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Atmospheric levels and cytotoxicity of polycyclic aromatic hydrocarbons and oxygenated-PAHs in PM 2.5 in the Beijing-Tianjin-Hebei region.

The chemical composition of PM2.5 and cellular effects from exposure to fine aerosol extracts were studied for samples collected in Beijing, Tianjin, Shijiazhuang, and Hengshui, China in winter 2015. Effects of priority polycyclic aromatic hydrocarbons (PAHs) and their oxygenated derivatives (OPAHs) in PM2.5 on cell cultures were a major focus of the study. Total quantified PAHs and OPAHs at Shijiazhuang and Hengshui were higher than at Beijing and Tianjin, and benz(a)anthracene, chrysene and 1,8-naphthalic anhydride were the most abundant species. Exposure to PM2.5 extracts caused a concentration-dependent decline in cell viability and a dose-dependent increase in nitric oxide production. Two cytokines, tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), also increased when A549 test cells were exposed to PM2.5 extracts. PAHs and OPAHs in PM2.5 can potentially cause cell damage and induce cytotoxicity and pro-inflammatory responses: benzo(a)anthracene-7,12-dione was highly correlated with NO production, dibenz(a,h)anthracene and 1,4-chrysenequinone were correlated with TNF-α production, and 1-naphthaldehyde was significantly correlated with IL-6 production. The study provides a new approach for evaluating relationships between air-quality and cell toxicity with respect to specific chemicals.

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