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BioMed Research International
Volume 2015 (2015), Article ID 892579, 10 pages
Research Article

Association of Environmental Arsenic Exposure, Genetic Polymorphisms of Susceptible Genes, and Skin Cancers in Taiwan

1Genomics Research Center, Academia Sinica, No. 128 Academia Road, Section 2, Nankang, Taipei 115, Taiwan
2Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei 100, Taiwan
3School of Public Health, College of Public Health and Nutrition, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan
4Department of Medical Research, Shuang Ho Hospital, Taipei Medical University, No. 291 Zhongzheng Road, Zhonghe District, New Taipei City 23561, Taiwan
5Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan
6Molecular and Genomic Epidemiology Center, China Medical University Hospital, China Medical University, Taichung 404, Taiwan
7Graduate Institute of Epidemiology, College of Public Health, National Taiwan University, 17 Xu-Zhou Road, Taipei 100, Taiwan

Received 26 August 2014; Revised 12 March 2015; Accepted 19 March 2015

Academic Editor: Marian K. Malde

Copyright © 2015 Ling-I Hsu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Deficiency in the capability of xenobiotic detoxification and arsenic methylation may be correlated with individual susceptibility to arsenic-related skin cancers. We hypothesized that glutathione S-transferase (GST M1, T1, and P1), reactive oxygen species (ROS) related metabolic genes (NQO1, EPHX1, and HO-1), and DNA repair genes (XRCC1, XPD, hOGG1, and ATM) together may play a role in arsenic-induced skin carcinogenesis. We conducted a case-control study consisting of 70 pathologically confirmed skin cancer patients and 210 age and gender matched participants with genotyping of 12 selected polymorphisms. The skin cancer risks were estimated by odds ratio (OR) and 95% confidence interval (CI) using logistic regression. EPHX1 Tyr113His, XPD C156A, and GSTT1 null genotypes were associated with skin cancer risk (OR = 2.99, 95% CI = 1.01–8.83; OR = 2.04, 95% CI = 0.99–4.27; OR = 1.74, 95% CI = 1.00–3.02, resp.). However, none of these polymorphisms showed significant association after considering arsenic exposure status. Individuals carrying three risk polymorphisms of EPHX1 Tyr113His, XPD C156A, and GSTs presented a 400% increased skin cancer risk when compared to those with less than or equal to one polymorphism. In conclusion, GSTs, EPHX1, and XPD are potential genetic factors for arsenic-induced skin cancers. The roles of these genes for arsenic-induced skin carcinogenesis need to be further evaluated.