Investigation of the chemical components of ambient fine particulate matter (PM2.5) associated with in vitro cellular responses to oxidative stress and inflammation.

Fine particulate matter (PM2.5) poses a significant risk to human health worldwide, by promoting oxidative stress and inflammation; however, the components responsible for these effects have not been fully evaluated. In this study, we investigated the cellular response of a macrophage cell line exposed to PM2.5 extracts in vitro. We obtained a dataset of chemical components of PM2.5 and determined those associated with the generation of reactive oxygen species (ROS) and secretion of inflammatory cytokines through an orthogonal partial least-squares (OPLS) regression. The results indicated that after water extracts exposure, both ROS and interleukin (IL)-1β levels were positively correlated with transition metals. In cells exposed to dichloromethane extracts, IL-1β secretion was significantly correlated with polycyclic aromatic hydrocarbons (PAHs); meanwhile, tumor necrosis factor (TNF)-α secretion was negatively associated with secondary nitrated PAHs, suggesting that atmospheric nitration process might modify the biological effects of PM2.5 components. We also performed source apportionment using a positive matrix factorization (PMF) model to explore the relative influence of different sources of components on cells. It was found that components from vehicle emissions promoted both ROS and TNF-α, while IL-1β secretion was induced mainly by those from coal combustion. This study provides information regarding PM2.5 components having biological effects, and the sources thereof, which could inform effective measures for controlling this type of air pollution.