TOXICOLOGY 
OR 
THE EFFECTS OF POISONS 
UNDERHILL TOXICOLOGY 
OR 
THE EFFECTS OF POISONS 
BY 
FRANK P. ^DERHILL/Ph.D. 
PROFESSOR OF PHARMACOLOGY AND TOXICOLOGY, 
SCHOOL OF MEDICINE, YALE UNIVERSITY 
PHILADELPHIA 
P. BLAKISTON'S SON & CO. 
1012 WALNUT STREET Copyright, 1924, by P. Blakiston's Son & Co. 
PRINTED IN U. S. A. 
BY THE MAPLE PRESS COMPANY, YORK, PA. TO 
L. R. U. PREFACE 
This volume has been compiled with the object of 
presenting a short, concise description of the effects of 
poisons upon the organism. No attempt has been made 
to enter into the details of the chemical reactions involved 
in the isolation and identification of poisons. Such mat- 
ters have been adequately treated in several well known 
books. On the other hand, a comparable treatise giving 
the essentials of the effects of poisons has not been 
published within recent years. It is hoped that this 
volume will fill this need and will be of service to medical 
students and physicians who wish to gain a clear concept 
of the essentials of the science of poisons. 
The subject matter has formed the basis of a course of 
lectures given to students in the Yale School of Medi- 
cine, and has been gathered from the standard text books, 
reference books and original literature upon the subject. 
In general, references have been given only to the later 
articles upon a given topic and then usually to those articles 
containing the earlier literature. 
Acknowledgement is made of the aid of Miss Mary 
Eloise Montague in preparation of the manuscript and in 
proof reading. 
New Haven, Conn. 
Frank P. Underhill. 
VII CONTENTS 
CHAPTER I 
Page 
The Principles of Toxicology i 
CHAPTER II 
Inorganic Poisons-Corrosive Acids and Alkalies ... 22 
CHAPTER III 
Poisonous Gases 36 
CHAPTER IV 
Metallic Poisons 72 
CHAPTER V 
Alkaloidal Poisons 121 
CHAPTER VI 
Miscellaneous Organic Poisons 164 
Index 265 
IX TOXICOLOGY 
CHAPTER I 
THE PRINCIPLES OF TOXICOLOGY 
Toxicology is the science of poisons. In its broadest 
use it is the science that treats of the origin, nature, prop- 
erties, effects and detection of poisons, and it includes 
treatment of poisoning. The science falls naturally into 
two divisions (a) that dealing with the effects of poisons 
and (b) that relating to their chemical identification and 
isolation. From this division it is readily seen that the 
first relates more especially to physiological action, whereas 
the latter is primarily concerned with chemical reactions. 
To give a general satisfactory definition of a poison is a 
somewhat difficult feat. Nevertheless various attempts 
have been made examples of which follow-"We define 
poisons as such inorganic or organic substances as are in 
part capable of artificial preparations, in part existing, 
ready formed, in the animal or vegetable kingdom, which 
without being able to reproduce themselves, through the 
chemical nature of their molecules under certain condi- 
tions, change in the healthy organism the form and general 
relationship of the organic parts, and through annihilation 
of organs, or destruction of their functions, injure health, 
or, under certain conditions, destroy life" (Husemann). 
According to Kobert-" Poisons are organic or inorganic 
unorganized substances originating in the organism itself, 
or introduced into the organism, either artificially pre- 
1 2 
TOXICOLOGY 
pared, or ready formed in nature, which through their 
chemical properties, under certain conditions, so influence 
the organs of living beings, that the health of these beings 
is seriously influenced temporarily or permanently." 
Blyth prefers the following-"A substance may be called 
a poison if it is capable of being taken into any living 
organism, and causes, by its own inherent chemical nature, 
impairment or destruction of function." Sollmann states 
that-"A poison is any substance which, acting directly 
through its inherent chemic properties, and by its ordi- 
nary action, is capable of destroying life, or of seriously 
endangering health, when it is applied to the body, 
externally, or in moderate doses (to 50 gms.) internally. 
CLASSIFICATION OF POISONS 
There are at least two ways in which poisons may be 
classified (a) according to chemical properties (b) accord- 
ing to physiological effects. From a scientific viewpoint 
neither system nor a combination is entirely adequate 
and one must either omit all attempts at classification or 
else be content to classify poisons from the standpoint of 
practical utility only. A chemical classification follows: 
1. Acids and Alkalies 
2. Metallic Poisons 
3. Gaseous Poisons 
4. Alkaloids 
5. Volatile Organic Poisons 
6. Miscellaneous Poisons 
The physiological classification recognizes the most 
prominent symptoms as the basis for division of poisons. 
According to this classification poisons may be divided 
into three great groups which is that adopted and defined 
by Sollmann. THE PRINCIPLES OF TOXICOLOGY 
3 
i. Irritants.-These produce inflammation; if they are 
taken by the mouth, there is pain throughout the alimen- 
tary canal, vomiting, purging, delirium, coma. So many 
poisons are to some extent irritant, that these symptoms 
are very commonly present. The irritants can be divided 
into corrosives, which produce destruction of tissue: and 
simple irritants which do not. If corrosives are taken by 
the stomach, the vomit is often bloody. 
2. Nerve Poisons.-These act on the neuromuscular 
apparatus, and include most of the poisons which are 
fatal in minute doses. They are subdivided into: Con- 
vulsants, which cause spasms; Somnifacients, causing 
sleep and coma; and Cardiac poisons, which stop the heart. 
3. Blood Poisons.-Those which alter the hemoglobin or 
blood corpuscles. These include the toxic gases, nitrites, 
etc. Their action is generally characterized by cyanosis. 
CONDITIONS MODIFYING THE EFFECTS OF POISONS 
The influence of a poison upon the organism is very 
materially modified by a variety of conditions. In general 
these may be divided into two great classes:-(A) Those 
relating to the poison itself and the manner of its adminis- 
tration, (B) Those relating to the organism itself. 
(2I) 1. The Physical State or Form of a Poison.-The 
physical state of a poison has a marked influence in modify- 
ing the action of a poison. Thus a poison is more rapidly 
absorbed in a gaseous form than in a solid or even a liquid 
state. In order that a substance may act as a poison it 
must be capable of solution, and absorption by the 
blood. No substance completely insoluble can be regarded 
as a true poison. Barium chloride which is readily soluble 
must be regarded as extremely toxic whereas the insoluble 
barium sulphate is devoid of toxic properties. In fact TOXICOLOGY 
4 
advantage is taken of this in the employment of barium 
sulphate in X-ray photography in diagnosis of gastro- 
intestinal disorders. The principle of the form of poison 
modifying its action is made use of in the treatment of 
various types of intoxication by means of antidotes, the 
object aimed at being to change the soluble substance to 
one insoluble and hence incapable of absorption. 
In general, dilution of a poison tends to favor rapid 
absorption and this in turn hastens and intensifies the 
toxic effect. An exception to this rule is seen in the case 
of those poisons with a corrosive action. These have 
their detrimental influence greatly decreased by dilution. 
Poisons taken into the stomach in the form of a dry powder 
may not manifest toxic symptoms for hours after adminis- 
tration. Usually the larger the dose the more rapid and 
severe are the effects. This, however, is not always true. 
Thus arsenic in large doses may act as an irritant to the 
stomach, causing vomiting, with prompt ejection of the 
poison so that few or no toxic symptoms result. On 
the other hand a very much smaller dose being devoid of 
irritant action on the stomach allows absorption of the 
poison with subsequent symptoms which may terminate 
fatally. Again the solvent containing the poison exerts a 
marked effect upon its action. Thus of alcoholic, aqueous 
or oily solutions the first is most rapidly absorbed, the last 
least so and in consequence more prompt and emphatic 
effects are to be expected the more rapid the absorption. 
Hot solutions are usually absorbed more rapidly than cold. 
2. The Path of Absorption.--In general a poison exerts 
its specific action irrespective of the mode of administra- 
tion. In other words it makes little difference through 
which path the poison reaches the circulation. The 
only modifying influence exerted by changing the path of 
absorption is the time of appearance of symptoms which THE PRINCIPLES OF TOXICOLOGY 
5 
varies directly with the rate of absorption. Thus symp- 
toms appear most rapidly when poisons are injected 
directly into the blood stream. Intraperitoneal injection 
and intramuscular stand next in order followed by 
subcutaneous and intra-dermal injection. 
Poisons are less rapidly absorbed when taken by mouth. 
The condition of the stomach greatly modifies the rate of 
absorption. A diseased stomach may markedly delay the 
absorption of a poison or on the other hand prove highly 
susceptible to an irritant poison. Food in the stomach 
may delay absorption either by retarding the emptying of 
this organ or by changing temporarily the physical state of 
the poison. Many apparent anomalies of the effects 
of poisons may be explained in this manner. Although 
it may be generally accepted that the path of absorption 
modifies the action of a poison only in its time relations and 
does not alter its specific effect, yet there are notable 
exceptions for in certain instances the mode of adminis- 
tration materially alters the action of the poison. This 
is particularly true of substances resembling proteins, 
hence capable of alteration by the digestive enzymes. 
Snake venom by mouth is entirely harmless even though 
highly poisonous when it gains direct entrance to the 
blood. The same is true of the toxic proteins, ricin and 
abrin, and various bacterial toxines fall into the same class. 
(B) The most important conditions residing in the 
organism that modify the action of poisons are (r) Age, (2), 
Idiosyncrasy, (3) Habit, (4) Tolerance, (5) Physical state 
of the individual. 
1. Age.-As might be assumed, the age of an individual 
distinctly modifies susceptibility to poison. Although as a 
rule the younger the individual the greater is the suscepti- 
bility, there are many notable exceptions. Thus for 
example, children are relatively less susceptible to the 6 
TOXICOLOGY 
action of strychnine, belladonna, and calomel. Con- 
versely, young children are particularly susceptible to the 
action of opium and its constituents and the same may 
be said of the other narcotic drugs. In old age, poisons 
may react with unusual severity, indicating a reduced 
resistance. 
2. Idiosyncrasy.-The term idiosyncrasy is applied 
when an individual exhibits peculiar, unusual reactions to 
certain poisons. Lack of knowledge of this peculiar 
personal susceptibility or tolerance may result in serious 
disturbances in bodily function or even terminate in death. 
In a given case of poisoning the possibility of this distinc- 
tive characteristic should always be taken into consider- 
ation. Idiosyncrasy may be manifested toward a large 
number of substances some of which are ordinarily non- 
toxic, so that this unusual sensitiveness may be both quali- 
tative and quantitative. This feature is brought into 
prominence in different individuals especially by morphine, 
calomel, arsenic, mercury, antipyrine, cocaine, etc. 
On the other hand, in some individuals a drug will 
induce an effect exactly opposite that usually produced. 
Thus morphine will cause wakefulness instead of sleep, or 
in larger doses convulsions simulating those of strychnine. 
Many individuals react with severe symptoms after eating 
or smelling of a large variety of substances, lobsters and 
other shellfish, honey, various fish, eggs, mutton, straw- 
berries, sewer gas, musk, smell of animals, and odor of 
flowers. 
3. Habit.-Repeated small doses of a poison generally 
lessen the effect. By gradually increasing the initial small 
dose of a poison relatively largedosesmay betaken without 
evidence of toxic symptoms. Habitual morphine users 
are pertinent examples, very large doses being necessary 
finally to produce the desired effect. Again in certain THE PRINCIPLES OF TOXICOLOGY 
7 
parts of Europe arsenic eating is notorious, huge quanti- 
ties being taken daily. Whether in the case of morphine 
the organism develops an ability to oxidize the drug to an 
unusual degree or whether the intestine acquires a resis- 
tance to absorption remains indicisive at present. So far 
as arsenic is concerned the assumption has been made for 
many years that there was a gradually increasing resis- 
tance to its effects. Very recently, however, it has been 
shown that the apparent habituation to arsenic may per- 
haps, in part at least, be ascribed to the quality of the 
arsenic consumed. Thus when arsenic made up of small 
crystals, or powdered, was ingested, much smaller 
doses were needed to produce toxic effects than when 
larger particles were introduced. From this it would 
appear that the whole matter may be explained on the 
basis of solubility of the arsenic, the powder or small 
crystals being much more readily soluble, hence more 
rapidly absorbed, than the larger, coarser crystals. 
This tolerance to poisons, acquired through habit, is not 
absolute since generally toxic effects and even death 
may be induced by slightly exceeding the limit of habitua- 
tion. It is this fact that largely explains the death of 
the habitue of morphine and of other similar poisons. 
Habit, however, cannot be acquired with all drugs, for 
antimony or mercury, for example, cannot be taken long 
with impunity even in relatively small doses. 
4. Tolerance.- Certain individuals exhibit a very note- 
worthy resistance to the action of certain poisons. 
This resistance or tolerance is natural, not having been 
acquired by habituation but it is rarely absolute so that 
it can hardly be regarded as a natural immunity. Thus 
some persons are capable of taking large doses of morphine 
without any apparent effect. The explanation of this 
peculiarity is not clear. In some instances it may be 8 
TOXICOLOGY 
due either to non-absorption, rapid elimination, unusual 
ability to neutralize or destroy the poison or to anatomic 
peculiarities. In some instances none of these hypotheses 
seems to hold. 
5. Disease.-Pathological conditions in the body may 
very naturally influence the action and effects of poisons. 
This modified action may be manifested as an increased 
susceptibility or the effect may be greatly diminished. 
These conditions that influence absorption and excretion 
play a particular role in this respect. Renal disease for 
example increases the susceptibility to arsenic and other 
drugs. In paralysis strychnine acts less readily. In 
peritonitis, delirium tremens, and in those states where 
intense pain exists the power of morphine is diminished 
whereas in conditions primarily associated with the nervous 
system as in inflammatory conditions of the brain an 
increased susceptibility may be noted. In insanity with 
maniacal characteristics and in convulsions narcotics 
may be almost without influence. Exhaustion tends to 
increase susceptibility. General reduction of vitality 
from whatever cause usually means a lowered resistance 
to poisons. On the other hand sleep, perhaps owing to 
lessened functional activity has a tendency to diminish or 
at least to retard the action of poisons. 
THE FATE OF POISONS 
After absorption, poisons rapidly leave the blood unless 
indeed they combine with the constituents of the blood 
and change its characteristics either temporarily or 
permanently. In general, however, poisons remain in the 
blood for a comparatively short time, being excreted 
through the urine, saliva, bile, sweat and feces. In 
certain instances more of the poison is eliminated by the THE PRINCIPLES OF TOXICOLOGY 
9 
feces than by the urine, lead for example. Usually 
however, most of the poison passes by way of the renal 
path. Poisons are promptly eliminated from the body 
but are deposited in all the principal organs and tissues. 
In general the liver contains the greater amount of stored 
poison, the amount deposited in the other organs varying 
with the type of poison. Gaseous poisons are not 
deposited but are promptly excreted by the lungs. 
So far as one may judge a poison deposited in an organ 
enters into some chemical combination with the cellular 
constituents and while thus deposited may be regarded 
as without special detrimental effect. Gradually this 
combination disrupts and the poison is thrown into the 
general circulation, injuring sensitive tissues in its passage 
to the excretory organs which indeed may suffer injury 
sufficient to cause death. Usually inorganic poisons are 
eliminated from the body unchanged, the organism being 
unable to alter them. On the other hand the natural 
response of the body is to change or modify the poison 
prior to elimination. Most of the organic poisons are 
altered in passage through the body by combination with 
constituents of the body or by undergoing oxidation, 
hydrolysis or other similar transformation. 
SYMPTOMATOLOGY OF POISONS 
There are certain outstanding features in poisoning that 
may be of value to the physician in diagnosis. These 
symptoms are general and although they do not indicate 
specific poisons their presence or absence exclude certain 
possibilities. Special symptoms relating to specific poisons 
will be considered under individual poisons. 
i. Nausea, Vomiting and Purging.-When these sud- 
denly appear in a normal individual it is indicative of 10 
TOXICOLOGY 
the presence of a gastro-intestinal irritant or of the onset 
of some acute disease. Many poisons, especially metals 
and food poisons, are characterized by initial symptoms of 
nausea, vomiting and purging. If the history of the case 
agrees with the possibility of poisoning, measures should 
be taken at once to assist the body in its efforts to rid itself 
of the noxious substances. 
2. Vasomotor Disturbances.-The effects of poisons 
upon the vasomotor centres is indicated by the fact that 
many poisons lead to marked changes in the skin. The 
color may be pale or the natural color much intensified 
and urticarial rashes are common. Heart action and 
respiration may be markedly modified in either direction. 
3. Cerebral Symptoms.-The influence of poisons upon 
the cerebrum lead to stupor or coma, or may partake of 
the nature of convulsions, illusions or hallucinations. 
Thus, hallucinations and temporary delusions may follow 
the use of salicylic acid and strychnine may cause convul- 
sions. Stupor and coma may be induced by narcotics 
or may be due to alcoholism or cerebral hemorrhage. 
4. Temperature.-The temperature changes in poison- 
ing have not been sufficiently studied to make definite 
statements concerning them. Certain it is that usually 
changes in temperature must be regarded as secondary 
effects rather than of specific effects of poison. Some 
poisons, like cocaine, in large doses may elevate temper- 
ature but usually in poisoning the temperature is either 
normal or is low in some instances being as low as 
95°F. 
5. Pulse.-Generally in acute poisoning the pulse is 
quick and feeble, the extent to which this is true begin 
determined by the degree of shock that may be present. 
Poisons that have a specific action upon the respiratory 
centre may influence the pulse only slightly if at all and the THE PRINCIPLES OF TOXICOLOGY 
11 
pulse may continue with a good tone for some time after 
respiration has ceased. 
6. Respiration.-The most common effect of poisons on 
the respiration manifests itself in dyspnea, which may be 
due to mechanical obstruction, as in edema of the glottis 
from local action of a corrosive poison, or to paralysis, 
as in chronic lead poisoning, or to muscular spasm, as 
in poisoning with strychnine, or to direct action on 
the respiratory centre, as may be observed with some 
poisons of bacterial origin. Cheyne-Stokes respiration 
marks the approaching termination of many cases of fatal 
poisoning. 
7. Motor Disturbances.-Motor disturbances are so 
characteristic in certain instances that they lead at once to 
a correct diagnosis. In lead poisoning the wrist drop is 
sufficient to arouse suspicion; tetanus due to strychnine 
poisoning is quite peculiar and the mydriasis of atropine 
poisoning is characteristic. Retention of urine occurs with 
narcotic poisons although a general reaction of fatal 
poisoning is paralysis of sphincters. 
8. The Eye.-Only a few reactions upon the eye are of 
particular value. Thus contraction of the pupil by mor- 
phine and dilatation by atropine are quite characteristic. 
Yellow vision with santonin and blindness from wood 
alcohol poisoning are quite specific. 
9. The Ear.-Quinine causes a ringing sensaiton in the 
ear, the hearing is more acute under the influence of 
strychnine, and salicylic acid causes a buzzing sensation. 
10. Modified Sensations.-Various changes of sensation 
in the skin, such as anesthesia, hyperesthesia, pins and 
needles sensation, etc., probably have their origin in some 
form of poisoning. Neuritis from lead, arsenic and alcohol 
are examples of abnormalities of sensation induced by 
intoxication. TOXICOLOGY 
12 
ii. Skin Lesions.-The long continued use of bromides 
or iodides may result in acnes or fungoid sores. Chronic 
arsenic poisoning gives rise to the peculiar coloring of 
the skin called arsenic melanosis, and silver causes the 
coloration known as argyria. Gangrene may be induced 
by ergot and members of the arsphenamine group may be 
responsible for varied skin eruptions partaking of the 
nature of urticarial, scarlatinoid and morbilliform erythe- 
mas together with itching or pruritus of the skin. 
THE DIAGNOSIS OF POISONING 
At times the diagnosis of poisoning is exceedingly 
difficult since with a few notable exceptions the effects of 
poisons are not characteristic. It is, of course, of the 
utmost importance to be able to make a diagnosis of 
poisoning so that proper treatment may be instituted. 
i. Suspicion of poisoning arises if any individual who 
has previously been in apparent good health suddenly 
manifests notable pathological symptoms which rapidly 
become intensified. This suspicion is strengthened if the 
symptoms appear a short time subsequent to the ingestion 
of some food or drink which may have had a peculiar odor 
or taste. Suspicion is further firmly established if the 
symptoms agree closely with those characteristic of a 
certain group of poisons and if they can be differentiated 
from disease. 
In general the physician is guided only by symptomatic 
evidence. This may entirely mislead him since a variety 
of diseases may cause symptoms simulating those induced 
by poisons. Thus, irritant poisoning may be simulated 
by gastro-enteritis, gastric and intestinal ulcers, acute 
indigestion, appendicitis, intestinal obstruction, peritoni- 
tis, etc. On the other hand, narcotic poisoning may be THE PRINCIPLES OF TOXICOLOGY 
13 
simulated by epilepsy, apoplexy, cerebral hemorrhage, 
certain heart diseases, inflammation of the cerebro-spinal 
system, uremia, etc. The symptoms of arsenic poisoning 
and those of cholera morbis are very similar. One may 
readily mistake apoplexy or uremia for opium poisoning. 
The resemblance between the symptoms of strychnine 
poisoning and tetanus is very close. 
In acute poisoning a careful examination will many 
times enable the physician to make an immediate accurate 
diagnosis. Evidences of corrosion on the lips, tongue, 
mouth and throat lead one to suspect that a corrosive 
poison has been taken. Chloroform, carbolic acid, 
potassium cyanide and other odoriferous substances may 
be detected on the breath, and examination of the vomitus 
and even of the feces may reveal important evidence. 
The urine is of considerable importance in examinations of 
this kind. 
2. The long continued use of sulphonal or trional gives 
the urine a red color from the presence of hematoporphy- 
rin which may be identified by the spectroscope. Methyl- 
ene blue imparts a green color to the urine and antipyrin 
and fuchsin cause it to assume a red hue. In santonin 
poisoning the fresh urine is normal in color but upon 
being made alkaline turns bright red. The urine turns 
dark green with phenol and cresol, the color deepening on 
standing. Quinine may cause hemoglobinuria which also 
results from the inhalation of arseniuretted hydrogen. 
Potassium chlorate induces methemoglobin and blood in 
the urine may follow the administration of any genito- 
urinary irritant such as cantharides or turpentine. Phos- 
phorus, mercury or lead may give the urine a brown or 
greenish brown color. 
Chronic poisoning is even more difficult of diagnosis 
than acute poisoning because the symptoms are usually 14 
TOXICOLOGY 
not sufficiently definite to arouse the suspicions of the 
physician. 
There are no definite rules to establish a diagnosis of 
poisoning during life except by chemical analysis of some 
of the excretions of the body such as urine, feces or 
vomitus. Any drink, food or medicine suspected should 
be subjected to analysis also. In no other way is it pos- 
sible to differentiate absolutely between the symptoms 
caused by disease and those induced by poisons. 
TREATMENT OF POISONING 
Each type of poisoning requires specific treatment. In 
many instances, however, the poison taken is unknown 
and it is therefore essential that general rules of treatment 
be established. These are (i) removal of the poison, (2) 
administration of antidotes, (3) symptomatic treatment. 
Removal of the Poison.-The measures taken will 
depend upon the site to which the poison was applied. 
If the skin or mucous membranes are concerned the best 
agent for removal of the poison is water copiously applied. 
This application not only dilutes the irritant agent but 
washes the site free from it. If the poison is not freely 
soluble in water (for instance, carbolic acid) alcohol may 
be employed. Chemical antidotes may be added to wash- 
water-thus for acids, soaps or Linimentum calcis; for 
alkalies, lemon juice or vinegar. It should be pointed 
out that strong acids or alkalies should never be used in 
the treatment of irritant poisons. After the site has 
been thoroughly freed from the toxic agent it should be 
covered with a bland oil or salve. 
Most poisons are taken by mouth, hence, in treatment 
the stomach should be emptied as soon as possible unless 
indeed sufficient time has elapsed to make this procedure THE PRINCIPLES OF TOXICOLOGY 
15 
useless. On the other hand it is always a good plan to 
follow since the cleansing of the stomach aids greatly in 
most cases of poisoning. There are only a few instances 
of poisoning where emptying the alimentary tract is con- 
traindicated. The most notable of these is in strychnine 
poisoning and in extensive corrosion of the alimentary 
canal. In emptying the stomach two types of procedure 
may be followed-the administration of emetics and 
lavage. Emetics are most easily given and have the 
advantage of not causing struggling on the part of the 
patient. If possible, however, lavage, employing the stom- 
ach tube, either through the mouth or nose, is to be 
preferred since it cleanses the stomach more thoroughly 
and also permits the introduction of chemical antidotes. 
Moreover, it is less depressing to the patient and must be 
employed when poisons have been taken that inhibit the 
vomiting centre-for example, chloral or morphine. 
If emetics are administered repetition should be prac- 
tised at intervals of 15 to 30 minutes if necessary. Apo- 
morphine (5 mgm. (grain ^0) in 1 Per cent solution = 5 
cc.,) subcutaneously is very rapid and effective in its 
action but has a distinctly depressing influence. Its 
great advantage lies in the fact that it is the only emetic 
that can be given hypodermically and is particularly 
useful when resistance to treatment is offered. Copper 
sulphate or zinc sulphate are safe and efficient emetics. 
Copper sulphate is perhaps more effective than zinc sul- 
phate but it is also more irritant. Both produce a mini- 
mum of depression. They should not be employed when 
irritant poisoning is under treatment. The dose of zinc 
sulphate is 2 gm. in a glass of water; for copper gm. at 
once or three doses of 0.3 gm. fifteen minutes apart. If 
vomiting does not occur the copper salt should be removed 
by lavage. In emergencies a dessert spoonful of ground 16 
TOXICOLOGY 
mustard stirred into a cup of tepid water may serve as an 
efficient emetic. At times it is desirable that the entire 
alimentary tract be cleansed and for this purpose cathartics 
should be employed. They need not be given, however, 
until the most acute symptoms have subsided. The 
saline cathartics are to be recommended for this purpose; 
oily cathartics in general should be avoided. Enemas 
are of little value. 
Administration of Antidotes.-An antidote neutralizes 
the action of a poison either by changing its physical state 
or its chemical composition, thereby preventing its action 
or retarding its absorption. Since the compounds formed 
by administration of antidotes may be only slightly less 
toxic than the original poison or may become poisonous 
by remaining in the stomach the giving of antidotes should 
be combined with lavage or the administration of emetics. 
If lavage is practiced the antidotes may be added to the 
wash-water; if emetics are used antidotes may be adminis- 
tered between the intervals of vomiting. In general anti- 
dotes should be given repeatedly at short intervals. In 
the selection of an antidote care should be exercised that it 
be as harmless as possible and that the substance resulting 
from its action is practically inert, at least, temporarily. 
Some antidotes, like raw eggs, acacia, milk, boiled starch 
or flour, which may be given in quantities as desired, act 
either by combining with the poison to form an insoluble 
compound-for example, eggs in the case of metals, espe- 
cially mercury, or by enveloping the poison temporarily 
in an impenetrable membrane, hence lessening absorption, 
accomplished in part by delaying the exit from the stom- 
ach. In the case of irritant poisons these antidotes also 
tend to allay inflammation. 
One of the most valuable antidotes is tannin which 
acts as a precipitating agent. This may be employed in THE PRINCIPLES OF TOXICOLOGY 
17 
the form of very strong hot tea which may be given 
ad libitum. Alcohol diminishes its efficiency since the 
precipitates formed are, for the most part, soluble in 
alcohol. The following antidotes will be found useful 
against specific poisons-Alkaloidal poisons-15 drops of 
tincture of iodine in half a glass of water. Barium- 
either sodium sulphate (Glauber's salt) or magnesium 
sulphate (Epsom salt). Oxalates-calcium either in the 
form of chalk, lime water, or whiting. Phosphorus-- 
copper sulphate or old turpentine. Acids-weak alkalies 
such as chalk, baking soda, soap, burnt magnesia. Alkalies 
-weak acids, as vinegar or lemon juice. Alkaloids, 
glucosides and phosphorus-- antidotes for these poisons are 
oxidizing agents which tend to oxidize and hence to nullify 
the action of the poison. Potassium permanganate, about 
2 grains of the crystals in a glass of water, repeatedly given 
if vomiting occurs or at least a liter of a 0.05 per cent solu- 
tion. In no case should any undissolved crystals be 
administered. For hydrocyanic acid poisoning potassium 
permanganate, hydrogen peroxide or sodium thiosulphate 
may be employed. 
In treatment of poisoning the hypodermic administra- 
tion of antidotes is sometimes useful, thus for hydrocyanic 
poisoning sodium thiosulphate may be employed and 
sodium carbonate may be injected to counteract the action 
of acids. After poisons have had opportunity for absorp- 
tion attempts to hasten elimination are sometimes made. 
The results have not been highly successful. At times, 
however, some of the measures to be employed are of value. 
It is, of course, evident that stimulation of the renal 
function will undoubtedly aid in ridding the body of poison. 
In choosing a diuretic it should be remembered that water 
is the best diuretic known. It should be given in large 
volumes, 4 to 8 liters in 24 hours, if maximum beneficial 18 
TOXICOLOGY 
results are to be realized. Hypodermic injection of 
0.9 per cent solution of sodium chloride repeatedly given 
in liter quantities will also increase urinary excretion. 
Intravenous infusion of the same solution may at times 
be employed. Venesection may be of value in some types 
of poisoning but the blood drawn (up to a liter) should be 
replaced immediately by an equal or double volume of 
isotonic salt solution. 
Another class of antidotes is the so-called group termed 
"physiological antidotes" or "physiological antagonists." 
These antidotes do not really nullify the effects of poisons; 
they merely mask the symptoms produced. They are 
employed only against absorbed poisons and tend to 
combat the symptoms produced by arousing the opposite 
action. In this way they sometimes are of value in 
carrying the patient over a critical period and aid in con- 
serving life. Some of the physiological antagonisms are 
atropine to pilocarpine, caffeine to morphine, strychnine 
to nicotine, chloral to strychnine, atropine to morphine, 
chloroform to strychnine, etc. 
Symptomatic Treatment.-In most cases of poisoning 
symptoms produced by the absorbed poison are the most 
dangerous and these should receive attention from the 
beginning of the treatment. One of the first functions to 
fail is the respiration. Treatment to sustain respiration 
should not be delayed until respiration has actually ceased 
but reflex stimulation of the respiratory centre should be 
begun as soon as any evidence is given of the weakening of 
respiration. For this purpose use may be made of inhala- 
tion of ammonia water, or smelling salts, or by administra- 
tion of aromatic spirits of ammonia (half a teaspoonful in a 
glass of water), whipping with wet towels, mustard plasters, 
etc. Or if desired, agents to act directly upon the respira- 
tion may be employed, as hot coffee, atropine (0.001 gram) THE PRINCIPLES OF TOXICOLOGY 
19 
or strychnine (0.002 gram). If none of these measures is 
effectual artificial respiration should be practiced. 
In certain types of asphyxiating gas as CO oxygen 
inhalation alone or inhalation of oxygen with small per- 
centages of CO2 may be of benefit. 
In attempting to stimulate the poisoned heart intrav- 
enous infusion of isotonic salt solution alone or with 
the addition of epinephrin (1:100,000) may be of value. 
Dilatation of the heart may be relieved by venesection. 
The patient should be kept quietly in bed, cooling 
prevented by application of heat; pain controlled by 
anodynes; convulsions counteracted by chloroform; and 
coma combatted by stimulants such as coffee or atropine. 
For poisoning cases the following suggestion by Soll- 
mann is highly recommended: 
"Antidotes for First Aid.-Every physician should 
keep the following antidotes together, in a special satchel 
(" Antidote Bag") so that they can be readily transported. 
The dose should be written on each container. Amyl 
nitrite pearls; Apomorphine tablets, 2 mg.; Atropine 
tablets, 1 mg.; Caffeine-Sodium Benzoate; Chloroform; 
Cocaine Hydrochloride tablets, 0.03 gm.; Tincture Iodine; 
Copper Sulphate, powdered; Lime water; Magnesia, cal- 
cined; Potassium Permanganate, 1 per cent solution (to 
be diluted twenty times); Sodium Sulphate; Spiritus 
Ammoniae Aromaticus; Strychnine Sulphate tablets, 
2 mg.; Whiskey; also a hypodermic syringe in good order, 
and a stomach tube with funnel. The following should be 
demanded at the house of the patient: Boiled water; 
Coffee (strong, hot, and black); Eggs; Hot-water 
bags; Milk; Mustard; Salad oil; Salt; Soap; Starch, 
boiled; Tea; Vinegar." 
In criminal cases of poisoning the physician should 
carefully note and record the symptoms observed and take TOXICOLOGY 
20 
possession of any suspected substances such as medicine, 
food, drink, and he should also preserve vomitus, urine and 
feces. In the event of an autopsy where a chemical analy- 
sis is anticipated it is desirable that the chemist be present. 
In this way much more satisfactory correlation may be 
obtained in tracing the origin of the organs than if they are 
delivered to the chemist by the physician. Moreover, the 
chemist will also be able to testify that the vessels con- 
taining the organs and tissues are chemically clean. 
In many instances it is deemed sufficient to examine the 
stomach and intestines for the presence of poisons. This, 
however, is not good practice. In addition to the tissues 
mentioned portions of all the principal organs including 
the brain, cord and urine of bladder should be secured, 
especially if the nature of the poison is unknown. In the 
event that a quantitative estimation of the poison will be 
called for the total weights of the organs selected should 
be determined. The various organs and tissues should be 
preserved in separate vessels without addition of antisep- 
tics and the chemical examination should be begun as soon 
as possible after the autopsy although in most instances 
poisons do not rapidly disappear from the body after death. 
On the other hand poisons that are gaseous or readily 
volatilized may disappear very rapidly after death. 
The autopsy itself may not reveal the cause of death. 
Indeed in most cases of death by poisoning the autopsy 
fails to show the cause of death. In this event chemical 
examination is relied upon to furnish the proof. At times 
even this fails for the poison may have been largely 
eliminated and exist in any particular organ in quantities 
too small to be detected by present day methods or it may 
be a poison for which there is no specific chemical test. 
In most instances, however, the chemical examination may 
be relied upon to give the desired information. THE PRINCIPLES OF TOXICOLOGY 
21 
The autopsy is of great value in suspected poison cases 
though no evidences of poisonous action on the organs and 
tissues can be demonstrated even on microscopic examina- 
tion, for it affords an opportunity to determine whether 
death could be ascribed to natural causes. In the event 
that the organs and tissues reveal no pathological aspects 
suspicion of poisoning is even more firmly established. 
References 
Bastedo: Materia Medica, 2nd Edition, Saunders and Company, 
1920. 
Blyth: Poisons: Their Effects and Detection, 5th Edition, Van 
Nostrand Company, 1920. 
Buchanan: Forsenic Medicine and Toxicology, 8th Edition, E. 
and S. Livingstone, Edinburgh, 1915. 
Cushny: Pharmacology and Therapeutics, or the Action of Drugs, 
7th Edition, Lea and Febiger, 1918. 
Kobert: Lehrbuch des Intoxicationen, 2nd Edition, Stuttgart, 
1902. 
Kunkel: Handbuch des Toxikologie, Jena, 1899. 
Peterson and Haines: Legal Medicine and Toxicology, ii, 2nd 
Edition, Saunders and Company, 1923. 
Sollmann: Manual of Pharmacology, 2nd Edition, Saunders and 
Company, 1922. 
Wttthaus: Manual of Toxicology, 2nd Edition, Wm. Wood and 
Company, 1911. CHAPTER II 
INORGANIC POISONS 
CORROSIVE ACIDS 
The action of mineral acids is entirely local and the 
effects produced depend upon the concentration of the 
acid. When brought into contact with the skin or mucous 
membrane these agents cause death of the tissues. 
Applied to the skin the concentrated mineral acids cause 
an intense inflammation which may be regarded as a char- 
acteristic reaction. When strong mineral acids are 
swallowed there is an immediate sensation of burning in 
the mouth and gullet. Intense pain is felt in the stomach, 
and vomiting of brown or black matter mixed with blood 
may occur. Portions of the mucous membrane of the 
stomach may be present in the vomited material; swallow- 
ing may be either very difficult or altogether impossible 
because of the swollen condition or stricture of the oeso- 
phagus. There is great thirst, scanty urine and constipa- 
tion. When the corrosive action has involved the larynx 
and trachea, there may be difficulty in speech and some 
cough. Respiration is difficult. The pulse is small and 
weak, the skin is usually clammy and cold. The face is 
intensely anxious. The mouth and lips are generally 
blistered although sometimes such signs are absent. 
Death occurs suddenly either from suffocation or from 
shock. Perforation of the stomach or intestines may take 
place. In those cases where recovery ensues the general 
health may be impaired, the coats of the stomach speci- 
fically suffering more or less permanent injury. When 
22 INORGANIC POISONS 
23 
only a small quantity of acid has been swallowed after 
effects of the poison are pyloric ulcerations and stenosis. 
The mineral acids are rarely employed for the purpose of 
homicide and in the few cases on record the victims have 
been either children or insane persons. The concentrated 
acids, especially sulphuric, have been used more frequently 
for disfiguring the face. Suicidal deaths by concentrated 
mineral acids are not uncommon. 
SULPHURIC ACID (Oil of Vitriol) 
(H2SO4) 
Pure concentrated sulphuric acid is a heavy, oily, 
colorless liquid (specific gravity 1.800 to 1.845) which when 
added to water causes a sharp rise of temperature. It 
has the property of blackening or charring organic 
substances. 
Local Action.-The contact of sulphuric acid with the 
skin causes great pain and the area of contact becomes 
first white, then brown. Shortly thereafter the surround- 
ing skin becomes red and swollen. A lasting scar occurs 
owing to the destruction of the epidermis. Sometimes 
the destructive action involves also the underlying deeper 
tissues. Thrown into the eyes an intense conjunctivitis 
follows or blindness may result. 
Treatment of sulphuric acid burns on the skin must be 
prompt. This consists of dilution of the acid with large 
volumes of water. If the face is involved it should be 
immersed in successive basins or pails of water or held 
under a tap of running water, and the eyes opened under 
water. Later treatment includes application of a paste of 
sodium bicarbonate, subsequent washing and bandaging 
the burned area with a bland oil, or coating with a low 
melting paraffin. Infection of the wounds should be 
guarded against by proper dressing. 24 
TOXICOLOGY 
Symptoms^-When sulphuric acid is taken by mouth 
there is instant pain which extends along the track of the 
acid from the mouth to the stomach, especially along the 
smaller curvature. The tongue may become so swollen 
that it fills the mouth. It has a white coating and may 
become a disorganized and shapeless mass of burned flesh. 
In certain instances swallowing is inhibited and the acid 
instead of passing down the esophagus runs out of the 
mouth on to the chin and neck characteristically corroding 
these areas. 
Salivation is profuse and may persist especially because 
of an inability to swallow owing to the inflamed condition 
of the pharynx. Sometimes the acid reaches the larynx 
with resulting spasmodic closure of the glottis causing a 
gasping respiration and a hoarse voice. 
Retching, vomiting and extreme thirst are quite charac- 
teristic. The vomitus is very acid, filled with mucus, 
sometimes blood stained and contains pieces of the 
mucous membranes of the oesophagus and stomach. 
The face shows extreme anxiety, the pulse is feeble, the 
respiration difficult, the skin clammy, the eyes sunken and 
the extremities convulsed. Death in asphyxia, coma or 
convulsion may occur in a few hours or be delayed for 
several days. If death does not occur there is usually a 
stricture of the oesophagus or pylorus. 
Post Mortem Appearances.-Post mortem appearances 
differ according to the period of life after swallowing the 
poison. In an early death the characteristic features are 
those of acute corrosion of the structures of the mouth, 
oesophagus and stomach. With the exception of the 
stomach the tissues are white or gray in color and give 
evidence of distinct erosion. The stomach may be red or 
brown from the formation of hematin from the hemoglobin 
of the blood, or black from the charring of the mucous INORGANIC POISONS 
25 
membrane. The membrane is swollen, and may be so 
softened that it peels readily. When death occurs only 
after several weeks characteristic appearances include 
ulceration and contraction of the oesophagus, absence of 
mucous membrane of the stomach with its walls thickened 
and red, and the presence of adhesions, the total capacity 
being greatly reduced by contraction of the scar tissue. 
Fatal Dose.-The fatal dose is quite variable, the out- 
come depending upon the portion of the alimentary canal 
most seriously injured. The smallest fatal dose on record 
for an adult is 3.8 grams. On the other hand, 20 drops 
may prove fatal to a young child. 
Treatment.-Treatment consists in neutralization and 
dilution of the acid and the relief of other symptoms that 
may appear, such as asphyxia induced by swelling of the 
larynx. Neutralization is best effected by the adminis- 
tration of weak alkalies, as the carbonates, or calcined 
magnesia. In an emergency, soap suds or whiting may 
be employed. It must be emphasized that all antidotes 
should be given suspended or dissolved in large volumes of 
fluid, water or milk. In the event that neutralizing 
agents are not available large volumes of water may be 
given with raw eggs. It may be necessary to perform 
tracheotomy or intubation, and morphine may be essential 
to allay the pain. Neutralization of the acid will, of 
course, only prevent further destruction of tissue; it will 
have no influence upon the tissue already destroyed. 
Whatever remedial measures are to be taken must be 
resorted to with great promptness. 
NITRIC ACID (HNO3) 
Pure nitric acid is a colorless liquid with a boiling point 
of 86°C. It is a strong oxidizing agent and in the presence 
of sunlight decomposes into water, oxygen and lower 26 
TOXICOLOGY 
nitrogen oxides. In medicine it finds a use as a caustic, 
corroding organic substances by oxidation. Protein sub- 
stances are turned a deep yellow and are dissolved 
by it. 
In general poisoning by nitric acid is less frequent than 
with sulphuric acid. When ingested in solutions of less 
than 20 per cent, local effects are not prominent. When, 
however, concentrations of 35 per cent or more are taken 
a very rapid destruction of tissue occurs. The action is 
very similar to that of sulphuric acid and the symptoms 
are quite alike except that the parts in contact with 
the acid are at first white and later become stained 
deep yellow. There is intense pain, vomiting and great 
thirst. 
Fatal Dose.-The fatal dose varies greatly in accord 
with the area with which the acid comes into contact. 
If it enters the larynx very small quantities are sufficient 
to produce death from asphyxia. In general, however, 
it may be stated that three fluid drams constitutes a fatal 
dose in adults. Death may occur within an hour or less 
or may be delayed for days or weeks. 
Post Mortem Appearances.-The post mortem appear- 
ances are those of erosion. The mucous membrane of the 
mouth and pharynx may be yellow, or greenish in color, 
much swollen and peels easily. The gullet, stomach or 
intestines may be perforated, or much contracted and 
very brittle. Portions or the entire mucous membrane 
of the stomach may be absent, or ulceration may be 
prominent. 
Treatment.--The general treatment for nitric acid poi- 
soning is similar to that outlined for sulphuric acid. 
Promptness is of great importance for strong nitric acid 
acts with such rapidity that aid must be given immediately 
to be of any value. INORGANIC POISONS 
27 
HYDROCHLORIC ACID (HCl) 
Pure hydrochloric acid is recognized as "a liquid com- 
posed of 31.9 per cent by weight of absolute hydrochloric 
acid, and 68.1 per cent of water. It is a colorless, fuming 
liquid, of a pungent odor, and intensely acid taste." Its 
specific gravity is about 1.158 at 25°C.; it is miscible with 
water in all proportions and also with alcohol. Formerly 
called Muriatic Acid it finds a useful place in the United 
States Pharmacopoeia where the official preparation is 
described. 
Symptoms.-Although hydrochloric acid is distinctly 
corrosive to mucous membranes it is not nearly so active 
in this respect as either sulphuric or nitric acid. For this 
reason when swallowed stricture of the esophagus is much 
more common as a sequel than perforation of the stomach. 
Inasmuch as hydrochloric acid is quite volatile its fumes 
may cause inflammation of the larynx and air passages. 
When taken by mouth there is instant pain which later 
extends to the esophagus, stomach and abdomen. At 
first the lips, tongue and the buccal cavity in general are 
white in color but later turn brown. Other symptoms 
are difficulty in swallowing, husky voice, irregular respira- 
tion, feeble pulse, general weakness, retching and vomiting. 
If recovery follows there is frequently stricture of the 
esophagus or pylorus. 
Fatal Dose.-The fatal dose varies with the manner in 
which the acid is ingested. A few drops entering the 
trachea may cause death while a fatal outcome is to be 
expected from a fluid dram taken directly into the 
stomach. 
Fatal Period.-The period of life may range from 2 
hours or less to 24 hours. 
Post Mortem Appearances.-Post mortem examination 
reveals no feature which would differentiate hydrochloric 28 
TOXICOLOGY 
acid effects from those induced by sulphuric or nitric acids 
except that with sulphuric acid the destruction of tissues 
is greater and with nitric acid the appearance of the tissues 
is quite peculiar. 
Treatment.-The treatment for hydrochloric acid 
poisoning is the same as outlined for sulphuric and nitric 
acids-namely, neutralization and dilution of the acid 
by a weak alkali in large volumes of fluid, either water or 
milk. 
POTASSIUM CHLORATE 
Commonly employed in saturated solution as a mouth 
wash in cases of sore throat and stomatitis, especially in 
mercury poisoning, potassium chlorate frequently gives 
evidences of toxicity if swallowed. It should not be taken 
internally since as far back as 1879 Jacobi pointed out the 
serious effects produced when the drug is absorbed. 
Upon absorption methemoglobin is formed, an indefinite 
amount of hemoglobin being used up in this way since the 
chlorate apparently does not enter into the reaction. As 
a result of this fact the action of chlorate may be very 
severe leading to a real asphyxia. Moreover the blood 
cells disintegrate resulting in embolism. Other secondary 
symptoms which may appear are jaundice, hemo- 
globinuria, anuria or suppression of urine, bloody-tube 
casts, delirium, coma and death from nephritis. The 
chlorate passes through the body unchanged. 
Symptoms.-The symptoms of poisoning indicate 
gastric irritation, nausea and vomiting, diarrhoea with 
pain in the abdomen, cyanosis, collapse and perhaps ter- 
minal convulsions may appear. The nephritic condition 
has already been mentioned. 
Fatal Dose.-There is great variation in susceptibility 
to the drug and herein lies one of the great dangers atten- INORGANIC POISONS 
29 
dant upon its use. If given in divided doses the toxic 
effect is greater than if administered in a single dose. Tne 
fatal dose varies from 15 to 30 grams, 10 grams producing 
toxic symptoms. In one instance death occurred with 
11.65 grams. 
Fatal Period.-Symptoms begin quickly and death may 
result in 5 or 6 hours but usually the fatal termination 
occurs in 6 or 7 days as a result of the nephritis 
produced. 
Post Mortem Appearances.-On autopsy the findings 
correspond with what might be expected from the symp- 
toms-gastro-enteritis, and inflammatory changes in the 
spleen, liver and kidneys. These organs are enlarged and 
dark brown in color from the contained methemoglobin. 
Treatment.-Treatment of poisoning with potassium 
chlorate consists of thorough lavage of the stomach, and 
treatment of the secondary symptoms as they arise. 
CORROSIVE ALKALIES 
SODA, POTASH, AMMONIA 
In general, poisoning by the caustic alkalies is accidental 
rather than intentional. Inasmuch as soda and potash 
are so similar chemically as well as in the effects they 
produce a single description will suffice for both. 
The forms of potash most commonly encountered are 
caustic potash or potassium hydroxide (KOH), either as a 
solid or in solution; potassium carbonate (K2CO3) or 
bicarbonate (KHCO3); pearl-ash an impure commercial 
product. Soda is found in commerce as sodium hydroxide 
(NaOH), carbonate (Na2CO3) washing soda, or bicarbon- 
ate (NaHCO3). In concentrated form all these substances 
produce similar toxicological effects differing only in 
degree. 30 
TOXICOLOGY 
Symptoms.-Applied locally the caustic alkalies destroy 
tissue in a manner similar to the concentrated mineral 
acids. As a rule the tissues affected are white and 
softened, in fact, somewhat gelatinous. The injury 
usually penetrates deeply and scar formation and contrac- 
tion of tissue are very much alike with acids and alkalies. 
Taken by mouth the caustic alkalies produce a strong 
soapy taste, which is nauseating. Pain is experienced in 
the mouth, throat, and stomach which later turns into 
pain of a colicky nature with great abdominal tenderness. 
Violent vomiting may take place at once, the vomitus 
containing mucous shreds and blood. The mucous mem- 
branes of the mouth and adjacent tissues become white 
and swollen, portions being destroyed and the lips and 
tongue may turn brown. There is difficult respiration 
due to constriction of the pharynx; the face is extremely 
anxious, the pulse rapid and feeble, and the entire body is 
bathed in perspiration, the skin being cold. If death 
does not occur immediately it may result within a few days 
from obstruction of the air passages, or unless surgical 
interference enters death from starvation may occur owing 
to constriction of the oesophagus. 
Fatal Dose.-Ordinarily the fatal dose is about ounce 
(15.5 grams) of the caustic hydroxide although as little as 
30 grains (2 grams) have caused death. 
Fatal Period.-Death may ensue within 3 hours although 
usually not so rapidly. Generally death occurs within 
24 hours. 
Post Mortem Appearances.-The post mortem picture 
reveals the mouth and esophagus much softened, swollen 
and white. The mucous membranes of the stomach and 
intestines are bright red or black, partially destroyed and 
disorganized in areas of patches. Ulcerations and stric- 
tures of the esophagus or pylorus are quite characteristic. INORGANIC POISONS 
31 
Treatment.-The treatment consists in neutralization 
of the alkali by large volumes of weak acid, such as lemon 
juice or vinegar. The stomach tube should not be passed 
owing to possible rupture of the injured walls of the 
stomach and esophagus. Pain may be allayed with 
morphine, collapse by suitable stimulants. 
AMMONIA (NH3) 
Ammonia is a colorless gas, with a characteristic odor, 
irritating to the eyes and mucous membranes of the air 
passages. A strong solution in water forms ammonium 
hydroxide which has all the chemical properties of the gas. 
Symptoms.-The character of the pathological effects 
produced by ammonia depend upon the concentration and 
the manner of administration. If the vapor penetrates 
the respiratory passages there is a feeling of suffocation 
followed by pain and the sense of weight in the chest. 
Death may occur in a very few minutes from asphyxiation. 
The gas is a strong irritant to the respiratory tract and 
even in low concentration is regarded as an irrespirable 
gas. The influence of ammonia upon the tissues in general 
is similar to that of sodium or potassium hydroxide, that is, 
the proteins are dissolved and water is withdrawn. 
Take by mouth in solution ammonia causes by its corro- 
sive action burning pain in the mouth, esophagus and 
stomach, salivation, vomiting, and difficulty in swallow- 
ing, or even complete inability to accomplish this reflex. 
Rapid absorption occurs and the absorbed poison may 
stop the action of the heart very quickly, or unconscious- 
ness may ensue. There may be delirium and as a sequel, 
if death does not occur soon, partial or complete stricture 
of the esophagus. 
Fatal Dose.-The fatal dose is quite variable since death 
has been caused by doses as small as a teaspoonful of con- 32 
TOXICOLOGY 
centrated ammonia, whereas recovery has followed the 
ingestion of a fluid ounce. 
Post Mortem Appearances.-The post mortem appear- 
ances are those characteristic for the other corrosive 
alkalies-the primary feature being an inflammatory 
condition of the alimentary canal brought into contact 
with the poison. The gas produces corresponding inflam- 
matory reactions in the respiratory tract. 
Treatment.-Treatment is identical with that outlined 
for the other corrosive alkalies-namely, neutralization 
and dilution of the poison. The best antidotes are weak 
vinegar, lemon juice, oil, butter or milk. Large volumes of 
fluid should be administered. Other symptoms should be 
treated as they arise. 
IRRITANT POISONS 
PHOSPHORUS (P) 
Phosphorus ordinarily occurs in' two forms-the 
crystalline, waxy phosphorus, and an amorphous form 
which is made from the first by high heat in an absence of 
oxygen. The waxy phosphorus is usually kept under 
water and turns yellow. This yellow phosphorus is 
extremely poisonous. Red phosphorus or the amorphous 
form is non-toxic. It spontaneously takes fire at 5o°C. a 
temperature which may be attained by friction of the 
hands. To avoid danger of burns phosphorus should al- 
ways be handled with forceps, never with the fingers. 
Yellow phosphorus smells and tastes somewhat like garlic. 
It is only slightly soluble in water, alcohol and gly- 
cerol. It is readily soluble in carbon bisulphide, ether and 
almond oil. White fumes of P2O3 are given off when 
it is exposed to the air, and in the dark a faint 
phosphorescence may be observed. INORGANIC POISONS 
33 
Phosphorus poisoning is not so common as in the past 
since in this country at least its use as the basis of matches 
has been forbidden. Previously when matches made with 
phosphorus were common, poisoning by phosphorus 
accidentally, or with suicidal intent was quite frequent. 
Even more serious perhaps was phosphorus poisoning 
from an industrial standpoint since many chronic cases 
were caused in match factories. In this form of poison- 
ing by phosphorus particularly characteristic were the 
necrosis of the jaw, especially the lower, and caries of the 
teeth. Various commercial preparations for the exter- 
mination of rats contain phosphorus as a basic principle. 
According to the researches of Tardieu there exist three 
acute forms of phosphorus poisoning-(i) the ordinary 
form, characterized by local irritation and jaundice, (2) 
hemorrhagic form in which both jaundice and blood 
effusions occur, and (3) a nervous form, in which jaundice 
is accompanied by outstanding symptoms indicating 
nervous action. Nearly all the cases show jaundice and 
changes in the blood. 
Symptoms.-The first symptoms are the garlic-like 
taste in the mouth, burning sensation in the throat, severe 
pains in the stomach, and generally intense thirst. Vomit- 
ing and purging occur and the breath may be phosphores- 
cent. The vomitus may contain blood, have a garlic-like 
odor and emit light. Sometimes the symptoms are delayed 
for many hours. The surface of the body is bathed in 
sweat, nervous and muscular debility is very great and even 
in the early stage of poisoning death may result from 
collapse. 
Usually, however, there is a distinct lessening of the 
symptoms of irritation and the patient may appear on the 
road to recovery. Jaundice soon appears, however. 
The liver increases in size, later, however, it may atrophy. TOXICOLOGY 
34 
Abdominal pain is severe, vomiting and diarrhoea set in, 
the ejected matters containing blood. Hemorrhages are 
common from mucous surfaces and under the skin. 
Headache, insomnia and itching eruptions of the skin 
usually occur. The temperature may be subnormal. 
The urine contains bile pigments, albumin, blood, casts 
and at times leucine and tyrosine. Additional symptoms 
are great prostration, rapid, feeble pulse, delirium, con- 
vulsions, and coma which gradually ends in death. Death 
may be caused primarily by the weakness of the heart 
muscle due to degeneration. At times it is hard to 
differentiate between the effects of phosphorus poisoning 
and acute yellow atrophy of the liver. 
Fatal Dose.-As small a quantity as grain has proved 
fatal but ordinarily grains may be regarded as the 
fatal dose. 
Fatal Period.-The fatal period varies from less than i 
hour to many weeks. 
Post Mortem Appearances.-Post mortem examination 
reveals one characteristic feature, namely, a widespread 
degeneration of both muscle and glandular tissues-the 
so-called fatty degeneration, the cellular contents being 
replaced in large measure by infiltration of fat. The 
liver, kidneys and muscles, particularly of the heart, are 
chiefly affected. 
