A compound that comes from the breakdown of once-common pest-control chemical DDT is linked with an increased risk of testicular cancer, a new study says.
Researchers measured pesticide levels, as well as levels of the chemicals that pesticides produce as they break down, in blood samples from more than 700 men who had been diagnosed with testicular cancer. They compared blood samples to more than 900 healthy men.
The study showed that men with the highest levels of DDE, the main chemical that DDT produces as it breaks down, had a 70 per cent increased risk of developing testicular cancer.
The research, led by Dr. Kathleen McGlynn of the National Cancer Institute in the United States, was published Tuesday in the Journal of the National Cancer Institute.
As was the case in the United States, the use of DDT in Canada was phased out in the mid-1970s. It was first used in Canada in the 1940s, primarily for pest control in crops.
Because it doesn't break down easily, DDE is still found in the environment. It is present in the air, water and soil, and is even found in breast milk.
"In the United States, over 95 per cent of the population that were examined still had detectable levels of DDE," McGlynn told CTV.ca.
"Even though DDT has been banned since the early seventies, its legacy lives on."
McGlynn said that she could not say exactly how DDE might influence the development of testicular cancer. However, because DDT has an estrogen-like effect in the body, she speculated that DDE also influences hormonal processes.
Abstract:
Persistent Organochlorine Pesticides and Risk of Testicular Germ Cell Tumors
Katherine A. McGlynn, Sabah M. Quraishi, Barry I. Graubard, Jean-Philippe Weber, Mark V. Rubertone, Ralph L. Erickson
Background: Exposure to endocrine-disrupting chemicals, such as persistent organochlorine pesticides, has been suggested to increase the risk of testicular germ cell tumors (TGCTs).
Methods: To study the relationship of POP exposure to TGCT risk, prediagnostic serum samples from 754 case subjects and 928 control subjects enrolled in the Servicemen's Testicular Tumor Environmental and Endocrine Determinants Study were analyzed for cis-nonachlor, trans-nonachlor, oxychlordane, total chlordanes, 锟�-hexachlorocyclohexane, mirex, p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE), and p,p'-dichlorodiphenyltrichloroethane. Adjusted odds ratios (ORs) and their associated 95% confidence intervals (CIs) for the risk of TGCT overall and for the histological subgroups, seminoma and nonseminoma, were estimated using multivariable logistic regression. All statistical tests were two-sided.
Results: TGCT risk was statistically significantly associated with higher plasma levels of p,p'-DDE (for highest quartile [Q4] vs lowest quartile [Q1], OR = 1.71, 95% CI = 1.23 to 2.38, Ptrend = .0002) and of two chlordane components, cis-nonachlor (Q4 vs Q1, OR = 1.56, 95% CI = 1.11 to 2.18, Ptrend = .009) and trans-nonachlor (Q4 vs Q1, OR = 1.46, 95% CI = 1.07 to 2.00, Ptrend = .026). Seminoma risk was statistically significantly associated with p,p'-DDE (Q4 vs Q1, OR = 1.91, 95% CI = 1.22 to 2.99, Ptrend = .0008), cis-nonachlor (Q4 vs Q1, OR = 1.93, 95% CI = 1.27 to 2.93, Ptrend = .0045), trans-nonachlor (Q4 vs Q1, OR = 1.72, 95% CI = 1.11 to 2.67, Ptrend = .033), and a chlordane metabolite, oxychlordane (Q4 vs Q1, OR = 1.64, 95% CI = 1.04 to 2.60, Ptrend = .048), whereas nonseminoma risk showed a statistically significant association with p,p'-DDE only (Q4 vs Q1, OR = 1.63, 95% CI = 1.10 to 2.42, Ptrend = .0044).
Conclusions: Increased exposure to p,p'-DDE may be associated with the risk of both seminomatous and nonseminomatous TGCTs, whereas exposure to chlordane compounds and metabolites may be associated with the risk of seminoma. 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.
