It has been reported (100) that diabetic males who smoke have a 50%
greater incidence of clinically detectable arteriosclerosis obliterans in the
legs than those who do not smoke. In general, however, there is little
information about the relation of smoking to peripheral arteriosclerosis.
Most experienced clinicians advise patients with obliterative peripheral arte-
rial disease to stop smoking (45).

Buerger’s disease, or thromboangiitis obliterans, has been traditionally
associated with smoking, and the literature contains numerous clinical re-
ports describing the arrest of Buerger’s disease when smoking is stopped
and its reactivation on resumption of smoking. The existence of Buerger’s
disease as an entity separate from arteriosclerosis obliterans has been re-
cently challenged (101), but well defended (61).

It is apparent that much mcre work will have to be done to determine
what relationship may exist between non-coronary occlusive vascular dis-
ease, aneurysmal disease, and smoking.

CHARACTERISTICS OF CIGARETTE SMOKERS

If it could be shown that cigarette smokers and non-smokers had signifi-
cant constitutional differences apart from any differences that might be caused
by smoking itself, then a possibility would exist that some predisposition of
smokers to a particular disease might also be of constitutional origin and not
caused by smoking. Cigarette smokers have, in fact, been found to differ
as a group from non-smokers, but the differences, such as serum cholesterol
concentration and resting heart rate, could have resulted from the smoking
habit itself, so far as present knowledge indicates.

The concentration of serum cholesterol has been found to be slightly higher
in smokers than in non-smokers by a number of investigators (6, 18, 49, 63,
95), but others have found no relationship (1, 54). Dawber (19) found
not only that serum cholesterol was higher in smokers than in non-smokers
but also that it remained higher in those who stopped smoking.

Smokers tend to be leaner than non-smokers, but to gain when they stop
smoking (3, 18, 49).

A few personality differences have been reported between cigarette smokers
and non-smokers. Friedman’s type A men (the coronary type) tended to be
heavy smokers (33). Smokers are said to be more easily angered and to eat
more when under stress (94). They have been reported to marry oftener.
to change jobs more frequently. to be more often hospitalized, and to par-
ticipate more actively in sports than non-smokers (60).

Thomas (94, 95) has reported that the parents of medical students who
smoke have a significantly higher incidence of arteriosclerotic and hyper-
tensive cardiovascular disease than parents of non-smokers. Clearly. this
finding is open to more than cne interpretation.

Smokers tend to have a higher heart rate than non-smokers (3, 94).

The matter of constitutional predisposition to smoking has been inves-
tigated in twins. It has heen found (27, 28. 32) that the smoking habits of
monozygotic twins are significantly more alike than those of dizygotic twins.
even when members of a twin pair are brought up separately.

326
In spite of some bits of suggestive evidence the existence of basic consti-
tutional differences between smokers and non-smokers is not presently
established. The constitutional hypothesis, which links smoking and predis-
position to disease, is discussed in detail in Chapter 9, Cancer.

PSYCHO-SOCIAL FACTORS OF SMOKING IN RELATION TO
CARDIOVASCULAR DISEASE

Even less conclusve information is available on the role of psycho-social
factors of smoking in relation to cardiovascular disease. Studies which have
focussed on this are limited in number according to Heinzelmann (44). Even
fewer, he found, are those which have specifically examined the relative
weight of these variables or their interaction. Reviewing those available,
he observes that the evidence is highly fragmentary and uncertain. The
findings suggest that the relationship between smoking behavior and coronary
heart disease may reflect the influence of stress factors and/or personality
mechanisms. However, they permit no definitive statements with respect
to the relative role of pyscho-social factors and smoking in relation to
etiology of the disease.