When death occurs quickly there may be extensive 
destruction of the stomach coats, ulceration, perforation 
or even gangrene. The stomach contents may give 
evidence of the presence of phosphorus, that is, garlicky 
odor and phosphorescence. Blood changes are profound, 
the red cells appearing almost colorless and transparent, 
the hemoglobin being dissolved in the plasma and the 
blood clotting only with difficulty. Hemorrhages may be INORGANIC POISONS 
35 
found in serous membranes, in the pleural and pericardial 
cavities, and on the surface of the brain and cord. 
Treatment.-Treatment of phosphorus poisoning con- 
sists in the use of the stomach tube at the first possible 
moment, the stomach being washed with i per cent potas- 
sium permanganate solution. Potassium permanganate 
oxidizes phosphorus to phosphoric acid which is harmless. 
The lavage with permanganate should be repeated fre- 
quently since any food in the stomach will unite with it 
also and thus leave little or none to act as an antidote. 
Dilute (1-3 per cent) hydrogen peroxide is perhaps even 
more effective. Old or oxidized turpentine forms with 
phosphorus an insoluble compound, hence, turpentine if 
old may be employed in this connection, one dram to a 
pint of water, frequently repeated. 
Copper sulphate has been recommended as an antidote 
and is of distinct value although its use in the doses neces- 
sary may aggravate the gastro-enteritis already present 
or may initiate this condition itself. Copper is said to form 
a coating on the phosphorus preventing its absorption. 
Further treatment consists in the administration of 
mucilaginous drinks containing magnesia in order to have 
free movements of the bowels. If the bowels do not move 
freely magnesium sulphate may be given. Oils and fats 
should be avoided, as they increase solution and absorption 
of phosphorus. From experiments on animals it is sug- 
gested that in acute phosphorus poisoning liquid petro- 
latum may be of benefit in treatment. 
Reference 
Atkinson: J. Lab. and Clin. Med., 1921, 7, p. 148. CHAPTER III 
POISONOUS GASES 
The group of poisonous gases is readily divisible into two 
subdivisions-(i) those producing toxic effects by com- 
binations with the hemoglobin of the blood, and (2) 
those causing poisoning because of their specifically irritant 
properties upon the mucous membrane of the respiratory 
tract. 
The first group comprises such substances as Carbon 
Monoxide, Hydrogen Sulphide, and Hydrocyanic Acid. 
The second group contains the war gases-Chlorine, 
Phosgene, Chlorpicrin and Mustard Gas, together with 
Bromine, Iodine and Fluorine. Other gases producing 
less specific effects are also included in this group. 
CARBON MONOXIDE (CO) 
Carbon monoxide is a colorless, odorless gas which is 
practically insoluble in water. As ordinarily encountered 
it arises from incomplete combustion,, of coal in stoves, for 
example, and is one of the chief ingredients of burning 
charcoal. It is also a constituent of illuminating gas. 
Owing to the fact that it is inodorous it may be insidious 
in its action, in many instances accidentally causing death, 
and it is a favorite method of suicide. It is probable that 
an atmosphere containing 0.5 per cent will cause death. 
Symptoms.-Although the sequence of symptoms which 
may be induced vary in individual cases the initial stage 
may be that of excitation. This is followed by intense 
headache, giddiness, throbbing of the temples, together 
36 POISONOUS GASES 
37 
with nausea and vomiting. At first there is a rise in blood 
pressure accompanied by a violent beating of the heart, 
later the pulse is very rapid but small. Breathing is 
deep and difficulty and as a result of deficient oxygena- 
tion there is diminished production of carbon dioxide. 
When the respiratory center is paralyzed respiration ceases. 
At times during the period of vomiting inspiration will 
draw the vomitus into the trachea producing death by 
suffocation. After a short time the individual loses con- 
sciousness and the period of unconsciousness may last for 
several days. Usually the muscular system is affected, 
a paralysis being observed which may be either general or 
may affect certain special groups of muscles. Sensation 
to pain may be absent for a long period.s There is redness 
of the face and loss of memory, vertigo, fainting, and the 
heart action, which is at first violent, may become weak 
and slow and stop/ The body temperature is subnormal 
and there may be an involuntary passage of excreta. A 
characteristic feature of carbon monoxide poisoning is 
the distribution of more or less extended patches of a bluish- 
red color on various parts of the skin. The inhalation of 
large amounts of carbon monoxide causes a very rapid 
onset of unconsciousness so that ordinarily the faces of 
those who have died are placid. The suddenness of loss 
of consciousness together with some of the other symptoms 
makes difficult the differentiation of this intoxication from 
that of the symptoms of drunkenness. Occasionally 
there are distinct deviations from this picture; for example, 
there may be tetanic strychnine-like convulsions and a 
continued condition of excitement in non-fatal cases which 
simulates alcohol poisoning. In still other cases tempo- 
rary mania may be seen. 
When the poisoning has been severe, but non-fatal, the 
symptoms are quite similar to those characteristic of 38 
TOXICOLOGY 
infectious fevers. There may be weakness of the intellect, 
thought may be irrational and disconnected, and insanity 
has been observed. There may be even softening of the 
brain and pneumonia frequently is a sequel. Other 
results of the intoxication are local inflammations, which 
may pass into gangrene, and hemorrhages, for example, in 
the lungs or in the brain. An apparent paralysis of 
the vasomotor mechanism, resulting in a distention of the 
capillaries, is evidenced by the red spots shown on the 
skin. Again there may be eruptions of the skin such as 
herpes or pemphigus. Generally there is glycosuria. 
Recovery in some cases is almost instantaneous with no 
memory on the part of the individual of his condition, 
whereas in other cases the recovery is very protracted. 
With chronic poisoning by carbon monoxide the symp- 
toms are mainly those of anemia. There is impaired 
digestion, the skin has a gray color, the tongue is coated, 
there is diminution of the intellectual powers,, and some- 
times convulsions may occur. There may be muscular 
weakness which is barely perceptible except by com- 
parative tests. 
In certain cases the acute symptoms entirely subside to 
be followed after some weeks by serious paralyses which 
often prove fatal. 
Poisonous Action.-The poisonous action of carbon 
monoxide is due to the fact that this gas is easily absorbed 
by the blood and enters into a definite chemical compound 
with the hemoglobin forming CO-hemoglobin, which is 
more stable than oxy-hemoglobin and hence prevents 
the hemoglobin from carrying oxygen to the tissues. The 
tissues, therefore, suffer, and particularly is this true of the 
nervous system. Lack of oxygen in the nerve structures for 
even a comparatively short period, less than five minutes, 
is capable of causing permanent damage to these structures. POISONOUS GASES 
39 
Fatal Dose.-The fatal dose of this gas is apparently 
quite variable. It has been shown that when the time 
of exposure in hours multiplied by the concentration of 
carbon monoxide in parts per ten thousand of air equals 
three there is no perceptible physiological effect; when it 
equals six there is a just perceptible effect; when it equals 
nine headache and nausea are induced; when it equals 
fifteen or more conditions are dangerous to life. From 
certain observations it would appear that about 0.8 of a 
gram of carbon monoxide is fatal to a man of seventy 
kilos. The rapidity of death depends more or less directly 
upon the quantity of gas which has been inhaled so that 
death has occurred in periods of a few hours to periods 
of several weeks. 
Post Mortem Appearances.-The characteristic features 
seen at autopsy are the clear rose-red or bluish-red colored 
patches usually of irregular form scattered over the 
anterior portions of the body and particularly the neck, 
face, chest, and abdomen. Since hydrocyanic acid also 
produces similar patches, in diagnosing, this fact must be 
kept in mind. As stated previously the cause of this 
phenomenon is due to the paralysis of the small arteries of 
the skin which, therefore, become injected with the carbon 
monoxide hemoglobin. The blood also has a character- 
istic reddish-blue color which is of diagnostic importance. 
Congestion of some of the internal organs is quite common 
and the membranes of the brain are strongly injected. 
Again the congestion may be localized in the lungs which 
may be more or less edematous. There is usually a right 
sided dilatation of the heart, and at times there may be 
areas of softening in the brain. 
Treatment of Carbon Monoxide Poisoning.-To be 
effective treatment of carbon monoxide poisoning should 
be carried out as soon as possible. The patient should be TOXICOLOGY 
40 
taken at once into the fresh air. Although the combina- 
tion between carbon monoxide and hemoglobin is much 
more stable than that between oxygen and hemoglobin 
nevertheless the carbon monoxide hemoglobin is gradually 
broken up and the carbon monoxide is breathed out. 
Moreover in carbon monoxide poisoning it has recently 
been shown that the blood alkali is greatly decreased. 
Oxygen deficiency induces excessive over-breathing, thus 
blowing off an abnormal amount of carbon dioxide from 
the blood. The result of this acapnial process is that the 
blood is left abnormally alkaline, and this alkalosis is 
gradually overcome by the passage of alkali out of the 
blood. Thus when a man is slowly asphyxiated by 
illuminating gas the oxygen deficiency, as the blood 
gradually takes up more and more carbon monoxide, 
induces such over-breathing that not only is the absorp- 
tion of the gas increased but an excessive amount of carbon 
dioxide is washed out of the tissues. As the normal 
stimulus of breathing is carbon dioxide a point is 
reached at which the lack of carbon dioxide results 
in failure of respiration. It is this condition that 
is chiefly responsible for the failure of breathing fre- 
quently observed after the victim of the gassing acci- 
dent is removed to fresh air. It is only as carbon dioxide 
reaccumulates in the blood that respiration gradually 
returns. It may then, for a time, be excessive because of 
the low alkali in the blood. In order to have correct 
respiration the alkali must be restored to the blood by the 
body itself. For this purpose and for the stimulation of 
respiration the subject is made to inhale oxygen containing 
ten per cent of carbon dioxide. If it is impossible to 
subject the patient to this treatment artificial respiration 
should be resorted to if necessary, or still better, the forced 
inhalation of oxygen. Transfusion of healthy blood has POISONOUS GASES 
41 
been strongly recommended and at times has proved very 
effective. The patient should be kept as warm as possible. 
Inasmuch as the carbon monoxide hemoglobin is decom- 
posed below the danger limit within an hour the carbon 
monoxide being practically eliminated in two to three 
hours, it is superfluous to use oxygen or transfusion after an 
hour has elapsed. If the coma continues longer this is due 
to the earlier injury of the nerve centers by the previous 
asphyxia. Once this injury has occurred it will not be 
helped by oxygen. Prognosis is bad if the coma has per- 
sisted for more than two days or if edema or cutaneous 
blebs have appeared. While recovery is usually slow the 
acute effects generally disappear within three hours. 
References 
Henderson: J.A.M.A., 1916, 67, p. 580. 
Henderson and Haggard: J. Ind. and Eng. Chem., 1922, 14, p. 
229; J.A.M.A., 1922, 79, p. 1137. 
Henderson and Haggard: J.A.M.A., 1923, 81, p. 385. 
HYDROGEN SULPHIDE (H2S) 
Hydrogen sulphide is a colorless, transparent gas which 
burns with a blue flame and possesses the odor of rotten 
eggs. It is soluble in water and is a common constituent 
of the atmosphere of sewers, cesspools, and of the products 
of putrefaction. In general, hydrogen sulphide is never 
met with outside of the chemists laboratory so that the 
few cases of poisoning by the use of the pure gas have been 
confined to laboratories. On the other- hand many cases 
of intoxication have occurred to men working in sewers or 
cleaning out cesspools. 
Symptoms.-In its pure form in sufficient concentration 
this gas is very rapidly fatal. In less concentrated form 
the symptoms produced are nausea, giddiness, cold skin, TOXICOLOGY 
42 
labored breathing, irregular action of the heart, great 
muscular weakness and headache. Death may be ushered 
in by coma or by convulsions. Even in very great dilu- 
tions symptoms may be experienced which are dizziness, 
headache and febrile symptoms which somewhat resemble 
those of typhoid fever. Continuous breathing of air 
contaminated with hydrogen sulphide induces chronic 
poisoning, the symptoms of which are conjunctivitis, 
headache, dyspepsia and anemia. Predisposition to boils 
has also been noticed. 
Poisonous Action.-It has been asserted that the toxic 
action of hydrogen sulphide is due to the formation of a 
relatively stable compound with hemoglobin, hydrogen 
sulphide hemoglobin which is not easily decomposed. 
According to this viewpoint the organs suffer from lack of 
oxygen and the symptoms induced result from tissue 
asphyxiation. Recently, however, it has been asserted 
that when the atmosphere containing hydrogen sulphide 
is inhaled no combination of the gas is formed with the 
hemoglobin of the blood nor is any appreciable amount of 
sodium sulphide formed in the plasma. In the absence 
of oxygen, blood plasma possesses the property of rapidly 
oxidizing hydrogen sulphide. These products of oxidation 
combine in part with the sodium of the plasma. Sodium 
sulphide is rapidly and completely hydrolyzed by blood or 
plasma. The absence of oxygen has no effect upon this 
process. If oxygen is prevent, however, a large part of the 
liberated hydrogen sulphide is oxidized. The reduction 
of blood by hydrogen sulphide or sodium sulphide is the 
result of withdrawal of oxygen from the corpuscles for the 
oxidation of the hydrogen sulphide. After inhalation of 
hydrogen sulphide, or the intravenous administration of 
sodium'sulphide, the sulphide in the blood exists only, as 
dissolved and as yet unoxidized hydrogen sulphide. POISONOUS GASES 
43 
The active physiological effects of sulphides are exerted 
by the hydrogen sulphide in the blood. During the 
administration of sulphide in any manner the hydrogen 
sulphide in solution in the blood is a factor in the reaction 
of oxidation. The rate of oxidation of hydrogen sulphide 
in the blood is such that in a comparatively short period 
many times the lethal amount of sodium sulphide may be 
administered intravenously to animals without any appar- 
ent effect. It is quite probable that hydrogen sulphide 
is not a cumulative poison. 
Fatal Dose.-Exact figures on the lethal dose of hydro- 
gen sulphide are lacking but one per cent in air is un- 
doubtedly destructive to life, and 0.02 per cent invariably 
produces toxic effects. The fatal period depends entirely 
upon the concentration of the gas. If the gas is in a suffi- 
cient concentration death is almost instantaneous. In 
more dilute concentration death may be delayed for 
variable periods. 
Post Mortem Appearances.-When death has been 
almost instantaneous the body shows little or no significant 
change. With slower poisoning the most frequent appear- 
ances are edema of the lungs, skin discoloration of the 
abdomen or of the skin of the whole body, and the offensive 
and characteristic odor from cavities and soft parts of the 
body. 
Treatment.-Treatment for intoxication of hydrogen 
sulphide consists in removing the patient to fresh air and 
if necessary the continuous employment of artificial 
respiration. The administration of stimulants is helpful. 
References 
Haggard: J. Biol. Chem., 1921, 49, p. 519. 
Haggard and Henderson: Am. J. Physiol., 1922, 61, p. 289. 44 
TOXICOLOGY 
HYDROCYANIC ACID (HCN) 
Hydrocyanic acid or Prussic acid is a colorless, trans- 
parent liquid, extremely volatile, intensely poisonous and 
possesses a peculiar peach blossom odor. This acid is 
known only in the laboratory except for a 0.2 per cent 
solution which is used at times medicinally. There are a 
number of salts of this acid, the cyanides particularly, 
potassium, sodium, mercury, silver, and gold being the 
best known. These are employed in commerce, some as 
constituents of insecticides, others in the process of electro- 
plating. All the cyanides possess very toxic properties 
and generally the poisoning results from the use of the salts 
rather than of the free acid. Usually either the acid or 
the salts are taken by mouth, but cases have been known 
where intoxication has resulted from inhalation of the 
gas itself. Hydrocyanic acid is also the product of numer- 
ous glucosides, the best known of which is amygdalin of 
the bitter almond. This glucoside when acted upon by an 
enzyme known as emulsin hydrolyzes amygdalin into 
glucose, hydrocyanic acid and oil of bitter almonds. This 
oil, benzaldehyde, is used as a perfume. Although 
instances of poisoning with benzaldehyde have been 
reported it is probable that these have been due to traces 
of the hydrocyanic acid contained in the oil. 
Hydrocyanic acid is rarely employed in criminal poison- 
ing because of its rapid action. Many instances of death 
by suicide, however, have been reported and such a death 
is made easy by the fact that the cyanides may be readily 
obtained. Whether taken by inhalation or by mouth 
intoxication may take two forms, namely, acute poisoning 
or chronic poisoning. 
Acute Poisoning. Symptoms.-The symptoms which 
come on very rapidly are chiefly dizziness, vertigo, palpi- 
tation, intense dyspnea, and unconsciousness. The salts, POISONOUS GASES 
45 
especially potassium and sodium, in a concentrated form 
produce corrosion of the mucous membranes with which 
they may come into contact producing vomiting. Respi- 
ration ceases previous to the heart. Heart action is very 
feeble and irregular, and the individual may go into 
violent convulsions which simulate those of epilepsy. 
Opisthotonos may be observed. The hands are usually 
clenched. The mortality is very high, being 95 per cent. 
If the patient survives for an hour recovery generally 
follows. 
Chronic Poisoning.-Repeated administration of small 
doses of cyanides or inhalation of small quantities of 
hydrocyanic acid lead to a chronic condition in which the 
symptoms are chiefly those of cachexia. There may be 
headache, dizziness, pallor, loss of appetite, and difficult 
respiration. Peripheral neuritis may also occur. 
Fatal Dose.-The smallest fatal dose of hydrocyanic 
acid is about dram (1.87 c.c. of a 2 per cent solution). 
In other words about 1 grain of hydrocyanic acid has 
caused death. In general the minimal fatal dose of 
hydrocyanic acid is about 2.4 grains. On the other hand 
recovery has followed much larger doses. 
Fatal Period.-Hydrocyanic acid enjoys the reputation 
of being one of the more powerful poisons, and this repu- 
tation is justified more by its extremely rapid action than 
by its toxic dose. In general, if fatal doses are taken death 
occurs within hour. On the other hand there have 
been cases reported in which the individuals did not die 
for a period of more than 3 hours. With the cyanides 
there are a few cases in which at least 24 hours have 
elapsed before death occurred. 
Poisonous Action.-Hydrocyanic acid must be regarded 
as a protoplasmic poison. It forms with hemoglobin a 
stable compound, cyanhemoglobin, thus depriving the TOXICOLOGY 
46 
tissues of oxygen and eventually leading to asphyxiation. 
The hydrocyanic acid in the body is changed to the 
sulpho-cyanides which are non-toxic and which are elimi- 
nated through the urine and saliva. 
Post Mortem Appearances.-The most characteristic 
feature is that various parts of the body, especially the 
dependent parts, and the finger nails, show bright red or 
purple patches. -The blood usually is coagulated and dark 
in color, and hemorrhages are found in various portions of 
the body such as the pleura and pericardium. If poison- 
ing has been induced by sodium or potassium cyanide 
characteristic lesions are found in the stomach which 
resemble those produced by the corrosive action of the 
strong alkalies. The odor of hydrocyanic acid persists 
in the body especially in the cavities for a considerable 
period. On the other hand if the body has undergone a 
considerable degree of putrefaction this odor may not be 
present. It is stated that the odor persists in the cavity of 
the skull for the longest period. In the post mortem 
examination of a suspected cyanide case, therefore, it 
would be desirable to open the skull cavity first. 
Treatment.-The treatment of hydrocyanic acid poison- 
ing must be prompt. In general the physician should 
wash out the stomach until the wash water no longer 
contains the odor of hydrocyanic acid. To this wash 
water may be added chemical antidotes such as the oxidiz- 
ing agents, namely, hydrogen peroxide or potassium per- 
manganate. Should a stomach tube not be available 
vomiting should be induced. Ordinarily, however, the 
absorption of the poison is so rapid and the effects so 
prompt that antidotes are usually ineffective. It has 
been suggested that the patient should be bled profusely, 
the blood being replaced by double the volume of salt 
solution. Inasmuch as the primary trouble is in the blood POISONOUS GASES 
47 
the last type of treatment deserves serious consideration. 
Attempts have also been made to transform the cyanide 
into the sulphocyanide by either hypodermic or intraven- 
ous injections of sodium thiosulphate. The sympto- 
matic treatment consists essentially in supporting the 
respiration. Artificial respiration should be begun at 
once and maintained so long as the heart beats. Counter- 
irritation and general stimulants may also be used. 
References 
Haskins: Bost. Med. and Surg. J., 1870, 82, p. 21. 
Hunt: Arch. int. Pharmacodyn, et de Ther., 1904, 12, p. 447. 
Flury and Heubaer: Biochem. Z., 1919, 95, p. 249. 
CARBON DIOXIDE (CO2) 
Carbon dioxide is a colorless gas with a slightly acid 
taste and smell, which does not burn and will not support 
combustion. It produces suffocation and under the names 
of "black damp" and "choke damp" it is dreaded in 
mines because of the possibility of its producing suffoca- 
tion. Although carbon dioxide is constantly in the 
atmosphere, even country air containing about 4 parts in 
10,000, it is only when it is in the air in excess' as in caves, 
wells, mines, vats, and badly ventilated rooms to the pro- 
portion of approximately 7 per cent that it can be said 
to have detrimental effects. In the atmosphere of rooms 
poorly ventilated discomfort is produced when about 0.1 
per cent of carbon dioxide is present in the air. If 1 per 
cent is present there is much greater discomfort and head- 
ache, dizziness and nausea may be caused by 3 per cent. 
The exact toxic concentration of carbon dioxide is not 
definite but it may be stated that an 8^ per cent by 
volume of carbon dioxide causes distinct dyspnea and 
rise of blood pressure. The untoward symptoms increase 
up to 15 per cent but are apparently not dangerous to men. 48 
TOXICOLOGY 
When 25 and 30 per cent is reached the symptoms are those 
of depression accompanied by diminished respiration, fall 
of blood pressure and coma. Much of the discomfort 
which is experienced in poorly ventilated rooms cannot be 
laid to the content of carbon dioxide in the atmosphere but 
to other factors such as increased temperatures, odors, etc., 
which produce psychic effects. 
Symptoms.-According to the degree of concentration of 
the gas inspired the symptoms may be either sudden or 
almost imperceptible. If the pure gas is breathed suffo- 
cation may be caused by a spasm of the glottis, insensi- 
bility results and death follows from apnea unless the 
patient is taken out of the atmosphere of the carbon dioxide. 
When the amount is smaller there may be cyanosis and 
dyspnea on exertion. Profuse perspiration and nausea are 
common. When a fatal concentration of gas has been 
breathed the symptoms are those of giddiness, loss of 
muscular power, sleepiness, pressure in the temples and 
singing in the ears. The body collapses, respiration stops, 
convulsions may ensue, the action of the heart ceases, 
sensibility is lost, and the limbs become flaccid, the 
countenance is livid, and death usually occurs without a 
struggle. 
Poisonous Action.-In carbon dioxide poisoning death 
is ascribed to excessive stimulation of the cerebral spinal 
system, producing asphyxia. 
Fatal Period.-The fatal period is indefinite. 
Post Mortem Appearances.-The post mortem appear- 
ances are those of typical asphyxia. There is nothing 
characteristic in the general appearance. Usually there 
is right-sided dilatation with the vessels of the lungs 
and brain congested. 
Treatment.-Treatment consists in inducing breathing, 
artificial respiration and administration of oxygen with POISONOUS GASES 
49 
stimulation such as application of cold and heat, friction, 
etc. The body temperature should be maintained. 
References 
Henderson: Trans. 15th International Conference of Hygiene, 
Vol. 2, No. 2, p. 622. 
Winslow: Am J. Public Health, 1917, 7, p. 827. 
NITRIC OXIDE (NO) 
Nitric oxide is a colorless gas which is feebly soluble and 
neither burns nor supports combustion. If brought into 
contact with oxygen of the air, brown-red fumes are formed 
which condense to a yellow liquid. In the manufacture of 
various products such as gun cotton, oil of vitriol, oxalic 
acid, and in metal working of various sorts, workmen 
are exposed to the fumes of this gas, which may produce 
effects of physiological importance. 
Symptoms.-In acute poisoning there is immediate 
dyspnea, coughing and cyanosis, fainting and diarrhoea 
and collapse may occur with death within 40 hours. If the 
poisoning is slight the symptoms may be delayed and are 
of a slightly different character. Headache, air hunger, 
thirst, and difficult breathing are quite characteristic. 
The body may be in a cold perspiration, the face anxious, 
the eye balls protruded, and there may be intervals of 
spasmodic coughing followed by vomiting. 
Poisonous Action.-The blood is thick and viscid 
probably owing to a change in its concentration. Inas- 
much as this is an irritating gas similar in its effects to 
those induced by the war gases, it is quite probable that 
death is provoked by the same type of mechanism (see 
page 60). 
Post Mortem Appearances.-The post mortem appear- 
ances are confined to the respiratory tract, inflamma- 50 
TOXICOLOGY 
tion being very prominent, together with edema of the 
lungs. 
Treatment.-Treatment is that followed in war gas 
poisoning (see page 63). 
NITROUS OXIDE (NzO) 
Nitrous oxide or laughing gas is colorless, possessing a 
sweet taste and smell, and supporting combustion. 
Symptoms.-Nitrous oxide is employed chiefly for its 
anesthetic effect but at times it assumes physiological 
importance. In the absence of oxygen asphyxia results. 
Post Mortem Appearances.-There are no characteristic 
changes to be observed. 
Treatment.-Treatment consists in the administration 
of fresh air or oxygen or artificial respiration if necessary, 
and stimulants. 
SULPHUR DIOXIDE (SO2) 
Sulphur dioxide is a colorless gas with a characteristic 
odor and taste reminding one of the odor of sulphur 
matches. It does not burn and is formed when sulphur 
burns. Sulphur dioxide is toxic to both plant and animal 
life and is a favorite method for fumigation in order to 
rid rooms of bugs, and fleas, or mosquitos, and bacteria. 
It is also used as a preservative of foods either as the gas 
or in the form of its salts, the sulphites and bisulphites 
(see page 255). 
Symptoms.-The first symptoms are those of suffoca- 
tion with spasms of the glottis, and irritation of the nose, 
trachea and bronchi, resulting in sneezing and coughing. 
A certain degree of habituation may be induced in both 
man and animals. Other effects produced are opacity of 
the cornea, dyspnea, cyanosis, and sometimes convulsions. POISONOUS GASES 
51 
If the poison is taken internally catarrh of the stomach and 
chronic sulphuric acid poisoning may result. 
Poisonous Action.-The primary actions are upon the 
respiratory tract producing either a catarrhal or an 
edematous condition. 
Post Mortem Appearances.-The post mortem appear- 
ances are those characteristic of asphyxia. The respira- 
tory tract presents evidence of an existing inflammatory 
reaction and the lungs at times may be either slightly or 
markedly edematous. 
Treatment.-For the effects upon the gastro-intestinal 
tract mild alkalies may be administered and lavage of the 
stomach should be carried out. For the systemic effects 
rest in bed and warmth are essential. If evidence of 
edema arises the treatment should follow that of the war 
gases (see page 63). 
ACETYLENE (C2H2) 
Acetylene has an odor of geranium and burns with a 
white flame. When mixed with air it is explosive. It is 
a product of incomplete combustion and is formed whenever 
lamps or gas-jets burn without a sufficient air supply. 
Symptoms.-In cases of poisoning there is restlessness, 
hallucinations, laughter. This period of excitement leads 
finally into deep sleep. These symptoms are associated 
with vomiting, cyanosis, small irregular pulse and dilated 
pupils. On coming out of the comatose condition there is 
dizziness, headache, restlessness and depression for a period 
of several hours. Acetylene is not a strong poison. 
Upon continuous exposure it produces edema, malnutrition, 
and nervous symptoms. So far as the blood is concerned 
it acts as an indifferent gas. 
Treatment.-Treatments consists in the administration 
of oxygen. 52 
TOXICOLOGY 
GASOLINE FUMES 
With the increase in the use of automobiles a relatively 
new hazard for life has been introduced. The exhaust 
gas of automobiles is extremely poisonous. Even when 
entirely odorless, colorless, and free from soot it is much 
more poisonous than any other ordinary form of smoke. 
Therefore neither smoke nor smell is a reliable index of 
the toxicity of exhaust gas. This gas owes its toxicity for 
the most part to its content in carbon monoxide, and the 
intoxication by the fumes from incomplete combustion 
of gas is due to the content of carbon monoxide. . It has 
been demonstrated recently that the quantity of carbon 
monoxide in ordinary city streets is considerable and 
offers a menace to general health. Moreover it has been 
shown that this low concentration causes and intensifies 
the development of fatigue. 
Every winter there occur throughout the country many 
deaths in private garages from the exhaust gas of auto- 
mobiles. Henderson has shown that even a small car 
produces i and a. large car or truck 2 or 3 cubic feet of 
carbon monoxide per minute. When the engine is run 
idle on a cold day with the garage doors closed the atmos- 
phere of a space large enough to hold a car is contaminated 
to a very dangerous extent, that is, 25 parts of carbon mon- 
oxide in 10,000 of air, within 5 minutes, and to a rapidly 
fatal extent in 10 minutes. The danger is insidious. The 
first indication that the victim receives is that his legs give 
way under him, he lies helpless until consciousness ceases 
a few minutes later, and in the accumulating gas death 
by asphyxia follows unless chance brings help within a short 
period thereafter. There is sufficient oxygen in the air 
for an engine to continue to run long after it has produced 
a fatal concentration of carbon monoxide. Although 
conditions are less threatening to life in public garages POISONOUS GASES 
53 
they are nevertheless more continuously dangerous to 
health. Inasmuch as very few garages have any system 
of ventilation other than that of simple diffusion of the 
gas outward and of air inward carbon monoxide headache 
is an almost daily occurrence with many of the employees 
in the larger garages. In repair shops the conditions are 
much worse inasmuch as the employees suffer from 
headache and nausea. These subacute effects are detri- 
mental to general health and should be recognized. 
For the general symptoms and treatment relative to 
carbon monoxide poisoning see Carbon Monoxide Poison- 
ing, page 36. 
Reference 
Henderson and Haggard: J.A.M.A., 1923, 81, p. 385. 
ETHYLENE (C2H4) 
Quite recently this gas has come into use as an anesthetic. 
It is a colorless, odorless gas constituting one of the com- 
ponents of ordinary illuminating gas to the extent of 4 
per cent. Ethylene burns and also supports combustion. 
It is extremely toxic to flowering plants but to animals and 
man its chief effect is that of general anesthesia. It pro- 
duces its anesthetic effects by existing in the blood in a 
state of physical solution rather than by combination with 
any of the constituents of the blood. The pure gas itself 
not only produces anesthesia but may give evidence of 
asphyxial symptoms. These, however, can be removed 
by the addition of oxygen without losing the narcotic 
effect from the ethylene itself. 
Ethylene apparently has a direct action on the nervous 
system, a concentration of 90 per cent maintaining the 
higher centers in a state of insensibility. The motor 
reflexes are also abolished at this concentration. 54 
TOXICOLOGY 
Reference 
Luckhardt and Carter: J.A.M.A., 1923, 80, pp. 765 and 1440. 
ARSENIURETED HYDROGEN (Arsin) (AsH3) 
Arseniureted hydrogen is a colorless gas possessing the 
odor of garlic. It burns with a bluish white flame, and 
condenses upon a cold body such as a porcelain plate. 
Symptoms.--The gas is extremely toxic, being one of 
the most deadly of the compounds of arsenic. When small 
quantities are breathed the respiration is slightly quick- 
ened with dryness and burning in the throat, temperature 
is normal, and the pulse rate is increased. If the arsenical 
atmosphere continues, nausea, shivering, dizziness, and 
prostration occur, together with chills of more or less 
severity, and pain in the kidneys. There may be jaundice, 
the blood becoming dark colored, and the urine may 
possess a brown or reddish color and perhaps be entirely 
suppressed. The conjunctiva and skin become yellow and 
later deepen to a bronze or copper color. The character- 
istic features by poisoning by arseniureted hydrogen are 
lumbar pain, icterus and hemoglobinuria. Arseniureted 
hydrogen besides producing hemolysis causes narcosis and 
paralysis. Possible contact with arseniureted hydrogen 
is in chemical laboratories and on board boats. In the 
latter instance deaths have occurred from ships carrying 
cargoes of electrolytic ferro silicon containing calcium 
phosphide, and also batteries of submarines, the 
arseniureted hydrogen being generated from the lead 
plates which may contain as much as 0.2 per cent arsenic. 
Fatal Dose.-Little or nothing is known relative to the 
fatal dose for man of arseniureted hydrogen. On the other 
hand it has been shown that 3^ c.c. per liter of air is 
rapidly fatal to mammals. POISONOUS GASES 
55 
Fatal Period.-Death occurs in a relatively short time, 
usually within 24 hours, although instances of death, at 
a later period up to 5 or 6 days have been reported. 
Post Mortem Appearances.-The characteristic post 
mortem appearances are those due to the condition of 
icterus, the skin assuming a dirty yellow or bronzed 
discoloration, the kidneys are brown, enlarged, and 
slightly congested, the mucous membrane of the stomach 
is slate colored or yellow. 
Treatment.-Inhalation of oxygen. It has also been 
suggested that bleeding followed by transfusion of blood is 
of great value. Other symptoms should be treated as 
they arise. The channels of excretion should be 
stimulated if possible. 
PHOSPHORETTED HYDROGEN (Phosphine) (PH3) 
Phosphoretted hydrogen is a colorless gas which is 
sparingly soluble and burns with a greenish flame, or if 
dry and insufficiently supplied with air the flame is white. 
This is an extremely toxic gas, although rarely do fatal 
accidents occur from it. 
Symptoms.-The symptoms are irritation of the skin, 
changed respiration and convulsions. 
Post Mortem Appearances.-The most typical of post 
mortem appearances are anemia of the brain, engorgement 
of the lungs, liver, and heart, with venous blood. 
WAR GASES 
CHLORINE, PHOSGENE, CHLORPICRIN, MUSTARD GAS, 
PALITE, SUPERPALITE 
Chlorine is a greenish, yellow gas, somewhat soluble 
in water, two and one-half times as heavy as air, and con- 
denses to a yellow liquid, which if perfectly dry, can be 
stored in steel cylinders. 56 
TOXICOLOGY 
Phosgene or carbonyl chloride (COC12) is a colorless 
gas with a peculiar odor described as that of "musty hay" 
by which it may be recognized. Phosgene was first 
prepared by exposing a mixture of equal parts of carbon 
monoxide and chlorine to sunlight. The name phosgene 
was given to the gas to suggest the part played by light in 
its formation. Phosgene is a liquid at a temperature of 
8°C. The toxic action of phosgene is slower than that of 
chlorine probably because to produce its effects it must 
undergo hydrolysis. 
Chlorpicrin or nitrochloroform (CCI3NO2) is a color- 
less liquid almost soluble in water, but soluble in alcohol. 
The vapor of chlorpicrin is almost six times as heavy as 
air. It is not as poisonous as some of the other gases but 
it was used chiefly because it has a specific action upon the 
vomiting center. It was used with other gases because it 
produced nausea and vomiting. This forced the removal 
of the masks from the soldiers at which time the enemy was 
overcome by the more poisonous gases which had been 
fired. In its action it stands mid-way between chlorine 
and phosgene, being slower in its effects than chlorine, 
but more rapid than phosgene. 
Mustard gas or dichlorethylsulphide (C2H4C1)2S, or 
yperite is a heavy oily fluid, sinking below water and not 
mixing with it, of a neutral reaction, having a sweet, 
ethereal odor and producing extensive burns in relatively 
small concentrations. 
PALITE (ClCOOCHsCl) AND SUPERPALITE (CICOOCh) 
OR DIPHOSGENE 
These two gases belong to the same group as phosgene 
and were extensively used in shells. They are both liquids 
and inasmuch as their physiological action is similar to 
phosgene will not be considered separately. POISONOUS GASES 
57 
Post Mortem Appearances. Chlorine.-From the 
pathological aspect chlorine produces injury to the organ- 
ism by causing immediate death of the epithelium lining 
the upper respiratory tract. Areas of focal necrosis in 
the lung itself are attributed to the direct action of chlorine 
on parts of the lung not protected by bronchiolar spasm. 
The destruction of the epithelium of the respiratory tract 
removes the normal protective mechanism and allows 
pathogenic bacteria from the mouth to find their way into 
the injured bronchioles within a very short period, result- 
ing in a pneumonia, lobar, lobular or necrotizing-the type 
depending on the organism concerned. The irritant action 
of chlorine results in a bronchiolar spasm which eventually 
causes an acute emphysema or atelectasis. Edema of 
the lungs, trachea, and bronchi is the most striking feature 
of acute death from chlorine gassing. It is probably 
brought about by the direct action of the gas which so 
damages the bronchi and alveoli as to render the adjacent 
capillary wall permeable. The coagulation of the plasma 
as it passes out through the alveolar wall leads to the 
deposition of fibrin in this situation which must thus 
seriously interfere with the inflow of blood through the 
lung, thus putting a strain on the right side of the heart. 
Phosgene.-With phosgene gassing the lesions seen at 
necropsy vary according to the length of time of survival 
after exposure to the gas. At first, a severe pulmonary 
edema is associated with extreme congestion and with an 
inflammatory exudation of fibrin and leucocytes which is 
most marked in and around the finer bronchioles and which 
spreads through the lung tissue to a variable extent. A 
typical lobular or pseudolobar pneumonia is the result. 
The pneumonia is frequently complicated by a necrotiza- 
tion of the wall of the bronchus, which may involve the 
adjacent alveoli to form abscesses. 58 
TOXICOLOGY 
The character of the phosgene lesion is explained by the 
localization of the action of the gas on the air tubes. The 
epithelium of the trachea and larger bronchi is not dam- 
aged, while that of the smaller bronchi and bronchioles is 
seriously injured, the more distal portions suffering most. 
In addition to the changes in the mucosa, the bronchi 
also show pathological contractions and distortions which 
result in the more or less complete obliteration of the 
lumen. These, in turn, lead to mechanical disturbances 
in the air sacs resulting in a chronic condition of atelectasis 
or emphysema. 
Chlorpicrin.-Chlorpicrin injures the epithelium of the 
entire respiratory tract, but all portions of the tract are 
not equally affected. The trachea and largest bronchi, 
though irritated, suffer only transient injury. The 
medium size and small bronchi are the most affected. 
There is a uniform and widespread damage of the alveolar 
walls which, however, is not severe enough to lead to 
necrosis. 
The overwhelming edema of the lungs rapidly follows 
exposure to Ihe lethal concentration of the gas. In 
extreme cases practically every alveolus is filled with fluid. 
In addition to the fluid in the lung itself there is also 
marked edema of the mediastinal tissues and pleura 
which is even more striking than in phosgene or chlorine 
gassing. Abscess formation, pleurisy, fibrinous or puru- 
lent, and organizing pneumonia are common complica- 
tions. Focal atlectatic emphysematous patches remain 
as prominent gross evidence of the gas injury. 
Mustard Gas.-Mustard gas differs from the other war 
gases thus far considered in that its effects are not confined 
to the respiratory tract. Very important actions on other 
parts of the body especially the skin are of great signifi- 
cance. At first the exposed skin reddens, becomes swollen POISONOUS GASES 
59 
and itches, later this skin erythema develops into blisters, 
sometimes of large size. The mustard burns resemble 
X-ray and drug dermatitis rather than simple heat burns. 
In general mustard burns are imperceptible when first 
received and they remain so until the blisters break. The 
lesions heal very slowly, due, perhaps, to injury of 
the blood vessels. They generally become more or less 
infected although only superficially. After three days 
exposure the blisters begin to become painful especially 
on contact with air or mechanical contact of any sort. 
The wound may remain painful for 3 or 4 weeks or it may 
take on a gangrenous form. Healing occurs after 5 to 7 
weeks by cauterization. Different individuals have a 
varying susceptibility to mustard gas. Negroes are not- 
ably tolerant, and moisture of the skin and prespiration 
increase the susceptibility. 
Symptoms.-Exposure to the gases elicits reactions 
which are slightly different with the different gases. With 
chlorine there is at first general excitement as indicated by 
restlessness, urination, irritation of the eyes, sneezing, 
copious salivation, retching and vomiting. This is 
followed by labored respiration with a distinct dyspnoea. 
The respiratory distress increases until eventually death 
may occur from apparent asphyxia. 
Very small doses of phosgene cause coughing, watering 
of the eyes and intense dyspnoea. The first symptoms are 
dizziness and cyanosis on exertion. It usually takes 
several hours for the symptoms to develop and in the inter- 
val there may be no sign of danger. Death is by failure of 
the respiration. 
Chlorpicrin produces coughing, nausea, vomiting, and in 
large quantity unconsciousness. Secondary effects are 
bronchitis, shortness of breath, a weak irregular heart and 
gastritis. A comparison of the three gases shows that 60 
TOXICOLOGY 
chlorine has a very strong irritating action, the individual 
becoming excited and in evident distress. With chlor- 
picrin the character of the reactions produced are very 
similar to those of chlorine except that they are less 
pronounced. Phosgene on the other hand appears to 
cause little or no immediate distress. All these gases 
have as their most prominent feature the development of 
an acute intensive pulmonary edema. 
With mustard gas an interval of 4 to 16 hours of freedom 
from distress exists between the actual gassing and the 
onset of symptoms. There may be a conjunctivitis, 
leucocytosis, bronchitis, and skin burns. The principal 
complications are early pulmonary edema and relatively 
late bronchopneumonia. 
Poisonous Action.-With the exception of mustard 
gas the action of these poisons is confined entirely to the 
mucous membrane of the respiratory tract. An intense 
inflammatory reaction is induced which is responsible for 
the early intensive pulmonary edema. Edema of the lungs 
causes a very marked concentration of the blood which in 
turn results in a failing circulation resulting in an inability 
to proper oxygenation of the tissues, causing death. 
Body temperature falls very distinctly and there is usually 
a right sided dilatation of the heart. Mustard gas acts 
in a similar manner but there is evidence that in addition 
some of the gas is absorbed and produces additional 
effects. 
On the basis of alterations in blood concentration quite 
definite stages in gas poisoning may be outlined. These 
stages stand out most clearly with phosgene, and there- 
fore the picture presented by this gas will be considered 
first. 
First Stage.-In the first few hours (5 to 8) after 
phosgene poisoning there is a notable decrease in the con- POISONOUS GASES 
61 
centration of the blood. The decrease occurs rapidly and 
then the blood gradually tends to assume the normal 
concentration. Accompanying the decreased concentra- 
tion of the blood there is a sharp drop in the chlorides of 
the blood and a marked increase in the chloride and water 
content of the lungs. The chlorides of the urine increase 
immediately after gassing, reaching a maximum between 
the third and seventh hours, then decreasing. The heart 
beat is distinctly slowed at first with a tendency to regain 
the normal or be somewhat above the normal before this 
period is over. The immediate effect on the respiration 
is a distinct increase in the rate. Oxygen capacity of the 
blood, the number of erythrocytes and hemoglobin 
follow a curve parallel with that of the changes in the 
blood throughout all stages of phosgene poisoning. The 
oxygen content of both arterial and venous blood decreases 
significantly. The saturation of hemoglobin with oxygen 
decreases somewhat. In general the decrease is more 
marked in the venous than in the arterial blood. 
Second Stage.-The period of blood dilution is followed 
by an interval during which the blood rapidly becomes 
concentrated to a point far above the normal value and 
remains near this level for several hours. In this stage 
the heart may be markedly decreased in size. During the 
period of increased blood concentration the chlorides of 
the blood show a tendency to regain the normal. The 
water and chloride content of the lungs reach a maximum 
and then gradually fall. The heart beat and respiration 
are both accelerated. The temperature drops to a degree 
or more below normal. Most of the fatalities occur in 
this stage. The oxygen content of arterial blood remains 
fairly stationary at a nearly normal value, whereas that of 
venous blood falls rapidly to a very low level. The satura- 
tion of hemoglobin with oxygen decreases rapidly in both 62 
TOXICOLOGY 
arterial and venous blood, but the fall is greater in venous 
blood. 
Third Stage-After the period of increased concentra- 
tion the blood gradually becomes more dilute until it is 
slightly under the normal value which is eventually gained, 
and recovery follows. The chlorides of the blood gradu- 
ally tend to regain the normal level. The chloride and 
water content of the lungs follows a similar course. The 
temperature rises to normal or above if recovery is to occur, 
whereas if death takes place during this period the heart 
beat and respiration rise but the temperature steadily 
falls. The oxygen content of arterial and venous blood 
tends to regain the normal. Chloride excretion by the 
kidney is markedly decreased but later is much augmented. 
It is generally assumed that the cause of death in gas 
poisoning is due directly to edema of the lungs aided, of 
course, by the accompanying congestion. It has been 
stated that death is caused by an individual literally drown- 
ing in the water of his lungs. The quantity of water may 
reach as high as a liter or more and such a conception as 
the cause of death is quite obvious. The most obvious 
condition, other than edema, which could lead to death is 
the concentration of the blood. It is evident that edema 
and blood concentration are closely associated. Edema 
is assuredly the cause for blood concentration and thus 
indirectly, at least, brings about death, but it would appear 
that blood concentration is much more likely to produce 
death than is the presence of fluid in the lungs. It has been 
conceded, however, that blood concentration is immediately 
responsible for death in these cases. Blood concentration 
means a failing circulation, an inefficient oxygen carrier, 
oxygen starvation of the tissues, fall of temperature, and 
finally suspension of vital activities. The whole aim of 
treatment in gas poisoning has been to prevent blood POISONOUS GASES 
63 
concentration or else/restore it to a level more nearly 
normal. Restoration of blood to a normal concentration 
permits survival even though an extensive edema exists. 
Treatment.-The principles of treatment of gases thus 
far considered having an effect upon the respiratory tract 
are very simple, venesection when the blood is diluted 
and infusion of salt solution during the initial period of 
blood concentration. Venesection tends to diminish the 
degree and extent of dilution. Infusion of salt solution 
tends to keep the blood concentration at a level where it 
is possible to maintain an approximately efficient circula- 
tion. Attempts to change the blood concentration are of 
little permanent value unless measures are taken in the 
early period after gassing. Once a highly concentrated 
blood has been assumed treatment is of little avail. 
The time and type of treatment is determined by follow- 
ing changes in the concentration of the blood by hemo- 
globin estimations. Oxygen alone is of little value in gas 
poisoning since theoretically, at least, there is not a defi- 
ciency of oxygen in the arterial blood, and the deficiency in 
the venous blood is due to the inability of the circulatory 
organs to push the concentrated fluid rapidly through the 
capillaries. If, however, the circulation is improved by 
venesection and salt infusion the addition of oxygen is of 
distinct value. 
The treatment of skin burns from mustard gas poisoning 
is most successful when the irritation is treated immedi- 
ately. The successful treatment of the rashes tends to 
abort the more severe burns. The skin should be scrubbed 
with kerosene, soap and hot water. The exposed part 
should be immersed for i or 2 hours in Dakin's solution of 
chlorinated soda or compresses may be applied to the 
affected part. A 1 per cent solution of alum or alumi- 
num acetate may be substituted for Dakin's solution 64 
TOXICOLOGY 
which may be too painful. Petrolatum dressings may be 
alternated with the baths. 
References 
Underhill: The Lethal War Gases; Physiology and Experimental 
Treatment, Yale University Press, 1920; J.A.M.A., 1919, 73, 
p. 686; Harvey Lectures, 1917-19, p. 234, Lippincott, Phila- 
delphia. 
Winternitz: Collected Studies on the Pathology of War Gas 
Poisoning, Yale University Press, 1920. 
Marshall, E. K.: J.A.M.A., 1919, 73, p. 684. 
Warthin and Weller: J. Lab. & Clin. Med., 1918, 3, p. 447; 1919, 
4, p. 265; 1919, 4, p. 833. 
IODINE (I) 
It is very unusual for iodine to be employed as a poison 
with criminal intent owing to the difficulty of disguising 
its color. It has, however, been used by suicides much 
more commonly and accidental poisoning is not rare. 
Iodine crystallizes in dark gray scales possessing an 
unpleasant taste and a characteristic odor. Even at 
ordinary temperature it gives off an invisible vapor which 
is very irritating to the nose and eyes. It becomes a liquid 
if heated to 2 2o°F. and then evaporates in violet colored 
fumes. It is soluble in water with great difficulty, but 
dissolves readily in alcohol, ether, carbon bisulphide and in 
water containing potassium iodide. Iodine itself is almost 
exclusively used externally as the tincture and the lini- 
ment. In strong solution iodine may act as a corrosive 
even when applied to the skin, producing typical blisters 
and burns. 
Symptoms.-The symptoms produced by iodine are 
those characteristic of irritants in general. Taken by 
mouth pain results there and follows its passage down the 
alimentary canal. Subsequently there is vomiting, purg- POISONOUS GASES 
65 
ing, extreme thirst, fainting attacks, and collapse. It 
may also be absorbed from raw surfaces and cause milder 
symptoms, such as headache, dizziness and gastric irrita- 
bility. It is excreted by way of the kidneys and may so 
involve these organs as to cause suppression of urine. As 
with chlorine and other pulmonary irritants its inhalation 
leads to inflammation of the lungs and pulmonary edema. 
Fatal Dose.-The fatal dose is about one fluid dram of 
the tincture. On the other hand, recovery has followed 
after taking one fluid ounce. 
Fatal Period.-The fatal period varies from i to 6 days. 
Post Mortem Appearances.-The post mortem appear- 
ances are those common to irritant poisons, namely, in- 
flammation and disorganization of mucous surfaces. 
Treatment.-Treatment should be aimed to dilute the 
stomach contents by large volumes of water, emptying 
this viscus either by inducing vomiting or by use of the 
stomach pump. Starch is the specific antidote and it 
should be given in the form of a decoction of ordinary 
laundry starch, boiled rice, barley water, etc., so long 
as it is colored blue by the stomach contents. 
For treatment of poisoning by fumes see that given for 
war gases under "Gaseous Poisons," page 63. 
Reference 
Luckhardt, Koch, Schroeder, and Wieland: J. Pharm. and 
Exp. Therap., 1920, 15, p. 1. 
IODIDES 
The employment of iodides, usually in the form of 
sodium or potassium iodide, may produce local irritation 
in the stomach and evidences of irritative reactions on the 
skin and mucous membranes. 66 
TOXICOLOGY 
Symptoms.-These reactions partake of the nature of 
rashes, or of coryza, headache, bronchitis, laryngitis, and 
conjunctivitis. Stomatitis, parotitis and anorexia may 
occur but much less commonly. In addition to the general 
irritation of the mucous membranes of the mouth, throat 
and trachea there may be salivation with general 
malaise. The symptoms referred to above lead the 
patient to believe he has influenza. At times the laryngi- 
tis may be so severe that edema of the glottis occurs. 
The skin lesions consist of irregularly scattered pimples, 
the chief sites being the face, shoulders, neck and back. 
In addition to this acne-like appearance "iodism" may 
manifest itself in the form of furuncles, erythema, purpura, 
urticaria and vesication, all of which may be accompanied 
by fever. The more serious eruptions usually occur in 
patients with a lowered vitality and are especially promi- 
nent in chronic nephritis, perhaps owing to inability to 
excrete iodides which in the normal individual are 
promptly eliminated. 
Usually the less severe skin eruptions are produced by 
smaller doses and they sometimes disappear when larger 
doses are given. 
Chronic iodism is characterized by anuria, emaciation, 
nervous irritability, tachycardia, and loss of sexual 
power. In general, even though definite symptoms are 
not in evidence large quantities, or long continued use of 
iodides, tend to lessen body tone and to depress the spirits. 
Susceptibility to iodide action varies greatly. In some 
patients the symptoms appear in a few hours even after 
a small dose; in others they are manifest only after long 
continued use. The reactions characteristically induced 
are not confined to iodides but may be caused by any 
iodine compound. Thus iodoform may produce the 
symptoms of iodism. It is probable, however, that these POISONOUS GASES 
67 
reactions occur only after dissociation of the compound 
with liberation of the iodide ion. Formerly the skin 
symptoms were referred to excretion of the drug by the 
sebaceous gland, the view being that free iodine was 
liberated by the fatty acids of the sebaceous secretions. 
This idea, however, is erroneous and similar symptoms may 
be induced by the sulphocyanides which in dissociation 
fail to liberate an irritative ion. 
Treatment of lodism.-The drug should be discon- 
tinued. Great cleanliness, particularly of the mouth, the 
administration of alkalies and arsenic, are indicated. The 
catarrhal symptoms may be cleared up in one or two days 
by the use of calcium lactate in doses of 4 grams per day 
but the calcium treatment should not be prolonged. 
IODOFORM (CHI3) 
Iodoform may produce general intoxication when applied 
as a surgical dressing over a large area. Less frequently 
it has caused poisoning by internal administration. 
Iodoform is a local irritant and may cause a dermatitis or a 
pustular rash. Iodoform is not excreted as such from the 
body. Instead it reappears in the urine as the iodide or 
the iodate and as other unknown compounds. 
Iodoform occurs in light yellow crystals possessing a 
penetrating and unpleasant odor and taste. It is insolu- 
ble in water, but is soluble in alcohol, ether, glycerol and 
oils. It melts at ii9°C. and volatilizes with steam. 
Symptoms.-The symptoms of iodoform poisoning may 
be of three types (a) gastro-intestinal disturbances as 
nausea and vomiting, (b) cerebral excitement or delirium, 
or (c) cerebral depression with melancholia. Death is 
caused by paralysis of the central nervous system. There 
may be great lassitude and weakness, hallucinations, 68 
TOXICOLOGY 
diminished reflexes, mental confusion, light convulsions 
and coma. The pulse is usually very rapid and there may 
be a high temperature. In some cases cerebral excite- 
ment may be entirely lacking, the only symptoms being 
those of cerebral depression-stupor and collapse. 
Fatal Dose.-Death has been caused by doses of 1.25 
grams to 2.0 grams of iodoform and recovery has followed 
the taking of more than 7 grams. 
Fatal Period.-Death may be a matter of less than 24 
hours or be delayed for several weeks. This variability 
depends upon the size of the dose and upon the manner of 
application. 
Post Mortem Appearances.-The characteristic patho- 
logical picture presented by iodoform poisoning is fatty 
degeneration of the liver, heart and kidneys. Edema of 
the lungs, acute nephritis and congestion of the meninges 
have also been observed. 
Treatment.--If poisoning has occurred from external 
application the treatment should be stopped. The 
strength of the patient should be sustained and according 
to whether there is cerebral stimulation or depression 
stimulants or sedatives should be administered. For 
specific treatment potassium iodide has been recom- 
mended. Subcutaneous or intravenous injection of large 
volumes of physiological salt solution are said to be of 
particular value. Sodium bicarbonate is an antidote. 
If taken by mouth, emesis and lavage of the stomach 
should be practised in addition to the measures indicated 
above for systemic effects. 
References 
Meltzer: Z. exp. Path., 1905, 1, p. 446. 
Crossman: Med. Record, 1920, 98, p. 772. POISONOUS GASES 
69 
BROMINE (Br) 
At ordinary temperatures bromine is a heavy, dark red 
liquid which if exposed to air is converted into a brownish- 
red vapor. It boils at 58°C. and at - 7-3°C. it is solid. 
It has an extremely disagreeable odor to which fact it owes 
its name which signifies a stench. It is soluble in water to 
a limited extent, and is soluble in alcohol and ether. It 
acts violently upon organic substances. It attacks the 
skin causing serious wounds and its effect upon the mucous 
membranes is very similar to that of chlorine. During the 
World War bromine was used in hand grenades. 
Symptoms.-When inhaled bromine acts as a respira- 
tory irritant. Taken by mouth it exerts a caustic action 
causing pain from the mouth throughout the alimentary 
canal producing such profound local effects that death 
from collapse may ensue in a few hours. The points of 
local action are characterized by a dark brown stain. The 
mucous membrane may be softened, inflamed or 
corroded. 
