The most serious criticism is the misclassification of the active
smoking status of the subjects, which can produce an apparent
increased risk with involuntary smoking. Moreover, it is likely to
result in differential misclassification because spouses tend to have
similar smoking habits (Burch 1981; Sutton 1981; Higgins et al.
1967). Speculation that the positive results reported in Japan and
Greece were due to cultural bias against the admission of smoking by
women in these more traditional societies may be discounted because
positive significant findings have now been observed in the United
States (Correa et al. 1983; Garfinkel et al. 1985) and in Sweden
(Pershagen et al., in press), where no comparable social stigma
exists. Moreover, in the studies by Garfinkel and coworkers (1985)
and Pershagen and coworkers (in press), the personal smoking status
of each subject was validated and verified at interview, usually by
next of kin, who presumably would have no reason to misrepresent
the true smoking status of the subject.

Misclassification of the lung as the primary site and the lack of
pathological confirmation are repeated concerns, but it must be
stressed that this bias would tend to dilute a true effect. Correa
(1983), Garfinkel (1985), and Pershagen (in press) and their respec-
tive colleagues addressed this issue by including only pathologically
confirmed lung cancers and considering histological cell type in their
analyses. In the study by Garfinkel and associates (1985), after an
independent pathological review was conducted, a significant associ-
ation of excess risk with involuntary smoking remained. Misclassifi-
cation of exposure to ETS cannot be dismissed, since an index based
solely on the smoking habits of a current spouse may not be
indicative of past exposure, cumulative exposure, or the relevant
dose to the respiratory tract.

The magnitude of risk associated with involuntary smoking
exposure is uncertain. Relative risks ranging from 2 to 3 were
generally reported for the highest level of exposure based on the
spouses’ smoking habits, but since sample sizes in most studies are
not large, the point estimates of effect are unstable, and confidence
limits are broad and generally overlap from one study to another. An
index of involuntary smoking based on the smoking habits of the
spouse is a simplistic and convenient measure. There is no reason to
believe, however, that the excess risk associated with involuntary
smoking is restricted to exposure from spouses. Nonsmokers married
to smokers are likely to be more tolerant of ETS exposure and to
experience more exposure to environmental tobacco smoke (Wald
and Ritchie 1984). Higher risk estimates for involuntary smoking
have been obtained in studies restricted to squamous cell and small
cell carcinomas of the lung.

Although involuntary smoking can be established as a cause of
lung cancer, important questions related to this exposure require

101
further research. More accurate estimates for the assessment of
exposure in the home, workplace, and other environments are
needed. Studies of sufficiently large populations should also be
performed. New data from such studies should yield more certain
risk estimates and describe the magnitude of the lung cancer risk in
nonsmokers.

Other Cancers

Several recent studies provide data on the relationship of ETS
exposure to cancer at sites other than the lung. Two published
reports address the risk of other cancers in adults from exposure to
tobacco smoke from spouses. Using the same Japanese cohort
described previously, Hirayama (1984a) reported excess mortality for
cancers of the paranasal sinus (N=28) and brain (N=34) among
nonsmoking women who were married to smokers. The standardized
mortality ratios (SMRs) for nasal sinus cancer were 1.00, 1.67, 2.02,
and 2.55 for women whose husbands never smoked, or had smoked
10 to 14, 15 to 19, or 20 or more cigarettes per day, respectively (one-
sided p for trend, 0.03). The corresponding SMRs for brain tumors
were 1.00, 3.03, 6.25, and 4.32, respectively (one-sided p for trend,
0.004). The total number of deaths due to nasal cancer and brain
tumors was small, and the numerators in the risk calculations were
unstable, based on five nasal cancers and three brain cancers in
women whose husbands were nonsmokers. In one study (Brinton et
al. 1984), active tobacco smoking was associated with an increased
risk of sinus cancer, particularly squamous cell tumors. Sidestream
smoke has also been suggested to be of etiological importance in
brain tumors in children (Preston-Martin et al. 1982).