SUMMARY

Smoking and nicotine administration cause acute cardiovascular effects
similar to those induced by stimulation of the autonomic nervous system,
but these effects do not account well for the observed association between
cigarette smoking and coronary disease. It is established that male ciga-
rette smokers have a higher death rate from coronary disease than non-
smoking males. The association of smoking with other cardiovascular
disorders is less well established. If cigarette smoking actually caused the
higher death rate from coronary disease, it would on this account be
responsible for many deaths of middle-aged and elderly males in the United
States. Other factors such as high blood pressure, high serum cholesterol,
and excessive obesity are also known to be associated with an unusually
high death rate from coronary disease. The causative role of these other
factors in coronary disease, though not proven, is suspected strongly enough
to be a major reason for taking countermeasures against them. It is also
more prudent to assume that the established association between ciga-
rette smoking and coronary disease has causative meaning than to suspend
judgment until no uncertainty remains.

CONCLUSION

Male cigarette smokers have a higher death date from coronary artery
disease than non-smoking males, but it is not clear that the association
has causal significance.

327
~I

10.

11.

12.

13.

14.

15.

16.

17.

18.

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Dawber, T, R., Moore, F. E., Mann, G. V, II. Coronary heart disease in
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Doll, R., Hill, A. B. Lung cancer and other causes of death in relation
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Dorn, H. F. Tobacco consumption and mortality from cancer and
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Doyle, J. T., Dawber, T. R., Kannel, W. B., Heslin, A. S., Kahn, H. A.
Cigaretie smoking and coronary heart disease. Combined experience
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331
Chapter 12

Other Conditions

714-429 06423
Contents

RELATIONSHIP OF PEPTIC ULCER TO TOBACCO USE .

Conclusion . . 2... ee ee ee ee ee ee
References . . 2. 20. ee eee ee ee ee

TOBACCO AMBLYOPIA...........0....0.4.

Conclusion . . 2 1. 1 we ee ee ee ee ee
References . 2... 1 1 6 eee ee te ee ee

SMOKING AND CIRRHOSIS OF THE LIVER ......

Conclusion... . 6. we ee ee ee ee ee
References . 2. 2 1 1 1 ee ee ee ee

MATERNAL SMOKING AND INFANT BIRTH WEIGHT .

Conclusions... WL ee ee ee
References . 2. 2. 1 0 cw ee ee ee ee ee

SMOKING AND ACCIDENTS ..............

Conclusion . 2. 1. 1 we ee ee ee
References . 2... ew ee ee ee ee ee ee

List of Tables

TaBLe 1. Summary of methods used in retrospective and cross-

sectional studies of peptic ulcer and smoking

Tassie 2. Summary of results of retrospective and cross-sectional
studies of peptic ulcer and smoking .......
TasLe 3. Expected and observed deaths and mortality ratios for
ulcer of stomach and duodenum among current
cigarette smokers, from seven prospective studies .

336

337

340
340

341
342
342
342
342
343
343

343
344

344

345
345

338

339

339
Chapter 12

 

 

 

RELATIONSHIP OF PEPTIC ULCER TO TOBACCO USE

There are five retrospective studies on the relationship of peptic (gastric
and duodenal) ulcer to smoking, in which data have been obtained about the
smoking habits of peptic ulcer patients and various kinds of control groups
(1, 2, 7, 14, 18). Also, in one cross-sectional study, the frequency of peptic
ulcer has been determined in a population of individuals with varying smoking
habits (11).

Tables 1 and 2 summarize the methods used and the results of these studies.
These studies demonstrate an association between cigarette smoking and
peptic ulcer which appears to be greater for gastric than for duodenal ulcers.
The proportion of non-smokers is higher among the controls than among the
ulcer patients in every one of these studies.

No differences were noted with respect to the frequency of heavy smokers
in the study of Doll (7) and no consistent relationship with amount smoked
was observed by Trowell (18).

In the cross-sectional study of Edwards, et al. (11), a larger proportion of
peptic ulcer cases was found among the cigarette smokers, and this proportion
increased with amount of cigarette smoking. The heavy cigarette smokers
had a frequency of peptic ulcer twice that of those who had never smoked
(12 percent as compared to 6 percent).

No association with pipe smoking was noted (1, 11. 14, 18).

