Background—A review by Glantz and Parmley published in 1995 and subsequently widely cited claims to demonstrate that passive smoke exposure increases the risk of heart disease. We have critically examined this claim in the light of the published evidence which they cite and of more recent publications.Methods and results—An updated review of the epidemiological evidence reveals no association between heart disease and ETS exposure in the workplace. Claims of an association with spousal smoking are weakened by the existence of various forms of bias in the studies. They are also undermined by recent reports from three large studies without evident major weaknesses which find essentially no association with spousal smoking. Interpretation of the experimental clinical studies is problematic because it is not possible to expose humans to ETS without their knowledge. For several reasons, short-term effects of exposure to unrealistically high concentrations of ETS throw no useful light on risk of coronary atherogenesis from long-term realistic exposure. In particular, the fact that humans can adapt to reduced ambient oxygen availability needs to be allowed for. Effects of counts of anuclear endothelial cell carcasses in circulating blood after ETS exposure are uninterpretable without basic information on the significance of this endpoint. The need for a realistic animal model for coronary atherosclerosis is not fulfilled by short-term studies in rats, rabbits, hamsters, birds or dogs in which aortic atheromatous plaque formation is used as a surrogate endpoint. Stress from confinement within cages, from the noise of fans and from irritation from high ETS concentrations needs to be controlled for, particularly in experiments on rabbits and birds. This has not been done and there is generally a serious dearth of information on the non-specific or specific effects of other environmental chemicals on many of the endpoints that have been used.Studies on the possible role of platelets in the aetiology of coronary heart disease are difficult to interpret because of confusion between their possible long-term role in atherogenesis and their putative involvement in thrombus formation which results in myocardial infarction. Evidence from an inadequately designed one-day study involving persons exposed to unmeasured amounts of ETS in a hospital corridor provides no insight into mechanisms involved in coronary atherogenesis. A study of the effect of exposure to ETS on the diameter of the brachial artery diameter is open to criticism because of the way in which subjects were recruited and failure to control for potentially important confounders.Conclusion — The available experimental and epidemiological evidence does not justify a conclusion that ETS exposure increases the risk of heart disease.