uan
Nonsmokers
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For Publication in ENVIRONMENT INTERNATIONAL, Pergamon Press, circa April, 1985.
QUANTITATIVE ESTIMATE OF NONSMOKERS' LUNG CANCER RISK FROM PASSIVE SMOKING
J.L. Repace'
Environmental Protection Agency
Washington, DC 20460
A.H. Lowrey'
Naval Research Laboratory
Washington, DC 20375
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ABSTRACT
This work presents a quantitative assessment of nonsmokers' risk of lung
cancer from passive smoking. The estimates given should be viewed as preliminary
and subject to change as improved research becomes available. It is estimated that
U.S. nonsmokers are exposed to from 0 to 14 milligrams of tobacco tar per day, and
that the typical nonsmoker is exposed to 1.4 milligrams per day. A phenomeno-
logical exposure-response relationship is derived, yielding 5 lung cancer deaths
per year per 100,000 persons exposed, per milligram daily tar exposure. This
relationship yields lung cancer mortality rates and mortality ratios for a U.S.
cohort which are consistent to within 5% with the results of both of the large
prospective epidemiological studies of passive smoking and lung cancer in the
U.S. and Japan.
Aggregate exposure to ambient tobacco smoke is estimated to produce about 5000
lung cancer deaths per year in U.S. nonsmokers aged 2. 35 years, with an average
loss of life expectancy of 17 +_ 9 years per fatality. The estimated loss of life
expectancy for the most-exposed passive smokers appears to be about 2/3 of that
reported for pipe smokers and 1/2 of that for cigar smokers. Mortality from
passive smoking is estimated to be about two orders of magnitude higher than that
estimated for carcinogens currently regulated as hazardous air pollutants under
the federal Clean Air Act.
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1.
INTRODUCTION \
Exposure of nonsmokers to indoor air pollution from tobaoco smoke (also known
as involuntary or passive smoking) has recently become a public health concern
(USSG, 1982) for several reasons: such exposure is widespread (Repace and Lowrey
1980; Friedman, et al. 1983); studies of the effects of tobacco smoke on smokers
worldwide have implicated it as the most important cause of lung cancer (USSG, 1982;
Doll and Peto, 1981); existence of a threshold for carclnogenesis is doubtful (USSG
1982; IRLG, 1979; USEPA, 1979a; IARC, 1979; Pitot, 1981), and there is suggestive new
evidence of lung cancer (and other serious health effects) in nonsmokers exposed
to ambient concentrations of tobacco smoke. (Trichopoulos, 1981; 1983; Hirayama,
1981a; 1981b; 1983a; 1983b; Garfinkel, 1981; Correa et al., 1983; Knoth et al.,
1983; Gillis et al.., 1983; Koo, et al. , 1983; Kabat and Wynder, 1984; Miller, 1984;
Sandier, et al., a; b, in press)
There are three important fractions of tobacco smoke: mainstream smoke,
which the smoker inhales directly into the lung; exhaled mainstream smoke, that
fraction of the mainstream smoke which is not retained in the lungs of the smoker,
and sidestream smoke, that fraction of tobacco smoke emanating directly from the
burning end of the cigarette into the air. Nonsmokers are commonly exposed to
tobacco combustion products in diluted sidestream and exhaled mainstream tobacco
smoke from cigarettes, cigars, and pipes (Repace and Lowrey, 1980). Tobacco smoke
contains 60 known or suspect carcinogens, including 51 in the phase containing
particulate matter; the carcinogenic activity of tobacco smoke appears to require
this phase(USSG, 1982). Animal bioassays indicate that sidestream tobacco tar is
more carcinogenic per unit weight than mainstream tar (USSG, 1982). For public
health purposes, it will be assumed that mainstream and sidestream smoke have
similar human carcinogenic potency.
In his 1982 report on cancer and smoking (USSG, 1982), the U.S. Surgeon
General asserted that despite the incompleteness of the evidence, nonsraokers
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should avoid exposure to second-hand smoke to the extent possible, a risk-management
judgement supported by the World Health Organization and the National Academy of
Sciences (TOO, 1979; NRC, 1981).
This raises the question of whether the quantity of tobacco tar to which the
average nonsmoker is exposed creates a significant risk of lung cancer. In order to
answer this question, a quantitative risk assessment is first justified and then
performed. Risk assessment is the use of science to define the health effects of
exposure of individuals or populations to hazardous materials or situations (NRC,
1983): Risk assessments contain some or all of the following four steps: (1).
Hazard identification — the determination of whether a particular chemical is or
is not causally linked to certain health effects. (2). Dose-response assessment —
the determination of the relation between the magnitude of exposure and the
probability of occurrence of the health effects in question. (3). Exposure
assessment — the determination of the extent of human exposure before or after
application of regulatory controls. (4). Risk characterization — the description
of the nature and often the magnitude of the human risk, including attendant
uncertainty. In other words, quantitative risk assessment deals with the question
of how much morbidity and mortality an agent is likely to produce given specified
levels of exposure. Typically utilized in the regulation of carcinogens, it is
important because control efforts cannot proceed without assurance that the
health gains are worth the costs (Lave, 1983; Albert, 1983). On the basis of
such assessments, informed risk management judgements can be made.
This work draws upon the epidemiology of lung cancer (USSG, 1982; Pitot, 1981;
USSG, 1979; Ives, 1983) and on indoor air pollution physics (Repace and Lowrey, 1980;
1982; NRC, 1981) to produce a risk analysis (IRLG, 1979; USEPA, 1979a; Lave, 1983;
COST, 1983; Fischoff, et al., 1981; NRC, 1983) in which nonsmokers' lifestyles
are correlated to exposure to airborne tobacco tar, and incidence of lung cancer.
This analysis first reviews estimates of the average exposure of the general
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population to ambient tobacco smoke. Second, it reviews studies linking tobacco-
related disease in nonsmokers to exposure-related variations in^ lifestyle.
Third, it couples these two factors to develop a phenomenological estimate for
the aggregate lung cancer risk to the U.S. nonsmoking population, and develops an
exposure-response relationship for the estimation of the risk to the most-exposed.
Fourth, it compares the estimated level of lung cancer mortality and resultant
loss of life expectancy from passive smoking to those from cigarette, pipe, and
cigar smoking. Fifth, it compares the predictions of alternate exposure-response
relationships with the results of two large prospective epidemiologic studies of
passive smoking and lung cancer, and performs a sensitivity analysis. Finally,
this work compares the estimated risk from ambient tobacco smoke to that from
various airborne carcinogens currently being regulated in the U.S. as hazardous
air pollutants, to place the significance of the estimated risk in perspective.
VARIATION OF EXPOSURE WITH LIFESTYLE
In earlier work (Repace and Lowrey, 1980; 1982; 1983; 1984; Repace, 1981;
1982; 1983; 1984; in press; Repace et al., 1980; 1984; Bock et al., 1982) factors
affecting nonsmokers1 exposures to tobacco smoke were studied, and field surveys
of the levels of respirable particles were conducted indoors and out, in both
smoke-free and smoky environments. This work established that ambient tobacco
smoke imposed significant air pollution burdens on nonsmokers, and, using control-
led experiments (Repace and Lowrey, 1980; 1982; 1983), a model was developed
to estimate those exposures. This model predicts that the exposure of U.S.
nonsmokers ranges from 0 to 14 mg of cigarette tar per day (mg/d), depending upon
the nonsmoker's lifestyle. As derived in Appendix A and shown in Table 1, the
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average population exposure for adults of working age, averaging over the work
and home micr©environments, is about 1.43 rag/d (Repace and Lowrey, 1983) with an
86Z exposure probability. Table 1, derived from the model in appendix A,
estimates probability-weighted exposure to the particulate phase of ambient
tobacco smoke for a typical U.S. adult nonsmoker. Exposures received in other
(Repace et al., 1980) indoor microenvironments, outdoors, and in transit, which
account for the remaining 127. of people's time, were omitted. Table 1 is
derived from considerations that ambient concentrations of tobacco tar have been
found to be directly proportional to the smoker density and inversely propor-
tional to the ventilation rate.(Repace and Lowrey, 1980) Ventilation rate tables
given by ASHRAE (1981), can be used to estimate both the range in ventilation
rate (from the design mechanical rates) and smoker density (from the design
occupancies), and thus upper and lower bounds and average concentrations for
model workplace and home microenvironments can be estimated. Table 1 suggests
that individuals receiving exposure both at home and at work constitute a high
exposure group, with the workplace appearing four times as strong a source of
exposure as the home; the reason for this differential is the generally higher
occupancy (i.e., smoker density) encountered in the workplace (Repace and Lowrey,
1982, ASHRAE, 1981). This estimate of exposures represents a modeled weighted
average taken over the entire population, including those who are not exposed.
Jarvis and Russell (in press), in a study of urinary cotinine (a nicotine
metabolite) in a sample of 121 self-reported nonsmokers, state that only 12Z of
subjects had undetectable cotinine levels, despite nearly 502 reporting no passive
smoke exposure. Matsukura (1984), in a study of 472 nonsmokers, examined the
relationship of urinary cotinine to the smokiness of their environment, and found
that nonsmokers who lived or worked with smokers had higher cotinine levels than
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those who did not. Matsukura et al (1984) also found that cotinine levels increa-
sed with the number of smokers present In the home and the workplace, although
none of the differences were statistically significant except the lowest urinary
cotinine level of the nonsmokers who were not exposed to tobacco smoke in the
home or the workplace. These studies respectively illustrate the widespread
exposure of nonsmokers to ambient tobacco smoke, and the relative importance of
the domestic and workplace microenvironments in such exposures.
EPIDEMIOLOGICAL EVIDENCE FOR THE VARIATION OF RISK WITH LIFESTYLE
PULMONARY EFFECTS
White and Froeb (1980) evaluated the effect of various degrees of long-term
(>20 yrs) workplace exposure to tobacco smoke on 2100 healthy middle-aged workers.
Of the workers, 83% held professional, managerial, or technical positions, while
the remaining 17% were blue collar workers. Relative to those not exposed at home
or at work, passive smokers of both sexes suffered statistically significant
declines in mid- and end-expiratory flow rates which averaged about 13.5 percent
and 22 percent respectively, and did not differ significantly from the values
measured in noninhaling or light smokers of cigarettes, pipes, and cigars. They
concluded that chronic exposure to tobacco smoke In the work environment reduces
small airways function to the same extent as smoking 1 to 10 cigarettes per day.
Kauffmann et al. (1983) compared pulmonary function in about 3800 people in
France: 849 male "true" nonsmokers (defined as those not exposed at home) 165
male passive smokers (defined as those exposed at home), 826 female "true" non-
smokers, and 1941 female passive smokers. The authors restricted the analysis to
subjects aged 40 years or older (I.e., to those who had been exposed for 15 or
more years to smoking by their spouses) and who were living In households with no
persons over the age of 18 years except their spouses. They found that nonsmoking
subjects of either sex whose spouses were current smokers of at least 10 g (about
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10 cigarettes) of tobacco a day had mid-expiratory flow rates averaging 11.52
lower than those married to nonsmokers. For women in social classes with the
highest percentage of paid work, the effect of workplace smoking appeared to
confound the effect of passive smoking at home. However, in the large subgroup
of women without paid work (i.e., not exposed to workplace smoking), a clear
dose-response relationship to amount of husbands' smoking was observed. They
concluded that women living with heavy smokers appeared to have the oaiae reduc-
tions in mid-expiratory flow rates as light smokers, and that after 15 years
exposure in the home environment, passive smoking reduces pulmonary function.
