Fine particulate matter (PM_2.5) is a significant health issue in Chinese megacities. However, little information is available regarding the PM_2.5‐bound toxic organics, especially their sources, atmospheric transformations, and health implications. In this study, we assessed the levels of polycyclic aromatic hydrocarbons (PAHs) and their nitrated, hydroxylated, and oxygenated derivatives (i.e., NPAHs, OHPAHs, and OPAHs, respectively) in PM_2.5collected in Beijing over a 1 year period. The median concentration of 23 PAHs, 15 NPAHs, 16 OHPAHs, and 7 OPAHs in PM_2.5was 53.8, 1.14, 1.40, and 3.62 ng m⁻³, respectively. Much higher concentrations and mass percentages for all species were observed in the heating season, indicating a higher toxicity of PM_2.5during this period of time. Positive matrix factorization was applied to apportion the sources of PAHs and their derivatives. It was found that traffic emissions in the nonheating season, and coal combustion and biomass burning in the heating season, were the major primary sources of PAHs and their derivatives. Secondary formation, however, contributed significantly to the derivatives of PAHs (especially NPAHs and OPAHs) in the nonheating season, suggesting significant impacts of atmospheric transformation on the toxicity of PM_2.5.

Particulate matter (PM), an important component of air pollution, induces significant adverse health effects. Many of the observed health effects caused by inhaled PM are associated with oxidative stress and inflammation. This association has been linked in particular to the particles’ chemical components, especially the inorganic/metal and the organic/polycyclic aromatic hydrocarbon (PAH) fractions, and their ability to generate reactive oxygen species (ROS) in biological systems. The transcription factor NF-E2 nuclear factor erythroid-related factor 2 (Nrf2) is activated by redox imbalance and regulates the expression of phase II detoxifying enzymes. Nrf2 plays a key role in preventing PM-induced toxicity by protecting against oxidative damage and inflammation. This review focuses on specific PM fractions, particularly the dissolved metals and PAH fractions, and their roles in inducing oxidative stress and inflammation in cell and animal models with respect to Nrf2 and mitochondria.

Water-soluble humic-like substances (HULIS_WS) are a major redox-active component of ambient fine particulate matter (PM_2.5); however, information on their sources and associated redox activity is limited. In this study, HULIS_WS mass concentration, various HULIS_WS species, and dithiothreitol (DTT) activity of HULIS_WS were quantified in PM_2.5 samples collected during a 1-year period in Beijing. Strong correlation was observed between HULIS_WS and DTT activity; both exhibited higher levels during the heating season than during the nonheating season. Positive matrix factorization analysis of both HULIS_WS and DTT activity was performed. Four combustion-related sources, namely coal combustion, biomass burning, waste incineration, and vehicle exhausts, and one secondary factor were resolved. In particular, waste incineration was identified as a source of HULIS_WS for the first time. Biomass burning and secondary aerosol formation were the major contributors ( > 59 %) to both HULIS_WS and associated DTT activity throughout the year. During the nonheating season, secondary aerosol formation was the most important source, whereas during the heating season, the predominant contributor was biomass burning. The four combustion-related sources accounted for > 70 % of HULIS_WS and DTT activity, implying that future reduction in PM_2.5 emissions from combustion activities can substantially reduce the HULIS_WS burden and their potential health impact in Beijing.

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.