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MATERNAL AND DEVELOPMENTAL TOXICITY OF PERFLUOROOCTANE SULFONATE (PFOS) IN THE MOUSE
Citation:
Thibodeaux, J R., R. G. Hanson, B E. Grey, B D. Barbee, J. H. Richards, J. L. Butenhoff, J M. Rogers, AND C Lau*. MATERNAL AND DEVELOPMENTAL TOXICITY OF PERFLUOROOCTANE SULFONATE (PFOS) IN THE MOUSE. Presented at Society of Toxicology, Salt Lake City, UT, March 09 - 13, 2003.
Description:
MATERNAL AND DEVELOPMENTAL TOXICITY OF PERFLUOROOCTANE SULFONATE (PFOS) IN THE MOUSE. J.R. Thibodeaux1, R.G. Hanson1, B.E. Grey1, B.D. Barbee1, J.H. Richards2, J.L. Butenhoff3, J.M. Rogers1, C. Lau1. 1Reprod. Tox. Div., 2Exp. Tox. Div., NHEERL, ORD, US EPA, Research Triangle Park, NC, 33M, Med. Dept, St. Paul, MN.
The maternal and developmental toxicity of PFOS, an environmentally persistent compound that has been used in the manufacture of surfactants and insecticides, were evaluated. Timed-pregnant CD1 mice were gavaged with 1, 5, 10, 15, or 20 mg/kg/day PFOS/K+ from GD 2 to term. Controls received an equivalent volume of 0.5% Tween-20 vehicle (10 ml/kg). Some dams were killed on GD 18 for teratological examination, while those remaining were allowed to deliver to monitor the postnatal growth and development of their offspring. PFOS levels in maternal serum and liver were determined at term. Maternal weight gain was suppressed by 20 mg/kg PFOS, indicating the general maternal toxicity of the chemical. Serum triglycerides and thyroxine in dams treated with greater than 5 mg/kg PFOS were significantly lower than controls. Dose-dependent maternal liver weight increases were observed at term. PFOS did not alter the number of implantations, live fetuses, or fetal weight at term. Cleft palate, sternal defects, cardiac ventricular septal defect, and enlargement of the right atrium were detected, primarily in the 20 mg/kg group. Live birth was observed in all groups; however, neonates in the 20 mg/kg group were moribund and died within 4-6 h. While newborns in the 15 mg/kg group appeared viable, all were found dead within 24 h. Postnatal viability was greater in the lower dose groups and surviving neonates appeared to thrive, but significant delays in eye opening were observed. These dose-dependent adverse effects will be compared to the body burdens of PFOS. These results are similar to the maternal and developmental toxicity of PFOS previously described in the rat, although the mouse appears to be a less sensitive species. This abstract does not necessarily reflect EPA policy.