A third study by Kasuga (1983) of urinary hydroxyproline-to-creatinlne (HOP-r)
ratios as a function of passive smoking status showed that HOP-r levels In nonsmo-
king wives and children varied in a dose-response relationship with husbands and
parental smoking habits, when adjusted for pre-existing respiratory disease.
Kasuga (1983) asserts that HOP-r serves as a marker to detect deleterious
active or passive smoking effects on the lung, before and after the manifestation
of clinical symptoms, and that urinary HOP-r in light smoking women is almost
equivalent to HOP-r in nonsmoking wives with heavy smoking husbands.
These three epidemlologic studies provide evidence that variations in the ex-
posure of adult nonsmokers to ambient tobacco smoke at home and particularly,
at work, can produce observable pulmonary effects. Like effects have been observed
in children exposed at home (Tager et al., 1983).
CANCER
Thirteen epidemiologlc studies have explicitly examined the lung cancer risk
incurred by the nonsmoking spouses of cigarette smokers. In all but one study, the
only exposure variable was the strength of the spouse's smoking habit. The
studies were conducted in Greece (Trlchopoulos et al., 1981; 1983), Japan (Hirayama,
1981a; 1981b; 1983a; 1983b), the U.S. (Garfinkel, 1981; Correa, et al., 1983;
Rabat and Wynder, 1984; Miller, 1984; Sandier, et al. a and b, in press), Germany
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(Knoth et al., 1983), Scotland (Gillis, et al., 1983), and Hong Kong (Chan and Fung,
1982; Koo, et al., 1983).
In the Greek study, Trichopoulos et. al. (1981, 1983) used the case-control
technique: involuntary exposure to cigarette smoke as measured by the husbands'
daily consumption was found to Increase the average risk of lung cancer by a
factor of 2.4 (p<0.01) when 77 lung cancer patients were compared to 225 controls,
and a dose-response relationship was observed. Divorce, remarriage, husband's
death, and change in smoking habits were considered.
In the Japanese study (1966-1981) of lung cancer in 91,540 nonsmoking women,
Hirayama (1981a, 1981b, 1983a, 1983b) used the prospective technique: relative to
those women not exposed at home (controls), involuntary exposure of wives of
smokers was found to increase the average risk of lung cancer by a factor of 1.78
(p<0.001), where the exposure was also estimated from husbands' daily consumption.
The annual lung cancer death (LCD) rate in the controls was 8.7 per 100,000.
Hirayama found that the exposed wives experienced an average annual increase in
lung cancer mortality rate of 6.8 per 100,000, with a range of from 5.3 to 9.4
per 100,000, in a dose-response relationship depending upon the degree of the
husband's smoking. Hirayama found further that the risk of lung cancer death in
nonsmoking women increased both with the time of exposure and number of cigarettes
smoked daily by the husband. Hirayama also reported a factor of 2.9 (jf 0.3, at
the 95% conf. level) for increased risk of lung cancer in 1010 nonsmoking
husbands with smoking wives. More recently. Hirayama extended his earlier work
to suggest increased risk of nasal sinus cancer, and ischemic heart disease in
passive smokers, and evidence of decreased lung cancer risk in nonsmoking wives
of exsmokers. With respect to cancer of the para-nasal sinuses in nonsmoking
wives (n=28) , Hirayama found standardized mortality ratios of 1.00, 2.27, 2.56,
and 3.44 when husbands were non-smokers, smokers of 1-14, 15-19, and >20 cigarettes
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per day respectively (p = 0.01). For ischemlc heart disease, risk elevations for
nonsmoking wives (n=494) with the extent of husbands' smoking were reported, with
standardized mortality ratios of 1.00, 1.10, and 1.31 when husbands were non-smo-
kers, smokers of 1-19, and >20 cigarettes per day respectively (p<0.02). For lung
cancer, the standardized mortality ratio of lung cancer In non-smoking women
(n=200) was 1.00, 1.36, 1.42, 1.58, and 1.91 when husbands were non-smokers,
ex-smokers, dally smokers of 1-14, 15-19, and >20 cigarettes/day, respectively.
In the first U.S. study, Garflnkel (1981) reported results from an analysis of
data collected from the American Cancer Society's (ACS) prospective study of lung
cancer risk in 176,739 nonsmoking white women (1960 to 1972) as a function of
involuntary exposure as indicated by their husbands' cigarette consumption. 72%
of the nonsmoking women were married to smokers. Three smoking categories were
identified: none, less than a pack (20 cigarettes) per day, or greater than a
pack per day. Garfinkel reported statistically insignificant risk ratios of
1.00, 1.27, and 1.10 respectively for the three categories (average 1.20 over
the exposed categories). Also reported were age-standardized death rates, which
were respectively 13.8, 12.9, and 13.1 lung cancer deaths per 100,000 person-years
for this cohort in 1960-1964, 1964-1968, and 1968-1972 (average 13.3 per 100,000
person-years for the period 1960-1972). The death rates were standardized to the
distribution of white men and women combined for the U.S. population in 1965,
which decreased the rates for females "slightly".
More recently, Correa, et al. (1983), studied 8 male and 22 female nonsmoking
lung cancer cases and 180 male and 133 female controls as part of a larger study
including smokers, with 1338 lung cancer cases and 1393 controls, in Louisiana.
They reported that nonsmokers married to heavy smokers had an increased risk of lung
cancer, as did smokers whose mothers smoked. Men with smoking wives had a nonsig-
nificant risk ratio of 2.0 compared to their counterparts with nonsmoking wives,
and women with smoking husbands had an average risk ratio of 2.07 (p<0.05) compared
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to women with nonsmoking husbands. An exposure-response relationship was observed,
with the peak risk reaching 3.52 (p<0.05). The combined data for men and women
passive smokers was significant (p<0.05) for the heavier smoking category (_>_ 41
pack-years).
A third U.S. case-control study, by Kabat and Wynder (1984), reported on
passive smoking and lung cancer in nonsmokers for 25 male cases and 25 controls,
and 53 female cases and 53 controls, where the majority of the patients were from
New York City. The controls consisted of patients hospitalized for non smoking-
related diseases, roughly two-thirds being cancer patients. No differences on
exposure to passive smoking at home or at work were found in the women. However,
the male passive smokers displayed a statistically significant (p=0.05) difference
in lung cancer (odds ratio 1.6) relative to the non-exposed group.
A fourth U.S. study by Miller (1984) of mortality from all forms of cancer
in 123 nonsmoking women (only 5 lung cancer cases) as a function of husband's
smoking history reported a non-significant odds ratio of 1.4 for all women (p=0.15)
for women whose husbands smoked relative to those who did not, and when employed
women were excluded the odds ratio increased to 1.94 and was statistically signi-
ficant (p<0.02).
A fifth U.S. study by Sandier, et al. (in press, a) also examined mortality
from all forms of cancer related to passive smoking, in both nonsmokers and smokers
(231 cases and 235 controls (70% white and 67% female); only 2 cases of lung
cancer in nonsmokers) as a function of spouses' smoking habits. Cancer risk
— adjusted odds ratio —(lung, breast, cervix, and endocrine) among individuals
ever married to smokers was 2.0 times that among those never married to smokers
(p<0.01). This increased risk was not explained by confounding individual
smoking habits, demographic characteristics, or social class.
In a sixth U.S. study, Sandier, et al. (in press, b) examined cancer risk
in adulthood in 197 cases and 223 controls, 66% female, from early life exposure
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to parents' smoking. They found that mothers' and fathers' smoking were both
associated with risk for hematopoletlc cancers (Hodgkln's disease, lymphomas,
and leukemlas), and a dose-response relationship was seen for the latter two.
The odds ratio for hematopoletlc cancers increased from 1.7 when one parent
smoked, to 4.6 when both smoked (p<0.001).
In the first of two studies from Hong Kong, Chan and Fung (1982) found a
lower Incidence of passive smoking among 34 female lung cancer cases (40.5Z) than
e
among 66 female controls (47.5%). All patients and controls were Interviewed con-
concerning their smoking habits and those of their spouses, their cooking habits,
Including types of cooking fuel used. Histological diagnoses of tumors were ob-
tained. Controls were taken from orthopedic patients.
In the second Hong Kong study, Koo et al. (1983) studied passive smoking in
56 female lung cancer cases and 85 female controls. Passive smoking cases had
an excess of 3.8 years of passive smoking (workplace plus domestic exposures)
compared with controls, but the differences were not statistically significant
(p £ 0.069). However, among a subgroup of 8 marine dwellers, cases had 11.8
years more exposure than controls (p - 0.0003).
Knoth et al. (1983) reported on a study of 39 nonsmoking German females with
lung cancer. 61.5Z were found to have smoking spouses. The authors state that
this percentage was threefold that expected on the basis of smoking habits of
German males.
Gillis et al. (1984) reported preliminary results of a study of passive smo-
king and lung cancer in 91 male controls (n-2) [the numbers in parentheses give
the numbers of cases] without domestic passive smoking and in 90 subjects exposed
at home (n-4), and in 40 female controls (n-2) and 58 subjects (n-6). No effects
of lung cancer were noted in the females, but elevated rates of myocardlal Infarc-
tion were reported (risk ratio 3.0). In the males, elevated rates of both lung
cancer (risk ratio 3.25) and myocardial infarction (risk ratio 1.45) were reported.
Gillis et al. state that since insufficient time has elapsed since the beginning
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of this study, no firm conclusions can be drawn relating to the incidence of cancer
or other diseases. Thus there are now a large number of studies providing evidence
for increased risk of lung cancer from Increased exposure to passive smoking.
It might be expected that subgroups of the population which proscribe smoking
among their membership would have a lower probability of passive smoking, and
therefore should also have a lower incidence of smoking-related disease than the
general nonsmoking population.
One such subgroup is the Church of Jesus Christ of the Latter Day Saints,
popularly known as the Mormon Church, which advises against the use of tobacco.
Enstrom (1978) found that active Mormons who were nonsmokers had standardized
mortality rates for lung cancer which were 21% of those in the general popu-
lation which includes smokers. This rate was found comparable to the rate of 19%
for a sample of the U.S. general population "who had never smoked cigarettes."
Interestingly, however, this result occurred despite the fact that 31% of the
active Mormon cohort were former smokers. This confounding factor was not present
for certain subgroups in the following study.
