Linn Salto Mamsen1, Bo A G Jönsson2, Christian H Lindh3, Rasmus H Olesen4, Agnete Larsen5, Erik Ernst6, Thomas W Kelsey7, Claus Yding Andersen8. 1. Laboratory of Reproductive Biology, Section 5712, The Juliane Marie Centre for Women, Children and Reproduction, University Hospital of Copenhagen, University of Copenhagen, Rigshospitalet, 2100 Copenhagen, Denmark. Electronic address: linn.salto.mamsen@regionh.dk. 2. Division of Occupational and Environmental Medicine, Department of Laboratory Medicine, Lund University, 223 61 Lund, Sweden. 3. Division of Occupational and Environmental Medicine, Department of Laboratory Medicine, Lund University, 223 61 Lund, Sweden. Electronic address: Christian.lindh@med.lu.se. 4. Department of Biomedicine - Pharmacology, Aarhus University, 8000 Aarhus C, Denmark. Electronic address: raho@biomed.au.dk. 5. Department of Biomedicine - Pharmacology, Aarhus University, 8000 Aarhus C, Denmark. Electronic address: Al@biomed.au.dk. 6. Department of Obstetrics and Gynaecology, University Hospital of Aarhus, Skejby Sygehus, 8000 Aarhus, Denmark. Electronic address: Erik.ernst@skejby.rm.dk. 7. School of Computer Science, University of St. Andrews, KY16 9SX St. Andrews, United Kingdom. Electronic address: twk@st-andrews.ac.uk. 8. Laboratory of Reproductive Biology, Section 5712, The Juliane Marie Centre for Women, Children and Reproduction, University Hospital of Copenhagen, University of Copenhagen, Rigshospitalet, 2100 Copenhagen, Denmark. Electronic address: Yding@rh.regionh.dk.
Abstract
BACKGROUND: Perfluoroalkyl substances (PFASs) are bio-accumulative pollutants, and prenatal exposure to PFASs is believed to impact human foetal development and may have long-term adverse health effects later in life. Additionally, maternal cigarette smoking may be associated with PFAS levels. Foetal exposure has previously been estimated from umbilical cord plasma, but the actual concentration in foetal organs has never been measured. OBJECTIVES: The concentrations of 5 PFASs and cotinine - the primary metabolite of nicotine - were measured in human foetuses, placentas, and maternal plasma to evaluate to what extent these compounds were transferred from mother to foetus and to determine if the PFAS concentrations were associated with maternal cigarette smoking. METHODS: Thirty-nine Danish women who underwent legal termination of pregnancy before gestational week 12 were included; 24 maternal blood samples were obtained together with 34 placental samples and 108 foetal organs. PFASs and cotinine were assayed by liquid chromatography/triple quadrupole mass spectrometry. RESULTS: In foetal organs, the average concentrations of perfluorooctanesulphonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluoroundecanoic acid (PFUnDa), and perfluorodecanoic acid (PFDA) were 0.6ng/g, 0.2ng/g, 0.1ng/g, 0.1ng/g, and 0.1ng/g, respectively. A significant positive correlation was found between the exposure duration, defined as foetal age, and foetal to maternal ratio for all five PFASs and cotinine. Smokers presented 99ng/g cotinine in plasma, 108ng/g in placenta, and 61ng/g in foetal organs. No correlation between the maternal cotinine concentrations and PFAS concentrations was found. CONCLUSIONS: PFASs were transferred from mother to foetus, however, with different efficiencies. The concentrations of PFOS, PFOA, PFNA, PFUnDA, and PFDA in foetal organs were much lower than the maternal concentrations. Furthermore, a significant correlation between the exposure duration and all of the evaluated PFASs was found. The health-compromising concentrations of these substances during foetal development are unknown.
BACKGROUND:Perfluoroalkyl substances (PFASs) are bio-accumulative pollutants, and prenatal exposure to PFASs is believed to impact human foetal development and may have long-term adverse health effects later in life. Additionally, maternal cigarette smoking may be associated with PFAS levels. Foetal exposure has previously been estimated from umbilical cord plasma, but the actual concentration in foetal organs has never been measured. OBJECTIVES: The concentrations of 5 PFASs and cotinine - the primary metabolite of nicotine - were measured in human foetuses, placentas, and maternal plasma to evaluate to what extent these compounds were transferred from mother to foetus and to determine if the PFAS concentrations were associated with maternal cigarette smoking. METHODS: Thirty-nine Danish women who underwent legal termination of pregnancy before gestational week 12 were included; 24 maternal blood samples were obtained together with 34 placental samples and 108 foetal organs. PFASs and cotinine were assayed by liquid chromatography/triple quadrupole mass spectrometry. RESULTS: In foetal organs, the average concentrations of perfluorooctanesulphonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluoroundecanoic acid (PFUnDa), and perfluorodecanoic acid (PFDA) were 0.6ng/g, 0.2ng/g, 0.1ng/g, 0.1ng/g, and 0.1ng/g, respectively. A significant positive correlation was found between the exposure duration, defined as foetal age, and foetal to maternal ratio for all five PFASs and cotinine. Smokers presented 99ng/g cotinine in plasma, 108ng/g in placenta, and 61ng/g in foetal organs. No correlation between the maternal cotinine concentrations and PFAS concentrations was found. CONCLUSIONS:PFASs were transferred from mother to foetus, however, with different efficiencies. The concentrations of PFOS, PFOA, PFNA, PFUnDA, and PFDA in foetal organs were much lower than the maternal concentrations. Furthermore, a significant correlation between the exposure duration and all of the evaluated PFASs was found. The health-compromising concentrations of these substances during foetal development are unknown.
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