9LS

Tanue 29.—Relatine risk of lung cancer for men, comparing cigar, pipe, and cigarette smokers with nonsmokers. A sums
mary of retrospective studies

 

 

 

 

Relative tisk ratto and Porcentage of cases and controls by typo of smoking
Author, reference Numbor
Nonsmoker Cigar only Plpeonly Total Pips = Clgnrotts Mixed
and clgar only
Levin, et al. (60); Relative risk..... 82 1.0 0.7 0.8 ..lL lll. 21 el.
Cases... 2. 236 = Percent cases_.._.. 15 ll 40 Leelee 66 Lele.
Controls__.2... eae eee ceeeuee 481 Percent controls... _. 22 23 2 le 4400 ell.
Schrek, et al. (81); Relative risk.3002 28. 1.0 6 07 lle | ns
Cases... 82 Percent cases......0. = 15 4 8 Leelee eee Bk
Controls... 522 Percent controls__...___. 22 23 VW eee 1! ee
Wynder and Graham (111) Relative risk...9..0 | 1.0 5. 1 3.6 2... 15.7 Joelle
Cases... 22. 605 Percent cases__.....___ | 1 4 $0 eee BL eel.
Controls... eee 780 Percent controls......._- 15 8 V2 lle 65 Lele
Doll and Hill (26): Relative risk.---. 00 1.0 welll BL eee l.. 96 oe ll
Bees 8 1,357 Percent cases___.... ne 4 lll T4 0 ell
Controls..... 2 1,357 Percent controls_....-_ G8 Lele TO eect eee 69 eee
Koulumies (66): Relative risk...02. 00 | al 9.6 -oel ll. 29.3 222 lll
Cases... 2.22. 812 Percent cases._..... 6. 6 Lele 2 ell TT lee
Controls... 2.222 300 Percent controls......__. Wo Le 6 Leelee M6 eel
Sadowsky, et al. (77) Relative risk... 8.088. 1.0 2.4 14 ll 3.7 5.6
Cases... 22... 477 Percent cases....00. 68 4 2 3 lle, 57 3h
Controls...02 222 fpeeeeee 615 Percent controls...... 13 3 7 knell. 53 19
LZL¢

Wynder and Cornfield (110):
Cases. 22... eee

Cases. eee

Cases. 2.2... teen

Cases_ 2.

Schwartz and Denoix (82) ;
Cases

Lombard and Snogireff (61);
Cases

13.5
96
78

89
78

95
75

50
82S

TABLE 29.—Relative risk of lung cancer for men, comparing cigar, pipe, and cigarette smokers with nonsmokers. A sum-
mary of retrospective studies—Continued

 

Rolativo risk ratio and percentage of casos and controls by typo of smoking

 

 

 

Author, reference Number
Nonsmoker Cigar only Pipsonly Total pipe Clgaretta Mixod
ond cigar only

Wicken (106): ‘Relative risk... 000 | LO eee Ll. 2.2 4.3 4.2

Cases... eee 803 Percent cases.__._..____ 4 lle eee loll. 10 78 7

Controls... eee 803 Percent controls.......__ ee 16 64 6
Abelin and Gsell (1): Relative risk... 20. 1.0 30.7 21.8 39. 9 31.0 24.7

Cases... 118 Percent cases.._....___| 2 28 7 58 25 24

Controls... 2... 524 Percent controls......._. 35 19 6 31 17 10
Wynder, et al. (116): Relative risk... 008. LO wee. lle 2.0 a
Cases--- 2. ee 210 Percent cases__._.. 2. 8 eee tlle 5 920 Lee
Controls... ee 420 Percent controls......... 21 eee ele 15 AT leas

 

 
62S

TABLE 30.—Changes in bronchial epithelium of male cigar, pipe, and cigarette smokers as compared to nonsmokers

 

 

Percont sectiona Percent 3 plus Percent Percent
Group Number of Sections with with epithelial callrows with atypical cells Total byperplasta and
subjects epithellum loslons cilia present sections goblet calls tao
ginods
Ist set (none vs. pipe vs. cigarette—matched
on 1:1 basis):
Nonsmoker_....-----------e2---- ee ee ee 20 985 21.7 11.2 2. 6 1, 031 10. 3
Pipe only-_... 2-2 eee ee eee eee eee eee 20 924 65.5 38, 1 37.0 979 35. 9
Cigarette only_-_--.------------------- 20 914 96. 8 88. 6 95. 2 982 72.1
2d set (none vs. pipe vs. cigarette—matched
on frequency basis):
Nonsmoker...-------------------- eee ee 25 1, 246 22.9 13. 4 7 1, 277 11.5
Pipe only.......---------------- eee 25 1, 164 68. 7 38.7 38. 2 1, 247 37.9
Cigarette only_..----------------- eee 25 1, 126 96.3 88. 7 89.5 1, 237 75.5
3d set (none vs. cigar vg. cigarette);
Nonsmoker_.--.----------+--+---e eee 35 1, 706 27.4 12.7 .8 1, 748 15.3
Cigar only......--2----.----------- eee 35 1, 733 90. 8 40. 0 73.6 1, 828 52.5
Cigarette only.......-..--------------- 35 1, 526 99. 0 92.7 97.8 1, 693 80. 2

 

Source: Auerbach et al. (8).
Tumorigenic Activity

The tumorigenic activity of tobacco smoke can be modified in botha
quantitative and qualitative sense. Physical or chemical changes in
tobacco that result in a reduction of total particulate matter upon
combusion of a given quantity of tobacco may result in a reduction
of carcinogenic potential. Such factors as tobacco selection, treatment,
blending, cut, end additives may quantitatively alter tar production.
Wrapper porosity and filtration may also affect tar production.

Quantitative changes in the tumorigenic activity of tobacco tar on
a gram-for-gram basis can be produced by the selection and treatment
of tobacco, the use of additives or tobacco sheets, or adjustments in the
cut and packing density.

Combustion temperature can also produce quantitative changes in
the particulate matter of tobacco smoke. Although high-temperature
burning produces less particulate matter in the smcke, it appears that
tumorigenic components occur in higher concentration when tobacco is
pyrolized at temperatures higher than 700° centigrade (34).

Cigars, pipes, and cigarettes are similar in that they are smoked
orally and have a common site of introduction to the body. The tissues
of the mouth, larynx, pharynx, and esophagus appear to receive ap-
proximately equal exposure to the smoke of these products. Inhalation
causes smoke to be drawn deeply into the lungs and also allows for
systemic absorption of certain constituents of tobacco smoke which
then can be carried further to other organs.

