Both episodic and long-term exposures to particulate air pollution are associated with an increased risk of ischemic heart disease. Time-series studies show an association between exposure to particulate air pollution and the exacerbation of ischemic heart disease on days of high pollution. Long-term effects of chronic exposure to polluted air are documented by several prospective cohort studies. These studies show that long-term exposure to ambient PM2.5 is associated with an increase in risk for atherosclerosis and traffic-related pollutants such as ultrafine particles. Several studies suggest that the cardiovascular effects of air pollution may be related to increases in blood coagulation and inflammation. Based on day-to-day fluctuation of particles, evidence for induction of ischemia by PM has been reported in patients with coronary artery disease. There seems to be immediate responses to particulate matter when assessed by personal measurements or within experimental settings. The link between acute changes in intermediate phenotypes of cardiovascular disease and chronic elevated risks are also subject of current research. The exact particle properties responsible for these associations are currently being investigated, but traffic-related particles seem to be the likely culprits. Exposure to traffic particles has been associated with the sudden onset of myocardial infarction. We have found an increase in the onset of myocardial infarction one hour after time spent in traffic. Incident coronary artery disease has also been linked to traffic density and it has been shown that traffic-related exposure is associated with an increase in measures of coronary atherosclerosis. Animal studies with ultrafine particles demonstrate that traffic might be especially potent in inducing atherosclerosis in experimental settings. Collectively, this evidence supports the view that exposure to traffic pollutants could have adverse effects on ischemic heart disease. Links between other forms of cardiovascular diseases also exist. The effects of traffic-generated pollutants on susceptible subgroups based on either genetic susceptibility or other co-morbidities are currently being investigated.