Philip Morris
Environmental Tobacco Smoke: A Compendium of Technical Information
Fields
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- Brunnemann, K.D.
- Haley, N.J.
- Hoffman, D.
- Mccarthy, J.
- Miesner, E.
- Samet, J.M.
- Shopland, D.
- Spengler, J.D.
- Haley, N.J.
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- American Lung Assn
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- Harvard School of Public Health
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- Natl Research Council
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- NCI, Natl Cancer Inst
- Office of Disease Prevention + Health Pr
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- Smoking + Tobacco Control Program
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- Akiba, S.
- Ames, B.N.
- Axelrad, R.
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- Behrens, R.
- Bennett, G.L.
- Best
- Biener, L.
- Borelli, T.
- Breslow
- Brownson, R.C.
- Brunnemann, K.D.
- Burrows
- Butler, C.
- Cain, W.S.
- Cano, J.P.
- Cederlof
- Chan, W.C.
- Chilcote, S.D., J.R.
- Correa, P.
- Coultas, D.B.
- Curvall, M.
- Dalager, N.A.
- Davis, J.W.
- Davis, R.
- Derrick, J.C.
- Dillon, H.
- Dockery, D.W.
- Doll, R.
- Dorn
- Dunn
- Dzubay, T.G.
- Effenberger, E.
- Elliott, L.P.
- Enstrom, J.E.
- Everson, R.B.
- Ferris, B.G., J.R.
- Feyerabend, C.
- First, M.W.
- Fischer, T.
- Foliart, D.
- Friberg
- Fung, S.C.
- Gao, Y.T.
- Garfinkel, L.
- Garland, C.
- Gillis, C.R.
- Glantz, S.A.
- Greenberg, R.A.
- Grufferman, S.
- Haley, N.J.
- Hammond, K.
- Harlos, D.P.
- Harmsen, H.
- Hill
- Hiller, F.C.
- Hinds, W.C.
- Hirayama, T.
- Hoffman, D.
- Hoffmann, I.
- Horn
- Hrubec
- Humble, C.G.
- Ingebrethsen, B.J.
- Jarvis, M.J.
- Josie
- Ju, C.
- Kabat, G.C.
- Kahn
- Keith, C.H.
- Klus, J.
- Knoth, A.
- Koo, L.C.
- Kristein, M.
- Kuhn, H.
- Kusama, M.
- Lam, T.H.
- Langone, J.J.
- Leaderer, B.P.
- Lebowitz
- Lebret, E.
- Lee, P.N.
- Letz, R.
- Lewtas, J.
- Linden
- Lorich
- Lowrey, A.H.
- Luck, W.
- Matsuki, T.
- Matsukura, S.
- Mccarthy, J.
- Mcginnis, M.
- Mcintosh, H.
- Meyer, M.
- Miesner, E.
- Miller, G.H.
- Morosco, G.
- Moschandreas, D.
- Mudarri, D.
- Muramatsu, M.
- Nau, H.
- Novotny, T.E.
- Parmley, W.W.
- Pathak, D.R.
- Pattishall, E.N.
- Pechacek, T.
- Pershagen, G.
- Peto, R.
- Pike, M.C.
- Porstendorfer, J.
- Prestonmartin, S.
- Quackenboss, J.J.
- Quant, F.R.
- Repace, J.L.
- Ritchie, C.
- Rogot
- Rothman, K.J.
- Rowe, D.R.
- Russell, Mah
- Sakuma, H.
- Samet, J.M.
- Sandler, D.P.
- Schmeltz, I.
- Schraub, A.
- Schwartzbickenbach
- Sears, S.B.
- Sepkovic, D.W.
- Shimizu, H.
- Shopland, D.
- Slade, J.
- Slattery, M.L.
- Spengler, J.D.
- Stadler, B.
- Stevens, R.K.
- Suguwara, S.
- Surgeon General
- Tosteson, T.D.
- Trichopoulos, D.
- Wald, N.J.
- Walker
- Wallace, L.A.
- Weber, A.
- Weir
- Weiss, S.T.
- Wells, A.J.
- Whitby, K.T.
- Wilcox, A.J.
- Wu, A.H.
- Wynder, E.L.
- Yamaguchi, K.
- Yamasaki, E.
- Ames, B.N.
- Document File
- 2040225000/2040225584/Epa Technical Compendium
- Litigation
- Stmn/Produced
- Author (Organization)
- Ahf, American Health Foundation
- Harvard School of Public Health
- NCI, Natl Cancer Inst
- Smoking + Tobacco Control Program
- Univ of Nm
- Harvard School of Public Health
- Master ID
- 2040225004/5288
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that of the nonsmoker. At the other extreme, even light smokers,
who consume only 1-9 cigarettes per day, see a quadrupling of the
risk of lung cancer.
An inverse dose-response relationship exists between an early
age of regular smoking and lung cancer mortality. In the U.S.
Veterans Study, those smokers who started smoking in their early
teens had substantially higher lung cancer death rates than those
who started in their late teens or twenties (Figure 3). Those who
began smoking before age 15 experienced a 19-fold greater lung
cancer mortality, compared to a slightly greater than 5-fold excess
risk for those who initiated their behavior after age 25.
