PFAS Exposure Pathways for Humans and Wildlife: A Synthesis of Current Knowledge and Key Gaps in Understanding

Abstract

We synthesize current understanding of the magnitudes and methods for assessing human and wildlife exposures to poly- and perfluoroalkyl substances (PFAS). Most human exposure assessments have focused on 2 to 5 legacy PFAS, and wildlife assessments are typically limited to targeted PFAS (up to ~30 substances). However, shifts in chemical production are occurring rapidly, and targeted methods for detecting PFAS have not kept pace with these changes. Total fluorine measurements complemented by suspect screening using high-resolution mass spectrometry are thus emerging as essential tools for PFAS exposure assessment. Such methods enable researchers to better understand contributions from precursor compounds that degrade into terminal perfluoroalkyl acids. Available data suggest that diet is the major human exposure pathway for some PFAS, but there is large variability across populations and PFAS compounds. Additional data on total fluorine in exposure media and the fraction of unidentified organofluorine are needed. Drinking water has been established as the major exposure source in contaminated communities. As water supplies are remediated, for the general population, exposures from dust, personal care products, indoor environments, and other sources may be more important. A major challenge for exposure assessments is the lack of statistically representative population surveys. For wildlife, bioaccumulation processes differ substantially between PFAS and neutral lipophilic organic compounds, prompting a reevaluation of traditional bioaccumulation metrics. There is evidence that both phospholipids and proteins are important for the tissue partitioning and accumulation of PFAS. New mechanistic models for PFAS bioaccumulation are being developed that will assist in wildlife risk evaluations. Environ Toxicol Chem 2021;40:631-657. © 2020 SETAC.

Keywords: Bioaccumulation; Drinking water; Exposure assessment; Organofluorine; Toxicants; Wildlife.

Figure 1.

Conceptual representation of key emission sources and global transport pathways of perfluoroalkyl acids (PFAA) and their polyfluorinated precursors.

Figure 2.

Components of the fluorine mass balance. Panel a) shows a conceptual diagram representing the relative fractions of total fluorine (TF) including fluoride, unextracted organofluorine, extractable organofluorine (EOF), and targeted PFAS. Panel b) shows actual data where unknown EOF was determined using targeted analysis of 50 PFAS congeners in blood plasma of first time mothers from Uppsala, Sweden (data from Miaz 2020).

Figure 3.

Schematic of exposure assessment steps for humans that relates PFAS sources to exposure media, and internal concentrations of PFAS in blood. Not all possible exposure routes (e.g., outdoor air) or arrows are shown. ADME = Absorption, distribution, metabolism and excretion.

Figure 4.

Key bioaccumulation processes, metrics and gaps associated with PFAS in wildlife. BMR = basal metabolic rate; BAF = bioaccumulation factor; BMF = biomagnification factor; TMF = trophic magnification factor; BCF = bioconcentration factor; BSAF = biota-sediment accumulation factor.

Figure 5.

Key elements for predicting the relationship between external exposure and internal dose of wildlife and human to PFAS. The internal distribution and dose are driven by the balance of absorption, distribution, metabolism, and elimination (ADME). For PFAS, unlike for neutral organic chemicals, internal distribution is substantially influenced by protein binding and transporter uptake and efflux, leading to accumulation in the liver and blood and species and sex-specific elimination half-lives.