Investigation of the chemical components of ambient fine particulate matter (PM_2.5) associated with in vitro cellular responses to oxidative stress and inflammation

Fine particulate matter (PM_2.5) 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 PM_2.5 extracts in vitro. We obtained a dataset of chemical components of PM_2.5 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 PM_2.5 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 PM_2.5 components having biological effects, and the sources thereof, which could inform effective measures for controlling this type of air pollution.