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This paper examines widely held beliefs about the six per- and polyfluoroalkyl substances (PFAS) addressed in the final U.S. Environmental Protection Agency's (EPA) rule on PFAS in drinking water (e.g., the Maximum Contaminant Levels - MCLs). Based on our understanding of the scientific literature and the comments submitted by stakeholders regarding the EPA's regulation that was promulgated in April 2024, we identified 15 misconceptions that had a weak scientific foundation. These are now memoralized in the MCLs for the six PFAS but remain debated due to ongoing ambiguous research findings. Many critics of the MCLs found the EPA's systematic review of the published relevant information, particularly the toxicology of perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), to be inadequate. The following seven views are among the most important. First, the EPA asserted that the toxicology of these six chemicals was poorly understood and lacked sufficient data to determine a safe daily intake level for chronic health effects; nonetheless, they promulgated what may be the costliest environmental regulation to date. Notably, adverse effects remain difficult to demonstrate in occupationally exposed individuals even at blood concentrations 50-100 times higher than current background PFAS levels. Second, the Agency indicated that the epidemiology data showed that exposure to PFOA and PFOS caused kidney and potentially other cancers, yet the data were equivocal and do not support that assertion. Third, it was stated that specific non-cancer effects, such as heart disease, would be prevented under the promulgated rule; however, the studies that they relied upon do not show an increased incidence of heart disease even in highly exposed populations. Fourth, the Agency relied on animal data to support its views on the likely toxic effects in humans, despite ample toxicology data that animals, particularly rodents, are poor predictors of the human response to PFAS exposures. Fifth, the EPA predicted a reduction in healthcare expenditures that would offset much of the cost of complying with the MCL, but, they did not have adequate data to support this prediction. Sixth, the EPA suggested that these six PFAS act through a shared mechanism of action (i.e., PPARα pathway induction); however, data indicate that PPARα induction in humans may be 80% less than what is observed in rodents. Also, induction of the PPARα pathway is not a cause of systemic disease. Seventh, the Agency failed to disclose that achieving the new MCL would yield negligible reductions in blood PFAS levels even among highly exposed populations, given drinking water accounts for only 20% or less of total PFAS exposure. The survey that could answer that question, the EPA's fifth Unregulated Contaminant Monitoring Rule, was only 25% complete at the time the MCL was promulgated. Overall, our analysis concluded that while the EPA's intent to regulate these chemicals due to their environmental presence was necessary, the derivation of the MCLs and the alleged health effects was based on the application of the precautionary principle rather than robust scientific evidence.
Paustenbach et al. (Sun,) studied this question.