National
Institute for Occupational Safety and Health
Current
Intelligence Bulletins (CIBs) are issued by the National Institute
for Occupational Safety and Health (NIOSH), Centers for Disease
Control, Atlanta, Georgia, to disseminate new scientific information
about occupational hazards. A CIB may draw attention to a
formerly unrecognized hazard, report new data on a known hazard,
or disseminate information on hazard control.
CIBs
are distributed to representatives of academia, industry,
organized labor, public health agencies, and public interest
groups, as well as to Federal agencies responsible for ensuring
the safety and health of workers.
Copies
are available to individuals upon request from the Division
of Standards Development and Technology Transfer, NIOSH (Robert
A. Taft Laboratories, 4676 Columbia Parkway, Cincinnati, Ohio
45226). We welcome suggestions concerning the content, style,
and distribution of these documents.
The
purpose of this bulletin is to disseminate information about
the potential risk of cancer to workers exposed to environmental
tobacco smoke (ETS). In 1964, the Surgeon General issued the
first report on smoking and health, which concluded that cigarette
smoking causes lung cancer. Since then, research on the toxicity
and carcinogenicity of tobacco smoke has demonstrated that
the health risk from inhaling tobacco smoke is not limited
to the smoker, but also includes those who inhale ETS. ETS
contains many of the toxic agents and carcinogens that are
present in mainstream smoke, but in diluted form. Recent epidemiologic
studies support and reinforce earlier published reviews by
the Surgeon General and the National Research Council demonstrating
that exposure to ETS can cause lung cancer. These reviews
estimated the relative risk of lung cancer to be approximately
1.3 for a nonsmoker living with a smoker compared with a nonsmoker
living with a nonsmoker. In addition, recent evidence also
suggests a possible association between exposure to ETS and
an increased risk of heart disease in non smokers. Although
these data were not gathered in an occupational setting, ETS
meets the criteria of the Occupational Safety and Health Administration
(OSHA) for classification as a potential occupational carcinogen
[Title 29 of the Code of Federal Regulations, Part 1990].
NIOSH therefore considers ETS to be a potential occupational
carcinogen and recommends that exposures be reduced to the
lowest feasible concentration. All available preventive measures
should be used to minimize occupational exposure to ETS. NIOSH
urges employers to disseminate this information to employees.
NIOSH also requests that professional and trade associations
and unions inform their members about the potential hazards
of exposure to ETS. Readers seeking more detailed information
about the studies cited in this bulletin are urged to consult
the original publications.
- J.
Donald Millar, M.D., D.T.P.H. (Lond.)
- Assistant
Surgeon General
- Director,
National Institute for
- Occupational
Safety and Health
- Centers
for Disease Control
The
National Institute for Occupational Safety and Health (NIOSH)
has determined that environmental tobacco smoke (ETS) is potentially
carcinogenic to occupationally exposed workers. In 1964, the
Surgeon General issued the first report on smoking and health,
which concluded that cigarette smoke causes lung cancer. Since
then, research on the toxicity and carcinogenicity of tobacco
smoke has demonstrated that the health risk from inhaling tobacco
smoke is not limited to the smoker, but also includes those
who inhale ETS. ETS contains many of the toxic agents and carcinogens
that are present in mainstream smoke, but in diluted form. Recent
epidemiologic studies support and reinforce earlier published
reviews by the Surgeon General and the National Research Council
demonstrating that exposure to ETS can cause lung cancer. These
reviews estimated the relative risk of lung cancer to be approximately
1.3 for a nonsmoker living with a smoker compared with a nonsmoker
living with a nonsmoker. In addition, recent evidence suggests
a possible association between exposure of nonsmokers to ETS
and an increased risk of heart disease.
Although
these data were not gathered in an occupational setting, ETS
meets the criteria of the Occupational Safety and Health Administration
(OSHA) for classifying substances as potential occupational
carcinogens [Title 29 of the Code of Federal Regulations,
Part 1990]. NIOSH therefore recommends that ETS be regarded
as a potential occupational carcinogen in conformance with
the OSHA carcinogen policy, and that exposures to ETS be reduced
to the lowest feasible concentration. Employers should minimize
occupational exposure to ETS by using all available preventive
measures.
This
bulletin was prepared by the Division of Standards Development
and Technology Transfer (DSDTT), Richard W. Niemeier, Ph.D.,
Director, and the Division of Surveillance, Hazard Evaluations,
and Field Studies (DSHEFS), Lawrence J. Fine, M.D., Director.
David M. Votaw, DSDTT, developed this document with the help
of Kyle Steenland, Ph.D., DSHEFS, who developed the epidemiology
section. The contributions of other National Institute for Occupational
Safety and Health (NIOSH) personnel are gratefully acknowledged:
David D. Bayse, Ph.D.; Philip J. Bierbaum; Robert M. Castellan,
M.D.; Jerome P. Flesch; Hugh J. Hansen, Ph.D.; Bryan D. Hardin,
Ph.D.; G. Kent Hatfield, Ph.D.; Frank J. Hearl; Marvin D. Mills;
William J. Moorman, Ph.D.; John E. Parker, M.D.; Edward L. Petsonk,
M.D.; Laurence D. Reed; Leslie T. Stayner, Ph.D.; and Ralph
D. Zumwalde.
Ruth
E. Grubbs and Anne C. Hamilton performed editorial review
and coordinated production; Vanessa L. Becks and Susan R.
Kaelin provided editorial assistance and produced camera-ready
copy; and Judith G. Curless typed the draft.
The
Surgeon General has concluded that tobacco smoke is a carcinogen
and an important risk factor for heart disease. The purpose
of this bulletin is to disseminate information about the potential
carcinogenicity of environmental tobacco smoke(1)
(ETS) in the workplace. Evidence is now clear that the health
risk from inhaling tobacco smoke is not limited to the smoker,
but also includes those who inhale ETS. Recent epidemiologic
studies of nonsmokers exposed to ETS have s own an increased
relative risk for lung cancer compared with unexposed nonsmokers.
In addition, recent evidence suggests that exposure of nonsmokers
to ETS may be associated with an increased risk of heart disease.
This bulletin describes the results and implications of these
studies.
The
conclusions and recommendations in this Current Intelligence
Bulletin (CIB) are based on the following:
Reports
of the Surgeon General on the health effects of tobacco smoke
Comparison of the chemical composition of ETS with that of
mainstream smoke(2) (MS). Results from
recent epidemiologic studies of nonsmokers exposed to ETS
Methods
for controlling involuntary exposures to ETS in the workplace
are also discussed.
In
1964, the Surgeon General issued the first report on smoking
and health, which concluded that cigarette smoke causes cancer
[DHEW 1964]:
Cigarette
smoking is causally related to lung cancer in men; the magnitude
of the effect of cigarette smoking far outweighs all other
factors. The data for women, though less extensive, point
in the same direction.... The risk of developing lung cancer
increases with duration of smoking and the number of cigarettes
smoked per day, and is diminished by discontinuing smoking.
Since
1964, evidence has continued to support the causal relationship
between exposure to cigarette smoke and lung cancer, demonstrating
that risk increases with amount and duration of smoking. Subsequent
research has increased our knowledge about the toxicity and
carcinogenicity of tobacco smoke and the risks of exposure.
