4E).

This is, however, a highly improbable scenario as there is evidence of both linear and branched precursor isomers being present in air samples ( Jahnke et al., 2007). Faster uptake of branched PFOS and precursors compared to linear PFOS and precursors, as was seen in rats and fish (Benskin et al., 2009a and Peng et al., 2014) would result in an enrichment of branched PFOS relative to linear PFOS. However, as increasing uptake efficiency and thus uptake rate was shown only to have little impact on the isomer pattern of total PFOS intake, it seems unlikely that uptake of branched isomers alone would result in isomer patterns that are enriched with branched PFOS as seen in human sera. Faster biotransformation of branched precursors relative to linear isomers (Benskin et al., 2009b) see more as well as faster urinary elimination of linear precursors relative to branched precursors in humans as was seen for FOSA (Zhang et al., 2013a) would result in increasing formation of branched PFOS relative to linear PFOS originating from indirect exposure. If this was a dominant Pifithrin-�� order pathway influencing the

isomer pattern in humans then enrichment of branched PFOS would be expected relative to the isomer Urease pattern of the total exposure. However, as discussed above (Fig. 4), it is unlikely that

biotransformation of precursors can fully explain the PFOS isomer pattern difference between total exposure and human serum, due to the low contribution of precursors to total PFOS exposure, which was estimated to be 16% in the intermediate-exposure scenario (Table S13). Another process that may alter the PFOS isomer pattern in human serum relative to the total exposure are isomer-specific differences in elimination half-lives between PFOS isomers. Both in rats and humans the major branched isomers are excreted faster relative to linear PFOS via urine (Benskin et al., 2009a and Zhang et al., 2013a). If this was the dominant elimination route, then the isomer pattern of total PFOS exposure (estimated as 84% linear) would become even more enriched with linear PFOS in humans. However, the PFOS elimination half-life calculated from blood serum measurements (representing overall human elimination through all processes) is shorter compared to the half-life estimated only from urinary excretion (Olsen et al., 2007 and Zhang et al., 2013a), indicating that there may be other significant elimination processes for PFOS, such as faecal excretion.