Fatal Dose.-The fatal dose is probably about one 
ounce of bromine. Generally the quantity taken is too 
small to cause death. 
Treatment.-Treatment of bromine poisoning is iden- 
tical with that for iodine. 
BROMIDES 
The more commonly employed bromides are those of 
potassium, sodium and ammonium and to a less degree 
those of lithium, strontium and calcium. So far as one 
may judge sodium bromide is quite capable of fulfilling 
all the functions and advantages ascribed to the others 
since it is to the Br ion that the remedial effect is due. 
The bromides are employed chiefly as sedatives to induce 70 
TOXICOLOGY 
sleep or to quiet conditions of hyperexcitability as in 
hysterical states, Basedow's disease, acute cerebral 
excitement and meningitis, delirium tremens, and con- 
vulsions as in epilepsy. 
Like the chlorides the bromides are rapidly eliminated 
through the urine although there is a tendency for the 
bromides to accumulate in the tissues. The administra- 
tion of chlorides tends to hasten the excretion of the 
bromides. 
Bromide rashes frequently occur, especially on the face 
when bromide administration has been continued for a 
considerable period. These rashes closely resemble those 
induced by iodides. The reason for the occurrence of 
these rashes is not clear, a variety of opinions being held 
but none being above criticism. It is quite probable that 
the nervous system is involved in some way since vaso- 
motor disturbances accompany the skin rashes. 
Symptoms.-Acute poisoning may occur from a single 
large dose. The symptoms observed are profound 
depression or apathy, or even a stupor which may last 
for several days. The respiration is slow and low blood 
pressure is in evidence. Bromides alone rarely, if ever, 
cause death. 
Bromism or chronic bromide poisoning results from 
repeated large doses. There is psychic deterioration, the 
patient being dull, stupid and apathetic; the face is with- 
out expression, pale and usually bears diffuse pimples; 
the memory is weak, speech is disturbed, voluntary move- 
ments are sluggish; there may be sexual impotence; 
somnolence; ataxia, tremors; malnutrition as shown by 
nausea, gastric irritation, diarrhoea or constipation lead- 
ing to a general cachexia and a lowered resistance. 
Treatment.-Treatment of bromism consists in stopping 
the administration of the drug and hastening its elimina- POISONOUS GASES 
71 
tion as much as possible. Pushing the intake of sodium 
chloride will aid in this process which should be further 
assisted by the ingestion of large volumes of water. The 
nutrition should be improved by careful diet and the 
depression counteracted by caffeine or strychnine. CHAPTER IV 
METALLIC POISONS 
TELLURIUM (Te) 
Tellurium occurs free in nature or in combination as a 
telluride. With other metals it forms grayish white 
crystals possessing a metallic luster. Chemically it is 
closely related to sulphur and forms anhydrides which with 
water produce tellurous (H2TeO3) and telluric (H2TeO4) 
acids which are analogous to sulphurous and sulphuric 
acid. With hydrogen it forms a gas, H2Te, which resem- 
bles hydrogen sulphide in its mode of formation, odor, 
and reaction with metallic solutions. These solutions, 
however, are stable and possess odors even more dis- 
agreeable than hydrogen sulphide. On combustion diox- 
ide is formed. The compounds which are most often met 
with are the oxides and the methyl compounds. In 
general the sodium salts are soluble in water. In medicine 
sodium tellurate has been employed to suppress sweating 
in tuberculosis. 
Although tellurium is, chemically, closely related to 
sulphur its pharmacological action resembles very closely 
that of arsenic. Fatalities from intoxication with tellu- 
rium are unknown and its interest from the viewpoint of 
toxicology is mainly from its employment in industry. 
In the separation of lead and copper it is met with in the 
form of fumes as hydrogen telluride, and in dust as 
tellurous oxide and tellurate. 
Symptoms.-The most pronounced symptoms are those 
of langour, sleepiness, loss of appetite, nausea, pronounced 
72 METALLIC POISONS 
73 
salivation, depression, garlic odor of the breath, and 
constipation. The garlic odor of the breath persists for 
a long time. The toxicity of tellurium is not very great, 
the oral toxic dose being much less than when the 
poison is given subcutaneously. The tellurite is much 
more toxic than the tellurate. Compared to hydrogen 
sulphide hydrogen tellurite is more irritant and toxic than 
hydrogen sulphide. 
Poisonous Action.-Tellurium compounds produce an 
action upon the blood which is very similar to that of 
arsenic, producing leucopenia, a decrease in red count, 
and hemolysis. With large doses the bone marrow 
appears red with hyperplasia of the white and red cells. 
The tellurium compounds are apparently methylated at 
least in part, and excreted as methyl telluride by the 
breath, urine and feces. Tellurium appears to diminish 
and suppress perspiration, and changes the tone of blood 
capillaries. 
Fatal dose and fatal period are unknown. 
Post Mortem Appearances.-In animals the post 
mortem appearances show that the mucosa of the duo- 
denum and jejunum is congested and swollen, contains 
small hemorrhages, and is covered with a pseudo-mem- 
brane. The kidney shows some irritation and the urine 
has casts, leucocytes and albumin. 
Treatment.-The treatment is purely symptomatic. 
Reference 
Mead and Gies: Am. J. Physiol., 1901, 5, p. 104. 
SELENIUM (Se) 
Selenium, like tellurium, is chemically closely related 
to sulphur. It occurs in two forms, either as an amor- 
phous variety which is a black or dark red solid which, on 74 
TOXICOLOGY 
heating, is transformed to a crystalline fluid possessing a 
gray color and a metallic luster. Pharmacologically it 
possesses properties similar to tellurium and arsenic, but 
is more toxic than tellurium. It has been employed in 
medicine as a specific treatment for tumors but its use 
has been discontinued. Selenium is sometimes encoun- 
tered in industrial plants as selenic acid and sulphates. It 
has an action in whitening ordinary glass. 
Symptoms.-One symptom of selenium poisoning is 
the typical odor of the breath which is very similar to 
that of tellurium, that is, a garlic odor, and is due to the 
production in the organism of the methyl compound. 
Selenium has a peculiar effect on the mucous membrane 
of the nose and throat, a catarrh which simulates that of a 
rose cold. Other symptoms are vomiting and pain in 
the abdomen and in the lumbar region. Introduction 
to dogs whether given by mouth or by peritoneal injec- 
tion speedily causes death. 
LEAD-PLUMBUM (Pb) 
Lead is a soft, bluish white metal which is very heavy 
and has a low melting point. If freshly cut the surface 
presents a brilliant luster which soon disappears owing to 
the formation of oxide on the surface by its contact with 
the air. Owing to its characteristic softness, pliability 
and low melting point it has many industrial uses, such 
as for solder, type metal, pewter, etc. Although there 
are a large number of lead salts, all of which possess toxic 
properties, those which are ordinarily concerned in lead 
poisoning are the lead acetate, lead carbonate, and lead 
sulphate. Lead acetate or sugar of lead is soluble in 
water and has a sweetish taste which later becomes 
metallic. It forms the basis of various pharmaceutical 
preparations. Lead carbonate, which is known as white METALLIC POISONS 
75 
lead or flake white, or "mineral white," is a mixture of 
lead hydroxide and neutral lead carbonate. It is em- 
ployed chiefly as a constituent of paint, and as such is the 
cause of the so-called painter's colic. Lead sulphate is 
used to give weight to white silk and is also employed 
in the painters trade. At times, however, salts, par- 
ticularly the oxides, cause poisoning owing to the lead 
dust which is formed in various trades such as lead smel- 
ters, zinc smelters, brass molders, workers in type metal, 
lead type, and shot. 
There are various ways in which lead poisoning may 
occur. In the first place there may be constant contact 
with lead and its salts in manufactories. It may be 
caused also by its use in the arts and as a pigment. This 
is especially noticeable among painters, in the glazing of 
cards or cardboard, and in makers of Brussels lace. 
Poisoning may occur by the application of various types 
of lead-containing ointments, plasters, cosmetics, and 
hair dyes. A fruitful source of chronic intoxication is 
from water which has either been stored or conveyed in 
leaden pipes. Many kinds of foods may contain lead 
owing to the fact that the containers or wrappers are 
made of materials of which lead is a constituent. Thus 
various farinaceous foods, chocolate and tea, may become 
contaminated and confectionary may contain lead from 
the use of lead chromate as a coloring agent. Lead 
poisoning may also occur from the use of tobacco, snuff, 
since these substances are contained in lead foil wrappers. 
Acute Lead Poisoning. Symptoms.-Lead is rarely, if 
ever, used for criminal poisoning. When poisoning does 
occur it is usually due to an accident. Lead salts in 
general act as astringents and are also irritant. They are 
absorbed slowly, chiefly from the alimentary canal, 
but may be absorbed from the lungs and other tissues or 76 
TOXICOLOGY 
even in the form of ointments through the skin. The 
first symptoms of poisoning are a metallic taste in the 
mouth with dryness of the throat, and intense thirst 
soon after the poison is swallowed. Within a relatively 
short period thereafter there is nausea and vomiting 
which may be persistent. The vomitus may be milky 
owing to the formation of lead chloride. There is paraly- 
sis in the esophagus and stomach with abdominal pain. 
Either obstinate diarrhoea or constipation may occur, the 
stools being black from the formation of lead sulphide. 
The urine may be diminished in volume, the face is 
anxious, there is a dry skin, the breath is foul, and the 
tongue is coated. There is more or less specific action 
upon the nervous system, and although the brain is clear 
there is pain and cramps in the legs, numbness and local 
palsies, and paralysis which appears somewhat later. 
The muscles undergo a form of fatty degeneration. The 
absorption of lead causes marked anemia with degenera- 
tion of the red corpuscles. The symptom which is quite 
characteristic of lead poisoning is the so-called "blue 
line" on the gums. This is not present invariably 
but should always be looked for. Fatal cases eventually 
pass into coma either with or without convulsions. If 
the case does not prove fatal apparent recovery takes 
place within a few days, only later to give rise to the 
phenomena of chronic poisoning. Perhaps the most 
characteristic features of lead poisoning are unmistakable 
colic and wrist-drop. 
Inasmuch as lead is a cumulative poison relatively large 
quantities may be found in the liver, kidneys, brain, 
muscles, and even in the blood. The excretion of lead is 
very slow and occurs over a long period of time even when 
the source of lead absorption has been stopped. The 
excretion takes place mainly by way of the feces, although METALLIC POISONS 
77 
it may be found to a smaller degree in the urine. Saliva 
and sweat also serve as channels of excretion. 
Poisonous Action.-Certain salts of lead possess an 
astringent property owing to the ease with which they 
combine with proteins, but this cannot be the entire cause 
for the toxicity of lead inasmuch as all of the lead salts 
are more or less corrosive compounds and possess proper- 
ties as poisonous as the others. -Lead appears to produce 
pathological changes in the kidneys leading to granular 
degeneration and the kidneys are hard and contracted. 
There are characteristic local paralyses with atrophy. 
The muscles involved are wasted and fatty, and there are 
changes in the large cells in the anterior cornua of the 
cord and in the peripheral nerve fibers. 
Fatal Dose.-According to Kobert the minimal fatal 
dose of lead acetate is 20 gms., that of white lead 25 gms. 
Fatal Period.-The fatal period -is quite variable 
although death usually occurs within a day or two. 
Post Mortem Appearances.--The post mortem appear- 
ances are not characteristic, the most prominent features 
being gastro-intestinal inflammation and evidences of 
inflammation in the liver and kidney. 
Treatment.-In acute poisoning it is desirable to rid 
the stomach as soon as possible of the toxic substances, 
and this may be accomplished by lavage followed by 
administration of soluble sulphates such as sodium and 
magnesium sulphate. If a stomach tube is not available 
emetics should be employed. For control of the colic and 
vomiting morphine and atropine are indicated. 
Chronic Poisoning. Symptoms.-Chronic poisoning is 
very much more common than the acute manifestations 
and usually occurs from contact of the metal in industry. 
Lead possesses a cumulative action and has independent 
influence upon the blood, upon nutrition, and upon muscu- 78 
TOXICOLOGY 
lar and nervous structures. The symptoms of chronic 
lead poisoning are very subtle. Generally the first 
symptoms are those of ordinary colic and of a general 
feeling of debility. The appetite is uncertain or may be 
lost. The mouth is parched, the breath is foul, the skin 
is sallow and dry, and more or less general emaciation 
occurs. Anemia, blue line on the gums, local paralysis, 
especially of the right forearm, presence of blood in the 
urine, disorders of the central nervous system, the presence 
of basophilic granules in the red blood cells are all symp- 
toins of chronic lead poisoning, none of which are 
absolutely peculiar to lead. The basophilic granules and 
the wrist-drop, lead in urine and feces are usually sufficient 
to lead to suspicion of chronic lead poisoning. If taken 
in time the prognosis of chronic poisoning is not 
unfavorable, if there are no complications such as alco- 
holism or degeneration of the liver, kidney, heart and blood 
vessels. If cerebral symptoms occur the prognosis is 
grave. These cerebral symptoms consist in hallucina- 
tions, illusions, delirium, melancholia, pseudoparalysis, 
coma and epileptiform convulsions. 
Chronic lead poisoning may produce changes in the heart 
and blood vessels leading to arteriosclerosis, valvular 
degeneration, cardiac hypertrophy, and renal changes 
with albuminuria. These conditions may be associated 
with arthritis and gout. The alterations in the vessels 
may lead to cerebral hemorrhages. 
Post Mortem Appearances.-The post mortem appear- 
ances in lead poisoning are not characteristic, although 
the intestines may be constricted with a gray-black dis- 
coloration of the mucous lining. The blue line around the 
gums is highly significant and changes in the cornua of the 
cord and in the peripheral nerve fibers together with 
those in the kidney may be prominent. METALLIC POISONS 
79 
Treatment.-Treatment in chronic lead poisoning is 
largely a matter of prophylaxis. The source of lead should 
be discovered and the patient should be guarded against 
further exposure to it. The special treatment consists in 
free bowel movement, best induced by doses of magnesium 
sulphate, or constipation may be treated with olive oil 
enemas. The symptomatic treatment is morphine against 
the pain of colic, hot applications or baths. The palsies 
may be treated with strychnine, massage and electricity. 
Although many efforts have been made to hasten the 
elimination of lead by means of potassium iodide, sweats 
and sulphur, doubt is expressed as to their efficiency. 
Perhaps the most promising is the iodide which may at 
first hasten the elimination but apparently soon loses its 
effect. Tonics are of considerable importance. Open 
air exercise and wholesome diet are, however, the best 
known means of combatting the detrimental effects of 
chronic lead poisoning. 
References 
Carlson and Woelfel: J.A.M.A., 1913, 61, p. 181. 
Harris: Arch. Int. Med., 1918, 22, p. 129. 
Hamilton: J.A.M.A., 1912, 59, p. 777. 
SILVER-ARGENTUM (Ag) 
Metallic silver is pure white in color with a high luster 
resisting the action of oxygen. It forms a large number 
of salts but in toxicology those of importance are the 
nitrate or protein compounds which are used because of 
the antiseptic properties of silver. Caustic silver nitrate 
is extensively employed locally in various affections for 
purposes of cauterization. In present day therapy argyr- 
ism, or a bluish-black discoloration of the skin, rarely 
occurs. In true argyrism the coloring is permanent but 
no symptoms arise. The application of silver salts to the 80 
TOXICOLOGY 
skin or mucous membranes causes stains which are quite 
distinct from argyrism. These stains may be removed by 
io per cent potassium iodide or cyanide. 
Symptoms.-Poisoning from silver usually occurs by the 
accidental swallowing of pieces of the caustic (Lunar 
Caustic) silver nitrate especially in infants during the 
treatment of various conditions of the mouth and lips. 
Swallowing the caustic causes pain in the throat and 
stomach, vomiting, gastritis, and later, diarrhoeal stools 
which may show blood. If absorption of the silver occurs 
dizziness, convulsions, and coma may supervene. 
Fatal Dose.-The fatal dose for an adult is approxi- 
mately 30 grains. 
Fatal Period.-Death may occur in a period of 6 hours 
or more. 
Post Mortem Appearances.-The post mortem 
appearances show the local action of the caustic. Stains 
on the mucous membranes of the esophagus and gastro- 
intestinal tract will be white at first but will turn black on 
exposure to light. Inflammation in the stomach and 
intestines is present. 
Treatment of Silver Nitrate Poisoning.-Large volumes 
of common salt and water (dilute solutions) should be 
given either as lavage or in combination with an 
emetic. Usually the salt water itself will act as an emetic. 
The salt forms the insoluble silver chloride which is not as 
irritating as the caustic silver nitrate. Lavage should be 
continued until the wash water no longer gives a test for 
silver. When this point is reached eggs and milk may be 
prescribed for their demulcent effect. 
MERCURY-HYDRARGYRUM (Hg) 
At ordinary temperatures mercury is in a liquid state. 
It vaporizes at room temperature and has a silver-white METALLIC POISONS 
81 
metallic luster. It forms two series of salts-the mer- 
curous and mercuric compounds. Salts of mercury may 
be regarded as protoplasmic poisons. In virtue of this 
property mercury salts are active germicidal agents. 
Their relative insolubility, ease of precipitation, distinctly 
irritative and toxic properties necessarily limit their wide 
application. In general, as with arsenic, poisoning occurs 
only when the salts are dissociated. In this instance, 
however, the poisonous action is associated with the 
mercury ion which is very reactive, chemically combining 
with protein and usually forming an insoluble compound. 
The mercurous salts in general are less irritative and less 
toxic than the mercuric salts because of greater insolubility. 
Certain of the organic mercury compounds, as "Mercuro- 
chrome 220," of Young, and mercurophen are not irritant 
although retaining antiseptic properties. The relatively 
low toxicity and non-precipitation of protein by these 
compounds are consequences of the non-ionized condition 
of the substances. Whatever type of mercury compound is 
employed it may, under favorable conditions, give rise to 
typical mercury intoxication. 
Some of the more common mercury compounds that 
may cause poisoning when employed medicinally are the 
various preparations containing metallic mercury, as Blue 
Mass or Blue Pill containing 33 per cent of mercury, 
and used similarly to calomel; Unguentum Hydrargyri 
for inunction-50 per cent mercury in suet or lard; or the 
more dilute Blue Ointment (30 per cent mercury) for cuta- 
neous parasites; Calomel; Calomel ointment; Yellow Mer- 
curous Iodide; Black Mercurial Lotion (Black Wash); 
Ammoniated Mercury in various compound ointment 
bases; Yellow Mercuric Oxide and Red Mercuric Oxide 
in various ointments; Corrosive Sublimate, Potassium 
Mercuric Iodide; Mercury Salicylate; Citrin Ointment; 82 
TOXICOLOGY 
organic mercury compounds as Mercurophen, Mercuro- 
chrome 220, and Chloromercurphlorescin. 
Mercury compounds are readily absorbed from mucous 
membranes and even from the skin. Mercury disappears 
rapidly from the blood and is deposited in the various 
organs probably as compounds of proteins of the cells. 
Excretion occurs both through the feces and urine and even 
after a single dose may continue for several days. When 
mercury has been given continuously for a considerable 
period its excretion may be a matter of months. Mercury 
poisoning may be classed into three types-acute, subacute 
and chronic. Usually the acute effects of mercury poison- 
ing are those induced by corrosive sublimate taken with 
suicidal or criminal intent. Chronic poisoning or mercur- 
ialism is the result of occupation, such as among workers 
in quick silver mines, in mirror makers, makers of ther- 
mometers, barometers, vacuum pumps, furriers and 
hatters, and munition workers. 
Acute Poisoning. Symptoms.-The earliest symptom of 
excessive therapeutic use of mercury is stomatitis. First 
the breath has a fetid odor, there is a metallic taste, the 
gums are sore (gingivitis) and salivation (ptyalism) occurs. 
This stomatitis occurs about as readily when mercury is 
given otherwise than per os. If the therapeutic adminis- 
tration is continued the edges of the gums become black 
and the teeth loosen. Later the gums and tongue are 
swollen and ulceration may occur. Infection sets in and, 
combined with the accompanying irritation, very severe 
salivation and progressive exhaustion develop. In the 
advanced stages the teeth may be lost and necrosis of the 
jaw may occur. Some grade of stomatitis may follow even 
the single administration of calomel in certain individuals. 
In the more acute types of poisoning the immediate 
effects are corrosion and irritation. There is a metallic METALLIC POISONS 
83 
taste, salivation is pronounced, the mouth and pharynx 
are ashy in appearance with a burning sensation, swelling 
of the mucous membrane may occur, and sometimes edema 
of the glottis is present. There is thirst with abdominal 
pain, colic, and vomiting with white or bloody mucous 
shreds. These symptoms usually yield to local treat- 
ment including fasting for i or 2 days and the patient seems 
quite well. Symptoms of stomatitis may appear during 
the first 24 hours. 
After absorption the poison appears to act chiefly upon 
the large intestine and upon the kidney. Generally 
within 2 or 3 days the urine contains albumin and is greatly 
diminished in volume, indeed, anuria may develop, 
followed by death without convulsions in about one week. 
If the kidneys have not been too severely injured a mem- 
branous colitis sets in accompanied by dysentery, tenes- 
mus, ulcerations, hemorrhages and degeneration of the 
liver. Death may not occur for weeks. In the most 
severe cases blood pressure may fall, due to cardiac involve- 
ment, and there may be vasomotor disturbances, feeble 
pulse, insensibility of the skin, coma and collapse. Con- 
sciousness is usually maintained unimpaired. Sometimes 
giddiness is experienced or the patient is sleepy and 
again anxiety and restlessness may be observed. 
Should recovery from the acute stage occur subacute 
poisoning may set in which is characterized by nephritis, 
stomatitis, and colitis. Sometimes skin eruptions are 
present. This syndrome is frequently seen in poisoning 
from the medicinal use of mercury. Usually the stomach 
and small intestines are not involved. 
When mercury poisoning occurs from use other than by 
mouth the local symptoms are absent. 
The kidney appears to be affected even after the 
ordinary medicinal use of mercury for some albuminuria 84 
TOXICOLOGY 
is frequently present owing, perhaps, to damage to the 
renal tissue in its effort to eliminate the poison. When 
the injury is slight the nephritis partakes of the nature of 
the interstitial form although the glomeruli and also the 
epithelium may be affected. Later cirrhosis may develop. 
If the nephritis is acute it involves the tubules primarily 
although with severe injury hemorrhagic glomerular 
nephritis may be induced. Sometimes various portions 
of the kidney may contain crystals of calcium carbonate. 
The formation of these crystals is not understood. 
The cause for stomatitis, colitis and nephritis is usually 
attributed to injury of membranes involved during the 
process of elimination. 
Fatal Dose.-The fatal dose varies probably from 3 to 5 
gms. of mercuric chloride. 
Fatal Period.-The fatal period varies from hour to 
2 weeks. 
Post Mortem Appearances.-If the poison has been 
taken by mouth the mucous membranes of the alimentary 
canal may be ashy colored, congested or corroded. The 
colon especially may be the seat of inflammation. The 
kidneys show acute inflammation with calcification. 
When mercury has been parenterally administered the 
colon and kidneys show the most change. 
Treatment of Stomatitis.-During the administration 
of mercury the mouth and teeth should be in the best 
condition possible. Both from the viewpoint of prophy- 
laxis and of treatment a mouth wash, hydrogen peroxide 
or potassium chlorate (a tablespoonful of the saturated 
solution to a glass of water) should be used several times 
daily. The addition of a little tincture of Myrrh will 
improve the taste of the mouth wash. 
Treatment of Acute Mercury Poisoning.-If the poison 
has been taken by mouth promptness in treatment is of METALLIC POISONS 
85 
prime significance and consists in precipitation in the 
stomach of the mercury as a non-corrosive albuminate. 
For this purpose white of egg or milk may be given. The 
mercury-protein compound thus formed should be 
promptly removed from the stomach by lavage preferably 
or by use of an emetic. If the poison has had time for 
absorption this treatment will be less effective. On the 
other hand frequent lavage of the stomach is of distinct 
value. Equally efficient but less convenient as an anti- 
dote is a hypophosphite-peroxide mixture (sodium hypo- 
phosphite i gm., water io c.c., and hydrogen peroxide 5 
c.c., estimated for each 0.1 gm. of mercuric chloride). 
Lavage with the diluted solution should follow this treat- 
ment. In order to protect the kidneys as much as pos- 
sible a light diet should be given with a plentiful supply of 
fluid so long as the kidney remains sufficiently active. 
The administration of sodium bicarbonate may also aid 
in protecting the kidney from damage. 
A detailed outline of treatment which embraces the above 
principles is that of Lambert and Patterson as follows: 
"The first indication is to give the patient the whites of 
several eggs and then to wash out the stomach thoroughly. 
This has usually been done before the patients are admitted 
to the hospital. On admission, the stomach contents are 
expressed and examined for mercury, the stomach is 
thoroughly washed, and a pint of milk introduced. If no 
stomach contents are obtained before lavage, then the 
lavage water is examined for mercury. The metal appears 
in the urine in from 3 to 24 hours after it has been 
swallowed. If more than a day has elapsed since the 
poisoning occurred, a stool should also be examined for 
the poison. If the first lavage does not allay the nausea 
and vomiting, it is repeated after an hour, and the follow- 
ing routine is begun as soon as the stomach will permit: 86 
TOXICOLOGY 
i. The patient is given every other hour 8 ounces of 
the following mixture: potassium bitartrate, i dram; 
sugar, i dram; lactose, ounce; lemon juice, i ounce; 
boiled water, 16 ounces. Eight ounces of milk are admin- 
istered every alternate hour. 
2. The drop method of rectal irrigation with a solution 
of potassium acetate, a dram to the pint, is given continu- 
ously. The amounts of urine secreted under the treat- 
ment are very large. 
3. The stomach is washed out twice daily. 
4. The colon is irrigated twice daily, in order to wash 
out whatever poison has been eliminated in that way. 
5. The patient is given a daily sweat in a hot pack. 
It is imperative to emphasize the necessity of keeping 
up the treatment with the colonic drip enteroclysis day and 
night without interruption." When poisoning is not 
severe a week may be sufficient time for treatment. When 
large or successive doses have been taken, or when there 
is a pre-existing kidney lesion, or when treatment begins 
several days after the poison has been taken, longer periods, 
even up to three weeks, are necessary. When cases have 
reached the stage of anuria favorable results cannot always 
be expected. 
A variety of treatments have been proposed aimed to 
render less active mercury that has been absorbed. None 
of these has proved of distinct advantage. 
Chronic Mercury Poisoning.-In chronic mercury poi- 
soning there is at first loss of appetite, nausea and 
gastro-intestinal symptoms with constipation or diarrhoea 
followed by loss of weight, anemia, and pains in the bones 
and joints. A general cachexia may result. Unlike lead 
poisoning there is no line on the gums but there may be 
a gingivitis. Nervous symptoms may be pronounced. 
The most prominent are tremors, usually of the hands and METALLIC POISONS 
87 
lips although the whole body may be affected. Psychic 
irritability, restlessness, mental weakness, loss of will 
power, various psychoses, and rarely a peripheral neuritis, 
muscular atrophy, decalcification of the -bone, are all 
symptoms that may be encountered. 
Treatment of Chronic Mercury Poisoning.-There is 
considerable doubt whether treatment materially modifies 
the patient's condition. Everything possible should be 
done to promote elimination of the poison, such as admin- 
istration of water and perhaps alkali. Potassium iodide 
is generally recommended but the efficacy of the treatment 
is very doubtful. For the rest treatment is purely 
symptomatic, attention being given to the malnutrition, 
the anemia, and to the nervous manifestations. 
References 
Toxicology of Mercury 
Schamberg, Kolmer and Raiziss: Bost. Med. and Surg. J., 1915, 
162, p. 826. 
Mercurophen 
Schamberg, Kolmer and Raiziss: J. Inf. Diseases, 1919, 24, p. 
547> 
Mercurochrome 
Young, White and Schwartz: J.A.M.A., 1919, 73, p. 1483. 
Treatment 
Lambert and Patterson: Arch. Int. Med., 1915, 16, p. 865. 
Rosenbloom: Am. J. Med. Sci., 1919, 57, p. 348. 
MacBride and Dennie: Arch. Derm, and Syphil., 1923, 7, p. 63. 
Gatewood and Byfield: Arch. Int. Med., 1923, 32, p. 456. 
COPPER (Cu) 
Copper is a heavy, bright red solid which on contact with 
air assumes a brown coating of the oxide. The salts which 88 
TOXICOLOGY 
are of interest toxicologically are those possessing irritant 
properties, namely, Copper Sulphate (Blue Vitriol), 
Copper Subacetate (Verdigris), and Copper Acetoarsenite 
(Paris Green). The salts of copper are extensively 
employed in industry and occasionally there are cases of 
poisoning among workers in such industries. It possesses 
toxic properties when given in large doses, and has been 
employed for purposes of suicide or criminal poisoning. 
In the latter instance it is not a favorite inasmuch as its 
taste militates against such use. Poisoning by copper 
may take the form of either acute or chronic poisoning. 
Usually the former is induced by ingestion of the copper 
salts, whereas the chronic poisoning arises from industrial 
employment or from the use of copper salts in foods. 
Acute Poisoning. Symptoms.-Immediately after tak- 
ing the copper salt there is a coppery, astringent taste 
and a feeling of dryness in the throat. Inasmuch as 
copper sulphate, for example, is an emetic, nausea and 
violent vomiting set in. The vomitus has a green color. 
The irritant action is continued by gripping pain of a 
colicky nature, the abdomen being distended, and accom- 
panied by thirst with violent purging. The stools possess 
a green coloration. Later the absorbed copper causes 
headache, giddiness, labored breathing with irregular 
pulse, muscular spasms which may be tetanic in character, 
paralysis, delirium and death. Inasmuch as the liver may 
be involved jaundice usually results. Copper is elimin- 
ated both through the urine and feces. 
Symptoms.-Copper causes the excretion of a urine 
containing albumin and casts, and it may also contain 
hemoglobin. 
Poisonous Action.-The action of copper may be two- 
fold. In the first place it may lead to death from its 
simple irritant properties or secondly from the influence METALLIC POISONS 
89 
upon the nervous tissues and upon the kidneys and 
liver. 
Fatal Dose.-The fatal dose is uncertain inasmuch as 
usually a portion of the ingested material is vomited. 
Fatal Period.-Usually life persists for several days even 
in fatal cases, though instances of death within 4 hours 
are on record. 
Post Mortem Appearances.-The post mortem appear- 
ances are those of an irritant poison, the gastro-intestinal 
tract showing congestion, swelling, softening, with perhaps 
ulcerations, and the mucous membrane may have a bluish 
color owing to the presence in it of copper. Fatty changes 
may be present in the liver, and the kidneys are swollen 
with the tubules clogged with bloody casts. 
Treatment.--Treatment consists in emptying the stom- 
ach either by means of the stomach tube or by vomiting, 
and the administration of white of egg or milk. Lavage 
of the stomach should be practised until it is certain 
practically all of the copper has been removed. The 
remaining measures to be taken are purely symptomatic. 
Chronic Poisoning. Symptoms.-Chronic poisoning is 
usually not fatal, the toxic phenomena extending over 
a long course, the symptoms indicating functional dis- 
turbances of the muscular nervous systems, anemia and 
cachexia. The so-called copper colic which simulates 
lead colic is less severe than the latter and is characterized 
by the fact that diarrhoea occurs instead of constipation. 
On the other hand there is evidence tending to show that 
copper does not produce a symptom complex of poisoning 
even though copper has been ingested to the point of 
a blue line on the gums and the urine gives a green color. 
Reference 
Huber: J. Pharm. and Exp. Therap., 1918, 11, p. 303. 90 
TOXICOLOGV 
BISMUTH (Bi) 
Under ordinary circumstances even very large doses of 
bismuth given by mouth are harmless. Under special 
conditions, however, bismuth salts may become poisonous. 
The insoluble bismuth salts are employed in X-ray diag- 
nosis, and as adhesive powders forming a protective mem- 
brane on inflamed mucous surfaces and on wounds. 
The subnitrate and subcarbonate are useful against 
diarrhoea, gastritis and gastric ulcers. Bismuth paste 
applied to chronic suppurative abscesses and sinus may 
give rise to toxic symptoms. A certain amount of the 
basic bismuth salts may be dissolved by the gastric juice, 
be absorbed into the circulation and find elimination 
through the intestine, kidney and mouth. Usually the 
amount thus absorbed is too small to produce symptoms. 
Quite recently a further possibility of poisoning by bis- 
muth salts has arisen since certain of these salts have been 
more or less extensively employed in medicine in the 
treatment of syphilis, especially in the form of an organic 
acid bismuth compound such as the tartro-bismuthate. 
In cases of poisoning bismuth may be found in the kidney, 
stomach, and liver. Formerly some samples of bismuth 
subnitrate contained traces of arsenic, antimony, lead and 
tellurium, and cases of poisoning from these impurities 
have been reported, arsenic being the chief offender. 
With more perfect methods of preparation contamination 
with these substances is no longer probable. 
Symptoms.-Poisoning from bismuth may manifest 
itself in several ways, (a) nitrite effects from reduction in 
the large intestine by bacteria of nitrate to nitrite, the 
toxic effects therefore being due to nitrite and not to 
bismuth itself. The symptoms are methemoglobin in the 
blood, cyanosis, diarrhoea, dyspnea and death from respira- 
tory failure, {b} Capillary thrombosis-this is formed from METALLIC POISONS 
91 
the precipitation of hydrogen sulphide in the intestinal 
vessels. Bismuth sulphide is black and very insoluble. 
When bismuth is absorbed into the blood precipitation of 
bismuth sulphide may take place in the capillaries of the 
large intestine causing capillary embolism. Later ulcera- 
tion occurs and vomiting, cramps, diarrhoea, colic and 
colitis may follow. The colitis produced is usually 
much less severe than that observed with mercury poison- 
ing. A "lead line" may appear upon the gums due to the 
deposition of bismuth sulphide. At times this spreads 
in patches on the mucous membrane of the mouth and 
indeed the entire mouth and tongue may become dis- 
colored; stomatitis and loosened teeth may also be in 
evidence, (c) Chronic Bismuth poisoning. The symp- 
toms observed in chronic bismuth poisoning are headache, 
fever, stomatitis, "lead line," and discoloration of mouth 
and tongue, gastro-intestinal disturbances, diarrhoea 
with black stools, colic, and albuminuria. Unlike lead, 
bismuth poisoning usually fails to show specific effects 
upon the nervous system and upon the blood. In some 
fatal cases convulsions and tetanus may occur. 
Bismuth is excreted both by the feces and the kidneys, 
and has been detected in the bile, milk and saliva. 
Post Mortem Appearances.-The most characteristic 
appearances of bismuth poisoning are evidences of liver 
and kidney lesions together with congestion of renal 
capillaries. The liver cells show cloudy swelling and 
necrosis. The convoluted tubules of the kidney are 
necrotic, and the lumen of the tubules is choked with 
cellular debris. 
Treatment.-For the nitrite effects emetics, or lavage 
of the stomach may be employed. To counteract the 
systemic influence epinephrine or strophanthin may be 
used. In treatment of specific bismuth poisoning the 92 
TOXICOLOGY 
administration or application of the drug should be 
stopped and everything possible done to favor elimination 
of the poison, for example, lavage of stomach, catharsis 
and administration of large volumes of water. For treat- 
ment of the stomatitis see under Mercury. 
Reference 
Lucke and Klauder: J. Pharm. and Exp. Therap., 1923, 21, p. 
3i3- 
ARSENIC (As) 
Arsenic is a steel black mineral with a metallic appear- 
ance and forms a series of salts all of which are toxic. 
The most common compounds of arsenic which may cause 
poisoning are vapors of arsenic, arsenite of copper, or 
Scheele's green, or the aceto-arsenite of copper (Paris 
green), or orpiment or yellow arsenic which has been 
employed in the arts for coloring of paper and coloring of 
toys, realgar or red arsenic employed for the same purpose, 
metallic arsenic in the form of fly powder or in the manu- 
facture of various colors such as magenta, aniline red, or 
fuchsin. For criminal purposes probably arsenic trioxide 
(which is also known as arsenic, white arsenic, ratsbane, 
or arsenious oxide) has been used more extensively than 
any other. 
The characteristic features of arsenic poisoning are elic- 
ited by arsenious acid (As2O3H3) and its salts or by the 
anhydride (As2O3) which is often spoken of as arsenic. 
The influence of arsenic is due to the ion of arsenious acid 
and not to the element. This conception readily explains 
the fact that compounds of arsenic such as arsenic acid 
(H3AsO4) and its salts, and organic compounds of arsenic, 
both of which dissociate less readily, are much less toxic 
than arsenious acid. Upon entrance into the body these 
latter substances only gradually dissociate forming METALLIC POISONS 
93 
arsenious acid in the tissues from which typical arsenic 
poisoning may occur. It is, therefore, quite evident that 
poisoning by arsenic is characteristic even though the 
source of arsenical compounds may be quite varied and 
the number of arsenical preparations may be large. 
The forms of arsenic most commonly prescribed follow: 
Arsenious oxide (As2O3): Fowler's solution (contains i 
per cent solution of arsenious anhydride rendered alkaline 
with potassium bicarbonate, to which compound tincture 
of lavender is added to give flavor and color): Sodium 
arsenate (Na2HAsO4 + 7H2O): Anhydrous sodium arsen- 
ate (NaHAsO4): Pearson's solution (i per cent solution 
of dried sodium arsenate; Arsenious iodide (Asl3): Dono- 
van's solution (contains i per cent of arsenic iodide 
and i per cent of red mercuric iodide): Cacodylates: 
Atoxyl or sodium arsenilate (NH2C6H4OAsOH.ONa): 
Arsacetin (Acetyl atoxyl): Arsphenamine (p. dihydroxy-m- 
diamino-arsenobenzene) (NH2OH.C6H3.As): Neo-arsphen- 
amine (Sod. diamino-dihydroxy-arseno-benzene-methanal 
sulphonylate) (AsC6H3OH.NH.CH2O.SO.Na): Silver 
arsphenamine. 
Irrespective of the method of administration arsenic 
exerts a poisonous action calling forth characteristic 
symptoms and inducing pathological changes. 
Types of Arsenic Poisoning.-There are at least three 
distinct types of arsenic poisoning-namely, an acute, 
a nervous and a chronic form. 
Acute Form.-The acute form of arsenic poisoning 
includes all those cases in which the inflammatory symp- 
toms are severe from the beginning and in which the 
patient dies within 24 hours or may survive for 2 or 3 days. 
Usually symptoms appear promptly but may be delayed 
for ¥ to 1 hour. This is especially true when large doses 
have been taken. The first symptoms appear to be dry- TOXICOLOGY 
94 
ness and constriction of the throat, with difficulty in 
swallowing and general discomfort in the stomach. Vio- 
lent pain with nausea and vomiting follow. The vomited 
matters at first consist of food substances together with 
part of the arsenic swallowed. Later the vomitus may 
contain bile, blood or consist of a clear fluid. Diarrhoea 
soon sets in with colicky pains. The fecal matter passed 
at first has the general characteristics of diarrhoeal stools; 
later, however, they may partake of the nature of the rice- 
water stools of cholera. As such they consist almost 
entirely of small particles or shreds of disintegrated mucous 
membrane suspended in a somewhat serous fluid. At 
times, however, the stools are clear. From the great 
extraction of water from the body by way of the gastro- 
intestinal tract there is thirst and the urine may be 
greatly diminished. Indeed, a condition of anuria may 
develop in large measure owing to the action of arsenic 
upon the kidney. If urine is excreted it may be albumin- 
ous or even bloody. Accompanying these gastro-intes- 
tinal manifestations nervous symptoms may intervene 
consisting of dizziness, headache and pain or cramps in the 
muscles, chiefly of the limbs. The skin is cold and damp 
and the extremities are cold; cyanosis may be present; 
there is a feeble pulse with weak, sighing respiration. 
Toward the end there is collapse which may pass into coma 
or there may be convulsions or general paralysis with 
death. Death is perhaps due in large part to exhaustion. 
In some instances death does not follow immediately, the 
patient recovering from the acute effects only to develop 
chronic arsenic poisoning. The fatal dose is uncertain, 
death having occurred from quantities as small as o.i gram 
(1^2 grains). 
Nervous Form.-In the nervous type of arsenic poison- 
ing the usual symptoms associated with gastro-intestinal METALLIC POISONS 
95 
disturbances may be slight or even entirely absent. This 
type is characterized by the influence upon the nervous 
system. The chief symptoms that may be manifested 
are narcotism, paresis, deepening into paralysis, delirium, 
and even acute mania and convulsions. These cases are 
not common but occasionally one occurs and attention is 
called to the possibility since the symptoms encountered 
are so unlike those usually seen in arsenic poisoning. 
Chronic Form.-Chronic arsenic poisoning may be initi- 
ated either by the ingestion of a single large dose or the 
repeated administration of small doses. The latter is the 
more common method of its induction. In the therapeu- 
tic use of arsenical preparations the earliest form oi 
intoxication is manifested by diarrhoea, colicky pains, 
conjunctivitis or swelling of the eyelids. There may be 
sensations of weakness, loss of appetite, nausea, occasion- 
ally vomiting, and even constipation may result. Should 
the arsenic be continued the second phase of chronic 
arsenic poisoning soon sets in. This is characterized by 
inflammation of the conjunctiva, coryza, sneezing, hoarse- 
ness and cough arising from an inflammatory reaction 
upon the mucous membranes of the nose and larynx. 
Jaundice may appear with swelling of the liver. Skin 
eruptions are usually quite marked, the so-called "eczema 
arsenicale." These may take the form of exfolation, the 
skin falling off in fine brownish flakes, or even in large 
flakes, especially on the hands and feet. The hair falls 
out and the finger nails may become loose or detached. 
Again an acne-like eruption may appear. A form of mel- 
anosis is also quite prominent which is probably caused by 
the formation in the layers of the skin of organic pigment 
granules. It has been erroneously assumed that the 
pigmentation is caused by deposition of arsenic in the skin. 
This symptom is much more prominent in individuals of 96 
TOXICOLOGY 
dark complexion than in those with a fair skin. In the 
latter it partakes more of the nature of freckles. Usually 
this arsenic melanosis, so-called, disappears when the 
individual becomes arsenic-free but in some instances the 
pigmentation is permanent. Chronic intestinal catarrh 
develops which ultimately may lead to ulceration. When 
the poisoning is very slow there is persistent capillary par- 
alysis leading to widespread fatty and other degeneration. 
The endothelium of the capillaries is first attacked, sub- 
sequently the cells of other organs and tissues, particularly 
the liver, kidney and heart-muscle. There is also consid- 
erable tendency for the development of local effusions. 
The symptoms referable to the third phase of chronic 
arsenic poisoning are indicative of an action upon the 
peripheral nerves giving rise to polyneuritis, atrophy of 
the muscles involved, disturbance and paralysis of sensa- 
tion which may involve the eye producing blindness. This 
phase of poisoning is initiated usually by intense headache, 
or acute pain in the knee, ankle or foot. It is less com- 
monly observed in the hand or wrist. The palms of the 
hands and the soles of the feet become red and swollen 
and are extremely sensitive to pressure. The sensory 
paralysis, especially of the extremities, closely resembles 
that of locomotor ataxia. In the later development of 
motor paralysis, which is usually confined to the extremi- 
ties, and generally although not invariably symmetrical, 
diagnosis of arsenic poisoning is sometimes quite difficult, 
the disturbances closely resembling those seen in lead 
poisoning and in alcoholic neuritis. If other differentia- 
tion fails the urine and hair should be tested for arsenic. 
If the period of poisoning is prolonged the individual sinks 
into an apathetic, semi-idiotic condition, or indeed may 
become epileptic. If the poison is removed the condition 
generally improves and the symptoms disappear although METALLIC POISONS 
97 
some trace of paralysis may persist for years. If the 
muscles are markedly degenerated little hope of improve- 
ment may be anticipated. Death usually results from 
malnutrition and exhaustion, emaciation being a striking 
feature. 
Pathology of Arsenic Poisoning.-The most marked 
changes to be observed are the fatty degeneration and 
infiltration of the liver and kidney. This change in the 
liver may proceed to such an extent that the entire organ 
is distinctly yellow. In acute poisoning there may or may 
not be evidences of an inflammatory reaction either in the 
stomach or intestines or in both. The inflammatory 
changes may be recognized many months after death since 
the presence of arsenic in tissues tends to prevent or at 
least to retard putrefactive changes. 
Treatment of Arsenic Poisoning.-Acute arsenic poison- 
ing is best treated by lavage with ^arm water. The 
lavage should be continued until one may be assured that 
all the arsenic has been removed from the stomach. If 
lavage is impossible emetics should be employed. They 
however, are not so effective as lavage and are detrimental 
inasmuch as they tend to induce depression. Whichever 
treatment is carried out should be prompt. Attempts to 
wash the intestine by high rectal tube are usually of little 
value. When the stomach has been thoroughly washed 
the intestine is best emptied by purgatives. For this 
purpose the saline cathartics are to be preferred since they 
act promptly. Chemical antidotes, such as the so-called 
" arsenic antidote," are of doubtful value. It is much 
better to rely upon repeated and copious lavage with sub- 
sequent purgation. The collapse usually observed in 
acute arsenic poisoning is to be treated by the ordinary 
measures employed, such as warmth and stimulants for 
example, caffeine and digitalis. In view of the water 98 
TOXICOLOGY 
deprivation of the body, incident to the extensive vomiting 
and diarrhoea, large volumes of fluid should be adminis- 
tered over a period of 3 or 4 days. Such a procedure will 
also facilitate the excretion of that portion of the arsenic 
absorbed. 
In the treatment of chronic poisoning the cause should 
be removed and symptomatic measures taken. The par- 
alysis may be combatted by stimulating the muscles with 
the galvanic current. 
Toxicology of the Arsphenamine Group.-In the use of 
arsphenamine and neo-arsphenamine there are a certain 
number of cases that exhibit systemic effects which are 
not completely understood. The percentage of cases in 
which the reactions occur varies from 1 to 15 per cent. In 
most instances the symptoms are alarming and distinctly 
annoying to the patient but only occasionally is there a 
fatality. There are several types of reaction elicited by 
these compounds. 
Type A. Nitritoid Reactions.-In the first type which is 
spoken of as the "nitritoid" reactions there may be vaso- 
dilatation, as in nitrite action, hence the name, which 
characterizes this group. If the reaction is very severe 
the symptoms partake of the nature of anaphylaxis. The 
symptoms may start during the intravenous injection or 
immediately after. There is flushing of the face, inflam- 
mation of the conjunctiva; an anxious expression, peculiar 
burning sensation of the tongue, nausea, vomiting and 
profuse perspiration, edema of the tongue and eyelids. 
Sometimes there is cough and dyspnea, precordial distress 
and cyanosis. The pulse is full at first then weak with a 
pallid skin. Unconsciousness with feeble pulse may 
intervene in the severe cases. At times during the 
period of injection there may be severe lumbar pain. 
The symptoms thus indicated may disappear within METALLIC POISONS 
99 
15 to 30 minutes or may grade into the group of 
symptoms described below as Type B. The symptoms 
observed immediately usually give place to speedy 
recovery even though there is a condition of actual 
collapse. The condition of actual collapse is much more 
frequent following the second dose. 
The cause of the nitritoid reactions has been variously 
given. It has been ascribed to lack of purity in the 
preparations employed, the impurity being spoken of as 
substance "X," to a "colloidal reaction," precipitation 
or "anaphylaxis;" to the liberation of decomposition 
products, which, however, are usually less toxic than the 
original substances; to the formation of an insoluble base, 
by certain salts of the blood, which forms emboli; to a 
special supersensitiveness to the drugs themselves. Of 
the foregoing hypotheses the most likely appear to be 
associated with the presence of substance X and the sus- 
ceptibility of the patient. 
Treatment of Nitritoid Reactions.-In the treatment of 
nitritoid reactions epinephrin may be employed prophy- 
lactically and after appearance of symptoms. If used as 
a prophylactic 1 mg. may be administered intramuscu- 
larly just before the injection of the arsphenamine com- 
pound. If symptoms have arisen to 1 mgm. may be 
given intravenously. Good results have been reported by 
this treatment. If the individual is susceptible to arsphe- 
namine it is quite possible that he will also exhibit sensi- 
tiveness to epinephrine resulting in symptoms quite as 
alarming as those induced by the arsphenamine compounds. 
Type B. Early Symptoms.-These symptoms consist 
of chilliness or a distinct rigor, headache, vertigo, nausea, 
vomiting, diarrhoea, and rise of temperature, usually 
ioo° to io2°F. All of these symptoms may not be present 
and the patient may merely feel "queer" or there may be TOXICOLOGY 
100 
chills, attacks of emesis and profuse and protracted diar- 
rhoea. Sometimes complaints are made of severe pains 
in the legs and back. This group of symptoms usually 
passes off in 12 to 14 hours and is followed by a feeling of 
lassitude and weakness. More rarely vomiting and 
diarrhoea with slight rise of temperature may continue for 
a number of days, nourishment not being retained during 
this period. Sometimes the urine is small in volume and 
may contain albumin and casts. Various types of erup- 
tions may appear within a few hours or not for several 
days. The most common are urticarial, scarlatinoid, 
morbilliform erythemas, rarely purpura. Sometimes an 
itching of the skin or pruritus without accompanying 
eruption may be observed. Generally these eruptions 
disappear within a day or two. Late eruptions occurring 
from 6 to 10 days after the administration of the drug 
are much more persistent, universal exfoliating dermatitis 
occurring which may last for weeks with fever and debility 
and at times ends in death. 
Type C. The Late Symptoms.-The reactions may be 
delayed for more than 24 hours, in which event they 
usually consist of vomiting, fever and diarrhoea, similar 
to the immediate reactions. More rarely serious and even 
fatal reactions may develop about 3 days after the adminis- 
tration of the drug. In these instances the symptoms are 
referable either to the brain or to the liver. In the severe 
cases there may be headache, vomiting, muscular twitch- 
ings, epileptiform convulsions, dilatation of the pupils, 
absent reflexes, coma and death. These symptoms are 
usually the expression of edema of the brain or of encepha- 
litis hemorrhagica. A rare syndrome subsequent to 
arsphenamine administration is characterized by severe 
jaundice accompanied by rise of temperature. This may 
appear in from 3 days to several weeks after treatment. METALLIC POISONS 
101 
Most cases pursue a favorable course but sometimes a 
fatality occurs with the symptoms and autopsy findings of 
acute yellow atrophy of the liver. 
The treatment of the later manifestations of poisoning 
by the arsphenamine group is purely symptomatic. 
References to Arsphenamine Group 
Schamberg, Kolmer and Raiziss: J. Cutaneous Diseases, 1917, 
35, p. 286. 
Schamberg, Kolmer, Raiziss and Weiss: Arch. Derm, and 
SyphiL, 1920, N.S. 1, p. 235. 
Hunt: J.A.M.A., 1921, 76, p. 854. 
ANTIMONY (Sb) 
Antimony is a solid with grayish white appearance. It 
is tasteless and odorless. Chemically it is closely related 
to arsenic and forms the same types of compounds. In 
general only two compounds of antimony are of toxi- 
cological importance. These are tartrated antimony and 
antimony chloride which is also known as butter of anti- 
mony. These substances have been employed in the 
past in medicine, the tartar emetic, as its name implies, 
being used as an emetic; the antimony chloride in the form 
of an external application. Antimony chloride is at the 
present time used in industry especially in certain forms 
of bronzing. 
There are two types of poisoning, the acute and the 
chronic. Previous to 1850 poisoning by antimony was 
rather common. To-day, however, antimony poisoning 
is very rare. 
Acute Poisoning. Symptoms.-Salts of antimony must 
be regarded as irritant poisons and the clinical picture 
of arsenic poisoning might be substituted for that of 
antimony. Soon after taking the poison violent, frequent 102 
TOXICOLOGY 
vomiting occurs, the vomitus sometimes being mixed with 
bloody matter. There is a sense of constriction in the 
throat and pain in the stomach. Vomiting may continue 
even though the stomach is completely empty. Colicky 
pains attended by diarrhoea with watery stools occur, and 
there may be fainting attacks with profuse sweating. 
Nervous symptoms may supervene as indicated by spas- 
modic contraction of the limbs, with delirium, convulsions 
or coma. The urine may be suppressed and the skin may 
be covered with an eruption. In general antimony poi- 
soning has a more hopeful prognosis than arsenic poisoning 
even though the case seems desperate. 
Poisonous Action.-The poisonous action consists in 
the local effects upon the gastro-intestinal tract with a 
remote influence upon the liver, kidneys, and the central 
nervous system. Elimination occurs both through the 
urine and feces. 
Fatal Dose -The exact fatal dose is uncertain owing to 
the fact that the antimony compounds produce vomiting. 
The smallest dose that has proved fatal to a child is % 
grain, and a healthy woman died from the effects of 
grains. On the other hand recovery has followed a 
dose of 170 grains. 
Fatal Period.-The fatal period varies from a few hours 
even to several months. 
Post Mortem Appearances.-The mucous membrane 
of the gastro-intestinal tract is softened and corroded. 
There may be fatty degeneration of the internal organs 
such as the liver and kidneys. This latter condition, 
however, is much more likely to occur after chronic poison- 
ing rather than from the acute intoxication. The mucous 
membranes of the stomach and intestine may show a 
varied coloration from yellowish to reddish color due to 
the presence of antimony salts. METALLIC POISONS 
103 
Treatment.-Usually vomiting is induced by the 
ingestion of antimony salts. If vomiting does not occur 
spontaneously it should be induced and the stomach 
emptied so far as possible from all the antimony. The 
stomach should be washed thoroughly with warm water 
containing tannic acid or tea, these tending to form the 
insoluble tannate of antimony. For the relief of pain 
morphine may be given and the depression treated by the 
administration of stimulants. The stomach and bowels 
may be soothed by demulcent drinks and the patient 
should be kept warm. 
References 
Gaehtgens: Centralb. med. Wissen., 1876, p. 321. 
Rowntree and Abel: Trans. Assn. Am. Physicians, 1910, 25, 
p. 403; J. Pharm. and Exp. Therap., 1912, 2, p. 101. 
TIN-STANNUM (Sn) 
Tin is a silver white metal which resists the action of air 
and water. It is also present in many forms of alloy such 
as that of bronze or Britannia metal, and in soft solder. 
Tin forms two types of salts, the stannus and the stannic 
compounds. Intoxication from tin is rather uncommon 
but occasionally it does occur. A considerable contro- 
versy has arisen as to the possibility of poisoning from tin 
containers for fruits and other foodstuffs. It has been 
demonstrated that if the contents of these cans possess 
an acid reaction a considerable portion of tin may be 
contained in the food products. The consensus of opinion 
appears to be that in this instance poisoning by the soluble 
tin is doubtful or if it does occur the effects are so subtle 
and vague as to escape detection. Inasmuch as very 
few cases of poisoning have been reported from this 
source some doubt has been expressed as to the absorb- 
ability of tin compounds. This matter, however, has 104 
TOXICOLOGY 
been settled in the affirmative, the tin finding its way into 
the urine within a relatively short time. The major 
portion of tin, however, is eliminated by way of the 
gastro-intestinal tract and may be distributed in the liver, 
skin, brain and spinal cord. 
Symptoms.-The salts of tin must be regarded as gastro- 
intestinal irritants, the symptoms produced being a 
metallic taste, nausea, vomiting, abdominal pain, diar- 
rhoea, cyanosis, and collapse. Tin poisoning may also 
give indications of an influence upon the nervous system, 
the effects being similar to those of ataxia. Again there 
may be sore throat, a feeling of coldness and a condition 
of marked anemia. 