In three prospective studies (Table 3) gastric ulcer has been classified
separately from duodenal ulcer. The mortality ratios of cigarette smokers
from gastric ulcer are high in all three studies (46/0, 5.1 and 4.3). For
duodenal ulcers the mortality ratios are more modest (2.2,2.3 and1.1). In
the remaining four prospective studies only the combined mortality ratios
for gastric and duodenal ulcers are available: their results being based on
small numbers of deaths, are erratic but their over-all average mortality
ratio is about the same as for the three large studies. Consequently. it ap-
pears likely that the excess mortality of cigarette smokers from peptic ulcer
can be attributed primarily to gastric ulcer. A breakdown by amount
smoked (Chapter 8, Table 23) shows no trend. For cigar and pipe smokers
the peptic ulcer mortality ratio (total over five studies) is 1.6 but in view
of the small number of deaths this elevation is not statistically significant.

Doll, et al., (7) conducted a clinical trial of the effect of stopping smoking
on the healing of gastric ulcers. The results were assessed by measuring
radiologically the reduction in the size of the ulcer niche. Patients advised
to stop smoking had an average 780 reduction in the size of the ulcer, com-
pared to 57% for those who continued to smoke. In view of the probable
existence of other factors which may have concomitantly been introduced
in the approach to the smokers. and the complex nature of the healing proc-
ess, it is difficult to interpret this ohservation.

337
BEE

Tasi_e L.—Summary of methods used in retrospective and cross-sectional studies of peptic ulcer and smoking

 

 

 

 

 

 

 

 

 

 

 

 

| Cases Controls
Investigator and) Year Country | Sexy oe ao a Collection of data
No. | Method of Selection No. Method of Selection

Barnett, (2) 1927 USA 'M 66 Gastric; 178 Patients admitted between 500 | Seleeted at random from the | 1. Retrospective review of
i Duodenal. 1913 and 1926. Only cascs general admissions males, records at Peter Bent

with complete smoking his- aged 20-60. Brigham Hospital.
tory selected. 2. Uleer diagnosis probably

well established.
Trowell, (18) 1934 England M 530 Duodenal | Not stated 400 | Selected at random from wards | 1. Interviewed by investigator.
of a general hospital. 2. Uleer diagnosis confirmed
by X-ray and/or surgery.

Mills, (14) 1950 U.S.A, M 55 Not stated 275 | Sample of population in | No details given.

Columbus, Ohio.

Allibone and Flint, (1) 1958 England M&F | 107 Consecutive admissions to hos-| 107 | Matched by age, sex, and | Patients and controls inter-
pital of patients with gastric time of admission from acute viewed by same observer.
and duodenal hemorrhage general surgical emergeney
or perforation. admissions.

Doll, Jones, and Pygott (7), | England M&F | 327 Gastric; 338 | Ulcer patients in Doll and /1,143 | Patients with non-uleer dis- | 1. Same interviewers and ques-

1958 Duodenal. Hil! Lung Cancer Study eases. Each case matched tionnaire in cases and
plus ‘additional patients in with 2 control patients of controls,
Central Middlesex Hospi- same sex, 5-year age group, | 2. Ulcer diagnosis probably
tal. and same type of place of well established.
residence. Male patients
matched by social class.
Edwards, McKeown, and | England M 1,737 men aged 60 and over on 11 General Practioners’ lists were examined and inter- | Of 143 considered to have a
Whitfield (11), 1959 viewed by these practitioners. Represents about 84% of all such men on these lists. peptic ulcer, 53 were con-
(9% non-response due to death and/or untraced.) firmed by X-ray.

 

 

 

 

 
TABLE 2.—Summary of results of retrospective and cross-sectional studies of
peptic ulcer and smoking

 

 

 

 

 

 

 

 

 

 

 

 

 

Percent Non-smokers Percent Heavy Smokers or Average
Amounts Used
Investigator _~
Cases | Controls Cases Controls
Barnett (2) Total 18 25 |
Gastric 15 |
Duodenal 20 |
Trowell (18) Duodenal 8 17 Cigarettes: 12.0 per day {111 per day.
Pipe: 1.6 0z. per week | 2.15 02. per
week.
Mills (14) ww} 35
_
Allibone and Flint () 38 54 |
ee
Doll et al. (7) Gastric Gastric :
M 1.3 4.7) M 10.6 11.3
F 51.1 66.8 | F 11 Lt
Duodenal Duodenal
M 2.1 5.8 | } 10,2 12.7
F 83.77 62.0 | F 1g 1.9
Edwards et al. (11) Percent of Peptic Uleer by Smoking Category
Never smoked_._._.0-.. 6.
Formerly smoked 6.

