They may be called forever chemicals because they can stay in your body for years, but we don’t have forever to enact health protective decisions on PFAS (per- and poly-fluorinated alkyl substances).
This is especially true given the large body of scientific evidence on prenatal exposures to PFAS and effects on fetal growth that the Program on Reproductive Health and the Environment (PRHE) has reviewed on PFAS using the Navigation Guide. This systematic review method integrates evidence from human and animal studies, appraises their quality, and determines the strength of the evidence. In 2014, PRHE published systematic reviews on a specific PFAS compound – perfluorooctanoic acid (PFOA) – and concluded that there was sufficient evidence of an association between prenatal exposure to PFOA and reduced fetal growth.
In December 2021, the Environmental Protection Agency (EPA) Office of Water published draft scientific documents regarding the health effects on two perfluorinated chemicals, PFOA and PFOS. The Agency determined that potential sources of PFOA in drinking water include firefighting foams, cosmetics, paints, stain-resistant treatments for clothes and furniture, and nonstick cookware. Now many water systems are contaminated with these chemicals; updated drinking water standards have the potential to reduce exposure to perfluorinated chemicals and thereby protect the health and water of millions of Americans.
To support its new drinking water standards, EPA used a systematic review approach that was largely consistent with EPA’s Integrated Risk Information System (IRIS) program as outlined in the draft IRIS handbook. EPA’s systematic review evaluated the science on PFAS exposures and multiple health outcomes, including cancer, developmental and reproductive outcomes, and neurological and cardiovascular diseases. Similar to PRHE’s systematic review on PFOA and birthweight, EPA evaluated studies that were relevant for fetal growth parameters, including birth weight, length, and size relative to gestational age at delivery.
Although the vocabulary was different from the Navigation Guide approach, EPA came to similar conclusions as PRHE on PFOA, stating that “there is suggestive evidence that PFOA may impact fetal growth restriction across a variety of birth weight related measures.” And across all developmental outcomes (gestational duration, fetal loss, birth weight, birth length, head circumference, and postnatal growth) EPA concludes that there is “moderate evidence of developmental effects related to PFOA based on the more recent epidemiological literature.”
EPA’s application of the IRIS handbook shares many features with our Navigation Guide systematic review methodology and incorporates recommendations from the National Academy of Sciences. However, there are areas of improvement that EPA must consider and revise in the systematic review methodology that was applied here for PFAS. The EPA needs to have a pre-published protocol outlining the systematic review methods, and its assessment of study quality (evaluation of the “risk of bias” in each study) should consider potential bias from industry funding. Evaluating risk of bias determines which factors of a study may be contributing to potential bias in the study. EPA should consider the factors that may influence risk of bias assessment independently, rather than combining these factors into an overall risk of bias, which has the potential to underestimate risk by excluding studies.
The report’s review of animal studies found that “the available animal toxicity data are in concordance with the data in humans and indicate the developing fetus is a target of PFOA toxicity.” It also reviewed developmental outcomes such as birth weight and stated that their “coherence with epidemiological evidence for other biologically related effects.” There was not an overall summary of the findings and whether the non-human findings were “sufficient” evidence for effects on fetal development. However, EPA’s conclusion that there is ‘coherence’ – or consistency – with the epidemiology literature is aligned with our own conclusion that the human and animal evidence together support PFOA being a risk factor for effects on fetal growth.
PRHE’s PFOA case study was the first in environmental health to apply systematic review methods throughout the process, including a protocol that prespecified methods for identifying, evaluating, and integrating both animal and human evidence. Now that systematic reviews have become the norm, EPA’s analysis of the health risks of PFOA and PFOS confirms that using our systematic review published over seven years ago would have accelerated timely interventions, including health-protective drinking water standards.
Overall, this body of evidence reviewed by EPA informs their process to develop a maximum contaminant level goal – which is the highest concentration at which adverse health effects are assumed to not occur and serves as an important step in the process of developing a drinking water regulation. It is critical that validated systematic review methods are applied to assess the body of evidence that will guide the estimation of these drinking water thresholds.
While there is no evidence that any level of PFAS in drinking water is safe, stricter regulations on PFAS in drinking water will be an important step forward for public health. With potentially hundreds or thousands of other chemicals polluting our water system, decisions on drinking water regulations must be timelier to prevent harm to people and communities. This is critical for emerging chemicals for which research groups like PRHE have published sufficient and timely evidence of health effects.
About the Author
Max Aung, PhD, MPH is an Assistant Professor at the University of Southern California Keck School of Medicine in the Department of Population and Public Health Sciences. Max’s research focuses on applying data science methods to investigate the impact of environmental pollution on child and maternal health to inform and pursue environmental justice. He was formerly an Associate Research Scientist for PRHE.