Associations between exposure to fine particulate matter and blood pressure responses have been reported in epidemiological studies but findings have proven inconsistent. The objective of this study was to measure effects of primary and secondary components of traffic-derived fine particulate matter (PM2.5) on blood pressure (BP). Sprague-Dawley rats were exposed to fresh primary vehicular particles (P), secondary organic aerosol (SOA), photochemically aged primary plus secondary organic aerosols (P + SOA) or filtered air for 5 h per day for three consecutive weeks. Particle concentration target was 50 mu g/m(3) for all exposures. Blood pressure parameters were measured continuously using implanted transmitters. Systolic (SBP) and diastolic blood pressure (DBP), mean pressure, pulse pressure, and heart rate responses were assessed using mixed effects models. Exposure to P resulted in increased SBP (p = 0.03) and DBP (p = 0.05) that was sustained across weeks. SOA exposure resulted in increases in SBP (p = 0.07) and DBP (p = 0.01) on the first day with this effect decreasing significantly across exposure days (p < 0.0001). P + SOA showed significant increases in SBP (p = 0.002) and DBP (p < 0.0001) across weeks with a magnitude of effect equaling the approximate average of the effect estimates of the P and SOA exposures. Double Sham exposures following SOA and P + SOA showed compensatory decreases in SBP and DBP. No exposure had a significant effect on heart rate. Primary and secondary traffic derived aerosols can substantially increase SBP and DBP, but these increases are lost with continued exposures. Compensatory BP responses resulting after exposure to secondary particles require further investigation to define BP control mechanisms.