As the US PFAS personal injury lawsuit grows, lawyers are preparing for the fight over the serious issues of PFAS causality.
Aqueous Film Formation Foam (AFFF) MDL is a docket of thousands of PFA-related cases for property damage and personal injury that alleges affff products containing PFA cause contamination or harm. Dockets are split into case type categories, with each track receiving its own scheduling order. One such category of cases is personal injury, and as PFAS litigators will closely follow the AFFF MDL in 2025, their attention focuses on issues related to causality that will be central to the court in a few months. However, the issue will attract a lot of attention in MDL, even before the court stage, as the court announced in early March 2025 that it intends to advance “Science Day.” This is an opportunity to present expert evidence on issues that include causality, and to assist the court in understanding the issue and determining whether a particular category of illness should be decorated for causal evidence.
A considerable amount of debate focuses on the issue of important litigation, whether the plaintiff can present enough evidence to establish a particular causal relationship for the first time in a PFAS case, i.e. whether he can present enough evidence that the level of exposure from a particular type of PFA in the particular product in question is sufficient to cause the plaintiff’s illness. What we pay little attention to, if not more important than a particular causal issue, is the general causal issue: can the type of PFA in question in the plaintiff’s case cause illness?
Part of the reason why common causal questions are too unattentional is that they are assumed to have already been positively established. However, if you look closely, the problem shows that it is far from being resolved, and that you must absolutely challenge yourself to properly defend any kind of PFAS litigation case, including personal injury, medical surveillance, and environmental pollution claims.
PFOA and PFOS: Causality must not be recognized
The two most commonly litigated types of PFAs are the original legacy PFAs, Perfluorooctano acid (PFOA) and Perfluorooctane sulfonic acid (PFOS). In a lawsuit against DuPont in connection with PFOA at its company’s facility in West Virginia in the early 2000s, the parties reached an agreement that a science panel of three epidemiologists would look into whether PFOAs were associated with human health effects. “C8 Science Panel” (C8 refers to the fact that PFOA has eight carbon atoms as its chemical backbone) spent eight years testing the blood of nearly 70,000 classes of plaintiffs, reporting the findings in 2013. The results are now well known not only to lawyers, but also to scientists, the media and citizens. “For six disease categories, the Science Panel concluded that there is a possible link to C8 exposure: diagnosis of high cholesterol, ulcerative colitis, thyroid disease, testicular cancer, kidney cancer, and pregnancy-induced hypertension. These findings are generally attributed equally to PFO due to the fact that both PFOA and PFO are “C8” PFA, but it is important to note that the C8 Science Panel studied PFOA alone.
The keyword in the summary survey results is “possibility of links.” Frequently, particularly in complaints filed in lawsuits, “possible links”[s]”It is depicted as a conclusion of actual causality, but in fact, a closer look at reports from the Science Panel shows that the conclusions are similar to relevance. The difference between “relevance” and “causality” is important for understanding not only from a scientific perspective, but also from a legal perspective. The “relevance” between two variables indicates that the two variables are somehow related to each other, while “causality” means that one variable causes another change. Therefore, causality is essentially definitive, but the association may or may not be the actual cause of something (e.g. – if people with lung cancer show that they tend to shoot dice, that is an interesting connection between the two variables, but it tells us nothing about the causality of lung cancer). It is important to note that Sir Bradford Hill, author of a well-known epidemiological guide to assessing causality, has listed the association as one of several factors to consider when determining causality.
Additionally, consider a more modern assessment of the PFOA/PFOS causal question published by the World Health Organization’s International Cancer Research Organization (IARC) in December 2023. On that face, the classification given to PFOA (Group 1 – Carcinogenicity in Humans) appears to be difficult to challenge, but it is important to look closely at specific findings in the context of the lawsuit. The IARC has reached the following conclusion regarding PFOA:
… Strong mechanical evidence in exposed humans (because epigenetic changes and immunosuppression) based on sufficient evidence of cancer in experimental animals. Also, there was limited evidence of cancer in humans (renal cell carcinoma and testicular cancer), with strong mechanical evidence (also for epigenetic changes and immunosuppression, and several other important features of carcinogens).
A review of the IARC literature points to evidence of PFOAs that can cause changes in the human body (“mechanical changes”), but the same review only showed “limited evidence” of actual cancer causality in humans. Instead, to arrive at a final conclusion, the IARC considered animal studies and leaned the balance in favor of group 1 classification. However, in the lawsuit, the actual human causality studies discussed by the IARC provide important evidence to clarify to the ju apprentice why causality regarding PFOA is not a resolved question.