Phillips et al. (1980a; 1980b) have studied mortality (1960-1976) in Seventh
Day Adventlsts (SDAs), a religious group who also follow rigorous proscriptions
against the use of tobacco. As with with the Mormons, SDAs have rates of mortality
from lung cancer and other smoking related cancers that are fractions, respectively
21% and 66%, of the rates for a demographically comparable group in the general
U.S. population (including smokers) (1980a). A sizable subgroup (35%) of SDAs
report prior cigarette use, especially among men (1980b). SDAs appear to be less
likely than the general population to be Involuntarily exposed to tobacco smoke,
as children or as adults, at home or in the workplace, because neither SDA homes
nor SDA businesses are likely to be places where smoking is permitted, and because
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the great majority of SDA family and social contacts are among other SDAs who do
not smoke (See Appendix C).
Phillips et al. (1980a; 1980b) compared mortality In two demographically
similar groups of Southern Californlans: SDAs (from 1960 to 1976) and non-SDAs
(from 1960 to 1971). In particular, for two select subgroups of each group,
25,264 SDAs and 50,216 non-SDAs who were self-reported nonsraokers who never
smoked, age adjusted mortality rates were compared for smoking-related and nonsmo-
king-related diseases. Table 2 compares age-adjusted lung cancer mortality
ratios for two SDA cohorts relative to nonsmokers in the general population who
never smoked. The first cohort consists of all SDA, and includes those who
never smoked, ex-smokers, and smokers. The first row of Table 2 gives the
mortality ratios relative to the never-smoked non-SDAs in the-general population.
The second row compares the second SDA cohort (those who never smoked) to the
non-SDA who never smoked. The values given are averaged over both sexes. From
Table 2 the results show that the non-SDA group of nonsmokers who never smoked
(but who were more likely to suffer involuntary exposure to tobacco smoke) had an
average lung cancer mortality rate of 2.4 times that of the never-smoked-SDAs (the
group less likely to have suffered such exposure by virtue of their lifestyle).
This concludes the review of evidence relating variations in lifestyle to variations
in lung cancer risk In nonsmokers.
DOES AMBIENT TOBACCO SMOKE POSE A CARCINOGENIC HAZARD?
The International Agency For Research on Cancer (IARC) criteria for
causality to be inferred between exposure and human cancer state that confidence
In causality increases when 1) independent studies agree; 2) associations are
strong; 3) dose-response relationships exist, and 4) reduction in exposure is
followed by reduction in cancer incidence (IARC, 1979).
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1. There are now 14 studies, covering 6 cultures, indicating a
relationship between exposure to ambient tobacco smoke and^ incidence of
lung cancer. If the studies are divided into substudies of men and women, this
yields 20 substudies, all but 2 of which suggested an increased cancer mortality
from passive smoking, and 12 of which attained statistical significance. Moreover,
the mortality ratios based on spouses' smoking as an exposure variable, cluster
around the value 2.0. Thus, many independent studies agree.
2. Mainstream tobacco smoke Is strongly associated with lung cancer. The
U.S. Surgeon General (USSG, 1982) asserts that mainstream cigarette smoke Is
a major cause of cancers of the lung, larynx, oral cavity, and esophagus, and
fs a contributory factor for the development of cancers of the bladder, pancreas,
and kidney, where the term contributory factor does not exclude the possibility
of causality. Both smokers and nonsmokers are exposed to exhaled mainsteam
and sldestream tobacco smoke. Sidestream smoke by animal bloassay has been
found to be of greater potency than mainstream smoke.
3. Five of the 14 studies reported dose-response relationships between
passive smoking and lung cancer. Dose-response relationships between lung cancer
and active cigarette smoking show increasing mortality with Increasing dosage
of smoke exposure, and an inverse relationship to age of initiation (USSG, 1982).
Dose-response relationships are also shown for smokers whose smoking habits are
like heavy passive smoking (Wynder and Goodman, 1983; Jarvis and Russell, in
press) I.e., In cigarette smokers who do not inhale, and in pipe and cigar smo-
kers, who also are unlikely to inhale (USSG, 1982; USSG, 1979).
4. Reductions in lung cancer incidence for reduction in exposure have been found
in all major studies of active smoking. (USSG, 1982) The one study of passive smo-
king and lung cancer which examined this question also found a similar result
(Hlrayama, 1983b). Further, the comparison of the SDA's who never smoked and who
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should have reduced exposure relative to the non-SDA's who never smoked, also
appears to exhibit this effect.
On the basis of the IARC criteria, the evidence appears to be sufficient
for reasonable anticipation of an increase in lung cancer mortality from passive
smoking, justifying a quantitive risk assessment. The significance of the
public health risk will now be estimated.
ESTIMATION OF TOTAL LCD RISK AND A PHENOMENOLOGICAL EXPOSURE-RESPONSE RELATIONSHIP
A phenomenological exposure-response relationship is now derived based on
consistency (Hirayama,1983b) of evidence provided by studies of lung cancer in
nonsmokers and from our exposure assessment. The Seventh Day Adventist Study
by Phillips et al (1980a;1980b) appears to provide the best evidence of the mag-
nitude of the lung cancer effect from passive smoking among"U.S. nonsmokers.
A calculation (Appendix C) based on the age-standardized differences In
lung cancer mortality rates between SDAs who never smoked and demographically
comparable nonSDAs who never smoked (age groups 35 to 85+) from the studies of
Phillips et al. (1980a; 1980b) yields an estimated 4700 lung cancer deaths for
the 62.4 million U.S. nonsmokers (USDC, 1980) at risk (USSG, 1979) aged >_ 35
years. This in turn yields an exposure-response relationship of 7.4 LCDs per
100,000 person-years (4700 LCDs/yr per 62,424,000 persons), in good agreement
with the value of 6.8 per 100,000 person-years reported in the Hirayama (1981)
study. To place the estimated mortality in perspective, 4700 deaths was about
5Z of the total annual LCDs, and about 30% of the LCDs in nonsmokers in 1982
(USSG, 1982).
The exposure of nonsmokers in the U.S. population of working age, taken
from the model results in Table 1, appears to be a weighted average of about
1.43 mg of tobacco tar per day, including the estimated 14% of the population
who receive no exposure at home or work. The carcinogenic risks will be
assumed to apply even to retired persons, whose exposures are reported
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to be less than the employed (Friedman, et al., 1983), because the risks of
lung cancer from smoking decline only slowly even with total cessation of
exposure (USSG, 1982), and because the risks of lung cancer Increase exponentially
with age (NCI, 1966).
Using the statistical risk of 7.4 LCDs per 100,000, and dividing by the
average exposure of 1.43 mg/d, we estimate a phenomenologlcal exposure-response
relation appropriate for the general U.S. population at risk, of about 5 LCDs
per 100,000 person-years at risk per 1 mg/d nominal exposure.
The range in nominal exposure has been estimated to be 0 to 14 mg/day (Re-
pace and Lowrey, 1980) Studies of lung cancer and passive smoking across three
cultures have shown an an exposure-response relationship. Thus, the assumption
of an exposure-response relationship is justified, and a linear exposure-response
function (Doll and Peto, 1981; IRLG, 1979; USEPA, 1979; Crump et al., 1976)
is assumed. With zero excess risk from tobacco smoke for zero exposure, and
applying the exposure-response relationship derived above, with the maximum
exposure of 14 mg/d, a maximum risk of about (14x5)= 70 LCDs per 100,000 person-
years is estimated for the most-exposed lifestyle. This lifestyle has been
previously typified by that of a nonsmoking musician who performs regularly in
a smoky nightclub and who resides in a small apartment with a chainsmoker; many
other scenarios may be drawn. (Repace and Lowrey, 1980)
ESTIMATED LOSS OF LIFE EXPECTANCY
Reif (1981 a;b) argues that there exists a genetically-determined distribu-
tion in natural susceptibility to lung cancer in people; the effect of exposure
to tobacco smoke is to shift this distribution toward death at earlier ages.
In other words, exposure to tobacco smoke produces a loss of life expectancy.
One method of presenting risk data involves calculation of the loss of life
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-16-
expectancy, in units of days of life lost per Individual, averaged over the
entire population at risk. When the average life-loss is multiplied by the
number of individuals at risk, the impact of the hazard on society in person-
years of life lost can be assessed. More importantly, one can display the
age-specific probabilities of death from the hazard, as well as the average
number of years of life lost by the average victim. Appendix C gives the
method of calculation.
Averaged over all of the population at risk, (i.e., including those who die
of other causes), the average loss of life expectancy from passive smoking is
calculated (appendix C) to be 15 days, which is equivalent to an ultimate loss
of 2.5 million person-years of life for the total at-rlsk U. S. population in
1979 over 35 years of age (62.7 million persons). The estimated worst-case
loss of life expectancy is 148 days, again averaged over all of the population
at risk. The estimated mean life expectancy lost by a passive-smoking lung
cancer victim Is 17+^9 years.
How does the calculated average loss -of life expectancy for very heavy
passive smoking compare with the the average loss of life expectancy found in
active smokers? The modeled worst-case lifestyle might be reasonably expected
to have lesser exposure, and hence lesser risk than active smokers. Table 3,
adapted from Cohen and Lee (1979) gives this comparison. The estimated most-
exposed lifestyle has about 2/3 the loss of life expectancy of the average pipe
smoker, about 1/2 the loss of the average cigar smoker, and 1/150 of that for
active cigarette smoking.
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ESTIMATE OF AN EXPOSURE-RESPONSE RELATIONSHIP BASED ON RISKS IN SMOKERS
An alternative extrapolated exposure-response relationship is now derived
from evidence provided by studies of lung cancer in cigarette smokers. Using
the Surgeon General's estimate that 85Z of all lung cancers are due to smoking
(USSG, 1982) a current annual LCD rate to smokers at risk of about 316 per '100,000
is estimated (see Appendix B). Assuming a one-hit model (see Appendix B) for
extrapolation of the risk (which in this range is functionally equivalent to
the linear assumption that that a milligram of tobacco tar inhaled by a nonsmoker
produces a response equivalent to that in a smoker) yields an estimate of about
0.87 LCDs/100,000 person-years. This corresponds to an exposure-response
relationship of 0.6 LCDs/ 100,000 person-years per mg/d, and an annual aggregate
risk estimate of about 555 LCDs per year, an order of magnitude lower than the
phenomenological estimate.
DISCUSSION OF ALTERNATE EXPOSURE-RESPONSE RELATIONSHIPS
We now speculate on why these two different methods produce such disparate
estimates of risk. One possibility is that nonsmokers may have a reduced tol-
erance to the effects of tobacco smoke. Another possibility is a "large dose"
effect (Jarvis and Russell, in press) whereby exposure to tobacco tar at the
lesser doses experienced by nonsmokers produces a greater risk per unit dose than
the greater doses experienced by active smokers, whose lung tissue is saturated
by carcinogenic tar. Large dose effects have been observed In cancer induction
by Ionizing radiation where the dose-response curve has a linear form at low
doses, a quadratic upward (positive) curvature at intermediate doses, but a
downward (negative) curvature at high doses.(NRC, 1980) Downturns in exposure-
response curves of lung cancer in smokers of more than 40 cigarettes per day
have been observed by Doll and Peto (1978) and Hirayama (1974).
