Vasoactive alteration and inflammation induced by polycyclic aromatic hydrocarbons and trace metals of vehicle exhaust particles

Exposure to particulate matter (PM) increases the incidence of cardiovascular disease, but the underlying mechanisms remain unclear. To characterise ambient PM collected from a coach station in an urban area, particulate polycyclic aromatic hydrocarbons (PAHs) and trace metals were evaluated, and diagnostic ratios were then used to determine the sources based on the PAHs identified in PM. To elucidate the mechanism of PM-induced vascular toxicology, human coronary artery endothelial cells (HCAECs) were exposed to PM, PM-free supernatant and residual PM, and the associations between PAHs and trace metals, nitric oxide (NO), endothelin-1 (ET-1) and interleukin-6 (IL-6) were investigated. Petrogenic-related particulate emissions, such as vehicle exhaust, accounted for 68.75% and 75.00% of mass in the 0.1–1-μm PM (PM0.1–1) and <0.1-μm PM (PM0.1) size fractions, respectively. Vehicle exhaust particles (VEPs) caused significant NO suppression and increase in ET-1 and IL-6, whereas residual PM caused an increase in NO, ET-1 and IL-6 compared with the effects of the corresponding supernatants. PAHs in PM, particularly those with 4–6 rings, were associated with NO suppression, and ET-1 and IL-6 were positively correlated with the amount of trace metal compounds. These findings suggest that chemical components affect the regulation of vasoactive function and inflammation.

► PAH diagnostic ratios were used to apportion PM collected from a coach station.
► NO, ET-1 and IL-6 induced by the physicochemistry of PM were determined.
► PAHs, particularly those with 4–6 rings, were associated with NO suppression.
► ET-1 and IL-6 were positively correlated with the amount of trace metal compounds.
► VEPs induced endothelial dysfunction and inflammations.