April 29, 2008 -- Men exposed to the lingering remnants of the once widely used pesticide DDT have an increased risk for the most common form of testicular cancer.
Scientists reporting in the April 29 issue of the Journal of the National Cancer Institute have found that men with the highest blood levels of DDE (dichlorodiphenyldichloroethylene), a DDT byproduct, were 1.7 times more likely to develop testicular germ cell tumors than those who had the lowest levels.
DDT (dichlorodiphenyltrichloroethane) is a synthetic bug killer known as an organochlorine pesticide. It was developed during the 1940s to kill mosquitos and prevent insect-borne diseases such as malaria. Farmers later sprayed it on crops to control insects.
The U.S. banned DDT in 1972 because of potential health risks. However, the chemical and its breakdown products, or metabolites, can persist in the environment for many years.
Studies have linked persistent exposure to DDT and similar pesticides to various health risks, including reproductive damage and cancer. But the findings regarding testicular cancer have not been replicated in an independent data set.
For the current study, Katherine McGlynn, PhD, of the National Cancer Institute, and colleagues evaluated the relationship between organochlorine pesticide exposure and a man's risk of testicular germ cell tumors (TGCTs). Germs cells are the cells that produce sperm. The majority of testicular cancers arise from these cells. The rate of TGCTs in the U.S. has been increasing for at least 30 years, since about the time DDT was banned.
McGlynn's team measured the amount of pesticides or their breakdown products in blood samples from healthy men and those who were later diagnosed with TGCTs. The men donated the blood about 14 years earlier as part of the U.S. Servicemen's Testicular Tumor Environmental and Endocrine Determinants study.
The researchers divided the men into groups based on the level of a particular pesticide in their blood and found that the highest levels of DDE were associated with an increased chance of developing testicular cancer compared with those with the lowest levels.
"If the relative risks calculated in this study are accurate ... the proportion of disease in the study population that is attributable to DDE exposure ... would be approximately 15 percent for all [testicular germ cell tumors]," the authors write.
McGlynn notes that it is impossible to determine when the men were exposed to the pesticide, but she adds that it may date back to the mother's pregnancy or shortly thereafter.
"Because evidence suggests that TGCT is initiated in very early life, it is possible that exposure to these persistent organic pesticides during fetal life or via breast feeding may increase the risk of TGCT in young men," she writes.
Although DDT is banned in the U.S., developing countries continue to use the product and more widespread use is being considered. The study authors encourage further studies to examine the link between the pesticides and testicular cancer in other populations.
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