Additional support for the Surgeon General's conclusion has
come from (1) animal studies that demonstrated the carcinogenicity
of tobacco smoke condensate, and (2) analytical studies demonstrating
that tobacco smoke contains carcinogens [DHEW 1972; DHHS 1982].
Cigarette smoking is the major cause of lung cancer (87% of
lung cancer deaths) and is estimated to account for 30% of
all cancer deaths [DHHS 1989].
The
1964 Surgeon General's report also pointed out that male cigarette
smokers have higher death rates from heart disease than nonsmokers.
Subsequent reports have concluded that cigarette smoking is
a major cause of heart disease and that smoking is a major
independent risk factor for heart attack [DHEW 1968; DHHS
1983].
On July
1, 1965, Congress approved the Federal Cigarette Labeling
and Advertising Act of 1965 (Public Use 89-92). This law,
which became effective on January 1, 1966, was the first of
a continuing series of Federal statutes enacting warning labels
to inform the public about the health hazards of smoking and,
subsequently, the use of other tobacco products. Presently,
the Comprehensive Smoking Education Act (Public Law 98-474)
[Title 15, SS 1331 of the U.S. Code] requires cigarette companies
o rotate four health warnings on all cigarette packages and
in advertisements.
ETS
contains many of the toxic agents and carcinogens that are present
in MS, but in diluted form [DHHS 1986]. The major source of
ETS is sidestream smoke(3) (SS), which contains
higher amounts of some toxic and carcinogenic agents than MS
when it is obtained in its undiluted form under laboratory conditions
[DHHS 1989]. For example, the release of volatile N-nitrosamines
and aromatic amines is higher in SS than in MS.
A major
reason that undiluted SS and MS have different concentrations
of toxic and carcinogenic agents is that peak temperatures
in the burning cone of a cigarette reach 800 to 900øC during
puffing, but only 600øC between puffs, resulting in less complete
combustion of tobacco during generation of SS. In addition,
most of the burning cone is oxygen deficient during smoldering
and produces a strongly reducing environment [NRC 1986]. Table
1 lists 26 toxic and carcinogenic agents identified in SS
and MS.
Table
1. Toxic and carcinogenic agents in undiluted cigarette
SS*,** |
Compound |
Type
of toxicity |
Amount
in SS (per cigarette) |
Ratio
of SS/MS |
Vapor
phase: |
Carbon
monoxide |
T |
26.8-61
mg |
2.5-14.9 |
Carbonyl
sulfide |
T |
2-3mg |
0.03-0.13 |
Benzene |
c |
400-500µg |
8-10 |
Formaldehyde |
c |
1,500µg |
50 |
3-Vinylpyridine |
SC |
300-450µg |
24-34 |
Hydrogen
cyanide |
T |
14-110µg |
0.06-0.4 |
Hydrazine |
c |
90ng |
3 |
Nitrogen
oxides |
T |
500-2,000µg |
3.7-12.8 |
N-nitrosodimethylamine |
C |
200-1,040ng |
20-130 |
N-nitrosopyrrolidine |
C |
30-390ng |
6-120 |
Particulate
phase: |
Tar |
C |
14-30mg |
1.1-15.7 |
Nicotine |
T |
2.1-46mg |
1.3-21 |
Phenol |
TP |
70-250µg |
1.3-3.0 |
Catechol |
CoC |
58-290µg |
0.67-12.8 |
o-Toluidine |
C |
3µg |
18.7 |
2-Naphthylamine |
C |
70ng |
39 |
4-Aminobiphenyl |
C |
140ng |
31 |
Benz(a)anthracene |
C |
40-200ng |
2-4 |
Benzo(a)pyrene |
C |
40-70ng |
2.5-20 |
Quinoline |
C |
15-20µg |
8-11 |
N'-nitrosonornicotine |
C |
0.15-1.7µg |
0.5-5.0 |
NNK |
C |
0.2-1.4µg |
1.0-22 |
N-nitrosodiethanolamine |
C |
43ng |
1.2 |
Cadmium |
C |
0.72µg |
7.2 |
Nickel |
C |
0.2-2.55µg |
13-30 |
Polonium-210 |
C |
0.5-1.6pCi |
1.06-3.7 |
*
- Sources: DHHS [1989]; Hoffmann and Hecht [1989].
** - Abbreviations: C, carcinogenic; CoC, cocarcinogenic;
MS, mainstream smoke; SC, suspected carcinogen; SS,
sidestream smoke; T, toxic; T?, tumor promoter; NNK,
4-(methyl-nitrosamino)-(3-pyridyl)- 1 -butanone.
|
ETS
is diluted in the air before it is inhaled and thus is less
concentrated than MS. However, active inhalation of MS is
limited to the time it takes to smoke each cigarette, whereas
exposure to ETS is constant over the period spent in the ETS-polluted
environment. This fact is reflected in measurements of nicotine
uptake by smokers and ETS-exposed nonsmokers [DHHS 1989].
Approximately
29% of the U.S. adult population smokes cigarettes, and exposure
to ETS is common [DHHS 1989]. Many people who report no exposure
to ETS have low concentrations of cotinine (a metabolite of
nicotine) in their urine, indicating exposure. The average concentration
of cotinine in the urine of nonsmokers has been reported to
be approximately 8 ng/ml compared with approximately 1,200 ng/ml
in smokers [Cummings et al. 1990]. The National Research Council
(NRC) estimated that nonsmokers exposed to ETS averaged 25 ng
of cotinine/ml, and active smokers averaged 1,825 ng/ml [NRC
1986]. Husgafvel-Pursiainen et al. [1987] found that nonsmoking
restaurant workers had an average urinary cotinine concentration
of 56 ng/ml, and nonsmokers not exposed to ETS had an average
concentration of 8.3 ng/ml. Other investigators have shown that
nonsmokers living with smokers have approximately two to three
times the amount of urinary cotinine as nonsmokers living with
nonsmokers [Haley et al. 1989].
Exposures
to ETS were measured by respirable suspended particulates
(<2.5 pm) and averaged 242 pg/m3 in public access
buildings [First 1984; NRC 1986; Repace and Lowrey 1980, 1982].
Studies reviewed by Repace and Lowrey [1990] suggested a 62%
probability of exposure to ETS for a nonsmoker in the workplace.
However, the relative contribution of work versus home environments
in ETS exposure has not been well quantified. In addition,
social settings outside the workplace or the home (e.g., restaurants
and bowling alleys) may contribute significantly to ETS exposure.
On the
basis of urinary cotinine concentrations, the NRC [1986] concluded
that nonsmokers exposed to ETS absorb the equivalent of 0.1
to 1.0 cigarette per day. On the basis of 1985 data, NIOSH
estimates that each cigarette smoker in the United States
smokes an average of about 21 cigarettes per day [NCHS 1988].
Blood and urine samples analyzed for vapor phase nicotine
indicate that nonsmokers exposed to ETS absorb about 1% of
the tobacco combustion products absorbed by active smokers
[NRC 19 6; DHHS 1986].