It is the IARC’s conclusion relating to PFO that is more open to scrutiny when applying legal standards.
PFOS may be carcinogenic to humans based on strong mechanical evidence (for epigenetic changes and immunosuppression, and some important properties of carcinogens) across test systems, including exposed humans (Group 2B). Also, there was limited evidence of cancer in experimental animals and insufficient evidence of cancer in humans.
The classification of PFOs was almost entirely dependent on evidence in the literature of human body changes caused by PFOs, but human and animal studies examining actual causal relationships have come to conclusions that are not legally sufficient for courts or ju judges to find causality. Indeed, this difference in the findings provides litigants with an interesting and viable opportunity to challenge the classification of IARCs in court.
Even stronger are the findings of the Toxic Substances and Disease Registry (ATSDR), a division of the Department of Health and Human Services’ Centers for Disease Control (CDC), which conducts assessments of substances that are potentially dangerous to human health. In 2019, ATSDR published an overview of the science and guidance of clinicians in “PFAS.” This is an assessment of human health risks based on literature available at the time. While ATSDR examined animal studies, some of them found a link between PFA and health effects on animals, noting that ATSDR “is difficult to compare the toxicity of half-life PFAs and is difficult due to the mechanism of toxicity and measured levels of exposure in epidemiological and experimental studies.” In other words, applying a direct correlation between animal research findings and effects on human health should not be done without considering human health research either.
The assessment of ATSDRs on human health research is important for litigation issues regarding the causality of PFA. The ATSDR report summary chart lists the 14 human health effects surveyed for certain types of PFA, including PFOA and PFO. Critical, ATSDR concluded that additional research is needed to determine whether there is a causal relationship between PFA and health effects, or that ATSDR “has not established a causal relationship.” Therefore, ATSDR concluded that the weight of evidence leads to the conclusion that “causality has not been established.”
Other PFAs: Even muddy causal water
At this point, maintaining the speed of all published non-PFOA/PFOS studies is essentially a full-time job. Each week, dozens of articles related to non-legacy PFAs are published in touch on areas ranging from research into potential ecological harms to potential impacts on human health. Generally, studies on these types of PFA are case studies, cohort studies, product testing studies, or animal studies. These types of studies can be considered in determining causality in the litigation context, but they certainly are inconclusive about causality and its impact on human health. At this point, there are few large (or average size) epidemiological human studies. In addition to the uncertainty surrounding this topic, the existing research is the fact that further research is needed or concluded that it is necessary to reach a definitive conclusion.
Nevertheless, too often, case complaints make widespread allegations of alleged toxicity of “all PFAs” given that only the EPA is aware of more than 15,000 PFAs. So far, federal regulators (particularly the Environmental Protection Agency) have not regulated PFA as a whole class. The EPA has been criticized for not adopting a “all PFA” regulatory approach, but it has also been criticized for allegedly ignored the science that Biden administration’s EPA weighed against the carcinogenic findings of certain PFAs that it announced regulations. However, it is not only the EPA’s motivation that is questioning the promulgated PFA regulations and causal findings that do not operate in blank spaces and cannot withstand pressure from external sources. Once chemical causal findings were reached, there were impacts and pressure engines that provided experimental nuances that allowed bias to be appropriately considered when comparing complex scientific evidence of cases.
Conclusion
The uncertain scientific environment regarding PFA and causality makes the issue of causal litigation in the case of PFAS interesting and challenging. However, the key to approaching the defense of PFAS cases is to understand the uncertainty regarding causal conclusions. Therefore, starting with Square 1 and defending general causal questions without acknowledging the points is important to effectively present your case to judges and ju judges.
reference
For more information about the C8 Science Panel, see
https://www.c8siencepanel.org
2. https://www.rtihs.org/sites/default/files/26902%20Rothman%201998%20the%20encyclopedia%20of%20biostatistics.pdf
https://www.iarc.who.int/news-events/iarc-monographs-evalute-the-carcinogenicity-of-perfluorooctanoic-acid-pfoa-and-perfluorocutanesulfonic-acid-pfos/ https://stacks.cdc.gov/842242242 Causal relationships were discovered in cancer, cholesterol, uric acid, liver effects, kidney effects, endocrine destruction, thyroid effects, ulcerative colitis, asthma, reproductive health, pre-lamp disease, and cancer. Health effects that require additional research to draw conclusions include immune and neurobehavioral effects. Regarding one health effect (birth weight) investigated, ATSDR concluded that “…the association between maternal PFA levels and reduced birth weight has not been consistently statistically significant.” pp. See 9-10.
This article will also be featured in the 23rd edition of Quarterly Publication.
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