948 
in subjects studied in the course of an expedition 
to Jungfraujoch (3,450 meters). 
485. Birren, J. E., M. B. Fisher, E. Vollmer, and B. 6. 
King. Effects of anoxia on performance at several simu- 
lated altitudes. /. exp. Psychol., 1946, 36: 35-49. 
486. Chapanis, A. A device for demonstrating the effects 
of anoxia on vision. J. Aviat. Med. 1946, 17: 348-356. 
487. Duguet, J. Le comportement de la parallaxe stereo- 
scopique en anoxemie. MSd. aeronaut., 1947, 2: 36-42. 
[Ch] [P] 
488 Dugnet, J. and J. P. Bailliart. Les modifications 
du champ visuel central sous 1’influence de 1’anoxemie et 
de Finhalation d’oxygene. Med. aeronaut., 1947, 2: 516— 
523. [P] [D] 
489. Duguet, J., P. Dumont, and J. P. Bailliart. The 
effects of anoxia on retinal vessels and retinal arterial 
pressure. J. Aviat. Med., 1947, 18: 516-520. [P] 
490. Ferrata, L. Sul comportamento degli angioscotomi 
retinici in anossia. Riv. Med. aero., Roma, 1950, 13: 
50-56. (English, French, Spanish, and German sum- 
maries. ) 
491. Giardini, A. Faticabilita del meccanismo accomo- 
dazione-convergenza in anossia acuta. Riv. Med. aero., 
Roma, 1949, 12: 511-525. (English, French, Spanish, and 
German summaries.) [P] 
492. Grandjean, E. and P. Zwahlen. Modifications de 
1’ophtalmotonus et de la pression arterielle retinienne en 
haute montagne. Helvet. physiol, pharm. Acta, 1948, 6: 
560-566. (English summary.) 
493. Halstead, W. C. Chronic intermittent anoxia and 
impairment of peripheral vision. Science, 1945, 101: 
615-616. [P] 
494. Hecht, S., C. D. Hendley, and S. Frank. The effect 
of anoxia on visual contrast discrimination. U. S. NRG— 
CAM. C. A. M. rept. no. 184, 15 August 1943, 13 pp. [P] 
495. Livingston, P, C. Report on effects of anoxia, 
carbon monoxide, and diabetes on the field of vision. Gt. 
Brit. FPRC. F. P. R. C. 451, undated, 2 pp. [P] 
496. Maynard, F. L. Low pressure chamber demonstra- 
tion of the effect of anoxia on night vision held at N. A. S. 
Grosse He, Michigan, 28 November 1945. U. S. Navy, 
Quonset Point. Project X-580 (Av-299-f), Kept. no. 3, 
12 December 1945, 8 pp. 
497. Motokawa, K. and K. Iwama. The electric ex- 
citability of the human eye as a sensitive indicator of 
oxygen deficiency. Tdhoku J. exp. Med., 1949, 50-51: 
319-328. 
498. Murray, G. D. The effect of acute anoxia upon 
flicker, dotting and handwriting tests in twenty untrained 
subjects. U. S. Navy, NATO, Pensacola, Fla., School of 
aviation medicine. Project X-lll (Av-R7-5), 15 Febru- 
ary 1943, 4 pp. [P] 
499. Peckham, R. H. Loss of visual contrast discrimina- 
tion. U. S. Navy. NATO, Pensacola, Fla., School of avia- 
tion medicine. Project X-153 {Av-R5-1), 4 June 1943, 
6 pp. [P] 
500. Posternak, J. L’adaptation visuelle a Pobscurite 
au Jungfraujoch. Helvet. physiol, pharm. Acta, 1948, 6: 
516-523. (English summary.) 
501. Posternak, J. Le champ visuel a 1’altitude. Helvet. 
physiol, pharm. Acta, 1948, 6: 524-527. [P] 
502. Scobee, R. G. The effect of exhaustion and of mod- 
erate anoxia on ocular muscle balance. U. S. AAF. 
Randolph Field, Tex. School of aviation medicine. 
Project 292, Rept. no. 1, 18 July 1944, 3 pp. [P] 
503. Seitz, C. P. and G. M. Smith. Auditory sensitivity 
under conditions of anoxia; A study of speech intelligi- 
bility. City College of New York, Psychological laboratory. 
29 January 1942, 10 pp. [P] 
504. Tschirren, B. and K. Wiesinger. Untersuchungen 
fiber den zeitlichen Verlauf des konsensuellen Pupil- 
lenreflexes beim Ubergang in die Hohe. Helvet. physiol, 
pharm. Acta, 1948, 6: 554-559. [P] 
505. Zwahlen, P. and E. Grandjean. Variation des 
sensibilites corneene et cutanee a Faltitude. Helvet. 
physiol, pharm. Acta, 1948; 6: 471-473. (English 
summary.) 
3. NERVOUS SYSTEM 
Reports by the following authors are devoted to 
investigations of the effects of decompression hy- 
poxia on psychological functioning and psycho- 
motor performance; Anthony, Clarke, Liberman, 
Miles, Nims, Tepperman, and Wesley {507) 1943; 
Fabre, Rougier, and Broussin {509) 1948; Gantt, 
Thorn, and Dorrance {512) 1949; Gerathewohl 
{514) 1951; Grandjean {515) 1948; Green {516) 
1947; Hall {518) 1950; Halstead {519) 1943; 
Klingman {523 and 524) 1947; Liberman, Miles, 
Nims, and Wesley {527) 1944; Mackenzie, Riesen, 
Bailey, Tahmisian, and Crocker {532) 1945; 
Ricketts, Adams, Alving, Bay, Bryan, Carmichael, 
Case, Halstead, and Landowne {534) 1945; Russell 
{535) 1948; Scow, Krasno, and Ivy {536) 1950; 
Smith {538) 1948; and Van Liere {541) 1942. 
These studies generally point out that of all tissues 
of the body, the nervous system is perhaps least 
capable of withstanding oxygen want. 
According to Gellhorn and Ballin {513) 1950, 
normal and adrenal-demedullated rats anesthetized 
with pentothal show a greater susceptibility to 
electroshock-induced convulsions under moderate LOW OXYGEN TENSIONS—NERVOUS SYSTEM 
degrees of hypoxia (280 mm. Hg for 10 minutes) 
than at normal barometric pressure. It was found 
that unanesthetized rats, shocked at a stage of 
hypoxia when righting reflexes are lost, responded 
more frequently with convulsions and showed more 
severe convulsions than under control conditions. 
On the contrary, it was observed that severe hypoxia 
leading to functional elimination of the cortex and 
brain stem reduced the susceptibility to convulsions. 
It was suggested by the authors that the increased 
susceptibility to convulsions in moderate anoxia was 
related to release of the subcortical structures. 
Hypoxia tends generally to reduce spinal reflex 
action. For papers on this subject, reports by the 
following authors may be consulted: Guibert {517) 
1951, Petrov {533) 1949, and Sillani {537) 1947. 
Beyne, Chauchard, and Chau chard, {508) 1947 
determined variations in chronaxie in man in a 
chamber subjected to a simulated altitude of 4,500 
to 5,000 meters. Chronaxie was determined on the 
median and radial nerves by inserted electrodes. 
It was found that under the conditions of these ex- 
periments chronaxie was doubled and sometimes 
quintupled. For a study of anoxic depolarization of 
frog nerves, a paper by Lorente de No {530) 1947 
should be consulted. 
For a detailed review of the histopathological 
changes within the central nervous system after ex- 
posure to high altitudes, hypoglycemia and other 
conditions associated with central hypoxia, a report 
by Hoff, Grenell, and Fulton {520) 1945 should be 
consulted. This report contains a very full bibliog- 
raphy. Under conditions of reduced barometric 
pressures, ganglian-cell changes correspond closely 
to those encountered in animals exposed to low 
oxygen mixtures at sea level. The cerebral cortex is 
usually spared. The medulla and cerebellar cortex 
are particular sites of election but damaged nerve 
cells are found scattered throughout the brain stem. 
In general, there are few or no changes in the spinal 
cord. In the affected ganglian cells the Nissl sub- 
stance is characteristically fragmented or broken up 
into fine dustlike particles. The cytoplasm may be 
vacuolated or homogeneously stained. There may 
be swelling or shrinkage of the cells. The nuclei may 
be displaced, irregular in shape, shrunken or darkly 
staining, and amorphous. Varicosities of the den- 
drites are sometimes characteristic. Animals sub- 
jected to a single lethal exposure at a simulated 
altitude of 12,000 meters for 40 to 110 minutes do 
not tend to show neuropathological changes, nor 
are the lesions present in the brains of animals 
sacrificed after repeated short, daily, sublethal de- 
compressions to this altitude. Exposure to single 
periods of decompression to 250 mm. Hg. for 33 
to 104 hours does not result in histologically demon- 
strable lesions if the animals are sacrificed immedi- 
ately after the experiment, although such animals 
usually die spontaneously some days later with 
marked changes in the brain. In general, pathologi- 
cal changes are most pronounced and widespread in 
animals succumbing to repeated decompression or 
dying some days after single exposures to low 
pressure. 
Titrud and Haymaker {540) 1947 have pre- 
sented a clinicopathological study of two cases of 
high altitude death with unusually long survival. 
They have also given a clinical report of a nonfatal 
case. In the two fatal cases, death occurred in 40 
hours and 3 weeks after exposure to altitude. The 
third case, the nonfatal one, was observed for 3 
weeks. The degree and duration of hypoxia in each 
case is not accurately known. In the first case, the 
accident occurred at higher than 20,000 feet. The 
patient was found unconscious 5 minutes after the 
completion of a bombing run. The second patient 
was exposed to an altitude of 24,000 feet for ap- 
proximately 10 minutes. In the third case, exposure 
was at an altitude of 27,000 feet. In the first fatal 
case there was conspicuous necrosis of ganglian cells 
in the cerebral cortex, basal ganglia, cerebellum, 
and the anterior horns of the spinal gray matter. 
There was also degeneration of myelin in the in- 
ternal capsule. In the second fatal case, the changes 
were virtually the same, except that the cerebral 
white matter, the brain stem, and spinal cord 
tended to be spared. In a report of observations at 
autopsy in 75 cases of high-altitude hypoxia, Lewis 
and Haymaker {525) 1949 found conspicuous evi- 
dence of circulatory failure. In most cases the blood 
in the heart and large vessels had not clotted. 
There were hemorrhages in the lungs, myocardium, 
submucosa of the intestinal tract, adventitia of the 
aorta, mastoid and petrosal sinuses, paranasal 
sinuses, and the middle and internal ear. Hemor- 
rhages in the brain were small and sparse. Intra- 
cellular vacuoles, containing inclusions, were found 
throughout the body, but were especially prominent 
in the liver and the heart. Though the periods of 
hypoxia in question were rarely longer than 20 
minutes, shrinkage and chromatolysis of ganglion 
cells were prominent. The cells of the cerebral cor- 
tex were mostly affected, especially in the hippo- 
campus. 
In an experimental series reported by Jensen, 
Becker, and Windle {522) 1949, young adult male 
guinea pigs were subjected to atmospheric condi- 
tions simulating an altitude of 30,000 feet in a 
decompression chamber for 6 hours daily, 6 days 
weekly up to 100, 150, 200, and 250 hours. At 506-519 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
appropriate times the experimental animals and 
controls were killed by perfusion of a solution of 
formaldehyde. The animals responded to reduced 
barometric pressure by remaining quiet, usually 
with episodes of physical distress, collapse, and ap- 
parent unconsciousness. After removal from the 
chamber, comparison with controls rarely revealed 
significant behavior changes or physical differences. 
No permanent neurological defects were observed. 
Exposure for 150, 200, and 250 hours resulted in 
retentive loss in ability to solve an alternation maze 
problem. All control animals solved the problem to 
the point of perfection. Focal areas of degeneration 
were discovered in the vermis of the cerebellum of 
all animals killed after 250 hours of exposure and in 
3 of the 7 animals after 100 and 150 hours. Else- 
where in the brain there were small areas of shrink- 
age of impaired staining. For the most part, the 
tissues of the brain appeared normal and most 
regions looked exactly like the controls. The his- 
tological studies failed to reveal an anatomical basis 
for the defect in memory. However, the most strik- 
ing memory defects occurred in the group of animals 
exposed to decompression for the maximum time, 
and it was in this group also that structural changes 
in the brain were most consistently revealed. 
Lindenberg {528) 1951 pointed out that the 
duration of hypoxia preceding death affects the 
post-mortem morphological appearance of ganglion 
cells. In instantaneous death, the ganglion cells ex- 
hibited homogenization with and without shrinkage, 
vacuolation, and incrustation of the Golgi appa- 
ratus. When the brain was kept at body tempera- 
ture, simple swelling appeared in 30 minutes, fol- 
lowed by homogenization and vacuolation in 6 
hours. If death was preceded by severe hypoxia last- 
ing 10 to 15 minutes, vacuolation seldom occurred 
and homogenization was incomplete; 30 minutes of 
hypoxia produced immediate post-mortem pyknosis 
and shrinkage; after hypoxia of 60 minutes the cells 
showed no noticeable changes between death and 
fixation. In a further report, Lindenberg {520) 
1951 reported that in all cases of acute death, with 
fixation of the brain 8 to 46 hours after death, clas- 
matodendrosis of the astrocytes occurred. If severe 
hypoxia of less than 30 minutes’ duration preceded 
death, clasmatodendrosis was accompanied by acute 
swelling, which did not occur if the hypoxic phase 
lasted 30 to 60 minutes. In cases of subacute death 
preceded by hypoxia lasting longer than 60 min- 
utes, the astrocytes revealed size variations and 
curling of the dendrites. Clasmatodendrosis was 
absent even 48 hours after death. Cell changes after 
acute death were principally those following fresh, 
local disturbance of the circulation by an embolism. 
For further studies on the effects of decompres- 
sion hypoxia on the nervous system, papers by the 
following authors should be consulted; Adams, 
Alving, Bay, Bryan, Carmichael, Case, Halstead, 
Landowne, and Ricketts {506) 1943; Fleisch and 
Grandjean {511) 1948; Hoffman, Clark, and 
Brown {521) 1945; Lifshits {526) 1949; di Macco 
{531) 1946; Suzuki and Masuda {539) 1951; Vol- 
ochov and Obraszova {542) 1950; and Fenn, Gal- 
ambos, and Rahn {510) 1950. 
506. Adams, W. R., A. S. Alving, E. B. Bay, A. H. 
Bryan, H. T. Carmichael, T. J. Case, W. C. Halstead, 
M. Landowne, and H. T, Ricketts. The effects of chronic 
intermittent anoxia in man; introduction, summary of 
results at 10,000 and 11,500 feet and conclusions. U. S. 
NRC-CAM. C. A. M. rept. no. 160, 20 July 1943, 7 pp. 
507. Anthony, R. A., R. W, Clarke, A. Liberman, W. R. 
Miles, L. F. Nims, J. Tepperman, and S. M. Wesley. 
A comparison of the psychological effects of first and 
second hours of exposure to anoxia at 15,000 feet. U. S. 
NRC-CAM. Yale aeromedical research unit. C. A. M. 
Rept. no. 141, 8 June 1943, 7 pp. 
508. Beyne, J., P. Chauchard, and B. Chauchard. 
Les facteurs conditionnant les variations d’excitabilite 
nerveuse en depression atmospherique chez 1’homme. C. R. 
Acad. Sci., Paris, 1947, 225: 437-439. 
509. Fabre, R., G. Rougier, and J. Broussln. Quelques 
experiences relatives a 1’apparition d’une activite psycho- 
physiologique inconsciente au cours de 1’anoxemie chez 
1’homme. Med. aeronaut., 1948, 3: 29-44. [P] 
510. Fenn, W. 0., R. Galambos, A. B. Otis, and 
H. Rahn. Corneo-retinal potential in anoxia and acapnia. 
J. appl. Physiol., 1950, 1: 710-716. Excerpta Medica. Sec- 
tion II. (Physiology, Biochemistry, and Pharmacology), 
1950, 3: 1256. 
511. Fleisch, A. and E. Grandjean. Der Tonus der 
Skelettmuskulatur im Hohenklima. Helvet. physiol, pharm. 
Acta, 1948, 6: 474-483. (English summary.) 
512. Gantt, W. H., G. W. Thorn, and C, Dorrance. 
Anoxia on conditional reflexes in dogs. Fed. Proc. Amer- 
Soc. exp. Biol., 1949, 8: 53. 
513. Gellhorn, E. and H. M. Ballin, Further investi- 
gations on effect of anoxia on convulsions. Amer. J. 
Physiol., 1950, 162: 503-506. Excerpta Medica. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1951, 
4: 647. Abstr. [P] 
514. Gerathewohl, S. J. Method for the analysis of 
psychomotor performance under hypoxia. J. Aviat. Med., 
1951, 22: 196-206.[P] 
515. Grandjean, E. Fonctions nerveuses a 1’altitude. 
Helvet, physiol, pharm. Acta, 1948, 6: 489-515. (English 
summary.) 
516. Green, D. M. Variations in the effect of anoxia on 
performance. Amer. J. Physiol., 1947, 151: 588-592. [P] 
517. Guibert R. Effet d’un sejour a une altitude 
moyenne sur les seuils de la sensibilite cutanee et du 
reflexe rotulien. These (Med.) Lausanne, 1951, 20 pp. 
518. Hall, F. G. Factors affecting consciousness time 
at altitude. Part II. USAF. Wright-Patterson air force 
base, Dayton, Ohio. Air materiel command. AF technical 
rept. no. 6009, September 1950, 24 pp. [P] 
519. Halstead, W. C. The effects of chronic inter- 
mittent anoxia. Neuropsychological aspects. U. S. NRC- 
CAM. C. A. M. rept. no. 159, 20 July 1943, 15 pp. [P] LOW OXYGEN TENSIONS—HEART AND CIRCULATION 
520-542 
620. Hoff, E. C., R. G. Grenell, and J. F. Fulton. 
Histopathology of the central nervous system after ex- 
posure to high altitudes, hypoglycemia and other condi- 
tions associated with central anoxia. Medicine, Baltimore, 
1945, 24: 161-217. 
521. Hoffman, C. E., R. T. Clark, and E. B. Brown, 
The rates of fall of blood oxygen saturations at simulated 
altitudes following mask removal. U. S. Navy. NATO, 
Pensacola, Fla. School of aviation medicine. Project 
X-572, 1 December 1945, 11 pp. 
522. Jensen, A. V., R. F. Becker, and W. F. Windle. 
Changes in brain structure and memory after intermittent 
exposure to simulated altitude of 30,000 feet. Arch. Neurol. 
Psychiat., Chicago, 1948, 60: 221-239. Abstr. World Med., 
1949, 6: 5. 
523. Klingman, W. 0. Disturbances of the nervous sys- 
tem due to anoxia and related factors in flying personnel. 
Arch. Neurol. Psychiat., Chicago, 1947, 59: 813-817. 
524. Klingman, W. 0. Nervous system disturbances from 
anoxia and related factors in flying personnel. J. nerv. 
ment. Dis., 1947, 106: 388-393. 
525. Lewis, R. B. and W. Haymaker. High altitude 
hypoxia. Observations at autopsy in 75 cases and an 
analysis of the causes of the hypoxia. J. Aviat. Med., 1948, 
19: 306-336. Abstr. World Med. 1949, 6: 395. 
526. Lifshits, A. V. Vliianiie gipoksemii na vysshuiu 
nervnuiu deiatel’nost’. [The effect of hypoxemia on the 
higher nervous functions.] Fiziol. Zh. S. S. S. R., 1949, 
35: 3-15. 
527. Liberman, A. M., W. R. Miles, L. F. Nims, and 
S. M. Wesley. The effects of acute anoxia upon psychologi- 
cal function in man at altitudes of 3,000, 10,000, 13,000, 
and 16,000 feet. U. S. NRC—CAM. Yale aeromedical re- 
search unit. Rept. no. 29, C. A. M. rept. no. 324, 15 July 
1944, 6 pp. 
528. Lindenberg, R. Neurohistological investigations on 
general oxygen deficiency of the brain. The morphological 
behavior of the ganglion cells after generalized acute and 
subacute hypoxia. USAF. Randolph Field, Tex. School 
of aviation medicine. Project 21-23-004, Rept. no. 1, 
February 1951, 22 pp. 
529. Lindenberg, R. Neurohistological investigations on 
general oxygen deficiency of the brain. II. The behavior 
of astrocytes after acute and subacute death. USAF. 
Randolph Field, Tex. School of aviation medicine. 
Project 21-23-004, Rept. no. 2, March 1951, 11 pp. 
530. Lorente de No, R. Anoxic depolarization of frog 
nerve. Stud. Rockefeller Inst. med. Res., 1947, 131: 
114-147. [P] 
531. Macco, G. di. Ipossia e sistema neurovegetativo. 
Boll. Soc. ital. Biol, sper., 1946, 22: 822. 
532. Mackenzie, C. G., A. H. Riesen, J. R. Bailey, T. N. 
Tahmisian, and P. L. Crocker. Duration of consciousness 
in anoxia at high altitudes. /. Aviat. Med., 1945, 16: 
156-164.[P] 
533. Petrov, I. P. O spinal’noi arefleksii u ozhivlennykh 
zhivotnykh. [Spinal areflexia in revived animals.] pp. 
123—127 in: Kislorodnoe golodanie golovnogo mozga; 
eksperimental’nye materialy [Oxygen deficiency of the 
cerebrum; experimental material.] Medgiz, Leningrad, 
1949, 204 pp. 
534. Ricketts, H. T., W. R. Adams, A. S. Alving, E. B. 
Bay, A. H. Bryan, H. T. Carmichael, T. J. Case, W. C. 
Halstead, and M. Landowne. The effects of mild anoxia 
on neuromuscular coordination in skilled investigators. 
J. Aviat. Med., 1945, 16: 429-431. 
535. Russell, R. W. The effects of mild anoxia on simple 
psychomotor and mental skills. /. exp. Psychol., 1948, 38: 
178-187. 
536. Scow, J., L. R. Krasno, and A. C. Ivy. The im- 
mediate and accumulative effect on psychomotor per- 
formance of exposure to hypoxia, high altitude and hyper- 
ventilation. /. Aviat. Med., 1950, 21: 79-81. Abstr. 
World Med., 1950, 8: 570. 
537. Sillani, L. Comportamento del riflesso patellare 
nel’anossia. Riv. Med. area., Roma, 1947, 10: 125-143. 
(Italian, English, French, Spanish, and German sum- 
maries. ) 
538. Smith, G, M. The differential effect of prolonged 
mild anoxia on sensory and sensory-motor reactions and 
on such subjective states as sleepiness, irritability and 
boredom. /. gen. Psychol., 1948, 38: 3-14. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and Phar- 
macology), 1949, 2: 242. Abstr. 
539. Suzuki, S. and M, Masuda. A study on changes of 
isoelectric points of the nucleoplasm of nervous cells in 
the hypothalamus and of motor cells in spinal cord of 
albino rats under the low atmospheric pressure. Osaka 
Univ. med. J., 1951, 3: (Japanese text pagination), 
189-196. (In Japanese with English summary), 189. 
540. Titrud, L. A. and W. Haymaker. Cerebral anoxia 
from high altitude asphyxiation. A clinico-pathologic 
study of two fatal cases with unusually long survival and 
a clinical report of a nonfatal case. Arch. Neurol. 
Psychiat., Chicago, 1947, 57: 397-416. 
541. Van Liere, E. F. Effect of anoxia on the nervous 
system, pp. 208-254 in: Anoxia. Its effect on the body. 
Chicago, The University of Chicago Press. 1942, 269 pp. 
542. Volochov, A. A. and G. A. Obraszova. [Influence of 
anoxia on the nervous system; disturbance of locomotor 
functions in anoxia.] Fiziol. Zh. S. S. S. R., 1950, 36: 
450-456. (Russian text.) 
4. HEART AND CIRCULATION 
For general studies of the effects of decompres- 
sion hypoxia upon the heart and circulation, papers 
by the following should be consulted: Houston and 
Riley (550) 1947, Starr and McMichael (561) 
1948, and Van Liere {565) 1942. The latter author 
has pointed out that under progressive hypoxia 
there is acceleration of the heart with alteration in 
systolic blood pressure, the pressure being main- 
tained, rising and then gradually falling. The pulse 
pressure remains unchanged or increases. Within 
certain ranges there may be an increase in cardiac 
output which may play an important part in the 
capacity of the individual to withstand hypoxia and 
to acclimatize to high altitude. Coronary flow is 
said to increase greatly when oxygen is reduced to 
8 or 9 percent. Moderate hypoxia may produce 
vagospasm and could in part account for the delay 
in the cardiac impulse. Severe anoxia probably 
produces delayed conduction by directly affecting 
conduction tissue. The electrocardiogram under 
conditions of hypoxia shows a diminished or in- 
verted T-wave, lengthening of the P-R interval, 
and deformity of the QRS complex. Severe anoxia 543-559 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
may result in cardiac dilatation. Continued exposure 
to hypoxia may produce cardiac hypertrophy. 
For studies on the effects of decompression hy- 
poxia upon cardiac action with particular refer- 
ence to the electrocardiogram, papers by the fol- 
lowing should be consulted: Baum, Malmo, and 
Sievers {544) 1945; Kirschbaum {551) 1951; Plas, 
Tabusse, Missenard, and Goujon [554) 1947; Rotta 
[555) 1947; Schutz [560) 1948; and Wyss-Dunant 
(569) 1950. 
For studies on the effects of decompression hy- 
poxia upon blood pressure, papers by the following 
may be consulted: Franzblau, Vawter, Pestel, and 
Marbarger [545) 1951; Rotta and Miranda [556) 
1949, Stavraky (562) 1945; Stavraky [563) 1946; 
Wezler and Frank (566) 1948; and Whitehorn 
(567) 1948. Papers on the effects of hypoxia on 
capillary circulation, fragility, and permeability 
have been reported by the following: Gabay [546) 
1951; Henry, Klain, Movitt, and Meehan [548) 
1946; Hopps and Lewis [549) 1947; Schmid [558) 
1949; and Wiemers, Maurer, and Niklas [568) 
1950. A paper on neurocirculatory collapse at alti- 
tude by Adler [543) 1950 and a study by Schneider 
[550) 1948 constituting a general review of the 
subject of circulation during hypoxia may be read. 
Mitchell, Thompson, and Arnold [553) 1951 
have studied the effects of intermittent exposure 
to high altitude on cardiovascular-renal lesions in 
hypersensitive rabbits. Sixty rabbits provided four 
treatment combinations; (1) controls; (2) hyper- 
sensitivity to horse serum; (3) acute exposure to 
high altitude; and (4) a combination of the hyper- 
sensitive state and altitude exposure. Qualitative 
and quantitative estimates of pathological lesions 
were made at the end of 28 days for the 4 groups of 
experimental animals. Under the conditions of this 
study, pathological evaluation of the animals 
showed that the protracted hypersensitive state 
when combined with the stress of altitude exposure 
resulted in a greater degree of heart and kidney 
damage than did either hypersensitivity or altitude 
stress alone. 
For further studies of the effects of hypoxia upon 
the heart and circulation, papers by the following 
may be referred to: Kramer and Luft (552) 1950, 
Schaefer (557) 1948, and Vacca and de Franciscis 
[564) 1947. 
543. Adler, H. F. Neurocirculatory collapse at altitude. 
USAF. Randolph Field, Texas. School of aviation medi- 
cine. Special Project. June 1950, 50 pp. 
544. Baum, W. S., R, B. Malmo, and R. F. Sievers. A 
comparative study of the effects of exercise and anoxia 
upon the human electrocardiogram. /. Aviat. Med., 1945, 
16: 422-428. [Pj 
545. Franzblau, S. A., G. F. Vawter, C. V. Pestel, and 
J. P. Marbarger. Effects of altitude stress on human 
circulatory system. Amer. J. Physiol., 1951, 167: 785. 
Abstr. 
546. Gabay, B. A, La fagilidad capilar en sujectos a 
nivel del mar, en anoxia cronica y en anoxia aguda; estu- 
dio hematologico complementario. Ann. fac. Med., Lima, 
1951, 34: 125-169. 
547. Henry, J. P., I. Klain, E. Movitt, and J. P. Meehan. 
The effects of anoxia on the capillary permeability of the 
human arm. Fed. Proc. Amer. Soc. exp. Biol., 1946, 5: 44. 
548. Henry, J. P., I. Klain, E. Movitt, and J. Meehan. 
On the effects of acute anoxia on the permeability of the 
capillaries in the human arm. U. S. NRG-CAM. OEM- 
cmr-288, C. A. M. rept. no. 497, 25 January 1946, 10 pp. 
[P] 
549. Hopps, H. C. and J. H. Lewis. Studies on capillary 
permeability as affected by anoxemia. Amer. J. Path., 
1947, 23: 829-836. [P] 
550. Houston, C. S. and R. L. Riley. Respiratory and 
circulatory changes during acclimatization to high altitude. 
Amer. J. Physiol., 1947, 149: 565-588. [P] 
551. Kirschbaum, H. Heart sounds in anoxia. /. Aviat. 
Med., 1951, 22: 212-213 (224). [P] 
552. Kramer, K. and IT. C. Luft. Activities of the 
vascular system during hypoxia. I. The activity of the 
spleen in hypoxia. USAF. Randolph Field, Tex. School of 
aviation medicine. Project 21—23—013, Rept. no. 1, De- 
cember 1950, 18 pp. [P] 
553. Mitchell, R. B., R. M. Thompson, and A. C. 
Arnold. Effects of stress associated with flight on the 
cardiovascular-renal lesions produced by hypersensitive 
reactions. 1. Cardiovascular-renal lesions in hypersensitive 
animals exposed to acute altitude stress. USAF. Randolph 
Field, Tex. School of aviation medicine. Project 21-32- 
020, Rept. no. 1, July 1951, 12 pp. ii. 
554. Plas, F., L. Tabusse, A. Missenard, and C. Goujan. 
Le comportement cardiovasculaire en altitude. Riv. Med. 
aero., Roma, 1947, 10: 275-302. (Italian, English, French, 
Spanish, and German summaries.) 
555. Rotta, A. Physiologic condition of the heart in the 
natives of high altitudes. Amer. Heart J., 1947, 33: 669- 
676. 
556. Rotta, A. and A. Miranda. Normal values of the 
arterial pressure and frequency of arterial hypertension in 
high altitudes. Amer. Heart ]., 1949, 37: 670. Abstr. 
557. Schaefer, K. E. The regulation of the blood circu- 
lation of man on submarines. The effect of a prolonged 
deficiency of oxygen associated with a prolonged increase 
of the carbon dioxide in the air. pp. G: 2—29 in; Mono- 
graph on submarine medicine, Folio 5. Germany. U. S. 
Zone. Office of naval advisor. 1948. 
558. Schmid, A. Die Kapillarresistenz und ihre Beein- 
flussung durch das Hohenklima, nebst einer Theorie des 
Messverfahrens. Helvet. physiol, pharm. Acta, 1949, 7: 
267-276. (English summary.) Med. aeronaut., 1950, 5: 
296. (French abstract.) 
559. Schneider, M. Der Kreislauf bei Sauerstoffmangel. 
pp. 97-108 in: Fiat Review of German Science 1939-1946. 
Physiology. Part I, Vegetative physiology. Senior author, 
Friedrich Hermann Rein. Office of military government 
for Germany. Field information agencies technical. Brit- 
ish, French, U. S. Printed under the supervision of 
Dieterich ’sche Verlagsbuchhandlung. Wiesbaden, Ger- 
many, 1948, 224 pp. [R] LOW OXYGEN TENSIONS—BLOOD 
560-569 
560. Schutz, E. Sauerstoff-Mangel-Wirkungen. pp. 191— 
194 in; Fiat Review of German Science 1939-1946. 
Physiology. Part I. Vegetative physiology. Senior author, 
Friedrich Hermann Rein. Office of military government 
for Germany. Field information agencies technical. Brit- 
ish, French, U. S. Printed under the supervision of 
Dieterich ’sche Verlagsbuchhandlung. Wiesbaden, Ger- 
many, 1948, 224 pp. [R] 
561. Starr, I., and M. McMicahel. Oxygen transport, 
circulation and respiration in healthy subjects at simulated 
altitudes of 16,000-18,000 feet. /. appl. Physiol., 1948, 1: 
430—440. Abstr. World Med., 1949, 6: 524. 
562. Stavraky, G. W. The effects of oxygen on the cir- 
culatory system in conditions of anoxia and asphyxia. 
Canad. ]. Res., 1945, 23 (E-F): 175-194. [P] 
563. Stavraky, G. W. The effects of oxygen on the cir- 
culatory system in conditions of anoxia and asphyxia. /. 
industr. Hyg., 1946, 28: abstract section 82. [P] 
564. Vacca C. and P. Franciscis, de. La curva di scom- 
parsa del tiocianato dal sangue di cane effetti della de- 
pressione barometrica. Riv. Med. aero., 1947, 10: 23-25. 
(English, French, Spanish, and German summaries.) [P] 
565. Van Liere, E. J. Effect of anoxia on the heart and 
circulation, pp. 73—87 in: Anoxia. Its effect on the body. 
Chicago, The University of Chicago Press. 1942, 269 pp. 
[R] 
566. Wezler, K. and E. Frank. Der Kreislauf im Sauer- 
stoffmangel bei Behaglichkeitstemperatur. Pfliig. Arch, 
ges. Physiol, 1948, 250: 248-276. [P] 
567. Whitehorn, W. V. Circulatory responses to expo- 
sure to barometric pressure of 30 mm. Hg. Fed. Proc. 
Amer. Soc. exp. Biol., 1948, 7: 133. 
568. Wiemers, K., W. Maurer, and A. Niklas. Uber die 
Permeabilitat der Bluthirnschranke im akuten Sauerstoff- 
mangel unter Versendung von radioaktivem Thorium als 
Indicator. Z. ges. exp. Med., 1950, 115: 688-698. [P] 
569. "Wyss-Dunant, E. The pulse rate at high altitudes. 
Schweiz, med. Wschr., 1950, 80: 224-227. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and 
Pharmacology), 1950, 3: 1504. Abstr. World Med., 1950, 
8: 117. 
5. BLOOD 
Papers by the following may be consulted for 
studies on the effects of decompression hypoxia on 
red cell formation and on polycythemia: Bons- 
dorff {571) 1948; Buhlmann, Wang, Wirz, and 
Verzar (575) 1951; Chiodi {579) 1951; Craven, 
Reissmann, and Chinn {580) 1951; Fave and Rin- 
genbach {582) 1950; Hurtado, Merino, and Del- 
gado {585) 1945; Merino {588) 1950; Merino and 
Reynafarje {589) 1949; Saathoff {592,593), 1950— 
51; Uzhanskii {595) 1949; and Van Liere {596) 
1942. Exposure to low barometric pressure environ- 
ments causes a polycythemic response with wide 
variations. In general, however, the polycythemic 
response is directly proportional to the degree of 
hypoxia and its duration and continuity. There 
seems to be a limit beyond which the hypoxic stimu- 
lus will not induce a hematological response. When 
extremely severe, the hypoxia may produce a de- 
pression rather than a further stimulation of 
hematopoiesis. The polycythemia observed immedi- 
ately on arrival at high altitude appears to be due 
to release of stored blood; for example, from the 
spleen. The polycythemia associated with repeated 
or constant exposure to low pressure environments 
is due to erythropoietic hyperactivity. Polycythemia 
of constant or intermittent hypoxia tends to show 
proportional elevation in circulating reticulocytes 
and in serum bilirubin. This latter suggests an in- 
creased rate of cellular destruction paralleling in- 
creased formation, but other factors such as insuffi- 
ciency of the liver in pigment excretion due to 
hypoxic conditions may also play an etiological role 
in hyperbilirubinemia. The stimulating influence of 
hypoxia upon the hematopoietic system is restricted 
to formation of red blood corpuscles. Leukopoiesis 
is not affected. Moderate and temporary leukocy- 
tosis is sometimes observed on arrival at high alti- 
tudes, probably related to the release and mobiliza- 
tion of stored blood. Chronic hypoxia does not 
modify erythropoietic activity permanently; a per- 
son who has lived since birth at high altitudes and 
is brought to sea level shows, after some time, 
characteristics similar to those in persons who have 
always lived at sea level. Abnormal decrease in red 
blood corpuscles and hemoglobin may occur during 
early adaptation to sea-level pressure (Hurtado, 
Merino, and Delgado (585) 1945). 
Regarding the effects of high-altitude hypoxia 
upon white blood count Grand] ean, Arnold, Bemey, 
Guibert, Jaquerod, and Magnin {583, 584) 1949 
found that in 8 healthy subjects who remained 
at an altitude of 1,750 meters for 3 weeks, there 
was a significant rise, not only in the red blood count 
and hemoglobin level, but also in the white blood 
count. There was an absolute increase in the num- 
bers of polymorphonuclear leukocytes, lymphocytes, 
and monocytes. 
Some reports, for example, that of Delachaux and 
Tissieres {581) 1946, indicate a rise not only of 
hemoglobin but also of the myoglobin level during 
acclimatization to high altitude. However, Bowen 
and Poel {573) 1948 and Bowen and Eads {572) 
1949 have found no increase but rather a diminu- 
tion in the myoglobin level in animals subjected to 
simulated high altitudes. In the former study {573), 
rats were exposed for 2 to 52 weeks, for 4 hours 
daily to 282 mm. Hg (a simulated altitude of 25,000 
feet). In these animals, the hematocrit and hemo- 
globin values increased to 25 and 66 percent, re- 
spectively, over the averages for the controls. The 
myoglobin, however, consistently showed no signifi- 
cant change from that of the controls. Also the re- 
sults showed that 2 to 8 times more hemoglobin was 
retained by the muscles of the exposed animals than SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
by the controls and that the amount retained varied 
directly with the hematocrit value. In the report of 
Bowen and Eads, dogs were exposed to a simulated 
altitude of 18,000 feet, 16 hours a day, 6 days a 
week for 6 months. At the end of the exposure 
period, the dogs were killed by deep anesthesia and 
exsanguination. Samples of various muscles includ- 
ing the heart and diaphragm were removed for 
analysis. In all the exposed dogs, the hemoglobin 
content increased markedly during the exposure, 
but the average myoglobin content of the muscles 
studied was less in the exposed dogs than in the 
unexposed. In a report by Reismann, Hoelscher, 
Topka, Criscuolo, and Burkhardt (591) 1951, the 
hemoglobin metabolism during the development 
and disappearance of polycythemia induced by 
hypoxia was studied by measuring the total circulat- 
ing hemoglobin and the daily bile pigment excretion 
in dogs with bile fistulas before, during, and after 
prolonged periods of exposure to a simulated alti- 
tude of 20,000 feet. The increased erythropoiesis 
during the first weeks of altitude exposure was ac- 
companied by a significant increase in bile-pigment 
output. No differences were seen in the life span of 
the red cells at ground level and during altitude 
exposure. The return of the number of red cells to 
normal after reaching ground level was achieved 
by the combined effect of a depression of erythro- 
poiesis and an increase in blood destruction. The 
latter accounted for 21 to 39 percent of the hemo- 
globin which disappeared from the circulation 
after return to sea level. 
The effect of acute hypoxia upon the blood hista- 
mine level has been studied by Burkhardt, Flick- 
inger, and Adler (576) 1949. These authors have 
reported that the blood histamine content of dogs 
as measured by biological assay may increase ten- 
fold or more in response to continuous hypoxia at a 
simulated altitude of 18,000 feet. The increase in 
histamine reached a peak on the fourth day of 
exposure and may be correlated with the clinical 
status of the dogs which at that time were apathetic, 
lethargic, and had lost appetite. After the peak had 
been reached on the fourth day, the histamine level 
began to decline until it again attained the control 
level about 7 or 8 days later; that is to say, after a 
total of about 12 days of continuous exposure. The 
decrease in histamine level seemed to be correlated 
with clinical symptoms in that gradually over the 
period of histamine decline, the animals lost their 
apathy and began to eat normally. When the dogs 
were returned to the ground level for 8 days, a 
reexposure to 18,000 feet failed to elicit the same 
marked degree of histamine response noted on the 
first exposure. A later study by Burkhardt, Flick- 
inger, Coulson, Criscuolo, and Adler (577) 1951 
revealed no increase in blood histamine in dogs, 
cats, and human beings subjected to acute hypoxia 
for periods of l/u hours. 
Plasma, cell and blood volumes, and total circu- 
lating hemoglobin were determined in a group of 
dogs before, during, and after acclimatization to 
20,000 feet simulated altitude by Reissmann (590) 
1951. During altitude exposure the plasma volume 
decreased gradually to a constant level, which was 
75 percent of the ground-level value. The cell vol- 
ume reached a plateau of 170 percent of the ground- 
level value in the fifth week of exposure and re- 
turned to normal within 6 weeks after exposure 
had been discontinued. The total circulating hemo- 
globin paralleled the cell volume, and in some 
animals increases of 200 grams of hemoglobin were 
observed during 5 weeks of exposure. The total 
blood volume remained almost constant during the 
first 2 weeks of exposure, then increased slowly and 
reached a plateau at 125 percent of the ground- 
level value in the fifth week of exposure. 
Mobilization of red cells from the spleen in severe 
hypoxia has been reported by Kramer and Luft 
(586) 1951. These observations recorded contrac- 
tion of the spleen in nembutalized dogs during acute 
hypoxia. This response did not appear early, but 
was a terminal event immediately preceding respira- 
tory failure. Loss in spleen weight during contrac- 
tion coincided with an increase in systemic hemo- 
globin content. During the refilling phase of the 
spleen in recovery from hypoxia, the same inverse 
relationship was evident as the systemic hemo- 
globin returned to the control level. An estimate of 
the hemoglobin concentration in stored blood based 
upon the amount of blood released by the spleen 
led the authors to the conclusion that the splenic 
stores consist almost entirely of packed red cells. 
Continuous records of the hemoglobin content in 
the splenic vein showed very rapid changes in the 
final stages of hypoxia, with peak values twice as 
high as in arterial blood. During recovery, the 
hemoglobin level in the splenic vein was slightly 
lower than in the artery, signifying the retention of 
red cells at this time. During control periods, with 
the animal breathing air, spontaneous rhythmic 
fluctuations were frequently observed in the hemo- 
globin content of blood in the splenic vein. During 
hypoxia, the oxygen saturation of venous blood 
from the spleen remained consistently higher than 
in arterial blood and even increased when splenic 
contraction reached its peak. It was concluded by 
the authors that in the critical phase of hypoxia, the 
spleen of the dogs releases large amounts of red IOW OXYGEN TENSIONS—RESPIRATION 
570-596 
cells with a relatively high oxygen content into the 
portal venous system. 
For further studies on the effects of decompres- 
sion hypoxia on the blood, papers by the following 
authors should be consulted: Beutler and Stampfli 
{570) 1948; Buhlmann and Hofstetter {574) 1951; 
Charnyi, Strltsov, Syrkina, and Kraspovitskaia 
{578) 1946; Malmejac, Cruck, and Neverre {587) 
1950; and Scano and Gnudi {594) 1950. 
570. Beutler, F. and R. Stampfli. Die Anderung der 
Blut- und Plasmaleitfahigkeit im Hohenklima. Helvet. 
physiol, pharm. Acta, 1948, 6: 688-698. [P] 
571. Bonsdorff, E. On the humoral mechanism in 
anoxic polycythaemia. Acta physiol, scand. {supple.), 
1948, 53: 8. 
572. Bowen, W. J. and H. J. Eads. Effects of 18,000 
feet simulated altitude on myoglobin content of dogs. 
Amer. J. Physiol, 1949, 159: 77-82. 
573. Bowen, W. J. and W. E. Poel. The effects of 
anoxia upon myoglobin concentration. Fed. Proc. Amer. 
Soc. exp. Biol, 1948, 7; 11. 
574. Biihlmann, A. and J. R. Hofstetter. Arbeitsver- 
suche in mittleren Hohen. Helvet, physiol. Acta, 1951, 
9: 222-226. [P] 
575. Buhlmann, A., S. I. Wang, H. Wirz, and F. Verzar. 
Die Erythrocytenzahl in mittleren Hohen. Schweiz, med. 
Wschr., 1951, 81: 80-82. [P] 
576. Burkhardt, W. L., D. Flickinger, and H. F. Adler. 
Blood histamine in hypoxia. Fed. Proc. Amer. Soc. exp. 
Biol, 1949, 8: 19. 
577. Burkhardt, W. L., D. Flickinger, C. K. Coulson, 
D. Criscuolo, and H. F. Adler. Production of histamine 
in the body during hypoxia. Blood histamine and acute 
hypoxia. USAF. Randolph Field, Tex. School of aviation 
medicine. Project 21-23-015, Rept. no. 1, April 1951, 
6 pp. ii. 
578. Charnyi, A. M., V. V. Strltsov, P. E. Syrkina, and 
S. E. Kraspovitskaia. Potreblenie kisloroda i krivaia dis- 
sotsoatsii oksigemoglobina v period posledeistviia vysotnoi 
anoksii. [Oxygen consumption and oxyhemoglobin dis- 
sociation curve in the phases of after effects of high 
altitude anoxia.] Arkhiv patol, Moskva, 1946, I: 22-25. 
579. Chiodi, H. Blood picture at high altitude. J. appl. 
Physiol, 1950, 2: 431-436. Abstr. World Med., 1950, 
8: 229. 
580. Craven, C. W., K. R. Reissmann, and H. I. Chinn. 
Mechanism of polycythemia occurring during high-alti- 
tude adaptation. III. The infrared absorption spectra for 
various porphyrins. USAF. Randolph Field, Tex. School 
of aviation medicine. Project 21-23-003, Rept. no. 3, 
June 1951, 2 pp. 
581. Delachaux, A. and A. Tissieres. L’adaptation tis- 
sulaire a 1’hypoxydose. Helvet, med. Acta, 1946, 13: 
333-338.[P] 
582. Fave, M. and G. Ringenbach. Haematological in- 
vestigations in high-altitude flight. The haemotoxic role 
of oxygen. J. Med., Bord., 1949, 126: 544-550. Abstr. 
World Med., 1950, 7; 569. 
583. Grandjean, E., E. Arnold, J. J. Berney, R. Guibert, 
R. Jaquerod, and P. Magnin. Effets d’un sejour a 
moyenne altitude (1750 m) sur la tonicite musculaire, la 
sensibilite tactile, le reflexe rotulien et la formule sanguine. 
Helvet. physiol, pharm. Acta, 1949, 7; 277—290. [P] 
584. Grandjean, E., E. Arnold, J. J. Berney, B. Gui- 
bert, R. Jaquerod, and P. Magnin. Recherches physio- 
logiques sur les effets d’un sejour a moyenne altitude, 
a 1750 m. Helvet. physiol, pharm. Acta, 1949, 7: Cll. [P] 
585. Hurtado, A., C. Merino, and E. Delgado. Influence 
of anoxemia on the hemopoietic activity. Arch, intern. 
Med., 1945, 75: 284-323. 
586. Kramer, K. and TJ. C. Luft. Mobilization of red 
cells and oxygen from the spleen in severe hypoxia. 
Amer. J. Physiol, 1951, 165: 215-228. [P] 
587. Malmejac, J., S. Cruck, and G. Neverre. Etude a 
Paide de 1’electrophorese des modifications de 1’equilibre 
protidique sanguin en anoxie. Med. aeronaut., 1950, 
5: 135—148. Excerpta Medica. Section II. (Physiology, 
Biochemistry, and Pharmacology), 1951, 4: 1129. [P] 
588. Merino, C. F. Studies on blood formation and de- 
struction in the polycythemia of high altitude. Blood, 
1950, 5: 1-29. [P] 
589. Merino, C. F. and C. Reynafarje. Bone marrow 
studies in the polycythemia of high altitudes. /. Lab. din. 
Med., 1949,34: 637-647. [P] 
590. Relssmann, K. R. Blood volume in the dog during 
altitude acclimatization. Amer. J. Physiol., 1951, 167: 
52-58. USAF. Randolph Field, Tex. School of aviation 
medicine. Project 21-23—003, Kept. no. 1, July 1951, 
8 pp. iii. [P] 
591. Reissmann, K. R., B. Hoelscher, E. Topka, D. 
Criscuolo, and W. L. Burkhardt. Mechanisms of high 
altitude adaptation. IV. Hemoglobin catabolism during 
and after prolonged exposure hypoxia. USAF. Randolph 
Field, Tex. School of aviation medicine. Project 21—23— 
003, Kept. no. 4, November 1951, 11 pp. ii. 
592. Saathoff, J. Uber die Latenzzeit des Reticulo- 
cytenanstieges bei Sauerstoffmangel. Virchows Arch., 
1950/51, 319: 107-115. [P] 
593. Saathoff, J. Medullare und extraraedullare Blut- 
bildung unter Sauerstoffmangel. Virchows Arch., 1950/51, 
319: 116-126. [P] 
594. Scano, A. and G. Gnndi. Sulla velocita di sedi- 
mentazione degli eritrociti umani nell’anossia provocata 
mediante rirespirazione e mediante depressione barome- 
trica. Riv. Med. aero., Roma, 1950, 13: 673-678. (French, 
German, Spanish, and English summaries.) 
595. Hzhanskii, I. G. K. Mekhanizmu stimulatsii kro- 
votvoreniia pri gipoksiakh. [On the mechanism of hemo- 
poiesis in hypoxia.] pp. 219-223 in: Gipoksiia, Kiev, 
Akad. Nauk. Ukr. SSR., 1949, 415 pp. 
596. Van Liere, E. J. Effect of anoxia on the blood, pp. 
33-58 in: Anoxia. Its effect on the body. Chicago, The 
University of Chicago Press, 1942, 269 pp. [R] 
6. RESPIRATION 
For studies of respiratory metabolism of human 
subjects during exposure to decompression hypoxia, 
papers by the following authors should be consulted: 
D’Angelo {597,598) 1946, Houston and Nez {602) 
1946, Riley and Houston {606) 1948, Rothschuch 
{608) 1947, and Schaefer and Alvis {610) 1951. 
The following authors have contributed reports 
dealing with alveolar and arterial gas tensions in 
hypoxia: Miller, Taylor, and Heagan {604) 1946; 
Lilienthal and Riley {603) 1946; Gemmill and 
and Malone (599) 1945; Grutering, Opitz, and 
Palme {600) 1944; Hoffman, Clark, and Brown 597-613 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
{601) 1945; Scano {609) 1951; and Winterstein 
{612) 1950. For general articles on the effects of 
hypoxia on respiration, papers by Nims {605) 1946 
and Van Liere {611) 1942 should be consulted. 
For other studies on respiration, the reader is re- 
ferred to papers by Rodbard {607) 1946 and Win- 
terstein {613) 1950. 
597. D’Angelo, S. A. The respiratory metabolism of 
human subjects during prolonged exposures to simulated 
altitudes of 8,000 and 10,000 feet. Amer. J. Physiol., 1946, 
146: 710-722. 
598. D’Angelo, S. A. The respiratory exchange in human 
subjects during prolonged exposures to moderately low 
simulated altitudes. Fed. Proc. Amer. Soc. exp. Biol., 1946, 
5: 20. 
599. Gemmill, C. L. and M. E. Malone. The physio- 
logical effects of anoxia and exercise. The relationship be- 
tween alveolar air oxygen tensions and arterial blood 
oxygen saturations. U. S. Navy. NATC, Pensacola, Fla. 
School of aviation medicine. Project X-484 (AV-258-f), 
Kept. no. 1,15 May 1945, 20 pp. [P] 
600. Griitering, F., E. Opitz, and F. Palme. Darstellung 
der Hohenanpassung im Gebirge durch Sauerstoffmangel. 
IV. Steigerung der alveolaren Hohenfestigkeit untersucht 
am Schriftbild. Pfliig. Arch. ges. Physiol., 1944, 248: 
376-386. [P] 
601. Hoffman, C. E., R. T. Clark, Jr., and E. B. Brown, 
Jr. Blood oxygen saturations and duration of consciousness 
in anoxia at high altitudes. Amer. J. Physiol., 1945, 145: 
685-692. 
602. Houston, C. S. and M. Nez. Relation of pulmonary 
ventilation to arterial oxygen. U. S. Navy. NATB, Pensa- 
cola, Fla. School of aviation medicine. Project X—675, 20 
January 1946, 11 pp. 
603. Lilienthal, J. L. and R. L. Riley. An experimental 
analysis in man of the oxygen pressure gradient from 
alveolar air to arterial blood during rest and exercise at 
sea level and at altitude. U. S. Navy. NATB, Pensacola, 
Fla. School of aviation medicine. Project X—484 (Av— 
258-f), Kept. no. 3, 23 February 1946, 33 pp. 
604. Miller, R. A., C. B. Taylor, and B. Heagan. The 
oxygen content of arterial blood of dogs exposed to di- 
minished pressures in a decompression chamber. U. S. 
AAF. Randolph Field, Tex. School of aviation medicine. 
Project 414, Kept. no. 1, 14 August 1946, 7 pp. 
605. Nims, L. F. Respiration. Annu. Rev. Physiol., 1946, 
8: 99-116. [R] 
606. Riley, R. L. and C. S. Houston. Composition of 
alveolar air and rate of pulmonary ventilation during long 
exposure to high altitude. U. S. Navy. NATC, Pensacola, 
Fla. School of aviation medicine and research. Project 
NM 001 013 (X-720) (Av-376-s), Kept. no. 7, 8 Sep- 
tember 1948, 5 pp. [P] 
607. Rodbard, S. The effect of oxygen, altitude, and 
exertion on breath-holding time. Fed. Proc. Amer. Soc. 
exp. Biol., 1946, 5; 88. 
608. Rothschuh, K, E. Zur Frage eines “Sparstoff- 
wechsels” bei kurzdauerndem Sauerstoffmangel. Pfliig. 
Arch. ges. Physiol, 1947,249: 175-190. [P] 
609. Scano, A. Ricerche sulla resistenza alia depressione 
barometrica. Nota I. Tensione dei gas alveolari, consumo 
di 02 e limiti de ricupero nel coniglio sottoposto a depres- 
sione barometrica. Riv. Med. aeronaut., 1950, 13: 507- 
550. Excerpta Medica. Section II. (Physiology, Biochem- 
istry, and Pharmacology), 1951, 4: 1213. 
610. Schaefer, K. E. and H. J. Alvis. The effect of in- 
halation of low oxygen concentration (10.5% 02 in N2) 
over a period of 33 minutes on respiration, pulse rate, 
arterial oxygen saturation (oximeter) and oxygen uptake. 
U. S. Navy. Submarine base, New London, Conn. Medical 
research laboratory. Project NM 002 015.03.02, Kept. no. 
175, 8 August 1951, 32 pp. [P] 
611. Van Liere, E. J. Effect of anoxia on respiration, 
pp. 101—127 in: Anoxia, Its effect on the body. Chicago, 
The University of Chicago Press. 1942, 269 pp. [R] 
612. Winterstein, H. Die alveolare Kohlensaurespan- 
nung in mittleren Hohen. (1800 m.) Arch. int. Pharma- 
codyn., 1950, 82: 67—79. Excerpta Medica. Section II. 
(Physiology, Biochemistry, and Pharmacology), 1950, 3: 
1210. 
613. Winterstein, H. Effets mecaniques de Pair 
rarefie. Concours med., 1950, 72: 233—234. [P] 
7. ALIMENTARY TRACT 
For an extensive monograph on the influence of 
law barometric pressure on the process of digestion, 
reference is made to a report by Razenkov (616) 
1948. This work includes material on the influence 
of decreased barometric pressure on salivary se- 
cretion and secretory activity of the gastric glands. 
An article by Van Liere {617) 1942 may also be 
consulted. This author pointed out that under con- 
ditions of hypoxia, hunger contractions in the dog 
were decreased in amplitude and that gastric mo- 
tility was reduced. There is a delay in gastric 
emptying time in both dogs and man. Anemic 
anoxia is stated to stimulate hunger contraction and 
delay gastric emptying. Histotoxic anoxia produced 
by barbiturates, bromides, and other drugs all 
caused prolonged gastric emptying. Compared with 
the central nervous system, the gastrointestinal tract 
is stated to be relatively resistant to hypoxia. Ranges 
of hypoxia compatible with life would not interfere 
with proper nourishment of the body so far as ab- 
sorption from the gut is concerned. Van Liere, Stick- 
ney, and Northup {618) 1950 and {619) 1951 
reported that the propulsive motility of the small 
intestine in rats was decreased by hypoxia. It was 
reasoned that if rats were acclimatized to low oxygen 
tensions, exposure to altitude would no longer pro- 
duce this effect. A group of albino rats were accord- 
ingly acclimatized by subjecting them to a simulated 
altitude of 24,000 feet by approximately 3 hours 
each day for 26 or 62 days. These acclimatized rats 
were paired with normal rats which were as nearly 
alike in weight and age as possible. A pair of these 
rats was given 2 cu. cm. of a charcoal-acacia mixture 
by stomach tube. After allowing 10 minutes for some 
of this material to enter the small intestine, both 
rats were placed in a low-pressure chamber at a 
pressure of 254 mm. Hg (simulated altitude, 28,000 
feet). At the end of 30 minutes they were removed 
from the chamber and decapitated. The small intes- LOW OXYGEN TENSIONS—METABOLISM 
614-619 
tine was removed, slit open, and the distance the 
charcoal had traversed measured. It was observed 
that the propulsive motility was significantly less in 
the unacclimatized than in the acclimatized ani- 
mals. This was interpreted by the authors to mean 
that the effect of hypoxia upon the propulsive mo- 
tility of the small intestine could be used as a 
criterion for acclimatization. 
MacLachlan {615) 1946 found that rats ex- 
hibited an initial acceleration of stomach emptying 
on exposure to diminished oxygen tension. He con- 
cluded that decreased rate of absorption of fat in 
rats subjected to hypoxia cannot be explained on 
the basis of prolonged gastric emptying time. In 
studies on the effects of hypoxia on gastric secretory 
functions, Karvinen and Karvonen {614) 1949 
subjected human subjects (3 normal and 1 achloro- 
hydric subject) to a simulated altitude of 5,000 
meters. Alcohol and carbaminolcholine were used 
as stimuli. In the carbaminolcholine tests the 
volume of gastric juice collected at 5,000 meters 
was, on the average, one-fifth of the corresponding 
value at sea level. The acid secreted was one-ninth 
and the amount of pepsin was one-twelfth of sea- 
level values. The total chloride value followed a 
course comparable to the values for titratable 
acidity, both at sea level and at 5,000 meters. In 
the alcohol tests, the secretion of the different com- 
ponents was fairly uniformly decreased at altitude. 
However, suppression of secretion was less pro- 
nounced than in the carbaminolcholine tests. The 
secretions of the achlorohydric stomach seemed un- 
affected by the degree of hypoxia imposed. 
614. Karvinen, E. and M. J. Karvonen. On the anoxic 
suppression of the gastric secretory functions. Ann. Med. 
exp. Fenn., 1949, 27; 59-72. [P] 
615. MacLachlan, P. L. Effect of anoxic anoxia on gas- 
tric emptying time of rats fed corn oil. Proc. Soc. exp. 
Biol., N. Y., 1946, 63: 147-148. 
616. Razenkov, I. P. Vliianie ponizhennogo barome- 
tricheskogo davleniia. [Influence of low barometric pres- 
sure on process of digestion.] Izdatelstvo Akademii Medi- 
zinskih Nayk S. S. S. R. Moskva, 1948, 167 pp. (Russian 
text.) 
617. Van Liere, E. J. Effect of anoxia on the alimen- 
tary tract, pp. 159—185 in: Anoxia. Its effect on the body. 
Chicago, The University of Chicago Press, 1942, 269 pp. 
[R] 
618. Van Liere, E. J., J. C. Stickney, and D, W. 
Northup. Effect of acclimatization on motility of small 
intestine during anoxia. Fed. Proc. Amer. Soc. exp. Biol., 
1950, 9: 128. 
619. Van Liere, E. J., J. C. Stickney, and D. W. 
Northup. The effect of acclimatization on the propulsive 
motility of the small intestine during anoxia. Proc. Soc. 
exp. Biol. Med., 1951, 76: 102-103. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharma- 
cology), 1951, 4: 1238. [P] 
8. METABOLISM 
For studies of weight loss and retardation of 
growth produced by decompression anoxia, papers 
by Stickney (648 and 649) 1946 and Altland {620) 
1948 should be consulted. A very complete article 
by Altmann {621) 1949 provides an excellent re- 
view of liver changes produced experimentally in 
cats by hypoxia. This article contains 463 references 
to the literature. References to articles by the follow- 
ing authors are recommended to readers desiring 
recent studies on the effects of hypoxia on carbo- 
hydrate metabolism: Boutwell, Gilley, Krasno, Ivy, 
and Farmer {625) 1951; Gellhorn and Safford 
{632) 1948; Keyes and Kelley {633 and 634) 1949; 
Langley, Nims, and Clarke {637) 1950; Langley, 
Nims, Harvey, and Clarke {638) 1943; McDonald 
{639) 1947; Nims, Langley, and Clarke {643) 
1946; Saviano and Vacca {646) 1950; Stickney, 
Northup, and Van Liere {650, 651) 1948; Van 
Liere, Stickney, and Northup {654, 655) 1948; Van 
Middlesworth {656) 1946; and Wickson and Mor- 
gan {661) 1946. In general, acute decompression 
hypoxia results in decreased glucose tolerance mani- 
fested by prolonged elevation of the blood sugar 
levels and by failure to return to normal fasting 
volumes as early as at ground level. Insulin toler- 
ance tests reveal a decreased insulin response in 
animals exposed to simulated altitudes. 
Murray and Morgan {641) 1946 found that 
ascorbic acid-deficient guinea pigs had a signifi- 
cantly higher blood sugar level and probably signifi- 
cantly lower liver and carcass glycogen levels than 
pair-fed normal animals 6 hours after they were fed 
glucose following a 24-hour fast. The intestinal ab- 
sorption of the sugar was less complete in the de- 
ficient animals. When similarly paired but fasting 
animals were exposed to hypoxia (349 mm. Hg for 
24 hours), the deficient group was able to maintain 
or increase blood sugar and glycogen stores more 
effectively than did the normal. Fasting, deficient 
guinea pigs at ordinary atmospheric pressure had 
lower carbohydrate stores than did those under 
hypoxia, but this was not true for the normal ani- 
mals. The ascorbic acid-deficient guinea pigs were 
found to have a significantly increased size of the 
adrenal glands, as compared with their paired con- 
trols. The lipid content of the livers and carcasses of 
the deficient animals was found to be nearly the 
same as in the normal, whether the animals had 
been subjected to hypoxia or not. The sudden loss of 
weight in the former was therefore considered to 
be due probably to dehydration. The liver-lipid 
values were increased in both groups after exposure 
to hypoxia. Oxygen consumption was not altered 620-627 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
by the ascorbic acid deficiency and no changes were 
seen in the thyroid glands. The reduced glycogen 
and increased blood sugar exhibited by the ascorbic 
acid-deficient guinea pigs following glucose feeding 
were considered by the authors to be in accord with 
the theory that the adrenal medullary mechanism is 
hyperactive in this deficiency. The increased size of 
the adrenal glands, rapid dehydration, and gluco- 
neogenesis of the deficient animals under hypoxia 
point, according to the authors, to similar compen- 
satory hyperactivity of the adrenocortical mecha- 
nism. 
According to Krasno, Gilley, Boutwell, Ivy, and 
Farmer (635) 1950, repeated exposure of human 
subjects to a simulated altitude of 18,000 feet with- 
out additional oxygen resulted in a decrease in the 
daily urinary excretion of ascorbic acid from an 
average of 33.6 mg. down to 12 mg. The plasma 
level of ascorbic acid decreased from an average 
control level of 0.73 mg. percent down to 0.58 mg. 
percent during the last week of exposure. The 
authors suggested liberal quantities of fruit or fruit 
juice in the diets of persons subjected to continuous 
or discontinuous hypoxia or hyperventilation. Re- 
peated exposure to a simulated altitude of 18,000 
feet without supplemental oxygen did not affect the 
urinary output of thiamine, riboflavin, alpha-ke- 
toglutaric acid, pyruvic acid, or acetone bodies. 
According to Mitchell and Edman (640) 1951, 
conditions of hypoxia may increase the require- 
ments for ascorbic acid, thiamine, and nicotinic 
acid. Vitamin supplements to adequate diets have 
not been proved to be effective in increasing toler- 
ance to hypoxia in man; particularly vitamin A 
supplement does not increase light sensitivity. 
For studies on the effects of hypoxia upon re- 
spiratory catalysts, papers by the following may be 
consulted: Beinert, Maier-Leibnitz, Richey, and 
Reissman (622) 1950; Lalli and Tagliamonte (636) 
1951; Seabra (647) 1947; Vannotti (659) 1946; 
and Voegtli (660) 1948. Tissue response to patho- 
logical oxygen deficiency is characterized by a sig- 
nificant increase of the levels of cytochrome C and 
of iron as well as biologically active complexes and 
of vitamins of the B group which are as coenzymes 
in the formation of the ferments indispensable to 
cellular metabolism. 
Exposure to decompression hypoxia tends to in- 
crease the excretion of 17-ketosteroids in the urine. 
For such studies, papers by the following may be 
consulted: Biget (623) 1950, Burrill and Ivy (628) 
1950, Cook (629) 1945, and Davidson (631) 1950. 
Van Middlesworth (657) 1950 and Van Middles- 
worth and Berry (658) 1951 have reported that 
hypoxia results in a decreased rate of uptake of 
radioactive iodine by the thyroid gland. In these 
experiments, rats fed a stock diet with a low iodide 
content were rapidly adapted to severe hypoxia 
by exposure to an equivalent altitude of 27,000 feet 
(258 mm. Hg) at 11 to 14° C. for 2 to 4 hours. 
After this exposure, the low iodide rats were injected 
intraperitoneally with 10 microcuries of carrier- 
free I181. The barometric pressure was then reduced 
to 177 mm. Hg (35,000 feet equivalent altitude) 
for 8 to 12 hours. The thyroid glands of the hypoxic 
series contained one-fourth as much radioactivity 
as controls. 
For studies on acid-base balance as affected by 
exposure to decompression hypoxia, papers by the 
following may be consulted; Boutwell, Farmer, and 
Ivy (626) 1950; Nims, Bunting, Ordway, and 
Clarke (642) 1943; Ochwadt (644) 1947; and 
Riley, Houston, and Jarvis (645) 1946. Additional 
references on the effects of decompression hypoxia 
upon metabolism are given as follows; Blood, 
Elliott, and d’Amour (624) 1946; Brobeck, Clarke, 
DuBois, Grenell, Liberman, Murphy, Nims, Patton, 
and Tepperman (627) 1943; Cook and Strajman 
(630) 1946; Tepperman, Tepperman, and Patton 
(652) 1944; and Van Liere (653) 1942. 
620. Altland, P. D, Recovery rate from some of the 
effect of chronic intermittent hypoxia in rats. Anat. Rec., 
1948,101: 668. Abstr. [P] 
621. Altmann, H. W. tlber Leberveranderungen bei 
allgemeinem Sauerstoffmangel nach Unterdruckexperi- 
menten an Katzen. Frankfurt. Z. Path., 1949, 60: 376- 
494. [R] [P] 
622. Beinert, H., H. Maier-Leibnitz, E. 0. Richey, 
and K, R. Reissmann. Further investigations on the in- 
jections of respiratory catalysts in an attempt to improve 
hypoxia tolerance. Studies on the incorporation of injected 
cytochrome C into tissue cells. USAF. Randolph Field, 
Tex. School of aviation medicine. Department of phar- 
macology and biochemistry. Project 21-02-054, Kept. no. 
I, May 1950, 11 pp. [P] 
623. Biget, P. Action de la depression atmospherique 
sur 1’elimination urinaire des ceto-17—steroides chez 
Phomme. C. R. Soc. Biol., Paris, 1950, 144: 1091-1092. 
[P] 
624. Blood, E. R., R. V. Elliott, and P. E. d’Amour. The 
physiology of the rat in extreme anoxia. Amer. J. Physiol., 
1946, 146: 319-329. [P] 
625. Boutwell, J. H., J. H. Gilley, L. R. Krasno, A. C. 
Ivy, and C. J. Farmer. Effect of repeated exposure of 
human subjects to hypoxia on glucose tolerance, excretion 
of ascorbic acid, and phenylalanine tolerance. /. appl. 
Physiol., 1950, 2: 388-392. Excerpta Medica. Section II. 
(Physiology, Biochemistry, and Pharmacology), 1951, 4: 
540. Abstr. 
626. Boutwell, J. H., C. J. Farmer, and A. C. Ivy. 
Studies on acid-base balance before and during repeated 
exposure to altitude, or to hypoxia and hyperventilation. 
J. appl. Physiol., 1950, 2: 381-387. 
627. Brobeck, J. R., R. W. Clarke, D. DuBois, R. G. 
Grenell, A. M. Liberman, H. T. Murphy, L. F. Nims, 
D. W. Patton, and J. Tepperman. A biochemical study of IOW OXYGEN TENSIONS—METABOLISM 
628-660 
the effect of anoxia on exercise performance in human 
subjects. U. S. NRG-CAM. Yale Aeromedical Research 
Unit. C. A. M. rept. no. 250, 1 December 1943, 18 pp. 
628. Burrill, M. W, and A. C. Ivy. Excretion of neutral 
17-ketosteroids in human subjects repeatedly exposed to 
hypoxia under conditions of simulated high altitude. /. 
appl. Physiol, 1950, 2: 437-445. Abstr. World Med., 1950, 
8: 232. 
629. Cook, S. F. The inhibition of animal metabolism 
under decompression, /. Aviat. Med., 1945, 16: 268-271. 
[P] 
630. Cooks, S. F. and E, Strajman. The effect of decom- 
pression on human metabolism during and after exercise. 
/. industr. Hyg., 1946, 28: abstract section: 47. U. S. 
NRG-CAM. Division of medical sciences. OEMcmr—196, 
C. A. M. rept. no. 406, 9 January 1945, 10 pp. 
631. Davidson, I. L. The excretion of urinary total 
neutral 17-ketosteroids during anoxia. Gt. Brit. FPRG. 
RAF Institute of aviation medicine. F. P. R. C. 739, July 
1950, 2 pp. [P] 
632. Gellhorn, E. and H. Safford. Influence of repeated 
anoxia, electroshock and insulin hypoglycemia on reac- 
tivity of sympathetico-adrenal system. Proc. Soc. exp. Biol, 
N. Y., 1948, 68: 74-79. [P] 
633. Keyes, G. H. and V. C. Kelley. Study of effects of 
altitude anoxia on glucose metabolism. 1. The glycogenic 
effect of adrenal cortical extract. USAF. Randolph Field, 
Tex. School of aviation medicine. Project 21-02—030, 
Rept. no. I, February 1949, 6 pp. [P] 
634. Keyes, G. H. and V, C. Kelley. A study of effects 
of altitude anoxia on glucose metabolism. The glucose 
tolerance of dogs as altered by atmospheric decompression. 
USAF. Randolph Field, Tex. School of aviation medicine. 
Project 21-02-030, Rept. no. 2, March 1949, 8 pp. [P] 
635. Krasno, L. R., J. H. Gilley, J. H. Bontwell, A C. 
Ivy, and C. J. Farmer. Effect of repeated exposure of 
human subjects to 18,000 feet without supplemental oxy- 
gen, to hyperventilation, and to 35,000 feet with 100 per- 
cent oxygen for one hour, on ascorbic acid excretion and 
plasma level and on urine pH. /. Aviat. Med., 1950, 21: 
283-292 and 312. 
636. Lalli, G. and B. Tagliamonte. Comportamento del 
ferro totale et di quello tissulare nella milza e nel fegato, 
nei suoi rapporti con 1’emoglo-binemia, in conigli sattoposti 
ad anossia discontinua ripetuta. Riv. Med. aero., Roma, 
1951, 14: 641-649. (English, French, German, and Span- 
ish summaries.) [P] 
637. Langley, L. L., L. F, Nims, and R. W. Clarke. 
Role of C02 in the stress reaction to hypoxia. Amer. J. 
Physiol, 1950, 161: 331-335. [P] 
638. Langley, L. L., L. F. Nims, T. S. Harvey, and 
R. W. Clarke. Anoxia, carbon dioxide and liver glycogen. 
U. S. NRC—CAM. Yale aeromedical research unit. C. A. 
M. rept. no. 108, January 1943, 9 pp. 
639. McDonald, R. Effects of altitude anoxia on glucose 
metabolism. USAF. Randolph Field, Tex. School of avia- 
tion medicine. Project 502, Rept. no. 1, 30 September 
1947, 1 p. [P] 
640. Mitchell, H. H. and M. Edman. Diet at altitude, 
pp. 96—151 in: Nutrition and climatic stress. Springfield, 
Charles C. Thomas. 1951, 234 pp. [R] 
641. Murray, H. C., and A. F. Morgan. Carbohydrate 
metabolism in the ascorbic acid-deficient guinea pig under 
normal and anoxic conditions. /. biol. Chem., 1946, 143: 
401-410. 
642. Nims, L. F., H. Bunting, IT. K. Ordway, and 
R. W. Clarke. Anoxic anoxia and acid-base balance. U. S. 
NRC—CAM. Yale aeromedical research unit. C. A. M. 
rept. no. 107, 18 January 1943, 5 pp. 
643. Nims, L, F., L. L. Langley, and R. W. Clarke. 
Anoxia, carbon dioxide and liver glycogen. Fed. Proc. 
Amer. Soc. esp. Biol., 1946, 5: 76. 
644. Ochwadt, B. t)ber Bicarbonatausscheidung und 
Kohlensauresystem in Harn wahrend akuter Hypoxie. 
Pfliig. Arch. ges. Physiol., 1947, 249: 452-469. [P] 
645. Riley, R. L., C. S. Houston, and W. H. Jarvis. A 
study of the physiological changes which occur during 
acclimatization to high altitude. U. S. Navy. NATG, 
Pensacola, Fla. School of aviation medicine. Project 
X-720, Rept. no. 4, 21 September 1946, 14 pp. 
646. Saviano, M. and C. Vacca. Richerche sui rapporti 
fra anossia e funzione insulare del pancreas. Riv. Med. 
aero., Roma, 1950, 13: 171-188. (English, French, 
Spanish, and German summaries.) 
647. Seahra, P. Oxidase and aviation. Influence of 
atmospheric decompression on the blood oxidase and 
resistance to infection. /. Aviat. Med., 1947, 18: 289-296. 
[P] 
648. Stickney, J. C. The effect of various degrees of 
intermittent anoxia on body weight loss in normal rats. 
Fed. Proc. Amer. Soc. exp. Biol., 1946, 5: 101. 
649. Stickney, J. C. Effect of anoxic anoxia on body 
weight loss in rats. Proc. Soc. exp. Biol., N. Y., 1946, 63: 
210-212. 
650. Stickney, J. C., D. W. Northup, and E. J. Van 
Liere. Blood sugar and dextrose tolerance during anoxia 
in the dog. Amer. J. Physiol., 1948,154: 423-427. 
651. Stickney, J. C., D. W. Northup, and E. J. Van 
Liere. Effect of anoxia on the glucose tolerance curve of 
dogs. Fed. Proc. Amer. Soc. exp. Biol., 1948, 7: 120. 
652. Tepperman, J., H. M. Tepperman, and B. W. 
Patton. Effects of low barometric pressure on the chemical 
composition of the adrenal glands and blood of rats. 
U. S. NRG-CAM. Yale aeromedical research unit. Rept. 
no. 26, 13 June 1944, 8 pp. Endocrinology, 1947, 41: 
356-363. 
653. Van Liere, E. J. Metabolism and anoxia, pp. 196- 
200 in: Anoxia. Its effect on the body. Chicago, The 
University of Chicago Press. 1942, 269 pp. 
654. Van Liere, E. J., J. C. Stickney, and D. W. 
Northup. Blood sugar response to anoxia during accli- 
matization. Amer. J. Physiol., 1948, 155: 10-14. [P] 
655. Van Liere, E. J., J. C. Stickney, and D. W. 
Northup. Effect of acclimatization on blood sugar response 
to anoxia. Fed. Proc. Amer. Soc. exp. Biol., 1948, 7; 
126-127. [P] 
656. Van Middlesworth, L. Glucose ingestion during 
severe anoxia. Amer. J. Physiol., 1946, 146: 491-495. [P] 
657. Van Middlesworth, L. Metabolism of I181 during 
acute adaptation to anoxia. Fed. Proc. Amer. Soc. exp. 
Biol, 1950, 9: 128-129. 
658. Van Middlesworth, L. and M, M. Berry. Iodide 
metabolism during anoxia, nephrectomy, trauma, avitami- 
noses and starvation in the rat. Amer. J. Physiol, 1951, 
167: 576-580. [P] 
659. Vannotti, A. The adaptation of the cell to effort, 
altitude and to pathological oxygen deficiency. Schweiz, 
med. Wschr., 1946, 76: 899-903. (French and German 
summaries.) [P] 
660. Voegtli, W. Das Verhalten der Erythrocytenphos- 
phatase bei 02 Mangel. Helvet, physiol, pharm. Acta, 
1948, 6: C69-C70. [P] SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
661-670 
661. Wickson, M. E. and A. F. Morgan. The effect of 
riboflavin deficiency upon carbohydrate metabolism in 
anoxia. J. biol. Chem., 1946, 162: 209—220. [P] 
9. KIDNEY 
Exposure of human subjects to low partial pres- 
sures of oxygen equivalent to 15,000 feet altitude 
for 2 hours in experiments carried out by Anthony, 
Clarke, Liberman, Nims, Tepperman, and Wesley 
{662) 1943 tended to alkalinize the urine. The data 
presented, together with evidence in the literature, 
indicated to the authors that the principal changes 
in kidney function consist in an increase in bicar- 
bonate elimination and a decreased phosphate 
elimination. Reduction of renal excretion of phos- 
phorus in human subjects during prolonged ex- 
posures to simulated altitudes of 8,000 and 10,000 
feet under conditions of restricted food and water 
intake was also reported by D’Angelo {663) 1946. 
No appreciable change in total urine output from 
ground-level values was found to occur in these 
experiments. According to D’Angelo {664) 1946, 
the most characteristic feature of urine elimination 
was the considerable degree of variation encoun- 
tered from run to run despite the carefully con- 
trolled food and water intake. The reduction of 
total urinary excretion of inorganic phosphorus be- 
came apparent early in the exposure period at 
either the 8,000-foot or 10,000-foot level. The rate 
of excretion increased with increasing exposure 
time. The reduced phosphorus output bore no rela- 
tionship to the total urine output, nor could it be 
directly correlated with changes in respiratory 
metabolism or in the sugar level. In experiments 
carried out on medical students by Kleinschmidt 
{667) 1948, exposure to 3,000 to 4,000 meters 
equivalent altitude resulted in a slight increase in 
urinary output. The increase was more definite at 
5,000 meters and at 6,000 meters. With further in- 
creases in altitude, a pronounced decrease in 
urinary secretion occurred. 
Observations on the effects of altitude hypoxia on 
renal function have been reported by Kelley and 
McDonald {666) 1948 and McDonald and Kelley 
{669) 1948. In the latter report, five dogs were 
subjected to renal function studies at ground level 
and at simulated altitudes of 18,000 feet and 24,000 
feet. The glomerular filtration rate in these animals 
was either decreased, increased, or unaffected, de- 
pending upon the reaction of the individual animal 
to reduced ambient pressure. The effective renal 
plasma flow was increased in all dogs at an altitude 
of 18,000 feet, and was further increased in one dog, 
but decreased below ground level values in the 
remaining dogs at 24,000 feet. In the former report 
it was stated that in 2 or 3 animals a decrease in 
the maximal ability to absorb glucose (Tmo) was 
observed at 18,000 feet as compared to the ground- 
level values, but in the third animal no change was 
evident. In none of the animals was there any ap- 
preciable difference between the value obtained at 
18,000 feet and the value at 24,000 feet. 
For a study of histopathological changes in the 
kidneys of mice subjected to hypoxia, a paper by 
Grattarola and Passerni {665) 1951 may be con- 
sulted. In animals subjected to a simulated altitude 
of 10,000 meters, there was intense cloudy swelling 
of the convoluted tubules with congestion in the 
glomeruli. 
For further studies on the effects of hypoxia on 
renal functions, papers by Lalli {668) 1950 and 
Ochwadt {670) 1947 may be consulted. 
662. Anthony, R. A., R. W. Clarke, A. Liberman, L. F. 
Nims, J. Tepperman, and S. M. Wesley, Renal function 
in man at reduced partial pressures of oxygen. U. S. 
NRC-CAM. Yale aeronautical research unit. C. A. M. 
rept. no. 138, 25 May 1943, 1 p. 
663. D’Angelo, S. A. Urinary output and phosphorus 
excretion in human subjects during prolonged exposures at 
low simulated altitudes. Proc. Soc. exp. Biol., N. Y., 1946, 
62: 13-17. [P] 
664. D’Angelo, S. A. Urine volume and phosphorus 
excretion in human subjects during prolonged exposures 
to moderately low simulated altitudes. Fed. Proc. Amer. 
Soc. exp. Biol., 1946,5: 21. 
665. Grattarola, G. V. and P. G. Passerni. Contributo 
sperimentale alio studio dell istopatologia del rene in 
ipossia. Riv. Med. aero., Roma, 1951, 14: 668-672. (Eng- 
lish, French, German, and Spanish summaries.) [P] 
666. Kelley, V. C. and R K. McDonald. Further ob- 
servations on the effects of altitude anoxia on renal func- 
tion. Amer. J. Physiol., 1948, 154: 201—206. 
667. Kleinschmidt, K. t)ber die Harnsekretion in 
akutem Os-Mangel. Pfliig. Arch. ges. Physiol., 1948, 250: 
79-90. 
668. Lalli, G. Contributo alio studio di alcuni aspetti 
della funzione renale in anossia; comportamento della 
diuresi, della densita urinaria, deU’eliminazione dei solidi, 
dei cloruri de delle basi totali. Riv. Med. aero., Roma, 
1950, 13: 483-495. (English, French, Spanish, and Ger- 
man summaries.) 
669. McDonald, R. K. and V. C. Kelley. Some observa- 
tions of the effects of altitude anoxia on renal function. 
USAF. Randolph Field, Tex. School of aviation medicine. 
Project 506, Rept. no. 1, 6 January 1948, 8 pp. [P] 
670. Ochwadt, B, t)ber Bicarbonatausscheidung und 
Kohlensauresystem im Harn wahrend akuter Hypoxie. 
Pfliig. Arch. ges. Physiol., 1947, 249: 452-469. [P] 
10. REPRODUCTION 
In general, decompression hypoxia depresses re- 
productive functions. According to Moore and 
Price {675) 1948, altitude levels greater than 14,260 
feet are required to produce marked interference 
with the reproductive capacity of rodents when ade- 
quate nutritional states and temperature control 
are maintained. Altland {671) 1949 examined the LOW OXYGEN TENSIONS—EFFECTS OF CARBON DIOXIDE 
671-682 
effects on growth and reproduction of discontinu- 
ous exposure of 247 rats to a simulated altitude of 
24.000 feet for 4 hours daily. Growth was retarded 
in the exposed rats of both sexes, the reduction being 
greater in the male. The body weights of exposed 
male rats never attained more than 80 percent of 
the control weights, whereas the body weights of 
the exposed females reached control levels after 10 
months. Exposure to altitude hypoxia did not affect 
the descent of the testis, but there was striking de- 
lay in the onset of sexual maturity. Spermatozoa 
were few in number as late as the 100th day of life. 
The vaginal orifice of exposed female rats opened 
1 to 6 weeks later than litter-mate controls. Com- 
plete failure of breeding experiments presents evi- 
dence that the testis is unable to acclimatize to this 
degree of hypoxic stress. Histological examinations 
of ovaries gave evidence that ovulation had oc- 
curred in exposed female rats. Five pregnancies de- 
veloped, but no living offspring were born. In a 
study of breeding performance in 131 rats exposed 
to 18,000 feet simulated altitude for 4 hours daily, 
Altland {672) 1949 found a significant reduction 
in the rate of reproduction in both sexes. In rats ex- 
posed only as adults, faulty gestation was observed. 
In those exposed from the 14th day of age there was 
a prevalence of implantation failure and early fetal 
death. Reproductive failures were also observed by 
Malmejac, Rossi, and Plane {674) 1950 in rats 
exposed to barometric pressures of 230 to 170 mm. 
Hg for 32 to 112 exposures at 4 hours each. After 60 
exposures these animals did not reproduce until 10 
months had elapsed. For further studies on repro- 
duction abnormalities produced by hypoxia, papers 
by di Macco {673) 1946, Shettles {676) 1947, and 
Walton and Uruski {677) 1947 may be consulted. 
671. Altland, P. D. Effect of discontinuous exposure to 
25.000 feet simulated altitude on growth and reproduc- 
tion of the albino rat. /. exp. Zool, 1949, 110: 1—16. [P] 
672. Altland, P. D. Breeding performance of rats ex- 
posed repeatedly to 18,000 feet simulated altitude. 
Physiol Zool, 1949, 22: 235-246. 
673. Macco, G. di, Gonadi e ipossia. Boll. Soc. ital. Biol, 
sper., 1946,22: 823. 
674. Malmejac, J., M. Rossi, and P, Plane. Effets de 
seances repetees au caisson a depression sur le comporte- 
ment de “families” de rats blancs. (Mus Decumanus, 
variete albinos.) C. R. Soc. Biol, Paris, 1950, 144: 271— 
272. [P] 
675. Moore, C. R. and D. Price. A study at high alti- 
tude of reproduction, growth, sexual maturity and organ 
weights. /. exp. Zool, 1948, 108: 171—216. 
676. Shettles, L. B. Effects of low oxygen tension on 
fertility in adult male guinea pigs. Fed. Proc. Amer. Soc. 
exp. Biol, 1947, 6: 200. 
677. Walton, A. and W. Uruski. The effects of low 
atmospheric pressure on the fertility of male rabbits. 
/. exp. Biol, 1947,23: 71-76. 
11. EFFECTS OF CARBON DIOXIDE ON HYPOXIA 
The effects of adding carbon dioxide to the in- 
spired air at lowered barometric pressures is dis- 
cussed in the references given in this section. Cer- 
tain favorable subjective and objective effects are 
reported. However, addition of carbon dioxide to 
respiratory mixtures as a means of improving alti- 
tude tolerance is probably not of practical value. 
678. Garasenko, V. M. The use of carbon dioxide at 
lowered barometric pressures. Amer. Rev. Soviet Med., 
1944, 2: 119-125. 
679. Garasenko, V. M. The use of carbon dioxide at 
lowered barometric pressures. Curr. Res. Anesth., 1945, 
24: 135-140. [P] 
680. Hall, F. G. and K. D. Hall. Effect of adding carbon 
dioxide to inspired air on consciousness time of man at 
altitude. Proc. Soc. exp. Biol, N. Y., 1951, 76: 140-142. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1951, 4: 1128. [P] 
681. Langley, L. L., L. F. Nims, and R. W. Clarke. 
Role of carbon dioxide in the stress reaction to hypoxia. 
Amer. J. Physiol, 1950, 161: 331-335. Excer pta Medica. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1951, 4: 412. Abstr. 
682. Petrov, I. P. O znachenii uglekisloty pri kislorod- 
nom golodanii. [Significance of carbon dioxide in oxygen 
deficiency.] pp. 184—200 in: Kislorodnoe golodanie golog- 
nogo mozga; eksperimentaPnye materialy. [Oxygen de- 
ficiency of the cerebrum; experimental material.] Lenin- 
grad, Medgiz, 1949, 204 pp. 
12. TOLERANCE 
Various factors are known to affect tolerance to 
decompression hypoxia. For studies on the effects 
of diets and enzymes on tolerance, papers by the 
following authors should be consulted; Craven 
{688) 1950; Davis {689) 1948; Eckman, Barach, 
Fox, Rumsey, and Barach {690) 1945; Green, 
Butts, and Mulholland {693) 1945; Harris, Ivy, 
and Friedemann {694) 1947; Noell and Chinn 
{700) 1950; Riesen, Tahmisian, and Mackenzie 
{704) 1946; Seitz {705) 1942; Venturi {707) 1951; 
and Wolff and Karlin {708) 1947. In general, 
inanition results in an increase in tolerance. It also 
appears {690) that a high carbohydrate diet is 
attended by a greater tolerance than high fat or 
high fat protein meals. The gain in altitude toler- 
ance with a high carbohydrate diet appears to be 
due to an increased respiratory quotient, a higher 
production of carbon dioxide with a given oxygen 
consumption, theoretically resulting in a propor- 
tionate rise in alveolar ventilation and oxygen 
tension. These findings have been confirmed by 
Green, Butts, and Mulholland {693) 1945 in hu- 
man subjects. However, Noell and Chinn {700) 
1950 found that intravenous glucose administration 
to rabbits did not affect the cerebral cortical sur- 
vival time under conditions of anoxia as measured 
by cortical responsiveness to visual stimuli. Riesen, 683-691 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
Tahmisian, and Mackenzie {704) 1946 concluded 
that preflight administration of a single dose of 
glucose in water to individuals on a normal diet 
produced a significant increase in the resistance to 
unconsciousness from hypoxia at 27,000 feet and 
30,000 feet. Protection afforded flying personnel 
by glucose administration was said to be greater 
30 to 50 minutes following its administration than 
after an interval of 60 to 80 minues. Ascorbic acid, 
either alone or in conjunction with glucose, had no 
demonstrable effect on the duration of conscious- 
ness at altitude. The literature presents evidence 
that resistance to hypoxia may be enhanced by 
thiamine {694) and riboflavin {694 and 708), but 
not by methionine {707) or cytochrome C {689). 
Investigations of drug prophylaxis against the 
lethal effects of hypoxia continue. Although some 
drugs can be shown to improve performance at low 
oxygen tensions, generally speaking, their use is 
dangerous and not of practical value. Investiga- 
tions of pharmacological means for improving hy- 
poxia tolerance are of great significance, however, 
in uncovering physiological and pathological effects 
of low oxygen tensions. The following recent reports 
should be consulted: Arnould and Lamarche {683) 
1950; Barach, Eckman, Ginsburg, Johnson, and 
Brookes {685) 1946; Barmack, Woodruff, and 
Rossett {686) 1942; Burkhardt, Eastman, and Hale 
{687) 1950; Emerson, Morrison, and Van Liere 
{691) 1947; and Gardner and Forbes {692) 1945. 
In studies of the effect of temperature on hypoxic 
failure in naval personnel in the altitude chamber, 
Houston, Cohen, Nuzie, and Bessen {686) 1944 
and Houston, Nuzie, Seitz, and Bessen {697) 1944 
found that at temperatures ranging from 84° to 
98° F. at the incidence of hypoxic failure at 18,000 
feet simulated altitude is slightly greater than in 
chilled runs at the same altitude. The severity of 
subjective complaints also increased with the in- 
crease in temperature. 
The effect of age upon resistance to hypoxia has 
been reported by the following; Arshavski {684) 
1945, Kolchinskaia (699) 1949, and Vail {706) 
1946. These authors confirm the well-known fact 
that newborn animals are more resistant to hypoxia 
than adult animals. 
Pace, Consolazio, and Lozner {701) 1945 have 
shown that polycythemia produced by transfusion 
of red blood cells in normal men affords increased 
tolerance to hypoxia. A group of 10 normal subjects 
were subjected to a simulated altitude of 15,500 
feet. From the 14th to the 17th day of the experi- 
ment a total of 2,000 ml. of a 50-percent suspension 
in dextrose and saline of red cells from blood drawn 
less than 24 hours before was injected intravenously 
in each of the experimental subjects and a total of 
2,000 ml. of dextrose and saline given to subjects 
in a control group. There was no increase in urinary 
pigment or hemoglobinuria. The oxygen capacity 
and arterial oxygen content of the blood increased 
significantly as a result of the transfusions. The 
arterial oxygen saturation at sea level and at alti- 
tude was unchanged by the transfusions. In the 
polycythemic period the pulse rate following exer- 
cise at low oxygen mixtures was significantly lower 
than the controls. The polycythemia persisted for 
approximately 6 weeks. There was no difference in 
the reticulocyte percentages of the two groups. 
From these studies, Pace, Lozner, Consolazio, Pitts, 
and Pecora {702) 1947 concluded that polycy- 
themia induced artificially and polycythemia which 
occurs during acclimatization to high altitude are 
very similar. Therefore, the latter must play an 
important part in the attainment of acclimatization 
and may represent the bulk of the acclimatization 
process. 
For other references to hypoxia tolerance, papers 
by the following may be consulted: Hiestand {695) 
1946, Kline {698) 1947, and Pitts and Pace {703) 
1947. 
683. Arnould, P. and M. Lamarche. Action d’un 
antihistaminique de synthese (2786 R. P. neo-antergan) 
sur la resistance du cobaye a 1’anoxemie. C. R. Soc. Biol, 
Paris, 1950, 144: 1088-1091. 
684. Arshavski, A. Adaptation to anoxia at different age 
levels. Amer. Rev. Soviet Med., 1945, 2: 508-512. 
685. Barach, A. L., M. Eckman, E. Ginsburg, A. E. 
Johnson, and R. D. Brookes. The effect of ammonium 
chloride on altitude tolerance. /. Aviat. Med., 1946, 17: 
123-136. [P] 
686. Barmack, J. E., J. L. Woodruff, and N. E. Rossett. 
The use of drug at high altitudes. The use of benzedrine 
and caffeine under conditions of oxygen want. City College 
of New York, Psychology laboratory, 9 July 1942, 17 pp. 
[P] 
687. Burkhardt, W. L., B. R. Eastman, and H. B. Hale. 
Production of histamine in the body during hypoxia; in- 
fluence of antihistaminics on respiratory response to hy- 
poxia. USAF. Randolph Field, Tex. School of aviation 
medicine. Project 21-24-015, Rept. no. 3, July 1950, 
4 pp. [P] 
688. Craven, C. W. Effect of carrot feeding and star- 
vation on the resistance of the rat to hypoxia. USAF. 
Randolph Field, Tex. School of aviation medicine. Proj- 
ect 21-02-139, March 1950, 10 pp. [P] 
689. Davis, S. K. Effects of cytochrome C on anoxia. 
USAF. Wright-Patterson air force base, Dayton, Ohio. Air 
materiel command, ENG, Aero medical laboratory. Serial 
No. MCREXD—696—112B, 19 January 1948, 8 pp. [P] 
690. Eckman, M., B. Barach, C. A. Fox, C. C, Rumsey, 
Jr., and A. L. Barach. Effect of diet on altitude tolerance 
J. Aviat. Med., 1945, 16: 328-340. [P] 
691. Emerson, G. A., J. L. Morrison, and E. J. Van 
Liere. Drug prophylaxis against lethal effects of severe 
anoxia: IV. A stand technique. Influence of body weight, 
injection of saline, muscular restraint, rate of ascent, and LOW OXYGEN TENSIONS—ACCLIMATIZATION 
692-720 
pre-treatment with oxygen or He-Oz in anoxic mice. Re- 
port filed with U. S. NRC-CMR. 14 January 1947, 14 pp. 
[P] 
692. Gardner, T. S. and F. B. Forbes. The effect of 
thiourea on mice undergoing an abrupt reduction of ex- 
ternal atmospheric pressure. J. Aviat. Med., 1945, 16: 
99-100. [P] 
693. Green, D. M., J. S. Butts, and H. F. Mulholland. 
The relationship of anoxia susceptibility to diet. J. Aviat. 
Med., 1945, 16: 311-327. [P] 
694. Harris, S. C., A. C. Ivy, and T. E. Friedemann. 
Work at high altitude. II. The effect of training and 
dietary restriction of thiamin and riboflavin on altitude 
tolerance and physical efficiency for work at a simulated 
altitude of 15,000 feet. Quart. Bull. Nthwest. Univ., 1947, 
21: 135-151.[P] 
695. Hiestand, W. A. A comparison of the effect of 
water starvation on anoxic death at ordinary barometric 
pressures with anoxic death caused by barometric decom- 
pression. Anat. Rec., 1946, 94: 420. Abstr. [P] 
696. Houston, C. S., E. J, Cohen, S. Nuzie, and G. E. 
Bessen. Effect of temperature on anoxic failure in naval 
personnel in altitude chamber. U. S. Navy. Naval air sta- 
tion, Miami, Fla. Altitude training unit. Project X-396, 
Rept. no. 1, 27 January 1944, 2 pp. [P] 
697. Houston, C. S., S. Nuzie, C. P. Seitz, and G. E. 
Bessen. Effect of temperature on anoxic failure in naval 
personnel in altitude chamber. U. S. Navy. Naval air sta- 
tion, Miami, Fla. Altitude training unit. Project X-396, 
Rept. no. 2, 8 August 1944, 4 pp. [P] 
698. Kline, R. F. Increased tolerance to severe anoxia 
on carbon dioxide administration. Amer. J. Physiol., 1947, 
151: 538-546. [P] 
699. Kolchinskaia, A. Z. K voprosy o gipoksii tsen- 
tral’noi nervnoi sistemy. [Hypoxia of the central nervous 
system.] pp. 105-112 in: Gipoksiia, Kiev, Akad. Nauk. 
Ukr. SSR, 415 pp. 
700. Noell, W. K. and H. I. Chinn, The effect of carbo- 
hydrates on cortical survival in anoxia. USAF. Randolph 
Field, Tex. School of aviation medicine. Project 21-23- 
012, Final Rept., December 1950, 3 pp. [P] 
701. Pace, N., W, V. Consolazio, and E. L. Lozner. The 
effect of transfusions of red blood cells on the hypoxia 
tolerance of normal men. Science, 1945, 102: 589—591. 
[P] 
702. Pace, N., E. L. Lozner, W. V. Consolazio, G. C. 
Pitts, and L. J. Pecora. The increase in hypoxia tolerance 
of normal men accompanying the polycythemia induced 
by transfusion of erythrocytes. Amer. J. Physiol., 1947, 
148: 152-163. [P] 
703. Pitts, G. C. and N. Pace. The effect of blood car- 
boxy hemoglobin concentration on hypoxia tolerance. Amer. 
J. Physiol, 1947,148: 139-151. [P] 
704. Riesen, A. H., T. N. Tahmisian, and C. G. Macken- 
zie. Prolongation of consciousness in anoxia of high alti- 
tude by glucose. Proc. Soc. exp. Biol, N. Y., 1946, 63: 
250-254. [P] 
705. Seitz, C. P. Diet and tolerance to high altitude. 
City College of New York, Psychological laboratories, May 
1942, 6 pp. [P] 
706. V. S. Ohvliianii temperatury okruzhaiushchei 
sredy na vozrastnye kolebaniia chuvstvitel’nosti k kislo- 
rodnomu golodaniiu. [The effect of surrounding tempera- 
ture on the sensitivity to oxygen deficiency in various age 
groups.] pp. 248—252 in: Trudy Voenno-Meditsinskoi 
Akademii im. Kirova, edited by L. A. Orbeli, N. N. 
Anichkova, I. P. Petrova, Moskva, A. V. Lebedinskogs, 
1946, 269 pp. 
707. Venturi, V. M. Azione della mentionina sulla re- 
sistenza all’ipossia sperimentale e sulla epatosi relativa. 
Riv. Med. aero., Roma, 1951, 14: 650-654. (English, 
French, German, and Spanish summaries.) [P] 
708. Wolff, E. and R. Karlin. La riboflavine hepatique 
et la resistance a 1’anoxie chez la souris. C. R. Soc. Biol., 
Paris, 1947,141: 772-774. [P] 
709. Anon. Glucose versus anoxia. /. Amer. med. Ass., 
1947, 133: 776-777. 
13. ACCLIMATIZATION 
The references cited below represent a selection 
of the recent literature on acclimatization to decom- 
pression hypoxia. That adaptation to conditions of 
low oxygen does occur is well established. Under 
certain circumstances acclimatization can be lost. 
The physiological adaptations involved in acclimati- 
zation are complex and include cardiovascular, 
respiratory, hemotological, and other changes. One 
of the principal experimental investigations of ac- 
climatization to high-altitude anoxia was “Opera- 
tion Everest,” carried out in 1946 at the U. S. Naval 
Air Station, Pensacola, Fla., School of Aviation 
Medicine. Reports of this study are given in refer- 
ences 719, 720, 721, and 735. 
710. Adams, W. Acclimatization to intermittent anoxia. 
/. din. Invest., 1946,25: 912. 
711. Adams, W. Acclimatization to intermittent anoxia. 
J. din. Invest., 1946, 25: 912. Excerpta Medica. Section II. 
(Physiology, Biochemistry, and Pharmacology), 1948, 1: 
185. Abstr. 
712. Adams, W. R., A. S. Alving, E. B. Bay, A. H. 
Bryan, H. T. Carmichael, T. J. Case, W. C. Halstead, 
M. Landowne, and H. T. Ricketts. Effects of chronic inter- 
mittent anoxia in man: miscellaneous observations. U. S. 
NRG—CAM. C. A. M. rept. no. 161, 5 July 1943, 4 pp. 
713. Altland, P. D. Effect of rest intervals on main- 
tenance of previously induced high altitude acclimatiza- 
tion. Fed. Proc. Amer. Soc. expt. Biol., 1949, 8: 3-4. 
714. Altland, P. D. and B. Highman. Acclimatization 
response of rats to discontinuous exposures to simulated 
high altitudes. Amer. J. Physiol., 1951, 167: 261—267. [P] 
715. Behnke, A. R., and S. W. Eyer. Notes on the inter- 
national symposium on high altitude biology—Lima, Peru. 
23-30 November 1949, U. S. Navy. BuMed. 19 pp. [D] 
716. Clinton, M., Jr., G. W. Thorn, and V. D. Daven- 
port. Studies on altitude tolerance. II. Studies on normal 
human subjects—effect of repeated short exposures to 
reduced atmospheric pressure. Johns Hopk. Hasp. Bull., 
1946, 79: 70-89. 
717. Dugal, L. P. and P. E. Fiset. Sensibility of man to 
light anoxia. /. Aviat. Med., 1950, 21: 362—374 and 404. 
718. Grandjean, E. L’adaptation de Forganisme humain 
a la montagne. Schweiz, med. Wschr., 1949, 79: 515-518. 
719. Graybiel, A., J. L. Patterson, and C. S. Houston. 
The changes in heart size in man during partial acclima- 
tization to simulated high altitudes. /. Aviat. Med., 1951, 
22: 548-549. Abstr. 
720. Houston, C. S. Operation Everest. A study of ac- 
climatization to anoxia. Nav. med. Bull., Wash., 1946, 
46: 1783-1792. [P] 
291222—54 5 721-744 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
721. Houston, C. S. The adaptations which produce 
acclimatization to oxygen lack. J. Aviat. Med., 1947, 
18: 237-243. [R] 
722. Ivanov, I. I. The mechanism of adaptation of 
animals to low partial oxygen pressures. C. R. Acad. Sci., 
U. S. S. R., 1946,51: 613-614. [P] 
723. Jequier-Doge, E. A propos du deficit-oxygene. 
Schweiz, med. Wschr., 1950, 80: 587—593. [D] 
724. Lipin, J. L. and W. V. Whitchorn. Role of metab- 
olism in the acclimatization of albino rats to reduced 
barometric pressure. /. Aviat. Med., 1950, 21: 405—413. 
725. McDonald, R. K. and V. C. Kelley. Study of 
acclimatization during a two-week exposure to moderate 
altitude. Some observations on the effects of altitude on 
metabolism. III. Hemoglobin metabolism and erythro- 
poiesis. USAF. Randolph Field, Tex. School of aviation 
medicine. Project 21—02—029, Rept. no. 3, October 1949, 
10 pp. [P] 
726. Opitz, E. Increased vascularization of the tissue 
due to acclimatization to high altitude and its significance 
for the oxygen transport. Exp. Med. and Surg., 1951, 
9: 389-403. [P] 
727. Opitz, E. and F. Palme. Darstellung der Hohenan- 
passung im Gebirge durch Sauerstoffmangel. II. Atmung 
und kritische alveolare Sauerstoffspannung bei Riickat- 
mung im Gebirge. Pfliig. Arch. ges. Physiol., 1944, 248: 
298-329.[P] 
728. Opitz, E. and F. Palme. Sauerstoffmangel zur 
Darstellung der Akklimatization im Gebirge. V. Abfla- 
chung von T in Elektrokardiogramm. Pfliig. Arch. ges. 
Physiol, 1944,248: 387-404. [P] 
729. Poel, W. E. Effect of anoxic anoxia on myoglobin 
concentration in striated muscle. Amer. J. Physiol, 1949, 
156: 44-51. 
730. Rahn, H. and A. B. Otis. Man’s respiratory re- 
sponse during acclimatization to high altitude. Fed. Proc. 
Amer. Soc. exp. Biol, 1948, 7: 96-97. 
731. Reynolds, 0. E. and N. E. Phillips. Adaptation of 
the albino rat to discontinuous chronic exposure to alti- 
tude anoxia. Amer. J. Physiol, 1947, 151: 147-154. [P] 
732. Rose, H. W. Study of acclimatization during a two- 
week exposure to moderate altitude (10,000 feet). Effect 
of altitude adaptation on night vision and ocular muscle 
balance. USAF. Randolph Field, Texas. School of avia- 
tion medicine. Project 21-02-029, Rept. no. 1, March 
1949, 16 pp. [P] 
733. Sanboz, L. M. Quelques aspects de I’adaptation a 
Paltitude. Med. aeronaut., 1950, 5: 94. (French abstract). 
Gesdh. Wohlfahrt, Schweiz, 1947, 27: 349-366. 
734. Thorn, G. W., M. Clinton, Jr,, S. Barber, and H. W. 
Edmonds. Studies on altitude tolerance. 1. Studies on 
normal rats—effect of repeated short exposures to reduced 
atmospheric pressure. Johns Hopk. Hasp. Bull, 1946, 79: 
59-69. 
735. U. S. Navy. School of aviation medicine. NAS, Pen- 
sacola, Fla., Operation Everest. 1946, 38 pp. 
736. Van Liere, E. J. Acclimatixation, pp. 140—158, in: 
Anoxia. Its effect on the body. Chicago, The University 
of Chicago Press, 1942, 269 pp. 
737. Van Middlesworth, L. Acute adaptation of rats to 
very low oxygen pressure. Proc. Soc. exp. Biol, N. Y., 
1949, 72: 476-478. [P] 
738. Wilhelm, R. E., M. S. Comess, and J. P. Marbarger. 
Performance under acute hypoxic stress in acclimatized 
mice. /. Aviat. Med., 1950, 21: 313-317. [P] 
739. Wyss, F. and A. Gianoli. Die Veranderung der 
Kapillarresistenz im Hdhenklima. Schweiz, med. Wschr., 
1946, 76: 626-630. [P] 
740. Zoll, M. Contribution d I’etude de I’adaptation d 
Valtitude. Les reactions d’acclimatement apres des sejours 
successifs en caisson a depression. Travail du Centre 
d’Etudes de Biologic Aeronautique du service de Sante 
de 1’Air. Dijon France, 1949, 64 pp. [R] [P] 
IV. PHYSIOLOGICAL EFFECTS OF HIGH CAR- 
BON DIOXIDE CONTENT IN ENVIRON- 
MENTAL AIR 
A. GENERAL STUDIES 
The existing literature on the physiological effects 
of high carbon dioxide concentration in environ- 
mental air gives extensive and valuable information 
on the acute and subacute effects of carbon dioxide 
upon man and animals. Although this information 
is valuable from a comparative as well as human 
standpoint, nevertheless there are significant de- 
fects in our understanding of the actions of high 
concentrations of high carbon dioxide over pro- 
longed periods of time. Long submergence in sub- 
marines imposes the hazard of intolerable concen- 
trations of carbon dioxide and it becomes important 
to have accurate information on the limits of carbon 
dioxide tolerance under conditions of actual opera- 
tions over long periods. Animal studies cannot be 
uncritically applied to the human situation and 
even dockside tests simulating periods of prolonged 
submergence do not fully reproduce the actual 
stresses of combat situations. A further difficulty 
is imposed by the problem of measuring accurately 
the limits to tolerance in terms of performance 
breakdown. 
In the present section, papers by the following 
authors are particularly valuable in affording a com- 
prehensive review of the physiological effects of 
high carbon dioxide content in the environmental 
air: Consolazio, Fisher, Pace, Pecora, Pitts, and 
Behnke {743) 1947; Fenn {746) 1948; Macintosh 
{748) 1946; Schaefer {749 and 750) 1951; and 
Schafer, Storr, and Scheer {751) 1949. 
741. Anselmo, J. E., D. E. Pesigan, G. D. Dizon, V. J. 
Luciano, and J. Y. Navarro. Fatal poisoning from carbon 
dioxide. Report of five cases with two deaths. J. Phil. Is. 
med. Ass., 1951, 27: 102-105. [CH] 
742. Chapin, J. L. The ventilatory response to, toxicity 
of, and acclimatization to carbon dioxide. Thesis 
(Physiol.), University of Rochester, Rochester, New York. 
1949, 164 pp. [P] 
743. Consolazio, W. V., M. B. Fisher, N. Pace, L. J. 
Pecora, G. C. Pitts, and A. R. Behnke. Effects on man of 
high concentrations of carbon dioxide in relation to vari- 
ous oxygen pressures during exposures as long as 72 hours. 
Amer. J. Physiol., 1947,151: 479-503. 
744. Cordier, D. and J. Chanel. Influence de la tension 
de 1’anhydride carbonique dans Pair inspire sur la vitesse PHYSIOLOGICAL EFFECTS OF HIGH CARBON DIOXIDE—NERVOUS SYSTEM 
745-752 
de 1’absorption intestinale des solutions isotoniques de 
glucose chez le rat. /. Physiol., Paris, 1950, 42: 459-462. 
745. Doro, B. Un case di asfissia in uncilindro di spinta. 
Rass. Med. indust., 1949,18: 67—74. 
746. Fenn, W. 0. Physiology of exposures to abnormal 
concentrations of the respiratory gases. Proc. Amer. phil. 
Sac., 1948, 92: 144-154. [R] 
747. Lvovich, D. B, [Accident in a well with great con- 
centration of carbon dioxide.] Gigiena San., Moskva, 1951, 
7: 50-51. 
748. Macintosh, F, C. Partial pressure of C02 in flooded 
submarine compartments. Gt. Brit. MRC-RNPRG. Pre- 
pared for Admiralty Committee on Submarine Escape. 
R. N. P. 46/285, May 1946, 12 pp. [P] 
749. Schaefer, K. E. Chronic carbon dioxide toxicity. 
Amer. J. Physiol., 1951,167: 823-824. 
750. Schaefer, K. E. Studies of carbon dioxide toxicity 
(1) Chronic carbon dioxide toxicity in submarine medi- 
cine. U. S. Navy. Submarine base. New London, Conn. 
Medical research laboratory. Project NM 002 015.03.05, 
21 August 1951, 20 pp. [R] 
751. Schafer, K. E., H. Storr, and K. Scheer. Uber 
langdauernde Einwirkung verschieden hoher C02—Kon- 
zentrationen auf Meerschweinchen. Pflug. Arch. ges. 
Physiol, 1949, 251: 741-764. [P] 
752. U. S. Navy, Memorandum from Force Medical 
Officer, COMNAVGER to Intelligence Officer, COM- 
NAVGER. Medical visit to French submarine and under- 
water research units. 12 December 1951, 4 pp. 
B. NERVOUS SYSTEM 
Lorente de No {767) 1947 has presented an 
analysis of the effect of carbon dioxide upon mem- 
brane potential and upon the functional ability of 
frog nerve. Carbon dioxide increases the membrane 
potential and it is this increase that raises the 
threshold of stimulation and decreases the speed 
of conduction as well as increases the height of the 
response. It appears that the effect of carbon di- 
oxide upon the nerve progressively decreases with 
increasing length of time of survival. Carbon di- 
oxide also increases the negative after potential 
following the supernormal phase. The membrane 
potential of a nerve kept in an atmosphere of 95 
percent oxygen and 5 percent carbon dioxide is the 
sum of 2 fractions. One fraction is restored at a 
slow rate after conduction of impulses and con- 
sequently disappears during tetanic stimulations of 
frequencies above 60 per second. This is called the 
L- (labile) fraction while the other fraction is 
larger and is restored with greater rapidity during 
the descending phase of the spike. For this reason 
this fraction is called the Q- (quick) fraction. 
During restoration of a potassium-treated nerve by 
the action of 5 percent C02, the membrane poten- 
tial is increased by an amount somewhat greater 
than the height of the negative afterpotential pro- 
duced by short tetani at moderate frequency. This 
difference is the increment of the Q-fraction and 
experimental observations indicate that this incre- 
merit is the direct cause of the relief of the potassium 
block. It can be said that the presence of 5 percent 
carbon dioxide increases the ability of the nerve to 
perform work, undoubtedly because the enzymatic 
mechanisms of the nerve utilize stores of metabolic 
energy more rapidly or more effectively in the pres- 
ence than in the absence of a certain concentration 
of carbon dioxide. The author believes that C02 acts 
upon the nerve by participating in reactions of the 
oxidative metabolism. It results in an increase of 
the membrane potential since the presence of car- 
bon dioxide displaces the point of equilibrium of 
respiratory reactions. 
In a study on five subjects who underwent a 
6-day exposure to an atmosphere containing 3 per- 
cent carbon dioxide, Schafer {775) 1949 measured 
their excitation time at the motor point (nerve 
point) of the brachiordalis muscle during exposure. 
Strength-duration curves were plotted and the 
chronaxie values obtained by extrapolation. Con- 
tinuous respiration of a 3-percent carbon dioxide- 
air mixture was found to have an exciting influence 
on the men in the first 24 hours, and a contrary 
effect in the following period. During the first and 
most of the second day of the exposure period, the 
chronaxie and simultaneously the rheobase were 
found to be decreased. From the third day onwards, 
the chronaxie and rheobase were increased to twice 
the control value. The author concluded that the 
changes in chronaxie and rheobase during acute 
and chronic exposure to 3 percent carbon dioxide 
are due to an acceleration followed by a retardation 
of the processes underlying excitation of the nerves. 
Early effects of carbon dioxide excess on spinal 
reflexes have been reported by Kirstein {763) 1951. 
In these studies, cats, decapitated by spinal section, 
were maintained by artificial respiration. The ven- 
tral roots T7 and S7 were cut and reflex discharges 
recorded by a five-stage condenser-coupled ampli- 
fier and a cathode-ray oscillograph. The effects of 
breathing nitrogen or breathing a mixture of 8.9 
percent carbon dioxide and 91.1 percent oxygen 
were determined. Studies were also made of the 
effects of clamping the aorta. After 20 seconds 
of breathing nitrogen, the monosynaptic extensor 
reflex was diminished in amplitude to 60 percent. 
Eighty seconds later the amplitude increased to 190 
percent, and finally after another 30 seconds the 
height of the reflex discharge decreased to 30 per- 
cent. As for the polysynaptic reflex there was no 
change in the first 20 seconds, but after 30 seconds 
there was an increase up to 140 percent followed 
by a gradual decrease. Aortic occlusion led to an 
immediate or early 35 percent decrease in the mono- 
synaptic extensor reflex followed by augmentation SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
after 15 seconds up to 300 percent and then a de- 
crease after 60 seconds. In animals breathing nitro- 
gen and anesthetized with Dial there was no initial 
depressive stage in the monosynaptic reflexes, but an 
increase of 120 percent was noted. Breathing the 
carbon dioxide mixture resulted in a gradual dimi- 
nution of the monosynaptic reflex to 40 percent in 4 
minutes. With the polysynaptic reflex no change 
was observed in the first minute, with a decrease of 
20 percent in 2 to 3 minutes. Thus the depressant 
action of carbon dioxide is confirmed as spinal in 
origin. In similar studies of submaximal two-neuron 
arc responses resulting from medial popliteal nerve 
stimulation, Bradley, Schlapp, and Spaccerelli 
(755) 1950 found that carbon dioxide in the in- 
spired air in amounts from 0.5 to 9 percent produced 
only depression of the response. The effects were 
not due to hypoxia or blood-pressure changes. Lac- 
tic acid injected intravenously in amounts sufficient 
to produce equivalent blood pH changes did not 
have a similar effect. Carbon dioxide did not in- 
crease the inhibition resulting from conditioning 
shocks applied to the lateral popliteral nerve. 
For a definitive and authoritative report on the 
action of carbon dioxide on the respiratory centers 
and other neurological mechanisms, a paper by 
Brazier (756) 1943 should be consulted. This paper 
contains an excellent review of the literature and 
comprises approximately 300 references. The author 
has discussed the mechanisms by which carbon diox- 
ide combats the effects of hypoxia through increase 
in respiratory volume due to direct stimulation of 
the respiratory centers; by a shift in the oxygen 
dissociation curve of blood so that oxygen is released 
more rapidly to the tissues; and through increase in 
the blood flow through the brain (by the action of 
carbon dioxide on cerebral vessels), increased sensi- 
tivity of vasomotor centers, reflex stimulation of the 
carotid and aortic bodies, and augmentation in the 
rise of blood pressure caused by hypoxia, improved 
venous return by the vasopressor effect of carbon 
dioxide, and the mechanical effects on the veins by 
respiratory pumping also play a role. 
On the subject of the specific action of carbon 
dioxide on the respiratory center, Leusen (765) 
1951 found that in dogs under morphine-chloralose 
anesthesia after vagosympathetic section and isola- 
tion of the carotid sinuses, perfusion of cerebral 
ventricles with solutions at various pH values, ob- 
tained by adding carbon dioxide led to respiratory 
stimulation at low pH and respiratory depression 
at high pH. When solutions without sodium bicar- 
bonate were used at pH values between 6.5 and 7.8, 
the changes in pH did not produce variations in 
respiratory activity. When sodium bicarbonate was 
added, a change of 0.3 pH unit produced a change 
in the central stimulation effect. According to 
Beyne, Chauchard, and Chauchard (753 and 754) 
1947, a minimal degree of carbon dioxide excess has 
a depressant effect upon the central nervous system. 
Measurement of chronaxie permits early detection 
of this narcotic effect of carbon dioxide before it 
becomes clinically manifest. Small doses of carbon 
dioxide produce this depressant action preceded by 
an excitation, indicated by an early diminution of 
chronaxie. There is a difference in sensitivity be- 
tween the cerebrum, which is excited only tran- 
siently by small doses, and the respiratory center, 
which continues to be excited by large doses. In the 
authors’ studies, the carbon dioxide percentages 
ranged from 0.25 percent to 3 percent. According to 
Heymans and Pannier {761) 1948, diminution of 
pressure at the level of the carotid sinus in dogs 
results in a hyperpnea while breathing air. This 
hyperpnea persisted for some time in spite of acap- 
nia. The hyperpnea initiated by inhalation of car- 
bon dioxide is pronounced when the pressure at the 
level of the carotid sinus is maintained above the 
normal level. 
Regarding the action of carbon dioxide on the 
excitability of sympathetic reflexes, Thieblot and 
Guilhem {780) 1946 found that dogs subjected to 
3 to 8 percent carbon dioxide in air showed an in- 
crease in the reflex excitability of the sympathetic 
vasomotor center and an increase of time of sum- 
mation measured in the hypogastric and splanchnic 
nerves. Carbon dioxide was found to be a weak 
mydriatic in dogs under chloralose anesthesia by 
Hoorens {762) 1948. 
The central action of carbon dioxide has also 
been investigated in studies of its effects upon cold 
shivering. Hensel {760) 1949 found that at a room 
temperature of 10° C. in normal air, cold shivering 
was produced only in predisposed subjects. Air con- 
taining 3 percent carbon dioxide elicited cold shiv- 
ering in all experimental persons. This carbon 
dioxide effect was enhanced by either hyperventila- 
tion with carbon dioxide or by increasing the carbon 
dioxide content of the air breathed by as little as 
0.2 percent. Cold shivering was held to be produced 
centrally. 
The central inhibitory effects of carbon dioxide 
have been studied by Pollock and associates {758, 
773, 774, and 778). In cats Pollock {773) 1949 
found that high concentrations of carbon dioxide in 
oxygen increase the frequency, but lowers the ampli- 
tude of the electroencephalographic waves. Carbon 
dioxide was found to antagonize seizures induced by PHYSIOLOGICAL EFFECTS OF HIGH CARBON DIOXIDE—NERVOUS SYSTEM 
metrazol and by electricity. It was found that 30 
percent carbon dioxide is more effective than 20 
percent. The 20 percent mixture is more effective 
than a 15 percent mixture and so on down through 
different dilutions to a 5-percent carbon dioxide 
mixture. The antagonism is present in low and high 
partial pressures of oxygen. Hyperventilation and 
breathing of pure oxygen seem to enhance the con- 
vulsive response to electric shock, whereas low 
oxygen (6 percent) and 100 percent nitrogen pro- 
duce antagonism to seizure activity. The duration 
of administration of the carbon dioxide mixtures 
and the strength of stimulus applied appear to be 
important factors in addition to the concentration 
of carbon dioxide. Utilizing the techniques de- 
scribed, it was found that the cerebellum did not 
respond with seizures to electrical stimulation. Stein 
and Pollock {778) 1949 found that concentrations 
of carbon dioxide over 20 percent prevented seizures 
due to electric stimulation when the mixture was 
inhaled for 3 minutes. The animals used in these 
studies were monkeys (Macacus rhesus). In a study 
on patients, Pollock, Stein, and Gyarfas {774) 1949 
produced seizures by stimulation with supra- 
threshold shocking current. It was found that con- 
centrations of carbon dioxide from 15 to 30 percent 
routinely prevented electrically induced seizures. 
With 30 percent carbon dioxide, 30 seconds of in- 
halation sufficed, whereas with 15 to 20 percent 
mixtures, slightly longer periods of time were re- 
quired. Gyarfas, Pollock, and Stein {758) 1949 
found that inhalation of 30 percent carbon dioxide 
and 70 percent oxygen in human subjects produced 
in all cases convulsive phenomena. There was ini- 
tial periocular twitching followed by either an 
extensor hypertonus in all extremities or, more often, 
slight flexor spasms in the arms and extension in 
the legs, consecutive transitory plastic tonus, in- 
creasing occipital rigidity and opisthotonus, and 
finally a high degree of extensor rigidity in all the 
limbs. The fingers were in the “main d’accoucheur” 
position and the toes were in flexion. The dilated 
pupils reacted to light on most occasions. The ten- 
don and skin reflexes could not be elicited on ac- 
count of the muscular rigidity. Pathological reflexes 
were not seen during or after the convulsion, though 
in some cases they preceded them. There was no 
biting of the tongue, incontinence, or postconvulsive 
stupor. The electroencephalogram, though obscured 
by muscular movements, was stated always to be 
clearly not of the grand mal type. The electrical 
activity of the cortex returned to normal shortly 
after discontinuing inhalation of carbon dioxide. 
The clinical symptoms, the electroencephalogram, 
and the absence of postseizure stupor, correspond to 
decerebrate seizures. Seizures produced by breath- 
ing high carbon dioxide concentrations in both ani- 
mals and man have been described by Meduna 
(768, 769) 1950. 
Moussatche (772) 1951 found that carbon di- 
oxide in high concentrations produced convulsions 
in rabbits, but not in the hind limbs after thoracic 
spinal cord section. Convulsions produced in 
morphinized dogs by application of strychnine or 
acetylcholine to the cerebral cortex were inhibited 
by breathing high carbon dioxide mixtures. The 
tension required for inhibition being less (12 to 20 
percent) for cortical than for spinal convulsions. 
Tension of carbon dioxide required to suppress 
spinal-cord convulsions induced by injected strych- 
nine was the same in spinal cord sectioned as in 
intact rabbits. Deafferentation of aortic arch and 
carotid sinus had no effect on the carbon dioxide 
level required for anticonvulsive effects. The action 
of carbon dioxide in these situations is evidently 
directly upon the centers. The mechanism of the 
inhibitory action of carbon dioxide has also been 
studied by Moussatche (777) 1950 on frogs in 
which it was shown that breathing a mixture of 
atmospheric air containing 30 percent carbon di- 
oxide for 20 minutes abolished attacks of cryo- 
epilepsy. Frogs subjected to concentrations of car- 
bon dioxide above threshold necessary to prevent 
attacks of cryoepilepsy did not show depression of 
the pH of the blood to values lower than those 
obtained with perfusion of acidified Ringer’s solu- 
tion. It was concluded by the author that the fall in 
pH is not the cause of inhibition by carbon dioxide 
of the cryoepilepsy. Changes in the brain pH re- 
sponse to carbon dioxide after prolonged hypoxic 
hypoventilation have been reported by Brown (757) 
1950. Carbon dioxide titration curves of brain 
homogenate were determined for guinea pigs. A 
given carbon dioxide tension produced a lower pH 
in the brain homogenates of the hyperventilated 
animals than in the controls, and it was suggested 
that this reduction in the buffering ability of the 
brain for carbon dioxide following prolonged hyper- 
ventilation may be the mechanism by which in- 
creased sensitivity of the respiratory center to 
carbon dioxide following such prolonged stress is 
brought about. 
For discussions of the effects of carbon dioxide 
upon cerebral functioning, several references may 
be consulted {766, 770, 776, 777, 779). Schafer 
(776) 1949 has described the effects of concentra- 
tions of 2 to 5 percent C02 upon brain action. The 
depression phase of carbon dioxide was expressed 
in two findings: (1) disappearance of the hyper- 
capnia effect after 3 days exposure to 3 percent 753-769 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
carbon dioxide, and (2) disappearance of the nor- 
mal inhibitory effect of sensory stimuli on the brain 
action potentials after 3 days in 3 percent carbon 
dioxide. This disappearance of the normal inhibi- 
tory effect of sensory stimuli was found to develop 
parallel with a general decrease of the excitability 
of the respiratory center. Observations on psycho- 
neurotic patients made by Meduna and Gyarfas 
{770) 1949 draw attention to widespread altera- 
tions of nervous activity ranging from primordial 
sensory phenomena to complicated dreams with or 
without emotional discharge, short temporary states 
of confusion, hallucinations, and complicated cor- 
tical or subcortical discharges. It was concluded 
that therapeutic administration of carbon dioxide 
produces decreased function of inhibitory cortical 
areas. Why this is of benefit in therapy can only be 
answered when there is an adequate physiological 
theory of the neuroses. Liest {766) 1949 has also 
reported personality mutation following carbon di- 
oxide inhalation. This author believes that carbon 
dioxide has its effects in descending order on (1) the 
cortex, (2) the basal ganglia and subcortical struc- 
tures, (3) the cerebellum, (4) sensory areas of the 
cord, (5) motor areas of the cord, and (6) the 
medulla. Side reactions of carbon dioxide were 
manifested in sensory, motor, psychosensory, and 
psychomotor changes. Carbon dioxide differs from 
other exogenous agents by the fact that it is in itself 
a powerful physiological agent in the regulation of 
intracranial metabolism. The author attributes the 
therapeutic effect of carbon dioxide inhalation to 
retrogressive, functional suppression of those cere- 
bral structures of specific gnosi-discriminative util- 
ity. He states that the inhalation of carbon dioxide 
is inhibitive, paralytic, and, broadly speaking, 
dyscratic rather than stimulative in its pharma- 
cological action. 
The effects of carbon dioxide upon the percep- 
tion of thermal cutaneous pain have been studied 
by Stokes {779) 1948 who found that carbon diox- 
ide can produce specific analgesia. He considers 
that the analgesic effect of carbon dioxide is not 
peripheral, but mainly central. According to Simon- 
son and Winchell {777) 1951, a mixture of 5 per- 
cent carbon dioxide and 95 percent oxygen in nor- 
mal healthy subjects caused a significant drop of 
fusion frequency of flicker within 12 minutes. The 
drop was faster and greater with the carbon dioxide 
mixture than with an air mixture containing 14 
percent oxygen and 86 percent nitrogen. For a re- 
port on confusion, dizziness, and headache from 
exposure to high concentrations of carbon dioxide 
(4 to 9 percent) subsequently breathing oxygen or 
normal air, a paper by Hayter and Duffner (759) 
1948 should be consulted. 
753. Beyne, J., B. Chauchard, and P. Chauchard. Les 
variations d’excitabilite nerveuse par respiration d’un air 
enrichi en gaz carbonique chez 1’homme. C. R. Soc. Biol., 
Paris, 1947, 141: 368-370. Excerpta Medica. Section II. 
(Physiology, Biochemistry, and Pharmacology), 1949, 2: 
91. Abstr. [P] 
754. Beyne, J., B. Chauchard, and P. Chauchard. Les 
modifications apportees par la presence de gaz carbonique 
aux effets sur 1’excitabilite nerveuse de 1’homme de la 
respiration de melanges anoxiques ou hyperoxiques. C. R. 
Soc. Biol., Paris, 1947, 141: 637-640. [P] 
755. Bradley, K., W. Schlapp, and G. Spaccerelli. 
Effect of carbon dioxide on the spinal reflexes in decapi- 
tated cats. /. Physiol., 1950, 3: abstract section: 62 P. [P] 
756. Brazier, M. A. B. The physiological effects of 
carbon dioxide on the activity of the central nervous system 
in man. Prepared for the Josiah Macy, Jr. Foundation, 
New York, N. Y., 1943, 58 pp. [R] 
757. Brown, E. B., Jr. Changes in brain pH response 
to C02 after prolonged hypoxic hyperventilation. /. appl. 
Physiol, 1950, 2: 549-552. 
758. Gyarfas, K., G. H. Pollock, and S. N. Stein. Central 
inhibitory effects of carbon dioxide. IV. Convulsive phe- 
nomena. Proc. Soc. exp. Biol, N. Y., 1949, 70: 292-293. 
759. Hayter, R. and G. J. Duffner. A study of the 
effect of breathing oxygen or normal air after exposure to 
an atmosphere having a high concentration of carbon 
dioxide. Nav. med. Bull, Wash., 1948, 48: 234—239. U. S. 
Navy. NMRI. Project X—678, Rept. no. I, 24 February 
1947, pp. 6. [P] 
760. Hensel, H. Auslosung von Kaltezittern durch 
Kohlensaureatmung. Pfliig. Arch. ges. Physiol, 1949, 252: 
107-110. 
761. Heymans, C. and R. Pannier. Presso-recepteurs 
du sinus carotidien et sensibilite du centre respiratoire au 
carbon dioxide. Arch. int. Pharmacodyn., 1948, 77: 
62-63. [P] 
762. Hoorens, A. Influences de 1’asphyxie, de 1’anemie, 
de Fhypoxemie et du carbon dioxide sur la pupille. Arch, 
int. Pharmacodyn., 1948, 77: 62-63. [P] 
763. Kirstein, L. Early effect of oxygen lack and carbon 
dioxide excess on spinal reflexes. Acta physiol, scand., 
fSuppl.), 1951, 80: 54 pp. [P] 
764. Klein, H. Die vakuolige Degeneration der Hypo- 
physenzellen unter langerer carbon dioxide Einwirkung. 
Verb, dtsch. path. Ges., 1949, 33: 89-95. [P] 
765. Leusen, I. Au sujet de la specificite de Faction du 
C02 sur le centre respiratoire. Arch. int. Physiol, 1950, 
57: 456—458. Excerpta Medica. Section II. (Physiology, 
Biochemistry, and Pharmacology), 1951, 4: 178. Abstr. 
766. Liest, L, J. Personality mutation following COs 
inhalation. Dis. nerv. Syst., 1949, 10: 333-338. [D] 
767. Lorente de No, R. Carbon dioxide and nerve 
function. Stud. Rockefeller Inst. med. Res., 1947, 131: 
148-194. [M] [R] 
768. Meduna, L. J. Central actions of carbon dioxide, 
pp. 3—8 in: Carbon dioxide therapy. A neurophysiological 
treatment of nervous disorders. Springfield, Charles G. 
Thomas, 1950, 225 pp. 
769. Meduna, L. J. The effect of carbon dioxide upon 
the function of the brain, pp. 17-36 in: Carbon dioxide 
therapy. A neurophysiological treatment of nervous dis- 
orders, Springfield, Charles C. Thomas, 1950, 225 pp. PHYSIOLOGICAL EFFECTS OF HIGH CARBON DIOXIDE—HEART 
770-780 
770. Meduna, L. J. and K. Gyarfas. Motor and sensory 
phenomena during therapeutical C02 inhalations. Dis. 
nerv. Syst., 1949, 10: 3-7. 
771. Moussatche, H. Inhibitory action of carbon dioxide 
on experimental convulsions: experiments on cryoepilepsy 
in the frog; mechanism of the inhibitory action of carbon 
dioxide on convulsions. Arch. int. Physiol., 1950, 57: 
399-410. 
772. Moussatche, H. AqSo inhibidora do gas carbonico 
nas convulsoes experimentias. I. Experiencias em coelhos 
com convulsoes estricninicas. II. Experiencias em caes com 
convulsoes pela excitagao quimica da cortex cerebral. 
Mem. Inst. Osw. Cruz., 1950, 47: 97-128. Excerpta 
Medico. Section II. (Physiology, Biochemistry, and Phar- 
macology), 1951, 4: 789. Abstr. 
773. Pollock, 6. H. Central inhibitory effects of carbon 
dioxide. /. N euro physiol., 1949, 12: 315-324. [P] 
774. Pollock, G. H., S. N. Stein, and K. Gyarfas. Central 
inhibitory effects of carbon dioxide. III. Man. Proc. Soc. 
exp. Biol., N. Y., 1949, 70: 291-292. [P] 
775. Schafer, K. E. Die Beeinflussung der Psyche und 
der Erregungsablaufe im peripheren Nervensystem unter 
langdauernder Einwirkung von 3% C02. Pflug. Arch. ges. 
Physiol., 1949, 251: 716-725. Excerpta Medico. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1948, 
4: 85, Abstr. [P] 
776. Schafer, K. E. Der Einfluss eines langdauernden 
Aufenthaltes in 3% COa auf die Hirnaktionsstrome. 
Pflug. Arch. ges. Physiol., 1949, 251: 726-740. [P] 
777. Simonson, E. and P. Winchell. Effect of high 
carbon dioxide and of low oxygen concentration on fusion 
frequency of flicker. J. appl. Physiol., 1951, 3: 637-641. 
778. Stein, S. N. and G. H. Pollock. Central inhibitory 
effects of carbon dioxide. II. Macacus rhesus. Proc. Soc. 
exp. Biol., N. Y., 1949, 70: 290-291. Excerpta Medico. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1950, 3: 83. [P] 
779. Stokes, J., W. P. Chapman, and L. H. Smith. 
Effects of hypoxia and hypercapnia on perception of ther- 
mal cutaneous pain. J. din. Invest., 1948, 27: 299—304. 
[P] 
780. Thieblot, L. and J. Guilhem. Etude electro- 
physiologique de Paction de C02 sur Pexcitabilite reflexe 
sympathique. C. R. Soc. Biol., Paris, 1946, 140: 997-999. 
[P] 
C. HEART AND CIRCULATION 
The effect of increased carbon dioxide on respira- 
tion and heart rate of hibernating hamsters and 
ground squirrels has been investigated by Lyman 
(799) 1951. The respiratory rate of deeply hibernat- 
ing hamsters and ground squirrels was increased by 
concentrations of carbon dioxide above 2.5 percent. 
The heart rate of ground squirrels usually increased 
with the respiratory rate, but concentrations of 
carbon dioxide above 5 percent were necessary to 
increase the heart rate of hamsters. Ground squir- 
rels remained in hibernation in spite of the higher 
heart rate, but the more easily aroused hamsters 
would waken if exposed for more than a few min- 
utes to concentrations of carbon dioxide higher than 
5 percent. It was concluded by the author that 
these rodents in the hibernating state retain homeo- 
static respiratory and cardiac mechanisms in spite 
of their low body temperature and apparently 
insensitive condition. 
Regarding the effect of breathing carbon dioxide 
on the output of the heart, Asmussen {783) 1943 
showed in human subjects that hyperventilation 
caused by carbon dioxide breathing has an increased 
effect on the cardiac output if the subject lies 
horizontally. There is no effect, however, if the sub- 
ject is tilted to an upright position. The author con- 
cluded that the effect of carbon dioxide breathing 
on the cardiac output must be due to the mechani- 
cal forces of hyperventilation and not to a chemical 
action of carbon dioxide on the circulation, as 
otherwise the difference of the effect in the two 
positions is unexplained. 
Meeter {801 and 802) 1948 found in dogs under 
chloralose anesthesia with both vagii cut that 
breathing 10 percent carbon dioxide resulted in a 
considerable reduction of oxygen consumption. The 
cardiac output decreased with oxygen consumption, 
but the heart rate did not change in these experi- 
ments. Dilatation of the heart under carbon dioxide 
was striking, but was reversible. With metabolic de- 
crease there was a reduction of stroke volume. The 
author found the pacemaker of the heart very in- 
sensitive to carbon dioxide. In a series of dogs in- 
haling an air mixture containing 5 percent carbon 
dioxide, 21 percent oxygen, and 74 percent nitro- 
gen, Patterson, Waits, and McPhaul {805) 1951 
found that the cardiac output either fell slightly or 
was unchanged. In chloralosed dogs not given 
tetraethylammonium chloride, carbon dioxide regu- 
larly produced a rise in mean arterial blood pressure 
and a fall in limb flow of 6 to 50 percent. In animals 
given tetraethylammonium chloride, there was a 
fall in arterial blood pressure of 4 to 23 mm. Hg 
and a rise in limb flow of 8 to 84 percent. In these 
latter cases, the cardiac output usually fell mod- 
erately. These studies suggested to the authors that 
the direct action of carbon dioxide and that medi- 
ated by nervous mechanisms are in competition. The 
fall in cardiac output with an associated rise in 
limb flow suggested that the direct dilatory effect 
of carbon dioxide on limb vessels must not be repre- 
sentative of the entire vascular system. In these 
studies tetraethylammonium chloride was given in 
dosages sufficient to cause complete ganglionic 
blockade. 
Regarding changes in the electrocardiogram, 
Altschule and Sulzbach {782) 1947 found that 
breathing of a mixture of 5 percent carbon dioxide 
and 95 percent oxygen in man resulted in a lower- 
ing of the arterial blood pH to about 6.9 with 
changes in the electrocardiogram indicative of SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
myocardial damage. These changes were rapidly 
reversible after cessation of each experiment and 
decreased in severity when the experiments were 
repeated several times in the same patient. The 
authors concluded that the human myocardium, 
although more tolerant to acidosis than was pre- 
viously believed, appears to be less tolerant than 
the canine heart. Christensen {787) 1946 recorded 
electrocardiographic signs of myocardial hypoxemia 
in normal human subjects hyperventilating volun- 
tarily. Continued hyperventilation of a mixture of 
5 percent carbon dioxide, 20 percent oxygen, and 
75 percent nitrogen resulted in a disappearance of 
the electrocardiographic changes in less than 1 
minute. It was suppposed that the changes are due 
to acapnia and alkalosis. On the basis of animal 
experiments, the authors concluded that myo- 
cardical hypoxemia may be caused either by con- 
striction of the coronary vessels or increased intra- 
myocardial tension, or a combination of the two. 
Large doses of nitroglycerin given immediately 
before the experiment did not prevent the occur- 
rence of the hypoxemic electrocardiographic 
changes. It was therefore concluded that they were 
not caused by coronary constriction alone, but were 
due chiefly to an increase intramyocardial tension. 
In studies on dogs, Spencer, Parry, Whitehead, 
and Draper {807) 1950 gave carbon dioxide per- 
centages of 10, 20, 30, and 40 percent to animals 
under thiopental sodium anesthesia. The venous 
blood pH was depressed roughly proportional to 
the carbon dioxide concentration in an amount 
approximating 0.2 of a unit for each increment of 
10 percent in carbon dioxide concentration. A 
marked increase in amplitude of the T-wave oc- 
curred, but there was no correlation between the 
amount of elevation of the T-wave and the con- 
centration of carbon dioxide inhaled. 
For studies on the effect of intravenous injections 
of carbon dioxide upon the electrocardiogram of 
dogs, papers by the following should be consulted; 
Durant, Long, and Oppenheimer {788) 1948; 
Durant, Long, Oppenheimer, and Wester {789) 
1947; and Durant, Long, and Oppenheimer {793) 
1947. In these studies, dogs under barbiturate anes- 
thesia were used. The chest was opened and the 
animal was ventilated through a tracheal canula. 
Fifty cu. cm. of carbon dioxide were rapidly in- 
jected into the femoral vein. The gas was collected 
in the right ventricle, preventing the passage of 
blood into the lungs. The right heart was found to 
dilate and the blood pressure fell. The initial “up” 
deflection was found to disappear entirely in the 
direct lead. Injections of carbon dioxide of 10 to 
15 cu. cm. resulted in lowering of the R-wave, while 
with 50 cu. cm. or more of carbon dioxide the 
R-wave disappeared entirely. The decrease in am- 
plitude of the R-wave was proportional in the 
amount of carbon dioxide injected. The P-wave 
was increased in amplitude and the ST segment 
raised. The T-wave was inverted. When 30 cu. cm. 
of 1 percent procaine was injected, the QRS inter- 
val increased, and when the action of carbon di- 
oxide was superimposed upon that of procaine, the 
pattern from the surface of the right ventricle re- 
sembled that of right bundle-branch block. Breath- 
ing gas mixtures containing 4 to 10 percent carbon 
dioxide in acute experiments in human subjects 
results in a rise in diastolic and systolic arterial 
blood pressure. 
Alella and Meda {781) 1948 exposed men to a 
gas mixture containing up to 4.7 percent carbon 
dioxide and 20 percent oxygen. In these studies the 
pulse rate was increased as well as diastolic, systolic, 
and mean arterial blood pressures and the minute 
volume. There was a decrease in peripheral resist- 
ance. In human subjects breathing various oxygen- 
nitrogen mixtures, Penneys {806) 1950 found that 
changing to 5 percent carbon dioxide in nitrogen 
and oxygen or 5 percent carbon dioxide in oxygen 
allayed symptoms in all cases. Both systolic and di- 
astolic arterial blood pressures were consistently 
higher with carbon dioxide in the gas mixtures, 
especially at 70 percent arterial saturation. In no 
cases was there so great an elevation in arterial 
blood pressure as to warrant termination of the test. 
The highest was 150 mm. Hg systolic pressure. 
Mayerson {800) 1946 has investigated the use of 
carbon dioxide in preventing postexercise orthostatic 
circulatory insufficiency. This author has called at- 
tention to the fact that many subjects faint when 
kept motionless in the upright position after per- 
forming a standard amount of moderate exercise. 
The postexercise response of these subjects is par- 
ticularly characterized by a low and rapidly falling 
systolic blood pressure and circulatory failure within 
5 to 10 minutes after the exercise is finished. In the 
author’s study, 10 such “fainters” were made to 
breathe air containing from 4 to 10 percent carbon 
dioxide for varying intervals after exercise. When 
carbon dioxide was given immediately after exercise, 
the postexercise systolic blood pressure level was 
high and dropped only gradually. Syncope did not 
occur and the pattern of response resembled that 
of the “nonfainter.” Also the administration of car- 
bon dioxide when syncope was imminent resulted 
in a reversal of the pattern of response and averted 
the collapse. Respiratory gas analyses indicated that PHYSIOLOGICAL EFFECTS OF HIGH CARBON DIOXIDE—HEART AND CIRCULATION 
the carbon dioxide content of the alveolar air in 
“fainters” is diminished after the exercise and re- 
mains from 25 to 40 percent lower than the pre- 
exercise level, whereas the drop in “nonfainters” is 
less (5 to 25 percent). The author suggested that 
under the conditions of his experiments the level of 
carbon dioxide in the “fainters” fell below that 
necessary to stimulate the vasomoter center, and 
that the rise in systolic blood pressure following the 
administration of carbon dioxide is due to stimula- 
tion of the vasomotor center and a consequent vaso- 
constriction which counteracts the local dilatation 
produced during exercise. Little, Avera, and Hoo- 
bler {798) 1949 found a rise of 21 percent in the 
mean arterial blood pressure in normotensive sub- 
jects and 16 percent in hypertensive subjects during 
inhalation of a gas mixture containing 10 percent 
carbon dioxide and 90 percent oxygen. The authors 
ascribed this rise in part to increased vasomotor 
tone, but also in part to an increase in cardiac out- 
put, since it also occurred after caudal anesthesia 
had been established to the third dorsal segment. 
The procedure also resulted in a reduction of renal 
plasma flow and an increase in renal resistance. 
These changes were greater in the hypertensive 
than in the normotensive group. 
Gibbs, Maxwell, and Gibbs {790) 1946 and 
{791) 1947 have studied the volume flow of blood 
through the brain of man at rest, during hyper- 
ventilation, and while breathing high concentra- 
tions of carbon dioxide. In the authors’ studies an 
0.2 percent solution of Evan’s Blue (T-1824) was 
injected into the right internal carotid artery of 
human patients at a rate of 1 cu. cm. per minute. 
Blood samples were drawn from the right internal 
jugular vein with or without occlusion of the left 
internal jugular vein, while simultaneous arterial 
samples were obtained from the femoral artery. 
The rate of injection and the difference in concen- 
tration of the dye in the arterial and venous samples 
gave the necessary information for estimating 
cerebral blood flow. With this value and the 
arteriovenous differences for oxygen it was possible 
to estimate oxygen consumption. This method was 
checked in one case against direct volumetric de- 
terminations of cerebral blood flow. The average 
resting blood flow for all subjects was found to be 
617 cu. cm. per minute and the average oxygen con- 
sumption was 39.2 cu. cm. per minute. Hyperventi- 
lation reduced the cerebral blood flow to approxi- 
mately one-half the control level. By breathing 10 
percent carbon dioxide it was possible to double 
the cerebral blood flow. Changes in arteriovenous 
differences for oxygen were in the same direction 
and of the same general magnitude as were to be 
expected from the changes in blood flow. 
The literature indicates that in acute experiments 
breathing of high concentrations of carbon dioxide 
in animals results in pulmonary vasoconstriction 
and rise of pulmonary arterial blood pressure. In 
the isolated perfused lungs of monkeys (Macacus 
rhesus), Hebb and Nimmo-Smith {794) 1948 
found that inhalation of carbon dioxide in rela- 
tively large amounts led to a rapid rise in pulmonary 
arterial blood pressure which was considered to be 
due to constriction of pulmonary vessels. These 
authors did not see this effect when similar tests 
were made on isolated perfused lungs of dogs. How- 
ever, Duke {792) 1949 exposed isolated dogs’ lungs 
to 5 and 10 percent carbon dioxide in air, and 
noted a diminution in the capacity of the pulmo- 
nary blood vessels and a 5 to 20 percent increase in 
pulmonary arterial blood pressure. The lung volume 
showed an inverse relationship to the carbon dioxide 
content of the arterial blood. The effect of adrena- 
line on pulmonary vessels was not altered during 
ventilation of the lungs with 5 percent carbon 
dioxide, and the response also was not inhibited by 
ergotoxine or by atropine. In isolated and perfused 
lungs of the cat, Nisell {804) 1948 found that in- 
halation of 6.5 percent carbon dioxide in oxygen 
increased the pulmonary blood pressure. The author 
considered that the response was due to a direct 
effect of carbon dioxide on pulmonary blood ves- 
sels. Van Euler and Liljestrand {808) 1946 found 
in cats that breathing 6.5 percent carbon dioxide in 
oxygen resulted in a moderate increase in pulmo- 
nary arterial blood pressure. Tests with higher car- 
bon dioxide concentrations gave the same result. 
In isolated dog lungs perfused with heparinized 
dog blood under constant pressure, Bean, Mayo, 
O’Donnell, and Gray {784) 1951 found that shift- 
ing from normal blood to high carbon dioxide blood 
for short periods resulted in a reversible decrease in 
outflow of blood from the ventilated and quiescent 
lung. This response was occasionally preceded by an 
initial light increase and not infrequently followed 
by a late tendency to an increase in flow. The 
authors concluded that the effect of carbon dioxide 
was to increase the resistance to outflow of blood as 
a consequence of a constrictive action of carbon 
dioxide on effluent vessels or on parenchymal smooth 
muscle and a passive or active dilatation of blood 
reservoir regions of the lung. Air was expelled from 
the lung as a result of the constrictive effect of car- 
bon dioxide on the smooth muscle of the bronchial 
tree and to some extent also to an encroachment of 
distended blood reservoirs upon the alveolar air 
volume. Shift to high carbon dioxide also caused a 
291222—54 6 781-800 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
predominant decrease of inflow of blood to the lung, 
following an initial transient increase of inflow. It 
was concluded that high carbon dioxide exerts a 
differential effect upon various parts of the pul- 
monary vascular bed. The authors consider that 
recognition of regional vasodilatation must qualify 
any generalization which might be arrived at simply 
from consideration of inflow or outflow of blood or 
of alterations in pulmonary arterial pressure alone 
that high carbon dioxide causes a pulmonary 
vasoconstriction. 
The effects of local alteration in carbon dioxide 
on the intestinal blood flow has been investigated 
by Mohamed and Bean {803) 1951 by perfusing the 
dog intestine either completely isolated, or isolated 
in situ with heparinized dog blood previously equil- 
ibrated with gas mixtures of various carbon dioxide 
content from 0 to 15 percent. Hypercapnemia in- 
variably increased the intestinal blood outflow and 
inflow, quite independently of any alterations in 
tone or motility, due to a direct vasodilating action 
of carbon dioxide on the intestinal blood vessels. 
There was commonly a predominant inhibition of 
motility and a diminished intestinal tone which was 
usually preceded by a transient initial augmenta- 
tion of motility and tone, occasionally followed by 
late sporadic tonic contractions. Local hypocapne- 
mia caused a vasoconstriction and decreased intes- 
tinal blood flow. Intrapulmonary administration of 
high carbon dioxide in respiratory gas mixtures 
caused vasoconstriction of central origin in the intes- 
tine isolated in situ except for its extrinsic nerve 
supply and perfused with normal heparinized blood. 
The high threshold and relatively low magnitude of 
this reflex vasoconstriction suggested to the authors 
that in the intact animal this central nervous regula- 
tion of intestinal vessels is not operative except 
under severe conditions. 
For further studies on the action of carbon diox- 
ide on the circulation, papers by the following may 
be consulted; Binet and Burstein (785) 1947; 
Campbell {786) 1950; Holmes, Parry, Draper, and 
Whitehead {795) 1950; Hood {796) 1947; and 
Jourdan, Collet, and Paulon {797) 1951. 
781. Alella, A. and E. Meda. Modification! nelTunano 
della pressione arteriosa e del volume minuto con 
respirazione di C02 a varie concentrazioni. Boll. Soc. ital. 
Biol, sper., 1948, 24: 491-492. Excerpta Medica. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1949, 
2: 775. Abstr. 
782. Altschule, M. D. and W. M. Snlzbach. Tolerance 
of the human heart to acidosis; reversible changes in 
RS—T interval during severe acidosis caused by administra- 
tion of carbon dioxide. Amer. Heart J., 1947, 33: 458- 
463. [P] 
783. Asmussen, E. CCVbreathing and output of the 
heart. Acta physiol, scand., 1943, 6: 176-186. [P] 
784. Bean, J. W., W. P. Mayo, F. O’Donnell, and G. W. 
Gray. Vascular response in dog lung induced by alterations 
in pulmonary arterial carbon dioxide tension and by 
acetylcholine. Amer. J. Physiol., 1951, 166: 723-732. [P] 
785. Binet, L. and M. Burstein. Action du C02 sur le 
tonus des vaisseaux peripheriques. C. R. Soc. Biol., Paris, 
1947, 141: 488-490. [P] 
786. Campbell, G. S. Effect of 10% carbon dioxide on 
the cardiac response to electrical stimulation of the vagus 
nerve. XVIII Intern, physiol. Congr., 1950, 142-143. 
787. Christensen, B. On the electrocardiographic 
changes in normal man brought about by changing the 
carbon dioxide tension in the arterial blood. Acta med. 
scand., (Suppi.), 1946,206; 20-28. 
788. Durant, T., J. Long, and M. J. Oppenheimer. The 
effect of carbon dioxide on the initial ventricular deflection 
of the EKG. Amer. J. med. Sci., 1947, 213: 633-634 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1948,1: 362. Abstr. 
789. Durant, T., J. Long, M. J. Oppenheimer, and 
M. R. Wester. Effect of carbon dioxide and other gases on 
electrocardiogram of the right ventricle. Proc. Soc. exp. 
Biol., N. Y., 1947, 66: 479—481. Excerpta Medica. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1949, 
2; 348. Abstr. 
790. Gibbs, F. A., H. P. Maxwell, and E. L. Gibbs. 
Volume flow of blood through the brain of man at rest, 
during hyperventilation and while breathing high C02. 
Fed. Proc. Amer. Soc. exp. Biol., 1946, 5: 33. 
791. Gibbs, F. A., H. Maxwell, and E. L. Gibbs. Volume 
flow of blood through the human brain. Arch. Neurol. 
Psychiat., Chicago, 1947, 57: 137—144. [P] 
792. Duke, H. IT. The action of carbon dioxide on 
isolated perfused dog lungs. Quart. J. exp. Physiol., 1949, 
35: 25-37. [P] 
793. Durant, T., J. Long, and M. J. Oppenheimer. The 
effect of carbon dioxide on the initial ventricular deflec- 
tion of the EKG. Amer. J. med. Sci., 1947, 213: 633—634. 
[P] 
794. Hebb, C. 0. and R. H. Nimmo-Smith. Pulmonary 
vasoconstriction in response to inhalation of carbon dioxide 
in the isolated perfused lungs of Macacus Rhesus. Quart. 
J. exp. Physiol, 1948, 34: 159-163. [P] 
795. Holmes, J. H., T. M. Parry, W. B. Draper, and 
R. W. Whitehead. Plasma volume changes produced by 
inhalation of carbon dioxide. J. din. Invest., 1950, 29: 
823. Abstr. 
796. Hood, B. Diodrastclearance under kolsyreinhala- 
tion. [Diodrast clearance under carbon dioxide inhalation.] 
Nord. Med., Stockholm, 1947, 33: 34-35. 
797. Jourdan, F,, A. Collet, and Y. Paulon. Sur la 
puissance et Tetendue de Taction vasculaire locale de 
Tanhydride carbonique. C. R. Soc. Biol, Paris, 1951, 145: 
732-734.[P] 
798. Little, W. J., J. W. Avera, and S. W. Hoebler. 
Effects of breathing C02 on blood pressure and renal 
circulation in normotensive and hypertensive subjects. 
Fed. Proc. Amer. Soc. exp. Biol, 1949, 8: 98-99. [P] 
799. Lyman, C. P. Effect of increased carbon dioxide on 
respiration and heart rate of hibernating hamsters and 
ground squirrels. Amer. J. Physiol, 1951, 167: 638-643. 
[P] 
800. Mayerson, S. The use of carbon dioxide in prevent- 
ing post-exercise orthostatic circulatory insufficiency. Fed. 
Proc. Amer. Soc. exp. Biol, 1946, 5: 72. PHYSIOLOGICAL EFFECTS OF HIGH CARBON DIOXIDE—BLOOD 
801-812 
801. Meeter, E. The effect of carbon dioxide breathing 
on the metabolism in the isolated heart-lung preparation. 
Acta brev. neerl. Physiol., 1948, 16: 31-32. [P] 
802. Meeter, E. De invloed van C02 in de ademhalings- 
lucht op de stofwisseling van het geisoleerde hart-long- 
praeparaat. [Influence of C02 in inspired air on the 
metabolism of isolated heart-lung preparation.] Ned. 
Tijdschr. Genesk., 1948, 92: 3032-3034. 
803. Moharaed, M. S. and J. W. Bean. Local and gen- 
eral alterations of blood carbon dioxide and influence of 
intestinal motility in regulation of intestinal blood flow. 
Amer. J. Physiol, 1951, 167: 413-425. [P] 
804. Nisell, 0. Effects of oxygen and carbon dioxide on 
the circulation of isolated and perfused lungs of the cat. 
Acta physiol, scand., 1948,76; 121-127. 
805. Patterson, J. L., Jr., E. J. Waits, and M. V. 
McPhanl. Studies on differential circulatory effects of car- 
bon dioxide. Fed. Proc. Amer. Soc. exp. Biol, 1951, 10: 
102. 
806. Penneys, R. A method of administering carbon 
dioxide at a constant degree of induced anoxemia and its 
cardiovascular effects. Johns Hopk. Hasp. Bull, 1950, 
86: 107-118. 
807. Spencer, J. N., T. M. Parry, R. W. Whitehead, and 
W. B. Draper, The tolerance of the dog under thiopental 
sodium anesthesia to high concentrations of carbon dioxide. 
/. Pharmacol, 1950, 98: 365-371. [P] 
808. Van Euler, U. S. and G. Liljestrand. Effects of 
inhalation of gas mixtures of varying oxygen and carbon 
dioxide content, pp. 309-312 in: Observations on the 
pulmonary arterial blood pressure in the cat. Acta physiol, 
scand., 1946, 12: 301-320. [P] 
D. BLOOD 
The effects of increased carbon dioxide concen- 
trations upon the electrolytes in the blood and tissues 
have been investigated by Malorny {809 and 810) 
1948. On the basis of animal experiments, the 
author finds that all the ion systems used to maintain 
the balance between acids and bases are affected by 
increased carbon dioxide. There is a considerable 
increase of serum calcium and a small diminution 
of ionized calcium with a resulting increase in the 
potassium-calcium quotient. Malorny found that 
this rise was particularly high with lower carbon 
dioxide tensions of 15 to 53 mm. Hg, whereas it was 
practically absent with higher tensions of more than 
80 mm. Hg. The process of exchange of anions in 
the blood corpuscle-plasma system was compared 
with the process of exchange of cations which occurs 
in the muscle cell-body fluid system and liver cell- 
body fluid systems. This shifting of ions also has a 
regulatory effect upon the metabolism of acids and 
bases. In order to increase the buffering capacity, 
the muscle cells take up the potassium and sodium 
ions, whereas, in proportion to its higher buffering 
power, the hepatic tissue releases these bases, even 
though not to a fully equivalent extent. The taking 
up of bases by the muscles at lower carbon dioxide 
tensions must be understood, according to the 
author, as a successful regulatory mechanism 
against acidification of the tissues. By this means the 
total alkali content of the muscles is increased by 
about 10 percent. At high carbon dioxide tensions 
this regulatory mechanism fails. The antagonistic 
effects of lower and higher carbon dioxide concen- 
trations is also shown in the behavior of the alkali 
reserve in the blood. If small quantities of carbon 
dioxide are present in the respired air, the alkali 
reserve of the animals is at first distinctly raised, 
dropping subsequently if the carbon dioxide tension 
is increased. 
809. Malorny, G. Das Verhalten der Elektrolyte im Blut 
und Gewebe bei erhohten C02—Spannungen der At- 
mungsluft. Arch. exp. Path. Pharmak., 1948, 205: 667- 
683. [P] 
810. Malorny, G. Mineral shifting between blood and 
tissue under the influence of increased C02 concentrations. 
Germany. U. S. Zone. Office of naval advisor, pp. C: I— 
1—C; 1-60 in: Monograph on submarine medicine. Folio 
IV, 1948. [P] 
E. CEREBROSPINAL FLUID 
Spencer, Goldensohn, Whitehead, Grover, and 
Draper {812) 1949 have investigated the pressure 
responses of the cerebrospinal fluid to diffusion 
respiration and carbon dioxide inhalation in dogs 
under light thiopental sodium anesthesia. With 
diffusion respiration and various concentration of 
carbon dioxide, the cerebrospinal fluid pressure 
was seen to rise consistently to at least twice the 
control value and to an average of times the 
control value. During inhalation of 40 percent car- 
bon dioxide in oxygen, the maximum rise in cere- 
brospinal fluid pressure was usually reached within 
5 minutes and amounted to 45/2 times the control 
pressure. Goldensohn, Whitehead, Parry, Spencer, 
Grover, and Draper {811) 1951 pointed out that 
the rise in mean cerebrospinal fluid pressure could 
not be correlated directly with changes in systemic 
arterial pressure or systemic venous pressure. They 
concluded that the rise in mean cerebrospinal fluid 
pressure produced by inhalation of high carbon 
dioxide concentrations is not dependent upon asso- 
ciated changes in the rate and force of respiratory 
movements. 
811. Goldensohn, E. S., R. W. Whitehead, T. M. Parry, 
J. N. Spencer, R. F. Grover, and W. B. Draper. Studies 
on diffusion respiration. IX. Effect of diffusion respiration 
and high concentrations of C02 on cerebrospinal fluid pres- 
sure of anesthetized dogs. Amer. J. Physiol., 1951, 165: 
334-340. [P] 
812. Spencer, J. N., E. S. Goldensohn, R. W. White- 
head, R. F. Grover, and W. B. Draper. Pressure responses 
of the cerebrospinal fluid to diffusion respiration and 
carbon dioxide inhalation. Fed. Proc. Amer. Soc. exp. Biol., 
1949, 8: 149. [P] SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
F. RESPIRATION 
graph of minute volume as a function of arterial 
blood pH shows a similar displacement in one sub- 
ject. The increase in response to carbon dioxide 
shown to exist after 24 hours of passively imposed 
hyperventilation cannot be explained entirely on 
the basis of reduced bicarbonate concentration of 
the blood which takes place with prolonged over- 
breathing. For a further report on the effect of 
hyperventilation on the response to inhalation of 
carbon dioxide, a paper by Brown, Campbell, 
Johnson, Hemingway, and Visscher {815) 1948 
may be consulted. That the respiratory responses to 
carbon dioxide are not altered by altitude hypoxia 
is indicated in a report by Weatherby and Burt 
{847) 1944. For a discussion of individual varia- 
tions in respiratory response to carbon dioxide at 
altitude, this report should be consulted. 
Effects of breathing high carbon dioxide concen- 
trations on animals are reported by the following: 
Chapin and Rahn {817) 1948; Eichenberger {824) 
1950; Hatsuzo {831) 1951; Miller, Brown, and 
Varco {836) 1950; Sass-Kortsak, Peyser, and 
Versar {841) 1947; Schaefer, Cornish, and Smith 
{842) 1951; and Valeriok and De Carli {845) 1950. 
These acute studies generally indicate an increase 
in respiratory activity from breathing high carbon 
dioxide mixtures. In the study by Miller, Brown, 
and Varco {836) 1950, it was found that respiratory 
depression occurred in dogs breathing mixtures 
containing carbon dioxide in concentrations greater 
than 15 percent. In rabbits, Eichenberger {824) 
1950 distinguished between an activating influence 
of carbon dioxide (with concentrations up to 7.5 
percent) and an inhibitory action on respiration 
(with concentrations above 7.5 percent carbon di- 
oxide). Valeriod and De Carli {845) 1950 found 
that breathing air containing 6 percent carbon di- 
oxide increased the depth and frequency of respira- 
tion of guinea pigs when in a horizontal position, 
but with animals in an orthostatic position there 
was only an increase in depth. These reactions dis- 
appeared entirely when animals were refrigerated 
below 23° C. In view of the very slight ventilatory 
response to carbon dioxide of diving mammals as 
compared to nondiving mammals, Chapin and 
Rahn {817) 1948 investigated the effect of inhala- 
tion of high carbon dioxide mixtures upon the 
ventilation of the unanesthetized beaver. The mi- 
nute ventilation during the control period was com- 
pared with the 6th to 10th minute after breathing 
the various carbon dioxide mixtures. With 3.8 per- 
cent carbon dioxide in air, there was a 27 percent 
increase in ventilation. With 6.5 percent carbon 
dioxide in air, the increase in ventilation was 84 
Dripps and Gomroe {822) 1947 and Comroe and 
Dripps {818) 1948 have investigated the respira- 
tory and circulatory responses of normal young men 
to inhalations of 7.6 and 10.4 percent of carbon 
dioxide mixtures. When 7.6 percent carbon dioxide 
in oxygen was inhaled, the average minute volume 
of respiration was increased to a maximum of 51.5 
liters per minute (range, 24 to 102 liters per min- 
ute) . The pulse rate was increased by 16.7 beats 
per minute and the blood pressure rose 30.8 mm. Hg 
systolic and 22.2 mm. Hg diastolic. When 10.4 per- 
cent carbon dioxide in oxygen was inhaled, the 
average maximal minute volume of respiration rose 
to 76.3 liters per minute (range, 40 to 130 liters per 
minute). The pulse rate increased 15.6 beats per 
minute, and the arterial blood pressure rose 33.4 
mm. Hg systolic and 25.0 mm. Hg diastolic. In these 
acute studies when the carbon dioxide inhalation 
was stopped, respiration and systolic blood pressure 
returned slowly to normal. The diastolic blood pres- 
sure fell abruptly upon removal of the mask and 
was often lower than the control figures. Comparing 
the maximal ventilation produced by (1) inhala- 
tion of 7.6 percent of carbon dioxide, (2) exhaustive 
muscular exercise, and (3) maximal voluntary 
hyperventilation, the authors found that the aver- 
age ventilation volume for voluntary hyperventila- 
tion was 166 liters per minute; that for exhaustive 
muscular exercise was 110 liters per minute, while 
the response to high concentrations of carbon diox- 
ide was least. 
Holman and Shires {833) 1949 carried out quan- 
titative studies of ventilation during inhalation of 
carbon dioxide in normal and emphysematous pa- 
tients. These subjects were exposed to 30 percent 
oxygen and 70 percent nitrogen mixture, and then 
to a mixture containing 67 percent nitrogen, 30 
percent oxygen, and 3 percent carbon dioxide. The 
subjects were in supine position and at rest. Both 
the normal subjects and the emphysematous patients 
showed a considerably variable increase in the 
minute volume of respiration. 
The effect of passive hyperventilation in human 
subjects for a 24-hour period upon the response to 
carbon dioxide inhalation has been investigated by 
Brown, Hemingway, and Visscher {816) 1950. 
Human subjects breathed 3 percent, 5 percent, or 
7 percent carbon dioxide in oxygen before and after 
24 hours of passively imposed hyperventilation. 
Plotting the minute volume of respiration against 
the arterial blood carbon dioxide tension, it was 
found that the slope of the curve was increased and 
displaced to the left after hyperventilation. The PHYSIOLOGICAL EFFECTS OP HIGH CARBON DIOXIDE—RESPIRATION 
813-831 
percent. With 11.4 percent carbon dioxide in air, 
the increase was 252 percent. These values are 
somewhat lower than those obtained on unanes- 
thetized dogs in the author’s laboratory and differed 
considerably from those obtained on human sub- 
jects. For studies of the action of carbon dioxide on 
central nervous respiratory mechanisms, papers by 
the following may be consulted: Gellhorn (826) 
1943; Gollwitzer-Meier and Pinotti {827) 1947; 
Heymans, Bouckaert, and Dautrebande {832) 
1950; Leusen {834) 1950; Gollwitzer-Meier {828, 
829) 1950; Gray {830) 1945; Santenoise, Grand- 
pierre, Biget, Cotlenko, Lemaire, and Ramana- 
manjary {840) 1950; and Wang and Nims {846) 
1948. 
The effects of carbon dioxide on pulmonary cir- 
culation have been discussed in a previous section 
(IV-C, heart and circulation (p. 59)). For further 
reports upon this subject, papers by the following 
are included; Bean and Mayo {814) 1951, Dirken 
and Heemstra {821) 1947-48, Duke {823) 1949, 
and Nisell {837) 1950. 
Meessen {835) 1948 exposed rats, guinea pigs, 
rabbits, and dogs to mixtures of carbon dioxide in air 
in which the carbon dioxide concentrations ranged 
from 1 to 26 percent while the oxygen pressure re- 
mained normal. These mixtures were inhaled for 
periods ranging from 5 to 6 weeks. The animals 
exhibited degenerative changes in the lungs, liver, 
kidney, and brain believed to be the result of in- 
creased carbon dioxide tension and not caused by 
anoxemia. The pulmonary reactions were similar 
to those elicited by experimental oxygen poisoning 
and by poisoning with phosgene. 
For further references on the effects of carbon 
dioxide on respiration, reference may be made to 
papers by the following: Beadle and Beadle {813) 
1949; Cordier and Cordier {819) 1950; Craig, 
Stubbs, and Marzulli {820) 1948; Fleisch and 
Lehner {825) 1949; Nisell {838) 1951; Pinotti 
{839) 1946; Shires and Eyer {843) 1950; and 
Travia and Cordone {844) 1946. 
813. Beadle, L. C. and S. F. Beadle. Carbon dioxide 
narcosis. Nature, Land., 1949, 164: 235. 
814. Bean, J. W. and W. P. Mayo. Influence of altera- 
tions in pulmonary arterial 0O2 on pulmonary volume and 
blood flow. Fed. Proc. Amer. Soc. exp. Biol, 1951, 10: 11. 
815. Brown, E. B., Jr., G. S. Campbell, M. H. Johnson, 
A. Hemingway, and M. B. Visscher. Changes in response 
to inhalation of C02 before and after 24 hours of hyper- 
ventilation in man. /. appl. Physiol, 1948, 1: 333-338. [P] 
816. Brown, E. B., Jr., A. Hemingway, and M. B. 
Visscher. Arterial blood pH and pC02 changes in response 
to C02 inhalation after 24 hours of passive hyperventila- 
tion. J. appl. Physiol, 1950, 2: 544-548. 
817. Chapin, L. L. and H. Hahn. The effect of C02 
upon the ventilation response of the beaver. Fed. Proc. 
Amer. Soc. exp. Biol., 1948, 7; 19-20. 
818. Comroe, T. H., Jr. and R. D. Dripps. The hyper- 
pnea produced in normal man by maximal voluntary 
hyperventilation, by inhalation of carbon dioxide and by 
severe muscular exercise. Amer. J. med. Sci., 1947, 213: 
246—247. Excerpta Medica. Section II. (Physiology, Bio- 
chemistry, and Pharmacology), 1948, 1: 141. Abstr. 
819. Cordier, J. and G, Cordier. Modifications du pH, 
de Pacide carbonique total et du sucre fibre de 1’humeur 
aqueuse au cours de Pacidose gazeuse. C. R. Soc. Biol., 
Paris, 1949, 143: 432-433. Excerpta Medica. Section II. 
(Physiology, Biochemistry, and Pharmacology), 1950, 3: 
797. 
820. Craig, F. N., J. Stuhhs, and F. N. Marzulli. Analysis 
of combined effects of exercise and carbon dioxide inhala- 
tion on pulmonary ventilation in man. Fed. Proc. Amer. 
Soc. exp. Biol., 1948, 7; 24. [P] 
821. Dirken, M. N. J. and H. Heemstra. Agents acting 
on the lung circulation. Quart. J. exp. Physiol, 1947-48, 
34: 227-241. [P] 
822. Dripps, R. D. and J. H. Comroe, Jr. The respira- 
tory and circulatory response of normal man to inhalation 
of 7.6 and 10.4 per cent C02 with a comparison of the 
maximal ventilation produced by severe muscular exercise, 
inhalation of C02 and maximal voluntary hyperventila- 
tion. Amer. J. Physiol, 1947, 149: 43-51. Med. J. Aust., 
1947, 2: 432. Abstr. [P] 
823. Duke, H. The effect of carbon dioxide on perfused 
lungs. /. Physiol, 1949, 108: 59P. Excerpta Medica. Sec- 
tion II. (Physiology, Biochemistry, and Pharmacology), 
1950, 3: 465. 
824. Eichenherger, E. t)ber die Wirkung der Kohlen- 
saure auf die Atmung des Kaninchens. Helvet. physiol, 
pharm. Acta, 1949, 7: 55—74. Excerpta Medica. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1950, 
3: 462. 
825. Fleisch, A. and F. Lehner. Die respiratorische 
Mittellage. Helvet. physiol, pharm. Acta, 1949, 7: 410- 
426. [P] 
826. Gellhorn, E. Adjustment reactions to carbon 
dioxide, pp. 21—36 in: Autonomic regulations. Their 
significance for physiology, psychology, and neuropsychia- 
try. New York, Interscience Publishers, Inc., 1943, 308 pp. 
827. Gollwitzer-Meier, K. and 0. Pinotti. Uber die 
Nachdauer (Hysteresis) der Erregung des Atemzentrums 
bei der Kohlensaureatmung. Pflug. Arch. ges. Physiol, 
1947, 249: 3-16. [P] 
828. Gollwitzer-Meier, K. Uber das Atemvolumen bei 
gleichzeitiger Einwirkung von Kohlensaureiiberschuss und 
Sauerstoffmangel. Bull. fac. Med., 1949, 12: 166-174. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1950,5; 1495. 
829. Gollwitzer-Meier, K. Uber das Atemvolumen bei 
der gleichzeitigen Einwirkung von Kohlensaureiiberschuss 
und Sauerstoffmangel. Pflug. Arch. ges. Physiol, 1949, 
251: 335-343. Excerpta Medica. Section II. (Physiology, 
Biochemistry, and Pharmacology), 1950, 3: 604. 
830. Gray, J. S. The multiple factor theory of respira- 
tory regulation: The isolation and quantification of the 
independent effects of H ion, C02, and 02 on respiratory 
ventilation. U. S. AAF. Randolph Field, Texas. School of 
aviation medicine. Project 386, Kept. no. 1, 7 May 1945, 
22 pp. [M] 
831. Hatsuzo, K. Studies on normal respiration of frog. 
Part I. Normal breathing and carbon dioxide effect on it. 832-850 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
Nihon Seiri. Z., 1951, 13: (Japanese text pagination), 
319-322. (English text pagination), 322. (In Japanese 
with English summary.) 
832. Heymans, C., J. J. Bouckaert, and L. Dautrehande. 
Importance comparative de Paction centrale directe et de 
Pinfluence reflexe du C02 sur la respiration. Experientia, 
1950, 6: 390. [P] 
833. Holman, J. and G. T. Shires. Quantitative studies 
of ventilation during inhalation of carbon dioxide in 
normal and emphysematous patients. Amer. Heart ]., 
1949, 37: 1101-1109.[P] 
834. Leusen, I. Concerning the specificity of the carbon 
dioxide action on the respiratory center. XVIII Intern, 
physiol. Congr., 1950, 336-337. Arch. int. Physiol., 1950, 
57: 456-458. Excerpta Medica. Section II. (Physiology, 
Biochemistry, and Pharmacology), 1951, 4: 541. Abstr. 
[P] 
835. Meessen, H, Chronic carbon dioxide poisoning. 
Arch. Path., Chicago, 1948, 45: 36-40. [P] 
836. Miller, E. A., E. B. Brown, and R. L. Varco. Cer- 
tain effects in dogs of inspiring 15—30% carbon dioxide. 
Fed. Proc. Amer. Soc. exp. Biol., 1950, 9: 89. 
837. Nisell, 0. I. The action of oxygen and carbon 
dioxide on the bronchioles and vessels of the isolated per- 
fused lungs. Acta physiol, scand. {Suppi.), 1950, 73: 7-59. 
[P] 
838. Nisell, 0. The influence of carbon dioxide on the 
respiratory movements of isolated perfused lungs. Acta 
physiol, scand., 1951,23; 352—360. 
839. Pinotti, 0. Influenza della tensione del C02 del 
sangue sulla eccitabilita riflessa del centre vasocostrittore. 
Boll. Soc. ital. Biol, sper., 1946, 22: 87—89. 
840. Santenoise, D., R. Grandpierre, P. Biget, V. 
Cotlenko, R. Lemaire, and W. Ramanamanjary. Influence 
de Pinhalation de doses progressivement croissantes de C02 
sur Pampliation thoracique. ]. Physiol., Paris, 1950, 42: 
721-724.[P] 
841. Sass-Kortsak, A., E. Peyser, and P. Versar. 
Sauerstoff und Kohlensaure der Einatmungsluft als Regu- 
lator des Lungenvolumens. Helvet. physiol, pharm. acta., 
1947, 5; C46-G47. [P] 
842. Schaefer, K, E,, E. R. Cornish, and F. S. Smith, 
Oxygen consumption and carbon dioxide excretion of 
guinea pigs under basal conditions on air and exposed for 
four hours to 3% carbon dioxide and 21% oxygen. U. S. 
Navy. Submarine base, New London, Conn. Medical re- 
search laboratory. Project NM 002 015.03.04, June 1951, 
8 pp. 
843. Shires, G. T. and S. W. Eyer. Studies in diffusion 
respiration. U. S. Navy. NMRI. Project NM 001 
056.03.01, 14 June, 1950. /. Aviat. Med., 1951, 22: 22-30. 
[P] 
844. Travia, L. and M. Cordone. L’anidrasi carbonica 
nel meccanismo respiratorio ed azione del C02 sull’atti- 
vita respiratoria dell’emoglobina. Riv. Med. aero., Roma, 
1946, 9: 111—120. (English, French, Spanish, and Ger- 
man summaries.) [P] 
845. Valerio, J. and F. De Carli. Azione dell’anidride 
carbonica sul reflesso respiratorio ortostatico nelle cavie a 
temperature corporea normale e con raffreddamento grad- 
uale. Boll. Soc. ital. Biol, sper., 1950, 26: 929-930. [P] 
846. Wang, S. C. and L. F. Nims. The effect of various 
anesthetics and decerebration on the COa stimulating 
action on respiration in cats. /. Pharmacol., 1948, 92: 
187-195. 
847. Weatherhy, J. H. and A. S. Burt. Individual 
variation in respiratory response to carbon dioxide at 
altitude. U. S. Navy. NATC, Pensacola, Fla. School of 
aviation medicine. Project X-402 {Av-216-f), Kept. no. 
7,25 July 1944,5 pp. 
G. ALIMENTARY TRACT 
Breathing high carbon dioxide mixtures by dogs 
was found in experiments of Stickney, Northup, 
and Van Liere (850) 1948 to delay the gastric 
emptying time proportionally to the concentration 
of carbon dioxide in the inspired air. When the car- 
bon dioxide range was between 6 and 8 percent, 
there was an average increase in gastric emptying 
time from 15 to over 100 percent. Between 8 and 
10 percent carbon dioxide caused an increase of 67 
to over 288 percent. Carbon dioxide concentrations 
between 10 and 12 percent produced an increase 
in gastric emptying time between 73 and over 300 
percent. Northup, Stickney, and Van Liere {849) 
1949 also found that high carbon dioxide mixtures 
in dogs and rats depressed the motility of the in- 
testines. In the dogs, intestinal motility was de- 
pressed by a concentration of carbon dioxide of 7.5 
percent or more and in the rats by a concentration 
of 15 percent or more. According to Cordier and 
Chanel {848) 1950, high carbon dioxide mixtures 
in the rat retard intestinal absorption of glucose. 
Exposure to hypoxia (5 percent oxygen) was found 
to reinforce the retarding effect of carbon dioxide 
on intestinal absorption of glucose in the rat. The 
narcotic effect of carbon dioxide was also aug- 
mented by hypoxemia. 
848. Cordier, D. and J. Chanel. Influence de la tension 
d’anhydride carbonique dans Fair inspire sur la vitesse 
de 1’absorption intestinale des solutions isotoniques de 
glucose chez le rat anoxique. /. Physiol., Paris, 1950, 42: 
574—576. Excerpta Medica. Section II. (Physiology, 
Biochemistry, and Pharmacology), 1951, 4: 760. [P] 
849. Northup, D. W., J. C. Stickney, and E, J. Van 
Liere. Effect of carbon dioxide on intestinal motility. 
Amer. J. Physiol., 1949,758; 119-121. [P] 
850. Stickney, J. C., D. W. Northup, and E. J, Van 
Liere. Effect of increased carbon dioxide in inspired air 
on gastric emptying in dogs. Amer. J. Physiol., 1948, 155: 
471. Abstr. 
H. METABOLISM 
For a comprehensive report on metabolism and 
other effects of increased carbon dioxide concen- 
trations in the inhaled air, a report by Schaefer 
{860) 1948 should be consulted. The author points 
out that prolonged exposure to 3 percent carbon 
dioxide in human subjects results in a distinct de- 
crease of the excitability of the respiratory center 
after 3 days. With physical exertion during pro- 
longed exposure to carbon dioxide, an improved 
oxygen intake and carbon dioxide release is found 
as compared with the same exertion during a short PHYSIOLOGICAL EFFECTS OF HIGH CARBON DIOXIDE—METABOLISM 
exposure to carbon dioxide. Under the influence of 
carbon dioxide, the acid-base balance is maintained 
at first by emergency measures such as an increased 
pulmonary ventilation, retention of bases by the 
kidneys, an increased ammonia excretion, and some- 
times by increased hydrochloric acid production of 
the stomach. After approximately 3 days in a carbon 
dioxide atmosphere of 3 percent, the buffer system 
of the blood is adapted by increase of the alkaline 
reserve to such an extent that it is able to keep the 
blood pH constant without the emergency measures. 
The author draws attention to a drop of pulse rate 
as exposure to carbon dioxide continues. The po- 
tassium-calcium quotient rises in several test sub- 
jects during the adaptation to carbon dioxide. At 
first there is a sympathicotonic phase which is fol- 
lowed by a vagotonia in the course of adaptation to 
carbon dioxide. The central nervous system shows 
a diminished efficiency and there is no evidence of 
adaptation here. There is a reduced chronaxie with 
simultaneous drop of the rheobase during the first 
day of exposure, while the chronaxie was prolonged 
to twice its basal value and the rheobase increased 
concurrently with prolonged action of carbon 
dioxide. 
In experiments reported by Endo {853) 1944, 
dogs were kept in an atmosphere containing 10 to 
14 percent carbon dioxide and the hemoglobin, 
protein, colloid osmotic pressure, sugar, lactic acid, 
carbon dioxide, and sodium chloride determined 
in the blood both entering and leaving the gastro- 
cnemius muscle while at rest and during work. 
During work in an atmosphere rich in carbon di- 
oxide, the carbon dioxide in the blood leaving the 
muscle was higher than when ordinary air was 
breathed. The protein was increased in the out- 
going blood, but the colloid osmotic pressure was 
decreased. This suggested that the protein is largely 
in the form of globulin. In a high carbon dioxide 
atmosphere there was found to be a smaller sugar 
utilization and lactic acid formation than with 
ordinary air. The formation of carbon dioxide in 
the muscle was also decreased and the oxygen debt 
increased. The blood circulating time was only 
slightly increased by high concentrations of carbon 
dioxide, but muscle fatigue was found to occur 
sooner. 
In normal anesthetized cats breathing 34 percent 
carbon dioxide in oxygen, Mackay {856) 1947 
found a rapid rise in plasma potassium reaching a 
peak in 5/s minutes, then gradually returning 
to about normal in approximately 30 minutes, while 
high carbon dioxide respiration was being con- 
tinued. Adrenalectomized cats breathing high car- 
bon dioxide showed a similar but smaller rise. These 
findings suggest to the author the possible partici- 
pation of adrenalhepatic mechanisms in the carbon 
dioxide effect, but they indicate definitely that some 
other mechanism must also be involved. Cats evis- 
cerated prior to administration of carbon dioxide 
showed a small rise in plasma potassium, probably 
released from the muscles to maintain the acid-base 
balance. In all of the cats high carbon dioxide levels 
resulted in initial stimulation of respiration followed 
by a sudden depression as the carbon dioxide passed 
from the excitatory to the narcotic level. The height 
of stimulation and depth of depression usually 
occurred within about five minutes on carbon di- 
oxide. Neither the adrenalectomized or eviscerated 
cats showed such a remarkable increase in respira- 
tion, as measured by minute volume after depres- 
sion, although the adrenalectomized cats did exhibit 
a very large increase in tidal volume. 
The literature does not contain reports of inves- 
tigation of metabolic changes following prolonged 
exposure in human subjects to carbon dioxide. 
However, Pointner (858) 1948 described a decrease 
in alkaline reserve in dogs given gas mixtures con- 
taining carbon dioxide from 12 to 20 percent in 
short experiments. Six human test subjects remained 
for 4 days with concentrations of 2.5 to 3 percent. 
Dogs remained for 10 days to 3 weeks under per- 
centages of 3 to 6 of carbon dioxide. In all cases, 
an increase of the carbon dioxide absorption curve 
could be observed. This increase of alkaline reserve 
did not occur when heavy work was done. Human 
subjects and dogs were given the short stress of a 
higher percentage of carbon dioxide (up to 20 
percent for the human subjects and 30 percent for 
the animals). While the alkaline reserve of the test 
subjects showed a considerable decrease, there was 
hardly any change in the case of the dogs which had 
become more readily adapted to prolonged inhala- 
tion of carbon dioxide than did human subjects. 
The author recommended that a potassium buffer 
salt be given to crew members during critical at- 
mospheric conditions. In animal studies conducted 
by Schaefer, Storr, and Scheer {861) 1948, guinea 
pigs were kept under various carbon dioxide con- 
centrations from 3 to 24 percent. Two animals were 
sacrificed within the first 3 days to determine the 
alkaline reserve and to get a whole blood count. 
Tissue was taken from the kidneys and liver to 
measure oxygen consumption. There was effective 
adaptation within 11 to 13 days. In all animals, the 
body weight was diminished in the early part of the 
tests, and weight loss was greater with 3 percent 
carbon dioxide than with higher concentrations. 
Within several days the weight became stabilized. 
With 3 percent carbon dioxide inhalation, the stable 851-8 1 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
weight level was below the basal value. With higher 
concentrations, it again reached the preexposure 
level. For a concentration of 3 percent carbon diox- 
ide and less, the amount of hyperventilation was 
adequate to prevent accumulation of carbon diox- 
ide. An accumulation of carbon dioxide did appear 
during the first days and with a further increase of 
carbon dioxide. This was overcome following the 
onset of a gradual increase of the alkaline reserve. 
After an initial, moderate drop in alkaline reserve, 
it became increased and the extent of this increase 
depended upon the concentration of the inhaled 
carbon dioxide. After transfer to normal air, the 
alkaline reserve dropped to the initial value. The 
blood sugar was found to be elevated during ex- 
posure to 3 percent and 12 percent carbon dioxide 
in the first days and subsequently dropped below 
the basal values. During the initial phase of excita- 
tion, there was an increase in nonprotein nitrogen, 
while the beginning of the second phase, the non- 
protein nitrogen in the urine decreased. Hence, 
during the first phase, the organism is not con- 
sidered accommodated to the carbon dioxide effect. 
In the second phase, the threshold for excitation 
of the central nervous system is raised to a higher 
level as contrasted to a lower level in the first phase. 
In an investigation of gas exchange in human 
subjects in submarines with carbon dioxide con- 
centrations at approximately 3.4 percent, Schaefer 
{859) 1948 reported a diminution of oxygen con- 
sumption and an increase in the release of carbon 
dioxide with an increased respiratory quotient. 
Haebisch {854) 1948, in reporting studies on crew 
members in submarines, draws attention to a 
respiratory quotient of one and a diminution of 
oxygen absorption. 
Studies of Bain and Klein {851) 1949 reveal a 
lowering of lactate and pyruvate levels in the brains 
of normal cats following respiration in 10 to 30 per- 
cent carbon dioxide mixtures. Brain tissue was 
analyzed after freezing with liquid air. In these ani- 
mals there was little change in the glucose or phos- 
phate concentrations. In convulsed animals there 
was considerable limitation of the expected rise in 
lactate, pyruvate, and inorganic phosphate. There 
was a rise in brain glucose level but little effect on 
the brain plasma-glucose ratios. Colldah {852) 
1949 has reported studies on tissue respiration, 
especially in the liver of animals exposed to high 
carbon dioxide concentrations before sacrifice. In- 
halation of carbon dioxide in narcotic concentra- 
tion (20 to 25 percent) lowered tissue respiration 
in the liver, even if oxygen deficiency had been 
avoided. Tissue respiration in the liver was normal 
with lower carbon dioxide concentrations without 
the narcotizing effect or reduction of the frequency 
of respiration. With narcotizing concentrations of 
carbon dioxide there was a great increase of inor- 
ganic phosphorus in the blood. 
For further studies of the effect of carbon dioxide 
on metabolic function, papers by Kuroda {855) 
1948 and Mason {957) 1947 may be referred to. 
851. Bain, J. A. and J. E,. Klein. Effect of carbon 
dioxide on brain glucose, lactate, pyruvate, and phos- 
phates. Amer. J. Physiol., 1949, 158: 478-484. [P] 
852. Colldah, H. On the changes in the organism re- 
sulting from insufficient gas exchange. III. On the cause 
of the lowered tissue respiration in insufficient gas ex- 
change and on the effect of high carbon dioxide concen- 
trations on tissue respiration. Acta med. sc and., 1949, 
132: 378-383.[P] 
853. Endo, K. Uber die Veranderungen der Stoffum- 
satze des Muskels in der Ruhe und bei der Arbeit unter 
C02 Atmung. Tdhoku J. exp. Med., 1944, 47: 223-235. 
(German text.) (English pagination.) [P] 
854. Haebisch, H. The gases contained in the air of 
submarines and gas metabolism during rest in the sub- 
marine environment, pp. C:III-1—C:III-17 in: Mono- 
graph on submarine medicine. Folio IV, Germany. U. S. 
Zone. Office of naval advisor. 1948. 
855. Kuroda, M. [The effect of inhalation of C02 for a 
long period of time upon the body, especially on the 
action of urinary function.] Jap. J. Hyg., 1948, 2: 21-25. 
(English pagination.) [P] 
856. Mackay, J. L. Effects of a narcotic level of carbon 
dioxide on the plasma potassium and respiration of cats. 
Amer. J. Physiol, 1947,151: 469-478. [P] 
857. Mason, E. C, The action of carbon dioxide in water 
mobilization. Ann. intern. Med., 1947, 26: 561-568. [P] 
858. Pointner, R. Carbon dioxide absorption curve and 
the mineral metabolism in an atmosphere containing car- 
bon dioxide and the influence effective on both of them, 
pp. C:II—1—C:II—24 in: Monograph on submarine 
medicine, Folio IV, Germany. U. S. Zone. Office of naval 
advisor. 1948. 
859. Schaefer, K. E. The content of oxygen and carbon 
dioxide in the submarine air. pp. B: 1—29—B: 1—30 in: 
Monograph on submarine medicine, Folio I, Germany. 
U. S. Zone, Office of naval advisor. 1948. 
860. Schaefer, K. E. The regulation of the blood circu- 
lation of man on submarines. The adaptation to increased 
C02 concentrations in the inhaled air. pp. G: 1-61 in: 
Monograph on submarine medicine, Folio 5, Germany. 
U. S. Zone. Office of naval advisor. 1948. 
861. Schaefer, K. E., H. Storr, and K, Scheer. Physio- 
logical and pathological investigations with guinea pigs 
exposed to various carbon dioxide concentrations. Part I. 
Physiological investigations, pp. C IX-1—G IX-18 in: 
Monograph on submarine medicine. Folio VI, Germany. 
U. S. Zone. Office of naval advisor. 1948. [P] 
I. ENDOCRINE GLANDS 
Schafer, Klein, and Zinck {863) 1950 found in 
experiments with dogs that adrenalin injections dur- 
ing acute exposure to 3 percent carbon dioxide pro- 
duced a strong increase of the blood sugar level. 
After prolonged exposure to carbon dioxide, adren- 
alin injection gave only a slight blood sugar rise. PHYSIOLOGICAL EFFECTS OF HIGH CARBON DIOXIDE—ACCLIMATIZATION 
862-863 
The blood sugar also decreased. Morphologically it 
was shown that after chronic carbon dioxide expo- 
sure, the chromaffin characteristic of the adrenal 
medullary cells was reduced. Gross vacuolation of 
the medullary and cortical cells was seen. The zona 
reticularis was hypertrophied with continuous car- 
bon dioxide exposure. Evidence indicated that the 
first 17 days of exposure constitute a rising phase of 
adrenal activity followed by a slow decrease of activ- 
ity. After prolonged exposure to 3 percent carbon 
dioxide, the epinephrine content of the adrenal 
medulla was found to be decreased as measured by 
the effect of extracts from the glands on the blood 
pressure of decerebrated cats. That exposure to 
high carbon dioxide is in itself an alarm reaction- 
producing stimulus, perhaps through its action on 
the acid-base balance of the blood, has been con- 
cluded by Fortier (862) 1949. Exposure of albino 
rats to an atmosphere containing 15 percent carbon 
dioxide, 19 percent oxygen, and 66 percent nitrogen 
for 38 hours resulted in significant hypertrophy of 
the adrenal cortex together with splenic and thymic 
involution. The object of this study was to examine 
whether alkalosis represents a necessary factor to 
the initiation of the alarm reaction or whether it is 
to be considered as but one form of nonspecific 
stress. The results indicated to the author that alka- 
line shift of the acid-base balance cannot be the 
necessary prerequisite to the development of the 
alarm reaction. 
862. Fortier, C. Effect of atmospheric carbon dioxide 
on adrenal cortical hyperplasia and associated changes 
due to stress. Proc. Soc. exp. Biol., N. Y., 1949, 70: 76—78. 
863. Schafer, K. E., H. Klein, and K. H. Zinck. Ex- 
perimented Untersuchungen iiber den Zusammenhang 
von Mark und Rinde der Nebenniere unter Langdauern- 
der CO2—Einwirkung. Klin. Wschr., 1950, 28: 179-184. 
[P] 
J. ACCLIMATIZATION 
Schafer (869) 1949 carried out experiments on 
human subjects involving continuous exposure to 
3 percent carbon dioxide and 21 percent oxygen 
over periods up to 6 days, followed by intermittent 
8-hour exposures to 3 percent carbon dioxide and 
21 percent oxygen over a period of 192 hours. The 
depressed state was reached during the first part 
of the experiment with 6 days of continuous ex- 
posure. This state of depression did not change 
during the second part of the experiment with 8 
days of intermittent exposure to carbon dioxide, in 
spite of relatively long time periods on ordinary air 
(16 hours a day). A period of 5 days on air was 
required before the urine suddenly showed a very 
large output of carbon dioxide and at the same 
time the pulse rate, blood alkaline reserve, and 
chronaxie returned to pretest levels. During the 
continuous and intermittent periods of exposure to 
carbon dioxide, the pulse rate was lowered, the 
blood alkaline reserve was increased, and the 
chronaxie prolonged. The carbon dioxide excretion 
in the urine was reduced to a minimum during the 
exposure to carbon dioxide. In 1950, Schafer {868) 
again called attention to a biphasic reaction pro- 
duced by exposure of men to 3 percent carbon 
dioxide in air over a period of 6 or more days. This 
reaction consists of an initial period of excitation 
followed by depression. Tests of letter canceling and 
hand steadying, chronaxie measurements and 
changes in the electroencephalographic pattern 
confirmed the subjective sensations. Excitability of 
the respiratory center decreased while the alkaline 
reserve of the blood increased, mainly due to reten- 
tion of alkalis by the kidney. Experiments with 
guinea pigs, rats, mice, and dogs using carbon 
dioxide concentrations from 3 to 24 percent also 
revealed biphasic variations. At lower carbon diox- 
ide concentrations around 3 percent, the excitatory 
phase was not regularly observed. Higher carbon 
dioxide concentrations of 12 percent or more ex- 
hibited both phases distinctly. 
According to Otis (867) 1949, the principal 
change in chronic exposure of mice to high carbon 
dioxide concentrations (up to 20 percent carbon 
dioxide) is an apparent increase of ventilation and 
an increase in the alkaline reserve of the blood. 
Mice subjected to gradually increasing carbon diox- 
ide tensions up to a final tension of 20 percent 
carbon dioxide had their tolerance increased, but 
when suddenly exposed to room atmosphere, con- 
vulsed and died. If the decrease in carbon dioxide 
percentage was gradually accomplished, the mice 
encountered no difficulty. This finding is of signifi- 
cance in view of the cases of collapse of submarine 
personnel coming out on deck after surfacing fol- 
lowing long periods of submergence. In man after 
3 days exposure to 3 percent carbon dioxide, there 
is an increase in blood bicarbonate. With continued 
exposure the hyperpnea diminishes. 
In healthy men working and resting in a chamber 
for 5 to 8 days in an atmosphere of 2.5 to 3 percent 
carbon dioxide, Habisch (865) 1949 found that 
the subjects became adapted to the increased car- 
bon dioxide concentration so long as this carbon 
dioxide tension was maintained for longer than 3 
days. This adaptation could be maintained through 
intermittent exposure in air with increased carbon 
dioxide tensions and also the adaptation reaction 
could be shortened by a continuous carbon dioxide 
stimulus. Habisch considered that adaptation to 
carbon dioxide was on an autonomic-humoral basis. 864-871 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
Adaptation manifested itself in a reduction of ven- 
tilation and a rise of alveolar carbon dioxide tension 
at rest and during exercise. There were marked in- 
dividual variations in the degree of adaptation. 
Karlin and Curtis (866) 1945 have reported 
observations on the efficiency of submarine per- 
sonnel during prolonged submergence, when the 
atmospheric oxygen was maintained at 17 percent 
and the carbon dioxide at 3 percent. The purpose 
of this investigation was to determine whether the 
operating efficiency of submarine personnel deteri- 
orated during submergence when the atmospheric 
oxygen was maintained at 17 percent and the carbon 
dioxide at 3 percent for extended periods. In these 
studies the air in the submarine reached 3 percent 
carbon dioxide after 18 hours of submergence, and 
this level was held for another 68 hours. The sub- 
jects showed a decreased capacity for physical work 
and a decrement in night visual efficiency in ap- 
proximately one-third of the ship’s company. There 
was striking reduction in mental efficiency of all 
hands and a decrease in efficiency of intercommuni- 
cations. A noticeable, but unproven, decrease in 
efficiency of radar, and bow and stem plane watches 
was reported. There was no reliable decrease of 
efficiency of sonar performance, “Christmas tree” 
watch, or in remembering numbers. 
For further studies on acclimatization, papers by 
the following may be consulted; Gray (864) 1945 
and White (870 and 871) 1948. 
864. Gray, J. S. The multiple factor theory of respira- 
tory regulation. III. Changes in sensitivity to C02 in pro- 
longed acapnia and hypercapnia. U. S. AAF. Randolph 
Field, Texas. School of aviation medicine. Project 386, 
Rept. no. 3, 21 November 1945, 47 pp. [M] [R] 
865. Habisch, H. t)ber den Gaswechsel bei Ruhe und 
Arbeit unter Kurz-und langfristiger Kohlensaureeinwir- 
kung. Pfliig. Arch. ges. Physiol., 1949, 251: 594-608. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1950,5: 1210. [P] 
866. Karlin, J. E. and J. F. Curtis. Observations on 
efficiency of submarine personnel during prolonged sub- 
mergence when the atmospheric oxygen is maintained at 
17% and the carbon dioxide at 3%. U. S. Navy. Sub- 
marine base. New London, Conn. Medical research 
department. Project X-516 {Sub. no. 105), Final rept., 
27 July 1945,46 pp. 
867. Otis, A. B. Acclimatization to carbon dioxide, 
carbon monoxide and low oxygen, pp. 23-25. U. S. 
NRG-CAM. Conference on acclimatization, 17 June 1949, 
29 pp. 
868. Schaefer, K. E. Adaptation of men and animals 
during prolonged exposure to increased carbon dioxide 
concentrations. Amer. J. Physiol., 1950, 163: 747. 
869. Schafer, K, Atmung und Saure-Basengleichgewicht 
bei langdauerndem Aufenthalt in 3% C02. Pfliig. Arch, 
ges. Physiol., 1949, 251: 689-715. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1950, 3: 1211. [P] 
870. White, C. S, Estimated tolerance of human sub- 
jects to various carbon dioxide time concentrations. Ap- 
pendix No. 1. Calculation of carbon dioxide percentage 
equivalents at sea level and various altitudes. Lovelace 
clinic. Project 200, Rept. no. 1, 12 October 1948. 
871. White, C. S. Estimated tolerance of human sub- 
jects to various carbon dioxide-time concentrations. 
Lovelace clinic. Project 200, Rept. no. 2, 27 July 1948. 
K. PATHOLOGICAL CHANGES 
The literature contains a number of studies of 
pathological changes resulting from experimental 
exposure to high concentrations of carbon dioxide. 
In 1947, Meessen (872) reported on exposure of 
rats, cats, and dogs to 4.5 percent carbon dioxide 
in air for 13 days. In these animals there were irre- 
versible changes including damage of the alveolar 
walls of the lungs and cell necrosis with dead cells 
and debris in the liver, kidney, and brain. In 1948, 
Meessen (873) subjected rats and guinea pigs to 
carbon dioxide concentrations of 1 to 26 percent 
for periods of 5 hours to 6 weeks. If animals were 
killed immediately after exposure, a high degree of 
hyperemia of the lung was found. Pulmonary 
edema was seen if the animal died in air with high 
carbon dioxide concentrations. In some cases fluid 
entirely obstructed the alveoli. On prolonged ex- 
posure, the alveoli of the lungs were dilated as in 
emphysema with dense infiltration of leukocytes in 
extensive areas. Hyperemia extended throughout 
the liver. In rats, after 4 days of exposure to 20 
percent carbon dioxide, there were extensive, irre- 
versible hepatic changes. In some liver cells the 
nuclei were pyknotic. After exposure to 14 percent 
carbon dioxide for 48 hours, the kidneys were 
hyperemic and nephrotic. In these same animals 
there were irreversible changes in the central neu- 
rons. In guinea pigs exposed to carbon dioxide 
concentrations of 3, 12, and 24 percent at an equal 
oxygen tension, Zinck (875) 1948 found that with 
up to 12 percent carbon dioxide there was a shifting 
of the blood from the splanchnic area towards the 
heart and lungs. With 24 percent carbon dioxide, 
the lungs were rather anemic and the abdominal 
organs showed a greater capillary vascularization. 
The musculature of the caudal extremities showed 
constricted capillaries in all experiments. The liver 
and kidneys appeared to be the first organs im- 
paired, showing changes which disappeared on 
recovery. In the liver there was reduction of the 
glycogen accompanied by moderate pericapillary 
and peripheral deposition of fat with simultaneous 
lipemia. The straight uriniferous tubules showed 
vacuolar degeneration and necroses. With high 
carbon dioxide concentrations, there were fat depos- 
its in renal pyramids. The glomeruli were swollen. HEAT AND HUMIDITY—GENERAL CONSIDERATIONS 
872-876 
There was a reduction of lipoid substances in the 
adrenal glands and the medullary cells were coarsely 
vacuolized, apparently indicating a reduction of 
epinephrine. There was atelectasis, interstitial 
pneumonia, hyperplasia of the alveolar epithelium 
and desquamation in the lungs. Glycogen disap- 
peared from the heart. Sometimes the striations of 
the heart muscle fibers became indistinct and edema 
was present. There was edema at the base of the 
left coronary artery. The spleen was contracted, and 
with 24 percent carbon dioxide an edema of the 
reticulum was observed. 
In a study of central nervous system changes re- 
sulting from increased concentrations of carbon 
dioxide, Stephens {874) 1951 exposed rats to an 
increase of carbon dioxide percentage to 20 percent 
within 2 hours and then up to 38 percent and finally 
to 43.2 percent. As the carbon dioxide percentage 
rose above 15 percent, the activity of the animals 
was greatly decreased. In chronic experiments, rats 
were exposed for periods of 10 to 166 days to carbon 
dioxide concentrations ranging between 6 and 10 
percent and the oxygen between 18 and 23 percent. 
Cells which are most sensitive to hypoxia (such as 
those of the cerebral cortex) were found to be 
protected from severe histopathological changes. 
The cells of the primitive levels of the brain (less 
sensitive to oxygen lack) sustained the greatest 
structural damage as result of high carbon dioxide. 
The nerve cell damage during carbon dioxide ex- 
posure in the prolonged experiments was believed 
by the author to be due to toxic cellular metabolites 
rather than hypoxia. The cell changes in animals 
exposed chronically to concentrations of carbon 
dioxide rarely exceeding 10 percent were reversible. 
Also in the acute exposures the cell changes were 
generally reversible. Irreversible changes were seen 
in some large motor cells. In the acute experiments, 
the neurons were slightly swollen and there was 
chromatolysis, more pronounced at the periphery 
of the cells. There was swelling of the nucleus and 
nucleolus, and also marked vacuolation. In the 
chronic experiments there was severe swelling of 
the cells with chromatolysis. 
In guinea pigs exposed to 3 percent carbon diox- 
ide with adequate oxygen, Klein {764) 1949 re- 
ported vacuolar degeneration of the cells of the 
hypophysis. Animals exposed for 12 to 14 days to 
this concentration of carbon dioxide demonstrated 
maximum vacuolation in the chromophobe cells. 
For studies on the pathological changes in the liver 
following exposure of guinea pigs to 12 percent car- 
bon dioxide, a report by Zinck {876) 1949 may be 
consulted. 
872. Meessen, H. Organveranderungen nach experimen- 
teller Kohlendioxydvergiftung. Schweiz. Med. Wschr., 
1947, 77; 1135-1136. [P] 
873. Meessen, H. Pathological findings after carbon 
dioxide intoxication, pp. C X-l—C X-9 in: Monograph 
on submarine medicine, Folio VI, Germany. U. S. Zone. 
Office of naval advisor. 1948. [P] 
874. Stephens, W. M. The central nervous system 
changes resulting from increased concentrations of car- 
bon dioxide. /. neuropath, din. neural., 1951, 1: 88-97. 
[P] 
875. Zinck, K. H. Physiological and pathological in- 
vestigations with guinea pigs exposed to various carbon 
dioxide concentrations. Part II. Pathological investiga- 
tions. Morphological findings with the carbon dioxide 
poisoning of guinea pigs compared with the damages of 
the tissues in cases of hypoxydosis and oxygen poisoning, 
pp. C IX-l—C IX-40 in: Monograph on submarine 
medicine, Folio VI, Germany. U. S. Zone. Office of naval 
advisor. 1948. [P] 
876. Zinck, K. H. Organveranderungen bei Kohlen- 
saureeinwirkung verschiedener Konzentration und Dauer 
auf das Meerschweinchen. Verb, dtsch. path. Ges., 1949, 
33: 89-95. [P] 
V. HEAT AND HUMIDITY PROBLEMS 
A. GENERAL CONSIDERATIONS OF TEMPERATURE, 
HUMIDITY, AND CLIMATE 
One of the foremost habitability problems in sub- 
marines arises from excess temperature and humid- 
ity. Conditions of insupportable heat and humidity 
may indeed be responsible for failure of the patrol, 
and it is reported that German submarines in World 
War II were forced to abandon patrols and turn 
back to port because of loss of efficiency of the crews 
due to heat and humidity. In the later stages of the 
war it was realized in the German submarine service 
that adequate air conditioning was essential, and 
some submarines were so conditioned. In the United 
States Navy, air conditioning is standard and its 
value has been fully demonstrated in terms of effi- 
ciency and lowered morbidity. Among the references 
given in this section, papers by the following are 
especially recommended to the reader who desires 
to familiarize himself with the general problems of 
temperature, humidity, and climate. Bazett (878) 
1948 and {879) 1949; Critchley {994) 1946; Gagge 
and Herrington (889) 1947; Grant {891) 1951; 
Hardy {892) 1950; Herrington {894) 1949; Her- 
rington and Hardy {895) 1949; Lee {899) 1948; 
Saunders {907) 1951; Spealman, Newton, and Post 
{909) 1947; Spealman, Yamamoto, Bixby, and 
Newton {910) 1949; and Yaglou, Baetjer, Machle, 
McConnell, Shaudy, Winslow, and Witheridge 
{912) 1950. A study of these reports and others 
given in this Sourcebook on heat and humidity 
problems indicates that our knowledge of the physi- 
ology and pathology of heat and humidity is quite 877-913 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
comprehensive. From the point of view of submarine 
medicine, the important consideration at this time 
is the application of this knowledge. 
877. Adolph, E. F. Acclimatization to heat and cold, 
pp. 488-496 in: Part IV. Physiology in: Advances in 
military medicine, Vol. II. Edited by E. C. Andrus, D. W. 
Bronk, G. A. Carden, Jr., G. S. Keefer, J. S. Lockwood, 
J. T. Wearn, and M. G. Winternitz. Boston, Little, Brown 
and Co., 1948, 472 pp. [R] 
878. Bazett, H. C. Human efficiency as affected by 
climate and its relation to social development. Advanc. 
Sci., 1948, 4: 348-353. 
879. Bazett, H. C. The regulation of body temperatures, 
pp. 109-192 in: Physiology of heat regulation and the 
science of clothing. Edited by L. H. Newburgh. Philadel- 
phia, W. B. Saunders Co., 1949, viii, 457 pp. [R] 
880. Bean, W. B, Treatment of conditions incident to 
hot climate, pp. 4-385—4-399 in: Treatment in general 
medicine. Volume 4. Edited by Hobart A. Reimann. 
Fourth edition. Philadelphia, F. A. Davis Co., 1948, 776 
pp. 
881. Bedford, T. Environmental warmth and its meas- 
urement. 1946, London, H. M. Stationery Office, 40 pp. 
Abstr: Bull. Hyg., Land., 1946, 21: 595—596. [R] 
882. Bedford, T., N. H. Mackworth, B. McArdle, and 
J. S. Weiner. Further research required into the effects 
of heat on human reactions. Gt. Brit. MRC—RNPRC, HS. 
R. N. P. 48/428, H. S. 224, undated, 3 pp. 
883. Buettner, K. Effects of extreme heat on man. 
II. Analysis of temperature changes caused by different 
kinds of heat application to the skin. USAF. Randolph 
Field, Texas. School of aviation medicine. Project 21-26- 
002, Rept. no. 2, November 1951, 10 pp. 
884. Critchley, M. Problems of naval warfare under 
climatic extremes. Lecture I. Milit. Surg., 1946, 98: 94— 
106. 
885. Dallav alle, J. M, The thermal environment, pp. 
80-101 in: The industrial environment and its control. 
New York, Pitman Publishing Corp., 1948, 225 pp. [D] 
886. Dohin, N. B., C. A. Neymann, and S. L, Osborne. 
Pathologic changes in the central nervous system resulting 
from experimentally produced hyperpyrexia. J. Neuropath, 
exp. Neurol, 1949, 8: 295—304. [P] 
887. Edwards, J., Jr. Electroencephalographic study of 
men transferred from the subtropic to the subarctic. 
USAF. Ladd air force base, Alaska. Arctic aeromedical 
laboratory. Project 21—01—004, Section IV, December 
1950, 18 pp. [P] 
888. Fischer, A., S. Gero, I. Rozsahegyi, and C. Sellei. 
Munkaartalmak pathogenesise es megelozese. [General 
study of pathogenesis of disturbances in high temperature 
exposures.] Orv. hetil, 1949, 90: 452—456. [P] 
889. Gagge, A. P. and L. P. Herrington. Physiological 
effects of heat and cold. Annu. Rev. Physiol, 1947, 9: 
409-428. [R] 
890. Glaser, E. M. Acclimatization to heat and cold. 
J. Physiol, 1950, 110: 330-337. Abstr. World Med., 1950, 
8: 5-6. [P] 
891. Grant, R. Physiological effects of heat and cold. 
Annu. Rev. Physiol, 1951, 13: 75—94. [M] [R] 
892. Hardy, J. D. Physiological responses to heat and 
cold. Annu. Rev. Physiol, 1950, 12: 119-144. [R & P] 
893. Hardy, J. D. and G. F. Soderstrom. Heat loss 
from the nude body and peripheral blood flow at tem- 
peratures of 22° to 35° C. /. Nutrit., 1938, 16: 493-510. 
[P] 
894. Herrington, L. P. The range of physiological re- 
sponse to climatic heat and cold. pp. 262-276 in: 
Physiology of heat regulation and the science of clothing. 
Edited by L. H. Newburgh. Philadelphia, W. B. Saunders 
Co., 1949, viii, 457 pp. 
895. Herrington, L. P. and J. D. Hardy. Temperature 
and humidity in relation to the thermal interchange be- 
tween the human body and the environment, pp. 269— 
309 in: A survey report on human factors in undersea 
warfare. Washington, D. C., National Research Council, 
1949, 541 pp. 
896. Hogger, D. Industrielle Arbeit bei grosser Hitze. 
Bern, Schweiz. Handelsamtsblatt, 1947, 74 pp. [R] [D] 
897. Lee, H. K. Special reports upon overseas visit 
1945-46. No. 1. Human climatology. Australian Army, 
NHMRC. 31 January 1946, 18 pp. 
898. Lee, D. H. K. Human climatology and tropical 
settlement. The John Thomson lecture for 1946. Univer- 
sity of Queensland, Brisbane, 1947, 34 pp. [P] 
899. Lee, D. H. K. Heat and cold. Annu. Rev. Physiol., 
1948, 10: 365-386. [R] 
900. Lee, D. H. K. Physiology as a guide to combating 
tropical stress. New Engl. J. Med., 1950, 243: 723-730. 
[D] 
901. Love, L. H. Heat loss and blood flow of the feet 
under hot and cold conditions. /. appl. Physiol., 1948, 1: 
20-34. [P] 
902. Machle, W. Control of heat in industry. Occup. 
Med., 1946, 2: 350-359. [D] 
903. MacPherson, R, K. Tropical fatigue. Univ. Qd. 
Dept. Physiol., 1949,1: 162 pp. 
904. Mole, R. H. The relative humidity of the skin. 
J. Physiol, 1948,107: 399-411. [M] 
905. Richardson, D. T. British Red Cross Society tropi- 
cal hygiene manual. No. 10. Revised, with additions by 
H. H. Scott. London, Cassell and Co., Ltd., 1946, 246 pp. 
906. Robinson, S., E. S. Turrell, and S. D. Gerking. 
Physiologically equivalent conditions of air temperature 
and humidity. Amer. J. Physiol, 1945, 143: 21-32. [P] 
907. Saunders, G. M. Hygiene in the tropics, pp. 1412— 
1450 in: Clinical tropical medicine. Edited by R. B. H. 
Gradwohl, Luis Benitex Soto, and Oscar Felsenfeld, St. 
Louis, The C. V. Mosby Company, 1951, 1647 pp. 
908. Shattuck, G, C. Tropical climates and health, pp. 
722—728 in; Diseases of the tropics. New York, Appleton- 
Century-Grofts, Inc., 1951, 803 pp. 
909. Spealman, C. R., M. Newton, and R. L. Post. 
Influence of environmental temperature and posture on 
volume and composition of blood. Amer. J. Physiol, 1947, 
150: 628-639. [P] 
910. Spealman, C. R., W. Yamamato, E. W. Bixby, 
and M. Newton. Observations on energy metabolism and 
water balance of men subjected to warm and cold en- 
vironments. /. industr. Hyg., 1949, 31: abstract section: 
67. [P] 
911. Stewart, W. Effects of heat with special reference 
to its occurrence in British troops in the Persian gulf area 
in 1941-1942. Nav arm. Cps. J., 1948, 90: 178-193. [D] 
912. Yaglou, C. P., A. M, Baetjer, W. Machle, W. J. 
McConnell, L. A. Shaudy, C, E. A, Winslow, and W. N. 
Witheridge. Thermal standards in industry. Amer. publ. 
Hlth. Yearb., Part II. 1950, 40: 131-143. 
913. Anon. Keeping cool. Roy. Nav. med. Bull, 1946, 
22: 18-24. [R] HEAT AND HUMIDITY—PHYSIOLOGICAL EFFECTS 
914-926 
R. TEMPERATURE AND HUMIDITY PROBLEMS ON 
SHIPBOARD AND IN SUBMARINES 
Prior to the installation of air-conditioning ma- 
chinery in submarines, high temperature and 
humidity constituted important limiting factors in 
efficient performance of combat duty. The sub- 
marine is a weapon of aggressive warfare and its 
chief function is to deliver torpedoes to enemy 
targets in the most efficient manner. Thus it is 
imperative that only such equipment be installed 
on board a submarine which will contribute to the 
carrying out of its military mission. Therefore, pro- 
visions which increase the habitability of the sub- 
marine from the human point of view must be 
judged in the light of overall military efficiency. 
Without adequate air cooling and ventilation, 
habitability on an active war patrol may become 
so poor that material defects and decreased per- 
sonnel endurance may compromise the effectiveness 
of the ship. The relationship of excess heat and 
humidity in the conning tower to the efficiency of 
control parties during long approaches to an enemy 
target is very important. For discussions of heat and 
humidity problems on shipboard and in submarines, 
the reader should consult the references listed below. 
914. Chubb, W., and F. E. Smith. Air temperature 
measurements in H. M. S. Vanguard. Gt. Brit. MRG- 
RNPRC, CES. R. N. P. 48/447, C. E. S. 247, W. V. P. 
18, May 1948, 16 pp. 
915. Critchley, M. Problems of naval warfare under 
climatic extremes. Lecture II. Milit. Surg., 1946, 98: 221— 
233. Brit. med. ]., 1945, 2: 146-148. 
916. Eggleton, H. G. E., and J. Campbell. Nutrition 
in relation to tropicalization. Canada NRG. Proceedings 
of the 4th meeting of the associated committee on naval 
medical research. Project C4105, 16 February 1945, 1 p. 
917. Ellis, F. P. Effects of a tropical climate on men 
In warships. Brit. med. Bull., 1947/48, 5: 13-19. /. industr. 
Hyg., 30: abstract section: 54. 
918. Gray, J. A. B. and F. E. Smith. Prediction of 
thermal conditions in H. M. ships in tropical waters. 
Gt. Brit. MRG-RNPRC, CES. R. N. P. 49/524, C. E. S. 
286, W. V. P. 34, March 1949, 26 pp. 
919. Gt. Brit. MRC—RNPRC, HS. Note on the working 
conditions of personnel in the tropics with reference to 
the paper by the late torpedo officer, H. M. A. S. Shrop- 
shire (T.05922/45) R. N. P. 293/46, H. S. 140. 3 pp. 
920. Gt. Brit. MRC-RNPRC, HS. Memorandum on the 
effect of thermal environment on efficiency with special 
reference to the bridge plotting room. R. N. P. 332/46, 
H. S. 163, Received 24 February 1950, 5 pp. 
921. Pace, N., W. V. Consolazio, and A. R. Behnke. 
Physiological observations made in men aboard ship dur- 
ing a shakedown cruise in tropical waters. U. S. NMRI. 
Project X-205, Rept. no. 3, 13 August 1945, 7 pp. 
922. Schaefer, K. E. Man and environment in the sub- 
marine. The heat metabolism of the submarine, pp. 
B; 5—14 in; Monograph on submarine medicine, Folio I. 
Germany. U. S. Zone. Office of naval advisor. 1948. 
923. Schaefer, K. E,, and H. Hensel. The regulation 
of the blood circulation of man on submarines. The heat 
regulation aboard submarines, pp. G: 2-30 in: Mono- 
graph on submarine medicine, Folio 5, Germany. U. S. 
Zone. Office of naval advisor. 1948. 
924. Thomson, M. L. Heat illness in H. M. S. Queen 
Elizabeth in the Indian Ocean. Gt. Brit. MRG-RNPRC, 
HS. R. N. P. 46/345, H. S. 149, October 1946, 18 pp. 
925. U. S. Navy, Technical mission to Japan. Effects 
of submergence in tropics, p. 43 in: Aero, surface, and 
submarine medicine and research in the Japanese Navy, 
Fascile, M-l, Target M-06, 4 September 1945, 72 pp. 
926. Yaglou, C. P. and W. V, Consolazio, A study 
of mean skin temperature and comfort of a large group of 
naval personnel living in a simulated battleship berthing 
compartment. U. S. Navy. NMRI. Project X-205, Kept, 
no. 8, 2 September 1947. [P] 
C. PHYSIOLOGICAL EFFECTS OF RAISED 
TEMPERATURES 
The following three references are given as source 
material on the general physiological effects of heat: 
Machle and Hatch (980) 1947, Wakim (1024) 
1948, and Wezler (1025) 1950. The maintenance 
of a constant body temperature under conditions of 
raised temperature and humidity involves wide- 
spread functional adaptation throughout the body. 
These adjustments include an increase in skin tem- 
perature, increase in evaporation of sweat, and in- 
crease in cardiovascular and respiratory activity. 
High humidity diminishes or abolishes the body’s 
capacity to give off heat by evaporation. The skin 
temperature rises steadily with rising air tempera- 
ture, though at a gradually decreasing rate. This 
rise in skin temperature is affected by dilatation of 
cutaneous vessels, including the arteriovenous an- 
astomoses. As the body temperature rises, there is 
an increase in pulse rate, stroke and minute volumes 
of the heart, and cardiac work. The increase in 
heart rate is estimated at 10 beats for every degree 
Fahrenheit rise in body temperature. This, however, 
is extremely variable. Under some circumstances, 
there may be a decrease of stroke volume of the 
heart with increase in heart rate. The blood pres- 
sure may rise or there may be a fall in diastolic 
pressure with no change in systolic pressure. Skin 
vasodilatation may be due to the stimulation of 
axon reflexes in the skin, liberation of vasodilator 
metabolites, and warming of the blood to the hypo- 
thalamus-evoking vasodilatation of central nervous 
origin. It has been estimated that there is an increase 
in respiratory rate of 5 to 6 respirations per minute 
for every degree Fahrenheit rise of body tempera- 
ture. This varies widely in unacclimatized persons. 
Metabolic activity may increase during hyperther- 
mia and the respiratory volume increases. Overheat- 
ing may result in heat collapse, heat stroke, or heat 
cramps. In heat collapse, there may be no rise in 
body temperature and the symptoms are mainly SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
those of hemodynamic failure. There is pallor, poor 
venous return, and rapid heart action. The condi- 
tion is mainly reversible. In heat stroke there is ele- 
vation of body temperature and symptoms asso- 
ciated with organic changes, especially in the brain. 
Heat cramps are caused by loss of water and chlo- 
ride in blood and tissues, especially in the central 
nervous system. There are tonic and chronic spasms, 
mild tetany, and twitching, with elevated leukocyte 
count, hemoconcentration, reduced serum sodium 
and chloride levels. Death from heat can occur as 
soon as the changes resulting from overheating, 
especially those in the brain, become irreversible. 
For further studies on general physiological prob- 
lems of hypothermia, papers by the following are 
cited: Bedford, Mackworth, McArdle, and Weiner 
{932) 1948; Carpenter {938) 1948; Glickman, 
Inouye, Keeton, and Fahnestock {952) 1948; Gt. 
Brit. MRC-RNPRC, HS (957) 1946; Gt. Brit. 
MRC-RNPRG, CES (958) 1949; Floughten, Gut- 
berlet, and Ferderber {961) 1943; Humphreys, 
Imatis, and Gutberlet {962) 1946; Humphreys, 
Imatis, and Gutberlet {963) 1946; Imrie {964) 
1950; Marbarger and Taylor {984) 1946; McArdle, 
Dunham, Holling, Ladell, Scott, Thomson, and 
Weiner (989) 1947; Pace, Fisher, Birren, Pitts, 
White, Consolazio, and Pecora {1002) 1945; Shel- 
ley and Horvath {1018) 1946; Spealman {1019) 
1945; Taylor {1021) 1947; and Taylor and Mar- 
barger {1022) 1946. 
Generally speaking, hyperthermia increases the 
activity of sense organs, peripheral nerves, and the 
central nervous system. The pain threshold tem- 
perature of the human skin irradiated with strong 
infrared radiant heat was found to be 44.8° C. by 
Buettner {935) in 1951. Marechaux and Schafer 
(985) 1950 reported on the temperature sensitivity 
of different parts of the body tested in a climate 
chamber. With increasing temperature, the warm 
sense sets in, in characteristic sequence from the 
upper to the lower parts of the body. With decreas- 
ing temperature, it disappears in the reverse order, 
first in the feet and last in the forehead. Typical 
of the studies of the effect of temperature on nerve 
activity is a report by Engelhardt {946) 1951 on the 
effect of temperature changes on conduction ve- 
locity in the sciatic nerve of frog and cat. 
As Rothstein and Towbin {1014) 1947 have 
stated, one of the important functions of the circula- 
tory system is the transport of heat from within the 
body to the surface. The rate of heat transfer de- 
pends upon the rate of blood flow to the skin and the 
temperature gradient between the internal organs 
and the skin surface. In the cardiovascular response 
to heat, it is more efficient to maintain a given 
cardiac output with a slower pulse and a larger 
stroke volume than with a faster pulse and a smaller 
volume. Such a shift represents a slow adjustment 
to the task of increased cardiac output imposed by 
heat and may be an important factor in the accli- 
matization to heat, for in the unacclimatized subject 
the pulse rate increases considerably and it is likely 
that in some subjects the stroke volume diminishes. 
An outstanding response to hyperthermia may be 
dehydration with loss of fluid from the blood. This 
imposes an additional cardiovascular strain, addi- 
tive to the peripheral vasodilatation caused by heat. 
This is balanced to an unknown extent by constric- 
tion in other vascular areas. With increased loss of 
water, the concentration of red blood corpuscles 
per unit volume of blood increases as does the 
plasma protein concentration. There is an increase 
in blood viscosity and the heart expends more 
energy to pump a given amount of blood. Dehy- 
dration in the heat is accompanied by increase in 
pulse rate and rectal temperature. The stress of 
dehydration is partitioned between cardiac strain 
as evidenced by pulse-rate increase and a storage 
of heat as evidenced by increased rectal tempera- 
ture. Pulse-rate and rectal-temperature increases 
are good indicators of total circulatory strain, one 
of the limiting factors in man’s performance in heat. 
For further studies of the cardiovascular responses 
to heat, papers by the following should be consulted: 
Cooper and Kerslake {940) 1948; Glaser, Berridge, 
and Prior {951) 1950; MacPherson {981) 1946; 
MacPherson {982) 1946; Miller and Moor {993) 
1947; Roos, Weisiger, and Moritz {1013) 1947; 
and Scott {1017) 1945. 
Johnson {965) 1943 has shown that in subjects 
with normal, healthy cardiovascular systems the 
peripheral circulation is maintained or even in- 
creased in the presence of dehydration with hemo- 
concentration due to exposure to heat. Evidence 
exists that generalized vasodilatation in the periph- 
ery occurs in response to afferent nerve stimuli aris- 
ing in locally heated areas of the skin. Further evi- 
dence supporting this hypothesis has been obtained 
by Cooper and Kerslake {941) 1949 by heating the 
chest and abdominal skin under a radiant heat 
cradle. The hand blood flow increased, the rise 
commencing within 12 seconds of switching on the 
lights. The time of onset of this dilatation was inde- 
pendent of the resting hand blood flow and of the 
intensity of the illumination within wide limits. 
Heating the front of the legs caused a similar in- 
crease in hand blood flow with the same time rela- 
tions. This response was unaltered when the circula- 
tion to the legs was arrested. The peripheral 
vasodilatation was found to be associated with a fall HEAT AND HUMIDITY—PHYSIOLOGICAL EFFECTS 
in mouth and rectal temperatures. Mead and 
Schoenfeld (992) 1950 reported mean blood flow 
in the vasodilated finger of five individuals, seated 
in an uncomfortably warm environment, ranging 
from 115 cu. cm. to 142 cu. cm. per 100 cu. cm. of 
tissue per minute. In one subject further warmed 
in a bathtub, a mean value of 173 cu. cm. per 100 
cu. cm. of tissue per minute was obtained. In 
vasodilated fingers, both arterial and venous flow 
were shown to be markedly pulsatile in character. 
This character of the venous flow in the vasodilated 
finger is consistent with the flow through structures 
such as the arteriovenous shunts known to be pres- 
ent in the finger. In a report on the reactions of the 
peripheral circulation to external heat, Grayson 
(955) 1949 measured finger blood flows, forearm 
blood flows, and skin temperatures on healthy hu- 
man subjects under varying conditions of environ- 
mental temperature. Finger blood flows and fore- 
arm blood flows were estimated separately to 
distinguish between vascular reactions of skin and 
muscle. The response of the skin circulation to rising 
environmental temperature consisted of (1) an in- 
crease in skin blood flow as the environment warms 
to approximately 36° C.; (2) a decrease in skin 
flow as the environment rises in temperature from 
36° to 40° G.; and (3) an increase in blood flow 
as the environmental temperature rises above 
40° C. During the phases (1) and (2) the body 
temperature remained steady or fell and there was 
no change in muscle blood flow. During the phase 
(3) the body temperature rose and there was an 
increase in forearm blood flow with the onset of 
perspiration. The vasoconstriction occurring in the 
skin when the environmental temperature rose 
above 36° C. was regarded as a possible tempera- 
ture regulating mechanism. The author stated that 
forearm blood flows do not respond to environ- 
mental temperature increases until the body tem- 
perature has begun to rise. Barcroft, Bonnar, and 
Edholm {930) 1948 made observations on blood 
flow in human subjects on normal forearms, sympa- 
thectomized forearms, on forearms with the skin 
flushed by mustard, and on those with the skin 
blanched with adrenalin. Body heating by putting 
both feet in hot water for a maximum of 50 min- 
utes increased the blood flow in the forearm from 
3.1 to 9.3 cu. cm. per 100 cu. cm. of forearm per 
minute. Since the effect was absent in sympathecto- 
mized forearms, the vascular reflex was held to 
have been mediated by the sympathetic nerves. 
Flushing of the forearm skin produced by mustard 
increased the forearm blood flow to the same extent 
as body warming. Since, however, in these experi- 
ments, the body warming did not flush the skin it 
was likely that the heat vasodilatation was for the 
most part deep to the skin. Body warming increased 
the blood flow in the forearm when the skin blood 
vessels were intensely constricted by adrenalin. It 
was concluded that the dilatation was for the most 
part deep in the skin, most probably in the 
skeletal muscle. 
The effect of thermal stimuli on the circulation in 
the human colon has been studied by Grayson (556) 
1949. The subject was a patient with a colostomy 
performed about 9 months previously. Needle ther- 
mocouples, inserted into a small knuckle of bowel 
exposed on the surface of the abdomen, recorded 
temperature changes in response to general body 
heating and to thermal stimuli applied to the ab- 
dominal wall near the colostomy. Skin-temperature 
changes from an index finger were recorded for 
purposes of comparison. A cold, ether-soaked pad 
applied to the abdomen produced a marked rise in 
colonic tissue temperature, whereas a hot pad pro- 
duced a definite fall. These responses were abolished 
by the surface application of novocaine to the colos- 
tomy. Gold applied to the colostomy itself was found 
to produce a generalized vasodilatation throughout 
the exposed tissue. Generalized body heating causes 
a vasoconstrictor response in the colon during the 
early stages of body heating followed by a vasodila- 
tor response after prolonged body heating. The 
vasoconstrictor phase in the colon accompanies an 
increase in cutaneous blood flow, whereas the vaso- 
dilator phase appears only after the rectal tempera- 
ture has risen. 
For further studies on vasomotor response to heat, 
papers by Ebaugh and Thauer {944) 1950 and 
Leusen and Demeester (979) 1951 may be 
consulted. 
For a discussion of temperature extremes and 
water and salt lacks, a chapter by Bartley and Chute 
{931) 1947 may be consulted. Three papers on 
water and salt depletion which appeared in 1947 by 
Marriott {986, 987 and 988) constitute a very com- 
plete discussion of the subject. As Brown and Tow- 
bin {933) 1947 have stated, a water deficit of 3 
percent of body weight or an air temperature of 
24° F. above average skin temperature increases 
man’s circulatory strain as much as does work which 
involves energy expenditure of twice the basal rate. 
The maximal rate of energy expenditure which man 
can endure depends directly on the air temperature 
and upon his body-water content. A working rate 
which is comfortable for a man in water balance 
becomes intolerable when he has attained sufficient 
dehydration. An increase of 10° F. air temperature 
is stated by the authors to increase man’s circulatory SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
strain as much as an energy expenditure of 29 cal- 
ories per square meter of body surface per hour. 
A dehydration of 1 percent of body weight increases 
circulatory strain as much as an energy expenditure 
of 24 calories per square meter of body surface per 
hour and an exposure to a temperature of 110° F. 
necessitates a 25 percent reduction in his working 
rate. A body-water deficit of 2.5 percent requires 
the same reduction of work output. According to 
Adolph {928) 1947, men who lose 1 to 11 percent 
of their body weight by rapid sweating in simulated 
desert conditions show a loss in volume of circulat- 
ing plasma. As measured by the method of dye 
dilution, the plasma volume diminishes 2.5 times as 
much as does an equal volume of the whole body. 
This decrease of plasma volume is paralleled by an 
increase in total serum concentration. For a further 
report on water loss in human subjects due to in- 
creased temperature, a paper by Brumsteyn {934) 
1950 may be consulted. Papers by McLean, Moritz, 
and Rods {991) 1947 and Pincus and Elmadjian 
{1003) 1946 contain data on blood changes caused 
by cutaneous exposure to excessive heat and the 
lymphocyte response to heat stress in normal and 
psychotic subjects. Changes in blood gas equilibria 
resulting from exposure to hypothermia have been 
reported by Gordon, Darling, and Shea {953) 1949. 
Exposure to elevated temperatures affects the 
gastric emptying time in both animals and men. 
Cordier and Piery {942) 1950 found that in male 
albino rats fasting 48 hours an increase of environ- 
mental temperature from 18° to 45° C. reduced the 
rate of passage through the stomach and delayed 
gastric emptying by an amount proportional to the 
temperature increase. Increase of external tempera- 
ture from 18° to 40° C. did not appreciably affect 
the rate of absorption of glucose in the same ani- 
mals. In 17 normal young men the gastric empyting 
times were observed at rest at environmental tem- 
peratures of 77° and 120° F. by Henschel, Taylor, 
and Keys {960) 1943. In all but one of the subjects 
the gastric emptying time was faster at the higher 
temperatures. Twelve of the subjects showed an 
average decrease of 30 percent in gastric emptying 
time when the temperature was 120° F. Observa- 
tions carried out on about 100 normal men during 
hard work at 120° F. failed to indicate any lack 
of appetite or any sign of decreased activity, except 
in actual heat exhaustion. Regarding food intake 
by healthy, physically fit soldiers in desert and jungle 
areas, Johnson and Kark {966) 1947 found that 
personnel tended to choose a diet with a lower 
caloric value at an environmental temperature of 
92° F. This is contrasted to higher caloric diets 
chosen by personnel in Arctic environments as low 
as —30° F. The authors stated that the caloric 
expenditure for a given task is greater in cold than 
in warm climate because of the hobbling effect of 
Arctic clothing and equipment. Also more heat is 
required in cold than in warm environments to 
maintain thermal equilibrium. The percent of pro- 
tein chosen is approximately the same in all en- 
vironmental conditions. According to Kark, Aiton, 
Pease, Bean, Henderson, Johnson, and Richardson 
(969) 1947, the most important considerations in 
troop feeding are variety of the food items, simi- 
larity to those the soldier usually eats in ordinary 
life, avoidance of caloric deficits, and high accept- 
ability insured by good food preparation. Tables of 
representative values of foods commonly used in 
tropical countries have been prepared by Platt 
{1005) 1945. 
From an experimental study of the effect of 
nutrition upon the reactions of animals to heat, 
Robinson and Lee (1008) 1947 concluded that the 
caloric value of the diet has a significant and at 
times practically important effect on the reactions 
of animals to hot conditions. However, the propor- 
tion of protein in the diet is not significant. Mitchell 
and Edman {994) 1951 have called attention to 
the conclusion from animal experiments that in 
hot environments the requirement for thiamin is 
markedly increased, while the riboflavin require- 
ment is decreased. The requirement for ascorbic 
acid may be increased if the body temperature is 
raised. These authors have pointed out that animal 
experiments constitute an insecure guide to human 
needs. Direct and field observations on human sub- 
jects show that the energy requirements are de- 
creased in hot climates due to diminished basal 
expenditure of energy or greater efficiency in certain 
types of muscular work, lighter clothing, lessened 
capacity or motivation for work. The water require- 
ments are increased with sweating and in proportion 
to the amount of sweat, whereas the daily water 
requirement in temperate climate may be 2*/a to 3 
liters. This will increase to 13 liters or more in a 
hot environment. Water losses must be covered by 
water intake at frequent intervals and thirst is not 
an adequate guide to water requirement. The salt 
requirement may be increased from a daily intake 
of 2 to 5 grams up to 15 to 17 grams under profuse 
sweating. This large increase in salt requirement is 
stated by the authors to be confined to the period 
of acclimatization. The authors believed that in 
acclimatizated individuals the salt replacement 
provided in food at meals is adequate. They con- 
sider that salt tablets are unnecessary except in 
unusual situations prior to acclimatization. There 
is no statistical evidence that men voluntarily select HEAT AND HUMIDITY—PHYSIOLOGICAL EFFECTS 
low-protein diets in hot climates and the authors 
consider that there is no benefit to body heat econ- 
omy from a low-protein diet. The protein require- 
ment may actually be increased slightly in the 
tropics. The vitamin requirements are stated not 
to be appreciably increased by residence or work 
in tropical climates. In hot environments, the re- 
quirement for iron and perhaps calcium is in- 
creased. The authors feel that attempts to increase 
tolerance or accelerate acclimatization by dietary 
modifications have not been as extensive as the im- 
portance of this problem warrants. In provision of 
rations for troops in the tropics, they stress the 
importance of a considerable variety of foods, items 
which the soldiers are accustomed to in ordinary 
life, but with emphasis on those of high biological 
value. A proper packaging and storing is important 
in preserving nutritional factors, particularly the 
vitamins. 
Pertinent to problems of nutrition and water in- 
take in man in environments at high temperatures 
is the question of thirst. Adolph and Wills (929) 
1947 have reviewed the current theories about the 
mechanisms of thirstiness. They found that increas- 
ing saliva flow did not give to the dehydrated man 
a sense that he had drunk water, nor did reducing 
his feeling of fatigue allow him to behave as if he 
had a normal body-water content. The authors con- 
cluded that, in practice, theories regarding thirst 
have proven useless. New theories are required. 
These must be so specific that they will show us how 
to cheat the body and so relieve some of the mental 
and physical distresses of thirst. They concluded 
that measures other than taking in water were not 
successful in improving the state of the dehydrated 
man, nor in relieving the urge to drink water. There 
is really no known substitute for water. 
There is an extensive amount of literature on 
water balance and sweating under conditions of 
high temperature, with or without elevated humid- 
ity. A representative study is that carried out by 
Nelson and Bean (997) 1942. Using 56 enlisted 
men living in a hot room of the laboratory, tem- 
peratures were maintained at 120° F. during the 
day and at 90° F. at night. Daily water require- 
ments were found to be contingent upon the en- 
vironmental temperature and the severity of physi- 
cal work. Water requirements, therefore, varied with 
the duties of the troops and the environment. In a 
hot climate, man dissipates the greater proportion of 
his heat by evaporation of sweat. Failure to supply 
sufficient water to make up for the loss in sweating 
results in depletion of body water. If continued, this 
leads to progressive loss in weight, physical dete- 
rioration, and reduced efficiency and capacity for 
work, and greatly impairs morale and motivation. 
Reduction of water consumption to levels below that 
required to maintain water balance will be followed 
by incapacitation, whether the reduction is gradual 
or abrupt. Schedules which require that a man dis- 
regard thirst and drink only at mealtimes results in 
no saving of water and may cause discomfort and 
reduced physical importance. Thirst is stated by the 
authors to be an inadequate indicator of rapid tissue 
dehydration at high rates of sweating which accom- 
pany even moderate work in heat. At high tempera- 
tures men will consistently drink less water than 
they are losing in sweat. Augmenting the water in- 
take so as to balance the fluid lost in the sweat will 
increase the amount of work which can be done and 
reduce injurious effects. It has been found that the 
daily water requirement is not significantly changed 
as men become acclimatized to heat. Regarding salt 
requirements, the authors have stated that the re- 
quirement for salt is in direct proportion to the 
amount of water taken. With exposure to heat, the 
need for extra salt is greater during the early drop 
than after acclimatization is established. The au- 
thors recommended that for light work 4 quarts of 
fluid per day be taken at 95° F., 6 quarts per day 
at 105° F., and 10 quarts at 115° F. For moderate 
work, the requirements are 5 quarts a day at 95° F., 
7 quarts at 105° F., and 11 quarts at higher temper- 
atures. For strenuous work, 7, 9, and 13 quarts are 
required for the respective temperatures. In a study 
on human subjects by Mitchell, Hamilton, and 
Shields (995) 1943, 4 men were subjected to 24 
consecutive weeks of observation. Two conditions 
were studied: (1) 112° F. with 20 percent humidity, 
and (2) 100° to 102° F. with 76 percent humidity. 
The authors concluded that sweating under hot, 
moist conditions is much more profuse and much 
more variable than under hot, dry conditions and is 
associated with a much greater increment in rectal 
temperature. The sweat under the humid condi- 
tions, besides being more profuse, has a higher con- 
centration of salt than the sweat excreted under the 
dry conditions. A man may lose an equivalent of 23 
grams of salt daily under hot, moist conditions and 
only 5.25 grams under hot, dry conditions. Sweat 
produced under muscular activity conditions is also 
more concentrated than that produced during re- 
pose. The rate of sweating is greatly increased by 
even a moderate degree of muscular work. Ascorbic 
acid is not secreted in appreciable concentrations in 
human sweat, even when the tissues and fluids of 
the body are physiologically saturated with vita- 
mins. The loss of thiamin in sweat is minimal under SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
all conditions of activity and environment, averag- 
ing only 0.2 microgram per hour. The average losses 
of nicotinic acid and riboflavin in sweat vary from 
7 to 29 micrograms per hour and 0.9 to 6.6 micro- 
grams per hour, respectively, and parallels the rate 
of sweating. Under conditions of excessive sweating 
of 1 liter per hour, the sweat may contain consider- 
able quantities of thiamin, riboflavin, nicotinic acid, 
iron, and calcium. For further studies on the physi- 
ology of sweat formation, papers by the following 
authors may be consulted: Adolph (927) 1947, 
Burch {936) 1948, and Ladell {976) 1947-48. For 
studies on the rate of sweating, the following refer- 
ences are useful: Gerking and Robinson {948) 
1946; Gosselin {954) 1947; MacPherson and Lee 
{983) 1948; Randall and McClure {1007) 1949; 
Robinson {1009) 1947 and {1010) 1949; Sato, 
Kikuta, and Hisao {1016) 1950; and Thomson 
{1023) 1948. 
A number of studies are available on salt concen- 
tration of sweat and factors influencing chloride 
excretion in sweat. Johnson, Pitts, and Consolazio 
(967) 1944 reported that in adequately nourished 
men under hot conditions the chloride in sweat 
increases as work is prolonged. There are definite 
individual differences, and the sweat chloride is 
decreased by drinking water during work. It is still 
further decreased by administration of an equal 
volume of saline instead of water. It increases as the 
rate of sweating increases. It is independent of 
acclimatization and increases with increasing body 
temperature. It also increases with local skin tem- 
perature and is independent, within limits con- 
sidered normal, of the plasma protein and plasma 
chloride. Ladell (975) 1945 stated that there was a 
great variation in chloride concentration of sweat 
in the same subject and in different subjects. The 
chloride concentration of the sweat was stated to 
increase with the duration of sweating and with the 
rate of sweating. The sweat, however, was always 
hypotonic. With salt deficiency, the chloride con- 
centration of sweat was reduced. In 1948, Ladell 
{978) measured the chloride content of whole body 
sweat as well as the chloride concentration of sweat 
samples obtained from an arm totally enclosed in a 
bag. These latter values were found to be the same 
as for whole body sweat. This did not indicate to 
the author that the chloride concentration in sweat 
is the same for all parts of the body. Johnston, 
Conn, Louis, and Steele {968) 1946 found that in 
men, fully acclimatized to heat and working suffi- 
ciently hard to produce 5 to 10 liters of sweat in 24 
hours, reasonably accurate balance studies for chlo- 
ride can be made when the averages of the daily 
concentration of salt in the hand sweat is used to 
represent the concentration in the total body sweat 
for the period. Given sufficient chloride in the diet 
to insure chloride equilibrium under these condi- 
tions, the authors predicted the average concentra- 
tion of chloride in body sweat for the period studied 
by applying the following formula: Total chloride 
intake minus total urinary chloride, divided by total 
sweat volume, equals average concentration of 
chloride in body sweat. When the predicted value 
for concentration of chloride in all of the body 
sweat produced in the period was compared with 
the determined value, good agreement was ob- 
tained. For further studies on the pattern of chloride 
excretion, papers by Robinson, Gerking, Turrell, 
and Kincaid {1012) 1950 and Kenney and Miller 
(972) 1949 may be consulted. 
Ladell (977) 1947 has carried out studies on 
creatinine losses in the sweat during work in hot, 
humid environments. These tests were conducted on 
4 young men fully acclimatized to work under the 
environmental conditions of the experiment. Each 
exposure lasted for 160 minutes in an air-condi- 
tioned chamber kept at a dry bulb temperature of 
100° F. (wet bulb, 93° F.) ; the relative humidity 
was 77 percent, the air movement was below 50 
feet per minute. The subjects were completely nude, 
except for a bag completely covering one arm in 
which the sweat was collected. Whereas the 
creatinine content of both saliva and blood increased 
threefold after an oral dose of 5 grams of creatinine, 
there was only a slight increase in the creatinine 
content of the sweat. The sweat creatinine appears 
to be more closely linked with the rate of sweating 
than with the level of creatinine in the blood. Sta- 
tistically, the author found a good correlation be- 
tween the reciprocal of the sweating rate and the 
sweat creatinine. This relationship between creati- 
nine content and sweating rate is the opposite of 
that observed for chloride concentration in sweat. 