Poisonous Action.-The poisonous action is probably 
caused by the local action of the tin as an irritant. In the 
more chronic types of cases the influence upon the nervous 
system and the blood are the characteristic features. 
Fatal Dose.-The quantity of tin salts necessary to 
produce death is unknown. 
Fatal Period.-The fatal period is unknown. 
Post Mortem Appearances.-The post mortem appear- 
ances are confined almost entirely to the gastro-intestinal 
tract which presents the picture of irritation. 
Treatment.-The stomach should be emptied and lavage 
employed. To sooth the irritated gastro-intestinal tract 
demulcent drinks should be given together with stimulants 
and agents to allay the pain. 
Reference 
Salant, Rieger and Treuhardt: J. Biol. Chern., 1914, 17, p. 265. 
CHROMIUM (Cr) 
Chromium is a white, hard crystalline metal which is 
insoluble in alkalies and in all acids except hydrochloric. METALLIC POISONS 
105 
The chromium compounds which are of interest from the 
toxicological standpoint are potassium chromate, chromic 
acid, and lead chromate. Lead chromate, known other- 
wise as chrome yellow, possesses quite toxic properties 
but the characteristic effects are undoubtedly elicited by 
the lead rather than by the chromium. The salts of 
chromium cause poisoning mainly from the industrial 
use since the salts of chromium are employed in various 
types of trade such as dyers, furriers, stainers, battery 
fluids, etc. In medicine, chromic acid has been employed 
externally as a caustic and even here its employment is 
attended with considerable danger. In dye works the 
employees occasionally suffer from irritation on the arms. 
Chromate dust produces ulcers which develop slowly 
but penetrate very deeply and heal with difficulty. It 
also causes ulceration of the mucous membrane of the 
septum of the nose. 
Symptoms.-Chromium compounds must be regarded 
as gastrointestinal irritants. After absorption they also 
have an effect upon the central nervous system. The 
acute symptoms are those characteristic of gastro- 
intestinal irritants. There is at first a disagreeable taste, 
with vomiting, diarrhoea, and pain. The pupils are 
dilated and respiration is greatly slowed. Muscular 
cramps ensue followed by collapse and unconsciousness. 
Chronic poisoning produces severe dermatitis and ulcers. 
After absorption a characteristic feature of chromate 
poisoning is the induction of a severe nephritis accom- 
panied by a glycosuria. In these respects chromium 
resembles uranium. 
Poisonous Action.-The poisonous action of chromium 
salts is three-fold. First, that of a gastro-intestinal 
irritant; secondly, the influence upon the nervous system; 
and thirdly, the action upon the kidneys. 106 
TOXICOLOGY 
Fatal Dose.-The fatal dose of potassium dichromate is 
less than 8 gms. and for chromic acid about 6 gms. 
Fatal Period.-The fatal period is variable, death having 
occurred in 40 minutes after the taking of 1 ounce. 
Post Mortem Appearances.-Upon necropsy there may 
be gastrointestinal inflammation and ecchymoses. The 
kidneys exhibit a parenchymatous nephritis. 
The chromium is found in the blood, urine, feces and 
gastric contents. The main avenue of excretion is by way 
of the kidney which causes a detrimental influence upon 
this organ, but it is also eliminated by way of the bowel 
and the bile. 
Treatment.-Treatment consists in evacuation and 
lavage of the stomach followed by demulcent drinks. 
For the pain the ordinary sedatives should be given, and 
cerebral and respiratory stimulants as indicated. 
References 
Macniven: Lancet, 1883, 2, p. 496. 
Brieger: Zeit. exp. Path. u. Therap., 1920, 21, p. 393. 
THALLIUM (Tl.) 
Thallium is a heavy metal resembling in its toxic prop- 
erties lead. All thallium compounds are toxic. They 
possess a toxicity almost equal to that of arsenic. Thal- 
lium acetate has been employed therapeutically, externally 
as a depilatory, and against the night sweats of tubercu- 
losis. The medicinal use has caused poisoning, the chief 
symptoms being stomatitis, diarrhoea and dyspnea. 
There is salivation, trembling and pain in the limbs fol- 
lowed by paralysis. The hair falls out and hemorrhages 
may occur in the stomach and from the lungs. The 
effects are cumulative, somewhat like those of mercury 
and inasmuch as it is eliminated through the kidney in METALLIC POISONS 
107 
part it produces a persistent nephritis which is charac- 
terized by albuminuria. Thallium is also found in the 
feces, the elimination being very slow. It is also excreted 
into the milk. It causes death from asphyxia. 
Reference 
Swain and Bateman: J. Biol. Chem., 1910, 7, p. 137. 
IRON-FERRUM (Fe) 
Iron generally occurs as oxides, carbonate, or the 
sulphides. Pure iron is of a silver white color and capable 
of being highly polished. It is plastic like wax and can 
be pressed or forged into all sorts of forms. It readily 
forms oxides and possesses two types of salts, the ferrous 
and the ferric. Iron occurs throughout the body particu- 
larly in the hemoglobin of the blood, and is a frequent 
constituent of food. Inasmuch as the organism has a 
need for iron, various salts have been extensively employed 
in medicine as tonics. Iron itself has no specific toxic 
action on protoplasm but the salts in sufficient quantities 
produce gastro-intestinal irritation. Iron salts are elimi- 
nated for the most part by the gastro-intestinal tract. 
The salts most commonly met with from a toxicological 
viewpoint are ferrous sulphate and ferric chloride. The 
ferrous sulphate or copperas or green vitriol, as it is 
sometimes called, has been administered as a poison but 
has been employed more frequently to produce abortion. 
Symptoms.-When these salts have been taken there is 
a metallic taste which resembles that of ink, accompanied 
by vomiting, abdominal pain and diarrhoea. Later there 
may be pain in the extremities together with paralysis, 
suppression of urine, convulsions and death. The feces are 
black from the formation of iron sulphide. 108 
TOXICOLOGY 
Poisonous Action.-The poisonous action must be 
regarded as that of a gastro-intestinal irritant, and after 
absorption has, however, an influence upon the central 
nervous system and upon the kidneys, leading to the sup- 
pression of urine. 
Fatal Dose.-The fatal dose is quite variable, recovery 
having followed after taking 3 ounces of the tincture of 
iron, and on the other hand death having followed from 
ounces. Bile and vomiting and urinary symptoms 
have resulted from the taking of 1 ounce. 
Fatal Period.-Acute death is uncommon, the fatal 
result usually occurring after several weeks although in 
one instance it followed after 4 hours. 
Post Mortem Appearances.--In acute cases the gastro- 
intestinal tract is covered with a greenish black substance. 
The kidneys and liver show congestion and swelling with 
ecchymoses. The brain and its membranes may give 
evidence of hyperemia. 
Treatment.-Treatment consists in the administration 
of emetics and lavage of the stomach with large volumes 
of water containing alkaline bicarbonates or carbonates. 
Further treatment is purely symptomatic. 
Reference 
Berenger-Ferand and Porte: Annales d'Hyg. Pub., 1879, 
3 S., i, pp. 312 and 508. 
ZINC (Zn) 
Zinc is a white, soft metal which at a high temperature 
volatilizes and burns. If the temperature is above ioo°C. 
it becomes soft and may be rolled into sheets. Zinc is a 
common constituent of many foods and probably is 
constant in the animal body. Chemically zinc resembles 
manganese and chromium, and forms a series of salts, METALLIC POISONS 
109 
especially the oxide, which is used in the preparation of 
paint. In general intoxication from zinc occurs with 
those salts which are soluble, either the sulphate or the 
chloride, which may be mistaken for other substances. 
In medicine zinc sulphate is employed as an emetic and 
locally as an astringent and antiseptic. It is less irritant 
to the gastro-intestinal tract than copper. Zinc chloride 
finds medicinal use in external application for purposes of 
its escharotic action. Spelter chills or brass founders' 
ague are conditions which result from the industrial use 
of zinc. The spelter chills are characterized by chilliness, 
sneezing, pains in the limbs and abdomen, and a 
heightened temperature. Irritated mouth, nausea, diar- 
rhoea, rapid pulse and prostration are sequels. Exhaus- 
tion, sweating, and a deep sleep follow the chills. The 
brass founders' ague is induced from inhalation of finely 
divided zinc oxide which gives rise to irritation of the 
throat, malarial chill, with temperature, and the other 
general symptoms already indicated. 
Zinc fumes may cause chronic lesions of the respiratory, 
digestive, excretory and nervous systems. 
Symptoms.-Poisoning from sulphate of zinc occurs 
only after large doses when it produces gastro-intestinal 
disturbances such as vomiting and purging resulting in a 
serious prostration. These symptoms may be entirely 
absent and death result from the depressant action on the 
nervous system. The symptoms from zinc chloride are 
immediate pain in the throat, mouth and stomach, 
swallowing is difficult and painful, and there is excessive 
salivation. There is vomiting, diarrhoea and collapse 
which may end in coma and death within a few hours. 
Should death be delayed nervous symptoms make their 
appearance which are particularly noticeable in the special 
senses, especially taste and smell. Again aphonia, muscu- TOXICOLOGY 
110 
lar and localized tetanic affections may be observed. The 
caustic action may result in stricture of the esophagus or 
pylorus and cause destruction of the mucons membrane of 
the stomach so that death from inanition may result. 
Handling zinc chloride which may be used in the preserva- 
tion of wood causes dermatoses and burns which are 
ascribed to the influence of the zinc chloride. 
Poisonous Action.-The poisonous action of the zinc 
salts is similar to that of the other metals, that is, the influ- 
ence which it exerts as a gastro-intestinal irritant and the 
action which it induces upon the nervous tissues after 
absorption. Like the other heavy metals it is present in 
the liver and muscles and is eliminated both by the 
gastro-intestinal tract and also in the urine. 
Fatal Dose.-The fatal dose of zinc sulphate may be 
taken as about ounces. So far as zinc chloride is 
concerned 6 gms. have caused death although recovery 
has followed after a dose of 200 grains. 
Fatal Period.-The fatal period varies greatly inasmuch 
as death has occurred in 4 hours from both zinc sulphate 
and zinc chloride, yet other cases are on record in which 
death followed more than 100 days because of the secon- 
dary constriction of the esophagus. 
Post Mortem Appearances.-The autopsy findings are 
those characteristic of irritant poisoning, and mainly more 
or less intense inflammation of the mucous membrane and 
intestine. With zinc chloride there may be in addition 
ulceration or even perforation. 
Treatment.-The stomach should be emptied as rapidly 
as possible, the stomach tube being employed carefully 
when vomiting is not readily induced. Large volumes of 
water or milk should be given. White of eggs and tannin, 
best in the form of tea, may be regarded as antidotes for 
zinc chloride. METALLIC POISONS 
111 
Reference 
McCord and Kilker: J.A.M.A., 1921, 16, p. 442. 
CADMIUM (Cd) 
Cadmium is chemically very similar to zinc and although 
it has similar toxicological properties is much more poison- 
ous. Kobert claims that cadmium sulphate is twice as 
toxic as zinc sulphate. The toxicological interest of 
cadmium compounds is the intoxication which results from 
its industrial use. Workers in zinc are exposed to cad- 
mium fumes and present symptoms which are typical for 
lead poisoning. Absorbed the cadmium is eliminated 
by the gastro-intestinal tract and the urine, inducing 
gastro-enteritis and nephritis together with degeneration 
of the liver and heart. Cadmium chloride is a powerful 
emetic and experimentally it produces nephritis. Its 
hypodermic injection induces local necrosis and when 
administered intravenously death is caused by failure of 
respiration. So far as one may find, no deaths have been 
reported from employment of cadmium salts and in man 
the acute effects are those of a gastro-intestinal irritant. 
Reference 
Stephens: J. Industrial Hygiene, 1920, 2, p. 129. 
MAGNESIUM (Mg) 
Magnesium is a white tough metal forming salts which 
are relatively little absorbed by the alimentary canal. 
Magnesium sulphate probably possesses the greatest 
importance toxicologically because of its frequent thera- 
peutic use as a purgative. Owing to obstruction or slug- 
gishness of the intestine the onward passage of the 
magnesium may be so delayed that a considerable degree 
of absorption occurs especially if the salt is given in high 112 
TOXICOLOGY 
concentration. In conditions of marked dehydration, in 
animals at least, the same action occurs. Under these 
circumstances typical magnesium effects are induced- 
namely a condition of general anaesthesia, scanty or 
suppressed urine with abolition of reflexes, and respiratory 
paralysis which may cause death. 
In treatment of tetanus magnesium sulphate has been 
employed to control the convulsions. Attempts to use 
the salt as a local and general anesthetic have caused 
magnesium poisoning. In fatal cases there are fatty 
changes in the liver with small hemorrhages of the pleura, 
and peri- and endocardium. 
Elimination occurs by way of the urine which in conse- 
quence may have a very high specific gravity a fact in itself 
pointing to magnesium sulphate poisoning. 
Treatment of poisoning aims to increase elimination and 
to counteract the respiratory depression. For the purpose 
of hastening excretion large volumes of saline may be given 
intravenously and the bowel may be emptied by calomel. 
Calcium is antagonistic in action to magnesium and the 
respiratory depression may be alleviated by calcium chlor- 
ide solution (0.02 per cent in physiological saline) up to 
600 c.c. or more. Physostigmine to 1 mgm. subcutane- 
ously will act in the same manner. In the absence of 
either remedy or as an adjuvant artificial respiration 
should be instituted. 
References 
Meltzer and Auer: Am. J. Physiol., 1905, 14, p. 366. 
Meltzer: J.A.M.A., 1916, 66, p. 931. 
CALCIUM (Ca) 
Calcium is a grayish white metal whose salts are 
widely distributed in nature. It is of minor significance METALLIC POISONS 
113 
from a toxicological viewpoint since its salts are relatively 
non-poisonous. Occasionally, however, cases of poisoning 
occur from the ingestion of some form of lime. The 
symptoms indicated are burning abdominal pain, intense 
thirst and obstinate constipation. Treatment of the 
condition is neutralization of the lime by large volumes 
of weak acid as lemon juice or vinegar and evacuation of 
the stomach. Demulcents, as white of egg, milk, barley 
or oatmeal gruel, control of pain, and saline purgatives as 
magnesium or sodium sulphate are indicated. 
BARIUM (Ba) 
Barium is a white metal belonging to the group of 
alkaline earths together with calcium and strontium. Its 
ion is toxic and the common salts-chloride, nitrate and 
carbonate, all irritant compounds, may give rise to poison- 
ing. Barium salts are employed in wood staining and 
glass-making. The carbonate mixed with arsenic con- 
stitutes "Rough on Rats" and common salt, sodium 
chloride, may contain significant quantities. Barium 
sulphate is employed in X-ray work and poisoning has 
occurred because of errors in using a barium salt other 
than the sulphate. The excretion of barium is largely by 
way of the feces. 
Symptoms.-Barium closely resembles digitalis in its 
physiological action but because of its toxicity is 
not employed therapeutically. Its principal effects are 
increased excitability of heart muscle, contraction of 
arterial muscle, causing rise of blood pressure, strong 
peristaltic action of the intestines, initial stimulation and 
final paralysis of the central nervous system. 
The first symptoms are those of gastro-intestinal irrita- 
tion-vomiting, abdominal pain (colic) and diarrhoea. 
When absorption occurs the pulse is slow and hard, and 114 
TOXICOLOGY 
the blood pressure is high. Later convulsions and paraly- 
sis may occur. Death results from arrest of the heart. 
Fatal Dose.-The fatal dose approximates i gram 
although much larger quantities have been taken with 
recovery. 
Fatal Period.-Death results after an hour or less, or 
may be delayed for several days. 
Post Mortem Appearances.-Autopsy reveals gastro- 
intestinal irritation and some degree of corrosion. The 
stomach, intestines and kidneys may show hemorrhages. 
Treatment.-Treatment consists in the first place of 
attempting to change any unabsorbed soluble barium 
salt into an insoluble form as the sulphate. For this 
purpose the best chemical antidote is magnesium sulphate 
or sodium sulphate. Gastric lavage with milk and water 
should be thoroughly carried out. Pain and cardiac 
depression should be treated by the usual appropriate 
measures. 
Reference 
Salant and Kleitman: J. Pharm. and Exp. Therap., 1922, 20, 
p. 247. 
LITHIUM (Li) 
Lithium is a silver-white metal closely resembling 
sodium in many of its properties. Lithium salts are 
present in many natural mineral waters and is a con- 
stituent of many foodstuffs. The chief interest in lithium 
salts from a medical standpoint lies in the fact that they 
were formerly employed quite extensively in therapeutics 
as uric acid solvents in rheumatic and gouty conditions. 
Toxicologically in animals lithium resembles potassium 
except that when taken into the body, irrespective of the 
avenue of introduction, gastro-enteritis is in evidence. 
Lithium is excreted by the urine, saliva and feces, the METALLIC POISONS 
115 
gastroenteritis probably being caused by the gastro- 
intestinal excretion. In man large doses of lithium salts 
produce general muscular weakness, tremors, vertigo, 
impaired vision and ringing in the ears, but gastro- 
intestinal disturbances, may at times be absent. 
References 
Good: Am. J. Med. Sci., 1903, 125, p. 273. 
Cleveland: J.A.M.A., 1913, 60, p. 722. 
ALUMINUM (Al) 
Aluminum is a bluish, silvery metal which has extensive 
use in industry. In the form of its salts it is widely 
distributed in nature, especially in soils. It forms a series 
of salts, the most important of which, from a medical 
viewpoint, are the double sulphates of aluminum and 
the alkalies, sodium, potassium, and ammonium, to which 
the name alum has been given. In medicine these salts 
have been employed as local caustics and as astringents 
against diarrhoea. In properties these salts are so similar 
that they may be interchanged without perceptible 
alteration of physiological effects. When alum is heated 
it loses its water of crystallization and is transformed 
from a crystalline form to a spongy white mass. This is 
called "burnt alum." Both types of alum possess 
marked caustic and astringent properties, the burnt alum 
to the greater degree. 
Aluminum salts are toxic to plants, animals and man 
exerting an irritant influence upon protoplasm. Alu- 
minum in the form of alum has caused violent irritant 
symptoms sometimes ending in death. The symptoms 
produced are gastro-intestinal disturbances as vomiting 
and pain, the vomitus containing blood stained mucus. 
The urine shows albumin and blood. 116 
TOXICOLOGY 
The chief interest in aluminum compounds centres 
around the employment of the alums, especially sodium 
alum, in baking powders, as an acid agent to liberate CO2 
from the sodium bicarbonate. There is left a residue of 
aluminum hydroxide, sodium sulphate and perhaps 
some unchanged alum. It has been held by some that 
the aluminum hydroxide is not absorbed, hence can- 
not exert a detrimental influence. Notwithstanding the 
report of the Referee Board to the contrary there is 
evidence that the aluminum contained in baked bread or 
biscuits is absorbed and is thus free to act upon any cells 
with which it may come into contact (Steel). Aluminum 
finding its way into the blood stream causes paralysis of 
sensation and motion, with fatty degeneration of the 
liver and kidneys (Siem). 
According to Mallet the aluminum of bread dissolves 
in the human gastric juice. "It is likely that the action 
of this soluble chemical would be deleterious to the gas- 
tric processes. Persons with temporary illness or those 
with permanently feeble digestion would suffer greater 
detriment than the many in health or of average peptic 
strength, whose power of resistance would enable them to 
withstand the tax without obvious harm. It is probable 
that the insidious strain repeated daily would in time 
be hurtful, and yet the cause of this effect go unrecog- 
nized" (Holland). 
"For these reasons it is just to demand that positive 
proof be furnished that these chemicals foreign to the 
normal body are harmless. This proof beyond a reason- 
able doubt is still lacking" (Holland). 
References 
House and Gies: Am. J. Physiol., 1906, 15, p. XIX. 
Steel: Am. J. Physiol., 1911, 28, p. 94. METALLIC POISONS 
117 
Siem: Schmidt's Jahrbuch., 1886, 211, p. 128. 
Holland: In Peterson, Haines and Webster's Legal Medicine and 
Toxicology, 2nd Edition, 1923, p. 165. 
Report of Referee Board, U. S. Dept. Agri. Bull. 103. 
URANIUM (U) 
Uranium, like radium, is a source of radiant energy and 
its salts have been employed in medicine for the treatment 
of diabetes. The soluble salts, the acetate and nitrate are 
the most common uranium preparations. Ingestion or 
injection of uranium salts leads to respiratory paralysis 
which is the cause of death. In sublethal doses uranium 
causes nephritis and glycosuria, the tubules and glomeruli 
both being affected. Other mechanisms that may be 
acted upon are the gastro-intestinal tract, blood vessels 
and the nervous system. At times the liver undergoes a 
degeneration, which is similar to that seen in mercury 
poisoning, and which is accompanied by acidosis. 
References 
MacNider: J. Exp. Med., 1916, 23, p. 171. 
Karsner, Reimann and Brooks: J. Med. Res., 1918, 39, pp. 163, 
169, 177. 
VANADIUM (V) 
Vanadium is a rare metal belonging to the nitrogen and 
phosphorus group. It is grayish-white with feebly basic 
and strong acid properties and has valences of 1, 2, 3, 4, 
and 5, the last being the most stable. Vanadium salts, 
especially the chloride and trioxide, are employed in indus- 
try chiefly in dyeing and in the manufacture of steel. 
Vanadium pentoxide has been used therapeutically in 
diseases of metabolism without sufficient justification. 
Vanadium poisoning, vanadiumism, is experienced by 
persons employed in manufactories where vanadium is 
produced, dust and fumes being responsible. Poisoning 118 
TOXICOLOGY 
may also result from using or wearing clothing dyed by 
vanadium chloride, trioxide or pentoxide. 
Symptoms.-Anemia is an early symptom (a peculiar 
cachexia) somewhat resembling chlorosis. At first there 
is an increase in hemoglobin content and red cell count 
followed shortly by a reduction of the cells and hemoglobin. 
Cough is a prominent and characteristic symptom. It is 
dry, irritating and paroxysmal, becoming so intense that 
hemorrhages are frequent and severe, even causing death. 
The victims of the poisoning are especially susceptible to 
tuberculosis. Emaciation, irritation of the nose, throat 
and eyes are always present. Gastro-intestinal distur- 
bances are indicated by anorexia, nausea, diarrhoea, alter- 
nating with constipation. The urine may contain albu- 
min, casts and blood. 
Later sequels of exposure to the poison are nervous dis- 
turbances, as headache, fine tremors of the extremities, neu- 
roretinitis, amaurosis, vertigo, hysteria and melancholia. 
Post Mortem Appearances.-The action of the poison 
seems directed on the gastro-intestinal tract, the lungs and 
the kidneys. The lungs show marked congestion and 
destruction of alveolar epithelium. The kidneys are 
highly congested and sometimes there is an acute hemor- 
rhagic nephritis. The gastro-intestinal tract is irritated 
and inflamed. The drug is excreted by the urine, feces, 
and saliva. 
Treatment.-The prognosis is good in the absence of 
serious renal, blood, nervous and lung involvement. The 
patient should be kept out of the poisonous environment, 
given open air exercise, tonics, and symptomatic treatment 
when needed, as for example, for cough. 
Reference 
Dutton: J.A.M.A., 1911, 56, p. 1648. METALLIC POISONS 
119 
MANGANESE (Mn) 
Manganese closely resembles iron in its physical and 
chemical properties. It has a reddish-gray lustrous color. 
Like iron it forms two series of salts, the ous and ic com- 
pounds. Manganese occurs in traces in the organs of 
man and animals due to the presence of manganese in the 
food. Salts of manganese in general produce no notice- 
able effects when taken by mouth. Absorption occurs to 
a certain extent and excretion takes place mainly by the 
intestines although some manganese is eliminated in the 
urine. Injected intravenously manganese salts produce 
fatty degeneration of the liver. Potassium permanganate 
which must be regarded as a strong oxidizing agent is a 
gastro-intestinal irritant, large doses causing death. 
Treatment of potassium permanganate poisoning consists 
in administration of white of egg and gastric lavage, the 
general symptoms being combatted as they arise. 
The main toxicological interest in manganese arises 
from its use in industry when workers are brought into 
contact with manganese dust. 
Symptoms.-According to Edsall, Wilbur and Drinker 
the symptoms which are clear cut and lend themselves 
readily to diagnosis are produced by contact with manga- 
nese dust for a period of three months. The characteristic 
signs are langour and sleepiness, stolid, mask-like facies, a 
low monotonous voice, muscular twitchings which may be 
generalized, cramps in the calves and stiffness of the leg 
muscles, cramps usually coming on at night and being 
worse after a day of exertion. There is a peculiar slapping 
gait, the patient maintaining a broad base. Occasionally 
there is uncontrollable laughter and sometimes crying. 
There are no disturbances of deep or superficial sensation, 
eye changes, genito-urinary or gastro-intestinal distur- 
bances, reactions of degeneration, blood, urine or spinal 120 
TOXICOLOGY 
fluid alterations. It is significant that, unlike lead, man- 
ganese does not shorten life by the production of degenera- 
tions. If severely poisoned the victims are life-long 
cripples. The metal apparently makes a very definite 
attack upon some non-vital portion of the neuro-muscular 
system, destroys it thoroughly, if time for action is per- 
mitted, and leaves the patient quite well in every other 
respect. There seems to be a certain degree of idiosyn- 
crasy to the action of manganese only a small proportion 
of workers being attacked. 
The disease is never fatal although autopsy has been 
performed by Casamajor upon a single case of advanced 
manganese poisoning, death being caused by pneumonia. 
No gross changes were present in the brain, kidneys, 
liver or spleen. Histologically examined there was a 
moderate chronic interstitial nephritis and in the liver 
there was considerable biliary cirrhosis. The brain showed 
evidences of digeneration in certain areas. 
When poisoning has actually occurred no form of treat- 
ment has any value. Prevention is the only known means 
of combatting the conditions. In incipient cases spontane- 
ous recovery follows when the patient is removed from the 
contaminating atmosphere. 
References 
Casamajor: J.A.M.A., 1913, 60, p. 646. 
Edsall, Wilber and Drinker: J. Ind. Hyg., 1919, 1, p. 183. 
Davis and Huey: J. Ind. Hyg., 1921, 3, p. 231. CHAPTER V 
ALKALOIDAL POISONS 
The alkaloids are organic nitrogenous bases occurring 
naturally, for the most part, in plants and they may be 
regarded as substituted ammonium compounds or amines, 
generally tertiary amines. Some contain oxygen whereas 
in others oxygen is absent. Certain of the alkaloids are 
liquid and volatile, others are solid and non-volatile. 
The oxygen-containing alkaloids belong to the latter group, 
the non-oxygen-containing alkaloids, like nicotine, and 
coniine are liquid and volatile. They are further divided 
into three great groups according to their chemical 
structure, thus derivatives of (a) pyridine, as atropine 
and nicotine, (6) quinoline, as quinine and strychnine, 
and (c) phenanthrene, as morphine and codeine. 
Several alkaloids may occur in the same plant and these 
may possess physiological actions similar or completely 
antagonistic to each other. On the other hand they all 
possess certain characteristic properties as a group. 
They are bitter, and give an alkaline reaction to litmus. 
As the free base they are generally insoluble in water, 
but form soluble crystalline salts with the common 
inorganic acids. The free bases are readily soluble in 
oils, ether, chloroform and alcohol, whereas the salts are 
relatively insoluble. They are precipitated from solution 
by forming compounds with a variety of reagents both 
organic and inorganic in nature and from this fact these 
substances are spoken of as "alkaloidal reagents." The 
list of alkaloidal reagents includes, mercuric chloride, 
121 122 
TOXICOLOGY 
potassium mercuric iodide (Mayer's Reagent), potassium 
bismuth iodide (Dragendorff's Reagent), phosphomolybdic 
acid and phosphotungstic acid, tannic acid, picric acid, 
platinic chloride, gold chloride, potassium dichromate, 
and picrolonic acid. Again many of the alkaloids give 
color changes with concentrated acids either with or 
without addition of oxidizing agents, the reaction aiding 
in the identification of a particular alkaloid. 
In general the alkaloids act upon the nervous system 
producing varied effects. 
CONIINE (Hemlock Alkaloid) 
Conium maculatum or "poison hemlock," is a plant 
growing wild in various parts of the United States. It 
closely resembles parsley and from this fact cases of 
poisoning have occurred. Coniine, a volatile alkaloid, 
is the principal active constituent of this plant and is a 
derivative of pyridine. The poison of hemlock has been 
well known since Socrates killed himself by drinking it. 
There are at least five other alkaloids in hemlock and they 
are closely related to coniine chemically. Formerly, the 
fluid extract of conium was employed as a sedative and 
antispasmodic but to-day it is not used to any extent. 
The concentrated free alkaloid is a local caustic. 
Pure coniine has been prepared synthetically but is of the 
racemic form whereas that occurring naturally is dextro- 
rotatory. Coniine is a colorless, oily liquid with a peculiar 
odor resembling that characteristic of mice. Its boiling 
point is i66°C. and has a specific rotation [a]D = 15.70 at ALKALOIDAL POISONS 
123 
i9°C. When the solid is sufficiently chilled coniine 
becomes a solid crystalline mass. It is relatively insoluble 
in water but easily soluble in alcohol, ether, chloroform, 
benzol and acetone. 
Symptoms.-The poisonous action develops very 
rapidly, the symptoms consisting of a burning, smarting 
sensation in the mouth and throat, pain in the head, 
drowsiness, faintness, lassitude, muscular weakness, 
muscular twitchings, stiffness and rigidity, and pupil 
dilation. Nausea is usually present and at times vomiting 
may occur, speech and deglutition being difficult. The 
intellect generally remains clear although the special 
senses may be dulled. Paralysis of the extremities may set 
in. The respiration is chiefly affected, at first being rapid, 
later slow and labored, eventually becoming weak and 
irregular, death resulting from respiratory failure. 
Poisonous Action.-Coniine causes paralysis of the ends 
of the motor nerves eventually extending to the trunks and 
the motor centre itself. The sensory nerves are less 
affected but may share in the paralysis. The final action 
is paralysis of the respiratory centre. Coniine is elimi- 
nated from the body by the lungs and by the kidneys. 
Probably a portion is burned or otherwise destroyed by 
the organism. 
Fatal Dose.-The fatal dose is between 2 and 3 grains. 
Fatal Period.-Death may occur within a few minutes 
and the longest case on record is fifty-two hours. 
Post Mortem Appearances.-There is nothing char- 
acteristic, the appearances being for the most part those 
peculiar to death by asphyxia. The gastro-intestinal 
membrane may be inflamed and congested. 
Treatment.-Treatment of coniine poisoning consists in 
lavage of the stomach, employing tannin as an antidote, 
stimulation and maintenance of the respiration. 124 
NICOTINE GROUP 
TOXICOLOGY 
American, Havana, French and Dutch tobaccos are in 
general obtained from the tobacco plant, Nicotina 
tobacum. Turkish, Syrian and Latakia tobaccos are 
derived mainly from Nicotina rustica. In either event 
there are at least four alkaloids present in the plant, chief 
of which is nicotine. It exists in all parts of the plant but 
occurs in largest quantity in the leaves, from which 
tobacco of commerce is prepared. 
Nicotine is a colorless, oily fluid with little odor but when 
allowed to stand or diluted with water the characteristic 
odor of tobacco develops. Its taste is sharp and irritating. 
In contact with air nicotine assumes a dark brown color 
and gradually becomes a resin. The free base is levoro- 
tatory [a]D= -166.4 at 2o°C. whereas its salts turn the 
plane of polarized light to the right. Nicotine is soluble in 
alcohol, ether and water. 
Symptoms.-Intoxication with nicotine, other than 
through the use of tobacco is rare although there are 
several cases on record. Irrespective of whether nicotine 
is taken in the form of the alkaloid or in the use of tobacco 
the symptoms produced are quite characteristic, the 
only significant difference being in the time of onset and 
development of symptoms. The pure nicotine acts with 
a rapidity equal to that of hydrocyanic acid, and if in ALKALOIDAL POISONS 
125 
concentrated form, leaves behind evidences of irritation 
since nicotine has some caustic action. 
If nicotine is taken by mouth there is a hot, burning 
sensation from the mouth to the stomach. Absorption 
occurs rapidly. The first symptoms are nausea, saliva- 
tion, vomiting, and purging with abdominal cramps. A 
considerable degree of dizziness, mental confusion and 
muscular weakness follow. The pulse is weak, slow and 
sometimes intermittent. There may be clonic convulsions 
and tetanic spasms. Respiration is rapid and labored and 
the eyes protrude, the pupils at first being contracted, later 
dilated. Later a condition of unconsciousness may set in, 
with symptoms of shock, or delirium, death resulting from 
respiratory failure. 
Poisonous Action.-Nicotine is readily absorbed as 
such and is then free to act upon the nerve centers. The 
first action is one of stimulation of the brain followed by 
depression. The convulsions are probably of cerebral 
origin, although nicotine acts powerfully upon the heart 
causing it to beat slowly and irregularly through vagus 
inhibition. Death does not occur from paralysis of the 
heart but from arrest of the respiration. Nicotine appears 
to possess a strong, almost specific effect upon the small 
intestines and uterus causing them to contract vigorously. 
Bile and saliva secretions are increased. It .is probable 
that a portion of nicotine is oxidized or otherwise changed 
in the body, the major portion, however, being eliminated 
by the urine and saliva. 
Fatal Dose.-One to four drops of pure nicotine will 
probably kill an adult in a few minutes. Perhaps the 
smallest fatal dose is about one grain. The fatal dose 
varies somewhat according to whether the individual 
has an established tolerance for nicotine through the use 
of tobacco. 126 
TOXICOLOGY 
Fatal Period.-Death may occur within a few seconds 
depending upon the rate of absorption of the nicotine, 
which in turn would be influenced by the state of the ali- 
mentary canal, food content, etc. A fatal outcome has 
been recorded as long as two days after ingestion of the 
poison. 
Post Mortem Appearances.-Post mortem appearances 
are not especially characteristic. The odor of nicotine 
may be present in the gastro-intestinal contents and the 
mucous membranes of the stomach and intestines may 
show signs of irritation. 
Treatment.-Evacuation of the stomach and thorough 
gastric lavage are indicated. To the wash-water may 
be added tannic acid or oxidizing agents as hydrogen 
peroxide. The symptoms are to be combatted by stimula- 
tion, maintenance of the respiration, and body temper- 
ature. Oxygen inhalation may be of value. 
THE USE OF TOBACCO 
Under ordinary circumstances the moderate use of 
tobacco in the form of smoking or chewing tobacco is not 
attended by any perceptible untoward effects except the 
establishment of a habit which in some instances is very 
difficult to break. Symptoms of poisoning which resem- 
ble mild nicotine intoxication, are, however, usually exper- 
ienced in the first use of tobacco in any form, and even 
in the experienced user of tobacco when an excess is 
consumed. In spite of statements to the contrary, it is 
quite generally accepted that the symptoms which may 
be called forth by the excessive use of tobacco are due to 
the nicotine content of the smoke or juice. Inhalation of 
the smoke produces more marked symptoms than are 
experienced when the smoke is not inhaled. This un- ALKALOIDAL POISONS 
127 
doubtedly is due to the greater absorption of nicotine by 
the blood vessels of the lungs. 
As stated previously the acute toxic symptoms which 
may be produced by the use of tobacco resemble those of 
acute nicotine poisoning. The long continued excessive 
use of tobacco may also give rise to chronic poisoning 
which is manifested especially upon the gastro-intestinal 
tract, the central nervous system and the heart. The 
symptoms indicative of chronic poisoning are loss of 
appetite, with various types of gastric inability to handle 
foods and chronic intestinal catarrh, which may lead 
to anemia and emaciation; nervous disturbances take the 
form of heightened reflexes, insomnia, tremors and lack 
of control of voluntary movements, and rarely nicotine 
blindness which may be completely cured by stopping the 
use of tobacco unless degeneration of the optic nerve 
has set in. The heart symptoms are so characteristic 
as to lead to the designation of the trouble as "tobacco 
heart." There is palpitation, increased rate, arythmia 
which is due to extra systoles of the auricles, and heart 
block. All these symptoms disappear on stopping the 
use of tobacco. The heart irregularity may become 
sufficiently grave to cause fainting. Angina pectoris is 
rare in these cases but arteriosclerosis is said to be favored 
by the use of tobacco. 
The therapeutic use of tobacco or nicotine at the present 
time is very limited. Numerous cases of poisoning have 
been recorded attendant upon the employment of tobacco 
therapeutically, as in the form of a poultice applied to local 
swellings or to stop bleeding, or as an enema. 
Analyses of tobacco of diverse origin have shown a wide 
variation in nicotine, the range being from 0.6 to 8.q per 
cent. It is often stated that different brands of cigarettes 
contain added opium derivatives. This is incorrect since 128 
TOXICOLOGY 
several investigations have failed to show the presence 
of any foreign narcotic drug. 
References 
Van Leeuwen: Arch. Need. Physiol., 1918, 2, p. 650; Arch. f. 
exp. Path. u. Pharm., 1918, 84, p. 282. 
Baumberger: J. Pharm. & Exp. Therap., 1923, 21, pp. 23, 35, 47. 
THE OPIUM GROUP 
When the unripe capsules of the garden or opium poppy, 
Papaver somniferum, are cut the juice flows out and this 
when air-dried is called opium. This brownish material 
contains twenty or more alkaloids which are divisible 
into two groups, namely, the morphine group and the 
papaverine group. The morphine group is the most 
important, and the members may be regarded as phen- 
anthrene derivatives. In addition to morphine this group 
contains esters formed by replacing the hydrogen of one 
or both hydroxyl groups in morphine. Codeine, or 
methylmorphine; thebaine, or dimethylmorphine are 
natural constituents of opium. Others, as dionine, or 
ethylmorphine, and heroine or diacetylmorphine are 
synthetic products. The second group of alkaloids in 
opium are iso-quinoline derivatives, the most important 
being papaverine and narcotine. The characteristic 
effects of this group is associated with the benzyl radicle. 
From a toxicological viewpoint the important con- 
stituents of opium are morphine, codeine, and heroine. 
The alkaloids of opium occur in combination with acids 
usually sulphuric and meconic acids although sometimes 
the combination is with acetic and lactic acids. In the 
dried form opium contains about 10 per cent of morphine. 
The structural relationships of the different opium 
derivatives may be represented by the following formulae: ALKALOIDAL POISONS 
129 
Pschorr's Formula 
for Morphine 
Pschorr's Formula 
for Codeine 
Pschorr's Formula 
for Thebaine 
Pschorr's Formula for 
Apomorphine 
Papaverine 130 
TOXICOLOGY 
OPIUM AND MORPHINE 
Inasmuch as opium and morphine are so similar in 
action toxicologically, the characteristic effects in either 
case being produced by morphine, a single description of 
the symptoms will suffice. The number of medicinal 
preparations into which morphine may enter as a con- 
stituent is very large and for the official preparations the 
reader is referred to the United States Pharmacopoeia. 
Morphine is found as a crystalline powder which may be 
made up of prisms or needles. This powder is without 
odor and is bitter to the taste. Relatively insoluble in 
water, ether and benzene it readily dissolves in chloro- 
form and alcohol especially if the latter is hot. Its 
aqueous solution is alkaline to litmus and dissolves readily 
in dilute acids and in an excess of the caustic alkalies. 
In small quantities of potassium and sodium hydroxides 
morphine is insoluble. Solutions of morphine in acid and 
alcohol turn the plane of polarized light to the left. 
Nearly all morphine salts are crystalline, soluble in water 
but insoluble in amyl alcohol, ether, chloroform and ben- 
zol. The most common morphine salts are the hydro- 
chloride and the sulphate which exist as white crystalline 
powders readily soluble in water. 
Symptoms.-The symptoms of poisoning in man may 
be divided into three stages (a) a period of excitement, 
(b) an interval of narcosis, and (c) coma. The rate at 
which symptoms begin to be manifested varies with the 
manner of administration, being earlier following hypo- 
dermic injection than when given by mouth. In the latter 
instance, usually in less than thirty minutes, there is a 
sensation of exhilaration and well being, the pulse rate 
is increased, the pupils contracted, and the face is flushed. 
Thus far the symptoms closely resemble those of alcohol. 
Immediately following these sensations there is a feeling ALKALOIDAL POISONS 
131 
of giddiness, and mental heaviness which gradually 
is succeeded by drowsiness, sometimes nausea and vomit- 
ing, the pulse being slow and reduced in volume. In 
certain cases skin eruptions may appear. An irresistible 
desire for sleep follows accompanied by feelings of great 
muscular relaxation and loss of sensation. The pupils 
become contracted, the bowels are generally constipated 
and voluntary control of the bladder is lost. Uncon- 
sciousness ensues which is succeeded by coma from which 
the patient cannot be aroused. The respiration is ster- 
torous and slow and gradually becomes shallower. Cya- 
nosis is present, the skin is covered with a cold sweat and 
near to death the pupils may dilate. Dilated pupils 
in a dead body, therefore, do not contraindicate mor- 
phine or opium poisoning. Death occurs from failure 
of respiration. As in other types of faulty respiration 
the blood shows typical features, accumulation of CO2, 
insufficient oxygen, etc. 
All cases of opium or morphine poisoning do not neces- 
sarily present the same train of symptoms. At times 
death is sudden without preliminary symptoms other 
than sleep, and death occurs quickly. Again in individu- 
als more or less accustomed to the drugs convulsions may 
be the characteristic feature. A relapsing form is also 
sometimes to be observed, the patient apparently being on 
the road to recovery, consciousness being restored, only to 
sink back into a fatal narcosis. Vomiting may or may not 
be present and the same is true with respect to diarrhoea. 
At times the diagnosis of opium or morphine poisoning 
is difficult since the symptoms so closely simulate those of 
disease and other types of intoxication. "Insensibility 
from chloral, from alcohol, from belladonna or atropine, 
and from carbon monoxide gas are all more or less like 
opium poisoning. With regard to chloral, it may be that 132 
TOXICOLOGY 
only chemical analysis and surrounding circumstances 
can clear up the matter. In alcohol poisoning the breath 
commonly smells very strongly of alcohol, and there is no 
difficulty in separating it from the contents of the stomach, 
etc., besides which the stomach is red and inflamed. 
Atropine and belladonna invariably dilate the pupil, 
and although just before death opium has the same effect, 
yet we must hold that mostly opium contracts, and that 
a widely dilated pupil during life would, per se, lead us to 
suspect that opium had not been used, although, as before 
mentioned, too much stress must not be laid upon the state 
of the pupils. In carbon monoxide, the peculiar rose-red 
condition of the body affords a striking contrast to the 
pallor which, for the most part, accompanies opium 
poisoning. In the rare cases in which convulsions are a 
prominent symptom, it may be doubtful whether opium 
or strychnine has been taken; but the convulsions hitherto 
noticed in opium poisoning seem to have been rather of 
an epileptiform character, and very different from the 
effects of strychnine. No rules can be laid down for cases 
which do not run a normal course; in medicine such are 
being constantly met with, and require all the care and 
acumen of the trained observer. Cases of disease render a 
diagnosis often extremely difficult, and the more so in 
those instances in which a dose of laudanum or other 
opiate has been administered. 
Apoplexy will only simulate opium poisoning during 
life; a post mortem examination will at once reveal the 
true nature of the malady. In epilepsy, however, it is 
different, and more than once an epileptic fit has occurred 
and been followed by coma-a coma which certainly 
cannot be distinguished from that produced by a narcotic 
poison. Death in this stage may follow, and on examining 
the body no lesion may be found" (Blyth). ALKALOIDAL POISONS 
133 
"In differential diagnosis of morphine poisoning it is 
observed that, as a rule, it differs from alcohol narcosis in 
the contraction of the pupil; from cerebral hemorrhage, in 
the two pupils being alike in contraction; from carbolic 
poisoning in showing no white stain in the mouth; and from 
the narcosis of chloroform or ether, in absence of the odor 
of these agents on the breath. In whatever diseases and 
from whatever poisons there are failure of respiration and 
excessive venosity of the blood, there are certain grave 
symptoms which are likewise found in morphine poisoning. 
Then the history of the case must be relied upon for a 
differential diagnosis, and, if possible, the question must be 
settled by a chemical analysis of the liquid vomited or 
drawn from the stomach " (Peterson, Haines and Webster). 
Morphine varies in its action on different animals. 
Thus in frogs, strychnine-like convulsions are caused; in 
the herbivora, as in the rabbit and goat, the narcotic 
influence is lacking but death follows from respiratory 
failure; in the cat and related species the feature is great 
excitement, culminating in convulsions and death; the 
dog behaves in a manner very similar to man. 
Morphine is rapidly absorbed from all mucous sur- 
faces. It is combined in the organs in part and in part is 
oxidized. As it is excreted into the stomach it may be 
reabsorbed. More is eliminated from the body by way of 
the feces than by the urine. 
Fatal Dose.-Doses of morphine above one grain are 
undoubtedly dangerous and death will generally occur 
after 2 grains. Doses of three to four grains of opium 
will probably cause death. Children are much more 
susceptible to morphine than are adults. 
Fatal Period.-The fatal period varies from about one 
to twelve hours. If respiration can be maintained for a 
period of 24 hours or more recovery is possible. 134 
TOXICOLOGY 
Post Mortem Appearances.-The only characteristic 
appearances after death are those common to other 
respiratory deaths, hyperemia of the brain and pulmonary 
congestion. 
Treatment.-The stomach should be evacuated as soon 
as possible even though the drug has been administered 
subcutaneously. Potassium permanganate gram per 
liter of water) is the best chemical antidote. Tannic acid 
is not very satisfactory. Every means should be taken 
to keep the patient awake and in motion if possible. Stim- 
ulation should be pushed, strong black hot coffee or 
strychnine. Atropine may aid if not more than grain 
is given. The patient should be kept warm and if the 
respiration shows signs of weakening artificial respiration 
should be instituted. When recovery is certain the bowels 
should be emptied by cathartics. The intestines should 
be emptied soon since a relapse may occur from reabsorbed 
morphine in the intestines. 
Reference 
Macht: J. Pharm. and Exp. Therap., 1915, 7, p. 339. 
The quantity of codeine present in opium is less than 
one-twentieth that of morphine. Codeine is very similar ALKALOIDAL POISONS 
135 
to morphine in its pharmacological and toxicological 
effects but very much weaker. Codeine occurs in crys- 
talline prisms which possess the same solubilities as 
morphine, being relatively insoluble in water, petroleum 
ether, and the hydroxides of sodium and potassium. It 
is soluble in ether, chloroform, benzol, amyl alcohol, acids 
and ammonium hydroxide. It is levorotatory in watery 
solutions. By treatment with strong acids it yields 
apomorphine under the same conditions as does morphine. 
The common salts of codeine are the phosphate and the 
sulphate which are readily soluble in water but insoluble 
in chloroform and ether. Unlike morphine codeine 
apparently does not readily form a habit. 
Symptoms.-Codeine produces less profound sleep than 
morphine and in large doses tends to increase excitability. 
The symptoms of poisoning are disturbances of vision, 
muscular weakness, slight delirium, increased heart rate, 
dyspnoea and collapse. Codeine does not appear to cause 
constipation. 
Fatal Dose.-Doses of more than 4.5 grains (0.3 grams) 
are dangerous. 
Treatment.-Treatment for codeine poisoning would be 
similar to that for morphine. 136 
TOXICOLOGY 
Heroine is a synthetic derivative of morphine, diacetyl- 
morphine. It forms a white powder of crystalline prisms 
which are difficultly soluble in water and ether but readily 
soluble in hot alcohol and chloroform. Treated with 
potassium hydroxide it yields morphine and acetic acid. 
With hydrochloric acid it forms heroine hydrochloride, 
a white crystalline powder, soluble in water and alcohol 
and insoluble in ether and chloroform. In the body 
morphine is formed from heroine. 
Symptoms.-Poisoning from heroine resembles closely 
morphine intoxication. In general there is a greater 
action on the respiratory mechanism, the cerebral symp- 
toms being less pronounced. The symptoms most char- 
acteristic are disturbed vision, headache, restlessness, 
slow pulse, slow, deep respiration, some cyanosis, pains 
in the extremities. Death is due to failure of respiration. 
In many instances death from heroine intoxication 
results from over-dosage by individuals with the heroine 
habit, acquired in many cases by the taking of the drug 
in the form of snuff. 
Fatal Dose.-The fatal dose is approximately 0.5 gram. 
Fatal Period.-This varies from a few hours to 2 or 3 
days. 
Post Mortem Appearances.-Autopsy of heroine victims 
reveals nothing characteristic beyond those features usual 
with deaths from respiratory failure. 
Treatment.-The treatment indicated for heroine poi- 
soning is exactly that outlined for morphine intoxication 
(see page 134). Inasmuch as heroine possesses an action 
upon the respiration more marked than morphine special 
attention should be given to its maintenance. 
Reference 
McNally: J. Lab. and Clin. Med., 1917, 2, p. 570. ALKALOIDAL POISONS 
137 
APOMORPHINE 
Apomorphine is a synthetic derivative of morphine 
made by the action of concentrated acids upon the 
alkaloid. It possesses little or no narcotic action but 
instead exercises an excitant action upon the nerve 
centres, particularly the vomiting centre. This is stimu- 
lated to a marked degree whether the drug is administered 
by mouth, vein or subcutaneously. Therapeutically 
and toxicologically its chief significance lies in its property 
of causing vigorous vomiting and advantage may be 
taken of its use in cases of other types of poisoning espe- 
cially when resistance is offered to treatment or coopera- 
tion on the part of the patient is lacking. In general, 
however, in poisoning with narcotics apomorphine fails 
to work. This statement is particularly true with respect 
to chloroform, chloral, morphine and its derivatives. 
Poisoning by apomorphine rarely occurs, its appearance 
for the most part resulting from accidents in therapeutic 
employment. 
Symptoms.-The chief symptoms of poisoning are 
marked excitement, anxiety, dizziness, fainting, irregular 
respiration, violent convulsions, and death from res- 
piratory failure. 
It is generally conceded that these untoward effects are 
produced by impurities, such as decomposition products, 138 
TOXICOLOGY 
in the apomorphine preparations employed. Accidents 
are particularly likely to occur if vomiting is not elicited, 
especially in lung and heart diseases, in patients with 
lowered resistance in general, and in children. 
The fatal dose is indefinite and treatment should be 
directed especially to the maintenance of respiration. 
References 
Harnack: Munch, med. Wochenschr., 1910, 57, p. 1745. 
Macht: J.A.M.A., 1917, 68, p. 1230; Proc. Soc. Exp. Biol, and 
Med., 1917, 15, p. 26. 
STRYCHNINE GROUP (Nux Vomica) 
STRYCHNINE AND BRUCINE 
Strychnine 
Brucine 
The seeds of Strychnos nux vomica, or Koochla tree, 
contain approximately three to four per cent of the 
alkaloids, strychnine and brucine, which occur in about 
equal quantities. The mixture obtained from dried ripe 
seeds constitutes the therapeutic preparation known as 
nux vomica. Both alkaloids have the same type of action 
in man, although the brucine effect is only about to ALKALOIDAL POISONS 
139 
as strong as the strychnine action. Practically, therefore, 
the action of nux vomica is represented by the strychnine 
present. 
The preparations of nux vomica commonly employed 
are nux vomica which officially must contain 2.5 per cent 
of alkaloids (1 grain = 0.06 gm.); the extract, 16 per cent 
of alkaloids (% grain = 0.01 gm.); the fluid extract, 
2.5 per cent (1 minim = 0.06 c.c.); the tincture, 0.25 per 
cent (10 minims = 0.6 c.c.). The official salts of strych- 
nine are the nitrate and the sulphate. 
Strychnine is insoluble in water but soluble in acids and 
chloroform. It has an intensely bitter taste and forms 
salts with acids which are soluble in water. 
Brucine is somewhat more soluble in water than 
strychnine and is readily soluble in chloroform and amyl 
alcohol. Its salts possess physical properties similar to 
those of strychnine. 
Symptoms.-The first signs of strychnine poisoning 
consist of restlessness, nervousness, abrupt movements, 
and stiffness of the face muscles. These symptoms are 
soon succeeded by more pronounced twitchings of the 
muscles which may partake of the nature of muscle spasm 
and lead to general convulsions of the spinal type. In 
these convulsions all the voluntary muscles are involved, 
so that of two opposing sets of muscles the stronger 
predominates. The extensor muscles usually being the 
stronger, the legs, arms and back are extended and the 
head is thrown back, the whole action at times being 
sufficiently aggravated so that the back is arched, the 
weight resting upon the heels and back of head (opis- 
thotonus). The hands are clenched, eyes open and the 
lips may part in a characteristic grin, the risus sardonicus, 
from the fact that the corners of the mouth are spas- 
modically drawn out. The patient's mind is clear which 140 
TOXICOLOGY 
leads to great anxiety and during the convulsions there is 
great pain from the muscle cramps. 
The convulsions at first are rapidly intermittent (clonic) 
but soon become tonic resulting in a typical tetanus. The 
muscles of the diaphragm are also involved so that ulti- 
mately it becomes rigid, and this together with the tense 
muscles of the thorax and abdomen stops respiration. 
Cyanosis is therefore present, the eyes protrude with 
dilated pupils and the pulse is small and tense and often 
cannot be detected. 
The convulsion usually lasts about a minute, the mus- 
cles relax, and a condition of depression almost amounting 
to paralysis sets in. An interval of io to 15 minutes may 
elapse before the next attack which usually follows some 
kind of stimulation. If death does not occur during a 
convulsion the remissions become progressively shorter, 
the convulsions become weaker and paralysis more 
prominent. 
Convulsions in the higher degrees of poisoning are 
induced usually by reflex stimulation such as the slamming 
of a door, a touch, a light, a puff of air, any voluntary 
movement, etc. In more serious cases the spasms are 
undoubtedly spontaneous but even in this instance just 
as few reflex stimuli as possible should be allowed to play 
upon the patient. Death follows usually from failure of 
respiration, the heart continuing to beat for some time 
after cessation of breathing. On the other hand, in long 
continued cases of strychnine poisoning the patient may 
die from the exhaustion induced by the tetanus. Strych- 
nine is excreted unchanged in the urine. Little is elimin- 
ated by the feces. 
Repetition of administration leads to increased suscepti- 
bility rather than to tolerance, hence the possible danger 
of too large doses continuously administered. ALKALOIDAL POISONS 
141 
At times it is difficult to differentiate strychnine tetanus 
from other types of tetanus, as traumatic tetanus, spinal 
meningitis, epilepsy or hysteria. In traumatic tetanus 
there has been previous malaise and slow development 
and the course of the condition will establish the diagnosis. 
If any doubt is present treatment for strychnine poisoning 
should be instituted. Fever and history will differentiate 
in spinal meningitis and in epilepsy consciousness is lost 
and the reflexes are normal. In certain cases of hysteria 
the diagnosis is impossible hence such cases should also 
be treated as for strychnine poisoning. 
Fatal Dose.-The smallest fatal dose on record is 
grain of strychnine sulphate. On the other hand a dose 
of 20 grains has been taken with recovery. 
Fatal Period.-The symptoms generally appear in about 
20 minutes after administration of the drug although they 
may be delayed for a much longer period, an hour or more. 
If the dose is very large death generally occurs within two 
hours although it may be delayed for many hours. Even 
when the patient has apparently recovered a sudden, severe 
spasm may occur terminating in death. 
Post Mortem Appearances.-The appearances after 
death are not characteristic beyond an early and main- 
tained rigor. 
