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PRENATAL WINDOW OF SUSCEPTIBILITY TO PERFLUOROOCTANE SULFONATE-INDUCED NEONATAL MORTALITY IN THE SPRAGUE-DAWLEY RAT
Citation:
Grasty, R. C., B E. Grey, C S. Lau, AND J M. Rogers. PRENATAL WINDOW OF SUSCEPTIBILITY TO PERFLUOROOCTANE SULFONATE-INDUCED NEONATAL MORTALITY IN THE SPRAGUE-DAWLEY RAT. BIRTH DEFECTS RESEARCH PART B: DEVELOPMENTAL AND REPRODUCTIVE TOXICOLOGY 68(6):465-471, (2003).
Description:
Abstract
The critical period for increased neonatal mortality induced by PFOS exposure was evaluated in the rat . Timed-pregnant Sprague-Dawley rats were treated by oral gavage with 25 mg/kg/d PFOS/K+ on four consecutive days during gestation (gestation days (GD) 2-5, 6-9, 10-13, 14-17 or 17-20). Controls received vehicle (10 ml/kg 0.5% Tween-20) daily on GD 2-20. Maternal weight gain was reduced in treated animals during dosing. Similar patterns were seen in food and water consumption. Litter size (postnatal day (PND) 0) was unaffected while litter weight was reduced in treated groups. All PFOS groups experienced decreases in neonatal survival while controls remained near 100%. Mortality increased as the dosing period fell later during gestation, with the GD 17-20 group approaching 100%. Deaths occurred before PND 4, most within the first 24 hours. Maternal serum levels on GD 21 were directly related to pup mortality. In a second dosing paradigm, pregnant rats were treated with 0, 25, or 50 mg/kg/d PFOS/K+ on GD 19-20. Dam weight gain was suppressed in both PFOS groups. Both groups experienced significant pup mortality within the first 12 hours. Mortality continued through PND 5, where mortality was 2, 34, and 97% for the 0, 25, and 50 mg/kg groups, respectively. Pup weight was also reduced in treated groups on these days. Gross dissection and histological examination of lungs revealed differences in maturation between control and treated animals on PND 0. We conclude that exposure to PFOS late in gestation is sufficient to induce 100% pup mortality and that inhibition of lung maturation may be involved.