From Chemical & Engineering News:

Two perfluorinated chemicals are linked to a delayed onset of puberty, according to a study of nearly 6,000 children living near a chemical plant (Environ. Sci. Technol., DOI: 10.1021/es1038694).

Since 1951, a DuPont plant near Parkersburg, W. Va., has released perfluorooctanoic acid (PFOA), a surfactant used in Teflon production, into the air and the nearby Ohio River. As a result, people living in the area have abnormally high levels of this compound in their blood.

In 2001, residents of the Mid-Ohio River Valley filed a class-action lawsuit against DuPont, alleging health problems that arose from drinking contaminated water. The company settled the lawsuit and agreed to fund research to determine whether PFOA exposure caused measurable health changes. Scientists had previously shown—in animals only—that PFOA causes cancer and disrupts sexual development.

Tony Fletcher, an epidemiologist at the London School of Hygiene & Tropical Medicine, sits on the scientific advisory panel established by the settlement. He wanted to know if PFOA alters sexual development in humans as it does in animals.

In 2005 and 2006, in research funded by the settlement, health care workers collected blood and medical histories from 69,030 people who lived in contaminated water districts surrounding the chemical plant. Fletcher and his colleagues analyzed data gathered from 3,067 boys and 2,931 girls between the ages of 8 and 18. They found that the median PFOA serum concentration was 26 ng/mL for boys and 20 ng/mL for girls. Both concentrations were much higher than the level in the general U.S. population, 4.2 ng/mL. The researchers also examined serum levels of a related chemical that has also been linked to altered timing of sexual maturation in animals. That chemical is perfluorooctane sulfonate (PFOS), which was not produced by the DuPont plant. The median level of PFOS in the children was only slightly higher than the national average.

To determine the age at which the children reached puberty, the researchers used a questionnaire and measured blood levels of sex hormones. When the investigators compared serum PFOA or PFOS levels with the age of onset of puberty, they found that girls with high concentrations of PFOA started puberty later than girls with low concentrations did. Meanwhile, both boys and girls with high levels of PFOS matured later than their low-concentration peers did. For both chemicals, the median delays in puberty were about 4 to 6 months—a significant change, but one that’s unlikely to cause health problems, Fletcher says.

“These results were surprising because many endocrine disrupters lead to earlier puberty rather than delayed puberty,” he says. Previous studies of the developmental effects of perfluorochemicals have used only small groups of people and produced inconclusive results, Fletcher says. But he hopes that his study, the largest yet to examine the effects of PFOA and PFOS on puberty in humans, will pave the way for studies of other populations exposed to perfluorochemicals early in life.