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Beginning in the late 1940s, doctors prescribed high doses of a potent synthetic estrogen to prevent miscarriages. In the United States alone, some 3 million pregnant women may have received the therapy. But this drug--diethylstilbestrol (DES)--was banned after studies in the early 1970s showed that daughters of the treated women faced an increased risk of gynecologic cancers and reproductive abnormalities, including sterility.

What about sons? Those exposed to DES exhibited an unusually high incidence of genitourinary and reproductive abnormalities at birth. However, a new study finds, in contrast to earlier indications, such prenatal exposures did not impair the fertility of sons--even those born with genital defects.

"On the face of it, that seems weird," acknowledges study leader Allen J. Wilcox of the National Institute of Environmental Health Sciences (NIEHS) in Research Triangle Park, N.C. In fact, animal studies conducted at NIEHS 20 years ago showed that such prenatal exposures could induce devastating male reproductive problems, including sterility.

DES is the most potent estrogenic compound known--more powerful even than nature's primary estrogen. As such, DES has served as a model for scientists investigating the risks associated with the growing number and amount of estrogen-mimicking pollutants being released into the environment (SN: 7/3/93, p.10).

"We regarded this study as a step towards testing that," Wilcox told Science News. "If DES had an effect on a man's fertility, it would support the idea that weaker estrogens might be having similar, if weaker, effects on male reproduction" (SN: 1/22/94, p.56).

In the new study, reported in the May 25 New England Journal of Medicine (NEJM), his team surveyed evidence of fertility among the sons of women who took part in a double-blind DES trial at the University of Chicago during the early 1950s. Wilcox's group located 548 of the 848 boys born during the trial and interviewed 90 percent of them--253 who had been exposed to DES in the womb, 241 who had not.

The researchers note that 15 percent of the men whose mothers had taken DES reported genital malformations (mostly minor ones, such as epididymal cysts). That was three times the rate in unexposed men.

However, "we found no evidence that DES impairs male fertility," the researchers said--at least as measured by length of time to conception, age at fathering first child, average number of children, whether a man had ever fathered a child, and sexual function.

A study of the same Chicago sons in the 1970s had reported lower sperm counts and more abnormal sperm among those exposed prenatally to DES. "While we don't know the current sperm characteristics of these men," Wilcox notes, "it is possible DES affected sperm and did not affect fertility."

Endocrinologist Richard J. Sherins of the Genetics and IVF Institute in Fairfax, Va., made a similar point in a Feb. 2 NEJM editorial accompanying the report of a 20-year decline in semen quality and sperm counts among men in Paris (SN: 2/25/95, p.127). The French data did not signal a drop in fertility, he argues, because "sperm count [alone] does not translate into fertility."

But that said, Sherins argues that even in the face of this new DES study, "you have to be cautious about putting the whole [reproductive] issue of environmental estrogens to rest."

Endocrinologist Niels E. Skakkebaek of University Hospital in Copenhagen agrees: "I certainly think this issue remains an open one."

At a minimum, Wilcox maintains, environmental estrogens "might be a problem in species other than humans--and in a way that deserves very serious consideration." Moreover, he notes, other classes of emasculating chemicals, such as those that block male sex hormones, may masquerade as estrogens (SN: 7/2/94, p.15).

For now, Sherins says, the best policy "is to stay concerned."