Philip Morris
Environmental Tobacco Smoke: A Compendium of Technical Information
Fields
- Author
- Behrens, R.
- Bennett, G.
- Cain, W.S.
- Glantz, S.A.
- Novotny, T.E.
- Parmley, W.W.
- Repace, J.L.
- Bennett, G.
- Area
- BORELLI,TOM/CARLSTADT
- Type
- REPT, REPORT, OTHER
- BIBL, BIBLIOGRAPHY
- CHAR, CHART, GRAPH, TABLE, MAPS
- BIBL, BIBLIOGRAPHY
- Site
- N329
- Request
- Stmn/R1-037
- Named Organization
- Communications Workers of America
- Control Data
- Dun Bradstreet
- Employee Advisory Council
- Employee Assistance Program
- Epa, Environmental Protection Agency
- FDA, Food and Drug Administration
- Fortune 500
- Gallup Org
- General Telephone of Ca
- Harvard Univ
- Hay Huggins
- Holiday
- Iarc
- Johnson Johnson
- La Pacific
- Louis Harris + Associates
- Mi Bell
- Milbank Quarterly
- Msi Insurance
- Nas, Natl Academy of Sciences
- Natl Center for Health Comm
- Natl Center for Health Statistics
- Natl Clearinghouse for Smoking + Health
- Natl Heart Lung + Blood Inst
- Natl Research Council
- Natl Restaurant Assn
- Nchs
- Non Smokers Inn
- Northwestern Univ
- Ny Times
- Nyserda
- Office of Prevention Education + Control
- Office of Technology Assessment
- Office on Smoking + Health
- Pa Blue Shield
- Pacific Mutual Life Insurance
- Pacific Northwest Bell
- Prevention Magazine
- Provident Indemnity Life Insurance
- Rainier Bancorporation
- Rainier Bank
- Ralston Purina
- Research + Forecasts
- Roper, Roper Org
- Sg
- Smoking Issues Steering Comm
- Speedcall
- Tx Instruments
- United Auto Workers
- United Steel Workers Union
- Unum Life Insurance
- US Bureau of Census
- US Congress
- US Dept of Transportation
- US Employee Relations
- US Gypsum
- US Public Health Service
- Ut State Dept of Health
- Wcbs Tv
- Wellness Comm
- Westlake Community Hospital
- Workplace Health Fund
- Ymca
- Acoustical Products
- Amalgamated Clothing + Textile Workers U
- American Academy of Family Physicians
- American Board of Family Practice
- American Family Insurance Group
- American Society of Personnel Administra
- Ashrae, American Society of Heating, Refrigerating + Air-Conditioning Engineers
- Bureau of Natl Affairs
- Canadian Pediatric Assn
- Cardinal Industries
- Center for Chronic Disease Prevention +
- Centers for Disease Control
- Control Data
- Named Person
- Albert, R.
- Allred, E.N.
- Aronow, W.
- Astrup, P.
- Baek, S.O.
- Becker, D.
- Beil, L.
- Benditt, E.
- Benditt, J.
- Berglund, L.G.
- Boleij
- Bonham, G.
- Broffman, P.
- Brunekreef
- Burghuber, O.
- Butler, T.
- Cain, W.S.
- Chesebro, J.
- Clark, R.E.
- Clausen, G.H.
- Coggins, E.I.
- Coghlin, J.
- Coultas
- Cuddeback
- Cummings, K.M.
- Davis, J.
- Davis, R.M.
- Deanfield, J.E.
- Dicorleto, P.
- Dietz, R.
- Dobson, A.
- Endicott
- Fanger, P.O.
- Fischer
- Fleming, D.W.
- Fox, P.
- Frederick
- Friedman, J.
- Fuster, V.
- Gallup
- Gann, P.H.
- Garland, C.
- Gierer, R.
- Gillis, C.
- Glantz, S.A.
- Grandjean, E.
- Green, C.E.
- Greenberg
- Grot, R.A.
- Gurlinger, A.
- Gvozdjak, J.
- Gvozdjakova, A.
- Hamilton
- Hammond, S.K.
- Hansen, E.
- Harris
- Haskins, R.
- Hawkins, L.H.
- Hawthorne
- He, Y.
- Helsing, K.
- Hirayama, T.
- Hole, D.
- Huey, R.J.
- Hugod, C.
- Humble, C.
- Humpreys, C.M.
- Hunter, M.
- Isseroff, R.
- Jarvis
- Jermini, C.
- Junkins, J.
- Kawachi, I.
- Kefalides, A.
- Kendall, D.A.
- Kerka, W.F.
- Khalfen, E.
- Kirk, Pww
- Kjeldsen, K.
- Klochkov, V.
- Kristein, M.M.
- Kristensen, T.
- Kuller
- Lamb, D.
- Leaderer, B.P.
- Lee, P.
- Leonardos, G.
- Lester, J.N.
- Lindquist
- Lipsitt, E.D.
- Lough, J.
- Lowrey, A.H.
- Luce, B.L.
- Luck
- Majesky, M.
- Mangels, J.D.
- Manning, W.G.
- Martin, M.
- Mason, R.
- Matsukura
- Mcmurray, R.
- Miesner
- Moller, S.B.
- Moschandreas, D.
- Moskowitz, W.
- Muhm, J.
- Murphy, C.L.
- Nau
- Nielsen, K.S.
- Nielson, C.
- Nitschke
- Nystrom, C.W.
- Oconnell, M.
- Oldaker, G.B.
- Olshan, A.
- Ott, W.R.
- Palmer, J.
- Parker
- Parmley, W.W.
- Pattishall
- Pearce, N.
- Penn, A.
- Perlman, D.
- Perry, R.
- Persily, A.
- Peterson, L.R.
- Pisha, S.
- Plischke, K.
- Pritchard
- Pukander, J.
- Randerath, E.
- Reinken, K.
- Remmer, H.
- Repace, J.L.
- Revis, N.
- Riboli, E.
- Rice, D.P.
- Rickert, W.S.
- Rigotti, N.A.
- Riley, E.C.
- Ritchie
- Rogers, C.C.
- Rogers, W.R.
- Roscovanu, A.
- Rosenstock, I.M.
- Ross, R.
- Rothman, K.
- Russell, L.B.
- Saba, S.
- Sahin, F.
- Schelling, T.C.
- Schlipkoeter, H.W.
- Schneiders
- Schweitzer, S.O.
- See, L.C.
- Sexton, K.
- Sheldon
- Sheps, D.
- Sinzinger, H.
- Spengler
- Sterling
- Stillman, F.A.
- Surgeon General
- Svendsen, K.
- Szalai
- Thomsen, H.
- Tosun, T.
- Vaughn, W.M.
- Virgolini, I.
- Visscher, W.
- Wald, N.
- Wall, M.A.
- Warner, K.E.
- Weber, A.
- Webertschopp, A.
- Weis, W.L.
- Wells, A.
- Wilkstrand, J.
- Williams, D.C.
- Wilson, R.W.
- Winneke, G.
- Yaglou, C.P.
- Allred, E.N.
- Document File
- 2040225000/2040225584/Epa Technical Compendium
- Litigation
- Stmn/Produced
- Author (Organization)
- Center for Chronic Disease Prevention +
- Centers for Disease Control
- Epa, Environmental Protection Agency
- Indoor Air Div
- John B Pierce Lab
- Natl Heart Lung + Blood Inst
- Office of Air + Radiation
- Office of Prevention Education + Control
- Office on Smoking + Health
- Univ of Ca San Francisco
- Wa Business Group on Health
- Yale Univ
- Centers for Disease Control
- Master ID
- 2040225004/5288
Related Documents: - Characteristic
- DRFT, DRAFT
- OVER, OVER SIZE DOCUMENT
- Date Loaded
- 24 May 1999
- UCSF Legacy ID
- edq02a00
Document Images
Draft - Do not cite or quote
CHAPTER 6
PASSIVE SMOKING AND HEART DISEASE:
EPIDEMIOLOGY, PHYSIOLOGY, AND BIOCHEMISTRY~
Stanton A. Glantz PhD
William W. Parffiley MeD.
Division of Cardiology
School of Medicine
University of California San Francisco, CA 94143
Introduction
The first disease linked to active smoking was lung cancer. It
is, therefore, not surprising that the first disease linked to
passive smoking was also lung cancer (USPHS, 1986). Before the
advent of mass marketed cigarettes, lung cancer was a rare disease.
The fact that smoking is the major identifiable cause of lung
cancer made identifying this link -- for both active and passive
smoking -- relatively straightforward. This situation contrasts
i4ith heart disease, which has many risk factors, so it is not
surprising that it took longer for the scientific community to
conclude that active smoking caused heart disease (USPHS, 1983).
Once the link between smoking and heart disease was established,
it became clear that smoking accounted for more heart disease
deaths than lung (and other) cancers because of the high prevalence
of heart disease. Similarly, smoking is the most important
preventable cause of coronary disease. Given this history, it is
not surprising that exposure to environmental tobacco smoke (ETS)
has now been linked to heart disease in nonsmokers (Wells, 1988;
Kristensen, 1989) and may result in a substantial number of
unnecessary coronary heart disease deaths in nonsmokers.
Most of the evidence linking ETS and coronary heart disease has
appeared since the US Surgeon General (USPHS, 1986) and National
Academy of Sciences (NRC, 1986) last reviewed the evidence on the
health effects of ETS. Based on the information available as of
early 1986, both these reports concluded that the evidence linking
ETS and heart disease was equivocal and that more research was
necessary before any definitive statements could be made. These
conclusions were reasonable at the time they were made. In the
four years since these reports were written, considerable
information on both the epidemiology and biological mechanisms by
which ETS may cause heart disease has accumulated from several
areas of scientific investigation. In fact, most of the results
1This chapter is an adaptation of a peer-reviewed manuscript
of the same title (Glantz and Parmley, 1990).
80
Draft - Do not cite or quote
presented in this chapter were published after the 1986 Surgeon
General and National Academy of Science reports.
First, there are now 11 epidemiological studies on the
relationship between exposure to environmental tobacco smoke in the
home and the risk of heart disease in the nonsmoking spouse of a
smoker. All but one of these studies yielded a relative risk
greater than 1.0. There are several lines of biologic evidence
which make this association plausible. There is evidence that
exposure to ETS reduces exercise tolerance of healthy individuals
as well as people with existing coronary artery disease. Such
reduced exercise capability is one of the landmarks of acute
compromises to the coronary circulation. There is evidence, from
both human and animal studies, that exposure to tobacco smoke,
including passive smoking, increases aggregation of blood
platelets. Such increases in platelet aggregation are an important
step in the genesis of atherosclerosis. In addition, increasing
platelet aggregation contributes to coronary thrombosis, the cause
of acute myocardial infarction. Finally, carcinogenic agents in
ETS, including benzo[a]pyrene have been shown to produce injuries
to the endothelial cells which line arteries. Such injuries are
the first step in the development of atherosclerosis. Thus,
exposure to ETS can contribute to both short term and long term
insults to the coronary circulation and the heart.
Effects of Primary Smokinq
Before reviewing the evidence linking ETS with coronary artery
disease, it is worth summarizing the evidence linking active
smoking with coronary artery disease. This evidence was summarized
in the 1983 Surgeon General's Report, which was devoted entirely
to cardiovascular disease (USPHS, 1983); it concluded:
In 1980, diseases of the circulatory system were responsible
for approximately one-half of the total U.S. mortality. CHD
was the sinale most important cause of death, accounting for
approximately 30 percent of all U.S. deaths.
Cigarette smoking is one of the three major independent CHD
risk factors. The magnitude of the risk associated with
cigarette smoking is similar to that associated with the
other two major CHD risk factors, hypertension and
hypercholesterolemia; however, because cigarette smoking is
present in a larger percentage of the U.S. population than
either hypertension or hypercholesterolemia, cigarette
smoking ranks as the largest preventable cause of CHD in the
United States. Cigarette smoking also acts synergistically
with the other major risk factors to greatly increase the
risk for CHD.
Arteriosclerosis is the predominant underlying cause of
cardiovascular disease, and atherosclerosis is the form of
81
Draft - Do not cite or quote
arteriosclerosis that most frequently causes clinically
significant disease, including CHD, atherothrombic brain
infarction, atherosclerotic aortic disease, and
atherosclerotic peripheral vascular disease. Cigarette
smoking contributes both to the development of
atherosclerotic lesions and to the clinical manifestations
of atherosclerotic vascular disease, including sudden death.
Although the precise pathophysiologic basis of these clinical
manifestations is not understood, it may be related to
several deleterious cardiovascular effects of cigarette
smoking, including production of an imbalance between
myocardial oxygen supply and demand, a decrease in threshold
for ventricular fibrillation, and an increase in platelet
aggregation. Nicotine and carbon monoxide are the tobacco
smoke constituents most closely associated with these adverse
effects; other cigarette smoke constituents such as hydrogen
cyanide, oxides of nitrogen, and carbon disulfide are being
studied for possible pathologic cardiovascular effects.
Since 1983, evidence has also mounted that the polycyclic aromatic
hydrocarbons in cigarette smoke can injure the arterial endothelium
and initiate the atherosclerotic process.
~ All the compounds implicated as damaging to the cardiovascular
system of smokers have been identified in ETS (USPHS, 1986; NRC,
1986).
Enidemioloaical Studies on ETS and Heart Disease
Since 1984, the epidemiological evidence linking exposure to
ETS with heart disease has rapidly accumulated. The results of the
eleven published studies are summarized in Table 1 and Figure 1;
four studies present data on men, nine on women, and one on both
sexes combined. Despite minor differences in methodology or end
points (some used death from ischemic heart disease of any origin
and some were limited to death from myocardial infarction), the
results of these studies are remarkably consistent. All the
studies on men yielded relative risks of death from heart disease
exceeding 1 for nonsmoking men married to smokers, with a median
risk of 1.2. All but one of the studies on women (Lee et al, 1986)
yielded relative risks exceeding 1, with a median relative risk of
1.4. Several studies also suggested an increase in the risk of
nonfatal coronary symptoms (Svendsen et al, 1987; Palmer et al,
1988; Hole et al, 1989; Dobson et al, 1990); quantitative results
in Table l only reflect risk of death, not coronary symptoms.
Consistency of an observation across different studies increases
the confidence one can have in the belief that an association is
causal, unless all studies have the same bias.
When interpreting the results of such epidemiological studies,
it is always important to consider biological plausibility and
potential confounding variables which could explain the results.
82
Draft - Do not cite or quote
Aside from noting that the compounds in mainstream smoke that have
been implicated in heart disease are in ETS, we will defer the
discussion of biological plausibility until later in this chapter,
when we discuss the effects of ETS on platelets and the atherogenic
agents in ETS. For now, we will concentrate on potential
confounding variables. These are particularly important in a
disease like heart disease, because it is known to be caused by
multiple risk factors.
All of the studies controlled for the most important confounding
variable, age, and several (Garland et al, 1985; Svedsen et al,
1987; He, 1989; Hole et al, 1989; Humble et al, 1990) controlled
for several known risk factors for coronary artery disease, in
particular levels of cholesterol, blood pressure and weight (or
body mass or body mass index). Most of the studies also included
one or more measures of socioeconomic status, such as the nature
of the housing or amount of education.
Lee (1988, 1989, 1990) has suggested that the elevated risk of
heart (and other) disease with passive smoking could be due to
misclassification of nonsmokers who are really smokers. In
addition, Wald (1986) has noted that some people who say they live
yith nonsmokers-Yrave detectable levels of the nicotine metabolite
cotinine in their blood, indicating that they are actually exposed
to ETS, either at work or at home. The former type of
misclassification will tend to lead to an overestimate of the risks
associated with ETS and the latter will lead to an underestimate
of the risk. Careful analysis of the question of misclassification
-- which applies generally to studies of ETS and not just heart
disease -- have demonstrated that the observed risks cannot be
explained by this technical problem (Wald, 1986; Wells, 1986, 1988,
1990; Kawachi and Pearce, 1989; Reinken, 1989). In addition, both
the Surgeon General (USPHS, 1986) and the National Academy of
Sciences (NRC, 1986) were presented with the argument that
misclassification errors accounted for the link between ETS and
lu W cancer and concluded that ETS caused lung cancer in healthy
nonsmokers. To date,.no compelling case has been made that this
technical error explains consistent findings linking ETS with heart
(or lung) disease. Indeed, the net effect of these two types of
misclassification errors is to lead to an underestimate of the
effects of passive smoking for lung cancer.
There is.always the possibility that there is some other
confounding variable relating to cultural factors,'such as the
nature of housing or employment or the nature of time spent outside
the home. Most studies look only at a crude measure of
exposure-spouse smoking-and it is possible that this is an
indicator variable for other things, such as poor diet, risky
lifestyle, or stress. The fact that results are similar from all
over the world in widely varying cultural settings -- including
several regions in the United States, the United Kingdom, Japan,
and China -- argues against this concern.
83
Draft - Do not cite or quote
Several authors also observed a dose-response relationship
(Table 1) between increasing amounts of smoking by the spouse and
the risk of heart disease in the nonsmoking spouse (Helsing et al,
1988 (statistically significant in women, but not men); Hole et al,
1989; Garland et al, 1985 (although not statistically significant);
Humble et al, 1990; He, 1989; Hirayama, 1984). The presence of
such dose-response effects across multiple studies, done in
different locations with different criteria supports the hypothesis
that the epidemiology is revealing a real effect of ETS on heart
disease in nonsmokers.
While all but one of the studies in Table 1 and Figure 1 yielded
relative risks greater than 1, the fact remains that 3 of the
studies in men and 4 of the studies in women had 95% confidence
intervals for the relative risk of passive smoking for heart
disease that fell below 1.0, meaning that the risk was not
statistically significantly elevated above 1.0 (with P<.05). It
is important to note that the 95% confidence intervals do not lie
symmetrically about 1.0, but rather are skewed towards higher
risks. To avoid false negative conclusions, Rothman (1978)
suggested examining the confidence interval, as we have done, in
concluding the exposure to ETS elevates the risk of heart disease.
One can assess formally how confident one can be in reaching a
negative conclusion by computing the power of the study to detect
an effect of specified size (Friedman et al, 1978). Table 1 shows
estimates of the power of each of the studies to detect a 20%
increase in risk-of heart disease (i.e., a relative risk of 1.2)
with the available samples. The power was computed as described
in Muhm and Olshan (1989), using a two-sided test for the relative
risk with a Type I risk of 5% (i.e., requiring the 95% confidence
interval for the relative risk to exclude 1.0 before concluding a
statistically significant elevation in risk in an individual
study). Most of the studies have low to moderate power. The two
(Helsing et al, 1988; Hole et al, 1989) that have power above the
desirable level of 80% both identified significant increases of
heart disease risk with ETS exposure. Interestingly, the study by
Lee (1986) which was the only one with a relative risk below 1,
also had the lowest power to detect an effect, only 3%.
It is possible to combine the results of these studies in a
formal analysis to derive a global estimate of the relative risk
and associated 95% confidence interval. By combining the studies,
the sample size and so the power to detect an effect increases.
Pooling the studies in Table 1 yields an estimate of the relative
risk of death from heart disease of 1.3 (95% CI 1.1-1.6) for men
and 1.3 (95% CI 1.2-1.4) for women. These results are consistent
with those reported by Wells (1988) who used the studies by Gillis
et al (1984), Lee et al (1986), and Helsing et al (1987) to compute
a pooled relative risk of 1.3 (with a 95% confidence interval from
1.1 to 1.6) for men and the studies by Hirayama (1984), Gillis et
84
Draft - Do not cite or quote
al (1984), Garland et al (1985), Helsing et al (1988), Lee et al
(1986), and Martin et al (1986) to compute a pooled relative risk
of 1.2 (with a 95% confidence interval from 1.1 to 1.4) for women.
Exposure to ETS significantly (p < 0.001) increases the risk of
death from heart disease in nonsmokers.
Finally, it is worth noting that all these studies are based on
the smoking habits of the nonsmoker's spouse, and so exposure to
ETS at home. Household exposures to ETS at home are generally much
smaller than exposures at work, where the density of smokers is
generally higher (Repace and Lowrey, 1985,1987). As a result,
these studies will generally underestimate the risk and attendant
public health burden due to ETS-induced heart disease if a
substantial proportion of the controls are exposed at work.
Kawachi et al (1989) have adjusted Wells' (1988) relative risks to
account for workplace exposures to ETS and found that the relative
risks increase to 2.3 (95% CI 104 - 3.4) for men and 1.9 (95% CI
1.4 - 2.5) for women. In addition, Wells (1988) and Kawachi et al
(1989) indicate that the number of heart disease deaths due to
passive smoking is an order of magnitude greater than the number
of lung cancer deaths due to passive smoking.
These epidemiological studies demonstrate a connection between
ETS exposure and death from heart disease. We now turn our.
attention to possible physiological and biochemical mechanisms
which could explain these observations.
Acute Effects of ETS Ex
osure
Chronic exposure to ETS exerts carcinogenic effects by
increasing the cumulative risk of a molecule of one of the
carcinogens in the ETS damaging the DNA in a cell and initiating
or promoting the carcinogenic process. To date, no one has
identified any effects of acute exposure to ETS (or, for that
matter, any other carcinogen) on cancer. The situation with heart
disease is different. In heart disease there are both important
chronic changes (i.e., the development of atherosclerotic lesions)
and acute changes. The latter include an increase in myocardial
oxygen demand which may outstrip the oxygen supply and produce
ischemia, and increased platelet aggregation which can lead to
coronary thrombosis and acute myocardial infarction.
When the coronary circulation cannot provide enough oxygen to
the myocardium to meet the demand, the result is ischemia which can
be silent or result in anginal chest pain. Earlier onset of angina
or hypotension during exercise is a reflection of more severe heart
disease. oxygen supply can be reduced by atherosclerotic narrowing
or vasoconstriction of the coronaries or by reducing the oxygen
carrying capacity of the blood by forming carboxyhemoglobin.
Khalfen and Klochkov (1987) confirmed earlier work by Aronow (1978)
demonstrating that exposure to ETS significantly reduced exercise
ability in patients with coronary artery disease and the rate
85
Draft - Do not cite or quote
pressure product (heart rate times systolic blood pressure). In
both studies, patients were exposed to realistic levels of ETS by
simply sitting in a waiting room while someone was smoking. These
effects were present in both smokers and nonsmokers (Khalfen and
Klochkov, 1987) and regardless of whether or not the room was
ventilated (Aronow, 1978; Khalfen and Klochkov, 1987). Exposure
to ETS also increased resting heart rate and systolic and diastolic
blood pressure, and resulted in a lower heart rate at the onset of
angina (Aronow, 1978). Blood carboxyhemoglobin was increased by
about 1% after exposure to ETS (Aronow, 1978). Sheps et al (1987)
found no change in cardiovascular function in subjects with angina
in response to mild elevation in blood carbon monoxide similar to
that experienced in passive smokers when they exposed their
subjects to pure carbon monoxide. In contrast, Allred et al (1989)
found a significant dose-response relation between
carboxyhemoglobin level and the change in the length of time to
both electrocardiographic and symptom manifestation in men with
angina pectoris exercising after exposure to CO. Even a small
increase in the carboxyhemoglobin level, representing a seemingly
minor reduction in the oxygen-carrying capacity of hemoglobin, was
associated with the statistically sIgnificant effects. Acute
exposure to ETS leads to an imbalance between myocardial oxygen
$upply and demand during exercise in patients with coronary artery
disease. While this discussion has concentrated on the carbon
monoxide in ETS as the active agent, it is likely that some other
component of the ETS is also contributing to this effect.
The effects of ETS on cardiac performance are, in fact, severe
enough to affect exercise performance in young healthy subjects
with no evidence of heart disease. McMurray et al (1985) blindly
exposed young healthy women to pure air and air contaminated with
ETS while they exercised on a treadmill. The results were similar
to those observed in patients with coronary artery disease.
Resting heart rate was increased during exposure to ETS, which
increased blood carboxyhemoglobin by about 1%. Exposure to ETS
significantly reduced maximum oxygen uptake (by 0.251/min and time
to exhaustion (by 2.1 min). Exposure to ETS also increased the
perceived level of exertion during exercise, maximum heart rate,
and COz output. It also significantly increased levels of lactate
in venous blood (from a mean of 5.5 mM during control period to
6.8 mM after exposure to ETS). This greater lactate at a lower
oxygen consumption during the passive smoking trials indicates a
greater reliance on anaerobic metabolism. The combined effect of
the reduced oxygen carrying capacity and increased lactate resulted
in a reduction in maximal aerobic power and 'the duration of
exercise. Thus, even in healthy subjects, exposure to ETS
adversely affects exercise performance.
The acute effects of CO and direct tobacco smoke on exercise
performance are well documented in the literature. Exposure to CO ~
(or CO in tobacco smoke), and the subsequent elevation of blood Q
carboxyhemoglobin levels to ca. 3%, has been shown to decrease
86 ~
~
~
~
~
~
Draft - Do not cite or quote
exercise duration in patients with ischemic heart disease and
decrease short-term maximal exercise duration in young healthy men.
It is conceivable, therefore, that elevations in COHb due to ETS
could have similar effects. While the association between active
smoking and cardiovascular disease is well known (USPHS, 1983),
little is known about the relative importance of each component of
tobacco smoke that may be responsible for this relationship. Most
experts agree, however, that both CO and nicotine are important,
and other constituents of the smoke may play a role as well.
Active smoking clearly aggravates the decrease in 02 capacity
induced by CO through an increase in the OZ demand of the heart
(Deanfield et al, 1986). Passive smoking exposes an individual to
all components in the cigarette smoke, but the CO component
dominates heavily because only 1%- or less of the nicotine is
absorbed from passive smoking compared to 100% in an active smoker
(Wall et al, 1988; Jarvis, 1987). Currently available information
indicates that acute exposure (1 to 2 h) to passive smoke will
increase a nonsmoker's COHb level by about 1% (Jarvis, 1987). This
small incremental increase in COHb due to ETS alone may not be
enough to trigger acute cardiovascular effects unless combined with
other sources of CO or with other components of ETS having a
similar effect (e.g., nicotine).
Lamb (1984) has suggested that at maximal exertion. levels, up
to 90% of the oxygen carrying capacity of the blood may be needed.
Because of the carbon monoxide, and perhaps other constituents, ETS
reduces this capacity, so the muscle cannot maintain its high rate
of aerobic metabolism unless cardiac output is further increased;
people with heart disease and reduced ventricular reserve have
difficulty meeting this demand. In sum, exposure to ETS increases
the demands on the heart during exercise and reduces the capacity
of the heart to respond. This imbalance increases the ischemic
stress of exercise in patients with existing coronary artery
disease and can acutely precipitate symptoms.
Moskowitz et al (1990) found evidence that adolescent children
of parents who smoked may suffer from chronic tissue hypoxia such
as that observed in anemia, chronic pulmonary disease, cyanotic
heart disease or high altitude. These children had significantly
elevated levels of 2,3-diphosphoglycerate (DPG), which suggests
that the body is attempting to compensate for hypoxia by increasing
DPG level in blood to meet tissue oxygen 'requirements, even after
correcting for age, weight, height and sex. These changes were
dose-dependent; the greater the exposure to ETS (measured both in
terms of parental smoking and serum thiocyanate in the children),
the greater the increase in DPG.
There is also evidence that acute exposure to ETS directly
affects the myocardial muscle at a cellular level. Gvozdjakova et
al (1984) exposed rabbits in a 50 liter child's incubator to the
smoke of three burning cigarettes smoked over a 30 minute period
and measured several variables related to the metabolism of cardiac
87
Draft - Do not cite or quote
mitochondria. (Mitochondria are the subcellular elements that
control cellular respiration; they convert oxygen into usable
energy in the form of ATP.) They had three groups of rabbits: one
group exposed to a single dose of ETS, one group exposed to 30 min
of ETS twice daily for two weeks, and one group exposed to 30
minutes of ETS twice a day for eight weeks. They measured
mitochondrial respiration (Q02) as the consumption of oxygen after
adding ADP to a vessel containing mitochondrial fragments. Using
pyruvate as a substrate, mitochondrial respiration QO was reduced
significantly compared to control (pure air) for all hses of ETS,
even a single exposure (Figure 2), to about half the control value.
The oxidative phosphorylation rate was also reduced significantly
at all exposures by about one-third. There were no significant
changes in the coefficient of oxidative phosphorylation (ADP:02)
with ETS exposure. Gvozdjakova et al concluded that pyruvate as
a substrate was a sensitive indicator of the toxic action of the
ETS on the oxidative process.
Later, to further isolate where in the process of mitochondrial
respiration, the ETS acted, Gvozdjak et al (1985, 1987) reported
data on succinate, NADH, and cytochrome oxidase activity in the
mitochondria in the four groups of rabbits. Figure 2 shows the
lFesults of exposure to ETS on the activity of NADH oxidase,
succinate oxidase and cytochrome oxidase of myocardial
mitochondria. The activity of the first two oxidases exhibited no
changes compared with the control group -- neither after a single
exposure to ETS or following exposures up to 2 weeks. Cytochrome
oxidase activity decreased both after a single exposure to ETS and
over time, with increasing effects as the duration of exposure to
ETS is extended. The observation that cytochrome oxidase and not
NADH or succinate oxidase activity was affected by ETS suggests
that the deleterious effects of ETS on myocardial mitochondrial
respiration occur at the terminal segment of the mitochondrial
respiration process.
Prolonged exposure to carbon monoxide has been shown in some
studies to induce ultrastructural changes in myocardium (Kjeldsen
et al, 1974; Thomsen and Kjeldsen, 1974; Lough, 1978). Later,
Kjeldsen and co-workers (Hugod et al, 1978), using a blind
technique and the same criteria to assess morphological myocardial
damage found no significant changes in the coronary arteries or
aorta in normocholesterolemic rabbits exposed to CO at
concentrations from 200 to 4000 ppm for' up to 12 weeks. They
suggested that the positive results obtained earlier were due to
the non-blind evaluation techniques and the small number of animals
used in these studies. Later, Hugod (1981): confirmed these
negative results using electron microscopy. In addition, the
earlier studies were conducted at "moderate" levels of CO (100 to
150 ppm) which are considerably higher than levels of CO found in
smoke-polluted environments (reported to be as high as 40-50 ppm,
but more typically are around 10 ppm) (NRC, 1986). These negative
studies only argue against an effect of CO in inducing coronary
88
Draft - Do not cite or quote
atherosclerosis, and not a direct effect of CO on myocardial oxygen
supply and demand (Deanfield et al, 1986).
Acute exposure to ETS not only increases the demand and
compromises the supply of oxygen to the heart as a whole, but also
reduces the myocardium's ability to use this oxygen to create ATP
to provide energy to support the heart's pumping activity. This
effect probably results from several of the compounds in ETS acting
simultaneously on the cardiovascular system.
Effects on Platelets
The action of ETS to increase platelet aggregation is another
way in which ETS can acutely increase the risk of a coronary event.
When blood platelets aggregate inappropriately and form a thrombus
(blood clot), this clot can form in a fissured plaque in the
coronary circulation and precipitate a myocardial infarction.
Platelets are important for the normal body process of hemostasis,
to prevent blood loss after an injury. Hemostasis depends on
complex interactions among the dynamics of blood flow, components
of the vessel wall, blood platelets and plasma proteins. A
thrombus can be considered as an inappropriate form of hemostasis
and is composed-of a mass of cellular material held together by a
network of fribrin. Definitive evidence has confirmed that
platelets play a major role in thrombus formation and embolization,
especially in the arterial system. In addition, increasing
evidence has shown that platelet deposition and thrombus formation
can contribute to the growth and progression of atherosclerotic
plaques (Fuster and Chesebro, 1981; Ross, 1986). An arterial
tbrombus appears to develop in three phases: platelet adhesion,
platelet aggregation, and activating of clotting mechanisms.
Passive smoking increases platelet aggregation and so increases the
likelihood of thrombus formation and myocardial infarction.
Table 2 summarizes the results of three studies (Davis et al,
1985a, 1986, 1989) on the effects of cigarette smoke on platelet
aggregation and damage to the arterial endothelium (lining). (We
will discuss the effects on the endothelium below.) Davis et al
(1989) also measured platelet aggregate ratios and endothelial cell
counts in nonsmokers before and after being exposed to 20 minutes
of ETS while sitting in a hospital atrium. Mean values before and
after passive smoking were 0.87 and 0.78 (P=.002) for platelet
aggregate ratios and 2.8 and 3.7 (P=.002) for counts~ of anuclear
endothelial cell carcasses in venous blood. These changes are in
between the effects observed after nonsmokers smoked two tobacco
cigarettes and the effects observed after smoking two non-tobacco
cigarettes (Davis et al, 1985a) and similar to the values observed
in nonsmokers who smoked two cigarettes while trying not to inhale
(Davis et al, 1986). These effects were not correlated with the
level of nicotine in the blood of the experimental subjects in any
of these or other (Davis et al, 1985, 1987), related studies on how
drugs modify platelet aggregation and endothelial cell counts. In
89
Draft - Do not cite or quote
particular, the effects observed in nonsmokers smoking without
inhaling were similar to the effects on smokers smoking two
cigarettes, despite the fact that the plasma nicotine levels in the
nonsmokers were a factor of 5 smaller than those observed in the
smokers (Davis et al, 1986). Other work in the same laboratory
comparing smoking with snuff use revealed similar changes in
platelet function in response to these two forms of tobacco use
(Davis et al, 1990). This result, combined with the finding that
smoking non-tobacco cigarettes (Davis et al, 1985a) failed to
produce changes in platelet function as large as observed with
tobacco cigarettes, suggests that nicotine is an important active
agent. Since non-tobacco cigarettes also 'affected platelet
aggregation somewhat, however, it is possible that carbon monoxide
or other combustion products are also influencing the platelets.
Sinzinger and Kefalides (1982) measured platelet sensitivity to
antiaggregatory prostaglandins (El, IZ, and D2) before, during and
after 15 minutes of exposure to ETS in healthy nonsmokers and
smokers (Table 3). Passive smoking reduced platelet sensitivity
to the antiaggregatory prostaglandins 12 and EZ significantly
(P<.01) by a factor of about 2 by the end of 15 minutes exposure
to ETS among nonsmokers. This effect persisted at 20 minutes after
the end of exposure, and was gone by 40 minutes. Platelet response
to prostaglandin Dz changed modestly in a similar pattern, but did
not reach statistical significance. Among smokers, the control
level of platelet aggregation was higher (P<.01) and the
prostaglandins had no significant effects on platelet aggregation
over time during or following exposure to ETS. Sinzinger and
Virgolini (1989) also showed that repeated exposure to ETS for one
hour per day for ten days produced lasting changes in platelet
function in nonsmokers similar to that observed in smokers. Thus,
nonsmokers' platelets seem much more sensitive to a single exposure
to ETS than do smokers' platelets, with platelet sensitivity to
disaggregating prostaglandins having similar effects in nonsmokers
acutely exposed to ETS as it does on the chronic levels of platelet
aggregation observed in long-term smokers.
Further evidence from the same_laboratory that passive smoking
increases platelet aggregation comes from work by Burghuber at al
(1986), who had smokers and nonsmokers smoke two cigarettes and
also exiosed a different group of smokers and nonsmokers to ETS in
an 18 m room in which 30 cigarettes had been smoked just before
exposing the nonsmokers. They measured the sensitivity. of
platelets to the disaggregating substance prostaglandin 12 (PGIz),
which is released by endothelium and inhibits platelet aggregation.
(PGI2 is also called prostacyclin.) Figure 3 shows the results of
this experiment. In smokers, neither smoking nor passive smoking
affected the sensitivity of the platelets to the disaggregating
effect of prostaglandin IZ. The sensitivity of platelets in
smokers was also significantly lower than nonsmokers. In contrast,
platelets were more sensitive to prostaglandin IZ in nonsmokers,
with both smoking and passive smoking producing similar reduction
90
Draft - Do not cite or quote
in platelet sensitivity to prostaglandin IZ. These results
suggest that the platelets of smokers are already desensitized to
the anti-aggregatory substance prostaglandin Iz, so that no further
decrease in aggregation is seen. The significant decrease in
platelet sensitivity to PGIZ after acute exposure to ETS suggests
that after ETS exposure platelets are more likely to aggregate,
with the adverse consequences described above.
Earlier work by Saba and Mason (1975) also indicated that
nicotine increased a variety of measures of platelet aggregation
in nonsmokers and smokers. While the effects of nicotine on
platelets from smokers was greater than in nonsmokers, the effect
generally did not vary with dose (between 2x10'9 and 2x10'4 molar),
suggesting that the effects of nicotine on platelets occur at low
doses and that the system saturates quickly. This observation may
explain why passive and active smoking have such similar effects
on platelets (Sinzinger and Kefalides, 1982; Burghuber et al, 1986;
Davis et al, 1989).
The probable link between nicotine and adverse physiologic
effects is nicotine-induced release of catecholamines.
catecholamines are then responsible for increased platelet
aggregation. This reasoning suggests that beta blockers might
provide some protection in smokers. This premise is borne out by
the MAPHY trial --a trial comparing the effects of the beta blocker
metoprolol to a thiazide diuretic in the control of moderate
hypertension (Wilkstrand, et al, 1988). For the same reduction in
blood pressure, the metoprolol treated group had a lower mortality
than the thiazide treated group. Virtually all of this reduction
in mortality, however, was seen in smokers, and not non-smokers.
This study provides evidence that blocking the effects of
catecholamines (released by nicotine) was the cause of the reduced
mortality in smokers who were receiving metoprolol.
In sum, passive smoking has significant effects on platelet
aggregation, of a magnitude similar to that observed in active
smoking. Moreover, the response of nonsmokers to both active and
passive smoking appears to be different from smokers, with
nonsmokers being more sensitive to low exposures to cigarette smoke
than smokers. This observation suggests that the pharmacology of
ETS in nonsmokers may be different than in smokers, with nonsmokers
being more sensitive to low doses of ETS. In particular, it
invalidates attempts to estimate "cigarette equivalent" doses of
ETS in nonsmokers or extrapolating from risks of smoking in smokers
to effects of ETS on nonsmokers. The resulting increase in
platelet aggregation can contribute to acute thrombus formation and
myocardial infarction.
In addition to the role of platelets in acute thrombus
formation, platelets are also important in the development of
atherosclerosis (Ross, 1986). Once there is damage to the arterial
endothelium, either through mechanical or chemical factors,
91
Draft - Do not cite or quote
platelets interact with or adhere to subendothelial connective
tissue and initiate a sequence which leads to atherosclerotic
plaque. When platelets interact with or adhere to subendocardial
connective tissue, they are stimulated to release their granule
contents. Endothelial cells normally prevent platelet adherence
because of the nonthrombogenic character of their surface and their
capacity to form antithrombotic substances such as prostacyclin.