Surgeon
General
The Surgeon
General first addressed the possible health effects of involuntary
smoking in 1972 [DHEW 1972]. Evidence associating adverse health
effects with ETS exposure continued to be reported, and in 1986,
the Surgeon General's report entitled The Health Consequences
of Involuntary Smoking focused entirely on this subject [DHHS
1986]. This report cited 3 cohort studies and 10 case-control
studies that together documented an approximately 1.3-fold increase
in the risk of lung cancer among nonsmoking women, usually wives
exposed to their husbands' ETS. The 1986 Surgeon General's report
concluded that involuntary smoking is a cause of disease (including
lung cancer) in healthy nonsmokers; however, more data on the
dose and distribution of ETS exposure in the population are
needed to accurately estimate the magnitude of risk in the U.S.
population [DHHS 1986].
NRC
[1986]The NRC
also reviewed the important epidemiologic data available in
1986 (3 cohort studies and 10 case-control studies) on the adverse
health effects of ETS exposure. These studies were the same
ones reviewed by the Surgeon General, except for one case-control
study. The statistical power of a single study is often small,
but it can be improved by analyzing all the data simultaneously
across all studies (meta-analysis). Using this approach, the
NRC estimated that the relative risk for nonsmokers married
to smokers was 1.25 compared with nonsmokers married to nonsmokers,
taking into account the possible misclassification of smokers
as nonsmokers. Using data from urinary cotinine tests to estimate
the extent of ETS exposure, the NRC also estimated that the
relative risk of lung cancer for nonsmokers exposed to ETS at
home, at work, or elsewhere was 1.42 compared with unexposed
nonsmokers, with a plausible range of 1.24 to 1.61. The NRC
concluded that "the weight of the evidence derived from epidemiologic
studies shows an association between ETS exposure of nonsmokers
and lung cancer that, taken as a whole, is unlikely to be due
to chance or systematic bias."
Wald
et al. [1986]In another
quantitative meta-analysis covering the same studies reviewed
by the NRC, Wald et al. [1986] reached similar conclusions.
Their analysis showed a 30% greater risk of lung cancer (relative
risk 1.30) for nonsmokers living with smokers relative to nonsmokers
living with nonsmokers. The authors concluded that this result
was unlikely to have occurred by chance and that it underestimated
the true risk associated with exposure to ETS because nonsmokers
living with nonsmokers are expose to ETS in other settings (e.g.,
at work). The relative risk is thus based on a reference group
that is partially exposed.
Blot
and Fraumeni [1986]Blot and
Fraumeni [1986] analyzed the same studies reviewed by the Surgeon
General and the NRC except for one case-control study. Combining
data across the reviewed studies, these investigators concluded
that the overall relative risk for nonsmoking women married
to husbands who smoked was 1.3 (95% confidence interval [CI],
1.1- 1.5) compared with nonsmoking women married to nonsmokers.
These authors also concluded that the relative risk for nonsmokers
exposed to heavy smoking was 1.7 (95% C , 1.4-2.1). They found
that the epidemiologic studies strongly suggested an increased
risk that was biologically plausible, but that limitations in
assessing ETS exposure had introduced uncertainty.
Eight
additional studies of lung cancer and ETS exposure among those
who never smoked have been published since the reviews by
the Surgeon General [DHHS 1986; NRC 1986; Wald et al. 1986;
Blot and Fraumeni 1986] (Table 2).
Table
2. Recent studies of lung cancer among ETS-exposed
persons who never smoked |
Study |
Design |
Exposure
definition |
Relative
risk* |
Comment |
Update
of Gillis et al. [1984] by Hole et al. |
12-yr
followup, 3,960 men and 4,037 women aged 45-64 in 1972-76 |
Living
with smoker or ex-smoker at the time of the survey |
2.41
(CI, 0.45-12.83; 7 observed |
Adjusted
for age, sex, and social class |
Brownson
et al. [1987] |
19
cases, 47 controls |
Exposure
for >4 hr\day |
1.68
(CI, 0.39-2.97) |
Adjusted
for age, income and occupation |
Humble
et al. [1987] |
28
cases, 54 controls |
Lived
with spouse who smoked |
For
cigarette ETS exposure: 2.2 (90% CI, 1.0-4.9) For any
type of ETS exposure: 2.6 (90% CI, 1.2-5.6 |
Adjusted
for ethnicity and age |
Gao
et al. [1987] |
246
cases, 375 controls |
Lived
with a smoker |
<20
yr, 1.0; 20-29 yr, 1.1 (CI, 0.7-1.8); 30-39 yr, 1.3 (CI,
0.8-2.1); >40yr, 1.7 (CI, 1.0-2.9) |
Adjusted
for age and education |
Lam
et al. [1987] |
199
cases, 375 controls |
Lived
with a smoker |
1.65
(CI, 1.16-2.35) |
Matched
for age and neighborhood |
Janerich
et al. [1990] |
191
cases, 335 controls |
Lived
with a spouse who smoked |
1.65
(CI, 1.16-2.35) |
Matched
for age, sex, and county of residence; relative risk for
spousal smoking = 0.9 |
Shimizu
et al. [1988] |
90
cases, 191 controls |
>25
smoker-yr of exposure during childhood |
2.07
(CI, 1.16-3.68) |
Matched
for age, sex, and hospital; relative risk for spousal
smoking = 1.1 |
Geng
et al. [1988] |
54
cases, 93 controls |
Lived
with spouse who smoked |
2.16
(CI, 1.03-4.53) |
Matched
for race, age, and marital status; positive dose response;
methodologic details not presented |
* Confidence interval is 95% unless otherwise indicated. |
Hole
et al. [1989]Hole et
al. [1989] updated an earlier cohort study [Gillis et al. 1984]
of 3,960 men and 4,037 women in Scotland. These men and women
had lived in the same households and had been followed for an
average of 11.5 years. They were aged 45-64 at the time of the
original interviews, which took place from 1972 to 1976. The
unexposed group was defined as persons who never smoked and
lived with nonsmokers at the time of interview. The exposed
group was composed of persons who never smoked and lived with
smokers. A third group was composed of persons who had smoked
during some period in the past. In the follow up study [Hole
et al. 1989], only 2 deaths from lung cancer occurred in the
unexposed group and 7 in the exposed group, compared with 147
deaths from lung cancer among smokers. The adjusted relative
risk for the exposed group was 2.41 (95% CI, 0.45-12.83), compared
with a relative risk of 10.64 for persons who had smoked in
the past. The risk for smokers was the same whether or not they
were exposed to ETS.
Brownson
et al. [1987]Brownson
et al. [1987] conducted a case-control study of persons diagnosed
with adenocarcinoma of the lung. A subset of 19 nonsmoking women
was identified from this group and was compared with 47 controls.
Exposure to ETS was classified as less than 4 hr/day or more
than 4 hr/day (there was no specification of when this exposure
occurred). The odds ratio for those exposed more than 4 hr/day
was 1.68 (95% CI, 0.39-2.97) after adjustment for confounders,
whereas the odds ratio for those expos d fewer than 4 hr/day
was 1.00. The study does not state whether the nonsmoking females
had ever smoked, but the implication is that they had never
smoked. Because many of the subjects were deceased, smoking
status was often determined from interviews with next of kin.
The study lacked sufficient sample size to draw substantive
conclusions, but it did suggest an increased risk for adenocarcinoma
among nonsmokers exposed to ETS.
