Outlawed Insecticide Linked to Prostate Cancer

by Todd Neale | MedPage Today | 06.21.2010

Exposure to the long-banned organochloride insecticide chlordecone may be associated with a greater chance of developing prostate cancer, a new case-control study showed.

Among residents of Guadeloupe, those who had the highest plasma levels of the chemical had 1.77-fold (95% CI 1.21 to 2.58) higher odds of being diagnosed with prostate cancer, according to Luc Multigner, MD, of the Institut National de la Santé et de la Recherche Médicale (INSERM) on the French West Indies island, and colleagues.

The findings, which were reported online in the Journal of Clinical Oncology, were similar when past exposure to chlordecone was assessed using a combination of years of residence in the French West Indies and plasma concentration of the insecticide, which was used in that country for over 30 years.

"Our results suggest that there is a causal relationship between chlordecone exposure and prostate cancer risk," Multigner and colleagues wrote.

Chlordecone, which was marketed as Kepone, is an estrogenic insecticide that has been banned for decades in several countries, including the U.S. (in 1975) and France (in 1993).

In the U.S., chlordecone was used as bait in household insect traps. In the French West Indies, the chemical was used extensively from 1973 until it was banned in 1993 to control pests on banana crops.

Chlordecone does not degrade in the environment, persisting in water and soil. The primary means of exposure in humans is through food.

The U.S. Environmental Protection Agency (EPA) considers the insecticide a likely carcinogen. It has been shown to cause hepatic tumors in rats and mice, and may act as a tumor promoter through hormone-mediated effects.

To explore a possible relationship with prostate cancer in the French West Indies, which has particularly high rates of prostate cancer, Multigner and his colleagues recruited men living in Guadeloupe -- 623 with prostate cancer and 671 without the disease.

Chlordecone was detected in about two-thirds of the cases and in the controls, with no difference between the two groups.

As plasma levels of the chemical increased, so did the odds of having a prostate cancer diagnosis (P=0.002 for trend). The finding persisted after controlling for age, total plasma lipid concentration, waist-to-hip ratio, and a history of prostate cancer screening.

Individuals with the highest levels of exposure assessed by a combination of years of residence in the French West Indies and plasma levels of chlordecone also had significantly increased odds of having prostate cancer (OR 1.73, 95% CI 1.04 to 2.88).

Stronger associations were seen among those with a family history of prostate cancer and among those who had lived in a Western country at some point (P<0.001). Individuals with both risk factors were nearly five-fold more likely to have prostate cancer (OR 4.94, 95% CI 1.15 to 21.23).

The researchers genotyped two single-nucleotide polymorphisms in the gene encoding chlordecone reductase. The variants result in low production of the enzyme and reduced clearance of the insecticide from the circulation.

Among individuals who had detectable plasma levels of chlordecone, carriers of the two genetic variants had a statistically nonsignificant higher chance of having prostate cancer (OR 5.23, 95% CI 0.82 to 33.32).

The study suggests that the association between chlordecone exposure and prostate cancer "may be affected by genetic background, together with environmental agents related to diet or lifestyle. These findings require further investigation," the authors wrote.

The study may be limited by virtue of being a patient-control study and also by unknown confounding factors, the authors said.

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