Once the endothelial cells have been damaged, the platelets can
stick to them. Once the platelets are bound to the endothelium,
they release mitogens such as platelet-derived growth factor
(PDGF), which encourage migration and proliferation of smooth
muscle cells in the region of the endothelial injury (Fox and
DiCorleto, 1984). If platelet aggregation is increased because of
exposure to ETS, the chances of platelets building up at an
endothelial injury will also be increased. Thus, in addition to
contributing to acute effects through increasing the likelihood of
thrombus formation, the effects of ETS on platelets also increase
the chances that endothelial injury will lead to arterial plaque.
ETS also plays a role in causing damage to the endothelium and
initiating the atherosclerotic process. As discussed above, Davis
et al (1989, 1986, 1985, 1987, 1985b, 1990) found that acute
exposure to ETS (1989), like active smoking (1986, 1985a, 1987,
1985b) and use of chewing tobacco (1990), lead to a significant
increase (P<.002) in the appearance of anu~:lear endothelial cell
carcasses in the blood of people exposed to ETS (or tobacco or
tobacco smoke) constituents. The appearance of these cell
carcasses indicates damage to the endothelium, which is the
initiating step in the atherosclerotic process. As noted above,
in nonsmokers the appearance of endothelial cells following passive
smoking is almost as great as following primary smoking (Table 2).
The process by which endothelial injury leads to the development
of an atherosclerotic plaque, including the role of platelets, is
described in Figure 4. Based on the information presented so far,
exposure to ETS appears to produce injuries similar to those
observed with exposure to primary smoke and also affects platelets
in a way that increases the chances that they will bind to the
injured area and promote growth of smooth muscle cells.
The Role of the Polycyclic Aromatic Hydrocarbons in ETS
Many atherosclerotic plaques in humans are either monoclonal or
possess a predominantly monoclonal component (Benditt and Benditt,
1973), which indicates that the smooth muscle cells of each plaque
have a predominant cell type. Several animal studies have also
shown that injections of polycyclic aromatic hydrocarbons (PAHs),
in particular 7,12-dimethylbenz(a,h)anthracene (DMBA),
benzo(a)pyrene (Albert at al, 1977; Revis, et al 1984; Penn et al,
1981; Penn et al, 1986; Majesky et al, 1983) accelerate the
development of atherosclerosis. Others (Rogers et al, 1980, 1988)
failed to find an effect of active smoking or the extent of fatty
92
Draft - Do not cite or quote
deposits in the coronary arteries of baboons. (There was a
significant effect on the carotid arteries.) Benzo(a)pyrene is an
important element in ETS (USPHS, 1986). The effects of PAHs or
other carcinogenic or mutagenic elements in ETS (Remmer, 1987)
relates directly to the response to injury theory of atherogenesis
discussed above (Ross, 1986). Changes in the underlying smooth
muscle stimulated by these agents could then initiate the "injury"
that leads to platelet aggregation and plaque formation. Thus,
chronic exposure to ETS could have effects on plaque formation
through mechanisms similar to that by which long term exposures
produce cancer in other organs.
Albert et al (1977) gave chickens weekly intramuscular
injections of DBMA and benzo(a)pyrene for up to 22 weeks, then
killed the chickens at various times beginning after 13 weeks and
measured the plaque volume in the chickenso aortas. They found
that both DBMA and benzo(a)pyrene significantly increased the
volume of plaque compared to control chickens who had just received
injections of the solvent used to carry these agents. This study
provided the first evidence that known carcinogenic chemicals could
be atherogenic as well.
Penn et al (1981) extended this result in a similar experiment
by showing that the effects of DBMA on the extent of plaque buildup
in chickens was dose-dependent. The median cross-sectional area
of plaques on individual aortic segments and the plaque volume
index (an approximate measure of the total volume of plaque per
aorta) increased in a nearly linear fashion with DBMA dose. In
contrast to the marked increase in plaque area in the DBMA-treated
animals, there was only a slight increase in the percentage of
aortic sections with plaques in carcinogen-treated animals than in
controls. Plaques with a small cross sectional area were present
in all animals. Lesions of widely differing cross sectional areas
appeared to be similar histologically under the light microscopeo
Together, these data suggest that a major effect of chronic DBMA
exposure is to increase the size of spontaneous aortic lesions.
Rather than inducing some sort of cancer-like change in an
individual cell that begins the process which ultimately leads to
formation of a plaque, Penn et al suggested that chronic DBMA
exposure causes preferential division of individual cells or
patches of cells within the preexisting spontaneous lesions. From
this perspective, DBMA and other exogenous compounds would be
acting as a mitogen, similar to that released by activated
platelets, to stimulate division of aortic smooth muscle.
Revis et al (1984) found similar results in White Carneau
pigeons injected with DMBA and benzo(a)pyrene weekly for 6 months,
beginning when the pigeons were 3 months old. Compared with the
work described above, they found a greater effect on atherogenesis
of benzo(a)pyrene than DBMA, and also failed to observe a dose-
response relationship between the dose given and the amount of
aortic plaque. These differences from the work just described may
93
Draft - Do not cite or quote
be related to species differences, differences in the carrier used
to inject the PAHs (DMSO in the previous studies vs. corn oil in
this one) or differences in the age of the pigeons or dosing
schedule. They also found an increase in aortic plaques in pigeons
treated with the PAH 3-methylcholanthrene, but not the carcinogen
2,4,6-trichlorophenol or the PAH benzo(e)pyrene, which is not
considered a carcinogen. This result suggests that carcinogenic
PAHs, rather than carcinogens or PAHs in general, are implicated
in the atherosclerotic process.
Revis et al also studied the distribution of these compounds
after they had been radiolabelled. Forty-eight hours after the
injection of PAHs, radioactivity in the liver, aorta and lung
accounted for 75% of the injected dose, whereas in animals injected
with 2,4,6-trichlorophenol, radioactivity in the liver and kidney
accounted for 80% of the dose. In addition, 80% of the
radioactivity observed in the plasma immediately following
injection of radiolabelled PAHs was associated with the LDL and HDL
cholesterol fractions, compared with only _24% of the 2,3,6-
trichlorophenol, suggesting that plasma lipoproteins are an
important vehicle for transporting PAHs to their sites of
activation in the arteries.
There is also some evidence that ETS directly affects plasma
lipoproteins. Moskowitz et al (1990) showed that adolescent
children whose parents smoked had elevated levels of cholesterol
and depressed levels of HDL, even after correcting for age, weight,
height and sex. These effects were dose dependent; the greater the
exposure to ETS, the greater the changes in these variables. High
cholesterol and low HDL are important for the development of
plaque. Data on cholesterol and HDL froi'n adults married to
smokers, however, do not show similar differences (Garland et al,
1985; Svendsen et al, 1987).
To further elucidate the possible mechanisms by which PAHs
induce atherosclerotic changes, Majesky et al (1983) gave White
Carneau and Show Racer pigeons a single injection of
benzo(a)pyrene, then looked for metabolites of the benzo(a)pyrene
in aortic and hepatic tissues 48 hours later. White Carneau
pigeons develop severe atherosclerosis by the time they are 3 years
old, whereas Show Racer pigeons are relatively resistant to aortic
atherosclerosis. Aortic preparations of the White Carneau strain
exhibited a much greater inducibility of the microsomal
monooxygenase system than did those of the Show Racer strain,
particularly in young pigeons. Aortic tissues from White Carneau
pigeons aged 6-12 months exhibited a 3-12 fold inducibility whereas
aortic tissues from the same strain at 2-5 years of age exhibited
only minor (maximum of 3.3 fold) and, for the most part,
statistically insignificant increases. No age differences in
inducibility could be detected in the Show Racer strain.
Interestingly, the differences in inducibility manifest in aortic
tissues were greater in aortic tissues than in hepatic tissues from
94
Draft - Do not cite or quote
the same birds. Thus, the PAHs seem to accelerate any preexisting
tendency to develop atherosclerosis.
Regardless of the ultimate mechanism by which PAHs exhibit
atherogenic effects, it seems logical to suppose that the reactive
intermediary metabolites of these chemicals are the proximate
atherogenic or co-atherogenic agents since the parent compounds are
relatively inert both chemically and biologically. Thus,
bioactivation and inactivation (and regulatory control of these
processes) may be presumed to play extremely important roles in
their atherogenic properties. Bioactivated chemicals vary in their
stability/reactivity according to four general categories: (i)
those which are extremely unstable and persist only at the
immediate site (enzyme) of bioactivation, (ii) those which persist
only within cells in which bioactivation occurs, (iii) those which
persist primarily only within tissues in which bioactivation
occurs, and (iv) those capable of being transferred in the
circulation from one organ to another. For the first three of
these four categories, biotransformation in the aorta ger se
(target tissue activation) would -be of prime interest and
importance. Thus, it appears that PAHs could be playing eith.er a
mutagenic or mitogenic role in beginning the atherosclerotic
process in susceptible cells or individuals, depending on how the
PAHs in ETS are metabolized in the aorta.
The finding that enzymes that metabolize DMBA and benzo (a) pyrene
are in the artery wall led Penn et al (1986) to search for specific
molecular events in plaque cells that would lead to DNA changes
similar to those previously found in tumors. Identification of
such processes would be supportive of the monoclonal hypothesis of
atherogenesis. They obtained human DNA samples from coronary
artery plaques as well as DNA from normal sections of the coronary
arteries at surgery to remove the plaque. These DNA samples were
tested with the NIH 3T3 cell transection assay. Foci arose in
cells transfected with each of the DNA samples obtained from the
huwn coronary plaque, with an efficiency (number of foci per gg
of DNA) ranging from 0:016 to 0.060 (mean 0.036). The transfection
efficiencies for DNA's from normal coronary artery, liver, spleen,
lung, kidney and trachea were all below 0.008. The transformed
cells were also injected into the scalps of nude mice, where they
developed tumors. These results provide direct evidence for
similarities on the molecular level in the development of plaques
and tumors. Human coronary artery plaque DNA contains sequences
capable of transforming NIH 3T3 cells and these transformed cells
can cause tumors after injection into nude .mice. Control
experiments verified that the transforming cells did indeed contain
human DNA and that the tumorigenic (or transforming) activity was
not due to the ras oncogene family. Although these results clearly
demonstrate that human plaque DNA has transforming ability, the
temporal expression of this activity in vivo is not known. The
plaques were taken from adult patients in late stages of vascular
disease. Thus, we cannot determine from these samples whether the
95
Draft - Do not cite or quote
manifestation of transformation is a relatively late event in
plaque development or an early but stable event. Oncogene
activation and expression is an important early event in
transformation and tumor genesis. These results identify specific
molecular events that may underlie the proliferation of smooth
muscle cells that is a hallmark of atherosclerotic plaque
development and demonstrates that plaque cells exhibit molecular
alterations that had previously only been thought to be present in
cancer-cell transformation and tumorigenesis. These results
provide direct support for the monoclonal hypothesis.
Randerath et al (1988) also demonstrated that constituents of
cigarette "tar," including benzo(a)pyrene, are preferentially
attracted to the heart and damage DNA there. They studied
molecular mechanisms of smoking-related carcinogenesis by examining
the induction and distribution of covalent DNA damage in internal
organs of the mouse following topic application of cigarette smoke
condensate daily for 1, 3, or 6 days then killed 24 hr later. DNA
samples were obtained from skin, lung, heart, kidney liver, and
spleen. Adducts containing benzo(a)pyrene-derived moieties were
identified, together with others. At all three times, the number
of adducts in heart and lung DNA was about five times higher than
that in liver and slightly higher than that in skin. Covalent DNA
damage was estimated to be 6.2, 5.7, 3.9, and 1.9 times higher,
respectively, in lung, heart, skin and kidney than in liver,
ranging from approximately 1 adduct in 5.4x106 DNA nucleotides in
lung to 1 adduct in 3.3xl0~ DNA nucleotides in liver. Spleen DNA
was virtually adduct free. While the DNA adduct prof.iles resembled
each other qualitatively among the different tissues, there were
major quantitative differences between the different tissues, with
the highest DNA binding occurring in the lung and heart. The
reasons for the high incidence of DNA adducts in the heart are not
known, but may be related to the role of plasma lipids in
transporting PAHs such as benzo(a)pyrene and preferential binding
of these lipids to cardiac tissue, as discussed earlier.
In sum, there is a growing body of evidence at a molecular level
supporting the monoclonal hypothesis of atherogenesis, with
compounds in tobacco smoke and ETS strongly implicated as agents
which stimulate the development of coronary lesions. Regardless
of whether the monoclonal hypothesis proves to be true (or, more
likely, one of several initiators of the atherosclerotic process),
the fact is that there is clear evidence that components of ETS,
in particular PAHs such as benzo(a)pyrene, initiate or accelerate
the development of plaque. These biochemical findings are
consistent with the epidemiological finding that chimney sweeps,
which are exposed to high levels of PAHs in soot, have an increased
risk of heart disease (as well as cancer) and tend to develop these
diseases younger than other, comparable, occupations which avoid
exposure to PAHs (Hansen, 1983).
Summary
96
Draft - Do not cite or quote
There are eleven epidemiological studies, done in a variety of
locations, which reflect a 30% increase in risk of death from
ischemic heart disease or myocardial infarction among nonsmokers
living with smokers. The larger studies also demonstrate a
statistically significant dose-response effect, with larger
exposure to ETS being associated with greater risks of death from
heart disease.
These epidemiological studies are complemented by a variety of
physiological and biochemical data from human studies which suggest
that ETS may adversely affect platelet function and damage arterial
endothelium in a way that increases the risk of heart disease.
Moreover, ETS, in realistic exposures, also exerts significant
effects on exercise capability of both normal people and people
with heart disease by affecting the body's ability to deliver and
utilize oxygen. In animal experiments, ETS also depresses cellular
respiration at the level of mitochondria. The polycyclic aromatic
hydrocarbons in ETS also accelerate, and may initiate, the
development of atherosclerotic plaque.
It is also important to note that the cardiovascular effects of
ETS appear to be different in nonsmokers and smokers. Nonsmokers
appear to be more sensitive to ETS than smokers, perhaps because
some of the affected systems are sensitive to low doses.of the
compounds in ETS, then saturate and also perhaps because of
physiological adaptions smokers undergo as a result of chronic
exposure to the toxins in cigarette smoke. In any event, these
findings indicate that, in terms of cardiovascular disease, it is
unreliable to"compute "cigarette equivalents" for passive exposure
to ETS, then try to extrapolate the effects of this exposure on
nonsmokers from the effects of direct smoking on smokers.
These results combine to suggest that heart disease is an
important consequence of exposure to ETS. The combination of
epidemiological studies with demonstration of physiological changes
with exposure to ETS, together with biochemical evidence that
elements of ETS have significant effects on the cardiovascular
system,'lead to the conclusion that ETS causes heart disease. This
increase in risk translates into about 10 times as many deaths from
ETS-induced heart disease as lung cancer, and contributes 37,000
to the estimated 53,000 deaths annually from passive smoking
(Wells, 1988). This toll makes passive smoking the third leading
preventable cause of death in the United States today, behind
active smoking and alcohol.
97
Draft - Do not cite or quote
References
Albert R, Vanderlaan F, Nishizumi M(1977) Effect of carcinogens
on chicken atherosclerosis. Cancer Res. 37: 2232-2235.
Alired EN, Bleecker ER, Chaitman BR, Dahms TE, Gottlieb SO, Hackney
JD, Pagano M, Selvester RH, Walden SM, Warren J (1989) Short-term
effects of carbon monoxide exposure on the exercise performance of
subjects with coronary artery disease. N. Engl. J. Med. 321: 1426-
32.
Aronow W (1978) Effect of passive smoking on angina pectoris. N.
Encjl. J. Med. 299 : 21-24.
Bardford-Hill A (1984) A Short Textbook of Medical Statistics
London: Hodder and Stoughton (11 ed.)
Barrett T, Gajdusek C, Schwartz S, McDougall J, Benditt E (1984)
Expression of the sis gene by endothelial cells in culture and in
vivo. Proc. Nat. Acad. Sci. 81: 6772-6774.
Benditt E, Benditt J (1973) Evidence for a monoclonal origin of
human atherosclerotic plaques. Proc. Nat. Acad. Sci. 70: 1753-.
1756.
Burghuber 0, Punzengruber C, Sinzinger H, Haber P, Silberbauer
(1986) Platelet sensitivity to prostacyclin in smokers and non-
smokers. Chest 90: 34-38.
Butler T (1990) The relationship of passive smoking to various
health outcomes among Seventh-Day Adventists in California.
Seventh World Conference on Tobacco and Health, 316 (abstract).
Davis J, Hartman C, Lewis H Jr, Shelton L, Eigenberg D, Hassanein
K, Hignite C, Ruttinger H (1985b), Cigarette smoking-induced
enhancement of platelet function: Lack of prevention by aspirin in
men with coronary artery disease.
483.
Davis J, Shelton L, Eigenberg D,
J. Lab. Clin. Med. 105: 479-
Hignite C, Watanabe I(1985)
Effects of tobacco and non-tobacco cigarette smoking on endothelium
and platelets. Clin. Pharmacol. Ther. 37: 529-533.
Davis J, Shelton L, Eigenberg D, Hignite C (1987) Lack of effect
of aspirin on cigarette smoke-induced increase in circulating
endothelial cells. Haemostasis 7: 66-69.
Davis J, Shelton L, Hartman C, Eigenberg D, Ruttinger H (1986)
Smoking-induced changes in endothelium and platelets are not
affected by hydroxyethylrutosides. Br. J. Exp. Path. 67: 765-771.
Davis J, Shelton L, Watanabe I, Arnold J (1989) Passive smoking
98
Draft - Do not cite or quote
affects endothelium and platelets. Arch. Intern. Med. 149: 386-
389.
Davis J, Shelton L, Zucker M (1990) A comparison of some acute
effects of smoking and smokeless tobacco on platelets and
endothelium. (submitted)
Deanfield JE, Shea MJ, Wilson RA, Horlock P, de Landsherre CM,
Selwyn AP (1986) Direct effects of smoking on the heart: silent
ischemic disturbances of coronary flow. Am. J. Cardiol 57: 1005-
1009.
Dobson A, Heller R, Alexander H, Lloyd D (1990) Passive smoking
and the risk of heart attack. Seventh World Conference on Tobacco
and Health, 102 (abstract).
Fox P, DiCorleto P (1984) Regulation of production of a platelet-
derived growth factor-like protein by cultured bovine aortic
endothelial cells. J. Cell. Ph sX iol. 121: 298-208.
Friedman J, Chalmers T, Smith H Jr, Keubler R (1978) The
importance of beta, the Type II error, and sample size in the
design and interpretation of the randomized controlled trial:
Survey of 71 "negative" trials. N. Engl. J. Med. 299: 690-694.
Fuster V, Chesebro J (1981) Antithrombotic therapy: Role of
platelet-inhibitor drugs: Io Current Concepts of Thrombogenesis:
Role of Platelets. Mayo Clin. Proc. 56: 102-112.
Garland C, Barrett-Connor E, Suarez L, Criqui M, Wingard D (1985)
Effects of passive smoking on ischemic heart disease mortality of
nonsmokers. Am J. Epidemiol. 121: 645-650.
Gillis C, Hole D, Hawthorne V, Boyle P (1984) The effect of
environmental tobacco smoke in two urban communities in the west
of Scotland. Eur. J. Resp. Dis. 65 (suppl 133): 121-126.
Glantz and Parmley (1990) Passive smoking and heart disease:
epidemiology, physiology and biochemistry. Circulation (in press).
Gvozdjak J, Gvozdjakova A,.Kucharska, Bada V (1987) The effect of
smoking on myocardial metabolism. Czech. Med. 10: 47-53.
Gvozdjakova A, Bada V, Sany L, Kucharska J, Kruty F, Bo ek,
Trstanksy L, Gvozdjak J (1984) Smoke cardiomyopathy: Disturbance
of oxidative process in myocardial mitochondria. Cardiovasc. Res.
18: 229-232.
Gvozdjakova A, Kucharska J, Sany L, Bada V, Bo ek, Gvozdjak J
(1985) Effect of smoking on the cytochrome and oxidase system of
the myocardium. Bratisl. lek. Listy. 83: 10-15.
99
Draft - Do not cite or quote
Hansen E (1983) Mortality from cancer and ischemic heart disease
in Danish chimney sweeps: A five-year follow-up. Am. J.
Epidemiol. 117: 160-164.
Hartman P (1983) Mutagens: Some possible health impacts beyond
carcinogenesis. Environ. Mutagen. 5: 139-152.
He Y (1989) Women's passive smoking and coronary heart disease.
ChunQ-Hua-Yu-Fang-I-Hsueh-Tsa-Chin 23: 19-22. (English translation
of entire article.)
Helsing K, Sandier D, Comstock G, Chee E (1988) Heart disease
mortality in nonsmokers living with smokers. Am. J. Epidemiol.
127: 915-922.
Hirayama T (1984) Lung cancer in Japan: Effects of nutrition and
passive smoking. In Lung Cancer: Causes and Prevention M. Mizell
and P Correa eds, pp 175-195. Verlag Chemie International, New
York.
Hole D, Gillis C, Chopra C, Hawthorne V (1989) Passive smoking and
cardiorespiratory health in a general population in the west of
Scotland. Br. Med. J. 299: 423-427.
Hugod C, Hawkins LH, Kjeldsen K, Thomsen HK, Astrup P(1978) Effect
of carbon monoxide on aortic and coronary intimal morphology in the
rabbit. Atherosclerosis 30: 333-342.
Hugod C (1981) Myocardial morphology in rabbits exposed to various
gas-phase constituents of tobacco smoke. Atherosclerosis 40: 181-
190.
Humble C, Croft J, Gerber A, Casper M, Hames C, Tyroler H (1990)
Passive smoking and twenty year cardiovascular disease mortality
among nonsmoking wives in Evans County, Georgia. Am. J. Pub. Health
80: 599-601.
Jarvis MJ (1987) Uptake of environmental tobacco smoke. In
Environmental carcinogens: methods of analysis and exposure
measurement: Vol 9: Passive Smokino O'Neill I, Bronnemann KD,
Dodet B, Hoffman D (eds), Lyon France: IARC, pp. 43-58.
Kawachi I, Pearce N (1989) Passive smoking in New Zealand
(letter). N. Zeal. Med. J. 102: 479.
Kawachi I, Pearce N, Jackson R (1989) Deaths from lung cancer and
ischaemic heart disease due to passive smoking in New Zealand. N.
Zeal. Med. J. 102:337-340.
Khalfen E, Klochkov V (1987) Effect of passive smoking on physical ~
4
tolerance of ischemic heart disease patients. Ter. Arkh. 59: 112- .~4
115
.
~
100
~
~
~
Draft - Do not cite or quote
Kjeldsen K, Thomsen H, Astrup P (1974) Effects of carbon monoxide
on myocardium: Ultrastructural changes in rabbits after moderate,
chronic exposure. Circ. Res. 34: 399-348.
Kristensen T (1989) Cardiovascular diseases and the work
environment: A critical review of the epidemiologic literature on
chemical factors. Scand J Work Environ Health 15:245-264.
Lamb D (1984) Physiology of exercise: Responses and adaptation
MacMillan Publishing Co.: New York.
Lee P (1988) Misclassification of smoking habits and passive
smoking. A review of the evidence International Archives of
Occupational and Environmental Health. Berlin: Springer-Verlag.
Lee P (1989) Deaths from lung cancer and ischaemic heart disease
due to passive smoking in New Zealand~(letter). N. Zeal. Med. J.
102: 448.
Lee P (1990) An estimate of adult mortality in the United States
from passive smoking: A response (letter). Environ. Int. 16:179-
181. :
Lee P, Chamberlain J, Alderson M (1986) Relationship of passive
smoking to risk of lung cancer and other smoking-associated
diseases. Br. J. Cancer 54: 97-105.
Lough J(1978) Cardiomyopathy produced by cigarette smoke. Arch.
Pathol. Lab. Med. 102: 377-380.
Majesky M, Yang H, Benditt E (1983) Carcinogenesis and
atherogenesis: Differences in monoxygenase inducibility and
bioactivation of benzo[a]pyrene in aortic and hepatic tissues of
atherosclerosis-susceptible versus resistant pigeons.
Ca=inocrenesis 4: 647-652.
Martin M, Hunt S, Williams R (1986) Increased incidence of heart
attacks in nonsmoking women married to smokers. Paper presented
at annual meeting of APHA, October.
McMurray R, Hicks L, Thompson D (1985) The effects of passive
inhalation of cigarette smoke on exercise performance. Eur. J.
Appl. Physiol. 54: 196-200.
Moskowitz W, Mosteller M, Schieken R, Bossano R, Hewitt J, Bodurtha
J, Segrest J(1990) Lipoprotein and oxygen transport alterations
in passive smoking preadolescent children: The MCV twin study.
Circulation 81: 586-592.
Muhm J, 0lshan A (1989) A program to calculate sample size, power,
and least detectable relative risk using a programmable calculator.
101
Draft - Do not cite or quote
Am. J. Epidemiol. 129: 205-11.
NRC (1986) Environmental Tobacco Smoke: Measuring Exposure and
Assessing Health Effects. Washington DC: National Academy Press.
Palmer J, Rosenberg L, Shapiro S (1988) Passive smoking and
myocardial infarction. CVD Epid. Newsletter 43: 29, 1988
(abstract)
Penn A, Batastini G, Soloman J, Burns F, Albert R (1981) Dose-
dependent size increases of aortic lesions following chronic
exposure to 7,12-Dimethylbenz(a)anthracene. Cancer Res. 41: 588-
592.
Penn A, Garte S, Warren L, Nesta D, Mindich B (1986) Transforming
gene is human atherosclerotic plaque DNA. Proc. Nat. Acad. Sci.
83: 7951-7955.
Pittilo R, Mackie I, Rowles P, Machin S, Woolf N (1982) Effects
of cigarette smoking on the ultrastructure of rat thoracic aorta
and its ability to produce prostacyclin. Thromb. Haemostas 48:
173-176.
Randerath E, Mittal D,- Randerath K (1988) Tissue distribution of
covalent DNA damage in mice treated dermally with cigarette 'tar':
preference for lung and heart DNA. Carcinogenesis 9: 75-80.
Reinken J (1989) Passive smoking in New Zealand (letter). N. Zeal.
Med. J. 102: 515.
Remmer H (1987) Passively inhaled tobacco smoke: A challenge to
toxicology and preventive medicine. Arch. Toxicol. 61: 89-104.
Repace J, Lowrey A (1985) A quantitative estimate of nonsmokers'
lung cancer risk from passive smoking. Environ. Int. 11: 3-22.
Repace J, Lowrey A (1987) Predicting the lung cancer risk of
domestic passive smoking. Am. Rev. Resp. Dis. 136: 1308.
Revis N, Bull R, Laurie D, Schiller C (1984) The effectiveness
of chemical carcinogens to induce atherosclerosis in the white
carneau pigeon. Toxicology 32: 215-227.
Rogers WR, Bass RL III, Johnson DE, Kroski AW, McMahan CA, Montiel
MM, Mott GE, Wilbur RL, McGill HC Jr (1980) Atherosclerosis-related
response to cigarette smoking in the baboon. Circulation 61: 1188-
1193.
Rogers WR, Carey KD, McMahan CA, Montiel MM, Mott GE, Wigodsky HS,
McGill HC Jr (1988) Cigarette smoking, dietary hyperlipidemia, and
experimental atherosclerosis in the baboon. Expt. Molec. Path. 48:
135-151.
102
Draft - Do not cite or quote
Ross R (1986) The pathology of atherosclerosis -- An Update. N.
Engi. J. Med. 314: 488-500.
Rothman K (1978) A show of confidence. N. Engl. J. Med. 299:
1362-1363. ~
Saba S, Mason R (1975) Some effects of nicotine on platelets.
Throm. Res. 7: 819-824.
Serabjit-Singh C, Bend J, Philpot R (1985) Cytochrome P-450
monooxygenase system: Localization in smooth_ muscle of rabbit
aorta. Molec. Pharmacol. 28: 72-79.
Sheps D, Adams K Jr, Brombarg P, Goldstein G, O'Neil J, Horstman
D (1987) Lack of effect of low levels of carboxyhemoglobin on
cardiovascular function in patients with ischemic heart disease.
Arch. Env. Health 42: 108-116.
Sinzinger H, Kefalides A (1982) Passive smoking severely decreases
platelet sensitivity to antiaggreatory prostaglandinso Lancet
2(8294): 392-393.
Sinzinger H, Virgolini I(1989) Are passive smokers at greater
risk of thrombosis? Wiener klinische Wochenschrift 20: 694-698.
Svendsen K, Kuller L, Martin M, Ockene J (1987) Effects of Passive
Smoking in the Multiple Risk Factor Intervention Trial. Am. J.
Epidemiol. 126: 783-795.
Thomsen H, Kjeldsen K (1974) Threshold limit for carbon monoxide-
induced myocardial damage. Arch. Environ. Health 29: 73-78.
USPHS (1983) The Health Consequences of Smoking: Cardiovascular
Disease: A report of the Surgeon General. DHHS(PHS) 84-50204.
USPHS (1986) The Health Consequences of Involuntary Smoking: A
report of the Surgeon General. DHS(CDC)87-8398.
Wald N (1986) Does breathing other people's tobacco smoke cause
lung cancer? Br. Med. J. 293: 1217-1222.
Wall MA, Johnson J, Jacob P, Benowitz NL (1988) Cot.inine in the
serum, saliva, and urine of nonsmokers, passive smokers, and active
smokers. Am. J. Pub. Health 78: 699-701.
Wells A (1986) Misclassification as a factor in passive smoking
risk. Lancet ii: 638.
Wells A (1988) An estimate of adult mortality in the United States
from passive smoking. Environ. Int. 14: 249-265.
103
Draft - Do not cite or quote
Wells A (1990) An estimate of adult mortality in the United States
from passive smoking: A response to criticism. Environ. Int. 16:
187-193.
Wikstrand J, Warnold I, Olsson G, , Tvomilehto J, Elmfeldt D,
Bergiund G (1988) Primary prevention with metoprolol in patients
with hypertension: Mortality results from the MAPHY trial. JAMA
259: 1976-1982.
104
Draft - Do not cite or quote
FIGURES AND TABLES, CHAPTER 6
105
Draft - Do not cite or quote
Passive Smoking and Heart Disease: Epidemiology, Physiology, and Biochemistry CR900213R3
TABLE 1.
Table 1
Epidemiological Studies of Environmentat Tobacco Smoke and Coronary Heart Disease Death
Author Type` Location Deaths Relative 95% Dose Power` Controlling for:
or Risk Confidence Response?b
Cases Interval
Mates
Gillis et ala P Scotland 32 1.3 0.7 2.6 - 5% age
(1984)
Lee et ate C United 41 1.2 0.6 - 2.6 4% age, marital status
(1986) Kingdom
Svendsen et P United States 13 2.1 0.7 - 6.5 Yes 3% age, blood pressure,
al'o (1987)d serum cholesterol,
weight, education,
alcohol
Hetsing et P Maryland 370 1.3 1.1 - 1.6 No 40% age, marital status,~
at " (1988) housing education
Pooted' 1.3 1.1 - 1.6
Females
Hirayama12 P Japan 494 1.2 0.9 - 1.4 Yes 40% age, diet
(1984)
Gitlis et ala P Scotland 21 3.6 0.9 -13.8 - 2% age
(1984)
Garland et P California 19 2.7 0.9 -13.6 - 2% age, blood pressure,
att3 (1985) plasma cholesterol,
weight years of marriage
Lee et at° C United 77 0.9 0.5 - 1.6 - 6% age, marital status
(1986) Kingdom
Martin et al" C Utah 23 2.6 1.2 - 5.7 - 3% age, family history of
(1986) CHD, hypertension,
diabetes, weight,
alcohol, exercise
Hetsing et P Maryland 988 1.2 1.1 - 1.4 Yes 92% age, housing, marital
atit (1988) status education
He (1989)i5 C China 34 1.5 1.3 - 1.8 Yes 3% age, race, residence,
occupation, hypertension,
family history of
hypertension or CHD,
alcohol, exercise,
h rli idemia
Humble et altQ P Georgia 76 1.6 1.0 - 2.6 Yes 8% age, serum cholesterol,
(1990) btood ressure weight
Butter/e P California 64 1.4 0.5 - 3.8 - 4% age
(1990)
Pooled 1.3 1.2 - 1.4
cA6lantz\manuscn'ktscols.doc
Draft - Do not cite or
Passive Smoking and Heart Diseasea Epidemiology, Physiology, and Biochemistry CR
0
9oa
ote
?1aR3
Table 1
Epidemiologiesl Studies of Environmental Tobacco Smoke and Coronary Heart Disease Death
Author Typet Location Deaths Relative 95% Dose Powero Corstrollin9 for:
or Risk Confidence Response?b
Cases Interval
Both sexes eo.bined
Hote et at'~ P Scotl" 84 2.0 1.2 - 3.4 - 10% age, sex, sociaL class,
(1989)t blood pressure,
cholesterol weight
Pooled® 1.3 1.2 - 1.4
`P = Prospective cohort, C= Case controi
No entry in this column indicates no eomaient on the presence or absence of dose-response
reiatiomhip
`'Power to detect relative risk of 1.2 with 95% confidence
dHigh risk populationl members of MRFIT trial
®Pooted relative risk computed as R= exp (M w% ln Ri /Mwj) where wi a (%y/ln R,)2
f
a
This report is a later follow-up of the population reported in Gillis et at
QALL studies combined without regard for sex, with Gillis et al° excluded because Hole et al'?
report later follow-up on the
same peopte. ""
-OW
c\gfa n tz\sna n uacnletscoIs. d oc
Draft - Do not cite or quote
Passive Smoking and Heart Disease: Epidemiology, Physiology, and Biochemistry CR900213R3
Table 2
Effect of Passive and Active Smoking on Platelet Aggregation and Endothetiat Cell Damage
Platelet Aggregate Ratio Endothelial Cell Count n
Before After Change Before After Change
Passive Smoking .87 .78 -.09 2.8 3.7 0.9 10
(nonsmoker)
Tobacco (nonsmoker) .80 .65 -.15 2.3 4.8 2.5 20
vs.
Non-tobacco .81 .78 -.03 2.5 3.0 0.5
cigarette
(nonsmoker)
%nhale cigarette .81 .68 -.13 4.0 5.4 1.4 24
(smoker) vs.
Not inhale cigarette .82 .73 -.09 3.3 4.7 1.4 22
(nonsmoker)
Smoke (smoker) vs. .85 .70 -.15 4.4 6.4 2.0 17
Snuff (smoker) .82 .76 -.06 3.9 4.7 0.8
Notes: All studies are paired and reflect significant differences (P<.005). Platelet aggregate ratio
is the ratio of platelet count of platelet-rich plasma, prepared imnediately after venipuncture with
a
solution containing edetic acid and formaldehyde, to that of platelet-rich plasma prepared in the
same
manner, except for the absence of formaldehyde. A decrease in the platelet aggregate ratio reflects
an
increased formation of platelet aggregates. Endothelial cell count is mean number of anuclear cell
carcasses in 0.9 µL chambers. Source: Davis et at47'48'Si'sz
c:lglantzlmanuscriktsco(s.doc
Draft ® Do not cite or quote
Ptatelet TabLe 3
Sensitivity to Prostaglandins Before and After Passive Smoking
(ng PG/mt piatetet rich p(asme)
Prostagiandin Before After 20 min 60 min
Norssmokers
Y 1.260.11 2.16t0.21' 1.76t0.210 1.35t0.14
E2 18.7t3.1 32.5t4.2* 28.234.1e 24.7t2.8
D 42.7s3.8 55.6t5.3 51.334.2 44.6t4.1
Smokers
I 1.75t0.26 2.0Em0.16 2.060.15 1.93±0.23
E2 27.8t2.3 30.6s3.5 31.034.1 29.1t2.9
D2 44.9t4.1 4So6s4.4 49.813.7 45.2±3.8
~Pe.01 comQared to control. Resuits are mean i SEM. Source. Sinzinger and Kefalides (1982)
c.\gtantz\Inanuscn7epa3.doc
Draft - Do not cite or quote
FIGURE CAPTIONS
Figure 1: Relative risk in epidemiological studies of the risk of
death from coronary heart disease or myocardial infarction among
nonsmokers living with smokers compared with nonsmokers living with
nonsmokers. Lines indicate 95% confidence intervals. (Note that
two studies have upper bounds to confidence interval off the scale
of the graph.)
Figure 2: Effect of passive smoking on myocardial mitochondrial
respiration. Q02(S3) = oxygen consumption in mitochondria in the
presence of the substrate and ADP; Q0z (S4) = capacity of respiratory
chain without ADP added; OPR = oxi.dation phosphorylation rate;
ADP:O = oxidation phosphorylation coefficient; RCI = respiratory
control index. Source: Gvozdjak et al (1987) Figures 1 and 2.
Figure 3: Effect of active (left) and passive (right) smoking on
platelet aggregation in smokers and nonsmokers. The sensitivity
index, SIPGIZ, is defined as the inverse of the concentration of
prostaglandln 12 necessary to inhibit ADP-induced platelet
aggregation by 50%. Lower values of SIPGIZ indicate greater platelet
aggregation. Source: Burghuber et al (1986) Figures 3 and 4.
Figure 4: Advanced intimal lesions of atherosclerosis may occur by
at least two pathways. The pathway demonstrated by the clockwise
(long) arrows to the right has been observed in experimentally
induced hypercholesterolemia. Injury to the endothelium (A) may
induce growth factor secretion (short arrow). Monocytes attach to
endothelium (B), which may continue to secrete growth factors
(short arrow). Subendothelial migration of monocytes (C) may lead
to fatty-streak formation and release of growth factors such as
platelet-derived growth factor (PDGF) (short arrow). Fatty streaks
may become directly converted to fibrous plaques (long arrow from
C to F) through release of growth factors from macrophages or
endothelial cells or both. Macrophages may also stimulate or
injure the overlying endothelium. In some cases, macrophages may
loose lose their endothelial cover and platelet attachment may
occur (D), providing three possible sources of growth factors --
platelets, macrophages, and endothelium (short arrows). Some of
the smooth-muscle cells in the possible lesion itself (F) may form
and secrete growth factors such as PDGF (short arrows). An
alternative pathway for the development of advanced lesions of
atherosclerosis is shown by the arrows from A to E to F. In this
case, the endothelium may be injured but remain intact. Increased
endothelial turnover may result in growth-factor formation by
endothelial cells (A). This may stimulate migration of smooth-
muscle as well as growth factor secretion from the "injured"
endothelial cells (E). These interactions could then lead to
fibrous-plaque formation and further lesion progression (F). The
PAHs in ETS probably act by the second pathway. Source: Ross
(1986) Figure 6.
