Inhalation of sidestream cigarette smoke accelerates development of arteriosclerotic plaques

• Published in: Circulation (New York, N.Y.) N.Y.), 1993-10, Vol.88 (4), p.1820-1825
• Main Authors: PENN, A, SNYDER, C. A
• Format: Article
• Language: English
• Subjects: Animals; Aorta, Abdominal - pathology; Aortic Diseases - etiology; Aortic Diseases - pathology; Arteriosclerosis - etiology; Arteriosclerosis - pathology; Atherosclerosis (general aspects, experimental research); Atmosphere Exposure Chambers; Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Chickens; Male; Medical sciences; Time Factors; Tobacco Smoke Pollution - adverse effects
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.cir.88.4.1820

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. To determine whether sidestream smoke inhalation affects arteriosclerotic plaque development, we exposed cockerels to sidestream smoke (n = 30) or to filtered air (n = 12) in inhalation chambers for 6 hours per day, 5 days a week from 6 to 22 weeks of age (0.4% of projected lifespan). Chamber levels of carbon monoxide, total suspended particulates, and nicotine were measured regularly during the exposures. The abdominal aorta from each cockerel was cut into 10 segments, and the plaque index (mean plaque cross-sectional area [mm2]/mean luminal circumference [mm] x 100) was calculated for each segment. There were no differences in plaque incidence or distribution between sidestream smoke-exposed and control cockerels; however, plaque indexes were significantly greater for sidestream smoke-exposed than control cockerels in all segments. Thus, relatively brief exposures to sidestream smoke early in life are sufficient to enhance arteriosclerotic plaque development.