PFAS (παντοτινά χημικά) – Per and polyfluoroalkyl substances (PFASs)

Per- and polyfluoroalkyl substances (PFASs)

have been in use since the 1950ies as ingredients of intermediates of surfactants and surface protectors for assorted industrial and consumer applications. Within the past decade, several long-chain perfluoroalkyl acids have been recognized as extremely persistent, bioaccumulative and toxic. Many have been detected globally in the environment, biota, food items, and in humans (OECD, 2015). It has been recognised more recently that shorter chain PFASs increasingly used as alternatives are also very persistent and thus very mobile in the environment, presumably leading to ground water contamination in future. To date many known and unknown alternatives of the so far regulated PFASs are used worldwide leading to environmental contamination und increasing human body burdens.

Substances included in the PFAS group

Based on the huge amount of available PFAS on the market and the knowledge gaps on identity, toxicity and uses (of the alternatives), the listing of chemicals in categories A-E is an attempt to categorize possibly relevant substances that contribute to the overall PFAS burden in humans. Several substances are listed in category A due to their restriction as PFOS- and PFOA-related substances, although limited or no HBM data are available. Efforts should be made to improve the methods to detect the broader spectrum of Category A substances. However, the priority for future HBM research should cover PFOS and PFOA alternatives with high production volume, wide dispersive use and identified or suspected hazardous properties which qualifies for Substance of Very High Convern (SVHC) identification.

Category A: PFOA, PFOS, PFNA, PFDA, PFU(n)DA, PFDoDA, PFTrDA, PFTeDA, PFHxS, FOSA, PFOSA, n-MeFOSA, N-Et-FOSAA, Et-PFOSA-AcOH, Et-FOSAA, N-EtFOSA, SULFLURAMID, N-EtFOSE, N-MeFOSE, 8:2 diPAP, 6:2/8:2 diPAP, 8:2 monoPAP

Category B: PFBA, PFPeA, PFHxA, PFHpA, PFBS, PFHpS, PFDS, N-Me-PFOSA-AcOH, Me-FOSAA, 6:2 FTSA, H4PFOS, THPFOS, 8:2 FTSA, PFODA, PfHxDA

Category C: PFBA, PFPeA, PFHxA, PFHpA, PFBS, PFHpS, PFDS, N-Me-PFOSA-AcOH, Me-FOSAA, 6:2 FTSA, H4PFOS, THPFOS, 8:2 FTSA, PFODA, PfHxDA

Category D: HFPO, PFCHS, 6:2/8:2 diPAP, 8:2 monoPAP, PFOPA, Perfluorinated Siloxane, FL16.119

Category E: 6:2 FTCA, 8:2 FTCA, 10:2 FTCA, PFECA, FBSA, MeFBSE, 6:2 PAP, 6:2 diPAP, PFHxPA, PFDPA, C8/C10 PFPiA, Denum SH, Krytox, Fomblin Z-DIAC, C3; C15-C20 PFCA, C3, C15-C20 PFSA, TFEE-5, polymers: PTFE, PVDF, PVF, TFE, HFP

Hazardous properties of PFAS

One of the major societal concerns is the irreversibility of contamination, together with endocrine disrupting effects, carcinogenicity, toxicity to reproduction, effects on immune system and on lipid metabolism for a broad range of PFASs.

A recent briefing provided by Chemtrust points out that children are currently not sufficiently being protected from chemicals that can disrupt brain development; they list per- and polyfluorinated compounds as one of the chemicals substance groups of concern (Chemtrust, 2017a). Chemtrust also raises the issue of use of PFASs as food contact materials and refers to a report on the implementation of the Food Contact Materials Regulation of the European Parliament which states that action at EU level is needed to address the lack of EU specific measures and the gaps in risk assessment, traceability, compliance and control (EU parliament, 2016) and an assessment of the Joint Research Center on the regulatory and market situation of the non-harmonised food contact materials in the EU (Simoneau et al., 2016). Also, European consumer organisations call for action on fluorinated compounds in fast food packaging (BEUC, 2017).

PFASs bind to proteins and partition to phospholipids. The elimination kinetics are highly species dependent, with humans showing the longest half-lives of up to e.g. 8.5 years for perfluorohexane sulfonic acid (PFHxS). A recent publication reports an estimated elimination range of 10.1 to 56.4 years – median 15.3 years for chlorinated polyfluoroalkyl ether sulfonic acids [Cl-PFESAs] (Shi et al., 2016). The CLP human health hazard classifications of the different substances are depicted in table 1. Substances which are best-known – perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) – are classified as carcinogenic (Carc. 2, suspected human carcinogens, such as kidney and testicular), toxic for reproduction (Repr. 1B, presumed human reproductive toxicants; Lact., may cause harm to breast-fed children), toxic to specific target organs (STOT RE 1, specific target organ toxicity – repeated exposure) and acute toxic (Acute Tox. 3-4) for different exposure routes. PFOS and PFOA belong to the so called long-chain perfluorinated compounds, which refers to perfluorocarboxylic acids with carbon chain lengths of 8 and higher, including PFOA; perfluoroalkyl sulfonates with carbon chain lengths of 6 and higher, including PFHxS and PFOS; and precursors of these substances that may be produced or may be present in products. A recent report showed that in product samples the detected individual PFAS constituted only a very minor part of the total organic fluorine (TOF), illustrating large data gaps in the current knowledge which PFASs that are being used in these products (Borg, 2017).

Several long-chain compounds beside PFOS and PFOA have also been identified as toxic to reproduction; further endpoints concern carcinogenicity, liver toxicity, neurotoxicity and immunotoxicity. Whether numerous other non-regulated PFASs show similar toxicity is currently less well established. In many cases data availability is poor and therefore no classification is possible. However, persistence is assumed to concerns largely all PFASs by reason of the extreme strength and stability of the carbon-fluorine bonds.

For PFOS and PFOA adverse effects on thyroid metabolism and lipid metabolism have been reported in a multitude of epidemiological studies suggesting endocrine disrupting potential (Barry et al., 2013).

Additional concerns include increased risk of miscarriage, reduced birth weight, increased weight in adult life, and reduced fertility among offspring as a result of early life exposures (Halldorsson et al., 2012; Jensen et al., 2015; Joensen et al., 2013; Timmermann et al., 2014). Postnatal exposures have also been associated with thyroid hormone imbalances and reduced immune response to vaccination (Grandjean and Budtz-Jørgensen, 2013). The US National Toxicology programme has listed both, PFOA and PFOS, as presumed to be an immune hazard to humans (NTP, 2016).

Grandjean and Clapp (2015) documented carcinogenicity, immunotoxicity and developmental toxicity of PFOA and highlighted the endocrine disrupting effects. A recent publication describes prenatal exposure to perfluoroalkyl substances and reduction in anogenital distance in girls at 3 months of age in a Danish mother-child cohort (Lind et al., 2017).

Since PFOS and PFOA can still be measured in highest concentrations in biota and in humans, exerting similar toxic effects along with and similar to a range of long-chain PFASs measured in blood, together with a range of unidentified PFASs the possibility of mixture effects is very high.

Since PFOS and PFOA can still be measured in highest concentrations in biota and in humans, exerting similar toxic effects along with and similar to a range of long-chain PFASs measured in blood, together with a range of unidentified PFASs the possibility of mixture effects is very high.