These results demonstrate that a dose-response relationship
exists for exposure to the carcinogens in cigarette smoke and the
risk of death from lung cancer: the greater the lifetime exposure
to tobacco smoke, the greater the risk.
Further evidence for the existence of a dose-response
relationship comes from follow-up of people who stop smoking and
so remove the exposure from the carcinogenic agents in mainstream
smoke. When an individual stops smoking, his or her lung cancer
risk declines relative to the continuing smoker. After about 15
years off cigarettes the former smoker's lung cancer risk
approaches that of the life-long nonsmoker. However, it appears
that some excess risk may be carried throughout life. This
residual risk is strongly influenced by the individual's total
lifetime exposure to the agent and the total number of years of
smoking cessation.
The presence of a dose-response relationship between smoking
and lung cancer, combined with the fact that there are significant
elevations in risk associated with even the lowest levels of
smoking, demonstrates that there is no threshold for the
carcinogenic effects of cigarette smoke. This result from active
smokers is consistent with the observed elevations of lung cancer
risk among nonsmokers exposed to ETS.
Coronary Heart Disease
In contrast to cancer, in which.smoking produces the disease
through the cumulative effects of long term exposure to the
carcinogens and co-carcinogens in the smoke, smoking effects the
cardiovascular system immediately as well as over the long term.
The carbon monoxide in the smoke reduces the oxygen carrying
capacity of the blood by binding to hemoglobin competitively with
oxygen. Nicotine is a vasoconstrictor, which increases blood
pressure and narrows coronary arteries. Smoking causes release of
catecholamine, which increase blood pressure and heart rate.
Smoking also increases platelet aggregation and adhesion, which
contributes to the development of atherosclerosis. All these
11
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effects occur immediately upon smoking and resolve relatively
quickly after stopping smoking. As a result, one year after
stopping smoking, the excess risk of death from heart disease falls
by half; the same drop in risk for lung cancer takes 10 years. As
with cancer, these effects exhibit a dose-response relationship,
with greater more smoking and smoking in combination with other
heart disease risk factors, increasing the risk of death from
coronary heart disease. As with cancer, there is no threshold for
these effects, so the effects of active smoking on the heart and
cardiovascular system support the biological plausibility of the
observed effects of ETS on the heart.
Coronary heart disease (CHD) continues to be this nation's
leading cause of death, and for nearly 20 years, medical research
has shown that smoking is one of the major independent risk factors
or causes of CHD (along with high blood pressure and high
cholesterol levels). In the final report of the Pooling Project,
an interaction between smoking and other risk factors was observed
(Figure 4). Each independent risk factor contributed about the
same increased level of risk, however, when two or more factors
were present, the risk of a major CHD event was increased beyond
the sum of the independent risk -- thus, synergistic effect was
created when two or more risk factors were present. Overall,
smokers have a 70% greater CHD death rate, a two- to fourfold
greater incidence of CHD, and a two- to fourfold greater risk for
sudden death than nonsmokers.
Dose-response relationships between cigarette smoking and CHD
mortality have been demonstrated for several measures of exposure
to cigarettes, including the number of cigarettes smoked per day,
the depth of inhalation, age at which smoking began, and the number
of years of smoking. Smoking cigarettes with reduced yields of tar
and nicotine does not reduce CHD risk, probably because these
cigarettes do not have reduced yields of carbon monoxide and other
combustion products which affect the cardiovascular system.
The independent risk of CHD for smoking is greater at the
younger age groups although the greatest number of excess CHD
deaths due to smoking actually occurs in the older age groups
(Figure 5). Smoking has also been shown to increase the risk for
other cardiovascular diseases, including peripheral vascular
disease, cerebrovascular disease (at younger age groups), and
aortic aneurysms. For women, smoking can interact with oral
contraceptives to greatly increase the risk factor for fatal and
nonfatal myocardial infarction and subarachnoid hemorrhage.
Smokers exhibit more atherosclerosis, both in the aorta and
coronary arteriese Cigarette smokers who continue to smoke
following transluminal coronary angioplasty appear more likely to
require repeat angioplasty than nonsmokers, suggesting that the
effects of smoking on atherosclerosis occur quickly. The
polycyclic aromatic hydrocarbons which result from the combustion
12
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of the smoking materials contribute to these effects. The
increase in platelet adhesion observed in smokers also contributes
to the development of atherosclerotic plaque.
Cigarette smoking aggravates the conditions of people with
CHD. Smokers have a more difficult course following coronary
artery bypass surgery. Smokers who experience angina pectoris have
a higher risk of death than nonsmokers, a poorer prognosis
following non-fatal myocardial infarction, and a greater risk of
sudden death. Smoking increases the risk of silent ischemia in
patients with stable angina.
Many public health estimates place the total number of excess
cardiovascular disease (including stroke) deaths due to smoking to
be.greater than those due to cancer (Figure 1). Up to 30 percent
of all CHD deaths may be due to cigarette smoking and its
interaction with other risk factors.
