title: Vasoactive alteration and inflammation induced by polycyclic aromatic hydrocarbons and trace metals of vehicle exhaust particles.
abstract: 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 (PM(0.1-1)) and <0.1-μm PM (PM(0.1)) 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.
authors.affiliation: School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan.
authors.forename: Hsiao-Chi
authors.initials: HC
authors.lastname: Chuang
authors.forename: Ching-Wen
authors.initials: CW
authors.lastname: Fan
authors.forename: Kuan-Yu
authors.initials: KY
authors.lastname: Chen
authors.forename: Guo-Ping
authors.initials: GP
authors.lastname: Chang-Chien
authors.forename: Chang-Chuan
authors.initials: CC
authors.lastname: Chan
mesh_terms: D002318:Cardiovascular Diseases / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology; D002460:Cell Line; D004305:Dose-Response Relationship, Drug; D042783:Endothelial Cells / Q000187:drug effects / Q000473:pathology; D019332:Endothelin-1 / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology; D015850:Interleukin-6 / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D052638:Particulate Matter / Q000633:toxicity*; D011084:Polycyclic Aromatic Hydrocarbons / Q000633:toxicity*; D018709:Statistics, Nonparametric; D014131:Trace Elements / Q000633:toxicity*; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D019332:Endothelin-1; D015850:Interleukin-6; D052638:Particulate Matter; D011084:Polycyclic Aromatic Hydrocarbons; D014131:Trace Elements; D001335:Vehicle Emissions; D009569:Nitric Oxide