PFOA is a carcinogen, liver toxicant, a developmental toxicant, an immune system toxicant, and also exerts hormonal effects including alteration of thyroid hormone levels. Animal studies show developmental toxicity from reduced birth size, physical developmental delays, endocrine disruption, and neonatal mortality. PFOA causes liver cancer in rodents and also induces testicular and pancreatic cancer through induction of Leydig cell tumors and pancreatic acinar cell tumors. PFOA alters lipid metabolism. It is an agonist of PPARα and is a peroxisome proliferator in rodents contributing to a well understood form of oxidative stress. Humans are considered less susceptible to peroxisome proliferation than rodents. However, PFOA has been found to be a liver carcinogen in rainbow trout via a potential estrogenic mechanism, which may be more relevant to humans. A study found PFOA to be an obesogen in female mice at mid-age—with altered levels of insulin and leptin—at the lowest dose of 0.01 milligrams per kilogram of body weight during development.
While a USEPA review notes PFOA has not "been shown to be mutagenic in a variety of assays" in 1991 researchers from Japan demonstrated oxidative liver DNA damage in an experiment with rats. PFOA has been described as a member of a group of "classic non-genotoxic carcinogens". However, a provisional German assessment notes that a 2005 study found PFOA to be genotoxic via a peroxisome proliferation pathway that produced oxygen radicals in HepG2 cells, and a 2006 study demonstrated the induction and suppression of a broad range of genes; therefore, it states that the indirect genotoxic (and thus carcinogenic) potential of PFOA cannot be dismissed. Criteria have been proposed that would allow PFOA, and other perfluorinated compounds, to be classified as "weakly non-specific genotoxic."
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