As the US PFAS personal injury litigation grows, attorneys are gearing up for battles over the critical issue of PFAS causation.
The aqueous film-forming foam (AFFF) MDL is a docket of thousands of PFAS-related cases for property damage and personal injury that all allege PFAS-containing AFFF as the product causing the contamination or harm. The docket is divided into case type categories, with each track receiving its own scheduling order. One such category of cases is personal injury cases, and as PFAS litigants follow the AFFF MDL closely in 2025, their attention is focused on issues related to causation that will be front and centre before the Court in a matter of months. The issue, though, will receive significant attention in the MDL even prior to the trial stage, as the Court announced in early March 2025 that it intends to proceed with a ‘Science Day’ – an opportunity for both sides to present abbreviated expert evidence on issues, including causation, to assist the Court in understanding the issues and determining whether certain disease categories need to be culled from the docket for lack of causative evidence.
Considerable debate has centred on the crucial litigation question of whether plaintiffs will be able to, for the first time in PFAS litigation, present sufficient evidence to establish specific causation – i.e., that the level of exposure from a specific type of PFAS in a specific product at issue was sufficient to cause the plaintiff’s disease. What receives far less attention, but is equally if not more important than the question of specific causation, is the question of general causation – i.e., is the type of PFAS at issue in a plaintiff’s case capable of causing disease?
Part of the reason that the general causation question receives too little attention is that it is assumed that the question is already established in the affirmative. However, a closer look shows that the question is far from settled and absolutely must be challenged to properly defend PFAS litigation cases of any kind, whether personal injury, medical monitoring, or environmental pollution claims.
PFOA and PFOS: Causation should not be conceded
The two most commonly litigated types of PFAS are the original legacy PFAS – perfluorooctanoic acid (PFOA) and perfluorooctane sulfonic acid (PFOS). In the early 2000s, in litigation against DuPont related to PFOA made at the company’s facility in West Virginia, the parties reached an agreement by which a science panel of three epidemiologists would examine whether PFOA has any associations between exposure and impact on human health. The ‘C8 Science Panel’¹ (C8 referring to the fact that PFOA has eight carbon atoms as its chemical backbone) spent eight years testing the blood of close to 70,000 class plaintiffs and in 2013, reported their findings. The results are now well known to not only attorneys, but scientists, media, and citizens – ‘for six disease categories, the Science Panel concluded that there was a probable link to C8 exposure: diagnosed high cholesterol, ulcerative colitis, thyroid disease, testicular cancer, kidney cancer, and pregnancy-induced hypertension.’ These findings are commonly attributed equally to PFOS due to the fact that PFOA and PFOS are both ‘C8’ PFAS, yet it is important to note that the C8 Science Panel only studied PFOA.
The key words in the summary findings are ‘probable link.’ Far too often, and particularly in Complaints filed in litigation, the ‘probable link[s]’ are painted as conclusions of actual causation, but in fact, a closer look at the reports from the Science Panel shows that the conclusions were more akin to associations. The difference between ‘association’ and ‘causation’ is critical to understand not only from a scientific perspective, but also from a legal perspective. An ‘association’ noticed between two variables indicates that the two variables are related to each other in some way, while ‘causation’ means that one variable causes a change in the other. A causal connection is therefore definitive in nature, while association either may or may not be an actual cause of something (e.g. – if studies showed that people with lung cancer tended to like to shoot dice, that is an interesting association between two variables, but it tells us nothing about the causation of lung cancer). It is important to note that Sir Bradford Hill, author of the renowned epidemiological guide for assessing causation, listed association as just one of several factors to consider when determining causation.² In this context, counsel must not concede the assertion that the C8 Science Panel conclusions end the debate of whether PFOA (and PFOS) can cause disease.
Further, consider the more modern assessment of the PFOA / PFOS causation question published by the World Health Organization’s International Agency for Research On Cancer (IARC) from December 2023, which reviewed existing literature related to PFOA and PFOS to reach its conclusions. On its face, the classification given to PFOA (Group 1 – carcinogenic to humans) appears difficult to challenge, but a closer look at the specific findings is important in the litigation context. IARC reached the following conclusion with respect to PFOA:
…on the basis of sufficient evidence for cancer in experimental animals and strong mechanistic evidence (for epigenetic alterations and immunosuppression) in exposed humans. There was also limited evidence for cancer in humans (renal cell carcinoma and testicular cancer) and strong mechanistic evidence in human primary cells and experimental systems (for epigenetic alterations and immunosuppression, as well as several other key characteristics of carcinogens).³
While IARC’s review of the literature noted evidence of PFOA capable of causing changes in the human body (‘mechanistic changes’), the same review showed only ‘limited evidence’ of actual cancer causality in humans. Instead, to reach its final conclusion, IARC considered animal studies, which tipped the balance in favour of a Group 1 classification. In litigation, however, the studies of actual causation in humans that IARC considered provide key pieces of evidence to articulate to a jury why the causation question as to PFOA is not a settled question.
