Poster-Systematic Evidence Map of the Mechanistic Evidence to Inform Human Health Outcomes Associated with Perfluorohexanesulfonic Acid (PFHxS)
On this page:
Background and Purpose: Per- and polyfluorinated substances (PFAS) are a group of manufactured chemicals widely used in consumer products and industrial processes. Exposure to PFAS has been associated with various adverse human health effects. Systematic Evidence Maps (SEMs) provide a useful tool to visualize trends and differences in the evidence base for a particular topic of interest. Mechanistic studies provide support to evidence from epidemiological and animal study evidence streams. Mechanistic evidence can also help elucidate the biological plausibility that a chemical can cause adverse health effects. Our goal was to develop a mechanistic evidence map of the available PFHxS evidence to identify potential research needs and areas of study to better support epidemiologic and animal data streams for adverse PFHxS-related health outcomes.
Methods: A literature search was performed to identify all the available PFHxS studies up to April 2023. 2441 unique studies were identified and screened in DistillerSR using a defined populations exposure comparators outcomes (PECO) eligibility criterion. Of the 2441 identified studies, 235 studies were tagged as mechanistic studies. The identified mechanistic studies were then mapped to the eleven health effects discussed in the IRIS PFHxS draft toxicological review including: Thyroid, immune, developmental, hepatic, cardiometabolic, male reproductive, female reproductive, neurodevelopmental, hematopoietic, and cancer.
Results: Mechanistic studies were available for 8 of the eleven health effects categories. Thyroid, immune, developmental, hepatic, male reproductive, female reproductive, neurodevelopmental, and cancer. Most of the mechanistic studies informed PFHxS related hepatotoxicity (45 out of 235) or developmental neurotoxicity (36 out of 235) related health outcomes. PFHxS-related thyroid and female reproductive health outcomes had 18 out of 235 studies each, whereas no mechanistic studies were identified for PFHxS related cardiometabolic or renal health outcomes.
Conclusions: The available mechanistic evidence to inform PFHxS-related adverse effects is relatively sparse. Our evidence map shows that most of the available evidence for PFHxS-related adverse health effects is focused on mechanisms of hepatotoxicity or developmental neurotoxicity. Studies of mechanisms of PFHxS-related cardiometabolic or renal adverse effects were not identified. Application of SEM toward the mechanistic literature was a useful and rapid approach for the identification of mechanistic evidence informing PFHxS health outcomes and contemporaneously identifies data gaps to focus potential areas of new research needed to substantiate potential hazards identified by epidemiologic and animal data streams. Disclaimer: The views expressed are those of the authors and do not necessarily represent the views or policies of the US EPA.