110
Draft - Do not cite or quote
FIGURES AND TABLES, CHAPTER 6
111
P-
~
~
~ -
~ Relative Risk
~
T
i
~ ~ Gillis (1984)
i
~
~ ' Lee (1988)
Svendsen (1987)
-}-- Helsing (1988)
~ Hirayama (1984)
~
Gillis (1984) ~
~
Garland (1985) c
c
i ~
i
~- Lee (1988)
~ i
m i ~ Helsing (1988)
i
i
i -~- He (1989)
~
i ~ Butler (1990)
i
r Humble (1990)
0
~
~
~
cD
x
(D
U)
O 1 N C,J -4 CP n 1
Hole (1989)
+ All studies combined
eqorib .zo a4to 4ou oQ - 4JP.zQ
-1
0.5~
y
.:
Si I
~ P <.0i 0.S
P 1<.03
SAtOKER } ics
0
®EFORE AFTER
0
BEFORE
AFTER
"1NJURY"
{mechanical, LDt,
homocystaine,
ImmunalogiC.
toxins, virusa .tC.)
FIGURE 4.
Draft - Do not cite or quote
lV
Deaths from Passive Smoking
Total Deaths: 53,000
Heart Disease
Lung Cancer
3700
Source: Wells, 1988
asISzz0102
Draft - Do not cite or quote
CHAPTER 7
EXPOSURE ASSESSMENT IN PASSIVE SMOKING
James L. Repace, MSc
indoor Air Division
Office of Air & Radiation
U.S. Environmental Protection Agency
Washington, DC 20460
introduction
This chapter will discuss some of the factors involved in the
assessment of exposure to indoor air pollution from tobacco smoke.
Exposures to environmental tobacco smoke (ETS) have been assessed
by questionnaires, personal air contaminant monitoring of ETS
constituents, modeling of concentrations, and biological markers.
(NRC, 1986) Most of the epidemiological studies of passive smoking
and disease have relied on questionnaires relating to the presence
or absence of a smoker at home, and have assumed that this is a
good surrogate for total exposure to ETS. To the extent that
nonsmokers are heavily exposed outside the home, e.g., the
workplace, this surrogate exposure variable will not differentiate
well between a more exposed and less exposed group, and tend to
cause epidemiologic studies of passive smoking and disease to find
no effect or to lack statistical significance. (Repace & Lowrey,
1990) For this reason, several workers, in assessing risk from
passive smoking, have attempted to correct for exposures outside
the home by adjusting for the finite urinary cotinine
concentrations in those who have reported "no exposure" to ETS.
(NRC, 1986; Wells, 1990) No studies have yet been performed which
yield a national probability sample of exposures to ETS. Thus, all
attempts to assess exposure in individual epidemiological studies
and otherwise have relied on some assumed paradigm of exposure.
This chapter will discuss the evidence for exposure, and emphasize
the insights which derive from a modeling approach.
Exposure to ETS occurs when an individual occupies a
microenvironment which possesses an ETS concentration. A dose is
,said to occur when the individual breathes the concentration. An
individual's total exposure to ETS is the time-weighted sum of the
individual microenvironmental ETS exposures encountered during the
day's activities. (Repace et al., 1980). The dose of ETS will be
affected by the individual's respiration rate during the exposures.
The dose of various ETS constituents to the body will be determined
by their relative rates of absorption and removal. The amount of
ETS inhaled is given by the product of the individual's respiration
rate during exposure, the ETS concentration in the building, and
the duration of the individual's stay in that microenvironment. In
112
Draft - Do not cite or quote
equilibrium, the ETS concentration is directly proportional to the
product of number of smokers, smoking rate, and emissions per
cigarette, pipe, or cigar, and is inversely proportional to the
product of space volume and removal rate. (Repace, IARC, 1987)
In the epidemiologic studies of passive smoking and lung cancer,
exposures are typically estimated on the basis of a questionnaire
which assesses smoking status, and typically ask simple questions
of the sort: "if you are a nonsmoker, do you live with, or work
with, or have regular contact with persons who are nonsmokers?"
(NRC, 1986) Some studies assess past exposure history and spouses'
smoking rate as well. This kind of question, though useful, is not
likely to be fully reliable or precise, particularly for non-
domestic exposures. (NRC, 1986; IARC, 1987) On the other hand, it
has been shown that those nonsmokers who report exposure to ETS at
home tend to have higher non-domestic exposures as well. (NRC, 1986;
Wald, 1986) Those individuals who have exposures both at home and
at work appear to have higher exposures than those who are exposed
at home only or at work only, as reflected by their urinary
cotinine excretion. (Riboli, et al., 1990) Riboli et al. (1990)
report data from a ten-country study of 1369 women, showing that
when appropriately questioned, nonsmoking women can provide a
reasonably accurate description of ETS exposure.
Ideally, the health effects of ETS might be assessed by
quantifying the time°dependent exposures for each of the several
thousand compounds in tobacco smoke and defining dose-response
relationships for these compounds in producing disease, both as
isolated compounds and in various combinations. However, the
enormity of this task has led to simpler approaches which attempt
to use measures of exposure to individual smoke constituents as
estimates of whole smoke exposure. For this reason, exposures to
ETS are often assessed using markers of the vapor phase or
particulate phase. Although biological markers show promise as
measures of exposure (and dose), they also have limitations.
Another consideration is duration of exposure. For chronic
diseases such as cancer, average exposures occuring over a year or
lifetime are of greater importance than short-term exposures.(SG,
1986)
. The two most promising atmospheric markers for ETS are
respirable suspended particles in the size range <3 um (RSP) and
nicotine.(NRC,1986; SG,1986; IARC,1987) A majority of field
studies have used RSP as an indicator of exposure to ETS because
of the substantial emission of RSP in indoor spaces from tobacco
combustion. ETS is the dominant contributor to the indoor levels
of RSP. The total RSP, as measured by personal monitors, has been
found to be substantially elevated for those who report exposure
to ETS relative to those who report no exposure. Both air
monitoring and modeling clearly indicate that RSP concentrations
will be elevated over background levels in indoor spaces when even
low smoking rates occur.(NRC, 1986) Although lacking specificity
113
Draft - Do not cite or quote
for tobacco smoke, the prevalence and number of smokers correlates
well with RSP levels in homes and other enclosed areas.(SG,1986)
RSP is the single largest component of ETS by weight, and RSP is
currently the best and most-utilized general category of air
contaminants to represent ETS.(NRC,1986) A recent study of week-
long averages of RSP and nicotine in about 100 homes with smokers
in New York State showed an RSP-to-nicotine ratio of about 11:1,
above a background of about 20 ug/m3.(Leaderer, 1990) Similar
results were obtained in a survey of 21 commercial buildings by
Miesner, et al. (1989), who found a RSP-to-nicotine ratio of about
10:1 for workday averages, above a background of about 23 ug/m3.
Biological markers in body fluids have also been used for
validating self-reports of exposures to ETS. For example, Haley
et al. (1989) and Cummings et al. (1990) found that cotinine levels
in the urine of those who reported exposure to ETS were more than
twice as high as those who denied having been exposed. Nicotine and
its metabolite cotinine, which derive exclusively from tobacco
products, are the most important markers. Almost all nicotine
shifts from the particulate phase in mainstream and fresh
sidestream smoke to the vapor phase in ETS. Nicotine and cotinine
can be quantified in saliva, blood, and urine. Generally,,the mean
concentrations of nicotine and cotinine in plasma or urine of
nonsmokers exposed to ETS under natural conditions is about 1
percent of the mean values in smokers, (NRC,1986) reflecting the
fact that smokers are present in nearly all environments, including
most workplaces, restaurants, and even in many vehicles, making it
almost impossible for nonsmokers to avoid exposure to ETS. (SG,1986)
A. Sources of ETS
,
In 1986, an estimated 50 million US smokers aged >17 yrs smoked
about 584 billion cigarettes annually. (NRC, 1986; Tobacco
Institute, 1987) They consumed an additional 3.2 billion cigars,
as well as an estimated 24.4 million pounds of tobacco for pipes
and hand-rolled cigarettes. (NRC, 1986) The average US cigarette
smoker smokes 32 cigarettes per day at a rate of 2 cigarettes per
hour and emits about 22 mg of RSP per cigarette. (Repace, IARC,
1987) Since the average person spends about 90% of the time
indoors, an estimated 12,000 metric tons of RSP are emitted into
US indoor microenvironments each year from cigarette smoking alone.
Assuming cigars produce 3 times as much RSP as cigarettes and that
pipes produce as much RSP as a cigarette, (Repace and Lowrey, 1982)
where pipes and hand-rolled cigarettes are assumed to contain 1 g
of tobacco, then all cigars are estimated to contribute as much RSP
indoors as 11 billion cigarettes, while all pipes and hand-rolled
cigarettes are estimated to contribute as much as 15 billion
regular cigarettes. This increases the estimated total RSP
generated in US indoor microenvironments from all cigarettes,
pipes, and cigars to nearly 13,000 metric tons per year. As
exemplified by data from EPA's TEAM study, ETS predominates over
114
Draft - Do not cite or quote
other sources of RSP indoors (see Fig. 1.)
Although the percentage of the population that smokes has
declined from nearly 50% in the 1960's to about 30% presently
(OSH,1988), the percent of smokers who are heavy smokers has
increased steadily over the past 30 years; thus although the
percentage of smokers has gone down, the increase in smoking rate
may tend to offset that trend towards lowering nonsmoker exposure
to ETS.(NRC,1986).
B. indoor air transport of ETS
Nonsmokers are exposed to ETS in indoor spaces. The
determinants of these enclosed-space exposures include smoking
occupancy, source air-contaminant emission characteristics, source
use, building characteristics, space volume, infiltration or
ventilation rates, efficiency of air mixing, surface sorption,
chemical transformation, and the efficiency of air cleaning
equipment. The interaction of these variables in determining the
resultant concentrations of ETS has been evaluated in both
eontrolled laboratory settings and in field studies within the
theoretical framework of the mass-balance equation. The mass-
balance equation-may be applied to tobacco smoke either as an
equilibrium model (time-independent) or as a dynamic model (time-
dependent). Dynamic and equilibrium models are useful in laboratory
studies; equilibrium models are best suited to evaluating and
predicting ETS concentrations in field studies, particularly when
average concentrations over a period of a workday or longer are of
interest. (NRC,1986)
Laboratory and field studies typically utilize some form of a
single-compartment equilibrium model to evaluate the input
parameters of the mass-balance equation, to evaluate field study
data, and to project RSP concentrations from ETS indoors. These
studies have reduced the general single-compartment mass-balance
equation to the following simplified form:
~
Ceq = G[m(NV + Ns)V]-' (1),
where C is the equilibrium concentration of ETS-generated RSP in
a space,~ expressed in units of micrograms per cubic meter (ug/m3),
G is the RSP generation rate from tobacco combustion in units of
micrograms per hour (ug/hr), N. is the ventilation or infiltration
rate in units of airchanges per hour (ach), Ns is. the loss rate of
RSP due to surface removal in a space in air changes per hour, V
is the volume of the space in cubic meters (m3), and m is the
mixing rate (Repace, IARC, 1987) expressed as a fraction. The
above model assumes no air-cleaning devices, either in the space
or recirculated air; Leaderer (1984) has given a detailed review
of this model. Under laboratory conditions, these input parameters
can be controlled and evaluated. In conducting field studies or
in estimating past RSP levels indoors, the values on the right side
115
Draft - Do not cite or quote
of eq.l have to be determined from available data. This equation
assumes equilbrium conditions, and to the extent that any of the
generation or removal terms are intermittent (e.g. smoking rate)
or variable (e.g. ventilation rate), errors are introduced.
(NRC,1986)
According to the National Research Council (1986) the most
extensive use of the mass-balance equation for assessing RSP levels
due to ETS in occupied spaces has been by Repace and Lowrey (1980),
who proposed and applied in field observations a condensed version
of the mass-balance equation for estimating RSP exposures due to
ETS in a variety of indoor microenvironments. Their model is:
Ceq = 650 Ds/Nv (2),
where C~ is the equilibrium concentration of RSP due to ETS in
units of micrograms per cubic meter, D is the density of active
smokers (burning cigarettes) observed in a space per 100 m3 over
the sampling time, and NV is the ventilation or infiltration rate
in ach. (NRC, 19 8 6) The constant term (650) is calculated from a
standard set of assumed conditions for smoking rates, RSP emission
rates, mixing factors, ventilation rates, and sink rates. These
standard sets of conditions are derived largely from experimental
data and building standards. In applying equilbrium mass balance
models such as eq.{2}, gathering data on easily measured input
parameters such as smoking rates or volume can substantially reduce
the variablity of the estimated RSP levels.(NRC,1986) Eq. 2 was
validated under controlled experimental conditions in real world
settings, and was found to predict the equilibrium values of ETS
within a high degree of accuracy in exposure chambers using real
smokers.(Repace & Lowrey,1980, 1982, Repace, IARC, 1987) Further,
the predictions of the model were found to be consistent with RSP
levels from ETS measured in the field. However, the NRC stated
that additional field testing of eq.{2} as well as a better
understanding of the variability of the input parameters was
needed.(NRC,1986) In 1987, Rickert et al.(1987) tested a key
theoretical assumption regarding the ratio between the effective
and ventilatory air exchange rates in the constant term in eq. 2
(Repace, IARC, 1987) and found that the model explained 87% of the
variation between observed and predicted values for RSP
concentrations from ETS in their experiments.
More recently, Repace(IARC,1987) has published a derivative of
eq.2 which incorporate advances in understanding. Eq.{2) assumes
a steady generation of tobacco smoke, which is generally only valid
when 3 or more smokers are present in a space. For less than 3
smokers, it represents an upper bound. It is also limited for
modeling purposes by being based on the room density of active
smokers. The derivative equation is based on the room density of
habitual smokers (number of habitual smokers per unit space
volume). Thus, the presence of an archetypical "habitual" smoker
(i.e., one who is assumed to smoke at an average rate of 2
116
Draft - Do not cite or quote
cigarettes per hour at 10 minutes per cigarette, with an emission
factor of about 22 mg of SS RSP per cigarette) is the modeling
parameter rather than the room density of burning cigarettes. (IARC,
1987) This derivative equation is given as follows:
Ceq = 217 Dhs/NY
(3),
where C is the equilibrium concentration in units of micrograms
per cubic meter, Dh$ is the number of habitual smokers per 100 cubic
meters of space volume, and NY is the number of space air changes
per hour. Eq. 3 assumes that tobacco smoke concentration is in
equilibrium, which occurs when the rate of generation equals the
rate of removal, and the concentration is in a steady state. This
assumption presumes three or more smokers, since the average smoker
smokes three cigarettes per hour and takes ten minutes to smoke a
cigarette. This means that with three smokers in a room, a
cigarette will always be burning. (During growth, e. (3) becomes
A = Ceq (1-exp-tNV) ; during decay, Ad (t>_T) = A exp~t v, where T is
Ae smoking duratione (Repace, 1987) A more (Yetailed description
of the derivation and validation of eq. 3 and the uses and
limitations of these models is given by Repace, (IARC, 1987,
chapter 3).)
If the number of habitual smokers being modeled is only 2 or 1,
steady-state conditions no longer apply, and other simple
approximations have been suggested, (Repace (IARC, 1987) in lieu
of using exact time-dependent growth and decay models. A one-
smoker-approximation model proposed by Repace (IARC, 1987) agrees
very well with the instantaneous predictions of an exact computer
simulation performed by Rickert (1988), but significantly
underestimates newly available field data, which represent time-
averaged concentrations. on the other hand, by contrast, eq.(3)
for less than 3 smokers represents an upper bound to the ETS
concentration, and as is illustrated below, produces reasonable
agreement with, and provides useful insights into, the analysis of
field data.
For example: As part of the the Harvard 6-City study of indoor
and outdoor air quality, Spengler and colleagues (1981) collected
RSP samples in 55 homes in 6 cities between May 1977 and April
1978. The number of smokers living in each home was recorded. The
quantity of tobacco smoked was not reported, nor were the number
of hours each smoker spent in the home or air exchange rates
measured. The daily average "background," or mean indoor RSP level
in the homes of nonsmokers was found to be about 24 ug/m3; using
regression analysis, the authors estimated that the average impact
of a single smoker (a composite averaged over both sexes) on 24-hr
average RSP levels from ETS in a residence was about 20 ug/m3 above
background. On average, two such habitual smokers would make about
40 ug/m3 above background (24-hr average), and so forth. Added to
a background of 24 ug/m3, this yields a daily average RSP
concentration for one smoker homes of 44 ug/m3, and for two-smoker
117
Draft - Do not cite or quote
homes of 64 ug/m3. What does eq. 3 predict?
Although'the air exchange rates were unknown, Fig. 2 shows a
histogram of the frequency of occurrence of various air exhange
rates (called infiltration rates) during the heating season for
typical middle income housing (R. Grot, personal communication) for
266 homes in 14 cities around the US in 1978 (SG,1986). Occupants
were asked to keep windows and doors closed during the tests. Under
these conditions, the mean air exchange rate found was 1.1 ± 0.9
ach (Grot & Clark, 1979); this value is likely to be somewhat lower
than a full seasonal average with no restrictions on door and
window openings.
The smoker density for a one-smoker home of volume 340 m3 has
been given by Re3pace and Lowrey (1985) as Dhs = 0.29 habitual
smokers per 100 m . Similarly, for a two-smoker home, Dhs = 0.58.
In-the absence of information on air exchange rates, let us assume,
from Grot and Clark (1979), a rate, N. = 1.1 ach. Then eq. 3
predicts a value of C = 217 x 0.29/1.1 = 57 ug/m3 during smoking,
for a one smoker home, and 114 ug/m3 for a two-smoker home. From
table Al for time budget studies in Repace and Lowrey (1985),
averaged over employed men and women, and homemakers, the average
amount of time spent awake in the home, (allowing for 8 hrs of
sleep per day) is about 7.9 hours per day. Converting our
calculations to a 24-hr average and adding a background of 24
ug/m3, yields an estimated 57 x 7.9/24 + 24 = 43 ug/m3 for a one-
smoker home, and 114 x 7.9/24 + 24 = 62 ug/m3 for the two smoker
home, in good agreement with the values of 44 ug/m3 and 64 ug/m3 from
the 6-City study above. A comparison of the predictions of eq. 3
with 17 months of RSP data on 55 homes in 6 Cities (Spengler, et
al., 1981) is given in fiq. 3. This example illustrates the
utility of models in estimating nonsmokers' domestic exposures to
ETS.
As a second example, consider the measured aerosol mass
concentration in a 700 m3 (25000 ft2 floor area) office with one
smoker (smoking rate not reported), and a measured air exchange
rate of 1 ach (see Fig. 4); the large impact on the office aerosol
concentration caused by smoking is apparent by comparing the
daytime and evening RSP concentrations.(IARC, 1987) The
predictions of eq. 3 for Dhs = 1 smoker per 7 hundred cubic meters
and N = 1 ach yields C = 31 ug/m3; with an 18 ug/m3 background
added, the predicted RSP~level is 49 ug/m3, in good agreement with
observations (fig 4). It is clear from fig. 4 and also from models,
that ETS can be very persistent in indoor environments: at an air
exchange rate of 1 ach, it takes 3 hrs for 95% of the smoke from
1 cigarette to be removed (Repace, IARC, 1987)
A third example, where more information is available on the
smoking rates, home volumes and air exchange rates, is provided by
the data obtained in the NYSERDA study of weekly average
residential aerosol concentrations in 141 homes with
118
Draft - Do not cite or quote
smokers.(Leaderer, et al., 1990) The measured weekly average RSP
levels were 43 3g/m3 in the smoking homes, the background levels
averaged 16 ug/m in the nonsmoking homes, the average air exchange
rates were 0.54 ach, the average house volumes 353 m3, the average
number of cigarettes smoked per week was 99.3, and the average
number of hours of smoking per day is calculated at 7.1 hrs/day
assuming 2 cig/smoker-hr (Repace and Lowrey, 1980). From this data,
using eq. 3 as before, we calculate R = 217 x 0.28/0.54 x 7.1/24
+ 16 = 49 ug/m3, in reasonable agreement with the observed average
of 43 ug/m3, but higher, as expected. Thus, although eq. 3 for
less than 3 smokers represents a simplified upper-bound
approximation, it has utility in producing estimates which are
reasonably consistent with field data, and has the advantage that
it is simple to use. However, since none of these studies were
specifically designed for model validation, further comparisons
with field data are important as new data sets become available.
A sampling of whole-building air-exchange rates in 8 large
federal office buildings in 7 states with different climates is
shown in Fig. 5, and these generally approximate the ASHRAE 62-81
ventilation standards for offices (20 cfm per occupant, equivalent
t-o 0.84 ach, for smoking buildings) , on average, although there are
some buildings significantly lower. A recent EPA study of air
exchange rates in 6 buildings (3 new, 3 old) did not show
significant differences between the new (.5 ach) and old (.5 ach)
buildings' airchange rates, although for a given building nighttime
measurements tended to be lower. (Sheldon, et al.,1987) Recent
research has revealed several interesting factors in large office
building air exhange. There are many pathways for floor-to-floor
air communication, particularly return air shafts, where the
existence of such pathways can cause a building's air exchange
characteristics to closely approximate those of a single large open
space; it does not require unusual numbers or sizes of openings to
create these conditions, (A. Persily, personal communication; Persily
and Grot,1986) a condition for which eq. 3 was designed. This
implies that ETS may diffuse throughout a large office building,
exposing nonsmokers even in private offices. Nicotine measurements
in office buildings support this observation. (Williams, et al.,
1985; Vaughn and Hammond, 1989)
In summary, limited field tests of the general equilibrium
model, in which some of the input parameters are measured and
others are estimated from either chamber studies or building codes,
have predicted RSP levels reasonably well over a wide range of
values of input parameters. It is clear that both models and
observations based on personal monitoring or area monitors in
various microenvironments yield consistent results: RSP levels when
smoking is allowed will result in substantial increases over RSP
levels in nonsmoking occupancy.(NRC,1986)
~
C. Tobacco Smoke and Ventilation Q
.t1
0
w
119
Draft - Do not cite or quote
Because of widespread public smoking, many buildings are
contaminated with tobacco smoke combustion products. Many building
owners and managers have assumed that ventilation is a viable
control mechanism for the clouds of smoke that are generated by
cigarettes, pipes, and cigars. In particular, the ventilation
standards proposed by ASHRAE (the American Society of Heating,
Refrigerating, and Air Conditioning Engineers) are often thought
to afford adequate control of tobacco smoke. However, ASHRAE
standards are not health-based standards designed to limit cancer
risk or eye irritation to levels acceptable to nonsmokers. They
are designed only to limit dissatisfaction with tobacco smoke odor
to a maximum of 20% for "visitors" (a test panel consisting of 50%
smokers and 50% nonsmokers) to a building where smoking occurs.
Currently ASHRAE recommends 20 cubic feet per minute per occupant
(cfm/occ) for this purpose. Providing ventilation adequate to
control cancer risk has been estimated to require 5400 cfm/occ, an
unrealistic ventilation rate.(Repace & Lowrey, 1985)
Air cleaners have three fundamental problems. One, most air
cleaners do not scrub gases from the air, and many of the harmful
tars appear in the gases. (Pritchard, 1990) Two, air cleaners
cannot remove smoke which encounters the nonsmoker before it
reaches the air cleaner. Three, even air cleaners which are close
to 100% effective in removing particles which reach them must
process hundreds of room air volumes per hour to reduce cancer risk
to an acceptable level.(Repace & Lowrey, 1985; Repace, 1989a)
Separation of smokers from nonsmokers within a space will expose
nonsmokers to smoke which diffuses from the smoking area.
Separation on the same ventilation system will reduce peak
concentrations to which nonsmokers are exposed, but will expose
nonsmokers to smoke recirculated by the ventilation system. (Repace,
1989; Repace and Lowrey, 1987)
The foregoing considerations demonstrate that source control,
i.e., removing the smoking from the air volume containing
nonsmokers, is the only viable control option. Source control
adequate to protect nonsmokers takes two forms: separation of
smokers from nonsmokers on separate ventilation systems, or
restriction of smoking from the building. (USEPA, 1989) Separation
of smokers in a designated smoking area exposes them to much higher
levels of exposure to ETS, and may significantly increase an
already considerable risk from active smoking.(Repace, 1989b)
D. Measured concentrations of ETS constituents:
RSP: Both field studies (Table 1) as well as chamber
studies have demonstrated that tobacco combustion has a major
impact on the mass of suspended particulate matter in occupied
spaces in the size range <2.5 um, defined here as RSP. RSP is a
major component of ETS. Even under conditions of low smoking
rates, easily measurable increases in RSP have been recorded above
background levels. The term RSP, however, encompasses a broad
120
Draft - Do not cite or quote
range of particulates of varying chemical composition and size
emanating from a number of sources (outdoors, cooking indoors,
kerosene heaters, etc.) (NRC, 1986) The apportionment of RSP
indoors depends primarily on the presence of these other sources.
However, in western society, there are few indoor sources
generating concentations which approach in strength those due to
ETSo There appears to be little variability between brands of
cigarettes or tobaccos for RSP emissions, although cigars will
produce greater emissions than cigarettes. Thus, it may be
inferred from Table 1 that from a comparison of smoking and
nonsmoking buildings, the bulk of the RSP found in buildings where
there is smoking is due to ETS. For example, by comparison of the
data of First (1984), Leaderer, et al (1986) and Repace and Lowrey
(1980,1982) for a total of 42 smoking buildings and 21 nonsmoking
buildings, the weighted average RSP level in the smoking buildinc~s
is 262 ug/m , while in the nonsmoking buildings it is 36 ug/m ,
suggesting that about 85% of the indoor RSP levels in those
buildings is due to ETS. Most of the buildings involved were
public access buildings. Hammond et al. (1988) measured personal
exposures to RSP in several hundred railroad workers. Mean
calculated ETS-derived RSP exposures for railroad office workers
averaged over 90 ug/m3; by comparison, all other sources of RSP for
these diesel-exhaust exposed workers averaged 39 ug/m3. The U.S.
Department of Transportation (1990) measured concentrations of RSP
in the smoking section of a random sample of 69 smoking and 23
nonsmoking flights. Nonsmoking flight attendants must work in the
smoking sections on aircraft. Levels of RSP on the smoking flights
averaged 175 ug/m3, whereas measurements in the same section of the
aircraft on nonsmoking flights averaged 35 to 40 ug/m3.
' Figure 6, (IARC, 1987) a plot of the data of Repace and Lowrey
(1980, 1982) illustrates the large impact of smoking on RSP levels;
smoking data points 'A' thru 'T' encompassed a wide variety
building microenvironments,including 10 restaurants, 3 cocktail
lounges, 3 bingo games, 2 dinner-dance halls, 1 bowling alley, 1
sports arena, 1 hospital waiting room, and a residence during a
dinher party. Studies of the dispersion of RSP from ETS in US
homes showed at most a factor of 2 difference among various rooms
in residences, averaged over 24 hrs. In a setting such as a work
environment, where the average exposure is several hours, ETS would
be expected to disseminate throughout the airspace where smoking
is occuring.(SG, 1986) Although most people spend approximately
90 percent of their time in just two microenvironments (home and
work), important exposures can also be encountered in other
microenvironents, e.g., in transit, which accounts for 0.5 to 1.5
hrs per day for most people..(SG, 1986) Exposures on aircraft can
also be considerable. (Repace and Lowrey, 1988; USDOT, 1989)
BENZENE: Wallace (1989) in reporting the results of EPA's TEAM
study with respect to the benzene exposure of the population, found
that ETS was a significant source of population benzene exposure,
accounting for about 5% of total nationwide exposure. Wallace
121
Draft - Do not cite or quote
reported that workplace exposures for nonsmokers not exposed to ETS
at home, but who report being exposed to ETS more than 50% of the
time at work showed significantly higher benzene concentrations
than those who report exposure to ETS less than 50% of the time.
Wallace estimates that ETS-benzene exposures are about equal at
home and at work.
NICOTINE: Leaderer and Hammond (in press) measured vapor phase
nicotine and RSP concentrations in 96 residences. Vapor phase
nicotine measurements were found to be closely related to number
of cigarettes smoked and highly predictive of RSP generated by
tobacco combustion. The mean RSP background in the absence of
measurable nicotine was found to be 15.2 ± 7 ug/m3. The mean RSP
value in the presence of nicotine was 44.1 ± 30 ug/m3. Weekly mean
nicotine concentrations in the residences was 1.1 ug/m3.
Stillman et al. (in press) measured weekly average nicotine
concentrations using the method of Leaderer and Hammond (above),
in 9 (F. Stillman, pers. comm.) university offices. Concentrations
averaged 2.1 ug/m3. After a smoking policy was implemented, the
nicotine levels decreased by 95%. Vaughn and Hammond (1990)
measured weekly average nicotine concentrations in offices in a
modern office building using both active and passive samplers.
Before the smoking control policy, nicotine vapor concentrations
at nonsmokers' desks were about 2 ug/m3, and were reduced by 95%
after a smoking policy was implemented, in good agreement with the
findings of Stiliman, above. Hammond et al. (1988) measured
nicotine and RSP in two employee smoking lounges at the University
of Massachusetts. RSP levels varied between 220 and 350 ug/m3
during smoking, with associated nicotine levels from 40 to 70
ug/m3. After charcoal-filter air cleaners were installed, nicotine
levels were virtually unchanged, and RSP levels varied between 100
and 310 ug/m3.
A study of personal exposures to airborne nicotine in 4 US
office workers showed about a 0.1 mg mean exposure (mean personal
nicotine concentration of 15 + 9 ug/m3, daily workday average,
times a 0.8 m3/hr inhalation rate times an 8-hr workday). The
nonsmokers were exposed to the smoke of a co-worker who smoked 9
cigarettes per workshift, about half the rate of the average US
smoker. (Hammond et al.,1987)
E. Exposure of nonsmoking populations to ETS
In the general population (both sexes) aged > 17 years in 1980
(160,798,000 persons), a majority has smoked at some time: 32.6%
were current smokers, and 21.3% were exsmokers, while 46.1% had
never smoked (see Table 2). Among current 1980 smokers, 53% were
male, and 47% were female, with some race- and gender-specific
differences white males, 35.9%, black males, 42.0%; white
females, 29.3%, black females, 29.7%. (R. Wilson, NCHS, personal
communication) In terms of the population at risk, both lifelong
122
Draft - Do not cite or quote
nonsmokers and former smokers, 66.7% of the adult population and
the overwhelming majority of children are potentially at risk from
involuntary exposure to ETS (in 1970, Bonham and Wilson (1970)
found in a national probability sample of children, that 62% of US
homes with children contained 1 or more smokers). Exposure to
various subpopulations or individuals, however, may vary
considerably. For example, the prevalence of smoking among
subgroups of the population who proscribe smoking on religious
grounds (such as Mormons and Seventh-Day Adventists) is much lower:
for example, in 1980, only 1.7% of Seventh Day Adventist men and
0.5% of Seventh Day Adventist women reported current smoking,
although 35% of the total were exsmokers. The incidence of lung
cancer -- a disease for which the majority of cases occur in
smokers -- among SDAs is 21% of that in the general population.
Thus, SDA homes would be, in general, expected to be ETS-free.
.The microenvironments of importance for exposure to ETS will be
those where the population spends the bulk of its time. As Table
3 (Ott, 1981) (based on 1972 data) shows, employed men spend an
estimated 56 % of their time at home, and 28 % of their time at work,
for a total of 84% of the time at home and at work; employed women
spend 64% of their time at home, and 22% of the time at work, for
total of 86% of the time at home and at work; while homemakers
spend 85% of the time at home. When time spent in other peoples'
homes and in non-work places of business are added in, the
population averages about 88% of its time in homes and workplaces.
These sites, therefore, must, on average, predominate as potential
sites for exposure to ETS for the general nonsmoking population.
A UK study of exposure to ETS in 20 nonsmoking men whose wives
smoked showed that 78% of the men's reported hours exposure came
from outside the home; by contrast, 90% of the ETS exposure of 101
nonsmoking men whose wives did not smoke was reported to come from
non-domestic microenvironments. (Table 4). Since the second
largest source of time spent by men is in the workplace (Table 3),
this suggests the workplace may be the major source of exposure
for nonsmoking men.
Cummings et al (1990) studied the prevalance of exposure to ETS
in 663 never- and ex-smokers who attended a cancer clinic in
Buffalo, N.Y. in 1986, by questionairre and urinary cotinine level.
76 % reported exposure to ETS in the 4 days preceding the interview,
while 91% had detectable urinary cotinine levels. Reported exposure
locations in order of frequency were workplace (28%), home (27%),
restaurants (16%), private social gatherings (11m), in transit
(10%), and in public buildings (8%), (total of 100%). 77% of
subjects reported being exposed to tobacco smoke at work, while 22 0
of the subjects lived with a smoker. In a second study, Cummings
et al. (1989) reported on 380 never smokers from the same study:
A total of 87% reported exposure to tobacco smoke at work. 24.3%
of the men reported spousal smoking, whereas 94.7% reported
workplace exposure; significantly, when asked to rate the severity
of exposure, on a scale where spousal smoking was normalized to 1,
123
Draft - Do not cite or quote
severity of workplace exposure was rated 5. 66% of women reported
spousal smoking, whereas 83.5% reported being exposed to smoking
in the workplace. The women studied rated the severity of spousal
smoking at about 30% higher than workplace exposures.
Coultas et al. (1990), in a pilot study of 15 nonsmokers in
Albuquerque, N.M., exposure questionnaires and saliva, urine, and
personal air samples were obtained pre- and post- workshift.
Nicotine and cotinine levels were quantified, as were atmospheric
nicotine and RSP samples. Statistically significant correlations
were obtained between RSP and nicotine and total reported hours of
exposure; between nicotine and total number of smokers, total hours
of exposure, and postshift urinary cotinine; between urinary
cotinine and total hours of exposure; and between salivary cotinine
and total number of smokers. Objective evidence of exposure to ETS
was obtained in various workplaces. Spengler et al. (1985) and
Sexton et al. (1984) demonstrated by personal monitoring of RSP and
the use of time-activity questionnaires that exposures to ETS both
at home and at work are significant contributors to personal
exposures.
A survey of exposure to ETS in a California population
subscribing to a health-maintainance plan indicated that 63% of
nonsmokers surveyed reported exposures to tobacco smoke (Friedman,
1983) ; this occurred despite the fact that in the 1980's California
has has been in the forefront of restrictions on smoking in public,
with 44% of its population currently living in communities that
have enacted workplace smoking restrictions.(SG, 1986) Garfinkel
(1981), in a study of 176,000 nonsmoking US women (1960-1972),
found 72% had smoking husbands. Kabat and Wynder (1986), in a
recent study of 215 sixty-year-old US women nonsmokers, found that
65% were exposed at home and 67% reported exposure at work,
averaged over adulthood. Studies of the concentration of nicotine
and cotinine in the body fluids of nonsmokers report similar
results (Table 4); Jarvis & Russell, (1984) showed that in a study
of about 100 UK nonsmokers, only 12% of the subjects had
undetectable cotinine levels. Moreover, in the latter study,
surprisingly, nearly 50% reported no exposure, suggesting that ETS
permeates indoor atmospheres to such an extent that many nonsmokers
are unwittingly exposed. This is borne out by a study of 46 US
infants, 40% of whom were reported by their mothers to be unexposed
to ETS, but only 20% had undetectable urinary cotinine
levels.(Greenberg, 1986) In a third UK study (Wald, 1986) of
urinary cotinine in 221 nonsmokers, the 20% who reported no
exposure had mean urinary cotinine levels which were 21% of the
remainder of the group who reported exposure.
The foregoing illustrates that exposure to ETS is very
widespread in the population, even among those nonsmokers who
believe themselves to be unexposed, however it tends to be greater
in those who say they are exposed at home, possibly indicating a
greater tolerance for ETS among men with nonsmoking spouses.
124
Draft - Do not cite or quote
Although there have been numerous measurements of ETS
concentrations in various indoor settings, these data do not
represent a comprehensive description of the actual distribution
of ETS exposures in the US population. However, additional data
on the distribution of smokers in the nonsmokers' environment as
well as the distribution of ETS levels in that environment, are
needed in order to characterize the actual ETS exposure of the
population. In the absence of such data, population exposures can
be estimated by models or by extrapolation from biological markers
from existing studies. (SG, 1986; IARC, 1987)
In summary, exposures to ETS can be assessed by personal air
contaminant monitoring, modeling of concentrations based upon air
sampling, time-activity patterns, and questionnaires, or upon
biological markers. The two best methods at present are based upon
the biological markers, nicotine and its metabolite, cotinine,
which are present in the saliva, plasma, and urine of active and
passive smokers, and upon atmospheric markers such as nicotine in
the vapor phase and RSP from the particulate phase of ETS, the
latter of which has been used in many field studies because of the
substantial emission of RSP from tobacco combustion. In US, ETS
f-s generated by 50 million smokers, who smoke the equivalent
(including pipes and cigars) of 610 billion cigarettes annually.
Although the number of smokers has been declining, the percentage
of heavy smokers has been increasing. There are models in use,
based on the massmbalance equation, and validated both under
laboratory and limited field conditions, which can predict the
concentrations of RSP from ETS to a reasonable degree of accuracy.
Application of such models, together with field studies of RSP
concentrations and sociological studies, has suggested that
exposure to ETS is very widespread in the population. Environmental
tobacco smoke is not readily controlled by either ventilation or
air cleaning. Field studies of RSP in buildings where smoking
occurs suggest that RSP from ETS contributes 80 to 90 percent of
the particulate load during the period of smoking, and that it
persists for long periods after smoking ends at typical building
air exchange rates, thus prolonging nonsmokers' exposures.
Available data suggest the workplace as a significant site of
exposure to ETS.
F. Integrated exposure analysis
Exposure to ETS can be quantified either by atmospheric or
biological markers. Of the latter, expired carbon monoxide,
carboxyhemoglobin, plasma thiocyanate, plasma, urinary or salivary
nicotine, and plasma, urinary, or salivary cotinine have been used
to evaluate exposure to ETS. However, successful attempts to
quantify the degree of exposure have been limited largely to
measurements of nicotine and cotinine. Urinary nicotine is a
sensitive indicator of recent ETS exposure, while cotinine appears
to be the short-term marker of choice for epidemiologic studies.
Nicotine and cotinine are the best markers currently available.
125
Draft - Do not cite or quote
Levels in body fluids may be elevated 10 or more times in the most
heavily exposed groups compared with the least exposed groups. Mean
levels of urinary nicotine and cotinine in body fluids increase
with an increasing self-reported ETS exposure and with an
increasing number of cigarettes smoked per day by active smokers.
(SG, 1986) Coghlin, Hammond, and Gann (1989), in assessing current
weekly ETS exposure in 53 nonsmoking volunteers by personal
nicotine monitors, diaries, and questionnaires, found that the best
predictor of total nicotine exposure was given by the formula hsp:
the number of hours of exposure (h), times the number of smokers
(s), times the proximity of those smokers (p), accounting for 83%
of total exposure. A significant finding was that exposures derived
from social situations (e.g. restaurants, bingo games, bars, and
bowling alleys) (which are workplaces for some persons) may
contribute significantly (34%) to total exposure.
