Studies on the toxicological effects of PFOA and PFOS on rats using histological observation and chemical analysis.

As an emerging class of environmentally persistent and bioaccumulative contaminants, perfluorinated compounds (PFCs), especially perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), have been ubiquitously found in the environment. Increasing evidence shows that the accumulated levels of PFCs in animals and the human body might cause potential impairment to their health. In the present study, toxicological effects of PFOA and PFOS on male Sprague-Dawley rats were examined after 28 days of subchronic exposure. Abnormal behavior and sharp weight loss were observed in the high-dose PFOS group. Marked hepatomegaly, renal hypertrophy, and orchioncus in treated groups were in accordance with the viscera-somatic indexes of the liver, kidney, and gonad. Histopathological observation showed that relatively serious damage occurred in the liver and lung, mainly including hepatocytic hypertrophy and cytoplasmic vacuolation in the livers and congestion and thickened epithelial walls in the lungs. PFOA concentrations in main target organs were in the order of kidney > liver > lung > (heart, whole blood) > testicle > (spleen, brain), whereas the bioaccumulation order for PFOS was liver > heart > kidney > (whole blood) > lung > (testicle, spleen, brain). The highest concentration of PFOA detected in the kidney exposed to 5 mg/kg/day was 228+/-37 microg/g and PFOS in the liver exposed to 20 mg/kg/day reached the highest level of 648+/-17 microg/g, indicating that the liver, lung, and kidney might serve as the main target organs for PFCs. Furthermore, a dose-dependent accumulation of PFOS in various tissues was found. The accumulation levels of PFOS were universally higher than PFOA, which might explain the relative high toxicity of PFOS. The definite toxicity and high accumulation of the tested PFCs might pose a great threat to biota and human beings due to their widespread application in various fields.