Linn Salto Mamsen1, Richelle D Björvang2, Daniel Mucs3, Marie-Therese Vinnars4, Nikos Papadogiannakis5, Christian H Lindh6, Claus Yding Andersen7, Pauliina Damdimopoulou8. 1. Laboratory of Reproductive Biology, Section 5712, The Juliane Marie Centre for Women, Children and Reproduction, University Hospital of Copenhagen, University of Copenhagen, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, Denmark. Electronic address: linn.salto.mamsen@regionh.dk. 2. Division of Obstetrics and Gynaecology, Department of Clinical Science, Intervention and Technology, K57 Karolinska University Hospital, Karolinska Institutet, 141 86 Stockholm, Sweden; Swetox, Karolinska Institute, Unit of Toxicology Sciences, Forskargatan 20, 151 36 Södertälje, Sweden. Electronic address: richelle.duque.bjorvang@ki.se. 3. Swetox, Karolinska Institute, Unit of Toxicology Sciences, Forskargatan 20, 151 36 Södertälje, Sweden; Unit of Work Environment Toxicology, Institute of Environmental Medicine, Box 210, Karolinska Institutet, 171 77 Stockholm, Sweden. Electronic address: daniel.mucs@ki.se. 4. Division of Obstetrics and Gynaecology, Department of Clinical Science, Intervention and Technology, K57 Karolinska University Hospital, Karolinska Institutet, 141 86 Stockholm, Sweden. Electronic address: marie-therese.vinnars@ki.se. 5. Division of Pathology, Department of Laboratory Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge H5, 141 83 Stockholm, Sweden. Electronic address: nikos.papadogiannakis@ki.se. 6. Division of Occupational and Environmental Medicine, Department of Laboratory Medicine, Medicon Village, Byggnad 402 A, Lund University, 223 61 Lund, Sweden. Electronic address: christian.lindh@med.lu.se. 7. Laboratory of Reproductive Biology, Section 5712, The Juliane Marie Centre for Women, Children and Reproduction, University Hospital of Copenhagen, University of Copenhagen, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, Denmark. Electronic address: claus.yding.andersen@regionh.dk. 8. Division of Obstetrics and Gynaecology, Department of Clinical Science, Intervention and Technology, K57 Karolinska University Hospital, Karolinska Institutet, 141 86 Stockholm, Sweden; Swetox, Karolinska Institute, Unit of Toxicology Sciences, Forskargatan 20, 151 36 Södertälje, Sweden. Electronic address: pauliina.damdimopoulou@ki.se.
Abstract
BACKGROUND: The persistent environmental contaminants perfluoroalkyl substances (PFASs) have gained attention due to their potential adverse health effects, in particular following early life exposure. Information on human fetal exposure to PFASs is currently limited to one report on first trimester samples. There is no data available on PFAS concentrations in fetal organs throughout all three trimesters of pregnancy. METHODS: We measured the concentrations of perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluoroundecanoic acid (PFUnA), and perfluorohexane sulfonic acid (PFHxS) in human embryos and fetuses with corresponding placentas and maternal serum samples derived from elective pregnancy terminations and cases of intrauterine fetal death. A total of 78 embryos and fetuses aged 7-42 gestational weeks were included and a total of 225 fetal organs covering liver, lung, heart, central nervous system (CNS), and adipose tissue were analyzed, together with 71 placentas and 63 maternal serum samples. PFAS concentrations were assayed by liquid chromatography/triple quadrupole mass spectrometry. RESULTS: All evaluated PFASs were detected and quantified in maternal sera, placentas and embryos/fetuses. In maternal serum samples, PFOS was detected in highest concentrations, followed by PFOA > PFNA > PFDA = PFUnA = PFHxS. Similarly, PFOS was detected in highest concentrations in embryo/fetal tissues, followed by PFOA > PFNA = PFDA = PFUnA. PFHxS was detected in very few fetuses. In general, PFAS concentrations in embryo/fetal tissue (ng/g) were lower than maternal serum (ng/ml) but similar to placenta concentrations. The total PFAS burden (i.e. the sum of all PFASs) was highest in lung tissue in first trimester samples and in liver in second and third trimester samples. The burden was lowest in CNS samples irrespective of fetal age. The placenta:maternal serum ratios of PFOS, PFOA and PFNA increased across gestation suggesting bioaccumulation in the placenta. Further, we observed that the ratios were higher in pregnancies with male fetuses compared to female fetuses. CONCLUSIONS: Human fetuses were intrinsically exposed to a mixture of PFASs throughout gestation. The compounds were detected in all analyzed tissues, suggesting that PFASs reach and may affect many types of organs. Collectively, our results demonstrate that PFASs pass the placenta and deposit to embryo and fetal tissues, calling for risk assessment of gestational exposures.
BACKGROUND: The persistent environmental contaminants perfluoroalkyl substances (PFASs) have gained attention due to their potential adverse health effects, in particular following early life exposure. Information on human fetal exposure to PFASs is currently limited to one report on first trimester samples. There is no data available on PFAS concentrations in fetal organs throughout all three trimesters of pregnancy. METHODS: We measured the concentrations of perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluoroundecanoic acid (PFUnA), and perfluorohexane sulfonic acid (PFHxS) in human embryos and fetuses with corresponding placentas and maternal serum samples derived from elective pregnancy terminations and cases of intrauterine fetal death. A total of 78 embryos and fetuses aged 7-42 gestational weeks were included and a total of 225 fetal organs covering liver, lung, heart, central nervous system (CNS), and adipose tissue were analyzed, together with 71 placentas and 63 maternal serum samples. PFAS concentrations were assayed by liquid chromatography/triple quadrupole mass spectrometry. RESULTS: All evaluated PFASs were detected and quantified in maternal sera, placentas and embryos/fetuses. In maternal serum samples, PFOS was detected in highest concentrations, followed by PFOA > PFNA > PFDA = PFUnA = PFHxS. Similarly, PFOS was detected in highest concentrations in embryo/fetal tissues, followed by PFOA > PFNA = PFDA = PFUnA. PFHxS was detected in very few fetuses. In general, PFAS concentrations in embryo/fetal tissue (ng/g) were lower than maternal serum (ng/ml) but similar to placenta concentrations. The total PFAS burden (i.e. the sum of all PFASs) was highest in lung tissue in first trimester samples and in liver in second and third trimester samples. The burden was lowest in CNS samples irrespective of fetal age. The placenta:maternal serum ratios of PFOS, PFOA and PFNA increased across gestation suggesting bioaccumulation in the placenta. Further, we observed that the ratios were higher in pregnancies with male fetuses compared to female fetuses. CONCLUSIONS:Human fetuses were intrinsically exposed to a mixture of PFASs throughout gestation. The compounds were detected in all analyzed tissues, suggesting that PFASs reach and may affect many types of organs. Collectively, our results demonstrate that PFASs pass the placenta and deposit to embryo and fetal tissues, calling for risk assessment of gestational exposures.
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