Pipe tobacco and cigars vary from cigarettes in a number of charac-
teristics that can produce both quantitative and qualitative changes in
the total particulate matter produced by their combustion. Experi
mental evidence suggests that although there is some difference in the
amount and quality of tar produced by cigars, this cannot account for
the reduced mortality observed in cigar smokers compared to cigarette

smokers.
Experimental Studies

Several experimental investigations have been conducted to examine
the relative tumorigenic activity of tobacco smoke condensates obtained _
from cigarettes, cigars, and pipes. Most of these studies were standard-
ized in an attempt to make the results of the cigar and pipe experiments
more directly comparable with the cigarette data and most used the
shaved skin of mice for the application of tar. Tars from cigars, pipes,
and cigarettes were usually applied on an equal weight basis so that
qualitative differences in the tars could be determined. In several ex-
periments, the nicotine was extracted from the pipe and cigar conden-
sates in an attempt to reduce the acute toxic effects that resulted in
animals from the high concentrations of nicotine frequently found in

these products.

580
Wynder and Wright (717) examined the differences in tumorigenic
activity of pipe and cigarette condensates. Tars were obtained by the
smoking of a popular brand of king-size cigarettes and the same ciga-
rette tobacco smoked in 12 standard-grade briar bowl pipes. Both the
cigarettes and pipes were puffed three times a minute with a 2-second
putf and a 35-ml. volume. Both the cigarettes and pipes attained similar
maximum combustion zone temperatures; however, the use of cigarette
tobacco in the pipe resulted in a combustion chamber temperature that
averaged about 150° centigrade higher than temperatures achieved
when pipe tobacco was used. Chemical fractionation was accomplished
and equal concentrations of the neutral fraction were applied in three
weekly applications to the shaved skin of CAF, and Swiss mice. The
results indicate that neutral tar obtained from cigarette tobacco smoked
in pipes is more active than that obtained in the usual manner from
cigarettes. About twice as many cancers were obtained in both the CAF,
and the Swiss mice, and the latent period was about 2 months shorter.

Extending these data, Croninger, et al. (20) examined the biologic
activity of tars obtained from cigars, pipes, and cigarettes, Each form
of tobacco was smoked as it was manufactured in a manner to simulate
human smoking or to maintain tobacco combustion. The whole tar was
applied in dilutions of one-to-one and one-to-two with acetone to the
shaved backs of female CAF, and female Swiss mice using three
applications each week for the life-span of the animal. The nicotine was
extracted from the pipe and cigar condensates to reduce the acute
toxicity of the solutions. The Swiss mice. pipe, cigar, and cigarette tars
produced both benign and malignant tumors. The incidence rates of
malignant tumors given as percents were: 44, 41, and 37, respectively.
These results suggested a somewhat higher degree of carcinogenic
activity for cigar and pipe tars than for cigarette tar.

Similar results were reported by Kensler (53) who applied conden-
Sates obtained from cigars and cigarettes to the shaved skin of mice.
The incidence of papillomas produced by cigar smoke concentrate was
no different from that of the cigarette smoke condensate. Similarly,
there was no difference between cigar and cigarette smoke condensates
when carcinoma incidences were conipared.

Homburger, et al. (45) prepared tars from cigar, pipe, and cigarette
tobaccos that were smoked in the form of cigarettes. In this way, all
tobaccos were smoked in an identical manner and uniform combustion
temperatures were achieved. Because of this standardization, differ-
ences in tumor yield could be attributed to tobacco blend and not the
manner in which the tars were prepared. The whole tars were diluted
one-to-one with acetone and applied to the shaved skin of CAF, mice
three times a week for the lifespan of the test animal. Skin cancers
Were produced more quickly with pipe and cigar smoke condensates
than with cigarette smoke condensates. This suggests that the smoking

425-028 O—73-_15

581
of pipe and cigar tobaccos in the form of cigarettes does not alter the
condensates to any significant degree.

Davies and Day (22) prepared tars from small cigars especially
manufactured from a composite blend of cigar tobacco representing
small cigar brands smoked in the United Kingdom, cigarettes espe-
cially manufactured from the same tobacco used for the cigars de-
scribed above, and plain cigarettes especially manufactured from a
composite blend of flue-cured tobacco representing the major plain
cigarette brands smoked in the United Kingdom. The whole tar was
diluted to four concentration levels and applied to the shaved backs
of female albino mice for their lifespan using four dosing regimens.
A statistically significant increase in mouse skin carcinogenicity was
shown with the cigar smoke condensate compared with the tars
obtained from either fiue-cured or cigar tobacco cigarettes. These
results are consistent with those of the previously reported
investigations.

The effect of curing on carcinogenicity was examined by Roe, et al.
(76). Bright tobacco grown in Mexico was either flue-cured or air-
cured and bulk fermented. Both flue-cured and air-cured tobaccos were
made into cigarettes standardized for draw resistance and were smoked
under similar conditions. Condensates from these cigarettes were ap-
plied to mouse skin three times each week in an acetone solution. The
development of skin tumors was higher in mice treated with the flue-
cured condensate than in mice treated with the air-cured condensate
(P<0.01). The difference may have been due to the use of equal —
weights of condensate rather than the use of extracts from an equal
number of cigarettes. The air-cured cigarettes produced a greater
weight of condensate than did the flue-cured cigarettes. A chemical
analysis of the two tobaccos and two condensates revealed only small
differences in composition. Evidently air curing of Bright tobacco
in the method used is not associated with a loss of reducing sugars.

A more detailed analysis of these experimental studies is presented
in table 31.

These experimental data suggest that cigar and pipe tobacco con-
densates have a carcinogenic potential that is comparable to cigarette
condensates. This is supported by human epidemiological data for
those sites ex posed equally to the smoke of cigars, pipes, and cigarettes.
The partially alkaline smoke derived from pipes and cigars is gen-
erally not inhaled, and as a result there appears to be a lower level
of exposure of the lungs and other systems to the harmful properties of
pipe and cigar smoke than occurs with cigarette smoking. It is antic-
ipated that modifications in pipe tobacco or cigars which would result
in a product that was more readily inhalable would eventually result
in elevated mortality from cancer of the lung, bronchitis and emphy-
sema, arteriosclerotic cardiovascular diseases, and the other condi-
tions which have been clearly associated with cigarette smoking.

582
8S

TABLE 31.—T'umorigenic activity of cigar, pipe, and cigaretle smoke condensates in skin painting experiments on animals
{[Key: A= Mothod, B=Froquoncy. CDuratlon, D=Matertal.]