Humble
et al. [1987]Humble et
al. [1987] evaluated the risk of lung cancer in a case-control
study of 28 lung cancer patients who never smoked and lived
with a smoking spouse compared with a control group of 54 persons
who never smoked and lived with a nonsmoking spouse. Surrogate
responses about smoking habits were used for 19 of the 28 cases,
with most of these data provided by the spouse.
The
adjusted odds ratio for nonsmokers living with a spouse who
smoked cigarettes was 2.2 (90% CI, 1.0-4.9), and it was 2.6
(90% CI, 1.2-5.6) for nonsmokers exposed to any type of ETS
(including pipes and cigars). There was no trend of increasing
risk with increased duration of exposure or increased amount
regularly smoked by the spouse. In addition, marriage to a
smoker did not increase the risk for persons who had ever
smoked. This study contained no data on exposure to ETS outside
the home or from other persons (nonspouses) living i the home.
Gao
et al. [1987]Gao et al.
[1987] studied 672 female lung cancer patients and 735 population-based
controls in Shanghai, China. Patients had been diagnosed as
having lung cancer between 1984 and 1986, and both patients
and controls were all interviewed directly. The odds ratio (adjusted
for age and education) was 0.9 (95% CI, 0.6-1.4) for persons
who had ever lived with a smoker during adulthood, and 1. 1
(95% CI, 0.7-1.7) for those who had ever lived with a smoker
during childhood. However, for 246 married patients and 375 married
controls, risk increased with increasing years of marriage to
a spouse who smoked, reaching 1.7 (95% CI, 1.0-2.9) among nonsmokers
who lived with a smoker for more than 40 years.
Lam
et al. [1987]Lam et al.
[1987] studied 445 female lung cancer patients in Hong Kong
matched by age with 445 female controls from the same neighborhood.
Analyses (unmatched) for exposure to ETS included 199 married
patients and 335 married controls who never smoked. A small
number of persons who were not married and never smoked (5%
to 6% of the patients and controls) were also included and treated
as unexposed to ETS. Wives exposed to ETS from a husband who
smoked had an odds ratio of 1.65 (95% CI, 1.16 2.35), with the
predominant type of cancer being adenocarcinoma (odds ratio
2.12). These odds ratios were not adjusted for any confounders.
Janerich
et al. [1990]Janerich
et al. [1990] conducted a population-based case-control study
of 191 persons who never smoked and were diagnosed with lung
cancer from 1982 to 1984; this group was compared with individually
matched controls who never smoked. Controls were matched by
age, sex, and county of residence. Surrogate interviews were
necessary for 62 cases and thus were also conducted for their
matched controls. The number of years of exposure to ETS in
the home was calculated by summing the number of smokers in
the home per year across all years of life. The number of years
exposed to ETS outside the home was also estimated, although
details were not given in the report. Childhood and adolescent
exposures in the home, adult exposures in the home, and adult
exposures outside the home all contributed about equally to
total lifetime exposure to ETS. For spouses, ETS exposure was
also calculated by multiplying the number of packs smoked per
day by the number of years the spouse smoked. The major finding
of the study was a trend of increasing lung cancer risk with
increasing years of exposure during childhood. Household exposure
to ETS for 25 or more years that included childhood doubled
the risk of lung cancer (odds ratio, 2.07; 95 % CI, 1.16-3.68).
No consistent increase in cancer risk occurred with increasing
years of adulthood exposure to all sources of ETS, but persons
exposed for the greatest number of years showed the highest
risk (odds ratio, 1.11; 95% CI, 0.56-2.20). Separate analyses
of exposure to ETS from spousal smoking found no excess risk
of lung cancer for individuals married to smokers, and no trend
of increased risk with increased years of exposure or with increased
amount smoked by the spouse. Odds ratios in this study were
not adjusted for any confounders, and odds ratios for exposure
to ETS from spousal smoking do not appear to have been adjusted
for childhood ETS exposures.
Shimizu
et al. [1988]Shimizu
et al. [1988] published a case-control study of 90 female lung
cancer patients who never smoked. Each patient was matched by
age, hospital, and admission date to 2 controls of the same
sex who did not have lung cancer (for 17 patients, only 1 control
was used). Information was gathered about occupation, exposure
to ETS, diet, and cooking fuels. The risk of lung cancer was
significantly elevated for women who never smoked and lived
in a home where the mother smoked (relative risk, 4. ; P<0.05)
or the paternal grandfather smoked (relative risk, 3.2; P<0.05).
Exposure to the ETS of other household members (including the
husband, the father, and the children) was not associated with
increased risk. The relative risk for exposure to ETS at work
was 1.2. The authors found no increasing trend in risk with
the number of cigarettes smoked by the mother or the paternal
grandfather. However, the authors indicated that the subjects
had trouble recalling the amount of smoking to which they had
been exposed. The authors also pointed out that in Japan, children
spend considerable time with their mother in the home, and less
with the father; it is also common for the retired father of
the husband to live in his son's home.
Geng
et al. [1988]Geng et
al. [1988] studied 54 nonsmoking (undefined) women with lung
cancer in Tianjin, China. These patients were matched with controls
by race, age, sex, and marital status. The authors reported
a significantly elevated odds ratio for the patients exposed
to ETS from spouses (odds ratio, 2.16; 95% CI, 1.03-4.53), but
it is not clear whether these women included former smokers.
Their risk increased with the amount and duration (years) of
the husband's smoking.
Summary
of Results from Lung Cancer Studies The studies
published since 1986 have concentrated on ETS exposure through
spousal smoking during adulthood [Hole et al. 1989; Brownson
et al. 1987; Humble et al. 1987; Gao et al. 1987; Lam et al.
1987; Janerich et al. 1990; Shimizu et al. 1988; Geng et al.
1988], although some studies include data on childhood exposures
[Janerich et al. 1990; Shimizu et al. 1988; Gao et al. 1987].
The data from these more recent studies do not individually
demonstrate a clear causal relationship between ETS exposure
and lung cancer, but their consistent finding of a relative
risk greater than 1.0 for nonsmokers exposed to ETS provides
evidence of a positive association. These data are consistent
with and reinforce the reviews by NRC [1986], DHHS [1986], Blot
and Fraumeni [1986], and Wald et al. [ 1986], all of which concluded
that ETS exposure is associated with an increased risk of lung
cancer for nonsmokers.
The
most important limitation observed in all studies reporting
lung cancer risks among persons who never smoked is the lack
of quantitative ETS exposure data. Most studies have defined
exposure to ETS for nonsmokers on the basis of living with
or being married to a smoker. All of the case-control studies
ascertained the potential for exposure by interviewing subjects
and controls (or surrogates) without any other independent
assessment of ETS exposure. Questionnaires often failed to
include specific questions about afl sources of ETS. Most studies
included limited or no information about the risk of lung
cancer from ETS exposure in the workplace.
