Perfluorooctane sulfonate: A review of human exposure, biomonitoring and the environmental forensics utility of its chirality and isomer distribution

Abstract

Perfluorooctane sulfonate (PFOS) found extensive use for over 60 years up until its restriction in the early 2000s, culminating in its listing under the Stockholm Convention on Persistent Organic Pollutants (POPs) in 2009. Efforts to minimise human body burdens are hindered by uncertainty over their precise origins. While diet appears the principal source for the majority of western populations (with other pathways like dust ingestion, drinking water and inhalation also important contributors); the role played by exposure to PFOS-precursor compounds followed by in vivo metabolism to PFOS as the ultimate highly stable end-product is unclear. Such PFOS-precursor compounds include perfluorooctane sulfonamide derivates, e.g., perfluorooctane sulfonamides (FOSAs) and sulfonamidoethanols (FOSEs). Understanding the indirect contribution of such precursors to human body burdens of PFOS is important as a significant contribution from this pathway would render the margin of safety between the current exposure limits and estimates of external exposure to PFOS alone, narrower than hitherto appreciated. Estimates derived from mathematical modelling studies, put the contribution of so-called "precursor exposure" at between 10% and 40% of total PFOS body burdens. However, there are substantial uncertainties associated with such approaches. This paper reviews current understanding of human exposure to PFOS, with particular reference to recent research highlighting the potential of environmental forensics approaches based on the relative abundance and chiral signatures of branched chain PFOS isomers to provide definitive insights into the role played by "precursor exposure".

Perfluoroalkyl substances with isomer analysis in umbilical cord serum in China

“…An in vitro study using human microsomes showed that branched chain perfluorooctane sulfonamides (PFOSAs, PFOS precursor) to be preferentially metabolized to PFOS relative to linear PFOSAs ). Studies show that exposure to PFOS precursors in becoming more important compared to direct exposure, suggesting more precautions should be taken in the further PFASs study (Miralles-Marco and Harrad 2015). A relative higher proportion of n-PFOS in maternal serum sample from Canada (80% n-PFOS, Benskin et al 2007), Norway (78% n-PFOS, Haug et al 2011), and Vietnam (83% n-PFOS, Rylander et al 2009b) may suggest that n-PFOS appears to undergo less facile cross-placental transport.…”

“…Results showed that in utero PFOS and PFOA exposure was associated with decreased measure of birth weight in most studies, but only some results were significant (Bach et al 2015). The chirality of PFAS isomers may have important environmental significance because different enantiomers can interact with various biological large molecules, leading to different toxicological responses (Miralles-Marco and Harrad 2015). Studies showed that branched PFASs were eliminated faster than the linear PFASs in rats ), fish (De Silva et al 2009b), and occupational workers (Gao et al 2015).…”

Exposure to per- and polyfluoroalkyl substances through the consumption of fish from lakes affected by aqueous film-forming foam emissions — A combined epidemiological and exposure modeling approach. The SAMINOR 2 Clinical Study

“…Seafood and freshwater fish have been identified as important contributors to dietary exposure to PFOS and long-chain PFCAs Berger et al, 2009;Fromme et al, 2009;Haug et al, 2010;Rylander et al, 2010), whereas a varied picture has been seen for other PFASs (Herzke et al, 2013;Vestergren et al, 2012). In addition, several biological factors play a role in the burden of PFASs in the body, including age, gender, reproductive factors, and compound specific toxicokinetics Denys et al, 2014;Harada and Koizumi, 2009;Haug et al, 2010;Lorber et al, 2015;Miralles-Marco and Harrad, 2015;Nost et al, 2014). In this context, toxicokinetic models are useful for the quantitative interpretation of biomonitoring data and exposure prediction (Hölzer et al, 2011;Zhou et al, 2014).…”

“…Human exposure to PFASs can occur via contact with consumer products, ingestion of house dust, transfer from food packaging, or via drinking water (Domingo, 2012;Fromme et al, 2009;Kotthoff et al, 2015;Miralles-Marco and Harrad, 2015). However, an increasing number of studies have emphasized the importance of dietary intake as an exposure pathway Fromme et al, 2009;Harada and Koizumi, 2009;Vestergren et al, 2008).…”

Chronic Exposure to Perfluorooctane Sulfonate Reduces Lifespan of Caenorhabditis elegans Through Insulin/IGF-1 Signaling

“…PFOS is globally distributed, persistent, bioaccumulative and potentially harmful to organisms, and so is of extensive concern. PFOS was categorized as a persistent organic pollutant (POP) in 2009 (Miralles-Marco and Harrad 2015).…”