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The effect of a leveling-off or downturn in the exposure-response curve at large
exposures would be to cause a linear model to underestimate the risk when
--"—• " *
extrapolated (Hoel, et al., 1975; 1983; NRC, 1980) over two orders of magnitude
to low exposures.
A third possibility is generated by modeling the dose, as opposed to the
exposure, of nonsmokers to tobacco smoke. Nonsmokers' exposure is translated
into dose by means of a simple single-compartment model for lung deposition and
clearance (Repace, 1983). This model suggests that tar may accumulate on the
surface of nonsmokers' lungs to an equilibrium dose an order of magnitude
higher than the nominal exposure, to a level of about 16 mg per day, due to the
long pulmonary residence times for respirable aerosols. If this 16 mg dose,
rather than the 1.4 mg exposure, is the operative factor, then the typical
passive smoker would have a risk, according to the one-hit model, of about 9 per
100,000, in agreement with the phenomenological estimate. In fact there is
support for this argument from Matsukura's study (1984), which showed that
heavy passive smokers had urinary cotinine levels comparable to active smokers
of less than 3 cigarettes per day, and from Kasuga's study (1983), which also
showed that heavy passive smokers had urinary hydroxyproline levels almost
equivalent to that of light smokers. Moreover, similar observations have been
found indicating that serum thiocyanate (Cohen and Bartsch, 1980) and benzpyrene
(Repetto and Martinez, 1974) levels in some passive smokers were comparable to
the elevated levels typically found in smokers.
Moreover, the simple model we have proposed ignores the effect of cancer
latency. The long latency period for lung cancer indicates that childhood
passive smoking may be an important factor affecting risk in adult life: Doll
and Peto (1981) have suggested that the effect of passive smoking may be surpri-
singly large because lifelong exposure may produce a lung-cancer effect four
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times as great as that which is limited to adult life (recall the observation of
Sandier et al.(in press): childhood passive smoking appeared to elevate the can-
cer risk of adults). As Bonham and Wilson (1981) have shown from a national
study of 40,000 children in 1970, 62% came from homes with one or more smokers,
indicating that many adults receive exposure during childhood.
SENSITIVITY ANALYSIS
Which of the two exposure-response relationships derived Is more useful in
explaining actual epidemiclogical data? The Garfinkel (1981) American Cancer
Society (ACS) study of passive smoking and lung cancer, which spanned the years
1960 to 1972, reported a standardised mortality ratio of 1.20 and an annual
lung cancer rate of 13.3 per 100,000 person-years. Of the 176,739 women
in the Garfinkel study, 28% had nonsmoking husbands. thus, the "controls"
numbered 49,487 and the total "exposed" were 127,252. According to census data
(BOC, 1980), female participation rates in the labor force ranged from 37.1% in
1960 to 38.8% in 1965, to 42.8% in 1970, and 43.7% in 1975, and was about 80%
of the 1965 level in 1947- Thus, it appears that about 38% of the women in
this study were in the labor force, and presumably exposed to passive smoking
while at work. It is assumed that for both groups of women, control and exposed,
38% were employed and exposed to ambient tobacco smoke while at work. As
indicated in table 1, typical U.S. nonsmoking adults are estimated to inhale
1.82 mg of tobacco tar per average day at work and 0.45 mg per average day at
home, an exposure ratio of 4:1; this is because, although domestic and workplace
air exchange rates are similar (appendix A) workplace smoker densities tend to
be far higher. Let the assumed basal rate of lung cancer deaths in these women
from causes other than passive smoking be 8.7 per 100,000 (the age-adjusted
rate for nonsmoking women married to non-smokers in Hirayama's (1981a) study).
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The Garfinkel (1981) ACS cohort can now be broken down as shown in Table 4a.
The Garfinkel (1981) study can be analyzed as follows, using the phenomeno-
logical exposure-response relationship of 5 LCDs/100,000 person-years-mg/d.
The lung-cancer deaths per 100,000 contributed by passive smoking are then
2.25 (0.45 x 5) for the home and 9.10 (1.82 x 5) for the workplace. Application
of these figures to the numbers of true and tainted controls and working and non-
working exposed women yields, after addition of the basal risk of 8.7 per 100,000,
the estimated rates for lung cancer deaths per 100,000 person-years as shown in
table 4b. The ratio of risks (all exposed:all controls) is thus 1.19. The ratio
(averaged over husbands' heavy and light smoking categories) in the Garfinkel
(1981) study was 1.20, less than a 1% difference. The lung-cancer death rate for
the weighted average of the "exposed" and "control" categories is 13.8 per
100,000. Over the 12 years of the Garfinkel study, the actual rate averaged
13.3 per 100,000, a less than 4% difference. In other words, this analysis
(Repace, 1984) appears to explain both the observed lung cancer death rate and
observed risk-ratio of the Garfinkel ACS cohort. Could this be due to chance?
Suppose instead of 38% of women in the workforce, that 100% of women worked.
Then the ratio of risks would be 1.13, a 6% difference from Garfinkel's
observation, but the annual lung cancer death rate would be 19.42, a 46%
difference. Suppose 0% of women worked. Then the ratio of risks would be
1.26, a 5% difference from Garfinkel's result, but the lung cancer death rate
would be 10.32 per 100,000, a 22% difference from Garfinkel's observation.
Suppose the exposure-response relationship of 0.6 LCDs/100,000 person-years
per mg/d yielded by extrapolation with the one-hit model from the risks in
smokers is used. The lung-cancer deaths per 100,000 contributed by passive
smoking are then 0.27 (0.45 x .6) for the home and 1.1 (1.82 x .6) for the
workplace. Application of these figures to the numbers of true and tainted
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-21-
controls and working and nonworklng exposed women yields, after addition of the
basal risk of 8.7 per 100,000, the figures shown in Table 4c. The ratio of
risks (all exposed:all controls) Is then 1.03. Compared with the risk ratio in
the Garfinkel (1981) study, this is a 14% difference. The lung-cancer death
rate for the weighted average of the "exposed" and "control" categories Is 9.3
per 100,000, a 30% difference from Garfinkel's result.
Finally, using the phenoraenologlcal exposure-response relation, the ratio
for "all exposed" and "true" controls Is 1.7. Hlrayama's (1981) average risk
ratio was 1.78 from passive smoking, a 4.5Z difference. Further, If lung cancer
risk rate calculation Is performed with the tainted controls Included as an
exposed group, the result is 14.8 per 100,000, compared with Hlrayama's observed
15.5 per 100,000, a 4% difference. In other words, the effect of moving the
confounding tainted controls from Garfinkel's control group into his exposed
group is to yield results within 5% of Hlrayama's.
When the one-hit model is used, the ratio of all-exposed to true controls
Is 1.09, a 38% difference with Hlrayama's ratio. The corresponding lung cancer
mortality rate Is 9.45, a 39% difference with Hlrayama's result.
Thus, on the basis of this sensitivity analysis, It would appear that the
phenomenological exposure-response relationship is better able to describe the
results of the Garfinkel (1981) study than the one-hit model, and In addition,
also appears to be able to explain quantitatively why the two large prospective
studies of passive smoking and lung cancer yielded different results.
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COMPARISON OP THE ESTIMATED RISK OF PASSIVE SMOKING WITH THOSE.OF HAZARDOUS
AIR POLLUTANTS CURRENTLY UNDER REGULATION
Although Che quantitative estimates presented should be regarded as preliminary
and subject to confirmation by further research, the evidence suggests that passive
smoking appears to be responsible for about one-third of the annual lung cancer
mortality among U.S. nonsmokers. To place these estimates in perspective, table
5 gives a comparison of the estimated risk of passive smoking to risks estimated
by the U.S. Environmental Protection Agency for the carcinogenic hazardous air
pollutants currently regulated under section 112 of the Clean Air Act (SCEP.1977).
As table 5 demonstrates, passive smoking appears to pose a public health risk
larger than the hazardous air pollutants from all regulated industrial emissions
combined.
ACKNOWLEDGEMENTS: The authors are grateful to R.L. Phillips of the Department of
Blostatistlcs and Epidemiology of Loma Linda University, Loma Linda, CA 92350,
for tabulations from his published studies of mortality in members of the Seventh Day
Adventlst Church. We also thank B. Fischoff, H. Gibb, J. Horowitz, D. Patrick,
G. Suglyama, W. Ott, and J. Wells for useful discussions, and J. DeMocker for assis-
tance with computer programming.
views presented In this article are those of the authors, and do not necessarily
reflect the policies of the agencies named.
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Al.
APPENDIX A: MODELING EXPOSURE OF NONSMOKING U.S. ADULTS TO AMBIENT TOBACCO SMOKE
INTRODUCTION
Lifestyle Is the integrated way of life of an individual; aspects of lifestyle
which will be considered here have to do with the amount of time a non-smoker
spends in contact with smokers, and therefore with their effluent. Exposure of
nonsmokers to tobacco smoke might be expected to be common in the U.S. because
one out of three U.S. adults smokes cigarettes at the estimated rate of 32 per
day (Repace and Lowrey, 1980), while an additional one out of six smokes cigars
or pipes, and because Indoor air pollution from tobacco smoke persists in indoor
environments long after smoking ceases (Repace and Lowrey, 1980; 1982).
Earlier work (Repace and Lowrey, 1980) presented a model of nonsmokers1
exposure to the partlculate phase of ambient smoke which was supported by control-
led experiments and a field survey of the levels of respirable particles indoors
and out, in both smokefree and smoky environments. This work, which established
that ambient tobacco smoke imposed significant air pollution burdens on nonsmokers,
was extended by later work (Repace and Lowrey, 1982) which further demonstrated
the predictive power of this model. The model predicts a range of exposure of
from 0 to 14 mg of cigarette aerosol per day, depending upon the nonsmoker's
lifestyle. Exposures of prototypical nonsmokers were modeled, but no attempt was
made to estimate the average population exposure. Concentrations of ambient
tobacco smoke encountered by nonsmokers can be approximated by equilibrium values
which are determined by the ratio of the average smoker density to the effective
ventilation rate (Repace and Lowrey, 1980; 1982), and that In practice, design
ventilation standards based on occupancy were useful surrogates for effective
ventilation rates. On the average, a characteristic value of this ratio can be
assigned to a particular microenvlronmental class, e.g., homes, offices, restau-
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A2.
rants, etc. (Repace, at al., 1980) Therefore, the average daily exposure of
Individuals can be estimated from the time-weighted sum of concentrations encoun-
tered in various oicroenvironments containing smoke. (Ott, in press; NRC, 1981;
Szalai, 1972; Repace, et al., 1980)
EXPOSURE AND LIFESTYLE
It is important to realize that moat persons' lifestyles are such that they
spend nearly 90% of their time in just two microenvironmental classes, thus
affording a great simplification of exposure modeling. Szalai (1972), as part of
The Multinational Comparative Time Budget Research Project, which studied the
habits of nearly 30,000 persons in 12 countries (1964-1966), has compiled data
reporting the average time spent in various locations or microenvironments. The
data for 44 cities in the U.S., as analyzed by Ott (in press) are summarized in
Table Al (see also NRC, 1981).