Nicotine is found in measurable concentrations in the saliva and
urine of most urban nonsmokers, and is present in higher
concentrations in those with some recent exposure. Estimating the
magnitude of the passive smoking dose is difficult, and it is of
doubtful validity to extrapolate from the uptake of one marker to
another. Over a period when one cigarette equivalent of carbon
monoxide is absorbed, the dose of nicotine appears to be only
between 1/10 and 1/3 of a cigarette equivalent. Similarly, under
extreme conditions of indoor pollution, it has been calculated that
a nonsmoker would inhale volatile nitrosamines equivalent to 10
nonfilter cigarettes or 35 filter cigarettes. (Hoffmann, IARC, 1987)
The average concentration of cotinine in the blood of habitual
smokers is about 300 ng/ml, and is calculated to represent the
consumption of about 36 mg of nicotine per day. On this basis, and
on the assumption that formation of cotinine from nicotine and
clearance from the body does not differ substantially from smokers
to nonsmokers, present data suggest that average urban nonsmokers
(in the UK) take in 0.2 mg of nicotine per day. (IARC, 1987) [.2 mg
represents .6% of the smokers' dose] The highest plasma cotinine
concentration observed in a nonsmoker corresponds to an approximate
maximum dose of 2.5 mg of nicotine per day, 10 times higher, and
7% of the average smoker's dose. Recent studies of salivary
cotinine in schoolchildren in the UK showed, in the case where both
parents smoked, average concentrations just over 1% of the levels
seen in heavy cigarette smokers.(IARC, 1987)
Although the ratio of nicotine to other tobacco smoke
constituents differs in MS and SS smoke, nicotine uptake may still
be a valid marker for total ETS exposure. Nicotine uptake in
nonsmokers has been estimated in terms of cigarette equivalents
from various studies to vary between 1/6 to 1/3 of a cigarette per
day. The NRC reports various estimates of cigarette equivalents
based upon cotinine in nonsmokers ranging from 0.1 to 1 cigarette
per day, and utilizes a ratio of urinary cotinine in ETS-exposed
nonsmokers (25.2 ng/ml) to that in active smokers (1826 ng/ml)
126
Draft - Do not cite or quote
yielding a 1.4% result.(NRC, 1986) [Assuming a usage of 32
cigarettes per day by habitual smokers based upon cigarette sales
(Repace and Lowrey, 1980), this yields 57 ng/ml/cigarette, or 0.44
cigarette equivalents per day. Adjusting this by multiplying by
the ratio of cotinine clearance in nonsmokers to that in smokers
reported in one study, 49.7 hrs/18.5 hrs = 2.67, yields a higher
value, 1.1 cigarette equivalents per day or 3.6% of the smokers'
dose.] In summary, based upon the limited studies (none of which
are a probability sample of US nonsmokers) of cotinine in body
fluids of nonsmokers (see Table 5), nonsmokers appear to have of
the order of 1% of the nicotine uptake of smokers. However, these
estimates must be interpreted with caution; relative absorption of
nicotine in smokers and nonsmokers may substantially underestimate
exposure to other components of ETS. (SG,1986)
Alternatively, human exposure to ETS can be estimated using
approaches similar to those used for other airborne pollutants.
Measures of exposure to individual atmospheric smoke constituents
can be used as estimates of whole smoke exposure. The accuracy of
this approach amy be limited by changes in the composition of ETS
with time and conditions of exposureo Although lacking specificity
Eor tobacco smoke, the prevalence and number of smokers correlates
well with RSP levels in homes and other enclosed areas. In the
Harvard study of indoor air pollution in 6 cities, Spengler et al.
and Sexton et al. demonstrated by the personal monitoring of RSP
and the use of time-activity questionnaires that exposures to ETS
at home and at work are significant contributors to personal
exposures. In general, measurements in a large number of locations
using measures of smoke generation such as the number of people
szioking or the number of cigarettes being smoked have shown a
definite relationship of smoke generation to particulate levels.
In US homes, there are few other sources of RSP, and therefore, the
relationships of RSP measurements to ETS are quite accurate.(SG,
1986)
Repace and Lowrey (1980) measured RSP concentration using a
piezobalance in severa.l public and private locations, in both the
presence and absence of smoking. They then developed an empirical
model utilizing the mass balance equation (Eq.2). Using both
measured and estimated parameters as input to the model, they
validated the model for predicting an individual's exposure to
ETS.(SG, 1986) Kuller et al (1986) in a review of estimates of the
nonsmoking population's exposure to ETS, observed that cigarette
smoking is probably the single most important source of indoor RSP;
that a higher percentage of nonsmokers appear to be exposed out of
the home, usually at work (Friedman, 1983); and that modeling of
RSP has estimated that the average exposure of the nonsmoking adult
population to tars from ETS was 1.43 mg/day, varying from 0 to 14
mg (Repace and Lowrey, 1985). Kuller et al. (1986) in reviewing the
latter estimate, observed that the ratio of average exposure in
passive smoking to that 'in active smoking, was about 0. 3%. This
translates into 3% of the smoker' exposure for the most-exposed
127
Draft - Do not cite or quote
passive smokers, reasonably consistent with estimates based on
doses from nicotine and cotinine, above.
Table 6 gives estimates of the probability-weighted exposures
to ETS for US nonsmoking adults at home and at work, the two most-
frequented microevironments.(Repace and Lowrey, 1985) Table 6 is
derived from RSP concentration modeling based upon Eq.'s 2-5, and
from assessments of exposure probability based on a limited
national survey of top management and health officials concerning
prevalence of smoking in the workplace in 3000 US corporations,
large, medium, and small (29% response), and a national probability
sample of the prevalence of smoking in homes with children (used
as a surrogate for all homes). Exposure probabilities were a
weighted average taken over the number of workers in white-collar
and blue-collar occupations, and including the different exposure
probabilities for white and blue collar workers. Air exchange rates
and building occupancies were taken from ASHRAE Standard
ventilation rate tables for white-collar workplaces (which were
used as surrogates for blue-collar workplaces).
_ Table 6 estimates average the workplace ETS exposure probability
at 63%, and the average estimated domestic ETS exposure probability
at 62%, where the focus was on estimation of ETS exposures in the
1950's to mid-1970's, since these exposures were held to be of
primary significance for the studies of passive smoking and lung
cancer, given the long latency for lung cancer. Comparison of
these exposure probability estimates to adult life ETS exposure
histories taken by Kabat and Wynder (1986) for 215 60-yr old female
nonsmokers, 65% at home and 67% at work, shows good agreement.
Table,6 estimates a 0.45 mg/day RSP exposure for nonsmokers at
home, (weighted for male and female time-activity pattern
differences, and for respiration rate) corresponding to a 19 ug/m3
24-hr average, in good agreement with results (19 ug/m3 per smoker)
published in the 6-City study.(Repace and Lowrey, 1985) Table 6
also estimates a 1.82 mg/day RSP exposure for workers, (again
weighted for male-female time-activity patterns and for respiration
rate) corresponding to about a 230 ug/m3 workplace concentration,
using ASHRAE Standard 62-73 for workplace occupancy and performing
a weighted average workday for the different hours worked by men
and women (Repace and Lowrey, 1985). This is in good agreement
with the weighted average concentrations (262 ug/m3) reported for
ETS in public access buildings.
Riboli et al. (1990) in a 10-country collaborative study of
exposure of nonsmoking women to ETS, examined the relationship
between smoking by spouse and urinary cotinine levels as an
indicator of exposure to ETS. Riboli et al.(1990) found that
cotinine values were significantly higher for women exposed to ETS
from the husband than from other sources; they also found that
questionairres in epidemiological studies based upon self-reports
of spousal smoking in fact identified a most-exposed population.
A clear increase in urinary cotinine levels was found from the
128
Draft - Do not cite or quote
women who were exposed neither at work or at home, to women who
were exposed both at work and at home, as suggested by the work of
Repace and Lowrey, above.
In summary, exposures to ETS can be assessed by personal air or
area contaminant monitoring, modeling of exposures, or by
biological markers of ETS contaminants in body fluids. Using
either the biological markers such as cotinine or the atmospheric
markers such as RSP produces a consistent assessment of ETS
exposure, i.e., of the order of 1% of that in smokers. The most-
exposed individuals appear to have levels about ten times higher.
Based upon limited data, the typical nonsmoker appears to carry a
daily body burden of about 0.2 milligrams (mg) of nicotine. The
cotinine-based estimates have the advantage that they reflect
actual dose of an ETS constituent. They have the disadvantage that
they do not reflect a wide distribution of target populations, are
based mostly on UK ETS exposures, and may substantially
underestimate exposures to other constituents of ETS. The RSP-
based estimates have the advantage that they are model-based, can
be used to estimate exposures in a variety of microenvironments,
represent the great bulk of ETS carcinogens, and can be compared
with atmospheric measurements of RSP. They have the disadvantage
that they do not represent whole smoke exposure, and do not reflect
absorbed dose. The greatest source of uncertainty is that neither
cotinine nor RSP measurements are based on a national probability
sample, and on an absolute scale, represent a limited amount of
data. Nevertheless, the NRC(1986), the SG(1986), and IARC(1987)
have found this data base acceptable for exposure assessment
purposes. Estimates of the adult nonsmoking population's exposure
to RSP from ETS suggest that the range of exposure is from 0 to 14
mg per day, with the population average put at 1.5 mg per day,
where the peak-to-mean ratio is about a factor of 10, consistent
with the biomarker-based findings.
Summary
1. Nonsmokers' exposures may be assessed by mathematical modeling,
as well as by biomarkers such as nicotine or cotinine in body
fluids or atmospheric indicators such as nicotine or RSP.
2. Despite limitations of the data base, mathematical models,
biological and atmospheric markers have produced: reasonably
consistent assessments of nonsmokers' ETS exposure.
3. Exposure to environmental tobacco smoke is inadequately
controlled by ventilation, air cleaning, spacial separation within
a space, or on the same ventilation system.
4. Data indicate that ETS is a significant indoor pollutant of
buildings, typically representing 80 to 90% of particulate indoor
air pollution during smoking, and that nearly all nonsmokers carry
a significant burden of tobacco combustion products in their body
129
Draft - Do not cite or quote
fluids.
130
Draft - Do not cite or quote
References
Bonham, G; Wilson, RW (1981). Children's health in families with
cigarette smokers. Amer. J. Public Health 71: 290-293.
Coghlin J, SK Hammond, PH Gann. "Development of epidemiologic tools
for measuring environmental tobacco smoke exposure." Amer. J.
Epidemiol. 130: 606m704 (1989).
Coultas DB, JM Samet, JF McCarthy, JD Spengler. "A personal
monitoring study to assess workplace exposure to environmental
tobacco smoke." AJPH 80: 988-990 (1990).
Cummings KM, SJ Markello, MC Mahoney, JR Marshall. "Measurement of
lifetime exposure to passive smoke.1° Am. J. Epidemiol. 130: 122-
132 (1989).
Cummings KM, M Mahoney, AK Bhargava, PD McElroy, JR Marshall.
"Measurement of current exposure to environmental tobacco smoke."
Arch. Env. Health 45:74-79.
Pirst; MW (1984). Environmental tobacco smoke measurement:
retrospect and prospect. Eur. J.Respir. Dis. 5(Suppl.):9-16.
Garfinkel, L (1981). Time trends in lung cancer mortality and a
note on passive smoking. J. Natl. Cancer Inst. 66:1061-1066
Greenburg, RA; Haley, NJ; Etzel, RA; Loda, FA. Measuring the
exposure of infants to tobacco smoke: Nicotine and cotinine in
urine and saliva. New England J. Med. 310: 1075-1078.
Grot, RA, & Clark, RE (1986). 178-194. Measured air infiltration
and ventilation rates in 8 large office buildings. ASTM Spec. Pub.
904, Ed. H. Trechsel & P. Lagus, ASTM, Philadelphia 151-183.
Haley, NJ; Colosimo, SG; Axeirad, CN; Harris, R; Sepkovic, DW.
Biochemical validation of self-reported exposure to environmental
tobacco smoke. Environmental Research 49:127-135 (1989).
Hammond, SK; Leaderer, BP; & Roche, A. (1987). Collection and
analysis of nicotine as a marker for environmental tobacco smoke
in personal samples.. Atmos. Env.
Hammond SK, TJ Smith, SR Woskie, BP Leaderer, & N Bettinger.
"Markers of exposure to diesel exhaust and cigarette smoke in
railroad workers. Am. Ind. Hyg. Assoc. J. 49:516-522 (1988).
Jarvis, MJ; Russell, MAH; Feyerabend, C; Eiser, JR; Morgan, M; et
al (1985). Passive exposure to tobacco smoke: saliva cotinine
concentrations in a representative population sample of nonsmoking
school children. Br. Med. J. 291: 927-929.
131
Draft - Do not cite or quote
Leaderer, BP; Cain, WS; Isseroff, G; Bergiund, LG. (1984).
Ventilation requirements in buildings. II Particulate matter and
carbon monoxide from cigarette smoking. Atmos. Environ. 18: 99-106.
Leaderer B, Koutrakis P, Briggs S, Rizzuto J. Impact of indoor
sources on residential aerosol concentrations. Proc 5th Int Conf
on Indoor Air Quality & Climate, V 2, 269-274. Toronto 29 July- 3
August 1990.
Leaderer, BP (1990). Risk Analysis 10: 19-26 (1990).
Leaderer, BP, and Hammond, SK. "An evaluation of vapor-phase
nicotine and respirable suspended particle mass as markers for
environmental tobacco smoke." Environmental Science & Technology,
in press.
Lofroth G, Burton RM, Forehand L, Hammond SK, Sella RL, Zweidinger
RB, and Lewtas J. Environ. Sci. Tech. 23: 610-614 (1989) .
Matsukura S., et al. Effects of environmental tobacco smoke on
urinary cotinine excretion in nonsmokers -- evidence for passive
smoking. New England J. Med. 311: 828-832 (1984).
Miesner EA, Rudnick SN, Preller L, Nelson W. Particulate and
nicotine sampling in public facilities and offices. JAPCA 39:
1577-1582 (1989).
National Research Council (1986). Environmental tobacco smoke --
measuring exposures and assessing health effects. National Academy
Press, Washington, DC.
,
Office on Smoking and Health (1988). Estimates of the mortality
from smoking. Centers for Disease Control, Washington, DC.
Ott, WR. Human activity patterns: A review of the literature for
estimation of exposure to air pollution. U.S. Environmental
Protection Agency, Washington, DC.
Pritchard et al. (1990).
Repace, JL (1989a) Smoking in the workplace: Ventilation. Smoking
Policy Questions and Answers, #5, National Cancer Institute,
Bethesda, MD.
Repace, JL (1989b) Protecting workers from the threat of secondary
smoke. Indoor Pollution Law Report, Cadwallader, Wickersham, &
Taft, Leader Publications, Washington, DC.
Repace, JL, and Lowrey, AH (1980). Indoor air pollution, tobacco
smoke, and public health. Science 208: 464-472.
Repace, JL, and Lowrey, AH (1982). Tobacco smoke, ventilation, and
132
Draft - Do not cite or quote
indoor air quality. ASHRAE Trans. 88: 894-914.
Repace, JL, and Lowrey, AH (1985). A quantitative estimate of
nonsmokers' lung cancer risk from passive smoking. Environment
International 11: 3-22.
Repace, JL, and Lowrey, AH (1990). Rebuttal to Lee/Katzenztein
commentary on passive smoking. Environment International, in
press.
Riboli E, Preston-Martin S, Saracci R, Haley NJ, Trichopoulos D,
Becher H, Burch JD, Fontham ETH, Gao YT, Jindal SK, Koo LC,
LeMarchand L, Segnan N, Shimizu H, Stanta G, Wu-Williams AH, and
Zatonski W. Exposure of nonsmoking women to environmental tobacco
smoke, a ten-country collaborative study. Cancer Causes and
Control, 10 243-252 (1990).
Rickert, WS; Robinson, JC; Collishaw, NE (1987). A study of the
growth and decay of cigarette smoke NOx in ambient air under
controlled conditions. Environ. Internat. 13: 399-408.
F2ickert, WS; and Labstat, Inc. (1988). Some considerations when
estimating exposure to ETS with particular reference to the home
environment. Canadian J. Publ.Health 79:S33-S37.
Sexton, K; Spengler, JD; Trietman, RD (1984). Personal exposure
to respirable particulates: a case-study in Waterbury, Vermonta
Atmos. Environ. 18: 1385-1398.
Surgeon General (1986). The Health Consequences of involuntary
smoking. U.S. Dept. of Health & Human Services, WAshington, DC.
Spengler, JD; Treitman, RD; Tosteson TD; Mage DT; and Soczek ML
(1985). Personal exposures to respirable particulates and
implications for air pollution epidemiology. Environ. Sci. &
Tec_~nol. 19:700-707.
Stillman FA, DM Becker, RT Swank, et al. "Ending smoking at the
Johns Hopkins medical institutions: an evaluation of smoking
prevalence and indoor air pollution. JAMA (1990), in press.
Tobacco Institute (1987). Tobacco industry profile, 1987.
Washington, DC.
U.S. Department of Transportation. U.S.. Department of
Transportation Study of Airliner Cabin Air Quality (1990).
U.S. Environmental Protection Agency, Indoor Air Facts #5,
Environmental Tobacco Smoke, Washington, DC, 1989.
Vaughn WM & SK Hammond. "Impact of 'Designated Smoking Area' Policy
on Nicotine vapor and particle concentrations in a modern office
~
.~
133 ~
~
~
~
~
~
Draft - Do not cite or quote
building. J.Air Waste Management Assoc. 40: 1012-1017 (1990)
Wald, NJ; Nanchanai, K; Thompson, SG; Cuckle, HS (1986). British
Med J. 293:1217-1222.
Wallace LA. "Major sources of benzene exposure." Environ. Health
Persp. 82: 165-169 (1989).
Williams DC, Whitaker JR, Jennings WG. Measurement of nicotine in
building air as an indicator of tobacco smoke levels. Environ
Health Persp 60:405-410 (1985)
134
Draft - Do not cite or quote
FIGURES AND TABLES FOR CHAPTER 6
~
~
.h
~
135 ~
~
TABLE 1 (NRC, 1986) Draft - Do not cite or quote
Study
Particulate Levels Measured in Indoor Environments, Including Smoking and Nonsmoking Occupancy
Type of
Premise
Concentrations
Volume. Ventilation Monitoring Mean (range),
Occupancy m3 Type/Rate Type/Time µg/m3
Comments
Brunekreef and 4 residences NS N/- G/2 mo 55(20-90) TSP, repeat measures
Boleij. 1982 0.2 mg
7 residences S = 1 N/- G/2 mo 125 (60-250) TSP sensitivity
14 residences S = 2 N/- G/2 mo 152 (60-340) TSP sensitivity
1 residence S = 3 N/- G/2 mo 335 (-) TSP sensitivity
Outdoors - - G/2 mo - (41-73)
Cuddeback 2 taverns S = 5-40 - N,M/1-6 ach G/9 h 446 (233-986) TSP ventilation
et al.. 1976 NS = 5-260 estimated
T = 10-300
Elliot and 3 arenas NS G/24 h 55(42-92) TSP
Rowe, 1975 3 arenas S M/- G/0.3 h 350(148-620) TSP
T = 2,000-
14,277
First, 1984 1 school
8 public NS
S M/-
N,M/- P/-
P/- 20 (-)
260 (40-660) TSP
TSP
HawtNrorne buildings
I1 residences
NS
150-674
M/0.18-0.96
QCMI/5-15 min
9-40 (-)
RSP, winter/summer-
et al.,
1984
8 residences
NS
150-674
M/0.26-1.98 (over 6 h)
QCMI/5-15 min
12-46 no sources
RSP, winter/summer-
2 residences
S
150-674
M/0.27-1.47 (over 6 h)
QCMI/5-15 min
96-106 sources'
RSP, winter/summer-
Leaderer
3 public
NS
163-1,326
M/0.37-5.6d (over 6 h)
G/4-21 h
17.8 (9.1-32.2) sources` + cig.
TSP, repeat measures,
et al..
personal buildings
7 public
1.7-4.57b
168-600
M/0.77-7.53d
G/2-24 h
z05.1 (58-452) all var.
Measured
communi buildings T = 2-6 (160.0 peak)
cation
Moschandreas
Outdoors
G/24 h
17.0 (-)
RSP, TSP also
et al.. 1981 measured
2 offices G/24 h 16.8-20.2 RSP, TSP also
5 residences
NS
-
N/0.5-1.3 ach
G/24 h (53 peak)
19.4-4.01 measured
RSP, TSP also
T = 2-6 (118.9 peak) measured
S residences S - N/0.5-1.3 ach G/24 h 36.9-99.9 RSP, TSP also
Nitschke
Outdoors
-
-
-
G/168 h
11.3 ± 6.0 (1-28) measured
RSP
et al.. 1985 19 residences NS 315-1,021 N/- G/168 h 26.0 ± 22.6 (6-88) RSP, repeat measures,
11 residences
S
290-800
N/-
G/168 h
59.2 ± 38.8(10-144) source mix"
RSP, repcat meatiures,
source mix'
Draft - Do not cite or quote
TaBL;: 1, contd.(NRC, 1986)
Continued
Study
Type of
Premise
Volume.
Occupancy m3
Ventilation
Type/Rate
Monitoring
Type/Time Concentrations
Mean (range).
µg/m3
Comments
Parker et al., I residence NS - N/0.2-1.9 ach 0/24 h <10(-) TSP
1984 T=3
2 residences S = 1-2 - N/0.2-0.7 ach 0/24 h 10-46 (-) TSP
T = 3-4
Repace and
Lowrey, Outdoots - P/2 min 42.9 (22-63) RSP, average of
2-min samples
1980,1982 27 Public 0.13-3.54j - M/- P/2 min 278 (86-1,140) RSP, average of
les
2-min sam
buildings p
Sexton et al., Outdoors G/24 h 17.0 t 1.6 (6-23) RSP, repeat samples
1984 19 homes
24 residences NS' N /- G/24 h 25.0 ± 1.0 (13-63) Used fireplaces
Spengler Outdoors - G/24 h 21.1 ± 11.9 (-) RSP, repeat measures
et al., 1981 35 residences NS N/- G/24 h 24.1 ± 11.6 (-) RSP, repeat measures
15 residences S = 1 N/- G/24 h 36.5 ± 14.5 (-) RSP, repeat measures
5 residences S = 2 N/- G/24 h 70.4 ± 42.9 (-) RSP, repeat measures
Spengler Outdoors - N/- G/24 h 18 ± 2.1 (-) RSP, repeat measures
et al., 1985 73 residences rNS°' G/24 h 28 ± 1.1 (-) RSP, repeat measures
28 residences S G/24 h 74 ± 6.6 (-) RSP, repeat measures
Sterling and I office S restr. G('?)/- 25.5 (15-36) TSP
Sterling, 1983 22 ofirices S G('?)/- 31.7 (-) TSP
U.S. Department 8 domestic S - M!- G/1-1/4, Not given (-) TSP
of Transpor- planes T = 27-110 2-1/2 h
tation, 1971 20 military S - M/- G/6-7 h < 10-120 (-) TSP
plancs T = 165-219
H'ebe? and 44 offices S - N,M/- P/2 min 133 ± 130 RSP, minus
Fischer, 1980 - (30 ea) (962 peak) background level
"Active smo~cers per 100 m3.
hGrams of tobacco consumed.
`Some smoking was reported during 9 of the 280 samples.
dMeasured during 24-h periods by the perfluorocarbon tracer tech-
nique.
`Some-Fesidences had combinations of sources (kerosene heaters,
wood stoves, etc.) and no cigarettes.
JActive smokers density per 100 ml.
ABBREVIATIONS:
ach = Air changes per hour
G = Gravimetric
M = Mechanical ventilation
N = Natural ventilation
NS = No smokers
0 = Optical monitor
P = Piezoelectric balance
QCMI = Quality Crystal Microbalance Cosade Impactor
RSP = Respirable suspended particles
S = Smokers
T = Tota4 occupants
TSP = Total susPenoyed particles
restr. = building wfth snwking restrictions
S
Table 2. Number of persons 17 years and over, by
United States, 1980. LNational Center for Health
Present Smokers Former Smokers
Regular
Regular
Regular
Regul
Regular All
Total All and/or smoker
and/or smoker Never occasional
Race Sex and A e Po ulation Smoker Occasional
onl
cca
sional onl smoked smoked
All races Num bers in Thousands
Both Sexes 17 yrs. 160798 86611 52442 51770 33130 30731 74086 3486
17-24 years 32176 13286 10069 9827 3009 2632 18890 652
25-44 years 61042 35258 22916' 22656 11985 11167 28754 1269
45-64 years 43556 27170 15336 15236 11474 10541 16330 1144
65 years & over 24024 10896 4121 4050 6664 6341 13112 421
Male > 17 years 75970 49048 27751 27445 20672 19297 26906 1994
17-24 years 15699 6640 5018 4866 1504 1303 9039 405
25-44 years 23549 19696 , .-'12591 12503 6886 6393 9837 692
45-64 years 20830 16238 8402 .8357 7612 7113 4593 645
65 year & over 9891 6473 1760 1718 4670 4488 3413 253
Female> 17 years 84828 37563 24690 24325 12452 11434 47180 1492
17-24 years 16477 6646 5051 4961 1504 1379 9832 248
25-44 years 22725 15562 10345 10152 5099 4774 15917 577
45-64 years 31472 10933 6933 6880 3862 3423 11737 499
65 years & over 14133 4423 2361 2333 1993 1853 9694 168
White> 17yrs. 139036 76041 45090 44515 30197 27976 62910 3045
17-24 years 2709.5 11525 8582 8400 2758 2463 15569 566
25-64 years 51889 30336 19723 19211 10728 9955 21471 1063 d
45-64 years 38470 24160 13383 13284 10480 9622 14269 1036 11
a
65 years & over 21635 10019 3676 3619 6231 5935 11600 380 fh
Male 65941 43124 23654 23435 19025 17732 22802 1735 rt
Female 73095 32917 21416 21079 11171 10244 40108 1310 1
Black> 17yrs. 16767 8314 5903 5831 2209 2045 8439 350 d
17-24 years 4094 1451 1264 1226 158 142 2643 * 56 0
25-44 years 6584 3656 2657 2624 874 829 2928 159 ~
45-64 years
4071
2471
1636
1636
785
711
1586 0
*108 rt
65 years & over 2018 736 346 346 391 369 1282 * 26 O
Male 7465 4512 3136 3078 1258 1192 2953 184 N
Female 9302 3802 2767 2753 950 853 5486 166
136
cigarett~ smoking
Comm.)
status, race, sex, and age:
~
LL 15ZZO~OZ °
ro
Draft - Do not cite or quote_
TABLE 3. (Repace and Lowrey, 1985)
Time spent in various rnicroenvironments by persons
in 44 C.'.S. cities, expressed in average hours per day.
(Ott, in press: NRC, 1981: Szala~. 1972).
Microenvironment Employed
Men,
AJI Days Employed
Women,
All Days Married
Housewives.
All Days
Inside one's home 13.4 15.4 20.5
Just outside one's home 0.2 0.0 0.1
At one's workplacet. 6.7 5.2 ®
In transit 1.6 1.3 1.0
In other people's homes 0.5 0.7 0.8
In places of business 0.7 0.9 1.1
In restaurants and bars 0.4 0.2 0.I
In all other locations 0.5 0.3 0.3
Total 24.0 24.0 24.0
Draft - Do not cite or quote_
TABLE 4. CoTININE IN NONSMOKERS FROM DOrESTIC AND NONDOMESTIC
EXPOSURES.(NRC, 198 6) 991% of the ETS exposure of the nonsmoking
husbands of smoking wives came from non-domestic sources compared
to 71% of the exposure of the nonsmoking husbands of smoking
wivest.. The most probable non-domestic source of exposure is the
workplace. -.
-----------------------------------------------------------------
Urinary Cotinine Concentration and Number of Reported
Hours of Exposure to Other People's Tobacco Smoke Within the Past 7
Days in Nonsmoking Married Men According to Smoking Habits of
Their W ives
Urinary Cotinine
W
ti
C Exposure to Other People's Smoke in
Preceding Week, h
Smoking
C
No.
f on.
o
centra
ng/ml
Total
Outside Home
ategory
of Wife o
Men Mean (SE) Median Mean (SE) Median Mean (SE) Median
Nonsmoker
Smoker 101
20 8.5(1.31'
25.2(14.8) 5.0
9.0 11.0(1.2)b
23.2(4.1) 6.5
21.1 2+?.0(1.2)`
i(3.4(3.3) 6.0
10.7
NOTE: Diffeiences (nonsmoking wife versus smoking wife): °p < 0.05; bp < 0.001;
`p < 0.06 (Wilcoxin rank sum test).
SOURCE: Wald and Ritchie (1984).
0
.~
.-1
N
...
a
~
~
_.a
0
00
3
~
i
I
111111111
1
1 I 1 1 1 1 1 1 I I 1
~~ x Z-
.~ ~~
2040225180
4
o ~ o w
. °
f
~
r
o~ha ..~ooa
1 1 1 1 1 1 1 1 I
1 1 1 1 1 I I 1 1
vvv,l4dAnn
~
2040225181
Draft - Do not cite or quote _
TABLE 6. Estimated average nonsmokers' exposures to RSP from
ETS at ho>!e and at work. (Repace and Lowrey, 1985) The
concentrations are calculated for model home and workplace
mic2'o* environments and are weighted by average respiration rates
and time budget-studies for percent ®f time spent at home and at
work by male and female nonsmokerso The typical nonsmoker is
estimated to be exposed to fros 0 to '14 mg of RSP from ETS per
day, with an average exposure of 1.5 mg/day.
-------------------------------- t--------------------------------
Lifestyle:
Daily Average P`tobability of Being Exposed
(Rounded Values)
Modeled
Daily Average Exposure (mg)
Daily
Probability Weighteg
At work and ai home: °'® 63 x 62 = 39 2.27 0.89
Ne4ther at work nor at home: 07s 37 x 38 =14 0.00 0,00
At home but not at work: r® 62 x 37 = 23 0.45 0.10
At work but not at home: ro 63 x38=24 1.82 0.44
_~...
Totai: we 100 1,43
The average nonexciusive probability of a nonsmoker being exposed
to ETS at work is estimated as 63%; the probability of not being
exposed at work is 37%; the nonexclusive probability of being
exposed to ETS at home is estimated as 62%; the probability of
not being exposed at home is 38%.
-----------------------------------------------------------------
Draft - Do not cite or quote
FIGtTRE 1 EPA's TEAM Study demonstrates that smoking provides the
dominant source of RSP in many buildings (Sheldon, et al, 1986)
------------------------------------- -----------------------------
3E:
Nine Smoxers
...
t r I
~
~ I
{
~
.-
- ~
=20J- ~
~
~
Q
A ..
~
.
~
~
12C 'hree Smokers ~ ~
ad ~
df1 e__. __.
i
M
i
/
t
C
ean
onCen
rat
on
~/ i n nonSTOki n9 area
S:OC PM / 5:30 6:00 6:30
-.}!E
N
0
~
Reso:ra:.e :ar..:~:a:es .. ?r: .oor .. ^s~e :f :~e e:ce-. Q
hone-: (3'. BJ`. N
N
t)'i
No Smokers i
00
W
Draft - Do not cite or quote
FIGURE 2 Air exchange rates in homes are one determinant of
nonsmokers' exposures to ETS. Low air exchange rates mean higher
exposures. Shown is a histogram of infiltration values in a
sample of 266 older US middle class homes around the country.
Average heating season values are shown. The median of the
distribution is 0.9 ach and the mean is 10 1± 0.9 ach. (Grot and
Clark, '1979) (NRC, 1986) _
-----------------------®-®-------------------------------------®-
ALL 14 CITIES
40
H No. OF NOUSES = 286
No. OF RfAOWS = 1048
0 30 Q=1.12 kRi
I t a = 0.86 NR ~
cc
66
20
~
I.- \
W ~
\
cc
'0
\
MEN
\\\
\
~\\\\\\ ~ ~ , ,
aa® 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 4.5
AIR EXCHANGE RATE (HR -
Figure 3. Histogram of measured natural air infiltration
rates for 14 veatherization sites
2040225185
¢
120
110
100
90
80
70
60
50
40
30
20
10
0
4 smokers
smokers
smokers
Nov. Dec. Jan. Feti Mar. Apr. May Jun. Jul. Aug. Sep. Oct. Nov. Dec. Jan. Feb. Mar. Apr.
1976 1977 1978
FIGURE 3. -- Comparison of predictions of RSP model for smoking
in single-family homes with field data (Spengler et al., 1981) for
monthly mean RSP concentrations for 55 homes in 6 Cities.
Theory (eq. 3)
= Indoor, 1 smoker
= Indoor, > 1 smoker
= Outdoor
= Indoor, no smokers
FIGtJI~ 4 The effect of smoking on ~~51ac~° 1~ ~Zevelsr ii °ae
Minneapolis office building. The contrast between daytime RSP
levels, when smoking occured, and night-time RSP levels, when it
did not, is marked.
300
~
so
2
~2
Oo
I
---------------------------------------------------------------
Aeresol mass concentration ,n a?00-m3 office with one smoker (Nalson et al . 1982! le
smoking #rqstrument and smoking rate were not specified. However, the air exchange rate tor
the space may be calculated by means of equation 2. For the decay of ETS on Thursday, July
9, a non-linear regression analysis of the RSP Peveis, with an 18 µg/m3 background level
subtraction, yields C, = 1.0 ach (r2 = 0.95). This value is close to the ASHRAE-recornmended
ventilation rate for office space.
~
I
~ I
I ~ I I ' ~ ' I
I ~ I
5®
0
WE ~~, ~
r 4"
0000
,200
?,A&V
TUE
0000
1200
i AAL s
WED
0000
1200
oJur
THU
0000
1200
10 Axr
FRI
0000
9200
/ 9 Jk r
SAT
Draft - Do not cite or quote
FIGURE 5?,ir exchange rates in commercial buildings are one
determinant of nonsmokers' exposures to ETS in the workplace.
Shown are air exchange rates (infiltration plus ventilation) in
eight..large federal office buildings in 8 US cities in 7 states.
Air exchange rates in the tighter bui-ldings failed to meet ASHRAE
standards for occupied office space, (20 cfm/occ or 0.84 ach).
The mean annual air exchange rate for all eight office buildings
is 0.71 ± 0.25 air changes per hour, about one third less than in
the sample of homes in fig. 2 . (Grot and Persily, 1986).
-----------------------------L-----------------------------------
Pittsfield
.Y
.-
FIG. 1-Location of the eight federal office buildings.
BUILDING DI?iF.NSIOxS (100 IK2 = 1000 ft2 )
Occupiable Fioor Volume, A.ir, exchanic
Le rate
Location Area, m2 mi ,
(ach)
Anchorage 45 500 174 000 ; 0.82 ± .35
Ann Arbor 4 900 31 700 1.04 + .69
Columbia 24 700 159 000 0.85 + .23
Fayetteville 3 400 21 300 0.37 + .09
Huron 6 420 2 7 500 0.32 + .16
Norfolk 17 300 60 300 0.79 + .19
Pittsfield 1 730 8 520 0.70 + .19
Springfield 13 500 5 7 700 0.79 + .18
Draft - Do not cite or quote
Figure 6. Indoor air pollution from ETS aerosol. Indoor levels
of respirable particles in buildings where tobacco is smoked (data
points (A-T)) greatly exceed those in which smoking is prohibited
(unlabeled), and exceed the levels for health-based U.S. ambient
air quality standards.
1200
i
1100
1000
800
NAAQS 24-H AV, SIGNIFICANT HARM LEVEL FOR TSP
900
~
v
3 700
~
~
~
c
d
~
0
400
NAAQS 24-H AV. AIR POLLUTION EMERGENCY LEVEL FOR TSP
a...-.-.-.-...e...-.-...-.-.-.-.-.-.-.-o....
T
®
SMOKER DENSITY ESTIMATED
0 MEASURED DATA
® CALCULATED EQUILIBRIUM LEVEL
B
eC
A
300
OG NAAQS 24-H PRIMARY LEVEL FOR TSP
_. H®.--6 -~------------------;,
200 1 J
100
K~a NAAQS 24H PRIMARY LEVEL FOR'(pM1p)
~'! ®.-.-.-.-<-.-.-.-._ -.-._...-.-.-.-.....-.
i : Li S
O o
`~R p Q
-~ 33 DATA POINTS
NAAQS ANNUAL ?RIMARY LEVEL FOR PM~~
i i i i 1
1.5 2.0 2.5 3.0 3.5
Active smoker density 000 x b,rrntna -taarettes ver m31
Draft - Do not cite or quote
~.C
~
~
Draft - Do not cite or quote
CHAPTER 8
DISCOMFORT ASSOCIATED WITH ENVIRONMENTAL TOBACCO SMOKE
William S. Cain PhD
John B. Pierce Laboratory and Yale University
New Haven, CT 06519
Introduction
The atmosphere inside buildings contains many
chemicals generated by the presence and activities of people.
People®s bodies give off small quantities of organic materials in
the breath and from the skin and alimentary tract. Although a
chemical analysis may reveal hundreds or even thousands of
materials, we usually perceive them in the aggregate as what we
call occupancy odor. We often notice it consciously when we enter
a hot, muggy room. Nevertheless, occupancy odor exists in occupied
spaces at essentially all other times, but remains at a low level
because of ventilation with outside air (Yaglou, Riley,and Coggins,
1936). When engineers and public health specialists began to study.
ventilation requirements for buildings quantitatively, they started
with the smell of occupancy (Cain, 1979). The fresh-air
requirements so derived exceeded those based on
metabolically-relevant gases (oxygen, carbon dioxide) several-fold.
In general, occupancy odor poses a mild challenge
to the.HVAC engineer. (HVAC refers to heating, ventilating, and
air-conditioning.) This odor constitutes the baseline case.
Anything else that people do in the space will increase ventilation
requirements. This would include cooking, painting, operating
machines (e.g., photocopier), woodworking, smoking, and so on. Of
these various activities, smoking has traditionally been the most
common. In a questionnaire study of odor problems in such spaces,
Leonardos and Kendall (1971) stated, "Tobacco smoke is by far the
most important odor contributor in enclosed space as indicated by
the consistent agreement of the panel [principally experts in
HVAC], and by their rankings. Also, it is considered a problem in
virtually all (11 of 14) of the enclosed spaces" (p. 101). Tobacco
smoke has accordingly received considerable attention historically
in studies of odor control via ventilation or filtration (e.g.,
Yaglou, 1955; Kerka and Humphreys, 1956; Weber, Jermini, and
Grandjean, 1976).
