Inhalation of sidestream cigarette smoke accelerates development of arteriosclerotic plaques.
Author(s) -
Arthur Penn,
C A Snyder
Publication year - 1993
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.88.4.1820
Subject(s) - sidestream smoke , tobacco smoke , medicine , carcinogen , cigarette smoke , passive smoking , smoke , inhalation , smoke inhalation , inhalation exposure , third hand smoke , toxicology , pathology , environmental health , chemistry , anesthesia , biochemistry , biology , organic chemistry
Environmental tobacco smoke has been blamed for approximately 40,000 excess deaths from heart disease annually in the United States. As yet, no pathophysiological process that could be responsible for these deaths has been identified. Environmental tobacco smoke is composed mainly of aged and diluted sidestream smoke but also contains 15% to 20% exhaled mainstream smoke. Carcinogens, including nitrosamines and polynuclear aromatic hydrocarbons, are present in mainstream smoke and sidestream smoke. Carcinogen levels in sidestream smoke, unlike those in mainstream smoke, are not reduced in filtered cigarettes. The US Environmental Protection Agency has designated environmental tobacco smoke as a human (class A) carcinogen. In cockerels, subtumorigenic doses of polynuclear aromatic hydrocarbons carcinogens accelerate aortic arteriosclerotic plaque development.
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