The exposure sources of perfluorooctane sulfonate (PFOS) in humans and wildlife are not well characterized. Human biomonitoring data show that PFOS profiles may consist of up to approximately 50% branched isomers, despite the fact that historical direct manufacturing of PFOS generally resulted in products containing no more than approximately 30% branched isomers. These observations cannot be explained based on what is known about the pharmacokinetics of branched PFOS isomers; thus, here we examined the relative isomer-specific biotransformation rates of a model PFOS-precursor (N-ethylperfluorooctane sulfonamide, NEtFOSA) with human microsomes and recombinant human cytochrome P450s (CYPs) 2C9 and 2C19. Using solid phase microextraction-gas chromatography-electron capture detection to monitor NEtFOSA disappearance, and liquid chromatography-tandem mass spectrometry to monitor product formation, we showed that, in general, human microsomes and CYP isozymes transformed the branched isomers more rapidly than linear NEtFOSA. Among branched isomers, perfluoroalkyl branching geometry significantly influenced the rate of biotransformation. As a result, PFOS isomer patterns in biota exposed predominantly to precursors could be much different than expected from the isomer pattern of the precursor. While these data are suggestive that the relatively high abundance of branched PFOS isomers present in some humans, or wildlife, may be explained by substantial exposure to PFOS-precursors, in vivo studies with other relevant PFOS-precursors are warranted to validate this as a biomarker of exposure source.
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