As he has with occupancy odor, the HVAC engineer
has confronted environmental tobacco smoke (ETS) via its sensory
characteristics, i.e., its odor and irritation, rather than via
its chemical or physical complexity. The chemical complexity of
ETS likely exceeds that of emissions from bodies and chemical
137
N)
0
.~i
0
N)
N
C)'I
1
~
0
Draft - Do not cite or quote
analysis of ETS-containing air has offered little of practical
significance regarding specific chemicals responsible for its odor
or irritation. Specification of the relevant chemicals might,
however, assist in the mitigation of offending characteristics
(National Research Council, 1986).
In what follows, we shall review how human beings
perceive ETS. We shall ask: How much ventilation air must be
introduced into a space in order to satisfy visitors to that space?
Will the amount of air required by smokers differ from that
required by nonsmokers? Does ETS-odor decay spontaneously after
smoking ceases? Do occupants accustomed to the environment impose
less stringent criteria for ventilation than visitors fresh from
a nonsmoking space? Does the odor and irritation of ETS come from
the smoke particles or from the vapors that accompany the
particles? Does filtration offer opportunities for control?
Ventilation Requirements Based on Responses of the 'Visitor'
A customary setting to explore how indoor
contaminants affect the senses is a climate-controlled
-environmental chamber with relatively inert surfaces, e.g.,
aluminum or stainless steel, and variable ventilation. Such a
model environment offers control over the physical and chemical
characteristics at the expense of what we may call ecological
realism, i.e., an everyday setting. For the study of occupancy
odor, human beings occupy the chamber in order to generate the odor
of interest. Judges may enter the chamber briefly or may place
their faces into a box fed with the atmosphere of the chamber. (In
so sampling the atmosphere, the judges essentially visit the
space.) The odor judgment may comprise a mark on an annotated
rating scale (e.g., 'no odor' to 'overpowering odor') or the choice
of a matching odor intensity. The latter judgment generally
entails the use of a device called an olfactometer that delivers
the vapor of some standard odorant, such as n-butyl alcohol
(1-butanol), at various concentrations. A matching odor has the
advantage of reproducibility from lab to lab.
Many modern investigations also obtain judgments of
acceptability in order to 'calibrate' intensity judgments.
Acceptability judgments address the question: How many people will
object to any given level of odor (or irritation)? The answer will
depend on individual differences in olfactory sensitivity and on
esthetic criteria. Whereas we can expect average intensity
judgments to remain constant through the decades for any fixed
stimulus, we can expect acceptability judgments to shift somewhat
with prevailing standards. Three or more decades ago, when
approximately half the adult population smoked and when
restrictions on smoking were relatively few, people seemed more
tolerant of tobacco smoke odor than today (see Cain,1979).
Figure 1 depicts how occupancy odor varied with
138
Draft - Do not cite or quote
ventilation rate per occupant under nonsmoking occupancy in a study
conducted in a 1200-ft 3 climate chamber (Cain, Leaderer, Isseroff,
Berglund, Huey, Lipsitt, and Perlman, 1983). Visitors made
judgments of air circulated through an outside sampling-box and
were therefore naive to the conditions of occupancy. The scale
refers to the concentration of 1-butanol matched to the occupancy
odor present after one hour of occupancy. Just as odor level
decreased with increases in ventilation rate, so also did
dissatisfaction, i.e., judgments that the odor was unacceptable.
The point of 20% dissatisfaction holds special interest.
The ventilation standard of the American Society of
Heating, Refrigerating, and Air-Conditioning Engineers (ASHRAE)
(1989) recommends a maximum of 20% dissatisfaction among visitors
to a space. By this criterion, the data from the investigation
imply the need for 17 cfm per occupant. The ASHRAE standard
suggests 15 cfm or more per occupant for most spaces, e.g., 15 cfm
for classrooms, libraries, auditoriums, dormitories; 20 cfm for
offices, conference rooms, dining rooms, lobbies; 25 cfm for
discos, beauty shops; 30 cfm for bars, casinos; 60 cfm for smoking
lounges (see Fig. 2). Hence, practice coincides with the
experimental data about as well as could be expected regarding the
baseline case.
When cigarettes were smoked in the climate chamber,
odor level increased markedly. Figure 3 displays ETS odor for
various conditions of smoking: intermittent (4 cig per hr) or
continuous (8 or 16 cig per hr). As Fig. 4 shows, the degree of
dissatisfaction mirrored the higher odor level. Based on the rule
of 20% maximum dissatisfaction, the ventilation rate required per
cigarette during active smoking exceeded 4,000 ft3. In order to
convert ventilation per cigarette into ventilation rate per person
for typical conditions of occupancy in a 'smoking-permitted' space,
it was assumed that 10% of occupants would be smoking at any given
time (see Repace and Lowrey, 1980). The resulting ventilation rate
equalled 53 cfm, three times that for nonsmoking occupancy. (The
average smoking rate will of course vary and the estimate of 10%
may be high for 1990. The assumption of a lower rate of smoking
would entail a proportional change in rate of ventilation.)
Does the higher ventilation rate for smoking imply
that the judges in the investigation showed a special aversion to
the odor of cigarettes? Apparently not. The judges, one-third of
whom were smokers and two-thirds of whom were not, seemed to base
their dissatisfaction strictly on odor intensity. Degree of
dissatisfaction varied with odor intensity in the same way for both
occupancy odor and tobacco smoke odor (Fig. 5)o Stronger odors
meant greater dissatisfaction irrespective of odor type.
How well does the higher rate implied by the
investigation compare with the ASHRAE standard? As indicated
above, the standard recommended 60 cfm per occupant in a smoking
139
lounge, where presumably most or all occupants w p~l°e smo~in~.~ote
If 100% rather than 10% were smoking simultaneously, then the rate
would need exceed an unachievable 500 cfm per occupant. If 50%
were smoking, perhaps a more realistic expectation, then the rate
would need to exceed a still unachievable 250 cfm per occupant.
(The maximum achievable rate for typical design occupancy in a
mechanically-ventilated space will usually equal about 60 cfm per
occupant, though as discussed below a generous allotment of space
per person can increase that value.) Fortunately, however, the
smoker seems less concerned about the odor of ETS than the
nonsmoker. As it turns out, smokers as a group seem satisfied with
about one quarter the ventilation air of a mixed group containing
a typical proportion of smokers and nonsmokers. Hence, a rate of
60 cfm per occupant may actually almost meet the customary ASHRAE
criterion of a maximum of 20% dissatisfaction.
How about nonsmokers? Just as a group of smokers
will hold a less stringent criterion than the mixed group, a group
of nonsmokers will hold a more stringent criterion. The data from
the investigation suggest that with 10% smoking at any given time,
nonsmokers would need over 100 cfm per occupant to hold
dissatisfaction at only 20% . At the present time, we do not know
whether the difference between smokers and nonsmokers derives from
=Olfactory sensitivity to ETS or to esthetic criteria.
Clausen (1986) confirmed differences in tolerance
of ETS odor between smokers and nonsmokers. For any given level
of odor (expressed as concentration of butanol), a group of
nonsmokers expressed much more dissatisfaction than smokers (Fig.
6). Both groups exhibited a lawful relation between odor intensity
and dissatisfaction, but the difference between the groups grew as
odor level increased. At the point where 20% of smokers expressed
dissatisfaction, almost half of nonsmokers did so.
As ETS enters the atmosphere, its many chemical
constituents react with each other and with surrounding materials
both chemically and physically. Does this behavior change the
nature of the contaminant over time? Yes and no. Irrespective of
whatever chemical changes occur, the odor of ETS behaves in the
short run like a stable contaminant. After the source has been
removed, ETS odor decays in a manner entirely predictable from
ventilation rate (Clausen, Fanger, Cain, and Leaderer, 1985). In
this respect, it differs from occupancy odor which has a half-life
of 55 min, presumably dictated by slow oxidation of its chemical
constituents into less odorous products (Clausen, Fanger, Cain, and
Leaderer, 1986). ETS odor offers no such easy benefit to the
engineer. Indeed, when ventilation fails -to eliminate the
contaminant entirely, ETS carries a penalty derived from its
physical interaction with surfaces. Because the ETS aerosol
adsorbs strongly to walls, fabrics, and so on, it becomes a source
of odor later. The background odor of the emitted products carries
its own demands for ventilation, predictable in part from the
140
Draft - Do not cite or quote
typical amount of smoking in a space (Clausen, Mcpller, Fanger,
Leaderer, and Dietz, 1986).
In a laboratory situation where other sources of
combustion can be eliminated, carbon monoxide can offer a gross
index of level of ETS. Figure 6 shows that Clausen could relate
dissatisfaction to concentration of carbon monoxide in ETS as well
as to matched level of butanol. This occurred because of a strong
correlation (r>0.90) between odor intensity and incremental carbon
monoxide due to smoking. Such a relationship makes it possible,
within limits imposed by brand-to-brand variability in emitted
carbon monoxide, to compare one study to another. We can ask, at
what concentration of carbon monoxide will ETS reach a given level
of dissatisfaction in one or another group? As Fig. 6 revealed,
the concentration at which 20% of nonsmokers expressed
dissatisfaction fell about eight times below that at which 20% of
smokers expressed dissatisfaction.
Responses of occupants
Up to this point, we have concerned ourselves only
with the reactions of visitors. Standards for ventilation have
tocused on the reactions of the visitor, rather than those of the
occupant, because the visitor will have a more sensitive, and hence
more critical, nose than the person adapted to the contaminant.
On the other hand, a focus on the visitor sidesteps another
important time-dependent sensory response of the occupant,
irritation. Whereas air containing an irritant may seem only
barely irritating at first, it may become intolerably so over time.
Figure 7 illustrates the time-course of eye
irritation experienced by occupants exposed to ETS at constant
concentrations of 2 or 5 ppm carbon monoxide, used here as a tracer
in the manner mentioned above (Cain, Tosun, See, and Leaderer,
1987). The lower concentration led to slight, though statistically
sighificant, irritation above pre-smoking baseline. The higher
concentration led to irritation that increased over time in sensory
magnitude and caused an increasing degree of dissatisfaction.
Whereas essentially none of the occupants found the irritation
objectionable at first, by the end of an hour about 30% found it
so. In an extension, Clausen, Nielsen, Sahin, and Fanger (1987)
found that an asymptotic level of 20% dissatisfaction would occur
at a concentration of 3.8 ppm carbon monoxide. A comparison with
the odor judgments of visitors in Fig. 6 reveals that only smokers
would find such a level tolerable by the '20% rule.' Clausen et
al. estimated that the ventilation rate necessary to control
irritation of occupants to a dissatisfaction of 20-% would equal
only one-tenth of that needed to control odor perceived by visitors
to the same level of dissatisfaction.
Although Clausen et al. did not argue in favor of
141
Draft - Do not cite or quote
lowering ventilation to meet only the dissatisfaction of occupants,
there could exist some temptation to do so (see Winneke, Plischke,
Roscovanu, and Schlipkoeter, 1984). Cain et al. (1987) cautioned
against the temptation to see irritation and odor in the same
light:
Apart from the issue of whether visitors or
occupants are more sensitive, there exists a question regarding
whether the '20% rule' should govern dissatisfaction based on
irritation just as it governs dissatisfaction based on odor alone.
Whereas odor may be interpretable narrowly on grounds of comfort,
irritation would seem interpretable on grounds of h e alt h.
Some people may find themselves quite neutral with respect to
one or another odor, but no one could plausibly argue neutrality
with respect to burning eyes. It could be argued, therefore,
that any consistent irritation above baseline should be deemed
unacceptable. [p.352]
Applicability of Chamber Studies
' The data presented above may raise two issues of
;concern: 1) Should chamber studies influence ventilation policy in
view of their remoteness from real-world circumstances? and 2)
Would small errors in the results lead to large differences in
recommended policies? The first issue has no simple answer. In
the real world, people engage in such a wide variety of activities
that any single field study, even assuming accurate execution,
would itself have very limited generality. Only a set of field
studies with a.variety of scenarios could even approach the
generality desired. Such field studies have not been done.
A group of subjects sitting in a chamber with no
task other than to focus attention on odors might seem likely to
behave very conservatively, i.e., to judge even weak odors
unacceptable, which would in turn imply the need for high
ventilation rates. We can neither confirm nor deny this tendency,
though circumstantial evidence runs against it. As already noted,
visitors in Cain et al.'s (1983) study found ETS odor no more
objectionable than occupancy odor at the same perceived intensity.
Could this just mean that subjects treat each odor equally
conservatively? Unlikely, since the recommended ventilation rates
for occupancy odor from that study converge with a great deal of
other lab and field evidence regarding the need for about 15 to 20
cfm of ventilation per occupant.
Even if the chamber experiment happened to encourage
conservatism, persons who choose to participate in it and hence
to expose themselves to potentially aversive environmental odors
may represent a less reactive fraction of the population. Persons
who find ETS odor aversive, for example, would seem unlikely to
accept such work. Concern about these matters might, however,
stimulate some productive research into the demographic factors
142
Draft - Do not cite or quote
that govern reactivity to indoor odors.
Chamber experiments on ETS can be criticized because
they have explored levels that largely exceed those of everyday
life. The tendency to explore high levels derives in part from a
desire to cover a wide range of cond4tions and in part from crude
estimates of levels of smoking in the countries and during the eras
when the experiments were performed. Even just ten years ago,
smoking in the U.S.A. occurred more commonly and at higher levels
than today. In countries such as Denmark, the location of some
recent studies, smoking occurs with a higher frequency and with
fewer restrictions than in the U.S.A.
Some recent field surveys have found surprisingly
low levels of ETS in common spaces, e.g., offices (Kirk, Hunter,
Back, Lester, and Perry, 1988; Oldaker, 1989). In order to
understand how to relate the chamber studies with such field data,
we need to factor in the ventilation rates in the field (see
Nystrom and Green, 1986, for a discussion of variables relevant to
the evaluation of ETS). Although a building code may specify a
ventilation rate of, say, 20 cfm per occupant, the actual
per-occupant rate will depend on the number of occupants actually
in the space. If a space typically contains only one-third the
design number of occupants, the ventilation rate will equal 60 cfm
per person. This situation occurs frequently since the design
occupancy listed in a standard commonly comes from fire regulations
regarding maximum density of occupancy. Accordingly, one cannot
argue, as has been done, that a putative low frequency of
complaints in field settings offers evidence against the
recommendations of chamber studies and in favor of lower
per-occupant rates. Field data, if collected in spaces occupied
well below design levels and if reported without actual
per-occupant ventilation rates, can give the illusion that rates
of ventilation suitable for occupancy odor can lead to adequate
control of ETS odor. When normalized to a per-cigarette
ventilation rate and hence when seen without assumptions regarding
occupancy, chamber studies have probably yielded quite valid data,
irrespective of the levels of smoking explored.
Regarding the second concern mentioned at the
beginning of this section, small errors in the estimate of
dissatisfaction could in fact lead to large errors in recommended
rate of ventilation since the relation between percent
dissatisfaction and ventilation rate for ETS has a rather low slope
(Fig. 4). Merely on general grounds, it would seem advisable to
replicate this relation with new participants in order to check its
stability and validity.
Alternatives to Ventilation
It might seem intuitively reasonable that the odor
of ETS should come from its vapor phase and the irritation from
143
Draft - Do not cite or quote
its particulate phase. At one time this seemed likely, but recent
investigations that have employed electrostatic air cleaning have
shown clearly that the gas phase accounts for the majority of odor
and irritation (cf. Hugod, 1984; Weber, 1984). Comparison of the
right and left sides of Fig. 7 will reveal that elimination of the
particulate phase had only a trivial effect on the eye irritation
caused ETS at 2 and 5 ppm carbon monoxide (Cain, Tosun, See, and
Leaderer, 1987). The same held true for judgments of odor and of
nose and throat irritation. Clausen, Nielsen, Sahin, and Fanger
(1987) confirmed these results. In finding that particles played
essentially no role in odor, both investigations also confirmed
Clausen et al.'s (1985) earlier experiments with visitors. Hence,
particle filtration holds no promise for immediate elimination of
the discomfort of ETS. The major advantage of such air cleaning
will derive from reduction of haze and collection of 'tar' that
would otherwise adsorb elsewhere in the space.
Although both the odor and irritation of ETS come
from the vapor phase, the chemical constituents that give rise to
the one probably do not give rise to the other. Undoubtedly, the
odor comes from a very large number of constituents. The sense of
smell will respond to almost all airborne organic materials present
:in sufficient concentration (Cain, 1988). For one substance,
however, a 'sufficient concentration' may fall a millionfold below
that of another. Furthermore, individual constituents will combine
perceptually in mixtures in complicated, nonlinear ways. Although
one or a few materials could in principle dominate the odor, it
seems unlikely.
Many fewer materials can cause irritation at the
concentrations present in ETS and its irritation could
realistically arise from a few or perhaps even one constituent.
Little is known about how irritants combine with each other
perceptually though it is known that odor and irritation interact
(Cain and Murphy, 1980). Irritation can suppress the perception
of odor and vice versa (Cain, See, and Tosun, 1986). In so far as
irritation may have a less complex origin than odor, it may offer
easier opportunities for control through filtration. As yet,
however, experiments on the origin of ETS have told more about what'
fails to cause irritation than about what causes it (Weber,
Jermini, and Grandjean, 1976; Weber-Tschopp, Fischer, and
Grandjean, 1977; Weber-Tschopp, Fischer, Gierer, and Grandjean,
.1977; Hugod, Hawkins, and Astrup, 1978).
The complexity of ETS more or less guarantees that
almost any means of air cleaning will eliminate part of it, even
though no simple procedure will eliminate all of it. Through the
use of air washing that presumably eliminated some water-soluble
constituents, Clausen, Moller, and Fanger (1987) achieved some
reduction in level of dissatisfaction though not in the perceived
intensity of ETS. The air-washed ETS smelled fresher. The results
offered little encouragement for the use air-washing alone, but
144
Draft - Do not cite or quote
showed that the odor character of ETS can play some role in degree
of acceptance.
Undoubtedly, a combination of particulate air
cleaning and vapor-phase cleaning via adsorption on activated
carbon or via chemisorption on oxidant-impregnated alumina can
control both the irritation and odor of ETS to some degree.
Unfortunately, there exist no standards to assess the efficacy of
vapor-phase filtration media. The installation of such media
occurs more commonly in special environments, e.g., libraries and
computer facilities, under expert guidance than in spaces designed
for general occupancy. In the overwhelming majority of cases,
attempts to control ETS rely on ventilation (dilution). As we have
seen, however, ventilation has its limitations.
SUMMARY
1. At an average smoking rate of 10% smoking at any one time,
nonsmokers would need in excess of 100 cfm/occupant to hold
dissatisfaction to the ASI3R.AE criterion of 20%. odor acceptibility.
2. Exposure to ETS generates odor and irritation in both nonsmokers
and smokers. Nonsmokers as a group are less tolerant of ETS than
smokers.
3. The irritation and odor from ETS appear to reside in the vapor
phase. The control of ETS irritation and odor by ventilation or
air cleaning can provide only limited results.
145
Draft - Do not cite or quote
References
American Society of Heating, Refrigerating, and Air-Conditioning
Engineers (ASHRAE) (1989). Ventilation for Acceptable Indoor Air
Quality. ANSI/ASHRAE 62-1989. Atlanta: ASHRAE.
Cain, W. S. (1979). Ventilation and odor control: prospects for
energy savings. ASHRAE Transactions, 85 (1), 784-792.
Cain, W. S. (1988). Olfaction. In R. C. Atkinson, R. J.
Herrnstein, G. Lindzey, and R. D. Luce (Eds.), Stevens' Handbook
of Exberimental Psycholoqy, Vol. 1: Perception and Motivation,
rev. ed. New York: Wiley. Pp. 409-459.
Cain, W. S. and Murphy, C. L. (1980). Interaction between
chemoreceptive modalities of odour and irritation. Nature, 284,
255-257.
Cain, W. S., See, L.-C., and Tosun, T. (1986). Irritation and
9dor from formaldehyde: chamber studies. In IAO '86: Managing
Indoor Air for Health and Energy Conservation. Atlanta: ASHRAE.
Pp. 126-137.
Cain, W. S., Tosun, T., See, L.-C., and Leaderer, B. (1987).
Environmental tobacco smoke: sensory reactions of occupants.
Atmospheric Environment, 21, 347-353.
Cain, W. S., Leaderer, B. P., Isseroff, R., Berglund, L. G., Huey,
R. J., Lipsitt, E. D., and Perlman, D. (1983). Ventilation
requirements in buildings - I. Control of occupancy odor and
tobacco smoke odor. Atmospheric Environment, 17, 1183-1197.
Clausen, G. H. (1986). Tobaksrog - lugtgener og ventilationsbehov.
Doctoral thesis, Technical University of Denmark.
Clausen, G. H., Fanger, P. 0., Cain, W. S., and Leaderer, B. P.
(1985). The influence of aging, particle filtration and humidity
on tobacco smoke odor. In P. 0. Fanger (Ed.), Clima 2000, Volume
4: Indoor Climate. Copenhagen: VVS Kongres - VVS Messe. Pp.
345-349.
Clausen, G. H., Fanger, P. 0., Cain, W. S., and Leaderer, B. P.
(1986). Stability of body odor in enclosed spaces. Environment
International, 12, 201-205. :
Clausen, G. H., Moller, S. B., Fanger, P. 0., Leaderer, B. P., and
Dietz, R. (1986). Background odor caused by previous tobacco
smoking. In IAO '86: Manaaing Indoor Air for Health and Energy
Conservation. Atlanta: ASHRAE. Pp. 119-125.
146
Draft - Do not cite or cluote
Clausen, G. H., Moller, S. B., and Fanger, P. 0. (1987). The
impact of air washing on environmental tobacco smoke odor. In B.
Seifert, H. Esdorn, M. Fischer, H. R_den, and J. Wegner (Eds.),
Indoor Air '87, Volume 2. Berlin: Institute for Water, Soil and
Air Hygiene. Pp. 47-51.
Clausen, G. H., Nielsen, K. S., Sahin, F., and Fanger, P. 0.
(1987). Sensory irritation from exposure to environmental tobacco
smoke. In B. Seifert, H. Esdorn, M. Fischer, H. R_den, and J.
Wegner (Eds.), Indoor Air '87, Volume 2. Berlin: Institute for
Water, Soil and Air Hygiene. Pp. 52-56.
Hugod, C. (1984). Indoor air pollution with smoke constituents
- an experimental investigation. Preventive Medicine, 13, 582-588.
Hugod, C., Hawkins, L. H., and _strup, P. (1978). Exposure of
passive smokers to tobacco smoke constituents. International
Archives of Occupational and Environmental Health, 42, 21-29.
Kerka, W. F. and Humphreys, C. M. (1956). Temperature and
humidity effect on odor perception. Heating, Pipinct,- and. Air
Conditioning, 22, 128-136.
Kirk, P. W. W.,+Hunter, M., Baek, S. 0., Lester, J. N., and Perry,
R. (1988). Environmental tobacco smoke in indoor air. In R.'
Perry and P. W. W. Kirk (Eds. ), Indoor and Ambient Air Ouality.
London: Selper. Pp. 99-112.
Leonardos, G. and Kendall, D. A. (1971). Questionnaire study on
odor problems of enclosed space. ASHRAE Transactions, 77
(1),101-112.
Leopold, C. S. (1945). Tobacco smoke control - A preliminary study.
ASHVE Transactions, 51, 255-270.
Nat.ional Research Council (1986). Environmental Tobacco Smoke -
Measuring Exposures and Assessing Health Effects Washington:
National Academy Press.
Nystrom, C. W. and Green, C. R. (1986). Assessing the impact of
environmental tobacco smoke on indoor air quality. In IAO '86:
Managing the Indoor Air for Health and Energy Conservation.
Atlanta: American Society of Heating, Refrigerating, and
Air-Conditioning Engineers. Pp. 213-233.
Oldaker, G. B. (1989). Environmental tobacco smoke (ETS): How much
is in the air? Presented at the International Tobacco Conference
Minisymposium on Environmental Tobacco Smoke and Scientific
Affairs, Winston-Salem, NC.
Repace, J. L. and Lowry, A. H. (1980). Indoor air pollution,
tobacco smoke, and public health. Science, 208, 464-472.
147
Draft - Do not cite or quote
Weber, A. (1984). Annoyance and irritation by passive smoking.
Preventive Medicine, 13, 618-625.
Weber, A., Jermini, C., Grandjean, E. (1976). Irritating effects
on man of air pollution due to cigarette smoke. American Journal
of Public Health, 66,.672-676.
Weber-Tschopp, A., Fischer, T., Grandjean, E. (1977).
Reizwirkungen des Formaldehyds (HCHO) auf den Menschen.
(Irritating effects of formaldehyde on men.) International
Archives of Occupational and Environmental Health 39, 207-218.
Weber-Tschopp, A., Fischer, T., Gierer, R., and Grandjean, E.
(1977). Experimentelle Reizwirkungen von Akrolein auf den
Menschen. (Experimentally induced irritating effects of acrolein
on men.) Archives of Occupational and Environmental Health, 40,
117-130.
Winneke, G., Plischke, K., Roscovanu, A., and Schlipkoeter, H.-W.
(1984). Patterns and determinants of reaction to tobacco smoke in
.:kn experimental exposure setting. In B. Berglund, T. Lindvall, and
J. Sundell (Eds.), Indoor Air, Vol. 2. Stockholm: Swedish Council
for Building Research. Pp. 351-356.
Yaglou, C. P. (1955). Ventilation requirements for cigarette
smoke. ASHAE Transactions, 61, 25-32.
Yaglou, C. P.,- Riley, E. C., and Coggins, E. I. (1936).
Ventilation requirements. ASHAE Transactions, 42, 133-162.
148
Draft - Do not cite or quote
Figure Captions
Figure 1. Showing the relation between level of
occupancy odor (indicated by concentration of 1-butanol matched to
the odor) and ventilation rate per occupant when 4 to 12 persons
occupied a climate chamber for an hour (filled squares) . Judgments
of odor were made by visitors who sampled the air of the chamber
at a remote sampling box. Also shown (unfilled squares) is the
frequency of dissatisfaction expressed by the visitors in response
to the question, Is the air acceptable or unacceptable ? Dashed
line shows ventilation rate that led to 20% dissatisfaction. Data
from Cain et al. (1983).
Figure 2. Frequency distribution of ventilation
rates recommended for various types of spaces (e.g., offices,
auditoriums, ticket booths, waiting rooms) by the ASHRAE standard
on ventilation and indoor air quality.
Figure 3. Showing the intensity of ETS odor
perceived by visitors to the sampling box during and after
intermittent (4 cig/hr) or continuous (8 and 16 cig/hr) smoking in
the climate chamber. Results are expressed relative to level of
butanol matched to odor during presmoking occupancy. The open
squares in the left panel show a function for nonsmoking occupancy
for comparison. Ventilation rate per occupant under smoking
conditions refers to smokers, who were the only occupants in the
chamber. From Cain et al. (1983).
Figure 4. Percent dissatisfaction among visitors
vs ventilation during the last 15 min of smoking in the experiment
shown in Fig. 3. Ventilation rate per cigarette based on 7.5-min
smoking time per cigarette. Ventilation rate per occupant adjusted
to conditions of smoking occupancy that assumed 10% of occupants
will be smoking at any give time. Modified from Cain et al.
(1983).
Figure 5. Percent dissatisfaction vs odor intensity
(graphic rating) for occupancy odor and for ETS odor. Data from
Cain et al. (1983).
Figure 6. Left: Percent dissatisfaction vs odor
intensity (matched level of butanol) judged by smokers and
nonsmokers. Right: Percent dissatisfaction vs increment in
concentration of airborne carbon monoxide. Modified from Clausen
(1986).
Figure 7. Perceived magnitude of eye irritation
and degree of dissatisfaction expressed by occupants exposed to
ETS for an hour. Concentrations of carbon monoxide were held
constant throughout the exposures and indicate severity of
exposure. Filtration refers to elimination of particles via
149
Draft - Do not cite or quote
electrostatic precipitation. Filtration had little effect on
irritation. From Cain et al. (1987).
150
Draft - Do not cite or quote
TABLES AND FIGURES FOR CHAPTER 8
N
O
-Ph.
151 O
N
N
CJ~
N
O
. ~
Draft - Do not cite or quote
e
so
...
E 60
a
a
O
~ 40
20
0
0 70 20
Ventilation Rate (cfm per occupant)
80
0
Figure 1
Draft - Do not cite or quote
Recommendations from ASHRAE Standard
Ventilation (cfm per occupant)
Figure 2
Figure 3
j
J
Q
.C
O 1000
900
800
700
~ 600
~
~
~ 500
1
Qei
L
~
400
300
200
100
4 Clqorelles/hr
I
i
i
Ls'Yocc. ctm/occ.
2.5
5.5
e
ro
12.s
17.5
34
I
~
I--smokln
30
60
90
120
8 C/yorelles/hr
30 60 90
Ttme (min)
11
120
I
ft
/6 C/gorelles/hr
30 - 60
90
120
O
0
:31
0
rt
0
`2
0
rt
m
LOZSZZOVOZ
Draft - Do not cite or quote
-0 80
~
~
~' 60
~ 20
U
~, 10
Ventilation Rate per Occupant (cfm)
5 10 20 50 , 100
200 500 1000 2000 5000
Ventilation Rate per Cigarette (ft3)
Figure 4
Draft - Do not cite or quote
80
60
40
° 20
5
2 3 4 5 6 7 8 910
Odor Intensity (cm)
Figure 5
Draft - Do not cite or quote
10
Smoker
a
C Nonsmoker
70 ~
a ao]
®utonol (ppm)
f
Smoker
Non-smoker
3 6 7 3 910
7 3 6 7 9 9,0
&CO (ppm)
Fi b 6
~
Draft - Do not cite or quote
NO FILTRATION
LS-i
1-1
O.S-i
j..
NO FlLTRATlON
,
s0-~
.0
30 ....
20
10 . +....,~.. . .'
~~... .,..
0
0 15 30 45
T I M E
FILTRATION
, 2 PPM
5 PPM
~ ~,y...
.'
.
` ~,..
..+'
~..
FTLTRATION
2 PPM
, 5 PPM
.......
--
0 1S 30 a5 60
(minutes)
.
Fig. 7
60
Draft - Do not cite or quote
CHAPTER 9
PASSIVE SMOKING--BELIEFS, ATTITUDES, AND EXPOSURES
IN THE UNITED STATES
Thomas E. Novotny, M.D.
Office on Smoking and Health
Center for Chronic Disease Prevention and Health Promotion
Centers for Disease Control
Introduction
The relationship among public attitudes, policies, and exposure to
certain health hazards is complex. With the release of the 18th
Surgeon General's report on smoking and health, The Health
Consequences of Involuntary Smoking (PHS 1986), public attention
on the issue of environmental tobacco smoke (ETS) was more strongly
focused than ever before. For many years, however, pollsters, the
tobacco industry; °'and the health promotion community have have been
surveying the public concerning attitudes toward ETS and toward
restrictions on smoking in public places. The Surgeon General's
Report described data from several of those surveys as well as
results from evaluations of worksite and local policy changes.
Additional detailed data on public beliefs and attitudes toward
smoking in general are found in the 1989 Surgeon General's Report:
Reducing the Health Consequences of Smoking -- 25 years of Progress
(PHS 1989). Recently, surveys have also included questions on
beliefs_about the harmfulness of ETS to the nonsmoker and on
respondents' reported exposure to ETS. In addition to such
measures of individual exposure to ETS, surveys of worksites and
of personnel managers have provided information about restrictions
on _,smoking in the workplace. Because changes in public attitudes
toward ETS usually precede laws or policies regarding ETS exposure
(PHS 1986), examining trends in these data over time is useful.
This chapter will summarize the most important findings from
several different nationally based data sources. Some of this
information was included in the 1989 Report of the Surgeon General
(PHS 1989)0
Data Sources and Methodology
Several surveys of public beliefs, attitudes, and reported
exposures to ETS are available (Table 1). Although these surveys
may report discrepant results, most discrepancies can be explained
by the differences in methodology, especially in the ways questions
are worded. To describe the effect of increasing numbers and
strength of laws and policies against smoking in public places,
152
Draft - Do not cite or quote
national surveys of worksites were also carried out in the 1980s
(PHS 1986). These surveys indicate the degree to which workers may
be protected from ETS exposure. The 1987 National Health Interview
Survey of Cancer Epidemiology and Control also collected
information about respondents' actions in response to ETS exposure.
Tobacco Industry Surveys
1. Roper Surveys: The Roper Organization conducted six biennial
national opinion surveys for The Tobacco Institute between 1966 and
1978. The 1974, 1976, and 1978 surveys focused on the passive
smoking/nonsmoker's rights issue (Roper 1978), whereas all six
surveys dealt with public attitudes toward the smoking and health
issue in general, toward the tobacco industry itself, and toward
government regulation of tobacco. The surveys were cross-
sectional, population-based telephone interviews. The sample
included over 2,000 adults, aged 17 years or older; other
information about the exact methodology and response rates is
unavailable. The 1974-1978 Roper surveys permit comparisons of
data collected for the tobacco industry with similar data collected
in the 1970s by the Office on Smoking and Health (OSH, formerly
known as the National Clearinghouse for Smoking and Health).
2. Hamilton, Frederick, and Schneiders: In December 1988, the
Tobacco Institute sponsored a telephone-based national adult survey
of 1,500 adults (401 smokers and 1,099 nonsmokers) which was
conducted by Hamilton, Frederick, and Schneiders (Hamilton,
Frederick and Schneiders, 1989). This survey asked about various
public policy issues and was designed to measure levels of support
for governmental'policy on smoking. The respondents were asked
what they thought about restrictions on smoking in restaurants and
worksites. Neither the response rates nor the results by smoking
status of the respondents were reported.
Other Public Opinion Surveys
1. Gallup Surveys: The Gallup Organization has published Gallup
Poll results monthly since 1965. Surveys are either personal
interviews or by telephone and have a population-based sample of
at least 1000 adults, aged 18 years or older. The sampling error.
for overall responses is reported to be no more than ±3% (Gallup
Report 1987). In addition, Gallup surveys may be commissioned by
a variety of organizations. The surveys reported here were
commissioned by the American Lung Association (1983, 1985, 1987,
and 1989) and the American Cancer Society (1988) to describe both
the prevalence of smoking and public opinions regarding smoking
issues. An additional Gallup Survey was commissioned by the
National Restaurant Association (1987) to obtain public opinion on
smo'r;ing in restaurants. The 1989 Gallup Survey sponsored by the
American Lung Association did not ask respondents about their
smoking status.
153
Draft - Do not cite or quote
2. Harris Poll: Louis Harris and Associates have performed eight
national surveys covering smoking between 1974 and 1987 using
probability samples of adults aged 18 years and older. These
surveys were conducted on behalf of various organizations,
including Prevention magazine and Pacific Mutual Life Insurance
Co., to ascertain health practices of Americans. In 1987, 1,250
persons were also asked about regulating smoking in public places.
Government Sponsored Surveys
1. Adult Use of Tobacco Surveys (AUTS): The Office on Smoking and
Health commissioned surveys of adult smoking behavior, attitudes,
and beliefs in 1964, 1966, 1970, 1975, and 1986. These surveys
oversampled persons who had ever smoked, but final results were
weighted to represent the United States resident population aged
21 years and older (1964, 1966, 1970, 1975). The 1986 AUTS
oversampled ever smokers but collected data from persons aged 17
and older. The final data in this survey (overall response rate,
7'4.3%) were weighted to reflect the educational, regional, racial,
and age distribution of the U.S. population on the basis of the
1986 Current Population Survey of the U.S. Bureau of the Census.
The 1986 AUTS collected detailed information on attitudes, beliefs,
and exposure regarding ETS.
2. National Health Interview Survey: The National Health
Interview Survey of Cancer Epidemiology and Control (NHIS-CEC)
collected data in-person from 22,000 adults aged 18 years and older
in households throughout the United States. The data were weighted
to reflect the adult U.S. population, and the overall response rate
for NHIS-CEC was 82%. Respondents were asked about the harmfulness
of ETS and about attitudes toward passive smoking. Questions
included items on perceived annoyance and whether smoking should
occur inside public places. Nonsmokers were asked how they would
act in response to smokers' lighting up in their presence.
Other Surveys
1. Bureau of National Affairs: The Bureau of National Affairs
(BNA) and the American Society for Personnel Administration (ASPA)
conducted a mail-in questionnaire survey of ASPA members, and 623
respondents reported on activities related to smoking in the
workplace. The response rate was 54%. A similar survey was
carried out by the BNA in 1986 on 662 businesses.
2. Office of Disease Prevention and Health Promotion: In 1988,
the Office of Disease Prevention and Health Promotion (ODPHP) of
the United States Public Health Service reported on worksite health
promotion activities, including smoking control. The survey,
carried out in 1985 on a sample drawn from the Dun and Bradstreet
154
Draft - Do not cite or quote
list of businesses, used telephone interviewing. To develop a
probability sample based on geographic region, size of firm, and
industry type, 320 worksites with 50-90 employees and 1,038
worksites with 100 or more employees were surveyed. Questions
about smoking restrictions were included.
3. American Board of Family Practice: In December 1984, the
American Board of Family Practice (ABFP) sponsored a national
telephone survey conducted by Research and Forecasts, Inc., of
1,007 adults aged 18 years and older and of 303 family physicians.
Questions were asked regarding beliefs about the harmfulness of
ETS, the rights of smokers and nonsmokers, and whether smoking
restrictions are effective in stopping or discouraging smoking.
The final sample response rates were 41% for the general public and
37% for physicians. Data for the general public portion of this
survey were weighted to reflect the estimated 1985 U.S. population.
The physicians surveyed represented a random sample of U.S. family
physicians. The results were published in a report entitled,
Rights and Responsibilities: Healthcare Options (ABFP 1985).
`Results of Surveys
1. Perceived Harmfulness of Environmental Tobacco Smoke
The Roper Surveys asked questions regarding harm and annoyance
caused by ETS. All AUT surveys asked about annoyance caused by
ETS, but only the 1986 AUTS asked if respondents believed that ETS
is harmful to the nonsmoker. The 1983 and 1988 Gallup Surveys
asked if respondents believed that smoking is hazardous to the
health of nonsmokers. The 1978 Roper Survey, the 1986 AUTS, and
the 1988 Gallup survey provide interesting information on the
change over the last several years in public beliefs about the
harmfulness of ETS to nonsmokers. The 1985 ABFP Survey asked both
adults and physicians if they believed nonsmokers are harmed by
breathing in the smoke of others in the same room.
Questions regarding harm caused by ETS showed that between 1974
and 1986, the percentage of smokers who believed that ETS is
harmful to the health of the nonsmoker more than doubled (Table
2). In 1974, most nonsmokers believed that ETS is harmful to
health in general, and the percentage of those who held this belief
increased substantially over time. In answering an additional
question on the 1986 AUTS, 69% of nonsmokers felt that ETS is
harmful to their own personal health. The results of the 1989
Gallup poll suggest that there is even stronger belief by
respondents (smokers and nonsmokers) in the harm of ETS to pregnant
women and children. These data show that there has been a major
change in the perception of ETS as a health hazard over the last
decade.