 

Cigarettes:
1-9 per day_
10-19 per day. _._
20 plus per day.

 

 

Aorowk US

 

 

TABLE 3.—Expected and observed deaths and mortality ratios for ulcer of

stomach and duodenum*

prospective studies

among current

cigarette smokers, from seven

Oe

 

 

 

 

Dorn (8)**

 

 

Number of Deaths |

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Investigator Type of Uleer Mortality
Ratio
Observed | Expected
Hammond and Horn (13)**_.- | Gastric. 2-22, 46 0 jeee ee eee
Duodenal....-2-2. 8 54 25 2.2
Both types. __..-. 2.2. 100 425 4.0
were eee eee Gastrie.-__. 22.22... 31 6.1 5.1
Duodenal... 36 15.45 2.3
Both types. _..--2-22 67 21.5 3.1
Hammond (12)... Gastric... 4a og 4.3
32 28.9 Ld
74 38. 6 19
Doll and Hill (6)_..--00 Both types..._....2.22 2. 14 | QO fell.
Dunn et al., Occupational (9).__.....__ Both types. weet 12 23.1 0.5
Dunn et al., Legion (10)... Both types. -.-...-2 2222... 12 18 6.8
Best et al. (5).--222-2- Both types. ---.--. 8, 54 7.9 a9

“Includes ISC numbers 540, 441.
**The Hammond and Horn d

ata are from their original published

report; the other results listed include

more recent data as tabulated for the Committee (see Chapter 8).

339
Numerous investigators have studied the clinical and physiological effects
of smoking on gastric motility and acid secretion in humans with and with-
out peptic ulcer. Great variation of gastric motility and secretion was
observed in response to cigarette smoking.

Some workers found inhibition of gastric motility (15, 17). Batterman
(3) showed three types of response in normal subjects and ulcer patients
after smoking one cigarette. In one-third no effect was observed, another
third complete inhibition of motor activity for a time, and in the rest a
period of hypermotility was followed by normal or subnormal activity,
Smoking appears to produce variable effects also on gastric secretion. In
a few studies. gastric secretion increased, while in others no change was
observed or there was depression of secretory activity (4,15, 16,17). Ad-
ditional studies of the effect of smoking on gastric secretory activity and
motility are needed to explain the biological meaning of the statistical asso-
ciation between cigarette smoking and peptic ulcer.

CONCLUSION

Epidemiological studies indicate an association between cigarette smoking
and peptic ulcer which is greater for gastric than for duodenal ulcer.

REFERENCES

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3. Batterman. R. C. The gzstro-intestinal tract. In: Wynder, E. L. ed.
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6. Doll, R.. Hill. A.B. Lung cancer and other causes of death in relation
to smoking: A second report on the mortality of British doctors.
Brit Med J 2: 1071-81, 1956.

- Doll. R.. Jones. F. A.. Pygott, F. Effect of smoking on the production
and maintenance of gastric and duodenal ulcers. Lancet 1: 657-62.
1958,

8. Dorn, H. F. Tobacco consumption and mortality from cancer and other

diseases. Public Health Rep 74: 581-93, 1959.

ww

~

340
9. Dunn, J. E., Linden, G., Breslow, L. Lung cancer mortality experience of
men in certain occupations in California. Amer J Pub Health 50:
1475-87, 1960.

10. Dunn, J. E., Jr., Buell, P., Breslow, L. California State Department of
Public Health, Special Report to the Surgeon General’s Advisory
Committee on Smoking and Health.

ll. Edwards, F., McKeown, T., Whitfield, A. G. W. Association between
smoking and disease in men over sixty. Lancet 1: 196-200, 1959.

