Prenatal PFOA Exposure and Long-term Health Impacts
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Background and Purpose. PFAS are known developmental toxicants that impact physiology, growth, and metabolism and are also associated with impacts to kidney health. Kidney disease is one the of well-established diseases associated with PFAS exposure. The environmental etiology of kidney disease and mechanisms that contribute to the disease have not been well studied and are largely unknown. The purpose of this study is to understand the impacts of prenatal PFOA exposure on metabolic endpoints and measures of kidney function in adulthood. Methods. Pregnant Sprague-Dawley rats were dosed via oral gavage with PFOA from gestation day (GD) 9-21 and their prenatally exposed offspring were examined for measures of metabolic function and kidney function in adulthood. To understand the impacts of prenatal PFOA (80mg/kg daily, GD9-21) metabolic endpoints (glucose tolerance testing) and measures of kidney function were measured in adult male and female offspring. Intraperitoneal glucose tolerance testing (IPGTT) was used to monitor the glucose response in offspring at two time periods (PND38-PND40 and at PND 88-90). At PND 90, offspring were assessed for impacts on kidney function with serum measurements of blood urea nitrogen (BUN), creatinine, urea, and serum proteins (albumin and globulin), proteins that may be important in immune function. Results. Prenatal PFOA exposure caused an elevated spike in glucose immediately after injection that returned to a normal response afterwards in animals of age PND38-PND40, an effect that did not persist in older animals (PND 88-90). Other time points in the glucose tolerance testing were unchanged in PFOA-exposed animals. Kidney function measures from adult F1 adult offspring showed significant effects at p<0.001 for BUN, urea, and BUN/creatine ratio. PFOA-dependent significant elevations versus control re seen for BUN, urea, and BUN/creatinine ratio. Serum creatinine and serum albumin were unchanged with PFOA exposure. Conclusions. Adult outcomes including kidney and metabolic function are adversely impacted by prenatal PFOA exposure. Prenatal exposure to PFOA significantly impacted various serum measures of kidney function (BUN, BUN: creatinine ratio, and urea). Metabolic function or glucose use, as measured with glucose tolerance testing, was also impacted by prenatal PFAS exposure. This study shows that developmental exposure to PFOA is associated with adverse health outcomes in adulthood. The views expressed in this abstract are those of the author(s) and do not necessarily represent the views or policies of the U.S. Environmental Protection Agency.