Traffic-related PM₂.₅ pollution in Hong Kong : component-specific and source-resolved health risks and cytotoxicity

Abstract

Current studies on the source apportionment of fine particulate matter (PM<inf>2.5</inf>) primarily emphasized the contributions of sources to mass concentrations, leaving the acute and chronic health effects caused by specific sources and components insufficiently addressed. In this study, we integrated source profiles with acute cytotoxicity and chronic health risk to assess the component-specific and source-resolved health effects of PM<inf>2.5</inf> in a coastal megacity, Hong Kong. An intracellular reactive oxygen species (ROS) analysis of 24-h integrated PM2.5 samples conducted on the BEAS-2b cell line revealed that trace metals dominantly drove PM<inf>2.5</inf>-induced ROS (contributing 52 % in roadside, 39 % in general urban, and 32 % for coastal background PM<inf>2.5</inf>). Among the analyzed metals, the primary culprits were Fe, Zn, and Cu, urging the need for non-exhaust pollution control. This study also provided quantitative evidence for the biological toxic potential of insoluble elemental carbon (EC), constituting 31 % and 22 % of overall ROS induction in roadside and general urban PM<inf>2.5</inf>, respectively. In conjunction with source profiles, our findings reveal a clear inequality in contributions attributed to the same source when assessed by mass, acute biological toxicity effect, and chronic health risks. For instance, local fresh on-road traffic emissions were predominant in accounting for the acute intracellular ROS induction (84 % in roadside and 63 % in general urban PM<inf>2.5</inf>). Meanwhile, regional sources brought in by long-rang transport, such as combustion & industrial emissions, posed more threats to chronic inhalation health risks induced by PM<inf>2.5</inf>, especially for general urban and coastal background aerosols in Hong Kong. This investigation has significant implications for developing toxicity-oriented pollution control strategies.