Table Al shows that U. S. urban people spend an average of 882 of their
time In just two microenvironments: in homes and in workplaces. Moreover, employed
persons in the U. S. cities are estimated to spend only 3Z of the day outdoors
while housewives spend only 27. outdoors (Ott, in press; NRC, 1981). Assume that
these values are representative of the entire population. (In 1970, approximately
three fourths of the population was urban) (USDC, 1980).
MODELING EXPOSURE OF NONSMOKERS AT WORK
Exposure of the population to the particulate phase of cigarette smoke can be
modeled to determine both range of exposure and the nominal inhaled dose, which is
the exposure multiplied by the respiration rate (Altman and Dltmer, 1971).
Repace and Lowrey (1980, 1982a) have shown that the ambient concentration of
tobacco smoke particles, Q, from cigarette smoking can be usefully represented by
an equilibrium model of the form Q - 650 DS/CV where D3 is the number of burning
cigarettes per 100m3, and Cy is the ventilatory air exchange rate in air changes
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A3.
per hour (ach). Rewriting this in terms of the occupancy of the space by habitual
smokers (Repace and Lowrey, 1980) (for every 3 habitual smokers, there Is one
cigarette burning constantly), D^gC- 3Dg):
Q - 217 Dhs/Cv (ug/m3) [Al ] ,
where Dvg is the habitual smoker density in unit«s of smokers per 100 m , and C is
the effective air change rate in units of air changes per hour (ach). Because
ASHRAE, The American Society of Heating, Refrigeration, and Ventilating Engineers
(Leaderer, et al . , 1981), a national engineering society, sets consensus standards
for ventilation rates in the U.S., and because those standards are tied to expected
building occupancy (e.g., ASHRAE, 1981), Eq. [1] offers the possibility of modeling
the range of nonsmokers ' exposures by estimating the ranges of occupancy and air
change rate. Appendix Al estimates that the average annual exposure to ambient
tobacco smoke particles by a typical nonsmoking U.S. worker is 1.8 mg/day, with a
exposure probability of 62. 5Z.
MODELING EXPOSURE OF NONSMOKERS AT HOME
By reviewing data from time budget and census studies, the average length of
time a person spends in the home microenvironment can be calculated. This time
differs for gender and employment status. Taking into account the different amounts
of time spent in the home by employed men, employed women, and homemakers, an estimate
of occupancy-weighted average number of cigarettes smoked in the home during a
16-hr waking day, assuming that if the entire waking day were spent at home, is 32
cigarettes per day (CPD) smoked in the house by a smoker of either sex. An esti-
mated occupancy-weighted average number of cigarettes equal to 22 CPD smoked in
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A4. .
Che typical home la derived In Appendix A2. Using Eq. 1, multiplied by the ratio
22/32, times a 1 m^/hr respiration rate for a 16 hr period, the.calculation is made
for a single family detached dwelling of 340 m^ volume (see Appendix A3), assuming
that on a 16 hr basis, the entire finished volume of the home is available for dis-
persion of the smoke. A typical nonsraoker of either sex appears to be exposed to an
average inhaled dose of 0.45 mg/day, assuming that occupancy of the home by smokers
and nonsmokers is coincident.
MEAN ESTIMATED DOSE TO A TYPICAL ADULT FROM THE MOST-FREQUENTED MICROENVIRONMENTS
A probability-weighted average exposure to a hypothetical typical U.S. adult is
estimated by combining the estimated dose to U.S. adults exposed In the workplace
and at home, by weighting the exposure received in each microenvlronment by the
probability of receiving it. Appendix Al estimates that nonsmoking U.S. workers
are exposed on the job to tobacco smoke with a probability of 63Z. Appendix A2
estimates that nonsmoking U.S. adults were exposed at home to tobacco smoke with a
probability of 62Z. Table 1 (main text) gives the combinations of these probabili-
ties, assuming that they are independent, i.e., that exposure at work is not corre-
lated to exposure at home. Table 1 suggests that only a relatively small percentage
(14Z) of the population may escape daily passive smoke exposure. By contrast,
individuals having exposure both at home and at work constitute a high exposure
group, with the workplace likely contributing more exposure than the home by a
ratio of 4 to 1.
On the basis of Table 1 it is estimated that the mean daily exposure to
tobacco tar and nicotine from the breathing of Indoor air contaminated by cigarette
smoke, to nonsmoking U.S. adults, is about 1.43 mg/day, averaged over the two most-
frequented mlcroenvironments. This may be compared to the estimate of 14 mg/day to
the hypothetical most-exposed individual (Repace and Lowrey, 1980). These results
indicate that the typical U.S. "nonamoker" appears to be exposed to a finite, non-
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A5.
zero amount of tobacco aerosol, equivalent in value to three low-tar cigarettes
(0.55 mg) per day.
In summation, it is possible, based on ASHRAE standards, time budget and cen-
sus surveys, the physics of indoor air pollution transport, and tables of
respiration rates, to estimate the average exposure of a typical nonsmoking
U.S. adult of working age. Using this methodology, estimates of the average
exposure of the U.S. adult population of working age to the particulate phase
of ambient tobacco smoke are made for the two most-frequented microenvlronments:
the workplace and the home. It Is estimated that 86Z of adults of working age
are exposed to ambient tobacco smoke on a daily basis, and 14% are not. It
Is estimated that the range of exposure varies from 0 to 14 mg of tobacco tar
per day. and that the typical exposure, averaged over 100% of the population,
is 1.43 mg/day. It also is estimated that those individuals who are exposed
both at home and at work receive a daily average exposure of 2.4 mg/day, and
that 39% of the adult worker population is in this category.• Those individuals
exposed only at home receive a daily exposure of 0.5 mg/day. and that 23% of
the adult population is in this category. Finally, it is estimated that those
individuals exposed only at work receive a daily exposure of 1.8 mg/day, and
that 24% of the worker population is In this category. Thus these estimates
suggest that the ratio of workplace dose to the exposure received at home Is
nearly 4:1, indicating that, on the average, the workplace is a more important
source of exposure than the home environment. Consistency of these estimates
of workplace and domestic exposure with field data is given in Appendices 1
and 2.
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Ab.
APPENDIX Al: MODELING THE AVERAGE DAILY EXPOSURE TO CIGARETTE SMOKE
FOR A TYPICAL U.S. NONSMOKING WORKER
It is possible to arrive at an estimated aggregate exposure because the range
of occupancies (I.e., smoker densities) is tied to the range of ventilation
rates, which in turn determine the range of concentration of ambient tobacco smoke
to which nonsmokers are exposed. A form of eq. [Al] Is given which can be related
directly to the ASHRAE Standards 62-73 (ASHRAE, 1973), promulgated in 1973, which
set standards for natural and mechanical ventilation. The practical range of
occupancy given in the ASHRAE Standard 62-1973 is from 5 persons/1000 ft2 to 150
persons/1000 ft2 [5.4 P/100 m2 to 161 P/100 m2], for Commercial and Institutional
buildings. [From 1946 to 1973, the operable engineering standard was descriptive
of general practice rather than prescriptive: The American Standard Building Code
Requirements for Light and Ventilation A53, Section 8 (ASA, 19.46) described
typical practice for mechanical ventilation based on floor area, not occupancy.
Section 8 described minimum values of .5 CFM/ft2 for offices, 1 to 1.5 CFM/ft2
[4.4 to 6.6 L/s-m2] for workrooms, and a range of .5 to 3 CFM/ft2 [2.2 to 13.2
L/s-m2] for public and institutional buildings, with the lower value applying to
museums, and the upper value to dance halls. This Implies air exchange rates
varying from 3 to 18 ach, and at the maximum of 75Z recirculation described, this
range reduces to .75 to 4.5 ach. In 1970, 60.72 of the U.S. workforce worked in
the white-collar and service occupations which Inhabit such buildings (USDC,
1980). A 1979 survey of 3000 employers in large, medium and small corporations
Indicated that smoking was prohibited in only 10.52 of white-collar workplaces
and in 27.5Z of blue-collar workplaces (NICSH, 1978). These percentages would
likely have been less In 1970. Eq. [A2] expresses the concentration, R, as a
function of occupancy, which is now a surrogate (Repace and Lowrey, 1980, 1982a)
for smoker density:
R - 25.6 Pa/Cy (ug/m3) [A2]
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A7.
7 ?
where Pa is the occupancy in persons per 1000 ft [100 m ], and C is the ventl-
3 V
latory air change rate in ach, as before. Exposures can be calculated by multiply-
ing R by the integrated average respiration rate expected for an adult nonsmoker
over an 8-hr workday. A reasonable value is 8 ra-^ per workshift, a value corres-
ponding to alternate sitting plus light work.(Table A3) Multiplying Eq. [A2] by
this rate yields the equation for the amount of tobacco tar Inhaled, N^:
Nd - 0.205 Pa/Cv (mg/8-hrs) [A3]
where the other parameters are defined as in Eq.[A2]. ASHRAE STANDARDS 62-73
yield the ranges in Pa of from 5 to 150 and In Cv of from 0.15 ach to 18 ach.
Table A2 expresses the variation of these parameters for the absolute minimum
airchange rate to the recommended minimum and maximum rates, and enables us to
bound the modeled dose for the workplace. The extreme bounds of workplace
exposure can be estimated to range from 1.35
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A8.
6.13 workhours/day, dally average. Thus, the daily average exposure Is Nj -
(6.13/8)x2.37- 1.82 mg/day.
It now remains to estimate the percentage of workers who are exposed to
cigarette smoke at work. The National Interagency Council on Smoking and Health
conducted a survey of top management and health officials of 3000 U.S. Corporations
In 1978 (NICSH, 1978). A 29% response rate was achieved. The survey Indicated
that of bluecollar companies surveyed, 30.6% had no restrictions on smoking, 42%
permitted smoking In designated areas, and 27.5% completely prohibited smoking.
The corresponding percentages for the white-collar companies were respectively
74.3%, 15.2%, and 10.52. Smaller companies were less likely to have restrictions.
Among companies with restrictions, about half imposed penalties for violations.
65% of the respondents Indicated that their policy was established after the
release of the 1964 Surgeon General's Report on Smoking.
In 1970, white collar workers constituted 48.3% of the workforce, blue collar
workers 35.3%, service workers 12.4%, and farmworkers 4% (USDC, 1980). The largest
change in any category from 1960 to 1979 was that of white collars, Increasing by
7%. Since about half of the blue collar companies Imposed penalties for smoking,
it will be assumed that 50% of the blue collar nonsmokers were not exposed on the
job. By contrast, it will be assumed that only 25% of the white collars were not
exposed. It will further be assumed that half of all workers follow white-collar
smoking rules, and the other half, consisting of blue-collar workers, service
workers,and farm workers, follow blue-collar rules. Thus, the estimated
weighted average percent of nonsmoking workers who are significantly exposed to
tobacco smoke on the job is: 0.50 x 50% +• 0.75 x 50% - 62.5%. By comparison,
a 1983 survey of 1515 white and blue collar businesses sampled at random reported
that "nearly two-thirds" had no smoking restrictions in the workplace. (Tobacco
Institute, 1984)
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A9.
