Penn A, Chen L C, Snyder C A
Nelson Institute of Environmental Medicine, New York University Medical Center, Tuxedo 10987.
Circulation. 1994 Sep;90(3):1363-7. doi: 10.1161/01.cir.90.3.1363.
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.
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.
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.
多项流行病学研究表明，在美国，每年环境烟草烟雾（二手烟）导致数万人死亡，其中大多数死于心脏病。环境烟草烟雾主要（80%至85%）由老化和稀释的侧流烟雾组成。其余部分是呼出的主流烟雾。在环境烟草烟雾中已鉴定出的数千种化合物中，有多种致癌物，包括多环芳烃致癌物，如苯并(a)芘。我们之前已经证明，包括苯并(a)芘在内的多种致癌物，在注射到公鸡体内后会促进斑块形成。几乎没有研究表明环境烟草烟雾对斑块形成有直接刺激作用。最近我们证明，暴露于侧流烟雾约其预期寿命0.4%时间的公鸡，动脉粥样硬化斑块发展加速。在该研究中，将特制吸入室内的公鸡每天暴露于5支香烟的稳态侧流烟雾中6小时，持续16周。这种暴露水平较高，但在环境中是可能出现的。暴露于烟雾的公鸡斑块大小有统计学意义的显著增加。
在本研究中，暴露水平降低了5倍。30只公鸡每天暴露于1支香烟的稳态侧流烟雾中6小时，持续16周。烟雾与过滤空气混合。10只对照公鸡仅暴露于过滤空气中。每天测量三次烟雾替代物水平，包括一氧化碳和总悬浮颗粒物。同样，暴露于烟雾的公鸡斑块大小有统计学意义的显著增加。为将这些研究置于环境相关背景下，在四个重度吸烟的酒吧中独立测量1至3小时的一氧化碳水平。测量的酒吧一氧化碳水平与1支香烟侧流烟雾研究中暴露室的水平一样高或更高。
实验性暴露于二手烟的水平等于甚至低于人们在烟雾弥漫环境中通常遇到的水平，就足以促进动脉粥样硬化斑块的发展。
