Observational studies have consistently demonstrated an association between exposure to air pollution and increased cardiovascular morbidity and mortality. This association is strongest for particulate matter (PM), of which combustion-derived particulate is an important component. Studies assessing the effects of PM exposure in vitro and in vivo have provided insight into the biological mechanisms underlying these observations. In this review we discuss the potential for inhaled particles to impact on the development and progression of atherosclerosis. Oxidative stress and inflammation are central to both the toxicology of PM and the pathogenesis of atherosclerosis. It is possible that nanoparticulates or soluble components of PM may translocate into the bloodstream, resulting in direct effects on atherosclerotic plaque stability, the vascular endothelium, platelet function, and thrombosis. We summarize the latest experimental research and relate this to current understanding of the role of inflammation and vascular dysfunction in the pathogenesis of atherothrombosis. Ongoing research in this area will continue to provide insight into the adverse vascular effects of PM, with the possibility of therapeutic interventions to reduce the impact of environmental air pollution on cardiovascular disease a realistic goal.