In a case-control study of adult cancers in relation to childhood
and adult exposure to involuntary smoking, Sandler and coworkers
(1985a, 1986) reported an overall cancer risk of 1.6 (95 percent CL.
1.2, 2.1) associated with exposure to spouses’ smoking, which was
more marked in nonsmokers than smokers. Significant increases
were observed for cancer of the breast (OR 1.8), cervix (OR 1.8), and
endocrine organs (OR 3.2). This study has been criticized in its choice
of controls and in the exclusion of certain cancers by the design of
the study. The biological plausibility of the study’s findings was also
questioned because the highest risk estimates were observed for
cancers that have not been consistently related to active smoking
and because higher risks were observed for nonsmokers than for
smokers. Failure to control for potential confounding factors and
known risk factors for the individual cancer sites under study may
have produced artifactual results (Friedman 1986; Mantel 1986;
Burch 1986). In a subsequent analysis of the same study population,
Sandler, Wilcox, and Everson (1985a,b) reported increasing cancer

102
risks with increasing exposure to involuntary smoking as measured
by the number of smokers in the household and by the time periods
of exposure. The biologic plausibility of these findings was also
questioned (Burch 1985; Higgins 1985; Lee 1985).

The effect of parental smoking on the development of cancers both
during childhood and in adult life is also of interest. The relationship
of parental smoking to overall cancer risk in children or in adults
has been assessed in three studies. A prospective survey (Neutel and
Buck 1971) of about 90,000 infants in Canada and the United
Kingdom followed for a maximum of 10 years found an overall
cancer risk of 1.3 (95 percent C.I. 0.8, 2.2) associated with maternal
smoking during pregnancy. No dose-response relationship was
observed, but there were few heavy smokers (>1 pack/day) in this
study. A Swedish case-control study (Stjernfeldt et al. 1986) of all
cancers found a risk of 1.4 (95 percent C.I. 1.0, 1.9) for maternal
smoking during pregnancy. A dose-response relationship was dem-
onstrated; the risk was highest in the most exposed group, those
smoking 10 or more cigarettes per day (RR 1.6, p< 0.01). On the basis
of the smoking habits of the parents of subjects up to 10 years of age,
Sandler, Everson, Wilcox, and Browder (1985) reported no significant
difference between all cancer cases and controls with respect to the
mother’s smoking (RR 1.1, 95 percent C.L. 0.7, 1.6), but the father’s
smoking was related to an overall increased risk (RR 1.5, 95 percent
C.l. 1.1, 2.0). In these three studies, analysis by specific cancer site
revealed an increased risk of leukemia associated with parental
smoking.

Neutel and Buck (1971) found an almost twofold increased risk of
leukemia in children of mothers who smoked during pregnancy, but
the association was not statistically significant. Stjernfeldt and
colleagues (1986) reported a significant positive association between
maternal smoking and acute lymphoblastic leukemia. The relative
risks were 1.0, 1.3, and 2.1 (p for trend, <0.01) for mothers who
smoked 0, 1 to 9, and 10 or more cigarettes per day, respectively.
Similar significant positive associations with maternal smoking were
not observed for other cancer sites, but the risk assessments were
based on a small number of cases. This study suggests that the
relationship between maternal smoking and leukemia was strongest
for smoking during the 5-year period before pregnancy, intermediate
for smoking during pregnancy, and lowest for smoking after
pregnancy. In the study by Sandler, Everson, Wilcox, and Browder
(1985), the mother’s smoking and the father’s smoking were sepa-
rately and jointly associated with an increased risk for leukemia and
lymphoma. The relative risk was 1.7 when one parent smoked and
4.6 when both parents smoked (p for trend, <0.001). The increased
risk with parental smoking was observed regardless of the personal
smoking status of the subject. No other cancer site was associated

103
with the mother’s smoking, although the father’s smoking was
associated with increased risks for other cancer sites, including the
brain and the cervix. Two studies of leukemia in children found no
relationship with parental smoking (Manning and Carroll 1957; Van
Steensel-Moll et al. 1985). In the study by Manning and Carroll
(1957), the mothers’ general smoking habits were assessed, whereas
Van Steensel-Moll and colleagues (1985) obtained information on the
smoking habits of both parents in the year before the pregnancy.
Stewart and colleagues (1958) reported a statistically significant risk
of 1.1 (p=0.04) for leukemia in association with the mothers’
smoking, but cautioned that the smoking information on the
mothers pertained to their habits at the time of interview, which
took place after the deaths of the patients and may have been
affected by bereavement.

