Impact of perfluorooctanesulfonate and perfluorooctanoic acid on human peripheral leukocytes.

Toxicol In Vitro

Institute of Immunology, Medical Faculty, RWTH Aachen University, Pauwelsstrasse 30, 52074 Aachen, Germany.

Published: June 2011

AI Article Synopsis

  • PFCs like PFOS and PFOA are widespread environmental contaminants that can affect immune functions in humans, but previous research mainly focused on rodents.
  • The study found that PFOS reduced natural killer-cell activity and decreased TNF-α release in response to stimulation, while also correlating with higher IL-6 release.
  • PFOA enhanced monocytic differentiation and showed a significant relationship between its plasma levels and pro-inflammatory cytokine release, highlighting the immune impact of these compounds on human leukocytes.

Article Abstract

Perfluorinated compounds (PFCs), such as perfluorooctanesulfonate (PFOS) and perfluorooctanoic acid (PFOA), are xenobiotics that can be detected worldwide in the environment, wildlife, and humans. So far, the immunotoxicity of PFCs has only been investigated in rodents, but not in humans. In this study, we explore the impact of PFOS and PFOA on selected functions of human leukocytes in vitro. PFOS induced a significant decrease of natural killer-cell activity and reduced the release of the pro-inflammatory cytokine TNF-α following lipopolysaccharide (LPS)-stimulation. Furthermore, the plasma PFOS concentrations (2.09-8.98 ng/ml) found in our study subjects correlated positively with the LPS-stimulated IL-6 release. PFOA augmented significantly calcitriol-induced monocytic differentiation of the HL-60 cell line. Additionally, there was a significant linear relationship between LPS-stimulated TNF-α and IL-6 release, and the plasma PFOA (1.20-6.92ng/ml) concentrations of the study subjects. In conclusion, the investigated PFCs affect human immune cells mainly with regard to natural killer-cell cytotoxicity and the pro-inflammatory cytokine release by stimulated macrophages.

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http://dx.doi.org/10.1016/j.tiv.2011.03.005DOI Listing

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