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Fine particulate matter (PM2.5) increases the risks of lung cancer. Epigenetics provides a new toxicology mechanism for the adverse health effects of PM2.5. However, the regulating mechanisms of PM2.5 exposure on candidate gene DNA methylation changes in the development of lung cancer remain unclear. Abnormal expression of the glutathione S transferase (GST) gene is associated with cancer. However, the relationship between PM2.5 and DNA methylation-mediated GST gene expression is not well understood. In this study, we performed GST DNA methylation analysis and GST-related gene expression in human A549 cells exposed to PM2.5 (0, 50, 100 µg/mL, from Taiyuan, China) for 24 h (n = 4). We found that PM2.5 may cause DNA oxidative damage to cells and the elevation of GSTP1 promotes cell resistance to reactive oxygen species (ROS). The Kelch-1ike ECH-associated protein l (Keap1)/nuclear factor NF-E2-related factor 2 (Nrf2) pathway activates the GSTP1. The decrease in the DNA methylation level of the GSTP1 gene enhances GSTP1 expression. GST DNA methylation is associated with reduced levels of 5-methylcytosine (5mC), DNA methyltransferase 1 (DNMT1), and histone deacetylases 3 (HDAC3). The GSTM1 was not sensitive to PM2.5 stimulation. Our findings suggest that PM2.5 activates GSTP1 to defend PM2.5-induced ROS and 8-hydroxy-deoxyguanosine (8-OHdG) formation through the Keap1/Nrf2 signaling pathway and GSTP1 DNA methylation. [ABSTRACT FROM AUTHOR]

The concentrations of ambient fine particulate matter (PM2.5) and its compositions in urban Taiyuan, China during a typical winter and summer time period in 2017 were measured to investigate the pollution characteristics, source apportionment and health risks assessment of PM2.5 pollution. The results demonstrated that the mean daily mass concentration of PM2.5 in winter (102.6 ± 6.2 μg/m3) was higher than that in summer (65.0 ± 17.2 μg/m3) during sampling. The relatively high concentrations of heavy metals (Zn, Pb, Cu, As, Ni, Cr and Cd), anion (SO42−, NO3−, Cl− and F−) and high-molecular-weight PAHs in PM2.5 were observed. The enrichment factors (EFs) values, special diagnostic ratios like ratios of NO3−/SO42− and individual PAHs concentration ratio showed that coal combustion and vehicle emissions were the major sources of PM2.5 pollution. Health risk assessment illustrated that mean hazard indices for non-cancer and cancer risk of all analyzed metals were within the safe range. However, inhalation exposure to PM2.5-bound PAHs had carcinogenic risk, while not indicating non-carcinogenic risk. Taken together, although PM2.5 pollution was alleviated to some extent, PM2.5 pollution in 2017 was still serious and PM2.5 was mainly originated from coal burning, especially, in which PM2.5-bound PAHs in Taiyuan may pose a potential health risk. [ABSTRACT FROM AUTHOR]

Taiyuan is a center of coal-based electricity production and many chemicals industries, where mixtures of sulfur dioxide (SO2) and particulate matter may be more prominent. The focus of the present study was to determine if there is a link between adverse effects in the brain and the combined-exposure to SO2and fine particulate matter (PM2.5). Rats were exposed alternately to PM2.5with different dosages (1.5, 6.0 and 24.0 mg/kg body weight) and SO2at the level of 5.6 mg/m3. The results showed that the combined exposure to PM2.5and SO2enhanced the mRNA expression and protein level of TNF-α and IL-6 in rat cortex and hippocampus relative to the control, SO2and PM2.5alone. Instead, TGF-β1 mRNA and protein level were down-regulated in the brain. Additionally, PM2.5at medium and/or high dose caused marked increase in Aβ42 level and PM2.5 + SO2induced further increase of Aβ42 level in the cortex and hippocampus. It suggests that SO2and PM2.5can synergistically exert inflammation responses and induce Aβ42 accumulation in the brain. Also, it is notable that the Aβ42 accumulation of rat cortex and hippocampus were closely associated with pro-/anti-inflammatory cytokines ratio. These results clearly demonstrated that the combined exposure to PM2.5and SO2can induce the imbalance of pro-/anti-inflammatory cytokine, resulting in Aβ42 accumulation of rat brain cortex and hippocampus. [ABSTRACT FROM AUTHOR]