{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,13]],"date-time":"2026-08-13T14:39:29Z","timestamp":1786631969096,"version":"build-2736575974"},"reference-count":74,"publisher":"American Chemical Society (ACS)","issue":"8","license":[{"start":{"date-parts":[[2017,12,29]],"date-time":"2017-12-29T00:00:00Z","timestamp":1514505600000},"content-version":"vor","delay-in-days":3854,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2007,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Arsenic exposure may alter the efficiency of DNA repair. UV damage is specifically repaired by nucleotide excision repair (NER), and common genetic variants in NER may increase risk for non-melanoma skin cancer (NMSC).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>We tested whether polymorphisms in the NER genes XPA (A23G) and XPD (Asp312Asn and Lys751Gln) modify the association between arsenic and NMSC.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Incident cases of basal and squamous cell carcinoma (BCC and SCC, respectively) were identified through a network of dermatologists and pathology laboratories across New Hampshire. Population-based controls were frequency matched to cases on age and sex. Arsenic exposure was assessed in toenail clippings. The analysis included 880 cases of BCC, 666 cases of SCC, and 780 controls.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>There was an increased BCC risk associated with high arsenic exposure among those homozygous variant for XPA [odds ratio (OR) = 1.8; 95% confidence interval (CI), 0.9\u20133.7]. For XPD, having variation at both loci (312Asn and 751Gln) occurred less frequently among BCC and SCC cases compared with controls (OR = 0.8; 95% CI, 0.6\u20131.0) for both case groups. In the stratum of subjects who have variant for both XPD polymorphisms, there was a 2-fold increased risk of SCC associated with elevated arsenic (OR = 2.2; 95% CI, 1.0\u20135.0). The test for interaction between XPD and arsenic in SCC was of borderline significance (p &amp;lt; 0.07, 3 degrees of freedom).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings indicate a reduced NMSC risk in relation to XPD Asp312Asn and Lys751Gln variants. Further, these data support the hypothesis that NER polymorphisms may modify the association between NMSC and arsenic.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1289\/ehp.10096","type":"journal-article","created":{"date-parts":[[2007,6,8]],"date-time":"2007-06-08T15:11:36Z","timestamp":1181315496000},"page":"1231-1236","source":"Crossref","is-referenced-by-count":71,"title":["Polymorphisms in Nucleotide Excision Repair Genes, Arsenic Exposure, and Non-Melanoma Skin Cancer in New Hampshire"],"prefix":"10.1021","volume":"115","author":[{"given":"Katie M.","family":"Applebaum","sequence":"first","affiliation":[{"name":"Department of Epidemiology and"},{"name":"Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Margaret R.","family":"Karagas","sequence":"additional","affiliation":[{"name":"Section of Biostatistics and Epidemiology, Department of Community and Family Medicine, and the Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, New Hampshire, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David J.","family":"Hunter","sequence":"additional","affiliation":[{"name":"Department of Epidemiology and"},{"name":"Channing Laboratory, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul J.","family":"Catalano","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA"},{"name":"Department of Biostatistical Science, Dana Farber Cancer Institute, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven H.","family":"Byler","sequence":"additional","affiliation":[{"name":"Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steve","family":"Morris","sequence":"additional","affiliation":[{"name":"Research Reactor Center, University of Missouri, Columbia, Missouri, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heather H.","family":"Nelson","sequence":"additional","affiliation":[{"name":"Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA"},{"name":"Division of Epidemiology and Community Health, Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"316","published-online":{"date-parts":[[2007,6,11]]},"reference":[{"key":"2026080504023928500_micit1","doi-asserted-by":"crossref","first-page":"123","DOI":"10.1016\/S0378-4274(03)00117-6","article-title":"DNA repair gene XPD and susceptibility to arsenic-induced hyperkeratosis","volume":"143","author":"Ahsan","year":"2003","journal-title":"Toxicol Lett"},{"key":"2026080504023928500_micit2","doi-asserted-by":"crossref","first-page":"1193","DOI":"10.1289\/ehp.9008","article-title":"Arsenic exposure is associated with decreased DNA repair in vitro and in individuals exposed to drinking water arsenic","volume":"114","author":"Andrew","year":"2006","journal-title":"Environ Health Perspect"},{"key":"2026080504023928500_micit3","doi-asserted-by":"crossref","first-page":"263","DOI":"10.1002\/ijc.10968","article-title":"Decreased DNA repair gene expression among individuals exposed to arsenic in United States drinking water","volume":"104","author":"Andrew","year":"2003","journal-title":"Int J Cancer"},{"key":"2026080504023928500_micit4","doi-asserted-by":"crossref","first-page":"672","DOI":"10.1093\/carcin\/bgl181","article-title":"Polymorphism in the ERCC2 codon 751 is associated with arsenic-induced premalignant hyperkeratosis and significant chromosome aberrations","volume":"28","author":"Banerjee","year":"2007","journal-title":"Carcinogenesis"},{"key":"2026080504023928500_micit5","doi-asserted-by":"crossref","first-page":"65","DOI":"10.1006\/taap.1999.8723","article-title":"Low levels of arsenic trioxide stimulate proliferative signals in primary vascular cells without activating stress effector pathways","volume":"159","author":"Barchowsky","year":"1999","journal-title":"Toxicol Appl Pharmacol"},{"key":"2026080504023928500_micit6","first-page":"994","article-title":"Cancer Mortality in Zones of Arsenical Waters of the Province of Cordoba, Argentine Republic. 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