1993CirculationRequires access

Inhalation of sidestream cigarette smoke accelerates development of arteriosclerotic plaques.

APenn, C ASnyder

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Abstract

BACKGROUNDEnvironmental 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.METHODS AND RESULTSTo determine whether sidestream smoke inhalation affects arteriosclerotic plaque development, we exposed cockerels to side...

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BACKGROUNDEnvironmental 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.METHODS AND RESULTSTo determine whether sidestream smoke inhalation affects arteriosclerotic plaque development, we exposed cockerels to side...

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Available abstract

BACKGROUNDEnvironmental 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.METHODS AND RESULTSTo determine whether sidestream smoke inhalation affects arteriosclerotic plaque development, we exposed cockerels to side...

Key concepts: Sidestream smoke, Carcinogen, Tobacco smoke, Cigarette smoke, Medicine, Inhalation, Smoke, Passive smoking

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Inhalation of sidestream cigarette smoke accelerates development of arteriosclerotic plaques. — Research Paper | ScholarLens