Exposure to fine particulate matter (PM2.5) from traffic affects heart-rate variability, thrombosis, and inflammation. This reanalysis investigated components potentially contributing to such effects in nonsmoking healthy male North Carolina highway patrol troopers. Nine officers were studied four times during their late shift. PM2.5, its elemental composition, and gaseous copollutants were measured inside patrol cars. Components correlated toPM2.5 were compared to cardiac and blood parameters measured 10 and 15 h, respectively, after each shift. Mixed effects models with control for PM2.5 were used. Components that were associated with health endpoints independently from PM2.5 were calcium (increased uric acid and von Willebrand Factor [vWF], decreased protein C), chromium (increased white blood cell count and interleukin 6), aldehydes (increased vWF, mean cycle length of normal R-R intervals [MCL], and heart-rate variability parameter pNN50), copper (increased blood urea nitrogen and MCL; decreased plasminogen activator inhibitor 1), and sulfur (increased ventricular ectopic beats). Control for gaseous copollutants had little effect on the effect estimates. The changes observed are consistent with effects reported earlier for PM2.5 from speed-change traffic (characterized by copper, sulfur, and aldehydes) and from soil (with calcium). The associations of chromium with inflammation markers were not seen before for traffic particles, but they are consistent with the toxicological literature although at low concentrations. Copper, sulfur, aldehydes, calcium, and chromium or compounds containing these elements seem to directly contribute to the inflammatory, coagulatory, and cardiac response to PM2.5 from traffic in the investigated patrol troopers. [Authors]