Concerns about possible cardiovascular and especially coronary effects of environmental tobacco smoke (ETS) derive from the reported effects of active smoking. Despite similarities, however, ETS has composition and physical characteristics different from the mainstream smoke (MS) that active smokers inhale and appears relatively more chemically inert and less biologically active. ETS doses to nonsmokers are small and often below the sensitivity of detection technologies. They are several orders of magnitude less than MS doses in active smokers. Numerous epidemiologic studies report that the active smoking of less than 10 cigarettes/day is not associated with measurable risk of coronary heart disease (CHD). Thus, even assuming that ETS and MS have equivalent biologic activities, conceivable ETS doses to nonsmokers are far below apparent no-effect thresholds for active smoking. Hence, it is no surprise that epidemiologic reports are inconclusive about a possible association of ETS exposure and CHD, some suggesting a slight elevation, others a reduction of risk. Often, the elevations reported are higher than the CHD risk values associated with active smoking. Such equivocations likely result from the presence of contrasting protective or aggravating confounders, of which more than 200 have been reported in the literature--confounders that were not and could not be adequately controlled by any epidemiologic study. By scientific standards, the weight of evidence continues to falsify the hypothesis that ETS exposure might be a CHD risk factor.