Porcent
Author, reference Animal Activity Treatmoat Numbor

nea enna
Papitlomas Carcinomas

 

Wynder and CAF, and A. Painting shaved skin, CAF:
Wright Swiss mice, B, 3 times a week, Pipe (cigarette tobacco)... 2. 30 GO 20
(117). C. Lifespan (24 months), Cigarette... 22 eee 30 30 3
D. Neutral fraction tar from Swiss:
cigarettes and cigarette Pipe (cigarette tobacco)__.._- 30 63 50
tobacco smoked in pipes. Cigarette... 2 30 63 33
Croninger, et Female Swiss A. Painting shaved skin, Cigar, nicotine free (1:1)... 46 65 4i
al. (£0). mice, B. 3 times a week. Pipe, nicotine free (1 eel 45 71 44
C. Lifespan. Cigar (1:2). 22 e 78 83 18
D. Whole tar diluted in Pipe, nicotine free (1 1) &9 30 16
acetone. Cigarette (lil). ee eel 86 47 37
Acctone controly.. 2 2222... 8 23 0 0
Kensler (68)_.. Swiss mice.._... A. Painting shaved skin. Cigar tar (J) 100 mg. per week__ 100 42 41
B. 3 times a week, Cigarette tar (G) 100 mg. per 100 40 28
C. Lifespan. week,
D. Whole tar diluted in Cigarette tar (E) 100 mg. per 100 34 34
acetone. week.
98S

TABLE 31.—Tumorigenic activity of cigar, pipe, and cigarette smoke condensates in skin painting
experiments on animals—Continued

(Key: A» Mothod, B= Frequoucy, C= Duration. D =Matortal.]

 

 

Porcent
Author, reference Anima! Activity Treatment Number
Papillomas Carcinomas
Homburger, et CAF, mice___..- A. Painting shaved skin, Cigar tobacco cigarettes 165 mg. 100 37.5 19
al. (44). B. 2 to 3 times a week. | per week.
C. Lifespan (2 years), Pipe tobacco cigarettes ! 64 mg. 100 23 20
D. Whole tar diluted 50 per- per week.
cent in acctone, Cigarettes } 62 mg. per week.__. 100 15 23
Acctone controls... ....20220--- 100 0 0
Davies and Female albino A. Painting shaved skin. Cigars, small 83 mm. long 150 144 44 27
Day (£8). mice. B. Varied. per week.
C. 116 weeks, Cigar tobacco cigarettes 150 72 32 14
D, Whole tar in 150 mg. per week.
acctone, Cigarettes 150 per week... _- 144 28 13
Roe, et al. Female Swiss A, Painting shaved skin. Flue-cured Bright tobacco 180 400 52 30
(76). mice. B. 3 times a week. mg. per week,
C. Lifespan. Air-cured Bright tobacco 180 400 68 23
D. Whole tar diluted in mg, per week,
acetone, Acctone controls 0.75 cc. per 400 1.3 0. 5

week,

1 Clygur, plpo, and clgarotto tobacco smokod us clgaretios at similar combustion tomporaturey,
CarpiovAsCULAR DiszasEs

The majority of deaths in the United States each year are due to
cardiovascular diseases. Cigarette smoking has been identified as a
major risk factor for the development of coronary heart disease
(CHD). However, pipe and cigar smokers experience only a small
increase in mortality from coronary heart disease above the rates of
nonsmokers. Cigarette smokers have higher death rates from cerebro-
vascular disease than nonsmokers, whereas pipe and cigar smokers have
cerebrovascular death rates that are only slightly above the rates of
nonsmokers. Table 32 summarizes the major prospective epidemiologi-
cal investigations that examined the association of smoking in various
forms and total cardiovascular diseases, coronary heart disease, and
cerebrovascular disease. Doll and Hill. (28), Best (9), and Kahn (50)
examined dose-response relationships for pipe and cigar smokers and.
reported a slight increase in mortality from coronary heart disease
with an increase in the number of cigars or pipefuls smoked.

Other prospective epidemiological studies have also examined the
relationship of smoking in various forms to coronary heart disease and
related risk factors. Jenkins, et al. (49) in the Western Collaborative
Group Study of coronary heart disease, reported an incidence of coro-
nary heart disease in men aged 50 to 59 who were pipe and cigar smok-
ers that was intermediate between the rates seen in cigarette smokers
and nonsmokers. No increase in incidence of coronary heart disease was
seen among the pipe and cigar smokers in the younger age groups.
Shapiro, et al. (8d), in a study of the health insurance plan (HIP)
population, reported incidence rates for myocardial infarction, angina
pectoris, and possible MI, in pipe and cigar smokers that were similar
to the incidence rates seen in cigarette smokers. These rates were con-
siderably higher than those of nonsmokers. Data from the pooling
project (47) suggested that the incidence of CHD deaths, sudden
death, and the first major coronary event in pipe and cigar smokers
was intermediate between the incidence experienced by cigarette smok-
ers and nonsmokers. In contrast to these-studies, Doyle, et al. (30)
reported no increase in CHD deaths, myocardial infarction, or angina
pectoris in pipe and cigar smokers over the rates of nonsmokers in the ~
Framingham study.

The retrospective studies of Mills and Porter (64), Villiger and
Hevden-Stucky (704), Schimmler, et al. (80), and Hood, et al. (46)
contained data suggesting that pipe and cigar smokers experience
mortality rates from coronary heart disease that are essentially similar
to those experienced by cigarette smokers. The retrospective study of
Spain and Nathan (8¢) reported lower rates of coronary heart dis-
ease in all smoking categories than were found in nonsmokers.

Van Buchem (703) and Dawber, et al. (23) examined serum choles-
terol levels in groups of individuals classified according to smoking

585
habits. In these two studies, pipe and cigar smokers had serum choles-
terol levels that were nearly identical with the levels found in
nonsmokers.

Tibblin (97) and Dawber, et al. (23) investigated the effect of smok-
ing on blood pressure. The proportion of smokers decreased in proups
with higher blood pressures, although this was not as dramatic for
pipe and cigar smokers as it was for cigarette smokers.

In an experimental study using anesthetized dogs, Kershbaum and
Bellet (54, 55) examined the effects of inhaled and noninhaled ciga-
rette, cigar, and pipe smoke on serum free fatty acid levels and urinary
catecholamine and nicotine excretion. In this study, inhalation of to-
bacco smoke from all these sources resulted in similar increases in
serum free fatty acids and in catecholamine and nicotine excretion.