Treatment of Nux Vomica Poisoning.-If the drug has 
been taken by mouth and prominent symptoms have not 
appeared thorough lavage of the stomach should be 
practiced, employing a chemical antidote in the washwater 
or administered at short intervals-potassium perman- 
ganate is probably the most effective teaspoonful of the 
crystals should be dissolved in one pint of warm water, 
carefully decanted so as not to include any crystals). 
Iodine (15 drops of the tincture in glass of water) or 
tannin (teaspoonful in glass of hot water) are also useful 142 
TOXICOLOGY 
since they render the alkaloids insoluble. They should, 
however, be immediately removed. Tea and coffee are 
less desirable since their content of caffein, if allowed time 
for absorption, acts synergistically to nux vomica or 
strychnine. 
When convulsions have already set in quick action is 
demanded and the patient should be anesthetized with 
ether or chloroform. Anesthesia with ether and chloro- 
form should not be continued longer than possible since 
both these anesthetics tend to depress the respiration. 
Ether is to be preferred since chloroform may give rise to 
delayed poisoning. For prolonged effect bromides in 
massive doses, 15 grams by mouth or rectum act in a 
manner antagonistic to nux vomica. Paraldehyde may 
also be useful since it does not depress the respiratory 
centre. Morphine should be employed with extreme 
caution owing to its marked depressant action upon the 
respiratory centre. If necessary artificial respiration 
must be given. A patient should be kept as quiet as 
possible. 
References 
Hatcher and Eggleston: J. Pharm. and Exp. Therap., 1917, 9, 
p. 359; 10, p. 281. 
Githens and Meltzer: J. Pharm. and Exp. Therap., 1911, 2, 
P- 357- 
ACONITINE 
Aconitum or monkshood contains several alkaloids of 
which aconitine is chief. The structure of aconitine has 
not yet been established. The principal therapeutic 
effects of aconitine are upon the circulation producing 
slowing of the pulse and fall of pressure. Employed 
locally as the tincture it has value for the relief of pain, in 
toothache, neuralgia and rheumatic conditions. The ALKALOIDAL POISONS 
143 
principal preparations are aconitum U.S.P. containing 
not less than 0.5 per cent of alkaloids; the extract repre- 
senting 2 per cent of alkaloids, the fluid extract containing 
0.5 per cent of alkaloids, and the tincture 10 per cent of 
drug or 0.05 per cent of alkaloids. A characteristic action 
of aconitine is the tingling sensation in the mouth which is 
followed by numbness and loss of sensation. This action 
is produced locally wherever the drug may be applied. 
Aconitine is unstable, decomposing readily and on 
hydrolysis yields benzoic and acetic acids and an inert 
base aconine. Aconitine is alkaline to litmus, soluble in 
chloroform, ether and benzene, and insoluble in water. 
It turns the plane of polarized light to the right; its salts 
to the left. 
Symptoms.-Symptoms of poisoning consist in tingling 
in the mouth, stomach and skin, and may be most pro- 
nounced in the finger tips. This characteristic feature 
is of considerable importance in the diagnosis of aconitine 
poisoning. There may be nausea, diarrhoea, vomiting and 
pain in the stomach. The burning and tingling sensations 
pass into anesthesia. There are peculiar chilly sensations, 
the pupils are dilated and vision is misty, the skin is cold 
and pallid, respiration is dyspnoeic, the pulse is weak and 
feeble and arhythmic. Speech may be impaired and 
convulsions are not infrequently encountered. Death 
occurs from respiratory failure or from heart block, or 
ventricular fibrillation. 
When large doses are taken death may result very 
rapidly from heart paralysis. 
Fatal Dose.-Aconitine is one of the most powerful 
poisons known and has caused death in amounts of Xo 
grain or less. 
Fatal Period.-Death usually occurs within 4 or 5 
hours, but in certain cases has been delayed for 3 or 4 days. 144 
TOXICOLOGY 
Post Mortem Appearances.- Sometimes the stomach is 
reddened and the liver, kidneys, lungs and brain may 
show congestion. 
Treatment.-Treatment of aconitine poisoning demands 
prompt administration of alkaloidal antidotes, emptying 
of the stomach and lavage. Body temperature must be 
maintained and artificial respiration may be necessary. 
The heart condition may be treated by epinephrine or 
strophan thin injected directly into the circulation. Atro- 
pine is of great value in aconitine poisoning to counteract 
the heart and respiratory disturbance. 
ATROPINE GROUP 
ATROPINE, HYOSCYAMINE AND SCOPALAMINE 
The group of atropine alkaloids comprises atropine, 
hyoscyamine and scopalamine, substances which have a 
close chemical relationship. Atropine and hyoscyamine 
are isomers, the following structure serving for both. 
c6h5 
Scopalamine is also closely related chemically but its 
exact structure has not been established. 
The atropine alkaloids are found in certain drugs 
obtained from plants belonging to the potato family. 
The principal drugs are Belladonna, Stramonium, Hyo- 
scyamus, Scopola, etc. The atropine alkaloids in general 
produce similar toxicological effects, differences being in 
relative rate of action rather than in markedly different 
type of reaction. ALKALOIDAL POISONS 
145 
Atropine occurs in the racemic form and may be 
obtained as crystalline plates. Difficulty soluble in water 
it readily dissolves in alcohol and chloroform. Atropine 
sulphate, a white crystalline powder, is the official prepara- 
tion which is soluble in water but relatively insoluble in 
chloroform and ether. 
Atropine actions fall into two groups (a) stimulation of 
nerve centres, principally cerebral and medullary, (b) 
depression of nerve endings as sensory nerve endings, 
motor nerve endings in the smooth muscle of the viscera, 
secretory nerve endings, the ends of the third nerve in the 
eye and vagus nerve endings. Poisoning may occur from 
administration of the isolated drug or from absorption 
through the skin by the use of plasters, oily or alcoholic 
preparations as ointments or liniments. Toxic symptoms 
in ophthalmic practise are fairly common. 
Symptoms.-The first warnings of toxic action are the 
dilated pupil, dry throat and mild cerebral symptoms. 
The symptoms occur promptly but may last several hours 
or days. In fatal cases the course of intoxication may run 
for two weeks or more. With severe poisoning there may 
be cerebral stimulation as evinced by delirium. Later this 
is followed by collapse, and coma. Death usually occurs in 
coma. Convulsions at the terminal stage are rare. 
During the stage of stimulation there is great thirst, 
burning and constriction of the throat, difficult swallowing, 
flushed skin, especially, of face and neck which resembles a 
scarlatinal rash. Accomodation of the eye is paralyzed so 
that vision is disordered. The pulse is rapid, respiration 
deep and rapid, arterial pressure is high, the temperature 
may rise several degrees, there is vertigo, muscular inco- 
ordination, often nausea and vomiting, and retention of 
urine. During the stage of delirium patients with atropine 
poisoning strongly resemble maniacs, and in the earlier 146 
TOXICOLOGY 
period of the poisoning the condition has been mistaken for 
scarlet fever. 
After the period of stimulation collapse follows which is 
characterized by feeble heart action, low blood pressure, a 
slow and shallow respiration, and coldness of the extremi- 
ties, death resulting usually from respiratory failure. 
Fatal Dose.-The fatal dose of atropine may be taken as 
o.i gram for adults and o.oi gram for children. The 
other members of the atropine group are less toxic. 
Fatal Period.-Death usually occurs within 24 hours, 
although it may be delayed for several days. 
Post Mortem Appearances.-The autopsy reveals 
findings typical of asphyxia. 
Treatment.-Treatment of atropine poisoning is quite 
effective since death does not usually occur rapidly, and it 
consists of lavage of the stomach, tannic acid or tea being 
added to the wash water. The general symptoms should 
be combatted by pilocarpine (10 mg. (% gr.) subcutane- 
ously repeated until mouth is moist). For the delirium, 
bromides and the ice cap. Because of their depressant 
effect upon the respiratory centre, morphine, chloral and 
chloroform should not be used, although the cautious use 
of morphine in the early excitement may be beneficial, or 
ether may be inhaled to lessen excitement. In the stage of 
collapse depression should be antagonized by strong coffee 
and artificial respiration persistently resorted to if necessary. 
Reference 
Cushny: J. Pharm. and Exp. Therap., 1921, 17, p. 41. 
VERATRINE GROUP 
There are three types of plants in which veratrine-like 
alkaloids may occur. Each type consists of a mixture of 
alkaloids, the classification differing widely and the whole 
subject being in more or less confusion. However, ALKALOIDAL POISONS 
147 
two substances stand out clearly, veratrine or cevadine, 
and protoveratrine. Cevadine (veratrine) is present in 
the seeds of Veratrum Sobadilla or Cevadilla. The 
active poisonous principle of both veratrum alba, or 
white hellebore, and veratrum viride, or green hellebore 
is protoveratrine. The official veratrine has as its princi- 
pal constituent cevadine. The official veratrum viride 
contains protoveratrine as its chief constituent. 
Therapeutically cevadine has been employed in the 
form of an ointment as a counterirritant in neuralgic 
conditions, especially of the face. As it is highly toxic 
its internal administration is not advised and poisoning 
has occurred from absorption through the skin. 
Protoveratrine (Veratrum viride) has been used to slow 
and soften the pulse and to lower blood pressure. Its 
chief action is that of a cardiac depressant from vagus 
stimulation, resulting in slowed pulse, fall of systemic 
blood pressure and reduction of temperature, the latter 
probably from the profuse sweating induced. It has 
enjoyed a wide use in conditions of high blood pressure 
particularly that associated with eclampsia. The prepara- 
tions most employed are veratrum viride, the fluid extract 
and the tincture. 
Symptoms.-Death from overdoses of veratrum viride 
is rare owing to the fact that it is a strong gastric irritant 
and promptly causes vomiting. Typical symptoms of 
veratrine poisoning consist of burning in the stomach, 
vomiting, diarrhoea, abdominal pain, increased saliva- 
tion, giddiness, headache, dilated pupils, irregular heart 
action, collapse, paralysis or convulsions, death from 
respiratory failure and accompanying cardiac collapse. 
Fatal Dose.-Little is known concerning the exact 
fatal dose although death may occur after taking 4 or 5 
c.c. of the fluid extract of veratrum viride. 148 
TOXICOLOGY 
Fatal Period.-Although death may occur rapidly it is 
usually delayed for more than 24 hours. 
Post Mortem Appearances.-These are not characteris- 
tic. There may be irritation of the gastro-intestinal tract 
and hyperemia of the brain and its linings, but these fea- 
tures are not constant. 
Treatment.-Alkaloidal antidotes and lavage of the 
stomach should be employed. For the collapse stimu- 
lants, as ammonia, brandy, atropine, strychnine and 
warmth, may be administered. Artificial respiration 
is of great value when indicated and the heart may be 
helped by intravenous injection of epinephrine or stro- 
phanthine should the need arise. 
References 
Pilcher and Sollmann: J. Pharm. and Exp. Therap., 1915, 7, 
P- 295- 
Pilcher: Ibid., 1917, 9, p. 350; Am. J. Physiol., 1917, 44, p. 1. 
PHYSOSTIGMINE 
Physostigmine (also called Eserine) is the principal 
alkaloid of Calabar bean, or the ordeal bean. It is a basic 
substance, containing nitrogen, and on treatment with 
potassium hydroxide yields carbon dioxide and meth- 
ylamine. It occurs in crystalline form, is tasteless, diffi- 
cultly soluble in water, readily soluble in alcohol, ether, 
chloroform and benzene, and turns the plane of polarized 
light to the left. Official preparations are the salicylate, 
the alkaloid itself, the extract and the tincture. The chief 
action of physostigmine is that of stimulating secretory 
nerve endings of glands and the nerve endings of striated 
and smooth muscle. It causes a powerful contraction of 
the smooth muscle of the eye and of the intestine. It is 
employed in diseases of the eye and in intestinal paresis. 
Paralytic effects may be observed as the action on the ALKALOIDAL POISONS 
149 
nervous system. It is antagonistic in its action to atro- 
pine. In many respects it resembles nicotine in its 
physiological effects. 
Symptoms.-The symptoms of poisoning by physostig- 
mine are marked muscular weakness without loss of con- 
sciousness, nausea, vomiting and sometimes purging. 
The pupils are noticeably contracted, the skin is covered 
with sweat, there is epigastric pain, salivation, lachryma- 
tion, palpitation with slow pulse, low blood pressure, 
dyspnoea, muscular twitchings, and convulsions. The loss 
of muscular power starts in the legs and travels upwards. 
Respiration is depressed and the breathing may be asth- 
matic in character from contraction of the bronchial 
muscles. Death is caused by failure of respiration. 
Fatal Dose.-The fatal dose is unknown. However, 
3 grains would be much beyond the minimum lethal dose. 
Fatal Period.-In the very few cases reported in the 
literature death has been a matter of a few hours. 
Post Mortem Appearances.-Autopsy reveals nothing 
characteristic, changes from the normal being those com- 
mon to an asphyxial death. 
Treatment.-Treatment consists of lavage of the 
stomach, stimulants, and atropine to i mg.). Magne- 
sium sulphate is also antagonistic to the action of physo- 
stigmine and its subcutaneous use in physostigmine 
poisoning has been recommended. 
References 
Robinson: Arch. Int. Med., 1915, 15, p. 645. 
Joseph and Meltzer: J. Pharm. and Exp. Therap., 1909, 1, p. 
369. 
PILOCARPINE 
Pilocarpine is the principal alkaloid of jaborandi leaves 
and it is distinctly antagonistic to the action of atropine, 150 
TOXICOLOGY 
peripherally stimulating the secretory nerves, the nerves 
governing smooth muscle, etc. The principal secretion 
affected is the sweat, pilocarpine being a powerful diaphor- 
etic. The preparations commonly employed are pilo- 
carpine the alkaloid, the fluid extract, the hydrochloride 
and the nitrate. 
Pilocarpine 
Pilocarpine the alkaloid is a soft gelatinous mass which, 
however, forms with mineral acids crystalline salts 
possessing the power of dextrorotation. 
Although the toxicology of pilocarpine is not very 
important cases of poisoning from overdoses occasionally 
occur. After toxic doses pilocarpine is an arterial dilator; 
it acts as a cardiac depressant, both from the action on 
the vagus and from its direct influence on the heart; in 
conditions of cardiac weakness collapse and death may 
follow even from relatively small doses; respiration is also 
depressed leading to pulmonary edema and asphyxia. 
Symptoms.-The symptoms of poisoning resemble those 
of muscarine and start with greatly increased secretion of 
saliva, sweat and tears. This may be followed by nausea, 
vomiting and diarrhoea with severe abdominal cramps. 
Changes in the eye are quite noteworthy, there being 
contraction of the pupil and spasm of accommodation. 
There is at first slowed heart beat, low blood pressure, 
and later collapse. These symptoms are due to the action 
of pilocarpine upon the vagus and upon the vasomotor 
centre, resulting respectively in vagus heart block and ALKALOIDAL POISONS 
151 
low pressure. Respiration is usually labored and of the 
asthmatic type and the lungs may give evidence of edema. 
Muscular relaxation which ascends from the lower limbs 
sometimes occurs. Generally consciousness is present 
although there may be confusion of ideas, vertigo, tremors, 
and feeble convulsions. Death results from paralysis 
of the heart or from pulmonary edema. 
Less dangerous symptoms of overdoses of pilocarpine 
manifest themselves by gastro-intestinal disturbances, 
nausea, and vomiting which may be long continued and 
very depressing. These symptoms may occur even 
though the drug is not introduced by mouth. Another 
characteristic symptom is a burning sensation in the ure- 
thra accompanied by an irresistible desire to urinate. A 
large portion is eliminated in the urine unchanged. 
Fatal Dose.-Two grains subcutaneously administered 
may be considered as a dangerous dose. 
Fatal Period.-Death ordinarily occurs quickly. 
Post Mortem Appearances.-There is nothing charac- 
teristic. 
Treatment.-Treatment for pilocarpine poisoning con- 
sists in the use of atropine to combat the pilocarpine effects 
and symptomatic treatment, especially artificial respira- 
tion for the collapsed state. The atropine tends to lessen 
bronchial secretion, hence prevent edema, modifies the 
asthmatic respiration and abdominal cramps and counter- 
acts the pilocarpine action upon the vagus, thus releasing 
the heart from its block. 
References 
McNally: J.A.M.A., 1915, 65, p. 1640. 
Eggleston and Hatcher: J. Pharm. and Exp. Therap., 1915, 7, 
p. 225. 
Eggleston: Ibid., 1916, 9, p. 11. 152 
TOXICOLOGY 
All portions of the common meadow-saffron, Colchicum 
autumnale, possess toxic properties because of the presence 
of the alkaloid colchicine. This alkaloid has been 
employed extensively for gouty conditions without definite 
indications for its use. Intoxication with colchicine is 
usually due to accident, mistaking the preparation for 
something else, or else from an overdose. At times, 
however, it has been administered with criminal intent. 
It is stated that the alkaloid itself is not toxic but upon 
oxidation in the body yields oxydicolchicine which induces 
the toxic symptoms. The excretion of the poison is slow. 
Symptoms.-The initial symptoms are burning in the 
throat and stomach, nausea, vomiting and purging, 
intense thirst, abdominal colic. Hematuria or anuria 
may follow. There is great depression and weakness. 
The pulse is irregular and weak, the respiration shallow, 
the pupils dilated, the mind may or may not be affected. 
At times there may be delirium or convulsions. Eventu- 
ally collapse results and death occurs from respiratory 
failure. 
Fatal Dose.-About grain (0.02 gram) of the pure 
alkaloid may cause death. 
Fatal Period.-Death usually occurs within 24 hours 
from a single dose although it may be delayed for several 
days. 
Post Mortem Appearances.-Autopsy reveals nothing 
characteristic. 
Treatment.-The stomach should be evacuated as soon 
as possible and to the wash-water add tannic acid or strong 
tea. For the irritated stomach demulcents (egg-white, ALKALOIDAL POISONS 
153 
milk, oatmeal group) may be given. Pain may be 
combatted by morphine and the collapse treated with 
strychnine and atropine. If necessary institute artificial 
respiration. 
References 
Dixon and Malden: J. Physiol., 1908, 37, p. 50. 
Denis: J. Pharm. and Exp. Therap., 1915, 7, p. 601. 
Cocaine is the principal alkaloid obtained from the leaves 
of Erythroxylon coca, a plant indigenous in South 
America. The natives of Peru, Chili and Bolivia have 
chewed these leaves from ancient time for the psychic 
stimulation produced. Cocaine exists in the dried leaves, 
to the extent of approximately 0.75 per cent. Other 
alkaloids are found with cocaine but they possess less 
significance. 
From a chemical viewpoint cocaine is closely related to 
atropine and occurs in three stereoisomeric forms, 1- 
cocaine, d-cocaine, and r-cocaine. It is the 1-cocaine that 
is of value from a medicinal standpoint. 
Cocaine occurs as a white crystalline powder which is 
almost insoluble in water and cold alcohol, but soluble in 
warm alcohol, ether, chloroform and olive oil. It forms 
cocaine hydrochloride which is the official preparation 
and constitutes a white crystalline powder, soluble in 
water and alcohol but insoluble in ether and olive oil. 
The solution in water is neutral to litmus and turns the 
plane of polarized light to the left. 154 
TOXICOLOGY 
Cocaine is rapidly absorbed, being partly destroyed in 
the organism, but is eliminated in large measure unchanged 
in the urine. Poisoning with cocaine resembles in some 
respects intoxication with epinephrine, namely, stimula- 
tion of the sympathetic nervous system. 
Symptoms.-Cocaine poisoning is not infrequent and 
fatal results may follow. In many instances intoxication 
results from carelessness in administration, mistakes in 
dosage or because of the idiosyncrasy of the individual. 
The first symptoms of cocaine intoxication are restless- 
ness or excitement, talkativeness, the speech is confused 
and incoherent, the individual laughs without cause, 
and there may be other evidences of mental disturbance, 
as delirium with hallucinations which may assume a mani- 
acal condition. The mouth and throat are dry, swallowing 
is difficult, there may be dizziness, a rapid pulse, quickened 
respiration, the pupils are dilated and exophthalmic, 
nausea, vomiting, abdominal pain and numbness and 
tingling of the hands and feet may be experienced. The 
heart is at first rapid and strong, later becoming weak and 
irregular. The skin is pale and covered with sweat and 
there may be creeping sensations. Dyspnea, Cheyne- 
Stokes respiration, unconsciousness, convulsions, cyanosis, 
and respiratory failure close the scene. 
In other instances fatal results are induced in a very few 
minutes, the severe symptoms appearing without warning. 
The patient may collapse, go into convulsions or uncon- 
sciousness and die. 
Chronic poisoning, induced through habit, is like other 
drug habits, characterized by peculiar features which, 
however, have no direct interest for the toxicologist. A 
discussion of the cocaine habit and its peculiarities is 
therefore not included here. ALKALOIDAL POISONS 
155 
Fatal Dose.-The fatal dose of cocaine depends upon the 
manner of the introduction. When taken by mouth prob- 
ably i gram may be considered as capable of producing 
death. Such a dose has caused death and in others large 
quantities have been taken with recovery. A dose of 0.03 
gram per urethra, 0.04 gram under the conjuctiva, have 
caused death. 
Fatal Period.-This depends upon the dosage and the 
rapidity of absorption. If the patient survives for 
an hour the chances of recovery are good. Death, 
however, may be delayed for several hours. 
Post Mortem Appearances.-With rapid death there is 
hyperemia of the brain, spinal cord, liver, spleen and 
kidneys. 
Treatment.-If cocaine has been taken by mouth the 
stomach should be emptied and well washed out. Chemi- 
cal antidotes, such as potassium permanganate, may be 
added to the wash-water. When the poison has been 
introduced parenterally every means should be employed 
to delay absorption, such as ligation, etc. If symptoms 
of poisoning have manifested themselves every means 
employed to delay death gives an opportunity for recovery 
since in the body cocaine is rapidly oxidized and thus 
rendered inert. For the depression or collapse, stimu- 
lants such as caffeine, aromatic spirits of ammonia, hot 
alcoholic drinks are indicated. The convulsion may be 
controlled by ether or chloral. Artificial respiration may 
be necessary. 
COCAINE SUBSTITUTES 
There are a large number of substitutes which are 
employed in medicine in place of cocaine. The purpose of 
their preparation was the endeavor to form a compound 
which would possess the anesthetic properties of cocaine 156 
TOXICOLOGY 
without its toxicity. In general these substitutes are less 
poisonous than cocaine but they still have a certain degree 
of toxicity. Even with these less toxic compounds cases 
of poisoning occasionally occur, the symptoms manifested 
resembling those induced by cocaine. Treatment indi- 
cated is symptomatic. 
The most important of the cocaine substitutes are- 
Eucaine-beta eucaine chloride or lactate (trimethyl- 
benzoyl oxypiperidine). 
Novocaine or Procaine.-(para-amino-benzoyl-diethyl 
amino euthanol) generally employed as the hydrochloride- 
Stovaine-(dimethyl-amino-benzoyl-pentanol chloride). ALKALOIDAL POISONS 
157 
Alypine-(the hydrochloride of tetra-methyl-diamino- 
dimethyl-ethyl-carbinyl-benzoate). 
Tropacocaine-(the benzoyl ester of pseudo-tropine 
chloride). 
References 
Eggleston and Hatcher: J. Pharm. and Exp. Therap., 1919, 13, 
p. 433; Proc. Soc. Exp. Biol, and Med., 1918, 16, p. 16. 
Roth: Hygienic Lab. Bull., 109, 1917. 
Hofvendahl: Biochem. Z., 1921, 1x7, p. 55. 
IPECAC 
Ipecac is obtained from the root of a Brazilian 
plant, which contains two potent alkaloids, emetine and 
cephaeline. Therapeutically they are employed for the 
production of nausea and emesis, as a sedative expectorant 
and as specifics in amebic dysentery. The emetic 
effects are not so prompt as with apomorphine. 
Chemically they are isoquinoline derivatives, emetine 
(C25H28N2(OCH3)4) being the mono-methyl ether of 
cephaeline (C25H28N2(OH) (OCH3)3). 
The therapeutic use of the various ipecac preparations 
has given rise to many cases of poisoning in some instances 
with fatal results. The toxic effects are particularly 158 
TOXICOLOGY 
prominent if the drug is given intravenously. Special 
care should, therefore, be exercised when it is so admin- 
istered. Emetine, for example, is excreted by the kidney 
but very slowly, appearing in the urine for several weeks. 
Symptoms.-In addition to the well marked gastro- 
intestinal irritation ipecac preparations may induce general 
edema consequent to renal insufficiency, hemoptysis, 
flaccid paralysis, peripheral neuritis, delirium, coma and 
failure of the heart. 
Fatal Dose.-Approximately 2 grams are fatal whether 
administered over a short or relatively long period since 
the drug appears to have a cumulative effect. Thus, 2 
grams administered subcutaneously in the course of 20 
days caused death. 
Fatal Period.-Most of the fatalities have occurred only 
after continued administration, hence little can be said 
relative to death after acute poisoning. 
Post Mortem Appearances.-Autopsy reveals severe 
gastro-intestinal irritation together with renal congestion. 
Treatment.-Since poisoning occurs generally only 
after repeated doses stoppage of the drug usually leads to 
cessation of symptoms and recovery. When acute intoxi- 
cation occurs the remedial measures are purely symp- 
tomatic, heart depression being the most serious symptom 
and most to be guarded against. 
References 
Levy and Rowntree: J. Pharm. and Exp. Therap., 1916, 8, p. 
120; Arch. Int. Med., 1916, 17, p. 420. 
Johnson and Murphy: Mil. Surg., 1917, 40, p. 58. 
ERGOT 
Ergot is a parasitic fungus which grows upon cereals. 
That which is obtained from rye constitutes the official 
preparation which may be either the extract or the fluid ALKALOIDAL POISONS 
159 
extract. There are several stages in the development of 
the fungus, the drug being obtained from the resting stage. 
The chemistry of ergot is complex, several basic substances 
being present which are responsible for the characteristic 
effects of the drug. The substances which are important 
in contributing to ergot pharmacological effects are ergo- 
toxine, tyramine and histamine. Ergo tine is perhaps 
responsible for ergot producing gangrene in the cock's 
comb; the rise of blood pressure is attributed to tyramine 
and the characteristic effect of ergot in stimulating 
the uterus to contraction is caused by histamine. The 
structure of ergotine has not been established. That of 
tyramine is p.hydro-xyphenylehylamine-which is closely 
related to tyrosine from which it may be formed by 
loss of CO2. and also to epinephrine- 
Tyramine 
Epinephrine 
Histamine, or /3-iminazolylethylamine, is closely related 
to the amino acid histidine from which it may be formed 
by loss of COo. 
Histamine TOXICOLOGY 
160 
In previous time ergot poisoning, or ergotism, was quite 
common. With better methods of handling grain ergo- 
tism has become of merely historic interest although 
it has been said that even to-day ergotism is present in 
certain portions of Russia. Intoxication from ergot is- 
caused either by overdosage in therapeutic use or its 
employment by women in attempts at abortion. Gener- 
ally therefore the symptoms produced are those of acute 
poisoning. 
Symptoms.-The early characteristic symptoms are 
those of intense gastro-intestinal irritation, vomiting, 
colic and diarrhoea being prominent. A second type of 
action is upon the cerebral nervous system as indicated 
by disturbances of vision, delirium, anesthesias, muscular 
weakness, convulsions, coma, suppression of urine, and 
death by respiratory failure. 
In pregnancy additional symptoms, abortion followed 
by severe hemorrhage, may ensue which may prove fatal 
to both mother and fetus. Recovery from ergot poison- 
ing is slow, several days elapsing before a normal condi- 
tion is regained. 
Fatal Dose.-Ergot preparations may vary widely in 
their content of the active principles and for this reason 
it is difficult to state definitely the fatal dose. There is 
also a certain degree of idiosyncrasy with respect to the 
drug which militates against positive statements concern- 
ing the toxic dose. Death has been produced by 12 grains 
(0.77 gram) whereas recovery has followed the adminis- 
tration of 150 grains (9.72 grams). 
Fatal Period.-Death is usually a matter of 3 or 4 days 
and is not so frequent after a single large dose as after 
small repeated doses for considerable periods which may 
induce the same symptoms as those produced by eating 
contaminated rye, namely, gangrene of the various por- ALKALOIDAL POISONS 
161 
tions of the body as fingers, toes, arms, legs, nose, or even 
the internal organs. 
Post Mortem Appearances.-The stomach and intes- 
tines show evidence of intense irritation. The lungs, 
kidney and uterus may be hyperemic. The tissues in 
general putrefy very quickly. 
Treatment.-The gastro-intestinal canal should be 
thoroughly cleaned out-the stomach by stomach tube 
and repeated lavage-the intestines by purgatives. If 
indicated, stimulants as tea, coffee or strychnine should 
be administered. 
References 
Barger: The Simpler Natural Bases, 1914. 
Koessler and Hanke: J. Pharm. and Exp. Therap., 1917, 9, p. 
360. 
EPINEPHRINE 
Epinephrine is the active principle of the medulla of 
the adrenal gland. It can be prepared synthetically and 
as its formula indicates is an amine closely related to the 
amino acid, tyrosine. It forms characteristic crystals 
which in solution in water readily decompose unless a 
preservative is present. The naturally occurring base is 
levo-rotatory, the synthetic is optically inactive. 
Therapeutically epinephrine is employed locally to stop 
hemorrhage by constriction of the arterioles; in bronchial 
asthma; and to stimulate circulatory failure. Its chief 
actions are as follows: in the intestines and bronchioles 
it produces relaxation; in the heart and blood vesselsit 162 
TOXICOLOGY 
causes constriction and raises blood pressure. In the body 
epinephrine is very quickly oxidized. 
Toxicologically epinephrine is of interest only because of 
over-dosage or hypersusceptibility of the individual. 
Symptoms.-The first indications of a toxic effect are 
excitement, anxiety, tremors, palpitation, precordial 
distress, rise in pulse and respiration, high blood pressure 
and increased temperature. If too great quantities are 
given intravenously, death may result from acute cardiac 
dilatation. Generally death results from failure of the 
respiration. There is also danger of intravenous admin- 
istration in cerebral artereosclerosis from rupture of a 
cerebral artery owing to the sudden increase in blood 
pressure. At times the condition of pulmonary edema 
may be aggravated when epinephrine is given intraven- 
ously in this condition. 
Fatal Dose.-The fatal dose is unknown. 
Fatal Period.-Death is usually sudden. 
Post Mortem Appearances.-Autopsy reveals nothing 
characteristic. 
Treatment.--This is purely symptomatic. 
References 
Cushny: J. Physiol., 1909, 38, p. 259. 
Hewlett: Arch. Int. Med., 1918, 21, p. 421. 
GELSEMIUM 
Obtained from the rhizome and roots of Gelsemium 
sempervirens, the yellow jasmine, the alkaloid gelsemin- 
ine acts in a manner similar to nicotine and coniine, 
although its influence upon the central nervous system is 
more depressing. Another alkaloid found in company 
with gelseminine is gelsemine which has a weak strychnine 
action. Official preparations are the fluid extract, dose ALKALOIDAL POISONS 
163 
i minim (0.06 c.c.), and the ten per cent tincture, dose 
io minims (0.6 c.c.). Although it has been employed 
therapeutically in neuralgias the mechanism of its action 
is not understood. 
Symptoms.-The symptoms consist of double vision, 
relaxation of the muscles of the eye and jaw, general 
muscular weakness and prostration. The pulse is slow 
and temperature falls. The respiration is slow and 
shallow. The mind remains clear up to the time of death 
which results from respiratory failure. 
Fatal Dose.-Relatively small doses may cause toxic 
symptoms and even death. A dram of the fluid extract 
has caused death and 15 minims have provoked evidences 
of poisoning. 
Fatal Period.-Death usually occurs in from 1 to 8 
hours. 
Post Mortem Appearances.-There is nothing especially 
noticeable beyond the appearances characteristic of a 
respiratory death. 
Treatment.-The stomach should be emptied and thor- 
oughly washed. Atropine and stimulants are indicated. 
Reference 
Cushny: Arch. f. exp. Path. u. Pharm., 1892, 31, p. 49. CHAPTER VI 
MISCELLANEOUS ORGANIC POISONS 
BENZOL (C6H6) 
The term benzol is used in two senses, first as a synonym 
for benzene and second to designate a variable mixture 
derived from the distillation of coal tar. When coal tar is 
subjected to fractional distillation there are four products 
that result: (i) crude naphtha, (2) dead oils or creosote 
oils, (3) green or anthracene oil, and (4) a pitch, the residue. 
Commercial benzol is obtained from the first fraction. 
Benzols of commerce vary widely in composition and in 
general they consist chiefly of benzene and its homologues, 
toluene (C6H5CH3), and xylene (C6H4(CH3)2), and small 
percentages of other substances. Benzine with which 
these two substances has been confused is a derivative not 
of coal tar but of petroleum, consisting chiefly of hexane 
(C6Hi4) and heptane (C7H16). Usually it contains no 
benzene (C6H6). The fate of benzol in the body, so far as 
it has been determined, is that from 15 to 30 per cent is 
oxidized to phenol, catechol, add quinol, and excreted 
as phenol sulphates. A part is changed to muconic acid 
and a considerable portion is excreted unchanged by the 
lungs. Two types of poisoning occur, acute poisoning 
and chronic poisoning. These intoxications are encoun- 
tered either from the industrial use of benzol or from 
its employment as a symptomatic remedy in the treatment 
of leucemia. 
Acute Poisoning.-The acute poisoning gives rise to the 
following symptoms-dizziness and confusion followed by 
164 MISCELLANEOUS ORGANIC POISONS 
165 
excitation, unconsciousness, and death from respiratory 
paralysis. The symptoms arising from its medicinal use 
are heart-burn, flatulence, nausea, vomiting, diarrhoea, 
bronchial irritation, minute hemorrhages of skin and 
mucous membranes (purpura hemorrhagica) albuminuria, 
ringing in the ears, and vertigo. 
Fatal Dose.-The fatal dose is undetermined but it is 
quite apparent that 15 mg. per liter of air produce listless- 
ness and confusion after hour, and exposure to 20 to 
30 mg. or from 2 to 3 parts per 100,000 parts of air for a 
few hours may cause loss of consciousness. 
Post Mortem Appearances.-The blood in the heart 
and vessels is fluid, and the veins of the abdomen are 
engorged. There are hemorrhages into the gastric mucosa 
and bloody foam in the air passages. Liver, kidney, 
and intestinal disturbances contraindicate benzol. 
Chronic Poisoning. Symptoms.-Chronic benzol poi- 
soning takes the form of an aplastic anemia with subcu- 
taneous hemorrhages and bleeding from the mucous 
membranes as terminal changes. There is a direct destruc- 
tion of leucocytes with reduced formation of the elements. 
A destructive action on blood platelets and the megakaryo- 
cytes of the marrow from which the platelets are formed is 
also in evidence. There is a destruction of the adult red 
corpuscles and the prevention of the formation of new 
ones. These changes occur in the order given, the effect 
on the red corpuscles being especially characteristic of 
very slow poisoning, the last to appear and the last to 
disappear with recovery. It may cause headache, vertigo, 
narcosis, and inability to walk, with vomiting. Bleeding 
from various mucous membranes together with bruise-like 
blotches on the body are quite characteristic. Some 
individuals are very much more sensitive than others, 
instances being cited of individuals dying from typical 166 
TOXICOLOGY 
benzine poisoning in air containing only i part of benzene 
to 10,000 of air. Benzol also exerts a catabolic influence 
upon the body tissues as a whole inasmuch as nitrogenous 
metabolism is stimulated by it. 
If after medicinal administration of benzol the leuco- 
cytes show a rapid fall in number the benzol should be 
stopped at once no matter how high the count, for this is 
an indication of severe aplasia, otherwise the leucocytes 
will continue to fall with fatal results. Under the cir- 
cumstances the bone marrow is very red with myelocytes, 
with much new connective tissue and new vessels and 
hemorrhages. 
Treatment.-Treatment is purely symptomatic. If 
swallowed the stomach tube should be used and ether and 
strychnine given hypodermatically. When overcome by 
the vapor removal to the open air, artificial respiration, 
oxygen inhalation, and stimulants are necessary. Poi- 
soning from a medicinal use may result in anemia which 
can be combatted successfully only by repeated transfu- 
sions of blood. 
References 
Hamilton: J.A.M.A., 1922, 78, p. 627. 
Underhill and Harris: J. Ind. Hyg., 1923, 4, p. 491. 
NITROBENZOL-NITROBENZENE 
(C6H5.NO2) 
By the action of nitric acid on benzene, nitrobenzene, 
which is also sometimes called "essence of mirbane," 
is formed. It is extensively employed in the preparation 
of aniline and various explosives, and because its odor 
resembles benzaldehyde, or oil of bitter almonds, finds 
considerable use as a substitute. Various flavoring 
extracts, perfumes, floor polishes, inks, shoe dyes, soaps, MISCELLANEOUS ORGANIC POISONS 
167 
alcoholic liquors, confectionery and pastry may contain 
nitrobenzene. It has also been used to induce abortion 
and with suicidal intent. Nitrobenzene must be regarded 
as a powerful narcotic poison. Poisoning has resulted 
from the external application, as by spilling upon the 
clothing, wearing dyed shoes, from employment as a 
delousing agent, from the use of soap containing it, etc. 
Needless to point out it should never be a constituent of 
any substance intended for internal administration. 
Industrially poisoning occurs chiefly in aniline plants. 
The vapor is even more toxic than the liquid. 
Nitrobenzene is an oily yellow liquid which may be 
obtained in crystalline form at low temperatures. It 
boils at 2O5°C. and has a specific gravity of 1.186. It is 
combustible, burning with a yellow flame. 
Symptoms.-Taken by mouth nitrobenzene may cause 
no symptoms for a period of three hours or more beyond a 
burning sensation in the throat and stomach which may 
be followed by numbness and tingling sensations. The 
vapor is more powerful than the liquid. In either case 
definite symptoms appear suddenly. In certain instances 
the victim has complained of feeling drunk. There is 
headache, giddiness, faintness, nausea and vomiting, 
the vomitus having the characteristic odor of nitrobenzene. 
The vision is disturbed, the face is steel gray in color, coma 
supervenes, sometimes ending in death. The general 
symptoms closely resemble prussic acid poisoning except 
that with nitrobenzene the coma is delayed for a consid- 
erable period and does not come on at once as with 
prussic acid poisoning. The temperature is lowered, 
respiration takes on the Cheyne-Stokes type and the pupils 
are not sensitive to light. The urine is dark in color, with 
an odor of nitrobenzene, and contains reducing substances. 
The phenolsulphonephthalein excretion may be consider- 168 
TOXICOLOGY 
ably decreased. The blood is chocolate colored. Death 
occurs from respiratory failure. After the acute symp- 
toms have subsided jaundice may persist for several days. 
Inhalation of relatively large quantities of the vapor 
may produce very sudden symptoms, chief of which are 
nausea, vomiting, unsteady gait and actions similar to 
those of alcoholic intoxication, stupor and coma finally 
appearing with intense cyanosis and respiratory failure. 
The habitual contact in industry produces a chronic 
condition having as outstanding features langour, breath- 
lessness, cyanosis and failing eye-sight. The urine is dark 
red in color, and there may be multiple neuritis, fatigue, 
indigestion, emaciation and anemia. 
Physiological Action.-Nitrobenzene has at least a 
two-fold action. In the first place it first stimulates, then 
paralyzes the central nervous system. Secondly it may 
be regarded as a blood poison since nitrobenzene so 
changes the blood that it is no longer capable of trans- 
porting oxygen. This is accomplished by nitrobenzene 
combining with hemoglobin to form nitrobenzene hemoglo- 
bin or acting upon hemoglobin in such a manner as to form 
methemoglobin. It is possible that both compounds may 
be formed. At any rate the action is temporary and in 
acute cases at least there is no destruction of red cells or 
diminution of hemoglobin. The oxygen capacity of the 
blood is markedly decreased. Some of the nitrobenzene 
appears in the urine as p.amino-phenol. 
Fatal Dose.-One gram will undoubtedly cause death 
in an adult, although recovery has followed from the 
ingestion of more than three ounces. Taken in an 
alcoholic mixture nitrobenzene appears to be more toxic 
than when taken alone. 
Fatal Period.-Death may occur in less than an hour 
although usually it is delayed for several hours and even MISCELLANEOUS ORGANIC POISONS 
169 
for several days. Generally, however, death takes place 
within 24 hours. 
Post Mortem Appearances.-The most characteristic 
features are the dark-brown or black color of the blood, 
which usually remains liquid, the appearance of ecchy- 
moses in the gastro-intestinal tract, hyperemia of the 
brain, venous engorgement, and the characteristic odor 
of nitrobenzene which may persist for several days. 
Treatment.-This consists in prompt evacuation of the 
stomach and thorough lavage. There are no special 
antidotes. When indicated general stimulation should 
be carried out. Since the most serious feature is due to 
the changed conditions in the blood this should be reme- 
died as soon as possible. Experience has demonstrated 
that this can be best accomplished by venesection and 
subsequent saline infusion or blood transfusion. Fatty 
or alcoholic substances are contraindicated. If the 
intoxication has been caused by spilling nitrobenzene on 
the body a bath should be given immediately so as to 
prevent absorption. 
References 
Scott and Hanzlik: J.A.M.A., 1920, 74, p. 1000. 
Hamilton: J. Ind. Hyg., 1919, 1, p. 200. 
Sanders: J.A.M.A., 1920, 74, p. 1518. 
Loeb, Bock and Fitz: Am. J. Med. Sci., 1921, 161, p. 539. 
PHENOL (Carbolic Acid) 
C6H5.OH 
Perhaps phenol poisoning is more frequent than any 
other type, since phenol is readily available and its use 
is a favorite method of suicide. It rarely occurs from a 
criminal motive. Many cases of accidental poisoning 
occur annually through the ingestion by mistake of 
phenol for other drugs or alcoholic fluids. Owing to its 170 
TOXICOLOGY 
valuable antiseptic properties it has been employed 
extensively as an antiseptic or disinfectant and such use 
has caused many cases of poisoning from absorption 
through the skin or wounds produced surgically. 
Pure phenol or carbolic acid obtained from coal tar 
synthetically is a white crystalline substance having a 
peculiar aromatic odor. The crystals melt at 4O°C. "It 
is soluble in about 15 parts of water, but becomes liquid 
when 10 parts of water are added to 90 parts of the 
crystals; the liquified phenol of the U.S.P. contains not 
less than 87 per cent of pure phenol. Phenol is readily 
soluble in alcohol, ether, chloroform, and glycerine. The 
aqueous solution is neutral, or at most only faintly acid 
to litmus." 
Phenol must be regarded as a general protoplasmic 
poison. It precipitates proteins forming with them a 
relatively loose chemical combination which is insufficient 
to prevent the diffusion of phenol into the deeper tissues 
of the body, where it causes necrosis. Upon its reaction 
with protein depends its antiseptic properties. As an 
antiseptic it is, however, not so powerful as corrosive 
sublimate or the cresols. Phenol exerts an anesthetic 
action upon sensory nerves and is employed as an anal- 
gesic against itching. In addition to the local action 
phenol in minute doses produces central effects which are 
at first in the nature of stimulation, later of depression. 
Phenol is readily absorbed from any mucous membrane, 
abraded skin, wound or even from the intact skin. A 
small portion of the phenol is burned in the body, the 
remainder being eliminated by the kidneys as the ethereal 
sulphates, and glycuronates of phenol, and as hydroquin- 
one and pyrochatechin. The latter substances are oxida- 
tion products of phenol. The urine generally assumes a 
smoky appearance. MISCELLANEOUS ORGANIC POISONS 
171 
Symptoms. Local Action.-Applied to the skin phenol 
causes local tingling and numbness or even complete 
anesthesia. The skin becomes wrinkled and soft, the 
color changing from a white stain to brown. The effect 
is not that of a direct corrosive action but rather a local 
necrosis. An eschar forms which eventually falls off with- 
out pus. The continued application may give rise to 
gangrene. Another distinct feature of the local applica- 
tion even in dilute solution is the production of a severe 
eczema. The absorption of phenol from local application 
may give rise to systemic effects. 
Systemic Effects.-Taken by mouth in more or less 
concentrated form phenol induces a burning pain in the 
mouth, pharynx and stomach. Vomiting may or may 
not occur. The contact of the poison produces local 
burns which generally heal promptly but which tempo- 
rarily leave brownish stains. The most characteristic 
symptom of phenol poisoning is the rapid collapse which 
may occur in a few minutes. The face is pale, and 
covered with a cold sweat. Unconsciousness ensues, the 
heart action is weak and rapid and the respiration is 
irregular. Cyanosis is intense. At times convulsions 
occur or there may be convulsive twitchings of the 
face or limbs. The pupils contract and the temperature 
is subnormal although this low temperature may be pre- 
ceded by a rise above normal. The urine, which is dimin- 
ished in volume, has a smoky appearance and may 
contain albumin, casts, blood or bile pigments. Little 
or no preformed sulphates are present, having been used 
up to form ethereal sulphates. Death occurs from respir- 
atory failure. Generally phenol may be detected on the 
breath. 
In less intense poisoning there may be headache, vertigo, 
excitement and mild delirium. The face is pale, the pulse 172 
TOXICOLOGY 
is feeble and respiration is irregular. Vomiting usually 
occurs and there may be evidences of renal irritation. 
From injudicious use of phenol dressings a form of 
chronic poisoning may occur which is characterized by 
disturbances of digestion, skin eruptions and renal irrita- 
tion ultimately causing death. 
Fatal Dose.-The fatal dose may be taken as 8 to 15 
grams, although recovery has followed the ingestion of 
three times the quantity and death has resulted from Xo 
the fatal dose as given above. Introduced by routes other 
than the alimentary canal death is induced by much 
smaller quantities. Thus, a uterine douche containing a 
dram of phenol in one quart of water caused death in less 
than two hours. 
Fatal Period.-Death may occur in a few minutes; 
nearly always in less than 24 hours. 
Post Mortem Appearances.-Autopsy reveals brown 
patches on the site of local application or about the mouth 
if ingested. In the latter instance the mouth, pharynx, 
esophagus and stomach membranes are white and when 
the acid has been taken in a concentrated form these 
mucous membranes are eroded. Sometimes the gastro- 
intestinal tract gives evidences of an intense inflammatory 
reaction. The odor of phenol may be present. The 
respiratory tract and the lungs may be congested. The 
blood vessels of the brain may be gorged with blood and 
there may be right sided dilatation of the heart since 
death usually occurs from asphyxia. When death is 
sudden, however, these appearances may be lacking. 
Treatment, (a) Local Effects.-The affected parts 
should be washed thoroughly with alcohol in which phenol 
is soluble, and oil dressings should be applied. Oils and 
fat solvents prevent the penetration of phenol into the 
tissues and indeed may absorb phenol from the tissues. MISCELLANEOUS ORGANIC POISONS 
173 
(b) Systemic Effects.-Since phenol stays in the stom- 
ach for a considerable period the stomach should be 
thoroughly washed out even though the poison has been 
ingested for a considerable period. The lavage fluid 
should be at first 10 per cent alcohol, later warm water. 
Potassium permanganate is perhaps the most valuable 
chemical antidote. Sulphates have been used but their 
employment seems without special benefit. White of egg 
by forming a compound with phenol may help to retard 
absorption but the compound thus formed should be 
promptly removed. In the period of circulatory depres- 
sion saline infusions may be of value. When collapse 
occurs the application of heat is indicated. 
References 
Clarke and Brown: J.A.M.A., 1906, 46, p. 782. 
Sollmann, Hanzlik and Pilcher: J. Pharm. and Exp. Therap., 
1910, 1, p. 409. 
Wilbert: Public Health Reports,-1916, 31, p. 1046. 
CRESOL 
Cresol occurs in three forms, the ortho, meta and para, 
so designated from the position of the alkyl radical in the 
phenol ring. Under ordinary conditions, however, the 
term cresol relates to the commercial preparation which is 
a mixture of the three cresols and is obtained from the dis- 
tillation of coal tar. This cresol is a liquid with a boiling 
point between 198° and 2O3°C. If sufficient ammonia is 
added it separates in crystalline scales. The same action 
is induced by 6 per cent soda solution. It is soluble in 
water and mixes in all proportions with alcohol, ether and 
glycerol. 174 
TOXICOLOGY 
Cresol enters into the composition of many of the com- 
mercial disinfectants of which perhaps lysol is the prepara- 
tion most often causing intoxication. 
The symptoms of poisoning with cresol and its deriva- 
tives are so similar to phenol intoxication that a separate 
discussion is unnecessary. Treatment of poisoning would 
likewise be that for phenol. 
Reference 
Hale: U. S. Hygienic Lab. Bull., 1913, No. 88. 
PYROGALLOL 
C6H3(OH)3 
Pyrogallol (pyrogallic acid) or trihydroxybenzene is a 
strong reducing agent which is closely related to phenol. 
The typical phenol effects, however, are lost in the over- 
whelming reducing action of the compound. Commer- 
cially pyrogallol is employed in photography, in hair dyes, 
and inks. In medicine it finds use externally in skin 
diseases, such as psoriasis, lupus and ring worm, as an 
ointment. Such use, however, is always dangerous as it is 
absorbed by the skin. It acts as a mild caustic to 
membranes and wounds. 
Pyrogallol occurs as colorless crystals possessing a bitter 
taste. It is soluble in water, less soluble in alcohol and 
ether and quite insoluble in chloroform and benzol. In 
alkaline solution it rapidly oxidizes changing to a brown 
or black color and staining skin or hair with which it may 
come into contact. 
Symptoms.-When absorbed pyrogallol acts chiefly 
upon the blood producing hemolytic effects and the out- 
standing symptoms are those induced by rapid destruction 
of the red corpuscles. The hemoglobin is thrown into the 
plasma and is transformed into methemoglobin. If this MISCELLANEOUS ORGANIC POISONS 
175 
change occurs to a sufficient degree asphyxial symptoms 
eventually appear and death occurs from respiratory fail- 
ure. The most prominent symptoms are at first headache, 
chills, vomiting, diarrhoea, cyanosis, and sometimes icterus. 
The urine is dark colored, contains hemoglobin and is 
diminished in volume. Intense nephritis with casts and 
protein may be observed. Coma and collapse usher in 
death. 
Fatal Dose.-The fatal dose has not been accurately 
determined but death has been caused by one-half ounce 
or less taken internally and from the use of the io per 
cent ointment applied to one-half the body in the 
treatment of psoriasis. 
Fatal Period.-Death usually occurs within 3 or 4 days. 
Post Mortem Appearances.-The internal organs are 
generally intensely congested, and the kidneys assume a 
purple or black color. 
Treatment.-The poison should be removed from the 
stomach if taken internally and this organ thoroughly 
washed with warm water. Inhalations of oxygen may 
help. Stimulation should be pushed and the body 
temperature should be maintained. Bleeding followed by 
saline infusions are recommended. If these measures 
fail blood transfusion should be carried out. 
References 
Neisser: Annal. d'Hyg. Pub., May, 1881. 
Reilly: Brit. Med. J., 1897, ii, p. 81. 
CREOSOTE 
Creosote is a mixture of crude phenols obtained in the 
distillation of wood. The principal substances present 
are guaiacol and creosol. 176 
TOXICOLOGY 
Guaiacol 
Creosol 
These substances partake of the nature of phenol but 
the toxic effects are less convulsive. Medicinally they 
have been employed in tuberculosis, as intestinal antisep- 
tics, and as local anesthetics in dentistry. 
Creosote is a yellow liquid with a characteristic smoky 
odor. 
The symptoms produced are those of phenol poisoning, 
the lethal dose approximating 7 grams and death occurring 
usually within 24 hours. Treatment would be similar to 
that of phenol. 
Thymol is allied to the creosote constituents and in its 
action resembles phenol. Contained in a number of 
aromatic oils, for example, thyme, it has high antiseptic 
value, low germicidal properties and relatively low toxicity. 
It is employed chiefly as an anthelmintic in the treatment 
of hookworm disease. In about one-half the cases treated 
unfavorable symptoms are observable and in rare instances 
severe poisoning occurs and even death. The symptoms 
resemble those of phenol except that convulsions do not 
occur, the chief action being depression of the central 
nervous system. In therapeutic use alcohol or oily solu- 
tions or mixtures should be avoided since toxicity is greatly 
favored owing to the more rapid absorption of the 
dissolved thymol. 
Treatment consists of emptying the stomach, lavage, 
saline cathartics (not castor oil) and stimulants for the 
central nervous system. MISCELLANEOUS ORGANIC POISONS 
177 
TRINITROTOLUENE (T.N.T.) 
C6H2(NO2)3CH3 
Trinitrotoluene poisoning came into prominence during 
the World War. It was used chiefly as an explosive, and 
in its manufacture and especially in the process of loading 
it into shells and grenades, many cases of intoxication 
resulted, of which a relatively large number were fatal. 
Trinitrotoluene may be absorbed from the skin, through 
the lungs or be introduced by way of the alimentary canal. 
While all three methods of introduction probably con- 
tribute to the poisoning in its industrial aspect the 
absorption through the skin is undoubtedly of prime 
importance. It must be classed with the irritant poisons 
and produces local irritation, the symptoms varying, of 
course, with the site of application. Contact with the 
skin induces dermatitis, with the alimentary canal gastric 
pain, etc., with the respiratory tract bronchitis, congestion 
and edema. Absorbed it exerts a specific influence upon 
the red cells of the blood transforming hemoglobin into 
methemoglobin, hematin and nitric-acid-hemoglobin. 
Ultimately there is red cell destruction resulting in an 
aplastic anemia. The poison also exerts a marked influ- 
ence upon the liver, jaundice being a prominent feature. 
In addition the kidneys may show irritation. It is 
excreted by the urine for the most part and in smaller 
measure by the bile and feces. Trinitrotoluene is a hard, 
pinkish yellow crystalline powder which melts and 
sublimes at 82°C. 
Symptoms.-The symptoms of intoxication vary with 
the manner of application of the poison. Thus, in the 
so-called acute gassing which occurs in the nitrating room 
it is probable that other substances than trinitrotoluene 
play a part. In this room there may be present large quan- 
tities of nitric acid, nitrous oxide, methane, hydrogen and 178 
TOXICOLOGY 
chlorine gases. The first symptoms are those of choking, 
cyanosis, and at times loss of consciousness. Upon 
removal from the room the sputum contains blood, and 
exposure to the gases results within a day of the onset in a 
chill, in bronchitis and moderate pulmonary edema, 
sometimes pneumonia. 
From swallowing the poison gastric intestinal distur- 
bances come to the front as evidenced by nausea, 
eructations, vomiting, bitter taste in the mouth, diarrhoea, 
or constipation, abdominal pain and colic. 
When in contact with the skin an intense itching derma- 
titis results partaking of the nature of an eczema usually 
most severe where sweating is greatest. The skin assumes 
an orange color. 
After absorption the systemic effects are associated 
with the action upon the blood cells, liver and kidneys. 
The symptoms include "pallor or cyanosis, dyspnea on 
exertion, dizziness, headache, fatigue, pains in the legs, 
drowsiness, blurring of visidn; those due to renal irritation, 
urgency and frequency of micturition and lumbar pain; 
those due to degeneration of the liver; pain and tenderness 
in the right epigastrium." In many instances death is 
preceded by delirium, anuria and coma. In the stage of 
liver degeneration a toxic jaundice is prominent. When 
death results primarily from the aplastic anemia there 
may be bleeding from the gums and nose, and death occurs 
in delirium and coma. In all severe poisonings the red 
cells and hemoglobin content of the blood are very mark- 
edly reduced. In some instances the hemoglobin may be 
30 per cent with a red cell count under one million. 