It has been reported that the greater the sweating 
rate the more nearly does the chloride content of 
sweat approach that of plasma. It would appear to 
the author that there are at least two mechanisms 
involved in the production of sweat from the body 
fluids. Some similarity between the mechanisms of 
sweat formation and urine formation has been sug- 
gested, but the fact that the creatinine content of 
sweat is little affected by that of blood, whereas the 
urinary creatinine is greatly affected by blood 
creatinine concentration, indicates that the mode 
of production of the two fluids must be very 
different. 
For further studies on sweating and water bal- 
ance, papers by the following may be consulted; 
Molnar, Towbin, Gosselin, Brown, and Adolph HEAT AND HUMIDITY—PHYSIOLOGICAL EFFECTS 
927-932 
(996) 1946; Chin {939) 1950; Sato, Fukuyama, 
Sakai, Naito, Katayama {1015) 1950; Kawahata 
(970 and 971) 1950; and Kuroda (973 and 974) 
1947. 
From a large source of literature on temperature 
regulation and thermal balance under hot condi- 
tions, papers by the following authors have been 
selected: Friedrich {947) 1948; Glaser {949) 1949; 
Glaser (959) 1949; McCutchan and Taylor (999) 
1950; Nelson, Eichna, Horvath, and Shelley {998) 
1946; Nelson, Eichna, Horvath, Shelley, and Hatch 
(999) 1947; Nelson, Shelley, Horvath, Eichna, and 
Hatch {1000) 1948; Robinson and Gerking {1011) 
1947; and Woodcock, Pratt, and Breckenridge 
{1027) 1952. 
For a study of heat production and energy re- 
quirements of tropical people, a paper by Cullum- 
bine {943) 1950 should be consulted. In these 
studies the basal heat production of 225 Ceylonese, 
males and females of various ages, was determined. 
The response of the endocrine glands to heat 
stress is a matter of importance and one which has 
been subjected to much experimental investigation. 
One such study is that carried out by Stein, Bader, 
Eliot, and Bass {1020) 1948. Three healthy, white 
males were exposed successively, after a preliminary 
2 weeks period of physical conditioning, to nineteen, 
five, and one 15-minute period of heat at a dry 
bulb temperature of 107° F. (wet bulb, 89° F.). 
They were then subjected to fourteen 5-hour 
periods of cold at 20° F. and following this to five 
reexposures to heat, and then to a 5-week interval 
of no exposure to environmental stress or rigorous 
exercise. Finally, there were three reexposures to 
heat. Measurements were made of the circulating 
eosinophile count, the absolute lymphocyte count, 
the urinary uric acid-creatinine ratio, the 24-hour 
17-ketosteroid excretion, and the effects of admin- 
istration of ACTH to evaluate adrenal cortical 
responses. Basal metabolic rates were studied as an 
indication of thyroid activity. The number of cir- 
culating eosinophiles was significantly reduced in 
daily counts during exercise, a combination of heat 
and exercise, and a combination of cold and exer- 
cise as compared to a baseline period without stress. 
There was no significant difference in the excretion 
of 17-ketosteroids in any of the experimental 
periods. This was also true of the daily urinary 
uric acid-creatinine ratio, and the absolute lympho- 
cyte count. Administration of ACTH for the assess- 
ment of adrenal cortical function yielded the same 
pattern of response after heat and cold stress as 
after control experiments. This indicated to the 
authors that this method is not sufficiently sensitive 
for this type of study. There was no significant 
change in the basal metabolic rate throughout the 
experimental period in any of the subjects. 
It is well known that high temperatures depress 
or inhibit spermatogenesis in the testes. An experi- 
mental study reported in 1950 by Elfving and 
Turpeinen {945) reveals that immersion of the 
scrotum of rats in water at 40.4° C. for 3 hours has 
no effect upon the production of spermatozoa. Tem- 
porary sterility is produced by immersion at this 
temperature for 5 to 8 hours. Immersion at 42.4° 
C. for 30 minutes produces temporary sterility and 
for 45 minutes produces permanent sterility. The 
animals tolerated a temperature of 46.3° C. for 
5 minutes with no effect, while exposure for 8 min- 
utes produced temporary sterility and exposure for 
15 minutes resulted in permanent sterility. The 
effects of the heat treatment on the testicular hor- 
mone production were also studied using the weight 
of the seminal vesicles as an indicator for the pres- 
ence of androgens. A 20-minute exposure to 44.3° 
C. had no appreciable effect on the vesicle weight. 
After an exposure to 46.3° C. for 20 minutes, a 
definite fall in the weight of the seminal vesicles 
was found 1 week after treatment. The vesicles, 
however, recovered rapidly and 1 week later had 
almost returned to their normal weight. It is evi- 
dent from these studies that the endocrine function 
of the testis is considerably more heat resistant than 
is spermatogenesis. 
Regarding the effects of environmental heat 
stress on renal functions, a paper by Radigan and 
Robinson {1006) 1949 may be consulted. 
927. Adolph, E. F. Heat exchanges, sweat formation, 
and water turnover, pp. 33-43 in: Physiology of man in 
the desert. Edited by E. F. Adolph and Associates. New 
York & London, Interscience Publishers, Inc., 1947, 
357 pp. 
928. Adolph, E. F. Blood changes in dehydration, pp. 
160—171 in: Physiology of man in the desert. Edited by 
E. F. Adolph and Associates. New York, Interscience 
Publishers, Inc., 1947, 357 pp. [P] 
929. Adolph, E. F. and J. H. Wills. Thirst, pp. 241-253 
in: Physiology of man in the desert. Edited by E. F. 
Adolph and Associates. New York, Interscience Publish- 
ers, Inc., 1947, 357 pp. [P] 
930. Barcroft, H., W. M. Bonnar, and 0. G. Edholm. 
Reflex vasodilatation in human skeletal muscle in response 
to heating the body. /. Physiol., 1947, 106: 271—278. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1948, 1: 650. Abstr. 
931. Bartley, S, H. and E. Chute. Temperature ex- 
tremes and water and salt lacks, pp. 99-134 in: Fatigue 
and impairment in man. New York, McGraw-Hill Book 
Co., Inc., 1947, 429 pp. [R] 
932. Bedford, T., N. H. Mackworth, B. McArdle, and 
J. S. Weiner, Further research required into the effects of 
heat on human reactions. Gt. Brit. MRC—RNPRC, HS. 
R. N. P. 48/428, H. S. 224, undated, 3 pp. 933-969 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
933. Brown, A. H, and E. J. Towbin. Relative influences 
of heat, work, and dehydration on blood circulation, pp. 
197—207 in: Physiology of man in the desert. Edited by 
E. F. Adolph and Associates. New York, Interscience Pub- 
lishers, Inc., 1947, 357 pp. [P] 
934. Brumsteyn, V. [Water loss in man during rest at 
different air temperatures.] Gigiena Truda, 1950, 15 {12): 
12-18. [P] 
935. Buettner, K. Effects of extreme heat on man. III. 
Surface temperature, pain, and heat conductivity of living 
skin in experiments with radiant heat. USAF. Randolph 
Field, Tex. School of aviation medicine. Project 21-26- 
002, Rept. no. 3, November 1951, 9 pp. 
936. Burch, G. E. Environmental conditions which 
initiate sweating in resting man. Proc. Soc. exp. Biol., 
N. Y„ 1948,67; 521-523. [P] 
937. Caplan, A. Observations on the effects of high en- 
vironmental temperatures in underground workers on the 
Kolar gold field. Fourth empire mining and metallurgical 
congress. Great Britain, 1949, London, Congress Salisbury 
House, 1949, 15 pp. [P] 
938. Carpenter, A. Comments on the use of combined 
estimates of the effect of hot climates on human beings. 
Gt. Brit. MRC-RNPRC, CES. R. N. P. 48/456, C. E. S. 
252, June 1948, 2 pp. 
939. Chin, T. Studies on water metabolism in the tropics. 
Hukuoka Acta med., 1950, 41 {11): 73—75. (English text 
pagination.) (In Japanese with English summary.) 
940. Cooper, K. E. and D. M. Kerslake. Changes in 
pulse rate during exposure of the skin to radiant energy. 
/. Physiol, 1948, 107: 42 P. [P] 
941. Cooper, K. E. and D. M. Kerslake. Vaso-dilatation 
in response to heating the skin. J. Physiol, 1949, 108: 
40P-41P. Abstr. [P] 
942. Cordier, D. and Y. Fiery, Influence des tempera- 
tures exterieures elevees sur la vitesse du transit gasterique 
et 1’absorption intestinale des solutions de glucose chez 
le rat. C. R. Soc. Biol, Paris, 1950, 144: 129-131. [P] 
943. Cullumbine, H. Heat production and energy re- 
quirements of tropical people. /. appl. Physiol, 1950, 
2: 640-653. 
944. Ebaugh, F. G., Jr., and R. Thauer. Influence of 
various environmental temperatures on the cold and 
warmth thresholds. /. appl. Physiol, 1950, 5; 173-182. 
[P] 
945. Elfving, G. and 0. Turpeinen. Effect of heat on 
the physiology of the testis. XVIII Intern, physiol. Congr., 
1950, 187. 
946. Engelhardt, A. Die Temperaturabhangigkeit der 
Erregungleitungsgeschwindigkeit im Kalt-und Warmblu- 
ternerven. Z. vergl. Physiol, 1951, 33: 125-128. Excerpta 
Medica, Section II. (Physiology, Biochemistry, and Phar- 
macology), 1951,4; 1148. 
947. Friedrich, H. Ertraglichkeitsgrenze fur wechselnde 
Raumtemperatur und -feuchte bei Ruhe und Arbeit. 
Pfliig. Arch. ges. Physiol, 1948, 250: 182-191. [P] 
948. Gerking, S. D. and S. Robinson. Decline in the 
rates of sweating of men working in severe heat. Amer. J. 
Physiol, 1946, 147: 370-378. [P] 
949. Glaser, E. M. The effects of cooling and of various 
means of warming on the skin and body temperature of 
men. J. Physiol, 1949, 109: 366-379. [P] 
950. Glaser, E, M, The effects of cooling and warming 
on the vital capacity, forearm and hand volume, and skin 
temperature of man. /. Physiol, 1949, 109: 421-429. [P] 
951. Glaser, E. M., F. R. Berridge, and K. M. Prior. 
Effects of heat and cold on the distribution of blood 
within the human body. Radiological investigations of the 
liver, lungs, and heart. Clin. Sci., 1950, 9: 181-186. 
952. (Hickman, N., T. Inouye, R. W. Keeton, and M. K. 
Fahnestock. Comparison of physiological adjustments of 
human beings during summer and winter. Trans. Amer. 
Soc. Heat. Vent. Engrs., 1948, 54: 307-319. [P] 
953. Gordon, E. E., R. C. Darling, and E. Shea. Effects 
of physical hyperthermia upon blood gas equilibria in man. 
/. appl. Physiol., 1949, 1: 496-510. [P] 
954. Gosselin, R. E. Rates of sweating in the desert. 
Appendix 4-B: Relation between rates of sweating and 
air temperature, pp. 69-72 in: Physiology of man in the 
desert. Edited by E. F. Adolph and Associates. New York, 
Interscience Publishers, Inc., 1947, 357 pp. [P] 
955. Grayson, J. Reactions of the peripheral circulation 
to external heat. /. Physiol., 1949, 109: 53-63. [P] 
956. Grayson, J. The effect of thermal stimuli on the 
circulation in the human colon. /. Physiol., 1949, 108: 
47P-48P. Abstr. 
957. 6t. Brit. MRC-RNPRC, HS. Environmental 
warmth and its measurement. R. N. P. 294/46, H. S. 134, 
1946, 10 pp. 
958. Gt. Brit. MRC-RNPRC, CES. Half-yearly report to 
31-12-48. R. N. P. 49/540, C. E. S. 294, July 1949, 12 pp. 
959. Henriques, F. C. and A. R. Moritz. Studies on 
thermal injury. I. The conduction of heat to and through 
skin and the temperatures attained therein. A theoretical 
and an experimental investigation. Amer. J. Path., 1947, 
23: 531-549. [P] 
960. Henschel, A., H. L. Taylor, and A. Keys. The 
gastric emptying time of man at high and normal environ- 
mental temperatures. U. S. OSRD-NDRC, O. E. M. cmr 
220, Medical nutrition report no. 5, 16 November 1943, 
1 p. Abstr. [P] 
961. Honghten, F. C., C. Gutberlet, and M. B, Ferder- 
ber. Physiological reactions applicable to workers in hot 
industries. Trans. Amer. Soc. Heat. Vent. Engrs., 1943, 
49: 188-194. [P] 
962. Humphreys, C, M., 0. Imalis, and C. Gutberlet. 
Physiological response of subjects exposed to high effective 
temperatures and elevated mean radiant temperatures. /. 
industr. Hyg., 1946, 28: abstract section: 124. 
963. Humphreys, C. M., 0. Imalis, and C. Gutberlet. 
Physiological response of subjects exposed to high effective 
temperatures and elevated mean radiant temperatures. 
Trans. Amer. Soc. Heat. Vent. Engrs., 1946, 52: 153-164. 
[P] 
964. Imrie, A. H. Physiological effects of heat. 
Physiother., 1950,56: 109-112. 
965. Johnson, C, A. Effects of heat and exercise associ- 
ated with dehydration on the peripheral circulation. 
USAF, Wright-Patterson air force base, Dayton, Ohio. 
Aero medical laboratory, Serial no. ENG-49-698-17, 28 
September 1943, 14 pp. [P] 
966. Johnson, R. E. and R. M. Kark. Environment and 
food intake in man. Science, 1947, 105: 378-379. [P] 
967. Johnson, R. E., J. C. Pitts, and F. C. Consolazio. 
Factors influencing chloride concentration in human sweat. 
U. S. OSRD-NDRC, O. E. M. cmr 328, 25 January 1944, 
15 pp. [P] 
968. Johnston, M. W., J. W. Conn, L. H. Louis, and 
B, F. Steele. Hand sweat values in the calculation of 
chloride and nitrogen balance under conditions of hard 
work in humid heat. Fed. Proc. Amer. Soc. exp. Biol., 
1946, 5: 234. 
969. Kark, R. M., H. F. Aiton, E. D. Pease, W. B, Bean, 
C. R. Henderson, R. E. Johnson, and L. M. Richardson. HEAT AND HUMIDITY—PHYSIOLOGICAL EFFECTS 
970-1003 
Tropical deterioration and nutrition. Clinical and bio- 
chemical observations on troops. Medicine, Baltimore, 
1947, 26: 1-40. 
970. Kawahata, A. Studies on the function of human 
sweat organs. (Report I.) /. Mie med. Coll., 1950, 1: 
25-41. 
971. Kawahata, A. Studies on the function of human 
sweat organs (Report II.) /. Mie med. Coll., 1950, 1: 
123-134. 
972. Kenney, R. A. and D. H. Miller. The effect of 
environmental temperature on water output and the 
pattern of chloride excretion. Acta med. scand., 1949, 
135: 87-90. [P] 
973. Kuroda, K. [Hydremia seen in laborers working in 
high temperatures.] Igaku & seibutugaku, 1947, 10: 
67—69. (In Japanese), (English text pagination). [P] 
974. Kuroda, K. [The cause of hydraemia of the persons 
engaging in work under high temperatures.] Igaku & 
seibutugaku, 1947, 10: 126-130. (In Japanese), (English 
text pagination). [P] 
975. Ladell, W. S. S. Thermal sweating. Brit. med. Bull., 
1945, 3: 175-179. 
976. Ladell, W. S. S. Effects on man of high tempera- 
tures with special reference to the work of the heat physi- 
ology team at the national hospital. Brit. med. Bull., 
1947/48, 5; 5-8. J. industr. Hyg., 1948, 30: abstract 
section: 53. [P] 
977. Ladell, W. S. S, Creatinine losses in the sweat 
during work in hot humid environments. J. Physiol., 1947, 
106: 237-244. 
978. Ladell, W. S. S. The measurement of chloride losses 
in the sweat. J. Physiol., 1948,107: 465-471. Abstr. World 
Med., 1950, 7; 7. [P] 
979. Leusen, I. and G. Demeester, Influence de la 
temperature sur les centres vasomoteurs. Arch. int. 
Physiol, 1951, 59: 40-48. [P] 
980. Machle, W. and T. F. Hatch. Heat: man’s ex- 
changes and physiological responses. Physiol. Rev., 1947, 
27: 200-227. [R] 
981. MacPherson, R. K. The effect of exposure to a 
humid tropical climate on circulatory responses to postural 
change. Australia, NHMRC, Fatigue laboratory. Rept. 
no. 6, 15 January 1946, 9 pp. [P] 
982. MacPherson, R. K. The effect of exposure to humid 
tropical climates on the resting pulse rate and arterial 
blood pressures. Australia, NHMRC, Fatigue laboratory. 
Rept. no. 7, 1 March 1946, 5 pp. [P] 
983. MacPherson, R. K. and D. H. K. Lee. Variations 
in human reactions to hot atmospheres as functions of 
temperature and humidity. Australia, NHMRC, Commit- 
tee on flying personnel research. Rept. no. FR133, no. 5, 
7 February 1948, 8 pp. 
984. Marbarger, J. P. and C. L. Taylor. The effect of 
air movement on human response to heat and humidity. 
Fed. Proc. Amer. Soc. exp. Biol., 1946, 5: 70-71. 
985. Marechaux, E. W., and K. E. Schafer. t)ber 
Temperaturembfindungen bei Einwirkung von Tempera- 
turreizen verschiedener Steilheit auf den ganzen Korper. 
Pfliig. Arch. ges. Physiol, 1949, 251: 765-784. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and Phar- 
macology), 1950, 3: 1663. 
986. Marriott, H. L. Water and salt depletion. Brit, 
med. ]., 1947, 1: 245-250. 
987. Marriott, H. L. Water and salt depletion. Part II. 
Brit. med. J., 1947, 1: 285-290. 
988. Marriott, H. L. Water and salt depletion. Conclu- 
sion. Brit. med. J., 1947, 1: 328-332. 
989. McArdle, B., W. Dunham, H. E. Holling, W. S. S. 
ladell, J. W. Scott, M. L. Thomson, and J. S. Weiner. 
The prediction of the physiological effects of warm and 
hot environments. Gt. Brit. RNPRC, HS. R. N. P. 47/391 
H. S. 194, October 1947, 21 pp. [P] 
990. McCutchan, J. W. and C. L. Taylor. Respiratory 
heat exchange with varying temperature and humidity of 
inspired air. USAF. Wright-Patterson air force base. Day- 
ton, Ohio. Air materiel command. AF Technical Kept. no. 
6023, October 1950, 38 pp. [P] 
991. McLean, R., A. R. Moritz, and A. Roos. Studies of 
thermal injury. VI. Hyperpotassemia caused by cutaneous 
exposure to excessive heat. /. din. Invest., 1947, 26: 
497-504. 
992. Mead, J. and R. C. Schoenfeld. The character of 
blood flow in the vasodilated finger. U. S. Army. Office 
Quartermaster General, Lawrence, Mass. Climatic research 
laboratory, Environmental protection section. Kept. no. 
161, 24 February 1950, 13 pp. [P] 
993. Miller, V. J. and E. B. Moor. Acute effects of a 
hot saturated atmosphere upon the human temperature, 
heart rate and blood-pressure, as influenced by age. Brit. 
J. phys. Med., 1947,10: 167-171. [P] 
994. Mitchell, H. H. and M. Edman. Diet in a hot 
environment, pp. 42—95 in: Nutrition and climatic stress. 
Springfield, Charles C. Thomas. 1951, 234 pp. [R] 
995. Mitchell, H. H., T. S. Hamilton, and J. B. Shields. 
The effect of high environmental temperatures, varied 
humidities and moderate muscular work on the losses of 
water-soluble vitamins and of minerals in the perspiration 
of adult human subjects. U. S. NRG-OSRD. OEM cmr— 
227, Medical Nutrition Rept. no. 9, 1 August 1943, 2 pp. 
[P] 
996. Molnar, G. W., E. J, Towbin, R. E. Gosselin, A. H. 
Brown, and E. F. Adolph. A comparative study of water, 
salt, and heat exchanges of men in tropical and desert 
environments. Amer. J. Hyg., 1946, 44: 411-433. 
997. Nelson, N. and W. B. Bean, Operations at high 
temperatures. U. S. ASF. Amored medical research labora- 
tory. Project no. 2-6, File no. 333.34, 12 November, 1942, 
18 pp. [P] 
998. Nelson, N. A., L. W. Eichna, S. M. Horvath, and 
W. B, Shelley. Operations at high temperatures, U. S. 
ASF. Armored medical research laboratory. Project 2-17, 
SPMEA 727.2, 21 February 1946, 20 pp. 
999. Nelson, N., L. W. Eichna, S. M. Horvath, W. B. 
Shelley, and T. F. Hatch. Thermal exchanges of man at 
high temperatures. Amer. J. Physiol., 1947, 151: 626-652. 
[P] 
1000. Nelson, N. A., W. B. Shelley, S. M. Horvath, L, W. 
Eichna, and T. F. Hatch, The influence of clothing, work, 
and air movement on the thermal exchanges of acclima- 
tized men in various hot environments. J. din. Invest., 
1948, 27: 209—216. J. industr. Hyg., 1948, 30: abstract 
section: 70. [P] 
1001. O’Connor, J. M, The influence of temperature on 
the tone of unstriped muscle. XVIII Intern, physiol. 
Congr., 1950, 377. 
1002. Pace, N., M. B. Fisher, J. E, Birren, G. C. Pitts, 
W. A. White, Jr., W. V. Consolazio, and L. J. Pecora. A 
comparative study of the effect on men of continuous 
versus intermittent exposure to a tropical environment. 
U. S. Navy, NMRI. Project X-205, Rept. no. 2, 9 May 
1945, 32 pp. [P] 
1003. Pincus, G. and F. Elmadjian. The lymphocyte 
response to heat stress in normal and psychotic subjects. 
/. din. Endocr., 1946, 6: 295-300. 1004-1027 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
1004. Pitesky, I. and J. H. Last. Effects of seasonal 
heat stress on glomerular and tubular functions in the 
dog. Amer. J. Physiol., 1951, 164: 497-501. [P] 
1005. Platt, B. S. Tables of representative values of 
foods commonly used in tropical countries. Gt. Brit. MRG. 
Special Kept., Series No. 253, 1945, 41 pp. 
1006. Radigan, L. R. and S. Robinson. Effects of en- 
vironmental heat stress and exercise on renal blood flow 
and filtration rate. /. appl. Physiol, 1949, 2: 185-191. [P] 
1007. Randall, W. C. and W. McClure. Quantitation of 
the output of individual sweat glands and their response 
to stimulation. /. appl. Physiol., 1949, 2: 72-80. [P] 
1008. Robinson, K. W. and D. H. K. Lee. The effect of 
the nutritional plane upon the reactions of animals to heat. 
J. anim. Sci., 1947,6: 182-194. 
1009. Robinson, S. The control of sweating in working 
men. Fed. Proc. Amer. Soc. exp. Biol., 1947, 6: 190. 
1010. Robinson, S. Physiological adjustments to heat, 
pp. 193-231 in: Physiology of heat regulation and the 
science of clothing. Edited by L. H. Newburgh. Philadel- 
phia, W. B. Saunders Co., 1949, viii, 457 pp. [R] 
1011. Robinson, S. and S. D. Gerking. Thermal balance 
of men working in severe heat. Amer. J. Physiol., 1947, 
149: 476-488. [P] 
1012. Robinson, S., S. D. Gerking, E. S. Turrell, and 
R. K. Kincaid. Effect of skin temperature on salt concen- 
tration of sweat. /. appl. Physiol., 1950, 2: 654-662. 
1013. Roos, A., J. R. Weisiger, and A. R. Moritz. Studies 
of thermal injury. VII. Physiological mechanisms re- 
sponsible for death during cutaneous exposure to excessive 
heat. /. din. Invest., 1947,26; 505-519. 
1014. Rothstein, A. and E. J. Towbin. Blood circula- 
tion and temperature of men dehydrating in the heat, 
pp. 172—196 in: Physiology of man in the desert. Edited 
by E. F. Adolph and Associates. New York, Interscience 
Publishers, Inc., 1947, 357 pp. [P] 
1015. Sato, T., T. Fukuyama, H. Sakai, Y. Naito, and 
K. Katayama. Physiology of workers in extremely hot 
environment (Report 3.)—blood analysis—/. Sci. Labour., 
1950, 26 (/); 34-37. (In Japanese with English sum- 
mary. ) 
1016. Sato, T., M. Kikuta, and S. Hisao. Physiology of 
workers in extremely hot environment (Report 4.)—on 
the sweating. /. Sci. Labour., 1950, 26 (2): 47. (English 
text pagination.) (In Japanese with English summary.) 
1017. Scott, J. W. The effect of moderate exercise on 
pulse, temperature and blood pressure while passing 
through the tropics. Gt. Brit. MRG-RNPRC, HS. R. N. 
P. 45/258, H. S. 101, December 1945, 4 pp. [P] 
1018. Shelley, W. B. and S. M. Horvath. The oral and 
rectal temperatures in hot environments. Bull. Army med. 
Dept., 1946, 5: 459-461. 
1019. Spealman, C. R. The effectiveness of partial im- 
mersion and periodic immersion in water for cooling men 
in hot spaces. U. S. Navy, NMRI. Project X-552, Rept. 
no. 1, 13 August 1945, 3 pp. 
1020. Stein, H. J., R. A. Bader, J. W. Eliot, and D. E. 
Bass. A study of hormonal alterations in men exposed to 
heat and cold stress. Amer. J. Physiol., 1948, 155: 425. 
Abstr. J. din. Endocrin., 1949, 9: 529—547. U. S. Army. 
Office of Quartermaster General, Lawrence, Mass., 
Quartermaster climatic research laboratory, Environ- 
mental protection section, Rept, no. 140, 27 December 
1948, 22 pp. [P] 
1021. Taylor, C. L. Physical exertion in the heat: some 
notes on its physiology and hygiene. J. industr. Hyg., 1947, 
29: abstract section: 3. /. Aviat. Med., 1946, 17: 137-145. 
1022. Taylor, C. L., and J. P. Marbarger. Some effects 
of extreme heat and humidity on man. Fed. Proc. Soc. 
exp. Biol., 1946, 5: 104. 
1023. Thomson, M. L. The effect of general ultra violet 
radiation on the sweating rate. Gt. Brit. MRG-RNPRC, 
GES. R. N. P. 48/439, C. E. S. 237, April 1948, 14 pp. [P] 
1024. Wakim, K. G. The physiologic effects of heat. 
J. Amer. med. Ass., 1948, 138: 1091-1097. [R] 
1025. Wezler, K, Physiological fundamentals of hyper- 
thermia and pathological physiology of heat injury, pp. 
792-827 in: German aviation medicine World War II, 
Vol. II. Department of the Air Force, Washington, D. G., 
1950, 1302 pp. [R] [P] 
1026. Wezler, K. and R. Thauer. Der Kreislauf im 
Dienste der Warmeregulation. Z. ges. exp. Med., 1943, 
112: 345-379. [P] 
1027. Woodcock, A. H., R, L. Pratt, and J. R. Brecken- 
ridge. A theoretical method for assessing heat exchange 
between man and a hot environment. U. S. Army. Office 
of Quartermaster General, Lawrence, Mass., Quarter- 
master climatic research laboratory. Environmental pro- 
tection branch, Kept. no. 183, January 1952, 41 pp. [M] 
D. TOLERANCE AND ACCLIMATIZATION TO HEAT 
AND HUMIDITY 
As Yaglou (1070) 1945 has stated, in several 
naval situations human tolerance to heat at various 
temperatures and humidities constitutes a limiting 
factor in operations. For short exposures, higher 
temperatures can be tolerated than for continuous 
exposures. For the latter, at a relative humidity of 
100 percent, 90° F. is the maximum dry bulb tem- 
perature tolerable. At a relative humidity of 20 
percent, a dry bulb temperature of 116° F. has been 
fixed as the maximum. Yaglou defined the heat- 
tolerable time as the time of exposure required to 
raise the mean pulse rate of a group of 5 subjects 
from an initial rate of 75 up to 125 beats per minute 
and the rectal temperature from an initial level of 
99° F. to 101° F. Serious discomfort does not occur 
until the pulse rate exceeds 135. A pulse of 160 is 
quite distressing and collapse may occur if the pulse 
rate exceeds 180 beats per minute. 
A series of reports by Blockley and associates 
(1031, 1032, 1033, and 1034) on tolerance to ex- 
treme heat may be consulted. In the first of these re- 
ports, Blockley and Taylor (1034) 1948 exposed 
human subjects to air temperature levels of 100°, 
140°, 160°, 180°, 200°, 220°, and 240° F. There 
was one exposure to 250° F. The average vapor 
pressure ranged from 0.25 to 0.9 in Hg. In most of 
the experiments the vapor pressure was about 0.8 in. 
Hg. The skin temperature rose during exposures, 
the rate of rise being greater with increased ambient 
temperature. A maximum skin temperature of 
107° F. was reached at an ambient temperature of 
240° F. in a subject wearing medium weight woolen 
clothing and cotton underwear. The heart rate in- 
creased in proportion to the skin temperature. HEAT AND HUMIDITY—TOLERANCE AND ACCLIMATIZATION 
usually reaching 140 to 160 beats per minute. The 
maximum rate was 172 beats per minute. The blood 
pressure showed individual differences. The systolic 
pressure rose during exposure in all cases, but the 
diastolic pressure declined continuously in one sub- 
ject and remained stable or slightly elevated in 
another. There were minor variations in the electro- 
cardiogram during and after exposure to heat, but 
no distinct electrocardiographic indications of heart 
damage were noted. Rectal temperature changes 
were slight and slow of onset. The authors con- 
sidered rectal temperature changes to be unreliable 
as an indication of the extent of temperature stress 
in short exposures. The highest rectal temperature 
recorded was 101° F. The maximum temperature 
of the exhaled air was recorded at 104° F. indi- 
cating that the mucous membranes exert a strong 
cooling influence. In these subjects, there was a 
feeling of air hunger associated with deep and 
irregular respiration. This was accompanied by 
restlessness and nervous irritability with waves of 
dizziness at the terminal stages. At an ambient tem- 
perature of 180° F. the mean tolerance time for 
4 exposures was 49 minutes; at 200° F. the mean 
tolerance time was 33 minutes; at 220° F. the mean 
tolerance time was 26 minutes, and at 240° F. sub- 
jects showed a mean tolerance time of 23/a minutes. 
Of physiological variables measured, Blockley and 
Taylor {1032) 1950 considered the skin tempera- 
ture constitutes the best single index of thermal 
strain. Blockley and Lyman {1031) 1950 have 
measured mental performance under heat stress as 
indicated by addition and number checking tests. 
These experiments were conducted at a vapor pres- 
sure of 0.8 in. Hg and at 3 levels of temperature; 
namely, 160°, 200°, and 235° F. The duration of 
each exposure was determined by the ability of the 
individual to tolerate the heat, and the work on the 
mental problems was continuous during the ex- 
posure except for a 15-second rest period in each 
3 minutes. In two of the experimental environ- 
ments, the performance in the final 6 minutes of 
heat exposure was found to be significantly poorer 
than in the preexposure period, but no significant 
differences were found for the 200° F. experiments. 
In a study of psychomotor performance of human 
subjects as indicated by a task simulating aircraft 
instrument flight, Blockley and Lyman {1033) 1951 
conducted experiments at 160°, 200°, and 235° F. 
with a vapor pressure of approximately 0.8 in. Hg, 
using a comfortable environment in the neighbor- 
hood of 80° F. as a control. The subjects were given 
an initial 1-hour practice period on experimental 
flight patterns before the first heat exposure. The 
task consisted of continuous repetitions of this 
flight pattern, which was 4 minutes in duration and 
included 4 turns combined variously with climbs, 
dives, and level flight. Although differing in level 
of competency or skill in the task, no subjects 
showed a change in proficiency within 80 minutes 
of “flight” in the comfortable environment. On 
exposure to heat, however, there was striking de- 
terioration of performance, commencing from 4 
to 13 minutes prior to the termination of exposure. 
Adolph {1028) 1946 pointed out that a practical 
limit to tolerance of high temperature is signaled by 
the premonition of circulatory collapse experienced 
by acclimatized subjects. Temperatures above 90° 
F. wet bulb can rarely be endured indefinitely. 
During work, the intolerable wet bulb temperature 
may be as low as 80° F. or less. There is an initial 
acclimatization in the majority of subjects which is 
nearly complete after 4 exposures of 2 hours each 
to limiting temperatures. There is a suggestion of 
additional slower acclimatization requiring a month 
or more. The variability in heat tolerances among 
individuals is reduced by their acclimatization. 
Adolph {1029) 1947 has ascertained the tolerance 
times of dogs, cats, rabbits, guinea pigs, rats, and 
mice to warm dry air at various temperatures. A 
consistent sign of lethal conditions was found in the 
rectal temperature which had different median 
critical values for each species, lying between 41.7° 
and 43.4° C. Heat stroke appeared to result from 
hyperthermia that injured unidentified regulatory 
tissues. Death might be delayed for periods up to 26 
hours after the animals had been sujected to criti- 
cal rectal temperatures and then cooled. Dehydra- 
tion through panting was limited in the mice, rats, 
rabbits, and guinea pigs, but was copious in the cats 
and dogs. Evaporation proceeded as rapidly after 
considerable dehydration as during periods of water 
balance. Dehydration resulted in a concentrated 
plasma and by inference a depleted plasma volume 
and limitation of circulation. This was considered 
important in sensitizing the animals to warm at- 
mospheres. The explosive rise of rectal tempera- 
ture was considered to develop through failure of 
the circulation to transport heat to the surface. 
Animals allowed an unlimited water intake did not 
drink enough to maintain body weight while in the 
hot atmospheres. If deprived of water they subse- 
quently drank less than enough to recover body 
weight except in the case of dogs with water deficits 
of less than 9 percent of body weight. 
Eichna, Ashe, Bean, and Shelley {1045) 1944 
have determined the upper limits and the safe limits 
of temperature and humidity at which acclimatized 
normal young men can work. At wet bulb tempera- SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
tures below 91° F., men worked easily, efficiently, 
and with only mild physiological changes. At wet- 
bulb temperatures from 91° F., and 94° F., pro- 
longed moderate hard work was rather difficult, 
resulting in loss of vigor and alertness, undesirable 
physiological responses, and occasional illness. Mod- 
erately hard work at wet-bulb temperatures of 
94° F. or higher rapidly lead to total disability in 
most men. Approximately 1 hour of sustained work 
was tolerated by most subjects, while those who 
worked longer did so inefficiently and with func- 
tional disturbances. Hatch {1050) 1945 has pointed 
out that resting human subjects can tolerate dry 
heat well above 200° F., providing the duration of 
exposure is very brief. Ellis {1049) 1950 has re- 
ported that experimental work has in general sup- 
ported the provisional recommendation for British 
sailors of an effective environmental temperature 
of 86° F. as the upper tolerable limit in any com- 
partment occupied for long periods of time. Ellis 
suggested that the effective temperature scale is 
inaccurate at higher levels of heat. For exposures 
of a few hours duration, skill deteriorates at levels 
of heat well below those at which men may carry 
out unskilled heavy work without loss of efficiency. 
For reports on measures for improving tolerance 
to high temperatures, papers by the following may 
be consulted: Bock {1035); Johnson, Pitts, and 
Consolazio {1052) 1943; Mills, Cottingham, and 
Taylor {1057) 1947; Napier {1058) 1946; and 
U. S. OSRD-NDRC {1068) 1943. 
Additional studies of tolerance to high tempera- 
tures are provided by the following authors; Burch 
and Sodeman {1036) 1944; Canada, Medical In- 
telligence Division, Ottawa {1037) 1945; Carpen- 
ter {1038) 1946; Consolazio, Pecora, and Pfeiffer 
{1042) 1944; Lee and MacPherson {1054) 1946; 
Mac Donald and Wyndham {1055) 1950; Taylor 
{1064) 1945 and {1065) 1946. 
In a laboratory study of acclimatization to high 
temperatures, Eichna, Bean, and Ashe {1046) 1943 
subjected 55 young enlisted men to dry-bulb tem- 
peratures ranging from 89° to 93.5° F. and relative 
humidities from 90 to 100 percent. In these studies 
carried out over a period of 6 months, it was found 
that soldiers exposed to moist heat became adapted 
by a process of acclimatization which enabled them 
to work more efficiently and with less risk of illness 
from heat than when first exposed. A man acclima- 
tized to humid or dry heat can work with a lower 
body temperature, lower heart rate, more stable 
blood pressure, and less discomfort than when not 
acclimatized. The rapidity of acclimatization varies 
from 3 to 10 days. Men in good physical condition 
acclimatize more rapidly and are capable of greater 
amounts of work than those in poor condition. For 
complete acclimatization, work in humid heat is 
necessary. The capacity to perform a maximum 
amount of work in hot environments is most quickly 
attained by beginning work at a low level and in- 
creasing it within the tolerance of the subject as 
heat exposure continues. Strenuous work on initial 
exposure to heat is not well tolerated. Acclimatiza- 
tion to desert environments increases ability to work 
in humid heat. The authors recommend an acclima- 
tization period of 2 weeks for troops with progres- 
sively increasing amounts of work and enough water 
to satisfy thirst. Alcohol should be prohibited. 
Eichna, Park, Nelson, Horvath, and Palmes {1047) 
1950 studied acclimatization in an environment of 
50.5° C. dry bulb and 15 percent relative humidity 
over a period of 10 days. The subjects carried out 
measured amounts of work. At the beginning of the 
acclimatization period, the heart rate increase was 
59 beats per minute above the mean rate in a cool 
environment, whereas at the end of the 10th day it 
was only 15 beats per minute above the mean rate. 
The rectal-temperature increase at the beginning of 
the experiment was 1.2° C., but only 0.1° C. at the 
end of the experiment. The authors believe that ac- 
climatization is mainly effected by an improvement 
in the loss of heat from the body by evaporation 
which lowers substantially the deep tissue tempera- 
ture and reduces the cardiovascular burden im- 
posed by the heat. Calorimetric measurements and 
clinical observations were made by Park and Palmes 
(1059) 1947 on three men working with a metabolic 
load of 180 calories per square meter per hour in a 
very dry, hot environment. On beginning work, deep 
and peripheral tissue temperatures rose rapidly 
owing to the retention of metabolic heat, as well as 
to heat gains by radiation and convection. The 
heavy load on the circulation probably accounted 
for many of the symptoms in the unacclimatized 
state. The principal thermal adjustment in the proc- 
ess of acclimatization was the development of a 
higher rate of sweat secretion. With acclimatization, 
signs of circulatory stress diminished greatly. The 
heat content of the body after acclimatization re- 
mained high, but the heat was absorbed in the 
peripheral tissues and the critical deep tissue tem- 
perature was maintained at a nearly normal value. 
Observations of Ladell {1053) 1950 indicated that 
acclimatization to work in moist, tropical heat is 
associated with increase in sweat production. For a 
study of individual variability in capacity to acclima- 
tize to high temperature, a report by Taylor, Metz, 
Henschel, and Keys {1066) 1951 may be consulted. HEAT AND HUMIDITY—TOLERANCE AND ACCLIMATIZATION 
1028-1032 
Acclimatization to heat is essentially related to 
improved cardiovascular efficiency. This is indi- 
cated by a report of Adolph (1030) 1949 who ob- 
served diminution of the frequency of the pulse 
during acclimatization. Enhanced cardiovascular 
and muscular efficiency in acclimatization are also 
reported by Critchley (1043) 1945. Robinson 
(1060) 1949 stated that after 6 or 8 days of work 
in hot environments a man can work in thermal 
equilibrium under conditions in which it would be 
impossible for him to continue unless acclimatized. 
Rectal temperature and metabolic rate were found 
to return to normal levels after few days of exposure. 
There is an increase in circulating blood volume and 
the maximal blood flow to the skin increases 10 to 
25 percent. There is greater stability of the circula- 
tion in different postural stresses and an increase in 
the efficiency of sweating. If water intake is limited 
and the demand for sweating is increased, the kid- 
neys may reduce the urinary output by 500 cu. cm. 
At first, the sodium chloride output of the kidneys 
is reduced, but later, normal output is resumed. 
In a study of cross-acclimatization to heat and 
cold, Eliot, Stein, and Bader (1048) 1948 exposed 
healthy, young male subjects to nineteen 5-hour 
periods of heat (107° F. dry bulb, 89° F. wet bulb, 
and 3 miles per hour wind velocity), 14 five-hour 
periods of cold (— 20° F., wind velocity 3 or 4 miles 
per hour), and 5 reexposures to heat. After 5 weeks 
without environmental stress, 3 more heat exposures 
were given. The most striking findings of these 
studies were those in men acclimatized to heat, loss 
of acclimatization was not accelerated by repeated 
cold exposures, as judged by cardiovascular and 
metabolic indices and subjective reactions. More 
rapid and effective vasoconstriction with successive 
cold exposures was demonstrated. Continuous 
diuresis and increased chloride loss were observed 
during the period of cold exposures, and these 
trends were only slowly reversed by reexposure to 
heat. No significant difference in basal metabolic 
rate was observed between the hot and the cold 
periods. Blood, plasma, and “available fluid” 
volume studies revealed no consistent changes dur- 
ing the hot or cold periods, but plasma protein and 
hematocrit values showed definite hemoconcentra- 
tion in the cold hemodilution in the heat. It was 
not demonstrated that increased tolerance to cold 
results from any of the changes observed. These 
same findings were reported by Stein, Eliot, and 
Bader (1063) 1948. 
In a study of the mechanism of acclimatization to 
heat, Conn (1041) 1949 has concluded that the 
major differences between unacclimatized and ac- 
climatized men consists of an improved peripheral 
circulation and an enhanced ability to resist deple- 
tion of body salt in the acclimatized subjects. This 
second difference manifests itself mainly as a capac- 
ity to produce sweat which is much lower in its con- 
centrations of sodium and chloride than in the 
unacclimatized subjects. Since, under conditions of 
work in the heat, the major loss of body salt occurs 
via sweating, this adjustment assumes primary im- 
portance. The author believes that the process of 
acclimatization to heat is linked with an increased 
secretion of the adrenocorticotropic hormone by 
pituitary gland and the resulting enhancement of 
production and liberation of adrenal cortical ste- 
roids. Under the conditions of the author’s experi- 
ments the need for conservation of body salt con- 
stitutes, it is believed, the stimulus which activates 
the mechanism and raises the level of activity of the 
pituitary-adrenal axis. According to a report of 
Robinson, Kincaid, and Rhamy (1062) 1951, men 
were able to perform work in an environmental 
temperature of 50° G. at 15 percent relative humid- 
ity under controlled conditions, with and without 
administration of desoxycorticosterone. On first 
exposure, subjects exhibited a rise in heart rate, body 
temperature, metabolism, and sweat sodium chlo- 
ride concentration. They underwent the normal 
course of acclimatization during 5 days of exposure. 
The only significant changes produced by desoxy- 
corticosterone were higher concentrations of plasma 
sodium and lower concentrations of sodium and 
chloride in the sweat during the first 2 days of 
exposure. 
For further studies of acclimatization to heat and 
humidity, papers by the following may be consulted: 
Christensen (1039) 1947; Clark (1040); Dreosti 
(1044) 1949; Horvath and Shelley (1051) 1946; 
Robinson, Dill, Wilson, and Nielson (1061) 1941; 
MacPhersen, Lee, and Furlonger (1056) 1947; 
U. S. NRC-CAM (1067) 1949; Winslow and Her- 
rington (1069) 1949. 
1028. Adolph, E. E. Tolerance of man toward hot at- 
mospheres. Publ. Hlth. Rep., Wash., 1946, Suppl. no. 192, 
38 pp. J. industr. Hyg., 1949, 27: abstract section: 44. [R] 
1029. Adolph, E. F. Tolerance to heat and dehydration 
in several species of mammals. Amer. J. Physiol., 1947, 
151: 564-575. [P] 
1030. Adolph, E. F. Acclimatization to warm climates, 
pp. 13—14 in. U. S. NRC-CAM. Conference on acclimati- 
zation. 17 June 1949, 29 pp. 
1031. Blockley, W. V. and J. Lyman. Studies of human 
tolerance for extreme heat. III. Mental performance under 
heat stress as indicated by addition and number checking 
tests. USAF. Wright-Patterson air force base, Dayton, 
Ohio. Air materiel command. Technical rept. no. 6022, 
October 1950, 54 pp. 
1032. Blockley, W. V. and C. L. Taylor. Studies in 
tolerance for extreme heat. Second summary report. USAF. 
291222—54—7 1033-1064 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
Wright-Patterson air force base, Dayton, Ohio. Air ma- 
teriel command. Technical rept. no. 5831, February 1950, 
84 pp. 
1033. Blockley, W. V. and J. Lyman. Studies of human 
tolerance for extreme heat. IV. Psychomotor performance 
of pilots as indicated by a task simulating aircraft instru- 
ment flight. USAF. Wright-Patterson air force base, Day- 
ton, Ohio, Aero medical laboratory. Technical rept. no. 
6521, May 1951, 45 pp. 
1034. Blockley, W. V. and C. L. Taylor. Studies of 
human tolerance for extreme heat. USAF. Wright-Pat- 
terson air force base, Dayton, Ohio, Air materiel command. 
Serial no. MCREXD-696-113A, contract W33-038 
ac-14504, 1 November 1948, 204 pp. [P] 
1035. Bock, A. V, Physiological adaptation of man to 
heat. U. S. OSRD. OEMcmr 328. Final rept., no date, 
6 pp. 
1036. Burch, G. E. and W. A. Sodeman. Effect of 
cooling isolated parts upon the comfort of man resting 
in hot humid environment. Proc. Soc. exp. Biol., N. Y., 
1944, 55: 190-194. [P] 
1037. Canada, Medical intelligence division, Ottawa. 
Acclimatization to heat. p. 15 in: General medical interest 
letter no. 13, 17 May 1945. [P] 
1038. Carpenter, A. The effect of room temperature 
on the performance of the resistance box test; A per- 
formance test of intelligence. Gt. Brit. MRC-RNPRG, 
HS. R. N. P. 46/318. H. S. 153, August 1946, 20 pp. [P] 
1039. Christensen, W. R. Long-term acclimatization to 
heat. Amer. J. Physiol., 1947, 148: 86-90. [P] 
1040. Clark, W. E. L. Notes on climatic research at 
Oxford (November 1948-November 1950). Gt. Brit. 
MRC-RNPRC, CES. R. N. P. 48/443, C. E. S. 236, 
undated, 4 pp. 
1041. Conn, J. W. The mechanism of acclimatization 
to heat. Advances intern. Med., 1949, 2: 373-393. [P] 
1042. Consolazio, W. V., L. J. Pecora, C. C. Pfeiffer. 
A new salt tablet for use in hot environments. U. S. Navy. 
NMRI. Project X-214, 13 October 1944, 11 pp. [P] 
1043. Critchley, M. Remarks on acclimatization. /. R. 
nav. med. Serv., 1945, 31: 245-248. 
1044. Dreosti, A. 0. The physiology of acclimatization 
in native mine labourers of the Witwatersrand gold mines. 
Fourth empire mining and metallurgical congress. Great 
Britain, 1949, London, Congress Salisbury House, 1949, 
14 pp. [P] 
1045. Eichna, L. W., W. F. Ache, W. B. Bean, and 
W. B. Shelley. Operations at high temperatures. U. S. 
ASF. Armored medical research laboratory. Project 2 
{11, 13, 17), File no. 727.2, 2 October, 1944. [P] 
1046. Eichna, L. W., W. B. Bean, and W. F. Ashe. 
Operations at high temperatures. U. S. ASF. Armored 
medical research laboratory. Project 2 {7, 11, 13, 15, 17, 
19), 727.3 GNOME, 18 October 1943. 
1047. Eichna, L. W,, C. R. Park, N. Nelson, S. M. Hor- 
vath, and E. D. Palmes. Thermal regulation during ac- 
climatization in a hot, dry (desert type) environment. 
Amer. J. Physiol., 1950, 163: 585-597. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharma- 
cology), 1951, 4: 1237. [P] 
1048. Eliot, J. W., H. J. Stein, and R. A. Bader. Cross- 
acclimatization to heat and cold. Amer. J. Physiol., 1948, 
155: 435. Abstr. 
1049. Ellis, F. P. The upper limits of warmth tolerated 
by man without loss of efficiency. Experimental studies at 
Singapore. Med. J. Malaya, 1950, 4: 175-189. Excerpta 
Medico. Section II. (Physiology, Biochemistry, and Phar- 
macology), 1951, 4: 60. Abstr. 
1050. Hatch, T. F. Upper limits of tolerance to heat 
and humidity. Trans, med. engr. Ind. Hyg. Found., 1945, 
Bull. 3: 24-31. 
1051. Horvath, S. M. and W. B. Shelley. Acclimati- 
zation to extreme heat and its effect on the ability to work 
in less severe environments. Amer. J. Physiol., 1946, 146: 
336-343. [P] 
1052. Johnson, R. E., J. C. Pitts, and F. Consolazlo. 
The effects of variations in dietary protein in the physical 
well being of men working in hot environments. U. S. 
OSRD-NDRC, OEMcmr 328, 15 August 1943, 3 pp. [P] 
1053. Ladell, W. S. S, Acquired heat tolerance of tem- 
perate climate men living in the tropics. XVIII Intern, 
physiol. Congr., 1950, 320-322. [P] 
1054. Lee, D. H. K. and R. K. MacPherson. Further 
considerations of the results obtained with the Harvard 
Pact test in RAAF ground crew on tropical service. 
Australia. NHMRG, Fatigue laboratory, Rept. no. 8, 12 
April 1946, 8 pp. 
1055. MacDonald, D. K. C. and C. H. Wyndham. Heat 
transfer in man. J. appl. Physiol., 1950, 3: 342-364. 
Excerpta Medico. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1951, 4: 1236. 
1056. MacPherson, R. K., D. H. K. Lee, and E. Fur- 
longer. Atmospheric conditions encountered during a 
survey of RAAF ground crew on tropical service and their 
relationship to both sweat loss and the results obtained 
with the Harvard Pack test. Australia. NHMRG, Fatigue 
laboratory. Rept. no. 9, 18 March 1947, 5 pp. 
1057. Mills, C. A., E. Cottingham, and E. Taylor. 
The influence of environmental temperature on dietary 
requirement for thiamine, pyridoxine, nicotinic acid, folic 
acid and choline in chicks. Amer. J. Physiol., 1947, 149: 
376-382. [P] 
1058. Napier, L. E. Measures for mitigating the effects 
of tropical climate, pp. 16-32 in: The principles and prac- 
tice of tropical medicine. New York, The Macmillan Com- 
pany, 1946, 917 pp. 
1059. Park, C. R. and E. D. Palmes. Thermal regula- 
tion during early acclimatization to work in a hot dry 
environment. U. S. Army, Fort Knox, Kentucky, Field 
research laboratory. MDFRL Project 2-17-1, 30 June 
1947, 15 pp. [P] 
1060. Robinson, S. Acclimatization of man to heat, 
pp. 9—12 in: U. S. NRG—CAM. Conference on acclima- 
tization. 17 June 1949, 29 pp. 
1061. Robinson, S., D. B. Dill, J. W. Wilson, and M. 
Nielson. Adaptations of white men and negroes to pro- 
longed work in humid heat. Amer. J. trop. Med., 1941, 
21: 261-287. 
1062. Robinson, S., R. K. Kincaid, and R. K. Rhamy. 
Effects of desoxycorticosterone acetate on acclimatization 
of men to heat. J. appl. Physiol., 1950, 2: 399-406. 
Abstr. World Med., 1950, 8: 228. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1951, 4: 59-60. Abstr. 
1063. Stein, H. J., J. W. Eliot, and R. A. Bader. Physio- 
logical reactions to cold and their effect on the retention 
of acclimatization to heat. U. S. Army. Office of Quarter- 
master General, Lawrence, Mass. Quartermaster climatic 
research laboratory. Environmental protection section. 
Rept. no. 142, 29 December 1948, pp. 26. J. appl. Physiol., 
1948, 1: 575-585. Abstr. World Med., 1949, 6: 262. [P] 
1064. Taylor, C. L. Human tolerance for short ex- 
posures to heat. USAF. Wright-Patterson air force base. HEAT AND HUMIDITY—EFFECT ON EFFICIENCY 
1065-1070 
Dayton, Ohio. Aero medical laboratory. Serial no. TSEAL- 
3-695-49 A, 28 February 1945, 22 pp. 
1065. Taylor, C. L. Human tolerance for short ex- 
posures to heat and humidity. USAF. Wright-Patterson 
air force base, Dayton, Ohio. Aero medical laboratory. 
Serial no. TSEAA 695-56B, 12 February 1946, 24 pp. 
1066. Taylor, H. L., B. Metz, A. Henschel, and A. Keys. 
Individual variability in capacity to acclimatize to high 
temperature. Amer. J. Physiol., 1951, 167: 813. Abstr/ 
1067. U. S. NRC—CAM, Conference on acclimatization. 
Acclimatization to heat. 17 June 1949, 29 pp. 
1068. U. S. OSRD-NDRC. Relation of diet and sub- 
sistence to the performance of work by men at high tem- 
peratures. OEMcmr 220, Medical nutrition, Final report, 
7 September 1943, 6 pp. 
1969. Winslow, C. E. A. and L. P. Herrington. The 
adaptations of the human body to varying thermal condi- 
tions. pp. 58-115 in: Temperature and human life. Prince- 
ton, Princeton University Press, 1949, 272 pp. [P] 
1070. Yaglou, C. P. Note on tolerance to various high 
levels of dry bulb temperature and relative 
U. S. Navy. NMRI. NH6-1/A11/X-205, 14 August 1945, 
2 PP- 
E. EFFECT OF HEAT ON EFFICIENCY 
Observations under conditions of operation in 
submarines and other naval vessels have generally 
shown that personnel operate more efficiently in 
correctly air-conditioned spaces. Many investiga- 
tions have been designed to examine under con- 
trolled conditions the influence of heat and humid- 
ity on working capacity. Bean, Eichna, Ashe, Hor- 
vath, and Nelson {1071) 1943 in such a study ex- 
posed men for 4 months, with only 5 minutes leave 
from the chamber a day, to temperatures ranging 
from 120° F. during the day to 90° F. at night, the 
relative humidity range was from 15-22 percent. 
The subjects became adapted to the heat and were 
able to carry out their duties more efficiently than 
at the beginning. Acclimatization was begun at the 
first exposure, and most of the acclimatization was 
acquired by the fourth day. Men in good physical 
condition acclimatized more quickly, and it was 
found that work in the heat was an aid to acclima- 
tization. Strenuous work on the first exposure to 
heat was not well tolerated and often resulted in 
disability. Eichna, Bean, Ashe, and Nelson {1077) 
1945 found that there is a measure of cross-accli- 
matization between hot, dry and hot, humid envir- 
onments. Performance of acclimatized men in 
humid heat is impaired most seriously by lack of 
adequate water intake and lack of physical fitness. 
Performance is also effected adversely, but not so 
severely by lack of rest and sleep, by added clothing 
equipment, by alcohol intake, and by prolonged 
periods of work. 
In a study of the effects of the thermal environ- 
ment on working capacity among Indian workers 
in the Kolar gold mine, Caplan and Lindsay {1074) 
1947 chose hand drilling as a performance test. The 
number of inches drilled per hour was taken as a 
quantative measure of performance. Six men of 
average fitness were acclimatized to. a wet-bulk 
temperature of 93° F. Each test lasted 3 hours and 
the number of inches drilled was measured at the 
end of each hour. The performance during the first 
hour of work at a wet-bulk temperature of 83° F. 
was taken as 100 percent. In these studies it was 
found that at a wet-bulb temperature of 89.5° F. 
the performance was 80 percent during the first, 
second, and third hours. The same performance was 
found for wet-bulb temperatures of 88.2° and 
86.6° F. Wet-bulb temperatures of 94.4°, 93.0°, 
and 91.3° F. were associated with a relative per- 
formance of 50 percent. In a normal working shift 
no serious diminution of work was found likely 
when the wet-bulb temperatures were below 85° 
F., but at 90° F. wet bulb temperature the relative 
performance over a 6-hour period was unlikely to 
be higher than 60 percent. It was considered that 
at 93° F. wet-bulb temperature it was improbable 
that any satisfactory work could be performed after 
the second hour and certainly not after the third 
hour. Macworth {1081) 1946 reported a study 
to determine if hot and moist atmospheres impair 
the accuracy with which trained telegraph operators 
can write down Morse messages heard over head- 
phones. Eleven physically fit men ranging in age 
from 18 to 34 years were used. It was found that 
when the room temperature was raised to a dry- 
bulb reading of 95° F. or a wet-bulb reading of 
85° F., there was a statistically definite fall in ac- 
curacy of wireless telegraphy reception compared 
with performance at a dry-bulb temperature of 85° 
F. or wet-bulb temperature of 75° F., or a dry-bulb 
temperature of 90° F. or 80° F. wet bulb. Since the 
velocity of the air was 100 feet per minute it was 
suggested that the effective temperatures of 79° F. 
to 83° F. were undoubtedly associated with a more 
effective wireless telegraphy reception than an ef- 
fective temperature of 87.5° F. In the Eastern Fleet 
of the Royal Navy, wireless telegraphy ratings have 
to work at temperatures above 84° F. and even 
under more severe conditions. The exceptionally 
able men were less affected by harassing atmospheric 
conditions than those less efficient. The deteriora- 
tion in performance as measured by the number 
of faulty wireless telegraphy messages bore a 
logarithmic relationship to the atmospheric tem- 
perature changes. This applied when the nature of 
the task was different, consisting simply of moving 
a heavy lever. There were no signs of phychological 
effects accumulating serially from day to day; in 
fact the men were usually better at the wireless SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
telegraphy test on the second day of a particular 
room temperature. The average number of wireless 
telegraphy errors per man per hour rose consider- 
ably and progressively within the third-hour watch 
period. Twice as many errors were made in the 
second hour and 3 or 4 times as many during the 
third hour. 
Pezechkian {1085) 1949 measured the rates of 
work of rats running in a revolving drum exposed to 
temperatures ranging from 13° to 40° G. The rectal 
temperature did not vary much beyond normal 
range. The maximum capacity for work was noted 
in the 31° to 34° G. temperature range, particularly 
at 31° to 32° G. Beyond these temperatures the 
work decreased as much as 34 percent. 
Mackworth {1083) 1948 administered perform- 
ance tests to a group of sailors subjected to effective 
temperatures from 79° F. to 97° F. Results showed 
that there is a critical region of temperature above 
which most acclimatized men dressed in shorts will 
not work so accurately or sleep restfully. The region 
lies between effective temperatures of 83° F. and 
87.5° F.; that is to say, between dry-bulb tempera- 
tures of 90° F. and 95° F. or wet-bulb temperatures 
between 80° F. and 85° F. The accuracy of very 
highly trained men was found to suffer to a less 
extent from the effects of high atmospheric tem- 
peratures than does the performance of men of 
ordinary ability. If a group of 12 to 20 men had been 
working at a sedentary task for 2 to 3 hours and if 
their average rectal temperature at the end of that 
time was found to be more than 100° F., then that 
group of men was not likely to have been working 
at full efficiency. This refers to acclimatized men 
dressed in shorts and cannot be used when the task 
entails heavy physical effort. There is no direct re- 
lationship between the rectal temperature and the 
incidence of mistakes. The association is noncasual, 
both rectal temperature and the error score being 
dependent upon the common factor of room tem- 
perature. These same conclusions have been re- 
ported by Mackworth {1084) in 1948. Mackworth 
{1082) 1946 has studied the effects of heat and 
high humidity on prolonged visual search as meas- 
ured by a clock test. This test was devised to incor- 
porate some of the main psychological features of a 
task in which the operator watches a radar tube. 
The task requires that the subject be sufficiently 
alert at all times to note faint and short-lasting 
visual signals, usually with no check on his working 
efficiency. During this test the optimum atmospheric 
temperature for accurate work was an effective 
temperature of 79° F. An increase in the effective 
temperature to 87.5° F. or a decrease to 70.0° F. 
produced an increase of 25 percent in the incidence 
of missed signals. Deterioration in the speed of work 
was not so striking as the decline in accuracy. At 
97° F. effective temperature the responses became 
sluggish. Training appears to help to maintain ac- 
curacy in hot atmospheres. Mackworth reported 
that there is a rise in rectal temperature of the men 
doing this sedentary test, and he found a weakly pos- 
itive association between the final rectal tempera- 
ture and the incidence of missed signals during the 
second hour of the test. However, this relationship 
could not be statistically validated. 
The performance of a motor coordination test by 
human subjects subjected to a hot, humid environ- 
ment was shown to be impaired in studies of Weiner 
and Hutchinson {1088) 1945. Acclimatization of 
motor coordination, as revealed by the tests and 
analogous to acclimatization to work, appears to be 
suggested by these experiments; but if such an ac- 
climatization to motor coordination does occur, the 
process must be different from acclimatization to 
work since the subjects already acclimatized in this 
respect gave an impaired coordination performance 
in the hot room. In a study of the performance of 
the pursuit-meter test under conditions of unfavor- 
able atmospheric heat, Carpenter {1075) showed 
deterioration in work performance with high room 
temperature and with handle load. The results sug- 
gested that the effects of handle load are greater 
at increased room temperature, but this effect is 
unreliable statistically. Rectal temperatures taken 
at the end of the test and the amount of weight lost 
in sweat showed the expected relationship with 
room temperature, but the individual readings re- 
vealed no correlation with performance. Mental 
performance under heat stress as indicated by addi- 
tion and number checking tests has been studied 
by Blockley and Lyman {1072) 1950. These experi- 
ments were conducted at a single humidity (vapor 
pressure of 0.8 in. of Hg) and at 3 levels of tem- 
perature: 160°, 200°, and 235° F. The duration 
of each exposure was determined by the ability of 
the individual to tolerate the heat. Work on the 
mental problems was continuous during the ex- 
posure, except for a 15-second rest period in each 
3 minutes. No significant differences in perform- 
ance were found for the 200° F. experiment, but 
in the two other experimental environments the 
performance in the final 6 minutes of heat exposure 
was found to be significantly poorer in the pre- 
exposure period. Cameron {1073) 1945 has made 
observations on the factors of stress operating on 
naval personnel based in India and Ceylon, and 
working under tropical conditions. His observations 
were based almost entirely upon the experiences HEAT AND HUMIDITY—HEAT DISEASE 
1071-1088 
of the psychiatrist dealing with men who had suf- 
fered from breakdown. While a psychiatric survey 
must deal with the whole picture, an attempt was 
made to underline the elements particularly related 
to the effects of heat and humidity and to suggest 
possible lines of investigation. The first element of 
importance appeared to be that associated with 
“tropical loss of memory.” This, the author con- 
sidered, is largely a metabolic phenomenon and not 
primarily emotionally determined. The author also 
described a “prepsychotic tropical syndrome.” This 
differs materially from the conditions that have 
been met with in men who experienced equal iso- 
lation and corresponding stress in nontropical over- 
seas service. A high proportion of breakdowns in 
naval personnel on tropical service are stated to be 
psychotic in character. This is not the case accord- 
ing to the author in naval service in temperate 
climates, however arduous. 
For further studies of the effects of heat on per- 
formance, papers by the following may be con- 
sulted: Carpenter {1076) 1949; G. Brit. MRC-R 
NPRG {1078) 1946; Henschel, Taylor, Brozek, 
Mickelsen, and Keys {1079) 1943; Lee {1080) 
1949; Trenchard {1086) 1946; and U. S. NRC 
{1087) 1945. 
1071. Bean, W. B., L. W. Eichna, W. F. Aslie, S. M. 
Horvath, N. Nelson. Influence of high temperatures on 
the efficiency of personnel. U. S. ASF. Armored medical 
research laboratory. File No. 727.2 GNOME, 3 April 1943. 
1072. Blockley, W. V. and J. Lyman. Studies of human 
tolerance for extreme heat. III. Mental performance under 
heat stress as indicated by addition and number checking 
tests. USAF. Wright-Patterson air force base, Dayton, 
Ohio. Air materiel command. Technical rept. no. 6022, 
October 1950, 54 pp. [P] 
1073. Cameron, K. The psychiatric aspects of tropical 
service in the navy. Gt. Brit. MRG-RNPRG, HS. R. N. P. 
45/252, H. S. 93, December 1945, 7 pp. [P] 
1074. Caplan, A. and J. K. Lindsay. An experimental 
investigation of the effects of high temperatures on the 
efficiency of workers in deep mines. Paper submitted for 
discussion at Meeting of Inst. Mining and Metallurgy, 
Oct. 17, 1946. Abstr: Bull. Hyg., Land., 1947, 22: 333- 
334. [P] 
1075. Carpenter, A. A comparison of the effects of 
handle load and of unfavourable atmospheric conditions 
on the performance of the pursuitmeter test. Gt. Brit. 
MRG-RNPRG, HS. R. N. P. 47/361, H. S. 182, undated, 
12 pp. [P] 
1076. Carpenter, A. Some effects of life in Singapore. 
Gt. Brit. MRG. The psychological laboratory, Cambridge. 
Applied psychology research unit. A. P. U. 103/49, June 
1949,14 pp. 
1077. Eichna, L. W,, W. B. Bean, W. F. Ashe, and N. 
Nelson. Performance in relation to environmental tem- 
perature. Reactions of normal young men to hot, humid 
(simulated jungle) environment. Johns Hopk. Hasp. Bull., 
1945, 76: 25-58. [P] 
1078. Gt. Brit. MRC-RNPEC, HS, Memorandum cm the 
effect of the thermal environment in efficiency. R. N. P. 
46/315, H. S. 151, March 1946, 5 pp. 
1079. Henschel, A., H. L. Taylor, J. Brozek, 0. Mickel- 
sen, and A. Keys. Vitamin C and ability to work in hot 
environments. U. S. NRC. OSRD Contract OEMcmr- 
220, 15 May 1943, 11 pp. [P] 
1080. Lee, D. H. K. Interactions of tropical environ- 
ments and human performance. U. S. Army. Office of 
Quartermaster General, Lawrence, Mass. Climatic research 
laboratory, Environmental protection section. Rept. no. 
154, March 1949, 2 pp. 
1081. Mackworth, N. H. Effects of heat on wireless 
telegraphy operators hearing and recording morse mes- 
sages. Brit. J. industr. Med., 1946, 3: 143-158. Bull. Hyg., 
Land., 1946, 21: 679-680. R. N. P. 45/243, H. S. 88, 
October 1945, 17 pp. /. industr. Hyg., 1947, 29: abstract 
section: 3 [P] 
1082. Mackworth, N. H. Effects of heat and high 
humidity on prolonged visual search as measured by the 
clock test. Gt. Brit. MRG-RNPRG, HS. R. N. P. 46/278 
H. S. 125, February 1946, 15 pp. [P] 
1083. Mackworth, N. H. Definition of the upper limit 
of environmental warmth by psychological tests of human 
performance. The Royal Society Empire Scientific Con- 
ference, June-July 1946, Volume I, 1948, 423-441. [P] 
1084. Mackworth, N. H. Researches on the measure- 
ment of human performance. Gt. Brit. MRC, Special re- 
port series no. 268, 1948, 77 pp. [P] 
1085. Pezechkian, M. Influence de la temperature 
exterieure sur la capacite de travail musculaire chez le rat. 
C. R. Soc. Biol., Paris, 1949, 143: 242-244. [P] 
1086. Trenchard, H. J. Inability to work in a tropical 
climate. Brit. med. J., 1946, 2: 416-418. 
1087. U. S. NRC. Subcommittee on clothing. Conference 
on “working efficiency and high temperatures”. 23 
October 1945, 15 pp. 
1088. Weiner, J. S. and J. C, D. Hutchinson. Hot humid 
environment: its effect on the performance of a motor 
co-ordination test. Brit. J. industr. Med., 1945, 2: 154— 
157. [P] 
F. HEAT DISEASE 
For general studies of heat disease, papers by the 
following should be consulted: Borden, Waddill, 
and Grier {1089) 1945; Conn {1091) 1940; Napier 
{1102) 1946; Reed and Harcourt {1103) 1941; 
Shattuck {1106) 1951; Talbott {1107) 1950; and 
Talbott, Dill, Edwards, Stumme, and Consolazio 
{1108) 1937. These authors divide heat disease 
into the following categories; (1) heat collapse or 
heat prostration, (2) heat exhaustion, (3) heat 
stroke, and (4) heat cramps. In heat prostration 
there is evidence of peripheral vascular collapse 
with poor venous return. There may be no rise in 
body temperature, and the symptoms are mainly 
those of hemodynamic failure. The patient may be 
anxious, the skin cold and clammy, the pupils 
dilated, and the blood pressure below normal. The 
condition is usually reversible. There is decrease of 
chloride in the urine, and in some cases a fall in 
the hemoglobin concentration. Such patients usually SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
are not in collapse long enough to require intra- 
venous administration of saline or whole blood, and 
administration of water and salt by mouth is con- 
sidered adequate therapy ordinarily. Heat exhaus- 
tion is characterized by weakness, lassitude, head- 
ache, dizziness, vomiting, mild cramps, sleepless- 
ness, rapid pulse, low blood pressure, and slight 
fever. The urinary chloride is low or absent. There 
may be fainting at work and psychological symp- 
toms. Peripheral vascular insufficiency is character- 
istic and the condition is described as akin to 
Addisonian crisis with diminution of extracellular 
fluid and sodum chloride reserve. There may be 
hemoconcentraton with elevated red and white 
blood counts. Treatment consists in removal of the 
patient from the surroundings causing the condition, 
regulation of diet and fluid intake, and replacement 
of fluid and salt. 
For reports on heat stroke, papers by the follow- 
ing should be consulted: Kirk {1097) 1946; Krai- 
ner {1098) 1949; Logue and Hanson {1099) 1946; 
Malamud, Haymaker, and Custer {1101) 1946; 
Schickele {1105) 1947; Waterlow {1109) 1947; 
and Wright, Repport, and Cuttino {1111) 1946. 
In heat stroke there is rise of body temperature 
and symptoms related to organic changes, especially 
in the nervous system. Krainer {1098) 1949 has 
drawn attention to severe degeneration of Purkinje 
cells with a picture of atrophy of the cerebellum in 
a case of fatal heat stroke with hyperpyrexia. This 
patient described by Krainer survived the hyper- 
pyrexial attack for 19 days in a state of unconscious- 
ness and coma. Logue and Hanson {1099) 1946 
have reported jaundice believed to be due to the 
toxic effect of the hyperpyrexia. The electrocardio- 
graphic changes are noted as confusing and similar 
to those of pericarditis, but without an elevation of 
the ST-segment. The report of Malamud, Hay- 
maker, and Custer {1101) 1946 is based on a study 
of 125 fatal cases of heat stroke which occurred in 
the U.S. Army during the summer months of 1941 
to 1944 in military installations in the Southern 
States. Soldiers were undergoing strenuous mus- 
cular exercise at high environmental temperatures. 
Lack of sufficient acclimatization seems to have 
been a predisposing factor. The clinical data estab- 
lished three categories of signs and symptoms: (1) 
those due primarily to hyperthermia, namely, mani- 
festations of the central nervous system, (2) those 
due secondarily to shock, and (3) those due to com- 
plications, such as bronchopneumonia, and lower 
nephron nephrosis arising during the illness. Some 
cases were of acute onset with early persistent coma 
or delirium. In other cases coma was the presenting 
symptom at the onset with remission or late relapse. 
In some cases the onset was insidious with a pro- 
gressive course and late development of coma. The 
duration of the disorder varied from less than an 
hour to 12 days. In 30 percent of the cases the illness 
lasted more than 24 hours. In the authors’ cases 
the most frequent laboratory findings were early 
development of leukocytosis, hemoconcentration, 
rise in the nonprotein nitrogen, and a decrease in 
the carbon dioxide combining power. Pathological 
changes in the central nervous system consisted of 
progressive degeneration of neurons with gliosis in 
the cerebellum, cerebral cortex, and basal ganglia, 
but not in the hypothalamus. There were also con- 
gestion, edema, and petechial hemorrhages. The 
hemorrhages occurred in a wide variety of struc- 
tures, regardless of the duration of the illness, and 
were seen especially in the lungs. According to the 
authors the clinical, laboratory, and pathological 
findings indicate two factors operative in heat 
stroke—hyperthermia and shock. It would seem that 
increased body temperature imparts to the disorder 
a specific character, affecting body tissues to varying 
degrees. The hypothesis is advanced that heat irre- 
parably damages the thermostatic function of the 
hypothalmus and that as a consequence the auto- 
nomic nervous system is no longer capable of re- 
establishing sweating or adequate peripheral cir- 
culation. Where anoxic anoxia or other conditions 
are combined with severe shock, the same sequence 
of clinical events may follow. The authors believed 
that although shock plays a significant part in heat 
stroke it is a secondary event and nonspecific. Pur- 
puric manifestations of heat stroke have been de- 
scribed by Wright, Repport, and Cuttino (1111) 
1946. Determinations of prothrombin time and 
platelet counts were made on 12 patients critically 
ill with heat stroke. It was concluded that the 
hemorrhagic phenomena associated with heat stroke 
are due to increase in capillary porosity and decrease 
in prothrombin and/or platelets. The prothrombin 
deficiency was thought to be secondary to hepatic 
damage. Early transfusions of whole blood and 
means to prevent or retard damage to the liver were 
considered as possibly of value in treating those 
patients who survive the first few hours. 
Although the pathogenesis of heat cramps is to 
some extent puzzling, it appears certain that the 
condition is due to excessive perspiration and resto- 
ration of fluids by drinking pure water so that 
chlorides lost in perspiration are not replaced. 
Heavy physical exertion in a hot environment is 
the predisposing factor. Heat is more important 
than humidity, and the condition is less likely to 
occur in environmental temperatures below 100° F. 
than those above. Vomiting is a further predis- HEAT AND HUMIDITY—HEAT DISEASE 
1089-1110 
posing factor since there may be additional loss in 
this way of chloride in the gastric contents. The 
skin may be pale and wet with perspiration, but 
signs or symptoms of shock are not usually present. 
The mortality rate is negligible. The principal 
symptom consists of muscle spasms in which the 
muscles may contract to a state of boardlike rigidity 
with agonizing pain. The cramps usually occur in 
muscles which are most used and may commence 
during or after work. The muscles of the fingers, 
forearms, arms, legs, pelvic girdle, and abdomen 
may be particularly affected. The involuntary 
muscles are spared. When the contraction passes, 
the pain is immediately relieved, but the muscles 
remain tender. The spasms may be reinitiated by 
active movements, trauma, or cold drafts on the 
body. There may be only a slight diminution in 
urinary output, but there is a decreased concen- 
tration of sodium and chloride in the serum and in 
the urine. In fact, chloride may be entirely absent 
in the urine. Plasma protein, potassium, phos- 
phorus, and calcium are increased, and there may 
be some hemoconcentration with increase in the 
red blood count. The cramps are relieved by re- 
placement of sodium and chloride as well as fluids. 
However, the replacement of fluids is considered 
of secondary importance. Relief of symptoms by 
sodium and chloride supports the hypothesis that 
the etiology of heat cramps relates to body de- 
pletion of essential electrolytes. Treatment consists 
of copious saline drinks of intravenous or rectal 
administration of saline solution if necessary. 
Morphine has been recommended for cramps, but 
some authors consider that morphine in therapeutic 
doses in severe cramps is not effective. Prevention 
of heat cramps may be successfully attained by 
administration of water containing salt tablets, 
from 10 to 30 grains of sodium chloride to each 
pint of water. Fleischmann {1095) 1947 has re- 
ported relief of pain in cramps from excessive water 
loss by active movement of antagonists of cramped 
muscles or passive movement of the limb in the 
direction opposed to that of the contracted muscle’s 
action. 
For further reports on heat disease, papers by 
the following may be referred to: Brown {1090) 
1947; Consolazio, Pecora, and Tusing (1092) 
1947; Daily and Harrison {1093) 1948; Fergusson 
{1094) 1948; Heilbrunn, Harris, Le Fevre, Wilson, 
and Woodward {1096) 1946; McCarthy {1100) 
1943; Rosenbaum {1104) 1946; and Weaver 
{1110) 1948. 
1089. Borden, D. L., J. F. Waddill, and G. S. Grier. 
Statistical study of 265 cases of heat disease. J. Amer. med. 
Ass., 1945, 128: 122-1205. 
1090. Brown, A, H. Dehydration exhaustion, pp. 208- 
225 in: Physiology of man in the desert. Edited by E. F. 
Adolph and Associates. New York, Interscience Publishers, 
Inc., 1947, 357 pp. [P] 
1091. Conn, J. W. The effects of heat. pp. 664 (I) — 
664 (16-12) in: Oxford medicine, Vol. IV, Part III. 
Edited by H. A. Christian. New York, Oxford University 
Press, 1940. [R] 
1092. Consolazio, W, V., L. J. Pecora, and T. Tusing. 
A slow dissolving, nonirritating salt tablet for use in hot 
environments. /. industr. Hyg., 1947, 29: 347-350. [P] 
1093. Daily, W, M. and T. R. Harrison. A study of the 
mechanism and treatment of experimental heat pyrexia. 
Amer. J. med. Sci., 1948, 215: 42-55. [P] 
1094. Fergusson, A. 6. Dermatological problems in 
tropical and sub-tropical areas, pp. 275-293 in: Modern 
trends in dermatology. Edited by R. M. B. MacKenna. New 
York, Paul B. Hoeber, Inc., 1948, 432 pp. 
1095. Fleischmann, S. Cramp and salt balance. Lancet, 
1947, 2: 492. 
1096. Heilbrunn, L. V., D. L. Harris, P. G. le Fevre, 
W. L. Wilson, and A. A. Woodward, Heat death, heat 
injury, and toxic factor. Physiol. Zool., 1946, 19: 404- 
429. [P] 
1097. Kirk, J. B. Heatstroke and sunstroke. Practitioner, 
1946, 157: 107-113. [R] 
1098. Krainer, L, Lamellar atrophy of the Purkinje 
cells following heat stroke. Arch. Neurol. Psychiat., Chi- 
cago, 1949, 61: 441-444. [CH] 
1099. logue, R. B. and J. F. Hanson. Electrocardio- 
graphic changes following heat stroke; report of a case. 
Ann. intern. Med., 1946, 24: 123-127. 
1100. McCarthy, L. Tropical mycoses. /. Amer. med. 
Ass., 1943, 123: 449-454. 
1101. Malamud, N., W. Haymaker, and R. P. Custer. 
Heat stroke. Milit. Surg., 1946, 99: 397-449. [CH] 
1102. Napier, 1, E. Diseases due to the direct effects 
of a tropical climate, pp. 34-51 in: The principles and 
practices of tropical medicine. New York, The Macmillan 
Company, 1946, 917 pp. 
1103. Reed, J. V. and A, K. Harcourt. Abnormalities 
of temperature. Excessive degrees of heat causing general 
disturbances, pp. 101-106 in: The essentials of occupa- 
tional diseases. Springfield, Charles G. Thomas, 1941, 
225 pp. 
1104. Rosenbaum, L. Significance of salt (NaCl) in 
torrid temperatures. Milit. Surg., 1946, 98: 43-47. [P] 
1105. Schickele, E. Environment and fatal heat stroke. 
An analysis of 157 cases occurring in the army in the U. S. 
during World War II. Milit. Surg., 1947, 100: 235-256. 
1106. Shattuck, 6, C. Acute effects of heat. pp. 729- 
740 in: Diseases of the tropics. New York, Appleton-Cen- 
tury-Crofts, Inc., 1951, 803 pp. [R] 
1107. Tolbott, J. H. Heat: pathologic effects, pp. 406- 
409 in: Medical physics. Volume II. Edited by Otto 
Glasser. Chicago, The Year Book Publishers, Inc., 1950, 
1227 pp. [R] 
1108. Talbott, J, H., D. B. Dill, H. T. Edwards, E. H. 
Stumme, and W. V. Consolazio. The ill effects of heat 
upon workmen. J. industr. Hyg., 1937, 19: 258-274. 
1109. Waterlow, J. C. Heat-stroke and heat-exhaustion 
in Iraq. Brit. med. Bull., 1947,5: 3-4. 
1110. Weaver, W. L. The prevention of heat prostration 
by use of vitamin C. Sth. med. J., Birmingham, 1948, 41: 
479-481. J. industr. Hyg., 1949, 31: abstract section; 
69-70. [P] SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
1111. Wright, D. 0., I. B,, Reppert, and J. T. Cuttino. 
Purpuric manifestations of heat-stroke. Studies of pro- 
thrombin and platelets in twelve cases. Arch, intern. Med., 
1946, 77: 27-36. 
G. SKIN DISEASES ASSOCIATED WITH HEAT AND 
HUMIDITY 
A number of affections of the skin may provide 
a hazard under conditions of military operations in 
hot climates or submarine action in tropical waters 
without adequate air conditioning and ventilation. 
For a consideration of common skin diseases of the 
tropics, a report by Napier {1120) 1946 should be 
consulted. Probably the most important and wide- 
spread of these skin conditions is prickly heat or 
heat rash, formally designated miliaria rubra. 
Prickly heat occurs in all tropical and many sub- 
tropical countries, especially during periods of high 
humidity. It is stated to be more common in newly 
arrived white men, and is more severe in infants 
and children than in adults. It is more common in 
men than in women and in thick-set individuals 
than in spare, thin persons. It appears to occur 
more usually in blond, fair-skinned people than in 
those with darker complexions and is more pro- 
nounced in obese subjects. Failure to bathe or 
change the clothes regularly may predispose towards 
prickly heat. The condition occurs on parts of the 
body where clothes are held in close contact by 
pressure, particularly around the waist and 
shoulders. Friction from clothes, especially in the 
groin, axilla, and backs of the wrists, may aggravate 
the condition. It occurs commonly in those areas 
where two skin surfaces are in continuous contact, 
as between folds of fat. The lesion consists of red 
papules and minute clear vesicles with a surround- 
ing red halo. The skin has a red granular appear- 
ance with a rough texture. Later there may be a 
white powdery desquamation. Factors causing hy- 
peremia of the skin, such as exercise or a hot bath, 
may result in an immediate exacerbation of the 
pricking sensation and the intolerable itching which 
is characteristic. The symptoms may be so insistent 
as to dominate the attention of the sufferer and 
interfere with sleep and performance of duty. From 
a series of clinical observations on a large group of 
naval officers, Fay and Susman {1115) 1945 con- 
cluded that the following factors increase liability 
to prickly heat: (1) age over 30, (2) fair skin, (3) 
highly strung emotional makeup, (4) large salt in- 
take, (5) working and sleeping below decks, (6) 
high temperatures in the work place, (7) long work- 
ing hours, and (8) battle dress or poorly ventilated 
clothing. It was stated by the authors that person- 
nel belonging to group O may have a greater pre- 
disposition to heat rash than those in other blood 
groups. The following factors were said to reduce 
liability: (1) age below 30, (2) previous suntan, 
(3) loose clothing, (4) working and sleeping in 
open air, (5) low temperature of the work place 
and, as a possible factor, (6) membership in blood 
group A. The following factors were listed as not 
affecting incidence: (1) weight, (2) sweat reac- 
tion, (3) open-neck shirts, and (4) effects of sun 
on the skin. Inconclusive factors listed included 
type of work, humidity, and brands of soap used. 
Sulzberger and Emik {1134) 1946 reported that 
66 percent of personnel of a research group on 
Guam suffered from prickly heat. These authors 
also indicated that the incidence of the condition 
was greater in blond, fair-skinned people or in red- 
headed persons than in others. They likewise re- 
ported no difference in incidence between over- and 
under-weight persons. Those who were working in 
particularly hot, humid spaces, as in the laundries 
or the kitchens, had no higher incidence than other 
members of the group, but the eruptions in the 
group working in the laundries and kitchens were 
longer lasting and more disagreeable. Work for 8 
hours in an air-conditioned environment during a 
24-hour day reduced the incidence. Prickly heat was 
found not to be related to race or former habitat. 
Sulzberger and Zimmerman {1135) 1946 observed 
that patches of prickly heat exhibited a reduction 
or absence of sweating as compared with normal 
areas of skin. Homy plugs were seen in the sweat- 
duct orifices, and edema was found around the ducts 
in the epidermis and upper corium. There was also 
periductal cellular infiltration. The acini of the 
sweat glands were found to be morphologically al- 
tered. These authors advanced the hypothesis that 
profuse sweating leads to maceration of the skin’s 
surface, faulty keratinization, occlusion of the sweat 
pores by horny plugs, and irritation of the tissues by 
substances derived from concentrated or retained 
sweat in the orifices and superficial portions of the 
ducts. This chain of events was believed to consti- 
tute the pathological process in the production of 
prickly heat. 
An experimental study of heat rash in volunteer 
subjects has been reported by Duffner {1114) 1946. 
Subjects carried out work 7 hours a day at a dry- 
bulb temperature of 108° F. (83° F. wet bulb, 
effective temperature 90° F.). They spent the re- 
maining 17 hours of the day in another room at a 
dry-bulb temperature of 95° F. (83° F. wet bulb, 
effective temperature 87° F.). Work consisted of 
walking on a treadmill. A similar group worked 7 
hours a day in the hot treadmill room, but spent HEAT AND HUMIDITY—SKIN DISEASES 
the remaining 17 hours in a temperature of 85° F. 
dry bulb (71° F. wet bulb, effective temperature 
78° F.). Each group carried out the program for 
10 days. All of the subjects in the “hot group” de- 
veloped heat rash, covering an average of 39 percent 
of the skin surface. One-half of these men com- 
plained that they were unable to sleep due to dis- 
comfort. Only one man in the “cool group” de- 
veloped heat rash, and in this case only 15 percent 
of the body surface was involved. In a further 
experimental series a “hot group” spent 3 hours a 
day in the hot treadmill room and the remaining 
21 hours in hot quarters. A “cool group” spent 3 
hours a day in the hot treadmill room, 9 hours a day 
in hot quarters, and 12 hours in cool quarters. 
These conditions were maintained for 30 days. 
Eleven out of 18 of the “hot group” developed heat 
rash as early as the third day in the hot atmosphere, 
with maximum severity on the 9 th to 13 th day. 
The “cool group” did not have heat rash. The 
author concluded that spending as little as 12 hours 
a day in an atmosphere in which one does not sweat 
at rest will prevent the occurrence of heat rash. 
Blum, Gersh, and Spealman {1113) 1945 have 
reported that heat rash is a rapidly reversible condi- 
tion, at least during the first week of exposure to hot 
environments. In these studies, exposure to ultra- 
violet radiation before entering the hot environ- 
ment inhibited the development of heat rash in all 
5 subjects of 1 experiment, but not in any of 6 sub- 
jects in another, a discrepancy not easily explained. 
Cold baths appear to have a slight ameliorating 
effect on the rash. Neither pressure nor friction, nor 
the inhibition of sweating by formalin, prevented 
the development of heat rash. Increase in white 
blood cell counts with relative lymphocytosis was 
observed in all 6 participants in 1 experiment in 
which blood counts were made. Change in pH of the 
sweat was not found to be associated with heat rash. 
There was no change in elasticity of the skin, in 
the rate of histamine wheal formations, or saline 
wheal disappearance in association with heat rash. 
Shelley and associates have reported a series of 
studies in which heat rash has been produced ex- 
perimentally in man. In the first report of this 
series, Shelley, Horvath, Weidman, and Pillsbury 
{1131) 1948 brought about local anhidrosis and 
sweat retention vesicles by a single treatment of the 
skin with iontophoresis. It appeared that a minor 
superficial epidermal injury was produced, not di- 
rectly affecting the acini of the sweat gland, with 
a resultant hyperkeratosis which led to a transitory 
sweat-duct obstruction. This resulted in local sweat 
retention anhidrosis and vesicles containing sweat. 
Various kinds of experimental stimulation were 
found by Shelley, Horvath, Weidman, and Pills- 
bury {1130) 1948 to be effective in the production 
of experimental heat rash in human subjects. These 
were: (1) iontophoresis, (2) ultraviolet light, (3) 
heat, (4) carbon dioxide ice, (5) maceration, 
(6) adhesive tape, (7) aluminum chloride, (8) 
soap, (9) phenol, and (10) chloroform. No im- 
mediate alteration was noted in the normal sweat- 
ing processes when the subjects were stimulated to 
vigorous sweating by means of heat. However, 
within 3 to 5 days definite changes were observed 
within the areas of the skin treated. They varied 
from slight to striking anhidrosis; in the areas of 
greatest anhidrosis, small, clear, superficial vesicles 
developed. These vesicles did not appear in areas 
in which the secretion of sweat was locally inhibited 
by atropine. These phenomena could be demon- 
strated repeatedly over a period of 1 to 2 weeks, 
after which the sweat function returned to normal. 
Microscopic studies revealed tiny plaques of hyper- 
keratosis in the treated areas. The vesicles were 
found to be situated entirely within the stratum 
corneum, and serial sections demonstrated that 
they were directly connected with the sweat ducts. 
It was concluded by the authors that the factor 
common to all stimuli applied was that of minor 
irritation, and the plugging of the sweat-gland 
orifices. These studies have also been reported by 
Shelley and Horvath {1127) 1950. In a further 
report Shelley and Horvath {1128) 1950 indicated 
that three separate factors are essential in the 
pathogenesis of experimental heat rash: (1) a 
minor epidermal injury, (2) intensive sweating for 
several hours, and (3) individual susceptibility. 
Alone, none of these factors was found to be suf- 
ficient. In a susceptible subject, hyperkeratotic 
plugging of the sweat duct results in sweat retention 
following which a single heat exposure of several 
hours leads to disorganization of the upper end 
of the sweat duct due to pressure of the entrapped 
sweat. Shelley {1126) 1951 distinguished four dis- 
tinct types of sweat retention which could be experi- 
mentally identified: (1) collection of sweat in a 
papulovesicle in the stratum corneum, (2) col- 
lection of sweat in an intramidepidermal papulo- 
vesicle, (3) collection of sweat in a dermal papulo- 
vesicle just beneath the epidermis, and (4) simple 
retention of sweat within the dermis without any 
clinical signs or symptoms. 
Sulzberger, Zimmerman, and Emerson {1136) 
1946 have inferred that ordinary prickly heat and 
tropical anhidrotic asthenia are different manifesta- 
tions of the same fundamental process. Distention 
291222—54 8 SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
and changes of pressure due to secretion of sweat 
into the plugged ducts contribute to the sensory 
disturbances in prickly heat, and these symptoms 
vanish in tropical anhidrosis following the relief of 
tension through rupture or other kinds of damage 
of the ducts and free drainage of sweat into the 
surrounding area. O’Brien {1121) 1947 has ad- 
vanced the suggestion that heat rash is a manifesta- 
tion of sebaceous deficiency of the skin, mainly the 
result of the many lipoid-depriving influences that 
act upon the skin from without. The stratum cor- 
neum, when deficient in lipoid, becomes the ob- 
structing agent plugging the sweat gland. The value 
of keratolytic substances in removing the keratin 
plugs produced in heat rash is stressed. The author 
recommended a routine of skin hygiene in the 
tropics designed to reduce lipoid deprivation of the 
skin to a minimum. In a discussion of tropical anhi- 
drotic asthenia, O’Brien {1122) 1948 pointed out 
that miliaria (heat rash) is distinguished by malaise, 
distaste for work, excessive fatigue, and loss of ac- 
climatization. Particularly there are asthenic symp- 
toms, exhaustion, headache, dyspnea, and giddiness 
when working in the heat. Also, after exercise there 
may be gross cardiorespiratory distress and an anhi- 
drosis on the covered areas of the body. The body 
temperature does not rise as high as could be ex- 
pected. The author postulated that the symptoms 
result from circulatory failure of a peripheral type. 
Miliaria predisposes toward hyperpyrexia. By caus- 
ing an increase in the sodium chloride concentration 
in the sweat miliaria may predispose toward heat 
exhaustion. Ladell {1118) 1951 found that an other- 
wise healthy subject on recovery from miliaria 
exhibited a diminished tolerance to heat and an 
increased rate of sodium chloride loss in the sweat, 
compared with figures on the same subject obtained 
before prickly heat had developed. 
Heat rash is easier to prevent than to cure. Under 
conditions of combat operations in the tropics it may 
be a cause of many lost man-days as well as a source 
of great annoyance and discomfort. It also imposes 
a heavy burden upon the medical department at an 
inopportune time. As Ribble, Luedemann, and Pea- 
body {1124) 1947 have stated, the most effective 
means of preventing heat rash is the provision of a 
suitable environmental temperature. Air condition- 
ing in the submarine will eradicate the condition. 
Reassignment of bunks should be effected when pos- 
sible to enable men working in hot places or per- 
forming heavy physical work to sleep in the coolest 
part of the vessel. Auxiliary precautions consist of 
the judicious use of electric fans, avoidance of very 
hot baths, frequent changes of underwear and other 
clothing, and avoidance of local overtreatment. It 
should be stressed that adequate air conditioning, 
in addition to its many other values, is effective 
prophylaxis against this condition which is so costly 
in its lowering of morale and overall efficiency of the 
crew. For further studies on treatment of heat rash 
the following references may be consulted: {1117, 
1123, and 1137). Attention may be particularly 
directed to a statement by Horne and Mole {1117) 
1950 that prickly heat is relieved by increasing fluid 
intake and by reducing salt intake. It can be made 
to relapse by increasing the intake of table salt. 
Radclyffe {1123) 1947 has recommended the use 
of benadryl to alleviate, but not cure, prickly heat. 
Within a period of several hours after taking 100 
mg. of benadryl there is a blanching of the affected 
area and relief from itching. After 1 or 2 days of 
taking benadryl there is stated to be a complete 
remission of symptoms. 
For a description of athlete’s foot (trichophytosis, 
epidermophytosis, Hong Kong foot, tinea pedis) 
an article by Napier previously referred to {1120) 
should be consulted. This condition is more wide- 
spread and serious in humid tropical environments 
and under conditions of naval operations on hot 
decks. The etiological organism is a fungus usually 
of the Trichophyton species. It may also be caused 
by Epidermophyton floccosum and by Candida 
albicans. The organisms penetrate the epidermis and 
the primary site is usually between the fourth and 
fifth toes. The condition spreads to other inter- 
digital spaces and to the soles of the feet, the dorsum 
and other sites on the feet, ankles, and nail beds. 
There are small vesicles surrounded by a halo of 
inflammation. Pieces of sodden epithelium separate, 
exposing the red corium. There may be bleeding as 
a result of scratching and the lesions may become 
infected with pyogenic micro-organisms. There may 
be areas of hyperkeratosis at the margins of the 
lesions. Serious cellulitis is a potential hazard. Pre- 
vention consists in avoiding infection by using 
washable slippers in shower quarters, by not going 
barefoot on wet floors, and not using towels and 
slippers in common. Changing the socks twice daily 
and washing the socks thoroughly may be helpful 
in reducing the seriousness of the condition. 
Hygiene of the feet is important; after washing they 
should be carefully dried and may be dusted with 
antiseptic powder. Several preparations for local 
application have been recommended, but it should 
be pointed out that the greatest danger is overtreat- 
ment. It is perhaps best to be content to keep the 
conditions inactive. 
Furunculosis may be present in submarine per- 
sonnel under conditions of operation. Reference is COLD EXPOSURE PROBLEMS—GENERAL CONSIDERATIONS 
1112-1138 
made to reports by the following: Barnes (1112) 
1943; Gant, Owens, and Schwartz (1116) 1942; 
Liles {1119) 1947; and Sukhtankar {1132) 1949. 
The paper by Gant, Owens, and Schwartz {1116) 
1942 discusses an epidemic of boils in a group of 
tunnel workers. This investigation reveals that the 
outbreak of boils was related to a combination of 
factors bringing about a lowering of skin resistance 
to bacteria. The causes of the outbreak were related 
to the humid atmosphere, perspiration, warm tun- 
nel water, friction from clothes and rubber coats 
infiltrated with rock dust, together with the unhy- 
gienic conditions of the tunnel, and the unsanitary7 
and dirty state of the working clothes. 
According to Sulzberger, Addenbrooke, Joyce, 
Greenberg, and Mack {1133) 1946, a varient of 
acne vulgaris had a high incidence and was a great 
cause of discomfort and loss of effectiveness among 
military personnel in the tropics. This form of acne 
differed from adolescent acne vulgaris in several 
significant respects, particularly age of onset, locali- 
zation, and course. It was found to be brought on 
or made worse by heat and high humidity, and 
tended to improve when the patients are removed 
to a cool, dry environment. Occlusion of the ducts 
of hyperactive sebaceous glands seems to be the 
essential pathological process. 
For further reports on skin diseases associated 
with heat and humidity, the following are listed: 
Robertson {1125) 1945, and Shelley, Horvath, and 
Pillsbury {1129) 1950. 
1112. Barnes, B. Furunculosis-etiology and treatment. 
J. din. Endocr., 1943,3: 243-244. [CH] 
1113. Blum, H., F. I. Gersh, and C. R. Spealman. 
Studies of experimental heat rash, U. S. NMRI. Project 
X-479, Kept. no. 1, 27 December 1945, 10 pp. [P] 
1114. Duffner, G. J. Heat rash as a problem in the 
naval service. Amer. J. trap. Med., 1946, 26: 539-541. 
1115. Pay, F. R. and E. Susman. On the prickly heat. 
Med. J. Aust., 1945,2: 453^156. 
1116. Gant, J. W., R. J, Owens, and L. Schwartz. An 
epidemic of boils in a group of tunnel workers Publ. Hlth. 
Rep., Wash., 1942, 57; 612-617. 
1117. Horne, G. 0. and R. H. Mole. The effect of water 
and salt intake on prickly heat. Lancet, Lond., 1949, 2; 
279-281. Abstr. World Med., 1950, 7; 295. [P] 
1118. Ladell, W. S. S. Changes in sweating after prickly 
heat. Brit. med. J., 1951, 1: 1358-1360. [CH] 
1119. Liles, J. H. The local treatment of furuncluosis 
with penicillin. U. S. nav. med. Bull., 1947, 47: 645-650. 
[CH] 
1120. Napier, L. E. Some common skin diseases of the 
tropics, pp. 570—585 in: The principles and practice of 
tropical medicine. New York, The Macmillan Co., 1946, 
917 pp. 
1121. O’Brien, J. P. A study of miliaria rubra, tropical 
anhidrosis and anhidrotic asthenia. Brit. J. Derm. Syph., 
1947, 59: 125-158. 
1122. O’Brien, J. P. Tropical anhidrotic asthenia. 
Arch, intern. Med., 1948, 81: 799-831. [R] [D] 
1123. Radclyffe, L. Alleviation of prickly heat. Brit. 
Med. J., 1947, 2; 1012. [D] 
1124. Kibble, G. B., W. S. Lnedemann, and S. M. 
Peabody. Epidemic of prickly heat on aircraft carrier. 
Nav. med. Bull., Wash., 1947, 47: 77-82. 
1125. Robertson, A. M. Prickly heat and tropical pem- 
phigus. J. R. nav. med. Serv., 1945, 31: 258-260. 
1126. Shelley, W. B. Experimental miliaria in man. 
IV. Sweat retention vesicles following destruction of termi- 
nal sweat duct. J. invest. Derm., 1951, 16: 53-64, 
1127. Shelley, W. B, and P. N. Horvath. Experimental 
miliaria in man. II. Production of sweat retention anidrosis 
and miliaria crystallina by various kinds of injury. /. 
invest. Derm., 1950, 14: 9-20. 
1128. Shelley, W. B. and P. N. Horvath. Experimental 
miliaria in man. III. Production of miliaria rubra (prickly 
heat). /. invest. Derm., 1950, 14: 193-204. 
1129. Shelley, W. B., P. N. Horvath, and D. M. Pills- 
bury. Anhidrosis; An etiologic interpretation. Medicine, 
Baltimore, 1950, 29: 195-224. 
1130. Shelley, W. B., P. N. Horvath, P. D. Weidman, 
and D. M, Pillsbnry. Experimental miliaria in man. 
I. Production of sweet retention anidrosis and vesicles by 
means of iontophoresis. /. invest. Derm., 1948, 11: 275- 
291. 
1131. Shelley, W. B., P. N. Horvath, P. D. Weidman, 
and D. II. Pillsbnry. Experimental miliaria in man. 
II. Production of sweat retention anidrosis and vesicles by 
various kinds of injury. Amer. J. Physiol, 1948, 155: 469. 
1132. Sukhtankar, K. M. A new treatment of furun- 
culosis with whole liver extract. /. Indian med. Ass., 1949, 
18: 245-246. 
1133. Suzberger, M. B., E. F. Addenbrooke, S. J. Joyce, 
S. Greenberg, and A. G. Mack. Tropical acne. Nav. med. 
Bull., Wash., 1946, 46: 1178-1184. 
1134. Sulzberger, M. B. and L. 0. Emik. Studies on 
prickly heat. I. Clinical and statistical findings. J. invest. 
Derm., 1946, 7: 53-60. 
1135. Sulzberger, M. B. and H. M. Zimmerman. 
Studies on prickly heat. II. Experimental and histologic 
findings. /. invest. Derm., 1946, 7; 61-68. 
1136. Sulzberger, M. B., H. M. Zimmerman, and K. 
Emerson. Tropical anidrotic asthenia (thermogenic an- 
hidrosis) and its relationship to prickly heat. /. invest. 
Derm., 1946, 7: 153-164. 
1137. H. S. Navy, Technical mission to Japan. Heat 
rash and fungus infection, p. 43 in: Aero, surface, and 
submarine medicine and research in the Japanese navy. 
Fascile M-l, Ter get M-06, 4 September 1945, 72 pp. 
1138. Anon. Prickly heat and tropical asthenia. Brit. 
Med. ]., 1947,2; 779. [D] 
VI. COLD EXPOSURE PROBLEMS 
A. GENERAL CONSIDERATIONS OP COLD 
In the compilation of references on cold exposure 
problems, the usefulness of these references as source 
material for the section on clothing (p. 284) has 
been kept in mind. In submarine operations, the 
cold problems are somewhat different from those 
encountered in surface ships in that conditions of 1139-1150 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
dampness as well as cold may prevail. Heating of 
surface vessels presents less of a problem, but the 
special conditions of submerged operations of sub- 
marines may make it difficult to adequately heat 
submarine compartments operating in Arctic 
waters. When the submarine is submerged, the only 
source of power is the batteries, and this power 
must be conserved for propulsion and other im- 
portant engineering functions. Snorkel operations 
and use of atomic power modify the heating situa- 
tion. Submarine crews encountered cold and wet 
weather on the deck, and cold exposure problems 
also come into the picture in connection with sub- 
marine rescue of survivors at sea. The following 
have prepared general reports which will serve to 
introduce the reader to the subject of physiological 
and pathological effects of cold: Brobeck {1141) 
1946; Josiah Mach, Jr., Foundation {1145a) 1952; 
Talbott {1149) 1940; and Weiner {1150) 1949. 
1139. Benitte, A. C. La guerre et le froid. Etude sur 
le comportement de 1’homme aux basses temperatures. 
Ministere de la Guerre. Du Bulletin d’Information Tech- 
nique et Scientifique. N 21 /G et N 22G, 1948. [D] 
1140. Brandis, H. J. von. General and local cold injury 
in war. U. S. AAF. Aero medical center. HQ. 3D. 
Central medical establishment, APO0172. Translated 25 
November 1946, 38 pp. 
1141. Brobeck, J. B. Physiology of heat and cold. Anna. 
Rev. Physiol, 1946, 8: 65-88. [R] 
1142. Gt. Brit. MRC—RNPRC, HS. Military require- 
ments for research into the effects of cold climates on 
man. R. N. P. 48/424, H. S. 223, January 1948, 3 pp. 
1143. Gt. Brit. MRC-RNPRC, HS. Memorandum on 
research problems into effects of cold environment. 
R. N. P. 48/423, H. S. 222, 10 June 1948, 4 pp. 
1144. Johnson, R. E., and C. G. Bly. Metabolic changes 
in heat acclimatized men during abrupt exposure to a 
very cold climate. /. din. Invest., 1949, 28: 792. Abstr. 
1145. McCollum, E. L. Survey of human adjustment 
problems in the northern latitudes. Morale survey of 
Alaskan air command. USAF. Ladd air force base, Alaska. 
Arctic aeromedical laboratory. Project 21-01-022, Pro- 
gram C, part 1-C, 1 August 1950, 12 pp. [P] 
1146. Metz, B. L’homme et le froid. Strasbourg-mid., 
1950, 1: 303—321. Excerpta Medica. Section II. (Physi- 
ology, Biochemistry, and Pharmacology), 1951, 4: 758. 
[R] 
1147. Park, R. G. Disorders due to cold. /. industr. 
Hyg., 1946,28: abstract section: 28. 
1148. Pugh, L. G. C. Physiological studies in H. M. S. 
Vengeance: Royal Navy cold weather cruise, 1949. Gt. 
Brit. MRG-RNPRG, CES. R. N. P. 49/561, C. E. S. 306, 
September 1949, 44 pp. [P] 
1149. Talbott, J. H. The effect of cold. pp. 664 
(20-1)—664 (20-45) in: Oxford medicine, Vol. IV, 
Part III. Edited by H. A. Christian. New York, Oxford 
University Press, 1940. [R] 
1150. Weiner, J. S. Progress report on Arctic cruise 
1949. Gt. Brit. MRG-RNPRC, CES. R. N. P. 49/508, 
C. E. S. 281, 1 February 1949, 5 pp. 
B. PHYSIOLOGICAL EFFECTS OF COLD 
For general studies on the physiological effects of 
cold, the reader is referred to papers by Nei and 
Tada {1197) 1950; Pugh {1199) 1950; Radsma 
{1200) 1950; and U. S. NRG {1215) 1943. In 
Radsma’s studies, normal human subjects remained 
for a whole morning either in an ordinary tropical 
room with an average dry-bulb temperature of 29° 
G. and a relative humidity of 70 percent, or in a 
cool room with a dry-bulb temperature of 22 to 24° 
C. and a relative humidity of 65 to 70 percent. It 
was found that the metabolic rate was depressed in 
the cool room and that body temperature fell. Un- 
der conditions of cold there was an increase in the 
volume of urine excreted with increased excretion 
of sodium and chloride. The pulse rate was higher 
in the warm room, but there were only slight 
changes in arterial blood pressure, oxygen satura- 
tion of the blood, and minute volume of circulation. 
In the cool room there was at first a slight increase 
in respiratory rate and alveolar carbon dioxide ten- 
sion, but no significant difference in the pH of the 
blood or urine. 
Numbness and pain in the extremities constitute 
a complicating hazard of cold. In a report of experi- 
ments carried out on 40 subjects at Fort Churchill, 
Mackworth {1189) has stated that there was much 
greater numbness in the subjects at temperatures 
between —30° and —35° C. than at —25° to —30° 
C. At these temperatures a wind velocity of greater 
than 6 miles an hour increased the loss of tactile 
discrimination and enhanced the numbing of the 
fingers. In 1949, Kunkle {1188) reported a study of 
phasic pains induced in 24 adult subjects by cold. 
One hundred and fifty experiments were performed 
in which the digit of one hand was immersed in a 
large crock of ice water maintained at 0° C. Im- 
mersion continued from 20 minutes to 2 hours. 
Reports of pain intensity were given by the subjects 
at 20-second intervals. After 10 to 60 seconds, an 
aching pain was reported in the digit, rising to a 
peak by the end of second to fourth minute. Super- 
ficial anesthesia and analgesia was observed by the 
end of the fourth to seventh minutes and at about 
the tenth minute, the finger felt numb. Following 
this, sensibility returned with a second pain peak 
which then slowly subsided until the fifteenth to 
twentieth minute, all pain was gone. Following re- 
moval of the digit from the ice water, there was pain 
for approximately 2 minutes. Some subjects devel- 
oped a brief presyncopal reaction with giddiness, 
sweating, facial pallor, and bradycardia after the 
second pain peak. The author associates the first 
pain peak with cold and vasoconstriction. This first COLD EXPOSURE PROBLEMS—PHYSIOLOGICAL EFFECTS 
pain peak is attributed to direct injury of chilled 
tissues or nerves and may be mediated by a metabo- 
lite locally released. The second pain is believed to 
be associated with reactive vasodilatation and con- 
sequent warming with return of function in sensory 
nerves earlier paralyzed by cold. These phenomena 
are relevant to the unusual susceptibility to cold 
pain commonly observed in the digits of patients 
with Raynaud’s disease and in injured tissues 
with impairment of local circulation and deep 
hyperalgesia. 
Blaisdell {1160) 1951 has reported variations in 
pain and temperature sensation accompanying cold- 
induced cyclic vasodilatation in fingers exposed to 
cold air of 0°, 5°, and 10° C. In these experiments, 
the initially appearing sensations of increasing cold 
and pain were spontaneously relieved by sensations 
of relative warmth and complete abatement of pain 
with the occurrence of each vasodilatation wave. 
These profound sensory changes occurred not only 
when the body as a whole was warm but also when 
it was cold. In certain unpredictable instances, 
spontaneous rewarming of the finger during a 
vasodilatation wave proceeded to a complete loss of 
sensation in air temperatures of 0° and 5° C. Three 
types of pain related to cold were observed: (1) 
“First pain,” a dull pain of increasing severity oc- 
curring during objective and subjective cooling; 
(2) “Second pain,” a burning and throbbing pain 
observed in a few instances, occurring only after a 
preceding numbness due to severe cooling during 
early spontaneous rewarming while the finger re- 
mained exposed to cold; and (3) “Afterpain,” also 
burning and throbbing in character and experienced 
upon removal of the finger from the cold, and also 
after the numbness of frostbite during exogenous 
rewarming. This latter pain was relieved by cir- 
culatory arrest but returned with the restoration 
of blood flow. Blaisdell considered that the “first 
pain” is due to the direct affect of cold upon neural 
sensory mechanisms. “Second pain” was believed to 
result from the return of function to nerves para- 
lyzed by cold and to reactive vasodilatation. “After- 
pain” seemed mainly a consequence of the reactive 
vasodilatation of exogenous rewarming. It was sug- 
gested that steep, spatial, thermal gradients estab- 
lished by warm blood entering the cool finger may 
contribute to “second pain” and “afterpain.” 
In environmentally produced hypothermia of the 
unanesthetized rat, mouse, or kitten, there occurs a 
progressive descending paralysis of the central 
nervous system. Hamilton {1179) 1937 has reported 
in these animals the abolition of higher nervous 
functions, locomotion, voluntary movements, atti- 
tudes, equilibration, hearing, and vision. Following 
this, swallowing, biting, and comeal and flexor re- 
flexes are abolished. Finally, the medullary centers 
are affected with resultant respiratory failure and 
death. The responses which are the last to disap- 
pear are the first to recover. The manner of central 
nervous system involvement nad recovery indicates 
to the author the narcotizing nature of hypothermia. 
Even at body temperatures below 70° F. the 
homeothermic animal attempts to resume a normal 
level of body heat. In body temperatures so low 
that nervous reactions and other evidences of life 
may be indiscernible, the animal can remain alive 
and subsequently recover. 
The effects of exposure of human subjects to 
ambient temperatures from —50° to +117° F. 
upon reaction time have been reported by Coakley, 
Forlano, and Barmack {1164) 1948. The perform- 
ance measured was simple discrimination and 
choice reaction time. Performance was found not 
to vary significantly with low ambient temperatures, 
provided that the body generally and the responding 
member in particular was properly protected. 
During exposures for several days to temperatures as 
low as —20° F., clothing was found adequately to 
protect the body without interfering significantly 
with the speed of simple reaction. For periods of 
about an hour, current-type clothing provides ade- 
quate protection against ambient temperatures as 
low as —50° F. Conditions which reduce strength 
and dexterity of movement were found to leave 
reaction time unchanged. Moreover, the reaction 
time did not vary significantly with high ambient 
temperatures up to +117° F., provided the wet- 
bulb temperature did not exceed about 86° F. 
Some evidence indicated that the reaction time 
varies inversely with body temperature over a re- 
stricted range of body temperatures. Possibly when 
conditions are such that the ambient temperature 
results in an alteration of body temperature, changes 
in reaction time may be expected. These conclu- 
sions are of practical importance in relation to the 
duties of submarine personnel in that if it is neces- 
sary to expose personnel to extreme temperatures it 
may predict that they will be able to perform with 
essentially normal speed, provided the activities 
are restricted to those kinds of performance involved 
in the reaction time experiment. Experimental 
studies upon the effects of cold on the nervous sys- 
tem find practical application also in the use of 
hypothermia in the treatment of psychiatric dis- 
orders as reported by Spradley and Marin-Foucher 
{1209) 1949 and in the application of hypothermia 
in certain types of surgery. 
In profound lethal hypothermia due to cold, 
death may be a result of the direct effect of cold SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
upon the heart muscle as stated by Baetjer {1156) 
1951. Graybiel and Dawe {1176) 1948 have re- 
ported the case of a previously healthy young man 
who nearly perished from hypothermia as the result 
of accidental immersion in ice water. Auricular 
fibrillation was among the clinical findings. The au- 
thors suggested that a possible cause of fibrillation 
was a local disturbance within the auricles. The 
cardiovascular effects of brief periods of exposure of 
human subjects to low temperatures have been re- 
ported by Miller and Miller {1194) 1949. Sixteen 
male subjects ranging in age from 19 to 40 years 
were exposed to temperatures of 34° to —15° F. 
with no perceptible air movement. Clothing had an 
insulating equivalent of 1 do. Subjects were ex- 
posed for 20 minutes after sitting in a warm room 
at a temperature of 70° to 85° F. Adequate sleep 
and food before cold exposure in these experiments 
appeared to increase body tolerance. Hemoconcen- 
tration was demonstrated in over 75 percent of the 
experiments. A sudden exposure to cold of moderate 
to severe degree appeared to be a strong enough 
stimulation to cause the early mobilization of this 
protective response. The immediate reaction to cold 
was a rise in both systolic and diastolic arterial 
blood pressure, with an early fall in pulse rate. 
There is a considerable volume of literature deal- 
ing with the effects of low temperatures upon blood 
flow through the extremities. Spealman {1206) 
1944 has made blood volume flow measurements on 
the skin on the hand immersed in water at various 
temperatures. With water temperatures of 15° to 
20° G., there was minimal blood volume flow in the 
skin of the hand. Skin temperature measurements 
made at the same time indicated that the difference 
between skin and water temperature was minimal 
in immersion in water within these temperature 
ranges. The effect of increasing the ambient air 
temperature was to increase this temperature differ- 
ence, except possibly in the case of very cold water 
of 10° G. or below. The author concluded that blood 
flow through the extremities is greater at very low 
skin temperatures than it is at more moderate skin 
temperatures. Regarding the implication of these 
studies to the problem of immersion foot, Spealman 
felt that it would seem that factors other than ische- 
mia contribute to the development of this condition. 
Spealman also reported {1207) 1945 that at any 
given temperature of the hands, the colder the body 
the smaller will be the blood supply to the hands. 
Calculations from blood-flow determinations re- 
vealed that much more heat is supplied to very 
cold hands than to moderately cold hands, and that 
the warmer the body the greater amount of heat 
supplied to the hands. Rapaport,, Fetcher, Shaub, 
and Hall {1202) 1949 have also indicated that the 
regulation of blood flow to the extremities at low 
ambient temperatures is primarily determined by 
the thermal state of the body as a whole. They car- 
ried out experiments on four young adult males at 
controlled ambient temperatures of 0°, —20°, and 
— 30° F. in a cold room. Studies of the exposed bare 
hands revealed that the vasoconstrictor effects of 
severe cold is subordinate to autonomic control of 
blood flow in extremities, since the hand-skin tem- 
perature could be sustained above 70° F. There- 
fore, the temperature of the extremities can remain 
nearly independent of ambient temperature and of 
insulation over a wide temperature range, and is 
dependent primarily upon the thermal state of the 
rest of the body. Under the circumstances of these 
experiments in which the body was protected by 
ventilated clothing, artificial application of heat to 
the extremities was unnecessary for the comfort of 
the subjects. 
Mead and Bader {1191) 1949 reported that 
when two inactive, seminude men were transferred 
to a cold environment, a very rapid reduction in 
blood flow to the fingers and toes, accompanied by 
a slower fall in skin temperatures, was observed. 
On return to a warm environment, there was a 
relatively rapid rise in digital skin temperature 
while blood-flow return was delayed, the time of 
onset of return varying with the duration of the 
prior cold exposure and requiring as long as 2 hours 
to reach precooling levels after a 2-hour cold ex- 
posure. Under these conditions, skin temperature 
was not even a qualitative index of blood flow, the 
changes in skin temperature depending largely upon 
the direct effect of the environment in warming 
the cooled tissues. In a further study, the same 
authors {1155) 1949 found that nearly maximal 
levels of blood flow may be maintained in the 
fingers of an individual otherwise under heat stress 
in the face of local ambient temperatures that 
would produce rapid freezing of the digits in cooled 
individuals. Blood flow through the fingers of an 
individual otherwise under cold stress may remain 
relatively low despite local heating of the fingers. 
When a subject was rewarmed after being cooled, 
the blood flow returned more rapidly to the fingers 
which had been maintained in a warm local en- 
vironment, than to fingers that had been kept in a 
cold local environment. None of these findings is 
inconsistent with the view that blood flow through 
the fingers depends primarily upon the overall body 
need to conserve or dissipate heat. 
In studies carried out by Greenfield and Shep- 
herd {1178) 1950, immersion of a finger in a water 
bath at 0° to 6° C. produced initial, nearly com- COLD EXPOSURE PROBLEMS—PHYSIOLOGICAL EFFECTS 
plete, cessation of blood flow. After a few minutes, 
the blood flow increased notably. Similar but lesser 
changes in blood flow occurred at 6° to 12° C. 
and at 12° to 15° G. There was no initial vaso- 
constriction and the blood flow per minute was 
lower than in the colder ranges. Gold pain was 
experienced by the subjects at 0° to 6° C. and this 
was believed not to be due to steep tissue thermal 
gradients, but it was postulated rather than vaso- 
constriction by lowering the internal finger tem- 
perature leads to pain. 
Further data indicating the dependence of the 
conditions in the extremities subjected to cold upon 
the state of thermal balance of the body are pro- 
vided by papers by Blaisdell {1159) 1951; Rapa- 
port, Fetcher, and Hall {1201) 1948; and Wynd- 
ham and Wilson-Dickson {1217) 1951. For further 
studies of local vessel reactions and body heat emis- 
sion resulting from immersing the extremities in 
cold water, papers by Aschoff {1152 and 1153) 
1944 may be consulted. As Miller {1193) 1947 has 
pointed out, vasodilatation in a part exposed to cold 
tends to protect that part against freezing. Vaso- 
constriction in an exposed part permits more rapid 
freezing. Miller {1193) found that chemical vaso- 
dilating agents, although capable of producing 
varying degrees of peripheral vasodilatation in ani- 
mals with a normal heat reserve, are entirely in- 
effective in eliciting vasodilatation in a cold-exposed 
ear of a chilled animal. Such vasodilating agents 
do not reduce the time or degree of freezing of the 
exposed ear. This is consistent with the transient 
vasodilatation produced locally by immersion of the 
hind limbs of a dog in warm water with the body 
in a cool room, followed by cutaneous vasoconstric- 
tion occurring with continued immersion, Heming- 
way and Lillehei {1182) 1950. It may be concluded 
that the addition of extra heat to the body of an 
animal is a much more effective means of achiev- 
ing peripheral vasodilatation than the use of chemi- 
cal vasodilators. Miller found that a rabbit having a 
normal heat reserve can prevent freezing in an ear 
exposed to a temperature of —55° C. over a period 
of 2 hours by means of vasodilatation. Miller also 
found that chemical vasoconstrictors are capable 
of producing vasoconstriction in an animal having 
a normal heat reserve to the extent that freezing 
will occur in an exposed ear within the same length 
of time as in a chilled animal without vasocon- 
strictors. Prevention of freezing in exposed areas 
of the extremities therefore depends upon the main- 
tenance of a normal body reserve of heat and 
avoidance of factors leading to peripheral vaso- 
constriction. 
For reports on body-temperature regulation un- 
der conditions of cold, the following papers should 
be consulted: Belding, Folk, Forbes, and Darling 
(1158) 1945; Geoghegan {1173) 1951; Glickman, 
Inouye, Telser, Keeton, Hick, and Fahnestock 
{1174) 1947; Hetherington, Luft, Moses, Wilks, 
Hale, Clamann, Aiken, and Briggs {1184) 1951; 
Malysheva {1190) 1950; and Spealman {1208) 
1949. In discussing heat loss from the body through 
the skin surface and by way of the respiratory tract, 
Spealman estimates that heat loss from the respira- 
tory tract may be as high as 50 calories per 1,000 
liters of respired air in extreme cold. 
The amount of water vapor evaporated from 
skin in a cold environment is importantly large and 
may be as high as 19 grams per man per hour in an 
uncomfortably cold environment and approximately 
4 grams less than that evaporated in a comfortable 
environment. In comfortably clothed men, vapori- 
zation of water removes approximately one-quarter 
of the total heat eliminated from the body. This 
relationship holds for both active and resting sub- 
jects over a wide range of environmental conditions. 
In cold conditions with peripheral vasoconstriction, 
approximately 9 calories of heat per square meter 
of body surface per hour are transferred to the sur- 
face of the body for each degree of difference in 
temperature between the deep body tissues and the 
body surface. Calculations indicate that the average 
blood flow in fully vasoconstricted skin is probably 
less than 15 cu. cm. per square meter of surface 
area per minute. During moderate vasodilatation, 
the flow may be 230 cu. cm. per square meter of 
surface area per minute, and the figure may rise to 
1,200 cu. cm. in severe exercise. Heat production in 
shivering is comparable to that during strenuous 
work. Men immersed in water up to the neck at 
20° C. showed an average heat loss, after body 
temperature stabilization, of 198 calories per square 
meter of surface area per hour. The difference in 
body and water temperature was 15.5° C. There- 
fore, the heat transferred per degree of difference in 
temperature was 13 calories per square meter of 
surface area per hour. Blood-flow values as low as 
0.2 to 0.5 cu. cm. per minute have been found in 
hands and fingers during experiments in moderately 
cold environments. Extreme degrees of relative 
ischemia can be withstood for long periods without 
harm. The blood flow in very cold extremities (5° 
to 10° C.) is many times greater than flow in moder- 
ately cold extremities 15° to 20° C.). Regarding 
chronic exposure to cold, there has been reported in 
rats and rabbits a rise in the resting metabolism of 
10 to 30 percent, probably the result of thyroid SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
activation. In human subjects exposed to a tempera- 
ture of 15° C. for about 2 weeks, there was a 7-per- 
cent rise in basal metabolic rate on the average. 
Numerous studies have suggested that hemodilu- 
tion occurs in hyperthermia and hemoconcentra- 
tion occurs in hypothermia. These deductions have 
been inferred from changes in the osmotic pressure 
or the plasma-protein concentration of the blood. 
Rodbard, Saiki, and Malin {1203) 1950 stated that 
so far as they were aware no data were available on 
the actual changes in blood volume and its relation 
to changes in the extracellular and intracellular 
fluid compartments. Their studies on physiological 
effects induced by body temperature changes were 
therefore extended to investigate possible fluid 
shifts in order to assay more adequately the effects 
of low temperature upon the cardiovascular system. 
In these experiments, rabbits and chicks were used 
as experimental animals. Lowering the body tem- 
perature to 25° C. resulted in only a slight increase 
in hematocrit and specific gravity. However, 
plasma and blood volumes and thiocyanate space 
were all reduced 30 percent below normal levels. 
Rewarming resulted in a return to normal values. 
Induced hyperthermia caused a slight decrease in 
hematocrit and plasma specific gravity. Plasma 
and blood volumes were slightly reduced, but thio- 
cyanate space was increased as much as 30 percent. 
These data suggested to the authors that induction 
of hypothermia results in a shift of fluid from the 
plasma and the interstitial spaces to the intracellu- 
lar phase. The fact that the hematocrit and specific 
gravity do not rise commensurate with the decreased 
volumes suggests that blood cells and plasma pro- 
teins are removed from the circulating plasma and 
stored. The reverse processes are brought about by 
rewarming to normal temperature levels. Induc- 
tion of hyperthermia causes water to leave the tissue 
cells, and causes commensurate quantities of plasma 
protein and blood cells to be released to the circu- 
lating bloodstream. 
Miller {1192) 1949 has reported a study of cer- 
tain blood properties in healthy young men trans- 
ferred from a subtropic to a subarctic environment. 
Thirty volunteer subjects were heat adapted during 
July, August, and part of September 1947 at Ran- 
dolph Field, Tex. In the latter half of September, 
the subjects were transferred to Ladd Field, Alaska, 
via train and ship. The lowest environmental tem- 
perature encountered was —40° F. The living 
quarters at Ladd Field were adequately heated. In 
these subjects complete blood studies were done 
both at Randolph Field and at Ladd Field. These 
included erythrocyte and leukocyte counts, differ- 
ential white counts, hematocrit ratios, coagulation 
times, sedimentation rates, specific gravity of whole- 
blood plasma, blood-sugar levels, total blood-pro- 
tein levels, and fasting serum chloride levels. The 
experimental results revealed no marked changes 
in the blood properties investigated, although there 
was the general tendency toward increase in red cell 
counts. All other differences were slight. The author 
concluded that the studies offered no evidence for 
the occurrence of acclimatization to cold for the 
factors studied. A further study on the mechanism 
of acclimatization to cold and loss of heat accli- 
matization in men subjected to prolonged cold ex- 
posures has been reported by Stein, Eliot, and Bader 
{1210) 1949. Three healthy, unacclimatized, white 
males were intermittently exposed successively to a 
2-week period of physical conditioning followed by 
19 periods of heat lasting 5*4 hours each. Following 
this, there were fourteen 5-hour periods of cold at 
— 20° F. with a wind velocity of 3 or 4 miles per 
hour. There were then 5 exposures to heat followed 
by a 5-week interval of no exposures to environ- 
mental stress, and finally 3 reexposures to heat. 
Throughout the entire experimental period, meas- 
ures were made of cardiovascular and metabolic 
function, water and chloride balance, and body- 
water partition. The results of the study indicated 
that in heat-acclimatized men, no acceleration of 
deacclimatization is caused by repeated, intermit- 
tent exposures to cold. Acclimatization to heat may 
be maintained for periods of several months by 
occasional reexposure to the original environmental 
stress. Toe temperatures during repeated cold ex- 
posures decreased more rapidly with successive 
exposures suggesting more rapid and complete 
vasoconstriction, which does not necessarily repre- 
sent acclimatization to cold since no increased 
tolerance to cold was demonstrated. Marked 
diuresis and negative chloride balance were ob- 
served throughout the period of cold exposures, 
tending to persist during subsequent reexposures to 
heat. No significant differences in total blood plasma 
or thiocyanate space volumes were found in any of 
the experimental periods, although plasma proteins 
and hematocrit values suggested hemodilution in 
heat and hemoconcentration in cold. The finding 
that heat acclimatization can persist even with 
fairly severe cold exposures intervening suggested 
to the authors that acclimatization to cold may be 
accomplished in part by mechanisms different from 
those involved in heat acclimatization. It may be 
that many of the fundamental changes which occur 
are the same in both types of acclimatization and 
one may actually reinforce the other. 
For a report on the effect of local cooling on 
fluid movement, effective osmotic pressure, and COLD EXPOSURE PROBLEMS—PHYSIOLOGICAL EFFECTS 
capillary permeability, a paper by Brown and 
Landis {1162) 1947 may be consulted. 
The effects of cold on the air passages and the 
lungs have been reported in papers by Moritz and 
Weisiger {1196) 1945 and Webb {1216) 1951. 
The former authors caused dogs to breathe ex- 
tremely cold air for periods ranging from 20 to 130 
minutes. The temperature of the air delivered to 
the larynx ranged between —50° and —28° C., 
and in no instance were the temperature readings 
lower than +18° C. at the bifurcation of the 
trachea, inhalation of cold air in circumstances such 
that intralaryngeal inspiratory temperatures as low 
as or lower than —30° C. were reached resulted in 
the development of a localized sublaryngeal 
tracheitis. In some adults, the disturbance was lim- 
ited to unusual activity on the part of the mucous 
secreting glands, and in others, there was focal de- 
struction of the superficial epithelium. There was 
no evidence of injury to the lower part of the 
trachea, to the bronchi, or to the lungs. According 
to the authors, the explanation of the rapid warm- 
ing of inhaled cold air and of the occurrence of the 
relatively mild and localized injury following in- 
halation of cold air lies in the fact that dry air has 
an extremely low heat capacity and that the number 
of calories required to produce a great rise in the 
temperature of dry air can be provided by the heat 
derived from the cooling of a small amount of tissue 
by a few degrees. Long exposure to cold air, accord- 
ing to the authors, might result in obstructive 
edema. Webb also measured the air temperature in 
the airway with a thermocouple and made air tem- 
perature tracings from the front, middle, and the 
back of the nose from 18 resting human subjects in 
the following ambient air temperature ranges; 23° 
to 28° G., 5° to 8° C., and -20° to -31° C. Aver- 
age minimum peak temperatures from these records 
demonstrated that the inspired air was rapidly 
warmed in its passage through the nose. At the back 
of the nose, inspired, warm ambient air had reached 
a temperature of 31.7° C.; cool air had reached a 
temperature of 30.0° C.; and cold air had reached 
a temperature of 25.4° G. Average maximum tem- 
perature peaks demonstrated that expired air at the 
back of the nose did not exceed 35.5° C., 34.9° C., 
and 31.9° C. at warm, cool, and cold ambient tem- 
peratures respectively. Measurements at the front 
of the nose showed that average maximum expired 
air temperature peaks had dropped to 34.1° C., 
29.2° C., and 26.2° C. under the same respective 
conditions. 
Grayson {1177) 1949 found that general body 
heating produces a vasoconstriction in the human 
bowel followed by a vasodilatation. His same tech- 
niques were used to investigate the effects of limb 
cooling. When the arm was immersed in ice water, a 
variable and transient vasodilatation of the bowel 
occurred at first and was always followed by a pro- 
nounced vasoconstriction and a fall in body tem- 
perature. With the circulation to the arm occluded, 
immersing the limb in ice-cold water always pro- 
duced a marked vasodilatation. On releasing the 
occluding pressure with the arm still in the water, a 
rapid fall in body temperature and a pronounced 
vasoconstriction in the bowel occurred. Vasocon- 
striction was never observed in response to limb 
cooling while the circulation to the limb was oc- 
cluded. The vasodilator effect of cold on the bowel 
circulation was, therefore, not conceived to be the 
result of direct cooling of the blood. The effect of 
circulating cooled blood appeared, in fact, to act as 
a vasoconstrictor stimulus so far as the bowel is con- 
cerned. In experimental studies, Cordier and Fiery 
{1165) 1950 studied the influence of cold on the 
speed of transit and intestinal absorption of glucose 
solutions in the rat. These animals were exposed to 
a temperature of —5° C. Exposure to this low tem- 
perature resulted in an acceleration of glucose move- 
ment in the stomach and an increase of intestinal 
absorption of glucose. This was ascribed by the 
authors not to an increased epinephrine secretion 
but to hypersecretion of the thyroid gland. In a 
study of nutritional requirements for men at work 
in cold, temperate, and hot climates, Gray, Conso- 
lazio, and Kark {1175) 1951 measured the caloric 
output of men doing hard work in these three differ- 
ent environments while wearing standard Arctic, 
temperate, and desert clothing. The subjects were 
healthy university students in excellent training. 
Their daily dietary intake exceeded the National 
Research Council’s recommended daily allowance 
for protein, calcium, phosphorus, irons, vitamin A, 
thiamin, riboflavin, niacin, and ascorbic acid. Their 
protein intake was largely of animal origin and their 
caloric intake was equal to their needs. Measure- 
ments of basal metabolic rate work output, oxygen 
consumption at work, and differences in body 
weight before and after exercise were made daily. 
The results of these studies showed that the caloric 
output for a given amount of external work per- 
formed at a constant temperature increased about 
5 percent when the clothing was changed from 
desert clothing and increased above 5 percent more 
when the clothing was changed from temperate to 
Arctic clothing. The caloric output for a given 
amount of external work performed in a given outfit 
of clothes decreased about 2 percent as the tem- 
perature was raised from —15° to 60° F., and de- SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
creased about 2 percent more when the temperature 
was raised from 60° to 90° F. 
In 1950, Swain, Toth, Gonsolazio, Fitzpatrick, 
Allen, and Koehn {1212) estimated the voluntary 
food consumption of troops at Fort Churchill dur- 
ing three 10-day periods in the winter of 1947-48. 
This location was chosen because it has about the 
highest wind-chill value of any inhabited area. The 
troops spent about 3 hours every day in the open. 
Food consumed in the messes was recorded and 
plate wastes were weighed. An attempt was made 
to estimate canteen food. An abundant ration of 
fresh and frozen food was provided, averaging 
5,500 calories per man per day. In these studies, all 
nutrient intakes equaled or exceeded the recom- 
mended allowances of the National Research 
Council for an active man. Continuous weight 
records of a small number of men showed a slight, 
mean rise during this period. It was concluded that 
the caloric intake varied inversely with the mean 
environmental temperature, and was directly cor- 
related with the mean wind chill. There was no 
preference for fats in the subarctic climate and the 
percentages of calories provided by protein, fat, 
and carbohydrate were about the same as those in 
temperature climates, being 13, 40, and 47 percent, 
respectively. It appeared that the troops regulated 
their food intake in relation to the severity of the 
weather, but it seemed that their appetite for par- 
ticular foods was not altered. Mitchel and Edman 
{1195) 1951 also concluded that cold environment 
in proportion to severity definitely increases caloric 
requirements of men. Water requirements were 
stated to be depressed except as sweating may occur 
during severe work in heavy Arctic clothing. 
Dietary modifications may definitely affect tolerance 
to cold. A high carbohydrate diet was stated to be 
superior to a high protein diet. The addition of 
dietary fat improves the relatively beneficial effects 
of carbohydrate. Tolerance to cold did not seem 
appreciably to be improved by the addition of 
thiamin, ascorbic acid, riboflavin, and niacin in pro- 
portions adequate in a comfortable environment. It 
was concluded that the extra calories required in 
cold were better supplied by increasing the carbo- 
hydrate intake and the fat intake rather than by 
increased proteins. The extent to which this can be 
put into effect in feeding communities of men de- 
pends upon acquired food habits, the duration of 
residence in Arctic environments, the motivation 
for such residence, and the extent to which a diet 
can be made palatable. In conditions of inactivity, 
high-protein intake may exert a temporary, favor- 
able effect upon cold tolerance. The authors be- 
lieved that decreasing the intervals between meals, 
especially if the foods are rich in fat, may increase 
the favorable effect on thermal balance in cold en- 
vironments. The authors warned that the results of 
animal experiments are not applicable to man and 
should not be applied to human situations before 
actual field tests on human subjects. For a further 
study of diet at low temperatures with particular 
reference to fat utilization, a paper by Butson 
{1163) 1950 may be consulted. 
Reference may also be made to 3 animal 
studies on the relation of low environmental tem- 
peratures to diet by Donhoffer and Vonotsky {1167) 
1947, Ershoff {1170) 1950, and Hegsted and Mc- 
Phee {1181) 1950. Donhoffer and Vonotsky re- 
ported an increase in food consumption in white 
mice at low temperatures (10° to 11° C.) and a 
decrease at high external temperatures (29° to 33° 
G.), It appears from the studies of Ershoff that 
prolonged exposure to cold increases the vitamin A 
requirements of the rat. Immature rats were fed 
purified rations deficient in vitamin A under cold- 
room conditions (2° C.) and room temperature 
conditions (23° C.). The rats became depleted more 
rapidly under the cold-room conditions than under 
ordinary room conditions. The body weight at the 
time of depletion was less in the cold-room rats than 
in the ordinary room temperature series, and finally 
the length of survival after depletion was signifi- 
cantly decreased in the cold-room series. Hegsted 
and McPhee found that there was an increased 
thiamin requirement in rats under cold-room 
conditions. 
Regarding the effect upon metabolic rate and 
heat output of exposure to cold in human subjects, 
Forstenberg, Newburgh, and Spealman {1172) 
1944 reported a slight increase in both basal metab- 
olism and total heat production after 10 days in a 
group of lightly dressed men who lived in a room at 
a temperature of 15° C. for 4 weeks. This tempera- 
ture was low enough to cause distinct discomfort, 
but not cold enough to produce shivering. In some 
subjects, the increase in metablic rate lasted for some 
days after the experiment was concluded. This de- 
layed response was attributed to a possible late pe- 
riod of thyroid response. A slight lowering of blood 
cholesterol levels was noticed. Discomfort gradually 
lessened or disappeared. This was not due to a 
change in skin temperature or increase of heat 
production. Energy exchange data were obtained by- 
Frantz and Roth {1171) 1948 on human subjects 
residing continuously for 9 days in a cold environ- 
ment at a temperature of —32° C. The subjects 
fasted in the same environment for a period of 6 
days to provide control data. Clothing assemblies COLD EXPOSURE PROBLEMS—PHYSIOLOGICAL EFFECTS 
and sleeping bags were adequate to maintain nor- 
mal body temperature and comfortable skin tem- 
perature without the necessity for fatiguing exercise 
during fasting or subsistence upon the ration. The 
ration used was the USAF emergency ration. Pro- 
gressive limitation of voluntary activity was noted in 
the fasting subjects. The respiratory quotient ap- 
proached 0.72 with continued fasting, especially for 
exercise requiring more rapid caloric expenditure. 
The metabolic cost for a standard workload on the 
treadmill was increased during low-temperature 
exposure. This was not observed during the activi- 
ties in which the hobbling effect of the clothing did 
not participate, that is to say, lying, sitting, and 
standing quietly. Considering ability to perform 
psychomotor tasks, gross work capacity, and main- 
tenance of body comfort in the fasting and nonfast- 
ing subjects, food appears to be of secondary im- 
portance to the adequacy of clothing and sleeping 
bags for survival at low ambient temperatures. 
In 1947, Horvath and Golden [1185) reported 
observations on men performing a standard amount 
of work in low ambient temperatures. Five sub- 
jects wearing light and heavy clothing walked at a 
standard rate of speed and grade of climb on a 
motor-driven treadmill in comfortable and very cold 
environments. The energy expenditure for the 
standard work was increased by 10 percent in the 
lower ambient temperatures. This increase seemed 
to be independent of the amount of clothing worn. 
Ability to work was not signficantly impaired even 
at ambient temperatures as low as —46.7° C., 
although there was a slight decrease of mechanical 
efficiency at certain of the environments. The loss 
of body heat was greater with the lightweight 
clothing, and the magnitude of the loss appeared 
to be directly related to the ambient temperature. 
Heat debts were less but quite variable when heavy 
clothing was worn. In all cases, the heat debts were 
accumulated in the early portion of exposure to 
the cold environment. 
Observations of metabolic rate, and skin and 
rectal temperatures of men exposed to extremely 
cold environments, have been made by Horvath, 
Golden, and Wager [1186) 1946. The experiments 
were carried out on 45 men dressed in Arctic uni- 
forms and sitting quietly in ambient temperatures 
ranging from 1.1° to —40° C. The heat production 
in the cold was observed to be above basal values 
during the entire test period. In the —40° C. 
environment, average metabolic increases of 13, 53, 
and 74 percent were recorded for the first, second, 
and third hours, respectively. The rise in heat out- 
put during the first hour could not be explained 
on the basis of shivering. In the third hour, shiver- 
ing was present in the majority of the subjects. 
The fall in rectal temperatures was moderate, 
although low values of 35.4° C. were occasionally 
observed. The absolute value was not correlated 
with the presence of shivering, and low rectal tem- 
peratures could not be considered as the stimulus 
for shivering. Mean skin temperatures fell pre- 
cipitously during the first hour of exposure and 
became stabilized before the end of the test period. 
Considerable variability was observed in both the 
rate and the extent of the fall, notably in different 
subjects but also in repeat tests on the same subject. 
Of all the skin areas, hands and feet exhibited the 
greatest temperature changes in both rate and de- 
gree of fall. Toe temperatures below 0° C. were 
observed in several instances. The susceptibility of 
the extremities to cold environments was related to 
their sensitive vasomotor mechanisms, and to the 
fact that they were provided with the least amount 
of insulative protection. The responses of men ex- 
posed to cold environments are subject to con- 
siderable variation, and extreme care must be exer- 
cised in the interpretation of data obtained, whether 
on a few or a large number of subjects. 
Although some authors have reported that ex- 
posure to cold increases the basal metabolic rate, it 
has been found by Ames and Goldthwait [1151) 
1948 that the basal metabolic rates of 10 out of 11 
subjects moved from Lawrence, Mass., to winter 
quarters at Churchill, Manitoba, Canada, were not 
apparently affected by the change in environment. 
However, the basal metabolic rate of one subject 
increased during the winter at Churchill, possibly 
as a result of exposure to cold. This subject received 
more exposure than any of the other ten, averaging 
5.1 hours a day out of doors. Contrasts between men 
and women in basal heat production and heat loss 
during exposure to environmental temperature ex- 
tremes have been reported by Hardy, Ebaugh, Ste- 
vens, and DuBois [1180) 1950. Thirteen normal 
young women were studied in the respiration calo- 
rimeter of the Russell Sage Institute of Pathology. 
They were under basal conditions and nude. Mea- 
surements were made of gas exchange, rectal and 
skin temperatures, total heat loss, and percentages 
lost by radiation, convection, and vaporization. On 
different days they were exposed to calorimeter 
temperatures in the range between 22° and 35° C. 
In the cold zone, even before the appearance of 
significant muscular tension or chills, there was 
often found a slight rise in heat production, suggest- 
ing a chemical regulation of metabolism. In 5 of the 
subjects, this was absent, but in 4 it was slight and 
in another 4 it was distinct. This was in contrast to 
the basal metabolism of men, which usually remains SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
constant in the cold until the abrupt onset of a chill. 
Some of the women showed a prolonged rise in 
metabolism with the onset of chill much later than 
in the case of the men. Some women appear to have 
a regulation of the balance between heat production 
and heat loss which is more adaptable than is usually 
found in male subjects. In 45 test subjects taking 
part in the test of the experimental Arctic Trial 
Ration (AT-1) in the vicinity of Fairbanks, Alaska, 
from 12 February to 4 March 1950, Sargent and 
Gonsolazio {1204) 1951 found no significant altera- 
tions in water or electrolyte balances. Albumin and 
sugar levels were observed in the urine only occa- 
sionally, and then in trace quantities. The signifi- 
cant biochemical finding was ketonuria. Changes in 
ketonuria observed during the Army ration trials 
were considered to be manifestations of the general 
adaptation syndrome, and alterations in ketone body 
metabolism are suggested by the authors as a means 
of investigating the metabolic aspects of adaptation 
to cold. As Brolin {1161) 1946 has stated, exposure 
to low temperatures is believed to produce an in- 
creased activity of the thyroid gland and the adrenal 
cortex. The response of the thyroid gland to a low 
environmental temperature has been studied by the 
use of radiactive iodine by Schachner, Gierlack, and 
Krebs {1205) 1949. Wistar-strain male albino rats 
were exposed to about 4° C. for periods from 2 
hours to 60 days, and the percent uptake of radio- 
active iodine by the thyroid glands measured. At 
exposure periods under 3 hours, there was a dimin- 
ished amount of radioactive iodine present in the 
experimental animals, while the amount present in 
animals exposed about 6 hours was the same as for 
controls. There was an increase in radioactive iodine 
uptake after 12 to 24 hours’ exposure. This increased 
iodine uptake was most pronounced at 7 to 9 days, 
and then gradually returned to control values after 
40 days. Tobin and Steeples {1214) 1942 found 
that in rats exposed to cold, there was a decrease in 
the cholesterol content of the adrenal glands. Male 
rats were more resistant to cold than were the 
females. The decrease in adrenal cholesterol was 
found to be less in heavier animals than in lighter 
ones exposed to the same low temperature. Admin- 
istration of an aqueous adrenal cortical extract pro- 
duced a diminution in the fall of adrenal cholesterol 
in all rats exposed to low temperatures. Dugal and 
Therien {1168) 1949 found a typical enlargement 
of the adrenal glands in rats and guinea pigs exposed 
to cold. This enlargement of the glands was com- 
pletely prevented by large doses of ascorbic acid. 
Ascorbic acid seems to play a compensatory role 
similar to adrenal cortical hormones. Not only was 
hypertrophy of the glands prevented, but also re- 
sistance to cold was increased. According to Her- 
mann, Chatonnet, and Vial {1183) 1949, rats ex- 
posed to cold (2° G.) for periods ranging from 15 
minutes to 2 hours showed a decrease in the epine- 
phrine level in the adrenal glands proportional to 
the length of exposure. This was ascribed to the 
excessive secretion of the hormone and implying a 
drainage of the gland. According to Osgood and 
Gimmerman {1198) 1949, the 17-ketosteroid excre- 
tion of seven healthy male subjects was not signifi- 
cantly changed during a field exercise at Fort 
Churchill, Canada, under conditions of extreme 
cold from the levels of excretion recorded for the 
same men during a similar exercise under temperate 
climatic conditions at Fort Knox, Ky. A diurnal 
variation in 17-ketosteroid excretion was observed 
in these subjects, the hourly excretion during the 
waking hours being consistently greater than that 
during sleep. These studies seem to indicate that the 
subjects may have already been adapted to the stress 
of cold and exercise during the period at Fort 
Churchill prior to the first urine collections. 
Renal and hormonal mechanisms of cold 
diuresis have been reported by Bader, Eliot, and 
Bass {1154) -1949. Men were exposed at 15° C., 
reclining nude except for shorts. Results on these 
subjects were compared with results of exposure at 
24° to 27° C., the subjects being covered by 
blankets. Endogenous creatinine clearances in nine 
experiments showed no significant change in glo- 
merular filtration, and in 16 experiments there was 
no significant change in either endogenous creati- 
nine or para-aminohippuric acid clearance during 
cold diuresis. In 12 experiments, there was a sub- 
stantial reduction in cold diuresis during standing, 
as compared with reclining. Cold diuresis was in- 
hibited following 15 minutes of walking. During 
cold diuresis, the specific gravity and chloride 
concentration of the urine fell as the volume rose, 
and each change appeared to be correlated with the 
previous state of hydration and chloride content of 
the diet. Use of an index of chloride reabsorption 
showed that chloride tended to be reabsorbed to a 
greater degree than water. In 27 experiments, 3 sub- 
jects received small intramuscular doses of either 
0.015, 0.03, 0.06, or 0.12 units per kilogram of body 
weight of pitressin at the beginning of each ex- 
posure, either cold or warm. Inhibition of cold 
diuresis was proportionately longer lasting following 
the larger doses, but even the smallest dose reduced 
urine flow for l/2 hours to the same small output 
seen in the warm exposures, with or without 
pitressin. The strong similarity between water and 
cold diuresis and the extreme sensitivity to pitres- COLD EXPOSURE PROBLEMS—PHYSIOLOGICAL EFFECTS 
1151-1166 
sin were presented by the authors as suggestive 
evidence that cold diuresis is controlled by the 
posterior pituitary gland. The same authors {1169) 
1949 alternated the order of exposure {2/% hours) 
to 27° G. and 15° C. between men and in each 
man from day to day. In 23 experiments, plasma 
proteins rose an average of 0.5 gram per 100 cu. 
cm. and the hematocrit rose 2.9 percent in the cold. 
In 12 experiments, the corrected sedimentation 
rate rose 76 percent in the cold. When warm ex- 
posure followed the cold, these values fell an aver- 
age of 0.5 gram per 100 cu. cm., 1.8 and 41 percent, 
respectively. In 18 experiments on 5 men, the aver- 
age increase in urine output in the cold over output 
in the warm was 287 cu. cm., which corresponded 
to an average plasma loss of 277 cu. cm. as calcu- 
lated from increase in plasma proteins, hematocrit, 
and an estimated plasma volume of 50 cu. cm. 
per kilogram of body weight. In a series of 15 ex- 
periments, cold diuresis was largely or completely 
abolished by the small doses of pitressin, but the 
plasma proteins rose 0.4 gram per 100 cu. cm. and 
the hematocrit rose 2.6 percent, indicating that 
there is no direct connection between changes in 
urine output and plasma volume in the cold. Fur- 
ther evidence of the role of the pituitary gland in 
cold diuresis has been provided by Stutinsky {1211) 
1949. The reader is also referred to a report by 
Talso, Crosley, and Clarke {1213) 1947, in which 
it was shown that the cold pressor test in 6 out of 
7 normal, male subjects resulted in a reduction 
of glomerular filtration rate and effective renal 
plasma flow. These changes occurred either during 
the application of the local cold stimulus, or within 
approximately 30 minutes thereafter. 
An important effect of cold is the stiffness in joint 
movements which may result in a loss in manual 
dexterity. For an experimental study of the factors 
responsible for joint stiffness in cold, a paper by 
Hunter and Whillans {1187) 1951 should be con- 
sulted. In experiments on the knee joint of the cat, 
stiffness was present under conditions of zero and 
subzero temperatures even after the joint had been 
freed from muscular attachment, with exception of 
the cruciate ligaments. It would appear, therefore, 
that a physiologically important component of joint 
stiffness resulting from exposure to cold must result 
from a local physical change in the joint tissues with 
an increase in friction of the joint. A final point of 
physiological importance concerns the relation of 
cold tolerance to age. De Boer and Ederstrom 
{1166) 1946 reveal that young puppies about a 
week old have a much greater tolerance to hypo- 
thermia than adult dogs. This is generally true for 
all animals. 
1151. Ames, A. and D. A. Goldthwait. Influence of cold 
climate on basal metabolism. U. S. Army. Office of the 
Quartermaster General, Lawrence, Mass. Quartermaster 
climatic research laboratory, Environmental protection 
section, Kept. no. 136, 22 September 1948, 12 pp. 
1152. Aschoff, J. Der Anstieg der Rectaltemperatur bei 
umschriebener Abkiihlung der Korperoberflache. Pfliig. 
Arch. ges. Physiol., 1944, 248: 149-157. [P] 
1153. Aschoff, J. Die Vasodilatation einer Extremitat 
bei ortlicher Kalteeinwirkung. Pfliig. Arch. ges. Physiol., 
1944, 178: 178-182. [P] 
1154. Bader, R. A., J. W. Eliot, and D. E, Bass. Renal 
and hormonal mechanisms of cold diuresis. Fed. Proc. 
Amer. Soc. exp. Biol., 1949, 8: 7. 
1155. Bader, M. E. and J. Mead. The effect of local 
thermal influences on blood flow through the fingers in 
various states of body heat balance. U. S. Army. Office of 
Quartermaster General, Lawrence, Mass. Quartermaster 
climatic research laboratory. Environmental protection 
section. Kept. no. 159, 21 December 1949, 14 pp. [P] 
1156. Baetjer, A. M. Temperature, pp. 937-965 in: 
Rosenau preventive medicine and hygiene. Edited by Ken- 
neth F. Maxcy. Seventh edition. New York, Appleton- 
Century-Crofts, Inc., 1951, 1462 pp. 
1157. Baxter, H. and M. A. Entin. Experimental and 
clinical studies of reduced temperatures in injury and 
repair in man. I. Structure and potentialities of human 
skin in temperature control and in defence against thermal 
trauma. Plast. reconstr. Surg., 1947, 2: 569-584. [P] [R] 
1158. Belding, H. W., G. E. Folk, W. H. Forbes, and 
R. C. Darling. Secretion and evaporation of sweat in cold 
weather. Fed. Proc. Amer. Soc. exp. Biol., 1945, 4: 7. 
1159. Blaisdell, R. K. Effect of body thermal state on 
cold-induced cyclic vasodilatation in the finger. U. S. 
Army. Office of the Quartermaster General, Lawrence, 
Mass. Quartermaster climatic research laboratory. En- 
vironmental protection section. Kept. no. 177, September 
1951, 25 pp. [P] 
1160. Blaisdell, R. K, Variations in pain and tempera- 
ture sensation accompanying cold-induced cyclic vaso- 
dilatation in fingers. U. S. Army. Office of the Quarter- 
master General, Lawrence, Mass. Quartermaster climatic 
research laboratory, Environmental protection branch. 
Kept. no. 182, December 1951, 18 pp. 
1161. Brolin, S. E. Yttertemperaturens inverkan pa 
insondringsorganen. [Influence of temperature on incretion 
organs.] Nord. Med., Stockholm, 1946, 30: 1401—1406. 
(English summary.) 
1162. Brown, E. and E. M. Landis. Effect of local 
cooling on fluid movement, effective osmotic pressure and 
capillary permeability in the frog’s mesentery. Amer. J. 
Physiol, 1947, 149: 302-315. 
1163. Butson, A. R. C. Utilisation of high-fat diet at low 
temperatures. Lancet, 1950, 258: 993-994. Abstr. World 
Med., 1950, 8: 458. 
1164. Coakley, J. D., G. Forlano, and J. E. Barmack. 
The effect of ambient and body temperatures upon re- 
action time. U. S. Navy. ONR. Special devices center. 
Contract N6-ori-l51, Task Order No. 1, Kept. no. 
151-1-13, 15 March 1948,43 pp. [R] 
1165. Cordier, D. and Y. Fiery. Influence du froid 
sur la vitesse du transit gastrique et 1’absorption intestinale 
des solutions de glucose chez le rat. C. R. Soc. Biol., 
Paris, 1950, 144: 1521-1523. [P] 
1166. De Boer, B. and H. E. Ederstrom. Lethal hypo- 
thermia in dogs of various ages. Anesthesiol, 1946, 7: 
518-521. 1167-1203 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
1167. Donhoffer, S. and J. Vonotsky, The effect of 
environmental temperature on food selection. Amer. J. 
Physiol, 1947,150: 329-333. [P] 
1168. Dugal, L. P. and M. Therien. The influence of 
ascorbic acid on the adrenal weight during exposure to 
cold. Endocrinology, 1949, 44: 420—426. 
1169. Eliot, J. W., R. A. Baser, and D. E. Bass. Blood 
changes associated with cold diuresis. Fed. Proc. Amer. 
Soc. exp. Biol, 1949,8: 41, [P] 
1170. Ershoff, B. H. Effects of prolonged exposure to 
cold on the vitamin A requirement of the rat. Proc. Soc. 
exp. Biol, N. Y., 1950, 74: 586-587. [P] 
1171. Frantz, J. A. and J. L. A. Roth. Metabolic bal- 
ances in the cold environment. II. Energy exchanges. 
Fed. Proc. Amer. Soc. exp. Biol, 1948, 7; 35-36. [P] 
1172. Furstenherg, A, C., X. H. Newburgh, and C. R. 
Spealman. Physiology of cold. U. S. OSRD. Contract no. 
O. E. M. cmr 269, 1 January 1944, 20 pp. [P] 
1173. Geoghegan, B. Thermal conditions at sea in the 
Arctic, 1950. (With a suggestion for temperature pre- 
diction with time of day.) Gt. Brit. MRG-RNPRC, CES. 
R. N. P. 51/648, C. E. S. 338, April 1951, 23 pp. 
1174. Glickinan, N., T. Inouye, S, E. Telser, R. W. 
Keeton, F. K. Hick, and M. Fahnestock. Physiological 
adjustments of human beings to sudden change in environ- 
ment. Trans. Amer. Soc. Heat. Vent. Engrs., 1947, 53: 
327-353. 
1175. Gray, E. L., F. C. Consolazio, and R. M. Kark. 
Nutritional requirements for men at work in cold, tem- 
perate and hot environments. J. app. Physiol, 1951, 4: 
270-275. 
1176. Graybiel, A. and C. J. Dawe. Auricular fibrillation 
resulting from hypothermia. A case report. U. S. Navy. 
NATC, Pensacola, Fla. School of aviation medicine. 
Project NM 001 019, Rept. no. 3, 27 December 1948, 4 
pp. [CH] 
1177. Grayson, J. Responses of the colonic circulation 
in man to cooling the body. /. Physiol, 1949, 110: 13P. 
1178. Greenfield, A. D. M. and J. T, Shepherd. A 
quantitative study of the response to cold of the circulation 
through the fingers of normal subjects. Clin. Sci., 1950, 
9: 323-347. [P] 
1179. Hamilton, J. B. The effect of hypothermic states 
upon reflex and central nervous system activity. Yale J. 
Biol. Med., 1937,9: 327-332. 
1180. Hardy, J. D,, F. G. Ehaugh, Jr., E. I. Stevens, 
and E, F, Du Bois. The basal heat production and heat 
loss of normal women exposed to hot and cold environ- 
ments. XVIII Intern, physiol. Congr., 1950, 245-246. 
1181. Hegsted, D. M. and G. S. McPhee. The thiamine 
requirement of the adult rat and the influence on it of a 
low environmental temperature. J. Nutrit., 1950, 41: 
127-135. [P] 
1182. Hemingway, A. and C. W. Lillehei. Thermal 
cutaneous vasomotor response in dogs. Amer. J. Physiol, 
1950,162: 301-307. [P] 
1183. Hermann, H., J. Chatonnet, and J. Vial. Influence 
du froid sur la teneur en adrenaline des capsules surrenales 
du rat. C. R. Soc. Biol, Paris, 1949, 143: 273-275. [P] 
1184. Hetherington, A. W., IT. C. Luft, X. E. Moses, S. S. 
Wilks, H. B. Hale, H. G. Clamann, D. W. Aiken, and 
R. W. Briggs. The cardiovascular and respiratory re- 
sponses of personnel suddenly exposed to very low tem- 
perature windblast. USAF. Randolph Field, Tex. School 
of aviation medicine. Project 21-23-028, July 1951, 35 pp. 
1185. Horvath, S. M. and H, Golden. Observations on 
men performing a standard amount of work in low ambient 
temperatures. /. din. Invest., 1947, 26: 311-319. 
1186. Horvath, S. M., H. Golden, and J. Wager. Some 
observations on men sitting quietly in extreme cold. /. 
din. Invest., 1946,25: 709-715. [P] 
1187. Hunter, J. and M. G. Whillans. Effect of cold on 
joints. Fed. Proc. Amer. Soc. exp. Biol., 1951, 10: 68-69. 
Canad. J. med. Sci., 1951,29: 255-262. 
1188. Kunkle, E. C. Phasic pains induced by cold. /. 
appl. Physiol, 1949,1: 811-824. [P] 
1189. Mackworth, N. H. Preliminary note on some re- 
cent experiments at Fort Churchill on the effects of 
exposure to cold. Gt. Brit. MRG-RNPRC, CES. 
R. N. P. 49/535, C. E. S. 293, May 1949, 2 pp. 
1190. Malysheva, A. E. Okhlazhdenie organizma pri 
mestnom deistvii kholodnykh poverkhnostei. [Cooling of the 
organism under the local effects of cold surfaces.] Gigiena 
San., Moskva, 1950, 15: 23-28. Abstr. World Med., 1950, 
8: 344. 
1191. Mead, J. and M. E. Bader. The rapidity of digital 
skin temperature and blood flow alterations in men exposed 
to sudden changes in environmental temperature. U. S. 
Army. Office of the Quartermaster General, Lawrence, 
Mass. Climatic research laboratory. Kept. no. 158, 11 
October 1949, 12 pp. [P] 
1192. Miller, A. J. Study of certain blood properties in 
healthy men transferred from a subtropic to a subarctic 
environment. /. Aviat. Med., 1949, 20: 201-206. [P] 
1193. Miller, M. R, The effect of vasodilators and 
vasoconstrictors on the vascular changes in the rabbits’ 
ear, rapidity of body cooling and the rapidity of freezing 
of the ear during exposure of an ear to cold. U. S. AAF. 
Randolph Field, Tex. School of aviation medicine. 
Project 490, Kept. no. 1, 5 June 1947, 4 pp. [P] 
1194. Miller, M. R. and A. J. Miller. Physiological 
effects of brief periods of exposure to low temperatures. 
/. Aviat. Med., 1949, 20: 179-185. [P] 
1195. Mitchell, H. H. and M. Edman. Diet in a cold 
environment, pp. 9-41 in: Nutrition and climatic stress. 
Springfield, Charles C. Thomas, 1951, 234 pp. [R] 
1196. Moritz, A. R. and J. R. Weisiger. Effects of cold 
on the air passages and lungs. Arch, intern. Med., 1945, 
75: 233-240. [P] 
1197. Nei, T. and N. Talda, Vital reactions by exposure 
to cold. Jap. med. ]., 1950,3: 185-193. [P] 
1198. Osgood, L. E. and W. J. Gimmerman. The urinary 
excretion of 17-ketosteroids by men under field conditions 
in extreme cold. U. S. Army. Fort Knox, Kentucky. Field 
research laboratory, MDFRL 6-64-12-4)2-{11), 27 Oc- 
tober 1949, 5 pp. [P] 
1199. Pugh, L. G. C. Aspects of the physiology of cold. 
Physiother., 1950, 36: 3-7. 
1200. Radsma, W. The influence of a temporary sojourn 
in a cool environment on various vegetative functions in 
inhabitants of the tropics. Acta Physiol. Pharmacol. Neerl, 
1950,/: 112-170. 
1201. Rapaport, S. I., E. S. Eetcher, and J. F. Hall. 
Physiological protection of the extremities from severe 
cold. Fed. Proc. Amer. Soc. exp. Biol, 1948, 7; 99. 
1202. Rapaport, S. I., E. S. Fetcher, H. 6. Shauh, and 
J. F. Hall. Control of blood flow to the extremities at low 
ambient temperatures. /. app. Physiol, 1949, 2: 61-71. 
1203. Rodhard, S., H. Saiki, and A. Malin. Body fluid 
redistribution in induced hypothermia and hyperthermia. 
Fed. Proc. Amer. Soc. exp. Biol, 1950, 9: 107. COLD EXPOSURE PROBLEMS—ACCLIMATIZATION AND TOLERANCE 
1204-1219 
1204. Sargent, F. and C. F. Consolazio. Biochemical 
observations made during Arctic winter ration trials, 1950: 
Stress and ketone body metabolism. U. S. Army. Chicago, 
Illinois. Medical nutrition laboratory. Kept. no. 82, 20 
February 1951, 59 pp. [P] 
1205. Schachner, H. G., Q. S. Gierlack, and A. T. Krebs. 
The response of the thyroid gland to a low environmental 
temperature as studied with radioiodine. U. S. Army. 
Fort Knox, Kentucky. Field research laboratory, M. D. F. 
R. L. no. 6-64-12-02-{6), 1 June 1949, 6 pp. [P] 
1206. Spealman, C. R. Blood flow through the extremi- 
ties at low temperatures and its possible relation to immer- 
sion foot. U. S. Navy. NMRI. Project X—297, Rept. no. 1, 
10 January 1944, 4 pp. [P] 
1207. Spealman, C. R. Effect of ambient air temperature 
and of hand temperature on blood flow through the hand. 
U. S. Navy. NMRI. Project X—297, Rept. no. 5, 30 July 
1945, 4 pp. [P] 
1208. Spealman, C. R. Physiologic adjustments to cold, 
pp. 232-239 in: Physiology of heat regulation and the 
science of clothing. Edited by L. H. Newburgh. Phila- 
delphia, W. B. Saunders Co., 1949, viii, 457 pp. 
1209. Spradley, J. B. and M. Marin-Foucher. Hypo- 
thermia. A new treatment of psychiatric disorders. Dis. 
nerv. Syst., 1949, 10: 235-238. 
1210. Stein, H. J., J. W. Eliot, and R. A. Bader. 
Physiological reactions to cold and their effects on the 
retention of acclimatization to heat. J. appl. Physiol., 1949, 
/: 575-585. [P] 
1211. Stutinsky, F. Action de la temperature sur la 
diurese provoquee chez le rat normal et hypophysectomise. 
C. R. Soc. Biol, Paris, 1949, 143: 195-198. [P] 
1212. Swain, H. L., F. M. Toth, F. C. Consolazio, W. H. 
Fitzpatrick, D. I. Allen, and C. J. Koehn. Food consump- 
tion of soldiers in a subarctic climate. J. Nutrit., 1949, 
38: 63-72. Abstr. World Med., 1950, 7: 8. 
1213. Talso, P. J., A. P. Crosley, Jr., and R. H. Clarke. 
Effects of the cold pressor test in glomerular filtration and 
effective renal plasma flow. U. S. Army. Fort Knox, Ken- 
tucky. Field research laboratory. M. D. F. R. L. no. 55-5, 
27 October 1947, 6 pp. [P] 
1214. Tobin, L. M. and J. L. Steeples. Effect of hypo- 
thermia on the adrenal cholesterol content of rats. U. S. 
Army. Fort Knox, Kentucky. Field research laboratory. 
M. D. F. R. L. no. 6-64-12-02 (3), 24 September 1942, 
9 pp. [P] 
1215. U. S. NRC. Subcommittee on clinical investigation. 
Third fitness conference. Discussion of physiological 
changes in man subjected to a cold environment and of 
means and methods of aiding and protecting him. Clinical 
investigation rept. no. 16, 5 October 1943, 16 pp. [P] 
1216. Webb, P. Air temperatures in respiratory tracts 
of resting subjects in cold. Amer. J. Physiol, 1951, 167: 
835. Abstr. 
1217. Wyndham, C. H. and W. G. Wilson-Dickson. 
Physiological responses of hands and feet to cold in rela- 
tion to body temperature. /. appl. Physiol, 1951, 4: 199- 
207. [P] 
C. CHILBLAINS 
Chilblains may constitute a problem in submarine 
personnel under conditions of operation in cold, 
damp environments. Chilblains are due to defective 
peripheral circulation. Sites of election are the fin- 
gers, the ulnar sides of the hands, the great toes, the 
heels, and the ears. Simple, first-degree chilblains 
are round, oval, or variably shaped macular areas 
which may be livid red or bluish in color. The skin 
is shiny and appears thin. There may be discomfort, 
pain, smarting, itching, cramp, and coldness. In 
second-degree chilblains, the skin may be broken or 
ulcerated, the swelling more intense, and the ery- 
thema more pronounced. There may be mottled and 
livid plaques. The lesions are painful and sometimes 
a sero-purulent liquid is found. Following healing 
there may be scars. Wigley {1219) 1946 has stressed 
the importance of warm clothing and the use of 
loose gloves and boots. The feet should be kept dry 
with frequent changes of socks. Cold-water baths 
should be avoided and tepid water used instead. 
The feet may be washed with weak potassium per- 
manganate. The author recommends various seda- 
tive solutions and suggests that penicillin cream may 
be used for ulcerated chilblains. Gourlay {1218) 
1948 has recommended the use of nicotinic acid in 
the treatment of chilblains. The adult dose by mouth 
is 50 mg. 3 times a day after meals. Gourlay reported 
a high percentage of cure of chilblains and stated 
that some patients reported an increased tolerance 
to cold. It was suggested that nicotinic acid be taken 
at the first sign of chilblains and continued until the 
cold, damp season has passed. 
1218. Gourlay, R. J. The problem of chilblains with a 
note on their treatment with nicotinic acid. Brit. med. ]., 
1948, / ; 336-339. [R] [P] [CH] 
1219. Wigley, J. E. M. Chilblains. Practitioner, 1946, 
147: 353-356. [R] 
D, ACCLIMATIZATION AND TOLERANCE TO COLD 
Tolerance to cold has been shown to be related 
to age in experimental animals. Adolph {1221) 1951 
and Adolph and Lawrow {1222) 1951 have shown 
in the cat, the golden hamster, and rat, and to 
some extent in the mouse, guinea pig, and rabbit 
that newborn animals will endure lower tempera- 
tures than older animals. There are also species 
differences in cold tolerance amongst the different 
laboratory animals, and Fetcher {1235) 1948 has 
shown that adult guinea pigs do not tolerate as 
severe reductions of body temperature as do adult 
rats. The former die at colonic temperatures of 
17.5° to 21° C. while the latter survive at a colonic 
temperature as low as 15° C. 
Vascular responses, principally of the fingers, and 
their relationship to cold tolerance have been in- 
vestigated by Bader and Mead {1227) 1949 and 
{1224) 1950. A variety of vascular responses were 
observed in a group of 24 men and compared with 
an evaluation of certain aspects of their individual 
cold tolerance. These studies were carried out under SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
controlled ambient conditions and at Fort Church- 
ill, Manitoba, Canada. Individuals in whom re- 
duction of finger blood flow during immersion of 
the feet in ice water was relatively transient showed, 
in general, a lower incidence of frostbite. They were 
able to work with unprotected hands in the cold for 
more prolonged periods than those in whom vaso- 
constriction was maintained throughout immersion 
of the feet in ice water. The authors stressed that, 
although correlation between digital vascular re- 
sponse and cold tolerance was demonstrated for 
certain experimental groups, there were notable in- 
dividual exceptions to the pattern. Hence, the cold- 
immersion response of a particular subject cannot 
be regarded as a specific indication of his per- 
formance under cold stress. No other physiological 
indices investigated were shown to have a significant 
relationship with cold tolerance. These indices in- 
cluded spontaneous variations in finger-pulse vol- 
ume and finger mean volume during the control 
period, finger-pulse reduction during the warming 
phase prior to cold immersion of feet, maximum 
finger-pulse-volume reduction during immersion, 
blood-pressure rises during immersion, and severity 
of pain experienced during immersion. Men studied 
before and after a field bivouac under cold stress 
experienced less pain and had smaller blood-pres- 
sure rises during immersion of the feet in ice water 
after bivouac. These changes were not observed in a 
control group. 
As has been pointed out by Booker, Dent, Jones, 
Hudson, and Hayes {1228) 1951, the mechanisms 
involved in protection against and recovery from 
various stresses such as cold remains largely an un- 
answered question. That the adrenal gland is in 
some way related to ascorbic acid metabolism in 
normal and in stressed condition is well known, al- 
though exactly what the relationship is cannot at 
present be explained. In an attempt to derive in- 
formation which might throw more light on these 
questions, the authors subjected adrenalectomized 
mice in a cold room to a temperature of 42° F. 
along with mice of approximately the same weight 
and sex with the adrenals intact. The survival time 
of the two groups was studied. The role of ascorbic 
acid, cortisone, and ACE, separately and in com- 
binations, was studied. The results show that 
ascorbic acid in low and in high doses is not effective 
in increasing the survival time of adrenalectomized 
animals. Both cortisone and ACE are effective in 
increasing the survival time of the animals in the 
cold room appears to be an important factor. Com- 
binations of cortisone and ascorbic acid, and ACE 
and ascorbic acid were found to be more effective 
than the steroids alone in increasing the survival of 
the mice in the cold. 
Lange, Gold, Weiner, and Kramer {1244) 1948 
found that rabbits restricted in their activity have 
a definitely shortened survival time compared with 
unrestricted controls when exposed to a temperature 
of —20° C. The restricted animals were unable to 
maintain a normal body temperature even when in 
the first few minutes of exposure the temperature 
drop was in a straight line. Superficial anesthesia 
simulating sleep also resulted in a more rapid loss 
of body temperature than occurred in the controls. 
Inebriating doses of alcohol likewise reduced sur- 
vival time. Treatment with thyroid hormone for sev- 
eral days before exposure resulted in a striking 
prolongation of survival time. Partial suppression of 
thyroid function by thiouracil lead to a more rapid 
fall of body temperature and a shortening of the 
survival time. There was a lag of 3 or 4 days before 
the protective effect of oral, subcutaneous, or intra- 
venous thyroid medication became noticeable. 
These findings regarding the effect of thyroxin are 
consistent with those of Turner {1252) 1946 who 
found that administration of thyroxin decreased the 
hypothermia of mice subjected for 1 hour to an 
environmental temperature of 5° C. In Turner’s ex- 
periments, administration of dinitrophenol in doses 
calorigenically equal to the thyroxin exaggerated 
the hypothermia. 
The effects of dietary modifications upon the 
tolerance of man to cold has been investigated by 
Keeton, Lambert, Glickman, Mitchell, Last, and 
Fahnestock {1243) 1946. The subjects were divided 
into two groups, the first receiving a high protein 
diet for 5*/2 months and the second a high carbo- 
hydrate diet for the same period. The daily food 
intake was consumed in four meals. The cold room 
was kept at — 20° F. The subjects were clothed in 
Army Quartermaster Corps Arctic clothing and the 
following measurements were carried out: rectal 
and skin temperatures, and psychomotor and visual 
efficiency tests such as critical fusion frequency of 
flicker, visual choice reaction time, speed of tapping, 
coordination time, and normal steadiness in holding 
a stated position and during voluntary movement. 
The following conclusions were derived from the 
data: There was an incomplete inversion of diurnal 
rhythm of physiological functioning in subjects re- 
cently changed from normal daytime to nighttime 
activity. High-protein diet was associated with the 
excretion of larger amounts of creatinine in the 
urine, but there were never any signs of kidney 
damage. The heat increment, that is to say, the 
specific dynamic effect of high-protein diet, was 50 
percent greater than for the high-carbohydrate diet COLD EXPOSURE PROBLEMS—ACCLIMATIZATION 
during 6 hours post prandium under cool condi- 
tions, and 76 percent greater under comfortable 
environmental conditions. Subjects on high-protein 
diet required for the maintenance of body weight 
an average total caloric intake of 162 percent of 
basal energy expenditures. For subjects on a high- 
carbohydrate diet, the figure was 191 percent. More 
complete protection by clothing of the trunk, upper 
arms, and thighs will retard the cooling of the body 
and of the skin, but not of the extremities during 
cold exposure. More complete clothing protection 
also obliterates the dietary effects on cold resistance. 
Additional clothing was found to retard the rate at 
which performance of psychomotor tests are ad- 
versely affected by cold, but only for the high-carbo- 
hydrate diet. Cooling of the internal body tissues on 
exposure to intense cold was greater on the high- 
protein diet. High-carbohydrate diet was found 
more potent in combating the effects of intense cold 
by slowing the rate of surface skin cooling. High- 
carbohydrate diet, more than high-protein diet, 
lessens the adverse effect of intense cold on psycho- 
motor performance. The superiority of the high- 
carbohydrate diet over the high-protein diet in 
increasing tolerance to cold of adult men under con- 
ditions in which caloric requirements are just satis- 
fied is associated with and probably causally related 
to increased requirement of food energy and pre- 
sumably increased heat production. It is not related 
to the differential specific dynamic effects of diets 
as revealed during the 6-hour period post prandium. 
In a further study, Mitchell, Glickman, Lambert, 
Keeton, and Fahnestock {1247) 1946 investigated 
the tolerance of man to cold comparing the values 
for carbohydrate diets versus high-fat diets and the 
effect of frequency of meals. Subjects given high- 
carbohydrate diets in the experiments reported 
above {1234) were given high-fat diets in the pres- 
ent experiments. Those given high-protein diets in 
the previous experiments were given high-carbohy- 
drate diets in the present study. All subjects were 
lightly clothed, that is to say, they did not wear 
fleece innerliner or the cotton-hooded parka, but 
wore all other warm clothing. It was concluded that 
the high-fat diet induced a mild ketonuria, but no 
hemolysis in blood samples taken under basal con- 
ditions. For the maintenance of body weight, the 
subjects on high-carbohydrate diet required a total 
caloric intake of 188 percent of basal energy expen- 
ditures. Those on high-fat diet required 200 percent. 
Cooling of the internal tissues of the body on expo- 
sure to intense cold was greater in the subjects on 
high-carbohydrate diet, but only when the interval 
between meals was reduced to 2 hours. Regarding 
cooling of the skin, there was no superiority of 
high-fat diet over high-carbohydrate diet in subse- 
quent 4-hour periods of exposure to cold. It ap- 
peared highly probable that the high-fat diet was 
superior to high-carbohydrate diet in maintaining 
general psychomotor performance and visual effi- 
ciency. The fat diet was clearly superior to the car- 
bohydrate diet in speed of tapping. Decreasing the 
interval between meals during cold exposure had 
no favorable effect on rectal temperature changes 
if the meals were largely carbohydrate, but there 
was a definitely favorable effect with high-fat meals. 
Decreasing the interval between meals progressively 
and strikingly increased the favorable effect on the 
maintenance of psychomotor functioning, but oblit- 
erated the differential effects produced by diets dif- 
fering widely in proportions of fat and carbohy- 
drates. The character of the meal consumed just 
prior to cold exposure exerted no appreciable effect 
upon the maintenance of psychomotor performance 
during exposure. The superiority of high-fat meals 
in maintaining tissue temperature in cold environ- 
ment is related to heat emission, and not heat pro- 
duction, and may involve a temporary deposition 
of dietary fat in the subdermal tissues following 
high-fat meals. It was concluded generally that 
dietary modifications may exert favorable effects 
upon the ability of man to withstand exposure to 
intense cold. High-fat and high-carbohydrate foods 
are preferred to high-protein diet, and small meals 
every 2 hours are considered better than large meals 
at 4 to 6 hours’ intervals. 
Glickman, Keeton, Mitchell, and Fahnestock 
(1240) 1946 also investigated the effects of intake 
of water-soluble vitamins on the tolerance of man 
to cold. The experiments were carried out on 12 
healthy young men over a 150-day period to deter- 
mine the effect of supplements of water-soluble 
vitamins to diets containing only borderline concen- 
trations of these vitamins. The cold stress was re- 
peated exposure of 8 hours’ duration either to in- 
tense cold ( — 20° F.) with considerable protective 
clothing or to a cool environment (60° F.) with 
little protective clothing. The basal diet consumed 
by all the subjects was considered adequate accord- 
ing to current standards in all essential nutrients 
except ascorbic acid, thiamin, riboflavin, and nico- 
tinic acid. The amounts of these vitamins in the 
basic diet was generally two-thirds or less than the 
recommended allowances of the National Research 
Council Food and Nutrition Board. The daily 
vitamin supplement consisted of 200 mg. of ascorbic 
acid, 8.8 mg. of thiamin, 8.0 mg. of riboflavin, 120 
mg. of nicotinamide, 10.2 mg. of pyriodoxine, and 
20.4 mg. of pantothenic acid. When not receiving SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
vitamins, the subjects received placebos indistin- 
guishable from the vitamin capsules. At no time 
were there clinical symptoms referable to the ex- 
perimental diets, and no biochemical evidence that 
the vitamin levels of the basic diet were inadequate 
for normal nutrition for the 89-day period. The re- 
sults of the study clearly indicated to the authors 
that the ability of men to withstand the damaging 
effects of repeated exposure to cold environments 
and maintain normal neuromuscular mental effi- 
ciency was not appreciably enhanced by supplemen- 
tary doses of ascorbic acid, thiamin, riboflavin, nico- 
tinamide, pyridoxine, and pantothenic acid in the 
amounts given in these experiments. A summary of 
these experiments is to be found in an unsigned 
article {1253) published in 1946. Similar conclu- 
sions have been expressed by Mitchell and Edman 
{1246) 1949. These authors express doubts that 
animal experimentation in this field of research may 
yield profitable results applicable to man’s situa- 
tion. Animal studies reported by Ershoff and 
Greenberg {1234) 1950 indicate that deficiency of 
vitamin A in rats may impair the ability of rats to 
withstand subsequent exposure to cold. Vitamins, 
including vitamin A, added to the diets of these 
animals may improve tolerance to cold. 
For a report of a nutritional investigation on 
British naval personnel under cold climatic con- 
ditions at sea, reference may be made to a paper 
by Geohegan and Sinclair {1237). 1949. In these 
studies, there was a significant loss of body weight 
among the men who were exposed to cold condi- 
tions, but none among those not exposed. Age was 
not a factor in the loss of weight. The daily caloric 
consumption was 3,800 calories. This diet seemed 
adequate in vitamins and minerals. Under cold 
climatic conditions, a diet of not less than 4,300 
calories was recommended for all personnel. For 
personnel exposed for 4 or more hours daily it was 
considered that there should be given an addi- 
tional meal of 1,000 calories. For watchkeepers, the 
authors recommended an increase in the diet of 
one-half ounce of sugar per man per watch. 
As Gladwin {1239) 1947 has stated, adaptation 
to extreme cold involves cultural devices as well as 
physiological adjustments. Studies by Bly, Johnson, 
Kark, Consolazio, Swain, Laudani, Maloney, Fi- 
gueroa, and Imperiale {1226) 1950 suggest that 
during the first few days of abrupt exposure to cold, 
unacclimatized soldiers exhibit a general adaptation 
syndrome, with stimulation of the pituitary-adreno- 
cortical system. According to Miller and Pecora 
{1245) and Pecora {1248) 1948, there is no im- 
paired renal function in men living in a subarctic 
environment under ordinary circumstances with a 
sufficient caloric and fluid intake. If the fluid and 
food intake is inadequate, there may be evidence of 
temporary renal dysfunction. Renal stress may be 
accentuated by living under the strain of a severely 
cold environment. Abnormal urinary constituents 
disappear as soon as men returned to a warm sit- 
uation. Red cell counts showed an increase in men 
transported from Texas to Alaska, and hematocrit 
levels tended to decrease. There was also a decrease 
in mean corpuscular volume. Sedimentation rates 
showed no particular direction of change, and co- 
agulation times tended to increase. There were no 
changes in the electrocardiogram of men exposed 
to short periods of severe cold. The diurnal tem- 
perature cycle seemed to be oriented at a somewhat 
lower level in men living in the subarctic as com- 
pared with cycles in the subtropic environment. 
From hand calorimeter studies on all the subjects, 
it could be said in general that men transferred 
from subtropic to a subarctic climate showed a 
decrease in the amount of heat loss through their 
hands. There were no significant changes in the 
basal metabolic rates in subjects transferred from 
Texas to the subarctic environment, although the 
Eskimos were found to have a generally increased 
basal metabolic rate. 
Change in the circulation of blood in the extremi- 
ties as a factor in acclimatization to cold was dis- 
cussed by Bazett {1225) 1949. He pointed out that 
seamen on long exposure to cold weather at sea 
become able to withstand immersion of the hands 
in water much better than do other individuals. It 
has not been established whether the local surface 
temperature of the exposed surface is allowed to fall 
to lower temperature levels or whether vascular re- 
actions are exaggerated and maintain abnormally 
high temperatures. The skin of acclimatized subjects 
appears to be thicker and coarser than that of un- 
acclimatized persons. It is possible that the tissues 
develop a capacity to withstand cooling so that 
deeper tissues can attain a somewhat lower tempera- 
ture without being damaged and without the oc- 
currence of inflammatory reactions. The sweat 
glands appear to show some atrophy from disuse on 
continued exposure to cold. Adaptation is also 
partly the result of certain habits in that, for 
example, trained individuals can sleep while shiver- 
ing, a feat not possible as a rule for the untrained 
subject. Daniels, Fainer, Bommarito, and Bass 
{1232) 1951 have emphasized from field reports 
that acclimatization to cold involves the role of 
many coordinated changes rather than striking 
changes in any one function. Animal studies of 
Sellers, Reichman, and Thomas {1249) 1951 and 
Sellers, Reichman, Thomas, and You {1250) 1951 COLD EXPOSURE PROBLEMS—ACCLIMATIZATION 
1220-1234 
have indicated that acclimatized rats show a greatly 
elevated metabolic rate in comparison with unac- 
climatized animals. Animals may be artificially 
acclimatized by pretreatment with a combination 
of cortisone and thyroxine. The increased rate of 
survival of the artificially acclimatized rats was not 
as great as in animals which had acclimatized 
naturally by previous cold exposure. 
A large increase in the ascorbic-acid content has 
been shown to occur in the tissues of the white rat 
after prolonged exposure and adaptation to cold 
(+4° to —4° C.). These studies were carried out 
by Dugal and Therien {1233) 1947 and Therien 
{1251) 1949. The increase in ascorbic acid is much 
smaller if the rats exposed to low temperatures re- 
ceive daily supplement of that vitamin. On the other 
hand, a decrease in ascorbic-acid content of the tis- 
sues has been found in rats unable to adjust them- 
selves to the cold environment. From these results 
on the white rat, it appears that acclimatization to 
low temperatures involves large quantities of ascor- 
bic acid. It is well known that the white rat is able 
to synthesize ascorbic acid while the guinea pig does 
not do so. Generally speaking, the tolerance of the 
guinea pig to cold environment is lower than that 
of the white rat, and results show that the tolerance 
of the guinea pig to a cold environment depends on 
the amount of ascorbic acid received daily. During 
the process of acclimatization to cold, more ascorbic 
acid is retained in the tissues of the guinea pig ex- 
posed to low temperatures than in the same tissues 
of control animals kept at room temperature. 
Finally, a direct relation has been observed by the 
authors between adaptability to cold environment 
and the content of ascorbic acid in the adrenal 
glands. For further studies on ascorbic-acid require- 
ment and acclimatization, a paper by Burton (1229) 
1949 may be consulted. Butson {1230) 1949 found 
an average increase of 10 mg. percent in the fasting 
blood-sugar level in men subjected to temperatures 
of 0° to —35° F. in the Antarctic. There was an 
increased sensitivity to adrenalin injection as indi- 
cated by blood-pressure changes, respiratory rate, 
pulse rate, and subjective sensations. A greater than 
normal rise in blood pressure was noted with the 
cold pressor test. 
For a report on acclimatization and the effects of 
cold on the human body as observed at Little Amer- 
ica III, on the United States Antarctic service expe- 
dition of 1939 to 1941, a paper by Frazier {1236) 
1945 may be consulted. Men consistently exposed to 
low temperatures in this expedition developed de- 
hydration of the skin and subcutaneous structures 
as a protective measure. The same was observed in 
other forms of animal life. There is an increase in 
the blood-sugar levels, and the author states that a 
vital factor in cold acclimatization is an increase in 
epinephrine output. For other papers relating to 
acclimatization and tolerance, reports by the fol- 
lowing authors should be consulted: Adolph {1220) 
1949; Adolph and Molnar {1223) 1946; Carlson, 
Burns, Quinton, and Bark {1231) 1949; Gilson 
{1238) 1950; Horvath, Friedman, and Golden 
{1241) 1947; and Irving {1242) 1951. 
1220. Adolph, E. E. Acclimatization to Arctic climates, 
pp. 1-2 in: U. S. NRG-GAM. Conference on acclimati- 
zation. 17 June 1949, 29 pp. 
1221. Adolph, E. F. Responses to hypothermia in several 
species of infant mammals. Amer. ]. Physiol., 1951, 166: 
75-91. 
1222. Adolph, E. F. and J. W. Lawrow. Acclimatization 
to cold air; hypothermia and heat production in the 
golden hamster. Amer. J. Physiol., 1951, 166: 62-74. 
1223. Adolph, E. F. and G. W. Molnar. Exchanges of 
heat and tolerances to cold in men exposed to outdoor 
weather. Amer. J. Physiol., 1946, 146: 507-537. [P] 
1224. Bader, M. E., and J. Mead, and M. E. Pillion. 
Individual differences in vascular responses and their 
relationship to cold tolerance. J. appl. Physiol., 1950, 2: 
608-618. Excerpta Medica. Section II. (Physiology, Bio- 
chemistry, and Pharmacology), 1951, 4: 888. 
1225. Bazett, H. C. Acclimatization to cold. pp. 2-5 in: 
U. S. NRG-GAM. Conference on acclimatization. 17 
June 1949, 29 pp. 
1226. Bly, C. G., R. E. Johnson, B. M. Hark, C. F. 
Consolazio, H, L. Swain, A. Laudani, M. A, Maloney, 
W. G. Figueroa, and L. E. Imperiale. Survival in the cold. 
Armed Forces med. ]., 1950,1: 615-628. 
1227. Bader, M. E. and J. Mead. Vascular responses in 
relation to cold tolerance. U. S. Army. Office of the 
Quartermaster General, Lawrence, Mass. Quartermaster 
climatic research laboratory. Environmental protection 
section. Kept. no. 157, 16 December 1949, 10 pp. [P] 
1228. Booker, W. M., F. M. Dent, W. M. Jones, M, L. 
Hudson, and B. L. Hayes. Factors influencing survival 
time of adrenalectomized mice in cold stress. Amer. J. 
Physiol., 1951, 769-770. 
1229. Burton, A. C. Acclimatization to cold. pp. 5-6 in: 
U. S. NRC-CAM. Conference on acclimatization. 17 
June 1949, 29 pp. 
1230. Butson, A. B. C. Acclimatization to cold in the 
Antarctic. Nature, Land., 1949, 163: 132—133. 
1231. Carlson, L. D,, H. L. Burns, W. E. Quinton, and 
B. S. Bark. Report of studies in acclimatization. Winter 
1948-1949. USAF. Wright-Patterson air force base, Day- 
ton, Ohio. Air materiel command. USAF Tech. Kept. 
5835, August 1949, 27 pp. 
1232. Daniels, F., Jr., D. C. Fainer, C. L. Boxnmarito, 
and D. E. Bass. Acclimatization to cold in man. Fed. Proc. 
Amer. Soc. exp. Biol., 1951,10: 32—33. 
1233. Dugal, L. P. and M. Therien. Ascorbic acid and 
acclimatization to cold environment. Canad. J. Res., 1947, 
25 Sec. E: 111-136. 
1234. Ershoff, B. H. and S. M. Greenberg. Effects of 
a transient vitamin A deficiency on subsequent resistance 
to cold. Proc. Soc. Exp. Biol., N. Y., 1950, 75: 604—607. 
[P] 1235-1257 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
1235. Fetcher, E. S. Study of temperature regulation, 
heat exchange, and tolerance of man and warm blooded 
animals in exposure to cold. USAF. Wright-Patterson air 
force base, Dayton, Ohio. Aero medical laboratory. Tech. 
Rept. no. MCREXD-696-113C, 3 November 1948, 105 
PP- [P] 
1236. Frazier, R, G. Acclimatization and the effects of 
cold on the human body as observed at Little America III, 
on the United States antarctic service expedition 1939— 
1941. Proc. Amer. phil. Soc., 1945, 89: 249—255. [P] 
1237. Geoghegan, B. and H. M. Sinclair. A nutritional 
investigation on naval personnel under cold climatic con- 
ditions. R. N. Operation “Rusty,” Arctic, 1949. Gt. Brit. 
MRC-RNPRC, CES. R. N. P. 49/546, C. E. S. 297, 
undated, 1 p. [P] 
1238. Gilson, S. B. Studies on adaptation to cold air in 
the rat. Amer. J. Physiol., 1950, 161: 87-91. [P] 
1239. Gladwin, T. Climate and anthropology. Amer. 
Anthrop., 1947, 49: 601-611. 
1240. Glickman, N., R. W. Keeton, H. H. Mitchell, 
and M. K. Fahnestock. The tolerance of man to cold as 
affected by dietary modifications: high versus low intake 
of certain water-soluble vitamins. Amer. J. Physiol., 1946, 
146: 538-558. [P] 
1241. Horvath, S. M., A. Friedman, and H. Golden, 
Acclimatization to extreme cold. Fed. Proc. Amer. Soc. exp. 
Biol, 1947, 6: 133. Amer. J. Physiol, 1947, 100: 99-108. 
[P] 
1242. Irving, L. Physiological adaptation to cold in 
arctic and tropic animals. Fed. Proc. Amer. Soc. exp. Biol, 
1951, 10: 543-545. 
1243. Keeton, R. W,, E. H. Lambert, N. Glickman, 
H. H. Mitchell, J. H. Last, and M. K. Fahnestock. The 
tolerance of man to cold as affected by dietary modifica- 
tions: proteins versus carbohydrates, and the effect of 
variable protective clothing. Amer. J. Physiol, 1946, 146: 
66-83. 
1244. Lange, K., M. M. A. Gold, D. Weiner, and M. 
Kramer. Factors influencing resistance to cold environ- 
ments. Bull. Army med. Dept., 1948, 8: 849-859. Abstr. 
World Med., 1949,6:5. [P] 
1245. Miller, A. J. and J. S. Pecora. Physiological and 
biochemical evaluation of long term acclimatization to a 
cold environment. USAF, Ladd air force base, Alaska. 
Arctic aeromedical laboratory. Quarterly research report, 
1 January 1946 to 31 March 1948, 17 pp. 
1246. Mitchell, H. H. and M, Edman. Nutrition and 
resistance to climatic stress with particular reference to 
man. U. S. Army. Quartermaster General, Research de- 
velopment board. November 1949, 112 pp. 
1247. Mitchell, H. H., N. Glickman, E. H. Lambert, 
R. W. Keeton, and M. K, Fahnestock. The tolerance of 
man to cold as affected by dietary modification; carbohy- 
drate versus fat and the effect of the frequency of meals. 
Amer. J. Physiol, 1946, 46: 84-96. [P] 
1248. Pecora, J. S. Physiological and biochemical evalu- 
ation of long term acclimatization to a cold environment. 
USAF. Ladd air force base, Alaska. Arctic aeromedical 
laboratory. Quarterly research report, Project I, 1 April 
1948 to 30 June 1948, 9 pp. 
1249. Sellers, E. A., S. Reichman, and N. Thomas. 
Acclimatization to cold: natural and artificial. Amer. J. 
Physiol, 1951,167: 644-650. [P] 
1250. Sellers, E, A., S. Reichman, N. Thomas, and 
S. S. Yon. Acclimatization to cold in rats: metabolic rates. 
Amer. J. Physiol, 1951, 167: 651-655. [P] 
1251. Therien, M. Contribution a la physiologic de 
1’acclimatation au froid. Laval, med., 1949, 14: 1062— 
1110. Excerpta Medica. Section II. (Physiology, Bio- 
chemistry, and Pharmacology), 1950, 3: 1049. [P] [R] 
1252. Turner, M. L. The effect of thyroxin and dinitro- 
phenol on the thermal responses to cold. Endocrinology, 
1946,58; 263-269. [P] 
1253. Anon. Physiologic performance and diet in cold 
environments. Nutrit. Rev., 1946, 4: 341-343. [R] 
E. EFFECT OF COLD ON EFFICIENCY 
Animal experiments of Dureuil and Ratsima- 
manga {1254) 1948 indicate that exposure to sud- 
den temperature drops does not generally alter the 
work output. Studies on human subjects similarly 
suggest that men may operate in the cold with un- 
impaired efficiency with proper protection. Horvath 
and Freedman {1256) 1947 exposed 70 men (50 
white and 20 negro) to a temperature environment 
of —10°, —14°, and —20° F, with zero wind 
velocity. The subjects wore the 6-piece Arctic 
assembly with mukluks and felt boots. The hand- 
wear was the M-1943 mitten combination. In these 
studies, the reaction time to visual stimuli was not 
altered during continuous exposure to a low environ- 
mental temperature for periods of 8 to 14 days. 
Finger dexterity and hand strength were strikingly 
diminished by exposure to low ambient tempera- 
tures, even when the duration of such exposures was 
relatively short. This loss of hand strength and 
finger dexterity in cold environments indicates a 
need for extreme care in the design of equipment 
for cold-weather operations. Similar conclusions are 
set forth in a paper by Forlano {1255) 1950. Miller 
{1257) 1949 has emphasized that the factor of 
motivation is highly important in evaluating the 
efficiency of men doing strenuous work in a cold 
environment. 
1254. Dureuil, M. and A. R. Ratsimamanga. Action 
des variations brusques de temperature sur la capacity 
de travail force du rat normal. C. R. Soc. Biol., Paris, 
1948,142: 720-723. 
1255. Forlano, G. The effect of ambient and body tem- 
perature upon reaction time. Tech. Data Dig., 1950, 
15: 18-24. [R] 
1256. Horvath, S. M, and A. Freedman. The influence 
of cold upon the efficiency of man. /. Aviat. Med., 1947, 
18: 158-164. [P] 
1257. Miller, A. J. Physical fitness for strenuous work 
in relation to the survival situation in a cold environment. 
/. Aviat. Med., 1949, 20: 65-67. [P] 
F. IMMERSION IN COLD WATER 
In a report on physiological responses to im- 
mersion in cold water, Newburgh and Spealman 
{1263) 1943 called attention to the fact that the 
complete curve of body cooling for the rat seems 
to be logarithmic in nature. It levels off at a body COLD EXPOSURE PROBLEMS—IMMERSION 
temperature a few degrees above the water tem- 
perature. The first signs of hypothermia in the rat 
are drowsiness and motor incoordination which be- 
gin to appear as the body temperature falls below 
30° C. As it approaches 20° C., unconsciousness 
supervenes. The initial fall of body temperature of 
men immersed in cold water progresses in a linear 
manner. The rate of fall is approximately propor- 
tional to the difference between water and body 
temperature, with a tendency for body temperature 
to fall more rapidly than expected in the case of 
lower water temperatures. From experimental evi- 
dence gained by the authors, it was inferred that 
survival time of men immersed in very cold water 
would be very short. This inference was in agree- 
ment with various reports of rapid death of men 
forced into the cold waters of the North. Immersion 
in water even as warm as 30° C. (86° F.) was 
found to cause a considerable fall in body tempera- 
ture during a 2-hour period of observation. Speal- 
man {1267) 1946 found that large dogs do not 
lose heat in water at 20° C. or above. In water at 
15° C. and below, cooling occurs, but some dogs 
can maintain normal body temperature for at least 
5 hours. Dogs become seriously impaired when the 
rectal temperature declines to about 27° C. In a 
study of cardiovascular responses of dogs to im- 
mersion hypothermia, Hegnauer, Shriber, and 
Haterius {1261) 1950 measured the pulse rate, 
arterial blood pressure, electrocardiogram, and 
blood viscosity in relation to temperature within the 
right heart during immersion hypothermia. In the 
early stages of hypothermia, the pulse rate reflects 
the algebraic sum of reflex excitatory and cold 
depressor influences. In the lower temperature 
range (25° to 14° G.) the reflex influence seems 
minimal or absent. The blood-pressure regression 
with diminishing temperature follows a course in- 
dependent of the pulse rate until a temperature of 
24° to 23° C. is reached, whence complete de- 
pendence on pulse rate is evident. The blood 
viscosity increases twofold to threefold between 
normal body temperature and 20° C., hemoconcen- 
tration accounting in a large measure for the 
changes. Both systole and isometric relaxation are 
prolonged progressively with cold, there being a 
fivefold or sixfold increase at 18° G. It is suggested 
by the authors that the cause of death in hypo- 
thermia is predominantly cardiac, occasioned by 
inadequate coronary blood flow, on the one hand, 
and diminished metabolic rate, on the other. The 
former stems from a fall in pressure head, increased 
blood viscosity, and prolongation of the tension 
phases of the cardiac cycle at the expense of the 
quiescent period. A developing respiratory inade- 
quacy may influence the temperature at which 
terminal events occur, but does not affect their 
nature. 
For further studies on experimental immersion 
hypothermia, papers by Penrod {1264) 1949 and 
Wolff and Penrod {1271) 1950 should be consulted. 
In the former paper, it was shown that the oxygen 
consumption in the dog varied directly with the 
shivering responses with rectal temperatures above 
23° C. Below 23° C. rectal temperature, shivering 
was no longer a factor and the oxygen consumption 
of all dogs fell to approximately one-third that of 
the precooling control level. During rewarming, all 
dogs shivered greatly when exposed to room air, 
beginning between 24° and 28° G. rectal tempera- 
ture. The shivering could be arrested almost at once 
by immersion in warm water. The oxygen-consump- 
tion pattern followed very closely that of the 
shivering. 
There is much evidence, as Spealman {1269) 
1949 has stated, that hypothermia may rank with 
asphyxia (drowning) as a cause of death following 
shipwreck in very cold water. Hence, considerable 
effort has been expended in devising measures for 
protecting men in these circumstances. The chief 
barrier to heat loss from the nude body in cold 
water is that afforded by the skin and other periph- 
eral tissues. Heat is removed from the nude body 
more rapidly in cold water than in air at the same 
temperature. This applied also when ordinary 
clothing was worn. Minimum water temperatures in 
which nude men can maintain body temperatures 
at normal levels is about 32° to 33° C. Most men as 
well as dogs are chilled fatally in less than 1 hour in 
water near freezing. Professional distance swim- 
mers use grease for supplying further insulation to 
their bodies. Large quantities must be applied to be 
effective, about 18 liters of grease for the average 
person. In 1945, Spealman {1266) supplied data 
supporting the conclusion that most unprotected 
men cannot survive long in water below 20° C. One 
pound of petrolatum spread over the body surface 
did not afford detectable protection against the 
cooling action of the cold water. Although 6 pounds 
afforded some protection, it is not practical in most 
situations to supply such large quantities of petro- 
latum for this purpose. Glaser {1258) 1950 calcu- 
lated that in water at 0° to 5° G. the average body 
temperature of a man would fall by about 0.18° to 
0.14° G. per minute and this was confirmed by ex- 
periment. A man will withstand a brief immersion 
at 3° C. without any subjective or objective signs 
of cooling. Further experiments showed that the 
heat production of slow swimming was about 230 
to 300 calories per square meter of body surface per SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
1258-1271 
hour, and that of moderately fast swimming about 
360 calories per square meter of body surface per 
hour. Such a heat production might roughly equal 
heat losses in water near the freezing point, and it 
was concluded that men who are immersed in icy 
water have a chance of surviving if they can swim 
or as long as they can swim. This conclusion has 
been supported by reports of survivors from ship- 
wreck. For a report on survival of men immersed in 
the ocean, a paper by Molnar {1262) 1946 should 
be consulted. Survival of men in rubber floats after 
brief immersion in icy water at 4.5° C. has been 
reported by Glaser and Hervey {1259) 1951. 
The symptoms of immersion hypothermia are 
described by Wayburn {1270) 1947. In this paper, 
a report is given of the cases of six patients who 
suffered from immersion in the North Sea on return 
from long combat flying missions. Four of the pa- 
tients showed transient electrocardiographic abnor- 
malities, and one revealed abnormal blood chemical 
findings. The clinical picture following immersion 
hypothermia is the resultant of the coldness of the 
water, the length of exposure, the emotional factors 
affecting the patient before and during the expo- 
sure, and the specific response of the person to cold. 
The chief effects are those on the cardiovascular 
system, and among the transient conditions observed 
were auricular fibrillation and flutter, ventricular 
extrasystoles, slight prolongation of the P-R inter- 
val, and falling of the arterial blood pressure with 
narrowing of the pulse pressure. The nervous system 
is also affected, and there may be partial to com- 
plete loss of consciousness with irrational behavior. 
There may be hemoconcentration and notable 
hyperglycemia. Wayburn recommended rapid 
restoration of normal body temperature by external 
heat, minimal activity, administration of warm 
fluids by mouth, and in severe conditions, use of 
blood plasma. No drugs were employed in the series 
reported, and the use of adrenalin was stated to be 
contraindicated. In a comment on Wayburn’s article 
on immersion hypothermia, Hamburger {1260) 
1948 discusses the question of rapid rewarming. As 
a prisoner for 2 years at Buchenwald during World 
War II, this author stated that he does not consider 
the so-called experiments at Buchenwald on re- 
warming to be worthy of serious scientific attention. 
For studies of the effects of immersion of the feet 
in cold water, papers by Spealman {1265) 1944 
and {1268) 1949 should be consulted. 
1258. Glaser, E. M. Immersion and survival in cold 
water. Nature. Land., 1950, 166: 1068-1069. [P] 
1259. Glaser, E. M. and G. R. Hervey. Survival in 
rubber floats after brief immersion in icy water. Gt. Brit. 
MRG-RNPRG. University of Cambridge, Department of 
experimental medicine. R. N. P. 51/650, S. S. 38, April 
1951, 5 pp. 
1260. Hamburger, R. J. Immersion hypothermia. Arch, 
intern. Med., 1948, 81: 109—110. 
1261. Hegnauer, A. H., W. J. Shriber, and H. 0. 
Haterius, Cardiovascular response of dog to immersion 
hypothermia. Amer. J. Physiol., 1950, 161: 455-465. 
1262. Molnar, G. W. Survival of hypothermia by men 
immersed in the ocean. J. Amer. med. Ass., 1946, 131: 
1046-1050. 
1263. Newburgh, L. H. and C. R. Spealman. Physiologi- 
cal responses to immersion in cold water. U. S. NRG— 
CAM. C. A. M. rept. no. 164, 1 August 1943, 10 pp. [P] 
1264. Penrod, K. E. Oxygen consumption and cooling 
rates in immersion hypothermia in the dog. Amer. J. 
Physiol, 1949, 157: 436-444. 
1265. Spealman, C. R. Early changes occurring in feet 
exposed to cold water and evaluation of insulation as a 
means of protection. U. S. Navy. NMRI. Project X-297: 
Rept. no. 3, 17 May 1944, 9 pp. 
1266. Spealman, C. R. Body cooling in water and effec- 
tiveness of petrolatum in retarding heat loss. U. S. Navy. 
NMRI. Project X—189, Rept. no. 4, 24 May 1945, 9 pp. 
1267. Spealman, C. R. Body cooling of rats, rabbits, and 
dogs following immersion in water, with a few observations 
on man. Amer. J. Physiol, 1946, 146: 262-266. [P] 
1268. Spealman, C. R. Laboratory and field studies. 
Wet cold. pp. 367—370 in: Physiology of heat regulation 
and the science of clothing. Edited by L. H. Newburgh. 
Philadelphia, W. B. Saunders Co., 1949, viii, 457 pp. 
1269. Spealman, C. R. Laboratory and field studies. 
Water, pp. 370—374 in: Physiology of heat regulation 
and the science of clothing. Edited by L. H. Newburgh. 
Philadelphia, W. B. Saunders Co., 1949, viii, 457 pp. 
1270. Wayburn, E. Immersion hypothermia. Arch, 
intern. Med., 1947, 79: 77-91. [CH] 
1271. Wolff, R. C. and K. E. Penrod. Factors affecting 
rate of cooling in immersion hypothermia in the dog. 
Amer. J. Physiol, 1950, 163: 580-584. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1951, 4: 1237. [P] 
G. REWARMING AFTER COLD EXPOSURE 
For experimental studies on treatment of hypo- 
thermia, papers by Hegnauer, Flynn, and D’Amato 
{1280) 1951 and Pichotka and Lewis {1282) 1951 
should be consulted. In the former report, dogs were 
subjected to immersion hypothermia and were suc- 
cessfully rewarmed from a mean heart temperature 
of 16.2° C. (approximately the lethal temperature) 
when placed in a bath of 45° C. There was return 
to normal of the pulse rate, blood pressure, P-R and 
Q-T intervals, and the duration of systole and the 
isometric relaxation following courses proportional 
to the increasing cardiac temperature. The relation- 
ships on rewarming are almost exactly the reverse of 
those observed in cooling. This complete reversibil- 
ity suggested to the authors that, within the tem- 
perature limits described, the cardiac phenomena 
which obtain in cooling represent merely a tempera- 
ture influence on metabolic rate rather than dys- 
function through cardiac pathology. From the ex COLD EXPOSURE PROBLEMS—REWARMING 
periments reported, there is no evidence that the 
subendocardial ecchymoses seen at autopsy influence 
the course of either cooling or rewarming. In the 
studies by Pichotka and Lewis, it was found that 
rapid thawing of the frozen legs of rabbits in water 
at 42° G. for 5 to 8 minutes almost entirely pre- 
vented superficial necrosis which generally occurs 
subsequent to exposures to either —12° G. or—15° 
C. for 30 minutes. Following the — 12° C. exposure, 
13 out of 51 rabbits rewarmed in room temperature 
developed skin necrosis, while none of 75 rapidly 
thawed animals developed such a complication. 
Following the — 15° C. exposure, 13 out of 33 spon- 
taneously rewarmed rabbits lost their legs and 17 
developed superficial necrosis, while only 3 out of 39 
rapidly thawed rabbits showed skin injury. Rapid 
rewarming also was apparently responsible for a 
decrease in the extent of muscle necrosis, although 
the difference was sometimes statistically insignifi- 
cant. Prolonged rewarming in water at 42° C. up to 
1 hour produced the same beneficial results as did 
rewarming for several minutes. Rapid thawing ap- 
parently caused severe pain; however, the animals 
with rapidly rewarmed legs exhibited a better gen- 
eral appearance and preserved better function of 
the injured limbs than the rabbits whose frozen 
legs were left to thaw spontaneously. 
In a review of work carried out at the Institut 
fur Luftfahrtmedizin, Munchen, whose director 
was G. A. Weltz, Alexander {1272) pointed out 
that experimental studies on human subjects had 
led to a recommendation of the method of rapid 
and intensive rewarming in a hot water bath at 
45° C. for people in shock from exposure to cold, 
especially in water, in the treatment of service per- 
sonnel in submarines. It was recommended that the 
victim should be undressed, immersed in a bath for 
10 minutes and then rubbed dry with towels, and 
placed in heated blankets. If the body temperature 
does not continue to rise, the hot treatment should 
be repeated, until the curve of rewarming ascends 
uniformly by at least 1 degree every 10 minutes. 
Grosse-Brockhoff {1277) 1950 likewise stresses the 
importance of rapid rewarming in the therapy of 
hypothermia. To minimize pain, he recommended 
that rewarming should be started at a water-bath 
temperature of about 34° C. and increased to ap- 
proximately 40° to 43° C. within the next 5 to 10 
minutes. The quickest possible rewarming is the 
first precept of this therapy. Medication was be- 
lieved to play a minor role in acute hypothermia. 
Atropine had some satisfactory effect by diminishing 
excessive vagal influences. Even without the pres- 
ence of hypoglycemia, infusion of glucose solutions 
had a favorable effect on circulation. In prolonged 
hypothermia, the primary measure is also rapid 
rewarming applied in the same way as for acute 
hypothermia. In the chronic cases, medication is 
much more important, and large infusions of glu- 
cose are stated to be necessary. Cardiac insufficiency 
is counteracted by strophanthin and atropine is 
recommended for vagotonia; adrenal extracts are 
also indicated, according to the author. It is sug- 
gested that in all cases of hypothermia, resuscitation 
by the means of intense heat supply should be at- 
tempted as long as the body temperature is not lower 
than 18° to 20° C. and so long as muscular rigidity 
still exists. Attempts at resuscitation should not be 
given up because the state resembles apparent 
death. 
Haterius {1278) 1948 investigated the ability of 
normal dogs to withstand and to recover from cool- 
ing of the body. Lightly anesthetized animals were 
submerged in ice water at about 0° C. until a 
cardiac or respiratory crisis occurred. Resuscitative 
measures included rapid rewarming in water at 42° 
to 45° C. and artificial respiration as required. 
Thirteen animals survived a reduction in deep rectal 
temperature to an average of 14.9° C., and re- 
covery was complete in all. The decline in body 
temperature in cooling was accompanied by a 
progressive fall in arterial blood pressure and by a 
bradycardia which became intensified as the tem- 
perature of the body fell below 20° C. The slow 
heart rate was uninfluenced by vagotomy or by 
atropinization. Eight animals failed to respond 
favorably or expired before rewarming was begun. 
In some cases death was due to respiratory failure 
and in others death was of cardiac origin. These 
same data are discussed in a paper by Haterius and 
Maison {1279) 1948. 
The physiological responses of human subjects to 
immersion in ice water and to slow and fast re- 
warming have been the subjects of reports by 
Behnke and Yaglou {1275) 1950 and {1276) 1951. 
In their studies, two nude subjects aged 22 and 46 
were immersed shoulder deep in ice water for about 
1 hour until the toes became numb. At this point 
exposure was terminated. The average water tem- 
perature varied from about 42° F. in the winter 
to as high as 50° F. in the summer. Following this 
drastic chilling, the subjects were rewarmed by 
exposure to air at 73° F. to 100° F., or to water 
at 100° F. or to water at 102° F. A third subject 
dressed in outdoor winter clothing was chilled in 
a cold chamber at — 20° F. for about 3 hours, until 
his toes became numb. He was then rewarmed in 
air at 100° F. without changing clothes. Rectal, 
gastric, and oral temperatures, following initial rise, 
fell linearly during the cold exposure period. The 1272-1279 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
conclusive finding in these tests was an abrupt fall 
of deep body temperatures in a compartively warm 
environment (air temperature, 73° to 100° F.) 
following immersion in the iced water or exposure 
to cold air. In one experiment, the fall of deep body 
temperature was greater during a period of 20 
minutes with the individual in air (73° F.) than it 
was during the previous 1-hour immersion in cold 
water (50° F.). There were no untoward effects 
from the exposures to cold. Reduction or absence 
of pain after the initial immersion shock, except in 
the toes, and at the waterline skin areas protruding 
from the water, was noted. A feeling of intense cold 
occurred during the initial period of rewarming, 
despite a high surface temperature. The onset and 
maintenance of shivering was associated not with 
the cooling of the skin, but with the fall in deep 
body temperature. The authors emphasized the 
need for rapid rewarming of the chilled body to 
lessen the duration of the precipitous “after drop” 
of deep temperatures under the conditions of chill- 
ing in these experiments. 
Ames, Griffith, Goldthwait, Macht, and fielding 
{1274) 1948 have reported a study of various meth- 
ods of rewarming men after exposure to extreme 
cold. In these experiments, oxygen consumption, 
skin temperatures, rectal temperatures, thermal 
comfort, and onset of shivering of 4 men were deter- 
mined during 15 experiments, each consisting of a 
1-hour exposure to —40° F., followed by 1 hour of 
rewarming and 1 hour of reexposure to —40° F. 
Rewarming was attempted by removal of the subject 
to higher ambient temperature, that is to say, 40° F. 
or 80° F. A second method consisted of moderate 
or strenuous exercise; namely, walking on a tread- 
mill at a rate of 2.5 miles per hour on the level or 
3.5 miles per hour on a 6.5 percent grade. A third 
method involved additional thermal insulation (a 
heavy sleeping bag). A final method consisted of 
irradiation of the hands or face. The order of effi- 
ciency of the various rewarming methods, as 
measured by change in total body heat, was (1) 
strenuous exercise, (2) ambient temperature of 
90° F., (3) the sleeping bag, (4) ambient tem- 
peratures of 40° F., (5) moderate exercise, 
(6) irradiation of the face, and (7) irradiation 
of the hands. The first four procedures caused in- 
creases in total body heat during the rewarming 
period, but only in the first was the original heat 
content approximated. Moderate exercise resulted 
in cessation of heat loss without gain during re- 
warming. Irradiation of the hands or face had no 
significant effect on the total heat content. In all 
cases, the body heat decreased during the second 
hour of cold exposure at approximately the same 
rate as during the first hour. The only indications 
of acclimatization, based on results of control ex- 
periments, were a progressive increase in thermal 
comfort and a progressive delay in the onset of 
shivering during successive exposures. Commenting 
upon these same experiments, Ames, Goldthwait, 
Griffith, and Macht {1273) 1948 reported that the 
ingestion of glucose had little effect on the reactions 
of men to cold. It slightly delayed the fall in internal 
temperature. Under the conditions of this investi- 
gation, taking alcohol did not cause significant 
peripheral vasodilatation in men who had been ex- 
posed to cold. It delayed the fall in internal tem- 
perature and increased thermal comfort. In quali- 
fication of this finding, it should be pointed out that 
there is good evidence that alcohol lowers resistance 
to cold. The repeated short periods of cold exposure 
used in this series of experiments did not produce 
evidence of acclimatization in terms of cooling 
curves. The subjects appeared to maintain thermal 
comfort longer as the experiment progressed, and 
the time elapsed before the onset of shivering was 
extended. For further studies on therapy after ex- 
posure to cold, three additional reports may be 
consulted {1281, 1283, and 1284). 
1272. Alexander, L. The treatment of shock from pro- 
longed exposure to cold especially in water. U. S. Army. 
Combined intelligence objectives subcommittee, APO 413, 
Allied forces. C. I. O. S. Target No. 24. 221 pages. 
1273. Ames, A., D. A. Goldthwait, R. S. Griffith, and 
M. B. Macht. An evaluation of methods of rewarming men. 
Including a brief investigation of the effects of glucose, 
alcohol and successive exposures on the reactions of men 
to cold. U. S. Army. Office of the Quartermaster General, 
Lawrence, Mass. Quartermaster climatic research labora- 
tory. Environmental protection section, Kept. no. 134, 
31 August 1948, 40 pp. 
1274. Ames, A., R. S. Griffith, D. A. Goldthwait, M. B. 
Macht, and H. S. Belding. A study of various methods of 
rewarming men after exposure to extreme cold. Fed. Proc. 
Amer. Soc. exp. Biol., 1948, 7: 2—3. 
1275. Behnke, A. R. and C, P. Yaglou. Responses of 
human subjects to immersion in ice water and to slow 
and fast rewarming. U. S. Navy. NMRI. Project X-189, 
Kept. no. 11, 23 March 1950, 16 pp. XVIII Intern, 
physiol. Congr., August 15, 1950, 98-99. 
1276. Behnke, A, R. and C. P. Yaglon. Physiological 
responses of men to chilling in ice water and to slow and 
fast rewarming. /. appl. Physiol., 1951, 3: 591-602. 
1277. Grosse-Brockhoff, F. Pathologic physiology and 
therapy of hypothermia. Therapy of acute hypothermia, 
pp. 839—842 in: German aviation medicine. World War 
II. Vol. II. Department of the Air Force, Washington, 
D. C., 1950,1302 pp. [R] 
1278. Haterius, H. 0. Experimental hypothermia and 
rewarming in the dog: recovery after severe reduction in 
body temperature. USAF. Wright-Patterson air force 
base, Dayton, Ohio. Aero medical laboratory. Tech. rept. 
no. MCREXD—696-113, 5 February 1948, 23 pp. [P] 
1279. Haterius, H, 0. and G. L. Maison. Experimental 
hypothermia and rewarming in the dog: recovery after COLD EXPOSURE PROBLEMS—PATHOLOGICAL EFFECTS 
1280-1284 
severe reduction in body temperature. USAF. Wright- 
Patterson air force base, Dayton, Ohio. Air materiel com- 
mand, ENG. Aero medical laboratory. Serial no. 
M CREXD-696-113, 5 February 1948, 23 pp. Amer. J. 
Physiol., 1948,152: 225-232. [P] 
1280. Hegnauer, A. H., J. Flynn, and H. D’Amato. 
Cardiac physiology in dog during rewarming from deep 
hypothermia. Amer. J. Physiol., 1951, 167: 69—75. [P] 
1281. Jaulmes ( ) and ( ) Benitte. Traitment de 
1’hypothermie. Med. aeronaut., 1950, 5; 73—74. 
1282. Pichotka, J. and R. B. lewis. Effect of rapid 
and prolonged rewarming on the extent of local cold 
injury. USAF. Randolph Field, Tex. School of aviation 
medicine. Project 21-23-006, Kept. no. 7, April 1951, 
14 pp. Armed Forces med. J., 1951, 2: 1293-1310. 
1283. Smith, S. Treatment of conditions arising from 
exposure to extreme cold. pp. 4-400—4-410 in: Treat- 
ment in general medicine. Volume 4. Edited by Hobart A. 
Reimann. Fourth edition. Philadelphia, F. A. Davis Co., 
1948, 776 pp. 
1284. Anon. Therapy after exposure to cold. Air-sea 
rescue bulletin. 1946,5; 22—23. 
H. PATHOLOGICAL EFFECTS OF COLD 
In a report on the epidemiology of trauma, 
Whayne {1301) 1950 has stressed the importance 
of trenchfoot and, to a less extent, frostbite as com- 
ponents of nonbattle trauma. In World War II, the 
average disability period per case was in excess of 50 
days, and only between 10 and 20 percent of cases, 
serious enough to receive hospital care, ultimately 
could be returned to full combat duty. The patho- 
logical process of cold injury has been compared 
with that of thermal burns, except that coagulation 
of serum components does not occur. Talbott 
{1298) 1950 has pointed out that trenchfoot occurs 
in wet environments with the air temperature near 
freezing. Immersion foot occurs usually at sea, on 
liferafts, and so forth, where temperatures may be 
higher. Heat loss is accelerated by a moist environ- 
ment because wet clothing has very little insulative 
value. The early symptoms are numbness, tender- 
ness, and muscle cramps, preceded by pain. Expo- 
sures of not more than 12 hours may be sufficient to 
produce immersion foot. Pulsations are absent in 
the peripheral arteries. There is loss of cutaneous 
sensation and the skin is pale and waxy white. When 
the victim is moved to a warm environment, the 
affected member develops a bright red flush and 
arterial pulsations become clear and bounding. 
There is rapid swelling and the foot becomes hot 
and dry. Blisters, ecchymoses, and areas of gangrene 
may appear. A patient is restless, toxic, and in need 
of sedation. Talbott recommends that the limbs be 
elevated but not rubbed. Asepsis must be main- 
tained and antibiotics are recommended. The feet 
should be exposed to moderately cool air (20° G.). 
Frostbite is a hazard at subzero temperatures (about 
—10° C. and below) with high winds. Inspection 
shows pearly white areas surrounded by pale-pink 
skin. The white area becomes suffused and red on 
return to warm environment. Tingling and pares- 
thesia may persist for 1 or 2 days, and the affected 
area may desquamate. The parts should not be 
rubbed, and antibiotics should be administered 
judiciously. 
The development of tissue damage due to cold 
has been reported and discussed by Kreyberg (1288) 
1946. As the skin is chilled, the initial changes are 
purely physiological adjustments to cold. At first, 
the blood vessels contract and the skin is cold and 
cyanotic. The skin then becomes very red with a 
high oxygen content, since metabolic processes are 
greatly slowed. Also there is a shift to the left in the 
oxyhemoglobin dissociation curve. The skin becomes 
numb and the extremities clumsy. Below 10° C., 
the skin is pink and there is pain with successive 
waves of blood-vessel constriction and dilation. 
Following this, where the temperature has fallen 
well below 0° C., actual freezing of the tissues oc- 
curs. Three types of cold exposure may be distin- 
guished : (1) Short exposure to moderate cold with 
return to normal, (2) freezing the tissues to ice and 
return to normal temperature, and (3) long expo- 
sure to moderate cold with a return to normal tem- 
perature. In all of these, the pathological reaction 
to cold is an acute aseptic inflammation which pro- 
duces hyperemia, edema, and necrosis. The necrosis 
is believed to result from blood stasis following loss 
of plasma through the very permeable capillary 
wall. In the treatment of tissue damage due to cold, 
rapid heating and rubbing are to be avoided. The 
author recommends that the limb be elevated and 
gradually rewarmed to normal temperatures. Krey- 
berg {1289) 1949 found that heparin did not in- 
fluence the development of stasis, and considered 
that heparinization is of little value in the preven- 
tion of necrosis after freezing. Increased permeabil- 
ity was considered the important element in the 
development of stasis. 
Friedman {1286) 1946 has stated that there is 
no essential dissimilarity between the lesions of 
trenchfoot and of high-altitude frostbite. He be- 
lieves that agglutinative thrombosis resulting in 
ischemic gangrene can account for the most severe 
lesions. Essex and Quintanilla {1285) 1946 have 
investigated experimentally the question of whether 
frostbite results in coagulation of the blood in the 
smaller vessels leading to anoxia and further de- 
struction of the frostbitten tissue. In his study, use 
was made of the Florey modification of the Clark 
transparent chamber inserted into the ears of rab- 
bits. Pieces of carbon dioxide ice were applied 
291222—54 9 SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
directly to the window for 30 seconds. The vessels 
that had grown into the chamber were completely 
frozen. Immediately after thawing, the vessels ap- 
peared normal in all respects. However, after 5 or 
10 minutes, it was apparent that serious injury had 
been done. The vessels became widely dilated and 
filled with red and white blood cells. The perme- 
ability of the vessel walls was increased and the 
plasma was drained from the vessels, leaving the 
formed elements concentrated in the vessels in con- 
glomerate masses. Coagulation was not a factor 
since an identical picture was seen in the vessels 
of animals whose blood had been rendered in- 
coagulable by injections of heparin. For a Russian 
report on the pathogenesis of frostbite, a paper by 
Piontkovskii {1296) 1949 may be consulted. This 
author states that the majority of the Soviet research 
workers recognize that one of the leading causes of 
frostbite seems to be tissue asphyxia. In the author’s 
experiments, chilling of isolated tissue reduced 
oxidative and glycolytic processes significantly. The 
damage to the tissue respiratory system was revers- 
ible or irreversible, depending upon the degree and 
duration of chilling. It was found that the respira- 
tory mechanism of the epidermal tissues was more 
resistant to chilling than that of muscular tissue. 
Regarding the treatment of frostbite, Lane and 
Bolleruf {1290) 1951 dressed all breaks in the skin 
or anticipated breaks with loose sterile vaseline 
dressings. Cases with open lesions were given peni- 
cillin. Whirlpool baths were administered to the 
majority of cases without open lesions. A very few 
cases required surgical intervention, the times be- 
tween exposure to cold and amputation being 58 
to 86 days. The authors stated that early surgery in 
frostbite cases seems contraindicated because of the 
possibility that such premature surgery might re- 
move tissue which would eventually survive. To 
determine whether cortisone is effective in decreas- 
ing the extent of necrosis resulting from standard- 
ized local cold injuries, Lewis and Frey tag {1293) 
1951 subjected rabbits to local cold injury for 7 
days with or without treatment with 5 mgs. of 
cortisone intramuscularly each day for 2 days be- 
ginning with the day of exposure followed by 3 
mgs. a day for 4 days. There was no significant 
difference between the cortisone treated and control 
animals in the extent of skin necrosis or muscle 
necrosis. Lewis (1292) 1951 has likewise determined 
the effect of rapid thawing of frostbitten rabbit 
legs with shortwave diathermy on the extent of skin 
and muscle necrosis. In these studies, it was found 
that the use of short wave diathermy did result in a 
decrease in the extent of muscle and skin necrosis 
in comparison with control frostbitten animals 
thawed at room temperature in air. Pichotka, Lewis, 
and Luft {1295) 1950 found that hypoxia did not 
influence the extent of necrosis due to local cold 
injury if present only during the exposure to cold 
and in a preparatory period up to 30 minutes. 
Hypoxia after local cold injury increased the extent 
of the resulting damage as measured by the pro- 
portion of necrotic tissue in the exposed leg. The 
increase was in direct relationship to the length of 
the period of hypoxia. It is conceivable, according 
to the authors, that general hypoxia induces this 
effect by local oxygen deficiency or by impairment of 
the peripheral circulation. Hypoxia preceding cold 
injury influenced the outcome in a complicated 
manner. Cases with a preparatory hypoxia period up 
to 60 minutes were not different in their results from 
controls exposed to cold injury alone. Slightly longer 
hypoxic periods (60 to 90 minutes or 60 to 120 
minutes) resulted in a striking increase in the extent 
of injury measured as proportion of necrotic muscle 
tissues and as extent of the superficial skin necrosis. 
A further prolongation of the preceding hypoxic 
period (120 to 180 minutes) brought the extent of 
injury back to that of the controls and, finally, with 
a duration of 180 to 300 minutes, the extent of 
injury was below that of the controls. The authors 
attribute the differences in extent of necrosis ob- 
served after different lengths of the hypoxic period 
prior to cold injury to factors secondary to general 
hypoxia. According to Pichotka, Lewis, and Frey- 
tag {1294) 1951, functional and anatomical 
changes in rabbit legs show a sequence of increas- 
ing local injury in proportion to the degree of cold. 
Exposure to 5° G., 0° C., and —5° C. for 30 min- 
utes resulted in temporary functional changes. The 
abnormalities noted were loss of muscular power 
in the leg and foot, absence of response or hyper- 
active reaction to pinprick, loss of the spreading 
reflex of the toes, and, in some cases, hyperexten- 
sion of the ankle joint. Muscle atrophy was observed 
in the more severe of these exposures and repre- 
sented extension into a second category of increas- 
ing injury. This second category included those 
animals exposed for 30 minutes to —10° C. to 
— 12° C. In these animals there was, in addition 
to the functional changes described for the first 
category, also isolated necrosis of muscle. In the 
third category, those animals exposed to tempera- 
tures below — 12° C. for 30 minutes, there was skin 
necrosis in addition to the abnormalities observed 
in the first and second categories. Often, the end 
result of these severe injuries was complete loss of 
the leg. 
For further reports on the pathological effects of 
cold, papers by the following may be consulted: VISUAL PROBLEMS—ACUITY 
1285-1308 
Hegnauer and Penrod {1287) 1949; Lange, 
Weiner, and Gold {1291) 1949; Sawatari {1297) 
1950; and U. S. Navy {1299,1300) 1948. 
1285. Essex, H. E. and R. Quintanilla. Effects of frost- 
bite on the minute blood vessels of a peripheral vascular 
bed. Fed. Proc. Amer. Soc. exp. Biol., 1946, 5: 25-26. 
1286. Friedman, N. B. The reactions of tissue to cold. 
The pathology of frostbite, high altitude frostbite, trench 
foot and immersion foot. Amer. J. din. Path., 1946, 16: 
634-639. 
1287. Hegnauer, A. H. and K. E. Penrod. Observations 
on the pathologic-physiology in the hypothermic dog. 
USAF. Wright-Patterson air force base, Dayton, Ohio. 
Air materiel command. Technical rept. no. 5912, August 
1949, 108 pp. vi. 
1288. Kreyberg, L. Tissue damage due to cold. /. 
industr. Hyg., 1946, 28: abstract section: 83. Lancet, 
1946,7: 338-340. 
1289. Kreyberg, L. Development of acute tissue damage 
due to cold. Physiol. Rev., 1949, 29: 156-167. [R, D] 
1290. Lane, F. H. and F. Bolleruf. Evaluation of 
methods for the treatment of frostbite. USAF. Ladd air 
force base, Alaska. Arctic aeromedical laboratory. Project 
21-01-012, January 1951,14 pp. 
1291. Lange, K., D. Weiner, and M. A, Gold. Studies on 
the mechanism of cardiac injury in experimental hypo- 
thermia. Ann. intern. Med, 1949, 31: 989-1002. [P] 
1292. Lewis, R, B. Microwave diathermy treatment of 
frostbite. USAF. Randolph Field, Texas. School of avia- 
tion medicine. Project 21-23-006, Rept. no. 11, August 
1951, 3 pp. 
1293. Lewis, R. B. and E. Freytag. Use of cortisone 
in the treatment of experimental frostbite. USAF. Ran- 
dolph Field, Tex. School of aviation medicine. Project 
21-23-006, Rept. no. 9, August 1951, 3 pp. [P] 
1294. Pichotka, J., R. B. Lewis, and E. Freytag. 
Sequence of increasing local cold injury. USAF. Randolph 
Field, Tex. School of aviation medicine. Project 21-23— 
006, Rept. no. 6, March 1951, 16 pp. 
1295. Pichotka, J., R. B. Lewis, and U. C. Lnft. The 
influence of general hypoxia on local cold injury. USAF. 
Randolph Field, Tex. School of aviation medicine. Project 
21-23-016, Rept. no. 2, July 1950, 8 pp. [P] 
1296. Piontkovskii, I. A. K voprosy o proiskhozhdenii 
tkanevoi asfiksii pri otmorozheniiakh. [Contributions to the 
etiology of tissue asphyxia in frostbite.] pp. 246-251 in: 
Gipoksiia, Kiev, Akad. Nauk Ukr. SSR., 1949, 415 pp. 
1297. Sawatari, J. Influence of atmospheric cold upon 
ear, nose, throat, and their diseases. J. oto-rhinolaryng. 
Soc., Tokyo, 1950, 53 (12): 428-435. (Japanese text 
pagination.) (English text pagination.) 53-54. 
1298. Talbott, J. H. Cold: pathologic effects, pp. 252- 
255 in: Medical physics. Volume II. Edited by Otto Glas- 
ses Chicago, The Year Book Publishers, Inc., 1950, 1227 
pp. [R] 
1299. U. S. Navy. Office of Naval Advisor, Office of 
Military Government for Germany, Medical Section. 
Effect of Cold. pp. 51-66 in: Report of the second con- 
ference of special medical consultants from 30 November 
to 3 December 1942 at the Military Medical Academy, 
Berlin. Project 1, Folio VII, 23 March 1948, 137 pp. 
1300. U. S. Navy. Office of Naval Advisor, Office of 
Military Government for Germany, Medical Section. 
Injuries due to cold. pp. 164-188 in; Report of the second 
conference of special medical consultants from 30 Novem- 
her to 3 December 1942 at the Military Medical Academy, 
Berlin. Project 1, Folio VIII, 23 March 1948, 226 pp. 
1301. Whayne, T. F. Cold injury in World War II. A 
study in the epidemiology of trauma. Thesis, (Med.), 
Harvard School of Public Health. Boston, Mass., 1 May 
1950, 364 pp. 
VII. VISUAL PROBLEMS 
A. GENERAL CONSIDERATIONS 
United States submarine medical activities have 
continued to play a significant role in visual re- 
search. For a review of this work, a report by 
Shilling {1306) 1951 should be consulted. Labora- 
tory research in vision is carried out at the U. S. 
Submarine Base, New London, Conn., and at the 
U. S. Naval School of Aviation, Pensacola, Fla., 
with field studies at Camp Lejeune and at the Naval 
Medical Research Institute, Bethesda. University 
laboratories and research institutes are also engaged 
in visual research in coordination with the U. S. 
Navy. A general introduction into the military 
visual problems is provided the reader in the gen- 
eral references that follow as well as in the refer- 
ences under specific headings below. The reader is 
particularly advised to consult the papers by Harris 
{1304) 1948 and Miles and Bronk {1305) 1948. 
1302. Chapanis, A. How we see: a summary of basic 
principles, pp. 3—60 in: A survey report on human factors 
in undersea warfare, Washington, D. C., National Research 
Council, 1949, 541 pp. 
1303. Chapanis, A., W. R. Garner, and C. T, Morgan. 
How we see. Basic problems of visibility, pp. 76-93 in: 
Applied experimental psychology. New York, John Wiley 
& Sons, Inc., 1949,421 pp. 
1304. Harris, J. D. Some relations between vision and 
audition. U. S. Navy. Submarine base, New London, 
Conn. Medical research department. Project NM 000-009, 
Kept. no. I, 21 July 1948, 22 pp. [R] 
1305. Miles, W. R., and D. W. Bronk. Visual problems, 
pp. 261-277 in: Part III. Aviation Medicine in: Advances 
in Military Medicine, Vol. I. Edited by E. C. Andrus, 
D. W. Bronk, G. A. Carden, Jr., G. S. Keefer, J. S. Lock- 
wood, J, T. Wearn, and M. C. Winternitz. Boston, Little, 
Brown and Co., 1948, 472 pp. [R] 
1306. Shilling, C. W. Visual research in the U. S. 
Navy. Trans. Amer. Acad. Ophthal. Oto-laryng., 1951 
56: 868-871. 
1307. Streltsov, V. The function of the eye in aviation. 
Amer. Rev. Soviet Med., 1944,2: 126-133. 
1308. Talbot, S. A. Vision. Annu. Rev. Physiol., 1949, 
11: 245-268. [R] 
B. ACUITY 
A number of studies on the measurement of visual 
acuity have been reported from the U. S. Submarine 
Base, New London, Conn. In 1945, Sulzman, 
Farnsworth, Cook, Bartlett, and Kindred {1326) 
reported a comparison of various screening devices 
with standard medical visual procedures. This re- 1309-1330 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
port gave results of work done to determine the 
validity and reliability of various visual screening 
devices including the Ortho-Rater. It was evident 
to the authors that clinical visual testing procedures 
were not sufficiently standardized to permit com- 
parisons of the performance of the various devices. 
In 1946, Sulzman, Cook, and Bartlett {1325) in- 
vestigated the comparative efficiencies of the Key- 
stone Telebinocular, the Bausch and Lomb Ortho- 
Rater, and the American Optical Sight Screener. 
Of the three, the Telebinocular proved inferior in 
both validity and reliability to the Ortho-Rater and 
the Sight Screener with no choice indicated between 
the latter two. In every instance the reliability of 
measures of acuity for distance was found to be 
greater than the reliability of measures for near 
vision. Reliability of measurements with screening 
instruments was found to be inferior to that of 
letter-chart tests conducted according to standard 
methods. Suggestions were made by the author for 
improvement of the Snellen charts. Similar results 
are given by Cook (1311 and 1312) 1948. Dimmick 
and Rudolph {1313) 1948 have examined checker- 
board visual acuity targets of various sizes to deter- 
mine whether they contain secondary cues which 
could distort visual acuity measurements taken with 
them. A series of valid targets have been obtained. 
Such a series is an essential element in a program of 
visual-acuity measurement. Dimmick and Rudolph 
(1314) 1948 and Pratt and Dimmick {1322) 1951 
have reported ophthalmological studies of visual 
acuity under dim illumination. 
For other studies on visual acuity, the reference 
list below may be consulted. 
1309. Beyne, P. J. E. La mesure correcte de 1’acuite 
visuelle chez 1’homme. Med. aeronaut., 1950, 5: 3—18. 
1310. Chapanis, A. Vision. Annu. Rev. Physiol, 1948, 
10: 133-156. [R] 
1311. Cook, E. B. Visual acuity measurements with 
three commercial screening devices. U. S. Navy. Sub- 
marine base, New London, Conn. Medical research de- 
partment, (A revision of progress report No. 2 of BuMed 
research. Project no. X-493 (Av-263-p) by Sulzman, 
Cook and Bartlett, 7 February 1946), 22 April 1948, 44 pp. 
[P] 
1312. Cook, E. B. Comparative performance of com- 
mercial screening devices and far and near wall charts 
utilizing the same test targets. U. S. Navy. Submarine 
base. New London, Conn. Medical research department. 
Project NM-003-011 {X-493), Rept. no. 5, 30 August 
1948, 56 pp. [P] 
1313. Dimmick, F. L. and L. M. Rudolph. Checker- 
board visual acuity targets: an experimental validation. 
U. S. Navy, Submarine base, New London, Conn. Medical 
research laboratory. Project NM-003-008 {X—423), Rept. 
no. 1, December 1948, 14 pp. 
1314. Dimmick, F, L. and L. M. Rudolph. Variations 
in visual acuity under different conditions of illumination. 
U. S. Navy. Submarine base, New London, Conn. Medical 
research department. Project NM-003-008 (X-423), 
Rept. no. 1, December 1948, 14 pp. 
1315. Feinberg, R. and S. E. Wirt. Visual acuity in 
relation to illumination in the Ortho-Rater. /. appl. 
Psychol, 1947, 31: 406-412. 
1316. Giese, W. J. The interrelationship of visual 
acuity at different distances. /. appl. Psychol, 1946, 30: 
91-106. [P] 
1317. Junes, ( ). Acuite visuelle et service militaire. 
Arch. Ophtal, Paris, 1951, 11: 358-369. 
1318. Kuntz, J. E. and R. B. Sleight. Effect of target 
brightness on “normal” and “subnormal” visual acuity. 
/. appl. Psychol, 1949,33: 83-91. [P] 
1319. Low, F. N. Studies and investigations in con- 
nection with a test for peripheral visual acuity; the devel- 
opment of simple form acuity in the retinal periphery dur- 
ing dark adaptation under scotopic conditions. U. S. NRC- 
CAM. OEMcmr—345, C. A. M. rept. no. 464, 7 June 1945, 
24 pp. 
1320. Low, F. N. The peripheral motion acuity of 50 
subjects. Amer. J. Physiol, 1947, 148: 124-133. 
1321. Mandelbaum, J. and L. L. Sloan. Peripheral 
visual acuity, with special reference to scotopic illumina- 
tion. Amer. J. Ophthal, 1947, 30: 581-588. [P] 
1322. Pratt, C. and F. L. Dimmick. An ophthalmologi- 
cal study of visual acuity under dim illumination. U. S. 
Navy. Submarine base, New London, Conn. Medical re- 
search department. Project NM 003 041.04.04, Rept. no. 
173, 6 June 1951, 15 pp. 
1323. Rose, H. W. Visual acuity and refraction. Effect 
of vibration on visual acuity, pp. 891-892 in: German 
aviation medicine World War II. Vol. II. Department of 
the Air Force, Washington, D. G., 1950, 1302 pp. 
1324. Senders, V. L. The physiological basis of visual 
acuity. Psychol. Bull, 1948, 45: 465-490. 
1325. Snlzman, J. H., E. B. Cook, and N. R. Bartlett. 
Visual acuity measurements with three commercial screen- 
ing devices. U. S. Navy. Submarine base. New London, 
Conn. Medical research department. Project X-493 (Av— 
263-p), Rept. no. 2, 7 February 1946, 43 pp. 
1326. Snlzman, J. H., D. Farnsworth, E. B. Cook, 
ET. R. Bartlett, and M. I. Kindred. Comparison of various 
screening devices with standard medical visual procedure. 
U. S. Navy. Submarine base, New London, Conn. Medical 
research department. Project X-493 (Av-263-p), Rept. 
no. 1, 23 November 1945, 50 pp. 
1327. Tufts College. Visual acuity. 12 pp. in: Hand- 
book of human engineering data for design engineers. 
Tufts College, Institute for applied experimental psychol- 
ogy. SDC Human Engineering Project 20-G-l, Project 
Designation NR-783-001, Technical Report 199—1—1, 1 
December 1949, 410 pp. 
1328. 11. S. Army. Staff, Personnel research section, 
Adjutant General’s office. Studies in visual acuity. Rept. 
no. 742. Washington, D. C., U. S. Government Printing 
Office, 1948, 161 pp. [P] 
1329. Warden, C. J. An investigation of motion acuity 
under scotopic conditions at various retinal positions. U. S. 
NRC-CAM. C. A. M. rept. no. 182, 6 August 1943, 17 pp. 
[P] 
1330. Warden, C. J. An investigation of motion acuity 
under scotopic conditions at various retinal positions. U. S. 
NRC-CAM. OEMcmr-264, C. A. M. rept. no. 477, 20 
October 1945, 23 pp. [P] VISUAL PROBLEMS—COLOR VISION 
1331-1335 
1331. Warden, C. J. and K. C. Brown. A preliminary 
investigation of form and motion acuity at low levels of 
illumination. /. exp. Psychol, 1944, 34: 437-449. 
C. COLOR VISION 
For United State naval research on color vision 
conducted chiefly at the U. S. Submarine Base, New 
London, Conn., the following references should be 
consulted: 1333, 1335, 1336, 1337, 1338, 1339, 
1340, 1341, 1348, 1351, 1353, 1356, and 1357. 
Farnsworth {1336) 1950 has pointed out that no 
hope for improvement of defective color vision can 
be expected from any treatment although education 
tends to improve somewhat the color discrimination 
of both normal and color defective individuals. 
Assignment of personnel in any kind of job should 
be preceded by an understanding of the degree of 
color perception required in positions to be filled. 
Farnsworth {1335) 1946 reported the development 
and trial of the New London navy lantern as a 
selection test for serviceable color vision. It was 
concluded that the new model lantern seems to rep- 
resent the most effective instrument for testing color 
vision of naval personnel. The New London navy 
lantern color-vision test has been evaluated by Rand 
and Ray {1351) 1950. On the basis of analysis of 
results for various conditions, the authors con- 
cluded that to enjoy maximum test-retest reliability, 
the New London test must be employed under con- 
ditions for which it was designed. Several possibili- 
ties for improving the New London test were con- 
sidered. Studies of the pseudo-isochromatic plates 
for color-vision testing have been carried out by 
Farnsworth {1337) 1951, Farnsworth and Reed 
{1338) 1944 and {1339) 1945. A preliminary re- 
port on color vision is given by Shilling {1356) 
1942. This author {1357) 1943 has also reported 
tests of the Royal Canadian Navy color-vision lan- 
tern in comparison with other tests of color vision. 
Farnsworth and Reed {1340) 1946 have reported 
on comparative reaction times to “Christmas tree” 
signal lights with respect to color deficiency. One of 
the most important color discriminations involved 
in the operation of a submarine is that of reading 
the “Christmas tree,” a panel of 30 to 60 small 
jewel-shaped lights, used to indicate whether hull 
openings, such as hatches and vents, are sealed or 
not. Electrical connections with the various open- 
ings cause the indicator board to light up. Each 
hatch controls a pair of lights on the board. If a 
hatch is open, the red member of this pair is lighted; 
if it is closed, the green light comes on. When the 
board is entirely green, the submarine is rigged for 
diving. Diving operations are performed with split- 
second timing, and in these moments the safety of 
the submarine depends upon the appearance of the 
“Christmas tree.” Since the colored lights are a 
vivid red and clear green, it may be assumed that 
all colorblind individuals except extreme cases 
could distinguish between the colors. However, it 
has been assumed that colorblind individuals 
would be slower or less accurate in making such dis- 
criminations than men with normal color vision. The 
authors have attempted t© check the accuracy of 
these assumptions. The “Christmas tree” was wired 
so that the observers’ reaction times to the red and 
green light signals could be measured. A group of 4 
colorblind subjects was compared with a group of 6 
color-normal individuals to determine the difference 
in mean reaction times when lights were at full 
brightness. Four hundred and sixty trials were given 
each man. Slight difference was found between the 
two groups. Since on patrol the lamps are custo- 
marily burned on reduced voltage, tests were car- 
ried out to approximate the appearance of a 
dimmed board. To accomplish this, the green jewel 
was changed slightly in color by the addition of a 
yellow filter. Two colorblind subjects and two men 
with normal-color vision were tested under these 
conditions. The change in color greatly lengthened 
the reaction time of the colorblind subjects but not 
of the normal subjects. It was concluded from the 
experiments that colorblind individuals are able to 
read the “Christmas tree” at full brightness nearly 
as rapidly as normal subjects. As the voltage sup- 
plying the lamps in the “Christmas tree” is dropped, 
the colorblind subjects may be expected to show 
progressively greater hesitancy in discriminating the 
red from the green jewels. The use of bluish-green 
glasses would be expected to decrease the confusion 
effect for colorblind subjects. 