The effect of parental smoking habits has been examined in
epidemiological studies of brain tumors, rhabdomyosarcoma, and
testicular cancer in children. Gold and colleagues (1979) reported an
association between maternal smoking prior to and during pregnan-
cy and brain tumors in children. A relative risk of 5.0 (p=0.22) was
found, but the result was based on a small number of patients and
was not statistically significant. No relationship between maternal
smoking during pregnancy (RR 1.1, one-sided p=0.42) and brain
tumors in children was found in another study (Preston-Martin et al.
1982), but a significantly increased risk (RR 1.5, one-sided p=0.03)
associated with mothers living with a smoker (usually the child’s
father) during pregnancy was observed. A significantly increased
risk with the father’s smoking, but not the mother’s smoking was
also reported in a study of rhabdomyosarcoma (Grufferman et al.
1982). The father’s smoking conferred a significant increase in risk
(RR 3.9, 95 percent C.I. 1.3, 9.6), but the mother’s smoking during
and after the pregnancy was not significantly different between
cases and controls (RR 0.8, 95 percent C.I. 0.3, 2.0). A history of
maternal smoking during pregnancy did not differ for testicular
cancer cases and controls (RR 1.0, p=0.57) in one study (Henderson
et al. 1979).

There are at present insufficient data to adequately evaluate the
role of involuntary smoking in adult cancers other than primary
carcinoma of the lung. In addition, active smokers necessarily
receive greater exposure to ETS than nonsmokers. Thus, effects
would not be anticipated in involuntary smokers that do not occur in
active smokers (IARC 1986), and the biological plausibility of
associations between ETS exposure and cancer of sites not associated

with active smoking must be questioned. The findings of Hirayama
(1984a) and Sandler, Everson, and Wilcox (1985) need confirmation
in studies that take into account the potential confounding factors
and the known risk factors for these individual sites. The evidence

104
for parental smoking and childhood cancer is also not clear, and
evaluation of this association is made difficult by the various
definitions of exposure that have been used, including maternal and
paternal smoking before, during, and after the pregnancy. Mothers
and fathers who smoke during a pregnancy generally smoked before
the conception and continue to smoke after the pregnancy. Thus, an
effect of involuntary smoking after birth cannot readily be distin-
guished from genetic or transplacentally mediated effects.

Cardiovascular Diseases

A causal association between active cigarette smoking and cardio-
vascular disease is well established (US DHHS 1983). The relation-
ship between cardiovascular disease and involuntary smoking has
been examined in one case-control study and three prospective
studies. In the case-control study by Lee and colleagues (1986),
described previously, ischemic heart disease cases and controls did
not show a statistically significant difference in their exposure to
involuntary smoking, based on the smoking habits of spouses or on
an index accounting for exposure at home, at work, and during
travel and leisure. In the Japanese cohort study, Hirayama (1984b,
1985) reported an elevated risk for ischemic heart disease (N=494) .
in nonsmoking women married to smokers. The standardized
mortality ratios when the husbands were nonsmokers, ex-smokers or
smokers of 19 or more cigarettes per day, and smokers of 20 or more
cigarettes per day were 1.0, 1.10, and 1.31, respectively (one-sided p
for trend, 0.019).

In the Scottish followup study (Gillis et al. 1984), nonsmokers not
exposed to tobacco smoke were compared with nonsmokers exposed
to tobacco smoke with respect to the prevalence of cardiovascular
symptoms at entry and mortality due to coronary heart disease.
There was no consistent pattern of differences in coronary heart
disease or symptoms between nonsmoking men exposed to tobacco
smoke and their nonexposed counterparts. Nonsmoking women
exposed to tobacco smoke exhibited a higher prevalence of angina
and major ECG abnormality at entry, and also a higher mortality
rate for all coronary diseases. However, rates of myocardial infarc-
tion mortality were higher for exposed nonsmoking men and women
compared with the nonexposed nonsmokers. The rates were 31 and 4
per 10,000, respectively, for the nonexposed nonsmoking men and
women, and 45 and 12 per 10,000, respectively, for the exposed
nonsmoking men and women. None of the differences were tested for
statistical significance.

