wAmbient particulate air pollution assessed as outdoor concentrations of particulate matter less than or equal to 2.5 mum in diameter (PM2.5) in urban background has been associated with cardiovascular diseases at the population level. However, the significance of individual exposure and the involved mechanisms remain uncertain. We measured personal PM2.5 and carbon black exposure in 50 students four times in 1 year and analyzed blood samples for markers of protein and lipid oxidation, for red blood cell (RBC) and platelet counts, and for concentrations of hemoglobin and fibrinogen. We analyzed protein oxidation in terms of gamma-glutamyl semialdehyde in hemoglobin (HBGGS) and 2-aminoadipic semialdehyde in hemoglobin (HBAAS) and plasma proteins (PLAAS), and lipid peroxidation was measured as malondialdehyde (MDA) in plasma. Median exposures were 16.1 mug/m(3) for personal PM2.5 exposure, 9.2 mug/m(3) for background PM2.5 concentration, and 8.1 x 10(-6)/m for personal carbon black exposure. Personal carbon black exposure and PLAAS concentration were positively associated (p <0.01), whereas an association between personal PM2.5 exposure and PLAAS was only of borderline significance (p = 0.061). A 3.7% increase in MDA concentrations per 10 mug/m(3) increase in personal PM2.5 exposure was found for women (P <0.05), whereas there was no significant relationship for the men. Similarly, positive associations between personal PM2.5 exposure and both RBC and hemoglobin concentrations were found only in women (p <0.01). There were no significant relationships between background PM2.5 concentration and any of the biomarkers. This suggests that exposure to particles in moderate concentrations can induce oxidative stress and increase RBCs in peripheral blood. Personal exposure appears more closely related to these biomarkers potentially related to cardiovascular disease than is ambient PM2.5 background concentrations.