Toxicological studies have demonstrated the associations between fine particle (PM2.5) components and various cytotoxic endpoints. However, few studies have investigated the toxicological eﬀects of source-specific PM2.5 at the individual level. To investigate the potential impact of source-specific PM2.5 on cytotoxic effects, we performed repeated personal PM2.5 monitoring of 48 adult participants in Hong Kong during the winter and summer of 2014–2015. Quartz filters were analyzed for carbonaceous aerosols and water-soluble ions in PM2.5. Teflon filters were collected to determine personal PM2.5 mass and metal concentrations. The toxicological effects of personal PM2.5 exposure—including cytotoxicity, inflammatory response, and reactive oxygen species (ROS) production—were measured using A549 cells in vitro. Personal PM2.5 samples collected in winter were more effective than those collected in summer at inducing cytotoxicity and the expression of proinflammation cytokine IL-6. By contrast, summer personal PM2.5 samples induced high ROS production. We performed a series of statistical analyses, Spearman correlation and a source apportionment approach with a multiple linear regression (MLR) model, to explore the sources contributing most significantly to personal PM2.5 bioreactivity. Secondary inorganic species and transition metals were discovered to be weak-to-moderately associated with cytotoxicity (rs: 0.26–0.55; p < 0.01) and inflammatory response (rs: 0.26–0.44; p < 0.05), respectively. Carbonaceous aerosols (i.e., organic and elemental carbon; rs: 0.23–0.27; p < 0.05) and crustal material (Mg and Ca) was positively associated with ROS generation. The PMF–MLR models revealed that tailpipe exhaust and secondary sulfate contributed to ROS generation, whereas secondary nitrate was the major contributor to PM2.5 cytotoxicity and inflammation. These results improve and variate the arguments for practical policies designed to mitigate the risks posed by air pollution sources and to protect public health.
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