By Janet Raloff
From Chicago, at the EPA Emerging Pollutants Workshop
A growing number of products designed to shun both water and oil rely on fluorine-based compounds. The nonstick chemicals also serve in stain-resistant coatings and as surfactants in fire-fighting foams, floor polishes, and insecticides. What these fluorine compounds don’t do is fully degrade.
In the environment, many break down only to perfluorooctane sulfonate (PFOS), a remarkably persistent pollutant that has started showing up in the blood of people and animals. Fetal exposures to this proliferating pollutant can harm newborn mice and rats, a new study shows.
Christopher Lau of the Environmental Protection Agency in Research Triangle Park, N.C., and his colleagues exposed female rodents to a range of PFOS doses throughout pregnancy. Though high doses of the compounds were tested, the study included exposures yielding blood concentrations of PFOS similar to those in some people exposed to the chemicals at factories that make the fluorine-based precursors of PFOS. Those amounts can be hundreds of times higher than those to which the general population is exposed.
The higher exposures in the new study proved toxic to pregnant rodents, which failed to gain much weight during gestation. Yet at birth, all pups looked normal, Lau notes. Only those pregnant rodents getting the highest doses in the study were a little more likely to bear with birth defects, such as cleft palate.
If the experiments had ended there, Lau says, PFOS wouldn’t look like much of a reproductive hazard. However, his team observed the pups for several days after birth, and that’s when PFOS’ more-devastating effects emerged.
All pups in the highest-exposure groups were born active and pink, but within an hour turned sickly and soon died. Nearly all rat pups from mothers getting the next-highest exposure to PFOS died within 8 to 12 hours. Even half of pups from the middle-exposure group eventually succumbed.
The exposed pups that managed to survive showed various problems. For example, they grew more slowly than unexposed newborns did. And the activity of their choline acetyltransferase, an important brain enzyme, was subtly but significantly impaired. Lau and his colleagues detail their new findings in the August Toxicological Sciences.
Although puzzled by the high mortality of newborns that had initially appeared healthy, the scientists suspect that those deaths trace to impaired lung development. At the workshop, Lau unveiled photos showing that as fetal exposure to PFOS climbs, the lungs don’t expand as fully after birth. He speculates that the effect might reflect the reduction in PFOS-exposed moms and newborns of certain thyroid hormones that are pivotal to the development of the lungs and other organs.
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