Perfluorooctanoic acid (PFOA) has been used used to manufacture Teflon and other non-stick and stain-resistant products. It is highly persistent in the environment and bioaccumulates efficiently through the foodchain and into biota. Therefore, PFOA contamination has been found in drinking water and house dust, and has been detected in significant portion of human blood samples. PFOA affects primarily the liver and can cause developmental and reproductive toxic effects at relatively low dose levels in experimental animals. It’s increased tumor incidence in rats, mainly in the liver. Epidemiological studies in PFOA-exposed workers do not indicate an increased cancer risk. Some have shown associations with elevated cholesterol and triglycerides, or with changes in thyroid hormones, but overall there is no consistent pattern of changes. In recent studies, PFOA exposure of pregnant women, measured by maternal and/or cord serum levels was associated with reduced birth weight. The European Food Safety Authority (EFSA) noted that these observations could be due to chance, or to factors other than PFOA. EPA has recently developed a drinking water health advisory, based on reproductive effects in laboratory animals.
PFOA exposure has been the subject of multiple class-action lawsuits, filed on behalf of residents who have been exposed through contaminated groundwater. More information about the regulatory and litigation issues can be found on SKAPP’s web site. According to a January 20th news item published in the InsideEPA.com Risk Policy Report (“PFOA Rulings May Stymie Plaintiffs’ Use of EPA Risk Methods in Tort Suits”), Federal judges in West Virginia and New Jersey declined class-action status to plaintiffs seeking medical monitoring from DuPont due to contamination from perfluorooctanoic acid (PFOA). These rulings were based in part because the plaintiffs used EPA-backed risk assessment methods to argue their cases.
According to the West Virginia court, plaintiffs seeking medical monitoring must show significant exposure, meaning exposure to higher levels or for a longer duration than the general public. Next, plaintiffs must show they experience a significantly increased risk of contracting a particular disease relative to that in the absence of exposure. The court agreed with DuPont that the plaintiffs as a class could not show an increased health risk, because each class member’s risk would vary based on variations in PFOA exposure and variations in each individual’s background risk in the absence of PFOA exposure (background risk may vary from person to person depending on individual characteristics and habits). Rejecting class action status creates an obstacle in the plaintiffs obtaining reimbursement from DuPont for the costs of medical monitoring. Just this month, the federal district court in New Jersey rejected a similar class action suit against DuPont.
An interesting development was the courts analyses of the role and limitations of regulatory risk assessment. In the opinion of the West Virginia judge, risk assessments were of limited utility in a toxic tort case especially for the issue of causation. Risk assessments have largely been developed for regulatory purposes, and serve a protective function in identifying levels below which there is no appreciable risk to the general population; they do not provide information about actual risk or causation. Risk assessments use appropriately prudent assumptions when there are limited data, and therefore intentionally present the upper range of possible risks. Other court decisions are cited for rejecting the use of regulatory standards as measures of causation because their role is to reduce exposure to harmful substances, and for determining that upper-bound risk estimates developed with EPA risk methods appropriately overstate risks for regulatory purposes (where caution is warranted), but are inappropriate for determining whether medical monitoring should be instituted.
The New Jersey court observed there is a difference between a “safe” level for public policy and regulatory purposes and the “significant exposure” that creates excessive risk triggering medical monitoring, and also concluded that a risk assessment methodology “does not work in the tort litigation context”, where a plaintiff must prove there is an actual increased risk of disease in order to receive medical monitoring.
Several things come to mind about the implications of these rulings, beyond setting the bar higher for plaintiffs exposed to toxic substances to be able to get relief through class-action suits. They reinforce the conventional wisdom that regulatory risk assessments are highly conservative and that they overstate the health risks associated with exposure to toxic substances:
While risk assessment information about a chemical can be somewhat useful in a toxic tort case, at least in terms of setting reasonable boundaries as to the likelihood of causation, the impetus for the development of risk assessment has been the regulatory process, which has different goals. Because of their use of appropriately prudent assumptions in areas of uncertainty and their use of default assumptions when there are limited data, risk assessments intentionally encompass the upper range of possible risks.
This isn’t a uniformly held view. There is a compelling argument made that the relationship between uncertainty and conservatism in risk assessment is complex, and that the conventional wisdom includes several unstated assumptions such as there is some underlying “true” risk that could be reflected by a “best estimate” of risk but which is being overstated by the regulatory risk assessment, and that decisions to manage that “true” risk can be made an unbiased manner without consideration of issues such as trust or equity.
In addition, it is possible that our current concepts of risk assessment, which grew out of the National Research Council’s (NRC) “Red Book”, and further articulated in the NRC’s “Blue Book” and the Presidential/Congressional Commission on Risk Assessment and Risk Management, have been superseded by more recent thinking about what biomarkers and toxicogenomics might be saying about the relationships between exposure and adverse effects, how cumulative risk concepts affect our notions of what’s a significant risk and what’s causation, and how risk assessors, regulators and the public (and judges and attorneys) should interact in understanding risks and decisions made to manage them. In particular, the variability in exposure that the courts used to reject the class action status might very well be the key to identifying the individuals who are at risk. However you can’t identify them without a monitoring program which evaluates variability. I think there is more work to be done here to get to a satisfactory remedy. Labels: environmental health policy, PFOA, risk assessment