For other studies on color vision and color- 
vision testing, the references given below should be 
consulted. 
1332. Christian, F., R. Haas, and V. V. Weizsacker. 
Uber ein Farbenphanomen. (Polyphane Farben.) Pfliig. 
Arch. ges. Physiol, 1948, 249: 655-701. [D] [P] 
1333. Farnsworth, D. The effect of colored lenses upon 
color discrimination. U. S. Navy. Submarine base, New 
London, Conn. Medical research department. Color vision 
rept. no. 9, N. L. Sub.—l—CV—17, Project X—502 (Av— 
269-p), 3 September 1945, 15 pp. 
1334. Farnsworth, D. and P. Foreman. A brief history 
of lanterns for testing color sensation and description of 
the essential principles. U. S. Navy. Submarine base, New 
London, Conn. Medical research department. Project 
X—457 {Av-241-k), Preliminary Kept., 15 April 1946, 
12 pp. 
1335. Farnsworth, D. Development and trial of New 
London navy lantern as a selection test for serviceable 
color vision. U. S. Navy. Submarine base, New London, 
Conn. Medical research department. Project X-457 (Av- 
241-k), Final Kept., 6 May 1946, 39 pp. [P] SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
1338-1359 
1336. Farnsworth, D. Color vision, pp. 309-311 in: 
Handbook of applied psychology. Volume 1. Edited by 
Douglas H. Fryer and Edwin R. Henry. New York, 
Rinehart and Co., Inc., 1950, ix, 380 pp. 
1337. Farnsworth, D. Proposed armed forces color vi- 
sion test for screening. U. S. Navy. Submarine base. New 
London, Conn. Medical research laboratory. Project NM 
003 041.10.01, 20 August 1951, 9 pp. 
1338. Farnsworth D. and J. D. Reed. The effect of 
changing the illumination on the colors in pseudo- 
isochromatic plates. U. S. Navy. Submarine base, New 
London, Conn. Medical research laboratory. Color Vision 
Rept. no. 5, 3 January 1944, 10 pp. 
1339. Farnsworth, D. and J. D. Reed. Comparison and 
evaluation of American Optical Co. pseudo-isochromatic 
plates, first and second editions. U. S. Navy. Submarine 
base. New London, Conn. Medical research department. 
Project X-480 {Av-255-p), Rept. no. 8, 19 March 1945, 
50 pp. 
1340. Farnsworth, D. and J. D. Reed. Comparative re- 
action times to Christmas tree signal lights with respect to 
color deficiency. U. S. Navy. Submarine base, New Lon- 
don, Conn. Medical research department. Project X-265 
(Av-153-c), Rept. no. 10, 5 February 1946, 11 pp. 
1341. Farnsworth, D., J. D. Reed, and C. W. Shilling. 
The effect of certain illuminants on scores made on 
pseudo-isochromatic tests. U. S. Navy. Submarine base, 
New London, Conn. Medical research laboratory. Color 
vision rept. no. 4, 22 November 1943, reissued 1 December 
1948, 9 pp. 
1342. Frick, D. C., E. L. Green, and J. M. Fry. The 
AAF. SAM color code test (Colcode); a performance test 
of color discrimination ability. USAF. Randolph Field, 
Tex. School of aviation medicine, Project 415, Rept. no. 
1, 18 September 1945, 15 pp. 
1343. Granit, R. A physiological theory of colour per- 
ception. Nature, Land., 1943,151: 11-14. 
1344. Hardy, L., G. Rand, and C. Rittler. Les epreuves 
de la vision des couleurs. Ann. Oculist., Paris, 1950, 183: 
515-518. [D] 
1345. Hardy, L., G. Rand, and C. Rittler. La vision des 
couleurs et les travaux recents sur les epreuves de la 
vision coloree. Ann. Oculist., Paris, 1950, 183: 519-532. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1951, 4: 1298. 
1346. Hartridge, H. A proposed colour blindness test. 
Proc. ninth intern. Congr. industr. Med., London, 1948, 
1052—1053. (French summary.) 
1347. Hartridge, H. Human colour vision. XVI Con- 
di. ophth. 1950 Acta, 1: 561-567. (French and Spanish 
summaries.) 
1348. Malone, F. L., M. S. Sexton, and D. Farnsworth. 
The detectability of yellows, yellow-reds, and reds, in air- 
sea rescue. U. S. Navy. Submarine base, New London, 
Conn. Medical research laboratory. Project NM 003 
041.35.01, 27 September 1951, 8 pp. 
1349. Motokawa, K. A physiological basis of color dis- 
crimination, Tohoku J. exp. Med., 1949, 51: 197-205. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1950, 3: 1257. [P] 
1350. Peckham, R. H. The influence of sun glasses on 
object-color perception. Temple University, Philadelphia. 
O. N. R. contract no. NR 142—565, 16 September 1949. 
28 pp. [P] 
1351. Rand, G. W. and J. T. Ray. Evaluation of the 
New London Navy lantern color vision test. U. S. Navy. 
NATO, Pensacola, Fla. School of aviation medicine. Joint 
report with Tulane University, Department of psychology. 
Report no. 1, 16 May 1950, 17 pp. [P] 
1352. Rose, H. W. and I. Schmidt. Physiological effects 
of reflective, colored, and polarizing ophthalmic filters. II. 
Effect of ophthalmic filters on color vision. USAF, Ran- 
dolph Field, Tex. School of aviation medicine. 2nd print- 
ing to replace issue distributed November 1949. Project 
21-02-040, Kept. no. 2, March 1950, 29 pp. [P] 
1353. Schelling, H., von. A method for calculating the 
effect of filters on color vision. U. S. Navy. Submarine base. 
New London, Conn. Medical research laboratory. Project 
NM 000 009, Kept. no. 3, 15 September 1949, 14 pp. [P] 
1354. Schmidt, I. New tests for the examination and 
training of color vision. 1. Pseudo-isochromatic plates. 
USAF. Randolph Field, Tex. School of aviation medicine. 
Project 517, Rept. no. 1, July 1948, 11 pp. [P] 
1355. Schmidt, I. Comparative evaluation of the New 
London Navy lantern for testing color perception. USAF. 
Randolph Field, Tex. School of aviation medicine. Proj- 
ect 21-29-009, August 1951, 10 pp. 
1356. Shilling, C. W. Preliminary report on color vision 
testing. U. S. Navy. Submarine base. New London, Conn. 
Medical research department. Project X-42 (V5-2), 
September 12, 1942, 14 pp. 
1357. Shilling, C. W. Royal Canadian Navy colour 
vision lantern in comparison with other tests of color 
vision. U. S. Navy. Submarine base, New London, Conn. 
Medical research division. Project X-42 (Av-5-2), 18 
January 1943, 21 pp. 
1358. Willmer, E. N. Retinal structure and colour vision. 
A restatement and a hypothesis. Cambridge, The Univer- 
sity Press, 1946, 231 pp. 
1359. Wright, W, D. Researches on normal and defec- 
tive colour vision. London, Henry Kimpton, 1946, 383 pp. 
D. VISUAL PERFORMANCE 
For United States naval studies on practical prob- 
lems concerned with visual performance, the fol- 
lowing references should be consulted: 1363, 1364, 
1371, 1373, 1374, and 1375. In 1948, Farnsworth 
{1363) reported proposed modifications of red and 
green navy signal lights. Standards for general- 
purpose sunglasses were given by Farnsworth 
{1364) in 1948. Sperling and Farnsworth {1371) 
1950 have discussed factors determining periscope 
acuity at night. 
A highly important task in the submarine is the 
reading of the dials of the TDC. Verplanck {1373) 
1946 has reported an experiment on the legibility 
of the TDC under several conditions of illumina- 
tion and adaptation. Two measures of efficiency in 
reading the dials of the TDC were obtained on six 
subjects, under several conditions of preadaptation 
and of conning-tower illumination. In both meas- 
ures of efficiency, changes associated with the pre- 
adaptation conditions were observable. Subjects 
who had previously adapted in red illumination for 
15 minutes read the TDC dials more quickly and 
with fewer errors than when they were not pre- VISUAL PROBLEMS—NIGHT VISION 
1360-1381 
adapted. For a comprehensive discussion of visual 
communication, a report by Verplanck {1375) 
1949 should be consulted. 
Other studies on visual performance are reported 
in the references given below. 
1360. Bartley, S, H. The basis of visual fatigue. Amer. 
J. Optom., 1947,24: 372-384. 
1361. Bitterman, M, E. Lighting and visual efficiency: 
the present status of research. Ilium. Engr., N. Y., 1948, 
43: 906-931. (Discussion by Mathew Luckiesh.) [R] 
1362. Bitterman, M, E., T. A. Ryan, and C. L. Cottrell. 
Muscular tension as an index of visual efficiency: A 
progress report. Ilium. Engr., N. Y., 1948, 43: 1074-1086. 
(Discussion by M. Luckiesh and S. K. Guth.) [P] 
1363. Farnsworth, D. Proposed specifications of red and 
green navy signal lights. U. S. Navy, Submarine base. 
New London, Conn. Medical research department. Project 
X—265 (Av-153—c), Adjunct Rept., 1 March 1948, 17 pp. 
1364. Farnsworth, D. Standards for general purpose 
sunglasses. U. S. Navy. Submarine base. New London, 
Conn. Medical research laboratory. Project NM 000 009, 
Rept. no. 2, 10 September 1948, 27 pp. 
1365. Holmes, J. G. Colour recognition of very small 
light sources. Docum. Ophth., 1949, 3: 240-250. [P] 
1366. Kravkov, S. V, Stimulating visual function. Amer. 
Rev. Soviet Med., 1944-45, 2: 353-355. 
1367. Saltzman, I. J., and W. R. Garner. The effects 
of size and brightness on the speed of identifying number 
of range rings. Johns Hopkins University, Psychological 
laboratory. Technical rept. no. SDC 166-1-79, 20 January 
1949, 13 pp. [P] 
1368. Saunders, E. E. Navy eye-correction, eye-protec- 
tion program. Trans. Amer. Acad. Ophthal. Oto-laryng., 
1947-48, 52: 562-565. 
1369. Simonson, E. and J. Brozek, Effects of illumina- 
tion level on visual performance and fatigue. /. opt. Soc. 
Amer., 1948, 38: 384-397. 
1370. Simonson, E., J. Brozek, and A. Keys. Effect of 
meals on visual performance and fatigue. /. appl. Physiol., 
1948, 1: 270-278. [P] 
1371. Sperling, H. G. and D. Farnsworth. Periscope 
acuity at night. 1. Central and paracentral acuity as a 
function of contrast and adaption. U. S. Navy. Submarine 
base, New London, Conn. Medical research laboratory. 
Project NM 003 041.39.01, 28 November 1950, 21 pp. 
1372. Stump, N. F. Industrial safety and visual func- 
tions. /. Psychol., 1945, 20: 369—379. 
1373. Verplanck, W. S. A brief experiment on the 
legibility of the TDC under several conditions of illumina- 
tion and adaptation. U. S. Navy. Submarine base, New 
London, Conn. Medical research department. Project 
X-519 (Av-273-p), Final Rept., 15 March 1946, 8 pp. 
1374. Verplanck, W. S. A field test of the use of filters 
in penetrating haze. U. S. Navy. Submarine base. New 
London, Conn. Medical research department. Project NM- 
011-003, Final Rept., 6 June 1947, 11 pp. [P] 
1375. Verplanck, W, S. Visual communication, pp. 
249-266 in: A survey report on human factors in undersea 
warfare. Washington, D. C., National Research Council, 
1949, 541 pp. 
1376. Williams, S. B. Visibility on cathode-ray tube 
screens: viewing angle. /. opt. Soc. Amer., 1949, 39: 
782-785. [P] 
1377. Williams, S. B. Visibility on radar scopes, pp. 
101-130 in: A survey report on human factors in undersea 
warfare. Washington, D. C., National Research Council, 
1949, 541 pp. 
E. ACCOMMODATION 
The status of this subject from the point of view of 
the submarine service remains virtually the same as 
at the time of preparation of the first volume of this 
Sourcebook. 
1378. Peterson, J. H. and E, Simonson. Effect of glare 
on accommodation near point. Amer. J. Ophthal., 1951, 
34: 1088-1092. [P] 
F. PHOBIA 
Cook {1379) 1948 has reported a factor analysis 
of acuity and phoria measurements obtained with 
commercial screening devices and by standard clini- 
cal methods. A comparative study of measures of 
heterophoria has been reported by Sulzman, Cook, 
and Bartlett (1381) 1946. Both of these papers indi- 
cate the need for further research. 
1379. Cook, E. B. A factor analysis of acuity and phoria 
measurements obtained with commercial screening devices 
and by standard clinical methods. U. S. Navy, Submarine 
base. New London, Conn. Medical research laboratory. 
Project NM-003-001 (X-493), Kept. no. 4, 15 August 
1948, 26 pp. 
1380. Duguet, J. Action de 1’anoxie sur les hetero- 
phories. Med. aeronaut., 1951, 6: 15—23. 
1381. Sulzman, J. H., E. B. Cook, and N. R. Bartlett. 
Comparative study of measures of heterophoria. U. S. 
Navy, Submarine base, New London, Conn. Medical re- 
search department. Project X-493 (Av-263-p), 22 Feb- 
ruary 1946, 39 pp, 
G. NIGHT VISION AND DARK ADAPTATION 
The large number of references in this section 
reflects the vital significance of night visual acuity 
in submarine operations. Nighttime provides con- 
ditions during which the striking power of the sub- 
marine is at its maximum. It is therefore particu- 
larly important that submarine personnel possess 
excellent night visual capacity. Studies of night 
vision and dark adaptation carried out at the U. S. 
Submarine Base, New London, Conn., are reported 
in the following items: 1396, 1429, 1435, 1436, 
1437, 1438, 1466, 1470, 1475, 1476, 1477, 1478, 
1479, and 1480. 
Verplanck has reported a number of tests of the 
radium plaque adaptometer. In field tests reported 
in 1943, Verplanck {1475) stated that the radium 
plaque adaptometer, as delivered, was subject to 
mechanical improvements, but aside from this, the 
adaptometer was satisfactory as a testing device. 
Addition of an intermediate filter was expected to 
improve its performance in the testing of difficult SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
subjects. For the proper development of necessary 
skill in testing personnel, supervised instruction of 
operators was considered essential. Modifications 
of the instruction manual were proposed. In 1944, 
Verplanck {1476) reported night-vision testing of 
5,750 men using the radium plaque adaptometer. 
Of all of the men tested, 82.5 percent passed the 
test. Although failing a first test, approximately 60 
percent passed the second test. Only 30 percent of 
those failing the two tests would be expected to 
pass a third test. Approximately 5 percent of the 
population failed the radium plaque adaptometer 
test on three consecutive tests. It was suggested by 
the author that these latter may constitute that 
section of the population who can be designated as 
nightblind. In 1945, Verplanck {1477) reported 
on the effect of increasing the difficulty of the 
radium plaque adaptometer test of night vision. It 
was asserted that the reliability of the test at a lower 
level of brightness is the same as at the standard 
level, and it was concluded by the author that no 
insignificant purpose would be served by altering 
the difficulty of the test. One result of increasing 
the difficulty of the test would be to fail a larger 
percentage of subjects, which would be of doubtful 
desirability in a test of undetermined validity. 
The predictive value of the radium plaque adap- 
tometer and other physiological measures of night 
vision for score on performance approximating the 
standing of a night lookout watch was discussed by 
Verplanck {1478) 1946. This report covered the 
development and use of the night lookout training 
stage at the Lookout School, U. S. Submarine Base, 
New London, Conn. On the basis of several years 
of experience with the night lookout trainer, it was 
concluded that 1 or 2 sessions on the night lookout 
trainer employing the basic drill serves satisfactorily 
to establish the fundamental habits of night lookout; 
namely, the use of off center vision. Further training 
sessions must stress realism and interest. These not 
only give additional practice in the use of night 
vision, but also, more important, they teach and 
drill correct scanning procedure. They also offer 
opportunity for correction of faulty reporting pro- 
cedures and give greater familiarity with relative 
bearings. The night lookout trainer cannot be made 
to yield a score or other basis upon which a man’s 
future ability as a lookout may be predicted. The 
trainer is not a testing device, although simulated 
“tests” on it may serve as a motivation of the men 
under training. In 1946, Verplanck {1480) reported 
on the reliability of the radium plaque adaptometer 
over long test-retest intervals. The radium plaque 
adaptometer scores of 723 men who took the radium 
each of two testing periods spaced more than 6 
months apart were analyzed. On the basis of this 
work, it was possible to state that the radium plaque 
adaptometer test systematically separates out a 
small portion of the population which is unable to 
perform satisfactorily a test requiring adequate red 
vision. 
The effect of night vision training on radium 
plaque adaptometer scores has been investigated by 
Orlansky {1438) 1945. This study was designed to 
ascertain if prior training on the Evelyn night- 
vision trainer would cut down the number of men 
failing the radium plaque adaptometer test. The 
author concluded that if there are any effects of 
training that can be measured by the radium plaque 
adaptometer they are transient in duration. 
The illumination of the conning tower of the 
submarine is a highly important matter because of 
the need for preservation of dark adaptation of 
officers who may use the periscope. In 1946, Ver- 
planck {1479) investigated the red illumination of 
the submarine conning tower. Verplanck’s experi- 
ments were designed to provide a practical evalua- 
tion of the red illumination in the conning tower. 
The visual performance simulated that of an officer 
at the periscope and the illumination conditions in- 
vluded complete absence of lights in the conning 
tower, full illumination of all night lights and of all 
instruments in a conning tower painted black, and 
full illumination of all night lights and of all instru- 
ments in a conning tower painted flat white. The re- 
sults of the experiments clearly indicated that with- 
out respect to the interior paint finish, the red light 
provided in the conning tower by two 50-watt red 
steamtight fixtures, although sufficient to permit 
casual reading and chartwork, was not sufficient to 
impair to any measurable extent practical night 
visual performance of personnel working in the 
conning tower. 
Dark adaptation of divers has been investigated 
in field tests by Everly and Kennett {1396) 1946. 
Data are presented on 120 dives in water of a depth 
of 15 to 18 feet in which the bottom was very muddy 
and the tide and current conditions such as to make 
the advantages of dark adaptation difficult to meas- 
ure. Subjective improvement was reported by 60 
divers. Measurable improvement was noted in 42 
dives in 170 feet of water by dark adapted divers. 
The practicability of dark adapting the divers by 
tfie use of dark adaptation goggles worn until the 
diver was on the bottom has been demonstrated. 
For other reports on night vision and dark adap- 
tation, the reference list below may be consulted. VISUAL PROBLEMS—NIGHT VISION 
1382-1418 
Various factors influencing dark adaptation are dis- 
cussed. Attention in the past has been given to the 
possibility of improving night vision by the adminis- 
tration of vitamin A. While it appears that defi- 
ciency of dark adaptation may be brought about by 
serious vitamin A lack, there is no evidence that 
dark adaptation of normal individuals is any way 
improved by addition of vitamin A to the diet, even 
in huge doses (1383). 
1382. Abramson, E. and T. Heyman. Dark adaptation 
and inhalation of carbon monoxide. Acta physiol, sc and., 
1944, 7; 303-305. [P] 
1383. Adler, F. H. Night blindness and vitamin A. pp. 
578-579 in: Physiology of the eye. St. Louis, C. V. Mosby 
Co., 1950,709 pp. 
1384. Adler, F. H. The effects of anoxia on dark-adapta- 
tion. pp. 579-581 in: Physiology of the eye. St. Louis, 
G. V. Mosby Co., 1950, 709 pp. 
1385. Babskii, E. B. and D. K. Sknlov. Vliianie adrena- 
lina na svetovuiu chuvstvitel’nost’ i temnovuiu adaptatsiiu 
glaza. [Effect of adrenalin on the light sensitivity and the 
dark adaptation of the eye.] Fiziol. Zh. S. S. S. R., 1946, 
32: 169-174. 
1386. Birren, J. E., M. W. Bick, and C. Fox. Age 
changes in the light threshold of the dark adapted eye. 
/. Gerontol, 1948, 3: 267-271. Abstr. World Med., 1949, 
6: 10. 
1387. Blystad, W. Dark adaptation in pigmented rats. 
The effect of overexposure to light. Acta Opthal, Kbh., 
1951, 29: 49-68. [P] 
1388. Campbell, D. A. A comparison of dark adaptation 
with the psychological state in miners. Brit. J. Ophthal, 
1948,32: 225-226. 
1389. Campbell, D. A., R. Harrison, and J. Vertigen. 
Binocular vision in light adaptation and dark adaptation 
in normal subjects and coal-miners. Part I. Normal sub- 
jects. Brit. J. Ophthal, 1951, 35: 395—405. [P] 
1390. Chapanis, A. The dark adaptation of the color 
anomalous. Amer. J. Physiol, 1946, 146: 689-701. [P] 
1391. Chapanis, A. and E. A. Pinson. AML portable 
radium plaque night vision tester. Air Surg. Bull, 1945, 
2: 285. 
1392. Chapanis, A., R. 0. Rouse, and S. Schachter. The 
effect of inter-sensory stimulation on dark adaptation and 
night vision. J. Exp. Psychol, 1949, 39: 425-437. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and 
Pharmacology), 1950, 3: 1099. [P] 
1393. Clark, B. and M, J. Johnson. The effect of sun- 
light on dark adaptation. Contact. Pensacola, 1945, 5: 
461-467. Amer. J. Ophthal, 1946, 29: 828-836. [P] 
1394. Clark, W. B. and M. L. Johnson. The course of 
dark adaptation after wearing orange dark adaptor 
goggles. U. S. Navy. NATB, Pensacola, Fla. School of 
aviation medicine. Project (Av-230-p), Rept. 
no. 1, 19 February 1945, 12 pp. 
1395. Cuppers, C. and E. Wagner. Zur pharmakologi- 
schen Beeinflussung der Netzhautfunktion. I. Teil: Die 
Dunkeladaptation des Normalen. Klin. Mbl Augenheilk., 
1950, 117: 59-69. [P] 
1396. Everley, I. A. and W. Kennett. Field test of dark 
adaptation of divers. U. S. Navy. Submarine Base, New 
London, Conn. Medical research department. Project 
X-663 {Av-241-p), Final Rept., 15 July 1946, 16 pp. 
1397. Fang, H. S. Comparative study of the effects of 
certain drugs on cone and rod dark adaptation. Tohoku J. 
exp. Med., 1950/51, 52-53: 115-124. [P] 
1398. Feldman, J. B. Practice of dark adaptation. Arch. 
Ophthal., Chicago, 1938, 19: 882-901. [R] 
1399. Ferree, C. E. and G. Band. The transition from 
day to night lighting. Personnel J., 1933, 11: 237-254. [P] 
1400. Grant, D. A. and F. A. Mote. Effects of brief 
flashes of light upon the course of dark adaptation. J. exp. 
Psychol, 1949, 39: 610-616. [P] 
1401. Grant, D. A. and E. B, Norris. Dark adaptation 
as a factor in the sensitization of the beta response of the 
eyelid to light. J. exp. Psychol, 1946, 36: 390-397. [P] 
1402. Gt. Brit. RNPRG—VPS. Letter from the electrical 
officer, H. M. S. Euryalus, 11 June 1951, V.P. S. 26, no 
date, 2 pp. 
1403. Hanaoka, T. Effect of melanophore-hormone upon 
the scotopic vision of human eye. Jap. J. Physiol, 1951, 
2: 9-16. 
1404. Hartline, H. K. Problems of visual physiology dur- 
ing the war. Fed. Proc. Amer. Soc. exp. Biol, 1946, 5: 
351-354.[R] 
1405. Hartline, H. K., L. J. Milne, and I. H. Wagman. 
Fluctuation of response of single visual sense cells. Fed. 
Proc. Amer. Soc. exp. Biol, 1947, 6: 124. 
1406. Hecht, S. Sunlight harms night vision. Air Surg. 
Bull, 1945, 2: 45. [P] 
1407. Hecht, S. and C. D. Hendley. The effect of sun- 
light on night vision. U. S. NRC-CAM. C. A. M. Report 
no. 420, 24 March 1945, 11 pp. [P] 
1408. Hecht, S., C. D. Hendley, S. Ross, and P. Rich- 
mond. Influence of exposure to intense sunlight on subse- 
quent night vision. U. S. Navy. Medical field research 
laboratory, Camp Lejeune, North Carolina. Project X— 
442 (Av-233-w), 26 April 1945, 32 pp. 
1409. Hecht, S., C. D. Hendley, S. Ross, and P. N. Rich- 
mond. The effect of exposure to sunlight on night vision. 
Amer. J. Ophthal, 1948, 31: 1573-1580. [P] 
1410. Hecht, S. and Y. Hsia. Dark adaptation following 
light adaptation to red and white lights. J. opt. Soc. Amer., 
1945, 35: 261-267. [P] 
1411. Hinn, G. J., and R. A. Montano. A case of night 
blindness. Air Surg. Bull, 1945, 2; 287. [CH] 
1412. Hodel-Boos, M. von. Untersuchungen fiber das 
Bewehungssehen bei Hell-und Dunkel-adaptation. Oph- 
thalmologic a., 1948, 115: 25-46. (French and English 
summaries.) Excerpta Medica. Section II. (Physiology, 
Biochemistry, and Pharmacology), 1949, 2: 510. Abstr. [P] 
1413. Holmes, W. J. Night vision. I. A comparison of 
the scotopic visual ratings of young Japanese and Cauca- 
sian adults living in Hawaii. Arch. Ophthal, Chicago, 
1946, 36: 141-154. 
1414. Holmes, W. J. Night vision. II. A comparison and 
critique of various procedures used for night vision testing. 
Arch. Ophthal, Chicago, 1946,56; 302—314. 
1415. Hosoya, Y., H. S. Fang, and M. T. Peng. The 
effect of nicotinic acid amide on dark adaptation. Tohoku 
J. exp. Med., 1951, 53: 103-108. [P] 
1416. Hosoya, Y., H. S. Fang, and M. T. Peng. Choline 
and dark adaptation in man. Tohoku J. exp. Med., 1951, 
53: 109-113. [P] 
1417. Johnson, E, P. The electrical response of the 
human retina during dark-adaptation. /. exp. Psychol, 
1949, 39: 597-609. [P] 
1418. Keil, F. C. Use of red light to facilitate dark adap- 
tation. U. S. AAF. Randolph Field, Tex. School of aviation 
291222—54—10 1419-1452 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
medicine. Project 118, Rept. no. 1, 19 February 1943, 
3 pp. 
1419. Kekcheev, K. K. Methods of accelerating dark 
adaptation and improving night vision. War. Med., Chi- 
cago, 1945, 8: 209-220. [P, R] 
1420. Lee, R. H., M. Pijoan, H. R, Catchpole, and E. M. 
Finch. Periodic fluctuations and threshold levels in dark 
adaptation and the effects produced by paredrine, oxygen, 
carbon dioxide, and ascorbic acid. U. S. Navy. NMRI. 
Project X-211, Rept. no. 2, 12 September 1944, 7 pp. 
1421. Livingston, P. C. The form and character of rod 
scotometry. Amer. J. Ophthal., 1944, 27: 349-353, 428. 
1422. Low, F. N. The peripheral visual acuity of 100 
subjects under scotopic conditions. Amer. J. Physiol., 
1945, 146: 21-25. [P] 
1423. Low, F, N. Studies and investigations in con- 
nection with a test for peripheral visual acuity: the night 
visual acuity of 100 normal night seers. U. S. NRC-CAM. 
C. A. M. Report no. 409, 25 January 1945, 4 pp. [P] 
1424. Low, F. N. Some characteristics of peripheral 
visual performance. Amer. J. Physiol., 1946, 146: 573-584. 
1425. Low, F. N. The development of peripheral visual 
acuity during the process of dark adaptation. Amer. J. 
Physiol, 1946, 146: 622-629. [P] 
1426. Lowery, E. A. and F. R. Brown. Instrument 
lighting—investigations of ultraviolet reflections. Part 3. 
A study of dark adaptation during observation of an ultra- 
violet activated aircraft instrument panel. U. S. Navy. 
BuAer. Aero medical laboratory, Philadelphia, Penna. 
Rept. TED no. NAM 31334, Part 3, 28 April 1950, 9 pp. 
[P] 
1427. McDonald, P. R. Evaluation of night vision. 
Amer. J. Ophthal, 1949, 32: 1535-1553. [P] Trans. 
Amer. ophthal. Soc., 1948, 46: 576-607. [R] [P] 
1428. MacGown, J. C. Night vision training and night 
vision in operational flying. Inter-allied conferences on 
war medicine, 1942—1945. 1947, 405-407. 
1429. MacMartin, L. S. and F. L. Dimmick. Mapping 
the central scotoma of the dark adapted retina: com- 
parison of a moving stimulus with a stationary presenta- 
tion. U. S. Navy. Submarine base, New London, Conn. 
Medical research laboratory. Project NM 003 041.09.02 
(formerly NM 003 024), 1 November 1949, 18 pp. 
1430. Mandelbaum, J. and W. M. Rowland. A pho- 
tometer for calibrating the AAF Eastman night vision 
tester. U. S. AAF. Randolph Field, Tex. School of avia- 
tion medicine. Project 262, Rept. no. 1, 1 May 1944, 5 pp. 
1431. Mann, I. and F. W. Sharpley. The normal visual 
(rod) field of the dark-adapted eye. J. Physiol, 1947, 
106: 301-304. [P] 
1432. Matthews, B. H. C. and A. K. Luczak. Some 
factors influencing dark adaptation. Gt. Brit., FPRC. 
F. P. R. C. Rept. no. 577, June 1944, 23 pp. [P] 
1433. Medvedev, Y. I, Ob izmenenii slukhovoi, 
taktil’noi i vibratsionnoi chuvstvitel’ nosti pri temnovoi 
adaptatsii glaza. [Modifications of aural, tactile and vi- 
bratory sensitivity in dark adaptation of the eye.] Fiziol. 
Zh. S. S. S. R., 1951,37: 35-40. 
1434. Millard, E. B. Jr., and W. S. McCann. Effect 
of vitmin A2 on the red and blue threshold of fully dark 
adapted vision. J. appl. Physiol, 1950, 1: 807-810. 
1435. Mitchell, R. T. The effect of low color tem- 
perature illumination and red illumination upon subse- 
quent dark adaptation. U. S. Navy. Submarine base. New 
London, Conn. Medical research department. Project 
NM 003 008, Rept. no. 2, 5 August 1949, 14 pp. 
1436. Mitchell, R. T., A. Morris, and F. L. Dimmick. 
The relation of dark adaptation to duration of prior red 
adaptation. U. S. Navy. Submarine base. New London, 
Conn. Medical research laboratory. Project NM 003 
041.49.01, 6 December 1950, 19 pp. 
1437. Morris, A. and F. L, Dimmick. Visual acuity 
at scotopic levels of illumination. U. S. Navy. Submarine 
base. New London, Conn. Medical research laboratory. 
Project NM 003 041.04, Kept. no. 3, 4 December 1950, 
26 pp. [P] 
1438. Orlansky, J. The effect of night vision training 
(Evelyn Trainer) on U. S. Navy radium plaque adaptom- 
eter scores. U. S. Navy. Naval air station, Quonset Point, 
R. I. Medical department. Project X-558 (w-289-p), 
16 April 1945, 8 pp. 
1439. Ourgaud, A. G. Vision nocturne et vitamine A. 
/. Med. Chir. prat., 1949,120: 171-179. [D] 
1440. Peckham, R. H. Night vision for military person- 
nel. Society proceedings. Amer. J. Ophthal., 1947, 30: 
1588-1589.[R] 
1441. Peckham, R. Protection and maintenance of night 
vision for military personnel. Arch. Ophthal., Chicago, 
1947, 38: 569-571. 
1442. Rees, W. L. Night visual capacity of neurotic 
soldiers. /. Neurol. Neurosurg. Psychiat., 1945, 8: 34-39. 
1443. Reid, D. D. Night visual capacity and its relation 
to survival in operational flying. Brit. J. Psychol., 1950, 
3: 141-149. [P] 
1444. Ripple, P. H. Appraisal of the Consolidated Night 
Vision Tester. USAF. Randolph Field, Tex. School of 
aviation medicine. Project 21-02-088, February 1949, 
6 pp. [P] 
1445. Rochon-Duvigneaud, A. L’adaptation et la vision 
nocturne chez les vertebres. Nature, Paris, 1946, 74: 
107-109. [D] 
1446. Rose, H. W. Night vision, pp. 931-965 in: 
German aviation medicine. World War II. Vol. II. De- 
partment of the Air Force, Washington, D. C., 1950, 
1302 pp. [P] 
1447. Rose, H. W. and I. Schmidt. Factors affecting 
dark adaptation. U. S. AAF. Wright-Patterson air force 
base, Dayton, Ohio. Aero medical laboratory. Tech. rept. 
U. 12-46-25 (Translated German document), 20 October 
1946, 11 pp. [P] 
1448. Rowland, L. S. Night visual efficiency in illumi- 
nations above the level of the cone threshold. U. S. AAF. 
Randolph Field, Tex. School of aviation medicine. Project 
258, Rept. no. 1, 31 May 1944, 13 pp. [P] 
1449. Rowland, W. M. Night vision: a review of in- 
vestigations at the AAF school of aviation medicine. 
U. S. AAF. Randolph Field, Tex. School of aviation 
medicine. Project 399, Rept. no. 1, 3 July 1945, 6 pp. 
1450. Rowland, W. M. and L. S. Rowland. Aspects of 
night visual efficiency. U. S. AAF. Randolph Field, Tex. 
School of aviation medicine. Project 106, Rept. no. 1, 
1 May 1943, 7 pp. [P] 
1451. Rowland, W. M. and L. S. Rowland. Studies of a 
number of men reporting difficulty in night operations. 
U. S. AAF. Randolph Field, Tex. School of aviation 
medicine. Project 251, Rept. no. 1, 10 May 1944, 10 pp. [P] 
1452. Rowland, L. S. and W. M. Rowland. Individual 
differences in the region of maximal acuity in scotopic 
vision: applications to night vision testing and training. 
U. S. AAF. Randolph Feld, Tex. School of aviation medi- 
cine. Project 220, Rept. no. 2, 19 February 1945, 10 pp. VISUAL PROBLEMS—NIGHT VISION 
1453-1484 
1453. Sasiain, M. R. Influencia de la aberracion mono- 
cromatica de apertura en la miopia nocturna. Arch. Soc. 
oftal. hisp.-amer., 1948,8; 925-938. 
1454. Schoen, Z. J. and F. L. Dimmick, Relative 
efficiency of goggles for dark adaptation. U. S. Navy. 
Submarine base. New London, Conn. Medical research 
laboratory. Project NM 003 024 (X—757 (Av—387—k)), 
Kept. no. 1, 9 April 1948, 10 pp. 
1455. Schwarz, F. Uber die elektrische Reizbarkeit des 
Auges bei Hell- und Dunkel-adaptation. Pfliig. Arch. ges. 
Physiol, 1947, 249: 76-86. [P] 
1456. Scobee, R. G. and H. I. Chinn. The effect of 
carbon monoxide on night visual efficiency. U. S. AAF. 
Randolph Field, Tex. School of aviation medicine. Project 
234, Kept. no. 1, 26 January 1944, 2 pp. [P] 
1457. Scott, J. W. and D. Y. Solandt. The relation of 
dark adaptation to colour vision. Canada NRG. Appendix 
B. Proceedings of the 4th meeting of associate committee 
on naval medical research. Project C4095, 16 February 
1945, 4 pp. [P] 
1458. Sexton, M., F. Malone, and D. Farnsworth. The 
effect of ultraviolet radiation from fluorescent lights on 
dark adaptation and visual acuity. U. S. Navy. Submarine 
base. New London, Conn. Medical research laboratory. 
Project NM 003 041.38.01, Kept. no. 169, 20 December 
1950, 316 pp. [P] 
1459. Sheard, C. Effects of anoxia, oxygen and increased 
intrapulmonary pressure on dark adaptation. Proc. Mayo 
Clin., 1945, 20: 230-236. 
1460. Sheard, C. Effects of increased intrapulmonary 
pressure on dark adaptation. U. S. NRC-CAM. 
OEMcmr-129, Kept. no. 449, 28 May 1945, 1 pp. 
1461. Sheard, C. The effects of smoking on the dark 
adaptation of rods and cones. Fed. Proc. Soc. exp. Biol., 
1946, 5: 94. 
1462. Sheard, C. Courses of dark adaptation and levels 
of vitamin A and carotene in normal and clinical condi- 
tions. Fed. Proc. Amer. Soc. exp. Biol., 1948, 7: 113. [CH] 
1463. Simonson, E., S. S. Blankstein, and E. J. Carey. 
The relationship between light adaptation and dark adap- 
tation and its significance for appraisal of the glare effect 
of different illuminants. Amer. J. Ophthal., 1946, 29: 
328-340. [P] 
1464. Sloan, L. L. Rate of dark adaptation and regional 
threshold gradient of the dark-adapted eye: physiologic 
and clinical studies. Amer. J. Ophthal, 1947, 30: 705-720. 
[P; CH] Excerpta Medica. Section II. (Physiology, Bio- 
chemistry, and Pharmacology), 1949, 2: 240. Abstr. 
1465. Smith, C. G. The report of the R. C. N. medical 
research unit test laboratories at Halifax and Deepbrook. 
Canada NRG. Proceedings of second meeting of the asso- 
ciate committee on naval medical research. Project C4054, 
7 October 1943, 3 pp. 
1466. Smith, J, A. and F. L. Dimmick. The parameters 
of scotopic sensitivity: (1) The effect of size. U. S. Navy. 
Submarine base, New London, Conn. Medical research 
laboratory. Project NM 003 041.09.03, MRL Rept. no. 
174, 20 June 1951, 19 pp. 
1467. Solandt, D. Y. and J. W. Dales. Preliminary re- 
port on a study of peripheral (scotopic) visual acuity of 
the normal human eye. Canada NRC. Proceedings of 
second meeting of associate committee on naval medical 
research. Project C4056, 7 October 1943, 1 pp. 
1468. Solandt, D. Y. and J. W. Scott. Visual function at 
low levels of illumination. Canada NRG. Proceedings of 
third meeting of associate committee on naval medical 
research. Project C4079, 15 May 1944, 2 pp. [P] 
1469. Steven, D. M. Relation between dark adaptation 
and age. Nature, Land., 1946, 153: 376-377. [P] [R] 
1470. Sulzman, J. H. A study of the physiological blind- 
spot of the dark adapted fovea. U. S. Navy. Submarine 
base. New London, Conn. Medical research laboratory. 
Project X-492 (Av—262—p), March 1, 1946, 8 pp. 
1471. Tufts College. Light sensitivity. 12 pp. in: Hand- 
book of human engineering data for design engineers. 
Tufts College, Institute for applied experimental psychol- 
ogy. SDC Human Engineering Project 20-G-l, Project 
Designation NM-783-001, Technical Kept. no. 199-1—1, 
1 December 1949, 410 pp. 
1472. IT. S. Navy. BuMed. Night vision board. The use 
of the eyes at night, undated, 16 pp. [D] 
1473. IT. S. Navy. Office of Naval Advisor, Office of 
Military Government for Germany, Medical Section. 
Dark adaptation and acuity of night vision, pp. 52-58 in: 
Report of the second conference of special medical con- 
sultants from 30 November to 3 December 1942 at the 
Military Medical Academy, Berlin. Project I, Folio II, 
23 March 1948, 128 pp. 
1474. U. S. Navy, IT. S. S. “Enterprise.” Study of dark 
adaptation and ships’ lighting. Project X-20, 23 March 
1942, 13 pp. [P] 
1475. Verplanck, W. S. Field tests of the radium plaque 
adaptometer. U. S. Navy. Submarine base. New London, 
Conn. Medical research laboratory. Project X-268 (Av- 
156-c), November 26, 1943,30 pp. 
1476. Verplanck, W. S. A report on the night vision 
testing of 5650 men. U. S. Navy. Submarine base, New 
London. Conn. Medical research department. Project 268 
(Av-156-c). Enclosure (A), 12 August 1944, 22 pp. 
1477. Verplanck, W. S. The effect of increasing the 
difficulty of the RPA test of night vision. U. S. Navy. 
Submarine base, New London, Conn. Medical research 
department. Project X—268 (Av—156—c), Interval Kept, 
no. 3, 25 September 1945, 18 pp. 
1478. Verplanck, W. S, Predictive value of the Navy 
radium plaque adaptometer and other physiological 
measures of night vision for score on performance ap- 
proximating the standing of a night lookout watch. U. S. 
Navy. Submarine base. New London, Conn. Medical re- 
search department. Project X—350 (Av-197-p), 1 March 
1946, 14 pp. 
1479. Verplanck, W. S. An investigation of the red 
illumination of the submarine conning tower. U. S. Navy. 
Submarine base. New London, Conn. Medical research 
department. Project X—519 (Av—273—p), 15 March 1946, 
50 pp. 
1480. Verplanck, W. S. Reliability of the RPA over long 
test-retest intervals. U. S. Navy. Submarine base. New 
London, Conn. Medical research department. Project 
X-268 (Av-156-c), Interval Kept. no. 4, 15 August 
1946, 23 pp. 
1481. Wald, G., P. V. Harper, Jr., H. C. Goodman, and 
H. P. Krieger. Respiratory effects upon the visual thresh- 
old. J. gen. Physiol., 1942,25: 891—903. [P] 
1482. Wendland, J. P. Effect of muscular exercise on 
dark adaptation. Amer. J. Ophthal., 1948, 31: 1429- 
1436. [P] 
1483. Wolf, E. Effects of exposure to ultra-violet light 
on human dark adaptation. Proc. nat. Acad. Sci., Wash., 
1946, 32: 219-226. 
1484. Wright, W. D. Night vision, pp. 22-33 in: Mod- 
ern trends in ophthalmology. Vol. II. Edited by A. Sorsby. 
New York, Paul B. Hoeber, Inc., 1947, 557 pp. [R] 1485-1506 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
1485. Wright, W. D. Photometry at low illuminations, 
pp. 66-87: Photometry and the eye. London, Hatton 
Press Ltd., 1949, 127 pp. 
H. UNDERWATER VISION 
Underwater vision is of concern to deep-sea divers 
and to underwater swimmers. The deep-sea diver 
works with an illuminating device, but even so, the 
visibility of objects in ocean water or river bottoms 
may be impaired by a number of circumstances. 
Jenkins, Bowen, and Rogers {1487) 1941 have 
investigated the visibility of objects in ocean water 
under various conditions of illumination. Attenua- 
tion by absorption and scattering and masking by 
the scattered light were found to be important 
factors- Even in the clearest water scattering is the 
chief factor. Because of selective absorption, color 
filters are of little use in increasing visibility. Tailliez, 
Dumas, Cousteau, Alinat, and Devilla {1488) 1949 
have pointed out that the field of vision as seen 
through the porthole of the diver’s helmet may be 
optically deformed. The factors determining effec- 
tiveness of vision in deep-sea diving are discussed 
by the authors. 
1486. Duntley, S. ft. The visibility of submerged objects. 
I. Optical effects of water waves. Massachusetts Institute 
of Technology, Visibility laboratory. Contract No. N5ori- 
07831 and NCbs—50378, 15 December 1950, 11 pp. 
1487. Jenkins, F. A., I. S. Bowen, and F. T. Rogers, Jr. 
Visibility in ocean water. University of California, San 
Diego, Calif. Radio and sound laboratory. NDRC Rept. 
no. C4-sr30-024, 18 October 1941, pp. 52. 
1488. Tailliez, P., F. Dumas, J. Y. Cousteau, J. Alinat, 
and F. Devilla. La vision en plongee. pp. 18-22 in: La 
plongee en scaphandre. Editions Elzevir, Paris, 1949, 119 
pp. 
VIII. AUDITORY PROBLEMS 
The references given in this section are princi- 
pally concerned with measurement of auditory 
function. These references have been included 
chiefly as source material in connection with the 
section on noise and vibration (p. 129) and the 
section on selection of sonar operators (p. 306). 
The reader’s attention is particularly directed to 
the reports by Harris and coworkers. For studies 
at the U. S. Submarine Base, New London, Conn., 
papers by the following authors should be con- 
sulted: Harris {1496 and 1497) 1948 and {1498) 
1950; Harris and Charney {1499) 1950; Harris and 
Myers {1500) 1948; Harris, Myers, Stover, and 
Stuntz {1501) 1949; Myers and Harris {1508) 1949 
and {1509) 1950; Rose and Harris {1516) 1948; 
Stuntz {1521) 1950; and Wing {1523) 1950. 
1489. Bunch, C. C. Clinical Audiometry. St. Louis, C. V. 
Mosby Company, 1943, 186 pp. [CH] 
1490. Curry, E. T. and G. H. Kurtzrock. A preliminary 
investigation of the ear-choice technique in threshold 
audiometry. /. Speech Dis., 16: 340-346. 
1491. Dickson, E. D. D., J. F. Simpson, D. B. Fry, G. E. 
Swindell, and R. E. C. Brown. A new method of setting 
the hearing efficiency of aviation candidates. /. Laryng., 
1946, 61: 139-203. [P] 
1492. Doughty, J. M. and W. R. Garner. Pitch char- 
acteristics of short tones. I. Two kinds of pitch threshold. 
/. exp. Psychol., 1947, 37: 351-365. 
1493. Eschweiler, H. Absolute eichung von audiometern. 
Z. Hals-Nas.-u. Ohrenheilk., 1936, 41: 190-198. [D] 
1494. Garner, W. R, and G. A. Miller. The masked 
threshold of pure tones as a function of duration. J. exp. 
Psychol, 1947, 37: 293-303. 
1495. Harris, J. D. Studies on the comparative efficiency 
of the free voice and the pure tone audiometer for routine 
testing of auditory acuity. U. S. Navy. Submarine base, 
New London, Conn. Medical research department. Proj- 
ect X-478 {Sub. no. 100), Kept. no. I, 8 October 1945, 
27 pp. 
1496. Harris, J. D. Pitch discrimination and absolute 
pitch. U. S. Navy. Submarine base, New London, Conn. 
Medical research department. Project NM 003 026, Kept, 
no. 1, 30 January 1948, 5 pp. [P] 
1497. Harris, J. D. Interpretations of measurements of 
auditory thresholds. U. S. Navy. Submarine base. New 
London, Conn. Medical research department. Project NM 
003-021, Kept. no. 1, 12 February 1948, 7 pp. 
1498. Harris, J. D. Studies in short duration auditory 
fatigue. II. The effect of the duration of the stimulating 
tone. III. The effect of the interval between stimuli. U. S. 
Navy. Submarine base. New London, Conn. Medical re- 
search laboratory. Project NM 003 041.34.02, 8 Decem- 
ber 1950, 9 pp. 
1499. Harris, J. D. and D. Charney. A revision of the 
Navy pitch-memory test, MRL Report no. 1, 9, 1-10 
(1950). U. S. Navy. Submarine base, New London, Conn. 
Medical research laboratory. Project NM 003 041.07.01, 
Kept. no. 152, 5 April 1950, 14 pp. 
1500. Harris, J. D. and C. K. Myers. Intensity discrimi- 
nation for white noise. U. S. Navy. Submarine base, New 
London, Conn. Medical research laboratory. Project NM 
003 020, Kept. no. 3, 13 August 1948, 25 pp. 
1501. Harris, J. D., C. K. Myers, A. D. Stover, and 
S. E. Stuntz. The effect of sensation level on intensity 
discrimination for white noise. U. S. Navy. Submarine 
base. New London, Conn. Medical research laboratory. 
Project NM 003 020, Rept. no. 4, 1 August 1949, 26 pp. 
1502. Huizing, H. C. Pure tone audiometry. Acta oto- 
laryng., Stockh., 1951, 40: 51-61. 
1503. Licklider, J. R. C. Auditory research and undersea 
warfare. U. S. NRC—CUW. Fourth undersea warfare 
symposium. NRC: C. U. W.: 0042, 16-17 May 1949, 
7 pp. 
1504. Lifshitz, S. Fluctuation of the hearing threshold. 
/. acous. Soc. Amer., 1939,11: 118—121. [M] 
1505. Liischer, E. and J. Zwislocki. The decay of sen- 
sation and the remainder of adaptation after short pure- 
tone impulses on the ear. Acta oto-laryng., Stockh., 1947, 
35: 428-445. 
1506. Liischer, E. and J. Zwislocki. The international 
standardization of audiometry. Acta oto-laryng., Stockh., 
suppl., 1949, 76: 27-35. (English, French, and German 
summaries.) NOISE AND GENERAL STUDIES 
1507-1537 
1507. Lumio, J. S. and P. Arni. Comparison of the 
hearing examination with the audiometer and with the 
set of Struycken’s tuning forks. Acta oto-laryng., Stockh., 
1949, 37: 71-79. 
1508. Myers, C. K. and J. D. Harris. The inherent 
stability of the auditory threshold. U. S. Navy. Submarine 
base, New London, Conn. Medical research laboratory. 
Project NM 003 021, Rept. no. 3, April 1949, 23 pp. [P] 
1509. Myers, C. K. and J. D. Harris. Variability of the 
auditory threshold with time. U. S. Navy. Submarine base. 
New London, Conn. Medical research laboratory. Project 
NM 003 041.21.06, Rept. no. 165, 5 December 1950, 28 
PP- [P] 
1510. Partridge, R. C., J. D. Brown, and G. K. Rose- 
blade. Certain details of the experiments on fatigue of 
pitch discrimination. Canada NRC. Proceedings of the 
third meeting of the associate committee on naval medical 
research. Project C4073, 15 May 1944, 5 pp. [P] 
1511. Partridge, R. C. and J. F. Fletcher. Fatigue and 
ability in pitch discrimination with reference notes of dif- 
ferent frequencies and fatigue of pitch discrimination with 
signals of various loudness levels. Canada NRC. Proceed- 
ings of third meeting of associate committee on naval medi- 
cal research. Project C4072, 15 May 1944, 5 pp. [P] 
1512. Partridge, R. C., J. P. Fletcher, and J. E. 
Goodwin. Studies on fatigue of pitch discrimination. 
Canada NRC. Appendix F. Proceedings of the fourth 
meeting of the associate committee on naval medical re- 
search. Project C4100, 16 February 1945, 8 pp. [P] 
1513. Partridge, R. C. and H. D. Hebb. The effect of 
training on pitch discrimination in asdic operators and 
fatigue of hearing in asdic operators. Canada NRG. Pro- 
ceedings of second meeting of the associate committee on 
naval medical research. Project C4045, 7 October 1943, 
8 pp. [P] 
1514. Reger, S. N. Standardization of pure tone audi- 
ometer testing technique. Laryngoscope, 1950, 60: 
161-185. 
1515. Reger, S. N. and H. A. Newby. A group pure 
tone hearing test. /. Speech Dis., 1947, 12: 61-66. 
1516. Rose, G. L. and J. D. Harris. Suggestions for 
constructing tests of pitch discrimination. U. S. Navy. 
Submarine base, New London, Conn. Medical research 
department. Project NM 003 026, Rept. no. 2, 10 Febru- 
ary 1948, 25 pp. [P] 
1517. Schubert, K. Auf Wegen zu neuen Horpruf- 
geraten. Arch. Ohr.-, Nas.-, u. KehlkHeilk., 1947/49, 
155: 656-666. 
1518. Shaw, W. A., E. B. Newman, and I. J. Hirsh. 
The difference between monaural and binaural thresholds. 
J. exp. Psychol, 1947, 37: 229-242. 
1519. Silverman, S. R. Recent developments in audi- 
tory tests. Proc. R. Soc. Med., 1949, 42: 675—686. 
1520. Snow, W. B. Change of pitch with loudness at 
low frequencies. J. acoust. Soc. Amer., 1936, 8: 14—19. 
1521. Stuntz, S. E. The effects of sound intensity level 
on judgments of “tonal range” and “volume level”; an 
interpretation of the loudness function. U. S. Navy. Sub- 
marine base. New London, Conn. Medical research 
laboratory. Project NM 003 041.20.5, 4 December 1950, 
20 pp. 
1522. Watson, L. A. and T. Tolan. Hearing tests and 
hearing instruments. Baltimore, The Williams & Wilkins 
Co., 1949, 597 pp. 
1523. Wing, K. G. The microphonic action of the 
cochlea; a selected bibliography. U. S. Navy. Submarine 
base, New London, Conn. Medical research laboratory. 
Project NM 003 041.27.2, 5 December 1950, 34 pp. 
1524. Witting, E. G. and W. Hughson. Inherent 
accuracy of a series of repeated clinical audiograms. 
Laryngoscope, St. Louis, 1950, 50: 259-269. 
1525. Anon. Recent research on hearing. /. Amer. med. 
Ass., 1938, 110: 900. 
IX. NOISE AND VIBRATION 
A. NOISE 
1. GENERAL STUDIES 
An examination of the literature cited in this sec- 
tion on noise reveals in aviation a concern for the 
possible pathological effects of engine noise upon 
hearing and sound communication. Submarine sur- 
geons have now become aware of similar problems 
in submarine operations. There may be temporary 
loss of auditory acuity and noise may complicate 
intercommunication. Among the general references 
listed, papers by the following are recommended as 
particularly useful: Berrien {1528) 1949; Harvard 
University Psycho-acoustic Laboratory {1537 and 
1538) 1950; Kryter {1542) 1950; Licklider {1543) 
1949; Sabine {1551) 1942; Suggit {1556) 1947; 
and U. S. NRC-CAM {1558) 1946. The latter re- 
port lists a bibliography of 59 unpublished docu- 
ments on noise, including noise measurements and 
control and effects of noise. 
1526. Baetjer, A. M. Noise, pp. 1005-1009 in: Rosenau 
preventive medicine and hygiene. Edited by Kenneth F. 
Maxcy. Seventh edition. New York, Appleton-Gentury- 
Crofts, Inc., 1951, 1462 pp. 
1527. Berrien, F. K. The effects of noise. Psychol. Bull. 
1946, 43: 141-161. [R] 
1528. Berrien, E. K. Relation of noise to the habitability 
of submarines, pp. 345—355 in: A survey report on human 
factors in undersea warfare. Washington, D. C., National 
Research Council, 1949, 541 pp. 
1529. Canfield, N. Trauma from noise in industry. Conn, 
med. ]., 1949, 13: 21-28. 
1530. Davis, H. How noise affects our behavior. U. S. 
Navy, ONR. Res. Rev., March 1951, pp. 18-22. [R] 
1531. Davis, R. C. Electrical skin resistance before, 
during, and after a period of noise stimulation. /. exp. 
Psychol., 1932, 15: 108-117. [P] 
1532. Eldredge, D. H. and H. 0. Barrack. Sound prob- 
lems in the Air Force. Armed Forces med. J., 1950, 1: 
449-461. 
1533. Finkle, A. L. and J. R. Poppen. Clinical effects 
of noise and mechanical vibrations of a turbo-jet engine 
on man. /. appl. Physiol., 1948, 1: 183-204. [P] [R] 
1534. Greene, R. An aviator and his ears. Industr. Med., 
1938, 7: 669-671. 
1535. Grove, W. E. Noise: will it damage your hearing? 
Trans. Amer. Acad. Ophthal. Oto-laryng., 1949, 53: 
574-575. 
1536. Grove, W. E. Will noise damage one’s hearing? 
/. Amer. med. Ass., 1949, 140: 674-677. 
1537. Harvard University psycho-acoustic laboratory. 
A bibliography in audition. Volume I. Cambridge, Har- 
vard University Press, 1950, 295 pp. [B] SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
1538-1563 
1538. Harvard University psycho-acoustic laboratory. 
A bibliography in audition. Volume II. Cambridge, Har- 
vard University Press, 1950, 322 pp. [B] 
1539. Johnson, N. C. Ear disorders in flying. Contact, 
Pensacola, 1947, 6: 177—188. 
1540. Kaser, R. Einfiihrung in das Problem des 
akustischen Traumas in Militardienst. Vjschr. schweiz. 
SanitOff., 1950, 27: 143-156. [R] 
1541. Kostelijk, P. J. Het acoustisch trauma. Ned. milit.- 
geneesk. Arch., 1951, 4: 95—114. 
1542. Kryter, K. D. The effects of noise on man. /. 
Speech Dis., 1950, Monogr. Suppl. no. 1: 1-95. [R] 
1543. Licklider, J. R, C. Auditory research and under- 
sea warfare. U. S. NRC-GUW. Serial no. N. R. C.- 
C. U. W. 0042,16 May 1949, 7 pp. 
1544. Lovell, G. D. Physiological and motor responses 
to a regularly recurring sound. Psychol. Bull., 1941, 38: 
715. 
1545. McCord, C. P., E. E. Teal, and W. N. Wither- 
bridge. Noise and its effect on human beings. Noise con- 
trol as a by-product of air conditioning. /. Amer. med. 
Ass., 1936, 110: 1553-1560. 
1546. McCoy, D. A. Industrial noise—its analysis and 
interpretation for preventive treatment. /. industr. Hyg., 
1944, 26: 120-123. 
1547. Muhlberg, 0. Akustisches Trauma und Dienst- 
tauglichkeit. Vjschr. schweiz, SanitOff., 1950, 27: 156- 
165. [D] 
1548. Nash, C. S. Industrial loss of hearing: medical 
aspects. Industr. med. surg., 1952,21: 171-173. 
1549. Peyser, A. Om det industriella bullrets allmanna 
inflytande pa organismen. [General effect of industrial 
noise on the organism.] Nord. Med. Stockholm, 1948, 38: 
1267-1270. 
1550. Pothoven, W. J. Some audiological aspects of air- 
craft noise. J. Aviat. Med., 1950, 21: 140—146. Ned. 
Tijdschr. Geneesk., 1949, 93: 2403—2408. 
1551. Sabine, P. E. Bibliography on noise. J. acoust. 
Soc. Amer., 1942, 13: 210. [B] 
1552. Sabine, P. E, The problem of industrial noise. 
Amer. J. publ. Hlth. 1944, 34: 265-270. 
1553. Seal, J. C. Noise deafness in industry and en- 
vironment. (Occupational deafness.) N. Y. St. J. Med., 
1933, 33: 1251-1254. 
1554. Spooner, H. J. Health problems involved in noise 
and fatigue. Nation’s Hlth., 1922, 4: 91-95. 
1555. Sterner, J, H. Standards of noise tolerance. 
Industr. med. surg., 1952, 21: 165—170. 
1556. Suggit, S. C. Noise and hearing in relation to the 
problems of the Royal Navy. Brit. med. ]., 1947, 5: 55—57. 
1557. Tufts College. Noise. 12 pp. in: Handbook of 
human engineering data for design engineers. Tufts Col- 
lege, Institute for applied experimental psychology. SDC 
Human Engineering Project 20-G-l, Project Designation 
NM-783-001, Technical Report 199-1-1, 1 December 
1949, 410 pp. [P] 
1558. U. S. NRC-CAM. Noise, pp. 404-409 in: Bibliog- 
raphy on aviation medicine. Vol. II. 1946, 802 pp. [B] 
1559. Von Gierke, H. E. Sound absorption at the surface 
of the body of man and animals. /. acoust. Soc. Amer., 
1949,27; 55. [P] 
1560. Von Gierke, H. E. Subharmonics generated in ears 
of humans and animals at intense sound levels. Fed. Proc. 
Amer. Soc. exp. Biol., 1950, 9: 130. 
1561. Walzl, E. M. Hearing. Acoustic trauma, pp. 235— 
242 in; Annu. Rev. Physiol., 1949, 11: 231-244. 
1562. Wever, E. 6. Loudness and fatigue, pp. 299-326 
in: Theory of hearing. New York, John Wiley & Sons, Inc., 
1949, xii, 484 pp. 
1563. Anon. Noise in industry. Arch. ind. Hyg. occufi. 
Med., 1951, 3: 232-235. 
2. PHYSIOLOGICAL AND PATHOLOGICAL EFFECTS 
OF NOISE 
The effects of noise upon psychological and 
physiological processes have been under investiga- 
tion for many years. Such a study is that of Harmon 
{1571) 1933 in which mental tasks (problems in 
addition) were carried out in the presence of noise 
from specially prepared phonograph records. One 
was made in a busy office room with a loudness 
from 50 to 65 decibels, the other made on a New 
York City street corner with a loudness from 65 to 
75 decibels. It was found that mental work, together 
with its physical concomitants, was accompanied 
by a small but consistent increase in metabolic rate, 
heart rate, and respiratory rate and volume. When 
complex noises were added, there were further in- 
creases observable at first. The increases caused by 
noises ran as high as 60 percent or more during the 
first days of the experiment. If the subject was pre- 
sented with the same noise situation day after day 
for several weeks, the noise effects gradually dis- 
appeared and working values tended to return to 
normal. In the author’s study there was no correla- 
tion between the attitude of the subjects and the 
effects of the noise. 
For studies on the effects of noise on sensory func- 
tions, papers by the following should be consulted: 
Bogoslovskii and Kravkov {1565) 1941; Cassel and 
Dallenbach {1566) 1918; Rosenblith, Galambos, 
and Hirsh {1577) 1950; and Theilgaard {1579) 
1951. The paper by Bogoslovskii and Kravkov 
{1565) is particularly interesting as an example of 
Russian investigations on the effect of sensory dis- 
tractions on perceptual acuity. 
As Archambault {1564) 1932 has pointed out, it 
can be demonstrated in many ways that noise may 
have damaging effects upon the functions of the 
nervous system. An example of such damage is to 
be found in the experimental sonogenic convul- 
sions which may be produced in laboratory animals. 
Reports by the following may be consulted on this 
subject: Brings and Brings {1569) 1950; Brings, 
Brings, and Kivert {1570) 1950; and Mirsky, 
Elgart, and Aring {1573) 1943. Various strains 
of mice were subjected to sounds at a frequency of 
10 kilocycles and an intensity of 110 decibels. There 
are interstrain and sex differences in behavior and 
incidence of seizure and even great individual varia- 
tion in susceptibility and pattern within the same 
litters. NOISE AND VIBRATION—PHYSIOLOGICAL AND PATHOLOGICAL EFFECTS OF NOISE 
In a study of the effect of sound distraction upon 
memory, Morgan {1574) 1917 indicated that noisy 
conditions reduce the amount of material retained 
in the memory and also decrease the effective range 
of attention. While adaptation to noise does occur, it 
does not counterbalance entirely the distraction 
effect. The motor effects of strong auditory stimuli 
have been measured in man by Davis {1568) 1948 
by recording muscular action potentials in both 
forearms under loud sound stimulation. In animals 
and man, noise has been shown to affect cardio- 
vascular function. Ruff and Strughold {1578) 
1939 found that exposure to noise increased the 
pulse rate and resulted in an elevation of systolic 
blood pressure. A change was also found in the 
patellar reflex, there being a decrease as exposure 
to noise continued. Yeakel, Shenkin, McCann, and 
Rothballer {1583) 1948 exposed rats for a year to 
the sound of a blast of compressed air for 5 minutes 
daily for 5 days a week. The average systolic blood 
pressure of gray Norway rats rose from an initial 
value of 113 up to 154 mm. Hg in the final 2 months 
of the experiment. The pressure rose from 124 to 
127 mm. Hg in the controls. Sixty-four percent of 
the experimental rats had a mean blood pressure 
of 150 mm. Hg at the end of the experiments. The 
results suggested to the authors that the auditory 
stimulus increased peripheral resistance. 
Laird {1572) 1932 has shown that in human 
subjects loud noises ranging in intensity from 45 to 
75 decibels reduce appreciably the secretion of saliva 
and gastric juice necessary for the proper function- 
ing of the digestive system. The author considers 
that noise is to a considerable degree responsible for 
the prevalence of digestive disorders in modern life. 
He found that sweat and aromatic foods or bever- 
ages tended to offset the depressing effects of noise 
on these secretions. These findings have been con- 
firmed by Vaughan and Van Liere {1580) 1940 in 
dogs. In these experiments, dogs with Pavlov 
pouches were subjected to noise of 30 to 100 deci- 
bels. Frequencies of 600 cycles and 2,000 cycles were 
used. At 600 cycles there was a significant reduction 
in the volume of gastric juice secreted, but no reduc- 
tion in the amount of acid. At 2,000 cycles there was 
a significant reduction in the amount of acid se- 
creted. Neither frequency produced any significant 
change in total chlorides or in the pH of the gastric 
juice. The authors concluded that there are striking 
individual variations in the effect of noise on gastric 
juice secretion, and that higher pitch noises have a 
greater depressing effect on both volume and total 
acid secretion than lower pitch noises. 
With the development of new types of engines 
and other sources of loud noises of unusual fre- 
quency, anxiety has been expressed not only for the 
possible damage to efficiency but also possible loss 
of hearing acuity and even more serious disturb- 
ances. A study of physiological effects of intense 
sound has been reported by Parrack, Eldredge, and 
Koster (1575) 1948. Two sound sources were used: 
(1) a turbojet engine (J-33-9) mounted appro- 
priately, and (2) a special siren. The intensity of 
the engine sound ranged from about 120 to 150 
decibels above the reference level. The siren-sound 
level was from about 120 to 160 decibels above the 
reference level. Severe, but so far temporary, losses 
of hearing followed exposure of project personnel 
to intense sound from both of these sources. Dur- 
ing exposure the subjects reported heating of the 
skin, a strong sense of vibration in various parts of 
the body, muscular weakness, and excessive fatigue. 
Guinea pigs and rats were killed by exposure to 
intense sound of the siren for as short as 8 minutes. 
The apparent cause of death was excessive elevation 
of body temperature caused in turn by absorption of 
acoustic energy in the fur with conversion to heat 
energy. It was concluded that noise fields of suffi- 
cient intensity to impair human hearing are pro- 
duced by turbojet powerplants. The frequency of 
the spectrum of the turbojet noise field was such 
that hearing loss produced in man interfered with 
the reception and understanding of speech. The 
frequencies having destructive effects on the experi- 
mental animals were within the audible range, al- 
though the effects were those usually attributed to 
action of “ultrasonic” frequencies. It was suggested 
by the authors that the important parameter may be 
intensity rather than frequency. 
In order to explain the heating and killing of 
small animals in sound fields, Von Gierke, Parrack, 
and Eldredge {1582) 1950 measured the sound 
absorption coefficient of the rat’s surface in terms 
of frequency. The absorption coefficient was found 
to decrease up to about 1,500 cycles, and then to 
increase up to 6,000 cycles. The behavior below 
1,500 cycles was determined largely by the tissue 
beneath the skin, while the increase above 1,500 
cycles was considered to be the result of the pres- 
ence of the fur. These absorption coefficients permit 
the estimation of the sound energy absorbed by a 
whole animal. By calculating the heat balance of 
the animal in a sound field, the sound intensity and 
time required to cause temperature rise can be cal- 
culated approximately. These calculated results 
agree with experimental data on the heat death of 
rats and establish overheating as the agent respon- 
sible for death. A clothed man may be expected to 
absorb some sound energy in his clothing just as a 
rat absorbs sound energy in his fur. 1564-1583 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
For further studies on the physiological effects 
of noise, papers by the following should be con- 
sulted: Davis, Galambos, Hawkins, Parrack, Lurie, 
and Leighton {1567) 1942; Peyser {1576) 1948; 
and Von Gierke {1581) 1950. 
1564. Archambault, L. The effect of noise of the nerv- 
ous system. A plea for official action by this society toward 
abatement of this damaging nuisance. N. T. St. J. Med., 
1932, 32: 1110-1115. 
1565. Bogoslovskii, A. I. and S. V. Kravkov. Vliinie 
shuma aviatsiannogo motora na zrenie. [The effect of 
aviation motor noise on the vision.] Prob. fziol. opt., 
Moskva, 1941, 7: 69-75. 
1566. Cassell, E. E. and K. M. Dallenbach. The effect 
of auditory distraction upon the sensory reaction. Amer. J. 
Psychol., 1918, 29: 129-143. [P] 
1567. Davis, H., R. Galambos, J. E. Hawkins, Jr., 
H. 0. Parrack, M. H. Lurie, and J. C. Leighton. Final 
report on physiological effects of exposure to certain 
sounds. U. S. NDRG. Division G. Section 5, Sound 
Sources. OSRD rept. no. 889, 31 July 1942, 88 pp. [P] 
1568. Davis, R. C. Motor effects of strong auditory 
stimuli. /. exp. Psychol., 1948, 38: 257-275. 
1569. Frings, H. and M. Frings. Studies on audiogenic 
seizures in laboratory mice. USAF. Wright-Patterson air 
force base, Dayton, Ohio. Air materiel command. Techni- 
cal Rept. no. 6369, December 1950, 13 pp. 
1570. Frings, H., M. Frings, and A. Kivert. Behavior 
patterns of the laboratory mouse under auditory stress. 
USAF. Wright-Patterson air force base, Dayton, Ohio. 
Air materiel command. Technical Rept. no. 6028, Sep- 
tember 1950, 23 pp. 
1571. Harmon, F. L. The effects of noise upon certain 
psychological and physiological processes. Arch. Psychol., 
N. Y., 1933, 23: 5-78. 
1572. Laird, D. A. Experiments on the influence of 
noise upon digestion, and the counteracting effects of 
various food agencies. Med. J. Rec., 1932, 135: 461—464. 
1573. Mirsky, I. A., S. Elgart, and C. D. Aring. Sono- 
genic convulsions in rats and mice. I. Control studies. 
J. comp. Psychol., 1943, 35: 249—253. 
1574. Morgan, J. J. G. The effect of sound distraction 
upon memory. Amer. J. Psychol., 1917, 28: 191-208. [P] 
1575. Parrack, H. 0., D. H. Eldredge, and H. F. Koster. 
Physiological effects of intense sound. USAF, Wright- 
Patterson air force base, Dayton, Ohio. Air materiel com- 
mand. MCREXD-695-71B, 24 May 1948, 8 pp. [P] 
1576. Peyser, A. Om det industriella bullret allmanna 
inflytande pa organismen. [The general effects of indus- 
trial noise on the organism.] Nord. Med. Stockholm, 1948, 
38: 1267-1270. [P] 
1577. Rosenblith, W. A., R. Galambos, and I. J. Hirsh. 
The effect of exposure to loud tones upon animal and 
human responses to acoustic clicks. Science, 1950, 111: 
569-571.[P] 
1578. Ruff, S. and H. Strughold. Mechanische 
Erschutterungen. pp. 153-157 in: Grundriss der Luft- 
fahrtmedizin. Leipzig, Johann Ambrosius Barth, 1939, 
190 pp. [P] [D] 
1579. Theilgaard, E, Investigations in auditory fatigue 
in individuals with normal hearing and in noise workers 
(weavers). Acta oto-laryng., Stockh., 1951, 39: 525-537. 
1580. Vaughan, P. E. and E. J. VanLiere. An experi- 
mental study of the effect of noise on gastric secretion in 
Pavlov dogs. J. Aviat. Med., 1940, II: 102-107. 
1581. Von Gierke, H. E. Measurement of the acoustic 
impedance and the acoustic absorption coefficient of the 
surface of the human body. USAF, Wright-Patterson air 
force base, Dayton, Ohio. Air materiel command. Tech- 
nical Kept. no. 6010, March 1950, 39 pp. 
1582. Von Gierke, H. E., H. 0. Parrack, and D. H. 
Eldredge. Heating of animals by absorbed sound energy. 
USAF, Wright-Patterson air force base, Dayton, Ohio. 
Air materiel command. Technical Kept. no. 6240, Octo- 
ber i960, 18 pp. [M] [P] 
1583. Yeakel, E. H., H. A. Shenkin, S. M. McCann, 
and A. B. Roghballer. The blood pressure of rats sub- 
jected to auditory stimulation. Amer. ]. med. Sci., 1948, 
215: 352. Abstr. [P] 
3. HEARING DEFECTS FROM EXPOSURE TO NOISE 
For a comprehensive report on professional deaf- 
ness due to exposure to noise, a paper by Larsen 
{1630) 1939 should be consulted. This comprehen- 
sive study includes a bibliography of about 200 
references. In a series of 123 boilermakers whose 
hearing was tested with the audiometer, the maxi- 
mum hearing decrement was found at 4,096 cycles. 
For further studies of the frequencies at which 
hearing is effected, several references may be con- 
sulted {1587, 1590, 1592, 1595, 1597, 1598, 1600, 
1603, 1607, 1613, 1619, 1621, 1625, 1626, 1628, 
1629, 1631, 1635, 1637, 1641, 1643, 1644, 1647, 
1648, 1649, 1650, 1652, 1653, 1654, 1655, 1656, 
1657, and 1661). 
Investigations of acoustic trauma in aviators indi- 
cate that the initial auditory damage tends to be 
manifested by a dip in the audiometer record at 
4.096 cycles. The notch in the hearing curve at 4,096 
cycles has been reported by many including Camp- 
bell and Hargreaves {1590) 1940; Castane {1592) 
1948; Meyer zum Gottesberge {1637) 1944; Ruedi 
and Furrer {1649) 1946; and von Russi {1650) 
1946. De Wit {1598) 1942 carried out investiga- 
tions of professional deafness among the naval air 
staff and submarine staff in the Swedish naval 
service. The submarine problem involved special 
features due to the noise of the diesel engines within 
a small space with steel resonating walls. Also, the 
control of equipment and apparatus in the engine- 
room must be made partly by spoken communica- 
tion so that the ears cannot be protected. Among 
torpedomen and engineers in the submarine staff, 
it was found that professional deafness occurred in 
the C5 dip (4,096 cycles). Studies of Senturia 
'1655) 1944 and {1656) 1949 indicate that loss of 
hearing among pilots may involve frequencies from 
1,024 to 5,792 cycles. From studies by Bunch 
{1587) 1941, Machle {1635) 1947, and Senturia 
{1652) 1943, it is apparent that a frequent hearing 
loss for those who have been exposed to loud noises 
is for tones near C4 (2,048 cycles) as well as for 
4.096 cycles. Hearing loss in the region of 2,896 NOISE—HEARING DEFECTS 
cycles is also stated to have a remarkably high inci- 
dence. Pastore (1641) 1941 found among experi- 
enced aviators that the range from 128 to 2,048 
cycles was hardly affected. It was the 4,096-cycle 
area where pilots were most deficient. According to 
Dickson (1600) 1947 and Perlman (1643) 1941, 
the maximum dip in the audiogram is usually an 
octave above the frequency of the fatiguing tone. 
Perlman found this true for frequencies of 512, 
1,024, 2,048, and 4,096 cycles. The results were not 
uniform for 256 cycles and a test could not be made 
for 8,192 cycles. A threshold curve commonly found 
in early acoustic trauma with a localized dip at 
4,096 cycles was obtained when subjects were ex- 
posed to a fatiguing tone of 2,048 cycles. Sounds 
of low frequency from 64 to 256 cycles produced 
less acoustic trauma than those of higher frequency 
and of approximately equal intensity. Exposure to a 
fatiguing tone of 4,096 cycles did not produce a 
threshold curve with a localized depression at 4,096 
cycles, but resulted in a curve with a localized drop 
for the tone an octave above it; namely, 8,192 cycles. 
A petrolatum-treated cotton earplug provided lim- 
ited protection from acoustic trauma. 
Certain kinds of noises may result in hearing 
defects at lower frequencies; for example, de 
Almeida (1597) 1950 reported that the apex of the 
deficit in hearing of subjects exposed to the noise of 
electric punchcard machines was recorded at a fre- 
quency of 256 cycles. In a study of the effect of 
intense and prolonged acoustical stimulation on the 
auditory sensitivity of guinea pigs, Horton (1625) 
1934 exposed guinea pigs for 110 hours to a tone 
of 1,000 cycles at 125 decibels above normal human 
threshold. A general loss of sensitivity was found 
to the eight octave-tones in the frequency range 
from 64 to 8,192 cycles, and this loss was no more 
confined to one tone than to another. Tests made 
at intervals up to 298 days after exposure revealed 
no recovery from this loss. Similar findings were 
reported in 1935 by Horton (1626). 
For studies on the intensity of noise required to 
produce hearing defects, several reports may be 
consulted (1584, 1591, 1596, 1604, 1610, 1615, 
1617, 1620, 1622, 1627, 1632, 1634, 1638, 1660, 
1662, and 1665). The findings of a number of work- 
ers indicate that exposure to sound intensities of 80 
to 100 or more decibels under daily working condi- 
tions for prolonged periods is likely to lead to severe 
auditory impairment. These conclusions are drawn 
from reports by Carhart (1591) 1950; Gt. Brit. 
FPRC, Otological committee (1615) 1950; Grove 
(1617) 1949; Jankowski (1627) 1950; McCoy 
(1634) 1944; Wessling (1662) 1948; and Wheeler 
(1665) 1951. In acute experiments on human sub- 
jects, Davis, Morgan, Hawkins, Galambos, and 
Smith (1596) 1950 exposed their subjects repeat- 
edly at intervals of several days to intense tones of 
frequencies of 500, 1,000, 2,000, and 4,000 cycles at 
intensities of 110, 120, and 130 decibels for periods 
of 1 to 64 minutes. A noise somewhat resembling 
an airplane in flight was also employed. Temporary 
impairment of hearing was regularly produced, but 
there was no evidence of cumulative injurious 
effects. No significant elevation of auditory thresh- 
old was produced for tones of frequency lower than 
the exposure tone. The greatest hearing loss oc- 
curred at a frequency about half an octave above 
the exposure tone. With brief exposures the loss was 
sometimes confined to the two ovtaves above, but 
with longer exposures the hearing loss was quite 
extensive for all tones above the exposure frequency. 
For reports relating the frequency of the hearing 
loss to damage of particular portions of the basilar 
membrane, papers by Davis, Derbyshire, Kemp, 
Lurie, and Upton (1594) 1935; Dickson and Ewing 
(1601) 1947; and Wheeler (1664) 1950 should be 
consulted. Dickson and Ewing (1601) point out 
that the basal turn of the cochlea, whose function 
it is to respond to high-pitched sound, is known to 
be highly susceptible, possibly because of its prox- 
imity to the oval window, which may expose it to the 
initial violence of thrusts of the stapes in response 
to impulsive sound. The phenomenon of high-tone 
deafness caused by a low-pitched engine noise may 
be explicable on the grounds that the chief com- 
ponents of engine noise are essentially impulsive and 
explosive in character. 
Studies of Wilson (1666) 1943 suggest that the 
ears of certain persons are more susceptible to acous- 
tic trauma than are those of others. Ears so predis- 
posed are fatigued more readily than normal. This 
relationship between abnormal auditory fatigue and 
irreversible traumatic loss of hearing affords a means 
of determining in advance those persons predis- 
posed to traumatic deafness. Such a means of screen- 
ing out susceptible persons might be of great value 
in noisy industry or in military services. Wheeler 
(1663) 1949 has pointed out that noise exposure 
initiates a continuum of events ranging from re- 
versible, temporary loss of hearing for short expo- 
sures at moderate noise levels to permanent, irre- 
versible loss induced by exposure to excessively 
intense sound pressures, such as produced by blast, 
explosion, or concussion. A significant aim is to de- 
termine the point at which the hearing loss ceases 
to be reversible and becomes a permanent impair- 
ment. This determination is involved in the question 
of susceptibility. The noise-susceptible ear is one 1584-1609 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
which displays significantly large losses of acuity in 
response to noise exposure and requires a long time 
for recovery to normal. The author concludes that 
the criteria for differentiating susceptible from non- 
suceptible subjects include: (1) the magnitude of 
the threshold shift, and (2) the recovery time from 
exposure. The latter is considered to have a greater 
differentiating value than the former. 
Individual differences in sensitivity to auditory 
fatigue have also been studied by Peyser {1645) 
1951 and Wilson {1667) 1950. Age and other fac- 
tors in susceptibility to hearing loss have been con- 
sidered by Fabritius {1606) 1948; Gruss {1618) 
1939; Hoople, Wolfe, and Bregande {1624) 1948; 
and Lumio {1633) 1949. 
The problem of psychogenic deafness in connec- 
tion to exposure to loud sounds has been discussed by 
Bleguad {1585) 1951. In many cases the defect is 
purely psychogenic in origin, while in others there 
may be an organic lesion with a C5 dip and a 
psychogenic overlay. 
For further studies on hearing defects from expo- 
sure to noise, papers by the following should be con- 
sulted: Brown {1586) 1942; Campbell {1588, 
1589) 1942; Causse and Chavasse {1593) 1943; 
Dickson {1599) 1946; Dickson, Ewing, and Littler 
{1602) 1939; Ewing and Littler {1605) 1935; 
Finch and Culler {1608) 1934; Firestone {1609) 
1938; Fowler {1611) 1945 and {1612) 1947; Gt. 
Brit. Advisory council on scientific research and 
technical development, Communications committee 
{1614) 1944; Grove {1616) 1947; Hoople, Wolfe, 
and Bregande {1623) 1947; MacLaren and Chaney 
{1636) 1947; Miller and Taylor {1639) 1948; 
Partridge, Fletcher, and Solandt {1640) 1947; 
Pattie {1642) 1927; Senseney {1651) 1947; Raw- 
don-Smith {1646) 1935-36; Sleight and Tiffin 
{1658) 1948; Smyth {1659) 1932; and Theilgaard 
{1660) 1949. Reference number 1668 may also be 
consulted. 
1584. Aubry, M. and S. Oumikov. L’action nocive du 
bruit sur 1’organe auditif. Ann Oto-laryng., 1944, 12: 
235-239. [R] 
1585. Bleguad, H. Tunh0rigbed opstaet ved staerke 
lyde. [Psychogenic deafness by loud sounds.] Ugeskr. 
Laeg., 1951,113: 16-20. [D] 
1586. Brown, C. H. Effect of flight upon hearing acuity. 
Gt. Brit. FPRG. F. P. R. C. Kept. no. 460 {a) 6 July 
1942, 3 pp. 
1587. Bunch, C. C. The problem of deafness in aviators. 
War Med., Chicago, 1941, 7 * 873-886. [D] 
1588. Campbell, P. A. The effect of flight upon hearing 
acuity. U. S. AAF. Randolph Field, Texas. School of 
aviation medicine. Project 5, Kept. no. 1, 22 January 1942, 
3 pp. Gt. Brit. FPRG. F. P. R. C. 460, 5 January 1942, 
3 pp. 
1589. Campbell, P. A. The effect of flight upon hearing. 
/. Aviat. Med., 1942,13: 56-61. 
1590. Campbell, P. A. and J. Hargreaves. Aviation 
deafness—acute and chronic. Arch. Otolaryng., Chicago, 
1940, 32: 417-428. [R] [P] 
1591. Carhart, R. The ears of industry. Arch, industr. 
Hyg., 1950, 2: 534-541. 
1592. Castand, A. El trauma sonoro y las sorderas pro- 
fesionales. Med. dep., 1948, 1410-1423. 
1593. Causse, R, and P. Chavasse. Etudes sur la fatigue 
auditive. Anne psychol., 1943, 9: 265-297. [P] 
1594. Davis, H., A. J. Derbyshire, E. H. Kemp, M. H. 
Lurie, and M. Tipton. Experimental stimulation deafness. 
Science, 1935, 81: 101-102. 
1595. Davis, H., C. T. Morgan, J, E. Hawkins, Jr., R. 
Galambos, and F. W. Smith. Temporary deafness follow- 
ing exposure to loud tones and noise. Laryngoscope, St. 
Louis, 1946, 56: 19-21. /. industr. Hyg., 1946, 28: ab- 
stract section; 87-88. [P] 
1596. Davis, H., C. T. Morgan, J. E. Hawkins, Jr., R. 
Galambos, and F. W. Smith. Committee on medical re- 
search of OSRD. Final report on temporary deafness 
following exposure to loud tones and noise. Acta oto- 
laryng., Stockh., 1950, Suppl. LXXXVIII: 1-55. 
1597. de Almeida, H. R. Influence of electric punchcard 
machines on the human ear. Arch. Otolaryng., Chicago, 
1950, 51: 215-222. [CH] 
1598. De Wit, G. Professional deafness in the naval staff. 
Acta oto-laryng., Stockh., 1942, 30: 373-382. (English, 
French, and German summaries.) [P] 
1599. Dickson, E. D. D. The bad effects of noise. Pharm. 
J., 1946, 102: 9-10. 
1600. Dickson, E. D. D. Aviation noise deafness and its 
prevention, pp. 37-39 in: Contributions to aviation 
otolaryngology. Edited by E. D. D. Dickson. London, 
Headley Brothers, 1947, 257 pp. 
1601. Dickson, E. D. D. and A. W. G. Ewing. The pro- 
tection of hearing, pp. 16-30 in: Contributions to aviation 
otolaryngology. Edited by E. D. D. Dickson. London, 
Headley Brothers, 1947, 257 pp. 
1602. Dickson, E. D. D., A. W. G. Ewing, and T. S. Lit- 
tler. The effects of aeroplane noise on the auditory acuity 
of aviators; some preliminary remarks. /. Laryng., 1939, 
54: 531-547. [P] 
1603. Dishoeck, H. van and J, van Gool. Adaptatie, 
vermoeidheid, en trauma. [Adaptation, fatigue, and 
trauma.] Ned. Tijdschr. Geneesk., 1951, 95: 1361-1365. 
[P] 
1604. Eldredge, D. H., H. 0. Parrack, and H. Davis. 
Some responses of the ear to intense high-frequency 
sound. USAF. Wright-Patterson air force base, Dayton, 
Ohio. Aero medical laboratory. Technical Kept. no. 6564. 
September 1951, 11 pp. 
1605. Ewing, A. W. G. and T. S. Littler. Auditory fa- 
tigue and adaptation. Brit. J. Psychol., 1935, 25: 284- 
307. [P] 
1606. Fabritius, H. F. Some remarks on occupational 
deafness; a comparative investigation. Acto otolaryng., 
Suppl, Stockh., 1948, 74: 136-140. 
1607. Fenner, E. Das Audiogramm des akustischen 
Traumas. Schweiz, med. Wschr., 1943, 73: 823-827. [D] 
1608. Finch, G. and E. Culler. Effects of protracted 
exposure to a loud tone. Science, 1934, 80: 41-42. [P] 
1609. Firestone, C. Bone conduction in the experienced 
pilot and a probable interpretation. Laryngoscope, St. 
Louis, 1938, 48: 168-175. NOISE—HEARING DEFECTS 
1610-1652 
1610. Flynn, J. P., I. P. Truscott, and E. B. Newman. 
Intensity discrimination as a function of signal-to-noise 
ratio and intensity level. Amer. psychologist., 1946, 1: 277. 
1611. Fowler, E. P,, Jr. Causes of deafness in flyers. 
Arch. Otolaryng., Chicago, 1945, 42: 21-32. 
1612. Fowler, E. P. Symposium on noise, (a) The per- 
centage of capacity to hear speech, and related disabilities. 
Laryngoscope, St. Louis, 1947, 57: 103-113. 
1613. Fujino, H. A combination to the knowledge on 
occupational deafness. J. otorhinolaryng. Soc., Tokyo, 
1950, 53 (7); (Japanese text pagination) 19-23. (Eng- 
lish text pagination), 4. 
1614. Gt. Brit. Advisory council on scientific research 
and technical development, Communications committee. 
Deafening and fatigue due to prolonged exposure to loud 
noise in A. F. V. A. C. 6611, Com. 234, E. A. 48, 15 
July 1944, 9 pp. [P] 
1615. Gt. Brit. FPRC. The otological committee. Min- 
utes of the 21st meeting. 6 January 1950, 12 pp. 
1616. Grove, W. E. Symposium on noise, (b) noise in 
industry. Laryngoscope, St. Louis, 1947, 57: 114—124. 
1617. Grove, W. E. The noise hazard. Industr. Med., 
1949,18: 25-28. 
1618. Gruss, L. The effect of noise on the hearing of 
industrial workers. Volta Rev., 1939, 41: 511-514, 
535-536. 
1619. Guild, E. Acoustic trauma in aircraft maintenance 
workers. J. Aviat. Med., 1951, 22: 477-490. 
1620. Harris, J. D. Pitch discrimination in noise. Amer. 
psychologist., 1946,1: 277. 
1621. Harris, J. D., A. I. Rawnsley, and P. A. Kelsey. 
Studies in short-duration auditory fatigue. I. Frequency 
differences as a function of intensity. U. S. Navy. Sub- 
marine base, New London, Conn. Medical research labora- 
tory. Project NM 003 041. 34.01, 8 December 1950, 12 pp. 
1622. Holway, A. H., R. C. Staton, and M. H. Zigler. 
The neurophysiology of hearing. I. The magnitude of 
threshold-stimuli during recovery from stimulation-deaf- 
ness. J. exp. Psychol., 1940, 27: 669-676. [P] 
1623. Hoople, G. D., W. C. Wolfe, and S. C. Bregande. 
Symposium on noise, (c) unrecognized battle noise 
trauma. Laryngoscope, St. Louis, 1947, 57: 125—136. [P] 
1624. Hoople, W., G. D, Wolfe, and S. C. Bregande. 
Traumatismos ignorados por intensos ruidos de guerra. 
Rev. oto-neurol. oftal., 1948, 23: 79-81. 
1625. Horton, G. P. The effect of intense and prolonged 
acoustical stimulation on the auditory sensitivity of guinea 
pigs. J. comp. Psychol., 1934, 18: 405-417. [P] 
1626. Horton, G. P. An experimental study of stimula- 
tion deafness in guinea pigs. Ann. Otol., etc., St. Louis, 
1935, 44: 252-259. 
1627. Jankowski, W. Leczniczego dla chor6b warstw 
pracowniczych przy Klinice Oto-laryngologicznej we 
Wroclawiu. Usledzenie sluchu u robotnikow panstwowej 
fabryki gwozdzi Archimedes. [Impaired hearing of the 
workers in the Archimedes screw factory in Wroclaw.] 
Oto-laryngol. slav., 1950, 4: 483-495. [CH] 
1628. Kipp, F. Gehoerschaedigungen durch flugzeug- 
laerm. U. S. AAF. Aeromedical center, HQ. 3D. Central 
medical establishment, APO 172, U. S. A., U8—46-18, 
26 May 1946, 25 pp. (English translation.) [CH] [P] 
1629. Kley, W. tlber die Schwehorigkeit wahrend und 
nach intensiver Larmeinwirkung. Arch. Ohr.-, Nas.-, u. 
KehlkHeilk., 1949/50, 156: 471-475. [P] 
1630. Larsen, B. Investigations of professional deafness 
in shipyard and machine factory labourers. Acta oto- 
laryng., Stockh., Suppl., 1939, 36: 5-255. [P] [CH] [D] 
1631. Larsen, B. Investigations in the fatigue of hearing. 
Acta oto-laryng., Stockh., 1942, 30: 525. 
1632. Lngli, G. and F. Pollice. Tempo di easurimento 
dei recettori acustici in funzione dell’intensita del suono 
affaticante. Ric. sci. ricostr., 1947, 17: 1620-1622. 
1633. Lumio, J. S. Studies on hearing loss of railway 
engine employes in Finland. Acta oto-laryng., Stockh., 
1949, 37: 539-550. 
1634. McCoy, D. A. The industrial noise hazard. Arch. 
Otolaryng., Chicago, 1944, 39: 327-330. 
1635. Machle, W. Industrial noise as it affects hearing. 
Conn., St. med., 1947, 11: 972-976. 
1636. MacLaren, W. R. and A. L. Chaney. An evalua- 
tion of some factors in the development of occupational 
deafness. Industr. Med., 1947, 16: 109-115. [R] 
1637. Meyer zum Gottesberge, A. Horschadigungen 
beim Flugpersonal. (Ein Beitrag zur Frage der c5—Senke.) 
Luftfahrtmed., 1944, 8: 256-264. 
1638. Miller, G. A. The perception of short bursts of 
noise. /. acoust. Soc. Amer., 1948, 20: 160-170. 
1639. Miller, G. A. and W. G. Taylor. The perception 
of repeated bursts of noise. /. acoust. Soc. Amer., 1948, 
20: 171-182. 
1640. Partridge, R. C., J. P. Fletcher, and D. Y. Solandt. 
Studies on pitch discrimination and acuity of hearing. 
Rev. Canad. Biol., 1947, 6: 176. 
1641. Pastore, P. N, Hearing among experienced avia- 
tors. Proc. Mayo Clin., 1941,16: 214-217. 
1642. Pattie, F. A. An experimental study of fatigue in 
the auditory mechanism. Amer. J. Psychol. 1927, 38: 
39-58. [P] 
1643. Perlman, H. B. Acoustic trauma in man. Clinical 
and experimental studies. Arch. Otol. N. Y., 1941, 34: 
429-452. 
1644. Perlman, H. B. The effects of noise and concus- 
sion on hearing. /. Speech Dis., 1943, 8: 289—295. 
1645. Peyser, A. Kroniskt akustiskt traumas forebyg- 
gande genom oronundersokningar. [Ear examinations in 
order to obviate chronic acoustic trauma.] Social med. 
tskr., 1951,28; 46. [M] 
1646. Rawdon-Smith, A. F. Experimental deafness. 
Further data upon the phenomenon of so-called auditory 
fatigue. Brit. J. Psychol., 1935-36, 26: 233—244. 
1647. Rosenblith, W. A. Industrial noises and industrial 
deafness. J. acoust. Soc. Amer., 1942, 13: 220-225. 
1648. Ruedi, L, and W. Furrer. Akustisches trauma 
und funktion des innenohres. Acta oto-laryng., Stockh., 
1945, 33: 460-470. (German, English, and French sum- 
maries.) [P] 
1649. Ruedi, L. and W. Furrer. Das akustische Trauma. 
Pract. oto-rhino-laryng., 1946, 8: 177—372. (French, Eng- 
lish, and Spanish summaries.) pp. 377—420 in: Medicine 
of the ear. Edited by Edmund Prince Fowler, Jr., with a 
foreword by John Devereux Kernan. Second edition. New 
York, Thomas Nelson and Sons. 1947, 777 pp. [P] 
1650. Russi, IT. von. t)ber Larmschadi gungen in indus- 
triellen Betrieben and ihre Verhiitung. Pract. oto-rhino- 
laryng., 1946,8; 71-113. [P] 
1651. Senseney, E. T. Symposium on noise, (e) A study 
of cases of acoustic trauma from a medicolegal standpoint, 
and a comparison of patterns of deafness. Laryngoscope, 
St. Louis, 1947,57; 142-157. 
1652. Senturia, B, H. A survey of auditory acuity among 
pilots and enlisted trainees. U. S. AAF. Randolph Field, 
Tex. School of aviation medicine. Project no. 171, Rept. 
no. 1, 14 September 1943, 5 pp. [P] 1653-1668 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
1653. Senturia, B. H. The effect of exposure to airborne 
noise on auditory acuity. U. S. AAF. Randolph Field, 
Tex. School of aviation medicine. Project 205, Kept. no. 1, 
11 December 1943, 5 pp. 
1654. Senturia, B. H. The effect of exposure to airplane 
noise on auditory acuity. U. S. AAF. Randolph Field, Tex. 
School of aviation medicine. Project 205, Kept. no. 2, 
26 May 1944, 4 pp. 
1655. Senturia, B. H. The effect of exposure to airplane 
noise on auditory acuity. U. S. AAF. Randolph Field, Tex. 
School of aviation medicine. Project 205, Rept. no. 3, 
4 August 1944, 4 pp. 
1656. Senturia, B. H. Hearing changes during pilot 
training. Milit. Surg., 1949,105: 205-208. [P] 
1657. Simonton, K. M. Hearing of airline pilots. A 10- 
year study. J. Aviat. Med., 1949, 20: 418-429. Abstr. 
World Med., 1950, 7: 569. 
1658. Sleight, R. B. and J. Tiffin. Industrial noise and 
hearing. /. appl. Psychol., 1948, 32: 476-488. [R] 
1659. Smyth, H. F. Noise in industry: its effect on the 
hearing and on general health (a review of the literature). 
Ann. Otol., etc., St. Louis, 1932, 41: 1110—1116. 
1660. Theilgaard, E. Testing of the organ of hearing 
with special reference to noise prophylaxis. Acta oto- 
laryng., Stockh., 1949, 37: 347-354. [P] 
1661. Ullmann, E. V. Traumatic deafness in combat 
flyers. Arch. Otolaryng., Chicago, 1944, 40: 374-381. 
1662. Wessling, G. Funktionsprovning av 300 horsel- 
skadade arbetare vid Gotaverken. [Functional examination 
of 300 workers with impaired hearing at Gotaverken 
(shipyards).] Nord. Med., Stockholm, 1948: 38: 1270. 
1663. Wheeler, D. E. Detection of noise-susceptible ears. 
Laryngoscope, St. Louis, 1949, 59: 1328-1338. 
1664. Wheeler, D. E. Noise-induced hearing loss. Arch. 
Otolaryng., Chicago, 1950, 51: 344-355. 
1665. Wheeler, D. Physical and physiological variables 
in noise-induced hearing loss. Arch. Otolaryng., Chicago, 
1951, 54: 267-272. 
1666. Wilson, W. H. Prevention of traumatic deafness. 
A preliminary report. Arch. Otolaryng., Chicago, 1943, 
37: 757-767. [P] 
1667. Wilson, W. H. Determination of susceptibility to 
abnormal auditory fatigue. Ann. Otol., etc., St. Louis, 
1950, 59: 399-405. [P] 
1668. Anon. Effects of noise. Flight Surgeons Reference 
File, U. S. AAF. Randolph Field, Tex. School of aviation 
medicine. AAF Manual 25-0-1, 8—6-178-6-9, 1 Novem- 
ber 1945. 
4. EAR DAMAGE 
Pathological changes occurring in the ear after 
exposure to intense noise include degeneration of 
the cochlear nerve {1691) and damage to the organ 
of Corti. In a report published in 1942, Davis, 
Galambos, Hawkins, Parrack, Lurie, and Leighton 
{1567) described the effects of exposure of guinea 
pigs to pure tones of various frequencies at intensi- 
ties from 140 to 153 decibels. The effects of 500 and 
1,000 cycles were most completely explored. The 
least detectable anatomical damage to the inner ear, 
namely, the disappearance of mesothelial cells from 
a limited area of the lower surface of the basilar 
membrane, was produced by 1,000 cycles at 140 
decibels for 3 minutes. More severe and extensive 
damage was produced by more intense tones and 
longer exposures. Such damage included degenera- 
tive changes in sensory cells, rupture of the organ 
of Corti, and dislocation of the organ of Corti from 
the basilar membrane. A few days or weeks after 
severe exposure, the organ of Corti was found to 
disappear where it had been severely damaged and 
the nerve fibers and cells were degenerated. Milder 
degrees of damage were localized, but a very severe 
exposure (150 decibels for several minutes) caused 
widespread permanent damage. The damage was 
found to be located near the helicotrema when 
caused by low tones and nearer the oval and round 
windows for high tones. Severe and extensive dam- 
age to the inner ear was caused by loud tones with- 
out apparent injury to the eardrum or the ossicles. 
The authors found that cats are far more resistant 
than guinea pigs to inner ear injury from intense 
sounds. Similar findings were reported by Hawkins, 
Lurie, and Davis {1680) 1943 and Lurie, Davis, 
and Hawkins {1682) 1944. For a further report on 
this research, an abstract by Hawkins, Davis, and 
Lurie {1679) 1946 should be consulted. 
Popoff {1685) 1930 subjected mice for weeks 
and months to a noise created by heavy hammers 
flattening out white-hot steel bars into scythes. The 
noise was graphically registered as to the prevalence 
of low tones (60 to 100 cycles) and high tones 
(2,000 to 3,000 cycles). The number of strokes of 
the hammer was 200 per minute. White mice were 
exposed for 8 hours daily for 20 days in the cage 
on the stand. These animals showed destructive 
changes at the commencement of the basilar mem- 
brane. The organ of Corti was destroyed, and 
changes were present in the neighboring ganglion 
cells. After 3 months’ exposure the destructive 
process had extended to the higher windings of the 
cochlea. There was destruction of the ganglion cells 
with their afferent and efferent fibres within the 
lamina spiralis and the corresponding portion of 
the modiolus. After 8 or 9 months all of the ganglion 
cells and nerve fibers of the upper convolutions had 
disappeared. It was concluded that the damaging 
effects on the inner ear were transmitted to the audi- 
tory apparatus through bone conduction and not 
vibrations transmitted through the air and the ex- 
ternal auditory meatus, since no changes were found 
under similar examinations in mice exposed to the 
same noise in cages suspended by a spring so that 
air transmission only was involved. Limitation of 
the degeneration to the superior section of the 
cochlea early in exposure was reported by Takezawa 
{1688) 1934 in guinea pigs exposed to noise levels 
of 90 to 95 decibels for 6 months. Although the 
degenerative changes were limited at first, after 3 NOISE—EAR DAMAGE 
1669-1678 
cells and also indicated to the authors support of 
the resonance theory of cochlear function. 
For a discussion of the mode of origin of the C5 
dip, a paper by Ruedi and Furrer [1687) 1946 
should be consulted. According to the authors, all 
natural sounds such as industrial noise have a broad- 
frequency spectrum, which, in the cochlear fluid, 
gives rise to many pairs of eddies. Each of these pairs 
changes direction at the perception point of ap- 
proximately 4,000 cycles. At this point the basilar 
membrane is subjected to great tension, which can 
lead to permanent deformation revealed as the C5 
dip. 
For further reports on ear damage, papers by the 
following may be consulted: Bender [1669) 1950; 
Bugard [1670) 1951; Causse and Falconnet [1672) 
1947; Friedenwald [1674) 1913; Fujino [1676 and 
1677) 1950; Kristensen [1681) 1947; Mancioli 
[1683) 1949; Nilsson [1684) 1950; Ruedi and 
Furrer [1686) 1946; Tissie [1689) 1948; Turner 
[1690) 1915; and Wolff [1692) 1942. 
1669. Bender, L. Affections causees par le bruit, les 
vibrations et les trepidations, pp. 313—322 in; Aledecine 
du travail. Edited by G. Simonin. Paris, Librairie Maloine, 
1950, 913 pp. [D] 
1670. Fugard, P. Action biologique de bruits complexes 
de niveau eleve. C. R. Soc. Biol., Paris, 1951, 145: 11—12. 
[p] 
1671. Causse, R. and P. Chavasse. Recherches sur les 
potentiels cochleaires du cobaye apres stimulation auditive 
intense. C. R. Soc. Biol., Paris, 1944, 138: 847-849. [P] 
1672. Causse, R. and P. Falconnet. La surdite profes- 
sionnelle de 1’aviateur. Med. aeronaut., 1947, 2: 414—429. 
[D] 
1673. Davis, H., A. J, Derbyshire, E. H. Kemp, M. H. 
Lurie, and M. Upton. Functional and histological changes 
in the cochlea of the guinea-pig resulting from prolonged 
stimulation. /. gen. Psychol., 1935, 12: 251—278. [P] 
1674. Friedenwald, H. Injuries effects of loud noises 
on the organ of hearing. Bull. med. chir. Fac. Md., 1913, 
5: 103-105. 
1675. Frings, H. and I. Senkovits. Destruction of the 
pinnae of white mice by high intensity air-borne sound. 
USAF. Wright-Patterson air force base, Dayton, Ohio. 
Air materiel command. Technical Rept. no. 6029, Sep- 
tember 1950, 23 pp. 
1676. Fujino, H. A contribution to the knowledge on 
occupational deafness. Nippon zibiinkoka gakkai kaiho, 
1950, 53: (Japanese text pagination), 19-23; (English 
text pagination), 4. (In Japanese with English summary.) 
[P] 
1677. Fujino, H, On the path of sound that causes 
inner ear deafness in repeated application. Nippon 
zibiinkoka gakkai kaiho, 1950, 53: (Japanese text pagina- 
tion), 344-349; (English text pagination), 36-37. (In 
Japanese with English summary.) [P] 
1678. Hamberger, C. A. H. Hyden, and G, Nilsson. 
The correlation between cytochemical changes in the 
cochlear ganglion and functional tests after acoustic stim- 
ulation and trauma. Acta oto-laryng., Stockh., suppl., 
1949, 75: 124-133. 
months the degeneration was seen in the whole 
cochlea and the cochlear nerve was also involved. 
That exposure of men to intense airborne sound 
may have deleterious effects, other than injury to 
the aural apparatus, is widely suspected. Exposure 
of animals to high-intensity sound has shown that 
death can be brought about if the exposure time is 
sufficiently long and the intensity of the sound suffi- 
ciently great. Death in this case results from the 
heat produced at the body surface as it absorbs the 
sound waves. Frings and Senkovits [1675) 1950 
have reported inflammatory changes in the pinnae 
of mice subjected to high-intensity airborne sound. 
Experimental studies have revealed a general 
correspondence between alterations in cochlear po- 
tentials and anatomical damage to the inner ear, 
but the parallelism is not exact or invariable. The 
anatomical changes are more consistent, and Davis, 
Galambos, Hawkins, Parrack, Lurie, and Leighton 
[1567) 1942 consider that the “electrical audio- 
gram” (cochlear potentials) is not as satisfactory 
or reliable a method of assessing injury to the ear 
as microscopic examination. Diminution in cochlear 
potentials in experimental animals associated with 
exposure to noise has been reported by Causse and 
Chavasse [1671) 1944 and Hamburger, Hyden, and 
Nilsson [1678) 1949. The former authors exposed 
dogs to 1,000 cycles at an intensity of 90 and 100 
decibels in an acoustic room for periods from 96 
to 408 hours. The 408-hour exposures resulted in 
complete deafness. Other animals showed a diminu- 
tion of cochlear potentials proportional to the dura- 
tion of exposure. The reduction in potentials was 
not uniform. Diminution of sensitivity was more 
pronounced at frequencies of 1,300 and 4,500 cycles. 
In the experiments of the latter authors, cochlear 
potentials in guinea pigs were registered at various 
times after acoustic stimulation at 6,000 cycles with 
an intensity of 80 decibels for 3 hours. No deviations 
from controls were found up to 14 days after stimu- 
lation. After detonations from a revolver there were 
severe changes in the cochlear potentials indicat- 
ing functional damage to the acoustic apparatus. 
Davis, Derbyshire, Kemp, Lurie, and Upton [1673) 
1935 found that noise at a frequency of 2,500 cycles 
and an intensity of 95 and 105 decibels for 40 to 45 
days in the guinea pig produced a fairly extensive 
degeneration of the outer hair cells centering in the 
middle of second cochlear whorl. The threshold of 
the electrical response was elevated corresponding 
to the severity and extent of the histological dam- 
age. In three cases, gross lesions of the cochlea were 
found to be correlated with highly abnormal elec- 
trical responses. The results indicated that the elec- 
trical respone of the cochlea is generated by the hair 1679-1692 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
1679. Hawkins, J. E., Jr,, H. Davis, and M, H. Lurie. 
Injury of the ear produced by exposure to loud tones. 
Fed. Proc. Amer. Soc. exp. Biol., 1946, 5: 42. 
1680. Hawkins, J. E. M., H. Lurie, and H. Davis. Injury 
of the inner ear produced by exposure to loud tones. 
U. S. OSRD. Supplementary Report. 31 December 1943, 
10 pp. [P] 
1681. Kristensen, H. K. Recherches sur 1’oreille interne 
de cobayes exposes aux bruits d’ateliers de tissage. Acta 
oto-laryng., 1947, 35: 220-224. [P] 
1682. Lurie, M, H., H. Davis, and J. E. Hawkins, Jr. 
Acoustic trauma of the organ of Corti in the guinea pig. 
Laryngoscope, St. Louis, 1944, 54: 375-386. [P] 
1683. Mancioli, G. Contribute alio studio delle otopatie 
professional!; richerche audiometriche sugli sbavatori. 
Ross. Med. indust., 1949, 18: 233-250. 
1684. Nilsson, G. Det akustiska traumat ur teoretisk 
synpunkt. Nord. Med., Stockholm, 1950, 43: 1058-1061. 
[D] 
1685. Popoff, N. F. Zur Frage der experimentell durch 
Fabrik-(Metall)-Gerausche erzeugten pathohistologischen 
Veranderungen im Gehororgan weisser Mause. (Kurzer 
Bericht iiber den auf dem 5, allrussischen Kongress der 
Oto-Laryngologen [Moskau, 26-30 April 1927] gehaltenen 
Vortrag. Der Vortrag wurde von Demonstrationen mikro- 
skopischer Praparate und Diapositive begleitet.) Bull. 
Hyg., Lond., 1930, 5: 574. Abstr. 
1686. Ruedi, L. and W. Furrer. Physics and physiology 
of acoustic trauma. J. acoust. Soc. Amer., 1946, 18: 
[D] [P] 
1687. Ruedi, L. and W. Furrer. Acoustic trauma. Its 
origin and prevention. Schweiz, med. Wschr., 1946, 76: 
843-851. (English, French, and German summaries. ) [P] 
[CH] 
1688. Takezawa, N. Experimentelle Untersuchungen 
iiber die professionelle Schwerhorigkeit. Mitt. med. Akad. 
Kioto, 1934, 12: 923-952. 
1689. Tissie, M. Les traumatismes sonores dans la 
pathologic du travail. Arch. Mai. prof., 1948, 9: 422-428. 
[R] [D] 
1690. Turner, A. L. Noise-deafness: a review of recent 
experimental work, and a clinical investigation into the 
effect of loud noise upon the labyrinth in boiler-makers. 
J. Laryng., 1915, 30: 91-105. [P] 
1691. Wittmaack, ( ). Uber Schadigung des Gehors 
durch Schalleinwirkung. Eine experimentelle Studie. Z. 
Ohrenheilk., 1907, 54: 37-80. [P] 
1692. Wolff, D. Microscopic examination of human 
labyrinths from patients exposed to loud noises. Arch. 
Otolaryng., Chicago, 1942, 36: 843-852. 
5. EFFECTS OF NOISE ON EFFICIENCY 
In 1948, Harris and Stover {1699) measured 
overall noise levels aboard the U. S. S. Raton. 
Interpretation of the data collected reveals that 
aside from the engine rooms no compartment in this 
submarine was noisy enough to reduce auditory 
acuity by a noticeable amount, or to reduce psycho- 
motor or physiological efficiency. In the engine 
rooms a noise level of 108 decibels was measured at 
standard surface cruising speed. This was considered 
to be sufficient to cause auditory fatigue in some 
individuals and to impair communication for some 
hours. This loss would not be permanent. The ex- 
tent of individual susceptibility was not determined. 
The noise spectrum in the engine room peaked at 
400 cycles, which is of a type least conducive to 
annoyance. Even though there may be no overall 
quantitative effect of noise on human performance, 
Chapanis, Garner, and Morgan {1696) 1949 found 
evidence that subjects require more energy to per- 
form the same kind of work in a noisy environment 
than in a quiet one. Several studies have shown 
quite consistently that the basal metabolism of sub- 
jects working in a noisy situation is higher than of 
those working in a quiet environment. This may 
account for the many reports of fatigue from work- 
ers in noisy spaces. In a report on noise in relation to 
efficiency, Behnke {1693) attributed noise fatigue 
to the fact of increased concentration incident to 
the maintenance of a satisfactory standard of work. 
His studies did not indicate any marked impairment 
resulting from noise but it was found that the sub- 
jects complained more of the annoyance or aggrava- 
tion incident to work performed in the noisy room 
than they did of bad effects of hot atmosphere. 
High noise levels slowed paristaltic activity and cut 
down the flow of saliva and gastric juice. Disturb- 
ance of sleep was the most obvious cause of fatigue 
associated with noise. In an experimental investi- 
gation of the effect of change in atmospheric con- 
ditions and noise upon performance, Viteles and 
Smith {1709) 1946 stated that noise intensities up 
to 90 decibels were of less importance than heat. In 
the opinion of these authors there is no justification 
for expenditures to reduce noise below the 90- 
decibel level. 
It has generally been found that noise reduces 
work output. Laird {1701) 1927 has stated that 
skilled workers are more adversely affected than 
mediocre workers. Weston and Adams {1710) 1932 
gave a figure of 1.5 to 3 percent output loss for 
weavers in a noisy environment as opposed to a 
quiet environment. Stevens, Egan, Waterman, 
Miller, Knapp, and Rome {1707) 1941 found that 
most types of mental, motor, and physiological ac- 
tivity are affected very little by noise as such. In 
these experiments human subjects were subjected 
to continuous 7-hour periods of work in airplane 
noise at 115 decibels. Performance in some tasks 
was impaired by as much as 5 percent, but pro- 
ficiency at other tests remained unaltered. 
Boulin {1694) has commented upon the effects 
of noise upon industrial production. It is contended 
that reducing noise in workshops increases produc- 
tivity and lowers defective output. Reduction in 
noise was also stated to lower the number of mistakes 
in telegraphy and typewriting. Pollock and Bartlett NOISE—EFFECTS ON EFFICIENCY 
1693-1710 
(1704) 1932, in commenting upon the experiments 
in this field, stated that the results were in general 
agreement that noise tends to produce slight and 
readily recoverable diminution of efficiency. The 
direct effects upon nonauditory performance are 
commonly greatly exaggerated. Individuals react 
differently to noises, pleasant or distasteful. Dis- 
continuous, loud mechanical noise was found to be 
more disturbing than continuous, loud mechanical 
noise, but even soft, pleasing, but interesting noise 
may be very distracting. Smith {1705) 1951 car- 
ried out a study on the effect of intermittent, loud 
noise on mental performance. The stimulus inten- 
sity was approximately 100 decibels for each subject. 
Bursts of sound ranged in duration between 10 
seconds and 50 seconds and were administered at 
irregular and unpredictable intervals. It was found 
that the effect of bursts of intense noise upon mental 
performance was to increase the quantity and de- 
crease the quality of the response. The author con- 
cluded that the allegedly malignant effects of ex- 
traneous noise may be expressed primarily in terms 
of depreciation in sustained performance, or of 
interference with factors other than adequate out- 
put. Hanley, Williamson, and Spilka {1698) 1950 
found that the amount of noise was not systemati- 
cally related to proficiency in performing mental 
tasks, and that such proficiency was not affected 
adversely or favorably by the presence of constant 
or variable noise. However, the tasks were simple, 
the noise duration short, and the levels low. 
For further reports on the effects of noise on 
efficiency, papers by the following may be con- 
sulted: Brandt {1695) 1947; Gilbert and Gawain 
{1697) 1950; Hood {1700) 1950; Morgan {1702) 
1917; Obata and Morita {1703) 1934; Stevens 
(1706) 1941; and Vernon {1708) 1930. 
1693. Behnke, A. R., Jr. Noise in relation to hearing and 
efficiency. N. Y. St. J. Med., 1940, 40: 1080-1088. [R] 
1894. Boulin, P. Le bruit et ses consequences au point 
de vue de de I’hygiene et de la capacity de 
production des ouvriers. Bull. Hyg., 1931, 6: 134. Ann. 
Hyg. publ., Paris, 1930, 8: 645-651. 
1695. Brandt, A. D. Industrial noise and its control, 
pp. 322—327 in: Industrial health engineering. New York, 
John Wiley & Sons, Inc., 1947, 395 pp. [P] 
1696. Chapanis, A., W. R. Garner, and C, T. Morgan. 
The working environment. Noise, pp. 414-417 in: Applied 
experimental psychology. New York, John Wiley & Sons, 
Inc., 1949, 421 pp. 
1697. Gilbert, P. F. and G. C. V. Gawain. Sonic and 
ultrasonic effects on maze learning and retention in the 
albino rat. USAF. Wright-Patterson air force base, Dayton, 
Ohio. Air materiel command. Tech. Kept. no. 6030, Sep- 
tember 1950, 49 pp. [P] 
1698. Hanley, T. D., R. J. Williamson, and B. Spilka, 
The effect of various noise levels on performance of three 
mental tasks. U. S. Navy. Special devices center, Port 
Washington, New York, Tech. Kept. 3DC-104-2-21, 15 
December 1950, 20 pp. [P] 
1699. Harris, J. D. and A, D. Stover. Noise levels 
aboard a fleet submarine. U. S. Navy. Submarine base. 
New London, Conn. Medical research department. Project 
NM-003-020, Kept. no. 2, 12 April 1948, 15 pp. 
1700. Hood, J. D. Studies in auditory fatigue and 
adaptation. Acta oto-laryng., Stockh., Suppl., 1950, 92: 57. 
1701. Laird, D. A. The measurement of the effects of 
noise on working efficiency. J. industr. Hyg., 1927, 9: 
431-434. 
1702. Morgan, J. J. G. The effect of sound distraction 
upon memory. Amer. J. Psychol., 1917, 28: 191-208. 
1703. Obata, J. and S. Morita. The effects of noise 
upon human efficiency. J. acoust. Soc. Amer., 1934, 5: 
255-261. 
1704. Pollock, K. G. and F. C. Bartlett. Psychological 
experiments on the effects of noise, pp. 1—37 in: Two 
studies in the psychological effects of noise. Gt. Brit. MRC, 
Industrial health research board. Kept. no. 65, 1932, 70 pp. 
[P] . 
1705. Smith, K. R. Intermittent loud noise and mental 
performance. Science, 1951, 114: 132—133. 
1706. Stevens, S. S. The effects of noise and vibrations 
on psychomotor efficiency. U. S. NRC. Committee on 
sound control. Progress report of Project 11, 31 March 
1941, 113 pp. [P] 
1707. Stevens, S. S., J. P. Egan, T. H. Waterman, J. 
Miller, R. H. Knapp, and S. C. Rome. The effects of noise 
on psychomotor efficiency. Noise reduction in aircraft as 
related to communication, annoyance and aural injury. 
U. S. NRC. Committee on sound control. Progress report 
of Project 2, 1 December 1941, 126 pp. [P] 
1708. Vernon, H. M. Noise. J. industr. Hyg., 1930, 12: 
235. Abstr. 
1709. Viteles, M. S. and K. R. Smith. An experimental 
investigation of the effect of change in atmospheric condi- 
tions and noise upon performance: /. industr. Hyg., 1946, 
28: abstract section; 124. Trans. Amer. Soc. Heat Vent. 
Engrs., 1946, 52: 167-180. [P] 
1710. Weston, H. C. and S. Adams. The effects of noise 
on the performance of weavers, pp. 38-70 in: Two studies 
in the psychological effects of noise. Gt. Brit., Industrial 
health research board, Kept. no. 65, 1932, 70 pp. [P] 
6. SOUND COMMUNICATION AND NOISE 
The problem of noise and speech intelligibility 
has been considered in a number of reports {1732, 
1735, 1736, 1738, 1739, 1743, 1744, 1745, 1746, 
and 1747). The effect on intelligibility of eliminat- 
ing either the high-frequency speech sounds or the 
low-frequency speech sounds was determined by 
Pollack {1739) 1948 by standardized articulation- 
testing procedures under the special circumstances 
of a background of white masking noise. In general, 
it was found that intelligibility increased as the fre- 
quency range and the intensity level of the speech 
signals were increased. Speech clipping and filter- 
ing circuits in voice communication systems so dis- 
tort transmitted speech as to raise the question of 
their effect upon intelligibilty. The results of experi- 
ments carried out by Stuntz {1745) 1950 indicate 
that speech clipping alone improves intelligibility SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
when the signals are partially masked by electrical 
noise entering the system between the transmitter 
and the receiver. Signals not so masked are similarly 
affected to almost the same degree. Intelligibility 
improves as clipping increases up to at least 24 
decibels. Under extreme noise masking, very heavy 
clipping (100 decibels or more) improves intelligi- 
bility, but reduces the intelligibility of signals not so 
masked. Other experiments revealed that intelligi- 
bility is not likely to suffer when voice frequencies 
below 580 cycles are sharply attenuated, with the 
possible exception that when masking white noise is 
very intense, restoring low frequencies causes slight 
increases in intelligibility. 
Tonndorf {1746) 1951 investigated the effect of 
three categories of noise upon the perception of 
sound signals; (1) conventional noises, (2) jet- 
powered noise, and (3) noises emanating from com- 
munication systems (static). The three kinds of 
noises affected the threshold of perception in dif- 
ferent manners. Shielding by ear cushions and espe- 
cially by earplugs was found to improve the ability 
to perceive signals in the presence of noise. As has 
been shown by Steer, Harris, Draegert, Hanley, and 
Kelly {1743 and 1744) 1948, speech intelligibility 
is generally diminished under stress. For discussions 
of training and other factors affecting speech in- 
telligibility, papers by the following may be con- 
sulted: Abrams {1711) 1949; Chapanis, Garner, 
and Morgan {1719) 1949; Chapanis, Garner, and 
Morgan {1770) 1949; and Egan and Wiener {1724) 
1946. 
Regarding voice communication in submarines, 
Abrams {1711) suggested that operators manning 
the more important communication posts should 
be selected for their inherent ability to speak in- 
telligibly as well as to interpret messages which 
have been altered by distortion and partially 
masked by noise. All operators can be trained to 
speak more intelligibly, to use their equipment effi- 
ciently, and improve their ability to interpret signals. 
All important messages can be standardized into 
short, simple, easy-to-say and easy-to-understand 
words. Chapanis, Garner, and Morgan {1719,1720) 
have pointed out that one of the prime determiners 
of speech intelligibility is the intensity of the speech 
in quiet and in noise. Intelligibility of speech is de- 
termined by how much more speech energy than 
nose energy there is in the listener’s environment. 
The speech-to-noise ratio is more important than 
the overall intensity of the noise. However, even 
with a constant speech-to-noise ratio, speech in- 
telligibility can be improved if the overall system is 
operated at a proper gain level. Under conditions 
where the noise and speech are coming from the 
same source, this overall level can be set with a 
simple gain control. When the noise and speech are 
coming from different sources, then the overall level 
can be changed only by decreasing the source of the 
sound at or near the eardrums. Regardless of where 
the masking noise comes from, it has the same effect. 
For the same total amount of energy, speech is by 
far the most effective masker of other speech. 
A wide variety of sounds have been investigated 
by Miller {1733) 1947 to determine the extent to 
which they interfere with vocal communication. 
The masking of speech was determined by articu- 
lation-testing methods and estimates of annoyance 
obtained by the method of paired comparisons. 
Sounds are classified as noises, tones, and voices. 
For all three types, the stimulus dimensions deter- 
mining both masking and annoyance are the in- 
tensity, frequency or spectrum, and the temporal 
pattern of the sound. Masking depends primarily 
on the speech-to-noise ratio over the range of fre- 
quencies involved in speech. Sounds of low fre- 
quency mask this range more effectively than sounds 
of high frequency. Interruptions in the sound de- 
crease the masking effectiveness. Annoyance also 
increases as the intensity is raised. Low-frequency 
sounds are less annoying than high-frequency 
sounds, and intermittent, irregular ones are more 
annoying than continuous sounds. Annoyance, how- 
ever, does not interfere with vocal communications 
in the laboratory situation. Miller pointed out 
{1734) 1949 that the effect of an interfering noise 
is to raise the threshold of detectability and intel- 
ligibility and so decrease the range of intensities 
available for vocal communication. This shift in 
threshold is the measure of masking. In a study of 
pitch discrimination in masking, Harris {1728) 
1948 concluded that loudness exerts a profound 
effect directly or indirectly on pure-tone pitch dis- 
crimination. This effect is complex and differs ac- 
cording to whether the tone is presented in quiet 
or is partially masked by noise. 
For studies on the effects of noise upon loudness 
of speaking, papers by the following should be con- 
sulted: Black {1713) 1949 and {1714) 1951; Black 
and Greybiel {1715) 1948; Black, Greybiel, Light- 
foot, and Morrill {1716) 1948; Broadbent {1717) 
1951; Hanley, Draegert, Buck, and Kelly {1727) 
1949; and Steer, Henley, Draegert, Buck, and Kelly 
{1742) 1949. Studies of Black and Greybiel {1715) 
1948 reveal that in repeating messages heard over 
headsets, the listener tends to respond with greater 
intensity as he hears more intense signals. It is also 
demonstrated that vocal loudness is similarly af- 
fected when the speaker is answering questions in- 
stead of repeating words. Moreover, the subjects NOISE—EFFECTS ON COMMUNICATION 
1711-1717 
were unable to maintain a constant intensity when 
saying back words that were heard at different 
levels of amplification. Two amounts of noise back- 
ground introduced into the headsets of the listeners 
did not significantly differentiate the levels of vocal 
response. Messages spoken by males and females 
elicited different intensities of response, the female 
being responded to the louder. Room illumination 
did not affect the intensity with which the listeners 
repeated words. Black {1713) 1949 also emphasized 
the tendency of subjects to talk with different inten- 
sities in keeping with the level of intensity of heard 
stimulus. The trends were the same whether the 
stimuli were words to be repeated or questions to be 
answered. Repeated words were spoken more in- 
tensely than answers to questions heard under the 
same conditions. In a further study, Black {1714) 
1951 exposed male subjects for 120 minutes to simu- 
lated cockpit noise. Following subjection to this 
noise there was an increase in vocal intensity which 
decreased linearly, but was not complete after 15 
minutes of silence. Steer, Hanley, Draeger, Buck, 
and Kelly {1742) 1949 found that distracting noises 
fed into the headphones worn by subjects reduced 
the speaking rate, increased the speech time, in- 
creased the mean syllable duration, and increased 
the mean speech-intensity level. Similar findings 
were reported by Hanley, Draegert, Buck, and Kelly 
{1727) 1949. The effect of speaking and listening 
simultaneously has been investigated by Broadbent 
{1717) 1951. It was concluded that in general one 
cannot attend perfectly both to the speech of others 
and to our own. Whether because we are attending 
to what we have just said or what we are just going 
to say is uncertain. 
Egan {1722) 1946 has demonstrated that al- 
though a sufficiently intense noise in one ear will 
mask speech heard in the contralateral ear, a weaker 
noise has the opposite effect, that is to say, it en- 
hances the loudness of speech heard in the other ear. 
Subjects reported that the monaural speech was 
more dense or more crisp when noise was intro- 
duced into the contralateral ear. Most observers 
reported a change in the localization in the speech. 
It was localized nearer to the center of the head 
when the noise was introduced into the opposite 
ear. Preliminary tests indicated that the intelligi- 
bility of speech heard monaurally is slightly in- 
creased when noise is introduced into the contra- 
lateral ear. These findings have also been discussed 
by Egan {1723) 1948. 
Pollack {1740) 1949 presented recorded speech 
passages against a background of white noise and 
against a quiet background. The effect of the noise 
on the loudness of speech was determined by having 
the listeners adjust a level of speech heard in quiet 
to sound equal in loudness to an assigned average 
level of speech presented against selected levels of 
background of noise. In general, it was found that 
low noise levels produce a proportionately lower 
depression in the loudness level of speech than 
higher noise levels. The effect of noise on the loud- 
ness of speech was found to be a function of the 
speech-to-noise ratio rather than of the level of the 
speech alone or of the noise alone. Under none of 
the conditons of the author’s experiments did white 
noise actually increase the loudness of speech (the 
Egan effect). 
For suggestions on speech reception testing, a 
paper by Harris {1729) 1948 may be consulted. 
Harris has also discussed {1730) 1950 the effect of 
sensation levels on intensive discrimination of noise. 
Loudness perception for pure tones and for speech 
was discussed in 1950 by Harris and Myers {1731). 
For studies of auditory discrimination in sonar 
operation, a paper by Neff {1737) 1949 should be 
consulted. Also a report evaluating auditory con- 
ditions in asdic cabins at sea by Solandt and Bunker 
{1741) 1944 may be referred to. 
For further studies on sound communication and 
noise, papers by the following may be consulted: 
Aleksenko {1712) 1949, Broadbent {1718) 1951, 
Davis {1721) 1951, Elliott {1725) 1951, and 
Garner {1726) 1949. 
1711. Abrams, M. H. Voice communications: personnel 
and phraseology, pp. 233-241 in: A survey report on 
human factors in undersea warfare. National research 
council, Washington, D. C., 1949, 541 pp. 
1712. Aleksenko, N, I. Vliianie neakusticheskikh raz- 
drazhenii na vospriiatie napravleniia zvuka. [Effect of 
nonacoustic stimulation on the perception of sound direc- 
tion.] Prob. fiziol. akust., Moskva., 1949, 1: 74-88. 
1713. Black, J. W. Loudness of speaking: the effect of 
heard stimuli on spoken responses. /. exp. Psychol., 1949, 
39: 311-315. [P] 
1714. Black, J. W. The effect of noise-induced tempo- 
rary deafness upon vocal intensity. U. S. Navy. NATB, 
Pensacola, Fla. School of aviation medicine. Project NM 
001 064.01.07, Kept. no. 7, 30 January 1951, 9 pp. 
1715. Black, J. W. and A. Graybiel. Loudness of 
speaking: the effect of heard stimuli on spoken responses. 
U. S. Navy. NATB, Pensacola, Fla. School of aviation 
medicine. Contract N7onr-411, Task Order no. 1, Project 
20-k-2, Rept. 411-1-2 Designation Number NR-782- 
004, 1 June 1948, pp. 39. [P] 
1716. Black, J. W., A. Graybiel, C. lightfoot, and 
5. N. Morrill. Loudness of speaking: the effect of the 
intensity of side-tone upon the intensity of the speaker. 
U. S. Navy, NATB, Pensacola, Fla. School of aviation 
medicine. Contract N7onr—411, Task Order no. 1, Project 
20-K-2, Rept. 411-1-4, Designation no. NR-782-004, 
12 June 1948, pp. 12. [P] 
1717. Broadbent, D. E. Speaking and listening simul- 
taneously. Gt. Brit. MRG. Cambridge. Applied psychology 1718-1747 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
research unit, the psychological laboratory. A. P. U. 146/ 
51, January 1951. [P] 
1718. Broadbent, D. E. Listening to one of two 
synchronous messages. Gt. Brit. MRG-RNPRC, OES. 
R. N. P. 51/681, O. E. S. 203, A. P. U. 157/51, October 
1951, 7 pp. [P] 
1719. Chapanis, A., W. R, Garner, and C. T. Morgan. 
Speech. Factors influencing speech intelligibility, pp. 220- 
239 in; Applied experimental psychology, New York, John 
Wiley & Sons, Inc., 1949, 421 pp. 
1720. Chapanis, A., W. R. Garner, and C. T, Morgan. 
Tonal signaling systems. Factors affecting discrimination 
of tones, pp. 256-261 in: Applied experimental psychol- 
ogy. New York, John Wiley & Sons, Inc., 1949, 421 pp. 
1721. Davis, H. Effects of noise on human behavior and 
communication. Arch. ind. Hyg. occup. Med., 1951, 3: 
227-231. 
1722. Egan, J. P. A noise in one ear increases the 
loudness of speech heard in the opposite ear. Amer. 
psychologist., 1946, 7; 277. 
1723. Egan, J. P. The effect of noise in one ear upon 
the loudness of speech in the other ear. /. acoust. Soc. 
Amer., 1948, 20: 58-62. [P] 
1724. Egan, J. P. and F. M. Wiener. On the intelligi- 
bility of bands of speech in noise. /. acoust. Soc. Amer., 
1946, 18: 435-441. 
1725. Elliott, E. A bibliography of the intelligibility of 
spoken orders. Gt. Brit. MRC-RNPRG, OES. R. N. P. 
51/682, O. E. S. 204, October 1951, 35 pp. 
1726. Garner, W. R, Auditory signals, pp. 201-217 in; 
A survey report on human factors in undersea warfare. 
National research council, Washington, D. C., 1949, 541 
pp. 
1727. Hanley, T. D., G. L. Draegert, M. W. Buck, and 
J. C. Kelly. Effect of level of distracting noise upon speak- 
ing rate, duration, and intensity. Purdue University, La- 
fayette, Ind. SDC Human Engineering Project 20—K—l, 
Project NR-782-003, Rept. no. 104-2-14, 24 June 1949, 
16 pp. 
1728. Harris, J. D. Studies on pitch discrimination in 
masking. II. The effect of signal noise differential. U. S. 
Navy. Submarine base. New London, Conn. Medical re- 
search department. Project NM 003 002 (X-747 (Sub. 
No. 154)), Rept. no. 3, 30 January 1948, 7 pp. [P] 
1729. Harris, J. D, Some suggestions for speech recep- 
tion testing U. S. Navy. Submarine base. New London, 
Conn. Medical research laboratory. Project NM 003-021, 
Rept. no. 2, 21 July 1948, 23 pp. [P] 
1730. Harris, J. D. The effect of sensation-levels on in- 
tensive discrimination of noise. Amer. J. Psychol., 1950, 
63: 409-421. [P] 
1731. Harris, J. D. and C. K. Myers. Loudness percep- 
tion for pure tones and for speech. U. S. Navy. Submarine 
base, New London, Conn. Medical research laboratory. 
Project NM 003 041.21.05, Rept. no. 156, 20 September 
1950, 28 pp. [P] 
1732. Mason, H. M., I. P. Brackett, and C. H. Talley. 
Studies of voice factors affecting the intelligibility of voice 
communication in noise: II. Pitch. U. S. OSRD. O. S. 
R. D. Project no. 5413, Rept. no. 16,4 August 1945, 16 
PP- [P] 
1733. Miller, G. A. The masking of speech. Psychol. 
Bull., 1947, 44: 105-129. 
1734. Miller, G. A, Voice communications: effects of 
masking and distortion, pp. 243—248 in: A survey report 
on human factors in undersea warfare. National research 
council, Washington, D. G., 1949, 541 pp. 
1735. Miller, G. A., G. A. Heise, and W. Lichten. The 
intelligibility of speech as a function of the context of 
the test materials. Harvard University, Psycho-Acoustic 
laboratory, Contract N5ori-76, Project Order II 
PNR-74, September 1950, 14 pp. 
1736. Miller, G. A. and J. C. R. licklider. The intelli- 
bility of interrupted speech. /. acoust. Soc. Amer., 1950, 
22: 167-173. 
1737. Neff, W. D. Auditory discrimination in sonar 
operation, pp. 219-230 in: A survey report on human 
factors in undersea warfare. National research council. 
Washington, D. C., 1949, 541 pp. 
1738. Newman, E. B. The problem of voice communica- 
tion in extremely high ambient noise. Amer. psychologist., 
1946,7; 276. 
1739. Pollack, I. Effects of high pass and low pass 
filtering on the intelligibility of speech in noise. J. acoust. 
Soc. Amer., 1948, 20: 259-266. [P] 
1740. Pollack, I. The effect of white noise on the loud- 
ness of speech of assigned average level. /. acoust. Soc. 
Amer., 1949,27; 255-258. 
1741. Solandt, D. Y. and M. L. Bunker. Evaluation of 
auditory conditions in asdic cabins at sea. Canada NRG. 
Proceedings of third meeting of associate committee on 
naval medical research. Project C4074, 15 May 1944, 9 
PP- [P] 
1742. Steer, M. D., T. D. Hanley, G. L. Draegert, M. W, 
Buck, and J. C. Kelly. Effect of level of distracting noise 
upon speaking rate, duration, and intensity. Purdue Uni- 
versity, Lafayette, Ind., Voice science laboratory. SDC 
human engineering Project 20—K—l, Contract N6ori—104, 
T. O. II. Project designation NR-782-003, 24 June 1949, 
9 pp. [P] 
1743. Steer, M. D., J. S. Harris, G. L. Draegert, T. D. 
Hanley, and J, C. Kelly. Voice communication: effect of 
stress conditions on speaker intelligibility. Purdue Univer- 
sity, Lafayette, Ind., Voice science laboratory, Contract 
N6ori-I04, Project 20-K-l, Task Order No. 2, Rept. no. 
10 104-2—10, 17 September 1948, pp. 9. 
1744. Steer, M. D., J. S. Harris, G. L. Draegert, T. D. 
Hanley, and J. C. Kelly. Voice communication; effect of 
stress on talkers-—a personality study. Purdue University, 
Lafayette, Ind., Voice science laboratory, Contract 
N6ori—104, Project 20-K—l, Task Order No. 2, Rept. 
no. 11 104-2-11 NR-78-003, 22 October 1948, pp. 4. 
1745. Stuntz, S. E. Premodulation speech clipping and 
filtering: a consideration of their effects on the intelligi- 
bility of speech. U. S. Navy, Submarine base, New Lon- 
don, Conn. Medical research laboratory. Project NM 
003 041.21.04, Rept. no. 155, 14 August 1950, 8 pp. [P] 
1746. Tonndorf, J. Auditory perception in noise. J. 
Aviat. Med., 1951, 22: 491-500, 529. 
1747. Tonndorf, J. The relation of pure-tone threshold 
to speech perception in white noise. USAF. Randolph 
Field, Tex. School of aviation medicine. Project 21-27- 
001, Rept, no. 2, December 1951, 5 pp. 
7. PROTECTION AGAINST NOISE 
A large volume of literature has developed on 
the subject of ear defenders. Walpole {1764) 1943 
points out that the prime purpose of ear protective 
devices is to provide adequate insulation against 
high-level sound intensities so that the magnitude of 
the sound reaching the ear drums is reduced to 
noninjurious levels. Walpole described a plastic ear NOISE AND VIBRATION—PROTECTION AGAINST NOISE 
1748-1756 
defender (the acousti-guard) which consisted of a 
hollow disk within a plastic diaphragm. The sound 
enters a small hole in the outer surface of the disk, 
passes around the diaphragm, and out through a 
cylindrical hole, continuing through a fitting shaped 
to fit into the outer ear. A cloth pad is attached 
around the cylinder on the inner surface of the disk. 
This is provided to keep the device tight over the ear 
opening and thus minimize noise leakage. The de- 
vice was designed to provide protection at higher 
sound levels by the action of the diaphragm forced 
against the discharge port by the pressure of the 
sound wave. At lower sound levels the pressure 
exerted is insufficient to close the diaphragm, thus 
permitting sound to pass through the device without 
serious diminution. Tests permitted the conclusion 
that the valve-action idea is good, but that this 
specific device did not have a good enough seal. 
Everley and Emrich {1755) 1944 carried out tests 
for estimating the sizes of ear defenders of the V-51 
(R) type. These authors found that measurements 
of head circumference did not correlate significantly 
with ear-defender size. Articulation tests were con- 
ducted by Kryter {1756) in 1946 to determine the 
intelligibility of speech in the presence of noise when 
listeners wore earplugs (NDRC ear wardens). It 
was found that with a reverberating signal from a 
public-address system and in the presence of noise 
that raises the open-ear speech threshold by 60 deci- 
bels or more, the wearing of ear wardens increased 
the intelligibility of speech, but in direct person-to- 
person speech the ambient noise must be of sufficient 
intensity to raise the speech threshold by 80 decibels 
or more before ear wardens may be used without 
interfering with the reception of speech. Since, in 
some military and industrial situations, noise is gen- 
erated that raises the threshold for hearing speech 
by more than 80 decibels, the use of suitable earplugs 
under these conditions will maximize the reception 
of speech and afford protection against the deafen- 
ing, fatiguing, and annoyance effects commonly 
attributed to sustained, intense noise. In a study of 
the effectiveness of various types of ear defenders, 
Schneider {1760) 1950 found that only 2 percent 
of men equipped with ear defenders acquired tem- 
porary hearing loss, whereas in those ears protected 
only by cotton wool, the percentage of temporary 
hearing loss amounted to 17.3. Parrack and Eld- 
redge {1758) 1951 considered that while the V-51 
(R) ear defender is not perfect, it is the best all- 
round ear protector for most cases. Cotton wool 
impregnated with petrolatum and paraffin is a suit- 
able substitute when not contaminated by grimy 
hands. For further studies on earplugs, papers by 
the following should be consulted: Allen {1748) 
1942, Davis {1752) 1945, Dickson {1753) 1942, 
and Siirala {1762) 1949. 
Borshehevskii {1749) 1938 has described a special 
helmet designed to protect against noise. This “sub- 
helmet,” as it is called, consists of noise-resistant 
insulation layers, covered by soft rubber. The sub- 
helmet is described as easy to put on and does not 
interfere with the wearing of the flier’s uniform 
and does not exert undue pressure on the helix. 
Wearing of the helmet is said to prevent pain in the 
ear and there is no stuffy feeling in the ear which 
is frequently observed in fliers without such pro- 
tection. Several other advantages are described. 
In a survey of engine- and boiler-room noise on 
vessels of the Royal Canadian Navy, a recommen- 
dation is made by the Canadian National Research 
Council {1750) 1942 for the use of sound-absorbent 
material on the bulkheads. This is recommended 
in addition to properly fitted ear defenders. 
For further reports on protection against noise, 
papers by the following may be consulted; Coates 
{1751) 1931, Edwards {1754) 1948, MacFarlan 
{1757) 1941, Perwitzschky and Lanig {1759) 1936, 
Shambaugh {1761) 1943, Taylor {1763) 1947, 
Watson and Knudson {1765) 1944, and Witheridge 
(1766) 1948. A letter describing the combat against 
noise which appeared in the Journal of the Ameri- 
can Medical Association in 1929 {1767) may also 
be consulted. 
1748. Allen, S. C. Ear plugs for flying personnel. U. S. 
AAF. Wright-Patterson air force base, Dayton, Ohio. 
Materiel center, ENG. Serial no. ENG—M—49—695—23, 
22 December 1942, 4 pp. [P] 
1749. Borshehevskii, I. A. Shum v aviatsii i mery bor’by 
s nim. [The noise in aviation and methods for its control.] 
Vyestn. Oto-rino-laring., 1938, 2: 162—171. 
1750. Canada NBC. Survey of engine- and boiler-room 
noise on vessels of the Royal Canadian Navy. Proceedings 
of second meeting of subcommittee on naval medical 
research. Appendix S, 28 January 1942, 3 pp. [P] 
1751. Coates, G. M. The prevention of deafness. Ann. 
Otol., etc., St. Louis, 1931, 40: 651—660. 
1752. Davis, H. Protection of workers against noise. 
Trans, med. engr. Ind. Hyg. Found., 1945, Bull. 3: 5—7. 
1753. Dickson, E. D. D. Aviation noise deafness and 
its prevention. /. Laryng., 1942, 57: 8-10. [D] 
1754. Edwards, D. A. W. Observations on the design 
and development of ear defenders. Gt. Brit. FPRG. 
F. P. R. C. Kept. no. 700a, May 1948, 20 pp. 
1755. Everley, D. A. and E. G. Emrich. Tests for 
estimating the sizes of ear defenders of the V-51 (R) 
type—n. D. R. C. U. S. Navy. Submarine base, New 
London, Conn. Medical research laboratory. Project 
X-233 {Sub. no. 45), February 28, 1944, 7 pp. 
1756. Kryter, K. D. Effects of ear protective devices 
on the intelligibility of speech in noise. J. acoust. Soc. 
Amer. 1946, 18: 413-417. [P] 1757-1767 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
1757. MacFarlan, D. Prevention and treatment of 
acoustic trauma in war and civil life. Trans. Amer. otol. 
Soc., 1941, 31: 272-277. 
1758. Parrack, H. 0. and D. H. Eldredge. Noise prob- 
lems associated with aircraft maintenance. /. Aviat. Med., 
1951,22:470-476. 
1759. Perwitzschky, R. and D. I. Lanig. Gehorschutz 
fur Arbeiten in Larmbetrieben. Z. Hals-Nas.-u. Ohren- 
heilk., 1936,41: 178-186. [D] 
1760. Schneider, R. Ohrenarztliche Reihenuntersuch- 
ungen und Schallschutzversuche bei der Fliegerabwehr- 
Truppe. Vjschr. schweiz. SanitOff., 1950, 27; 165-178. 
[P] 
1761. Shambaugh, G. E., Jr. Prevention and treatment 
of acoustic trauma. /. Speech Dis., 1943, 8: 369-372. 
1762. Siirala, XT. Ett nytt horselskydd. [A new ear- 
guard] Nord. Med., Stockholm., 1949, 42: 1406-1407. 
1763. Taylor, H. M. Symposium on noise, (d) ear 
defenders. Laryngoscope, St. Louis, 1947, 57: 137-141. 
1764. Walpole, R. H. Test of acousti-guard (ear pro- 
tective device). U. S. Army, Fort Knox, Ky. Armored 
medical research laboratory. Project 12.741.7 GNOML, 
5 November 1943, 5 pp. [P] 
1765. Watson, N. A. and V. 0. Knudsen. Ear defenders. 
/. acoust. Soc. Amer., 1944, 15: 153—159. 
1766. Witheridge, W. N. Sound conditioning, pp. 
127-130 in: Industrial hygiene and toxicology. Edited by 
Frank A. Patty. New York, Interscience Publishers, Inc., 
1948, 531 pp. 
1767. Anon. Combat against noise. Foreign Letter. 
Berlin. /. Amer. med. Ass., 1929, 92: 2119. 
B. VIBRATION 
1. PHYSIOLOGICAL EFFECTS OF VIBRATION 
In an experimental study on human subjects of 
the physiological effects of mechanical vibration, 
Loeckle {1777) 1950 found that a rise in frequency 
of the vibratory stimulus was, in general, more dis- 
agreeable than an increase in amplitude. Subjective 
sensations were most impressive when the subject 
was seated and tense. The sensations are associated 
with uneasy, vegetative sensations, change in respir- 
atory rhythm, tension in the lower extremities, and 
pain in the head. The human organism can vibrate 
with a critical frequency below 10 cycles per second. 
Above 140 cycles per second damping by the body 
is complete. Damping is directly proportional to the 
quotient of body size to body weight. Damping is 
better when the subject is standing. Shaking vibra- 
tions are superimposed on respiratory movements, 
and shaking movements of the heart and stomach 
may be seen on the fluoroscopic screen. Maximum 
subjective comfort depends not upon critical fre- 
quency or damping effect but upon alternating 
acceleration of the skull. Impairment of visual 
acuity is directly associated with the transmission 
factor. Lines not parallel to the direction of vibra- 
tion appear vague, blurred, or broadened. Measure- 
ments of binocular vision showed that above 16 
cycles per second, the phenomenon has a constant 
relationship to amplitude transmitted to the skull. 
The patellar reflex and the Achilles reflex, as well 
as other proprioceptive reflexes, were inhibited. In 
experiments to explain this reflex behavior, it was 
found that the reflexes were changed only quanti- 
tatively and could be revived by various facili- 
tatory stimuli. Investigations an animals revealed 
no pathological changes in the spinal cord or brain. 
Efficiency tests on man before, during, and after 
vibrations showed some apathy, but little sensory 
effect. According to the author, injuries to health 
attributable to vibration have been demonstrated 
reliably, as yet only in men using pneumatic tools 
for extended periods; or workers on certain ham- 
mering machines in shoe factories. Generally speak- 
ing, men and animals are surprisingly resistant to 
vibration. For other general reports on the effects 
of vibratory motion on the human body, papers by 
Goldman {1774) 1948 and Reiher and Meister 
{1781) 1946 should be consulted. 
For studies on the absorption and propagation of 
vibratory energy by the body, papers by the follow- 
ing should be consulted: Franke, von Gierke, 
Oestreicher, Parrack, and von Wittern {1772) 1951; 
Francke, von Gierke, Oestreicher, and von Wittem 
{1780) 1950; and Ernsthausen {1771) 1950. Par- 
rack, von Gierke, Oestreicher, and von Wittem 
made measurements of the response of the body 
surface to mechanical vibrations in overlapping 
frequency ranges so as to span a total frequency 
range of 20 to 20,000 cycles per second. The results 
were consistent and described the mechanical im- 
pedance of the body surface and the elastic prop- 
erties of the tissue. The impedance consists of a 
frictional resistance and reactance. The resistance 
was found to be proportional to the square root of 
the frequency. The reactance is an elastance vary- 
ing inversely with the frequency up to about 50 
cycles per second, where it becomes zero. Above this 
frequency the reactance is proportional to the fre- 
quency throughout the measured range. The 
vibratory energy absorbed at the body surface and 
converted to heat in the tissue may be calculated 
from the impedance. From these results the authors 
developed a theory on the mechanical behavior of 
the vibrating body tissue that considered the tissue 
as an elastic medium with viscosity. 
For studies on the effects of vibration upon sense 
organs, papers by the following may be consulted: 
Mercier {1778) 1948, Temkin {1793) 1933, and 
Yamamoto {1796 and 1797) 1949. Experimental 
studies on the influence of vibration upon the 
auditory organ have been reported by Yamamoto 
1796 and 1797). This author applied a vibratory 
stimulus with a frequency of 40 cycles per second to VIBRATION—PHYSIOLOGICAL EFFECTS 
guinea pigs which were confined on the plate of a 
vibrator in free postures. The guinea pigs received 
2 or 4 hours of vibration a day for a total exposure 
of 10 to 160 hours in different groups of animals. 
As the vibrator produced a noise of 150 decibels, the 
author subjected another group of guinea pigs to 
the noise of the vibrator without the vibration. 
Rotary nystagmus was reduced for animals receiv- 
ing an exposure of 10 hours of vibration which also 
reduced the strength of auricular reflex. The effects 
were apparently due to vibration and not the noise. 
Histological examination of the auditory organ of 
the guinea pigs used in these experiments revealed 
atrophy of the organ of Corti, more marked in the 
upper than in the lower coils of the cochlea. There 
were few changes in the cochlear nerve and cells 
of the spiral ganglion. In the acoustic maculae there 
was reduction and disappearance of the otoliths, the 
otolith membrane, and the hair cells with disturbed 
arrangement of the epithelium. There was disturbed 
arrangement and impaired clearness of the boun- 
daries of the epithelial cells of the cristae acusticae, 
but little change in the nerve fibres. The effects of 
vibration were thus mainly on the maculae acous- 
ticae and the christae acousticae. Temkin {1793) 
1933, in a discussion of industrial deafness, at- 
tributed severe lesions to vibrations within the en- 
vironment rather than to the noise. He localized 
the apex of the hearing losses in the frequency of 
256 cycles per second. In a discussion of the in- 
fluence of vibration on vision, Mercier {1778) 1948 
described reduction of visual acuity attributed to 
exposures of long duration (more than 1 hour) to 
vibration. 
Investigations by Schaefer {1783) in the diesel- 
engine room of a submarine yielded vibrations of a 
frequency of 16 to 40 cycles per second. The ampli- 
tude of the vibration ranged between 0.05 and 0.3 
mm. The largest amplitude of vibration was on the 
platform next to the engines. A rubber mat reduced 
only the vibration amplitude. Electric-motor vibra- 
tions were not measurable. In subjects tested after 
duty in the engineroom, there was reduced perform- 
ance on attentiveness tests, and the skin over the 
ankle and knee joints revealed hypesthesia. There 
was no change in the patellar reflexes, but a de- 
creased accuracy in estimating weights. The studies 
revealed that, in the case of vibrations of 15 cycles, 
there is 90 percent transmission to the head. Hence 
aboard submarines a particularly unfavorable type 
of mechanical vibration occurs. 
For further studies on the effect of mechanical 
vibration on the patellar reflex, a paper by Goldman 
{1775) 1948 should be consulted. His observations 
on the effect of mechanical vibration on the patellar 
reflex of the cat confirmed those of previous investi- 
gators that vibration produces an inhibition. Fre- 
quencies of 10 to 600 cycles per second were used 
and decerebrate and lumbar-sympathectomized cats 
were subjected to the vibratory stimuli. The inhibi- 
tion of the patellar reflex was found to be inde- 
pendent of the autonomic nervous system and evi- 
dence was presented to support the concept that 
mechanical vibration acts by preempting the stretch 
reflex pathway. The inhibition was found to appear 
between 10 and 30 cycles, and to fade out between 
300 and 600 cycles per second. 
A number of reports have been given by Sueda on 
the effect of vibration upon body-weight, lifespan, 
and body temperature of experimental animals. In 
1937, Sueda {1787) subjected rabbits to vertical 
or up-and-down vibration and other animals to a 
side-to-side vibration simulating lurching move- 
ment. The vibrating speed was 140 cycles per min- 
ute. It was found that the vertical vibration caused 
relatively slight injuries. The bodyweight decreased 
rather slowly at first but, after a certain period, the 
weight loss was arrested despite continuance of the 
vibrations. The body weight thus lost was not recov- 
ered, however, even after a long rest. Some animals 
lived for a long period under these conditions. 
Those subjected to the lurching side-to-side motions 
died after 9 to 21 days (mean, 16.5). The rate at 
which the body weight declined was much more 
rapid than in the case of the animals shaken verti- 
cally. Just before death, the weight of the animals 
suffered an additional sudden decrease. The same 
author {1789) in 1938 reported that administra- 
tion of glucose to animals receiving continuous vi- 
bration enhanced the animals’ capacity to with- 
stand the harmful influences of vibration. If mice 
were subjected to alternate periods of vibration and 
rest of 12 hours’ duration, it was found that the body 
weight was only slightly decreased and that repose 
facilitated recovery. Lurching motion in rabbits 
produced a gradual decrease of about 30 percent 
in quantity of food intake, a gradual decrease of 
about 50 percent in urinary output, a decrease of 
about 65 percent in respiratory rate, and an increase 
of about 10 to 20 percent in pulse rate {1788). 
Sueda {1791) 1939 found that rabbits subjected to 
lurching vibrations for 24 hours continuously ex- 
hibited a rise of body temperature of about 0.2° C. 
during the shaking process. The temperature quickly 
fell about 0.3° C. after termination of the stimula- 
tion. The effect of vibrations upon the estrous cycle 
of white rats has been investigated by Sueda {1786) 
1937. Mature, female white rats were subjected to 
horizontal vibration of a frequency of 140 cycles a 1768-1785 
SPECIAL ANATOMY, PHYSIOLOGY, AND BIOCHEMISTRY 
minute and an amplitude of 4 cm. Animals shaken 
for a mean of 13.6 days suffered disturbances of the 
estrous cycle, but over half of them recovered rather 
quickly after the vibrations were stopped. Another 
group of animals shaken for a mean of 27.1 days 
exhibited a complete disruption of the cycle. After 
23 days of shaking the estrous cycle of 71.4 percent 
of the animals was still completely interrupted while 
the rest were recovering poorly. 
Schreiber {1784) 1950 subjected rats and mice to 
vibrations at a frequency of 160 cycles per minute 
and an amplitude of 4 cm. The concentration of 
ascorbic acid in the adrenal glands fell after shaking 
for one-half hour. In 2 hours, it fell to less than 
30 percent of the prestimulation value. The author 
reported a decrease in total lipoid concentration in 
the adrenal cortex and stated that after one-half- 
hour shaking, the total white blood count was 
significantly increased. After 4 hours, there was a 
decrease in white blood count as well as the absolute 
lymphocyte count. The number of polymorpho- 
nuclear neutrophile cells was relatively decreased 
after one-half hour of shaking with a significant rise 
after 4 hours. After 5 minutes of shaking there was 
a hypoglycemia* The liver glycogen content was 
reduced by 50 percent 1 hour after shaking. After 
4 hours there was still a reduction of liver glycogen. 
In chronic experiments, Schreiber {1785) 1950 
found a reduction of weight of the pituitary, thy- 
roid, and thymus glands. There was no change in 
the weight of the gonads or the adrenal glands. 
After shaking, there was a reduced tolerance to 
decompression hypoxia. 
Reference may be made to a report by Restarski 
{1782) 1945 on the effect of vibration upon the 
dental pulp and periosteum of white rats. In the 
author’s studies, the animals were exposed to vibra- 
tion at a frequency of 2,600 cycles per minute 8 
hours daily, 6 days per week for 28 days. This ex- 
posure did not affect the rate of growth of the 
incisor teeth or the calcification of the dentin. 
Histological examination of the dentin, pulp, alve- 
olar periosteum, alveolar bone, and the structures 
of the temporomandibular articulation failed to dis- 
close any greater variation of cellular changes than 
those occurring normally. 
For further studies of the physiological effects of 
vibration, papers by the following may be con- 
sulted: Bekesy {1768) 1940; Castellanos {1769) 
1948; Dalla Valle {1770) 1948; Grognot {1776) 
1947; Tadokoro, Saito, and Horie {1792) 1944; 
Tinker {1794) 1948; and Wulff, Fry, Tucker, Fry, 
and Melton {1795) 1951, 
1768. Bek6sy, 6. The neural terminations responding 
to stimulation of pressure and vibration. J. exp. Psychol., 
1940, 26: 514-519. [P] 
1769. Castellanos, F. J, Accion de las vibraciones sobre 
el organism©. Rev. san. aero., 1948, 1: 121-124. 
1770. Dalla Valle, J. M. Noise, vibration, and fatigue, 
pp. 68—79 in: The industrial environment and its control. 
New York, Pitman Publishing Corp., 1948, 225 pp. [D] 
1771. Ernsthausen, W. Sound and vibration in aircraft. 
The human body as a vibration receptor, pp. 669-685 in: 
German aviation medicine World War II. Vol. II. De- 
partment of the Air Force, Washington, D. C., 1950, 1302 
pp. [R] 
1772. Franke, E. K., H. E. von Gierke, H. L. 
Oestreicher, H. 0. Parrack, and W. W. von Wittern. 
Physics of vibrations in living tissues. USAF. Wright-Pat- 
terson air force base, Dayton, Ohio. Air materiel corn- 
man. Technical rept. no. 6367, February 1951, 28 pp. 
1773. Franke, E. K., H. E. von Gierke, H. I. 
Oestreicher, and W. W. von Wittern. The propagation 
of surface waves over the human body. USAF. Wright- 
Patterson air force base, Dayton, Ohio. Aero medical lab- 
oratory. Technical rept. no. 6464, June 1951, 13 pp. 
1774. Goldman, D. E. A review of subjective responses 
to vibratory motion of the human body in the frequency 
range 1 to 70 cycles per second. U. S. Navy. NMRI. Project 
NM 004 001, Rept. no. 1, 16 March 1948, 6 pp. [R] 
1775. Goldman, D. E. The effect of mechanical vibra- 
tion on the patellar reflex of the cat. U. S. Navy. NMRI. 
Project NM 004 001, Rept. no. 2, 17 March 1948. Amer. 
J. Physiol, 1948,155: 78-81. [P] 
1776. Grognot, P. Bruits et vibrations ressentis en avion. 
Med. aeronaut., 1947, 2: 327-341. [P] 
1777. Loeckle, W. E. The physiological effects of me- 
chanical vibration, pp. 716—722 in: German aviation 
medicine World War II, Vol. II. Department of the Air 
Force, Washington, D. G., 1950, 1302 pp. [R] 
1778. Mercier, A. L’influence des vibrations sur la 
vision. Med. aeronaut., 1948, 3: 154-162. [D] 
1779. Oestreicher, H. A theory of the propagation of 
mechanical vibrations in human and animal tissue. USAF. 
Wright-Patterson air force base, Dayton, Ohio. Air ma- 
teriel command. Technical Rept. no. 6244, November 
1950, 18 pp. [P] [M] 
1780. Parrack, H. 0., H. von Gierke, H, Oestreicher, 
and W. W. von Wittern. Absorption of vibratory energy 
by human body surface. Fed. Proc. Amer. Soc. exp. Biol, 
1950, 9: 97-98. 
1781. Reiher, H. and F. J. Meister. The sensitiveness 
of the human body to vibrations. U. S. AAF. Wright- 
Patterson air force base, Dayton, Ohio. Aero medical 
laboratory. Technical rept. no. TS 616 (Translated 
German document), 16 August 1946, 15 pp. [P] 
1782. Restarski, J. Effect of vibration upon the dental 
pulp and periosteum of white rats. /. dent. Res., 1945, 
24: 57-60. [P] 
1783. Schaefer, K. E. Technical influences. III. Vi- 
brations. pp. B: 1-51—B; 1-58 in: Monograph on sub- 
marine medicine, Folio I. Germany, U. S. Zone. Office 
of naval advisor. 1948. 
1784. Schreiber, V. Pusobeni otfesu na 
endocrinni system. Akutni nasledky otfesu. [The effect of 
mechanical shaking on the endocrine system. Immediate 
results of shaking.] Prakt. Lik., 1950, 2; 153-164. (English 
summary.) [P] 
1785. Schreiber, V. Pflsobenf otfesft na 
endokrinni system. Chronicke nasledky otfesfi a zmgny 1787-1799 
VIBRATION—EFFECTS ON PERFORMANCE 
zkfiiene resistence. [The effect of mechanical shaking on 
the endocrine system. Part II. End-result of shaking and 
changes of the crossed resistance.] Prakt. Lek., 1950, 2: 
210-215, (English summary.) [P] 
1786. Sueda, M, On the effect of vibrations upon the 
oestrous cycle of white rats. Mitt. med. Akad. Kioto, 1937, 
21: 1290. (English Abstr.) 
1787. Sueda, M. The influences of vibration. I. Report. 
The effect upon the body-weight and life period of animals. 
Mitt. med. Akad. Kioto, 1937, 21: 1703. (English Abstr.) 
1788. Sueda, M. The influences of vibration. II. Re- 
port. The effect upon the body temperature, quantity of 
food, quantity of urine, quantity of faeces, rates of respira- 
tion and pulse. Mitt. med. Akad. Kioto, 1938, 22: 391- 
392. (English Abstr.) 
1789. Sueda, M. Experimental study of the effect of 
some medicines upon the general conditions, body-weight 
and life period of animals subjected to continuous vibra- 
tions. II. Report. The effect of the injection of 1.6%, 
3.2%, and 5% glucose solution. Mitt. med. Akad. Kioto, 
1938, 22: 1335. (English Abstr.) 
1790. Sueda, M. Experimental study of the effect of 
alternate vibration and repose upon the body weight of 
animals. Mitt. med. Akad. Kioto, 1939, 25: 209-210. 
(English Abstr.) 
1791. Sueda, M. The body temperature of rabbits dur- 
ing and after vibration. Mitt. med. Akad. Kioto, 1939, 
25: 397. (English Abstr.) 
1792. Tadokoro, T., T. Saito, and Y. Horie. [The in- 
fluence of a long period of vibration upon glycosuria in 
rats.] Igaku & Seibutugaku, 1944, 6: 309—311. (English 
pagination.) (Japanese text.) [P] 
1793. Temkin, J. Die Schadigung des Ohres durch 
Larm und Erschiitterung. Mschr. Ohrenheilk., 1933, 67: 
257-299; 450-479; 705-736; 823-834. [P] [GH] 
1794. Tinker, M. A. Effect of vibration upon reading. 
Amer. J. Psychol, 1948, 61: 386-390. [P] 
1795. Wulff, V. J., W. J. Fry, D. Tucker, F. J. Fry, and 
C. Melton. Effects of ultrasonic vibrations on nerve tissues. 
Proc. Soc. exp. Biol, N. Y., 1951, 76: 361—366. 
1796. Yamamoto, K. Experimental studies on the in- 
fluence of vibration upon the auditory organ. (I) Influence 
of vibration of rotary nystagmus and Preyer’s auricular 
reflex. J. oto-rhinolaryng. Soc., Tokyo, 1949, 52 (7): 
(Japanese text pagination), 229-233. 
1797. Yamamoto, K. Experimental studies on the in- 
fluence of vibration upon the auditory organ. (II) The 
pathological and histological change of the auditory organ 
as influenced by the vibration. J. oto-rhinolaryng. Soc., 
Tokyo, 1949, 52 (7): (Japanese text pagination), 233- 
237. 
2. EFFECTS OF VIBRATION ON PERFORMANCE 
There is some suggestion in the literature (1798, 
1799) that vibration may result in impairment of 
performance and increase in fatigue. 
1798. Knudsen, V. 0. and I. H. Jones. The effect of 
audible and of subaudible vibrations on the acuity of 
hearing. Arch. Otolaryngol, 1929, 10: 472-479. 
1799. IT. S. Navy. Technical mission to Japan. Vibra- 
tion effects, pp. 9—10 in: Aero, surface, and submarine 
medicine and research in the Japanese Navy, Fascile M—l, 
Target M-06, 4 September 1945, 72 pp. Biology of Very High Hydrostatic 
Pressures 
In the first volume of this Sourcebook (pp. 85- 
89) there is to be found a discussion of the literature 
on the effects of raised hydrostatic pressures upon 
the activity of living cells and tissues as well as upon 
biochemical reactions. It is not intended in the 
present volume to cover this literature again since 
the subject lies at the fringe of interest in com- 
pressed air, diving, and submarine medicine. At- 
tention may be called, however, to three representa- 
tive reports. 
Boyd {1800) 1946 has investigated the effect of 
high hydrostatic pressures on hemagglutinating 
antibodies. It was found that pressures of the order 
of magnitude which have previously been found to 
coagulate proteins will destroy anti-A agglutinins 
investigated. Destruction was found to be complete 
at pressures above 4,000 atmospheres. A definitely 
higher pressure was required to destroy anti-Rh 
“blocking” antibody than was required for anti-Rh 
agglutinating antibody or anti-A or anti-B agglu- 
tinins. The author’s results seemed to indicate that 
the effect of high pressures on plasma proteins is 
not to break up the molecules but to induce 
polymerization. Johnson and Schlegel {1802) 1948 
found that high hydrostatic pressures up to 10,000 
lbs. per sq. in. have no appreciable effect on the 
hemoglobin-oxyhemoglobin equilibrium of 0.1 per- 
cent bovine hemoglobin in 0.8 percent sodium 
chloride solution. 
The effect of high pressures on the activation of 
chymotrypsinogen by trypsin has been studied by 
Curl and Jansen {1801) 1950 in connection with a 
general investigation of the effect of high pressures 
on enzymes; in particular, crystalline proteinases. 
Chymotrypsinogen was not activated by pressure 
in the absence of trypsin. No significant change in 
the extent of activation by trypsin was found under 
pressures up to 700 bars. About 10 percent less 
activation than in an unpressed system was observed 
under a pressure of 1,000 bars. The inhibition of the 
reaction increased with increase in pressure and 
practically no reaction occurred at 3,000 bars. Up to 
this pressure the activation proceeded after release 
of the pressure at practically the same rate as ini- 
tially in the control. Following release of systems 
at higher pressures than this, progressively less ac- 
tivity was obtained, until after pressing at 5,700 
bars on active enzymes was formed. The effect on 
the mixture of chymotrypsinogen and trypsin was 
much greater than on either protein alone. 
1800. Boyd, W. C. The effect of high pressures on he- 
magglutinating antibodies. /. exp. Med., 1946, 83: 
401-407. 
1801. Curl, A. L. and E. F. Jansen. Effect of high pres- 
sures on activity of proteinases. Fed. Proc. Amer. Soc. 
exp. Biol., 1950, 9: 165. 
1802. Johnson, F. H. and F. M. Schlegel. Hemoglobin 
oxygenation in relation to hydrostatic pressure. /. cell, 
comp. Physiol, 1948, 31: 421-425. [P] Diseases and Accidents in Submarine 
Personnel, Divers, and Compressed 
Air W orkers 
I. DISEASES AND ACCIDENTS IN NAVAL 
PERSONNEL: MORBIDITY 
Pugh {1809) 1950 has drawn attention to the 
fact that colds, constipation, and skin diseases con- 
stitute the principal disorders suffered by submarine 
personnel. At the time of departure on a patrol, a 
few members of the crew may have upper respir- 
atory infections. Infection is spread to others within 
48 hours, but by the end of a week or perhaps 
longer, the incidence of upper respiratory infections 
subsides. Colds remain infrequent for the remainder 
of the patrol and the incidence does not rise again 
normally until new contacts are made. Constipation 
is probably the result of lack of physical exercise, a 
diet of starchy foods, and natural reluctance to use 
the cold, clammy, cramped, wet watercloset. Heat 
rash and fungus growth present a problem in hot, 
humid atmospheres and bunk sharing helps spread 
these conditions. Venereal disease necessitates re- 
moval of personnel in peacetime. During wartime, 
when removal is not carried out, there is created 
a detriment to morale which taxes the ingenuity of 
the pharmacist’s mate. Vertical ladders, narrow 
passageways, and slippery decks are productive of 
falls, and operation of machinery may add to the 
incidence of injuries from other causes. Pugh refers 
also to hazards to personnel arising from the use 
of the snorkel. In some cases the change in atmos- 
pheric pressure produced by closing of the valve 
may cause ear pain and even some otological dam- 
age. In normal snorkeling operations, however, ex- 
perience has revealed that little or no discomfort is 
experienced. Hazards associated with escape from 
a disabled submarine are discussed. Escape may be 
attempted either by the submarine escape apparatus 
(the “lung”) or without apparatus (free escape). 
In the latter mode of escape, the escapee exhales 
during the entire ascent through the water. Failure 
to breathe out during the ascent may be followed by 
rupture of the alveoli, leading to air embolism with 
grave consequences. Pugh points out that World 
War II submarine experience indicated that it was 
unprofitable to keep submarines on patrol longer 
than 60 days. There seems to be a definite corre- 
lation between efficient endurance and the amount 
of time spent submerged. Either the fact of de- 
creased endurance must be accepted or personnel 
selection methods must produce persons of excep- 
tionally high endurance. The importance of sound 
selection techniques is stressed. 
Insight into the medical problems of submarine 
patrols is given by reports of the following authors; 
Duff {1803) 1947, {1804) 1949, Duff and Shilling 
{1805) 1949, and Shilling and Duff {1812 and 
1813) 1947. Duff {1803) has pointed out that only 
62 deaths occurred in submarine operations in 
World War II, exclusive of deaths in the case of 
52 overdue submarines. Twenty-six persons were 
lost by asphyxiation, 17 were drowned over side, 
12 were killed in battle, 3 were killed by accidents, 
1 committed suicide, 1 died of malignancy, 1 of 
pneumonia, and 1 died of unknown causes. Twenty- 
nine patrols returned because of illness. A large 
number of patrols returned because of excessive 
personnel fatigue, carbon monoxide poisoning, and 
battle casualties. Four patrols returned because of 
a limitation of potable water supply. Of injuries 
encountered in submarine patrols, poorly illumi- 
nated hatches accounting for many. The tempera- 
ture in the submarine sometimes rose to 125° F. 
in the maneuvering room during “silent” running. 
With a sea temperature of 27° F. the single hull 
portions of the boat could not be heated adequately. 
Ice formed in the bilges and in pipes containing 
water, such as the shower drains. Cold, rough 
weather, and seasickness reduced morale in some 
291222—54 11 DISEASES AND ACCIDENTS 
patrols as did lack of targets. Duff {1804) states 
that excessive fatigue limited the duration of 9 
patrols. Illness due to carbon monoxide poisoning 
limited the duration of 6 patrols. In 5 patrols, battle 
casualties caused the patrol to be curtailed, while 
in 2 patrols a case of acute appendicitis was the 
limiting factor. The following conditions limited 
the duration of 1 patrol each: multiple axphyxia- 
tion, serious injury, pneumonia, mumps, mental 
disease, copper sulfate poisoning, and unknown 
fever. Duff and Shilling {1805) reported disturb- 
ances of the digestive tract and urogenital system. 
The incidence of tuberculosis was low, being 0.43 
percent. Shilling and Duff {1812) points out that 
the pharmacist’s mate is medical officer, dentist, 
nurse, and chaplain all rolled in one. In 685 patrols 
studied by Shilling and Duff, some 1,208 injuries 
were considered sufficiently important to justify 
mention in the official patrol report. Injuries were 
listed in the following decreasing order of fre- 
quency: lacerations, contusions, sprains, abrasions, 
burns, shrapnel and gunshot wounds, fractures, and 
heat exhaustion. Many crew members sustained 
injury on the bridge watch where extremely rapid 
maneuvers were necessary to clear the bridge in 
seconds or where heavy seas flung the men against 
the steel surfaces. The routine of checking the tor- 
pedoes was also hazardous and resulted in 1 fatal 
intracranial injury. One hundred and ten subma- 
rines in 200 pickup operations recovered 542 avia- 
tors. Ten percent of these airmen were suffering 
from severe wounds and shock, but only 2 of the 
aviators died on board. 
Gastric and gastrointestinal disturbances and 
constipation are common in submarines, and oc- 
casional cases of acute appendicitis occur. These 
are a cause of anxiety to submariners. Diagnosis is 
difficult to make sometimes because of frequent 
gastrointestinal disturbances in submariners. Con- 
servative treatment is recommended. With con- 
servative treatment more cases will recover than if 
surgery is atttempted aboard the submarine. No 
food is to be given by mouth; fluid may be given by 
mouth or intravenously. Cathartics must never be 
administered. The patient is to have absolute bed 
rest, sedation to produce quiet sleep, and an icebag 
over the lower right quadrant of the abdomen. 
Antibiotics should be given in adequate doses. Dur- 
ing World War II pharmacist’s mates made the 
diagnosis of acute appendicitis in 127 instances on 
116 war patrols. There were no fatalities. In 11 cases 
the patrols were terminated and it was stated in 10 of 
these that the appendix would have ruptured if 
the submarine had not returned. The performance 
of three appendectomies aboard submarines has 
been reported. As previously stated, this procedure 
is contraindicated since it carries with it a higher 
mortality than conservative treatment under sub- 
marine operating conditions. 
The influence of weather, combat, and over- 
crowding on the rate of incapacitation from disease 
and accident aboard 9 ships of the line has been 
studied and reported by Morales and Tarver 
{1808) 1946. Most of the major types of vessels 
are represented in the study. With regard to 
respiratory diseases, cold weather increased the in- 
cidence, whereas neither overcrowding nor combat 
seemed to produce any observable effect on inci- 
dence. The incidence of gastrointestinal diseases 
was not affected by overcrowding or combat, but 
was somewhat more prevalent during steady hot 
weather. Skin diseases seemed to be more prevalent 
in hot weather, but were unaffected by overcrowd- 
ing or combat. The number of accidents was slightly 
higher during the months of steady hot weather, 
and was slightly higher during combat but was not 
affected by overcrowding. 
Schaefer {1810) 1948 has reported on health 
conditions in German submarines. It was stated 
that during the first few weeks of a cruise 68 per- 
cent of the men lost weight, even though on re- 
stricted activity. The men of the deck force showed 
the earliest loss of weight and later the engineering 
force. Three weeks were required for the diesel- and 
motor-room force to regain their weight. Members 
of the crew began to lose weight later than the of- 
ficers, and this was attributed to the greater psychic 
strain under which the latter were believed to be 
operating. Tonndorf {1814) 1948 reports that, in 
the first phase of World War II, radio operators per- 
formed medical services aboard German sub- 
marines. This was arranged so that they would be 
familiar with symptoms and terms when radioing 
for instructions for the care of the sick. The medical 
manual for submarines was considered insufficient 
because of lack of detailed instructions. Laymen 
performed such procedures as setting a broken 
bone, opening an abscessed gum, and amputating 
a foot. All were described as successful. Anesthesia 
was by morphine and oral administration of alco- 
hol. In 1942, a naval surgeon was attached to every 
submarine tender, 1 for every 10 submarines. Later 
on, medical assistants were trained to take over 
duties of the medical officers aboard submarines. 
These assistants began to man the submarines in 
1944. They were trained in naval hospitals and had 
2 months special training on submarine problems. 
Information on health conditions on Japanese sub- 
marines is given by Tonndorf {1814) and also in a 
U. S. Navy, ONI report {1816). It appears that EAR, NOSE AND THROAT—GENERAL STUDIES 
1803-1822 
there was a high incidence of pulmonary tubercu- 
losis among Japanese submariners. 
For further studies on special medical problems 
aboard submarines, papers by the following may be 
consulted: Ingraham and Wheeler {1806) 1943, 
Shilling and Kohl {1811) 1947, and U. S. Navy, 
BuNavPers {1815) 1949. 
1803. Duff, I. F. Medical aspects of submarine warfare 
in the human factor as reflected in war patrol reports, 
pp. 156-183 in; History of submarine medicine in World 
War II. Edited by Shilling, C. W., and J. W. Kohl. U. S. 
Navy. Submarine Base, New London, Conn. Medical 
research laboratory. 25 May 1947, 328 pp. 
1804. Duff, I. F. Medical aspects of submarine warfare. 
Arch, intern. Med., 1949, 84: 246-260. [R] 
1805. Duff, I. F. and C. W. Shilling. Medical care on 
wartime operating submarines. Nav. med. Bull., Wash., 
1949, 49: 580-591. 
1806. Ingraham, H. S. and S. M. Wheeler. Study of 
respiratory infections on submarines with special reference 
to the spread of infection through the air. U. S. Navy. 
NMRI. Project X-45 {Sub. no. 15), 25 February 1943, 
38 pp. 
1807. Knap, J. Laerebok i skipshygiene og skipsmedisin. 
Oslo, Johan Grundt Tanum, 1948, 327 pp. 
1808. Morales, M. and E. Tarver. The influence of 
weather, combat status, and overcrowding on the incidence 
of disease and accidents aboard naval vessels. U. S. Navy. 
NMRI. Research Project X—205, Report no. 5, 9 April 
1946, 18 pp. [R] 
1809. Pugh, L. Medical problems encountered in under- 
sea craft. J. Amer. med. Ass., 1950, 144: 230-233. [R] 
1810. Schaefer, K. E. Technical influences. IV—D. The 
process of adaptation to the entire environment of sub- 
marines. pp. B: 1-59—B: 1—79 in; Monograph on sub- 
marine medicine, Folio I. Germany, U. S. Zone. Office 
of naval advisor. 1948. 
1811. Shilling, C. W. and J. W. Kohl. Special care of 
submarine personnel, pp. 63-76 in; History of submarine 
medicine in World War II. U. S. Navy. Submarine Base, 
New London, Conn. Medical research laboratory, 25 May 
1947, 328 pp. 
1812. Shilling, C. W. and I. F. Duff. Analysis of patrol 
reports: surgical care on a wartime operating submarine, 
pp. 94-114 in: History of submarine medicine in World 
War II. Edited by Shilling, C. W., and J. W. Kohl. 
U. S. Navy. Submarine Base, New London, Conn. Medical 
research laboratory. 25 May 1947, 328 pp. 
1813. Shilling, C. W. and I. F. Duff. Medical care on 
wartime operating submarines, pp. 115-156 in: History 
of submarine medicine in World War II. Edited by 
Shilling, G. W., and J. W. Kohl. U. S. Navy. Submarine 
Base, New London, Conn. Medical research laboratory. 
25 May 1947, 328 pp. 
1814. Tonndorf, J. The medical service on the sub- 
marines. Germany, U. S. Zone, Office of naval advisor, 
pp. A: 1-9 in; Monograph on submarine medicine. Folio 
I, 1948. History of medical service of German armed 
forces. Edited by W. Kittel. U. S. Naval forces. Germany. 
Technical section (medical), 12 May 1948, 105 pp. 
1815. U. S, Navy. BuNavPers. (B) Medical problems in 
submarines, pp. 142-150 in: Submarine medicine practice. 
NavPers 10838, March 1949, 182 pp. 
1816. TJ. S. Navy, ONI. Germany, U-boat medical re- 
search. O. N. I. serial no. X-1250, 21 June 1945, 1 p. 
II. EAR, NOSE AND THROAT DISTURBANCES 
A. GENERAL STUDIES OF 0T0RHIN0IARYNG0L06- 
ICAL DISTURBANCES 
Sternstein {1826) 1946 has presented a descrip- 
tion of the common ear, nose, and throat conditions 
of clinical importance to the naval medical officer, 
not trained in the specialty, who may be assigned 
to independent duty. The paper discusses practical 
measures necessary for effective management of 
otorhinolaryngological disturbances. Consideration 
is given to otitis media among aviators, submariners, 
and divers. 
A paper by Tonndorf {1827) 1948 on the in- 
fluence of service on submarines on the auditory 
organ may be consulted. This paper discusses the 
effects of pressure variations within the submarine, 
particularly on snorkel operations in which tran- 
sient ear disturbances may occur. In some cases 
there is vascular injection of the tympanum after 
being at sea for many days. The phenomena are 
transient and cannot be demonstrated by audiom- 
eter tests after return to the base. In the author’s 
experience, the irritation of the tympanum dis- 
appeared after 3 to 4 weeks at sea. Gases of acute 
otitis media are described, including suppurative 
cases. German submarine trainees underwent tests 
in the diving tank. Only 1 percent of men under- 
going diving training suffered ear disorders. Four 
percent of the personnel complaining of the ear 
trouble during diving training had acute purulent 
otitis media. The author describes eczematous con- 
ditions of the external ear, furuncles, and other 
conditions. For other papers giving an introduction 
to the general subject of ear, nose, and throat dis- 
turbances, papers in the reference list given below 
should be consulted. 
1817. Eagle, W. W. Secretory otitis media. Ann. Otol., 
etc., St. Louis, 1946, 55; 55-67. Trans. Amer. Laryng. 
rhin. otol. Soc., 1946, 23-37. [GH] 
1818. Farrior, J. B. Lymphoid eustachian salpingitis: 
its effect on tubal patency. Arch. Otolaryng., Chicago, 
1948, 48: 221-232. [CH] 
1819. Hayashi, S. Statistic study of mastoid cell devel- 
opment in cases of chronic otitis media, as observed in 
X-ray pictures. /. oto-rhinolaryng. Soc., Tokyo, 1951, 54 
(6): (English text pagination), 28-29. 
1820. Hitschler, W. J. The relationship of swimming 
and diving to sinusitis and hearing loss. Laryngoscope, St. 
Louis, 1949, 59: 799-819. 
1821. Hoople, G. D. Otitis media with effusion—a chal- 
lenge to otolaryngology. Laryngoscope, St. Louis, 1950, 
60: 315-329. 
1822. Kurozumi, S. What influences on the hearing 
acuity were found when the pressure in the tympanic 1823-1827 
DISEASES AND ACCIDENTS 
cavity was changed experimentally? Nippon zibiinkoka 
gakkai kaiho, 1950, 53: (Japanese text pagination), 331— 
335; (English text pagination), 35-36. (In Japanese with 
English summary.) [P] 
1823. Lewis, R. S. Common accidents to the ears and 
their treatment. Med. Pr., 1948, 219: 579-582. 
1824. Ortiz, R. B. Barotrauma otico. Rev. Otorrinolar- 
ing., 1948, 8: 41-66. (English summary.) 
1825. Simpson, W. L. and J. E. Witcher. A study of 
the eustachian tubes and their orifices and lumens in 
patients with large operative defects giving direct visual- 
ization. Ann. Otol., etc., St. Louis, 1947, 56: 357-367. 
1826. Sternstein, H. J. Management of common eye, 
ear, nose, and throat conditions in naval practice. Nav. 
med. Bull., Wash., 1946,46: 1041-1052. 
1827. Tonndorf, J. The influence of service on sub- 
marines on the auditory organ, pp. D II-l—D 11-54 in: 
Monograph on submarine medicine. Germany, U. S. Zone. 
Office of naval advisor. 1948. [R] [CH] 
B. 0T0L0GICAL EFFECTS OF COMPRESSION AND 
DECOMPRESSION 
Two papers on the effects of pressure variations 
in snorkel operations upon the clearing of the mid- 
dle ear are cited. The first study, by Irvine {1833) 
1950, reports observations made during an Arctic 
snorkel cruise of H. M. submarine Ambush in 1948. 
During pressure changes, 17 out of 19 sleeping men 
were awakened. Seven of these had difficulty in 
clearing the ears and eight of the men showed in- 
jection of the tympanic membrane. One man had a 
bilateral serous effusion. In an experimental study 
on an anesthetized goat, it was found that under 
pressure the animal behaved in a manner similar 
to human beings. The animal was taken to an 
equivalent depth of about 30 feet of water. No 
change was noted in the mouth of the Eustachian 
tube under direct visualization at the onset of the 
pressure drop, but later the mouth of the Eustachian 
tube opened and the tube cleared, a stream of 
bubbles being seen to issue forth from the mouth of 
the tube. Once the tube had cleared, the mouth shut 
down and remained closed until the next clearing. 
The clearing of the tube occurred at a pressure 
difference about 1 to lbs. per sq. in. This was 
repeated at similar intervals until atmospheric 
pressure was again reached. No swallowing move- 
ments occurred while the pressure was decreasing. 
Uffenorde {1840) 1948 reported that otological 
examinations of men returning from snorkel opera- 
tions in German submarines revealed turbid tym- 
panic membranes which were highly retracted and 
not transparent. There was an increased vascular 
injection of the ear membranes, and sometimes cir- 
cumscribed hemorrhages were observed. Only one- 
fourth of all the eardrums inspected were normal. 
In one-third of the men, hearing impairments were 
proven by whispered voice and tuning-fork tests. 
Behnke {1828) 1945 has pointed out that, in de- 
compression, release of air from patent sinus and 
middle-ear cavities can take place almost instan- 
taneously without abnormal symptoms. Equalization 
of pressure between the middle ear and the external 
atmosphere is more difficult during compression. 
The nature of the valvular action of the Eustachian 
tube in relation to changes of atmospheric pressure 
has been investigated by McGibbon {1837) 1947. 
In these studies, passive opening of the Eustachian 
tube recurred on an average at each successive de- 
crement of extratympanic pressure corresponding 
to an ascent of 435 feet. Closure took place immedi- 
ately, leaving a residual intratympanic positive 
pressure of about 3.6 mm. Hg. Less than 3.6 mm. 
Hg pressure is insufficient to maintain passive 
patency of the tube. Schubert {1839) 1950, in a 
study of the resistance of the eardrum to high pres- 
sure, carried out experiments on cadavers in which 
23 normal tympanic membranes ruptured at a 
maximum pressure of 1,292 mm. Hg and at a 
minimum of 532 mm. Hg. In tympanic membranes 
presenting atrophic scars, the highest pressure for 
rupture was 380 mm. Hg, the lowest being 304 
mm. Hg. The maximum pressure to be safely en- 
dured by a normal tympanic membrane amounts to 
about 160 mm. Hg, according to the author. 
Three reports on pressure changes and baro- 
trauma in the middle ear of monkeys resulting from 
decompression and recompression have been given 
by Chang, Margaria, and Gelfan {1830, 1831) 
1949 and {1832) 1950. Pressure changes in the 
middle ear of 12 monkeys during decompression and 
recompression were measured directly by means of 
a membrane-mirror manometer and recorded. 
During a slow rate of decompression (50 mm. Hg 
per minute), the Eustachian tube opened periodi- 
cally to keep the tympanic pressure always close to 
the ambient pressure. A differential pressure of 
about 52 mm. Hg was required to open the 
Eustachian tube initially. Thereafter, the required 
pressure was less, apparently diminishing gradually 
toward the later stages of decompression. A decom- 
pression rate greater than 120 mm. Hg per minute 
resulted in a sustained patency of the Eustachian 
tube. At the instant of explosive decompression, the 
middle-ear pressure increased abruptly to a value 
which tended to approach the pressure difference 
between the pre- and post-explosive decompression 
altitudes and then to return quickly to ambient 
pressure. During recompression, anesthetized mon- 
keys were not able to equalize the tympanic and 
ambient pressures, and there developed in the mid- 
dle ear a negative pressure, the magnitude of which 
was determined by the range of recompression. EAR, NOSE AND THROAT—AEROTITIS MEDIA 
1828-1843 
Unanesthetized monkeys were able to accomplish 
pressure equalization by active opening of the 
Eustachian tube unless they were subjected to very 
fast recompression rates. The critical negative pres- 
sure for tympanic hemorrhage was about 300 mm. 
Hg. A negative pressure of 38 mm. Hg over a pro- 
longed time led to the same degree of damage as 
the higher negative pressure. 
For studies on the effects of barometric pressure 
changes on hearing, papers by the following may be 
consulted: Jones and Edmonds {1834) 1949; Kos 
{1835) 1945; Rasmussen {1838) 1946; Wever, 
Lawrence, and Smith {1841) 1948 and {1842) 
1949. For other studies on the effects of changing 
barometric pressure, the following references should 
be consulted: 1829, 1836, and 1843. 
1828. Behnke, A. R. Physiologic effect of pressure 
changes with reference to otolaryngology. Arch. Oto- 
laryng., Chicago, 1945, 42: 110-116. 
1829. Byrne, J. G. Studies on the physiology of the 
middle ear. H. K. Lewis & Co. Ltd., London. 1938, 298 pp. 
1830. Chang, H. T., R. Margaria, and S. Gelfan. Pres- 
sure changes and hemorrhage in the middle ear of monkeys 
resulting from decompression and recompression. Fed. 
Proc. Amer. Soc. exp. Biol., 1949, 8: 23. [P] 
1831. Chang, H. T., R. Margaria, and S. Gelfan. A 
quantitative study of pressure changes in the middle ear 
of monkeys and otitic barotrauma resulting from decom- 
pression and recompression. Yale aero-medical research 
unit, Yale University School of Medicine. Navy contract 
Task Order VIII, 16 April 1949, 33 pp. [P] 
1832. Chang, H. T., R. Margaria, and S. Gelfan. Pres- 
sure changes and barotrauma resulting from decompres- 
sion and recompression in the middle ear of monkeys. 
Arch. Otolaryng., Chicago, 1950, 51: 378-399. [P] 
1833. Irvine, G. S. Report of an investigation into the 
clearing of the eustachian tube in unconscious (anaes- 
thetised) goats. Gt. Brit. MRC-RNPRG, UPS. R. N. P. 
50/Sol, U. P. S. 112, February 1950, 5 pp. [P] 
1834. Jones, M. E. and F. C. Edmonds. Acoustic and 
vestibular barometery. Air pressure effects on hearing and 
equilibrium of unoperated and fenestrated ears. Ann. Otol., 
etc., St. Louis, 1949, 58: 323-344. [P] 
1835. Kos, C. M. Effect of barometric pressure changes 
on hearing. Arch. Otolaryng., Chicago, 1945, 41: 322-326. 
[R] 
1836. Lieherman, A. T. Aero-otitis media in pressure 
chamber “flights.” Arch. Otolaryng., Chicago, 1946, 43: 
500-507. 
1837. McGihhon, J. E. 6. The nature of the valvular 
action (passive opening) of the eustachian tube in rela- 
tion to changes of atmospheric pressure and to aviation 
pressure deafness, pp. 53-59 in: Contributions to aviation 
otolaryngology by E. D. D. Dickson. London, Headley 
Brothers, 1947, 257 pp. [R] 
1838. Rasmussen, H. Studies on the effect upon the 
hearing through air conduction brought about by varia- 
tions of the pressure in the auditory meatus. Acta oto- 
laryng., Stockh., 1946, 34: 415-424. [P] 
1839. Schubert, H. Uber die Widerstandsfahigkeit des 
Trommelfells gegen Uberdruck der Aussenluft. Z. Hals- 
Nas.-u. Ohrenheilk., 1949, 1: 357-358. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1950, 3: 945. 
1840. Uffenorde, H. Otological experience with 
“Schnorchel” equipped submarine. D III-l—D III-41 
in: Monograph on submarine medicine Folio VII. 
Germany, U. S. Zone. Office of naval advisor. 1948 [P] 
[CH] [R] 
1841. Wever, E. G., M. Lawrence, and K. R. Smith. 
The middle ear in sound conduction. Arch. Otolaryng., 
Chicago, 1948, 48: 19-35. [P] 
1842. Wever, E. G., M. Lawrence, and K. R. Smith. 
The effects of negative air pressure in the middle ear. 
Ann. Otol., etc., St. Louis, 1949, 57: 418-428. [P] 
1843. Anon. Effect of changing barometric pressure. 
Flight Surgeon’s Reference File. U. S. AAF. Randolph 
Field, Tex. School of aviation medicine. AAF Manual 
25-0-1, 8-3-1 /8-3-6, 1 November 1945. 
C. AEROTITIS MEDIA AND AEROSINUSITIS 
Barometric pressure changes occurring in diving 
and also in snorkel operations may be of sufficient 
magnitude to cause inflammation of the middle 
ear and sinuses. These effects on the middle ear 
and sinuses may range from minor hyperemia to 
serious pathological changes with effusion, hemor- 
rhage, suppuration, and rupture of the eardrum. 
There is an extensive amount of literature on 
aerotitis media and aerosinusitis, and a rather wide 
selection from this literature has been included in 
the reference list given below. In the U. S. sub- 
marine service, investigations of aerotitis media 
have been principally carried out in connection with 
the selection and indoctrination program at the 
escape training tank, U. S. Submarine Base, New 
London, Conn., and the diving schools. 
In 1944, Shilling {1876) presented a report on 
aerotitis media and auditory acuity loss in submarine 
escape training. This paper presents an analysis of 
the extent of the damage associated with sub- 
marine escape training and outlines possible pre- 
ventive and therapeutic procedures. Thirty percent 
of the men undergoing escape training at New Lon- 
don were found to have difficulty leading to aerotitis 
media and resultant loss of auditory acuity. Of the 
152 cases diagnosed as aerotitis media in the series 
under consideration, 18 of the more severe cases 
showed an average drop in acuity of 12.7 to 23.9 
decibels as compared with a control group. By 
otoscopy and nasopharyngoscopy, it was possible 
to predict with fair accuracy which ear would 
suffer damage during the 50 lbs. pressure test. By 
means of a thorough preselection examination com- 
bined with a routine check on the ability of each 
subject to perform the Valsalva maneuver, a group 
could be selected in which otopathology could be 
reduced to 2 to 3 percent of the cases instead of 
the 27.5 to 30 percent found in 2 separate groups 
of 858 and 708 men. It was found that for low 1844-1850 
DISEASES AND ACCIDENTS 
tones the ears were relatively unaffected, but, for 
tones of 2,046 and above, a loss of acuity was the 
rule for ears affected by pressure. In some cases 
permanent damage may result. However, in some 
ears with considerable otopathology, the losses in 
acuity may be slight. In all the cases with severe 
damage to the ears, the author noted flattening 
of the Eustachian-tube orifices caused by lymphoid 
hyperplasia. It was thus predicted that X-ray or 
radium treatment of the Eustachian orifice should 
be of benefit. It was stated that, with more careful 
preselection of candidates and proper administra- 
tion of pressure, severe otopathology with associated 
hearing loss need not be as common as formerly. 
Shilling, Haines, Harris, and Kelly {1877) 1947 
stated that the effect on auditory acuity was actu- 
ally less than might have been anticipated and very 
severe loss in hearing acuity was associated only 
with maximum damage to the drum and with 
effusion into the middle ear. 
A report by Haines and Harris {1861) 1947 is 
based on a study of 6,149 submariners examined by 
means of the otoscope, the nasopharyngoscope, and 
the audiometer before and after they were given 
the 50 lbs. pressure test at the escape training tank. 
Five experimental groups were given different types 
of treatment; (1) psychological treatment, (2) 
topical treatment, (3) X-ray treatment, (4) radium 
treatment, and (5) treatment of dental malocclu- 
sion. Only slightly beneficial effects resulted from 
tropical treatment consisting of 5 drops of 0.25 
percent neosynephrine in an isotonic solution ap- 
plied to the nasopharynx every 2 hours or several 
hours before the pressure test. The results of X-ray 
therapy to the Eustachian tube were inconclusive. 
The radiumtherapy consisted in the application for 
8 to 10 minutes to the nasopharyngeal orifice of the 
Eustachian tube a small metal cylinder containing 
50 mg. of radium salt. This dose after two to eight 
applications at intervals of a month was found ef- 
fective in reducing the amount of lymphoid tissue 
around the opening of the Eustachian tube. Ninety 
percent of the patients thus treated became able to 
sustain pressure without developing aerotitis media. 
Dental therapy was investigated in cases in which 
improper jaw motion was suspected of hindering 
normal opening and closing of the Eustachian tube. 
Striking success was reported for this procedure. 
For another report on aerotitis media based on 
experience at the U. S. Submarine Base, New 
London, Conn,, a paper by Teed {1879) 1949 may 
be consulted. A case history is given in detail and 
the author describes four grades of severity of the 
condition. He prefers the term “salpingotympanitis” 
rather than “aerotitis media” in that the former 
term emphasizes the important role of the Eusta- 
chian tube in the evolution of the disease. In grade 
I, blood vessels expand, congestion is noted, and 
the eardrum is retracted. If the subject is removed 
from pressure at this stage, congestion and pain 
disappear. A vasoconstrictor drug helps to relieve 
pain. In grade II, the eardrum is retracted and red 
in all quadrants, and the patient complains of 
severe otalgia and loss of hearing. Catheterization 
of the Eustachian tube may correct retraction of the 
drum, but will not reduce inflammation or pain. It 
is evident that the blood vessels in this grade have 
expanded beyond the limit of nervous control and 
are temporarily paralyzed. Time only will bring 
about return of adequate vascular function. The 
author recommends sedation and bed rest. In grade 
III, there is transudation of serum and the 
tympanum may be completely filled with fluid caus- 
ing the eardrum to have a yellow appearance. De- 
crease in expansion of the blood vessels in this 
grade may be due to a splinting action of the fluid 
or to tissue edema. Treatment consists of daily 
shrinkage of the tubal mucosa and inflation of the 
Eustachian tubes. If fluid is not absorbed within a 
week, myringotomy, followed by suction, is indi- 
cated. About 0.5 percent of men passing through 
the training tank at New London developed so- 
called grade IV salpingotympanitis characterized by 
hemorrhage into the middle ear and/or perforation 
of the eardrum. The entire middle ear may be filled 
with blood and the eardrum appear black. Dissect- 
ing hemorrhages may occur in the eardrum with 
rupture into the external canal. 
1844. Aschan, G. K. Aero-otitis media and aerosinusitis. 
Acta otolaryng., Stockh., Suppl., 1946, 69: 1-116. [P] 
1845. Ballenger, W. L., H. C. Ballenger, and J. J. Bal- 
lenger. Injuries and diseases of the tympanic membrane, 
pp. 637-641 in: Diseases of the nose, throat and ear. 
Philadelphia, Lea & Febiger, 1947, 993 pp. 
1846. Ballenger, W. L., H. C. Ballenger, and J. J. Bal- 
lenger. Diseases of the Eustachian tubes, pp. 642-651 in: 
Diseases of the nose, throat and ear. Philadelphia, Lea 
& Febiger, 1947, 993 pp. 
1847. Bateman, G. H. The effect of sinusitis on flying 
personnel, pp. 162-172 in: Contributions to aviation 
otolaryngology. By E. D. D. Dickson. London, Headley 
Brothers, 1947, 257 pp. 
1848. Bierman, H. R. and I. W. Brickman. The rela- 
tionship of dental malocclusion to vacuum-otitis media 
and the use of dental splints during descent from altitudes. 
Ann. Otol., etc., St. Louis, 1946, 55: 5-12. [P] 
1849. Boies, L. R. Acute otitis media, pp. 61-69 in; 
Fundamentals of Otolaryngology. Philadelphia, W. B. 
Saunders Company, 1949, 443 pp. 
1850. Caneghem, ( ) van. La pathogenese des devia- 
tions successives de la tete au cours des otites aigiies. 
Acta oto-rhino-iaryng., Belg., 1947, 1: 270-274. [D] EAR, NOSE AND THROAT—OTITIS MEDIA 
1851-1886 
1851. Carruthers, D. G. Diseases of the middle ear. pp. 
201-210 in: Diseases of the ear, nose, and throat. Balti- 
more, The Williams & Wilkins Co., 1948, 344 pp. 
1852. Carruthers, D. 6. The complications of suppura- 
tive otitis media, pp. 211—288 in: Diseases of the ear, nose, 
and throat. Baltimore, The Williams & Wilkins Co., 1948, 
344 pp. 
1853. Chester, L. and J. C. Drooker. Aero-otitis media 
and aero-sinusitis. Laryngoscope, St. Louis, 1943, 53: 
203-209.[R] 
1854. Coronel, M. C, Las otitis medias. Sanid. mil., 
1949, 2: 229-235.[D] 
1855. Crowe, S. J. and E. W. Hagens. Otis media with 
effusion—challenge to otolaryngology, pp. 273-274 in; 
The 1950 yearbook of the eye, ear, nose, and throat. 
Chicago, The Year Book Publishers, Inc., 1951, 446 pp. 
[R] 
1856. Dickinson, R. J. and C. A. Voelker. Aerosinusitus 
with hematoma. U. S. Air Surg. Bull., 1945, 2; 444. [CH] 
1857. Dickson, E. D. D., J. E. G. McGibbon, and A. C. P. 
Campbell. Acute otitic barotrauma—clinical findings, 
mechanism and relationship to the pathological changes 
produced experimentally in the middle ears of cats by 
variations of pressure, pp. 60-83 in: Contributions to avia- 
tion otolaryngology. By E. D. D. Dickson. London, 
Headley Brothers, 1947, 257 pp. [R] [P] 
1858. Dysart, B. R. Otitis media and complications. 
Arch. Otolaryng., Chicago, 1950, 51: 106-123. [R] 
1859. Eggston, A. A. and D. Wolff. Inflammation of 
the middle ear (otitis media), pp. 333-353 in: Histo- 
pathology of the ear, nose, and throat. Baltimore, The 
Williams & Wilkins Co., 1947, viii, 1080 pp. 
1860. Gt. Brit. FPRC. Head measurements in cases of 
recurrent otitic baratrauma. F. P. R. C. Rept. no. 608, 
6 February 1945,4 pp. [P] 
1861. Haines, H. L, and J. D, Harris. Aerotitis media 
in submariners. /. industr. Hyg., 1947, 29: abstract sec- 
tion: 40. Ann. Otol., etc., St. Louis, 1946, 55: 347—371. 
[P] 
1862. Harvey, W. Investigation and survey of malocclu- 
sion and ear symptoms, with particular reference to otitic 
barotrauma (pain in ears due to change in altitude). 
Brit. dent. J., 1948,85: 219-225. [P] 
1863. Hoilien, M. J. An improvement in technique of 
the Proetz method of treating paranasal sinusitis. J. Aviat. 
Med., 1945,16: 358-359. 
1864. Hollender, A. R. Purulent otitis media, pp. 513- 
534. in; Office treatment of the nose, throat, and ear. 
Chicago, The Year Book Publishers, Inc., 1950, 620 pp. 
[R] 
1865. Jordan, R. Chronic secretory otitis media. Laryn- 
goscope,St. Louis, 1949,59: 1002—1015. 
1866. Kerekes, G. Y. Oto-rhinologiai tapasztalatok a 
Caisson-betegsegnel. [Oto-rhinological experiences in 
caisson disease.] Oto-rhino-laryng. Danub., 1948, 1: 181. 
Abstr. [CH] [R] 
1867. Lentine, J. A review of one hundred cases of 
acute aero-otitis. Arch. Otolaryng., Chicago, 1946, 43: 
293-297. 
1868. Lieberman, A. T. Aero-otitis media in pressure 
chamber “flights”. Arch. Otolaryng., Chicago, 1946, 43: 
500-508. [P] 
1869. McGuckin, F. Chronic otitis media. /. Laryng., 
1949, 63: 328-336. 
1870. Morrison, W. W. Acute inflammation of the tym- 
panic cavity and mastoid cells, pp. 107—134 in: Diseases 
of the ear, nose, and throat. New York, Appleton-Century- 
Crofts, Inc., 1948, 772 pp. 
1871. Nielsen, J. C. Studies of the aetiology of acute 
otitis media. Copenhagen, Ejnar Munksgaard, 1945, 191 
pp. [P, R] 
1872. Ogden, F. W. A study of altitude chamber aero- 
otitis media. U. S. AAF. Randolph Field, Tex. School of 
aviation medicine. Project 147, Kept. no. 1, 5 May 1943, 
6 pp. 
1873. Ogden, F. W. Tubal resistance and aero-otitis 
media. U. S. AAF. Randolph Field, Tex. School of aviation 
medicine. Project 268, Kept. no. 1, 24 June 1944, 4 pp. 
[P] 
1874. Patton, R. A. Purulent otitis media in albino rats 
susceptible to sound-induced seizures. /. Psychol., 1947, 
24: 313-317. 
1875. Samwatari, Z. [Otitis media.] Nippon rinsyo, 
1948,6; 127-130. (English pagination.) 
1876. Shilling, C. W. Aero-otitis media and auditory 
acuity loss in submarine escape training. U. S. Navy. Sub- 
marine base. New London, Conn. Medical research de- 
partment. Project X-434 {Sub. no. 90), Kept. no. 1, 
8 October 1944,8 pp. [CH] 
1877. Shilling, C. W., H, L. Haines, J. D. Harris, and 
W. J. Kelly. Aerotitis media. A brief presentation of its 
symptomatology, prevention and treatment. J. Aviat. Med., 
1947, 18: 48-55. 
1878. Tauride, D. Sumbole eis ten meses aerotitos 
{Spoude tesnosou epi toon hellenoon Iptamenoon). [Con- 
tribution to the study of aero-otitis media. A study of the 
disease among flying personnel of the Royal Hellenic Air 
Force.] Thesis (Medecine), Athens, 1950, 105 pp. 
1879. Teed, R. W. A contribution of war experience to 
the etiology of otitis media. Trans. Amer. Acad. Ophthal. 
Oto-laryng., 1949, 53: 254-260. [R] 
1880. Tobey, H. G. Acute catarrhal otitis media with 
effusion. Trans. Amer. otol. Soc., 1948, 36: 51-71. 
1881. Anon. Diver’s ear (otitic barotrauma). Roy. Nav. 
med. Bull., 1943,5; 13-14. 
1882. Anon. Barotrauma. Roy. Nav. med. Bull., 1946, 
22: 53-57. [R] 
D. OTITIS MEDIA THERAPY 
1. GENERAL CONSIDERATIONS 
The following references are included as introduc- 
tory source material of particular interest to the 
general reader and to those desiring brief reports 
on therapy of acute otitis media. 
1883. Fox, S. A. The management of the acute ear. 
Laryngoscope, St. Louis, 1946, 56: 312-319. 
1884. Pompe, J. Otitis media acuta in njegova terapija. 
[Acute otitis media and its therapy.] Med. Glasn., 1949, 3: 
102-107. 
1885. Singleton, J. D. Acute otitis media; its manage- 
ment by the general practitioner and pediatrician. J. Okla. 
med. Ass., 1946, 39: 325-328. 
1886. Trapasso, T. J. Aerotitis program in the Fifteenth 
Air Force. Ann. Otol., etc., St. Louis, 1945, 54: 716-721. 
2. USE OF VASOCONSTRICTOR AND ANALGESIC 
DRUGS 
Ogden (1887) 1943 reported that the use of 
various vasoconstrictor sprays just prior to simu- 
lated flights in an altitude chamber did not reduce 1887-1920 
DISEASES AND ACCIDENTS 
the occurrence of aerotitis media to a degree con- 
sidered statistically significant. However, in the 
group of subjects who had received tuamine (2- 
amino heptane sulphate) as a nasal spray, the total 
incidence of aerotitis media was definitely reduced. 
Reid {1888) 1946 has used ephedrine solutions in- 
stilled into the ear in the treatment of acute otitis 
media with advantage in early cases. Unger {1889) 
1947 has described a process of cocainization of the 
tympanum via the Eustachian tube. 
1887. Ogden, F. W. A study of the effects of vaso- 
constrictor solutions on altitude chamber aero-otitis 
media. U. S. NRG-CAM. C. A. M. rept. no. 170, 1 June 
1943, 8 pp. [P] 
1888. Reid, W. 0. Treatment of acute otitis media by 
decongestion. Brit. med. ]., 1946, 1: 648-649. [P] 
1889. Unger, M. Cocainizing the tympanum via the 
eustachian tube. A new method. Arch. Otolaryng., Chi- 
cago, 1947, 45: 693-696. 
3. CHEMOTHERAPY 
None of the references given below refers to 
aerotitis media incurred in military situations in- 
volving pressure changes. Most of them refer to 
acute or chronic otitis media with bacterial infection 
in which antibiotic treatment is indicated. These 
references are included because aerotitis media may 
be complicated by infection with suppuration, and 
in such cases or if such a condition is feared, 
recourse to antibiotics is indicated. 
1890. Baba, S. Fundamental studies on the penicillin 
treatment of otitis media. /. oto-rhinolaryng. Soc., Tokyo, 
1951, 54 {11): (English text pagination), 53-54. 
1891. Bateman, G. H. The place of chemotherapy and 
penicillin in the treatment of acute otitis media. Irish J. 
med. Sci., 1947, 6th Series, 457-464. 
1892. Belfort, F. Nova tecnica de tratamento de otites 
m6dias agudas por meio de antibioticos. Med. cir. pharm., 
1950, 96-98. 
1893. Crowe, S. J., W. E. loch, and E. N. Broyles. 
Diseases of the ear, nose, and throat. Ann. rev. Med., 
1950, 1: 339-354. [R] 
1894. Evans, M. 6. The treatment of acute suppurative 
otitis media. The relative merits of chemotherapy and 
myringotomy in avoiding surgical mastoiditis. Ann. Otol. 
etc. St. Louis, 1951, 60: 638-647. 
1895. H6troy, M. Les sulfamides dans les otites aigiies 
et subaigiies. Concours med., 1946, 68: 505. [D] 
1896. House, H. P. Otitis media. A comparative study 
of the results obtained in therapy before and after the 
introduction of the sulfanomide compounds. Arch. Oto- 
laryng., Chicago, 1946, 43: 371-378. 
1897. Jezek, K. Ambulantni leeba akutnich otitid peni- 
cilinem. Gas Lek. ces., 1951, 90: 1128-1132. [D] 
1898. Karatay, S. Treatment of otitis media and 
sinusitis with penicillin. Arch. Otolaryng., Chicago, 1947, 
45: 288-293. 
1899. Kucera, M. Penicilin u akutnich zangtft stfed- 
ousnich. [Penicillin and acute otitis media.] Prakt. Lek., 
Praha, 1948, 28: 208-209. 
1900. Landgren, N. Penicillinterapi vid akuta otiter. 
Nord. Med. Stockholm, 1949, 42: 1401-1403. [CH] 
1901. Monteiro, A. Sulfas e penicilina no tratamento 
das otites medias agudas e suas complicaqoes. Estudo com- 
parative. Hospital, 1949, 36: 23-53. 
1902. Nielsen, J. C. Effect of dipencillin administered 
once daily on acute otitis media, with particular reference 
to the bacteriology. Acta oto-laryng., 1951, 39: 222-237. 
[CH] 
1903. Ohsawa, R., and M. Kamata. A new form of 
chemotherapy in treatment of otitis media purulenta 
chronica. /. oto-rhinolaryng. Soc., Tokyo, 1950, 53 (8): 
(Japanese text pagination), 265-267. (English text pagi- 
nation), 28—29. 
1904. Piquet, J. La sulfamidotherapie dans les otites 
aigiies d’apres les publications des auteurs nordiques. Ann. 
Oto-laryng., 1946, 13: 344-347. [D] 
1905. Rajner, V. Pfispevek k leebe akutnich otitid 
penicinilem. Gas Lek. hes., 1951, 90: 1124-1128. [CH] 
1906. Ramadier, J. A. A propos d’une serie de deboires 
avec la sulfamido-penicillo therapie dans le traitement 
des otites aigiies. Sem. Hop., Paris, 1947, 23: 2579-2583. 
[CH] 
1907. Reimann, H. A. Acute otitis media, pp. 1-293— 
1—294 in; Treatment in general medicine. Volume I. 
Fourth edition. Philadelphia, F. A. Davis Co., 1948, 780 
pp. 
1908. Riskaer, N. Penicillin treatment of simple acute 
otitis media. Acta oto-laryng., Stockh., 1949, 37: 230-238. 
1909. Rodel, A. Zur Behandlung der akuten Mittelohr- 
entziindungen mit Sulfonamiden. Tract, oto-rhino-laryng., 
1946, 8: 499-504. [CH] 
1910. Royal Society of Medicine, Section of otology. 
Society proceedings, 5 December 1947. Discussion on 
penicillin treatment in acute otitis media. J. Laryng., 1948, 
62: 608-612. 
1911. Salinger, A. Antibiotics in ear, nose, and throat. 
Wis. med. J., 1948, 47: 997-998. 
1912. Simpson, J. F. Otorhinolaryngology, pp. 317—331 
in: Penicillin. Its practical application. Edited by A. Flem- 
ing. London, Butterworth & Co., Ltd., 1950, 454 pp. 
1913. Sobieski, J. Penicillinotherapie locale des otites 
moyennes aigiies. Concours med., 1949, 71: 1193—1194. 
[CH] 
1914. Tobey, H. 6. The sulfonamide drugs in the treat- 
ment of acute otitis media. Ann. Otol., etc., St. Louis, 
1942, 51: 945-954. 
1915. Vicencio, A. B. Treatment of chronic otitis media 
with a mixture of glycerite of hydrogen peroxide, strep- 
tomycin and penicillin. Arch. Otolaryng., Chicago, 1951, 
53: 87-88. 
1916. Volkmar, E. Soli man bei der akuten otitis media 
Sulfonamide verordnen? Med. Klinik., 1943, 43: 390- 
391. [D] 
1917. Weiss, J. A. Transtubal instillation of penicillin 
in acute otitis media. Arch. Otolaryng., Chicago, 1946, 
43: 17-18. 
1918. Wilcox, J, G. Penicillin treatment of acute middle 
ear and mastoid infections. Penn. med. J., 1947, 50: 574— 
577. [CH] 
1919. Wilson, C. P. Report of 110 cases of acute in- 
fection of the ear treated with penicillin. J. Laryng., 1946, 
61: 404-410. 
1920. Young, A. and I. S, Hall. Penicillin treatment 
in acute suppurative otitis media with special reference 
to long-term hearing. /. Laryng., 1948, 62: 551-556. [CH] EAR, NOSE AND THROAT—OTITIS MEDIA 
1921-1931 
4. IRRADIATION THERAPY 
1922. Dickson, E. D. D. and J, E. G. McGibbon. The 
treatment of recurrent otitic barotrauma by irradiation 
(with special reference to lymphoid tissue in the sub- 
mucosa of the eustachian tube). /. Laryng., 1949, 63: 
647-671. 
1923. Fowler, E. P,, Jr. Irradiation of the Eustachian 
tube. Arch. Otolaryng., Chicago, 1946, 43: 1—11. 
1924. Glauber, J. J., J. W. Smith, and D. H. Earl. 
Report of the Third Air Force irradiation unit, 31 August 
1945. Ann. Otol., etc., St. Louis, 1945, 54: 686-693. 
1925. Hendricks, J. E. and A. T. Lieberman. Activities 
of the irradiation clinic at Westover Field, Massachusetts. 
Ann. Otol., etc., St. Louis, 1945, 54: 662-683. 
1926. Mikell, J. S. The use of radium in the aerotitis 
control program in the Twelfth Air Force. Ann. Otol., 
etc., St. Louis, 1945,54: 708—715. 
1927. Northington, P. Radium therapy in aerotitis 
media. Nav. med. Bull., Wash., 1946, 46: 1559-1567. [M] 
1928. Proctor, D. F. Irradiation for the elimination of 
nasopharyngeal lymphoid tissue. Arch. Otolaryng., Chi- 
cago, 1946, 43: 473-480. 
1929. Shilling, C. W., H. L. Haines, J. D. Harris, and 
W. J. Kelley. The prevention and treatment of aerotitis 
media. Nav. med. Bull., Wash., 1946, 46: 1529—1558. [P] 
1930. Weymuller, E. A. and P. L. Magnuson. Report 
of 52 cases of recurrent aerotitis, First Air Force, Mitchel 
Field, New York. Ann. Otol., etc., St. Louis, 1945, 54: 
684-685. 
1931. Anon. The use of radium in the aerotitis control 
program of the Army air forces. Ann. Otol., etc., St. Louis, 
1945, 54: 650-660. 
5. DENTAL THERAPY 
Kelly {1932, 1933, 1934, and 1935) 1946 and 
Kelly and Langheinz {1936) 1946 have reported 
successful investigations of dental treatment for the 
prevention of aerotitis media. Success claimed 
earlier in relieving ear symptoms in aviators with 
over-closure of the mandible by inserting a splint be- 
tween the back teeth to open the bite suggested to 
Kelly that the muscles concerned with the move- 
ment of the jaw are also in some way involved with 
the functions of the Eustachian tube. Kelly rea- 
soned that abnormally strained muscular activity 
during jaw movement might exert a deleterious ef- 
fect on the function of the Eustachian tube. Dental 
treatment was accordingly devised and carried out 
to correct occlusion and provide free movement of 
the mandible and normal unstrained muscle action 
during all jaw movements. Casts of the jaws were 
made and X-rays were taken in the open and closed 
positions, and points on the teeth which hampered 
excursions were corrected. 
A group of 50 subjects with severe aerotitis media 
{1936) who demonstrated defective mandibular 
functions were selected for treatment of the occlu- 
sion defect. Following treatment, 46 of these pa- 
tients were able to undergo pressure without 
otological symptoms or signs. These findings were 
based upon objective examination of each ear with 
the otoscope in the hands of an experienced oto- 
Faulty opening of the mouth of the Eustachian 
tube, especially during compression, lies at the basis 
of aerotitis media. Lymphoid hyperplasia around 
the mouth of the tube is believed to be a cause of 
this defective function. Accordingly, a therapeutic 
and preventative procedure has been developed in 
which recession of the lymphoid tissue is effected 
by means of local irradiation. For this purpose, 
radium, radon, and X-rays have been utilized. 
Shilling, Haines, Harris, and Kelly {1929) 1946 
have reported that the use of X-ray is of inconclu- 
sive value and has been discontinued. Other evi- 
dence indicates that the administration of X-ray 
therapy presents particular problems. The use of 
radium, however, has proved successful, according 
to the authors, in well over 90 percent of the cases. 
Irradiation treatment has been widely employed 
in the U. S. Air Force and evaluations of results 
are given in the following references: 1921, 1923, 
1924, 1925, 1926, 1930, and 1931. These reports 
indicate that irradiation is not a cure-all and will 
not affect symptoms having a functional basis. 
However, it appears that there is objective improve- 
ment in approximately 90 percent of cases {1925, 
1926). For an anlysis of 28 failures out of 1,177 
patients treated at the Third Air Force Irradiation 
Unit, a paper by Glauber, Smith, and Earl {1924) 
1945 should be consulted. 
The reader is advised to consult a carefully pre- 
pared report by Dickson and McGibbon {1922) 
1949 for a cautionary and critical treatment of the 
subject of irradiation therapy for otitis media. The 
authors draw attention to the possible dangers of 
haphazard introduction of powerful sources of 
radio-activity into the nasopharynx. Positioning is of 
vital importance if the lymphoid tissue is actually 
to be affected. The authors pointed out in 1949 
that at that time it was still too early to express any 
opinion as to the occurrence of delayed, local ill 
effects. The authors stated that in order to irradiate 
adequately the entire Eustachian tube from a single 
nasopharyngeal source, the dosage with radium 
would need to be such as would be dangerous to 
tissues adjacent to the source. It was considered 
consequently that deep X-irradiation was the only 
acceptable procedure. A safe method of applica- 
tion of X-irradiation was described which would 
not cause damage to the skin or tissues in the region 
of Eustacian tube. A disadvantage of X-irradiation 
is that a considerable volume of tissue must be 
irradiated. 
1921. Collins, B. E., J. W. Eschenbrenner, Jr., and 
P. L. Lyle. Aerotitis and radium therapy in the Eighth 
Air Force. Ann. Otol., etc., St. Louis, 1945, 54: 694-707. 
291222—54 12 1932-1947 
DISEASES AND ACCIDENTS 
laryngologist. Three out of the four unsuccessful 
cases responded to radium therapy. One case resisted 
all attempts at therapy. In explanation of the ra- 
tionale of dental therapy in aerotitis media, the 
authors suggested that normally the action of the 
superior pharyngeal constrictor muscles stimulates 
the lymph vessels draining the Eustachian tube. 
Dysfunction of that muscle may lead to stasis of the 
tube. The action of the buccinator muscle is inti- 
mately interrelated with the action of the superior 
pharyngeal constrictor muscle through the pterygo- 
mandibular raphe, and it was argued that the 
rationale of dental therapy lay in restoring normal, 
unstrained function to the buccinator and hence 
to the superior pharyngeal constrictor muscle. This 
was believed to reduce an abnormal tourniquet 
effect of the latter upon the lymphatics and so re- 
store the normal massaging effect, thereby stimulat- 
ing lymphatic drainage and thus reducing conges- 
tion of the Eustachian tube. This theory of 
lymphatic stasis is substantiated by the fact that the 
amount of lymphoid tissue present in the naso- 
pharynx has little bearing upon the success or fail- 
ure of the dental method of treatment. 
1932. Kelly, W. J. The results of dental therapy in 50 
cases of aerotitis media in submarine personnel based upon 
a new functional concept of eustachian tube blockage. 
U. S. Navy. Submarine base, New London, Conn. Medical 
research department. Project X-434 {Sub. no. 90), Inter- 
val report no. 1, 21 January 1946, 15 pp. [P] 
1933. Kelly, W. J. Dental treatment of trismus, tinnitus, 
otalgia and obscure neuralgias. U. S. Navy. Submarine 
base, New London, Conn. Medical research department. 
Project X-434 (Sub. no. 90), Interval Report no. 2, 31 
January 1946, 17 pp. 
1934. Kelly, W. J. A rapid dental treatment for the 
prevention of aerotitis media. U. S. Navy. Submarine base, 
New London, Conn. Medical research department. Project 
X-434 (Sub. no. 90), Interval Report no. 3, 1 February 
1946, 11 pp. [CH] 
1935. Kelly, W. J. An evaluation of a dynamic concept 
of dental treatment based upon a functional classification 
of malocclusion. U. S. Navy. Submarine base, New Lon- 
don, Conn. Medical research department. Project X-434 
(Sub. no. 90), Interval Report no. 4, 15 February 1946, 
10 pp. 
1936. Kelly, W. J. and H. W. Langheinz. Dental treat- 
ment for the prevention of aerotitis media. Ann. Otol., 
etc., St. Louis, 1946,55; 13-28. [P] 
6. SURGICAL AND PHYSICAL PROCEDURES 
Various methods to inflate the middle ear and to 
facilitate drainage of fluid from the middle ear have 
been devised. These and other surgical procedures 
in otitis media are described in the references that 
follow. 
1937. Dagg'ett, W. I. Operative treatment of chronic 
suppurative otitis media. /. Laryng., 1949, 63: 635-646. 
1938. Fowler, E. P. Treatment of otitis media, pp. 626— 
629 in; The specialties in general practice. Edited by 
Russell L. Cecil. Philadelphia, W. B. Saunders Co., 1951, 
818 pp. 
1939. Ogden, F. W. Modified Politzerization in treatment 
of aero-otitis media. U. S. AAF. Randolph Field, Tex. 
School of aviation medicine. Project 173, Kept. no. I, 
3 August 1943, 5 pp. 
1940. Ogden, F. W. Continuous pressure politzerization 
in the prevention of altitude chamber aero-otitis media. 
U. S. AAF. Randolph Field, Tex. School of aviation 
medicine. Project 177 Kept. no. 1, 31 August 1943, 5 pp. 
[P] 
1941. Olmsted, F. Modifications of a device for testing 
patency of the Eustachian tube. Rept. no. 53 in: Studies 
in Aviation Medicine. Yale aero-medical research unit, 
Yale University School of Medicine, New Haven, Conn., 
1941-1946. 
1942. Seltzer, A. P. Newly designed paracentesis needle 
for use in aerotitis media. Arch. Otolaryng., Chicago, 1951, 
53: 672-674. 
1943. Trowbridge, B. C. A new treatment of acute aero- 
otitis media. Arch. Otolaryng., Chicago, 1949, 50: 
255-263. [CH] 
1944. Unger, M. A new method of treatment for nasal 
sinusitis: oxygen inflation. Arch. Otolaryng., Chicago, 
1945, 41: 353-354. [M] [CH] 
E. OTITIS EXTERNA 
Otitis externa is a clinical entity with high mor- 
bidity in military personnel on tropical duty. It is 
also a condition to which underwater swimmers are 
subject unless effective preventive measures are 
taken. Otitis externa in underwater swimmers is 
discussed in the section on diseases prevalent in 
swimmers (p. 332). The causative organism may be 
any of a variety of bacteria and fungi. Ashley {1945) 
1946 classifies the condition into three groups. In 
group I, the external auditory canal is moist and 
filled with exudate and debris. In group II, there 
is a cellulitis of the deep tissue of the canal. Group 
III cases are more chronic with persistent itching 
and other symptoms. Cases will occur under con- 
tinuous exposure to hot, humid environments, espe- 
cially after swimming or taking showers, unless care 
is taken to keep the ear canals dry. Most cases of 
bacterial otitis externa are considered to be caused 
by various species of the genus Pseudomonas (1946, 
1947,1948,1952,1953, and 1956). The role of fungi 
in the etiology of otitis externa is believed by Syver- 
ton, Hess, Krafchuk, Josselyn, and Freyvogel {1956) 
1946 to have been overemphasized, and Senturia 
{1953) 1945 states that fungi played little part in 
the inception or persistence of otitis externa seen at 
Randolph Field, Tex. 
1945. Ashley, P. External otitis in the tropics. Nav. med. 
Bull., Wash., 1946, 46: 1230-1236. 
1946. Beach, E. W. and L. L. Hamilton. Tropical otitis 
externa. Ear. fungus. Nav. med. Bull., Wash., 1945, 44: 
599-602. 
1947. Clark, J. V. Acute otitis externa in India. /. 
Laryng., 1946, 61: 586-593. DECOMPRESSION SICKNESS—GENERAL CONSIDERATIONS 
1948-1956 
1948. Gill, E. K. and W. D. Gill. Otitis externa. Some 
comments concerning the present status of therapy. Sth. 
med. J., Birmingham, 1950, 43: 428-431. [CH] 
1949. Jewell J. H. A. Otitis externa and acute otitis 
media. Brit. Guiana med. Annu., 1947, 28: 77-84. 
1950. Koch, H. Allergical investigations of chronic 
otitis. Acta oto-laryng., Stockh., Suppl., 1947, 62: 201 pp. 
1951. Lumsden, R. B. External otitis. /. Laryng., 1951, 
65; 33-37. [D] 
1952. Salvin. S. V. and M. L. Lewis. External otitis, 
with additional studies on the genus pseudomonas. J. Bact., 
1946, 51: 495-506. 
1953. Senturia, B. H. Etiology of externa otitis. U. S. 
AAF. Randolph Field, Tex. School of aviation medicine. 
Project 349, Kept. no. 1, 15 January 1945, 15 pp. 
1954. Senturia, B. H., J. I. Matthews, and B. C. Adler. 
External otitis. IV. Cytologic study of secretions. Laryn- 
goscope, St. Louis, 1950, 60: 543-550. [P] 
1955. Simonton, K. M. Study of acute otitis externa with 
special reference to secondary myringitis and otitis media. 
Milit. Surg., 1947, 100: 156-164. 
1956. Syverton, J. T., W. R. Hess, J. Krafchuk, E, H. 
Josselyn, and 6. H. Freyvogel, Jr. Otitis externa. Clinical 
observations and microbiologic flora. Arch. Otolaryng., 
Chicago, 1946, 43: 213-225. 
F. OTITIS EXTERNA THERAPY 
Correct hygiene of the external ear is essential in 
preventing otitis externa. The canal should be kept 
clean and dry and free from moisture. Treatment is 
most successful, according to McLaurin {1957) 
1951, when the otologist limits himself to a few anti- 
bacterial or fungicidal agents and supplements this 
treatment by thorough cleansing of the external 
auditory canal and by utilizing resources for the 
relief of discomfort. The use of “iso-par” ointment 
in the treatment of otitis externa in Okinawa in 
1946 was described by Senturia {I960) 1946. 
Senturia and Broh-Kahn {1961) 1947 described 
the use of streptomycin locally in the form of an 
ointment in 54 patients with diffused otitis externa 
in the San Antonio area. These cases showed a high 
number of cultures of Pseudomonas. Successful 
treatment was accompanied by a rapid disappear- 
ance of Pseudomonas from infected ears. Treatment 
of otitis externa with 250 micrograms and 1 mg. 
of streptomycin per gram of ointment base was no 
more effective than treatment with the base alone. 
Treatment with 5 mg. of streptomycin per gram of 
ointment base gave beneficial results where simple 
cleansing of the ear canal and drying failed to pro- 
duce favorable clinical effects. The use of various 
vehicles and antibiotics in the external auditory 
canal in the treatment of otitis externa has been dis- 
cussed in detail in a report by Senturia and Doubly 
{1962) 1947. When both streptomycin and peni- 
cillin were incorporated in an aqueous vehicle, a 
potentiated antibiotic effect was obtained. This 
combination was valuable in mixed infections. 
Senturia and Wolf {1963) 1945 found that sulfanil- 
amide had marked fungistatic effects when applied 
to the surface of cultures of a number of fungi. 
Sulfathiazole, sulfadiazine, sulfaguanidine, and 
sulfamerazine had no observable effect upon the 
growth of these fungi. The authors recommended 
local application of powdered sulfanilamide in 
cases of otomycocis. Sulfanilamide was found not to 
affect cultures of monilia. Local and systemic use 
of sulfonamides has also been discussed by Simon 
{1964) 1945, and Sullivan and Smith {1965) 1950. 
1957. McLaurin, J. W. Principles of therapy in otitis 
externa. Laryngoscope, St. Louis, 1951, 61: 66-87. 
1958. Ochs, I. L. Treatment of external otitis; a simple 
and effective technic. J. Amer. med. Ass., 1950, 142: 
1361-1362. [CH] 
1959. Reardon, W. T. Use of “iso-par” ointment in the 
treatment of otitis externa. Arch. Otolaryng., Chicago, 
1947, 45: 294-297. 
1960. Senturia, B. H. Penicillin therapy in external 
otitis. Ann. Otol, etc., St. Louis, 1946, 55: 90-107. [CH] 
1961. Senturia, B. H. and R. H. Broh-Kahn. The use 
of streptomycin in the treatment of diffuse external otitis. 
U. S. AAF. Randolph Field, Tex. School of aviation medi- 
cine. Project 486, Kept. no. 1, February 1947, 8 pp. 
[CH] [P] 
1962. Senturia, B. H. and J. A. Doubly, Treatment of 
external otitis. III. The use of vehicles and antibiotics in 
the external auditory canal. In vitro studies. Laryngo- 
scope, St. Louis, 1947, 57: 633-656. [P] 
1963. Senturia, B. H. and F. T. Wolf. Treatment of 
external otitis. II. Action of sulfonamide compounds on 
fungi isolated from cases of otomycosis. Arch Otolaryng., 
Chicago, 1945, 41: 56-63. 
1964. Simon, E. Otitis externa and its treatment. Arch. 
Otolaryng., Chicago, 1945,42; 123-130. 
1965. Sullivan, J. A. and J. B. Smith. The office treat- 
ment of chronic otitis. Ann. Otol., etc., St. Louis, 1950, 
59: 364-380. 
III. DEC0MPEESSI0N SICKNESS 
A. GENERAL CONSIDERATIONS 
For a comprehensive review of the literature on 
decompression sickness up to 1 January 1946, refer- 
ence should be made to appropriate sections (pp. 
108-162) in the first volume of this Sourcebook. 
The references given below provide access to the 
general subject of decompression sickness as it has 
developed since the beginning of 1946. The reader 
will find especially helpful the reports by Behnke 
{1968) 1945, {1969) 1947, {1970) 1940, {1971) 
1950, {1972) 1951; and Fulton {1978) 1948, 
{1979) 1951; and Fulton and Nims {1980) 1941- 
46. 
The term “decompression sickness” refers to the 
signs, symptoms, and underlying pathological proc- 
esses arising from rapid reduction of barometric 
pressure from high pressures to 1 atmosphere as in 
caisson work, tunneling operations, or in diving. 1966-1987 
DISEASES AND ACCIDENTS 
The term also covers the deleterious effects of de- 
compression to levels of less than 1 atmosphere as 
experienced in high-altitude flights or in experi- 
mental decompression chambers. The symptoms 
include pain (bends), painful breathing (chokes), 
and paralysis. There may also be visual and other 
sensory disturbances, involvement of the integu- 
ment, convulsive seizures and other central nervous 
symptoms, and even sudden death. Decompression 
sickness appears to have as its etiological basis the 
liberation of gas bubbles directly into various tissues 
or into the bloodstream in which they are carried 
to find lodgment in various parts of the body. 
Lesions may be found in the central nervous system, 
the eye, the internal ear, as well as in the bones and 
joints and other areas. The condition may be pre- 
vented by following appropriate decompression 
procedures breathing air or helium-oxygen mix- 
tures. At safe depths not sufficient to cause oxygen 
intoxication, pure oxygen may be breathed during 
decompression. Treatment includes recompression 
in a pressure chamber to an appropriate depth with 
administration of oxygen down to 50 feet. Various 
special symptoms and signs require special treat- 
ment. The acute symptoms are usually transient 
and there is ordinarily no permanent damage, pro- 
viding recompression treatment has been carried 
out adequately. However, chronic disturbances 
following repeated decompression over the years 
may supervene. Chronic lesions of the bone and 
joints, for example, may be due to this cause. 
1966. Alpers, B. J. Caisson disease, pp. 311-312 in: 
Clinical neurology. Second edition. Philadelphia, F. A. 
Davis Co., 1949, 846 pp. 
1967. Antnnez, Nieto. Efectos del aumento de la pre- 
sion. El mal del buzo. pp. 117—118 in; Higiene naval y 
nociones de anatomia y fisiologia. Moret, La Coruna, 1950, 
321 pp. 
1968. Behnke, A. R. Decompression sickness incident 
to deep sea diving and high altitude ascent. Medicine, 
Baltimore, 1945, 24: 381-402. /. industr. Hyg., 1946, 28: 
abstract section: 47. 
1969. Behnke, A, R. A review of physiologic and clinical 
data pertaining to decompression sickness. U. S. Navy. 
NMRI. Project X—443, Rept. no. 4, 13 May 1947, 35 pp. 
[R] 
1970. Behnke, A. R. Decompression sickness (caisson 
disease, compressed air illness, bends, aero-embolism), 
pp. 664 (47)—664 (54-19) in: Oxford medicine, Vol. IV, 
Part III. Edited by H. A. Christian. New York, Oxford 
University Press, 1940. [R] 
1971. Behnke, A. R. Decompression sickness, pp. 257- 
267 in: Medical physics Volume II. Edited by Otto 
Glasser. Chicago, The Year Book Publishers, Inc., 1950, 
1,227 pp. [R] 
1972. Behnke, A. R. Decompression sickness following 
exposure to high pressures, pp. 53-89 in: Decompression 
sickness. Caisson sickness, diver’s and flier’s bends and 
related syndromes. Edited by J. F. Fulton for the Subcom- 
mittee on decompression sickness. National Research 
Council. W. B. Saunders Co., Philadelphia, 1951, 437 pp. 
1973. Best, C. H. and N. B. Taylor. Caisson disease— 
compressed air sickness—aeroembolism—“the bends”— 
“explosive” decompression, pp. 426-427 in: The physio- 
logical basis of medical practice. A text in applied physi- 
ology. Fifth edition. Baltimore, The Williams & Wilkins 
Co., 1950, 1,330 pp. 
1974. Bjurstedt, H. Tryckfallssjukan i nutida belysning. 
[Decompression sickness in modern light.] Kungl. Krigsvet. 
akad. handl. tidsskr., 1949 153: 1-24. [D] 
1975. Brown, B. R. The incidence and relation of syn- 
cope to decompression sickness. J. Aviat. Med., 1946, 17: 
257-264. [P] 
1976. Cedrangolo, E. and R. Gaudio. Studio sull- 
apparato cardio-vascolare nei caissonisti. Rass. med. in- 
dust., 1951, 20: 203-204. 
1977. Darling, R. C. Diseases due to physical agents. 
Decompression illness (caisson disease) : pp. 502—504 in: 
A Textbook of medicine. Eighth edition. Edited by R. L. 
Cecil, and R. F. Loeb. Philadelphia, W. B. Saunders Co., 
1951, 1549 pp. 
1978. Fulton, J. F. Altitude decompression sickness, 
pp. 318-330 in: Part III, Aviation Medicine in; Advances 
in Military Medicine, Vol. I. Edited by E. G. Andrus, 
D. W. Bronk, G. A. Carden, Jr., G. S. Keefer, J. S. Lock- 
wood, J. T. Wearn, and M. C. Winternitz. Boston, Little, 
Brown and Co., 1948, 472 pp. [R] 
1979. Fulton, J. F. Historical introduction, pp. 1—3 in: 
Decompression sickness. Caisson sickness, diver’s and 
flier’s bends and related syndromes. Edited by J. F. Fulton 
for the Subcommittee on decompression sickness. National 
Research Council. Philadelphia, W. B. Saunders Co., 1951, 
437 pp. 
1980. Fulton, J. F. and L. F. Nims. Decompression 
sickness. Anoxia in man and animals. III. Scientific in- 
vestigations. pp. 6-9 in Final Rept. in: Studies in Aviation 
Medicine. Yale aero-medical research unit, Yale Uni- 
versity School of Medicine, New Haven, Conn., 1941— 
1946. [P] 
1981. Jakohsson, S. G. Tryckfallssjukan i nutida belys- 
ning. [Decompression sickness in modern light.] Kungl. 
Krigsvet. akad. handl. tidsskr., 1949, 153: 27—50. [D] 
1982. Jung, F. P. Compressed air work in bridge cais- 
sons. Amer. industr. Hyg. Ass., Quart., 1947, 8: 83-88. 
1983. Lund, D. W. Decompression sickness (caisson 
disease, compressed air illness, barotrauma), pp. 4-371— 
4-377 in: Treatment in general medicine. Volume 4. 
Edited by Hobart A. Reimann. Fourth edition. Philadel- 
phia, F. A. Davis Co., 1948, 776 pp. 
1984. Malmejac, J. Action physique de la depression 
barometrique. Degagement gazeux et aeroembolies. Med. 
aeronaut., 1948, 3: 67—89. Excerpta Medica. Section II. 
(Physiology, Biochemistry, and Pharmacology), 1949, 2: 
796. [R] 
1985. Olsen, C. G. Decompression illness. Amer. J. Nurs., 
1951, 51: 190-192. 
1986. Reed, J. V. and A. K. Harcourt. Compressed air 
disease or caisson disease, pp. 106-109 in: The essentials 
of occupational diseases. Springfield, Charles C. Thomas, 
1941, 225 pp. 
1987. Rozanov, L. S. Sravnitel’naia otsenka razlichnykh 
sposobov vedeniia kessonnykh rabot (opyt gigienicheskoe 
kharakteristiki). [Comparative evaluation of various con- 
struction methods in caisson work (experience in the 
characteristics of industrial hygiene).] Gigiena San., 
Moskva, 1951, 9: 31-36. 1988-2000 
DECOMPRESSION SICKNESS—CASE REPORTS 
1988. Anon. Decompression sickness. /. Amer. med. Ass., 
1946, 130: 82. [R] 
B. CLINICAL PICTURE OF DECOMPRESSION 
SICKNESS 
The recent literature does not add any essen- 
tially new contribution to knowledge of the actual 
symptomatology of decompression sickness beyond 
that set forth on pages 115 to 137 of the first volume 
of this Sourcebook. Of the references given below, 
items 1989, 1993, and 1996 describe the clinical 
picture of decompression sickness following decom- 
pression from pressures higher than 1 atmosphere. 
References 1990, 1991, 1992, 1994, 1995, 1997, 
1998, 1999, and 2000 describe the symptomatology 
of decompression sickness as encountered in rapid 
ascent to altitude. 
1989. Aldao, C. N. G. Formas cutaneas de la enfermedad 
del aire comprimido. Rev. or gent, Dermato-sif., 1949, 33: 
20-25. [D] 
1990. Bridge, E. V., F. M. Henry, 0. L. Williams, and 
J. H. Lawrence. “Chokes”; A respiratory manifestation of 
aeroembolism in high altitude flying. Ann. intern. Med., 
1945, 22: 398-407. C. A. M. Kept. no. 382, 23 October 
1944, 1 p. 
1991. Goggio, A. and G. H. Houck. Physiologic abnor- 
malities and pathologic changes following exposure to 
simulated high altitudes. War. Med., Chicago, 1945, 7: 
152-156. [CH] [P] 
1992. Gray, J. S. The location, severity, and altitude of 
disappearance of the bends. U. S. AAF. Randolph Field, 
Tex. School of aviation medicine. Project 117, Kept. no. 1, 
5 February 1943, 6 pp. [P] 
1993. Hanns, A. Accidents causes par le travail dans 
Pair comprime. pp. 335—344 in: Medecine du travail. 
Edited by G. Simonin. Paris, Librairie Maloine, 1950, 
913 pp. [D] 
1994. Hartrijsen, F. B. Tarmgas og hoydeflyging. [In- 
testinal gas and high altitude flying.] Nord. Med., 
Stockholm, 1949,42: 1319-1321. 
1995. Inman, V. T. and J. B. M. Saunders, deC. Re- 
ferred pain from skeletal structures. J. nerv. ment. Dis., 
1944, 99:660-667. [P] 
1996. Jacobs, M. H. and D. R. Stewart. Observations 
on the blood of albino rats following rapid decompression. 
U. S. NRG-CAM. C. A. M. Kept. no. 76, October 1942, 
5 pp. [P] 
1997. McDonough, F. E. Roentgenographic observations 
on the amount and distribution of intestinal gas at altitude 
in relation to abdominal symptoms. U. S. NRC-CAM. 
C. A. M. Kept. no. 216, 1 November 1943, 9 pp. [P] 
1998. Romano, J., G. L. Engel, J. P. Webb, E. B. Ferris, 
H, W. Ryder, and M. A. Blankenhorn. Syncopal reactions 
during simulated exposure to high altitude in decompres- 
sion chamber. War Med., Chicago, 1943, 4: 475-489. 
1999. Tobias, C. A. Decompression sickness in actual 
flights, pp. 360—377 in: Decompression sickness. Caisson 
sickness, diver’s and flier’s bends and related syndromes. 
Subcommittee on decompression sickness. National Re- 
search Council, Philadelphia, W. B. Saunders Co., 1951, 
437 pp. [CH] [D] 
2000. Whitten, R. H. Scotoma as a complication of 
decompression sickness. J. industr. Hyg., 1947, 29: ab- 
stract section: 82. Arch. Ophthal., Chicago, 1946, 36: 
220-224. [P] 
C. CASE REPORTS 
A large number of case histories of decompression 
sickness are referred to on pages 121 to 137 of the 
first volume of this Sourcebook. Reference should 
be made to these histories for basic information on 
the clinical pattern of decompression sickness. The 
references listed below report specific cases of de- 
compression sickness due to decompression from 
high pressures as well as decompression to altitude 
or simulated altitude. 
Van Der Aue {2011) 1948 reported a case of 
decompression sickness in a diver aboard the U. S. S. 
Chanticleer. The diver descended to 356 feet, re- 
mained there for 10 minutes, and ascended to 50 
feet without symptoms. After completing the 60- 
foot stop and the 50-foot stop he breathed oxygen. 
He was then asked to unshackle and reported that 
he had done so. Mumbling sounds then ensued and 
at 30 feet, telephone contact was lost. When the 
diver was brought to the surface he was found to 
be unconscious and suffering convulsive body move- 
ments. The face was pink, the body was limp. He 
was carried to a recompression chamber in his 
diving suit and was recompressed to a simulated 
level of 165 feet 6 minutes later. He began thrash- 
ing about and required restraint. He was uncon- 
scious for 29 minutes. Table 2A was used for de- 
compression. On regaining consciousness the diver 
was mildly disoriented and complained of headache 
and soreness in the ears. There was some bleeding 
from the mouth. At the simulated 40-foot level, 
otoscopic examination revealed hemorrhagic ear- 
drums, but no perforations. Some blood streaked 
the posterior pharyngeal wall. This blood probably 
came from the Eustachian tubes or the nasal sinuses. 
The patient said he remembered nothing after he 
unshackled. The patient had never before experi- 
enced any symptoms. 
A case history is described by van Keuren {2012) 
1946 of decompression sickness in a diver attached 
to the U. S. S. Coucal. The U. S. S. Coucal was 
anchored for diving activity 12 miles from Pearl 
Harbor. Lead-line soundings indicated a depth of 
130 feet. Divers overside were paid out 200 feet of 
hose on air. After 4 minutes on the bottom, the 
diver started up according to the standard table for 
air dives. Pain was experienced in the chest at 10 
feet, and the diver was brought to the surface and 
recompressed in the chamber on the ship. Complete 
relief was experienced at 30 feet. Two or three 
minutes after treatment, the diver noted a tingling 2001-2011 
DISEASES AND ACCIDENTS 
sensation in the left leg, but nevertheless went to 
chow. The condition became more serious and 
weakness developed. The diver was put back into 
the chamber 42 minutes after the onset of symptoms 
and was taken to a simulated depth of 165 feet 
where he remained for 20 minutes. During the first 
hour of treatment, the weakness rapidly increased 
until the diver was unable to walk, stand, or crawl. 
When the ship reached dock, a medical examination 
revealed impaired touch and pain perception from 
the level of the umbilicus downward. There was 
weakness of lower back movements and weakness 
of motion in the right hip, knee, ankle, and toes, 
and complete inability to move the left hip, knee, 
ankle, and toes. Position sense was normal. The 
superficial abdominal and cremasteric reflexes were 
absent bilaterally. The patellar, knee, and ankle 
jerks were hyperactive and bilaterally equal. The 
Babinski reflex was positive on both sides. There 
was mild clonus on the left ankle. Pinprick percep- 
tion was impaired, but not absent from the level of 
the 10th thoracic segment downward. It was con- 
sidered that bubbles had lodged in the anterior horn 
of the spinal cord at about the level of the 10th 
thoracic segment and had been there for 40 min- 
utes before treatment was begun. Apparent pro- 
gression of the symptoms was considered possibly 
due to nerve injury already done, plus involvement 
of a surrounding area by edema and hemorrhage. 
