Exposure to wood smoke, HPV infection, and genetic susceptibility for cervical neoplasia among women in Colombia
Cervical cancer is the second leading cause of death from cancer among women in Colombia (16/100,000). Infection with high‐risk human papillomavirus (HPV) plays a major role in the etiology of high‐grade squamous intraepithelial lesions (HSILs). Exposure to chemical agents may be a cofactor for tumo...
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Published in | Environmental and molecular mutagenesis Vol. 47; no. 7; pp. 553 - 561 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.08.2006
Wiley-Liss |
Subjects | |
Online Access | Get full text |
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Summary: | Cervical cancer is the second leading cause of death from cancer among women in Colombia (16/100,000). Infection with high‐risk human papillomavirus (HPV) plays a major role in the etiology of high‐grade squamous intraepithelial lesions (HSILs). Exposure to chemical agents may be a cofactor for tumor induction, and individual genetic differences in the metabolism of these chemical agents may affect the susceptibility of individuals towards the development of HSIL. In this case–control study, a total of 91 cases with HSIL and 92 healthy controls, frequency‐matched by age and place of origin, were recruited, and their frequencies of CYP2E1, GSTM1, and GSTT1 polymorphism were determined. We then evaluated the association of these polymorphisms, by themselves and in combination with wood smoke exposure and HPV‐infection status, with the risk of HSIL. The results indicate that GSTM1 and GSTT1 polymorphism were not associated with HSIL, although a small increase in risk was observed for individuals who were GSTT1 null (OR = 1.4, 95% CI = 0.57–3.44). Contrary to other investigations, the c2/c2 variant of the CYP2E1 gene was associated with a significant increase in risk after adjusting for wood smoke exposure (OR = 6.3, 95% CI = 1.10–36.38) or wood smoke exposure and HPV‐infection status (OR = 10.7, 95% CI = 1.76–65.58). Wood smoke exposure also increased the risk of HSIL among CYP2E1 c2/c2 HPV‐positive women (OR = 3.3, CI = 0.50–22.50); however, the increase did not achieve statistical significance. Our study provides tantalizing evidence that genetic differences in the metabolism of wood smoke carcinogens, particularly metabolism by CYP2E1, may confer susceptibility for HSIL development. Further investigations with larger populations will be needed to confirm this association, which may provide important information for improving cervical cancer prevention programs. Environ. Mol. Mutagen., 2006. © 2006 Wiley‐Liss, Inc. |
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Bibliography: | Colciencias, Observatorio Colombiano de Ciencia y Tecnología - No. 1103-04-11087 ark:/67375/WNG-KQ4N6J95-N istex:DAF46965740AB22BFD396DA0EE54D10E1804BAD6 ArticleID:EM20228 Presented at the 9th International Conference on Environmental Mutagens and 36th Annual Meeting of the Environmental Mutagen Society, San Francisco, CA, September 3-8, 2005. Presented at the 9th International Conference on Environmental Mutagens and 36th Annual Meeting of the Environmental Mutagen Society, San Francisco, CA, September 3–8, 2005. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0893-6692 1098-2280 |
DOI: | 10.1002/em.20228 |