Exposure to fine particulate matter causes oxidative and methylated DNA damage in young adults: A longitudinal study

An increased understanding is needed of the physiological effects and plausible biological mechanisms that link PM2.5 (particulate matter with an aerodynamic diameter below 2.5μm) exposure to mortality and morbidities such as atherosclerosis and respiratory disease. PM2.5 causes carcinogenic health...

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Published inThe Science of the total environment Vol. 598; pp. 289 - 296
Main Authors Lai, Ching-Huang, Huang, Han-Bin, Chang, Yue-Cune, Su, Ting-Yao, Wang, Ying-Chuan, Wang, Gia-Chi, Chen, Jia-En, Tang, Chin-Sheng, Wu, Trong-Neng, Liou, Saou-Hsing
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 15.11.2017
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Summary:An increased understanding is needed of the physiological effects and plausible biological mechanisms that link PM2.5 (particulate matter with an aerodynamic diameter below 2.5μm) exposure to mortality and morbidities such as atherosclerosis and respiratory disease. PM2.5 causes carcinogenic health effects. Biomonitoring in humans has suggested that 8-oxo-7, 8-dihydro-2-deoxyguanosine (8-oxodG) and N7-methylguanine (N7-MeG) are correlated with oxidative and methylated DNA damage. Thus, it is meaningful to explore the mechanisms of mutagenesis and carcinogenesis associated with oxidative and methylated DNA damage by simultaneously measuring these two markers. We recruited 72 participants from 2 areas (residential and commercial as well as residential and industrial) in the greater Taipei metropolitan area at baseline. Personal samplers were used to collect 24-hour PM2.5-integrated samples. All participants completed an interview, and blood and urine samples were collected the next morning. All collection procedures were repeated twice after a two-month follow-up period. Urinary 8-oxodG and N7-MeG were assayed as biomarkers of oxidative and methylated DNA damage, respectively. Plasma superoxide dismutase (SOD) and glutathione peroxidase-1 (GPX-1) were measured as biomarkers of antioxidants. Urinary 1-hydroxypyrene (1-OHP) was used as a biomarker of exposure to polycyclic aromatic hydrocarbons (PAHs). The mean PM2.5 level was 37.3μg/m3 at baseline. PM2.5 concentrations were higher during winter than during spring and summer. After adjusting for confounds through a generalized estimating equation (GEE) analysis, N7-MeG was significantly increased by 8.1% (β=0.034, 95% CIs=0.001–0.068) per 10μg/m3 increment in PM2.5. 8-oxodG levels were positively correlated with N7-MeG according to both cross-sectional and longitudinal analyses, and 1-OHP was significantly associated with increasing 8-oxodG and N7-MeG concentrations. Exposure to PM2.5 increases methylated DNA damage. The mean level of urinary N7-MeG was 1000-fold higher than that of 8-oxodG. [Display omitted] •Exposure to fine particulate matter is carcinogenic.•Limited information is available concerning the effects of PM2.5 exposure on urinary N7-MeG levels.•This study examined the relationships between personal exposure to PM2.5 and oxidative and methylated DNA damage markers.•N7-MeG is likely PAH metabolite dependent.•Elevated levels of PM2.5 might be associated with increases in urinary N7-MeG.
ISSN:0048-9697
1879-1026
DOI:10.1016/j.scitotenv.2017.04.079