Based on our Decitabine research buy findings, our initial hypothesis that the isomer pattern of total PFOS exposure can help to explain the isomer pattern found in human serum is rejected. Furthermore, current knowledge on isomer-specific differences in pharmacokinetics and metabolism of PFOS and/or precursors combined with the present data cannot explain the difference in the isomer pattern of the intake relative to the pattern in human serum. This discrepancy between PFOS isomer patterns in external and internal exposure could potentially be explained by: i) inaccurate estimation of the daily exposure (e.g., due to unknown precursors, missing or poorly quantified exposure pathways and/or poorly quantified isomer ratios of PFOS and

precursors) or ii) an incomplete understanding of the human pharmacokinetic processes (e.g., biotransformation and elimination kinetics of precursors, intermediates and PFOS isomers). The estimated daily intakes for all PFCAs and individual precursors (assuming no biotransformation) are provided in Table S11. Based on these intakes and biotransformation factors for precursors as given

in Section 2.2, the highest Baf-A1 chemical structure total daily exposures among individual PFCAs are estimated for PFOA with 44 pg/kg/d, 270 pg/kg/d, and 3000 pg/kg/d for the low-, intermediate-, and high-exposure scenarios, respectively (Table 1, Fig. 2). Direct PFOA intake is dominant in the low- and intermediate-exposure scenarios (87% and 73% of total exposure, respectively), while in the high-exposure scenario precursor-based (indirect) intake is more important, contributing 64% to the total exposure (Tables S12–S14). Lower daily exposures are estimated for PFHxA and PFDA, ranging from 15 to 520 pg/kg/d for PFHxA and from 24 to 660 pg/kg/d for PFDA, depending on the exposure scenario (Table 1). For both PFHxA and PFDA, direct intake is dominant

in the low- and intermediate-exposure scenarios, contributing between 72% and 96% of the total exposures. In the high-exposure scenario, direct PFHxA intake is still dominant (66%), whereas for PFDA the major daily exposure (66%) originates from precursor-based intakes. The lowest daily exposures are estimated for PFBA and PFDoDA, ranging between 6.3 and 190 pg/kg/d for PFBA and between 23 and 180 pg/kg/d for PFDoDA, depending on the exposure scenario (Table 1). nearly For both PFBA and PFDoDA, daily exposures originate almost entirely from direct intakes regardless of the scenario (i.e., 75%–99%). Based on these results, our hypothesis that the estimated total exposure to PFOA is greater than to other PFCA homologues, and that contributions of direct and indirect exposure vary widely by homologue, is verified. Furthermore, the exposure scenario has a strong influence on the estimated relative importance of direct and indirect intakes, with precursors becoming more important the higher the exposure scenario (Table 1).