A short-term increase in fine particulate matter air pollution (PM(2.5)) concentration increases the risk for myocardial infarctions, strokes, and heart failure exacerbations. An important mechanism likely contributing to these associations is an elevation in arterial blood pressure (BP). Exposure to ambient PM(2.5) even at present-day concentrations can increase BP within a period of a few days while long-term exposure might also promote the development of chronic hypertension. Controlled human and animal experiments have corroborated the veracity of these findings and elucidated plausible biological mechanisms. PM(2.5) deposition within the pulmonary tree is capable of rapidly triggering autonomic nervous system imbalance, thereby increasing BP within minutes of inhalation. In addition, fine particles can instigate a systemic pro-inflammatory response over a more prolonged period of exposure. Higher circulating levels of activated immune cells and inflammatory cytokines could consequently cause vascular endothelial dysfunction leading to an imbalance in vascular homeostatic responses. Indeed, chronic PM(2.5) exposure augments pro-vasoconstrictive pathways while blunting vasodilator capacity. Finally, certain particle constituents (e.g., metals, organic compounds, and ultra-fine particles) might also be capable of reaching the systemic circulation upon inhalation and thereafter directly impair vascular function. At the molecular level, the generation of oxidative stress with the consequent up-regulation of redox sensitive pathways appears to be a common and fundamental mechanism involved in the instigation of these pro-hypertensive responses. Due to the ubiquitous, continuous and often involuntary nature of exposure, PM(2.5) may be an important and under-appreciated worldwide environmental risk factor for increased arterial BP.