At this stage It must be asked whether the numbers calculated are reasonable
in terms of measurements of ambient tobacco smoke under natural conditions.
Repace and Lowrey (1980; 1982a) in a field survey of ambient tobacco smoke in 23
commercial buildings in the metropolitan Washington, D.C. area during 1979-1980,
found concentrations ranging from about 100 ug/m-^ to more than 1000 ug/nH. This
range is quite compatible with the the concentrations Q derived In table Al. The
average of all values measured under a variety of smoking conditions and ventila-
•B
tion rates by Repace and Lowrey was 242 ug/m^ (range 100 to 1000 ug/m^) for
these 23 locations, corrected for background. This Is compatible with the values
calculated in Table A2. Breathing 242 ug/m^ of ambient" tobacco smoke for 8
hours at a rate of .99 m^/hr yields an exposure of 1.92 mg/8hrs or on a daily
average basis, 1.92 x (6.13/8) - 1.47 mg.
In terms of relative exposures, these results also appear to be reasonable.
In Appendix A2, an average smoking rate of 32 CPD was used (Repace and Lowrey, 1980)
At current sales-weighted average tar plus nicotine values (14 mg) (USFTC 1984),
the typical smoker would inhale (14mg/cig) x 32 CPD = 448 mg/d. In Table 1, the
typical passive smoker was calculated to inhale 1.43 mg/d. This Is a relative
exposure ratio of 313:1. Wald et al (1984A), in a study of urinary cotinine levels
in smokers and nonsmokers, found the ratio (1645 ng/mL)/(6 ng/mL)- 274:1. Thus, the
ratio of exposures calculated theoretically using the model derived here differs
by only 14% from an experimentally derived value based on a biological marker of
exposure.
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A10.
APPENDIX A2. CALCULATION OF THE ESTIMATED DAILY AVERAGE NUMBER OF CIGARETTES
SMOKED IN THE AVERAGE HOME
Since Che source strength depends upon the length of time smokers spend in
indoor mlcroenvironments, it is necessary to review pertinent information from
time budget (Ott, in press; Szalai, 1972; NRC, 1981) and census (USDC, 1980)
studies, which gives the average length of time that persons spend in various
mi croenvi ronments.
From Table Al, It is seen that, allowing for 8 hours of sleep, employed
men spend 34.42 of the waking day In the home; employed women spend 45.9Z of the
waking day in the home; "housewives" spend 81Z of the waking day in the home. In
1979, approximately 42Z of families with both the husband and wife present, both
were employed. Thus for homes occupied by married couples, 66Z of the waking day
(weighted mean averaged over 42% working wives and 58Z homemakers) the home is
occupied by a wife, and 34Z of the day, by a husband. If the average habitual
smoker smokes 32 cigarettes per day (CPD), then the wife will smoke 21 CPD in the
house, and the husband will smoke 11 CPD in the house.
Bonham and Wilson (1981) found that 62Z of U.S. homes with children in 1970
contained one or more smokers, and 25Z contained two or more. Thus we may assume
that of homes with one or more smokers, 40Z have two smokers, and 60Z have one
smoker. We have three cases to consider: a) Husband and Wife Both Smoke, b) Only
Wife Smokes, and c) Only Husband Smokes. In 40Z of the smoking homes, (a) is
true, and in 60Z of those homes, either (b) or (c) is true. 38% of men and 30Z
of women smoke.(16) Then the probability of (c) being true is 34Z (38/68 x 60Z),
and the probability of (b) being true is 26Z (30/68 x 60Z). The weighted mean of
these is given by the sum of the products of the percent of homes with a given
number of smokers of either or both sexes, times the number of cigarettes per day
smoked by either or both sexes: .40 x 32 + .26 x 21 + .34 x 11 - 22 CPD, estimated
-------
All.
to be smoked daily in the average U.S. home, or about a pack, per day. Is this
theoretical estimate a reasonable number?
Dockery and Spengler (1981a; 1981b) in a one-year study of Indoor air pollu-
tion in 68 homes In 6 U. S. cities, found that cigarette smoking was the dominant
source of respirable particles (RSP), and that in a typical house in the study,
the average 24-hr RSP levels were Increased by 0.88 ug/nH per cigarette smoked,
and in a tightly sealed house, by a value of 2.11 ug/m^. At an estimated occu-
pancy-weighted average in-the-home smoking rate of 22 cigarettes per day, a 24-hr
average RSP level of about 19 ug/m3 (22 CPD x 0.88 ug/tn^-cpo) is calculated for
the typical house; in fact, Spengler, et. al. (quoted in NRC, 1981) observed, in
22 of the homes in the study where there was only 1 smoker, a 24-hr average of 19
ug/m3. This number corresponds to an air exchange rate of 1.5 ach using the
model (see Appendix A3). Since this air exchange rate is within the expected
range,(Repace and Lowrey, 1980, 1982) an average of 22 CPD smoked in the home
provides a reasonable basis for estimating exposure.
The theoretical in-the-home number of cigarettes smoked in the home is
weighted for occupancy during the waking day. Since there is no data differen-
tiating occupancy for smokers and nonsmokers, it is assumed that the statistical
occupancy of the nonsmoker is coincident with that of the smoker, i.e., that
there is a nonsmoker present to receive the exposure. In order to calculate the
daily dose received, Eq. Al is used with the parameters D^s» 0.29 smokers/100m ,
Cv- 1.5 ach, times an occupancy factor of 22/32, times a respiration rate of 0.99
m^/hr, times a 16 hr maximum exposure day, yielding an estimated average exposure
of 0.45 mg/day, for an adult nonsmoker, with an exposure probability of 62Z.
A reasonable approximation to the probability of a typical nonsmoking adult
-------
A12.
being exposed Co ambient tobacco smoke at home Is 622, the same as Bonham and
Wilson (1981) above found for adults with children (in 1970, 562 of families had
*
one or more children under 18) (DSDC, 1980) No differentiation is made between
male and female nonsmokers since Friedman et al.(1983) observed that degree of
passive smoking had little correlation with gender. In households with 2 or more
smokers, there might not be an adult nonsraoker to be exposed; in this case, the
probability of passive smoking (for a nonsmoker) reduces from 622 to 372. However,
the estimated total exposure (Table 1) only decreases by 82, from 1.46 mg/day to
1.34 mg/day. In the absence of data on this point, it will be assumed that a
nonsmoking adult is present.
APPENDIX A3.
CALCULATION OF THE RATIO OF THE HABITUAL SMOKER DENSITY TO THE EFFECTIVE VENTILATION
RATE FOR A TYPICAL U.S. SINGLE FAMILY HOUSE
The typical range of annual closed-window air exchange rates in U.S. residences
is generally considered to be of the order or 0.5 ach to 1.5 ach, with the range
for the average residence of the order of 0.7 to 1.1. ach, and that of the tighter
and newer residences of the order of 0.5 to 0.8 ach (Fuller, 1981). So-called
energy-efficient structures have rates of the order of 0.3 to 0.5 ach. (Repace,
1982) A typical U.S. single-family detached house is estimated to have a floor
area of 1500 sq.ft. [139 m2] with an 8-ft [2.4 m] ceiling, for a volume of 340 m3
(NAHB, 1981).
Thus, per habitual smoker, the ratio Dhs/Cv - (1/3.4)/ 1.0 - 0.29 habitual smokers
per hundred cubic meters per air change per hour. In 1978, nearly 2/3 of occupied
housing units were single-family detached dwellings (USDC, 1980). It is assumed
that the ratio calculated above is valid for multifamily dwellings as well (the
volume of an apartment in a multi-family building is likely to be less, but the
air exchange rate is likely to be greater).
-------
APPENDIX B; EXTRAPOLATED ESTIMATE OF RISK FROM PASSIVE SMOKING
An alternative method of estimation of risk from passive -smoking is calcula-
ted as follows. In 1980, 108,504 individuals in the D.S. were reported to have
died from lung cancer (USPHS, 1983). The 1982 Surgeon General's report on Smoking
and Cancer estimated that 85Z of LCDs are due to cigarette smoking (USSG.1982) this
yields 92,228 LCDs/yr. Lung cancers occur primarily in smokers over the age of
35 (NCI Monograph 19, 1966); in 1980, there were an estimated 29,225,000 smokers
of all races and both sexes in this age bracket (USPHS, in press). It follows that ir
1980, there were 3.156 x 10"^ LCDs per smoker of lung cancer age. In 1978 the
average cigarette was 17 mg tar, and the average smoker smoked 32 per day (Re-
pace and Lowrey, 1980), for an estimated tar Intake of 544 mg/day-smoker. (A
1980 lung cancer death reflects a 20 to 40 year smoking history, during which
smoking rates increased by, and tar levels decreased by, about 502 (USSG, 1979).
Thus, 3.156 x 10" ^ LCDs/smoker divided by 544 mg/day-smoker yields a rate of
about 5.8 x 10"^ LCDs/yr per mg/day per smoker of lung cancer age.
Using a one-hit model (Hoel, et al., 1983; Crump, 1976) for the extrapolation
of the risk from the estimated exposure of smokers down to the estimated exposure
of nonsmokers provides an alternate exposure-response relationship. Crouch and
Wilson (1981) have used this model which saturates at high exposures, but which is
linear at low exposures. This model has the form P(D) = 1 - exp (bD), where P(D)
is the estimated risk, b is the exposure-response function, and D is the exposure.
This model, because of its functional form, can be considered as the first stage of
the more complex multistage model. (USEPA, 1983a; Hoel, et al., 1983) Whenever
the data can be fitted adequately by the one-hit model, estimates of both models
will be comparable (USEPA, 1983a; Crump, 1976; Hoel, et al., 1983).
-------
B-2
From above, b - 5.8 x 10~^ LCDs per year per mg/day. D » 1.5 mg/day, from Che esti-
mated average exposure for the typical U.S. nonsmoker (Appendix A), assuming that
per milligram, tobacco tar produces the same carcinogenic response In nonsmokers as
It does in smokers. This calculation yields an estimated annual LCD risk of about
0.87 x 10~5 from passive smoking, or about an order of magnitude lower than the
phenomenological estimate made earlier. In this exposure range, this result is
essentially the same as would be obtained from a linear extrapolation.
The primary age group at risk of lung cancer is that _>. 35 years (Reif, 1981a;b).
Therefore, in the calculation that follows only nonsmokers >^ 35 yrs will be assumed
to be at risk of lung cancer. In 1980, there were about 63.8 million nonsmokers
aged >^ 35 (USPHS, in press). Thus, the alternative risk estimate is derived from
multiplying 0.87 LCDs/yr per 100,000 passive smokers times 63.8 x 10^ passive
smokers at risk yielding 555 LCDs per year in U.S. nonsmokers from passive smoking,
using the one-hit model of carcinogenesis for extrapolation.
