BACKGROUND: Studies show that exposure to air pollution damages human health, but the mechanisms are not fully understood. One suggested pathway is via oxidative stress. OBJECTIVES: This study examines associations between exposure to air pollution and oxidative DNA damage, as indicated by urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) concentrations in ageing participants during 2006-2008. METHODS: We fit linear regression models to examine associations between air pollutants and 8-OHdG adjusting for potential confounders. RESULTS: 8-OHdG was significantly associated with ambient particulate matter ≤2.5 μm in aerodynamic diameter (PM(2.5)), nitrogen dioxide (NO(2)), maximal 1 h ozone (O(3)), sulphate (SO(4)(2-)) and organic carbon (OC), but not with black carbon (BC), carbon monoxide (CO), the number of particles (PN) or elemental carbon (EC). Effects were more apparent with multi-week averages of exposures. Per IQR increases in 21-day averages of PM(2.5), PN, BC, EC, OC, CO, SO(4)(2-), NO(2) and maximal 1 h O(3) were associated with 30.8% (95% CI 9.3% to 52.2%), -13.1% (95% CI -41.7% to 15.5%), 3.0% (95% CI -19.8% to 25.8%), 5.3% (95% CI -23.6% to 34.2%), 24.4% (95% CI 1.8% to 47.1%), -2.0% (95% CI -12.4% to 8.3%), 29.8% (95% CI 6.3% to 53.3%), 32.2% (95% CI 7.4% to 56.9%) and 47.7% (95% CI 3.6% to 91.7%) changes in 8-OHdG, respectively. CONCLUSIONS: This study suggests that ageing participants experienced an increased risk of developing oxidative DNA injury after exposure to secondary, but not primary, ambient pollutants.
BACKGROUND: Studies show that exposure to air pollution damages human health, but the mechanisms are not fully understood. One suggested pathway is via oxidative stress. OBJECTIVES: This study examines associations between exposure to air pollution and oxidative DNA damage, as indicated by urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) concentrations in ageing participants during 2006-2008. METHODS: We fit linear regression models to examine associations between air pollutants and 8-OHdG adjusting for potential confounders. RESULTS:8-OHdG was significantly associated with ambient particulate matter ≤2.5 μm in aerodynamic diameter (PM(2.5)), nitrogen dioxide (NO(2)), maximal 1 h ozone (O(3)), sulphate (SO(4)(2-)) and organic carbon (OC), but not with black carbon (BC), carbon monoxide (CO), the number of particles (PN) or elemental carbon (EC). Effects were more apparent with multi-week averages of exposures. Per IQR increases in 21-day averages of PM(2.5), PN, BC, EC, OC, CO, SO(4)(2-), NO(2) and maximal 1 h O(3) were associated with 30.8% (95% CI 9.3% to 52.2%), -13.1% (95% CI -41.7% to 15.5%), 3.0% (95% CI -19.8% to 25.8%), 5.3% (95% CI -23.6% to 34.2%), 24.4% (95% CI 1.8% to 47.1%), -2.0% (95% CI -12.4% to 8.3%), 29.8% (95% CI 6.3% to 53.3%), 32.2% (95% CI 7.4% to 56.9%) and 47.7% (95% CI 3.6% to 91.7%) changes in 8-OHdG, respectively. CONCLUSIONS: This study suggests that ageing participants experienced an increased risk of developing oxidative DNA injury after exposure to secondary, but not primary, ambient pollutants.
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