12. Hammond, E. C. Special report to the Surgeon General’s Advisory
Committee on Smoking and Health.

13. Hammond, E. C., Horn, D. Smoking and death rates—Report on
forty-four months of follow-up of 187,783 men. II. Death rates by
cause JAMA 166: 1294-1308, 1958,

14, Mills, C. A. Tobacco smoking: Some hints of its biologic hazards.
Ohio Med J 46: 1165-70, 1950.

15. Packard, R. S. Smoking and the alimentary tract: A review. Gut 1:
171-4, 1960.

16. Schnedorf, J. G., Ivy, A. C. The effect of tobacco smoking on the
alimentary tract. JAMA 112: 898-903, 1939.

17. Steigmann, F., Dolehide, R. U., Keminski, L. Effects of smoking
tobacco on gastric acidity and motility of hospital controls and pa-
tients with peptic ulcer. Amer J Gastroent 22: 399-409, 1954.

18. Trowell, O. A. The relation of tobacco smoking to the incidence of
chronic duodenal ulcer. Lancet 1: 808-9, 1934.

TOBACCO AMBLYOPIA

For more than a century clinicians have attributed certain cases of
amblyopia—dimness of vision unexplained by an organic lesion—to the use
of tobacco.

The distinguishing characteristic of tobacco amblyopia is a specific type
of centrocecal scotoma. Since this disease was defined as a distinct clinical
entity for the first time in 1930 (4) , the medical literature prior to this date
is of relatively little value in the critical evaluation of the problem (3). No
epidemiological studies with adequate controls are available to establish for
this disease a relative risk among smokers and nonsmokers.

Clinical impressions associate tobacco amblyopia with pipe and cigar
smoking and very rarely with cigarette smoking.

It has been suggested that this disease, which is now rare in the United
States, occurs mainly in individuals with a nutritional deficiency which
presumably renders the retina or optic nerve unduly sensitive to tobacco
(1, 5).

Objective attempts at experimentation have been extremely rare and most
of the literature is related to uncontrolled clinical impressions (2).

34]
CONCLUSION

Tobacco amblyopia had been related to pipe and cigar smoking by clinical
impressions. The association has not been substantiated by epidemiological
or experimental studies.

REFERENCES

1. Heaton, J. M., McCormick, A. J. A., Freeman, A.G. Tobacco Amblyopia:
A clinical manifestation of vitamin B-12 deficiency. Lancet 2: 286~
90, 1958.

2. Potts, A.M. Special report to the Surgeon General’s Advisory Commit-
tee on Smoking and Health.

3. Schwartz, J. T. Special report to the Surgeon General’s Advisory Com-
mittee on Smoking and Health.

4, Traquair, H. M. Toxic Amblyopia, including retro-bulbar neuritis.
Trans Ophthal Soc U K 50: 351-85, 1930.

5. von Sallmann, L. Special report to the Surgeon General’s Advisory
Committee on Smoking and Health.

SMOKING AND CIRRHOSIS OF THE LIVER

Epidemiological studies have noted an association between cigarette smok-
ing and mortality from cirrhosis of the liver. The mean mortality ratio for
cirrhosis of the liver calculated from all prospective studies was 2.2 (Table
19, Chapter 8). The individual ratios in six of these studies ranged from 1.3
in the Canadian veterans study (1) to 4.0 in the California occupational study
(3). The earliest prospective study, by Doll and Hill (2) reported no
deaths from cirrhosis of the liver among non-smokers.

The small amount of information on the biological effects of nicotine and
tobacco smoke on the liver of experimental animals is contradictory (5).

In several studies (4, 6, 7) it has been reported that heavy smokers also
tend to drink alcoholic liquors excessively. It is well established that heavy
consumption of alcohol and nutritional deficiencies are associated with in-
creased mortality from cirrhosis of the liver. The increased death rate from
cirrhosis among smokers may reflect the consumption of alcohol and asso-
ciated nutritional deficiencies rather than the effect of cigarette smoking.

CONCLUSION

Increased mortality of smokers from cirrhosis of the liver has been shown
in the prospective studies. The data are not sufficient to support a direct or
causal association.

342
REFERENCES
1. Best, E. W. R., Josie, G. H., Walker, C.B. A Canadian study of mortality

in relation to smoking habits, a preliminary report. Canad J Pub
Health 52: 99-106, 1961.

