Abstract
Testicular germ cell carcinoma (TGCC) is the most common malignancy among men ages 20 to 34 years. Although the pathogenesis of TGCC is poorly understood, suboptimal androgen levels or impaired androgen signaling may play a role. Some persistent organochlorine pesticides commonly found in human tissue possess antiandrogenic properties. We examined whether the risk of TGCC is associated with serum levels of 11 organochlorine pesticides, including p,p′-DDE, and whether the p,p′-DDE-TGCC association is modified by CAG or GGN repeat polymorphisms in the androgen receptor gene. We conducted a population-based case-control study among 18- to 44-year-old male residents of three Washington State counties. Cases (n = 246) were diagnosed during 1999 to 2003 with a first, primary TGCC. Controls (n = 630) were men of similar age with no history of TGCC from the same population identified through random-digit telephone dialing. Questionnaires elicited information on demographic, medical, and lifestyle factors. A blood specimen provided serum for gas chromatography-high-resolution mass spectrometry analysis of organochlorine pesticide residues and DNA for genotyping. We observed no clear patterns between TGCC risk and concentrations of any of the organochlorines measured, nor did we observe that the risk associated with p,p′-DDE was modified by androgen receptor CAG (<23 versus ≥23 repeats) or GGN (<17 versus ≥17 repeats) genotype. This study does not provide support for the hypothesis that adult exposure to organochlorine pesticides is associated with risk of TGCC. Due to uncertainty regarding how well organochlorine levels measured in adulthood reflect exposures during early life, further research is needed using exposure measurements collected in utero or during infancy. (Cancer Epidemiol Biomarkers Prev 2008;17(8):2012–8)
- testicular cancer
- organochlorines
- DDE
- pesticides
- androgen receptor
Footnotes
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Grant support: National Cancer Institute, NIH grants R01CA095790 and R01CA085914 and National Institute of Environmental Health Sciences, NIH grants T32ES007262 and 5P30ES007033.
- Accepted May 30, 2008.
- Received January 12, 2008.
- Revision received April 17, 2008.