TABLE 32.—Mortality ratios for cardiovascular deaths in male cigar and
pipe smokers. A summary of Prospective epidemiological studies

 

 

 

Type of smoking
Author, reference Category
Non-  Clpar PI Total Clga-
smoker only only pipe and rette only Mixed
cigar
Hammond and Cardiovascular 1.00 1.26 1.07 _____. 157 _LLL__
Horn (40). total.
Coronary.__.___ 100 128 £03 ______ 1.70 2.
Cerebrovascular_____ 1.00 1.31 1.23 1 | 1.30 2.2L.
Doll and Hill Cardiovascular 100-2022 LLlL le 0.99 1.26 1.13
(26, 27). total.
Coronary_..___.___. 1.00 22-0 oo. 94 123 1.18
Cerebrovascular. ____ 100-22. LL lle -95 113 97
Best (9)__._._ Cardiovascular 1.00 £14 -95 _ Le 1.52 ___.o
total.
Coronary._________. 1. 00 99 1.00 _____. 1.60 _..___
Cerebrovascular__ --- 100 1.28 85 22 ~ 83 2. LL
Hammond ! Cardiovascular 1.00 -_-.. lll. 1.06 1.90 ______
(38). total.
Coronary_____._____. 100 135 21.19 |__| 184 1.58
Cerebrovascular_____ 1.00 2020 2 1.09 1. 1.40
Kahn (60)____ Cardiovascular 100 105 £06 105 1 752 ee
total
Coronary eae ee eee 1.00 104 108 1.05 1.74 LLL
Cerebrovascular. ____ 1.00 108 109 106 1.52 __.___

 

 

' Mortality ratios for ages 33 to 64 only are presented.
Curonxic Oxstrective Pcusox ary Disease (COPD)
Chronic bronchitis and pulmonary emphysema account for most of

the morbidity and mortality from chronic respiratory disease in the
United States. Cigarette smokers have higher death rates from these

586
diseases and have more pulmonary symptoms and impaired pul-
monary function than nonsmokers. Cigarette smokers also have more
frequent and more severe respiratory infections than nonsmokers.
The relationship between smoking pipes and cigars and these diseases
is summarized in this chapter. The major prospective epidemiological
studies are summarized in table 33.

In a retrospective study of 1,189 males and matched controls in
Northern Ireland, Wicken (406) investigated smoking in various
forms and mortality from bronchitis. ‘Che relative risk ratios com-
pared to nonsmokers for mortality from chronic bronchitis were 1.98
for all smokers, 1.55 for pipe and cigar smokers, 2.95 for cigarette
smokers, and 1.49 for mixed smokers.

From a review of these prospective and retrospective studies, it
appears that pipe and cigar smokers experience mortality rates from
bronchitis and emphysema that are higher than the rates of non-
smokers. Although these morality rates approach those of cigarette
smokers, in most instances they are intermediate between the rates
of cigarette smokers and nonsmokers.

Pipe and cigar smokers have significantly more respiratory symp-
toms and illnesses than nonsmokers. Those studies which contain data
on pipe and cigar smoking as related to respiratory symptoms are
summarized in table 34. ,

Only a few studies have examined pulmonary function in pipe and
cigar smokers. There appears to be little difference in pulmonary func-
tion values for pipe and cigar smokers as compared to nonsmokers
(table 35).

Naeye (67) conducted an autopsy study on 322 Appalachian coal
workers who were classified according to the type of coal mined and
tobacco usage. Emphysema was slightly greater in cigarette smokers,
as were anatomic evidences of chronic bronchitis and bronchiolitis.
Those changes found in pipe and cigar smokers were intermediate
between those of cigarette smoking miners and nonsmoking miners.

Changes in pulmonary histology in relation to smoking habits and
age were examined by Auerbach, et al. (8). Fibrosis, alveolar rupture,
thickening of the walls of small arteries, and thickening of the walls
of the pulmonary arterioles were found to be highly related to the
smoking habits of the 1,340 male subjects examined, The 91 pipe and
cigar smokers over the age of 60 were found to have somewhat more
alveolar rupture than the men of the same age distribution who never
smoked regularly. However, pipe and cigar smokers as a group had
far less rupture than cigarette smokers. The same relations as described
above were found for fibrosis, thickening of the walls of the arterioles
and small arteries, and padlike attachinents to the alveolar septums.

Tobacco smoke has been shown experimentally to have a ciliostatic
effect on the respiratory epithelium. The interval between puffs, the

587
amount of volatile and particulate compounds in the smoke, and the
exposure volume have been shown to influence the toxic effect of
tobacco smoke. Dalhamn and Rylander (27) exposed the upper trachea
of anesthetized cats to the smoke of cigarettes and cigars, observing
the effect on ciliary activity through an incident-light microscope.
A chemical analysis of the gas and particulate phases revealed that
the cigar smoke was more alkaline and, in general, contained higher
concentrations of isoprene, acetone, acetonitrile, toluene, and total
particulate matter compared to cigarette smoke. The average number
of puffs required to arrest ciliary activity was found to be 73 for the
cigarette smoke and 114 for the cigar smoke. The difference is statisti-
cally significant (P <0.01). Of the two smokes, the smoke with the
highest concentration of volatile compounds was found to be the least
ciliostatic. This suggests that the degree of ciliotoxicity of a smoke is
not necessarily correlated to the level of one or several of the substances
found in the smoke.

Passey, et al. (70.71, 72) studied the effect of smoke from flue-cured
cigarette tobacco cigarettes and air-cured cigar tobacco cigarettes on
the respiratory system of rats. In two separate but similar experi-
ments, a total of 48 animals were exposed to English cigarette tobacco
smoke, 48 were exposed to air-cured cigar tobacco smoke, and 12 were
exposed to an air-cured Burley tobacco smoke. The rats in groups were
exposed to the specific smoke in a smoke-filled cabinet. Animals ex-
posed to the smoke. from air-cured tobaccos remained healthy through-
out the experiments, even at high levels of smoke exposure. The three
deaths that occurred within this group were from nonrespiratory
causes. In both experiments, the rats exposed to cigarette tobacco smoke
began to die within 1 or 2 months, and in each experiment most of the
animals died within a week or two of the first deaths. At autopsy the
rats exposed to flue-cured tobacco smoke on gross examination were
found to have greatly enlarged lungs, the trachea was often full of
mucus, and there was evidence of pneumonia. On microscopic examina-
tion it was found that the trachea and bronchi contained purulent
cellular exudates, evidence of metaplastic changes, an absence of cilia,
and goblet cell hpyerplasia. Typically, the cause of death was a lobar
or bronchopneumonia. The author concluded that, “the smokes of flue-
cured tobaccos are more dangerous to man and to animals than those

of air-cured tobaccos.”

588
Unfortunately, few details were published concerning the method
used to expose the animals to the different types of smoke. The fre-
quency and duration of exposure were not specified. and the extent of
actual inhalation of smoke by the different groups of rats was either
not determined or not reported. It is also difficult to determine the
effect of smoke exposure on the frequency and severity of respiratory
infections when animals are exposed to smoke in groups where common
exposure occurs. The rat strain used was not identified, but it was
noted that animals appeared to suffer from an endemic rat. bron-
chiectasis. It is not known to what extent epidemics of respiratory
infections occurred among these animals. Because of these difficulties,
no firm conclusion can be drawn concerning the effect of smoking flue-
cured or air-cured tobaccos on the incidence of respiratory infections
in rats.