As to further treatment, oxygen was given but was 
stopped because of increased nervousness and finger 
twitchings. Helium-oxygen mixtures and air were 
alternated every half hour. The following morning 
a small amount of urine was passed and catheteriza- 
tion was done. Later, the deep reflexes in the lower 
extremities became depressed and disappeared. 
Subsequently the patient was left with residual 
symptoms and was surveyed from the naval service. 
This case stresses the importance of immediate re- 
compression to an adequate depth. 
Welham and Waite {2013) 1951 reported two 
unusual cases of decompression sickness. The first 
was a 21-year-old diver who reported to the diving 
school with complaint of pain, weakness, and numb- 
ness of the right upper arm and shoulder, and 
mottling of the entire right arm. The last dive had 
been made 36 hours prior to the onset of symptoms. 
The dive had been made to 25 to 35 feet in the 
Anacostia River. The patient had been recom- 
pressed with relief at 20 feet and surfaced several 
minutes later, but the symptoms had returned 1 
hour subsequently. The patient was recompressed 
according to table I of the treatment tables in the 
U. S. Navy Diving Manual and surfaced symptom 
free. The second case was that of a 24-year-old 
student diver who made a dive to 27 feet for 96 
minutes and who 7 hours later suffered a sharp 
pain in the wrist. Hot soaks at home brought no 
relief. Chamber recompression gave relief at 56 
feet. This patient was treated according to table I 
and surfaced symptom free. Twenty-one hours after 
initial treatment, the patient again complained of 
pain in the affected area. When no relief was 
afforded at 165 feet, the case was determined not 
to be bends. X-ray investigation at the U. S. Naval 
Hospital at Bethesda revealed no fracture, and the 
final diagnosis was that of a sprain. 
Two further cases of decompression sickness in 
divers are given by Laane {2004) 1949 and Bayul- 
kem and Akyol {2001) 1950. Parodi {2010) 1948 
has presented five cases of decompression sickness 
in caisson workers who experienced acute pain in 
the extremities and abdomen, vertigo, and general 
malaise. 
For reports of cases of decompression sickness due 
to high altitude or simulated high altitude, the fol- 
lowing references are given: 2002, 2003, 2005, 
2006, 2007, 2008, and 2009. 
2001. Bayulkem, F. and N. Akyol. Caisson hastaligi. 
Turk Tip Cem. Mec., 1950, 16: 99-106. (French and 
English summaries.) 
2002. Gibson, W. C. Relative resistance to decompres- 
sion sickness 8 years after multiple, severe injuries. Asso- 
ciate committee on aviation medical research, Canada 
NRG. N. R. C. Grant no. A. M. 17-5, C. T. U., Kept. no. 
33, 29 January 1943, 1 pp. [GH] 
2033. Grulee, C. G. Eleven cases of “aeroembolism” re- 
quiring hospitalization. U. S. NRC—CAM. C. A. M. Kept, 
no. 172, 29 October 1942, 21 pp. [CH] 
2004. Laane, C. L. Et tilfelle av dykkersykdom. [A case 
of caisson disease.] Tskr. Norske Laegeforen., 1949, 69: 
396-397. 
2005. Lund, D. W., J. H. Lawrence, and L. B. Lawrence. 
Case report on a severe, delayed reaction with cerebral 
involvement following decompression. U. S. NRC-CAM. 
C. A. M. Kept. no. 396, 15 December 1944, 5 pp. [CH] 
2006. Lund, D. W., J. H. Lawrence, and L. B. Lawrence. 
Latent neurologic manifestations following decompression. 
Occup. Med., 1946, /: 75-80. [CH] 
2007. Masland, R. L. Review of cases of collapse occur- 
ring in altitude chambers. U. S. NRC-CAM. C. A. M. 
Kept. no. 179, 10 August 1943, 13 pp. [CH] 
2008. Masland, E,. L. Injury of the central nervous 
system resulting from decompression to simulated high 
altitudes. Arch. Neurol. Psychiat., Chicago, 1948, 59: 
445-456. [CH] 
2009. Motley, H. L., H. I. Chinn, and F. A. Odell. 
Studies on bends. J. industr. Hyg., 1946, 28: abstract 
section: 47. 
2010. Parodi, V. M. Rilievi semeiologici e clinici nelle 
forme osteomioartralgiche della malattia dei cassoni. 
Med. d. Lavoro, 1948, 39: 73-79. [CH] 
2011. Van der Aue, 0. E. Caisson disease—in the case 
of Ferguson, Charles P., GM1, 250-54—57. U. S. Navy. 
Naval gun factory, EDU. (aboard U. S. S. Chanticleer 
ASR-7), Rept. to Chief, BuMed, 6 November 1948. DECOMPRESSION SICKNESS—INCIDENCE, DIAGNOSIS, PROGNOSIS 
2012-2039 
2012. Van Keuren, H. C. Air embolism in the case of 
Miller, William B., SF3c, 283-93-12, USN. U. S. S. 
Coucal (ASR-8). Report of to Chief, BuMed, 12 March 
1946, 6 pp. 
2013. Welham, W. and C. L. Waite. Decompression 
sickness. Report of two unusual cases. Armed Forces med. 
J., 1951, 2: 1201-1204. 
D. INCIDENCE, DIAGNOSIS, AND PROGNOSIS OF 
DECOMPRESSION SICKNESS 
The references given below are principally con- 
cerned with altitude decompression sickness. How- 
ever, they are included because they provide useful 
source material for the reader who is concerned 
with factors affecting incidence and prognosis of 
decompression sickness. 
2014. Allan, J. H. Traumatic calcifications; a precipi- 
tating factor in “bends” pain. /. industr. Hyg., 1946, 28: 
Abstract section: 47. [CH] 
2015. Anthony, R. A., R. W. Clarke, A. Liberman, I. F. 
Nims, J. Tepperman, and S. M. Wesley. Temperature and 
decompression sickness. U. S. NRC-CAM. C. A. M. Rept. 
no. 136, 26 May 1943, 3 pp. 
2016. Anthony, R. A., R. W. Clarke, A. Liberman, 
L. F. Nims, J. Tepperman, and S. M. Wesley. Effects of 
local compression, impairment of venous return and 
arterial tournequet upon the intensity of established 
“Bends” pain. U. S. NRC-CAM. C. A. M. Rept. no. 143, 
16 June 1943, 6 pp. 
2017. Bierman, H. R. The relationship of age to the 
incidence of decompression in aviation. U. S. Navy. 
NATO., Pensacola, Fla. School of aviation medicine. 
Project X-10 (Av-R7-1), 13 July 1943, 5 pp. [P] 
2018. Burkhardt, W. L., H. F. Adler, A. F. Thometz, 
A. J. Atkinson, and A. C. Ivy. Decompression sickness; 
some factors which affect the incidence of bends at alti- 
tude. /. industr. Hyg., 1947, 29: abstract section; 58. 
J. Amer. med. Ass., 1947,133: 373-377. 
2019. Burkhardt, W. L., A. F. Thometz, and A. C. Ivy. 
The effect of deliberate hyperventilation on the incidence 
of “intolerable” cases of bends and chokes. U. S. NRC- 
CAM. C. A. M. Rept. no. 438, June 1945, 4 pp. 
2020. Cook, S. F. Role of exercise, temperature, drugs 
and water balance in decompression sickness, pp. 223-241 
in; Decompression sickness. Caisson sickness, diver’s and 
flier’s bends and related syndromes. Edited by J. F. Fulton 
for the Subcommittee on decompression sickness, National 
Research Council. Philadelphia, W. B. Saunders Co., 
1951,437 pp. [D] 
2021. Evxard, E, Observations experimentales relatives 
aux effets vitesses ascensionnelles rapides sur 1’organisme 
de 1’aviateur (suit et fin). Brux. med., 1949, 29: 3689— 
3706. Excerpta Medica. Section II. (Physiology, Bio- 
chemistry, and Pharmacology), 1950, 3: 1003. 
2022. Gray, J. S. The effect of exercise at altitude on 
aeroembolism in cadets. U. S. NRC-CAM. C. A. M. 
Rept. no. 169, 2 June 1943, 5 pp. [P] 
2023. Gray, J. S. Aeroembolism induced by exercise in 
cadets at 23,000 feet. U. S. AAF. Randolph Field, Tex. 
School of aviation medicine. Project 227, Rept. no. 1, 
26 January 1944, 3 pp. [P] 
2024. Gray, J. S. Constitutional factors affecting 
susceptibility to decompression sickness, pp. 182-191 in: 
Decompression sickness. Caisson sickness, diver’s and 
flier’s bends, and related syndromes. Edited by J. F. Fulton 
for the Subcommittee on decompression sickness, National 
Research Council. Philadelphia, W. B. Saunders Co., 
1951,437 pp. [D] 
2025. Griffin, D. R,, S. Robinson, H. S. Belding, R. C. 
Darling, and E. Turrell. The effects of cold and rate of 
ascent on aero-embolism. U. S. NRC-CAM. C. A. M. 
Kept. no. 174, 22 June 1943, 12 pp. [P] 
2026. Griffin, D. R., S. Robinson, H. S. Belding, R. C. 
Darling, and E. S, Turrell. The effects of cold and rate 
of ascent on aero-embolism. /. Aviat. Med., 1946, 17: 
56-66. 
2027. Hodes, R. and M. G. larrabee. The relation be- 
tween alveolar carbon dioxide tension and susceptibility 
to decompression sickness. Amer. J. Physiol., 1946, 147: 
603-615.[P] 
2028. Henry, F. M. The role of exercise in altitude pain. 
U. S. NRG—CAM. OEMcmr—196, Kept. no. 460, Septem- 
ber 1945, 2 pp. Abstr. 
2029. Henry, F. M. The role of exercise in altitude pain. 
Amer. J. Physiol., 1945,145: 279-284. [P] 
2030. Houston, C. S., S. Nuzie, C. P. Seitz, and G, E. 
Bessen. Studies on factors affecting incidence of bends in 
low pressure chamber runs. U. S. Navy. Naval air station, 
Miami, Fla. Altitude training unit. Project X-374, Repts. 
nos. 1, 2, and 3, 27 July 1944, 25 pp. 
2031. Ivy, A. C., A. J. Atkinson, H. F. Adler, W. 
Burkhardt, and A. F. Thometz. Incidence of symptoms of 
“bends and chokes” at 47,500 feet for 1 hour without 
exercise with intermittent pressure breathing. U. S. NRC- 
CAM. C. A. M. Kept. no. 370, 6 October 1944, 1 p. 
2032. Ivy, A. C., W. L. Burkhardt, and A. F. Thometz. 
The effect of pecuniary incentive on the incidence of 
“intolerable” cases of bends and chokes. U. S. NRC- 
CAM. C. A. M. Kept. no. 422, 23 March 1945, 2 pp. [P] 
2033. Karpovich, P. V. Relation between bends and 
physical fitness. U. S. AAF. Randolph Field, Tex. School 
of aviation medicine. Project 192, Rept. no 1, 25 October 
1943, 2 pp. C. A. M. Rept. no. 217, 25 October 1943, 2 
PP- [P] 
2034. Knisely, M. H., S. Gray, H. M. Peck, R. L. Nichols, 
I/. Warner, and J. A. Orcutt. The effect of elevation of a 
limb on the development and severity of bends pain. U. S. 
NRC-CAM. C. A. M. Rept. no. 196, 1 October 1943, 
2 pp. [P] 
2035. Robinson, T. W. Factors correlated with resistance 
to decompression sickness. Fed. Proc. Amer. Soc. exp. 
Biol, 1949, 8: 133. 
2036. Rodbard, S. Recurrence of decompression sickness 
on reascent to high altitude. Fed. Proc. Amer. Soc. exp. 
Biol, 1945, 4: 59-60. J. industr. Hyg., 1948, 30: abstract 
section: 19. [P] 
2037. Smedal, H. A. and E. B. Brown, Jr. Incidence of 
bends pain in a short exposure to simulated altitudes of 
26,000, 28,000, and 30,000 feet. U. S. Navy, NATC., 
Pensacola, Fla. School of aviation medicine. Project 
X-609 (Av-311-h), 1 September 1945, 8 pp. [P] 
2038. Smith, H. W. The effect of anoxia on the inci- 
dence of decompression sickness at 35,000 feet. Canada 
NRG. Associate committee on aviation medical research. 
N. R. G. Grant no. A. M. 17—5, C. I. U., Rept. no. 29, 28 
January 1943, 6 pp. 
2039. 1JSAF. Wright-Patterson air force base, Dayton, 
Ohio. Aero medical laboratory. Decompression sickness, 
pp. 7—11 in: Synopsis of the aero medical aspects of jet- 
propelled aircraft. January 1949, 46 pp. 2040-2051 
DISEASES AND ACCIDENTS 
2040. Van Der Aue, 0. E., R. J. Kellar, and E. S. 
Brinton. The effect of exercise during decompression 
from increased barometric pressures on the incidence of 
decompression sickness in man. U. S. Navy. Naval gun 
factory, EDU. Project NS-186-051, Rept. no 1, E. D. U. 
no. 8-49, March 1949, 44 pp. [P] 
E. ETIOLOGY OF DECOMPRESSION SICKNESS 
Catchpole and Gersh [2043) 1947 and Gersh 
and Catchpole [2046) 1951 have pointed out that 
the evidence is overwhelming that gas bubbles are 
the primary pathogenic agent in decompression 
sickness, whether due to decompression from high- 
pressure atmospheres or decompression to altitude. 
The authors believe that the gas bubbles are chiefly 
intravascular and these are held to be responsible 
for nearly all important phases of the syndrome of 
decompression sickness. Extravascular gas bubbles 
are also believed to occur under certain circum- 
stances in decompression from high-pressure atmos- 
pheres, but they are restricted to certain lipid-rich 
structures. The pathological effects may be vastly 
greater after decompression from high-pressure at- 
mospheres than at altitude. Bean [2042) 1950 con- 
siders that extravascular bubble formation is more 
important because there is no local cyanosis, pallor, 
or cooling to implicate defective blood supply. Also, 
he points out that X-rays reveal no consistent 
vascular distribution of bubbles. Bean accepts the 
possibility that intravascular bubbles may accentu- 
ate focal changes. Intravascular bubbles are found 
in divers dying with bends or in the vena cava of 
decompressed animals. He considers that intra- 
vascular bubbles may be secondary and arise after 
symptoms occur. He states that bubbles may go on 
forming after death. He considers that the weight 
of evidence supports the secondary formation of 
intravenous bubbles in animals after stasis or stag- 
nation following vasospasm. 
Nims [2053) 1947 and [2054) 1951 has pro- 
pounded a physical theory of decompression sick- 
ness. Gas bubbles growing in tissues must displace 
and deform adjacent structures. If the deformation 
pressure exceeds a threshold value, nerve fibers or 
endings are stimulated by the mechanical defor- 
mation of the tissues. Decompression sickness pain 
is stated not to differ in kind from the pain pro- 
duced by excessive stretching of the eardrum or the 
pain due to unequalized pressure in the sinuses. 
Reduction of the deformation pressure to below 
threshold values provides immediate relief of pain- 
ful stimuli. It is not the size of the bubble that deter- 
mines the appearance of the symptons, but rather 
the magnitude of the distortion pressure that is pro- 
duced. Nims believes that bends pain comes from 
extravascular bubbles because reascent to altitude 
produces pain in exactly the same area as before. 
When the deformation pressure is near threshold 
value, a slight increase in carbon dioxide level or 
nitrogen in diving could well be the critical deter- 
minant in decompression sickness. 
For other studies relating to the etiology of de- 
compression sickness, particularly at altitude, the 
following references may be consulted: 2041, 2044, 
2045, 2047, 2048, 2049, 2050, 2051, 2052, 2055, 
2056, 2057, 2058, and 2059. 
2041. Aird, R. B. and C. Pfaffmann. Pressure stimula- 
lation of peripheral nerves. Proc. Soc. exp. Biol., N. Y., 
1947, 66: 130-132. [P] 
2042. Bean, W. Physical and toxic agents. Syndromes 
produced by free gas. pp. 737-742 in; Pathologic physi- 
ology. Mechanisms of disease. Edited by W. A. Sodeman. 
Philadelphia, W. B. Saunders Co., 1950, 774 pp. 
2043. Catchpole, H. R, and I. Gersh. Pathogenetic 
factors and pathological consequences of decompression 
sickness. Physiol. Rev., 1947, 27: 360-397. /. industr. 
Hyg., 1948, 30: abstract section: 47. 
2044. Clarke, R. W., A. M. Liberman, L. F. Nims, J. 
Nyboer, and J. Tepperman. Peripheral circulation during 
decompression—digital volume-pulse. U. S. NRC-CAM. 
C. A. M. rept. no. 232, 29 November 1943, 4 pp. 
2045. Ferris, E. B., Jr. and G. L. Engel. The clinical 
nature of high altitude decompression sickness. With a 
note on psychologic reactions by J. Romano, pp. 4—52 in: 
Decompression sickness. Caisson sickness, diver’s and flier’s 
bends and related syndromes. Edited by J. F. Fulton for 
the Subcommittee on decompression sickness, National 
Research Council. Philadelphia, W. B. Saunders Co., 
1951,437 pp. [R] 
2046. Gersh, I. and H. Catchpole. Decompression sick- 
ness: physical factors and pathologic consequences, pp. 
165—181 in: Decompression sickness. Caisson sickness, 
diver’s and flier’s bends and related syndromes. Edited by 
J. F. Fulton for the Subcommittee on decompression sick- 
ness, National Research Council. Philadelphia, W. B. 
Saunders Co., 1951, 437 pp. [D] 
2047. Ivanov, D. I. Castro-intestinal reflex in caisson 
disturbances during rapid rise to high altitudes. Amer. 
Rev. Soviet Med., 1947/48, 5: 49-51. [P] 
2048. Kaufman, S. S., L. F. Nims, and J. Nyboer. 
Peripheral circulation and decompression illness at 38,000 
feet. U. S. NRC-CAM. C. A. M. rept. no. 318, OEMcmr— 
38, 15 June 1944, 5 pp. 
2049. Knisely, M. H., S. Gray, H. M. Peck, R. L. Nichols, 
L. Warner, J. A. Orcutt, and N. Anderson, A brief review 
of some of the evidences indicating the necessity for con- 
trolling the circulatory homeo-static reactions of decom- 
pressed men. Appendix II in Methods and testing of 
therapeutic agents in relation to bends by M. H. Knisely. 
U. S. NRC-CAM. OEMcmr-290, C. A. M. rept. no. 473, 
September, 1945, 13 pp. 
2050. Lazarow, A., P. R. Patek, E. Bartosh, and G. H. 
Scott. Observations on the capillary circulation in skeletal 
muscle of frogs at simulated high altitudes. U. S. NRC- 
CAM. C. A. M. rept. no. 162, 15 June 1943, 3 pp. [P] 
2051. Lund, D. W. and J. H. Lawrence. An hypothesis 
as to a cause of “bends” pain with observations on mas- 
sage at high altitude. U. S. NRC-CAM. C. A. M. rept. 
no. 404, 10 January 1945, 9 pp. [M] DECOMPRESSION SICKNESS—PATHOLOGICAL 
2052-2059 
2052. Lund, D. W. and J. H. Lawrence. Studies on the 
cause of pain in high altitude “bends.” Fed. Proc. Amer. 
Soc. exp. Biol., 1946,5: 66. 
2053. Nims, L. F. A physical theory of decompression 
sickness. Yale University, New Haven, Conn. Aeromedi- 
cal research unit. Rept. no. 55, Contract N6—ori—44, T. O. 
VII, 1 May 1947,27 pp. 
2054. Nims, L. F. A physical theory of decompression 
sickness, pp. 192-222 in: Decompression sickness. Caisson 
sickness, diver’s and flier’s bends and related syndromes. 
Edited by J. F. Fulton for the Subcommittee on decom- 
pression sickness. National Research Council. Philadelphia, 
W. B. Saunders Co., 1951, 437 pp. [D] 
2055. Patek, P. R., A. Lazarow, E. Bartosh, and G. H. 
Scott. Observations on living periosteum and peritoneum 
at simulated high altitudes. U. S. NRG-CAM. C. A. M. 
rept. no. 244, 17 January 1944, 3 pp. [P] 
2056. Sureda, F. L. Effets des changements de pression 
atmospherique sur 1’organisme humain. Bull. int. Serv. 
Sante Arm., 1946, 19: 180—182. 
2057. Swindle, P. F. The possible relationship between 
intravascular agglutination of erythrocytes and decom- 
pression sickness. U. S. NRC-CAM. C. A. M. rept. no. 178, 
13 August 1943, 8 pp. [P] 
2058. Thometz, A. F. The etiology of aeroembolism and 
aeroemphysema and hyperventilation as a prophylactic 
and therapeutic measure. Contact, Pensacola, 1948, 6: 
237-246. 
2059. Tobias, C, A., W. F. Loomis, and J. H. Lawrence. 
Studies on skin temperature and circulation in decom- 
pression sickness. Amer. J. Physiol., 1947, 149: 626-633. 
[P] 
F. PATHOLOGICAL LESIONS 
For a detailed description of pathological lesions 
encountered in decompression sickness, the appro- 
priate section (pp. 142-162) in the first volume of 
this Sourcebook should be consulted. The litera- 
ture that has appeared since the first volume was 
published has been mainly concerned with bone and 
joint lesions. With more effective modern treatment 
of acute symptoms, it would appear that lesions of 
the central nervous system, and visual and auditory 
apparatus, are less common than previously. Fewer 
cases are now being reported with serious, obvious 
neurological and other sequelae. On the other hand, 
chronic bone and joint lesions detected in caisson 
workers and divers, often many years after exposure 
to decompression, have caused interest and aroused 
concern. Improved radiological techniques have 
made possible the more accurate and detailed study 
of these lesions, and considerations of workmen’s 
compensation renders important an accurate evalu- 
ation of their relationship to exposure to decom- 
pression. Often bone and joint symptoms are com- 
plained of by former divers and caisson workers who 
give no history of episodes of severe decompression 
sickness. It is possible that lesions in bones or joints 
may follow even a single attack of decompression 
sickness, provided it is of sufficient intensity. 
For review articles on bone and joint lesions due 
to decompression sickness, references by the follow- 
ing may be consulted: Brailsford {2062) 1948, 
Geschickter and Copeland {2064) 1949, Pugh 
{2079) 1951, Mouchet and Mouchet {2076) 1941, 
Nicoulaud {2078) 1940, and Raymond {2080) 
1948. The bone and joint lesions are characterized 
by multiple areas of localized necrosis in the bone 
and joint surfaces and are believed to be the result 
of air emboli {2062 and 2064). Examination of per- 
sons who work in compressed air shows a high inci- 
dence of skeletal lesions {2079). These are often 
extensive and multiple, and in some instances are 
bilateral. As mentioned above, they often occur in 
divers or caisson workers who have never had symp- 
toms of bends. Their high incidence in divers and 
caisson workers leaves little doubt in the mind of 
Pugh {2079) that they are the direct result of 
exposure to decompression. The lesions are most 
frequently found in the long bones, usually of the 
lower extremity. Hands and feet are spared. The 
lesions involve the distal ends of the shaft and per- 
haps the epiphyseal portion of the bone. At first, the 
lesion consists merely of a region of rarefaction 
which represents an aseptic necrosis of the cancel- 
lous portion of the bone. As healing takes place, 
there is replacement of the necrotic bone by new 
bone which is irregular in architecture and is of 
greater density than normal. The lesion is often well 
circumscribed from the surrounding normal bone 
by a zone of calcification and ossification at the 
periphery of the lesion. In some cases, the central 
portion remains rarefied, but usually the entire lesion 
becomes irregularly calcified. When the end of the 
bone is affected, the changes are greater than those 
involving the diaphysis. Aseptic necrosis involves the 
articular surface and is accompanied by devitaliza- 
tion of the articular cartilage. Infarction through 
the articular surface takes place, and the surface 
becomes irregular and rough. The bone beneath the 
articular surface becomes rarefied in places with 
spotty zones of increased density. As revasculariza- 
tion occurs, the affected bone becomes more rare- 
fied and is abnormally soft so that, with weight bear- 
ing, deformity results. The final appearance in a 
weight-bearing joint is one of secondary osteo- 
arthritis. Because the lesions are often symmetrical 
it is only by the recognition of areas of old dia- 
physeal infarction or knowledge that the patient 
has been a caisson worker or diver that the changes 
in the joint can be distinguished from primary osteo- 
arthritis. 
A number of case histories are given in which 
bone and joint complications were significant. In 
1941, de La Marnierre {2069) reported three cases 2060-2065 
DISEASES AND ACCIDENTS 
with bony and articular complications. The first 
case was that of a 26-year-old man who had been 
working in caissons for 3 years. He complained of 
pain in his limbs half an hour after leaving the 
chamber. He returned some months later with pain 
and partial immobilization of his legs. When ex- 
amined in the hospital about a year later, he still 
showed limitation of movement of the left leg. X-ray 
revealed clearly a necrosis at the level of the inferior 
part of the head of the femur. A second X-ray taken 
3 years subsequently showed extension of the lesion. 
The second case is that of a man of 42 who had 
worked in caissons since 1938 and who presented 
himself to the clinic with painful rheumatism. In 
1939, after working for 5 hours in a caisson, he de- 
veloped symptoms half an hour after decompres- 
sion. These included vertigo, excessive perspiration, 
and pain in the legs, particularly the hip. The pa- 
tient returned to work in 15 hours. Six months 
later, he returned after having been injured by a 
winch. The pain of the left thigh persisted. On 
examination about 18 months later, the patient was 
walking with difficulty. There was limitation in the 
movement of the hip joint. X-rays revealed chronic 
lesions of the head of the left femur. The third case 
was that of a 42-year-old man who had worked in 
caissons for 2 years. In June 1939, he had a violent 
crisis with pain in the legs, more accentuated in 
the lower left leg, thigh, hip, and elbow. The pain 
appeared 2*4} hours after leaving the chamber. One 
month later, he was still complaining of pain in the 
left hip region. The lesions appeared in the superior 
part of the head of the femur. 
Wertheimer and Mansuy (2082) 1941-42 re- 
ported the case of a 34-year-old patient who ap- 
peared for the first time in the hospital for an 
abscess of the right big toe. The patient returned 
2 years later, suffering from a painful toe with ul- 
ceration. X-rays showed arthritic lesions and the 
toe was amputated. On return to the hospital 6 
months later, the patient had a pain in his left hip. 
He stated that he had had hip pain 8 years pre- 
viously after exposure to decompression in caissons. 
There was no history of syncope, abdominal pain, 
respiratory symptoms, or hemorrhages. The patient 
had blamed the pain on the caisson work and had 
stopped work 3 months after the onset of the symp- 
toms. On examination, there was a limitation of 
movement of the left hip and X-rays showed a con- 
siderable deformity of the head of the femur, the 
internal part being very dense and compact. The 
articular areas were deformed. Osteophytes were 
seen at the inferior part of the articulation. 
Guillain and Crossiord (2065) 1943 reported the 
case of a 34-year-old patient who presented him- 
self to the clinic in 1940 with a history of having 
worked in a caisson for 3 years. On his first trip into 
the caisson he worked for 8 hours at 2/2 atmos- 
pheres. On decompression he was surfaced too rap- 
idly and bled through the nose and ears. One-half 
hour after coming out of the caisson he had extreme 
pain in his extremities, particularly in the shoulders. 
The patient complained of insomnia and joint pain. 
The patient was seen 8 months later with pain in 
the right shoulder and left tibia, and soon after 
with pain in the opposite members. Six months 
subsequently, he was seen again and was unable to 
work. Examination 4 months later revealed further 
limitation of joint movement. X-rays of the glenoid 
fossa and surrounding bone showed pathological 
changes. The inferior part of the articulation ap- 
peared healthy, but the superior part was nipped 
and there was bony erosion. The head of the hu- 
merus was flattened and atrophied. The lesions in 
this case were not attributed to gaseous arterial 
embolism but to liberation of gas bubbles in the 
bone marrow. Such bubbles may be liberated, ac- 
cording to authors, in a region of poor circulation, 
diminishing the chance of resorption and producing 
a necrotic lesion. 
Mazel and Bourret (2071) 1945 have listed 2 
case histories, one a man of 33 and the other of 34. 
In both of these cases, X-rays revealed decalcified 
areas in the bone. Fischgold, Coville, and Doassans 
(2063) 1948 presented a case in which radiological 
evidence of alterations in osseous tissue was ob- 
tained 2 years after the decompression sickness 
episode. 
For other studies of pathological lesions in de- 
compression sickness, the reference list below may 
be consulted. 
2060. Alamercery, D. Les osteo-arthropathies des ou- 
vriers travaillant dans les caissons a air comprime. These 
(med.) Lyon, Bose and Riou, 1945, 60 pp. Arch. mal. 
prof., 1946, 7: 317-318. Abstr. 
2061. Bourret, J., P. Fraisse, and H. Fraisse, La mala- 
die des caissons: contribution k 1’etude des lesions osteo- 
articulaires des tubistes. Arch. mal. prof., 1948, 9: 309- 
311. [CH] 
2062. Brailsford, J. F. Caisson disease, pp. 648—649 in: 
The radiology of bones and joints. Baltimore, Williams & 
Wilkins Co., 1948, 760 pp. [D] 
2063. Fischgold, H., R. Coville, and P. Doassans. Al- 
teration chronique des epiphyses dans la maladie des 
caissons. J. Radiol. Electrol., 1948, 29: 230-231. [CH] 
2064. Genschickter, C. F. and M. M. Copeland. Caisson 
disease, p. 783 in: Tumors of hone. Philadelphia, J. B. 
Lippincott, 1949, 810 pp. [D] 
2065. Guillain, 6. and A. Grosslord. L’osteo-arthrite 
de la “maladie des caissons.” Paris mid., 1943, 33 • 329- 
333. [CH] DECOMPRESSION SICKNESS—PREVENTION AND TREATMENT 
2066-2086 
2066. Hare, C. C. Compressed air illness (Caisson dis- 
ease). pp. 675-680 in: Injuries of the brain and spinal 
cord and their coverings. Edited by Samuel Brock. Third 
edition. Baltimore, Williams & Wilkins Co., 1949, 783 pp. 
2067. Haymaker, W. and C. Davison. Fatalities result- 
ing from exposure to simulated high altitudes in decom- 
pression chambers. A clinicopathologic study of five cases. 
J. Neuropath, exp. Neurol, 1950, 9: 29-56. Abstr. World 
Med., 1950, 8: 93. [GH] 
2068. Herget, ( ). Gelenkveranderungen bei Tauchern. 
Klin. Wschr., 1948, 26: 288. [CH] 
2069. La Marnierre, P. de. and A. Salann. Compli- 
cations osseuses et articulaires de la maladie des caissons. 
J. Chir., Paris, 1941,57: 40-49. [R] [CH] 
2070. La Marnierre, P. de, and A. Salann. A propos des 
lesions osteo-articulaires de la maladie des caissons. Pr. 
mid., 1944, 52: 248-249. [CH] 
2071. Mazel, P. and J. Bourret. Osteo-arthropathies 
consecutives au travail dans Fair comprime. /. med. Lyon, 
1945, 26: 55-61. [CH] 
2072. Michelis, F. de. Lee altarazioni dell’apparato 
masticatorio nei lavatori dei cassoni. Rass. med. indust., 
1951, 20: 151-158. 
2073. Molfino, F. Contribute alia diagnostica differen- 
ziale dell’osteoartrosi cronica da malattia dei cassoni. Rass. 
med. indust., 1950, 19: 274-275. 
2074. Molfino, F. Contribution au diagnostic differen- 
tiel de Fosteoarthrite chronique, consequence de la maladie 
des caissons. Arch. mal. prof., 1951, 12: 271—274. [CH] 
2075. Molfino, F. and G. Balestra. L’osteonecrose asep- 
tique et Fosteorthrose de la maladie des caisson. Arch, 
mal. prof., 1950, 11: 411-412. Abstr. [D] 
2076. Mouchet, A., and A. Mouchet. Les lesions des os 
et des articulations dans la “maladie de caissons.” Pr. 
mid., 1941, 49: 670-673. [R] 
2077. Nicolas, M. Notions nouvelles sur la maladie de 
Fair comprime et son traitement dans le travail en tube 
caissons. Med. usine., 1949, 11: 321—328. Arch. mal. prof., 
1950, 11: 411. Abstr. [D] 
2078. Niconlaud, M. D. M. La maladie des caissons a 
forme d’arthrite de la hanche. These (med.), Paris, 1940, 
75 pp. 
2079. Pugh, D. G. Caisson disease, pp. 227-230 in: 
Roentgenologic diagnosis of diseases of bones. New York, 
Thomas Nelson and Sons, 1951, 316 pp. [D] 
2080. Raymond, M. V. Les osteo-arthrites pneumatiques. 
Lesions osseuses des tubistes et des scaphandriers. Arch, 
mal prof., 1948, 9: 437—442. [R] 
2081. Thomas, S. F. and 0. L. Williams. High-altitude 
joint pains (bends): their roentgenographic aspects. 
Radiology, 1945, 44: 259—261. 
2082. Wetheimer, P. and L. Mansuy. Troubles tro- 
phiques des orteils, arthrite chronique de la hanche et 
maladie des caisson. Lyon chir., 1941-1942, 37: 26-29. 
[CH] 
G. PREVENTION AND TREATMENT OF DECOMPRES- 
SION SICKNESS, INCLUDING PRESELECTION 
TESTS 
1. GENERAL STUDIES 
A comprehensive review of the literature dealing 
with prevention and treatment of decompression 
sickness up to 1 January 1946 is to be found on 
pages 260 to 300 of the first volume of this Source- 
book. The sections that follow in the present volume 
are not designed to reevaluate the material already 
published in the first volume but are planned to 
provide a guide to newer literature. For general 
considerations of prevention and treatment, refer- 
ences 2084, 2085, and 2086 are especially useful. 
2083. Gray, J. S. The effects of pressure breathing on 
decompression sickness and circulatory reaction in cadets. 
U. S. AAF. Randolph Field, Tex., School of aviation medi- 
cine. Project 248, Kept. no. 1, 15 March 1944, 8 pp. [P] 
2084. Huston, J. W. and W. J, Alexander. Diving at 
U. S. Naval Torpedo Station, Newport, R. I. Nav. med. 
Bull, Wash., 1946, 46: 348-352. 
2085. IT. S. Navy. BuMed. Deep-sea diving, pp. 213- 
226 in; A manual of naval hygiene. Washington, D. G., 
Government Printing Office, 1943, 340 pp. 
2086. IT. S. Navy. BuNavPers. Lecture on (B) com- 
pressed air illness, pp. 74—80 in: Submarine medicine 
practice. NavPers 10838, March 1949, 182 pp. [D] 
2. DECOMPRESSION PROCEDURES 
The reader may consult references 2089 and 2090 
for description of the decompression tables in use 
in the U. S. Navy. Figure 1 reproduces the decom- 
pression table for air dives taken from the U. S. 
Navy Diving Manual 1943 which is in current use. 
This figure gives depths from 40 feet to 300 feet 
for various exposure times in minutes. For each 
particular depth at a given time from leaving the 
surface to beginning of ascent, stops at different 
depths in minutes are set forth. 
Surface decompression is also described in items 
2089 and 2090, and Van Der Aue, Kellar, Brinton, 
Barron, Gilliam, and Jones {2091) 1951 have re- 
ported calculations and tests of decompression tables 
for air dives employing the procedure of surface 
decompression and the use of oxygen. These authors 
point out that the average total times of decompres- 
sion using tables which they have derived is about 
45 percent less than that necessary with the current 
air surface decompression procedure. Oxygen was 
administered at 40 feet instead of 50 feet because of 
some cases of nausea. In many instances, bends 
symptoms would rapidly disappear when the diver 
was recompressed to 40 feet to receive oxygen de- 
compression only to reappear or lead to additional 
symptoms after final decompression was completed. 
This was attributed to “silent” bubble formation 
which occurs as a result of a supersaturation of the 
tissues during this critical period of the dive. The 
authors therefore recommended a recalculation to 
correct defective tables using decompression ratios 
which offer deeper and longer water stops (see 
fig. 2). DISEASES AND ACCIDENTS 
For British {2087), French {2088), and Swedish 
{2092) comments on decompression procedures, 
papers by Davidson, Sutton, and Taylor {2087) 
1950; Tailliez, Dumas, Cousteau, Alinat, and De- 
villa {2088) 1949; and von Dobeln {2092) 1948 
should be consulted. 
Figure 1.—Decompression table (Air) (U. S. Navy Diving Manual—1943). 
Depth 
up 
to— 
Time from 
leaving 
surface to 
beginning 
of ascent 
Stop at 
different 
depths in 
minutes 
Depth 
up 
to— 
Time from 
leaving 
surface to 
beginning 
ofascent 
Stop at 
different 
depths in 
minutes 
Depth 
up 
to— 
Time from 
leaving 
surface to 
beginning 
ofascent 
Stop at different depths in minutes 
Feet 
Minutes 
30' 
20' 
10' 
Feet 
Minutes 
40' 
30' 
20' 
10' 
Feet 
Minutes 
90' 
80' 
70' 
60' 
50' 
40' 
30' 
20' 
10' 
40 
120 
0 
100 
25 
0 
160 
15 
9 
40 
180 
2 
100 
40 
12 
160 
34 
27 
28 
40 
240* 
4 
100 
60 
18 
16 
160 
45* 
17 
28 
43 
40 
300 
6 
100 
75 
27 
21 
160 
75 
3 
19 
23 
34 
68 
100 
85* 
6 
28 
21 
50 
78 
0 
100 
90 
8 
27 
24 
170 
15 
11 
50 
120 
2 
100 
120 
17 
28 
48 
170 
30 
24 
27 
SO 
150 
5 
170 
40* 
19 
28 
46 
50 
190*.. 
9 
no 
20 
0 
170 
75 
9 
19 
23 
38 
68 
50 
300 
12 
no 
35 
12 
no 
55 
22 
21 
185 
15 
25 
60 
55 
0 
no 
75* 
14 
27 
37 
185 
26 
24 
37 
60 
75 
2 
no 
105 
2 
22 
29 
50 
185 
35* 
19 
28 
46 
60 
110 
13 
185 
65 
18 
18 
23 
37 
65 
51 
60 
150* 
5 
15 
120 
18 
0 
60 
180 
7 
16 
120 
30 
11 
200 
15 
32 
60 
210 
8 
18 
120 
45 
18 
21 
200 
23 
23 
37 
120 
65* 
13 
28 
32 
200 
35* 
22 
28 
46 
70 
43 
0 
120 
100 
5 
22 
27 
69 
200 
60 
5 
18 
18 
23 
37 
65 
51 
70 
60 
4 
70 
75 
13 
130 
15 
0 
210 
15 
35 
70 
90 
4 
16 
130 
35 
11 
15 
210 
30* 
5 
16 
28 
40 
70 
120* 
13 
16 
130 
52 
6 
28 
28 
210 
55 
6 
18 
18 
23 
37 
65 
51 
70 
150 
18 
21 
130 
60* 
13 
28 
28 
70 
180 
2L 
32 
130 
90 .. 
9 
22 
28 
69 
225 
15 
6 
35 
225 
27* 
22 
26 
35 
48 
80 
35 
0 
140 
15 
4 
225 
60 
13 
18 
18 
23 
47 
65 
83 
80 
50 
6 
140 
30 
8 
21 
80 
70 
6 
16 
140 
45 
5 
27 
27 
250 
15 
17 
37 
80 
100 
20 
16 
140 
55* 
15 
28 
32 
250 
25* 
2 
23 
26 
35 
51 
80 
115* 
22 
26 
140 
85 
14 
22 
32 
69 
250 
50 
12 
14 
17 
19 
29 
49 
65 
83 
80 
150 
28 
29 
150 
15 ... 
7 
300 
12 
20 
37 
90 
30 
0 
150 
30 
13 
21 
300 
20 
9 
23 
26 
35 
51 
90 
45 
6 
150 
38 
28 
30 
300 
45 
6 
14 
15 
17 
18 
31 
49 
65 
83 
90 
60 
9 
16 
150 
50* 
16 
28 
32 
90 
75 
18 
14 
150 
80 
18 
23 
32 
68 
90 
95* 
2 
27 
21 
Note.—*Optimum exposure 
time. 
90 
130 
9 
27 
29 
Rate of ascent 
not 
to exceed 25 feet 
per minute. 
[168] DECOMPRESSION SICKNESS—PREVENTION AND TREATMENT 
1** 
Depth 
in feet 
2** 
Time 
•j** 
Time (min.) at 
water stops 
breathing air at— 
4** 
Time 
(min.) at 
40'cham- 
ber stop 
oxygen 
6** 
■j** 
Approxi- 
mate total 
decom- 
pression 
time 
(min.) 
Depth 
in feet 
2** 
Time 
3** 
Time (min.) at 
water stops 
breathing air at— 
4** 
Time 
(min.) at 
40'cham- 
ber stop 
oxygen 
6** 
•j** 
Approxi- 
mate total 
decom- 
pression 
time 
(min.) 
60' 
50' 
40' 
30' 
60' 
50' 
40' 
30' 
70 
52 
0 
0 
0 
0 
0 
3 
120 
70 
0 
0 
0 
4 
39 
54 
70 
90 
0 
0 
0 
0 
15 
24 
120 
80 
0 
0 
0 
5 
46 
62 
*70 
120 
0 
0 
0 
0 
23 
32 
120 
90 
0 
0 
3 
0 
51 
72 
70 
150 
0 
0 
0 
0 
31 
40 
120 
100 
0 
0 
6 
15 
54 
86 
70 
180 
0 
0 
0 
0 
39 
48 
130 
15 
0 
0 
0 
0 
7 
5 
80 
40 
0 
0 
0 
0 
0 
3 
130 
30 
0 
0 
0 
0 
12 
23 
80 
70 
0 
0 
0 
0 
14 
23 
130 
40 
0 
0 
0 
0 
21 
32 
80 
85 
0 
0 
0 
0 
20 
G 
29 
130 
50 
0 
0 
0 
3 
29 
G 
43 
80 
100 
0 
0 
0 
0 
26 
bO 
35 
*130 
60 
0 
0 
0 
5 
37 
GO 
53 
*80 
115 
0 
0 
0 
0 
31 
X 
X 
40 
130 
70 
0 
0 
0 
7 
45 
* 
63 
80 
130 
0 
0 
0 
0 
37 
o 
46 
130 
80 
0 
0 
6 
7 
51 
o 
76 
80 
150 
0 
0 
0 
0 
44 
txo 
•S 
53 
130 
90 
0 
0 
10 
12 
56 
.sf 
90 
90 
32 
0 
0 
0 
0 
0 
oi 
4 
140 
13 
0 
0 
0 
0 
0 
■M 
<L> 
6 
90 
60 
0 
0 
0 
0 
14 
V-i 
PQ 
24 
140 
25 
0 
0 
0 
0 
11 
23 
90 
70 
0 
0 
0 
0 
CD 
<u 
20 
jj 
30 
140 
30 
0 
0 
0 
0 
s 
w 
15 
JJ 
27 
90 
80 
0 
0 
0 
0 
p 
25 
3 
35 
140 
35 
0 
0 
0 
0 
p 
G 
20 
-a 
32 
*90 
90 
0 
0 
0 
0 
30 
£ 
40 
140 
40 
0 
0 
0 
2 
s 
24 
£ 
38 
90 
100 
0 
0 
0 
0 
34 
<D 
44 
140 
45 
0 
0 
0 
4 
29 
U 
45 
90 
110 
0 
0 
0 
0 
39 
. ci 
MH 
49 
140 
50 
0 
0 
0 
6 
33 
U 
51 
90 
120 
0 
0 
0 
0 
o 
43 
3 
53 
*140 
55 
0 
0 
0 
7 
<u 
u 
38 
P 
CO 
57 
90 
130 
0 
0 
0 
0 
u 
X 
48 
o 
58 
140 
60 
0 
0 
0 
8 
X 
W 
43 
o 
63 
w 
U 
140 
65 
0 
0 
3 
7 
o 
48 
u 
70 
100 
26 
0 
0 
0 
0 
H 
0 
o 
4 
140 
70 
0 
2 
7 
7 
H 
51 
XI 
80 
100 
50 
0 
0 
0 
0 
4-> 
14 
a 
24 
b 
G 
100 
60 
0 
0 
0 
0 
z 
20 
-a 
30 
150 
11 
0 
0 
0 
0 
z 
0 
~G 
u 
6 
100 
70 
0 
0 
0 
0 
26 
36 
150 
25 
0 
0 
0 
0 
oi 
> 
13 
G 
25 
*100 
80 
0 
0 
0 
0 
> 
32 
42 
150 
30 
0 
0 
0 
0 
u 
aj 
18 
•M 
30 
100 
90 
0 
0 
0 
0 
*-> 
38 
<U 
O 
48 
150 
35 
0 
0 
0 
4 
s 
23 
39 
100 
100 
0 
0 
0 
0 
44 
tP 
54 
150 
40 
0 
0 
3 
6 
<u 
27 
Q 
49 
100 
110 
0 
0 
0 
0 
u 
49 
59 
150 
45 
0 
0 
5 
7 
. ci 
33 
rf 
58 
100 
120 
0 
0 
0 
3 
53 
a 
66 
*150 
50 
0 
2 
5 
8 
P 
38 
6 
o 
66 
CO 
£ 
150 
55 
2 
5 
9 
4 
44 
£ 
78 
no 
22 
0 
0 
0 
0 
0 
5 
4-i 
no 
40 
0 
0 
0 
0 
12 
G 
<u 
23 
160 
9 
0 
0 
0 
0 
0 
<L) 
U 
7 
no 
50 
0 
0 
0 
0 
19 
(S3 
30 
160 
20 
0 
0 
0 
0 
11 
< 
24 
no 
60 
0 
0 
0 
0 
26 
37 
160 
25 
0 
0 
0 
0 
16 
o 
29 
*110 
70 
0 
0 
0 
0 
33 
4-» 
P 
44 
160 
30 
0 
0 
0 
2 
21 
p 
35 
no 
80 
0 
0 
0 
1 
40 
• S 
52 
160 
35 
0 
0 
4 
6 
26 
49 
no 
90 
0 
0 
0 
2 
46 
il 
59 
160 
40 
0 
3 
5 
8 
32 
62 
no 
100 
0 
0 
0 
5 
51 
rsl 
67 
*160 
45 
3 
4 
8 
6 
38 
73 
no 
110 
0 
0 
0 
12 
54 
77 
* 
170 
7 
0 
0 
0 
0 
0 
7 
120 
18 
0 
0 
0 
0 
0 
5 
170 
20 
0 
0 
0 
0 
13 
26 
120 
30 
0 
0 
0 
0 
9 
20 
170 
25 
0 
0 
0 
0 
19 
32 
120 
40 
0 
0 
0 
0 
16 
27 
170 
30 
0 
0 
3 
5 
23 
44 
120 
50 
0 
0 
0 
0 
24 
35 
170 
35 
0 
4 
4 
7 
29 
58 
•120 
60 
0 
0 
0 
2 
32 
45 
*170 
40 
4 
4 
8 
6 
36 
73 
•These are the optimum exposure times for each depth which represent 
the best balance between length of work period, safety and amount of 
useful work for the average diver. Exposure beyond these times is 
permitted only under special conditions. 
••Notes on columns. 
Column 1. Depth—In feet, gage (art. 836). 
Column 2. Time—Interval from leaving the surface to leaving the bottom. 
Column 3. Water stops—Time spent at tabulated stops using air. 
If no water stops are required, use a 25-foot-per-minute rate of ascent 
to the surface. When water stops are required use a 25-foot-per-minute 
rate of ascent to first stop. Take an additional minute between stops. 
Use 1 minute for the ascent from 30 feet to the surface. 
Column 4. Surface interval—The surface Interval shall not exceed 
6 minutes and is composed of the following elements; 
(o) Time of ascent from the 30-foot water stop, or from 30 feet if no 
water stops are necessary, to the surface (1 minute). 
(6) Time on surface for landing the diver on deck and undressing 
(not to exceed 3IS minutes). 
(c) Time of descent in the recompression chamber from the surface 
to 40 feet (about Vi minute). 
Column 5. During the period while breathing oxygen, the chamber 
shall be ventilated as outlined in article 674. 
Column 6. Surfacing—Oxygen breathing during this 2-minute period 
shall follow the period of oxygen breathing tabulated in column 5 without 
interruption. 
Column 7. Total decompression time—This includes— 
(а) Time of ascent from bottom to first stop, or to 30 feet if no water 
stop is required, at 25 feet per minute. 
(б) Sum of tabulated water stops, column 2. 
(c) 1 minute between water stops. 
(d) Surface interval. 
(e) Time at 40 feet in recompression chamber, column 4. 
(/) Time of ascent, an additional 2 minutes, from 40 feet in the recom- 
pression chamber to the surface, column 5. 
The approximate Total Decompression Time may be shortened only 
be decreasing the time required to undress the diver on deck. 
Figure 2.—Surface decompression table using oxygen. 2087-2093 
DISEASES AND ACCIDENTS 
where it is probable that at least part of the in- 
creased respiratory effort is due to changes in tissue 
elasticity. Where respiratory obstruction exists in 
larger passages, there are good theoretical grounds, 
supported by experimental evidence, for expecting 
relief with helium. 
For information on the thermodynamic prop- 
erties of helium, a report by Norris and Akin {2103) 
1947 may be consulted. The effect of helium on 
gas exchange of mice has been discussed by Cook, 
South, and Young {2096) 1951. Greenspan {2099) 
1949 and {2100) 1950 has reported on the velocity 
and attenuation of sound in rarefied helium. 
The rationale for the use of helium-oxygen mix- 
tures in diving has been given on page 295 of the 
first volume of this Sourcebook. Consolazio {2095) 
1948 has reported an economical and uniform 
method of mixing oxygen and helium for diving use. 
Molumphy {2101 and 2102) 1950 has given tables 
for helium-oxygen decompression. In order to re- 
duce the incidence of oxygen intoxication, the oxy- 
gen stops have been moved up to 50 and 40 feet. 
Time to all stops for various depth dives and dura- 
tion has been computed. Tests of the helium-oxygen 
diving tables have been reported by Van Der Aue, 
Molumphy, Tacke, and Blockwick {2106) 1949. 
Block wick {2094) 1951 has given a detailed review 
of helium-oxygen diving. He points out that dives 
in excess of 150 feet on air are unsatisfactory be- 
cause of the impairment of the mental processes of 
the diver. This anesthetic effect is caused by the 
high partial pressure of nitrogen. A helium-oxygen 
mixture is an excellent breathing medium for dives 
to greater depths because the mental facilities are 
practically unimpaired. To keep the carbon dioxide 
concentration within acceptable limits, a ventila- 
tion rate of 1.5 to 4.0 cubic feet per minute is neces- 
sary. Provision of this amount of gas is impractical 
and expensive. This problem was partially solved 
by the use of a carbon dioxide absorbent used in 
conjunction with a venturi recirculating system 
which permitted the gas to be used over again. 
This system was limited to 350 feet because at 
greater depths the carbon dioxide exceeded 3 per- 
cent effective. The solution to this problem was the 
improvement of the efficiency of the recirculating 
system. It was found that the new circulating system 
reduced the effective carbon dioxide concentration 
by 43 percent. Dives have been made to 561 feet 
with the new venturi recirculating system with good 
results. 
For further reports on helium-oxygen diving, the 
following references may be consulted; 2097 and 
2105. 
2087. Davidson, W. M., B. M. Sutton, and H. J. Taylor. 
Investigation into the decompression tables. Report I. De- 
compression ratio for goats following long exposure and 
return to atmospheric pressure without stoppages. Appen- 
dix “A” by Case, R. A. M. Statistical analysis of the site 
of bends. Gt. Brit. RNPRG-MRC, UPS. R. N. P. 50/582, 
U. P. S. 110, D. P. 2, February 1950, 12 pp. [P] 
2088. Tailliez, P., F, Dumas, J. Y. Cousteau, J. Alinat, 
and F. Devilla. Tables de plongee du G. R. S. pp. 97-108 
in: La plongee en scaphandre. Paris, Elzevir, 1949, 119 pp. 
2089. U. S. Navy. BuNavPers. Lectures on (A) de- 
compression tables, pp. 69—74 in: Submarine medicine 
practice. Nav Pers 10838, March 1949, 182 pp. [D] 
2090. U. S. Navy. BuShips. Decompression tables, pp. 
78—81 in: Chapter 94. Salvage section II. Diving. 25 Jan- 
uary 1951, U. S. Government printing office, Washington, 
D. C., 1951,93 pp. 
2091. Van Der Aue, 0. E., B. J. Kellar, E. S. Brinton, 
G. Barron, H. D. Gilliam, B. J. Jones. Calculation and 
testing of decompression tables for air dives employing 
the procedure of surface decompression and the use of 
oxygen. U. S. Navy. Naval gun factory, EDU. Project 
NM 002 007, Kept. no. I, November 1951, 52 pp. [M] [P] 
2092. Dobeln, W., von. Surface decompression in deep 
diving. Acta physiol, scand., suppl., 1948, 53: 17. 
2093. Yarbrough, 0. D. Calculation of decompression 
tables. U. S. Navy. Naval gun factory, EDU. No date, 
46 pp. 
3. HELIUM-OXYGEN ADMINISTBATION 
Effect of respiratory gas density on resistance to 
respiratory gas flow in man has been investigated 
by Otis and Bembower {2103a) 1951. A comparison 
was made of the resistance to the respiratory gas 
flow in man breathing air, or an 80 percent helium- 
20 percent oxygen mixture, or oxygen in a low- 
pressure chamber at equivalent altitudes of 18,000 
and 36,000 feet. The results indicate that less 
alveolar pressure is required to produce a given 
velocity of gas flow when a person breathes the 
helium mixture at altitude than when he breathes 
air at ground level. Theoretical treatment of the 
data indicates that this effect is due to a decreased 
turbulence with the less dense gas. Specht, Marshall, 
and Spicknell {2104) 1950 have indicated that with 
helium-oxygen mixtures, respiratory flow is facili- 
tated. 
Since an 80 percent helium-20 percent oxygen 
mixture is less dense than air or pure oxygen, it has 
been used in the treatment of asthma. Doll {2098) 
1946 has reported the use of the helium-oxygen 
mixture in six cases of mild to severe asthma. Two 
of these patients were unable to tolerate respiration 
of the mixture through a B. L. B. mask. In the rest 
of the patients some improvement was noted com- 
parable to that obtained from 100 percent oxygen. 
The author considered that helium was not likely 
to be of great value in asthma, where the obstruc- 
tion is in the smallest respiratory passages and DECOMPRESSION SICKNESS—HYDROGEN-OXYGEN 
2094-2112 
2094. Blockwick, T. N. Helium-oxygen diving and the 
evaluation, redesign and testing of the helium-oxygen re- 
circulating system. Thesis, (Eng.), University of Mary- 
land, June 1951, 73 pp. 
2095. Consolazio, W. V. Preparation of compressed 
helium-oxygen gas mixtures. U. S. Navy. NMRI. Project 
NM Oil 015, Kept. no. 3, 17 January 1948, 11 pp. 
2096. Cook, S. E., E. E. South, Jr., and D. R. Young. 
Effect of helium on gas exchange of mice. Amer. J. Physiol., 
1951, 164: 248-250. [P] 
2097. Davis, R. H. Helium and oxygen in deep diving. 
The United States Navy oxy-helium tables, pp. 180-196 
in: Deep diving and submarine operations. A manual for 
deep sea divers and compressed air workers. London, The 
Saint Catherine Press, Ltd., 1951, 670 pp. [D] 
2098. Doll, R. Helium in the treatment of asthma. 
Thorax, 1946, 1: 30-38. 
2099. Greenspan, M. Attenuation of sound in rarefied 
helium. Physiol. Rev., 1949, 75: 197-198. 
2100. Greenspan, M. Propagation of sound in rarefied 
helium. /. acoust. Soc. Amer., 1950,22: 568-571. 
2101. Molumphy, G. G. Computation of helium-oxygen 
decompression tables. U. S. Navy. Naval gun factory, 
EDU. Project NS 186—201, Sub-task 4, Kept. no. 7—50, 
25 September 1950, 25 pp. [P] 
2102. Molumphy, G. G. He02 decompression tables. 
U. S. Navy. Naval gun factory, EDU. Project NS-186- 
201, Sub-task 4, Kept. no. 8-50. 26 September 1950, 26 pp. 
2103. Norris, R. H. and S. W. Akin. Thermal con- 
ductivity and viscosity of helium, supplement to the main 
report entitled “The thermodynamic properties of helium 
at high pressures and temperatures.” U. S. General Electric 
Company, Schenectady, N. Y. General Engineering and 
Consulting Laboratory, Kept. no. 55141—supplement, for 
Project Hermes, U. S. Army Ordnance, July 1947, 5 pp. 
2104. Specht, H., L. H. Marshall, and B. H. Spicknall. 
Effects of helium and altitude on respiratory flow patterns. 
J. appl. Physic!., 1950, 2: 363-372. 
2105. TJ. S. Navy, BuNavPers. Medical aspects and 
decompression procedures of diving with helium-oxygen, 
pp. 103—117 in: Submarine medicine practice. NavPers 
10838, March 1949, 182 pp. [D] 
2106. Van der Aue, 0. E., G. G. Molumphy, A. W. Tacke, 
and T. N. Blockwick, Tests of present He02 tables, the 
determination of C02 and 02 percentages at various stages 
of the dives and the comparison of the present venturi 
recirculation system with the revised type with special 
regard to the effective C02 concentration at depths ranging 
from atmospheric to 429'. U. S. Navy. Naval gun factory, 
EDU. Project NS 186-026, Kept. no. 13-49, 12 December 
1949, 16 pp. 
4. HYDROGEN-OXYGEN ADMINISTRATION 
Zetterstrom {2108) 1948 has devised an ingeni- 
ous method of diving with a gas mixture containing 
hydrogen instead of helium. This hydrogen must be 
mixed with oxygen in a proportion in which the 
partial pressure of oxygen will be sufficient for 
breathing. However, the gas mixture must be safe 
from explosion. It will not explode if the oxygen 
content is less than 4 percent, regardless of the 
hydrogen or nitrogen content. If the gas mixture 
contains 4 percent oxygen, the partial pressure of 
the oxygen will not suffice until a depth of 30 meters 
or more has been reached. The diver must descend 
to 30 meters with ordinary air and then change to 
the hydrogen-oxygen mixture. So as to have suf- 
ficient quantities of gases, these must be manu- 
factured aboard the vessel. By an ammonia-cracking 
process, a gas mixture containing 75 percent hydro- 
gen and 25 percent nitrogen can be evolved. By 
adding 4 percent oxygen to the mixture, the final 
composition of the resulting gas will be 72 percent 
hydrogen, 24 percent nitrogen, and 4 percent 
oxygen. The author used the gas mixture in dives 
to 40 meters, 110 meters, and 160 meters. It was 
found at 110 meters that respiratory resistance was 
small and the narcotic effect of nitrogen negligible. 
An evaluation of hydrogen-oxygen diving in the pre- 
vention of decompression sickness and nitrogen 
narcosis has been given by Bjurstedt and Severin 
{2107) 1948. 
2107. Bjurstedt, H. and G. Severin. The prevention of 
decompression sickness and nitrogen narcosis by the use 
of hydrogen as a substitute for nitrogen (the Arne Zetter- 
strom Method for deep-sea diving). Milit. Surg., 1948, 
103: 107-116. 
2108. Zetterstrom, A. Deep-sea diving with synthetic 
gas mixtures. Milit. Surg., 1948, 103: 104-106. /. industr. 
Hyg., 1949, 31: abstract section: 23-24. 
5. OXYGEN ADMINISTRATION 
Preoxygenation has been shown to be valuable in 
the prevention of decompression sickness in flying 
and in decompression chambers. Breathing oxygen 
acts by washing out nitrogen from the body. The 
following references on this topic have been se- 
lected: 2110, 2114, 2115, 2120, 2121, 2122, 2123, 
2124,2125,2126, 2127,2128,2129,2132,2135, and 
2139. It has also been found that oxygen inhalation 
reduces abdominal distension in flying by removal of 
nitrogen from the alimentary tract. 
For further studies on the physiological effects 
of oxygen, the references given below may be 
consulted. 
2109. Alella, A. and E. Meda. Frequenza cardiaca du- 
rante la respirazione di 02 nell’ uomo ed importanza del 
vago. Boll. Soc. ital. Biol, sper., 1948, 24: 581-582. 
2110. Bateman, J. B .Review of data on value of pre- 
oxygenation in prevention of decompression sickness, pp. 
242—277 in: Decompression sickness. Caisson sickness, 
diver’s and flier’s bends and related syndromes. Edited by 
J. F. Fulton for the Subcommittee on decompression 
sickness, National Research Council. Philadelphia, W. B. 
Saunders Co., 1951, 437 pp. [D] 
2111. Berger, L. B. and S. J. Davenport. Effects of the 
inhalation of oxygen. U. S. Bureau of mines. Information 
circular 7575, July 1950, 36 pp. [R] 
2112. Beznak, A. B. L. and G. liljestrand. The effect 
of variations in oxygen tension on the lymph flow. Acta 
physiol, scand., 1949, 19: 170—186. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1950, 3: 1075. 2113-2139 
DISEASES AND ACCIDENTS 
2113. Campbell, A. and E. P. Poulton. Decompression 
after deep-sea diving, pp. 45-46 in: Oxygen and carbon 
dioxide therapy. London, Oxford University Press, 1938, 
202 pp. 
2114. Clarke, R. W., F. D. Humm, and L. F. Nims. The 
efficacy of preoxygenation in the prevention of decom- 
pression sickness. U. S. NRG-CAM. C. A. M. rept. no. 31, 
4 November 1944, 5 pp. 
2115. Clarke, R. W., F. D. Humm, and L. F. Nims. The 
efficacy of preflight denitrogenation in the prevention of 
decompression sickness. U. S. NRG-CAM. OEMcmr-38, 
C. A. M. rept. no. 472, 5 September 1945, 13 pp. 
2116. Comroe, J. H. and P. Walker. Normal human 
arterial oxygen saturation determined by equilibration with 
100 percent Oz in vivo and by the oximeter. Amer. J. 
Physiol, 1948, 152: 365-371. [P] 
2117. Fasciolo, J. C. and H. Chiodi. Arterial oxygen 
pressure during pure 02 breathing. Amer. J. Physiol, 1946, 
147: 54-65. [P] 
2118. Fowler, W. S. and J. H, Comroe, Jr. The rate of 
increase of arterial oxygen saturation following inspira- 
tion of 100 percent oxygen. Fed. Proc. Amer. Soc. exp. 
Biol, 1947, 6: 104. [P] 
2119. Fowler, W. S. and J. H. Comroe, Jr. Lung func- 
tion studies. I. The rate of increase of arterial oxygen 
saturation during the inhalation of 100 percent 02 J. din. 
Invest., 1948, 27: 327-334. [P] 
2120. Gray, J. S. The effect of varying periods of deni- 
trogenation on aeroembolism in cadets. U. S. AAF. Ran- 
dolph Field, Tex. School of aviation medicine. Project 
164, Rept. no. 1, 17 June 1943, 7 pp. [P] 
2121. Gray, J. S. The effect of varying periods of deni- 
trogenation on aeroembolism in cadets. U. S. NRG- 
CAM. C. A. M. rept. no. 168, 17 June 1943, 7 pp. [P] 
2122. Gray, J. S. Effect of denitrogenation at various 
altitudes on aeroembolism in cadets. U. S. NRG-CAM. 
C. A. M. rept. no. 258, 5 January 1944, 7 pp. 
2123. Gray, J. S. and S. C. F. Mahady. The prevention 
of aeroembolism in cadets at 45,000 feet by denitrogena- 
tion. U. S. AAF. Randolph Field, Tex. School of aviation 
medicine. Project 252, Rept. no. 1, 29 March 1944, 7 pp. 
[P] 
2124. Gray, J. S., S. C. F. Mahady, and R. L. Masland. 
Studies on altitude decompression sickness. III. The ef- 
fects of denitrogenation. /. Aviat. Med., 1946,17: 606-610. 
[P] 
2125. Henry, F. M. and S. F. Cook. Effectiveness of 
pre-flight oxygen breathing in preventing decompression 
sickness. /. Aviat. Med., 1945, 16: 350-355. [P] 
2126. Henry, F. M., S. F. Cook, E. Strajman, and D. W. 
Lund. Effectiveness of preflight oxygen breathing in pre- 
venting decompression sickness. U. S. NRG-CAM, 
C. A. M. rept. no. 384, 30 October 1944, 17 pp. 
2127. Jones, H. B. Preoxygenation and the rate of nitro- 
gen elimination with regard to decompression sickness. 
U. S. NRG-CAM. OEMcmr-196, C. A. M. rept. no. 491, 
October 1945, 3 pp. [P] 
2128. Karel, L. and R. E. Weston. Femoral arterial 
and venous blood nitrogen content of dogs during 
denitrogenation by continuous oxygen inhalation. Fed. 
Proc. Amer. Soc. exp. Biol, 1947, 6: 342-343. [P] 
2129. Karel, L. and R. E. Weston. Nitrogen content of 
femoral arterial and venous blood in anesthetized dogs 
denitrogenated by continuous inhalation of 99.6 percent 
oxygen. Amer. J. Physiol, 1947, 151: 71-79. 
2120. Kline, R. F. Effects of severe anoxia and their 
amelioration. Fed. Proc. Amer. Soc. exp. Biol., 1947, 6: 
143-144. 
2131. Linde Air Products Company. Bibliography on 
oxygen therapy. Revised edition. Linde Air Products Go., 
New York, N. Y., 1947, 99 pp. [B] 
2132. McGoldrick, T. A., J. F. Lally, and L. L. Largby. 
Influence of demand and air dilutor demand oxygen sys- 
tems used from sea level on the incidence of bends. U. S. 
Navy. NATO, Pensacola, Fla. School of aviation medicine. 
Project X-201 (Av-R6-6), Kept. no. I, 2 November 
1943,3 pp. [P] 
2133. Meda, A. and A. Allella. Diminuzione del volume- 
minuto nella respirazione di oxygen. Richerche nell’uomo. 
Boll. Soc. ital. Biol, sper., 1948, 24: 492-493. 
2134. Miller, A. T., Jr. The influence of oxygen admin- 
istration on the cardiovascular response to exercise. Fed. 
Proc. Amer. Soc. exp. Biol., 1948, 7; 81. [P] 
2135. Murray, G. D. Effect of preoxygenation on resist- 
ance to decompression illness. U. S. Navy. NATC, Pensa- 
cola, Fla. School of aviation medicine. Project X—141 (Av- 
R6-4), 26 March 1943, 7 pp. [P] 
2136. Nahas, G. G. and E. H. Morgan. Direct measure- 
ments of alveolar-arterial differences in oxygen tension in 
man breathing 100% oxygen. Fed. Proc. Amer. Soc. exp. 
Biol., 1951, 10: 96. 
2137. Pogrund, R. S. and F. R. Steggerda. Studies on 
the removal of gas from the colon by oxygen inhalation. 
J. industr. Hyg., 1949, 31: abstract section: 84-85. [P] 
2138. Preston, S. N. and N. K. Ordway. Observations 
of arterial oxygen content in children during the inhala- 
tion of air and 100 percent oxygen. Amer. J. Physiol., 
1948, 152: 696-702. [P] 
2139. Weston, R. E. and L. Karel. The influence of 
denitrogenation on the response of anesthetized dogs to 
intravenously injected oxygen. /. din. Invest., 1947, 26: 
837-848. [P] 
6. RECOMPRESSION TREATMENT AND PROCEDURES 
For basic information on the treatment of decom- 
pression sickness by recompression, papers by the 
following should be consulted: U. S. Navy, BuShips 
{2140) 1951, Van Der Aue, Duffner, and Behnke 
{2141) 1947, and Van Der Aue, Hayter, Brinton, 
Kellar, and Behnke {2142) 1945. 
In figure 3 are given the treatment tables for use 
in the recompression treatment of caisson disease 
and air embolism. The figure shows in tables 1 and 
1A the decompression schedule in the case of those 
suffering with bends pain in which the pain is re- 
lieved at recompression depths less than 66 feet. 
Tables 2 and 2A (of fig. 3) are used if the pain is 
relieved at recompression depths greater than 66 
feet. If pain does not improve within 30 minutes at 
165 feet, the case is probably not bends. The victim 
should be decompressed on table 2 or 2A. Table 3 
and table 4 (of fig. 3) are for use with serious 
symptoms, including unconsciousness, convulsions, 
weakness, or inability to use the arms or legs, any 
visual disturbances, dizziness, loss of speech or hear- 
ing, or severe shortness of breath or chokes. Table 3 DECOMPRESSION SICKNESS—RECOMPRESSION 
(of fig. 3) gives the decompression schedule in those 
cases where the symptoms are relieved within 30 
minutes at 165 feet. Table 4 (of fig. 3) is used in 
those cases where the symptoms are not relieved 
within 30 minutes at 165 feet. If the symptoms re- 
turn while breathing air during treatment with any 
of the tables given, the victim is to be recompressed 
to the depth of relief, but never less than a depth of 
30 feet and then is to be decompressed from this 
depth according to table 4. If symptoms reoccur fol- 
lowing treatment with any of the tables given in 
figure 3, the diver is to be recompressed to a depth 
giving relief. If relief occurs at depths less than 30 
feet, the diver is to be taken to 30 feet and decom- 
pressed from the 30-foot stop to the surface accord- 
ing to table 3 in figure 3. If relief occurs deeper 
than 30 feet, the diver is to be retained at the depth 
of relief for 30 minutes and then is to complete the 
remaining stops of table 3 of figure 3, using air 
throughout. 
Figure 3.—Treatment of caisson disease and air embolism (U. S. Navy Diving Manual—1952). 
Stops 
Bends—Pain only 
Serious symptoms 
Rate of Descent—25 ft. 
per min. 
Rate of Ascent—1 min- 
ute between stops. 
Pain relieved at depths 
less than 66 ft. 
Use Table 1-A if °2 is not 
available. 
Pain relieved at depths 
greater than 66 ft. 
Use Table 2-A if °2 is not 
available. 
If pain does not improve 
within 30 min. at 165 
ft., the case is probably 
not bends. Decompress 
on Table 2 or 2-A. 
Serious symptoms include any one of the following: 
1. Unconsciousness. 
2. Convulsions. 
3. Weakness or inability ot use arms or legs. 
4. Any visual disturbances. 
5. Dizziness. 
6. Loss of speech or hearing. 
7. Severe shortness of breath or chokes. 
Symptoms relieved 
within 30 minutes 
at 165 ft. Use 
Table 3. 
Symptoms not relieved within 
30 minutes at 165 ft. 
Use Table 4. 
Lbs. 
Ft. 
Table 1 
Table 1-A 
Table 2 
Table 2-A 
Table 3 
Table 4 
73.4 
165 
30 (Air). . 
30 (Air).... 
30 (Air) 
30 to 120 (Air). 
62.3 
140 
12 (Air). . 
12 (Air). . 
12 (Air) 
30 (Air). 
53.4 
120 
12 (Air). . 
12 (Air) 
12 (Air) 
30 (Air). 
44.5 
100 
30 (Air). . 
30 (Air) 
12 (Air). . 
12 (Air) 
12 (Air) 
30 (Air). 
35.6 
80 
12 (Air). . 
12 (Air)... . 
12 (Air). . 
12 (Air) 
12 (Air) 
30 (Air). 
26.7 
60 
30 (°2)*. . 
30 (Air) 
30 (°2)*.. 
30 (Air) 
30 (°2)* or (Air). . . 
6 hrs. (Air). 
22.3 
50 
30 (°2)* . 
30 (Air) . 
30 (°2)*.. 
30 (Air) 
30 (°2)* or (Air). . . 
6 hrs. (Air). 
17.8 
40 
30 (°2). . . 
30 (Air) 
30 (°2)... 
30 (Air) 
30 (°2) or (Air) 
6 hrs. (Air). 
13.4 
30 
60 (Air) 
60 (°2).. . 
2 hrs. (Air). . 
12 hrs. (Air) 
First 11 hrs. (Air), then 
1 hr. (°2) or (Air). 
8.9 
20 
60 (Air) 
2 hrs. (Air). . 
2 hrs. (Air) 
First 1 hr. (Air), then 
5 (°2). . . . 
1 hr. (°2) or (Air). 
4.5 
10 
2 hrs. (Air). . 
■5 (°2). . . . 
• 4 hrs. (Air). . 
2 hrs. (Air) 
First 1 hr. (Air), then 
1 hr. (°2) or (Air). 
Surface 
1 min. (Air). 
,1 min. (Air). 
1 min. (Air) 
1 min. (°2). 
TIME AT ALL STOPS IN MINUTES UNLESS OTHERWISE INDICATED 
If symptoms return while breathing air during treatment with any of the above tables, recompress to depth of relief but never less 
than a depth of 30 ft., and then complete decompression from this depth according to Table 4. 2140-2149 
DISEASES AND ACCIDENTS 
Some prime considerations in the recompression 
treatment of decompression sickness may be given. 
Experience has shown that failure to give treatment 
in doubtful cases is a frequent and important error. 
Another frequent error consists in delaying the re- 
compression procedure. It has been found in the 
past that the longer the delay the deeper the diver 
will have to be taken for relief of symptoms. Failure 
to treat the serious cases adequately according to 
table 3 or 4 of figure 3 is a serious error. In all cases, 
the treated diver should be kept near the chamber 
for a 24-hour period in case symptoms return. 
Bends symptoms may occasionally become tem- 
porarily worse if pressure is applied too rapidly. 
If this occurs, compression should be stopped mo- 
mentarily and the pressure then slowly raised at a 
rate which the diver can tolerate. In all cases, par- 
ticularly in serious cases with paralysis, the ability 
of the diver to stand up and walk the length of the 
chamber should always be tested. This test should 
be made routinely before the diver leaves the depth 
of relief of symptoms and also at the completion of 
the 30-foot stops. Additional treatment of bends 
symptoms includes first-aid measures. The patient 
should be lying down during the treatment to pre- 
vent, if possible, the movement of bubbles up into 
the brain. Again, it should be stressed that on the 
completion of treatment, the diver patient should 
always be kept near the chamber for not less than 
24 hours in order to treat any recurrences immedi- 
ately. When oxygen is administered in the treatment 
of decompression sickness, a fire hazard is always 
present. Smoking is prohibited and the chamber 
should be ventilated frequently to keep the oxygen 
concentration low. The highest concentration of 
oxygen, preferably above 95 percent, should be de- 
livered to the diver patient. The mask should be 
leakproof in order to make treatment tables effec- 
tive in the cases where oxygen is used. If possible, 
the oxygen should be humidified to avoid dryness 
of the nose and throat. Personnel giving treatment 
for recompression sickness using oxygen should al- 
ways be conscious of the possible development of 
oxygen intoxication. At maximum pressures of 
treatment, helium-oxygen mixtures (about 80-to-20 
ratio) may be used to advantage instead of air in 
all types of treatment. 
Tenders must always be present in the chamber 
with divers breathing oxygen. Tenders require 60 
minutes of oxygen during the last 60 minutes of the 
oxygen-therapy period outlined in tables 1 and 2 
of figure 3. If the diver is treated as outlined in 
tables 3 and 4 of figure 3, the tender will neces- 
sarily be subjected to the same treatment. Decom- 
pression for additional tenders who may subse- 
quently enter the decompression chamber for short 
periods will be carried out in accordance with the 
standard diving tables. 
2140. U, S. Navy. BuShips. Compressed air illness and 
treatment tables, pp. 81-85 in: Chapter 94. Salvage 
section II. Diving. U. S. Government Printing Office, 
Washington, D. C., 25 January 1951, 93 pp. 
2141. Van Der Aue, 0. E., G. J. Duffner, and A. R. 
Behnke. The treatment of decompression sickness: an 
analysis of one hundred and thirteen cases. /. industr. 
Hyg., 1947, 29; 359-366. 
2142. Van Der Aue, 0. E., W. A. White, Jr., R. Hayter, 
E. S. Brinton, R. J. Kellar, and A, R. Behnke. Physiologi- 
cal factors underlying the prevention and treatment of 
decompression sickness. U. S. Navy. NMRI. Project 
X-443, Kept. no. 1, 26 April 1945, 12 pp. 
7. DRUGS IN PREVENTION AND TREATMENT OF 
DECOMPRESSION SICKNESS 
During World War II, investigations were con- 
ducted to evaluate the use of various drugs in the 
prevention and relief of pain and other symptoms 
of decompression sickness. Such studies were vir- 
tually limited to decompression sickness of altitude. 
The references given below indicate the trends of 
these studies. 
2143. Comroe, J. H., Jr. The use of morphine and 
demerol for the relief of pain of bends. U. S. NRC-CAM. 
C. A. M. rept. no. 198, September 1943, 6 pp. [P] 
2144. Ivy, A. C., A. J. Atkinson, H. Adler, and W. 
Burkhardt. Pertaining to the effect of B2B (dextro- 
amphetamine) and of preoxygenation plus B2B on the 
incidence of “bends” and “incapacitating bends and 
chokes” at 40,000 ft. for 1 hour. U. S. NRC-CAM. 
C. A. M. rept. no. 113, 23 December 1942, 4 pp. [P] 
2145. Knisely, M. H. Methods and testing of therapeutic 
agents in relation to bends. U. S. NRC-CAM. OEMcmr- 
290, C. A. M. rept. no. 473, September 1945, 8 pp. [R] 
[P] 
2146. Knisely, M. H., S. Gray, H. M. Peck, R. L. 
Nichols, L. Warner, and J. A. Orcutt. Specific individual 
controls for some types of decompression experiments on 
human subjects. U. S. NRC-CAM. C. A. M. rept. no. 194, 
1 October 1943, 1 p. [P] 
2147. Knisely, M. H., S. Gray, H. M. Peck, R. L. 
Nichols, L. Warner, J. A. Orcutt, and N. Anderson. Pre- 
liminary tests of the effect of intravenous aminophyllin 
in preventing or alleviating bends and chokes. U. S. 
NRC-CAM. C. A. M. rept. no. 195, 1 October 1943, 7 pp. 
[P] 
2148. Ryder, H. W., G. L. Engel, J. Romano, J. P. 
Wehb, M. A. Blankenhorn, E. B. Ferris, and W. E. Brown. 
An assay of dextro-amphetamine for its protective value 
in decompression sickness. U. S. NRC-CAM. C. A. M. 
rept. no. 112, 28 January 1943, 6 pp. [P] 
2149. Williams, 0. L., W. R. Lyons, E. V. Bridge, and 
S. F. Cook. The use of drugs for the prevention of decom- 
pression sickness. J. Aviat. Med., 1946, 17: 602-605. [P] 
8. PRESELECTION TESTS 
As indicated in the references given below (2ISO- 
2171) , much time and effort has been expended on 
methods and procedures of evaluating differences EXPLOSIVE DECOMPRESSION—GENERAL STUDIES 
2150-2171 
in susceptibility to decompression sickness due to 
high altitude. Preselection tests have been devised 
by the use of which the incidence of decompression 
sickness in a preselected group of men is less than 
the incidence in an unselected group. The exact 
incidence in the selected group depends upon a 
number of factors including the type of test, pro- 
portion of men rejected, flight conditions, and pre- 
oxygenation, as well as diurnal and seasonal fluctua- 
tions in bends susceptibility. 
Regarding preselection of divers, high standards 
of physical fitness are paramount. Welham, Blanch, 
and Behnke {2171) reported in 1944 a procedure 
of selecting diving and aviation personnel resistant 
to decompression sickness based on tests in a low- 
pressure chamber. These and other preselection 
tests require further validation studies. 
2150. Gray, J. S. Symptoms experienced during re- 
peated low-pressure chamber flights, and their significance 
for high altitude classification. U. S. NRC-CAM. C. A. M. 
rept. no. 71, 1 July 1942, 5 pp. [P] 
2151. Gray, J. S. The reliability of procedures for high 
altitude classification. U. S. NRC-CAM. C. A. M. rept. 
no. 98, 5 November 1942, 4 pp. [P] 
2152. Grenell, R., F. D. Humjn, L. F. Nims, and H. M. 
Somherg. The reliability of the decompression subcommit- 
tee’s 90-minute preselection test. U. S. NRC-CAM. C. A. 
M. rept. no. 355, 5 September 1944, 4 pp. 
2153. Henry, F. The reliability of chamber classifica- 
tion for “bends” susceptibility and validity of the inert 
gas-exchange method. U. S. NRC-CAM. C. A. M. rept. 
no. 176, 2 September 1943, 10 pp. [P] 
2154. Henry, F. M. The relation of pain to impairment 
in motor function in decompression sickness. U. S. NRC- 
CAM. C. A. M. rept. no. 397, 15 December 1944, 6 pp. 
2155. Henry, F. M. Altitude pain. A study of individual 
differences in susceptibility to bends, chokes, and related 
symptoms. /. Aviat. Med., 1946, 17: 28-55. [P] 
2156. Henry, F. M., S. F. Cook, H. B. Jones, and E, 
Strajman, Decompression sickness classification tests at 
30.000 feet with preoxygenation and exercise, and at 
38.000 feet with light exercise. U. S. NRC-CAM. 
OEMcmr-196, C. A. M. rept. no. 454, July 1945, 2 pp. [P] 
2157. Henry, F. M., S. F. Cook, J. H. Lawrence, and 
D. W. Lund. Decompression sickness classification tests 
with leg exercise and combined arm-leg exercise. U. S. 
NRC-CAM. OEMcmr-196, C. A. M. rept. no. 446, July 
1945, 9 pp. 
2158. Henry, F. M., S. F. Cook, and D. W. Lund, An 
effective decompression sickness classification test, and a 
method for evaluating its usefulness. U. S. NRC-CAM. 
C. A. M. rept. no. 421, 24 February 1945, 14 pp. 
2159. Henry, F. M. and A. C. Ivy. Preselection tests, 
pp. 322-359 in: Decompression sickness. Caisson sickness, 
diver’s and flier’s bends and related syndromes. Edited by 
J. F. Fulton for the Subcommittee on decompression sick- 
ness, National Research Council. Philadelphia, W. B. 
Saunders Co., 1951, 437 pp. [D] 
2160. Henry, F. M., H. B. Jones, J. B. Mohney, and C. A. 
Tobias. The reliability of decompression chamber classi- 
fication using the step-up exercise, and the relation of 
inert-gas exchange and other factors to bends-resistance. 
U. S. NRC-CAM. C. A. M. rept. no. 264, 2 December 
1944, 16 pp. 
2161. Jones, H, B., C. Tobias, W. F. Loomis, J. B, Ma- 
honey, W. N. Sears, J. C. Larkin, J. G. Hamilton, and 
J. H. Lawrence. An objective method for the study of the 
physiology of aeroemphysema and for the selection of 
high altitude aircrew using the radioactive isotopes of 
inert gases. U. S. NRC-CAM. C. A. M. rept. no. 81, 
November 1942, 6 pp. [P] 
2162. Larrabee, M. G., J. C. Lilly, J. H. Comroe, Jr., 
and R. Hodes. Decompression sickness during exposures to 
38,000 feet, accompanied by exercise. Evaluation of a 
classification procedure. U. S. NRC-CAM. C. A. M. rept. 
no. 137, 9 June 1943, 20 pp. [P] 
2163. Nims, L. F. Decompression sickness selection tests 
using denitrogenation. Yale Aero-medical research unit, 
Rept. no. 43, 16 April 1945, 2 pp. 
2164. Robinson, T. W. High-altitude endurance tests. 
U. S. NRC-CAM. C. A. M. rept. no. 205, 10 August 
1943, 5 pp. [P] 
2165. Robinson, T. W, High-altitude tolerance tests. 
U. S. NRC-CAM. C. A. M. rept. no. 316, 12 May 1944, 
30 pp. [P] 
2166. Ryder, H. W., C. D. Stevens, J. P. Webb, and 
M. A. Blankenhorn. The measurement of decompression 
sickness. U. S. NRC-CAM. C. A. M. rept. no. 412, 15 
February 1945, 46 pp. [M] 
2167. Savely, H. E. High altitude classification tests. 
U. S. NRC-CAM. C. A. M. rept. no. 99, 31 October 
1942, 14 pp. [P] 
2168. Stevens, C. D., M. Inatome, H. W. Ryder, E. B. 
Ferris, and M, A. Blankenhorn. The rate of nitrogen 
elimination from the lungs and its relation to individual 
susceptibility to decompression sickness. U. S. NRC-CAM. 
OEMcmr—36, C. A. M. rept. no. 456, July 1945, 19 pp. 
2169. TJ. S. AAF. Wright-Patterson air force base. Day- 
ton, Ohio. Materiel command, ENG. Aero medical labora- 
tory. Preselection test for susceptibility to aeroembolism 
ENG-49-095-27, 30 March 1943, 9 pp. [P] 
2170. Walder, D. N. Serum surface tension and its rela- 
tion to the decompression sickness of aviators. J. Physiol., 
1948, 107: 43P—44P. Excerpta Medica. Section II. 
(Physiology, Biochemistry, and Pharmacology), 1949, 2: 
632. Abstr. 
2171. Welham, W., J. J. Blanch, and A. R. Behnke. 
A procedure for selection of diving and aviation personnel 
resistant to decompression sickness based on tests in a 
low-pressure chamber. U. S. Navy, Naval gun factory, 
EDU. Project X-338 (Av-191-h), January 1944, 5 pp. [P] 
IV. EXPLOSIVE DECOMPRESSION 
A. GENERAL STUDIES 
This section on explosive decompression has been 
included because some of the pathological effects of 
explosive decompression are similar to those pul- 
monary lesions found in escape accidents. Also, air 
embolism occurs in explosive decompression to high 
altitudes as in decompression sickness caused by too 
rapid ascent from pressures greater than 1 atmos- 
phere. In explosive decompression, there is generally 
a short initial rise of arterial blood pressure followed 
by a prolonged slowing of the heart and fall of ar- 
terial blood pressure in part due to decompression 2172-2179 
DISEASES AND ACCIDENTS 
effects and in part due to anoxia. There is a brief 
rise in cerebrospinal fluid pressure, paralleling the 
rise in intrathoracic pressure. Following the period 
of explosive decompression there is apnea. Tempera- 
ture within the lungs drops due to evaporation of 
moisture and to gas expansion. There is an increase 
in the alveolar carbon dioxide and oxygen. In some 
cases there are hemorrhages and liver-like consolida- 
tion of the lungs. Pulmonary blood flow is impeded. 
Intravascular bubbles are observed in animals ex- 
plosively decompressed to 30 mm. Hg. Anoxic 
anoxia and air embolism are considered the major 
lethal factors in explosive decompression injury. 
Intrapulmonary gas expansion, while a cause of 
lung lesions, is not considered so important as a 
lethal agent. 
For general studies on explosive decompression, 
the references given below should be consulted. 
2172. Clamann, H. G. Explosive decompression tests on 
human subjects. 1. Interim report: tests of explosive de- 
compression without oxygen. U. S. AAF. Wright-Patterson 
air force base, Dayton, Ohio. Aero medical laboratory. 
Technical rept. S2-46-9, (Translated German document), 
25 March 1946, 6 pp. [P] 
2173. Comfort, E. Anoxia following explosive decom- 
pression from altitudes below 10,000 feet. USAF. Wright- 
Patterson air force base, Dayton, Ohio. Aero medical lab- 
oratory. Technical rept. MCREXD-696-111 A, 10 May 
1948, 10 pp. [P] 
2174. Fulton, J. F. Altitude sickness and acclimatiza- 
tion. The history of oxygen, pp. 3-48 in: Aviation medicine 
in its preventive aspects. An historical survey. London, 
Oxford University Press, 1948, 174 pp. [R] 
2175. Gelfan, S. Explosive decompression of monkeys 
to extreme altitudes (motion picture). Fed. Proc. Amer. 
Soc. exp. Biol., 1950, 9: 47. 
2176. Haber, F. Physical process of explosive decom- 
pression. /. Aviat. Med., 1950, 21: 495-499. USAF. School 
of aviation medicine, Randolph Field, Tex. Department 
of space medicine, Special Rept., October 1950, 7 pp. 
2177. Millet, P. Decompression explosive au cours d’une 
montee a 40.000 pieds. MSd. aeronaut., 1950, 5: 151-153. 
[D] 
2178. Wilson, J. W. Explosive decompression at high 
altitude. USAF. Wright-Patterson air force base, Dayton, 
Ohio. Aero medical laboratory. Technical rept. TSEAA— 
696-104B, 11 August 1947, 21 pp. [P] 
2179. Wilson, J. W. Explosive decompression to 30 mm. 
Hg. USAF. Wright-Patterson air force base, Dayton, Ohio. 
Aero medical laboratory. Technical rept. MCREXD-696- 
1041, 18 June 1948, 76 pp. [P] 
B. EFFECTS OF EXPLOSIVE DECOMPRESSION ON 
HEART AND CIRCULATION 
Experimental animals explosively decompressed 
show a drop in systemic arterial blood pressure and 
bradycardia. Whitehorn, Lein, and Edelmann 
{2189) 1945 decompressed anesthetized dogs at 
rates greater than 20 lbs. per sq. in. per second 
over a range of 435 mm. Hg. The extent of the 
blood-pressure fall in these animals was found to 
vary directly with the rate and range of the decom- 
pression. Increasing the resistance to respiration 
markedly increased the severity of blood-pressure 
drops at a given rate and range of decompression. 
Increased intrathoracic pressure with distention of 
the lungs, occurring when the rate of decompression 
of the chamber exceeded the rate at which the lungs 
could decompress, was considered to be the primary 
cause of the fall in arterial pressure. Reflexes from 
distended abdominal organs were believed to play a 
contributing part. Livingston {2187) 1951 and 
Gelfan and Werner (2184 and 2185) 1951 have 
given reports on blood-pressure changes following 
explosive decompression of monkeys to extreme alti- 
tudes. Monkeys can withstand the stress of sudden 
decompression to altitudes as high as 75,000 feet 
simulated altitude provided that they are recom- 
pressed at free-fall rates in 100 percent oxygen. At 
the moment of decompression there is a brief reflex 
cardiac slowing that is a function of the decom- 
pression rate but independent of anoxia {2182 and 
2187). This initial slowing is probably mediated by 
the vagus nerve and appears to be initiated by 
pressor receptors responding to the mechanical 
effects of decompression. After a latent period of 
about 40 seconds, a prolonged bradycardia super- 
venes caused by the effects of complete anoxia on 
the central nervous system with some direct in- 
fluences on the heart itself. Negative middle-ear 
pressure may initiate reflex bradycardia occurring 
in the unanesthetized animals during recompres- 
sion at a free-fall rate. Reversible blood-pressure 
changes following sudden decompression to very 
high altitudes are due to mechanical factors and 
the very rapidly induced total anoxia {2184 and 
2185). The extremely rapid rate of ambient pressure 
change has an initial Valsalva-like effect and causes 
an instantaneous blood-pressure rise. This sudden 
rise of blood pressure elicits from the carotid sinus 
and the aortic arch an immediate, but brief, reflex 
cardiac slowing and slight lowering of blood pres- 
sure. The vagal discharge is usually intense enough 
to produce sinus arrest for a period of 1 to 4 cardiac 
cycles. The entire duration of this decompression 
response is less than 10 seconds. Following decom- 
pression to altitudes at which a positive intra- 
abdominal pressure inevitably develops, the result- 
ing interference with venous return from the lower 
part of the body causes an additional lowering of 
the arterial blood pressure. Within 20 seconds, the 
blood pressure may drop precipitously to 50 percent 
of the predecompression level. This precipitous drop 
is due also to the rapidly induced total anoxia at EXPLOSIVE DECOMPRESSION—HEART AND CIRCULATION 
2180-2187 
altitudes above 52,000 feet, even in 100 percent 
oxygen. Although the rate of establishing total 
anoxia is explosive, the latent period for the be- 
ginning of the anoxic fall in arterial blood pressure 
is about 20 seconds. The mechanical effects thus 
precede the anoxic ones. This circulatory impair- 
ment probably hastens the establishment of tissue 
anoxia. The evidence suggests that the rapidly in- 
duced total anoxia and simultaneous acapnia 
quickly render the vasomotor center unresponsive 
to chemoreceptor influence. Recovery is prompt if 
the animal chamber is recompressed within the 
latent period for the anoxic cardiovascular effects. 
With free-fall descent rates in oxygen, blood-pres- 
sure recovery to within 10 percent of control levels 
is a function of the time interval to reach altitudes. 
Intra-abdominal pressure equalization occurs dur- 
ing free-fall when the monkeys are still at com- 
pletely anoxic altitudes during free-fall descent. 
The mechanical interference with adequate dias- 
tolic filling of the heart is thus first to be eliminated 
during descent just as this factor is the first to in- 
fluence the blood pressure immediately after decom- 
pression. Contrary to previous reports, Gelfan and 
Werner {2184) 1951 stated that the pulse pressure 
throughout the period beginning immediately upon 
decompression never disappears, even at final 
ambient pressures of 20 to 26 mm. Hg. 
Cardiac changes following explosive decompres- 
sion to simulated altitudes as high as 75,000 feet 
were studied in anesthetized monkeys by Dowling 
and Gelfan {2181) 1949 by means of unipolar lead 
electrocardiography, recording simultaneously from 
three extremity leads. The first observable change 
in the electrocardiogram complex is displacement 
of the S-T segment, which occurs between 5 to 30 
seconds after the sudden decompression. This 
change is quickly followed by an increase in the 
P-R interval and simultaneously an absolute short- 
ening of the Q-T interval, even during the marked 
bradycardia that develops. The Q-T interval short- 
ening indicates an acceleration of repolarization, 
and there are indications that it is the left anterior 
ventricle that repolarizes faster than the rest of the 
heart. The increase in irritability of this part of the 
heart is indicated not only by electrocardiographic 
changes but also by the extrasystoles that arise from 
the left anterior ventricle. Heart block ranging from 
first degree to complete block is also observed. The 
electrocardiographic complex returns to normal 
after recompression to sea level. These cardiac 
changes are believed by the authors to be due to 
anoxia rather than pressure changes since the same 
alterations have been observed in nitrogen anoxia 
without pressure changes. Also, sudden decompres- 
sion from sea level to 40,000 feet simulated altitude 
in oxygen, at which altitude the anoxia is insignifi- 
cant, does not alter the electrocardiographic com- 
plex. Electrocardiographic changes following explo- 
sive decompression of dogs to 30 mm. Hg have been 
reported by Burch {2180) 1949. In a previous com- 
munication, this author had reported that dogs ex- 
plosively decompressed to a terminal pressure of 
30 mm. Hg died of venticular fibrillation, which de- 
veloped about 80 seconds after the explosion. This 
conclusion was derived from direct observation on 
the heart through a plastic window sutured to the 
anterior chest wall. The radical surgery involved 
may have been a factor in producing the fibrillation, 
and to test this possibility the author explosively 
decompressed a series of intact, anesthetized dogs 
recording the electrocardiograms continuously. 
About 60 seconds after the explosion, changes in 
rhythm were noted. There was auriculoventricular 
block, interventricular block, and idioventricular 
rhythms but no evidence of ventricular fibrillation. 
About 2 minutes after the explosion a severe slow- 
ing of the heart occurred. This was considered sig- 
nificant since previous chest-window observations 
showed that cessation of the heart occurred within 
2 seconds after such explosions. The author con- 
cluded that the surgical procedure tended to pre- 
cipitate ventricular fibrillation. 
For further studies on the cardiovascular effects 
of explosive decompression, papers by Hitchcock, 
Beman, and Kemph (2186) 1948 and Vail and 
Hitchcock {2188) 1949 should be consulted. 
2180. Burch, B. H. Electrocardiographic observations 
following explosive decompression of dogs to 30 mm. Hg. 
Fed. Proc. Amer. Soc. exp. Biol., 1949, 8: 19. 
2181. Dowling, R. and S. Gelfan. Cardiac changes in 
monkeys following explosive decompression to extreme 
altitudes. Fed. Proc. Amer. Soc. exp. Biol., 1949, 8: 36-37. 
2182. Gelfan, S. Explosive decompression of Macaque 
monkeys to extreme altitudes and recompression at free- 
fall rates. J. appl. Physiol., 1950, 3: 254-281. [P] 
2183. Gelfan, S. and G. D. Davis. Explosive decompres- 
sion of monkeys at extreme altitudes. Fed. Proc. Amer. Soc. 
exp. Biol., 1948, 7; 41. 
2184. Gelfan, S. and A. Y. Werner. Blood pressure 
changes following explosive decompression of monkeys to 
extreme altitudes. Fed. Proc. Amer. Soc. exp. Biol., 1951, 
10: 48. 
2185. Gelfan, S. and A. Y. Werner. Cardiovascular 
responses following explosive decompression of Macaque 
monkeys to extreme altitudes. /. appl. Physiol., 1951, 4: 
280-310. 
2188. Vail, E. G. and F. A. Hitchcock. Effects of explo- 
Estimation of subcutaneous pressure in animals explosively 
decompressed to pressures of 30 mm. Hg. Fed. Proc. Amer. 
Soc. exp. Biol., 1948, 7: 55. [P] 
2187. Livingston, R. B. Addendum, pp. 396-397 in: 
Decompression sickness. Caisson sickness, diver’s and flier’s 
bends and related syndromes. Edited by J. F. Fulton for 2188-2190 
DISEASES AND ACCIDENTS 
the Subcommittee on decompression sickness, National 
Research Council. Philadelphia, W. B. Saunders Co., 1951, 
437 pp. 
2188. Vail, E. G. and F. A. Hitchcock. Effects of explo- 
sive decompression on blood temperature in the right and 
left heart. Fed. Proc. Amer. Soc. exp. Biol., 1949, 8: 168. 
2189. Whitehorn, W. V., A. Lein, and A. Edelmann. 
The effect of explosive decompression on the blood pres- 
sure of anesthetized dogs. U. S. NRC—CAM. OEMcmr—74. 
C. A. M. rept. no. 479, 13 September 1945, 9 pp. 
C. EFFECT OF EXPLOSIVE DECOMPRESSION ON 
CEREBROSPINAL FLUID PRESSURE 
The effect of both slow and explosive decompres- 
sion upon cerebrospinal fluid pressure of anesthe- 
tized dogs was measured by Whitehorn, Lein, Edel- 
mann, and Hitchcock {2190) 1947 by means of a 
closed optical manometer system. The cerebrospinal 
fluid pressure was recorded from a needle inserted 
in the cisterna magna. Decompression to 141 mm. 
Hg in about 10 minutes resulted in an average rise 
of 3.0 mm. Hg cerebrospinal fluid pressure which 
persisted as long as the reduced pressure was main- 
tained. Explosive decompression from a pressure of 
522 mm. Hg to 141 mm. Hg in 0.01 or 0.08 second 
resulted in cerebrospinal fluid pressure rises of 22.5 
mm. Hg and 11.6 mm. Hg, respectively, and per- 
sisting for only 1.5 seconds. No bubbles were ob- 
served. The rise in cerebrospinal fluid pressure was 
considered by the authors to be a reflection of a 
similar rise in intrathoracic pressure. The brief 
duration of the rise in cerebrospinal fluid pressure 
and its relationship to the rate of decompression 
indicated to the authors that the causal factor is the 
change in intrathoracic pressure rather than the 
increased abdominal pressure. 
2190. Whitehorn, W. V., A. Lein, A. Edelmann, and 
F. A. Hitchcock. The effect of explosive decompression on 
cerebrospinal fluid pressue. Amer. ]. Physiol., 1947, 148: 
253-258. [P] 
D. EFFECTS OF EXPLOSIVE DECOMPRESSION ON 
THE RESPIRATORY SYSTEM 
Hitchcock and Edelmann {2196) 1947 explo- 
sively decompressed a series of dogs to 30 mm. Hg 
and kept them at this pressure for 15 to 120 seconds. 
The sequence of events following explosion was as 
follows; first, the respiration became deep and 
rapid, then abdominal distention occurred and the 
animals collapsed, and there were mild convulsions. 
The animals then became quiescent except for occa- 
sional gasping movements. Lacrimation, salivation, 
and urination occurred. All visible respiratory move- 
ments ceased about 30 seconds after the explosive 
decompression. Shortly after this, subcutaneous 
swelling started in the lower abdomen and pro- 
gressed headward. Thirty to 35 seconds after the 
explosion the eyes were glazed and the animals 
appeared to be dead, and remained in this condi- 
tion until recompression. When the animals were 
recompressed to about 55 mm. Hg the distention 
of the body decreased, and at 100 mm. Hg the dogs 
were almost back to normal size. When normal 
barometric pressure was reached and the chamber 
was opened, the animals had invariably ceased 
breathing but the heart was still beating. Respira- 
tion reappeared within 30 seconds after return to 
atmospheric pressure. The corneal reflexes returned 
3 to 7 minutes later. Several dogs kept at terminal 
pressure for 1 minute or longer showed decerebrate 
rigidity. This developed about 6 minutes after the 
explosion and lasted for about 3 minutes. The dogs 
were usually on their feet 12 to 13 minutes after the 
explosion, and 20 minutes after return to normal 
barometric pressure, the animals were behaving 
without symptoms or signs. The authors considered 
that all of the effects except the swelling of the body 
are due to acute anoxia. 
The volume and composition of air expelled from 
the lungs during explosive decompression has been 
studied by Hitchcock, Edelmann, Shelden, and 
Whitehorn {2197) 1946. The effect of explosive 
decompression upon the temperature of the lungs 
in anesthetized dogs has been investigated by Vail 
and Hitchcock {2200) 1948. A thermistor located in 
the trachea recorded the temperature of the in- 
spired and expired air. The temperature of expired 
air never reached the temperature recorded in the 
deep lung. Measurements of the temperature at 
various levels in the pulmonary tract wave a mean 
temperature in the trachea of 34.5° C., and in the 
deep lung of 37.1° C. At explosive decompression, 
tank temperatures were found to decrease an aver- 
age of 2.0 C. for all terminal pressures. The greatest 
drop occurred in 0.2 second. Respiratory patterns 
showed many variations. The point in a respiratory 
cycle at which the explosion occurred had a pro- 
nounced effect upon the respiratory pattern. The 
tracheal temperature fell during decompression and 
remained at a low level until recompression. The 
average decrease in tracheal temperature was 8.8° 
C. Although attempted respiratory movements were 
observed in these animals, no ventilation of the 
lungs occurred. The temperature drop in the lungs 
occurred in two phases. The first phase was con- 
sidered to be due probably to the expanding lung 
gases and the second to the vaporization of water. 
Regarding the relationship between the phases 
of respiration and the amount of lung damage pro- 
duced by explosive decompression, Berg, Baum- 
berger, Crescitelli, Rapaport, and Greeley {2191) 
1943 carried out experimental studies on the rat. EXPLOSIVE DECOMPRESSION—RESPIRATORY SYSTEM 
2191-2192 
The respiration of individual rats was photo- 
graphically recorded, using a string galvanometer 
in conjunction with sensitive thermocouples which 
gave electrical variations due to the difference in 
temperature between inspired and expired air. 
Explosive decompression produced a sudden deflec- 
tion of the string which was caused by the rapid 
expiration of expanded air from the lungs. This 
served accurately to place the time of decompres- 
sion in the respiratory cycle. All rats were explosively 
decompressed from ground level to 40,000 feet 
simulated altitude in approximately 0.02 second. 
They were breathing 100 percent oxygen and were 
returned to the ground level in about 30 seconds. 
Lung damage occurred throughout inspiration and 
during the first one-third of expiration. Slight or no 
damage was found during the last two-thirds of 
expiration. A period of apnea always followed the 
decompression. 
Alveolar gases were analyzed by Luft, Clamann, 
and Adler {2198) 1951 in subjects before and im- 
mediately after rapid decompression to various 
equivalent altitudes up to 52,000 feet. Alveolar 
oxygen as well as carbon dioxide percentages in- 
creased immediately after decompression when air 
was breathed. The higher the equivalent altitude 
reached, the greater was the increase in alveolar 
oxygen and carbon dioxide. At 50,000 feet the 
alveolar oxygen reached a value of 27 percent and 
the carbon dioxide 40 percent. When oxygen was 
breathed during the decompression, alveolar oxygen 
was reduced at the expense of carbon dioxide, the 
latter reaching a value of 56 percent after decom- 
pression to 52,000 feet simulated altitude. These 
results are explained by the authors by the fact that 
the normal carbon dioxide and oxygen tensions are 
suddenly reduced below the level existing in the 
pulmonary blood. Thus both of these gases pass 
from the blood to the alveoli and crowd out the 
nitrogen when air is breathed. When oxygen is 
breathed, only carbon dioxide, oxygen, and water 
vapor compete for the alveolar space. 
In an experimental study of the effects of explo- 
sive decompression, Corey {2193) 1947 carried out 
300 tests on rats and cats explosively decompressed 
to an altitude equivalent of 80,000 feet. Recompres- 
sion was carried out usually at a rate to simulate that 
of a freely falling man until the level of 18,000 feet 
was reached. Thereafter, a rate of fall of 20 feet per 
second, simulating a parachute descent, was main- 
tained. No fatal injuries were observed in explosive 
decompressions below 35,000 feet. From this level 
up to 80,000 feet, slightly more than 50 percent of 
the animals succumbed. Even at the latter level, 
however, a few animals survived following very 
rapid recompression. The injuries produced were 
limited to the lungs and gastro-intestinal tract. Pul- 
monary hemorrhage and bleeding into the gastro- 
intestinal tract with occasional perforations were 
observed. In cases of fatal decompression, the heart 
rate fell progressively and the rhythm became irreg- 
ular. The severity of the injury from explosive de- 
compression would appear, according to the author, 
to depend upon the volume of gas within the lungs 
(that is to say, the phase of respiration) and the 
gastrointestinal tract at the moment of decompres- 
sion. The severity of the injury also depends upon 
the length of time the animal is maintained at the 
simulated high altitude. It was observed that in all 
cases in which the expansion of the lungs was re- 
stricted by a simple strap around the upper part 
of the body, no fatality occurred from explosive de- 
compression. Also in tests in which very rapid (in- 
stantaneous) recompression was made, a much 
larger number of animals survived. Multiple explo- 
sive decompressions carried out on dogs were found 
to increase the extent of pulmonary hemorrhage in 
comparison with animals decompressed only one 
time (Burkhardt, Coulson, Criscuolo, and Adler 
{2192) 1951). 
Pathological changes in rats explosively decom- 
pressed to high altitudes have been examined by 
Wilson {2201) 1947. In Wilson’s studies more than 
200 rats were explosively decompressed in a cham- 
ber from a simulated altitude of 20,000 feet up to 
altitudes ranging to a maximum of 75,000 feet. 
Grossly visible, intravascular bubbles were infre- 
quently found and when they did occur, tended to 
be seen most often in the veins of rats decompressed 
to above 50,000 feet. Hemorrhages into the cochlea 
occurred in more than one-third of the animals de- 
compressed to above 45,000 feet. Rats dying at 
altitudes above 50,000 feet tended to show liverlike 
consolidation of the lungs. In these rats there was 
nearly complete obstruction to blood flow through 
the pulmonary bed. 
For further studies on the effects of explosive de- 
compression upon the lungs, papers by the follow- 
ing may be consulted: Hall {2194) 1950; Hall and 
Hall {2195) 1951; and USAF, Wright-Patterson 
Air Force Base, Dayton, Ohio, Aero Medical Lab- 
oratory {2199) 1949. 
2191. Berg1, W. E., J. P, Baumberger, F. Crescitelli, S. 
Rapaport, and P. 0. Greeley. Explosive decompression; 
lung damage correlated with the respiratory cycles in 
explosive decompression. U. S. NRC—CAM. C. A. M. 
rept. no. 173, 16 August 1943, 7 pp. [P] 
2192. Burkhardt, W. L., C. K. Coulson, D. Criscuolo, 
and H. F. Adler. Explosive decompression. II. The me- 
chanical effect of multiple explosive decompressions. 2193-2203 
DISEASES AND ACCIDENTS 
USAF. Randolph Field, Tex. School of aviation medicine. 
Project 21-23-005, rept. no. 2, August 1951, 8 pp. 
2193. Corey, E, L. Tests on explosive decompression. 
Fed. Proc. Amer. Soc. exp. Biol., 1947, 6: 91. 
2194. Hall, F. G. Pattern of gas expulsion from human 
lungs during rapid decompression. Fed. Proc. Amer. Soc. 
exp. Biol., 1950, 9: 55. USAF. Wright-Patterson air force 
base, Dayton, Ohio. Air materiel command. Technical 
rept. no. 6239, September 1950, 16 pp. 
2195. Hall, F. G. and K. D. Hall. Expulsion of respira- 
tory gases from lungs of human subjects during rapid 
decompression. J. appl. Physiol., 1951, 4: 1-6. 
2196. Hitchcock, F. A. and A. Edelmann. The response 
of normal dogs to explosive decompression to 30 mm. of 
Hg. Fed. Proc. Amer. Soc. exp. Biol., 1947, 6: 130. 
2197. Hitchcock, F. A., A. Edelmann, F. F. Shelden, 
and W. V. Whitehorn. The volume and composition of 
air expelled from the lungs during explosive decompres- 
sion. Fed. Proc. Amer. Soc. exp. Biol., 1946, 5: 48. 
2198. Luft, U. C., H. G. Clamann, and H. F. Adler. 
Alveolar gases in rapid decompression to high altitudes. 
J. appl. Physiol., 1949, 2: 37-48. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1951, 4: 300. Abstr. 
2199. USAF. Wright-Patterson air force base, Dayton, 
Ohio. Air materiel command. Aero medical laboratory, 
ENG. Explosive decompression, pp. 11—13 in: Synopsis 
of the aero medical aspects of jet propelled aircraft. 
January 1949, 46 pp. [R] 
2200. Vail, E. G. and F. A. Hitchcock. Effect of explo- 
sive decompression on the temperature of the lungs. 
Amer. J. Physiol., 1948, 155: 473—474. Abstr. 
2201. Wilson, J. W. Pathology in rats explosively de- 
compressed to high altitudes. USAF. Wright-Patterson air 
force base, Dayton, Ohio. Air materiel command. Aero 
medical laboratory. Technical rept. TSEAA-696—104C, 
12 August 1947, 17 pp. [P] 
E. EFFECT OF EXPLOSIVE DECOMPRESSION ON 
OCCURRENCE OF INTRAVASCULAR BUBBLES 
Whitehorn, Lein, and Hitchcock {2203) 1947 
subjected animals to explosive decompression and 
subsequent brief periods of exposure to reduced 
barometric pressures. Of 13 guinea pigs dying dur- 
ing such exposures, 7 showed intravascular gas 
bubbles after recompression. No bubbles were found 
in animals surviving the exposure. In dogs subjected 
to explosive decompression, Kemph and Hitchcock 
{2202) 1948 found no intravascular bubbles 30 
seconds after explosive decompression to barometric 
pressures greater than 55 mm. Hg. Bubbles were a 
frequent finding within 30 seconds at lower baro- 
metric pressures and a constant finding after 1 
minute exposure to 30 mm. Hg. Bubbles were ob- 
served in superficial arteries within 30 seconds, and 
in veins within 3 minutes after explosive decom- 
pression to 30 mm. Hg. The authors concluded that 
intravascular bubbles were formed centrally rather 
than peripherally; that is to say, in the large veins, 
heart, or pulmonary system. The circulation was 
probably blocked by these bubbles. Determinations 
of blood gases showed considerable oxygen present 
after explosive decompression to pressures less than 
50 mm. Hg. Therefore, stagnation anoxia and other 
factors, rather than anoxic anoxia, were considered 
significant in the etiology of the effects of rapid 
decompression to barometric pressures below the 
vapor pressure of body fluids. Whitehorn, Lein, and 
Hitchcock {2203) considered that intravascular 
bubble formation was a negligible hazard in explo- 
sive decompression. It was observed that the out- 
standing feature associated with death was abdomi- 
nal distention. It seemed likely to the authors that 
anoxia, probably intensified by interference with 
respiratory movements as the result of abdominal 
distention, was the prime cause of fatalities. 
2202. Kemph, J. P. and F. A. Hitchcock. Changes in 
the blood following explosive decompression. Amer. J. 
Physiol., 1948, 155: 477. Abstr. 
2203. Whitehorn, W. V., A. Lein, and F. A. Hitchcock. 
The effect of explosive decompression on the occurrence 
of intravascular bubbles. J. Aviat. Med., 1947, 18: 392— 
394. [P] 
F. LETHAL FACTORS IN EXPLOSIVE 
DECOMPRESSION INJURY 
In explosively decompressed rats and cats, Corey 
{2204) 1947 observed pulmonary hemorrhage in 
all animals exposed to pressure equivalents of 50,- 
000 feet and 80,000 feet. No pulmonary lesions were 
found in animals decompressed to simulated alti- 
tudes below 35,000 feet. The left lung showed less 
extensive trauma than did the right. In both lungs 
the apical poles, the posterior surfaces, and the thin, 
pulmonary margins appeared to be the most vulner- 
able areas. Hall and Corey {2213) 1950 considered 
that anoxic anoxia was of major importance as a 
causative factor in death resulting from explosive 
decompression injury in animals decompressed to 
an altitude equivalent of 80,000 feet. According to 
Corey and Lewis {2207) 1950, the duration of post- 
decompression anoxia represents the major factor 
in determining the outcome of explosive decompres- 
sion. Injection of atropine or mecholyl significantly 
reduced the mortality in rats exposed to a standard- 
ized decompression invariably lethal to untreated 
animals. Anesthesia with ether, evipal, or pentothal 
permitted all rats tested to survive explosive de- 
compression which was uniformly fatal to control 
animals. 
Corey (2205 and 2206) 1949 explosively decom- 
pressed rats to normal atmospheric pressure after 
exposure to positive pressures of 2 to 20 atmospheres 
for varying intervals of time. Decompression from 
2 to as much as 6 atmospheres (equivalent to a gas- 
expansion differential of 18,000 to 42,000 feet) was 
well tolerated and such decompressions may be con- EXPLOSIVE DECOMPRESSION—TOLERANCE 
2204-2219 
sidered to be entirely innocuous in the rat. Of rats 
decompressed after 30 minutes’ exposures to 7 to 11 
atmospheres, 77 percent died. Air embolism was 
present in 82 percent of these animals, with pul- 
monary lesions in 18 percent of all cases. All ani- 
mals succumbed following decompression from 11 
atmospheres (a gas-expansion equivalent of 55,000 
feet) when so maintained for 30 minutes prior to 
release of pressure. Without exception these ani- 
mals exhibited gas emboli, while pulmonary hemor- 
rhages were seen in only 15 percent. All rats dying 
following explosive decompression from 20 atmos- 
pheres gave evidence of severe aeroembolism, while 
pulmonary lesions could be demonstrated in only 
43 percent of such animals. Decompression after a 
50-second exposure to 30 atmospheres was invari- 
ably fatal. On the other hand, all animals survived 
this pressure change when the time under pressure 
was reduced to 10 seconds. These experiments indi- 
cated to the author that anoxic anoxia and aeroem- 
bolism constitute the major factors in the etiology 
of explosive decompression injury, and that intra- 
pulmonary gas expansion may be considered of 
relatively minor importance as a lethal agent. 
In considering the pathological lesions caused by 
explosive decompression, Edelmann, Whitehorn, 
Lein, and Hitchcock {2208) 1946 believed sudden 
increases in intrapulmonary pressure produced by 
explosive decompression to be the primary etiologi- 
cal agent in producing lesions in dogs explosively 
decompressed and rapidly recompressed to avoid 
anoxia as a complicating factor. Fusco, Mellette, 
and Hitchcock {2210) 1948 found that edema and 
hemorrhage of the lungs could be produced in rats 
exposed to nitrogen, but these lung lesions were not 
as great as in rats explosively decompressed to 30 
mm. Hg. Therefore, it was considered that only a 
part of the effects of explosive decompression on 
the lungs are due to anoxia. Whitehorn, Lein, and 
Hitchcock (2277) 1947 reported that binding the 
abdomen and lower thorax of dogs did not protect 
against the occurrence of pulmonary hemorrhages. 
They stated that binding seems to increase the 
tendency to pathological lesions through the bruis- 
ing action of the lungs against rigid thoracic walls. 
For further studies on lethal factors in explosive 
decompression injury, papers by the following may 
be consulted: Fulton {2209) 1941; Gelfan, Nims, 
and Livingston (2277) 1947; Grossly and Meakin 
(2272) 1943; Kemph and Hitchcock {2214) 1951; 
Mahoney (2275) 1949; and Smith {2216) 1946. 
2204. Corey, E. L. An experimental study of explosive 
decompression injury. Amer. J. Physiol, 1947, 150: 607- 
612. /. industr. Hyg., 1948, 30: abstract section: 85-86. 
[P] 
2205. Corey, E. L. Factors in explosive decompression 
injury. Amer. J. Physiol, 1949, 157: 88-93. [P] 
2206. Corey, E. L. Conditions influencing explosive de- 
compression injury. Fed. Proc. Amer. Soc. exp. Biol., 
1949, 8: 29. [P] 
2207. Corey, E. L. and E. G. Lewis, Etiology of explo- 
sive decompression injury. Amer. J. Physiol, 1950, 162: 
452—457. Fed. Proc. Amer. Soc. exp. Biol, 1950, 9: 25. 
2208. Edelmann, A., W. V. Whitehorn, A. Lein, and 
F. A. Hitchcock. Pathological lesions produced by explo- 
sive decompression. /. Aviat. Med., 1946, 17: 596-601. [P] 
2209. Fulton, J. F. Explosive decompression and pres- 
sure cabin aircraft. U. S. NRC-CAM. C. A. M. rept. no. 
33, 11 November 1941, 4 pp. 
2210- Fusco, M., H. Mellette, and F. A. Hitchcock. 
Determination of the etiology of pathological effects of 
explosive decompression on the lungs of rats. Fed. Proc. 
Amer. Soc. exp. Biol, 1948, 7: 39. [P] 
2211. Gelfan, S., L. F. Nims, and R. B. Livingston. 
Cause of death from explosive decompression at high 
altitudes. Fed. Proc. Amer. Soc. exp. Biol, 1947, 6: 110. 
2212. Grossly, D. W. and L. W. Meakin. Explosive 
decompression—effects on human subjects. U. S. NRC- 
CAM. C. A. M. rept. no. 220, 24 April 1943, 4 pp. [P] 
2213. Hall, W. M. and E. L. Corey. Anoxia in explosive 
decompression injury. Amer. J. Physiol, 1950, 160: 361- 
365. Abstr. World Med., 1950, 8: 456. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1950, 3: 1211. [P] 
2214. Kemph, J. P. and F. A. Hitchcock. X-ray studies 
of effects of high intrapulmonic pressures on heart, lungs 
and thoracic cage of dogs at 30 mm. Hg ambient pressure. 
Amer. J. Physiol, 1951, 167: 801-802. Abstr. 
2215. Mahoney, D. I. Repeated explosive decompres- 
sion. Fed. Proc. Amer. Soc. exp. Biol, 1949, 8: 104. 
USAF. Wright-Patterson air force base, Dayton, Ohio. 
Air materiel command. Memo. Rept. MCREXD-696- 
107H, 15 December 1948, 3 pp. 
2216. Smith, J, J. The physiological and pathological 
effects of explosive decompression. Northwestern Univer- 
sity, Summaries of doctoral dissertations. 1946, 15: 215- 
217. 
2217. Whitehorn, W. V., A. Lein, and F. A. Hitchcock. 
The effect of binding of the abdomen and thorax on pul- 
monary lesions produced by explosive decompression. /. 
Aviat. Med., 1947.18: 102-104. [P] 
G. TOLERANCE OF EXPLOSIVE DECOMPRESSION 
Experiments of Hitchcock (2225) 1951 have led 
him to conclude that explosive decompression at 
rates and over ranges likely to occur with modem 
aircraft is not a serious hazard. For other studies 
of tolerance of explosive decompression, references 
listed below should be consulted. 
2218. Allen, S. C. Ability of human subjects to with- 
stand “explosive decompression.” Fed. Proc. Amer. Soc. 
exp. Biol, 1947, 6: 68. [P] 
2218a. Burkhardt, W. L., R. E. Hedblom, A. W. Hether- 
ington, and H. F. Alder. Extent of pathological damage to 
animals explosively decompressed in a cold environment. 
/. Aviat. Med., 1950, 21: 304-308; 320. 
2219. Gagge, A. P., and R. S. Shaw, Explosive decom- 
pression. pp. 49—50 in: Medical physics. Volume II. 
291222—54 13 2220-2226 
DISEASES AND ACCIDENTS 
Edited by Otto Glasser. Chicago, The Year Book Pub- 
lishers, Inc., 1950, 1227 pp. [R] 
2220. Gelfan, S., L. F. Nims, and R. B. Livingston. 
Explosive decompression at high altitude. Amer. J. 
Physiol, 1950, 162: 37-53. [P] 
2221. Hall, W. M. and E. L. Corey. Anoxia in explosive 
decompression injury. Amer. J. Physiol, 1950, 160: 
361-365. 
2222. Hiestand, W. A. and F. W. Stemler. Rapidly 
acquired tolerance to decompression in insects. Fed. Proc. 
Amer. Soc. exp. Biol, 1951,10: 63-64. 
2223. Hitchcock, F. A. Explosive decompression, pp. 
378-395 in: Decompression sickness. Caisson sickness, 
diver’s and flier’s bends and related syndromes. Edited 
by J. F. Fulton for the Subcommittee on decompression 
sickness. National Research Council. Philadelphia, W. B. 
Saunders Co., 1951, 437 pp. [D] [P] 
2224. Hitchcock, F. A., W. V. Whitehorn, and A. Edel- 
man. Tolerance of normal men to explosive decompres- 
sion. J. appl. Physiol, 1948, 1: 418-429. [P] 
2225. Pivovarov, ML A. and G. L. Komendantov. O 
trenirovke organizma k rezkim perepadam barometric- 
hesogo davleniia. [Training of the organism to sharp falls 
in barometric pressure.] pp. 252-266 in: Trudy Voenno- 
Meditsinskoi Akademii Im. Kirova, edited by: L. A. 
Orbeli, N. N. Anichkova, I. P. Petrova, A. V. Lebedin- 
skogo. Moskva, 1946, 269 pp. 
2226. Rockhold, W. T., F. W. Stemler, J. E. Wiehers, 
and W. A. Hiestand. Survival time of the mouse as related 
to ambient p02 produced by explosive decompression. 
Proc. Soc. exp. Biol, N. Y., 1950, 73: 331-332. [P] 
V. OXYGEN INTOXICATION 
A. EFFECTS OF INCREASED OXYGEN TENSION 
NOT IN EXCESS OF ONE ATMEOSPHERE 
1. GENERAL STUDIES 
For a comprehensive review of the literature on 
oxygen intoxication, the reader should consult the 
section on this subject (pp. 163-194) in the first 
volume of this Sourcebook. Reference should be 
made to the classical studies of Paul Bert cited in 
the first volume of the Sourcebook and to the work 
of Bean also cited there. The toxic effects of an 
excess of oxygen have always been and still remain 
a subject of interest and importance. The mecha- 
nisms of these toxic effects are still not entirely 
clear. Observations and investigations of the past 
have distinguished two principal manifestations of 
oxygen poisoning. The first is the so-called Lorrain 
Smith effect or subacute poisoning, which consists 
of an irritation of the pulmonary alveoli and de- 
velops as a result of exposure to oxygen tensions of 
about 0.7 to 0.8 atmosphere of oxygen. The second 
manifestation is the so-called Paul Bert effect and 
consists of generalized epileptiform convulsions pro- 
duced by prolonged inhalation of oxygen at pres- 
sures greater than 1 atmosphere. Although the pul- 
monary manifestations are characteristically ob- 
served at relatively lower oxygen tensions, while the 
convulsive effects are characteristic of high oxygen 
tensions, nevertheless, the lungs may also be involved 
at very high pressures of oxygen. 
Exposure to oxygen in concentrations above 60 
percent of 1 atmosphere for sufficient lengths of time 
produces toxic effects on both animals and human 
beings. The severity of these effects is proportional 
to the concentration and to the duration of ex- 
posure and varies from individual to individual as 
well as from one species to another (2235). Under 
these conditions, oxygen acts adversely upon the 
lungs, the blood, and other tissues of the body, in- 
cluding to some extent the central nervous system. 
Symptoms in human subjects include substernal 
distress, nasal congestion or coryza, conjunctival 
irritation, significant decrease in vital capacity, dis- 
comfort in the ears, and fatigue. Schmidt and 
Brooks {2234) 1949 elicited respiratory symptoms 
in 90 healthy, young men between the ages of 19 
and 31 years who were exposed to oxygen for 24 
hours at 1 atmosphere. Substernal distress was pro- 
duced in 82 percent of the subjects and there was a 
significant decrease in vital capacity. Signs of nose 
and throat irritation were common. Intermittence 
of oxygen supply produced by 15 minutes breathing 
of normal air every 3 hours did not decrease the 
incidence of complaints. In anesthetized cats and 
dogs breathing pure oxygen at normal barometic 
pressure, Beznak and Liljestrand (2228) 1949 found 
a reduction of lymph flow from the right thoracic 
duct amounting to about 30 percent. Intestinal 
movements showed an increase. The authors con- 
sidered that oxygen inhalation under the condition 
of their experiments produced alteration of the per- 
meability of the capillaries or the colloid osmotic 
pressure or both. With regard to the lungs, a block- 
ing effect of the dilated precapillaries upon the 
lymphatic seemed possible. 
In studies carried out by Comroe, Dripps, Dumke, 
and Deming {2231) 1945, the administration of 
100 percent oxygen to a large group of healthy men 
continuously for 24 hours at normal barometric 
pressure produced substernal distress in 86 percent 
of the subjects. Breathing 75 percent oxygen pro- 
duced symptoms in only 55 percent of the subjects, 
and breathing 50 percent oxygen led to no symp- 
toms. Breathing 100 percent oxygen at a simulated 
high altitude of 18,000 feet did not produce symp- 
toms, suggesting that the symptoms are due to high 
oxygen tension and not to elimination of nitrogen. 
The authors believed that the administration of 100 
percent oxygen for short periods up to 12 hours 
is probably completely safe, but when oxygen must 
be given in excess of 12 hours it should be reduced 
to 60 percent unless this is insufficient to saturate 
the arterial blood. If 100 percent oxygen must be OXYGEN INTOXICATION AT ATMOSPHERIC PRESSURE—NERVOUS SYSTEM 
2227-2237 
administered, a careful check should be made of the 
symptoms most likely to occur as result of high 
tensions of oxygen. 
For other general studies on the effects of in- 
creased oxygen tension not in excess of 1 atmos- 
phere, papers by the following may be consulted: 
Baetjer {2227) 1951, Binet and Bochet {2229) 
1951, Comroe and Dripps {2230) 1950, Gotten and 
Walton {2232) 1951, and Patel {2233) 1946. 
2227. Baetjer, A. M. The effects of high and low baro- 
metric pressures, pp. 996—1004 in: Rosenau preventive 
medicine and hygiene. Edited by Kenneth F. Maxcy. 
Seventh edition. New York, Appleton-Century-Crofts, 
Inc., 1951, 1462 pp. 
2228. Beznak, A. B. L. and G. Liljestrand. The effect of 
variations in oxygen tension on the lymph flow. Acta 
physiol, scand., 1949, 19: 170-186. [P] 
2229. Binet, L. and ( ) Bochet. Le sejour prolonge 
dans 1’oxygene pur. Biol, med., Paris, 1951, 40: 85-95. [R] 
2230. Comroe, J. H. and R. D. Dripps. Inhalation of 
oxygen by normal man. pp. 3-18 in: The physiological 
basis for oxygen therapy. Springfield, Charles C. Thomas, 
1950, 85 pp. [D] 
2231. Comroe, J. H., Jr., R. D. Dripps, P. R. Dumke, 
and M. Deming. The effect of inhalation of high concen- 
trations of oxygen for 24 hours upon normal men at sea 
level and at a simulated altitude of 18,000 feet. U. S. 
NRC-CAM. OEMcmr-28, C. A. M. rept. no. 414, 5 
March 1945, 1 p. 
2232. Gotten, M. de V. and R. P. Walton. The effects 
of high oxygen atmospheres on drug induced convulsions. 
Anesthesiol., 1951, 12: 491-499. 
2233. Patel, J. C. Toxicity of oxygen. Indian Physician, 
1946, 5: 242-246. 
2234. Schmidt, C. F. and J. W. Brooks. Oxygen. 5 pp. 
from: Basic Science Notes. U. S. Army. Medical depart- 
ment, Research and graduate school. Volume No. 6, 1949, 
Department of Army, Washington, D. C. [P] 
2235. Snapp, F. E., and H. F. Adler. Oxygen toxicity. 
USAF. Randolph Field, Tex. School of aviation medicine. 
Project Rept. 9, November 1948, 4 pp. [R] 
2. EFFECTS ON THE CENTRAL NERVOUS SYSTEM 
Although the effects of oxygen-air mixtures or 
pure oxygen at normal barometric pressure are pre- 
dominantly upon the respiratory, circulatory, and 
metabolic functions, nevertheless, some effects upon 
the central nervous system have been elucidated. 
Of particular interest in connection with the central 
nervous system effects of oxygen at normal baro- 
metric pressure is the so-called parodoxical oxygen 
effect which is often observed on administration of 
oxygen under conditions of preexisting hypoxia. 
For a consideration of the oxygen paradox, the ap- 
propriate section in this Sourcebook may be con- 
sulted (p. 197). 
Beyne, Chauchard, and Chauchard {2236) 1946 
found in guinea pigs that respiration of a hyper- 
oxygenated atmosphere produces a lengthening of 
chronaxie of motor nerves. In 42 students breathing 
pure oxygen at normal atmospheric pressure, Binet, 
Strumza, and Levy {2237) 1951 found an increase 
in the number of errors in intellectual performance 
tests as compared to performance when breathing 
ordinary air. 
2236. Beyne, J., B. Chauchard, and P. Chauchard. 
Effects de la respiration en atmosphere suroxygenee sur 
1’excitabilite nerveuse de 1’homme. C. R. Soc. Biol., Paris, 
1946, 140: 411-412. [R] 
2237. Binet, L., M. V. Strumza, and J. Levy. Effects de 
1’inhalation d’oxygene pur, a la pression atmospherique, 
sur les facultes intellectuelles de 1’homme normal. C. R. 
Acad. Sci., Paris, 1951, 232: 1527-1529. [P] 
3. EFFECTS ON THE CARDIOVASCULAR SYSTEM 
The evidence of the literature is in general agree- 
ment that respiration of oxygen or hyperoxygenated 
air at normal atmospheric pressure results in a slow- 
ing of the heart. Cardiac slowing occurred in most 
of the subjects who inhaled 100 percent oxygen in 
experiments carried out by Dripps and Comroe 
{2240) 1947. In these subjects there was an im- 
mediate decrease in pulse rate and respiratory min- 
ute volume. This suggested to the authors that some 
chemoreceptors of the carotid and aortic bodies are 
tonically active at the oxygen tension present in the 
arterial blood of many normal men breathing room 
air at sea level. In resting human subjects, Meda 
{2242 and 2243) 1950 found that oxygen at normal 
barometric pressure caused a decrease in the heart 
rate of 3.7 to 11 percent. This reduction lasted only 
10 to 35 minutes, even when oxygen breathing was 
continued. This bardycardia was not observed in 
subjects breathing an air mixture containing less 
than 50 percent of oxygen. The magnitude of the 
response was proportional to the percentage of 
oxygen in the air mixture. 
To gain additional information on circulatory 
changes in normal men during inhalation of 100 
percent oxygen at normal barometric pressure, 
Whitehorn, Edelmann, and Hitchcock {2245) 1946 
have determined cardiac minute volume and sys- 
temic blood pressure under these conditions. The 
subjects of these experiments were young male sub- 
jects of 18 to 35 years of age in the basal state, lying 
quietly. Cardiac output was determined from bal- 
listocardiograms. Cardiac minute volumes were 
consistently lower during inhalation of 100 percent 
oxygen as compared with determinations on the 
same subjects breathing air. Slowing of the heart 
was considered to be almost entirely responsible for 
the reduction in cardiac output during the first 10 
minutes of oxygen breathing. On continued inhala- 
tion of 100 percent oxygen, reduction of stroke vol- 
ume contributed to the total effect. Systolic blood 
pressure did not change but diastolic pressure 2238-2249 
DISEASES AND ACCIDENTS 
showed a slight but significant rise. The average 
diastolic pressure after 60 minutes of 100 percent 
oxygen breathing was 7 mm. Hg higher than the 
control value. The maintenance of the arterial blood 
pressure level in spite of reduced cardiac output 
was interpreted by the authors as evidence of an 
increase in the general peripheral vascular resist- 
ance. It was suggested that the cardiovascular effects 
of oxygen inhalation be kept in mind in conditions 
of hyperoxygenation of the blood, such as denitroge- 
nation, and that they may play a part in the physio- 
logical responses to changes in barometric pressure. 
In experiments on seven healthy young men, it 
was shown by Alella and Meda {2238) 1948 that 
administration of atropine prevented the decrease 
of pulse frequency caused by inhalation of 100 per- 
cent oxygen. Gijon and Lorenzo {2241) 1947 ad- 
ministered pure oxygen under normal barometric 
pressure to 30 healthy young guinea pigs for 48 to 
72 hours. The electrocardiographic tracings did not 
reveal any symptoms of cardiac hypoxia under these 
conditions. There were no significant deviations in 
the glycogen content of the heart. 
For a further study of cardiovascular changes 
occurring during oxygen breathing, a paper by 
Alveryd and Brody {2239) 1948 may be consulted. 
2238. Alella, A. and E. Meda. Frequenza cardiaca 
durante la respirazione di 02 nell’uomo ed importanza del 
vago. Boll. Soc. ital. Biol, sper., 1948, 24: 581-582. Ex- 
cerpta Medica. Section II. (Physiology, Biochemistry, and 
Pharmacology), 1949,2: 771. Abstr. [P] 
2239. Alveryd, A. and S. Brody. Cardiovascular and 
respiratory changes in man during oxygen breathing. Acta 
physiol, scand., 1948, 15: 140-149. 
2240. Dripps, R. D. and J. H. Comroe, Jr. The effect 
of the inhalation of high and low oxygen concentrations 
on respiration, pulse rate, ballistocardiogram and arterial 
oxygen saturation (oximeter) of normal individuals. Amer. 
]. Physiol., 1947, 149: 277-291. Excerpta Medica. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1948, 
I: 368. Abstr. [P] 
2241. Gijon, F. R. and P. L. Lorenzo. El contenido 
de glicogeno del corazon de cobayas sometidos a respira- 
cion de oxigeno puro. Farmacoter. act. 1947, 4: 394-398. 
2242. Meda, E. I. Effetti della respirazione di miscele 
ricche di 02 sull’apparato cardiovascolare dell’uomo. II. 
Variazioni elettrocardiografiche nell’uomo durante la 
respirazione di 02. Boll. Soc. ital. Biol, sper., 1950, 26: 
930-931. [P] 
2243. Meda, E. Ricerche elettro cardiografiche durante 
la respiratione di miscele ricche di ossiggeno. Riv. Med. 
aero., Roma, 1950, 13: 441—453. Excerpta Medica. Section 
II. (Physiology, Biochemistry, and Pharmacology), 1951, 
4: 1242. 
2244. Whitehorn, W. V. and A. Edelmann. The cardio- 
vascular response to the breathing of 100% oxygen at 
normal barometric pressure. U. S. NRC-CAM. OEMcmr- 
74, C. A. M. rept. no. 474, 13 September 1945. Abstr. 
2245. Whitehorn, W. V., A, Edelmann, and F. A. Hitch- 
cock. The cardiovascular responses to the breathing of 
100 percent oxygen at normal barometric pressure. Amer. 
J. Physiol., 1946, 146: 61-65. [P] 
4. EFFECTS ON THE BLOOD 
Many workers have observed a decrease in the 
red blood count in subjects exposed to oxygen or 
hyperoxygenated air at normal atmospheric pressure 
for prolonged periods of time. Tinsley, Moore, Du- 
bach, Minnich, and Grinstein {2249) 1949 sub- 
jected patients and normal persons to high oxygen 
concentrations for 8 to 14 days by means of a mask. 
Seventy percent oxygen was administered to the 
normal subjects for a period of 10 days. Results in- 
dicated that high oxygen tensions of inspired oxygen 
depress erythrocytogenesis in human subjects. The 
authors considered that their experiments provide 
further evidence that the oxygen tension of the 
arterial blood is one of the principal regulators of 
erythropoietic activity. These findings are in har- 
mony with those of Cooperberg and Singer {2246) 
1951 who investigated erythropoetic activity in the 
bone marrow of guinea pigs exposed to high oxygen 
tensions. In normal animals breathing high oxygen 
mixtures, there was a reticulocytopenia which was 
definitely caused by erythrocytic hypoplasia of the 
red bone marrow. 
According to Donnell, Jensen, and Alt {2247) 
1946, exposure of guinea pigs to intermittent high 
oxygen tension failed to depress erythropoiesis. 
These animals were intermittently exposed to 80 to 
100 percent oxygen at normal atmospheric pressure 
for 57 days. The periods of exposure covered 6 hours 
a day, 6 days a week. There was no significant dim- 
inution in the erythrocyte counts and hemoglobin 
values in any of these animals. 
For a further study of the relation of oxygen to 
erythropoiesis, a paper by Grant and Root {2248) 
1947 may be consulted. 
2246. Cooperberg, A. and K. Singer. The reaction of 
the bone marrow to high oxygen tension in normal and 
anemic guinea pigs. /. Lab. din. Med., 1951, 37: 936—947. 
2247. Donnell, W. S., A. V. Jensen, and H. L. Alt. 
Exposure of guinea pigs to intermittent high oxygen tension 
and its failure to depress erythropoiesis. Proc. Soc. exp. 
Biol., N. Y., 1946, 63: 64-66. [P] 
2248. Grant, W. C. and W. S. Root. The relation of 
O2 in bone marrow blood to posthemorrhagic erythro- 
poiesis. Amer. J. Physiol., 1947, 150: 618-627. 
2249. Tinsley, J. C., Jr., C. V. Moore, R. Dubach, 
V. Minnich, and M. Grinstein. The role of oxygen in the 
regulation of erythropoiesis. Depression of the rate of 
delivery of new red cells to the blood by high concen- 
trations of inspired oxygen. /. din. Invest., 1949, 28: 
1412-1421. Excerpta Medica. Section II. (Physiology, 
Biochemistry, and Pharmacology), 1950, 3: 1075. Ahstr. 
World Med., 1950, 8: 343. [CH] [P] OXYGEN INTOXICATION AT ATMOSPHERIC PRESSURE—BLOOD 
5. EFFECTS UPON THE RESPIRATORY SYSTEM 
Although there is lack of unanimity as to the 
effects of oxygen or hyperoxygenated air at normal 
barometric pressures upon respiration, the more 
reliable evidence indicates that oxygen adminis- 
tration does cause changes in breathing although 
these may not be large and may be masked by the 
techniques used in their measurements. The older 
literature indicates that in animals the respiratory 
minute volume is reduced by inhalation of oxygen, 
and in man, Patterson, Heyman, and Duke (2258) 
1951 have found depression of pulmonary venti- 
lation in patients with chronic pulmonary emphy- 
sema breathing 85 to 100 percent oxygen at normal 
barometric pressure. 
Binet and Strumza (2251) 1947 recorded a drop 
in respiratory rhythm from 17 down to 14 per 
minute in dogs under chloralose anesthesia given 
pure oxygen at normal barometric pressure. The 
minute volume of respiration fell from 4.02 liters 
to 3.38 liters. This depressive effect of oxygen upon 
respiration was found to be transient. According 
to Gollwitzer-Meier (2253) 1948, breathing 100 
percent oxygen by men (10 minutes) and narcotized 
dogs (6 to 7 minutes) was associated with an 
immediate drop in ventilation rate. Upon recovery 
on air, there was a gradual return within 1 to 7 
minutes in man, while in dogs a hyperventilation 
was maintained for at least 6 minutes. Hypoventi- 
lation was not observed in dogs in which the sinus 
nerves were ligatured. The reaction of man to 
carbon dioxide in the inspired air before and after 
recovery from oxygen breathing indicates no change 
in the sensitivity of the respiratory system to carbon 
dioxide. These results are interpreted by the author 
on the theory that the chemoreceptors are inhibited 
by high oxygen pressure, but that the central con- 
trol is stimulated. During the initial period of 
oxygen breathing, the chemoreflex drive is dominant 
but is soon overruled by the central drive, which 
persists and is slow to recover during the recovery 
period on air. 
In 1948, Barach (2250) reviewed experimental 
and clinical studies on the effects of high concen- 
trations of oxygen. Inhalation of 100 percent oxygen 
for periods under 7 hours has been shown to have 
no after-effects. The difficulty of obtaining high 
oxygen concentrations in oxygen tents or with nasal 
catheters minimizes the likelihood of oxygen poison- 
ing by these methods of treatment. In administra- 
tion of oxygen with masks, an intermittent schedule 
of administration is desirable. 
Studies of pathological changes produced in the 
lungs by breathing oxygen or highly oxygenated air 
mixtures at normal barometric pressure have been 
described on pages 174 to 176 of the first volume of 
this Sourcebook. These pathological changes in- 
clude inflammation, congestion, edema, atelectasis, 
fibrin formation, and consolidation of the lungs. 
There may be pneumonia of various types, bron- 
chitis with bronchiectasis, and hypertrophy, hyper- 
plasia, desquamation, and degenerative changes in 
alveoli. There may be also sclerotic changes with 
narrowing, thickening, and hyalinization of the 
pulmonary arteries. 
Pulmonary edema and vascular congestion of the 
lungs have been described by Hemingway (2254) 
1951 in guinea pigs subjected to almost pure oxygen 
at normal barometric pressure. There was little 
edema during the first 24 to 48 hours of the high 
oxygen environment. Subsequently, edema progres- 
sively developed, causing death in 5 to 6 days. Kuhn 
and Pichotka (2256) 1948 exposed guinea pigs and 
rabbits to 90 to 98 percent oxygen mixtures at nor- 
mal barometic pressure for 60 to 122 hours. These 
animals showed a hyalinelike membrane in the 
lungs as well as necrosis of the bronchial epithelium. 
There was an alveolar exudate consisting of fibrin 
and leucocytes. In an experimental investigation on 
3 adult and 9 infant guinea pigs, exposed to 98 
percent oxygen at normal barometic pressure for 
several days, Bruns and Shields (2252) 1951 found 
a hyalinelike membrane in the lungs after 50 to 64 
hours. The general pathological findings in all ani- 
mals dying in high concentrations of oxygen were 
paradoxically those of anoxia. The authors carried 
out their investigations in an attempt to explain 
the formation of hyalinelike membranes in the 
lungs of stillborn infants and infants dying neo- 
natally. 
In a study of the pathogenesis of pulmonary dam- 
age caused by breathing oxygen at normal baro- 
metric pressure, Ohlsson (2257) 1947 reported that 
the pulmonary damage in oxygen poisoning at 1 
atmosphere seems to be caused by a lesion of the 
capillary wall. The damaging effects of oxygen are 
considerably higher in experiments in which 3 to 
3.5 percent carbon dioxide is added to the respira- 
tory mixture. The author considers that the decrease 
in vital capacity observed in high oxygen breathing 
is due partly to the dilating effect of the oxygen on 
the pulmonary vessels and partly to an exudation 
into the pulmonary tissue caused by oxygen at high 
partial pressure. The author considers that there is 
no experimental basis for the view that pulmonary 
damage in oxygen poisoning is produced by a direct 
effect of oxygen in the pulmonary tissue. He sug- 
gests rather that the pulmonary damage in oxygen 
poisoning is caused by disturbance of the carbon 
dioxide transport in the venous blood. 2250-2262 
DISEASES AND ACCIDENTS 
For an experimental study on the resistance of 
animals to chronic oxygen poisoning, a paper by 
Hempleman {2255) 1951 may be consulted. 
2250. Barach, A. L. Oxygen poisoning, pp. 303-309 
in: Physiologic therapy in respiratory diseases. Second 
edition. Philadelphia, J. B. Lippincott Co., 1948, 408 pp. 
2251. Binet, L. and M. V. Strumza, Sur 1’effet depres- 
seur respiratoire de 1’inhalation brusque d’oxygene pur. 
C. R. Soc. Biol., Paris, 1947, 141: 3-5. [P] 
2252. Bruns, P. D. and L. V. Shields. The pathogenesis 
and relationship of the hyalinelike pulmonary membrane 
to premature neonatal mortality. Amer. J. Obstet. Gynec., 
1951, 61: 953-965. [P] 
2253. Gollwitzer-Meir, K. Uber die Wirkung der 
Sauerstoffatmung auf das Atemzentrum und uber ihre 
Nachdauer. Pfliig. Arch. ges. Physiol., 1947, 249: 32-43. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1948, / ; 629. Abstr. 
2254. Hemingway, A. Effect of hypoxia and oxygen 
poisoning on pulmonary edema. Fed. Proc. Amer. Soc. 
exp. Biol., 1951, 10: 62. 
2255. Hempleman, H. V. The reistance of animals to 
chronic oxygen poisoning. Gt. Brit. MRC-RNPRC, UPS. 
Royal naval physiological laboratory, Alverstoke. R. N. P. 
51/652, U. P. S. 127, 8 pp. [P] 
2256. Kuhn, H. A. and J. Pichotaka. Uber die Morpho- 
genese der Lungenveranderungen bei der Sauerstoffver- 
giftung. Arch. exp. Path. Pharmak., 1948, 205: 667-683. 
[P] 
2257. Ohlsson, W. T. L. A study of oxygen toxicity 
at atmospheric pressure with special reference to the path- 
ogenesis of pulmonary damage and clinical oxygen therapy. 
Acta med. scand., 1947, Suppl., 190: 1-93. [P] 
2258. Patterson, J. L., Jr., A. Heyman, and T. W. Duke. 
The cerebral circulation and metabolism in chronic pul- 
monary emphysema with observations on the effects of 
inhalation of oxygen. U. S. Navy. NATC, Pensacola, Fla. 
School of aviation medicine. Project NM 001 050.01.02, 
26 July 1951, 11 pp. 
6. EFFECTS ON METABOLISM 
Analysis of the literature on the effects of oxygen 
and hyperoxygenated air at normal barometric 
pressure upon the metabolic processes reveals no 
consistent and dependable evidence that breathing 
oxygen-rich air or pure oxygen causes any change 
in metabolism manifested by alteration in exchange 
of respiratory gases. Most reports support the view 
that the respiratory exchange is not a function of 
oxygen tension except under those conditions in 
which the oxygen tension falls below normal. A 
number of metabolic responses to high oxygen ten- 
sion may be discerned, however. Mann and Quastel 
{2264) 1946 found that the respiration of minced 
brain tissue falls off to a greater extent in the pres- 
ence of oxygen than in the presence of air, particu- 
larly when the respiration of the brain tissue takes 
place in the presence of glucose, sodium lactate, 
or sodium pyruvate. The respiration of minced brain 
in the presence of sodium succinate appears not to 
be so oxygen sensitive. The evidence points to the 
pyruvate oxidizing system as constituting that part 
of the brain respiratory system most sensitive to 
oxygen. Mann and Quastel suggest that pyruvate 
oxidase is the substance which is poisoned by high 
tensions of oxygen. 
Regarding the effect of prolonged inhalation of 
oxygen upon the emptying time of the stomach and 
speed of intestinal absorption of isotonic solutions 
of glucose in the rat, Cordier and Chanel {2261) 
1950 found no changes in these functions in rats 
kept in pure oxygen at atmospheric pressure. It 
appears that inhalation of oxygen may bring about 
improvement in patients with impaired liver func- 
tion. Kaufman, Hollo, Rosenthal, Stone, Beck, and 
Fink {2263) 1950 found in patients with depressed 
hepatic function that breathing of 10 percent oxygen 
with 90 percent nitrogen for 35 minutes impaired 
BSP excretion to a significant degree. Breathing 100 
percent oxygen for 4 hours improved in certain 
cases the excretion of the dye. Other liver function 
tests carried out in combination with hypoxia or 
hyperoxia gave inconclusive results. 
Binet and Bargeton {2260) 1941 have reported 
experiments on the action of oxygen inhalation on 
muscular work in rats. The animals were anesthe- 
tized and the gastrocnemius exposed and stimulated 
electrically. The work level of the stimulated muscle 
was augmented when the rats breathed oxygen. In 
human subjects, Asmussen, von Dobeln, and Nielsen 
{2259) 1948 found that breathing pure oxygen in- 
creased the capacity for work. In this study healthy 
males exercising on a bicycle ergometer were sub- 
jected to acute changes in oxygen tension of the 
inspired air. The maximum blood lactate concen- 
tration was practically the same as under normal 
air conditions. 
For further studies of the effects of high oxygen 
tensions on metabolism, papers by the following may 
be consulted; Dediulin {2262) 1949, Massey and 
Rogers {2265) 1950, and Ruiz Gijon and Lopez 
Lorenzo {2266) 1947. 
2259. Asmussen, E., W. von Dobeln, and M. Nielsen. 
Blood lactate and oxygen debt after exhaustive work at 
different oxygen tensions. Acta physiol, scand., 1948, 15: 
57-62. [P] 
2260. Binet, L. and D. Bargeton. Action de 1’inhala- 
tion de melanges riches en oxygene sur le travail muscu- 
laire fourni par le rat normal et par le rat decapsule. C. R. 
Soc. Biol, Paris, 1941,135: 1523-1526. [P] 
2261. Cordier, D., and J. Chanel. Influence de 1’in- 
halation prolongee d’oxygene sur la vitesse du transit 
gastrique et 1’absorption intestinale des solutions isoto- 
niques de glucose chez le rat. C. R. Soc. Biol., Paris, 1950, 
144: 1373-1374. [P] 
2262. Dediulin, I. M. K probleme kislotno-shchelo- 
chnogo ravnovesiia v organizme cheloveka pri ponizhen- 
nom i pri povyshennom partsial’nom davlenii kisloroda. OXYGEN INTOXICATION ABOVE ONE ATMOSPHERE—GENERAL STUDIES 
2263-2267 
[Acid-base equilibrium in the human organism in increased 
and decreased oxygen pressure.] pp. 44-45 in: Gipoksiia, 
Kiev, Akad. Nauk Ukr. SSR., 1949, 415 pp. 
2263. Kaufman, P., J. Hollo, J. Rosenthal, J. Stone, 
R. D. Beck, and V. Fink. The effect of 10% and 100% 
oxygen inhalation on certain liver-function tests. New 
Engl. J. Med., 1950, 242: 90-92. [P] 
2264. Mann, P. J. G. and J. H. ftuastel. Toxic effects 
of oxygen and of hydrogen peroxide on brain metabolism. 
Biochem. J., 1946, 40: 139-144. [P] 
2265. Massey, V. and W. P. Rogers. Effects of oxygen 
carriers and oxygen tensions on fluoroacetate inhibition 
of citrate utilization. Nature, Land., 1950, 166: 951. 
2266. Ruiz, G. J. and P. Lopez Lorenzo. El contenido 
de glicogeno del corazon de cobayas sometidos a respira- 
cion de oxigeno puro. Farmacoter. act., 1947, 4: 394-398. 
[P] 
2267. Stevenson, I. P. and L. Smith. The influence of 
oxygen tension upon the respiration of rat kidnev slices. 
Arch. Biochem., 1948, 17: 61-73. [P] 
B. EFFECTS OF OXYGEN TENSION IN EXCESS OF 
ONE ATMOSPHERE 
1. GENERAL STUDIES 
If oxygen is breathed at a sufficiently high pres- 
sure above 1 atmosphere for a sufficient length of 
time, generalized convulsions supervene. The requi- 
site length of exposure varies inversely with the 
partial pressure of oxygen breathed. The cause of 
the convulsions still remains unclear in spite of the 
large number of experimental investigations that 
have been brought to bear upon this important sub- 
ject. After the bibliographical lists of this volume of 
the Sourcebook had been compiled, and therefore 
too late for inclusion, two important papers on 
oxygen toxicity appeared in the March 1953 issue 
of the Journal of Applied Physiology. The first of 
these, by C. J. Lambertsen, R. H. Kough, D. Y. 
Cooper, G. L. Emmel, H. H. Loeschke, and 
G. F. Schmidt, is entitled “Oxygen Toxicity; Effects 
in man of oxygen inhalation at 1 and 3.5 atmos- 
pheres upon blood gas transport, cerebral circula- 
tion, and cerebral metabolism.” The second paper, 
by C. J. Lambertsen, M. W. Stroud, R. A. Gould, 
R. H. Kough, J. H. Ewing, and C. F. Schmidt, is 
entitled “Oxygen toxicity: Respiratory responses of 
normal men to inhalation of 6 to 100 percent oxygen 
under 3.5 atmospheres pressure.” These papers 
should be consulted for excellent bibliographical 
lists, critical discussions of previous research, and 
significant experimental contributions. Lambertsen 
and coworkers point out that, at present, the ex- 
planation of the convulsions resulting from expo- 
sure to high oxygen pressures appears to rest upon 
one or more of the following: (1) a direct toxic 
effect of high oxygen pressures upon certain con- 
stituents of brain cells; (2) an accumulation of 
carbon dioxide in toxic quantities in the central 
nervous system because of breakdown in the nor- 
mal transport function of hemoglobin for this gas; 
and (3) changes in the cerebral circulation. They 
conclude that central accumulation of carbon diox- 
ide on breathing oxygen at increased ambient pres- 
sures does not contribute to the toxicity of oxgyen, 
but rather may reduce indirectly the exposure of 
brain tissue to toxic levels of oxygen tension by 
producing hyperventilation and cerebral vasocon- 
striction. 
For three reports from overseas giving general 
material on the toxic action of oxygen, papers by 
the following should be consulted: Ruiz Gijon 
(2272) 1951; Spurway-Haldane and Haldane 
{2274) 1945; and Tailliez, Dumas, Cousteau, Ali- 
nat, and Devilla (2275) 1949. 
A particularly significant series of papers on oxy- 
gen poisoning in man is that presented by Donald 
(2270) 1946 and (2268 and 2269) 1947. The first 
of these gives a full explanatory and historical back- 
ground of the subject of oxygen poisoning in man. 
The first series of experiments reported by Donald 
(2268) was carried out to determine the oxygen 
tolerance of a group of healthy male subjects at a 
fixed oxygen tension corresponding to 3.7 atmos- 
pheres absolute. These experiments were carried out 
in a pressure chamber of 100-cubic-foot capacity 
and all subjects breathed oxygen at pressure until 
acute symptoms developed. Symptoms in 36 subjects 
included prolonged “dazzle,” and severe spasmodic 
vomiting to severe lip twitching. The most striking 
finding was an enormous variation in oxygen toler- 
ance in this group of human subjects. The subjects 
were also exposed to high oxygen tension in wet runs 
in a diving tank. The respiratory apparatus worn 
was a modification of the Davis submarine escape 
apparatus. A light rubberized canvas suit with a 
soft helmet was worn. The subjects breathed oxygen 
at atmospheric pressure for 10 minutes before arriv- 
ing at the experimental depth. The compression 
time was 90 seconds. The temperature of the water 
was 65° F. The first series of experimental dives was 
to 50 feet (2.5 atmospheres absolute). One hundred 
subjects were used. If a subject convulsed or had 
other severe symptoms, he was hauled out immedi- 
ately. Out of 100 subjects, 26 had convulsions, 24 
had other symptoms, and 50 had no symptoms. A 
series of dives was undertaken to compare the tol- 
erance of subjects in compressed air and under 
water at 60 feet and 90 feet of sea water. The ex- 
perimental data indicated that tolerance is greatly 
decreased when under water as compared with dry 
runs. After a large number of experiments, a new 
factor became increasingly evident. It became clear 
that the tolerance of individual subjects varied from DISEASES AND ACCIDENTS 
was not given (by accident), another attack oc- 
curred 30 seconds later. The attack is followed by 
confusion, dissociation, headache, nausea, and 
vomiting. A majority of the subjects in the post- 
convulsive period were subdued and ataxic, and 
usually fell asleep after 15 minutes. There tended to 
be amnesia for the experience and the subjects com- 
plained of stiffness in the trunk. In some subjects, 
the onset of air breathing seemed to bring on con- 
vulsions. To avoid these convulsions associated with 
transfer from oxygen to air, subjects were not de- 
compressed until symptoms were gone. In the wet 
dives, 9.2 percent of the subjects experienced con- 
vulsions, 60.6 percent showed lip twitching, and 
vertigo was experienced in 8.8 percent. Nausea was 
recorded in 8.3 percent, respiratory disturbances in 
3.8 percent, general twitching in 3.2 percent, drowsi- 
ness and confusion in 3.2 percent, visual disturb- 
ances in 1 percent, and acoustic hallucination in 0.6 
percent. Regarding pulmonary symptoms, Donald 
found no irritation of the lungs after wet dives at 
50 feet for 30 minutes. At depths greater than 30 
feet, nervous symptoms necessitated termination of 
the dive long before any pulmonary irritation oc- 
curred. X-rays taken of the exposed men over 
periods of 2 years yielded no positive findings. In 
some cases, the pulse slowed after long exposures to 
60 feet, and some of the convulsed subjects did not 
recover normal rate until several hours after ex- 
posure. There was no relation between bradycardia 
and tolerance. X-rays revealed no cardiac enlarge- 
ment. Within a 3-year period, no aftereffects were 
observed in neurological integrity, intellectual abil- 
ity, or personality. No unusual reflex effects were 
observed acutely at 60 and 90 feet dry runs. Some 
subjects showed pupillary dilation at the end of ex- 
posure. Exposure to oxygen at 120 feet had no im- 
mediate effects upon the electroencephalogram. At 
no time was any attack akin to petit mal observed 
either clinically or electrically. Donald concluded 
from his studies that variations of tolerance between 
individuals and impairment of tolerance with work 
and underwater conditions all make diving on pure 
oxygen at depths greater than 25 feet of sea water a 
hazardous undertaking. It is emphasized that no 
signs or symptoms can be given that will insure a 
timely cessation of oxygen breathing in all cases. 
Experimental studies of oxygen poisoning at 
raised atmospheric pressures have been reported by 
Pichotka and Kuhn (2277) 1947. Guinea pigs and 
rabbits breathing oxygen at 3.5 to 5.8 atmospheres 
died within a period of 1 hour. Pathological changes 
in the lungs and liver are described. 
Schaefer, Alvis, Webster, and Willmon (2275) 
1949 have investigated symptoms produced by ex- 
day to day, and it was impossible to plot a curve for 
a single subject. The findings seem to indicate that 
diving on oxygen to any toxic pressure involves a 
risk impossible to determine in advance, even if the 
diver’s tolerance has been previously measured. In 
wet oxygen dives carried out by groups of subjects 
at 50, 60, 70, 80, 90, and 100 feet, the toxic effects 
became greater as the depth increased. The varia- 
bility of the group was found to be independent of 
depth. In a series of experiments to discover at what 
pressure under water oxygen begins to cause toxic 
nervous symptoms, the author elicited no symptoms 
at 25 feet. It was surprising to find oxygen convul- 
sions at as low a pressure as 33 feet of sea water. 
Tolerance to oxygen was markedly diminished by 
vigorous work consisting of lifting a large bag of 
weights by a pulley. The physiological basis for this 
effect is not definitely known. 
The signs and symptoms of oxygen poisoning 
have been investigated by Donald (2269) 1947. 
Facial pallor occurs within a few minutes after the 
beginning of the exposure. Fasciculation of the lips 
or face is often seen early in the experiment and 
sometimes throughout the exposure. This is attrib- 
uted partially to fatigue from the mouthpiece. 
Some subjects show facial perspiration, and in some 
cases there is generalized sweating associated with 
more severe stress. Salivation seems to increase, but 
this is probably a reflex response to the presence of 
the mouthpiece. There may be nausea, vertigo, 
malaise, apprehension, or choking sensations. Palpi- 
tations may also occur. As the intoxication becomes 
more intense, there are changes in mood. Severe 
irrational apprehension, sometimes amounting to 
acute terror is observed, and sometimes the subjects 
complain of feeling “far away.” Some subjects fall 
asleep and can be aroused only with difficulty. 
Visual or auditory hallucinations are late symptoms. 
Patients complain of flashes of light in the center of 
the visual field, halos around objects, lateral move- 
ment of images, micropsia, and changes in apparent 
brightness of illumination. There may be a sense of 
ringing in the ears, deafness, or hyperacuity. Un- 
pleasant tastes or odors are complained of in the 
wet dives, but not in the dry environment. Constric- 
tion of the visual fields is gradual. Shortly before 
the convulsive attack, there is definite twitching of 
the lips which is powerful and sustained. These con- 
vulsive movements of the lips pass into generalized 
jactitations. Occasionally isolated twitching of the 
arm, leg, or trunk occurs. There may be rapid, pant- 
ing movements. Convulsive attacks due to oxygen 
poisoning were found to be about 2 minutes in 
duration and only one attack usually resulted if air 
was given immediately. On one occasion when air OXYGEN INTOXICATION ABOVE ONE ATMOSPHERE—NERVOUS SYSTEM 
2268-2275 
posure of underwater swimmers to oxygen during 
swimming trials in a tank under pressure. Subjects 
swam at a rate of about 0.9 mile an hour. Fifty trials 
were made. The average exposure time to produce 
symptoms was 61.7 ±21.5 minutes at a depth of 
22.1 ±9.9 feet. The authors concluded that at 10 
feet, 6 to 29 percent of the men would be expected 
to show symptoms. At 20 feet, symptoms would be 
shown by 10 to 33 percent. At 30 feet, symptoms 
would be found in 15 to 39 percent, while at 40 feet, 
20 to 46 percent would show symptoms. At 50 feet, 
26 to 55 percent would show symptoms, and at 60 
feet, 34 to 65 percent of the subjects would be ex- 
pected to complain of symptoms. 
2268. Donald, K. W. Oxygen poisoning in man. Brit, 
med. J., 1947, 1: 667-672. Arch. Mai. Prof., 1948, 9: 
83-85. /. industr. Hyg., 1947, 29: abstract section: 100. 
[P] 
2269. Donald, K. W. Oxygen poisoning in man. II. 
Signs and symptoms of oxygen poisoning. Brit. med. J., 
1947, 1: 712-717. [P] 
2270. Donald, K. W. Oxygen poisoning in man. Gt. 
Brit. Royal Navy, Admiralty experimental diving unit, 
H. M. S. Vernon. Report No. XVI, 1946, 208 pp. [P] [R] 
2271. Pichotka, J. and J. A. Kiihn. Experimented 
und morphologische Untersuchungen zur Sauerstoffver- 
giftung. Arch. exp. Path. Pharmak., 1947, 204: 21-36. [P] 
2272. Ruiz, G. J. La accion toxica del oxigeno. Med., 
Madrid, 1951, 18: 264-281. 
2273. Schaefer, K. E., H. J. Alvis, A. P, Webster, and 
T. 1. Willmon. Studies of oxygen toxicity. 1. Preliminary 
report on underwater swimming while breathing oxygen. 
U. S. Navy. Submarine base, New London, Conn. Medical 
research laboratory. Project NM 002 015.03.01, 22 October 
1949, 9 pp. 
2274. Spurway-Haldane, H. and J. B. S. Haldane. 
La vie humaine h haute pression. C. R. Soc. Biol., Paris, 
1945, 139: 1062-1063. 
2275. Tailliez, P., F. Dumas, J. Y. Cousteau, J. Alinat, 
and P. Devilla. Intoxication par 1’ oxygene. pp. 52—54 in; 
La plongee en scaphandre. Paris, Editions Elzevir, 1949, 
119 pp. 
2. CONVULSIONS AND OTHER DISTURBANCES OF 
THE CENTRAL NERVOUS SYSTEM 
In studies reported by Yarbrough, Welham, 
Britton, and Behnke {2289) 1947, it was con- 
firmed that naval personnel given oxygen under 
pressure supported dry chamber runs for a longer 
period than underwater runs. Subjects at rest 
tolerated a simulated depth of 60 feet with oxygen 
in the dry chamber for 2 hours without neurological 
symptoms. At the same depth under water at rest, 
32 out of 107 exposures had to be terminated prior 
to 60 minutes. The average time of termination was 
30 minutes, the range being 8 to 58 minutes. In 
2 subjects convulsive seizures occurred, 1 after 13 
minutes and 1 after 24 minutes. At a depth of 80 
feet, 74 out of 99 exposures ended prior to 60 
minutes. At a depth of 100 feet, 43 out of 46 ex- 
posures ended prior to 60 minutes. The authors 
concluded that moderate work can be done safely 
at 30 feet or less. At this depth in 35 exposures, 
symptoms were manifest in 2 men at 87 and 111 
minutes. At 40 feet, symptoms occurred in 19 out 
of 71 exposures prior to 2 hours. At 50 feet, symp- 
toms occurred in 3 out of 5 exposures. Symptoms 
responsible for termination of 168 quiescent ex- 
posures in dry and wet chambers at 60, 80, and 
100 feet were nausea, twitching, vertigo, visual dis- 
turbances, restlessness, irritability, numbness, and 
convulsions. The latter were reported in 4 percent 
of the subjects. The symptoms were found rapidly 
to disappear when air was substituted for oxygen. 
Convulsions induced in psychotic patients by 
oxygen inhalation at increased ambient pressures 
have been described and studied by Gould, Lam- 
bertsen, Kough, Stroud, Ewing, and Frehan {2284) 
1951. This report is part of a broad study of the 
effects of oxygen at high pressure. As part of this 
investigation, the possibilities of oxygen convulsions 
as a new form of convulsive psychiatric therapy are 
being studied. Kough, Cooper, Emmel, Louschcke, 
Lambertsen, and Schmidt (2285) 1950 have meas- 
ured the effects of high tensions of inspired oxygen 
on the cerebral blood flow, cerebral oxygen con- 
sumption, and cerebral vascular resistance in three 
groups of healthy young men. The original source 
may be consulted for a tabulation of results. 
For experimental studies on transient and per- 
manent aftereffects of exposure of rats to oxygen at 
high pressures, three papers by Bean and Siegfried 
(2276 and 2277) 1945 and {2278) 1946 should be 
consulted. Young adult, unanesthetized rats were 
subjected to oxygen at 65 lbs. gage pressure in short, 
single, or successive exposures {2276). The cham- 
ber temperature was maintained at 24° C., and 
carbon dioxide was absorbed. The acute reactions 
occurring during compression or immediately after 
the acute reactions included stupor, coma, catato- 
nia, hyperexcitability, hypotonia, and hypertonia, 
as well as tonic convulsive reactions, motor dysfunc- 
tions, and dyspnea. Recovery was rarely immediate 
even after single exposures. After apparent complete 
recovery from acute reactions following single ex- 
posure, alterations persisted for some time. Chronic 
effects were characterized by spastic motor paralysis, 
which in the less severe cases involved only the fore- 
legs, but which in more pronounced cases affected 
almost the entire body musculature. The chronic 
effects were induced by successive exposures given 
2 to 4 times a day and were usually permanent. The 
animals showed a wide individual variation in sus- 
291222—54—-14 DISEASES AND ACCIDENTS 
ceptibility to the chronic effects {2276 and 2277). 
Permanent motor paralysis supervened in some ani- 
mals that had failed to show acute reactions. The oc- 
currence of convulsive attacks or lesser disturbances 
during either the exposure to or decompression from 
oxygen at high pressure was not an essential prelude 
to the production of the permanent motor disabili- 
ties by successive exposures. The susceptibility of 
the animals to the toxic action of oxygen at high 
pressure was progressively increased with successive 
exposures, but this increase did not continue indefi- 
nitely. After a plateau had been attained, the suscep- 
tibility remained relatively constant unless the pro- 
gram of exposures was altered. The authors viewed 
the reactions occurring during exposure to and 
decompression from oxygen at high pressure, as well 
as the more transient of the acute postdecompres- 
sion reactions, as due to the toxic influence of an 
accumulation of endogenous carbon dioxide in the 
tissues, increased tissue acidity, and a direct action 
of oxygen at high pressure on tissue enzymes. The 
more persistent of the acute postdecompression 
effects are attributed by the authors to more slowly 
reversible alterations in the tissues, conceivably a 
slowly reversible tissue injury by these same transient 
toxic agents. In regard to the chronic postdecom- 
pression effects, manifest by permanent motor dis- 
ability, the authors consider that irreversible tissue 
damage and degenerative changes within the central 
nervous system have been induced by the same 
toxic agents. The nature of the permanent disability 
points to the upper motor neuron as the permanent 
site of disturbance, although other portions of the 
central nervous system are possibly also involved. 
Bean and Siegfried {2278) 1946 have pointed out 
that some rats exposed to oxygen at 65 pounds gage 
pressure for 10 to 25 minutes, 2 to 4 times a day 
for many days, show permanent motor disability 
characterized by chronic, spastic paralysis involving 
the limbs and body musculature for as long as 18 
months after exposure. Eight-day-old chicks exposed 
to oxygen at 90 and 65 lbs. gage pressure in a similar 
manner over a period of days were similarly af- 
fected, and the disability thus induced persisted into 
adult life. 
The syndrome of oxygen poisoning in cats has 
been reported by Gersh {2280) 1944 and {2281) 
1945. These animals were exposed to pressures of 
60, 70, 90, or 100 pounds gage pressure in oxygen. 
The cats appeared quiet until a few minutes before 
the onset of the motor seizure. They then showed 
restlessness and began to explore the inside of the 
pressure tank. The pupils became widely dilated, 
and stringy saliva drooled from the mouth. There 
was piloerection and panting. Just before the onset 
of the seizure, the muscles of the ears, forelegs, and 
neck began to twitch. Generalized convulsive move- 
ments were initiated with explosive violence, and 
continued during decompression and even 3 to 10 
minutes after removal of the animal from the tank. 
Frequently, there was micturition and defecation. 
As the involuntary movements subsided, the animals 
showed exaggerated tone in the antigravity or in 
flexor muscles. The animals were insensitive to vis- 
ual, auditory, or painful stimuli, and the pupils were 
widely dilated. As sensory functions gradually re- 
turned, the cats became difficult to arouse to motor 
activity. When the animals were subjected repeat- 
edly to oxygen seizures, there were signs of cumu- 
lative neurological damage manifested by deteriora- 
tion of hopping, placing, and dropping reactions, 
especially in the forelegs. There was also persistent 
increase in extensor tone. These changes tended to 
disappear after prolonged rest. The author con- 
cluded that the motor seizures originate in the cere- 
bral cortex in which the neurons are probably most 
sensitive to the toxic action of oxygen. This conclu- 
sion and interpretation is supported by the electro- 
encephalographic findings. Gersh {2281) 1945 and 
Gersh and Cohn {2282) 1944 found that the brain- 
wave pattern during oxygen convulsions in the cat 
resembles that observed in other well-defined clin- 
ical and experimentally induced seizures. Slow brain 
waves appear before the onset of the seizure and 
become progressively more permanent, alternating 
with periods of high frequency activity and with 
phases of exhaustion during which no activity is 
elicited. Drugs most effective in delaying the seiz- 
ures were depressants of central nervous system 
activity. Pathological changes in cats repeatedly 
exposed to oxygen under pressure were found to 
be slight. 
Stein and Sonnenschein {2288) 1950 have re- 
ported on the electrical activity and oxygen tension 
of the brain during hyperoxic convulsions in cats. 
In animals exposed to 100 percent oxygen at an 
increasing pressure of 2l/i lbs. per minute, it was 
found that convulsions appeared within 2 to 10 
minutes after a pressure of 75 lbs. gage pressure 
had been reached. The seizures lasted for a few 
seconds to 2 minutes, followed by a quiet phase of 
1 to 5 minutes before the next seizure started. 
Twenty to forty such seizures may occur in one-half 
to 1 hour at a sustained pressure of 45 lbs. gage 
pressure. After 1 hour, brain activity diminished 
and disappeared. During the seizures and the period 
of decreased activity, the electroencephalogram 
showed no marked changes in rate or rhythm. The OXYGEN INTOXICATION ABOVE ONE ATMOSPHERE—NERVOUS SYSTEM 
2276-2288 
authors concluded that the convulsions may start 
elsewhere than in the cerebral cortex. 
Gersh, Davies, and Larrabee {2283) 1945 found 
in cats in an atmosphere of oxygen under high 
pressure that the “oxygen tension” value of the 
cerebral cortex rises very early and then falls 
abruptly to a plateau which slopes to a slightly lower 
value at the time of death of the animal. Cortical 
damage may occur at the time of the sharp peak 
in oxygen tension, and after a latent period becomes 
manifest in the characteristic convulsive seizure. As 
stated, drugs which depress the central nervous 
system showed some effect in reducing the incidence 
or severity of the convulsions. Pfeiffer and Gersh 
{2286) 1944, in a study on 250 cats, investigated 
48 drugs. Of these, only a few compounds were 
found to be effective. These were glutamic acid, 
lactic acid, sodium lactate, ammonium chloride, 
cysteine, and central nervous system depressants. 
All drugs depressing the central nervous system 
showed some degree of activity, but the short-acting 
barbiturates were the most effective. When daily 
oxygen convulsions were prevented with pento- 
barbital sodium, temporary functional impairment 
of the central nervous system occurred. Metrazol, 
mecholyl, carbon dioxide, and sodium bicarbonate 
shortened the preconvulsive period. Atropine and 
methylene blue increased the severity of the con- 
vulsions. Various combinations of effective drugs 
were tried, but the only evidence of possible 
synergistic action was found with combinations of 
pentobarbital and lactic acid or sodium lactate. 
Degenerative changes induced in the central nerv- 
ous system of albino rats by exposure to oxygen at 
high pressure have been described by Siegfried and 
Bean {2287) 1946. In these experiments, albino 
rats were exposed to oxygen at increased pressure, 
usually 65 lbs. gage pressure, for short periods from 
10 to 25 minutes, 2 to 4 times a day, over a period 
of time necessary to produce definite permanent 
motor impairment. Because of wide variations in 
individual susceptibility, the program of exposures 
varied considerably for different animals. Decom- 
pression was such as to preclude the possibility of 
bubble formation. Following the last exposure, an 
interval of about 14 days was permitted to elapse 
to allow degenerative changes to become demonstra- 
ble histologically. The animals were then sacrificed, 
and brain and cord preparations examined. Histo- 
logical examination revealed numerous sites of de- 
generative changes, varying in degree from slight 
to severe. The most common and permanent degen- 
eration was found in the corticospinal tract. Less 
permanently and less consistently, degenerative in- 
volvement was found in the fasiculus gracilis and 
also the spinocerebellar tracts, the brachiumpontis, 
the cerebral peduncles, and corpus callosum. In a 
few preparations, there was evidence of optic-nerve 
involvement. The severity and extent of the histo- 
pathological lesions were not uniformly commen- 
surate with the severity and extent of the motor 
dysfunction manifest by the animal prior to sacri- 
fice. These results indicate a widespread deleterious 
effect of oxygen at these pressures on the central 
nervous system. 
For a further study of the nervous system symp- 
toms of oxygen poisoning, a note by Culpin {2279) 
1947 may be consulted. 
2276. Bean, J. W. and E. C. Siegfried. Transient and 
permanent aftereffects of exposure to oxygen at high 
pressure. Amer. J. Physiol., 1945, 143: 656-665. [P] 
2277. Bean, J. W. and E. C. Siegfried. Permanent 
motor disabilities induced by successive exposures to oxygen 
at high pressures. Fed. Proc. Amer. Soc. exp. Biol., 1945, 
4: 6. 
2278. Bean, J. W. and E. C. Siegfried. Chronic motor 
disability resulting from repeated exposure to oxygen at 
high pressure. Fed. Proc. Amer. Soc. exp. Biol., 1946, 
5: 6. 
2279. Culpin, M. Oxygen poisoning in man. Brit. Med. 
J., 1947, 2: 70-71. 
2280. Gersh, I. The syndrome of oxygen poisoning in 
cats. U. S. Navy. NMRI. Project X-192, Rept. no. 1, 
30 October 1944, 9 pp. [P] 
2281. Gersh, I. Syndrome of oxygen poisoning in cats. 
War Med., Chicago, 1945, 8: 221-228. 
2282. Gersh, I. and R. Cohn. Changes in brain poten- 
tials during convulsions induced by oxygen under pressure. 
U. S. Navy. NMRI. Project X-192, Rept. no. 4, 30 
October 1944, 5 pp. [P] 
2283. Gersh, I., P. W. Davies, and M. G. Larrabee. 
“Oxygen tension” of the cerebral cortex of cats during 
oxygen poisoning. U. S. Navy. NMRI. Project X-192, 
Rept. no. 6, 7 May 1945, 5 pp. [P] 
2284. Gould, R. A,, C. J. Lambertsen, R. H. Rough, 
M. W. Stroud, J. H. Ewing, and F. A. Freyhan. Convul- 
sions induced in psychotic patients by oxygen inhalation 
at increased ambient pressures (motion picture). Fed. 
Proc. Amer. Soc. exp. Biol., 1951, 10: 53. 
2285. Rough, R. H., D. Y. Cooper, Jr., G. L. Emmel, 
H. H. Loeschcke, C. J. Lambertsen, and C. F. Schmidt. 
Effect of inhalation of oxygen at high partial pressure 
upon cerebral circulation and cerebral oxygen consump- 
tion in man. Fed. Proc. Amer. Soc. exp. Biol., 1950, 9: 
72. 
2286. Pfeiffer, C. C. and I. Gersh. The prevention of 
the convulsions of oxygen poisoning by means of drugs. 
U. S. Navy. NMRI. Project X-192, Rept. no. 2, 30 
October 1944, 7 pp. [P] 
2287. Siegfried, E. C. and J. W. Bean. Degenerative 
changes induced in the C. N. S. of albino rats by exposure 
to 02 at high pressure. Fed. Proc. Soc. exp. Biol., 1946, 
5; 95. 
2288. Stein, S. N. and R. R. Sonnenschein. Electrical 
activity and oxygen tension of brain during hyperoxic 
convulsions. J. Aviat. Med., 1950, 21: 401—404. [P] 2289-2295 
DISEASES AND ACCIDENTS 
2289. Yarbrough, 0. D., W. Welham, E. S. Britton, 
and A. R. Behnke. Symptoms of oxygen poisoning and 
limits of tolerance at rest and at work. U. S. Navy. Naval 
gun factory, EDU. Project X-337 {Sub. no. 62) Kept, 
no. 1, January 1947, 9 pp. 
3, EFFECTS ON RESPIRATION 
In a consideration of the possible harm from in- 
halation of oxygen at high pressure, Comroe and 
Dripps (2299) 1950 draw attention to the occur- 
rence of oxygen apnea in subjects whose respiratory 
center is no longer regulated normally by carbon 
dioxide and who have no important reflexes other 
than chemoreceptor reflexes maintaining respira- 
tion. Lamhertsen, Cooper, Emmel, Loeschcke, 
Kough, and Schmidt (2295) 1950; Lamhertsen, 
Emmel, Cooper, Loeschcke and Kough (2294) 
1950; and Lamhertsen, Kough, Cooper, Emmel, 
Loeschcke, and Schmidt (2295) 1950 have reported 
the effects in man of inhalation of oxygen at high 
partial pressure upon oxygen content, carbon di- 
oxide content, oxygen and carbon dioxide tensions, 
and pH in arterial and internal jugular blood. In 
these experiments significant changes were produced 
by oxygen at 3.5 atmospheres. At 3.5 atmospheres 
the arterial plasma oxygen content almost met cere- 
bral oxygen requirements as indicated by the near 
arterial level of internal jugular hemoglobin satura- 
tion. Hemoglobin base available for carbon dioxide 
transport by reduction of hemoglobin decreased 60 
percent, producing an 8-millimeter increase in the 
arteriovenous carbon dioxide tension difference. A 
rise in venous oxygen tension reflects an increased 
brain-tissue carbon dioxide tension which probably 
contributed to the decreased arterial carbon dioxide 
tension by an increased pulmonary ventilation ob- 
served in subsequent experiments. Pulmonary irri- 
tation by oxygen has not been excluded as a factor 
in the respiratory stimulation. The small increase in 
venous carbon dioxide tension indicates that reten- 
tion of carbon dioxide in the brain during exposure 
to oxygen at high partial pressure is not an important 
factor in acute oxygen poisoning. 
Gersh (2297) 1944 has investigated pneumo- 
thorax and extrapulmonic emphysema in cats ex- 
posed to oxygen under pressure. Gross and micro- 
scopic observations on the lungs and associated 
structures of cats subjected to oxygen at high pres- 
sures showed spontaneous atelectasis. The primary 
defect appears to be a rupture of a few alveoli into 
the retropleural connective tissue in the manner of 
a one-way valve. The next state is the escape of this 
gas into the hilus, posterior mediastinal tissue and 
the pleural spaces. The final stage takes place during 
decompression and is due to the expansion of the 
gases in these sites, with a coincident compression 
of the lung. Spontaneous atelectasis was observed 
only in old cats. 
Methods for the estimation of the tissue fluid were 
utilized by Hawkinson and Gersh (2292) 1945 in 
the investigation of pulmonary edema, which de- 
velops on exposure to oxygen at 1 atmosphere and 
at high pressures. The outstanding pulmonary 
change resulting from exposure of guinea pigs to 8 
atmospheres of oxygen is a significantly decreased 
chloride concentration of the tissue fluid and of the 
lung as a whole without any important variation in 
the water content. This unexpected finding is inter- 
preted by the authors to mean that a change in per- 
meability of cells in the lungs has taken place as a 
result of the toxic action of oxygen under pressure. 
In contrast to the high-pressure experiments, ex- 
posure of guinea pigs to 1 atmosphere of oxygen 
resulted in an increased chloride and water content 
consistent with pulmonary edema. 
2290. Comroe, J. H. and R. D. Dripps. Possibilities of 
harm from the inhalation of oxygen, pp. 58—75 in: The 
physiological basis for oxygen therapy. Springfield, Charles 
G. Thomas, 1950, 85 pp. [D] 
2291. Gersh, I. Pneumothorax and extrapulmonic 
emphysema in cats exposed to oxygen under pressure. 
U. S. Navy. NMRI. Project X—I92, Kept. no. 5, 30 Octo- 
ber 1944, 4 pp. [P] 
2292. Hawkinson, G. E. and I. Gersh. Biochemical 
study of pulmonary edema of guinea pigs exposed to high 
oxygen atmospheres. U. S. Navy. NMRI. Project X-I92, 
Kept. no. 7, 24 September 1945, 7 pp. [P] 
2293. Lamhertsen, C. J., Y. D. Cooper, G. L. Emmel, 
H. H. Loeschcke, R. H. Kough, and C. E. Schmidt. Some 
observations on the role of carbon dioxide in acute oxygen 
toxicity at 3]/? atmospheres inspired oxygen tension. 
Amer. J. med. Sci., 1950, 219: 581-582. 
2294. Lamhertsen, C. J., G. L. Emmel, D. Y. Cooper, 
H. H. Loeschcke, and R. H. Kough. Effects of inhalation 
of oxygen at high partial pressures upon arterial and 
internal jugular blood gas content, tension and pH. Fed. 
Proc. Amer. Soc. exp. Biol., 1950, 9: 73. 
2295. Lamhertsen, C. J., R. H. Kough, D. Y. Cooper, 
G. L. Emmel, H. H. Loeschcke, and C. E. Schmidt, Some 
effects upon man of oxygen inhalation at high partial pres- 
sures. XVIII. Intern, physiol. Congr., 1950, 322-323. 
4. EFFECTS ON METABOLISM 
Dickens (2297) 1946 has reported that the respi- 
ration of brain tissue is slowly and irreversibly 
poisoned by exposure of the isolated tissue to oxygen 
at high pressure. Even at 1 atmosphere, very slow 
poisoning by oxygen occurs, and above this pressure 
the rate of poisoning steadily increases. No restora- 
tion of brain metabolism was observed when the 
oxygen-poisoned tissue was returned to normal pres- 
sure nor could it be restored by any of the methods 
tried. From the data, it was concluded that if the 
oxygen poisoning of brain respiration is responsible 
for the convulsion produced by oxygen at high pres- OXYGEN INTOXICATION ABOVE ONE ATMOSPHERE—METABOLISM 
sure, the clinical effects must occur when only a 
small percentage of brain respiration has been 
poisoned by oxygen. The order of sensitivity to oxy- 
gen of the respiration of various rat tissues was 
given in the following diminishing sequence: cere- 
bral cortex, spinal cord, liver, testis, kidney, lung, 
and muscle. In addition to poisoning the oxidation 
of glucose, oxygen also was found to poison the capa- 
city of the brain tissue to oxidize fructose, lactate, 
and pyruvate. The capacity of the brain slices to 
oxidize succinate is much less affected than for the 
other substrates. Feeding the rats a diet rich or 
poor in the B-factors had no significant effect upon 
brain metabolism. It was suggested that oxygen may 
poison primarily the pyruvate oxidase system, prob- 
ably attacking the essential SH group of the enzyme. 
Attention was drawn to a parallelism between the 
action of narcotics and of oxygen on cell metabolism. 
Both interfere with pyruvate oxidation, but they 
may act upon different links in the enzyme complex. 
For a further study on the toxic effects of oxygen 
on tissue enzymes, a paper by Dickens {2298) 1946 
should be consulted. 
For further investigations of the metabolic 
changes produced by oxygen poisoning, papers by 
the following should be consulted: Stadie, Riggs, 
and Haugaard {2302, 2303) 1945, and Stadie and 
Haugaard {2301) 1946. Stadie, Riggs, and Hau- 
gaard {2302) determined metabolic activity in 
vitro of surviving tissues exposed to high oxygen 
pressures in comparison with similar tissues under 1 
atmosphere of oxygen. Thin slices of brain from 
animals killed by high-pressure oxygen showed no 
significant change in total oxygen uptake or respira- 
tory quotient when these were subsequently deter- 
mined by the Warburg technique at 1 atmosphere 
of oxygen. Similar preparations of brain slices and 
homogenates from normal animals exposed in a 
preliminary period to high oxygen pressures and 
subsequently observed in a Warburg apparatus at 1 
atmosphere of oxygen showed a steadily decreasing 
rate of oxygen uptake in proportion to the pressure 
of oxygen and the time of exposure. Inhibition of 
brain metabolism by high oxygen pressures was 
similar with glucose, fructose, pyruvate, or lactate 
as the substrate. Similar results were obtained when 
normal tissues was observed at 8 atmospheres of 
oxygen. The initial rate of oxygen uptake was 
halved in approximately 1 hour’s time. The time re- 
quired for appreciable reduction in the rate of oxy- 
gen uptake was found to be far greater than for the 
production of serious symptoms, convulsions, and 
deaths when intact animals were subject to the same 
oxygen pressure. Brain slices subjected to relatively 
high pressures of carbon dioxide (up to 107 mm. 
Hg) in addition to 8 atmospheres of oxygen were 
no more susceptible to oxygen poisoning than those 
exposed to 8 atmospheres of oxygen alone. The 
metabolism of brain in vitro, although diminished, 
was not altered from its predominantly carbohy- 
drate character by high oxygen pressure. Attempts 
to reverse lowered oxygen uptake of poisoned brain 
tissue by early return to 1 atmosphere failed. The 
rate of oxygen uptake of brain tissue in vitro at 1 
atmosphere of oxygen was not affected by 7 addi- 
tional atmospheres of nitrogen or helium. On the 
basis of these experiments, the author concluded 
that generalized tissue anoxia is not the cause of 
acute oxygen poisoning. Alternative hypotheses are 
discussed. 
Stadie, Riggs, and Haugaard {2303) 1945 have 
investigated the effects of high oxygen pressures 
upon the metabolism of liver, kidney, lung, and 
muscle tissue. Regarding the liver, they found that 
at high pressures of oxygen, the rate of oxygen up- 
take during the first hour in the case of isolated 
tissue did not differ significantly from that at 1 
atmosphere. As in the case of brain tissue, the rate 
of oxygen uptake in liver tissue fell slowly and stead- 
ily during exposure, but the rate reached 50 percent 
of the control rate only after hours as opposed 
to 1 hour in the case of brain. As with brain tissue, 
although there is a definite effect of high oxygen 
pressure on oxygen uptake of liver slices, the extent 
of the effect is negligible until long after the time 
required to distinguish the last signs of life in intact 
animals under similar conditions. In experiments on 
kidney slices, it was found that long preliminary 
exposures were required to reduce the oxygen up- 
take significantly. The sensitivity of the kidney 
slices to high oxygen pressure lies midway between 
that of brain and liver slices. Again it was seen 
that the falling off in respiration takes place long 
after an intact animal would have succumbed. The 
mean respiratory quotient was not significantly dif- 
ferent from that observed at 1 atmosphere. Oxygen 
uptake of rat diaphragm was measured during ex- 
posure of isolated tissue to 8 atmospheres of oxygen. 
This muscle was found to be more resistant to 
oxygen poisoning than all other tissues examined. 
The initial rate under high oxygen pressure was not 
significantly different from that under 1 atmos- 
phere, and fell off very slowly. The authors con- 
clude that the slow development of loss of metabolic 
activity indicates that this plays little or no role in 
the acute phase of oxygen poisoning or early death 
of intact experimental animals. Stadie and Hau- 
gaard {2301) 1946 showed that intact animals un- 
der 8 atmospheres of oxygen rapidly developed 2296-2306 
DISEASES AND ACCIDENTS 
severe symptoms of oxygen poisoning without show- 
ing decreases of oxygen consumption. 
Riggs {2300) 1945 found that the tone of the 
pyloric sphincter muscle of rabbits is depressed by 
exposure to oxygen under high pressure at a rate 
similar to that at which the intact animal succumbs 
under similar conditions to convulsions and death. 
The total oxygen uptake of the muscle was found to 
be not significantly affected by high oxygen pressure 
during the time at which its tone was depressed. 
According to Bean {2296) 1951, repeated short 
exposure of baby albino rats to oxygen at high 
pressure interferes with normal growth. This and 
the recognition that conditions of stress alter ad- 
renal cortical activity suggested that exposure to 
oxygen at high pressure might also induce gross 
and microscopic changes in the adrenals. Experi- 
ments were therefore carried out in which each of 
several litters of baby and young adult rats were 
divided into test and control groups. The test ani- 
mals were exposed to oxygen at about 70 lbs. gage 
pressure for several minutes, followed by a long 
interval of rest, 4 times a day over periods from 2 
weeks to 3 months. The adrenal glands of the test 
animals exposed over the longer periods followed 
by 7 months of nonexposure were significantly larger 
and heavier than adrenals of control animals. The 
adrenal glands of animals killed immediately fol- 
lowing the termination of the shorter exposure 
schedules were also distinctly larger and heavier 
than their controls. Gersh and Wagner {2299) 1944 
found in cats that hypothyroidism lengthened the 
time of onset of the convulsive seizures and de- 
creased the cumulative neurological damage. Con- 
versely, hyperthyroidism was found to increase the 
sensitivity of the animals to oxygen at high pressure. 
For further studies on metabolic changes in oxy- 
gen poisoning, papers by Van Goor and Jongbloed 
{2304) and {2305) 1949, and {2306) 1950 may 
be consulted. 
2296. Bean, J. W. Adrenal alteration induced by 
oxygen at high pressure. Fed. Proc. Amer. Soc. exp. Biol., 
1951, 10: 11. 
2297. Dickens, F. The toxic effects of oxygen on brain 
metabolism and on tissue enzymes. 1. Brain metabolism. 
Biochem, J., 1946, 40: 145-171. Gt. Brit. MRC-RNPRC, 
UPS. R. N. P. 44/146, U. P. S. 51, March 1944, 80 pp. 
[P] 
2298. Dickens, F. The toxic effects of oxygen on brain 
metabolism and on tissue enzymes. 2. Tissue enzymes. 
Biochem. J., 1946, 40: 171-187.'[P] 
2299. Gersh, I. and C. E. Wagner. Metabolic factors 
in oxygen poisoning. U. S. Navy. NMRI. Project X-192, 
Kept. no. 3, 30 October 1944, 8 pp. [P] 
2300. Riggs, B. C. The effect of exposure to oxygen 
at high pressure upon the tonus and respiration of pyloric 
muscle from the rabbit. Amer. J. Physiol., 1945, 145: 
211-217. [P] 
2301. Stadie, W. C. and N. Haugaard. Oxygen poison- 
ing. X. The effect of oxygen at eight atmospheres upon 
the oxygen consumption of the intact mouse. /. biol. 
Chem., 1946, 164: 257-263. [P] 
2302. Stadie, W. C., B. C. Riggs, and N. Haugaard. 
Oxygen poisoning. III. The effect of high oxygen pressures 
upon the metabolism of brain. /. biol. Chem., 1945, 160: 
191-208. [P] 
2303. Stadie, W. C., B. C. Riggs, and N. Haugaard. 
Oxygen poisoning. IV. The effect of high oxygen pres- 
sures upon the metabolism of liver, kidney, lung, and 
muscle tissue. /. biol. Chem., 1945, 160: 209-216. 
2304. Van Goor, H. and J. Jongbloed. Oxygen poison- 
ing. Enzymologia, 1949,13: 313—324. [P] 
2305. Van Goor, H. and J. Jongbloed. Zuurstofver- 
giftiging in vitro en in vivo. Ned. Tijdschr. Geneesk., 1949, 
93: 2118-2120. 
2306. Van Goor, H. and J. Jongbloed. Oxygen poison- 
ing in vitro and in vivo. Acta brev. neerl. Physiol., 1950, 
17: 49-52. [P] 
C. MECHANISMS OF INTOXICATION 
1. ROLE OF CARBON DIOXIDE AND OTHER FACTORS 
IN OXYGEN INTOXICATION 
A discussion of the literature on the mechanism of 
the poisonous action of oxygen is found on pages 193 
and 194 of the first volume of this Sourcebook. We 
have also discussed the problem in the present vol- 
ume under general studies in the section on the 
effects of oxygen tension in excess of 1 atmosphere 
(p. 187). Reference is made there to recent papers 
by Lambertsen and coworkers who have indicated 
that the cause of convulsions remains uncertain, but 
that at present the explanation appears to rest upon 
one or more of the following: (1) a direct toxic 
effect of high oxygen pressures upon certain con- 
stituents of brain cells, (2) an accumulation of car- 
bon dioxide in toxic amounts in the central nervous 
system due to the breakdown in normal transport 
function of hemoglobin for this gas, and (5) 
changes in cerebral circulation. Too late for inclu- 
sion in the bibliographical lists of the present volume 
is a report by Lambertsen and his colleagues in the 
Journal of Applied Physiology, Volume V, No. 10, 
1953, on the role of carbon dioxide. 
A number of workers have reported accumula- 
tion of carbon dioxide in oxygen poisoning. Camp- 
bell and Poulton {2307) 1938 stated that an effect 
of oxygen breathing is to increase the carbon di- 
oxide content of tissues; they suggested that con- 
vulsions are due in some measure to a great increase 
of carbon dioxide pressure in the tissues. Pichotka 
{2313) 1946 subjected guinea pigs and rabbits to 
oxygen tensions ranging from 3.5 to 5.8 atmospheres. 
The author believed that oxygen poisoning is due to 
carbon dioxide accumulation in the periphery. Dur- 
ing acute oxygen poisoning, the oxygen tension of OXYGEN INTOXICATION ABOVE ONE ATMOSPHERE—MECHANISMS 
2307-2308 
the tissues reached 300 mm. Hg and the carbon 
dioxide tension reached 200 mm. Hg. When animals 
were exposed to 20 to 35 percent carbon dioxide 
in a normal oxygen atmosphere, it was found that 
the histological picture in the lung and liver were 
the same as in oxygen poisoning, although the clin- 
ical picture was different. The author considered 
that oxygen poisoning is an indirect carbon dioxide 
poisoning. 
Seelkopf and von Werz {2314) 1948 also found 
an accumulation of carbon dioxide in the tissue in 
oxygen poisoning in guinea pigs exposed to oxygen 
under pressure. This carbon dioxide congestion was 
considered mainly due to the delay of carbon di- 
oxide pickup and transport. Taylor {2316 and 2317) 
1949 placed cats in a glass chamber in which they 
breathed oxygen at atmospheric pressure. Breathing 
oxygen at atmospheric pressure led to convulsions 
and there was a progressive fall in tissue oxygen ten- 
sion and a progressive rise in tissue carbon dioxide 
tension until death or convulsions occurred. The 
tissue oxygen tension of cats exposed intermittently 
to oxygen and air at atmospheric pressures showed 
a fall and then a rise to a consistent value, this be- 
ing somewhat less than the original normal value 
when the animal was breathing air. The tissue car- 
bon dioxide tension showed little change. Animals 
thus treated were acclimatized to subsequent con- 
tinuous oxygen exposure. This effect was not per- 
manent, but was still present 7 weeks after ac- 
climatization. When the cats convulsed, the tissue 
oxygen tension was near the value for normal cats 
breathing air. Convulsions were considered by the 
author to be due neither to increased oxygen ten- 
sion in the tissues nor to anoxia. Since the carbon 
dioxide tissue gas tensions were much higher than 
normal, this was believed to support the view that 
one factor in the production of convulsions is the 
accumulation of carbon dioxide in the tissues. In a 
subsequent paper published in 1949, Taylor {2317) 
found in cats breathing oxygen at high pressure 
that both the oxygen and the carbon dioxide tissue 
tensions reached high values. Additional carbon 
dioxide shortened the time required for the onset 
of oxygen convulsions. This effect was most striking 
in cats whose convulsion time in oxygen without 
added carbon dioxide is comparatively long. 
Stroud, Lambertsen, Kough, Gould, and Ewing 
{2315) 1951, in a study of the effect of oxygen 
inhalation at increased ambient pressures upon 
tissue carbon dioxide tension in small animals and 
psychotic patients, were not able to find a marked 
immediate rise of subcutaneous carbon dioxide ten- 
sion. The rises observed were slow in onset and 
accompanied by pulmonary damage and respiratory 
failure in the small animals. No appreciable increase 
of “tissue” carbon dioxide tension occurred in 
human subjects prior to the onset of oxygen con- 
vulsions. The rapid rise of carbon dioxide tension 
found by previous workers is considered by the 
authors to be probably not due to the loss of the dual 
function of hemoglobin, but appears to be the result 
of other factors such as (1) pulmonary damage by 
oxygen and by decompression, (2) respiratory de- 
pression, and (3) diffusion of carbon dioxide into 
the depot during decompression of the animal for 
gas sampling. In the authors’ experiments, gas sam- 
pling was performed at the pressure of exposure to 
oxygen. 
Kough, Lambertsen, Stroud, Gould, and Ewing 
{2312) 1951 carried out four types of experiments 
using human subjects at 3/2 atmospheres of in- 
spired oxygen in an attempt to evaluate the role of 
carbon dioxide in acute oxygen toxicity. In four men 
carried to convulsions, the highest carbon dioxide 
tension in subcutaneous gas depots was 50 mm. Hg. 
In 12 subjects, the internal jugular carbon dioxide 
tension increased 3 mm. Hg, while the arterial 
carbon dioxide tension decreased 5 mm. Hg. In 
seven subjects, cerebral blood flow decreased 25 per- 
cent. Cerebral vascular resistance increased 50 per- 
cent, while the cerebral oxygen consumption was 
unchanged so that the internal jugular oxygen ten- 
sion was only 75 mm. Hg. In man, it appears, there- 
fore, that any elevation of tissue carbon dioxide 
tension accompanying acute oxygen poisoning at 
3/2 atmospheres is adequately explained by loss of 
the dual function of hemoglobin and changes in 
blood flow, and that elevation of tissue carbon diox- 
ide tension is not sufficient per se to produce con- 
vulsions. The significant finding in 7 experiments on 
4 subjects who breathed 2 percent carbon dioxide in 
oxygen at 3*/a atmospheres was a decrease in the 
cerebral arteriovenous oxygen difference resulting 
in an increase in the internal jugular oxygen ten- 
sion to a mean value of 800 mm. Hg. One way that 
the breathing of carbon dioxide may conceivably 
hasten the onset of oxygen convulsions is by increas- 
ing the cerebral blood flow so that a larger bulk of 
the brain is exposed to higher and presumably more 
toxic levels of oxygen. 
2307. Campbell, A, and E. P. Ponlton. Oxygen poison- 
ing. pp. 42-45 in: Oxygen and carbon dioxide therapy. 
Oxford University Press, London, Humphrey Milford, 
1938, 202 pp. [R] 
2308. Cass, R. E. Effects of high oxygen tensions upon 
the carbon dioxide production of skeletal muscle and other 
tissues of the frog. Amer. J. Physiol., 1947, 148: 490-506. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1948,1: 495. Abstr. [P] 2309-2317 
DISEASES AND ACCIDENTS 
2309. Haldane, J. B. S. Oxygen poisoning in man. Brit. 
Med. ]., 1947,2: 226. 
2310. Hill, L. Oxygen poisoning in man. Brit. Med. ]., 
1947, 2: 396. 
2311. Hough, R. H., C. J. Lambertsen, M. W. Stroud, 
R. A. Gould, and J. H. Ewing. Some observations on the 
role of carbon dioxide in acute oxygen toxicity at 8/2 
atmospheres inspired oxygen tension. Amer. J. med. Sci., 
1951, 221: 354. 
2312. Kough, R. H., C. J. Lambertsen, M. W. Stroud, 
R, A. Gould, and J. H. Ewing. Role of carbon dioxide in 
acute oxygen toxicity at 3/2 atmospheres inspired oxygen 
tension. Fed. Proc. Amer. Soc. exp. Biol., 1951, 10: 76. 
2313. Pichotka, J, Experimented Untersuchungen zur 
Ursache der Sauerstoff-Vergiftung. (lecture translation). 
U. S. AAF. Aero medical center, HQ. 3D. Central medical 
establishment. D2-46-35, 28 February 1946, 9 pp. [P] [R] 
2314. Seelkopf, K. and R. von Werz. Uber die Rolle 
der Kohlensaure bei der Sauerstoffvergiftung. Arch. exp. 
Path. Pharmak., 1948, 205: 351-366. [P] 
2315. Stroud, M. W., C. J. Lambertsen, R. H. Kough, 
R. A. Gould, and J. H. Ewing, Effect of oxygen inhalation 
at increased ambient pressures upon tissue carbon dioxide 
tension. Fed. Proc. Amer. Soc. exp. Biol., 1951, 10: 338. 
2316. Taylor, H. J. The effect of breathing oxygen at 
atmospheric pressure on tissue oxygen and carbon dioxide 
tensions. /. Physiol., 1949, 108: 264-269. [P] 
2317. Taylor, H, J. The role of carbon dioxide in 
oxygen poisoning. J. Physiol., 1949, 109: 272-280. [P] 
2. DISTURBANCES OF CELLULAR METABOLISM IN 
THE PRODUCTION OF OXYGEN INTOXICATION 
For studies on the effects of oxygen at high pres- 
sure on metabolism, the reader is referred to appro- 
priate sections on pages 192 and 193. Many experi- 
mental findings support the theory that oxygen poi- 
soning is the result of interference with cellular 
metabolism. Factors which increase aerobic meta- 
bolic requirements decrease the time of onset of oxy- 
gen seizures, and those which decrease the metabolic 
rate prolong the time of onset. Gersh and Wagner 
{2319) 1945 found that hyperthyroidism produced 
in animals by oral administration of thyroid de- 
creased the time of onset of convulsions. Thyroidec- 
tomy increased the time of onset of seizures due to 
breathing oxygen at high pressure in cats. Adminis- 
tration of thiourea or thiouracil could not be shown 
to have an effect, and in these experiments no his- 
tological evidences of thyroid inhibition were seen. 
Changes in environmental temperature (within 
the range between 22° C. and 41° C.) had no 
effect on oxygen seizures, whereas either elevation 
or depression of body temperature increased the 
susceptibility of the cat to seizures. Administration 
of oxygen under pressure (105 lbs. gage pressure) 
did not cause marked fall in temperature. Young 
cats were found to be more resistant to oxygen 
seizure than older ones, and the authors suggested 
that the greater reliance of the young brains on 
anaerobic metabolism is the explanation of this 
finding. A significant correlation between thyroid 
activity and susceptibility to the poisonous action 
of oxygen at high pressure has been determined by 
Grossman and Penrod (2527) 1949. Seventy-five 
rats of approximately 200 grams each were divided 
equally into three groups. All were fed a stock diet 
to which was added propyl-thiouracil for 22 days 
for one group and desiccated thyroid powder for 8 
days for the second group. The third group served 
as controls. Oxygen consumption was determined at 
1-atmosphere pressure, after which all the animals 
were exposed to 5.5 atmospheres of oxygen for 1 
hour. There was a highly significant inverse corre- 
lation between oxygen consumption and survival 
rate in the three groups. In the hypothyroid rats, 80 
percent of the animals survived. In the control 
group, there was a 56-percent survival. In the 
hyperthyroid group, there was a survival of 29 per- 
cent of the animals. The authors suggested that 
carbon dioxide production and accumulation is an 
important factor in the etiology of high oxygen 
poisoning. Five and one-half atmospheres of oxygen 
for 1 hour is considered to be the approximate LD50 
for the strain and age of rats used. 
In a study of the relation between inactivation 
of enzymes by oxygen and essential sulfhydryl 
groups, Haugaard (2522) 1946 reported that some 
sulfhydryl enzymes while stable in the presence of 
air are inactivated by oxygen at high pressure. 
Succinic dehydrogenase is inactivated by 2 to 4 
hours of exposure to oxygen at 7 atmospheres. 
Lactic acid dehydrogenase is rapidly inactivated at 
38° C. at 7 atmospheres in air or oxygen. At 26° C. 
there was no appreciable inactivation. Exposure to 
7 atmospheres of oxygen for 4 hours at 38° C. did 
not affect acid phosphatase activity of rat-kidney 
homogenate. Phosphorylation of glucose (rabbit- 
kidney extract) was unaffected by high-pressure 
oxygen. Enzyme reactions inhibited by exposure to 
7 atmospheres of oxygen at 38° C. were malic de- 
hydrogenase, pyruvic oxidase, choline dehydrogen- 
ase, glutamic acid dehydrogenase, and alpha-keto- 
glutaric oxidase (all rat tissue). Only one of the 
enzymes studied contained the sulfhydryl group— 
cholinesterase—was resistant to the action of oxygen 
at high pressure. The toxic action of oxygen is slow 
in intact tissue, making it difficult to correlate 
enzyme inhibition with the rapid onset of symptoms 
exhibited in intact rats exposed to oxygen at high 
pressure. 
Lenggenhager (2525) 1950 found that animals 
exposed to 3 to 6 atmospheres of oxygen die within 
a few hours. The idea that accumulation of tissue 
carbon dioxide is the cause of high oxygen death 
was rejected by this author. He based his con- OXYGEN INTOXICATION—OXYGEN PARADOX 
2318-2325 
clusion in part on the finding of normal carbon 
dioxide values in the cerebrospinal fluid of 2 human 
subjects exposed to 3 atmospheres of pure oxygen 
for 30 minutes. The clinical picture preceding oxy- 
gen death points to a predominantly cerebral cause. 
However, no histological alterations could be traced 
in the brains of animals killed by oxygen. Injection 
of a redox indicator revealed that the reducing 
power of an excised brain can be markedly lowered 
by storing the brain under high pressure of oxygen. 
However, when the dye was injected into the brain 
of an animal freshly killed by oxygen, the method 
failed to demonstrate an abnormally low reducing 
power. It was argued by the author that oxygen 
death must be brought about by changes in redox 
potentials too small to be detected by present tech- 
niques, yet sufficient to impair cerebral function. 
For further studies on metabolic factors in the 
production of oxygen intoxication, papers by Allen 
and Mortarotti {2318) 1948 and White {2324) 
1945 may be consulted, 
2318. Allen, S. C. and T. G. Mortarotti. The effect of 
rutin on oxygen toxicity in rats. Fed. Proc. Amer. Soc. 
exp. Biol., 1948, 7; 202. [P] 
2319. Gersh, I. and C. E. Wagner. Metabolic factors in 
oxygen poisoning. Amer. J. Physiol., 1945, 144: 270-277. 
/. industr. Hyg., 1946, 28: abstract section: 13. [P] 
2320. Grossman, M. S. and K. E. Penrod. Relationship 
of hypothermia to high oxygen poisoning. Amer. J. 
Physiol, 1949, 156: 177-181. [P] 
2321. Grossman, M. S. and K. E, Penrod. The thyroid 
and high oxygen poisoning in rats. Amer. J. Physiol, 1949, 
156: 182-184. Excerpta Medica. Section II. (Physiology, 
Biochemistry, and Pharmacology), 1950, 3: 321. [P] 
2322. Haugaard, N. Oxygen poisoning. XI. The rela- 
tion between inactivation of enzymes by oxygen and essen- 
tial sulfhydryl groups. /. biol. Chem., 1946, 164: 265—270. 
[P] 
2322. Lenggenhager, K. Warum wirkt Sauerstoffuber- 
druck rasch todlich? Z. ges. exp. Med., 1950, 116: 
353-377. [P] 
2324. White, W. A. Oxygen poisoning in man, effect 
of cysteine hydrochloride and ammonium chloride on the 
time of onset of toxic symptoms. U. S. Navy. NMRI. 
Project X-435, Kept. no. 1, 13 August 1945, 3 pp. 
D. EFFECT OF HIGH OXYGEN TENSIONS ON 
MICRO-ORGANISMS 
The older literature (see p. 189 of the first volume 
of this Sourcebook) indicates that oxygen under 
high pressure inhibits or deleteriously affects the 
activity of certain micro-organisms. A more recent 
study by Porter and Bean {2325) 1946 may be con- 
sulted for a report of the adverse influence of in- 
creased oxygen pressure on malarial parasites in 
vitro and in vivo. In these studies, the parasite 
Plasmodium lophurae was used. The viability of 
these parasites in duck or chick bloods exposed to 
oxygen at various pressures was compared with that 
in control bloods kept under room conditions. Ex- 
posure to oxygen for 6 hours at 30 to 60 lbs. gage 
pressure reduced the parasite viability to 68 percent 
or more below that of controls. Six hours of ex- 
posure at 15 lbs. gage pressure did not lower 
viability appreciably. Exposure to oxygen for 12 
hours at 15 lbs. gage pressure gave moderate reduc- 
tion of viability, but no reduction at atmospheric 
pressure. Previous in vivo studies revealed no detect- 
able effect on the proportion of parasitized erythro- 
cytes in infected chicks given repeated short ex- 
posures to oxygen at 50 and 90 lbs. gage pressure. 
Because of the toxicity of these pressures, the 
authors utilized pressures below 15 lbs. gage pres- 
sure. Infected chicks were kept 5 or 6 days in oxygen 
at atmospheric pressure or at 300 to 500 mm. Hg 
gage pressure for about 10 hours a day. At the peak 
of infection, the proportion of parasitized erythro- 
cytes in test chicks was 64 to 86 percent lower than 
in controls. The data indicate that increased oxygen 
pressure enhances the destruction of Plasmodium 
lophurae in drawn blood, and suppresses para- 
sitemia in infected birds. 
2325. Porter, R. J. and J. W. Bean. Adverse influence 
of increased oxygen pressure on malarial parasites in 
vitro and in vivo. Fed. Proc. Amer. Soc. exp. Biol., 1946 
5: 82. 
E. OXYGEN PARADOX 
Under certain circumstances rapid recompression 
to sea level from simulated high altitudes or admin- 
istration of oxygen following a period of hypoxia 
results in untoward psychological, cardiovascular, 
and neuromotor symptoms. There may be mental 
confusion, cardiovascular collapse, and muscular 
incoordination or convulsions. These effects are 
spoken of as the oxygen paradox. 
A thesis by Bouverot (2326) 1949 reviews com- 
pletely the subject of the oxygen paradox. Dogs 
given oxygen following hypoxia showed a slowing 
of the respiratory rate, reduction of cardiac rate, 
and a drop in arterial blood pressure. An incoordi- 
nation of movements was also observed. Sometimes 
convulsions occurred, these being either clonic or 
tonic. In man, there were psychic disturbances in- 
cluding euphoria and defects of judgment. 
A description of the paradoxic response following 
oxygen administration in patients with chronic an- 
oxemia is given by Comroe, Bahnson, and Coates 
{2327) 1950. Psychic changes were noted in 8 of 65 
patients. No patient became somnolent unless (a) 
the initial arterial pCo2 was 50 mm. Hg. or more, 
(b) the arterial oxygen saturation was below 90 
percent, and (c) oxygen therapy relieved the anox- 2326-2339 
DISEASES AND ACCIDENTS 
emia. The authors believe that the mechanism for 
the paradoxic response may possibly involve carbon 
dioxide narcosis, cerebral vasospasm, reflex depres- 
sion, increased cerebrospinal fluid pressure, or direct 
depression of the cerebral cortex by high oxygen 
tensions. 
For experimental studies on paradoxic effects of 
oxygen in human hypoxia, the reader is referred to 
papers by Latham {2333) 1948 and {2334) 1951. 
Sixty exposures of 52 people at 20,000 feet simulated 
altitude were made; 13 of these manifested para- 
doxic symptoms during oxygen administration. 
Writing-test errors reached a peak 12 seconds after 
oxygen inhalation. Cardiovascular responses fol- 
lowed approximately 40 seconds later, and these 
were accompanied by musuclar incoordination and 
mental confusion. Later, there was threat of cardio- 
vascular collapse associated with a fall in blood 
pressure and an increase in peripheral flow. 
Lemaire, Franck, and Grandpierre {2335) 1950 
recorded electroencephalograms of nonanesthetized 
subjects during a 3-minute exposure to 7-percent 
oxygen in nitrogen followed by oxygen inhalation. 
During the experiment the subjects were kept in a 
dark and silent room with their eyes closed and 
were ignorant of the actual changes in the respira- 
tory air. During the anoximic phase, the usual de- 
crease in the frequency of the electroencephalo- 
graphic waves was observed. After the inhalation of 
pure oxygen a phase of “electrical silence” appeared, 
flattening of the waves starting after 3 or 4 respira- 
tions in pure oxygen and lasting from 15 to 20 sec- 
onds. Following this, the EEG pattern returned to 
that manifested at the beginning of the experiment. 
According to Grandpierre, Franck, and Lemaire 
(2329, 2330) 1948, there is a depression of the 
respiratory center in chloralosed dogs given 100- 
percent oxygen after a brief period of anoxemia. 
For other general reports on the oxygen paradox, 
the reader may consult articles by Franck, Grand- 
pierre, and Royer {2328) 1948; Grandpierre, 
Franck, and Lemaire {2331) 1948 and {2332) 
1950; Malmejac, Chardon, and Neverre {2336) 
1947 and {2337) 1949; and U. S. Army {2338) 
1945. 
2326. Bouverot, P. Contribution a Tetude de Taction 
paradoxale de Toxygene. These. (Med.) Paris, Lyon, 1949, 
144 pp. 
2327. Comroe, J. H., Jr., E. R. Bahnson, and E. 0. 
Coates, Jr. Mental changes occurring in chronically anox- 
emic patients during oxygen therapy. /. Amer. med. 
1950, 143: 1044-1048. [GH] 
2328. Franck, C., R. Grandpierre, and P. Royer. Apnee 
provoquee chez Thomme par inhalation d’un melange 
gazeux riche en oxygene au cours de 1’anoxemie. C. R. 
Soc. Biol, Paris, 1948, 142: 376-378. [P] 
2329. Grandpierre, R., C. Franck, and R. Lemaire. 
L’excitabilite du centre respiratoire dans Taction para- 
doxale de Toxygene. C. R. Soc. Biol., Paris, 1948, 142: 
1028-1029. [P] 
2330. Grandpierre, R., C. Franck, and R. Lemaire. Les 
modifications du rythme cardiaque dans Taction para- 
doxale de Toxygene. C. R. Soc. Biol., Paris, 1948, 142: 
1030-1031. [P] 
2331. Grandpierre, R., C. Franck, and R. Lemaire. 
L’action paradoxale de Toxygene. Son interet en medecine 
aeronautique. Med. aeronaut., 1948, 3: 199-226. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and Phar- 
macology), 1949, 2: 641. Abstr. [R] 
2332. Grandpierre, R., C. Franck, and R. Lemaire. 
Travaux originaux-Taction paradoxale de Toxygene. J. 
Physiol, Paris, 1950, 42: 5-30. [R] [P] 
2333. Latham, F. Studies on the oxygen paradox. Gt. 
Brit. FPRC. Institute of aviation medicine, Farnborough. 
F. P. R. C. rept. no. 705, December 1948, 10 pp. 
2334. Latham, F. The oxygen paradox. Experiments on 
the effects of oxygen in human anoxia. Lancet, 1951, 1: 
77-81. [P] 
2335. Lemaire, R., C. Franck, and R. Grandpierre. Les 
modifications de Tactivite electrique du cerveau dans 
Taction paradoxale de Toxygene chez Thomme. C. R. Soc. 
Biol, Paris, 1949, 143: 1111—1112. Excerpta Medica. Sec- 
tion II. (Physiology, Biochemistry, and Pharmacology), 
1950, 3: 1098. 
2336. Malmejac, J., G. Chardon, and G. Neverre. Ac- 
tion paradoxale de Toxygene sur les centres vasomoteurs. 
C. R. Soc. Biol, Paris, 1947,141: 396-398. [R] 
2337. Malmejac, J., G. Chardon, and G. Neverre. Role 
eventuel de Tinfluence excitante directe du deficit en oxy- 
gene sur les centres vaso-moteurs dans la production de 
Taction paradoxale de Toxygene. C. R. Soc. Biol, Paris, 
1949, 143: 694-696. [P] 
2338. TJ. S. Army, Combined intelligence objectives sub- 
committee. Part I. Aviation medicine, pp. 4-19 in: Avia- 
tion medicine, general medicine, veterinary medicine, and 
chemical warfare. C. I. O. S. Target nos. 24/17 and 
25/82, 27 April 1945, 48 pp. 
VI. NOXIOUS AGENTS 
A. GENERAL STUDIES OF NOXIOUS AGENTS 
Du Bois has carried out pioneer research on nox- 
ious gases and other agents occurring in submarines. 
A classical paper on this subject by Du Bois {2340) 
1919 should be read. The reader is also recom- 
mended to examine the standard texts and mono- 
graphs on toxicology. Reference is made to the 
monograph by Elkins {2341) 1950 for up-to-date 
discussions of industrial toxic hazards, organic and 
inorganic compounds, prevention methods, max- 
imal allowable concentrations of toxic agents, sam- 
pling and measuring devices, and analytical meth- 
ods and procedures. Maximum allowable concen- 
trations of atmospheric contaminants have also been 
listed by Cook {2339) 1945. 
2339. Cook, W. A. Maximum allowable concentrations 
of industrial atmospheric contaminants. Industr. Med., 
1945, 14: 936-946. NOXIOUS AGENTS—CARBON MONOXIDE 
2340-2362 
2340. Du Bois, E. F. Gases occurring in submarines, 
pp. 9-19 in; Review of recent work on air purification in 
submarines. U. S. Navy. BuMed. Submarine ventilation. 
Bulletin No. 4 {126632), March 15, 1919, 47 pp. 
2341. Elkins, H. B. The chemistry of industrial toxi- 
cology. New York, John Wiley & Sons, Inc., 1950, ix, 
406 pp. [R] 
B. NOXIOUS GASES, DUSTS, AND VAPORS 
1. CARBON MONOXIDE 
(a) General Studies of Carbon Monoxide Poisoning 
New problems of possible carbon monoxide haz- 
ards are posed by the development of snorkeling. 
With strong following winds, engine exhaust gases 
may not be carried away completely from the air 
intake. Leaks in the exhaust lines within the sub- 
marines may also give rise to carbon monoxide poi- 
soning. In deep-sea diving, faulty compressors may 
carry down carbon monoxide to the diver himself. 
A similar problem may exist in caisson operations. 
A further carbon monoxide hazard arises in connec- 
tion with regeneration of the air in submarines. 
Chemical generation of oxygen by means of the 
chlorate candle may introduce some carbon monox- 
ide into the air. Concentrations of carbon monoxide 
in the air become more hazardous in proportion to 
reduction of the partial pressure of oxygen or in- 
creased atmospheric pressure as in deep-sea diving. 
Although there is a considerable bulk of literature 
on carbon monoxide poisoning, knowledge of the 
actual mechanism of carbon monoxide intoxication 
has not advanced far beyond that reported in the 
first volume of this Sourcebook. Among the general 
references that follow, papers by the following are 
particularly significant; Campbell and Fulton 
{2342) 1938, Gt. Brit. Factory Department, Minis- 
try of Labour and National Service {2350) 1945, 
Hamilton and Hardy {2351) 1949, Jacobs {2352) 
1949, McConnell {2354) 1951, Reed and Harcourt 
{2358) 1941, Rossiter {2359) 1947, and Sayers 
{2360) 1951. 
2342. Campbell, A. and E. P. Poulton. Carbon monox- 
ide poisoning, etc. pp. 113-119 in: Oxygen and carbon 
dioxide therapy. London, Oxford University Press, 1938, 
202 pp. 
2343. Dahlstrbm, H., G. Obreschkow, and T, Sjbstrand. 
A comparison between the effects of carbon monoxide 
poisoning and inhalation of air with low oxygen content 
upon respiration, circulation, alkaline reserve of the plasma 
and patellar reflex in normal subjects and in cases of 
“Chronic Producer Gas Poisoning.” Acta pharm. toxicol., 
Kbh., 1947, 3: 105-123. Excerpta Medica. Section II. 
(Physiology, Biochemistry, and Pharmacology), 1948, 1: 
693. Abstr. [P] 
2344. Flandin, C. and J. Guillemin. L’intoxication oxy- 
carbonee. {Etude clinique et therapeutique). Paris, Masson 
et Cie, 1942, 156 pp. [R] 
2345. Forssman, S., B. Gullberg, and A. Svensson. Gen- 
gasforgiftnings problemen. Nord. Med., Stockholm, 1946, 
32: 2716-2722. [P] 
2346. Fourcade, J. Intoxications par 1’oxyde de carbone. 
pp. 172—196 in; Medecine du travail. Edited by C. 
Simonin. Paris, Librairie Maloine, 1950, 913 pp. [D] 
2347. Fridliand, I. G. K pathogenezy otravlenii okis’iu 
ugleroda v Leningrade v 1941-1943 gg. [Pathogenesis of 
carbon monoxide poisoning in Leningrad in 1941—1943.] 
pp. 65—88 in: Otravleniia okis’iu ugleroda v osazhdennom 
Leningrade v 1941—1943 gg. [Carbon monoxide poisoning 
in besieged Leningrad in 1941-1943.] Leningrad, S. M. 
Korova, 1947, 118 pp. 
2348. Fridliand, I. G. Nekotorye osobennosti kliniki in- 
toksikatsii okis’iu ugleroda v Leningrade v 1941-1943 gg. 
[Certain characteristics in the clinical aspects of carbon 
monoxide poisoning in Leningrad, 1941-1943.] Sovetsk. 
Vrach. Zh., 1947, 5: 13-17. 
2349. Fridliand, I. G. Nekocorye voprosy terapii. [Ther- 
apeutic problems.] pp. 93-106 in: Otravleniia okis’iu 
ugleroda v oxazhdennom Leningrade v 1941—1943 gg. 
[Carbon monoxide poisoning in the besieged Leningrad 
in 1941-1943.] Leningrad, S. M. Kirova, 1947, 118 pp. 
2350. Gt. Brit., Factory department, Ministry of la- 
bour and national service. Memorandum on carbon 
monoxide poisoning. Form 827, May 1945, 32 pp. 
2351. Hamilton, A. H. and H. L. Hardy, Asphyxiants, 
pp. 219-267 in: Industrial toxicology. New York, Paul B. 
Hoeber, Inc., 1949. 
2352. Jacobs, M. B. Carbon monoxide, carbon dioxide, 
cyanides, and nitriles, pp. 401-466 in: The analytical 
chemistry of industrial poisons, hazards, and solvents. 
New York, Interscience Publishers, Inc., 1949, 788 pp. 
2353. Kohn-Abrest, M. Sur 1’oxycarbonemie. Arch. mal. 
Prof., 1949,10: 37-38. [D] 
2354. McConnell, W. J. Diseases due to chemical agents. 
Carbon monoxide poisoning, pp. 507-508 in: A textbook 
of medicine. Edited by R. L. Cecil and R. F. Loeb. 
Philadelphia, W. B. Saunders Co., 1951, 1549 pp. 
2355. Moeschlin, S. Zum Problem der Kohlenoxydven- 
giftung (Leuchtgas). Schweiz, med. Wschr., 1946, 76: 
508-510. Abstr. [R] 
2356. Pierquin, L. Acquisitions recentes concernant 1’in- 
toxication oxycarbonee professionnelle. Med. usine, 1950, 
12:101-102. [D] 
2357. Raymond, V. and A. Vallaud. L’oxyde de carbone 
et I’oxycarbonisme. Institut national de securite pour la 
prevention des accidents du travail et des maladies pro- 
fessionnelles, Paris, 1948, 367 pp. 
2358. Reed, J. V., and A. K. Harcourt. Carbon monox- 
ide pp. 24-31 in: The essentials of occupational diseases. 
Springfield, Charles C. Thomas, 1941, 225 pp. 
2259. Rossiter, F. S. Carbon monoxide, pp. 113-129 
in: Introduction to industrial medicine. Edited by T. 
Lyle Hazlett. Second edition. Chicago, Industrial Medicine 
Publishing Co., 1947, 260 pp. 
2360. Sayers, R. R. Carbon monoxide poisoning, pp. 
123—129 in: Practice of medicine. Volume 8. Edited by 
Frederick Tice. Hagerstown, W. F. Prior Co., Inc., 1951, 
627 pp. 
2361. Wohlfart, G., B, Gullberg, and A. Svensson. 
Differential diagnostiska synpunkter pa akut och kronisk 
koloxidforgiftning. Nord. Med., Stockholm, 1946, 32: 
2726-2734. 
2362. Zahle, V. Om den akute kulilteforgiftning. 
Ugeskr. Laeg., 1948,110: 1024. 2363-2368 
DISEASES AND ACCIDENTS 
2363. Anon. Case 37. Carbon monoxide poisoning. 
Amer. Practit., 1947/48,2: 411-414. 
(b) Carbon Monoxide in Submarines and Other Naval 
Vessels 
Although there are a variety of carbon monoxide 
problems on board submarines, experience has 
shown that carbon monoxide poisoning rarely oc- 
curred in normal submarine operations prior to the 
use of the snorkel. In normally functioning sub- 
marines in the presnorkel period, practically no 
carbon monoxide was forced into the boat. Malorny, 
in 1948 {2365), reporting on carbon monoxide in 
submarines in the German submarine fleet during 
World War II, stated that the content of carbon 
monoxide in diesel exhaust gases was rather low. 
Malorny reported that during normal snorkel oper- 
ations, concentrations of carbon monoxide of 0.01 
up to 0.04 volume percent developed. The crew 
was exposed to such concentrations for many hours 
without interruption. During submerged operations 
with the snorkel there was an increase of negative 
pressure within the boat if a wave broke over the 
snorkel head or if an inexperienced planesman did 
not maintain correct snorkel depth. Under such 
circumstances reduction of oxygen partial pressure 
resulted in increased toxicity of the carbon mon- 
oxide, especially in the engineroom. In submerged 
snorkel operations the carbon monoxide concentra- 
tion in the engineroom sometimes attained toxic 
values from 0.10 to 0.24 volumes percent of carbon 
monoxide. Many cases of central nervous system 
damage occurred as a sequel to carbon monoxide 
poisoning, and it is known that there were deaths 
attributed to carbon monoxide poisoning in the 
German submarine fleet. 
Malorny {2366) in 1948 gave a report on meas- 
urements of carbon monoxide in the air of small 
submarines of the German Navy. In these one-man 
submarines fatal carbon monoxide poisoning oc- 
curred repeatedly in craft equipped with gasoline 
engines. The exhaust gases from these engines have 
a high carbon monoxide content, and the slightest 
leakages of the exhaust line in the confined spaces 
permitted the accumulation of dangerous concen- 
trations of carbon monoxide. It was unexpectedly 
found that in craft operated with electric motors 
toxic concentrations of carbon monoxide were also 
found if the electric charge was too high. Whether 
this was due to sparking of the brushes or heating 
up of insulating material is not entirely clear. 
Schaefer {2367) in 1948 similarly drew attention 
to the danger in snorkel operations of the addition 
of carbon monoxide to the submarine atmosphere 
from the engines and stated that subtoxic and 
sometimes toxic concentrations of carbon monoxide 
developed. 
Ellis {2364) gave an account in 1947 of another 
potential hazard from carbon monoxide in sub- 
marine operations. A torpedo motor started by ac- 
cident when the torpedo tube of a submarine was 
being loaded at Malta in May 1941. It filled the 
torpedo compartment with exhaust fumes. An offi- 
cer entered the compartment to rescue one of his 
men who had collapsed. The officer lost conscious- 
ness and was exposed to the toxic environment for 
6 to 10 minutes. The officer was delirious after re- 
covering consciousness and suffered from mental 
confusion for a long time. For many days he was 
completely blind. His vision then returned gradu- 
ally. He was still unable to write for 2 months after 
the incident, partly because incoordination of fine 
movements and partly because of loss of memory 
and word pattern. Later he made a complete re- 
covery. The man rescued from the compartment 
died later. A similar incident followed the firing of a 
practice salvo of torpedos at Malta later in the same 
year, when several of the torpedo firing party were 
overcome. 
Solandt and Bunker {2368) reported in 1944 that 
under normal and blackened ship conditions the 
average level of carbon monoxide in the engine- 
room of “Fairmiles”-class vessels in the Royal Ca- 
nadian Navy does not rise significantly above 0.009 
percent. The authors stated that this level does not 
constitute a danger. Some cases of carbon monoxide 
poisoning were reported which were stated to be 
due to defect in the exhaust system with leakage of 
exhaust fumes. 
2364. Ellis, E. P. The hazards of toxic gases in warships 
excluding agents of chemical warfare. /. R, nav. med. 
Serv., 1947, 33: 25-37. [R] 
2365. Malorny, G. Carbon monoxide on submarines, 
pp. B: III—1—B: III—49 in: Monograph on submarine 
medicine, Folio III, Germany. U. S. Zone. Office of naval 
advisor. 1948. 
2366. Malorny, G. The development of carbon monox- 
ide on minature submarines (one man submarines), 
pp. B: IV—1—B: IV-24 in: Monograph on submarine 
medicine. Folio III, Germany. U. S. Zone. Office of naval 
advisor. 1948. 
2367. Schaefer, K. E. Technical influences. I. Carbon 
monoxide, admixtures of the air, and trace substances, 
pp. B: 1—35—B: 1—38 in: Monograph on submarine 
medicine, Folio I, Germany. U. S. Zone. Office of naval 
advisor. 1948. 
2368. Solandt, D. Y., and M. L. Bunker. Investigation 
of carbon monoxide hazards in naval vessels. Canada 
NRG. Proceedings of third meeting of associated com- 
mittee on naval medical research. Project C4076, 15 May 
1944, 9 pp. [P] NOXIOUS AGENTS—CAEBON MONOXIDE 
(c) Clinical Picture, Functional Changes, and Patho- 
logical Effects of Carbon Monoxide Poisoning 
Carbon monoxide poisoning continues to be a 
potential hazard in industry as well as in submarine 
operations. After prolonged moderate exposure to 
carbon monoxide, there may be symptoms of acute 
intoxication, or symptoms of chronic carbon mon- 
oxide poisoning may develop without preceding 
acute intoxication symptoms. There may be head- 
ache, lassitude, drowsiness during the day, insomnia 
at night, irritability, loss of memory, vertigo, tremor, 
paresthesiae, and slight confusion. There may also 
be such symptoms as palpitation, precordial pain, 
dyspnea, colic, attacks of diarrhea, polyuria, im- 
potence, and reduced tolerance for alcohol. There 
may be attacks of elevated temperature and dis- 
turbances of vision and hearing. Grut (2390) drew 
attention to the importance of differentiation of 
chronic carbon monoxide poisoning from recurring 
acute intoxication, and from the sequele of severe 
acute intoxication. In the course of studies carried 
out in English motorcar factories to determine the 
risk of carbon monoxide intoxication of workers, 
Feil (2387) reported in 1948 that the highest blood 
concentrations of carbon monoxide were detected 
among those workmen in the heating section, 
workers in foundries, truck drivers, and those super- 
vising gas production. Among those working in 
parts of factories not particularly exposed to carbon 
monoxide intoxication, 83 percent of the workers 
had a blood carbon monoxide concentration of less 
than 0.6 cu. cm. per 100 cu, cm. of blood and only 
4 percent had more than 1 cu. cm. of carbon mon- 
oxide per 100 cu. cm. of blood. Feil reported that 
a high content of carbon monoxide in the blood 
does not necessarily imply industrial poisoning. 
After a slight inhalation of gas there may be a 
transient carbon monoxide hemoglobinemia with- 
out injury to the health. He stated that chronic 
carbon monoxide poisoning can be affirmed only 
if carbon monoxide is found in the blood in con- 
siderable amounts several weeks after cessation of 
the dangerous occupation. 
Bonnevie and Grut (2374) reported in 1948 that 
90 percent of workers in foundries showed acute 
symptoms on the molding day while only slight 
symptoms of chronic carbon monoxide poisoning 
were encountered. This the authors attributed to 
the short and infrequent exposure. They encoun- 
tered few chronic and acute cases in gasworks, and 
then only under defective outdated working pro- 
cedures. After moderate exposure to carbon mon- 
oxide gas for 8 hours daily, 8 out of 15 female 
workers showed symptoms of chronic intoxication 
which disappeared after ventilation improvements. 
In locomotive running sheds and tunnels the air 
may contain high concentrations of carbon mon- 
oxide causing acute symptoms, but generally chronic 
intoxication does not occur. The authors reported 
that although 42 percent of bus drivers showed 
symptoms of acute intoxication, the occurrence of 
chronic carbon monoxide poisoning was not greater 
than in controls. For a further study of carbon 
monoxide poisoning in drivers or conductors, a 
paper by Peloquin (2403) published in 1951 may 
be consulted. 
Chinn (2380), in a paper published in 1949, in- 
dicated the potential hazard of carbon monoxide 
poisoning in workers employed in airplane-engine 
repair shops. In 11 workers exposed to concen- 
trations of less than 0.005 percent of carbon mon- 
oxide, there was no significant increase in the car- 
boxyhemoglobin concentration in the blood after a 
normal 8-hour working day. In those workers ex- 
posed to an air concentration of 0.005 to 0.015 
percent carbon monoxide, there was an average 
increase of 4.1 percent carboxyhemoglobin observed 
in the blood at the end of the day. These latter 
carbon monoxide concentrations in the air were 
found in poorly ventilated areas of the engine test 
section, the pickup line, and the engine storage 
room. Among those workers breathing less than 
0.005 percent carbon monoxide in the air, no blood 
samples contained more than 6 percent carboxy- 
hemoglobin. Among the persons breathing 0.005 to 
0.015 percent carbon monoxide, 77 percent had 
carboxyhemoglobin concentrations exceeding this 
figure; 54 percent had over 8 percent carboxyhemo- 
globin; 17 percent had over 10 percent carboxy- 
hemoglobin. Chinn reported that about 30 percent 
of all workers in this study claimed occasional or 
recurring headaches which were attributed to the 
working conditions. 
Kugelberg (2394) in 1946 investigated 215 cases 
of carbon monoxide gas injuries, mainly among 
bus drivers in Stockholm. In at least 91 cases there 
was fusion reduction and conversion weakness 
leading to temporary diplopia and error in 
judging distances. In some cases there was weak- 
ness of accommodation, but no case of limitation 
of the field of vision, color discrimination, or any 
reduction of vision or ordinary paralysis of the eye 
muscles. Almgren (2369) in 1950 stated that the 
symptoms of carbon monoxide poisoning may be 
subjective and that there may also be definite oph- 
thalmological signs present. In 197 cases of carbon 
monoxide poisoning with opthalmological findings 
at the author’s clinic, 78 showed conversion defects, 
69 showed convergence and fusion disturbances, 
and 50 fusion disturbances only. A followup study DISEASES AND ACCIDENTS 
of 66 cases revealed that these disturbances lasted 
as long as 6 months, 2/z years, or longer. A case 
was reported in 1951 by Fink {2388) of a 30-year- 
old white man who accidentally inhaled a quantity 
of illuminating gas from a faulty heater who, after 
a period of unconsciousness for 2 days, was afflicted 
with complete blindness, a weakness in the right 
upper extremity, and a depression of mental func- 
tions. During the following weeks, there was an 
improvement in vision and motor capacity. After 
the condition had become static, opthalmological 
examination revealed marked loss of visual acuity 
in each eye, with good color perception and active 
pupillary responses. The visual fields were markedly 
constricted. Restriction of the visual field following 
carbon monoxide poisoning in a driver continually 
exposed to carbon monoxide was also reported by 
Mercier {2401) in 1947. In this case, there was also 
a reduction in dark adaptation. Halperin, Niven, 
McFarland, and Roughton {2391) in 1947 reported 
an investigation of the comparative and the com- 
bined effect of carbon monoxide and hypoxic 
hypoxia on human visual intensity discrimination. 
In previous studies they had found that the meas- 
urement of the visual, intensity discrimination 
thresholds at a low level of illumination provide a 
sensitive, useful, and precise quantitative index of 
the physiological disturbances resulting from oxy- 
gen deprivation, and they applied the same tech- 
nique in measuring the defect of small concentra- 
tions of carbon monoxide. They report that a given 
increase in the percentage of carboxyhemoglobin 
in the blood at sea level produces an effect approxi- 
mately equal to that of a comparable decrease in 
the percentage of oxyhemoglobin due to hypoxic 
hypoxia. At simulated altitudes, a given percent- 
age of carboxyhemoglobin produces an impair- 
ment equivalent to a further ascent which would 
cause an equal additional decrement in the per- 
cent of oxyhemoglobin. They have stated that 
the visual threshold is much more sensitive to car- 
bon monoxide than are other physiological func- 
tions so far investigated. The authors found in a 
study of the recovery from carbon monoxide that 
inhalation of pure oxygen was more beneficial than 
inhalation of air in producing recovery. In a fur- 
ther study, McFarland, Niven, and Halperin 
{2400) in 1948 found that carbon monoxide was 
significantly effective even in small quantities in 
accentuating the effect of hypoxia. The change in 
oxygen tension of the blood was shown to be the 
determining factor in the elevation of the visual 
threshold. This was true whether it was associated 
with a loss in the oxygen-carrying capacity of the 
blood due to saturation with carbon monoxide, or 
a loss in the arterial oxygen saturation due to alti- 
tude, or to a combination of both factors. The 
saturation of the blood with carbon monoxide 
therefore results in defects equal to those caused by 
lowered arterial oxygen saturation of the same 
magnitude. 
During World War II, a shortage of gasoline in 
the Scandinavian countries led to the use of carbon 
monoxide for motorcar power. This gave rise to 
large numbers of cases of carbon monoxide poison- 
ing. Lumino {2398) reported in 1948 a total of 700 
patients exposed to the influence of gases, especially 
carbon monoxide, in daily work and who were 
examined in the otolaryngological clinic of the Uni- 
versity of Helsinki between 1 December 1945 and 
31 May 1947. Of these, 263 suffered with chronic 
carbon monoxide poisoning. Detailed examination 
revealed hearing deficiency in 78.3 percent of all 
patients with chronic carbon monoxide poisoning, 
and 26.7 percent in patients having no definite ob- 
jective symptoms of poisoning. The hearing loss 
dropped steeply between 1,000 and 2,000 cycles, and 
when the vibration rate was increased the hearing 
decreased steadily. Although the audiometric exam- 
inations revealed defective hearing in 78.3 percent 
of the patients tested, only 47.9 percent complained 
of reduction in hearing. Followup examination 
showed an improvement in auditory acuity in 26.7 
percent of the cases. Improvement was always slight 
and occurred chiefly in those patients with only a 
slight initial hearing disturbance. In 10.7 percent of 
the cases, hearing returned to normal. Lumio con- 
cluded on the basis of these studies that carbon 
monoxide poisoning is frequently responsible for 
hearing impairment. Lumio further reported in 
1948 {2399) that followup examinations 1 to 3 
months later in some cases revealed subjective im- 
provement in hearing, but no great improvement in 
the audiometric findings. 
The symptoms of chronic carbon monoxide poi- 
soning have been reported by Bourguignon {2376) 
in 1950. This author also described audiometric and 
other tests for chronic carbon monoxide poisoning. 
The poisoning effects of carbon monoxide particu- 
larly involved the central nervous system. There may 
be a disturbance of intellect, behavior, and con- 
sciousness with maniacal shouting, extreme rest- 
lessness, and struggling. The basal ganglia may be 
affected, and there may be hypertonia, increased or 
absent deep reflexes, clonus, and bilateral Babinski 
responses. Corkhill {2381) in 1947 commented 
upon cerebral edema with rise of cerebrospinal fluid 
pressure in these cases, and he recommended intra- 
venous injections of 100 cu. cm. of 15 percent NOXIOUS AGENTS—CARBON MONOXIDE 
saline solution to relieve headache and mental con- 
fusion. Four cases of carbon monoxide poisoning, 
showing characteristic extrapyramidal rigidity re- 
sembling Parkinson’s syndrome, were described in 
1949 by de Lehoczky {2395). These cases were also 
characterized by mental confusion and dementia. 
Pathological examination revealed a bilateral soft- 
ening of the globus pallidus. In one case there were 
minimal lesions in the cerebral cortex, while in 
others there were severe alterations, not specifically 
localized but observed diffusely in nerve cells. 
Wohlfart, Gullberg, and Swensson {2411) stated 
in 1947 that subjective sensations are noted when 
the carboxyhemoglobin level reaches 30 percent. 
A saturation of 50 percent usually connotates mental 
involvement with cerebral as well as cardiac lesions. 
The author has discussed cases of Parkinsonism, 
hyperkinesis, hemiplegia, nystagmus, severe loss of 
equilibrium of the vestibulspinal type, and confu- 
sion. All of these cases have been attributed to 
chronic carbon monoxide poisoning. In a study of 
carbon monoxide poisoning in Finland between 
1940 and 1947, Sumari {2407) reported in 1948 
on the examination of 2,139 persons working in 
carbon monoxide-contaminated environments. In 
these cases arterial blood pressure was found to be 
above normal in 30 percent. Asymmetry and exag- 
geration of the reflexes with slight disturbances of 
the sensory and the sympathetic nervous systems 
were found in 70 percent. Vestibular disturbances 
were seen in 56.1 percent, and 67.7 percent of the 
cases had bilateral symmetrical deficiency in hear- 
ing. About 80 percent of the cases showed constric- 
tion of the visual field, particularly to blue light. 
The most commonly observed neuropsychiatric dis- 
turbance was a so-called toxic neurastenia. In fol- 
lowup examinations it was ascertained that in mild 
cases the symptoms disappeared in 1 to 4 months. 
In those cases of medium or moderate severity the 
symptoms disappeared in 6 months, and in the severe 
cases there were residual subjective and objective 
symptoms. 
A report by Zahle {2412), published in 1947, 
indicates that peripheral neuritis is a rare but im- 
portant sequel to acute carbon monoxide poisoning. 
Zahle’s report is based upon a review of the litera- 
ture and a study of his own material 
1,308 cases. Zahle concluded that peripheral nerve 
lesions following carbon monoxide poisoning most 
often affect the branches of the sciatic nerve. 
Regarding psychiatric complications of carbon 
monoxide intoxication, Benon {2372), reported in 
1949, considered that the first effect of carbon 
monoxide poisoning was a psychic and muscular 
asthenia. This condition, the author stated, dis- 
sipates gradually and is replaced by a hyperasthenia, 
sometimes with manic excitation, and this may give 
way to a periodic manic psychosis referred to by the 
author as a periodic dysthenia. Courville (2382) 
stated in 1948 that the danger of psychotic reaction 
or pyramidal or extrapyramidal disabilities is 
greater if the coma lasts longer than 36 hours. 
Cardiovascular changes in acute carbon mon- 
oxide poisoning have been reported by Loeper, 
Varay, Cottet, and Leveille (2397) in 1947. In 17 
cases of acute carbon monoxide poisoning, the 
authors found no evidence of angina pectoris. In 
one patient there was a transitory hypertension, 
while in two the arterial pressure remained essen- 
tially normal. In the others there was a hypotension. 
In some cases, the heart was abnormally slowed and 
in others there was tachycardia. Occasional extra- 
systoles were observed. There were many and 
variable electrocardiographic changes, the out- 
standing ones being disphasic changes in the 
P-wave, enlargement of the QRS complex, and 
flattening of the T-wave. It was found that prog- 
nosis depends upon individual predisposition, and 
is more grave in the presence of circulatory defects. 
