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Effects of particulate air pollution on BPDE-DNA adducts, telomere length, and mitochondrial DNA copy number in human exhaled breath condensate and BEAS-2B cells.

Naruporn Pedklang·Panida Navasumrit·Chalida Chompoobut·Jeerawan Promvijit·Potchanee Hunsonti·Mathuros Ruchirawat
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Abstract

Traffic-related particulate matter (PM) and polycyclic aromatic hydrocarbons (PAHs) have been linked to respiratory diseases and cancer risk in humans. Genomic damage, including benzo[a]pyrene diolepoxide (BPDE)-DNA adducts as well as alterations in telomere length (TL) and mitochondrial DNA copy number (mtDNA-CN) are associated with respiratory diseases. This study aimed to investigate the association between exposure to traffic-related particulate pollutants and genomic damage in exhaled breath condensate (EBC) in human subjects and a bronchial epithelial cell line (BEAS-2B). Among the 60 healthy recruited subjects, residents living in high-traffic-congested areas were exposed to higher concentrations of PM2.5 (1.66-fold, p&#xa0;<&#xa0;0.01), UFPs (1.79-fold, p&#xa0;<&#xa0;0.01), PM2.5-PAHs (1.50-fold, p&#xa0;<&#xa0;0.01), and UFPs-PAHs (1.35-fold, p&#xa0;<&#xa0;0.05), than those in low-traffic-congested areas. In line with increased exposure to particulate air pollution, the high-traffic-exposed group had significantly increased BPDE-DNA adducts (1.40-fold, p&#xa0;<&#xa0;0.05), TL shortening (1.24-fold, p&#xa0;<&#xa0;0.05), and lower mtDNA-CN (1.38-fold, p&#xa0;<&#xa0;0.05) in EBC. The observations in the human study linking exposure to PM2.5, UFPs, PM2.5-PAHs, and UFPs-PAHs with the aforementioned biological effects were confirmed by an in vitro cell-based study, in which BEAS-2B cells were treated with diesel exhaust particulate matter (DEP) containing fine and ultrafine PM and PAHs. Increased BPDE-DNA adducts levels, shortened TL, and decreased mtDNA-CN were also found in treated BEAS-2B cells. The shortened TL and decreased mtDNA-CN were in part mediated by decreased transcript levels of hTERT, and SIRT1, which are involved in telomerase activity and mitochondrial biogenesis, respectively. These results suggest that exposure to traffic-related particulate pollutants can cause genomic instability in respiratory cells, which may increase the health risk of respiratory diseases and the development of cancer.

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HumansDNA AdductsParticulate MatterDNA, MitochondrialMaleAir Pollutants7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxideCell LineFemaleAdultMiddle AgedDNA Copy Number VariationsBreath TestsPolycyclic Aromatic HydrocarbonsTelomereVehicle EmissionsEpithelial CellsExhalationBPDE-DNA adductExhaled breath condensateMitochondrial DNA copy numberParticulate matterPolycyclic aromatic hydrocarbonTelomere lengthJournal ArticleResearch Support, Non-U.S. Gov't

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Naruporn Pedklang, Panida Navasumrit, Chalida Chompoobut, Jeerawan Promvijit, Potchanee Hunsonti, Mathuros Ruchirawat. 2024-11-18. Effects of particulate air pollution on BPDE-DNA adducts, telomere length, and mitochondrial DNA copy number in human exhaled breath condensate and BEAS-2B cells.. https://doi.org/10.1016/j.ijheh.2024.114488

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