Per- and polyfluoroalkyl substances (PFAS) are a class of over 5,000 individual synthetic fluorinated chemicals used extensively in numerous products and processes. Sub-groups of “long-chain” PFAS that contain more than six or eight carbons and sulfonic or carboxylic acid functional groups have been phased out of production and use in the U.S. and several European countries due to persistence, bioaccumulation, and toxicity (PBT). Replacements for phased out PFAS are being detected in environmental media and biota, and many replacement compounds are understudied with respect to PBT. One perceived limitation associated with the management of PFAS is that a unifying mechanism of toxicological action for adverse health effects in humans has not been agreed upon, even for the well-studied PFAS. However, numerous mechanisms have been posited, ranging from cytotoxicity (necrosis and apoptosis), activation of peroxisome proliferator-activated receptors, and other nuclear receptors, induction of oxidative stress, endocrine disruption, alteration of inflammatory pathways, and modification of cell-cell communication. Some of these mechanisms of toxicological action have been dismissed as not being relevant to human health, not relevant to more than just a few individual PFAS, or only relevant to a limited number of adverse health outcomes. Regardless, these mechanisms demonstrate that PFAS interfere with biological molecules to disrupt physiology and produce toxicity. This presentation will provide an overview of these different mechanisms of PFAS toxicological action, discuss what is known about their operability across cell types, tissues, and organisms, and address their relevance to adverse health effects associated with PFAS exposure in human populations.

Mechanisms of toxicity for per- and polyfluoroalkyl substances: Are we there yet?

ACS Fall 2020 Virtual Meeting

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.