In the Japanese and the Scottish studies, other known risk factors
for cardiovascular diseases, i.e., systolic blood pressure, plasma
cholesterol, were not accounted for in the analysis.

105
In a study of heart disease, Garland and coworkers (1985) enrolled
82 percent of adults aged 50 to 79 between 1972 and 1974 in a
predominantly white, upper-middle-class community in San Diego,
California. Blood pressure and plasma cholesterol were measured at
entry, and all participants responded to a standard interview that
asked about smoking habits, history of heart disease, and other
health-related variables. Excluding women who had a previous
history of heart disease or stroke or who had ever smoked, 695 |
currently married nonsmoking women were classified by their
husbands’ self-reported smoking status at enrollment. After 10 years
of followup, there were 19 deaths due to ischemic heart disease; the
age-standardized mortality rates.for nonsmoking wives whose hus-
bands were nonsmokers, ex-smokers, and current smokers were 1.2,
3.6, and 2.7, respectively (one-sided p for trend, <0.10). After
adjustment for age, systolic blood pressure, total plasma cholesterol,
obesity index, and years of marriage, the relative risk for death due
to ischemic heart disease for women married to current or former
smokers at entry compared with women married to never smokers
was 2.7 (one-sided p <0.10).

The study’s findings are not convincing from the point of view of
sample stability. The total number of deaths due to ischemic heart
disease was small, and the denominator in the relative risk
calculation is unstable, based on the deaths of two women whose
husbands had never smoked. Moreover, it is well established that the
risk of coronary heart disease is substantially lower among those
who have stopped smoking (US DHHS 1988), although the amount of
time required for this change after cessation of smoking is not clear
(Kannel 1981). In this study, 15 of 19 deaths occurred in nonsmoking
women married to husbands who had stopped smoking at entry, and
the age-standardized rate for ischemic heart disease was highest in
this group. The high proportion of deaths in nonsmoking women
married to men who became ex-smokers implies that the excess
resulted from a sustained effect of involuntary smoking. More
detailed characterizations of exposure to ETS and specific types of
cardiovascular disease associated with this exposure are needed
before an effect of involuntary smoking on the etiology of cardiovas-
cular disease can be established.

One study (Aronow 1978a,b) suggested that involuntary smoking
aggravates angina pectoris. This study was criticized because the end
point, angina, was based on subjective evaluation, and because other
factors such as stress were not controlled for (Coodley 1978; Robinson
1978; Waite 1978; Wakehan 1978). More important, the validity of
Aronow’s work has been questioned (Budiansky 1983).

106
Conclusions

1. Involuntary smoking can cause lung cancer in nonsmokers.

2. Although a substantial number of the lung cancers that occur
in nonsmokers can be attributed to involuntary smoking, more
data on the dose and distribution of ETS exposure in the
population are needed in order to accurately estimate the
magnitude of risk in the U.S. population.

3. The children of parents who smoke have an increased frequen-
cy of hospitalization for bronchitis and pneumonia during the
first year of life when compared with the children of nonsmok-
ers.

4. The children of parents who smoke have an increased frequen-
cy of a variety of acute respiratory illnesses and infections,
including chest illnesses before 2 years of age and physician-
diagnosed bronchitis, tracheitis, and laryngitis, when com-
pared with the children of nonsmokers.

5.Chronic cough and phlegm are more frequent in children
whose parents smoke compared with children of nonsmokers.
The implications of chronic respiratory symptoms for respirad
tory health as an adult are unknown and deserve further
study.

6. The children of parents who smoke have small differences in
tests of pulmonary function when compared with the children
of nonsmokers. Although this decrement is insufficient to
cause symptoms, the possibility that it may increase suscepti-
bility to chronic obstructive pulmonary disease with exposure
to other agents in adult life, e.g., active smoking or occupation-
al exposures, needs investigation.

7. Healthy adults exposed to environmental tobacco smoke may
have small changes on pulmonary function testing, but are
unlikely to experience clinically significant deficits in pulmo-
nary function as a result of exposure to environmental tobacco
smoke alone.