These effects all exhibit a dose-response relationship with
no threshold in active smokers, with detectable damage even among
light smokers. These facts support the biological plausability of
the evidence linking ETS with heart disease in nonsmokers.
" Nonmalignant Respiratory Diseases
In addition to causing lung cancer, smoking causes or
aggravates several related nonmalignant respiratory diseases,
including emphysema, asthma, chronic bronchitis, and chronic
obstructive pulmonary disease (COPD). While the number of
sZnoking-induced deaths classified due to chronic obstructive
pulmonary disease (COPD) is smaller than for cancer or
cardiovascular disease (Figure 1), COPD afflicts about 12 million
Americans. Even if not fatal, COPD and related disorders such as
emphysema severely debilitate the victim and represent a
substantial number of people who become disabled due to their
condition, unable to work or even seek employment.
~
For many years cigarette smoking has been known to increase
the risk of developing and dying from COPD. Even the first Surgeon
General's Report issued in 1964 identified a causative role between
smoking and chronic bronchitis. As with lung cancer, the risk of
contracting and dying from COPD is substantially elevated among
smokers (Figure 6) and this risk increases with an increased dose
of cigarette smoke received; as with the other smoking-induced
diseases discussed in this chapter, there is :a positive dose-
response relationship. Mortality rations for COPD in smokers
versus nonsmokers are very high, exceeding 30 to 1 for heavy
smokers (Figure 7).
Smoking also has a dramatic effect on lung function. The
normal rate of lung function decline with increasing age is
accelerated in cigarette smokers (Figure 8). These effects
13
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probably reflect damage to the small airways of the lungs as well
as a thickening and increased reactivityof the airways in response
to chronic exposure to the irritants in cigarette smoke. The
volume an individual and exhale in one second of forced expiration
(FEVj) is a measure of small airway function. Figure 9 shows that
FEV9 falls in a dose-dependent manner as the amount of smoking
increases. There is no safe level of exposure: there is a
measurable decrement in pulmonary function even among light
smokers.
Stopping smoking partially reverses the nonmalignant effects
of the respiratory system (Figure 8). When one stops smoking, the
decline in lung function with age resembles that of a nonsmoker,
but a permanent decrement in lung function remains, indicating some
permanent damage. The amount of this permanent deficit depends on
the duration and intensity of smoking.
ETS exposure produces similar, but more modest nonmalignant
pulmonary effects. FEV1 is reduced in passive smokers among both
children and adults to levels similar to that observed in light
smokers. Children of parents who smoke develop more asthma,
bronchitis and other respiratory problems. The rate of lung
development in children exposed to ETS is smaller than that of
unexposed children. These effects of ETS are what one would expect
based on the effects of active smoking.
conclusions
This chapter has reviewed the effects of active smoking in on
those cancers, heart disease, and nonmalignant pulmonary diseases
which have also been identified with passive smoking. In each
case, cigarette smoking significantly increased the risk of disease
in smokers in a dose-dependent manner. There is no evidence of a
threshold level for adverse effects. Because ETS is similar to
(but more toxic than) mainstream smoke, these effects on the smoker
help provide evidence for the biological plausibility for the
epidemiological evidence linking ETS with lung cancer, heart
disease, and nonmalignant respiratory disorders, after accounting
for the lower dose the involuntary smoker receives.
1. There is a dose-response relationship between exposure to
tobacco smoke and the diseases of smoking.
2. There are no discernable thresholds of exposure for the diseases
of smoking.
3. Adverse health effects observed in smokers provide biological
plausibility for the occurrence of those diseases in nonsmokers.
14
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TABLES AND FIGURES, CHAPTER 1
N
Q
~
~
2- Q
N
- W
US Deaths Attributed to Srnoking in 1985
Source: US Surgeon General, 1989
CVD
28000
Cancer, lung
106000
30000
Vzoszz9'Pfl~
Draft - Do not cite or quote
~-~ Zy, ----
I
0s
Men
6005 1000% 16005 2000% 26005
' Cwrent Smoker --~ Former Smoker
3000%
0%
600%
1000%
16005
= Ourrent Smokrtr ''GFormer Smoicer
2000s
EZGURE 2 c Percent increased cancer morality risk, by site and qender, in current and former smoke,a
as deri ed fron: the
American Car.cer Socir.ty 50-State Study.
Draft - Do not cite or quote
Ndrle
At1 SM
410 14-19 20
Nos at c1garettes daJly
,
FIGURE 3.
(1989 SURGEON GENERAL'S REPORT, p. 49)
21-30
310
FIGURE 4.
Lung cancer' mortality ratios for males, by age
began smoking - U.S. Veterans' Study
20
<
18.7
0
Q
0
Ct
(D
4Z aSZZa~ ~?; ,
FIGiUR4 5.
Major risk factor combirrations,10-year
incidence of first major coronary events,
men age 30-59 at entry, Pooling project
w
200
SM
Only
C or ti
Only
SM&C C&H
or (No SM)
SM&H
189
None
of 3
AII 3
to
0
rt
0
~.
rt
Risk Factor Status at Entry ~
SM =smokerB C = cholesterol, H = hypertension
®
~
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