155
Draft - Do not cite or quote
2. Annoyance Caused by Environmental Tobacco Smoke
The AUT surveys show an increasing trend in the percentage of
respondents who are annoyed by ETS (Table 3a). Data regarding
annoyance to ETS from Roper Surveys other than the 1978 survey are
not available. However, the results of both the 1978 Roper Survey
and the AUTS suggest that increasing numbers of Americans are
annoyed by ETS exposure.
The results of the 1987 NHIS-CEC also indicate increased annoyance
from ETS. In this survey, a smaller percentage of current smokers
reported annoyance than on the 1986 AUTS, but this difference may
be due to different methodologies. The NHIS-CEC also collected
information about what nonsmokers did in response to exposure to
ETS (Table 3b). About half of respondents moved away from the
exposure source, 40% did nothing, 3% did something else, and only
4% asked the person not to smoke. Despite their high positive
responses to perceived harm caused by ETS and annoyance from ETS,
most nonsmokers remain rather passive in their behavior toward
smokers (Davis et al., 1990).
3. Limiting or Banning Smoking in Public Places
The majority of respondents to the 1978 Roper Survey felt that
smokers should at least be segregated in all the public places
cited (Table 4). After being asked about segregation of smokers'
and nonsmokers, respondents were then asked if smoking should be
banned outright in selected public places. The majority of
respondents favored smoking bans in retail stores, physicians' or
dentists' waiting rooms, and elevators (Table 5a). The narrative
description of the survey results pointed out that after
recognizing the option to segregate smokers, respondents were
probably less likely to be in favor of a total ban (Roper 1978).
The two most important reasons given by Roper Survey respondents
before 1978 as to why smoking should be restricted had to do with
dangers to others, specifically, cigarette smoking as a fire hazard
and ETS as a health hazard to nonsmokers. In 1978, the chief
reason respondents gave in favor of public laws against smoking was
that the "health of nonsmokers is harmed by other people smoking
in their presence."
In 1983, 1985, 1987, and 1989, the Gallup Organization conducted
telephone surveys for the American Lung Association (ALA) that
asked if smokers should refrain from smoking in the presence of
nonsmokers. Overall, the percentage of respondents to these
surveys who agree that smokers should not smoke in the presence of
nonsmokers has increased from 69% in 1983 to 82% in 1989 (Table
6a). This trend holds true for both smokers and nonsmokers.
Unfortunately, the 1989 survey did not differentiate between
smokers and nonsmokers.
156
Draft - Do not cite or quote
The ALA Gallup Surveys also included questions on where smoking
should be restricted or banned. With regard to smoking in hotels,
motels, and restaurants, the majority of respondents in 1983, 1987,
and 1989 felt that certain areas should be set aside for smoking
(Table 7). Complete bans were less favored, especially by persons
who currently smoked.
In addition, respondents to the ALA Gallup Surveys were asked in
1983, 1985, and 1987 if companies should have a policy on smoking
at work. By 1985, almost 90% of all respondents, including 80% of
smokers and 89% of nonsmokers, felt that smoking should be assigned
to certain areas of the worksite or that it should be totally
banned at work (Table 7).
In 1987, the monthly Gallup Polls (not commissioned by the ALA)
asked if respondents favored or opposed a complete ban on smoking
in all public places. The results of these polls are much more
strongly in favor of total bans on smoking in public places. These
results contrast sharply with the Roper results of almost a decade
ago and are even more in favor of increased restrictions on smoking
in public places than the ALA-sponsored surveys in the same year.
Fn the Gallup Survey conducted for the National Restaurant
Association in 1987, 61% of adults reported that they preferred
no-smoking sections in restaurants. These included 20% of smokers,
65% of former smokers, and 83% of never smokers (Gallup 1987).
These results are similar to those of the AUTS on preferences
concerning no-smoking sections described later in this chapter.
The 1987 NHIS-CEC.asked a slightly different question than either
the Gallup Surveys or the AUTS. This question restricted the
respondent to consider indoor public places. The percentage of
all respondents, especially former smokers, agreeing that smoking
should not be allowed inside public places, was higher on this
survey than on the 1987 Gallup survey (Table 6b). The Gallup
question applied to a general statement about refraining from
smoking in the presence of nonsmokers.
Interestingly, the Tobacco Institute-sponsored survey by Hamilton,
Frederick, and Schneiders in 1988 showed even stronger preferences
for restaurant and worksite restrictions than the ALA surveys
mentioned previously (Table 5b).. For each of these sites, the
question referred to the "current policy" ~s a response choice; for
restaurants, the "current policy" meant that customers must select
smoking vs. nonsmoking sections; for worksites, employers and
employees should decide on worksite restrictive policies. In this
survey, 2% of respondents favored no restrictions on smoking in
restaurants compared with 8% in the ALA survey, and 3% favored no
restrictions on smoking in worksites compared with 10% in the ALA
survey.
N
Between 1964 and 1975, the percentage of respondents to the AUT 0
.P
0
157 N
N)
C)'I
N
Draft - Do not cite or quote
surveys who favored restrictions on smoking in public places
increased from 52% to 70% (strongly agree and mildly agree) (Table
8). However, the question asked in 1986 was quite different from
the questions asked in the earlier surveys (Table 8). Between 1964
and 1975, AUTS respondents who favored more restrictions increased
by 18 percentage points. About half of respondents in 1986 felt
that restrictions against smoking were adequate, perhaps because
many more restrictions were in place by 1986.
In 1966 and 1975, respondents were also asked if employers have a
right to regulate smoking in their places of business. In 1966,
92% felt that the "employer has a right to tell a person when or
where he can smoke while on the job," whereas in 1975, 78% felt
that "management should have the right to prohibit smoking in their
places of business." These are very different questions: the first
concerns management's right to regulate employees, and the second
concerns management's right to regulate customers, visitors, and
employees.
In 1987, respondents to the Harris Poll that was performed for
Prevention magazine were asked if laws should prohibit smoking in
public places or require separate smoking and nonsmoking sections,
or should smoking in public places not be regulated by law. Among
all respondents, -23% felt that laws should prohibit smoking in
public places, 61% felt that laws should require separate smoking
and nonsmoking sections, and only 13% felt that laws should not
regulate smoking in public places at all (3% were unsure). Again,
more than 80% of respondents, smokers and nonsmokers, favored
restrictions against smoking in public places.
4. Public Opinion on Restrictions After Enactment of Laws
Few evaluations of the acceptability of laws banning smoking in
public places have been performed. New York City enacted a ban on
smoking in most public places, including restaurants, in April
19&Z© Three months after the ban took effect, a telephone poll of
676 randomly sampled New Yorkers (New York Times/WCBS-TV poll)
revealed that 73% of respondents approved of the law, including
84% of nonsmokers and 43% of smokers (New York Times, July 5,
1988).
The 1986 AUTS asked respondents if they.would select nonsmoking
sections in airplanes, restaurants, and other public places if
given a choice. Overall, 61% choose nonsmoking seating, including
82% of never smokers, 69% of former smokers, and even 14% of
current smokers (CDC 1988).
Finally, a clean- indoor-air ordinance that took effect in March
1987 in Cambridge, Massachusetts was evaluated by researchers at
Harvard University after three months of implementation. This
evaluation study revealed that 78% of Cambridge residents favored
158
Draft - Do not cite or quote
the restriction, including 41% of smokers and 90% of nonsmokers
(Rigotti 1988).
5. Exposure to ETS
Many studies have demonstrated the biochemically measurable
exposure of nonsmokers to ETS (PHS 1986). However, only the 1986
AUTS has asked a nationally representative sample of residents
about exposure to ETS. PA subsample of 8,600 working respondents
from the AUTS was analyzed with respect to reported exposure at
the worksite and reported policies restricting smoking at their
worksites (Table 9). Fifty-three percent of respondents who worked
in environments with restrictive smoking policies still reported
exposure to ETS. Of these, 11%.reported that their worksite is
"very smoky." Even among the 2.5% of respondents reporting a total
ban on smoking in the workplace, 21% reported still being at least
somewhat exposed to ETS at work. These data help confirm the notion
that worksite restrictions decrease but do not eliminate reported
exposure to ETS at the worksite.
6. The Increasing Number of Policies/Laws Restricting Smokincr at
the Worksite
In 1987, 54% of respondents to the BNA/ASPA survey reported that
their worksites had restrictive smoking policies, up from 36% in
1986 (BNA 1987). The 1986 figure was nearly the same as the
percentage of individual workers reporting the presence of such
policies in the 1986 AUTS.
Among respondents to the 1985 ODPHP Worksite Survey, 35.6% of
worksites reported offering smoking control activities, including
classes, information, special events, or contests. Of those
companies, 76.5% also had formal smoking policies (restriction or
prohibition). In addition to frequently cited benefits--such as
improved employee morale, improved employee health--respondents
reported cleaner air and work environments, fewer smokers in the
workforce, and fewer complaints from nonsmokers (PHS 1988).
7. Perceived Future Effect of Restrictive Smoking Policies
The National Survey of Healthcare Opinions sponsored by the ABFP
and carried out by Research and Forecasts, Inc., in 1985 asked
adults and family physicians if restrictions on smoking in medical
facilities or on the job would be effective. in stopping or
discouraging smoking. Among the nonphysicians, 57% felt that
restrictions in medical facilities would be effective, and 40% felt
that restrictions by employers against smoking on the job would be
effective. Among physicians, 83% felt that such restrictions would
be effective in health care facilities, and 67% felt that
restrictions would be effective on the job. These responses should
be differentiated from those in other surveys that ask about
support for restrictive smoking policies. The ABFP survey tried
159
Draft - Do not cite or quote
to ascertain if respondents thought policies were an effective
intervention for smokers to refrain from using tobacco, whereas the
Gallup surveys tried to ascertain what people want in terms of
protecting the nonsmoker from exposure to ETS.
Few studies have actually been able to assess the effect of
restrictive smoking policies on smokers' behavior, but some studies
from individual worksites show decreased numbers of cigarettes
smoked per day without a change in the prevalence of smoking
(Peterson et al., 1987, Rosenstock et al., 1986).
Conclusions
These data indicate an important shift in public beliefs and
attitudes toward ETS over the last decade or more. The majority
of U.S. citizens have recognized that cigarette smoking directly
harms the health of smokers (89% of men and 90.9% of women in 1975
[AUTS 1975]; 92% of men and 91.8% of women in 1986 [AUTS 1986]).
Moreover, the percentage of survey respondents who believe that ETS
also harms the health of nonsmokers has increased dramatically (46%
overall in 1974 [Roper 1978] to 81% overall in 1986 [AUTS 1986,
Gallup 1988]). Even more Americans agree that ETS harms vulnerable
populations such as pregnant women and children.
Many laws and local ordinances that were put into place during the
last decade undoubtedly increased public awareness of ETS issues
(PHS 1989). The National Academy of Sciences Report and the
Surgeon General's Report on involuntary smoking were released in
late 1986. However, not all of the change in belief about
harmfulness to ETS can be attributed to the publication of these
reports, even though they received enormous media attention; most
of the 1986 AUTS had been completed by late 1986. Therefore, the
increase in reported beliefs about the harmfulness of ETS likely
reflects a growing and sustained awareness among U.S. residents
rather than merely a public response to the highly visible Surgeon
General's Report. This report may have convinced more persons
about the harmful effects of ETS, as evidenced by the results of
the 1989 Gallup Survey.
The slightly discrepant results on attitudes toward laws regarding
restricting smoking in public places found in the 1986 AUTS and the
1988 Harris Poll may be explained by the differences in the way the
question was asked in this survey. Many laws were put into place
by 1986, and respondents may have felt less concerned about
increasing regulations than they did in earlier surveys, before
these laws were in effect. These laws have been evaluated directly
by researchers in some jurisdictions and indirectly by surveys, and
they are apparently widely accepted by both smokers and nonsmokers.
There appears to be a trend towards limiting smoking in workplaces.
It is unclear whether laws and regulations restricting smoking in
160
Draft - Do not cite or quote
public places (which became widespread in the late 1970s) were the
stimuli for policies restricting smoking in the workplace (which
are mostly a phenomenon of the 1980s) or whether simply the concern
for the health of nonsmokers is the stimulus for this trend. The
1986 AUTS results, which show that even with a total ban on smoking
in the workplace some workers are exposed to ETS, suggest that
there is incomplete enforcement of restrictions. In worksites where
smokers and nonsmokers are segregated, exposure to ETS may result
from the inefficiency of separating smokers and nonsmokers within
the same airspace. The 1986 Surgeon General's Report concluded
that this level of restriction was inadequate to protect the
nonsmoker from ETS (PHS 1986). The 1990 Health Objectives for the
Nation, which were endorsed by the U.S. Public Health Service,
recommend that all 50 states have laws by 1990 that both prohibit
smoking in enclosed public places and require separate smoking
areas in the workplace and in dining establishments (PHS 1980).
The number and strength of these "clean indoor air" laws continues
to increase at both the state and local level.(PHS, 1989)
As of late 1988, 31 states had laws restricting smoking in public
worksites, 13 had laws restricting smoking in private worksites,
and 26 had laws restricting smoking in restaurants (PHS 1989).
Continuing to assess public knowledge and beliefs regarding tobacco
use remains important as new information becomes available. These
survey results assist public health providers in measuring the
success of policies to control health hazards such as ETS. In
addition, these data emphasize the change in the social milieu
surrounding tobacco use. The shift in public attitudes away frpm
the social acceptability of smoking may increase the pressure for
smokers to quit and for potential smokers to avoid smoking.
Policy-makers may also find it easier to address tobacco issues
more directly if they understand the public opinions expressed
through these surveys.
SUMMARY
1. The majority (81%) of U.S. citizens have recognized that
cigarette smoking harms the health of nonsmokers.
2. As of late 1988, 31 states had laws restricting smoking in
public worksites, 13 had laws restricting smoking in private
worksites, and 26 had laws restricting smoking in restaurants.
3. There appears to be a trend towards limiting smoking in
workplaces; however, there are indications. of incomplete
enforcement of restrictions.
161
Draft - Do not cite or quote
References
Bureau of National Affairs. Where there's smoke: problems and
policies concerning smoking in the workplace. A BNA special report
2nd ed. Rockville, Maryland: Bureau of National Affairs, 1987.
CDC. Cigarette smoking in the United States, 1986. MMWR
1987;36(35):581-585.
CDC. Passive smoking: Beliefs, attitudes, and exposures--United
States, 1986. MMWR 1988;37(15):239-241.
Davis RM, Boyd GM, Schoenborn CA. 'Common Couresty' and the
elimination of passive smoking. Results of the 1987 National
Health Interview Survey. JAMA 1990; 263: 2208-2210.
Gallup. Survey of attitudes toward smoking. Conducted for the
American Lung Association. Princeton, New Jersey: Gallup
Organization, July 1985.
Gallup. Attitudes toward smoking in restaurants and fast food
establishments. Conducted for the National Restaurant Association.
Princeton, New Jersey: Gallup Organization, February 1987.
Gallup. Majority backs ban on smoking in public places. Gallup
Report No. 258. Princeton, New Jersy: Gallup Organization, March
1987.
Gallup. On-the-go Americans prefer smoke-free air. Am J Pub Health
1988;78(5):563.
Gallup. A telephone survey of 1549 adults conducted in 1988 for
the American Cancer Society. The Gallup Report 1988, No. 268.
Princeton, New Jersey: Gallup Organization, September 1988.
Gallup. Survey of attitudes toward smoking. Conducted for the
American Lung Association. Princeton, New Jersey: Gallup
Organization, August 1989.
Harris, Louis and Associates. Prevention in America V steps people
take or fail to take for better health, 1987. Survey~performed for
Prevention Magazine. May 13, 1988. Appendix B:page 8.
Hamilton, Frederick, and Schneiders. National Survey of American's
Attitudes on Various Public Policies and Practices. Conducted for
The Tobacco Institute, December 1988.
National Center for Health Statistics. Smoking and other tobacco
use: United States, 1987. Hyattsville, Maryland: National Center
for Health Statisitics. DHHS Pub. No. 89-1597. NCHS Series 10,
# 169.
162
Draft - Do not cite or quote
National Clearinghouse for Smoking and Health. Adult use of tobacco
1970. Rockville, Maryland: US Department of Health, Education, and
Welfare. Public Health Service. June 1973.
National Clearinghouse for Smoking and Health. Adult use of
tobacco 1975. Rockville, Maryland: US Department of Health,
Education, and Welfare. Public Health Service. Center for Disease
Control, June 1977.
National Clearinghouse for Smoking and Health. Use of tobacco:
practices, attitudes, knowledge, and beliefs, United States--Fall
1964 and Spring 1966. Washington D.C.: U.S.Department of Health,
Education, and Welfare. Public Health Service July 1969.
Office of Health Promotion and Disease Prevention. National
Survey of Worksite Health Promotion Activities. Washington, D.C.:
U.S. Department of Health and Human Services. Public Health
Service. Summer 1987.
Peterson LR, Helgerson SD, Gibbons CM, Calhoun CR, Ciacco KH, and
Pitchford KC. Employees smoking behavior changes and attitudes
following a restrictive policy on worksite smoking in a large
company. Public Health Rep 1988;103(2):115-120.
Public Health Service. Promoting health/preventing disease:
objectives for the nation. Washington, D.C.: US Department of
Health and Human Services, Public Health Service, 1980.
Public Health Service. The health consequences of involuntary
smoking: a report of the Surgeon General. Rookville, Maryland: US
Department of Health and Human Services, Public Health Service,
Centers for Disease Control, 1986; DHHS publication no. (CDC)
87-8398.
Public Health Service. Reducing the Health Consequences of
Smoking--25 Years of Progress. A Report of the Surgeon General.
Rockville, Maryland: U.S. Department of Health and Human Servics,
Public Health Service, Centers for Disease Control, 1989; DHHS
publication no. (CDC) 89-8411.
Public Health Service.* Major local smoking ordinances in the
United States. A detailed matrix of the provisions of workplace,
restaurant, and public places smoking ordinances. Bethesda, MD:
U.S. Department of Health and Human Services, Public Health
Service, National Institutes of Health, 1989. DHHS Publ. # (NIH)
90-479.
Research and Forecasts, Inc. Rights and responsibilities -- a
national survey of health care opinions sponsored by the American
Board of Family Practice. Lexington, Kentucky: American Board
of Family Practice, 1985.
163
Draft - Do not cite or quote
Rigotti NA, Stoto MA, Kleiman M, Schelling TC. Implementation and
impact of a Cambridge, Massachusetts, ordinance restricting
smoking in public places and the workplace. In Aoki et al., eds.
Smoking and Health 1987. Proceedings of the 6th World Conference
on Smoking and Health, Tokyo, 9-12 November 1987. Amsterdam:
Excerpta Medica, 1988.
Roper Organization. A study of public attitudes toward cigarette
smoking and the tobacco industry in 1978. New York: Roper
Organization, May 1978.
Rosenstock IM, Stergachis A, Heaney C. Evaluation of smoking
prohibition policy in a health maintainance organization. Am J
Public Health 1986a76(8):1014-1015.
Anonymous. Support for smoking ban. New York Times, July 5,
1988:B2.
164
Draft - Do not cite or quote
FIGURES AND TABLES FOR CHAPTER 9
N
O
165 -A
O
N)
N)
CTt
N
N
CT1
Draft - Do not cite or quote
Table 1. Surveys With Information on Beliefs, Attitudes,
and Exposures to Environmental Tobacco Smoke
Survey Year Sponsor
Adult Use of Tobacco '64,'66,'70,'75,'86 Office on Smoking and
Health
Roper Organization '74,'76,'78
Gallup Survey '83,'85,'87,'89 Tobacco Institute
American Lung
Association
Research & Forecasts '85 American Academy of
Family Physicians
Gallup Survey
Harris Poll
Gallup Survey
Hamilton, Frederick '87
'87
'88
'88 National Restaurant
Association
Prevention Magazine
American Cancer Society
Tobacco Institute
& Schneiders
166
Draft - Do not cite or quote
Table 2. Beliefs About Harmfulness of
Environmental Tobacco Smoke to Nnonsmokers (% of Respondents)
by Smoking Status
Smoking Status
Survey Year Current Former Nonsmokers Never All
Smokers Smokers Smokers Respondents
Roper '74 30 57 46
Roper '76 38 61 52
Roper '78 40 69 58
Gallup '83 64 80 84
Research
Forecasts'85 77
(Physicians=87)
AUTS '86 69 82 85 87 81
NHIS-CEC '87 67 84 89 82
Gallup '88 64 86 89 81
Gallup '89
Harmful to adults 86
Harmful to pregnant women 88
Harmful to children 89
Source: Roper Organization 1978; Gallup Surveys 1983, 1988; Adult Use
of Tobacco Survey 1986, Research and Forecasts 1985
167
Draft - Do not cite or quote
Table 3a. Annoyance Caused by
Environmental Tobacco Smoke
(% of Respondents Reporting Annoyance)
by Smoking Status
Annoyed by ETS
Smoking Status
Survey Curr ent Former Nonsmokers Never A11
Smoke rs Smokers Smokers Respondents
AUTS 1964 20 49 64 69 46
AUTS 1966 26 52 70 48
AUTS 1970 34 63 73 78 59
AUTS 1975 35 72 79 79 63
ROPER 1978 5 60
AUTS 1986 42 73 80 83 69
° NHIS-CEC 198 7 34 75 88 69
Source: Adult Use of Tobacco Surveys 1964, 1966, 1970, 1975, 1986;
Roper Organization 1978, NHIS-CEC 1987.
168
N
O
-h
0
N
N
Cn
N
N
00
Draft - Do not cite or quote
Table 3b. Reactions to Secondhand Smoke in Public Places, 1987*
Former Never A11
Smokers Smokers Nonsmokers
a o a
~ o =
Ask person not to smoke 4 5 4
Move away 52 46 52
Do nothing 40 47 40
Do something else 3 3 3
*Not asked of current smokers
Source: 1987 NHIS-CEC (Davis et al.; 1990)
169
Draft - Do not cite or quote
Table 4. Public Opinion (% of Respondents Who Agree)
on Separating Smokers and Nonsmokers
in Selected Public Places, 1978
Smoking should be permitted:
In separate
sections Anywhere
In trains, airplanes, and buses 91 7
In theaters 83 11
In eating places 73 25
At indoor sporting events 73 22
At public meetings 67 28
In train, plane, bus stations 62 34
In work places or.offices 61 34
In barber or beauty shops 53 42
Source: Roper Organization 1978
-IM
170
Draft - Do not cite or quote
Table 5a. Public Opinion (% of Respondents Agreeing)
on Banning Smoking in Selected Public Places, 1978
Should smoking be:
Banned Not banned
o %
In elevators 86 12
In doctors' or dentists' waiting rooms 69 27
In retail stores 55 41
In theaters 44 47
At indoor sporting events 34 57
At.:public meetings 32 58
In city, state, or federal buildings 32 63
In taxis 32 64
In trains, planes, buses 26 65
In eating places 23 68
In barber or beauty shops 21 70
In work places or offices 17 73
In train, plane, bus stations 16 75
Source: Roper organization 1978
171
Draft - Do not cite or quote
Table 5b. Public Opinion (% of Respondents Agreeing)
on Prohibiting Smoking or Retaining Current Policies
in Selected Public Places, 1988
"Current Policy" Prohibit all Smokina No Restriction
In Restaurants 74 24 2
In Worksites 76 20 3
Source: Hamilton, Frederick, and Schneiders 1988
N
O
172 ~
O
N
N
CJ7
N
W
N
L
Draft - Do not cite or quote
Table 6a. Should Smokers Refrain from Smoking
in the Presence of Nonsmokers? (% of Respondents)
by Cigarette Smoking Status, 1983, 1985, 1987, and 1989
Agree Disagree Don't Know
Survey Year: '83 '85 '87 '89 '83 '85 '87 '89 '83 '85 '87 '89
SmokincT Status
Current Smokers 55 62 64 39 37 31 6 1 5
Former Smokers 70 78 76 22 22 19 8 0 5
Nonsmokers 82 85 86 14 15 10 4 * 4
All Respondents 69 75 77 82 25 24 19 15 6 1 4 2
*Less than 0.5%
Source: Gallup Surveys 1983, 1985, 1987, 1989
N
0
~
173 p
IV
N
CTt
N
W
W
Draft - Do not cite or quote
Table 6b. "If People Want to Smoke, They Should Not Do So
Inside Public Places Where it Might Disturb Others"
(% of 1~espondents Agreeing) 1987
Acrree Disaaree No Opinion
Current smokers 67 22 9
Former smokers 80 10 8
Never smokers 89 5 5
All respondents 81 11 7
Source: NHIS-CEC 1987 (Davis et al., 1990)
N
0
4
0
174 N)
N
CJ1
N
w
~
2040225235
N Table 7. Opinions Regarding Smoking in Selected Public Places
0
and Worksites, (% of Respondents With the Opinion)
N
~ by Smoking Status,
1983, 1985, 1987,
1989
v Hotels and Motels
_P
0 Set Aside Totally Ban
r_ Certain Areas Smoking No Restriction s Don't Know
0
0 '83 '87 '89 '83 '87 '89 '83 '87 '89 '83 '87 '89
I
,N Current Smokers
49
61
7 6
42
30
2 3
44Former Smokers 54 72 13 9 27 16 6 3
A Nonsmokers 60 68 15 14 20 15 5 3
All Respondents 54 67 63 12 10 12 30 20 18 4 3 6
Restaurants
Set Aside
Certain Areas Totally Ban
Smoking
No Restriction
s Don't Know
'83 '87 '89 '83 '87 '89 '83 '87 '89 '83 '87 '89
Current Smokers 74 79 12 7 13 13 1 1
Former Smokers 71 74 19 19 9 6 1 1
Nonsmokers 65 71 26 23 7 5 2 1
All Respondents 69 74 66 19 17 23 10 8 8 2 1 3
Worksites
Set Aside
Certain Areas Totally Ban
Smoking
No Restrictions
Don't Know
'83 '85 '87 '89 '83 '85 '87 '89 '83 '85 !87
'89 '83 '85 '87 '89
Current Smokers 64 76 72 11 4 8 21 19 __
_
18 4 1 2
Former Smokers 68 80 73 14 12 16 14 6 8 4 2 3
Nonsmokers 63 80 67 24 9 23 9 10 8 4 1 2
All Respondents 64 79 70 65 17 8 17 21 15 12 11 10 4 1 2 4
Source: Gallup Surveys 1983, 1985, 1987, 1989
175
1
Draft - Do not cite or quote
Table 8. Restrictions on Smoking in Public Places
(% of respondents favoring increase)
by Smoking Status, 1964, 1966, 1970, 1975, and 1986
Smoking Status 1964 1966 1970 1975 1986*
Current smokers - 34 35 42 51 23
Former smokers ' 56 58 61 77 53
Never smokers 68 67 68 82 63
All Respondents 52 52 57 70 50
*The question for the first four surveys read "The smoking of
cigArettes should be allowed in fewer places than it is now." The
question in 1986 read "There are already enough restrictions on where
people can smoke."
Source: Adult Use of Tobacco Surveys 1964, 1966, 1970, 1975, and 1986.
--W
176
Draft - Do not cite or quote
Table 9. Reported Worksite Smoking Policies and Worksite
Exposure to Environmental Tobacco Smoke (% of Respondents), 1986
Worksite Policy ~ Reporting Policy % Reporting Exposure to ETS
Not Restricted 55.4 64.8
Restrictive 42.1 53.2
Total Ban 2.5 21.1
Source: Adult Use of Tobacco Survey 1986
177
BLANK PAGE
Draft - Do not cite or quete
178
Draft - Do not cite or quote
BLANK PAGE
N
O
~
O
179 N
C11
N
W
(0
Draft - Do not cite or quote
CHAPTER 10
THE EFFECTS OF PASSIVE SMOKING AND DAY CARE
ON RESPIRATORY ILLNESSES
Glen Bennett MPH
Office of Prevention, Education, and Control
National Heart, Lung, and Blood Institute
Bethesda, MD 20892
1. INTRODUCTION
Reports of the Surgeon General (43) and the National Research
Council (27) concluded that children of parents who smoke have more
lower respiratory diseases and otitis media. Other reviews (1, 17)
showed that children in day care have more upper respiratory
illnesses, especially otitis media. The overlap in these findings
Zaises a new concern. Does passive smoking and day care attendance
interact to increase the rate of respiratory diseases in infants
and young children? This chapter examines the data to determine
if evidence exist to support this concern. The chapter begins with.
a review of the day-care market to show its complexity. Ignoring
the diversity of day care might lead to faulty conclusions and
recommendations.
2. DAY CARE IN THE U. S.
,2.1. GENERAL CHARACTERISTICS
In 1982, 6 million mothers (48.2%) with a child under the age of
5 were in the civilian work force. (28) The most drastic change
has been the return of parents to work while their children are
infants. (26) These children get care in three basic types of day
care delivery systems. They are inmhome care, family day care, and
group day care.
Parents, relatives, or non-relatives provide in-home care in the
home of the child. They also give family day care (day care homes)
in a private home other than the child's. (2, 50) Day care
centers, including nurseries, provide care for 12 or more children
in nonresidential buildings. (17, 49) This sector is almost always
subject to government regulation and is the smallest of the 3
sectors. (17) However, centers are the fastest growing segment in
the day care market. (1, 24, 28)
180
N
O
4
O
N)
N
01
N
~
O
Draft - Do not cite or quote
Table 1 lists the percent distribution of the type of child day
care used by the age of the child. Nine percent (9%) of working
mothers were able to care for their children while working. Almost
one-third (30.5%) arranged for in-home care of their children.
However, day care homes were the predominate source of care,i.e.,
40.2%. Table 2 describes the percent distribution of care-givers
by the age of the child. Relatives provided child care to 29% and
non-relatives provided 27.5% of all day care to children of working
mothers. Data in Table 3 show that 22% of all children and almost
25% of infants and toddlers got care in the home of a non-relative.
(28)
2.2. REGULATIONS
The U.S. does not have a national policy on child care and efforts
to develop one have reached a stalemate. (35) Sponsors have
withdrawn the 1980 Federal Interagency Day Care Requirements.
However, they continue to serve as a guideline for minimum
standards. (49)
Each state regulates its own day care facilities. They have
. written very tough requirements but enforcement is poor. (35)
,_ All states have passed regulations which contain some
provisions for health and safety. However, they are not
consistent. (17) Licensing practices also vary from state to
state. (24) Forty-four (44) states now regulate family day
care homes. (49) However, children cared for in their own
home are beyond the reach of federal and state policy (17).
2.3. PREVALENCE OF SMOKING
In a 1980 survey, 28.9% of female child care workers smoked
cigarettes. This is less than females in general. However, their
rates are much higher than those for female elementary school
teachers (19.8%) and higher than secondary school teachers (24.8%).
(44)
3. RESPIRATORY INFECTIONS
3.1. MAGNITUDE OF THE PROBLEM
Upper respiratory infections are the most common diseases affecting
children under 5 years of age. They 'are important causes of
childhood illness and their treatment consumes a large portion of
health care resources. (8, 14, 17) Infants average 7-8 acute
respiratory infections per year. Older children; 1-5 years of age,
average one or two fewer infections than infants. (17)
Acute otitis media (AOM) is the most common complication of upper
respiratory diseases in infants and young children. (16, 1~, 31,
47) AOM is the largest single cause of morbidity with possible
sequelae in children. (47) Recurrent episodes are also very common
181
Draft - Do not cite or quote
in children during the first years of life. (23) AOM account for
one-third of pediatric office visits (31) and three-fourths of
follow-up visits. (16) Nearly all children have at least one
episode with effusion (OME) during their first 6 years of life.
Some develop chronic OME or chronic otitis media with perforation
and discharge. (45) Repeated episodes of OME in early life may
lead to transient or permanent hearing loss and impeded speech.
These conditions may then lead to developmental or educational
delays. (17, 47)
Bronchiolitis is the most common manifestation of lower respiratory
infections in infants and small children. The true incidence is
unknown. However, about 10 per 1,000 infant are hospitalized with
bronchiolitis. The mean age for respiratory syncytial virus (RSV)
bronchiolitis is 7.8 months and the peak age is 2 months. Half of
children hospitalized for the condition are under 3 months of age.
(42)
3.2. DAY-CARE AND RESPIRATORY INFECTIONS
Respiratory diseases are the most common ailments affecting
e_~hildren in day care. (1) Today, infants and pre-school age
children get infections at earlier ages and are spending more time
outside the home. A common factor in this changing pattern is the
increasing popularity of day-care centers. (24) Day care centers.
with many children in the same place create favorable conditions
for respiratory epidemics. (30) However, the total burden of
respiratory diseases seems no greater for the day care child. They
simply occur at younger ages. (1)
The association of day care and respiratory diseases began in the
1920's. (17) In the 1970's, Scandinavian researchers (19, 23, 31,
32, 39, 41, 45) found an increased rate of otitis media among
children in day care. Children in centers had the highest rate.
Those in family day care held an intermediate position between
centers and in-home care. Moreover, home-reared children with
abnormal findings at first testing were significantly more likely
to have normal results at subsequent testings.
There are obvious difficulties in transferring the results from
studies conducted in Scandinavian countries. However, Haskins (17)
concluded that the high quality of these studies make the findings
worthy of careful attention. They show that children in day care
are at 2-3 times the risk of otitis media as those reared at home.
Two American research teams (14, 42) confirmed the Scandinavian
results. Visscher and colleagues (47) studied patients in a large
pediatrics group practice in Minneapolis. They collected data on
every child attending the clinic during a 2-week period in
February, 1982. Cases were patient presenting with AOM on a study
day. Controls had a diagnosis other than AOM and no prior history
of otitis. Attending a day care facility was the second most
182
Draft - Do not cite or quote
important risk factor. The risk increased with the number of other
children at the facility. Exposure to smokers was not a risk
factor.
Fleming and colleagues (14) also studied childhood infections in
Atlanta. They found that children attending day care were
significantly more likely to have an upper respiratory tract
infections during a 2-week. Maternal smoking also increased the
risk. The effects of attending day care and smoking mothers were
independent. Age and living in crowded conditions were also risk
factors. The researchers estimated that 31% of upper respiratory
infections can be attributed to day care attendance.
Most studies of bronchiolitis focused on children in hospitals.
Comprehensive studies of this disease in ambulatory patients or
day-care centers are lacking. (42) However, a Chapel Hill, NC
study compared the rates of bronchiolitis in a day care center and
a pediatric practice. The rate was much higher in the day care
center for children 6 months of age or younger. However, the
proportion of cases requiring medical treatment and hospitalization
was less among day care children. (10)
Reviewers (1, 17, 18, 19) have identified problems which limits the
generalization of the findings from these studies. They are:
1. Control groups were less than satisfactory. Researchers
observed children in day care more frequently than those
in home care.
2. Some studies reported symptoms while others used
diagnostic categories.
3. The ages of children studied and the manner of reporting
illnesses by age category differed widely.
4. The reliability of case-controlled and cohort studies
depends on the accurate quantification of disease
occurrence. This raises the questions of whether day
care parents seek a physician for their children's
illnesses more frequently. When a day care provider
suggests taking a child to a physician this might have
important effects on parents.
5. Most studies did not control for other factors that
probably influence the incidence of respiratory
illnesses. These factors include housing, humidity,
ventilation, passive smoking, and other air pollution.
Nonetheless, reviewers concluded that most studies have shown an
increase in respiratory diseases among children in day care. There
is stronger evidence for initial and recurrent otitis media. (17)
The rate of otitis is greater in large group day care centers and
183
Draft - Do not cite or quote
probably smaller day care homes. (2, 17, 18, 31) Studies also show
reduced rates of both symptoms and acute illnesses with increasing
age in all sites. However, there is very little evidence of an
excessive rate of illness in day care children for the more serious
respiratory diseases. (17) Asymptomatic children do not have
higher levels of respiratory tract pathogens or even different
pathogens than children reared at home. (1, 17, 40) However, The
true incidence of infectious disease in family day care is unknown
since most of it is unlicensed. (2)
3.3. PASSIVE SMOKING AND DISEASES IN INFANTS AND CHILDREN
A number of studies have demonstrated a positive association
between passive smoking and lower respiratory symptoms (4, 5, 13,
36) and diseases. (11, 12, 22, 29, 48) The effect was stronger in
infants. Maternal smoking, when measured, showed a high
correlation. However, paternal smoking was rarely significant.
Studies on the relationship of passive smoking to the development
of bronchiolitis are less clear. Two studies (32, 38) showed a
positive association with maternal smoking. However, another study
(29) did not find a relationship.
Otitis media is the only upper respiratory disease reported in the
literature as being associated with passive smoking. Five studies
(3, 20, 21, 30, 34) showed an increased incidence of otitis media
with maternal smoking. However, in five other studies (14, 39, 45,
46, 47) parental smoking was not significant. However, the study
by Fleming and colleagues (14) included only 34 cases among the 575
children with upper respiratory illnesses. Pukander and colleagues
(30) also suggested that day care attendance may mask the effect
of parental smoking.
Two comprehensive reviews (27, 43) concluded that lower respiratory
diseases and otitis media occur more frequently in children with
mothers who smoke. Two researchers (29, 48) offered explanations
for the association with only maternal smoking. They argued that
children are more likely to be with their mothers at the times
smoking occur. Some mothers also remain at home with the child.
This suggests that the duration of exposure to smoke rather than
just the presence of a smoker is the more important factor.
Both reports (27, 43) emphasized the need for caution in the
interpretation of these studies. Independent risk factors, such
as age and sex, were not always taken into account. The use of
questionnaires to collect information on symptoms are prone to
recall bias. Most studies examined only the effects of exposure
to parental smoking, excluding exposures outside the immediate
family. Future studies must control for potential confounding
variables.
184
N
O
~
O
N
N
01
N)
~
P
Draft - Do not cite or quote
3.4. DAY CARE AS A CONFOUNDING VARIABLE
Passive smoking increases the risk of upper and lower
respiratory diseases in infants. Day care attendance also
increases the occurrence of upper respiratory infections and
perhaps some lower respiratory illnesses in infants and
toddlers. However, studies focusing primarily on the effects
of passive smoking did not control for day care attendance.
Many of the studies on day care infections did not consider
parental smoking as a possible confounding variable.
Moreover, none of the studies in either area considered the
smoking habits of day care workers.
Seven of the day care studies (14, 19, 30, 39, 45, 46, 47) did
consider parental smoking. Two of these studies (14, 30) found an
independent effect for both day care attendance and maternal
smoking. The effect of day care was strongest in both cases. The
remaining studies showed a statistical significance for day care
attendance only.
It is unfortunate that researchers have ignored the smoking habits
pf day care givers. Especially since the duration of exposure is
'important. (29,-4-8) Smoking by day care workers exposes the child
to smoke. The Section on Allergy o,f the Canadian Pediatric
Association (37) provided support for this premise. They reported
that infants admitted to hospitals for chest problems had
significantly more day care givers who smoke than did control
infants.
