Inhalation of ambient particulate matter (PM) increases cardiovascular mortality and morbidity, but the systemic mechanisms are unclear. The purpose of this study was to determine if pulmonary exposure to a PM surrogate, such as residual oil fly ash (ROFA), alters systemic microvascular function. Rats were exposed to ROFA (0.1, 0.25, 1 or 2 mg/rat), TiO2 (0.25 mg/rat), or saline by intratracheal instillation 24 hrs prior to experiments. Intravital microscopy of the spino trapezius muscle was used in conjunction with lumenal delivery of the Ca2+ ionophore A23187 to study arteriolar dilator responses. Bronchoalveolar lavage (BAL) samples were analyzed to monitor pulmonary inflammation and damage. A23187 dilated arterioles up to 72+/-% of maximum in saline treated rats. ROFA or TiO2 exposure significantly attenuated these dilations. BAL fluid analysis revealed pulmonary inflammation and damage after exposure to >1 mg ROFA (but not TiO2, or <1 mg ROFA) , as evidenced by significantly higher polymorphonuclear leukocyte (PMNL) counts, enhanced BAL albumin levels, and lactate dehydrogenase activity. Histological sections from lungs of rats exposed to 0.1 mg ROFA indicated focal alveolitis. ROFA exposure produced systemic inflammation as evidenced by: PMNL adherence in paired venules, increased fMLP-induced chemiluminescence from isolated blood PMNL, and increased dihydroethidium oxidation in the arteriolar wall. These results suggest that pulmonary PM exposure is associated with systemic microvascular dysfunction and inflammation.