Prenatal DDT Exposure and Testicular Cancer: A Nested Case-Control Study

ABSTRACT

The authors examined maternal serum levels of DDT-related compounds in relation to son's risk of testicular cancer 30 years later. Fifteen of 9,744 live-born sons were diagnosed with germ cell testicular cancer and had maternal serum samples. Cases were matched to three controls on race and birth year. Maternal serum DDT-related compounds, measured in the early postpartum, were associated with her son's risk of testicular cancer. Despite low statistical power, we observed that mothers of cases had a significantly higher ratio of p,p′-DDT (1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane) to p,p′-DDE (1,1′-dichloro-2,2′-bis(p-chlorophenyl)ethylene) and lower o,p′-DDT (1,1,1-tricholoro-2-(p-chlororphenyl)-2-(o-chlorophenyl)ethane). These findings are consistent with earlier exposure to DDT and with slower p,p′-DDT elimination among mothers of cases. Whether these associations could be direct, or operate via other pathways is unknown. Further research on interindividual differences in DDT metabolism could provide clues to testicular cancer etiology.

KEYWORDS:

• DDT
• DDE
• pregnancy
• prospective
• testicular cancer

Acknowledgments

We acknowledge Julie A. Booher and the late Theodore E. Cohn who encouraged us to undertake this study and helped find funding to support it, the late Jacob Yerushalmy who designed and initiated the CHDS; Barbara van den Berg, the second Director of the CHDS, for comments on earlier versions, Mary Wolff for performing the assays and for comments on an earlier version of the manuscript, Morgana Mongraw-Chaffin and Richard Cohen who performed data analysis and contributed to early drafts of the manuscript, Ruthann Rudel who advised on interpretation of findings, and the California Cancer Registry for their ongoing work in maintaining the high quality of the cancer linkage in California.

The collection of cancer incidence data used in this study was supported by the California Department of Public Health as part of the statewide cancer reporting program mandated by California Health and Safety Code Section 103885; the National Cancer Institute's Surveillance, Epidemiology and End Results Program under contract N01-PC-35136 awarded to the Northern California Cancer Center, contract N01-PC-35139 awarded to the University of Southern California, and contract N02-PC-15105 awarded to the Public Health Institute; and the Centers for Disease Control and Prevention's National Program of Cancer Registries, under agreement #U55/CCR921930-02 awarded to the Public Health Institute. The ideas and opinions expressed herein are those of the author(s) and endorsement by the State of California, Department of Public Health, the National Cancer Institute, and the Centers for Disease Control and Prevention or their contractors and subcontractors is not intended nor should be inferred.

This project was made possible by funding from the Lance Armstrong Foundation and the National Institutes of Health (N01 DK63422). The point of view and conclusions expressed in this paper are those of the authors and do not necessarily represent the official position or policies of the Lance Armstrong Foundation or the Department of Health and Human Services.

The study sponsors had no role in study design, collection, analysis, or interpretation of the data, the writing of the report, or the decision to submit the paper for publication.