The
potential exists for a positive bias, particularly in the
case-control studies, where ex-smokers with lung cancer might
have been misclassified as never having smoked. The misclassified
ex-smokers are more likely to be married to smokers and to
develop lung cancer than those who never smoked. However,
the NRC [1986] estimated that the effect of such misclassification
would have been relatively slight and could not entirely account
for the increased risk of lung cancer following exposure o
ETS. This conclusion by the NRC is based on calculations that
assume a degree of misclassification (based on nonsmoker urinary
cotinine data) and its likely effect on the observed lung
cancer risk. In addition, the risk of lung cancer in these
studies is based on a reference group of nonsmokers living
with nonsmokers who are exposed to ETS in other settings.
This background exposure results in underestimation of the
true risk.
Several
risk assessments have been performed for persons who never
smoked and were exposed to ETS. The NRC [1986] estimated that
of the 7,000 lung cancer deaths reported in 1985 among U.S.
women who never smoked, 2,010 (29%) were attributable to ETS.
The corresponding number for men was 820 (16%) of the 5,200
lung cancer deaths among U.S. males who never smoked. Wells
[1988] estimated that approximately 3,000 of the lung cancer
deaths reported in 1985 among persons who never smoked occurred
as a result of ETS exposure. Repace and Lowrey [1990] estimated
that approximately 5,000 of the lung cancer deaths reported
in 1988 among persons who never smoked and ex-smokers occurred
as a result of ETS exposure. These risk assessments used a
1.3 to 1.5 relative risk of lung cancer for nonsmokers exposed
to ETS at home or elsewhere compared with unexposed persons.
The number of deaths attributable to ETS exposure was derived
using standard formulas for attributable risks [Kleinbaum
et al. 1983] with the estimated number of annual lung cancer
deaths in the United States for persons who have never smoked.
Surgeon
General
The Surgeon
General [DHHS 1986] reviewed four epidemiologic studies of cardiovascular
disease in persons exposed to ETS [Lee et al. 1986; Hirayama
1984; Gillis et al. 1984; Garland et al. 1985] (Table 3). He
concluded that further studies on the relationship between involuntary
smoking and cardiovascular disease are needed in order to determine
whether involuntary smoking increases the risk of cardiovascular
disease. 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 cardiovascular disease can be established.
NRC
[1986]
The NRC
[1986] reviewed four epidemiologic studies that evaluated the
association between heart disease and ETS exposure [Garland
et al. 1985; Gillis et al. 1984; Hirayama 1984; Svendsen et
al. 1985, 1987(4)] (Table 3). The same NRC
review examined studies of the effects of ETS exposure on heart
rate and blood pressure among healthy individuals. No statistically
significant increases were found in heart disease or effects
on heart rate and blood pressure. The NRC report concluded that
with respect to chronic cardiovascular morbidity and mortality,
although biologically plausible, there is no evidence of statistically
significant effects due to ETS exposure, apart from the study
by Hirayama (see Table 3) in Japan."
Other
Epidemiologic and Experimental Studies Since publication
of the reports by the NRC and the Surgeon General, researchers
have published two epidemiologic studies of heart disease and
ETS exposure [Humble et al. 1990; Helsing et al. 1988], and
one update [Hole et al. 1989] of an earlier cohort study [Gillis
et al. 1984] (Table 3). Experimental studies of the effects
of ETS on the heart have also been published [Davis et al. 1989;
Allred et al. 1989; Sheps et al. 1990].
Table
3. Recent studies of hear disease among ETS-exposed
persons who never smoked |
Study |
Design |
Exposure
definition |
Relative
risk |
Comment |
Update
of Gillis et al. [1984] by Hole et al. [1989]** |
12-yr
followup, 3,960 men and 4,037 women aged 45-64 in 1972-76 |
Living
with a smoker or ex-smoker in early 1970's |
2.01
(CI, 1.21-3.35; 485 observed) |
Adjusted
for cardiovascular risk factors***, positive dose response |
Humble
et al. [1990] |
20-yr
followup, 513 women aged 40+ |
Living
with smoker in 1960 |
1.59
(CI, 0.99-2.57) |
Adjusted
for cardiovascular risk factors, dose response in some
strata |
Helsing
et al. [1988] |
12-yr
followup, 4,162 men and 14,873 women, aged 25+ in 1963 |
Living
with smoker or ex-smoker in 1963 |
Men:
1.31 (CI, 0.99-2.57) |
Adjusted
for cardiovascular risk factors, dose response among women
only |
Svendsen
et al. [1985, 1987]**** |
7-yr
average followup, 1,245 men aged 35-57 in 1973-82 |
Married
to smoker or ex-smoker |
1.61
(CI, 0.96-2.71; 90 observed) |
Adjusted
for cardiovascular risk factors, positive dose response |
Garland
et al. [1985] |
10-yr
followup, 695 women aged 50-79 in 1972-74 |
Married
to a smoker or ex-smoker |
2.9
(estimate; 19 observed) |
Adjusted
for age |
Hiryama
[1984] |
16-yr
followup, 91,540 women aged 40+ |
Married
to a smoker or ex-smoker |
Low
exposure: 1/10 (90% CI, 0.91-1.33) |
Significant
dose response |
*
- Confidence interval is 95% unless otherwise indicated.
** - Hole et al. [1989] provide updated results of the
same population studied by Gillis et al. [1984].
*** - Serum cholesterol, blood pressure, and body mass
index.
**** - Svendsen et al. [1987] is the full report of the
abstract published by Svendsen et al. [1985]. |
The
studies reported by Hole et al. [1989], Helsing et al. [1988],
and Humble et al. [1990] associated ETS exposure with an increase
of heart disease among persons who never smoked. The studies
by Hole et al. [1989] and Helsing et al. [1988] are both large
follow-up cohort studies that used direct interviews of men
and women who lived in the same household. Study of these
cohorts demonstrated an excess of heart disease in persons
who lived with smokers and never smoked compared with persons
ho lived with nonsmokers and never smoked. Furthermore, Hole
et al. [1989] and Humble et al. [1990] show an increasing
risk for heart disease mortality with increasing exposure
to ETS at home. Helsing et al. [1988] found a similar trend
in women but not men.
Experimental
studies support the hypothesis that ETS exposure has deleterious
effects on platelets and the endothelium [Davis et al. 1989]
and can decrease the time to onset of angina pectoris in patients
with coronary artery disease [Allred et al. 1989]. Allred
et al. [1989] reported that the time to angina decreased in
heart disease patients who exercised after exposure to airborne
carbon monoxide (CO) at concentrations producing 2% and 3.9%
carboxyhemoglobin (COHb) in the blood. Sheps et l. [1990]
observed that arrhythmias in heart disease patients increased
when they exercised after exposure to airborne CO at concentrations
producing 6% COHB in the blood. Persons exposed to ETS in
unventilated areas have been shown to have COHB concentrations
of 2% to 3% [NRC 1986].
Wells
[1988] estimated that among nonsmokers in the United States,
32,000 deaths from heart disease each year were attributable
to ETS exposure. Wells used estimated rates for death from
heart disease among nonsmokers and a relative risk of 1.30
for ETS-exposed nonsmokers compared with unexposed nonsmokers.
Glantz
and Parmley [1991] recently reviewed the epidemiologic literature
on exposure to ETS and heart disease (including the studies
in Table 3) from 1984 to the present. These researchers estimated
a 30% increase (relative risk, 1.30; 95% CI, 1.2-1.4) in the
risk of death from ischemic heart disease or myocardial infarction
in nonsmoking individuals exposed to ETS at home. Glantz and
Parmley also noted that several of these studies found a dose-response
relation between the amount of smoking by the spouse and the
risk of heart disease in the nonsmoking spouse; they concluded
that exposure to ETS can cause heart disease.