TABLE 33. —Mortality ratios for chronic obstructive pulmonary deaths
im male cigar and pipe smokers. A summary of prospective epidemio-
logical studies

 

Type of smoking

 

 

Author, reference Category
Non- Cigar P Total Cigs-
smoker only only pipe and rette only Mixed
cigar
Hammond and COPD total._______ 1.00 829 L777 LL 2.85 .__..e
Horn (40). Emphysema__.---2. 2222 22-2. Lee Le. Le
Bronchitis.-.--.---22 22. 28 nee ee
Doll and Hill COPD total. 22-22 ee ee ee ee
(26, 27). Emphysema__.-.2-- _222 22-2. @2-e ee Le
Bronchitis.._______. 1.00 _.2 0) LLL Le 4.00 7.00 6.67
Best (9)... COPD total... 2-22. Lee. ee eee ee
Emphysema_______. 1.00 3.33 .75 ____. 5.85 22 _
Bronchitis._._._____ 1.00 3.57 2.11 _____ 11.42 _____.
Hammond ($8).. COPD total_._-..-. 222. 22-2. eee eee 8
Emphysema________ 1.00 L202. LLL 1.37 '°655 _._.2-
Bronchitis_._-....222 _-2. © Le pene eee
Kahn (60)______ COPD total._______ 100 .79 2.36 .99 1008 ______
Emphysema________ 100 £24 2.13 1.31 1417 _____.
Bronchitis..._______ 1.00 21.17 1.28 1.17 449 |

 

' Only mortality ratios for ages 55 to 64 re presented.

495-028 O—73-—_16

589
TasLe 34.—Prevalence of respiratory symptoms and illness by type of

 

 

smoking
Percent prevalence
Autbor, reference Number and type of Tiinass
population Noo- Total Cigs-
smoker pipe and rette Mixed
cigar only
Boake (10)_._ Parents of 59 Cough__..2-2 2. 32 32 48...
families. Sputum 24 15 20 _-.--
production.
Chest iliness______ 5 4 nn
Edwarda, et 1,737 male Chronic bronchitis. 17 19 31 14
al. (38). outpatients.
Ashford, et 4,014 male Bronchitis________ IO '35 21 37
al. (4). workers in 3. Pneumoconiosis___. 1k 6134 14 2
Scottish
collieries.
Bower ({f1)__. 95 male bank Cough... 2 Le 0 0 29 __LL_e
employees. Sputum 8 15 33 .__L_.
production.
Wheeze._.__-.___. & 31 33 LL.
Chest iliness._____ 15 54 40 _____.
Wynder, etal. 315 male pa- Cough (New 14 33 56 51
(114). tients in York).
New York Cough 22 30 67 66
and 315 male (California).
patients in Influenza (New ll 21 24 2 LLL
California. York).
influenza 28 24 3b LLL.
(California).
Chest illness 9 10 12 LLL.
(New York).
Chest illness 7 6 WLLL
(California).
Densen, et al. 5,287 male Persistent cough. . 7 11 25 22
(24). postal and Persistent 11 16 26 LL
7,213 male sputum
transit production.
workers in Dyspnea___.______ 16 19 26 _.__L-
New York Wheeze___._-._-_- 14 21 32 Le
City. Chest illness______ 13 16 18 ___L_.
Cederlof, et 4,379 twin pairs, Cough. 22.22 Le 4 7 WF _ 1.
al. (18). all U.S. Prolonged cough... 2 4 lE Llllle
veterans. Bronchitis. _._.._- 2 3 10 _.. LL.
Rimington 41,729 male Chronic bronchitis. 5 1g |
(78). volunteers.

590
TABLE 34.— Prevalence of respiratory symptoms and illness by type of

 

 

 

smoking—Continued
Percent prevalence
Autbor, references Number and type of Tiness
population Noo- Total Ciga-
smoker pipe and rette Mired
cigar only
Comstock, et 670 male tele- Persistent cough. _ 10 16 41 _.2LL.
al. (19). phone Persistent 13 20 cn
employees. sputum.
Dyspnea___.____. 33 39 44 28.
Chest illness in 14 18 20 _____-
past 3 years.
Lefcoe and 310 male phy- Chronic respira- 9 18 44 _
Wonnacott Sicians in tory disease.
(69). London, Chronic bronchitis_ 1 12 34 _..__.
Ontario. Obstructive lung 1 3 4 Lie.
disease,
Asthma____.____. 7 3 6 .. 2 -
Rhonchi.....---.- oO 3 9__--L.

 

1 Figures for pipe only.

TABLE 35.—Pulmonary function values for cigar and pipe smokers as
compared to nonsmokers

 

Type of smoking

 

 

 

Auther, reference Number and type Function
of population Non- Total pipe Cigarette Mized
smoker and cigar only

Ashford, et 4,014 male FEV, 0..----- 3.39 12,59 3.14 2.62
al. (4). workers in

3 Scottish
collieries.

Goldsmith, 3,311 active Puffmeter__.. 313.63 299.26 303.44 _..__-
et al. (37). or retired FEV).0-_.---- 2.99 2. 80 2.91 2. LL

longshore- TVC_.._____- 3. 87 3. 68 3.88 --- 22
men. _

Comstock, 670 male FEV, .c._-_--- 3.12 3. 26 2.82 ...--
et al. (19). telephone

employees.

Lefcoe and 310 male FEV, .9-__---- 3. 39 3.17 31D Lee
Wonnacott physicians MMFR liters 4.09 4.17 3.64 -.----
(89). in London, per second.

Ontario.
5 Figures for pipe only.

591
GASTROINTESTINAL D1soRDERS

Cigarette smokers have an increased prevalence of peptic ulcer
disease and a greater peptic ulcer mortality ratio than is found in
nonsmokers. These relationships are stronger for gastric ulcer than
for duodenal ulcer. Cigarette smoking appears to reduce the effective-
ness of standard peptic ulcer treatment regimens and slows the rate
of ulcer healing. Cigar and pipe smokers experience higher death
rates from peptic ulcer disease than nonsmokers. These rates are higher
for gastric ulcers than for duodenal ulcers but are somewhat less than
those rates experienced by cigarette smokers, Table 31 presents the
mortality ratios for ulcer disease in cigar and pipe smokers as reported
in the prospective epidemiological studies.

Retrospective or cross-sectional studies by Trowell (95), Allibone
and Flint (2), Doll, et al. (29), and Edwards, et al. (33) contain
data on ulcer disease in pipe smokers as well as cigarette smokers. No
association was found between pipe smoking and ulcer disease in these

investigations.

