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Carcinogenesis Advance Access published online on June 19, 2008
Carcinogenesis, doi:10.1093/carcin/bgn153
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Renal cell carcinoma, occupational pesticide exposure, and modification by glutathione S-transferase polymorphisms

S Karami1, P Boffetta2, N Rothman1, RJ Hung2,3, T Stewart1, D Zaridze4, M Navritalova7, D Mates9, V Janout5, H Kollarova5, V Bencko6, N Szeszenia-Dabrowska8, I Holcatova6, A Mukeria4, J Gromiec11, S Chanock10, P Brennan2, W-H Chow1 and LE Moore1

1 Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, MD, USA
2 International Agency for Research on Cancer, Lyon, France
3 University of California, School of Public Health, Berkeley California
4 Institute of Carcinogenesis, Cancer Research Centre, Moscow, Russia
5 Department of Preventive Medicine, Faculty of Medicine, Palacky University, Olomouc, Czech Republic
6 Institute of Hygiene and Epidemiology, Charles University, First Faculty of Medicine, Prague, Czech Republic
7 Department of Cancer Epidemiology and Genetics, Masaryk Memorial Cancer Institute, Brno, Czech Republic
8 Department of Epidemiology, Institute of Occupational Medicine, Lodz, Poland
9 Institue of Public Health, Bucharest, Romania
10 Core Genotyping Facility at the Advanced Technology Center of the National Cancer Institute, NIH, Department of Health and Human Services
11 Nofer Institute of Occupational Medicine, Department of Chemical Hazards, Lodz, Poland

This study investigated associations between occupational pesticide exposure and renal cell carcinoma (RCC) risk. To follow-up on a previous report by Buzio and colleagues, we also considered whether this association could be modified by glutathione S-transferase M1 and T1 (GSTM1 and GSTT1) genotypes. 1,097 RCC cases and 1,476 controls from Central and Eastern Europe were interviewed to collect data on lifetime occupational histories. Occupational information for jobs held for at least 12 months duration were coded for pesticide exposures and assessed for frequency and intensity of exposure. GSTM1 and T1 gene deletions were analyzed using TaqMan® assays. A significant increase in RCC risk was observed among subjects ever exposed to pesticides (OR: 1.60; 95% CI: 1.00-2.55). After stratification by genotypes, increased risk was observed among exposed subjects with at least one GSTM1 active allele (OR: 4.00; 95%CI: 1.55-10.33) but not among exposed subjects with two GSTM1 inactive alleles, compared to unexposed subjects with two inactive alleles (P-interaction: 0.04). Risk was highest among exposed subjects with both GSTM1 and GSTT1 active genotypes (OR: 6.47; 95% CI: 1.82-23.00; P-interaction: 0.02) compared to unexposed subjects with at least one GSTM1 or T1 inactive genotype. In the largest RCC case-control study with genotype information conducted to date, we observed that risk associated with pesticide exposure was exclusive to individuals with active GSTM1/T1 genotypes. These findings further support the hypothesis that GST polymorphisms can modify RCC risk associated with occupational pesticide exposure.

Key Words: RCC • glutathione transferase • GSTM1 • GSTT1 • pesticide

Received April 12, 2008; revised June 5, 2008; accepted June 14, 2008.


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