The smoking practices of workers in day care homes deserve special
attention. This sector includes more children and is especially
popular with mothers of infants and toddlers. Day care providers
who smoke probably spend as much time with these children as their
mothers. Thus, the smoking habits of these workers potentially
confound the results of studies of the effect of parental smoking.
4.~ RECOMMENDATIONS
4.1. REGULATIONS
Existing day care regulations clearly are deficient in mandating
a safe and healthy day care environment. Federal regulation, while
desirable, is not possible now. The prevailing attitude today is
away from federal intervention and toward state and personal
responsibility. (49) The regulation of day care homes, which
contain the most children, is an especially: delicate issue.
Increased regulation of homes might have the effect of actually
decreasing the availability of this mode of child care. (2)
Moreover, the sheer number of providers and the small size of these
units would make effective oversight difficult. (17)
185
Draft - Do not cite or quote
The most important interim steps are to give parents better
information and improve state regulations that relate to health.
(17) Requiring all facilities to have written policies on health
and give copies to parents is a start. Parents should also be
informed about the potential interaction between passive smoking
and day care on the risk of early childhood infections. (14)
4.2. RESEARCH
The sparse data available regarding family day care make it
important to pay more attention to this mode. Since day care homes
includes more children, particularly infants and toddlers, it is
important to understand the disease experiences in these homes. (2)
Surveys are needed to determine the smoking patterns of day care
workers. Data from the National Health Interview Surveys,
1978-1980 put the prevalence of smoking among female child care
workers at 28.9%. However, these data excluded private household
child care workers.
4.3. EDUCATION
Presently, Parents must judge for themselves the quality of care
given to their children. However, most parents do not know what
to look for in a day care setting and there are no federal
standards. (35, 50) There are, however, guidelines that the child~
development community supports. (35) There is also a checklist
that can differentiate between centers of high and low quality.
The checklist includes one item on smoking: "Adults do not smoke
in rooms where children are." (7, 35) Education efforts to
disseminate this information are needed. Low-cost materials must
also be available to day care providers. (1)
5. CONCLUSION
The children of working parents are receiving day care primarily
in their own home, family day care homes, and day care centers.
Family day care is the largest of the three sectors but day care
centers represent the fastest growing segment. Studies, mostly in
Scandinavian countries, have demonstrated that children attending
day care have more respiratory infections. The effect was stronger
among infants and toddlers.
Another group of studies have linked parental smoking, primarily
maternal smoking, with an increase in respiratory diseases among
infants. However, most of these studies did' not control for
attending day care. The few studies that controlled for parental
smoking and day care showed a consistent and positive association
for day care. Parental smoking was less clear. None of the
studies, however, controlled for the exposure to smoke from day
care workers.
186
Studies controlling for potential confoundiDng SactoDs a~~~ ~~n~y ~ote
needed in this area. The smoking practices of day care workers,
particularly day care homes, may have been a major uncontrolled
factor in past studies.
In the interim, parents must be educated. They must know about the
harmful effects of parental smoking and the potential for added
exposure from day care workers. Some 58% of one sample attended
full-time day care, i.e., 40 hours or more per week. (14) Thus,
children of nonsmoking parents are not without risk. Staying with
day care smokers may increase their exposure to smoke similar to
that with smoking parents. Children of smoking parents may face
as much as twice the exposure. This has special implications for
day care homes. First, the children are younger. They also spend
most of the time in a smaller environment with other children and
the day care worker. If smoking occurs, the exposure should not
be materially different from that found in the home.
Day care providers must also know about the possible interaction
of passive smoking and day care attendance. Those in day care
homes, particularly, should not smoke in the presents of the
children. Since strict regulations of this sector in not possible,
the parents must insist upon this practice.
Day care centers, while providing a different environment, should
adhere to the same principle. They are similar to the school
system where teachers can not smoke in the classroom. State
regulatory agencies should also include this provision in the
licensing of day care facilities.
SUMMARY
1. Studies have linked both parental smoking and day care
attendance with increased respiratory infections. Smoking by
daycare workers may have been a major uncontrolled confounding
factor in studies of infections caused by maternal passive smoking.
2. Parents and daycare providers should be educated to know
about the harmful effects of parental smoking and the potential for
added exposure from day care workers, which could double total ETS
exposure.
3. State regulatory agencies should include prohibitions
against smoking in daycare as they do in classrooms.
187
Draft - Do not cite or quote
6. REFERENCES
1. Aronson, SS; Osterholm, M. "Infectious Diseases in Child
Care: Management and Prevention. Summary of the Symposium
and Recommendations;" Review of Infectious Diseases; 1986,
July-Aug; 8(4): 672-679
2. Bartlett, AV; Orton, P; Turner, M "Day Care Homes: The
Silent Majority of Child Care;" Review of Infectious
Diseases; 1986, July-August; 8(4): 663-671
3. Black, N. "The Aetiology of Glue Ear: A Case-Control
Study," International Journal of Pediatric
Otorhinolaryngology, 9(2): 121-133; July, 1985
4. Burchfiel, CM; Higgins, MW; Keller, JB; Butler, WJ; Howatt,
WF; Higgins, ITT; "Passive Smoking in Childhood:
Respiratory Conditions and Pulmonary Function in Tecumseh,
® Michigan," American Review of Respiratory Disease, 133(6):
966-973, June, 1986
5. Charlton, A. "Children's Coughs Related to Parental
Smoking," British Medical Journal, 288(6431): 1647-1649;.
June 2, 1984
6. Cherian, A and Feldman, W. Personal communications reported
in: Section Allergy, Canadian Pediatric Association;
"Secondhand Smoke Worsens Symptoms in Children With Asthma;"
Canadian Medical Association Journal; 1986, August 2;
135(4): 321-323
7. Clarke-Stewart, A. Daycare, Cambridge, MA: Harvard
University Press, 1982
8. Cypress, BK; "Pattern of Ambulatory Care in Pediatrics: The
National Ambulatory Medical Care Survey: U.S., January 1980
- December 1981," in Vital Health Statistics, Series 13, No.
75; U.S. Department of Health and Human Services;
Publication No. 94-1736; Government Printing Office, 1983
9. Denny, FW; "Childhood Acute Respiratory Tract Infections
Deserve Our Attention;" American Journal of Public Health;
1988, January; 78(1): 16-17
10. Denny, FW; Collier, AM; Henderson, FW; Clyde, WA; "The
Epidemiology of Bronchiolitis," Pediatric Research, 11:
234-236, 1977
11. Evans, D; Levison, M; Feldman, C; Clark, N; Wasilewiski, Y;
Levin, B; Mellins, R. "The Impact of Passive Smoking on
188
Emergency Room Visits of Urban CIPKIOten DA)i=t Atitkvna:~21 quote
American Review of Respiratory Diseases; 1987; 135:
567-572
12. Fergusson, DM; Horwood, LJ; Shannon, FT; Taylor, B.
"Parental Smoking and Lower respiratory Illness in the First
Three Years of Life," Journal of Epidemiology and Community
Health, 35(3): 180-184; September, 1981
13. Ferris, BG; Ware, JH; Berkey, CS; Dockery, DW; Spiro III, A;
Speizer, FE; "Effects of Passive Smoking on Health of
Children," Environmental Health Perspectives, 62: 289-295;
1985
14. Fleming, DW; Cochi, SL; Hightower, AW; Broome, CV;
"Childhood Upper Respiratory Tract Infections: To What
Degree is Incidence Affected By Day Care Attendance;"
Pediatrics; 1987, January; 79(1): 55-60
15. Fosburg, S; Family Day Care In The United States: Summary
of Findings; Government Printing Office, 1981
16. Giebink, GS; "Epidemiology and Natural History of Otitis
Media;" in Lim, DJ; et al; Recent Advances in Otitis Media
With Effusion; 1984; 5-8
17. Haskins, R; '!Day Care and Illness: Evidence, Costs, and
Public Policy;" Pediatrics; 1986; 77: 951-982
18. Henderson, FW; Giebink, GS; "Otitis Media Among Children in
Day Care: . Epidemiology and Pathogenesis;" Review of
Infectious Diseases; 1986, July-August; 8(4): 533-538
19. Ingvarsson, L; Lundgren, K; 0lofsson, B; "Epidemiology of
Acute Otitis Media in Children-A Cohort Study in an Urban
Population;" in Lim, DJ; et al; Recent Advances in Otitis
Media With Effusion; Philadelphia: B C Decker; 1984;
19-22
20. Iverson, M; Birch, L; Lundqvist, G; Elbrond, 0. "Middle Ear
Effusion in Children and the Indoor Environment: An
Epidemiological Study," Archives of Environmental Health
40(2): 74-79; March-April, 1985
21. Kraemer, MJ; "Risk Factor for Persistent Middle Ear
Effusions;" Journal of American Medical Association; 1983,
February 25; 249(8): 1022-1025
22. Leeder, SR; Corkhill, RT; Irwig, LM; Holland, WW. "Influence
of Family Factors on the Incidence of Lower Respiratory
Illness During the First Year of Life," British Journal of
N
0
189 4~6
O
N
N
C~'1
N
-D.,
(0
Draft - Do not cite or quote
Preventive and Social Medicine, 30(4): 203-212, December,
1976
23. Lundgren, K; Ingvarsson, L; Olofsson, B; "Epidemiological
Aspect in Children With Recurrent Acute Otitis Media;" in
Lim, DJ; et al; Recent Advances in Otitis Media With
Effusion; Philadelphia: B C Decker; 1984; 22-25
24. Marwick, C; Simmons, K; "Changing Childhood Disease Pattern
Linked With Day-Care Boom;" Journal of American Medical
Association; 1984, March 9; 251(10): 1245-1247, 1250-1251
25. McConnochie, K; Hall, C; Barker, W; "Lower Respiratory Tract
Illness in the First Two Years of Life: Epidemiologic
Patterns
American
34-39 and Costs in a Suburban Pediatric Practice;"
Journal of Public Health; 1988, January; 78(1):
26. Morgan, G; Stevenson, C; Fiene, R; Stephens, K; "Gaps and
Excesses in the Regulation of Child Care: Report of a
Panel;" Review of Infectious Diseases; 1986, July-August;
8(4): 634-643
27. National Research Council; Environmental Tobacco Smoke -
Measuring Exposure and Assessing Health Effects; Washington,
DCo National Academy Press; 1986
28. O'Connell, M; Rogers , CCe "Child Care Arrangements of
Working Mothers: Ju ne 1982;°1 Current Population Reports
(Bureau of Census); 1982; Special Studies P-23; No. 129
i
29. Pedreira, F; Guandolo, V; Feroli, E; Mella, G; Weiss, I;
"Involuntary Smoking and Incidence of Respiratory Illness
During the First Year of Live," P ediatrics, 1985; 75:
594-5970
30. Pukander, J; Luotonen, J; Timonen, M; Karma, P; "Risk
Factors Affecting the Occurrence of Otitis Media Among 2-3
Year Old Urban Children;" Acta Otolaryngology [Stockholm];
1985, September-October; 100(3-4): 260-265
31. Pukander, J; Sipira, M; Karma, P; ."Occurrence of and Risk
Factors in Acute Otitis Media;" iri Lim, DJ; et al; Recent
Advances in Otitis Media With Effusion; Philadelphia: B C
Decker; 1984; 9-13
32. Pullan, CR; Hey, EN. "Wheezing, Asthma, and Pulmonary
Dysfunction 10 Years After Infection With Respiratory
Syncytial Virus in Infancy," British Journal of Medicine,
284(6330): 1665-1669, June 5, 1982
190
N)
0
~
O
N)
N
CT1
N
CTt
0
33. Ruopp, R; Travers, J; Glantz, F; Coelen~f C. CDhildren Ate the quOte
Center: Summary Findings and their Implications; Cambridge,
MA: Abt Books; 1979
34. Said, G; Zalokar, J; Lellouch, J; Patois, E; "Parental
Smoking Related To Adenoidectomy and Tonsillectomy in
Children," Journal of Epidemiology and Community Health,
32(2): 97-101; June, 1978
35. Scarr, S; Mother Care, Other Care; New York: Basic Books;
1984
36. Schenker, MB; Samet, JM; Speizer, FE "Risk Factors for
Childhood Respiratory Disease: The Effect of Host Factors
and Home Environmental Exposure," American Respiratory
Disease, 128: 1038-1043; 1983
37. Section Allergy, Canadian Pediatric Association; "Secondhand
Smoke Worsens Symptoms in Children With Asthma;" Canadian
Medical Association Journal; 1986, August 2; 135(4):
38.
- 321-323
Sims, DG;. Downham, M; Gardner, PS; Webb, J; Weightman, D.
"Study of'8-Year-Old Children With A History of Respiratory
Syncytial Virus Bronchiolitis in Infancy," British Journal
of Medicine, 1(6104): 11-14, January 7, 1978
39. Stahlberg, MR; "The Influence of Form Day Care on the
Occurrence of Acute Respiratory Tract Infections Among
- Children;" Acta Paediatric Scandinavia [Supplement]; 1980;
282: 1-87 '
40. Strangert, K; Carlstrom, G; Jeansson, S; Nord, CE;
"Infections in Preschool Children In Group Day Care," Acta
Paediatric Scandinavia, 65: 455-463, 1976
41" Strangert, K; ."Respiratory Illness in Preschool Children
With Different Forms of Day Care," Pediatrics, 57(2):
191-196; February, 1976
42. Task Force on Epidemiology of Respiratory Diseases;
Epidemiology of Respiratory Diseases; Division of Lung
Diseases, National Heart, Lung & Blood Institute; November,
1981
43. Public Health Service, The Health Consequences of
Involuntary Smoking: A Report of the Surgeon General, U.S.
Department of Health and Human Services, Rockville,
Government Printing Office, 1986 MD:
44. Public Health Service, The Health Consequences of Smoking:
Cancer and Chronic Lung Disease in the Workplace, U.S.
191
Draft - Do not cite or quote
Department of Health and Human Services, DHHS (PHS)
85-50207, 1985
45. Van Cauwenberge, PB; Kluyskens, PM; "Some Predisposing
Factors in Otitis Media With Effusion;" in Lim, DJ; et al;
Recent Advances in Otitis Media With Effusion; Philadelphia:
B C Decker; 1984; 28-32
46. Vinther, B; Elbrond, CB; "A Population Study of Otitis Media
in Childhood," Acta Otolaryngology, [Stockholm] Supplement
360: 135-137; 1979.
47. Visscher, W; Mandel, JS; Batalden, PB; Russ, JN; Giebink; GS;
"A Case-Control Study Exploring Possible Risk Factors for
Childhood Otitis Media;" in Lim, DJ; et al; Recent Advances
in Otitis Media With Effusion; Philadelphia: B C Decker;
1984; 13-15
48. Ware, JH; Dockery, D; Spiro, A; Speizer, F; Ferris, B.
"Passive Smoking, Gas Cooking and Respiratory Health of
Children Living in 6 Cities;" American Review of Respiratory
Diseases; 1984, March; 129(3): 366-374
219. Young, KT and Zigler, E; "Infant and Toddler Day Care:
Regulations and Policy Implication," American Journal of
Orthopsychiatry, 1986, January; 56(1): 43-55
50. Zigler, E; Muenchow, S; "Infectious Diseases in Day Care:
Parallels Between Psychologically and Physically Healthy
Care;" Review of Infectious Diseases; 1986, July-August;
8(4): 514-520
e
--192
Draft - Do not cite or quote
7. TABLEB
TYPE OF CHILD CARE BY AGE OF CHILD
AGE < 1 Year Table 1
1-2 Years
3-4 Years
TOTAL
IN-HOME CARE 3 4. 3% 3 3. 3% 2 4. 6% 30 . 5%
DAYCARE HOME 42.7% 43.0% 35.4% 40.2%
GROUP CARE 5. 3% 11. 7% 2 5. 8% 14 . 8%
MOTHER 9.2% 8.6% 9.9% 9.1%
TOTAL 91. 5% 96. 6% 95. 7% 94.6%
Source: O'Connell and Rogers, 1982 (28)
193
Draft - Do not cite or quote
CARE GIVER BY AGE OF CHILD
Table 2
AGE < 1 Year 1-2 Years 3-4 Years TOTAL
FATHER 13.9% 15.8% 11.0% 13.9%
MOTHER 9.2% 8.6% 9.9% 9.1%
GRANDPARENT 22.4% 16.8% 14.6% 17.2%
OTHER RELATIVE 11.3% 12.3% 12.8% 12.1%
NONRELATIVE 29.4% 31.4% 21. 6% 27.5%
GROUP CARE 5.3% 11.7% 25.8% 14.8%
TOTAL 91.5% 96.6% 9507% 94.6%
Source: O'Connell and Rogers, 1982 (28)
194
Draft - Do not cite or quote
CAREGIVERS BY TYPE OF CHILD CARE AND AGE OF CHILD
Table 3
AGE < 1 Year 1-2 Years 3-4 Years TOTAL
IN-HOME CARE
Father 13.9% 15.8% 11.0% 13.9%
Grandparent 8.9% 6.3% 3.6% 5.9%
Other Relative 5.1% 5.0% 5.7% 5.2%
Non-relative 6.4% 6.2% 4.3% 5.5%
'DAY CARE HOME
Grandparent
13.5%
10.5%
11.0%
11.3%
Other Relative 6.2% 7.3% 7.1% 6.9%
Non-relative 23.0% 25.2% 17.3% 22.0%
GROUP CARE
Nursery
1.7%
3.2%
11.7%
5.6%
Day Care Center 3.6% 8.5% 14.1% 9.2%
MOTHER 9.2% 8.6% 9.9% 9.1%
TOTAL 91.5% 96.6% 95.7% 94.6%
Source: O'Connell and Rogers, 1982 (28)
195
Draft - Do not cite or qtiots
FIGURES AND TABLES FOR CHAPTER 10
1
196
N
O
~
O
N
N)
CT~
N
(11
~
Draft - Do not cite or quote
CHAPTER 11
NO SMOKING POLICIES AT THE WORKSITE
A Look at What Companies Are Doing Today
Ruth Behrens*
Washington Business Group on Health
The movement of businesses to develop and implement smoking
control policies appears to be strong, and may even by gaining
momentum.
A national survey released in 1987 by the Office of Disease
Prevention and Health Promotion, U. S. Department of Health and
Human Services, found that 27 percent of all U.S. companies with
50 or more employees had a formal smoking policy. Of these, 40
percent reported the policy was in place to protect nonsmokers; 40
percent reported the policy was designed to comply with
regulations; 13 percent reported a need to protect equipment; and
=t'percent advised that the policy was designed to protect employees
at high risk for health problems.'
A more recent study that looked only at large and medium-sized
companies, the 42nd annual Northwestern University Lindquist-
Endicott Report, found that 70 percent had restricted, or were
prepared to limit, smoking in the workplace. The study was
released in early'1988.Z
Another study of 916 large and mid-sized U.S. companies, conducted
in 1989 by Hay/Huggins, a management consulting firm, found that
81 percent of surveyed firms with revenues of $1 billion or more
restrict smoking; the percent dropped to 65 percent for companies
grossing less than $200 million per year.3
A 1989 survey by the Gallup Organization commissioned by the
American Lung Association found that 21 percent of individuals
surveyed supported a total ban on smoking at the worksite, with an
additional 65 percent in favor of smoking only in designated
areas.4
The development and implementation of a no smoking policy within
a business is a multi-faceted process. Experiences of the growing
number of companies that have developed written statements spelling
out how smoking will be limited or prohibited illustrates vividly
that the process involves many individuals and groups, and that
deliberations often are emotionally charged.
197
Draft - Do not cite or quote
This chapter contains a series of case studies outlining how
several companies have successfully approached this process. But
before discussing company-specific examples, there is merit in
examining some of the key issues that must be looked at by any
company considering developing a no smoking policy. Among the
questions to be answered are:
o What kind of specific smoking restrictions are best for the
company?
o What benefits can be realistically anticipated from the
policy?
o How should employees be involved?
o How should unions be involved?
o What kind of education should be offered and to whom?
o What kind of incentives should be offered?
o How should the policy be enforced?
,.
Further details about each of these steps are contained within the
"Case Studies" section of this chapter.
Options for Smoking Restrictions
Restrictions on smoking in the worksite are not new.
For years--even decades--businesses have had policies that banned
smoking in specific areas such as elevators, hallways, auditoriums,
sections of cafeterias, laboratories, rooms with delicate
equipments, etc. In many instances, these restrictions were
imposed because of laws or ordinances requiring them or to protect
property. Before the 1980s, they were seldom implemented for
health reasons. The assumption was, of course, the entire company
is considered a Smoking Permitted area unless otherwise specified.
Another type of policy began appearing with regularity in the mid
and late 1980s. It banned smoking throughout the company except
in designated areas. While many of 'these policies did 'not
necessarily put greater limits on smoking--often allowing offices
and work areas, special lounges, large parts of the cafeterias,
etc, to be designated as Smoking Permitted areas, they did set the
precedent that the company is Smoke Free except in specified areas.
While the difference between these two types of policies may seem
subtle at first glance, there is a strikingly different corporate N
O
198 .p
O
N
N
CJ1
K)
Cl7
00
Draft - Do not cite or quote
philosophy underlying the two approaches. And in the late 1980s,
it was this latter approach--establishing a smoke free company,
possibly with a few, carefully selected areas that permit smoking-
-that appeared to be setting the pattern for worksite smoking
policies.
According to a spokesperson for Texas Instruments, Inc. (TI),
determining what approach to take in limiting smoking was the most
difficult aspect of developing and implementing its policy.
As TI and many other companies have found, designating even a few
smoking areas within a company can still pose serious health
hazards for employees. Smoke from lounges, cafeterias, hallways,
and enclosed offices, gets into the ventilation system and is
circulated throughout the building, including into no smoking
sections. (See "Case Studies: Pacific Northwest Bell.") As an
interim step in a phased-in nonsmoking work environment, Pacific
Mutual Life Insurance Company, Newport Beach, California, installed
electronic filters in the temporary smoking area of its cafeteria.
TI chose to avoid this problem by eliminating smoking from the
worksite except for designated smoking areas which were, to the
extent possible, separately ventilated. Similarly, the
headquarters complex of General Telephone of California prohibited
smoking in all areas except a small portion of the cafeteria that
has its own ventilation system.
For others like American Family Insurance Group, Madison,
Wisconsin, Pennsylvania Blue Shield, and UNUM Life Insurance
Company, Portland, Maine, the choice to provide separate
ventilation was either too expensive or physically impossible, so
they chose to ban smoking completely at the worksite. On October
1, 1987, Ralston Purina's headquarters in St. Louis, Missouri,
became the first Fortune 500 company to completely ban smoking in
its facilities.
Clearly, more and more companies are banning smoking or severely
limiting it. Most require that all visitors abide by the company's
regulations. Some will not allow smoking on company property,
including grounds and parking lots. Groups like Michigan Bell,
which has a large number of motor vehicles, are expanding their
bans to all company-owned vehicles. However, others are voiding
a ban in company cars and trucks because they believe enforcement
will be virtually impossible.
A few companies have gone even further, and may be bellwethers for
a future tend. These companies require that all new employees sign
a statement that they are nonsmokers, even on their own time.
Company policies prohibiting the hiring of smokers got nationwide
publicity when Acoustical Products Company, a subsidiary of
Chicago-based US Gypsum Corporation, announced that because of
exposures to fibers that could have adverse health effects, all
present workers were required to quit smoking or face termination,
199
Draft - Do not cite or quote
and in the future, only nonsmokers would be hired. The Non-Smokers
Inn in Dallas, Texas, provides only nonsmoking rooms and hires only
individuals who do not smoke. At Cardinal Industries, Columbus,
Ohio, new employees must state on the application form whether or
not they smoke, and only nonsmokers will be hired; but the company
does not make any effort to validate applicants' statements.
Louisiana Pacific Corporation, a Portland, Oregon-based national
timber company with 15,000 employees, does not hire smokers in any
of its plants or in corporate offices "because of the medical
costs, absenteeism, environment of smoke in the workplace, the fire
problems in the mills, and lung cancer."Z
The vast majority of companies still do not require that new
employees be nonsmokers. But many companies with strict bans are
seeing fewer smokers apply. "Why would a smoker want to work for
us," one company spokesman said, "when we deprive him of his habit
for eight hours every workday?"
Benefits of No Smoking Policies
Developing and implementing a worksite no smoking policy may not
be easy and may cause some discomfort for smokers and management
alike. So why do companies do it? What benefits do they receive?
In a recent national survey of all types of worksites with 50 or~
more employees, the Office of Disease Prevention and Health
Promotion, U. S. Department of Health and Human Services, asked
those with smoking programs what benefits they perceived.
0 41 percent said smoking control policies and programs
improved employees' health;
0 16 percent said they increased employees' productivity;
0
9 percent said they improved morale, and
8 percent said smoking control activities reduced costs.'
Some companies have conducted evaluations of the results from their
smoking control efforts. Several of these studies, along with some
anecdotal findings, are reported in this chapter's Appendix, "The
Economic Justification for No Smoking Policies."
To many companies, a reduction in the number or percent of
employees who smoke is benefit enough from a policy. Smokers
dropped from 21 percent of the workforce to 16 percent in two years
at UNUM Life Insurance Company. In addition, 87 percent of the
smokers reported they were smoking less after the policy was
implemented.6 At Pacific Northwest Bell, smokers dropped from 28
percent at the time the ban was implemented to just 20 percent of
employees two years later.
N
0
200 .41
O
N
N
CTI
N
O)
0
Draft - Do not cite or quote
Employee Involvement
Some companies, especially those wanting quick results that can be
controlled, develop smoking policies at the top executive or
management level and announce them to the employees. But a more
frequently seen pattern today involves employees in the process of
formulating and implementing a policy from the outset--but with
varying degrees of direction from management. Companies have found
that involvement of employees, including smokers, facilitates
compliance with the resulting policy.
In some companies, the involvement takes the form of responding to
a charge. For example, an employee committee might be asked to
examine the issues and problems related to smoking at the worksite
and to present to management within three months recommendations
for a policy and implementation plan to deal with them. In others,
management may decide that smoking is a serious health hazard to
its employees and that smoking is to be eliminated in 12 months.
This organization's charge to employees might be to review how
other companies have successfully moved to a smoke free workplace
and to present recommendations for steps the company should
tindertake during the next 12 months to make that transition both
smooth and as painless for smokers as possible.
Regardless of the approach, if employees are to be involved, it is
important that their contributions have meaning and be listened to
objectively by management.
When tracing the history of smoking policies in organizations, it
is not unusual to find that the initial push to limit or eliminate
smoking came not from management, but from the employees,
themselves.
At UNUM Life Insurance Company, employees' complaints, coupled with
a Maine law requiring employers to reduce smoking, resulted in the
company-wide ban. Pacific Northwest Bell emphasizes that no
company officer or executive advocated its move to implement a
smoking policy. Rather, the impetus came from employees. A grass
roots group conducted a survey of workers and eventually
recommended that PNW Bell ban smoking. The Employee Advisory
Council at Cardinal Industries' Sanford, Florida, plant initiated
the idea of a tough no smoking stand. (See "Case Studies--Cardinal
Industries and Pacific Northwest Bell")
At Holiday Corporation, Memphis, Tennessee, a task force of
employees developed a Clean Air Policy covering its headquarters
offices. The task force was originally set up as a Weilness
Committee a full year before work began on the smoking policy. The
employee group researched various aspects of the smoking problem
by gathering data, talking to other companies that had already done
201
N
O
~
O
N
N
CTt
N
0)
~L
Draft - Do not cite or quote
it, and working with the local cancer society and lung association.
A survey was conducted of all employees to identify their habits
and attitudes related to smoking. The task force, itself, created
the phased-in process that resulted in Holiday Corporation
headquarters and several of its subsidiary groups going smoke free
on January 1, 1987.
But the act of involving employees is not always as easy as it
might seem, according to Charles Nielson of Texas Instruments.
It is important to involve employees in the process of developing
a policy as early as possible, and a survey of their habits and
attitudes provides invaluable data to management, says Nielson.
Because TI has so many locations, however, timing of an employee
survey was sometimes very difficult; in some locations, the policy
had already been set by corporate headquarters before the attitude
survey could be conducted. As a result, some employees felt they
were being manipulated. "Data is vital to planning, but timing is
also important so that the company maintains its credibility,"
cautions Nielson.
Union Involvement
fn any unionized organization, consideration must be given at the
outset to how and when unions will be involved. Popular thinking
just a few years ago was that unions would block most company-
sponsored wellness efforts, particularly those that interfered with
individual lifestyle choices, such as smoking. But through the
work of several pioneering unions such as the Amalgamated Clothing
and Textile Workers Union, the United Steelworkers Union, and the
United Auto Workers, as well as the efforts of national groups
including the Workplace Health Fund, more and more labor groups are
willing to cooperate with management in reducing smoking if they
are approached properly--and early in the process.7
Unions also recognize that their membership reflects closely the
national averages, therefore the vast majority of their members do
not smoke. As a result, many unions are receiving increased
pressure from their membership to help control smoking in the
workplace. After having been involved in all aspects of policy
development, the Communications Workers of America sent a memo to
its 8,000 members at Pacific Northwest Bell acknowledging that the
company was implementing a smoking ban, but stating that CWA would
not oppose it because of the possibility that nonsmoking members
would sue the union--and probably win. (See "Case Studies:
Pacific Northwest Bell.")
In late 1985, the Workplace Health Fund, in cooperation with the
®ffice of Disease Prevention and Health Promotion, (US DHHS), held
a conference of union people to discuss the merits and value of
health promotion. One of the outcomes of the meeting was a set of
criteria for union involvement in worksite wellness efforts.
202
Draft - Do not cite or quote
Among the recommendations were two that placed heavy emphasis on
the need to have a good working relationship between the union and
management before attempting to implement any kind of wellness
program. "Worksites in which labor and management are not
cooperating to bring health and safety hazards under control should
not be sites for health promotion activities." In addition, "where
the worksite is not under control or the employer is uncooperative,
and where the union has established the need for health P romotion,
the programs should be conducted outside the worksite."
But for any unionized company considering a smoking policy, the
first step must be to look carefully at its union contracts,
particularly for any wording that might guarantee members the right
to smoke. If such agreements exist, the likelihood of the union
supporting a no smoking policy is slim.
Sue Pisha, area director of the northwest region of the
Communication Workers of America, believes that with motivational
information and education, there is the potential for unions to
eventually become a proactive force for nonsmoking policies.
"Policies seem to eliminate in-fighting," she says. "Withoiut a
.policy, the issue.is messy and polarizing."$
Education
A companion element of virtually every successful workplace no
smoking policy is an educational program designed to inform
employees about the new rules and to provide opportunities for
smokers to kick the habit. While behavior modification programs
are the most commonly presented, some companies have offered
innovative approaches such as acupuncture, hypnosis, self-help
materials, hot lines, incentives for nonsmoking employees to
encourage and assist their co-workers to quit, and multi-day
intensive programs for hard-core smokers.
Now that the nicotine in tobacco is widely recognized as an
addictive substance, in much the same way that alcohol and drugs
are considered addictive, other education techniques also have come
into use. They include aversion techniques such as satiation and
rapid smoking, relaxation training,9 coping skills training,
stimulus control, and nicotine fading.
In addition to on-site opportunities, businesses have gotten good
results by encouraging participation in community-sponsored stop
smoking classes merely by providing lists of sessions available
through reputable groups such as cancer and lung associations,
hospitals, Y's, and for-profit organizations.
Because quitting can be very difficult and often is greatly
enhanced by peer and family support, many companies make cessation
203
Draft - Do not cite or quote
opportunities available to spouses and other immediate family
members, as well. (See "Incentives.")
UNUM Life Insurance Company offers classes for a usually over-
looked group, nonsmokers. The classes are designed to help those
who do not smoke understand the problems faced by smokers trying
to quit and to urge them to encourage fellow workers to quit or to
refrain from smoking. At Rainier Bank, Seattle, Washington, stress
management classes were offered to help smokers adjust to the
policy as well as to assist those who were trying to quit.
While no national data are available on worksite quit rates, strong
worksite programs claim anywhere from 20 to 50 percent quit rates
after one year. However, most published studies report six-month
abstinence rates of 30.percent or less.10 As a result of an
intensive smoking cessation campaign, Johnson & Johnson, New
Brunswick, New Jersey, reports a two-year success rate of 23
percent of all smokers in the company, not just 23 percent of those
who went through a program or completed it.i1
Incentives
Piany companies go a step beyond offering cessation classes by
providing incentives for smokers to quit. Some also have devised
rewards.for non-smokers. The most widely used incentives for
smokers are monetary, often tied to completing a cessation program
and/or stopping smoking. Many companies offer cessation classes
free to employees and their families, often during company time,
or reimburse them for the cost of taking a community-based class.
Others, like the Utah State Department of Health, reward smokers
who actually quit. The "Healthy Utah" programs pays $25 to smokers
who quit at the end of three smoke-free months, another $225 after
six months, and $50 at the end of a year of not smoking.
Nonrnonetary incentives, too, can be appealing. Employees who
participated in a 24-hour "Cold Turkey" stop smoking day at MSI
Insurance, Arden Hills, Minnesota, became eligible for a drawing
for a frozen turkeyo Those who quit for six months were eligible
for a drawing for a free YMCA membership, and anyone who stayed off
cigarettes for a full year was eligible for a weekend vacation.13
Some companies also have gotten creative in finding ways to rereiard
employees who are nonsmokers or who quit before a policy goes into
effect. Employees who take a health risk appraisal at Westlake
Community Hospital, Melrose Park, Illinois, receive a $50 "bounty"
for participating plus several "good health bonuses" including $25
for not smoking. Weekly paychecks at Speedcall Corporation,
Hayward, California, include an extra $7.00 for those who do not
smoke at work. Backsliders who light up one week and lose their
reward are encouraged to get back quickly to not smoking; so the
next week without smoking earns the $7.00 bonus again.12
204
N
0
4
O
N
N
CJ1
N)
~
~
Draft - Do not cite or quote
Businesses also offer nonsmokers discounts on life and health
insurance, a very visible and tangible incentive to stop smoking
and improve health.
Smoking Policy Enforcement
Without a doubt, one of the most difficult questions asked by
companies considering a smoking policy is "How can a no smoking
policy be enforced?" The response from most businesses that have
moved to a ban is that the company must first demonstrate to
employees that it is serious about eliminating smoking in all or
parts of the building. Second, it must handle violations in the
same way that infractions of all other personnel policies are dealt
with.
Cardinal Industries had a highly visible and dramatic way of
demonstrating its commitment. Its president, Austin Gurlinger, a
cigar smoker, stated to all employees that he would refrain from
smoking at the workplace.
Uaking certain that each employee receives a copy of the policy in
advance of its implementation and posting signs clearly delineating
where workers may and may not smoke are small steps that can help
show a company's commitment to smoking controls and increase
compliance, as well.
Some companies are enforcing their no smoking policies by referring
employees who are unable to quit because they are addicted to
nicotine to an Employee Assistance Program. These companies may
apply the same enforcement guidelines to addicted smokers as they
do to users of alcohol or drugs, requiring that they overcome the
habit in order to remain with the company.
Most companies say that no employees have quit their jobs because
of the new rules. However, most also point out that a few have
"tested" the policy, with some pushing it all the way to probation.
According to Dick Becker, employee services representative for
American Family Insurance Group, "Some employees tested the waters,
sneaking cigarettes in the rest rooms. Supervisors let it be known
that smoking would be treated like any other violation of policy,
for example, inappropriate dress."6 Holiday Corporation follows
its usual procedure for violation of any company rule--first a
verbal warning, then a written warning, followed by a "final"
warning, and if necessary, termination.
But all agree, termination is not the objective. Everything
possible should be done to encourage employees to comply, and most
feel that peer pressure is the best policing mechanism. However,
when an employee continues to break the rules, he or she must be
205
Draft - Do not cite or quote
disciplined appropriately, or the entire policy will crumble. (See
"Case Studies.")
CASE STUDIES
The following case studies illustrate how four widely different
companies approached the development and implementation of a policy
to reduce or eliminate smoking within their organizations.
CARDINAL INDUSTRIES, INC.
Overall Policy: A total ban on smoking on any company property
exists; all new employees must attest to being nonsmokers.
Beginning January 1, 1987, the 8,650 employees of Cardinal
Industries were assured of a totally smoke free work environment.
One year prior to the ban, Cardinal, the nation's largest
manufacturer of modular homes, had taken an even more dramatic step
by instituting a multi-faceted policy that included hiring only
nonsmokers as new employees.
Benefits Anticipated
Although insurance carriers are saying it will take 12 to 18 months
to see any decrease in insurance rates, Cardinal's management
expects to significantly lower operating costs, increase
productivity, reduce absenteeism, and eventually pay lower
insurance premiums as a result of the new policy. Even more
importantly, it expects to improve the health of its key asset--
its human resources.
But employees at Cardinal's Sanford, Florida, location--one of four
regional sites throughout the country--are convinced they would
have gone smoke free even without the corporate edict. Why?
Because employees wanted it, and because management recognized the
negative impact of smoking on employees' health and productivity.
The passage of Florida's Clean Indoor Air Act in October, 1985,
focused attention on the plant's efforts and established it as one
of the most progressive worksite no-smoking policies in the state,
stimulating a letter of commendation from the governor.
Employee Involvement
Because of the nature of materials used at Cardinal, the second
largest residential builder in the country, the company had a long-
standing policy prohibiting smoking in its five manufacturing
plants. But at the Sanford location, the real push for a tough
206
Draft - Do not cite or quote
policy that extended beyond the manufacturing facility came through
its Employee Advisory Council in late 1985. Made up of employees
elected by the workers within each department, the Council meets
regularly with top management.
Based on employees' suggestions, a three-phase policy was developed
and implemented Jan. 1, 1986, that gradually eliminated smoking in
meeting rooms, the cafeteria, and other common areas over the next
12 months. As part of the policy, which was designed to make
Cardinal smoke-free by the end of the year, the company began
hiring only non-smoking personnel. Current employees' smoking
privileges (in designated areas) were grandfathered for the
remainder of the year.
But before the policy was implemented, it required approval by top
management, including the company's 33 year-old founder and
president who was a cigar smoker--a situation that has stopped many
other companies with good intentions. "We had been looking for
ways to reduce our health care costs and at the same time improve
efficiency and productivity," said a company spokesperson, "and the
evidence about the health consequences of smoking were too powerful
to ignore. When you add the fact that Cardinal pays for ;00% of
.employees' health insurance, the decision seemed inevitable."
Enforcement
In many ways, the fact that the chief executive at Sanford was a
smoker aided in convincing employees that the plant was serious.
The announcement that only nonsmokers would be hired and that there
would be no exceptions to the rule--even the president--helped
overcome one of company's biggest obstacles to successful
implementation...convincing employees that the company is serious
about the ban.
