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Original article
Exposure to traffic exhausts and oxidative DNA damage
  1. C-H Lai1,
  2. S-H Liou1,
  3. H-C Lin2,
  4. T-S Shih3,
  5. P-J Tsai4,
  6. J-S Chen5,
  7. T Yang1,
  8. J J K Jaakkola6,
  9. P T Strickland7
  1. 1Department of Public Health, National Defence Medical Center, Taipei, Taiwan 114, ROC
  2. 2Department of Pharmacology, National Defence Medical Center, Taipei, Taiwan 114, ROC
  3. 3Institute of Occupational Safety and Health, Council of Labour Affairs, Executive Yuan, Taipei, Taiwan 221, ROC
  4. 4Department of Environmental and Occupational Health, National Cheng Kung University, Tainan, Taiwan 70428, ROC
  5. 5Tri-Service General Hospital, Department of Internal Medicine, Division of Nephrology, Taipei, Taiwan 114, ROC
  6. 6Institute of Occupational and Environmental Medicine, The University of Birmingham, Edgbaston, Birmingham B15 2TT, UK
  7. 7Department of Environment Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA
  1. Correspondence to:
 Dr C H Lai
 Department of Public Health, National Defence Medical Center, Taipei, Taiwan 114, ROC; lghndmctsgh.edu.tw

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

https://doi.org/10.1136/oem.2004.015107

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    Footnotes

    • Funding: this research was supported by the National Science Council in Taiwan (NSC 92-2320-B-016-062)

    • Competing interests: none declared