1,3 Butadiene, a Vapor Phase Component of Environmental Tobacco Smoke, Accelerates Arteriosclerotic Plaque Development

Background Our recent results support predictions from epidemiology studies that thousands of excess heart disease–related deaths result yearly in the United States from involuntary exposure to environmental tobacco smoke (ETS). Limited exposures of cockerels to ETS significantly accelerate arteriosclerosis. Despite little direct in vivo support, tar fraction rather than vapor phase compounds are considered largely responsible for the plaque-promoting effects of cigarette smoke. Here, we evaluate the effects of two ETS components on plaque development: the vapor phase component, 1,3 butadiene, and the tar component, the tobacco-specific N-nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). At relatively high doses, injected NNK is carcinogenic in rodents. Epidemiology studies have identified increased mortality from arteriosclerotic heart disease among black men working in the butadiene rubber industry. Neither butadiene nor NNK has been tested experimentally for a possible role in plaque d...