4.7 Review

Epigenetic changes by per- and polyfluoroalkyl substances (PFAS)

Journal

ENVIRONMENTAL POLLUTION
Volume 279, Issue -, Pages -

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.envpol.2021.116929

Keywords

Three to ten pertinent; Environmental epigenetics; per-and polyfluoroalkyl substance (PFAS); Persistent organic pollutants (POPs); Perfluorooctane sulfonate (PFOS); Perfluorooctanoic acid (PFOA); Molecular mechanisms; Mechanistic toxicology; Endocrine disrupting chemicals (EDCs)

Funding

  1. National Research Foundation of Korea (NRF) [2019R1A6A3A03031711]
  2. Strategic Environmental Research and Development Program [W912HQ19C0050]
  3. Baylor University
  4. National Research Foundation of Korea [2019R1A6A3A03031711] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Studies have shown that per- and polyfluoroalkyl substances (PFAS) can cause epigenetic modifications, including DNA methylation, histone modification, and microRNA expression. Different types of research have revealed the potential harm of PFAS to human health, and further studies are needed to understand the specific effects of PFAS.
Increasing studies are examining per-and polyfluoroalkyl substances (PFAS) induced toxicity and resulting health outcomes, including epigenetic modifications (e.g., DNA methylation, histone modifi-cation, microRNA expression). We critically reviewed current evidence from human epidemiological, in vitro, and animal studies, including mammalian and aquatic model organisms. Epidemiological studies identified the associations between perfluorooctane sulfonate (PFOS) or perfluorooctanoic acid (PFOA) exposure and epigenetic changes in both adult populations and birth cohorts. For in vitro studies, various cell types including neuroblasts, preadipocytes, and hepatocytes have been employed to understand epigenetic effects of PFAS. In studies with animal models, effects of early life exposure to PFAS have been examined using rodent models, and aquatic models (e.g., zebrafish) have been more frequently used in recent years. Several studies highlighted oxidative stress as a key mediator between epigenetic modi-fication and health effects. Collectively, previous research clearly suggest involvement of epigenetic mechanisms in PFAS induced toxicity, though these efforts have primarily focused on specific PFASs (i.e. mainly PFOS and PFOA) or endpoints (i.e. cancer). Additional studies are necessary to define specific linkages among epigenetic mechanisms and related biomarkers or phenotypical changes. In addition, future research is also needed for understudied PFAS and complex mixtures. Studies of epigenetic effects elicited by individual PFAS and mixtures are needed within an adverse outcome pathways framework, which will advance an understanding of PFAS risks to public health and the environment, and support efforts to design less hazardous chemicals. (c) 2021 Elsevier Ltd. All rights reserved.

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