Circulation, Vol 90, 1363-1367, Copyright © 1994 by American Heart Association
A Penn, LC Chen and CA Snyder
BACKGROUND: A number of epidemiologic studies have suggested that every
year environmental tobacco smoke (second-hand smoke) is responsible for
tens of thousands of deaths, mostly from heart disease, in the United
States. Environmental tobacco smoke is composed mainly (80% to 85%) of aged
and diluted sidestream smoke. The remainder is exhaled mainstream smoke.
Among the thousands of compounds that have been identified in environmental
tobacco smoke are a number of carcinogens, including polynuclear aromatic
hydrocarbon carcinogens, such as benzo(a)pyrene. We have demonstrated
previously that a number of carcinogens, including benzo(a)pyrene, promote
plaque development after injection into cockerels. There have been almost
no studies showing a direct stimulatory effect of environmental tobacco
smoke on plaque development. Recently we demonstrated that cockerels
exposed to sidestream smoke for approximately 0.4% of their projected
lifespan exhibited accelerated development of arteriosclerotic plaques. In
that study, cockerels in specially designed inhalation chambers were
exposed to the steady-state sidestream smoke from 5 cigarettes for 6 h/d
for 16 weeks. This level of exposure is high but environmentally plausible.
Statistically significant increases in plaque size were demonstrated in the
smoke-exposed cockerels. METHODS AND RESULTS: In the present study,
exposure levels were decreased by a factor of 5. Thirty cockerels were
exposed to the steady-state sidestream smoke from 1 cigarette for 6 hours
per day for 16 weeks. The smoke was mixed with filtered air. Ten control
cockerels were exposed to filtered air only. Levels of smoke surrogates,
including carbon monoxide and total suspended particulates, were measured
three times a day. Again, there was a statistically significant increase in
plaque size in the smoke-exposed cockerels. To place these studies within a
context of environmental relevance, levels of carbon monoxide were measured
independently over 1 to 3 hours in four bars where there was heavy smoking.
Measured carbon monoxide levels were as high or higher in the bars than
they were in the exposure chambers during the 1-cigarette sidestream-smoke
study. CONCLUSIONS: Experimental exposure to secondhand smoke at levels
equal to or even below those routinely encountered by people in
smoke-filled environments is sufficient to promote arteriosclerotic plaque
development.
ARTICLES
Inhalation of steady-state sidestream smoke from one cigarette promotes arteriosclerotic plaque development
Nelson Institute of Environmental Medicine, New York University Medical Center, Tuxedo 10987.
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