Toxicological effects of personal exposure to fine particles in adult residents of Hong Kong

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.