Comparison of cytotoxicity induced by PM2.5-bound polycyclic aromatic compounds from different environments in Xi'an, China

Abstract The chemical and bioreactivity properties of fine particulate matter (PM2.5) in indoor and outdoor environments in Xi'an were characterized, and the lung function of various participants was investigated. The concentrations of polycyclic aromatic hydrocarbons (PAHs), oxygenated polycyclic aromatic hydrocarbons, and nitrated polycyclic aromatic hydrocarbons were higher in outdoor environments than in indoor environments; in addition, urban areas had higher concentrations of these compounds than did suburban areas, with fossil fuel combustion likely being the primary source. Moreover, PM2.5-induced inflammation was higher in urban areas than in suburban areas. Indoor environments with coal combustion emissions showed relatively higher oxidative potential and inflammation. Moderate (phenanthrene) to strong (acenaphthylene and benzo(a)pyrene) correlations were observed between selected PAHs against interleukin 6 (IL-6), 8-hydroxy-desoxyguanosine (8-OHdG), and necrosis factor-α (TNF-α). Moreover, 9-fluorenone, 9,10-anthraquinone, and 5,12-naphthacenequinone exhibited higher oxidative stress and inflammation than did their parent PAHs. Forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) were negatively correlated with 8-OHdG, and FEV1/FVC was negatively correlated with TNF-α and IL-6. These findings—which integrates PM2.5 with lung function and bioreactivity analyses—suggest that coal burning, especially indoors, could elevate the cytotoxicity of PM2.5 to the occupants and that chronic exposure may lead to a decline in lung function.