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Occup Environ Med 2004;61:692-696 doi:10.1136/oem.2003.007435
  • Original article

Increased urinary excretion of 8-hydroxydeoxyguanosine in engine room personnel exposed to polycyclic aromatic hydrocarbons

  1. R Nilsson1,
  2. R Nordlinder1,
  3. B E Moen2,
  4. S Øvrebø3,
  5. K Bleie4,
  6. A H Skorve4,
  7. B E Hollund2,
  8. C Tagesson5
  1. 1Department of Occupational Medicine, The Sahlgrenska Academy at Göteborg University, Sweden
  2. 2Section for Occupational Medicine, University of Bergen, Norway
  3. 3Department of Toxicology, National Institute of Occupational Health, Oslo, Norway
  4. 4Department of Occupational Medicine, Haukeland Hospital, Bergen, Norway
  5. 5Department of Occupational and Environmental Medicine, University Hospital, Linköping, Sweden
  1. Correspondence to:
 Dr R Nilsson
 Department of Occupational Medicine, Göteborg University, St Sigfridsgatan 85, SE 41266 Göteborg, Sweden; ralph.nilssonymk.gu.se
  • Accepted 26 October 2003

Abstract

Background: Previous investigations indicate that engine room personnel on ships are exposed to polycyclic aromatic hydrocarbons (PAH) from oil and oil products, with dermal uptake as the major route of exposure. Several PAH are known carcinogens and mutagens.

Aims: To investigate the urinary excretion of a marker for oxidative DNA damage, 8-hydroxydeoxy-guanosine (8OHdG), in engine room personnel, and to study the association between 8OHdG and 1-hydroxypyrene (1OHP), a biological marker for PAH exposure.

Methods: Urine samples were collected from engine room personnel (n = 36) on 10 Swedish and Norwegian ships and from unexposed controls (n = 34) with similar age and smoking habits. The exposure to oils, engine exhaust, and tobacco smoke 24 hours prior to sampling was estimated from questionnaires. The urinary samples were frozen for later analyses of 8OHdG and 1OHP by high performance liquid chromatography.

Results: Excretion in urine of 8OHdG (adjusted to density 1.022) was similar for controls (mean 18.0 nmol/l, n = 33), and for those who had been in the engine room without skin contact with oils (mean 18.7 nmol/l, n = 15). Engine room personnel who reported skin contact with oil had increased excretion of 8OHdG (mean 23.2 nmol/l, n = 19). The difference between this group and the unexposed controls was significant. The urinary levels of ln 1OHP and ln 8OHdG were significantly correlated, and the association was still highly significant when the effects of smoking and age were accounted for in a multiple regression analysis.

Conclusion: Results indicate that exposure to PAH or possibly other compounds from skin contact with oils in engine rooms may cause oxidative DNA damage.

Footnotes

  • Present affiliation for R Nordlinder: Department of Environment and Chemistry, Volvo Technology Corporation, Göteborg, Sweden

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