Perfluorooctanoic acid and perfluorononanoic acid in fetal and neonatal mice following in utero exposure to 8-2 fluorotelomer alcohol.
8-2 Fluorotelomer alcohol (FTOH) and its metabolites, perfluorooctanoic acid (PFOA) and perfluorononanoic acid (PFNA), are developmental toxicants but metabolism and distribution during pregnancy are not known. To examine this, timed-pregnant mice received a single gavage dose (30 mg 8-2 FTOH/kg body weight) on gestational day (GD) 8. Maternal and neonatal serum and liver as well as fetal and neonatal homogenate extracts were analyzed using gas chromatography coupled with mass spectrometry. During gestation (GD9 to GD18), maternal serum and liver concentrations of PFOA decreased from 789 +/- 41 to 668 +/- 23 ng/ml and from 673 +/- 23 to 587 +/- 55 ng/g, respectively. PFOA was transferred to the developing fetuses as early as 24-h posttreatment with concentrations increasing from 45 +/- 9 ng/g (GD10) to 140 +/- 32 ng/g (GD18), while PFNA was quantifiable only at GD18 (31 +/- 4 ng/g). Post-partum, maternal serum PFOA concentrations decreased from 451 +/- 21 ng/ml postnatal day (PND) 1 to 52 +/- 19 ng/ml (PND15) and PFNA concentrations, although fivefold less, exhibited a similar trend. Immediately after birth, pups were cross-fostered with dams that had been treated during gestation with 8-2 FTOH (T) or vehicle (C) resulting in four treatment groups in which the first letter represents in utero (fetal) exposure and the second represents lactational (neonatal) exposure: C/C, T/C, C/T, T/T. On PND1, neonatal whole-body homogenate concentrations of PFOA from T/T and T/C groups averaged 200 +/- 26 ng/g, decreased to 149 +/- 19 ng/g at PND3 and this decreasing trend was seen in both neonatal liver and serum from PND3 to PND15. Based on detectible amounts of PFOA in neonatal serum in the C/T group on PND3 (57 +/- 11 ng/ml) and on PND15 (58 +/- 3 ng/ml), we suggest that the neonates were exposed through lactation. In conclusion, exposure of neonates to PFOA and PFNA occurs both pre- and postnatally following maternal 8-2 FTOH exposure on GD8.
Henderson
W Matthew
WM
Interdisciplinary Toxicology Program, College of Public Health, University of Georgia, Athens, Georgia 30602, USA. Henderson.matt@epa.gov
Smith
Mary Alice
MA
D000818:Animals; D000831:Animals, Newborn; D001822:Body Burden; D001835:Body Weight / Q000187:drug effects; D002210:Caprylates / Q000032:analysis* / Q000097:blood; D004785:Environmental Pollutants / Q000493:pharmacokinetics / Q000633:toxicity*; D005233:Fatty Alcohols / Q000493:pharmacokinetics / Q000633:toxicity*; D005260:Female; D005466:Fluorocarbons / Q000032:analysis* / Q000097:blood; D005865:Gestational Age; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D051379:Mice; D008815:Mice, Inbred Strains; D009929:Organ Size / Q000187:drug effects; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000097:blood / Q000139:chemically induced / Q000378:metabolism; D014018:Tissue Distribution
C505284:1,1,2,2-tetrahydroheptadecafluorodecanol-3,3,4,4,5,5,6,6,7,7,8,8,9,9,10,10,10-heptadecafluoro-1-decanol; D002210:Caprylates; D004785:Environmental Pollutants; D005233:Fatty Alcohols; D005466:Fluorocarbons; C018959:hexadecafluoro-nonanoic acid; C023036:perfluorooctanoic acid