In 29 cases of renal involvement following carbon 
monoxide poisoning, the authors found elevated 
blood urea nitrogen in 14 patients. Urinary exami- 
nation disclosed but a few cases with albumin, casts, 
or red cells in the specimens. In two cases the 
elimination of PSP was reduced. It was concluded 
that the renal impairment in carbon monoxide 
poisoning is a result of renal asphyxia. Dahlstrom, 
Obreschkow, and Sjostrand {2383) reported in 
1947 a comparison between the effects of carbon 
monoxide poisoning and inhalation of air with low 
oxygen content upon respiration, circulation, alka- 
line reserve of the plasma, and the patellar reflex 
in normal subjects and in cases of “chronic producer 
gas poisoning.” Generally speaking, the effects were 
comparable. Similar findings have been reported by 
Swann and Brucer {2408) in 1949. For case his- 
tories of acute carbon monoxide poisoning with 
sample electrocardiograms, the reader is referred 
to a paper published in 1948 by Borst and Otten 
{2375). 
The effects of experimental carbon monoxide in- 
halation in dogs upon peripheral vasomotor reac- 
tions have been reported in 1948 by Binet and Bur- 
stein {2373). In the perfused paws of dogs with the 
innervation intact, carbon monoxide inhalation re- 
sulted at first in an intense vasoconstriction, stated 
by the authors to be of central origin, giving way 
in the terminal phase to an ’equally intense phase DISEASES AND ACCIDENTS 
of dilatation. This latter phase was considered by 
the authors to be of humoral origin. In 1948, Sjost- 
rand (2405) investigated the effect of carbon mon- 
oxide upon the diameter of the blood vessels in the 
pia mater. A glass window was mounted in the 
cranial wall of cats under light dial or ether anes- 
thesia, and through this window the effect of carbon 
monoxide administered via the lungs upon the di- 
ameter of the blood vessels in the pia mater was 
observed directly with an ocular micrometer. The 
brain volume was estimated by determining the dis- 
tance between the brain surface and the window 
surface. Intracranial pressure was measured by a 
water manometer connected to a cannula fastened 
into the cranial window. During absorption of car- 
bon monoxide, the diameter of the blood vessels in 
the pia mater enlarged. The brain increased in vol- 
ume and the intracranial pressure rose. After the 
administration of carbon monoxide, the brain vol- 
ume and the diameter of the blood vessels slowly 
decreased approximately to their original level. 
The intracranial pressure, however, fell considerably 
below the prestimulation level. These observations 
are considered by the author to explain the head- 
aches accompanying carbon monoxide poisoning 
and other very profound effects which this gas may 
have upon central nervous functions. 
Asmussen and Knudsen (2370) reported, in 
1943, studies on acute, moderate carbon monoxide 
poisoning in two normal men (25 to 32 percent car- 
boxyhemoglobin in the blood). In these investiga- 
tions, it was found that the relative cell volume of 
the blood as well as the plasma protein concen- 
tration were augmented after inhalation of carbon 
monoxide, suggesting a leakage of fluid from the 
vessels, presumably associated with peripheral vaso- 
dilatation. An increased rate of filtration could not 
be detected in the lower extremity. The concentra- 
tion of glucose and lactic acid in the blood was un- 
affected by this degree of carbon monoxide intoxi- 
cation so long as the subject remained quiet. In 
moderate work, the concentration of lactic acid in- 
creased, whereas the blood-sugar level remained 
normal. Glucose tolerance was unaffected by this 
degree of carbon monoxide poisoning. In a series 
of 17 cases of chronic carbon monoxide poisoning, 
Helve (2393) in 1949 found no striking differences 
from normal in the figures for blood phosphorus in 
various forms or cholesterol. 
Cameron and Collins (2377) reported in 1946 a 
study of reproduction and lactation in albino rats 
during prolonged exposure to carbon monoxide. 
Adult female rats were exposed to sublethal amounts 
of carbon monoxide twice every 24 hours for 12 to 
24 days. These animals gave birth to normal litters, 
but histological examination of the gonads of the 
exposed rats revealed extensive damage and degen- 
eration. Females in which lactation was inhibited 
recovered before the next litter was produced. The 
same authors (2378) in 1948 reported placing male 
rats in an atmosphere consisting of 20 percent car- 
bon monoxide and 80 percent room air for 1 to 2 
minutes every 24 hours. At sacrifice on the 21st day 
there was failure of spermatogenesis, with very few 
spermatids and spermatozoa found in the testes. 
For other studies of pathological changes in 
carbon monoxide poisoning, papers by Fornari 
(2389) 1949; Moniatte, Schwartz, Treussard, Mal- 
huret, and Alt (2402) 1949; and Tosetti (2409) 
1948, may be consulted. According to Lhermitte 
and De Ajuriaguerra (2396) 1947, the changes in 
the brain in carbon monoxide poisoning differ 
widely, depending upon the time elapsed between 
the exposure and the time of death. In those cases 
in which death occurred rapidly, the picture is 
characterized by hemorrhages, necrobiosis, necrosis, 
and edema. These changes may involve primarily 
the basal ganglia, but also the subcortical white 
matter, the hippocampus, the substantia nigra, and 
the cerebellum. Changes in the vascular network 
with infiltration of the walls by neutral lipids and 
by a peculiar substance containing iron salts, cal- 
cium, and lipids may be observed in cases in which 
the poisoning continues for a prolonged period or 
in which death is delayed. A diffuse demyelination 
of the entire white matter of the brain similar to 
Schilder’s disease may be observed in cases in which 
death occurs after a long period of remission. It is 
suggested that in carbon monoxide poisoning there 
is, in addition to the anoxic factor, a toxic factor 
which affects the neuroglia and the vascular net- 
work. Ceresa (2379) in 1948 examined the central 
nervous system of a patient with acute carbon 
monoxide poisoning who died 24 hours after ex- 
posure. Comparing the findings in this case with 
another patient who died 26 days after intoxication, 
the author concluded that the alterations within 
the nervous tissue are not determined by a direct 
action of carbon monoxide on the nerve cell, but 
by asphyxia caused by vasoconstriction resulting 
from the carbon monoxide. Pathological changes in 
the brain of a 33-year-old man dying 3 months after 
exposure to carbon monoxide were described in 
1951 by Fazekas and Gereb (2386). They described 
ganglion-cell changes in the cerebral cortex and in 
the basal ganglia, with perivascular changes and 
marked gliosis. There was widespread demyelina- 
tion and fatty degeneration. Regarding the patho- 
logical mechanism of carbon monoxide poisoning, NOXIOUS AGENTS—CARBON MONOXIDE 
2369-2400 
the author considered that anoxia is the primary 
factor. 
For other studies of the clinical picture, func- 
tional changes, and pathological effects of carbon 
monoxide poisoning, the reader is referred to papers 
by Asmussen and Knudsen {2370) 1940, Asmussen 
and Vinther-Paulsen {2371) 1950; Doumer and 
Merlen {2384) 1946; Enzer {2385) 1946; Ham- 
burger, Collins, Shaver, and Gall {2392) 1949; 
Helve {2393) 1949; Perrin {2404) 1949; Sklyan- 
skaya {2406) 1946; Vollmer, King, Fisher, and 
Birren {2410) 1945. 
2369. Almgren. S. Oftalmoneurologiska forandringar 
vid koloxid-och nagra forgiftningar. [Ophthalmoneurologic 
changes in carbon-monoxide and some other forms of 
poisoning.] Nord. Med., Stockholm, 1949,42: 1898-1901. 
Abstr. World Med., 1950,8: 17. 
2370. Asmussen, E. and E. 0. E. Knudsen. Studies in 
acute but moderate CO-poisoning. Acta physiol, scand., 
1943, 6: 67-78. [P] 
2371. Asmussen, E. and N. Vinther-Paulsen. On the 
circulatory adaptations to arterial hypoxemia (CO poison- 
ing). Acta physiol, scand., 1949, 19: 115-124. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and Phar- 
macology), 1950, 5; 1443. 
2372. Benon, R. Intoxication par Foxyde de carbone. 
Troubles mentaux. Sem. Hop., Paris, 1949, 25: 1222— 
1223. [D] 
2373. Binet, L. and M. Burstein, Intoxication par 
Foxyde de carbone et tonus des vaisseaux peripheriques. 
C. R. Soc. Biol., Paris, 1948, 142: 1487-1488. [P] 
2374. Bonneville, P. and A. Grut. Carbon monoxide 
poisoning in industry. Proc. ninth intern. Congr. industr. 
Med., London, 1948, 908-910. (French summary.) 
2375. Borst, J. R. and K, Often. Enkele moeilijkheden 
bij de diagnostiek en beoordeling van gevallen van acute 
kodmonoxydeverkiftiging. Ned. Tijdschr. Geneesk., 1948, 
92: 1235-1239. (French, German, and English summa- 
ries.) [CH] 
2376. Bourguignon, A. L’oxycarbonisme chronique; 
(Donnees nouvelles). Sem. Hop. Paris, 1950, 26: 4449- 
4453. 
2377. Cameron, J. A. and C. K, Collings. Reproduction 
and lactation in albino rats during prolonged exposure to 
carbon monoxide. Anat. Rec., 1946, 96: 523. Abstr. [P] 
2378. Cameron, J. A, and C. K. Collings. Failure of 
spermatogenesis after daily exposure to carbon monoxide. 
Anat. Rec., 1948,100: 647. Abstr. [P] 
2379. Ceresa, C. Sulla eziopatogenesi delie alterazioni 
dell’encefalo nella intossicazione acuta da ossido di car- 
bonic. Med. d. Lavoro, 1948, 39: 19-22. (English sum- 
mary.) [CH] [P] 
2380. Chinn, H. I. Carbon monoxide-hemoglobin levels 
of workers employed in airplane engine repair shops. /. 
industr. Hyg., 1949, 31: 258-260. Abstr. World Med., 
1950, 7: 453. 
2381. Corkill, A. B. Some clinical aspects of carbon 
monoxide poisoning. Med. J. Aust., 1947, 2: 289-291. 
[R] [CH] 
2382. Courville, C. B. Cerebral anoxia and its residuals. 
IV. The asphyxial syndromes—acute, subacute, and 
chronic. Med. Arts Sci., 1948, 2: 67—79. [D] 
2383. Dahlstrom, H., G. Obreschkow, and T. Sjostrand. 
A comparison between the effects of carbon monoxide 
poisoning and inhalation of air with low oxygen content 
upon respiration, circulation, alkaline reserve of the plasma 
and patellar reflex in normal subjects and in cases of 
“chronic producer gas poisoning.” Acta pharmacol., 
toxicol., 1947,5; 105-123. [P] 
2384. Doumer, E. and J. F. Merlen. Syndrome de 
Wolff, Parkinson et White au cours d’une intoxication 
aigue par 1’oxyde de carbone. Acta cardial., Brux., 1946, 
1: 302-304. [GH] 
2385. Enzer, N. Gangrene of lower extremity following 
carbon monoxide asphyxia. Amer. J. din. Path., 1946, 16: 
111-116. 
2386. Fazekas, I. G. and T. Gereb. Adatok a CO- 
mergezes agyszovettani elvaltozassaihoz es azok keletkezes- 
modjahoz. [Cerebral histological changes and their patho- 
mechanism in CO poisoning.] Mag. belorv. Arch., 1951, 
4: 4. 
2387. Fell, A. Chronic carbon monoxide poisoning in 
the mortor-car industry. Proc. ninth intern. Congr. industr. 
Med., London, 1948, 919-923. (French summary.) 
2388. Fink, A. I. Carbon-monoxide asphyxia with visual 
sequelae. With report of a case. Amer. J. Ophthal., 1951, 
34: 1024-1026. [CH] 
2389. Fornari, A. Cosiderazioni attorno a 33 casi 
mortali di intossicazione ossicarbonica non provocata da 
gas illuminante. Arch. Antrop. crim., 1949, 69: 113-124. 
[CH] 
2390. Gmt, A. Chronic carbon monoxide intoxication. 
Proc. ninth intern. Congr. industr. Med., London, 1948, 
911-913. (French summary.) 
2391. Halperin, M. H., J. I. Niven, R. A. McFarland, 
and F. J. W. Houghton. Variations in visual thresholds 
during carbon monoxide and hypoxic anoxia. Fed. Proc. 
Amer. Soc. exp. Biol., 1947, 6: 120. [P] 
2392. Hamburger, M., W. T. Collins, M. R. Shaver, 
and E. A. Gall. Clinical pathological conference. Cincinn. 
J. Med., 1949, 30: 200-204. [CH] 
2393. Helve, 0. A study of the blood phosphorus and 
certain lipids in chronic carbon monoxide poisoning. Ann. 
Med. exp. Fenn., 1949, 27: 41-45. [CH] [P] 
2394. Kugelberg, I. Ogonsymtom vid gengasfor- 
giftning. [Eye symptoms in cases of producer gas poison- 
ing.] Bull. Hyg., Lond., 1946, 21: 246. Abstr. 
2395. Lehoczky, T. de Du mecanisme physiopatholo- 
gique des lesions centrales de 1’intoxication oxycarbonee. 
Acta neural, belg., 1949, 49: 488-495. [CH] 
2396. Lhermitte, J. and ( ), De Ajuriaguerra. Lesions 
of central nervous system produced by carbon monoxide 
poisoning. /. industr. Hyg., 1947, 29: abstract section: 
73. 
2397. Loeper, M., A. Varay, J. Cottet, and J. Reveille. 
The visceral consequences of acute carbon monoxide 
poisoning. /. industr. Hyg., 1947, 29: abstract section: 11. 
[CH] [P] 
2398. Lumio, J. S. Hearing deficiencies caused by 
carbon monoxide (generator-gas). Acta oto-laryng., 
Stockh., 1948, Suppl. 71: 1-112. [R] [P] 
2399. Lumio, J. S. Audiometric testing of patients with 
producer gas poisoning. Acta otolaryng., Suppl., Stockh., 
1948, 74: 150-154. 
2400. McFarland, R. A., J. I. Niven, and M. H. Hal- 
perin. Visual thresholds as an index of physiological 
imbalance caused by anoxia, carbon monoxide, and low 
blood sugar. Proc. ninth intern. Congr. industr. Med., 
London, 1948, 519-522. (French summary.) 2401-2412 
DISEASES AND ACCIDENTS 
2401. Mercier, A. Troubles visuels causes par 1’oxyde 
de carbone. Soc. Frangaise Ophthal., 1947, 60: 314-318. 
[CH] 
2402. Moniatte, ( ), ( ), Schwartz, ( ), Treussard, 
( ) Malhuret, et ( ) Alt. Eruption a type d’erytheme 
polymorphe bulleux due a une intoxication oxycarbonee. 
Bull. Soc. frang. Derm. Syph., 1949, 56: 102—103. [CH] 
2403. Peloquin, M. Au sujet de 1’ “oxycarbonisme 
chronique.” Arch. Mai. prof., 1951, 12: 313-314. 
2404. Perrin, M. Granulocytopenic consecutive a une 
intoxication oxycarbonee prolongee et discontinue. Paris 
med., 1949, 39: 461-462. [CH] 
2405. Sjostrand, T. Brain volume, diameter of the 
blood-vessels in the pia mater, and intracranial pressure 
in acute carbon monoxide poisoning. Acta physiol, scand., 
1948, 15: 351-361.[P] 
2406. Sklyanskaya, R. M. Action of carbon monoxide 
at elevated temperatures. /. industr. Hyg., 1946, 28: 
abstract section: 11. [P] 
2407. Sumari, P. Carbon monoxide poisoning in Fin- 
land, 1940—1947. Proc. ninth intern. Congr. industr. Med., 
London, 1948, 603-607. (French summary.) 
2408. Swann, H. G., and M. Brucer. The cardiorespira- 
tory and biochemical events during rapid anoxic death. 
IV. Carbon monoxide poisoning. Texas Rep. Biol. Med., 
1949, 7: 569-592. Abstr. World Med., 1950, 8: 230. 
2409. Tosetti, R. Sopra una particolare modalita di 
anossia miocardica. Folia cardiol., Milano, 1948, 7: 183- 
194. (French summary.) [CH] 
2410. Vollmer, E. P., B. G. King, M. B. Pisher, and 
J. E. Birren. The effects of carbon monoxide on three 
types of performance at simulated altitudes of 10,000 and 
15,500 feet. U. S. Navy. NMRI. Project X-417, Kept, 
no. 7, 27 February 1945, 9 pp. J. exp. Psychol., 1946, 36: 
244-251. 
2411. Wohlfart, G., B. Gullherg, and A. Swensson. 
Quelques aspects neurologiques et psychiatriques de 1’in- 
toxication aigue et de 1’intoxication chronique par 1’oxyde 
de carbon. Acta psychiat., Kbh., 1947, 46: 353-369. [D] 
2412. Zahle, V. Perifere nervelaesioner ved acut kulilte- 
forgiftning. [Peripheral nerve lesions by acute carbon mon- 
oxide poisoning.] Nord. Med. Stockholm, 1947, 35: 1665. 
(d) Mechanisms of Carbon Monoxide Poisoning 
A major action of carbon monoxide on the body 
depends upon interference with the oxygen trans- 
port mechanism in the blood. Pappenheimer {2417) 
in 1947 stated that moderate, acute carbon mon- 
oxide poisoning is believed to be the result solely 
of the effect of carbon monoxide on the equilibria 
between oxygen and hemoglobin. However, Lilien- 
thal {2415) pointed out in 1951 that a wide selec- 
tion of biological processes other than the oxygen- 
hemoglobin relationship is affected by carbon mon- 
oxide. Evidence is to be found in the literature that 
carbon monoxide may exert a direct toxic action up- 
on the heart, for example. It is well known that car- 
bon monoxide poisoning produces selective lesions in 
the central nervous system, and the mechanism for 
such selection as, for example, the special vulner- 
ability of subcortical ganglia is not clear (Barthe 
and Paris {2413) 1949, and Van der Horst {2414) 
1948). Pappenheimer {2417) has stated that the 
partial pressure of carbon monoxide necessary to 
produce a given percentage saturation of carboxy- 
hemoglobin is 1/200 of the partial pressure of oxy- 
gen necessary to produce the same percentage 
saturation of oxyhemoglobin. Until recently it was 
believed that the rate of absorption of carbon mon- 
oxide by the blood was close to the maximum 
possible rate, but evidence indicates that it is ap- 
proximately one-half the maximum possible rate. 
Elimination of carbon monoxide from the blood is 
stated to take place entirely by diffusion from the 
lungs. Evidence has been adduced that carbon 
monoxide in moderate amounts is not metabolized. 
Lilienthal {2415) stated that many animal tis- 
sues, especially cardiac and skeletal muscle, can 
oxidize carbon monoxide to carbon dioxide. Recent 
studies have helped to deepen our understanding 
of the Douglas-Haldane blood-gas laws and to re- 
veal the mechanisms of tolerance to carbon mon- 
oxide. Lilienthal, Riley, Proemmel, and Franke 
{2416) in 1945 reported on the relationship be- 
tween carbon monoxide, oxygen, and hemoglobin 
in the blood of man at altitude. Three male sub- 
jects were studied at varying pressure altitudes 
while in equilibrium with inspired gas mixtures 
containing from 0.005 to 0.015 percent carbon 
monoxide. The distribution of carboxyhemoglobin, 
oxyhemoglobin, and reduced hemoglobin and their 
related gas tensions confirmed in vivo the funda- 
mental laws first defined by Haldane for the equili- 
bria obtaining in vitro. A simple rearrangement of 
the Haldane equation makes possible an accurate 
prediction of the amount of carboxyhemoglobin 
obtaining when man is in equilibrium with a carbon 
monoxide-contaminated atmosphere at any given 
altitude. The total barometric pressure was found 
to play no role in the distribution of carbon mon- 
oxide and oxygen at equilibrium. It appears that 
the hemoglobin of individuals who smoke does not 
differ from that of nonsmokers in its affinity for 
carbon monoxide and for oxygen. The symptoms 
produced by carbon monoxide are proportional not 
only to the blood concentration of carboxyhemo- 
globin but also to the duration of exposure to a 
given concentration. Sroka {2419) in 1951 stated 
that a volume percentage of 0.02 carbon monoxide 
replaces 12.5 percent of oxygen in the circulating 
blood in the form of carboxyhemoglobin. Carbon 
monoxide concentrations below this level may be 
considered harmless even over extended periods. 
Air containing 0.05 percent carbon monoxide 
puts approximately 30 percent of the hemoglobin 
in the blood out of action as far as its oxygen-carry- 
ing capacity is concerned. It is reported that symp- 
toms arise when 18 to 20 percent of the hemoglobin NOXIOUS AGENTS—CARBON MONOXIDE 
2413-2420 
has been converted into carboxyhemoglobin. In- 
halation of 0.1 percent carbon monoxide for 1 hour 
results in a conversion of 50 percent of the hemo- 
globin into carboxyhemoglobin, giving rise to a 
critical anoxia. The limit of tissue viability is be- 
lieved to have been reached when 70 percent of the 
hemoglobin is bound as carboxyhemoglobin. This 
dangerous limit is attained when 0.4 percent carbon 
monoxide in air is inhaled for 25 to 30 minutes. 
For further reports on the mechanism of action 
of carbon monoxide, the reader is referred to papers 
by Pitts and Pace {2418) 1944 and Wallgren 
{2420) 1950. 
2413. Barthe, R. and J. Paris. L’atteinte du systeme 
neuro-vegetatif dans intoxication chronique profession- 
nelle par 1’oxyde de carbone dysthyroidies oxycarbonees. 
Pr. mid., 1949, 57: 217-218. [CH] 
2414. Horst, L. Van der. Clinische lessen over Ver- 
giftiging met Koolmonoxyde. [Clinical picture of carbon 
monoxide poisoning.] Ned. Tijdschr. Geneesk., 1947, 91: 
846-851. Excerpta Medica. Section II. (Physiology, Bio- 
chemistry, and Pharmocology), 1948, 1: 695. 
2415. Lilienthal, J. L., Jr. Carbon monoxide. /. 
Pharmacol., 1950, 99: 324-354. Excerpta Medica. Sec- 
tion II. (Physiology, Biochemistry, and Pharmacology), 
1951, 4: 487. Abstr. 
2416. Lilienthal, J. L. Jr,, R. L. Riley, D. D. Proemmel, 
and R. E. Franke. The relationships between carbon 
monoxide, oxygen, and hemoglobin in the blood of man at 
altitude. Amer. J. Physiol., 1945, 145: 351-358. [P] 
2417. Pappenheimer, J. R. Notes on the physiology of 
moderate acute carbon monoxide poisoning. U. S. NRC- 
CAM. Special C. A. M. report, 6 February 1947, 3 pp. 
2418. Pitts, G. C. and N. Pace. The relationship between 
various levels of COHb in the blood and the equivalent 
physiological altitude. U. S. Navy. NMRI. Project X-417, 
Rept. no. 3, 30 October 1944, 20 pp. [P] 
2419. Sroka, K. H. Beitrag zur Frage der Kohlenoxy- 
dentgiftung. Ther. Umschau, 1950, 7: 72—74. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and Phar- 
macology), 1951, 4: 603. Abstr. 
2420. Wallgren, G. R. Some observations on serum- 
copper in chronic carbon monoxide poisoning. Scand. J. 
Clin. lab. Invest., 1950,2: 328-334. 
(e) Carbon Monoxide Uptake, Absorption, and 
Elimination 
Pace {2436 and 2437) in 1945 constructed a 
nomograph for the estimation of the uptake of car- 
bon monoxide by flying personnel breathing air up 
to altitude of 15,000 feet. The data required are 
toxic concentrations of carbon monoxide, altitude, 
and exposure time. The original nomograph was 
modified so as to make it possible to estimate the car- 
bon monoxide uptake when personnel breathe vary- 
ing quantities of ambient air containing carbon 
monoxide through a diluter demand regulator. In 
1945, Lilienthal and Pine {2434) reported a study 
of the effect of oxygen pressure on the uptake of 
carbon monoxide by nine subjects at sea level and at 
altitude. Seventy-eight separate observations were 
made on 8 men and 1 woman. The duration 
of exposure to the carbon monoxide mixture 
varied from 20 to 66 minutes, and the variety 
of partial pressures of oxygen in the inspired 
air was used. In accordance with the laws 
of combination of carbon monoxide with hemo- 
globin in the presence of oxygen, the rate of uptake 
of carbon monoxide is inversely proportional to the 
partial pressure of oxygen. Using a formula decided 
on by the authors, the rate of uptake of carbon 
monoxide may be predicted with considerable accu- 
racy for sea-level and altitude conditions. The total 
barometric pressure plays no discernible role in the 
uptake of carbon monoxide. The authors stated that 
the effect of minimal hypoxia due to altitude sums 
with the effect of small amounts of circulating car- 
boxyhemoglobin to produce moderately severe 
symptoms of hypoxia. The same authors {2433) 
concluded that the correct use of oxygen equipment 
under normal conditions should prevent undue 
effect of carbon monoxide in aircraft. 
Goldman (2430 and 2431) in 1947 constructed 
formulae for determining the rate of uptake of 
carbon monoxide by man. The rate of uptake is 
linear with time up to about one-third of the 
equilibrium value of carboxyhemoglobin in the 
blood. For this range the rate depends on the 
alveolar diffusion coefficient and the alveolar 
respiratory minute volume, as well as the ambient 
gas concentration. If an individual is exposed to an 
atmosphere containing carbon monoxide, his blood 
carboxyhemoglobin concentration increases at first 
linearly with time as stated, but more slowly as 
equilibrium is approached. It most often occurs 
that these equilibrium values are so high as to be 
dangerous, and it is thus of practical importance 
to deal primarily with the initial portion of the 
absorption curve. A formula is given which explains 
the fact that somewhat less than one-half of the 
carbon monoxide inhaled is absorbed into the blood. 
In vitro studies reported in 1947, Pace, Strajman, 
and Walker {2438) found that a 50-percent sus- 
pension of finely divided blood-free rat or guinea- 
pig liver in Tyrode’s solution took up essentially no 
carbon monoxide when the suspension was shaken 
with this gas. It appears that there is no material 
in the liver capable of taking up sufficiently large 
amounts of carbon monoxide to explain the tem- 
porary retention of carbon monoxide by the liver 
in the intact animal. The authors describe a new 
type of Geiger-Muller counter tube for in vivo 
detection of gamma radiations by which it is pos- 
sible to measure the disappearance curves of tagged DISEASES AND ACCIDENTS 
carbon monoxide in human subjects simultaneously 
in various parts of the body, including the heart, 
liver, and thigh. Preliminary studies indicated that 
in addition to fast and slow components observed 
in the heart and the liver, it is possible to resolve a 
third, very fast component with a half time of 0.28 
to 0.88 minute. The authors believed that the very 
fast component and the fast component represent 
mixing phases in the disappearance curve, and that 
the slow component represents the true elimination 
of carbon monoxide from the blood via the lungs. 
No retention of tagged carbon monoxide in the liver 
was observed when doses of 80 cu. cm. or less of 
inert carrier carbon monoxide were used. This was 
presumed by the authors to indicate that the tem- 
porary retention of carbon monoxide by the liver 
is due to a transient local hypoxemia with an 
engorgement of the liver with blood. 
In a study of the rate of carbon monoxide uptake 
by the blood, Behnke, White, Consolazio, and Pace 
{2421) in 1943 exposed 26 men on 42 occasions to 
various concentrations of carbon monoxide in air 
from 5 to 20 parts per 10,000. They found that in 
blood concentrations up to 35 percent carboxyhemo- 
globin, the uptake apparently follows a straight line. 
The principal factors affecting the rate of carbon 
monoxide accumulation in normal men were ex- 
pressed quantitatively in an equation based upon 
experimental data. A simplified form of the equation 
for use as a gross approximation was obtained as 
follows: 
Time of exposure p e rc e n t carboxyhemoglobin 
(m minutes) = 200 X 77:— ;—;— 
Minute volume of respiration 
(in liters) X parts of carbon 
monoxide per 10,000 
In the application of this equation, if the carboxy- 
hemoglobin is limited to 20 percent, and the min- 
ute volume is limited to 18 liters, i. e., in moderate 
exercise, then 20 parts per 10,000 of carbon mon- 
oxide can be breathed for 11 minutes; 15 parts per 
10.000 can be breathed for 15 minutes; 10 parts per 
10.000 can be breathed for 22 minutes. A constant 
amount of carbon monoxide is removed from tidal 
air throughout the course of the exposure. There- 
fore, the quantity of carboxyhemoglobin present in 
the blood does not appear materially to influence 
further uptake of carbon monoxide, at least up to 
concentrations of 35 percent carboxyhemoglobin. 
The rate of uptake up to 35 percent saturation is 
therefore represented by a straight line and not by 
an exponential curve which holds for the absorp- 
tion of many of the inert gases. Carbon monoxide is 
held in such close combination with hemoglobin 
that a steep diffusion gradient is apparently main- 
tained between lung carbon monoxide and blood 
carbon monoxide until the carboxyhemoglobin satu- 
ration reaches a fairly high figure, at least above 35 
percent. The blood flow through the lung capillaries 
does not appear to be a limiting factor under these 
conditions. The blood appears to be capable of as- 
similating all of the carbon monoxide available in 
the lungs at each breath. In 1945, Pitts and Pace 
{2440) reported 2 tests of 12 and 7 hours’ duration, 
respectively, at sea level upon supine subjects breath- 
ing, by means of a demand system and an A-14 
mask, carbon monoxide concentrations of 89 parts 
per million and 156 parts per million to determine 
the rate of absorption. The percentage saturation of 
hemoglobin with carbon monoxide was determined 
each hour. The subjects ventilated at a rate of ap- 
proximately 6.7 liters per minute. After 12 hours 
of exposure to 89 parts per million of carbon mon- 
oxide, one subject had a carboxyhemoglobin con- 
centration of 11.0 percent. The second subject ex- 
posed to 156 parts per million of carbon monoxide 
for 7 hours had a final carboxyhemoglobin concen- 
tration of 16.6 percent. The course of the respective 
carbon monoxide uptake curves indicated that dur- 
ing the time of exposure neither subject maintained 
final equilibrium with the carbon monoxide con- 
centration being breathed. 
For a study of special methods of computation of 
the diffusion of carbon monoxide and oxygen 
through the membrane of the red blood corpuscles 
and the subsequent diffusion and binding of these 
substances within the red blood corpuscles, the 
reader is referred to a report published in 1951 by 
Nicolson and Roughton {2435). 
An experimental study of the fate of carbon 
monoxide in the body during recovery from mild 
carbon monoxide poisoning in man was reported 
in 1945 by Roughton and Root {2441). In normal 
men breathing oxygen or air, it was found that the 
carbon monoxide recovered from the expired air 
amounts to only 60 to 70 percent of that currently 
lost from the blood during the first hour after car- 
bon monoxide administration. Independent theo- 
retical calculations confirm the validity of this 
result, according to the authors. If the subjects con- 
tinued to breathe oxygen for 4 hours after the 
carbon monoxide administration, about 96 percent 
of the carbon monoxide initially absorbed by the 
subjects was recovered in the expired air over this 
more prolonged period. It was inferred that the 30 
to 40 percent fraction of the carbon monoxide lost 
from the blood during the first hour and unac- 
counted for in the expired air must have combined 
reversibly with hemoglobinlike pigments outside NOXIOUS AGENTS—CARBON MONOXIDE 
the main bloodstream. Subsequently, as the blood 
carbon monoxide content falls, the carbon monox- 
ide dissociated reversibly from these combinations, 
diffuses back into the blood and then into the ex- 
pired air. The results of the 4-hour experiments 
confirm previous views stating that there is no sig- 
nificant loss of carbon monoxide through the skin, 
sweat, urine, or feces, or by oxidation or other forms 
of metabolism, in all events, in mild carbon mon- 
oxide poisoning and with an adequate oxygen sup- 
ply. Experimental studies of the elimination of car- 
bon monoxide from the human body with reference 
to the possible conversion of carbon monoxide to 
carbon dioxide were reported in 1945 by Tobias 
and Lawrence {2444), and Tobias, Lawrence, 
Rough ton, Root, and Gregersen {2445). In these 
experiments several normal men were each given, 
via the lungs, a relatively large amount of radio- 
active carbon monoxide mixed with about 150 cu. 
cm. ordinary carbon monoxide. Thereafter, the sub- 
jects breathed oxygen for a period up to 1 hour 
during which their expired carbon dioxide was 
absorbed in soda lime. Tests of the latter for radio- 
activity showed that the carbon monoxide oxidized 
to carbon dioxide by the body under these condi- 
tions amounted to less than 0.1 percent of the car- 
bon monoxide currently lost from the blood. The 
time course of the radioactivity in three parts of 
the body, namely, the thigh muscles, the region of 
the spleen and heart, and the region of the liver, 
was studied by placing Geiger counters over these 
regions. The curves for the muscles and for the 
spleen-heart areas could be reasonably interpreted 
in terms of the average amount of blood present in 
them at any given time, and the rate of blood flow. 
The liver curve, however, showed an unexpectedly 
high and prolonged initial phase difficult to explain 
completely in terms of amount of blood present 
at any given time and the rate of blood flow. The 
nature of the possible additional factor present in 
this region was discussed by the authors. 
Evidence for the conversion of carbon monoxide 
to carbon dioxide by isolated tissues and by the in- 
tact animal was reported in 1948 and in 1949 by 
Clark, Stannard, and Fenn {2424, 2425, and 2426). 
Various tissues of the frog were exposed to a gas 
mixture containing 80 percent carbon monoxide 
and 20 percent oxygen for periods ranging from 5 
to 10 hours. The rate of gas consumption in the 
carbon monoxide-oxygen mixture and in air were 
measured in a respirometer. The radioactive isotope 
C14 was used in the carbon monoxide-oxygen mix- 
ture, and the amount of carbon monoxide burned 
to carbon dioxide was calculated from radioactivity 
measurements of the respired carbon dioxide. The 
amount of carbon monoxide burned to carbon diox- 
ide was found to agree with the excess gas consump- 
tion in the respirometer, thereby showing that the 
excess gas consumption was due to the burning of 
carbon monoxide to carbon dioxide. The rate of 
carbon monoxide oxidation by frog tissue was found 
to be highest for heart muscle, next for skeletal 
muscle, low in nerve, and negligible in skin. The 
amount of carbon monoxide burned to carbon diox- 
ide but retained within the tissues was found to be a 
small fraction of the total amount of carbon monox- 
ide burned. Other reports by Clark, Stannard, and 
Fenn {2425) 1949, {2423) 1950, and {2427) 1950 
and Clark {2422) 1950 give additional details of 
the experimental evidence in tissues and in animals 
for the conversion of carbon monoxide to carbon 
dioxide. In general, the technique used by these 
authors consists in measuring (1) the total gas con- 
sumed by the tissues or the animal in the presence 
of a carbon monoxide-oxygen mixture minus the 
amount of oxygen consumed in air over an equiv- 
alent period, and (2) the radioactivity of the car- 
bon dioxide collected during exposure of tissues or 
animals to the carbon monoxide-oxygen mixture 
containing radioactive carbon monoxide and the 
calculation of the amount of carbon monoxide 
which would have been oxidized to produce the 
measured amount of activity in the carbon dioxide 
collected. Turtles over an 8-to-13-day period con- 
sumed from 30 to 52 percent of the carbon monox- 
ide, while mice over a 4-day period used 0.24 cubic 
millimeter of carbon monoxide per gram body 
weight per hour. Mice were reported to convert 
0.28 cubic millimter of carbon monoxide to carbon 
dioxide per gram of body weight per hour. The rate 
of conversion of carbon monoxide to carbon dioxide 
by mice was 10 times greater than would have been 
expected by a straight-line extrapolation from the 
findings in isolated muscles in an 80-percent carbon 
monoxide-20 percent oxygen mixture. 
In an experimental study of the influence of age 
on carbon monoxide desaturation in man, Pace, 
Strajman, and Walker {2439) 1948 have found 
that the half time of desaturation of carbon monox- 
ide from the blood shows a 1-percent increase for 
each increase in year of age of the subject. The 
authors consider that respiratory and circulatory 
changes must occur with increasing age which are 
reflected in the rate of gas exchange between the 
blood and the ambient air. 
For further studies on carbon monoxide uptake, 
absorption, and elimination, the reader is referred 
to papers by Fox {2428) 1948; Gemmill, Bierman, 
Lilienthal, and Fugitt {2429) 1944; Gullberg and 2421-2445 
DISEASES AND ACCIDENTS 
Svensson [2432) 1946; Sjostrand [2442) 1950; and 
Sjostrand [2443) 1951. 
2421. Behnke, A. R., W. A. White, Jr., W. V. Con- 
solazio, and N. Pace. Measurements of CO absorption in 
man: a formula for computing concentration vs. time of 
exposure. U. S. Navy. NMRI. Project X—160, Kept. no. 2, 
15 June 1943, 16 pp. 
2422. Clark, R. T,, Jr. Evidence for conversion of 
carbon monoxide to carbon dioxide by the intact animal. 
Amer. J. Physiol., 1950, 162: 560-564. [P] 
2423. Clark, R. T., J. N. Stannard, and W. 0. Fenn. 
Evidence for the conversion of carbon monoxide to carbon 
dioxide by the intact animal. Science, 1949, 109: 615—616. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1950, 3: 393. 
2424. Clark, R. T., Jr., J. N. Stannard, and W. 0. Fenn. 
Further evidence on conversion of CO to C02 by tissues 
including experiments with radioactive carbon. Amer. J. 
Physiol., 1948,155: 430. Abstr.. 
2425. Clark, R. T., Jr., J. N. Stannard, and W. 0. Fenn. 
Oxidation of CO to C02 by the intact animal. Fed. Proc. 
Amer. Soc. exp. Biol., 1949, 8: 26. 
2426. Clark, R. T., Jr,, J. N. Stannard, and W. 0. Fenn 
The oxidation of carbon monoxide to carbon dioxide by 
animal tissues as shown by experiments with C 14. I. The 
oxidation of carbon monoxide by isolated tissues. II. Evi- 
dence for the conversion of carbon monoxide to carbon 
dioxide by the intact animal. University of Rochester, 
U. S. Atomic Energy Project. Contract W-7401-eng-49, 
UR-97, 27 October 1949, 26 pp. [P] 
2427. Clark, R. T,, Jr., J. N. Stannard, and W. 0. Fenn. 
The burning of CO to C02 by isolated tissues as shown by 
the use of radioactive carbon. Amer. J. Physiol., 1950, 
161: 40-46. [P] 
2428 Fox, H. M. Carbon monoxide affinity of chloro- 
cruorin and haemoglobin. Nature, Land., 1948, 162: 20. 
2429. Gemmill, C. L., H. R. Bierman, J. L. Lilienthal, 
and C. H. Fugitt. A. The concentration of carbon mon- 
oxide in various training aircraft. B. The blood concen- 
tration of carboxy hemoglobin in personnel in various 
training aircraft. U. S. Navy. NATC., Pensacola, Fla. 
School of aviation medicine. Project X—129 {Av-R9-1), 
Final report, 9 March 1944, 5 pp. [P] 
2430. Goldman, D. E. The dependence of carbon mon- 
oxide uptake of the body on respiratory minute volume. 
Fed. Proc. Amer. Soc. exp. Biol., 1947, 6: 112. [M] 
2431. Goldman, D, E. The physics of respiratory gas 
exchange=CO uptake in man. U. S. Navy. NMRI. 
Project X-417, Rept. no. 12,9 September 1947, 3 pp. [R] 
2432. Gullberg, B. and A. Svensson. Experimentella 
undersokningar over nagra koloxid-problem. Nord. Med., 
Stockholm, 1946, 32: 2722-2726. 
2433. Lilienthal, J. L. and M. B. Pine. The effect of 
varying partial pressures of oxygen and carbon monoxide 
on the uptake of carbon monoxide in man. U. S. Navy. 
NATC., Pensacola, Fla. School of aviation medicine. 
Project X-129: (Av-R9-1), Rept. no. 1, 15 October 
1943, 8 pp. [P] 
2434. Lilienthal, J. L., Jr. and M. B. Pine. The effect 
of oxygen pressure on the uptake of carbon monoxide by 
man at sea level and at altitude. Amer. J. Physiol., 1945, 
145: 346-350. J. industr. Hyg., 1946, 28: abstract section; 
51-52. 
2435. Nicholson, P. H. and F. J. W. Ronghton. A 
theoretical study of the influence of diffusion and chemical 
reaction velocity on the rate of exchange of carbon mon- 
oxide and oxygen between the red blood corpuscle and the 
surrounding fluid. Proc. r. Soc., Series B, 1951, 138: 
241-264. [P] 
2436. Pace, N. A nomograph for the estimation of the 
uptake of carbon monoxide by the blood of flying per- 
sonnel. U. S. Navy. NMRI. Project X-417, Kept. no. 8, 
18 July 1945, 6 pp. 
2437. Pace, N. A nomograph for the estimation of the 
uptake of carbon monoxide by flying personnel breathing 
air or breathing through a diluter demand regulator. 
U. S. Navy. NMRI. Project X-417, Kept. no. 9, 9 August 
1945, 5 pp. 
2438. Pace, N., E. Strajman, and E. Walker. The func- 
tion of the liver in carbon monoxide metabolism. Univer- 
sity of California, Berkeley, Calif. Division of medical 
physics. Contract N7onr O 295, Task Order IV, Kept, 
no. 1, 26 June 1947. [P] 
2439. Pace, N., E. Strajman, and E. Walker. Influence 
of age on carbon monoxide desaturation in man. Fed. 
Proc. Amer. Soc. exp. Biol., 1948, 7: 89. [P] 
2440. Pitts, G. C. and N. Pace. The rate of blood 
absorption of low concentrations of carbon monoxide at 
sea level. U. S. Navy. NMRI. Project X-417, Kept. no. 6, 
26 February 1945, 5 pp. 
2441. Houghton, F. J. W. and W. S. Root. The fate of 
CO in the body during recovery from mild carbon monox- 
ide poisoning in man. Amer. J. Physiol., 1945, 145: 239— 
252. /. industr. Hyg., 1946, 28: abstract section: 62. [P] 
2442. Sjostrand, T. Endogenous formation of carbon 
monoxide in man under normal and pathological condi- 
tions. Scand. J. din. lab. Invest., 1941, 1: 201—214. Abstr. 
World Med., 1950, 7: 457. 
2443. Sjostrand, T. The in vitro formation and disposal 
of carbon monoxide in blood. Nature, Lond., 1951, 168: 
729-730. [P] 
2444. Tobias, C. A, and J. H. Lawrence. The elimina- 
tion of carbon monoxide from the human body with 
reference to the possible conversion of CO to C02. 
U. S. NRG-GAM. Acting for OSRD-CMR. OEMcmr- 
196, Kept. no. 458, September 1945, 10 pp. 
2445. Tobias, C. A., J. H. Lawrence, F. J. W. Roughton, 
W. S. Root, and M. I. Gregersen. The elimination of 
carbon monoxide from the human body with reference to 
the possible conversion of CO to C02. Amer. J. Physiol., 
1945, 145: 253-263. J. industr. Hyg., 1946, 28: abstract 
section: 62. [P] 
(f) Tolerance and Acclimatization to Carbon Monoxide 
The circulatory adaptation to severe carbon mon- 
oxide poisoning for 10 days with blood concentra- 
tions of carboxyhemoglobin up to 46 percent was 
studied in dogs by Asmussen and Vinther-Paulsen 
[2446) in 1949. The authors found a slight increase 
in cardiac output together with an increase in hemo- 
globin concentration. The latter was attributed in 
part to an acute, probably splenogenic, increase and 
partly to a slow increase caused by the new forma- 
tion of red blood corpuscles. In spite of these adapta- 
tive reactions, the venous oxygen tension was low 
in chronic carbon monoxide poisoning. Gorbatow 
and Noro (2448) reported in 1948 that rats and 
mice which were exposed daily to carbon monoxide 
in concentrations of 0.25, 0.4, and 0.5 percent be- 
came acclimatized easily to these concentrations, NOXIOUS AGENTS—CARBON MONOXIDE 
2446-2449 
so that in 8 to 15 days the tolerance was increased 
2 to 4 times the control value. Only slight acclimati- 
zation to a concentration of 1 percent carbon mon- 
oxide was observed. An intermission of several days 
in the exposure diminished the tolerance. The longer 
the intermission, the greater the loss of tolerance. 
Polycythemia was observed with the acclimatiza- 
tion, but this later disappeared and there was in- 
creased tolerance without polycythemia. In the ac- 
climatized animal there was noted no decrease in the 
percentage of carboxyhemoglobin in the blood. 
Clark {2447) in 1950 presented data indicating that 
mice exposed to concentration of carbon monoxide 
up to 0.15 percent for 3 weeks could survive an 
acute exposure to a simulated altitude of 34,000 
feet much longer than mice unacclimatized to car- 
bon monoxide. Conversely, mice that had been ex- 
posed to low oxygen, simulating an altitude of 18,- 
000 feet for 3 weeks, were able to survive in an 
atmosphere containing 0.25 percent carbon mon- 
oxide for a considerably longer time than mice 
unacclimatized to low oxygen. In an attempt to de- 
termine the factors responsible for acclimatization 
to carbon monoxide and to low oxygen, the author 
found an increase in the oxygen capacity of the 
blood of about 60 percent, and in the hematocrit of 
about 85 percent in both the carbon monoxide and 
the low oxygen animals. The carbon dioxide capa- 
city of the plasma was found to decrease for the 
mice exposed to low oxygen, but showed no change 
from the controls for animals exposed to carbon 
monoxide. Since the carbon dioxide capacity is a 
measure of the alkaline reserve, and the alkaline 
reserve is known to vary with the ventilation, the 
results seemed to indicate that mice in low oxygen 
environments hyperventilated, whereas those ex- 
posed to carbon monoxide exhibited no change in 
ventilation. The rate of oxygen consumption was 
measured on all the animals under normal atmos- 
pheric conditions and during acclimatization to car- 
bon monoxide and low oxygen. The rate during 
acclimatization did not vary from that under nor- 
mal atmospheric conditions. In none of these groups 
was there any significant alteration in acclimatiza- 
tion to low oxygen, although an increase in hemo- 
globin is a constant finding in acclimatization to 
high altitude. The results of these studies would 
seem to indicate that there are also other pertinent 
adjustments made by the animal during the process 
of acclimatization. 
In a study of the nature of acclimatization oc- 
curring during repeated exposure of a human sub- 
ject to atmospheres containing low concentrations 
of carbon monoxide Killick {2450) in 1948 sub- 
jected a man repeatedly to concentrations of carbon 
monoxide of 0.019 to 0.045 percent for 1 hour in 
an airtight chamber. Each exposure was prolonged 
until the carboxyhemoglobin percentage attained a 
steady value. Acclimatization was indicated by a 
diminution in the severity of symptoms and a dis- 
crepancy between the observed carboxyhemoglobin 
percentage at the end of exposure and the greater 
carboxyhemoglobin percentage obtained in vitro 
when the subject’s blood was equilibrated with a 
mixture containing oxygen and carbon monoxide at 
the same partial pressure as in alveolar air. In this 
acclimatized subject there was no change in red 
blood count, proportion of reticulocytes, or in blood 
volume. Thus, there was acclimatization without 
evidence of a hematopoietic response. The author 
also indicated that there was no appreciable de- 
struction of carbon monoxide in the body, and 
stated that the value of the constant for partition 
of hemoglobin between oxygen and carbon monox- 
ide, as determined in vitro, remained unaltered as 
acclimatization developed. 
For a study of safe human tolerance for high 
concentrations of carbon monoxide over short peri- 
ods of time, reference may be made to a paper 
published in 1951 by Hall, Patterson, and Colehour 
{2449). 
2446. Asmussen, E,, and N. Vinther-Panlsen, On the 
circulatory adaptations to arterial hypoxemia (CO-poison- 
ing). Acta physiol, scand., 1949, 19: 115—124. [P] 
2447. Clark, E, T., Jr. Comparative studies on the ac- 
climatization of mice, hamsters, and rats to carbon monox- 
ide and low oxygen. XVIII Intern, physiol. Congr., 1950, 
157-159. 
2448. Gorbatow, 0. and L. Noro. On acclimatization in 
connection with acute carbon monoxide poisonings. Acta 
physiol, scand., 1948, 15: 77-87. [P] 
2449. Hall, A. L., C. A. Patterson, and J. K. Colehour. 
Safe human tolerance for high concentrations of CO over 
short periods of time. /. Aviat. Med., 1951, 22: 501-508, 
517. 
(g) Treatment of Carbon Monoxide Poisoning 
Several reports are on record in the literature on 
the value of intravenous administration of procaine 
hydrochloride in the treatment of asphyxia due to 
carbon monoxide. In 1943, Besancon and Laroche 
{2453) described the successful treatment of four 
cases of carbon monoxide poisoning with novocaine 
in amounts from 400 to 700 milligrams. These au- 
thors cited the use of novocaine in a case with coma 
following ablation of an intercranial tumor. In this 
case 5 cu. cm. of a 1-percent solution of novocaine 
was given, and the patient recovered. Amyes, Ray, 
and Brockman {2451) reported in 1950 the treat- 
ment of 23 patients with procaine hydrochloride 
injected intravenously after carbon monoxide poi- 
soning. All of these patients showed neurological or DISEASES AND ACCIDENTS 
mental abnormalities. The usual dose of procaine 
hydrochloride was 500 milligrams given intrave- 
nously in 500 cu. cm. of 5 percent dextrose in water 
or isotonic saline solution. The solution was given 
over a 2-hour period. In each case a skin test for 
procaine sensitivity was carried out before injection. 
If the patient was conscious and there was no respir- 
atory depression, an injection of 0.13 gram of so- 
dium phenobarbital was given intramuscularly. 
Seventeen patients made good recoveries, while 6 
died or did not fully recover. These six had received 
procaine administration late. Also, the average age 
of this latter group was 67. Moreover, they consti- 
tuted a group more susceptible to hypoxia and also 
there were some who had had previous neurological 
disturbances or a history of coronary disorder. 
These cases are also discussed by Beckman {2452) 
in the 1950 Yearbook of Drug Therapy, published 
in 1951. Beckman pointed out that the earlier the 
procaine was given the better were the results. 
Olsen, Marinacci, Ray, and Amyes {2456) in 
1949 described several cases of asphyxia due to car- 
bon monoxide treated by intravenous injection of 
procaine hydrochloride. A 27-year-old male patient 
had gone to sleep in a closed room with a lighted 
gas heater. The deep reflexes were hypoactive, ab- 
dominal reflexes were absent, and Babinski’s sign 
was positive bilaterally. The temperature was 100.4° 
F., the pulse was 104, and the respiration 22. The 
patient was given 500 milligrams of procaine hy- 
drochloride intravenously in a 1-percent solution in 
physiological saline. The blood pressure rose from 
130/90 to 140/95. There was a restoration of nor- 
mal cerebral rhythm as demonstrated by the electro- 
encephalogram, and the patient was discharged 
improved after 3 days. A 61-year-old woman who 
had been poisoned with carbon monoxide was still 
moderately cyanotic after 24 hours of oxygen ad- 
ministration. There were choreiform movements, 
hyperkinesis, and quasipurposive motor activity. In 
addition to oxygen, the patient received a trans- 
fusion of 500 cu. cm. of whole blood on the day of 
admission and 10 cu. cm. of 1 percent procaine 
intravenously the following day. The patient left the 
hospital with no symptoms. The rationale for the 
use of procaine hydrochloride has not been ade- 
quately described in the literature cited. However, 
its value, if any, probably depends upon the central 
action of procaine in stimulating the central nervous 
system from above downward. As is well known, the 
first recognizable action of procaine is on the cere- 
bral cortex and is manifested in restlessness and 
excitement, with some evidence of increase of 
mental power and capacity for muscular work. Pro- 
caine acts upon the medulla as a respiratory stim- 
ulant and also excites the vasomotor centers. The 
use of a drug for its central effect is fraught with 
danger since central stimulation is often followed 
by depression. Eventually, the medullary centers 
may be depressed and death may result from respir- 
atory failure. Although procaine is stated to be 
the least toxic of all local anesthetics, it sometimes 
causes sympathetic effects in sensitive subjects. 
Death has been reported in the literature from the 
injection of as little as 0.01 to 0.13 gram of procaine. 
The use of barbiturates along with procaine makes 
for greater safety. 
The literature on the use of oxygen in the treat- 
ment of patients asphyxiated with carbon monoxide 
can be only briefly alluded to here. There is some 
difference of opinion as to whether pure oxygen is 
preferable or whether a better result is obtained 
from a mixture of 93 percent oxygen and 7 percent 
carbon dioxide. Claim for the superiority of both 
has been made, but the recent trend is to regard 
the use of carbon dioxide-oxygen mixture as of 
questionable value in the treatment of carbon mon- 
oxide poisoning. In some forms of asphyxia, it is 
asserted that the use of carbogen may be actually 
harmful. Respiratory physiologists and anesthesiol- 
ogists generally tend to prefer 100 percent oxygen 
to carbogen in artificial respiration, although many 
reports suggest that pure oxygen or carbon dioxide 
mixtures are equally effective. Reports indicate that 
the use of the carbon dioxide-oxygen mixture has- 
tens the elimination of carbon monoxide from the 
blood. Vining, Whittenberger, and Wollack {2462) 
1946 came to this conclusion in an experimental 
study of carbon monoxide poisoning in animals. In 
these experiments a mixture of 7 percent carbon 
dioxide and 93 percent oxygen was used for 10 
minutes as inhalation therapy on goats as well as 
dogs, sustaining an arterial saturation of 60 to 80 
percent carbon monoxide. The rate of elimination 
of carbon monoxide and the effect on the blood 
carbon dioxide levels, on blood pressure, and on 
minute volume of respiration were compared with 
similar data on two groups of goats and dogs simi- 
larly asphyxiated but treated with pure oxygen 
or room air. The animals treated with the carbon 
dioxide-oxygen mixture eliminated an average of 
10 percent more carbon monoxide than those 
treated with pure oxygen. In the authors’ experi- 
ments there was no evidence of respiratory or cir- 
culatory depression during the period of inhalation 
of the carbon dioxide-oxygen mixture or following 
its use. For a further report on the clinical use of 
carbogen in the treatment of cases of carbon mon- 
oxide poisoning, reference may be made to a paper NOXIOUS AGENTS—CARBON MONOXIDE 
published in 1948 by Desoille, Griffon, Assouly, 
Feldstein, and Le Breton {2454). 
Pace, Strajman, and Walker {2457) 1951 have 
found that the elimination of carbon monoxide 
from human subjects can be accelerated by breath- 
ing oxygen under high atmospheric pressure. In 
their experiments, 10 subjects, 5 males and 5 fe- 
males, breathed a mixture containing 250 milliliters 
of carbon monoxide and 2 liters of air from a bag 
for 30 seconds. Each subject was then placed in a 
compression chamber and the ambient pressure 
raised to 2.5 atmospheres. Oxygen breathing was 
begun and the venous blood analyzed every 15 
minutes for carboxyhemoglobin. In these experi- 
ments, the half time of carbon monoxide elimina- 
tion was of the order of 20 minutes for the male 
subjects and faster in the females. These findings 
were compared with the half-time elimination val- 
ues when the subjects breathed 20 percent oxygen 
and 100 percent oxygen at 1 atmosphere. In these 
latter experiments, the half-time elimination of 
carbon monoxide with 20 percent oxygen was 249 
minutes, and for the 100 percent oxygen experi- 
ment 47 minutes. The elimination in the female 
subjects was 30 percent faster than in the males. 
Reference may also be made to the alleged benefit 
of ozone inhalation in lowering the carbon mon- 
oxide content of blood when carbon monoxide is 
present in the air. In an experimental study on 
white mice, Pitts and O’Neal {2458) 1948 exposed 
adult white mice to atmospheres containing physi- 
ologically tolerable concentrations of ozone (from 
0.01 to 0.1 part per million) at two different con- 
centrations of carbon monoxide; namely, 118 parts 
per million and 553 parts per million. Under these 
conditions the blood carbon monoxide saturation 
curves showed no effect whatever of ozone. The 
authors attributed previous positive results reported 
in the literature to experimental inadequacy. 
Many of the questions at issue in the treatment 
of carbon monoxide poisoning have been settled by 
the work of Schwerma and his colleagues. Their 
studies include evaluation of methods of artificial 
respiration in conjunction with administration of 
pure oxygen or carbogen. Schwerma, Ivy, and 
Friedman {2459) in 1948 reported a comparative 
study of the effectiveness of several commonly used 
methods of resuscitation in dogs asphyxiated with 
commercial cylinder carbon monoxide diluted with 
air. Carbon monoxide concentrations of 0.3, 2, and 
5 percent were used. One hundred and fifty-seven 
dogs were exposed to 0.3 percent carbon monoxide 
until the onset of the first respiratory gasp. Of 20 
animals in this group receiving no treatment except 
removal from the asphyxiating chamber, three sur- 
vived. Thirty animals were treated by manual arti- 
ficial respiration with inhalation of 7 percent 
carbogen, and of these, 15 survived. A further 30 
animals were treated with mechanical artificial 
respiration of the “suck and blow” type with 100 
percent oxygen, and of these, 14 survived. Thirty 
animals were treated with mechanical artificial 
respiration of the “suck and blow” type with 7 
percent carbogen, and of these, 15 survived. Thirty 
animals were treated with mechanical artificial 
respiration of the positive pressure type with 7 per- 
cent carbogen, and of these, 12 survived. Seventeen 
animals were kept in the asphyxiating chamber for 
1 minute after the last respiratory gasp and were 
then treated with mechanical artificial respiration 
of the “suck and blow” type with 7 percent carbo- 
gen. None of these animals survived. Ten animals 
were exposed to 5 percent carbon monoxide until 
the onset of the first respiratory gasp. Except for 
one dog, which did not manifest air hunger, all 
were resuscitated with mechanical artificial respira- 
tion of the “suck and blow” type with 7 percent 
carbogen. Fifty-nine percent of all dogs exposed 
to 0.3 percent carbon monoxide longer than the 
mean time of 60.5 minutes survived, and 82 percent 
of the survivors suffered neurological sequelae of 
more than transitory duration. Thirty percent of 
the dogs exposed to 0.3 percent carbon monoxide 
less than the mean time of 60.5 minutes survived, 
and of these, 48 percent suffered neurological 
sequelae of more than transitory duration. From 
the survival data in these experiments, the authors 
concluded that artificial respiration induced by the 
mechanical resuscitators has no advantage over 
manual respiration with inhalation of 7 percent 
carbogen. In previous studies in which a large num- 
ber of animals were asphyxiated with illuminating 
gas, it was found that mechanical artificial respira- 
tion was unquestionably more effective than manual 
methods. Since the experimental conditions were 
identical, except for the source of carbon monoxide, 
the authors considered that the differing results 
must be due to some difference in the action of the 
asphyxiating gas. The authors suggested that the 
carbon monoxide has a histotoxic effect based on 
the combination of carbon monoxide with iron- 
containing enzymes related to hemoglobin, and that 
the presence of some constituents in natural gas 
prevents or delays this combination and thus 
decreases the toxicity of carbon monoxide. 
In 1948, Schwerma, Wolman, Sidwell, and Ivy 
{2461) reported further studies in which dogs were 
given various types of resuscitation treatment after 
exposure to air containing 0.3 percent carbon mon- 
291222—54 15 2450-2459 
DISEASES AND ACCIDENTS 
oxide until acute respiratory distress in the form of 
air hunger or gasping appeared. In these experi- 
ments, the rate of clearance of carbon monoxide 
from the blood of the dog was studied. The follow- 
ing methods of resuscitation were used: (1) manual 
artificial respiration with inhalation of air, (2) 
mechanical artificial respiration of the “suck and 
blow” type using 100-percent oxygen, (3) the 
same device using 7-percent carbogen, and (4) me- 
chanical artificial respiration of the positive pres- 
sure type using 7-percent carbogen. In the authors’ 
experiments no direct relationship was found be- 
tween the concentration of hemoglobin present in 
the blood and the chances of survival from carbon 
monoxide asphyxia. The average difference in the 
hemoglobin values between the survivors (15.3 
grams per 100 cc.) and the nonsurvivors (14.5 
grams per 100 cc.) was stated to be suggestive, but 
not specifically significant, since individuals with 
high and low hemoglobin concentrations were pres- 
ent in each group. There was an evident and strik- 
ing individual variation in the susceptibility to 
effects of carbon monoxide asphyxia. The mean 
carbon monoxide saturation in animals at the time 
of the first gasp was 74.3 percent. Twenty dogs with 
a saturation of 74 percent or less were exposed for 
an average of 52 minutes before showing the first 
gasp, whereas 21 dogs showing a saturation of 74 
percent or more withstood the exposure for an aver- 
age of 76 minutes. The latter group of animals were 
obviously more tolerant to carbon monoxide poison- 
ing for some reason other than the hemoglobin con- 
tent of the blood, and the answer to the question 
raised by this experiment is not evident in the data. 
The conclusion is that inhalation of oxygen is an 
efficient means of rapidly reducing the carbon mon- 
oxide content of the blood. The authors asserted 
also that administration of oxygen forces the dis- 
sociation of carboxyhemoglobin and thereby pro- 
motes rapid elimination of carbon monoxide. The 
only effects of administration of exogenous carbon 
dioxide are the slightly more rapid excretion of 
carbon monoxide and in some cases a more rapid 
restoration of respiratory movements. The signifi- 
cance of these effects has been exaggerated, accord- 
ing to the authors, while the much greater signifi- 
cance of adequate cardiac function has in large 
part been overlooked. Since carbon dioxide plays no 
demonstrable part in fortifying cardiac function, its 
addition to oxygen in the inhalation of the mixture 
confers no further value in resuscitation. It is, there- 
fore, concluded that the carbon dioxide is an un- 
necessary therapeutic adjunct. 
In view of the importance of cardiac support in 
the therapy of victims of carbon monoxide poison- 
ing, Schwerma, Ivy, and Friedman {2460) in 1948 
gave intracardiac injection of epinephrine and 
atropine in conjunction with 100-percent oxygen 
administration by a mechanical resuscitator to dogs 
asphyxiated with 0.3 percent carbon monoxide. 
The use of epinephrine and atropine appeared to 
confer an additional advantage, and the authors 
believed that this treatment was worthy of trial as 
a last resort in human cases of cardiac arrest fol- 
lowing carbon monoxide asphyxia. 
The literature on the use and design of gas respi- 
rators to protect against carbon monoxide in the air 
cannot be reviewed here. The reader is referred to 
a description by Forbes and Grove {2455) 1948 of 
a pocket-size gas respirator that protects the wearer 
against carbon monoxide in the air for one-half 
hour. 
2450. Killick, E. M. The nature of the acclimatization 
occurring during repeated exposure of the human subject 
to atmospheres containing low concentrations of carbon 
monoxide. /. Physiol., 1948, 107: 27-44. [P] 
2451. Amyes, E. W., J. W. Ray, and N. W. Brockman. 
Carbon monoxide anoxia. Intravenous administration of 
procaine hydrochloride in the treatment of acute and 
chronic effects. /. Amer. med. Ass., 1950, 142: 1054-1058. 
Abstr. World Med., 1950, 8: 353. [R] [CH] 
2452. Beckman, H, Carbon monoxide anoxia: intra- 
venous administration of procaine hydrochloride in treat- 
ment of acute and chronic effects, pp. 342-343 in; The 
1950 Year Book of Drug Therapy. Chicago, The Year 
Book Publishers, Inc., 1951, 566 pp. [CH] 
2453. Besancon, L. J, and C. Laroche. L’injection in- 
traveineuse de novocain e au cours des commas prolonges 
consecutifs a Pintoxication oxycarbonee. Bull. Soc. med. 
Hop. Paris, 1943, 59: 431-432. [CH] 
2454. Desoille, H., ( ) Griffon, ( ) Assonly, ( ) Feld- 
stein, and ( ) Le Breton. Traitement par le carbogene de 
Poxycarbonemie chronique professionnelle. Arch. Mai. 
prof., 1948,9: 549-551. [CH] 
2455. Forbes, J. J. and G. W. Grove. Protection against 
mine gases. U. S. Bureau of Mines. Miners’ Circular 35, 
1948, 58 pp. [R] 
2456. Olsen, C. W., A. A. Marinacci, J. W. Ray, and 
E. W. Amyes. Intravenous procaine hydrochloride in the 
treatment of asphyxia due to carbon monoxide. Bull. Los 
Angeles neural. Soc., 1949, 14: 23—31. [CH] 
2457. Pace, N., E. Strajman, and E. L. Walker. Accel- 
eration of carbon monoxide elimination in man by high 
pressure oxygen. Science, 1950, III: 652-654. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and Phar- 
macology), 1951, 4: 834. Abstr. Abstr. World Med., 1950, 
8: 583. 
2458. Pitts, G. C. and J. D. O’Neal. Effect of ozone on 
CO uptake. U. S. Navy. NMRI. Project X-417, Kept, 
no. 13, 10 February 1948, 4 pp. 
2459. Schwerma, H., A. C. Ivy, and H. Friedman. Re- 
suscitation from nearly fatal effects of exposure to “pure” 
carbon monoxide. /. appl. Physiol., 1948, 1: 157-168. [P] NOXIOUS AGENTS—CARBON MONOXIDE 
2460-2476 
2460. Schwerma, H., A. C. Ivy, and H. Friedman. Car- 
diac stimulation in carbon monoxide asphyxia. /. appl. 
Physiol., 1948,1: 364-368. [P] 
2461. Schwerma, H., W, Wolman, A. E. Sidwell, Jr., 
and A. C. Ivy. Elimination of carbon monoxide from the 
blood of acutely poisoned dogs. J. appl. Physiol., 1948, 
1: 350-363. Abstr. World Med., 1949, 6: 148. [P] 
2462. Vining, K. K., Jr., J. L. Whittenberger, and A. C. 
Wollack. A comparison of the effect of 7% carbon dioxide 
with 93% oxygen, and pure oxygen, on goats and dogs, 
acutely asphyxiated with carbon monoxide. Fed. Proc. 
Soc. exp. Biol., 1946, 5: 209. 
(h) Carbon Monoxide Detection in Air and Blood 
Methods for detection of carbon monoxide in the 
air and in the blood will not be discussed in detail, 
nor will the literature be exhaustively summarized. 
Reference is made to the section on gas analysis in 
air and blood (p. 2). Regarding methods for de- 
tection of carbon monoxide in the air, a classical 
method utilizes the hoolamite or activated iodine 
pentoxide indicator. The white hoolamite granules 
are changed to bluish green, then to violet brown, 
and finally to black, depending upon the concentra- 
tion of carbon monoxide in the air. For references 
to this method, papers by Forbes and Grove {2472) 
1937; Consolazio, Pecora, MacDonald, Collison, 
Kreuger, Platt, O’Neal, and Rae {2471) 1945; and 
Pitts {2481) 1947 may be consulted. The following 
papers deal with the hopcalite indicator: Mueller, 
Pope, Sharpe, Vollmer, and Walker {2478) 1944; 
Salsbury, Cole, and Yoe {2484, 2485) 1947; and 
Yoe and Lindsley {2494) 1944. 
Shepherd {2486) in 1946 developed a colorimet- 
ric indicating gel for the rapid determination of 
small amounts of carbon monoxide in the air. This 
gel will detect and estimate less than one part of 
carbon monoxide in 500 million parts of air in 
approximately 1 minute. Field use requires a small, 
inexpensive apparatus without maintenance prob- 
lems, and involves procedures so simple that un- 
trained personnel can obtain reliable results. Yoe, 
Cole, and Salsbury {2493) 1943 have also de- 
scribed carbon monoxide indicators of the impreg- 
nated silica gel type. The determination of carbon 
monoxide in air by the use of red mercuric oxide 
has been described by McCullough, Crane, and 
Beckman {2476) 1948, and Beckman, McCullough, 
and Crane {2465) 1948. Other methods include a 
silver permanganate zinc oxide method described 
by Katz and Katzman {2474) 1949; an infrared 
analyzer described by Siebert {2487) 1948, and Nel- 
son {2479) 1945; and methods using the absorption 
or fixing of carbon monoxide by hemoglobin solu- 
tion described by Soucek {2489) 1949 and Chinn 
{2469) 1946. For other indicators, the reader may 
consult the following references: 2468, 2480, 2483, 
and 2495. 
For a description of methods of estimation of 
carbon monoxide in the blood, the following refer- 
ences should be consulted: 2463, 2464, 2466, 2467, 
2470, 2473, 2475, 2477, 2482, 2488, 2490, 2491, 
and 2492. 
2463. Baldi, A. Su di un nuovo metodo per la determina- 
zione del GO nel sangue. Arch. Antrop. crim., 1949, 69: 
125-128. 
2464. Barthe, ( ), ( ) Paris, ( ) Duchemin, and ( ) 
Thomas, Etude comparee des resultats obtenus par les 
methodes eudiomertique et d’absorption par le chlorure 
cuivreux pour le dosage de 1’oxyde de carbone du sang. 
Arch. Mai. prof., 1949, 10: 581—588. Excerpta Medica. 
Section II. (Physiology, Biochemistry, and Pharmacology), 
1951,4: 126. Abstr. 
2465. Beckman, A. 0., J. D. McCullough, and R. A. 
Crane, Microdetermination of carbon monoxide in air: a 
portable instrument. /. industr. Hyg., 1948, 30: abstract 
section: 123. [P] 
2466. Bellessimo, B. Su alcuni metodi per la determina- 
zione rapida del “coefficiente d’intossicazione, ossicar- 
bonica.” Folia med., Napoli, 1947, 30: 144-150. 
2467. Castagnou, R. and H. Golse. Contribution a 
1’etude du dosage de Poxyde de carbone dans le sang par 
le methode de Wolff. Arch. Mai prof., 1952, 13: 39-41. 
2468. Cherry, R. H. and G. A. Perley. Development of 
a direct-indicating carbon monoxide instrument. U. S. 
OSRD-NDRG. O. S. R. D. rept, no. 4111, 8 September 
1944, 51 pp. 
2469. Chinn, H. I. A method for the determination of 
CO in alveolar air. U. S. AAF. Randolph Field, Tex. 
School of aviation medicine. Project 233, Rept. no. 2, 
24 April 1946, 11 pp. 
2470. Consolazio, W. V. and L. J. Pecora, Preservation 
of blood containing carbon monoxide for transportation 
from the field to the laboratory. U. S. Navy. NMRI. 
NH6-1 /All/NMRI-69, 6 June 1944, 3 pp. 
2471. Consolazio, W. V., L. J. Pecora, E. MacDonald, 
H. A. Collison, N. L. Kreuger, W. T. Platt, J. D. O’Neal, 
and J. A. Rae. The evaluation of methods for determining 
the concentration of CO. U. S. Navy. NMRI. Project 
X—417, Rept. no. 5, 23 February 1945, 4 pp. 
2472. Forhes, J. J. and G. W. Grove. Mine gases and 
methods for their detection. U. S. Bureau of Mines. 
Miners’ Circular 33, 1937, 82 pp. [R] 
2473. Gray, C, H. and M. Sandiford. Micro-diffusion 
method for the estimation of carbon monoxide in blood. 
Analyst, 1946, 71: 107—110. 
2474. Katz, M. and J. Katzman. Rapid determination 
of low concentrations of carbon monoxide in air. Analyst, 
1949, 74: 467. Abstr. Canad. J. Res., 1948, 26, Section F: 
318-329. 
2475. Lenggenhager, K. and K. Lottenbach. Fine neue, 
einfache Methode zur Bestimmung des CO-Gehaltes im 
Blute. Schweiz, med. Wschr., 1948, 78: 370—371. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and Phar- 
macology), 1949, 2: 691. Abstr. 
2476. McCullough, J. D., R. A. Crane, and A. 0. Beck- 
man. Determination of carbon monoxide in air by use of 
red mercuric oxide. J. industr. Hyg., 1948, 30: abstract 
section: 64. [P] 2477-2495 
DISEASES AND ACCIDENTS 
2477. Meigs, J. W. Carbon monoxide poisoning. Bull. 
U. S. Army med. Dept., 1948, 8: 542-546. /. industr. 
Hyg., 1949,57; asbtract section: 46. [CH] [P] 
2478. Mueller, L. E., L. J. Pope, L. M. Sharpe, E. P. 
Vollmer, and E. L. Walker. Comparison of MSA portable 
hopcalite carbon monoxide indicator and bulb type color- 
imeter. U. S. Navy. Naval Air Station, San Diego, Calif. 
Project X-362, Rept. no. 1, March 1944,4 pp. [P] 
2479. Nelson, N, NDRC infra-red analyzer for deter- 
mination of rapidly changing carbon monoxide concen- 
trations. Final report. U. S. Army. Fort Knox, Ky. 
Armored medical research laboratory. Project T—9, 
SPMEA 723,13-1,18 May 1945, 5 pp. 
2480. Pecora, L. J. and W. V. Consolazio. An evalua- 
tion of the Sjostrand carbon monoxide indicator. U. S. 
Navy. NMRI. Project Rept. no. 10,4 June 1946, 
3 pp. 
2481. Pitts, G. C. A modification of the iodine pentox- 
ide method for the analysis of carbon monoxide in small 
gas samples. U. S. Navy. NMRI. Project X-417, Rept. no. 
11, 7 March 1947, 5 pp. 
2482. Pitts, G. C. and A. R. Behnke. Reevaluation of 
the NIH midget photometer for determining carboxy- 
hemoglobin and total hemoglobin. U. S. Navy, NMRI. 
Project X—146, 25 September 1945, 5 pp. 
2483. Roughton, P. J. W. and W. S. Root. Estimation 
of small amounts of carbon monoxide in air. Analyst, 1946, 
71: 149-150. Abstr. /. industr. Hyg., 1946, 28: abstract 
section: 127-128. 
2484. Salsbury, J. M., J. W. Cole, and J. H. Yoe. Micro- 
gravimetric method for the determination of carbon mon- 
oxide. Analyst, 1947, 72: 418. Abstr. 
2485. Salsbury, J. M., J. W. Cole, and J. H. Yoe. De- 
termination of carbon monoxide; a micro-gravimetric 
method. /. industr. Hyg., 1947, 29: abstract section: 57. 
[P] 
2486. Shepherd, M. A preliminary report on the N. B. S. 
colorimetric indicating gel for the rapid determination of 
small amounts of carbon monoxide. U. S. Department of 
Commerce, National Bureau of Standards, 29 June 1946, 
27 pp. 
2487. Siehert, W. [The infrared absorption recorder and 
its application in mining.] Gliickauf, 1948, 84: 113-118. 
2488. Siosteen, S. M. and T. Sjostrand. A method for 
determination of low concentrations of carbon monoxide 
in the blood and the relation between the CO concentra- 
tion in the blood and that in the alveolar air. Acta physiol, 
scand., 1951, 22: 129-136. 
2489. Soucek, B. Quantitative estimate of carbon mon- 
oxide in air. /. industr. Hyg., 1949, 31: abstract section: 
27. [M] 
2490. Stacy, R. W. Pyrotannic acid method for deter- 
mination of the carbon monoxide content of blood. USAF. 
Wright-Patterson air force base, Dayton, Ohio. Aero med- 
ical laboratory. Technical rept. TSEAL 3-696-41F, 9 May 
1945, 3 pp. 
2491. Van Slyke, D. D., A. Hiller, J, R. Weisiger, and 
W. 0. Cruz. Determination of carbon monoxide in blood 
and of total and active hemoglobin by carbon monoxide 
capacity. Inactive hemoglobin and methemoglobin con- 
tents of normal human blood. J. hiol. Chem., 1946, 166: 
121-148. Analyst, 1947, 72: 257-260. Abstr. 
2492. Wolff, E. Une methode tres simple pour la deter- 
mination de petites quantites d’oxyde de carbone dans le 
sang. Ann. Med. leg., 1947, 27: 221-222. 
2493. Yoe, J. H., J. W. Cole, and J. M. Salsbury. Car- 
bon monoxide indicators of the impregnated silica gel 
type. U. S. OSRD-NDRC. O. S. R. D. rept. no. 1958, 
25 October 1943, 27 pp. 
2494. Yoe, J. H. and C. H. Lindsley. Acidimetric and 
iodometric methods for analysis of carbon monoxide in 
air. U. S. OSRD-NDRG. O. S. R. D. rept. no. 3410, 27 
March 1944, 39 pp. 
2495. Anon. Carbon monoxide indicator guards Hol- 
land tunnel. Heat. Vent., 1950,47: 68. 
2. ARSINE 
Poisoning of submarine personnel by arsine is a 
hazard which is now of historical concern only. 
This is true because of improved industrial methods 
in providing lead-battery grids free of contamina- 
tion with arsenic. Insistence upon the purity of the 
lead is essential in the protection of personnel and 
the virtual elimination of arsine poisoning in sub- 
mariners should not blind us to the dangers in- 
volved. Rigid enforcement of material standards for 
batteries and of adequate ventilation of battery 
compartments is a continuing requirement. 
Arsine is primarily a hemolytic agent. It is pro- 
duced when an acid and a metal, either or both con- 
taining arsenic, are brought into contact, with a 
resulting liberation of nascent hydrogen which 
combines with arsenic to form the toxic gas, arsine. 
In a chapter on arsenic poisoning, McConnell 
{2504) 1951 called attention to arsine poisoning in 
galvanizing works, submarines (from battery plates 
or acid) or ships carrying ferrosilicon. Inhalation of 
arsine over a period of several hours in a concentra- 
tion of 30 parts per million will cause poisoning and 
lethal doses range from 100 milligrams to over 500 
milligrams. There are individual variations in sus- 
ceptibility. The symptoms usually manifest them- 
selves about 6 hours after inhalation of the toxic 
gas, and consist of malaise, vertigo, weakness, head- 
ache, nausea, and vomiting. There may be abdom- 
inal pain and diarrhea. A few hours later, hemoglo- 
binuria or hematuria and albuminuria are observed. 
The pulse may be rapid and feeble, and the respira- 
tory rate increased. Within a day or two, there may 
be a coppery cyanosis with jaundice. The leucocytes 
are not normally involved. There may be transitory 
toxic polyneuritis with pain or anesthesia, but there 
is usually no motor involvement. The condition 
carries a 30-percent mortality and in fatal cases, 
death occurs usually within a week. Oxygen should 
be administered immediately and inhalation of 
oxygen should be prolonged. Blood transfusion may 
be necessary. BAL (2,3-dimercaptopropanol) de- 
veloped as an antidote to arsenical blister gases, 
appears promising in the treatment of arsenical 
poisoning. McConnell recommended that 3 milli- 
grams of BAL per kilogram of body weight be given 
intramuscularly every 4 hours for the first 2 days, NOXIOUS AGENTS—ARSINE 
followed by 4 injections on the third day, with in- 
jections twice daily for 10 days thereafter or until 
complete recovery. 
Reed and Harcourt (2507) 1941 pointed out 
that arsine as such is not used in industry, but is a 
dangerous byproduct of several industrial processes. 
It is a hazard to acid dippers, hydrogen balloon 
workers, battery workers, and makers of bleaching 
powder and fertilizers. Much of the arsine poisoning 
in the United States occurs in workers cleaning out 
tanks and tank cars which have contained concen- 
trated hydrochloric or sulfuric acid with arsenic 
as an impurity. Arsine is probably the most poison- 
ous of all the inorganic gaseous compounds, and 
amounts ranging from 0.1 to 1.0 percent in air often 
prove fatal. These authors point out that it may 
take 6 to 36 hours to produce an effect, depending 
upon the size of the dose. They draw attention to 
the fact that arsine is a hemolytic poison and that 
the essential pathological process is a rapid exten- 
sive destruction of the red cells with cellular debris 
from the destroyed red cells clogging the capillaries 
and producing ischemia of certain organs. The 
symptoms are those associated with a destruction of 
red cells; namely, dizziness, nausea, general weak- 
ness, vomiting, epigastric pain, prostration, and 
death if poisoning increases. If the patient survives 
the first few hours, the urine may be bloody, and in 
24 hours there may be jaundice with the red blood 
count as low as 2 million cells per cubic millimeter. 
Regarding treatments, the authors recommend that 
the patient be removed from the influence of the 
poison as quickly as possible and given continuous 
inhalation of oxygen until out of danger. If respira- 
tion is embarrassed, they recommend the addition of 
carbon dioxide to the respiratory mixture. They 
also suggest immediate blood transfusion, and as the 
patient recovers, massive doses of iron. For further 
general studies of arsine poisoning, the reader is 
referred to papers by Assouly and Griffon (2496) 
1949, and Fourcade (2498) 1950. The paper by 
Assouly and Griffon is a particularly good biblio- 
graphical source. 
For reports of clinical cases of arsine poisoning, 
the reader is referred to papers by Hawlick and Ley 
(2499) 1946; Lievre, Bloch-Michel, and Solignac 
(2503) 1948; Spolyar and Harger (2509) 1950; and 
Wills (2501) 1948. These studies also reveal that 
arsine poisoning is an acute hemolytic process often 
fatal, and sometimes followed in nonfatal cases by 
a chronic involvement of the kidneys. Wills (2510) 
reported the case of a 51-year-old man who cleaned 
a Heroult steel furnace which contained drosses of 
calcium arsenide, calcium phosphide, and calcium 
carbide from a process treating manganese ore. The 
furnace had been empty for 1 month and the victim 
worked in the furnace for 3 hours. Medical examin- 
ation the day before exposure had revealed that the 
worker was in normal condition. Signs and symp- 
toms began on the day of exposure and there was 
dark, port-wine urine with muscular aches, slight 
fever, a parboiled redness of the skin, and acute red- 
ness of the sclera. The tongue was dry and coated, 
there was a metallic odor of the breath, and the 
temperature was 101.2° F. orally. The pulse was 
86 and the blood pressure was 84/52, the normal on 
previous examination having been 112/80. There 
was mild tenderness in the midepigastric region. In 
the hospital, blood hemoglobin had fallen to 8 
grams, or 51.5 percent. There were 2,350,000 red 
blood cells, and 14,450 white blood cells. Later, the 
red blood cell count fell to 1,500,000 and the hemo- 
globin to 38.2 percent. Daily whole-blood transfu- 
sions were given together with fluid orally, and 
2,000 cu. cm. of 10-percent glucose in saline intra- 
venously. Every 4 hours, 1.35 cu. cm. of BAL were 
administered intramuscularly. Diagnosis of blood 
destruction due to heavy metal poisoning was based 
on the findings of marked destruction of red blood 
cells with symptoms of anoxemia and anemia, uri- 
nary suppression, hemoglobinuria, and pulmonary 
edema. 
Josephson, Pinto, and Petronella (2500) 1951 
have reported electrocardiographic changes in 
human patients with arsine poisoning and have 
called attention to characteristic elevation of the 
T-wave in all leads from 2 to 12 days after arsine 
exposure. In four deaths occurring after arsine 
poisoning, the authors ascribed the fatal outcome 
to rapid myocardial failure. Pathological examina- 
tion in two fatal cases revealed myocardial de- 
generation. This was ascribed either to the direct 
action of arsine on cardiac musculature, or to the 
action of metabolites (arsinites) formed from the 
reaction of arsine poisoning have been reported by 
Firket (2497) 1951; Moureau, Ponsart, and Warin 
(2505) 1951; and de Scoville (2508) 1949. In one 
case reported by Firket (2497), post-mortem ex- 
amination revealed pulmonary parenchymal con- 
gestion; a flaccid, dilated heart with a pale myo- 
cardium; and a congested liver. Microscopically, 
there were extravasations of plasma into the pul- 
monary alveoli, red blood cells in the lumen of the 
renal glomeruli, and tumefaction of the renal epi- 
thelium. Firket considered that it is the excessive 
lowering of the arterial blood pressure which leads 
to the anuria, and not just the mechanical block- 
age of the nephrons. In the cases which came to 
autopsy, reported by Moureau, Ponsart, and Warin 2496-2510 
DISEASES AND ACCIDENTS 
{2505), there was icterus of the conjunctivae and 
pallor of the myocardium. The surface of the heart 
showed small hemorrhagic suffusions. There was 
pulmonary edema and pallor of the liver; the kid- 
neys showed the classical picture of hemoglobinuria 
with albuminous precipitate and cellular debris in 
the intracapsular space. In a case in which death 
supervened in 54 hours, de Scoville {2508) indi- 
cated that the damage to the nephrons was gen- 
eralized, but that the most significant lesions were 
localized in the distal convoluted tubules. The 
characteristic lesions in arsine poisoning are similar 
to those observed in nontraumatic muscular ische- 
mic necrosis, crush syndrome, and burns. Apart 
from the tubular necrosis in the distal convoluted 
tubules, there were intratubular casts in the same 
portion. No gross interstitial edema was observed. 
The author considered that mechanical blockage 
produced by intratubular necrosis and precipitate 
could not alone account for the anuria. The possi- 
bility of diversion of blood from the renal cortex to 
the juxta-medullary region was discussed. 
In a discussion of the mechanisms of the lethal 
action of arsine, Nau {2506) 1948 listed (1) the 
hemolysis of red blood corpuscules with the liber- 
ation of toxic arsenic-containing substances, (2) 
blockage of the kidney tubules by products of the 
hemoglobin breakdown, and (3) decrease of the 
oxygen-carrying capacity of the blood. The author 
also suggested that some arsine escapes red blood 
corpuscle fixation long enough to be carried to vital 
organs where its toxic effects are manifested. This 
corresponds to the conclusions of Levvy {2501) 
1947-48 that the toxicity of arsine in the higher 
concentration ranges may in part be due to the 
action on vital organs of the unchanged gas reach- 
ing them in physical solution in the blood plasma. 
Arsine is believed to be lytic only under aerobic 
conditions. The mechanism of lysis is not known. 
Arsenic trioxide and arsenic pentoxide are stated 
by Nau {2506) not to be lytic. He calls attention 
to the fact that arsine inhibits the respiration of 
various organ tissue slices, including kidney. 
In 1946, Kensler, Abels, and Rhoaes {2502) 
reported animal experimental studies on the treat- 
ment of arsine poisoning. These authors assumed 
that if compounds could be found which would 
effectively prevent the hemolysis of erythrocytes by 
arsine in vitro, or would protect the respiration of 
the tissue slices from inhibition by arsine in vitro, 
these compounds should be effective in the treat- 
ment of the clinical condition. Some dithiols were 
found to prevent the lysis of red cells by arsine in 
vitro when added 5 minutes after the cells had been 
exposed to the toxic gas. Some dithiols also pro- 
tected tissue respiration from inhibition by arsine 
or by arsenite. Several dithiols were found to be 
effective in saving the lives of rabbits, dogs, and 
monkeys poisoned with arsine. 
2496. Assouly, ( ) and ( ), Griffon. L’intoxication par 
1’hydrogene arsenic au cours du detartrage par les acides. 
Arch. Mai. prof., 1949,10: 337-346. [D] 
2497. Firket, J. A propos des intoxications aigues par 
1’hydrogene arsenic, de leur anurie et des essais pour la 
prevenir. Arch, beiges M6d. soc., 1951, 9: 23—30. [CH] 
2498. Eourcade, J. Intoxications professionnelles par 
1’hydrogene arsenic, pp. 140-142 in: Medecine du travail. 
Edited by C. Simonin. Paris, Librairie Maloine, 1950, 
913 pp. [D] 
2499. Hawlick, G. F. and E. B. Ley. Arsine poisoning. 
Occup. Med., 1946,1: 388-390. [CH] 
2500. Josephson, C. J., S. S. Pinto, and S. J. Petronella. 
Arsine: electrocardiographic changes produced in acute 
human poisoning. Arch. ind. Hyg. occup. Med., 1951, 4: 
43-52 [CH] 
2501. Levvy, G. A. A study of arsine poisoning. Quart. 
J. exp. Physiol., 1947/48, 34: 47-67. /. industr. Hyg., 
1948, 30: abstract section: 13. [P] 
2502. Kensler, C. J., J. C. Abels, and C. P. Rhoads. 
Arsine poisoning, mode of action and treatment. /. Phar- 
macol., 1946, 88: 99-108. 
2503. Lievre, J. A., H. Bloch-Michel, and H. Solignac. 
Ictere hymolytique par hydrogene arsenic. Bull. Soc. 
med. Hop. Paris, 1948, 64: 195-198. [CH] 
2504. McConnell, W. J. Diseases due to chemical agents. 
Arsenic poisoning, pp. 514-516 in: A textbook of medi- 
cine. Edited by R. L. Cecil and R. F. Loeb. Philadelphia, 
W. B. Saunders Go., 1951, 1549 pp. 
2505. Moureau, P., E, Ponsart, and J. Warin. Quelques 
aspects particuliers de 1’intoxication par I’hydrogene 
arsenic. Arch, beiges MSd. soc., 1951, 9: 23-30. 
2506. Nan, C. A. The accidental generation of arsine gas 
in an industry. Sth. med. J., Birmingham, 1948, 41: 
341-344.[R] 
2507. Reed, J. V. and A. K. Harconrt. Arsine AsH3 or 
arseniurated hydrogen, pp. 11-13 in: The essentials of 
occupational diseases. Springfield, Charles C. Thomas, 
1941, 225 pp. 
2508. Scoville, A. de. Etude histo-pathologique et 
histo-physiologique d’un cas d’intoxication par 1’hydrogene 
arsenic. Considerations sur le mecanisme de son anurie. 
Rev. beige Path., 1949,19: 195-213. [CH] 
2509. Spolyar, L, W. and R. R. Harger. Arsine poison- 
ing. Arch, industr. Hyg., 1950, 1: 419-436. Arch, industr. 
Hyg. occup. Med., 1950, 1: 419-436. Abstr. World Med., 
1950, 8: 586. 
2510. Wills, R. A. Arsine gas poisoning—report of a 
case. Industr. Med., 1948,17: 208. [CH] 
3. BERYLLIUM 
Beryllium is extracted from beryl ore which is 
mined in Brazil, Germany, Russia, India, and the 
United States of America. Since the 19th century, 
beryllium has been used as an alloy with copper, and 
is now also employed as an alloy with aluminum to 
make it resistant to corrosion and to increase resist- 
ance to stress and strain. Beryllium is also used in 
radio tubes, neon-sign tubing, and electric heating 
elements. Some of the first cases of pneumonitis NOXIOUS AGENTS—BERYLLIUM 
from beryllium were reported in the fluorescent 
lamp industry {2522, 2528). 
A major source of information on beryllium 
poisoning is Vorwald’s volume {2538) published in 
1950. As Vorwald and others have pointed out, 
beryllium poisoning manifests itself in an acute form 
and in a chronic form. In acute beryllium poison- 
ing, the clinical manifestations are dermal and 
respiratory. These are contact dermatitis, conjunc- 
tivitis, corneal burns, and ulcers. Regarding the 
respiratory effects, the symptoms vary from rhinitis 
to pneumonitis. Treatment for the acute manifes- 
tations is supportive with prevention of further ex- 
posure, absolute rest, and oxygen administration. 
Benadryl and pyribenzamine are stated to be some- 
times beneficial. The chronic form of beryllium 
poisoning is characterized by the long latent period 
often seen between the last exposure to beryllium 
compounds and the development, sometimes years 
later, of respiratory symptoms. The clinical features 
of the chronic disease are dyspnea, loss of weight, 
and a chronic pulmonary granulomatosis. The diag- 
nosis is established by ruling out pulmonary tubercu- 
losis, silicosis, and Boeck’s sarcoid. Hasterlik {2525) 
1949 has pointed out that beryllium poisoning 
should be understood as a disease of the entire body, 
although the most prominent and incapacitating 
features are centered in the respiratory system. 
Beryllium poisoning has been produced by exposure 
to many beryllium compounds as well as the finely 
powdered beryllium metal. Tracer studies on ani- 
mals with Be7 indicate that a large and significant 
portion of the injected dose of a soluble beryllium 
salt is rapidly deposited in the bone, where it re- 
mains almost indefinitely. This finding of deposition 
of beryllium in the bone gives a clue to the mecha- 
nism of the delayed appearance of the disease. It is 
possible that various “trigger mechanisms” act to 
release beryllium stored in the bones into the general 
circulation. Hasterlik believes that it is not possible 
at present to set “safe” levels of concentration of 
beryllium in the air. It is known that exposure to 
air concentrations of a beryllium compound of 25 
micrograms of beryllium per cubic meter of air has 
produced the acute form of the disease. This, then, 
represents a level which should never be permitted. 
The danger of beryllium poisoning in work spaces 
emphasizes the importance of continual air purifica- 
tion. Sax {2531) 1951 indicated that the maximal 
allowable concentration of beryllium in air in a 
working area is 2 micrograms per cubic millimeter 
of air. Vorwald {2538) has drawn attention to defi- 
nite species differences in the susceptibility of the 
common laboratory animals to beryllium com- 
pounds inhaled experimentally. In studies on the 
dog, rabbit, guinea pig, mouse, hamster, and rat, 
mice were found to be most susceptible. There is 
striking pulmonary damage in all species with a 
consistant rise in the leukocyte counts in the dog, 
rabbit, and rat. None of the animal studies repro- 
duces exactly the type of pulmonary lesion seen in 
the clinical disease in man. For further studies on 
the general problems of acute and chronic beryl- 
lium poisoning and the medical control of beryllium 
poisoning, the reader is referred to reports by Hardy 
(2523) 1949, and Tabershaw, Dustan, and Gold- 
water {2534) 1949. 
The exact mechanism of the poisonous action of 
beryllium compounds is not known. Studies of Hys- 
lop, Palmes, Alford, Monaco, and Fairhall {2526) 
1943 indicate that no particular toxicity can be 
established for beryllium itself. It appears that the 
toxicity of beryllium salts is due to the toxicity of 
the acid radical such as the fluoride or the oxyfluo- 
ride, or to some objectionable condition brought 
about by the hydrolysis of certain of its salts, such 
as the chloride and the sulfate. Hyslop and his co- 
workers carried out animal experiments in which 
a number of beryllium compounds were injected 
intraperitoneally into guinea pigs at various concen- 
trations. Beryllium compounds were also adminis- 
tered orally to young rats and guinea pigs, and, in 
addition, guinea pigs were exposed to the dust of 
beryllium compounds in high concentrations and 
over long intervals of time. These experiments gave 
no indication that beryllium is inherently toxic. 
Exposure of both guinea pigs and rats to the fumes 
arising from the electrolysis of molten fluorides con- 
taining beryllium fluoride or oxyfluoride indicated 
that these fumes are decidely toxic. In the authors’ 
experiments, exposure to large amounts of beryllium 
by mouth, by inhalation, or by intraperitoneal in- 
jection resulted in very little storage of beryllium in 
the body. More beryllium was found to be stored 
in the liver than in the kidneys, and still more beryl- 
lium was found in the bone tissue. No significant 
changes in hemoglobin values were obtained, nor 
was there any evidence of polycythemia, or any 
other blood dyscrasia. Certain salts of beryllium, 
such as the fluoride and the sulfate, hydrolyze read- 
ily and these were found to have an irritant effect 
upon the skin, but this effect was absent in the case 
of the neutral salts. Recovery experiments indicated 
that absorption of beryllium from the alimentary 
tract is slight and that beryllium is excreted mainly 
in the feces. The absorption of beryllium carbonate 
from the lungs was also found to be very slight. 
A comparison of the relative toxicities of beryl- 
lium, magnesium, and zinc by intraperitoneal injec- DISEASES AND ACCIDENTS 
tion revealed beryllium to be the least toxic and 
zinc the most toxic. Microscopic examination of the 
tissues of animals that had been exposed to beryl- 
lium by inhalation of beryllium dust or fumes, in- 
jection of beryllium compounds, or the oral admin- 
istration of this material, indicated no specific 
relationship between beryllium and rickets, and no 
consistent pathological change which could be at- 
tributed to beryllium. The authors therefore con- 
cluded that since no particular toxicity could be 
established for beryllium, no safe permissible work- 
ing standards should be based upon beryllium itself. 
Safe operating conditions must therefore depend 
upon other considerations than an implied toxicity 
of beryllium. 
In initial studies of the inhalation toxicity of 
beryllium sulfate, Sprague, Pettengill, and Stock- 
inger {2533) 1948 collected data from 66 animals 
representing 6 species on the toxic effects caused by 
inhalation of beryllium sulfate tetrahydrate at a 
concentration approximating 90 micrograms of the 
salt per cubic meter of air. The animals were exposed 
for 6 hours daily for a 2-week period in a small 
inhalation exposure chamber. The mortality for all 
species was 43 percent of the exposed animals. 
Weight response data showed that all species except 
the guinea pig were adversely affected by the ex- 
posure. The rat and the hamster revealed the great- 
est weight depression, losing 11 percent of their 
original weight. There was indication of renal im- 
pairment, with some subsequent regeneration in 
the rabbits. Much less serious kidney damage and 
hepatic injury in the dogs was indicated. The study 
showed an upward trend in the leukocyte count 
during the second week of exposure. The symptoms 
differed in each species. Ocular opacity developed 
in the dog, mouse, and guinea pig, whereas the rat 
developed rales. Other species were unaffected ex- 
ternally. Pulmonary edema was found in the mouse, 
rabbit, and rat. Hepatic injury was seen in mice 
dying during the first 9 days, not thereafter. Renal 
changes were seen in the rabbit and the rat, with 
some regeneration of the tubular epithelium in the 
former species. The authors believed that the sulfate 
ion contributed significantly to the toxicity of this 
beryllium salt. 
LaBelle, Morrow, Booth, Wescott, and Melville 
(2527) 1949 have reported a study of beryllium 
poisoning on 325 rats and 18 rabbits, plus a smaller 
number of mice, guinea pigs, monkeys, and dogs 
receiving beryllium by intratracheal injection, usu- 
ally as an insoluble compound, at levels ranging 
from 5 to 100 micrograms of beryllium per kilogram 
of body weight. In studies covering a period of 1 year 
after the injection, it was found that the chronic 
type of lesion developed in the lungs of most of the 
exposed animals. The characteristics of the lung le- 
sions were specific within a given species and for a 
given compound, but were in no case identical with 
the human chronic pulmonary lesions. During the 
year’s period most of the commonly measured vari- 
ables in the blood and serum remained normal. The 
outstanding changes were increases in the blood 
platelets and the absolute polymorphonuclear leuko- 
cyte content of the circulating blood. In a study on 
the mechanism of action of beryllium, DuBois, 
Doull, and Cochran (2577) 1949 observed the acute 
effect of beryllium chloride upon carbohydrate me- 
tabolism and on various enzymatic reactions. Aque- 
ous solutions of beryllium chloride were admin- 
istered intraperitoneally to rats and the LD-50 value 
was found to be 0.6 milligram of beryllium per kilo- 
gram of body weight. Following acutely toxic doses 
of beryllium, there was a striking hyperglycemia. 
This hyperglycemia could be prevented by insulin, 
ergotamine, or removal of the adrenal medulla, 
suggesting that the effect was induced by epineph- 
rine. Five hours after administration of 7.5 milli- 
grams of beryllium salts per kilogram of body 
weight, there was a 50-percent decrease in liver 
glycogen, and 48 hours after this dose of beryllium 
there was a depletion of phosphocreatine and a 
striking increase in inorganic phosphorus in the 
liver. High concentrations of beryllium did not 
inhibit the oxidation of glucose or anaerobic gly- 
colysis. Alkaline phosphatases activated by calcium 
or magnesium were strongly inhibited by beryllium. 
Caccuri (2574) 1941 has reported alteration of 
the liver and the kidneys in beryllium poisoning. 
Daily doses of 1 milligram per kilogram body weight 
of beryllium (as carbonate, nitrate or oxide) were 
injected into rabbits and the animals were sacri- 
ficed 30 to 90 days later. At the end of 1 month, 
the liver and kidneys were still normal, but there 
was a slight hyperglycemia in all animals given the 
nitrate. There was venous congestion of the liver 
and sometimes venous dilatation. At the end of 2 
months, this congestion became more pronounced 
in both the liver and the kidneys, and the former 
began to show fatty degeneration. The renal 
tubules were enlarged and filled with proteinaceous 
material. The author concluded that the nitrate is 
the most toxic beryllium compound of those used 
in the experiments reported. 
Regarding the diagnosis of acute or chronic 
berylliosis, Dutra, Chalak, and Hubbard (2579) 
1949 have reported that in some cases the diagnosis 
may be supported by the analysis of the urine for 
beryllium. In their study, beryllium was isolated NOXIOUS AGENTS—BERYLLIUM 
from the urine of persons working in beryllium 
plants who had no symptoms of berylliosis, although 
some had previously had the acute pulmonary con- 
dition. During acute or chronic berylliosis, the 
beryllium urinary excretion varies from day to day 
so that a few negative results do not exclude the 
diagnosis and an occasional case may never excrete 
beryllium in the urine. Appreciable amounts of 
beryllium were recovered from the lungs of all 
patients dead from berylliosis, except in one chronic 
case of nonoccupational origin. In some cases, 
beryllium was also recovered from other tissues. 
As Vorwald has stated (2557) 1948, the patho- 
logical manifestations of the disease seen in beryl- 
lium workers are observed principally in the lungs 
and the tracheobronchial lymph nodes. Two dis- 
tinct types of changes are recognized: (1) the acute 
form which resembles a pneumonic process and is 
attended by edema, hemorrhage, and exudate, but 
without the polymorphonuclear leukocytic re- 
sponses that accompanies an acute infectious proc- 
ess, and (2) the chronic form characterized by a 
diffuse pulmonary reaction and scattered granulo- 
matous lesions throughout both lungs. Dutra (25/5) 
1948 described a boggy, generalized consolidation 
of both lungs in the acute pneumonitis which simu- 
lates to some extent the stage of gray hepatization 
in lobar pneumania. Microscopically, in the acute 
form there is a diffuse intraalveolar exudate com- 
posed of large mononuclear phagocytes and edema 
fluid. In the chronic condition, the lungs are volu- 
minous and emphysematous. Enlargement of the 
right ventricle of the heart is constantly present. 
Cases of acute pneumonitis in workers exposed to 
beryllium oxide and metallic beryllium have been 
reported by Aub and Grier (25//) 1949. These 
cases indicate to the authors that the beryllium ion 
is toxic in its own right, and that the effects of 
exposure are not always attributable to the acid 
radicals of soluble beryllium salt. For information 
on acute dermatitis and pneumonitis in beryllium 
workers, the reader is referred to a review of 406 
cases in a 6-year period reported by DeNardi, Van 
Ordstrand, and Carmody (25/5) 1949. The report 
concerns acute dermatological and respiratory tract 
manifestations of beryllium poisoning encountered 
in three plants in the Cleveland area. More than 
25 percent of the new employees in contact with 
beryllium inorganic salt fumes and dusts suffered 
skin reactions within 10 days after exposure, A seri- 
ous problem was the development of acute beryllium 
ulcers of the skin which sometimes became chronic. 
These ulcers result from a deposition of minute 
beryllium sulfate tetrahydrate crystals in the 
skin through abrasion portals. Treatment con- 
sists of an incision of the papule, removal of the 
crystals in the acute ulcers, and curettage of the 
fibrous base in both the acute and chronic phases. 
The incidence and mortality of pneumonitis, the 
severest form of the respiratory tract disorders 
arising from the beryllium contamination, are the 
cause of concern. The irritative phenomena present 
in these cases are stated by the author to be the 
result of reactions in the bronchioles to some in- 
organic salts of beryllium or histaminelike by- 
products, which cause spasm and partial blocking 
of the finer respiratory passages. There is inter- 
ference with gas exchange in the alveoli, resulting 
in local anoxia, a colloidal imbalance, and in alve- 
olar edema. The intermittant use of oxygen and 
hospitalization are recommended. 
Serious, acute pulmonary changes resulting from 
beryllium sodium fluoride dusts in experimental 
animals have been reported by Policard (2530 and 
2542) 1948. In these experiments, there is early and 
violent pulmonary edema with death of the animals 
within 24 hours. Beryllium oxide dusts, on the other 
hand, result in hyperplasia of the mesenchyma of 
the lung. Three types of reaction were reported, 
the first being a histiocyte pneumonia; the second, 
granulomatous nodules, often with giant-cell for- 
mation; and the third, thickening of the alveolar 
walls. The granulamatous nodules were seen after 
a few weeks of exposure and persisted for several 
months. In Policard’s experiments, metallic beryl- 
lium and beryl did not seem to affect the lungs of 
the experimental animals. Carriere, Fraisse, Rich- 
ard, and Roche (25/5) 1949 and Wilson (2539) 
1948 have described cases of delayed chemical 
pneumonitis or diffuse granulamatosis of the lung 
due to beryllium inhalation. These cases were all 
characterized by a delayed onset and somewhat 
chronic course. Carriere and his coworkers describe 
symptoms including irritation of the eyes, nose and 
air passages, varying in intensity with individual 
cases. The ocular and nasal irritation subsided in 
several days or a few weeks, but then the cough and 
dyspnea appeared to get worse, keeping the patients 
from work. The dyspnea followed effort and some- 
times drifted into asthmatic attacks occurring fre- 
quently at night. Symptoms gradually disappeared, 
leaving behind a sensitivity of the air passages to 
vapors or fumes. In 1 or 2 cases, the X-ray showed 
shadows indicative of some discrete reticulonodular 
lesions, which in their turn tended to disappear in 
time. The distinctive features of these cases are the 
short exposure, the delayed onset of severe pulmo- 
nary symptoms, and final complete recovery after 
several months. For further reports of respiratory 
291222—54 16 2511-2524 
DISEASES AND ACCIDENTS 
tract involvement in beryllium poisoning, papers by 
Hardy and Tabershaw (2524) 1946; Pascucci 
(2529) 1948; Van Ordstrand, Hughes, and Car- 
mody (2555) 1943; Van Ordstrand, Hughes, 
DeNardi, and Carmody (2555) 1945 may be 
consulted. 
Reference may be made to experimental beryl- 
lium rickets reported in 1931 by Branion, Guyatt, 
and Kay (2572). These authors found that by 
replacing the calcium carbonate in Steenbock’s 
rachitogenic ration 2965 with an equivalent amount 
of beryllium carbonate, bone lesions were produced 
in young rats which were similar to rickets. These 
changes were brought about by quantities of beryl- 
lium as low as 1 percent of the diet. Both the X-rays 
and histological sections revealed an almost com- 
plete failure of calcium deposition immediately 
proximal to the epiphyseal disc of the long bones. 
The onset of this type of rickets was not found to 
be preventable by cod-liver oil or irradiated ergos- 
terol, both in generous quantities, or by irradiation 
with ultraviolet light. In 1949, Branion, Tisdall, 
and Drake (25/5) reported that while the addi- 
tion of 0.5 percent beryllium carbonate to the ra- 
tion had little or no effect on long bone formation 
in the chick, nevertheless the addition of 1 to 2 
percent beryllium carbonate resulted in beryllium 
rickets, characterized by low levels of inorganic 
plasma phosphorus, subnormal percentage of ash 
in leg bones, and failure in calcification and bone 
development. It was found that chickens were more 
resistant to beryllium rickets than were rats. 
Pathological pulmonary changes in 12 chronic 
cases that came to autopsy have been reported by 
Gardner (252/) 1946. In these cases there were 
minute compact granulomatous nodules barely vis- 
ible to the naked eye, distributed more or less uni- 
formly within the walls of the airspaces throughout 
both lungs. In a case reported in England in 1948 
(2540 and 2541), death was due to granulomatous 
fibrosis of the lungs and failure of a hypertrophied 
right heart. Microscopically, the lungs resembled 
silicosis and sarcoidosis, but were not typical of 
either of these. The patient in question was a 36- 
year-old physicist who had been working with 
beryllium oxide from December 1941 to December 
1942 in connection with research on fluorescent 
lamps. He remained apparently well until 1945. 
The patient then began to complain of cough, 
breathlessness, and great loss of weight. He was 
eventually admitted to the London Hospital, where 
he died on 4 November 1945. Autopsy showed that 
death was due to beryllium poisoning. Gardner 
(252/) has also emphasized the chronicity and the 
high mortality rate which characterize beryllium 
poisoning. He points out that the patients suffering 
from this condition have lived from 6 months to 4 
years, finally dying with cachexia, progressive 
dyspnea, and heart failure. The onset of the disease 
may be delayed as long as 3 or 4 years after apparent 
cessation of exposure. 
Although the characteristic pulmonary changes 
seen in human cases of chronic beryllium poisoning 
have not been reproduced exactly in animals under 
experimental conditions, nevertheless definite path- 
ological changes have been observed in animals, 
and for such a study of the effects of inhalation of 
beryllium dust in guinea pigs, the reader is referred 
to a report by Fabroni (2520) 1935. A report by 
Shilen, Galloway, and Mellor (2552) 1944 on the 
health hazards in a plant manufacturing alloys of 
beryllium should be consulted. 
2511. Aub, J. C. and R. S. Grier. Acute pneumonitis in 
workers exposed to beryllium oxide and beryllium metal. 
Chem. Abstr., 1949, 43: 7606. /. industr., Hyg., 1949, 31: 
123-133. 
2512. Branion, H. D., B. L. Guyatt, and H. D. Kay. 
Beryllium rickets. /. biol. Chem., 1931, 92: xi. 
2513. Branion, H. D., F. F. Tisdall, and T, 6. H. Drake. 
Beryllium rickets in chickens. Chem. Abstr., 1949, 33: 
2946. 
2514. Caccnri, S. The alteration of the liver and the 
kidneys in beryllium poisoning. Chem. Abstr., 1941, 35: 
1521. Rass. Med. industr., 1940, 11: 307-314. 
2515. Carriere, G., P. Fraisse, L. Richard, and L. Roche. 
Occupational diseases of the lungs caused by inhaling 
beryllium. /. industr. Hyg., 1949, 31: 99. (Abstr.) 
2516. DeNardi, H. M., H. S, Van Ordstrand, and M. 6. 
Carmody. Acute dermatitis and pneumonitis in beryllium 
workers: review of 406 cases in 8-year period with fol- 
lowup on recoveries. Nuclear Sci., Abstr., 1949, 3: 50. 
Ohio St. med. J., 1949, 45: 567-575. 
2517. DuBois, K. P., J. Doull, and K. W. Cochran. 
Effects of acute beryllium poisoning on carbohydrate 
metabolism. Nuclear Sci., Abstr., 1949, 3: 420. 
2518. Dutra, F. R. The pneumonitis and granulomatosis 
peculiar to beryllium workers. Amer. J. Path., 1948, 24: 
1137-1152. [R] [CH] 
2519. Dutra, F. R., J. Chalak, and D. M. Hubbard. The 
value of beryllium determinations in the diagnosis of beryl- 
liosis. Chem. Abstr., 1949, 43: 4366. Amer. J. din. Path., 
1949, 19: 229-234. 
2520. Fabroni, S. M, Patologia polmonare da polveri de 
berillio. Med. d. Lavoro, 1935, 26: 297-303. 
2521. Gardner, L. U. Generalized pulmonary granu- 
lomatosis occurring among workers believed to be exposed 
to beryllium or its compounds. Trans. 11th annual meeting 
of Industrial Hygiene Foundation of America, Inc., 1946 
p. 89. 
2522. Hamilton, A, and H. L. Hardy. Beryllium, pp. 
172-187 in: Industrial toxicology. Second edition. New 
York, Paul B. Hoeber, Inc., 1949, 574 pp. 
2523. Hardy, H. L. Acute and chronic beryllium poison- 
ing. Nuclear Sci., Abstr., 1949, 3: 477. 
2524. Hardy, H. L. and I. R. Tabershaw. Delayed 
chemical pneumonitis occurring in workers exposed to 
beryllium compounds. Chem. Abstr., 1946, 40: 7015. 
/. industr. Hyg., 1946, 28: 197-211. NOXIOUS AGENTS—CADMIUM 
2525-2542 
2525. Hasterlik, R. J. Beryllium poisoning. Nuclear Sci. 
Abstr., 1949, 3: 421. 
2526. Hyslop, 3?., E. D. Palmes, W. C. Alford, A. R. 
Monaco, and L. T. Fairhall. The toxicology of beryllium. 
Nat. Inst. Hlth Bull., 1943,181: 56 pp. 
2527. LaBelle, C. W., P. Morrow, C. Booth, F. Wescott, 
and G. Melville. Beryllium poisoning: II. One-year studies 
by intratracheal injection. Fed. Proc. Amer. Soc. Pharm. 
exp. Ther., 1949, 8: 311. 
2528. Osol, A., G. E. Farrar, E. E. Leuallen, W. F. 
Verwey, H. W. Youngken, D. K. Detweiler, and H. C. 
Wood, Jr. Beryllium, p. 1363 in: The dispensatory of the 
United States of America. 24th edition, 1947. Philadelphia, 
J. B. Lippincott Co., 1928 pp. 
2529. Pascucci, L. M. Pulmonary disease in workers 
exposed to beryllium compounds: its roentgen character- 
istics. Radiology, 1948, 50: 23—36. (Spanish summary.) 
[CH] 
2530. Polieard, A. Diseases of the lungs. Lancet, 1948, 
255: 506. 
2531. Sax, N. I. Beryllium, pp. 46-48 in: Handbook of 
dangerous materials. New York, Reinhold Publishing 
Corp., 1951, 848 pp. vii. 
2532. Shilen, J., A. E. Galloway, and J. F, Mellor. 
Beryllium oxide from beryl—health hazards incident to 
extraction—. Industr. Med., 1944, 13: 464-469. 
2533. Sprague, G. F., A. G. Pettengill, and H. E. 
Stokinger. Initial studies of the inhalation toxicity of 
beryllium sulfate. Fed. Proc. Amer. Soc. exp. Biol., 1948, 
7; 257. 
2534. Tabershaw, I. R., C. Dustan, and L. J. Goldwater. 
Medical control of beryllium poisoning. Nuclear Sci., 
Abstr., 1949, 2: 306. Chem. Abstr., 1949, 43: 8073. J. 
industr. Hyg., 1949, 31: 227-233. 
2535. Van Ordstrand, H. S., R. Hughes, and M. G. 
Carmody. Chemical pneumonia in workers extracting 
beryllium oxide. Cleveland Clin. Quart., 1943, 10: 10-18. 
[CH] 
2536. Van Ordstrand, H. S., R. Hughes, J. M. DeNardi, 
and M. G. Carmody. Beryllium poisoning. J. Amer. med. 
Ass., 1945, 129: 1084-1090. [CH] 
2537. Vorwald, A. J. Pathologic aspects of acute pneu- 
monitis and pulmonary granulomatosis in beryllium work- 
ers. Occup. Med., 1948, 5: 684-689. 
2538. Vorwald, A. J,, M. Bowditch, T. M. Durkan, and 
T. C. Waters. Pneumoconiosis. New York, Paul B. Hoeber, 
Inc., 1950, 659 pp. 
2539. Wilson, S. A. Delayed chemical pneumonitis or 
diffuse granulomatosis of the lung due to beryllium. Radiol- 
ogy, 1948, 50: 770—779. (Spanish summary.) Chemical 
Abstr., 1948, 42: 7461. [CH] 
2540. Anon. Beryllium as a cause of death. Brit. Med. J., 
1948, 4588: 1042. 
2541. Anon. Death from exposure to beryllium. Lancet, 
1948, 255: 937. [CH] 
2542. Anon. International congress of industrial medi- 
cine. Nuclear Sci., Abstr., 1948,1: 444. 
4. CADMIUM 
For information on the general subject of cad- 
mium poisoning, papers by Hamilton and Hardy 
{2543) 1949, Johnstone {2545) 1948, Ross {2547) 
1944, and the U. S. National Institute of Health 
{2549) 1942 should be consulted. Cadmium has 
probably more lethal potentialities than any other 
of the metals which may cause acute or chronic 
illness. It has for a long time been a rare metal in 
industry, but has now become widely used in the 
manufacture of alloys and for electroplating. Cad- 
mium is extracted from zinc ores as a condensation 
product. It is also found in the sludge after the 
electrolytic recovery of zinc. Cadmium is used in 
making storage batteries, in metal bearings, ceram- 
ics, cadmium vapor lamps, and in rustproofing. 
Cadmium poisoning usually occurs from the acci- 
dental absorption of cadmium fumes or dusts 
through the respiratory system, seldom by ingestion. 
The maximum allowable concentration of cadmium 
dust or fumes is given by Jacobs {2544) 1949 as 
0.1 mg. per cu. mm. of air. 
The lungs bear the brunt in all cases of cadmium 
fume inhalation. The first symptoms are usually 
smarting of the eyes and dryness and irritation of 
the throat. This is followed by severe, constricting 
pain in the chest and marked dyspnea. There may 
be coughing and a feeling of prostration, and some- 
times giddiness and headaches. Three or four hours 
after exposure, the respiratory distress becomes in- 
creased in severity and gastric disturbances make 
themselves manifest with nausea, retching, vomiting, 
and occasionally diarrhea. There is frequently 
pyrexia with rigors and striking prostration. In the 
event of prolonged exposure to cadmium, pneu- 
monia may supervene, and in fatal cases there may 
be signs of kidney and liver involvement. In mod- 
erate cases of cadmium intoxication, the patient is 
pale, dyspneic, prostrated, inclined to retch, and the 
pulse rate and temperature rise. The serious case 
shows evidence of diffuse bronchopneumonia, best 
revealed by X-ray. Ross {2547) has reported 23 
cases of cadmium poisoning with no fatalities. Osol, 
Farrar, Leuallen, Verwey, Youngken, Detwiler, and 
Wood {2546) 1947 have pointed out that death 
may occur after the fifth or seventh day. They call 
attention to the fact that acid foods dissolve cad- 
mium from metal containers containing this ele- 
ment. A concentration of only 30 p. p. m. of cad- 
mium in solution causes, within 10 to 30 minutes, 
nausea, vomiting, abdominal cramps, weakness, and 
diarrhea, with recovery usually in 5 or 6 hours after 
this amount of cadmium ingestion. In a fatal case of 
cadmium poisoning described in 1943 in the Journal 
of the American Medical Association {2550), a 
worker died within 4 days after a prolonged expo- 
sure to a high concentration of cadmium fumes in 
an Indiana plant. The deceased worker undertook 
a job of “flanging” a cadmium-plated, stainless-steel 
pipe. To produce the flange, the pipe was heated 
with a blowtorch until it became cherry red. Soon 2543-2550 
DISEASES AND ACCIDENTS 
after beginning the operation, employees com- 
plained of irritation of the nose and throat as well 
as the thick blue smoke present in the environment. 
Within 4 hours, 2 employees became violently ill 
and were taken home. Vomiting, chest pains, and 
shortness of breath were the chief symptoms at this 
time. The chest symptoms of one worker increased, 
and within 4 days this man died. Four case histories 
are described by Johnstone (2545), who also has 
discussed treatment, recommending the immediate 
use of an oxygen tent for relief of air hunger. A 
method for the microscopic detection of cadmium 
oxide particles in lung tissue of experimental ani- 
mals is described by Thiers, Arthur, Mills, Hamly, 
and Beamish {2548) 1947. 
2543. Hamilton, A. and H. L. Hardy. Cadmium, pp. 
145—156 in: Industrial toxicology. Second edition. 1949. 
New York, Paul B. Hoeber, Inc., 574 pp. [R] 
2544. Jacobs, M. B. Cadmium, pp. 261—263 in: The 
analytical chemistry of industrial poisons, hazards, and 
solvents. Second edition. 1949. New York, Interscience 
Publishers, Inc., 788 pp. 
2545. Johnstone, R. T. Cadmium, pp. 265—276 in: Oc- 
cupational medicine and industrial hygiene. St. Louis, 
The C. V. Mosby Co., 1948, 604 pp. [GH] 
2546. Osol, A., G. E. Farrar, E. E, leuallen, W. F. Ver- 
wey, H. W. Youngken, D. K. Detweiler, and H. C. Wood, 
Jr. Cadmium, pp. 1376—1377 in: The dispensatory of the 
United States of America. 24th edition, 1947. Philadel- 
phia, J. B. Lippincott Co., 1928 pp. 
2547. Boss, P. Cadmium poisoning. Brit. med. J., 1944, 
1: 252-253. 
2548. Thiers, B. E., E. M. S. Arthur, J. B. Mills, D. H. 
Hamly, and F. E. Beamish. Microscopic detection of cad- 
mium oxide particles in lung tissue. Chem. Abstr., 1947, 
41: 3163. J. Ind. Hyg. Tax., 1947, 29: 129-133. 
2549. H. S. National Institute of Health, Division of 
Industrial Hygiene. Cadmium poisoning. Pub. Hlth Rep., 
Wash., 1942, 57: 601-612. 
2550. Anon. Fatal case of cadmium poisoning. /. Amer. 
med. Ass., 1943, 123: 1057. [CH] 
5. CHLORINE 
Chlorine gas is a powerful lung irritant, and was 
the first chemical war gas used in World War I. 
In the past, chlorine has been liberated in sub- 
marine compartments through leakage of salt water 
into the storage batteries. Victims of inhaled chlo- 
rine gas show dyspnea, cyanosis, and coma. There 
is a sense of suffocation, constriction in the chest, 
and tightness in the throat, and death may ensue 
if resuscitation procedures are not promptly carried 
out. The patient is likely to recover if immediately 
removed to fresh air. There may be areas of slough- 
ing of the mucous membranes of the nose, throat, 
or bronchi. If the gas is swallowed, there may be 
necrosis of the mucosa of the esophagus or stomach. 
Marked irritation of the conjuntivae is also a char- 
acteristic feature. Nearly all cases of chlorine poison- 
ing tend to recover completely if the victims survive 
the first 24 hours. Secondary infection of mucous 
surfaces is a possible complication. Reed and Har- 
court {2563) 1941 believe that chronic exposure to 
chlorine gas does not result in real occupational 
disease so far as serious disability is concerned. The 
inhalation of small concentrations of chlorine over 
long periods of time may cause dental caries, acne- 
form dermatitis, and chronic bronchitis. For reports 
on maximum allowable concentrations of chlorine 
gas in the environment, the reader is referred to 
papers by Fairhall {2554) 1949, Heyroth {2556) 
1948, Jacobs {2558) 1949, and Skljanskaja and 
Rappoport {2565) 1934-35. Fairhall {2554) has 
pointed out that concentrations of chlorine of 
40 to 60 p.p.m leads to pneumonitis and edema of 
the lungs. It is stated that 30.2 p.p.m. cause cough- 
ing, and with 3.5 p.p.m. there is a detectable odor 
of chlorine. The maximum allowable concentration 
is described as 0.35 to 4.0 p.p.m. for exposures of 
one-half to 1 hour. Skljanskaja and Rappoport 
{2565) have observed catarrh-like changes in the 
upper respiratory tract with hemorrhage and 
emphysema in the lungs of rabbits exposed to a 
chlorine concentration of 0.7 to 1.7 p.p.m., and 
these authors assert that chlorine appears to sensi- 
tize the respiratory tract to infection. Heyroth 
{2556) has stated that 1,000 p.p.m. is a fatal con- 
centration for even large laboratory animals. If 
death does not occur, there may be pulmonary 
edema. The conjunctivae become inflamed and 
there is coughing and dyspnea. The respiratory 
rate of experimental animals subjected to this con- 
centration of chlorine becomes increased during ex- 
posure. When the concentration is 1,000 or more 
p.p.m., inspiration becomes slower and deeper. The 
author has stated that men may work without 
interruption in air with 0.003 to 0.006 mg. of chlo- 
rine per liter. Exposures to low concentrations of 
0.01 to 0.02 mg. per liter or 3 to 6 p.p.m. cause 
stinging and burning of the eyes, nose, and throat, 
and sometimes headache. There may be redness 
and watering of the eyes, sneezing, coughing, and 
laryngitis. Bleeding of the nose may occur and the 
sputum may be bloodtinged. Exposure for one-half 
to 1 hour to 0.04 to 0.06 mg. per liter, that is to 
say, 14 to 21 p.p.m., is dangerous and a concen- 
tration of 0.29 mg. per liter, that is to say, 100 
p.p.m., cannot readily be borne longer than 1 
minute. Dangers of low concentrations are limited 
to the nose and throat because of the solubility of 
chlorine in water. Higher concentrations give rise 
to pulmonary congestion and edema, the seriousness 
of which is increased by bronchoconstriction. Hey- 
roth has pointed out that men lose their ability to 
detect chlorine in small concentrations. He also NOXIOUS AGENTS—CHLORINE 
states that workers exposed in bleaching rooms to 
concentrations of 0.015 mg. per liter, that is to 
say, 5 p.p.m., suffer from bronchial diseases and 
tend to be predisposed to tuberculosis. The teeth 
become corroded, and ulceration of the mucous 
membrane of the nose occurs. 
Many experimental studies of the toxicity of 
chlorine were carried out during and immediately 
following World War I. Two such investigations 
are reported by Barbour (2551) 1919-20 and Klotz 
(2559) 1917. Barbour called attention to the effect 
of chlorine in concentrations of 20 to 30 p.p.m. of 
air in producing considerable increase in the body 
temperature of dogs. He stated that dogs gassed 
with lethal concentrations of chlorine tend to be- 
come poikilothermous, that is to say, they lose their 
capacity to regulate body temperature in environ- 
mental extremes. Barbour considered that periph- 
eral nerve irritation produced by chlorine exerts 
inhibitory effects upon the temperature centers of 
the nervous system and may thus contribute sub- 
stantially to the derangement of the heat-regulating 
mechanism seen with the concentrations of chlorine 
employed in his experiments. On the basis of his 
studies, he recommended that, in the treatment of 
gassed cases, an excessively warm environment may 
be as dangerous as one which is too cold. A further 
paper on the toxic effects of chlorine upon the lungs 
is that published by Barbour and Williams in 
1919-20 (2552). 
For descriptions of clinical cases of chlorine 
poisoning, papers by Doub (2553) 1933; Olliver 
and Charpin (2561) 1947; and Smith, Chassis, 
Bannon, Helm, and McLeod (2566) 1944 may be 
consulted. The latter gives an account of the well- 
known Brooklyn chlorine accident. On 1 June 1944, 
a truck carrying 27 cylinders of chlorine from 
Bayonne, N. J., to Brooklyn, N. Y., was found to 
contain a leaky cylinder. When the driver dis- 
covered the leak, he came to a stop approximately 
30 feet from a subway entrance and 18 inches from 
a series of gratings covering ventilation shafts lead- 
ing from the sidewalk to the subway station plat- 
form. Liquid chlorine spilled into the gutter ad- 
jacent to the gratings. Sufficient chlorine gas entered 
the station to cause a number of passengers to leave 
the train and go to the street. Some left the train 
at the next stop to obtain medical aid. There were 
104 cases of chlorine poisoning, and 102 of these 
were from the subway. A total of 418 persons ex- 
posed were examined at 8 hospitals. Two hundred 
and eight were admitted for observation. Thirty- 
three victims were hospitalized for 1 to 2 weeks. 
The symptoms occurring after the first few hours 
after exposure consisted of burning of the eyes, nose, 
and mouth, with increased salivation, cough, chok- 
ing sensation, and substernal pain accompanied by 
nausea, vomiting, headache, and dizziness. There 
was syncope in 8 out of the 33 cases. Six to ten 
hours after exposure, the casualties were perturbed 
and acutely ill, and suffered from moderate to severe 
respiratory distress. Cyanosis of the mucous mem- 
branes was frequent. The respiratory rate was in- 
creased and was costoabdominal in type. Dry and 
moist rales were a universal finding. Symptoms 
tended to subside within 24 hours. Oxygen was 
given to all acutely ill victims over a period of 96 
hours, and pressure breathing in 20 cases reduced 
respiratory distress and resulted in the disappear- 
ance of pulmonary sounds. Bronchodilating drugs, 
such as epinephrine and aminophyllin, were stated 
to be beneficial. 
The reader is referred to a report on respiratory 
studies made during the late stages of gas poisoning 
by Pearce (2562) 1920. This author found that the 
majority of men complained of symptoms which 
they believed to be due to gas fail to show any signs 
of cardiac or pulmonary impairment. These pa- 
tients suffered from subjective symptoms similar to 
those of the so-called effort syndrome. One patient 
who had been gassed with chlorine 1 year previously 
showed no cardiovascular or pulmonary impair- 
ment, save some bronchitis. He complained of in- 
ability to work without becoming restless and faint. 
Treatment of chlorine gas poisoning includes 
early administration of oxygen. Oxygen treatment 
for chlorine-gas exposure has been described by 
Nale (2560) 1946. On experimental grounds, Hjort 
and Taylor (2557) 1919 concluded that the admin- 
istration of morphine exerts, if anything, an unfav- 
orable influence upon the ultimate outcome of 
chlorine poisoning. They reported that in dogs 
gassed with chlorine, the administration of mor- 
phine in 10 mg. per kilo body weight doses may 
temporarily prolong the maintenance of a high 
alkali reserve level and so tend to counteract a 
rapidly advancing acidosis produced by chlorine 
gas inhalation. The bronchoconstriction resulting 
from inhalation of chlorine gas has been studied by 
Gunn (2555) 1919-20. The author concluded that 
the immediate bronchoconstriction is produced re- 
flexly by the first contact of the irritant chlorine 
vapor with the bronchial mucous membrane. Con- 
tinued inhalation of the gas produces thereafter an 
apparent slight and gradual bronchoconstriction, 
but from histological observation it appeared to the 
author that this is due rather to edema of the bron- 
chial mucous membrane than to contraction of the 
bronchial muscle. In Gunn’s experiments, a num- 2551-2567 
DISEASES AND ACCIDENTS 
ber of bronchodilator drugs were investigated, and 
it was concluded that, for practical purposes, atro- 
pine or epinephrine might be the most useful. 
For experimental investigations of the pathologi- 
cal changes resulting in animals from exposure to 
chlorine gas, papers by Klotz (2559) 1917; Schultz 
and Hunt {2564) 1918; and Weedon, Hartzell, and 
Setterstrom (2567) 1940 may be consulted. Weedon, 
Hartzell, and Setterstrom (2567) exposed rats and 
mice to various concentrations of chlorine from 63 
p.p.m. to 1,000 p.p.m. With the highest concen- 
trations, the brain was congested. The lungs were 
distended, pale, and waxy, and the cut surfaces 
foamy. The right heart was greatly distended, the 
liver was congested, the stomach moderately to 
greatly distended, and there was distention of the 
intestines and congestion of the kidney. Klotz 
(2559) found that the acute reaction in the lungs 
of animals exposed to chlorine was mainly an in- 
tense congestion with edema and capillary throm- 
bosis. Animals surviving for a longer period ex- 
hibited pulmonary infiltration of inflammatory cells, 
mainly lymphocytes. The acute capillary throm- 
bosis appears of importance in acute death when 
the concentration of chlorine is great. There is 
a tendency toward increased viscosity of the blood, 
and this, together with capillary thrombosis, im- 
pedes the ready flow of blood through the lungs 
and leads to a fall in systematic arterial blood 
pressure. Post-mortem study of the lungs of cats 
and dogs exposed to chlorine gas by Schultz and 
Hunt (2564) revealed varying degrees of edema 
together with separation of the epithelium from 
wide areas of the respiratory tract. The alveoli and 
the finer air passages were invaded by serous 
exudate. 
2551. Barbour, H. G. The effects of chlorine upon the 
body temperature. J. Pharmacol., 1919/1920, 14: 65-73. 
2552. Barbour, H. G. and H. W. Williams. The effects 
of chlorine upon isolated bronchi and pulmonary vessels. 
/. Pharmacol, 1919/1920, 14: 47-53. 
2553. Doub, H. P. Pulmonary changes from inhalation 
of noxious gases. Radiology, 1933,21: 105-113. 
2554. Eairhall, L. T. Chlorine, pp. 51-53 in: Industrial 
toxicology. Baltimore, The Williams & Wilkins Co., 1949, 
471 pp. 
2555. Gunn, J. A. The action of chlorine, etc., on the 
bronchi. Report to the chemical warfare committee. Quart. 
J. Med., 1919/1920, 13: 121-127. 
2556. Heyroth, P. F. Chlorine, pp. 545-549 in: Indus- 
trial hygiene and toxicology. Edited by Frank A. Patty. 
New York, Interscience Publishers, Inc., 1948, 1138 pp. 
2557. Hjort, A. M. and F. A. Taylor. The effect of 
morphine upon the alkali reserve of the blood of dogs 
gassed with fatal concentrations of chlorine. /. Pharmacol, 
1919, 13: 407-416. [P] 
2558. Jacobs, M. B, Common poisonous compounds of 
the halogens. A. Chlorine, pp. 373-390 in: The analytical 
chemistry of industrial poisons, hazards, and solvents. 
Second edition. New York, Interscience Publishers, Inc., 
1949, 788 pp. 
2559. Klotz, 0. Acute death from chlorine poisoning. 
/. Lab. din. Med., 1917,2: 889-895. 
2560. Hale, T. W. Oxygen treatment for chlorine gas 
exposures. W. Va. med. ]., 1946, 42: 178—180. 
2561. Ollivier, H. and J. Charpin. A propos d’une in- 
toxication accidentelle collective par le chlore. Ann. Med. 
leg., 1947,27; 150-151. [CH] 
2562. Pearce, R. G. Note on some respiratory studies 
made on late stages of gas poisoning. /. Lab. din. Med., 
1920, 5: 411-417. [CH] 
2563. Reed, J. V. and A. K. Harcourt, Chlorine and 
chloride of lime CaOCfi. pp. 34-35 in: The essentials of 
occupational diseases. Springfield, Charles G. Thomas, 
1941, 225 pp. 
2564. Schultz, W. H. and H. R, Hunt. Some pathologi- 
cal phenomena following inhalation of chlorine gas. J. 
Pharmacol., 1918, 11: 181-183. 
2565. Skljanskaja, R. M,, and J. L. Rappoport. Experi- 
mentelle Studien fiber chronische Vergiftung von Ka- 
ninchen mit geringen Ghlorkonzentrationen und die En- 
twicklung der Nachkommenschaft der chlorverfigteten 
Kaninchen. Arch. exp. Path., Lpz., 1934/1935, 177: 276- 
286. [P] 
2566. Smith, H. W., H. Chassis, J. H. Bannon, J. Helm, 
and C. M. McLeod. Brooklyn chlorine accident. A technical 
and medical report. U. S. Army. Chemical warfare serv- 
ice, Medical division. Contract W~49-036-csw-l with 
New York University, College of Medicine. 1 July 1944, 
36 pp. xci. [CH] 
2567. Weedon, E. R., A. Hartzell, and C. Setterstrom. 
Toxicity of ammonia, chlorine, hydrogen cyanide, hydro- 
gen sulphide, and sulphur dioxide gases. V. Animals. 
Contr. Boyce Thompson Inst., 1940, 11: 365-384. [P] 
6. LEAD 
Brown (2572) has reported that the incidence of 
lead poisoning among U. S. Navy personnel de- 
creased between 1922 and 1944. Two factors re- 
sponsible for this reduction in incidence were the 
changes in 1931 from a paint containing 70 percent 
red lead to one containing only 29.5 percent and 
the changeover to zinc chromate paint in 1941. 
Probably improvements in hygienic control were of 
even greater importance. So far as can be ascer- 
tained, shipbreaking during the 2 years immediately 
following World War II produced very few cases 
of plumbism, a condition very common in this occu- 
pation after World War I. The route by which lead 
enters the organism most rapidly is the respiratory 
tract, and lead absorbed by this route produces the 
most serious symptoms. Next in danger comes the 
continued ingestion of lead compounds by mouth, 
and least harmful of all the possible routes is a slow 
cutaneous absorption in persons with broken or 
irritated skin. Lead compounds may reach the 
mouth via contaminated hands, or lead fumes may 
be inhaled during grinding or filing, during paint- 
ing with lead paints, or cutting, burning, or chipping 
of lead painted surfaces. The upper limit of safety NOXIOUS AGENTS—LEAD 
for industrial lead exposure has been given by Kehoe 
{2583) 1948 as 1.5 mg, per 10 cubic meters of air. 
The upper limit of safe urinary excretion of lead 
does not exceed 0.15 mg. per liter of urine. Kehoe 
{2582) indicated that the safe level for the inges- 
tion of lead in food and drink is greater than 0.3 
mg. and less than 0.6 mg. per day. It is significant 
physiologically that from 95 to 98 percent of lead 
present in the body in lead poisoning is found in 
the erythrocytes in the blood. Only a small quantity 
of the lead ingested is absorbed into the body. The 
absorbed portion is distributed to the tissues, in- 
cluding the liver, from which it is partially secreted 
back into the alimentary tract with the bile. This 
action of the liver in withdrawing lead from the 
body and secreting it into the alimentary tract is 
responsible for the fact that the ingestion of lead is 
less dangerous than its inhalation. Lead poisoning 
is stated by Jacobs {2580) 1949 as 10 times more 
likely to occur through inhalation than by ingestion. 
The toxicity of lead depends upon a number of 
factors—its solubility in body fluids; the length of 
time in contact with the body fluids; the quantity 
ingested, inhaled, or absorbed; and the quantity in 
the circulation at a given time. Inhalation of 1.45 
mg. of lead per day is stated by Jacobs to produce 
lead poisoning within l/z years. Hamilton and 
Hardy {2578) 1949 have pointed out that various 
compounds of lead differ in their toxicity. Metallic 
lead particles in the lung act much as do silica 
particles, setting up a fibrotic process, which paves 
the way for a pulmonary tuberculosis. Absorption 
by the respiratory tract is extremely rapid. Skin 
absorption is slight, except in the case of tetraethyl 
lead. Absorption of lead by the alimentary tract is 
minimized by excess of phosphate ions which keep 
the lead insoluble. Lead is carried in the blood as 
the dibasic phosphate or as the glycerophosphate, 
and is deposited in the skeleton as the very slightly 
soluble tribasic phosphate. The liver, spleen, lungs, 
and kidneys may retain lead for a short period, 
during which the excretion rate is highest (a few 
weeks). Redistribution of lead results in a shift of 
most of the remaining amount to the bony skeleton 
with small amounts retained in the liver and spleen. 
The most consistently harmful effect of abnormal 
lead absorption is on the blood cells. Anemia is 
invariably present. Basophilic stippling is always 
seen in the acute stage of lead intoxication, but is 
not pathognomonic of plumbism since basophilic 
stippling may be present in other diseases of the 
blood. The mechanism of intestinal colic in lead 
poisoning is not clearly understood. Usually other 
symptoms precede the colic. The gastrointestinal 
symptoms usually begin with anorexia, disagreeable 
sweetish taste in the mouth, dyspepsia, and obstinate 
constipation. There is also lassitude and malaise 
with pain around the umbilicus, and spasmodic 
contraction of the abdominal wall. The colic is 
typically decreased by pressure, and there is no 
tenderness. This colic has been ascribed by some 
authors to vagal irritation produced by the lead. A 
characteristic phenomenon is wrist drop due to 
paralysis of the extensor muscles of the forearm. 
There may be considerable wasting of the muscles. 
The lead line may be present, a bluish black stip- 
pling along the lower incisors at the gum margin. 
The reader is referred to several comprehensive 
treatises on lead poisoning. These include mono- 
graphs or articles by Aub, Fairhall, Minot, and 
Reznikoff {2568) 1925, Cantarow and Trumper 
{2573) 1944, Hamilton and Hardy {2578) 1949, 
and Johnstone {2581) 1948. The review by Aub 
and coworkers contains an excellent bibliography 
of 500 references. Papers by Brandt and Reichen- 
bach {2571) 1943 and Heyroth {2579) 1948 may 
also be consulted. Fine {2576) 1923-24 has indi- 
cated that metallic lead is less readily phagocytosed 
than is basic lead carbonate. The presence of soluble 
lead impairs the phagocytic properties of the leuko- 
cyte, and in the presence of metallic lead the 
phagocytosis of carbonate is retarded. The rate of 
phagocytosis of metallic lead by leukocytes is of the 
same low order of magnitude as that of quartz. 
These facts suggest to the author that metallic lead, 
like quartz, remains as a foreign body in the lung 
and excites fibrosis. 
Regarding the absorption and excretion of lead 
under normal conditions and in lead poisoning, the 
reader is referred to papers by Cholak and Bambach 
{2574) 1943 and Kehoe, Thamann, and Cholak 
{2584, 2585) 1933. The latter authors point out 
that the normal adult American excretes lead at a 
rate of 0.02 to 0.08 mg. per liter of urine and at a 
rate of 0.03 to 0.1 mg. per gram of ash in the feces. 
The mean daily individual output of lead for vari- 
ous groups of normal persons varies from 0.25 to 
0.38 mg. The lead intake in food of selected normal 
subjects is approximately equivalent to the lead 
content of their feces, and this may be taken as 
evidence, not only of the passage of the great pro- 
portion of the ingested lead through the alimentary 
tract unabsorbed, but also of the predominant 
source of the lead which is absorbed and excreted 
by normal persons. It is calculated from direct 
analytical observations on food and from indirect 
interpretation of the fecal lead content of a large 
group of normal subjects that the daily intake of 
lead in the food is normally of the order of 0.16 to DISEASES AND ACCIDENTS 
0.28 mg. Normal persons whose lead metabolism 
is followed for prolonged periods show no evidence 
of lead accumulation, but appear to have estab- 
lished an equilibrium with their environment, in 
which the excretion of lead keeps pace with the 
absorption. Post-mortem analysis of the tissues of 
normal subjects indicates a total lead content in 
the adult body of 135 mg. Administration to a 
human subject of 1 mg. and 5 mg. of lead chloride 
daily for short periods resulted in the elimination 
of the greater portion of the lead unabsorbed, and 
in the absorption of amounts slightly less than 0.5 
mg. daily for the former dosage and approximately 
1 mg. daily for the latter. These amounts of ab- 
sorbed lead are sufficient to produce a measurable 
increase in the rate of urinary lead excretion during 
a period of active absorption and for a time there- 
after. Persons who have absorbed abnormally large 
amounts of lead excrete lead at a higher than 
normal rate after the cessation of lead exposure. 
The duration of the period of increased lead excre- 
tion depends upon the extent of lead absorption. 
The rate of lead output diminishes rapidly for a 
period of several weeks, after which there is a 
prolonged and gradual diminution in excretory rate 
until the normal level is reached. The relative in- 
tensity of the lead exposure is indicated by the 
initial height of the excretory level, by the sharp- 
ness of the decline in the excretory rate during 
the early weeks of freedom from exposure, and by 
the duration of the period of high excretory rate. 
Persons abnormally exposed to lead show unusually 
large amounts of lead in their circulating blood 
during life, and in their tissues at necropsy for 
variable periods of time after the discontinuance of 
exposure. The total amount of lead in the body 
depends upon the severity of the lead exposure and 
the interval between exposure and death. The de- 
tection of an abnormally high rate of lead excre- 
tion or an unusual amount of lead in the tissues is 
useful in estimating the severity of the lead ex- 
posure. It does not constitute proof of the existence 
of lead intoxication. 
Cholak and Bambach {2574) 1943 have reported 
normal lead concentrations in human subjects of 
0.030 mg. per 100 grams of blood, 0.027 mg. per 
liter of urine, and 0.27 mg. per 24-hour fecal sample. 
Exposure in industry causes a definite increase in 
the mean lead concentration in proportion to the 
severity of exposure. The lead content of either the 
urine or the blood serves as a better criterion of 
lead exposure than the concentration in the feces. 
Analytical data from large representative groups of 
workmen may be set up in the form of histograms 
to determine the character of exposure in a plant. 
Distribution of results and mean values obtained 
over extended periods of time can be used as meas- 
ures of the uniformity and efficacy of means em- 
ployed to control lead exposure. For further reports 
on the subject of absorption and excretion as well as 
differential diagnosis of lead poisoning, papers by 
Aub, Minot, Fairhall, and Reznikoff {2569) 1924 
and Belknap {2570) 1949 may be consulted. 
For case histories of lead poisoning, the reader 
is referred to papers by Cotter (2575) 1946, Gent 
(2577) 1945, d’Onofrio (2587) 1950, and a paper 
in the Journal of Industrial Medicine (2591) 1947. 
Ten cases cited by Cotter (2575) were from a group 
of 30 workers who were demolishing an elevated 
railroad with blowtorches which involved cutting 
through layers of steel and paint. Unless positive 
pressure respirators were worn, the incidence of 
inhaled lead poisoning ran as high as 80 percent. 
Most of the patients had cramps, nausea, consti- 
pation, and abdominal tenderness, and showed a 
lead gumline. Some complained of muscular weak- 
ness. There was an elevation of the reticulocyte 
count in the blood and a lowering of granulocytes 
and hemoglobin. The blood cholesterol, nonprotein 
nitrogen, carbon dioxide content, phosphorus, and 
protein were all within normal limits. The lead con- 
tent of the urine varied from 0 to 0.2 mg. per 100 
cu. cm. A high lead content of the urine is usually 
considered unfavorable, but the author believed that 
in this series it indicated a high rate of elimination 
with a more favorable prognosis. Reference 2591 
reports an unusual case of lead poisoning in a man 
who worked in a shooting gallery for 2 years. Air 
analysis in the shooting gallery showed toxic air 
concentrations of lead dust of 7 to 60 times the 
maximum allowable concentration. The source of 
lead in the air was from bullets hitting the targets. 
As Wilentz {2590) 1949 has stated, treatment 
should be directed towards overcoming the intesti- 
nal colic, correcting the anemia, and restoring the 
patient to his job symptom free with no disability. 
Depending upon the severity of symptoms, hospitali- 
zation may be necessary in the acute stage. It is 
probable that the storage of lead may be minimized 
by keeping the bones filled with calcium by means 
of a high calcium diet. The colic may be relieved 
by antispasmodics, such as atropine, or by intra- 
venous administration of calcium gluconate. 
Wilentz does not recommend the use of narcotics. 
Cases should be followed with complete blood cell 
count and stippling determination, also estimation 
of lead in the urine and a complete urinalysis. 
Wilentz does not recommend measures to hasten 
the excretion of lead from the body since this 
involves certain dangers, prolongs hospitalization NOXIOUS AGENTS—MERCURY 
2568-2591 
and disability, and because the results are considered 
uncertain. Calcium immobilization therapy is ad- 
vocated because of its safety and simplicity and 
because of favorable results. Cotter (2575) also 
speaks favorably of the antispasmodic action of 
intravenous calcium gluconate. However, he points 
out that calcium gluconate is not a curative agent 
and that there is an attendant danger of renal 
calculi. 
The use of sodium citrate has been recommended 
as a prophylactic or therapeutic procedure. Shiels, 
Thomas, and Palmer {2589) 1951 have recom- 
mended the administration of sodium citrate in 
oral doses of 4 or 5 grams in water once a day as a 
preventive procedure in employees exposed to lead. 
Evidence from a study of stippled cell counts and 
lymphocytes before and after commencing this 
prophylaxis suggests that sodium citrate is useful 
in preventing ill-effects of increased lead absorp- 
tion. The authors are careful to point out that 
sodium citrate prophylaxis is not a substitute for 
improved working conditions, but is a useful ad- 
junct. Kety and Letonoff {2586) 1943 have re- 
ported the results of sodium citrate therapy in 15 
cases of lead poisoning in adults. Sodium citrate 
administration resulted in a significant fall in the 
blood lead concentration, and an early and per- 
sistent amelioration of the symptoms of lead poison- 
ing. Intravenous administration of sodium citrate 
resulted in the immediate relief of severe colic in 
2 of 4 patients presenting this symptom. There were 
no ill-effects of sodium citrate nor any recurrence 
of symptoms following therapy. For a further dis- 
cussion of the treatment of lead poisoning, the 
reader is referred to an article by Osol, Farrar, 
Leuallen, Verwey, Youngken, Detweiler, and Wood 
{2588) 1947. 
2568. Aub, J. C., L. T. Fairhall, A. S. Minot, and P. 
Reznikoff. Lead poisonin. Medicine, 1925, 4: 1-250. 
2569. Aub, J. C., A. S. Minot, L. T. Fairhall, and P. 
Reznikoff. Recent investigations of absorption and excre- 
tion of lead in the organism. /. Amer. med. Ass., 1924, 83: 
588-592. [P] 
2570. Belknap, E. L, Differential diagnosis of lead pois- 
oning. J. Amer. med. Ass., 1949, 139: 818-823. 
2571. Brandt, A. D., and G. S. Reichenbach. Lead ex- 
posures at the government printing office. /. industr. Hyg., 
1943, 25: 445-450. 
2572. Brown, E. W. Health hazards from lead paint and 
zinc chromate paint. Incidence in modern construction, 
maintenance and scrapping of ships. Occup. Med., 1948, 
5: 739-758. Abstr. World Med., 1949, 6: 259. 
2573. Cantarow, A. and M. Trumper. Lead poisoning. 
Baltimore, The Williams & Wilkins Co., 1944, 264 pp. [R] 
2574. Cholak, J, and K. Bambach. Measurement of 
industrial lead exposure by analyses of blood and excreta of 
workmen. /. industr. Hyg., 1943, 25: 47-54. 
2575. Cotter, L. H. Lead intoxication by inhalation. /. 
industr. Hyg., 1946, 28: 44-46. [CH] 
2576. Fine, J, The phagocytosis of lead compounds and 
their influence on the activity of the leukocyte. /. industr. 
Hyg., 1923/1924, 5: 138-144. 
2577. Gent, J, C. An unusual case of lead poisoning. 
/. R. nav. med. Serv., 1945, 31: 117—118. 
2578. Hamilton, A., and H. L. Hardy. Lead. pp. 49- 
103 in: Industrial toxicology. Second edition. New York, 
Paul B. Hoeber, Inc., 1949, 574 pp. [R] 
2579. Heyroth, F. F. The metals (except lead). pp. 675- 
738 in: Industrial hygiene and toxicology. Edited by 
Frank A. Patty. New York, Interscience Publishers, Inc., 
1948, 1138 pp. [R] 
2580. Jacobs M. B. Lead, mercury, and arsenic, pp. 191— 
219 in: The analytical chemistry of industrial poisons, 
hazards, and solvents. Second edition. New York, Intersci- 
ence Publishers, Inc., 1949, 788 pp. 
2581. Johnstone, R. T. Lead. pp. 234-264 in; Occupa- 
tional medicine and industrial hygiene. St. Louis, The 
C. V. Mosby Co., 1948,604 pp. [CH] 
2582. Kehoe, R. A. Exposure to lead. Occup. Med., 
1947, 3: 156-171. [P] 
2583. Kehoe, R. A. Industrial lead poisoning, pp. 643— 
673 in: Industrial hygiene and toxicology. Edited by Frank 
A. Patty. New York, Interscience Publishers, Inc., 1948, 
1138 pp. [R] 
2584. Kehoe, R. A., F. Thamann, and J. Cholak. On the 
normal absorption and excretion of lead. I. Lead absorp- 
tion and excretion in primitive life. /. industr. Hyg., 1933, 
15: 257-288.[P] 
2585. Kehoe, R. A., F. Thamann, and J. Cholak. Lead 
absorption and excretion in relation to the diagnosis of 
lead poisoning. /. industr. Hyg., 1933, 15: 320—339. 
2586. Kety, S. S. and T. V. Letonoff. The treatment of 
lead poisoning by sodium citrate. Amer. J. med. Sci., 1943, 
205: 406-414. [CH] 
2587. Onofrio, V. d’. Lead poisoning in the pottery in- 
dustry. Rass. Med. Lav. industr., 1949, 18: 155-171. 
Abstr. World Med., 1950,7: 239-240. 
2588. Osol, A., G. E. Farrar, E. E. Lenallen, W. F. Ver- 
wey, H. W. Youngken, D. K. Detweiler, and H. C. Wood, 
Jr. Lead. pp. 623-625 in: The dispensatory of the United 
States of America. 24th edition, 1947. Philadelphia, J. B. 
Lippincott Co., 1928 pp. 
2589. Shiels, D. 0., W. C. Thomas, and G. R. Palmer. 
The effects of sodium citrate in lead poisoning and lead 
absorption. Med. J. Aust., 1951, 2: 922-928. [P] 
2590. Wilentz, W. C. Treatment of lead intoxication. 
J. Amer. med. Ass., 1949, 139: 823-825. 
2591. Anon. Shooting gallery lead poisoning. Industr. 
Med., 1947,16: 421. [CH] 
7. MERCURY 
Mercury poisoning is a potential hazard in any 
situation in which mercury vapor may be released 
into the air and taken in via the lungs. Under some 
circumstances mercury may also be ingested via 
contaminated hands. Beauchamp and Tebbens 
(2592) 1951 and Shepherd, Schuhmann, Flinn, 
Hough, and Neal (2606) 1941 have reported on the 
hazards of mercury vapor in university and other 
scientific laboratories. As Hamilton and Hardy 
{2598) 1949 have pointed out, mercury vaporizes 
even at the temperature at which water freezes. DISEASES AND ACCIDENTS 
Mercury may enter the body via the lungs, the 
alimentary tract, and the skin. Industrial mer- 
curialism is characterized by three features: in- 
flammation of the mouth, muscular tremors, and 
psychic irritability. According to Osol and coauthors 
(2603) 1947, the first signs of mild mercury poison- 
ing are metallic taste in the mouth, slight soreness 
of the gums, and an unpleasant sensation in the 
sockets of the teeth when the jaws are firmly closed. 
Later the gums become swollen and a black line 
may be seen along the gingival margin. There is an 
increase in the quantity and viscidity of the saliva. 
The gums, tongue, throat, and face may all become 
swollen. The acute form of industrial mercurialism 
is largely a disease of the oral mucous membranes. 
The chronic intoxication is a disease primarily of 
the nervous system, and occurs from inhalation of 
metallic mercury vapor. Hazardous concentrations 
can result from seemingly negligible spillage of 
mercury, and probably as little as 1 part in 50 
million parts of air is toxic in long air exposures. 
The acute effects are characterized by spongy 
gingivitis, anorexia, weakness, and dyspepsia. Fol- 
lowing chronic exposure, there may be weight loss, 
pallor, and nervousness, plus a tremor which in- 
creases on the use of the limbs. There may be 
muscular pain with tension and cramps manifested 
at night. Dermographia, excessive perspiration, and 
blushing, together with exaggerated tendon reflexes, 
have also been observed. The nervous lesion is 
thought to be located in the basal ganglia, but the 
cerebral cortex may be the site of involvement. 
Advanced neurological defects due to mercurialism 
are extremely refractory to treatment. For further 
general studies of mercury poisoning, the reader is 
referred to articles by Fourcade (2596) 1950, 
Howard (2600) 1951, and Johnstone (2601) 1948. 
Reports by Fourcade (2596) and Hamilton and 
Hardy (2598) contain discussions of severe damage 
to the kidneys. 
Nine cases of mercury poisoning from the use 
of antifouling plastic paint have been reported by 
Goldwater and Jeffers (2597) 1942. Plastic paint 
heated to a temperature of 350° F. prior to appli- 
cation was sprayed on ships at a Navy yard. Many 
men worked as long as 13 hours a day for several 
days at this operation. Toxic fumes containing 
mercury vapor were liberated during the heating 
and the spraying process. Men wearing gold rings 
observed a silvery coating of mercury amalgam 
on the rings. Personnel had been given charcoal 
respirators to wear, but were lax in the use of these 
protective devices. Among the 17 painters engaged 
in the operation, 9 developed illness diagnosed as 
mercury poisoning. Symptoms consisted of consti- 
pation, anorexia, nausea, vomiting, hoarseness, sore 
throat, tightness of the chest, sore gums, bad taste 
in the mouth, fatigue, nervousness, headache, dizzi- 
ness, and bloody urine. There were tremors of the 
hands in five cases. 
Turner (2608) 1924 reported that daily exposure 
to an atmosphere containing as small a quantity 
as 0.02 mg. of mercury per cubic foot of air results 
in signs and symptoms of poisoning. Clinical his- 
tories indicated that daily exposure must continue 
for 2 or 3 months, or more, before symptoms ap- 
pear. It was estimated that in exposure to these 
quantities of mercury for 3 to 5 hours daily, there 
was a total daily absorption of mercury ranging 
from 0.771 to 1.285 mg., according to the duration 
of exposure. The author called attention to copper- 
colored discoloration of the mucous membrane of 
the pharynx, the pillars of the fauces, and the gums. 
This discoloration was constant in all cases, and 
the gums were swollen with enlargement of the 
capillaries. Superficial erosions appeared upon the 
mucous membrane of the gums and upon the buccal 
mucous membrane in the vicinity of the upper 
molar teeth. Perialveolar abscesses frequently oc- 
curred and caused considerable discomfort. Occa- 
sionally there was an appreciable increase in the 
flow of saliva. Urinalysis and differential blood 
counts showed the urine and the blood to be un- 
affected by the mercury absorbed. There was sub- 
jective tenderness of the gums and hypersensitive- 
ness of the teeth, particularly those containing amal- 
gam fillings. Intestinal peristalsis was slightly in- 
creased, occasionally developing into mild attacks 
of diarrhea. Shifting neuralgic pains were occasion- 
ally felt in various joints and in the chest. 
Chronic mercurialism is a potential hazard in the 
hatters’ fur-cutting industry and for reports of cases 
of mercury poisoning in this industry, papers by 
Neal, Jones, Bloomfield, and Dallavalle (2602) 
1937 and Vigliani and Baldi (2609) 1948 may be 
consulted. The authors of the former paper stress the 
neurological and psychic disturbances. There may 
be tremor varying in degree from a slight tremor of 
the hand, eyelids, or tongue to marked, generalized 
tremor. Psychic imbalance may be present as indi- 
cated by irascible temper, discouragement without 
cause, feeling of depression or despondency, exces- 
sive embarrassment in the presence of strangers, 
timidity, desire for solitude, anxiety, excitability, 
inability to take orders, or a strong sense of self- 
consciousness. Christensen, Krogh, and Nielsen 
(2595) 1937 reported cases of acute mercury pois- 
oning in a respiration chamber in personnel under- 
going carbon dioxide experiments over a prolonged 
period. These subjects became ill with bronchial NOXIOUS AGENTS—STIBINE 
2592-2609 
irritation, violent coughing, and severe headache. 
After 3 days there was inflammation of the mouth. 
The cases were due apparently to spillage of metal- 
lic mercury. Gases of chronic mercury poisoning in 
a thermometer workshop have been described by 
Buckell, Hunter, Milton, and Perry {2594) 1946, 
and the reader is referred to a report on two deaths 
from exposure to the fumes of a diethyl mercury 
published in 1943 by Hill {2599). 
Prophylaxis includes all of those procedures de- 
signed to prevent contamination of the environment 
with mercury. The treatment of contaminated sur- 
faces such as floors is important. Renes and Seifert 
{2604) 1946 reported that the treatment of con- 
taminated surfaces with polysulfides was not found 
to be an adequate control measure. Thorough wash- 
ing of the contaminated surfaces followed by wax- 
ing was the most effective procedure for reducing 
the hazard of exposure. A brief report on prophy- 
laxis by Sappington {2605) 1946 may be consulted. 
The reader may also consult papers by Brigatti and 
Baldi {2593) 1947 and Slutzky {2607) 1951. 
2592. Beauchamp, I. L. and B. D. Tebbens. Mercury 
vapor hazards in the university laboratories. Amer. industr. 
Hyg. Ass. Quart., 1951, 72: 171—174. [P] 
2593. Brigatti, L. and G. Baldi. La crasi ematica nel 
mercurialismo cronico. Med. d. Lavoro, 1947, 38: 192- 
198. [CH] 
2594. Buckell, M., D. Hunter, R. Milton, and K. M. A. 
Perry. Chronic mercury poisoning. Brit. J. industr. Med., 
1946, 3: 55-63. 
2595. Christensen, H., M. Krogh, and M. Nielsen. 
Acute mercury poisoning in a respiration chamber. Nature, 
Land., 1937, 139: 626-627. [CH] 
2596. Fourcade, J. Intoxications par le mercure et ses 
composes, pp. 117-126 in: Medicine du travail. Edited by 
C. Simonin. Paris, Librairie Maloine, 1950, 913 pp. [D] 
2597. Goldwater, L. J. and C. P. Jeffers. Mercury 
poisoning from the use of antifouling plastic paint. J. 
industr. Hyg., 1942, 24: 21-23. [CH] 
2598. Hamilton, A. and H. L. Hardy. Mercury poison- 
ing. pp. 115-126 in: Industrial toxicology. Second edition. 
New York, Paul B. Hoeber, Inc., 1949, 574 pp. 
2599. Hill, W. H. A report on two deaths from ex- 
posure to the fumes of a di-ethyl mercury. Canad. J. publ. 
Hlth, 1943, 34: 158-160. [CH] 
2600. Howard, T, Mercury-poisoning, pp. 75-81 in: 
Practice of medicine. Volume 8. Edited by Frederick Tice. 
Hagerstown, W. F. Prior Co., Inc., 1951, 627 pp. 
2601. Johnstone, R. T. Mercury, chromium, copper, 
and aluminum, pp. 310-316 in: Occupational medicine 
and industrial hygiene. St. Louis, The C. V. Mosby Co., 
1948, 604 pp. [CH] 
2602. Neal, P. A., R. R. Jones, J. J. Bloomfield, J. M. 
Dallavalle. A study of chronic mercurialism in the hatters’ 
fur-cutting industry. Publ. Hlth. Bull., Wash., 1937, 234: 
70. 
2603. Osol, A., G. E. Farrar, E. E. Leuallen, W. F. 
Verwey, H. W. Youngken, D. K. Detweiler, and H, C. 
Wood, Jr. Mercury, pp. 690-692 in: The dispensatory 
of the United States of America. 24th edition, 1947. 
Philadelphia, J. B. Lippincott Co., 1928 pp. 
2604. Renes, L. E, and H. E, Seifert. Mercury vapor 
hazards in certain chemical laboratories. Amer. industr. 
Hyg. Ass. Quart., 1946, 7: 21-25. [P] 
2605. Sappington, C. 0. Mercury exposures: evaluation 
and prophylaxis. Amer. industr. Hyg. Ass. Quart., 1946, 
7: 26-28. 
2606. Shepherd, M., S. Schuhmann, R. H. Elinn, J. W. 
Hough, and P. A. Heal. Hazard of mercury vapor in 
scientific laboratories. J. Res. nat. Bur. Stands., 1941, 
26: 357-376. 
2607. Slutzky, Z. Variaciones hematologicas en las 
intoxicaciones mercuriales agudas. Prensa med. argent., 
1950, 37: 380—382. Excerpta Medica. Section II. (Physi- 
ology, Biochemistry, and Pharmacology), 1951, 4: 1493. 
2608. Turner, J. A. Mercurial poisoning. A report on 
poisoning from small quantities of mercurial vapor. Pub. 
Hlth. Rep., Wash., 1924,39: 329-341. 
2609. Vigliani, E. C. and G. Baldi. An unusual out- 
break of mercurialism in the felt-hat industry. Proc. ninth 
intern. Congr. industr. Med., London, 1948, 574-580. 
(French summary.) 
8. STIBINE 
Antimony hydride (SbH3), known as anti- 
moniuretted hydrogen and later as stibine, was dis- 
covered by Thomson working in England and 
independently by Pfaff in Germany in 1837. Both 
of these investigators were studying the Marsh test 
for arsenic. 
Since battery grids often contain from 5 to 10 
percent antimony, the production of stibine in per- 
ceptible quantities during overcharging of batteries 
is a potential hazard in submarines. That stibine 
is present in the air of submarines during battery- 
charging operations has been demonstrated by 
Webster, Liljegren, Fairhall, and Neal {2614) 
1943. The stibine content of battery gas was in- 
vestigated by these authors on five submarines under 
various operating conditions. Two regular charges, 
2 equalizing charges, 1 equalizing charge followed 
by a rapid 6-hour discharge, and a normal dis- 
charge were studied. Chemical and spectrographic 
tests were carried out to establish the presence of 
antimony and/or arsenic compounds in battery 
gases. No stibine was detected during either the 
normal or rapid discharge of the batteries. How- 
ever, stibine was regularly present during the latter 
part of the charging operations after gassing had 
begun. It was present when the hydrogen content 
amounted to 0.6 percent or more. When the battery 
gas was exhausted outboard via the main induction 
valve or via the vents in the conning tower, hardly 
a trace of stibine could be detected inside the boat. 
Under these circumstances, the stibine content was 
not more than 0.2 p. p. m. When the battery gas 
was discharged inboard, stibine could be quickly 
detected in various parts of the boat, A test carried DISEASES AND ACCIDENTS 
out on the U. S. S. Paddle showed an average of 
0.6 p. p. m. during charging. From measurements 
made under usual dockside operating conditions, it 
is concluded that the concentration of stibine in the 
interior of a submarine is not likely to rise above a 
few tenths of a part per million unless the gas is 
exhausted inboard. 
A major report on the toxicology of stibine ap- 
peared in 1951 under the authorship of Webster, 
Liljegren, Zimmer, and Dunn {2617). These studies 
were carried out on 775 animals of 9 species com- 
prising mice, rats, guinea pigs, rabbits, cats, dogs, 
monkeys, frogs, and chicks. The animals received 
one or more exposures to stibine-air mixtures of 
known concentrations in order to study both the 
acute and chronic toxic effects. Concentrations of 
stibine from 9 p.p.m. to about 700 p.p.m. with 
durations of exposure varying between 4 minutes 
and one-half hour for a single exposure were used. 
The usual exposure period was 1 hour. These studies 
indicate that stibine is a highly toxic gas capable of 
inducing profound changes in the several experi- 
mental animals investigated. There is a wide species 
variation in susceptibility, dogs being most easily 
affected and the frogs the least. Stibine appears to 
act mainly as an irritant affecting primarily the 
deeper structures of the lung and with increasing 
concentrations and length of exposure producing 
pulmonary congestion followed by edema and even 
hemorrhages. With the lower concentrations, there 
is sometimes irritation of the nose and mouth, and 
watering of the eyes. There may be symptoms of 
shock such as hemoconcentration, asthenia, shallow 
rapid breathing, restlessness, reduced body tempera- 
ture, and reduced peripherial circulation. Death 
may occur within 48 hours, and in most of these 
cases, fatality is due to involvement of the lungs and 
respiratory failure. In animals surviving for 48 
hours, there may be secondary or delayed effects 
of stibine poisoning which may be fatal. In these 
delayed deaths the lethal action of stibine or its 
decomposition products is on the blood. The hemo- 
lytic action appears to vary not only with the con- 
centration of stibine but also with the type of animal 
used. The red-cell count frequently increases im- 
mediately after exposure, suggesting hemoconcen- 
tration. The white-cell count usually drops immedi- 
ately after exposure, and this is frequently followed 
the next day by leukocytosis. The red-cell count may 
fall for several days before the minimal value is 
reached. Providing sufficiently high concentrations 
of stibine are used, severe anemia may supervene as 
a result of a single exposure. In fatal cases, other 
complications such as severe liver damage are 
usually present. There may be hemoglobinuria; 
albuminuria is of frequent occurrence following the 
disappearance of hemoglobinuria. Sometimes bili- 
rubin can be detected in the urine of animals, and 
urobilinogin regularly appears when severe liver 
damage occurs. The authors state that bile forma- 
tion appears to be stimulated by the increased de- 
struction of erythrocytes. However, bilirubin is 
hardly ever found in the plasma, since the animals 
are apparently able to excrete bilirubin rapidly via 
the liver. Consequently, frank jaundice was not 
seen in any of the species suffering from stibine 
poisoning with exception of the rabbits. In the dogs 
and the cats, there was vomiting, and in the rodents, 
diarrhea. At moderate to high concentrations of sti- 
bine, anoxia was commonly seen in all of the ani- 
mals investigated, particularly the cats. There were 
other symptoms such as convulsions, exophthalmos, 
weakness of the hind quarters, and cyanosis. 
With repeated exposures in the animal experi- 
ments, the authors found a successively lessened 
susceptibility to the action of stibine, and they at- 
tributed this to changes in the lung structure affect- 
ing the breathing pattern or to diminished breath- 
ing on successive exposures. In either case, less 
stibine would be inhaled as the exposures were 
repeated, and less marked effects would be ex- 
pected. This apparent tolerance is lost on waiting 
several months between exposures and on raising 
the exposure level. The outstanding pathological 
findings revealed that autopsy include pulmonary 
involvement, congestion of the kidneys and spleen, 
fatty changes in the liver, and sometimes enlarge- 
ment of the right heart. There are species differ- 
ences in the toxicity of stibine which depend to 
some extent on body weight and activity. The 
smaller and more active animals appear to be more 
susceptible to the action of stibine. On the basis of 
these highly toxic effects of stibine on laboratory 
animals, the authors consider that stibine would 
probably be very toxic to man. Comparison of its 
toxicity with that of arsine using experimental 
animals suggested to the authors that the order of 
toxicity of arsine and stibine would be approxi- 
mately the same for man. 
Earlier reports by Webster, Liljegren, and Zim- 
mer (2615 and 2616) 1944 and 1945 may be con- 
sulted. These reports include a description of meth- 
ods of generating stibine. An outline of the rhoda- 
mine B method for the analysis of stibine content of 
air in chambers is given. For further studies on the 
methods of production and determination of small 
quantities of stibine, the reader may wish to consult 
papers by Rabideau and Thomas {2611) 1943 
and Webster and Fairhall {2613) 1943. NOXIOUS AGENTS—TOBACCO SMOKE 
2610-2617 
Using radioactive antimony administered as 
stibine gas, Smith, Steele, Eakin, and Gowie 
(2612) 1948 measured the distribution of this sub- 
stance in blood and tissues at successive time inter- 
vals following administration. The concentration 
of antimony in the blood stream exhibited a 
smoothly decaying curve, decreasing more rapidly 
in the guinea pig than in the chick. The red cells 
contained initially a much higher concentration of 
antimony than plasma, although the difference be- 
came reduced in time. The concentration curves 
in the lung, brain, muscles, and fat, were generally 
similar to those of blood. The curves for the liver 
and to a lesser extent the spleen, passed through a 
maximum about one hour following exposure. 
Approximately four hours after exposure, tissue 
antimony levels became constant; those for the 
liver, spleen, and kidneys were greater than for 
whole blood. All other tissues showed concentra- 
tions of antimony less than for blood, but were equal 
to or greater than the concentrations in plasma. 
The authors adduced evidence to show that the 
rate of elimination from the body is higher for the 
guinea pig than for the chick. 
A chapter on stibine by Jacobs (2610) 1949 may 
be consulted. 
2610. Jacobs, M. B. Stibine. pp. 259-261 in: The 
analytical chemistry of industrial poisons, hazards, and 
solvents. Second edition. New York, Interscience Publish- 
ers, Inc., 1949, 788 pp. 
2611. Rabideau, S. W. and E. S. Thomas. A method 
of production and determination of small quantities of 
stibine. U. S. Navy. NRL. No. P—2130, Kept. no. 3, 3 
August 1943, 6 pp. 
2612. Smith, R. E., J. M. Steele, R. E. Eakin, and D. B. 
Cowie. The tissue distribution of radioantimony inhaled 
as a stibine. /. Lab. din. Med., 1948, 33: 635-643. [P] 
2613. Webster, S. H. and L. T. Eairhall. Progress re- 
port on the study of the toxicity of stibine. U. S. National 
Institutes of Health, Bethesda, Md. (Coordinate Navy 
Project X-I66, Kept. no. 2), 26 July 1943, 3 pp. 
2614. Webster, S, H,, E. J. Liljegren, L, T. Eairhall, 
and P. A. Neal. Report on a field trip to the U. S. sub- 
marine base at New London, Conn., to investigate the 
stibine content of storage battery gases. U. S. National 
Institutes of Health, Bethesda, Md. (Coordinate Navy 
Project X—166, Kept. no. I), 9 June 1943, 13 pp. 
2615. Webster, S. H., E. J. Liljegren, and D. J, Zimmer. 
An interim report on the stibine study. U. S. National 
Institutes of Health, Bethesda, Md. (Coordinate Navy 
Project X—166, Kept. no. 4), 15 June 1944, 37 pp. 
2616. Webster, S. H., E. J. Liljegren, and D. J. Zimmer. 
An interim report on the stibine study. U. S. National 
Institutes of Health, Bethesda, Md. (Coordinate Navy 
Project X-166, Kept. no. 5), 23 May 1945, 30 pp. 
2617. Webster, S. H., E. J. Liljegren, D. J. Zimmer, 
and R. C. Dunn. The toxicology of stibine. National in- 
stitute of arthritis and metabolic diseases, U. S. National 
Institutes of Health, Public Health Service, Bethesda, Md., 
4 October 1951, 193 pp. 
9. TOBACCO SMOKE 
Smoking has become a virtually universal habit, 
and the use of tobacco has certain definite morale 
values. Conditions of submarine operation, how- 
ever, impose certain definite restrictions upon smok- 
ing. The study of the physiological and pathological 
effects of tobacco constitutes an important field of 
investigation which cannot be discussed in detail 
here. From the large body of literature on this sub- 
ject, only a few representative reports are discussed 
and considered. The major effects of tobacco are 
due to its nicotine content. However, tobacco smoke 
also contains a definite amount of carbon monoxide 
and it appears also that the resins present in tobacco 
smoke may exert a significant action, particularly 
when taken into the lungs over a prolonged period. 
The action of tobacco smoke may be adverse when 
added to unfavorable environmental conditions such 
as low oxygen and high carbon dioxide content of 
the air. Smoking may also be inadvisable under con- 
ditions of stress and intense bodily activity. More- 
over, there are certain pathological conditions in 
which smoking is contraindicated. For a general 
consideration of tobacco, a chapter by Osol and col- 
leagues {2628) 1947 may be consulted. Attention is 
drawn to the action of nicotine in producing periph- 
eral vasoconstriction with a rise in blood pressure. 
There is also an inhibition of hunger contractions 
resulting in a diminution of appetite. Salivary and 
gastric secretion may be increased. There is also an 
increased output of epinephrine with an increase 
in the blood-sugar level. Extreme views on the bi- 
ological hazards of tobacco smoking are expressed by 
Mills (2626) 1950 who cites the opinion that smok- 
ing predisposes to pulmonary tuberculosis. He also 
claims an abnormally high incidence of cigar and 
pipe smoking in male victims of malignant disease 
of the upper and lower respiratory passages. Post- 
operative pneumonia is stated to be more frequent 
among smokers than nonsmokers, and the author 
quotes the view that patients with peptic ulcer 
should abstain from smoking. He also states that 
smoking is a handicap to nursing mothers, and 
voices the opinion that smoking mothers are more 
likely to bear malformed infants than those who do 
not smoke. There is no confirmation in the litera- 
ture for this view regarding malformation. Mills 
states that only tobacco smokers are afflicted with 
thromboangitis obliterans, and this is virtually true. 
In a report on some effects on the circulation of 
smoking cigarettes with varying nicotine content, 
Mather, Patterson, and Levy (2624) 1949 have 
pointed out that the degree of reaction varies di- 
rectly with the nicotine content of the smoke. There 
is a definite individual difference in the response, 2618-2624 
DISEASES AND ACCIDENTS 
and the variability in response in different persons 
is stated to depend to a greater extent upon indi- 
vidual susceptibility than upon the presence of car- 
diac disease. Acceleration of the heart is the most 
sensitive index of the nicotine effect, and a measure 
of individual differences in susceptibility is possible 
on a single reading. The authors suggest that an in- 
crease in the heart rate of 25 beats per minute after 
smoking one cigarette with inhalation may be re- 
garded as evidence of hypersensitivity to the imme- 
diate effects of nicotine. The authors have found 
that smoking cigarettes with a nicotine content as 
low as 0.23 percent results in a significant heart-rate 
increase. In 1935, Lampson (2623) carried out a 
quantitative study of peripheral vasoconstriction 
induced by smoking. He determined peripheral 
blood flow in human subjects by recording changes 
in hand volume. Blood pressure and pulse were also 
recorded. Normal young men and patients from the 
peripheral circulatory clinic of the Massachusetts 
General Hospital, Boston, were the subjects. With 
one exception, smoking produced marked reduction 
of peripheral circulation in both the normal indi- 
viduals and patients with thromboangitis obliterans. 
Smoking and inhaling cigarette smoke caused a 
sudden marked peripheral vasoconstriction, lasting 
about 60 minutes. When inhaling was avoided there 
was vasoconstriction lasting, however, only 15 min- 
utes. So-called “denicotinized” cigarettes were 
found to produce less effect than ordinary cigarettes. 
Cigar and pipe smoking also induced vasoconstric- 
tion. Patients with thromboangitis obliterans re- 
sponded in the same manner as normal subjects. 
The author recommended that smoking was contra- 
indicated in patients with peripheral vascular 
disease. 
Evans and Stewart (2619) 1943 also found that 
normal male subjects experienced a decrease in 
peripheral blood flow as a result of smoking, regard- 
less of the type of cigarette smoked. After cessation 
of smoking, the peripheral blood flow continued to 
decrease in some cases, but began to return to nor- 
mal levels in other cases. In all subjects a return 
toward normal had begun by the end of 30 minutes 
after cessation of smoking. Evans and Stewart found 
that the increase in blood pressure and pulse rate 
was essentially of the same magnitude and duration 
from smoking every type of cigarette. The average 
skin temperature decreased in all but five experi- 
ments. Herrell and Cusick (2621) 1938 emphasized 
the significance of the vasospastic response following 
inhalation of tobacco smoke among those who have 
a tendency towards hypertension, and stated that 
such a patient has everything to gain and nothing 
to lose by discontinuing the use of tobacco. These 
authors have demonstrated photographically the 
vasospactic changes in the retina. Mulinos and 
Shulman (2627) 1940 concluded that deep breath- 
ing alone can account for the greater part of the 
decreased blood flow rate, loss of hand volume, and 
drop of skin temperature resulting from the inhala- 
tion of cigarette smoke. The subjects who did not 
inhale cigarette smoke showed a greater vascular 
response of the hand from 10 deep breaths than 
from puffing the cigarette, and a lesser response 
than those who inhaled the cigarette smoke. Inhal- 
ing smoke from so-called denicotinized cigarettes 
resulted in as great a vasoconstriction as inhaling 
smoke from a standard-brand cigarette. Occasion- 
ally the vasoconstrictor effect from the “denicotin- 
ized” cigarettes was greater. These authors also 
draw attention to significant individual differences 
in susceptibility to cigarette smoke. For further re- 
ports on the effect of smoking on circulatory and 
respiratory phenomena, papers by Jourdan and 
Collet (2622) 1951 and Med and Sramek (2625) 
1950 should be consulted. 
The effect of smoking in diminishing hunger has 
been explained by Haggard and Greenberg (2620) 
1934 as an action of nicotine on the adrenal glands 
with a production of hyperglycemia. These authors’ 
study was carried out on human subjects and should 
be consulted. For an experimental study of the 
effect of nicotine on maze learning ability of albino 
rats, the reader is referred to a report by Essenberg 
(2618) 1948. 
2618. Essenberg, J. M. The effect of nicotine on maze 
learning ability of albino rats. Fed. Proc. Amer. Soc., exp. 
Biol., 1948, 7: 31-32. 
2619. Evans, W. E. and H. J. Stewart. The effect of 
smoking cigarettes on the peripheral blood flow. Amer. 
Heart J., 1943, 26: 78-89. [P] 
2620. Haggard, H. W. and L. A. Greenberg. The effects 
of cigarette smoking upon the blood sugar. Science, 1934, 
79: 165-166. 
2621. Herrell, W. E. and P. L. Cusick. Vascular and 
retinal abnormalities following inhalation of tobacco 
smoke: preliminary report. Proc. Mayo Clin., 1938, 13: 
273-279. [CH] 
2622. Jourdan, F. and A. Collet. Effects compar6s de 
1’inhalation de fumee de tabac par les voies respiratoires 
superieures et par les poumons chez le chien. C. R. Soc. 
Biol., Paris, 1950, 144: 861-863. Excerpta Medica. Sec- 
tion II. (Physiology, Biochemistry, and Pharmacology), 
1951, 4: 1359. 
2623. Lampson, R. S. A quantitative study of the vaso- 
constriction induced by smoking. /. Amer. med. Ass., 1935, 
104; 1963-1966. 
2624. Mather, J. A. L., M. C. Patterson, and R. L. 
Levy. Some effects on the circulation of smoking cigarettes 
with varying nicotine content. Amer. Heart J., 1949, 37: 
612-619. [P] NOXIOUS AGENTS—BENZENE 
2625-2640 
2625. Mecl, A. and J. Sramek. tJCinek nikotinu na 
pracovni obehu krevniho a dychani. [The effect of 
cigarette smoking on the circulation and respiration at 
work.] Arch bohem. med., 1949, 51: 377-410. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and Phar- 
macology), 1950, 3: 1443. 
2626. Mills, C. A. Tobacco smoking: some hints of its 
biologic hazards. Ohio St. med. J., 1950, 46: 1165-1170. 
2627. Mulinos, M. G, and I. Shulman. The effects of 
cigarette smoking and deep breathing on the peripheral 
vascular system. Amer. J. med. Sci., 1940, 199: 708-719. 
[P] 
2628. Osol, A., G. E. Farrar, E. E. Leuallen, W. F. 
Verwey, H. W. Youngken, D. K. Detweiler, and H. C. 
Wood, Jr, Tobacco, pp. 1631-1633 in: The dispensatory 
of the United States of America. 24th edition, Philadelphia, 
J. B. Lippincott Co., 1947, 1928 pp. 
10. 0B.GANIC SOLVENTS 
(a) Benzene 
Benzene is one of the best organic solvents known, 
and is widely used for the purpose of dissolving 
grease from small parts and for other extraction 
purposes. Therefore, benzene may be present on 
the submarine and does constitute a potential health 
hazard. The acute symptoms from inhaling a high 
concentration of benzene may begin with a sense 
of exhilaration followed by drowsiness, fatigue, diz- 
ziness, nausea, and headache. If exposure is pro- 
longed or if higher concentrations are inhaled, 
there may be tonic-clonic spasms succeeded by 
paralysis and loss of consciousness. The respiration 
at first becomes rapid but soon slows, and there 
may be circulatory collapse. The victim of severe 
exposure may succumb quickly from respiratory 
paralysis. The chronic inhalation of even small 
amounts of benzene may be potentially dangerous. 
The classical picture of chronic benzene poisoning 
is a profound anemia, loss of clotting capacity with 
resultant hemorrhage and loss of white blood cells 
and substances concerned with the defense of the 
organism against infection. There may also be a 
regenerative response to the destructive effect of 
benzene, and a normal red and white blood cell 
count may indicate only a compensatory action 
which veils the chronic destruction. In workers 
suffering from chronic benzene poisoning, the 
harmful effects can occur in advance of detectable 
blood changes, and may even continue to develop 
after removal from exposure. In persons poisoned by 
benzene, the bone marrow may be normal, aplastic, 
or hyperplastic. The maximum allowable concen- 
tration of benzene in the atmosphere has been gen- 
erally accepted at 100 p.p.m. However, Hardy and 
Elkins {2630) 1948 have stated that 75 p.p.m. of 
benzene is too high, and that the maximum per- 
missible concentration should be reduced to 35 
p.p.m. They recommended that workers exposed to 
benzene should have routine complete blood studies 
done and that there should be a routine preemploy- 
ment medical evaluation including history of re- 
peated infections, chronic blood loss, and ingestion 
of drugs known to depress bone-marrow activity. 
The hematological base line should be established 
by laboratory study and a follow up blood count 
should be done at intervals, depending upon the 
circumstances of benzene exposure. For further 
reports on benzene poisoning, papers by Foulger 
{2629) 1949 and Hutchings, Drescher, McGovern, 
and Coombs {2631) 1947 may be consulted. 
2629. Foulger, J. H, Physiologic effects of industrial 
solvents. /. Amer. med. Ass., 1949, 139: 826—829. 
2630. Hardy, H. L. and H. B. Elkins. Medical aspects 
of maximum allowable concentrations: benzene. /. in- 
dustr. Hyg., 1948, 30: 196-200. 
2631. Hutchings, M., S. Drescher, E. B. McGovern, and 
F. A. Coombs. Investigation of benzol and toluol poisoning 
in Royal Australian Air Force workshops. Med. J. Aust., 
1947,2: 681-692. [P] 
(b) Carbon Tetrachloride 
The use of carbon tetrachloride as a cleaning 
solvent for greasy equipment may incur severe 
poisoning effects following the use of this fluid in 
poorly ventilated working areas. Cases of nephrosis 
due to carbon tetrachloride inhalation are described 
in the literature cited below. 
2632. Abbott, G. A. and M, J. Miller. Carbon tetra- 
chloride poisoning. A report on 10 cases at the U. S. 
Marine Hospital, Seattle, Wash., since 1937. J. industr. 
Hyg., 1949, 31: abstract section: 102. Publ. Hlth. Rep., 
Wash., 1948, 63: 1619-1624. [CH]. 
2633. Amouroux, P. L’intoxication par les extincteurs 
d’incendie au gas ardexine. Rev. Mid. nav., 1948, 
3: 133-147. [D] 
2634. Andre, L. Intoxication par le tetrachlorure de car- 
bone dans la marine. Rev. Med. nav., 1946, 1: 213—234. 
[D] [CH] 
2635. Elkins, H. B. Maximal allowable concentrations. 
I. Carbon tetrachloride. /. industr. Hyg., 1942, 24: 233— 
235. [CH] 
2636. Farrier, E.. M. and B. H. Smith. Carbon tetra- 
chloride nephrosis. A frequently undiagnosed cause of 
death. /. Amer. med. Ass., 1950, 143: 964—967. Abstr. 
World Med., 1950, 8: 585. 
2637. Glynn, L. E, and H. P. Himsworth. The intra- 
lobular circulation in acute liver injury by carbon tetra- 
chloride. Clin. Sci., 1948, 6: 235-245. [P] 
2638. Gray, I. Carbon tetrachloride poisoning. Report 
of seven cases with two deaths. N. Y. St. J. Med., 1947, 
47: 2311-2315. [CH] 
2639. King, B. G. High concentration-short time expo- 
sures and toxicity. /. industr. Hyg., 1949, 31: 365—375. 
[R] 
2640. Laqueur, W. and F. Nashat. Dietary protein and 
carbon tetrachloride intoxication. Histological changes in 
the rat’s liver in acute poisoning. Arch. int. Pharma- 
codyn., 1948, 78: 449-455. Abstr. World Med., 1949, 
6: 148. 2641-2664 
DISEASES AND ACCIDENTS 
2641. Lehmann, K. B. and F. Flury. Carbon tetrachlo- 
ride. pp. 145-154 in: Toxicology and hygiene of indus- 
trial solvents. Translated by E. King and H. F. Smyth, Jr. 
Baltimore, The Williams & Wilkins Co., 1943, 378 pp. 
2642. McCord, C. P., J. H. Sterner, L. L. Kline, and 
P, E. Williams. The thymol-barbital test in experimental 
carbon tetrachloride poisoning. Occup. Med., 1946, 1: 
160-167. [P] 
2643. Moon, H. D. Pathology of acute carbon tetrachlo- 
ride toxicity. Amer. J. Pathol., 1949, 25: 788-789. Ex- 
cerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1950, 3: 252. 
2644. Moon, H. D. The pathology of fatal carbon tetra- 
chloride poisoning with special reference to the histo- 
genesis of the hepatic and renal lesions. Amer. J. Pathol., 
1950, 26: 1041-1057. [GH] 
2645. Mushett, C. W. Influence of crystalline vitamin 
B12 on carbon tetrachloride poisoning. Fed. Proc. Amer. 
Soc. exp. Biol., 1950, 9: 339. 
2646. Reed, J. V. and A. K. Harcourt. Carbon tetra- 
chloride CGh. pp. 31—34 in: The essentials of occupa- 
tional diseases. Springfield, Charles C. Thomas, 1941, 
225 pp. 
2647. Sirota, J. H. Carbon tetrachloride poisoning in 
man. I. The mechanisms of renal failure and recovery. 
/. Clin. Invest., 1949, 28: 1412-1421. [R] [P] 
2648. Stewart, A. and L, J. Witts. Chronic carbon 
tetrachloride intoxication. Brit. J. industr. Med., 1944, 
I: 11-19. [CH] 
2649. Snndareson, A. E. Protective action of nucleic 
acid on the liver in carbon tetrachloride poisoning. J. In- 
diana med. Assn., 1948, 17: 287-290. [P] 
2650. Thompson, C. M. Pulmonary changes in carbon 
tetrachloride poisoning. Amer. J. Roentgenol., 1946, 
55: 16-19. 
2651. Wilson, R. H. Diagnosis and treatment of indus- 
trial solvent poisoning. /. Amer. med. Assn., 1949, 139: 
906-909. 
2652. Woods, W. W. The changes in the kidneys in 
carbon tetrachloride poisoning, and their resemblance to 
those in the “crush syndrome.” /. Path. Bact., 1946, 
58: 767-773. [M] [R] [CH] 
11. OTHER NOXIOUS AGENTS 
For references concerning other toxic gases and 
substances, the reader is referred to the following 
papers. 
2653. Baetjer, A. M. Chronic exposures to air pollutants 
and acute infectious respiratory diseases. Arch. ind. Hyg. 
occup. Med., 1950,2: 400-406. 
2654. Baetjer, A. M. Atmospheric pollution, pp. 1010- 
1021 in: Rosenau preventive medicine and hygiene. 
Edited by Kenneth F. Maxcy. Seventh edition. Appleton- 
Century-Crofts, Inc., New York, 1951, 1462 pp. 
2655. Cauer, H. Chemical climatology of the trace sub- 
stances in the air of submarines, pp. B: II-l—B: 11—108 
in: Monograph on submarine medicine, Folio II, Ger- 
many, U. S. Zone. Office of naval advisor. 1948. 
2656. Finland, M., M. Ritvo, C. S. Davidson, and S. M. 
Levenson. Roentgenologic findings in the lungs of victims 
of the Cocoanut Grove disaster. Amer. J. Roentgenol., 
1946, 55: 1-15. [CH] 
2657. Gray, M. G. Toxicity of ozone under simulated 
industrial conditions. Fed. Proc. Amer. Soc. exp. Biol., 
1949, 8: 296. 
2658. Lushbaugh, C. C., J. W. Green, Jr., and C. E. 
Redemann. Effects of prolonged inhalation of oil fogs on 
experimental animals. Arch, industr. Hyg. occup. Med., 
1950, 1: 237—247. Excerpta Medica. Section II. (Physi- 
ology, Biochemistry, and Pharmacology), 1950, 3: 1580. 
2659. Osol, A., G. E. Farrar, E. E. Leuallen, W. F. Ver- 
wey, H. W. Youngken, D. K. Detweiler, and H. C. Wood, 
Jr. Acrolein, pp. 1306-1307 in: The dispensatory of the 
United States of America. 24th edition, Philadelphia, 
J. B. Lippincott Co., 1947, 1928 pp. 
2660. Schaefer, K. E. Technical influences. II. Con- 
densation droplets, ions and gamma-rays contained in the 
air of submarines, pp. B: 1-38—B: 1-50 in: Monograph 
on submarine medicine, Folio I, Germany, U. S. Zone. 
Office of naval advisor. 1948. 
2661. Sendroy, J., J. D. O’Neal, and G. C. Pitts. Com- 
position and effect of vapors emanating from insulated 
electrical equipment under conditions of simulated sub- 
marine operation. U. S. Navy. NMRI. Project NM004 
005.02.01, 8 August 1950, 22 pp. [P] 
2662. Shea, T. E., Jr., G. C. Pitts, and J. D. O’Neal. 
Effect of temperature and operation time upon the pro- 
duction of noxious gases from silicone insulated electrical 
equipment under conditions of simulated submarine 
operation. U. S. Navy. NMRI. Project X—755, Kept. no. 
1, 9 December 1947, 6 pp. [P] 
2663. Thorp, C. E. The toxicity of ozone. A report and 
bibliography. Industr. med surg., 1950, 19: 49-57. 
2664. U. S. Army. Chemical Corps. Medical Division. 
Health hazards of propellant fuels and treatment therefor. 
Project 4-16-17-01, Summary Kept., 30 June 1949, 35 
PP- [P] 
VII. MOTION SICKNESS 
A. GENERAL STUDIES ON MOTION SICKNESS 
Of the general references to motion sickness listed 
below, particular attention is called to articles by 
the following authors: Bard {2667) 1948; Chap- 
anis, Garner, and Morgan {2669) 1949; Heming- 
way {2673) 1945; McEachern, Morton, and Leh- 
man {2674) 1942; Schwabb {2677) 1940; Spiegel 
and Sokalchuk {2678) 1950; Tufts College {2679) 
1949; and Tyler and Bard {2680) 1949. 
Tyler and Bard’s review {2680) sets forth the sub- 
ject of motion sickness in detail. These authors 
point out that motion sickness became of utmost 
importance during World War II when vast num- 
bers of men were being carried to combat zones 
or were flying. Animals as well as men are subject 
to motion sickness, and it is believed that almost any 
human being can be made ill if the stimuli are 
sufficiently strong. Dogs are especially susceptible 
and are similar to human beings in their suscepti- 
bility. Monkeys and cats are very resistant. Suscepti- 
bility appears to depend upon a rather specific 
constitutional capacity to respond to certain pat- 
terns of vestibular stimulation and can be modified 
by several extralabyrinthine influences. About 95 
percent of susceptible persons are capable of adap- 
tation to motion. Adaptation to one type of move- MOTION SICKNESS—SIGNS AND SYMPTOMS 
2665-2682 
ment does not necessarily adapt the individual to 
motion produced by a different device or vessel. 
It is estimated that 3 to 5 percent of the population 
are extremely susceptible to motion sickness and 
cannot be adapted. Experimental methods of pro- 
ducing motion sickness use devices which reproduce 
movements of ships, elevators, and swings. Appa- 
ratus which rotates and tilts the head may also be 
used. Composite motion is more effective than any 
one type. It appears that the most significant struc- 
ture concerned in the production of motion sickness 
is the labyrinth. Bilateral labyrinthectomy will ren- 
der susceptible dogs immune to motion sickness. 
Human deaf-mutes, lacking in labyrinthine reac- 
tions, are generally not susceptible to motion sick- 
ness. The labyrinthine sense organs essentially in- 
volved in motion sickness are the cristae of the 
semicircular canals and the utricular maculae. 
Addition of small angular accelerations to a motion 
which has only linear changes in velocity augments 
its nauseating properties. Motion sickness can be 
produced by either angular or linear accelerations, 
the semicircular canals being involved in the former 
and the utricles being stimulated in the latter. Any 
head position in which the vertical canals assume 
a nearly horizontal position is the least conducive to 
the production of swing sickness. It has been shown 
that extirpation of the cerebellum or portions of 
the cerebellum prevents motion sickness in animals. 
The central nerve pathway apparently leads from 
the labyrinth to the vestibular nuclei in the medulla, 
and thence to cerebellar, thalamic, and spinal cen- 
ters. Vagal centers in the medulla are also essen- 
tially involved. The extent of cortical involvement 
is uncertain, and experimental studies show that 
decortication does not affect susceptibility to motion 
sickness. Psychological factors appear to have very 
little to do with the cause of motion sickness. No 
entirely satisfactory tests for preselecting motion- 
sickness-resistant candidates for submarine, flight, 
or other military training have yet been devised. 
It has been recommended that actual motion sick- 
ness in the early phases of operational training is 
the most practical selective procedure. 
2665. Antnnez, N. Mal de mar y su tratamiento. pp. 
192-196 in: Higiene naval y nociones de anatomia y 
fisiologia. Moret, La Coruna, 1950, 321 pp. 
2666. Babkin, B, P., and S. Dworkin. Experimental 
studies of motion sickness. Canada NRC. Proceedings of 
conference on motion sickness, Project 736, 28 August 
1942, 9 pp. 
2667. Bard, P. Motion sickness, pp. 278-295 in: Part 
III. Aviation Medicine in: Advances in Military Medicine, 
Vol. I. Edited by E. C. Andrus, D. W. Bronk, G. A. Car- 
den, Jr., C. S. Keefer, J. S. Lockwood, J. T. Wearn, and 
M. C. Winternitz. Boston, Little, Brown and Co., 1948, 
472 pp. [R] 
2668. Blackham, R. J. Sea-sickness. Brit. med. J., 1939, 
2: 163-167. [R] 
2669. Chapanis, A., W. R. Garner, and C. T. Morgan. 
The working environment. The effects of motion, pp. 408— 
414 in: Applied experimental psychology. New York, John 
Wiley & Sons, Inc., 1949, 421 pp. 
2670. Cipriani, A. and D. McEachern. Montreal motion 
sickness machine. Canada NRC. Proceedings of conference 
on motion sickness. Project C615, 28 August 1942, 5 pp. 
2871. Dragotti, 6. Rivista sintetica; il mal di movimento. 
Policlinico. 1948, 55: 1329-1336. [D] 
2672 Green, D. M. Air sickness in bomber crews. /. Aviat. 
Med., 1943, 14: 366-372. 
2673. Hemingway, A. Survey of research on the problem 
of air sickness in the Army Air Forces. U. S. AAF. Ran- 
dolph Field, Tex. School of aviation medicine. Project 
381, Kept. no. 1, 20 April 1945, 45 pp. [R] 
2674. McEachern, D., G. Morton, and P. Lehman. Sea 
sickness and other forms of motion sickness. I. A general 
review of the literature. War Med., Chicago, 1942, 2: 
410-428. [R] 
2675. Monaco, L. Per i passeggeri che coffrono di mal 
d’aria. Riv. Med. aero., 1947, 10: 370-372. [D] 
2676. Rubin, H. J. Air sickness in a primary air force 
training detachment. J. Aviat. Med., 1942, 13: 272-276. 
2677. Schwab, R. S. Motion sickness, pp. 664 (54-20)— 
664 (54-30) in; Oxford medicine, Vol. IV, Part III. 
Edited by H. A. Christian. New York, Oxford University 
Press, 1940. [R] 
2678. Spiegel, E. A. and A. Sokalchuk. Motion sickness, 
pp. 572-580 in: Medical physics, Vol. II. Edited by Otto 
Glasser. Chicago, The Year Book Publishers, Inc., 1950, 
1227 pp. [R] ~ 
2679. Tufts College. Motion sickness. 6 pp. in: Hand- 
book of human engineering data for design engineers. 
Tufts College, Institute for applied experimental psychol- 
ogy. SDC Human Engineering Project 20-G—l, Project 
Designation NR-783-001, Technical Report 199—1—1, 1 
December 1949, 410 pp. 
2680. Tyler, D. B. and P. Bard. Motion sickness. 
Physiol. Rev., 1949, 29: 311-369. [R] 
2681. U. S. NRC-CAM. Bibliography of air sickness and 
sea sickness. Bibliography of labyrinthine studies in relation 
to motion sickness. List of reports of British flying person- 
nel research committee (F. P. R. C.) and of the National 
Research Council, Canada, in relation to motion sickness 
up to September 1942. C. A. M. Rept. no. 82, November 
1942, 44 pp. [B] 
2682. IT. S. Navy, 0NR. Psychophysiology Branch. Re- 
port of conference on motion sickness. 9 September 1950, 
15 pp. 
B. SIGNS AND SYMPTOMS OF MOTION SICKNESS 
(PHYSIOLOGICAL AND PATHOLOGICAL CHANGES) 
For general studies of the symptomatology of 
motion-sickness, papers by the following should be 
consulted: Brett (2684) 1942, Hewlett (2688) 
1942, and Palmisano (2691) 1951. Cold sweating 
in motion sickness has been investigated by Heming- 
way (2685) 1944 by an electrical device which 
measures the onset of sweating. A calcium chloride 
water absorption device was also used to measure 
the rate of sweating. In Hemingway’s study, sub- 
jects were men between the ages of 20 and 30 who DISEASES AND ACCIDENTS 
had passed the Army physical examination. The 
men were subjected to periodic motion involving 
changing linear and centrifugal accelerations vary- 
ing between 1.0 and 2.0 g. It was found that sweat- 
ing occurred as a result of motion, and at the same 
time the mouth temperature fell. According to Hem- 
ingway, there appears to be no physiological pur- 
pose in cold sweating, and the motion sickness 
mechanism is probably a part of a primitive defense 
reaction. In a further study by Hemingway {2686) 
1945, motion sickness was produced in normal young 
men by means of a 20-minute swing test. Blood pres- 
sure, pulse rate, body and skin temperature, and the 
rate of sweating were measured. Motion sickness 
was not associated with any significant change in 
systolic pressure, diastolic pressure, or pulse rate. 
Cold sweating was present during motion sickness 
with a drop in skin and mouth temperature, and 
this was seen in environments with air temperatures 
near freezing. Hyperventilation frequently occurred 
with tingling sensations in the feet and hands, and 
occasionally carpopedal spasm. In a few instances 
the latter was so severe that the hands were “frozen” 
to the supports and the fingers had to be pried loose. 
X-ray examination after a barium meal showed 
loss of gastric tone and delayed emptying of the 
stomach associated with motion sickness. In a fur- 
ther report, Hemingway {2687) 1945 reported that 
of a group of 489 normal young adults who were 
exposed to the swing, sickness occurred in 29 per- 
cent of those tested. There was a slight tendency 
for elevation of blood pressure immediately follow- 
ing vomiting, but otherwise (as just stated) there 
were no significant changes in systolic pressure, 
diastolic pressure, or pulse rate associated with 
motion sickness. 
Sokalchuk {2694) 1947 reported blood-pressure 
readings in seasick crew members of a destroyer sub- 
jected to a combination of rolling, pitching, yawing, 
and up and down motion. An average of 6 percent 
of the men became seasick. In 37 men, systolic and 
diastolic blood pressures were repeatedly measured 
in port and during seasickness. Rise as well as fall 
of the systolic pressure appeared in five cases. Fall in 
the systolic pressure of 1 to 10 mm. of Hg was more 
frequent (15 cases) than a corresponding rise (2 
cases). Fifteen men showed an average fall of 11 
to 27 mm. of Hg, and 13 men showed a maximal 
fall of more than 15 mm. of Hg. The reaction of the 
diastolic pressure was somewhat similar. 
Ventilation rates and respiratory patterns during 
exposure to the swing test for motion sickness have 
been studied by Rushmer {2693) 1943. Ventilation 
rates were recorded on 35 subjects. In 15 subjects, 
respiratory movements and period of the swing were 
simultaneously recorded to determine how fre- 
quently they tended to breathe in rhythm with the 
motion of swing. Ventilation rates were found al- 
most invariably to be elevated during the swing 
test. The increase tended to be greater in persons 
suffering from symptoms of motion sickness than 
in those subjects not so affected by the swing test. 
There was a poor correlation in this group of sub- 
jects between increase in ventilation rate and sub- 
jective complaint of symptoms. With one excep- 
tion, every subject tended to synchronize respiratory 
rhythm with the motion of the swing. Overventila- 
tion was not considered of importance in the etiol- 
ogy of swing sickness. Several subjects exhibiting the 
greatest increases in ventilation rates during the 
swing test admitted they were apprehensive and 
excited during the test. 
Regarding the effect of swinging on motility of 
the stomach, Babkin and Bornstein {2683) 1943 
have carried out experimental studies on dogs. A 
combination of a horizontal and vertical accelera- 
tion with a minimum of rotatory movement pro- 
duced motion sickness in dogs susceptible to this 
form of disturbance. Swinging of dogs susceptible 
to motion sickness immediately inhibited all the 
movements of the fasting stomach, as evidenced by 
cessation of hunger contractions and a fall of gastric 
tone. Continuation of swinging induced vomiting 
within 5 to 15 minutes. The aftereffect of swinging 
in animals susceptible to motion sickness was, in the 
minority of cases, a gradual recovery of gastric tone 
and return of hunger contractions. More often, 
there appeared within 15 to 120 minutes special 
rhythmic contractions of the stomach which de- 
veloped gradually with lowered tone. This latter 
form of gastric hypermotility was not affected by 
atropine and could not be induced by prostigmine. 
In a dog less susceptible to motion sickness, swinging 
likewise arrested the hunger contractions, but vomit- 
ing did not occur until after about 2 hours of 
continuous swinging. The special rhythmic con- 
tractions of the stomach appeared during swinging, 
but they were relatively weak and irregular. Bi- 
lateral labyrinthectomy abolished all symptoms of 
motion sickness in the susceptible dogs. It was con- 
cluded, therefore, that the chief cause of the diverse 
phenomena observed in the stomach during hori- 
zontal and vertical acceleration is excessive stimu- 
lation of the vestibular apparatus. 
Repeated vomiting associated with motion sick- 
ness may have serious consequences. Pumphrey, 
Kuh, Johnson, and Day {2692) 1946 reported the 
case of a 25-year-old crewman aboard an attack 
transport who was seasick for 3 days. He vomited 
repeatedly and hyperventilated. His arms and MOTION SICKNESS—SUSCEPTIBILITY 
2683-2694 
fingers became stiff, and he fell unconscious with 
carpopedal spasm. He was given 20 cc. of 10 percent 
calcium gluconate and rebreathed into a paper bag. 
There was relaxation of the spasm within 10 
minutes. A slight chill with vomiting supervened. 
One thousand cu. cm. of 5 percent glucose in saline 
were given. 
For vestibular symptoms, papers by Lewy {2689) 
1947 and Palmisano {2690) 1951 maybe consulted. 
2683. Babkin, B. P. and M. B. Bernstein. The effect of 
swinging on the motility of the stomach in dogs. Canada 
NRC. Proceedings of second meeting of associated com- 
mittee on naval medical research. Project C4030, 7 Octo- 
ber 1943, 12 pp. 
2684. Brett, J. R. Symptomatology of swing sickness. 
Canada NRC. Proceedings of conference on motion sick- 
ness. Appendix “R” 5f, 28 August 1942, 1 p. 
2685. Hemingway, A. Cold sweating in motion sickness. 
Amer. J. Physiol., 1944, 141: 172-175. 
2686. Hemingway, A. Physiological changes during 
motion sickness. Fed. Proc. Amer. Soc. exp. Biol., 1945, 
4: 33. 
2687. Hemingway, A, Cardiovascular changes in motion 
sickness. /. Aviat. Med., 1945,16: 417-421. [P] 
2688. Hewlett, P. A. I. Symptomatology of air sickness. 
Canada NRG. Proceedings of conference on motion sick- 
ness. Appendix “R” 5d, 28 August 1942, 3 pp. [P] 
2689. lewy, A. The symptomatology of vertigo. Ann. 
Otol., etc., St. Louis, 1947,56: 534-540. 
2690. Palmisano, C. Ossevazioni sulla fisiopatologia 
neuro-vegetativa, vestibolare e oculare nella naupatia, di 
soggetti imbarcati su navi di superficie. Ann. Med. nav. 
trap., 1951, 56: 164-176. 
2691. Palmisano, C. Studio delle caratteristiche oculari 
e del riflessi oculari neurovegetativi in condizioni di mare 
calmo e ricerche sulle loro variazioni fisio-patologiche nella 
naupatia, in soggetti imbarcati su navi di superficie Ann. 
Med. nav. trap., 1951, 56: 687-710. [P] 
2692. Pumphrey, R. E,, J. R. Kuh, M. A. Johnson, and 
A. L, Day. Unusual conditions aggravated by sea sickness. 
Nav. med. Bull, Wash., 1946, 46: 742-743. [GH] 
2693. Rushmer, R. P. Overventilation in subjects dur- 
ing the swing test. U. S. AAF. Randolph Field, Tex. School 
of aviation medicine. Project 133, Rept. no. 1, 1 May 1943, 
6 pp. [P] 
2694. Sokalchuk, A. Blood pressure in seasickness. Fed. 
Proc. Amer. Soc. exp. Biol, 1947, 6: 207. [P] 
C. SUSCEPTIBILITY TO MOTION SICKNESS 
Birren {2699) 1949 has pointed out that it is 
improbable that a totally motion-sickness-resistant 
group could ever be screened because of the large 
population of persons who may be made motion 
sick. Susceptibility to motion sickness may be re- 
garded as a general factor for all situations involv- 
ing acceleration. With available means of detecting 
susceptibility to motion sickness, including ques- 
tionnaires and surveys, a significant reduction could 
be made in the number of unadaptable or very 
susceptible persons being assigned to critical tasks 
in the services. Although there are striking indi- 
vidual differences in susceptibility to motion sick- 
ness, the basis for these differences is not entirely 
apparent. Few individual traits, either physiological 
or psychological, have been found to be related to 
susceptibility. Personality factors do not contribute 
in an important degree to variations in suscepti- 
bility. Motion sickness is not a psychological afflic- 
tion, although there appear to be persons in whom 
unusual emotional stress may favor the onset of 
symptoms. 
Hemingway {2710) 1946 has discussed a num- 
ber of methods for evaluating susceptibility to mo- 
tion sickness. The Barany chair test has been 
abandoned. History of motion sickness may be of 
value, but should not by itself be used as a reason 
for rejecting a candidate. The swing test is a simple 
method for producing motion sickness and is su- 
perior to the motion-sickness history in its correla- 
tion with incidence of airsickness. Hemingway 
believes that the swing-test results should by them- 
selves not be considered disqualifying. He considers 
the record of airsickness in flight training the best 
means of evaluating motion-sickness susceptibility. 
He has recommended that the motion-sickness 
history and the swing-test results be considered in 
preflight evaluation for flying fitness, and that the 
airsickness record be kept for the first 10 flights. 
If the trainee is airsick once after the fifth flight, 
the case should be reviewed for possible elimina- 
tion. If the trainee is sick twice after the fifth flight, 
he should be eliminated. In general, it would seem 
that these recommendations are valid. 
A number of reports have appeared in the litera- 
ture on the value of the motion-sickness history in 
predicting airsickness or other forms of motion sick- 
ness under operational conditions. For such studies, 
papers by the following should be consulted: Alex- 
ander, Cotzin, Hill, Ricciuti, and Wendt {2695) 
1945; Birren {2698) 1947; Birren and Fisher 
{2700) 1947; Birren, Fisher, and Stormont {2701) 
1944; Hewlett and Brett {2712) 1942; and 
Mathewson {2721) 1942. Beginning with the early 
years of World War II, histories of previous motion 
sickness were derived from men subjected to the 
swing test as well as those interviewed at flying 
schools in the various services both in the United 
States and abroad {2712). Mathewson {2721) 
1942 pointed out that it was impossible by the his- 
tory method to ascertain accurately the prevalence 
of susceptibility to motion sickness. He found that 
the incidence of positive histories increased as the 
inquiries became more searching. From data assem- 
bled from a closely supervised group of 308 men, 
it would appear that some correlation exists be- 
tween a previous history of motion sickness and DISEASES AND ACCIDENTS 
airsickness occurring during flight training. The 
positive correlation depends to a large extent on 
the care with which the history was obtained. Bir- 
ren, Fisher, and Stormont {2701) 1944 admin- 
istered a motion-sickness questionnaire to 277 male 
naval personnel whose susceptibility to motion sick- 
ness was known from the person’s own judgment 
of his susceptibility, from susceptibility ratings of 
men by officers at sea, and from judgment of boards 
of medical survey. From an item analysis of the 
questionnaire it appeared that susceptibility to 
motion sickness is a rather specific factor. No evi- 
dence was found of a correlation between general 
psychosomatic complaints and susceptibility to mo- 
tion sickness. Alexander, Gotzin, Hill, Ricciuti, and 
Wendt {2695) 1945 reported a series of five ex- 
periments, using a total of 477 naval officer candi- 
dates, in which the incidence of motion sickness 
resulting from a 20-minute exposure of blindfolded 
subjects on a vertical accelerator was analyzed for 
its relationship to previous history of motion sick- 
ness as determined by a questionnaire. The overall 
results showed a reliable and moderately high rela- 
tion between motion-sickness history and experi- 
mentally produced sickness. The results were inter- 
preted by the authors as indicating that machine 
sickness has factors in common with other forms of 
motion sickness. It was also suggested that a ques- 
tionnaire might yield a useful prediction of motion 
sickness in military situations and might be used 
as an elimination or selection device. 
As a result of an experimental study with 
a revised motion-sickness questionnaire, Birren 
{2698) 1947 believed it of sufficient validity and 
reliability to screen out those who would be severely 
affected by motion sickness. There was a tendency 
for men to rate themselves more susceptible than 
did their associates. No relation was found between 
questions of general somatic and psychosomatic 
import and susceptibility to seasickness. There was 
no indication that fear of naval duty was related 
to susceptibility to seasickness. There seems little 
evidence to justify a purely psychogenic interpreta- 
tion of motion sickness. In 48 men incapacitated 
for sea duty because of extreme susceptibility to 
motion sickness, the most distinctive group was 
sensitive to all forms of motion sickness. The group 
was also characterized by excessive body sway, 
proneness to nausea and vomiting from the action 
of centrally acting emetic drugs, and ease with 
which symptoms were produced on a rolling plat- 
form. No severe psychological defects were revealed 
which could account for susceptibility. Results of 
a questionnaire given to 1,560 male naval personnel 
suggest that motion sickness is relatively common. 
Distress, nausea, and vomiting are produced by a 
wide variety of situations involving periodic motion. 
Birren and Fisher {2700) 1947 studied the validity 
of the questionnaire method by comparing the 
questionnaire scores of 150 officers and men with 
sea experience on a destroyer as reported by officers 
who were in a position to know the relative sus- 
ceptibility to seasickness of each man. About 10 
percent of the 150 men were indicated as highly 
susceptible. A person’s questionnaire score corre- 
lated more highly with his own estimate of suscepti- 
bility than with another individual’s estimate of his 
susceptibility. The 10 percent of the destroyer- 
escort crew having the highest questionnaire scores 
included about half of those who were rated highly 
susceptible to seasickness. Elimination of this 10 
percent would therefore have reduced the number 
of susceptibles from 10 in 100 to about 5 in 100. 
Greater predictive efficiency of the questionnaire 
was indicated when self-judgments, rather than 
judgments by associates, were used as the criterion. 
It was concluded by the authors that the question- 
naire seems to have sufficient validity and reliability 
for screening out persons very susceptible to sea- 
sickness. Brown, Brett, and Hewlett {2703) 1943 
concluded that use can be made of a well-taken 
history of susceptibility to motion sickness in indi- 
cating those men who may experience airsickness 
in flight training. 
The swing test for the production of motion sick- 
ness has been used both in experimental animals 
and in man. Induced motion-sickness techniques 
have provided not only a method whereby the 
mechanisms of motion sickness may be studied but 
also have permitted differentiation of the persist- 
ently motion-sick group from the non-motion-sick 
group with fair accuracy. For studies of the relation 
of swing-test results to actual incidence of motion 
sickness in military operations, papers by the fol- 
lowing authors should be consulted: Fields {2705) 
1942; Hemingway {2707) 1943; Hemingway 
{2708) 1943; Hemingway {2709) 1946; Hewlett 
{2711) 1942; Hewlett and Brett {2713) 1942; 
Jasper, Battista, Bornstein, and Noble {2716) 
1943; McDonough {2719) 1943; Morton {2722) 
1942; Morton, Cipriani, and McEachern {2723) 
1942; and Noble {2726) 1948. 
Attempts to establish a significant relationship 
between psychological defects and susceptibility to 
motion sickness have not yielded reliable positive 
findings {2730). Wendt {2729) 1949 believes that 
no absolute distinction can be made between psy- 
chological and physiological factors in motion sick- 
ness. Factors such as the character of the motion, 
the position of the head, and the physiological state MOTION SICKNESS—SUSCEPTIBILITY 
2695-2697 
as affected by drugs, are considered the major de- 
terminers of motion-sickness rates. Army and Navy 
subjects did not become motion sick unless the 
combination of physiological and physical factors 
was appropriate. The author concluded that, al- 
though psychological factors are demonstrably oper- 
ative, physical and physiological factors outweigh 
them in practical importance. Wendt has stressed 
the need of a better understanding of the kinds of 
motion sickness and a better understanding of the 
physiology of motion sickness so that prophylactic 
drugs may be more adequately studied. 
A number of factors have been investigated in 
relation to motion-sickness susceptibility. Head po- 
sition and character of motion have been investi- 
gated by Morton and McEachern (2724) 1942. In 
these authors’ studies, vertical up and down motion 
with the head fixed in the erect position provided 
the situations most likely to cause motion sickness. 
Birren, Stormont, and Pfeiffer (2702) 1945 have 
studied reactions to neostigmine and apomorphine 
as an indication of susceptibility to seasickness. Neo- 
stigmine was administered intramuscularly to 14 
control subjects and to 14 enlisted personnel sur- 
veyed to shore duty because of chronic seasickness. 
Vomiting did not occur in either group. The symp- 
tomatology following neostigmine did not aid in 
distinguishing between the seasick susceptibles and 
the normals. Apomorphine was administered sub- 
cutaneously to 18 controls and 22 chronic seasick- 
ness personnel. Nausea and vomiting occurred in 7 
of the 22 seasick susceptible subjects and in 3 of 
the 18 control subjects. Reactions elicited after ad- 
ministration of apomorphine thus allowed a very 
rough differentiation between susceptibility and 
nonsusceptibility to seasickness. 
Birren (2697) 1945 initiated observations on the 
basis for susceptibility to seasickness on 48 men who 
were so susceptible to seasickness that they were 
unable to work effectively at sea. These men were 
given a series of tests, three of them involving equi- 
librium. The susceptible men were not different 
from the normal seamen in their ability to balance 
themselves in the railwalking test which requires the 
subject to walk a 10-foot 1-inch wide rail. Postrota- 
tional nystagmus was slightly, but not significantly, 
longer in the susceptible men for both the horizontal 
and vertical positions in the Barany chair. The fall- 
ing reaction to the vertical position appeared exag- 
gerated in several of the susceptible men. The 
Barany chair test as a whole did not bring out any 
striking differences between the normal and suscep- 
tible men. A difference did appear between the 
susceptible and normal men in the amount of body 
sway. 
It seems from studies of Goehring {2706) 1942 
and Benedict and Schwab (2696) 1945 that men 
suffering from seasickness or who are susceptible to 
seasickness show characteristic abnormalities of the 
stomach and duodenum (loss of gastric motility and 
spasm of the pyloric sphincter) as examined by X- 
ray. Kirkner (2718) 1949 attempted to design a 
test for the prediction of airsickness on the hypothe- 
sis that skin resistance changes characteristically 
during spatial displacement. Various stimulations 
were used including subcutaneous injection of apo- 
morphine, caloric irrigation, rotation, and swabbing 
the throat with a light cotton swab. The most violent 
vomiting reaction was obtained with apomorphine. 
The data failed to show any consistent relationship 
between sweating and relative decrease in palmar 
resistance. According to the data, a relative decrease 
in palmar resistance does not appear to be a reliable 
measure of the rate of sweating or of nausea. It was 
concluded that relative palmar resistance change is 
not a satisfactory measure for nausea induced by 
labyrinthine stimulation. 
According to Jasper and Morton (2717) 1942, 
there is no significant correlation between instability 
in electroencephalographic records and past history 
of motion sickness. Thorner (2728) 1943 concluded 
that the electroencephalogram cannot be used effec- 
tively as a means of preselecting navigation cadets 
who will be most susceptible to airsickness, although 
the electroencephalograms of airsickness-susceptible 
groups differ markedly from those of a correspond- 
ing group of healthy adults in the general popula- 
tion. Morton, McNally, and Stuart (2725) 1942 
carried out caloric tests on 31 subjects and con- 
cluded that there is no definite correlation between 
the reaction to minimum caloric stimulation and 
susceptibility to motion sickness, unless the nystag- 
mus, nausea, and vomiting are unusually severe. 
For further studies on susceptibility to motion 
sickness, papers by the following should be con- 
sulted: Eyer (2704) 1943, Hewlett and Brett 
(2714) 1942, Hewlett and Brown (2715) 1942, 
MacPhee and Pennington (2720) 1946, and Schwab 
(2727) 1942. 
2695. Alexander, S. J., M. Cotzin, C. J. Hill, Jr., E. A. 
Ricciuti, and G. R. Wendt. Wesleyan University studies 
of motion sickness: VI. Prediction of sickness on a vertical 
accelerator by means of a motion sickness history question- 
naire. /. Psychol., 1945, 20: 25—30. [P] 
2696. Benedict, E. B. and R. S. Schwab. Gastroscopic 
studies in naval personnel with chronic seasickness. New 
Engl. J. Med., 1945, 233: 237. [GH] 
2697. Birren, J. E. Equilibrium and susceptibility to 
seasickness. Fed. Proc. Amer. Soc. exp. Biol., 1945, 4: 7. 2698-2730 
DISEASES AND ACCIDENTS 
2698. Birren, J. E. Psychophysiological studies of motion 
sickness. Abstract: Northwestern University, Summaries 
of doctoral dissertations, 1947, 15: 254-257. 
2699. Birren, J. E. Motion sickness: its psychophysi- 
ological aspects, pp. 375-414 in: A survey report on 
human factors in undersea warfare. Washington, D. C., 
National Research Council, 1949, 541 pp. 
2700. Birren, J. E., and M. B. Fisher. Susceptibility to 
seasickness: a questionnaire approach. J. appl. Psychol., 
1947, 31: 288-297. [P] 
2701. Birren, J. E., M. B. Fisher, and R. T. Stormont. 
An evaluation of a motion sickness questionnaire in pre- 
dicting susceptibility to seasickness. U. S. Navy. NMRI. 
Project X-278, Rept. no. 2, 15 August 1944, 8 pp. [P] 
2702. Birren, J. E., R. T. Stormont, and C. C. Pfeiffer. 
Reactions to neostigmine and apomorphine as indication 
of susceptibility to seasickness. U. S. Navy. NMRI. 
Project X-278, Rept. no. 4, 26 February 1945, 9 pp. [P] 
2703. Brown, B. R., J. R. Brett, and J. G. Hewlett. 
Swing sickness and a history of motion sickness in relation 
to airsickness. Canada NRC. Proceedings of a conference 
on motion sickness. Project C2504, 18 May 1943, 8 pp. 
2704. Eyer, A. W. The incidence of airsickness among 
aviation cadets in patrol aircraft. U. S. Navy. NATG., 
Pensacola, Fla. School of aviation medicine. Project no. 
X-72 (Av-F10-1), 29 January 1943, 10 pp. [P] 
2705. Fields, W. S. Induced motion sickness in naval 
ratings. Canada NRG. Proceedings of conference on 
motion sickness. Project C738, 28 August 1942, 5 pp. [P] 
2706. Goehring, H. D. Gastrointestinal tract in seasick- 
ness. U. S. Navy. Naval Hospital, Chelsea, Mass. Project 
no. X-375, 26 December 1942, 3 pp. [P] 
2707. Hemingway, A. Incidence of swing sickness in 
eight categories of army personnel. U. S. AAF. Randolph 
Field, Texas. School of aviation medicine. Project 170, 
Rept. no. 1, 30 July 1943, 3 pp. [P] 
2708. Hemingway, A. Motion sickness history and re- 
sults of the swing test of one hundred and seven (107) 
airsick eliminees from flight training. U. S. AAF. Ran- 
dolph Field, Tex. School of aviation medicine. Project 170, 
Rept. no. 2, 7 September 1943, 6 pp. [P] 
2709. Hemingway, A. The relationship of airsickness to 
other types of motion sickness. J. Aviat. Med., 1946, 17: 
80-85, 95. [P] 
2710. Hemingway, A. Selection of men for aeronautical 
training based on susceptibility to motion sickness. /. Aviat. 
Med., 1946, 17: 153-163. [P] 
2711. Hewlett, F. A. L. Swing test followup. Canada 
NRC. Proceedings of conference on motion sickness. 
Appendix R, 5i, 28 August 1942, 1 p. 
2712. Hewlett, F. A. L, and J. R. Brett. History of 
motion sickness and its relation to airsickness. Canada 
NRG. Proceedings of conference on motion sickness. 
Appendix R, 5c (2), 28 August 1942, 1 p. 
2713. Hewlett, F. A. L. and J. R. Brett. Airsickness in- 
vestigation (A. S. 5). Canada NRC. Proceedings of con- 
ference on motion sickness. Appendix R, 5g, 28 August 
1942, 6 pp. 
2714. Hewlett, F, A. I. and J. R. Brett. Blood pressure 
and motion sickness. Canada NRC. Proceedings of con- 
ference on motion sickness. Appendix R, 5j, 28 August 
1942, 2 pp. [P] 
2715. Hewlett, J. G. and B. R. Brown. Incidence of air- 
sickness at training schools. Canada NRC. Proceedings of 
conference on motion sickness. Appendix R, 5b, 28 Au- 
gust 1942, 2 pp. [P] 
2716. Jasper, H. H., A. Battista, M. Bornstein, and 
R. H. Noble. Reliability of the swing test of motion sick- 
ness. Canada NRG. Proceedings of second meeting of 
associated committee on naval medical research. Project 
C4038, 7 October 1943, 3 pp. 
2717. Jasper, H. H. and G. Morton, Electroencephalog- 
raphy in relation to motion sickness in volunteers. Canada 
NRC. Proceedings of conference on motion sickness. Proj- 
ect C745, 28 August 1942, 2 pp. 
2718. Kirkner, F. J. Psychophysiological studies of 
motion sickness and airsickness. /. comp, physiol. Psychol., 
1949, 42: 273-285. [P] 
2719. McDonough, F. E. Airsickness in navigation train- 
ing. U. S. NRG-CAM. C. A. M. rept. no. 181, 5 July 
1943, 18 pp. 
2720. MacPhee, H. M. and L, A. Pennington. The 
identification of cases of chronic motion sickness during 
military screening examinations. J. soc. Psychol., 1946, 
23: 61-64. 
2721. Mathewson, F. A. L. History of motion sickness 
and relationship to incidence of airsickness. Canada NRG. 
Proceedings of conference on motion sickness. Appendix R, 
5c, 28 August 1942, 3 pp. [P] 
2722. Morton, G. Susceptibility of animals to induced 
motion sickness. Canada NRG. Proceedings of conference 
on motion sickness. Project C746, 28 August 1942, 1 p. [P] 
2723. Morton, G., A. Cipriani, and D. McEachern. 
Susceptibility to motion sickness in volunteers. Canada 
NRC. Proceedings of conference on motion sickness. Proj- 
ect C742, 28 August 1942, 5 pp. [P] 
2724. Morton, G. and D. McEachern. Experimental 
studies on a susceptible individual. Canada NRC. Proceed- 
ings of conference on motion sickness. Project C750, 28 
August 1942, 2 pp. [P] 
2725. Morton, G., W. J. McNally, and E. A. Stuart. 
Caloric vestibular tests in relation to susceptibility to 
motion sickness. Canada NRC. Proceedings of conference 
on motion sickness. Project C743, 28 August 1942, 1 p. [P] 
2726. Noble, R. L. Adaptation to experimental motion 
sickness in dogs. Amer. J. Physiol., 1948, 154: 443-450. [P] 
2727. Schwab, R. S. Chronic seasickness. Neurological, 
psychiatric, and naval aspects. Nav. med. Bull., Wash., 
1942, 40: 923-936. 
2728. Thorner, M. W. Cortical activity in airsick per- 
sonnel. U. S. AAF. Randolph Field, Tex. School of avia- 
tion medicine, Project 169, Rept. no. I, 24 July 1943, 6 pp. 
[P] 
2729. Wendt, G. R. Of what importance are psycho- 
logical factors in motion sickness? /. industr. Hyg., 1949, 
31: abstract section: 69. J. Aviat. Med., 1948, 19: 24-32. 
[R] 
2730. Zwerling, I. Psychological factors in susceptibility 
to motion sickness. /. Psychol., 1947,23: 219-239. 
D. MECHANISMS OF MOTION SICKNESS 
For general studies on the mechanisms of motion 
sickness, papers by the following may be consulted: 
Byrne {2742) 1912, Cojazzi {2744) 1950, Harbert 
and Schiff {2747) 1950, Hatcher {2748) 1924, 
Morales {2768) 1949, and Sjoberg {2773) 1931. 
The volume by Byrne is a large, definitive work on 
the physiology of the semicircular canals and their 
relation to seasickness. Cojazzi’s paper {2744) is 
an excellent critical review of present views on the MOTION SICKNESS—MECHANISMS 
pathogenesis of seasickness and contains a long ref- 
erence list. Sjoberg [2773) has prepared an article 
giving approximately 160 references on the general 
subject of motion sickness and the labyrinthine 
mechanism. Hatcher’s long review [2748) gives a 
historical survey of the literature covering the 
mechanisms of vomiting itself. Harbert and Schiff 
[2747) have pointed out that motion sickness is not 
the result of stimulation of a single organ, but is 
the result of a break in accommodation by the 
spinal, medullary, and cerebellar centers from con- 
tinual, unusual stimuli arising in several organs. 
In order of importance, the sensory stimuli are prob- 
ably vestibular, proprioceptive, visual, and others. 
An important factor in this breakdown is a discrep- 
ancy in the sensations from various sources. Sensa- 
tions from the labyrinth and so forth are not un- 
pleasant by themselves. It is the abnormal reflexes 
produced by these sensations that are unpleasant. 
When the cerebellar, medullary, and spinal centers 
are repeatedly subjected to unusual stimuli, partic- 
ularly when the stimuli are incompatible, a point is 
finally reached when they cause more than normal 
reflex responses. Morales’ report [2768) discusses 
physical factors in the etiology of motion sickness 
and is concerned with the characteristics of the 
motion patterns as well as responses of the receptor 
systems. 
Noble [2770) 1950 made extensive observations 
on the motion factors causing vomiting in dogs. He 
found horizontal motion to be most effective. The 
vertical component has some effect and the angular 
component probably none. No one component of 
motion was as effective as composite motion. The 
rate of horizontal motion was an important factor, 
resulting in an increased effect. The effectiveness 
of vertical movement in producing motion sickness 
could be increased by increasing the distance tra- 
versed. Increasing the rate was ineffective. Swings 
with six different radii and swinging through three 
different angles were reported. The optimum radius 
appeared to be about 14 feet, longer or shorter 
radii causing a diminution of susceptibility. Reduc- 
ing the angle of swinging lowered the incidence of 
vomiting, except where a very short radius was used. 
In this case an increased response occurred, prob- 
ably related to the increase in rate of swinging. 
Wendt and his associates have carried out detailed 
studies to discover the physical conditions of motion 
sickness. Using a wave machine similar to an ele- 
vator, Alexander, Cotzin, Hill, Ricciuti, and Wendt 
[2731) 1945 exposed subjects to waves having a 
period of constant velocity during the up-and-down 
motions. It was found that a wave with a 1.1-second 
period of constant velocity produced the most sick- 
ness; it was concluded that the time interval be- 
tween accelerations is a factor in production of 
motion sickness. Alexander, Cotzin, Klee, and 
Wendt (2733) 1947 used waves with constant ac- 
celeration of 0.2 g., the frequency being controlled 
by control of duration of application of upward and 
downward acceleration. By this means, wave fre- 
quencies of 13, 16, 22, and 32 cycles per minute were 
obtained, having amplitudes of 9 feet, 5 feet 4 inches, 
2 feet 6 inches, and 1 foot 1 inch. Other significant 
variables were counterbalanced or controlled. Re- 
sults on 120 subjects showed motion sickness varied 
with the energy per wave. The largest wave pro- 
duced the most sickness, the smallest wave the least. 
Sickness rates of 37, 37, 10, and 7 percent were 
obtained in that order, proceeding from the large, 
slow wave to the small, fast wave. In general, it was 
found that some waves are as much as 20 times more 
nauseating than others per unit of energy. Motion- 
sickness-producing capacity depends upon at least 
four factors: (1) wave duration, (2) acceleration 
level, (3) distribution of acceleration, and (4) 
energy per wave. Fraser and Manning [2746) 
1950 have examined the effects of variation in swing 
radius and arc upon the incidence of swing sickness. 
The incidence of swing sickness increased from 4 to 
58 percent when the frequency was decreased from 
22 per minute on a 6-foot swing to 15 per minute on 
a 16-foot swing. The incidence was reduced from 
50 to 22 percent by reducing the oscillation angle 
from 90° to 50°, or by a g change from 0.9 to 0.25. 
Increasing the angle from 90° to 130° did not in- 
crease the incidence of swing sickness. The authors 
suggested that the tangential component of force on 
the swing was necessary for the production of motion 
sickness. 
Body and head position affect susceptibility to 
motion sickness. Manning and Stewart [2763) 1942 
and [2764) 1949 concluded from a series of 1005 
swing experiments carried out on 825 men swung 
in 14 various body positions, that the maximal inci- 
dence of swing sickness occurs in the sitting position 
with the subject completely inclosed in a cabinlike 
arrangement. The minimal incidence occurred in 
the supine position with the eyes open. Apprehen- 
sion, time of day, and meals did not appear to be 
factors affecting the occurrence of swing sickness. 
These experiments, according to the authors, sup- 
port the view that motion sickness is primarily a 
labyrinthine disturbance which tends to be sup- 
pressed or compensated by visual orientation. 
Stewart and Manning [2776) 1943 stated that the 
sitting position with the head tilted back 90° from 
the horizontal is the least susceptible position on the DISEASES AND ACCIDENTS 
four-pole swing. Hewlett, Wardill, and Brett {2753) 
1943 carried out swing tests on 50 unselected air- 
crew trainees who were swung through an angle of 
80° in the supine position with the head resting 
on the middle of the occiput and the reference plane 
perpendicular to the swing base. These trainees were 
also swung in the supine position through an angle 
of 62° with the head rotated backwards so that the 
reference plane formed an angle of 13° with the 
base of the swing. The incidence of swing sickness 
was low when the subjects were swung through an 
angle of 80° in the supine position with the head 
resting on the middle of the occiput and with the 
reference plane perpendicular to the swing base. 
According to Johnson, Stubbs, Kelk, and Franks 
{2754) 1951, individual susceptibility to motion 
sickness produced by a simple harmonic swing 
shows a significant correlation with the degree of 
concomitant head movement. Swing sickness, ac- 
cording to the authors, can be almost totally over- 
come by preventing this head movement. 
Regarding the sensory and central nervous 
mechanisms involved in motion sickness, a number 
of studies have been reported which are contribu- 
tory. For such studies, papers by the following 
should be consulted: Barany {2734) 1910 and 
{2735) 1912; Bard {2736) 1945 and {2737) 1946; 
Bard, Woolsey, Snider, Mountcastle, and Bromiley 
{2738) 1947; Borison and Wang {2740) 1949; 
Hewlett and Brett (2752) 1943; McNally {2758) 
1944 and {2759) 1947; McNally and Stuart {2760) 
1942; McNally, Stuart, and Morton {2761) 1942; 
Meda {2766) 1947; Morales {2767) 1946; Oka- 
wachi (2777) 1951; Palmisano (2772) 1951; Spie- 
gel {2774) 1946; Spiegel, Oppenheimer, Henny, 
and Wycis (2775) 1944; Trotter (2777) 1946; 
Wang and Borison {2778) 1950; and Wendt {2779) 
1951. The paper by Wendt (2779) is particularly 
useful as an excellent review of the history and de- 
velopment of research on vestibular functions. 
The reports by Bard and colleagues {2736, 2737 
and 2738) are of especial interest as casting fresh 
light upon the central nervous mechanisms. The role 
of the cerebral cortex was evaluated and tested 
{2736) and it was found that temporal, occipital, 
and parietal areas are not essentially involved in the 
motion-sickness mechanism. Bilateral temporal lo- 
bectomy, removal of both frontal poles, or ablation 
of all the neocortex except one or both frontal poles 
did not significantly alter susceptibility to motion 
sickness. The effect of complete decortication was 
not determined {2738). Decerebration by removing 
a wedge of tissue rostral to a plane passing from 
the anterior colliculi to a level just behind the mam- 
millary bodies did not alter the emetic response to 
swing tests between 26 and 53 days following the 
operation. After uncomplicated removal of the en- 
tire cerebellum, a highly susceptible dog failed to 
vomit or show any premonitory symptoms in 15 
tests carried out during a survival period of 17 
months. Removal of the nodulus and uvula rendered 
very susceptible dogs immune, but did not affect 
the emetic response to apomorphine {2737). 
A number of experimental investigations have 
been carried out to study physiological and chemi- 
cal changes associated with motion sickness. For 
the most part, these studies have not yielded sig- 
nificant correlations that would permit the use of a 
physiological or chemical change in prediction of 
motion-sickness susceptibility. Cipriani and Morton 
{2743) 1942 found no constant or significant 
changes in heart rate, blood pressure, or respira- 
tory rate as a result of motion. According to Best, 
Sellers, and Stephenson {2739) 1942, motion sick- 
ness does not cause a significant change in the acid- 
base balance in dogs. The level of ionized calcium 
does not seem to be connected in any way with the 
susceptibility of a dog to motion sickness. The 
potassium ion showed a slight decrease in dogs 
subjected to motion. High potassium or high so- 
dium diet had no apparent effect on the suscepti- 
bility of dogs to motion sickness. There seemed to 
be a slight increase in plasma protein in motion- 
sick dogs, especially those that salivated profusely. 
There appeared to be little evidence to support 
chemical changes in the blood as important causes 
of motion sickness. According to Fields, Meakins, 
and McEachern {2745) 1942, there was no change 
in blood sugar, calcium, phosphorus, sodium, or 
potassium before and after motion in human sub- 
jects. Meakins, Morton, and McEachern {2765) 
1942 found no changes in the carbon dioxide con- 
tent, oxygen content, oxygen capacity, or oxygen 
saturation in pre- and post-motion specimens of 
arterial dog blood. These same findings were re- 
ported in 1942 by McEachern and Lehmann 
(2757). Morton, Cipriani, and McEachern {2769) 
1947 reported that determinations of the sugar, 
phosphorus, and various bases in the blood in human 
subjects showed a moderate increase in sugar and 
a reduction of phosphorus as a result of motion. 
These changes occurred whether or not the subject 
became sick. They were attributed possibly to the 
liberation of epinephrine, due to motion or appre- 
hension. Studies of gases in the arterial blood of 
animals revealed no significant changes as a result 
of motion. Cholinesterase determinations were 
carried out before and after swinging in human 
subjects who became motion sick in experiments 
carried out by Manning {2762). No significant MOTION SICKNESS—MECHANISMS 
2731-2763 
differences in cholinesterase activity before and 
after swing sickness in both airsick-susceptible and 
nonairsick individuals were found. For other studies 
on cholinesterase activity and its possible relation 
to motion sickness, papers by Himwick, Essig, 
Hampton, Bales, and Freedman {2751) 1949, and 
Laborit and Morand {2755) 1946 may be 
consulted. 
For other reports on the mechanisms of motion 
sickness, papers by the following should be con- 
sulted : Alexander, Cotzin, Hill, Ricciuti, and 
Wendt {2732) 1945; Bortolotti {2741) 1940; 
Hemingway {2749) 1943 and (2750) 1946; and 
Landahl {2756) 1950. 
2731. Alexander, S. J., M. Cotzin, C. J. Hill, Jr., E. A. 
Ricciuti, and G. R. Wendt. Wesleyan University studies 
of motion sickness: I. The effects of variation of time 
intervals between accelerations upon sickness rates. /. 
Psychol., 1945, 19: 49-62. [P] 
2732. Alexander, S. J., M. Cotzin, C. J. Hill, Jr,, E. A. 
Ricciuti, and G. R. Wendt. Wesleyan University studies 
of motion sickness: V. Incidence of sickness at various 
hours of the day. J. Psychol., 1945, 20: 19-24. [P] 
2733. Alexander, S. J., M. Cotzin, J. B. Klee, and 
G. R. Wendt. Studies of motion sickness: XVI. The 
effects upon sickness rates of waves of various frequencies 
but identical acceleration. /. exp. Psychol., 1947, 37: 
440-448.[P] 
2734. Barany, R. Versuche zur Erklarung der See- 
krankheit. Mschr. Ohrenheilk., 1910, 44: 723-725. [D] 
2735. Barany, R. Die Seekrankheit. pp. 864-873 in: 
Handbuch Der Neurologie. Dritter Band Spezielle Neurol- 
ogie II. Edited by M. Lewandowsky. Berlin, Verlag Von 
Julius Springer. 1912, 1165 pp. [D] 
2736. Bard, P. Physiological investigation of causes and 
nature of motion sickness. U. S. NRG—CAM. OEMcmr— 
257, C. A. M. rept. no. 485, 30 September 1945, 12 pp. 
IP] 
2737. Bard, P. Motion sickness. Johns Hopk. Hasp. 
Bull, 1946, 79: 359-360. [P] 
2738. Bard, P., C. N. Woolsey, R. S. Snider, V. B. 
Mountcastle, and R. B. Bromiley. Delimitation of central 
nervous mechanisms involved in motion sickness. Fed. 
Proc. Amer. Soc. exp. Biol, 1947, 6: 72. [P] 
2739. Best, C. H., E. A. Sellers, and N. R. Stephenson. 
Seasickness—animal experiments. Canada NRG. Proceed- 
ings of conference on motion sickness. Project C735, 28 
August 1942, 21 pp. [P] 
2740. Borison, H. L., and S. C. Wang. Localization of 
the central nervous mechanism of emesis. Fed. Proc. Amer. 
Soc. exp. Biol, 1949,8; 13. 
2741. Bortolotti, R. II VII nel punto di passaggio 
dalla seconda alia sua terza porzione. Rass. ital. Oto- 
rinolaring., 1940, 14: 11-32. 
2742. Byrne, J. On the physiology of the semicircular 
canals and their relation to seasickness. New York, J. T. 
Dougherty, 1912, 569 pp. 
2743. Cipriani, A., and G. Morton. Studies of blood 
pressure, electrocardiograms, and respiratory tracings in 
volunteers. Canada NRC. Proceedings of conference on 
motion sickness. Project C744, 28 August 1942, 3 pp. [P] 
2744. Cojazzi, L. Attuali canoscenze sulla patogenesi 
del mal di mare. Clin, otorinolaring., 1950, 2; 357-383. 
2745. Fields, W. S., J. C. Meakins, and D. McEachern. 
Blood chemistry studies in motion sickness. Canada NRC. 
Proceedings of conference on motion sickness. Project 
C740, 28 August 1942, 2 pp. [P] 
2746. Fraser, A. M. and G. W. Manning. Effect of 
variation in swing radius and arc on incidence of swing 
sickness. /. appl. Physiol., 1950, 2: 580-584. 
2747. Harbert, F. and M, Schiff. Motion sickness. 
Armed Forces med. J., 1950, 1: 979-984. [D] 
2748. Hatcher, R, A. The mechanism of vomiting. 
Physiol. Rev., 1924, 4: 479-504. [R] 
2749. Hemingway, A. The effect of environmental tem- 
perature on motion sickness. U. S. AAF. Randolph Field, 
Tex. School of aviation medicine. Project 170, Kept. no. 3, 
2 November 1943, 4 pp. [P] 
2750. Hemingway, A. Environmental temperature and 
swing sickness. J. Aviat. Med., 1946, 17: 86-88; 99. [P] 
2751. Himwich, H. E., C. F. Essig, J. L, Hampson, 
P. D. Bales, and A. M. Freedman. Cholinergic nature 
of the vestibular receptor mechanism; forced circling 
movements (motion picture). Fed. Proc. Amer. Soc. exp. 
Biol., 1949, 8: 75. 
2752. Hewlett, J. G. and J. B. Brett. A speculation 
on the mechanism of utricular response to stimulation in 
motion sickness. Canada NRG. Proceedings of conference 
on motion sickness. Project C2509, 7 May 1943, 6 pp. [P] 
2753. Hewlett, J. G., T. E. M. Wardill, and J. B. Brett. 
The effect of position on the incidence of swing sickness. 
Canada NRC. Proceedings of conference on motion sick- 
ness. Project C2508, 7 May 1943, 6 pp. [P] 
2754. Johnson, W. H., B. A. Stubbs, G. F. Kelk, and 
W. B. Franks. Stimulus required to produce motion sick- 
ness. I. Preliminary report dealing with importance of 
head movements. /. Aviat. Med., 1951, 22: 365-374. 
2755. Laboria, H. and P. Morand. L’activite choli- 
nesterasique et son role probable dans le mal de mer. Rev. 
Med. nav., 1946, 1: 23-24. 
2756. Landahl, H. D. An application of the theory of 
neural nets to the study of motion sickness. Bull. math. 
Biophys., 1950, 12: 353-357. [M] 
2757. McEachern, D. and P. Lehmann. Summary of 
reports presented to committee on motion sickness. Canada 
NRC. Proceedings of conference on motion sickness. Proj- 
ect C751, 9 September 1942, 9 pp. [R] 
2758. McNally, W. J. Recommendation for further in- 
vestigation to be carried on in solving the problem of 
motion sickness. Canada NRC. Proceedings of third meet- 
ing of associate committee on naval medical research. 
Project C4063, 15 May 1944, 1 p. 
2759. McNally, W. J. The physiology of the vestibular 
mechanism in relation to vertigo. Ann. Otol., etc., St. 
Louis, 1947, 56: 514-533. 
2760. McNally, W. J. and E. A. Stuart. Physiology of 
the labyrinth reviewed in relation to seasickness and other 
forms of motion sickness. War Med., Chicago, 1942, 2: 
683-771. [R] 
2761. McNally, W. J., E. A. Stuart, and G. Morton. 
Effect of labyrinthectomy on motion sickness in animals. 
Canada NRG. Proceedings of conference on motion sick- 
ness. Project C748, 28 August 1942, 1 pp. [P] 
2762. Manning, G. W. Choline esterase activity in 
relation to airsickness. Canada NRC. Proceedings of con- 
ference on motion sickness. Project C2513, 1 p. (sum- 
mary.) [P] 
2763. Manning, G. W. and W. G. Stewart. The effect 
of position on the incidence of swing sickness. Canada 
291222-54- 17 2764-2780 
DISEASES AND ACCIDENTS 
NRC. Proceedings of conference on motion sickness. Proj- 
ect C2511,12 December 1942, 2 pp. [P] 
2764. Manning, G. W. and W. G. Stewart. Effect of 
body position on incidence of motion sickness. /. appl. 
