The trouble with PFOA: testing, regulation and science concerning perfluorooctanoic acid and implications for future litigation.

• Author: Berger, Bruce J.
• Position: Perfluorooctanoic acid

IN THE April 2007 Defense Counsel Journal, we wrote about "endocrine disrupters" ("EDs"), widely used synthetic chemicals that are believed to disrupt the body's normal hormonal functions. (1) This article will provide an update on this topic, reviewing recent testing, regulation, science, and litigation regarding one alleged ED, perfluorooctanoic acid ("PFOA").

1. Background

   PFOA, also known as C8, is a synthetic chemical that has been used in the manufacture of commercial products such as non-stick cookware, stain-resistant clothing and carpets, food wrappers, and firefighting foam, and has many industrial uses as well. Although "[t]here is still controversy over PFOA's toxicity," (2) PFOA has raised health concerns because it is persistent in the environment, found at low levels in the blood of the general U.S. population, remains in the human body for a long time, and has been linked to adverse health effects in laboratory animals. (3)

   In 2006, the United States Environmental Protection Agency ("EPA") instituted--and eight manufacturers signed onto--a Global Stewardship Program designed to phase out PFOA by the year 2015. (4) Recent findings of contaminated soil and drinking water and new and continuing studies on human health effects, however, ensure the potential for future litigation. (5)

2. Testing and Regulation

   PFOA fears have spurred recent action in several states. In Alabama, allegedly high levels of PFOA and other perfluorochemicals ("PFCs") were found in grazing land near Decatur, prompting concern that they had spread to milk and meat and seeped into the water supply. (6) In response, EPA issued a short-term Provisional Health Advisory limit for PFOA in drinking water of 0.4 parts per billion (ppb). (7) Tests of nearby wells and ponds revealed that, out of 51 samples, 25% exceeded that limit, (8) although PFOA was present in local drinking water systems at levels "well below anything that could be a health risk." (9) The exact source of the chemicals is unknown, but a public meeting held in June 2009 discussed the status of the EPA investigation. (10) The director of the EPA's water protection division has ordered potential contributing companies to "expand a survey of private wells." (11)

   Drinking water supplies are also being tested in Georgia and Minnesota. In the former, the local news rushed to report elevated PFOA levels before the EPA had even seen test results. (12) In the latter, the suspected source of local contamination is a firefighting foam made by 3M that allegedly "is flushed into storm sewers or left to seep into the ground" after being used "in training exercises, often on city-owned property adjacent to municipal wells." (13) Indeed, plaintiffs' attorneys are trolling for clients. (14) California may be another future site for lawsuits, as the Carcinogen Identification Committee, which advises the state EPA's Office of Health Hazard Assessment (OEHHA), recently recommended PFOA for "the highest priority review" for inclusion in its Proposition 65 list of hazardous chemicals. (15)

   As part of a 2005 settlement with EPA, DuPont is testing whether fluorotelomers in its consumer products are breaking down into PFOA and other perfluorinated chemicals. (16) On January 8, 2009, the federal Environmental Appeals Board (17) approved a three-year extension for the completion of the tests, provoking some public outcry. (18) Under the program, "DuPont must provide replacement water supplies for anyone whose drinking water contains more than the EPA-recommended level of 0.4 parts per billion." (19) Residents near the company's Chamber Works plant in New Jersey, however, are calling for a stricter measure, the 0.04 micrograms per liter (equivalent to 0.04 ppb in water) level recommended by the state's Department of Environmental Protection (DEP). (20)

3. Science

   i. Environmental Studies

   Environmental testing in Alabama, Minnesota, and elsewhere involves sampling the PFOA levels in the water or soil of a given area and, using a "safety" level extrapolated from the limited health studies available, determining whether the local human population is at risk. There are several problems with this approach, including the uncertain derivation of the safety level, as illustrated by the competing figures promulgated by the EPA and New Jersey's DEP.

