You are here:
Disposition of Perfluorooctanoic Acid (PFOA) in Pregnant and Lactating CD-1 Mice and Their Pups
Citation:
FENTON, S. E., J. L. REINER, S. F. NAKAYAMA, A. DELINSKY, J. STANKO, E. P. HINES, S. WHITE, A. B. LINDSTROM, M. STRYNAR, AND S. E. PETROPOULOU. Disposition of Perfluorooctanoic Acid (PFOA) in Pregnant and Lactating CD-1 Mice and Their Pups. Presented at Teratology Society Annual Meeting, Rio Grande, PUERTO RICO, June 26 - July 01, 2009.
Impact/Purpose:
For submission to Teratology Society Annual Meeting, Rio Grande, Puerto Rico
Description:
Previous studies in mice prenatally-exposed to PFOA demonstrate growth and developmental effects, including impaired body weight gain and mammary gland development, delayed eye opening, and increased mortality. Those dose dependent effects appeared to worsen if offspring exposed in utero nursed from PFOA-exposed dams. PFOA disposition in pregnant and lactating mice and their offspring following a single gestational exposure was characterized in this study. Timed-pregnant CD-1 mice were dosed by gavage with 0, 0.1, 1, or 5 mg PFOA/kg (N=25/dose group) on gestation day (GD)17. Maternal fluids and tissues, pup serum, or whole pups (N=5 litters/dose) were collected between GD18 and postnatal day (PND)18. PFOA concentrations were measured in amniotic fluid, maternal serum, urine, mammary tissue, milk, pup serum, and whole pups by ultra performance liquid chromatography-tandem mass spectrometry. On GD18, amniotic fluid PFOA concentrations were 68.8, 51.8, and 40% of that in dam serum at 0.1, 1, and 5 mg/kg, respectively. On PND1, pups exhibited significantly higher serum PFOA concentrations than their respective dams (p<0.05). Maternal mammary gland tissue, milk, and serum PFOA concentrations were highest in early (PND1-4) and late lactation (PND18), and lowest at mid-lactation (PND8), regardless of dose. The distribution ratio of milk vs. maternal serum PFOA (milk:serum) was greatest in early and late lactation (PND2 and 18), ranging from 0.15-0.56 (averaging 0.33 early and 0.26 late), whereas near the peak of lactation (PND8 and 11), milk:serum PFOA ranged from 0.11-0.27 (mean 0.18). Whole pup PFOA body burden (ng) increased from birth to PND8; decreasing by PND18. The U-shaped concentration curves are likely due to temporal dilution and concentration of PFOA in milk and maternal/offspring serum, inversely following blood and milk volumes over the course of lactation. In a concentration-based comparison, prenatally-exposed pups exhibited a significantly larger serum PFOA load than their dam. These data suggest that milk is a substantial PFOA exposure route to mouse offspring following a single gestational exposure and that accumulation of pup PFOA body burden over time results from early lactational transfer of PFOA, an exposure that had previously been ill-defined in other species. This abstract does not necessarily reflect EPA policy.