Physiol, 1949, 1: 619-627. [P] 
2765. Meakins, J. C., G. Morton, and D. McEachern. 
Studies of blood gases in animals. Canada NRC. Proceed- 
ings of conference in motion sickness. Project C747, 28 
August 1942, 2 pp. [P] 
2766. Meda, E. Effetti di ripetuti eccitamenti rotatori 
dell’apparato vestibolare sui fenomeni soggettivi da cam- 
biamento di posizione del capo durante e dopo la rota- 
zione. Riv. Med. aero., Roma, 1947, 10: 316-323. (Italian, 
English, French, Spanish, and German summaries.) 
2767. Morales, M. F. Asynchrony of labyrinthine re- 
ceptors as a physical factor in motion sickness. Bull. math. 
Biophys., 1946, 8: 147-157. [M] 
2768. Morales, M. F. Motion sickness: physical con- 
siderations regarding its etiology, pp. 399-414 in: A 
survey report on human factors in undersea warfare. 
Washington, D. C., National Research Council, 1949, 
541 pp. 
2769. Morton, G., A. Cipriani, and D. McEachern. 
Mechanism of motion sickness. Arch. Neurol Psychiat., 
Chicago, 1947, 57: 58-70. 
2770. Noble, R. L. Observations on various types of 
motion causing vomiting in animals. Canad. J. Res., 1945, 
23 (E-F): 212-225. 
2771. Okawachi, K. Experimental study on labyrinthine 
vomiting. Nippon zibiinkoka gakkai kaiho, 1951, 54: 
(Japanese text pagination), 1-8; (English text pagina- 
tion), 1. (In Japanese with English summary.) [P] 
2772. Palmisano, C. Studio del tono labirintico e dei 
riflessi vegetativolabirintico in soggetti imbarcati su navi 
di superficie e studio delle variazioni dell’eccitabilita 
vestibolare per lo stimolo fisico di movimenti nave nella 
naupatia. Ann. Med. nav. trap., 1951, 56: 424-446. 
2773. Sjdberg, A. A. Experimentelle Studien iiber den 
Auslosungsmechanismus der Seekrankheit. Acta oto- 
laryng., Stockh., Suppl, 1931, 15: 136 pp. (English sum- 
mary.) [P] [R] 
2774. Spiegel, E. A. Effect of labyrinthine reflexes on 
the vegetative nervous system. Arch. Otolaryng., Chicago, 
1946, 44: 61-72. [R] 
2775. Spiegel, E. A., M. J. Oppenheimer, G. C. Henny, 
and H. T. Wycis. Experimental production of motion 
sickness. War Med., Chicago, 1944, 6: 283-290. 
2776. Stewart, W. G. and G. W. Manning. The effect 
of tilting the head back on the incidence of sickness on 
the four-pole swing. Canada NRG. Proceedings of con- 
ference on motion sickness. Project C25I0, 1 June 1943, 
2 pp. 
2777. Trotter, W. R. Sea sickness. Practitioner, 1946, 
157:45-49. [R] 
2778. Wang, S. C. and H. L. Borison. The vomiting 
center; a critical experimental analysis. Arch. Neurol. 
Psychiat., Chicago, 1950, 63: 928-941. XVIII Intern, 
physiol. Congr., 1950, 503—504. Excerpt a Medica. Sec- 
tion II. (Physiology, Biochemistry, and Pharmacology), 
1951,4; 1129. 
2779. Wendt, G. R. Vestibular functions, pp. 1191- 
1223 in: Stevens—Handbook of experimental psychology. 
New York, John Wiley & Sons, Inc., 1951, xi. 1436 
pp. [R] 
E. EFFECT OF MOTION SICKNESS ON 
PERFORMANCE 
Practical experience under combat conditions re- 
veals that motion sickness may seriously impair per- 
formance. This performance deficit is, however, 
difficult to demonstrate significantly under labora- 
tory test conditions. Effects of exposure to experi- 
mental motion upon performance of laboratory 
motor performance tests have been studied by Alex- 
ander, Cotzin, Hill, Ricciuti, and Wendt {2780) 
1945. Certain performance tests were administered 
to human subjects before and after exposure to mo- 
tion on the vertical accelerator. The data were 
analyzed to determine whether those who became 
motion sick showed deficits in performance. Of four 
tests used, only one, the Mashburn Complex Co- 
ordinator, showed a statistically reliable harmful 
effect of motion sickness, the obtained deficit being 
about 4 percent. These results were interpreted by 
the authors as indicating that brief exposure to 
motion for 20 minutes or until vomiting occurred 
probably had no important effects upon laboratory 
motor performance tests. 
2780. Alexander, S. J., M. Cotzin, C. J. Hill, Jr., E. A. 
Ricciuti, and G. R. Wendt. Wesleyan University studies 
of motion sickness. VII. The effects of sickness upon per- 
formance. /. Psychol., 1945,20; 31-39. 
F. PREVENTION AND TREATMENT OF MOTION 
SICKNESS 
Search for effective motion-sickness-preventive 
drugs and effective combinations of these drugs has 
gone on for many years. Investigation of motion- 
sickness preventives was accelerated during World 
War II; and, as the reference list given below indi- 
cates, these studies are continuing unabated. A num- 
ber of drugs, such as hyoscine, dramamine, other 
antihistaminics, and the barbiturates, are recognized 
as effective. Some studies seem to indicate that cer- 
tain combinations of these drugs may be particularly 
effective, and other synthetic substances have also 
been under test. While these substances may reduce 
the incidence of motion sickness, they may produce 
undesirable side effects, such as somnolence, which 
may render personnel unfit for various types of 
military duty while under the influence of the drugs. 
For example, it is not desirable that aviators be in 
the actual control of aircraft while under the in- 
fluence of motion-sickness-preventive drugs. Passen- 
gers in aircraft, surface vessels, and submarines may 
safely take motion-sickness drugs, provided that the 
effects of these substances will have worn off by the 
time such personnel are required to carry out essen- 
tial military duties. For papers on the general sub- MOTION SICKNESS—PREVENTION 
2781-2803 
ject of prevention and treatment of motion sickness, 
the following references may be consulted: 2782, 
2788, 2789, 2790, 2793, 2794, 2795, 2803, 2804, 
2810, and 2812. 
The use of hyoscine has been investigated as indi- 
cated in the following references: 2784, 2785,2792, 
2796, 2797, 2800, 2802, 2806, 2807, 2808, 2809, 
2813, 2815, 2819, 2825, 2832, 2833, 2838, 2839, 
2840, 2841, 2842, 2843, 2848, 2849, 2854, 2855, 
2856, 2857, 2858, 2859, 2863, 2864, 2874, 2876, 
2882,2883,2885,2886,2890,2891,2893, and 2894. 
For studies on dramamine, the following refer- 
ences are given: 2805,2818,2821,2822,2823,2826, 
2836, 2837, 2844, 2845, 2847, 2865, 2866, 2868, 
2871, 2872, 2873, 2887, 2888, 2889, 2896, 2898, 
2900, and 2901. 
Studies on other antihistaminic drugs are given 
in the following references: 2798, 2799, 2801, 2820, 
2831, 2834, 2835, 2860, 2867, 2873, 2884, 2895, 
and 2899. 
The barbituric acid derivatives have been used 
singly and in combination with other substances. 
Studies on these compounds are reported in the 
following references: 2814, 2829, 2850, 2852, 2853, 
2861, 2879, 2880, 2881, and 2892. 
The following substances have also been used in 
the prevention of motion sickness: pyridoxine 
{2878), sodium bicarbonate and other inorganic 
compounds {2787, 2817 and 2828, and bromides 
{2786). 
For other studies on motion-sickness prevention, 
the following references may be consulted: 2781, 
2791, 2811, 2816, 2824, 2827, 2830, 2846, 2851, 
2862, 2869, 2870, 2875, 2877, and 2897. 
2781. Albrecht, F. K. A therapeutic evaluation of ben- 
zedrine sulfate in the treatment of seasickness: results in 
100 cases. Med. Clin. N. Amer., 1943, Philadelphia 
number; 1652—1658. 
2782. Alvarez, J. S. A. Estado actual de la fisiopatologia 
y tratamiento del mal de mar. Medicina, Madr., 1949, 
17: 223-235. 
2783. Ambrus, J. L, and C. M. Ambrus. Motion sick- 
ness and antihistamines, Lancet, 1950, 258: 326. Excerpta 
Medica, Section II. {Physiology, Biochemistry, and Phar- 
macology), 1950, 3: 969. 
2784. Amouroux, P. Traitement du mal du mer par les 
seasickness tablets. Rev. Med. nav., 1947, 2: 167-168. 
[D] 
2785. Armstrong, H. G. Treatment of air sickness. Post- 
grad. Med., 1950, 8: 55-56. [D] 
2786. Babkin, B. P. and M. Schachter. The effect of 
cortical-inhibitory drugs and the effect of decortication 
in dogs susceptible to motion sickness. A preliminary re- 
port. Canada NRC. Proceedings of second meeting of 
associate committee on naval medical research. Project 
C4059. 7 October 1943,4 pp. [P] 
2787. Beckman, Harry. Prevention of motion sickness 
by intravenous injection of sodium bicarbonate, pp. 390- 
392 in: The 1950 Year Book of Drug Therapy. Chicago. 
The Year Book Publishers, Inc., 1951, 566 pp. [P] 
2788. Beckman, Harry. Effectiveness of newer drugs 
in seasickness, pp. 392-394 in: The 1950 Year Book of 
Drug Therapy. Chicago. The Year Book Publishers, Inc., 
1951, 566 pp. 
2789. Beckman, Harry. Effectiveness of various drugs in 
prevention of airsickness, pp. 394 in: The 1950 Year 
Book of Drug Therapy. Chicago. The Year Book Pub- 
lishers, Inc., 1951, 566 pp. [P] 
2790. Birren, J. E., R. T. Stormont, and M. B. Fisher. 
Side effects of three motion sickness preventives. U. S. 
Navy. NMRI. Project X-278, Kept. no. 1. 26 June 1944, 
7 pp. [P] 
2791. Birren, J. E., R. T. Stormont, and C. C. Pfeiffer. 
An evaluation of the potentiality of bulbocapnine as a 
motion sickness preventive. U. S. Navy. NMRI. Project 
X-278, Rept. no. 3. 16 August 1944, 5 pp. [D] 
2792. Boland, J. D, and A. D. Grinstad. Comparison of 
scopolamine hydrobromide and dramamine in the treat- 
ment and prevention of airsickness. /. Aviat. Med., 1951, 
22: 137-145. 
2793. Chinn, H. I. Motion sickness in the military serv- 
ice. Milit. Surg., 1951,108: 20-29. 
2794. Chinn, H, I. Motion sickness. USAF. Randolph 
Field, Tex. School of aviation medicine. Special Report, 
December 1951, 8 pp. 
2795. Chinn, H. I., W. K. Noell, and P. K. Smith. 
Prophylaxis of motion sickness: evaluation of some drugs 
in seasickness. USAF. Randolph Field, Tex. School of 
aviation medicine. Project 21—32-014, Rept. no. 4 (for- 
merly Project 21-02-169), October 1950, 20 pp. Arch, 
intern. Med., 1950, 86: 810. [P] 
2796. Chinn, H. I. and F. W. Oherst. Effectiveness of 
various drugs in prevention of airsickness. Proc. Soc. exp. 
Biol., N. Y., 1950, 73: 218-219. [P] 
2797. Chinn, H. I. and F. W. Oherst. Effectiveness of 
various drugs in prevention of airsickness. 1. Effects of 
chemical components of dramamine. USAF, Randolph 
Field, Tex. School of aviation medicine. Project 21-32- 
014 {formerly project 21-02-169), Rept. no. 1, August 
1950, 5 pp. [P] 
2798. Chinn, H. I., F. W. Oherst, and S. S. Wilks. Anti- 
histaminics and motion sickness prophylaxis. Tex. Rep. 
Biol. Med., 1950, 8: 320-325. 
2799. Chinn, H. I., F. W. Oherst, and S. S. Wilks. Effec- 
tiveness of various drugs in prevention of airsickness. III. 
Study of additional antihistaminics in airplane and 
swing. USAF. Randolph Field, Tex. School of aviation 
medicine. Project 21-32-014 {formerly project 21-02- 
169), Rept. no. 3, August 1950, 7 pp. [P] 
2800. Chinn, H, I. and B. A. Strickland, Jr. Effective- 
ness of various drugs in prevention of airsickness. II. Com- 
parison of hyoscine with benadryl-hyoscine mixture during 
navigation training flights. USAF. Randolph Field, Tex. 
School of aviation medicine. Project 21-32-014, Rept. no. 
2 {formerly project 21-02-169), December 1950, 3 pp. 
[P] 
2801. Chinn, H. I., B. A. Strickland, F. W. Oherst, S. S. 
Wilks, and M. Tinkham. Evaluation of some drugs in 
motion sickness. /. Aviat. Med., 1950, 21: 424-429. [P] 
2802. Chinn, H. I., B. A. Strickland, 0. H. Waltrip, 
and S. H. Gainer. Prevention of airsickness by benadryl- 
scopolamine mixtures. USAF Med. /., 1951, 2: 401-404. 
2803. Chinn, H. I., 0. H. Waltrip, and H. W. Massen- 
gale. Further studies on the effectiveness of various drugs 
against airsickness. J. Aviat. Med., 1951, 22: 535-539. 2804-2842 
DISEASES AND ACCIDENTS 
2804. Chinn, H. I., 0. H. Waltrip, and H. W. Massen- 
gale. Effectiveness of various drugs in prevention of air- 
sickness. V. Comparison of additional preparations in air- 
craft. USAF. Randolph Field, Tex. School of aviation 
medicine. Project 21-32-014, Rept. no. 5, July 1951, 
4 pp. 
2805. Christiansen, M. Experience with “dramamine,” 
“ncptusan” in seasickness. Ugeskr. Laeg., 1950, 112: 86- 
87. Excerpta Medica. Section II. (Physiology, Biochem- 
istry, and Pharmacology), 1950, 3: 969. 
2806. Corning, J. L. The suppression of rotary vertigo; 
its bearing on the prevention and cure of seasickness. N. Y. 
med. J., 1904, 80: 297-299. 
2807. Crosfill, J. W. L., E. M. Glaser, and G. R. Hervey. 
The prevention of seasickness by various drugs, Report on 
tests at sea. Gt. Brit. MRG-RNPRC, SS. R. N. P. 51/653, 
S. S. 40. 14 pp. [P] 
2808. Crosfill, J. W. L., E. M. Glaser, and 6. R. Hervey. 
Further experiments on the prevention of motion sickness. 
Report on tests carried out in Portobello Bathing Pool. 
Gt. Brit. MRC-RNPRG, SS. R. N. P. 51/679, S. S. 43, 
October 1951, 20 pp. [P] 
2809. Damrau, F. Motion sickness and its relief. Med. 
World. Phil ad., 1947, 65: 353-354, 356, and 386. Med. 
Rec., N. Y., 1947, 160: 408-412. 
2810. Duguet, J. Trois consultations avant un voyage 
cn avion. Maroc med., 1949, 28: 325-333. 
2811. Elliott, K. A. C. and Noble, R. L. Control of car 
sickness in a dog by V-12 (mosidal). Canad. med. Ass. ]., 
1948, 59: 277. 
2812. Engquist, S. Ett nytt svenskt sjosjukemedel. [A 
new Swedish remedy for seasickness.] Svenska Lakartidn., 
1950, 47: 1464-1467. [P] 
2813. Evans, R. G. The prevention and treatment of 
travel sickness. Med. World, Land., 1947, 66: 300—302. 
2814. Fields, W. S. Therapeutic trials with barbiturates 
and vasano compounds. Canada NRC. Proceedings of 
conference on motion sickness. Project C4034, 16 June 
1943.2 pp. 
2815. Fields, W. S. Further therapeutic trials with bella- 
donna alkaloids. Canada NCR. Proceedings of conference 
on motion sickness. Project C4035, 16 June 1943, 4 pp. 
[P] 
2816. Fields, W. S. Observations of seasickness trials of 
U. S. Pacific Coast. Canada NRC. Proceedings of the 
fourth meeting of associate committee on naval medical 
research. Project C4117, 16 February 1945, 2 pp. [P] 
2817. Fields, W. S. and W. Penfield. Preliminary thera- 
peutic experiments. Canada NRC. Proceedings of con- 
ference on motion sickness. Project C741, 28 August 
1942.3 pp. [P] 
2818. Fleming, J. F. New drug effective in motion 
sickness. Hasp, topics and buyer., 1949, 27: 26-28. 
2819. Foucar, F. H., B. S. Gordon, and S. Kaye. Fatal 
poisoning from motion sickness preventive. /. Amer. med. 
Ass., 1946,137: 971-972. [CH] 
2820. Frinberg, S. M., S. Malkiel, and A. R. Feinberg. 
Motion sickness, nausea and vomiting, pp. 159—161 in: 
The antihistamines. Chicago, Year Book Publishers, Inc., 
1950, 291 pp. 
2821. Gay, L. N. A subsequent report on dramamine. 
The prophylactic and therapeutic control of motion sick- 
ness and vestibular disturbances. Milit. Surg., 1951, 108: 
324-331. 
2822. Gay, L. N. and P. E. Carliner. The prevention 
and treatment of motion sickness. Bull. Johns-Hopkins 
Hasp., 1949, 84: 470-487. 
2823. Gay, L. N. and P. E. Carliner. Motion sickness, 
p. 529 in: Current Therapy. Edited by Howard F. Conn. 
Philadelphia, W. B. Saunders Co., 1951, pp. 699. 
2824. Gibson, W. C., G. W. Manning, and B. Kirkpat- 
rick. The effect of active vestibular training on motion 
sickness. Canada NRC. Proceedings of conference on 
motion sickness. Project C2512, 2 pp. [P] 
2825. Gt. Brit. MRC-RNPRC, SS. Minutes of the 9th 
meeting. R. N. P. 51/684, S. S. 46. 14 November 1951, 
6 pp. 
2826. Gutner, L. B., W. J. Gould, and R. C. Batterman. 
Action of dimenhydrinate (dramamine) and other drugs 
on vestibular function. Arch. Otolaryng., Chicago, 1951. 
53: 308-315. 
2827. Harper, J. and M. B. Belf. Prevention and treat- 
ment of travel sickness with promethazine chlorotheophyl- 
linate. Lancet, 1951, 1: 1141-1143. 
2828. Hasegawa, T. Prevention of motion sickness by 
intravenous injection of sodium bicarbonate. Arch. Oto- 
laryng., Chicago., 1949, 50: 708-715. 
2829. Hemingway, A. and P. K. Smith. Effect of bar- 
bital on swing sickness. U. S. AAF. Randolph Field, Tex. 
School of aviation medicine. Project 104, Kept. no. I, 9 
January 1943, 4 pp. [P] 
2830. Hemingway, A. and P. K. Smith. Effect of vasano 
on swing sickness. U. S. AAF. Randolph Field, Tex. School 
of aviation medicine. Project 110, Kept. no. 1, 2 March 
1943, 3 pp. [P] 
2831. Heully, M. F. Action d’un antihistaminique de 
synthese dans le mal des transports. Rev. med. Nancy, 
1951, 76: 258-261. 
2832. Holling, H. E. Wartime investigations into sea- 
and air-sickness. Brit. med. Bull., 1947/48, 5; 46-50. J. 
industr. Hyg., 1948, 30: abstract section: 71. [P] 
2833. Holling, H. E., B. McArdle, and W. R. Trotter. 
Prevention of seasickness by drugs. Lancet., 1944, 246: 
127-129. [P] 
2834. Hunter, R. B. and D. M. Dunlop. A review of 
antihistamine drugs. Quart. J. Med., 1948, 17: 271—290. 
[R] 
2835. Johns, R. J. and H. E. Himwich. A central action 
of some antihistamines. Correction of forced circling 
movements and of seizure brain waves produced by the 
intracarotid injection of di-isopropyl fluorophosphate. 
Amer. J. Psychiat., 1950,107: 362-372. [P] 
2836. Klayman, M. I. Dramamine vs. motion sickness. 
Tufts med. J. 1950,17: 56-58 and 70. 
2837. Lessard, R. Dramamine. Pour la prophylaxie et le 
traitement de la maladie des transports. Laval med., 1949, 
14: 809-811. 
2838. Lilienthal, J. L. The effect of hyoscine on motion 
sickness in aircraft. U. S. Navy. NATO., Pensacola, Fla. 
School of aviation medicine. Project X-252 (Av-138-6), 
1 May 1944, 8 pp. 
2839. Lilienthal, J. L., Jr. The effect of hyoscine on 
airsickness. /. Aviat. Med., 1945, 16: 59—68. [P] 
2840. Lilienthal, J. L. The effect of hyoscine on motion 
sickness in aircraft: individual therapy of motion sus- 
ceptible subjects. U. S. Navy. NATC., Pensacola, Fla. 
School of aviation medicine. Project X-252 (Av-138-6), 
2 March 1945, 5 pp. [P] 
2841. Longmore, D. B. Travel sickness. Guy’s Hasp. 
Gaz., 1950, 64: 237-240. [D] 
2842. Luykx, H. M. C. Motion sickness preventives. 
Canada NRC. Proceedings of third meeting of associate 
committee on naval medical research. Project C4066, 
Rept. no. 1,15 May 1944, 9 pp. MOTION SICKNESS—PREVENTION 
2843-2880 
2843. Luykx, H. M. C. Motion sickness preventives. 
Canada NRC. Proceedings of third meeting on naval 
medical research. Project C4067, Rept. no. II. 15 May 
1944, 6 pp. 
2844. M, H. J. L. Recent studies on the treatment of 
motion sickness. Ann. intern. Med., 1951, 35: 1383-1389. 
2845. MacKay, R. A. and J. K. W. Ferguson, Influence 
of certain antimotion-sickness drugs on psyshomotor and 
mental performance. J. Aviat. Med., 1951, 22: 194-195. 
2846. Merrell, M. Analysis of Dr. David B. Tyler’s ex- 
periments on motion sickness remedies, by individual boats, 
June 1-December 5, 1944. U. S. NRC-CAM. C. A. M. 
rept. no. 408, January 1945, 9 pp. 
2847. Montandon, A. Existe-t-il une prophylaxie du mal 
de mer, et d’une maniere generate du mal des transports? 
Rev. med. Suisse Rom., 1951, 71: 528—530. 
2848. Monto, R. W. Treatment of motion sickness. /. 
Mich. med. soc., 1947, 46: 1164-1168. 
2849. Moulis, A. La scopolamine dans le traitement du 
mal des voyages. Toulouse med., 1950, 51: 755-756. 
2850. Noble, R. L. Motion sickness in cats treated by 
barbiturate Canada NRG. Proceedings of 
conference on motion sickness. Project C695, 28 August 
1942, 8 pp. [P] 
2851. Noble, R. L. The prevention of motion sickness in 
experimental animals by treatment with VI. Canada 
NRC. Proceedings of conference on motion sickness. 
Project C737, 28 August 1942, 2 pp. [P] 
2852. Noble, R. L. The experimental use of barbiturates 
in motiqn sickness. Canada NRG. Proceedings of con- 
ference on motion sickness. Project C883, 16 June 1943, 
2 pp. 
2853. Noble, R. L. Methods of assaying motion sickness 
preventives on dogs. Canad. J. Res., 1945, 23 (E-F): 
226-234. 
2854. Noble, R. L. Studies on experimental motion sick- 
ness. Bull. New Engl. med. Center, 1946, 8: 49—53. 
2855. Noble, R. L. Treatment of experimental motion 
sickness in humans. Canad. J. Res., 1946, 24 Section E: 
10-21. 
2856. Noble, R. L. Motion sickness; with special refer- 
ence to airsickness. Practitioner, 1948, 160: 453-458. [P] 
2857. Noble, R. L., E. A. Sellers, and C. H. Best. The 
treatment of motion sickness. Canad. med. Ass. ]., 1947, 
56: 417-424. [R] 
2858. Parker, J. M. Report of trials of seasickness 
remedies on board Canadian army transport, S. S. Lady 
Rodney. (Halifax to St. John’s, Newfoundland, and return, 
3 December-9 December 1943.) Canada NRC. Proceed- 
ings of third meeting of associate committee on naval 
medical research. Project X4068, 15 May 1944, 4 pp. [P] 
2859. Parker, J. M. Motion sickness studies at 
H. M. C. S. York. Canada NRC. Proceedings of the fourth 
meeting of the associate committee on naval medical re- 
search. C4116, 16 February 1945, 5 pp. [P] 
2860. Parker, J. M, and W. S. Fields. Report on trials 
of seasickness remedies conducted in the United Kingdom. 
Canada NRC. Proceedings of third meeting of associate 
committee on naval medical research. Project C4069, 15 
May 1944, 9 pp. [P] 
2861. Parker, J. M., W. S. Fields, and E. A. Sellers. 
Progress report on therapeutic trials conducted in Montreal 
and Toronto. Canada NRC. Proceedings of conference on 
motion sickness. Project C4036, 16 June 1943, 5 pp. 
2862. Parker, J. M,, W. S. Fields, E. A. Sellers, and 
C. H. Best. Report on sea trials with R. C. N. experimental 
seasickness remedy no. 1. Canada NRC. Proceedings of 
second meeting of associate committee on naval medical 
research. Project C4053, 7 October 1943, 7 pp. 
2863. Plichet, A. Le traitement du mal de 1’air. Pr. 
rued., 1949, 57: 892. [D] 
2864. Ricciardi, R. La sindrome naupatica. Attuali 
verdute in tema di patogenesi e di terapia. Diagnosi, 
Napoli., 1949, 5: 209-230. 
2865. Rust, S. M. and F. W. A. Foshery. Prevention of 
sea-sickness. Brit. med. /., 1949, 2: 98. [D] 
2866. Sabrie, R. La maladie des transports maritimes, 
terrestres, aeriens. Son importance aux armees, sa thera- 
peutique. Rev. gen. Clin., 1951, 65: 359—361. 
2867. Salter, W. T. Therapeutics and toxicology. Ann. 
rev. Med., 1950, 1: 391-413. [R] 
2868. Santesson, G. Det nya sjosjukemedlet B-dimet- 
hylamino-etylbens-hydryleter-8-klorteofyllinat. A new sea- 
sickness remedy (Almosyt ordramamine). Svenska Ldkar- 
tidn., 1949, 46: 2492-2496. 
2869. Schwab, R, S. Interim report on the study of 
chronic seasickness at the naval hospital. U. S. Navy. Naval 
Hospital, Chelsea, Mass. Project no. X-118 {Av-F10-2), 
3 March 1943, 8 pp. [P] 
2870. Sellers, E. A. Experiments on the dosages of 
various agents used to prevent or modify seasickness. 
Canada NRC. Proceedings of third meeting on naval medi- 
cal research. Project C4065, 15 May 1944, 5 pp. [P] 
2871. Shaw, C. C. Dramamine trials in the U. S. Navy. 
(Presented on 10 November 1949, before the 56th annual 
convention of the association of military surgeons, Wash- 
ington, D. G.) U. S. Navy. BuMed., Washington, D. G., 
17 pp. 
2872. Shaw, C. C. Dramamine trials in the United States 
Navy. Milit. Surg., 1950, 106: 441-449. [R] 
2873. Simon, S. W. and L. E. Seyler. Dramamine in 
pilots. /. Aviat. Med., 1949, 20: 371—379. Excerpta Med- 
ico. Section II. (Physiology, Biochemistry, and Pharma- 
cology.) 1950,5; 969. [D] 
2874. Smith, P, K. Effect of hyoscine (scopolamine) on 
swing sickness. U. S. NRC-CAM. C. A. M. rept. no. 156, 
19 April 1943, 4 pp. [P] 
2875. Smith, P. K, The effectiveness of some motion 
sickness remedies in preventing airsickness. U. S. AAF. 
Randolph Field, Tex. School of aviation medicine. Project 
261, Rept. no. I, 30 June 1944, 5 pp. 
2876. Smith, P. K. The effectiveness of some motion 
sickness remedies in preventing airsickness in navigation 
students. U. S. AAF. Randolph Field, Tex. School of 
aviation medicine. Project 261, Rept. no. 2, 18 January 
1945, 6 pp. [P] 
2877. Smith, P. K. Effects on swing sickness and side 
effects of some atropine-like drugs. U. S. AAF. Randolph 
Field, Tex. School of aviation medicine. Project 297, Rept. 
no. 1, 19 January 1945, 9 pp. [P] 
2878. Smith, P. K. Effect of pyridoxine hydrochloride 
on swing sickness. U. S. AAF. Randolph Field, Tex. 
School of aviation medicine. Project 333, Rept. no. 2, 
24 August 1945, 4 pp. [P] 
2879. Smith, P. K. Effect of various substances on swing 
sickness. Proc. Soc. exp. Biol., N. Y., 1946, 63: 209-210. 
[P] 
2880. Smith, P. K, Present status of drugs for use in 
motion sickness with particular reference to airsickness. 
U. S. AAF. Randolph Field, Tex. School of aviation medi- 
cine. Project 468, Rept. no. 1, 14 June 1946, 33 pp. 2881-2901 
DISEASES AND ACCIDENTS 
2881. Smith, P. K. Treatment of airsickness with drugs. 
Amer. J. Med., 1948, 4: 649-651. Excerpta Medico. Sec- 
tion II. (Physiology, Biochemistry, and Pharmacology), 
1949, 2: 661. Abstr. [R] 
2882. Smith, P. K. Effect of various substances on swing 
sickness. Excerpta Medico. Section II. (Physiology, Bio- 
chemistry, and Pharmacology), 1948, I: 186. Abstr. Proc. 
Soc. exp. Biol., N. Y., 1946, 63: 209-210. 
2883. Smith, P. K. and A. Hemingway. Effect of 
hyoscine (scopolamine) on swing sickness and on perform- 
ance. U. S. AAF. Randolph Field, Tex. School of aviation 
medicine. Project 111, Kept. no. 1, 2 March 1943, 7 pp. 
[P] 
2884. Smith, P. K. and A. Hemingway. Effect of some 
atropine-like drugs on swing sickness. Proc. Soc. exp. Biol., 
N. Y., 1946, 63: 206-208. [P] 
2885. Sollmann, Torald. Scopolamine (hyoscine). pp. 
321—324 in: A manual of pharmacology and its applica- 
tions to therapeutics and toxicology. Philadelphia. W. B. 
Saunders Co., 1948, 1132 pp. [R] 
2886. Spiegel, E, A. and A. Sokalchuk. Influence of 
medication upon blood pressure in seasickness. Fed. Proc. 
Amer. Soc. exp. Biol., 1947, 6: 209. [P] 
2887. Strickland, B. A. Jr. and G. L. Hahn. The 
effectiveness of dramamine in the prevention of airsick- 
ness. Science, 1949, 109: 359-360. [P] 
2888. Strickland, B. A., Jr., G. L. Hahn, and H. Adler. 
Studies on airsickness. J. Aviat. Med., 1950, 21: 90-97, 
163. Abstr. World Med., 1950, 8: 569-570. [P] 
2889. Strickland, B. A,, Jr,, G. L. Hahn, and H. Adler. 
Effects of dramamine on airsickness. USAF. Randolph 
Field, Tex. School of aviation medicine. Project 21-32- 
007, Kept. no. I, February 1951, 14 pp. 
2890. Tru, C. and C. Debrnille. The comparative 
toxicity and effectiveness of scopolamine hydrobromide 
(CiiHjiCbN-HBr) and scopolamine aminoxide hydro- 
bromid- fC„H2106N-HBr). Amer. J. Pharm., 1945, 117: 
319-326. [P] 
2891. Tyler, D. B. A comparison of the efficacy of motion 
sickness preventative, army development type, seasickness 
remedy, R. C. N. type, ND 0.6 mg. of hyoscine in pre- 
venting seasickness during landing craft operations. U. S. 
NRG-CAM. C. A. M. rept. no. 300, 20 April 1944, 6 pp. 
[P] 
2892. Tyler, D, B. A summary of the findings of the 
studies on motion sickness, fatigue and prolonged wake- 
fulness. U. S. NRC-CAM. OEMcmr-282, C. A. M. rept. 
no. 505, 15 December 1945, Abstr. 
2893. Tyler, D. B. The influence of a placebo, body 
position and medication on motion sickness. Amer. J. 
Physiol., 1946, 146: 458-466. [P] 
2894. Tyler, D. B. Effect on marksmanship of some 
motion sickness preparations containing barbiturates and 
hyoscine. J. appl. Physiol., 1950, 1: 737-742. 
2895. Van Proosdij-Hartzema, E. G. Dimenhydrinaat 
bij misselikjheid als symptoom van enige aandoeningen. 
[Dimenhydrinate in nausea of various etiology.] Geneesk. 
Gids., 1950, 3: 41-46, 
2896. Vogel, J. A field study of the therapeutic effect 
of dramamine. U. S. Navy. Submarine base, New London, 
Conn. Medical research laboratory. Project NM 002 
015.5.01, Rept. no. 172, 30 April 1951, 7 pp. [P] 
2897. Wendt, G. R. Special conference on seasickness 
remedies. Canada NRC. Proceedings of third meeting on 
naval medical research. Project C4064, 15 May 1944, 
5 pp. 
2898. Winston, J., A. Rubin, J. S. Lewis, and J. M. 
Rehherger. The effect of dramamine upon cochlear func- 
tion and the vestibular responses to turning in normal 
subjects. Ann. Otol., etc., St. Louis, 1950, 59: 622-630. [P] 
2899. Wright, W. L. Effectiveness of newer drugs in 
seasickness. Armed Forces med. J., 1950, 1: 570-577. [P] 
2900. Yetwin, I, J. Dramamine for prevention of air- 
sickness in airborne troops. Milit. Surg., 1950, 107: 453- 
455. 
2901. Anon. Prevention of seasickness. Brit. med. J., 
1949, 1: 855. [D] 
VIII. SUBMARINE ESCAPE PROBLEMS 
A. BREATH HOLDING 
All submariners, divers, and underwater swim- 
mers in the U. S. Navy are trained to use the 
submarine escape apparatus (referred to as the 
“lung”) at the escape training tank, Submarine 
Base, New London, Conn., or the Submarine Base, 
Pearl Harbor, T. H. Free escape, that is to say, 
escape without the use of any apparatus, is also 
practiced by the instructors at the escape training 
tanks and certain of the more proficient trainees. 
With regard to free escape, correct breath control 
is absolutely essential. The air in the lungs must 
be exhaled rather slowly to begin with, and then 
with steadily increasing volume so as to avoid 
dangerously high positive pressure in the lungs. If 
exhalation is impaired, there may be an excess 
pressure sufficient to tear the lung tissue. Too rapid 
exhalation slows the ascent rate and may destroy 
positive buoyancy. However, it is considered safer 
to err on the side of too rapid exhalation, since lost 
buoyancy can relatively easily be compensated for 
by swimming up a few strokes. The references on 
breath holding which follow have been included 
and are discussed here because of the manifest im- 
portance of breath control in escape and because 
from the literature on breath holding are to be 
derived data of importance needed for the design 
and operation of escape apparatus and underwater 
swimming gear. 
The breath-holding breakpoint at various in- 
creased pressures has been reported by Alvis {2904) 
1951. His investigation was undertaken to deter- 
mine what factors force a person to inspire when 
he voluntarily holds his breath. It was hypothesized 
that carbon dioxide accumulation might be the 
critical factor rather than blood pH or oxygen de- 
pletion when the partial pressure of oxygen was 
above some undetermined level. It was further 
hypothesized that the blood pH would not vary 
significantly under increased pressure or during a 
series of breath holds conducted within an elapsed 
time of 1 to 2 hours. Alveolar carbon dioxide 
tension was found to be a more consistent value SUBMARINE ESCAPE—ESCAPE PROCEDURES 
2902-2911 
at the breath-holding breakpoint than alveolar 
oxygen tension or duration of breath holding. This 
was found to be true for various increased ambient 
pressures. Subjects were found to be able to hold 
their breath after breathing air for longer periods 
and to higher alveolar carbon dioxide tension levels 
as the ambient pressure was increased. Oxygen was 
presumed to play no important role in limiting 
breath holding beyond 33 feet depth. Rahn, Otis, 
and Fenn {2909) 1947 and Otis, Rahn, and Fenn 
{2910) 1948 found that at high oxygen tensions 
the breath-holding time was long, whereas at low 
oxygen tensions (corresponding to an altitude of 
18,000 feet) breath-holding time was short. 
In a respiratory and circulatory study during 
breath holding, Muxworthy {2908) 1950 found in 
trained subjects that a linear relationship does not 
exist between lung volume and the maximum time 
of apnea. At the breakpoint of breath holding, the 
carbon dioxide tension was higher with the greater 
lung volumes while the oxygen saturation remained 
approximately the same. The smaller lung volumes 
resulted in lower carbon dioxide tension while there 
was little change in oxygen saturation of the blood as 
compared to breath holding with lung volumes 
within the range of normal tidal volume. The car- 
bon dioxide tension is higher and the oxygen ten- 
sion lower during exercise, both with normal respira- 
tion and at the end of maximum breath holding, as 
estimated from alveolar air samples. The heart rate 
decreased as the blood pressure increased during 
breath holding, and did not begin to increase until 
the pressure decrease during the recovery period 
reached approximately the same level that stimu- 
lated the rate to decrease. Rate of blood flow, pulse 
volume, and total finger volume all indicate that 
vasoconstriction occurs during breath holding and 
lasts about 8 to 10 seconds beyond the breakpoint. 
Stroud {2911) 1950 found that establishment of 
acidosis by ingestion of 15 grams of ammonium 
chloride a day for 3 days resulted in shorter breath- 
holding time than normal. The resting alveolar car- 
bon dioxide tension was lowered and the oxygen 
tension increased, and at the breakpoint the carbon 
dioxide tension was lower in all cases. 
For further reports on breath holding, papers by 
the following may be consulted: Akira {2902,2903) 
1950, Andre and Boxus {2905) 1947, Fenn and 
DuBois {2906) 1950, and Montoye {2907) 1951. 
2902. Akira, N. Studies on the breath holding. (6) On 
the comparison of the breath holding with the rebreathing. 
Nihon Seiri. Z., 1950, 12: (Japanese text pagination), 
121-127. (English text pagination), 127. (In Japanese 
with English summary.) 
2903. Akira, N. Studies on the breath holding. (7) In- 
fluence of the inhalation of pressed air on the human body. 
Nihon Seiri. Z., 1950, 12: (Japanese text pagination), 
128-131. (English text pagination), 131. (In Japanese 
with English summary.) 
2904. Alvis, H. J. Breath-holding breakpoint at various 
increased pressures. U. S. Navy. Submarine base. New 
London, Conn. Medical research laboratory. Project NM 
002 014.01, Kept. no. 1, 10 August 1951, 10 pp. 
2905. Andre M. J. and V. Boxus. Le temps d’apnee 
voluntaire du sujet sain dans diverses conditions experi- 
mentales. Rev. beige Path., 1947, 18: 42-77. [P] 
2906. Penn, W. 0. and A. B. DuBois. Carbon dioxide 
in the alveolar air, muscles and bones. XVIII Intern, 
physiol. Congr., 1950: 199-200. 
2907. Montoye, H. J. An analysis of breath-holding 
tests. Res. Quart Amer. Phys. Educ. Ass., 1950, 21: 322— 
330. Excerpta Medica. Section II. (Physiology, Biochem- 
istry, and Pharmacology), 1951, 4: 881. 
2908. Muxworthy, J. F., Jr. A respiratory and circula- 
tory study during breath holding. Thesis, (Physiol.) Uni- 
versity of Rochester. Rochester, New York. 1950, 64 pp. [P] 
2909. Rahn, H., A. B. Otis, and W. 0. Fenn. Alveolar 
gas changes during breath holding. Fed. Proc. Amer. Soc. 
exp. Biol, 1947, 6: 183. [P] 
2910. Otis, A. B., H. Rahn, and W. 0. Fenn. Alveolar 
gas changes during breath holding. Amer. J. Physiol, 
1948, 152: 674-686. [P] 
2911. Stroud. R. C. Alterations in the sensitivity of the 
respiratory drives as measured by breath holding. Thesis, 
(Physiol.). University of Rochester School of Medicine 
and Dentistry, Rochester, N. Y. 1950, 66 pp. [P] 
B. ESCAPE PROCEDURES 
For reports on training in escape procedures and 
a commentary on actual escapes in a submarine 
disaster, a paper by Willmon, Duff, and Shilling 
{2917) 1947 should be consulted. An ONI report 
{2916) 1951 also contains a general discussion of 
submarine escape. The former paper describes the 
submarine training tank and the submarine escape 
apparatus. The authors consider that training with 
the submarine escape apparatus not only provides 
a sense of security but also a prognostic test for 
identifying personnel not adapted to submarine 
service. The history is given of an accident off 
Formosa in 1944 when the U. S. S. Tang was sunk 
by its own torpedo. The boat sank quickly by the 
stern and remained for 15 minutes at least at a 
very acute angle, the stern resting on the bottom 
and the bow sticking out of water. The upper 
conning tower hatch was open as the boat sank. 
Those in the control room managed to shut the 
lower conning tower hatch, but it was strained by 
the explosion and leaked. The confusion at this 
stage with men and gear falling around due to 
the acute angle was great. All but two of those 
in the conning tower were probably drowned almost 
at once. One of these two found himself breathing 
in an airpocket. He struggled out of this and reached DISEASES AND ACCIDENTS 
a larger pocket at the forward end of the conning 
tower. Very shortly thereafter this officer ducked 
out from his airpocket and made a successful free 
ascent through the conning tower hatch without 
breathing apparatus or lifebelt. The officer had been 
instructed in the technique of exhaling during free 
ascent at the submarine school. He described his 
ascent as follows: “I began to swim up, using both 
hands as hard as I could. The whole idea was to 
get up. I wanted air and lots of it. I had no sen- 
sation of being under pressure, but thought about 
letting the air out, and knew as I came up that 
I would have to force the air out so I heaved it 
out all at once and then just as I thought I would 
have to swallow some salt water I burst out on the 
surface and began swimming.” He was none the 
worse, had no pains in his chest, and swam around 
for about 8 hours before he was picked up. The 
second man alive in the conning tower was dazed 
and frightened. He was to have held on to the 
officer’s trouser leg as he ducked out, but appears 
to have let go and was probably drowned without 
attempting to escape. Meanwhile, many men were 
alive (probably about 45 in the control room and 
compartments forward, and in the engineroom and 
after battery room). Approximately 15 to 30 min- 
utes after the accident, an enlisted man in the con- 
trol room opened a tank vent by hand and the sub- 
marine sank to the bottom and leveled off without 
any very serious angle. The depth was now 180 feet. 
The men made their way forward until 45 of them 
were collected in the forward torpedo room. One 
of them had his face smashed in when the door 
into the forward torpedo room was opened. The 
emergency lights were working. Not long after this 
an officer and some men tried to pass through the 
door aft, but as they cracked the door dense smoke 
and fumes poured in through the door. This smoke 
was serious for some time. Men complained of 
irritation of throat and lungs and eyes and seemed 
actually to choke to death in it. One survivor stated 
that this smoke did more to kill the men who did 
not get out than any other thing. Within 20 minutes 
or so, however, these conditions improved. There 
seems little doubt that there was a bad battery 
fire in the forward battery room which continued 
right up to the end as the lower part of the bulk- 
head at the after end of the torpedo room got 
hotter and hotter until the paint began to peel. 
There had previously been another fire forward 
when the forward plane rigging and tilting motor 
burned out completely. There was probably a con- 
tinuous buildup of pressure from the flooded portion 
aft as the escape proceeded. Some survivors were 
said to have noticed the heightened pressure, but 
there was no definite evidence of it. The first at- 
tempt to escape from the forward torpedo room 
was made about 4 hours after the accident, and 
the last about 6 to 7 hours after the accident. In 
all, it seems that five attempts to escape were made. 
In the first attempt, four men entered the escape 
trunk taking a rubber boat with them. There was 
a difference of opinion among them as to pro- 
cedures. There was also difficulty in getting the line 
out. One man did not wait for the line and went 
out alone. This man had already been injured 
about the head in the first crash and is reported 
to have used his escape apparatus and taken two 
pistols and a bayonet with him. He was not seen 
again, and whether he reached the surface is not 
known. Some 40 minutes later, as there was no 
signal from the trunk, those in the compartment 
drained it down. The three remaining in the trunk 
must therefore have been under pressure equal to 
180 feet of water for 40 minutes. The failure of the 
three men to escape after 40 minutes in the trunk 
must have discouraged those in the compartment, 
especially as one of them stated that he did not care 
to attempt the escape again. Summarizing the 
escapes from the forward torpedo room, it appears 
that probably 13 tried to escape, and 8 or 9 reached 
the surface and 5 survived. Of those who died on 
the surface, one was probably already injured, one 
had been exposed to a pressure 180 feet of water 
for a long time twice, and all had been subjected 
to rising pressure and smoke inside the submarine 
for several hours. 
Commenting upon this disaster, Willmon, Duff, 
and Shilling recommended that provisions must be 
made for vocal communication between the escape 
trunks and adjacent compartments. Personnel in 
the compartment did not know what trouble those 
in the trunk were having. It was also recommended 
that an oxygen supply be provided for the escape 
trunk. Emergency lights were controlled from below 
instead of being turned on from the trunk. This 
should be corrected. It was considered important 
that personnel know that in the absence of oxygen, 
compressed air or even one’s own breath can be used 
to fill the submarine escape apparatus. Also person- 
nel should know that free escape can be made in 
event the “lung” comes loose. All officers should be 
indoctrinated in escape procedures, and all person- 
nel should be given detailed instruction on how to 
operate the escape trunks. The authors felt that 
more leadership training was needed to handle such 
stressful situations. 
Reports of survivors from the German submarine, 
U-1195, sunk in April 1945 in the English channel 
off the Nab, provide valuable data of significance SUBMARINE ESCAPE—ESCAPE PROCEDURES 
in planning safer escape procedures and more re- 
alistic escape training. This boat was submerged at 
approximately 75 feet when she was holed by a 
depth charge forward. She rested on the bottom in 
96 feet of water. All of the crew were alive, approx- 
imately 50 in all. These split into two parties. One 
lot of 33 went into the afterpart, the remaining 17 
went into the control room. Out of the conning 
tower and control room 6 reached the surface and 
survived, 3 were without Draeger gear and 3 with it. 
It is of interest that these 3 with Draeger gear 
were submerged completely for what must have 
been several minutes before they could come out 
of the conning tower. Of the 50 crew members alive 
in the submarine after she sank, 14 actually came 
to the surface and lived. Of these, 7 came up with 
no Draeger gear, 1 came up using the Draeger only 
as a lifebelt with the mouthpiece cock shut, and the 
remaining 6 had Draeger gear in operation. Six 
had survived from the control room and conning 
tower, 6 from the twill trunk hatch, and 2 from the 
afterhatch with no twill trunk at all. An escape via 
the twill trunk may be described in some detail; 
This escapee was an officer. As his oxygen bottle 
was not working, he blew up his Draeger bag with 
his mouth while his head was in the air at the top 
of the compartment. The compartment had been 
flooded so that the twill trunk hatch could be 
opened. The officer took a deep breath and tried to 
get out, but was caught by his gear fouling the 
twill trunk. He repeated the procedure a second 
time and again got caught. The third time he went 
right under by holding on to the deck and got safely 
through the trunk. For the ascent he had his Draeger 
blown up as a lifebelt, the mouthpiece in his mouth 
but the mouthpiece cock shut. He stated afterwards 
that he put the mouthpiece into his mouth as the 
mouthpiece cock was leaking and he did not want 
the air to exhaust from his Draeger bag. He swal- 
lowed a little water during his struggle to get under 
and through the trunk. He considers that he must 
have been a minute struggling under the water be- 
fore he got clear. After getting out, and on his way 
up, he let air escape out of his mouth as he had been 
taught. His minute of struggling in the trunk plus 
the air he had deliberately let escape finally made 
him want to breathe in before he reached the sur- 
face. Although he wanted to breathe in very badly 
he managed to keep his mouth firmly shut. Some 
water came in through his nose which finally stopped 
him trying to breathe in. He distinctly felt the ex- 
panding pressure in his lungs on his way up. He 
was in the water about 10 to 15 minutes before he 
was picked up on the surface. He stated that his 
eyes and the lower part of his chest hurt after the 
rescue. The pains in his chest made him feel that he 
could not get in enough air, but these pains sub- 
sided after about 20 minutes. His nose was perma- 
nently running for about 3 hours. He had no other 
pain and no visual disturbances, although his eyes 
continued to hurt him for a long while during cold 
weather. A survivor who made a free escape from 
the conning tower described in detail how he and 
the others were breathing very rapidly in a tiny 
airpocket immediately prior to opening the conning- 
tower hatch. He also stated he was unable to take a 
deep breath before leaving as there was so little air 
left and that this little amount contained much 
carbon dioxide. He stated that in this high concen- 
tration of carbon dioxide he found it very hard to 
hold his breath. Although he had been panting 
hard and found it difficult to breathe before the 
hatch was opened, as soon as he started ascending 
he no longer wanted to breathe in. As he ascended, 
he let air escape out of his mouth as he had been 
taught to do. He stated, “I just opened my mouth 
and away it went.” He let out air all the way up. 
At first after leaving the boat he felt he was ascend- 
ing too slowly. He therefore let more air into his life- 
jacket (presumably from a C02 cartridge). He then 
went up faster and at no time did he attempt to 
check his ascent. He felt no ill effects after reaching 
the surface. He stated quite clearly that he had no 
desire to inhale on the way up. On the contrary, he 
had too much air and wanted to get rid of it. 
For descriptions of British escape procedures, 
papers by Davis {2912) 1951; Donald, Davidson, 
and Shelford {2913) 1948; and Taylor {2915) 
1947 should be consulted. In evaluating self-con- 
tained escape apparatus, Davis {2912) stated that 
they should fulfill the following requirements: (1) 
they should be compact and light; (2) they should 
be instantly and easily put on; (3) they should 
have adequate air-regenerating devices to insure 
the wearer an air supply; (4) they should render 
him immune against poisonous gases; (5) they 
should be so designed as to allow the escapee free 
passage through hatchways; (6) they should per- 
mit him to breathe freely under water, no matter 
of what pressure; (7) they should be capable of 
retarding the velocity of ascent; (8) on the surface, 
they should provide buoyancy with the head up; 
and (9) they should not impede swimming 
progress. Escape training and procedures used in 
the Royal Navy are described. Two methods of 
escape are now used: (1) the collapsible trunk 
attached to an escape hatch, in which the whole 
compartment of the submarine is flooded (this is 
called the twill trunk); and (2) an escape cham- 
ber in which the escapees enter, 1 or 2 at a time 
291222—54 18 2912—2917 
DISEASES AND ACCIDENTS 
and which is flooded to enable them to emerge by 
an escape hatch. British escape procedures are 
further described by Donald, Davidson, and Shel- 
ford {2913). Considerable attention has been given 
to the procedure of free, unaided escape both by 
the U. S. Navy and the Royal Navy. A British 
report by Taylor {2915) 1947 describes unevent- 
ful free escapes made by goats from 220 feet and 
300 feet. These results suggested to the author that 
for man such ascents are feasible. Reference may be 
made to a Russian report by Klimenko, Pavlovskii, 
and Maksimenko {2914) 1948. This report is to 
be found in the Soviet manual for divers of the 
navy, primarily a training manual. Means of escape 
are described and examples of escape are given. 
A submarine rescue chamber similar to the U. S. 
Navy chamber is explained. An escape training 
chamber resembling the training chamber at New 
London is diagramed and discussed. 
2912. Davis, Robert H. Escape from sunken submarines, 
pp. 257-289 in: Deep diving and submarine operations. 
A manual for deep sea divers and compressed air workers. 
London, The Saint Catherine Press Ltd., 1951, 670 pp. 
[D] 
2913. Donald, K. W., W. M. Davidson, and W. 0. Shel- 
ford. Submarine escape breathing air. J. Hyg., Camb., 
1948, 46: 176-183. [P] 
2914. Klimenko, N. A., K. A. Pavlovskii, and V. P. 
Maksimenko, Escape of personnel from the damaged sub- 
marine. pp. 136—169 in: Manual for divers of the navy. 
Moskow, Military Printing office, 1948, 172 pp. (Russian 
text.) 
2915. Taylor, H. J. Simulated unaided ascents of goats 
in water from depths of (A) 220 feet, (B) 300 feet. Gt. 
Brit. MRG-RNPRC, UPS. R. N. P. 47/348, U. P. S. 79, 
January 1947, 2 pp. [P] 
2916. IT. S. Navy, ONI. Norway-Submarine personnel, 
training in escape procedures. O. N. I. serial 62-U-51, 
12 June 1951, 2 pp. 
2917. Willmon, T. L., I. F. Duff, and C. W. Shilling. 
Submarine escape (“lung”) training pays off. pp. 199—214 
in: History of submarine medicine in World War II. 
Edited by Shilling, C. W., and J. W. Kohl. U. S. Navy 
Submarine Base, New London, Conn. Medical research 
laboratory, 25 May 1947, 328 pp. 
C. ESCAPE ACCIDENTS FROM SUBMARINES OR 
ESCAPE TRAINING TANKS 
Excerpts from accounts of escape attempts from 
disabled submarines given in the previous section 
(p. 251) provide examples of the hazards involved. 
The operation of escape training tanks has con- 
tinued over the years with a remarkable safety rec- 
ord. The following escape training fatal accident 
was reported by Cole {2918) in 1947: this accident 
occurred at the Submarine Base, Pearl Harbor, 
T. H. The man entered the escape tank from the 
100-foot lock for ascent; as he passed the 50-foot 
lock, the attendant observed that the mouthpiece 
was out of the trainee’s mouth. He was ascending 
rapidly and when he reached the 35-foot level, one 
of the attendants caught him and compressed his 
chest region. He was still conscious at that time, 
but was unconscious when he reached the surface. 
Within 6 minutes, he was placed in the recompres- 
sion chamber and taken to a simulated depth of 
165 feet. The pulse was rapid and the respiration 
deep, fast, and stertorous. He remained at 165 feet 
for 2 hours, during which time he had several con- 
vulsive seizures. Phenobarbital was ineffective. 
Eight hours after he entered the tank, the patient 
had a very violent convulsion. Spontaneous respira- 
tion ceased about an hour later and artificial respira- 
tion was given. The pulse was rapid and fairly 
strong. After another hour the patient had a further 
convulsion and required restraint. After this the 
heart began to fail. Caffeine was given in an effort 
to stimulate respiration but without benefit. The 
patient was pronounced dead 1 hour later. Death in 
this case was considered to be due to brain injury 
from air embolism. Loss of the breathing apparatus 
was considered to have caused panic with forced 
closure of the glottis. As the patient rose, the ex- 
panding air within the lungs resulted in excessive 
intrapulmonary pressure which exceeded the 
strength of the alveolar walls. Rupture of the alveo- 
lar walls allowed air to enter the pulmonary vessels 
and eventually the arterial circulation of the brain. 
A case of air embolism occurring at the escape 
training tank at the Submarine Base, New London, 
Conn., was reported in 1947 by Hay ter {2919). The 
patient was one of a group of 10 men making a free 
escape from a depth of 35 feet. On the first day of 
his training, he made 2 escapes from 12 feet, 2 from 
18 feet, and 1 from 35 feet. On the final run the 
patient said he exhaled continuously until the 10- 
foot level and said he exhaled all he could. From 
the 10-foot level he swam to the surface. On reach- 
ing surface, he collapsed and sank. When he was 
removed from the water he was unconscious, and 
pale and bloody saliva was issuing from the mouth. 
There was gurgling in the throat. The pulse was 
weak, slow, and regular. Placed in the recompres- 
sion chamber at a simulated depth of 165 feet, he 
became conscious, but was confused and appeared 
to be in mild shock. There was involuntary defeca- 
tion. Blood pressure was 90/60 mm. Hg. Tendon 
reflexes, abdominal, and cremasteric reflexes were 
all absent. Percussion of the chest revealed hyper- 
resonance of the lungs. The region of cardiac dull- 
ness was not abnormal. Examination showed sub- 
cutaneous emphysema in the supraclavicular fossae SUBMARINE ESCAPE—GAS EMBOLISM 
2918-2919 
confirmed by X-ray findings. There was no evidence 
of pneumothorax. 
It seems evident that the major hazard in making 
a free escape arises from inadequate exhalation of 
air from the lungs. Under such a circumstance 
positive pressure will be built up within the lungs 
which may cause the lung tissue to tear, followed 
either by hemorrhage into the lungs or the forcing 
of air into the blood stream. Since cases of air em- 
bolism have been described from depths as shallow 
as 10 feet (implying a positive pressure of not more 
than 4.5 lbs. per sq. in.), it is essential that trainees 
be taught to exhale during the whole ascent, and 
enough so that there is never any sense of distention 
in the chest. Although trainees always express con- 
cern as to whether they will have enough air to reach 
the surface in making free escape, observation of 
free escapes in many trainees indicates that the air 
in the lungs is more than adequate to last the sub- 
ject until he reaches the surface insofar as oxygen 
content is concerned. Even if he does exhale a bit 
too much, a few deliberate strokes swimming up- 
ward will cause the air in the lungs to expand and 
fill the chest. 
In free escapes under actual operational condi- 
tions, a serious potential hazard may be loss of sense 
of direction in dark water, particularly to negatively 
buoyant individuals with high specific gravity. It is 
possible for a man to become disoriented in the 
water if there is not light above to show or if vision 
is not sufficiently good to give a reference point. A 
man may think he is ascending when really he is 
sinking. One solution to this problem seems to be 
to take along some buoyant object, such as a pillow- 
case, a lifejacket, or some other object holding 
entrapped air. 
In escapes made with the aid of the submarine 
escape apparatus, it is important that the subjects 
inhale and exhale regularly. 
2918. Cole, G. M. Escape training diving accident in the 
case of Singer, Earl C., StD2, 894-06-15, USN. U. S. 
Navy. Submarine base, Pearl Harbor, T. H. Report of to 
Chief, BuMed, 27 March 1947. 
2919. Hayter, R, Air embolism in the case of Holst, 
Richart R., Em3c, 321-96-63, USN. U. S. Navy. Sub- 
marine base. New London, Conn. Medical research de- 
partment. Report of to Chief, BuMed, 30 June 1947, 2 pp. 
D. GAS EMBOLISM 
Gas in the circulation constitutes a potential 
hazard not only in lung damage in escape accidents, 
but also as a part of the picture of decompression 
sickness. The references give below have been se- 
lected as source material for the reader particularly 
concerned with the mechanism of air embolism in 
free escape accidents. In this condition, air is forced 
under pressure into the pulmonary circulation 
through ruptures in the lung tissue and is admitted 
into the left heart and thence into the systemic 
arteries. 
For studies of pulmonary air embolism resulting 
from injection of air on the venous side of the 
systemic circulation, papers by the following authors 
may be consulted: Auer and Krueger [2920) 1946; 
Blood and D’Amour (2925) 1950; Cameron, De, 
and Sheikh (2926) 1951; and Durant, Long, and 
Oppenheimer (2931) 1947. 
Cooper, Marchand, and North (2927) 1945 have 
investigated air embolism from passive overventi- 
lation of the rat through a tracheal cannula. 
Animals received air under pressure sufficient to 
cause maximal respiratory excursions of the chest 
and abdomen. They developed multiple hemor- 
ragic patches in the lung parechyma, followed by 
a terminal episode of pulmonary edema with a sud- 
den evolution of pink foam from the trachea. Still 
greater pressures caused immediate air embolism 
and death. With each passively overventilated rat, 
a control animal was anesthetized and cannulated 
in the same way, but not connected to the air valve. 
These control animals survived the interval of the 
experiment by spontaneous respiration through the 
cannula and exhibited no evidence of lung injury 
at autopsy. Some degree of overventilation occurred 
in this control group as a result of operative manip- 
ulation of the trachea. There seems little doubt but 
that these authors have succeded in producing ex- 
perimentally the conditions responsible for death 
in free escape accidents. 
An early study on cerebral gas embolism reported 
by Villaret, Cachera, and Fauvert (2947) 1937 
deserves comment. Working with dogs, these au- 
thors concluded that gas emboli in the brain are 
capable of stopping the circulation in the small 
vessels. They consider that the air emboli behave 
as plugs which impede the .flow of blood. This 
provokes a state of temporary ischemia which can 
last long enough to injure the neurons. The authors 
stated that they had never observed cerebral vaso- 
constriction from the flow of gaseous emboli. They 
consider that the emboli do not act by producing 
vascular spasm, but believe that the mechanism of 
injury following air embolism of the brain is 
cerebral ischemia of simple mechanical origin 
through gaseous obstruction. 
For a report on methods of testing for air 
embolism, a paper by Karsner (2937) 1949 may be 
consulted. He points out that when air is injected 
into the dog’s superior cava a bubbling sound can 
be heard through the stethoscope as the air enters 2920-2925 
DISEASES AND ACCIDENTS 
the heart and the same is said to be true of man. 
The author also discusses the effects of gas bubbles 
in the brain and cord as a part of the picture of 
decompression sickness. He points out that if the 
breath is held during decompression the expansion 
of air in the lungs may rupture the alveoli so that air 
enters the tissues to produce interstitial emphysema 
and may also pass into the blood vessels with 
consequent air embolism. 
In a discussion of the origin and clinical picture 
of arterial gas embolism in the greater circulation, 
Rdssle {2943) 1947 stated that he considered that 
arterial gas emboli in connection with primary ven- 
ous air embolism can arise out of passage of the 
gas through an open foramen ovale or passage of 
air through arteriovenous anastomoses. He states 
that air may pass into the arterial circulation in 
contusion of the lungs through compression of the 
thorax, through crushing of the lungs “from within” 
by maximum expansion of the lungs, injection of air 
by means of a catheter in both men and animals, and 
through air impact on the lungs in consequence of 
detonation. He points out that in detonation in- 
juries, gas bubbles are usually found in the coronary 
arteries and in the base of the brain as well as upper 
parts of the brain. They are rarely found in the fine 
mesenteric arteries. Durant {2930) 1948 pointed out 
that arterial gas embolism is commonly associated 
with localized cerebral or coronary effects. The fact 
of gas buoyancy determines to a considerable extent 
the effects of arterial gas embolism in that gas which 
reaches the aorta will be distributed to those 
branches which are superiorly located with respect 
to the trunk. The degree of obstruction of the ves- 
sels involved is determined not only by the size of the 
gas bubbles but also by associated vasospasm in- 
duced by the irritant action of the gas in the lumen 
of the vessel, a view in contradiction with findings 
of Villaret, Cachera, and Fauvert {2947) 1937. 
Aside from symptoms of pain in the chest, hemi- 
plegia, hemiparesis, hemianaesthesia, monoplegia, 
nystagmus, convulsions, giddiness, and cyanosis, 
there may also be observed gas in the retinal vessels. 
These vessels show pale, silvery sections, represent- 
ing small columns of air. Durant suggests that in 
embolism the patient should be placed immediately 
in a position such that the head is dependent and 
the trunk is alined midway between the left lateral 
and prone positions. He considers that this position 
minimizes the amount of gas reaching the cerebral 
and coronary arteries. 
Cerebral air embolism from air entering the pul- 
monary venous circulation has also been described 
bv Hare {2935) 1949. He has drawn attention to 
the early signs of cerebral air embolism consisting 
of vertigo and pallor, followed by cyanosis and 
respiratory difficulty, loss of consciousness, sharp 
drop in blood pressure, bradycardia, apnea, convul- 
sions, urinary and fecal incontinence, focal neuro- 
logical disturbances, and, in some instances, death. 
Courville {2929) 1945 has drawn attention to the 
fact that marked cerebral symptoms or sudden death 
from air embolism are usually due to an overwhelm- 
ing invasion of air into the pulmonary veins as in 
injuries to the chest and lungs in pulmonary opera- 
tions. 
Rdssle {2944) 1949 has described several cases 
of arterial gas embolism in which the patients sur- 
vive for periods varying from several hours to sev- 
eral days. This paper describes in detail the histo- 
logical findings in the cerebral vessels. The cerebral 
capillaries are dilated, and air penetrates into the 
perivascular spaces. There is also penetration of air 
into the glial tissue and the pericellular spaces of 
ganglion cells. There are small necrobiotic areas in 
the cerebral tissue and small hemorrhages. 
The management of cases of escape accident in- 
cludes immediate placing of the head in the depend- 
ent position and carrying the victim in this position 
at once to the recompression chamber when this is 
available. The patient should remain in the head- 
down, feet-up position as for shock during and 
after rapid recompression to a simulated depth of 
165 feet. Convulsions and other symptoms must be 
treated as they arise. 
For other studies on gas embolism, papers by the 
following authors should be consulted: Barach 
{2923) 1948; Binet and Burstein {2924) 1947; Gt. 
Brit. Medical Research Council {2932) 1947; 
Leriche {2939) 1947; Milwidsky {2940) 1948; 
Neuhof {2941) 1948; Whitteridge {2948) 1951; 
and Zilliacus {2949) 1946. 
2920. Auer, J. and H. Krueger, Accidental air embo- 
lism and fibrin formation in the heart of rabbit. Proc. Soc. 
exp. Biol., N. Y., 1946, 61: 166-169. [P] 
2921. Bageant, W. E. and L. A. Rapee. The treatment 
of pulmonary embolus by stellate block. Anesthesiol., 
1947, 8: 500-505. [CH] 
2922. Baker, D. V., Jr., R. Warren, J. Homans, and D. 
Littman. Pulmonary embolism. Evaluation of a policy for 
prophylaxis and therapy. New Engl. J. Med., 1950. 242: 
923-928. 
2923. Barach, A. L. Pulmonary embolism and infarc- 
tion. pp. 215-217 in Physiologic therapy in respiratory 
diseases. Second edition, Philadelphia. J. B. Lippincott 
Co., 1948, 408 pp. 
2924. Binet, L. and M. Burstein. Sur le mecanisme de 
la mort part embolie pulmonaire. Etude experimentale. 
/. franq. Med. Chir. thor., 1947, 1: 363-366. 
2925. Blood, F, R. and F. E. D’Amour, Cardiac output 
in the rat and its relationship to air embolism. Fed. Proc. 
Amer. Soc. exp. Biol., 1950, 9: 13. SPECIAL DIVING ACCIDENTS 
2926-2949 
2926. Cameron, G. R., S. N. Be, and A. H. Sheikh. 
Cardio-vascular responses to air embolism. J. Path. Bact., 
1951, 63: 181-194. 
2927. Cooper, M. R., J. F. Marchand, and N. North. 
Carbon dioxide depletion and air embolism from passive 
overventilation of the rat by tracheal cannula. U. S. 
NRC-CAM. C. A. M. rept. no. 478, 4 October 1-945, 
4 PP- 
2928. Cort, J. H. and G. D. Davis. Observations on the 
role of vagal activity in the effects of pulmonary embolism. 
Yale J. Biol. Med., 1950, 22: 213-218. [P] 
2929. Conrville, C. B. Diseases of the intracranial and 
intraspinal blood vessels, pp. 87-148 in: Pathology of 
the central nervous system. Mountain View, California. 
Pacific Press Publishing Association, 1945. 450 pp. 
2930. Durant, T. M. Cardiovascular accidents due to 
gas embolism. Trans. Amer. Climat. (din.) Ass., 1948, 
60: 87-98. [D] 
2931. Durant, T. M., J. Long, and M. J. Oppenheimer. 
Pulmonary (venous) air embolism. Amer. Heart ]., 1947, 
33: 269-281.[P] 
2932. Gt. Brit. MRC-RNPRC, TTPS. Minutes of the 25th 
meeting of the underwater physiology subcommittee. 
R. N. P. 47/365, U. P. S. 80, 23 April 1947, 3 pp. 
2933. Groedel, F. M., B. Kisch, and M. Miller. Electro- 
cardiographic changes following air embolism in man. 
Exp. Med. Surg., 1949, 7: 73-77. [CH] 
2934. Kara, M. and J. R. Smith, Experimental observa- 
tions on embolism of pulmonary lobar arteries. J. thorac. 
Surg., 1949,18: 536-542. [P] 
2935. Hare, C. C. Cerebral air embolism, pp. 683-685 
in; Injuries of the brain and spinal cord and their cover- 
ings. Edited by Samuel Brock. Third edition. Baltimore. 
The Williams & Wilkins Co., 1949, 783 pp. 
2936. Haynes, F. W., T. D. Kinney, H. K. Hellems, and 
L. Dexter. Circulatory changes in experimental pulmonary 
embolism. Fed. Proc. Amer. Soc. exp. Biol., 1947, 6: 
125-126. [P] 
2937. Karsner, H. T. Air and gas embolism, pp. 124- 
126 in: Human pathology. Seventh edition. Philadelphia. 
J. B. Lippincott Co., 1949, 927 pp. 
2938. Kelly, H. G., W. C. Gibson, and J. F. Meakins. 
Cerebral air embolism following artificial pneumothorax; 
treatment with prolonged inhalation of oxygen. Canad. 
med. Ass. J., 1947, 56: 388-391. (French summary.) [GH] 
2939. Leriche, R. Les embolies de Vartere pulmonaire 
et des arteres des membres. Physiologie pathologique et 
traitement. Paris, Masson & Cie, 1947, 126 pp. [R] 
2940. Milwidsky, H. Therapeutischer Paravertebral- 
Block des Sympathicus bei peripherer arterieller Embolie. 
Schweiz, med. Wschr., 1948, 78: 301-302. [CH] 
2941. Neuhof, H. Venous thrombosis and pulmonary 
embolism. New York. Grune & Stratton, 1948, 159 pp. 
2942. Pratt, C. L. G. and H. J. Taylor. The risk of 
bends or vascular embolism during simulated escapes 
from (a) 300 ft. (b) 150 ft. Gt. Brit. MRC-RNPRC, UPS. 
R. N. P. 47/347, U. P. S. 78, January 1947, 5 pp. 
2943. Rossle, R. Ursachen und Folgen der arteriellen 
Luftembolien des grossen Kreislaufes. Virchows, Arch., 
1947, 314: 511-533. [R] [CH] 
2944. Rossle, R. t)ber die ersted Veranderungen des 
menschlichen Gehirns nach arterieller Luftembolie. Abstr. 
World Med., 1949, 6: 37. Virchows Arch., 1948, 315: 
461-480. 
2945. Smith, J. R. and M. Kara. Experimental embo- 
lism of selected portions of pulmonary arterial bed. Fed. 
Proc. Amer. Soc. exp. Biol., 1948, 7: 117. [P] 
2946. Stallworth, J. M., J. B. Martin, and R. W. Pos- 
tlethwait. Aspiration of the heart in air embolism. J. 
Amer. med. Ass., 1950, 143: 1250-1251. [GH] 
2947. Villaret, M., R. Cachera, and R. Fauvert. L’em- 
bolie gazeuse cerebrale; ses effets circulatoires locaux. 
C. R. Soc. Biol., Paris, 1937, 125: 108-111. 
2948. Whitteridge, D. Multiple embolism of the lung 
and rapid shallow breathing. Physiol. Rev., 1950, 30: 
475—486. Excerpta Medica. Section II. (Physiology, Bio- 
chemistry, and Pharmacology), 1951, 4: 881. 
2949. Zilliacus, H. On the specific treatment of throm- 
bosis and pulmonary embolism with anticoagulants, with 
particular reference to the post-thrombotic sequelae. Acta 
med. scand., Suppl., 1946, 171: 221 pp. (French, German 
and Russian summaries.) [R; P] 
IX. SPECIAL DIVING ACCIDENTS 
Divers are subject to certain special accidents in- 
cluding “blowing up,” “squeeze,” and underwater 
confinement. The accidents known as “blowing 
up” and divers’ “squeeze” have been described in 
the first volume of this Sourcebook (pp. 228-230). 
Under certain circumstances, the diver may be 
forced rapidly to the surface because of filling of 
the diving dress with air. These accidents (“blowing 
up”) are associated with acute manifestations of 
decompression sickness. Cases have been described 
of almost immediate death from too rapid surfac- 
ing. For consideration of special accidents to divers, 
papers by Buyard (2950) 1946 and U. S. Navy, 
BuNavPers {2954) 1949 should be consulted. 
As a diver descends, the air pressure within the 
helmet and the suit must be correspondingly in- 
creased with the increasing pressure of the column 
of water against the body surface. At any depth, 
the air pressure within the helmet in the suit must 
be maintained. If the pressure within the helmet 
suddenly falls or if the hydrostatic pressure on the 
outside of the body increases suddenly without a 
corresponding increase in the air pressure within 
the helmet, a differential pressure is created which 
interferes with respiration and drives blood into the 
head and neck or may even force portions of the 
body itself up into the helmet. This condition, 
known as divers’ “squeeze,” occurs if a diver falls 
off a ledge on the bottom to a new level without a 
corresponding increase in helmet pressure. Roer 
(2952) 1948-49 has given an excellent and com- 
plete review of divers’ “squeeze,” including a com- 
prehensive bibliography and some very complete 
case histories. Three autopsy reports are included. 
The author has also provided experiments on rabbits 
subjected to “squeeze.” The minimum depth at 
which the condition may become fatal is 1.40 meters 
in the lying-down position and about 3 meters stand- 
ing up, corresponding to a suction of 100 mm. Hg 
within the helmet-lung area. In fatal cases of divers’ 2950-2955 
DISEASES AND ACCIDENTS 
“squeeze,” there is always, according to the author, 
emphysema of the skin. 
Three cases of underwater confinement have 
been described by Romney {2953) 1946. The first 
was that of a 26-year-old qualified deep-sea diver, 
working beneath a sunken LST, who was trapped 
for 72 hours at 55 feet of water. There were no 
symptoms of compressed-air illness. When the diver 
was examined on being brought finally to the sur- 
face, he was alert, calm, cooperative, and physi- 
cally exhausted. He was recompressed to 100 feet 
simulated depth for 30 minutes, decompressed, and 
later hospitalized. The second case was that of a 
24-year-old qualified deep-sea diver who was work- 
ing with the diver just described. He became excited 
and frantic. It is stated that he became disoriented 
and irrational, and lost telephonic contact. When he 
was brought to the surface 75 hours after descent, 
his suit and helmet were found to be intact and 
contained an adequate air supply. This man did not 
survive. The third case was that of a 36-year-old 
qualified diver who went to rescue the two previous 
divers. Another cave-in trapped him for 17 hours 
at a depth of 45 feet. A modified type of surface 
decompression was employed. The subject was co- 
operative, but extremely tired. He recuperated 
within 2 weeks. It was assumed and seems probable 
that the fatal outcome in the second case was due 
in part to intense emotional stress. 
For a report on the circumstances, opinions, and 
recommendations in connection with further diving 
accidents, papers by Van der Aue {2955) 1949 
and Dietrich, Behnke, and McDonald {2951) 1949 
should be consulted. 
2950. Buyard, P. Guide therapeutique des scaphan- 
driers. Rev. Med. nav., 1946, 1: 267—284. [D] 
2951. Dietrich, W. P., A. E. Behnke, and J. H. Mc- 
Donald. The proceedings, findings of facts, opinions and 
recommendations of the board of investigation in the case 
of death of Egnacio Lopez Huerta, 381-34-88, chief 
metalsmith. U. S. Navy. Naval gun factory, EDU. 3 June 
1949, 75 pp. 
2952. Eoer, H. Ueber das Blaukommen der Taucher 
(Morbus caerulescens). Dtsch. Z. ges. gerichtl. Med., 
1948/49, 39: 378-420 [CH] [R] [P] 
2953. Romney, S. L. Underwater confinement—report 
of three cases. Nav. med. Bull., Wash., 1946, 46: 1259- 
1264. 
2954. U. S. Navy, BnNavPers. Surface decompression 
procedure, pp. 118-132 in: Submarine medicine practice. 
NavPers 10838, March 1949, 182 pp. [CH] [D] 
2955. Van der Aue, 0. E. Diving accident in the case of 
Huerta, Ignacio L., MEG, 381-34-88, U. S. Navy. Naval 
gun factory, EDU. Report to Chief, BuMed. 6 March 
1949, 6 pp. 
X. BLAST INJURIES 
Underwater blast constitutes an important prob- 
lem to the underwater swimmer, deep-sea diver, and 
survivor of disaster at sea. During World War II, 
underwater blast was a far greater cause of casual- 
ties than air blast. Detonation of armed charges on 
a sinking vessel, accidental explosion of mines, or 
countermeasure explosions by the enemy are a con- 
stant threat to the buoyant or submerged swimmer. 
It is not intended under this heading to include 
in its entirety the literature on air blast. The reader 
should consult reports such as those by Baron {2956) 
1948, Burnett {2960) 1948, Corey and Gersh 
{2968) 1944, Friedman {2970) 1948, Ruskin and 
Beard {2975) 1948, and Smith {2976) 1949. Refer- 
ence should be made to an excellent review on blast 
published in 1949 by Clemedson {2964). 
Martin {2973) 1943 describes a case of rectal 
perforation resulting from immersion blast. A 28- 
year-old seaman was swimming in the water follow- 
ing the torpedoing of his ship, while destroyers made 
depth-charge attacks on the submarine. Examina- 
tion of the survivor 14 hours later revealed no ex- 
ternal bruises or fractures. A small amount of blood 
had been passed from the anus. His temperature 
was 100° F. and his pulse was 120. Abdominal 
rigidity was present, especially over the right iliac 
fossa. Laparotomy following saline and glucose in- 
fusion revealed pus in the peritoneal cavity and a 
1-cm. laceration on the anterior surface of the rec- 
tum. The perforation was oversewn and buried with 
a pursestring suture. After draining the pelvis, the 
abdomen was closed and 2 pints of blood adminis- 
tered, The following day the patient exhibited 
jaundice, and on the third day he presented a para- 
lytic ileus accompanied by vomiting and a pulse of 
140. Duodenal drainage, intravenous saline drip, 
and morphine administration were of no avail. The 
patient died 52 hours after the operation. Autopsy 
showed a general peritonitis having originated in 
the pelvis. The paralytic ileus involved the whole 
left bowel; the right lung showed a contusion on 
the anterior surface near the medial and inferior 
borders. 
For detailed studies of immersion injuries, the 
reader is referred to the section on water or immer- 
sion blast injuries in Submarine Medicine Prac- 
tice {2977) 1949. A description is given of cases 
admitted to the Pearl Harbor Naval Hospital from 
the naval battle near Midway Island. Approxi- 
mately 5 days had elapsed between the battle and 
arrival at the hospital, and out of the group of 33 
admitted to the hospital, over half walked in and 
required very little definite treatment. The mor- 
tality rate was very high for those seriously injured. 
The characteristic finding for the seriously injured 
group as a whole was a distended and silent ab- BLAST INJURIES 
domen. Those critically ill on arrival presented a 
picture of intestinal obstruction of the adynamic or 
paralytic type. In several there was a superimposed 
general peritonitis. Roentgenograms revealed free 
gas beneath the diaphragm in two cases. In one of 
these instances the patient was moribund and died 
within a few hours following admission. A Levin 
or Miller-Abbott tube was introduced in all bed- 
ridden patients, and fluids including 5 percent glu- 
cose, electrolytes, vitamins, and blood plasma were 
given generously by vein. All received intravenous 
sulfadiazine in amounts sufficient to maintain a 
concentration of 15 mg. per 100 cu. cm. of blood. 
Surgery was resorted to in only two cases in this 
entire group. All except two of those having post- 
mortem examination showed one or more per- 
forations of the bowel with general peritonitis. The 
majority of these perforations were through local- 
ized necrotic areas in the jejunum or ileum. In one, 
there were two perforations in the large bowel in 
addition to one or more in the small intestine. In 
one patient perforation was demonstrated, but 
his cecum and ascending colon were a formless, 
hemorrhagic, necrotic mass. It is stated that the se- 
verity of injury from immersion blast depends upon 
several factors: (1) proximity to the blast; (2) in- 
tensity of the blast; (3) whether almost completely 
submerged or only partially submerged; (4) whether 
swimming on the stomach or on the back; and (5) 
whether the thoracic and abdominal areas are pro- 
tected by a life jacket. It appears that the under- 
water concussion wave produces tissue injury by 
shredding the tissue as it passes from a solid to a 
gaseous medium within the body. With the body in 
the supine position in the water or protected over 
the thorax and abdomen by kapok or foam rubber, 
the injurious effects of the compression wave may 
be minimized. 
According to Clemedson {2963) 1948, animals 
exposed to underwater blast are more severely in- 
jured when they are immersed 1 meter below the 
water’s surface than when floating on the surface. 
Death in rabbits seemed to be due to suffocation 
by extensive pulmonary hemorrhages and blood 
clots in the respiratory tract. The usual lesions of 
the abdominal viscera were seen, and in the more 
severe cases a diffuse edema in the mucosa and sub- 
mucosa of the gut was noted. The gut exhibited 
maximal contraction and, when squeezed, felt like 
a tendon. 
An experimental study of physical and subjective 
sensations of deep-sea divers and underwater demo- 
lition team members exposed to blast was carried 
out by Corey {2967) 1946. The divers acting as 
subjects were subjected to concussion from charges 
of 1 to 300 pounds in weight. It was found that 
divers can tolerate calculated explosion pressures 
up to 50 lbs. per square inch without serious dis- 
comfort or injury. During the work performed on 
the stage in deep water, the divers’ heads were at 
times thrown with different degrees of violence 
against portions of the helmet and breastplate, but 
in no instance was the blow to the head of sufficient 
violence to break or bruise the skin or render the 
subject dizzy or unconscious, or to interfere in any 
way with prompt mental or physical reactions. 
To determine lethal blast pressures, strips of beef 
intestine were suspended inside a diving dress, at 
the level corresponding to the umbilicus, by means 
of a weight and a cord attached to the chin valve 
of the helmet. The suit was then lowered into the 
water and exposed to blasts from 114-pound 
charges. The calculated pressure at which rupture 
of the intestinal sample occurred was considered 
“lethal.” From the results of the experiment, the 
author concluded that a calculated underwater 
blast pressure of 300 lbs. per square inch may be 
considered lethal for divers wearing standard deep- 
sea diving dress. It was found that the British anti- 
blast vest offered a measure of protection against 
underwater concussion, the “lethal” pressure being 
raised to at least 525 lbs. per square inch. 
Corey also exposed underwater swimmers to blast 
from 110-pound demolition charges. Six men wore 
swimming trunks, and one of these wore, in addi- 
tion, an inflatable lifebelt, while four were equipped 
with the standard Navy kapok lifejacket. The water 
was 5 feet deep over a soft mud bottom, and the 
charges were detonated at a depth of 3 feet with the 
men immersed to the neck. The underwater con- 
cussion produced definite abdominal sensations at 
rather low pressures (22.5 lbs. per square inch), but 
no impact of the shock wave against the thorax 
could be detected. It was concluded that calculated 
explosion pressures up to 70 lbs. per square inch 
may be readily tolerated in shallow water. 
Draeger, Barr, and Sager {2969) 1946 state that 
underwater blast pressures over 250 lbs. per square 
inch will result in intestinal perforation. Because 
the body has a density approximately equal to 
water, only air-containing portions of the body are 
subjected to sudden compression and expansion, 
causing a rupture of tissues adjacent to the con- 
tained air. The authors recommend that the patients 
be treated for shock and given bed rest. Handling 
and excessive transportation should be avoided. 
Fluids should be given to maintain the electrolyte 
balance and a Miller-Abbott tube should be used in 
cases of paralytic ileus. 2956-2980 
DISEASES AND ACCIDENTS 
The reader is advised to consult reports by Ben- 
zinger (2958 and 2959) 1950-51 for an excellent 
discussion of the mechanics and physiological effects 
of air and water blast. Arterial air embolism, caused 
by rupture of the boundaries between alveolar spaces 
and alveolar capillaries, was shown in dogs to be 
the chief cause of death from blast in air as well as 
under water. Cerebral focal symptoms were found 
when the head of the animal was protected from 
the blast, while its trunk was exposed. With the head 
exposed and the trunk shielded, cerebral focal symp- 
toms were not observed. Post-mortem examination 
revealed air emboli in the cardiac and cerebral ar- 
teries. It thus appears that the cerebral symptoms 
arose from air emboli reaching the brain from the 
exposed trunk areas. 
According to Clemedson and Granstom {2965) 
1950, lung hemorrhages and rib markings are the 
result of tearing forces produced by pressure differ- 
ences between the lungs and the pleural space. 
These pressure differences are stated to be due to 
different accelerations of the structural thoracic ele- 
ments. The risk of tearing is expected to be greatest 
in those parts of the lung which correspond to the 
costal interspaces, and that is where the rib mark- 
ings were observed in the experimental animals. 
Protection of divers against underwater explosions 
is outlined in a report by the Great Britain Medical 
Research Council {2972) 1945. It is stated that the 
intensity of damage to the diver from underwater 
blast may be reduced if the diver wears a kapok 
garment surrounding his chest and abdomen. It is 
recommended that a shockabsorbing headdress be 
worn inside the rigid helmet. Protection afforded by 
kapok jerkins is based on the layer of air held within 
the kapok, the efficiency of the kapok being reduced 
if it becomes wet or soggy. Wearing kapok jerkins 
has been shown to protect a man from peak pres- 
sures up to 225 lbs. per square inch. A momentary 
discomfort may be experienced at peak pressure. 
For other general reports on underwater blast, 
the reader may consult articles by Bebb {2957) 
1951, Cameron {2962) 1947, Cole {2966) 1948, 
Gala {2971) 1947, Netter {2974) 1948, U. S. Navy 
{2978) 1950, Wright {2979) 1947, and Young 
{2980) 1945. 
2956. Baron, S. H. The repair of the eardrum in blast 
injuries. Ann. Otol., etc., St. Louis, 1948, 57: 143-152. 
[CH] 
2957. Bebb, A. H. Underwater blast injury—some 
physical factors. Gt. Brit. MRC-RNPRC, UWB. Royal 
naval physiological laboratory, Alverstoke, Hants. R. N. P. 
51/641, U. W. B. 22, January 1951, 11 pp. 
2958. Benzinger, T. Physiological effects of blast in 
air and water, pp. 1225—1259 in: German aviation medi- 
cine World War II. Vol. II. Department of the Air Force, 
Washington, D. G., 1950, 1302 pp. [R] 
2959. Benzinger, T. Causes of death from blast. Amer. 
J. Physiol., 1951, 167: 767. Abstr. 
2960. Burnett, H. A. Early evaluation of blast injury. 
Milit. Surg., 1948, 103: 275-278. [CH] 
2961. Cameron, G. R. A survey of the effects of under- 
water blast on human beings and animals. Gt. Brit. MRG- 
RNPRG, UWB. R. N. P. 47/380,'U. W. B. 4, September 
1947, 4 pp. 
2962. Cameron, G, R. Summary of literature on the 
effects of underwater blast on human beings and animals 
(1940-47). Gt. Brit. MRG-RNPRC, UWB. R. N. P. 47/ 
381, U. W. B. 5, September 1947, 23 pp. [R] 
2963. Clemedson, C. J. Om undervattensdetonations- 
skador [Immersion Blast Injuries]. Tidskr. milit. Hdlsov., 
1948, 73: 1-34. 
2964. Clemedson, C. J. An experimental study on air 
blast injuries. Acta physiol, scand., Suppl., 1949, 61: 
1-200. [P] 
2965. Clemedson, C. J. and S. A. Granstom. Studies 
of the genesis of “Rib markings” in lung blast injury. 
Acta, physiol., scand., 1950, 21: 131-144. [P] 
2966. Cole, R. H. Underwater explosions. Princeton, 
Princeton University Press, 1948, 437 pp. [D] 
2967. Corey, E. L. Medical aspects of blast. Nav. med. 
Bull., Wash., 1946, 46: 623-652. [R] 
2968. Corey, E. L. and I, Gersh. Observations on the 
effects of air blast on the central nervous system and 
viscera of cats and rabbits. U. S. Navy. NMRI. Project 
X-219, 24 June 1944, 4 pp. [P] 
2969. Draeger, R. H., J. S. Barr, and W. W. Sager. 
Blast injury. J. Amer. med. Ass., 1946, 132: 762-767. 
/. industr. Hyg., 1947, 29: abstract section: 38-39. [RJ 
2970. Friedman, 0. Blast injuries of the ears. Arch. 
Otolaryng., Chicago, 1948, 47: 471-484. [CH] 
2971. Gala, P. Syndrome des phenomenes d’explosion. 
Rev. Med. nav., 1947,2: 31-50. [D] 
2972. Gt. Brit. MRC-RNPRC, UWB. Protection of 
divers against underwater explosions. R. N. P. 47/374, 
V. W. B. 1, 1 November 1945, 6 pp. 
2973. Martin, P. G. C. Perforation of rectum from 
immersion blast. Lancet, 1943: II: 605-606. [CH] 
2974. Netter, Frank H. Immersion blast injuries of the 
abdomen, pp. 153 in: The Ciba collection of medical illus- 
trations. Ciba Pharmaceutical Products, Inc., Summit, 
N. J., 1948, 222 pp. 
2975. Ruskin, A. and 0. W. Beard. The Texas City 
disaster—cardiovascular studies, with followup results. 
Tex. Rep. Biol. Med., 1948, 6: 234-259. [CH] 
2976. Smith, H. E. Accommodative defect following 
atmospheric concussion. Amer. J. Opthal., 1949, 32: 959- 
966. [CH] 
2977. U. S. Navy. BuNavPers. Water or immersion blast 
injuries, pp. 55-68 in: Submarine medicine practice. 
NavPers 10838, March 1949, 182 pp. [CH] [D] 
2978. U. S. Navy, Naval medical school, Bethesda, Md. 
Blast injury, pp. 176-177 in: Color atlas of pathology. 
Philadelphia, J. B. Lippincott Co., 1950, 546 pp. [CH]1 
2979. Wright, H. C. Subjective effects of distant under- 
water explosions. Gt. Brit. MRC-RNPRC, UWB. R. N. P. 
47/375, U. W. B. 2, April 1947, 25 pp. 
2980. Young, M. W. Mechanics of blast injuries. War. 
Med., Chicago, 1945, 8: 73-81. [R] [P] SPECIAL PROBLEMS OF SNORKEL 
2981-2986 
XI. DROWNING 
The danger of drowning in submariners, divers, 
and caisson and tunnel workers is probably greater 
than in other occupations, but because of the gen- 
eral nature of this particular subject it is recom- 
mended that the reader consult standard works on 
medicine and occupational diseases. The section 
on resuscitation and respiratory devices (p. 290) 
includes information pertaining to resuscitation 
from drowning, while the data presented here are 
concerned primarily with the physiological and 
biochemical events transpiring during drowning. 
Swann, Brucer, Moore, and Vezien {2985) 1947 
conducted drowning experiments on 8 healthy dogs 
under local procaine anesthesia. Drowning was 
accomplished by flooding a sealed face mask with 
fresh or salt water. Blood oxygen was found to drop 
to zero within 3 minutes after the beginning by 
water inhalation, but the carbon dioxide, after a 
transitory rise, fell again to the normal range. The 
pH declined to approximately 7.1. During fresh- 
water drowning there was an abrupt hemodilution, 
indicated by a rapid drop in plasma protein, hemo- 
globin, and chloride. In sea-water drowning, hemo- 
concentration occurred. During fresh-water drown- 
ing, ventricular fibrillation occurred in 4 out of 6 
dogs after 3 to 5 minutes of submersion. Fibrillation 
was not observed in any of the dogs drowned in sea 
water. 
Franko {2981) 1949 subjected anesthetized rab- 
bits to drowning by pouring water or Ringer’s solu- 
tion down the trachea. Circulation and respiration 
ceased most rapidly when the water at 20° C. was 
used. Dilution of arterial blood was rapid and 
powerful. Vagotomy, atropine injection, 38° C. 
water, or pregnancy slightly lengthened the time 
of survival. The author presumed that the injurious 
effects of water in the lungs are in principle due to 
the following factors: (1) prevention of external 
interchange of gases by liquid in the respiratory 
tract; (2) hydremia caused by absorbed water; 
(3) osmotic injuries in the lung tissue; and (4) the 
possible liberation of substances capable of decreas- 
ing the blood pressure. 
Anesthetized and unanesthetized rats drowned by 
submersion demonstrated four respiratory phases 
before cessation of respiratory movements. Gray 
{2982) 1951 describes these phases as: (1) a short 
period of apnea; (2) a period of dyspnea; (3) a 
long period of anoxic apnea; and (4) a short series 
of respiratory movements of about the amplitude of 
normal respirations, but accompanied by neck and 
facial movements. Rats submerged in water at 1.0° 
C. reached the beginning of the fourth phase in 
about 155 seconds, while in water at 40° C. the time 
required was approximately 95 seconds. The time 
of survival increased further as the temperature was 
raised to 55° C., and then decreased at higher 
temperatures. A report by Veen {2986) 1947 states 
that following the submersion of dogs in water, the 
volume of air remaining in the lungs decreased to 
approximately 107 cu. cm. 
Changes observed in the lungs and liver following 
drowning are reported by Shkaravskii {2983) 1949. 
In all cases observed, the fundamental argyrophil 
substances in the lungs and liver outlast the phases 
of dilution. The dilution of the fundamental argyro- 
phil substances occurs quickly, even in the short- 
duration drownings observed in human and in 
experimental animals. The quick onset of lung and 
liver edema during drowning was attributed to 
increased permeability of the filtering membranes. 
2981. Franko, 0. and A. Vartiainen, Effects of intra- 
tracheally poured water on blood pressure and respiration 
in rabbit, with reference to the pathologic physiology of 
drowning. Ann. Med. exp. Fenn., 1949, 27: 110-127. [P] 
2982. Gray, S. W. Respiratory movement of rat during 
drowning and influence of water temperature upon sur- 
vival after submersion. Amer. J. Physiol, 1951, 167: 95- 
102. [P] 
2983. Shkaravskii, F. I. Izmenenie osnovnogo argiro- 
filnogo veshchetva v legkikh i pecheni pri utoplenii. 
[Changes of fundamental argyrophil substances in the lungs 
and in the liver after drowning.] pp. 288-293 in; Gipok- 
siia, Kiev, Akad Nauk. Ukr. SSR., 1949, 415 pp. 
2984. Swann, H. G. and M. Brucer. The cardiorespira- 
tory and biochemical events during rapid anoxic death. 
VI. Fresh water and sea water drowning. Texas Rep. Biol. 
Med., 1949, 7: 604-618. Abstr. World Med., 1950, 8: 230. 
2985. Swann, H. G,, M. Brucer, C. Moore, and M, L. 
Vezien. Fresh water and sea water drowning: a study of 
the terminal cardiac and biochemical events. Texas Rep. 
Biol. Med., 1947, 5: 423-437. [P] 
2986. Veen, H. The air content of the lungs after 
drowning. Arch. need. Physiol, 1947, 28: 451-461 [P] 
XII. SPECIAL PROBLEMS OP SNORKEL 
In 1945, Hay ter and Bateman {2992) reported 
observations made during simulated snorkel opera- 
tions carried out at Portsmouth Navy Yard aboard 
the U. S. S. Sir age {SS 485) in September of 1945. 
At no time did the drop in barometric pressure 
approach levels dangerous to human life. The 
highest carbon monoxide concentration was only 
0.002 percent, which may be considered to be of 
no importance. The tests demonstrated that sub- 
mergence of the snorkel head for 45 seconds will 
not cause a dangerous drop in barometric pressure. 
Cycling operations in which the head valve is closed 
up to two-thirds of the time will reach pressure 
equilibrium at a safe pressure if the cycles are of 
short duration. Submergence of the snorkel head DISEASES AND ACCIDENTS 
for over 2 minutes will produce less of a reduction 
in pressure than that found at an altitude of 10,000 
feet. The incidence of aerotitis media encountered 
among personnel involved in these tests was high 
and indicated to the authors the need for further 
study along this line. It was noted that the condi- 
tions of the experiment were more severe than 
would probably be encountered in actual snorkel 
operations. The 19 men aboard were examined 
with an otoscope. Ten ears in eight men showed 
evidence of mild aerotitis media (grades 1 and 2), 
and one man had severe bilateral aerotitis media. 
The authors believed that the large number of 
involved ears encountered in these tests was due pri- 
marily to the sudden rise in barometric pressure 
encountered when the engines shut off. 
In 1947, Hayter (2991) gave a medical report on 
snorkel operations in the U. S. S. Amber jack (SS- 
522). The observations recorded in this report were 
made during two periods of snorkeling, one lasting 
55)/2 hours and the other 40 hours. The fluctuation 
of barometic pressure was usually 1 to 2 in. of Hg. 
Sleep was undisturbed by snorkeling under the con- 
ditions of these observations. During one period 
there was sufficient pain to awaken personnel when 
at the request of the medical officer maximum pres- 
sure fluctuations were produced. At this time, per- 
sonnel showed redness of the eardrums. Ventilation 
of the boat during snorkeling was found to be ade- 
quate. In 1947, a report was given by Bateman, 
Hayter, Haines, and Cook (2987) of a preliminary 
study of the medical aspects of snorkel operations 
carried out on American personnel manning the 
captured German submarine, U-873. Fifty-six 
American crew members were involved in the 
study. There were 4 days of snorkeling divided into 
two sessions a week apart. The short period of opera- 
tions and the limited number of subjects, as well as 
the differences between this submarine and those to 
which snorkels might be adapted prevents, accord- 
ing to the authors, any final, clear-cut answers to 
the many problems associated with snorkel opera- 
tions. It was found that the pressure variations were 
usually less than 1 in. of Hg during ordinary snorkel- 
ing, and personnel soon became accustomed to the 
constant pressure variations. During simulated loss 
of depth control, the pressure dropped to 18.5 in. 
of Hg (equivalent to an altitude of 12,400 feet) in 
a period of A/2 minutes. The most rapid rise in pres- 
sure recorded during the return of pressure to nor- 
mal was at a rate of 0.1 in. of Hg per second (aver- 
age, 0.03 in. of Hg per second). The limiting factor 
during simulated loss of depth control was the pres- 
ence of exhaust fumes in the engine room. The high- 
est carbon monoxide concentration there at these 
times was 4.7 parts per 10,000. The irritant char- 
acter of the fumes was such that exposure for more 
than a short time could not be tolerated. In these 
studies, 40 percent of the personnel developed aero- 
titis media of grade 2, 3, or 4. Grade 4 ears with 
free bleeding into the middle ear were present in 
16 percent of the subjects. The same incidence and 
severity of ear damage was encountered in ordinary 
snorkel operation as in simulated loss of depth 
control. During ordinary snorkel operations, no 
pain was associated with the damage and there 
was no apparent awareness of it, whereas dur- 
ing simulated loss of depth control it was neces- 
sary voluntarily to clear the ears. Some subjects 
with colds complained of moderate pain. In the 
subjects of these tests, the presence or absence 
of aerotitis media during the first snorkel session 
was a valid predictor of the presence or absence of 
aerotitis media during the second session. Admin- 
istration of the routine 50-lb. pressure test did not 
satisfactorily predict the occurrence of aerotitis 
media during snorkeling. The authors stated that in 
this regard more observations were necessary to de- 
termine the need for changing the test procedure in 
the selection of personnel for snorkel operations. A 
higher than ordinary incidence of aerotitis media 
was encountered in those personnel who slept dur- 
ing the snorkel operations (63 percent in the sleep- 
ing group as compared with 29 percent in the wak- 
ing group), and those who were suffering from cold 
(66 percent in those with colds as compared with 
31 percent in controls). No nausea, dizziness, or 
diarrhea were experienced by any of the crew, al- 
though these effects have previously been ascribed 
to snorkeling in the German reports. Subsequent 
experiences with snorkeling in the U. S. Navy and 
in the British Navy have revealed that aerotitis 
media is not a special hazard of normal snorkeling 
operations. 
Schaefer {2994), describing German operations 
in 1948, drew attention to periodic pressure drops 
of 200 and 300 millibars recorded within short in- 
tervals. He also reported middle-ear damage and 
defects of hearing in submariners in snorkel subma- 
rines. In discussing fluctuating atmospheric pres- 
sures under trial conditions with British prototype 
snorkel equipment, Ellis (2989) 1949 found no 
evidence to suggest that special conditions will 
occur in snorkel-fitted submarines to influence ad- 
versely the health or efficiency of the crews. Report- 
ing in 1949, Davidson (2988) found that carefully 
selected submariners experienced no special ear 
problems in snorkel submarines; in fact, hearing 
improved in some cases. DENTAL PROBLEMS 
2987-2995 
The effect of prolonged snorkeling on the health 
of officers and men and on the general habitalibity 
of the submarine has been a subject which has en- 
gaged the attention of submarine surgeons. Ritch 
{2993) 1948 has described medical aspects of a 
cruise of the guppy-snorkel submarine U. S. S. 
Trumpetfish (SS-425), in which the submarine 
was submerged for 330 hours. Of this time, 309 
hours were spent in snorkeling. Pressure fluctuations 
within the submarine of sufficient magnitude to 
require equalization within the middle ear occurred 
only during relatively short periods of time of the 
snorkel cruising. During the cruise, seven men ex- 
hibited tympanic membrane trauma visible on oto- 
scopic examination. Ritch discussed the following 
problems which may be enhanced in guppy-snorkel 
submarines; (1) boredom and tendency toward 
apathy of personnel; (2) general overcrowding, 
particularly in berthing facilities; (3) ventilation 
problems; (4) air-conditioning problems; (5) prob- 
lems of fresh-water distillation and sewage disposal; 
and (6) problems of garbage and refuse disposal. 
In these studies, 48 percent of the personnel re- 
ported that their ears were cleared automatically. 
Fifty-two percent of the men complained of some 
disturbance of sleep. Men with head colds experi- 
enced moderate to severe headaches associated with 
the pressure fluctuations. It was expected by the 
author that snorkeling in heavy seas would raise the 
percentage of ear trauma. 
Willmon and Ritch {2995) 1948 have reported 
on the general health and morale of officers and 
crew during a 30-day simulated war patrol aboard 
the U. S. S. Irex (SS-482). The U. S. S. Irex, 
an experimental snorkel submarine with conven- 
tional superstructure, was on patrol during the 
period from 1 to 30 March 1948 during which 
time she was submerged for 615 hours: 390 by 
snorkel and 225 on battery propulsion. During this 
patrol the morale and health were good. The 
authors considered that the increased monotony 
and emotional stress incident to a largely or totally 
submerged patrol makes mandatory an even more 
stringent personnel selection program and efforts 
toward increased physical and emotional comfort, 
proper illumination, pleasing interior color and 
design, and all diversions that may be practical. 
The effect on personnel of atmospheric pressure 
fluctuation due to opening and closing of the 
snorkel head valve presented no problem during this 
patrol. However, the conditions of operations were 
not considered to afford a critical evaluation of the 
problem in that only negligible pressure fluctuations 
were experienced. The authors emphasized the im- 
portance of an appraisal of the effect on personnel 
of prolonged snorkeling during periods of sleep, 
and recommended that this could be most easily 
accomplished by a proposed dockside study. 
Reference may also be made to a British com- 
mentary on problems of motion and time study in 
snorkel-fitted submarines {2990). 
2987. Bateman, J. G., R. Hayter, H. L. Haines, and 
N. L. Cook. A preliminary study of the medical aspects 
of schnorchel operations. U. S. Navy. BuMed., Project 
X-606 (Sub 131), 15 January 1947, 23 pp. [M] 
2988. Davidson, W, M. Physiological problems in snort- 
fitted submarines. /. R. nav. med. Serv., 1949, 35: 26-29. 
[R] 
2989. Ellis, F. P. Fluctuating atmospheric pressures. A 
novel environmental variant observed in submarines. 
Brit. J. industr. Med., 1949, 6: 24-30. [M] 
2990. Gt. Brit. MRC-RNPRC, OES. Notes on a meeting 
to discuss problems of motion and time study in snort- 
fitted submarines. R. N. P. 48/464, O. E. S. 151, 5 July 
1948, 5 pp. 
2991. Hayter, R. Medical report on snorkel operations 
of U. S. S. Amber jack (SS-522) U. S. Navy. Submarine 
base. New London, Conn. Medical research department. 
Project NM 002 009 (X—753, Sub. no. 156), Interim 
rept. no. 1, 16 December 1947, 7 pp. 
2992. Hayter, R. and J. G. Bateman. Observations 
made during simulated Schnorchel operations carried out 
at Portsmouth Navy Yard aboard the U. S. S. Sirage 
(SS-485) on 11, 12, and 13 September 1945. U. S. Navy. 
NMRI. Interim report, Project X-605 and X-606, 1 
November 1945, 6 pp. 
2993. Ritch, T. G. Report on the effects of prolonged 
snorkeling on the health of the officers and men and on 
the general habitability of the guppy-snorkel submarine 
U. S. S. Trumpetfish (SS-425). U. S. Navy. Submarine 
base, New London, Conn. Medical research department. 
Project NM 002 009 {X—753, Sub. no. 156), Rept. no. 2, 
12 April 1948, 9 pp. 
2994. Schaefer, K. E. Technical influences. IV. Air- 
pressure. Pp. B: 1-56—B: 1-59 in: Monograph on sub- 
marine medicine. Folio I, Germany. U. S. Zone. Office 
of naval advisor. 1948. 
2995. Willmon, T. L. and T. G. Ritch. The general 
health and morale of the officers and crew during a 
30-day simulated war patrol aboard a snorkel submarine. 
U. S. Navy. Submarine base, New London, Conn. Medi- 
cal research laboratory. Project NM 002 009, Rept. no. 3, 
4 November 1948, 8 pp. 
XIII. DENTAL PROBLEMS 
The problem of dental pain is one of particular 
concern not only in divers but also in aviators. 
Susceptibility to the traumatic effects of pressure 
changes on oral tissues depends primarily on a 
hyperemic pulp, pulpitis, or necrosis of the pulp. 
Exposure by Orban {2999) 1945 of dogs decom- 
pressed to a simulated altitude of 38,000 feet after 
their teeth had been test filled with amalgam, ce- 
ment, cilicate, zinc oxide and eugenol, and croton 
oil, showed no pathological changes in the teeth. 
One dog sacrificed at altitude and with the teeth 
fixed at altitude showed blood vessels surrounded by 2996-3002 
DISEASES AND ACCIDENTS 
polymorphonuclear leukocytes. Another dog sacri- 
ficed in the chamber revealed extensive hyperemia 
in the pulp with some microscopic bleeding. Addi- 
tional studies by Orban, Ritchey, and Zander 
{3000) 1945 on asphyxiated dogs revealed hypere- 
mia and hemorrhage in all teeth checked; both con- 
ditions were more or less independent of the cavity 
preparation or the use of croton oil. The control 
teeth showed similar findings. 
Kennon and Osborn {2996, 2997) in 1945 
ascribed pain in the oral tissue during decompres- 
sion or recompression to imperfect ventilation of 
the maxillary sinuses. Usually the pain was felt in 
the upper bicuspids or the first or second molars, 
the pain being sporadic or constant but not local- 
ized in any one tooth. Sometimes a burning or 
tingling occurred at the mucobuccal fold and this 
was sometimes accompanied by headache under 
the eyes, numbness, and pain in the maxilla or sinus- 
itis. Negative X-ray findings, slight sensitivity to 
percussion, and conspicuous absence of fillings lead 
the authors to believe that maxillary pain during 
changes in atmospheric pressure is the result of 
aerosinusitis. They recommend that zinc oxide and 
eugenol be used as a base material for cavity prepa- 
rations when dental pain is the result of pulpitis. 
Dental services aboard a submarine are rendered 
by the pharmacist’s mate only during dental emer- 
gencies. Routine care is given aboard the submarine 
tender for the personnel of submarines tied up 
alongside, and secondarily for relief crews and per- 
sonnel of the tender. It is imperative that oral 
tissues of submariners be placed in good condition 
prior to extensive patrol periods in war areas. 
Toothache or tissue infection render a man im- 
potent as a fighter at a time when his efficiency is 
a vital factor in the success of a submarine attack. 
Aboard the submarine, dental caries is rampant 
and can be attributed to poor oral hygiene and a 
diet very high in carbohydrates. Martin {2998) 
1946 reminds the reader that submariners are heavy 
coffee drinkers, drinking it “black and sweet.” 
Cakes and pies are usually in evidence in the galley. 
There is lots of bread and jam, lots of potatoes and 
gravy—carbohydrate galore! A continued carbo- 
hydrate diet of this type increases susceptibility to 
dental caries. 
Men with apparently sound teeth may, after sev- 
eral patrols, show evidence of caries activity. Such 
activity is difficult to detect by the regular mouth 
mirror and explorer examination. By the use of 
bite-wing X-rays these areas of caries activity may 
be demonstrated. As a general rule, all teeth with 
carious exposed pulps should be removed, and pulp 
cappings of exposed pulps are not recommended. 
In cases where the carious process has not pro- 
gressed to such a degree, intermediate bases should 
be inserted in most cavities prior to placing the 
alloy filling material. This is particularly desirable 
in the 2 and 3 surface cavities. 
Water distilled aboard the submarine is adequate 
for drinking and cooking purposes, but insufficient 
for frequent bathing. The shower room is secured 
most of the time unless a water reserve is built up. 
Dental hygiene is closely allied with bathing habits 
and many of the men admit that their toothbrushes 
remain unused day after day. Martin feels that the 
submariner just isn’t “tooth-conscious” and con- 
siders brushing of the teeth too much trouble on a 
war patrol. A program of dental education for sub- 
marine personnel should be made a part of general 
hygiene and first-aid instruction, and could be 
accomplished by pamphlets, slide pictures, or 
lectures. 
Disease of the gingival tissue may occur among 
personnel confined to a submarine for a long period 
of time. The etiology and treatment are adequately 
described in the dental literature elsewhere, and 
will not be included here because of lack of space. 
The factors listed for caries may contribute to the 
etiology of these conditions. 
For other reports on dental problems, the reader 
may consult articles by Pigott {3001) 1944 and 
Schuessler {3002) 1947. 
2996. Kennon, R. H. and C. M. Osborn. Relation of 
areodontalgia to aerosinusitis. Air Surg. Bull., 1945, 2: 
434-435.[P] 
2997. Kennon, R. H. and C. M. Osborn. Causes and 
treatment of aerodontalgia. Air Surg. Bull., 1945, 2: 
442-443. [CH] 
2998. Martin, W. B. Dental problems on submarines. 
Nav. med. Bull., Wash., 1946,46: 898-900. 
2999. Orban, B. Problems in aviation dentistry: Experi- 
mental studies of pulp changes produced in the decom- 
pression chamber. U. S. NRC-GAM. OEMcmr-5779, 
C. A. M. Kept. no. 481, 31 October 1945, 1 pp. [P] 
3000. Orban, B,, B. Ritchey, and H. A. Zander. Experi- 
mental study of pulp changes produced in the decom- 
pression chamber (1), (2). U. S. NRC-CAM. Final rept., 
OEMcmr-559, March 1946, 12 pp. [P] 
3001. Pigott, J. P. Dental pain at high altitudes: origin 
and treatment. U. S. NRC-CAM. C. A. M. Rept. no. 
383, OEMcmr-38, 23 October 1944, 8 pp. 
3002. Schuessler, C. The effect of high altitude on oral 
tissues. Milit. Surg., 1947, 100: 318-322. 
XIV. EFFECTS OF RADIOACTIVITY ON 
PERSONNEL 
Modern warfare imposes additional dangers to 
the combatant man, and the advent of nuclear 
power and atomic bomb explosions has introduced 
radiation exposure as a real hazard. It is possible for 
a ship or submarine to be sound mechanically after 
an atomic explosion, yet radiological contamination EFFECTS OF RADIOACTIVITY ON PERSONNEL 
may make its operation temporarily dangerous to 
deck personnel. Underwater swimmers operating in 
radioactive waters are also subject to radiation from 
fission-product particles. The danger in handling or 
even approaching contaminated objects lies primar- 
ily in the harmful gamma radiation, although beta 
and alpha particles are an additional, if minor, 
hazard. 
The literature included under this title is ad- 
mittedly not complete. The papers selected have 
been chosen principally because they have been re- 
ferred to in reports dealing with radiation sickness. 
For more complete descriptions of technical pro- 
cedures and physiological effects of radiation, ref- 
erence should be made to the classified literature. 
For general studies on radiation, papers by the 
following may be consulted: Behrens {3005) 1949 
and {3006) 1951; Brues {3010) 1948; Cronkite 
and Chapman {3014) 1949; Dobson and Lawrence 
{3016) 1948; Dunham, Cronkite, Le Roy, and 
Warren {3017) 1951; Warren {3033) 1942; War- 
ren and Bowers {3037) 1950; and Warren and 
Draeger {3038) 1946. An anonymous paper {3040) 
1951 is also listed. 
The clinical picture in radiation sickness has been 
described by Brues {3011) 1950. Following a single, 
brief exposure of the total body to a lethal dose of 
ionizing radiation, there is a latent period of one 
or more hours during which no manifestations are 
seen. This is followed by a period of prostration, 
which varies somewhat with the species. In dog and 
man, vomiting and listlessness are observed. Super- 
ficial hyperemia and evidence of transudation of 
plasma from the capillaries are noted during this 
period. There is some evidence that the initial re- 
sponse is mediated through the parasympathetic 
system, since it may be alleviated in part by atropine 
and vagotomy. 
Subsequent to the initial reaction there is a loss 
of appetite accompanied by greatly decreased food 
and water intake, and examination of the blood 
shows a precipitous fall of total white-cell count 
and the various cell types, ordinarily preceded by 
an increase in granular leukocytes, as seen in acute 
pyogenic infections. During the acute phase, which 
usually appears during the second week, the white- 
cell count is greatly depressed. This is ordinarily ac- 
companied by widespread gastrointestinal ulcera- 
tion and gingivitis. The anemia seen in this stage is 
due to failure of red-cell formation and to destruc- 
tion of red cells already present. Fever, tachycardia, 
increased rate of red-cell formation, and sedimenta- 
tion rates are observed in the third and fourth 
weeks. The delayed blood clotting and spontaneous 
bleeding into various sites have been shown to be 
the result of an increased concentration of heparin 
in the blood and can be counteracted by judicious 
use of protamine or toluidine blue, which combine 
with heparin. 
In addition, there is impairment of intestinal glu- 
cose absorption and a shift in the salt and water 
balance. Sublethal doses result in sterility in the 
male but, as a general rule, survivors recover the 
ability to form sperm within a few months. Termi- 
nally, the state resembles irreversible shock follow- 
ing massive trauma or hemorrhage or the terminal 
stages of overwhelming infectious disease. The blood 
pressure is depressed and renal function approaches 
zero. 
For other reports on clinical symptoms of radia- 
tion sickness, papers by the following may be con- 
sulted: Cronkite {3012) 1949; Hempelman, Lisco, 
and Hoffman {3021) 1952; Le Roy {3025) 1947; 
Nims {3026) 1949; Prosser {3028) 1947; and Raper 
{3029) 1950. 
The bleeding tendency, attributed to an increase 
of circulating heparin, was investigated by Allen 
and Jacobson {3003) 1947. Both bleeding and clot- 
ting times are prolonged, and this is accompanied 
by a thrombocytopenia. At death, hemorrhage is 
first seen in organs of motion such as the heart, 
intestines, lungs, urinary bladder, and skeletal mus- 
cle. The clotting time is returned to normal by anti- 
heparin substances, and therefore thrombocytopenia 
does not, per se, appear to play an important role 
in hemorrhage. The administration of vitamins K 
and G, calcium salts, and fresh, whole blood did not 
prevent hemorrhage. 
Experimental work by Cronkite {3013) 1950 and 
Cronkite, Ulrich, Eltzholtz, Sipe, and Schork 
{3015) 1949 on the hemorrhagic syndrome of acute 
ionizing radiation indicates that this phenomenon 
is the result of increased vascular fragility and 
thrombocytopenia. Evidence was presented suggest- 
ing that serum fibrinolysis may have been activated 
also. 
Observations on the radiation effect of atomic 
bombing are reported by Beck and Meissner {3004) 
1946. Bone-marrow studies on 20 Nagasaki patients 
demonstrated an anemia, neutropenia, and throm- 
bycytopenia. Seven post-morten examinations con- 
firmed this bone-marrow damage. Recovery of the 
bone marrow was noted clinically. Lawrence {3023) 
1949 investigated the urinary excretion pattern of 
17-ketosteroids in 11 dogs following exposure to a 
minimal lethal dose of total body X-radiation. All 
animals exhibited a significant increase in steroid 
excretion at some time between the 5th and 12th 
day following radiation. These values then fell to 
normal or subnormal levels by the 30th to 40th day. 3003-3021 
DISEASES AND ACCIDENTS 
This excretion pattern is interpreted to indicate an 
alteration of adrenal cortical and/or testicular 
activity. 
The cellular effects of radiation are reported in 
papers by Failla {3019) 1940, Lea {3024) 1946, 
and Warren {3032) 1942 and {3035) 1944. The 
review by Warren {3035) gives the following most 
recognizable cell changes after radiation exposure: 
(1) inhibition of mitosis; (2) breakage of chromo- 
somes; (3) lagging of chromosomes; (4) complete 
or partial adhesion of chromosome pairs; and (5) 
asymetry of mitosis. Vacuolation of the cytoplasm 
is the most consistent feature. Lea {3024) 1946 be- 
lieves that decomposition of proteins and other cell 
constituents by radiation may be injurious even in 
low concentrations, and recommends investigation 
of this matter. The overall chemical change may be 
small, but locally it may be high. 
For general studies on radiation pathology, papers 
by the following may be consulted: Benkwith 
{3007) 1946; Bloom {3008) 1948; Brown, Harden- 
bergh, and Tullis {3009) 1951; Schlaegel {3030) 
1947; Tullis and Warren {3031) 1947; Warren 
{3034) 1942 and {3036) 1946; and Zirkle {3039) 
1951. The study by Bloom is a large, definitive 
volume on the histopathology of irradiation pub- 
lished as one of the health volumes in Division IV 
of the National Nuclear Energy Series. Zirkle has 
reported gross effects of beta irradiation on re- 
stricted surfaces of rabbits following varying doses 
of radiation. The main effects in order of appear- 
ance were (1) erythema; (2) pigmentation; (3) 
epilation; (3) loss of outer layer of skin; (5) crust 
formation; (6) healing; and (7) regrowth of hair. 
Damage to the skin produced by massive doses of 
beta rays resembled thermal burns but showed two 
important differences. The various stages of beta 
damage required 4 to 7 times as long to develop, 
and secondly, the indirect action was confined to 
superficial tissue. Gross effects to total-surface beta 
irradiation includes (1) inflammation of the eye- 
lids; (2) erythema in the ears and feet; (3) closure 
of the eyes; (4) epilation and desquamation around 
the eyes, mouth, and nostrils; (5) ulceration; (6) 
regrowth of hair; and (7) tumor formation. 
3003. Allen, J. G. and L. 0. Jacobson. Hyperhepari- 
nemia: cause of the hemorrhagic syndrome associated with 
total body exposure to ionizing radiation. Science, 1947, 
105: 388-389. [R] 
3004. Beck, J. S. P. and W. A. Meissner. Radiation 
effects of the atomic bomb among the natives of Naga- 
saki, Kyushu. Amer. J. din. Path., 1946, 16: 634-639. 
3005. Behrens, C. F. Atomic medicine. New York, 
Thomas Nelson & Sons, 1949, 416 pp. 
3006. Behrens, C. F. Permissible dosage and considera- 
tions of calculated risk. U. S. Navy. NMRI. Lecture and 
review series no. 51-7, 2 July 1951, 21 pp. 
3007. Benkwith, K. B. Retinal hemorrhage as seen in 
an atomic-bomb casualty. Amer. J. Ophthal., 1946, 29: 
799-800. [CH] 
3008. Bloom, W. Histopathology of irradiation from 
external and internal sources. New York, McGraw-Hill 
Book Co., Inc., 1948, xxv, 808 pp. 
3009. Brown, C. S., E. Hardenbergh, and J. L. Tullis. 
The biochemical, cellular, and bacteriologic changes in 
thoracic duct lymph of dogs exposed to total body irradi- 
ation. U. S. Navy. NMRI. Project NM 006 012.04.29, 
14 pp. 
3010. Brues, A. M. Pathologic effects of ionizing radia- 
tions and radioactive materials. Proc. Soc. exp. Biol., 
N. Y., 1948, 42: xxii. 
3011. Brues, A. M. Radiation sickness, pp. 778-781 in: 
Medical physics. Volume II. Edited by Otto Glasser. 
Chicago, The Year Book Publishers, Inc., 1950, 1227 
pp. [R] 
3012. Cronkite, E. P. The clinical manifestations of 
acute radiation illness in goats. Nav. med. Bull., Wash., 
1949, 49: 199-215. 
3013. Cronkite, E. P. The hemorrhagic syndrome of 
acute ionizing radiation illness produced in goats and 
swine by exposure to the atomic bomb at Bikini, 1946. 
U. S. Navy. NMRI. Project NM 006 012.04.33, 21 De- 
cember 1950, 45 pp. Blood, 1950, 5: 32-45. [P] 
3014. Cronkite, E. P. and W. H. Chapman. A critical 
analysis of the syndrome of acute total body radiation 
illness, its role in atomic warfare and its influence on the 
future practice of military medicine. U. S. Navy. NMRI. 
Project NM 007 039, Kept. no. 13, 3 January 1949, 23 
pp. Milit. Surg., 1949, 104: 7—21. 
3015. Cronkite, E. P., F. W. Ullrich, D. C. Eltzholtz, 
C. R. Sipe, and P. K. Schork. The response of the periph- 
eral blood of swine to whole body X-ray radiation in the 
lethal range. U. S. Navy. NMRI. Project NM 007 039. 
Kept. no. 21, 7 April 1949, 11 pp. 
3016. Dobson, R. L. and J. H. Lawrence. Physiological 
effects of radiant energy. Annu. Rev. Physiol., 1948, 10: 
479-500.[R] 
3017. Dunham, C. L., E. P. Cronkite, G. V. Le Roy, S. 
Warren, The syndrome of acute radiation injury due to 
exposure of the whole body to the initial nuclear radia- 
tion of an atomic bomb. U. S. Navy. NMRI. Lecture 
and review series no. 51-10, 7 August 1951, 11 pp. 
3018. Ellinger, F. Newer concepts of radiation sickness 
and its treatment. U. S. Navy. NMRI. Lecture and review 
series no. 51—6, 23 May 1951, 14 pp. 
3019. Failla, G. Some aspects of the biological action 
of ionizing radiations. Amer. J. Roentgenol., 1940, 44: 
649-664. 
3020. Fulton, J. D., A. C. Arnold, R. B. Mitchell, and 
M. B. Danford. The antibody response of animals exposed 
to X-radiation. III. The protective effect of chemothera- 
peutic agents of a specific immune status of X-radiated 
mice. USAF. Randolph Field, Tex. School of aviation 
medicine. Project 21—47—002, Rept. no. 3, October 1951, 
iii, 15 pp. 
3021. Hempelmann, L. H., H. Lisco, and J. G. Hoffman. 
The acute radiation syndrome: A study of nine cases and a 
review of the problem. Ann. Intern. Med., 1952, 36: 279— 
510. [CH] EFFECTS OF RADIOACTIVITY ON PERSONNEL 
3022-3040 
3022. Kaplan, S. J., C. D. Tait, Jr., P. D. Wall, and 
R. B. Payne. Behavioral changes following radiation. I. 
Study of retention of a partially learned maze habit. USAF. 
Randolph Field, Tex. School of aviation medicine. (Un- 
numbered project), Rept. no. 1, March 1951, 33 pp. 
3023. Lawrence, G. H. The effect of total body X-radia- 
tion on 17-ketosteroid excretion in dogs. U. S. Navy. 
NMRI. Project NM 007 039, Rept. no. 22, 14 June 1949, 
12 pp. [P] 
3024. Lea, D. E. Actions of radiations on living cells. 
Cambridge, University Press. 1946, xii, 402 pp. 
3025. LeRoy, G. V. The medical sequelae of the atomic 
bomb explosion. J. Amer. med. Ass., 1947,134: 1143-1148. 
3026. Nims, L. E. Radiation. Anna. Rev. Physiol., 1949, 
11: 527-544. [R] 
3027. Pickering, J. E. Evaluation of the Land Self- 
Developing Film Badge dosimeter. USAF. Randolph 
Field, Tex. School of aviation medicine. Special rept.. 
May 1951, 4 pp. 
3028. Prosser, C. L. The clinical sequence of physiologi- 
cal effects of ionizing radiation in animals. Radiology, 
1947, 49: 299-313. (Spanish summary.) 
3029. Raper, J. R. Beta rays: biologic effects, pp. 66-71 
in: Medical physics. Volume II. Edited by Otto Glasser. 
Chicago, The Year Book Publishers, Inc., 1950, 1227 pp. 
[R] 
3030. Schlaegel, T. F., Jr. Ocular histopathology of 
some Nagasaki atomic-bomb casualties. Amer. J. Ophthal., 
1947, 30: 127-135. 
3031. Tullis, J. L. and S. Warren. Gross autopsy obser- 
vations in the animals exposed at Bikini. /. Amer. med. 
Ass., 1947, 134: 1155-1158. 
3032. Warren, S. Effects of radiation on normal tissues. 
Arch. Path., Chicago, 1942, 34: 443-450. [R] 
3033. Warren, S. Effects of radiation on normal tissues. 
Dunlap, C. E. III. Effects of radiation on the blood and 
the hemopoietic tissues, including the spleen, the thymus 
and the lymph nodes. Arch. Path., Chicago, 1942, 34: 
562-608. [R] 
3034. Warren, S. Effects of radiation on normal tissues. 
V. Effects on the respiratory system. Arch. Path., Chicago, 
1942, 34: 917-931. [R] 
3035. Warren, S. The histopathology of radiation le- 
sions. Physiol. Rev., 1944, 24: 225-238. 
3036. Warren, S. The pathologic effects of an instan- 
taneous dose of radiation. Cancer Res., 1946, 6: 449-453. 
[D] 
3037. Warren, S. and J. Z. Bowers. The acute radia- 
tion syndrome in man. Ann. intern. Med., 1950, 32: 207- 
216. 
3038. Warren, S. and R. H. Draeger. The pattern of 
injuries produced by the atomic bombs at Hiroshima and 
Nagasaki. Nav. med. Bull., Wash., 1946, 46: 1349-1353. 
3039. Zirkle, R. E. Effects of external beta radiation. 
First edition. New York, McGraw-Hill Book Co., Inc., 
1951, 242 pp. 
3040. Anon. Atomic-powered submarine. Mech. Engr., 
1951, 73: 17. Protection and Preservation of 
Personnel 
I. GENERAL STUDIES 
It is not sufficient to select personnel with high 
physiological and psychological reserves and with 
high tolerance of stress. Superimposed upon a 
realistic and efficient selection program must be 
efforts to protect personnel from intolerable stresses 
by attention to habitability, food and water supply, 
clothing, and special equipment and devices. In all 
procedures and plans for protection and preserva- 
tion of personnel, it must be borne in mind that the 
submarine is a fighting vessel. The effective fighting 
power of the submarine is the primary considera- 
tion, and all matters of protection and comfort of 
personnel are important in the degree to which 
they contribute to this. 
3041. 6t. Brit. Ministry of labour and national serv- 
ice. Part VI. Diving operations, pp. 29-30 in: Factories 
acts, 1937 and 1948, Work of engineering construction. 
London, His Majesty’s Stationary office, 1951, 55 pp. 
3042. Kopecky, E, E,, L. M. Biggs, and H. A. Lindsey. 
Comparison of the semirigid stretcher (NMRI Model A) 
now carried by most submarines with the Peters emergency 
stretcher. U. S. Navy. Submarine base. New London, 
Conn. Medical research department. Project NM Oil 019, 
Kept. no. 1, 31 March 1948, 5 pp. 
3043. Pointner, R. Clinical investigations with sub- 
mariners. pp. D:I-1—D:I-22 in; Monograph on sub- 
marine medicine. Folio VII, Germany. U. S. Zone. Office 
of naval advisor. 1948. [P] 
3044. Southwell-Sander, G. H. G. Recent advances in 
naval hygiene and preventive medicine. /. R. nav. med. 
Serv., 1947, 33: 294-305. [R] 
3045. U. S. Navy. BuMed. Submarine medicine, pp. 
198-212 in: A manual of naval hygiene. Government 
Printing Office, Washington: 1943, 340 pp. 
II. HABITABILITY 
A. LIGHTING 
The subject of artificial illumination is of basic 
importance in all inside working and living environ- 
ments, including the submarine. To maintain 
healthful and efficient visual function, it is neces- 
sary to provide adequate lighting. In the submarine 
only artificial illumination is used, and a unique 
situation is provided by this environment for the 
study of basic lighting requirements and the appli- 
cation of new lighting technique. The overheads 
tend to be low, and much of the overhead and wall 
space is occupied by pipes, conduits, dials, and other 
machinery. The deck space is confined largely to 
narrow passageways and walks. It is evident there- 
fore that special lighting problems are presented, 
and that in most cases illumination layouts of home 
and office cannot be transferred without modifica- 
tion to the submarine situation. 
A report by Tinker (3062) 1949 surveys the light- 
ing and painting conditions in several submarines. 
The most common deficiencies were found to be: 
(1) insufficient light at the places where visual dis- 
criminations have to be made; (2) marked bright- 
ness contrasts in adjoining surfaces; (3) lack of 
adequate uniformity in distribution of illumination; 
(4) disturbing spectral reflections from shiny sur- 
faces such as highly polished valve and switch 
handles; and (5) glare from excessively bright and 
poorly located light sources. The author reviews 
the spectral quality of color of light as it applies 
to submarine problems. He states that for threshold 
seeing, spectral yellow, or yellow light from sodium 
vapor lamps, is slightly more effective than other 
artificial illuminations. No illuminant is better than 
diffused daylight. 
Intensity of illumination was considered in rela- 
tion to visual acuity, size of object to be discrimi- 
nated, speed of vision, brightness contrast, and 
efficiency of performance. There are indications 
that visual efficiency of normal eyes increases 
rapidly as illumination is increased from a fraction 
of 1 up to 5 foot-candles, more slowly from there 
up to about 10 foot-candles, and very slowly from 
10 to about 20 foot-candles. When the object is 
small, visual efficiency improves by practical 
amounts up to 40 or 50 foot-candles. 
Visual efficiency and visual comfort are reduced 
by two factors of distribution: (1) glare from bright 
spots in the field of vision, and (2) marked bright- 
ness contrast between areas in the field of vision. 
Tinker {3063) 1950 recommends that illumination 
be as uniform as possible, and that brightness con- 
trasts between adjoining areas be small. Painted 
bulkheads, overheads, and furnishings should be 
pleasing and should provide reflecting surfaces. HABITABILITY—LIGHTING 
3046-3054 
The paint should be light enough to reflect a large 
portion of incident light: overheads, 70 to 80 per- 
cent; bulkheads, 40 to 50 percent; desk tops, 30 to 
40 percent; and floors, 20 to 25 percent. Good 
decorative schemes can be executed with a low 
brightness contrast of around 3 to 1. 
Interior decoration of the U. S. S. Cutlass in 1949 
is described by Dewey {3051) 1950. “Operation 
Rainbow” was initiated at the Philadelphia Navy 
Yard to increase the habitability of the submarine 
by the medium of color and lighting. Three differ- 
ent colors were used, making each compartment 
different from its neighbor. The color shades were 
green-gray, yellow-gray, and medium gray. Ladders 
and apparatus were painted also to give a feeling 
of expansiveness. Strong colors were not used be- 
cause it was felt that such visual stimulation caused 
fatigue. Individual bedlamps were used to increase 
the opportunity for sleep of crew members in the 
same compartment. Continuously lighted compart- 
ments were illuminated by indirect lighting to add 
to the feeling of depth and expansiveness, and the 
decks were tiled in brown to give an “earthy” 
atmosphere. 
The general subject of illumination is discussed 
by Farnsworth {3052 and 3053) 1950 with emphasis 
on intensity of illumination and spectral quality of 
light as they apply to the job performed. Insuf- 
ficient illumination may cause fatigue and ineffi- 
ciency, and continued effort under these conditions 
may result in eyestrain, astigmatism, myopia, and 
headaches. Differences in work efficiency while ex- 
posed to white and monochromatic light are in- 
significant. The author states that a room may be 
correctly lighted from a visual hygiene and working 
efficiency standpoint, but still may cause an un- 
pleasant feeling. A flatly lighted area is less pleasant 
than one with gradations. The light should diffuse 
over the room or compartment and blend into other 
lights with a moderate amount of contrast. The 
Tufts College report {3064) 1949 states that an 
objection against modern lighting arises from the 
uncomfortable effects of high brightness.'When the 
general brightness level is low, then relatively high 
brightness ratios become acceptable, and when the 
adaptive level is raised, then the brightness ratio 
must be reduced to remain acceptable. 
For a review of illumination problems as related 
to the working environment, the reader should con- 
sult reports by Brandt {3048) 1947; Chapanis, Gar- 
ner, and Morgan {3049) 1949; Crouch {3050) 
1945; and Hoffman {3057) 1947. A report by 
Schaefer {3060) in 1948 indicated that the re- 
searcher, when studying the effects of illumination, 
must also consider the photodynamic effect; i. e., 
optical sensitization by which the fluorescing sub- 
stances of the organism are rendered sensitive to rays 
of light which normally are inactive. These sub- 
stances are adrenalin, biliary pigments, vitamin D, 
and the carotinoids. He states that the withholding 
of chemotonic and sensutonic effects of light from 
the organism could cause a persistent condition of 
vagotonia. Stimulation of the vegetative system is 
reduced in montonous and gloomy environments. 
Lack of sunlight experienced by submarine per- 
sonnel during World War II was a cause for some 
concern, and the possibility of longer periods away 
from sunlight presented by snorkel operation may 
heighten interest in this field again. During World 
War II, ultraviolet lamps were used in a few sub- 
marines for sunbathing by the crew and disinfec- 
tion of the air by installing these lamps in the air 
ducts. A report by Blum {3046) in 1944 indicated 
that few if any beneficial effects were derived from 
irradiation by mercury arc lamps. There was a 
value associated with morale. Reports by Boeder 
{3047) 1950 and Ludwigh and Kinsey {3059) 
1946 state that ultraviolet radiations longer than 
365 millimicrons are without deleterious effect on 
the functions of the normal eye. 
For other general reports on illumination, the 
reader may consult articles by Grether {3054) 
1948; Hall and Greenbaum {3055) 1950; Hanes 
{3056) 1950; Kuhn {3058) 1950‘Tinker {3061) 
1946; U. S. Navy {3065) 1943; and Witheridge 
{3066) 1948. 
3046. Blum, H, F. The advisability of mercury arc 
lamps for irradiation of personnel of submarines. U. S. 
Navy. NMRI. NH6-1/All/NMRI-47, 25 February 1944, 
pp. 5. 
3047. Boeder, P. The effect of ultraviolet on the human 
eye. Amer. J. Optom., 1950, 27: 437-447. 
3048. Brandt, A. D. Industrial illumination, pp. 298—321 
in; Industrial health engineering. New York, John Wiley 
& Sons, Inc., 1947, 395 pp. [D] 
3049. Chapanis, A., W. B. Garner, and C. T. Morgan. 
The working environment. Light and color, pp. 417-419 
in: Applied experimental psychology. New York, John 
Wiley & Sons, Inc., 1949, 421 pp. 
3050. Crouch, C. L. The relation between illumination 
and vision. Ilium. Engn., N. Y., 1945, 40: 747—784. [D] 
3051. Dewey, H. S. Interior decoration for submarines. 
Proc. U. S. nav. Inst., 1950, 76: 1183-1185. 
3052. Farnsworth, D. Illumination, pp. 60-68 in: 
Handbook of applied psychology. Volume I. Edited by 
Douglas H. Fryer and Edwin R. Henry. New York, Rine- 
hart & Co., Inc., 1950, ix, 380 pp. [R] 
3053. Farnsworth, D. Illumination. U. S. Navy. Sub- 
marine base. New London, Conn. Medical research labora- 
tory. Project NM 003 041.18, Kept. no. 5, 1950, 9 pp. 
3054. Grether, W. F. Dial reading performance as 
related to illumination variables. II. Spectral distribution. 
USAF. Wright-Patterson air force base, Dayton, Ohio. 3055-3075 
PROTECTION AND PRESERVATION OF PERSONNEL 
Aero medical laboratory. Tech. rept. no. MCREXD-694- 
21 A, 1 December 1948, 26 pp. [P] 
3055. Hall, M. V. and L. J. Greenbaum. Areas of vision 
and cockpit visibility. Trans. Amer. Acad. Opthal. Oto- 
laryng., 1950, 55: 74-88. [R] [P] 
3056. Hanes, R. M. Some effects of shape on apparent 
brightness. /. exp. Psychol., 1950, 40: 650-654. 
3057. Hoffman, A. C. Luckiesh and Moss on reading 
illumination. /. appl. Psychol., 1947, 31: 44-53. 
3058. Kuhn, H. S. Illumination, pp. 287—306 in; Eyes 
and industry. Second edition. St. Louis, C. V. Mosby Co., 
1950, 378 pp. 
3059. Ludvigh, E. and V. E. Kinsey. Effect of long 
ultraviolet radiation on the human eye. Science, 1946, 
104: 246-247. [P] 
3060. Schaefer, K. E. Deficiency of light, pp. B: 
1-30-—B: 1—32 in; Monograph on submarine medicine, 
Folio I. Germany. U. S. Zone. Office of naval adviser. 
1948. 
3061. Tinker, M. A, Illumination standards. Amer. J. 
publ. Hlth., 1946, 36: 963-973. 
3062. Tinker, M. A. Lighting and color, pp. 357-374 
in: A survey report on human factors in undersea war- 
fare. Washington, D. C., National Research Council, 
1949, 541 pp. 
3063. Tinker, M. A. Building illumination, pp. 283—288 
in: Handbook of applied psychology. Volume I. Edited 
by Douglas H. Fryer and Edwin R. Henry. New York, 
Rinehart & Co., Inc., 1950, ix, 380 pp. 
3064. Tufts College. Illumination. 12 pp. in: Hand- 
book of human engineering data for design engineers. 
Tufts College, Institute for applied experimental psy- 
chology. SDC Human Engineering Project 20-G—l, 
Project Designation NR—783—001, Technical Report 
199-1-1, 1 December 1949, 410 pp. 
3065. U. S. Navy. BuMed. Lighting of ships, pp. 55—64 
in: A manual of naval hygiene. Government Printing 
Office, Washington, D. C., i943, 340 pp. 
3066. Witheridge, W. N. Light condition, pp. 119-127 
in: Industrial hygiene and toxicology. New York, Inter- 
science Publishers, Inc., 1948, 531 pp. 
B. VENTILATION AND AIR CONDITIONING 
1. GENERAL STUDIES 
Existence on a submarine is characterized by very 
crowded living and sleeping conditions, limited 
water supply, frequent high temperatures and hu- 
midity resulting from engineroom heat and shutting 
down of ventilation during certain periods of enemy 
contact and, finally, toxic levels of carbon dioxide 
and decreased concentrations of oxygen. A number 
of reports dealing with general problems of ventila- 
tion and air purification have been selected from the 
large volume of literature on air conditioning as 
being of possible application to the problems as 
encountered in the submarine service. References 
of a general nature have been listed below. 
3067. Bedford, T. The quality of the air. pp. 129-152 
in: Basic principles of ventilation and heating. London, 
H. K. Lewis & Co., Ltd., 1948, 401 pp. 
3068. Behnke, A. R., F. C. Houghten, W. V. Con- 
solazio, and N. Pace. Physiologic principles underlying 
naval ventilation. U. S. Navy. Naval medical school, De- 
partment of atmospheric hygiene, Bethesda, Md. Novem- 
ber 1942, 69 pp. 
3069. Bennet, M. G. Notes on visit to H. M. Submarine 
Tradewind. Gt. Brit. MRC-RNPRC, CES. R. N. P. 49/ 
520, C. E. S. 284, 26 January 1949, 2 pp. 
3070. Brandt, A. D. Heating, ventilating, and air con- 
ditioning for temperature, humidity, comfort, and odor 
content, pp. 280—290 in: Industrial health engineering. 
New York, John Wiley & Sons, Inc., 1947, 395 pp. [D] 
3071. Chapanis, A., W. R. Garner, and C. T. Morgan. 
The working environment. Atmospheric effects, pp. 396— 
408 in: Applied experimental psychology. New York, John 
Wiley & Sons, Inc., 1949, 421 pp. 
3072. Dewey, H. S. Submariner explains importance 
of undersea air conditioning. Heat Pip. Air Condit., 1950, 
22: 102-103. 
3073. Du Bois, E. F. Methods of air purification, pp. 
23-31 in: Review of recent work on air purification in 
submarines. U. S. Navy. BuMed. Submarine ventilation. 
Bulletin no. 4 (126632), March 15, 1919, 47 pp. 
3074. Gt. Brit. MRC-RNPRC, CES. Memorandum on 
air hygiene in warships. R. N. P. 48/446, C. E. S. 243, 
April 1948, 3 pp. 
3075. Herrington, L. P. Industrial ventilation, pp. 
288-297 in: Handbook of applied psychology. Volume I. 
Edited by Douglas H. Fryer and Edwin R. Henry. New 
York, Rinehart & Co., Inc., 1950, ix, 380 pp. 
2. AIR FLOW AND VOLUME 
Air-conditioning requirements vary according to 
the special conditions of the installation, which 
may be in a theater, factory, store, submarine, or 
any other enclosure occupied by human beings. 
Modern engineering practice of air conditioning 
involves two phases: (1) actual conditioning of 
air, that is, the controlled alteration of its tempera- 
ture, humidity, purity, carbon dioxide level, and 
oxygen concentration; and (2) ventilation, or re- 
placement of stale air in an enclosure by condi- 
tioned air. Correct air conditions are essential for 
proper functioning of mechanical equipment. 
Apart from the mechanical reaction, considerations 
of health, efficiency, and morale of the human 
occupants require that the air be fit to breathe. 
This requires the removal of fumes from a ship’s 
galley, engineroom, battery room, and waterclosets. 
Stale air must be replaced by fresh air. Moreover, 
the body gives off excess heat and moisture in the 
expired air and the air in contact with the surface 
of the body. 
Of interest experimentally were the responses of 
men exposed to wind velocities ranging between 10 
and 100 feet per minute and wet-bulb temperatures 
above 80° F. The subjects were observed over 4- 
hour periods during which they either sat still or 
worked. Dunham, Holling, Ladell, McArdle, Scott, 
Thomson, and Weiner {3091) 1946 found that 
environments with the air moving at speeds between 
10 and 75 feet per minute were extremely uncom- 
fortable when the men were working in overalls HABITABILITY—HUMIDITY CONTROL 
3076-3089 
at high dry- and wet-bulb temperatures. An in- 
crease in the velocity of air movement above 75 
feet per minute partially alleviated this condition, 
but speeds above 300 feet per minute gave no sig- 
nificant increases in comfort. When the tempera- 
ture of the air was above 100° F., conditions were 
made more intolerable by raising the rate of air 
movement above 300 feet per minute. Ventilation 
conditions in the submarine are reported by Schae- 
fer {3096) 1948. In this report on the problems of 
ventilation encountered on German submarines 
during World War II, the author describes the un- 
comfortable effects of high-velocity air movement 
channeled to men from small air ducts. In a report 
by Ellis {3092) 1948, the author states that sub- 
marine crews in northern waters are subjected to 
cold air drawn aft from the conning tower to the 
engineroom, but while in tropical waters this move- 
ment of warm air reduces the efficiency of the air- 
conditioning plant. It was found that the volume 
of breathable air available for each man in the 
submerged submarine is somewhere between 300 
and 500 cu. ft. 
In an investigation of the minimal quantity of 
replenishment air required in a living space to 
keep odors at an acceptable level in conjunction 
with the use of air cooling and activated carbon, 
Consolazio and Pecora {3090) 1946 found that, 
with air cooling alone, 5 cu. ft. per minute per 
man (3 cu. ft. per minute per bunk) of replenish- 
ment air would keep the odors at acceptable levels. 
The odor level in an air-cooled space was found to 
be dependent upon the following factors: (1) 
quantity of replenishment air; (2) temperature and 
humidity of the compartment air; (3) quantity of 
water condensed in the cooling coils; (4) hygiene 
of the occupants and cleanliness of the space; and 
(5) activity of the occupants. With activated car- 
bon the replenishment air could be further reduced 
to values as low as 1 cubic foot per minute per man. 
For additional reports on volume and air flow, 
the reader should consult reports by Gt. Brit. MRC- 
RNPRC {3093) 1950; Nelson, Eichna, Shelley, 
and Horvath {3094) 1946; and Nothdurft {3095) 
1946. 
3076. Chuiton, [ ]le. Les problemes d’hygiene que pose 
la vie a bord des sous-marins. Sem. Hop. Paris, 1948, 24: 
198-201. 
3077. Leopold, C. S. Conditions for comfort. Trans. 
Amer. Soc. Heat, and Vent. Engrs., 1947, 53: 295—304. 
[R] 
3078. Nothdurft, H. The necessity of air conditioning 
in combat submarines in the German navy. Gt. Brit. 
MRC-RNPRC, HS. R. N. P. 46/286, H. S. 131, undated, 
5 pp. 
3079. Scott, J. W. Conditions in H. M. S. Devonshire 
en route from Devonport, England, to Sydney, Australia, 
in September and October 1945. Gt. Brit. MRC-RNPRC, 
HS. R. N. P. 45/259, H. S. 102, December 1945, 6 pp. 
3080. Scott, J. W. and D. Y. Solandt. Survey of lighting 
and ventilation in barracks and in ships of the Royal 
Canadian Navy. Canada NRG. Proceedings of second 
meeting of associate committee on naval medical research. 
Project C4050, 7 October 1943, 2 pp. 
3081. Sellers, E. A. and J. M. Parker. Outline of pro- 
posed trials of air conditioning in frigates. Canada NRG. 
Proceedings of the fourth meeting of associate committee 
on naval medical research. Project C4118, 16 February 
1945, 7 pp. 
3082. Smith, K. R. Ventilation, pp. 68-74 in: Hand- 
book of applied psychology. Volume I. Edited by Douglas 
H. Fryer and Edwin R. Henry. New York, Rinehart & 
Co., Inc., 1950, ix, 380 pp. 
3083. Stiening, E. H. Air conditioning. Factors affect- 
ing human comfort and health: Fundamental require- 
ments of an air conditioning system, pp. 202-209 in: 
Introduction to industrial medicine. Edited by T. Lyle 
Hazlett. Second edition. Chicago, Industrial Medicine 
Publishing Co., 1947, 260 pp. 
3084. Urdahl, T. H. and W. C. Whittlesey. Warship 
ventilating, heating and air conditioning. Trans. Amer. 
Soc. Heat, and Vent. Engrs., 1943, 49: 35-48. Discussion 
by J. W. Markert. [R] 
3085. U. S. Navy. BuMed. Ventilation of submarines, 
pp. 31-36 in: A manual of naval hygiene. United States 
Government Printing Office, Washington, D. C., 1943, 
340 pp. 
3086. U. S. Navy. BuNavPers. Habitability and subma- 
rine health, pp. 156-174 in: Submarine medicine practice. 
NavPers 10838, March 1949, 182 pp. [D] 
3087. Winslow, C. E. A. and L. P. Herrington. The 
objectives of air conditioning, pp. 163—197 in; Tempera- 
ture and human life. Princeton, Princeton University 
Press, 1949, 272 pp. 
3088. Witheridge, W. N. Air conditioning, pp. 107- 
119 in: Industrial hygiene and toxicology. Edited by 
Frank A. Patty. New York, Interscience Publishers, Inc., 
1948, 531 pp. 
3089. Witheridge, W. N. Ventilation, pp. 275-348 in: 
Industrial Hygiene and Toxicology. Volume I. Edited by 
F. A. Patty. New York, Interscience Publishers, Inc., 1948, 
ix, 531 pp. [R] 
3. HUMIDITY CONTROL 
There is in the submarine a continuous evapora- 
tion of moisture into the air from four main sources: 
(1) storage batteries, (2) cooking, (3) human oc- 
cupants, and (4) bilges. Space can be made avail- 
able for sufficient air-conditioning machinery to 
control the dewpoint. Control of the dewpoint 
means control of the relative humidity, and it is 
the relative humidity more than the mere tempera- 
ture of the air that causes discomfort. With a build- 
up of a thousand pounds of moisture per day in 
the air of a submarine, relative humidity becomes a 
factor of major significance. 
Humidity control in submarines is important, but 
it is just as important a problem in industry. Be- 
cause of the engineering ramifications it is not in- 
tended under this heading to discuss the extensive 3090-3097 
PROTECTION AND PRESERVATION OF PERSONNEL 
literature on methods of regulating humidity. For 
a report on humidity problems aboard the sub- 
marine, a paper by Schaefer {3097) 1948 should 
be consulted. The relative humidity levels usually 
range between 70 and 90 percent in submarines 
operating in the middle latitudes. Lower relative 
humidities are present in the enginerooms where 
the temperatures are higher, but when calculated 
as vapor pressure, they are equivalent to the rest 
of the boat. Under long periods of submergence, 
moisture is dammed up in the submarine at an air 
temperature of 20° C. 
3090. Consolazio, W. V. and L. J. Pecora. Minimal re- 
plenishment air required for living spaces under conditions 
of mechanical cooling and in conjunction with the removal 
of odors by activated carbon and other means. U. S. Navy. 
NMRI. Project X-533, Kept. no. 4, 26 July 1946, 23 pp. 
[P] 
3091. Dunham, W., H. E. Holling, W. S. S. Ladell, B. 
McArdle, J. W. Scott, M. L. Thomson, and J. S. Weiner. 
The effects of air movements in severe heat. Gt. Brit. 
MRC-RNPRC, HS. R. N. P. 46/316, H. S. 152, August 
1946, 20 pp. [P] 
3092. Ellis, F. P. Environmental factors affecting 
health and efficiency in warships. Publ. Hlth., Lond., 1948, 
61: 104-107. Brit. med. ]., 1948, 1: 587-592. J. industr. 
Hyg., 1948, 30: abstract section: 86. [R] 
3093. Gt. Brit. MRC-RNPRC, CES. Recirculation of air 
in warships. R. N. P. 50/635, C. E. S. 333, 15 November 
1950, 3 pp. 
3094. Nelson, N., L. W. Eichna, W. B. Shelley, and 
S, M. Horvath. The effect of air movement on the loss 
of heat by evaporation, convection, and radiation from 
nude and clothed individuals. Fed. Proc. Amer. Soc. exp. 
Biol, 1946, 5: 76. 
3095. Nothdurft, H. The necessity of air conditioning 
in combat submarines in the German navy. Gt. Brit. MRC- 
RNPRC, HS. R. N. P. 46/286, H. S. 131, 18 December 
1946, 5 pp. 
3096. Schaefer, K. E. Conditions of ventilation on board, 
pp. B: 1-16—B: 1—28 in: Monograph on submarine medi- 
cine, Folio I, Germany. U. S. Zone. Office of naval advisor. 
1948. 
3097. Schaefer, K, E. The humidity aboard the sub- 
marine. pp. B: I—14—B: 1-16 in: Monograph on subma- 
rine medicine, Folio I, Germany. U. S. Zone. Office of 
naval advisor. 1948. 
4. TEMPERATURE CONTROL 
When the ocean or tropical air is warmer than 
the submarine, there is a passage of heat from the 
water into the boat. Heat is also added internally 
by hot engines, storage batteries, galley stove, elec- 
tric lights, radio and radar equipment, and the 
human occupants. An adult, when engaged in light 
work, gives off approximately 500 B. t. u. per hour. 
In comparison, a 25-watt electric light bulb gives 
off 85 B. t. u. per hour. Therefore, in a small en- 
closure as in the submarine, the rise in temperature 
and moisture of the air caused by the presence of 
a number of people is considerable. 
Information concerning the indices of comfort 
in moving air may be obtained from papers by 
Yaglou (3108 and 3110) 1947 and 1949. According 
to the author, the effective temperature scale over- 
estimates greatly the influence of humidity at the 
lower temperatures, and not enough allowance is 
made for humidity at the higher temperatures 
which approach the limit of man’s endurance to 
heat. This disability is attributed to absorption and 
adaptation phenomena, which had been overlooked 
in the index. A rational method is proposed for 
correcting the index on the basis of mean skin 
temperature. Kellogg {3104) published a paper 
in 1946 on the critical factors in minimal air cooling 
of living quarters. Studies were made on a group 
of 12 men, previously acclimatized to severe heat 
and maintained continuously for periods of \/<x 
days at each of a series of humidities in the dry-bulb 
temperature range from 76° to 93° F. (73° and 
83° E. T.). The skin temperature rose to 94° and 
95° F. at a dry-bulb temperature of 81° to 83° F., 
and remained in this range at the higher dry-bulb 
temperatures. Evaporative water loss during light 
activity varied with dry-bulb rather than with ef- 
fective temperature, and was doubled with in- 
creases in dry-bulb temperatures between 79° and 
86° F. The subjective response to temperature and 
skin wetness varied with the effective temperature 
rather than the dry-bulb temperature. The “just 
right” temperature arrived at by interpolation was 
found to be about 76° E. T. Practically all skins 
appeared to be “dry” at temperatures below 76° 
E. T. For the regimen employed, the threshold for 
producing heat rash seemed to lie between 82° 
and 84° F. with high humidities, and between 87° 
and 89° F. at low humidities. The men slept com- 
fortably and did not develop heat rash when the 
effective temperature did not exceed 78° and the 
dry-bulb temperatures did not extend beyond 
85° F. 
For a discussion of factors contributing to pleas- 
ant environments as related to temperature, the 
reader should consult a monograph by Bedford 
{3100 and 3101) 1948. The author found that with 
the cool-air, warm-wall environment the mean skin 
temperature is lower than when the air and walls 
were at the same temperature. A sudden drop of 
temperature (10° F.) is harmful to man in the 
tropics when the skin and clothing are wet with 
perspiration. The initial chilling suppresses sweat- 
ing and may reduce man’s ability to withstand heat 
for some time after returning to the hot atmosphere. 
Maximum comfort was attained when the skin tem- 
perature on the head, sternum, cheek, and the area 
over the carotid artery was 92.3° F. Man feels HABITABILITY—DISINFECTION OF AIR 
3098-3111 
“too cool” when the temperature of the skin over 
these areas is below 89° F., and temperatures 
above 96° F. give the sensation of being “too warm.” 
A report by the Climatic Efficiency Subcommittee 
of the Great Britain Medical Research Council 
{3103) 1951 stated that the 80° F. effective tem- 
perature should represent the upper desirable limit 
for environmental standards with 86° F. effective 
temperature as the upper tolerable limit. 
The American Society of Heating and Ventilat- 
ing Engineers {3098) 1951 presents evidence that in 
machinery spaces it is more practicable to use spot 
cooling of personnel at working areas than to at- 
tempt to obtain uniform ambient temperature. 
They also state that the minimum quantity of 
ventilation air required for sleeping spaces should 
be that which will limit the temperature rise over 
that of the outside air to not more than 10° F., 
or a minimum of 30 cu. ft. per minute per person, 
whichever is greater. The optimum temperature 
for berthing spaces is stated to be 70° F. Galley and 
food-handling spaces should have the air changed 
once every 1 to 4 minutes. 
The use of electrically heated foot-warming 
panels as a means of alleviating foot discomfort in 
naval personnel on duty in cold bridge areas of 
ships was investigated by Yaglou {3111) 1950. The 
efficient use of the heating panel was found to be 
limited to conditions of low wind velocities and 
temperatures above 0° F. In the presence of appre- 
ciable winds the panel’s effectiveness is greatly re- 
duced and the power consumption becomes too 
great in comparison with that of other methods 
of keeping the feet, or the whole body, warm. Addi- 
tional data on this subject are supplied in the papers 
by Nielsen {3105 and 3106) 1948. 
It is suggested that readers wishing to obtain 
further information on temperature control consult 
papers by the American Society of Heating and 
Ventilating Engineers {3099) 1951; Crowden and 
Angus {3102) 1947; Reese {3107) 1947; and 
Yaglou {3109) 1949. 
3098. American Society of Heating and Ventilating 
Engineers. Transportation air conditioning, pp. 981-996 
in: Heating ventilating air conditioning guide. 1951. 
Baltimore, Waverly Press, Inc., 1951, 1456 pp. 
3099. American Society of Heating and Ventilating 
Engineers. Instruments and measurements, pp. 1021-1040 
in: Heating ventilating air conditioning guide. 1951. 
Baltimore, Waverly Press, Inc., 1951, 1456 pp. 
3100. Bedford, T. Warmth and comfort, pp. 86-107 in; 
Basic principles of ventilation and heating. London, H. K. 
Lewis & Co., Ltd., 1948, 401 pp. 
3101. Bedford, T. Stimulating and pleasant environ- 
ments. pp. 115-128 in; Basic principles of ventilation and 
heating. London, H. K. Lewis & Co., Ltd., 1948, 401 pp. 
3102. Crowden, G. P. and T. C. Angus. Modern views 
on ventilation, warming and cooling. Practitioner, 1947, 
159: 210-217. [R] 
3103. Gt. Brit. MRC—UNPEG, CES. Review of activities. 
R. N. P. 50/638, C. E. S. 335, 23 November 1951, 7 pp. 
3104. Kellogg, R. H. Critical factors in minimal air 
cooling of living quarters. U. S. NMRI. Project X-205, 
Kept. no. 7, 26 November 1946, 17 pp. [P] 
3105. Nielsen, M, Unders0gelser over relationen mellem 
behagelighedsfornemmelser, opvarmningstilstand og fysio- 
logiske reaktioner ved stillesiddende arbejde. (Studies on 
the relation between sensations of comfort, degree of 
heating and physiological reactions.) Contribution no. 3. 
Committee for the study of domestic heating, Copen- 
hagen, 1947, 82 pp. 
3106. Nielsen, M. Undersogelser over betydningen af 
gulvopvarmning for behagelighedsfornemmelser og fod- 
temperaturer. (On the importance of heating of floors 
for the sensation of comfort and the temperatures of the 
lower extremities.) Contribution no. 4. Committee for 
the study of domestic heating, Copenhagen, 1948, 28 pp. 
[P] 
3107. Reese, J. M. The measurement of the thermal 
environment afloat. /. R. nav. med. Serv., 1947, 33: 
200-204. [R] 
3108. Yaglou, C. P. A method for improving the effective 
temperature index. Trans. Amer. Soc. Heat, and Vent. 
Engrs., 1947, 53: 307-312. [M] [R] 
3109. Yaglou, C. P. Thermometry, pp. 70-77 in: Physi- 
ology of heat regulation and the science of clothing. 
Edited by L. H. Newburgh. Philadelphia, W. B. Saun- 
ders Co., 1949, viii, 457 pp. 
3110. Yaglou, C. P. Indices of comfort, pp. 277—287 in: 
Physiology of heat regulation and the science of clothing. 
Edited by L. H. Newburgh. Philadelphia, W. B. Saunders 
Co., 1949, viii, 457 pp. 
3111. Yaglou, C. P. Performance characteristics of 
BuShips footwarming panel designed for use in semi- 
exposed bridge areas of ships. U. S. Navy. NMRI. 
Project X-189, Rept. no. 12, 21 December 1950, 13 pp. 
5. DISINFECTION OF AIR 
Most airborne diseases are spread in enclosed 
spaces where people are in close proximity. Recent 
studies on air disinfection have indicated two dis- 
tinct control measures: (1) suppression of dust and 
lint, and (2) disinfection of droplet nuclei. The con- 
trol of relative humidity is also an important factor. 
In the submarine the suppression of dust and lint 
is not of prime concern because of the deterring 
effect on dust formation by spilled oil from machin- 
ery parts. For general studies on air disinfection, the 
reader should consult papers by the American So- 
ciety of Heating and Ventilating Engineers {3112) 
1951; Wolman, Fair, Hardenbergh, Lawrence, 
Maxcy, Tiedeman, Whittaker, and Yaglou {3143) 
1947; and Yaglou and Wilson {3144) 1942. The 
following anonymous papers may also be consulted: 
{3145 and 3146) 1946 and 1947. 
The mechanism of aerosols in aerial disinfection 
was discussed by Puck {3128 and 3129) 1947. Theo- 
retical analysis of chemical action reveals that the 
rapid killing properties of aerial disinfectants can- PROTECTION AND PRESERVATION OF PERSONNEL 
not be accounted for by a collision process between 
germicidal aerosol particles and the airborne bac- 
teria. However, a mechanism involving condensa- 
tion of germicide molecules in the vapor state on 
the bacteria-containing droplets results in a theoret- 
ical velocity of the correct order of magnitude. Ex- 
perimental tests by the author showed that pure 
germicide vapors free of aerosol droplets are almost 
instantly lethal to airborne bacteria. Conversely, 
pure germicidal areosols in the absence of vapor 
had no effect on airborne bacteria within 20 minutes 
or more. Puck concluded that rapid air sterilization 
requires the existence of the germicide in the vapor 
state. According to Lester, Kaye, Robertson, and 
Dunklin {3124) 1950, minute quantities of tri- 
ethylene glycol vapor (2.5 micrograms per liter of 
air) are sufficient to produce maximum rates of 
bacterial action. Relative humidity limits the max- 
imum concentration of glycol which can accumulate 
within the airborne particle. The authors state that 
the glycol-water content of the particle should al- 
ways maintain an equilibrium with the vapor con- 
centration of these substances in the air. Humidity 
controls the staturation concentration according to 
physicochemical principles, and at high humidities 
the particles in equilibrium contain so much water 
that highly bactericidal concentrations of glycol are 
unattainable. 
In an experiment on the efficacy of triethylene 
glycol for air sterilization, medical personnel at the 
U. S. Naval Training Center, Great Lakes, 111. 
{3140 and 3141) 1951, treated naval barracks with 
this substance. Each of these barracks housed 240 to 
320 persons. Epidemics of influenza, streptococcal 
infections, and other acute respiratory infections 
occurred during the experimental period. The air 
in the dormitories contained triethylene glycol vapor 
in concentrations exceeding 2.5 micrograms per liter 
of air. It was found that the counts of airborne 
bacteria were reduced approximately 65 percent in 
the glycol-treated barracks. Beta-hemolytic strepto- 
cocci were recovered from the environment during 
the last 2 months of the study. No consistent reduc- 
tion in acute respiratory diseases was found to occur 
in the 661 men living in the experimental dormi- 
tory. Additional information provided by the work 
of Bigg, Jennings, and Olson {3113) 1947 showed 
a 42-percent reduction of disease incidence (colds, 
atypical virus pneumonia, streptococcal infections, 
measles, mumps, etc.) in men living and working in 
triethylene-glycol-vapor-treated buildings. 
Gedda {3116) 1950 published a report on the 
effectiveness of triethylene-glycol-vapor disinfection 
in an ear, nose, and throat clinic and a children’s 
home. In the clinic waiting room the bacterial con- 
centration of the air was reduced approximately 30 
percent, and a 40-percent reduction was reported 
in the children’s home. For related articles, the 
reader may wish to consult reports by Bigg, Olson, 
Garlock, and Jennings {3114) 1946; Lester, Rob- 
ertson, Puck, and Wise {3125) 1949; Loosli, Smith, 
Gauld, Robertson, and Puck {3126) 1947; Puck 
and Chaney {3130) 1946; Robertson {3132) 1947; 
Jennings and Bigg {3122) 1943; Robertson, Appel, 
Puck, Lemon, and Ritter {3133) 1948; Robertson 
and Lester {3134) 1951, and Rosebury, Meiklejohn, 
Kingsland, and Boldt {3137) 1947. 
Ultraviolet radiation for the control of airborne 
infections has been studied extensively at the Naval 
Training Center, Great Lakes, 111. In these studies 
the floors were oiled, and oil-processed blankets were 
issued. Ultraviolet lamps were suspended from the 
ceiling and radiated upward; they were turned on 
100 hours before the recruits entered the buildings. 
Miller, Jarrett, Willmon, Hollaender, Brown, Le- 
wandowski, and Stone {3127) 1948 found that 
ultraviolet radiation of the floors and upper air in 
these barracks housing recruits resulted in a 19.2- 
percent overall reduction in total respiratory disease. 
Streptococcal disease rates were at a very high level 
during this particular test period, and a 24-percent 
reduction in rate was obtained. Followup studies 
by Willmon, Hollaender, and Langmuir {3142) 
1948 covering a 4-year period showed that respira- 
tory admission rates at sickbay, irradiated groups 
were consistently lower than rates from comparable 
control groups. Reductions as great as 20 to 25 per- 
cent were frequently observed. The authors con- 
cluded that ultraviolet radiation has a partial effect 
on certain types of respiratory diseases among re- 
cruits, but they caution that the results warrant 
continuing research. 
It is quite natural to assume that men returning 
from leave bring pathogenic organisms aboard the 
submarine. Infections—especially respiratory infec- 
tions—can be traced to contacts with shore-based 
personnel, lowered individual resistance, and in- 
clement weather during the leave period. Quoting 
from one patrol report, “Ninety percent of the crew 
had colds due more or less to the sudden change of 
climate from Pearl Harbor to Dutch Harbor.” The 
effects of ultraviolet lamps installed in the air ducts 
of submarines on airborne bacteria was investigated 
by Ingraham {3120) 1944. The lamps were of the 
low-pressure mercury-vapor type and were rated at 
8 watts. Eighty percent of the emitted radiation is 
at the level of 2,537 Angstrom units. It was found 
that the bacterial counts were lower with the lights HABITABILITY—DISINFECTION OF AIR 
3112-3133 
on, except in one instance of simulated submergence 
at the dock. 
In general, the evidence does not indicate a clear- 
cut value of ultraviolet lighting in reducing infec- 
tions of personnel in closed spaces. For other studies 
of the role of ultraviolet radiation in the conti ol of 
airborne infections, reports by the following authors 
should be consulted: Coblentz {3115) 1942; Hama 
{3117) 1949; Hart {3118) 1942; Hollaender 
{3119) 1942; Jarrett {3121) 1949; Laurens {3123) 
1942; Rentsehler {3131) 1942; Robinson {3135) 
1942; Ronge {3136) 1948; Scott and Locke {3138) 
1944; and Scott and Locke {3130) 1945. 
3112. American Society of Heating and Ventilating 
Engineers. Air conditioning in the prevention and treat- 
ment of disease, pp. 137-156 in; Heating ventilating air 
conditioning guide. 1951. Baltimore, Waverly Press, Inc., 
1951, 1456 pp. 
3113. Bigg, E., B. H. Jennings, and F. C. W, Olson. 
Triethylene glycol vapor distribution for air sterilization. 
Trans. Amer. Soc. Heat, and Vent. Engrs., 1947, 53: 
397-406. [P] 
3114. Bigg, E., F. C. W. Olson, F. C. Garlock, and B. H. 
Jennings. The control of airborne infections by the use of 
triethylene glycol. Proc. cent. Soc. din. Res., 1946, 19: 
67. [P] 
3115. Coblentz, W. W. Standardization of ultraviolet 
lamps used as sources of germicidal radiation, pp. 138-141 
in: Aerobiology. Edited by Forest Ray Moulton. Ameri- 
can Association for the Advancement of Science. Wash- 
ington, D. C., 1942, 289 pp. 
3116. Gedda, E. Triethyelene glycol in air disinfection. 
Abstr. World. Med., 1950, 7: 561. Nord. Med., Stockholm, 
1949, 41: 363-371. 
3117. Hama, 6. M. Ultraviolet exposure from germicidal 
lamps. Industr. Med., 1949, 18: 75—76. [CH] 
3118. Hart, D. The importance of airborne pathogenic 
bacteria in the operating room: a method of control by 
sterilization of the air with ultraviolet radiation, pp. 186— 
192 in: Aerobiology. Edited by Forest Ray Moulton. 
American Association for the Advancement of Science. 
Washington, D. C., 1942, 289 pp. 
3119. Hollaender, A. Abiotic and sublethal effects of 
ultraviolet radiation on micro-organisms, pp. 156—165 in: 
Aerobiology. Edited by Forest Ray Moulton. American 
Association for the Advancement of Science. Washington, 
D. C., 1942, 289 pp. 
3120. Ingraham, H. S. Evaluation of the bactericidal 
power of ultraviolet lamps on the air of the submarine 
U. S. S. Angler. With supplementary report on tests for 
the presence of stibine. U. S. Navy. NMRI. Project X-45 
{Sub. no. 15), 4 April 1944, 18 pp. 
3121. Jarrett, E. T. The evaluation of ultraviolet radia- 
tion for control of airborne infections in naval barracks. 
U. S. Navy, Naval training center. Great Lakes, 111., 
Medical research unit no. 4. Project 005 051.01 (NM 
005 008). 10 August 1949, 33 pp. [P] 
3122. Jennings, B. H., and E. Bigg. Studies and in- 
vestigations in connection with ventilating problems in- 
volved in utilization of propylene and triethylene glycol 
vapors for air sterilization. U. S. OSRD. Northwestern 
University Contract no. OEMcmr-175, Final Kept., July 
1943, 26 pp. 
3123. Laurens, H. The physiological effects of ultra- 
violet radiation, pp. 142-155 in: Aerobiology. Edited by 
Forest Ray Moulton. American Association for the Ad- 
vancement of Science. Washington, D. G., 1942, 289 pp. 
3124. Lester, W., Jr., S. Kaye, 0. H. Robertson, and 
E. W, Dunklin. Factors of importance in the use of tri- 
ethylene glycol vapor for aerial disinfection. Amer. J. 
publ. Hlth., 1950, 40: 813-820. [R] 
3125. Lester, W., 0. H. Robertson, T. T. Puck, and 
H. Wise. The rate of bactericidal action of triethylene 
glycol vapor on micro-organisms dispersed into the air in 
small droplets. Amer. J. Hyg., 1949, 50: 175-188. 
3126. Loosli, C. G., M. H. D. Smith, R. L. Gauld, 0. H. 
Robertson, and T. T. Puck. Control of cross-infections in 
infants’ wards by the use of triethelyene glycol vapor. 
Amer. J. publ. Hlth., 1947, 37: 1385-1398. 
3127. Miller, W. R., E. T, Jarrett, T. L. Willmon, A. 
Hollaender, E. W. Brown, T. Lewandowski, and R. S. 
Stone. Evaluation of ultraviolet radiation and dust control 
measures in control of respiratory disease at a naval train- 
ing center. J. infect. Dis., 1948, 82: 86-100. 
3128. Puck, T. T. The mechanism of aerial disinfection 
by glycols and other chemical agents. I. Demonstration 
that the germicidal action occurs through the agency of 
the vapor phase. J. exp. Med., 1947, 85: 729-739. 
3129. Puck, T. T. The mechanism of aerial disinfection 
by glycols and other chemical agents. II. An analysis of the 
factors governing the efficiency of chemical disinfection of 
the air. /. exp. Med., 1947, 85: 741-757. 
3130. Puck, T. T. and A. L, Chaney. The dispersal and 
control of triethylene glycol vapor for aerial disinfection. 
Amer. industr. Hyg. Ass. Quart., 1946, 7; 10—16. 
3131. Rentsehler, H. C. Production and control of bac- 
tericidal ultraviolet radiation, pp. 166-170 in: Aerobiology. 
Edited by Forest Ray Moulton. American Association for 
the Advancement of Science. Washington, D. C., 1942, 
289 pp. 
3132. Robertson, 0. H. New methods for the control of 
airborne infection with especial reference to the use of 
triethylene glycol vapor. Wis. med. ]., 1947, 46: 311-317. 
[D] 
3133. Robertson, 0. H., E. M. Appel, T. T. Puck, H. M. 
Lemon, and M. H. Ritter. A study of the bactericidal 
activity in vitro of certain glycols and closely related com- 
pounds. /. infect. Dis., 1948, 83: 124-137. 
3134. Robertson, 0. H. and W. Lester, Jr. The lethal 
effect of triethylene glycol vapor on dried airborne bac- 
teria. Amer. J. Hyg., 1951, 53: 69—79. [P] 
3135. Robinson, E. W, Practical considerations in the 
design and maintenance of ultraviolet air sanitation equip- 
ment. pp. 181-183 in: Aerobiology. Edited by Forest Ray 
Moulton. American Association for the Advancement of 
Science. Washington, D. G., 1942, 289 pp. 
3136. Ronge, H. E. Ultraviolet irradiation with artificial 
illumination. A technical, physiological, and hygienic study. 
Acta physiol, scand., Suppl., 1948, 49: 7-183. [P] 
3137. Rosebury, T., G. Meiklejohn, L. C. Kingsland, 
and M. H. Boldt. Disinfection of clouds of meningopneu- 
monitis and psittacosis viruses with triethylene glycol 
vapor. /. exp., Med., 1947, 85: 65-76. 
3138. Scott, J. W. and W. Locke. A survey of methods 
for air sterilization. Canada NRG. Proceedings of third 
meeting of associate committee on naval medical research. 
Project C4081. 15 May 1944, 3 pp. 
3139. Scott, J. W. and W. Locke. The sterilization of 
air with ultraviolet light. Canada NRG. Proceedings of 
the fourth meeting of the associate committee on naval 3140-3150 
PROTECTION AND PRESERVATION OP PERSONNEL 
medical research. Project C4097, 16 February 1945, 5 
PP- [P] 
3140. IT. S. Navy. U. S. Naval training center, Great 
Lakes, 111. Naval medical research unit no. 4. The use of 
triethylene glycol for control of acute respiratory diseases 
in Navy recruits. I. Physical factors and the effect on air- 
borne bacteria. Project NM 005 051.05.01, 15 October 
1951, 40 pp. 
3141. XL S. Navy. U. S. Naval training center, Great 
Lakes, 111. Naval medical research unit no. 4. The use of 
triethylene glycol for control of acute respiratory diseases 
in Navy recruits. I. Physical factors and the effect on 
airborne bacteria. Project NM 005 051.05.02, 15 Septem- 
ber 1951,45 pp. 
3142. Willmon, T. I., A. Hollaender, and A. D. Lang- 
muir. Studies of the control of acute respiratory diseases 
among naval recruits. I. A review of a 4-year experience 
with ultraviolet irradiation and dust suppressive measures, 
1943 to 1947. Amer. J. Hyg., 1948, 48: 227-232. [P] 
3143. Wolman, A., G. M. Fair, W. A. Herdenhergh, 
R. E. Lawrence, K. F. Maxcy, W. D. Tiedeman, H. A. 
Whittaker, and C. P. Yaglou. Recent studies on disin- 
fection of air in military establishments. Amer. J. publ. 
Hlth., 1947, 36: 189-198. [R] 
3144. Yaglou, C. P., and U. Wilson. Disinfection of air 
by air conditioning processes, pp. 129-132 in: Aerobiol- 
ogy. Edited by Forest Ray Moulton. American Association 
for the Advancement of Science. Washington, D. G., 1942, 
289 pp. 
3145. Anon. Recent studies in disinfection of air in 
military establishments. Amer. J. publ. Hlth., 1947, 37: 
189-198. 
3146. Anon. The problem of airborne infection in war- 
ships. Roy. Nav. med. Bull., 1946, 22: 1—9. [R] 
6. ELIMINATION OF DUST, GASES, FUMES, AND 
ODORS FROM AIR 
In confined spaces intended for human occu- 
pancy, the processes of ventilation and air condition- 
ing simultaneously control the moisture content, 
temperature, movement, and quality of air. Con- 
sidering the quality of air, it is generally accepted 
that when the only source of contamination is the 
human occupant, the minimal quantity of outdoor 
air needed is that required to remove objectionable 
body odors, galley vapors, and tobacco smoke. The 
odor level in a space depends primarily upon a num- 
ber of factors, including characteristics of the en- 
vironment, dietary and hygenic habits of the oc- 
cupants, the amount of outdoor air supplied, 
whether smoking is permitted or not, the space 
allowed per person, the capacity of the wet-coil 
cooling surface to remove odors, and the tempera- 
ture and relative humidity. 
Odors complained of most frequently by sub- 
marine personnel are those emanating from the 
waste products from the lavatories and galleys which 
are collected in sanitary tanks. Military security 
prevents emptying the tanks during hostilities, ex- 
cept upon surfacing under cover of darkness. The 
tanks are then “blown” dry with compressed air. 
During long patrols, despite frequent emptying and 
the use of various disinfectants, the tanks become 
unpleasantly odorous. The removal of odors from 
submarine air by various methods has been investi- 
gated by Consolazio and associates {3150, 3151, 
3152 and 3155). Under conditions of mechanical 
cooling in conjunction with the use of activated car- 
bon, Consolazio and Pecora {3152) 1947 found that 
the odor level for a circulation rate of 5 cu. ft. per 
minute per man at 78° F. effective temperature was 
of the same order of magnitude as that for 53 cu. ft. 
per minute per man for weather air. Odoriferous 
substances were condensed on the cooling coils and 
subsequently removed along with the water con- 
densed from the air. With activated carbon, the 
replenishment air necessary for maintenance of an 
acceptable odor condition could be reduced below 
5 cu. ft. per minute per man. The use of ozone did 
not reduce the odor level. 
According to Korotianskii and Mirskii {3157) 
1946, the soiling of air in caissons is attributable to 
three major factors: (1) contamination of the air 
by oil vapor; (2) soiling of the air as a result of the 
nature of work; and (3) contamination of the air 
by infiltration of outside natural gases (methane, 
carbon dioxide, etc.) from the river or sea bottom. 
The authors give quantitative evaluations of the 
methods used for air purification. The air purifiers 
were tested under varying conditions of pressure, 
temperature, and oil concentration. 
McCord and Witheridge {3162) 1946 in their 
excellent text state that offensive odors unfavorably 
influence health only through the possibilities of 
lessening food and water intake, disturbing sleep, 
and promoting nausea and vomiting. For related 
articles, the reader may wish to consult reports by 
the American Society of Heating and Ventilating 
Engineers {3147, 3148 and 3149) 1951; Florida 
Chemical Research Co. {3156) 1950; Kuehner 
{3158) 1947; Loosli {3159) 1948; Luaces {3160) 
1946; McCord {3161) 1952; Policard {3163) 1947; 
Ray {3164) 1952; U. S. National Research Council 
{3165) 1949; and Watson {3166) 1948. 
3147. American Society of Heating and Ventilating 
Engineers. Air contaminants, pp. 157-172 in: Heating 
ventilating air conditioning guide. 1951. Baltimore, Wa- 
verly Press, Inc., 1951, 1456 pp. 
3148. American Society of Heating and Ventilating 
Engineers. Physiological principles, pp. 117-136 in: 
Heating ventilating air conditioning guide. 1951. Balti- 
more, Waverly Press, Inc., 1951, 1456 pp. 
3149. American Society of Heating and Ventilating 
Engineers. Air cleaning, pp. 709-724 in: Heating venti- 
lating air conditioning guide. 1951. Baltimore, Waverly 
Press, Inc., 1951, 1456 pp. 
3150. Consolazio, W. V. and D. G. Doherty. Evaluation 
of an activated carbon canister (Dorex) and blower de- HABITABILITY—CARBON DIOXIDE ABSORBENTS 
3151-3166 
signed especially for removal of offensive odors. U. S. 
Navy. NMRI. Project X-533, Kept. no. 1, 25 June 1945, 
5 pp. [P] 
3151. Consolazio, W. V, and J. D. O’Neal. An evalua- 
tion of activated carbon as a means of odor control in meat 
and garbage lockers. U. S. Navy. NMRI. Project X-533, 
Kept. no. 5, 21 August 1946, 6 pp. [P] 
3152. Consolazio, W. V. and L. J. Pecora. Minimal 
replenishment air required for living spaces: under condi- 
tions of mechanical cooling and in conjunction with the 
removal of odors by activated carbon and other means. 
/. industr. Hyg., 1947, 29: abstract section: 83. [P] 
3153. Dautrebande, L., W. C. Alford, and B. Highman. 
Studies on aerosols. I. Reduction of dust deposition in 
lungs of rabbits by aqueous aerosols. /. industr. Hyg., 1948, 
30: 103-107. [P] 
3154. Dautrebande, L., W. C. Alford, and B. Highman. 
Studies on aerosols. II. Coating and agglutinating of dust 
particles by aqueous aerosols. /. industr. Hyg., 1948, 30: 
108-113. [P] 
3155. Doherty, D. G. and W. V, Consolazio. Evaluation 
of six commercial means of odor control for use in inhab- 
ited space. U. S. Navy. NMRI. Project X-533, Kept. no. 
3, 13 May 1946, 5 pp. [P] 
3156. Florida Chemical Research Co., New York. Odors 
and the sense of smell. New York, Airkem Incorporated, 28 
December 1950, 342 pp. [B] 
3157. Korotianskil A. M., and M. IA. Mirskii. Ochist- 
ka szhatogo vozdukha podavaemogo v kesson. [Purifying 
of compressed air in caissons.] Gigiena i Sanitaria, 1946, 
5: 23-28. 
3158. Kuehner, R. L. The effects of moisture content on 
the diffusion of odors in the air. Trans. Amer. Soc. Heat, 
and Vent. Engrs., 1947, 53: 77-88. [P] 
3159. Loosli, C. G. Problem of dust control for the dis- 
infection of air. Amer. J. publ. Hlth., 1948, 38: 409-415. 
[R] 
3160. Luaces, E, L. Vapor adsorbent carbons, pp. 840- 
848 in: Colloid chemistry. Theoretical and applied. Vol- 
ume VI. General principles and specific industries syn- 
thetic polymers and plastics. Edited by Jerome Alexander. 
New York, Reinhold Publishing Corp., 1946, 1215 pp. 
3161. McCord, C. P. Properties, physiology, and psychol- 
ogy of odors, pp. 248-250 in: Air pollution. Proceedings 
of the United States technical conference on air pollution. 
Louis C. McCabe, Chairman. New York, McGraw-Hill 
Book Co., Inc., 1952, 847 pp. 
3162. McCord, C. P. and W. N. Witheridge. Odors 
physiology and control. New York, McGraw-Hill Book Co., 
Inc., 1949, 405 pp. 
3163. Policard, A. First stages of the dust cell formation 
in pulmonary tissue. Occup. Med., 1947, 4: 100-103. [R] 
3164. Ray, A. B. Role of activated carbon in practical 
control of atmospheric contamination, pp. 357-372 in: 
Air pollution. Proceedings of the United States technical 
conference on air pollution. Louis C. McCabe, Chairman. 
New York, McGraw-Hill Book Co., Inc. Toronto. London. 
1952, 847 pp. 
3165. TT. S. NRC. Committee on sanitary engineering 
and environment. Subcommittee on shelter and clothing. 
Minutes of the fifth meeting, 15 November 1949, 1 p. 
3166. Watson, H. H. Dust sampling in a haematite mine 
with the P. R. U. hand pump. Brit. J. industr. Med., 1948, 
5: 198-203. [P] 
7. CARBON DIOXIDE ABSORBENTS, CARBON DIOXIDE 
ABSORPTION, AND TOLERABLE CONCENTRA- 
TIONS OF CARBON DIOXIDE AND OXYGEN 
Limiting values of carbon dioxide, after submerg- 
ing without snorkel, are theoretically not attained 
until expiration of a period of hours calculated from 
Q 
the formula: X=0.04 — where C = net air space of 
N 
me submarine in cubic feet, N — the number of men 
in the crew, and X = the time in hours. If submer- 
gence under ordinary operating conditions is less 
than 17 hours, oxygen or compressed air replenish- 
ment and C02 absorption are not normally neces- 
sary. Under abnormal conditions, when the environ- 
ment is damp and cold and metabolic rates are 
above averages, the validity of this formula may not 
hold. During World War II, adequate instruments 
to measure the concentration of carbon dioxide and 
oxygen in the air were not available. Need for car- 
bon dioxide absorption was commonly based on sub- 
jective evidence, as headache, dyspnea, and failure 
of the air to sustain a flame. When the need became 
obvious, carbon dioxide absorbent, in varying 
amounts, was spread out on rubber mattress covers 
in the bunk. This haphazard procedure is entirely 
inadequate for submarines of advanced design and 
long submergence capacity. 
Miller {3175) 1945 has reported on the experi- 
mental control of carbon dioxide aboard a U. S. 
Navy submarine. The atmosphere in the submarine 
was maintained within narrow limits at 3 percent 
carbon dioxide and 17 percent oxygen. The total 
submerged period was 68 hours. For the first 24 
hours, oxygen was replenished with chlorate candles 
and lithium hydroxide was used for carbon dioxide 
absorption. During the remaining hours of sub- 
mergence, the air for the 90 men was purified with 
KOX (potassium tetroxide). This compound re- 
acts with carbon dioxide and water vapor to pro- 
duce oxygen. Three canisters of KOX running 
simultaneously removed the carbon dioxide and fur- 
nished sufficient oxygen. One chlorate candle was 
used each 55 minutes, and oxygen was generated at 
the rate of 1 cubic foot per minute during the 
period when lithium hydroxide was used as a car- 
bon dioxide absorbent. Both methods of air regen- 
eration satisfied the submariners’ requirements. 
According to Malorny {3173 and 3174) 1948, the 
air of miniature submarines is more difficult to 
maintain at habitable levels than the larger fleet- 
type submarines. The carbon dioxide content in 
these small vessels is more easily maintained at safe 
levels (by absorbents), while the oxygen concen- 
tration is more labile because of the many individ- 
ual variations in metabolic rates of the crew mem- 
291222—54 19 3167-3178 
PROTECTION AND PRESERVATION OF PERSONNEL 
bers. Two methods of air purification for miniature 
submarines are described by the author. One method 
requires that crew members wear masks which ab- 
sorb carbon dioxide during exhalation and permit 
the use of compartment air during inspiration. The 
oxygen supplied to the boat is either bled in from 
oxygen tanks or compressed air banks. The other 
process, not requiring the use of face masks, utilizes 
an air injection valve resembling that used in deep- 
sea diving helmets for air recirculation and carbon 
dioxide absorption. It is an application of the ven- 
turi principle. The energy of the oxygen or oxygen- 
air mixture leaving the narrow V-shaped nozzle 
serves to draw in the compartment air. The air mix- 
ture is then forced through a carbon dioxide absor- 
bent. 
A report by the U. S. Navy {3178) 1945 de- 
scribes the “alka-cellulose” which replaced sodium 
hydroxide as a carbon dioxide absorbent on Japa- 
nese submarines. This commercial preparation, ob- 
tained by processing staple fiber, is the result of 
an alkalinization process. The material was packed 
in 4 kg. tins, and when needed the fiber was spread 
out on the deck. One tin of this material supposedly 
absorbed 400 liters of carbon dioxide. Tests of a 
service-type lithium hydroxide hopper for carbon 
dioxide removal are described by McConnaughey 
and Woods {3172) 1951. The results indicated that 
two such hoppers, each using about 21.6 pounds of 
lithium hydroxide pellets, will maintain the atmo- 
sphere in an 80-man submarine at an average car- 
bon dioxide concentration of 1. to 1.5 percent for 4 
hours without recharging. Blower requirements have 
been established as 75 to 85 cu. ft. per minute, at 
2.5 in. of water static pressure. The reader may also 
care to refer to reports by the following authors; 
Adriani {3167) 1945; Davidson and Hempleman 
{3168) 1950; Foregger {3169) 1948; Henson and 
Pender {3170) 1944; Kindrick and Reitmeier 
{3171) 1950; Miller and Tanning {3176) 1941; 
and Mousel, Weiss, and Gilliom {3177) 1946. 
3167. Adrian!, J. The effect of varying the moisture con- 
tent of soda lime upon the efficiency of carbon dioxide 
absorption. Anesthesiol., 1945, 6: 163-172. [P] 
3168. Davidson, W. M., and H. V. Hempleman. Carbon 
dioxide absorption trial carried out in H. M. submarine 
Trespasser, 23rd-24th March 1950. Gt. Brit. MRC— 
RNPRC, UPS. R. N. P. 50/595, U. P. S. 115, April 1950, 
5 pp. 
3169. Foregger, R. The regeneration of soda lime fol- 
lowing absorption of carbon dioxide. Anesthesiol., 1948, 
9: 15-20. [P] 
3170. Henson, M., and J. W. Pender. Evaluation of 
baralyme as a carbon dioxide absorbent. U. S. Navy. 
NMRI. Project X-75, 14 July 1944, 2 pp. 
3171. Kindrick, R. C. and R. E. Reitmeier. Recom- 
mendations for the selection of amines for the absorption 
of C02 from air. U. S. Girder Corp. Kept. no. T2. 
20-2-6, 26 July 1950, 11 pp. 
3172. McConnaughey, W. E. and F. J. Woods. A pellet- 
ized lithium hydroxide hopper to remove carbon dioxide 
from submarine atmospheres. U. S. Navy. NRL. NRL 
Kept. no. 3868, 12 October 1951, 12 pp. 
3173. Malorny, 6. Investigations of compartment air 
in miniature submarines. Use of injector, pp. B: V—21— 
B: V—32 in: Monograph on submarine medicine. Folio 
III, Germany, U. S. Zone. Office of naval advisor. 1948. 
3174. Malorny, 6. Investigations of compartment air in 
miniature submarines. The significance of climatic factors, 
pp. B: V-36—V—37 in: Monograph on submarine medi- 
cine, Folio III, Germany. U. S. Zone. Office of naval 
advisor. 1948. 
3175. Miller, R. R. Experimental control of carbon diox- 
ide and oxygen concentrations aboard the U. S. S. Sail- 
fish. U. S. Navy, NRL. NRL Rept. no. P-2665, October 
1945, 30 pp. [P] 
3176. Miller, R. R. and W. C. Fanning. The seventh 
partial report on oxygen source material. U. S. Navy. 
NRL. NRL Rept. no. P-1691, 4 February 1941, 20 pp. 
3177. Mousel, L. H., W. A. Weiss, and L. A. Gilliom. 
A clinical study of carbon dioxide absorption during 
anesthesia. Anesthesiol., 1946, 7: 375-398. 
3178. IT. S. Navy, Technical mission to Japan. Carbon 
dioxide absorption, p. 44 in: Aero, surface, and submarine 
medicine and research in the Japanese Navy, Fascile M—l, 
Target M-06, 4 September 1945, 72 pp. 
8. OXYGEN GENERATORS 
To maintain the air of a submarine within the 
limits of safety, it is necessary not only to limit the 
increasing carbon dioxide concentration by chemical 
absorbents but also to replenish the decreasing sup- 
ply of oxygen by adding oxygen or air at regular 
intervals. Future demands imposed on submarine 
activity by the atomic power plant will extend its 
submerged range beyond the limits of oxygen endur- 
ance as supplied by conventional methods. 
It is not intended under this heading to include 
in its entirety the extensive literature on the various 
types and evaluation of oxygen-producing systems. 
A few selected reports have been included {3183, 
3185, 3187, 3188, 3191 and 3194). Of interest is 
the report by Geissman {3183) 1946 describing the 
operating characteristics of “Salcomine” (salicyl- 
aldehyde ethylenediamine). This compound pro- 
duced oxygen at satisfactory temperature and 
pressure ranges. Animal and human experiments 
demonstrated that the dust of “Salcomine” was 
irritative to the bronchial passages, digestive tract, 
and liver. In the 11 men exposed, the dust produced 
an irritation of the eyes, nose, larynx, and bronchial 
tubes. Removal of the men from the dust environ- 
ment relieved the symptoms. 
Information concerning alkali oxides for sub- 
marine air purification may be obtained from a 
paper by Grand, Ramskill, and Burgess {3185) 
1942. These alkali oxide canisters were developed HABITABILITY—BUNKING FACILITIES 
3179-3194 
for carbon dioxide absorption and oxygen genera- 
tion in submarines. 
In 1930, an individual oxygen generator was de- 
veloped for use in mine-rescue work. This generator 
utilized oxygen from a chlorate briquet manufac- 
tured in Berlin under the trade name “Naszogen.” 
The apparatus was later tested by the British Ad- 
miralty for oxygen replenishment in submarines, 
but was rejected because the oxygen liberated was 
contaminated with chlorine. 
Pappenheimer (3187 and 3188) in 1945 pub- 
lished observations on the Japanese chemical oxygen 
generator developed for aircraft. The oxygen was 
evolved by the decomposition of potassium chlorate. 
Flow rates at 25°, —20°, and —55° G. were 4.1, 
3.4, and 2.8 liters of oxygen per minute. The gas 
mixture produced contained 96 to 97 percent oxy- 
gen, 3 to 4 percent carbon dioxide, and 0.1 percent 
carbon monoxide. The blood of one observer con- 
tained 20 percent carboxyhemoglobin after 50 min- 
utes at a simulated altitude of 18,000 feet, while the 
equipment supplied oxygen to the chamber. The 
improved candle produced in the United States 
contained NaC103, Fe, Ba02, and fiberglass. The 
use of reduced iron as an accessory heat source di- 
minished production of carbon monoxide and car- 
bon dioxide. The Ba02 eliminated the formation of 
free chlorine. The reader should also consult the 
report published by the U. S. Office of Scientific Re- 
search and Development {3194) 1946 for a com- 
plete bibliography on oxygen generator equipment. 
Other references are included without comment. 
3179. Berner, F. W. Aircraft oxygen generator. U. S. 
AAF. Wright-Patterson air force base, Dayton, Ohio. 
Air materiel command, ENG. Serial no. ENG-49-660— 
45-1, 6 July 1944, 4 pp. 
3180. Calvin, M. Manufacture of oxygen by use of 
regenerative chemicals. U. S. OSRD-NDRG. Division B. 
O. S. R. D. no. 403, Serial no. 186, 23 February 1942, 
10 pp. 
3181. Diebold, V. B. Laboratory and flight test of the 
Bendix 8-liter liquid oxygen converter (Model XE795826— 
1), U. S. AAF. Wright-Patterson air force base, Dayton, 
Ohio. Air materiel command. Serial no. MCREXD-660- 
104-J, 3 March 1950, 15 pp. 
3182. Dodge, B. F. The production of liquid oxygen. 
U. S. OSRD-NDRC. Division B. Serial no. 59, 14 August 
1941, 36 pp. 
3183. Geissman, T. A. Oxygen generation from regenera- 
tive chemicals, pp. 242-267 in: Improved equipment for 
oxygen production. Summary technical report of Divi- 
sion 11, U. S. OSRD-NDRC. Washington, D. C., 1946, 
428 pp. 
3184. Giaugne, W. F. Cascade oxygen system, U. S. 
OSRD-NDRC. Division B. O. S. R. D. no. 491, Serial 
no. 201, 28 February 1942, 44 pp. 
3185. Grand, J. A., E. A. Ramskill, and D. S. Burgess. 
Eleventh partial report on oxygen source material. Use 
of the alkali oxides in canisters for submarine air purifi- 
cation. U. S. Navy. NRL. NRL Rept. no. P-1904, 11 
July 1942, 65 pp. 
3186. Latimer, W. M. The production of oxygen by the 
use of a regenerative chemical. U. S. OSRD-NDRG. 
O. S. R. D. Serial no. 64, 25 August 1941, 6 pp. 
3187. Pappenheimer, J. R, Notes on the Japanese chem- 
ical oxygen generator for aircraft. U. S. NRC-CAM. 
OEMcmr-26, C. A. M. Rept. no. 427, April 1945, 14 
PP- [P] 
3188. Pappenheimer, J. R. Development of oxygen 
candle apparatus for use in aircraft. U. S. NRC-CAM. 
C. A. M. Rept. no. 499, June 1946, 52 pp. 
3189. Prentiss, S. S. Oxygen generation from nonre- 
generative chemicals, pp. 268-294 in: Improved equip- 
ment for oxygen production. Summary technical report 
of Division 11, U. S. OSRD-NDRC. Washington, D. C., 
1946, 428 pp. 
3190. Prentiss, S. S. Liquid oxygen vaporizers for 
aeronautical, medical and engineering uses. pp. 295-308 
in: Improved equipment for oxygen production. Sum- 
mary technical report of Division 11. U. S. OSRD- 
NDRG. Washington, D. C., 1946, 428 pp. 
3191. Prentiss, S. S. Submarine problems, pp. 330-342 
in: Improved equipment for oxygen production. Sum- 
mary technical report of Division 11, U. S. OSRD- 
NDRC. Washington, D. C., 1946, 428 pp. 
3192. Rahtgen, H. G. Description and instruction for 
operation and maintenance of oxygen charging apparatus 
10—100 3—1. U. S. AAF. Wright-Patterson air force base, 
Dayton, Ohio. Air materiel command. Serial no. ENG 
49-660-15-0,-1. (German translation no. 373), 16 Jan- 
uary 1944, 31 pp. 
3193. U. S. AAF. Wright-Patterson air force base, 
Dayton, Ohio. Air materiel command, ENG. Aero medical 
laboratory. Design requirements and test results on air- 
craft type liquid oxygen converts. Technical rept. 
TSEAL-3-660-61-J, 25 March 1945, 21 pp. 
3194. TJ. S, OSRD-NDRC. Improved equipment for 
oxygen production. Summary technical report of Divi- 
sion 11, Volume 1. Washington, D. C., 1946, 428 pp. [B] 
C. BUNKING FACILITIES 
There has been a lack of extensive concern for 
the adequacy of bunking facilities as a phase of 
habitability which calls for an investigation of the 
sleeping quarters and the type, size, and arrange- 
ments of bunks. In a standard, fleet-type submarine, 
enlisted personnel are provided 17 bunks in the 
forward torpedo room, 18 in the after torpedo 
room, 27 in the after battery compartment, and 5 
in the chief petty officers’ cabin. The bunks are only 
to 26 inches wide and 73 to 75 inches long. 
To make matters worse, some bunks are arranged in 
3 or even 4 tiers, so close to each other vertically 
that it is impossible for a sleeper to turn over with- 
out hitting and scraping against the sagging ham- 
mock-type spring of the bunk above. Both the 
narrowness of the bunks and their vertical crowd- 
ing discourage frequent changes in sleeping postures 
essential for restful sleep. Probably the absence of 
complaints concerning sleeping accommodations 
can be explained only by the esprit de corps of the 3195-3197 
PROTECTION AND PRESERVATION OF PERSONNEL 
submarine service and the well-adapted type of 
person obtained through selection procedures. 
Substitution of neoprene sponge mattresses for 
hair mattresses has been tried as a means of im- 
proving bunking conditions aboard submarines. An 
evaluation of this trial by Spealman, Trumper, 
Fisher, Birren, and Duggan {3196) 1944 showed 
that the neoprene mattresses were preferred to hair 
mattresses by 9 out of the 10 subjects, primarily 
because they were softer. The neoprene mattresses 
were not irritating to the skin nor did they absorb 
appreciable quantities of water during the experi- 
ment. It was recommended that a fungistatic be 
applied to mattresses to prevent the growth of cer- 
tain fungi. 
Crowded conditions, as indicated by prevailing 
bunking arrangements, certainly must have some 
effect upon the incidence of acute respiratory 
diseases. This problem will not be discussed here 
but is considered under the section on disinfection of 
air (p. 273). For pertinent references on this subject 
as applied to bunking arrangements, the reader 
should consult papers by the U. S. Army {3197) 
1946 and Breese, Stanbury, Upham, Calhoun, Van 
Buren, and Kennedy {3195) 1945. 
3195. Breese, B. B., J. Stanbury, H. Upham, A. J. Cal- 
houn, B,. L. Van Buren, and A. S. Kennedy. Influence of 
crowding on respiratory illness in a large naval training 
station. War Med., Chicago, 1945, 7: 143-146. 
3196. Spealman, C. E,., M. Trumper, M. B. Fisher, J, E. 
Birren, and T. L. Duggan. Investigation of the suitability 
of neoprene sponge mattresses for use aboard submarines. 
U. S. Navy. NMRI. Project X-221, Kept. no. 2, 8 No- 
vember 1944, 6 pp. 
3197. U. S. Army. Commission on acute respiratory 
diseases. Fort Bragg, N. C. The effect of double-bunking 
in barracks on the incidence of respiratory disease. Amer. 
J.Hyg., 1946, 43: 65-81. [P] 
m. FOOD AND WATER SUPPLY 
When proper precautions have been taken and 
when the distilling machinery functions in a routine 
manner, water delivered to the submarine crew for 
drinking purposes will normally be potable. Mul- 
tiple runs of the water through the distilling plant 
will yield salt-free water, adequate for the batteries 
and pure enough to drink. First consideration is 
given to the battery supply, while the remainder 
is rationed to the men for drinking, cooking, and 
bathing purposes. The supply for bathing is often 
inadequate. 
During World War II a few submarines reported 
the occurrence of gastrointestinal symptoms among 
the crew which were presumed to be due to the 
consumption of impure drinking water. It was no- 
ticed that 2 or 3 weeks after the start of a patrol 
the fresh water tasted “metallic” and that cigarettes 
had a sweet taste when smoked after drinking the 
water. Some of the men developed nausea, vomit- 
ing, and malaise of varying severity. On one boat 
the majority of the crew was incapacitated by the 
symptoms and it became necessary to retire from 
patrol. The onset of nausea and vomiting occurred 
most frequently after the consumption of water in 
the morning before breakfast. The toxic manifesta- 
tions in most cases were relieved when the men 
abstained from drinking water and derived their 
fluid intake from canned fruit juices and coffee. 
At the time the drinking water developed the 
bad taste it was also noticed that the water turned 
a blue-green color when soap was added to it. This 
condition was reported by submarines operating 
in widely scattered localities—in the Gulf of Mex- 
ico, in transit from the Canal Zone to Hawaii, in the 
Coral Islands area, in the Inland Sea, and other 
parts of the Pacific Ocean. 
Submarines start on a war patrol with fresh- 
water tanks filled with water from the dock or 
tender. In 1 to 3 weeks, depending on the rate of 
water consumption, this water is diluted 50 to 90 
percent with the water distilled on board. A modem 
submarine during a war patrol will consume about 
500 gallons of fresh water a day for cooking, drink- 
ing, and engine water makeup. In addition to this, 
the main storage batteries require about 500 gallons 
of battery water a week. 
An investigation of the cause of drinking-water 
contamination on the U. S, S. Icefsh by Duffner 
and Hay ter {3203) 1946 revealed that the un- 
pleasant taste of the water was due to the con- 
centration of copper salts. The copper was found to 
have come from the distilling plant. The tubes in 
the distillation units are made of a copper-nickel 
alloy and over one-half of the fixed residue in the 
samples collected from the distillation units and 
from the distillate collecting tank is derived from 
the copper-nickel source. It is reasonably certain 
that these substances in the water are formed by 
the action of the compressed vapor and hot water 
on the metal tubes. 
The water delivered at the crews’ scuttlebutt 
contained approximately twice as much copper 
(8.18 p. p. m.) as did the water delivered at the 
distilling units (3.67 p. p. m.). Bacteriological ex- 
amination of samples collected from each of the 
fresh-water tanks, the crews’ scuttlebutt, the tap 
at the galley sink, and the distillate collecting tank 
did not reveal evidence of coli-aerogenes contam- 
ination. FOOD AND WATER SUPPLY 
The effect of drinking water with a copper con- 
centration of 3 p, p. m. was investigated by Hayter 
and Consolazio {3205) in 1945. Twenty-five men 
drank daily for 8 days 1 pint of distilled water con- 
taining 3 p. p. m. of copper and 25 men drank this 
water daily for 7 days. Controls drank tap water. 
Seventy to eighty percent of the men noticed the 
taste of the copper in the water and thought it was 
unpleasant. One man had nausea, one had nausea 
with vomiting, and a third man had nausea twice 
and nausea with vomiting once. The authors felt 
that it would be advisable to keep the copper levels 
in the water below 3 p. p. m. This is the limit 
recommended by the U. S. Public Health Service 
for drinking and culinary water supplied by com- 
mon carriers in interstate commerce. 
The water supplied to the crew must be free of 
disease-producing bacteria. A submarine as a mat- 
ter of necessity may have to distill water pumped 
into the boat from a foreign contaminated harbor 
and therefore the stills must operate at tempera- 
tures which are lethal for pathogenic bacteria. 
Malfunctioning of the distilling plant under these 
circumstances would supply the crew with con- 
taminated water which might lead to sickness of 
epidemic proportions miles from home. 
Payne {3210) 1945 carried out a very complete 
investigations of the bactericidal efficiency of a low- 
pressure, double-effect distilling plant capable of an 
output of 40,000 gallons per day. In all runs suf- 
ficient sewage was introduced into the feed water 
to produce an average probable number of coliform 
organisms of 605,000 per 100 cc., and an average 
bacterial content of 41,000 per cc. as determined 
by the plate count at 37° C. Results showed that 
the condensate was free of coliform bacteria, and 
the number of other bacteria was inconsequential 
even when highly polluted water was used. The fact 
that some bacteria were carried over into the con- 
densate when the separators were removed and the 
salinity exceeded 0.6 grain per gallon indicates the 
need for efficient separators or eliminators in all 
plants. In cases where the eliminators are not 
known to be effective in keeping the salinity con- 
sistently below one-fourth grain per gallon, other 
means must be provided for killing the harmful 
bacteria. If heat is used to kill the bacteria, a mini- 
mum temperature of 165° F. is satisfactory. It was 
found that this temperature killed all coliform 
organisms, but not the more heat-resistant bacteria. 
In other words, a 165° F. temperature will not 
produce sterile water but apparently it is sufficient 
to kill the pathogenci bacteria. 
Burrows, Gordon, Porter, and Moulder {3201) 
1949 state that the most efficient method of killing 
bacteria is with dry heat. The pathogenic bacteria 
are less resistant to heat, the spores being more 
resistant and sometimes 16 hours of boiling is re- 
quired to kill them. As a rule, exposure to 120° G. 
for 15 minutes suffices for complete destruction of 
both vegetative and spore forms of bacteria. Water 
at 100° C. for a few minutes kills all vegetative 
forms. 
Zobell and Conn {3221) 1950 heated samples 
of sea water and mud to 30° C. for 10 minutes and 
found that about 25 percent of the bacteria present 
were killed. Only 20 percent of the bacteria sur- 
vived 40° C. for 10 minutes. The authors stated 
that prolonged exposure at 40° to 42° C., or instan- 
taneous exposure at temperatures a few degrees 
higher than 42° C., is lethal for a large percentage 
of the bacteria from the ocean. Marine bacteria are 
thermosensitive because many live at colder temper- 
atures at the depths of the ocean. Chang {3202) in 
1950 investigated the survival of cysts of Entameba 
histolytica in water temperatures ranging from 45 
to 50° C. He found that at 45° C. for 135 minutes’ 
contact time, approximately 115 minutes were 
needed to get 100 percent killing; at 47° C. for 32 
minutes’ contact time, 30 minutes were needed; at 
49° C. with a contact time of 9 minutes, 7.5 minutes 
were required; and at 50° C., contact time of 3 
minutes, 2 minutes were needed for 100 percent 
destruction. The pH of the culture was 6.8. 
For other articles concerned with the general sub- 
ject of water purification and testing, the reader is 
advised to consult reports by the following: Ameri- 
can Public Health Association and the American 
Water Works Association {3198) 1946; Bateman 
{3199) 1943; Black and Spaulding {3200) 1944; 
Futcher, Consolazio, Pace, and Gerrard {3204) 
1943; Jones and Newton {3206) 1950; Lamanna 
{3207) 1942; Moore {3208) 1950; Otto {3209) 
1951; Prescott, Winslow, McCrady {3211) 1946; 
Taylor {3213) 1949; U. S. Public Health Service 
{3217, 3218) 1946 and {3219) 1951; and Zobell 
{3220) 1946. 
That portion of the food problem pertaining to 
the preparation of foods will be alluded to briefly 
here, while a more thorough coverage of food as it 
applies to diet will be discussed in the succeeding 
section (p. 282). The radarange or electronic 
cooking device was not considered by Sussman 
{3212) 1947 to be practical for use on submarines. 
He listed the following disadvantages: (1) cook- 
ing is limited to a penetration of 3 inches, (2) the 
oven is too small, (3) the life of the magnetron 3198-3221 
PROTECTION AND PRESERVATION OF PERSONNEL 
tube is too short, and (4) the timing device is de- 
fective. It was found to be superior to the standard 
oven in that (1) no smoke or fumes were produced 
during cooking, (2) there was little heat radiation, 
and (3) it possessed good “short-order” cooking 
qualities. Vegetables were found to retain their 
natural flavor and color. Thomas, Brenner, Eaton, 
and Craig {3214) 1949 compared the nutritive 
value of foods cooked on the radarange with those 
prepared in gas and electric ovens. They found 
almost no difference between the retention of nico- 
tinic acid and of riboflavin in beef roasts or meat 
patties when cooked electronically and when grilled. 
Electronic cooking caused slightly greater loss of 
aneurin in beef and slightly less in patties. With 
electronic cooking, less ascorbic acid, riboflavin, and 
aneurin were retained than with pressure cooking 
while still less was retained with saucepan cooking. 
These results with vegetables are chiefly due to 
differences in the amount of water, most vitamins 
being retained with pressure cooking in which the 
smallest amount of water is used. For additional 
papers on food problems, the reader is referred to 
articles by the U. S. Navy {3215) 1949 and {3216) 
1945. 
3198. American Public Health Association and the 
American Water Works Association. Standard methods 
for the examination of water and sewage. American Public 
Health Association, New York 19, N. Y., 1946, Ninth 
edition—second printing {1947), 286 pp. 
3199. Bateman, J. B. Supply of fresh water at sea. 
Canada NRC. Proceedings of second meeting of associate 
committee on naval medical research. Project C4051, 
7 October 1943, 2 pp. 
3200. Black, H. H. and C. H. Spaulding. Diatomite 
water filtration for field troops. J. Amer. Wat. Wks. Ass., 
1944, 36: 1208-1221. [P] 
3201. Burrows, William, Francis Byron Gordon, Rich- 
ard Janvier Porter, and James William Moulder. The 
lethal effects of heat. pp. 138-140 in: Jordan-Burrows 
textbook of bacteriology. Fifteenth edition. Philadelphia, 
W. B. Saunders Co., 1949, 981 pp. 
3202. Chang, S. L. Kinetics in the thermodestruction of 
cysts of endamoeba histolytica in water. Amer. J. Hyg., 
1950, 52: 82-90. 
3203. Duffner, G. J. and R. Hayter. An investigation 
into the cause of drinking water contamination aboard the 
U. S. S. Icefish (SS-367). U. S. Navy. NMRI. Project 
X-588, Rept. no. 1, 30 January 1946, 8 pp. 
3204. Futcher, P. M., W. V. Consolazio, N. Pace, and 
E. J. Gerrard. The tablet emergency ration for lifeboats, 
rafts and floats. U. S. Navy. NMRI. Project X-127, Rept. 
no. 4, 10 November 1943, 15 pp. 
3205. Hayter, R. and W. V. Consolazio. Determination 
of the effect of drinking water containing 3 p. p. m. 
copper. U. S. Navy. NMRI. Project X-588, Rept. no. 2, 
3 May 1945,4 pp. [P] 
3206. Jones, M. F., and W. L. Newton. The survival of 
cysts of endamoeba histolytica in water at temperatures 
between 45° C. and 55° C. Amer. J. trap. Med., 1950, 
30: 53-58. 
3207. Lamanna, C. Relation of maximum growth tem- 
perature to resistance to heat. /. Bact., 1942, 44: 29-35. 
[P] 
3208. Moore, E. W. The desalting of saline waters: a 
review of the present status. U. S. NRC. Committee on 
sanitary engineering and environment, Subcommittee on 
water supply, 24 May 1950, 13 pp. [D] 
3209. Otto, G. F. Diseases and infections due to intesti- 
nal protozoa, pp. 227-242 in: Rosenau preventive medi- 
cine and hygiene. Edited by Kenneth F. Maxcy. Seventh 
edition. New York, Appleton-Century-Crofts, Inc., 1951, 
1462 pp. 
3210. Payne, W. W. Report of study of bactericidal 
efficiency of low-pressure, double-effect distilling plant. 
U. S. Public Health Service in cooperation with U. S. 
Maritime Commission. November 1945, 100 pp. [P] 
3211. Prescott, S. C., C.-E. A. Winslow, and M. H. 
McCrady. The bacteria in natural waters, pp. 1-23 in: 
Water bacteriology. With special reference to sanitary 
water analysis. Sixth edition. New York, John Wiley & 
Sons, Inc., 1946, 368 p. [P] 
3212. Snssman, L. Evaluation of electronic cooking 
device (radarange) for submarines. U. S. Navy. Sub- 
marine base. New London, Conn. Medical research de- 
partment. Project NM Oil 016, October 1947, 17 pp. 
3213. Taylor, Edwin Windle. The examination of 
waters and water supplies. London, J. & A. Churchill, 
Ltd., 1949. Sixth edition, 819 pp. 
3214. Thomas, M. H., S. Brenner, A. Eaton, and V. 
Craig. Effect of electronic cooking on nutritive value of 
foods. /. Amer. diet. Ass., 1949, 25: 39—45. Abstr. World 
Med., 1949,6; 138. 
3215. II. S. Navy. BuNavPers. Analysis of submarine 
food problems in World War II. pp. 165—174 in: Sub- 
marine medicine practice. NavPers. 10838, March 1949, 
182 pp. [D] 
3216. U. S. Navy, Technical mission to Japan. Rations 
for submarine crews, pp. 41-42 in; Aero, surface, and 
submarine medicine and research in the Japanese Navy, 
Fascile M-l, Target M-06, 4 September 1945, 72 pp. 
3217. IT. S. Public Health Service. Drinking water 
standards 1946. Publ. Hlth. Rep., Wash., 1946, 61: 371— 
384. 
3218. U. S. Public Health Service. Manual of recom- 
mended water-sanitation practice. Public Health Bulletin 
no. 296, U. S. Government Printing Office, Washington, 
D. C., 1946, 40 pp. 
3219. IT. S. Public Health Service. Potable water, pp. 
1-20 in: Handbook on sanitation of vessels in operation. 
PHS publication no. 68, U. S. Government Printing Office, 
Washington, D. C., 1951, 44 pp. 
3220. ZoBell, Claude E. Characteristics of marine bac- 
teria. pp. 114-128 in: Marine microbiology. A mono- 
graph on hydrobacteriology. Waltham, Mass., Chronica 
Botanica Co., 1946, 240 pp. 
3221. ZoBell, C. E. and J. E. Conn. Studies on the 
thermal sensitivity of marine bacteria. /. Bact., 1950, 40: 
223-238. 
IV. DIET AND PHYSICAL FITNESS 
There is at present very little nutritional research 
directly involving submariners and therefore the 
dietary problems of submarine personnel must be 
projected onto the general background of available 
nutritional knowledge. Since there are few events DIET AND PHYSICAL FITNESS 
in his daily routine besides his meals to which the 
submariner really looks forward, he is likely to in- 
dulge in excessive eating. This habit, in addition to 
the possible immediate effects of reducing alertness 
and capacity to concentrate on complex tasks may 
permanently affect dietary practices. 
Ordinarily physicians are not greatly concerned 
with the details of food supplies. The naval medical 
officer is specifically charged with the duty of “in- 
specting, as to quality, all fresh provisions issued as 
authorized mess”. A review of the patrol reports by 
Shilling and Duff (5226) 1947 and (5227) 1948 
indicated that this duty too often was not assumed 
by medical officers associated with the submarine 
force. It was recommended by the authors that sub- 
marine squadron medical officers should actively 
concern themselves not only with the quality of 
food issued to submarines but with the planning of 
menus to provide a dietetically acceptable ration. 
This should be accomplished by close cooperation 
of the medical staff officers, commissary personnel, 
and commanding officers. 
The ration provided a submarine must fulfill 
certain requirements. It must occupy a minimum 
space and must evidence excellent keeping qualities 
in stowage. From it a daily well-balanced menu 
incorporating a maximum of food value and variety 
and a minimum of waste should be easily prepared. 
Submarines have always had a more generous ration 
allowance than other ships or stations with a similar 
complement. 
Indication of the role which food supplies may 
have in influencing the length and success of patrols 
is shown by reports of commanding officers. “Food 
supply was low; the decision to remain on station 
was based on a 5-day supply of food. The patrol 
could not have continued for a longer period with- 
out a serious reduction in efficiency and health due 
to an unbalanced ration”. “The ice cream freezer 
paid for itself many times over, it being estimated 
that one ton of ice cream was consumed during the 
patrol, cold weather notwithstanding”. 
Meat—its quality and quantity—was the one 
article of the submarine ration commented upon 
most frequently, according to Shilling and Duff. 
Early in the war, for reasons of space economy, 
boneless beef was made available to submarines. 
It was supplied as steak and roasting, stewing and 
boiling, and chopped beef. Regulations of the Bu- 
reau of Supplies and Accounts for all ships required 
that 30 percent of the meat was to be drawn in 
inferior quality. Submarines starting on patrol were 
issued beef in the following proportions: (1) roast 
and steaks 50 percent; (2) hamburger 25 percent; 
and (3) stewing and boiling meat 25 percent. The 
result of such a situation evoked the following com- 
ments in one of the patrol reports: “This is a satis- 
factory proportion but since stewing and boiling 
meat is not considered worth the icebox space, it is 
generally left at the base and other frozen items, 
as shrimps, frozen foods, and sausage are taken in 
quantity to fill the space.” Duff and Shilling recom- 
mended that this entire problem be restudied in a 
less hurried atmosphere with the view toward con- 
structing a master ration plan for the submarine 
service, sufficiently exact to be helpful as a guide 
and at the same time flexible enough to allow for 
satisfying individual preferences. 
An excellent review of nutritional problems in 
submarines by Brozek and Mickelsen (5222) 1949 
indicates that physiologically no acute nutritional 
problems exist as far as the submarine personnel 
are concerned. The requirements for calories, vita- 
mins, minerals, proteins, carbohydrates, and fats 
appear to be the same as those of other moderately 
active men. Consequently, improvement in sub- 
marine nutrition depends on general progress in 
the physiological understanding of the role of food 
in the overall metabolism of the human organism 
and on technological developments of food grow- 
ing, preservation, and preparation. There is a gap 
in our knowledge of the changes occurring, during 
prolonged patrols, in food preferences, likes, and 
dislikes, and the overall position of food in the life 
of the submarine personnel. When men are sub- 
jected to confining and trying circumstances, some 
of them may find an escape in eating. On the 
other hand, nervousness and anxiety may result in 
a loss of appetite. 
Schulte (5225) 1950 found that 3,800 calories 
per man per day were consumed by submariners in 
a simulated war patrol in the arctic zone and this 
was supplied by 120 grams of protein, 480 grams 
of carbohydrate and 120 grams of fat. The ingested 
diet contained more than the established minimum 
adult requirements of thiamin, riboflavin, ascorbic 
acid, and vitamin A. From this patrol it was deter- 
mined that the consumption by this crew was not 
appreciably greater or less than the nutritional re- 
quirements since there were no significant weight 
changes. 
For further studies on food and physical fitness, 
reference may be made to reports by Dugal, Le- 
blond, Therien (5225) 1945 and Ellis (5224) 1948. 
3222. Brozek, J. and 0. Mickelsen. Diet. pp. 311-327 
in: A survey report on human factors in undersea warfare. 
National research council. Washington, D. C. 1949, 541 
pp. 3223-3246 
PROTECTION AND PRESERVATION OF PERSONNEL 
3223. Dugal, 1. P., C. P. Leblond, and M. Therien. 
Resistance to extreme temperatures in connection with 
different diets. Canad. J. Res., 1945, 23 (E-F): 244-258. 
3224. Ellis, F. P. Victuals and ventilation and the 
health and efficiency of seamen. Brit. ]. industr. Med., 
1948,5: 185-197. 
3225. Schulte, J. H. A dietary study of a submarine 
patrol in the arctic. U. S. Navy. Submarine base. New 
London, Conn. Medical research laboratory. Project NM 
002 015.06.01, Kept. no. 1, 1950, 33 pp. 
3226. Shilling, C. W. and I. F. Duff. Analysis of sub- 
marine food problems in World War II. pp. 215-241 in: 
History of submarine medicine in World War II. Edited 
by Shilling, C. W. and J. W. Kohl. U. S. Navy. Sub- 
marine base, New London, Conn. Medical research labora- 
tory, 25 May 1947, 328 pp. 
3227. Shilling, C. W. and I, F. Duff. Analysis of sub- 
marine food problems in World War II. Nav. med. Bull. 
Wash., 1948, 48: 683-697. 
V. CLOTHING 
A. GENERAL STUDIES 
The references that follow provide a general in- 
troduction to the problems of clothing under a wide 
variety of environmental conditions. 
3228. Burton, A. C. Clothing and heat exchanges. 
Fed. Proc. Amer. Soc. exp. Biol., 1946, 5; 344-351. [R] 
3229. Critchley, M. Problems of naval warfare under 
climatic extremes. Lecture I. Milit. Surg., 1946, 98: 94- 
106. [R] 
3230. Gagge, A. P, Research on military clothing. 
U. S. NRC-CAM. C. A. M. rept. no. 39, 5 January 1942, 
4 pp. 
3231. Gt. Brit. MRC-RNPRC. Special meeting clothing 
panel. C. P. rept. no. 6, 18 January 1951, 3 pp. 
3232. Lee, D. H. K. and H. Lemons. Clothing for global 
man. Geogr. Rev., 1949, 39: 181-213. [R] 
3233. Robinson, S. and H. S. Belding. Protective 
clothing, pp. 497-519 in: Part IV Physiology in: Ad- 
vances in military medicine. Vol. II. Edited by E. C. 
Andrus, D. W. Bronk, G. A. Carden, Jr., C. S. Keefer, 
J. S. Lockwood, J. T. Wearn, and M. C. Winternitz. 
Boston, Little, Brown and Co., 1948, 472 pp. [R] 
3234. Siple, P. A. Clothing and climate, pp. 389-442 
in: Physiology of heat regulation and the science of cloth- 
ing. Edited by L. H. Newburgh. Philadelphia, W. B. 
Saunders Go., 1949, viii, 457 pp. 
3235. U. S. Navy. BuMed. Naval clothing, pp. 65-91 
in: A manual of naval hygiene. U. S. Government Print- 
ing Office, Washington, D. G., 1943, 340 pp. 
3236. U. S. NRC. Subcommittee on clothing. Minutes 
of the third meeting. 17 June 1943, 16 pp. 
3237. U. S. NRC. Subcommittee on clothing. Minutes 
of the fourth meeting on jungle clothing. 6 October 1943, 
12 pp. 
3238. U. S. NRC. Subcommittee on clothing. Minutes 
of the seventh meeting. 15 December 1943, 8 pp. 
3239. U. S. NRC. Subcommittee on clothing. Minutes 
of the meeting. 10 March 1944, 6 pp. 
3240. U. S. NRC. Subcommittee on clothing. Minutes 
of the meeting. 6 May 1944, 14 pp. 
3241. U. S, NRC. Subcommittee on clothing. Minutes 
of conference on climatic stresses. 9 March 1945, 11 pp. 
3242. IT. S. NRC. Subcommittee on clothing. Minutes 
of conference on climatic stresses. 16 April 1945, 4 pp. 
3243. TJ. S. NRC. Subcommittee on clothing. Minutes 
of meeting. 19 June 1945, 10 pp. 
3244. U. S. NRC, Subcommittee on clothing. Minutes 
of meeting. 24 October 1945, 22 pp. 
3245. U. S. NRC. Subcommittee on shelter and cloth- 
ing. Committee on sanitary engineering and environment. 
Medical advisory commission. Minutes of first meeting. 
Bulletin, shelter and clothing, 1 June 1948, 5 pp. 
3246. U. S. NRC. Subcommittee on shelter and cloth- 
ing. Commission on sanitary engineering and environment. 
Medical advisory commission. Minutes of third meeting. 
Bulletin, shelter and clothing. 17 June 1949, 9 pp. 
B. PHYSICAL PROPERTIES, TESTING, AND 
STANDARDS 
With the advent of the newer types of subma- 
rines where streamlining leaves little protection for 
bridge personnel, the need for more effective protec- 
tion of watchstanders on the bridge becomes press- 
ing. In rough seas and cold weather, the physical 
tolerance of watchstanders is limited, the periods 
sometimes being as short as 30 minutes. To keep 
men dry, when waist-deep seas are encountered, 
something comparable to a diving suit is required; 
and the solution is made more difficult by the special 
needs of the submarine service, in that not only is 
adequate protection required, but maximum mo- 
bility must be maintained for such actions as clear- 
ing the bridge under emergency conditions. 
For general references on the subject of physical 
properties, testing, and standards of clothing, papers 
by the following should be consulted: Bartell, Pur- 
cell, and Dodd {3248) 1943; Burton {3255) 1948; 
Coke, Kitching, and Page {3256) 1944; Christen- 
sen {3257) 1948; Fourt and Harris {3261) 1949; 
Fourt and Parrish {3262) 1945; Goodings, Coles, 
Kitching, Burton, Coke, and Bazett {3264); Her- 
rington {3266) 1945; Lee, White, and Kelso 
{3269) 1945; Newburgh and Harris {3272) 1945; 
and Perry {3273) 1949. Fourt and Harris limit 
their discussion of clothing fabrics to those prop- 
erties relating to human comfort and efficiency, 
e. g., effects of fabrics on the passage of air, heat, 
and water vapor. When a large amount of insula- 
tion is needed, a quilted combination shows superior 
thermal effectiveness per unit of weight. The sur- 
face characteristics determining the warm or cool 
feel of fabrics is the result of rapid local cooling of 
the skin by drawing heat into the fabric. Since fab- 
rics do not differ greatly in their specific heats, this 
effect depends on the fraction of gross surface which 
is in actual contact and the mass of fibres behind it. 
Therefore, fabrics woven of filament yarns and 
linen, with their long straight fibres, tend to feel 
cooler than the more hairy cotton fabrics, while wool CLOTHING—PHYSICAL PROPERTIES 
3247-3263 
with its springy, hairy surface feels warmest of all. 
The authors {3261) stress the important relation- 
ship between the absorption capacity of clothing 
and water vapor. 
Regarding the transfer of heat to the environ- 
ment by fabrics and the thermal insulation of 
ambient air, a number of studies have been reported 
which are contributory. For such studies, papers 
by the following should be consulted: Barker {3247) 
1951; Blum {3250) 1945; Burton {3253 and 3254) 
1945; Fetcher, Rapaport, Hall, and Shaub {3259) 
1949; Forbes {3260) 1949; Herrington {3267) 
1947; Mendelson, Hosbach, Tibet, and Bazett 
{3270) 1945; Wulsin {3286) 1945; and Yaglou 
{3287) 1945. Burton {3253) points out that the 
do determination of the insulating value of clothing 
depends on the knowledge of the amount of heat 
passing through the clothing via radiation and con- 
vection. The heat debt is equal to the thermal 
capacity of the body times the fall of body tem- 
perature. It is recommended that a specific heat 
value of 0.83 for the body be used until further 
experimental determinations on the whole human 
body suggest another value. 
Yaglou {3287) 1945 cautions the researcher 
against the unlimited use of insulation value for- 
mulas for the estimation of protection afforded by 
low temperature clothing assemblies because the 
overall figure gives no idea of protection of those 
areas particularly sensitive to cold, such as the 
shoulders, back, hands, knees, and feet. Inadequate 
protection of these critical areas greatly reduces 
endurance to cold. A method is described for evalu- 
ating local insulation of critical areas, as well as 
insulation of individual articles of clothing. 
For further studies on thermal insulation pro- 
vided by clothing, papers by the following should be 
consulted: Belding, Darling, Griffin, Robinson, and 
Turrell {3249) 1945; Burton {3251) 1943 and 
{3252) 1944; Herrington {3265) 1945; Rinecker 
{3274) 1950; Siple {3275 and 3276) 1945; U. S. 
National Research Council {3281) 1944; {3282) 
1945; and {3283) 1948; Winslow {3285) 1949; 
and Yaglou {3289 and 3290) 1948. 
For papers concerning special problems of cloth- 
ing design, papers by the following may be con- 
sulted: Debons {3258) 1950; Law, Wright, and 
Gotlieb {3268) 1950; Talbot {3277, 3278 and 
3279) 1945; U. S. National Research Council 
{3280) 1942; Van Dilla, Day, and Siple {3284) 
1949; and Yaglou {3288) 1946. 
3247. Barker, M. E, Warm clothes. What fabrics or 
combinations of fabrics best insulate the body against the 
loss of heat? An account of an unusual study that pro- 
duced some objective and practical answers to this ques- 
tion. Sci. Amer., 1951, 184: 56-60. [R] 
3248. Bartell, F. E., W. P. Purcell, and C. G. Dodd. 
Development of fabrics with desirable surface properties. 
U. S. OSRD-NDRG. OSRD contract no. O. E. M. cmr 
252, 1 November 1943, 50 pp. 
3249. Belding, H. S., E. C. Darling, D. B. Griffin, 
S. Eobinson, and E. S. Turrell. Evaluation of thermal 
insulation provided by clothing, pp. 9-21 in: Clothing 
test methods, Edited by L. H. Newburgh and Milton Har- 
ris. Ann Arbor, Michigan, Edwards Brothers, Inc., 1945, 
325 pp. 
3250. Blum, H. E. Solar heat load. pp. 23-36 in: 
Clothing test methods. Edited by L. H. Newburg and 
Milton Harris. Ann Arbor, Michigan, Edwards Brothers, 
Inc., 1945, 325 pp. 
3251. Burton, A. C. The use of the “table of wind chill 
values” prepared by the climatic research unit. Canada 
NRG-ACAMR. A. C. A. M. R. rept. no. C 2454, S. P. C. 
115, 5 April 1943, 2 pp. 
3252. Burton, A. C. Standard values for the thermal 
insulation of ambient air with different degrees of air 
movement. Canada NRG-ACAMR. A. C. A. M. R. rept. 
no. C 2753, S. P. C. 185, 16 November 1944, 5 pp. 
3253. Burton, A. C. Calculation of the heat debt. pp. 
5-7 in: Clothing test methods. Edited by L. H. Newburgh 
and Milton Harris. Ann Arbor, Michigan, Edwards Broth- 
ers, Inc., 1945, 325 pp. 
3254. Burton, A. C. Transfer of heat to the ambient 
air, and the thermal insulation of the ambient air. pp. 37- 
40 in: Clothing test methods. Edited by L. H. Newburgh 
and M. Harris. Ann Arbor, Michigan, Edwards Brothers, 
Inc., 1945, 202 pp. 
3255. Burton, A. C. On the science of field testing as 
applied to clothing and personal equipment. University 
of Western Ontario, Canada, 1948, 31 pp. 
3256. Coke, C. E., J. A. Hitching, and E. Page. Dis- 
posal of body moisture in subjects wearing various types 
of exposure suits. Canada NRG-ACAMR. A. C. A. M. R. 
rept. no. C 2689, S. P. C. 165, 18 May 1944, 8 pp. [P] 
3257. Christensen, W. E. Effects of physical character- 
istics of fabrics upon physiological heat load and subjec- 
tive reactions. /. industr. Hyg., 1948, 30: 251-255. 
3258. Debons, A. Gloves as a factor in reduced dexterity 
USAF. Ladd air force base, Alaska. Arctic aeromedical 
laboratory, Alaska. Project no. 21-01-018, February 
1950, 6 pp. [P] 
3259. Fetcher, E. S., S. I. Eapaport, J. F. Hall, and 
H. G. Shaub. Biophysical requirements for the venti- 
lation of clothing. /. appl. Physiol., 1949, 2: 49-60. 
3260. Forbes, W. H. Laboratory and field studies. 
General principles, pp. 320-329 in: Physiology of heat 
regulation and the science of clothing. Edited by L. H. 
Newburgh. Philadelphia, W. B. Saunders Go., 1949, viii, 
457 pp. 
3261. Fourt, L. and M. Harris. Physical properties 
of clothing fabrics, pp. 291-319 in: Physiology of heat 
regulation and the science of clothing. Edited by L. H. 
Newburgh. Philadelphia, W. B. Saunders Co., 1949, viii, 
457 pp. [P] 
3262. Fourt, L. and M. E. Parrish. Quamco cloth 
(bonded silica aerogel fabrics). U. S. NRC-CAM. 
OEMcmr-506, C. A. M. rept. no. 459, July 1945, 2 pp. 
Abstr. [P] 
3263. Galligan, A. and E. L. Day. Statistical consider- 
ation of data. pp. 63 in: Clothing test methods. Edited 
291222—54 20 3264-3290 
PROTECTION AND PRESERVATION OE PERSONNEL 
by L. H. Newburgh and Milton Harris. Ann Arbor, Michi- 
gan, Edwards Brothers, Inc., 1945, 325 pp. 
3264. Goodings, A. C., B. C. Coles, J. A. Hitching, 
A. C. Burton, C. E Coke, and H. C. Bazett. Investigation 
of physiological factors influencing water loss from the 
body and humidity of clothing. Canada NRC-ACAMR. 
A. C. M. R. rept. no. 114, no date, 6 pp. 
3265. Herrington, L. P. Measurement of skin and 
clothing temperatures, p. 3 in: Clothing test methods. 
Edited by L. H. Newburgh and Milton Harris. Ann Arbor, 
Michigan, Edwards Brothers, Inc., 1945, 325 pp. 
3266. Herrington, L. P. Moisture loss and moisture 
evaporated, pp. 21-22 in: Clothing test methods. Edited 
by L. H. Newburgh and Milton Harris. Ann Arbor, 
Michigan, Edwards Brothers, Inc., 1945, 325 pp. 
3267. Herrington, L. P. Basic procedures in the cal- 
culation of the heat exchange of the clothed human body. 
Yale J. Biol. Med., 1946/47,19: 735-755. 
3268. Law, N. C., L. A. Wright, and C. C. Gotlieh. 
Problems in assessing winter flying clothing. /. Aviat. Med., 
1950,21: 419-423. 
3269. Lee, D. H. K., C, White, and W. T. Kelso. Studies 
of evaporation from an artificial “skin” underneath service 
cloths. Australia, NHMRC, Fatigue laboratory. Univer- 
sity of Queensland. Report no. 2, 27 September 1945, 
4 pp. [P] 
3270. Mendelson, E. S., L. Hoshach, B. Lihet and H. C. 
Bazett. The testing of insulation in gloves by the use of a 
cold box for cooling the hands only and calorimetric esti- 
mations of the heat exchange under these conditions. U. S. 
NRC—CAM. OEMcmr—380, C. A. M. rept. no. 435, 
1 June 1945, 2 pp. [P] 
3271. Murphy, G. E. Physiological facts facilitating the 
enunciation of a statement of policy on military clothing. 
Gt. Brit. M. P. R. C. Subcommittee on clothing and per- 
sonnel. M. P. R. C./S/C/P/{50) 13a, 14 June 1950, 6 pp. 
3272. Newburgh, L. H., and M. Harris. A survey of 
tests for physical properties of clothing, pp. 75-98 in: 
Clothing test methods. Edited by L. H. Newburgh and 
Milton Harris. Ann Arbor, Michigan, Edwards Brothers, 
Inc., 1945, 325 pp. 
3273. Perry, W. 0. Development of insulating cloth for 
cold weather clothing. USAF. Wright-Patterson air force 
base, Dayton, Ohio. Air materiel command. Technical 
rept. 5753, January 1949, 5 pp. [P] 
3274. Rinecker, F. G. Thermal characteristics of multi- 
layer combinations of aluminum foil and nylon and cotton 
fabric in clothing. USAF. Wright-Patterson air force base, 
Dayton, Ohio. Air materiel command. Serial no. 
MCREXD-666—23H, 16 August 1950, pp. 5. 
3275. Siple, P. Definition of adequacy of clothing in 
cold climates, pp. 65-72 in; Clothing test methods. 
Edited by L. H. Newburgh and Milton Harris. Ann Arbor, 
Michigan, Edwards Brothers, Inc., 1945, 325 pp. 
3276. Siple, P. A. General principles governing se- 
lection of clothing for cold climates. Proc. Amer. phil. 
Soc., 1945, 89: 200-234. [R:P] 
3277. Talbott, J. H. Standardization of subjects, pp. 
41-45 in; Clothing test methods. Edited by L. H. New- 
burgh and Milton Harris. Ann Arbor, Michigan, Edwards 
Brothers, Inc., 1945, 325 pp. 
3278. Talbott, J. H. Tolerance time. pp. 47—48 in: 
Clothing test methods. Edited by L. H. Newburgh and 
Milton Harris. Ann Arbor, Michigan, Edwards Brothers, 
Inc., 1945, 325 pp. 
3279. Talbott, J. H. Grading of sensation, pp. 49-50 
in: Clothing test methods. Edited by L. H. Newburgh and 
Milton Harris. Ann Arbor, Michigan, Edwards Brothers, 
Inc., 1945, 325 pp. 
3280. IT. S. NRG. Subcommittee on clothing. Minutes 
of first meeting. 17 June 1942, 14 pp. 
3281. U. S. NRG. Subcommittee on clothing. Minutes 
of the meeting. 13 September 1944, 7 pp. 
3282. IT. S. NRG. Subcommittee on clothing. Minutes 
for meeting January 26, 1945, 4 pp. 
3283. 11. S. NRG. Subcommittee on shelter and cloth- 
ing. Minutes of second meeting: (Insulation character- 
istics of fibrous glass lined garments), 30 November 1948, 
14 pp. 
3284. van Dilla, M., R. Day, and P. A. Siple. Labora- 
tory and field studies. Special problem of hands, pp. 
374-388 in: Physiology of heat regulation and the science 
of clothing. Edited by L. H. Newburgh. Philadelphia, 
W. B. Saunders Co., 1949, viii, 457 pp. 
3285. Winslow, C.-E. A. and L. P. Herrington. The 
thermal protective influence of clothing, pp. 116—162 in: 
Temperature and human life. Princeton, Princeton Uni- 
versity Press, 1949, 272 pp. [P] 
3286. Wulsin, F. R. Metabolic rates for military activi- 
ties. pp. 51-61 in: Clothing test methods. Edited by L. H. 
Newburgh and Milton Harris. Ann Arbor, Michigan, Ed- 
wards Brothers, Inc., 1945, 325 pp. 
3287. Yaglou, C. P. A rational method for determining 
local and overall insulation of low temperature clothing. 
U. S. Navy. NMRI. Kept. no. 8, Project X—189, 19 
September 1945, 8 pp. 
3288. Yaglou, C. P. Pressures in the interior of army 
footgear. Report to the Office of the Quartermaster Gen- 
eral, 21 January 1946, 10 pp. [P] 
3289. Yaglou, C. P. Thermal insulation and comfort 
characteristics of fibrous glass-lined garments. /. Industr. 
Hyg., 1948, 30: 312-315. [P] 
3290. Yaglou, C. P. Thermal insulation of clothing. 
Trans. Amer. Soc. Heat, and Vent. Engrs., 1948, 54: 
291-298. [R] 
C. EFFECTS OF CLOTHING ON PHYSIOLOGICAL 
RESPONSES TO ENVIRONMENTAL CHANGES 
Physiological adjustments to sudden changes in 
ambient environment of 7 subjects wearing standard 
summer weight clothing compared with subjects 
wearing cotton, full length union suits were investi- 
gated by Glickman, Inouye, Keeton, Telser, and 
Fahnestock (3292) 1950. Exposure for one hour 
in a comfortable room at 24.4° C. with a vapor 
pressure of 9.2 and 24.4 kilodynes per sq. cm. was 
followed by 1 or 2 hours in the hot room at 37° C. 
with a vapor pressure of 41.1 kilodynes per sq. cm. 
Only slight differences in the physiological adjust- 
ments of the subjects was noted, these occurring 
primarily during the first 10 minutes of exposure. 
The buffering effect of clothing was evident on 
entering the hot room. Greater pulse rate increases 
were noted in the subjects wearing full length union 
suits during the first hour of exposure. 
Fourt {3294) 1949 states that summer clothing 
should possess good “wetting out” characteristics so 
that “blobs” of sweat can be spread out over large CLOTHING—PROTECTIVE 
3291-3308 
clothing areas for rapid evaporation. The author 
also believes that individual sweat glands may alter- 
nate in activity and that there is “hunting around” 
for the optimal rate of heat loss. 
The effect of body warmth, foot exercise, and 
surrounding insulation on foot comfort in cold water 
was investigated by Spealman {3298 and 3299) 
1944. The author concluded that when the body is 
cold, large amounts of insulation will not maintain 
the feet at a temperature greatly above that at which 
immersion foot is known to occur. On the basis of 
the information obtained under conditions where 
the body is warm, it appears that measures for con- 
serving body heat are of greater importance in 
maintaining elevated foot temperatures than is local 
insulation. Foot exercise also helped to maintain 
adequate foot temperatures when the feet were 
insulated (cellular rubber). 
For further reports on clothing in relation to 
physiological adjustments to environmental changes, 
papers by the following should be consulted; 
Belding, Russell, Darling, and Folk {3291) 1947; 
Folk and Peary {3293) 1951; Griffin, Folk, and 
Belding {3295) 1944; Horvath {3296) 1948; Lif- 
son and Visscher {3297) and U. S. National 
Research Council {3300) 1942. 
3291. Belding, H. S., H. D. Russell, R. C. Darling, and 
G. E. Folk. Analysis of factors concerned in maintaining 
energy balance for dressed men in extreme cold; effects 
of activity on the protective value and comfort of an 
arctic uniform. Amer. J. Physiol., 1947, 149: 223-239. 
3292. Clickman, N., T. Inouye, R. W. Keeton, S. E. 
Telser, and M. K. Fahnestock. The effect of clothing on 
the physiological adjustments of human beings to sudden 
change in environment. Fed. Proc. Arner. Soc. exp. Biol., 
1950, 9: 48. 
3293. Folk, G. E. and R. E. Peary, Penetration of 
water into the human foot. U. S. Army. Office of the 
Quartermaster General. Lawrence, Mass. Quartermaster 
climatic research laboratory. Environmental protection 
section. Rept. no. 181, October 1951, 44 pp. [R] 
3294. Fourt, L, Effect of clothing on heat exchange of 
man in hot environments, pp. 14—16 in: U. S. NRG-CAM. 
Conference on acclimatization. 17 June 1949, 29 pp. 
3295. Griffin, D. R., G. E. Folk, and H. S. Belding. 
Physiological studies of exposure suits in hot and cold 
environments. U. S. OSRD-CMR. Harvard fatigue lab- 
oratory, Harvard University. OEMcmr 54 and 328, Rept. 
no. 26, 9 March 1944, 4 pp. [P] 
3296. Horvath, S. M. Ventilation of clothing and toler- 
ance of man to low environmental temperatures. J. industr. 
Hyg., 1948, 30: 133-139. [P] 
3297. Lifson, N., and M. B. Visscher. Effect of wet 
garments on body weight loss at high environmental tem- 
peratures. U. S. NRC. Committee on clinical investiga- 
tion. No date, 7 pp. [P] 
3298. Spealman, C. R. The relationship between foot 
temperature and amount of insulation surrounding the 
foot immersed in cold water. U. S. Navy. NMRI. Project 
X-297, Rept. no. 2, 11 March 1944, 6 pp. [P] 
3299. Spealman, C. R. The effect of body warmth and 
foot exercise on the temperature of feet immersed in ice 
water. U. S. Navy. NMRI. Project X-297, Kept. no. 4, 
28 August 1944, 5 pp. 
3300. IT. S. NRC. Subcommittee on clothing. Minutes of 
the second meeting. 10 August 1942, 32 pp. 
D. CLOTHING FOR COLD AND DRY CONDITIONS 
The lack of adequate protection for watch stand- 
ers on the bridge of the newer type submarines 
exposes these personnel to heavy, cold seas. Refer- 
ences in this section have been included because 
they provide clothing data which may be applied 
to clothing research where conditions of cold, wet 
environments will be encountered. 
3301. Bearn, F. A. Clothing for war in arctic climates: 
experiences in Iceland. Inter-allied conferences on war 
medicine. 1942-1945, published 1947: 282-283. 
3302. Belding, H. S. Protection against dry cold. U. S. 
Army. Office of the Quartermaster General. Lawrence, 
Mass. Quartermaster climatic research laboratory. En- 
vironmental protection section. Kept. no. 155, 2 August 
1949, 19 pp. 
3303. Blair, E. A. and C. W. Gottschalk. Efficiency of 
signal corps operators in extreme cold. U. S. Army. Fort 
Knox, Kentucky. Armored medical research laboratory. 
Project 57, 22 January 1947, 17 pp. [P] 
3304. Busby, J. C. and S. V. Gianola, Arctic clothing 
for naval personnel. A report to the chief of Bureau of 
Supplies and Accounts on the work of the arctic clothing 
expedition at Point Barrow, Alaska, 12 October 1948 to 
30 April 1949. U. S. Navy, Naval clothing depot, Brook- 
lyn, New York. 1 May 1949, 123 pp. 
3305. Critchley, M. Medical observations during passage 
on northern convoy; in Russia; and in Iceland. Gt. Brit. 
MRC-RNPRC, CES. R. N. P. 48/454, C. E. S. 251, 
May 1948, 53 pp. 
