Stroke is a leading cause of morbidity and mortality in the United States with 795,000 people experiencing a new or recurrent stroke every year. Identifying modifiable risk factors for stroke should therefore be considered a research priority. While associations between ambient exposure to air pollution and other cardiovascular diseases are well established in the literature, the evidence linking particulate matter (PM) air pollution exposures to the risk of ischemic or hemorrhagic stroke remains equivocal. Furthermore, the exact pathophysiologic mechanisms by which exposure to PM may lead to cerebrovascular events are not yet fully understood. Hypothesized pathways include the mediation of effects through a combination of inflammatory responses, autonomic dysregulation, and/or vascular endothelial disturbances. This dissertation addresses existing gaps in the literature in three separate studies. Two time-stratified case-crossover studies examined the association between short-term PM exposures and stroke risk, one in the Health Professionals Follow-up Study (HPFS) and the other among a large database of Maryland stroke hospitalizations. Conditional logistic regression models were used to examine associations by stroke subtype, population subgroups, and clinically-relevant variables. Our third study took place within the Nurses’ Health Study cohort. Multivariable linear regression models were used to examine the associations between PM and residential distance to road exposures and four inflammatory biomarkers (CRP, IL-6, fibrinogen, and ICAM-1). We found positive significant associations between PM10 and ischemic stroke events in the HPFS cohort, and associations were elevated for nonsmokers, aspirin nonusers, and those without a history of high cholesterol. Concentrations were elevated for both CRP and IL-6 among participants who lived close to a major roadway, but no significant results were found by estimated PM exposure. This work provides additional evidence that PM exposure is associated with ischemic stroke and adds to the current literature that those not currently taking aspirin and those without a history of high cholesterol may be at elevated risk. Although the direct role of inflammatory processes requires more investigation, this work does provide additional evidence that proximity to traffic may influence cardiovascular-related inflammation.