2. Doll, R., Hill, A. B. Lung cancer and other causes of death in relation
to smoking: A second report on the mortality of British doctors. Brit
Med J 2: 1071-81, 1956.

3. Dunn, J. E., Linden, G., Breslow, L. Lung cancer mortality experience
of men in certain occupations in California. Amer J Pub Health 50:
1475-87, 1960.

4. Heath, C. W. Differences between smokers and non-smokers. AMA
Arch Int Med 101: 377, 1958.

5. Larson, P. S., Haag. H. B., Silvette, H. Tobacco—experimental and
clinical studies. A comprehensive account of the world literature.
Balliere, Tindall & Cox. London, 1961. p. 319-321.

6. Matarazzo, J. D., Saslow, G. Psychological and related characteristics
of smokers and non-smokers. Psychol Bull 57: 493, 1960.

7. McArthur, C., Waldron, E., Dickinson, J. The psychology of smoking.
J Abnorm Soc Psychol 56: 267-275, 1958.

MATERNAL SMOKING AND INFANT BIRTH WEICHT

Five retrospective and two prospective studies have shown an association
between maternal smoking during pregnancy and birth weight of the infant
(2, 4, 5, 6, 8, 9, 10). Women smoking during pregnancy have babies of
lower birth weight than non-smokers of the same social class. They have
also a significantly greater number of premature deliveries (defined as
birth weight of 2,500 grams or less) than the non-smoking controls.

While several studies reported a slightly greater neonatal death rate of
the children of smokers (2, 5), others did not demonstrate any significant
difference in the fetal and neonatal death rates of the two groups (6, 7).

Studies on alterations of placental morphology and function as a response
to smoking are insufficient for judgment. The difference in infant weight
may be due to vasoconstriction of the placental blood vessels (1) or to toxic
substances such as CO in the circulation of the smoker and fetus (3).

It is not known whether the lower birth weight of the infants of smokers
has any clinical significance. In one of the groups studied (5) there was
less need for surgical induction of labor among mothers who smoked.

CONCLUSIONS

1. Women who smoke cigarettes during pregnancy tend to have babies
of lower birth weight.

2. Information is lacking on the mechanism by which this decrease in
birth weight is produced.

3. It is not known whether this decrease in birth weight has any influ-
ence on the biological fitness of the newborn.

343
REFERENCES

1. Essenberg, J. M., Schwind, J., Patras, A. The effects of nicotine and
cigarette smoke on pregnant female albino rats and their offsprings.
J Lab Clin Med 25: 708-17, 1940.

2. Frazier, T. M., Davis, G. H{., Goldstein, H., Goldberg, I. D. Cigarette
smoking and prematurity: a prospective study. Amer J Obstet Gynec
81: 988-96, 1961.

3. Haddon, W. Jr., Nesbitt, R. E. Smoking and pregnancy: carbon mon-
oxide in blood during gestation and at term. Obstet Gynec 18: 262-7,
1961.

4. Herriot, A., Billewicz, W. F., Hytten, F. E. Cigarette smoking in preg-
nancy. Lancet 1: 771-3, 1962.

5. Lowe, C.R. Effect of mother’s smoking habits on birth weights of their
children. Brit Med J 2: 673-6, 1959.

6. O’Lane, J. M. Some fetal effects of maternal cigarette smoking. Obstet
Gynec 22: 181-4, 1963.

7. Savel, L. E., Roth, E. Effects of smoking on fetal growth. Obstet Gynec
20: 313-6, 1962.

8. Simpson, W. J. A preliminary report on cigarette smoking and the in-
cidence of prematurity. Amer J. Obstet Gynec 73: 808-15, 1957.

9. Villumsen, A. L. Cigarette smoking and low birth weights: A prelimi-
nary report. Ugeskr Laeg 124: 630-1, 1962.

10. Yerushalmy, J. Statistical considerations and evaluation of epidemio-
logical evidence. In: James, George and Rosenthal, Theodore eds.
Tobacco and Health. Springfield, Nl. Charles C. Thomas, 1962.
p. 208-30.

