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Cancer Epidemiology Biomarkers & Prevention Vol. 9, 271-277, March 2000
© 2000 American Association for Cancer Research

Risk of Breast Cancer and Organochlorine Exposure1

Mary S. Wolff2, Anne Zeleniuch-Jacquotte, Neil Dubin3 and Paolo Toniolo

Department of Community and Preventive Medicine, Mount Sinai School of Medicine, New York, New York 10029 [M. S. W.], and Departments of Obstetrics and Gynecology [P. T.] and Environmental Medicine [A. Z-J., N. D., P. T.] and Kaplan Comprehensive Cancer Center [A. Z-J., N. D., P. T.], New York University School of Medicine, New York, New York 10016

A prospective investigation of breast cancer and organochlorine (OC) exposures was undertaken in the New York University Women’s Health Study. Cases (n = 148) and individually matched controls (n = 295) were identified among women whose blood had been obtained 6 months or more prior to breast cancer diagnosis. In addition, among 84 cases and 196 controls, two or more consecutive annual blood samples were available to estimate half-lives of 1,1-dichloro-2,2-bis(p-chlorophenyl) ethene (DDE) and polychlorinated biphenyls (PCBs). Cases and controls had similar levels of DDE (geometric mean, 6.95 versus 7.27 ng/ml; lipid-adjusted geometric mean, 977 versus 1100 ng/g) and PCBs (5.04 versus 4.97 ng/ml; lipid-adjusted geometric mean, 683 versus 663 ng/g). These differences remained nonsignificant when estrogen receptor status of tumors was considered. DDE and PCB half-lives did not differ in case versus control patients. In control patients, DDE and PCB half-lives were strongly correlated (rs = 0.71), and the half-life of DDE (but not that of PCB) was inversely correlated with body mass index (BMI), yet the blood serum levels of PCB (but not those of DDE) were correlated with BMI. We conclude that there is no evidence for an association of breast cancer risk with DDE or PCB levels in blood (based on samples collected during the period 1987–1992) nor with their elimination half-lives. However, changes in DDE and PCBs over time are influenced by metabolism, BMI, and current OC exposures, and each may affect interpretation of OC levels in risk assessment models.




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