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Carcinogenesis Advance Access originally published online on April 29, 2007
Carcinogenesis 2007 28(8):1697-1702; doi:10.1093/carcin/bgm099
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
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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, Quazzi Quamruzzaman4, Mahmuder Rahman4, Golam Mahiuddin4, Louise Ryan5, Li Su2 and David C. Christiani2

1 Department of Epidemiology and Public Health, Division of Environmental Health Sciences, Yale University School of Medicine, Epidemiology and Public Health, New Haven, CT, 06520 USA
2 Department of Environmental Health, Harvard School of Public Health, Boston, MA, 02115 USA
3 Department of Dermatology, Massachusetts General Hospital, Boston, MA, 02114 USA
4 Dhaka Community Hospital, 1217 Dhaka, Bangladesh
5 Department of Biostatistics, Harvard School of Public Health, Boston, MA, USA

* To whom correspondence should be addressed. Tel: +1 203 785 6062; Fax: +203 737 6023; Email: kathleen.mccarty{at}yale.edu

Background: Single-nucleotide polymorphisms in genes related to DNA repair capacity and ultraviolet 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 Xeroderma Pigmentosum complementation group D (XPD) (Lys751Gln and Asp312Asn) genes, tendency to sunburn and arsenic-related skin lesions. Methods: Unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Result: No significant association was observed between skin lesions and the XPD 312 Asp/Asn (adjusted OR = 0.87, 95% CI = 0.65–1.15) Asn/Asn (adjusted OR = 0.76, 95% CI = 0.50–1.15) (referent Asp/Asp); XPD 751 Lys/Gln (adjusted OR = 0.92, 95% CI = 0.69–1.23) Gln/Gln (adjusted OR = 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 with 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 with 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: XPD polymorphisms modified the relationship between tendency to sunburn and skin lesions in an arsenic exposed population. Further study is necessary to explore the effect of XPD polymorphisms and sun exposure on risk of arsenic-related skin lesions.

Abbreviations: BMI, body mass index; CI, confidence interval; LRT, likelihood ratio test; NER, nucleotide excision repair; OR, odds ratio; UV, ultraviolet; XPD, Xeroderma Pigmentosum complementation group D

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


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