Fatal Dose.-The fatal dose of trinitrotoluene is 
unknown. 
Fatal Period.-Death may occur within 24 hours but is 
usually delayed for days or even weeks. MISCELLANEOUS ORGANIC POISONS 
179 
Post Mortem Appearances.-The most striking post 
mortem appearances are those of an extensive hepatic 
necrosis and atrophy closely resembling the liver of acute 
yellow atrophy. In the kidney the glomeruli are 
congested and the tubules contain casts, cellular debris 
and in some instances the lumen is closed by the swollen 
cells. Fatty degeneration may also be present. 
Treatment.-Treatment is largely preventative. All 
possible care should be taken to prevent contact of the 
patient with the dust. Especially should the skin be 
protected. Thorough cleansing of the skin is particularly 
recommended. Rest is essential for patients suffering 
from the effects of contact. The channels of elimination 
should be stimulated by the use of purgatives and the 
ingestion of large volumes of fluid. A well balanced diet 
containing a sufficiency of meat is recommended in 
attempts to combat the anemia. In the incipient form 
this treatment will undoubtedly prove successful but in 
the stage of aplastic anemia the prognosis is unfavorable. 
References 
Martland: 1917, 68, p. 835. 
Voegtlin, Hooper and Johnson: U. S. Pub. Health Report, 
1919, 34, P- 1307- 
Haythorn: J. Ind. Hyg., 1920, 2, p. 298 (literature). 
Hamilton: Ibid., 1921, 3, p. 102. 
ANILINE (C6H5.NH2) 
Aniline is a colorless, oily liquid, with a characteristic 
odor and a burning taste. It is inflammable, and on 
exposure to air gradually turns brown. Its boiling point is 
i84°C. It is slightly soluble in water but dissolves readily 
in alcohol, ether and chloroform. Formed by the reduc- 
tion of nitrobenzol it possesses basic properties and forms 180 
TOXICOLOGY 
typical salts. It is readily absorbed by the unbroken skin 
as well as by mucous membranes. 
In general poisoning by aniline occurs from its industrial 
use. Under these circumstances pure aniline intoxication 
is not to be considered but rather the effects of aniline oil 
which contains several impurities, such as the toluidines, 
and xylidine. Poisoning may occur in the manufacture of 
aniline dyes, yarious pharmaceutical preparations, photo- 
graphic materials, and in dyeing establishments and in 
rubber industries. Absorption may occur through the 
skin, which is the ordinary method of poisoning, by spilling 
upon clothing, etc., by inhalation of vapors and dust, and 
by swallowing of the dust with saliva or food. There are 
on record a few cases of suicide by the use of aniline. 
Aniline must be regarded as a blood poison causing 
methemoglobin and disintegration of the red cells, and in 
addition an influence upon the nervous system. It has 
been stated that in the blood aniline black is formed. 
Aniline is excreted in the urine, in part, unchanged, in 
part as an ethereal sulphate. 
Symptoms.-Pallor is the first symptom of aniline 
poisoning. A blue color, especially on the lips and finger 
nails succeeds this pallor. There is weariness, sleepiness, 
flushed face, fulness in the head, mental confusion. There 
is dryness of the throat, difficulty in swallowing, weak 
pulse, low temperature, severe headache, dizziness, a 
staggering gait, nausea, loss of consciousness, convulsions, 
coma and death. In mild poisoning there may be pallor 
with cyanosis, weakness, unsteady gait, labored speech, 
irritability, and defective orientation with other symptoms 
resembling alcoholic intoxication. At a later period there 
may be loss of appetite, constipation, marked air hunger, 
and cyanosis, loss of reflexes, jaundice, vomiting, painful 
micturition and bloody urine. MISCELLANEOUS ORGANIC POISONS 
181 
In chronic poisoning the chief characteristic is anemia, 
with slow pulse, disturbances of digestion, headache, 
dizziness, head noises, and muscular pains. Skin erup- 
tions of an eczematous and pustular character on various 
parts of the body especially on the scrotum are common. 
Perhaps the most reliable means of diagnosing aniline 
poisoning, particularly of the chronic type, is by estimation 
of hemoglobin content. A reduction of 15 to 20 per cent 
accompanied by stippling of the cells is indicative of 
aniline poisoning. A dark colored urine, due to the 
presence of hemoglobin and aniline decomposition prod- 
ucts is quite characteristic. 
Fatal Dose.-The fatal dose is unknown. Death has 
been caused by quantities varying from 25 c.c. to 100 c.c. 
although recovery has followed the ingestion of 75 c.c. 
On the other hand, 0.1 to 0.25 gram aniline will produce 
serious symptoms. 
Fatal Period.-In acute cases death has generally 
followed within 24 hours. In chronic poisoning recovery 
takes several weeks and in many instances the individual 
is unable to return to his former work because of increased 
susceptibility. 
Post Mortem Appearances.-Beyond the finding of 
methemoglobin autopsy reveals nothing characteristic 
of aniline poisoning. 
Treatment.-For acute symptoms treatment consists 
in removing the patient to the fresh air. If aniline has 
been swallowed lavage of the stomach should be instituted. 
The saline purgatives and stimulants (hot, black coffee) are 
recommended. If the case is serious and the patient can 
stand it bleeding with saline infusion may be carried out 
or bleeding with transfusion of blood. Oxygen inhalations 
may help and body temperature should be maintained. 182 
TOXICOLOGY 
References 
Harrington: Boston Med. and Surg. J., 1918, 179, p. 497. 
Luce and Hamilton: J.A.M.A., 1916, 66, p. 1441. 
Hamilton: J. Ind. Hyg., 1919, 1, p. 200. 
Birge: J.A.M.A., 1914, 62, p. 314. 
Poisoning from acetanilid usually results from the 
careless or ignorant use of this antiseptic for its analgesic 
effect, usually in the form of headache powders. When 
employed for its action in lowering a febrile temperature 
care must also be taken for the side action of the drug 
may result in sudden collapse. Both acute and chronic 
poisoning may occur, death resulting from either. Pre- 
viously intoxication resulted from absorption of acetanilid, 
which has some antiseptic properties, applied to wounds. 
Acetanilid crystallizes in lustrous white plates, which 
possess no odor and only a slight burning taste. It melts 
at ii3°C. and is sparingly soluble in cold water. It dis- 
solves readily in hot water, alcohol and ether, and when 
heated with acids or alkalies decomposes to aniline and 
acetic acid. Acetanilid is rapidly absorbed and reappears 
promptly in the urine transformed into para-aminophenol 
combined either with sulphuric or glycuronic acids. This 
derivative of acetanilid gives to the urine the "indophenol 
reaction." 
Acetanilid produces toxic effects chiefly by its action 
upon the red blood cells forming methemoglobin and 
causing destruction of the erythrocytes. This blood 
destruction gives rise to a characteristic cyanosis. MISCELLANEOUS ORGANIC POISONS 
183 
Symptoms.-The outstanding features of acetanilid 
poisoning are cyanosis, profuse perspiration, muscular 
weakness, prostration and collapse. The pulse is weak, 
the extremities are cold, the respiration is shallow and 
dyspnoeic, the temperature is subnormal, and there may 
be unconsciousness, convulsions or delirium. Death 
occurs from circulatory failure. The blood has a lowered 
oxygen capacity, and contains methemoglobin. Nephritis 
with anuria and an acute jaundice may be observed. 
There have been reported a number of cases of chronic 
acetanilid poisoning, the characteristic symptoms being 
weakness, insomnia, increased nervous excitability, diges- 
tive disturbances, dyspnoea, cyanosis and anemia. The 
heart sounds are indistinct and there may be murmurs. 
The urine contains methemoglobin and is generally brown 
in color. 
Fatal Dose.-With a weak heart small doses (io to 20 
grains (0.6 to 1.3 grams) may cause alarming symptoms. 
With individuals with normal hearts death has been caused 
by doses varying from 8 to 30 grains although recovery has 
followed the administration of 60 to 120 grains. 
Fatal Period.-Death may be sudden or be delayed for a 
period of several days. 
Post Mortem Appearances.-In acetanilid poisoning 
autopsy reveals nothing characteristic beyond the choco- 
late colored blood due to the presence of methemoglobin. 
Treatment.-The alimentary canal should be thor- 
oughly cleansed by lavage and saline purgatives. Stimu- 
lants, such as strychnine, camphor, ammonia, brandy, 
warmth, are indicated. In desperate cases venesection 
with subsequent saline infusion is recommended. Epine- 
phrine or strophanthin may be used intravenously to stimu- 
late the heart. Perform artificial respiration if necessary. 
For chronic poisoning the treatment is symptomatic. 184 
TOXICOLOGY 
References 
Arculi: Lancet, 1921, 1, p. 965. 
McEllroy: J.A.M.A., 1919, 73, p. 1927. 
Nadler: Ibid., 1920, 74, p. 1717. 
Shuman: Ibid., 1921, 77, p. 526. 
ACETPHENETIDIN (Phenacetin) 
Acetphenetidin is closely allied to acetanilid both chemi- 
cally and toxicologically. In general it is less toxic than 
acetanilid and its effects are produced more slowly. As 
with acetanilid para-aminophenol is formed which may 
be the cause of the toxic symptoms. 
Acetphenetidin occurs in white glistening crystals or 
powder. It is odorless, slightly bitter and causes a faint 
numbness of the tongue. In water solution it is neutral to 
litmus. It is rather difficulty soluble in cold water but 
readily soluble in hot water, in alcohol and chloroform. 
It is less soluble in ether although appreciable quantities 
are dissolved by this solvent. It melts between 1330 
and i35°C. 
Symptoms.-Symptoms of poisoning are practically 
identical for those of acetanilid (which see). The skin 
eruptions, however, appear to occur more frequently 
than with acetanilid. 
Fatal Dose.-This is indefinite since in most of the fatal 
cases some pathological condition has contributed to the 
outcome. Doses as small as 10 to 15 grains have caused 
death under these circumstances. MISCELLANEOUS ORGANIC POISONS 
185 
Fatal Period.-Death may be sudden or be delayed for 
several days. 
Post Mortem Appearances.-Autopsy reveals nothing 
characteristic beyond the brown color of the blood due to 
the presence of methemoglobin. 
Treatment.-Treatment is identical with that for ace- 
tanilid (which see). 
References 
West: Lancet, 1895, 1, p. 91. 
Tobey: Mon. Bull. State Board Mass., Jan., 1908. 
In general antipyrin (phenyl-dimethyl-pyrazolon) has 
a toxicological action similar to that of acetanilid. It 
causes a tumultuous action of the heart and there may be 
erythematous or herpetic eruptions of the skin. These 
eruptions may be accompanied by edema and itching. 
Poisoning generally results from overdoses and a habit 
may be formed. Unlike acetanilid and acetphenetidin it 
does not cause the formation of methemoglobin. It is in 
part eliminated as such in the urine and in part in combina- 
tion with sulphuric acid. 
Antipyrin occurs as a white crystalline powder or as 
tubular crystals. It is odorless and possesses a slightly 
bitter taste. It is soluble in water, alcohol and chloroform 
but relatively insoluble in ether. It melts between m° 
and ii3°C. 
Symptoms.-The symptoms are principally those of 
depression, rapid, feeble pulse, collapse, cyanosis, cold 186 
TOXICOLOGY 
perspiration, loss of body temperature, nervous symptoms 
(restlessness, convulsions, sense disturbances) delirium, 
coma, sometimes albuminuria. A type of chronic poison- 
ing is characterized by skin eruptions, digestive distur- 
bances and muscular weakness. 
Fatal Dose.-Death has followed the administration 
of doses varying from 15 to 30 grains. 
Fatal Period.-Death in acute cases is generally sudden. 
Post Mortem Appearances.-Nothing characteristic is 
revealed by necropsy. 
Treatment.-Follow that outlined for acetanilid. 
References 
Report of Therapeutic Committee, B.M.A. Brit. Med. J., 1891, 1, 
p. 85. 
Blakeney: Ibid., 1899, ii, p. 85. 
CAMPHOR 
Camphor, a substance closely related chemically to 
terpene, is a solid obtained by distillation of the wood of 
camphor-laurel growing in China, Japan and the East 
Indies. Recently it has been made from turpentine. 
Medicinally it is employed as a mild irritant and antiseptic, 
as a counterirritant, or as a stimulant to the central ner- 
vous system. It assumes toxicological importance mainly 
with children, being given either by mistake for something 
else or in overdoses. On the other hand it has been MISCELLANEOUS ORGANIC POISONS 
187 
employed as an abortifacient with fatal results and 
it may cause poisoning through its use as a common 
cold remedy. 
Camphor may be regarded chemically as a solid ketone, 
insoluble in water but readily soluble in alcohol, ether, 
benzene, oils and chloroform. In the body it is oxidized 
to camphorol and eliminated in the urine in combination 
with glycuronic acid. 
Symptoms.-Camphor produces toxic effects mainly 
through its action upon the central nervous system. At 
first stimulation is in evidence followed by depression and 
paralysis of the central nervous system. The symptoms 
induced are nausea, vomiting, a burning sensation in the 
mouth, throat and stomach, thirst, disturbed vision, 
ringing in the ears, excitement, incobrdinated movements, 
dizziness, headache, rapid pulse, hallucinations, delirium, 
epileptiform convulsions, especially in children, sometimes 
anuria, unconsciousness. Death is rather rare in adults 
and results from asphyxia and collapse. The breath smells 
of camphor. 
Fatal Dose.-For an adult the fatal dose is unknown 
although one gram or less will cause toxic symptoms. 
This dose, however, is fatal to young children. 
Fatal Period.-With fatal doses death usually occurs 
within 24 hours. 
Post Mortem Appearances.-There are no characteristic 
post mortem appearances. The tissues generally smell of 
camphor. 
Treatment.-In camphor poisoning the stomach should 
be emptied and thoroughly washed. All use of oils and 
alcohol is contraindicated since they tend to hasten the 
absorption of camphor. The bowels should be purged 
with saline purgatives or calomel. The convulsions 
may be relieved by morphine or bromides. Stimulation 188 
TOXICOLOGY 
should be practiced and if necessary artificial respiration 
should be instituted. 
References 
Austragesillo: J.A.M.A., 1915, 64, p. 1694. 
Macleod: Brit. Med. J., 1896, 1, p. 1556. 
Benz: J.A.M.A., 1919, 72, p. 1217. 
TURPENTINE 
Turpentine is obtained from various species of pine by 
distillation. When purified turpentine consists chiefly of 
pinene which is closely related chemically to camphor. 
Pinene 
Camphor 
Turpentine is a thin, colorless, or slightly yellowish oil- 
It is inflammable, somewhat soluble in alcohol, only 
slightly soluble in water, and possesses a characteristic 
odor and taste, which increases on exposure and becomes 
more unpleasant. It is employed in medicine internally 
to diminish bronchial secretions. Externally it finds use 
as a counterirritant. It has also been used to induce 
abortion and as a means of suicide. The vapors are toxic. 
Whether inhaled or taken by mouth absorption into the 
blood occurs, excretion taking place mainly through the 
urine, turpentine leaving the kidney in the form of a 
glycuronate. The urine has the odor of violets. Poison- 
ing may be either acute or chronic. The latter usually 
occurs from exposure of workmen to the fumes in varnish 
factories, etc. MISCELLANEOUS ORGANIC POISONS 
189 
Symptoms.-Taken internally the symptoms induced 
by turpentine are those of gastro-intestinal irritation. 
The respiration is slow, the pulse weak, and nervous 
symptoms are present, resembling in part alcoholic intoxi- 
cation. There is excitement, muscular incoordination, 
and sometimes delirium. The urinary tract is greatly 
irritated as indicated by painful micturition, bloody urine, 
albuminuria, and at times anuria. In some cases skin 
eruptions of a scarlatinoid type are in evidence. 
In the chronic cases of poisoning the chief symptoms are 
headache, dizziness, rapid respiration, palpitation, ataxia, 
pain in chest, bronchitis, nephritis, stupor, unconscious- 
ness and convulsions. 
Fatal Dose.-The fatal dose of turpentine is unknown. 
Death in an adult has occurred from swallowing six 
ounces and in children from a teaspoonful to one ounce 
has caused death. 
Fatal Period.-Death usually occurs within 24 hours. 
Post Mortem Appearances.-There is nothing 
characteristic except the action upon the gastro-intestinal 
tract and the kidney. 
Treatment.-The stomach should be emptied and 
thoroughly washed, the lavage being followed by 
demulcents to allay the gastro-intestinal irritation. 
Stimulation by hot black coffee is indicated. 
References 
Harris: Arch. Int. Med., 1918, 22, p. 12g. 
Blackwood: J.A.M.A., 1913, 61, p. 412. 
ALCOHOLS 
ETHYL ALCOHOL-CeHs.OH 
Alcohol poisoning is extremely common, the chronic 
type, however, being much more usual than the acute. In TOXICOLOGY 
190 
the chronic type the toxicologist has only slight interest. 
Death from acute alcoholism is infrequent but not rare. 
It has resulted in children from administration of relatively 
large quantities of alcoholic drinks, and in adults as the 
result of wagers or sprees. 
Alcohol, also called ethyl or grain alcohol and ethanol, 
"is a transparent, colorless, mobile, and volatile liquid 
having a characteristic odor, and a burning taste." "It 
is very hygroscopic, specific gravity not higher than 
0.797 at I5°C. (6o°F.). It boils at 78.4°C. (173.i°F.), 
and is congealed at -130.5°C. (- 202.9°F.). It burns 
with a non-luminous flame. It dissolves resins, fats, 
volatile oils, bromine, iodine, etc., also many salts and 
gases. On oxidation it is converted into aldehyde and 
acetic acid. The alcohol of commerce always contains 
some water (usually about nine parts by weight) and 
various impurities. The different alcoholic beverages 
vary widely in the percentage of alcohol they contain: 
beers have from 2 to 6 per cent; light wines from 7 to 12 
per cent; strong wines, such as port and sherry, from 15 to 
20 per cent; spirits, such as whiskey, brandy, rum, and 
gin, have from 45 to 60 per cent of alcohol by weight. It 
is the latter class of beverages (spirits) that is responsible 
for most cases of acute poisoning with alcohol. These 
beverages, which contain in addition to ethyl alcohol 
higher alcohols of the same series, such as amyl alcohol or 
"fusel oil," and certain little known bodies called 
"enanthic ethers," are, as a rule, slightly more poisonous 
than pure alcohol diluted to the same extent with water; 
there is no justification, however, for the view, sometimes 
held, that the toxicity of these spirits is due more to the 
impurities than to the ethyl alcohol." 
Alcohol must be regarded as a local irritant. If applied 
to the skin or mucous membrane it produces redness and a MISCELLANEOUS ORGANIC POISONS 
191 
burning sensation with some anesthesia. It hardens 
tissues by withdrawing water, causing precipitates of the 
proteins. In a concentration of 70 per cent alcohol is an 
effective germicide. In concentrations above or below 
this figure it is almost inactive. Taken by mouth in 
relatively large volumes it causes irritation of the gastric 
membrane resulting in nausea and vomiting. 
Alcohol has long enjoyed a reputation as a general 
stimulant to the body. At the present time the concensus 
of pharmacological opinion is to the effect that alcohol is in 
reality, especially in large doses, a distinct depressant. 
The apparent stimulating effects, namely, the increase 
in heart and respiration rate, the rise in blood pressure, the 
sensations of flushing and warmth, are to be ascribed to 
the paralysis of inhibitory functions. 
Alcohol readily passes into the blood and in alcoholic 
intoxication the blood may contain 0.13 per cent. In 
large measure (about 90 per cent) alcohol is oxidized in the 
tissues to carbon dioxide and water, the remainder being 
eliminated by the lungs and kidneys. It also passes into 
the milk and probably permeates every tissue in the body. 
It appears to have a specific influence upon the germ cells 
causing degenerative changes which induce abnormalities 
in the offspring. 
Symptoms.-Four stages of intoxication are recognized, 
namely, the "stimulant" stage, the narcotic stage, the 
anesthetic stage and the paralytic stage. In the "stimu- 
lant" stage a flushing of the skin and a feeling of warmth 
constitute the first symptoms. Excitement quickly fol- 
lows and assumes various forms of expression, some indi- 
viduals becoming foolish in speech and action, others 
angry or violent. 
The narcotic stage quickly follows and is characterized 
by diminished psychic activity. There is generally 192 
TOXICOLOGY 
nausea, vomiting, vertigo, loss of coordinated movement 
and more or less incoherent speech. The individual 
is drowsy. 
In the anesthetic stage there is a gradual loss of 
consciousness, sensation and muscular tone, and the 
patient may be partially aroused from the stupor but soon 
relapses. 
The paralytic stage is characterized by medullary 
paralysis, slow and stertorous respiration, small, slow 
pulse, cold cyanotic skin, dilated pupils, lost reflexes, low 
temperature (86°F. or lower). The breath smells of 
alcohol. Death results from respiratory failure. Death 
may not be the immediate result of the alcohol poisoning 
but may result from pneumonia. 
During acute alcohol intoxication acute insanity may 
develop in which the patient may attempt acts of violence, 
or suicidal melancholia may be present. Various forms of 
unconsciousness or coma may complicate the diagnosis of 
alcohol poisoning. The breath, however, is generally 
diagnostic. 
Fatal Dose.-The fatal dose of alcohol is variable, being 
conditioned by several factors, such as the state of health 
of the individual, the period of digestion, habituation, the 
strength of the solution and the manner of administration. 
One to two pints of whiskey or brandy taken at one time 
may perhaps be considered a fatal dose, although recovery 
has followed the ingestion of even larger quantities. In 
terms of pure alcohol the above figures would correspond 
to 8 to 16 ounces of pure alcohol. The smallest fatal dose 
of pure concentrated alcohol varies from 3^ to 7 ounces. 
Children require much smaller doses, since 2^ ounces 
have caused death in children from 5 to 7 years of age. 
Fatal Period.-Death usually occurs within a few hours 
(6 to 12), although in some instances it was delayed for 5 or MISCELLANEOUS ORGANIC POISONS 
193 
6 days. The prognosis is unfavorable if the coma persists 
for more than 12 hours. 
Post Mortem Appearances.-The most characteristic 
autopsy findings are inflammation of the stomach mucous 
membrane with punctiform ecchymoses. The membranes 
of the brain are generally hyperemic and there may be 
well marked edema of the brain or of the lungs. The 
stomach contents and the brain especially may have a 
noticeable odor of alcohol which may persist for a 
considerable period after death. 
Treatment of Acute Alcohol Poisoning.-The stomach 
should be emptied, best by apomorphine since this also 
serves as a hypnotic, and thorough lavage with warm water 
is advisable. Stimulation should be instituted by the 
administration of strong hot coffee, or aromatic spirits of 
ammonia, or strychnine. The body temperature should 
be maintained by hot applications and the rubbing of the 
limbs. Restlessness and headache, may be combatted by 
caffeine and bromides. Morphine is not recommended 
except to control mania. With respiratory failure 
artificial respiration should be instituted. 
References 
Dodge and Benedict: Psychologic Effects of Alcohol, Carnegie 
Institute, 1915. 
Special Report Series No. 31, 34, 56, Med. Res. Com., London, 
1919-20. 
Miles: J. Pharm. and Exp. Therap., 1922, 20, p. 265. 
METHYL ALCOHOL (Wood Alcohol) 
CH3.OH 
Methyl alcohol is obtained by distillation of wood. It 
is also known as wood alcohol, methyl hydrate, methanol, 
wood spirit, wood naphtha, and carbinol. When purified 
it is commercially known as acetone alcohol, Columbian 
spirits, Colonial spirits, Eagle spirits, Lion d'Or, etc., and 194 
TOXICOLOGY 
is employed in the manufacture of paints, shellac, dyes, 
rubber, essences, bay rum, perfumes, and in the denatura- 
tion of grain alcohol. Commercial wood alcohol occurs 
in varying conditions of purity, some of the impurities 
being acetone, ethyl-methyl-ketone, methyl and dimethyl 
acetate, furfural, and allyl alcohol. The admixture of 
these substances may impart an unpleasant taste and 
odor to the fluid. On the other hand, it is difficult if not 
impossible to differentiate between methyl and ethyl 
alcohol by taste or smell. 
Methyl alcohol, when pure, is colorless with a specific 
gravity of 0.8021 at i5.5°C. It boils at 66°C. It readily 
yields formaldehyde and formic acid when subjected to 
oxidation. 
Poisoning from wood alcohol has come into prominence 
since the establishment of prohibition in the United States 
by passage of the 18th Amendment to the Constitution. 
In many instances ignorance has led to death by drinking 
methyl alcohol as a substitute for ethyl alcohol in various 
preparations sold for beverage purposes. Poisoning has 
also resulted from inhalation of the fumes in factories, 
from external application, and from the drinking of 
denatured alcohol. 
Even though death has not always resulted from wood 
alcohol poisoning, a characteristic result of severe intoxica- 
tion is impairment of vision which may be temporary or 
permanent, partial or complete blindness, due to atrophy 
of the optic nerve. Usually a central scotoma develops. 
At times the color sense is chiefly affected. In some 
instances the only untoward symptom of poisoning has 
been the blindness. 
Poisoning in man by wood alcohol differs distinctly 
from ethyl alcohol intoxication. Although in animal 
experiments methyl alcohol is less toxic than ethyl alcohol MISCELLANEOUS ORGANIC POISONS 
195 
yet in man the reverse is true. This may perhaps be 
explained by the fact that methyl alcohol seems to possess 
a degree of specificity for the nervous structures and man 
being more highly organized than animals in the develop- 
ment of the nervous system is therefore more susceptible. 
From animal experimentation it has been shown that the 
intoxication from wood alcohol does not markedly differ 
from that of ethyl alcohol except that the onset of symp- 
toms is much slower and the effects are much more pro- 
longed. This influence is explained by the difference in 
the fate of the two alcohols. Ethyl alcohol is, in large 
measure, quickly burned in the body to carbon dioxide 
and water, whereas methyl alcohol is only slowly oxidized, 
one product of combustion being formic acid which 
undoubtedly plays a part in the symptoms produced. An 
acidosis also results but it is questionable how large a share 
this plays in the serious features of the intoxication. The 
formic acid formed from the incomplete oxidation of 
methyl alcohol is only slowly eliminated from the body 
which accounts in a measure at least for the prolonged 
period of intoxication. The ingestion of repeated doses 
of ethyl alcohol establishes a degree of tolerance; with 
methyl alcohol the same procedure induces a cumulative 
effect. 
Symptoms.-With methyl alcohol poisoning the stage 
of excitement characteristic of ethyl alcohol intoxication 
is usually absent. Instead the most outstanding feature 
is depression and weakness. There is headache, nausea, 
vomiting, violent abdominal pains, muscular incoordina- 
tion, weak, rapid pulse, dyspnoea, cyanosis, restlessness, 
non-sensitive dilated pupils, low temperature, cold, 
moist skin, sometimes delirium, generally coma, infre- 
quently convulsions, and death from respiratory failure. 
Total blindness may be sudden. Eye effects are usually 196 
TOXICOLOGY 
manifested within 48 hours by pain sensations around the 
eyes, tenderness on pressure of the eye balls, some photo- 
phobia, pupil dilatation, blurring of vision, blindness. 
At times .complete or nearly complete vision is regained 
which may remain but frequently is again permanently 
lost. It is only when the optic nerve atrophies sufficiently 
that total blindness occurs. 
Fatal Dose.-Individuals show remarkable variations 
in their susceptibility to wood alcohol. It may be stated, 
however, that, in general, the fatal dose varies between 1 
to 2 ounces. Blindness or disturbances of vision have 
been reported after taking quantities as small as ounce. 
It has been stated that if 4 ounces of wood alcohol were 
drunk by each of 10 persons all would have abdominal 
pain within 3 hours, 4 would die, 2 of these being blind 
before death, 6 would ultimately recover, but 2 of these 
would be blind permanently. 
Fatal Period.-Usually death occurs within 36 hours, 
but may be delayed for 3 or more days. Death has 
occurred within 1 hour. 
Post Mortem Appearances.-The stomach and duo- 
denum are inflamed, the lungs may be edematous and the 
brain and its membranes may show edema and congestion. 
Treatment.-The stomach should be emptied and 
repeatedly washed with warm water. Methyl alcohol is 
in part eliminated into the stomach hence the need for 
lavage at intervals after the evacuation of the organ. 
Stimulation by caffeine or strychnine should be instituted 
if deemed necessary. Sodium bicarbonate by mouth or 
intravenously may be given to overcome the acidosis 
present. The evidence seems to show, however, too much 
dependence should not be placed upon this measure since 
it is quite probable that the acidosis is only an accompany- 
ing factor. Acidosis is not responsible for the condition. MISCELLANEOUS ORGANIC POISONS 
197 
Pain may be controlled by morphine. It has been stated 
that the eye symptoms are relieved by the use of pilo- 
carpine, potassium iodide, strychnine and purgatives. 
For mania hyocine may be given. Venesection may be 
useful in edema of the lungs. If indicated give artificial 
respiration. Large volumes of fluid are of value in hasten- 
ing elimination of the products of combustion. 
References 
Buller and Wood: 1904, 43, pp. 972, 1058, 1117, 1213, 
1289. 
Baskerville: Second Report Factory Invest. Committee, 1913, 
2, p. 921. 
Hunt: Johns Hopkins Hosp. Bull., 1902, 13, p. 213. 
Sollmann: J. Pharm. and Exp. Therap., 1920, 16, p. 291. 
Harrop and Benedict: J.A.M.A., 1920, 74, p. 25. 
Isaacs: Ibid., 1920, 75, p. 718. 
Haskell, Hileman and Gardner: Arch. Int. Med., 1921, 27, 
p. 71. 
AMYL ALCHOL (Fusel Oil) 
(CH3)(C2H3) = CH-CH2OH 
In general the different alcohols increase in toxicity 
with increase of the size of the molecule. Amyl alcohol, 
therefore, possesses a greater degree of toxicity than either 
methyl or ethyl alcohol. There are eight amyl alcohols 
possible; seven are known. Only isoamyl alcohol is of 
significance in toxicology at present. It occurs as the 
principal constituent of the so-called 11 fusel oil" formed 
in fermentation. 
Isoamyl alcohol is an oily liquid with a penetrating odor 
and acrid taste. It is only slightly soluble in water but 
mixes in all proportions with alcohol, ether and benzene. 
It boils at i3i.6°C. and has a specific gravity of 0.8148. 
Fusel oil is employed in industry and several cases of 
poisoning by it have occurred. 198 
TOXICOLOGY 
The symptoms of amyl alcohol poisoning are character- 
ized by coma, glycosuria and sometimes methemoglobin. 
The toxic dose of amyl alcohol for man is unknown but 
from animal experiments it may be stated that it is about 
five times as toxic as ethyl alcohol. 
References 
Futcher: Am. Med., 1901, 2, p. 210. 
Macht: J. Pharm. and Exp. Therap., 1920, 16, p. 1. 
Ether poisoning is rare although there are records of 
deaths by suicide and as a result of chronic poisoning 
induced by its habitual use as an intoxicant. In certain 
types of industry, such as the manufacture of smokeless 
powders, acute ether intoxication may occur by inhalation 
of the vapor. A certain degree of tolerance may be 
induced by ether as with alcohol. In certain parts of 
Europe ether drinking has been recognized for a long time. 
The quantities thus consumed may amount to as much 
as a pint or more, daily. 
Symptoms.-Ether is a colorless, readily volatile liquid, 
with a characteristic penetrating odor and a sweet, sharp 
taste. Evaporated on the skin it causes cold sensations. 
It possesses a specific gravity of 0.713 and boils at 35°C. 
Ether burns readily and when mixed with air forms an 
explosive mixture. It is practically insoluble in water but 
mixes with alcohol and chloroform. 
Death from ether during anesthesia is rare. The danger 
signals of overdosage of ether occur suddenly and consist 
of pupil dilatation, pallor and a changed facial expression. MISCELLANEOUS ORGANIC POISONS 
199 
Usually death in deep anesthesia is caused by respiratory 
paralysis with more or less involvement of the circulation. 
Respiration ceases even while the heart action is good. 
Serious but not necessarily fatal sequalae to ether 
anesthesia may be exhibited upon the respiratory organs 
and the kidney. Thus, bronchitis, pulmonary edema, 
and the flaring up of an old tuberculous lesion of the lung 
are some of the common after effects of ether induced in 
part perhaps by the irritative properties of the ether. 
Albuminuria and nephritis also sometimes occur. 
Ether taken by mouth produces a strong burning 
sensation in the throat and stomach. The intoxication 
resulting from absorption is in every respect similar to 
that of alcohol except that the onset is much more rapid 
and the duration is much shorter. Owing to the volatility 
of ether the stomach may be greatly dilated soon after 
the ether is swallowed. This gastric dilatation at times 
causes serious interference with respiration. 
Fatal Dose.-The fatal dose of ether by inhalation is 
very indefinite. The important factor is one of concen- 
tration rather than the total quantity inspired. The 
maintenance of surgical anesthesia requires a concentration 
of nearly 7 per cent ether vapor by volume in the air 
inspired. A marked depressing effect is caused by con- 
centrations of 9 per cent and concentrations of 11 per cent 
or more cause paralysis of the respiratory centre. Taken 
by mouth it is stated that one ounce of ether would 
probably be fatal to most adults. 
Fatal Period.-From ether narcosis death may occur 
suddenly or be delayed for days. In delayed death 
complications, such as pneumonia and nephritis, usually 
play a predominating part. 
Post Mortem Appearances.-Autopsy fails to reveal 
characteristic features in death from ether. Usually the TOXICOLOGY 
200 
brain and lungs are greatly congested, sometimes also the 
liver and kidneys. The odor of ether may often be 
recognized in the different tissues and organs. 
Treatment.-In anesthesia if the pulse is weak, rapid or 
irregular the administration of the ether should be 
stopped. In case of collapse the head should be lowered 
giving the patient free access to air. Maintain body 
temperature. Artificial respiration should be instituted 
if indicated. Give hot saline by rectum or slow intra- 
venous infusion containing i c.c. epinephrine per liter. 
For collapse strychnine or caffeine may be injected sub- 
cutaneously or ammonia by inhalation is often effective. 
For stoppage of the heart rapid rhythmic pressure over the 
heart or on the epigastrum should be tried. 
References 
Boothby: J. Pharm. and Exp. Therap., 1914, 5, p. 379. 
Report of Anesthesia Committee: J.A.M.A., 1912, 5, p. 1908. 
CHLOROFORM 
(CHCI3) 
Chloroform plays little role in toxicology from the stand- 
point of administration with criminal intent. At times it 
figures in suicide from swallowing the liquid and death is 
sometimes caused by drinking it in mistake for some 
other fluid. Chloroform, therefore, is of more significance 
from the accidents that have occurred in its use as an anes- 
thetic. 
Chloroform is a heavy, colorless liquid with a charac- 
teristic odor and a sweet taste. It is neutral in reaction, 
difficulty soluble in water but is miscible in all proportions 
with alcohol and ether. Its specific gravity is 1.491 and 
iCboils at 62°C. Chloroform is not inflammable. 
Symptoms.-Chloroform must be regarded as an irritant 
whether applied to mucous membranes or to the skin. MISCELLANEOUS ORGANIC POISONS 
201 
When taken by mouth chloroform induces pain, vomiting 
and sometimes diarrhoea. 
Chloroform anesthesia is attended by at least three 
sources of danger (i) early heart failure, (2) depression of 
the heart with limited margin of safety, (3) delayed chloro- 
form poisoning. In the early stages of chloroform 
anesthesia the common symptoms are sudden cessation of 
respiration, asphyxia leading to dilatation of the heart, 
vagus stimulation, and finally failure of the heart because 
of the asphyxial condition. In light chloroform narcosis 
the heart muscle becomes over-stimulated sometimes 
inducing ventricular fibrillation followed by death. It is 
probable that this type of action is due to excessive reflex 
inhibition of the vagus and the direct action of the chloro- 
form upon the heart muscle, chloroform being recognized 
as a protoplasmic poison. Even after the heart has 
stopped respiration may be resumed but generally the 
heart cannot be revived. In most instances therefore the 
heart ceases before respiration and the former must be 
regarded as the real cause of death. When death occurs 
in deep anesthesia with chloroform the blood pressure 
steadily falls, respiration fails and the heart stops. Gen- 
erally, however, the pulse cannot be felt before respiration 
ceases. Usually such accidents occur when the concentra- 
tion of the chloroform vapor has been too high. Warning 
signs of this type of chloroform poisoning are shallow or 
irregular respiration, a pulse that is either very slow or very 
rapid, dilatation of the pupil and cyanosis. 
Delayed Chloroform Poisoning.-By delayed chloro- 
form poisoning is meant the condition which develops in 
some patients a few hours or days after chloroform adminis- 
tration and which is marked by great prostration, delirium, 
coma and death. The symptoms may appear suddenly 
or gradually. When the onset is sudden recovery from 202 
TOXICOLOGY 
the anesthesia has hardly been attained before the unto- 
ward symptoms appear. These consist of shrieking and 
struggling alternating with intervals of stupor or coma; 
profuse vomiting which may be blood stained; cyanosis; 
jaundice, edema, renal hemorrhage, acetone breath. The 
urine contains albumin and casts and the ammonia coeffi- 
cient may be high. The urine also usually contains ace- 
tone, diacetic and /3-oxybutyric acids. The blood shows 
retention of non-protein nitrogen, urea and amino acids. 
Fatal Dose.-By mouth the probable fatal dose of 
chloroform is ounces. By inhalation of chloroform 
death has been caused by 15 drops. Much larger quanti- 
ties (20 ounces) have not caused fatality. Patients should 
not receive air containing more than 3.5 per cent of chloro- 
form by volume even for a short period. 
Post Mortem Appearances.-Autopsy shows extensive 
vacuolization and fatty degeneration of the liver, swelling 
and necrosis of the cells, especially about the central veins. 
Fatty degeneration also occurs in the kidney and sometimes 
in the heart and arteries. Children are especially suscep- 
tible to this type of chloroform poisoning and patients with 
diabetes, hepatic diseases, cyclic vomiting, rickets or 
wasting diseases, renal disease, alcoholism and anemia are 
particularly likely to succumb to this condition. In 
general, delayed chloroform poisoning almost certainly 
causes death, very few cases ever having recovered. 
Impurities in the anesthetic are not responsible for the 
untoward effects, contrary to popular opinion. They 
may contribute to the local irritative symptoms but are 
probably not concerned in the dangerous effects. Swal- 
lowing of chloroform may cause gastritis and the 
phenomena characteristic of delayed chloroform poisoning. 
Treatment.-Treatment of chloroform poisoning (exclud- 
ing delayed chloroform poisoning) consists in stopping MISCELLANEOUS ORGANIC POISONS 
203 
the anesthetic, the head lowered, and artificial respiration 
resorted to immediately. This prevents asphyxia and 
aids in the elimination of the poison. In order to aid the 
action of the heart the cardiac region should be strongly 
compressed at the rate of 40 times per minute. Saline 
solution containing 1 c.c. of 1:1000 solution of epinephrin 
per liter should be injected into the cardiac end of an 
artery. None of these measures are of value unless they 
can be taken immediately. 
References 
Report of Anesthesia Committee: J.A.M.A., 1912, 58, p. 1908. 
Schoenhof: Beitr. path. Anat., 1914, 58, p. 130. 
Levy: Heart, 1913, 4, p. 320. 
Graham: J. Exp. Med., 1915, 22, p. 48; J.A.M.A., 1917/69, p. 
1666. 
Underhill and Kapsinow: J. Met. Research., 1922, 2 p. 57. 
Gunn and Martin: J. Pharm., & Exp. Ther., 1915, 7, p. 31. 
CARBON DISULPHIDE 
(CS2) 
Acute poisoning with carbon disulphide is rare. From 
the fact that this substance is employed to a considerable 
extent in industry as a solvent for sulphur, phosphorus, 
oils, resins, rubber, etc., and as a disinfectant, chronic 
poisoning is much more common. 
Carbon disulphide is a colorless, volatile fluid possessing 
the property of refracting light. When impure its odor is 
most offensive and disagreeable. The pure substance 
lacks this repulsive odor. Its specific gravity is 1.293 
at o°C. and it boils at 47°C. Very inflammable, it burns 
with a blue flame, forming sulphur dioxide. It is difficulty 
soluble in water but readily dissolves in alcohol or ether. 
Symptoms.-Carbon disulphide!* must be regarded as a 
blood poison forming methemoglobin and destruction of 
(CS2) TOXICOLOGY 
204 
the red cells. It produces total anesthesia and causes 
death by respiratory failure. 
The symptoms prominent in acute intoxication are 
pallor, dilated pupils, rapid, weak pulse, lowered tem- 
perature, and convulsions. Carbon disulphide is elimi- 
nated through the lungs and the kidneys. In chronic 
poisoning two stages are recognized-a stage of excite- 
ment and a stage of depression. In the first stage, there 
is headache and gastro-intestinal disturbances. There is 
increased sensitiveness of the skin, head noises, irritable 
temper, pain in the limbs and spasmodic contractions of 
various groups of muscles. 
Anesthesia of the skin and mucous membranes ushers in 
the second stage-that of depression. Digestive distur- 
bances, weakness of the muscular system and mental 
debility may be prominent and paralysis of the limbs may 
occur. Recovery from the effects of chronic poisoning by 
carbon disulphide may take a year or more and if paralysis 
has taken place the injury may be permanent. 
Fatal Dose.-The fatal dose of carbon disulphide is 
unknown. Two ounces or more have failed to produce 
death when taken with suicidal intent. 
Fatal Period.-This is generally prolonged being a 
matter of days and sometimes of weeks. 
Post Mortem Appearances.-Autopsy reveals appear- 
ances with acute poisoning quite similar to those of delayed 
chloroform poisoning. 
Treatment.-If taken by mouth, evacuation and lavage 
of the stomach and general stimulation should be 
attempted. If indicated, blood transfusion is recom- 
mended. Artificial respiration and maintenance of body 
temperature should be carried through. 
Reference 
Hamilton: U. S. Bur. Labor Bull., 1915, p. 179. MISCELLANEOUS ORGANIC POISONS 
205 
CHLORAL-CHLORAL HYDRATE 
cci3.cho.h2o 
Chloral has been extensively employed as a hypnotic. 
Most cases of poisoning have resulted from overdoses 
prescribed by physicians, from self-medication by individu- 
als or from the use of proprietary preparations advertised 
as remedies for insomnia. A few instances are on record 
where it has been given with criminal intent. Death from 
chloral by suicides is not uncommon. Chloral constitutes 
the so-called "knock-out drops" which have been 
administered for purposes of robbery or rape. Generally 
poisoning has occurred from chloral taken by mouth 
although there are records of deaths from its injection into 
the blood stream and introduction by rectum. 
Chloral, which is an oily liquid, is generally used in the 
form of its hydrate, CC13.CHO.H2O. The latter occurs in 
the form of white crystals. At ordinary temperature it is 
somewhat volatile, melts at 5&°C. and boils at 97.5°C. 
Easily soluble in water and alcohol it possesses a melon- 
like odor and an unpleasant taste which may be completely 
masked by solution in alcoholic fluids. The addition of 
alkalies to chloral solutions decomposes it into chloroform, 
formic acid and water. 
The general action of chloral hydrate is depression and 
paralysis of the central nervous system. In these respects 
it closely resembles alcohol and chloroform. It has been 
extensively employed for the purpose of inducing sleep 
which closely resembles natural sleep. The analgesic 
effect is not pronounced until large doses have been given. 
Continued use of chloral may lead to fatty degeneration 
of different organs. Chloral must be regarded as a local 
irritant possessing some antiseptic properties, which 
might be anticipated from its aldehyde nature. It is 
excreted in the urine as a conjugated glycuronate which 206 
TOXICOLOGY 
imparts to the urine a reducing action, hence, may simu- 
late the appearance of sugar in the urine. 
Symptoms.-Generally with doses up to 2 grams drowsi- 
ness and heavy sleep are the only symptoms. With 
large doses uncontrollable narcosis results. The intoxica- 
tion may closely resemble that induced by alcohol or 
chloroform. With weak heart death may occur in a short 
period from heart failure. Nausea and vomiting may 
occur induced by the local action of chloral upon the 
gastric membrane. The temperature declines sharply 
in from 5 to 20 minutes after taking the drug. Respira- 
tion is shallow, the pupils are usually contracted and 
cyanosis may be prominent. Sleep may pass directly into 
death without marked change or may be preceded by 
collapse or delirium and convulsions. Death results from 
respiratory failure. Pulmonary edema at times con- 
tributes to a fatal outcome. 
In chronic poisoning by chloral the symptoms may be 
so varied as to render diagnosis extremely difficult. 
Types of symptoms are digestive disturbances; skin 
troubles, as rashes, vesicle formation, ulceration at the 
nail roots; inflammation of the eyes; nervous symptoms, 
insomnia, depression, or melancholia; at times a condition 
resembling delirium tremens, especially on withdrawal of 
the drug, or a type of dementia. In chloral habitues 
death from sudden heart failure is frequent. 
Fatal Dose.-The fatal dose of chloral is extremely 
variable death having been caused by 2 grams and 
recovery following 30 grams. Children are less suscepti- 
ble than adults but old individuals are particularly 
susceptible to its effects. It is quite probable that doses 
of 8 grams or under may not prove fatal, especially if 
proper treatment is instituted, but with doses of more 
than 10 grams it is probable that death will surely result. MISCELLANEOUS ORGANIC POISONS 
207 
Fatal Period.-The fatal period is determined in large 
measure by the size of the dose and the condition of the 
individual. Sudden death, that is, within 15 minutes, to 
an hour, is common after large doses or in persons with a 
weak heart. Most of the deaths appear to occur during a 
period of 6 to 10 hours. 
Post Mortem Appearances.-The post mortem appear- 
ances are not characteristic. The esophagus and stom- 
ach membranes may show an inflammatory reaction 
and the odor of chloral may sometimes be detected in the 
stomach contents. Edema of the lungs may be present 
in acute intoxication. In chronic poisoning there may be 
fatty degenerations, especially of the heart and muscles. 
Treatment.-Lavage of the stomach should be instituted 
especially if the drug has not had time for absorption. 
Owing to the depressant action of chloral on the nervous 
system emetics may fail to act. Owing to the rapid 
absorption of chloral other measures are likely to be more 
successful than gastric lavage. General stimulation is 
indicated and this is best attained by subcutaneous injec- 
tions of strychnine and hot coffee by mouth or rectum. 
Atropine and camphor may also be useful. The body 
temperature demands maintenance by application of hot 
water bags, etc. At times artificial respiration is essential. 
Chronic chloral poisoning is best treated in the hospitals 
especially conducted for the cure of drug addicts. 
References 
Wood: J.A.M.A., 1906, 46, p. 1220. 
Bennett: Ibid., 1922, 79, p. 1048. 
FORMALDEHYDE 
(H.CHO) 
Formaldehyde is a colorless irritant gas formed by the 
oxidation of methyl alcohol. The official solution of 208 
TOXICOLOGY 
formaldehyde contains about 37 per cent by weight of the 
gas with small amounts of methyl alcohol. Formaldehyde 
is soluble in water and these solutions tend to decompose, 
on standing, but particularly on heating, into insoluble 
decomposition products. By treatment with ammonia 
formaldehyde is transformed into hexamethylenamine. 
Because of its antiseptic properties formaldehyde has been 
extensively employed for disinfectant purposes and to 
some extent as a food preservative, especially for milk. 
At present, however, its use as a food preservative is 
prohibited by law in the United States. It possesses 
an irritant action for the skin and mucous membranes and 
according to concentration its solutions by continued appli- 
cation may induce an eczema or ulcerations and gangrene. 
Its vapor is extremely irritating to mucous membranes and 
it may produce bronchitis and pneumonia. 
Formaldehyde is absorbed by all mucous surfaces and in 
small quantities is oxidized to formic acid in the tissues. 
Some of the formaldehyde may be eliminated as such or be 
transformed into hexamethylenamine. 
Symptoms.-Poisoning by formaldehyde is not very 
common but there are a number of cases on record. "The 
symptoms consist of immediate and severe abdominal 
pain; often sudden and prolonged loss of consciousness, 
and collapse." There is sometimes diarrhoea, sore mouth, 
irritation of the respiratory tract, and an action upon the 
central nervous system resembling that of acute alcohol 
intoxication, such as staggering gait, stupor, coma and 
sometimes convulsions. The urine may be suppressed 
for several hours and then it may contain casts and blood. 
If recovery occurs it is usually rapid and complete. 
Fatal Dose.-An ounce of "formalin" (40 percent 
commercial solution) has caused death, and the largest 
quantity from which recovery has occurred is 2 ounces. MISCELLANEOUS ORGANIC POISONS 
209 
Fatal Period.-Death may be sudden, that is, within 2 
to 3 hours but generally takes place within 36 hours. 
Post Mortem Appearances.-Autopsy reveals gastritis 
with erosions, and the kidneys may show congestion. 
Treatment.-Gastric lavage should be practised 
promptly and should be followed by administration of 
dilute ammonia and ammonium acetate with the purpose 
of transforming the irritating formaldehyde into the 
non-irritating and non-toxic hexamethylenamine. 
References 
MacLachlan: Cleveland Med. J., 1909, 8, p. 606. 
Salkowski: Biochem. Z., 1921, 115, p. 159. 
PARALDEHYDE 
(CH3.CHO)3 
Poisoning by paraldehyde is rare. A few deaths have 
resulted from overdoses either given therapeutically or 
from overdosage as the result of the formation of a habit. 
Paraldehyde, a polymer of acetaldehyde, is a volatile, 
colorless liquid with an ethereal odor which is penetrating 
and disagreeable. It has a burning taste and resembles 
ether inasmuch as it irritates the mouth, throat and 
stomach. It is soluble in water, alcohol, ether and oils 
and becomes a solid at low temperatures. Its boiling 
point is i24°C. 
Rapidly absorbed it produces sleep, and in its action it 
resembles chloral but does not cause noteworthy depres- 
sion of the nervous centers. It is eliminated in part by 
the lungs and imparts a characteristic odor to the breath. 
A portion is also excreted by the kidneys. 
Symptoms.-Toxic doses of paraldehyde result in 
stupor, muscle relaxation, depression of medullary centers, 
collapse and death. 210 
TOXICOLOGY 
With chronic paraldehyde poisoning the symptoms 
closely resemble those of chronic alcoholism. These may 
be followed by delirium tremens, convulsions, high tem- 
perature, marked thirst, profuse sweating, weak pulse 
and polyuria. 
Fatal Dose.-The toxicity of paraldehyde is low. As 
much as 100 grams have been followed by recovery. 
Fatal Period.-Little is known concerning this. When 
death has occurred it has taken place within a few hours. 
Post Mortem Appearances.-Autopsy reveals nothing 
except possibly gastric irritation. The stomach contents, 
lungs and in fact most of the organs may have the odor of 
paraldehyde. 
Treatment.--Gastric lavage is indicated in acute 
intoxication. Stimulation by strychnine, hot coffee, 
atropine and camphor are recommended. The body 
temperature should be maintained by hot water bags, 
blankets, etc. Artificial respiration may be necessary. 
Chronic paraldehyde poisoning should be treated in a 
manner similar to treatment for chronic alcoholism. 
References 
Kraepelin: Biochem. Bull., 1916, 5, p. 223. 
Fornaca and Quarelli: Berl. klin. Woch., 1912, 49, p. 2451. 
CARBON TETRACHLORIDE 
(CC14) 
Carbon tetrachloride has recently become of toxi- 
cological importance chiefly because of its extended 
employment in various fields. It is used in industry as a 
rubber solvent, as an ingredient of certain types of paint, 
as a fire extinguisher, and as a shampooing agent. In 
medicine it has been quite extensively employed as an 
anthelmintic, and to a small degree as a delousing agent. MISCELLANEOUS ORGANIC POISONS 
211 
In the presence of heat carbon tetrachloride may form 
phosgene and hydrochloric acid which may cause serious 
poisoning. Such possibilities exist under suitable circum- 
stances when carbon tetrachloride is used as a fire 
extinguisher. 
Carbon tetrachloride is a colorless liquid with a pleasant 
odor. It solidifies to a solid mass at - 3o°C. and has a 
boiling point of y6°C. It possesses a narcotic action some- 
what similar to that of chloroform. The physiological 
action at times is obscured by the influence of carbon 
disulphide which is often present in carbon tetrachloride 
as an impurity. 
Symptoms.-The symptoms of poisoning by carbon 
tetrachloride are nausea, vomiting, abdominal pain, at 
first stupor later deepening into coma, absence of reflexes, 
cloflic convulsions, weak pulse, increased temperature and 
death. 
Fatal Dose.-The fatal dose is unknown but is several 
times the therapeutic dose (3 to 4 c.c.). 
Fatal Period.-Death usually occurs within 36 hours. 
Post Mortem Appearances.-The most characteristic 
feature on necropsy is severe necrosis of the liver. The 
kidneys are not affected. 
Treatment/-The treatment is purely symptomatic. 
References 
Lambert: J,A.M.A., 1923, 80, p. 526. 
Smillie and Pessoa: Am. J. Hyg., 1923, 3, p. 35. 
Lamson and McLean: J. Pharm. and Exp. Therap., 1923, 21, p. 
237- 
NITRITES 
The nitrite group of drugs includes the inorganic 
nitrites, the nitrous esters, as amyl nitrite, ethyl nitrite or 212 
TOXICOLOGY 
"Sweet Spirits of Niter," and those nitrates which are 
reduced to nitrites in the body. 
Amyl Nitrite.-(C5H11NO2) is a clear yellow fluid with a 
peculiar ethereal fruit odor and aromatic taste. It is 
practically insoluble in water but mixes with alcohol and 
ether. It is very volatile, even at low temperatures and is 
inflammable. 
Nitroglycerine.-(CsH^NOs^) is a clear yellow, oily 
liquid insoluble in water but soluble in alcohol, ether and 
chloroform. Upon concussion it will explode. 
Symptoms.-Although death rarely, if ever, occurs 
after the therapeutic use of the nitrites it is quite common 
for untoward symptoms to appear which, however, usually 
pass over rapidly. The effects seem to be aggravated if 
the patient is in an upright position. The symptoms 
most obvious are a pounding heart, flushing of the face and 
neck, throbbing and fulness of the head "as if the top of 
the head were coming off," and intense headache. There 
may also be confusion of ideas, visual disturbances, dizzi- 
ness, a feeling of faintness, or indeed actual fainting may 
occur. At times there may be localized edema and exces- 
sive sweating. The symptoms are probably referable to 
low cerebral blood-pressure. 
There is a wide range of susceptibility to the action of the 
nitrites, some patients displaying marked toxic symptoms 
with very small doses, others being unaffected with very 
great quantities. 
In general the nitrites in large doses form methemo- 
globin which produces cyanosis and asphyxia. Exces- 
sive doses of nitroglycerine may produce nausea, vomiting, 
colic, and at times bloody diarrhoea. There is a flushed 
and perspiring skin; headache is persistent; vertigo is 
present; and very rarely blindness and delirium. Respi- 
ration is markedly altered, hyperpnea at first obtaining, MISCELLANEOUS ORGANIC POISONS 
213 
being followed by dyspnea. The body surface is cold with 
cyanosis, the heart is slowed, paralysis occurs, convulsions 
appear and death results within seven or eight hours from 
respiratory failure. 
Nitrite poisoning may also occur from the administra- 
tion of bismuth subnitrate (which see). 
Fatal Dose.-The fatal dose of amyl nitrite is unknown. 
With nitroglycerine a few drops may prove fatal. 
Fatal Period.-With nitroglycerine death may occur 
within an hour or two or may be delayed for several hours. 