SMOKING AND ACCIDENTS

Smoking has heen associated with a variety of accidents. Among these.
fires have the most obvious and important consequences. —

In a special study of home accident fatalities in 1952 through 1953, the
Public Health Service and the National Safety Council reported that 231
(18°) of 1,274 deaths from fires of known origin were due to cigarettes.
cigars or pipes (1).

The Metropolitan Life Insurance Company reported that of 352 deaths in
1956 and 1957 among their polievholders from fires and burns with known
causes in and about the home. 57 (16° ) were due to smoking (2).

Of physiological responses related to driving. smoking degrades detectably
only the differential brightness threshold and this effect increases with
amount of smoking i41. The epidemiological data available on the effects
of smoking on traffic accidents are inconclusive.

It has been shown that a level of carboxyhemoglobin of 5 percent--a level
which js not uncommon among heavy cigarette smokers (3. 6)—depresses
visual perception to as great an extent as anoxia at 8.000 to 10,000 feet

altitude (4, 5).

344
CoNcLUSION

Smoking is associated with accidental deaths from fires in the home. No
conclusive information is available on the effects of smoking on traffic
accidents.

REFERENCES

1. Home Accident Fatalities: 1952-1953. National Office of Vital Statistics,
U.S. Public Health Service, 1956. Mimeographed report. Table 12.

2. How fatal accidents occur in the home. Metrop Life Insur Statist Bull 40:
6-8, November—December, 1959.

3. Larson, P. S., Haag, H. B.. Silvette, H. Tohacco: Experimental and
Clinical studies. Baltimore, Williams and Wilkins. 1961. Carboxy-
hemoglobin, p. 107-110.

4. McFarland, R. A., Moseley, A.L. Carbon monoxide in trucks and buses
and information from other areas of research on carbon monoxide.
altitude and cigarette smoking. In: Conference proceedings: Health,
medical and drug factors in highway safety. National Academy of
Sciences—National Research Council Publication 328, 1954. Sect.
4.17-4.33.

0. McFarland, R. A., Roughton, F. J. W., Halperin, M. H., Niven, J. 1. The
effects of carbon monoxide and altitude on visual thresholds. J Aviat
Med 15: 6, 381-94, 1944.

6. Schrenk, H. H. Results of laboratory tests. Determination of concen-
tration of carbon monoxide in blood. Pub Health Bull 278: 36-49,
1942.

345
Chapter 13

 

Characterization of the
Tobacco Habit and
Beneficial Effects of Tobacco
Contents

CHARACTERIZATION OF THE TOBACCO HABIT... .

Nicotine . 2... 1 ee ee ee ee ee ee ee
Distinction Between Drug Addiction and Drug Habituation .
Tobacco Habit Characterized as Habituation . . . . . . .
Relationship of Smoking to Use of Addicting Drugs . . . .
Measures for Cure of Tobacco Habit. . . 2... 1...

Summary... 1. ee ee ee ee ee
References . . 1... 1 eee et ee ee et te

Page
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Chapter 13

 

CHARACTERIZATION OF THE TOBACCO HABIT

NICOTINE

Of the known chemical substances present in tobacco and tobacco smoke,
only nicotine has been given serious pharmacological consideration in rela-
tionship to the tobacco habit. Lewin (17) stated. “The decisive factor in the
effects of tobacco, desired or undesired, is nicotine . . . and it matters little
whether it passes directly into the organism or is smoked.” Support for this
statement is based mostly on rationalizations from smoking behavior, analogy
to other habits involving pharmacological agents and, to a much lesser extent,
on established scientific fact. The latter may be summarized briefly as
follows:

1. Only plants with active pharmacological principles have been employed
habitually by large populations over long periods; e.g., tobacco (nicotine) ;
coffee, tea, and cocoa (caffeine) ; betel nut morsel (arecoline) ; marihuana
(cannibinols) ; khat (pseudoephedrine) ; opium (morphine); coca leaves
(cocaine) ; and others (see Lewin, 17).

2. Denicotinized tobacco has not found general public acceptance as a
substitute (16, pp. 531-532).

3. Chewing tobacco and using snuff, although providing oral gratification,
also furnish nicotine for absorption to produce systemic effects (34).

