Common pollutants undermine masculinity

 Some widespread pesticides and chemicals in plastics can induce reproductive impairment in males, according to seven new animal studies. These compounds wreak their havoc by blocking the action of male sex hormones as they program sexual development.

 Phthalates, ubiquitous oily solvents that make plastics flexible, have become the most abundant synthetic chemicals in the environment. One of the new studies examines the effects of fetal exposure to either diethylhexyl phthalate (DEHP), a softening agent found in most polyvinyl chloride (PVC) products, or di(n-butyl) phthalate (DBP), an additive in mosquito repellents.

 L. Earl Gray Jr. and his colleagues at the Environmental Protection Agency in Research Triangle Park, N.C., administered the chemicals to female rats from weaning through lactation. They gave doses of 200 to 1,000 milligrams per kilogram of body weight. Then, they examined the exposed animals' offspring.

 Compared with rats whose mothers had no phthalate exposure, these offspring produced far less testosterone and exhibited a range of abnormalities. Sometimes one testicle was absent or appeared as just a sac of blood. Says Gray, "We've never seen anything like this."

 Prenatal exposure to either phthalate also markedly reduced the size of a muscle that runs from the colon to the base of the penis. In some offspring, the epididymis, a sperm-storing organ, was similarly just a fraction of its normal size.

 Gray's team catalogued these and also many abnormalities that had already been seen with compounds that block male sex hormones, or androgens. Many test animals bore classically feminine features such as permanent nipples. The data were presented at the Society of Toxicology meeting in New Orleans 2 weeks ago and in the just-released January-March issue of Toxicology and Industrial Health.

 Paul M.D. Foster and his coworkers at the Chemical Industry Institute of Toxicology in Research Triangle Park, N.C., have also been exploring the antiandrogenic effects of phthalates. At the toxicology meeting, they reported that developmental defects in males can be triggered by as little as 100 mg of DBP per kg of body weight in the mom.

 DBP halves testosterone production by the fetal testis, their data show. Foster says that the testis responds by making twice as many cells, a proliferation that resulted in testicular tumors after the animals became adults.

 Many commercial chemicals possess antiandrogenic activity. In four other papers in Toxicology and Industrial Health, Gray's group describes two fungicides (vinclozolin and procymidone), an herbicide (linuron), an insecticide (methoxychlor), and several other compounds that provoke various degrees of reproductive-organ abnormalities.

 Linuron's devastating effect had a surprising aspect. Usually, external genital abnormalities hint at disruption of internal organs. However, although few linuron-exposed offspring had external malformations, "50 percent had a missing epididymis or malformed testis," Gray observes.

 His group also showed that exposing young male animals to an antiandrogenic pesticide just before puberty dramatically delays the maturation of their sexual organs.

 The doses at which all these adverse effects occurred in the rats approach the "range where people are actually being exposed," says Boston physician Ted Schettler, science director of the Science and Environmental Health Network. Dialysis patients and people receiving fluids in most plastic intravenous bags get substantial exposure to DEHP, he notes. Many PVC-based teething toys also leach this phthalate.

 Peter L. deFur of Virginia Commonwealth University in Richmond worries, "I think there is more than just a possibility that [current human] exposures to antiandrogens are having measurable health effects."