Exposure to particulate air pollution is associated with acute and chronic cardiovascular morbidity and mortality. The mechanisms involved in these effects are not fully elucidated. Research has proved that fine particles, principally the ultrafine fraction, which are predominantly derived from combustion of fossil fuel, are the most toxic. Recent clinical and experimental studies have reported mechanistic observations linking fine and ultrafine particles to the coagulation cascade, platelet function, and subsequent development of atherosclerosis and thrombosis. These effects have been explained either by release of soluble mediators by the lungs, which affect blood coagulation parameters, or by the direct translocation of ultrafine particles into the systemic circulation or the alteration of autonomic cardiac control. Despite recent advances, additional studies are needed to investigate the pathophysiologic mechanisms linking particulate air pollution and hemostasis.