A second advantage Cardinal has in terms of enforcement is a highly
desirable work environment. It pays top benefits and offers
excellent working conditions. An employee must balance sacrificing
his/her smoking habit for eight hours each day with sacrificing a
job at Cardinal. So far, Cardinal has won every time. Not only
has no one quit, but the ban has not even been tested. "They know
we are serious, and if they test us, they must be willing to live
with the consequences." Management also believes that the long-
standing positive environment among employees and management has
contributed to the easy transition.
Education
During the 12 months between the announcement and the
implementation, various company-paid educational programs and
cessation classes were offered. In addition to regular stop
207
Draft - Do not cite or quote
smoking seminars provided after business hours, employees and their
families also were offered a hypnosis program, and for those who
felt they were addicted to smoking, an intensive two-day, off-site
treatment program was provided. FDA approved pharmaceuticals also
were offered as quitting aides. During the period preceding the
ban, smoking areas within the locations were gradually restricted
until, on January 1, 1987, the entire company became smoke free.
Blue Collar Workers
Although no survey has been taken to determine how many employees
have quit smoking, a survey taken before the ban was implemented
revealed that more white collar employees than blue collar workers
were smokers. At the Florida location, for example, some 40 to 45
percent of employees could be classified as "blue collar." But
partly because the manufacturing plants were always nonsmoking,
there has been no particular problem in implementation.
Off-Job Smoking
In a Position Paper discussing its policy, Cardinal Industries
states, "The program only concerns itself with smoking in the
workplace'and not what employees do on their own personal time.
Cardinal Industries never has, and never will try to regulate the
activities of its employees on their own personal time." Thus,
while Cardinal's application form asks prospective employees
whether or not they smoke, and while its policy prohibits the
hiring of smokers, no attempt is made to test employees or to check
on their off-work habits.
TEXAS INSTRUMENTS
Overall Policy: Smoking is prohibited in all owned and leased
facilities except in specific locations in each facility that
are designated as smoking areas and, to the extent possible, are
separately ventilated.
In late 1985 and early 1986, several of the 37 major sites of Texas
Instruments began implementing their own smoking policies as a
result of employee complaints and local' Clean Air legislation.
Rather than be faced with 37 different policies to implement, TI
made a decision to implement a single corporate-wide policy.
Employee Habits and Attitudes
Before embarking on policy development, TI surveyed its employees
to learn how many smoked and how they viewed worksite smoking
restrictions. About half of the more than 50,000 workers surveyed
208
Draft - Do not cite or quote
took the time to respond, revealing that 77 percent of TI employees
were nonsmokers or exsmokers, and that just 23 percent were current
smokers. Of those who smoked, over 40 percent said they wanted to
quit.
Corporate Obiectives and Policy
Before designing the Clean Air Policy, top corporate management
agreed on three objectives that would form its underlying
philosophy. There were to:
o provide a healthful and safe working environment;
o ensure high quality in all TI products; and
o initiate the company's clean air approach rather than be
forced to react to legislation (including the possibility of
legislation from many different states,and municipalities).
From these objectives grew TI's Clean Air Policy.
. "It is the goal of Texas Instruments to provide for its
employees a healthful and safe working environment. In accord
with this goal, Texas Instruments will prohibit smoking in all
TI owned and leased facilities, except for specific locations
in each facility which are designated as smoking areas."
Education and Training
To underscore the importance of the new policy, the eight-month,
phased=in implementation process took a top-down track, with the
President and CEO Jerry Junkins working directly with a key
operating manager and the personnel director from each location
th=ughout the organization. During the session, Mr. Junkins
emphasized the organization's complete commitment to the new
personnel policy and each individual manager's responsibility for
its successful implementation. These teams then headed up similar
training programs in their own locations. Training sessions were
conducted for selected managers using a centrally prepared manual
to ensure consistency among the.37 locations. Specially developed
brief video tapes offered all employeesI an introduction to'the
policy (3 minutes), briefed managers and supervisors on issues
related to- smoking (10 minutes), and assisted managers and
supervisors in learning techniques for resolving smoking-related
problems at the worksite (16 minutes).
Making every effort to assist smoking employees to prepare for the
new policy, TI provided company-paid smoking cessation programs on
company time during the initial phase-in of the clean air program.
Classes were scheduled to accommodate workers on all three shifts,
209
Draft - Do not cite or quote
and "maintenance sessions" were offered to provide additional
support.
More than 4,700 employees signed up for cessation classes,
representing 40 percent of the company's smokers--almost exactly
the percent that said they wanted to quit in the employee survey.
Of the group, 3,235 completed all the required classes (including
maintenance classes), with 1887, or 58 percent, reporting they had
quit by the end of the program.
As a further aid, a Tip Sheet, "How to Make Life Easier Until the
Next Cigarette Break" provided "some practical suggestions to help
you when you need to change your regular smoking routine." A "Wrap
Sheet: Daily Cigarette Count," designed to be wrapped around a pack
of cigarettes, offered an easy place to keep track of how much was
smoked, when and why, in the hope that the information would assist
the smoker in altering his/her habits.
However, all communication was not downward! Employees were given
opportunities to ask questions and voice concerns during
educational programs. Special attention was paid to employees
concerns and complaints in in-house communication vehicles, as
wel l .
Facilities Modification
Because TI chose to designate a limited number of areas in each
building as smoking areas rather than to completely ban tobacco,
it faced the problems of recirculating contaminated air. Thus,
where necessary and possible, facilities were modified to provide
separate ventilation. In addition, all cigarette machines were
removed from TI facilities and a decision was made that no new ones
would be installed.
Enforcement
TI made it clear from the beginning that a new personnel policy had
been established that would be monitored and enforced in the same
way as all other policies, such as attendance. Thus, anyone found
smoking in non-designated areas would be given an oral warning.
If there were no further problems, no 'further action would be
taken. However, with subsequent smoking incidents, the employee
would be given written guidance, followed by probation for
additional infractions, with termination as a final step. But TI
stressed to all supervisors that they should make every effort to
educate smokers about the importance of the policy, rather than to
be heavy-handed. After nine months, "two or three cases" have gone
to probation, but no one has been terminated because of smoking.
Considering that 50,000 to 60,000 employees are covered by the
210
Draft - Do not cite or quote
policy, this is an excellent record, says Charles Nielson, Vice
President and Manager of U.S. Employee Relations.
Advice: Keep Policy's Purpose in Perspective
Nielson cautions other companies considering establishing a no
smoking policy that one of the most difficult problems they face
will be keeping the desire to eliminate the health hazards of
smoking at the worksite in proper perspective.
TI made a corporate decision to eliminate smoking at the worksite
except in designated areas. The decision was a business decision,
not a moral or a value judgement. TI, which has 50 percent of its
business in semiconductors, is facing intense competition,
according to Nielson. Therefore, it must have productive
employees. And that means it must have good relationships with all
its employees. But smoking is an emotional issue for many people,
both smokers and nonsmokers. "I'm not sure those of us in the
personnel field have yet learned how to deal with this kind of
highly charged issue and still maintain our productivity," states
Nielson. "It takes a lot of hard work to achieve the desired
atmosphere of teamwork, rather than an adversarial relationship."
RAINIER BANK/RAINIER BANCORPORATION
Overall Policy: Following a one year phase in period, smoking
is banned in 411 200 domestic facilities and in car pool
vehicles.
In September, 1985, the 5,800 employees of Rainier Bancorporation's
U.S. facilities received a communication from their President, John
D. Mangels stating that "We are committed to insuring a healthful
and comfortable environment for all employees." As part of that
commitment, he announced, the corporation would become smoke-free
on October 1, 1986. As part of a transition plan, beginning
October 15, 1985, smoking would be restricted to designated areas,
and the company would sponsor and pay for smoking cessation classes
to assist employees who choose to quit.
Rainier Bancorporation is headquartered in Seattle, Washington,
with 200 offices in Washington, plus Alaska, Oregon, California,
Hawaii, Arizona, New York, and the Far East.
Health Threats, Employee Complaints, Legal Concerns Prompt Policy
According to Peter Broffman, personnel officer for Rainier Bank,
the major subsidiary of Rainier Bancorporation, the policy resulted
from three converging issues, the major one being a concern for
211
Draft - Do not cite or quote
employee health and wellness. Additional factors were an
increasing number of employee complaints about smoke in the
workplace, and the changing legal and regulatory climate. In July,
1985, the state of Washington had adopted a Clean Indoor Air Act
that prohibited smoking in public places, including public areas
of banks, and there was reason to believe that unless employees
acted on their own initiative, there might also be legislation
regarding private workspace. That, coupled with an increasing
number of court cases upholding the right of employees to have a
smoke free workplace, added impetus to the development of a policy.
Communications Vital to Implementation
once the decision was made to go forward with a phased-in ban,
communications with employees became a key link to successful
implementation. Emphasis was placed on the fact that Rainier was
prohibiting smoking at the workplace, not smokers.
Phase-In Period
During the transition period, managers were given discretion to
determine the most appropriate way to make the transition. The
company policy stated that "The needs and 'comfort level' of both
smokers and non-smokers should be considered during this period."'
Guidelines for Phase I stated, in part:
o All common areas, including lobbies, elevators, conference
rooms, hallways, libraries, rest rooms and computer rooms
will be smoke free.
o In open-office work environments, managers should use
discretion in deciding whether those areas should be smoke
free. Individual employees may, of course, designate their
assigned immediate work space as a no-smoking area.
o Employees with enclosed offices may designate their area as
a smoking or no-smoking area. However, the rights of non-
smokers who must come into an enclosed office to conduct
business should be respected.
o Lunchroom and lounge areas will be divided into areas for
smokers and non-smokers. Managers are given discretion to
divide the rooms as appropriate for their locale.
According to Broffman, there were relatively few difficulties in
the initial phase of implementation. The few problems that did
exist were due largely to differences in the ways various managers
chose to implement and police their smoking restrictions.
Occasionally disputes arose over what areas should be smoking and
212
Draft - Do not cite or quote
nonsmoking, especially in the smaller branch offices where there
were few options for allocating space. For the most part, Broffman
says, the problems were minor and easily resolved when the total
prohibition was enforced.
However, in retrospect Broffman believes that a shorter transition
period might have been more desirable. "A three to six month
phase-in period probably would have been adequate," he says.
"Many smokers go through a adjustment period. A few indicated that
putting off the inevitable ban for too long really isn't doing them
a favor because it prolongs the period of anxiety and allows them
to procrastinate in making the adjustment. Also, a shorter
transition emphasizes the resolve of the company to become smoke
free." In addition, any employees who want to defeat the policy
will use the entire phase-in period to rally support. A shorter
transition period would shorten the debate and lessen the
possibility that the detractors will succeed.
Enforcing the Ban
Phase II, the total smoking ban, was introduced in a low-key,
-matter-of-fact manner: a simple "reminder" that smoking would be
prohibited in all work areas. With the exception of minor, final
protests by a few "die-hards", employees accepted the new policy.
Rainier has received no formal complaints, has had no problem with
recruiting, and no one has resigned. The only complaint Broffman
is aware of is that a few employees who still smoke do so
immediately outside company building during breaks, and some
employees are concerned about the impression this gives to
customers entering the bank.
Because of its stance that Rainier is eliminating smoke, not
smokers, the organization makes no attempt to discriminate against
hiring smokers.
Bicrgest Obstacle to Policy: Fear
Broffman acknowledges that when the policy was first proposed,
there was concern on the part of a few senior manager of "What
might happen." Although the majority and the leadership of senior
management supported the policy, a few were initially concerned
that there could be mass defections, that disagreements about
smoking would cause major disruptions in work units, and that it
could turn into an "employee rights" issue. However, these things
did not happen at Rainier.
"We had more complaints from nonsmokers before the policy was
implemented than we got from smokers after it was enforced."
Broffman says. His advice to other companies considering a smoking
ban? "Do it! You can make it work!"
213
Draft - Do not cite or quote
PACIFIC NORTHWEST BELL
Overall Policy: Because of health concerns related to smoke,
PNB does not allow smoking in any company facility.
On October 15, 1985, Pacific Northwest Bell became the first large
company (15,000 employees in 750 buildings) to go completely smoke
free. Its policy is simple:
"To protect the health of PNB employees, there will be no smoking
in any company facility."
Options for Smoking Restrictions
Prior to the establishment of the policy, PNB had allowed each work
group to decide, itself, whether or not it would be a smoking area.
Problems arose, however, when adjacent work groups had differing
approaches. Smoke would drift around barriers, waft across no-
smoking desks, and generally infiltrate all areas of the building.
Smokers assigned to no smoking areas would merely walk into work
groups that permitted smoke, making the atmosphere even worse for
nonsmokers in the area. Difficulties occurred even within
individual units that voted to eliminate smoking. If 60 percent
voted to be a clean air area and 40 percent voted for smoking, the
question arose as to whether the wishes of four-out-of-ten
employees could really be ignored.
,
While this kind of democratic approach had initially sounded like
an easy way to avoid forcing a company-wide policy, it was seen as
unfair and inequitable by most workers. No one was really
satisfied and all the underlying problems still existed.
Eventually both managers and employees began exerting pressure on
PNB to develop a company-wide policy.
Employee Involvement
In January, 1983, a Smoking Issues Steering Committee was
established consisting of smokers, nonsmokers, and a group often
forgotten, former smokers. Employees representing their unions and
from the legal, health services, safety, and many operating
departments were part of the task force. One of its first
undertakings, an employee survey, brought an astonishing 74 percent
response rate, attesting to the importance of the issue among
workers. In addition to comments from those who were randomly
surveyed, 151 people who were not part of the survey group made the
effort to get copies from their friends so they, too, could have
their view heard. They included 135 nonsmokers and 16 smokers.
214
Draft - Do not cite or quote
Results of the 1983 questionnaire showed that 28 percent of PNB
employees smoked, but that the majority of employees were bothered
at least occasionally by smoke at the workplace, and almost 80
percent said the company should be concerned about smoking at the
worksite.
Two-and-one-half years after its inception--following a great deal
of research and discussion by the task force, as well as
involvement in the issue by numerous Quality of Work Life teams and
various ad hoc groups--the employee committee recommended to the
officers that smoking be eliminated at PNB.
Union Involvement
At PNB, unions were instrumental in all phases of policy
development. Not only were they included in the employee committee
making recommendations about a future policy, but leaders of both
unions were part of the June 1985 presentation to the company
president of the committee's recommendation. "They were not there
as advocates for a no smoking worksite," cautions Len Beil,
director of hum&n resources planning and employee involvement.
"They were present, rather, to state that they had been involved
in the process and what their positions would be on a strong
policy. While they did not endorse the complete elimination of
smoking in all buildings, they stated that their unions would not
formally fight its implementation, either."
Beil adds that tHe union members on the committee were "extremely
helpful" in all aspects of policy development, and that while they
never fought against the policy, they negotiated successfully for
several compromises that proved to be fair and beneficial for all
employees. Initially, the company wanted to reimburse employees
for smoking cessation classes after successful completion. The
union position was that PNB's goal was to assist and encourage
employees to live with the policy and comply with it--not necessary
to get them to stop smoking. Therefore, they pressed, the company
should reimburse totally for cessation classes, whether or not the
employee completed the series. On the issue of smoking in company
vehicles, union representatives stressed the difficulty of
enforcement and potential problems if cigarette butts were found
in a company car or truck ash tray. On both issues, PNB went with
the unions', requests. All employees got full reimbursement for
taking a cessation class and smoking in company vehicles is a
matter of "common courtesy." The unions also urged that any policy
be consistent throughout all company locations and for all
employees.
Education
215
Draft - Do not cite or quote
The day the policy was announced, which was 90 days before the
policy was to go in effect, PNB provided two telephone hot lines
to answer questions about the policy and provide information on
free cessation programs for employees and their dependents. 14 A wide
range of quit opportunities were made available, many on company
time, with PNB paying all fees following completion. But PNB also
garnered kudos from many employees by allowing them to take classes
outside the company and still get reimbursement. The ability to
choose their own quit method seemed to add to their commitment to
succeed and helped encourage a friendlier attitude toward the
policy.
Benefits
Within the first two years, 1,738 people had gone through cessation
programs--1,353 of them employees, 360 spouses, and 25 dependents-
-receiving full reimbursement from the company for a cost of about
$250,000. Is this investment worth it to PNB? "Yes," says Beil.
"It is money well spent. This equals the cost of just two or three
cancers cases. And.we would much rather pay for 1,738 to try to
quit smoking than pay the results of their continued habit."
Enforcement
PNB reports that there have been "no real problems" with
enforcement. On the first day, there were reports that one or two
people were smoking behind closed doors in several locations. But
"word got around" and by the second day they were abiding by the
rules. Although several people threatened to contact lawyers and
a few employees tried to organize a Smokers Rights day, nothing
significant came from any of the attempts to block implementation.
The bottom line: After two years, no one has quit because of the
no smoking policy, there have been no grievances, and smokers at
PNB have dropped from 28 percent to 20 percent in the two years
since implementation. All in all, the company views its no smoking
policy as an unqualified success.
StJMMARY
1. The movement of businesses to develop and implement smoking
control policies appears to be strong, and gaining momentum.
2. Employees and unions should be involved in the developement and
implementation of workplace smoking policies.
3. Enforcement of smoke-free workplace policies has not proved to
be a real problem for business.
216
Draft - Do not cite or quote
REFERENCES
1. Office of Disease Prevention and Health.Promotion, National
Survey of Worksite Health Promotion Activities, U.S.
Department of Health and Human Services, 1987, Washington,
DC.
2. The Washington Post, "Around the nation: Many firms limit
smoking," Washington, DC, February 23, 1988.
3. Hay/Huggins Benefits Report, November 17, 1989, Philadelphia.
4. American Lung Association, "Summary of results of the 1989
survey on public attitudes toward smoking," Nov. 1989, New
York.
5. Tripp, J, "Tobacco smoke disappearing in workplace: Employers
impose ban" The Oregonian, March 17, 1986.
6. Read, K. "Smoking bans: Corporate cold turkey," Corporate
. Fitness: The Journal for Employee Health and Weilness
Programs, Aug/Sept 1987.
7. Kaiser, J and Behrens, R, Health Promotion and the Labor
Union Movement, Washington Business Group on Health, July
1986. Washington, DC.
8. Smoking Pol-icy Institute, "Smoking policies and the unions."
1986. Seattle, WA.
9. U.S. Department of Health and Human Services, The Health
Consequences of Smoking: Nicotine Addiction--A Report of the
Surgeon General, 1988, Office on Smoking and Health,
Rockville, Md
10. U.S. Department of Health and Human Services, Office on
Smoking and Health. The Health Consequences of Smoking--
,Cancer: A Report of the Surgeon General. U. S. Government
Printing Office, Washington, DC. Secondary Source: Office
of Disease Prevention and Health Promotion, A Decision
Maker's Guide to Smoking at the Worksite, 1985.
11. Office of Disease Prevention and Health Promotion. A
Decision Maker's Guide to SmokincT at the Worksite. U.S.
Department of Health and Human Services, 1985..
12. Yenney, SL, Using Incentives to Promote Employee Health,
Washington Business Group on Health, 1985. Washington, DC.
13. Behrens, R. Reducing Smoking at the Workplace, Washington
Business Group on Health, 1985. Washington, DC.
217
Draft - Do not cite or quote
14. Bureau of National Affairs, Where There's Smoke: Problems
and Policies Concerning Smoking in the Workplace, Washington,
DC.
N
O
~
O
N
218
N
01
N
v
00
Draft - Do not cite or quote
CHAPTER 11, APPENDIX
IS THERE ECONOMIC JUSTIFICATION FOR
NO SMOKING POLICIES AT THE WORKSITE?
By Ruth Behrens*
Washington Business Group on Health
The health hazards of smoking--including smoking at the workplace-
-have been well documented. Smoking greatly increases an
individual's chances of contracting serious illnesses, such as
cancer, chronic bronchitis, emphysema, and coronary heart disease,
and of dying prematurely as a result of these diseases. There is
little doubt that smoking also has a significant economic impact.
It.-is estimated that businesses pay over $100 billion per year in
health care costs. A significant portion of this bill is the
result of smoking, and is paid out through insurance premiums for
employees, dependents, and retirees who smoke or breathe second-
hand smoke, as well as for nonemployees who smoke or breathe
others' smoke through programs supported by state and local taxes.
Zn other words, smoking is costing businesses a lot of money.
How much does smoking cost U.S. businesses? No one knows exactly.
But a growing list of researchers are tackling the difficult job
of attempting to identify these costs.
Costs of Smoking to the Nation
At least three major studies have addressed the question of what
smoking is costing the nation.
In 1978, Luce and Schweitzer estimated the economic costs of
smoking in the United States to be $47.6 billion. They further
broke this down to $811 per adult smoker, or $1.56 per pack of
cigarettes sold.~
In 1985, the Office of Technology Assessment, U.S. Congress (OTA),
estimated that smoking costs the nation about $65 billion per year
in lost productivity and health care costs alone. OTA estimates
that smoking-caused illness results in $43 billion in lost
productivity annually (or $1.45 for each pack of cigarettes sold),
expenses borne largely by employers. Businesses also pay a
significant portion of another $22 billion in smoking-related
health care costs, since nearly two-thirds of the costs are
incurred by those under 65. According to the OTA, combined lost
productivity and health costs related to smoking equal $2.17 per
pack of cigarettes sold.2
219
Draft - Do not cite or quote
Most recently in 1986, a group of researchers, which included the
former director of the government's National Center for Health
Statistics, concluded that smoking costs the United States at least
$53.7 billion each year in direct medical costs and salary losses
alone. These cost estimates were calculated by comparing the
health costs and income losses from smokers in excess of the same
amounts incurred by nonsmokers. The study concluded that smokers
are sicker and require more medical care than nonsmokers.3
The components of the $53.7 price tag were broken out as follows.
o Direct medical costs such as doctor bills, drugs, and
hospital and nursing home expenses were $23.3 billion more
for smokers than the average of nonsmokers.
o A total of nearly $9.3 billion was lost in salaries due to
smokers being sick with smoking-related diseases including
lung cancer, heart attacks, stroke, emphysema, and other
respiratory illnesses.
o In 1984, lifetime earning losses from smoking related deaths
were approximately $21.1 billion.
The authors characterize their findings as "conservative" since
they "did not take into account the adverse effects of passive
smoking, risks of abortions, stillbirths, and neonatal deaths, or.
deaths under age 20 that might be associated with smoking."
In their paper published in The Milbank Quarterly, Rice et al
translated all three of these studies to 1984 dollars. The result
is three analyses of the economic impact of smoking on the nation
that demonstrate enough similarity to underscore that smoking does,
indeed cost our country a staggering amount:'
o Luce & Schweitzer show a cost to the nation of $52.8 billion
per year in 1984 dollars;
o OTA, $62.2 billion in 1984 dollars; and
o Rice et al, $53.7 billion in 1984 dollars.3
Differing Methodologies Make Pinpointing Worksite Costs Hard
A number of researchers also have attempted to assess the specific
costs of smoking to businesses. But many problems arise when
attempting to identify one, or even a "best" methodology for
arriving at these costs.
Among the difficulties in conducting any study of the costs of
smoking is the fact that smokers differ from nonsmokers in several
genetic, social, and economic characteristics that may contribute
to disease. For example, the prevalence of smoking varies by race
(more blacks smoke that whites), education (fewer college graduates
220
Draft - Do not cite or quote
smoke than persons with only some high school), income (males with
lower income smoke more, while the opposite holds for women), and
occupation (blue collar workers smoke more than professional or
technical workers). If factors known to be related to health
status and smoking habits are not controlled, the impact of smoking
on health and the costs of smoking may be overstated.3
When examining smoking in the worksite, specifically, other
methodologic issues must be resolved. Marvin M. Kristein and
William Weis both published studies in the early 1980s identifying
the cost to business of each smoking employee. Kristein estimated
the cost in 1980 dollars to be between $336 and $601 per smoker
annually,4 while Weis placed the figure nearer $4500. These
findings are now outdated; in an article published in 1989,
Kristein has stated that "...the typical smoking employee in 1988
cost the typical employer at least $1000 in excess costs" compared
to a similar nonsmoker.6 However, a look at why their conclusions
differed 10 fold dramatically illustrates two points: 1) the
difficulty of pinpointing the cost of smoking to businesses, and
2) the wide range of business costs that can be affected by
environmental tobacco smoke.
Much of the rathe'r staggering discrepancy between the two studies
is attributable to their selection of different categories of costs
to include in the equation, the weight given each category, and the
salary assigned to the average smoker.
According to Weis, business costs in at least ten areas are
affected by smoking or smoking controls, including no smoking
policies: health insurance; incremental absenteeism; life and
disability insurance; fire, liability and industrial accident
insurance; ventilation and energy consumption for heating and air
conditioning; legal liability; property damage, depreciation and
maintenance; time lost to the smoking ritual, employee morale, and
corporate image.7 Kristein factors in health and life insurance,
fir~ losses, workers' compensation costs, absenteeism,
productivity, and occupational health costs. (In a 1984 article,
Kristein looked at only short-term costs and included fire,
accidents, ventilation, cleaning, productivity, and occupational
health risks.) g
To help illustrate the differences between Kristein and Weis's
total smoking-related costs, one can look at how each calculates
the costs of absenteeism to employers due to smoking.
Weis uses government data that shows a smoker is absent 2.2 days
per year more than a nonsmoker. Using $30,000 per employee as the
average annual wage and salary, including fringe and payroll taxes,
the- company pays approximately $120 per working day for every
employee on the payroll. Assuming a 25 percent return on payroll
dollars, the direct cost to the employer is $150 per absence,
excluding the cost of temporary replacements. According to this
221
Draft - Do not cite or quote
formula, the total cost per smoker per year due to absenteeism is
$310. A similar system is used by Weis in determining costs in
other categories.7
Kristein, on the other hand, used 1979 data showing smokers are
absent 33 to 45 percent more than nonsmokers, or 2.0 days more per
year, and assigns a daily salary of just $40.per smoker due to
smoking (versus $150 for Weis). Thus Kristein includes from $40
to $80 per smoker per year r attributable to absenteeism in his total
(versus $310 for Weis).
While Kristein's estimates are based on what he called "real
numbers" drawn from insurance companies, U.S. government
statistics, and detailed academic studies, he cautions, "We lack
meaningful 'case controlled' company comparisons of experience with
smoking employees versus nonsmoking employees...oIn general, the
emphasis is on underestimating the costs to business."9
Economic Impact of Smokers on the Worksite
ividence also shows that, in addition to excess absences of two or
more days per year, smokers exert other types of economic impacts
on businesses over their nonsmoking counterparts. Studies have
shown that:
o smokers have twice as many job related accidents as
nonsmokers.10
o Smokers are 50 percent more likely to be hospitalized than
those who do not smoke.
o Employers have been held legally responsible for at least
part of the disability cost for smoking employees who
contracted smoking related illnesses, in addition to claims
from nonsmoking employees who were adversely affected by the
smoke of others.
o Companies with certain occupational hazards can expect
greatly increased costs related to smoking. For example, an
asbestos worker who smokes is ten times more likely to die
prematurely than his nonsmoking coworkers. A smoking uranium
miner has six times the risk of contracting lung cancer as
a nonsmoker in the same job.4
In addition, many health consequences of smoking translate directly
into increased health care costs, since employers pay for a major
portion of these costs for their employees, dependents, and
retirees.
o Heavy smokers (two or more packs a day) are 15 to 25 times
more likely to die of lung cancer than nonsmokers, and
222
Draft - Do not cite or quote
overall, smokers are ten times more likely to die of lung
cancer than nonsmokers.12
o Eighty to 90 percent of such long term severe lung diseases
as emphysema and chronic bronchitis are related to smoking. 13
o It is estimated that 30 percent of all cancers are caused by
smoking. That means that38,000 Americans died of cancer in
1986 because of smoking. 13
o Heavy smokers are three to four times more likely to die of
cancer than nonsmokers and overall, the risk to smokers is
two times greater than for those who don't smoke.12
o More than 550,000 Americans will die of coronary heart
disease this year, and up to 30 percent of those deaths will
be attributable to cigarette smoking.
o Heavy smokers have a 200 percent greater risk of dying from
coronary heart disease than nonsmokers, and overall, the risk
for all smokers regardless of the amount smoked, is 70
percent greater than for those who don't smoke.1 4
o Evidence demonstrates that smoking during pregnancy has a
significant adverse effect upon the well being of the fetus
and the health of the newborn, including causing lower birth
weight infants and increasiong the risk of spontaneous
abortion and neonatal deaths.
o Children of smoking parents have increased prevalence of
respiratory symptoms and have an increased frequency of
bronchitis and pneumonia early in life.13
Two studies relate smoking directly with costly health-related
events, stroke and automobile accidents.
A study has concluded that smokers who quit can decrease their risk
of having a stroke by more than half when compared to those who
continue to smoke, thus cutting dramatically their potential health
care costs.15
A two-year study in Worcester County, Massachusetts, comparing the
motor vehicle driving records of smokers with nonsmokers found that
smokers had 50 percent more accidents than nonsmokers and 46
percent more traffic violations. The study identified several
reasons for the smokers' increased risk of being involved in costly
accidents and violations, including
o smokers' more frequent use of alcohol and drugs,
o smokers' greater risk-taking behavior, and
223
Draft - Do not cite or quote
o smokers' diminished attention to ~driving due to the
distractions associated with smoking.
Individual Companies Document Costs, Consequences of Smokincr
While studies conducted by individual companies have varying
degrees of validity, they do offer some further insights into the
price businesses pay for their smoking employees.
In a study of 40,000 employees at 27 locations of the Control Data
Corporation, CDC found that smokers cost the company substantially
more in health related costs than nonsmokers. The study, using
health data collected from 1981 to 1984, found:
o* Smokers of one pack of cigarettes per day or more generate
health claims 18 percent higher than nonsmokers.
o Smokers of one cigarette to one pack per day accrue claims
costs 10 percent higher than nonsmokers.
o Heavy smokers have 25 percent more inpatient days than their
counterparts who do not smoke.
o Heavy smokers are 29 percent more likely to have health
claims over $5,000 than those who do not smoke.17
One Los Angeles company estimates production losses alone at $675
per smoker per year. Adding longer term costs such as absenteeism,
premature death, and illness would raise the cost to at least
$1,000 per year for each smoker.' $
Provident Indemnity Life Insurance Company charges its smoking
employees the excess rate of their insurance coverage over that of
nonsmokers, an amount in the vicinity of $300 per year.19
Smoking and the Bottom Line
When viewed in the aggregate, these studies may appear to make a
compelling case for the potential of smoking control programs and
.policies to significantly cut long-term business costs. However,
a number of researchers, including health promotion and smoking
control advocates, point out that this conclusion may not be
justified. In some cases, the studies presented have significant
methodological problems or their underlying assumptions may be
flawedo Equally important, the total costs of developing and
implementing smoking control programs and policies, coupled with
the increased costs associated with longer life resulting from
quitting smoking (pensions, retiree and dependent health care
costs), may eliminate any financial gain for the company.
224
Draft - Do not cite or quote
Following are several examples and studies illustrating how these
supposed cost savings may not be what they initially appear to be.
As is pointed out in this appendix, many of the costs associated
with smoking can be attributed to characteristics of smokers (risk-
taking style, alcohol and drug use, low socioeconomic status).
However, it is unlikely that these basic characteristics would
change, even if the individual employee was induced to stop
smoking.
A portion of the supposed economic penalty associated with hiring
smokers results from an increase in absenteeism seen in employees
who smoke. Statistics indicate that people who smoke are eight
times more likely than nonsmokers to have alcoholism. Thus,
helping current employees stop smoking might not have the expected
effect on absenteeism, since in some, alcoholism also is a root
cause of the absenteeism.20
Some argue that smokers already are "paying their own way" through
cigarette excise taxes. In examining the lifetime costs that
smokers impose on others through collectively financed health
insurance, pensions, disability insurance, group life insurance,
fires, motor-vehicle accidents, and the criminal justice system,
Willard G. Manning, et al, conclude that on balance, smokers
probably pay for their own costs to society under the current level
of excise tax on cigarettes.21
According to Kenneth E. Warner,, Ph.D., a successful workplace
smoking cessation program will reduce certain health care costs,
life.insurance costs, disability costs, and absenteeism, and it may
increase productivity as well. "However," he adds, "one thing that
it is almost certain to do, by virtue of its success, is to extend
the lives of a subset of employees well into retirement, implyin
both pension and health care (and other) cost implications....11
~
Warner concludes that when all costs are taken into account--such
as, for example, the increased costs of pensions, health care, and
disability for retired workers who live longer because they stopped
smoking, versus the decreased costs for workers who continued to
smoke, die prematurely, and are replaced by a younger, less
expensive employee--businesses might very well conclude that, from
a purely economic point of view it may be cheaper to allow
employees to continue smoking.Z2 Louise Russe11,23 Thomas
Schelling,24 and others have come to similar conclusions based on
cost savings alone.
Individuals such as these, who debunk the idea that smoking control
programs will result in cost savings for businesses, do not,
however, conclude that it is in best the interest of businesses and
society to advocate smoking or to shun smoking control policies.
225
Draft - Do not cite or quote
There are obvious short term benefits of a smoke free workplace,
over and above the health-related savings Warner lists above. They
include reduced building and equipment cleaning and maintenance
costs, reduced costs from fire damage and insurance, reduced energy
consumption cost because of reduced ventilation needs, and reduced
turnover. In addition, there are the less tangible benefits of a
working environment that is perceived as being better by the
overwhelming majority of employees, as well as an improved company
image.
But for many, the potential of better health for employees, and of
eliminating or delaying the onset of degenerative or fatal diseases
is the most compelling reason to implement a company-wide smoking
control policy.
So the real bottom line for companies considering whether or not
to implement a smoking control policy or a smoking ban may not be
a simple dollars and cents formula. But rather, the bottom line
may be as pragmatic as the need to comply with local legislation,
or the desire to improve productivity, as paternalistic as the
desire to have happy, loyal employees, or as altruistic the desire
to "do the right thing" by providing the most healthful environment
for its employees. If costs savings follow, these companies may,
themselves, have received a bonus.
SLJ14MARY
1. Smoking in the workplace increases business costs because the
diseases of smoking increase absenteeism and hospitalization, and
may increase insurance, disability and legal dosts. However, these
costs may be offset by the longer lifespan of employees who quit
smoking as a result of workplace restrictions, increasing pension
costs to employers.
2. The most compelling reason to restrict smoking in the
workplace is the potential for better health for both nonsmoking
and smoking employees, by eliminating or delaying the onset of
degenerative or fatal diseases.
226
Draft - Do not cite or quote
REFERENCES
1. Luce, BL and SO Schweitzer, "Smoking and Alcohol Abuse: A
Comparison of their Economic Consequences," New England
Journal of Medicine 298, 569-571. 1978
2. Office of Technology Assessment, U.S. Congress. "Smoking-
Related Deaths and Financial Costs." (OTA Staff Memorandum).
1985 Washington, DC.
3. Rice, DP, TA Hodgson, P Sinsheimer, W Browner and AN
Kopstein. "The Economic Costs of the Health Effects of
Smoking, 1984" The Milbank Quarterly. Vol. 64 , No. 4, 1986.
Cambridge University Press.
4. Kristein, MM, "How Much Can Business Expect to Profit from
Smoking Cessation?" Preventive Medicine, 12, 358-381, 1983.
5. Weis, WL. "No Ifs, ands or Buts: Why Workplace smoking
should be banned" Management World, 339-44, Sept 1981.
b. Kristein,: MIIM, "Economic issues related to smoking in the
workplace." N.Y. State J Med. 89: 44-47 (1989).
7. Smoking Policy Institute, "The Costs of Smok ing in the
Workplace," 1986, Seattle, WA.
8. Kristein,MM "Wanted: Smoking Policies for the Work Place,"
Business and Health, Washington Business Group on Health,
Nov. 1984. Washington, DC.
9. Bureau of National Affairs, "Where There's Smoke: Problems
& Policies Concerning Smoking in the Workplace," 1986,
Washington, DC.
~
10. U.S. Department'of Health, Education and Welfare, Office on
Smoking and Health. Smoking and Health: A Report of the
Surgeon General. U.S. Government Printing Office, 1979,
11. Washington, DC.
American Lung Association, "Smoking at the Workplace:
The
Changing Legal Situation. More Facts & Features for
Nonsmokers & Smokers. 1983. New York, New York.
12. U.S. Department of Health and Human Services, Office on
Smoking and Health. The Health Consequences of Smokincr--
Cancer: A Report of the Surgeon General. U.S. Government
Printing Office. 1982. Washington, DC.
13. U.S. Department of Health and Human Services, Office on
N
Smoking and Health. The Health Consequences of Smoking-- 0
4
227 O
N
N
U1
N
00
j
Draft - Do not cite or quote
Chronic Obstructi.v Lung Disease: A Report of the Suraeon
General. U.S. GoVrernmeuit Printi"g Office, 1984. Washington,
DC.
14. U.S. Department of Health and Human Services, Office on
Smoking and Health. The Health Consequences of Smoking--
Cardiovascular Disease: A Report of the Surgeon General
U. S. Government Printing Office, 1983. Washington, DC.
15. Abbott, RD, et a., "Risk of Stroke in Male Cigarette
Smokers," New England Journal of Medicine, Sept. 18, 1986
315:717-20.
16. DiFranza, JR, et al, "The relationship of smoking to motor
vehicle accidents and traffic violations," New York State
Journal of Medicine, Sept. 1986.
17. Milliman & Robertson, Inc. Health Risk and Behavior: The
Impact on Medical Costs. 1987, Brookfield, WI.
18. Rice, DP and TA Hodgson, "Economic Costs of Smoking: An
Analysis of Data for the U.S.," presented at the Allied
Social Science Association annual meeting, San Francisco, CA
~ Dec. 28, 1983.
19. Behrens, RA. Reducing Smoking at the Workplace. Washington.
Business Group on Health. Oct 1985. Washington, DC.
20. Warner, KE, Wickizer, TM, Wolfe, RA, Schildroth, JE,
Samuelson, riH. "Economic implications of workplace health
promotion programs: review of the literature. J. Occ. Med.
30: 106-112 (1988).
21. Manning, WG, et al, "The Taxes of Sin: Do Smokers and
Drinkers Pay Their Way," Journal of the American Medical
Association Vol. 261, No. 11, March 17, 1989.
22. Warner, KE, "Selling Health Promotion to Corporate America:
Uses and Abuses of the Economic Argument," Health Education
Quarterly, Vol. 14, No. 1, Spring 1987.
23. Russell, LB, Is Prevention Better than Cure? Brookings
Institute, 1986, Washington, DC. .
24. Schelling, TC, "Economics and Cigarettes," Preventive
Medicine, Vol. 15, 1986.
--®----------®---------m--®®m--------------------------
* present address: 3026 East Marlette, Phoenix, AZ 85016
N
228 O
~
0
N
N
01
N
O
00