Post Mortem Appearances.-Beyond the reddish-brown 
color of the blood, due to the presence of methemoglobin, 
the only noteworthy features of nitrite poisoning revealed 
on autopsy are hyperemia of various organs and tissues. 
Treatment.-Gastric lavage is indicated in the case of 
nitroglycerine. To hasten further elimination purgation 
may be induced by saline cathartics. When the case is 
desperate venesection with subsequent infusion of physi- 
ological saline is recommended. For the attendant severe 
headaches caffeine in the form of large volumes of black 
coffee is useful. 
References 
Cadwallader: Med. Record, 1896, 50, p. 816. 
Evans: J.A.M.A., 1912, 58, p. 550. 
DIGITALIS 
The active principles of digitalis, or foxglove, are 
obtained from the leaves of Digitalis purpurea an orna- 
mental garden flower which also grows wild both in Europe 
and America. The active constituents are glucosides and 
therefore prone to chemical change. The glucosides pres- 
ent in digitalis are divisible into at least four groups (a) 
digitoxin, is a crystalline alcohol soluble compound of the 214 
TOXICOLOGY 
formula C34H45O11 which is probably the most important 
substance of the leaves. On hydrolysis digitoxin yields 
a hexose and digitoxigenin, (b) Digitalin, an amorphous 
alcohol-soluble compound of the formula C35H360i4 which 
on hydrolysis yields dextrose, digitaligenin and digitalose. 
It is about one-half as active as digitoxin, (c) Digitalein, 
an amorphous water-soluble substance which is probably 
a mixture of closely related compounds. They have 
typical digitalis effects. (J) Digitonin, which is a water- 
soluble saponin occurring in both a crystalline and an 
amorphous form. The digitonin has properties similar to 
saponins, that is, irritant and hemolytic effects and the 
typical digitalis action is lacking. 
Various other glucosides, notably the strophan thins, 
have digitalis effects, the action differing quantitatively 
rather than qualitatively. There is considerable con- 
fusion relative to the chemistry of the different commercial 
preparations. The official strophanthin, is strophanthin 
amorphous, although the same plant, the Kombe, also 
yields a crystalline strophanthin whose action is very 
similar. Oubain is a crystallized strophanthin which has 
about twice the toxicity of strophanthin. It is of particu- 
lar value for intravenous administration. 
Digitalis and strophanthins are of great importance in 
therapeutics in correcting irregularities of the heart beat 
as in auricular fibrillation or in chronic dilatation of the 
heart. 
Great care in administration must, however, be exer- 
cised since digitalis and its allies are highly toxic. The 
best preparations of digitalis are undoubtedly the tincture 
and the infusion. 
Poisoning from the clinical use of digitalis is not rare, 
indeed the border line between the necessary efficient ther- 
apeutic dose and the toxic dose is so narrow that toxic MISCELLANEOUS ORGANIC POISONS 
215 
symptoms may appear simultaneously with the desired 
therapeutic effects. This toxic action is not permanently 
harmful if care in administration and dosage is properly 
regulated. 
Symptoms.-Early indications of toxicity are nausea, 
malaise and headache which may be very severe. Diar- 
rhoea sometimes occurs but is more common with stro- 
phanthin. The dosage of the drug should either be 
reduced or stopped altogether when these symptoms make 
their appearance. In one or two days they usually 
disappear. 
In advanced digitalis poisoning various heart irregu- 
larities may be noted. The most common and the earliest 
to appear being the result of overstimulation of the vagus, 
the b^art beat dropping to 50 or lower. Extra systoles are 
frequent although the rhythm may be maintained. The 
next stage of poisoning is partial heart block which may 
be permanent. Finally there may be muscular irritability 
of the heart, with extra systoles and high blood pressure. 
Acute poisoning from digitalis is characterized by the 
symptoms appearing late and the course of the intoxica- 
tion being prolonged, death in many instances not occur- 
ring for a week or more. The most notable symptoms are 
nausea, vomiting, diarrhoea, slow arhythmic pulse, lassi- 
tude, sensory and muscular disturbances. Sudden death 
with asphyxial convulsions is quite characteristic. 
Fatal Dose.-The fatal dose of digitalis is quite variable, 
2.5 grams having caused death whereas with 4.0 grams 
recovery has been noted. The difference in results 
appears to be associated with the different degrees of 
absorption taking place, and the effect of vomiting, 
diarrhoea, etc. upon this absorption. 
Fatal Period.-Death is usually delayed for a period of 
several days. 216 
TOXICOLOGY 
Post Mortem Appearances.-Sometimes there is evi- 
dence of gastric irritation. 
Treatment.-In the simplest type of poisoning treat- 
ment consists in stopping the drug and keeping the patient 
quiet in bed until the symptoms have disappeared. To 
counteract over-stimulation of the vagus atropine sulphate 
in doses of %5 grain (o.ooi gram) may be given subcu- 
taneously. Atropine action, however, is short lived, its 
influence lasting not more than i hour. Bromides 
(i to 2 drams (4 to 8 grams) of sodium bromide or morphine 
sulphate, grain (0.015 gram) and a hot water bag, or 
ice bag over the heart may reduce excessive irritability. 
When severe poisoning is present absolute quiet and 
freedom from exertion must be maintained, since even 
the slightest effort may cause circulatory failure and 
sudden death. The other measures to be followed are 
purely symptomatic, warmth, stimulants, etc. 
In acute poisoning, evacuation of the stomach, catharsis, 
quiet and general symptomatic treatment are advocated. 
Reference 
Hatcher and Eggleston: J. Pharm. and Exp. Therap., 1912, 4, 
p. 113. 
PICROTOXIN (C30H34Oi3) 
Picrotoxin may be taken as the pharmacological repre- 
sentative of the active principles of a number of plants. 
It occurs in the seed, Cocculus indicus, of the plant 
Anamirta paniculata. The fruit is also known as fish 
berries and in powdered form has been employed as fish 
and bird poison, and as a remedy against parasites and 
vermin. Poisoning has been induced by eating the berries, 
or the flesh of fish poisoned with it, by drinking beer to 
which it has been added as an adulterant and as an 
ingredient of so-called "knock-out" drops. MISCELLANEOUS ORGANIC POISONS 
217 
Active principles of other plants capable of inducing 
picrotoxin-like effects upon the organism are Cicutoxin 
from the root of Cicuta virosa or "Water Hemlock" 
which has been eaten for parsley; Coriamyrtin from 
Coriaria myrtifolia and Tutin from Coriaria tutu, both 
glucosidal in nature. 
Pure picrotoxin occurs as colorless crystals with a 
neutral reaction, slightly soluble in cold water, more 
readily soluble in warm water and easily soluble in alcohol, 
ether and chloroform. The solutions are odorless but 
possess an intensely bitter taste. The crystals melt at 
I92 -200 C. 
Picrotoxin stimulates the medullary centres and the 
spinal cord causing typical convulsions. The stimulation 
is followed by paralysis. Picrotoxin is excreted by the 
urine in part at least in unchanged form. Picrotoxin is 
not employed therapeutically. 
Symptoms.-The initial symptoms of poisoning are a 
burning sensation in the mouth, throat, esophagus and 
stomach with subsequent salivation, nausea, vomiting, 
abdominal pain, and diarrhoea. Closely following these 
symptoms are profuse sweating, pallor, weakness, head- 
ache, shallow respiration, palpitation. Confusion and 
stupor soon pass into unconsciousness. Early in the 
intoxication convulsions, both clonic and tonic, may set in 
and opisthotonus may be in evidence. Sometimes the 
jaws are firmly closed, thus resembling strychnine poison- 
ing. The convulsions ultimately cease and paralysis 
ensues, death resulting from respiratory failure. 
Fatal Dose.-No cases of fatal poisoning have occurred 
in man from the pure picrotoxin, hence, the exact fatal dose 
is unknown. From animal experimentation it has been 
inferred that the fatal dose probably varies between 0.13 
and 0.20 gram. Death has been caused, however, from 218 
TOXICOLOGY 
eating 2.4 grams of the powdered berries which contained 
much less than the toxic dose given above. 
Fatal Period.-Death may be very rapid-30 to 60 
minutes-or be delayed for several hours. In some 
recorded cases several days elapsed before death occurred. 
Post Mortem Appearances.-The post mortem appear- 
ances are those of death by asphyxia. 
Treatment.-If vomiting has not been free, emetics 
should be administered. The convulsions may be con- 
trolled by ether, chloroform or chloral. Ether presents 
less danger than the others, chloroform may lead to 
delayed chloroform poisoning, and chloral possesses a 
depressant action on respiration. Stimulation by hot 
mustard baths and minimal doses of atropine may be 
given in the later stages. 
References 
Brown: Brit. Med. J., 1875, i, p. 540. 
Gruenwald: Arch. f. exp. Path. u. Pharm., 1909, 60, p. 249. 
SULPHONAL 
Sulphonal was introduced into medicine as a hypnotic 
by Baumann and Kast in 1888. Since then at least 34 
fatal cases have been recorded due either to overdosage 
from a single administration or from long continued use. 
Its effects are cumulative and it is possible that it may 
form a habit without the induction of tolerance. 
Sulphonal is a strong hypnotic but has only slight analgesic 
properties. It is excreted by the urine in part as ethyl- 
sulphonic acid and partly unchanged, but the elimination 
is very slow. MISCELLANEOUS ORGANIC POISONS 
219 
Sulphonal occurs in the form of crystals which are 
odorless and almost tasteless. It is almost insoluble 
in cold water but dissolves readily in hot water, alcohol 
and ether. The crystals melt at i25°C. 
Symptoms. Acute Poisoning.-Large doses of sul- 
phonal are followed by stupor, unconsciousness, and 
sometimes convulsions. The respiration is profoundly 
affected, being stertorous and irregular, and cyanosis 
develops. The pulse is weak, the temperature may be 
increased and the urine may be partially or entirely sup- 
pressed. At times the urine becomes red in color from the 
presence of hematoporphyrin from disintegration of the 
red corpuscles. Diagnostically this condition is regarded 
as an unfavorable symptom. 
Chronic Poisoning.-The use of the drug for long 
intervals leads to a type of poisoning which is character- 
ized by disturbances of digestion, nausea, vomiting, either 
constipation or diarrhoea, headache, noises in the head, 
vertigo, mental and physical incapacity, difficulty in 
speech, more or less paralysis, great emaciation, albumi- 
nuria, hematoporphyrin in the urine, and various skin 
eruptions. 
Fatal Dose.-Death has been reported from the use of 
doses varying from 5 to 30 grams. Much larger doses 
(100 grams for instance), have been followed by recovery. 
The use of sulphonal over a period of several months 
has caused death in daily doses varying from 0.6 to 1.3 
grams. 
Fatal Period.-Death may be rapid from single doses 
varying from a few hours or may be delayed for several 
days. Death from chronic poisoning is usually a matter 
of months. 
Post Mortem Appearances.-The post mortem appear- 
ances are not characteristic. TOXICOLOGY 
220 
Treatment.-In acute poisoning the stomach should be 
emptied and washed out. Excretion should be hastened 
by the use of purgatives, saline cathartics preferably, the 
administration of diuretics, best large volumes of water. 
Stimulation is indicated, strychnine and other stimulants 
may be given. In chronic poisoning the drug should be 
discontinued. Rest, regular diet, free movement of the 
bowels, large volumes of fluid, and tonics are recom- 
mended. Recovery is generally slow and prognosis 
is unfavorable when hematoporphyrin appears in the urine. 
References 
Taylor and Sailer: Contributions from Pepper Laboratory, 1900, 
p. 120. 
Rogers: J.A.M.A., 1912, 58, p. 1510. 
TRIONAL 
Trional is closely related both chemically and 
pharmacologically to sulphonal. A few cases of acute 
poisoning have been described and at least one instance of 
chronic intoxication is on record. The symptoms are so 
similar to those induced by sulphonal that a separate 
description is unnecessary. Treatment would also follow 
that of sulphonal poisoning. The fatal dose is not defi- 
nitely known, but it probably smaller than that for sul- 
phonal since trional is more soluble and its effects are 
therefore correspondingly more rapid and intense. 
Trional occurs in crystalline scales, which are colorless, 
odorless, and possess a bitter taste. In aqueous solution 
it is neutral to litmus and has a melting point between 740 
and 76°C. Above this temperature it decomposes yielding 
sulphur dioxide. MISCELLANEOUS ORGANIC POISONS 
221 
References 
Coleman: Med. News, 1900, 77, p. 129. 
v. Noorden: Therap. Mon., 1916, 30, p. 426. 
BARBITAL (Veronal) 
Barbital, as may be seen from its structure is an urea 
derivative, which was first introduced into medicine in 
1903-05 as an hypnotic. In many ways it possesses dis- 
tinct advantages over other preparations having similar 
pharmacological effects. Compared with chloral it is 
more powerful and agreeable and it is not a local irritant. 
There is also a greater range between the therapeutic dose 
(0.5 gram) and the dose likely to produce toxic symptoms 
(8-10) grams). On the other hand it has certain dis- 
advantages, for example, it acts more slowly than chloral, 
and after depression effects are more usual than is true 
for chloral. These depression effects, however, are rather 
exceptional for in therapeutic doses there is generally little 
or no influence upon the circulation and respiration. The 
general action of the therapeutic use of barbital is to 
produce a deep, dreamless sleep from which the individual 
awakes without bad after effects. Certain individuals, 
however, exhibit a variety of symptoms such as lassitude, 
dizziness, headache, diarrhoea, nausea and skin eruptions. 
Barbital is chiefly eliminated through the urine although 
small quantities may appear in the feces. Usually more 
than one-half is excreted unchanged. Excretion is very 
slow, hence cumulative effects appear and constitute a 
menace if continuous doses are maintained for a consider- 
able period of time. Tolerance is not readily established 
although the barbital habit may be formed. 222 
TOXICOLOGY 
It has been stated that the toxic action of barbital is 
especially directed to the blood vessels. It resembles 
arsenic in this action. In addition to its employment as 
a general hypnotic barbital has been used in epilepsy, 
delirium tremens, prolonged labor, pernicious vomiting 
of pregnancy and sea sickness. 
A large number of deaths have been reported from the 
use of barbital. Most of these have been caused either 
by overdosage of the drug taken in single doses or from 
continued use. A number of deaths by suicide are also 
on record. 
Barbital is a white crystalline powder with a slightly 
bitter taste. It is soluble in hot water and alcohol and 
ether. The sodium salt is readily soluble and generally 
barbital sodium is the form in which barbital is prescribed. 
Symptoms.-The acute symptoms of poisoning with 
barbital consist of coma, low blood pressure, weak heart 
action, slow and shallow respiration, increased reflexes, 
temperature either high or subnormal, cyanosis, and 
asphyxia. There may be renal irritation, the urine secre- 
tion may be suppressed either partially or completely, 
skin eruptions, death from respiratory failure. 
Symptoms of chronic poisoning are gastro-intestinal 
disturbances, nausea, vomiting, diarrhoea, confusion, 
staggering gait, loss of memory, general debility, delusions, 
anemia, hematoporphyrinuria and skin rashes somewhat 
resembling those of measles. 
Fatal Dose.-The fatal dose varies enormously probably 
depending upon the rate of absorption and the factors 
present which may modify this. Quantities as small as i 
gram have caused death whereas recovery has followed 
the administration of more than 8 grams. It is probably 
fair to state that the usual fatal dose lies somewhere 
between 8 and io grams. MISCELLANEOUS ORGANIC POISONS 
223 
Fatal Period.-Death rarely occurs under 24 hours, and 
may be delayed for 2 or 3 days. 
Post Mortem Appearances.-Autopsy reveals no 
characteristic symptoms although there may be present 
hyperemia of various organs, notably, the brain and liver 
and kidneys, and the latter may show tubular degenera- 
tion. At times from the nature of the death edema of 
the lungs may be observed. 
Treatment.-Prompt lavage of the stomach is indicated 
together with measures for stimulating excretion, such as 
the administration of diuretics (best large volumes of 
fluid) and saline purgatives. Since a failing circulation 
is one of the most prominent features of barbital poisoning 
attempts should be made to increase blood pressure. 
Hypodermic injections of camphor may help. The 
extremities should be bandaged and caffein is especially 
useful. At times saline infusion may tide the patient over 
the critical period. Artificial respiration may be necessary. 
References 
Zornlaib: Wien. med. Wochen., 1906, 56, p. 2544. 
Willcox: Lancet, 1913, ii, pp. 734 and 1178. 
Raemer: Deut. med. Wochen., 1919, 45, p. 1305. 
Hassin and Wien: J.A.M.A., 1920, 75, p. 671. 
LUMINAL 
Luminal, which is the trade name for phenylbarbital, 
is closely allied in properties and effects to barbital. It 
is a more powerful hypnotic than barbital and usually is 
given as the sodium salt which is freely soluble whereas 
the free acid is insoluble. There is perhaps more dange^ 224 
TOXICOLOGY 
of poisoning with luminal than with barbital since the 
zone between the therapeutic dose and the toxic dose is 
very narrow. 
The symptoms of poisoning so closely resemble those of 
barbital that a separate discussion is unnecessary. 
References 
Farnell: J.A.M.A., 1913, 61, p. 192. 
Shonle and Moment: J. Am. Chem. Soc., 1923, 45, p. 243. 
NAPHTHOL 
There are two naphthols, the Alpha and Beta com- 
pounds. The first is very toxic and has not been used in 
medicine, ^-naphthol has an action similar to that of 
phenol and is even more germicidal. It has been used 
especially in the form of ointment in various skin diseases, 
such as psoriasis, acne, etc., and internally it is employed 
as an anthelmintic especially in hookworm disease. 
/3-naphthol is a white crystalline powder with a burning 
taste and the odor of phenol. It is difficultly soluble in 
water but dissolves easily in alcohol, ether, chloroform, 
glycerol and alkalies. 
In the body /3-naphthol has an influence similar to that 
of phenol. It destroys the red cells and is irritant to the 
kidney. It is absorbed from the skin and its application 
to the diseased skin has led to several cases of poisoning. 
Symptoms.-The symptoms of poisoning apparently 
vary according to conditions of administration. In some MISCELLANEOUS ORGANIC POISONS 
225 
cases the application to the skin produces a severe nephri- 
tis, whereas in others vomiting, stupor, and unconscious- 
ness were most in evidence. Taken by mouth as in 
the treatment of hookworm disease nausea, vomiting, 
abdominal pain, destruction of red cells, with resulting 
anemia, large spleen and liver may be the chief symptoms, 
or again an acute nephritis may develop. The urine is 
dark in color from the conjugated glycuronate and sulphate 
formed. 
Fatal Dose.-The precise fatal dose is unknown. Death 
has been caused by the absorption of the 2 per cent oint- 
ment applied to the skin of children or by 3 or 4 grams in 
adults. By mouth doses of 18 grams cause serious symp- 
toms. 
Fatal Period.-The fatal period is usually delayed for 
many days. Death may occur in from 24 hours to a 
month. 
Post Mortem Appearances.-The most characteristic 
feature is the presence of an acute nephritis. 
Treatment.-Follow the treatment for phenol poisoning 
-see page 173. 
References 
Smillie: J.A.M.A., 1920, 74, p. 1503. 
Busquet: J.A.M.A., 1921, 79, p. 51. 
CUBEB AND COPAIBA 
The oleoresins of copaiba and cubeb are employed as 
urinary antiseptics in subacute and chronic urethritis. 
They are used as aids to local treatment to diminish pain 
and the discharge and to hasten healing. Cubeb is also 
sometimes used in bronchitis. The oleoresins are rich in 
terpenes and resin acids which are mildly irritant. This 
irritant action is induced along the urinary tract as a 226 
TOXICOLOGY 
stimulus to repair, the terpenes at the same time acting as 
antiseptics. 
These substances are also irritating to the gastro- 
intestinal tract causing anorexia, colic, eructations and 
diarrhoea. Scarlatinal rashes occur in some patients 
whether from the direct action of the drugs or secondary to 
the gastro-intestinal disturbance is uncertain. With 
large doses there is intense irritation of the urinary tract 
resulting in renal pain and albuminuria. 
OIL OF SAVIN 
Savin is a volatile oil present in the leaves of the common 
savin plant (Juniperus Sabina or Sabina Communis) 
which is indigenous in Europe and certain parts of the 
United States. The tops of this evergreen have been 
employed in the form of a decoction from time 
immemorial to produce abortion and most of the fatalities 
have occurred from such use. The intoxication with savin 
resembles turpentine poisoning except that it is much more 
serious. 
Symptoms.-There is a burning sensation in the throat 
and stomach followed by nausea, vomiting, violent 
abdominal colic, and bloody diarrhoea. There is severe 
congestion in the pelvic organs including the uterus upon 
which it may exert a specific effect. If the uterus is 
pregnant the fetus is generally expelled. The menstrual 
flow is said to be greatly increased. The urinary organs 
are intensely irritated, blood and protein appearing in the 
urine, the passing of which is painful and may be entirely 
suppressed. The respiration is irregular. Later uncon- 
sciousness and convulsions may be manifested and death 
occurs in collapse. 
Fatal Dose.-Since death generally occurs from 
home made decoctions it is impossible to state the exact MISCELLANEOUS ORGANIC POISONS 
227 
fatal dose. According to Lewin 6 drops of the oil may 
produce toxic effects. 
Fatal Period.-Death usually occurs only after several 
days but may result in a few hours. 
Post Mortem Appearances.-In a case described by 
Blyth the pharynx was much reddened, and the gullet 
even congested. The stomach was inflamed and con- 
tained some greenish matter in which savin tops could 
be identified. The odor of savin may be detected in the 
gastro-intestinal contents. The kidneys are irritated. 
Treatment.-Treatment of savin poisoning consists in 
evacuation of the stomach and lavage. The administra- 
tion of demulcents and stimulants is indicated. 
Reference 
Blyth: Poisons, 5th Edition, 1920, p. 485. 
OIL OF CEDAR 
Oil of cedar is contained in the tops of the red cedar 
(Juniperus Virginiana) indigenous in the United States. 
This oil resembles closely the oil of savin and like the latter 
has caused toxic effects and death mainly from its use by 
the laity as an abortifacient. On the other hand it has 
been taken by mistake and also with suicidal intent. It 
rarely produces abortion. 
Symptoms.-The symptoms produced are somewhat 
similar to those evoked by savin-burning in the throat 
and stomach, nausea, vomiting, the vomitus at times con- 
taining blood, convulsions, irregular respiration, slow, inter- 
mittent pulse, unconsciousness, coma and death in collapse. 
The kidneys are irritated and there may be anuria. 
Fatal Dose.-The smallest fatal dose on record is one 
ounce. As small a quantity as 00 minims (5.5 c.c.) have 
caused serious symptoms. 228 
TOXICOLOGY 
Fatal Period.-Death may occur within an hour or be 
delayed for more than a day. 
Post Mortem Appearances.-There is gastro-intestinal 
irritation and congestion of the renal organs. The stom- 
ach contents have the odor of oil of cedar. 
Treatment.-The treatment should be prompt, evacua- 
tion of the stomach with lavage and general stimulation 
if indicated. 
References 
McNally: Med. Record, 1916, 89, p. 330. 
DeNeen: Am. J. Surg., 1919, 33, p. 277. 
CROTON OIL 
Croton oil is a fixed oil which is obtained by pressure 
from the seeds of Croton Tiglium. It is a pale yellow 
liquid, with a faint fatty odor, and contains about 10 per 
cent of the active constituent " croton resin." Poisoning 
has occurred accidentally from mistaking it for castor oil, 
from overdoses and from homicidal motives. The 
ingestion of the seeds of the plant has also caused intoxica- 
tion. In medicine it has been employed as a purgative 
in obstinate constipation when other measures have 
failed. 
Symptoms.-The chief symptoms are gastro-intestinal 
irritation with subsequent collapse. Applied to the 
surface of the body croton oil is an irritant, producing 
sensations of burning, redness of the face and formation 
of vesicles, which may develop pus, and sometimes slough- 
ing of the tissues. 
Taken by mouth croton oil produces a burning sensation 
in the mouth and throat, irritation, salivation and vomiting. 
Intense abdominal pain occurs accompanied by profuse 
diarrhoea, the stool often containing blood. The skin MISCELLANEOUS ORGANIC POISONS 
229 
is moist and cold, the face pinched, the respiration is slow 
and shallow, the pulse small and thready, and the tem- 
perature falls. There may be delirium. Collapse sets 
in, cyanosis develops and death occurs from respiratory 
failure. It is reported that death may take place without 
special gastro-intestinal disturbances, as purging. 
Fatal Dose.-Death has been caused by the ingestion of 
20 drops of the oil whereas recovery has followed the 
administration of one-half dram. The toxicity of different 
specimens of the oil varies considerably. In general the 
freshly prepared samples are less toxic than those which 
have stood for a considerable period. 
Fatal Period.-Death usually occurs in from 4 to 12 
hours, although there are cases of poisoning on record 
where death was delayed for several days. 
Post Mortem Appearances.-The characteristic features 
observable on necropsy are intense inflammation of the 
gastro-enteric tract, sometimes with erosion. 
Treatment.-The stomach should be emptied either by 
the tube or by an emetic as apomorphine. The stomach 
should be washed with warm water, and after thorough 
lavage demulcent drinks are indicated. The circulation 
and respiration should be stimulated. This may be 
accomplished by aromatic spirits of ammonia, strychnine 
and strong coffee. 
SANTONIN (C15H18O3) 
Santonin is the inner anhydride or lactone of santonic 
acid obtained from Levant wormseed, Santonica. San- 
tonin forms colorless crystals, which become yellow on 
exposure to light. They are odorless and at first tasteless, 
leaving an after bitter taste. The crystals are only 
slightly soluble in water but dissolve readily in alcohol. 
The crystals melt at 17o°C. 230 
TOXICOLOGY 
Santonin is employed medicinally as an anthelmintic 
and nearly all the cases of intoxication have been due to 
overdoses generally by the laity in attempts at self- 
medication. Most deaths have occurred among children 
although occasionally adults have succumbed. Santonin 
is changed in the intestine to sodium santoninate and the 
major portion is passed out as such through the feces. 
The portion absorbed is changed in the organism, probably 
by oxidation, and the decomposition products impart a 
yellow color to the urine. Upon rendering the urine 
alkaline the yellow color becomes pink. 
Symptoms.-The symptoms observed in santonin 
poisoning are gastro intestinal disturbances and an influ- 
ence upon the central nervous system. The symptoms of 
gastro-intestinal trouble are nausea, vomiting, abdominal 
pain and diarrhoea. The nervous symptoms are headache, 
vertigo, weakness, sleepiness. Later unconsciousness, 
clonic convulsions, and fall of temperature may occur. 
There seems to be a special influence upon the eye since 
even with large therapeutic doses there may be "yellow 
vision" which in severe poisoning may result in temporary, 
partial or complete blindness. The blindness may last 
for a week or more. At times taste, smell and hearing are 
also affected. At times also there may be skin eruptions, 
fever, nephritis, hematuria, and urine suppression. Death 
is due to respiratory failure. 
Fatal Dose.-The fatal dose of santonin for children 
between the ages of four to seven years lies somewhere 
between 2 and 3 grains (0.06 to 0.16 gram). With adults 
as much as 1 gram has been taken without fatal results. 
Fatal Period.-The fatal period is variable. Some 
deaths have occurred in less than 1 hour, others in 15 
hours and in other cases death has been delayed for 1 
or 2 days. MISCELLANEOUS ORGANIC POISONS 
231 
Post Mortem Appearances.-Beyond the possibility 
of gastro-intestinal irritation autopsy reveals no charac- 
teristic features of santonin poisoning. 
Treatment.-The stomach should be emptied and 
thoroughly washed with warm water. The bowels should 
be emptied preferably by saline cathartics, as magnesium 
sulphate. The convulsions may be controlled by ether or 
chloral hydrate. Chloroform may be used but it is not 
advisable because of the danger of delayed chloroform 
poisoning. For the collapse stimulants are indicated. 
References 
Binz: Arch. f. exp. Path. u. Pharm., 1877, 6, p. 308. 
Harnack: Ibid., 1901, 45, pp. 272 and 447. 
MALE FERN 
The employment of male fern, Aspidium filix-mas, as an 
anthelmintic dates from ancient times. The form in 
which it is generally employed is that of the dried ethereal 
extract, the constituents of which are a number of closely 
related substances, filicic acid, aspidium, flavaspidin, 
etc., of which filicic is probably the active ingredient. 
The oleoresin is a green, oily liquid sometimes containing 
a crystalline deposit which should be discarded. It pos- 
sesses a disagreeable taste and odor. The active con- 
stituent, filicic acid, is a derivative of phloroglucin. It is 
insoluble in water but soluble in oils. 
Nearly all the cases of poisoning by male fern have been 
due to overdoses or to the administration of castor oil 
with or subsequent to its administration. Being soluble 
in castor oil it is thought that the toxic effect is increased 
owing to the better absorption of the drug. Filicic acid 
is decomposed in the body yielding trimethylphloroglucin. 232 
TOXICOLOGY 
Symptoms.-The symptoms of poisoning induced by 
male fern are indicative of gastro-intestinal disturbance 
and an action upon the nervous system. The gastro- 
intestinal disturbance is manifested by nausea, vomiting, 
abdominal pain, and profuse diarrhoea. The influence 
upon the nervous system is indicated by headache, muscu- 
lar twitching, dizziness, confusion, sleepiness, dyspnoea, 
sometimes convulsions, delirium, muscle cramps, coma, 
collapse and death by respiratory failure. Glycosuria 
sometimes occurs and albuminuria with casts may be 
present. In many instances icterus may be observed. 
Male fern also causes serious trouble by an action upon 
the eye resulting in temporary and sometimes permanent 
blindness. Out of 78 cases of poisoning 18 became perma- 
nently blind in both eyes, and 15 lost the vision of one eye. 
In others while actual blindness was not permanent the 
vision was distinctly impaired. The influence upon the 
eye is caused by spasm of the retinal vessels with subse- 
quent atrophy of the optic nerve. 
Fatal Dose.-For adults the fatal dose varies from 5 to 
6 drams (18.5 to 22.2 c.c.) although death has resulted from 
1 dram. For children the fatal dose is probably from 1 to 
2 drams (3.7 to 7.4 c.c.). 
Fatal Period.-Death usually occurs within 24 hours. 
Post Mortem Appearances.-The gastro-intestinal 
tract is much congested and the small intestine may 
contain many hemorrhagic areas. The kidneys may show 
nephritis. 
Treatment.-The stomach should be emptied and saline 
cathartics should be administered. Fats and oil are 
contra-indicated. Demulcent drinks are recommended. 
In the period of convulsions ether may be given and stimu- 
lants in the stage of collapse. Artificial respiration may be 
necessary. MISCELLANEOUS ORGANIC POISONS 
233 
References 
Stuelp: Zent. f. Biochem. u. Biophys., 1904, 12, p. 470. 
Sidler-Huguenin: Correspondenzbl. f. schweiz. Aertze., 1898, 
28, p. 512. 
OIL OF CHENOPODIUM 
Oil of Chenopodium has caused fatal poisoning almost 
entirely from overdosage in its therapeutic use as an 
anthelmintic. Severe intoxication may result even with 
ordinary therapeutic doses. During fasting the drug is 
more toxic than when food is given, especially fatty food 
and carbohydrates. This fact is recognized by the present 
manner of therapeutic administration during which period 
liquid food is given. The probable active principle of the 
oil is Ascaridole which is more toxic than the oil itself. The 
oil is distinctly constipating and for this reason its adminis- 
tration is followed by castor oil. The oil is absorbed from 
the stomach and intestines and is in part eliminated by 
the lungs. 
The oil of Chenopodium is obtained by distillation of the 
American wormseed, Chenopodium ambrosioides anthel- 
miniticum. 
Symptoms.-The symptoms of poisoning are gastro- 
intestinal irritation and depression of the nervous system. 
The first indications of intoxication are nausea, vomiting, 
abdominal pain and colic, diarrhoea with bloody or mucous 
stools, headache, and tingling in the hands and feet. 
There may be temporary deafness which may last as long 
as two years'but usually clears up in a few days or weeks. 
The pulse becomes irregular and drowsiness is prominent. 
Hallucinations, clonic convulsions, paralysis, collapse and 
coma may intervene and death close the scene by respira- 
tory failure. 234 
TOXICOLOGY 
Fatal Dose.-The fatal dose is unknown. Four drops 
of the oil 3 times a day for seven doses caused the death 
of an infant of one year, and death has occurred in an adult 
after 2 doses of 3 c.c. each. 
Fatal Period.-Death may occur within a few hours and 
may be delayed for several days. 
Post Mortem Appearances.-The only noteworthy 
autopsy findings are gastro-intestinal irritation. 
Treatment.-Treatment of oil of Chenopodium intoxica- 
tion consists in immediate purgation, and central stimula- 
tion by strychnine or caffiene, in the form of hot, black 
coffee. 
References 
Preuschoff: Zeit. f. exp. Path. u. Pharm., 1920, 2, p. 425. 
Darling, Barber and Hacker: J.A.M.A., 1918, 70, p. 499. 
Salant and Livingston: J. Pharm. and Exp. Therap., 1916, 8, 
p. 119. 
CANTHARIDIN 
Cantharidin is the active principle of the commercial 
cantharides which is either dried entire, or the dried and 
powdered blister beetle, Spanish fly (Cantharis vesica- 
toria). It is highly toxic and many cases of poisoning 
have resulted from its supposed action of stimulating 
sexual feeling and from its abortifacient properties. 
Poisoning has also resulted from its use as a vesicant 
and as a counterirritant in pleurisy, neuralgia and rheu- 
matic pains. In a few cases it has been used to cause 
death with criminal intent. 
Cantharidin is probably the lactone of a ketonic acid, 
cantharidic acid. It is insoluble in water and difficulty 
soluble in alcohol, chloroform and ether, but readily dis- 
solves in alkaline solutions. With bases, cantharidin 
forms salts. The pharmaceutical preparations are the 
plaster, tincture and the dried beetle. MISCELLANEOUS ORGANIC POISONS 
235 
Symptoms.-Cantharides is an irritant to the skin and 
mucous membranes. Consequently irrespective of the 
manner of administration local irritation will be in evi- 
dence. Taken by mouth there is a burning sensation in 
the mouth and throat succeeded by swelling and blistering, 
thirst and difficulty in swallowing. Generally there is 
salivation, nausea, vomiting, the vomitus sometimes 
bloody, abdominal pain, and bloody diarrhoea. The 
poison exerts a specific action upon the genito-urinary 
mechanism resulting in renal pain, pain in the penis with 
sometimes erection, urethral burning, frequent micturition, 
scanty urine, albuminuria, hematuria, casts, and in preg- 
nant women abortion. The pulse is weak and slow, chills 
may occur, delirium and tetanic convulsions have been 
observed and death is preceded by collapse and coma. If 
recovery occurs chronic nephritis may result, although 
this is by no means constant. In many instances the 
urine regains its normal aspects within a few days. 
Fatal Dose.-Death has been caused by doses varying 
from 1.5 to 3.0 grams although recovery has followed the 
ingestion of larger amounts. Distinctly toxic symptoms 
may be produced by 0.5 gram or less. 
Fatal Period.-In the acute deaths, which occur from 
shock, the period varies from a few hours to a day or two. 
In those instances in which a fatal outcome is due to the 
induced nephritis death may be delayed for many days. 
Post Mortem Appearances.-Autopsy reveals blistering 
of the mouth and pharynx, and gastro-enteritis, which may 
be accompanied by intestinal perforation. An acute 
nephritis is generally present and there may be evidences 
of an urethritis. 
Treatment.-The type of treatment to be carried out 
depends upon the conditions in the alimentary canal. The 
first step is to empty the stomach and whether this shall be 236 
TOXICOLOGY 
done by lavage depends upon the degree of injury to the 
mucous membrane of the throat, esophagus and stomach. 
If the inflammatory reaction appears to be sufficiently 
severe so that the passage of the stomach tube would prob- 
ably cause further damage to the mucous membrane, the 
stomach should be emptied by apomorphine. To sooth the 
pain demulcent drinks and opiates are indicated. Oils 
and fats are contraindicated. The body temperature 
should be maintained. Large volumes of water are 
recommended. 
References 
Avery: Lancet, 1908, ii, pp. 800 and 1100. 
Folin, Karsner and Denis: J. Exp. Med., 1912, 16, p. 789. 
Lipsitz, Fuerth and Cross: Arch. Int. Med., 1917, 20, p. 913. 
Morgulis and Muirhead: Ibid., 1919, 23, p. 190. 
ACETIC ACID (CH3.COOH) 
In concentrated form, that is, as glacial acetic acid, acetic 
acid is a corrosive. In dilute solution it acts as an irritant. 
As pure glacial acid it occurs as crystals melting at' i7°C. 
The liquid is colorless and dropped upon the skin or 
mucous membranes it forms blisters and erodes the tissues 
beneath. 
In some European countries, particularly Russia, 
poisoning with acetic acid is quite common although quite 
infrequent in England and the United States. 
Symptoms.-The symptoms resemble those of the 
concentrated mineral acids so closely that a detailed 
description need not be repeated. The parts exposed to 
the action of the acid become softened and turn yellowish 
in color. Since the acid is very volatile the larynx may be 
involved. MISCELLANEOUS ORGANIC POISONS 
237 
Fatal Dose.-The fatal dose has not been accurately 
estimated although it is said that 2 tablespoonfuls have 
proved fatal. 
Post Mortem Appearances.-Post mortem examination 
reveals typical evidences of corrosive action throughout 
the mouth and those portions of the alimentary canal with 
which the acid came into contact. 
Treatment.-Treatment consists in neutralization of 
the acid by large volumes of weak alkali, as magnesia, 
emptying the stomach by vomiting and dilution of any 
remaining acid by more dilute alkali. Other symptoms 
should be treated as they arise, and may even include 
tracheotomy because of the swollen condition of the 
larynx. 
OXALIC ACID GROUP 
COOH 
OXALIC ACID (Acid of Sugar) | 
COOH 
Oxalic acid, or its acid potassium salt (salt of lemons) 
COOH 
occurs in many types of plants, as rhubarb, sorrel, 
COOH 
dock, etc. It possesses marked bleaching properties and 
is used in commerce to remove rust and ink from linen, to 
bleach straw for hats, to polish metals, etc. Owing to its 
close resemblance to Epsom Salts (Magnesium Sulphate) 
accidental poisoning is not infrequent with oxalic acid. 
Its acid taste prevents its employment by criminals. 
On the other hand, owing to the ease with which it may be 
bought, it is frequently used by suicides. Salt of lemons 
so closely resembles in appearance cream of tartar that 
poisoning may easily result if a mistake in identity is made. 
In large doses oxalic acid acts as a corrosive. With 
small doses it is an irritant or may produce serious results TOXICOLOGY 
238 
by its remote inhibitory action on the respiratory or 
cardiac centres. With large doses death sometimes occurs 
so rapidly that treatment cannot be instituted. 
Symptoms.-With large doses there is an acid taste with 
burning pain in the throat, esophagus and stomach. 
There is vomiting, the vomitus consisting of mucus, or 
mucus admixed with blood, presenting a coffee-ground 
appearance. The pulse may be imperceptible and weak- 
ness is pronounced at first, later, leading to complete 
collapse owing to the action of the poison on the heart. 
Should a dose of oxalic acid insufficient to produce death, 
be taken, the absorbed poison produces characteristic 
effects indicative of an action upon the nervous system. 
These consist of headache, cramps, tetany, convulsions, 
delirium and coma. It is probable that these effects are 
associated with a combination of the acid with calcium 
which temporarily at least eliminates the normal function 
of this element. Convalescence is very slow. During this 
period the patient complains of numbness and tingling, 
soreness of the mouth and throat, and painful swallowing. 
The urine may contain significant quantities of protein. 
Oxalic acid differs from the other corrosive acids in that it 
is still poisonous even after dilution which has eliminated 
its corrosive and irritant properties. Sometimes subse- 
quent to the ingestion of a small dose immediate symptoms 
are lacking, later nervous phenomena being the first 
indication of poisoning. 
Fatal Dose.-The fatal dose varies between i and 3 
drams. In general death follows to 1 ounce. With 
large doses vomiting usually occurs which offers a degree 
of relief and may lead to recovery. When more than 1 
ounce has been retained death usually follows in spite of 
proper treatment. MISCELLANEOUS ORGANIC POISONS 
239 
Fatal Period.-The shortest fatal period on record is 
three minutes. There is an individual variation in this 
respect even when the same dose has been taken. Death 
generally occurs within 4 or 5 hours although it may not 
ensue for an equal number of days. 
Post Mortem Appearances.-Post mortem appearances 
are not especially characteristic, the acid leaving no stain 
upon the lips, face or mouth. On the other hand, the tis- 
sues with which it has come into contact are white in 
color and mucous membranes are loose giving evidence of 
erosion in spots and there may be areas of contraction. 
The stomach may contain bloody or coffee ground matter. 
The walls may be white and smooth or present a highly 
inflamed appearance. Generally perforation does not 
take place. The kidneys show marked congestion and 
contain large amounts of oxalates. 
Treatment.-Treatment calls for special attention inas- 
much as alkalies and water cannot be employed. Alkalies 
transform the acid into its salts which are more soluble 
than the acid and which are about equally toxic and much 
more readily absorbed. Water increases the solubility 
and accordingly correspondingly increases the quantity 
immediately available for absorption. The best antidote 
is some preparation containing calcium or magnesium 
which uniting with the acid or its salt forms an insoluble 
salt. Finely divided chalk, calcined magnesium, or whit- 
ing from the wall suspended in large volumes of water 
may be given. The stomach tube should be used with 
caution since its contact against the corroded mucous 
membrane may cause perforation. Emetics, especially 
apomorphine, are indicated. When an antidote is to be 
given its administration should be prompt since oxalic acid 
acts with great rapidity. TOXICOLOGY 
240 
PICRIC ACID 
At present picric acid is one of the most common 
therapeutic agents for the local treatment of small super- 
ficial burns. It has been advised in a number of affections 
of the skin-acute eczema, intertrigo, and herpes labialis. 
For the unbroken skin alcoholic solutions may be used but 
in superficial burns only the aqueous solution should be 
employed, otherwise poisonous symptoms may arise. 
Picric acid is a yellow, crystalline substance, without 
odor, and possessing an extremely bitter taste. It is 
somewhat soluble in water, readily soluble in alcohol, 
ether and chloroform. It explodes when subjected to 
percussion or heated rapidly. 
Symptoms.-Evidences of the toxic action of picric acid 
applied locally consist of an acute inflammation of an 
erythematous nature, the later appearance of vesicles and 
considerable local edema. The usual constitutional 
symptoms are headache and an annoying insomnia. 
Itching of the affected part is almost unendurable. Later 
the acute lesions involute to an erythemato-aqueous type 
accompanied by considerable thickening and possibly 
infiltration of the skin. This stage is not unlike an 
eczema. 
Taken internally picric acid is probably absorbed as the 
sodium salt. The picric acid is in part reduced to picramic 
acid by the liver and other tissues of the body as a method 
of detoxication. Elimination is chiefly through the urine 
to which an intense yellow color is imparted, or the urine 
may be colored a peculiar red or reddish-brown. After a MISCELLANEOUS ORGANIC POISONS 
241 
single dose of a gram, the excretion of picric acid may 
continue for a week. 
The symptoms of intoxication are referred to either the 
gastro-intestinal, nervous, circulatory, or urinary systems 
or more commonly to several of these locations. Depend- 
ing on the degree of the intoxication the gastro-intestinal 
symptoms vary from a mild anorexia, dyspepsia and 
flatulence to a severe diarrhoea accompanied by gastro- 
dynia, abdominal cramps and emesis, the vomited matter 
being stained yellow. The irritant action of picric acid on 
the mucous membranes is responsible for the gastritis 
found. The nervous manifestations vary from a slight 
headache and vertigo to stupor with convulsions followed 
by collapse in the extremely severe cases. Picric acid is a 
respiratory and cardiac depressant, but symptoms referable 
to these systems are rare. At times a primary tachy- 
cardia with a subsequent slowing of the pulse rate may be 
noted. Occasional symptoms are strangury and anuria. 
Asthenia and fever may accompany the above constitu- 
tional manifestations of internal picric acid poisoning. 
Toxic doses may also destroy the red corpuscles, and 
induce hemorrhagic nephritis and acute hepatitis. 
Yellow pigmentation of the mucous membranes is 
usually observed and superimposed upon this may be an 
erythema or even a generalized eruption of eczematous 
character and itching in nature. This dermatitis may 
partake of the nature of a measle rash. 
Fatal Dose.-The fatal dose is unknown. Six grams 
have failed to cause death. 
Fatal Period.-The fatal period is unknown. 
Post Mortem Appearances.-The only characteristic 
feature revealed by autopsy is the yellow color of the 
organs and skin. 242 
TOXICOLOGY 
Treatment.-(a) Taken internally and with constitutional 
effects. Lavage of the stomach with administration of 
large volumes of water to hasten elimination is indicated. 
(6) Local evidences of poisoning. The treatment to be 
followed is identical with that for acute eczema. 
Reference 
Pack: J. Ind. Hygiene, 1923, 4, p. 501. 
TARTARIC ACID 
CHOH.COOH 
CHOH.COOH 
Tartaric acid in concentrated solution acts as an 
irritant producing an intense inflammatory reaction on the 
stomach. Toxicologically it is of little importance, 
poisoning rarely occurring and then only when taken in 
mistake for some other substance. Some cases of poison- 
ing are on record in which tartaric acid was taken in con- 
centrated form as a fruit acidulant. Injected under the 
skin of animals or given by mouth in large doses tartaric 
acid and its salts cause acute nephritis leading to death. 
The quantities necessary to produce this effect are very 
greatly in excess of those ever employed in therapeutic 
application of this acid and its salts. 
References 
Underhill, Wells and Goldschmidt: J. Exp. Med., 1913, 18, 
P- 3i7- 
Post: J.A.M.A., 1914, 62, p. 592. 
CITRATES 
From the toxicological point of view the citrates are of 
little importance since given by mouth they are harmless 
even in large quantities. Since 1915 when Weil suggested MISCELLANEOUS ORGANIC POISONS 
243 
the use of sodium citrate to prevent blood coagulation 
during transfusion there have been numerous cases show- 
ing untoward symptoms which although not dangerous 
or of much practical significance are nevertheless suffi- 
ciently outstanding to be worthy of note. The symptoms 
consist of fairly severe chill and fever of 2.50 F. in about 
one-half hour subsequent to transfusion of citrate blood 
but within 4 to 8 hours normal conditions are restored. 
Varied views have been held relative to the cause of 
such symptoms and perhaps the most likely hypothesis is 
that the corpuscles and platelets are changed or injured 
by the citrate withdrawing calcium from the blood ele- 
ments and combining with it to form a stable compound. 
Reference 
Drinker and Brittingham: Arch. Int. Med., 1918, 23, p. 133. 
SALICYLATES 
Because of their close relationship to phenol one might 
suspect that the salicylates would possess toxic properties. 
In general the early evidences of toxicity are nausea, 
vomiting and sometimes diarrhoea, or headache, ringing 
in the ears, and deafness or mental excitement. 
Salicyiism resembles cinchonism although the ear symp- 
toms are not so common as with quinine. These may be 
due to either congestion or anemia or to changes in the 
nervous tissue of the cochlea. Disordered vision may also 
occur which is associated with degenerative changes in the 
retina or optic nerve. Other characteristic symptoms are 
a feeling of fulness of the head, angioneurotic swelling of 
the face and throat, general urticaria, mental dulness and 
apathy, muscular weakness, or mental excitement with 
loquacity, a talkative delirium, the so-called "Salicylic 
jag" the cerebral symptoms of which resemble those of 244 
TOXICOLOGY 
atropine. Alcoholics are especially susceptible to this 
type of reaction. 
With very large doses, or because of idiosyncrasy, there 
may be weakening of the heart and depression of respira- 
tory and vasomotor centres followed by collapse. Hanzlik 
asserts that even with full therapeutic doses albumin, 
leucocytes and casts appear in the urine of both normal 
individuals and rheumatic patients. The administration 
of bicarbonate with the salicylate has practically no 
demonstrable influence upon the albuminuria and renal 
functional changes produced by the salicylate. This 
evidence of inflammation of the kidney promptly ceases 
upon stopping administration of the drug. With full 
therapeutic doses there may be diminution of the urine 
with corresponding increase of body weight due to fluid 
retention in the tissues. Although edema is not visible 
this is probably an edemic condition. 
All toxic effects of salicylates are usually without danger 
disappearing as soon as the drug is stopped. On the 
other hand, a few deaths have been reported from large 
doses or because of idiosyncrasy. It is, however, difficult 
to determine whether death in these cases was induced by 
the drug or whether the accompanying disease was 
responsible. Autopsy findings in these instances show 
hyperemia of the brain and its membranes, of the kidneys 
and lungs and ecchymoses of the pericardium. 
In a clinical statistical study of the toxicity of different 
salicylates in adult males and females, respectively, 
Hanzlik found the toxic dose to be as follows: 180 and 140 
grains of the synthetic salicylates; 200 and 135 grains of 
the natural sodium salicylate; 120 minims of the methyl 
salicylate; 165 and 120 grains of acetyl salicylate; 100 and 
83 grains of salicylo-salicylic acid. For females the toxic 
dose was approximately 80 per cent of that for males. MISCELLANEOUS ORGANIC POISONS 
245 
The toxic dose of the different salicylates was uninfluenced 
by age between 16 and 75 years; by racial differences; 
various diseased conditions, and therapeutic response with 
the synthetic salicylate. Individuals showed idiosyncrasy 
toward toxic doses of the synthetic salicylate, but no rela- 
tionship was found to exist between this and such factors 
as age, race and diseased condition. Idiosyncrasy varies 
in the same patient, and was not influenced by previous 
salicylate medication. The toxic dose for children is 
higher than would be calculated for the age. 
Treatment.-The drug should be stopped. Usually the 
symptoms quickly disappear. Bromides control, in a 
measure at least, the cerebral excitement. Renal excre- 
tion should be stimulated, best by large volumes of water. 
References 
Hanzlik: The Salicylates; Annual Report for 1914 for the Thera- 
peutic Research Committee of the Council on Pharmacy and 
Chemistry of the American Medical Association. 
Hanzlik, Scott and Thoburn: Arch. Int. Med., 1917, 19, p. 1029 
Hanzlik, Scott and Reycraft: Ibid., 1917, 20, p. 329. 
FOOD POISONING 
Food poisoning may be due to a variety of causes. The 
idiosyncrasy of the individual toward some special type 
of food, as in the case of eggs, milk, oatmeal, strawberries, 
etc., must be regarded as a condition of food sensitization 
or alimentary anaphylaxis. The symptoms in such 
poisonings are usually some form of skin affection (such 
as urticaria or eczema) sneezing, nausea, vomiting and 
diarrhoea. Such symptoms usually do not lead to serious 
consequences, disappearing without sequelae after a short 
interval. By food poisoning, however, is generally meant 
an intoxication due to some peculiarity of the food 
itself rather than to some idiosyncrasy of the individual. 246 
TOXICOLOGY 
According to this concept food poisoning may be due to 
substances inadvertantly added to the food in their 
preparation or preservation as in the case of metals (lead, 
arsenic, tin, etc.); to the presence of poisons occurring 
naturally, as in mushrooms, or to toxic substances eaten 
by animals themselves subsequently eaten and their flesh 
giving rise to poisonous effects; and finally to products 
produced by bacterial activity or to infection induced by 
the ingestion of food contaminated with pathogenic 
organisms. 
For many years the term "ptomaine poisoning" has 
been applied to that condition induced by the ingestion of 
spoiled or contaminated foods. By this term was meant 
originally the presence in the food of certain bases formed 
by putrefaction which are assumed to be responsible for 
the effects produced. A few such substances have been 
isolated from spoiled foods but their effects do not cor- 
respond with those originally produced by the foods them- 
selves. The term "ptomaine poisoning," therefore, has 
come to have an indefinite meaning and is really applied 
in many instances when no more definite description seems 
adequate. Nevertheless the significance of its meaning 
has been lost and the term should be discarded as obso- 
lete. Food decomposed by putrefactive organisms is not 
so toxic as hitherto has been supposed which explains the 
apparent paradox of the harmless custom of eating 
"ripened " cheeses or game well on the road to putrefaction. 
A misconception of the toxicity of such products has been 
engendered by the method of testing experimentally the 
toxicity of products contained in spoiled foods, that is 
these substances are usually injected either subcutaneously 
or intravenously into animals rather than given by mouth, 
the way in which the food would naturally be taken. 
When spoiled food is given by mouth to animals, even very MISCELLANEOUS ORGANIC POISONS 
247 
young cats, no untoward symptoms result, which leads 
Savage to state that 11 a study of the evidence along these 
accessory lines of inquiry singularly fails to bring forward 
any evidence associating the consumption of food in a 
state of incipient putrefaction with illness in those who 
consume it." 
Food poisoning today means contamination with the 
paratyphoid group or other organisms, or the type of 
intoxication produced by B. botulinus. Two types of food 
poisoning are therefore recognized. Investigation reveals 
that food poisoning in the United States is steadily increas- 
ing. Generally poisoning occurs from food preserved 
either commercially or in the home. Of the commercially 
prepared foods, meat products, as beef, are responsible 
for most of the cases of poisoning; of fish, salmon is first 
and sardines second; of the vegetables and fruits the list 
is as follows, the incrimination of the product being in the 
order given-tomatoes, corn, beans, string beans, pork and 
beans, peas, peaches and olives. Of the home prepared 
products the order is for meat products, beef, sausage and 
pork; of fish, salmon; of vegetables, string beans, corn, 
and asparagus; of fruits, apricots and peaches. 
The season of the year appears to play little role in the 
outbreaks of food poisoning and the physical appearance, 
taste and odor of the food do not necessarily bear any 
relation to the toxic symptoms produced. 
Food Poisoning by the Paratyphoid Group.-"The 
diagnosis of food infection depends on: the history of 
exposure to the suspected food; symptoms suggestive of 
food poisoning, isolation of the infecting organisms from 
the suspected food and also from the blood, urine, feces or 
viscera of the patient; specific identification of the causa- 
tive organism by agglutination tests; demonstration of 
agglutinins in the blood serum of patients." 248 
TOXICOLOGY 
All degrees of poisoning are encountered from rapid 
fulminating cases fatal within 24 hours to those of slight 
diarrhoea and general malaise insufficient to keep the 
patient from work. The incubation period varies con- 
siderably, in some instances symptoms arising in less 
than four hours, in others being delayed for two or 
three days. 
Symptoms.-The symptoms are chiefly those of gastro- 
intestinal disturbances, nausea, vomiting, abdominal pain 
diarrhoea and fever. The diarrhoea may continue for 
several days and be associated with tetany or suppression 
of urine. In other instances there may be a more or less 
generalized erythema. Great mental depression is 
marked. 
Treatment.-Treatment consists of gastric lavage, 
purgation and stimulants as indicated. 
Food Poisoning from Botulinus.-Botulism has been 
recognized for a great many years but its significance has 
only recently received merited attention and study due 
undoubtedly in large measure to the many recent out- 
breaks identified as this condition. It differs funda- 
mentally from most types of food poisoning in that acute 
gastro-intestinal disturbances are lacking. Although 
some cases exhibit pain in the abdomen, nausea, vomiting, 
and diarrhoea, these symptoms are not outstanding. On 
the contrary an obstinate constipation appears to be a 
prominent symptom. 
