The objective of the present study was to conduct metal element analysis and carcinogenicity risk assessment of particulate matter with an aerodynamic diameter <2.5 μm (PM2.5) from Shenzhen and Taiyuan. Samples of PM2.5 were collected in Shenzhen and Taiyuan during the yeas 2017 and 2018. Ten heavy metal elements were detected by inductively coupled plasma mass spectrometry. Health risk was assessed using the recommended US Environmental Protection Agency model. Metal elements found in PM2.5 samples from Shenzhen included (in decreasing order of concentration) Al, Pb, Mn, Cr, Cu, V, As, Ni, Cd, and Co. Metal elements found in Taiyuan included (in decreasing order of concentration) Al, Mn, Pb, Cr, Cu, As, Ni, V, Cd, and Co. There were significant differences in Pb, Mn, Al, As, and Ni levels between Shenzhen and Taiyuan (p < 0.05); but the remaining element levels did not show significant differences between the 2 cities. Risk‐assessment data showed higher total risk from 5 carcinogenic metal elements in Taiyuan (3.79 × 10−4) compared to Shenzhen (2.44 × 10−4): Cr had the highest carcinogenicity risk (>10−4), followed by As, Ni, and Cd (10−6 ~ 10−4), and Pb had the lowest risk (<10−6). The results indicated that some of the metal elements in PM2.5 samples from Shenzhen and Taiyuan pose a carcinogenicity risk; further research and measures for prevention and control should be considered. Environ Toxicol Chem 2020;39:1273–1276. © 2020 SETAC

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This current study explored the effects of fine particulate matter (PM2.5) on deoxyribonucleic acid methylation in human bronchial epithelial cells. Human bronchial epithelial cells were exposed to PM2.5 for 24 h after which, deoxyribonucleic acid samples were extracted, and the differences between methylation sites were detected using methylation chips. Subsequent gene ontology functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed for the differential methylation sites. Functional epigenetic modules analysis of the overall differential methylation site interactions was also conducted. A total of 127 differential methylation sites in 89 genes were screened in the PM2.5 10 μg/ml group, of which 55 sites demonstrated increased methylation, with methylation levels decreasing in a further 72 sites. Following an exposure of 50 μg/ml PM2.5, a total of 238 differentially methylated sites were screened in 168 genes, of which methylation levels increased in 127 sites, and decreased in 111. KEGG analysis showed that the top 10 enrichment pathways predominantly involve hepatocellular carcinoma pathways and endometrial cancer pathways, whereas functional epigenetic modules analysis screened eight genes (A2M, IL23A, TPIP6, IL27, MYD88, ILE2B, NLRC4, TNF) with the most interactions. Our results indicate that exposure to PM2.5 for 24 h in human bronchial epithelial cells induces marked changes in deoxyribonucleic acid methylation of multiple genes involved in apoptosis and carcinogenesis pathways, these findings can provide a new direction for further study of PM2.5 carcinogenic biomarkers.