Tas_Le 36.—Afortality ratios for peptic ulcer disease in male cigar and
pipe smokers. Summary of prospective studies

Type of smoking

 

 

Author, reference Tiiness Total Cigs-
Non- Cigar Pipe pipe rette Mixed
smoker only only and only
cigar
Hammond and Ducdenal ulcer_..... 1.00 0.25 1.67 ..-__- 2.16 _-.---
liorn (40).
Doll and Hill Gastric ulcer__...__. 1.00 -...- -.--- 4.00 7.00 5.30
(26, 27).
Hammond (38).. Gastric ulcer_..----- 1.00 __--- ----- 2.04 2.95 ____--
Duodenal ulcer_____- 1.00 ___.. ----- 92 2.86 __----
Kahn (60)___..- Gastric ulcer___.---- 1.00 2.90 2.84 2.48 4.13 _.._--
Duodenal ulcer. __--- 1.00 1.58 1.59 1.39 2.98 -_.__-

 

Little Cigars

In the past year, several new brands of little cigars (weighing 3
poundsor less per 1,000) have appeared on the national market. These
cigarette-sized products are manufactured, packaged, advertised, and
sold in a manner similar to cigarettes, Little cigars enjoy several legal
advantages over cigarettes: They have access to television advertising ;
they are taxed by the Federal Government and by most States, at much
lower rates than cigarettes, resulting in a significant price advantage;

592
and they do not carry the warning label required on cigarette pack-
ages and in cigarette advertising. A market appears to be developing
for these products, as there has recently been a sharp increase in the
shipment of little cigars destined for domestic consumption (table 37).

It is important to estimate the potential public health impact of
these little cigars. An adequate epidemiological evaluation of the ef-
fect of Jittle cigar smoking on health could take 10 or 15 years and is
probablv an impractical consideration ; however, a review of the epide-
miological, autopsy, and experimental data concerning the health con-
sequences of cigarette, pipe, and cigar smoking summarized in this and
previous reports 19 helpful in considering the potential impact on
health of smoking little cigars. An analysis of the chemical constit-
uents suggests that both cigarettes and cigars contain similar com-
pounds in similar concentrations. Two exceptions are reducing sugars,
which are not found in quantity in the fermented tobaccos commonly
used in cigars, and the pH of the inhaled smoke. The pH of the smoke
from U.S. commercial cigarettes is below 6.2 from the first to the last
puff, whereas the smoke from the last half of a cigar may reach as high
as pH 8 to 9. With increasing pH, nicotine is increasingly present in
the smoke as the free base. Skin painting experiments in mice indicate
that tumor yields with cigar or pipe “tars” are nearly identical with
those obtained with cigarettes “tars”. In addition, the epidemiological
data suggest that depth of inhalation probably accounts for the fact
that cigarettes are so much more harmful than cigars and pipes in con-
tributing to the development of lung cancer, coronary heart disease,
and nonneoplastic respiratory disease. For such diseases as cancer of
the oral cavity, larynx, and esophagus, where smoke from cigars, pipes,
and cigarettes is available to the target organ at comparable levels, the
mortality ratios are very similar for all three forms of tobacco use.
Several factors, including “tar,” nicotine, and the pH of the smoke,
probably operate to influence inhalation patterns of smokers. The
relative contribution of individual factors to the inhalability of a
tobacco product has not been determined.

Smoking those brands of little cigars which can be inhaled by a
significant portion of the population in a manner similar to the pres—
ent use of cigarettes would probably result in an increased risk of de-
veloping those pulmonary and cardiovascular diseases which have
been associated with cigarette smoking. On the other hand, smoking
those little cigars which are used like most large cigars whereby the
smoke is rarely inhaled would probably result in lower rates of those
pulmonary and cardiovascular diseases than would be found among
cigarette smokers,

Only a limited analysis is available comparing the chemical com-
pounds found in little cigars, cigarettes, and large cigars. The FTC
analyzed the tar and nicotine content of all the little cigars (24) and
cigarettes (97) currently available on the market. Little cigars have

593
generally a higher “tar” and nicotine level than cigarettes, although
considerable overlap results in some little cigar brands having “tar”
and nicotine levels comparable to those of some brands of cigarettes
(figs. £ and 5). Hoffmann and Wynder (44) recently compared three
brands of little cigars with an unfiltered cigarette, a filtered cigarette,
and a large cigar. They measured a number of smoke constituents, in-
cluding: “tar,” nicotine, carbon monoxide, carbon dioxide, reducing
sugars, hydrogen cyanide, acetaldehyde, acrolein, pyridines, phenols,
benz(a)anthracene, and benzo(a)pyrene (table 32). Cigarette A was
the Kentucky reference cigarette, cigarette B was a popular brand of
filter cigarette. Cigar A was an 85 mm, little cigar, cigar B was an
85 mm. little cigar, cigar C was a 95 mm. small cigar, and cigar D was
a 112 mm. popular brand of medium sized cigar.

The smoke pH was analyzed puff by puff (table 39). Cigarette
smoke was found to be acidic (pH less than 7) for the entire cigarette.
The smoke from little cigars became alkaline only in the last puff or
two, whereas about the last 40 percent of the puffs from the larger
cigar were alkaline. Although the pH of the total condensate obtained
from cigarettes is usually acidic and the total condensate obtained
from cigars is usually alkaline, the above data indicate that smoke
pH of tobacco products changes during the combustion process. Smoke
from large cigars may be acidic during the first portion of the smoke
and not become alkaline until the last half of the cigar is smoked.

Brunnemann and Hoffmann (7/5), using the same techniques de-
scribed above, examined the effect of 60 leaf constituents on smoke pH.
For several varieties of cigarette tobacco, they found a high correlation
between the total aklaloid and nitrogen content and smoke pH. Stalk
position also affected smoke pH. Tobacco leaves near the top of the
plant, which contain high levels of tar and nicotine, yielded a smoke
with a much higher pH than leaves lower on the plant. At present it is
not known to what extent these factors influence the pH of the smoke
of tobaccos commonly used in cigars or how these kinds of pH changes
influence the inhalability of tobacco smoke.

The inhalation of smoke, however, appears to be the most important
factor determining the impact a cigar will have on overall health.
Those physical and chemical characteristics of a tobacco product
which most influence inhalation of tobacco smoke have not been
accurately determincd. Nevertheless, it appears likely that the smoke
of some brands of cigars may be compatible with inhalation by a sig-
nificant portion of the smoking population, since: (2) Little cigars
have tar and nicotine levels which, in some brands, are similar to the
levels found in cigarettes, and (6) the pH of the smoke of some little
cigar brands is acidic for the major portion of the little cigar and
becomes alkaline only in the last puff or two.