4. Many but not all smokers can detect a reduction in nicotine content of
cigarettes (9).

5. The administration of nicotine mimics the subjective effects of
smoking (13). In uncontrolled experiments Johnston administered nicotine
hypodermically, intravenously, or orally to smokers and non-smokers. Non-
smokers found the effects “queer,” whereas many smokers, including John-
ston himself, claimed the subjective effects to be identical to those obtained
by inhaling cigarette smoke and found that the urge to smoke was greatly
reduced during nicotine administration.

In spite of the anecdotal nature of most of this information, the facts are
that nicotine is present in tobacco in significant amounts, is absorbed readily
from all routes of administration, and exerts detectable pharmacological
effects on many organs and structures including the nervous system. The
classical pharmacological characterization of nicotine—cellular stimulation
followed by depression which is noted in isolated tissue and organ systems—
has been invoked to explain the widely differing subjective responses of
smokers, many of whom describe the effects as stimulating (“smoking relieves
the depression of the spirits”), while others obtain a soothing and tranquiliz-
ing effect (16, p. 533).

Wilder (33) summarized the literature by noting “. . . observations that
cigarette smoking obviously serves a dual purpose: it will mostly pick us up

349
when we are tired or depressed and will relax and sedate us when we are
tense and excited.” In order to ascribe such biphasic effects solely to the
direct action of nicotine it would be necessary to discount psychological re-
sponses and alterations in mood from all other types of stimuli associated
with smoking or the use of tobacco, an obvious impossibility. Although
Knapp and Domino (15) have shown nicotine in small amounts to exert
potent arousal effects in the electroencephalogram in animals, this evidence
is difficult to interpret as it relates to smoking in man. A consensus among
modern authors (27) appears to be that smoking, and presumably nicotine,
exert a predominantly tranquilizing and relaxing effect. The act of smoking
is of such complexity that the difficulties associated with objective analysis
of whether smoking induces pleasure by creating euphoria or by relieving
dysphoria renders objective analysis virtually impossible. The anecdotal
literature suggests that sedation plays a more important subjective role in
pipe and cigar smoking than with cigarette smoking. Since most pipe and
cigar smokers do not inhale, this suggests that bronchial and pulmonary
irritation from cigarette smoke after inhaling may contribute an important
sensory input to the central nervous system which could modify the sedative
effects of nicotine, so that some individuals would describe the experience as
stimulating rather than sedative. Heavy cigarette smokers who inhale often
describe the act as a pleasant sensory experience which constitutes for them
one of the prime drives to continue to smoke. Freedman (10) used the term
“pulmonary erotism.” Mulhall (19) and Robicsek (22) have commented on
this concept. An interesting psychoanalytical approach by Jonas (14),
which postulates central nervous system counterirritation to constant pul-
monary irritation from smoking, is based upon this concept. If pulmonary
irritation is a pleasure factor it probably is not related to nicotine alone but
to other irritants in smoke and could represent a non-specific increase in
afferent sensory discharge from the whole respiratory tract. A gap in knowl.
edge exists in this area. Furthermore, until carefully controlled experiments
with nicotine are conducted in man, the literature will be burdened further
with anecdote and hypothesis rather than fact.

DistINCTION BETWEEN Druc ADDICTION AND Druc HABiITuATION

Smokers and users of tobacco in other forms usually develop some degree
of dependence upon the practice. some to the point where significant emo-
tional disturbances occur if they are deprived of its use. The evidence indi-
cates this dependence to be psychogenic in origin. In medical and scientific
terminology the practice should be labeled habituation to distinguish it clearly
from addiction, since the biological effects of tobacco, like coffee and other
caffeine-containing beverages, hetel morsel chewing and the like, are not
comparable to those produced by morphine, alcohol, barbiturates, and many
other potent addicting drugs. In fact, to make this distinction, the World
Health Organization Expert Committee on Drugs Liable to Produce Addiction
(35) created the following definitions which are accepted throughout the
world as the basis for control cf potentially dangerous drugs.

350