Cellular effects of PM2.5from Suzhou, China: relationship to chemical composition and endotoxin content

Exposure to PM(2.5)can cause adverse health outcomes. In this study, we analyzed PM(2.5)samples collected from suburban and urban sites, including a traffic tunnel in Suzhou, China, for their physicochemical properties, endotoxin contents, and effects on HepG2 and A549 cells in vitro. The greatest cellular responses, including oxidative stress, cytotoxicity, genotoxicity, inflammatory, and transcriptional activation of stress-responsive genes (i.e.,HSPA1A,GADD45 alpha), were observed in cells treated with traffic tunnel PM2.5. Cytokine expression was also measured and closely correlated with endotoxin content, while other toxic effects were largely related to PM2.5-bound metals and polycyclic aromatic hydrocarbons (PAHs). These findings suggested that chemical and biological composition of PM2.5, including adsorbed trace metals, PAHs, and endotoxin, may contribute significantly to their toxicity. In addition to commonly used in vitro toxicity tests,HSPA1AandGADD45 alpha promoter-driven luciferase reporter cells may provide a potential new tool for rapid screening and quantification of PM(2.5)toxicity.

Automated summary

Exposure to PM(2.5) can have adverse health outcomes, particularly when it comes from traffic tunnels. The study found that PM(2.5) from traffic tunnels had the most significant negative effects on cells, including oxidative stress, cytotoxicity, genotoxicity, inflammation, and activation of stress-responsive genes. Cytokine expression was correlated with endotoxin content, while other toxic effects were mainly linked to PM(2.5)-bound metals and polycyclic aromatic hydrocarbons (PAHs).