-------
APPENDIX C; AGE-STANDARDIZED CALCULATION OF ESTIMATED ANNUAL U.S. MORTALITY AND
LOSS OF OF LIFE EXPECTANCY FROM INVOLUNTARY EXPOSURE TO AMBIENT TOBACCO SMOKZ
Approximately 501 of SDAs in Che cancer age range (>35 yrs old) are adult
converts to the church; others were either born Into an SDA home or joined the
church prior to age 20, typically with other immediate family members. A
large proportion of SDAs tend to be heavily Involved In church activities. Only
a very small proportion of SDAs report current use of cigarettes (males, 1.7Z;
females 0.5Z) (Phillips,et al., 1980b). (By contrast, in 1970, 43.5Z of adult
males and 31.12 of adult females In the general population aged _>. 17 years
reported smoking) (USDHHS, 1979).
Moreover, a substantial portion of SDAs work for "an organization owned and
operated by the SDA Church" (nearly 45Z of SDA females and 40Z of SDA males in
the study group, (aged _> 25 years), reported working for the SDA Church. (Phil-
lips et al.. 1980a; 1980b). Clearly, SDAs are less likely than the general
population to be involuntarily exposed to tobacco smoke, as children or as
adults, at home or in the workplace, because neither SDA homes nor SDA businesses
are likely to be places where smoking Is permitted, and because the great
majority of SDA family and social contacts are among other SDAs who do not
smoke (Phillips et al. 1980b).
Table Cl shows the age-standardized calculation of estimated loss of life
expectancy and annual lung cancer mortality from passive smoking. The calculation
is based on the lung cancer mortality difference between two Southern California
cohorts of self-reported nonsmokers who never smoked. Based on lifestyle
differences, they appear to have different average levels of involuntary smoke
exposure. The more-exposed group are designated non-SDAs, and the less-exposed
group SDAs (see text).
Columns 1, 2, 5, and 6 are tabulations from which age-adjusted mortality
rates were calculated In the study of mortality In the Seventh-Day Adventlst
-------
C-2
(SDA) by Phillips et al. (1980a; 1980b). Columns 1 and 2 an*d 5 and 6 give the
age-apecific lung cancer deaths and person-years at risk respectively for the
SDA and the non-SDA. The fractional number of LCDs in column 1 Is due to a
correction for out-migration of the SDA population from the study area.
Columns 3, 7, 10, and 11 show the average numbers of Individuals at risk
annually during the study, allowing for those who died during the study.
Cols. 4 and 8 show the annual average lung-cancer death rate (LCD) per 100,000
persons, and Col. 9 gives the differences between the non-SDAs and SDAs in those
rates. Col. 12 gives average LCD rates weighted to reflect the fact that there
were three times as many women as men in the study, and that the female data
attained statistical significance whereas the male did not although the
combined data were significant. (Phillips et al., 1980a; 1980b) A common LCD
rate is assumed for both sexes in the calculation that follows. Also, It will
be assumed that the entire LCD rate difference is due to passive smoking (see
discussion on confounding factors in Appendix D).
Next, this calculation will be extrapolated to the entire U.S. nonsmoking
population aged >_ 35 years. Col. 13 gives the mean age of the individuals in
the 5-year age group, and Col. 14 gives the number of persons alive at that
mean age per 100,000 born alive. Col. 15 gives the total number of persons In
the 5-year age group (5 x Col. 14) per 100,000 born alive (whites only) from
the 1974 U.S. Life Tables (USDHHS, 1975). Col. 16 gives the age-specific LCD
rates attributed to passive smoking, standardized to (i.e., weighted by) the
age specific population distribution in 1974 for U. S. whites (col. 12 times
col. 15).
Col. 17 gives the average life expectancy corresponding to the mean age
-------
C-3
given in Col. 13, which is taken Co represent that of the entire five-year age
group. Col. 18, the product of Cols. 16 and 17, gives the estimated age-specific
age-standardized person-years of life lost due to lung-cancer from passive
smoking.
The sum of the values of Col. 18 gives an estimated 3932 person-years
of life lost due to passive smoking per 100,000 persons alive at age 35 in the
U. S. population in 1979. 3932 person-years, when divided by the 94,724 persons
(USDHHS, 1975) at risk at age 40 (LCDs were not observed at earlier ages in the
SDA study; however, they are observed in the general nonsmoking 0. S. population
at age 35) (USSG, 1979) yields 15 days, the mean number of days of life lost,
and multiplying by the peak-to-mean exposure ratio, 112 days for the maximum
number of days lost (where the risks of the non-white population are taken to
be the same as for the white population.)
Col. 19 is col. 16 times 62.424 million divided by the sum of col. 15.
The sum of Col. 19 gives an estimated age-standardized mortality total of
4,665 LCDs per year in U.S. nonsmokers from passive smoking (where there were
93,636,000 persons aged >_ 35 years in 1979, and two-thirds or 62,424,000 of
these were nonsmokers).
Examining Col. 19, shows that of those individuals assumed to contract
lung cancer from passive smoking, that approximately 1-1/2Z do so at
each year of age from 40 to 69, and that over age 70, approximately 3Z do so
each year. Of those who actually contract fatal lung cancer from passive
smoking, the mean life expectancy lost is about 17 +_ 9 years, and about 8Z lose
as much as 33 years.
-------
APPETOIX D; DISCUSSION OF CONFOUNDING FACTORS
The IARC criteria for causality and human cancer spectfy that possible
sources of bias and confounding error should be considered (IARC, 1979). What
factors other than passive smoking could account for a lung cancer difference
between two cohorts?
The most obvious one Is mlsclassification. Some of the individuals clas-
sified as nonsmokers could have been smokers or exsmokera, giving rise to a
spurious effect. Workplace or residential exposure to lung carcinogens or
dietary differences between the cohorts might also give rise to spurious differ-
ences. However, this is not likely to be an effect constant over nine positive
studies in five different countries, all of which report about a doubling of
risk when the exposure variable Is spouses' smoking.
Arsenic, asbestos, beryllium, chloroethers, chromium, coke oven emissions,
nickel, radon, and vinyl chloride, as well as tobacco smoke, have been implica-
ted in the etiology of lung cancer (Ives, 1983; Sellkoff, 1981). Possible
differences due to industrial exposures should be expected primarily in blue-
collar workers. Phillips et al. (1980a; 1980b) have stated that the SDA/non-SDA
subgroups were demographically and educationally similar, suggesting similar
occupational distributions, although there is no information on this point.
There Is no reason to believe that domestic radon levels, which are a property
of the soil, would b« any different in SDA homes than Non-SDA homes. Finally,
it should be considered that co-exposures to other lung carcinogens (e.g.
radon) may Increase the effect of passive smoking (Bergman and Axelson, 1983).
It is also possible that dietary differences between the two groups might
have contributed to the SDA/nonSDA lung cancer difference. 54Z of SDAs follow
a lacto-ovarlan diet and 41Z rarely use caffeine beverages. However, Hirayama
-------
D-2
(I981a; 1981b; 1983a; 1983b) observed a dose-response relationship between
exposure Co passive smoking and lung cancer even in those with an apparently
cancer-inhibiting diet. Also SDA/non-SDA cancer differences are not significant
for other smoking-related cancer sites; this runs counter to a protective
effect of diet as a confounding factor. Finally, Hirayama (1983a) observed
e
that the magnitude of this effect varied from mortality ratio of 1 for passive
smoking women who did not follow a protective diet to 0.82 for women who used
green-yellow vegetables only occasionally, to 0.72 for women who ate them
daily. Thus the magnitude of the effect does not appear to be sufficient to
account for the observed SDA/NonSDA lung cancer difference. Moreover, If 40Z
of the SDAs work for church-run organizations, 60Z do not:- these 607. surely
must be subject to some passive smoking in the workplace, at least partially
offsetting the effects of potential dietary or occupational differences with
the nonSDAs.
-------
TABLE 1. ESTIMATED PROBABILITIES OF NONSMOKERS EXPOSURE TO TOBACCO SMOKE
AT HOME AND AT WORK (after Repace and Lowrey, 1983; Appendix A)
Non-«zcluslve probability of being exposed at work: 63%
Probability of not being exposed at-work: 377.
Non-exclusive probability of being exposed at home: 622
Probability of not being exposed at home: 38%
Exposure (mg)
Lifestyle: Daily Average Probability Modeled Dally Daily Proba
of being exposed (Rounded Values) Average bility-Welg
At work and at home: % 63 x 62 - 39 2.27 0.89
Neither at work nor at hom«: Z 37 x 38 - 14 0.00 0.00
At home but not at work: % 62 x 37 - 23 0.45 0.10
At work but not at home: % 63 x 38 - 24 1.82 0.44
Total: % 100 1.43
Table 1. The estimated exposure to the partlculate phase of ambient tobacco smok
for U.S. adults of working age, at work and at home (chese two microenvironments
account for an estimated 88% of the average person's — both smokers and nonsmoki
time), determined from average concentrations of tobacco sooke calculated for
model workplace and home microenvironments, weighted for average occupancy, as
derived in Appendix A.
-------
TABLE 2: AGE-ADJUSTED SDA-TO-NONSDA RATIO OF LUNG CANCER
MORTALITY (after Phillips, et al.(!980b^
By Health Habit Index
I. All SDAs
Average
0.54
Beat
Third
0.54
Average
Third
0.40
Worst
Third
0.96
II. SDAs who Never
Smoked
0.41
0.41
0.32
0.78
Values shown are adjusted by Mantel-Raenzel procedure (p £ 0.01),
Lung cancer mortality ratios taken from a prospective study of two deaogra-
phlcally similar cohorts. The non-SDA coma from Che general south California
population, and were self-reported nonsmokers who never smoked. The SDA come
from a southern California subgroup less likely to engage in passive smoking by
virtue of lifestyle differences. The health habit index is a measure of how
faithfully individuals adhered to the Church's teachings; the worst third were
also more likely to have a non-SDA spouse) (Values quoted in text are the
reciprocals of numbers given here.) Phillips, et al.(1980a; 1980b) reported
results for all SDA, and reported replicating these data for SDA who never
smoked, aa shown (R.L. Phillips, Department of Biostatistics and Epidemiology,
Looa Linda University. Loaa Linda, CA 92350). The SDA subjects and nonSDA
subjects for this study consisted of white California respondents to the same
four-page self-administered questionnaire collected by the Aatrican Cancer
Society study of 1 million subjects throughout the United States (NCI Monograph
19, 1966; Garfiukel, 1981; Phillips et al., 1980a; 1980b).
-------
TABLE 3. ESTIMATED LOSS OF LIFE EXPECTANCY FROM ACTIVE SMOKING (ALL CAUSES)
AND PASSIVE SMOKING (LUNG CANCER (WLY) — adapted from Cohen and Lee(1979).
