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12-17 September 2010

Perfluoroalkylated substances (PFAS) is the collective name for a vast group of fluorinated compounds, including oligomers and polymers, which consist of neutral and anionic surface active compounds with high thermal, chemical and biological inertness. Perfluorinated compounds are generally hydrophobic but also lipophobic and will therefore not accumulate in fatty tissues as is usually the case with other persistent halogenated compounds. An important subset is the (per)fluorinated organic surfactants, to which perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) belong. The analytical detection method of choice for PFOS and PFOA is currently liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS), whereas both LC-MS/MS and gas chromatography-mass spectrometry (GC-MS) can be used for the determination of precursors of PFOS and PFOA. There are few reports of analysis of food items using these methods. Due to the substantial lack of suitable analytical data, many assumptions have been made in order to derive exposure estimates. Therefore, figures on levels in food and exposure provided in this opinion should be taken as indicative. PFOS, PFOA and other perfluorinated organic compounds have been widely used in industrial and consumer applications including stain- and water-resistant coatings for fabrics and carpets, oil-resistant coatings for paper products approved for food contact, fire-fighting foams, mining and oil well surfactants, floor polishes, and insecticide formulations. A number of different perfluorinated organic compounds have been widely found in the environment.

PFAS (perfluoroalkyl substances) are considered non-genotoxic. However, PFAS exposure has been associated with the induction of oxidative stress in vitro and in vivo, and the possible induction of indirect genotoxic effects under sustained PFAS exposure has not been investigated. In order to shed light on this aspect, in this study a comprehensive assessment of genotoxicity was carried out in mice administered with perfluorooctanoic acid (PFOA, 0.1, 1 and 5 mg/kg body weight) and its C4 analogue perfluorobutyric acid (PFBA, 5 mg/kg body weight) for five weeks through drinking water. Markers of cell toxicity, oxidative stress and DNA strand breaks were measured in liver, the main target of toxicity of PFOA in rodents; systemic genotoxicity was also assessed by the analysis of micronuclei in reticulocytes and spleen lymphocytes, and germ cell effects by the Comet assay on testis cells. PFOA administration at the highest dose (5 mg/kg body weight) induced marked liver hypertrophy with signs of cell injury (elevated ALT and AST), with no concurrent evidence of lipid peroxidation and oxidative stress (decreased antioxidant capacity). Only mild liver hypertrophy, with no other signs of toxicity, was determined by PFBA administration. No evidence of treatment related genotoxicity was observed in any experimental group. Overall, data indicate that under the experimental conditions of this study, severe liver toxicity induced by PFOA administration is not associated with oxidative stress. Accordingly, no genotoxic effect is observed in liver and in the other tissues examined. Milder evidence of liver toxicity, with no genotoxicity, and a lower tendency to bioaccumulation were observed in PFBA treated mice.