3306. Gt. Brit. MRC-RNPRC, CES. Clothing panel. 
(Summary of R. N. P. 49/564 ‘Observations on physio- 
logical and clothing problems in the arctic during Opera- 
tion “Rusty” ’, by C. H. Wyndham and W. G. Wilson- 
Dickson). (Revision of C. P. 4). C. E. S. 332, C. P.4 (A), 
23 November 1951, 5 pp. [D] 
3307. IT. S. Navy. BuY&D. Report on arctic clothing 
experience. NavDocks P-13, May 1948, 29 pp. [D] 
3308. Anon. Footwear for frigid feet. U. S. Navy. ONR. 
Res. Rev., March 1951, pp. 7-8. 
E. PROTECTIVE CLOTHING FOR IMMERSION 
AND RAIN 
The clothing requirements of immersion suits for 
aviators and cold weather deck clothing for sub- 
marine personnel are quite similar. The protective 
clothing must be water-tight for immersion in 
water or exposure to heavy seas, must possess quali- 
ties of warmth, and must be durable enough to re- 
sist tearing against bridge gear in heavy seas, and 
trim enough to fit through small hatches. 
An exposure suit tested for shipboard use by 
Margolis {3316) 1946 was found to be satisfactory 
for immersion in sea water ranging in temperature 3309-3322 
PROTECTION AND PRESERVATION OF PERSONNEL 
between 28° and 48° F. The suit is made of a water- 
impermeable laminated fabric composed of two 
plies of olive drab cotton sheeting with a waterproof 
coating between the layers. It envelops the body up 
to the neck and is seated by a drawstring. The 
sleeves have an extra cuff of rubber and standard 
Navy boots are cemented and sewed to the legs. 
Concerning the protective properties of clothing 
for subjects immersed in cold water, Newburgh and 
Spealman {3318 and 3319) 1943 found that the 
rate of cooling was greatly retarded when dry cloth- 
ing was worn underneath the watertight suit. The 
nude subject enclosed in the watertight suit cooled 
as quickly as the entirely naked man. 
For further studies on immersion suits and water 
repellent clothing, reference may be made to the fol- 
lowing reports: Cowan and Grant {3309) 1944; 
Fonash {3310) 1947 and {3311) 1949; Bazett 
{3312) 1942; Gerking and Robinson {3313) 1945; 
Gerking, Robinson, and Turrell {3314) 1944; 
Lombard and Creedon {3315) 1946; Murrell 
{3317) 1951; Pugh {3320) 1951; Spealman and 
Margolis {3321) 1945; and U. S. Navy, BuNavPers 
{3322) 1949. 
3309. Cowan, C. R. M. and R. Grant. Royal Canadian 
Navy participation in clothing trials. Canada NRG. Pro- 
ceedings of third meeting of associate committee on naval 
medical research. Project C4077, 15 May 1944, 3 pp. [P] 
3310. Fonash, R. L. Test and evaluation of four experi- 
mental modifications of the MK 2 exposure suit. U. S. 
Navy. Aero medical laboratory, Philadelphia, Penna. Rept. 
TED no. NAM 2574—.4, 15 October 1947, 11 pp. [P] 
3311. Fonash, R. L. Test and evaluation of four experi- 
mental modifications of the MK 2 exposure suit. U. S. 
Navy. Air materiel center, Philadelphia, Penna. Aero- 
nautical medical equipment laboratory. Rept. TED no. 
NAM 25704.4, BuAer Ur Aer-AE-52, 08474, 30 June 
1949, 11 pp. 
3312. Bazett, H. C. Watertight suits. Canada NRC- 
ACAMR. A. C. A. M. R. rept. no. C 2339, S. P. C. 59, 
19 October 1942, 3 pp. 
3313. Gerking, S. D, and S. Robinson. Physiological 
comparisons of water repellent and water absorbent cloth- 
ing. U. S. NRC—CAM. OEMcmr—351, C. A. M. rept. no. 
432, 24 April 1945, 7 pp. 
3314. Gerking, S. D., S. Robinson, and E. S. Turrell. 
A physiological study of raincoats and ponchos. U. S. 
OSRD-CMR. Contract no. OEMcmr—351, Interim rept. 
no. 13, 17 July 1944, 10 pp. 
3315. Lombard, B. F. and W. E. Creedon. Evaluation 
of exposure suits designed and manufactured by H. K. 
Shaw. U. S. Coast Guard. Field testing and development 
unit. A Coast Guard Yard, Curtis Bay, Md. Project 
CGTD—55—02—45, Rept. no. 1, 1 October 1946, 31 pp. [P] 
3316. Margolis, S. I. Field trial of an exposure suit for 
shipboard use. U. S. Navy. NMRI. Project X-189, Rept. 
no. 10, 26 June 1946, 4 pp. 
3317. Murrell, H. Job classification of naval activities 
undertaken above deck. Gt. Brit. MRG-RNPRC. Depart- 
ments of operational research and of the senior psychol- 
ogist. Naval motion study unit report no. 44, September 
1951, 7 pp. 
3318. Newburgh, L. H. and C. R. Spealman, Protective 
clothing for subjects immersed in cold water. U. S. Navy. 
NMRI. Project X-189, Kept. no. 1, 10 July 1943, 4 pp. 
3319. Newburgh, L. H. and C. R. Spealman. Protective 
clothing for subjects immersed in cold water. Part A. 
Some characteristics of the “Paske” suit. Part B. Degree 
of protection against evaporating cooling afforded by 
water-tight suits. U. S. Navy. NMRI. Project X-189, 
Rept. no. 2, 10 August 1943, 5 pp. 
3320. Pugh, L. G. C. Summary of physiological observa- 
tions during operation “Rusty”, with particular reference 
to clothing. (Revision of G. P. 3). Gt. Brit. MRC- 
RNPRG, CES. C. E. S. rept. 334, C. P. 3(a), 23 Novem- 
ber 1951, 5 pp. 
3321. Spealman, C. R. and S. I. Margolis. Comparative 
comfort of the combination rain suit-exposure suit (Red 
Star Rubber Co.) and Navy Parka Rain Clothing. U. S. 
Navy. NMRI. Project X-189, Rept. no. 9, 29 October 
1945. 
3322. U. S. Navy. BuNavPers. (A) Submarine clothing, 
pp. 175-176 in: Submarine medicine practice NavPers 
10838, March 1949, 182 pp. [D] 
F. CLOTHING FOR CONDITIONS OF HEAT AND 
HUMIDITY 
Experiments carried out by Yaglou and Rao 
(3328) 1947 on men, wearing loose and close- 
fitting clothing exposed to a chamber temperature 
of 85° F. with a relative humidity of 85 percent 
and an air movement of 70 feet per minute, demon- 
strated that the loose-fitting clothing was more com- 
fortable under these conditions. The subjects felt 
that it was more comfortable because when the 
loose clothing became wet it did not stick to the 
skin as much as the close-fitting clothing. 
Shelley, Eichna, and Horvath {3326) 1946 in- 
vestigated the effects of two types of clothing on 
the ability of acclimatized men to work at upper 
heat limits. The upper limiting wet bulb tempera- 
ture for successful group performance of four hours 
marching at three miles per hour (dry bulb tem- 
perature, 120° F.) was 92° F. for nude men, 90° F. 
for men wearing herringbone twill, and 88° F. for 
men wearing impregnated herringbone twill uni- 
forms. At upper limits of environmental heat, wear- 
ing of a single layer herringbone twill uniform (8 
ounces) imposes a heat load which is equivalent 
to a 2° F. increase in wet bulb temperature. 
Robinson {3325) 1945 states that the physiologi- 
cal difference between the hottest and coolest suit 
is much less than the difference between the coolest 
suit and shorts. When the subjects wore shorts, skin 
temperature, sweating and heart rates were lower. 
The actual amount of sweat evaporated was less 
when the subjects wore shorts, suggesting that the 
efficiency of evaporation in cooling the body may DEEP SEA DIVING EQUIPMENT 
3323-3334 
be greater when it takes place directly from the 
skin than when it takes place from clothing surfaces. 
For reports on clothing under conditions of heat 
and humidity, reference may be made to papers by 
Buettner and Richey {3323) 1951, Gerking and 
Robinson {3324) 1945, and U. S. National Re- 
search Council {3327) 1943. 
3323. Buettner, K. and E. 0. Richey. Effects of extreme 
heat on man. IV. Mechanism of heat transfer in an 
open gasoline fire. USAF. Randolph Field, Texas. School 
of aviation medicine. Project 21-26-002, Kept. no. 4, 
July 1951, 4 pp. 
3324. Gerking, S. D. and S. Robinson. The physiologi- 
cal effects of double layers of cloth on summer flying suits. 
U. S. OSRD. Contract no. OEMcmr 351, interim rept. 
no. 23, 19 February 1945, 3 pp. [P] 
3325. Robinson, S. Laboratory and field studies. Tropics, 
pp. 338-351 in: Physiology of heat regulation and the 
science of clothing. Edited by L. H. Newburgh. Phila- 
delphia, W. B. Saunders Co., 1949, viii, 457 pp. [P] 
3326. Shelley, W. B., L. W. Eichna, and S. M. Horvath, 
The effect of clothing on the ability of men to work in 
intense heat. /. din. Invest., 1946, 25: 437-446. 
3327. IT. S. NRC. Subcommittee on clothing. Minutes 
of the second meeting on jungle clothing. 19 August 1943, 
3 pp. 
3328. Yaglou, C. P. and M. N. Rao. Loose versus close- 
fitting clothing for work in “tropical heat”. /. industr. 
Hyg., 1947, 29: 140-142. [P] 
VI. DEEP SEA DIVING EQUIPMENT AND 
PROCEDURES 
Diving with apparatus is usually considered by 
the layman to be divided into deep sea and shallow 
water diving, the distinction being made in terms 
of depth. These two terms have been used so fre- 
quently that the whole subject of diving has popu- 
larly come to be divided into these two categories. 
Deep sea diving has tended to imply diving to more 
than 36 feet with shallow water diving referring to 
diving to less than 36 feet. In diving, the type of 
work to be undertaken, location of the work, the 
extent of the operations, and the climatic conditions, 
in addition to depths, are the determining factors 
in deciding upon the personnel and type of equip- 
ment to be used and the method of accomplishing 
the task. Therefore, the distinction between deep 
sea and shallow water diving is not a sharp one. 
For reasons of convenience the present section deals 
with diving in which the respiratory gas mixture 
is supplied to the diver from surface equipment. 
The discussion of self-contained diving apparatus 
is included in the section on special problems of 
shallow water diving (p. 329), 
The deep sea diving rig is composed essentially 
of a helmet and water-tight dress, weighted belt and 
shoes, a hose and control valve whereby air is 
furnished and the quantity of air controlled, and 
a nonreturn valve used to prevent air from escaping 
from the dress in the event of an accidental rupture 
of the air hose. 
For an excellent description of deep sea diving 
equipment the reader is referred to a U. S. Navy 
publication {3339) 1951 which has now been in- 
corporated into the Bureau of Ships Diving Manual, 
1952, and can be obtained from the U. S. Govern- 
ment Printing Office, Washington 25, D. C. The 
section of the book devoted to diving equipment 
includes a description of the apparatus with pictures 
and cross-sectional diagrams. Additional informa- 
tion on this subject is supplied in a descriptive 
monograph by Davis {3319 and 3330) 1951. 
Tests by Molumphy {3336) 1948 on the U. S. 
Navy deep sea diving helmet at depths of 0, 75, 
150, and 225 feet, with supply pressures of 25, 50, 
75, and 100 lbs. per square inch over bottom in- 
dicated that the ratio of total recirculation of high 
pressure-nozzle flow for helium-oxygen mixtures is 
about 7 to 1 and it was found to increase somewhat 
with depth. Practically no difference was found to 
exist in recirculation by the venturi system when the 
high-pressure nozzle was one-fourth inch away or 
flush with the mouth of the venturi discharge nozzle. 
All high-pressure nozzle and recirculation flows de- 
creased with depth. For additional information on 
this subject the reader should avail himself of 
papers by Molumphy {3335 and 3337) 1948. 
For other reports on diving procedures and 
equipment, the reader may consult papers by 
Delorme and Locke {3331) 1944; Klimenko, Pav- 
livskii, and Maksimenko {3332, 3333, and 3334) 
1948, and the U. S. Navy {3338) 1949. 
3329. Davis, Robert H. A summary of the present state 
of the art of deep diving, pp. 1-25 in: Deep diving and 
submarine operations. A manual for deep sea divers and 
compressed air workers. London. The Saint Catherine 
Press Ltd., 1951, 670 pp. [D] 
3330. Davis, Robert H. The physics and physiology of 
deep diving, pp. 26—40 in: Deep diving and submarine 
operations. A manual for deep sea divers and compressed 
air workers. London. The Saint Catherine Press Ltd., 
1951, 670 pp. [D] 
3331. Delorme, E. J. and W. Locke. Report in the medi- 
cal aspects of diving practice of interest to the Royal 
Canadian Navy. Canada NRC. Proceedings of 3rd meeting 
of associate committee on naval medical research. Project 
C4080, 15 May 1944, 6 pp. 
3332. Klimenko, K. A., K. A. Pavlovskii, and V. P, 
Maksimenko, The physics of diving, pp. 10-25 in: Man- 
ual for divers of the navy. Moskow, Military Printing 
office, 1948, 172 pp. (Russian text.) 
3333. Klimenko, N. A., K. A. Pavlovskii, and V. P. 
Maksimenko. Safety rules for descent, pp. 64-78 in: 
Manual for divers of the navy. Moskow, Military Printing 
office, 1948, 172 pp. (Russian text.) 
3334. Klimenko, N. A., K. A. Pavlovskii, and V. P. 
Maksimenko. Care and repair of diving equipment, pp. PROTECTION AND PRESERVATION OF PERSONNEL 
3335-3339 
127-135 in: Manual for divers of the navy. Moskow, 
Military Printing office, 1948, 172 pp. (Russian text.) 
3335. Molumphy, C. G, Test of recirculation and jet 
flow of He-(D2 helmets from USS Thinga and USS Petrel. 
U. S. Navy. Naval gun factory, EDU. Project no. 
11 March 1948, 7 pp. 
3336. Molumphy, C. 6. Test of total recirculation, jet 
flow and vacuum of a He-02 helmet submitted by the USS 
Kittiwake. U. S. Navy. Naval gun factory, EDU. 25 
March 1948, 8 pp. 
3337. Molumphy, C. G. Determination of total recircula- 
tion, vacuum, high pressure nozzle discharge and other 
general characteristics of the recirculating system of the 
standard U. S. Navy He-02 deep sea diving helmet under 
various conditions of depth and venturi supply pressures, 
with air and He-02 mixtures. U. S. Navy. Naval gun 
factory, EDU. Project no. SRD 235/46, 22 April 1948, 
12 pp. 
3338. U. S. Navy, BuNavPers. The descent, pp. 81-102 
in; Submarine medicine practice. NavPers 10838, March 
1949, 182 pp. [D] 
3339. U. S. Navy. BuShips. Description and care of 
standard diving equipment, pp. 3—19 in: Chapter 94. 
Salvage section II. Diving. 25 January 1951. U. S. Gov- 
ernment printing office, Washington, D. C., 1951, 93 pp. 
VII. RESUSCITATION AND RESPIRATORY 
DEVICES 
Aboard ships at sea during war many occasions 
are presented when life may be saved by prompt 
administration of artificial respiration. The main 
emergencies in which it is required are drowning 
and electric shock. Because the subject extends far 
beyond the scope of this volume, it has not been 
considered pertinent to include an extensive bibli- 
ography of the literature on artificial respiration 
or respiratory devices. 
For general studies on artificial respiration, pa- 
pers by the following authors should be consulted: 
Andre {3340) 1949; Behrens {3343); Davis {3350) 
1947; Groesbeck {3359) 1951; Jellinek {3362) 
1947 and {3363) 1951; Murray {3372) 1945; Whit- 
tenberger and Sarnoff {3392) 1950; Wiggin, Saun- 
ders, and Small {3393 and 3394) 1949; Wilson 
{3395) 1948; and U. S. National Research Coun- 
cil {3397) 1951. Reference 3398 may also be 
consulted. 
In drowning and electric shock, respiratory fail- 
ure occurs first and failure of the heart secondarily. 
When the activity of the medulla oblongata is de- 
pressed respiration becomes sluggish and may cease 
but the heart continues to beat independently of 
the central nervous system, provided it receives 
an adequate supply of oxygen. Therefore, if oxygen 
can be supplied to the patient’s blood promptly the 
circulation will continue and the respiratory center 
may recover its rhythmic activity for natural and 
sustained respiration. 
It is stated {3393 and 3394) that in the human 
being complete cerebral anoxia for 10 seconds 
produces unconsciousness, 20 to 30 seconds causes 
cessation of brain waves, and 3 to 5 minutes pro- 
duces irreversible pathological changes in nervous 
tissue. Damage to the myocardium by anoxia is im- 
portant because although it develops less rapidly 
than that to the brain, it is responsible for the inabil- 
ity of the heart to recover from cardiorespiratory 
arrest in cases in which cardiac resuscitation is un- 
successful. Wiggin, Saunders, and Small also state 
that if cardiorespiratory arrest has not lasted longer 
than 2 to 4 minutes, recovery may be expected. For 
another excellent review of resuscitation, the reader 
should consult the paper by Andre {3340) 1949. 
When cardiac massage is resorted to, this author 
favors the injection of one-half mg. of atropine as 
soon as the myocardial contractions have reap- 
peared to avoid vagal inhibition when spontaneous 
respiratory movements reappear. 
Conclusions drawn from the National Research 
Council conference on methods of artificial respi- 
ration {3397) indicate that the prone pressure 
method is unsatisfactory and should be abandoned. 
Because the arm-lift back-pressure method gives 
adequate ventilation and is easy to teach and can 
be carried out by a single operator for long periods 
of time, it was advised that this method be adopted 
for military use. The arm-lift chest-pressure method 
provides sufficient ventilation but is not conducive 
to a clear airway. Difficulty in teaching and learn- 
ing the hip-roll back-pressure method was stated to 
be a deterrent to its acceptance and the hip-lift 
back-pressure method was stated to be too fatiguing 
for a single operator. This latter method gave the 
fullest pulmonary ventilation. 
Experimental evidence presented by Gordon, 
Free, Wedell, Sadove, Raymon, Nelson, and Ivy 
{3355) 1951 indicated no significant differences in 
the mean arterial oxygen saturation when hip-lift 
back-pressure, arm-lift back-pressure, hip-roll back- 
pressure and Eve methods were used. Fifteen nor- 
mal male subjects (23 to 45 years old) were given 
curare to produce complete apnea. The right heart 
was catheterized via the external jugular or ante- 
cubital vein with the tip in the pulmonary artery 
one inch beyond the bifurcation. Another catheter 
was introduced into the right auricle and a third 
catheter was inserted in the femoral artery. High 
cardiac outputs of over 5.5 liters per minute were 
obtained for all methods. Great differences in pul- 
monary arterial pressures (inspiratory and expira- 
, tory) were found in all methods except for the 
I Schaefer method. The mean level of arterial oxygen 
saturation for the Schaefer method was only 77 
percent while for other methods it ranged between RESUSCITATION AND RESPIRATORY DEVICES 
89 and 100 percent. In the manual push-pull 
methods, a high carbon dioxide output and respira- 
tory quotient indicated a high rate of enforced gas 
exchange. The Eve method gave uniform respira- 
tory quotients with only small fluctuations. 
Swann and Brucer {3386) 1948 found in dogs 
that the first sign of recovery during resuscitation 
was a sharp rise in systolic pressure but not neces- 
sarily a rise in diastolic pressure. Soon thereafter 
breathing was reinstated. Animals were given air 
mixtures of 2.4 percent oxygen in nitrogen and when 
death was imminent, various lung ventilation meas- 
ures were instituted to resuscitate the animals. The 
first rise in blood pressure occurred within 100 sec- 
onds or not at all, even though pulmonary venti- 
lation was continued for 20 minutes. When cardiac 
massage, as well as artificial respiration, was insti- 
tuted, recovery was facilitated. However, return of 
blood pressure and respiration was slower. 
For additional papers of cardiovascular responses 
occurring during resuscitation, the reader should 
consult reports by Binet and Strumza {3345) 1951; 
Fainer, Martin, and Ivy {3352) 1951; Handford, 
Ricchiuti, and Bodenlos {3360) 1951; Lapin 
{3370) 1945; and Wilson {3396) 1949. 
Respiratory studies by Asmussen and Nielsen 
{3341) 1950 on 6 male and 5 female subjects given 
artificial respiration by the Schaefer, Nielsen and 
Eve methods gave tidal air values of 180 cu. cm. 
for the Schaefer method, 450 cu. cm. for the Nielsen, 
and 540 cu. cm. for the Eve method. Two patients 
with respiratory arrest were subjected to different 
methods of artificial respiration by Comroe and 
Dripps {3349) 1946. The tidal air from the Schaefer 
method varied from 71.5 to 117 cu. cm. while the 
Eve method produced exchanges ranging from 286 
to 500 cu. cm. per cycle. Because the Schaefer 
method depends primarily on the elastic recoil of 
the lungs and tone of the respiratory muscles and 
since these are absent in the deeply asphyxiated 
patient, this method is of least value when needed 
most. Conversely, the Eve method is efficient when 
tone and elasticity of these structures is absent. It 
was also found that intratracheal insufflation with 
oxygen is not as effective as actual expansion and 
collapse of the lungs for the movement of carbon 
dioxide from the alveolar surfaces. This is explained 
by the fact that carbon dioxide has a greater mo- 
lecular weight than oxygen and does not diffuse as 
rapidly as oxygen, despite the greater ease with 
which it diffuses through water and living mem- 
branes. The accumulation of lactic acid due to 
severe tissue anoxia and fixed retention resulting 
from intense renal vasoconstriction caused by too 
low blood pressure were probably responsible for 
some of the acidosis that developed. These studies 
by Comroe and Dripps emphasize that artificial 
respiration must not only raise blood oxygen levels 
to normal levels but must also reduce the blood 
carbon dioxide. 
Additional papers by Gordon, Affeldt, Sadove, 
Raymon, Whittenberger, and Ivy {3354) 1951; 
Nims, Conner, Botelho, and Comroe (3373) 1951; 
Thompson {3387) 1948; and Whittenberger, 
Affeldt, Goodale, and Sarnoff {3391) 1951 indi- 
cate that tidal air volumes for the Schaefer method 
are considerably lower than those obtained by the 
other methods of manual artificial respiration. 
These other push-pull methods have been found to 
be at least 2 times more efficient for pulmonary 
ventilation than the Schaefer method. Pneumo- 
tachographic studies dictate that active inspiration 
and active expiration should ideally occupy approx- 
imately one and a half second each. Best perform- 
ance was obtained by a 5 to 6 second cycle with 10 
to 12 cycles per minute. Although the Nielsen 
method produced less pulmonary ventilation than 
the hip-lifting procedures, it appeared to be a con- 
venient and practical method for giving artificial 
respiration for long periods of time. It is recom- 
mended {3373) that since the blood carbon dioxide 
level has risen in the apneic patient, a breathing 
frequency in excess of 10 to 12 per minute should 
be used. 
Further studies on respiratory effects of resuscita- 
tion have been reported by Carson and Pinto 
{3348) 1947; De Forest and Potthoff {3351) 
1951; Gordon, Sadove, Raymon, and Ivy {3357) 
1951; Karpovich, Hale, and Bailey {3367) 1951; 
Pask {3374) 1948; Sadove, Gordon, Nelson, and 
Ivy {3377) 1951; Spiro, Aaron, and Thompson 
{3382) 1947; Spiro, Goltra, and Thompson {3383) 
1948; and Swann {3384) 1948 and {3385) 1949. 
Karpovich and Hale {3365) 1951 measured the 
energy expenditure of 20 men and women perform- 
ing 5 methods of artificial respiration. Oxygen con- 
sumption for the methods was as follows: Schaefer, 
547 cu. cm. for men and 445 cu. cm. for women; 
Silvester, 706 cu. cm. and 480 cu. cm.; Nielsen, 706 
cu. cm. and 657 cu. cm.; hip-roll back-pressure, 
1,045 cu. cm. and 746 cu. cm.; and the hip-lift 
back-pressure, 1,050 cu. cm. and 713 cu. cm. Work 
by Gordon, Raymon, Sadove, Wedell, and Ivy 
{3356) 1951 leads them to conclude that the 
Schaefer method is least taxing; the hip-lift back- 
pressure requires the greatest energy expenditure 
while the Silvester and Nielsen methods are 
intermediary. 3340-3366 
PROTECTION AND PRESERVATION OF PERSONNEL 
The ease of teaching the various methods of 
manual artificial respiration was investigated by 
Karpovich and Hale {3364) 1941 and {3366) 
1951. One hundred academy cadets and 67 college 
students were instructed in 5 methods of artificial 
respiration. From the standpoint of ease of learning 
and operation, these methods have been arranged 
in the following order of increasing difficulty: 
prone pressure, arm-lift back-pressure, arm-lift 
chest-pressure, hip-roll back-pressure, and hip-lift 
back-pressure. Gordon, Star, Meier, Hale, and Ivy 
{3358) 1951 found that the arm-lift back-pressure 
and variations of the hip-lift back-pressure methods 
could be successfully taught to naval recruits, in- 
cluding Waves, in relatively brief training sessions. 
Of these methods, the arm-lift back-pressure sur- 
passes all the variations of the hip method in accu- 
racy of performance, ease of learning, and physical 
ease of performance. 
For additional papers on artificial respiration the 
reader should consult papers by Baetjer {3342) 
1951; Brucer and Swann {3346) 1951; and 
Schwerma, Ivy, Friedman, and La Brosse {3380) 
1948. 
It is not intended under this heading to include 
in its entirety the extensive literature on resuscita- 
tive equipment. A paper by Schwerma and Ivy 
{3379) 1946 contains information on pathological 
damage of lungs resulting from excessive positive 
and negative pressures of respirators in dog experi- 
ments. The reader should also consult reports such 
as those by Campbell and Poulton {3347) 1938 and 
Fisher {3353) 1950 for discussions and descriptions 
of respiratory devices now in use. 
3340. Andrg, M. J. La ranimation en chirurgie traite- 
ment physiologique de la syncope (A 1’exclusion de 1’oxy- 
gdno-carboth6rapie). Anest. & Analges., Paris, 1946-49, 
6: 128-165. [R] 
3341. Asmussen, E. and M. Nielsen. Efficacy of artifi- 
cial respiration. J. appl. Physiol, 1950, 5: 95-102. 
3342. Baetjer, A. M. Resuscitation, pp. 1022-1027 in; 
Rosenau preventive medicine and hygiene. Edited by Ken- 
neth F. Maxcy. Seventh edition. New York, Appleton- 
Century Crofts, Inc., 1951, 1462 pp. [R] 
3343. Behrens, C. F. Asphyxia in naval operations. U. S. 
Navy. NMRI. Lecture and review series. No. 51-8. 12 
June 1951, 7 pp. 
3344. Berger, L. B. Supplemental list of respiratory 
protective devices approved by the Bureau of Mines. Ad- 
ditions to list published in Information Circular 7444. 
U. S. Bureau of Mines. Information Circular 7513. April 
1949, 3 pp. 
3345. Binet, L. and M. V. Strumza. C02 total plasma- 
tique art6riel et d6clenehement de la reprise respiratoire 
apr£s apnee primaire anoxique. C. R. Soc. Biol. Paris, 
1951, 145: 192-195. [P] 
3346. Brucer, M. and H. G. Swann. Requirements for 
resuscitation by artificial respiration in fulminating anoxia. 
J. appl. Physiol, 1951, 3: 479-488. 
3347. Campbell, A. and E. P, Poulton. Artificial respira- 
tion. pp. 147-150 in: Oxygen and carbon dioxide therapy. 
London, Oxford University Press, 1938, 202 pp. 
3348. Carson, L. D. and J. C. Pinte. The Eve method of 
resuscitation. Nav. Med. Bull., Wash., 1947, 47: 650-656. 
J. industr. Hyg., 1948, 30: abstract section: 3. [P] [R] 
3349. Comroe, Jr., J. H. and R. D. Dripps. Artificial 
respiration. J. Amer. med. Ass., 1946, 130: 381-383. J. 
industr. Hyg., 1946, 28: abstract section: 71-72. [R] [CH] 
3350. Davis, R. H. Breathing in irrespirable atmospheres 
and, in some cases, also under water. London, The Saint 
Catherine Press Ltd., 1947, 374 pp. 
3351. De Forest, R. E. and C. J. Potthoff. Back pressure- 
arm lift method for administering artificial respiration 
recommended. /. Amer. med. Ass., 1951, 147: 1454-1455. 
3352. Fainer, D. C., C. G. Martin, and A. C. Ivy. 
Resuscitation of dogs from fresh water drowning. J. appl. 
Physiol., 1951, 3: 417-426. [P] 
3353. Fisher, H. E. Resuscitation, pp. 876-878 in: 
Medical physics. Volume II. Edited by Otto Glasser. Chi- 
cago, The Year Book Publishers, Inc., 1950, 1227 pp. [R] 
3354. Gordon, A. S., J. E. Affeldt, M. Sadove, F. Ray- 
mon, J. L. Whittenberger, and A. C. Ivy. Air-flow pat- 
terns and pulmonary ventilation during manual artificial 
respiration on apneic normal adults. /. appl. Physiol., 
1951, 4: 408-420. [P] 
3355. Gordon, A. S., 0. Free, H. Wedell, M. S. Sadove, 
F. Raymon, J. T. Nelson, and A. C. Ivy. Circulatory 
studies during artificial respiration on apneic normal 
adults. III. /. appl. Physiol., 1951, 4: 421-438. [P] 
3356. Gordon, A. S., F. Raymon, M. S. Sadove, H. 
Wedell, and A. C. Ivy. Energy expenditure of operators 
during manual artificial respiration. IV. /. appl. Physiol., 
1951, 4: 439-446. [P] 
3357. Gordon, A. S., M. S. Sadove, F. Raymon, and 
A. C. Ivy. Critical survey of manual artificial respiration. 
J. Amer. med. Ass., 1951,147: 1444-1453. [R] 
3358. Gordon, A. S., S. Star, F, Meier, C. Hale, and 
A. C. Ivy. Pedagogical and performance factors of manual 
artificial respiration with naval personnel. V. J. appl. 
Physiol, 1951, 4: 447-457. [P] 
3359. Groesbeck, B., Jr. Survival, rescue, and resuscita- 
tion. J. Amer. med. Ass., 1951, 147: 1406-1408. 
3360. Handford, S. W., N. V. Ricchiuti, and L. J. 
Bodenlos. Positive and alternating positive-negative pres- 
sure resuscitation from curare poisoning. /. appl. Physiol, 
1951,5: 535-553. 
3361. Jacobs, H. J. Artificial respiration and the pneu- 
matic balance resuscitator. Army med. Bull, 1947, 7: 
707-717. 
3362. Jellinek, S. The technique of life-saving—long- 
standing evils—new guiding principles, pp. 158-203 in: 
Dying, apparent-death and resuscitation. Baltimore, The 
Williams & Wilkins Co., 1947, 246 pp. 
3363. Jellinek, S. Artificial respiration. Sci. Amer. July 
1951. 185: 18-21. 
3364. Karpovich, P. V. The best method of manual 
artificial respiration. Res. Quart. Amer. phys. Educ. Ass., 
1941, 12: 50-60. 
3365. Karpovich, P. F. and C. J. Hale. Energy ex- 
pended in administering artificial respiration. /. appl. 
Physiol, 1951, 4: 467-471. [P] 
3366. Karpovich, P. V. and C. J, Hale. Manual artificial 
respiration. Pedagogical and fatigue factors involved in its 
use. J. appl. Physiol, 1951, 4: 472-475. [P] DIFFUSION RESPIRATION 
3367-3398 
3367. Karpovich, P. V., C. J. Hale, and T. L, Bailey. 
Pulmonary ventilation in manual artificial respiration. 
/. appl. Physiol., 1951,4: 458-466. [P] 
3368. King, B. G., E. P. Vollmer, D. E. Goldman, and 
J. B, Dorner, Evaluation of the Heidbrink model-70 and 
army item no. 37261 positive pressure resuscitators and 
Kreiselman hand bellows resuscitator with field tests in 
collaboration with Naval Air Station, Lakehurst, New 
Jersey. U. S. Navy. NMRI. Project X-486, Rept. no. 2, 
7 May 1945, 13 pp. 
3369. King, B. G., E. P. Vollmer, A. W. Urban, and 
H. E. Newton. An improved positive pressure resuscitator- 
inhalator assembly designed for general navy use (Heid- 
brink stock no. 3804-0063). U. S. Navy. NMRI. Project 
Rept. no. 3, 22 May 1945,6 pp. 
3370. Lapin, S. B. Modification of the Eve method of 
resuscitation. Army med. Bull., 1945, 3: 110-111. 
3371. Motley, H. L., A. Cournand, L. Werko, D. T. 
Dresdale, A. Himmelstein, and D. W. Richards, Jr. In- 
termittent positive pressure breathing. A means of admin- 
istering artificial respiration in man. /. Amer. med. Ass., 
1948, 137: 370—382. Excerpta Medica (Section II. 
Physiology, Biochemistry, and Pharmacology), 1949, 2: 
497. Abstr. [R] 
3372. Murray, S. D. Application of the Eve rocking 
method of resuscitation on shipboard. Nav. med. Bull., 
Wash., 1945,44: 161-165. 
3373. Nims, R. 6., E. H. Conner, S. Y. Bothelho, and 
J. H. Comroe, Jr. Comparison of methods for performing 
manual artificial respiration on apneic patients. J. appl. 
Physiol, 1951,4: 486-495. [P] 
3374. Pask, E. A. Artificial respiration. Proc. R. Soc. 
Med., 1948, 41: 138-142. Anesthesiol., 1948, 9: 667. 
Abstr. [R] 
3375. Patty, Frank A. Respirators and respiratory pro- 
tective devices, pp. 455-465 in: Industrial hygiene and 
toxicology. Edited by Frank A. Patty. New York, Inter- 
science Publishers, Inc., 1948, 531 pp. 
3376. Rahn, H., A. B. Otis, M. Hodge, M. Brontman, 
J. Holmes, and W. 0. Fenn. The pneumatic balance re- 
suscitator. U. S. NRC-CAM. OEMcmr—147, C. A. M. 
rept. no. 424, 5 March 1945, 1 pp. (Summary) 
3377. Sadove, M. S., A. S. Gordon, J, T. Nelson, and 
A, C. Ivy. Barbiturate-curare-induced apnea for artificial 
respiration studies on normal adults. J. appl. Physiol., 
1951, 4: 403-407. [P] 
3378. Schrenk, H. H. List of respiratory protective de- 
vices approved by the Bureau of Mines. U. S. Bureau of 
Mines. Information circular 7444, March 1948. 
3379. Schwerma, H. and A. C. Ivy. Safety of modern 
alternating positive and negative pressure resuscitators. 
J. Industr. Hyg., 1946, 28: abstract section: 42. [P] 
3380. Schwerma, H., A. C. Ivy, H. Friedman, and E. 
La Brosse. A study of resuscitation from the juxtalethal 
effects of exposure to carbon monoxide. Occup. Med., 
1948,5: 24-48. [P] 
3381. Severinghaus, J. W. Electrophrenic respirator: 
description of a portable all-electronic apparatus. 
Anesthesiol, 1951, 12: 123-128. 
3382. Spiro, R. K., R. S. Aaron, and J. S. Thompson. 
Experiments on the Eve rocking method of artificial 
resuscitation. Fed. Proc. Amer. Soc. exp. Biol, 1947, 6: 
209-210. [P] 
3383. Spiro, R. K., E. R. Goltra, and J. S. Thompson. 
Experiments with the Eve method of artificial resuscita- 
tion. /. appl. Physiol, 1948,1: 285-297. 
3384. Swann, H. G. Studies in resuscitation. USAF. 
Wright-Patterson air force base, Dayton, Ohio. ENG. Air 
materiel command. Contract no. W-33-038-ac—14379, 
rept. no. 696-79G, 28 April 1948, 128 pp. [P] 
3385. Swann, H. 6. Studies in resuscitation. USAF. 
Wright-Patterson air force base, Dayton, Ohio. Air ma- 
teriel command. Technical rept. no. 5972, August 1949, 
20 pp. [P] 
3386. Swann, H. G. and M. Brucer. The recovery 
period after resuscitation. Fed. Proc. Amer. Soc. exp. Biol., 
1948, 7: 121. [P] 
3387. Thompson, T. M. Modern methods of resuscita- 
tion. Industr. Med., 1948, 17: 325-328. [R] 
3388. Vollmer, E. P. Appraisal of two resuscitation de- 
vices made up of obsolete oxygen equipment. U. S. Navy. 
NMRI. Project X—486, Rept. no. 4, 25 June 1945, 3 pp. 
3389. Yollmer, E. P,, B. G. King, and J. A. Peck. Evalu- 
ation of the Burns pneumatic balance resuscitator. U. S. 
Navy. NMRI. Project X-486, Rept. no. 5, 2 July 1945, 
6 pp. 
3390. Vollmer, E. P., B. G. King, and J. A. Peck. Evalu- 
ation of the Emerson automatic positive pressure resusci- 
tator and inhalator assembly—“Defense Model.” U. S. 
Navy. NMRI. Project X-486, Rept. no. 7, 13 August 
1945, 7 pp. 
3391. Whittenberger, J. L., J. E. Affeldt, W. T. Goodale, 
and S. J. Sarnoff. Mechanics of breathing in relation to 
manual methods of artificial respiration. J. appl. Physiol., 
1951, 4: 476-485. [P] [CH] 
3392. Whittenberger, J. L., and S. J, Sarnoff. Physio- 
logic principles in the treatment of respiratory failure. 
Med. Clin. N. Amer., 1950,34: 1335-1362. 
3393. Wiggin, S. C., P. Saunders, and 6. A. Small. 
Resuscitation. New Engl. J. Med., 1949, 241: 370-378. 
[R] 
3394. Wiggin, S. C., P. Saunders, and G. A. Small. 
Resuscitation (concluded). New Engl. J. Med., 1949, 
241: 413-420. 
3395. Wilson, J. W. Studies in resuscitation. USAF. 
Wright-Patterson air force base, Dayton, Ohio. Aero 
medical laboratory. Technical rept. MCREXD-696-79G, 
28 April 1948, 128 pp. [P] 
3396. Wilson, J. W. Studies in resuscitation by Dr. 
H. G. Swann. USAF. Wright-Patterson air force base, 
Dayton, Ohio. Aero medical laboratory. Technical rept. 
MCREXD-696-79G, 28 March 1949, 89 pp. [P] 
3397. U. S. NBC. Division of Medical Sciences. Ad hoc 
conference on manual methods of artificial respirations. 
Minutes of first meeting, 1 October 1951, 16 pp. 
3398. Anon. Artificial respiration: Its importance to 
you. Clin. Med., 1945,52: 192-194. 
VIII. DIFFUSION RESPIRATION 
It is not intended under this heading to make any 
attempt to include in its entirety the literature 
relating to diffusion respiration. The selected refer- 
ences on diffusion respiration which follow are dis- 
cussed here because from this literature are to be 
derived data which can be applied to respiratory 
problems of divers and underwater swimmers. 
Alveolar carbon dioxide levels of dogs subjected 
to 45 minutes of apnea after oxygen inhalation were 
measured by Roth, Whitehead, and Draper (3404) 3399-3405 
PROTECTION AND PRESERVATION OF PERSONNEL 
1947. Following denitrogenation, breathing was 
arrested by continuous infusion anesthesia. After 
collection of air samples, the animals were revived 
by artificial respiration. After 30 minues of diffusion 
respiration the alveolar carbon dioxide concentra- 
tion had risen to 13.3 percent and after 45 minutes 
had risen to 43.0 percent. In the 4 dogs exposed to 
room air 3 minutes after their removal from the 
oxygen chamber, the alveolar carbon dioxide con- 
centration had fallen to 9.9 percent. 
Similar work by Binet and Strumza {3399) 1947 
on 15 dogs showed plasma carbon dioxide levels of 
55.8 volumes percent after 20 minutes, 73.7 after 
60 minutes, and 88.9 volumes percent after 2 hours. 
The hypercapnia was associated with a lowering 
of pH, a value of 6.8 being manifested after 2 hours. 
Blood pH levels of 6.78 after 45 minutes of apnea 
were reported by Draper, Whitehead, and Spencer 
{3401) 1947. An hour after institution of artificial 
respiration the pH of the venous blood had risen 
to 7.32. Of 12 dogs subjected to apnea after oxygen 
inhalation, one died 96 hours after resuscitation. 
The authors attribute the survival and ultimate 
recovery of these dogs to the suction inward of 
respiratory gases to the hemoglobin-oxygen “pump”. 
Dogs subjected to diffusion respiration for two 
45-minute period demonstrated an initial fall of 
systolic pressure, but thereafter this was well main- 
tained during the remaining period of respiratory 
arrest. Parry, Spencer, Whitehead, and Draper 
{3403) 1948 also reported ventricular extrasystoles 
during the first phase of diffusion respiration which 
disappeared during the latter phase of apnea. These 
authors {3405) 1948 also reported that in dogs 
given thiopental after denitrogenation, the oxygen 
uptake decreased approximately 11 percent. Simi- 
lar values were obtained with curare. This level 
was maintained for 30 minutes, then gradually fell 
to reach a level 30 percent less than the control 
value. The maximum negative intrapulmonary 
pressure developed in this series of experiments ex- 
ceeded 10 cm. of water. 
For other articles concerned with diffusion 
respiration, the reader is recommended to consult 
reports by the following authors: Draper and 
Whitehead {3400) 1951 and Ferris {3402) 1951. 
3399. Binet, L. and M. V. Strumza. Vie en apnee dans 
un milieu d’oxygene pur. C. R. Acad. Sci., Paris, 1947, 
225: 12-14. 
3400. Draper, W. B. and E. W, Whitehead. The 
phenomenon of diffusion respiration. Curr. Res. Anesth., 
1949, 28: 307—318. Excerpta Medico, (Section II. 
Physiology, Bio-chemistry and Pharmacology), 1951, 4: 
302. Abstr. 
3401. Draper, W. B., E. W. Whitehead, and J. N. 
Spencer. Studies on diffusion respiration. III. Alveolar 
gases and venous blood pH of dogs during diffusion 
respiration. Anesthesiol, 1947, 8: 524-533. [P] 
3402. Ferris, B. G., Jr. Problems of diffusion in the 
lungs. Bull. New Engl. med. Center., 1950, 12: 144-153. 
Excerpta Medico,. (Section II. Physiology, Biochemistry 
and Pharmacology), 1951, 4: 646, Abstr. 
3403. Parry, T. M., J, N. Spencer, E. W. Whitehead, 
and W. B. Draper. Changes in heart rate, blood pressure 
and electrocardiogram in dogs during diffusion respiration. 
Amer. J. Physiol., 1948,155: 459. Abstr. 
3404. Both, L. W., E. W. Whitehead, and W. B. Draper. 
Studies on diffusion respiration. II. Survival of the dog 
following a prolonged period of respiratory arrest. 
Anesthesiol, 1947,8: 294-302. [P] 
3405. Spencer, J. N„ W. B. Draper, T. M. Parry, and 
E. W. Whitehead, Studies on diffusion respiration, v. The 
hemoglobin-oxygen pump. Fed. Proc. Amer. Soc. exp. 
Biol, 1948, 7: 119. 
IX. PRESSURE BREATHING 
Aside from therapeutic applications of pressure 
breathing, information arrived at from research in 
this respiratory field is also applicable to the design 
and development of underwater swimming gear 
for shallow water swimmers. Impetus was given to 
this field by military research during World War II, 
the primary purpose being to increase the ceiling of 
aviators at very high altitudes by raising the partial 
pressure of oxygen in the lungs. Many modifications 
of pressure breathing equipment have been devel- 
oped for delivering gases under pressure to the 
lungs, giving almost every conceivable pattern of 
pressure breathing. 
In 1947, Barach, Fenn, Ferris, and Schmidt 
{3409) reviewed the literature on the physiology of 
pressure breathing. It is stated that pressure breath- 
ing will not lead to serious difficulties provided the 
pressures within the mask do not exceed 15 mm. of 
Hg. The difficulty of expiring against a continuous 
pressure can be avoided by the use of intermittent 
pressure breathing devices which keep the pressure 
high on inspiration and low on expiration. This 
usually results in hyperventilation and will prob- 
ably lead to decreased performance if the alveolar 
carbon dioxide tension falls below 25 mm. of Hg. 
Decreases of function produced by exposures to 
47.000 feet in men breathing with a continuous 
positive pressure of 15 mm. of Hg. have been re- 
ported by Barach, Eckman, Bloom, Eckman, Rule, 
Rumsey, and Wortis {3406) 1947. Exposures to 
42.000 feet with a continuous positive pressure of 
15 mm. Hg. produced no measurable decrease in 
performance. All subjects complained of a post- 
flight fatigue which became progressively worse as 
the number of exposures was increased. The occur- 
rence of two cases of syncope and three of imminent 
collapse in 17 subjects breathing with a positive 
pressure of 15 mm. Hg. during flights at 44,800 PRESSURE BREATHING 
feet while runs to 42,000 feet resulted in no syncope 
or collapse indicated that the stability of the indi- 
vidual may be impaired by pressure breathing at 
this critical altitude. 
Regarding the effect of increased positive intra- 
pulmonary pressure on the muscular response, Bean 
and Elwell {3412) 1950 found that there was an 
augmentation of tibialis anticus contractions elicited 
by slow single shock motor nerve stimulation. This 
has been ascribed to an influence on the myoneural 
junction induced by the alteration in blood flow 
which results from positive intrapulmonary pres- 
sure. The finding that augmentation occurred in 
direct stimulation of the normal muscle, but was 
missing in such stimulation of the chronically de- 
nervated muscle supports this interpretation. 
According to De Lalle {3418) 1948 the reduction 
in skin temperature of men using pressure breathing 
apparatus is the result of peripheral vasoconstric- 
tion. In his studies, subjects wore the U. S. Air 
Force A-13 mask connected to a pump and tank 
giving intermittent pressures ranging between — 20 
to + 20 cm. of water. These pressures were admin- 
istered for 10 minutes. Navy pneumatic vests were 
also worn by the eleven subjects. All subjects ex- 
perienced a —0.3° G. fall of finger skin temperature 
being reduced somewhat after 7 minutes of pressure 
breathing. The inflated vests seemed to increase the 
magnitude of skin cooling. This vasoconstrictor re- 
sponse did not depend on expansion of the chest 
because it occurred in negative pressure breathing 
or when expansion of the chest was prevented by 
expansion of the pneumatic vest. Bateman and 
Sheard {3410 and 3411) 1946 also reported a slight 
decrease in skin temperature during pressure breath- 
ing but this fall was followed by a slow rise which 
as a rule exceeded the initial decrease so that the 
peripheral vessels became more dilated than they 
were in the control period at ambient pressure. 
Experimentally, Werko {3440) 1947 found that 
intermittent pressure breathing produced small 
blood pressure changes in persons with normal cir- 
culatory systems and variable changes in patients 
with cardiovascular disease. When a mixture of 
10 percent oxygen in nitrogen was used, the pul- 
monary arterial pressure was increased and was 
accompanied by an increase in pulmonary vascular 
resistance. In one case with normal circulation 
using a continuous pressure breathing device, there 
was a reduction in cardiac output corresponding to 
a low mean mask pressure accompanied by increases 
in arterial, right ventricular and pulmonary arterial 
pressures. The automaticity of the intermittent pres- 
sure devices reduces labored breathing. When the 
mean mask pressure and consequently the rise in 
pleural pressure is small, no decreases in cardiac 
output should occur. The author states that when 
intermittent pressure equipment is used for arti- 
ficial respiration, the inspiratory period with a high 
pressure should be short and the expiratory period 
long. Expiratory mean mask pressure should be as 
near atmospheric pressure as possible so as not to 
produce any added adverse effects on the circu- 
lation. 
According to Cournand, Motley, Werko, and 
Richards {3417) 1948, cardiac output is decreased 
in proportion to the increase in mean mask pres- 
sure when respirators are used having expiratory 
times equivalent to inspiratory periods with ex- 
piratory pressures above atmospheric. Decreased 
cardiac output is also produced when the inspira- 
tory pressure is rapidly increased and then dropped 
rapidly during expiration, the latter pressure being 
above atmospheric. The net filling pressure of the 
right ventricle was decreased during the phase of 
increased mask pressure and increased during the 
phase of decreasing mask pressure. Conversely, 
when cardiac output was increased, the mean net 
filling pressure was increased. The authors inter- 
preted these changes as being suggestive of a deficit 
in cardiac output during the inspiratory phase, com- 
pensated for in the expiratory phase. When the 
pressure drop is rapid in expiration with a resulting 
low intrapleural pressure, compensation is complete, 
provided the expiratory period is of sufficient dura- 
tion. Expiratory time must equal or exceed inspira- 
tory time in order that the number of heart beats 
during expiration may equal or exceed the number 
present during inspiration. It was recommended 
that intermittent positive pressure breathing appa- 
ratus should allow for a gradual increase in pressure 
during inspiration, a rapid drop in pressure after 
cycling, a mean mask pressure practically equiva- 
lent to atmospheric pressure during expiration, and 
an expiratory time equal to or greater than the 
inspiratory phase. 
Studies by Fenn and associates (3422 and 3423) 
1947 demonstrated, with a newly designed finger 
plethysmograph, a decrease in finger volume when 
men respired with a positive pressure respirator. A 
pressure of 30 cm. of water was applied to the lungs 
through the medium of a pressurized helmet. It 
was felt that this decrease in blow-flow due to posi- 
tive pressure breathing was chiefly the result of a 
vasoconstriction and only to a small extent due to 
an increase in venous pressure. Volume measure- 
ments of the legs during positive pressure breathing 
showed an increase in volume, as measured by a 
boot plethysmograph. This is believed to be due to 
a passive inflation of the veins. PROTECTION AND PRESERVATION OF PERSONNEL 
Information concerning fluid shifts in men using 
positive pressure breathing respirators can be ob- 
tained from papers by Henry {3426) 1951; Henry, 
Hendrickson, Movitt, and Meehan {3427) 1948; 
Henry, Jacobs, Meeham, and Karstens {3428) 
1948; and Jacobs, Karstens, and Henry {3433) 
1948. According to Henry {3426), when man 
breathes against pressures as high as 60 mm. of Hg., 
the available blood reserve is lost into the limbs in 
two ways: (1) by venous distention and (2) by 
cutting down the blood volume through fluid filtra- 
tion caused by high pressures in minute vessels, the 
loss being greater in a warm environment. Because 
the blood volume is inadequate, diastolic filling of 
the heart is impaired and may decrease to a point 
where ventricular emptying will be completed be- 
fore the systolic phase has been terminated. This 
results in an abnormal squeezing and rubbing of 
the empty ventricular walls which may result in 
afferent firing of the vagus to initiate reflex 
peripheral vasodilatation and collapse character- 
istic of vasovagal syncope. The author concludes 
from this that pressure suits should be used in 
ascending from the 40,000 foot level to prevent the 
loss of blood into the limbs. 
Henry, Jacobs, Meeham, and Karstens {3428 and 
3433) 1948 reported an increase in mean venous 
pressure during pressure breathing when the intra- 
thoracic pressure had reached levels of 20 to 60 mm. 
Hg. Hematocrit and hemoglobin measurements on 
8 subjects indicated a hemoconcentration which in- 
creased in proportion to the pressure used. At 30 
mm. Hg. mean intrathoracic pressure the fluid 
loss in 30 minutes was 4.0 ±0.5 cu. cm. per 100 
cu. cm. of blood. Aside from fluid losses during 
pressure breathing, an increase in venous pressure 
occurred in those vessels lying outside of the raised 
pressure areas of the head and trunk. The distention 
of these vessels aided the pooling of blood outside 
of the pressure areas. Determinations of volume 
changes were made by measuring the differences 
in volume of the blood in both legs and one arm 
isolated by arterial occlusion cuffs. The estimated 
volume decrease of 300 cu. cm. of 6 percent of total 
volume was in fair agreement with estimations made 
with plethysmographic and teeter-board methods. 
When pressures above 40 mm. Hg. were used, the 
fluid losses were greater. These changes are in them- 
selves adequate to account for the frequent de- 
velopment of syncope during periods of raised 
intrathoracic pressure. 
An experimental study was conducted by Cain, 
Wood, and Mahoney {3415) 1950 to determine the 
time tolerance of a group of individuals breathing 
at various positive pressures from 30 to 60 mm. Hg. 
at room temperatures of 65° and 95° F. A fairly 
narrow time range of tolerance occurred with the 
high pressures of 50 and 60 mm. Hg. This range 
widened considerably at 30 and 40 mm. Hg., ap- 
proximating time tolerance of 1 minute at 60, 7 min- 
utes at 50, and 15 minutes at 40 mm. Hg. When 
breathing against 30 mm. Hg., the time was ex- 
tended to 1 to 2 hours and the exposures were 
terminated because of fatigue, rather than impend- 
ing syncope. 
Subjects exposed to 40,000 feet using positive 
pressure breathing equipment developing a mask 
pressure of 15 mm. Hg. had an increase in arterial 
oxygen saturation equivalent to that obtained by a 
15 mm. Hg. increase in barometric pressure. 
Barach, Eckman, Eckman, Ginsburg, and Rumsey 
{3407) 1947 stated that their data gave no indica- 
tions which would suggest a change in the opera- 
tion of the laws concerned with the transfer of gas 
from the lungs to the blood at very high altitudes. 
For an authoritative review of the respiratory 
effects of positive pressure breathing, the reader is 
referred to the article by Wyss {3443) 1949. The 
capacity and resistance of the pulmonary vascular 
bed and the effects of airway pressure on the altera- 
tion of fluid exchange in the lungs during intermit- 
tent positive pressure breathing have been investi- 
gated by Maloney and Whittenberger {3436) 1951. 
In a series of dog experiments, measurements of 
intrapleural pressure, alveolar pressure, and pul- 
monary “capillary” pressure were made. From the 
data collected it became apparent that two factors 
of major importance were: (1) the effects of 
alteration of venous return brought about by 
changes of pressure relationships in the venous 
system within and without the thorax, and (2) the 
effects of lung volume change. At a given lung 
volume it was found that intrapleural pressure, 
alveolar pressure, and pulmonary “capillary” pres- 
sure bore the same relationship to each other, re- 
gardless of the method used to inflate the lungs. It 
was concluded that the hemodynamic effects of 
pressure breathing were due to effects on venous 
return, and not to any direct effect on the lungs 
other than volume change. 
According to Barach, Eckman, Ginsburg, Rum- 
sey, Korr, Eckman, and Besson {3408) 1946, 
breathing under a positive pressure of 15 mm. Hg. 
with a demand pressure regulator resulted in in- 
crease of functional residual air and frequently 
elevation of minute and tidal volumes. These 
changes were reduced when a vest or vest-pants 
apparatus was used, the pressure applied being 
equal to that of the mask. The effects resulting from PRESSURE BREATHING 
3406-3411 
added resistance to respiration were investigated by 
Cain and Otis {3414) 1949. In resting subjects 
breathing through a “Y” tube, to which was con- 
nected a flow meter, resistance disc, and strain gage, 
the inspiratory and expiratory work required to 
overcome breathing resistance was measured. The 
average efficiency for the extra work of a complete 
respiratory cycle on a resistance of 0.385 mm. water 
per cu. cm. per second was 33 percent. The ex- 
piratory reserve increased 275 cu. cm. This change 
in expiratory reserve favors the muscles of expira- 
tion. It was found that breathing against a resist- 
ance decreases the total ventilation and brings 
about an increase of alveolar pC02 and a decrease 
in p02. Ballistocardiograms showed an increase in 
cardiac minute volume during inspiration and a 
decrease during expiration against a resistance of 
0.385 mm. Hg. per cu. cm. per second. Cardiac 
minute volume was decreased 4 percent. Ivy, Adler, 
Snapp, and Bancroft {3432) 1949 subjected 
nembutalized dogs to respiration pressures ranging 
from 4 to 29 cm. of water and measured changes 
in intracranial pressure. When the intracranial 
pressure was at a level of 25 to 50 cm., pressure 
breathing caused an infrequent rise of 10 cm, in 
the intracranial pressure. A fall in intracranial pres- 
sure of the order of 15 cm. was observed during 
pressure breathing when the intracranial pressure 
was at a level of 60 to 80 cm. of cerebrospinal fluid. 
In studies on kidney function in men exposed to 
30-minute periods of continuous pressure breath- 
ing at 10, 20, 30, and 40 mm. Hg. above ambient 
pressure, Drury, Henry, Goodman {3420) 1947 
found a progressive reduction of kidney function 
which, with the higher pressures, reached approxi- 
mately 20 to 50 percent of normal values. This de- 
pression in function persisted for 1 or 2 hours 
after the cessation of pressure breathing. The au- 
thors believe that these results support the view 
that estimations of kidney function may be used as 
a measure of the circulatory stress induced by a 
reduction of effective blood volume. 
Hyman and North {3431) 1941-1946 decom- 
pressed men to 35,000 feet using pressure breathing 
equipment operating at pressures of 6 and 8 in. of 
water. No great effect on the frequency of occur- 
rence of decompression sickness was found when 
compared with the occurrence of these symptoms in 
the same subjects decompressed with normal oxy- 
gen supply equipment. Hardy and Barach {3425) 
1945 describe the beneficial use of positive pressure 
respiration in the therapy of an 11-year-old boy 
having pulmonary edema incurred by inhalation of 
chlorine gas. Prompt improvement was noted 
when a pressure of 4 cm. of water was imposed 
during expiration. This patient had inhaled in a 
single inspiration some freshly prepared chlorine. 
Painful, persistent coughing ensued for 2 hours. 
Some relief was given by one-half grain of codeine. 
One hour later the cough returned with labored, 
rapid breathing, exhaustion, vomiting, and a fast, 
thin pulse. Loud rhonchi were heard throughout 
the chest bilaterally. The patient was placed in an 
oxygen tent containing 40-percent oxygen. After 4 
hours in the tent, fine moist rales were present in 
the left lower lobe laterally and at the left border 
of the heart. Fifteen hours later the pulse was feeble, 
irregular and cyanosis was recognizable. A mask 
was applied delivering 50-percent oxygen at 4 cm. 
pressure. The following day most of the moist 
sounds had disappeared. A normal pulse did not 
return for 3 days. 
For further studies on pressure breathing, refer- 
ence may be made to papers by Bickerman and 
Beck {3413) 1950; Carr and Essex {3416) 1946; 
Drinker {3419) 1945; Fenn {3421) 1950; Gillick 
and Schneider {3424) 1949; Hyman and Goodman 
{3429) 1948; Hyman and Klain {3430) 1946; 
Kaufman, Nims, Nyboer, and Somberg {3434) 
1944; Maloney {3435) 1950; Otis, Suskind, and 
Rahn {3437) 1948; Ryder and Kehoe {3438) 
1948; Tatum and Himmelfarb {3439) 1945; 
Whittenberger {3441) 1950; and Wilson {3442) 
1946. 
3406. Barach, A. L., M. Eckman, W. L. Bloom, I. Eck- 
man, C. Rule, C, C. Rumsey, Jr., and J, Wortis. Studies on 
positive pressure respiration. IV. Subjective, clinical and 
psychological effects of continuous positive pressure breath- 
ing at high altitudes. /. Aviat. Med., 1947, 18: 252-258. 
[P] 
3407. Barach, A. L., M. Eckman, I. Eckman, E. Gins- 
burg, and C. C. Rumsey, Jr. Studies on positive pressure 
respiration. III. Effect of continuous pressure breathing 
on arterial blood gases at high altitude. /. Aviat. Med., 
1947, 18: 139-148. [P] 
3408. Barach, A. L., M. Eckman, E. Ginsburg, C. C. 
Rumsey, Jr., I. Korr, I. Eckman, and G. Besson. Studies 
on positive pressure respiration. I. General aspects and 
types of pressure breathing. II. Effects on respiration and 
circulation at sea level. J. Aviat. Med., 1946, 17: 290—320. 
[P] 
3409. Barach, A. L., W. 0. Fenn, E. B. Ferris, and C. F. 
Schmidt. The physiology of pressure breathing: a brief 
review of its present status. U. S. NRG—CAM. C. A. M. 
rept. no. 494, September 1945, 20 pp. /. Aviat. Med., 
1947, 18: 73-87. [R] 
3410. Bateman, J. B. and C. Sheard. The effect of 
pressure breathing upon the skin temperatures of the 
extremities. U. S. NRC-GAM. OEMcmr-129, C. A. M. 
rept. no. 428, 2 May 1945, 8 pp. 
3411. Bateman, J. B. and C. Sheard. The effect of 
pressure breathing on the cutaneous temperatures of the 
extremities. J. Aviat. Med., 1946, 17: 568—578, 583. 3412-3443 
PROTECTION AND PRESERVATION OF PERSONNEL 
3412. Bean, J. W. and L. E. Elwell. Dual effect of 
positive intrapulmonic pressure on muscular response. 
Fed. Proc. Amer. Soc. exp. Biol., 1950, 9: 9. 
3413. Bickerman, H. A. and G. J, Beck. Pressure 
breathing with oxygen and helium-oxygen in pulmonary 
edema and obstructive dyspnea. Bull. N. Y. Acad. Med., 
1950, 26: 410-423. [CH] [P] 
3414. Cain, C. C. and A. B. Otis. Some physiological 
effects resulting from added resistance to respiration. 
/. Aviat. Med., 1949,20: 149-160. [P] 
3415. Cain, C. C., J. A. Wood, and D. I. Mahoney. 
Human tolerance and responses to high positive pressure 
breathing. Fed. Proc. Amer. Soc. exp. Biol., 1950, 9: 21. 
3416. Carr, D. T. and H. E. Essex. Certain effects of 
positive pressure respiration on the circulatory and respir- 
atory systems. Amer. Heart ]., 1946, 31: 53-73. [P] 
3417. Cournand, A., H. I. Motley, L. Werko, and 
D. W. Richards, Jr. Physiological studies of the effects 
of intermittent positive pressure breathing on cardiac out- 
put in man. Amer. J. Physiol., 1948, 152: 162-174. [P] 
3418. Be Lalla, V. Causes of skin cooling in pressure 
breathing, deep inspiration and deep expiration. Amer. 
]. Physiol., 1948, 152: 122-130. [P] 
3419. Drinker, Cecil K. Pulmonary edema and in- 
flammation. Cambridge, Harvard University Press, 1945, 
viii, 106 pp. 
3420. Drury, D. R., J. P. Henry, and J. Goodman, 
The effects of continuous pressure breathing on kidney 
function. /. din. Invest., 1947,26: 945—951. 
3421. Fenn, W. 0. Pressure breathing, pp. 3-8 in: 
Chemical Corps medical division report no. 236, A Con- 
ference on treatment of chemical warfare casualties with 
acute lung injury. U. S. Army. Army chemical center, 
Edgewood, Maryland, 13 March 1950, 69 pp. 
3422. Fenn, W. 0. and L. E. Chadwick. Effect of pres- 
sure breathing on blood flow through the finger. Amer. J. 
Physiol, 1947,151: 270-275. [P] 
3423. Fenn, W. 0., A. B. Otis, H. Rahn, L. E. Chadwick, 
and A. H. Hegnauer. Displacement of blood from the 
lungs by pressure breathing. Amer. J. Physiol, 1947, 151: 
258-269. [P] 
3424. Gillick, F. G. and J. Schneider. Electrokymo- 
graphic studies of lung field pulsations with exhalation 
against pressure. J. appl. Physiol, 1949, 2: 30—36. [P] 
3425. Hardy, C. and A. L. Harach. Positive pressure 
respiration in the treatment of irritant pulmonary edema 
due to chlorine gas poisoning. /. Amer. med. Ass., 1945, 
128: 359. [CH] 
3426. Henry, J. P. The significance of the loss of blood 
volume into the limbs during pressure breathing. J. Aviat. 
Med., 1951,22: 31-38. 
3427. Henry, J. P., I. Hendrickson, E. Movitt, and J. P. 
Meehan. Estimations of the decrease in effective blood 
volume when pressure breathing at sea level. /. din. 
Invest., 1948, 27: 700-705. U. S. NRC-CAM. OEMcmr- 
288, CAM 452, 11 July 1945, 16 pp. [P] 
3428. Henry, J. P., H. Jacobs, H. Meeham, and A. 
Karstens. The effect of pressure breathing on circulating 
blood volume. (1) Fluid loss into the tissue spaces. Fed. 
Proc. Amer. Soc. exp. Biol, 1948, 7: 53. [P] 
3429. Hyman, C. and J. Goodman. Fluid shifts in ani- 
mals during pressure breathing. Amer. J. Physiol, 1948. 
155: 208-214. [P] 
3430. Hyman, C. and A. Klain. Fluid loss during pres- 
sure breathing. USAF. Wright-Patterson air force base, 
Dayton, Ohio. Air materiel command. ENG. Serial no. 
TSEAA-696-104, contract W33-038-ac 14711, 27 Sep- 
tember 1946, 5 pp. 
3431. Hyman, C. and N. North. The effect of pressure 
breathing on the occurrence of decompression sickness. 
Kept. no. 49 in: Studies in Aviation Medicine. Yale 
University School of Medicine, New Haven, Conn. Aero- 
medical research unit. 1941-1946. [P] 
3432. Ivy, J. H., H. F. Adler, F. E. Snapp, and R. W. 
Bancroft. The effect of pressure breathing on intracranial 
pressure. USAF. Randolph Field, Texas. School of aviation 
medicine. Project 21-02-018, March 1949, 17 pp. [P] 
3433. Jacobs, H., A. Karstens, and J. P. Henry. The 
effect of pressure breathing on circulating blood volume. 
(2) Distension of the venous reservoirs. Fed. Proc. Amer. 
Soc. exp. Biol., 1948, 7: 60—61. USAF. Wright-Patterson 
air force base, Dayton, Ohio. Air materiel command. 
MCREXD-696-104K, 29 October 1948, 14 pp. [P] 
3434. Kaufman, S. S., L. F. Nims, J. Nyboer, and H. M. 
Somberg. The value of carbon dioxide in intermittent 
pressure breathing. U. S. NRC-CAM. C. A. M. rept. no. 
321, June 1944, 4 pp. 
3435. Maloney, J. V., Jr. Effect on the circulation, pp. 
15—26 in: Chemical Corps medical division report no. 
236, A Conference on treatment of chemical warfare 
casualties with acute lung injury. U. S. Army. Army 
chemical center, Edgewood, Maryland, 13 March 1950, 
69 pp. 
3436. Maloney, J. V., Jr. and J. L. Whittenberger. 
Direct pulmonary effects of pressure breathing. Fed. Proc. 
Amer. Soc. exp. Biol., 1951, 10: 88-89. 
3437. Otis, A. B., M. Suskind and H. Rahn. Effect of 
pressure breathing and posture upon the respiratory gas 
exchange and heart rate. Fed. Proc. Amer. Soc. exp. 
Biol, 1948, 7: 89. 
3438. Ryder, H. W. and R. A. Kehoe. Rationale and 
hazards of pressure breathing and oxygen therapy. 
Anesthesiol., 1948, 9: 21-31. [R] [CH] 
3439. Tatum, H. J. and S. Himmelfarm. A comparison 
of the effect of breathing air and 100% oxygen under 
atmospheric and increased pressure upon the arterial oxy- 
gen saturation of CG gassed dogs. U. S. Army. Chemical 
warfare service, Edgewood arsenal, Maryland. Medical 
division report no. 53. Publication control no. 5030-53, 
19 August 1945, 11 pp. [P] 
3440. Werko, L. The influence of positive pressure 
breathing on the circulation in man. Acta med. sc and., 
Suppl., 1947, 193: 125 pp. 
3441. Whittenberger, J. L. Pulmonary effects of pres- 
sure breathing, pp. 9-14 in: Chemical corps medical 
division report no. 236, A conference on treatment of 
chemical warfare casualties with acute lung injury. U. S. 
Army. Army chemical center, Edgewood, Maryland, 13 
March 1950, 69 pp. 
3442. Wilson, J. W. Fluid loss during pressure breath- 
ing. USAF. Wright-Patterson air force base, Dayton, Ohio. 
Air materiel command. Aero medical laboratory. Serial 
no. TSEAA-696-104, 27 September 1946, 16 pp. [P] 
3443. Wyss, 0. A. M. Respiration. Annu. Rev. Physiol., 
1949, 11: 469-492. [R] Selection and Training of Submarine 
Personnel, Divers, and Compressed 
Air Workers 
I. SELECTION 
For general discussions of the subject of selection 
of submarine personnel in the U. S. Navy, the fol- 
lowing references should be consulted; 3457, 3464, 
3485 and 3495. Cronbach {3457) 1949 has in- 
dicated that selection research has increased the 
effectiveness of military forces by placing superior 
men in responsible posts. Selection and placement 
of men can be improved by mathematical studies of 
mass processing, the multiple cut-off method, and 
factor analysis. Billets should be studied in terms of 
human requirements and the significant human 
aptitudes should be classified. Test design should be 
deliberate, based on principles of measurement 
rather than a trial and error process. Basic studies of 
test design are considered by the author to be much 
needed. Improved technical methods of classifying 
men must be supplemented by careful use of the 
methods. A frontier barely explored is personality 
assessment. The author stresses that tests of per- 
sonality can be improved. Future studies should 
consider how normal men function rather than 
identify potential break-down cases only. Research, 
according to the author, has been handicapped by 
inadequate criteria of proficiency. Procedures for 
judging effectiveness of men on the job should be 
further developed. Herrick {3464) 1951 has pointed 
out that the selection system at first was a negative 
one, involving the weeding out of those men who 
might be potentially dangerous due to marked de- 
ficiencies of speech or motor-coordination. 
In general {3485) the submariner is considered to 
be an individual who is average or above average in 
mental capacity and education, who is strong and 
in good health, who is well adjusted emotionally 
and temperamentally to himself and to his fellow 
men, and desires submarine duty. A selection screen- 
ing program involves the elimination of personnel 
below median intelligence and the maintenance of 
rigorous standards of physical requirements—par- 
ticularly with reference to special senses—and free- 
dom from chronic disease. It is agreed that only 
those men should be accepted for submarine service 
who are highly motivated. This involves, however, 
an evaluation of the basis for motivation, the qual- 
ity of motivation, and the sustained character of 
motivation. 
Willmon {3495) 1948 has stated that selection 
of officers and men for submarines resolves itself 
into a process of determining the adequacy of the 
individual as regards intelligence and education, 
physique and health, emotionality and personality. 
Attrition is seen to be due for the most part to in- 
adequate scores in classification tests, over-age, and 
defective vision. As Willmon has emphasized, there 
is no place in submarines for the emotionally im- 
mature, the emotionally unstable, the neurotics, or 
psychopaths. Only one serious mistake is made in 
the life of a submarine. Clues to personality disturb- 
ances may be given by a bad civilian or military 
record, a history of repeated shifting of jobs for no 
real reason, repeated discharges from employment, 
multiple divorces, or repeated family difficulties. A 
history of nail-biting, constipation, frequently upset 
stomach, diarrhea, frequent headache, somnam- 
bulism, somniloquism, tachycardia, hypertension, 
and wet palms may all serve to identify the tempera- 
mentally ill-adapted candidate. Four of the follow- 
ing traits are suggested as placing a candidate in a 
doubtful category and 6 or more are offered as 
predicting probable break-down under stress: (1) 
bed-wetting beyond the age of 4 years; (2) thumb- 
sucking or nail-biting beyond 6 years; (3) failure 
to engage in competitive games involving risk of SELECTION AND TRAINING OF PERSONNEL 
injury; (4) tantrums in childhood; (5) abnormal 
shyness or sensitiveness; (6) preference for playing 
alone; (7) repeating grades in school, chronic tru- 
ancy or difficulty with teachers; (8) abnormal 
fears; (9) shunning girls after puberty; (10) faint- 
ing; (11) excessive autonomic system reactions to 
emotion (tremor, abnormal sweating, tachycardia, 
etc.); (12) sulkiness under discipline; (13) abnor- 
mal attachment to mother after puberty; (14) 
stammering; (15) obsessional traits. 
In a paper on the development of selection pro- 
cedures, Shilling and Kohl {3482) 1945 have 
pointed out that at the onset of the war, the physical 
examination was the only examination for entry 
into submarine duty. Some requirements were un- 
realistic and underwent modification. Selection of 
sonar operators brought about new testing pro- 
cedures. Psychological testing came into the picture 
with various paper and pencil tests and other 
methods. In 1943 a trained psychiatrist was used 
at New London in selection, interviewing those 
candidates who failed the paper and pencil tests. 
Submarine crews returning from combat were re- 
examined with the result that many were elimi- 
nated who should never have been assigned to 
submarine duty in the first place. In 1943 an inter- 
view board traveled to officer indoctrination units to 
interview aspirants for submarine training. These 
same board members served on a final review board 
for all officer candidates. Checking their findings 
with final accomplishments of personnel indicated 
a high proficiency of selection procedures. The 
escape training tank was used not only for escape 
training directly but also in providing stressful sit- 
uations in which emotional adaptability could be 
evaluated. Two U. S. Navy reports published in 
1946 {3486 and 3487) may be consulted for com- 
ments on submarine personnel classification. These 
reports stressed the following defects of wartime 
classification: (1) undue complexity, (2) misplaced 
emphasis, and (3) inadequate indoctrination of 
forces afloat in use of classification data. Various 
suggestions on methods of classification were set 
forth. 
In 1944 Willmon and Bartlett {3496) reported a 
standard form that would provide some indication 
of the performance of every graduate of the sub- 
marine school. Previously, general information on 
performance of men at sea had been obtained in- 
formally from the commanding officers. It was 
anticipated that the new procedure would afford 
detailed information to guide selection. An account- 
ing method was established to trace every candidate 
reporting for examination for submarine school 
until either he left the submarine service or com- 
pleted one patrol on a submarine. Data on each of 
the steps in processing a man were referred to a 
common information center where machine ac- 
counting facilities were available. An early study 
of the data collected in this manner pertained to 
the problem of age or maturity of submariners and 
led to the conclusion that it might be advisable to 
set the lower age limit at 19, thus eliminating the 
17- and 18-year old groups. 
Bartlett {3445) 1945 also contended that, other 
factors being equal, older men are preferred to 
young men of 17 and 18 years of age. In a .correla- 
tion of tests with grades in submarine school, Bart- 
lett found that a combination of scores for the 
general classification test, the arithmetic reasoning 
test, and the mechanical knowledge test, is a better 
index of grades in submarine school than is the 
general classification test score alone. From statis- 
tical data presented in an earlier report in 1942 
{3488) it was apparent that sole reliance could not 
be placed on the general classification test for selec- 
tion of personnel. It was also apparent at that time 
that some more comprehensive study would have 
to be completed to determine a more reliable stand- 
ard than had been presented by any of the reports 
to that date. Bartlett {3445) concluded that the 
population of the submarine schools could be im- 
proved with respect to training performance by 
further selection on the basis of test scores. The 
ages of students were found to be related to grades 
in submarine school, but the degree of relationship 
did not seem to warrant any change in the then 
present age standard in order to improve training 
performance. Similarly no change in standards for 
educational level seemed indicated. 
In 1945 Bartlett {3447) made an evaluation of 
the officer classification test as a device for selecting 
officer candidates for submarine school. He reported 
that officer classification test scores were correlated 
significantly with performance in submarine school. 
A score combining sections of the test was found 
to be the most significant index of subsequent 
academic standing, but if any single section score 
had to be employed the mathematical score was 
probably the most satisfactory of the different 
scores. Candidates with previous submarine indoc- 
trination achieved higher standings than did those 
without indoctrination. The class standings of 
officers with previous indoctrination could be pre- 
dicted with more confidence from the aptitude 
scores than could the standings of officers without 
indoctrination. In 1946 Bartlett {3449) carried out 
an investigation of the billet qualifications blank 
(NavPers 16418) to test its suitability with combat- SELECTION 
experienced candidates for submarine training. 
His studies warranted the assumption that person- 
ality tests could be utilized to good effect with a 
combat-experienced population. In 1946 Bartlett 
presented two reports {3450 and 3451) describing 
an abstract of the service record for analysis of ex- 
aminations of experienced submarine personnel re- 
ceived for reassignment. This record was developed 
to allow a systematic accounting of examinations 
of experienced submarine personnel received at the 
U. S. Submarine Base, New London, Conn., for 
reassignment. The record was designed to list men 
examined for reassignment by rate, age, and by 
experience and to analyze reasons for failure in 
medical examinations. The record also made it 
possible to tabulate failures in examinations for 
specialties, such as sonar, radar, and night vision, 
and to allow analysis of such failures by rate, age, 
and collateral test scores. The record also made it 
possible to maintain psychological quality control 
data on men examined and to accumulate gradu- 
ally a master file of enlisted submarine personnel 
with pertinent experience data from their service 
record. 
From the date of the entrance of the United 
States into World War II to the middle of 1945 a 
total of 33,011 enlisted men were received for 
training in the submarine service of the U. S. Navy. 
Of this number, 6,040 were disqualified by the 
examiners. A total of 24,752 men were enrolled in 
the submarine school where 771, or approximately 
3 percent were disqualified. A further 3 percent 
were lost in the advanced rate training school. A 
total of 2,408 officers applied for training and of 
these 2,043 were graduated. It was found that Otis 
test scores obtained on enlisted men permitted a 
rough prediction of the general level of school per- 
formance, but gave only little more than chance 
prediction of rejections in training. Other tests are 
also discussed in the report. The officer qualification 
test was found to be a useful index for screening the 
officer candidates for submarine school. 
In 1949 a study was reported by Cook and 
Wherry {3455) of the interrelationships of some 
330 physiological and psychological measures ob- 
tained on a population of 120 submarine enlisted 
candidates. It was hoped by the authors that on 
the basis of this fundamental study it would be pos- 
sible to establish a simple selection battery, consist- 
ing of the primary physiological and psychological 
factors which emerge significant. This could then 
be validated on a large, independent sample of 
applicants. In 1943 Graham, Riggs, Bartlett, Berry, 
Verplanck, Solomon, and Mueller {3462) reported 
a summary of research conducted at the U. S. Sub- 
marine Base, New London, Connecticut concerned 
with development of tests for identifying men who 
are unfit. Three criteria of unfitness were adopted: 
(1) psychiatric evaluation, (2) officers’ judgment 
of men as operating crews of submarines, and (3) 
escape tank performance. The tests used were the 
NRG inventory, the New London-NDRC confi- 
dential questionnaire, the personal inventory, and 
a 2 hand coordination test. Data in the Otis intelli- 
gence test scores were also analyzed. The authors’ 
report considered results obtained from 3 batteries, 
each made up of the 2 hand test and the Otis test 
in combination with one of the inventories. All of 
the individual tests related significantly to psychi- 
atric criteria. The individual test combined with 
the New London and the personal inventory bat- 
teries, according to the procedure described, pre- 
dicted the psychiatric dichotmy into good and bad 
in a highly significant degree and to an extent which 
improved considerably on results obtained by the 
intelligence test alone. A battery involving items of 
the New London inventory related significantly to 
officers’ judgment of men from operating crews of 
submarines. 
Graham, Mote, and Berry {3461) 1944 reported 
the relation of selection test scores to tank escape 
performance. In the course of escape training at 
the Submarine School, U. S. Submarine Base, New 
London, Conn, about V/2 percent of prospective 
submarine crew men were disqualified on the 
grounds of escape performance of an emotional 
type. A study of the relation of selection test scores 
to tank escape performance indicated that the test 
battery predicts tank failures to a degree consider- 
ably better than chance. 
For reports describing and analyzing disqualifi- 
cation of enlisted applicants for submarine train- 
ing, papers by Malinosky and Bartlett {3469) 1945, 
Bartlett {3480) 1946, and Shilling and Bartlett 
{3481) 1947 should be consulted. 
Comparisons of various visual screening devices 
with standard medical procedures have been re- 
ported by the following: Farnsworth, Bartlett, and 
Kindred {3459) 1945; Farnsworth, Sperling, and 
Kimble {3460) 1949, and Sulzman, Farnsworth, 
Bartlett, and Kindred {3484) 1945. For an investi- 
gation of selection of candidates for enlisted sub- 
marine radar school a paper by Bartlett {3448) 
1945 should be consulted. 
For reports of studies on the development and 
validation of methods for the selection of sonar 
personnel, papers by Shilling {3479) 1942 and Har- 
ris {3463) 1946 should be consulted. The latter 
report gives a history of the submarine sonar selec- 3444-3459 
SELECTION AND TRAINING OF PERSONNEL 
tion program. For other reports the following refer- 
ences should be consulted: 3472, 3489, and 3492. 
For a discussion of problems encountered in 
selection of submarine personnel in the French 
submarine service, a paper by Rosenstiel {3477) 
1946 should be consulted. According to Curran and 
Critchley {3458) 1946 methods of selection for 
U-boat personnel in the German service were not 
essentially different from the undersea warfare 
services in other nations. The authors considered 
that morale in the German Navy generally appears 
to have been excellent and the incidence of break- 
down low in comparison with other branches of 
the armed services in Germany. Deficiencies in 
neuropsychiatric practice were stated to be striking 
in the German Navy and the standard of available 
treatment low in comparison with that of other 
nations. For wartime selection standards for per- 
sonnel in the Japanese submarine service, a report 
published by the U. S. Navy in 1945 {3490) may 
be consulted. 
For reports on selection of Naval, Coast Guard, 
and Marine personnel, papers by the following may 
be consulted: Cornehlsen {3456) 1946; Leavitt 
and Adler {3466) 1946; McCain {3467) 1947-48; 
Newman, Bobbitt, and Cameron {3473) 1946; 
Rodger {3475) 1947; USNRG Committee on Den- 
tistry {3491) 1949, and Williams, Leavitt and 
Blair {3494) 1946. For a few selected reports on 
selection and classification procedures in the U. S. 
Air Force papers by the following may be referred 
to: Buel and Melton {3454) 1943; McCollum 
{3468) 1951; Matthews {3470) 1943; Roff {3476) 
1951. A number of reports on personnel selection, 
job assignment and personality tests have appeared 
and a few of these have been listed as follows: 
Alexander {3444) 1944; Bechtoldt {3453) 1951; 
Hunt and Stevenson {3465) 1946; Moore {3471) 
1950; Richardson {3474) 1950; Rundquist {3478) 
and Shipley, Gray, and Newbert {3483) 1946. 
For additional papers on selection, reports by 
the following may be referred to: Bartlett {3446) 
1945, and Wiggin and Bartlett {3493) 1944. 
3444. Alexander, F. A. Personnel selection and job as- 
signment. pp. 89-103 in: Human behaviour and its 
relation to industry. Edited by D. Ewen Cameron and 
H. Graham Ross. Montreal, McGill University, 1944, 211 
pp. 
3445. Bartlett, N. R. Correlations of tests with grades 
in submarine school. U. S. Navy. Submarine base. New 
London, Conn. Medical research department. Project 
X-243 {Sub no. 47) Report no. 2, 13 February 1945, 
13 pp. 
3446. Bartlett, N. R. Submarine duty completed by 
enlisted personnel ordered to New London for assignment 
to new construction. U. S. Navy. Submarine base, New 
London, Conn. Medical research department. Project 
X-243 {Sub. no. 47) Third Interim Report, 31 May 1945, 
11 pp. 
3447. Bartlett, N. R. An evaluation of the officer 
classification test as a device for selecting officer candidates 
for submarine school. U. S. Navy. Submarine base, New 
London, Conn. Medical research department. Project 
X-530 {Sub. no. 107) Final Kept., 7 July 1945, 17 pp. 
3448. Bartlett, N. R. Investigation of the combat in- 
formation center test (NavPers 16680) as a selection 
device for enlisted submarine radar school. U. S. Navy. 
BuMed. Project no. X—496 {Sub. no. 103), Final Kept., 
22 October 1945, 13 pp. 
3449. Bartlett, N. R. An investigation of the billet 
qualifications blank (NavPers 16418) for its suitability 
with combat-experienced candidates for submarine train- 
ing. U. S. Navy. BuMed. Project X—598 {Sub. no. 129), 
14 January 1946, 12 pp. 
3450. Bartlett, N. R. Description of an abstract of the 
service record for analyses of examinations of experienced 
submarine personnel received for re-assignment. U. S. 
Navy. BuMed. Project X—596 {Sub. no. 128), Kept. no. 1, 
23 January 1946, 3 pp. 
3451. Bartlett, N. R. Description of an abstract of the 
service record for analyses of examinations of experienced 
submarine personnel received for re-assignment. U. S. 
Navy. BuMed. Project X—596 {Sub. no. 128) Kept. no. 2, 
24 January 1946, 3 pp. 
3452. Bartlett, K. R. Review of research and develop- 
ment in examination for aptitude for submarine training. 
U. S. Navy. Submarine base, New London, Conn. Medical 
research laboratory. Project NM—003—041.13.2 {formerly 
NM-003-036), 22 May 1950, 42 pp. 
3453. Bechtoldt, H. P. Selection. Handbook of experi- 
mental psychology. Edited by S. S. Stevens. New York, 
John Wiley & Sons, Inc., 1951, 1362 pp. [M] [R] 
3454. Buel, J. and A. W. Melton. The S. A. M. two- 
hand coordination test for the classification of aviation 
cadets: I. Apparatus and procedures. U. S. AAF. Ran- 
dolph Field, Texas. School of aviation medicine. Project 
124, Kept. no. 1, 11 March 1943, 10 pp. [P] 
3455. Cook, E. B. and R. J. Wherry. A study of the 
interrelationships of psychological and physiological meas- 
ures on submarine enlisted candidates: I. History, experi- 
mental design, and statistical treatment of data. U. S. 
Navy. Submarine base, New London, Conn. Medical re- 
search laboratory. Project NM—003—017, Kept. no. 1, 
9 March 1949, 45 pp. 
3456. Cornehlsen, J. H., Jr. The selection and classifi- 
cation of naval officer personnel. Amer. psychol., 1946, 1: 
349-352. 
3457. Cronbach, L. J. Selection and training, pp. 
491—513 in; A survey report on human factors in under- 
sea warfare. Washington, D. C., National Research 
Council, 1949, 541 pp. 
3458. Curran, D. and M. Critchley. German neuro- 
psychiatry with special reference to the Kriegsmarine (and 
with a note on habitability of the Prinz Eugen). Gt. Brit. 
MRC-RNPRC, HS. R. N. P. 46/320 H. S. 156, August 
1946, 37 pp. 
3459. Farnsworth, D., N. R. Bartlett, and M. I. 
Kindred. Comparison of various screening devices with 
standard medical procedure. U. S. Navy. Submarine base, 
New London, Conn. Medical research department. Project 
X-493 {Av-263-p), Prelim, rept. 24 January 1945, 15 
PP- [P] SELECTION 
3460-3490 
3480. Farnsworth, D., H. G. Sperling, and P. F. Kimble. 
A battery of pass-fail tests for detecting degree of color 
deficiency. U. S. Navy. Submarine base. New London, 
Conn. Medical research laboratory. Project NM 003 018, 
Rept. no. 1, 10 August 1949, 29 pp. 
3461. Graham, C. H., F. A. Mote, and R. N. Berry. 
The relation of selection test scores to tank escape per- 
formance. Submarine school. U. S. OSRD-NDRC. Ap- 
plied psychology panel. Project N—113, Rept. no. 3, 31 
January 1944, 7 pp. 
3462. Graham, C. H,, L. A. Riggs, N. R. Bartlett, R. N. 
Berry, W. S Verplanck, R. L. Solomon, and C. G. Mueller. 
A report of research on selection tests at the U. S. Sub- 
marine base, New London, Conn. U. S. OSRD—NDRG. 
Project 44, Rept. no. 1770, 25 pp. 
3463. Harris, J. D. Comprehensive validation of sub- 
marine sonar selection tests. U. S. Navy. Submarine base, 
New London, Conn. Projects X—327 {Sub. no. 56), X—331 
{Sub. no. 60), X-632 {Sub. no. 137), Final rept., 30 
September 1946, 32 pp. 
3464. Herrick, J. Personnel selection and training, 
pp. 109—117 in: Subsurface warfare. The history of Divi- 
sion 6, National defense research committee. U. S. OSRD, 
Washington, D. C., 1 January 1951, 200 pp. 
3465. Hunt, W. A. and I. Stevenson. Psychological 
testing in military clinical psychology: II. Personality 
testing. Psychol. Rev., 1946, 53: 107—115. 
3466. Leavitt, H. J, and N. Adler, Validation of 
officer selection tests by means of combat proficiency 
ratings. U. S. Navy. Camp Lejeune, N. G. Medical field 
research laboratory. Project X-620 {Sub. no. 135), KC/ 
All {P-11) X-620, 16 May 1946, 45 pp. 
3467. McCain, J. A. The enlisted selection program of 
the United States Navy during world war II. Stanford 
University, Calif. Abstracts of Dissertations. 1947—48, 23: 
304-311. 
3468. McCollum, E. L. Selection of men best qualified 
for subarctic and arctic duty. An eighteen month longi- 
tudinal study of airmen assigned to Alaskan duty. USAF. 
Ladd air force base, Alaska. Project 2-01-007, Part B, 
March 1951, 8 pp. 
3469. Malinosky, A. T. and N. R. Bartlett. Analysis 
of rejections in examinations for submarine school. U. S. 
Navy. Submarine base. New London, Conn. Medical re- 
search department. Project X-566 {Sub. no. 119) Third 
interim rept., 27 June 1945, 3 pp. 
3470. Matthews, J. L. Physical standards for selection 
of radar operators. U. S. AAF. Randolph Field, Texas. 
School of aviation medicine. Project 167, Rept. no. 1, 20 
July 1943, 9 pp. [P] 
3471. Moore, B. V. Personnel interviewing, pp. 142-147 
in: Handbook of applied psychology. Volume I. Edited 
by Douglas H. Fryer and Edwin R. Henry. New York, 
Rinehart and Company, Inc., 1950, ix, 380 pp. [R] 
3472. Neff, W. D. Memorandum on the use of audi- 
grams in the selection of sound operators. U. S. Navy. 
Submarine base, New London, Conn. Medical research 
department, 14 December 1942, 5 pp. 
3473. Newman, S. H., J. M. Bobbitt, and D. C. Cameron. 
The reliability of the interview method in an officer can- 
didate evaluation program. Amer. psychol, 1946, 1: 103— 
109. 
3474. Richardson, M. W. Effectiveness of selection de- 
vices. pp. 192—194 in: Handbook of applied psychology. 
Volume I. Edited by Douglas H. Fryer and Edwin R. 
Henry. New York, Rinehart and Company, Inc., 1950, 
ix, 380 pp. 
3475. Rodger, A. Personnel selection in the Royal Navy. 
Brit. med. J. 1947, 5: 37-38. 
3476. Roff, M. F. Personnel selection and classification 
procedures: spatial tests. A factorial analysis. USAF. 
Randolph Field, Texas. School of aviation medicine. Proj- 
ect 21-29-002, Final Kept., January 1951, 46 pp. 
3477. Rosenstiel, M. Pathologic des sous-mariniers. 
Rev. Med. nav., 1946, 1: 175-179. [D] 
3478. Rundquist, E. A. Personality tests and pre- 
diction. pp. 182—191 in: Handbook of applied psychology. 
Volume I. Edited by Douglas H. Fryer and Edwin R. 
Henry. New York, Rinehart and Company, Inc., 1950, 
ix, 380 pp. 
3479. Shilling, C. W. The development of methods for 
the selection of sound listening personnel. U. S. Navy. 
Submarine base, New London, Conn. Medical research 
department. 1 March 1942, 15 pp. 
3480. Shilling, C. W. and N. R. Bartlett. A description 
of disqualifications of enlisted applicants for submarine 
training. U. S. Navy. Submarine base, New London, 
Conn. Medical research department. Project X-566, 
{Sub. no. 119),8 February 1946, 25 pp. 
3481. Shilling, C. W. and N. R. Bartlett. A description 
of disqualifications of enlisted applicants for submarine 
training. Nav. med. Bull., Wash., 1947, 47: 59-76. 
3482. Shilling, C. W. and J. W. Kohl. Development of 
use of selection procedures, pp. 18-29 in: History of sub- 
marine medicine in World War II. U. S. Navy. Submarine 
base, New London, Conn. Medical research department, 
25 May 1945, 328 pp. 
3483. Shipley, W. C., F. E. Gray, and N. Newbert. 
The personal inventory—its derivation and validation. 
/. din. Psychol, 1946, 2: 318-322. 
3484. Sulzman, J. H., D. Farnsworth, N. R. Bartlett, 
and M. I. Kindred. Comparison of various screening de- 
vices with standard medical procedure. U. S. Navy. Sub- 
marine base, New London, Conn. Medical research de- 
partment. Project X-493 {Av-263-p) 2nd prelim, rept., 
27 April 1945, 21 pp. [P] 
3485. U. S. Navy, BuNavPers. (A) Submarine personnel 
selection, pp. 135—142 in: Submarine Medicine practice. 
NavPers 10838, March 1949, 182 pp. [D] 
3486. U. S. Navy. Submarine base, New London, Conn. 
Medical research department. A comment on submarine 
personnel classification. “Analysis of examinations of per- 
sonnel received for new construction submarines.” Proj- 
ect X-596 {Sub. no. 128), 28 January 1946, 4 pp. 
3487. U. S. Navy. Submarine base, New London, Conn. 
Medical research department. A comment on submarine 
personnel classification. Project X-596 {Sub. no. 128) 
Rept. no. 3, 28 January 1946, 5 pp. 
3488. IT. S. Navy. Submarine base, New London, Conn. 
Medical research department. Memorandum comparing 
the scores obtained by testing submarine school candi- 
dates with the Otis self-administering test of mental ability 
with the scores received on the general classification test, 
as recorded in the service records of these candidates. 
28 December 1942, 10 pp. 
3489. U. S. Navy. Submarine base, New London, Conn. 
Medical research department. Selection and training of 
sound listening personnel. 22 September 1942, 6 pp. 
3490. U. S. Navy. Technical mission to Japan. Selection 
of personnel, pp. 39-40 in: Aero, surface, and submarine 
medicine and research in the Japanese Navy. Fascile M—l, 
Target M-06, 4 September 1945, 72 pp. 3491-3496 
SELECTION AND TRAINING OF PERSONNEL 
3491. U. S. NEC. Committee on dentistry. Minutes of 
the eighth meeting. 14 November 1949, 2 pp. 
3492. Wever, E. G. and W. D. Neff. Classification of 
audigrams for use in the selection of sound operators. 
U. S. Navy. Submarine base. New London, Conn. Medical 
research department. 1 August 1942, 11 pp. 
3493. Wiggin, B. E. and N. B. Bartlett. Development 
of a method for obtaining personal preferences from within 
small groups, and the relationship of such evaluations to 
other psychiatric and psychological data. U. S. Navy. Sub- 
marine base. New London, Conn. Medical research de- 
partment. Project X-246 {Sub. no. 50), 25 January 1944, 
7 pp. 
3494. Williams, S. B., H. J. Leavitt, and C. L. Blair. 
Validation of officer selection tests by means of combat 
ratings. Kept. no. 1; The prediction of successful combat 
leadership. U. S. Navy. Camp Lejeune, N. C. Medical 
field research laboratory. Project X-620 {Sub. no. 135), 
KC/All {P-11) X-620, 18 January 1946, 18 pp. 
3495. Willmon, T. L. Outline and discussion of methods 
for selection of submarine reserve personnel. U. S. Navy. 
Submarine base. New London, Conn, Medical research 
department. 16 February 1948, 16 pp. [R] 
3496. Willmon, T. L. and N. R. Bartlett. Relationship 
of personnel selection devices to the behavior criteria of 
school performance and overall performance on a sub- 
marine patrol. U. S. Navy. Submarine base, New London, 
Conn. Medical research laboratory. Project X-243 {Sub. 
no. 47) Report no. 1, 25 October 1944, 8 pp. 
II. TRAINING 
During World War II the training program 
operating within the submarine service reached an 
unbelievably high level of efficiency. Courses of 
instruction were developed, and techniques of 
training were perfected; new and improved equip- 
ment for training and indoctrination were instituted. 
The center of much of this training was at the Sub- 
marine School, U. S. Submarine Base, New London, 
Conn. However, training activity within the sub- 
marine force was located at almost every submarine 
base, notably Pearl Harbor. 
That portion of the training program coming 
under the cognizance of the Medical Department 
is reviewed by Shilling and Kohl (3502) 1947. 
One of the most important training activities of 
submarine force candidates and personnel is the 
Escape Training Tank. Aside from the actual train- 
ing value of the escape tank, an excellent means of 
selection is provided by this activity to eliminate 
those individuals not particularly suited for under- 
water activity. This particular aspect has been re- 
viewed more completely in the foregoing section on 
selection (p. 299). 
The submarine Escape Training Tank was de- 
signed to permit thorough training of all submarine 
personnel in the use of the “lung” or submarine 
escape appliance, under conditions which would 
simulate as closely as possible those prevailing dur- 
ing an actual escape from a disabled submarine. 
This 280,000-gallon tank contains a vertical column 
of water 100 feet high and 18 feet in diameter. 
Integrated with the tank are escape locks or com- 
partments which duplicate those installed in sub- 
marines. These locks are located at depths from 
the top of the tank of 18 feet, 50 feet, and 100 feet, 
permitting escapes under conditions identical to 
those existing at similar depths at sea. All sub- 
marines are supplied with submarine escape appa- 
ratus and the crew must be properly trained in the 
use of the lung, either at the tank located at New 
London or at the one at Pearl Harbor. Active sub- 
marine personnel must requalify every year at either 
one of these tanks at the 12-foot and 30-foot stops. 
To escape from a sunken submarine, it is neces- 
sary that the pressure within the compartment from 
which egress is to be made be equalized with the 
outside water pressure. To do this, the compart- 
ment is flooded by admitting water through various 
valves; as the water rises, it compresses the air in 
the upper part of the compartment. When the water 
rises to the top of the escape door or telescope trunk, 
it creates a pressure within the compartment equal 
to the sea pressure. At this stage it is possible for 
the hatch or door to be opened by hand. After the 
pressure is equalized, the hatch is opened and a 
buoy with an ascending line is released through 
the open hatch and escape is made to the surface 
with the use of the “lung.” 
Qualification at the tank consists of the following 
essentials: (1) a pressure test of 50 lbs. per sq. in. 
in the recompression chamber; (2) a lecture on 
construction, operation, safety features, and pre- 
cautions in the use of the “lung”; (3) shallow water 
training for confidence in breathing under water; 
(4) 12-foot training to attain proper relaxation and 
confidence; (5) 18-foot and 50-foot escapes to 
train in the use of the “lung” so that should he 
be called upon to use this device under stress, he 
could most effectively use its life-saving qualities. 
It is of particular interest that the sumarine serv- 
ice was the first in the U, S. Navy to inaugurate 
night lookout training and that this training was 
developed under auspices of the Medical Research 
Laboratory at the U. S. Submarine Base, New 
London, Conn. Also, the Medical Research Labora- 
tory, through its advice, helped to modify the Navy’s 
Recognition Program at Ohio State University so 
that night lookout training was combined with and 
added to all recognition training by the Navy. 
Through this training a realistic horizon was 
provided upon which the trainee was required to 
sight and identify small ship models which were 
placed upon it. The apparatus provided also repro- 
duction of distant gunfire, of moonlight, and of PERFORMANCE—SUBMARINE OPERATIONS 
3497-3505 
recognition lights. Its advantages as a training de- 
vice lay in its realism, and the interest which it 
aroused in the men. In operation, lookouts were 
posted in pairs and located and reported in proper 
phraseology the position and type of ships. 
As a result of liaison work of the Applied Psy- 
chology Panel of the Office of Scientific Research 
and Development and the Medical Research Lab- 
oratory, U. S. Submarine Base, New London, 
Conn., the Telephone Talker School was officially 
established in July 1944. The name of this school 
was later changed to Interior Voice Communica- 
tions School as it took over a broader field of in- 
struction. One of the most important features of 
the training program was the teaching of the use 
of standard procedures, a type of practical drill 
which greatly facilitated instruction in voice com- 
munication procedures, phraseology, and terminol- 
ogy while simulating the actual operations. During 
the course the student participated in practical 
drills, torpedo approach, battle surface, and other 
standard patrol operations. An additional paper 
by Abrams, Miller, Mallory, Hibbitt, Temple, Neff, 
and Jenkins {3497) 1945 concerning submarine 
voice communication should be consulted. 
For other general reports on training and the 
problems involved, the reader may consult articles 
by Bartlett {3498) 1946; Brown {3499) 1945; 
Molumphy {3500) 1949; Shilling and Kohl {3501) 
1947; Verplanck {3503 and 3504) 1946; and Wolfle 
{3505) 1951. 
3497. Abrams, M. H., J. Miller, L. A. Mallory, G. W. 
Hibbitt, W. J. Temple, W, D, Neff, and W. J. Jenkins. 
A project for standardizing submarine phraseology and 
developing a training program in submarine voice com- 
munications. Final report. U. S. OSRD-NDRG, O. E. M. 
sr 658, 830, and 1128, Rept. no. 4795, 28 February 1945, 
31 pp. 
3498. Bartlett, N. R. An evaluation of shipboard indoc- 
trination of officer candidates for submarine training. 
U. S. Navy. Submarine base. New London, Conn. Medi- 
cal research department. Project X-531, 5 February 1946, 
11 pp. [R] 
3499. Brown, W. B. The ship recognition trainer. U. S. 
Navy. Submarine base, New London, Conn. Medical re- 
search department. Project X-271 (Av-159-c) First in- 
terval rept., 25 September 1945, 39 pp. [M] 
3500. Molumphy, C. G. Report of diving training in 
U. S. S. Chanticleer, off Key West, during the period 19 
October to 8 December 1948. U. S. Navy. Naval gun 
factory. EDU. Project NS 186-042, 1 July 1949. 
3501. Shilling, C. W. and J. W. Kohl. Medical per- 
sonnel. pp. 3—18 in; History of submarine medicine in 
World War II. U. S. Navy. Submarine base, New London, 
Conn. Medical research laboratory, 25 May 1947, 328 pp. 
3502. Shilling, C. W. and J. W. Kohl. Training activi- 
ties. pp. 32-62 in: History of submarine medicine in 
World War II. U. S. Navy. Submarine base, New London, 
Conn. Medical research laboratory. 25 May 1947, 328 pp. 
3503. Verplanck, W. S. Night lookout training stage. 
U. S. Navy. Submarine base, New London, Conn. Medi- 
cal research department. Project X-350 (Av-197-p) 
Final rept. 1 March 1946, 14 pp. 
3504. Verplanck, W. S. Experimental evaluation of the 
ship recognition trainer. U. S. Navy. Submarine base, 
New London, Conn. Medical research department. Proj- 
ect X-271 (Av-159-c), 14 March 1946, 10 pp. 
3505. Wolfle, B. Training, pp. 1267-1286 in: Hand- 
book of experimental psychology. Edited by S. S. Stevens. 
New York, John Wiley & Sons, Inc., 1951, 1362 pp. 
[M & R] 
III. PERFORMANCE—SUBMARINE 
OPERATIONS 
For a definitive report on United States sub- 
marine operations in World War II, reference 
should be made to the excellent and comprehensive 
volume by Roscoe {3512) published in 1949. In 
this exhaustive study of submarine operations many 
glimpses into human factors and their bearing on 
operational results are given. The author has pre- 
sented numerous examples of performance of per- 
sonnel under hazardous conditions and has discussed 
the almost mystical bond that welds submarine 
crewmen together. The relationships between skip- 
pers and their crews are illustrated by many stories. 
Closely related to morale are seen to be various 
psychological aspects of living aboard submarines. 
Most submariners find it more difficult to take 
severe depth charging when lying helplessly on the 
bottom than when maneuvering to evade. The com- 
mand “battle surface” is sounded as a welcome 
break in the routine. The author stresses the psycho- 
logical advantage of air-conditioning. Habitability 
of the submarine is discussed in many places in the 
volume and there is a consideration of the recouper- 
ation program during periods of leave. Weather 
conditions affected the men greatly and the worst 
conditions were said to be in the cold climate of the 
Aleutian Islands. The color of the interior of the 
submarine is considered to be of great importance. 
Submarine rescue work is referred to. The author 
states that 504 airmen were rescued by submarines 
during World War II. The work of hospital corps- 
men attached to submarines is praised many times. 
Accounts of appendectomies performed by hospital 
corpsmen are given. 
For a section on the history of the development 
of submarine warfare, reference should be made to 
Cope and Karig’s volume {3506) published in 
1951. In summing up battle operations the authors 
point out that odds were never better than even. 
That so many of our submarines survived scores of 
battles deeper into enemy territory than even air- 
craft could penetrate except during the last phases 3506-3514 
SELECTION AND TRAINING OF PERSONNEL 
of the war is testimony to the skill and resource- 
fulness of the young Americans who manned them 
from the bridge to the galleys. In a popular article 
Schwed and Wolters {3513) 1949 have pictured 
the U. S. S. Tusk inside and outside during a cruise. 
Life in a midget submarine in the British Navy has 
been described by Galway {3509) 1947. These 
midget submarines of the British Navy, spoken of 
as X-craft, spent many hours submerged reconnoit- 
ering off the Normandie beaches on D-day. Three 
British X-craft torpedoed the giant German battle- 
ship, Tirpitz in a Norwegian fjord. The author de- 
scribes the effects of hypoxia and carbon dioxide 
in midget submarines. He points out that when sur- 
faced after a 10-hour dive one usually got head- 
aches. The rule while submerged was to avoid ex- 
ertion and lead a languid existence. Food was 
cooked in an electric pot and electric kettle. Most 
of the meals consisted of sandwiches washed down 
with orange juice or condensed milk. The toilet was 
situated in the escape chamber and known as “wet 
and dry” because it could be flooded and pumped 
dry at will. It was hardly ever dry. It was described 
as an unsalubrious spot in which there was little 
temptation to dally and only just room to move. 
The tank was pumped out only at night. Washing 
was limited to shaving and brushing the teeth. Many 
men took a swim at night to get clean. The first 
lieutenant of one of the boats indulged in a swim 
overside during the Tirpitz adventure. Members 
of the crew became accustomed to each other’s odor 
and tended to be avoided by submarine tender 
crews until they had taken a bath. The inside of 
the boats was wet with condensation from hot drinks 
and water brought by men from the watch into the 
interior. There were meager bunking facilities in the 
battery room and the engine room. The bunk in 
the control room was usually filled with food 
supplies. 
The Germans made use of three different types 
of midget submarines {3514). These were the 
“Biber,” the “Molch,” and the “Seehund.” The 
“Seehund” was the largest of the midget submarines 
and was prefabricated with an overall length of 39 
feet, a depth of 6 feet, and a displacement of about 
16 tons. This craft had a surface speed of 8 knots 
and a submerged speed of 3 or 4 knots. Propulsion 
was by diesel engine and electric motors. The “See- 
hund” carried two 21-inch modified electric tor- 
pedoes. The range of the submarine at 8 knots was 
275 miles plus 50 miles at 3 knots submerged. The 
“Biber” was the smallest of these submarines and 
was a one-man boat. Its overall length was 29 
feet with a beam of 4 feet 9 inches. It was equipped 
with 2 outboard torpedos. In this submarine the 
pilot conned through 6 rectangular armoured glass 
scuttles. The hatch was also fitted with a glass 
scuttle for upward observation. At normal trim the 
conning tower rose about 2 feet above the water 
and was fitted with a projector compass about 18 
inches in height, a periscope 4 feet 6 inches in 
height and an air intake. The boat was propelled 
by a gasoline engine and an electric motor and the 
air intake was designed so that the submarine could 
proceed on her engines with the hatch closed. The 
maximum speed was 6J/2 knots, the submerged 
speed being 6 knots. The maximum endurance was 
48 hours or 100 miles. The submarine operated to 
a depth of 60 feet. The “Molch” was a one-man 
submarine 46 feet long and 7 *-4 feet deep. Its 
armourment was similar to that of the “Biber.” 
For other reports on performance, the reader 
may consult the section on general studies of sub- 
marine medical problems (p. 1) and the section 
on diseases and accidents in naval personnel, mor- 
bidity (p. 149). For reference to manuals and text- 
books issued to pharmacist’s mates on submarines, 
the following items in the bibliography are given; 
3508, 3510, and 3511. 
For an excellent and graphic study of the job 
carried out by tunnel diggers, a paper by Corcoran 
and Wolters {3507) 1947 should be read. 
3506. Cope, Harley, and Walter Karig. The submarine, 
pp. 3—16 in: Battle submerged. Submarine fighters of 
World War II. First edition. New York, W. W. Norton & 
Company, 1951, 244 pp. 
3507. Corcoran, J. and D. Wolters. The tunnel diggers. 
Sci. III., 1947, 2: 50-59. 
3508. Cullen, Stuart C. and E. G. Gross. Manual of 
medical emergencies. Chicago, The Year Book Publishers, 
Inc., 1949, 267 pp. 
3509. Galwey, G. V. Life in a midget submarine. Proc. 
U. S. nav. Inst., 1947, 73: 421-425. 
3510. Jensen, Julius and Deborah Maclurg Jensen. 
Nursing in clinical medicine. Third edition. New York, 
The Macmillan Company, 1949, 791 pp. 
3511. Rehfuss, Martin Emil and Alison Howe Price. 
A course in practical therapeutics. Second edition. Balti- 
more, The Williams & Wilkins Company, 1951, 938 pp. 
3512. Roscoe, Theodore. United States submarine opera- 
tions in World War II. U. S. Naval Institute, Annapolis, 
Maryland, 1949, 577 pp. 
3513. Schwed, W. W. and D. Wolters. Snorkel, sub- 
marine that breathes. Sci. III., 1949, 4: 34-41, 86. 
3514. Anon. German midget submarines. Engineer, 
Land., 1945, 179: 428-429. 
IV. SPECIAL SONAR PROBLEMS 
The submarine acquires information about its 
environment by various methods: visual contact, 
radar, radio, and sonar. Sonar utilizes sound waves 
which are transmitted through water, the sound SPECIAL SONAR PROBLEMS 
3515-3519 
signals being picked up from the water, amplified, 
and finally analyzed in various ways. These are 
presented to the operator as useful items of infor- 
mation about objects and their movements in the 
water around them. The submarine is made aware 
of the position of floating mines and the position, 
type, speed, and course of a surface vessel or another 
submarine. 
The sound man using sonar apparatus must de- 
tect a sound signal presented to him in a background 
of noise. The signal will differ from the background 
in one or more of the following characteristics: 
rhythm, loudness, and quality. Capacity for rapid 
and successful differentiation of changes in these 
characteristics of auditory signals determines to a 
great extent the success of the sound man and the 
life of the submarine. Therefore, improvement of 
selection procedures will depend immediately upon 
answers to auditory problems arrived at through 
psycho-physical studies. Solutions to the more far- 
reaching problems will depend on physiological 
information. 
For an excellent description of auditory problems 
arising out of sonar operation, a chapter by Neff 
and Thurlow in the monograph, Human factors in 
undersea warfare. National Research Council, 
Washington, D. G., 1948, should be consulted. 
Other chapters in this monograph are referred to 
elsewhere (1726 and 1737). Auditory tasks of the 
sonar operator, methods of investigation, and results 
of relevant research and suggestions for future re- 
search are discussed. Experimental evidence pro- 
vided in a paper by Harris {3517) 1945 has shown 
that 0.27 decibels is the negative time-error for an 
average group of subjects. For poor subjects the 
magnitude of the negative time-error was 0.6 
decibel. No sound change was reported from sub- 
jects presented a standard sound stimulus, the sig- 
nal then being increased or decreased 0.28 decibel 
in intensity. No correlation was found to exist be- 
tween the test and final sound school grades but 
when correlated against specific auditor sonar per- 
formance to which loudness discrimination may 
reasonably be presumed contribute, correlations of 
the order of 0.21 to 0.51 were obtained. Significant 
differences in performance were found between 
those who do poorly and those who do average or 
better on the test. 
Additional data obtained by Myers and Harris 
{3520 and 3521) 1948 indicates that a zone of de- 
tectability of the order of two to three decibels exists 
between the intensity at which a tone is just de- 
tected 50 percent of the time and the intensity at 
which it may be assigned a pitch quality 50 percent 
of the time. This zone where some unidentified 
sound can be heard is somewhat less for the medium 
tones. The zone of detectability of the frequencies 
500, 1,000, 2,000, 4,000, 8,000, and 14,000 cycles 
per second varied at random from 2 to 4 decibels, 
independently of frequency. For the higher fre- 
quencies, an experienced subject can select a certain 
criterion of tonality and maintain it with consider- 
able precision. The matching of variable frequencies 
of low sensation levels to a standard frequency of 
10 decibels showed improvement in matching as 
the intensity increased from 0 to 10 decibels. It was 
reasoned that the subjective criterion of tonality 
which a subject can select and maintain is one of 
pitch rather than of loudness. The authors con- 
cluded that the phenomenon depends upon the in- 
tensity of the stimulus rather than upon a change 
in its frequency composition. 
Group audiometry, as contrasted to individual 
auditory testing, was tried and evaluated by Myers, 
Harris, and Fowler {3522) in 1948. Complete audi- 
ometric examinations were given to 1448 men in 
seven days. It was found that with a college popu- 
lation, the group technique is effective within a two 
percent error. Effectiveness of this examination pro- 
cedure requires a psychological impetus which will 
force the subject to use his last 10 decibels of hear- 
ing ability. A history of childhood disease was found 
to be slightly related to high-tone deafness and of 
the 94 men who had had aerotitis media, 5.3 per- 
cent had a low-tone average loss of 25 decibels. 
Aerotitis media contributes slightly to high tone loss. 
For further reports on special sonar problems, 
papers by the following may be consulted: Harris 
{3515) 1944; {3516 and 3518) 1945; and {3519) 
1946; Neff {3523, 3524, and 3525) 1942; Schafer 
{3526) 1949; U. S. Navy {3527) 1942 and {3528) 
1946; and U. S. National Research Council {3529) 
1950. 
3515. Harris, J. D. Propeller noise discrimination. U. S. 
Navy. Submarine base. New London, Conn. Medical re- 
search department. Preliminary report, Project X—53, 
26 December 1944, 14 pp. 
3516. Harris, J. D. Functions of pitch in submarine 
sonar operation. U. S. Navy. Submarine base. New Lon- 
don, Conn. Medical research department. Project X-330 
{Sub. no. 59), 30 January 1945, 15 pp. 
3517. Harris, J. D. Functions of loudness discrimination 
in submarine sonar operation. U. S. Navy. Submarine 
base, New London, Conn. Medical research department. 
Interval report, Project X-53, 5 April 1945, 19 pp. 
3518. Harris, J. D. The relation between the audiogram 
at high frequencies and proficiency in sonar performance. 
U. S. Navy. Submarine base, New London, Conn. Medical 
research department. Interim report no. 1, Project X-329 
(Sub. no. 58), 4 June 1945, 9 pp. 
3519. Harris, J. D. Comprehensive validation of sub- 
marine sonar selection tests. U. S. Navy. Submarine base, 
New London, Conn. Medical research department. Final 3520-3529 
SELECTION AND TRAINING OF PERSONNEL 
report on Projects X-327 {Sub. no. 56), X-330 {Sub. no. 
59), X-331 {Sub. no. 60), X-632 {Sub. no. 137), 30 
September 1946, 32 pp. 
3520. Myers, C. K. and J. D. Harris. Detection thresh- 
olds and pure tone thresholds in auditory acuity. U. S. 
Navy. Submarine base. New London, Conn. Medical 
research department. Project NM-003-022 {X-747 {Sub. 
no. 154)) Kept. no. 2, 22 January 1948, 7 pp. 
3521. Myers, C. K. and J. D. Harris. The emergence of 
a tonal sensation. U. S. Navy. Submarine base, New Lon- 
don, Conn. Medical research laboratory. Project NM- 
003-022, Kept. no. 4, 31 March 1948, 14 pp. 
3522. Myers, C. K., J. D. Harris, and E. P. Fowler, Jr. 
The feasibility of group audiometry. U. S. Navy. Sub- 
marine base, New London, Conn. Medical research de- 
partment. Project NM 006 007 {X-761 {Sub. no. 163)) 
Terminal report, 12 February 1948, 54 pp. 
3523. Neff, W. D. Memorandum on the selection and 
training of sound operators. U. S. Navy. Submarine 
base, New London, Conn. Medical research department. 
7 July 1942, 43 pp. 
3524. Neff, W. D. Memorandum on test-retest reliabil- 
ity of pitch discrimination tests. U. S. Navy. Submarine 
base, New London, Conn. Medical research department, 
14 December 1942, 2 pp. 
3525. Neff, W. D. Memorandum on inventory of musical 
background, Form B. U. S. Navy, Submarine base, New 
London, Conn. Medical research department. 15 Decem- 
ber 1942, 4 pp. 
3526. Schafer, T. H. Detection of a signal by several 
observers. U. S. Navy, NEL, San Diego, Calif. U. S. N, 
E. L. Kept. no. 101, 26 January 1949, 9 pp. 
3527. U. S. Navy. Submarine base, New London, Conn. 
Medical research department. Memorandum on an abbre- 
viated procedure for the determination of audiograms in 
the selection of sound operators. 1 August 1942, 3 pp. 
3528. H. S. Navy. NEL, San Diego, Calif. Studies of 
the recognition of submarine echoes. Contract NObs-2074, 
File no. 01-41, 30 September 1946, 108 pp. [R] [P] 
3529. U. S. NRG—CUW. Panel on underwater acoustics. 
A survey report on basic problems of underwater acoustics 
research. 1950, 137 pp. Special Psychological and Psychiatric 
Problems 
I. GENERAL STUDIES 
Two items are listed as general source material 
on military psychological problems. The first is a 
monograph published by Bray [3530) in 1948. This 
work constitutes a history of the applied psychology 
panel of the National Defense Research Committee. 
The second item is a survey report on human factors 
in undersea warfare published by the National Re- 
search Council in 1949. In addition, Kennedy’s 
chapter [3531) on personnel resources for research 
in Applied Experimental Psychology may also be 
consulted. 
It has become increasingly apparent in modern 
times that the peculiar complexity of military oper- 
ations in general and submarine warfare in partic- 
ular creates psychological problems which can no 
longer be successfully handled haphazardly or with- 
out recourse to special skills available to the dis- 
cipline of psychology. Some of the special problems 
include those arising in selection and classification 
of personnel, training, performance, and the design 
of controls, displays, and work spaces to conform to 
human capacities and limitations. Present and pro- 
jected submarine operations impose excessive stress 
on personnel under certain conditions and prob- 
lems of fatigue and morale take on new significance. 
Questions of sleep-wakefulness cycles and duty 
and rest periods can no longer be left unanswered 
or handled by chance alone. There seems little 
doubt but that if adequate attention is given to 
human factors in submarine operations with proper 
consideration for habitability and good morale, the 
incidence of psychiatric breakdown may be kept 
at a minimum. 
3530. Bray, C. W. Psychology and military proficiency. 
A history of the applied psychology panel of the national 
defense research committee. Princeton, Princeton Univer- 
sity Press, 1948, 235 pp. 
3531. Kennedy, J. L. Personnel resources for research 
in applied experimental psychology, pp. 517-518 in: A 
survey report on human factors in undersea warfare. 
Washington, D. C. National Research Council, 1949, 541 
pp. 
H. HUMAN FACTORS IN ENGINEERING 
DESIGN 
This section, although focused on the submarine, 
covers material not limited to this branch of the 
service, either for experimental data or applications. 
Industry and the allied military services have con- 
tributed much information relative to the problem 
of instrument, control, and panel design as they 
apply to the human operator. For example, research 
on cockpit design for aircraft has a relation to the 
design of submarine control rooms and systems re- 
search on the GIG for surface ships applies also to 
submarines. 
In a control system, man has been regarded as a 
chain consisting of sensory devices, a computing 
system to reduce misalignments on the basis of 
previous experience, an amplifying system render- 
ing small afferent nerve activity effective to initiate 
muscle action, and finally a mechanical linkage 
system. Graik [3546) 1948 also states that the pri- 
mary problem of human engineering consists in 
discovering in detail the characteristics of this hu- 
man chain as it compares to an automatic system. 
Although satisfactory data on many human engi- 
neering design problems have been gathered, Stellar 
[3581) states that many of the gaps have been 
filled in rather liberally with opinions and hypoth- 
eses. There has been a tendency of the literature in 
this area to formulate general principles of panel 
design prematurely and to offer them as recom- 
mendations to the design engineer. Actually it has 
turned out that many of these principles are little 
more than the common sense opinions of experi- 
enced engineers and psychologists. Keeping in mind 
the need for separation of fact from opinion, the 
author lists 6 general principles which one should 
try to adhere to in planning panel layouts: (1) All 
controls and displays should be located within a 
practical working distance from the operator. 
291222—54 21 SPECIAL PSYCHOLOGICAL AND PSYCHIATRIC PROBLEMS 
(2) Within the working area, each control and 
display should be situated in a position where it 
may be most efficiently used. (3) Where two or 
more controls or displays on a panel have the same 
optimal position, the more important and more fre- 
quently used items should be given the preferred 
positions. (4) Controls and displays should be 
grouped in patterns that make for the easiest oper- 
ation and observation from the point of view of the 
operator. (5) No one part of the body should be 
overloaded with work that could be assigned to 
other body parts. (6) Any possible confusion of 
controls or of displays by the operator should be 
avoided by proper design or placement. 
For additional general studies of human engineer- 
ing design, papers by the following should be con- 
sulted: Bartley and Chute [3533) 1947; Channell 
and Tolcott [3536) 1948; Chapanis [3537) 1951; 
Fitts [3553) 1949; Lawrence [3564) 1946; Mack- 
worth [3569) 1949; and Tufts College [3582) 
1949. 
The sensory signal is presented to the operator 
by instrument dials or gages. The problem of design 
for each type of instrument is somewhat special, in 
terms of the way in which the information is pre- 
sented or the varied conditions under which it will 
be used. According to Kappauf [3561) 1949, there 
are in general, two kinds of instruments: one which 
proposes to be accurate and quantitative, the other, 
a monitoring or checking type of instrument. Read- 
ings from either type of instrument should conform 
with stated tolerances or operating requirements. 
How well these tolerances are met depends upon 
the restrictive nature of the conditions of instrument 
use and on the adequacy with which display design 
variables have been manipulated to take particular 
account of the operator’s characteristics. Two differ- 
ent types of instrument reading conditions are 
recognized in submarine service: (1) Some instru- 
ments must be illuminated in such a way that the 
operator and his neighbors will remain as well 
dark-adapted as possible for night observation. (2) 
Other instruments are used at stations where opera- 
tor dark-adaptation is not a consideration and so 
these indicators and devices may be well illumi- 
nated. The author discusses problems of instrument 
marking, instrument illumination, instruments for 
presenting quantitative data, check reading instru- 
ments, and design of specific instruments. 
Experimental observations by Kappauf [3562) 
1951 indicated that the best design for a simple 
dial numbered every 10 units and quantitatively 
at any and all scale values, is one which has a scale 
break at zero, locates the zero near the bottom of 
the dial, and locates the numbers outside the scale. 
Additional data by Kappauf [3563) 1951, obtained 
on 20 subjects reading a series of simply designed, 
straight scales, graduated every unit and numbered 
every 10 units, demonstrated that reading to the 
nearest unit as compared to reading to the nearest 
10 unit required about l/i seconds additional read- 
ing time. In addition to this there were about 50 
percent more reading errors. 
For a complete discussion of visual displays, the 
reader should consult the lengthy monograph by 
Chapanis, Garner, and Morgan (3538 and 3539) 
1949. It is stated that a direct-reading counter is 
better than a circular scale. Markers that change in 
value from one part of the scale to another or from 
one dial to another have been found to be very con- 
fusing. To increase accuracy and decrease the num- 
ber of errors, a scale should increase from zero in a 
clockwise direction. 
Poulton [3578) 1950 investigated the effect of 
practice on the accuracy of tracking with a two- 
pointer display as compared with a one pointer 
display. Results of the investigation provided con- 
firmation of the prediction that performance with 
a one pointer display could be improved by pre- 
senting the subject with additional information. 
It was found that practice resulted in a relative im- 
provement in tracking with a one pointer display, 
principally because the subject showed so little 
anticipation initially with the one pointer. Learning 
with one pointer displays could be accelerated by 
presenting the subject from time to time with an 
additional pointer showing the “stimulus” move- 
ment. For further studies on instrument design and 
dial legibility, reference may be made to papers by 
Barber and Garner [3532) 1951; Chapanis and 
Leyzorek [3541) 1950; Crook, Harker, Hoffman, 
and Kennedy [3549) 1948; Fitts [3554) 1951; 
Loucks [3566, 3567, and 3568) 1944; Saltzman 
[3579) 1950; and White [3590) 1951. 
As has been stated, two different lighting situa- 
tions exist in the submarine. The conditions under 
which low levels of illumination are needed to 
preserve night vision in the submarine were investi- 
gated by Lee and Finch [3565) 1945 at the Naval 
Medical Research Institute at Bethesda. It was 
decided that red light of wave lengths longer than 
590 units should be used in submarine conning 
towers during night operations. Patches of red light 
may be used to locate instruments and hatches if 
the intensity is kept below 0.003 millilamberts. In- 
strument markings should be red on a black dial 
and the intensity of numbers which subtend 18 min- 
utes of arc by 14 minutes of arc at the observer’s 
eye may be set as high as 0.003 millilamberts with- 
out disturbing night vision, provided the ratio of HUMAN FACTORS IN ENGINEERING DESIGN 
luminous to total dial area is less than one-tenth. At 
this intensity the dial numbers will be clearly visible 
to a light adapted observer as well as to a dark 
adapted person. 
The experimental results obtained by Chalmers, 
Goldstein, and Kappauf {3535) 1950 from 8 sub- 
jects reading 12 different types of dials at various 
levels of illumination indicated a progressive in- 
crease in the number of errors as illumination de- 
creased. Gross errors and reading times changed 
very little with decreasing brightness until a critical 
level was reached. This level was found to be equiv- 
alent for all dials with a given size of lettering. 
Additional data on the effect of illumination on 
dial legibility can be obtained from papers by Crook 
and Baxter {3548) 1951; Gleason {3558) 1947; 
Partridge and Solandt {3575) 1943; Spragg {3580) 
1948; and Wise {3591) 1948. 
Reacting to adequate auditory or visual stimuli, 
the operator may have to make adjustments with 
hand or foot controls. Although the control system 
in some instances may consist of only one single 
element, more often it consists of a number of ele- 
ments linked together. The designer’s choice there- 
fore depends to a great extent on the nature of the 
task which the system must perform. A complete 
discussion of the factors relating to control design 
is provided in a paper by Craig and Ellson {3544) 
1949. Traditional attempts to link a better man to 
the machine and, through changes in existing equip- 
ment, to provide a better link between man and 
machine, have masked the fact that the operator 
and his controls are transmission elements in the 
control system and that the control task is per- 
formed by the control system as a whole. The 
designer of control systems needs to know the trans- 
mission characteristics of the operator, his operating 
ranges, and his susceptibility to expected operating 
conditions. The designer must constantly be re- 
minded of the fact that “the operator” as an ele- 
ment in the design of the system is an abstraction 
from the operator who, as an individual, is the 
embodiment of a multiplicity of transmission 
systems. 
Chapanis, Garner, and Morgan {3540) 1949 
emphasize the importance of selecting appropriate 
controls for the task and the use of controls which 
are psychologically realistic. Controls should be ad- 
justed not only to the force which operators are able 
to exert but also for values at which changes can 
be discriminated. Remarkable increases in efficiency 
can result from adjusting the ratio between control 
movement and indicator movement. 
A study of positioning reactions involving move- 
ments from a point of rest to a terminal position at 
varying distances was carried out by Brown, 
Knauft, and Rosenbaum {3534) 1948. The reac- 
tions were made in total darkness after a 2.5 second 
visual presentation at one of the following positions: 
0.6, 2.5, 10, or 40 cm. distant. Various planes of 
movement were studied. It was found that a greater 
variability occurred in positioning movements di- 
rected away from the body when compared to those 
movements directed toward the body at distances 
of 10 and 40 cm. The relationship was reversed for 
distances of 0.6 and 2.5 cm. This effect is attributed 
to the position of the terminal points with respect 
to the body, since the larger variabilities were asso- 
ciated with the more remotely located points. 
Studies by Weitz {3587 and 3588) 1944 and 
{3589) 1945 indicated that changing the position of 
controls and shape of handlers in transfer tasks had 
the greatest detrimental effect on speed and accu- 
racy of performance. Changing position alone pro- 
duced some loss in performance whereas keeping the 
position of the controls constant but varying the 
shape of the handles showed practically no loss in 
performance. Following learning of control posi- 
tions, changing of these positions was found to have 
detrimental effects on speed and accuracy of per- 
formance. This effect is minimized to a degree when 
the control handles are coded with respect to color 
and shape. For additional papers on design of con- 
trols, reports by the following may be referred to: 
Glutton-Baker {3542) 1951; Kelson {3559) 1949; 
Jenkins {3560) 1947; and Mitchell and Vince 
{3570 and 3571) 1951. 
The human operator is usually included as a 
matter of necessity rather than choice. If the de- 
signer is to include the operator in the design, he 
will require the same sort of information about the 
operator as he does about the other elements. He 
will need to know his operating characteristics and 
limits and his susceptibility to task conditions. 
Craik {3545) 1947 describes the place of the 
operator in control systems. The human operator 
behaves basically as an intermittent correction servo. 
This is evidenced by the periodic or “wavy” nature 
of a time record of tracking errors showing a spec- 
trum with a predominant frequency of about 0.5 
seconds and a smaller cluster of frequencies from 
0.25 to 1.0 second. 
Reference may also be made to a report from 
Tufts College {3584) 1949 on motor responses in- 
volved in control systems. The stimulus which 
evokes motor responses usually involves some type 
of sensory discrimination and this can be either 
visual, auditory, tactual, kinesthetic or combina- 
tions of any of these. The basic factors involved in 
motor responses are reaction time, speed, force, 
and precision. 3532-3558 
SPECIAL PSYCHOLOGICAL AND PSYCHIATRIC PROBLEMS 
A review article by Conrad {3543) 1951 dis- 
cusses the principles involved in skilled behavior. 
It is believed that varying the nature of one motion 
element of a cycle alters the time taken for the re- 
maining element. The visual requirements of a 
task are the predominant factors determining 
optimum conditions. These visual requirements can 
be slightly modified after the task has been become 
a habit because the eyes leave the scene of action 
before the action is completed. 
A number of reports may be consulted on the 
general aspects of the physical and physiological 
characteristics of the human operator acting as a 
transmission unit in the control system. Items by 
the following authors have been selected because of 
their special bearing on this subject; Darcus and 
Maynard {3550) 1951; Elbel {3551) 1945; Fisher 
and Birren {3552) 1945; Gagne and Foster {3555 
and 3556) 1948; Gibbs {3557) 1951; Newman and 
White {3572) 1951; Norris and Spragg {3573 and 
3574) 1950; Paulsen {3576 and 3577) 1935; Tufts 
College {3583 and 3585) 1949; and Weddell and 
Darcus {3586) 1947. 
3532. Barber, J. L. and W. R. Garner. The effect of 
scale numbering on scale-reading accuracy and speed. 
/. exp. Psychol., 1951, 41: 298-309. 
3533. Bartley, S. H. and E. Chute. Personal factors 
in the work situation, pp. 324-340 in: Fatigue and im- 
pairment in man. New York, McGraw-Hill Book Com- 
pany, Inc., 1947, 429 pp. [M] 
3534. Brown, J. S., E. B. Knauft, and G. Rosenbaum. 
The accuracy of positioning reactions as a function of 
their direction and extent. Amer. J. Psychol., 1948, 61: 
167-182. 
3535. Chalmers, E. L., M. Goldstein, and W. E. 
Kappauf. The effect of illumination on dial reading. 
USAF. Wright-Patterson air force base, Dayton, Ohio, 
Aero medical laboratory. Technical rept. no. 6021, 1 
August 1950, 25 pp. [P] 
3536. Channell, R. C. and M. A. Tolcott. The use of 
human engineering data in equipment design problems. 
U. S. Navy. Special devices center, Port Washington, 
New York, Rept. 151-1-16, Project 20-F-2, 20 May 1948, 
31 PP- [D] 
3537. Chapanis, A. Theory and methods for analyzing 
errors in man-machine systems. Ann. N. Y. Acad. Sci., 
1951, 51: 1179-1203. [M] 
3538. Chapanis, A., W. R. Garner, and C. T. Morgan. 
Instrument dials and legibility, pp. 118-156 in: Applied 
experimental psychology, New York, John Wiley & Sons, 
Inc., 1949, 421 pp. 
3539. Chapanis, A., W. R. Garner, and C. T. Morgan. 
Visual displays, pp. 156-189 in: Applied experimental 
psychology, New York, John Wiley & Sons, Inc., 1949, 
421 pp. 
3540. Chapanis, A., W, R. Garner, and C. T. Morgan. 
Controls for human use. pp. 297-330 in: Applied experi- 
mental psychology, New York, John Wiley & Sons, Inc., 
1949, 421 pp. 
3541. Chapanis, A. and M. Leyzorek. Accuracy of 
visual interpolation between scale makers as a function 
of the number assigned to the scale interval. J. exp. 
Psychol., 1950, 40: 655-667, 
3542. Glutton-Baker, J. Some alternative control lever 
arrangements in a compensatory tracking task. Gt. Brit. 
MRC-RNPRC, OES. R. N. P. 51/655, O. E. S. 199, 
July 1951, 11 pp. [P] 
3543. Conrad, R. Study of skill by motion and time 
study and by psychological experiment. Research, 1951, 
4: 353-358. 
3544. Craig, D, R. and D. G. Ellson. The design of 
controls, pp. 133—151 in: A survey report on human factors 
in undersea warfare. Washington, D. C., National Research 
Council, 1949, 541 pp. 
3545. Craik, K. J, W. Theory of the human operator 
in control systems. I. The operator as an engineering 
system. Brit. J. Psychol., 1947, 38: 56-61. 
3546. Craik, K. J, W. Theory of the human operator 
in control systems. II. Man as an element in a control 
system. Brit. J. Psychol., 1948, 38: 142-148. 
3547. Crook, M. N. Printed materials, maps, and charts, 
pp. 61—76 in; A survey report on human factors in under- 
sea warfare. Washington, D. C., National Research Coun- 
cil, 1949, 541 pp. 
3548. Crook, M. N. and F. S. Baxter, Recognition time 
for dial-type numerals as a function of size and brightness. 
USAF. Wright-Patterson air force base, Dayton, Ohio. 
Aero medical laboratory. Technical rept. no. 6465, March 
1951, 26 pp. [P] 
3549. Crook, M. H., G. S. Barker, A. C. Hoffman, and 
J. L. Kennedy. Studies of the effect of typographical 
spacing on the legibility of numerals under vibration. 
USAF. Wright-Patterson air force base, Dayton, Ohio. 
Aero medical laboratory. Technical rept. no. MCREXD- 
694-10, 23 September 1948, 18 pp. [P] 
3550. Darcus, H. D. and G. C. Maynard. The ‘universal’ 
naval seat. Gt. Brit. MRC-RNPRC, OES. R. N. P. 51/ 
660, O. E. S. 201, July 1951, 16 pp. 
3551. Elbel, E. R, Leg strength and leg endurance in 
relation to height, weight, and other body measurements. 
U. S. AAF. Randolph Field, Texas. School of aviation 
medicine. Project 318, Rept. no. 1, 15 August 1945, 26 pp. 
3552. Fisher, M. B. and J. E. Birren. Standardization 
of a test of hand strength. U. S. Navy. NMRI. Project 
X-293, Rept. no. 5, 16 April 1945, 14 pp. [P] 
3553. Fitts, P. M. Psychological aspects of equipment 
design. USAF. Wright-Patterson air force base, Dayton, 
Ohio. Air materiel command, ENG. Technical rept. 5829, 
August 1949, 99 pp. 
3554. Fitts, P. M. Engineering psychology and equip- 
ment design, pp. 1287—1340 in: Handbook of experi- 
mental psychology. Edited by S. S. Stevens, New York, 
John Wiley & Sons, Inc., 1951, 1362 pp. 
3555. Gagne, R. M. and H. Foster. A study of transfer 
in a motor task with varying display-control relationships. 
Connecticut College, Conn. Contract N7onr-316, Task 
Order I, Rept. 316-1-3, 28 April 1948, 29 pp. 
3556. Gagne, R. M. and H. Foster. Transfer to a 
motor skill from practice on a pictured representation. 
Connecticut College, Conn. SDC Project No. 20-M-la, 
Designation no. NR-783—003, Rept. no. 316-1—4, 1 June 
1948, 30 pp. 
3557. Gibbs, C. B. Transfer of training and skill as- 
sumptions in tracking tasks. Quart. J. exp. Psychol., 1951, 
3: 99-110. 
3558. Gleason, J. G. The design of numerals for use in 
counter-type instruments; a review of the literature. Pur- HUMAN FACTORS IN ENGINEERING DESIGN 
3559-3587 
due University. Department of education and applied 
psychology. O. N. R. contract 166-1-39, 20 December 
1947, 24 pp. 
3559. Kelson. H. Design of equipment and optional 
human operation. Amer. J. Psychol., 1949, 62: 473-497. 
3560. Jenkins, W. 0. The discrimination and repro- 
duction of motor adjustments with various types of air- 
craft controls. Amer. J. Psychol., 1947, 60: 397-406. [P] 
3561. Kappauf, W. E. The design and use of instru- 
ments. pp. 77-99 in: A survey on human factors in under- 
sea warfare. Washington, D. C., National Research Coun- 
cil, 1949, 541 pp. 
3562. Kappauf, W. E. Design of instrumental dials for 
maximum legibility. Part V. Origin location, scale break, 
number location, and contrast direction. USAF. Wright- 
Patterson air force base, Dayton, Ohio. Aero medical 
laboratory. Technical rept. 6366, May 1951, 26 pp. 
3563. Kappauf, W. E. Some data on the influence of 
attempted interpolation on the speed and errors of scale 
reading. USAF. Wright-Patterson air force base, Dayton, 
Ohio. Air development center. Technical rept. 6530, May 
1951, 14 pp. 
3564. Lawrence, M. and J. W. Macmillan. Annotated 
bibliography on human factors in engineering design. 
U. S. Navy. BuMed. Project X-651 {Av-340-a), February 
1946, 209 pp. 
3565. Lee, R. H. and E. M. Finch. Instrument lighting 
and low level illumination in submarine conning towers. 
U. S. Navy. NMRI. Project X-380, Rept. no. 1, 17 Jan- 
uary 1945, 7 pp. 
3566. Loucks, R. B. Legibility of aircraft instrument 
dials: The relative legibility of tachometer dials. U. S. 
AAF. Randolph Field, Texas. School of aviation medicine. 
Project 265, Rept. no. 1, 30 May 1944, 12 pp. 
3567. Loucks, R. B. Legibility of aircraft instrument 
dials: A further investigation of the relative legibility of 
tachometer dials. U. S. AAF. Randolph Field, Texas. 
School of aviation medicine. Project 265, Rept. no. 2, 27 
October 1944, 7 pp. 
3568. Loucks, R. B. Legibility of aircraft instrument 
dials: the relative legibility of various climb indicator 
dials and pointers. U. S. AAF. Randolph Field, Texas. 
School of aviation medicine. Project 286, Rept. no. 1, 
25 November 1944, 11 pp. [P] 
3569. Mackworth, N. H. Human problems of work 
design. Nature, Land., 1949,164: 982-984. 
3570. Mitchell, M. J. H. and M. A. Vince. The di- 
rection of movement of machine controls. Gt. Brit. MRC. 
The psychological laboratory, Cambridge. Applied psy- 
chology research unit. A. P. U. 137/50, February 1951. 
[P] 
3571. Mitchell, M. J. H. and M. A. Vince. The di- 
rection of movement of machine controls. Quart. J. exp. 
Psychol, 1951, 3: 24-35. 
3572. Newman, R. W. and R. M. White. Reference 
anthrompometry of army men. U. S. Army. Quartermas- 
ter climatic research laboratory, Lawrence, Mass. En- 
vironmental protection section. Rept. no. 180, September 
1951, 173 pp. 
3573. Norris, E. B. and S. D. S. Spragg. Studies in 
complex coordination. I. Performance on the two-hand 
coordinator as a function of the planes of operation of 
the controls. University of Rochester, Department of 
psychology. SDC Human Engineering Project 20-M-ld, 
Project NR-783-006, Rept. no. 241-6-3, August 1950, 
15 pp. 
3574. Norris, E. B. and S. D. S. Spragg. Studies in 
complex coordination. II. Performance of the two-hand 
coordinator as a function of the relations between direc- 
tion of rotation of controls and direction of movement of 
display. University of Rochester, Department of psychol- 
ogy. SDC Human Engineering Project 20—M—ld, Project 
NR-783-006, Kept. no. 241-6-5, November 1950, 17 pp. 
3575. Partridge, R. C. and D. Y. Solandt. Suggestions 
for rendering asdic trace visible under red illumination. 
Canada NRC. Proceedings of second meeting of associate 
committee on naval medical research. Project C4046, 
7 October 1943, 2 pp. 
3576. Paulsen, G. B. The reliability and consistency 
of individual differences in motor control. /. appl. Psychol., 
1935, 19: 29-42. 
3577. Paulsen, G. B. The reliability and consistency 
of individual differences in motor control. /. appl. Psychol., 
1935, 19: 166-179. 
3578. Poulton, E. C. Two pointer and one pointer 
displays in tracking. Gt. Brit. MRG. The psychological 
laboratory, Cambridge. Applied psychology research unit. 
A. P. U. 142/50, December 1950, 21 pp. 
3579. Saltzman, D. C. and W. R. Garner, Accuracy 
of visual estimation of azimuth position. /. Psychol., 1950, 
29: 453-467. 
3580. Spragg, S. D. S. Dial reading performance as 
related to illumination variables: I. Intensity. USAF. 
Wright-Patterson air force base, Dayton, Ohio. Aero med- 
ical laboratory. Technical rept. MCREXD-694-21, 1 
October 1948, 32 pp. [P] 
3581. Stellar, E. Human factors in panel design, pp. 
153-175 in: A survey report on human factors in under- 
sea warfare. Washington, D. C., National Research 
Council, 1949, 541 pp. 
3582. Tufts College. Human engineering. 3 pp. in: 
Handbook of human engineering data for design engi- 
neers. Tufts College. Institute for applied experimental 
psychology. SDC Human Engineering Project 20-G-l, 
Project Designation NR-783-001, Technical Report 199- 
1-1, 1 December 1949, 410 pp. 
3583. Tufts College. Anthropometries. 8 pp. in: Hand- 
book of human engineering data for design engineers. 
Tufts College. Institute for applied experimental psychol- 
ogy. SDC Human Engineering Project 20-G-l, Project 
Designation NR-783-001, Technical Report 199-1-1, 1 
December 1949, 410 pp. 
3584. Tufts College. Motor responses. 45 pp. in; Hand- 
book of human engineering data for design engineers. 
Tufts College. Institute for applied experimental psychol- 
ogy. SDC Human Engineering Project 20-G-l, Project 
Designation NR-783-001, Technical Report 199-1-1, 
1 December 1949, 410 pp. 
3585. Tufts College. Physiological conditions as deter- 
minants of efficiency. 53 pp. in: Handbook of human 
engineering data for design engineers. Tufts College. In- 
stitute for applied experimental psychology. SDC Human 
Engineering Project 20—G—l, Project Designation NR- 
783-001, Technical Report 199-1—1, 1 December 1949, 
410 pp. 
3586. Weddell, G. and H. D. Darcus. Some anatomical 
problems in naval warfare. Brit. J. industr. Med., 1947, 
4: 77-83. 
3587. Weitz, J. Effect of the shape of handles and 
position of controls on speed and accuracy of perform- 
ance. U. S. AAF. Randolph Field, Texas. School of avia- 
tion medicine. Project 266, Rept. no. 1, 12 June 1944, 
7 pp. 3588-3596 
SPECIAL PSYCHOLOGICAL AND PSYCHIATRIC PROBLEMS 
3588. Weitz, J. Effect of shape and color coding of air- 
plane controls on speed and accuracy of performance. 
U. S. AAF. Randolph Field, Texas. School of aviation 
medicine. Project 336, 23 December 1944, 9 pp. [P] 
3589. Weitz, J. Effect of shape of handles and position 
of controls on speed and accuracy of performance when 
visual cues are restricted. U. S. AAF. Randolph Field, 
Texas. School of aviation medicine. Project 351, Kept. no. 
I, 29 March 1945, 5 pp. [P] 
3590. White, W. J. The effect of pointer design and 
pointer alignment position on the speed and accuracy of 
reading groups of simulated engine instruments. USAF. 
Wright-Patterson air force base, Dayton, Ohio. Aero med- 
ical laboratory. AF Technical rept. no. 6014, July 1951, 
17 pp. 
3591. Wise, H. G., Jr. A survey of current research and 
development on cockpit and instrument panel lighting 
systems by airlines and aircraft manufacturers. USAF. 
Wright-Patterson air force base, Dayton, Ohio. Air mate- 
riel command. Aero medical laboratory. MCREXD-9/ 
HGW/mec, 24 May 1948, 12 pp. 
III. PSYCH0M0T0H RESPONSES 
Of the extensive literature on psychomotor reac- 
tions only a small number of papers have been 
selected. Lewis’ report {3595) on the double-disk 
pursuit apparatus for studying interference in psy- 
chomotor performance may be consulted. Reference 
may also be made to a report by Poulton {3596) 
1950 on anticipation in sensorimotor skills. By an- 
ticipating the time of occurrence of a signal the 
subject can make the appropriate response syn- 
chronously with the signal. A classification of sen- 
sorimotor skills into open and closed types is sug- 
gested by the author, the position of any particular 
skill on this continuum depending upon the degree 
of predictability of the environmental signals. One 
advantage of closed skills is the reduced attention 
which environmental signals require. A second ad- 
vantage, shared by open skills allowing receptor 
anticipation, is that voluntary compensation is sel- 
dom required. In a report on speed and load stress 
in a sensorimotor skill, Conrad {3593) 1951 found 
with all loads an increase in speed of signals gives 
a statistically significant increase not only in the 
absolute number of errors but also in the propor- 
tion of presented signals which are missed. Increas- 
ing the speed 3 times increased the errors at least 
30 times with the 4 dial displays used in the appa- 
ratus with which these studies were carried out. 
Without altering the number of signals per minute, 
doubling the load much more than doubled the 
number of errors of omission. Therefore, the au- 
thor concluded that load alone is an important 
factor in skilled deterioration. Of the responses 
made, the size of errors of timing is not affected by 
the speed of the task. Doubling the load approxi- 
mately doubles the timing error. The subjects were 
never asked to deal with more than two series of 
events although there is no obvious theoretical 
justification for this limit. The author states that 
little is known of psychological functions that un- 
derlie the ability to perceive selectively, to ignore 
some signals, to store others, to combine yet others, 
and to withhold responses until the critical moment. 
Not much is known about the factors that disturb 
the operation of these functions. 
That operation of a pursuit meter represents a 
stressful situation reflected in the lymphocyte re- 
sponse and the output of 17-ketosteroids is indi- 
cated by Hoagland, Elmadjian, and Pincus {3594) 
1946. In these studies, three normal men, three 
normal women, two cooperative, schizophrenic 
patients and one cooperative psychopathic patient 
operated the Hoagland-Werthessen pursuit meter 
breathing a 12 percent oxygen mixture with the 
carbon dioxide absorbed. It was found in the nor- 
mal subjects that the lymphocyte count fell with 
the stress of the experiments, whereas in the case of 
the patients it generally rose with the stress. In the 
normal group, the stress was shown to increase the 
output of 17-ketosteroids as it lowered the lympho- 
cyte count. The patients revealed anomolous 
changes in 17-ketosteroid output. 
In 1944, Brown (3592) discussed the use of psy- 
chomotor tests in the selection of radar operators. 
He pointed out that the principal psychomotor as- 
pect of radar operators’ tasks appears to be the 
ability to memorize and perform several complex 
series of rather precise manual actions. Although 
few of the individual actions are inherently diffi- 
cult, the psychomotor complexity arises from the 
necessity for performing them in the correct order 
with speed and precision. In certain instances the 
actions involve coordinated preceptual judgments 
and clear conceptual standards of what constitutes 
accurate judgment. 
3592. Brown, J. S. Psychological aptitudes involved in 
operating the AN/APS-15 radar equipment. U. S. AAF. 
Randolph Field, Texas. School of aviation medicine. Proj- 
ect 329, 11 December 1944, 6 pp. [P] 
3593. Conrad, B. Speed and load stress in a sensori- 
motor skill. Brit. J. industr. Med., 1951, 8: 1-7. [P] 
3594. Hoagland, H., F. Elmadjian, and G. Pincus. 
Stressful psychomotor performance and adrenal cortical 
function as indicated by the lymphocyte response. /. din. 
Endocr., 1946, 6: 301-311. 
3595. Lewis, D. Devices for studying interference in 
psychomotor performance: III. The double-disk pursuit 
apparatus. State University of Iowa. SDC Human En- 
gineering Project 20-M-l, Project NR-783-002, Kept, 
no. 57-2-13, undated, 18 pp. 
3596. Poulton, E. C. Anticipation in open and closed 
sensorimotor skills. Gt. Brit. MRG. The psychological 
laboratory, Cambridge. Applied psychology research unit. 
A. P. U. 138/50, September 1950, 18 pp. STRESS 
3597-3601 
IV. PSYCHOLOGICAL FACTORS IN 
PERFORMANCE 
It has frequently been observed that under cer- 
tain emergency circumstances combat personnel rise 
above various adverse environmental conditions 
and perform at an unusually high level of com- 
petence, at least for a limited period of time. The 
exact nature of the psychological factors in such 
performance is not known. Mackworth {3599) 
1947 has approached the problem by investigating 
the question as to whether high incentive will enable 
men to surmount difficulties of working in hot and 
humid atmospheres and satisfactorily complete a 
series of tasks. In laboratory experiments he chose 
the task of lifting and lowering a 15 lb. weight by 
bending and straightening the arm in time to a 
metronome. The subject was to continue this task 
until completely exhausted. High incentive was 
provided by letting him have the results as he 
worked and giving a running commentary of en- 
couragement. Powerful incentive failed to delay 
deterioration in physical output when the men 
were working to complete exhaustion in high atmos- 
pheric temperatures. High incentives failed to alter 
the critical level on the room temperature scale 
above which performance began to deteriorate. 
However, the incentive used did greatly raise the 
total output of work. Extra incentives were particu- 
larly effective with the better subjects. The per- 
formance increase was found to be larger when the 
atmospheric temperature was normal than when 
unusually high. 
For other reports on psychological factors in per- 
formance, papers by the following may be con- 
sulted: Cane and Horn {3597) 1951; Gibbs {3598) 
1951; Seashore {3600) 1951; and Vince {3601) 
1948. 
3597. Cane, V. R. and V. Horn. The timing of responses 
to spatial perception questions. Quart. J. exp. Psychol., 
1951, 3: 133-145. 
3598. Gibbs, C. B, Transfer of training and skill assump- 
tions in tracking tasks. Quart. J. exp. Psychol., 1951, 3: 
99-110. 
3599. Mackworth, N. H. High incentives versus hot and 
humid atmospheres in a physical effort task. Brit. J. 
Psychol, 1947, 38: 90-102. [P] 
3600. Seashore, B. H. Work and motor performance, 
pp. 1341—1362 in: Handbook of experimental psychology. 
Edited by S. S. Stevens. New York, John Wiley & Sons, 
Inc., 1951, 1362 pp. [M] [R] 
3601. Yince, M. A. The intermittency of control move- 
ments and the psychological refractory period. Brit. J. 
Psychol, 1948, 38: 149-157. [P] 
V. STRESS 
For a detailed report of the effects of combat 
stress, the important monograph of Grinker and 
Spiegel {3606) 1945 should be considered. These 
authors have differentiated two groups of psycho- 
logical casualties. In the first, minimal stress has 
produced severe symptoms due to previous emo- 
tional disorders which lessen psychological pre- 
paredness. In the second group, severe stress has 
produced symptoms only after long exposure in 
men who are psychologically stable. The authors 
give histories of cases where previous disorders have 
rendered men incapable of withstanding combat 
stress. The authors define operational fatigue as “a 
reactive state in which the ego loses power to con- 
trol intense anxieties and hostilities and to maintain 
functional efficiency”. The symptoms of combat 
fatigue are varied and are classified as free anxiety 
states, phobic states, conversion states, psychoso- 
matic reactions, and depressions. Treatment of com- 
bat reactions in the theaters of operations fell into 
two phases: first, the prevention and early treat- 
ment at the level of the combat group and, second, 
removal of the individual from the combat organ- 
ization for definitive psychiatric care. In the Army 
Air Force the flight surgeon was accorded respon- 
sibility for the first phase while psychiatric con- 
sultants took responsibility for the second. The flight 
surgeon, like the family doctor, bears a heavy re- 
sponsibility for the general welfare of the men. He 
is an important contribution to the success of the 
mission and he must have a thorough understand- 
ing of himself and a familiarity with the problems 
facing his men. Early handling of psychiatric cas- 
ualties involves an attempt to increase insight, to 
neutralize ineffective or crippling methods of deal- 
ing with anxiety, to permit abreaction of anxiety 
and hostility, to modify the superego, to support 
dependent needs, and to estimate the limits of tol- 
erance for anxiety. When these attempts fail prompt 
removal of the individual from the combat group 
becomes necessary. The problem facing the psy- 
chiatrist is a difficult one. He must decide whether 
the patient is able to tolerate further combat stress 
and whether with further psychotherapy he can be 
returned to combat in a short time. If this is not pos- 
sible, it must be decided whether he can carry out 
a new assignment in flying or on the ground. A 
decision may also have to be made whether the 
patient should be returned to the zone of interior for 
prolonged treatment. While the authors have dis- 
cussed these problems from the point of view of 
combat flying, their experience and conclusions 
bear significantly on submarine warfare as well. 
Haggard {3607) 1949 has analyzed those factors 
which determine the effects of stress on the indi- 
vidual, particularly in submarine operations. The 
author stresses the importance of the childhood de- SPECIAL PSYCHOLOGICAL AND PSYCHIATRIC PROBLEMS 
velopment of the individual, his reactions to his 
parents, siblings and others. A necessary aspect of 
military life in general and of submarine operations 
in particular is the relationship between the officers 
and the enlisted men. The officers give commands, 
exert dominance, and look out for the men, who in 
turn take orders and are dependent on the officers. 
Both must be able to assume their proper roles. As 
a rule the greater the emotional stress experienced 
by all members of the submarine group, the more 
they become fused together into a group and the 
more the welfare of the group supersedes that of 
any one individual. Often men who had traumatic 
childhood experiences or histories of neurotic diffi- 
culties did not break down under the stress of battle. 
Haggard stresses that in an emergency where an 
individual’s welfare, safety, and integrative capaci- 
ties are threatened, he mobilizes energy to cope 
with the threat whereby he may escape or, if prop- 
erly directed, will fight effectively. If aggressive 
impulses do not find adequate outlet they express 
themselves in chronic anxiety, fatigue, accident 
proneness, or physical illness. It is difficult and 
enervating to do nothing when one is stimulated to 
activity, as being compelled to submit to depth 
charging without being able to do anything about 
it. As a person becomes progressively adapted to a 
stress situation, he learns that by keeping his head 
he will subject himself to minimal danger and will 
be able to react more effectively than otherwise. 
Realistic training under realistic conditions is a 
necessary procedure in the prevention of psychiatric 
casualties in combat. Breakdown may occur after 
the stress situation is over and may be due to relaxa- 
tion of the person’s defense against aggressive im- 
pulses and a return, in overwhelming intensity, of 
anxiety previously held in check. Emotional stress 
is intensified where cognitive structure is lacking. 
To have been through an experience and to have 
executed duties successfully usually imparts self- 
confidence and enhanced efficiency to a man. 
Motivation is also brought out as a critical factor 
in the individual’s adjustment to emotional stress. 
Undesirable motivations found in unstable, highly 
egocentric individuals stem from the desire to 
escape from something distasteful or to gain status 
and self-respect through short cuts. Emotional 
strain may also result from a conflict of motives. 
Situational conditions may also precipitate collapse 
of the individual’s adjustive mechanisms. For in- 
stance, he may be caught off guard after a series of 
moderate stimuli or by the presentation of stimuli 
which recurred too frequently or for too long to 
permit adequate rest. Strict adherence to a highly 
rigid time schedule or forced delay of a response 
after the signal to act is given or being forced to 
alternate between action and restraint may all be 
factors in breakdown. 
Darrow and Henry [3604) 1949 have given a 
report on the psycho-physiology of stress in sub- 
marine activities. They describe severe physiological 
responses to environmental conditions such as oxy- 
gen deficiency, carbon dioxide excess, high tem- 
perature, odors, etc. They also call attention to 
stresses imposed in the performance of duty in- 
volving fatigue, loss of sleep, and hunger. Emotion 
under stress, as in depth bomb attacks, may result 
in combat fatigue. Finally, factors such as boredom, 
poor morale and so forth may aggravate the other 
effects of stress. The authors describe several means 
of recording and evaluating emotionally-induced 
organic changes which may be symptomatic of 
effects within the central nervous system. These in- 
clude studies of the electromyogram, the galvanic 
skin reaction, blood pressure, heart action, respira- 
tion, blood oxygenation, vasomotor changes in the 
extremities, blood sugar, metabolic activity, endo- 
crine function, electroencephalographic action, etc. 
Performance of psychomotor and other psycho- 
logical tests may be significantly altered under con- 
ditions of stress and experimental studies of such 
alterations have been carried out. An example of 
such studies is that by Vince (3615) 1950 on learn- 
ing and retention of an unexpected control-display 
relationship under stressful conditions. 
A familiarity with the work of Selye is essential 
for an intelligent examination of the responses to 
stress. The following references to Selye’s work are 
given: {3610) 1946,{3611) 1950,and {3612) 1951. 
Apart from many specific defense reactions to stress 
there is an integrated syndrome of closely interre- 
lated adaptive reactions to nonspecific stress itself. 
This has been termed by Selye the “general adapta- 
tion syndrome”. This syndrome may be defined as 
the sum of all nonspecific systemic reactions of the 
body which ensue upon long-continued exposure 
to stress. It evolves in three distinct stages: (1) the 
stage of alarm reaction; (2) the stage of resistance; 
and (3) the stage of exhaustion. The alarm reaction 
is the sum of all known specific systemic phenomena 
elicited by sudden exposure to stimuli to which the 
organism is quantitatively or qualitatively not 
adapted. Sometimes two phases of the alarm re- 
action appear: (a) shock and (b) counter-shock. 
Most of the characteristic manifestations of the 
alarm reaction disappear or are actually reversed 
during the second stage—that of resistance. How- 
ever, even a highly adapted organism cannot in- 
definitely maintain itself at the stage of resistance. 
If exposure to abnormal conditions continues the STRESS 
adaptation fails and manifestations characteristic 
of the alarm reaction reappear and the stage of 
exhaustion develops. The references cited contain 
discussions of the various theories which have been 
advanced to explain the various stages of the gen- 
eral adaptation syndrome. The general adaptation 
syndrome never occurs in its pure form but is always 
complicated and modified by superimposed specific 
actions of eliciting stressors. 
There is a considerable volume of literature on 
the effects of stress and emotional reactions upon 
heart rate, breathing, and arterial blood pressure. 
It appears that the cardiovascular responses in ques- 
tion vary in character, intensity, and duration ac- 
cording to the characteristics of the stressing sit- 
uation and the personality structure of the individ- 
ual. Two earlier papers on this subject are those 
of Landis and Gulette {3608) 1925 and Skaggs 
{3613) 1926. 
Alterations in colonic function are well known 
to occur in human beings under stress and a recent 
report on this subject is that of Almy, Abbot, and 
Hinkle {3602) 1950. These authors made continu- 
ous kymographic records of the motility of the sig- 
moid colon in 18 patients suffering from “irritable 
colon.” The symptoms tended to be worse during 
emotional conflicts. In general, it was found that a 
sudden reduction in tone and motility occurred 
when the patient’s mood was one of inadequacy, 
self-reproach, and hopelessness. Often at such times 
weeping occurred. 
It is known that stress produces an increase in 
the output of those urinary constitutents particu- 
larly representative of adrenal cortical activity. 
Associated with this response is a decrease in the 
eosinophile profile. Pincus in 1950 {3609) reported 
that responsiveness to stress may not be impaired in 
men surviving to old age without ill health or 
infirmity and that in these subjects the pituitary- 
adrenal mechanism involved in the response to 
acute stress may be relatively intact. Domanski, 
Swan, Wells, and Hughes {3605) 1951 have in- 
vestigated the existence and character of the rela- 
tionship between the eosinophile response and 
selected forms of exercise applied to normal human 
subjects with the aim of facilitating subsequent 
design of test stresses. The subjects were nine 
healthy males from 19 to 37 years of age. For the 
most part submaximal exercise was employed. This 
consisted of walking on a treadmill at a constant 
velocity of 3*/a miles an hour with progressively in- 
creased elevation of the treadmill for 12 minutes or 
until attainment of a pulse rate of 180 per minute. 
Using the same technique, 6 subjects also walked 
to exhaustion. Exercise was not invariably asso- 
ciated with the negative eosinophile profile and the 
magnitude of the eosinophile response was different 
for different individuals. With exhaustive exercise 
in only 2 of 6 subjects was there any decrease in 
eosinophile profile as compared with exercise to a 
pulse of 180. In general, the rise in pulse rate fol- 
lowed a similar pattern in all 3 tests. Increase in 
duration of treadmill exercise accentuated the simi- 
larity, with pulse rate data for the exhaustion test 
being a near extension of the 180 pulse rate test 
findings. The exercise employed emerges as a rela- 
tively uncomplicated form of stress. Such stress of 
itself probably does not provoke a major emotional 
response. 
In an attempt to use the urinary excretion of 17- 
and 20-ketosteroids as a measurement of stress, 
Stern {3614) 1949 measured the output of these 
substances during 6- or 7-hour flights. The output 
of 17-ketosteroids was increased on the average 
to an extent which could be judged to be just 
significant. 
A somewhat similar study was carried out in 
1950 by Cook and Wherry (3603). In this investi- 
gation the urinary 17-ketosteroid output of enlisted 
candidates for submarine service was measured dur- 
ing two stressful situations. One hundred and 
twenty subjects selected at random from the general 
group of enlisted candidates undergoing routine 
processing for submarine school were chosen. Two 
groups of 6 subjects each were tested during an 
intensive 3-day experimental period. The psycholog- 
ical stress situation consisted of administering the 
short group form of the Minnesota multiphasic 
personality inventory and the officers classification 
test. Finishing times were repeatedly stressed. The 
tank stress situation consisted of 2 escapes for each 
man from the training bell at 12 feet and 2 escapes 
from each of the 18- and 50-foot locks. Urine sam- 
ples were taken on rising in the morning, 15 minutes 
before the stress, 15 minutes after the stress, and 2 
hours after the stress ended. The output of andro- 
gens was positively related to the general level of 
17-ketosteroid output and negatively related to age. 
The 17-ketosteroid output of subjects increased 
significantly over basal samples during both types 
of stressful situations. A greater output was evi- 
denced during the tank stress than during the 
psychological stress situation. The amount of 17- 
ketosteroid increase during stress was considered by 
the authors a reliable measure of individual 
differences. 
3602. Almy, T. P., F. K. Abbot, and L. E. Hinkle. Al- 
ternations in colonic function in man under stress. IV. 
Hypomotility of the sigmoid colon, and its relationship 
291222—54 22 3603-3615 
SPECIAL PSYCHOLOGICAL AND PSYCHIATRIC PROBLEMS 
to the mechanism of functional diarrhea. Gastroenterology, 
1950, 15: 95-103. Abstr. World Med., 1950, 8: 542. 
3603. Cook, E. B. and R. J. Wherry. The urinary 17- 
ketosteroid output of naval submarine enlisted candidates 
during two stressful situations. Hum. Biol., 1950, 22: 104— 
124. [P] 
3604. Darrow, C. W. and C. E. Henry. Psychophysiol- 
ogy of stress, pp. 417—439 in: A survey report on human 
factors in undersea warfare. Washington, D. C., National 
Research Council, 1949, 541 pp. 
3605. Domanski, T. J., A. G. Swan, J. G. Wells, and 
L. B. Hughes. Physiological relationships in human stress 
response. I. Eosinophil response to muscular activity. 
USAF. Randolph Field, Texas. School of aviation medi- 
cine. Project 21-32-025, Kept. no. I, October 1951, 
13 pp. 
3606. Grinker, R. R. and J. P. Spiegel. Men under 
stress. Blakiston. Philadelphia, 1945, 484 pp. 
3607. Haggard, E. A, Psychological causes and results 
of stress, pp. 441-461 in: A survey report on human fac- 
tors in undersea warfare. Washington, D. C., National 
Research Council, 1949, 541 pp. 
3608. Landis, C. and R. Gullette. Studies of emotional 
reactions. III. Systolic blood pressure and inspiration- 
expiration ratios. /. comp. Psychol., 1925, 5: 221-252. 
3609. Pincus, 6. Measures of stress responsivity in 
younger and older men. Psychosom. Med., 1950, 12: 225- 
228. 
3610. Selye, H. The general adaptation syndrome and 
the diseases of adaption. /. din. Endocr., 1946, 6: 117— 
196. [R] 
3611. Selye, H. The physiology and pathology of ex- 
posure to stress. Montreal, Acta Incorporated, 1950, 822 
pp. 
3612. Selye, H. Annual report on stress. Montreal, Acta, 
Incorporated, 1951, 644 pp. 
3613. Skaggs, E. B. Changes in pulse, breathing and 
steadiness under conditions of startledness and excited 
expectancy. J. comp. Psychol., 1926, 6: 303-317. [P] 
3614. Stern, M. I. The determination of urinary total 
neutral 17 and 20 ketosteroids in “Stress.” Gt. Brit. FPRC. 
F. P. R. C. rept. no. 719, July 1949, 11 pp. [P] 
3615. Vince, M. A. Learning and retention of an “un- 
expected” control-display relationship under stress con- 
ditions. Gt. Brit. MRG-APU. The psychological labora- 
tory, Cambridge. A. P. U. 125/50, August 1950, 8 pp. 
VI. FATIGUE 
For general references on the subject of fatigue, 
papers by the following may be consulted: Ash 
{3616) 1914; Chapinis, Garner, and Morgan 
{3622) 1949; Katzell {3627) 1950; Laird {3628) 
1948; Sayers {3633) 1942; and Smith {3635) 
1916. Of these references the reports by Ash {3616) 
1914 and Smith {3635) 1916 constitute early 
studies. The former is an excellent discussion of the 
general subject in both its somatic and psychological 
aspects. There is a good bibliography. Katzell 
{3627) 1950 has pointed out that fatigue is a com- 
plex psycho-physiological condition presenting at 
least three aspects: (1) a decline in the quantity 
and quality of production for a given amount of 
effort; (2) feelings of strain, irritation, and un- 
pleasantness; and (3) a disturbed physiological 
state characterized by acceleration of catabolic 
processes and an accumulation of toxins and other 
chemical products of these catabolic processes. 
Changes in motivation also complicate the analysis 
and control of fatigue. Work decrement studies 
show that work output improves during the early 
stages of any segment of work. The production 
reaches a peak and later declines. As fatigue super- 
venes, effort may cause increased pulse rate, rise 
of blood pressure, alterations in differential white 
blood count, changes in blood sugar level, blood 
lactic acid level, oxygen consumption, etc. Al- 
though no precise physiological criteria of fatigue 
have been clearly established, measurements of 
physiological changes do reflect strain and have a 
value in attempting to identify work methods least 
taxing to workers. Feelings of strain usually develop 
earlier than decline in quantity and quality of pro- 
duction. Boredom is sometimes confused with 
fatigue but is to be differentiated from it in its 
subjective and objective characteristics. In boredom 
there is a desire for change rather than for rest. 
The work curve is irregular. Boredom may be re- 
lieved by variation of work methods, rotation of 
duties, and broadening the scope of the job. Fatigue 
may be reduced by steps to minimize its occurrence 
and provision for its dissolution after it appears. 
These steps include rest, shortening of long work 
periods, improving the pace of work, improving 
technique and equipment, controlling environ- 
mental factors such as noise, vibration, illumination, 
and atmospheric conditions, and improving per- 
sonal factors such as clothing, rest and sleep habits, 
diet, drugs, and emotional state. 
Sayers {3633) 1942 has pointed out that psycho- 
logical and environmental factors are more im- 
portant causes of fatigue than are physiological 
factors. He distinguishes 2 types of fatigue; (1) 
fatigue originating in the central nervous system 
and (2) fatigue originating partly in the central 
nervous system and partly in active muscles. Re- 
garding the factor of effect on muscles in fatigue, 
the author considers that muscles are probably not 
injured directly by overwork under usual conditions. 
Two papers on fatigue associated with visual per- 
formance may be consulted. The first of these by 
Simonson, Brozek, and Keys {3634) 1947 presents 
a laboratory study of visual fatigue. The second by 
Mackworth {3631) 1948 is a quantitative investi- 
gation of the breakdown of vigilance during pro- 
longed visual search under laboratory conditions. 
The experimental situation was developed for the 
automatic presentation of occasional, brief, and 
barely visible signals throughout long watchkeeping FATIGUE 
periods, the stimuli being given at irregular inter- 
vals. It was found that the efficiency of the subject 
during a 2-hour spell was definitely lower after the 
subject had been watching for about half an hour. 
During a 1-hour spell there was the same ad- 
vantage in favor of the first half-hour. A half-hour 
rest period following a half-hour watch allowed a 
further one-half-hour spell with no detrimental 
effect on accuracy. Even a sudden, short telephone 
message in the middle of a 2-hour watch gave a 
temporary improvement. 
Bast and co-workers have reported a series of ex- 
perimental exhaustion due to lack of sleep and 
have examined the effects of such fatigue upon 
nerve cells in the spinal cord and medulla oblongata. 
In these studies, rabbits were prevented from going 
to sleep by being rotated in cylindrical cages. This 
rotation forced the animals to change their position 
about 8 times a minute. The animals were kept 
awake continually until exhaustion supervened. 
(Bast and Loevenhart (3618) 1927). Bast, Schacht, 
and Vanderkamp (3619) 1927 reported chroma- 
tolysis with vacuolation of the cytoplasm, particu- 
larly in the zone midway between the cell wall 
and the nucleus. Bast and Bloemendal (3717) 1927 
found chromatolytic cells constantly in the reticular 
formation, and other nuclei of the medulla. The 
Nissl substance was granular and the cytoplasm was 
vacuolar. The nuclei of the cells were stained deeply 
but there was no migration of the nucleus. Cells of 
the hypoglossal nucleus showed no chromatolysis or 
other changes as a result of exhaustion by loss of 
sleep and this was true for all motor nerve cells 
supplying somatic musculature. 
The fatigue of standing has been studied by Lar- 
sen (3629) 1948. In 17 observations on 12 healthy, 
young women the height of the center of gravity 
was lowered by an average of 0.216 percent of the 
body height as a result of 15 minutes of natural 
standing. In 21 observations on 17 similar young 
women, static effort produced a similar fall of 0.253 
percent. It was suggested by the author that stance 
fatigue has its origin in excessive generation of nerve 
impulses brought about by repetitive stimulation of 
the antigravity musculature and by subacute cere- 
bral hypoxia arising from the circulatory dis- 
turbance. 
Circulatory changes are a part of the physiological 
pattern characteristic of fatigue. Leake, Grab, and 
Senn (3630) 1927 reported in rabbits fatigued to 
the point of collapse by deprivation of sleep that 
there was a fall in body temperature and a rise in 
pulse rate above normal followed by marked fall. 
There was a gradual fall in the respiratory rate. 
In studies reported by Bjerner (3621) 1950 normal 
human subjects responded to a reaction time test. 
Sleep deprivation was associated with poor per- 
formance and it was found that the poorest per- 
formance in the test, which usually occurred at 
0400 to 0600, was associated with a transient fall in 
pulse rate as well as a depression of alpha activity 
of the electroencephalogram. In four out of the five 
subjects there was evidence of diurnal variation in 
the alpha frequency, the lowest rate coinciding with 
a tendency to a high percentage of error in responses 
to auditory stimuli. Hinrichs (3623) 1951 has re- 
ported hematological changes before and after 
fatiguing exercise in 87 athletes. Following the exer- 
cise there was a significant decrease in the percent- 
age of polymorphonuclear leukocytes in 67 percent 
of the subjects and a significant increase in the per- 
centage of lymphocytes in 70 percent. There was 
also a slight, but significant increase in the average 
number of nuclear lobes of the polymorphonuclear 
cells. 
Watkins, Copp, Finesinger, Brazier, Shands, and 
Pincus (3636) 1948 conducted psychiatric and 
physiological studies of fatigue in psychoneurotic 
patients who complained of feelings of tiredness, 
weariness, or lassitude. Guilt and rejection situa- 
tions precipitated fatigue episodes. Using a standard 
braking resistance on a bicycle ergometer for 3 
minutes at 37 rotations per minute for men and 30 
rotations per minute for women, the patients com- 
pared with normal controls showed significant in- 
creases in blood lactate and pyruvate, heart and 
ventilation rate, but no change in blood cholin- 
esterase or in the electroencephalogram. A one- 
minute grip test on a spring dynamometer with ten- 
sions of 20 kg. for men and 15 kg. for women also 
gave significant increases in lactic acid production. 
Stimulation of the ulnar nerve for 4 minutes by 
unidirectional square wave impulses gave from 100 
to 120 percent rise in blood lactate and pyruvate 
in both patients and controls, but no change in blood 
cholinesterase. Two-thirds of the patients reacted 
to stress situations by a drop in the lymphocyte 
count and an increase in uric acid in the urine, but 
not in the blood. The authors attributed this to an 
increased production of cortical steroids. Accord- 
ing to Bast, Supernaw, Lieberman, and Munro 
(3620) 1928 exhaustion due to lack of sleep in ani- 
mals resulted in vacuolation of the cytoplasm with 
pyknotic nuclei in the cells of the adrenal glands. 
Scattered patches of eosinophile cells were found 
in the adrenal cortical sinuses in 36 percent of the 
rabbits. There was marked congestion of the cortical 
sinuses and the vessels of the medulla with colloid- 
like material and cellular debris. 3616-3637 
SPECIAL PSYCHOLOGICAL AND PSYCHIATRIC PROBLEMS 
Ivy and Seashore (3626) have reported on the 
effects of analeptic drugs in relieving fatigue from 
prolonged military activity. A volunteer group of 
two officers and 14 men participated in 18 to 20 
mile hikes with 20 pounds of equipment followed 
by all-night guard duty without relief. Caffein, ben- 
zedrine, and desoxyephedrinc had measurable 
effects of relieving fatigue as demonstrated by vari- 
ous means including a visual flicker fusion test. 
Speed of visual discrimination reaction time was 
slightly, but reliably improved by all 3 drugs. Hand- 
arm sway was improved slightly by caffein and mod- 
erately by benzedrine and desoxyephedrinc. Of all 
the 3 drugs the best all-round results were obtained 
from benzedrine. Caffein produced desirable sub- 
jective improvements but with little improvement 
in motor performance. Desoxyephedrinc resulted in 
little change in subjective reports, but improve- 
ments in motor performance were as good as or 
slightly better than for benzedrine. 
For further studies on fatigue, papers by the 
following authors should be consulted; Holling- 
worth {3624) 1914; Ishizuka {3625) 1951; Ota 
{3632) 1950; and Welford and Brown {3637) 1951. 
3616. Ash, I, E, Fatigue and its effects upon control. 
Arch. Psychol, 1914,31: 1-61. [D] 
3617. Bast, T. H. and W. B. Bloemendal. Studies in 
experimental exhaustion due to lack of sleep. IV. Effect 
on the nerve cells in the medulla. Amer. J. Physiol, 1927, 
82: 140-146.[P] 
3618. Bast, T. H. and A. S. Loevenhart. Studies in 
exhaustion due to lack of sleep. I. Introduction and 
methods. Amer. J. Physiol, 1927, 82: 121-126. [P] 
3619. Bast, T. H., F. Schacht, and H. Venderkamp. 
Studies in experimental exhaustion due to lack of sleep. 
III. Effect on the nerve cells of the spinal cord. Amer. J. 
Physiol, 1927, 82: 131-139. [P] 
3620. Bast, T. H., Supernaw, J, S., B. Lieherman, and 
J. Munro. Studies in exhaustion due to lack of sleep. 
V. Effect on the thyroid and adrenal glands with special 
reference to mitochondria. Amer. J. Physiol, 1928, 85: 
135-140. 
3621. Bjerner, H. Alpha depression and lowered pulse 
rate during delayed actions in a serial reaction test. A 
study in sleep deprivation. Acta physiol, scand., 1949, 19: 
5-93. Excerpta Medica. Section II. (Physiology, Bio- 
chemistry, and Pharmacology). 1950, 3: 941. 
3622. Chapanis, A., W. R. Garner, and C. T. Morgan. 
Working and resting, pp. 365—392 in: Applied experi- 
mental psychology. New York, John Wiley & Sons, Inc. 
1949, 421 pp. 
3623. Hinrichs, M. A. Further studies on some effects 
of physical fatigue on the peripheral circulation of ath- 
letes. Res. Quart. Amer. Phys. Educ. Ass., 1950, 21: 
175-181. Excerpta Medica. Section II. (Physiology, Bio- 
chemistry, and Pharmacology), 1951, 4: 768. Abstr. 
3624. Hollingworth, H. L. Variations in efficiency dur- 
ing the working day.. Psychol Rev., 1914, 21: 473-491. 
3625. Ishizuka, T. On the relation between the fatigue; 
measured by flicker-test and the quantity of labour; 
counted by step-counter. Osaka Univ. med. J., 1951, 3: 
(Japanese text pagination) 217-222; (In Japanese with 
English summary) 217. 
3626. Ivy, A. C. and R. H. Seashore. Effects of analeptic 
drugs in relieving fatigue from prolonged military activity. 
U. S. OSRD-NDRG. O. E. M. cmr. 46, M. R. P. D. 
project 26, no date, 4 pp. [P] 
3627. Katzell, R. A. Fatigue and its alleviation, pp. 
74-84 in: Handbook of applied psychology. Volume I. 
Edited by Douglas H. Fryer and Edwin R. Henry. New 
York, Rinehart and Company, Inc., 1950, ix, 380 pp. [R] 
3628. Laird, D. A. Work and fatigue, pp. 738 (l)-738 
(6) in Oxford Medicine. Volume I, Part II. Edited by 
H. A. Christian. New York, Oxford University Press, 1948. 
3629. Larsen, E. M. The fatigue of standing. Amer. J. 
Physiol., 1947, 150: 109-121. Excerpta Medica. (Section 
II. Physiology, Biochemistry and Pharmacology), 1948, 
I: 182. Abstr. 
3630. Leake, C., J. A. Grab, and M. J. Senn. Studies in 
exhaustion due to lack of sleep. II, Symptomatology in 
rabbits. Amer. J. Physiol., 1927, 82: 127-130. [M] 
3631. Mackworth, N. H. The breakdown of vigilance 
during prolonged visual search. Quart. J. exp. Psychol., 
1948, 1: 6-21. 
3632. Ota, H, On the changes of nervous function in 
fatigue. Hukuoka Acta med., 1950, 41 (6): (English text 
pagination) 63. (In Japanese with English summary). 
3633. Sayers, R. R. Major studies of fatigue. War Med., 
Chicago, 1942, 2: 786-823. 
3634. Simonson, E., J. Brozek, and A. Keys. Visual 
fatigue. Fed. Proc. Amer. exp. Biol., 1947, 6: 202. 
3635. Smith, M. A contribution to the study of fatigue. 
Brit. J. Psychol, 1916, 8: 327-350. 
3636. Watkins, A. L., S. Cobb, J. E. Einesinger, 
M. A, B. Brazier, H. C. Shands, and G. Pincus. Psychiatric 
and physiologic studies on fatigue. Preliminary report. 
Arch. phys. Med., 1947, 28: 199-206. Excerpta Medica. 
(Section II. Physiology, Biochemistry and Pharmacology), 
1948, /; 183. Abstr. 
3637. Welford, A. T. and R. A. Brown. Two experi- 
ments on fatigue as affecting skilled performance in ci- 
vilian air crew. Brit. J. Psychol, 1950, 40: 195-211. Ex- 
cerpta Medica. (Section II. Physiology, Biochemistry, and 
Pharmacology), 1951, 4: 840. 
VII. MORALE 
It has been universal experience that good morale 
in a competent group is essential to fighting effec- 
tiveness. However, it is not easy to define exactly 
the components which make for good or bad morale 
or to say precisely what are the factors valuable in 
maintaining morale. The latter question has been 
discussed by Bassan {3638) 1947. This report tells 
of conditions existing aboard “The Sullivan” dur- 
ing 12 months of active war operation in the Pacific 
area and shows how care and foresight made a 
happy ship with no morale breakdown during the 
period. The men received long and careful indoc- 
trination training during the fitting out and shake- 
down period. Each cruise lasted about 30 days dur- 
ing which time the crew was divided into three 
sections. Each section stood the same watch during 
the cruise. They could thus become familiar with SLEEP-WAKEFULNESS 
3638-3640 
their routine. Care was given to planning tasty 
meals and the men were told of their mission and 
destination and felt their part and responsibility in 
the operation. News was given the men as soon as 
possible and they were provided with music, books, 
movies, and whenever possible, athletic sports. 
Shore parties were made possible whenever condi- 
tions permitted. Medical care was provided as 
needed. The author considered none of the factors 
mentioned could be thought of singly as the thing 
that kept the men going. Above and beyond any 
one single factor, there was an intangible element 
that seemed to produce harmonious interpersonal 
relationships between the officers themselves, the 
officers and men, and among the men themselves. 
Leadership appears to be one of the significant 
factors in morale. French has discussed this in a 
paper {3639) published in 1949. He discusses vari- 
ous methods of appraising morale or group effec- 
tiveness, involving use of questionnaires, observa- 
tion and interview methods, sociometric procedures, 
projective techniques, group indices, and situation 
tests. The author considers it a pertinent question 
as to whether a group functions better if it is com- 
posed of individuals of similar or dissimilar charac- 
teristics. He states that mutual selection of members 
often works for better adjustment of the group. 
Satisfaction with job assignment is considered per- 
haps the single most important factor in morale. 
Length of time spent in an assignment or locality is 
often important. Since the manipulation of varia- 
bles related to morale is primarily the responsibility 
of appointed leaders, the factor of leadership as- 
sumes central significance in the quality of morale. 
A large share of research on this problem of leader- 
ship and morale has been dominated by the con- 
cept of leadership as a personality trait in the leader. 
A newer concept now developing views leadership 
as a process of interaction between individuals in 
which the characteristics of the leader are impor- 
tant only in relation to the situation, that is to say, 
the goals and other characteristics of the group and 
relevant external circumstances. The author con- 
siders intensive analysis of leader-follower inter- 
action essential to intelligent research in selection 
and training of leaders. 
Insight into problems of morale and leadership 
in German submarines has been given by Lueth 
{3640) 1947. This author considers that morale 
of the crew depends upon discipline, success of 
operation, well organized daily routine, example 
and correct attitude of officers, and real spiritual 
leadership for the men together with a genuine con- 
cern for their personal welfare. In this paper a 
description is given of various procedures instituted 
for the comfort of the crew, including music, books, 
etc. It appears that the discipline was stern with 
authoritarian control over even quite minute ele- 
ments of personal conduct. 
With new and more rigorous conditions of oper- 
ation inevitably to be imposed by modern warfare 
and new type submarines it is imperative that the 
problem of morale be constantly reevaluated. It is 
likely in the future that good morale will play an 
even more important part than in the past in the 
success of patrols. 
3638. Bassan, M. E. Some factors found valuable in 
maintaining morale on a small combatant ship. Bull. 
Menninger Clin., 1947,11: 33-42. 
3639. French, R. L. Morale and leadership, pp. 463- 
488 in: A survey report on human factors in undersea 
warfare. Washington, D. C., National Research Council, 
1949, 541 pp. 
3640. Lueth, W. Problems of leadership in a submarine. 
A lecture by a German submarine commander, 17 Decem- 
ber 1943. U. S. Navy. ONI. Kept. no. 11746, 1947, 15 pp. 
VIII. SLEEP-WAKEFULNESS 
For papers on the general subject of sleep, reports 
by the following authors should be consulted: Bart- 
ley and Chute {3646) 1947; Endres and von Frey 
{3651) 1930; Gillespie {3656) 1929; Hess {3658) 
1949; Johnson and Swan {3662) 1930; Kayser 
{3663) 1949; Pieron {3685) 1913; and Ranson 
{3687) 1934. 
Much has been written on the mechanisms of 
sleep. The following significant references to theo- 
ries of sleep should be consulted: Atkinson {3642 
and 3643) 1947; Drogendijk {3649) 1949; Ivy and 
Schnedorf {3661) 1937; Learoyd {3677) 1950; 
Pavlov {3683 and 3684) 1927; Singh and Singh 
{3694) 1946; and Stern, Marijan, and Eisen 
{3696) 1950. Sleep is envisiged as a process of in- 
ternal inhibition {3683, 3684, and 3694). It is gov- 
erned by the central nervous system and both the 
cortical and sub-cortical mechanisms are involved 
in the process {3642 and 3643). The source of the 
central nervous inhibition may be a chemical sub- 
stance—a “fatigue fluid” or “hypnotoxin” {3649 
and 3661). Stern, Marija, and Eisen {3696) 1950 
have reported experimental studies on the role of 
calcium in the activation of the cholinergic system 
during sleep. Animals treated with hypnotic doses of 
medinal after calcium had been removed with sodi- 
um oxalate fell asleep after a longer interval than 
controls. Rats and rabbits in which calcium had been 
removed by sodium oxalate showed a decreased 
cholinesterase activity in the hypothalamus while 
the cholinesterase in the cortex did not change. Ad- 
ditional small amounts of calcium chloride restored 
the cholinesterase activity to almost normal rate. SPECIAL PSYCHOLOGICAL AND PSYCHIATRIC PROBLEMS 
Clinical as well as experimental investigations of 
cerebral localization of the sleep mechanism have 
implicated various nuclei in the diencephalon and 
mesencephalon as well as higher centers. Papers by 
the following may be consulted on this subject: von 
Economo {3650) 1930; Harrison ( 3657) 1940; 
Manceau and Jorda {3678) 1948; Ranstrom 
{3688) 1947; Rowe {3692) 1935; and Scrota 
{3693) 1939. According to von Economo {3650) 
1930 the sleep center has its location in the area 
of the brain affected by encephalitis lethargica. Von 
Economo conceived that the virus of encephalitis 
has an affinity for the sleep center and that the 
action of sleep-regulating center probably consists 
in a coordination of the changes in vegetative and 
psychic functions which occur in sleep. According 
to von Economo, normal sleep may be considered as 
an inhibitory action brought about by the center 
of sleep regulation acting upon the cerebral cortex 
and thalamus. Circulating toxins may set the sleep 
center into action. 
Rowe {3692) 1935 concluded from a survey of 
the literature that evidence favoring localization of 
the sleep mechanism in the diencephalon is incon- 
clusive and not entirely satisfactory. On the basis 
of cases studies he suggested that disturbances of 
sleep result from lesions of a rather diffuse, central 
correlating mechanism involving the thalamus, hy- 
pothalamus, and mesencephalon. A correlation be- 
tween hypothalamic activity and sleeping and 
waking states has been experimentally determined 
in cats by Serota {3693) 1939. This author found 
by direct measurements that the hypothalamus was 
warmer than the cortex. This was true in uncon- 
scious, anesthetized animals and it was found that 
the absolute temperature fluctuated during the 
waking state, sometimes in a rhythmic manner. 
The positive temperature difference between the 
hypothalamus and the cortex was found to increase 
in an irregular fashion with activity. Emotional 
state, such as fear, rage, or anticipation of food, 
increased the relative temperature of the hypo- 
thalamus. Sleep decreased the hypothalamic tem- 
perature and stabilized it. On awakening, the hypo- 
thalamic temperature rose earlier and higher than 
that of the cortex, caudate nucleus of Ammon’s 
horn. The specific temperature decrease of the 
hypothalamus in sleep was shown to be due to 
lowered cell metabolism rather than to a marked 
change in hypothalamic blood flow. This indicated 
to the author that sleep is associated with decreased 
rather than increased activity of the hypothalamic 
sleep center. 
An attempt to produce sleep by diencephalic 
stimulation was reported by Harrison {3657) in 
1940. This author applied destructive and stimu- 
lating electric currents to the hypothalamus, thal- 
amus, head of the caudate nucleus, septum pellu- 
cidum, and the region of the anterior commissure 
in waking cats. Somnolence was produced by de- 
structive action of currents when applied to the 
lateral hypothalamic area. Catalepsy tended to 
develop when lesions involved the medial and 
posterior part of the hypothalamus. Somnolence was 
produced by destructive electric currents applied to 
the lateral group of thalamic nuclei, but the strength 
and duration of these currents was much greater 
than in the hypothalamic experiments. Extensive 
lesions of the head of the caudate nucleus did not 
produce somnolence. The author considers that his 
experiments offer no evidence to support the theory 
that sleep is a phenomenon of active inhibition. 
In a report published in 1947, Ranstrom (3688) 
points out that the literature on the physiology and 
pathology of sleep infers that the regulation set up 
for sleep-wakefulness must exist within the posterior 
part of the hypothalamus. In the author’s experi- 
ments, electrolytic lesions placed by an X-ray 
stereotaxic method within the posterior part of the 
hypothalamus of cats produced sleep of some days 
duration. The period of sleep set in after an interval 
of some hours following the operation and not im- 
mediately after placing the lesion. The sleep effect 
was presumably brought about by substances 
liberated by necrosis. The author considers that 
these are not nonspecific products of necrosis but 
substances which occur performed in this part of 
the brain. Lesions in the posterior part of the hypo- 
thalamus of rabbits brought about no sleep effects 
and it was presumed that rabbits lack a regulatory 
center for sleep in this area. Histological character- 
istics of neurones in the hypothalamic region sug- 
gested to the author that cells of this part of the 
brain are capable of secretory function. Sleepiness 
produced experimentally by electrolytic lesions in 
the hypothalamus was considered to be brought 
about by liberation of hormonal substances from the 
neurones themselves. 
A number of papers have been written on the 
physiological and biochemical changes occurring 
during sleep. Richter and Dawson (3690) 1948 
found that the lactic acid content of the rat brain 
was reduced in sleep and increased in emotional 
excitement. The rise in lactic acid content in the 
brain during emotion was not due to concomitant 
muscular activity since the effect was still observed 
in animals immobilized by d-tubocurarine. The 
onset and termination of sleep is not accompanied 
by significant change in blood flow through the 
brain according to Gibbs, Gibbs, and Lennoux SLEEP-WAKEFULNESS 
{3655) 1935. According to Barker and Burgwin 
{3645) 1950 much misunderstanding is produced 
by trying to identify the hypnotic state with sleep. 
The hypnotic trance leaves the alpha rhythm un- 
changed except for short periods following sugges- 
tions or instructions. However, when true sleep is 
induced by hypnosis the sleep patterns are those 
observed as in natural sleep. Euziere, Passouant- 
Fontaine, Passouant, and Latour {3652) 1950 have 
carried out electrocardiographic studies of spon- 
taneous sleep and sleep provoked by pentothal in 
neurological patients. On the basis of 30 tracings 
of spontaneous sleep and 70 tracings of sleep pro- 
duced by pentothal obtained from patients with 
encephalitis, epilepsy, cerebral atrophy, and tu- 
mours, it was concluded that in diffuse brain 
lesions there is a decrease in the number of transi- 
tory stages between sleep and wakefulness. In local- 
ized brain lesions there is a dissimilarity in the 
EEG tracings from different regions. In epilepsy 
characteristic bursts may appear in wakefulness, 
normal sleep, induced sleep, and semi-sleep, but 
particularly in the frontal region. According to the 
authors the frontal lobe may be the last link between 
the cortex and the subcortical regions to disappear 
during sleep and the first to reappear as a result of 
external stimulation. Regarding the effect of sleep 
on cerebrospinal fluid circulation, Cans {3654) 
1950 has offered the hypothesis that sleep influences 
the flow of the cerebrospinal fluid so that it passes 
from the ventricles to the subarachnoid spaces en- 
tirely or partly by a transcerebral route, bringing 
nourishment to, and removing waste products from 
the brain cells. For studies on the effects of sleep 
on metabolism papers by the following may be con- 
sulted: Banche {3644) 1950; Collip {3647) 1920; 
Frommel, Beck, Favre, and Vallette {3653) 1947; 
and Mason and Benedict {3679) 1934. 
Research on the physiology of sleep and sleep 
rhythms is associated with the name of Kleitman 
and his colleagues {3648, 3665, 3666, 3667, 3668, 
3669, 3670, 3671, 3672, 3673, 3674, and 3675). 
Kleitman {3665) 1923 reported on the effects of 
prolonged wakefulness on man. More phosphorus 
was said to be excreted in the urine per hour during 
sleep than during wakefulness, independently of the 
volume of urine secreted {3666). It was suggested 
that this increase in the excretion of phosphorus 
during sleep is due to more complete muscular re- 
laxation in that state. Kleitman and Camille 
{3671) 1932 reported that decorticated dogs have 
several periods of sleep alternating with periods of 
activity each 24 hours. The activity consisted of al- 
most incessant walking in circles. Most constantly oc- 
curring period of sleep followed shortly upon feed- 
ing. It was concluded that diurnal sleep in dogs 
depends for its establishment and persistence upon 
the integrity of the cerebral cortex. According to 
Kleitman and Doktorsky (3672) 1933 assumption 
of horizontal position generally leads to a fall in 
body temperature. Onset of sleep tends to accentu- 
ate the downward trend of temperature preceding 
sleep. Awakening is not characteristically followed 
by change in body temperature. According to Coop- 
erman, Mullin, and Kleitman {3648) 1934 sleep fol- 
lowing 60-hour periods of wakefulness is character- 
ized by decrease in the frequency of movements, in 
time spent in stirring, and in the total number of 
movements. 
For studies on the sleep-wakefulness cycle, 3 par- 
ticular papers by Kleitman should be consulted 
{3668, 3669, and 3670). The latter report concerns 
the sleep-wakefulness cycle of submarine personnel. 
Although there is nothing physiologically compel- 
ling about the 24-hour alternation of sleep and 
wakefulness, according to the author, the cycle 
stems from the fact of the succession of day and 
night and community life is adapted to this. A sim- 
ple test of the degree of adaptation of the in- 
dividual to this cycle is the fixity of the diurnal body 
temperature curve which may, however, be changed 
by following a new schedule of activities for a length 
of time. Efficiency of performance and degree of 
alertness during the waking phase of the cycle are 
seen by the author to conform to the rise and fall of 
body temperature. On awakening, the temperature 
is about the same as at retiring and performance is 
very similar. Both temperature and performance 
level rise and reach a peak or plateau in the early 
afternoon. Later on, sometime in the evening, the 
body temperature turns downward and at the same 
time there is a progressive decline in efficiency of 
performance. The author carried out studies of the 
sleep-wakefulness cycle on the U. S. S. Dogfish 
carrying 8 officers and 66 men aboard. The mean 
age of the officers and crews was 25 years. Some had 
been on submarines as long as 14 years. Hours of 
watches were fixed for the entire cruise with meal 
hours coinciding with watch changes. According to 
the schedule someone was asleep at all times and 
the total duration of sleep per 24-hour period aver- 
aged 8/2 hours per man. This was obtained usually 
in 2 or 3 periods. There was a tendency for wake- 
fulness to be concentrated during the afternoon and 
evening. Temperature recording on 9 subjects 
showed that it was possible while isolated in a sub- 
marine to preserve the shore type of 24-hour body 
temperature curve by following a customary routine 
of living. It was also possible to establish 2 equal 
12-hour curves on a 4 hours on and 8 hours off 3641-3670 
SPECIAL PSYCHOLOGICAL AND PSYCHIATRIC PROBLEMS 
watch schedule. It was considered that personnel 
overestimated their ability to become fully alert on 
short notice. Both the narrowness of the bunks and 
their vertical crowding discouraged frequent 
changes in sleeping posture essential for restful 
sleep. Very few subjects complained of their bunks 
and most considered them but little less adequate 
than on shore stations. In the new schedule of 
watches, the most revolutionary feature was the 
necessity for preparation of 9 meals a day. Trial 
runs showed that cheerful acceptance of the new 
schedule by the crew would be a necessary pre- 
requisite before such could be adopted. 
A report by Husband (3660) 1935 indicates that 
there is no significant difference between the value 
of continuous and interrupted sleep. In Husband’s 
experiments a subject slept for 8 consecutive hours 
nightly for one month while during the second 
month he slept 3 hours, remained awake 3 hours 
and then slept 3 hours more. Various performance 
tests indicated no change in efficiency of the subject 
during the total time of the study. 
For studies on the effects of loss of sleep, papers 
by the following may be consulted: Laslett {3676) 
1924; Rakestra and Whittier {3686) 1923-24; 
Robinson and Herrmann {3691) 1922; and Wei- 
skotten {3697) 1925. For studies on the effects of 
hypoxia and drugs upon sleep papers by the follow- 
ing may be consulted: Smith {3695) 1946; Mullin, 
Kleitman, and Cooperman {3680) 1933; and Hol- 
lingworth {3659) 1912. Other references on sleep 
are given as follows: Andreyeff {3641) 1951; King 
{3664) 1946; Page {3682) 1935; and Reed and 
Kleitman {3689) 1926. 
3641. Andreyeff, B. Investigation of the dynamics of 
sleep in man by means of recording eye-lid movements. 
Fisiol. Zh. S. S. S. R., 1950, 36: 429-435. Excerpta 
Medica. (Section II. Physiology, Biochemistry, and Phar- 
macology), 1951, 4; 1279. 
3642. Atkinson, J. B. The anatomy and physiology of 
the sleep mechanism. MD. 1947,2: 9—15. 
3643. Atkinson, J, B. The anatomy and physiology of 
the sleep mechanism. MD. 1947, 2: 26-30. 
3644. Banche, M. La secrezione gastrica notturna 
durante il sonno. Minerva med. Roma, 1950, 1: 428—434. 
Excerpta Medica. (Section II. Physiology, Biochemistry, 
and Pharmacology), 1950, 3: 1485. 
3645. Barker, W. and S. Burgwin. Brain wave patterns 
during hypnosis, hypnotic sleep and normal sleep. Arch. 
Neurol. Psychiat., Chicago, 1949, 62: 412-420. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and Phar- 
macology), 1950,5; 1095. 
3646. Bartley, S. H. and E. Chute. Sleep and other 
periodicities, pp. 240-279 in: Fatigue and impairment in 
man. McGraw-Hill Book Company, Inc., New York, 1947, 
429 pp. 
3647. Collip, J. B. Effect of sleep upon the alkali reserve 
of the plasma. J. biol. Chem., 1920, 41: 471-472. 
3648. Cooperman, N. R., F. J. Mullin, and N. Kleitman. 
Studies on the physiology of sleep. XI. Further observa- 
tions on the effects of prolonged sleeplessness. Amer. J. 
Physiol, 1934, 107: 589-593. 
3649. Drogendijk, A. C. La nature du sommeil. Schweiz, 
med. Wschr., 1949, 79: 100-103. 
3650. Economo, C. von. Sleep as a problem of localiza- 
tion. /. nerv. merit. Dis., 1930, 71: 249-259. [D] 
3651. Endres, G. and W. von Frey. Ueber Schlaftiefe 
und Schlafmenge. Z. Biol, 1930, 90: 70-80. [R] [P] 
3652. Euziere, J., Th. Passouant-Fontaine, P. Pas- 
souant, and H. Latour. Etude electroencephalographique 
du sommeil spontane et provoque par le pentothal au cours 
de divers etats pathologiques. J. Physiol, Paris, 1949, 
41: 167-A-172-A. Excerpta Medica. (Section II. Physi- 
ology, Biochemistry, and Pharmacology), 1950, 3: 1097. 
3653. Frommel, E., I. T. Beck, M. Favre, and F. 
Vallette. Etudes dans le domaine du sommeil. Helvet. 
physiol pharm. acta., 1947, 5: 361—363. 
3654. Gans, M. Der Schlaf und die dritte Zirkulation. 
Der Versuch einer Losung des Schlafproblems. Schweiz. 
Arch. Neurol Psychiat., 1949, 64: 88-100. Excerpta 
Medica. Section II. (Physiology, Biochemistry, and Phar- 
macology), 1950, 5; 1397. 
3655. Gibbs, F. A., E. L. Gibbs, and W. G. Lennox. The 
cerebral blood flow during sleep in man. Brain. 1935, 
58: 44-48. 
3656. Gillespie, R. D. Sleep and the treatment of its 
disorders. London, Bailliere, Tindall and Cox, 1929, 267 
pp. 
3657. Harrison, F. An attempt to produce sleep by 
diencephalic stimulation. /. Neurophysiol, 1940, 5: 
156-165. 
3658. Hess, W. R. Le sommeil comme fonction 
physiologique. /. Physiol, Paris, 1949, 41: 61-67A. [P] 
3659. Hollingworth, H. L. The influence of caffein 
alkaloid on the quality and amount of sleep. Amer. J. 
Psychol, 1912, 23: 89-100. 
3660. Husband, R. W. The comparative value of con- 
tinuous versus interrupted sleep. /. exp. Psychol, 1935, 
18: 792-796. 
3661. Ivy, A. C. and J. G. Schnedorf. On the hypnotoxin 
theory of sleep. Amer. J. Physiol, 1937, 119: 342. 
3662. Johnson, H. M. and T. H. Swan. Sleep. Psychol. 
Bull, 1938, 27: 1-39. [R] 
3663. Kayser, C. Le Sommeil. /. Physiol, Paris, 1949, 
41: 1-5 3A. [R] 
3664. King, C. D. Electrometric studies of sleep. /. gen. 
Psychol, 1946, 35: 131-159. 
3665. Kleitman, N. Studies on the physiology of sleep. 
I. The effects of prolonged sleeplessness on man. Amer. 
J. Physiol, 1923, 66: 67-92. 
3666. Kleitman, N. Studies on the physiology of sleep. 
III. The effect of muscular activity, rest and sleep on the 
urinary excretion of phosphorus. Amer. J. Physiol, 1925, 
74: 225-237. 
3667. Kleitman, N. Sleep. Physiol. Rev., 1929, 9: 624- 
665. [R] 
3668. Kleitman, N. Sleep and wakefulness. As alternat- 
ing phases in the cycle of existence. Chicago, The Uni- 
versity of Chicago Press, 1939, 638 pp. 
3669. Kleitman, N. Biological rhythms and cycles. 
Physiol Rev., 1949, 29: 1-30. [R, D] 
3670. Kleitman, N. The sleep-wakefulness cycle of 
submarine personnel, pp. 329-341 in: A survey report 
on human factors in undersea warfare. Washington, 
D. C., National Research Council, 1949, 541 pp. DUTY AND REST PERIODS 
3671-3697 
3671. Kleitman, N. and N. Camille. Studies on the 
physiology of sleep. VI. The behavior of decorticated dogs. 
Amer. J. Physiol, 1932, 100: 474-480. 
3672. Kleitman, N. and A. Doktorsky. Studies on the 
physiology of sleep. VII. The effect of the position of the 
body and of sleep on rectal temperature in man. Amer. J. 
Physiol, 1933, 104: 340-343. 
3673. Kleitman, N. and D. P. Jackson. Body tempera- 
ture and performance under different routines. J. appl 
Physiol, 1950, 3: 309-328. [P] 
3674. Kleitman, N. and A. Ramsaroop. Periodicity in 
body temperature and heart rate. Endocrinology, 1948, 
43: 1-20. 
3675. Kleitman, N., S. Titelbaum, and H. Hoffmann. 
The establishment of the diurnal temperature cycle. Amer. 
J. Physiol, 1937, 119: 48-54. 
3676. Laslett, H. R. An experiment on the effects of 
loss of sleep. /. exp. Psychol 1924, 7: 45-58. 
3677. Learoyd, C. 6. The mechanism of sleep. Practi- 
tioner., 1950, 164: 261-269. Excerpta Medica. Section II. 
(Physiology, Biochemistry, and Pharmacology), 1950, 3: 
1249. 
3678. Mancean, A, and M. Jorda. Les centres meso- 
diencephaliques du sommeil. Sem. Hop., Paris, 1948, 24: 
3193-3202. 
3679. Mason, E. D. and F. G. Benedict. The effect of 
sleep on human basal metabolism, with particular ref- 
erence to South Indian women. Amer. J. Physiol, 1934, 
108: 377-383. 
3680. Mullin, F. F., N. Kleitman, and N. R. Copperman. 
Studies on the physiology of sleep. X. The effect of alcohol 
and caffein on motility and body temperature during sleep. 
Amer. J. Physiol, 1933, 106: 478-487. [P] 
3681. Nekhorocheff, I, L’electroencephalogramme du 
sommeil chez 1’enfant. Rev. Neurol, 1950, 82: 487-495. 
Excerpta Medica. Section II. (Physiology, Biochemistry, 
and Pharmacology), 1951, 4: 910. 
3682. Page, J. D. An experimental study of the day and 
night motility of normal and psychotic individuals. Arch. 
Psychol,N. Y., 1935,28: (192) 1-40. 
3683. Pavlov, I. P. Lecture XV. Internal inhibition and 
sleep as one and the same process with regard to their 
intimate mechanism, pp. 250—264 in: Conditioned re- 
flexes. An investigation of the physiological activity of the 
cerebral cortex. London, Oxford University Press, 1927, 
xv, 430 pp. 
3684. Pavlov, I. P. Lecture XVI. Transition stages be- 
tween the alert state and complete sleep: hypnotic stages, 
pp. 265-283 in: Conditioned reflexes. An investigation of 
the physiological activity of the cerebral cortex. London, 
Oxford University Press, 1927, xv, 430 pp. 
3685. Pieron, H. Le probleme physiologique du sommeil. 
Paris, Masson et Cie, Editeurs, 1913, 520 pp. 
3686. Rakestra, N. W., and F. 0. Whittier. The effect 
of loss of sleep on the composition of the blood and urine. 
Proc. Soc. exp. Biol. Med., 1923-24, 21: 5-6. [P] 
3687. Ranson, S. W. Sleep. Sci. Mon., N. Y., 1934, 38: 
473-476. 
3688. Ranstrom, S. The hypothalamus and sleep regula- 
tion. An experimental and morphological study. Acta path, 
microbiol, scand., Suppl., 1947, 70, 90 pp. [P] 
3689. Reed, C. I. and N. Kleitman. Studies on the 
physiology of sleep. IV. The effect of sleep on respira- 
tion. Amer. J. Physiol, 1926, 75: 600-608. 
3690. Richter, D. and R. M. C. Dawson. Brain metabo- 
lism in emotional excitement and in sleep. Amer. J. 
Physiol, 1948, 154: 73-79. [P] 
3691. Robinson, E. S. and S. 0. Herrmann. Effects of 
loss of sleep (I). /. exp. Psychol., 1922, 5: 19—32. 
3692. Rowe, S. H. Localization of the sleep mechanism. 
Brain, 1935, 58: 21-43. [R] 
3693. Serota, H. M. Temperature changes in the cortex 
and hypothalamus during sleep. J. Neurophysiol., 1939, 
2: 42-47. 
3694. Singh, I. and S. I. Singh. Sleep as an adaptation 
phenomenon. Curr. Sci., 1946,15: 307—308. [D] 
3695. Smith, G. M. The effect of prolonged mild anoxia 
on sleepiness, irritability, boredom, and other subjective 
conditions. J. gen. Psychol., 1946, 35: 239-250. 
3696. Stern, P., N. Marijan, and V. Eisen. Znaiienje 
kalcija za aktivaciju holinergickog sistema u snu. [The 
role of calcium in activation of the cholinergic system 
during sleep.] Excerpta Medica. Section II. (Physiology, 
Biochemistry, and Pharmacology), 1950, 3: 85. Acta med. 
lugo., 1948, 2; 113-130. 
3697. Weiskotten, T. F. On the effects of the loss of 
sleep. J. exp. Psychol., 1925, 8: 363-380. 
IX. DUTY AND REST PERIODS 
Most civilian enterprises employ the majority of 
their personnel between the hours of 0800 and 1800 
and the daily routine of these employees and their 
families is built around these conventional working 
hours. Since operation of a ship under way requires 
a round-the-clock schedule of activities, the crews 
work under a rotation of watches which usually 
involves a “4 hours on and 8 hours off” routine. 
This type of watch schedule places some duty sec- 
tions at a disadvantage with respect to meals and 
recreation, as well as sleep. Apart from this, during 
general quarters all hands must be at their battle 
stations. Some of the stress brought on by odd watch 
hours is lessened by “dogging” the watch: viz the 
2000 to 2400 watch is split in two, with the new 
section going on watch at 2200. This type of watch 
scheduling may appear to be fair to all hands but 
it probably wreaks havoc with the normal diurnal 
cycle of sleep and wakefulness. It is probably true 
that efficiency is lowered during the hours of dark- 
ness when the body temperature is low and these 
are important hours to a fighting ship since oppor- 
tunities for enemy attack are at a maximum. 
Normally aboard the operating submarine there 
are three watch sections. Section I (2 officers and 
16 men) has the 0400 to 0800 and 1600 to 2000 
watches; Section II (2 officers and 18 men), the 
0800 to 1200 and 2000 to 2400 watches; Section III 
(2 officers and 17 men), the 0 to 0400 and 1200 to 
1600 watches. Personnel of Section IV (2 officers 
and 15 men) are not required to stand watches, 
but either followed a frankly shore-type schedule 
of activities (cooks and messmen) or are on call at 
all hours. The hours of watches are fixed for the 
entire cruise (except for the officers), and the meal 
hours are made to coincide with watch changes— 3698-3702 
SPECIAL PSYCHOLOGICAL AND PSYCHIATRIC PROBLEMS 
breakfast at 0730 to 0800, dinner at 1130 to 1200 
and supper at 1930 to 2000. 
Pioneer work in the revision of the older standard 
watch schedules has been carried out by Kleitman 
and the report by Kleitman and Jackson (3700) 
1950 describes and evaluates a schedule which per- 
mitted the continuance of a normal diurnal tem- 
perature cycle. The two-fold purpose of this study 
was to determine the ease with which naval per- 
sonnel adapted themselves to various watch sched- 
ules as judged by their diurnal body temperature 
curves, and to discover the existence, if any, of a 
correlation between body temperature and alert- 
ness, as indicated by performance in several tests 
and in other aspects of behavior. Results obtained 
indicated a variability in adjustment. On the rotat- 
ing (dogged) schedule of watches the pattern of 
the diurnal body temperature changes was the same 
as on shore. Color naming, and to a lesser extent, 
reaction time and Link trainer performance, showed 
a diurnal variation particularly on the dogged 
watch routine, the only one which permitted testing 
around the clock. In general, the higher the body 
temperature the better was the performance. 
Operationally, the original Kleitman schedule 
has proven to be impractical because of its require- 
ment of 9 meal servings each day. Aside from this, 
the duration and distribution of on-and-off watch 
periods are not equal for all sections. 
Another watch schedule was tried and tested 
physiologically and psychologically at sea by Utter- 
back and Ludwig (3702) 1949. This schedule re- 
quires 3 watches of 3, 3, and 2 hour durations by 
each section of the crew, and provides a continuous 
period off duty of 10 to 12 hours. These studies were 
made on 3/s, 4, 19, and 21 day cruises aboard the 
U. S. S. Tusk, U. S. S. Sirago, and U. S. S. Cuhera. 
The schedule was compared with the present system 
of 4-hour watches separated by 8 hours off. The 
rapidity with which the men adapted to the sched- 
ule was determined by means of oral temperature 
cycles, which also afforded an indication of the 
alertness and efficiency of men on watch. On the 
basis of body temperature studies, the proposed 
schedule was found to be a definite improvement 
over the present one. The advantages accrued were 
similar to those found by Kleitman. An extra ad- 
vantage was the requirement of only 4 meals for 
a 24-hour period, each section receiving 3 meals per 
day. As with the Kleitman watch bill, the duration 
and distribution of on-and-off watch periods were 
not uniform for all sections. 
The adjustment of watch schedules to match 
body temperatures and the attempt to alter temper- 
ature curves to fit an unusual routine are based 
upon information obtained from normal sleep- 
wakefulness cycles and efficiency measurements 
correlated with body temperature. A more complete 
review of the physiological process of sleep and 
sleep-wakefulness cycles is provided in section on 
sleep-wakefulness (p. 321). 
Studies by Kleitman and Engelmann (3699) in 
1947 on the activity of rabbits as related to body 
temperature showed that with continuous access to 
food, activity was lowest during daytime hours when 
the rectal temperature was low. When food was 
available only from 9-10 a. m. to 3-4 p. m., activity 
became decidedly monophasic, increasing sharply 
in the morning, prior to the time of feeding and 
continuing at a high level during the day. The rec- 
tal temperature showed a marked rise during the 
feeding period, reaching its high level in the after- 
noon, instead of late in the evening. Although 
usually considered polyphasic, rabbits under ordi- 
nary laboratory conditions show a distinct 24-hour 
cycle of activity and body temperature. The tend- 
ency to a night-time high, when access to food was 
continuous, could easily be modified by making food 
available for only a few hours during the day. 
Earlier experiments by Kleitman, Titelbaum, and 
Feiveson (3701) 1938 on the effects of body tem- 
perature on reaction times in man showed that the 
best performance was obtained in the afternoon 
with poorer performance records during the morn- 
ing hours. This variation appeared to be depend- 
ent upon the diurnal body temperature. A spon- 
taneous or induced change in body temperature was 
reflected in a change in the opposite direction of 
reaction time. 
3698. Benedict, F. G. Studies in body-temperature. I. 
Influence of the inversion of the daily routine; the tem- 
perature of night-workers. Amer. J. Physiol., 1904, 11: 
145-169. 
3699. Kleitman, N. and T. Engelmann. Diurnal cycle 
in activity and body temperature of rabbits. Fed. Proc. 
Amer. Soc. exp. Biol., 1947, 6: 143. 
3700. Kleitman, N. and D, P. Jackson. Variations in 
body temperature and in performance under different 
watch schedules. U. S. Navy. NMRI. Project NM 004 
005.01.02, 15 February 1950, 58 pp. 
3701. Kleitman, N., S. Titelbaum, and P. Feiveson. 
The effect of body temperature on reaction time. Amer. 
J. Physiol, 1938, 121: 495-501. [P] 
3702. Utterback, R. A. and G. D. Ludwig. A compara- 
tive study of schedules for standing watches aboard sub- 
marines based on body temperature cycles. U. S. Navy. 
NMRI. Project NM 004 003, Rept. no. 1, 24 March 1949, 
24 pp. [P] PSYCHIATRIC BREAKDOWN 
X. PSYCHIATRIC BREAKDOWN 
The situational stresses of submarine war patrols 
during World War II were often extremely trying. 
The experiences of some of these patrols have been 
summarized by Duff and Shilling {3704) 1947. 
Depth charging, heat, and other environmental 
stresses took their toll and sometimes taxed beyond 
the limits the endurance of the crews. One account 
describes a terrific explosion within a submarine. 
All hands not holding onto something were knocked 
from their feet. Thick toxic smoke filled the maneu- 
vering room and the after torpedo rooms. All hands 
were violently ill. Another account tells of the intol- 
erable conditions imposed by heat and humidity. 
In one case the maneuvering room temperature 
was 125° F. All hands were stripped down to their 
shorts and shoes were removed. Men perspired so 
profusely that in an hour or more the decks were 
slippery with sweat. Towels used to keep perspira- 
tion out of the eyes became wringing wet; socks 
could be wrung out like rags. Everyone drank large 
quantities of water and took salt and aspirin tablets. 
As time went by the air became so oppressive and 
stifling that it was difficult to breathe. Headaches 
were prevalent and severe. It was impossible to 
sleep. 
On many patrols heat rash caused serious discom- 
fort. The enervation from the heat became so strik- 
ing that physical exertion such as required to change 
and maintain depth control would exhaust a plane- 
man. Controllermen had to be spelled frequently. 
Efficiency and reaction times were strikingly re- 
duced. Errors were prevalent, even among experi- 
enced men. There was an increase in accident rate. 
Tempers were short. Nerves were on edge. Some- 
times, apathy developed. As the younger crewmen 
folded up, older and more phlegmatic men would 
take over. Some without permission, others after 
requesting relief would quietly shove off and lie 
down on the cooler spots of decking. Sometimes, two 
men would take turns, the off watchman resting on 
the deck beside his station. Generally, there was no 
evidence of hysteria, the men carrying out their 
duty to the limit of physical and mental endurance. 
Oftentimes, upon surfacing there was distressing 
nausea and vomiting. Under such conditions, sub- 
marines were no longer in a position to fight or de- 
fend themselves. Though the more serious of these 
symptoms passed off quickly with rest and fresh 
air, the men were often fatigued and extremely 
tense for days thereafter. 
These brief pictures, which by no means repre- 
sent the most dangerous or stressing experiences of 
submarine crewmen, afford insight into the severity 
of submarine operations. It is remarkable that under 
conditions often similar to and exceeding these 
there were only approximately 56 psychiatric cas- 
ualties out of a total of 126,160 man-patrols during 
World War II. Duff and Shilling have analyzed 
the possible reasons for such remarkable perform- 
ance. These include sound selection techniques, 
training, morale, medical care, rest camps, rotation 
of duty, and confidence in officers. Psychiatric 
casualties in submarine warfare have also been dis- 
cussed by Duff and Shilling in another publication 
{3703) 1947. 
It was not uncommon in the 24-hour period 
following a depth charge attack to see a number of 
cases of mild gastric disturbance with nausea, ab- 
dominal cramps, diarrhea, indigestion, and head- 
aches usually with rapid recovery without treatment 
{3709). Occasionally the entire crew exhibited gen- 
eralized impairment of appetite after a depth- 
charge attack. Symptoms also included anxiety, 
dizziness, and insomnia. These occurred not only in 
inexperienced personnel, but also in veteran sub- 
mariners. 
Psychiatric reactions developing in operators of 
antisubmarine sound gear have been described by 
Will {3710) 1945. Case histories are given of 2 
sound operators who developed acute schizophrenic 
episodes while at sea. The author emphasized the 
importance of careful preselection of men for these 
duties and more frequent rotation of the watch 
with additional brief rest periods. 
For 16 months during 1943 and 1944 McHarg 
{3707) 1946 had the opportunity of studying 
psychiatric disabilities in submariners of the British 
submarine service in a home-based submarine 
flotilla. One-half of the cases seen were referred to 
neuropsychiatric specialists and one-third eventually 
became permanently unfit for submarine duty. The 
rate of admission to hospital was less than one per- 
cent per annum. The rate of invaliding from the 
Navy on psychiatric grounds was less than 0.3 per- 
cent. This study of 71 cases undertaken by the 
author was carried out to verify the impression that 
the incidence of serious psychiatric illness among 
submariners is very small. Stress plays a large part 
in the majority of cases. Indications are that sub- 
mariners are stable individuals. Less stable men do 
not reach the submarine service or are eliminated 
in early stressful situations. 
Several case histories of submariners with nervous 
symptoms have been reported by Essen {3705) 
1948. This paper is of particular importance since 
the submariners in question were members of the 
German submarine service. The author has de- 
scribed psychosomatic and other symptoms of 3703-3710 
SPECIAL PSYCHOLOGICAL AND PSYCHIATRIC PROBLEMS 
patients entering the clinic with symptoms of fatigue 
and nervous exhaustion. 
The remarkably low incidence of psychiatric 
breakdowns in the U. S. submarine service in World 
War II does not justify complacency as to the im- 
portance of the psychiatric problems or the potential 
hazards in the future. It becomes increasingly 
essential to eliminate the psychiatrically unstable in 
the early stages and to improve techniques for the 
recognition of those candidates for submarine train- 
ing who are likely to become psychiatric casualties. 
The selection program developed during World 
War II undoubtedly was effective in eliminating 
most of the unfit. For example, the low incidence 
of claustrophobic fears among submariners is un- 
doubtedly due to the fact that many applicants with 
serious personality defects were eliminated by the 
selection procedures, not the least important of 
which was the escape training tank program (3706 
and 3708). 
3703, Duff, I. F. and C. W. Shilling. Psychiatric casual- 
ties in submarine warfare, pp. 183-198 in: History of sub- 
marine medicine in World War II. Edited by C. W. Shill- 
ing and J. W. Kohl. U. S. Navy. Submarine base, New 
London, Conn. Medical research laboratory, 25 May 
1947, 328 pp. 
3704. Duff, I. F. and C. W. Shilling, Psychiatric casual- 
ties in submarine warfare. Amer. J. Psychiat., 1947, 103: 
607-613. 
3705. Essen, K. W. The nervous syndrone of subma- 
riners. Clinical findings, pathogenesis, attempt at therapy, 
pp. D IV—1—D IV—40 in: Monograph on submarine 
medicine. Folio VII, Germany. U. S. Zone. Office of naval 
advisor. 1948. [R] [CH] 
3706. Lewin, B. D. Claustrophobia. Psychoanal. Quart., 
1935, 4: 227-233. 
3707. McHarg, J. F. The mental health of submariners, 
with special reference to 71 cases examined psychiatrically. 
J. Ment. Sci., 1946, 92: 343-356. 
3708. Schmideberg, M. A note on claustrophobia. 
Psychoanal. Rev., 1948, 35: 309-311. 
3709. XI, S. Navy. BuNavPers. (C) Psychiatric casual- 
ties in submarine warfare, pp. 150-155 in: Submarine 
medicine practice. NavPers 10838, March 1949, 182 pp. 
[D] [CH] 
3710. Will, 0. A., Jr. Certain psychiatric reactions in 
operators of antisubmarine sound gear. Report of two 
cases. Nav. med. Bull., Wash., 1945, 44: 746-748. Special Problems of Swim-Diving 
I. GENERAL STUDIES 
World War II and the years following have seen 
an increasing awareness of the military potentialities 
of individual men swimming, “skin-diving,” or using 
self-contained diving equipment independent of 
connections to the surface. The advantages of free- 
dom of movement and of stealth fit such men for a 
variety of tasks which can be accomplished by other 
means only with great difficulty, if at all. Their 
accomplishments have included penetration of 
harbor defenses and sinking large warships, recon- 
naissance of beachheads, clearing of underwater 
obstacles before and after assaults, and location and 
disposal of mines. Self-contained apparatus has ad- 
vantages in certain operations where conventional 
diving gear is generally used but where lifeline and 
airhose may be more of an encumbrance than a safe- 
guard, where heavy surface equipment is a handi- 
cap, or where conventional mooring and other 
time-consuming preparations are impractical. 
In addition to increasing military and commer- 
cial applications, this form of diving has gained 
widespread recreational use in spear fishing and 
underwater “sightseeing.” It has also become a 
recognized scientific technique in marine biology, 
oceanography, and submarine archeology. These 
developments strongly suggest that what may be 
called “swim-diving” will have continuously in- 
creasing importance in underwater work. Since it 
involves problems peculiar to itself in addition to 
those associated with conventional diving and 
swimming, and since these peculiar problems have 
received only a fraction of the attention they de- 
serve, it is to be hoped that the next few years will 
see many new studies on this subject. 
In discussing equipment for underwater warfare 
in World War II, Davis [3713) 1951 provides in- 
formation not only on breathing apparatus and 
midget submersible craft, but also about a variety 
of applications of such apparatus. These include 
the “human minesweepers” and “human torpe- 
does,” and the history and work of “frogmen.” 
Excellent references are included. Waldron and 
Gleeson [3722) 1950, give an exciting account of 
the background and development of “frogmen” 
techniques, beginning with the operations of Italian 
divers who rode two-man torpedoes and success- 
fully damaged several large warships by attaching 
limpet mines. Subsequently, the British adopted 
the idea and solved many engineering and research 
problems involved in such operations. The Nor- 
mandy invasion was greatly facilitated by port clear- 
ance parties which gave individual attention to 
enemy mines. The partial destruction of the cele- 
brated Remagen bridge appears to be the only no- 
table achievement by the Germans in this type of 
activity. 
The United States Navy Underwater Demolition 
Teams (U. D. T.) had their beginning in 1943. 
Robb [3719) 1951 describes the costly lesson 
learned at Tarawa concerning their potential value. 
It was such lessons that greatly stimulated U. D. T. 
development. Subsequent operations and the tech- 
niques employed, mainly without the use of breath- 
ing apparatus, are described. An account of the 
U. D. T. techniques of screening applicants pro- 
vides a graphic illustration of the gruelling physical 
and mental stresses imposed upon trainees: “For 6 
days and nights of ‘hell week’ the trainees are sub- 
jected to every trial of stamina and nerves their 
resourceful instructor can devise * * * early 
morning swims, each progressively longer, are made 
in overcoat weather. As late as early December, 
trainees take daily swims in the Atlantic wearing 
only swim trunks.” Lambertsen [3718) 1947, who 
developed a closed-circuit oxygen unit and partici- 
pated in the training and operations of the U. S. 
Office of Strategic Services’ “operational swim- 
mers,” reports on the problems which arose during 
more than 5,000 man-hours of underwater swim- 
ming with the equipment. Medical problems en- 
countered by an underwater demolition team are 
discussed by Waite [3721) 1951. 
Dugan [3715) 1948 discusses the “diving lung” 
developed by Cousteau and Gagnon for the French 
navy. With this equipment, an open-circuit com- 
pressed air unit, Cousteau was able to reach a depth 
of 210 feet; and dives to 100 feet without connec- 
tions to the surface became commonplace. Divers 3711-3722 
SPECIAL PROBLEMS OF SWIM-DIVING 
using this equipment were observed medically for 
several years without detecting any pulmonary, cir- 
culatory, or auditory changes. Details of training 
and requirements for this type of work in the Italian 
navy as of 1942 are included in its manual for 
shallow water divers {3717). 
Schenk and Kendall {3720) 1950 provide a pop- 
ularized approach to the construction and opera- 
tion of shallow-water and self-contained equipment. 
Wartime underwater research activities of the Cana- 
dian navy, including some of interest in “swim- 
diving,” are reported by Delorme and Locke 
{3714) 1944. Further information on diving with 
open-circuit gear is incorporated in a text on diving 
by Tailliez, Dumas, Cousteau, Alinat, and Devilla 
{3802) 1949. 
3711. Akashi, K. Morphological study of AMA (women 
divers). Part I. Morphology of the chest. Folia endocrin. 
japon., 1951, 27 (4): (English text pagination) 121-122. 
(In Japanese with English summary). 
3712. Akashi, K. Morphological study of the AMA 
(women divers). Part II. Morphology of the lower torso. 
Folia endocrin. japon., 1951, 27 (4) : (English text pagi- 
nation) 123-124. (In Japanese with English summary). 
3713. Davis, Robert H. Diving equipment for under- 
water warfare in the second World War. pp. 290-324 in: 
Deep diving and submarine operations. A manual for deep 
sea divers and compressed air workers. London, The Saint 
Catherine Press Ltd., Fifth edition, 1951, 670 pp. [D] 
3714. Delorme, E. J. and W. Locke. Report on the 
medical aspects of diving practice of interest to the Royal 
Canadian Navy. (Summary of report). Canada. NRG. 
Proceedings of the third meeting of the Associate com- 
mittee on naval medical research. Appendix R, Report 
no. C4080, 15 May 1944, 6 pp. 
3715. Dngan, J. The first of the menfish. Sci. III., 1948, 
3: No. 12: 30-32, 68-69. 
3716. Gay-French, S, Oto-rhinological problems of 
offensive diving. J. Laryng., 1946, 61: 417-440. 
3717. Italian Royal Navy. [Royal Navy manual for 
shallow water divers.] Underwater department of the Royal 
Navy, Divers School, 1942, 47 pp. 
3718. Lamhertsen, C. J. Problems of shallow water 
diving. Occup. Med., 1947, 3: 230-245. 
3719. Robb, J. E. UDT pays off. Milit. Rev. Fort 
Leavenw., 1951, 13: 3-14. 
3720. Schenk, H., Jr. and H. Kendall. Shallow water 
diving for pleasure and profit. Cambridge, Maryland, Cor- 
nell maritime press, 1950, 138 pp. 
3721. Waite, C. L. Medical problems of an underwater 
demolition team. U. S. Armed Forces med. J., 1951, 2: 
1317-1326. 
3722. Waldron, T. J, and James Gleeson. The frogmen. 
The story of the wartime operators. London, Evans Broth- 
ers Limited. 1950, 191 pp. 
II. PHYSIOLOGICAL PROBLEMS OF SWIMMING 
AND SWIM-DIVING 
Many problems encountered in conventional 
diving have already been discussed in foregoing 
sections. These include such topics as the physi- 
ological effects of elevated atmospheric pressures 
(p 7), decompression sickness (p. 159), ear, nose, 
and throat disturbances (p. 151), oxygen intoxica- 
tion (p. 182), anoxia (p. 17), carbon dioxide tox- 
icity (p. 54), “squeeze” (p. 257), air embolism (p. 
255), immersion in cold water (p. 112), and under- 
water blast (p. 258). Physiologically, a man is div- 
ing when he exposes himself to the underwater 
environment, regardless of his method. Hence, all of 
these discussions concern swimming and the use of 
self-contained apparatus, although in some cases 
with unusual application or emphasis. 
Studies primarily concerned with surface swim- 
ming have been included in this section, not only 
for their potential significance in swim-diving but 
because swimming itself has achieved a measure of 
military importance. As has been pointed out, 
swim-diving involves not only factors which are 
common to all types of underwater work and those 
related primarily to swimming but also a number 
of problems which are essentially different. These 
unique problems constitute a major area of needed 
study. A review of some of the principal difficulties 
encountered in swim-diving is provided by Lam- 
bertsen {3718) 1947. 
Several of the problems most peculiar to swim- 
diving arise from the fact that the diver, who lacks 
a helmet and partially inflated suit, is exposed not 
only to the hydrostatic pressure at a given depth but 
also to the different pressures of the various depths 
subtended by his body and equipment. While these 
differences in hydrostatic pressure are small when 
compared to the total pressure, they assume sig- 
nificance in a delicately balanced mechanism such 
as that of respiration, where pressure differences of 
a few centimeters of water are important. The 
hydrostatic pressure of water acts upon the thoracic 
cage, tending to produce a certain pressure therein. 
It also acts upon any exposed, nonrigid portion of 
his breathing apparatus such as a rebreathing bag 
or demand valve. If these pressures are not essen- 
tially balanced, the mechanical work of breathing 
may be greatly increased with consequent respira- 
tory fatigue. There is also a possibility of secondary 
circulatory impairment and actual pulmonary dam- 
age. The implications of such imbalances can best 
be appreciated by referring to studies on the me- 
chanics of breathing and the effects of breathing 
resistance such as those of Fenn {3726a) 1951 and 
Cain and Otis {3414) 1949, and to the extensive 
literature on pressure-breathing (p. 294). 
Paton and Sand {3736) 1947 undertook to de- 
termine the optimum position for breathing bags or 
valves in self-contained apparatus and the permissi- 
ble limits of pressure differences for respiratory PHYSIOLOGICAL PROBLEMS OF SWIMMING 
function. They designated the bag pressure which 
comfortably balanced intrapulmonary pressure as 
the “eupneic pressure” and expressed this in terms 
of the position of the bag or demand valve with 
reference to body landmarks. Eupneic pressure in 
the standing position at rest was provided when 
the bag or valve was 5 to 10 cm. below the external 
auditory meatus, increasing to 10 to 15 cm. with 
hypernea from any cause. In all other positions, 
eupneic pressure was attained by positioning the 
bag or valve at the suprasternal notch. Variations 
as great as minus 15 or plus 20 cm. had no signifi- 
cant effect on minute volume, tidal air, or shape of 
the respiratory cycle in the steady state although 
subjects could readily detect departures from eup- 
neic pressure. The authors also report that vital 
capacity was reduced by vertical immersion, fur- 
ther reduced by negative intrapulmonary pressure, 
and partially restored by positive pressure. Reserve 
air (expiratory reserve volume) was diminished 
during vertical immersion at eupneic pressure with 
a corresponding increase in complemental air (in- 
spiratory capacity). Residual air (residual volume) 
was slightly diminished. In the horizontal position, 
these volumes were essentially the same as in air. 
Karpovich {3730) 1939, states that tidal volume 
of respiration in swimming may vary from less than 
0.5 liter to almost 3 liters. He found that the extra 
work of breathing in water amounted to 2.77 to 
5.97 calories per square meter of body surface for 
each liter of air. This work had an efficiency of 6 
to 22.6 percent. The importance of teaching cor- 
rect breathing in swimming was emphasized by the 
observations that respiratory movements interfere 
with propulsion and that improper breathing is 
apparently capable of disturbing blood pressure to 
the point of causing headaches and epistaxis in 
beginners. The study included experiments in 
breathing while submerged at various depths which 
indicated that submersion to a depth of 4.25 feet 
may preclude any possibility of breathing through 
an open tube to the surface. In a study of the energy 
requirements of swimming, Karpovich and Mill- 
man {3732) 1944 discovered that swimming in 
excess of 2 feet per second (about 1.2 knots) ele- 
vated metabolism to more than 10 times the basal 
rate, while speeds beyond 5 feet per second (about 
3 knots) might cause a 100-fold increase. They also 
reported that untrained swimmers expend 2 to 5 
times as much energy as skilled swimmers. The 
study permitted ranking the various strokes in order 
of increasing energy costs: crawl, back, breast, and 
side. The greater fatiguing effect of the butterfly 
stroke as compared to conventional breast stroke 
was tentatively explained by greater local fatigue of 
shoulder-girdle muscles. (Swimming with “fins,” 
using the legs only, which is the style generally used 
in operational swimming, was not investigated.) 
Karpovich and Le Maistre {3731) 1940, investi- 
gated a method of predicting swimming perform- 
ance based on a man’s maximum oxygen intake, 
maximum oxygen debt, and oxygen requirements 
for various speeds. With this information, obtained 
in test swims of 180 feet or less, it was possible to 
predict breast-stroke swimming times for distances 
up to 1,320 feet. They conclude that an improve- 
ment in swimming can be obtained only through 
improved efficiency of the stroke and increased 
capacity for oxygen intake and debt. The work was 
confined to one subject. The effect of prior oxygen 
inhalation on swimming performance was also 
studied by Karpovich {3729) 1934. He states that 
an increase of speed in the hundred yard dash re- 
sulted from oxygen inhalation immediately prior to 
swimming but not from inhalation 4 to 5 minutes 
before. The effect apparently lasted about 1 
minute, provided the subject remained quiet. 
Oxygen inhalation after a 100-yard dash appeared 
to relieve respiratory and circulatory embarrass- 
ment but did not influence performance on a second 
swim 20 minutes later. 
An early study of respiration in swimming is that 
of Aycock, Graaff, and Tuttle {3724) 1932, who 
describe a method of recording respiratory rhythms 
of swimmers. They found that as stroke rate is in- 
creased, both respiratory and expiratory phases are 
shortened but that the latter shows the greatest 
change. Saviano and Boeri {3737) 1946 compared 
respiratory and circulatory data in two expert and 
two less skilled Italian “frogmen.” They found that, 
at rest, the less skilled men had lower blood-oxygen 
capacity and more variable alveolar carbon dioxide 
tensions. At work, their oxygen consumption-venti- 
lation ratio was lower (i. e., they tended to increase 
their ventilation out of proportion to the increase 
in oxygen consumption) and their circulatory rates 
were slower. All 4 subjects breathed 100 percent oxy- 
gen while working. All experienced syncope, head- 
ache, and dyspnea under various circumstances. 
Arnold {3723) 1937 reports that swimming in- 
creases oxygen consumption more than any other 
sport and that the largest lung capacities are found 
in trained swimmers. Swimming seriously depletes 
the alkaline reserve of the blood, according to 
Hewitt and Calloway {3727) 1936. The influence 
of cold-water swimming on pulse and blood pres- 
sure was studied by Miyama {3734) 1930-31, who 
states that pulse rate, systolic pressure, and pulse 
pressure return gradually to normal after such 
exertion but that diastolic pressure returns at a 3723-3740 
SPECIAL PROBLEMS OF SWIM-DIVING 
much slower rate. Protein, erythrocytes, and leu- 
kocytes, previously absent, were found in the urinary 
sediment of many subjects after swimming. Vladysik 
and Turkeltaub {3739) 1936 attribute electro- 
cardiographic changes in swimming to a shift of the 
blood volume, the rate of return to normal being 
influenced by the duration and intensity of exertion 
as well as individual differences in cardiovascular 
apparatus. 
Lanoue {3733) 1950 studied swimming cramps 
and concluded they are not very likely to occur in 
usual indoor swimming and are of little consequence 
to trained swimmers unless speed or power is re- 
quired. Most cramps occur in the calf of the leg 
and can be remedied (or prevented in the incipient 
stage) by stretching the affected muscle. Lanoue 
states that stomach cramps are probably much 
overrated as a factor in drowning. He also con- 
cludes that the amount of fat, minor variations of 
water temperature, and swimming ability have little 
influence on the occurrence of cramps and that 
swimming directly after meals has no harmful 
effects on college indoor swimmers except when 
speed is required. Muido {3735) 1946 found that 
improved swimming speed resulted from increasing 
the rectal temperature by passive (hot bath) or 
active (exercise) warming prior to swimming. 
Active warming was the most effective. An increase 
of 0.6° C. in rectal temperature from stationary 
bicycling improved the time by 1.4 to 2.6 percent. 
Lowering the temperature by 1° C. decreased 
efficiency by 3.6 to 6.3 percent. 
For further studies related to swimming, refer- 
ence should be made to papers by Dummer {3726) 
1940; Zosiaka {3740) 1943; Jaedicke {3728) 1937; 
and Akashi {3711 and 3712) 1951. 
3723. Arnold A. Zur physiologic des Schwimmens. 
Gesundh. u. Erzieh., 1937, 50: 39-44. [D] 
3724. Aycock, T. M., L, H. Graaff and W. W. Tuttle. 
An analysis of the respiratory habits of trained swimmers. 
Res. Quart. Amer. phys. Educ. Ass., 1932, 3: 199-217. [P] 
3725. Dannehi, ( ). Ohr und Schwimmdienst. Dtsch. 
Militararzt., 1912, 41: 418-422. [D] 
3726. Dummer, G. Die gesundheitliche Bedeutung des 
Schwimmsportes. Med. Welt, 1940, 14: 168-170. [D] 
3726-a. Fenn, W. 0. Mechanics of respiration. Amer. 
J. Med., 1951, 10: 77-91. 
3727. Hewitt, J. E. and E. 0. Callaway. Alkali reserve 
of the blood in relation to swimming performance. Res. 
Quart. Amer. phys. Educ. Ass., 1936, 7: 83-93. [P] 
3728. Jaedicke, H. G. Aus dem arztlichen Schrifttum 
zur physiologic des Schwimmens. Gesundh. u. Erzieh., 
1937, 50: 52-53. [D] 
3729. Karpovich, P. V. The effect of oxygen inhalation 
on swimming performance. Res. Quart. Amer. phys. Educ. 
Ass., 1934, 5: 24-30. [P] 
3730. Karpovich, P. V. Respiration in swimming and 
diving. Res. Quart. Amer. phys. Educ. Ass., 1939, 10: 
3-14. 
3731. Karpovich, P. V. and H. Le Maistre. Prediction 
of time in swimming breast stroke based on oxygen con- 
sumption. Res. Quart. Amer. phys. Educ. Ass., 1940, 11: 
40-44. [P] 
3732. Karpovich, P. V. and N. Millman, Energy ex- 
penditure in swimming. Amer. J. Physiol., 1944, 142: 
140-144. [P] 
3733. Lanoue, F. Some facts on swimming cramps. 
Res. Quart. Amer. phys. Educ. Ass., 1950, 21: 153-157. 
[P] 
3734. Miyama, A. [Investigation into the influence of 
bodily exercise on the function of the circulatory system. 
V. The influence of cold-water swimming upon the pulse 
rate and blood pressure.] Acta Sch. med. Univ. Kioto, 
1930/31, 13: 51-55 (English pagination). [P] 
3735. Muido, L. The influence of body temperature on 
performances in swimming. Acta physiol, scand., 1946, 
12: 102-109.[P] 
3736. Paton, W. D, M. and A. Sand. The optimum 
intrapulmonary pressure in underwater respiration. J. 
Physiol., 1947, 106: 119-138. 
3737. Saviano, M. and E. Boeri. Osservazioni su 
“sommozzatori”. Arch. Sci. biol. Napoli, 1946, 31: 29-38. 
3738. Stafford, J. Protect your sinuses. Precautions 
necessary when swimming because humans lack workable 
muscle for closing nostrils in water. Sci. News Lett., Wash., 
1941, 40: 90-91. 
3739. Vladysik, M. M. and M. Turkeltaub. O vliianii 
morskikh kupanii i dalnikh zaplyvov na serdechno-sosu- 
distuiu sistemu. [The effect of ocean bathing and distance 
swimming on the cardiovascular system.] Terap. Arkh., 
1936, 14: 609-623.[P] 
3740. Yosioka, Z. [The influence of swimming on the 
functions of the body—the changes in gases (02 and C02) 
with fresh water swimming and different types of swim- 
ming.] Keio Igaku, 1943, 23: 1143—1161. (English text 
pagination.) 
III. DISEASES PREVALENT IN SWIMMERS 
The most common infections found to occur in 
personnel in swim-diving while operating in warm, 
moist climates are those attributed to the fungi. 
The ears, feet, hands, and groins are the sites most 
commonly affected. Dermatomycoses, or fungus 
affections of the skin, include all the pathologic 
alterations of the skin and/or its appendages which 
are produced by fungi or their products. 
A discussion of fungus infections found in swim- 
mers operating in tropical waters is given in a paper 
by Waite {3721) 1951. Otomycosis, a subacute or 
chronic mycotic infection of the ear, is characterized 
by an exudate. The common complaint is pruritis 
and pain, especially at night. Hearing is frequently 
impaired, and in the subacute phase the external 
auditory meatus may be swollen shut, red, and 
weeping and the entire ear may be exquisitely ten- 
der to palpation. A superimposed secondary bac- 
terial infection is not uncommon. The author DISEASES PREVALENT IN SWIMMERS 
3741-3756-a 
recommends treatment of a soothing nature for the 
acute phase: compresses applied to reduce edema 
and irrigation of the external canal with a solution 
of hydrogen peroxide and sodium bicarbonate. 
Wicks saturated with Burow’s solution should be 
placed in the canal. When the infection has sub- 
sided the affected parts should be painted with 1 
percent gentian violet. 
While on a training cruise with an underwater 
demolition team in a semi tropical climate Waite 
instituted a program to prevent fungus infections. 
After every swim the ears were swabbed dry and a 
fungicidal powder (undecylenic acid and zinc un- 
decylenate) was blown into the external auditory 
meatus with an atomizer. In a 6-week period, dur- 
ing which the personnel involved were in the water 
almost every day, there were no cases of fungus 
infection of the ears as compared with the high 
incidence observed on previous trips to the same 
area. The following important factors predisposing 
to fungus infection have been listed by Pillsbury, 
Sulzberger, and Livingood {3760) 1942: (1) ex- 
cessive sweating; (2) circulatory instability or vas- 
cular disease of the extremities; (3) encasement of 
the feet in heavy shoes; (4) prolonged wearing of 
foot gear; and (5) extended immersion. Further 
studies of fungus infections and therapy have been 
reported by Conant, Martin, Smith, Baker, and 
Callaway {3743) 1944; Dowding and Levy {3744) 
1939; Downing and Conant {3745) 1945; Duggan 
{3746) 1944; Frazier and Deeper {3747) 1950; 
Glauser {3749) 1944; Gohar and Manson-Bahr 
{3750, 3751) 1948; Haley {3752, 3753, 3754, 
and 3755) 1950; James {3756) 1943; Lewis {3758) 
1951; Peck {3759) 1943; Shattuck {3762) 1951; 
Smith {3763) 1949; Sneddon {3764) 1942; Sutton 
and Sutton {3765) 1951; Swartz {3766) 1949; 
Whalen {3767) 1938; Wiltshire {3768) 1944; and 
Wolf {3769) 1945. 
In addition to fungus infections, acute bacterial 
infections of the external ear contribute to the 
reduction of the total number of man-hours in oper- 
ational swim-diving. For a description of acute bac- 
terial infection of the external ear, a paper by 
Mitchell {3756a) 1937 may be consulted. At times 
the condition is clinically indistinguishable from 
the early phase of otomycosis. A small furuncle may 
be found if the infection is seen early but in the 
later stages the edema and tenderness make thor- 
ough examination of the ear impossible. The ear 
drum is normal in appearance and if it can be 
visualized no discharge can be seen. Treatment con- 
sists of hot compresses to reduce edema and either 
penicillin or sulfadiazine for the infection. 