Summary
of Results from Heart Disease Studies The principal
limitation found in the lung cancer studies also applies to
the studies of heart disease in persons exposed to ETS-that
is, the indirect method of assessing exposure to ETS (usually
defined as spousal smoking). The second limitation of these
heart disease studies is the difficulty in controlling for all
known cardiovascular risk factors (e.g., blood pressure, serum
cholesterol, and body mass index). In addition, the risk of
heart disease for ETS-exposed persons who never smoked seems
large compared with the risk of heart disease for smokers. Unlike
lung cancer mortality, where the relative risk for smokers compared
with nonsmokers is 22.4 for men and 11.9 for women, the relative
risk of heart disease mortality for smokers compared with nonsmokers
is 1.9 for men and 1.8 for women [DHHS 1989]. Note that the
nonsmoking comparison group for these risk estimates includes
those exposed to ETS.
In
1964 the Surgeon General concluded that cigarette smoke Causes
lung cancer. Since that time, additional research on the toxicity
and carcinogenicity of tobacco smoke has demonstrated that the
health risks from inhaling tobacco smoke are not limited to
smokers, but also include those who inhale ETS. ETS contains
many of the toxic agents and carcinogens found in MS, but in
diluted form. Recent epidemiologic studies support and reinforce
the conclusions of the reviews by the Surgeon General and the
NRC demonstrating that exposure to ETS can cause lung cancer.
These reviews estimated the relative risk for lung cancer to
be approximately 1.3 for nonsmokers living with smokers compared
with nonsmokers living with nonsmokers. In addition, recent
evidence also suggests a possible association between exposure
to ETS and an increased risk for heart disease in nonsmokers.
The recent epidemiologic studies (including those associating
ETS with other adverse health effects) point to a pattern of
health effects that is similar for both smokers and nonsmokers
exposed to ETS.
NIOSH
recognizes that these recent epidemiologic studies have several
shortcomings: lack of objective measures for characterizing
and quantifying exposures, failure to adjust for all confounding
variables, potential misclassification of ex-smokers as nonsmokers,
unavailability of comparison groups that have not been exposed
to ETS, and low statistical power. Nonetheless, NIOSH has
determined that the collective weight of evidence (i.e., that
from the Surgeon General's reports, the similarities in composition
of MS and ETS, and the recent epidemiologic studies) is sufficient
to conclude that ETS poses an increased risk of lung cancer
and possibly heart disease to occupationally exposed workers.
The epidemiologic data are not sufficient to draw conclusions
about other health effects such as cervical cancer, ischemic
stroke, spontaneous abortion, and low birth weight.
Several
systems exist for classifying a substance as a carcinogen. Such
classification systems have been developed by NTP [1989], IARC
[1987], and OSHA [29 CFR 1990]. NIOSH considers the OSHA classification
system (Identification, Classification, and Regulation of Potential
Occupational Carcinogens [29 CFR 1990], also known as the OSHA
carcinogen policy) the most appropriate for use in identifying
occupational carcinogens(5). The Surgeon
General has concluded that cigarette smoke causes lung cancer
as well as heart disease. Table 1 lists 21 known or suspected
carcinogens, cocarcinogens, and tumor promoters identified as
components of ETS and MS in analytical studies. Furthermore,
a large body of evidence indicates that exposure to ETS has
produced lung cancer in nonsmokers. NIOSH therefore considers
ETS to be a potential occupational carcinogen in conformance
with the OSHA carcinogen policy [29 CFR 1990]. The risk of developing
cancer should be decreased by minimizing exposure to ETS. Employers
should therefore assess conditions that may result in worker
exposure to ETS and take steps to reduce exposures to the lowest
feasible concentration.
Workers
should not be involuntarily exposed to tobacco smoke. To prevent
worker exposures to any hazardous substance, employers should
first eliminate hazardous workplace emissions at their source.
If elimination is not possible, emissions should be removed
from the pathway between the source and the worker [NIOSH 1983].
Therefore, the best method for controlling worker exposure to
ETS is to eliminate tobacco use from the workplace and to implement
a smoking cessation program. Until tobacco use can be completely
eliminated, employers should protect nonsmokers from ETS by
isolating smokers. Methods for eliminating tobacco use from
the workplace and isolating smokers are described here briefly.
- Prohibit
smoking at the workplace and provide sufficient disincentives
for those who do not comply
- Distribute
information about health promotion and the harmful effects
of smoking
- Offer
smoking-cessation classes to all workers
- Establish
incentives to encourage workers to stop smoking
Further
information regarding workplace smoking policies and smoking
cessation programs can be found in No Smoking: A Decision
Maker's Guide to Reducing Smoking at the Worksite [American
Cancer Society et al. 1985].
Warning
signs should be posted at the entrances to the workplace in
both English and the predominant language of non-English-reading
workers. These signs should state that smoking is prohibited
or permitted only in designated smoking areas. If designated
smoking areas are provided, they should be clearly identified
by signs.
Research
is needed to investigate the following issues:
- More
accurate quantification of the increased risk of lung cancer
associated with ETS exposure, including determination of
other contributing factors (e.g., occupational exposures)
that may accentuate the risk.
- Determination
of the concentration and distribution of ETS components
in the workplace to help quantify the risk for the U.S.
working population.
- The
association of ETS exposure with cancer other than lung
cancer.
- The
relationship between ETS exposure and cardiovascular disease.
- The
relationship between ETS exposure and nonmalignant respiratory
diseases such as asthma, bronchitis, and emphysema, and
the effects of ETS on lung function and respiratory symptoms.
- Possible
mechanisms of ETS damage to the cardiovascular system, such
as increased platelet aggregation, increased CORB leading
to oxygen deprivation, or damage to the endothelium.
- Effects
of workplace smoking restrictions on the ETS exposure of
nonsmokers and ETS related health effects in nonsmokers.
The
Occupational Safety and Health Administration (OSHA) and the
Mine Safety and Health Administration (MSHA) have not established
permissible exposure limits (PEU) for ETS in the workplace.
OSHA is now preparing to address this issue as part of an
indoor air quality standard.
The
U.S. Environmental Protection Agency (EPA) states that ETS
is a known cause of lung cancer and respiratory symptoms and
that it has been linked to heart disease. EPA also recommends
that exposure to ETS be minimized wherever possible by restricting
smoking to separately ventilated areas directly exhausted
to the outside, or by entirely eliminating smoking in buildings
[EPA 1989].
The
International Agency for Research on Cancer [IARC 1986] stated
that epidemiologic studies have demonstrated an increased
risk of lung cancer for nonsmoking spouses of smokers. Although
researchers had substantial difficulty in determining exposure
to ETS and other risk factors for the cancers studied, IARC
concluded that passive smoking gives rise to some risk of
cancer. IARC also concluded that there is sufficient evidence
that tobacco smoke is carcinogenic to humans," and that there
is sufficient evidence that inhalation of tobacco smoke as
well as topical application of tobacco smoke condensate cause
cancer in experimental animals."