Symptoms.-Early symptoms of botulism are an 
indefinite, indisposition associated with fatigue, some- 
times headache or giddiness, muscular weakness and 
constipation. Eye symptoms, dimness of vision, mydria- 
sis, loss of accomodation, etc., due to retrobulbar neuritis, 
occur early in the intoxication. Shortly after the eye 
symptoms are noted the patients complain of difficulty MISCELLANEOUS ORGANIC POISONS 
249 
in swallowing and talking and a sense of constriction in 
the throat. The tongue is generally heavily coated. 
Inability to speak is caused by paralysis of the laryngeal 
and pharyngeal muscles. The mouth is very dry which 
undoubtedly increases the difficulty in swallowing. 
Extreme muscular weakness is a striking feature of botu- 
lism and if it progresses sufficiently simulates paralysis. 
The patient is usually apathetic, semicomatose, or 
frequently restless with insomnia. At times there may be 
loss of memory, loss of sight or hearing, neuralgia in the 
neck, disturbance or loss of sensation in the arms or fingers. 
The secretions in general tend to diminish and the skin 
becomes hard and dry. The pulse is rapid, reaching in 
some cases to 150 per minute and the heart sounds may be 
distinct and weak. Usually the temperature is below 
normal ranging between 96° and q8°F. and unless compli- 
cations set in the low temperature continues until death. 
Sometimes fever develops when pneumonia intervenes. 
Respiration at first normal, later becomes irregular with 
extreme dyspnoea which may merge into partial or 
complete asphyxia. Death may occur from cardiac or 
respiratory failure, usually the latter. The length of 
the period of illness shows great variation; some patients 
die within 48 hours but in the majority of cases death 
occurs in from 4 to 6 days, although it may be delayed for 
as long as 3 weeks. If recovery occurs convalescence 
is slow. Difficulty in swallowing disappears first, but the 
muscular weakness persists for several weeks. Eye dis- 
turbances are the last to regain the normal, and the 
patient may retain a tendency to constipation. 
The diagnosis of botulism is sometimes difficult but 
"when one has decided that he is dealing with cases of 
food-poisoning the disturbances of vision, the difficulty in 
swallowing and talking, the absence of sensory dis- TOXICOLOGY 
250 
turbances, the marked muscular weakness, and the sub- 
normal temperature at once suggest botulism" (Dickson). 
Botulism may be confused with acute poliomyelitis, cere- 
brospinal syphilis, bulbar paralysis, various toxic ophthal- 
mophgias, and poisoning from belladonna, gelesemium, 
hyocyamus, and methyl alcohol. The average mortality 
in the United States is 64 per cent. 
Post Mortem Appearances.-Beyond congestion and 
hyperemia of various organs, autopsy reveals nothing 
characteristic in deaths from botulism. 
Treatment.-Treatment has not been especially effec- 
tive as the high mortality figures testify. That which has 
been most often employed is the institution of emesis and 
lavage with active purgation induced by magnesium 
sulphate or castor oil. The colon should be thoroughly 
irrigated. The patient should remain in bed and be kept 
quiet. Simple nourishing food with plenty of water 
should be given but care should be taken that none gets 
into the trachea because of the difficulty in swallowing. 
Water by rectum or salt solution under the skin are recom- 
mended. Strychnine is advocated for stimulation of the 
central nervous system and may be given freely. Pilo- 
carpine is given to increase the secretion and in many cases 
affords temporary relief. Cardiac stimulants, as digitalis 
or strophanthin, should be administered as indicated and 
artificial respiration with oxygen administration should be 
continued so long as the heart beats. 
References 
Bernstein and Fish: J.A.M.A., 1916, 66, p. 167. 
Rosenau and Weiss: J.A.M.A., 1921, 77, p. 1948. 
Savage: J. Hygiene, 1921, 20, p. 69. 
Dickson: Monographs of the Rockefeller Institute for Medical 
Research, No. 8, 1918. 
Geiger: J.A.M.A., 1923, 81, p. 1275. MISCELLANEOUS ORGANIC POISONS 
251 
POISONING FROM FOOD PRESERVATIVES AND DYES 
The preservation of food by addition of chemicals has 
long been practised and it is probable that upon no other 
topic has a greater controversy been waged than upon the 
question of the influence upon health of the addition of 
these chemicals to food. In spite of the great amount of 
work that has been done upon the subject an actual 
demonstration is lacking that the addition of preservatives 
to food, as practised, is harmful. On the other hand it is 
granted that in sufficient doses these substances must be 
regarded as distinct poisons and occasionally, in circum- 
stances other than from their use as preservatives, 
poisoning occurs. 
So far as dyes or coloring matters are concerned some, 
such as annatto, employed to color butter are believed to 
be entirely harmless, whereas others, for example the salts 
of copper and other metals, as well as various aniline 
derivatives, are either known to yield distinctly toxic 
effects or else are regarded with definite suspicion. Indeed 
in many states of this country, and in European countries 
in general, specific laws are in force against their employ- 
ment to color foods since these substances are classed as 
poisons. 
Below is given a brief resume of the toxicology of the 
most commonly employed food preservatives that are of 
interest in this connection. Our knowledge concerning 
the specific toxic action of aniline dyes as employed in 
foods is not sufficiently definite to allow a detailed account 
of the toxicology of these substances. 
Poisoning from addition of salts of toxic metals is, 
however, different, a short review of the toxicology of 
substances usually employed being given below. 252 
TOXICOLOGY 
Both boric acid and borax have been extensively 
employed as food preservatives. One must assume that 
they exert an identical influence upon the nutrition of the 
body and as ordinarily consumed in small quantities occa- 
sionally there is little or no evidence that any deleterious 
influence is exerted. On the other hand there is no ques- 
tion concerning the continued use of even relatively small 
quantities of the substances for they tend to accumulate 
in the body, the digestion becomes somewhat deranged, 
body weight is lost, and the feces become more fluid 
without actual diarrhoea being present. The effects 
may be even more detrimental for individuals with diges- 
tive or renal disturbances. Indeed it has been shown that 
if an albuminuria were present it is increased under admin- 
istration of food containing borax or boric acid. 
In general borax and boric acid are excreted through the 
urine, little or none being eliminated by the bowel. When 
doses of i to 3 grams per day are ingested pronounced 
effects follow so that it may be stated that doses of more 
than 2 grams per day are distinctly harmful, the effects 
being seen mainly in gastro-intestinal and renal 
disturbances. 
Symptoms.-With acute poisoning from larger doses 
the following symptoms are to be observed-gastro- 
enteritis, skin eruptions resembling those of scarlet fever, 
disturbances of vision, muscular weakness, lack of co- 
ordination, fall of temperature and collapse. 
Post Mortem Appearances.-On post mortem examina- 
tion evidences of fatty degeneration are present rather 
generally. 
Treatment.-Treatment of the chronic type of poisoning 
consists of preventing ingestion of these substances and 
measures to hasten elimination. For acute poisoning 
BORIC ACID AND BORAX MISCELLANEOUS ORGANIC POISONS 
253 
lavage of the stomach, catharsis, and stimulants are 
advocated. 
References 
Tunnicliffe and Rosenheim: J. Hygiene, 1901, 1, p. 168. 
Wiley: U. S. Bur. Chern. Circular, 13, 1904. 
SALICYLIC ACID 
Salicylic acid exists in combination in the volatile oils 
of birch and wintergreen and possesses about the same anti- 
septic powers as benzoic acid and phenol. It is irritant 
to mucous membranes and in strong solution effects 
destruction of the skin. It possesses a biting taste and 
distinctly retards gastric digestion. It is rapidly absorbed 
from the intestines and has analgesic properties resembling 
acetanilid in this respect. Rapidly excreted by all the 
secretions but principally through the urine it leaves the 
body mainly as the salicyluric acid, a compound of salicylic 
acid and glycocoll. In large doses the urine may give a 
green color. 
The toxic effects of salicylic acid, aside from the local 
irritant action are characteristic of salicylates, which see. 
BENZOIC ACID AND BENZOATES 
Benzoic acid occurs in the balsams, in cranberries, and in 
various vegetables and fruits. The free acid even in con- 
centrations as low as 0.1 is distinctly irritant whereas the 
salts are not. The toxicity of benzoic acid is low due 
probably to its being transformed in the organism to hip- 
puric acid by union with glycocoll. 
Investigations by various Governmental commissions 
have led to the conclusion that the presence of small 
quantities of benzoate in food is without evidence of harm- 
fulness although in larger doses the conclusions do not 254 
TOXICOLOGY 
appear to be concordant. It is quite apparent that 
benzoate in food as ordinarily preserved may be taken by 
normal individuals without serious detriment. With 
patients with gastro-intestinal or kidney lesions the inher- 
ent irritant properties of the acid may prove deleterious. 
Symptoms.-In sufficient doses benzoic acid and its 
salts exhibits symptoms of toxicity strikingly similar to 
those of phenol poisoning. There is gastric irritation, 
nausea and vomiting. The respiration is dyspnoeic in 
character, the reflexes are diminished, and either coma or 
convulsions may ensue. 
Treatment.-Treatment consists of evacuation and 
lavage of the stomach and stimulants. 
References 
Chittenden, Long and Herter: Report 88, U. S. Department of 
Agriculture. 
Wiley: Report 84, Ibid. 
SACCHARIN 
Saccharin, or benzosulphinid, has an intense sweet 
taste, even in greatly diluted solution. It passes through 
the body practically unchanged within a period of 24 
hours almost all being eliminated by the kidneys. It 
has a sweetness about 500 times that of sugar and has 
been extensively employed to give a sweet taste to the 
food of diabetics and as an adulterant of sweet foods. 
Although the older literature reveals reports of various 
digestive and other disorders following the use of saccharin 
later work has all tended to demonstrate its low toxicity 
although even here large doses tend to produce minor 
derangements. Distinctly poisonous effects in man are 
unknown. 
Reference 
Herter and Folin: Report 94, U. S. Department of Agriculture. MISCELLANEOUS ORGANIC POISONS 
255 
FORMALDEHYDE 
Formaldehyde at times has been employed as a food 
preservative especially of milk, but its characteristic 
irritant properties renders its employment in this connec- 
tion extremely dangerous. When large doses have been 
swallowed there is immediate agonizing abdominal pain, 
loss of consciousness and general collapse. Death usually 
occurs within 48 hours. Post mortem examination reveals 
acute and extensive gastritis. When death does not 
occur the urine may be suppressed for 24 hours and usually 
when secretion is resumed the urine contains blood, 
albumin and casts. Sometimes there is diarrhoea. (See 
also p. 207.) 
Formaldehyde is probably oxidized to formic acid, a 
part of which may appear in the urine. 
References 
MacLachlan: Cleveland Med. J., 1909, 8, p. 606. 
Wiley: U. S. Bureau of Chemistry Circular, 42, 1908. 
Tunnicliffe and Rosenheim: J. of Hygiene, 1901, 1, p. 321. 
SULPHITES 
By the term sulphites is meant sulphurous acid, sodium 
sulphite and sodium thiosulphite. The substances are 
strongly reactive and readily combine with oxygen to form 
sulphates which tends to render harmless their native 
toxicity. Even in large quantities this transformation 
into sulphates prevents a general systemic intoxication, 
their employment in food being associated with deleterious 
action because of local irritant properties through the 
liberation of sulphuric acid. 
Symptoms.-Systemic effects are in evidence only when 
quantities sufficient to overwhelm the oxidative capacity of 
the body have been ingested. Under these circumstances 256 
TOXICOLOGY 
blood pressure is lowered, there is central nervous depres- 
sion and depression of the musculature of the heart and 
arteries. At times violent colic and diarrhoea may be 
observed. Death results from paralysis of the respiratory 
centre. 
Treatment.-Treatment consists in evacuation of the 
gastro-intestinal tract by lavage and catharsis and general 
stimulation. 
NITRATES 
Potassium nitrate, or Saltpeter, has been and still 
is extensively employed in the preservation of meats. In 
general it acts like other neutral salts although it probably 
is distinctly more irritant to the stomach and intestine. 
Readily absorbed it is chiefly eliminated by the urine and 
has diuretic properties. 
Symptoms.-With large doses the characteristic symp- 
toms include severe abdominal pain, vomiting and 
at times bloody stools. The pulse becomes irregular, 
convulsions occur and collapse ensues. The urine may be 
entirely suppressed or if passed may contain albumin and 
blood. Death may result from the gastro-intestinal 
disturbances provoked by the salt action. 
Treatment.-Potassium nitrate poisoning should be 
treated by administration of large volumes of water and 
by gastric lavage. To allay the irritation of the gastro- 
intestinal tract milk, eggs, etc., should be given. * 
COPPER 
Copper in food is employed mainly for the purpose of 
giving a green color to peas and beans. It combines with 
the chlorophyll of young vegetables to form a stable com- 
pound but with older vegetables the combination is not so 
firm. Consequently in the ingestion of these colored foods 
more copper gains entrance into the tissues when the older MISCELLANEOUS ORGANIC POISONS 
257 
vegetables are eaten than when the young peas and beans 
colored with copper are taken. Even though the maximum 
quantities of the latter are eaten distinct toxic symptoms 
are not in evidence. With large quantities of old 
vegetables colored with copper gastro-intestinal dis- 
turbances may occur. 
Symptoms.-The symptoms of poisoning are associated 
with the gastro-intestinal tract since copper is irritant 
and causes vomiting, diarrhoea, and pain. Lesions in the 
kidney and spleen are characteristic. 
Treatment.-Treatment of copper poisoning consists in 
the prompt administration of precipitants as white of egg, 
milk or acacia, with thorough lavage of the stomach, and 
stimulants if indicated. 
Reference 
Long: Preservatives, Trans. Internat. Congress of Hygiene, 1912. 
MUSHROOM POISONING 
Mushroom poisoning has been well recognized from 
ancient times. Certain varieties of mushrooms are edible, 
others are toxic at certain seasons of the year and still 
others always possess poisonous properties. The toxic 
properties of these fungi may perhaps be modified by 
climate since reports concerning the toxicity of various 
species vary in some degree, at least, according to the 
locality in which they have grown. In Italy and Hungary 
certain mushrooms are eaten which are regarded as poison- 
ous in England, and the same holds true for others eaten 
in Russia and France. Some mushrooms are more toxic 
to certain individuals than to others, so that it is quite 
likely that idiosyncrasy may play a part in the severity 
of the effects produced. 
Although the number of mushrooms considered capable 
of causing toxic symptoms is large most attention has 258 
TOXICOLOGY 
been directed to two species, namely, Amanita phalloides 
and Amanita muscaria or "fly mushroom." The fungus 
most often responsible is Amanita phalloides perhaps 
because of its widespread and abundant distribution and 
its pleasant taste. Moreover, it is perhaps possessed of 
greater toxicity than any other mushroom. In the United 
States it is popularly termed " toadstool." Because of the 
deadly character of the two species cited above consider- 
able attention has been devoted to their toxicology and 
the knowledge gained constitutes our definite knowledge 
of the nature of the toxic substances present in mushrooms. 
On the other hand, more than 70 species are capable of 
producing toxic symptoms in man. 
Amanita Phalloides. Symptoms.-Several hours usu- 
ally elapse before any symptoms appear. The first effects 
are great abdominal pain, vomiting, and diarrhoea. The 
vomitus and stools may contain blood. There may be 
periods when vomiting and pain may cease. These 
intervals are usually brief. The suffering is intense and 
rapidly leads to loss of strength. The period of intoxica- 
tion may last in adults for six or eight days, in children for 
a shorter period, and during this time a variety of symp- 
toms may develop. Especially important is the partial 
or complete suppression of urine due to acute nephritis. 
There may be jaundice, cyanosis and lowered temperature. 
Death is usually preceded by deep coma. 
An influence upon the nervous system may also be 
observed as indicated by convulsions and delirium in some 
cases. In some instances death occurs rapidly-within 
24 hours. 
If recovery occurs health is regained very slowly. In 
rare cases a chronic poisoning may result, death being 
delayed for several weeks. MISCELLANEOUS ORGANIC POISONS 
259 
Post Mortem Appearances.-Autopsy shows that 
amanita phalloides contains a poison which causes an 
extensive disintegration of cells, especially the endothelial 
cells of the blood vessels, renal cells, cells of the liver and 
central nervous system. The liver and kidney show 
extensive fatty degeneration. In general when large 
quantities of the poison have been ingested the cellular 
destruction is so widespread as to render impossible con- 
tinued functional activity of the organism as a whole and 
death results. This destruction of cells once established is 
so great as to render treatment of little use. 
The Poison of Amanita Phalloides.-The active princi- 
ple of Amanita phalloides has been isolated and is prob- 
ably closely related to indole. It partakes of the nature 
of an amine and contains C, H, N, and S. When injected 
into animals the lesions produced closely resemble those 
induced in man by ingestion of the fungus. 
Amanita Muscaria. Symptoms.-Poisoning by amanita 
muscaria may be readily diagnosed because of the charac- 
teristic symptoms. Soon after eating the mushrooms 
there is salivation, perspiration and weeping together with 
violent gastro-intestinal disturbances as indicated by 
vomiting, watery stools, and great thirst. There is a 
slow, irregular pulse, rapid respiration with dyspnoea. 
An influence upon the nervous system becomes apparent. 
In some cases there are present the symptoms charac- 
teristic of alcoholic intoxication, or there may be merely 
mental confusion and dizziness. In other cases the ner- 
vous effects may be so great as to lead to delirium, convul- 
sions, profound coma, and eventually death from respiratory 
paralysis. In still other cases after the preliminary 
exhibition of gastro-intestinal upset sleep overtakes the 
patient from which he awakes after several hours, greatly 
weakened but out of danger. The pupils of the eye are 260 
TOXICOLOGY 
usually contracted and do not respond to light. This fact 
is of importance in diagnosis. 
Post Mortem Appearances.-Beyond the fact that the 
alimentary tract shows great congestion with hemorrhages, 
little is known concerning changes in man induced by the 
active principle of amanita muscaria. Certain it is that 
this poison does not lead to widespread degeneration so 
typical of Amanita phalloides. 
The Poison of Amanita Muscaria.-It has been assumed 
for many years that the active principle of Amanita 
muscaria is muscarine, a base stronger than ammonia and 
closely related to choline. 
Choline 
Muscarine 
Its chief action is the production of typical peripheral 
stimulation of the parasympathetic system. It provokes 
the characteristic pilocarpine reactions and in addition 
possesses a nicotine and curare effect. Muscarine and 
atropine are antagonistic, atropine depressing the nerves 
stimulated by muscarine, in particular the inhibitory 
nerve endings of the vagus. Muscarine paralyzes the 
heart and respiration by stimulating the inhibitory fibres 
of the vagus-atropine depresses these fibers and is there- 
fore a physiological antidote for muscarine. 
Classification of Mushroom Poisoning.-Although the 
symptoms of poisoning characteristic of Amanita phal- 
loides and Amanita muscaria have been presented in some 
detail other symptoms are at times observed by ingestion 
of different mushrooms which may be quite dissimilar to 
those described. The classification most widely adopted 
is that of Huseman who recognized three types. Mush- 
room poisoning was designated by him by the term myce- MISCELLANEOUS ORGANIC POISONS 
261 
tismus. According to Huseman the three forms were 
mycetismus intestinalis, mycetismus choleriformis and 
mycetismus cerebralis-the terms being sufficiently 
descriptive. More recently Ford has modified and 
extended this classification so that five types are 
recognized. 
FORD'S CLASSIFICATION OF SYMPTOMS 
i. Mycetismus Gastro-mtestinalis.-The symptoms are 
mainly gastro-intestinal and are short lived. Death 
is only infrequent. The symptoms are characteristic of 
the Boleti, certain of the Entolomas, Lactarii znALepiotas. 
2. Mycetismus Choleriformis.-Gastro-intestinal dis- 
turbances are prominent at first. Later the characteristic 
features are weakness, pain, nephritis, anuria, delirium 
and coma. Death occurs in nearly 50 per cent of cases. 
This type of poisoning is produced by A manita phalloides 
and closely related species. 
3. Mycetismus Nervosus.-Initial gastro-intestinal dis- 
turbances accompanied by excessive perspiration, 
salivation and by lachrymation. Later there may be 
delirium, mental confusion, convulsions and coma. Death 
is unusual but may occur. The muscarine-containing 
fungi are responsible for this group of symptoms- 
especially Amanita muscaria, the Inocybes and the 
Clitocybes. 
4. Mycetismus Sanguinareus.-Gastro-intestinal 
symptoms are prominent at first. Jaundice and anemia 
develop later. The urine may contain hemoglobin from 
hemolysis of the red cells. The symptoms are character- 
istic of the fungus Helvetia esculenta. 
5. Mycetismus Cerebralis.-Only temporary excite- 
ment and hallucinations are characteristic. There is 262 
TOXICOLOGY 
dilatation of the pupils and collapse may result. The 
patient generally recovers. Only two fungi are known 
definitely to produce the effects, namely, Panceolus 
campanulalus and Panceolus papilionaceous. 
Treatment of Mushroom Poisoning.-In order that the 
best type of treatment be instituted it is very desirable to 
learn the nature of the mushroom taken. This may, 
perhaps, be learned from descriptions of the fungus by 
the patient or better by examination of the vomited 
material. Such identification, however, may be impossi- 
ble and no time should be lost in applying treatment 
irrespective of the type of mushroom eaten. Even though 
vomiting and diarrhoea may be present the gastro-intes- 
tinal canal should be cleaned out by gastric lavage and if 
possible by saline purgatives. If these are not retained 
high enemas may be given. The possibility exists that 
amanita muscaria may be the cause of the symptoms and 
atropine should be administered even though this hypo- 
thesis fails to be substantiated. Atropine will do no harm 
and if muscaria has been eaten it will act as a physiological 
antidote. Other general measures to employ, especially 
with symptoms of collapse, are stimulants as strychnine, 
digitalis, application of heat, and large volumes of fluid. 
If it is known that Amanita phalloides is responsible 
for the symptoms there is nothing specific that can be 
done. The measures outlined above for general treatment 
are applicable here and in line with the best type of 
treatment. 
If amanita muscaria is the cause of the symptoms 
atropine is the specific antidote. It should be given 
repeatedly hypodermically or even intravenously. The 
collapse should be combatted by strychnine and digitalis. 
Large volumes of fluid are especially recommended. MISCELLANEOUS ORGANIC POISONS 
263 
References 
Clark, Marshall and Rowntree: J.A.M.A., 1915, 64, p. 1230. 
Ford: In Peterson, Haines and Webster: Toxicology, 1923, 2, 
p. 817. 
Schlesinger and Ford: J. Biol. Chem., 1907, 3, p. 279. 
Ford: J. Inf. Diseases, 1908, 5, p. 116. 
Ford: J. Inf. Diseases, 1906, 3, p. 191. 
Ford: J. Pharm. and Exp. Therap., 1911, 6, p. 195. 
Krieger: National Geographic Magazine, 1920, 37, p. 387. INDEX 
Acetaldehyde, 209 
Acetanilid, 182 
fatal dose of, 183 
poisoning, fatal period of, 183 
post mortem appearances of, 183 
symptoms of, 183 
treatment of, 183 
Acetate, lead, 74 
fatal dose of, 77 
thallium, 106 
Acetic acid, 236 
fatal dose of, 237 
poisoning, post mortem appearances of, 237 
symptoms of, 236 
treatment of, 237 
Acetoarsenite of copper, 88 and 92 
Acetone, 194 
Acetphenetidin, 184 
fatal dose of, 184 
poisoning, fatal period of, 185 
post mortem appearances of, 185 
symptoms of, 184 
treatment of, 185 
Acetylene, 51 
poisoning, symptoms of, 51 
treatment of, 51 
Acid, acetic, 236 
arsenic, 92 
arsenious, 92 
benzoic, 253 
boric, 252 
cantharidic, 234 
carbolic, 169 
chromic, 105 
ethyl sulphonic, 218 
filicic, 231 
formic, 195 and 208 
hydrochloric, 27 
265 266 
INDEX 
Acid, hydrocyanic, 44 
muconic, 164 
muriatic, 27 
nitric, 25 
of sugar, 237 
oxalic, 237 
picramic, 240 
picric, 240 
prussic, 44 
pyrogallic, 174 
salicylic, 253 
santonic, 229 
selenic, 74 
sulphuric, 23 
sulphurous, 255 
tartaric, 242 
telluric, 72 
tellurous, 72 
Acids, corrosive, 22 
Aconitine, 142 
fatal dose of, 143 
poisoning, fatal period of, 143 
post mortem appearances of, 144 
symptoms of, 143 
treatment of, 144 
Aconitum, alkaloids of, 142 
Alcohol, amyl, 197 
allyl, 194 
ethyl, 189 
isoamyl, 197 
methyl, 193 
poisoning, fatal period of, 192 
post mortem appearances of, 193 
symptoms of, 191 
treatment of, 193 
wood, 193 
Alcohols, 189 
Alkalies, caustic, poisoning by, 30 
corrosive, 29 
Alkaloid, definition of, 121 
Alkaloidal poisons, 121 
reagents, 121 
Alkaloids of atropine, 144 
nux vomica, 138 
opium, 128 INDEX 
267 
Alkaloids of tobacco, 124 
veratrum, 146 
properties of, 121 
Allyl alcohol, 194 
Aluminum, 115 
poisoning, 115 
symptoms of, 115 
Alums, 115 
Alypine, 157 
Amanita muscaria, poison of, 260 
poisoning, post mortem appearances of, 260 
symptoms of, 259 
treatment of, 262 
phalloides, poison of, 259 
poisoning, post mortem appearances of, 259 
symptoms of, 258 
treatment of, 262 
Ammonia, 31 
fatal dose of, 31 
poisoning, post mortem appearances of, 32 
symptoms of, 31 
treatment of, 32 
Ammoniated mercury, 81 
Amygdalin, 44 
Amyl alcohol, 197 
fatal dose of, 198 
poisoning, symptoms of, 198 
Amyl nitrite, 212 
fatal dose of, 213 
Aniline, 179 
fatal dose of, 181 
poisoning, fatal period of, 181 
post mortem appearances of, 181 
symptoms of, 180 
treatment of, 181 
Annatto, 251 
Antidote, arsenic, 97 
definition of, 16 
for first aid, 19 
for specific poisons, 17 
Antimony, 101 
butter of, 101 
fatal dose of, 102 
poisoning, fatal period of, 102 
post mortem appearances of, 102 268 
INDEX 
Antimony, poisoning, symptoms of, ioi 
treatment of, 103 
poisonous action of, 102 
tartrated, 101 
Antipyrin, 185 
fatal dose of, 186 
poisoning, fatal period of, 186 
post mortem appearances of, 186 
symptoms of, 185 
treatment of, 186 
Apomorphine, 137 
fatal dose of, 138 
poisoning, symptoms of, 137 
Argentum, 79 
Argyrism, 79 
Arsenic, 92 
acid, 92 
antidote, 97 
fatal dose of, 94 
poisoning, acute, 93 
chronic, 95 
nervous form, 94 
pathology of, 97 
symptoms of, 93, 94, 95 
treatment of, 97 
trioxide, 92 
white, 92 
Arsenious acid, 92 
oxide, 92 
Arsenite of copper, 92 
Arseniureted hydrogen, 54 
fatal dose of, 54 
poisoning, fatal period of, 55 
post mortem appearances of, 54 
symptoms of, 54 
treatment of, 55 
Arsin, 54 
Arsphenamine, 93 
group, nitritoid reactions of, 98 
toxicity of, 98 
Ascaridole, 233 
Aspidium, 231 
Atoxyl, 93 
Atropine, 144 
alkaloids, 144 INDEX 
269 
Atropine, fatal dose of, 146 
poisoning, fatal period of, 146 
post mortem appearances of, 146 
symptoms of, 145 
treatment of, 146 
Barbital, 221 
fatal dose of, 222 
poisoning, fatal period of, 223 
post mortem appearances of, 223 
symptoms of, 222 
treatment of, 223 
Barium, 113 
fatal dose of, 114 
poisoning, fatal period of, 114 
post mortem appearances of, 114 
symptoms of, 113 
treatment of, 114 
Belladonna, 144 
Benzene, 164 
Benzine, 164 
Benzoate, in food, 253 
Benzoic acid, 253 
poisoning, symptoms of, 254 
treatment of, 254 
Benzol, 164 
fatal dose of, 165 
poisoning, post mortem appearances of, 165 
symptoms of, 164, 165 
treatment of, 166 
Benzosulphinid, 254 
Bird poison, 216 
Bismuth, 90 
poisoning, post mortem appearances of, 91 
symptoms of, 90 
treatment of, 91 
Black damp, 47 
wash, 81 
Blood poisons, 3 
Blue line, lead, 76 
mass, 81 
ointment, 81 
pill, 81 
vitriol, 88 
Boleti, 261 INDEX 
270 
Borax, 252 
Boric acid, 252 
poisoning, post mortem appearances of, 252 
symptoms of, 252 
treatment of, 252 
Botulism, 248 
diagnosis of, 249 
post mortem appearances of, 250 
symptoms of, 248 
treatment of, 250 
Bromides, 69 
Bromine, 69 
fatal dose of, 69 
poisoning, symptoms of, 70 
treatment of, 70 
Bromism, 70 
Brucine, 138 
poisoning, 138 
Butter of antimony, 101 
Cacodylates, 93 
Cadmium, in 
fumes, in 
poisoning, in 
Calcium, 112 
poisoning, 112 
symptoms of, 113 
treatment of, 113 
Calomel, 81 
Camphor, 186 
fatal dose of, 187 
poisoning, fatal period of, 187 
post mortem appearances of, 187 
symptoms of, 187 
treatment of, 187 
Cantharides, 234 
Cantharidic acid, 234 
Cantharidin, 234 
poisoning, fatal period of, 235 
post mortem appearances of, 235 
symptoms of, 235 
treatment of, 235 
Carbinol, 193 
Carbolic acid, 169 
poisoning, 169 INDEX 
271 
Carbon dioxide, 47 
fatal dose of, 47 
poisoning, fatal period of, 48 
post mortem appearances of, 48 
symptoms of, 48 
treatment of, 48 
poisonous action of, 48 
Carbon disulphide, 203 
as solvent, 203 
fatal dose of, 204 
poisoning, fatal period of, 204 
post mortem appearances of, 204 
symptoms of, 203 
treatment of, 204 
Carbon monoxide, 36 
fatal dose of, 39 
poisoning, fatal period of, 52 
post mortem appearances of, 39 
symptoms of, 36 
treatment of, 39 
poisonous action of, 38 
Carbon tetrachloride, 210 
fatal dose of, 211 
poisoning, fatal period of, 211 
post mortem appearances of, 211 
symptoms of, 211 
treatment of, 211 
Cardiac poisons, 3 
Catechol, 164 
Caustic alkalies, 30 
fatal dose of, 30 
poisoning, fatal period of, 30 
post mortem appearances of, 30 
symptoms of, 30 
treatment of, 31 
lunar, 80 
Cedar, oil of, 227 
Cephaeline, 157 
Cevadine, 147 
Chenopodium, oil of, 233 
poisoning, fatal period of, 234 
post mortem appearances of, 234 
symptoms of, 233 
treatment of, 234 
Chloral, 205 272 
INDEX 
Chloral, fatal dose of, 206 
hydrate, 205 
poisoning, fatal period of, 207 
post mortem appearances of, 207 
symptoms of, 206 
treatment of, 207 
Chlorine, 55 
poisoning, post mortem appearances of, 57 
symptoms of, 59 
treatment of, 63 
poisonous action of, 60 
Chloroform, 200 
fatal dose of, 202 
poisoning, delayed, 201 
post mortem appearances of, 202 
symptoms of, 200 
treatment of, 202 
Chloromercurphlorescin, 82 
Chlorpicrin, 56 
poisoning, post mortem appearances of, 58 
symptoms of, 59 
treatment of, 63 
Choke damp, 47 
Choline, 260 
Chromic acid, 105 
Chromium, 104 
fatal dose of, 106 
poisoning, fatal period of, 106 
post mortem appearances of, 106 
symptoms of, 105 
treatment of, 106 
poisonous action of, 105 
Citrate poisoning, symptoms of, 243 
Citrates, 242 
Citron ointment, 81 
Classification of mushroom poisoning, 260 
poisons, 2 
Clitocybes, 261 
Cocaine, 153 
fatal dose of, 155 
poisoning, fatal period of, 155 
post mortem appearances of, 155 
symptoms of, 154 
treatment of, 155 
substitutes, 155 INDEX 
273 
Codeine, 134 
fatal dose of, 135 
poisoning, symptoms of, 135 
treatment of, 135 
Colchicine, 152 
fatal dose of, 152 
poisoning, fatal period of, 152 
post mortem appearances of, 152 
symptoms of, 152 
treatment of, 152 
Colchicum, 152 
Colic, painter's, 75 
Colonial spirits, 193 
Columbian spirits, 193 
Coniine, 122 
fatal dose of, 123 
poisoning, fatal period of, 123 
post mortem appearances of, 123 
symptoms of, 123 
treatment of, 123 
poisonous action of, 123 
Conium, 122 
Convulsants, 5 
Copaiba, 225 
Copper, 87 
acetoarsenite, 88 
arsenite, 92 
fatal dose of, 89 
in food, 88, 256 
poisoning, acute, fatal period of, 89 
post mortem appearances of, 89 
symptoms of, 88, 257 
treatment of, 89, 257 
chronic, symptoms of, 89 
poisonous action of, 88 
Corrosive acids, 22 
alkalies, 29 
sublimate, 81 
Corrosives, 3 
Creosote, 175 
poisoning, symptoms of, 176 
treatment of, 176 
Cresol, 173 
poisoning, symptoms of, 174 
treatment of, 174 INDEX 
274 
Croton oil, 228 
poisoning, fatal period of, 229 
post mortem appearances of, 229 
symptoms of, 228 
treatment of, 229 
tiglium, 228 
Cubeb, 225 
Delayed chloroform poisoning, 201 
symptoms of, 201 
Diagnosis of poisoning, 12 
Digitalein, 214 
Digitaligenin, 214 
Digitalin, 214 
Digitalis, 213 
fatal dose of, 215 
poisoning, fatal period of, 215 
post mortem appearances of, 216 
symptoms of, 215 
treatment of, 216 
Digitalose, 214 
Digitonin, 214 
Digitoxigenin, 214 
Digitoxin, 213 
Dimethylacetate, 194 
Diphosgene, 56 
Disease and poisons, 8 
Donovan's solution, 93 
Dyes, poisoning from food, 251 
Eagle, spirits, 193 
Eczema arsenicale, 95 
Emetine, 157 
Emulsin, 44 
Enanthic ethers, 190 
Entolomas, 261 
Epinephrine, 161 
fatal dose of, 162 
poisoning, fatal period of, 162 
post mortem appearances of, 162 
symptoms of, 162 
treatment of, 162 
Ergot, 158 
fatal dose of, 160 
poisoning, fatal period of, 160 INDEX 
275 
Ergot, poisoning, post mortem appearances of, 161 
symptoms of, 160 
treatment of, 161 
Ergotine, 159 
Ergotism, 160 
Ergotoxine, 159 
Eserine, 148 
Essence of mirbane, 166 
Ethanol, 190 
Ether, 198 
fatal dose of, 199 
poisoning, fatal period of, 199 
post mortem appearances of, 199 
symptoms of, 198 
treatment of, 200 
Ethers, enanthic, 190 
Ethyl alcohol, 189 
Ethyl nitrite, 211 
sulphonic acid, 218 
Ethylene, 53 
toxicity of, 53 
Ethylmethylketone, 194 
Eucaine, 156 
Fate of poisons, 8 
Fern, male, 231 
Ferrum, 107 
Filicic acid, 231 
First aid antidotes, 19 
Fish poison, 216 
Flakewhite, 75 
Flavaspidin, 231 
Food poisoning, 245 
by botulinus, 248 
by paratyphoid, 247 
Foods, copper in, 88 
Formaldehyde, 207 
fatal dose of, 208 
in food, 255 
poisoning, fatal period of, 209 
post mortem appearances of, 209 
symptoms of, 208 
treatment of, 209 
Formalin, 208 
Formic acid, 195, 208 276 
INDEX 
Fowler's solution, 93 
Foxglove, 213 
Fumes, cadmium, nr 
gasoline, 52 
vanadium, 117 
zinc, 109 
Furfural, 194 
Fusel oil, 190, 197 
Gas, mustard, 55 
Gases, poisonous, 36 
war, 36, 55 
Gasoline fumes, 52 
toxicity of, 52 
Gelsemine, 162 
Gelseminine, 162 
Gelsemium, 162 
alkaloids of, 162 
fatal dose of, 163 
poisoning, fatal period of, 163 
post mortem appearances of, 163 
symptoms of, 163 
treatment of, 163 
Green vitriol, 107 
Guaiacol, 175 
Habit and poisons, 6 
Helvella esculenta, 261 
Hematoporphyrin, 219, 220, 222 
Hemlock, poison, 122 
water, 217 
Heptane, 164 
Heroine, 135 
fatal dose of, 136 
poisoning, fatal period of, 136 
post mortem appearances of, 136 
symptoms of, 136 
treatment of, 136 
Hexamethylenamine, 208 
Hexane, 164 
Histamine, 159 
Hydrargyrum, 80 
Hydrochloric acid, 27 
fatal dose of, 27 
poisoning, fatal period of, 27 INDEX 
277 
Hydrochloric acid poisoning, post mortem appearances of, 27 
symptoms of, 27 
treatment of, 28 
Hydrocyanic acid, 44 
fatal dose of, 45 
poisoning, fatal period of, 45 
post mortem appearances of, 46 
symptoms of, 44 
treatment of, 46 
poisonous action of, 45 
Hydrogen, arseniureted, 54 
phosphoretted, 55 
sulphide, 41 
fatal dose of, 43 
poisoning, fatal period of, 43 
post mortem appearances of, 43 
symptoms of, 41 
treatment of, 43 
poisonous action of, 42 
telluride, 72 
Hydroquinone, 170 
Hyoscyamine, 144 
Idiosyncracy and poisons, 6 
Inocybes, 261 
Inorganic poisons, 22 
Iodide poisoning, symptoms of, 66 
treatment of, 67 
potassium mercuric, 81 
Iodides, 65 
Iodine, 64 
fatal dose of, 65 
poisoning, fatal period of, 65 
post mortem appearances of, 65 
symptoms of, 64 
treatment of, 65 
lodism, 66 
Iodoform, 67 
poisoning, fatal period of, 68 
post mortem appearances of, 68 
symptoms of, 67 
treatment of, 68 
Ipecac, 157 
fatal dose of, 158 
poisoning, fatal period of, 158 278 
INDEX 
Ipecac poisoning, post mortem appearances of, 158 
symptoms of, 158 
treatment of, 158 
Iron, 107 
fatal dose of, 108 
poisoning, fatal period of, 108 
post mortem appearances of, 108 
symptoms of, 107 
treatment of, 108 
poisonous action of, 108 
Irritant poisons, 32 
Irritants, 3 
Iso-amyl alcohol, 197 
Jaborandi, 149 
Jasmine, 162 
Knock-out drops, 205, 216 
Lactarii, 261 
Lead, 74, 106 
acetate, 74 
fatal dose of, 77 
blue line, 76 
carbonate, 74 
chromate, 105 
line, from bismuth, 91 
poisoning, acute, 75 
chronic, 77 
fatal period of, 77 
post mortem appearances of, 77, 78 
symptoms of, 75, 77 
treatment of, 77, 79 
sugar of, 74 
sulphate, 74 
white, 74 
Lemons, salt of, 237 
Lepiotas, 261 
Lion d'Or, 193 
Lithium, 114 
poisoning, symptoms of, 114 
Luminal, 223 
poisoning, symptoms of, 224 
Lunar caustic, 80 INDEX 
279 
Magnesium, in 
poisoning, symptoms of, 112 
treatment of, 112 
Male fern, 231 
Manganese, 119 
in food, 119 
poisoning, post mortem appearances of, 120 
symptoms of, 119 
treatment of, 120 
Mercuro-chrome, 81 
Mercurophen, 81 
Mercury, 80 
salicylate, 81 
salts, as protoplasmic poisons, 81 
poisoning, acute, 84 
fatal period of, 84 
post mortem appearances of, 84 
treatment of, 84 
chronic, 86 
treatment of, 87 
stomatitis, treatment of, 84 
Metallic poisons, 72 
Methanol, 193 
Methyl acetate, 194 
alcohol, 193 
fatal dose of, 196 
poisoning, fatal period of, 196 
post mortem appearances of, 196 
symptoms of, 195 
treatment of, 196 
hydrate, 193 
selenium, 74 ' 
Mineral white, 75 
Mirbane, essence of, 166 
Miscellaneous organic poisons, 164 
Monkshood, 142 
Morphine, 130 
fatal dose of, 133 
poisoning, fatal period of, 133 
post mortem appearances of, 134 
symptoms of, 130 
treatment of, 134 
Muconic acid, 164 
Muriatic acid, 27 
Muscarine, 260 280 
INDEX 
Mushroom poisoning, 257 
classification of symptoms, 261 
symptoms of, 261 
treatment of, 262 
Mustard gas, 56 
burns, 58 
treatment of, 63 
poisoning, post mortem appearances of, 58 
symptoms of, 60 
treatment of, 63 
Mycetismus, 260 
classification of symptoms, 261 
Naphthol, 224 
poisoning, fatal period of, 225 
post mortem appearances of, 225 
symptoms of, 224 
treatment of, 225 
Neoarsphenamine, 93 
Nerve poisons, 3 
Nicotine, 124 
fatal dose of, 125 
poisoning, fatal period of, 126 
post mortem appearances of, 126 
symptoms of, 124 
treatment of, 126 
poisonous action of, 125 
Niter, sweet spirits of, 212 
Nitrate, of silver, 80 
poisoning, symptoms of, 256 
treatment of, 256 
Nitrates, in food, 256 
Nitric acid, 25 
fatal dose of, 26 
poisoning, fatal period of, 26 
post mortem appearances of, 26 
symptoms of, 26 
treatment of, 26 
oxide, 49 
poisoning, fatal period of, 49 
poisonous action of, 49 
post mortem appearances of, 49 
symptoms of, 49 
treatment of, 50 
Nitrite poisoning, fatal period of, 213 INDEX 
281 
Nitrite poisoning, post mortem appearances of, 213 
symptoms of, 212 
treatment of, 213 
Nitrites, 211 
Nitritoid reactions, symptoms of, 99, 100 
treatment of, 99 
Nitrobenzene, 166 
Nitrobenzol, 166 
fatal dose of, 168 
physiological action of, 168 
poisoning, fatal period of, 168 
post mortem appearances of, 169 
symptoms of, 167 
treatment of, 169 
Nitroglycerine, 212 
fatal dose of, 212 
Nitrous oxide, 50 
poisoning, post mortem appearances of, 50 
symptoms of, 50 
treatment of, 50 
Novocaine, 156 
Nux vomica, 138 
poisoning, symptoms of, 139 
treatment of, 141 
Oil, croton, 228 
of cedar, 227 
fatal dose of, 227 
poisoning, fatal period of, 228 
post mortem appearances of, 228 
symptoms of, 227 
treatment of, 228 
of chenopodium, 233 
fatal dose of, 234 
fusel, 197 
of savin, 226 
fatal dose of, 226 
of vitriol, 23 
Opium, 128 
alkaloids of, 128 
fatal dose of, 133 
poisoning, fatal period of, 133 
post mortem appearances of, 134 
symptoms of, 130 
treatment of, 134 
Opium, 128 282 
INDEX 
Ordeal bean, 148 
Organic poisons, miscellaneous, 164 
Ou bain, 214 
Oxalic acid, 237 
fatal dose of, 238 
poisoning, fatal period of, 239 
post mortem appearances of, 239 
symptoms of, 238 
treatment of, 239 
Oxide, red mercuric, 81 
yellow mercuric, 81 
Painters colic, 75 
Palite, 56 
Panaeolus campanulatus, 262 
papilionaceous, 262 
Para-aminophenol, 182, 184 
Paraldehyde, 209 
fatal dose of, 210 
poisoning, fatal period of, 210 
post mortem appearances of, 210 
symptoms of, 209 
treatment of, 210 
Paratyphoid, 247 
food poisoning, symptoms of, 248 
treatment of, 248 
Paris green, 88, 92 
Pearl ash, 29 
Pearson's solution, 93 
Phenacetin, 184 
Phenanthrene, 121 
Phenol, 169 
as protoplasmic poison, 170 
fatal dose of, 172 
poisoning, fatal period of, 172 
post mortem appearances of, 172 
symptoms of, 171 
treatment of, 172 
Phloroglucin, 231 
Phosgene, 56 
poisoning, post mortem appearances of, 57 
symptoms of, 59 
treatment of, 63 
poisonous action of, 60 
Phosphine, 55 INDEX 
283 
Phospho retted hydrogen, 55 
poisoning, post mortem appearances of, 55 
symptoms of, 55 
Phosphorus, 32 
fatal dose of, 33 
poisoning, fatal period of, 34 
post mortem appearances of, 34 
symptoms of, 33 
treatment of, 35 
Physostigmine, 148 
fatal dose of, 149 
poisoning, fatal period of, 149 
post mortem appearances of, 149 
symptoms of, 149 
treatment of, 149 
Picramic acid, 240 
Picric acid, 240 
fatal dose of, 241 
poisoning, fatal period of, 241 
post mortem appearances of, 241 
symptoms of, 240 
treatment of, 242 
Picrotoxin, 216 
fatal dose of, 217 
poisoning, fatal period of, 218 
post mortem appearances of, 218 
symptoms of, 217 
treatment of, 218 
Pilocarpine, 149 
fatal dose of, 151 
poisoning, fatal period of, 151 
post mortem appearances of, 151 
symptoms of, 150 
treatment of, 151 
Pinene, 188 
Plumbum, 74 
Poison, bird or fish, 216 
definition of, 1 
hemlock, 122 
of amanita muscaria, 260 
amanita phalloides, 259 
Poisoning, by acetani id, 182 
acetic acid, 236 
acetphenetidin, 184 
aconitine, 142 284 
INDEX 
Poisoning, by aluminum, 115 
amanita muscaria, 259 
amanita phalloides, 258 
ammonia, 31 
amyl alcohol, 197 
aniline, 179 
antimony, 101 
antipyrin, 185 
apomorphine, 137 
arsenic, 92 
arseniuretted hydrogen, 54 
arsin, 54 
atropine, 144 
barbital, 221 
barium, 113 
benzol, 164 
bismuth, 90 
borax, 252 
boric acid, 252 
bromides, 69 
bromine, 69 
brucine, 138 
cadmium, in 
camphor, 186 
cantharidin, 234 
carbolic acid, 169 
carbon dioxide, 47 
disulphide, 203 
monoxide, 36 
caustic alkalies, 29 
chloral, 205 
chlorine, 55 
chloroform, 200 
chlorpicrin, 55 
chromium, 104 
cocaine, 153 
codeine, 135 
colchicine, 152 
coniine, 122 
copper, 87 
in food, 257 
creosote, 175 
cresol, 173 
croton oil, 228 
digitalis, 215 INDEX 
285 
Poisoning, by diphosgene, 56 
epinephrine, 161 
ergot, 158 
ether, 198 
ethyl alcohol, 189 
ethylene, 53 
food, 245 
dyes, 251 
preservatives, 251 
formaldehyde, 207 
in food, 255 
gasoline fumes, 52 
gelsemium, 162 
heroine, 135 
hydrochloric acid, 27 
hydrocyanic acid, 44 
hydrogen sulphide, 41 
iodides, 65 
iodine, 64 
iodoform, 67 
ipecac, 157 
iron, 107 
lead, 74 
lithium, 114 
luminal, 223 
magnesium, in 
male fern, 231 
manganese, 119 
mercury, 80 
methyl alcohol, 193 
morphine, 130 
mushrooms, 257 
mustard gas, 55 
naphthol, 224 
nicotine, 124 
nitrates in food, 256 
nitric oxide, 49 
nitrites, 211 
nitrobenzol, 166 
nitrous oxide, 50 
oil of cedar, 227 
chenopodium, 233 
savin, 226 
opium, 128 
oxalic acid, 237 286 
INDEX 
Poisoning, by palite, 56 
paraldehyde, 209 
phenacetin, 184 
phenol, 169 
phosgene, 55 
phosphine, 55 
phosphuretted hydrogen, 55 
physostigmine, 148 
picric acid, 240 
picrotoxin, 216 
pilocarpine, 149 
potassium permanganate, 119 
prussic acid, 44 
pyrogallol, 174 
saccharin in food, 254 
salicylic acid, 253 
santonin, 229 
selenium, 73 
silver, 79 
strychnine, 138 
sulphites in food, 255 
sulphonal, 218 
sulphur dioxide, 50 
sulphuric acid, 23 
superpalite, 56 
tartaric acid, 242 
thallium, 106 
thymol, 176 
tin, 103 
T.N.T., 177 
tobacco, 127 
trinitrotoluene, 177 
trional, 220 
turpentine, 188 
uranium, 117 
vanadium, 117 
veratrine, 146 
veronal, 221 
yperite, 56 
delayed chloroform, 201 
diagnosis of, 12 
symptomatic treatment for, 18 
treatment of, 14 
Poisonous gases, 36 
Poisons, alkaloidal, 121 INDEX 
287 
Poisons and disease, 8 
and habit, 6 
antidotes for, 16 
specific, 17 
blood, 3 
cardiac, 3 
classification, 2 
conditions modifying effects of, 3 
convulsants, 3 
fate of, 8 
idiosyncrasy to, 6 
inorganic, 22 
irritant, 3, 32 
metallic, 72 
miscellaneous organic, 164 
nerve, 3 
somnifacients, 3 
symptomatology of, 9 
tolerance to, 7 
Potash, poisoning by, 29 
Potassium chlorate, 28 
fatal dose of, 28 
poisoning, fatal period of, 29 
post mortem appearances of, 29 
symptoms of,. 28 
treatment of, 29 
chromate, 105 
mercuric iodide, 81 
permanganate poisoning, 119 
symptoms of, 119 
treatment of, 119 
Preservatives, poisoning from food, 251 
Procaine, 156 
Protoveratrine, 147 
Prussic acid, 44 
Ptomaine poisoning, 246 
Pyridine, 121 
Pyrochatechin, 170 
Pyrogallic acid, 174 
Pyrogallol, 174 
fatal dose of, 175 
poisoning, fatal period of, 175 
post mortem appearances of, 175 
symptoms of, 174 
treatment of, 175 288 
INDEX 
Quinol, 164 
Quinoline, 121 
Ratsbane, 92 
Red mercuric oxide, 81 
Rough on rats, 113 
Saccharin, 254 
in food, 254 
Salicylate, mercury, 81 
poisoning, post mortem appearances of, 244 
symptoms of, 244 
treatment of, 244 
Salicylates, 243 
toxic dose of, 244 
Salicylic acid, 253 
jag, 243 
Salicylism, 243 
Salt, of lemons, 237 
Saltpeter, 256 
Santonic acid, 229 
Santonin, 229 
fatal dose of, 230 
poisoning, fatal period of, 230 
post mortem appearances of, 231 
symptoms of, 230 
treatment of, 231 
Savin, oil of, 226 
poisoning, fatal period of, 227 
post mortem appearances of, 227 
symptoms of, 226 
treatment of, 227 
Scheele's green, 92 
Scopalamine, 144 
Selenic acid, 74 
Selenium, 73 
methyl, 74 
poisoning, symptoms of, 74 
Silver, 79 
arsphenamine, 93 
nitrate, 80 
fatal dose of, 80 
poisoning, fatal period of, 80 
post mortem appearances of, 80 
symptoms of, 80 
treatment of, 80 INDEX 
289 
Soda, poisoning by, 29 
Somnifacients, 3 
Spanish fly, 234 
Spelter's chills, 109 
Stannum, 103 
Stomatitis, mercury, 82 
treatment of, 84 
Stovaine, 156 
Stramomium, 144 
Strophanthins, 214 
Strychnine, 138 
fatal dose of, 141 
poisoning, fatal period of, 141 
post mortem appearances of, 141 
symptoms of, 139 
treatment of, 141 
Sugar, acid of, 237 
of lead, 74 
Sulphite poisoning, symptoms of, 255 
treatment of, 255 
Sulphites, in food, 255 
Sulphonal, 218 
fatal dose of, 219 
poisoning, fatal period of, 219 
post mortem appearances of, 219 
symptoms of, 219 
treatment of, 220 
Sulphur dioxide, 50 
poisoning, post mortem appearances of, 51 
poisonous action of, 51 
symptoms of, 50 
treatment of, 51 
Sulphuric acid, 23 
fatal dose of, 25 
local action of, 23 
treatment of local effects, 23 
poisoning, post mortem appearances of, 24 
symptoms of, 24 
treatment of, 25 
Sulphurous acid, 255 
Superpalite, 56 
Sweet spirits of nitre, 212 
Symptomatic treatment, 18 
Symptomatology of poisons, 9 INDEX 
290 
Tartaric acid, 242 
poisoning, 242 
Tartrated antimony, 101 
Tartro-bismuthate, 90 
Telluric acid, 72 
Telluride, hydrogen, 72 
Tellurium, 72 
fatal dose of, 73 
poisoning, fatal period of, 73 
in industry, 72 
post mortem appearances of, 73 
symptoms of, 73 
treatment of, 73 
poisonous action of, 73 
Tellurous acid, 72 
Thallium, 106 
acetate, 106 
poisoning, 106 
Thymol, 176 
poisoning, symptoms of, 176 
treatment of, 176 
Tin, 103 
fatal dose of, 104 
in foods, 103 
poisoning, fatal period of, 104 
post mortem appearances of, 104 
symptoms of, 104 
treatment of, 104 
poisonous action of, 104 
T.N.T., 177 
Tobacco, alkaloids of, 124 
analyses of, 127 
heart, 127 
poisoning, symptoms of, 127 
use of, 126 
Tolerance, 7 
Toluene, 164 
Toxicology, definition of, 1 
Treatment of poisoning, 14 
Trimethylphloroglucin, 231 
Trinitrotoluene, 177 
fatal dose of, 178 
poisoning, fatal period of, 178 
post mortem appearances of, 179 
symptoms of, 177 INDEX 
291 
Trinitrotoluene poisoning, treatment of, 179 
Trional, 220 
fatal dose of, 220 
poisoning, symptoms of, 220 
treatment of, 220 
Tropacocaine, 157 
Turpentine, 188 
fatal dose of, 189 
poisoning, fatal period of, 189 
post mortem appearances of, 189 
symptoms of, 189 
treatment of, 189 
Tyramine, 159 
Unguentum hydrargyri, 81 
Uranium, 105, 117 
acetate, 117 
nitrate, 117 
poisoning, symptoms of, 117 
Vanadium, 117 
fumes, 117 
poisoning, post mortem appearances of, 118 
symptoms of, 118 
treatment of, 118 
Vanadiumism, 117 
Veratrine, 146 
fatal dose of, 147 
poisoning, fatal period of, 148 
post mortem appearances of, 148 
symptoms of, 147 
treatment of, 148 
Veratrum, alkaloids of, 147 
viride, 147 
Verdigris, 88 
Veronal, 221 
Vitriol, green, 107 
oil of, 23 
War gas poisoning, post mortem appearances of, 57 
symptoms of, 59 
treatment of, 63 
gases, 36, 55 
poisonous action of, 60 
Water hemlock, 217 292 
INDEX 
White arsenic, 92 
lead, 74 
Wood alcohol, 193 
naphtha, 193 
spirit, 193 
Wormseed, 229, 233 
Wrist drop, 78 
Xylene, 164 
Yellow mercuric oxide, 81 
vision, 230 
Yperite, 56 
Zinc, 108 
fatal dose of, no 
fumes, 109 
in foods, 108 
poisoning, fatal period of, 110 
post mortem appearances of, no 
symptoms of, 109 
treatment of, no 
poisonous action of, no