Article Text
Abstract
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) (β = 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.
- 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
- traffic exhaust
- air pollution
- 1-hydroxypyrene-glucuronide
- nitric oxide
- 8-hydroxydeoxyguanosine
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Footnotes
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Funding: this research was supported by the National Science Council in Taiwan (NSC 92-2320-B-016-062)
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Competing interests: none declared