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Carcinogenesis Advance Access published online on April 29, 2007
Carcinogenesis, doi:10.1093/carcin/bgm099
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Polymorphisms in XPD (Asp312Asn and Lys751Gln) genes, sunburn and arsenic related skin lesions

Kathleen M. McCarty1,2, Thomas J. Smith2, Wei Zhou2, Ernesto Gonzalez3, Quazi Quamruzzaman4, Mahmumder Rahman4, Golam Mahiuddin4, Louise Ryan5, Li Su2 and David C. Christiani2

1 Yale University School of Medicine, Epidemiology and Public Health, Division of Environmental Health Sciences, New Haven, CT, USA
2 Harvard School of Public Health, Department of Environmental Health, Boston, MA, USA
3 Massachusetts General Hospital, Department of Dermatology, Boston, MA, USA
4 Dhaka Community Hospital, Dhaka, Bangladesh
5 Harvard School of Public Health Department of Biostatistics, Boston, MA, USA

Correspondence to: Kathleen M. Mc Carty Division of Environmental Health Sciences, Yale University School of Public Health, LEPH, 60 College St, New Haven, CT 06520, USA. (203) 785-6062 fax (203) kathleen.mccarty{at}yale.edu

Background: Single nucleotide polymorphisms in genes related to DNA repair capacity and UV exposure have not been well investigated in relation to skin lesions associated with arsenic exposure. This population based case-control study, of 600 cases and 600 controls, frequency matched on age and gender in Pabna, Bangladesh in 2001-2002, investigated the association and potential effect modification between polymorphisms in XPD (Lys751Gln and Asp312Asn) genes, tendency to sunburn and arsenic related skin lesions.

Methods: Unconditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI).

Result: No significant association was observed between skin lesions and the XPD 312 Asp/Asn (AOR 0.87, 95%CI (0.65-1.15)) Asn/Asn (AOR 0.76, 95%CI (0.50-1.15)) (referent Asp/Asp); XPD 751 Lys/Gln (AOR 0.92, 95% CI (0.69-1.23)) Gln/Gln (AOR 0.98, 95%CI (0.66-1.45)) (referent Lys/Lys. While we did not observe any evidence of effect modification of these polymorphisms on the association between well arsenic concentration and skin lesions; we did observe effect modification between these polymorphisms and sunburn tendency and arsenic related skin lesions. Individuals with the heterozygote or homozygote variant forms (Asp/Asn or Asn/Asn) had half the risk of skin lesions (OR 0.45 95%CI 0.29-0.68) compared to those with the wild type XPDAsp312Asn genotype (Asp/Asp) and individuals with heterozygote or homozygote variant forms (Lys/Gln or Gln/Gln) had half the risk of skin lesions (OR 0.47 95%CI 0.31-0.72) compared to those with the wild type XPDLys751Gln genotype (Lys/Lys), within the least sensitive strata of sunburn severity. We observed effect modification on the multiplicative scale for XPD 751 and XPD 312.

Conclusion: Tendency to sunburn modified the relationship between XPD polymorphism and skin lesions. Further study is necessary to explore the effect of XPD polymorphisms and sun exposure on risk of arsenic related skin lesions.

Key Words: Arsenic • Sun • DNA repair • XPD • hyperkeratosis • melanosis • ERCC2 • molecular epidemiology • environmental health

Received December 24, 2006; revised March 20, 2007; accepted April 17, 2007.


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