More open to scrutiny when applying legal standards are IARC’s conclusions related to PFOS:
PFOS is possibly carcinogenic to humans (Group 2B), on the basis of strong mechanistic evidence across test systems, including in exposed humans (for epigenetic alterations and immunosuppression, as well as several other key characteristics of carcinogens). There was also limited evidence for cancer in experimental animals, and inadequate evidence regarding cancer in humans.
The PFOS classification relied almost entirely on evidence in the literature of changes in the human body caused by PFOS, yet human and animal studies that examined actual causation reached conclusions that are not legally sufficient for a Court or jury to find causation. Certainly, this divergence in findings provides litigants with interesting and viable opportunities to challenge IARC’s classifications in court or at least cast doubt on whether they truly meet the legal standard for causation.
Even more strongly on point are the findings of the Agency for Toxic Substances and Disease Registry (ATSDR), a division of the Department of Health and Human Services’ Centers For Disease Control (CDC) that conducts assessments on substances that are potentially hazardous to human health. In 2019, ATSDR issued ‘An Overview of the Science and Guidance For Clinicians On PFAS’⁴, an assessment of human health risk based on available literature at the time. While ATSDR did examine animal studies, some of which found associations between PFAS and health effects on animals, ATSDR was quick to point out that ‘the comparison of the toxicity of PFAS across species is difficult because of the differences in half-lives, mechanisms of toxicity, and measured exposure levels in epidemiological and experimental studies.’ In other words, applying a direct correlation between animal study findings and human health impacts should not be done without also examining human health studies.
ATSDR’s assessment of the human health studies is critical to the litigation question of causation for PFAS. In a summary chart in ATSDR’s report, it lists fourteen human health impacts that were examined for specific types of PFAS, including PFOA and PFOS. Critically, ATSDR found that either additional studies were needed to determine if there is a causal connection between PFAS and the health impact, or the ATSDR concluded that ‘no causal relationship has been established.’⁵ Notably, with respect to cancers, ATSDR specifically examined IARC’s findings related to PFOA and PFOS, but noted that while IARC was correct that some studies suggest links between PFOA, PFOS and cancer, others do not. As such, ATSDR concluded that the weight of the evidence leads to the conclusion that ‘no causal relationship has been established.’
Other PFAS: Even murkier waters on causation
At this point, remaining up to speed on all of the non-PFOA/PFOS studies that are published is essentially a full-time job. Every week, dozens of articles are published related to non-legacy PFAS that touch on areas ranging from studying potential ecological harms to potential impacts on human health. By and large, the studies on these types of PFAS are case studies, cohort studies, product testing studies, or animal studies. While these types of studies can be considered when determining causation in the litigation context, they are certainly not conclusive on the question of causation and human health impacts. Large-scale (or even average-sized) epidemiological human studies are few and far between at this point in time. Adding to the uncertainty surrounding this topic is the fact that the studies that do exist reach polar opposite conclusions or conclude that further studies are needed to reach definitive conclusions.
Nevertheless, far too often, case Complaints make broad-sweeping allegations regarding the alleged toxicity of ‘all PFAS’, which is a truly broad-sweeping statement when considering that the EPA alone recognises over 15,000 PFAS. Thus far in the United States, federal regulatory agencies (most notably the Environmental Protection Agency) have not regulated PFAS as an entire class. While EPA has received criticism for not taking the ‘all PFAS’ regulatory approach, it has also received criticism for allegedly ignoring science that weighed against a carcinogenicity finding for certain PFAS for which the Biden administration’s EPA put forth regulations. Yet, it should not just be the EPA’s motives that are called into question for promulgated PFAS regulations or causation findings – all agencies, research groups, etc. do not operate in a vacuum and are not immune to pressures from outside sources. Any influences or pressures agencies were under when reaching chemical causation findings make for trial nuances that can result in the jury appropriately considering biases when weighing the complex scientific evidence in cases.
Conclusion
The uncertain scientific environment with respect to PFAS and causation makes litigating questions of causation in PFAS cases both interesting and challenging. The key to approaching the defence of PFAS cases, however, is to understand that there is uncertainty as to causation conclusions. Thus, starting at square one and defending the general causation question without conceding the point is critical for presenting your case effectively to the judge and jury.
References
- More information about the C8 Science Panel can be found at
https://www.c8sciencepanel.org
- https://www.iarc.who.int/news-events/iarc-monographs-evaluate-the-carcinogenicity-of-perfluorooctanoic-acid-pfoa-and-perfluorooctanesulfonic-acid-pfos/
- https://stacks.cdc.gov/view/cdc/84242
- Health impacts where no causal relationship was found were cancer, cholesterol, uric acid, liver effects, kidney effects, endocrine disruption, thyroid effects, ulcerative colitis, asthma, reproductive health, preeclampsia, and cancer. Health impacts where additional studies are needed to draw conclusions include immune effects and neuro-behavioural effects. For one health impact examined (birth weight), ATSDR concluded “…the association between the maternal PFAS level and decreased birth weight does not consistently show statistical significance.” See pp. 9-10.
Please note, this article will also appear in the 23rd edition of our quarterly publication.
