Despite legislation, leading to dramatic decreases in levels of air pollution since the time of the great smogs, a large body of epidemiological evidence has demonstrated that pollution continues to have adverse effects on human health. One striking finding from the epidemiological data is that patients with cardiovascular disease are susceptible to acute rises in ambient pollutants. Mortality and hospital admissions for myocardial infarction, congestive cardiac failure and cardiac arrhythmia all increase with a rise in the concentration of both particulate and gaseous pollutants. Before concluding that this association is a causal one, plausible pathophysiological mechanisms are required. Evidence is accumulating in support of two mechanistic hypotheses: inhalation of pollutants might provoke a local inflammatory response with the consequent release into the circulation of pro-thrombotic and inflammatory cytokines. A systemic response of this nature would put individuals with coronary atheroma at increased risk of cardiac events; exposure to pollutants may have an adverse effect on cardiac autonomic control, leading to an increased risk of arrhythmia in susceptible patients. Clarification of the pollutants involved and the precise mechanisms of action is essential in designing measures by which susceptible individuals might be protected from the adverse cardiovascular effects of air pollution.