The majority of investigations into the immunotoxic effects of perfluoroalkyl acids have focused on immunosuppression following the oral route of exposure. The potential for dermal exposure exists not only in the manufacturing of products and reformulations but also in use of end products such as fire-retardants. Recent studies have demonstrated that as compared to oral dosing, dermal exposure results in qualitatively similar immunosuppressive effects and additionally, that while not allergenic itself, dermal exposure to PFOA simultaneously with exposure to a respiratory allergen augments the IgE response to that allergen. This presentation will discuss the modulation of immune related genes following PFOA exposure, helping to explain the reciprocal relationship between the mechanisms governing immune suppression and augmentation of IgE-mediated hypersensitivity and demonstrating the kinetics of absorption and penetration of PFOA through human and mouse skin. Genetic diversity in these immune responses was also demonstrated between Th1 and Th2 strains of mice.
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