The cellular effects of PM2.5 collected in Chinese Taiyuan and Guangzhou and their associations with polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs and hydroxy-PAHs.

Numerous studies have demonstrated adverse effects on human health after exposure to fine particulate matter (PM2.5). However, it is still not clear how the toxicological effects and the health risks vary among PM samples of different compositions and concentrations. In this study, we examined effects of region- and season-dependent differences of PM2.5 on cytotoxicity, and the contributions of PAHs, nitro-PAHs (N-PAHs) and hydroxy-PAHs (OH-PAHs) to PM2.5 toxicity by determining different toxicological indicators in three lung cell lines. The results illustrated significant differences in components concentrations and biological responses elicited by PM2.5 collected in different cities and seasons. The concentrations of most PAHs, N-PAHs and OH-PAHs were much higher in Taiyuan than in Guangzhou. PM2.5 from Taiyuan exhibited lower cell viability and higher reactive oxygen species (ROS) and interleukin-6 (IL-6) release on lung cells than those from Guangzhou. Specifically, PM2.5 collected in summer from Taiyuan caused higher levels of pro-inflammatory responses and oxidative potential than those collected in winter. The correlation analysis between 19 PAHs, 17 N-PAHs and 12 OH-PAHs and the measured indicators demonstrated that PAHs were more related to PM2.5-induced CCK-8 cytotoxicity and IL-6 release in Taiyuan while N-PAHs and OH-PAHs were more related to PM2.5-induced CCK-8 cytotoxicity and dithiothreitol (DTT)-based redox activity in Guangzhou, suggesting that the toxicity of PM2.5 from Taiyuan was mostly correlated with PAHs while the toxicity of PM2.5 from Guangzhou was closely associated with N-PAHs and OH-PAHs. These results revealed that composition differences in PM2.5 from different regions and seasons significantly accounted for the differences of their toxicological effects.

Mass spectrometry-based metabolomics reveals the mechanism of ambient fine particulate matter and its components on energy metabolic reprogramming in BEAS-2B cells.

Exposure to airborne fine particulate matter (PM2.5) is associated with various adverse effects. However, the molecular mechanism involved in PM2.5-elicited energy metabolic reprogramming and the toxic chemical determinants within PM2.5 are not well elucidated. In this study, nontargeted and targeted metabolomics research were conducted to investigate the overall metabolic changes and relevant toxicological pathways caused by Taiyuan winter total PM2.5 and its water soluble and organic soluble fractions in human lung bronchial epithelial cells (BEAS-2B). The results showed that significant metabolome alterations in BEAS-2B cells were observed after the exposure of total PM2.5 and its organic soluble fraction. Purine metabolism, arginine and proline metabolism, glutathione (GSH) metabolism, tricarboxylic acid (TCA) cycle and glycolysis were mainly affected. Along with a significant increase of reactive oxygen species (ROS), malondialdehyde (MDA), nitric oxide (NO) and pro-inflammatory cytokines (TNF-α, IL-6 and IL-1ß), obvious metabolic phenotype remodeling from oxidative phosphorylation to glycolysis was found in BEAS-2B cells treated with total PM2.5 and its organic soluble fraction. Compared with water soluble fraction, organic soluble fraction was found to play the dominant role in PM2.5 toxicity. Our study provided novel insights into the mechanism of PM2.5-elicited toxicity.