Table
4. Commonly used abbreviations in this Current
Intelligence Bulletin |
Abbreviations |
Meanings |
ASPH |
Association
of Schools of Public Health |
c |
carcinogenic |
CO |
carbon
monoxide |
COHb |
carboxyhemoglobin |
CoC |
cocarcinogenic |
CI |
confidence
interval |
CIB |
Current
Intelligence Bulletin |
°C |
degree
Celsius |
DSDTT |
Division
of Standards Development and Technology Transfer |
DSHEFS |
Division
of Surveillance, Hazard Evaluations, and Field Studies
EPA U.S. Environmental Protection Agency |
EPA |
U.S.
Environmental Protection Agency |
ETS |
environmental
tobacco smoke (tobacco smoke in the ambient atmosphere
composed of sidestream smoke and exhaled mainstream
smoke) |
IARC |
International
Agency for Research on Cancer |
m |
meter |
MS |
mainstream
smoke (smoke drawn through the tobacco and into
the smoker's mouth) |
mg |
milligram |
ml |
milliliter |
mm |
millimeter |
MSHA |
Mine
Safety and Health Administration |
ng |
nanogram |
NIOSH |
National
Institute for Occupational Safety and Health |
NNK |
4-(methyl-nitrosamino)-(3-pyridyl)-
1-butanone |
NRC |
National
Research Council |
OSHA |
Occupational
Safety and Health Administration |
P |
probability |
pCi |
picocurie |
PEL |
permissible
exposure limit |
SC |
suspected
carcinogen |
sec |
second |
SS |
sidestream
smoke (smoke generated by smoldering tobacco between
puffs and smoke diffusing through the cigarette
paper and escaping from the burning cone during
puffing) |
T |
toxic |
TP |
tumor
promoter |
µg |
microgram |
µm |
micrometer |
|
Table 4
lists commonly used abbreviations in this Current Intelligence
Bulletin.
- ACGIH
[1986]. Industrial ventilation: a manual of recommended
practice. 19th ed. Cincinnati, OH: American Conference of
Governmental Industrial Hygienists.
- Ahlborg
G Jr. [1990]. Epidemiologic studies on occupational factors
and pregnancy outcome. Arbete och Halsa 14:1-65.
- Allred
EN, Bleecker ER, Chairman BR, Dahms TE, Gottlieb SO, Hackney
JD, et al. [1989]. Short term effects of carbon monoxide
exposure on the exercise performance of subjects with coronary
artery disease. N Engl J Med 321(21):1426-1432.
- American
Cancer Society, American Heart Association, American Lung
Association [1985]. No smoking: a decision maker's guide
to reducing smoking at the worksite. Washington, DC: U.S.
Department of Health and Human Services, Public Health Service,
Office of Disease Prevention and Health Promotion, and Office
on Smoking and Health.
- ANSI
[1979]. American national standard fundamentals governing
the design and operation of local exhaust systems. New York,
NY: American National Standards Institute, Inc., ANSI Z9.2-1979.
- ASHRA.E
[1989]. Ventilation for acceptable indoor air quality. Atlanta,
GA: American Society of Heating, Refrigerating, and Air-Conditioning
Engineers, Inc., ASHRAE 62-1989.
- Blot
WJ, Fraumeni JF Jr. [1986]. Passive smoking and lung cancer.
JNCI 77(5): 993-1000.
- Brownson
RC, Reif JS, Keefe TJ, Ferguson SW, Pritzl JA [1987]. Risk
factors for adenocarcinoma of the lung. Am J Epidemiol 125(l):25-34.
- 29
CFR 1990. Code of Federal regulations. Washington, DC: U.S.
Government Printing Office, Office of the Federal Register.
- Cummings
KM, Markello SJ, Mahoney M, Bhargava AK, McElroy PD, Marshall
JR [1990]. Measurement of current exposure to environmental
tobacco smoke. Arch Environ Health 45(2):74-79.
- Davis
JW, Shelton L, Watanabe IS, Arnold J [1989]. Passive smoking
affects endothelium and platelets. Arch Intern Med 149:386-389.
- DHEW
[1964]. Smoking and health. Report of the advisory committee
to the Surgeon General of the Public Health Service. Rockville,
MD: U.S. Department of Health, Education, and Welfare, Public
Health Service, Center for Disease Control, PHS Publication
No. 1103.
- DHEW
[1968]. The health consequences of smoking. A public health
service review: 1967. U.S. Department of Health, Education,
and Welfare, Public Health Service, PHS Publication No.
1696.
- DHEW
[1972]. The health consequences of smoking. A report of
the Surgeon General: 1972. Rockville, MD: U.S. Department
of Health, Education, and Welfare, Public Health Service,
Health Services and Mental Health Administration, DHEW Publication
No. (HSM) 72-7516.
- DHHS
[1982]. The health consequences of smoking: cancer. A report
of the Surgeon General. U.S. Department of Health and Human
Services, Public Health Service, Office on Smoking and Health,
DHHS Publication No. (PHS) 82-50179.
- DHHS
[1983]. The health consequences of smoking: cardiovascular
disease. A report of the Surgeon General. Rockville, MD:
U.S. Department of Health and Human Services, Public Health
Service, Office on Smoking and Health, DHHS Publication
No. (PHS) 84-50204.
- DHHS
[1986]. The health consequences of involuntary smoking.
A report of the Surgeon General. Rockville, MD: U.S. Department
of Health and Human Services, Public Health Service, Centers
for Disease Control, Center for Health Promotion and Education,
Office on Smoking and Health, DHHS Publication No. (CDC)
87-8398.
- DHHS
[1989]. Reducing the health consequences of smoking: 25
years of progress. A report of the Surgeon General. Rockville,
MD: U.S. Department of Health and Human Services, Public
Health Service, Centers for Disease Control, Center for
Chronic Disease Prevention and Health Promotion, Office
on Smoking and Health, DHHS Publication No. (CDC) 89-841
1.
- Donnan
GA, Adena NU, O'Malley HM, McNeil JJ, Doyle AE, Neill GC
[1989]. Smoking as a risk factor for cerebral ischaemia.
Lancet, September 16, pp.643-647.
- EPA
[1989]. Indoor air facts: environmental tobacco smoke. No.
5. Washington, DC: U.S. Environmental Protection Agency,
Office of Air and Radiation (ANR-445).
- First
MW [1984]. Environmental tobacco smoke measurement: retrospect
and prospect. Eur J Respir Dis 5(Suppl):9-16.
- Gao
YT, Blot WJ, Zheng W, Ershow AG, Hsu CW, Levin L et al.
[1987]. Lung cancer among Chinese women. Int J Cancer 40(5):604-609.
- Garland
C, Baffett-Connor E, Suarez L, Criqui NM, Wingard DL [1985].
Effects of passive smoking on ischemic heart disease mortality
of nonsmokers. Am J Epidemiol 121(5):645-650.
- Geng
G-Y, Liang ZH, Zhang AY, Wu GL [1988]. On the relationship
between smoking and female lung cancer. In: Aold M, Hisamichi
S, Tominaga S, eds. Smoking and health 1987: proceedings
of the 6th World Conference on Smoking and Health, Tokyo,
9-12 November 1987. Amsterdam, The Netherlands: Elsevier
Science Publishers, pp. 483-486.