   Researchers from DEP and Rutgers University (21) used a "risk assessment approach" to derive "a health-based drinking water concentration protective for lifetime exposure" to PFOA of 0.04 micrograms per liter. (22) This figure was based on two main assumptions: first, that there is a quantifiable connection between PFOA in drinking water and the blood serum of the local population; second, and more importantly, that PFOA in human blood relates to identifiable adverse health effects. The researchers determined that there is approximately a 100:1 serum to drinking water concentration ratio using two different studies. The 100:1 ratio was observed in one study of a highly contaminated area in Ohio. (23) The researchers then found "a similar ratio" by reviewing data from five Ohio and West Virginia water districts with lower PFOA concentrations. (24) While PFOA serum levels seemed to rise with the level in drinking water in these five lower-concentration areas, the researchers caution that, because of various unknowns, "the mean or median drinking water concentrations in these districts cannot be accurately estimated from the range of concentrations." (25)

   To determine at what level PFOA in drinking water may pose a risk to humans, the researchers turned to a 2005 EPA draft risk assessment, which "identified toxicological end points in experimental animals," mainly rats. (26) We have previously noted the limited usefulness of animal studies in determining potential human health effects. (27) Many problems arise in attempting to extrapolate results in animals to human beings. (28) For example, any correlation between the effect of high blood concentration of PFOA in animals and the minuscule concentrations in humans is purely speculative. As one science panel notes, although "[a]nimal studies suggest that [PFOA] exposure can cause some cancers, but up to this point the few human studies which have been done have shown no clear increase in cancer.... Animal evidence indicates C8 can damage the liver, but again, the few human studies which have been done do not support this." (29) In addition, animal studies have not always proven consistent, even with each other. There is a "tremendous species difference in elimination" of PFOA, and "also gender differences" found in some animals, but not in others. (30) In fact, studies have concluded that "[i]t is clear that there are vast species differences in the toxicokinetics of PFAAs." (31)

   The New Jersey researchers used an uncertainty factor ("UF") (32) of 10 to account for interspecies extrapolation, but note that there was some question at EPA of "whether comparison on this basis fully addresses interspecies toxicokinetic differences, and whether an interspecies UF of 3 rather than 10 is appropriate." (33) The New Jersey study also used a "standard UF of 10 for subchronic to chronic exposure" to explain the difference between their 0.04 ppb figure for lifetime PFOA exposure and the 0.4 ppb provisional level for short-term exposure advised by EPA. (34) Although a factor of 10 generally is applied to extrapolate chronic exposure from subchronic exposure, the assumption on which these levels are based are not necessarily valid. At least one study has questioned the necessity of using such a high factor. (35) Finally, the New Jersey study notes that there have been recent "data not considered" by EPA in developing its endpoints. (36) Mice, the study asserts, may be a more appropriate model for health effects extrapolation than rats, and "[r]ecent mouse developmental studies show significant effects not seen in the rat." (37) These effects also have not been seen in humans. (38) The New Jersey researchers also assert that evaluation of "other studies of similar or shorter duration not considered by USEPA. .. could result in a short-term health-based concentration below" 0.4 micrograms per liter. (39) However, the referenced studies are animal studies, and therefore should be seen only as hypothesis-generating, potentially indicating the need for further study. (40)

   Because PFOA is pervasive both in the environment and in human beings, (41) it is difficult to pinpoint its exact source, and the mechanism for its transfer to the human body is still unknown. (42) One recent study found that dust inhalation may contribute to human exposure to PFOA. (43) Another group of researchers found polyfluoroalkyl phosphoric acid diesters ("diPAP"s), a group of PFCs that break down into PFOA and are used in food wrappers, at low-level concentrations in human blood. (44) The findings "suggest that diPAPs are contributing a significant portion of the PFOA found in human blood ... maybe 10 percent or more." (45) According to the New Jersey study, non-drinking water sources "are assumed to provide 80%...