An unusual condition found in swimmers exposed 
to cold water is reported by Adams (3741 and 3742) 
1951. Lowering the external auditory canal tem- 
perature to approximately 65° F. by cold water is 
stated to be a major contributing factor in the de- 
velopment of exostoses and hyperostoses of the bony 
meatus. 
For further articles concerned with clinical prob- 
lems encountered in swimming the reader is ad- 
vised to consult reports by the following authors: 
Davies {3748) 1938; Mood, Clarke, and Gelperin 
{3757) 1951; and Rochaix {3761) 1936. 
3741. Adams, W, S. The aetiology of swimmer’s exos- 
toses of the external auditory canals and of associated 
changes in hearing. Part. I. /. Laryng., 1951, 65: 133-153. 
[D] [CH] 
3742. Adams, W. S. The aetiology of swimmer’s exos- 
toses of the external auditory canals and of associated 
changes in hearing. Part II. /. Laryng., 1951, 65: 232-250. 
[CH] 
3743. Conant, Norman F., Donald Stover Martin, 
David Tillerson Smith, Roger Denio Baker, and Jasper 
Lamar Callaway. Manual of clinical mycology. Phila- 
delphia, W. B. Saunders Company, 1944, 348 pp. 
3744. Dowding, E. S. and M. R. Levy. A mould from 
the ear. Canad. med. Ass. J., 1939, 41: 336-339. 
3745. Downing, J, G. and N. F. Conant. Mycotic in- 
fections. New Engl. J. Med., 1945,233: 153-161. 
3746. Duggan, T, L. Investigation of the fungistatic 
activity of reagents that might be suitable for use in the 
treatment of epidermophytosis. U. S. Navy. NMRI. Proj- 
ect X-A69, Kept. no. 1, 5 October 1944,4 pp. 
3747. Frazier, C. N. and R, W. Deeper. The treatment 
of common skin diseases. Med. Clin. N. Amer., 1950, 34: 
1473-1486. 
3748. Daviess, G. B. Sinusitis and ear infections as 
related to swimming and diving. /. Hlth. phys. Educ., 
1938,9; 308. 
3749. Glauser, F. Management of fungus infection of 
the feet. Nav. med. Bull., Wash., 1944,43: 525—526. 
3750. Gohar, N. and P. Manson-Bahr. The mycoses, 
pp. 14-16 in: Mycoses and practical mycology. Baltimore, 
The Williams & Wilkins Company, 1948, 234 pp. 
3751. Gohar, N. and P. Manson-Bahr. Fungicides: fun- 
gistatics: prescriptions: media: poisonous fungi. Pp. 209- 
221 in: Mycoses and practical mycology. Baltimore, The 
Williams & Wilkins Company, 1948, 234 pp. 
3752. Haley, L. D. Etiology of otomycosis. I. Mycologic 
flora of the ear. Arch. Otolaryng., Chicago, 1950, 52: 
202-207. 
3753. Haley, L. D. Etiology of otomycosis. II. Bacterial 
flora of the ear. Arch. Otolaryng., Chicago, 1950, 52: 
208-213. 
3754. Haley, L. D. Etiology of otomycosis. III. Observa- 
tions on attempts to induce otomycosis in rabbits. Arch. 
Otolaryng., Chicago, 1950, 52: 214—219. 
3755. Haley, L. D. Etiology of otomycosis. IV. Clinical 
observations. Arch. Otolaryng., Chicago, 1950, 52: 220— 
224. 
3756. James, A. P. R. The fungi go to war. Nav. med. 
Bull, Wash., 1943, 41: 1065-1067. 
3756-a. Mitchell, J. H. Streptococci dermatoses of the 
ears. J. Amer. med. Ass., 1930, 108: 361—366. 3757-3769 
SPECIAL PROBLEMS OF SWIM-DIVING 
restriction from water work, cleansing of the ulcer 
with a three-percent solution of hydrogen peroxide, 
and a dry dressing. 
A very large jellyfish or a concentration of jellyfish 
can incapacitate the operator and cause failure of 
the mission. On the tentacles of the jellyfish are 
thousands of specialized cells called nematocysts 
which are concerned with food getting. When the 
small sensitive elements of the nematocyst are 
touched a microscopic barb is projected to pierce 
the prey. The injected toxin is capable of paralyzing 
small fish and other life. A report of two jellyfish 
sting cases in 1943 by Stuart and Slagle {3786) 
describes pain of a burning character at the site of 
contact, with redness followed by an urticaria-like 
wheal about 10 minutes later. A person stung by 
jellyfish experiences immediate, severe pain usually 
accompanied by nausea and weakness and possibly 
shock. Moderate dilatation of the pupils may be 
accompanied by congestion of the respiratory mu- 
cous membrane and spasm of the respiratory mus- 
cles. The authors recommended intravenous use of 
10 cu. cm. of 10 percent calcium gluconate. Since 
this is usually not practical in the field, no treatment 
beyond local cold compresses, analgesics and rest 
may be available to swim-divers stung by jellyfish. 
Frachtman and McCollum {3776) 1945 reported 
the case of a sailor who was stung by a Portuguese 
man-of-war across the arms and thighs. Severe 
muscular spasms ensued, followed by the threat of 
respiratory failure. Administration of calcium salts 
intravenously failed to relieve the muscular spasms 
but barbiturates appeared to be of value in control- 
ling them. For additional information on jellyfish 
poisoning, reports by Light {3781) 1914, Old 
{3782) 1908, and Wade {3788) 1928 may be 
consulted. 
Sea urchins {Strongylocentrotus drobachiensis) 
are found in large numbers along coral reefs in 
tropical waters. According to Waite {3721) 1951 it 
is not uncommon for a swimmer to come away from 
an encounter with a sea urchin with 30 or more 
spines in his skin. These spines, which vary from 
about 2 to 15 cm. in length, have hundreds of 
microscopic barbs, making extraction difficult. The 
unfortunate diver who steps or sits on one of these 
animals suffers a severe, stinging pain as the spines 
penetrate deep into his tissues and break off. Broken 
spines buried deeply in the skin may be left alone 
for they will be absorbed. After the removal of as 
many spines as possible, the area should be cleansed 
with an antiseptic solution and cushioned with a 
large dressing. Penicillin and sulfadiazine should be 
administered prophylactically because the spines 
carry bacteria deep into the tissues. Waite recom- 
3757. Mood, E. W., C. C. Clarke, and A. Gelperin. The 
effect of available residual chlorine and hydrogen-ion con- 
centration upon the eyes of swimmers. Amer. J. Hyg., 
1951, 54: 145-159. [P] 
3758. Lewis, G. M. Superficial fungous infections, pp. 
665-671 in: The specialties in general practice. Edited by 
Russell L. Cecil. Philadelphia, W. B. Saunders Company, 
1951, 818 pp. 
3759. Peck, S. M. A practical plan for the treatment of 
superficial fungus infections. Publ. Hlth. Rep., Wash., 
1943, 58: 337-345. 
3760. Pillsbury, Donald M., Marion B. Sulzberger, 
and Clarence S. Livingood, Fungous infections, pp. 201- 
219 in: Manual of dermatology. Philadelphia. W. B. 
Saunders Company, 1942, 421 pp. 
3761. Rochaix, A. Natation et dangers d’infection. C. R. 
Congr. int. Med. educ. phys. {1934) 1936, pp. 331—336. 
[D] 
3762. Shattuck, George Cheever. Dermatomycoses. pp. 
623-629 in; Diseases of the tropics. New York, Appleton- 
Century-Crofts, Inc., 1951, 803 pp. 
3763. Smith, D. T. Fungous infections in the United 
States. /. Amer. med. Assoc., 1949,141: 1223-1225. 
3764. Sneddon, I. B. Epidermophyton infections of the 
skin. /. R. nav. med. Serv., 1942, 28: 154-160. 
3765. Sutton, R. L. and B. L. Sutton, Jr. The mycoses, 
pp. 115—170 in: Practice of medicine. Volume 4. Edited 
by Frederick Tice. Hagerstown, W. F. Prior Company, 
Inc., 1951, 733 pp. 
3766. Swartz, Jacob Hyams. Elements of medical my- 
cology. Second edition. New York, Grune & Stratton, 1949, 
240 pp. 
3767. Whalen, E. J. Fungous infections of the external 
ear. /. Amer. med. Assoc., 1938, 111: 502-504. 
3768. Wiltshire, S. P., C. Wilcocks, and J. T. Duncan. 
An annotated bibliography of medical mycology 1943. 
Kew, Surrey, The Imperial Mycological Institute, 1944, 
32 pp. [B] 
3769. Wolf, F. T. The action of sulfonamides on certain 
fungi pathogenic to man. U. S. AAF. Randolph Field, 
Tex. School of aviation medicine. Project 346, Rept. no. 1, 
16 January 1945, 7 pp. [P] 
IV. HAZARDS FROM DANGEROUS FISH AND 
OTHER MARINE ORGANISMS 
The underwater swimmer working in tropical 
waters has as much to fear from invertebrate ani- 
mals such as barnacles, coral, jellyfish, and sea 
urchins, as from vertebrates such as barracudas, 
sharks, and seals. The Moray eels will bite severely 
if molested and sting rays will inflict a wound if 
stepped on. According to Levin and Behrman 
{3780) 1941, abrasions by coral are notoriously 
slow to heal and it has been supposed that a toxic 
material on the coral is responsible. The affected 
skin shows intense serous exudation and a sloughing 
ulcer may appear within 24 hours. Immediate 
cleansing of all abrasions with soap and water, fol- 
lowed by application of sulfanilamide powder and 
dry dressings will aid prompt healing. Lambertsen 
{3718) 1947 recommends that when cases of re- 
tarded healing occur, treatment should consist in UNDERWATER BREATHING GEAR 
3770-3788 
mends wearing canvas shoes to protect the feet from 
both sea urchins and coral. 
The shark problem resembles somewhat the dog 
problem ashore and it is recommended that the 
swimmer in shark-inhabited areas keep moving and 
not become panicky. Actual instances of attacks on 
man by sharks are rare. Lambertsen {3718) 1947 
states that the two species apparently guilty of at- 
tack on man are the tiger and gray nurse sharks. 
Experiences of operational swimmers tend to sup- 
port the impression that sharks exhibit primarily a 
nonaggressive behavior towards man under the 
water’s surface. Lambertsen reported no cases of 
shark attack on men operating with him during 
10,000 man-hours of swim-diving in the Caribbean 
Sea, Indian Ocean, and Bay of Bengal. Although 
large sharks of unidentified species approached 
within a few feet of divers on many occasions, in 
each instance the approach was leisurely and in 
no way resembled an attack. Because it is believed 
that the shark is excited by the presence of blood 
in the water, any diver suffering a laceration was 
required to leave the water. A report by Springer 
{3784) 1943 describes with pictures and geographic 
location the habits and size of the various generic 
members of the shark family. 
Shark repellents, aside from their actual pro- 
tective qualities, give a boost to the morale of 
personnel in or near shark-infested waters. Springer, 
McBride, Todd, and Schmidt {3785) in 1943 re- 
ported on the effectiveness of copper acetate dif- 
fusing at a rate of 0.1 lb. per hour or more, under 
the field conditions experienced at that time, acting 
as a shark repellent. In tests performed by the U. S. 
Navy {3787) 1943, ethanol extract and maleic 
anhydride were found to be ineffective as shark 
repellents. Decomposition of shark meat yielded 
ammonium acetate suggesting the use of copper 
acetate. The latter compound proved effective as 
a deterrent when the diffusion rates exceeded 0.1 
lb. per hour. The shark repellent (specification no. 
Mil.-S-2785) attached to the inflatable life jackets 
of naval aviators includes copper acetate, a black 
dye, and a wax binder. Further references on the 
hazards from marine life by the following authors 
may be consulted; Amaral {3770) 1951; Bayley 
{3771) 1940; Burden {3772) 1945; Clench and 
Kondo {3773) 1943; Evans {3774) 1921; Gudger 
{3775) 1930; Halstead and Modglin {3777) 1950; 
Halstead {3778) 1951; Jarcho and Van Burkalow 
{3779) 1951 and Shattuck {3783) 1951. 
3770. Amaral, A. D. Poisoning by fish and other ani- 
mals. pp. 1265—1272 in: Clinical tropical medicine. 
Edited by R. B. H. Gradwohl, Luis Benitex Soto, and 
Oscar Felsenfeld. St. Louis, The C. V. Mosby Company, 
1951, 1647 pp. 
3771. Bayley, H. H. Injuries caused by scorpion fish. 
Trans. R. Soc. trap. Med. Hyg., 1940, 34: 227-230. 
3772. Burden, W. D. Development of a shark deterrent. 
Air Surg. Bull., 1944-45, 2: 344-347. 
3773. Clench, W. J. and Y. Kondo. The poison cone 
shell. Amer.J. trap. Med., 1943,25: 105-121. 
3774. Evans, H. M. The poison organs and venoms of 
venomous fish. Brit. med. J., 1921, 2: 690-692. 
3775. Gudger, E. W. Poisonous fishes and fish poison- 
ings, with special reference to ciguatera in the West In- 
dies. Amer. J. trap. Med., 1930, 10: 43-55. 
3776. Frachtman, H. J. and W. T. McCollum. Portu- 
guese man-of-war stings: a case report. Amer. J. trap. 
Med., 1945, 25: 499-500. [CH] 
3777. Halstead, B. W. and F. B. Modglin. A prelimi- 
nary report on the venom apparatus of the bat-ray, Hol- 
orhinus californicus. Copeia, 1950,5; 165-175. 
3778. Halstead, B. W. Injurious effects from the sting 
of the scorpionfish, Scorpaena guttata. Calif. Med., 1951, 
74: 395-396 
3779. Jarcho, S. and A. Van Burkalow. Geographical 
study of “swimmers’ itch” in the United States and 
Canada. Geogr. Rev., 1951, 42: 212-226. 
3780. Levin, 0. L. and H, T. Behrman. Coral derma- 
titis. Arch. Derm. Syph., 1941, 44: 600-603. [CH] 
3781. Light, S. F. Another dangerous jellyfish in Phil- 
ippine waters. Philipp. J. Sci. (b), 1914, 9: 291-295. 
3782. Old, E. H. H. A report of several cases with un- 
usual symptoms caused by contact with some unknown 
variety of jellyfish (scyphozoa). Philipp. J. Sci. (b), 1908, 
5; 329-333. [CH] 
3783. Shattuck, George Cheever. Various noxious ani- 
mals. pp. 755-760 in: Diseases of the tropics. New York, 
Appleton-Century-Crofts, Inc., 1951, 803 pp. 
3784. Springer, S. Sharks and their behavior. U. S. 
Navy. Office of coordinator of research and develop- 
ment. Emergency rescue equipment section, Washington, 
D. G., 29 September 1943, 10 pp. [R] 
3785. Springer, S., A. F. McBride, D. Todd, A. H. 
Schmidt. Tests of shark repellents—Gulf of Guayaquil. 
U. S. NRG. OEMcmr-184, 6 December 1942-10 Febru- 
ary 1943, 3 pp. [P] 
3786. Stuart, M. A. and T, D. Slagle. Jellyfish stings, 
suggested treatment, and report on two cases. Nav. med. 
Bull., Wash., 1943, 41: 497-501. [CH] 
3787. TJ. S. Navy. Office of coordinator of research and 
development. Report of conference. Protection of sea sur- 
vivors against shark attack. Washington, D. C., 29 Sep- 
tember 1943. [P] 
3788. Wade, H. W. Post-mortem findings in acute jelly- 
fish poisoning with sudden death in status lymphaticus. 
Amer. J. trap. Med., 1928, 8: 233-241. [CH] 
V. UNDERWATER BREATHING APPARATUS 
AND RELATED GEAR 
For many underwater operations, the advantages 
of apparatus independent of surface connections 
are obvious. Work requiring mobility, stealth, or 
freedom from heavy surface equipment can be car- 
ried out expeditiously with suitable self-contained 
underwater breathing apparatus. For a valuable 
review of such equipment, the reader is referred to SPECIAL PROBLEMS OF SWIM-DIVING 
sections of a lengthy monograph by Davis {3713, 
3797) published in 1951. 
Development of self-contained underwater 
breathing apparatus has followed three major lines: 
(1) the closed-circuit apparatus; (2) the open- 
circuit apparatus; and (3) the semi-closed circuit 
apparatus. These resulting types of equipment have 
characteristics which are distinct and which are 
advantageous in some types of work and undesira- 
ble in others. The first type in general use was the 
closed-circuit (oxygen rebreathing) equipment, the 
elements of which are a cylinder of oxygen, a 
breathing bag, and a canister containing a carbon 
dioxide absorbent. Such apparatus has the advan- 
tages of virtually complete utilization of the gas 
which is carried and the resulting absence of bub- 
bles. It is thus well adapted to work where the pres- 
ence of the user must not be detected from the 
surface. The main disadvantage lies in the possibil- 
ity of oxygen poisoning, which strictly limits the 
depth at which it can be safely used. 
Blockwick {3790 and 3792) 1950 reports com- 
parative evaluations of 3 closed-circuit units; Lam- 
bertsen, Mine Safety Appliance Co., and Browne. 
The studies included swimming runs with determi- 
nation of oxygen and carbon dioxide levels and 
overall endurance. Breathing resistance, dead air 
space, and the visual angles of mask eyepieces were 
measured, and general ease of use and repair were 
evaluated. Improvements in the Lambertsen unit 
were discussed in a U. S. Army report {3803) in 
1951. Modifications included increased operating 
duration through larger oxygen supply and in- 
creased carbon dioxide absorption capacity, incor- 
poration of a demand valve for automatic oxygen 
supply and buoyancy control, and improved vision 
through the use of smaller eyepieces mounted closer 
to the eyes. Report 3807 includes historical material 
on self-contained breathing equipment and de- 
scribes the Pirelli closed-circuit apparatus. This 
employs a valve system intended to supply oxygen 
at a constant rate. Waite {3806) 1951 reports an 
American evaluation of a British closed-circuit unit 
known as the Varbell. 
Perhaps the simplest form of self-contained un- 
derwater breathing apparatus is that which consists 
of cylinders containing compressed air with a de- 
mand valve which releases the amount of air 
required for each inspiration. Since the exhaled 
breath is simply expelled into the water, the term 
“open-circuit” is generally applied to this type of 
equipment. The volume of gas which must be car- 
ried for a dive of given duration is obviously much 
larger than for closed-circuit equipment. The dura- 
tion of the supply is further diminished at greater 
depths where the respiratory volume remains rel- 
atively unchanged while the elevated ambient pres- 
sure increases the actual mass of gas removed from 
the cylinders by each inspiration. Open-circuit ap- 
paratus can be used at much greater depths than 
oxygen-rebreathing systems, depth limits being im- 
posed primarily by duration of the air supply and 
by the danger of decompression sickness. Talliez, 
Dumas, Cousteau, Alinat, and Devilla {3802) 
1949, include in their monograph on diving a dis- 
cussion of the problems and principles of design of 
open-circuit apparatus. 
In his evaluation of open-circuit apparatus, 
Blockwick {3794) 1950, emphasizes the simplicity 
of this equipment but calls attention to the in- 
creased breathing resistance which demand valves 
may offer under conditions of hard work and in- 
creased depth. He also stresses the desirability of 
limiting the use of such units to those depths and 
times which do not require stage decompression. 
For further information on open-circuit compressed 
air equipment, reference may be made to Fulton 
and Blockwick {3798) 1951, Bussoz {3796), and 
reports 3800 and 3801. 
The third major type of self-contained under- 
water breathing apparatus involves a “semi-closed” 
circuit in which the gas supply is conserved by re- 
breathing but in which a controlled rate of inflow 
and spillage permits reasonably safe use of breath- 
ing media other than pure oxygen. Reports by 
Waite {3805) 1951, and Fulton, Welham, and 
Blockwick {3799) 1951, discuss the performance of 
such equipment and point out its advantages over 
the simpler open- and closed-circuit types. The per- 
centage of nitrogen in the respired gas, and thus 
also the danger of decompression sickness, can be 
reduced by using a gas mixture containing a higher 
percentage of oxygen than that found in air. Pro- 
vided that the increase in oxygen content is not 
sufficient to introduce the danger of oxygen poison- 
ing and that consumption of oxygen does not exceed 
the amount supplied, use of this apparatus permits 
significant extension of the depth-time limits. In 
addition, the reduction of bubble formation renders 
detection more difficult than in the use of open- 
circuit gear. Reference may also be made to Block- 
wick {3789 and 3793) 1950, and report 3804 for 
further information on subjects relating to self-con- 
tained underwater breathing apparatus. 
In many locations, the effect of exposure to cold 
water limits the activities of swim-divers much more 
severely than do problems of breathing apparatus. 
Development of protective suits is thus a vital task 
which demands extensive study. Problems of buoy- 
ancy-control introduced by the use of insulating UNDERWATER BREATHING GEAR 
3789-3807 
suits to conserve body heat can be discerned in a 
study by Blockwick (3791) 1950, in which a light- 
weight diving dress and an underwater swim suit 
were investigated from this standpoint with various 
amounts of clothing beneath. The obvious advan- 
tages of a positive method of supplying heat led 
to an investigation of electrically heated clothing 
by Blockwick (3795) 1951. It was concluded that 
150 to 250 watts are required to keep hands and 
feet warm in water colder than 45° F. and that it 
is not feasible for a swimmer to carry batteries 
which will meet these power requirements. The 
study also indicated that two suits of heavy diving 
underwear would suffice without additional heat 
in water at 55° F., but that immersion at 45° F. 
would require the same amount of underwear in 
addition to heated gloves and boots. 
3789. Blockwick, T. N. Determination of the potentiali- 
ties of the mine safety appliance self-contained swimming 
outfit for descents to 400 ft. using helium-oxygen breath- 
ing mixtures. U. S. Navy. Naval gun factory. EDU. S94— 
(3)-(l)-{694D) of 4 November 1949, Rept. no. 10-50, 
4 December 1950. 
3790. Blockwick, T. N. Determination of C02 and 02 
at various stages of the dives using 3 different types of self- 
contained breathing apparatus under identical conditions 
and the appraisal of them from a standpoint of comfort, 
breathing resistance, duration, visibility and other factors 
pertinent to their practical use. U. S. Navy. Naval gun 
factory. EDU. Project NS 186-012, Rept. no. 1—50, 21 
February 1950, 8 pp. 
3791. Blockwick, T. N. The determination of the basic 
condition of lightness that can be attained by the present 
lightweight diving outfit and the underwater swim suit 
and the evaluation of their operating characteristics. 
U. S. Navy. Naval gun factory. EDU. Project NS 186- 
052, Rept. no. 2-50, 21 March 1950, 9 pp. 
3792. Blockwick, T. N. Determination of C02 and 02 
at various stages of the dives using three different types of 
self-contained breathing apparatus under identical condi- 
tions and the appraisal of them from a standpoint of 
comfort, breathing resistance, duration, visibility and 
other factors pertinent to their practical use. U. S. Navy. 
Naval gun factory. EDU. Project NS 186-012, Rept. no. 
4-50, 12 June 1950, 10 pp. 
3793. Blockwick, T. N. Determination of the potentiali- 
ties of the Bendix, MSA and Cousteau-Gagnon demand 
breathing appliances for descents to 400 feet and the 
measurement of the amounts of gas required for the various 
depths. U. S. Navy. Naval gun factory. EDU. S94-{3)- 
(1 )—{694D) of 4 November 1949, Rept. no. 5-50, 2 
August 1950, 9 pp. 
3794. Blockwick, T, N. Evaluation of the performance 
of the aqua lung self-contained swimming outfit as fur- 
nished and also when it is modified by the substitution of 
the mouthpiece for a face mask. U. S. Navy. Naval gun 
factory. EDU. Project NS-186-012, Test no. 17, Kept, 
no. 6-50, 12 September 1950,5 pp. 
3795. Blockwick, T. N. Test of electrically heated 
clothing. U. S. Navy. Naval gun factory. EDU. Project 
NS 186-012, Test no. 12, Kept. no. 3—51, 13 February 
1951, 15 pp. 
3796. Bussoz, R. Self-contained diving. U. S. Divers Co., 
Los Angeles, Calif, (no date), 23 pp. 
3797. Davis, Robert H. Self-contained and armoured 
diving apparatus, pp. 204-213 in: Deep diving and sub- 
marine operations. A manual for deep sea divers and com- 
pressed air workers. London, The Saint Catherine Press 
Ltd., Fifth edition, 1951, 670 pp. [D] 
3798. Fulton, H. T. and T. N. Blockwick. Test of the 
Scott model 8300 self-contained underwater breathing 
apparatus. U. S. Navy. Naval gun factory. EDU. Project 
NS 186-012, Test no. 23, Kept. no. 9-51, 22 June 1951, 
6 pp. 
3799. Fulton, H. T., W. Welham and T. N, Blockwick. 
Preliminary report of nitrogen-oxygen self-contained un- 
derwater breathing equipment. U. S. Navy. Naval gun 
factory. EDU. Project NS 186-201, Sub task no. 5, Kept, 
no. 8-51, 11 June 1951, 13 pp. 
3800. Scott Aviation Corporation. Descriptive specifica- 
tions of the Scott model 8300 self-contained shallow water 
diving equipment. Lancaster, New York, (no date), 10 pp. 
3801. Siebe, Gorman, and Company, Ltd. “Essjee” self- 
contained compressed air diving apparatus (single cylinder 
type). Descriptive information circular. Siebe, Gorman 
and Company, Ltd., London, 1 p. 
3802. Tailliez, P., F. Dumas, J. Y. Cousteau, J. Alinat, 
and F. Devilla. Principe des scaphandres. Scaphandres a 
casque, pp. 23—36 in: La plongee en scaphandre. Paris, 
Elzevir, 1949, 119 pp. 
3803. U. S. Army. Engineer research and development 
laboratory. Fort Belvoir, Va. Water Supply Equipment 
branch. Improvement of Lambertsen type diving unit. 
Project 8-80-11-002, Final rept., 1 October 1951, 44 pp. 
3804. U. S. Navy. BuShips. Use of shallow water diving 
mask. NavShips No. 394 0007, 1943, 18 pp. 
3805. Waite, C. L. Evaluation of the British Admiralty 
“P” party suit. U. S. Navy. Naval gun factory. EDU. 
Project NS 186—201, Sub task no. 5, Rept. no. 2—51, 
1 February 1951, 8 pp. 
3806. Waite, C. L. Evaluation of the British Varbell 
self-contained swimming suit. U. S. Navy. Naval gun 
factory. EDU. Project NS 186-012, Rept. no. 4-51, 2 
March 1951, 4 pp. 
3807. Anon. Pirelli underwater oxygen self-contained 
breathing apparatus. Model L. S. 901. Pirelli, Inc. New 
York, N. Y., 19 pp. Key to Abbreviations of Journals 
and Handbooks Cited 
Abbreviations not included in A World List of Scientific Periodicals Published in the 
Years i goo-30, 3d Ed., London, 1952 are marked with an asterisk 
Abstr. Diss. Stanf. Univ. Abstracts 
of Dissertations for the Degree of 
Doctor of Philosophy. Stanford 
University, Palo Alto. 
Abstr. World Med. Abstracts of 
World Medicine. London. 
Acta brev. neerl. Physiol. Acta 
brevia Neerlandica de Physiologia, 
Pharmacologia, Microbiologia, e. a. 
Amsterdam. 
Acta cardiol., Brux. Acta Cardio- 
logica. Bruxelles. 
Acta med. scand. Acta medica Scan- 
dinavica. Stockholm. 
Acta neural, belg. Acta neurologica 
et psychiatrica Belgia. Bruxelles. 
Acta opthal., Kbh. Acta opthalmo- 
logica. Kjpbenhavn. 
Acta oto-laryng., Stockh. Acta oto- 
laryngologica. Stockholm. 
Acta oto-rhino-laryng. belg. Acta 
oto-rhino-laryngologica Belgica. 
Bruxelles. 
Acta path, microbial, scand. Acta 
pathologica et microbiologica 
Scandinavica. Kpbenhavn. 
Acta pharm. toxicol., Kbh. Acta 
pharmocologica et toxicologica. 
Kpbenhavn. 
Acta physiol, pharm neerl. Acta 
physiologica et pharmacologica 
Neerlandica. Amsterdam. 
Acta physiol, scand. Acta physio- 
logica Scandinavica. Stockholm. 
Acta psychiat., Kbh. Acta psychi- 
atrica et neurologica. Kj0ben- 
havn. 
Acta Sch. med. Univ. Kioto. Acta 
Scholae Medicinalis Universitatis 
Imperialis in Kioto. Kioto. 
Advanc. internal Med. Advances in 
Internal Medicine. New York. 
Advanc. Sci., Land. Advancement 
of Science, London. 
Air sea-rescue Bull* Air sea-rescue 
Bulletin. Washington D. C. 
Air Surg. Bull. Air Surgeon’s Bul- 
letin. Dayton, Ohio. 
Algerie. med. Algerie medicale. 
Alger. 
Amer. Anthrop. American Anthro- 
pologist. Lancaster, Pa. 
Amer. Heart J. American Heart 
Journal. St. Louis. 
Amer. ind. Hyg. Ass. Quart. Amer- 
ican Industrial Hygiene Association 
Quarterly. 
Amer. J. din. Path. American Jour- 
nal of Clinical Pathology. Balti- 
more. 
Amer. J. Hyg. American Journal of 
Hygiene. Baltimore. 
Amer. J. Med. The American Jour- 
nal of Medicine. New York. 
Amer. J. med. Sci. American Jour- 
nal of the Medical Sciences. Phil- 
adelphia. 
Amer. J. Nurs. American Journal of 
Nursing. Philadelphia. 
Amer. J. Obstet. Gynec. American 
Journal of Obstetrics and Gyne- 
cology. St. Louis. 
Amer. J. Ophthal. American Jour- 
nal of Ophthalmology. St. Louis. 
Amer. J. Optom. The American 
Journal of Optometry. Minne- 
apolis. 
Amer. J. Path. American Journal of 
Pathology. Boston. 
Amer. J. Physiol. American Journal 
of Physiology. Boston. 
Amer. J. Psychol. American Journal 
of Psychology. Worcester. 
Amer. J. publ. Hlth. American 
Journal of Public Health. New 
York. 
Amer. J. Roentgenol. American 
Journal of Roentgenology (and 
Radium Therapy). New York. 
Amer. J. trop. Med. American Jour- 
nal of Tropical Medicine. Balti- 
more. 
Amer. Practit. American Practi- 
tioner. Philadelphia. 
Amer. Psychol. The American Psy- 
chologist. Baltimore. 
Amer. Publ. tilth. Yearbk, Pt. II .* 
American Public Health Associa- 
tion Yearbook. New York. 
Amer. Rev. Sov. Med. American 
Review of Soviet Medicine, New 
York. 
An. Fac. Med. Lima. Anales de la 
facultad de Medicina. Universi- 
dad (nacional Mayor de San 
Marcos) de Lima. 
Analyst. The Analyst. London. 
Anat. Rec. Anatomical Record. Phil- 
adelphia. 
Anest. Analg. Anesthesie et analgesic. 
Paris. 
Anesthesiology. Anesthesiology. Lanc- 
aster, Pa. 
Ann. Hyg. publ., Paris. Annales d’hy- 
giene publique et de medecine 
legale (industrielle et sociale). 
Paris. 
Ann. intern. Med. Annals of Internal 
Medicine. Ann Arbor. 
Ann. Med. exp. Fenn. Annales medi- 
cinae experimentalis et biologiae 
Fenniae. Helsinki. 
Ann. Med. leg. Annales de medecine 
legale. Paris. 
Ann. Med. nav. colon. Annali di med- 
icina navale e coloniale. Roma. 
Ann. N. Y. Acad. Sci. Annals of the 
New York Academy of Sciences. 
N. Y. 
Ann. Oculist., Paris. Annales d’ocu- 
listique. Paris. 
Ann. Oto-laryng. Annales d’oto- 
laryngologie. Paris. 
Ann. Otol., etc., St. Louis. Annals of 
Otology, Rhinology and Laryngol- 
ogy. St. Louis. 
Ann. trop. Med. Parasit. Annals of 
Tropical Medicine and Parasitol- 
ogy. Liverpool. 
Annee psychol. Annee psychologique. 
Paris. 
Annu. Rev. med. Annual Review of 
Medicine. Stanford University, 
Palo Alto. JOURNAL ABBREVIATIONS 
Ann-Cli 
Annu. Rev. Physiol. Annual Review 
of Physiology. Stanford University, 
Palo Alto. 
Arch. Anthrop. crim. Archives d’an- 
thropologie criminelle, de medecine 
legale et de psychologic normale et 
pathologique, Lyon. 
Arch, beiges Med. soc. Archives bei- 
ges de medecine sociale, hygiene, 
medecine du travail et medecine 
legale. Bruxelles. 
Arch. Biochem. Archives of Biochem- 
istry. New York. 
Arch. Derm. Syph., N. Y. Archives 
of Dermatology and Syphilology. 
New York. 
Arch. exp. Path. Pharmak. Naunyn- 
Schmiedebergs Archiv fur experi- 
mentelle Pathologic und Pharma- 
kologie. Leipzig. 
Arch, industr. Hyg. Archives of In- 
dustrial Hygiene and Occupational 
Medicine. Baltimore. 
Arch, indust. Hyg., Chicago. Archives 
of Industrial Hygiene. Chicago. 
Arch. int. Pharmacodyn. Archives In- 
ternationales de pharmacodynamic 
(et de therapie). Bruxelles-Paris, 
Gand. 
Arch. int. Physiol. Archives Interna- 
tionales de physiologic. Liege et 
Paris. 
Arch, intern. Med. Archives of In- 
ternal Medicine. Chicago. 
Arch. Mai. prof. Archives des Mala- 
dies professionelles; Hygiene et 
Toxicologic industrielles. Paris. 
Arch. Mai. prof. Archives des mala- 
dies professionelles de Medecine 
du travail et de securite sociale. 
Paris. 
Arch, neerl. Physiol. Archives neer- 
landaises de physiologic de Phom- 
me et des animaux. Amsterdam. 
Arch. Neurol. Psychiat., Chicago. 
Archives of Neurology and Psychi- 
atry. Chicago. 
Arch. Ohr.-, Nas.-, u. KehlHeilk. 
Archiv fur Ohren—, (Nasen— 
und Kehlkopf) heilkunde, Leipzig. 
Arch. Ophthal., N. Y. Archives of 
Ophthalmology. New York. 
Arch. Ophtal., Paris. Archives d’oph- 
talmologie. Paris. 
Arch. Otol., N. Y. Archives of Otol- 
ogy. New York. 
Arch. Otolaryng., Chicago. Archives 
of Otolaryngology. Chicago. 
Arch. Path., Chicago. Archives of 
Pathology (and Laboratory Medi- 
cine). Chicago. 
Arch. phys. Med. Archives of Physi- 
cal Medicine. Omaha. 
Arch. Psychol., N. Y. Archives of 
Psychology. New York. 
Arch. Sci. biol., Napoli. Archivio di 
scienze biologische. Napoli. 
Arch. Sci. med. Archivio per le 
scienze mediche. Torino. 
Arch. Soc. oftal. hisp.-amer. Archives 
de la Sociedad oftalmologica his- 
pano-americana. Barcelona. 
Arch. Surg., Chicago. Archives of 
Surgery. Chicago. 
Arkh. Pat. Arkhiv Patologii. Moskva. 
Army med. Bull. Army Medical Bul- 
letin. Carlisle, Pa. 
Beitr. path. Anat. Beitrage zur pa- 
thologischen Anatomic und zur 
allgemeinen Pathologic. Jena. 
Bibl. Laeger. Bibliotek for laeger. 
Published in Kj0benhavn. 
Biochem. J. Biochemical Journal. 
Cambridge. 
Biol. med. Biologic medical. Paris, 
Blood. Blood. The Journal of Hema- 
tology. New York. 
Boll. Soc. ital. Biol. sper. Bollettino 
della Societa italiana di biologia 
sperimentale. Napoli. 
Brain. Brain; a journal of neurology. 
London. 
Brit. dent. J. British Dental Journal. 
London. 
Brit. Guiana med. Annu. British 
Guiana Medical Annual and Hos- 
pital Reports. Demerara. 
Brit. J. Derm. British Journal of 
Dermatology (and Syphilis). 
London. 
Brit. J. industr. Med. British Journal 
of Indutrial Medicine. London. 
Brit. J. Opthal. British Journal of 
Ophthalmology. London. 
Brit. J. phys. Med. British Journal 
of Physical Medicine and Indus- 
trial Hygiene. London. 
Brit. J. Psychol. British Journal of 
Psychology. Cambridge. 
Brit. med. Bull. British Medical Bul- 
letin. London. 
Brit. med. J. British Medical Journal. 
London. 
Bull. Acad. nat. Med. Bulletin de 
P Academic nationale de medecine. 
Paris. 
Bull. Hyg., Land. Bulletin of Hygiene. 
London. 
Bull. int. Serv. Sante Arm. Bulletin 
international des services de sante 
des armees de terre, de mer et de 
Pair. Liege. 
Bull. Los Angeles neural. Soc. Bul- 
letin of the Los Angeles Neuro- 
logical Society. Los Angeles. 
Bull. math. Bio phys. Bulletin of 
Mathematical Biophysics. Chicago. 
Bull. med. chir. Fac. Md. Bulletin of 
the Medical and Chirurgical Fac- 
ulty of Maryland. Baltimore. 
Bull. Menninger Clin. Bulletin of the 
Menninger Clinic. Topeka, Kans. 
Bull. New Engl. med. Cent. Bulletin 
of the New England Medical 
Centre. Boston, Mass. 
Bull. N. Y. Acad. Med. Bulletin of 
the New York Academy of Medi- 
cine. New York. 
Bull, pract. Ophthal. Bulletin of 
Practical Ophthalmology. San 
Francisco. 
Bull. Soc. Franq. Derm. Syph. Bulle- 
tin de la Soci6te frangaise de der- 
matologic et de syphiligraphie. 
Paris. 
Bull. Soc. Franq. Ophtal. Bulletin et 
memoires de la Societe fran$aise 
d’ophtalmologie. Paris. 
Bull. Soc. m£d. Hop. Paris. Bulletin 
et memoires de la Societe medicale 
des hopitaux de Paris. 
Byull. eksp. Biol. Med. Byulletin ek- 
sperimentalnoy Biologii i Medit- 
siny. Moskva. 
C. R. Acad. Sci., Paris. Compte rendu 
hebdomadaire des seances de P- 
Academie des sciences. Paris. 
C. R. Acad. Sci., U. R. S. S. Compte 
rendu de 1’Academic des sciences 
de FU. R. S. S. Moskva. Lenin- 
grad. 
C. R. Congr. int. med. Educ. Compte 
rendu; Congres international de 
Medecine appliquee a 1’education 
physique et aux sports. 
C. R. Soc. Biol., Paris. Compte rendu 
hebdomadaire des seances et mem- 
oires de la Societe de biologic. 
Paris. 
Calif. Med. California Medicine. 
San Francisco. 
Canad. J. Med. Sci. Canadian Jour- 
nal of Medical Sciences. Ottawa, 
Canada. 
Canad. J. publ. Hlth. Canadian Jour- 
nal of Public Health. Toronto. 
Canad. J. Res. Canadian Journal of 
Research. Ottawa. 
Canad. med. Ass. J. Canadian Medi- 
cal Association Journal. Toronto. 
Cancer Res. Cancer Research. Balti- 
more. 
Cas. Lek. ces. Casopis L6kafu 
Ceskych. v Praze. 
Chem. Abstr. Chemical Abstracts. 
Easton, Pa. 
Cincinn. J. Med. Cincinnati Journal 
of Medicine. Cincinnati. 
Circulation. Circulation. New York. 
Cleveland Clin. Quart. Cleveland 
Clinical Quarterly. Cleveland. 
Clin. Sci. Clinical Science, incorpo- 
rating Heart. London. 
Clin, otorinolaring. Clinica otorino- 
laringo-iatrica. Roma. XVI Con—J. Lab 
JOURNAL ABBREVIATIONS 
XVI Concil. ophth. 1950 Acta. 
XVI Concilium Ophthalmologi- 
cum 1950 Britannica London Acta. 
London. 
Conn. St. med. J. Connecticut 
State Medical Journal. New 
Haven. 
Contact. Pensacola. Contact. U. S. 
Naval Air Station. Pensacola, Fla. 
Contr. Boyce Thompson Inst. Con- 
tributions from Boyce Thompson 
Institute for Plant Research. Me- 
nasha, Wis. 
Curr. Res. Anesth. Current Re- 
searches in Anesthesia and Anal- 
gesia. Rocky River, Ohio. 
Curr. Sci. Current Science. Ban- 
galore. 
Dent. Surv. Dental Survey. Minne- 
apolis. 
Diagnosi. Napoli. Diagnosi; rivista 
di medicina pratica. Napoli. 
Dis. nerv. Syst. Diseases of the Nerv- 
ous System. Chicago. 
Docum. ophthal. Documenta oph- 
thalmologica. Zurich, Paris. 
Dtsch. Militdrarzt. Deutsche Mili- 
tararzt. Berlin. 
Dtsch. militdrdrztl. Deutsche Mili- 
tararztliche Zeitschrift. Berlin. 
Endocrinology. Endocrinology. Glen- 
dale, Calif. 
Engineer, Lond. Engineer. Lon- 
don. 
Enzymologia. Enzymologia. Den 
Haag. 
Excerpta med. Excerpta medica. 
Amsterdam. 
Excerpta med. Excerpta medica. 
Basel, Leipzig. 
Experientia. Experientia. Basel. 
Exp. Med. Surg. Experimental Med- 
icine and Surgery. Brooklyn Med- 
ical Press. 
Farmacoter. act. Farmacoterapia ac- 
tual. Madrid. 
Fed. Proc. Federation Proceedings. 
(American Societies for Experi- 
mental Biology). Baltimore. 
Fed. Proc. Amer. Soc. Pharm. exp. 
Ther. Federation Proceedings for 
the Society for Pharmacology and 
Experimental Therapeutics, Inc. 
Fiziol. Zh. S. S. S. R. Fiziologi- 
cheskiy Zhurnal. S. S. S. R. 
Moskva. Journal of Physiology of 
the U. S. S. R. Moscow. 
Folia cardiol., Milano. Folia cardi- 
ologica. Milano. 
Folia endocrin. jap. Folia endocrin- 
ologica japonica. Kyoto. 
Folia med., Napoli. Folia medica. 
Napoli. 
Frankfurt Z. Path. Frankfurter 
Zeitschrift fur Pathologic. Wies- 
baden. 
Fukuoka Acta med. Fukuoka Acta 
medica. Fukuoka. 
Gastroenterology. Gastroenterology. 
Baltimore. 
Geneesk. Gids. Geneeskundige 
Gids.’s Gravenhage. 
Geogr. Rev. The Geographical Re- 
view. New York. 
Gesundh. u. Erzieh. Gesundheit und 
Erziehung. Leipzig. 
Gesundh. u. Wohlf. Gesundheit und 
Wohlfahrt. Zurich. 
Gigiena San., Moskva. Gigiena i 
sanitariya. Moskva. 
Gigiena Truda. Gigiena truda. 
Moskva. 
Gipoksiia. Gipoksiia. Moskva. 
Gluckauf. Gluckauf! Berg-u. Hut- 
temann Zeitschrift. Essen. 
Guy’s Hasp. Gaz. Guy’s Hospital 
Gazette. London. 
Heat. Pip. Air Condit. Heating, 
Piping, and Air Conditioning. 
New York. 
Heat. & Ventilating. Heating and 
Ventilating. New York. 
Helv. med. acta. Helvetica medica 
acta. Basel. 
Helv. physiol, acta. Helvetica phy- 
siologica et pharmacologica acta. 
Basel. 
Hasp. top. & buyer* Hospital Top- 
ics & Buyer. Chicago. 
Hospital. Rio de J. Hospital. Rio 
de Janeiro. 
Hum. Biol. Human Biology; a rec- 
ord of research. Baltimore. 
Industr. Med. Industrial Medicine. 
Chicago. 
Igaku & Seibutugaku* Tokyo. 
Ilium. Engr., N. Y. Illuminating 
Engineer. New York. 
Indian Physician. Indian Physician. 
Bombay. 
XVIII Intern, physiol. Congr. In- 
ternational Physiological Congress. 
Copenhagen. 
Irish J. med. Sci. Irish Journal of 
Medical Science. Dublin. 
J. acoust. Soc. Amer. Journal of the 
Acoustical Society of America. 
Menasha, Wise. 
J. Amer. med. Ass. Journal of the 
American Medical Association. 
Chicago. 
/. Amer. Wat. Wks. Ass. Journal of 
the American Water Works Assoc., 
Baltimore. 
J. Anim. Sci. Journal of Animal 
Science. Menasha, Wise. 
J. appl. Physiol. Journal of Applied 
Physiology. Washington. 
/. appl. Psychol. Journal of applied 
Psychology. Worcester, Mass. 
/. Aviat. Med. Journal of Aviation 
Medicine. New Orleans. 
/. biol. Chem. Journal of Biological 
Chemistry. Baltimore. 
/. cell. comp. Physiol. Journal of 
Cellular and Comparative Physiol- 
ogy. Philadelphia. 
/. Chir., Paris. Journal de chirurgie. 
Paris. 
/. din. Endocrin. Journal of Clinical 
Endocrinology. Springfield, 111. 
/. din. Invest. Journal of Clinical 
Investigation. Baltimore. 
/. din. Psychol. Journal of Clinical 
Psychology. Burlington. 
/. comp. Psychol. Journal of Com- 
parative Psychology. Baltimore. 
/. dent. Res. Journal of Dental Re- 
search. Baltimore. 
/. Egypt, med. Ass. Journal of the 
Egyptian Medical Association. 
Cairo. 
J. Endocrin. Journal of Endocrinol- 
ogy. Oxford, Cambridge. 
/. exp. Med. Journal of Experimen- 
tal Medicine. New York. 
/. exp. Psychol. Journal of Experi- 
mental Psychology. Princeton, 
N. J. 
J. exp. Zool. Journal of Experimen- 
tal Zoology. Philadelphia. 
/. frang. Med. Chir. thor. Journal 
de medecine et chirurgie 
thoracique. Paris. 
/. gen. Physiol. Journal of General 
Physiology. Baltimore. 
J. gen. Psychol. Journal of General 
Psychology. Worcester, Mass. 
/. Geront. Journal of Gerontology. 
Springfield, 111. 
J. Hlth. phys. Educ. Journal of 
Health and Physical Education. 
Springfield, Mass. 
J. Hyg., Camb. Journal of Hygiene. 
Cambridge. 
/. Indian med. Aw. Journal of the 
Indian Medical Association. Cal- 
cutta. 
/. Ind. med. Ass. Journal of the In- 
diana State Medical Association. 
Indianapolis. 
J. industr. Hyg. Journal of Indus- 
trial Hygiene (and Toxicology). 
New York, Boston, Baltimore. 
J. infect. Dis. Journal of Infectious 
Diseases. Chicago. 
/. invest. Derm.* Journal of Inves- 
tigative Dermatology. Baltimore. 
/. Lab. din. Med. Journal of Lab- 
oratory and Clinical Medicine. 
St. Louis. JOURNAL ABBREVIATIONS 
J. Lar-Niss 
/. Laryng. Journal of Laryngology 
(Rhinology) and Otology. Lon- 
don. 
/. Med. Chir. prat. Journal de mede- 
cine et de chirurgie pratiques. 
Paris. 
J. Med. Lyon. Journal de medecine 
de Lyon. 
/. med. Soc. N. J. Journal of the 
Medical Society of New Jersey. 
Newark. 
/. Ment. Sci. Journal of mental 
Science. London. 
J. Mich. med. Soc. Journal of the 
Michigan State Medical Society. 
Detroit. 
J. Mie med. Coll. Journal of Mie 
Medical College. 
J. nerv. ment. Dis. Journal of Ner- 
vous and Mental Diseases. New 
York. 
/. Neurol. Psychiat. Journal of Neu- 
rology (Neurosurgery) and Psy- 
chiatry. London. 
]. Neuropath. Journal of Neuropa- 
thology and Experimental Neurol- 
ogy. Baltimore. 
J. Neurophysiol. Journal of Neuro- 
physiology. Springfield, III. 
]. Nutrit. Journal of Nutrition. 
Philadelphia, Pa. 
/. Okla. med. Ass. Journal of the 
Oklahoma State Medical Associa- 
tion. Muskogee. 
/. opt. Soc. Amer. Journal of the 
Optical Society of America. Phila- 
delphia. 
/. oto-rhinolaryng. Soc., Tokyo. 
Journal of the Oto-rhino-laryngo- 
logical Society of Japan. Tokyo. 
J. Path. Bact. Journal of Pathology 
and Bacteriology. London. 
J. Pharmacol. Journal of Pharma- 
cology and Experimental Thera- 
peutics. Baltimore. 
J. Phil. Is. med. Ass. Journal of the 
Philippine Islands Medical Asso- 
ciation. Manila. 
J. Physiol. Journal of Physiology. 
London; Cambridge. 
J. Physiol. Path. gen. Journal de 
physiologic (et de pathologic gen- 
erate). Paris. 
/. Psychol. Journal of Psychology. 
Worcester, Mass. 
J. R. nav. med. Serv. Journal of the 
Royal Naval Medical Service. 
London. 
/. Radiol. Electrol. Journal de radi- 
ologic et d’electrologie (et Archives 
d’electricite medicale). 
/. Res. nat. Bur. Stand. Journal of 
Research. National Bureau of 
Standards. Washington. 
/. Sci. Labour. The Journal of 
Science of Labour. Tokyo. 
/. Speech Dis. Journal of Speech 
(and Hearing) Disorders. Colum- 
bus, Ohio. 
/. thorac. Surg. Journal of Thoracic 
Surgery. St. Louis. 
Jap. J. Hyg* Japanese Journal of 
Hygiene. Tokyo. 
Jap. J. Physiol. Japanese Journal of 
Physiology. Nagoya. 
Jap. med. J. The Japanese Medical 
Journal. Tokyo. 
Johns Hopk. Hasp. Bull. Johns Hop- 
kins Hospital Bulletin. Baltimore. 
Keio Igaku.* Keio Igaku. Tokyo. 
Klin, Mbl. Augenheilk. Klinische 
Monatsblatter fur Augenheilkunde. 
Stuttgart. 
K. Krigsvet. handl. tidsskr* Kung- 
liga Krigsvetenskaps - akademien 
Handlingar och tidsskrift. Stock- 
holm. 
Lancet. Lancet. London. 
Laryngoscope. St. Louis. Laryngo- 
scope. St. Louis. 
Laval med. Laval medical. Que- 
bec. 
Lek wojsk. Lekarz Wojskowy. 
Warszawa. 
Luftfahrtmedizin. Luftfahrtmedizin. 
Berlin. 
Mag. belorv. Arch. Magyar Belor- 
vosi Archivum es Ideggyogyaszati 
Szemle. Budapest, Hungary. 
Mar. News. Marine News. New 
York. 
Maroc med. Maroc medical. Casa- 
blanca. 
MD. MD. Chicago. 
Mech. Engr. Mechanical Engineer. 
Manchester. 
Med. aero. Medicine aeronautique. 
Paris. 
Med. Arts Sci. Medical Arts and 
Sciences. Washington. 
Med. Cirurg. Pharm. Medicina, cir- 
urgia, pharmacia. Rio de Janeiro. 
Med. Clin. N. Amer. Medical 
Clinics of North America. Phila- 
delphia. 
Med. d. Lavoro. Medicina del la- 
voro. Milan%. 
Med. Departe y Trab. Medicina del 
deporte y del trabajo. Buenos 
Aires. 
Med. et Hyg., Anvers. Medecine et 
hygiene. Anvers. 
Med. Glasn. (Russian).* Medicin- 
ski. Glasnik. Belgrade. 
Med. J. Aust. Medical Journal of 
Australia. Sydney. 
Med. J. Malaya. Medical Journal of 
Malaya. Singapore. 
Med. J. Rec. Medical Journal and 
Record. New York. 
Med. Klinik. Medizinische Klinik. 
Wien. 
Med. Pr. Medical Press (and Cir- 
cular). London. 
Med. usine. Le Medecin d’usine. 
Edition du Medecin d’usine. 
Paris. 
Med. Welt. Medizinische Welt. 
Berlin. 
Med. World. Land. Medical World. 
London. 
Med. World. Philad. Medical 
World. Philadelphia. 
Medicina. Madr. Medicina. Ma- 
drid. 
Medicine. Baltimore. Medicine. 
Baltimore. 
Mem. Inst. Osw. Cruz. Memo ias do 
Institute Oswaldo Cruz. Rio de 
Janeiro. 
Milk. Rev. Fort Leavenw. Com- 
mand and General Staff School 
Military Review. Fort Leaven- 
worth, Kansas. 
Milk. Surg. Military Surgeon. 
Washington. 
Mitt. med. Akad. Kioto. Mitteilun- 
gen aus der Medizinischen Akade- 
mie zu Kioto. Kyoto-Ikadaigaku- 
Zasshi, 
Mschr. Ohrenheilk. Monatsschrift 
fur Ohrenheilkunde und Laryngo- 
Rhinologie. Wien & Berlin. 
N. Y. med. J. New York Medical 
Journal. New York. 
N. Y. St. J. Med. New York State 
Journal of Medicine. New York. 
Nat. Inst. Hlth. Bull. National In- 
stitute of Health Bulletin. United 
States Public Health Services. 
Washington. 
Nation’s Hlth. Nation’s Health. 
Chicago. 
Nature. Land. Nature. London. 
Nature. Paris. Nature. Paris. 
Nav. arm. med. Cps. J* Naval Army 
Medical Corps Journal. Wash- 
ington. 
Nav. med. Bull., Wash. Naval Medi- 
cal Bulletin. Washington. 
Nav. med. Res. Inst. Rept. Naval 
medical Research Institute Re- 
ports. Washington. 
Ned. milk.-geneesk. Arch. Neder- 
landsch militairgeneeskundig ar- 
chief. Utrecht. 
Ned. Tijdschr. Gene esk. Neder- 
landsch tijdschrift voor genees- 
kunde. Amsterdam. 
New Engl. J. Med. New England 
Journal of Medicine. Boston . 
Nippon rinsyo* Nippon Rinsyo. 
Osaka. 
Nippon Seiri. Z. Nippon Seirigaky 
Zassi. Japan. 
Nissin Igaku. Nissin Igaku. Tokyo. 
291222—54 23 Nor—Sem 
JOURNAL ABBREVIATIONS 
Nord. med. Nordisk medicin. 
Stockholm. 
Nuclear Sci. Abst. Nuclear Science 
Abstracts. Oak Ridge, Tenn. 
Nutrit. Rev. Nutrition Reviews. 
New York. 
Occup. Med. Occupational Medi- 
cine. Chicago. 
Ophthalmologica. Ophthalmologica. 
Basel. 
Orv. Hetil. Orvosi Hetilap. Honi 
es kvilfoldi gyogyazat es korbuvar- 
lat kozlonye. Budapest. 
Osaka Univ. med. J. Osaka Daigaku 
Igaku Zassi. Osaka. 
Otolaryng. slav. Otolaryngologia 
slavica. Prag. 
Oto-rhino-laryng., Danub* Oto- 
rhino-laryngologica Danubiana. 
Budapest. 
Paris med. Paris medical. La se- 
maine du clinicien. Paris. 
Penn. med. J. Pennsylvania Medical 
Journal. Pittsburgh. 
Personnel J. Personnel Journal. 
Baltimore. 
Pfliig. Arch. ges. Physiol. Pfliigers 
Archiv fiir die gesamte Physiologic 
des Menschen und der Tiere. 
Bonn. 
Pharm. J. Pharmaceutical Journal 
and Pharmacist. London. 
Pharmacol. Rev. Pharmacological 
Reviews. Baltimore. 
Philipp. J. Sci. (b). Philippine 
Journal of Science, (b) Medicine. 
Manila. 
Physiol. Rev. Physiological Reviews. 
Baltimore. 
Physiol. Zool. Physiological Zoology. 
Chicago. 
Physiother., Land. Physiotherapy. 
London. 
Plast. reconstr. Surg. Plastic and 
Reconstructive Surgery. Balti- 
more. 
Pol. med. Wkly. Polski Tydgodnik 
Lekarski. Warszawa. 
Policlinico. Policlinico. Roma. 
Postgrad. Med. Postgraduate Medi- 
cine. Milwaukee. 
Pr. med. Presse medicale. Paris. 
Pract. oto-rhino-laryng. Practica 
oto-rhino-laryngologica. Basel. 
Practitioner. Practitioner. London. 
Prakt. Lek., Praha. Praktick# Lekaf. 
Praha. 
Prensa med. argent. Prensa medica 
argentina. Buenos Aires. 
Probl. fiziol. Akust. Problemy Fizi- 
ologicheskoi Akustiki. Moskva. 
Proc. Amer. phil. Soc. Proceedings 
of the American Philosophical So- 
ciety. Philadelphia. 
Proc. cent. Soc. din. Res. Proceed- 
ings of the Central Society for 
Clinical Research. Chicago. 
Proc. Mayo Clin. Proceedings of 
the Staff Meetings of the Mayo 
Clinic. Rochester, Minn. 
Proc. nat. Acad. Sci., Wash. Pro- 
ceedings of the National Academy 
of Sciences. Washington. 
Proc. ninth intern, congr. industr. 
med. 1948. Proceedings of the 
ninth international congress of in- 
dustrial medicine. 1948. 
Proc. R. Soc. Med. Proceedings of 
the Royal Society of Medicine. 
London. 
Proc. roy. Soc. Proceedings of the 
Royal Society. London. 
Proc. Soc. exp. Biol., N. Y. Pro- 
ceedings of the Society for Ex- 
perimental Biology and Medicine. 
New York (Utica, N. Y.). 
Proc. U. S. nav. Inst. Proceedings 
of the United States Naval Insti- 
tute. Annapolis, Md. 
Psychoanal. Quart. Psychoanalytic 
Quarterly. Albany, N. Y. 
Psychoanal. Rev. Psychoanalytic Re- 
view. New York. 
Psychol. Bull. Psychological Bul- 
letin. Lancaster, Pa. 
Psychol. Rev. Psychological Re- 
view. Lancaster, Pa. 
Psychosom. Med. Psychosomatic 
Medicine. Experimental and 
Clinical Studies. Washington. 
Publ. Hlth., Land. Public Health. 
London. 
Publ. Hlth. Bull., Wash. Public 
Health Bulletin. Washington. 
Publ. Hlth. Rep., Wash. Public 
Health Reports. Washington. 
Quart. Bull. Nthwest. Univ. Quar- 
terly Bulletin of Northwestern 
University, (b) Medical. Evan- 
ston, 111. 
Quart. J. exp. Physiol. Quarterly 
Journal of Experimental Physiol- 
ogy. London. 
Quart. J. exp. Psychol. Quarterly 
Journal of Experimental Psychol- 
ogy. Cambridge. 
Quart. J. Med. Quarterly Journal 
of Medicine. Oxford. 
Quart. Phi Beta Pi med. Frat.* 
Quarterly. Phi Beta Pi Medical 
Fraternity. Menasha, Wis. 
Radiology. Radiology. Syracuse, 
N. Y. 
Rass. ital. Otorinolaring. Rassegna 
italiana di oto-rino-laringologia. 
Napoli. 
Rass. Med. industr. Rassegna di 
medicina industriale. Torino. 
Res. Rev. Research Reviews. Lon- 
don. 
Research, Land. Research: a jour- 
nal of science and its applications. 
Res. Quart. Amer. Phys. Educ. Ass. 
Research Quarterly of the Amer- 
ican Physical Education Associa- 
tion. Ann Arbor. 
Rev. argent. Dermato-sif. Revista 
argentina de dermato-sifilologica. 
Buenos Aires. 
Rev. beige Path. Revue beige de 
pathologic et de medecine experi- 
mentale. Bruxelles. 
Rev. canad. Biol. Revue canadienne 
de biologic. Montreal. 
Rev. gen. Clin. Revue generate de 
clinique et de therapeutique. 
Paris. 
Rev. med. Nancy. Revue medicale 
de Nancy. 
Rev. Med. nav. Revue de medecine 
navale (metropole et outremer). 
Paris. 
Rev. oto-neuro-oftal., B. Aires. Re- 
vista oto-neuro-oftalmologica y de 
cirurgia neurologica. Buenos 
Aires. 
Rev. Otorinolaring., Santiago. Re- 
vista de otorinolaringologia. San- 
tiago de Chile. 
Rev. Sanid. Aero., B. Aires. Re- 
vista de sanidad de aeronautica. 
Buenos Aires. 
Rev. sci. Instrum. Review of Scien- 
tific Instruments. New York. 
Ric. sci. Mem. Ricerca scientifica 
(e reconstruzione) Memorie. 
Roma. 
Rinsyo & Kenkyo. Japanese Journal 
of Clinical and Experimental Med- 
icine. Hokuoka. 
Riv. Med. aero. Rivista di medi- 
cina aeronautica. Roma. 
Roy. Nav. med. Bull. Royal Naval 
Medical Bulletin. London. 
Scand. J. din. lab. Invest. Scandi- 
navian Journal of Clinical and 
Laboratory Investigation. Oslo. 
Schweiz. Arch. Neurol. Psychiat. 
Schweizer Archiv fiir Neurologic 
und Psychiatric. Zurich. 
Schweiz, med. Wschr. Schweizer- 
ische medizinische Wochenschrift. 
Basel. 
Sci. Amer. Scientific American. 
New York. 
Sci., III. Science. Illinois. 
Sci. Mon., N. Y. Scientific Monthly. 
New York. 
Sci. News Lett., Wash. Science 
News Letter. Washington. 
Science. Science. New York. 
■Sem. Hop. Paris. Semaine des ho- 
pitaux de Paris. AGENCY ABBREVIATIONS 
Set—Z. Hal 
Settim. med. Settimana medica. 
Palermo. 
Soc. med. tskr.* Social medicinsk 
tidskrift. Stockholm. 
Sovetsk. Vrach. Zh. Sovetskiy vra- 
chebniy zhurnal. Leningrad. 
Sth. med. J., Birmingham. Southern 
Medical Journal. Journal of the 
Southern Medical Association. 
Birmingham, Ala. 
Strasbourg-med. Strasbourg-medi- 
cal. Strasbourg. 
Stud. Rockefeller Inst. med. Res. 
Studies from the Rockefeller In- 
stitute for Medical Research, New 
York. 
Summ. Diss. Northw. Univ. Sum- 
maries of Dissertations. North- 
western University, Chicago. 
Surg. Gynec. Obstet. Surgery, Gyn- 
ecology and Obstetrics. Chicago. 
Svenska Ldkartidn. Svenska Lak- 
artidningen. Stockholm. 
Tech. Data Dig. U. S. Air Cps* 
Technical Data Digest. U. S. Air 
Corps. Dayton, Ohio. 
Terap. Arkh. Terapevticheskii 
Archiv. Moskva. 
Tex. Rep. Biol. Med. Texas Reports 
on Biology and Medicine. Gal- 
veston. 
Ther. Umsch. Therapeutische Um- 
schau. Bern. 
Thorax. Thorax. London. 
Tidskr. milit. Hdlsov. Tidskrift i 
militar halsovard. Stockholm. 
Tidsskr. norske Laegeforen. Tids- 
skrift for den Norske Laegefore- 
ning. Kristiania, Kjpbenhavn. 
Tohoku J. exp. Med. Tohoku Jour- 
nal of Experimental Medicine. 
Sendai. 
Toulouse med. Toulouse medical. 
Toulouse. 
Trans. Amer. Acad. Ophthal. Oto- 
laryng. Transactions of the Amer- 
ican Academy of Ophthalmology 
and Oto-laryngology. St. Louis. 
Trans. Amer. climat. {din.) Ass. 
Transactions of the American 
Climatological (and Clinical) As- 
sociation. Philadelphia. 
Trans. Amer. laryng. rhin. otol. Soc. 
Transactions of the American 
Laryngological, Rhinological and 
Otological Society. New York. 
Trans. Amer. ophthal. Soc. Trans- 
actions of the American Ophthal- 
mological Society. New York. 
Trans. Amer. otol. Soc. Trans- 
actions of the American Otological 
Society. Boston. 
Trans. Amer. Soc. Heat. Vent. Engrs. 
Transactions of the American So- 
ciety of Heating and Ventilating 
Engineers. New York. 
Trans. Ass. Amer. Phycns. Trans- 
actions of the Association of Amer- 
ican Physicians. Philadelphia. 
Trans, med. engr. Ind. Hyg. Found. 
Transactions, medical and engi- 
neering section. Tra ns action 
Series, Bulletin no. 3 Industrial 
Hygiene Foundation. Pittsburgh. 
Trans. R. Soc. trap. Med. Hyg. 
Transactions of the Royal Society 
of Tropical Medicine and Hygiene. 
London. 
Tufts med. J. Tufts medical Jour- 
nal. Boston. 
Turk Tip Cem. Mec. Turk Tip 
cemiyeti mecmuasi. Istanbul. 
Ugeskr. Laeg. Ugeskrift for Laeger. 
Kj0benhavn. 
Univ. Qd. Dept. Physiol. Univer- 
sity of Queensland Papers. De- 
partment of Physiology. 
U. S. Forces med. J. United States 
Armed Forces Medical Journal. 
Washington. 
Verh. dtsch. path. Ges. Verhand- 
lungen der Deutschen Pathologi- 
schen Gesellschaft. Jena. 
Virchows Arch. Virchows Archiv 
fur pathologische Anatomic und 
Physiologic und fur klinische 
Medizin. Berlin, 
Vjschr. schweiz. Sanitoff. Viertel- 
jahrsschrift fur Schweizerische 
Sanitatoffiziere. Basel. 
Volta Rev. Volta Review. Wash- 
ington. 
Vyestn. Otorhinolaryng., Leningr. 
Vyestnik Otorhinolaryngologii. 
Leningrad. 
W. Va. med. J. West Virginia Medi- 
cal Journal. Wheeling. 
War. Med., Chicago. War Medi- 
cine. Chicago. 
Wis. med. J. Wisconsin Medical 
Journal. Milwaukee. 
Yale J. Biol. Med. Yale Journal of 
Biology and Medicine. New Ha- 
ven. Conn. 
Z. Biol. Zeitschrift fixr Biologic. 
Berlin & Miinchen. 
u. ges exp. Med. Zeitschrift fur die 
gesamte experimentelle Medizin. 
Berlin. 
Z. Hals- Nas — u. Ohrenheilk. Zeit- 
schrift fur Hals- Nasen- und 
Ohrenheilkunde. Miinchen & Ber- 
lin. 
KEY TO AGENCY ABBREVIATIONS 
In listing reports from a given source the abbreviations in the corporate entries and serial listings have 
been adopted from those employed by the agency; when these were lacking, a suitable abbreviation has been 
devised by the authors. An alphabetical listing of all such abbreviations follows, together with a few addi- 
tional symbols. The italicized words in each case form the basis of the abbreviation. 
AAF U. S. Army air forces. 
ACAMR Canada. National research council of Can- 
ada. Associate committee on aviation medi- 
cal research. 
AMRL U. S. Army service forces. Armored medical 
research laboratory, Fort Knox, Ky. 
APU Gt. Brit. Medical research council. Applied 
psychology unit. Psychological laboratory, 
Cambridge. 
ASF U. S. Army service forces. 
BuAer U. S. Navy. Bureau of aeronautics. 
BuMed U. S. Navy. Bureau of medicine and surg- 
ery. 
BuNavPers U. S. Navy. Bureau of naval personnel. 
BuShips U. S. Navy. Bureau of ships. 
BuY & D U. S. Navy. Bureau of Yards and Docks. 
CAM U. S. National research council. Committee 
on aviation medicine. 
CES Gt. Brit. Medical research council. Royal 
naval personnel research committee. Cli- 
matic efficiency subcommittee. 
CUW U. S. National research council. Committee 
on undersea warfare. 
EDU U. S. Navy. Naval Gun Factory. Experi- 
mental diving unit. 
ENG U. S. Air force. Air technical service com- 
mand. Engineering division. 
FPRG Gt. Brit. Royal Australian air force. Flying 
personnel research committee. AGENCY ABBREVIATIONS 
HS Gt. Brit. Medical research council. Royal 
naval personnel research committee. Habit- 
ability subcommittee. 
MRG Gt. Brit. Medical research council. 
NATB U. S. Navy. Pensacola, Fla. Naval air 
training base. 
NDRG U. S. office of scientific research and develop- 
ment. National defense research committee. 
NEL U. S. Navy. Naval electronics laboratory, 
San Diego, Calif. 
NHMRG Australia. National health and medical re- 
search council. 
NMRI U. S. Navy. Naval medical research insti- 
tute, Bethesda, Md. 
NRG National research council. 
NRL U. S. Navy. Naval research laboratory, 
Anacostia, D. C. 
OES Gt. Brit. Medical research council. Royal 
naval personnel research committee. Opera- 
tional efficiency subcommittee. 
ONI U. S. Navy. Office of naval intelligence. 
ONR U. S. Navy. Office of naval research. 
OpNav U. S. Navy. Office of the chief of naval 
operations. 
OSRD U. S. Office of scientific research and devel- 
ment. 
RNPRG Gt. Brit. Medical research council. Royal 
naval personnel research committee. 
SS Gt. Brit. Medical research council. Royal 
naval personnel research committee. Sur- 
vival subcommittee. 
TSEAL U. S. Air force. Air technical service com- 
mand. Engineering division. Aero medical 
laboratory. 
UPS Gt. Brit. Medical research council. Royal 
naval personnel research committee. Under- 
water physiology subcommittee. 
USAF U. S. Air force. 
UWB Gt. Brit. Medical research council. Royal 
naval personnel research committee. Under- 
water blast subcommittee. 
VPS Gt. Brit. Medical research council. Royal 
naval personnel research committee. Visual 
problems subcommittee. Index of Authors 
Reference is given to serial numbers 
Aaron, R. S., 3382 
Abbot, F. K., 3602 
Abbott, G. A., 2632 
Abels, J. G., 2502 
Abrams, M. H., 1711,3497 
Abramson, E., 1382 
Adams, S., 1710 
Adams, W., 711 
Adams, W. R., 506, 534, 
712 
Adams, W. S., 3741, 3742 
Addenbrooke, E. F., 1133 
Adler, B. G., 1954 
Adler, F. H., 1383, 1384 
Adler, H. F., 454, 456, 457, 
464,576,577,877,2018, 
2031, 2192, 2198, 2235, 
3432 
Adler, H., 2144, 2888, 2889 
Adler, N., 3466 
Adolph, E. F., 446, 543, 
927, 928, 929, 996, 1028, 
1029, 1030, 1220, 1221, 
1222, 1223 
Adriani, J., 3167 
Affeldt, J. E., 3354, 3391 
Aiken, D. W., 1184 
Aird, R. B., 2041 
Aiton, H. F., 969 
Akashi, K., 3711, 3712 
Akin, S. W., 2103 
Akira, N., 2902, 2903 
Akyol, N., 2001 
Alamercery, D., 2060 
Albrecht, F. K., 2781 
Aldao, C. N. G., 1989 
Aleksenko, N. I., 1712 
Alella, A., 306, 307, 781, 
2109, 2133, 2238 
Alexander, F. A., 3444 
Alexander, J. D., 310 
Alexander, L., 1272 
Alexander, S. J., 2695, 
2731, 2732, 2733, 2780 
Alexander, W. J., 2084 
Alford, W. C., 2526, 3153, 
3154 
Alinat, J., 1488, 2088, 
2275, 3802 
Allan, D. I., 1212 
Allen, J. H., 2014 
Allen, J. G., 3003 
Allen, S. C., 1748, 2218, 
2318 
Allen, W. J., 308 
Almgren, S., 2369 
Almy, T. R, 3602 
Alpers, B. J., 1966 
Alt, ( ), 2402 
Alt, H. L., 2247 
Altland, P. D., 620, 671, 
672, 713, 714 
Altmann, H. W., 621 
Altschule, M. D., 782 
Alvarez, J. S. A., 2782 
Alveryd, A., 2239 
Alving, A. S., 506, 534 
Alvis, H. J., 610, 2273, 
2904 
Amaral, A. D., 3770 
Ambrus, C. M., 2783 
Ambrus, J. L., 2783 
Ames, A., 1151, 1273, 1274 
Amouroux, P., 2633, 2784 
Amyes, E. W., 2451, 2456 
Anderson, D. P., 308 
Anderson, I. F., 45 
Anderson, N., 2049 
Andre, L., 2634 
Andre, M. J., 2905, 3340 
Andreyeff, B., 3641 
Angus, T. C., 3102 
Anselmo, J. E., 741 
Anthony, R. A., 507, 662, 
2015, 2016 
Antunez, N., 1967, 2665 
Appel, E. M., 3133 
Archambault, L., 1564 
Airing, G. D., 1573 
Armstrong, H. G., 2785 
Arni, P., 1507 
Arnold, A., 3723 
Arnold, A. C., 553, 3020 
Arnold, E., 583, 584 
Arnould, P., 683 
Arshavski, A., 684 
Arthur, E. M. S., 2548 
Aschan, G. K., 1844 
Aschoff, J., 1152, 1153 
Ash, I. E., 3616 
Ashe, W. F., 1045, 1046, 
1071, 1077 
Ashley, P., 1945 
Asmussen, E., 783, 2259, 
2370, 2371, 2446, 3341 
Assouly, ( ), 2454, 2496 
Atkinson, A. J., 2018, 2031, 
2144 
Atkinson, J. B., 3642, 3643 
Atwell, R. J., 309 
Aub, J. G., 2511, 2568, 
2569 
Aubry, M., 1584 
Auer, J., 2920 
Avera, J. W., 798 
Aycock, T. M., 3724 
Aykut, R., 251 
Baba, S., 1890 
Babkin, B. P., 2666, 2683, 
2786 
Babskii, E. B., 1385 
Bader, M. E., 1155, 1191, 
1224, 1227 
Bader, R. A., 1020, 1048, 
1063, 1154, 1155, 1210 
Baetjer, A. M., 912, 1156, 
1526, 2227, 2653, 2654, 
3342 
Bageant, W. E., 2921 
Bahnson, E. R., 2327 
Bailey, J. R., 532 
Bailey, T. L., 3367 
Bailliart, J. P. 488, 489 
Bain, J. A., 851 
Baker, D. V., Jr., 2922 
Baker, R. D., 3743 
Balanina, N. V., 465 
Baldi, A., 2463 
Baldi, G., 2593, 2609 
Bales, P. D., 2751 
Balestra, G., 2075 
Ballenger, H. C., 1845, 
1846 
Ballenger, J. J., 1845, 
1846 
Ballenger, W. L., 1845, 
1846 
Ballin, H. M., 513 
Bambach, K., 2574 
Banche, M., 3644 
Bancroft, R. W., 3432 
Bannon, J. H., 2566 
Barach, A. L., 466, 685, 
690, 2250, 2923, 3406, 
3407, 3408, 3409, 3425 
Barach, B., 690 
Barany, R., 2734, 2735 
Barber, J. L., 3532 
Barbour, H. G., 2551, 2552 
Barcroft, H., 308, 930 
Bard, P., 2667, 2680, 2736, 
2737, 2738 
Bardeen, A., 17 
Barger, A. G., 18 
Bargeton, D., 2260 
Bark, R. S., 1231 
Barker, M. E., 3247 
Barker, W., 3645 
Barmack, J. E., 686, 1164 
Barnes, B., 1112 
Barnes, D. K., 173, 177 
Baron, S. H., 2956 
Barr, J. S., 2969 
Barron, G., 2091 
Bartell, F. E., 3248 
Barthe, ( ), 2464 
Barthe, R., 2413 
Bartlett, F. G., 1704 
Bartlett, N. R., 1325, 1326, 
1381, 3445, 3446, 3447, 
3448, 3449, 3450, 3451, 
3452, 3459, 3462, 3469, 
3480, 3481, 3484, 3493, 
3496, 3498 
Bartley, S. H., 467, 931, 
1360, 3533, 3646 
Bartosh, E., 2050, 2055 
Baser, R. A., 1169 
Bass, D. E., 1020, 1154, 
1169, 1232 
Bassan, M. E., 3638 
Bast, T. H., 3617, 3618, 
3619, 3620 
Bateman, G. H., 1847, 1891 
Bateman, J. B., 148, 149, 
3199, 3410, 3411 
Bateman, J. G., 2110, 2987, 
2992 
Batterman, R. G., 2826 
Battista, A., 2716 
Baum, W. S., 544 
Baumberger, J. P., 2191 
Baxter, F. S., 3548 
Baxter, H., 1157 
Bay, E. B., 506, 534, 712 
Bayley, H. H., 3771 
Bayulkem, F., 2001 
Bazett, H. C., 878, 879, 
1225, 3264, 3270, 3312 
Beach, E. W., 1946 Bea—Bue 
INDEX OE AUTHORS 
Beadle, L. C., 813 
Beadle. S. F.. 813 
Beamish, F. E., 2548 
Bean, J. W., 143, 144, 145, 
784, 803, 814, 2276, 
2277, 2278, 2287, 2296, 
2325, 3412 
Bean, W., 2042 
Bean, W. B., 880, 969, 997, 
1045, 1046, 1071, 1077 
Beard, E. F., 310 
Beard, O. W., 2975 
Bearn, F. A., 3301 
Beauchamp, I. L., 2592 
Bebb, A. H., 2957 
Bechtoldt, H. P., 3453 
Beck, G. J., 3413 
Beck, I. T., 3653 
Beck, J. S. P., 3004 
Beck, R. D., 2263 
Becker, R. F., 522 
Beckman, A. O., 2465, 2476 
Beckman, H., 2452, 2787, 
2788, 2789 
Bedford, T., 881, 882, 932, 
3067, 3100, 3101 
Behnke, A. R., 1, 2, 3, 4, 
167, 193, 208, 221, 222, 
229, 715, 743, 921, 1275, 
1276, 1693, 1828, 1968, 
1969, 1970, 1971, 1972, 
2141, 2142, 2171, 2289, 
2421, 2951, 3068 
Behrens, C. F., 3005, 3006, 
3343 
Behrman, H. T., 3780 
Behrmann, V. G., 19 
Beinert, H., 622 
Beischer, D. E., 20, 21 
Bekesy, G., 1768 
Belding, H. S., 1273, 1274, 
2025, 2026, 3233, 3249, 
3291, 3295, 3302 
Belding, H. W., 1158 
Belf, M. B., 2827 
Belfort, F., 1892 
Belknap, E. L., 2570 
Bellessimo, B., 2466 
Beman, F. M., 2186 
Bembower, W. C., 2103a 
Bender, L., 1669 
Benedict, E. B., 2696 
Benedict, F. G., 3679, 3698 
Benitte, ( ), 1281 
Benitte, A. C., 1139 
Benkwith, K. B., 3007 
Bennet, M. G., 3069 
Benon, R., 2372 
Benson, O. O., Jr., 4, 194 
Benzinger, T., 2958, 2959 
Benzinger, T. H., 22, 129 
Berg, W. E., 23, 150, 151, 
168, 198, 200, 2191 
Berger, E. Y., 218, 236, 
448, 452 
Berger, L. B., 91, 2111, 
3344 
Berk, L., 370 
Berner, F. W., 3179 
Berney, J. J., 583, 584 
Bernthal, T. G., 311, 312, 
313 
Berridge, F. R., 951 
Berrien, F. K., 1527, 1528 
Berry, M. M., 658 
Berry, R. N., 3461, 3462 
Besancon, L. J., 2453 
Bessen, G. E., 696, 697, 
2030, 3408 
Best, C. H., 1973, 2739, 
2857, 2862 
Betourne, C., 314 
Beutler, F., 570 
Beyer, R. E., 47 
Beyne, J., 252, 414, 508, 
753, 754, 2236 
Beyne, P. J. E., 1309 
Beznak, A. B. L., 2112, 
2228 
Bick, M. W., 1386 
Bickerman, H. A., 3413 
Bierman, H. R., 315, 1848, 
2017, 2429 
Bietti, G. B., 239, 240, 248 
Biget, P., 623, 840 
Bigg, E., 3113, 3114, 3122 
Biggs, L. M., 3042 
Binet, L., 253, 316, 382, 
383, 455,468, 785, 2229, 
2237, 2251, 2260, 2373, 
2924, 3345, 3399 
Binger, G., 268 
Birren, J. E., 485, 1002, 
1386, 2410, 2697, 2698, 
2699, 2700, 2701, 2702, 
2790, 2791, 3196, 3552 
Bitterman, M. E., 1361, 
1362 
Bixby, E. W., 910 
Bjerner, B., 3621 
Bjornstad, J. M., 98 
Bjurstedt, A. G. H., 384, 
1974, 2107 
Black, H. FI., 64, 3200 
Black, J. W., 1713, 1714, 
1715, 1716 
Blackham, R. J., 2668 
Blair, C. L., 3494 
Blair, E. A., 3303 
Blaisdell, R. K., 1159, 1160 
Blanch, J. J., 2171 
Blankenhorn, M. A., 1998, 
2148, 2168 
Blankstein, S. S., 1463 
Bleguad, N., 1585 
Blinks, L. R., 152, 168, 184, 
186, 187, 188, 189 
Bloch-Michel. H., 2503 
Blockley, W. V., 1031, 
1032, 1033, 1034, 1072 
Blockwick, T. N., 24, 83, 
84, 113, 2094, 2106, 
3789, 3790, 3791, 3792, 
3793, 3794, 3795, 3798, 
3799 
Bloemendal, W. B., 3617 
Blood, F. R., 624, 2925 
Bloom, W. L., 3008, 3406 
Bloomfield, J. J., 2602 
Blum, H. F., 1113,3046 
Blum, H. R., 3250 
Bly, G. G., 1144, 1226 
Blystad, W., 1387 
Bobbitt, J. M., 3473 
Bochet, ( ), 2229 
Bock, A. V., 1035 
Bodenlos, L. J., 3360 
Boder, M. E., 1155 
Boeder, P., 3047 
Boeri, E., 3737 
Bogoslovskii, A. I., 1565 
Boies, L. R., 1849 
Boland, J. D., 2792 
Boldt, M. H., 3137 
Bolleruf, F., 1290 
Bollman, J. L., 415 
Bommarito, G. L., 1232 
Bonnar, W. M., 930 
Bonnevie, P., 2374 
BonsdorfF, E., 571 
Booker, W. M., 1228 
Booth, C., 2527 
Boothby, W. M., 194, 195 
Borden, D. L., 1089 
Borison, H. L., 2740, 2778 
Bornschein, H., 241 
Bornstein, M. B., 2683, 
2716 
Borshehevskii, I. A., 1749 
Borst, J. R., 2375 
Bortolotti, R., 2741 
Botelho, S. Y., 3373 
Bouckaert, J. J., 832 
Boulin, P., 1694 
Bourguignon, A., 2376 
Bourret, J., 2061, 2071 
Boutwell, J. FL, 429, 625, 
626, 635 
Bouverot, P., 411, 2326 
Bowditch, M., 2538 
Bowen, I. S., 1487 
Bowen, W. J., 572, 573 
Bowers, J. Z., 3037 
Boxus, V., 2905 
Boy, G., 414 
Boyd, W. C., 1800 
Boyer, M. FL, 25 
Brackett, F. S., 54 
Brackett, I. P., 1732 
Bradley, K., 755 
Brailsford, J. F., 2062 
Brandt, A. D., 1695, 2571, 
3048, 3070 
Branion, FF. D., 2512, 2513 
Bray, G. W., 3530 
Brazier, M. A. B., 254, 756, 
3636 
Breckenridge, J. R., 1027 
Breese, B. B., 3195 
Bregande, S. C., 1623, 1624 
Brenner, S., 3214 
Brett, J. R., 2684, 2703, 
2712, 2713, 2714, 2752, 
2753 
Brewer, G., 386, 387 
Brice, R., 114 
Brickman, I. W., 1848 
Bridge, E. V., 1990,2149 
Brigatti, L., 2593 
Briggs, R. W., 1184 
Brin, B. M., 416 
Brinkman, R., 26 
Brinton, E. S., 2040, 2091, 
2142, 2289 
Broadbent, D. E., 1717, 
1718 
Brobeck, J. R., 627, 1141 
Brockman, N. W., 2451 
Brodie, B. B., 218, 236 
Brody, S., 2239 
Broh-Kahn, R. H., 1961 
Brolin, S. E., 1161 
Bromiley, R. B., 2738 
Bronk, D. W., 1305 
Brontman, M., 3376 
Brookes, R. D., 685 
Brooks, G. M., 219, 255 
Brooks, J. W., 2234 
Broussin, J., 509 
Brown, A. FF., 933, 996, 
1090 
Brown, B. R., 1975, 2703, 
2715 
Brown, C. FF., 1586 
Brown, G. S., 3009 
Brown, E., 1162 
Brown, E. B., 52, 521, 601, 
757, 815, 816, 834, 2037 
Brown, E. W., 2572, 3127 
Brown, F. R., 1426 
Brown, H. C., 1331 
Brown, J. O., 1510 
Brown, J. S., 3534, 3592 
Brown, R. A., 3637 
Brown, R. E. C., 1491 
Brown, W. B., 3499 
Brown, W. E., 2148 
Broyles, E. N., 1893 
Brozek, J., 220, 1079, 1369, 
1370, 3222, 3634 
Brubach, H. F., 126 
Brucer, M., 362, 363, 364, 
365, 385, 2408, 2984, 
2985, 3346, 3386 
Brues, A. M., 3010, 3011 
Brull, L., 317, 449 
Brumsteyn, V., 934 
Bruns, P. D., 2252 
Bryan, A. H., 506, 534, 712 
Buck, M. W., 1727, 1742 
Buckell, M., 2594 
Buel, J., 3454 
Buettner, K., 883, 935, 
3323 INDEX OF AUTHORS 
Bug—Cot 
Bugard, P., 1670 
Biihlmann, A., 574, 575 
Bunch, G. C., 1489, 1587 
Bunker, M. L., 1741,2368 
Bunting, H., 642 
Burch, B. H., 2180 
Burch, G. E., 936, 1036 
Burchenal, J. H., 370 
Burden, W. D., 3772 
Burdy, L. M. J., 53 
Burgess, D. S., 3185 
Burgwin, S., 3645 
Burkhardt, W. L., 576, 577, 
591, 687, 2018, 2019, 
2031, 2032, 2144, 2192, 
2218a 
Burnett, H. A., 2960 
Burns, H. L., 82, 1231 
Burrill, M. W., 429, 628 
Burrows, W., 3201 
Burstein, M., 785, 2373, 
2924 
Burt, A. S., 847 
Burton, A. C., 1229, 3228, 
3251, 3252, 3253, 3254, 
3255 
Busby, J. C., 3304 
Bussot, R., 3796 
Butson, A. R. C., 1163, 
1230 
Butts, J. S., 693 
Buyard, P., 2950 
Byrne, J. G., 1829,2742 
Caccuri, S., 2514 
Cachera, R., 2947 
Cain, C. C., 3414, 3415 
Caldwell, F. T., 450 
Calhoun, A. J., 3195 
Callaway, E. G., 3727 
Callaway, J. L., 3743 
Callebaut, G., 256 
Calvin, M., 3180 
Cameron, D. C., 3473 
Cameron, G. R., 2926, 
2961, 2962 
Cameron, J. A., 2377, 2378 
Cameron, K., 1073 
Camille, N., 3671 
Campbell, A., 2113, 2307, 
2342, 3347 
Campbell, A. C. P., 1857 
Campbell, D. A., 1388, 
1389 
Campbell, G. S., 789, 815 
Campbell, J., 916 
Campbell, P. A., 1588, 
1589, 1590 
Cane, V. R., 3597 
Caneghem, ( ), van, 1850 
Canfield, N., 1529 
Cantarow, A., 2573 
Caplan, A., 937, 1074 
Carey, E. J., 1463 
Carhart, R., 1591 
Carli, F. de, 845 
Carliner, P. E., 2822, 2823 
Carlson, L. D., 82, 1231 
Carmichael, H. T., 506, 
534, 712 
Carmody, M. G., 2516, 
2535, 2536 
Carpenter, A., 938, 1038, 
1075, 1076 
Carr, D. T., 3416 
Carriere, G., 2515 
Carruthers, D. G., 1851, 
1852 
Carson, L. D., 3348 
Case, R. A. M., 2087 
Case, T. J., 506,534, 712 
Cass, R. E., 2308 
Cassel, E. E., 1566 
Castagnou, R., 2467 
Castaigne, P., 469 
Castane, A., 1592 
Castellanos, F. J., 1769 
Castle, W. B., 370 
Catchpole, H. R., 153, 154, 
155, 156, 157, 163, 164, 
1420, 2043, 2046 
Cauer, H., 2655 
Causse, R., 1593, 1671, 
1672 
Cedrangolo, E., 1976 
Ceresa, C., 2379 
Cerletti, A., 257 
Chadwick, L. E., 458, 3422, 
3423 
Chalak, J., 2519 
Challoner, A. R., 130 
Chalmers, E. L., 3535 
Chambers, A. H., 286, 387 
Chanel, J.,410, 744,2261 
Chaney, A. L., 1636, 3130 
Chang, H. T., 1830, 1831, 
1832 
Chang, S. L., 3202 
Channel!, R. C., 3556 
Chapanis, A., 107, 486, 
1302, 1303, 1310, 1390, 
1391, 1392, 1696, 1719, 
1720, 2669, 3049, 3071, 
3537, 3538, 3539, 3540, 
3541, 3622 
Chapin, J. L., 742,817 
Chapman, W. H., 3014 
Chapman, W. P., 779 
Chardon, G., 284, 285, 286, 
287, 288, 289, 318, 319, 
343, 344, 345, 346, 347, 
348, 349, 381, 417, 418, 
437, 438, 439, 2336, 
2337 
Charney, D., 1499 
Charnyi, A. M., 578 
Charpin, J., 2561 
Chassis, H., 2566 
Chatonnet, J., 1183 
Chauchard, B., 252, 508, 
753, 754, 2236 
Chauchard, P., 252, 508, 
753, 754, 2236 
Chavasse, P., 1593, 1671 
Cherry, R. H., 2468 
Chester, L., 1853 
Chin, T., 939 
Chinn, H. I., 247,291,292, 
403, 580, 700, 1456, 
2009, 2380, 2469, 2793, 
2794, 2795, 2796, 2797, 
2798, 2799, 2800, 2801, 
2802, 2803, 2804 
Chiodi, H., 579, 2117 
Cholak, J., 2574, 2584, 
2585 
Christensen, B., 787 
Christensen, H., 2595 
Christensen, W. R., 1039, 
3257 
Christian, P., 1332 
Christiansen, M., 2805 
Chubb, W., 914 
Chute, E., 467, 931, 3533, 
3646 
Gilley, J. H., 429, 625, 635 
Cipriani, A., 2670, 2723, 
2743, 2769 
Citroni, M., 246 
Claff, C. L., 70 
Clamann, H. G., 1184, 
2172, 2198 
Clark, B., 1393 
Clark, J. V., 1947 
Clark, K. B., 249 
Clark, R. T., Jr., 521, 601, 
2422, 2423, 2424, 2425, 
2426, 2427, 2447 
Clark, W. B., 1394 
Clark, W. E. L., 1040 
Clarke, C. C., 3757 
Clarke, B. H., 1213 
Clarke, R. W., 115, 507, 
627, 637, 638, 642, 643, 
662, 681, 2015, 2016, 
2044, 2114 
Clemedson, G. J., 2963, 
2964, 2965 
Clench, W. J., 3773 
Clinton, M., Jr., 716, 734 
Clutton-Baker, J., 3542 
Coakley, J. D., 1164 
Coates, E. O., Jr., 2327 
Coates, G. M., 1751 
Cobb, S., 3636 
Coblentz, W. W., 3115 
Cochran, K. W., 2517 
Cohen, E. J., 696 
Cohn, R., 2282 
Cojazzi, L., 2744 
Coke, C. E., 3256, 3264 
Cole, G. M., 2918 
Cole, J. W., 2484, 2485, 
2493 
Cole, R. H., 2966 
Colehour, J. K., 2449 
Coles, B. C., 3264 
Colldahl, H., 852 
Collet, A., 797, 2622 
Ceilings, C. K., 2377, 2378 
Collins, B. E., 1921 
Collins, W. T., 2392 
Collip, J. B., 3647 
Collison, H. A., 2471 
Colonna, P. C., 158 
Comess, M. S., 738 
Comfort, E., 2173 
Comroe, J. H., Jr., 320, 
322, 388, 818, 822, 2116, 
2118, 2119, 2143, 2162, 
2230, 2231, 2240, 2290, 
2327, 3349, 3373 
Conant, N. F., 3743, 3745 
Conn, J. E., 3221 
Conn, J. W., 968, 1041, 
1091 
Connell, S. C., 98 
Conner, E. H., 3373 
Conrad, R., 3543, 3593 
Consolazio, F. G., 967, 
1052, 1175, 1204, 1212, 
1226 
Consolazio, W. V., 57, 701, 
702, 743,921,926, 1002, 
1042, 1092, 1108, 2095, 
2421, 2470, 2471, 2480, 
3068, 3090, 3150, 3152, 
3155, 3204, 3205 
Cook, E. B., 1311, 1312, 
1325, 1326, 1379, 1381, 
3455, 3603 
Cook, N. L., 2987 
Cook, S. F., 629, 630, 
2020, 2096, 2125, 2126, 
2149, 2156, 2157, 2158 
Cook, W. A., 2339 
Cook, W. E., 142 
Coombs, F. A., 2631 
Cooper, D. Y., 2285, 2293, 
2294, 2295 
Cooper, K. E., 940, 941 
Cooper, K. W., 174, 175, 
176, 178, 183 
Cooper, M. R., 2927 
Cooperberg, A., 2246 
Cooperman, N. R., 3648, 
3680 
Cope, H., 3506 
Copeland, M. M., 2064 
Corcoran, J., 3507 
Cordier, D., 258, 371, 372, 
410, 419, 420, 421, 422, 
744, 848, 942,1165,2261 
Cordier, G., 258, 819 
Cordier, J., 819, 848 
Cordone, M., 844 
Corey, E. L., 2193, 2204, 
2205, 2206, 2207, 2213, 
2221, 2967, 2968 
Corkill, A. B., 2381 
Cornehlsen, J. H., Jr., 3456 
Corning, J. L., 2806 
Cornish, E. R., 842 
Coronel, M. C., 1854 
Cort, J. H., 2928 
Cotlenko, V., 840 Cot—Edh 
INDEX OF AUTHORS 
Gotten, M. V. de., 2232 
Cotter, L. H., 2575 
Cottet, J., 2397 
Cottingham, E., 1057 
Cottrell, C. L., 1362 
Cotzin, M., 2695, 2731, 
. 2732, 2733, 2780 
Coudier, R., 371, 372 
Coulson, C. K., 577, 2192 
Cournand, A., 352, 3371, 
3417 
Courville, C. B., 259, 260, 
261, 262,263,2382, 2929 
Cousteau, J. Y., 1488, 2088, 
2275, 3802 
Coville, R., 2063 
Cowan, C. R. M., 3309 
Cowie, D. B., 2612 
Craig, D. R., 3544 
Craig, F. N., 820 
Craig, V., 3214 
Craik, K. J. W., 3545, 3546 
Crane, R. A., 2465, 2476 
Craven, G. W., 580, 688 
Creedon, W. E., 3315 
Crescitelli, F., 2191 
Crickard, R. G., 54 
Criscuolo, D., 577, 591, 
2192 
Critchley, M., 884, 915, 
1043, 3229, 3305, 3458 
Crocker, P. L., 532 
Cronbach, L. J., 3457 
Cronkite, E. P., 3012, 3013, 
3014, 3015, 3017 
Crook, M. N., 3547, 3548, 
3549 
Crosfill, J. W. L., 2807, 
2808 
Crosley, A. P., Jr., 1213 
Crossland, J., 264 
Crouch, C. L., 3050 
Crowden, G. R, 3102 
Crowe, S. J., 1855, 1893 
Cruck, S,. 375, 587 
Cruz, W. O., 2491 
Cullen, S. C., 3508 
Culler, E., 1608 
Cullumbine, H., 943 
Culpin, M., 2279 
Cuppers, C., 1395 
Curl, A. L., 1801 
Curran, D., 3458 
Curry, E. T., 1490 
Curtis, J. F., 866 
Cusick, P. L., 2621 
Custer, R. P., 1101 
Cuttino, J. T., 1111 
Daggett, W. I., 1937 
Dahlberg-Parrow, R., 265 
Dahlene, O., Jr., 321 
Dahlstrom, H., 2343, 2383 
Daily, W. M., 1093 
Dales, J. W., 1467 
Dallavalle, J. M., 885, 
1770, 2602 
Dallenbach, K. M., 1566 
d’Amato, H., 1280 
d’Amour, F. E., 624, 2925 
Damrau, F., 2809 
Danford, M. B., 3020 
d’Angelo, S. A., 597, 598, 
663, 664 
Daniels, F., Jr., 1232 
Dannehi, ( ), 3725 
Daoud, F., 303 
Darcus, H. D., 3550, 3586 
Darling, R. C., 953, 1158, 
1977, 2025, 2026, 3249, 
3291 
Darrow, C. W., 3604 
Dautrebande, L., 832, 
3153, 3154 
Davenport, H. W., 386, 387 
Davenport, S. J., 2111 
Davenport, V. D., 716 
Davidson, C. S., 2656 
Davidson, I. L., 631 
Davidson, W. M., 2087, 
2913, 2988, 3168 
Davies, R W., 2283 
Daviess, G. B., 3748 
Davis, F. H., 136 
Davis, G. D., 2183, 2928 
Davis, H., 1530, 1567, 
1594, 1595, 1596, 1604, 
1673, 1679, 1680, 1682, 
1721, 1752 
Davis, R. C., 1531, 1568 
Davis, R. H., 116, 117, 121, 
2097, 2912, 3329, 3330, 
3350, 3713, 3797 
Davis, S. K., 689 
Davison, G., 2067 
Dawe, C. J., 1176 
Dawson, R. M. C., 3690 
Day, A. L., 2692 
Day, R. L., 3263, 3284 
De, S. N., 2926 
de Ajuriaguerra, ( ), 2396 
de Almeida, H. R., 1597 
De Boer, B., 1166 
Debons, A., 3258 
Debruille, C., 2890 
Dediulin, I. M., 2262 
De Forest, R. E., 3351 
Delachaux, A., 581 
De Lalla, V., 3418 
Delgado, E., 585 
Delorme, E. J., 3331, 3714 
Demeester, G., 979 
Deming, M., 2231 
DeNardi, J. M., 2516, 2536 
Dent, F. M., 1228 
Derbyshire, A. J., 1594, 
1673 
Dessaux, G., 420, 421 
Desoille, H., 2454 
Detweiler, D. K., 2528, 
2546, 2588, 2603, 2628, 
2659 
Devilla, F., 1488, 2088, 
2275, 3802 
Dewey, H. S., 3051,3072 
Dexter, L., 2936 
Dickens, F., 2297, 2298 
Dickinson, R. J., 1856 
Dickson, E. D. D., 1491, 
1599, 1600, 1601, 1602, 
1753, 1857, 1922 
Diebold, V. B., 3181 
Dietrich, W. F., 2951 
Dill, D. B., 1061, 1108 
Dimmick, F. L., 1313, 
1314, 1322, 1429, 1436, 
1437, 1454, 1466 
Dirken, M. N. J., 821 
Dishoeck, H. van, 1603 
Divry, A., 317, 449 
Dizon, G. D., 741 
Doassans, P., 2063 
Dobeln, W. von, 2092, 
2259 
Dobin, N. B., 886 
Dobson, R. L., 3016 
Dodd, C. G., 3248 
Dodge, B. F., 75,3182 
Doherty, D. G., 3150, 3155 
Doktorsky, A., 3672 
Dolatkowski, A., 5 
Doll, R., 2098 
Domanski, T. J., 3605 
Donald, K. W., 2268, 2269, 
2270, 2913 
Donhoffer, S. Z., 1167 
Donnell, W. S., 2247 
Dorner, J. B., 3368 
Doro, B., 745 
Dorrance, G., 512 
Doub, H. R, 2553 
Doubly, J. A., 1962 
Doughty, J. M., 1492 
Douglas, A. S., 266 
Doull, J., 2517 
Doumer, E., 2384 
Dowding, E, S., 3744 
Dowling, R., 2181 
Downing, J. G., 3745 
Draeger, R. H., 94, 104, 
2969, 3038 
Draegert, G. L., 1727, 
1742, 1743, 1744 
Dragotti, G., 2671 
Drake, T. G. H., 2513 
Draper, W. B., 795, 807, 
811, 812, 3400 , 3401, 
3403, 3404, 3505 
Dreher, R. E., 1393 
Dreosti, A. O., 1044 
Drescher, S., 2631 
Dresdale, D. T., 352, 3371 
Drinker, G. K., 3419 
Dripps, R. D., 320, 322, 
388, 818, 822, 2230, 
2231, 2240, 2290, 3349 
Drogendijk, A. C., 3649 
Drooker, J. C., 1853 
Drury, D. R., 3420 
Dubach, R., 2249 
DuBois, A. B., 2906 
DuBois, D., 627 
DuBois, E. F., 27, 1180, 
2340,3073 
DuBois, K. R, 2517 
Duchemin, ( ), 2464 
Duff, I. F., 1803, 1804, 
1805, 1812, 1813, 2917, 
3226, 3227, 3703, 3704 
Duffner, G. J., 759, 1114, 
2141, 3203 
Dugal, L. R, 717, 1168, 
1233, 3223 
Dugan, J., 3715 
Duggan, T. L., 3196, 3746 
Duguet, J., 487, 488, 489, 
1380, 2810 
Duke, H. N., 323, 324, 792, 
823 
Duke, T. W., 2258 
Dumas, F., 1488, 2088, 
2275, 3802 
Dumke, P. R., 2231 
Diimmer, G., 3726 
Dumont, P., 489 
Duncan, J. E., 85 
Duncan, J. T., 3768 
Dunham, C. L., 3017 
Dunham, W., 989, 3091 
Dunklin, E. W., 3124 
Dunlap, G. E., 3033 
Dunlop, D. M., 2834 
Dunn, R. C., 2617 
Dunning, M. F., 218, 236 
Duntley, S. Q., 1486 
Dupertuis, C. W., 221, 222 
Durant, T. M., 788, 789, 
793,2930, 2931 
Dureuil, M., 1254 
Durkan, T. M., 2538 
Dustan, C., 2534 
Dustin, E. H., 461 
Dutra, F. R., 2518, 2519 
Dworkin, S., 2666 
Dysart, B. R., 1858 
Eads, H. J., 572 
Eagle, W. W., 1817 
Eakin, R. E., 2612 
Earl, D. H., 1924 
Eastman, B. R., 687 
Eaton, A., 3214 
Ebaugh, F. G., Jr., 944, 
1180 
Eccles, J. C., 255 
Eckman, I., 3406, 3407, 
3408 
Eckman, M., 685, 690, 
3406, 3407, 3408 
Economo, C. V., 3650 
Edelman, I. S., 235 
Edelmann, A., 2189, 2190, 
2196, 2197, 2208, 2224, 
2244, 2245 
Ederstrom, H. E., 1166 
Edholm, O. G., 308, 930 INDEX OF AUTHORS 
Edm—Fuk 
Edman, M., 640, 994, 1195, 
1246 
Edmonds, F. G., 1834 
Edmonds, H. W., 734 
Edwards, D. A. W., 1754 
Edwards, H. T., 1108 
Edwards, J., Jr., 887 
Efimov, V. V., 325 
Egan, J. P., 1707, 1722, 
1723, 1724 
Eggleton, P., 146 
Eggleton, H. G. E., 916 
Eggston, A. A., 1859 
Eichenberger, E., 824 
Eichna, L. W., 998, 999, 
1000, 1045, 1046, 1047, 
1071, 1077, 3094, 3326 
Eisen, V., 3696 
Elbel, E. R., 3551 
Eldredge, D. H., 1532, 
1575, 1582, 1604, 1758 
Elfving, G., 945 
Elgart, S., 1573 
Eliot, J. W., 1020, 1048, 
1063, 1154, 1169, 1210 
Elkins, H. B., 2341, 2630, 
2635 
Ellinger, F., 3018 
Elliott, E., 1725 
Elliott, K. A. G., 2811 
Elliott, M. A., 28 
Elliott, R. V., 624 
Ellis, F. P., 917, 1049, 
2364, 2989, 3092, 3224 
Ellson, D. G., 3544 
Elmadjian, F., 1003, 3594 
Elsden, S. R., 146 
Eltzholtz, D. C., 3015 
Elwell, L. E., 3412 
Emerson, G. A., 691 
Emerson, K., 1136 
Emik, L. O., 1134 
Emmel, G. L., 2285, 2293, 
2294, 2295 
Emrich, E. G., 1755 
Endo, K., 423, 853 
Endres, G., 3651 
Engel, G. L., 1998, 2045, 
2148 
Engelhardt, A., 946 
Engelmann, T., 3699 
Engquist, S., 2812 
Entin, M. A., 1157 
Enzer, N., 2385 
Ernsthausen, W., 1771 
Ershoff, B. H., 1170, 1234 
Eschenbrenner, J. W., Jr., 
1921 
Eschweiler, H., 1493 
Essen, K. W., 3705 
Essenberg, J. M., 2618 
Essex, H. E., 1285, 3416 
Essig, C. F., 2751 
Euler, U. S. von, 389, 808 
Euziere, J., 3652 
Evans, G. T., 431 
Evans, H. J., 67 
Evans, H. M., 3774 
Evans, M. G., 1894 
Evans, R. G., 2813 
Evans, W. F., 2619 
Everley, I. A., 1396, 1755 
Evrard, E., 470, 2021 
Ewing, A. W. G., 1601, 
1602, 1605 
Ewing, J. H., 2284, 2311, 
2312, 2315 
Eyer, A. W., 2704 
Eyer, S. W., 715, 843 
Fabinyi, M., 390, 391,424 
Fabre, R., 267, 326, 509 
Fabritius, H. F., 1606 
Fabroni, S. M., 2520 
Fahnestock, M. K., 952, 
1174, 1240, 1243, 1247, 
3292 
Failla, G., 3019 
Fainer, D. C., 1232, 3352 
Fair, G. M., 3143 
Fair hall, L. T., 2526, 2554, 
2568, 2569, 2613, 2614 
Falconnet, P., 1672 
Fang, H. S., 1397, 1415, 
1416 
Farah, A., 413 
Farber, S., 734 
Farmer, C. J., 429, 625, 
626, 635 
Farnsworth, D., 95, 96, 97, 
111, 1326, 1333, 1334, 
1335, 1336, 1337, 1338, 
1339, 1340, 1341, 1348, 
1363, 1364, 1371, 1458, 
3052, 3053, 3459, 3460, 
3484 
Farr, L. E., 141 
Farrar, C. B., 447, 462 
Farrar, G. E., 2528, 2546, 
2588, 2603, 2628, 2659 
Farrier, R. M., 2636 
Farrior, J. B., 1818 
Fasciolo, J. C., 2117 
Faulconer, A., Jr., 415 
Fauvert, R., 2947 
Fave, M., 582 
Favre, M., 3653 
Fay, F. R., 1115 
Fazekas, I. G., 2386 
Fazio, A. N., 415 
Fegler, J., 146 
Feil, A., 2387 
Feinberg, A. R., 1315, 2820 
Feiveson, P., 3701 
Feldman, J. B., 1398 
Feldman, M., 327 
Feldstein, ( ), 2454 
Fender, F. A., 268 
Fenn, W. O., 59, 269, 510, 
746, 2423, 2424, 2425, 
2426, 2427, 2906, 2910, 
3376, 3409, 3421, 3422, 
3423, 3726a 
Fenner, E., 1607 
Ferderber, M. B., 961 
Ferguson, J. K. W., 2845 
Fergusson, A. G., 1094 
Ferrata, L., 490 
Ferree, C. E., 1399 
Ferris, B. G., Jr., 3402 
Ferris, E. B., Jr., 214, 1998, 
2045, 2148, 2168, 3409 
Ferro-milone, F., 392 
Fetcher, E. S., 1201, 1202, 
1235, 3259 
Fields, W. S., 2705, 2745, 
2814, 2815, 2816, 2817, 
2860, 2861, 2862 
Figueroa, W. G., 1226 
Finch, E. M., 1420, 3565 
Finch, G., 1608 
Fine, J., 2576 
Finesinger, J. E., 302, 3636 
Fink, A. I., 2388 
Fink, V., 2263 
Finkle, A. L., 1533 
Finland, M., 2656 
Firestone, C., 1609 
Firket, J., 2497 
Fischer, A., 888 
Fischgold, H., 2063 
Fiset, P. E., 717 
Fisher, H. E., 3353 
Fisher, M. B., 94, 105, 485, 
743, 1002, 2410, 2700, 
2701, 2790, 2791, 3196, 
3552 
Fisher, R. L., 135 
Fitts, P. M., 3553, 3554 
Fitzpatrick, W. H., 1212 
Flandin, C., 2344 
Fleisch, A., 511, 825 
Fleischmann, S., 1095 
Fleming, J. F., 2818 
Flemister, S. G., 29, 68 
Fletcher, D. E., 270 
Fletcher, J. P., 1511, 1512, 
1640 
Flickinger, D., 576, 577 
Flinn, R. H., 2606 
Flury, F., 2641 
Flynn, J. P., 1280, 1610 
Folk, G. E., 1158, 3291, 
3293, 3295 
Fonash, R. L., 3310, 3311 
Fontanille, P., 289 
Forbes, F. B., 692 
Forbes, J. J., 2455, 2472 
Forbes, W. H., 1158, 3260 
Foregger, R., 3169 
Foreman, P., 1334 
Forlano, G., 1164, 1255 
Fornari, A., 2389 
Forssander, G. A., 86 
Forssman, S., 2345 
Fortier, C., 862 
Fosbery, F. W. A., 2865 
Foster, H., 3555, 3556 
Foucar, F. H., 2819 
Foulger, J. H., 2629 
Fourcade, J., 2346, 2498, 
2596 
Fourrier, A., 318, 319 
Fourt, L., 3261, 3262, 3294 
Fowler, E. P., Jr., 1611, 
1612, 1923, 1938, 3522 
Fowler, N. O., 368 
Fowler, W. S., 2118, 2119 
Fox, G., 1386 
Fox, C. A., 690 
Fox, H. M., 2428 
Fox, S. A., 1883 
Frachtman, H. J., 3776 
Fraisse, H., 2061 
Fraisse, P., 2061, 2515 
Franciscis, P. de., 564 
Franck, G., 333, 334, 335, 
336, 396, 397, 426, 2328, 
2329, 2330, 2331, 2332, 
2335 
Frank, E., 566 
Frank, S., 494 
Franke, E. K., 1772, 1773 
Franke, R. E., 63, 2416 
Franklin, K. J.,451 
Franko, O., 2981 
Franks, W. R., 2754 
Frantz, J. A., 1171 
Franzblau, S. A., 545 
Fraser, A. M., 2746 
Frayser, R., 38 
Frazier, C. N., 3747 
Frazier, R. G., 1236 
Freedman, A., 1256 
Freedman, A. M., 2751 
Freeman, S., 429 
French, R. L., 3639 
Frey, F. E. J., 30, 329 
Frey, W. von, 3651 
Freyhan, F. A., 2284 
Freytag, E., 1293, 1294 
Frick, D. C., 1342 
Fridliand, I. G., 2347, 
2348, 2349 
Friedemann, T. E., 429, 694 
Friedenwald, H., 1674 
Friedman, A., 1241 
Friedman, H., 2459, 2460, 
3380 
Friedman, N. B., 1286 
Friedman, O., 2970 
Friedrich, H., 947 
Friis-Hansen, B. J., 235 
Frinberg, S. M., 2820 
Frings, H., 1569, 1570, 
1675 
Frings, M., 1569, 1570 
Frommel, E., 3653 
Fry, D. B., 1491 
Fry, F. E. J., 1795 
Fry, J. M., 1342 
Fry, W. J., 1795 
Fugitt, C. H., 2429 
Fujino, H., 1613, 1676, 
1677 
Fukas, H. K., 425 
Fukuyama, T., 1015 Ful—Gya 
INDEX OF AUTHORS 
Fulton, H. T., 3798, 3799 
Fulton, J. D., 3020 
Fulton, J. F., 159, 471, 
473, 520, 1978, 1979, 
1980, 2174, 2209 
Furchgott, R. F., 304, 305 
Furlonger, E., 1056 
Furrer, W., 1648, 1649, 
1686, 1687 
Furstenberg, A. C., 1172 
Fusco, M., 2210 
Futcher, P. H., 3204 
Gabay, B. A., 546 
Gabb, J. E., 3637 
Gagge, A. P., 889, 2219, 
3230 
Gagne, R. M., 3555, 3556 
Gaillard, R., 279 
Gainer, S. H., 2802 
Gala, P., 2971 
Galambos, R., 510, 1567, 
1577, 1595, 1596 
Galdston, M., 448, 452 
Gall, E. A., 2392 
Galligan, A., 3263 
Galloway, A. E., 2532 
Galvao, P. E., 223 
Galwey, G. V., 3509 
Gans, M., 3654 
Gant, J. W., 1116 
Gantt, W. H., 512 
Garasenko, V. M., 678, 679 
Gardner, L. U., 2521 
Gardner, T. S., 692 
Garlock, F. C.,3114 
Garner, W. R., 1303, 1367, 
1492, 1494, 1696, 1719, 
1720, 1726, 2669, 3049, 
3071, 3532, 3538, 3539, 
3540, 3579, 3622 
Gaspa, P., 114 
Gaudio, R., 1976 
Gauer, O., 330 
Gauld, R. L., 3126 
Gawain, G. C. V., 1697 
Gay, L. N., 2821, 2822, 
2823 
Gay, French, S., 3716 
Gedda, E., 3116 
Geissman, T. A., 3183 
Gelfan, S., 1830, 1831, 
1832, 2175, 2181, 2182, 
2183, 2184, 2185, 2211, 
2220 
Gellhorn, E., 242, 271, 272, 
273, 513, 632, 826 
Gelperin, A., 3757 
Gemmill, C. L., 6, 599, 
2429 
Gent, J. C., 2577 
Geoghegan, B., 1173, 1237 
Georg, J., 331, 393, 394 
Geraci, J. E., 31 
Gerathewohl, S. J., 514 
Gereb, T., 2386 
Gerking, S. D., 906, 948, 
1011, 1012, 3313, 3314, 
3324 
Germanov, V. A., 373 
Gero, S., 888 
Gerrard, E. J., 3204 
Gerschman, R., 269 
Gersh, I., 153, 154, 155, 
156, 157, 160, 161, 162, 
163, 164, 165, 166, 167, 
224, 1113, 2043, 2046, 
2280, 2281, 2282, 2283, 
2286, 2291, 2292, 2299, 
2319, 2968 
Geschickter, G. F., 2064 
Gianola, S. V., 3304 
Gianoli, A., 739 
Giardini, A., 239, 491 
Giaugue, W. F., 3184 
Gibbs, C. B., 3557, 3598 
Gibbs, E. L., 790, 791, 3655 
Gibbs, F. A., 790, 791, 3655 
Gibson, W. C., 2002, 2824, 
2938 
Gierlack, G. S., 1205 
Giese, W. J., 1316 
Gijon, F. R., 2241 
Gilbert, P. F., 1697 
Gill, E. K., 1948 
Gill, W. D., 1948 
Gillespie, R. D., 3656 
Gilliam, H. D., 2091 
Gillick, F. G., 3424 
Gilliom, L. A. 3177 
Gilson, S. B., 1238 
Gimmerman, W. J., 1198 
Ginsburg, E., 685, 3407, 
3408 
Giulio, L., 243, 244 
Gladwin, T., 1239 
Glaser, E. M., 890, 949, 
950, 951, 1258, 1259, 
2807, 2808 
Glauber, J. J., 1924 
Glauser, F., 3749 
Gleason, J. G., 3558 
Gleeson, J., 3722 
Glickman, N., 952, 1174, 
1240, 1243, 1247, 3292 
Glynn, L. E., 2637 
Gnudi, G., 594 
Goebel, A., 425 
Goehring, H. D., 2706 
Goggio, A., 1991 
Gohar, N., 3750, 3751 
Golay, M. J. E., 134 
Gold, M. M. A., 1244, 1291 
Golden, H., 1185, 1186, 
1241 
Goldensohn, E. S., 811, 812 
Goldman, D. E., 32, 33, 
1774, 1775, 2430, 2431, 
3368 
Goldschmidt, S., 386, 387 
Goldstein, M., 3535 
Goldthwait, D. A., 1151, 
1273, 1274 
Goldwater, L. J., 2534, 
2597 
Gollwitzer-Meier, K., 395, 
827, 828, 829, 2253 
Golse, H., 2467 
Goltra, E. R., 3383 
Goodale, W. T., 3391 
Goodings, A. C., 3264 
Goodman, H. C., 1481 
Goodman, I., 34 
Goodman, J., 3420, 3429 
Goodwin, J. E., 1512 
Gool, J. van, 1603 
Gorbatow, O., 2448 
Gordon, A. S., 3354, 3355, 
3356, 3357, 3358, 3377 
Gordon, B. S., 2819 
Gordon, E. E., 953 
Gordon, F. B., 3201 
Gordon, I., 332 
Gosselin, R. E., 954, 996 
Gotlieb, C. C., 3268 
Gottschalk, C. W., 3303 
Goujon, C., 554 
Gould, R. A., 2284, 2311, 
2312,2315 
Gould, W. J., 2826 
Gourlay, R. J., 1218 
Gover, J., 436 
Graaff, L. H., 3724 
Grab, J. A., 3630 
Graham, C. H., 3461, 3462 
Grand, J. A., 3185 
Grandjean, E., 492, 505, 
511, 515. 583, 584, 718 
Grandpierre, R., 333, 334, 
335, 336, 396, 397, 426, 
840, 2328, 2329, 2330, 
2331, 2332, 2335 
Granit, R., 1343 
Granstom, S. A., 2965 
Grant, D. A., 1400, 1401 
Grant, R., 891, 3309 
Grant, W. C., 35, 2248 
Grattarola, G. V., 665 
Gray, C. H., 2473 
Gray, E. L., 1175 
Gray, F. E., 3483 
Gray, G. W., 784 
Gray, I., 2638 
Gray, J. A. B., 918 
Gray, J. S., 398, 472, 830, 
864, 1992, 2022, 2023, 
2024, 2083, 2120, 2121, 
2122, 2123, 2124, 2150, 
2151 
Gray, M. G., 2657 
Gray, S., 2034, 2049, 2146, 
2147 
Gray, S. W., 2982 
Graybiel, A., 719, 1176, 
1715, 1716 
Grayson, J., 955, 956, 1177 
Greeley, P. O., 2191 
Green, D. M., 516, 693, 
2672 
Green, E. L., 1342 
Green, J. W., Jr., 2658 
Greenbaum, L. J., 3055 
Greenberg, L. A., 2620 
Greenberg, S., 1133 
Greenberg, S. M., 1234 
Greene, R., 1534 
Greene, W., Jr., 312 
Greenfield, A. D. M., 1178 
Greenspan, M., 2099, 2100 
Gregersen, M. I., 2445 
Grenell, R. G., 274, 520. 
627, 2152 
Gressly, D. W., 2212 
Grether, W. F., 98, 3054 
Grier, G. S., 1089 
Grier, R. S., 2511 
Griffin, D. R., 2025, 2026, 
3249, 3295 
Griffith, R. S., 1273, 1274 
Griffiths, E., 130 
Griffon, ( ), 2454, 2496 
Grinker, R. R., 3606 
Grinstad, A. D., 2792 
Grinstein, M., 2249 
Grodins, F. S., 456, 457, 
472 
Groedel, F. M., 2933 
Groesbeck, B., Jr., 3359 
Grognot, P., 1776 
Gross, A., 285, 286, 287, 
288, 318, 319, 346, 381, 
417, 453 
Gross, E. G., 3508 
Grosse-Brockhoff, F., 1277 
Grossiord, A., 2065 
Grossman, M. S., 2320, 
2321 
Grove, G. W., 87, 2455, 
2472 
Grove, W. E., 1535, 1536, 
1616, 1617 
Grover, R. F., 811,812 
Grulee, C. G., 2003 
Grundfest, H., 127 
Grundmann, E., 337 
Gruss, L., 1618 
Grut, A., 2374, 2390 
Griitering, F., 600 
Gudger, E. W., 3775 
Guibert, R., 517, 583, 584 
Guild, E., 1619 
Guilhem, J., 780 
Guillain, G., 2065 
Guillemin, J., 2344 
Gullberg, B., 2345, 2361, 
2411, 2432 
Gullette, R., 3608 
Gullickson, G., 36 
Gunn, J. A., 2555 
Gurdjian, E. S., 460 
Gustavson, R. G., 34 
Gutberlet, C., 961, 962, 963 
Gutner, L. B., 2826 
Guyatt, B. L., 2512 
Gyarfas, K., 758, 770, 774 INDEX OF AUTHORS 
Haa—Hop 
Haas, R., 1332 
Haber, F., 2176 
Habisch, H., 37, 854, 865 
Hadden, G., 413 
Hagens, E. W., 1855 
Haggard, E. A., 3607 
Haggard, H. W., 2620 
Hahn, G. L., 2887, 2888, 
2889 
Haines, H. L., 1861, 1877, 
1929, 2987 
Haldane, J. B. S., 2274, 
2309 
Hale, C. J., 3358, 3365, 
3366, 3367 
Hale, H. B., 687, 1184 
Haley, L. D., 3752, 3753, 
3754, 3755 
Hall, A. L., 2449 
Hall, F. G., 518, 680, 2194, 
2195 
Hall, I. S., 1920 
Hall, J. F., 1201, 1202, 
3259 
Hall, K. D., 680, 2195 
Hall, M. V., 3055 
Hall, W. M., 2213, 2221 
Halperin, M. H., 2391, 
2400 
Halstead, B. W., 3777, 3778 
Halstead, W. C., 493, 506, 
519, 534, 712 
Hama, G. M., 3117 
Hamberger, C. A., 1678 
Hamburger, M., 2392 
Hamburger, R. J., 1260 
Hamilton, A., 2351, 2522, 
2543, 2578, 2598 
Hamilton, J. B., 1179 
Hamilton, J. G., 215, 2161 
Hamilton, L. L., 1946 
Hamilton, T. S., 995 
Hamly, D. H., 2548 
Hampson, J. L., 2751 
Hanaoka, T., 1403 
Handford, S. W., 3360 
Hanes, R. M., 3056 
Hanley, T. D., 1698, 1727, 
1742, 1743, 1744 
Hanns, A., 1993 
Hanson, J. F., 1099 
Kara, M., 2934, 2945 
Harbert, F., 2747 
Harcourt, A. K., 1103, 
1986, 2358, 2507, 2563, 
2646 
Hardenbergh, E., 3009 
Hardenbergh, W. A., 3143 
Hardy, C., 3425 
Hardy, H. L., 2351, 2522, 
2523, 2524, 2543, 2578, 
2598, 2630 
Hardy, J. D., 131,892, 893, 
895, 1180 
Hardy, L., 1344, 1345 
Hare, C. C., 2066, 2935 
Harfenist, M., 231 
Harger, R. N., 2509 
Hargreaves, J., 1590 
Harker, G. S., 3549 
Harmon, F. L., 1571 
Harper, J., 2827 
Harper, P. V., 1481 
Harris, A. S., 399 
Harris, D. L., 1096 
Harris, J. D., 1304, 1495, 
1496, 1497, 1498, 1499, 
1500, 1501, 1508, 1509, 
1516, 1620, 1621, 1699, 
1728, 1729, 1730, 1731, 
1861, 1877, 1929, 3463, 
3515, 3516, 3517, 3518, 
3519, 3520, 3521, 3522 
Harris, J. S., 1743, 1744 
Harris, M., 151, 168, 3261, 
3272 
Harris, S. C., 694 
Harrison, F., 3657 
Harrison, R., 1389 
Harrison, T. R., 1093 
Hart, D., 3118 
Hartline, H. K., 1404, 1405 
Hartman, F. W., 19 
Hartridge, H., 1346, 1347 
Hartrijsen, F. B., 1994 
Hartzell, A., 2567 
Harvey, E. N., 169, 170, 
171, 172, 173, 174, 175, 
176, 177, 178, 183 
Harvey, T. S., 638 
Harvey, W., 1862 
Hasegawa, T., 2828 
Hasterlik, R. J., 2525 
Hatch, T. F., 980, 999, 
1000, 1050 
Hatcher, R. A., 2748 
Haterius, H. O., 1261, 
1278, 1279 
Hatsuzo, K., 831 
Hauenstein, V. D., 368 
Haugaard, N., 2301, 2302, 
2303, 2322 
Hawkins, J. E., Jr., 1567, 
1595, 1596, 1679, 1680, 
1682 
Hawkinson, G. E., 165, 166, 
167, 2292 
Hawlick, G. F., 2499 
Hayashi, S., 1819 
Hayes, R. L., 1228 
Haymaker, W., 525, 540, 
1101, 2067 
Haynes, F. W., 2936 
Hayter, R., 88, 141, 759, 
2142, 2919, 2987, 2991, 
2992, 3203, 3205 
Heagan, B., 604 
Hebb, C. O', 146, 794 
Hebb, H. D., 1513 
Hecht, S., 494, 1406, 1407, 
1408, 1409 
Hedblom, R. E., 2218a 
Hedes, R., 2027 
Heemstra, H., 821 
Hegnauer, A. H., 1261, 
1280, 1287, 3423 
Hegsted, D. M., 1181 
Heilbrunn, L. V., 1096 
Heise, G. A., 1735 
Hellems, H. K., 2936 
Helm, J., 2566 
Helmholz, H. F., Jr., 195 
Helson, H., 3559 
Helve, O., 2393 
Hemingway, A., 36, 52, 90, 
353, 427,815,816, 1182, 
2254, 2673, 2685, 2686, 
2687, 2707, 2708, 2709, 
2710, 2749, 2750, 2829, 
2830, 2883, 2884 
Hempelmann, L. H., 3021 
Hemphill, R. W., 250 
Hempleman, H. V., 2255, 
3168 
Henderson, C. R., 969 
Hendley, C. D., 494, 1407, 
1408, 1409 
Hendricks, J. E., 1925 
Hendrickson, I., 3427 
Henny, G. C., 2775 
Henriques, F. C., 959 
Henry, C. E., 3604 
Henry, F. M., 200, 1990, 
2028, 2029, 2125, 2126, 
2153, 2154, 2155, 2156, 
2157, 2158, 2159, 2160 
Henry, J. P., 548, 3420, 
3426, 3427, 3428, 3433 
Henschel, A., 220, 960, 
1066, 1079 
Hensel, H., 760, 923 
Henson, M., 3170 
Herber, F. J., 428 
Herget, ( ), 2068 
Herman, G. L., 385 
Hermann, H., 1183 
Herrell, W. E., 2621 
Herrick, J., 3464 
Herrington, L. P., 889, 894, 
895, 1069, 3075, 3087, 
3265, 3266, 3267, 3285 
Herrmann, S. O., 3691 
Hervey, G. R., 1259, 2807, 
2808 
Hess, W. R., 1956, 3658 
Hesse, R., 400 
Hetherington, A. W., 1184, 
2218a 
Hetroy, M., 1895 
Heully, M. F., 2831 
Hewitt, J. E., 3727 
Heyman, A., 2258 
Heyman, T., 1382 
Heymans, C., 273, 761, 832 
Heyroth, F. F., 2556, 2579 
Hibbitt, G. W., 3497 
Hibert, Y., 326 
Hick, F. K., 1174 
Hickam, J. B., 38, 309 
Hiestand, W. A., 695, 2222, 
2226 
Higgs, P. M., 128 
Highman, B., 714, 3153, 
3154 
Hill, C. J., Jr., 2695, 2731, 
2732, 2780 
Hill, J. M., 99 
Hill, L., 2310 
Hill, T. L., 179 
Hill, W. H., 2599 
Hiller, A., 2491 
Himmelfarb, S., 3439 
Himmelstein, A., 352, 3371 
Himsworth, H. P., 2637 
Himwich, H. E., 275, 2751, 
2835 
Hinkle, L. E., Jr., 3602 
Hinn, G. J., 1411 
Hinrichs, M. A., 3623 
Hirsh, I. J., 1518, 1577 
Hisao, S., 1016 
Hitchcock, F. A., 41, 76, 
2186, 2188, 2190, 2196, 
2197, 2200, 2202, 2203, 
2208, 2210, 2214, 2217, 
2223, 2224, 2245 
Hitschler, W. J., 1820 
Hjort, A. M., 2557 
Hoagland, H., 3594 
Hodel-Boos, M. von, 1412 
Hodes, R., 2162 
Hodge, M., 3376 
Hoelscher, B., 591 
Hoff, E. C., 473, 474, 475, 
476, 520 
Hoffman, A. C., 3057, 3549 
Hoffman, C. E., 521, 601 
Hoffman, J. G., 3021 
Hoffmann, H., 3675 
Hofstetter, J. R., 574 
Hogger, D., 896 
Hoilien, M. J., 1863 
Hollaender, A., 3119, 3127, 
3142 
Hollender, A. R., 1864 
Holler, M. K., 92 
Holling, H. E., 989, 2832, 
2833, 3091 
Hollingworth, H. L., 3624, 
3659 
Hollo, J., 2263 
Holman, J., 833 
Holmes, F. E., 39 
Holmes, J., 3376 
Holmes, J. G., 1365 
Holmes, J. H., 795 
Holmes, W. J., 1413, 1414 
Holway, A. H., 1622 
Homans, J., 2922 
Hoobler, S. W., 798 
Hood, B., 796 
Hood, J. D., 1700 
Hoople, G. D., 1623, 1821 
Hoople, W., 1624 
Hoorens, A., 762 
Hopps, H. C., 549 Hor—Kle 
INDEX OE AUTHORS 
Horie, Y., 1792 
Horiuti, K., 180 
Horn, V., 3597 
Horne, G. O., 1117 
Horowitz, S. A., 448, 452 
Horst, L. van der, 2414 
Horton, G. P., 1625, 1626 
Horvath, P. N., 1127, 1128, 
1129, 1130, 1131 
Horvath, S. M., 998, 999, 
1000, 1018, 1047, 1051, 
1071, 1185, 1186, 1241, 
1256, 3094, 3296, 3326 
Horwitz, S. A., 448,452 
Hosbach, L., 3370 
Hosoya, Y., 1415, 1416 
Houck, G. H., 1991 
Hough, J. W., 2606 
Houghten, F. C., 136, 961, 
3068 
House, H. P., 1896 
Houston, C. S., 401, 550, 
602, 606, 645, 696, 697, 
719, 720, 721, 2030 
Howard, T., 2600 
Howell, T. W., 310 
Hewlett, F. A. L., 2688, 
2711, 2712, 2713, 2714, 
2715 
Hewlett, J. G., 2703, 2752, 
2753 
Hoyos, J. M., 338 
Hsia, Y., 1410 
Hubbard, D. M., 2519 
Hudson, M. L., 1228 
Huerkamp, B., 339 
Hughes, L. B., 3605 
Hughes, R., 2535, 2536 
Hughson, W., 1524 
Huizing, H. C., 1502 
Hull, W. E., 40 
Humm, F. D., 2114, 2115, 
2152 
Humphreys, C. M., 962, 
963 
Hunt, H. R., 2564 
Hunt, W. A., 3465 
Hunter, D., 2594 
Hunter, J. A., 41, 76,118 
Hunter, R. B., 2834 
Hurtado, A., 585 
Husband, R. W., 3660 
Huston, J. W., 2084 
Hutchings, M., 2631 
Hutchinson, J. G. D., 1088 
Hyden, H., 1678 
Hyman, C., 3429, 3430, 
3431 
Hyslop, F., 2526 
landolo, G., 276 
Ikui, H., 245 
Imalis, O., 962, 963 
Imdahl, H., 425 
Imperiale, L. E., 1226 
Imrie, A. H., 964 
Imus, H. A., 100, 112 
Inatome, M., 214, 2168 
Ingraham, H. S., 1806, 
3120 
Inman, V. T., 1995 
Inouye, T., 952, 1174, 3292 
Irvine, G. S., 1833 
Irving, L., 68,69, 1242 
Ishizuka, T., 3625 
Ivanov, D. I., 2047 
Ivanov, I. I., 722 
Ivy, A. C., 191, 477, 536, 
635, 694, 2018, 2019, 
2031, 2032, 2144, 2159, 
2459, 2460, 2461, 3352, 
3354, 3355, 3356, 3357, 
3358, 3377, 3379, 3380, 
3626, 3661 
Ivy, J. H., 3432 
Ivy, R. C., 200, 429, 456, 
457, 625, 626, 628 
Iwama, K., 277, 497 
Jackenthal, R., 218 
Jackson, D. P., 3673, 3700 
Jacobs, H. J., 3361, 3428, 
3433 
Jacobs, M. B., 2352, 2544, 
2558, 2580 
Jacobs, M. H,, 1996, 2610 
Jacobson, L. O., 3003 
Jaedicke, H. G., 3728 
Jaggi, F., 402 
Jakobsson, S. G., 1981 
James, A. P. R., 3756 
Jankowski, W., 1627 
Jansen, E. F., 1801 
Jaquerod, R., 583, 584 
Jarcho, S., 3779 
Jarrett, E. T., 3121,3127 
Jarvis, W. H., 645 
Jasper, H. H., 2716,2717 
Jaulmes, ( ), 1281 
Jeannoel, G., 418 
Jeffers, C. P., 2597 
Jehn, K. H., 132 
Jellinek, S., 3362, 3363 
Jenkins, F. A., 1487 
Jenkins, W. J., 3497 
Jenkins, W. O., 3560 
Jenney, E. H., 166 
Jennings, B. H., 3113, 3114, 
3122 
Jensen, A. V., 522, 2247 
Jensen, D. M., 3510 
Jensen, J., 3510 
Jequier-Doge, E., 723 
Jewell, J. H. A., 1949 
Je2ek, K., 1897 
Johns, R. J., 2835 
Johnson, A. E., 685 
Johnson, C. A., 965 
Johnson, E. P., 1417 
Johnson, F. H., 1802 
Johnson, H. M., 3662 
Johnson, M. A., 2692 
Johnson, M. L., 1393, 1394 
Johnson, M. N., 815 
Johnson, N. C., 1539 
Johnson, R. E., 966, 967, 
969, 1052, 1144, 1226 
Johnson, W. H., 2754 
Johnston, M. W., 968 
Johnstone, R. T., 2545, 
2581, 2601 
Jones, E. D., 158 
Jones, E. S., 49 
Jones, H. B., 196, 197, 198, 
200,209,215,216, 2127, 
2156, 2160, 2161 
Jones, I. H., 1798 
Jones, M. F., 1834,3206 
Jones, R. J., 2091 
Jones, R. R., 2602 
Jones, W. M., 1228 
Jongbloed, J., 2305, 2306 
Jorda, M., 3678 
Jordan, R., 1865 
Josephson, C. J., 2500 
Jourdan, F., 797, 2622 
Joyce, S. J., 1133 
Junes, ( ), 1317 
Jung, F. P., 1982 
Kabat, H., 274 
Kallenberger, A., 257 
Kamata, M., 1903 
Kaplan, N., 42 
Kaplan, S. J., 3022 
Kappauf, W. E., 3535, 
3561, 3562, 3563 
Karatay, S., 1898 
Karel, L., 2128, 2129, 2139 
Karig, W., 3506 
Kark, R. M., 966, 969, 
1175, 1226 
Karlin, J. E., 866 
Karlin, R., 708 
Karpovich, P. V., 2033, 
3364, 3365, 3366, 3367, 
3729, 3730, 3731, 3732 
Karsner, H. T., 2937 
Karstens, A. K., 3428, 3433 
Karvinen, E., 614 
Karvonen, M. J., 614 
Kaser, R., 1540 
Katayama, K., 1015 
Katz, L. N., 256, 327, 360, 
361, 366, 445 
Katz, M., 2474 
Katzell, R. A., 3627 
Katzman, J., 2474 
Kaufman, P., 2263 
Kaufman, S. S., 2048, 3434 
Kawahata, A., 970, 971 
Kay, H.D., 2512 
Kaye, S., 2819, 3124 
Kayser, G., 3663 
Keeton, R. W., 952, 1174, 
1240, 1243, 1247, 3292 
Kehoe, R. A., 2582, 2583, 
2584, 2585, 3438 
Keil, F. C., 1418 
Kekcheev, K. K., 1419 
Kelk, G. F., 2754 
Kellar, R. J., 2040, 2091, 
2142 
Kelley, V. C., 633, 634, 
666, 669, 725 
Kellogg, R. H., 3104 
Kelly, H. G., 2938 
Kelley, J. C., 1727, 1742, 
1743, 1744 
Kelly, W. J., 1877, 1929, 
1932, 1933, 1934, 1935, 
1936 
Kelsey, P. A., 1621 
Kelso, W. T., 3269 
Kemp, E. H., 1594, 1673 
Kemph, J. P., 2186, 2202, 
2214 
Kendall, H., 3720 
Kennedy, A. S., 3195 
Kennedy, J. L., 3531, 3549 
Kennett, W., 1396 
Kenney, R. A., 972 
Kennon, R. H., 2996, 2997 
Kensler, G. J., 2502 
Kerekes, G. Y., 1866 
Kerslake, D. M., 940, 941 
Kety, S. S., 199, 430, 2586 
Keyes, G. H., 633, 634 
Keys, A., 220, 960, 1066, 
1079, 1370, 3634 
Kikuta, M., 1016 
Killick, E. M., 324, 2450 
Kimble, P. F., 3460 
Kincaid, R. K., 1012, 1062 
Kindred, M. I., 1326, 3459, 
3484 
Kindrick, R. C., 3171 
King, B. G., 485, 2410, 
2639, 3368, 3369, 3389, 
3390 
King, C. D., 3664 
Kingsland, L. C., 3137 
Kinney, T. D., 2936 
Kinsey, V. E., 3059 
Kipp, F., 1628 
Kirk, J. B., 1097 
Kirkner, F. J., 2718 
Kirkpatrick, B., 2824 
Kirschbaum, H., 551 
Kirstein, L., 278, 763 
Kisch, B., 2933 
Kitching, J. A., 3256, 3264 
Kitzinger, C., 22, 129 
Kivert, A., 1570 
Klain, A., 3430 
Klain, I., 548 
Klante, W., 425 
Klayman, M. I., 2836 
Klee, J. B., 2733 
Klein, H., 764, 863 
Klein, J. R., 851 
jKleinberg, W., 177< 
’Kleinschmidt, K., 667 INDEX OF AUTHORS 
Kle—Loe 
Kleitman, N., 3648, 3665, 
3666, 3667, 3668, 3669, 
3670, 3671, 3672, 3673, 
3674, 3675, 3680, 3689, 
3699, 3700, 3701 
Kley, W., 1629 
Klimenko, N. A., 8, 122, 
2914, 3332, 3333, 3334 
Kline, L. L., 231, 2642 
Kline, R. F., 698, 2130 
Klingman, W. O., 523, 524 
Klotz, O., 2559 
Knap, J., 1807 
Knapp, R. H., 1707 
Knauft, E. B., 3534 
Knight, R. T., 52 
Knisely, M. H., 2034, 2049, 
2145, 2146, 2147 
Knudsen, E. O. E., 2370 
Knudsen, V. O., 1765, 1798 
Koch, H., 1950 
Koch, W., 101 
Koehn, C. J., 1212 
Kohl, J. W., 16, 1811,3482, 
3501, 3502 
Kohn-Abrest, M., 2353 
Kolchinskaia, A. Z., 699 
Komendantov., G. L., 2225 
Kondo, Y., 3773 
Konig, H., 359 
Kopala, J., 460 
Kopecky, E. F., 3042 
Korkes, S., 403 
Korotianskil, A. M., 3157 
Korr, I., 3408 
Kos, C. M., 1835 
Kostelijk, P. J., 1541 
Koster, H. F., 1575 
Kottke, F. J., 431 
Rough, R. H., 2284, 2285, 
2293, 2294, 2295, 2311, 
2312, 2315 
Krafchuk, J., 1956 
Krainer, L., 1098 
Kramer, K., 137, 330, 342, 
464, 552, 586 
Kramer, M., 1244 
Krasno, L. R., 429, 536, 
625, 635 
Kraspovitskaia, S. E., 578 
Kravkov, S. V., 1366, 1565 
Krebs, A. T., 1205 
Kreienberg, W., 340 
Krejci, F., 241 
Kreuger, N. L., 2471 
Kreyberg, L., 1288, 1289 
Krieger, H. P., 1481 
Krimsky, E., 102 
Kristensen, H. K., 1681 
Krivosheenko, N. K., 140 
Krogh, M., 2595 
Krueger, H., 2920 
Kryter, K. D., 1542, 1756 
Ku£era, M., 1899 
Kuehner, R. L., 3158 
Kugelberg, I., 2394 
Kuh, J. R., 2692 
Kuhn, H. A., 2256, 2271 
Kuhn, H. S., 3058 
Kunkle, E. C., 1188 
Kuntz, J. E., 1318 
Kuroda, K., 973, 974 
Kuroda, M., 855 
Kurozumi, S., 1822 
Kurtzrock, G. H., 1490 
Kvacek, J., 89 
Laane, C. L., 2004 
Labaw, L. W., 212 
LaBelle, C. W., 2527 
Laborit, H., 2755 
La Brosse, E., 3380 
Ladell, W. S. S., 975, 976, 
977, 978, 989, 1053, 
1118, 3091 
Laget, P., 279 
Laird, D. A., 1572, 1701, 
3628 
Lalli, G., 636, 668 
Lally, J. F., 2132 
Lamanna, C., 3207 
Lamarche, M., 683 
Lambert, E. H., 1243, 1247 
Lambertsen, C. J., 2284, 
2285, 2293, 2294, 2295, 
2311, 2312, 2315,3718 
Lampson, R. S., 2623 
Landahl, H. D., 2756 
Landgren, N., 1900 
Landis, C., 3608 
Landis, E. M., 18, 1162 
Landowne, M., 506, 534, 
712 
Lane, F. H., 1290 
Lange, K., 1244, 1291 
Langheinz, H. W., 1936 
Lanig, D. L, 1759 
Langley, L. L., 637, 638, 
643, 681 
Langmuir, A. D., 3142 
Lanning, W. C., 3176 
Lanoue, F., 3733 
Lapin, S. B., 3370 
Laquer, W., 2640 
Largby, L. L., 2132 
Larkin, J. C., 2161 
Laroche, C., 2453 
Larrabee, M. G., 2027, 
2162, 2283 
Larsen, B., 1630, 1631 
Larsen, E. M., 3629 
Lash, J. J., 43 
Laslett, H. R., 3676 
Last, J. H., 1004, 1243 
Latham, F., 2333, 2334 
Latimer, W. M., 3186 
Latour, H., 3652 
Laudani, A., 1226 
Laurens, H., 3123 
Lavigne, S., 279 
Law, N. C., 3268 
Lawrence, G. H., 3023 
Lawrence, J. H., 200, 201, 
215, 216, 1990, 2005, 
2006, 2051, 2052, 2059, 
2157, 2161, 2444, 2445, 
3016 
Lawrence, L. B., 2005, 2006 
Lawrence, M., 250, 1841, 
1842, 3564 
Lawrence, R. E., 3143 
Lawrow, J. W., 1222 
Lazarow, A., 2050, 2055 
Lazarow, L., 44 
Lea, D. E., 3024 
Leake, C., 3630 
Learoyd, C. C., 3677 
Leavitt, H. J., 3466, 3494 
Lebensohn, J. E., 103 
Leblond, C. P., 3223 
Le Breton, ( ), 2454 
Le Chuiton, ( ), 3076 
Lee, D. H. K., 897, 898, 
899, 900, 983, 1008, 
1054, 1080, 3232, 3269 
Lee, R. H., 94, 104, 105, 
1420, 3565 
Leeper, R. W., 3747 
Le Fevre, P. G., 1096 
Lehmann, K. B., 2641 
Lehmann, P., 2674, 2757 
Lehner, F., 825 
Lehoczky, T. de, 2395 
Leighton, J. G., 1567 
Lein, A., 2189, 2190, 2203, 
2208, 2217 
Lemaire, R., 181, 335, 336, 
397,411,426, 840, 2329, 
2330, 2331, 2332, 2335 
Le Maistre, H., 3731 
Lemley, J. M., 341 
Lemon, H. M., 3133 
Lemons, H., 3232 
Lenggenhager, K., 404, 
2323, 2475 
Lennox, W. G., 3655 
Lentine, J., 1867 
Leonardi, G., 432, 433 
Leopold, C. S., 3077 
Leriche, R., 2939 
LeRoy, G. V., 3017, 3025 
Lessard, R., 2837 
Lester, W., Jr., 3124, 3125, 
3134 
Letonoff, T. V., 2586 
Leuallen, E. E., 2528, 2546, 
2588, 2603, 2628, 2659 
Leusen, I., 765, 834, 979 
Leveille, J., 2397 
Levenson, S. M., 2656 
Levey, M. R., 3744 
Levin, O. L., 3780 
Levy, J, 2237 
Levy, R. L., 2624 
Lewy, G. A., 2501 
Lewandowski, T., 3127 
Lewin, B. D., 3706 
Lewis, D., 3595 
Lewis, E. G., 2207 
Lewis, G. M., 3758 
Lewis, J. H., 549 
Lewis, J. S., 2898 
Lewis, M. L., 1952 
Lewis, R. A., 376 
Lewis, R. B., 525, 1282, 
1292, 1293, 1294, 1295 
Lewis, R. S., 1823 
Lewy, A., 2689 
Ley, E. B., 2499 
Leyzorek, M., 3541 
Lhermitte, J., 2396 
Liberman, A. M., 527, 662, 
2015, 2016, 2044 
Libet, B., 3270 
Lichten, W., 1735 
Licklider, J. R. C., 1503, 
1543, 1736 
Lieberman, A. T., 507, 627, 
1836, 1868, 1925 
Lieberman, B., 3620 
Liest, L. J., 766 
Lievre, J. A., 2503 
Lifshits, A. V., 526 
Lifshitz, S., 1504 
Lifson, N., 3297 
Light, S. F., 3781 
Lightfoot, G., 1716 
Liles, J. H., 1119 
Lilienthal, J. L., Jr., 62, 63, 
603, 2415, 2416, 2429, 
2433, 2434, 2838, 2839, 
2840 
Liljegren, E. J., 2614, 2615, 
2616, 2617 
Liljestrand, G., 389, 808, 
2112, 2228 
Lillehei, C. W., 1182 
Lilly, J. C., 45,2162 
Lindenberg, R., 528, 529 
Lindgren, I., 46 
Lindsay, J. K., 1074 
Lindsey, H. A., 3042 
Lindsley, C. H., 2494 
Lipin, J. L., 724 
Lisco, H., 3021 
Little, W. J., 798 
Littler, T. S., 1602,1605 
Littman, D., 2922 
Littmann, H., 106 
Livingood, G. S., 3760 
Livingston, P. C., 495, 1421 
Livingston, R. B., 2187, 
2211, 2220 
Loch, W. E., 1893 
Locke, W., 3138, 3139, 
3714 
Loeckle, W. E., 1777, 3331 
Loeper, M., 2397 
Loeschicke, G., 434 
Loeschicke, H. H., 280, 
434, 2285, 2293, 2294, 
2295 
Loevenhart, A. S., 3618 Log—Mer 
INDEX OF AUTHORS 
Logue, R. B., 1099 
Lombard, B. F., 3315 
Long, J., 788, 789, 793, 
2931 
Longmore, D. B., 2841 
Loomis, T. A., 47 
Loomis, W. F., 201, 216, 
2059, 2161 
Loosli, G. G., 3126, 3159 
Lorente de No, R., 530, 767 
Lorenzo, P. L., 2242, 2266 
Lottenbach, K., 2475 
Loucks, R. B., 3566, 3567, 
3568 
Louis, L. H., 968 
Love, L. H., 901 
Lovell, G. D., 1544 
Lovett-Doust, J. W., 281 
Low, F. N., 1319, 1320, 
1422, 1423, 1424, 1425 
Lowenbach, H., 282 
Lowery, E. A., 1426 
Lozner, E. L., 701, 702 
Luaces, E. L., 3160 
Lucas, G. B., 283 
Luciano, V. J., 741 
Luczak, A. K., 1432 
Ludvigh, E., 3059 
Ludwig, G. D., 3702 
Luedemann, W. S., 1124 
Lueth, W., 3640 
Luft, U. G., 194, 342, 552, 
586, 1184, 1295, 2198 
Lugli, G., 1632 
Lumio, J. S., 1507, 1633, 
2398, 2399 
Lumsden, R. B., 1951 
Lund, D. W., 478, 1983, 
2005, 2006, 2051, 2052, 
2126, 2157, 2158 
Lundin, G., 195, 435 
Lurie, M. H., 1567, 1594, 
1673, 1679, 1680, 1682 
Liischer, E., 1505, 1506 
Lushbaugh, G. G., 2658 
Luykx, H. M. C., 2842, 
2843 
Lvovich, D. B., 747 
Lyle, P. L., 1921 
Lyman, C. P., 799 
Lyman, J., 1031, 1033, 
1072 
Lyons, W. R., 2149 
McArdle, B., 882, 932, 989, 
2833, 3091 
MacArthur, J. J., 48 
McBride, A. F., 3785 
McCain, J. A., 3467 
McCance, R. A., 225 
McCann, S. M., 1583 
McCann, W. S., 1434 
McCarthy, L., 1100 
McCay, C. M., 228 
McClure, W., 1007 
Macco, G. di, 531, 673 
McCollum, E. L., 1145, 
3468 
McCollum, W. T., 3776 
McConnaughey, W. E., 
3172 
McConnell, W. J., 912, 
2354, 2504 
McCord, C. P., 1545, 2642, 
3161, 3162 
McCoy, D. A., 1546, 1634 
McCrady, M. H., 3211 
McCullough, J. D., 2465, 
2476 
McCutchan, J. W., 990 
MacDonald, D. K. C., 1055 
MacDonald, E., 2471 
McDonald, J. H., 2951 
McDonald, P. R., 1427 
McDonald, R. K., 639, 666, 
669, 725 
McDonough, F. E., 1997, 
2719 
McEachern, D., 2670, 
2674, 2723, 2724, 2745, 
2757, 2765, 2769 
McElroy, W. D., 173, 174, 
175, 176, 177, 178, 182, 
183, 217 
MacFarlan, D., 1757 
McFarland, R. A., 2391, 
2400 
McGee, L. E., 328, 451 
McGibbon, J. E. G., 1837, 
1857, 1922 
McGoldrick, T. A., 2132 
McGovern, F. B., 2631 
MacGown, J. C., 1428 
McGuckin, F., 1869 
McGuire, J., 368 
McHarg, J. F., 3707 
Machle, W., 902, 912, 980, 
1635 
Macht, M. B., 1273, 1274 
Macintosh, F. C., 748 
Mack, A. G., 1133 
MacKay, R. A., 2845 
Mackay, J. L., 856 
Mackenzie, C. G., 532, 704 
Mackworth, N. H., 882, 
932, 1081, 1082, 1083, 
1084, 1089, 3569, 3599, 
3631 
MacLachlan, P. L., 436, 
615 
MacLaren, W. R., 1636 
McLaurin, J. W., 1957 
McLean, R., 991 
McLeod, C. M., 2566 
MacMartin, L. S., 1429 
McMichael, M., 350, 561 
MacMillan, J. W., 3564 
McNally, W. J., 2725, 
2758, 2759, 2760, 2761 
McPhaul, M. V., 805 
McPhee, G. S., 1181 
MacPhee, H. M., 2720 
MacPherson, R. K., 903, 
981,982, 983, 1054, 1056 
Macradyen, A., 133 
Maegraith, B. G., 49 
Magnin P., 583, 584 
Magnuson, P. L., 1930 
Magnussen, J. D., 374 
Mahady, S. G. F., 2123, 
2124 
Mahler, S. L., 393 
Mahoney, D. L, 2215, 3415 
Mahoney, J. B., 2161 
Maier-Leibnitz, H., 50, 622 
Maison, G. L., 1279 
Maksimenko, V. P., 8, 122, 
2914, 3332, 3333, 3334 
Malamud, N., 1101 
Malhuret, ( ), 2402 
Malin, A., 1203 
Malinosky, A. T., 3469 
Malkiel, S., 2820 
Mallory, L. A., 3497 
Malm, E., 51 
Malmejac, J., 284, 285, 
286, 287, 288, 289, 343, 
344, 345, 346, 347, 348, 
349, 375, 381, 437, 438, 
439, 453,587,674, 1984, 
2336, 2337 
Malmo, R. B., 544 
Malone, F. L., 1348, 1458 
Malone, M. E., 599 
Maloney, J. V., Jr., 3435, 
3436 
Maloney, M. A., 1226 
Malorny, G., 809, 810, 
2365, 2366, 3173, 3174 
Malysheva, A. E., 1190 
Manceau, A., 3678 
Mancioli, G., 1683 
Mandelbaum, J., 1321, 
1430 
Mann, I., 1431 
Mann, P. J. G., 2264 
Manning, G. W., 308, 2746, 
2762, 2763, 2764, 2776, 
2824 
Manson-Bahr, P., 3750, 
3751 
Mansuy, L., 2082 
Marbarger, J. P., 545, 738, 
984, 1022 
Marchand, J. F., 2927 
Marechaux, E. W., 985 
Margaria, R., 202, 211, 
1830, 1831, 1832 
Margolis, S. I., 3316, 3321 
Marin-Foucher, M., 1209 
Marine, D. N., 219 
Marijan, N., 3696 
Marinacci, A. A., 2456 
Markert, J. W., 3084 
Marnierre, P. de la, 2069, 
2070 
Marriott, H. L., 986, 987, 
988 
Marriott, W., 403 
Marshall, J. M., 203 
Marshall, L. H., 2104 
Martin, D. S., 3743 
Martin, J. B., 2946 
Martin, G. G., 3352 
Martin, P. G. C., 2973 
Martin, W. B., 2998 
Marzulli, F. N., 820 
Masland, R. L., 2007, 2008, 
2124 
Mason, E. C., 857 
Mason, E. D., 3679 
Mason, H. M., 1732 • 
Massengale, H. W., 2803, 
2804 
Massey, V., 2265 
Master, A. M., 351 
Masuda, M., 539 
Mather, J. A. L., 2624 
Mather, G. G., 353 
Mathewson, F. A. L., 2721 
Mathis, J. A., 32, 33 
Matthews, B. H. C., 1432 
Matthews, J. I., 1954 
Matthews, J. L., 3470 
Maurer, W., 568 
Maxcy, K. F., 3143 
Maxwell, H. P., 790 
Mayerson, S., 800 
Maynard, G. C., 3550 
Maynard, F. L., 496 
Mayo, W. P., 784, 814 
Mazel, P., 2071 
Mead, J., 992, 1155, 1191, 
1224, 1227 
Meakin, L. W., 2212 
Meakins, J. C., 2745, 2765 
Meakins, J. F., 2938 
Mecl, A., 2625 
Meda, E., 781, 2109, 2133, 
2238, 2242, 2243, 2766 
Meduna, L. J., 768, 769, 
770 
Medvedev, V. I., 1433 
Meeham, H., 3428 
Meehan, J. P., 548, 3427 
Meessen, H., 835, 872, 873 
Meeter, E., 801, 802 
Meier, F., 3358 
Meigs, J. W., 2477 
Meiklejohn, G., 3137 
Meissner, W. A., 3004 
Meister, F. J., 1781 
Melik-Megrabov, A. M., 
405 
Mellette, H., 2210 
Mellor, J. F., 2532 
Melton, A. W., 3454 
Melton, C., 1795 
Melville, G., 2527 
Mendelson, E. S., 3270 
Meneely, G. R., 341 
Mercier, A., 1778, 2401 
Merino, C. F., 585, 588, 
589 
Merlen, J. F., 2384 INDEX OF AUTHORS 
Mer—Orb 
Merrel, M., 2846 
Metz, B., 1066, 1146 
Meyer zum Gottesberge, A., 
1637 
M, H. J. L., 2844 
Michelis, F. de, 2072 
Mikell, J. S., 1926 
Mickelsen, O., 1079, 3222 
Miles, W. R., 507, 527, 
1305 
Millard, E. B., 1434 
Miller, A. J., 1192, 1194, 
1245, 1257 
Miller, A. T., Jr., 2134 
Miller, D. H., 972 
Miller, F. A., 52, 90, 836 
Miller, F. S., 447, 462 
Miller, G. A., 1494, 1638, 
1639, 1733, 1734, 1735, 
1736 
Miller, J., 1707, 3497 
Miller, J. A., Jr., 447, 462 
Miller, M., 2933 
Miller, M. J., 2632 
Miller, M. R., 1193, 1194 
Miller, R. A., 604 
Miller, R. R., 3175, 3176 
Miller, V. J., 993 
Miller, W. R., 3127 
Millet, P., 2177 
Millman, N., 3732 
Mills, C. A., 1057, 2626 
Mills, J. R., 2548 
Milne, L. J., 1405 
Milton, R., 2594 
Milwidsky, H., 2940 
Minnich, V., 2249 
Minot, A. S., 2568, 2569 
Minter, C. C., 53 
Miranda, A., 556 
Mirskil, M. I., 3157 
Mirsky, I. A., 1573 
Missenard, A., 554 
Mitchell, H. H., 640, 994, 
995, 1195, 1240, 1243, 
1246, 1247 
Mitchell, J. H., 3756a 
Mitchell, M. J. H., 3570, 
3571 
Mitchell, R. B., 553, 3020 
Mitchell, R. T., 1435, 1436 
Miyama, A., 3734 
Modglin, F. R., 3777 
Moeschlin, S., 2355 
Mohamed, M. S., 803 
Mohney, J. B., 59, 2160, 
2161 
Mole, R. H., 904, 1117 
Molfino, F., 2073, 2074, 
2075 
Molnar, G. W., 996, 1223, 
1262 
Molumphy, C. G., 123, 
2101, 2102, 2106, 3335, 
3336, 3337, 3500 
Monaco, A. R., 2526 
Monaco, L., 2675 
Moniatte, ( ), 2402 
Montandon, A., 2847 
Montano, R. A., 1411 
Monteiro, A., 1901 
Montgomery, G. E., Jr.,-31. 
Monto, R. W., 2848 
Montoye, H. J., 2907 
Mood, E. W., 3757 
Moon, H. D., 2643, 2644 
Moon, V. H., 440 
Moor, F. B., 993 
Moore, B. V., 3471 
Moore, G., 2985 
Moore, C. R., 675 
Moore, C. V., 2249 
Moore, E. W., 3208 
Moore, F. D., 226, 235 
Morales, M. F., 204, 205, 
206, 207, 208, 213, 227, 
1808, 2767, 2768 
Morand, P., 2755 
Morgan, A. F., 641, 661 
Morgan, G. T., 1303, 1595, 
1596, 1696, 1719, 1720, 
2669, 3049, 3071, 3538, 
3539, 3540, 3622 
Morgan, E. H., 2136 
Morgan, J. J. G., 1574, 
1702 
Morita, S., 1703 
Moritz, A. R., 959, 991, 
1013, 1196 
Morone, G., 246 
Morrill, S. N., 1716 
Morris, A., 1436, 1437 
Morrison, J. L., 691 
Morrison, L. R., 290 
Morrison, W. W., 1870 
Morrow, P., 2527 
Mortarotti, T. G., 2318 
Morton, G., 2674, 2717, 
2722, 2723, 2724, 2725, 
2743, 2761, 2765, 2769 
Moses, L. E., 1184 
Mote, F. A., 1400, 3461 
Motley, H. L., 352, 2009, 
3371, 3417 
Motokawa, K., 497, 1349 
Mouchet, A., 2076 
Moulder, J. W., 3201 
Moulis, A., 2849 
Mountcastle, V. B., 2738 
Moureau, P., 2505 
Mousel, L. H., 3177 
Moussatche, H., 771, 772 
Movitt, E., 548, 3427 
Mueller, C. G., 3462 
Mueller, L. E., 2478 
Miihlberg, O., 1547 
Muido, L., 3735 
Mulholland, H. F., 693 
Mullin, F. J., 3648, 3680 
Mulinos, M. G., 2627 
Munro, J., 3620 
Muralt, A. von, 479 
Murphy, G. E., 3271 
Murphy, H. T., 627 
Murray, G. D., 498, 2135 
Murray, H. G., 641 
Murray, S. D., 3372 
Murrell, H., 3317 
Mushett, G. W., 2645 
Muxworthy, J. F., Jr., 2908 
Myers, C. K., 1500, 1501, 
1508, 1509, 1731, 3520, 
3521, 3522 
Myers, E., 198 
Nahas, G. G., 353, 427, 
2126 
Nairn, R. C., 354 
Naito, Y., 1015 
Nakano, K., 245 
Nale, T. W., 2560 
Napier, L. E., 1058, 1102, 
1120 
Nash, C. S., 1548 
Nashat, F., 2640 
Nau, C. A., 2506 
Navarro, J. Y., 741 
Neal, P. A., 2602, 2606, 
2614 
Neff, W. B., 268 
Neff, W. D., 1737, 3472, 
3492, 3497, 3523, 3524, 
3525 
Nei, T., 1197 ' 
Neilson, M., 1061 
Nekhorocheff, I., 3681 
Nelson, J. T., 3355, 3377 
Nelson, N. A., 997, 998, 
999, 1000, 1047, 1071, 
1077, 2479, 3094 
Netter, F. H., 2974 
Neuhof, H., 2941 
Neverre, G., 289, 347, 348, 
349,375,418,587, 2336, 
2337 
Newbert, N., 3483 
Newburgh, L. H., 1172, 
1263, 3272, 3318, 3319 
Newby, H. A., 1515 
Newlin, H. E., 228 
Newman, E. B., 1518, 1610, 
1738 
Newman, R. W., 3572 
Newman, S. H., 3473 
Newton, H. E., 3369 
Newton, M., 909, 910 
Newton, W. L., 3206 
Neymann, C. A., 886 
Nez, M., 602 
Nichols, R. L., 2034, 2049, 
2146, 2147 
Nicolas, M., 2077 
Nicolson, P. H., 2435 
Nicoulaud, M. D. M., 2078 
Nielsen, J. C., 1871, 1902 
Nielsen, M., 1061, 2259, 
2595, 3105, 3106, 3341 
Niemeyer, H., 70 
Nier, A. O. C., 52, 90 
Niklas, A., 568 
Nilsson, G., 1678, 1684 
Nimmo-Smith, R. H., 794 
Nims, L. F., 471, 480, 507, 
527, 605, 627, 637, 638, 
642, 643, 662, 681, 846, 
1980, 2015, 2016, 2044, 
2048, 2053, 2054, 2114, 
2115, 2152, 2163, 2211, 
2220, 3026, 3434 
Nims, R. G., 3373 
Nisell, O. I., 355, 804, 837, 
838 
Niven, J. I., 2391, 2400 
Noble, R. L., 2716, 2726, 
2770, 2811, 2850, 2851, 
2852, 2853, 2854, 2855, 
2856, 2857 
Noell, W. K., 247, 291, 292, 
700, 2795 
Noro, L., 2448 
Norris, E. B., 1401, 3573, 
3574 
Norris, R. H., 2103 
North, N., 2927, 3431 
Northington, P., 1927 
Northup, D. W., 412, 618, 
619, 650, 651, 654, 655, 
849, 850 
Nothdurft, H., 3078, 3095 
Nuzie, S., 696, 697, 2030 
Nyboer, J., 2044, 2048, 
3434 
Obata, J., 1703 
Oberst, F. W., 2796, 2797, 
2798, 2799, 2801 
Obraszova, G. A., 301, 542 
Obreschkow, G., 2343, 
2383 
O’Brien, J. P., 1121, 1122 
Ochs, I. L., 1958 
Ochwadt, B., 644, 670 
O’Connor, J. M., 1001 
Odell, F. A., 2009 
O’Donnell, F., 784 
Oestreicher, H. L., 1772, 
1773, 1779, 1780 
Ogden, F. W., 1872, 1873, 
1887, 1939, 1940 
Ohlsson, W. T. L., 2257 
Ohsawa, R., 1903 
Ohsio, S., 245 
Okawachi, K., 2771 
Old, E. H. H., 3782 
Ollivier, H., 2561 
Olmsted, F., 1941 
Olsen, C. G., 1985 
Olsen, C. W., 2456 
Olson, F. C. W., 3113, 3114 
Olson, R. A., 54 
O’Neal, J. D., 2458, 2661, 
2662, 3151 
Onofrio, V. d’, 2587 
Opitz, E., 400, 600, 726, 
727, 728 
Oppenheimer, M. J., 788, 
789, 793, 2775, 2931 
Orban, B., 2999, 3000 Ore—Ray 
INDEX OF AUTHORS 
Orcutt, J. A., 2034, 2049, 
2146, 2147 
Ordway, N. K., 642, 2138 
Orlansky, J., 1438 
Orth, O. S., 17 
Ortiz, R. B., 1824 
Osborn, G. M., 2996, 2997 
Osborne, S. L., 886 
Osgood, L. E., 1198 
Osol, A., 2528, 2546, 2588, 
2603, 2628, 2659 
Osserman, E. F., 221, 222, 
229 
Oster, R. H., 444 
Ota, H., 3632 
Otis, A. B., 59, 458, 510, 
730, 867, 2103-a, 2909, 
2910, 3376, 3414, 3423, 
3437 
Otten, K., 2375 
Otto, G. F., 3209 
Oumikov, S., 1584 
Ourgaud, A. G., 1439 
Owens, R. J., 1116 
Pace, N., 227, 230, 231, 
232, 233, 701, 702, 703, 
743, 921, 1002, 2418, 
2421, 2436, 2437, 2438, 
2439, 2440, 2457, 3068, 
3204 
Page, E., 3256 
Page, E. B., 309 
Page, J. D., 3682 
Palme, F., 400, 600, 727, 
728 
Palmer, G. R., 2589 
Palmes, E. D., 1047, 1059, 
2526 
Palmisano, C., 2690, 2691, 
2772 
Pannier, R., 761 
Pappenheimer, J. R., 2417, 
3187, 3188 
Paris, J., 2413, 2464 
Park, G. R., 1047, 1059 
Park, R. G., 1147 
Parker, J. M., 2858, 2859, 
2860, 2861, 2862, 3081 
Parkes, A. S., 441 
Parodi, V. M., 2010 
Parrack, H. O., 1532, 1567, 
1575, 1582, 1604, 1758, 
1772, 1780 
Parrish, M. E., 3262 
Parry, T. M., 807, 811, 
3403, 3405 
Partridge, R. C., 1510, 
1511, 1512, 1513, 1640, 
3575 
Pascucci, L. M., 2529 
Pask, E. A., 3374 
Passerni, P. G., 665 
Passouant, P., 3652 
Passouant-Fontaine, T., 
3652 
Pastore, P. N., 1641 
Patek, P. R., 2050, 2055 
Patel, J. G., 2233 
Paton, W. D. M., 3736 
Patterson, G. A., 2449 
Patterson, J. L., 719, 805, 
2258 
Patterson, M. C., 2624 
Pattie, F. A., 1642 
Patton, B. W., 627, 652 
Patton, R. A., 1874 
Patty, F. A., 3375 
Paul, W., 55 
Pauling, L., 56 
Paulon, Y., 797 
Paulsen, G. B., 3576, 3577 
Pavlov, I. P., 3683, 3684 
Pavlovskii, K. A., 8, 122, 
2914, 3332, 3333, 3334 
Payne, R. B., 3022 
Payne, W. W., 3210 
Peabody, S. M., 1124 
Pearce, R. G., 2562 
Pearce, S. J., 91 
Peary, R. E., 3293 
Pease, D. G., 173, 174, 175, 
176, 177, 178, 183, 184, 
189 
Pease, E. D., 969 
Peck, H. M., 2034, 2049, 
2146, 2147 
Peck, J. A., 3389, 3390 
Peck, S. M., 3759 
Peckham, R. H., 499, 1350, 
1440, 1441 
Pecora, J. S., 1245, 1248, 
2470, 2471, 2480, 3090 
Pecora, L. J., 57, 185, 702, 
743, 1002, 1042, 1092, 
3152 
Peloquin, M., 2403 
Pender, J. W., 3170 
Penfield, W., 2817 
Peng, M. T., 1415, 1416 
Penneys, R., 356, 376, 806 
Pennington, L. A., 2720 
Penrod, K. E., 1264, 1271, 
1287, 2320, 2321 
Perley, G. A., 2468 
Perlman, H. B., 1643, 1644 
Perrin, M., 2404 
Perry, K. M. A., 2594 
Perry, W. O., 3273 
Perwitzschky, R., 1759 
Pesigan, D. E., 741 
Pestel, G. V., 545 
Peterson, J. H., 1378 
Petronella, S. J., 2500 
Petrov, I. P., 293, 294, 533, 
682 
Pettengill, A. G., 2533 
Peyser, A., 1549, 1645 
Peyser, E., 406, 841, 1576 
Pezechkian, M., 1085 
Pfaffmann, C., 2041 
Pfeiffer, C. C., 1042, 2286, 
2702 
Phalen, J. S., 431 
Phillips, N. E., 731 
Piccard, J., 185 
Pichotka, J., 1282, 1294, 
1295, 2256, 2271, 2313 
Pickering, J. E., 3027 
Pieron, H., 3685 
Pierquin, L., 2356 
Piery, Y., 942, 1165 
Pigott, J. P., 3001 
Pijoan, M., 1420 
Pillion, M. E., 1224 
Pillsbury, D. M., 1129, 
1130, 1131, 3760 
Pincus, G., 1003, 3594, 
3609, 3636 
Pine, M. B., 2433, 2434 
Pinotti, O., 827, 839 
Pinson, E. A., 107, 1391 
Pinto, J. C., 3348 
Pinto, S. S., 2500 
Pinotkovskii, I. A., 1296 
Piquet, J., 1904 
Pitesky, I., 1004 
Pitts, G. C., 221, 222, 229, 
702, 703, 743, 1002, 
2418, 2440, 2458, 2481, 
2482, 2661, 2662 
Pitts, J. C., 967, 1052 
Pivovarov, M. A., 2225 
Plambeck, H., 295 
Plane, P., 674 
Plas, F. L., 554 
Platt, B. S., 1005 
Platt, W. T., 2471 
Plichet, A., 2863 
Poel, W. E., 573, 729 
Pogrund, R. S., 2137 
Pointner, R., 858, 3043 
Policard, A., 2530, 3163 
Pollack, I., 1739, 1740 
Pollice, F., 1632 
Pollock, G. H., 758, 773, 
774,778 
Pollock, K. G., 1704 
Polonovski, M., 414 
Pompe, J., 1884 
Ponsart, E., 2505 
Pope, L. J., 2478 
Popoff, N. F., 1685 
Poppen, J. R., 1533 
Porter, R. J., 2325, 3201 
Post, R. L., 909 
Posternak, J., 500, 501 
Postlethwait, R. W., 2946 
Pothoven, W. J., 1550 
Potthoff, C. J., 3351 
Poulton, E. C., 2307, 3578, 
3596 
Poulton, E. P., 2113, 2342, 
3347 
Pratt, C., 1322 
Pratt, C. L. G., 2942 
Pratt, R. L., 1027 
Prec, O., 3355 
Prentiss, S. S., 58, 3189, 
3190, 3191 
Prescott, S. G., 3211 
Preston, S. N., 2138 
Price, A. H., 3511 
Price, D., 675 
Prior, K. M., 951 
Proctor, D. F., 1928 
Proemmel, D. D., 63, 2416 
Prokop, L., 340 
Proosdij-Hartzema, E. G. 
van, 2895 
Prosser, G. L., 3028 
Pryor, W. W., 309 
Puck, T. T., 3125, 3126, 
3128, 3129, 3130, 3133 
Pugh, D. G., 2079 
Pugh, L., 1809 
Pugh, L. G. G., 1148, 1199, 
3320 
Pumphrey, R. E., 2692 
Purcell, W. R., 3248 
Quastel, J. H., 2264 
Quenon, E. E., 87 
Quintanilla, R., 1285 
Quinton, W. E., 1231 
Quinton, W. F., 82 
Rabideau, S. W., 2611 
Rachmilewitz, M., 379 
Radclyffe, L., 1122 
Radigan, L. R., 1006 
Radsma, W., 1200 
Rae, J. A., 2471 
Rahn, H., 59, 458, 510, 
730, 817, 2909, 2910, 
3376, 3423, 3437 
Rahtgen, H. G., 3192 
Raiford, M. B., 108 
Rajner, V., 1905 
Rakestra, N. W., 3686 
Ralph, F. T., 99 
Ramadier, J. A., 1906 
Ramanamanjary, W., 840 
Ramsaroop, A., 3674 
Ramskill, E. A., 3185 
Rand, G., 1344, 1345, 1399 
Rand, G. W., 1351 
Randall, W. C., 1007 
Ranson, S. W., 3687 
Ranstrom, S., 3688 
Rao, M. N., 3328 
Rapaport, S., 2191 
Rapaport, S. I., 1201, 1202, 
3259 
Rapee, L. A., 2921 
Raper, J. R., 3029 
Rappoport, J. L., 2565 
Rasmussen, H., 1838 
Rathbun, E. N., 167, 227, 
232, 233 
Ratsimamanga, A. R., 1254 
Rawdon-Smith, A. F., 1646 
Rawnsley, A. I., 1621 
Ray, A. B., 3164 
Ray, J. T., 1351 
Ray, J. W., 2451, 2456 
Raymon, F., 3354, 3355, 
3356, 3357 
Raymond, M. V., 2080 INDEX OF AUTHORS 
Ray—Sch 
Raymond, V., 2357 
Razenkov, I. P., 616 
Reardon, W. T., 1959 
Redemann, C. E., 2658 
Reed, G. I., 3689 
Reed, E. A., 184, 186, 187, 
188, 189 
Reed, J. D., 1338, 1339, 
1340, 1341 
Reed, J. V., 1103, 1986, 
2358, 2507, 2563, 2646 
Rees, W. L., 1442 
Reese, J. M., 3107 
Reger, S. N., 1514, 1515 
Rehberger, J. M., 2898 
Rehfuss, M. E., 3511 
Reichenbach, G. S., 2571 
Reichman, S., 1249, 1250 
Reid, D. D., 1443 
Reid, W. O., 1888 
Reiher, H., 1781 
Reimann, H. A., 1907 
Rein, F. H., 442 
Reissmann, K. R., 310, 377, 
580, 590, 591, 622 
Reitmeier, R. E., 3171 
Renes, L. E., 2604 
Rentschler, H. C., 3131 
Reppert, L. B., 1111 
Restarski, J., 1782 
Reufin, A., 312 
Reynafarje, C., 589 
Reynolds, O. E., 731 
Reznikoff, P., 2568, 2569 
Rhamy, R. K., 1062 
Rhoads, C. P., 2502 
Ribble, G. B., 1124 
Ricardson, L. M., 969 
Ricchiuti, N. V., 3360 
Ricciardi, R., 2864 
Ricciuti, E. A., 2695, 2731, 
2732, 2780 
Richard, L., 2515 
Richards, C. H., 131 
Richards, D. W., Jr., 3371, 
3417 
Richardson, D. T., 905 
Richardson, G. S., 18 
Richardson, L. M., 969 
Richardson, M. W., 3474 
Richey, E. O., 50, 622, 
3323 
Richmond, P. N., 1408, 
1409 
Richter, D., 264, 3690 
Ricketts, H. T., 506, 534, 
712 
Riesen, A. H., 532, 704 
Riggs, B. G., 2300, 2302, 
2303 
Riggs, L. A., 3462 
RikkP, A. V., 140 
Riley, R. L., 60, 61, 62, 63, 
550, 603, 606, 645, 2416 
Rinecker, F. G., 3274 
Ringenbach, G., 582 
Ripple, P. H., 1444 
Riska, N., 378 
Riskaer, N., 1908 
Ritch, T. G., 2993, 2995 
Ritchey, B., 3000 
Ritter, M. H., 3133 
Rittinghaus, F. W., 339 
Rittler, C., 1344, 1345 
Ritvo, M., 2656 
Robb, J. E., 3719 
Robertson, A. M., 1125 
Robertson, J. S., 209 
Robertson, O. H., 3124, 
3125, 3126, 3132, 3133, 
3134 
Robinson, E. S., 3691 
Robinson, F. W., 3135 
Robinson, K. W., 1008 
Robinson, S., 906, 948, 
1006, 1009, 1010, 1011, 
1012, 1060, 1061, 1062, 
2025, 2026, 3233, 3249, 
3313, 3314, 3324, 3325, 
Robinson, T. W., 2035, 
2164, 2165 
Rochaix, A., 3761 
Roche, L., 2515 
Rochon - Duvigneaud, A., 
1445 
Rockhold, W. T., 2226 
Rodbard, S., 190, 256, 327, 
360, 361,607, 1203, 2036 
Rodel, A., 1909 
Rodger, A., 3475 
Roer, H., 2952 
Roff, M. F., 3476 
Rogers, F. T., Jr., 1487 
Rogers, W. P., 2265 
Rolf, D., 450 
Romano, J., 1998, 2148 
Rome, S. C., 1707 
Romney, S. L., 2953 
Ronge, H. E., 3136 
Roos, A., 64, 991, 1013 
Root, W. S., 2248, 2441, 
2445, 2483 
Roscoe, T., 3512 
Rose, G. L., 1516 
Rose, H. W., 732, 1323, 
1352, 1446, 1447 
Roseblade G. K., 1510 
Rosebury, T., 3137 
Rosenbaum, G., 3534 
Rosenbaum, L., 1104 
Rosenblith, W. A., 1577, 
1647 
Rosenstiel, M., 3477 
Rosenthal, J., 2263 
Rosin, A., 379 
Ross, P., 2547 
Ross, S., 1408, 1409 
Rossett, N. E., 686 
Rossi, M., 674 
Rossiter, F. S., 2359 
Rossle, R., 2943, 2944 
Roth, J. L. A., 1171 
Roth, L. W., 3404 
Rothballer, A. B., 1583 
Rothschuh, K. E., 608 
Rothstein, A., 1014 
Rotta, A., 555, 556 
Roughton, F. J. W., 2391, 
2435, 2441, 2445, 2483 
Rougier, G., 267, 326, 509 
Rouse, R. O., 1392 
Rowe, S. N., 3692 
Rowland, L. S., 1448, 1450, 
1451, 1452 
Rowland, W. M., 1430, 
1449, 1450, 1451, 1452 
Royer, P., 296, 2328 
Rozanov, L. S., 9, 1987 
Rozsahegyi, I., 888 
Rubin, A., 2898 
Rubin, H. J., 2676 
Rudolph, L. M., 1313, 1314 
Ruedi, L., 1648, 1649, 
1686, 1687 
Ruff, S., 1578 
Ruiz, G. J., 2266, 2272 
Rule, C., 3406 
Rumsey, C. C., Jr., 690, 
3406, 3407, 3408 
Rundquist, E., A., 3478 
Rushmer, R. F., 2693 
Ruskin, A., 2975 
Russell, H. D., 3291 
Russell, R. W., 535 
Russi, U. von, 1650 
Rust, S. M., 2865 
Ryan, T. A., 1362 
Ryder, H. W., 214, 1998, 
2148, 2168, 3438 
Saathoff, J., 592, 593 
Sabine, P. E., 1551, 1552 
Sabrie, R., 2866 
Sadove, M. S., 3354, 3355, 
3356, 3357, 3377 
Safford, H., 632 
Sager, W. W., 2969 
Saiki, H., 1203 
Saito, T., 1792 
Sakai, H., 1015 
Salaun, A., 2069, 2070 
Salinger, A., 1911 
Salsbury, J. M., 2484, 2485, 
2493 
Salter, W. T., 2867 
Saltzman, D. C., 3579 
Saltzman, I. J., 1367 
Salvin, S. V., 1952 
Sanboz, L. M., 733 
Sand, A., 3736 
Sandiford, M., 2473 
Santenoise, D., 840 
Santesson, G., 2868 
Sappington, C. O., 2605 
Sargent, F., 1204 
Sarkisian, S. S., 234 
Sarnoff, S. J., 3391, 3392 
Saruwatari, Z., 1875 
Sasiain, M. R., 1453 
Sass-Kortsak, A., 406, 841 
Sato, T., 1015, 1016 
Saunders, E. E., 1368 
Saunders, G. M., 907 
Saunders, J. B. de C. M., 
1995 
Saunders, P., 3393, 3394 
Savely, H. E., 2167 
Saviano, M., 646, 3737 
Sawatari, J., 1297 
Sax, N. I., 2531 
Sayers, R. R., 2360, 3633 
Seal, J. C., 1553 
Scano, A., 240, 248, 594, 
609 
Scardigli, G., 358 
Schachman, H. K., 231 
Schachner, H. G., 1205 
Schacht, F., 3619 
Schaghter, M., 2786 
Schachter, S., 1392 
Schaefer, K. E., 210, 557, 
610, 749, 750, 751, 775, 
776, 842, 859, 860, 861, 
863, 868, 869, 922, 923, 
985, 1783, 1810, 2273, 
2367, 2660, 2994, 3060, 
3096, 3097 
Schafer, T. H., 3526 
Scheer, K., 210, 751, 861 
Schenk, H., Jr., 3720 
Schickele, E., 1105 
Schiff, M., 2747 
Schiffer, T., 340 
Schlaegel, T. F., Jr., 3030 
Schlapp, W., 755 
Schlegel, F. M., 1802 
Schloerb, P. R., 235 
Schmid, A., 558 
Schmideberg, M., 3708 
Schmidt, A. M., 3785 
Schmidt, C. F., 430, 2234, 
2285, 2293, 2294, 2295 
Schmidt, I., 109, 1352, 
1354, 1355, 1447 
Schmidt-Nielsen, B., 65 
Schnedorf, J. G., 3661 
Schneider, J., 3424 
Schneider, M., 559 
Schneider, R., 1760 
Schober, H., 110 
Schoen, Z. J., 1454 
Schoenfeld, R. C., 992 
Scholander, P. F., 66, 67, 
68, 69, 70 
Schork, P. K., 3015 
Schreiber, V., 1784, 1785 
Schrenk, H. H., 3378 
Schubert, H., 1839 
Schubert, K., 1517 
Schuessler, C., 3002 
Schuhmann, S., 2606 
Schulte, J. H., 3225 
Schultz, W. H., 2564 
Schupfer, F., 248 
Schutz, E., 560 
Schwab, R. S., 2677, 2696, 
2727, 2869 
Schwartz, ( ), 2402 
Schwartz, L., 1116 
291222—54 24 Sch—Ste 
INDEX OF AUTHORS 
Schwarz, F., 1455 
Schwed, W. W., 3513 
Schwerma, H., 2459, 2460, 
2461, 3379, 3380 
Scobee, R. G., 502, 1456 
Scott, G. G., 71 
Scott, G. H., 2050, 2055 
Scott, J. W., 989, 1017, 
1457, 1468, 3079, 3080, 
3091, 3138, 3139 
Scott, R. G., 368 
Scoville, A. de, 2508 
Scow, J., 429, 536 
Sculthorpe, H. H., 49 
Seabra, P., 647 
Sears, W. N., 2161 
Seashore, R. H., 3600, 3626 
Sebelien, J., 10 
Seelkopf, K., 2314 
Seifert, H. E., 2604 
Seitz, C. P., 249, 299, 503, 
697, 705, 2030 
Sellei, G., 888 
Sellers, E. A., 1249, 1250, 
2739, 2857, 2861, 2862, 
2870, 3081 
Seltzer, A. P., 1942 
Selye, H., 3610, 3611, 3612 
Senders, V. L., 1324 
Sendroy, J., Jr., 202, 211, 
2661 
Senkovits, I., 1675 
Senn, M. J., 3630 
Senseney, E. T., 1651 
Senturia, B. H., 1652, 1653, 
1654, 1655, 1656, 1953, 
1954, 1960, 1961, 1962, 
1963 
Scrota, H. M., 3693 
Setterstrom, C., 2567 
Severin, G., 2107 
Severinghaus, J. W., 3381 
Sexton, M. S., 1348, 1458 
Seyler, L. E., 2873 
Shambaugh, G. E., Jr., 
1761 
Shands, H. C., 3636 
Shapiro, B., 238 
Sharpe, L. M., 2478 
Sharpley, F. W., 1431 
Shattuck, G. C., 908, 1106, 
3762, 3783 
Shaub, H. G., 1202, 3259 
Shaudy, L. A., 912 
Shaver, M. R., 2392 
Shaw, C. C., 2871, 2872 
Shaw, R. S., 2219 
Shaw, W. A., 1518 
Shea, E., 953 
Shea, T. E., Jr., 2662 
Sheard, C., 1459, 1460, 
1461, 1462, 3410, 3411 
Sheikh, A. H., 2926 
Shelden, F. F., 2197 
Shelford, W. O., 2913 
Shelley, W. B., 998, 999, 
1000, 1018, 1045, 1051, 
1126, 1127, 1128, 1129, 
1130, 1131, 3094, 3326 
Shenkin, H. A., 1583 
Shepherd, J. T., 1178 
Shepherd, M., 2486, 2606 
Shettles, L. B., 676 
Shields, J. B., 995 
Shields, L. V., 2252 
Shiels, D. O., 2589 
Shilen, J., 2532 
Shilling, C. W., 16, 1306, 
1341, 1356, 1357, 1805, 
1811, 1812, 1813, 1876, 
1877, 1929, 2917, 3226, 
3227, 3479, 3480, 3481, 
3482, 3501, 3502, 3703, 
3704 
Shipley, W. C., 3483 
Shires, G. T., 833, 843 
Shkaravskii, F. I., 2983 
Shorr, E., 304, 305 
Shriber, W. J., 1261 
Shulman, I., 2627 
Sidwell, A. E., Jr., 2461 
Siebert, W., 2487 
Siegfried, E. G., 2276, 
2277, 2278, 2287 
Sievers, R. F., 544 
Siirala, U., 1762 
Sillani, L. S., 407, 443, 537 
Silverman, S. R-, 1519 
Simon, E., 1964 
Simon, S. W., 2873 
Simonson, E., 777, 1369, 
1370, 1378, 1463, 3634 
Simonton, K. M., 1657, 
1955 
Simpson, J. F., 1491, 1912 
Simpson, W. L., 1825 
Sinclair, H. M., 1237 
Singer, K., 2246 
Singh, I., 3694 
Singh, S. I., 3694 
Singleton, J. D., 1885 
Siosteen, S. M., 2488 
Sipe, C. R., 3015 
Siple, P. A., 3234, 3275, 
3276, 3284 
Siri, W. E., 72, 209 
Sirota, J. H., 2647 
Sjoberg, A. A., 2773 
Sjostrand, T., 73, 2343, 
2383, 2405, 2442, 2443, 
2488 
Skaggs, E. B., 3613 
Skulov, D. K., 1385 
Sklyanskaya, R. M., 2406 
Skljanskaja, R. M., 2565 
Slagle, T. D., 3786 
Sleeth, D. K., 436 
Sleight, R. B., 1318, 1658 
Sloan, H. E., 297 
Sloan, L. L., 1321, 1464 
Slutzky, Z., 2607 
Small, G. A., 3393, 3394 
Smedal, H. A., 2037 
Smith, G. G., 1465 
Smith, D. C., 444 
Smith, D. T., 3743, 3763 
Smith, F. E., 914 
Smith, F. S., 212, 463, 842 
Smith, F. W., 1595, 1596 
Smith, G. M., 249, 298, 
299, 503, 538, 3695 
Smith, H. E., 2976 
Smith, H. W., 2038, 2566 
Smith, J. A., 1466 
Smith, J. B., 1965 
Smith, J. H. C., 74 
Smith, J. J., 2216 
Smith, J. R., 2934, 2945 
Smith, J. W., 1924 
Smith, K. R., 1705, 1709, 
1841, 1842, 3082 
Smith, L. H., 779, 2267 
Smith, M., 3635 
Smith, M. H. D., 3126 
Smith, P. K., 2795, 2829, 
2830, 2874, 2875, 2876, 
2877, 2878, 2879, 2880, 
2881, 2882, 2883, 2884 
Smith, R. E., 204, 205, 206, 
207, 208, 213, 227, 408, 
459, 2612 
Smith, R. H., 2636 
Smith, S., 1283 
Smith, W. W., 463 
Smyth, H. F., 1659 
Snapp, F. E., 456, 457, 464, 
918, 2235, 3432 
Sneddon, I. B., 3764 
Snider, R. S., 2738 
Snow, W. B., 1520 
Snyder, G. H., 350 
Sobieski, J., 1913 
Sodeman, W. A., 1036 
Soderstrom, G. F., 893 
Sokalchuk, A., 2678, 2694, 
2886 
Solandt, D. Y., 1457, 1467, 
1468, 1640, 1741, 2368, 
3080, 3575 
Solignac, H., 2503 
Sollmann, T., 2885 
Soloman, A. K., 235 
Solomon, R. L., 3462 
Somberg, H. M., 2152, 
3434 
Sonne, L. M., 331, 393, 
394 
Sonnenschein, R. R., 2288 
Soucek, B., 2489 
South, F. E., Jr., 2096 
Southwell-Sander, G. H. G., 
3044 
Spaccarelli, G., 755 
Spaulding, C. H., 3200 
Spealman, C. R., 909, 910, 
1019, 1113, 1172, 1206, 
1207, 1208, 1263, 1265, 
1266, 1267, 1268, 1269, 
3196, 3298, 3299, 3318, 
3319, 3321 
Specht, H., 126, 147, 2104 
Spector, N. A., 75 
Spencer, J. N., 807, 811, 
812, 3401, 3403, 3405 
Sperling, H. G., 1371, 3460 
Spicknall, B. H., 2104 
Spiegel, E. A., 2678, 2774, 
2775, 2886 
Spiegel, J. P., 3606 
Spilka, B., 1698 
Spiro, R. K., 3382, 3383 
Spolyar, L. W., 2509 
Spooner, H. J., 1554 
Spradley, J. B., 1209 
Spragg, S. D. S., 3573, 
3574, 3580 
Sprague, G. F., 2533 
Springer, S., 3784, 3785 
Spurway-Haldane, H., 2274 
Sramek, J., 2625 
Sroka, K. H., 2419 
Stacy, R. W.,41,76, 2490 
Stadie, W. G., 2301, 2302, 
2303 
Stafford, J., 3738 
Stallworth, J. M., 2946 
Stampfli, R., 570 
Stanbury, J., 3195 
Stannard, J. N., 2423, 
2424, 2425, 2426, 2427 
Star, S., 3358 
Starr, I., 561 
Staton, R. C., 1622 
Stavraky, G. W., 562, 563 
Steegmann, A. T., 300 
Steele, B. F., 968 
Steele, J. M., 218, 236, 
2612 
Steeples, J. L., 1214 
Steer, M. D., 1742, 1743, 
1744 
Steffensen, K. A., 237 
Steggerda, F. R., 2137 
Stein, H. J., 1020, 1048, 
1063, 1210 
Stein, S. N., 758, 778, 2288 
Steinmann, B., 359 
Stellar, E., 3581 
Stelzner, H., 11 
Stemler, F. W., 2222, 2226 
Stephens, W. M., 874 
Stephenson, N. R., 2739 
Stern, M. I., 3614 
Stern, P., 3696 
Sterner, J. H., 1555, 2642 
Sternstein, H. J., 1826 
Steven, D. M., 1469 
Stevens, C. D., 214, 2168 
Stevens, E. I., 1180 
Stevens, S. S., 1706, 1707 
Stevenson, I., 3465 
Stevenson, I. P., 2267 
Stewart, A., 2648 
Stewart, D. R., 1998 
Stewart, H. J., 2619 
Stewart, W., 911 
Stewart, W. G., 2763, 2764, 
2776 INDEX OF AUTHORS 
Sti—Ver 
Stickney, J. C., 412, 618, 
619, 648, 649, 650, 651, 
654, 655, 849, 850 
Stiening, F. EL, 3083 
Still, M. A., 224 
Stokes, J., 779 
Stokinger, H. E., 2533 
Stone, J., 2263 
Stone, R. S., 3127 
Stone, W. E., 460 
Stormont, R. T., 2701, 
2702, 2790, 2791 
Storr, H., 751, 861 
Stover, A. D., 1501, 1699 
Strajman, E., 630, 2126, 
2156, 2438, 2439, 2457 
Straut, C. B., 250 
Streltsov, V. V., 587, 1307 
Strickland, B. A., Jr., 2800, 
2801, 2802, 2887, 2888, 
2889 
Strom, G., 435 
Stroud, M. W., 2284, 2311, 
2312, 2315 
Stroud, R. C., 2911 
Strughold, H., 1578 
Strumza, M. V., 253, 316, 
382, 383, 455, 468, 2237, 
2251, 3345, 3399 
Stuart, E. A., 2725, 2760, 
2761 
Stuart, M. A., 3786 
Stubbs, J., 820 
Stubbs, R. A., 2754 
Stumme, E. H., 1108 
Stump, N. F., 1372 
Stuntz, S. E., 1501, 1521, 
1745 
Sturdivant, J. H., 56 
Stutinsky, F., 1211 
Sueda, M., 1786, 1787, 
1788, 1789, 1790, 1791 
Suggit, S. C., 1556 
Sukhtankar, K. M., 1132 
Sullivan, J. A., 1965 
Sulzbach, W. M., 782 
Sulzberger, M. B., 1133, 
1134, 1135, 1136,3760 
Sulzman, J. H., 1325, 1326, 
1381, 1470, 3484 
Sumari, P., 2407 
Sundareson, A. E., 2649 
Supernaw, J. S., 3620 
Sureda, F. L., 2056 
Surtshin, A., 360, 361, 366, 
445 
Suskind, M., 3437 
Susman, E., 1115 
Sussman, L., 3212 
Sutton, B. M., 2087 
Sutton, R. L., 3765 
Sutton, R. L., Jr., 3765 
Suzuki, S., 539 
Svensson, A., 2345, 2361, 
2432 
Swain, H. L., 1212, 1226 
Swan, A. G., 3605 
Swan, T. H., 3662 
Swann, H. G., 362, 363, 
364, 365, 385, 2408, 
2984, 2985, 3346, 3384, 
3385, 3386 
Swartz, J. H., 3766 
Swensson, A., 2411 
Swindell, G. E., 1491 
Swindle, P. F., 2057 
Syr kina, P. E., 578 
Syverton, J. T., 1956 
Szebehelyi, J., 390, 391, 
424 
Tabershaw, I. R., 2524, 
2534 
Tabusee, L., 554 
Tacke, A. W., 2106 
Tada, N., 1197 
Tadokoro, T., 1792 
Tagliamonte, B., 380, 636 
Tahmisian, T. N., 532, 704 
Tailliez, P., 1488, 2088, 
2275, 3802 
Tait, C. D., Jr., 3022 
Takezawa, N., 1688 
Talbot, S. A., 1308 
Talbott, J. H., 1107, 1108, 
1149, 1298, 3277, 3278, 
3279 
Talley, C. H., 1732 
Talso, P. J., 1213 
Tarver, E., 1808 
Tatum, H. J., 3439 
Tauride, D., 1878 
Taylor, C. B., 431,604 
Taylor, C. L., 984, 990, 
1021, 1022, 1032, 1034, 
1064, 1065 
Taylor, E., 1057 
Taylor, E. W., 3213 
Taylor, F. A., 2557 
Taylor, H. J., 2087, 2316, 
2317, 2915, 2942 
Taylor, H. L., 960, 1066, 
1079 
Taylor, H. M., 1763 
Taylor, N. B., 1973 
Taylor, W. G., 1639 
Teal, E. E., 1545 
Tebbens, B. D., 2592 
Teed, R. W., 1879 
Telser, S. E., 1174, 3292 
Temkin, J., 1793 
Temple, W. J., 3497 
Tepperman, H. M., 652 
Tepperman, J., 507, 627, 
652, 662, 2015, 2016, 
2044 
Thamann, F., 2584, 2585 
Thauer, O., 944 
Thauer, R., 1026 
Theilgaard, E., 1579, 1660 
Therien, M., 1168, 1233, 
1251, 3223 
Thiebaux, R., 296 
Thieblot, L., 780 
Thiers, R. E., 2548 
Thomas, ( ), 2464 
Thomas, G. B., 356, 376 
Thomas, F. S., 25, 2611 
Thomas, M. H., 3214 
Thomas, N., 1249, 1250 
Thomas, S. F., 2081 
Thomas, W. C., 2589 
Thometz, A. F., 2018, 2019, 
2031, 2032, 2058 
Thompson, G. M., 2650 
Thompson, J. S., 3382, 
3383 
Thompson, R. M., 553 
Thompson, T. M., 3387 
Thomson, M. L., 924, 989, 
1023, 3091 
Thorn, G. W., 512, 716, 
734 
Thorner, M. W., 2728 
Thorp, G. E., 2663 
Tiedeman, W. D., 3143 
Tiffin, J., 1658 
Timmons, D. E., 137 
Tinker, M. A., 1794, 3061, 
3062, 3063 
Tinkham, M., 2801 
Tinsley, J. C., Jr., 2249 
Tisdall, F. F., 2513 
Tissie, M., 1689 
Tissieres, A., 581 
Titelbaum, S., 3675, 3701 
Titrud, L. A., 540 
Tobey, H. G., 1880, 1914 
Tobias, C. A., 201, 215, 
216, 1999, 2059, 2160, 
2161, 2444, 2445 
Tobias, J. M., 77 
Tobin, L. M., 1214 
Todd, D., 3785 
Tolan, T., 1522 
Tolcott, M. A., 3536 
Tonndorf, J., 1746, 1747, 
1814, 1827 
Topka, E., 591 
Tosetti, R., 2409 
Toth, F. M., 1212 
Touze, M., 422 
Towbin, E. J., 933, 996, 
1014 
Trapasso, T. J., 1886 
Travia, L., 844 
Trenchard, H. J., 1086 
Treussard, ( ), 2402 
Trotter, W. R., 2777,2833 
Trowbridge, B. C., 1943 
Trumper, M., 2573, 3196 
Truscott, I. P., 1610 
Tschirren, B., 504 
Tucker, D., 1795 
Tui, C., 2890 
Tullis, J. L., 3009, 3031 
Turkeltaub, M., 3739 
Turner, A. L., 1690 
Turner, J. A., 2608 
Turner, M. L., 1252 
Turner, R., 332 
Turpeinen, O., 945 
Turpin, F. H., 201, 216 
Turrell, E., 2025 
Turrell, E. S., 906, 1012, 
2026, 3249,3314 
Tusing, T., 1092 
Tuttle, W. W., 3724 
Twitty, V. C., 151, 152, 168 
Tyler, D. B., 2680, 2891, 
2892, 2893, 2894 
Uffenorde, H., 1840 
Ullmann, E., 328, 451 
Ullmann, E. V., 1661 
Ullrich, F. W., 3015 
Unger, M., 1889, 1944 
Upham, H., 3195 
Upton, M., 1594, 1673 
Urban, A. W., 3369 
Urdahl, T. H., 3084 
Uruski, W., 677 
Utterback, R. A., 3702 
Uzhanskii, I. G., 595 
Vacca, C., 79, 482, 564, 
646 
Vail, E. G., 2188, 2200 
Vail, V. S., 706 
Valerio, J., 845 
Valk, J. M., van der, 93 
Vallaud, A., 2357 
Vallette, F., 3653 
Van Buren, R. L., 3195 
Van Burkalow, A., 3779 
Van Der Aue, O. E., 92, 
2011, 2040, 2091, 2106, 
2141, 2142, 2955 
Vanderkamp, H., 3619 
Van Dilla, M., 3284 
Van Goor, H., 2305, 2306 
Van Keuren, H. C., 2012 
Van Liere, E. J., 412, 541, 
565, 596, 611, 617, 618, 
619, 650, 651, 653, 654, 
655, 691, 736, 849, 850, 
1580 
Van Loo, A., 366, 445 
Van Middlesworth, L., 656, 
657, 658, 737 
Vannotti, A., 367, 659 
Van Ordstrand, H. S., 
2516, 2535, 2536 
Van Slyke, D. D., 138, 
2491 
Van Slyke, K. K., 138 
Varay, A., 2397 
Varco, R. L., 52, 90, 836 
Vartiainen, A., 2981 
Vaughan, P. E., 1580 
Vawter, G. F., 545 
Veen, H., 2986 
Venturi, V. M., 707 
Vernant, P., 316 
Vernon, H. M., 1708 Ver—Woo 
INDEX OF AUTHORS 
Verplanck, W. S., 1373, 
1374, 1375, 1475, 1476, 
1477, 1478, 1479, 1480, 
3462, 3503, 3504 
Versar, F., 406, 841 
Vertigen, J., 1389 
Verwey, W. F., 2528, 2546, 
2588, 2603, 2628, 2659 
Verzar, F., 575 
Verzeano, M., 302 
Vezien, M. L., 2985 
Vial, J., 1183 
Vicencio, A. B., 1915 
Vigliani, E. C., 2609 
Villaret, M., 2947 
Vince, M. A., 3570, 3571, 
3601, 3615 
Vining, K. K., Jr., 2462 
Vinther-Paulsen, N., 2371, 
2446 
Visscher, M. B., 353, 431, 
815, 816, 3297 
Viteles, M. S., 1709 
Vladysik, M. M., 3739 
Voegtli, W., 660 
Voelker, C. A., 1856 
Vogel, J, 2896 
Volkmar, E., 1916 
Vollmer, E. P., 485, 2410, 
2478, 3368, 3369, 3388, 
3389, 3390 
Volochov, A. A., 301, 542 
Von Brandis, H. J., 1140 
Von Gierke, H. E., 1559, 
1560, 1581, 1582, 1772, 
1773, 1780 
Vonotzky, J., 1167 
Von Schelling, H., Ill, 
1353 
Von Tavel, F., 483 
Von Wittern, W. W., 1772, 
1773, 1780 
Vorwald, A. J., 2537, 2538 
Vuorelainen, O., 51 
Waddill, J. F., 1089 
Wade, H. W., 3788 
Wager, J., 1186 
Wagman, I. H., 1405 
Wagner, G. E., 192, 2299, 
2319 
Wagner, E., 1395 
Waite, C. L., 2013, 3721, 
3805, 3806 
Waits, E. J., 805 
Wakim, K. G., 1024 
Wald, G., 1481 
Walder, D. N., 2170 
Waldfogel, S., 302 
Waldron, T. J., 3722 
Walker, E. L., 2438, 2439, 
2457, 2478 
Walker, P., 2116 
Wall, P. D., 3022 
Wallgren, G. R., 2420 
Walpole, R. H., 1764 
Walton, A., 677 
Walton, R. P., 2232 
Waltrip, O. H., 2802, 2803, 
2804 
Walzl, E. M., 1561 
Wang, S. C., 846, 2740, 
2778 
Wang, S. L, 575 
Warden, C. J., 1329, 1330, 
1331 
Wardill, T. E. M., 2753 
Warin, J., 2505 
Warner, L., 2034, 2049, 
2146, 2147 
Warren, G. H., 176, 177, 
183 
Warren, R., 2922 
Warren, S., 3017, 3031, 
3032, 3033, 3034, 3035, 
3036, 3037, 3038 
Waterlow, J. C., 1109 
Waterman, T. H., 1707 
Waters, T. C., 2538 
Watkins, A. L., 3636 
Watkins, E., Jr., 80 
Watson, H. H., 3166 
Watson, L. A., 1522 
Watson, N. A., 1765 
Wayburn, E., 1270 
Weatherby, J. H., 847 
Weaver, W. L., 1110 
Webb, J. P., 1998, 2148 
Webb, P., 1216 
Webster, A. P., 2273 
Webster, J. E., 460 
Webster, S. H., 2613, 2614, 
2615, 2616, 2617 
Weddell, G., 3586 
Wedell, H., 3355, 3356 
Wadral, J. W., 191 
Weedon, F. R., 2567 
Weidman, F. D., 1130, 
1131 
Weiner, D., 1244, 1291 
Weiner, J. S., 882, 932, 
989, 1088, 1150, 3091 
Weisiger, J. R., 138, 1013, 
1196, 2491 
Weiskotten, T. F., 3697 
Weiss, J. A., 1917 
Weiss, W. A., 3177 
Weitz, J., 3587, 3588, 3589 
Weizsacker, V. V., 1332 
Welford, A. T., 3637 
Welham, W. C., 221, 222, 
229, 2013, 2171, 2289, 
3797 
Wells, J. G., 3605 
Wendland, J. P., 1482 
Wendt, G. R., 2695, 2729, 
2731, 2732, 2733, 2779, 
2780, 2897 
Werkb, L., 352, 3371, 3417, 
3440 
Werner, A. Y., 2184, 2185 
Wertheimer, E., 238 
Wertheimer, P., 2082 
Werz, R. von, 2314 
Wescott, F., 2527 
Wesley, S. M., 507, 527, 
662, 2015, 2016 
Wessling, G., 1662 
West, T. C., 413 
Westcott, R. N., 368 
Wester, M. R., 789 
Weston, H. C., 1710 
Weston, R. E., 2128, 2129, 
2139 
Weterings, P. A. A., 409 
Wever, E. G., 250, 1562, 
1841, 1842, 3492 
Weymuller, E. A., 1930 
Wezler, K., 566, 1025, 1026 
Whalen, E. J., 3767 
Whayne, T. F., 1301 
Wheeler, D. E., 1663, 1664, 
1665 
Wheeler, S. M., 1806 
Wherry, R. J., 3455, 3603 
Whillans, M. G., 1187 
Whitaker, D. M., 151, 152, 
168 
White, C., 3269 
White, C. S., 870, 871 
White, H. L., 450 
White, M. S., 484 
White, R. M., 3572 
White, W. A., Jr., 135, 136, 
141, 1002, 2142, 2324, 
2421 
White, W. J., 3590 
Whitehead, R. W., 807, 
811, 812, 3400, 3401, 
3403, 3404, 3405 
Whitehorn, W. V., 567, 
724, 2189, 2190, 2197, 
2203, 2208, 2217, 2224, 
2244, 2245 
Whiteley, A. H., 81, 173, 
174, 175, 176, 177, 178, 
182, 183, 217 
Whittaker, H. A., 3143 
Whitten, R. H., 2000 
Whittenberger, J. L., 2462, 
3354, 3391, 3392, 3436, 
3441 
Whitteridge, D., 2948 
Whittier, F. O., 3686 
Whittlesey, W. C., 3084 
Wickson, M. E., 661 
Widdowson, E. M., 225 
Wiebers, J. E., 2226 
Wiemers, K., 568 
Wiener, F. M., 1724 
Wiesinger, K., 504 
Wiggin, B. E., 3493 
Wiggin, S. C., 3393, 3394 
Wigley, J. E. M., 1219 
Wilcocks, G., 3768 
Wilcox, J. G., 1918 
Wilentz, W. C., 2590 
Wilhelm, R. E., 738 
Wilks, S. S., 1184, 2798, 
2799, 2801 
Will, O. A., Jr., 3710 
Williams, H. W., 2552 
Williams, O. L., 1990, 
2081, 2149 
Williams, P. E., 2642 
Williams, S. B., 1376, 1377, 
3494 
Williamson, R. J., 1698 
Willmer, E. N., 1358 
Willmon, T. L., 12, 13, 14, 
2273, 2917, 2995, 3127, 
3142, 3495, 3496 
Wills, J. H., 929 
Wills, R. A., 2510 
Wilson, G. P., 1919 
Wilson, J. W., 1061, 2178, 
2179, "2201, 3395, 3396, 
3442 
Wilson, R. H., 2651 
Wilson, S. A., 2539 
Wilson, U., 3144 
Wilson-Dickson, W. G., 
1217 
Wilson, W. H., 303, 1666, 
1667 
Wilson, W. L., 1096 
Wiltshire, S. P., 3768 
Winchell, P., 777 
Windle, W. F., 522 
Wing, K. G., 139, 1523 
Winslow, C. E. A., 912, 
1069, 3087, 3211, 3285 
Winston, J., 2898 
Winterstein, H., 251, 612, 
613 
Wirt, S. E., 1315 
Wirz, H., 575 
Wise, H., 3125 
Wise, H. G., Jr., 3591 
Wit, G. de, 1598 
Witherbridge, W. N., 1545 
Witheridge, W. N., 912, 
1766, 3066, 3088, 3089, 
3162 
Witting, E. G., 1524 
Wittmaack, ( ), 1691 
Witts, L. J., 2648 
Wohlfart, G., 2361, 2411 
Wolf, E., 1483 
Wolf, F. T., 1963, 3769 
Wolfe, G. D., 1624 
Wolfe, W. C., 1623 
Wolff, D., 1692, 1859 
Wolff, E., 2492 
Wolff, R., 708 
Wolff, R. C., 1271 
Wolfle, D., 3505 
Wollack, A. C., 2462 
Wolman, A., 3143 
Wolman, W., 2461 
Wolpaw, B. J., 112 
Wolters, D., 3507, 3513 
Wood, E. H., 31 
Wood, H. G., Jr., 2528, 
2546, 2588, 2603, 2628, 
2659 
Wood, J. A., 3415 
Wood, R. E., 56 INDEX OF AUTHORS 
Woo—Ano 
Wood, T., 370 
Woodcock, A. H., 1027 
Woodcock, C. C., Jr., 313, 
369 
Woodruff, J. L., 685 
Woods, F. J., 3172 
Woods, W. W., 2652 
Woodward, A. A., 1096 
Woolsey, C. N., 2738 
Worth, H. M., 71 
Wortis, J., 3406 
Wright, D. O., 1111 
Wright, H. 'C., 2979 
Wright, L. A., 3268 
Wright, W. D., 1359, 1484, 
1485 
Wright, W. L., 2899 
Wulff, V. J., 1795 
Wulsin, F. R., 3286 
Wycis, H. T., 2775 
Wyndham, G. H., 1055, 
1217 
Wyss, F., 739 
Wyss, O. A. M., 3443 
Wyss-Dunant, E., 569 
Yaglou, G. R, 912, 926, 
1070, 1275, 1276, 3108, 
3109, 3110, 3111, 3143, 
3144, 3287, 3288, 3289, 
3290, 3328 
Yamamato, W., 910 
Yamamoto, K., 1796, 1797 
Yarbrough, O. D., 15, 2093, 
2289 
Yeakel, E. H., 1583 
Yetwin, I. J., 2900 
Yoe, J. H., 2484, 2485, 
2493, 2494 
Yosioka, Z., 3740 
You, S. S., 1250 
Young, A., 1920 
Young, A. C., 82 
Young, D. R., 2096 
Young, M. H., 142 
Young, M. W., 2980 
Youngken, H. W., 2528, 
2546, 2588, 2603, 2628, 
2659 
Zahl, H. A., 134 
Zahle, V., 2362, 2412 
Zander, H. A., 3000 
Zetterstrom, A., 2108 
Zigler, M. J., 1622 
Zilliacus, H., 2949 
Zimmer, D. J., 2615, 2616, 
2617 
Zimmerman, H. M., 1135, 
1136 
Zinck, K. H., 863, 875, 876 
Zirkle, R. E., 3039 
Zobell, G. E., 3220, 3221 
Zoll, M., 740 
Zwahlen, P., 492, 505 
Zwerling, I., 2730 
Zwislocki, J., 1505, 1506 
Anon., 709, 913, 1138, 
1253, 1284, 1525, 1563, 
1668, 1767, 1843, 1881, 
1882, 1931, 1988, 2363, 
2495, 2540, 2541,, 2542, 
2550, 2591, 2901, 3040, 
3145, 3146, 3308, 3398, 
3514, 3807 Index of Sources for Unpublished 
Reports 
Reference is given to serial numbers 
American Public Health Association 
and the American Water Works 
Association, 3198 
American Society of Heating and 
Ventilating Engineers, 3098, 3099, 
3112,3147, 3148, 3149 
Australia. NHMRC, 897 
Australia. NHMRC. Fatigue lab- 
oratory, 1054, 1056, 3269 
Canada. Medical intelligence divi- 
sion. Ottawa, 1037 
Canada. NRC-ACAMR, 3251, 
3252, 3256, 3264, 3312 
Canada. NRC. Proceedings of the 
associate committee on naval re- 
search, 916, 1457, 1465, 1467, 
1468, 1510, 1511, 1512, 1513, 
1741, 1750, 2002, 2038, 2368, 
2683, 2716, 2758, 2786, 2816, 
2842, 2843, 2858, 2859, 2860, 
2862, 2870, 2897, 3080, 3081, 
3138, 3139, 3309, 3331, 3575, 
3714 
Canada. NRC. Proceedings of 
conference on motion sickness, 
2670, 2684, 2688, 2703, 2705, 
2711, 2712, 2713, 2714, 2715, 
2717, 2721, 2722, 2723, 2724, 
2725, 2739, 2743, 2745, 2752, 
2753, 2757, 2761, 2762, 2763, 
2765, 2776, 2814, 2815, 2817, 
2824, 2850, 2851, 2852, 2861 
Connecticut College, 3555, 3556 
Florida Chemical Research Com- 
pany, New York, 3156 
Gt. Brit. Advisory council on scien- 
tific research and technical devel- 
opment, 1614 
Gt. Brit. FPRC, 495, 631, 1432, 
1586, 1615, 1754, 1860, 2333, 
3614 
Gt. Brit. Industrial health research 
board, 1710 
Gt. Brit. Ministry of Labor and 
National Service, 7, 118, 2350, 
3041 
Gt. Brit. MPRG. Subcommittee on 
clothing and personnel, 3271 
Gt. Brit. MRG, 1005, 1076, 1084 
Gt. Brit. MRC, APU, 1717, 3515, 
3570, 3578, 3596 
Gt. Brit. MRC-RNPRC, 748, 3231, 
3317 
Gt. Brit. MRC-RNPRC, CES, 914, 
938, 958, 1023, 1040, 1148, 1150, 
1173, 1189, 1237, 3069, 3074, 
3093, 3103, 3305, 3306, 3320 
Gt. Brit. MRC-RNPRC, HS, 882, 
918, 919, 920, 932, 957, 989, 1017, 
1038, 1073, 1075, 1078, 1082, 
1142, 1143, 3078, 3079, 3091, 
3095, 3458 
Gt. Brit. MRC-RNPRC, OES, 
1718, 1725, 2990, 3542, 3550 
Gt. Brit. MRC-RNPRC, SS, 1259, 
2807, 2808, 2825 
Gt. Brit. MRC-RNPRC, UPS, 
1833, 2087, 2255, 2915, 2932, 
2942, 3168 
Gt. Brit. MRC-RNPRC, UWB, 
2957, 2961, 2962, 2972, 2979 
Gt. Brit. MRC-RNPRC, VPS, 1402 
Gt. Brit. Royal Navy, Admiralty ex- 
perimental diving unit. HMS 
Vernon, 2270 
Harvard University, Psycho-acoustic 
laboratory, 1537, 1538, 1735 
John Hopkins University, Psycho- 
logical laboratory, 1367 
Italian Royal Navy, 3717 
Linde Air Products Company, 2131 
Massachusetts Institute of Technol- 
ogy. Visibility laboratory, 1486 
Purdue University, Voice science 
laboratory, 1727, 1742, 1743, 
1744, 3558 
Royal Society of Medicine, Section 
of otology, 1910 
Scott Aviation Corporation, 3800 
Siebe, Gormann & Co., Ltd., 119, 
124,3801 
Stanford University, 3467 
State University of Iowa, 3595 
Temple University, 1350 
Tufts College, 481, 1327, 1471, 1557, 
2679, 3064, 3582, 3583, 3584, 3585 
University of California, Division of 
medical physics, 2438 
University of California, Radio and 
sound laboratory, 1487 
University of Maryland, 2094 
University of Rochester, Department 
of psychology, 3573, 3574 
University of Rochester, School of 
Medicine and Dentistry, 2911 
University of Rochester, U. S. atomic 
energy project, 2426 
University of Western Ontario, Can- 
ada, 3255 
U. S. AAF. Aeromedical center, 
Hq, 3d. Central medical estab- 
lishment, APO 172, 1628, 2313 
USAF. Ladd air force base, Alaska. 
Arctic aeromedical laboratory, 887, 
1145, 1245, 1248, 1290, 3258, 
3468 
USAF. Randolph Field, Texas. 
School of aviation medicine, 50, 
194, 292, 310, 403, 454, 457, 464, 
502, 528, 529, 543, 552, 553, 577, 
580, 590, 591, 604, 622, 633, 634, 
639, 687, 688, 700, 725, 732, 864, 
883, 935, 1184, 1193, 1282, 1292, 
1293, 1294, 1295, 1342, 1352, 
1354, 1355, 1418, 1430, 1444, 
1448, 1449, 1450, 1451, 1452, 
1456, 1588, 1652, 1653, 1654, 
1655, 1668, 1747, 1843, 1872, 
1873, 1939, 1940, 1953, 1961, 
1992, 2023, 2033, 2083, 2120, 
2123, 2192, 2469, 2673, 2693, 
2707, 2708, 2709, 2710, 2728, 
2749, 2794, 2795, 2797, 2800, 
2804, 2829, 2830, 2875, 2876, 
2877, 2878, 2880, 2883, 2888, 
2889, 3020, 3022, 3027, 3323, 
3432, 3454, 3470, 3476, 3551, 
3566, 3567, 3568, 3587, 3588, 
3589, 3592, 3605, 3769 INDEX OF SOURCES FOR UNPUBLISHED REPORTS 
USF—U.S. NRC 
USAF. Wright-Patterson air force 
base, Dayton, Ohio. Air materiel 
command. Aero medical labora- 
tory, 40, 98, 461, 518, 689, 965, 
990, 1031, 1032, 1033, 1034, 
1064, 1065, 1072, 1231, 1278, 
1279, 1287, 1447, 1569, 1570, 
1575, 1581, 1582, 1604, 1675, 
1697, 1748, 1772, 1773, 1779, 
1781, 2039, 2169, 2172, 2173, 
2178, 2179, 2199, 2201, 2490, 
3054, 3179, 3181, 3192, 3193, 
3273, 3274, 3384, 3385, 3395, 
3396, 3430, 3442, 3535, 3548, 
3549, 3553, 3562, 3563, 3580, 
3590, 3591 
U. S. A. S. F. Armored medical re- 
search laboratory, 997, 998, 1045, 
1046, 1059, 1071, 1198, 1205, 
1213, 1214, 1764, 2479, 3303 
U. S. Army. Chemical Corps, Med- 
ical division, 2664, 3441 
U. S. Army. Chemical warfare serv- 
ice, Medical division, 2566, 3439 
U. S. Army. Combined Intelligence 
objectives subcommittee, APO 413, 
1272, 2338 
U. S. Army. Commission on acute 
respiratory diseases, Fort Bragg, 
N. C., 3197 
U. S. Army. Engineer research and 
development laboratory. Fort Bel- 
voir, Va., 3803 
U. S. Army. Medical department. 
Research and graduate school, 
2234 
U. S. Army. Medical nutrition lab- 
oratory, Chicago, 111., 1204 
U. S. Army. Office of the Quarter- 
master General, Lawrence, Mass. 
Climatic research laboratory, 992, 
1020, 1027, 1063, 1080, 1151, 
1155, 1159, 1191, 1227, 3288, 
3293, 3302, 3572 
U. S. Army. Office of the Quar- 
termaster General. Research de- 
velopment board, 1246 
U. S. Army. Staff, Personnel re- 
search section. Adjutant General’s 
Office, 1328 
U. S. Bureau of Mines, 2472, 3378 
U. S. Coast Guard. Field testing 
and developing unit, Curtis Bay, 
Md., 3315 
U. S. Department of Commerce, 
National Bureau of Standards, 
2486 
U. S. National Institute of Health, 
Bethesda, Md., 2549, 2613, 2614, 
2615, 2616, 2617 
U. S. Naval Institute, Annapolis, 
Md., 3512 
U. S. Navy. BuAer. Aero medical 
laboratory, Philadelphia, Penna., 
1426, 3310, 3311 
U. S. Navy. BuMed., 27, 715, 1472, 
2085, 2871, 2987, 3045, 3065, 
3073, 3085, 3235, 3448, 3449, 
3450, 3451, 3486, 3564 
U. S. Navy. BuNavPers., 1815, 
2086, 2089, 2105, 2954, 2977, 
3086, 3215, 3322, 3338, 3485, 
3709 
U. S. Navy. BuShips., 120, 125, 
2090, 2140, 3339, 3804 
U. S.Navy. BuY. & D., 3307 
U. S. Navy. Medical field research 
laboratory, Gamp Lejeune, N. G., 
1408, 3466, 3494 
U. S. Navy. Naval air station, Mi- 
ami, Fla. Altitude training unit, 
696, 697, 2030 
U. S. Navy. Naval air station, San 
Diego, Calif., 2478 
U. S. Navy. Naval Clothing Depot, 
Brooklyn, New York, 3304 
U. S. Navy. Naval Gun Factory, 
EDU, 24, 83, 84, 113, 123, 2011, 
2040, 2091, 2101, 2102, 2106, 
2171, 2289, 2951, 2955, 3335, 
3336, 3337, 3500, 3789, 3790, 
3791, 3792, 3793, 3794, 3795, 
3798, 3799, 3805, 3806 
U. S. Navy. Naval Hospital, Chel- 
sea, Mass., 2706, 2869 
U. S. Navy. Naval medical school, 
Bethesda, Md., 2978, 3068 
U. S. Navy. Naval training center. 
Great Lakes, 111. Naval medical 
research unit no. 4, 3121, 3140, 
3141 
U. S. Navy. NATB, Pensacola, Fla. 
School of aviation medicine, 20, 
21, 60, 61, 62, 100, 112, 498, 499, 
521, 599, 602, 603, 606, 645, 735, 
847, 1176, 1351, 1394, 1714, 1715, 
1716, 2017, 2037, 2132, 2135, 
2258, 2429, 2704, 2838, 2840 
U. S. Navy. NEL, San Diego, Calif., 
3526, 3528 
U. S. Navy. NMRI, 22, 32, 45, 57, 
88, 94, 104, 105, 129, 135, 136, 
141, 153, 154, 157, 160, 161, 163, 
165, 166, 167, 179, 192, 202, 204, 
206, 208, 213, 221, 222, 224, 227, 
230, 232, 233, 759, 843, 921, 926, 
1002, 1019, 1042, 1070, 1113, 
1206, 1207, 1265, 1266, 1275, 
1420, 1774, 1775, 1806, 1808, 
1969, 2142, 2282, 2283, 2286, 
2291, 2292, 2324, 2410, 2418, 
2421, 2431, 2433, 2436, 2437, 
2440, 2470, 2471, 2480, 2481, 
2482 
U. S. Navy. NRL, 25, 28, 53, 2611, 
3172, 3175, 3176, 3185 
U. S. Navy. Office of coordinator 
of research and development, 3784, 
3787 
U. S. Navy. Office of Naval Ad- 
visor, Office of Military Govern- 
ment for Germany. Medical sec- 
tion, 1299, 1300, 1473 
U. S. Navy. ONI. Germany, 1816, 
2916, 3640 
U. S. Navy. ONR. Psychophysiol- 
ogy branch, 2682 
U. S. Navy. ONR. Special devices 
center, 1164, 1698, 3536 
U. S. Navy. Quonset Point, R. I., 
496, 1438 
U. S. Navy. Submarine base, New 
London, Conn. Medical research 
laboratory, 16, 95, 96, 97, 111, 
139, 142, 610, 750, 842, 866, 1304, 
1311, 1312, 1313, 1314, 1322, 
1325, 1326, 1333, 1334, 1335, 
1337, 1338, 1339, 1340, 1341, 
1348, 1353, 1356, 1357, 1363, 
1364, 1371, 1373, 1374, 1379, 
1381, 1396, 1429, 1435, 1436, 
1437, 1454, 1458, 1466, 1470, 
1475, 1476, 1477, 1478, 1479, 
1480, 1495, 1496, 1497, 1498, 
1499, 1500, 1501, 1508, 1509, 
1516, 1521, 1523, 1621, 1699, 
1728, 1729, 1731, 1745, 1755, 
1803, 1811, 1812, 1813, 1876, 
1932, 1933, 1934, 1935, 2273, 
2614, 2896, 2904, 2917, 2919, 
2991, 2993, 2995, 3042, 3053, 
3212, 3225, 3226, 3445, 3447, 
3452, 3455, 3459, 3460, 3463, 
3469, 3472, 3479, 3480, 2482, 
3484, 3486, 3487, 3488, 3489, 
3492, 3493, 3495, 3496, 3498, 
3501, 3502, 3503, 3504, 3515, 
3516, 3517, 3518, 3519, 3520, 
3521, 3522, 3523, 3524, 3525, 
3527, 3703 
U. S. Navy. Submarine base. Pearl 
Harbor, T. H., 2918 
U. S. Navy. Technical Mission to 
Japan, 1799, 3178, 3216, 3490 
U. S. Navy. U. S. S. Enterprise, 
1474 
U. S. NDRC. Division G, Section 
5, Sound sources, 1567 
U. S. NRG. Committee on Dentis- 
try, 3491 
U. S. NRG. Committee on sanitary 
engineering and environment, 
Subcommittee on shelter and cloth- 
ing, 3165, 3245, 3246, 3283 
U. S. NRG. Committee on sanitary 
engineering and environment, 
Subcommittee on water supply, 
3208 
U. S. NRG. Committee on sound 
control, 1706, 1707 
U. S. NRG. Division of medical 
sciences, 3397, 3785 
U. S. NRG. Subcommittee on clin- 
ical investigation, 1215, 3297 U.S. NRC—Yale 
INDEX OF SOURCES FOR UNPUBLISHED REPORTS 
U. S. NRC. Subcommittee on 
clothing, 1087, 3236, 3237, 3238, 
3239, 3240, 3241, 3242, 3243, 
3244, 3280, 3281, 3282, 3300, 
3327 
U. S. NRC-CAM, 23, 59, 173, 174, 
175, 176, 177, 183, 184, 186, 187, 
188, 189, 198, 216, 350, 429, 494, 
506, 507, 519, 527, 548, 627, 630, 
638, 642, 652, 662, 691, 712, 867, 
1030, 1060, 1067, 1220, 1225, 
1229, 1263, 1319, 1329, 1330, 
1407, 1423, 1460, 1558, 1887, 
1996, 1997, 2003, 2005, 2007, 
2015, 2016, 2019, 2022, 2025, 
2028, 2031, 2032, 2034, 2044, 
2048, 2049, 2050, 2051, 2055, 
2057, 2114, 2115, 2121, 2122, 
2126, 2127, 2143, 2144, 2145, 
2146, 2147, 2148, 2150, 2151, 
2152, 2153, 2154, 2156, 2157, 
2158, 2160, 2161, 2162, 2164, 
2165, 2167, 2168, 2189, 2191, 
2209, 2212, 2231, 2244, 2417, 
2444, 2681, 2719, 2736, 2846, 
2874, 2891, 2892, 2927, 2999, 
3000, 3001, 3230, 3262, 3270, 
3294, 3313, 3376, 3409, 3410, 
3434 
U. S. NRC-GUW. Panel on un- 
derwater acoustics, 1503, 1543, 
3529 
U. S. NRC-OSRD, 995, 1079, 1172, 
1567 
U. S. OSRD, 1680, 1732, 3122, 
3324, 3464 
U. S. OSRD-CMR, 3295, 3314 
U. S. OSRD-NDRC, 58, 78, 960, 
967, 1035, 1052, 1068, 1567, 2468, 
2493, 2494, 3180, 3182, 3183, 
3184, 3186, 3189, 3190, 3191, 
3194, 3248, 3461, 3462, 3497, 
3626 
U. S. Public Health Service, 3210, 
3217, 3218, 3219 
Yale University School of Medicine. 
Yale aero-medical research unit, 
1831, 1941, 2053, 2163, 3431 Index of Subjects 
Reference is given to page numbers 
Aerotitis media and aerosinusitis— 
153, 262 
Air compressors—6 
Air disinfection—273 
Alimentary tract, effects of carbon 
dioxide on—62, 66 
cold—101 
heat—76 
low oxygen—46 
motion sickness—238 
noise—131 
vibration—145 
Alkaline reserve, in carbon dioxide 
excess—67 
Anoxia, see Low oxygen. 
Apparatus, respiratory—4 
air compressors—6 
chambers—5 
pressure gages—6 
temperature measurement—6 
visual—5 
Appendectomies—150 
Argon-oxygen mixtures—9 
Arsine—216 
Artificial respiration—35, 290 
Auditory problems—128 
Benzene—235 
Beryllium—218 
Blast injuries, underwater—258 
Blood, effects of carbon dioxide on— 
63 
carbon monoxide—202 
cold—100 
heat—74 
lead poisoning—226 
low oxygen—28, 43 
oxygen intoxication—184, 192 
radioactivity—264 
vibration—146 
“Blowing up”—257 
Bones, erythrocyte formation in 
hypoxia—28, 43 
lesions in decompression sickness— 
165 
Breath holding—250 
Bubbles, circulatory effects of—11 
formation of—9 
in decompression sickness—162, 
164, 166, 167 
inert gas effects on—10 
in explosive decompression—180 
location of—9 
physical factors in—12 
preoxygenation effects on—11 
Bunking facilities—279 
Cadmium—223 
Caisson disease, see Decompression 
sickness. 
Carbon dioxide absorbents and ab- 
sorption—277 
Carbon dioxide, accumulation in 
oxygen intoxication—194 
Carbon dioxide excess, effects on ac- 
climatization—6 9 
alimentary tract—62, 66 
alkaline reserve—67 
autonomic nervous system—56 
blood—63, 67 
blood pressure—60, 64 
blood sugar—69 
cardiac output—59 
carotid sinus—56 
cerebral blood flow—61 
cerebrospinal fluid—63 
chronaxie—55 
convulsions—57 
electrically induced convulsions—■ 
57 
electrocardiogram—59 
electroencephalogram—56 
endocrine glands—68 
heart and circulation—59 
metabolism—66 
nerve conduction—55 
nervous system—55 
orthostatic response—60 
oxygen intoxication—190, 192, 
194 
psychomotor response in nervous 
disorders—58 
pulmonary function—61 
respiration—64 
respiratory center—56 
respiratory quotient—68 
spinal reflexes—55 
tissue gases—68 
tolerance to hypoxia—35 
vasoconstriction—61 
Carbon dioxide excess, pathological 
effects of—65, 70 
Carbon monoxide poisoning—199 
clinical picture, functional changes, 
and pathological effects—201 
detection in air and blood—215 
mechanisms of carbon monoxide 
poisoning—206 
tolerance and acclimatization—210 
treatment—211 
uptake, absorption, an(d elimina- 
tion—207 
Carbon tetrachloride poisoning—235 
Cardiovascular system, effects of 
carbon dioxide on—59 
cold—97 
diving accidents—254 
explosive decompression—176 
heat—73, 82 
low oxygen—23, 41 
motion sickness—238 
noise—131 
oxygen intoxication—183, 195 
pressure breathing—297 
raised atmospheric pressures—7 
resuscitation—2 91 
Case histories of decompression sick- 
ness—161 
Chambers, recompression—5 
in submarine escape—254 
Chlorine intoxication—224 
Clothing—284 
for cold and dry conditions—287 
for heat and humidity conditions— 
288 
for immersion and rain—287 
effects of clothing on physiological 
responses to environmental 
changes—286 
physical properties, testing, and 
standards—284 
Cold exposure, effects on acclimati- 
zation and tolerance to cold— 
107 
alimentary tract—101 
blood flow—98 
blood volume—100, 113 
cardiovascular system—98 
chilblains—107 
efficiency—112 
electrocardiogram—110, 114 
endocrine glands—104, 108 
immersion in cold water—112 
lungs—101 
metabolism—102 
nutritional requirements—101, 
108 
pain production—96 
pathological changes—117 
renal function—104 
rewarming after cold exposure— 
114 
shivering—113 
vasoconstriction—99 
Communication, effects of noise on— 
139 
training in—305 
Compressed air intoxication—7 
Compressors, air—6 
heat—74 INDEX OF SUBJECTS 
Controls, human factors in (design 
of—309 
operation of—314 
Convulsions, in decompression sick- 
ness—161 
in escape accidents—254 
in gas embolism—256 
in high carbon dioxide tensions— 
57 
in high intensity sound—130 
in oxygen intoxication—188 
Decompression, physiological ef- 
fects—9 
on bubble formation—9 
on fat and water content of the 
body—16 
on saturation and desaturation of 
gases—15 
Decompression sickness—159 
bone lesions in—165 
case histories—161 
cerebral symptoms—161 
clinical picture—161 
convulsive seizures in—161 
decompression procedures—167 
diagnosis—163 
drugs in prevention and treat- 
ment—174 
ear lesions in—165 
etiology of—164 
frequency of symptoms—163 
incidence—163 
joint lesions in—162 
lesions of the central nervous sys- 
tem—161 
motor disturbances—162 
nervous system in—161 
pain in—164 
pathological lesions—9, 165 
prevention—167 
prognosis—163 
sensory disturbances—162 
signs and symptoms—162, 163 
time of onset of symptoms—161 
treatment—167, 172 
Deep sea diving equipment and pro- 
cedures—289 
Dental problems—263 
Dental treatment of otitis media— 
154, 157 
Diet and physical fitness—282 
Diffusion respiration—293 
Disasters, submarine—251 
Diseases and accidents in submarine 
personnel, divers, and com- 
pressed air workers, morbidity— 
149 
Diuresis, effects of cold on—104 
Diurnal temperature variations—323 
Divers, decompression of—167 
Diving accidents—257 
Diving dress—289, 335 
Dramamine, use in motion sickness— 
246 
Drowning—261 
Dust, elimination of—276 
Duty and rest periods—325 
Ear, effects of raised atmospheric 
pressure on—152 
Ear, nose, and throat disturbances— 
151 
aerotitis media and aerosinusitis— 
153 
otological effects of compression 
and decompression—152 
Electrocardiogram, effects of carbon 
dioxide on—59 
cold—110, 114 
explosive decompression—177 
hypoxia—24, 41 
oxygen intoxication—184 
swim-diving—332 
Electrolyte balance, effects of carbon 
dioxide on—63 
cold—100 
heat—78 
Embolism, gas—162, 164, 180, 255 
Enzyme activity, effect of, high hy- 
drostatic pressures on—148 
high oxygen tensions—186, 192 
Escape accidents—254 
Escape procedures—251 
Escape training tank—299, 304 
Eupneic pressure—331 
Explosive decompression, effects on 
alveolar gases—179 
blood pressure—176 
cerebrospinal fluid pressure—178 
electrocardiogram—177 
heart and circulation—176 
intravascular bubbles—180 
lethal factors—180 
lung temperature—178 
pathological changes—179, 181 
respiratory system—178 
tolerance—181 
Fat, body content of—9 
Fatigue—318 
Food and water supply—280 
Fumes, elimination of—276 
Fungus infections—332 
Gas analysis in air and blood—2, 216 
Gas elimination—276 
Gas embolism—255 
Germicidal aerosols—274 
Habitability—268 
Hearing in submarine personnel— 
132, 152, 261 
Heart and circulation, see Cardiovas- 
cular system. 
Heat and humidity, effects on ali- 
mentary tract—75, 76 
blood—74 
cardiovascular system—74, 82 
efficiency—87 
endocrine glands—79 
heat cramps—90 
heat disease—89 
heat prostration—89 
Heat and humidity—Continued 
heat stroke—90 
metabolism—7 6 
pathological changes in heat 
stroke—90 
performance—83, 87 
problems in submarines—71, 271, 
327 
sense organs—74 
skin diseases associated with heat 
and humidity—92 
sweating—78, 85 
tolerance and acclimatization to— 
82, 327 
vasodilatation—7 4 
water and salt depletion—75 
Heat collapse—89 
Heat Cramps—90 
Heat exhaustion—89 
Heat stroke—90 
Heat rash—92 
Helium, effect on bubble forma- 
tion—9 
use in diving—170 
High hydrostatic pressures, biological 
effects on—148 
Human engineering design—309 
Hydrogen-oxygen mixtures in div- 
ing—170 
Hyoscine, use in motion sickness— 
246 
Hypoxia, see Low oxygen. 
Illumination of submarines—268 
Immunology—273 
Intoxication, by compressed air—7 
by oxygen—182 
Joint lesions in decompression sick- 
ness—165, 180 
Kidney, see Renal function. 
Lead poisoning—226 
Lighting—268 
Lorrain-Smith effect in oxygen in- 
toxication—182 
Low oxygen tensions, resulting from 
decompression, physiological ef- 
fects on acclimatization—53 
alimentary tract—46 
blood—43 
blood sugar—47 
chronaxie—39 
electrically induced convulsions— 
39 
electrocardiogram—41 
ery thropoiesis—4 3 
heart and circulation—41 
histamine response—44 
kidney—50 
metabolism—47 
nervous system—38 
pathological changes—39 
reproduction—50 
respiration—45 
special senses—37 INDEX OF SUBJECTS 
Low oxygen tensions—Continued 
spleen—44 
tolerance—51 
urine—50 
Low oxygen tensions, without de- 
compression, physiological ef- 
fects on bile secretion—31 
blood—28 
chemoreceptors—19 
cortical sensitivity—20 
electrically induced convulsions— 
20 
electrocardiogram—24 
epinephrine response—32 
erythropoiesis—28 
heart and circulation—23 
kidney—34 
lymphatics—29 
metabolism—31 
muscular activity—23 
nervous system—18 
pathological changes—21 
performance—21 
pulmonary function—25 
respiration—29 
respiratory center—19 
scotoma formation—17 
special senses—17 
spleen—24 
temperature control—19, 32, 33 
thyroid—36 
tolerance—35 
urine—34 
vasoconstriction—19, 34 
vasodilatation—19 
Lung injury, blast—258 
escape accidents—254 
oxygen intoxication—182 
Lung rupture—255 
Lymph, effects of low oxygen—29 
Mercury poisoning—229 
Metabolism, effects of carbon dioxide 
on—66 
cold-102 
heat and humidity—76 
low oxygen—31, 47 
oxygen intoxication—186, 192, 
196 
Midget submarines—306 
Morale—320 
Moray eels—334 
Motion sickness—236 
alimentary tract—238 
blood—244 
blood pressure—238 
body position—243 
central nervous mechanisms—244 
effects on performance—246 
emetic drugs—241 
labyrinthine responses—243 
mechanisms—242 
prevention and treatment—246 
respiratory rate—238 
signs and symptoms—237 
susceptibility—239 
sweating—237 
Motor disturbances, in decompres- 
sion sickness—162 
in escape accidents—254 
in high carbon dioxide—57 
in noise—131 
in oxygen intoxication—189 
Muscular activity, effects of low oxy- 
gen on—23 
oxygen intoxication—187 
Nervous system, effects of carbon 
dioxide on—55 
cold—96 
decompression sickness—162 
escape accidents—254 
low oxygen—18, 38 
oxygen intoxication—183, 189 
Night vision and dark adaptation—■ 
123 
Nitrogen, saturation and desatura- 
tion—9, 15, 164, 170 
Noise, effects on efficiency—138 
hearing defects—132 
physiological and pathological ef- 
fects—130 
protection against noise—142 
sound communication—139 
Noxious agents—198 
Odor elimination—276 
Otitis externa—158 
therapy—159 
Otitis media, see Aerosinusitis media 
and aerosinusitis. 
Otitis media, therapy—155 
chemotherapy—156 
dental therapy—157 
irradiation therapy—157 
surgical and physical procedures— 
158 
vasoconstrictor and analgesic 
drugs—155 
Oxygen administration during de- 
compression—171 
Oxygen intoxication, resulting from 
pressures in excess of one atmos- 
phere, effects on 
cerebral blood flow—189 
cerebral vascular resistance—195 
convulsions and nervous system 
disturbances—189 
electroencephalogram—190 
endocrine glands—194 
hemoglobin—192 
metabolism—192 
mechanisms of intoxication—194 
micro-organisms—197 
pathological changes—191 
pupils—190 
pyloris—194 
pyruvic oxidase—193, 196 
respiration—192 
sequelae—189 
signs and symptoms—187 
SH group—193 
Oxygen intoxication, resulting from 
pressures not exceeding one at- 
mosphere, effects on blood—184 
blood pressure—184 
cardiac output—183 
cardiovascular system—183 
chronaxie—183 
electrocardiogram—184 
erythropoiesis—184 
lymph flow—182 
metabolism—186 
nervous system—183 
nose and throat irritation—182 
pathological changes—182, 185 
pulse rate—183 
pyruvic oxidase—186 
respiratory minute volume—185 
respiratory system—185 
ventilation rate—185 
Oxygen generation—278 
Oxygen paradox—197 
Pain, in cold—97 
in decompression sickness—164 
Pathological lesions in, beryllium poi- 
soning—218 
carbon monoxide poisoning—201 
chlorine poisoning—224 
decompression sickness—161, 165 
escape accidents—254 
noise—130 
oxygen intoxication—182, 185 
underwater blast—258 
Phoria—123 
Physical fitness—282 
Portuguese man-of-war—334 
Post-mortem findings in carbon diox- 
ide intoxication—65, 70 
in decompression sickness—164 
in escape diving accidents—254 
in explosive decompression—180 
in oxygen intoxication—191 
Pressure breathing—294 
Pressures, high, physiological effects 
on heart and circulation—7 
nervous system—7 
respiration—8 
Pressures, hydrostatic—148 
Protection and preservation of per- 
sonnel—268 
Psychiatric breakdown—327 
Psychological and psychiatric prob- 
lems—309 
Psychological factors in perform- 
ance—315 
Psychomotor responses—314 
Radioactivity, effects on naval per- 
sonnel—264 
Radium treatment of otitis media— 
157 
Recompression treatment in decom- 
pression sickness—172 
Renal function, effects of carbon di- 
oxide on—69 
carbon tetrachloride poisoning— 
235 INDEX OF SUBJECTS 
Renal function, etc.—Continued 
cold—104 
heat—78 
low oxygen—26, 34, 50 
Respiration, effects of breath hold- 
ing on—250 
carbon dioxide—64 
decompression sickness—160 
diffusion respiration—293 
explosive decompression—178 
low oxygen—29, 45 
motion sickness—238 
oxygen intoxication—185, 192 
oxygen paradox—197 
pressure1 breathing—294 
resuscitation—290 
Respirators—292 
Resuscitation and respiratory de- 
vices—35, 290 
Saturation and desaturation of gases 
in the body—15 
Sea urchins—334 
Selection of submarine personnel and 
divers—299 
Sharks—334 
Signs and symptoms of oxygen in- 
toxication—182, 187 
Sleep, wakefulness—321 
Snorkel problems—261 
Sonar problems—306 
Spleen, effect of low oxygen—24, 44 
“Squeeze”—257 
Stibine poisoning—231 
Stress—315 
Submarine escape problems—250 
Submarine operational perform- 
ance—305 
Sweating, effects of heat on—77, 85, 
92 
in motion sickness—237 
Swim-diving—329 
blood pressure—331 
cramps—332 
dangerous fish and other marine 
organisms—334 
diseases prevalent in swimmers— 
332 
electrocardiogram—3 3 2 
eupneic pressure—331 
fungus infections—332 
hydrostatic pressure—330 
oxygen consumption—331 
residual volume—331 
treatment of fungus—332 
underwater breathing apparatus— 
335 
vital capacity—331 
Tables, decompression—168 
treatment—173 
Tidal volume in artificial respira- 
tion—290 
breathholding—251 
carbon dioxide—64 
Tobacco smoke—233 
Training of personnel—304 
U. D. T., see Swim-diving. 
Ultraviolet light, use for submarine 
crews—274 
Ultraviolet radiation—274 
Underwater blast—258 
U. S. S. Gubera—326 
U. S. S. Icefish—280 
U. S. S. Irex—263 
U. S. S. Sirage—261 
U. S. S. Tang—251 
U. S. S. Trumpetfish—263 
U. S. S. Tusk—326 
Vasoconstriction, effects of carbon 
dioxide on—61 
cold—98 
heat—75 
low oxygen—25 
oxygen intoxication—195 
pressure breathing—295 
Vasoconstrictor and analgesic drugs 
in the therapy of otitis media— 
156 
Vasodilatation, as affected, by heat— 
73, 74 
low oxygen—19 
pressure breathing—296 
Ventilation and air-conditioning— 
270 
air flow and volume—270 
disinfection of air—273 
dust, gas, fume, and odor elimina- 
tion—276 
humidity control—271 
temperature control—272 
Vibration, effects on performance— 
147 
physiological effects—144 
Visual problems, accommodation— 
123 
acuity—119 
color vision—121 
night vision and dark adaptation— 
123 
phoria—123 
underwater vision—128 
visual performance—122 
Water balance, effects of heat on—77 
X-craft—306 
X-ray treatment of otitis media—157 
U. S. GOVERNMENT PRINTING OFFICE: 1954