ORIGINAL ARTICLE

Exposure to traffic exhausts and oxidative DNA damage

C-H Lai¹, S-H Liou¹, H-C Lin², T-S Shih³, P-J Tsai⁴, J-S Chen⁵, T Yang¹, J J K Jaakkola⁶ and P T Strickland⁷

¹ Department of Public Health, National Defence Medical Center, Taipei, Taiwan 114, ROC
² Department of Pharmacology, National Defence Medical Center, Taipei, Taiwan 114, ROC
³ Institute of Occupational Safety and Health, Council of Labour Affairs, Executive Yuan, Taipei, Taiwan 221, ROC
⁴ Department of Environmental and Occupational Health, National Cheng Kung University, Tainan, Taiwan 70428, ROC
⁵ Tri-Service General Hospital, Department of Internal Medicine, Division of Nephrology, Taipei, Taiwan 114, ROC
⁶ Institute of Occupational and Environmental Medicine, The University of Birmingham, Edgbaston, Birmingham B15 2TT, UK
⁷ Department of Environment Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA

Correspondence to:
Correspondence to:
Dr C H Lai
Department of Public Health, National Defence Medical Center, Taipei, Taiwan 114, ROC; lgh{at}ndmctsgh.edu.tw

Aims: To assess the relations between exposure to traffic exhausts and indicators of oxidative DNA damage among highway toll station workers.

Methods: Cross-sectional study of 47 female highway toll station workers exposed to traffic exhausts and 27 female office workers as a reference group. Exposure assessment was based on average and cumulative traffic density and a biomarker of exposure, urinary 1-hydroxypyrene-glucuronide (1-OHPG). Urinary 8-hydroxydeoxyguanosine (8-OHdG) was used as a biomarker of oxidative DNA damage. Plasma nitric oxide (NO) was measured as an indicator of oxidative stress related to traffic exhaust exposure.

Results: The mean concentration of urinary 8-OHdG was substantially higher among the exposed non-smokers (13.6 µg/g creatinine) compared with the reference non-smokers (7.3 µg/g creatinine; difference 6.3, 95% CI 3.0 to 9.6). The mean concentration of NO among the exposed (48.0 µmol/l) was also higher compared with the reference non-smokers (37.6 µmol/l; difference 10.4, 95% CI –0.4 to 21.2). In linear regression adjusting for confounding, a change in log(8-OHdG) was statistically significantly related to a unit change in log(1-OHPG) (ß = 0.372, 95% CI 0.081 to 0.663).

Conclusions: Results indicate that exposure to traffic exhausts increases oxidative DNA damage. Urinary 8-OHdG is a promising biomarker of traffic exhaust induced oxidative stress.

Abbreviations: 1-OHP, 1-hydroxypyrene; 1-OHPG, 1-hydroxypyrene-glucuronide; 8-OHdG, 8-hydroxydeoxyguanosine; eNOS, endothelial nitric oxide synthase; iNOS, inducible nitric oxide synthase; NO, nitric oxide; PAHs, polycyclic aromatic hydrocarbons; ROS, reactive oxygen species; RNS, reactive nitrogen species

Keywords: traffic exhaust; air pollution; 1-hydroxypyrene-glucuronide; nitric oxide; 8-hydroxydeoxyguanosine

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