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Institute of Public Health, University of Copenhagen, DK-2200 Copenhagen N [M. S., L. E. K., S. L.]; The Department of Environmental and Occupational Medicine, University of Aarhus, DK-8000 Aarhus [H. A.]; National Environmental Research Institute, DK-4000 Roskilde [O. H.]; and National Institute of Occupational Health, DK-2100 Copenhagen Ø [H. W.], Denmark
Ambient particulate air pollution assessed as outdoor concentrations of particulate matter
2.5 µm in diameter (PM2.5) has been associated with an increased cancer risk. However, outdoor PM2.5 concentrations may not be the best measure of the individual particle exposure that is a sum of many sources besides outdoor particle levels, e.g., environmental tobacco smoke and cooking. We measured personal PM2.5 and black smoke exposure in 50 students four times over 1 year and analyzed for biomarkers of different types of DNA damages. Ambient PM2.5 concentrations were also measured. Exposure was measured for 48 h, after which blood samples were collected and analyzed for DNA damage in lymphocytes in terms of 7-hydro-8-oxo-2'-deoxyguanosine (8-oxodG), strand breaks, endonuclease III- and fapyguanine glycosylase-sensitive sites, and polyaromatic hydrocarbon adducts. Twenty-four-h urine collections were analyzed for 8-oxodG and 1-hydroxypyrene. Personal PM2.5 exposure was found to be a predictor of 8-oxodG in lymphocyte DNA with an 11% increase in 8-oxodG/10 µg/m3 increase in personal PM2.5 exposure (P = 0.007). No other associations between exposure markers and biomarkers could be distinguished. The genotype of glutathione S-transferase M1 (GSTM1), T1 (GSTT1), and P1 (GSTP1) and NADPH:quinone reductase was also determined, but there were no effects of genotype on DNA polyaromatic hydrocarbon adducts or oxidative damage. The results suggest that moderate exposure to concentrations of PM can induce oxidative DNA damage and that personal PM2.5 exposure is more important in this aspect than is ambient PM2.5 background concentration.
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