Circulation, Vol 83, 1-12, Copyright © 1991 by American Heart Association
SA Glantz and WW Parmley
The evidence that ETS increases risk of death from heart disease is similar
to that which existed in 1986 when the US Surgeon General concluded that
ETS caused lung cancer in healthy nonsmokers. There are 10 epidemiological
studies, conducted in a variety of locations, that reflect about 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 significant dose-response effect, with greater exposure to
ETS associated with greater risk of death from heart disease. These
epidemiological studies are complemented by a variety of physiological and
biochemical data that show that ETS adversely affects platelet function and
damages arterial endothelium in a way that increases the risk of heart
disease. Moreover, ETS, in realistic exposures, also exerts significant
adverse effects on exercise capability of both healthy people and those
with heart disease by reducing 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. Of
note, the cardiovascular effects of ETS appear to be different in
nonsmokers and smokers. Nonsmokers appear to be more sensitive to ETS than
do smokers, perhaps because some of the affected physiological 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
long-term exposure to the toxins in cigarette smoke. In any event, these
findings indicate that, for cardiovascular disease, it is incorrect to
compute "cigarette equivalents" for passive exposure to ETS and then to
extrapolate the effects of this exposure on nonsmokers from the effects of
direct smoking on smokers. These results 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 adverse effects on the cardiovascular system, leads 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; these deaths contribute greatly to the estimated 53,000 deaths
annually from passive smoking. This toll makes passive smoking the third
leading preventable cause of death in the United States today, behind
active smoking and alcohol.
ARTICLES
Passive smoking and heart disease. Epidemiology, physiology, and biochemistry
Department of Medicine, University of California, San Francisco 94143- 0124.
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