594
It is reasonable to conclude that smoking little cigars may result in
health effects similar to those associated with smoking cigarettes if
little cigars are smoked in amounts and with patterns of inhalation
similar to those used by cigarette smokers, for the reasons cited nbove,
and these additional reasons: (a) In those little cigars for which pre-
liminary data are available, the concentrations of carbon monoxide,
hydrogen cyanide, acetaldehyde, acrolein, pyridine, phenol, and poly-
cyclic hydrocarbon levels are comparable to those found in cigarettes:
(4) cigarette smokers who switch to cigars appear to be more likely
to inhale cigar smoke than cigar smokers who have always smoked
cigars (14); and (c) cigarette smokers who switch to little cigars may
be inclined to use them as they did cigarettés because of the physical
similarities between the little cigars and cigarettes, including their
size and shape, the number in a package, the burning rate, and the
time it takes to smoke them.

Figure 4.—Percent distribution of 130 brands of cigarettes and 25 brands of little cigars by

 

 

 

 

 

 

 

 

 

 

 

 

“tar’’ content.
50 f
ast 7) [Cigarettes Z 77]
40}
35} 4
. 30} q | 7]
Soa
= D 4
60 S 25} A
5 3
é |
20+ 1
15} I
4
10 J
5 i]
g
olf —n
Mg. ‘tar’ 0 0 0 16.0 8.0 32.0 32.0 0 8.0 4.0
Cigarettes O4 5-9 10-14 15-19 20-24 25-29 30-34 35-39 40-44 45-49
Little Cigars 3.1 3.1 10.0 46.2 23.1 10.0 3.9 0.8 9 0

 

SOURCE: U.S. Department of Health, Education, and Welfare (97) and Federal Trades Commission (34).

595
Figure 5.—Percent distribution of 130 brands of cigarettes and 25 brands of little
cigars by nicotine content.

 

 

 

 

 

 

 

 

 

50
Cigarettes
» Little Cigaee
40 7]
2 Y
= 3 Y
2 30
3°
iY)
e? Z
@ 20 ,
@ 15
g
10
4
5 | Y
ota al.
2 & 8s & & @ © & © F 4
; > ; > “ “ “ “ nN nN
ee i 8
si 22 284 a8 2228
Sd a 0 ~m <+
m n o n ) 2 , oO
gu oo 4 § ¢ 4a aa
<§
Sd oO o
S 2 ° ° ° 2 ° 4
ee ° 3 8 + 8 £ & ¥ OOS
o
&
eS

SOURCE: US. Department of Health, Education, and Welfare (97) and Fedaral Trade Com-
mission (34).

596
Tasie 37.—Shipment of small and large cigars destined for domestic

 

 

consumption (1970, 1971, 1972)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Year 1970 1971 1072
Small cigars

January.-220 02 58, 328, 520 85, 753, 780 123, 477, 550
February....---_) 63, 431, 580 72, 092, 205 179, 817, 839
March. .-22- 222 85, 881, 860 46, 542, 800 198, 165, 593
Aprile. 101, 613, 500 59, 059, 920 125, 335, 740
May_.--- 2 81, 093, 180 93, 237, 473 159, 334, 565
June... 82, 471, 120 94, 560, 140 180, 582, 243

Subtotal__._. 472, 819, 760 451, 246, 318 966, 713, 530
July. 62, 143, 140 70, 332, 500 127, 713, 320
August... 22-2 68, 220, 365 127, 709, 310 670, 936, 869
September_.____._____ 79, 101, 045 95, 027, 340 422, 534, 705
October___..-_- 90, 752, 880 109, 567, 900 708, 116, 830
November___.____-______ 64, 290, 600 106, 666, 107 551, 326, 888
December__.____._._ 8, 63, 806, 010 123, 809, 553 485, 587, 014

Subtotal... oo. 428, 314, 040 633, 112, 710 2, 966, 215, 626

Yearly total... 901, 133, 800 1, 084, 359, 028 3, 932, 929, 156

 

 

 

 

 

Large cigars

 

573, 039, 120
586, 810, 844
665, 998, 099
655, 850, 213
670, 064, 933
692, 436, 529

534, 565, 488
562, 414, 577
654, 827, 796
554, 242, 048
719, 489, 529
578, 501, 068

 

January... 581, 742, OOL
February...--.. 595, 249, 522
March____.._---_ 629, 977, 375
April.” 652, 800, 200
May____.--2- 748, 040, 796
June_.----e ee, 644, 539, 031

Subtotal. | 3, 852, 348, 925
July. 647, 397, 547
August.____ ween elle 673, 082, 971
September... | a 721, 561, 449
October._2- 797, 601, 253
November_...0 696, 526, 464
December_.__..--. 596, 244, 159

Subtotal... | 4, 132, 413, 843

Yearly total. __ 8, 084, 762, 763

Boures: 0.8. Department of the Treasury (101).

3, 844, 199, 738

619, 838, 386
662, 970, 148
680, 476, 418
679, 420, 968
742, 948, 802
516, 879, 415

3, 902, 534, 137

7, 746, 733, 875

3, 604, 040, 506

520, 873, 339
682, 331, 630
594, 843, 957
693, 150, 668-
650, 746, 540
437, 429, 996

3, 579, 356, 130

7, 183, 396, 636

597
TaBLe 38.—Selected compounds in mainstream smoke

 

 

Smske compound Cigarette A Cigarette 3B Little Littles Small
(nonaiter) (filter) cigar A clear B ciaar C

“Tar, milligram per cigarette___ 36. t 20, 3 17.4 31.8 40.6
Nicotine, milligram per cigarette - 2.7 14 -6 1.8 3.1
Carbon monoxide, volume per-

cent.._-_.._.--------------- 4.6 4.5 5. 3 Mi 7.7
Carbon dioxide, volume percent__ 9.4 9.6 8.3 13. 2 12.7
Reducing sugars, percent of

tobacco weight__._-_.-_----- 9.3 7.9 L5 2.9 2.7
Hydrogen cyanide, microgram

per Cigarette__.__----.-.-.-- 536.0 361.0 381.0 697.0 1,029.0
Acetaldehyde, microgram per

Cigarette_...__.------------- 770.0 774.0 630.0 1,238.0 1,150.0
Acrolein, microgram per cigar-

ette._. eee eee 105. 0 71.0 41.0 54.0 66. 0
Total pyridines, micrograms per

Cigarette... _..- 2-2-2 ------ 82.8 27.3 58. 0 85. 3 80. 3
Phenol, microgram per cigsrette_. 124.2 33. 0 35.1 63.4 94.1
Benz(s)anthracene, nanogram

per cigarette__ 22-2 2 -- 74.0 31.0 34.0 25.0 39. 0
Benzo(s)pyrene, nanogram per

cigsrette_.--- ee 47.0 20.0 18. 0 22.0 30. 0

 

Source: Hoffmann, D., Wynder, E. L. (44).

