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Despite exposure levels estimated to be equivalent to smoking only 0. 1-1.0 cigarettes per day, exposure to environmental tobacco smoke (ETS) is estimated to increase the risk of death from coronary heart disease (CHD) between 25 and 35% above the risk of nonexposed persons. This surprisingly large risk associated with a seemingly small exposure has raised doubts about the validity of attributing the increased CHD risk to ETS exposure. This paper reviews various biases that have been hypothesized to account for the increased CHD risk associated with ETS in the epidemiologic studies and characterizes the adverse effects of ETS on thrombosis, vascular endothelium, and exercise tolerance observed in experimental studies of humans and laboratory animals. None of the identified factors that has been proposed to introduce a spurious association between ETS and heart disease seem to invalidate the epidemiologic findings, either separately or in combination. In addition, experimental studies of ETS and heart disease demonstrate that acute exposure of humans and other species to ETS affects platelet function, vascular endothelium, and myocardial exercise tolerance at exposure concentrations widely prevalent in the workplace. Because exposure to ETS affects multiple physiologic pathways, it appears biologically plausible that ETS could cause the substantial increase in CHD risk that has been observed in epidemiologic studies.

environmental health perspectives

Why is environmental tobacco smoke more strongly associated with coronary heart disease than expected? A review of potential biases and experimental data.