Cause Days
Cigarette smoking — male 2250
Cigarette smoking — female 800
Cigar smoking 330
Pipe smoking 220
Passive Smoking1' (Eat. most exposed lifestyle) 148
Passive smoking* (Est. average lifestyle) 15
^Estimated this work (see Appendix C); averaged over all nonamokera at risk, i.e.,
those who are presumed to die from passive snsoklng-induced lung cancer, and those
do not. Estimates given for passive smoking are phenomenologlcal estimates.
-------
TABLE 4a. NUMBER OF WOMEN IN EACH EXPOSURE CATEGORY IN THE GARFINKEL(1981) STUDY
OF PASSIVE SMOKING AND LUNG CANCER
Group - No.
Total cohort 176,739
"True" controls: do not work, husbands do not smoke 30,682
"Tainted" controls: work, husbands do not smoke 18,805
Total "controls" 49,487
"Exposed" workers: work, husbands smoke 48,356
"Exposed" non-workers: do not work, husbands smoke 78,896
Total "exposed" 127,252
TABLE 4b: CALCULATED LUNG CANCER RISKS FOR EACH SUBGROUP IN THE GARFINKEL (1981) STUD
USING THE 5 LCDs/100,000 person-years/mg/d EXPOSURE-RESPONSE RELATION.
Group Rate
True controls 8.7
Tainted controls 17.8 (8.7 + 9.1)
All controls (weighted mean) 12.16
Exposed workers . 20.05 (8.7 + 2.25 +9.10)
Exposed non-workers 10.95 (8.7 + 2.25)
All exposed (weighted mean) 14.41
TABLE 4c. CALCULATED LUNG CANCER RISKS FOR EACH SUBGROUP IN THE GARFINKEL (1981)
STUDY USING THE 0.6 LCDs PER 100,000 person-years/mg/d EXPOSURE-
RESPONSE RELATION.
Group Rate
True controls 8.7
Tainted controls 9.8 (8.7 + 1.1)
All controls (weighted mean) 9.11
Expoaed workers 1°'°7 (8.7*0.27 + 1.1)
Exposed non-workers 8.97 (8.7 * 0.27)
All exposed (walghted mean) 9.39
-------
Table 5. COMPARISON OF ESTIMATED RISKS FROM VARIOUS HAZARDOUS AIR POLLUTANTS
Risks have been assessed for non-occupational exposures of Che general popu.
tion Co several hazardous air pollucancs. All are airborne carcinogens; all buc
passive smoking are being regulated by society. The statistical aortality given
is b«fore control.
POLLUTANT ESTIMATED ANNUAL MORTALITY Reference
Passive Smoking 5000 LCDs per year (this work)
Vinyl Chloride <27 CDs per year (USEPA,1975)
Radionuclides
(world-wide impact
from Department of 17 CDs per year (USEPA,1983b)
Energy facilities)
Coke Oven Emissions <15 LCDs per year (USEPA,1984)
Benzene <8 CDs per year (USEPA,1979b)
Arsenic <5 LCDs per year (USEPA,1980)
CD « Cancer Death; LCD - Lung Cancer Death
Risks for passive smoking and radlonuclides are best estimates, and risks for
other pollutants are upper bound.
-------
Table Al. TIME SPENT IN VARIOUS MICROENVIRONWENTS BY PERSONS IN 44 U. S.
CITIES. EXPRESSED IN AVERAGE HOURS PER DAY. Ott- (in press); NRC (1981);
Szaial(1972)
Married House- • • •
Mlcroenvironment Employed Men. All Days Employed Woman, All Days wives, All pa_i | | |
Inside one's home 13.4 15.4 20.5
Just outside one's
home 0.2 0.0 0.1
at one's workplace 6.7 5.2
in transit 1.6 1.3 1.0
in other people's 0.5 0.7 0.8
homes
in places of business 0.7 0.9 1.2
in restaurants and bars 0.4 0.2 0.1
in all other locations 0.5 0.3 0.3
Total 24.0 24.0 24.0
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TABLE A2
CALCULATION OF THE RANGE OF CONCENTRATION Q, and EXPOSURE Nd TO WHICH NONSMOKERS
ARE SUBJECT UNDER TEE MODEL GIVEN BY EQUATIONS 2 and 3 ASSUMING ASHRAE STANDARD VENTILA1
A. USING ASHRAE 62-73 RECOMMENDED MAXIMUM MAKEUP AIR BASED ON OCCUPANCY
Occupants air- Exposure - Concentration
OCCUPANCY per 1000 ft2 changes/
[per 100 m2] hour (ach) (mg/8hrs) (ug/m3)
MAXIMUM
MINIMUM
OFFICES
150
5
10
18
0.5
1.5
1.69
2.03
1.35
213
256
170-
B. USING ASHRAE 62-73 ABSOLUTE MINIMUM MAKEUP AIR BASED ON OCCUPANCY
MAXIMUM 150 4.5 6.77 853
MINIMUM 5 0.15 6.77 853
OFFICES 10 0.3 6.77 853
C. USING ASHRAE 62-73 RECOMMENDED MINIMUM MAKEUP AIR BASED ON OCCUPANCY
MAXIMUM 150 9 3.38 655
MINIMUM 5 0.3 3.38 655
OFFICES 10 0.9 2.26 284
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TABLE A3 RANGE OF TYPICAL ADULT RESPIRATION RATES FOR DIFFERENT LEVELS OF EFFORT
after Aitman and Dltmer (1971).
ACTIVITY LEVEL
Resting
Sitting
Alternate Sitting & Light Work
Light Work
Heavy Work
RESPIRATION RATE (m3/hr)
0.36
0.60
0.99
1.47
2.04
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C-4
APPENDIX C
AGE-STANDARDIZED ESTIMATION OF LUNG CANCER DEATHS FROM PASSIVE SMOKING
Females
SDANever Spokers
Non-SDA Never smokers
S yr. Age
>roup
35-39
40-44
45-49
50-54
55-59
60-64
65-69
70-74
75-79
80-84
85+
Total
5-yr Age Group
35-39
40-44
45-49
50-54
55-59
60-64
65-69
70-74
75-79
80-84
85+
Total
1.
Total
LCDs
(17 yr
period
0
0
0
1.119
1.000
1.101
1.148
0
1.000
7.775
2.258
15.401
SDA
0
0
0
0
1.119
1.000
3.401
1.115
0
1.143
2.235
10.013
2.
Person
yr at
Risk
3791
11494
18757.5
24808.5
24702
24051.5
23326.5
21809
18822
13435.5
10017.5
195,015
3.
Average
Annual
No. of Per-
sons
223.0
676.1
1103.4
1459.3
1453.1
1414.8
1372.1
1282.9
1107.2
790.3
589.5
11,472
4.
LCDs
per 100,000
Person
Years
0
0
0
4.5106
4.0483
4.5777
4.9214
0
5.3219
57.869
22.541
103.7899
Males
Never Smokers
1926.5
5732.5
9177
11480
10359.5
8763.5
7386.5
6360.5
5278.5
3957.0
3160.0
73581.5
113.0
337.2
539.8
675.3
609.4
515.5
434.5
374.1
310.5
232.8
185.9
4328
0
0
0
0
10.8017
11.440
46.0435
17.5301
0
28.8855
70.7278
185.4286
5.
Total
LCDs
(12.58 yr
period)
0
1
2
4
8
7
4
9
10
6
10
61
6.
Person yrs
At Risk
5766
16466
38319
61630
71289
65054
55614
44248
29250
15301
7891
410.828
Non-SDA Never
0
0
0
1
2
4
8
0
2
4
2
23
1581
3479
9662
19313
23848
19535
14105
9786
6541
3517
1671
113,038
7.
Average
Annual No.
of Persons
at Risk
458.3
1308.3
3046.9
4899.0
5666.9
5171.2
4420.8
3517.3
2325.1
1216.3
627.3
32,657
Suckers
119.3
276.6
768.0
1535.2
1895.6
1552.9
1121.2
777.9
520.0
279.6
132.8
8979. 1
8.
LCDs
per 100,000
Person
Yrs.
0
6.0731
5.2193
6.4909
11.222
10.760
7.1924
20.340
34.188
39.213
126.73
267.4287
0
0
0
5. 1779
8.3865
20.4761
56.7!75
0
30.5764
IS3.733
119.689
354.7564
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C-5
APPENDIX C
ACE-STANDARDIZED ESTIMATION OF LUNG CANCER DEATHS FROM PASSIVE SMOKING (con't.)
Feaale
Male/Female
5 yr Age
Croup
35-39
40-44
45-49
50-54
55-59
60-64
65-69
70-74
75-79
80-84
85+
Total
9.
Annual
LCDs
per 100,000
(Non-SDA-
SDA
0
6.0731
5.2193
1.9803
7.1737
6.1823
2.2710
20.340
28.875
-18.656
104.189
163.6477
10.
Average
Age-Specific
No. of SDA
& Non SDA
at Risk
681
1985
4149
6358
7120
6586
5793
4800
3432
2006
1217
44,127
11.
Average
Age-Spec! fie
No. of SDA
& Non SDA
at Risk
913
2599
5457
8569
9625
8654
7349
5952
4263
2518
1536
57,435
12.
Annual
Weighted
Mean LCD
per 100,000
(unisex)
0
4.64
4.50
2.81
4.67
6.87
4.05
13.0
29.2
2.35
92.6
164.69
13.
Mean
age of
5 yr
Group
37.5
42.5
47.5
52.5
57.5
62.5
67.5
72.5
77.5
82.5
87.5
14.
Mean No.
of Persons
At Risk at
each yr of
5 yr Croup
95,201
94,122
92,339
89,590
85,477
79,396
71,177
60,455
46.689
31,209
11,913
(1974
Census
(whites
per 100,000
at Birth)
15.
Mean No.
of Persons
At Risk In
Entire 5 yr
Age Group
476,005
470,610
461,645
447,950
427,385
396,980
355,885
302,275
233,445
156,045
59,565
3,787,790
16.
Age
Specific
Age Stand
(1974 U.S.
White
Populat ion)
LCDs
0
21.84
20.77
12.59
19.96
27.27
14.41
39.30
68.17
3.67
55.16
203.14
5 yr. Age
Males
35-39
40-44
45-49
50-54
55-59
60-64
65-69
70-74
75-79
80-84
0
0
0
5.1779
-2.4152
9.0651
10.6740
-17.5301
30.5764
84.8475
232
614
1308
2211
2505
2068
1556
1152
831
512
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APPENDIX C
C-6
5 Yr. Age
Group
35-39
40-44
45-49
50-54
55-59
60-64
65-69
70-74
75-79
80-84
85+
17.
Average life
Expectancy
for the 5-
year Age
Group
_
33.1
28.7
24.6
20.8
17.2
14.0
11.1
8.6
6.6
3.1
17 + 9
18.
Person
years of
life
lost due
to LCDs
f roa
passive
SEBoklng
0
723
596
310
415
469
202
436
586
24
171
3932
19.
LCDs per
year In age
group In entire
1979 U.S.
nonsmoking
population
aged 2.
35 years
0
360
343
207
329
449
237
647
1123
61
909
4665
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