8. A number of studies report that chronic middle ear effusions
are more common in young children whose parents smoke than
in children of nonsmoking parents.

9. Validated questionnaires are needed for the assessment of
recent and remote exposure to environmental tobacco smoke in
the home, workplace, and other environments.

10. The associations between cancers, other than cancer of the
lung, and involuntary smoking require further investigation
before a determination can be made about the relationship of
involuntary smoking to these cancers.

11. Further studies on the relationship between involuntary
smoking and cardiovascular disease are needed in order to

107
108

determine whether involuntary smoking increases the risk of
cardiovascular disease.
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CHAPTER 3

ENVIRONMENTAL TOBACCO
SMOKE CHEMISTRY
AND
EXPOSURE OF NONSMOKERS
CONTENTS

Introduction
Laboratory Smoking
Human Smoking

 

 

Sidestream Smoke
Formation and Physicochemical Nature
Chemical Analysis

 

Radioactivity of Tobacco Smoke

 

Environmental Tobacco Smoke

 

Comparison of Toxic and Carcinogenic Agents in Main-
stream Smoke and in Environmental Tobacco Smoke

 

Number and Size Distribution of Particles in Environ-
mental Tobacco Smoke

 

Estimating Human Exposure to Environmental Tobacco
Smoke
Time-Activity Patterns
Temporal and Spatial Distribution of Smokers

 

Determinations of Concentration of Environmental
Tobacco Smoke
Microenvironmental Measurements of Concentration
Monitoring Studies

 

Conclusions

 

References

123
Introduction

The physicochemical nature of environmental tobacco smoke
(ETS) is governed by the type and form of the tobacco product or
products burned, by the prevailing environmental conditions, and by
secondary reactions. Mainstream smoke (MS) is the complex mixture
that exits from the mouthpiece of a burning cigarette, cigar, or pipe
when a puff is inhaled by the smoker. Sidestream smoke (SS) is
formed between puff-drawings and is freely emitted into the air
surrounding a smoldering tobacco product. Sidestream smoke repre-
sents the major source for ETS. The exhaled portions of MS and the
vapor phase components that diffuse through the wrapper into the
surrounding air constitute minor contributors to ETS.

In the scientific literature, the terms “passive smoking,” “involun-
tary smoking,” and “inhalation of ETS” are frequently used inter-
changeably (US DHEW 1979; US DHHS 1982, 1984).

Laboratory Smoking

Data on the composition of MS and SS originate from laboratory
studies. For such studies, cigarettes, cigars, or pipes are smoked by
machines under standardized reproducible conditions. It is a major
goal of these measurements to compare the yields of the specific
components in the MS or SS or both of a variety of experimental or
commercial tobacco products and to simulate, though not to repro-
duce, human smoking habits. The most widely used standard
conditions for machine smoking cigarettes and little cigars (< 1.5 g)
are one 35 mL puff of 2-second duration drawn once a minute to a
butt length of 23 mm, or the length of the filter tip plus the overwrap
plus 3 mm (Brunnemann et al. 1976). The annual reports of the U.S.
Federal Trade Commission on the tar, nicotine, and carbon monox-
ide content of the smoke of U.S. commercial cigarettes are based on
these laboratory smoking conditions. For cigars, the standard
smoking conditions are a 20 mL puff of 1.5-second duration taken
once every 40 seconds, and a butt length of 33 mm (International
Committee for Cigar Smoke Study 1974). The most frequently used
pipesmoking conditions call for the bowl to be filled with 1 g of
tobacco and a 50 mL puff of 1-second duration to be taken every 12
seconds (Miller 1964).

A number of devices for collecting sidestream smoke have been
developed (Dube and Green 1982). The most widely used device is a
collection apparatus made of glass and cooled by water circulating
through an outer jacket. The air entering the chamber through a
distributor has a flow rate of 25 mL per second (4.5 L/min)
(Brunnemann and Hoffmann 1974). Under these conditions, the
yields of mainstream smoke components from a cigarette approxi-
mate those obtained from the same cigarette when it is being smoked

125