TasLe 39.—The pH of the mainstream smoke of selected tobacco products

{Numbers fu parentheses Indicate number of last puff.]

 

 

Average pH CizarettoA Cigarette B Little Little Small Cigar D
(nonfilter) (filter) cigar A clgar B cigac C
3d puff_____ 6.19 6.15 6. 44 6. 55 6. 53 6. 47
5th puff__.. 6.14 6. 12 6. 34 6. 46 6.49 _LiL--.-
7th puff... 6.09 6. 01 7.03 6. 51 6.56  _L_Lee-
9th puff___._ 6.02 5.83 __.-.--- 6. 98 6. 59 6. 27
13th puff... 2-2-e eee eee ee eee eee eee eee we ++ --- 6. 39
18th puff ee eee eee eee eee eee 6. 41
23d puff... -----e-- eee eee eee eee eee eee eee 6. 81
28th puff..§ 8 eee eee eee nee 7. 22
33d puff..-2 Lee eee eee eee eee eee eee 7. 53
38th puff..8 22 eee eee eee eee eee 7. 78
Last puff_.. 5.96(11) 5.76(10) 7.73 (8) 7.25(10) 7.11(41) 7. 96(43)

 

Source: Hoffmann, D., Wynder, FB. L. (44).

598
Conclusions

Pipe and cigar smokers in the United States as a group experience
overall mortality rates that are slightly higher than those of nonsmok-
ers, but these rates are substantially lower than those of cigarette
smokers. This appears to be due to the fact that the total exposure to
smoke that a pipe or cigar smoker receives from these products is
relatively low. The typical cigar smoker smokes fewer than five cigars
a day and the typical pipe smoker smokes less than 20 pipefuls a day.
Most pipe and cigar smokers report that they do not inhale the smoke.
Those who do inhale, inhale infrequently and only slightly. As a
result, the harmful effects of cigar and pipe smoking appear to be
largely limited to increased death rates from cancer at those sites which
are exposed to the smoke of these products. Mortality rates from
cancer of the oral cavity, intrinsic and extrinsic larynx, pharynx, and
esophagus are approximately equal in users of cigars, pipes, and ciga-
rettes. Inhalation is evidently not necessary to expose these sites to
tobacco smoke. Although these are serious forms of cancer, they account
for only about 5 percent of the cancer mortality among men.

Coronary heart disease, lung cancer, emphysema, chronic bronchitis,
cancer of the pancreas, and cancer of the urinary bladder are diseases
which are clearly associated with cigarette smoking, but for cigar and
pipe smokers death rates from these diseases are not greatly elevated
above the rates of nonsmokers. These diseases seem to depend on mod-
erate to deep inhalation to bring the smoke into direct contact with
the issue at risk or to allow certain constituents, such as carbon mon-
oxide, to be systematically absorbed through the lungs or to affect the
temporal patterns of absorption of other constituents such as nicotine
that can be absorbed either through the oral mucosa or through the
lungs. Evidence from countries where smokers tend to consume more
cigars and inhale them to a greater degree than in the United States
indicates that rates of lung cancer become elevated to levels approach-
ing those of cigarette smokers.

Available data on the chemical constituents of cigar, pipe, and
cigaretta smoke suggest that there are marked similarities in the cam-=
position of these products. Pipe and cigar smoke, however, tends to
be more alkaline than cigarette smoke, and fermented tobaccos com-
monly used in pipes and cigars contain less reducing sugars than the
rapidly dried varieties commonly used in cigarettes.

Experimental evidence suggests that little difference exists between
the tumorigenic activities of tars obtained from cigar or cigarette

599
tobaccos. Malignant skin tumors appear somewhat more rapidly and
in larger numbers in animals whose skin has been painted with cigar
tars than in those animals painted with cigarette tars.

One must conclude that some risk exists from smoking cigars and
pipes as they are currently used in the United States, but for most
diseases this 1s small compared to the risk of smoking cigarettes as they
are commonly used. Nevertheless, changes in patterns of usage that
would bring about increased exposure either through increased indi-
vidual use of cigars and pipes or increased inhalation of pipe and cigar
smoke have the potential of producing risks not unlike those now
incurred by cigarette smokers. Mechanical or chemical modifications
of pipe tobacco and cigars that would result in a smoke more compat-
ible with inhalation could have this effect.

Pipe and Cigar References

(1) ABELIN, T., GSELL, O. T. Relative risk of pulmonary cancer in cigar and
pipe smokers. Cancer 20(8) : 1288-1296. August 1967.

(2) ALumoNe, A., Fount, F. J. Bronchitis, aspirin, smoking, and other factors
in the aetiology of peptic ulcer. Lancet 2: 179-182, July 26, 1958.

(3) Agstirace, A. K., Turner, D. M. Absorption of nicotine in cigarette and
cigar smoke through the oral mucosa. Nature 226(5252) : 1231-1232,
June 27, 1970.

(4) AsHrForpD, J. R., Brown, S., DuFFierp, D. P., Sstitu, C. S., Pay, J. W. J.
The relation between smoking habits and physique, respiratory symp-
toms, ventilatory function, and radiological pneumoconiosis amongst
coal workers at three Scottish collieries. British Journal of Preventive
and Social Medicine 15: 106-117, 1961.

(5) Aversacu, O., Hasssconn, E. C., GanFinxe., L. Histologic changes in the
larynx in relation to smoking habits. Cancer 25(1) : 92-104, January 1970.

(6) Aurepacn, O., Srout. A. P., Hastmonp, E. C., GARFINKEL, L. Changes in
bronchial epithelium in relation to sex, age, residence, smoking and
pneumonia. New England Journal of Medicine 267(3) : 111-119, July 19,
1962.

(7) Aversacu, O., Strout, A. P., Hamsconp, E. C., GaRFINKEL, L. Histologic
changes in esophagus in relation to smoking habits. Archives of Environ-
mental Health 11(1): £15, July 1965.

(8) AvERBacH, O., Strout, A. P., Hasmsonp, E. C., GARFINKEL, L. Smoking
habits and age in relation to pulmonary changes. Rupture of alveolar
septumss, fibrosis and thickening of walls of smail arteries and arterioles.
New England Journal of Medicine 269(20) : 1045-1054, Nov. 14, 1963.

(9) Best, E. W. R. A Canadian Study of Smoking and Health. Ottawa, Depart-
ment of National Health and Welfare, 1966, 137 pp.

(10) Boake, W. C. A study of illness in a group of Cleveland families. XVHL
Tobacco smoking and respiratory infections. New Engtand Journal of
Medicine 259(26) : 1245-1249, Dec. 25, 1958

(11) Bower, G. Respiratory symptoms and ventilatory function in 172 adults
employed in a bank. American Review of Respiratory Diseases 83:

684-689, 1961.

600