A new study finds evidence that people may be exposed through drinking water to a persistent chemical — one used to make nonstick products  — at levels approaching concentrations that trigger adverse effects in laboratory animals.

The fluorine-based chemical, PFOA or perfluorooctanoic acid, has been in production for more than 50 years. One primary use has been the production of chemicals that long served as the basis of DuPont's Teflon line of nonstick products. Ironically, earlier studies have shown that the PFOA itself sticks around a very, very long time — potentially forever.

The chemical appeared in roughly two-thirds of some 30 public water systems sampled by New Jersey’s Department of Environmental Protection between 2006 and 2008, researchers report online and in an upcoming issue of Environmental Science & Technology.

In five of the New Jersey water systems sampled, PFOA concentrations exceeded a safety limit developed by the researchers — sometimes by a factor of two or three. In each of those instances, says toxicologist Keith Cooper of Rutgers University in New Brunswick, the affected water came from groundwater or from well water. However, he adds, where contaminated water entered a water-treatment plant, “[PFOA] concentrations in the intake water and the output water were basically the same.” So it looks like the treatment plants didn’t remove the pollutant.

How PFOA gets into water remains largely unknown, although the chemical has been used in everything from carpeting and frying pans to popcorn bags. So, Cooper says, “I think the values we saw in New Jersey water probably are representative of [water supplies] around the country.”

Human data have shown that blood concentrations of PFOA tend to be 100 times higher than the values in drinking water. To gauge whether the concentrations of PFOA found in the state’s aquifers, wells and surface waters were likely to pose health risks, the researchers used blood concentrations of PFOA associated with toxicity in animals. The scientists then calculated how low water concentrations of PFOA would need to be to fall below the adverse-effects level. For added safety, they cut this value to a 10th of the starting value — a common practice when toxicologists need to extrapolate between animals or human life stages.

As a result of this analysis, the researchers propose a drinking water limit of 0.04 micrograms per liter. On January 8, the Environmental Protection Agency proposed a “provisional health advisory” for PFOA that was 10 times higher. At the time, EPA explained it was issuing the advisory “in response to an urgent or rapidly developing situation” involving unregulated pollution.

One explanation for the difference: EPA’s value was set to deal with short-term emergencies such as a spill, Cooper says, whereas “ours was designed to deal with chronic exposure over a lifetime.”

Abby D. Benninghoff, a PFOA toxicologist at Oregon State University in Corvallis, finds the proposed New Jersey safety limit for PFOA pretty convincing. “I looked through the math pretty carefully and I am familiar with most of the studies that they based it on. So it [the proposed limit] strikes me as reasonable.”

But the implications are a bit unsettling. She’s been studying PFOA activity in trout, a surprisingly good model for testing the chemical’s human cancer risk (SN Online: 5/21/08), and in human cells. These data show that the 8-carbon PFOA molecule and its 9- and 10-carbon analogs — which also show up in the environment — all bind to and activate the estrogen receptor. In trout, this estrogen action promotes the development of liver cancer.

Concentrations of any of these chemicals needed to turn on this hormone mimicry in human cells are fairly low, she reported at a toxicology conference last November. Indeed, she now notes, such levels are in the same ballpark as what would likely develop in the blood of people drinking water from the more contaminated sites described by Cooper’s team.

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