Endocrine Disruptors and Persistent Organic Pollutants: Their Impact on the Environment and Human Health

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Exposome Analysis and Risk Assessment".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 885

Special Issue Editors


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Guest Editor
Department of Chemistry, University of Crete, 70013 Heraklion, Greece
Interests: environmental analytical chemistry of toxic organic compounds; DBPs; endocrine disruptors; POPs; human exposure studies of legacy and emerging toxic organic contaminants and endocrine disruptors

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Guest Editor
Section of Biomolecular Medicine, Department of Metabolism, Digestion and Reproduction, Imperial College London, London W12 0NN, UK
Interests: metabolomics; volatolomics; exposomics; mass spectrometry; enviromental exposures; human health
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Special Issue Information

Dear Colleagues,

Endocrine disruptors (EDCs) and persistent organic pollutants (POPs) are environmental contaminants that persist in ecosystems and bioaccumulate through food chains. EDCs disrupt hormone functions, leading to reproductive and developmental disorders, cardiovascular diseases, and cancer. POPs are linked to diabetes, cancer, neurodevelopmental issues, and reproductive disorders.

Key EDCs include BPA, phthalates, parabens, triclosan, and PFAS, which are found in personal care products and plastics. Key POPs include organochlorine pesticides (OCPs) and polybrominated diphenyl ethers (PBDEs), which are used as flame retardants.

Human exposure to these substances occurs through environmental contact, food, and product use, primarily via inhalation, skin contact, and ingestion. Persistent EDCs like PFAS accumulate in the blood, requiring repeated measurements to be taken during pregnancy and early childhood.

Research and review articles are needed to support the regulatory efforts essential to mitigate the environmental and health impacts of EDCs and POPs. Understanding their mechanisms of action and long-term effects is crucial for developing effective protection strategies.

Prof. Dr. Euripides G. Stephanou
Dr. Antonis Myridakis
Guest Editors

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Keywords

  • biomonitoring of EDCs and POPs
  • Prenatal exposure to mixtures of endocrine-disrupting chemicals and respiratory health in children
  • exposure to POPs and emotional and behavioral outcomes from early childhood to adolescence

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Published Papers (1 paper)

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Research

16 pages, 9832 KB  
Article
Gestational GenX Exposure Induces Maternal Hepatotoxicity by Disrupting the Lipid and Bile Acid Metabolism Distinguished from PFOA-Induced Pyroptosis
by Jin-Jin Zhang, Yu-Kui Chen, Ya-Qi Chen, Qin-Yao Zhang, Yu Liu, Qi Wang and Xiao-Li Xie
Toxics 2025, 13(8), 617; https://doi.org/10.3390/toxics13080617 - 24 Jul 2025
Viewed by 597
Abstract
Perfluorooctanoic acid (PFOA) and its replacement, GenX, are per- and polyfluoroalkyl substances (PFASs) widely used in industrial and consumer applications. Pregnant women are a vulnerable population to environmental pollutants. The maternal effects of GenX and PFOA exposure during pregnancy have not been fully [...] Read more.
Perfluorooctanoic acid (PFOA) and its replacement, GenX, are per- and polyfluoroalkyl substances (PFASs) widely used in industrial and consumer applications. Pregnant women are a vulnerable population to environmental pollutants. The maternal effects of GenX and PFOA exposure during pregnancy have not been fully elucidated. In this study, pregnant mice received daily oral doses of GenX (2 mg/kg/day), PFOA (1 mg/kg/day), or Milli-Q water (control) throughout gestation. Histopathological analyses revealed significant liver abnormalities in both exposure groups, including hepatocyte swelling, cellular disarray, eosinophilic degeneration, karyopyknosis, lipid vacuolation, and increased inflammatory responses. Through transcriptomics analyses, it was found that multiple metabolic and inflammatory pathways were enriched in both exposure groups. In the GenX group, overexpression of CYP4A, c-Myc, and Oatp2 proteins and decreased expression of EGFR and β-catenin in the liver suggested disruption of lipid and bile acid metabolism. In the PFOA group, significantly upregulated protein levels of NLRP3, GSDMD, caspase-1, IL-18, and IL-1β indicated hepatic pyroptosis. Despite these distinct pathways, both compounds triggered inflammatory cytokine release in the liver, consistent with the results of the transcriptomics analysis, suggesting shared mechanisms of inflammatory liver injury. Taken together, our findings provided novel insights into the hepatotoxicity mechanisms of GenX and PFOA exposure during pregnancy, underscoring the potential health risks associated with PFAS exposure. Full article
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