- Gillis
CR, Hole DJ, Hawthorne VM, Boyle P [1984]. The effect of
environmental tobacco smoke in two urban communities in
the west of Scotland. Eur J Respir Dis 65(Suppl 133):121126.
- Glantz
SA, Partnley WW [1991]. Passive smoking and heart disease:
epidemiology, physiology, and biochemistry. Circulation
83(l):1-12.
- Hagopian
JH, Bastress EK [1976]. Recommended industrial ventilation
guidelines. Cincinnati, OH: U.S. Department of Health, Education,
and Welfare, Public Health Service, Center for Disease Control,
National Institute for Occupational Safety and Health, DHEW
(NIOSH) Publication No. 76-162.
- Haley
NJ, Colosimo SG, Axelrad CM, Harris R, Sepkovic DW [1989].
Biochemical validation of self-reported exposure to environmental
tobacco smoke. Environ Res 49:127-135.
- Helsing
KJ, Sandler DP, Conistock GW, Chee E [1988]. Heart disease
mortality in nonsmokers living with smokers. Am J Epidemiol
12 7(5):915 922.
- Hirayama
T [1984]. Lung cancer in Japan: effects of nutrition and
passive smoking. In: Nfizell M and Correa P, eds. Proceedings
of the International Lung Cancer Update Conference. Tokyo,
Japan: Verlag Chemie International, pp. 175-195.
- Hoffmann
D, Hecht SS [1989]. Advances in tobacco carcinogenesis.
In: Grover P, ed. Handbook of experimental pharmacology
1988. New York, NY: Springer Verlag.
- Hole
DJ, Gillis CR, Chopra C, Hawthorne VM [1989]. Passive smoking
and cardiorespiratory health in a general population in
the west of Scotland. Br Med J No. 6696, 299:423-427.
- Humble
C, Croft J, Gerber A, Casper M, Hames CG, Tyroler HA [1990].
Passive smoking and 20-year cardiovascular disease mortality
among nonsmoking wives, Evans County, Georgia. Am J Public
Health 80(5):599-601.
- Humble
CG, Samet JM, Pathak DR [1987]. Marriage to a smoker and
lung cancer risk. Am J Public Health 77(5):598-602.
- Husgafvel-Pursiainen
K, Sorsa M, Engstrm K, Einist P [1987]. Passive smoking
at work: biochemical and biological measures of exposure
to environmental tobacco smoke. Int Arch Occup Environ Health
59:337-345.
- IARC
[1986]. IARC monograph on the evaluation of the carcinogenic
risk of chemicals to humans: tobacco smoking. Vol. 38. Lyon,
France: World Health Organization, International Agency
for Research on Cancer.
- IARC
[1987]. IARC monographs on the evaluation of carcinogenic
risks to humans: overall evaluations of carcinogenicity;
an updating of IARC monographs. Vols. 1 through 42, Suppl.
7. Lyon, France: World Health Organization, International
Agency for Research on Cancer, pp. 17-34.
- Janerich
DT, Thompson WD, Varela LR, Greenwald P, Chorest S, Tucci
C, et al. [1990]. Lung cancer and exposure to tobacco smoke
in the household. N Engl J Med 323(10):632-636.
- Kleinbaum
L, Kupper L, Morganstern H [1983]. Epidemiologic research.
San Jose, CA: Lifetime Publications.
- Lam
TH, Kung ITM, Wong CM, Lam WK, Kleevens JWL, Saw D, et al.
[1987]. Smoking, passive smoking, and histological types
in lung cancer in Hong Kong Chinese women. Br J Cancer 56:673-678.
- Lee
PN, Chamberlain J, Alderson MR [1986]. Relationship of passive
smoking to risk of lung cancer and other smoking-associated
diseases. Br J Cancer 54:97-105.
- NCHS
[1988]. Vital and health statistics: health promotion and
disease prevention, United States, 1985. Hyattsville, NM:
U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control, National Center for
Health Statistics, DHHS Publication No. (PHS) 88-1591.
- NIOSH
[1983]. NIOSH comments to the U.S. Department of Labor:
comments of the National Institute for Occupational Safety
and Health. Presented at the Advance Notice of Proposed
Rulemaldng (ANPR) meeting to OSHA for Docket H-160: health
standards; methods of compliance, June 1983. NIOSH policy
statements. Cincinnati, OH: U.S. Department of Health and
Human Services, Public Health Service, Centers for Disease
Control, National Institute for Occupational Safety and
Health.
- NIOSH
[1986]. Proposed national strategy for the prevention of
leading work-related diseases anl injuries: a proposed national
strategy for the prevention of occupational lung diseases.
Cincinnati, OH: U.S. Department of Health and Human Services,
Public Health Service, Centers for Disease Control, National
Institute for Occupational Safety and Health, DHHS (NIOSH)
Publication No. 89-128.
- NRC
[1986]. Environmental tobacco smoke. Measuring exposures
and assessing health effects. National Research Council,
Board on Environmental Studies and Toxicology, Committee
on Passive Smoking. Washington, DC: National Academy Press.
- NTP
[1989]. Fifth annual report on carcinogens: summary 1989.
Research Triangle Park, NC: U.S. Department of Health and
Human Services, Public Health Service, National Institute
of Environmental Health Sciences, National Toxicology Program,
NTP 89-239.
- Repace
JL, Lowrey AH [1980]. Indoor air pollution, tobacco smoke,
and public health. Science 208:464-472.
- Repace
JL, Lowrey AH [1982]. Tobacco smoke, ventilation, and indoor
air quality. ASHRAE Trans. 88:894-914.
- Repace
JL, Lowrey AH [1990]. Risk assessment methodologies for
passive smoking-induced lung cancer. Risk Analysis 10(l):27-37.
- Sheps
DS, Herbst MC, Hinderliter AL, Adams KF, Ekelund LG, O'Neil
JJ, et al. [1990]. Production of arrhythmias by elevated
carboxyhemoglobin in patients with coronary artery disease.
Ann Intern Med 113:343-351.
- Shimizu
H, Morishita M, Nfizuno K, Masuda T, Ogura Y, Santo M, et
al. [1988]. A case-control study of lung cancer in nonsmoking
women. Tohoku J Exp Med 154:389-397.
- Slattery
ML, Rebison LM, Schuman KL, French TK, Abbott TM, Overall
JC, Gardner JW [1989]. Cigarette smoking and exposure to
passive smoke are risk factors for cervical cancer. JAMA
261:1593-1598.
- Svendsen
KH, Kuller LH, NeatonJ [1985]. Effect of passive smoldng
in the multiple risk factor intervention trial. American
Heart Association 58th Scientific Sessions.
- Svendsen
KH, Kuller LH, Martin MJ, Ockene JK [1987]. Effects of passive
smoking in the multiple risk factor intervention trial.
Am J Epidemiol 126:783-795.
- Wald
NJ, Nanchahal K, Thompson SG, Cuckle HS [1986]. Does breathing
other people's tobacco smoke cause lung cancer? Br Med J
293:12171222.
- Wells
AJ [1988]. An estimate of adult mortality in the United
States from passive smoking. Environ Int 14:249-265.
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