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PERFLUOROOCTANE SULFONATE (PFOS) DISRUPTS THE THYROID STATUS IN LABORATORY RODENTS
Citation:
Lau*, C, J R. Thibodeaux, R. G. Hanson, B E. Grey, AND J M. Rogers. PERFLUOROOCTANE SULFONATE (PFOS) DISRUPTS THE THYROID STATUS IN LABORATORY RODENTS. Presented at Society of Toxicology, Salt Lake City, UT, March 09 - 13, 2003.
Description:
PERFLUOROOCTANE SULFONATE (PFOS) DISRUPTS THE THYROID STATUS IN LABORATORY RODENTS. C. Lau, J.R. Thibodeaux, R.G. Hanson, B.E. Gray and J.M. Rogers. Reprod. Tox. Div. NHEERL, US EPA, Research Triangle Park, NC.
PFOS is an environmental contaminant ubiquitously found in humans and wildlife. Reproductive and developmental toxicity of this fluorochemical have been indicated in laboratory animals. The current study examines if alterations of thyroid status are involved in PFOS toxicity. Timed pregnant Sprague-Dawley rats and CD-1 mice were given PFOS/K+ (1, 2, 3, 5 or 10 mg/kg for rats, and 1, 5, 10, 15 or 20 mg/kg for mice) daily by oral gavage throughout pregnancy; while controls received 0.5% Tween-20 vehicle. Maternal blood was collected at intervals of several days during pregnancy, and serum T4, T3 and TSH were analyzed by specific RIA. Some animals were allowed to give birth and thyroid status of the neonates were monitored. PFOS in itself did not interfere with the RIA. During pregnancy, a marked decline of serum T4 concentration, and to a less extent T3, was seen in the control rat, with a feedback elevation of serum TSH. Superimposed on the hormonal decline, total and free T4 as well as T3 levels were significantly further reduced in the PFOS-treated dams at all dose groups and time points evaluated. In contrast, while elevation of TSH was also seen in the PFOS-treated rats, their levels did not exceed that of the controls. Similar findings were observed in the mice. Because the thyroid hormones fluctuate during pregnancy, these findings were extended to non-pregnant rats where 90-day old male and females were given similar doses of PFOS daily. At as little as 3 days after treatment, reduction of serum T4 was already apparent, while significant reductions of both T4 and T3 were seen after 20 days of treatment; however, an absence of feedback rise of TSH was also noted. In the developing rats, hypothyroxinemia was observed without concurrent changes of T3 or TSH. These results indicate that PFOS can be considered as an environmental endocrine disruptor, and the underlying mechanisms of this hormonal imbalance as well as its physiological consequences warrant further investigation. (This abstract does not reflect US EPA policy.)