Moms’ POPs, Sons’ Problems: Testicular cancer tied to a fetus’ pollutant contact

Women who’ve had substantial exposure to certain environmental pollutants are more likely than others to bear sons who develop testicular cancers. These findings of a new epidemiological study jibe with a current hypothesis that contact with hormonelike chemicals before birth raises a male’s risk of various genital problems.

In the United States, the testicular cancer rate climbed 67 percent between 1973 and 1999. A similar trend has affected parts of Europe, and past research suggested a link between this epidemic and rising exposures to artificial estrogens (SN: 2/26/94, p. 138), also known as endocrine disruptors.

Such hormonally active chemicals include persistent organic pollutants (POPs) such as hexachlorobenzene (HCB), polychlorinated biphenyls (PCBs), and chlordanes. These contaminants, which chemically resemble estrogen, the primary female sex hormone, break down slowly in the environment and accumulate in fatty tissues of people and animals.

To examine the relationship between POPs and testicular cancer, Lennart Hardell of Örebro University in Sweden and his colleagues took blood from 58 Swedish men, average age 30, who had the cancer. They then measured each sample’s concentrations of 46 POPs, including PCBs, HCB, and several chlordanes. They also made the same measurements on blood samples from a comparable number of healthy Swedish men of similar age and from most mothers of the men in either group.

Men with testicular cancer averaged higher concentrations of one POP, cis-nonachlordane, than other men did, but for all other chemicals examined, differences between the two groups were not significant.

Among the men’s mothers, however, relatively high blood concentrations of all PCBs, HCB, cis-nonachlordane, and one other chlordane were linked to sons’ cases of testicular cancer, Hardell and his colleagues report in an upcoming issue of Environmental Health Perspectives.

“This is the first time [testicular cancer researchers] have looked at persistent organic pollutants in mothers,” comments Niels E. Skakkebaek of Rigshospitalet in Copenhagen. Although the Swedish team sampled the mothers’ blood years after their sons were born, it’s reasonable to suspect that the women had elevated concentrations of the long-lasting pollutants in question during their pregnancies, he says. Release of most of these pollutants peaked in the 1970s.

In a current model for the disease’s origin, Richard Sharpe of the University of Edinburgh and Skakkebaek have proposed that exposure to endocrine disruptors before birth can alter testicular-cell development so that some cells become likely to turn cancerous after puberty (SN: 1/22/94, p. 56: Moreover, they say that these pollutants may explain the rising rates of male fertility problems and genital abnormalities such as undescended testicles and malformed penises.

While international environmental agreements now limit releases of some POPs, “there may be other chemicals out there that are endocrine disruptors, and we need to be very cautious about [using] those,” says Hardell.


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