Traffic Exhausts and Oxidative Stress

Abstract

MS7-10 Abstract: Traffic exhausts constitute a complex mixture of byproducts of the combustion process, including hundreds of pollutants in gaseous and particulate phases. Traffic exhausts such as metabolites of polycyclic aromatic hydrocarbons (PAHs) may form an electrophilic derivative that binds to DNA and may involve reactive oxygen species. Oxidative stress has been considered as a feature underlying the toxic effects of traffic exhausts. We assessed the relation between exposure to traffic exhausts and indicators of oxidative stress and antioxidant status among highway toll station workers. We conducted a cross-sectional study of 47 female highway toll station workers and 27 female office workers as a reference group. Exposure assessment was based on average and cumulative traffic density and urinary 1-hydroxypyrene-glucuronide (1-OHPG), which has shown to be a promising biomarker of exposure to traffic exhausts (Lai et al. Arch Environ Health. 2004;59:61–69). The urinary 8-hydroxydeoxyguanosine (8-OHdG) and urinary isoprostane levels were determined as a biomarker of oxidative DNA damage and lipid peroxidation, respectively. Markers of antioxidant status were measured in blood. Our previous results showed that the mean concentration of urinary 8-OHdG was substantially higher among the exposed nonsmokers (13.6 μg/g creatinine) compared with the reference nonsmokers (7.3 μg/g creatinine, difference, 6.3, 95% confidence interval [CI]: 3.0–9.6) (Lai et al. Occup Environ Med. 2005;62:216–222). In linear regression adjusting for confounding, a change in log(8-OHdG) representing oxidative DNA damage was statistically significantly related to a unit change in log(1-OHPG) (β = 0.372, 95% CI: 0.081–0.663) representing exposure to traffic exhausts. A positive relation was found between the log(8-OHdG) and log(isoprostane) (r = 0.41, P = 0.001). Our results indicate that exposure to traffic exhausts increases oxidative stress.