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Emerging Plastic-Related Toxicity: From Environmental Exposure to Human Health
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Emerging Plastic-Related Toxicity: From Environmental Exposure to Human Health

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (20 April 2026) | Viewed by 4452

Special Issue Editors

Dr. Antonietta Santoro

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Guest Editor
Department of Medicine, Surgery and Dentistry, University of Salerno, 84081 Baronissi, Italy
Interests: the effects of environmental pollutants on human health; the role of the endocannabinoid system in the processes of carcinogenicity, inflammation, neurogenesis and neuronal differentiation
Special Issues, Collections and Topics in MDPI journals
Dr. Marta Anna Szychlinska

E-Mail Website
Guest Editor
Department of Precision Medicine in Medical, Surgical and Critical Care (MEPRECC), University of Palermo, Palermo, Italy
Interests: cartilage tissue engineering; mesenchymal stem cells; osteoarthritis; articular cartilage morphology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Over the past decade, the rise in plastics and their accumulation in the environment has become a public concern. To limit petroleum-based plastic pollution, bioplastics—comprising bio‐based and/or biodegradable polymers—have been publicized as “green” alternatives with the positive connotation of “environmental sustainability”. As technological advancements refine their properties, plastics and bioplastics are increasingly permeating industries. However, their rapid integration into daily-use products requires the scientific scrutiny needed to assess their potential implications for human health. New insights are emerging suggesting that exposure to plastics—especially in the form of microplastics and nanoplastics—and their additives could cause adverse health effects by compromising cell metabolism and inducing oxidative stress, inflammation, and apoptosis in both in vitro systems and animal models. Therefore, this Special Issue welcomes reviews and research papers aiming to assess the acute and chronic toxicity of plastics (including micro- and nanoplastics) on human health by analyzing toxic and epigenetic effects, metabolic alterations, and molecular mechanisms of action in human and mammal experimental model systems.

Dr. Antonietta Santoro
Dr. Marta Anna Szychlinska
Guest Editors

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Keywords

  • (bio)plastic- and (bio)polymer-related toxicity
  • microplastic and nanoplastic accumulation/degradation in mammals
  • cell cultures
  • human health
  • in vivo models
  • epigenetics effects
  • endocrine disruptor properties of bioplastics
  • plastics and inflammation
  • plastics in neurodegeneration and neuroinflammation
  • reproduction
  • cell metabolism
  • immunomodulation

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Published Papers (3 papers)

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Research

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22 pages, 4549 KB  
Article
Hepatotoxic Mechanisms of Polyethylene Terephthalate Microplastics Revealed by Network Toxicology, Molecular Docking, and In Vivo Validation
by Xuemei Tan, Min Zhang, Jingying Lu, Shuo Shi, Xueting Shi and Zhouhua Hou
Int. J. Mol. Sci. 2026, 27(7), 3256; https://doi.org/10.3390/ijms27073256 - 3 Apr 2026
Viewed by 594
Abstract
Polyethylene terephthalate microplastics (PET-MPs) are emerging environmental pollutants, but the molecular mechanisms underlying their hepatotoxicity remain poorly understood. Here, we combined network toxicology with experimental validation to investigate how PET-MPs induce liver injury. In silico, we investigated the PET-repeating unit as the molecular [...] Read more.
Polyethylene terephthalate microplastics (PET-MPs) are emerging environmental pollutants, but the molecular mechanisms underlying their hepatotoxicity remain poorly understood. Here, we combined network toxicology with experimental validation to investigate how PET-MPs induce liver injury. In silico, we investigated the PET-repeating unit as the molecular basis for target interactions. We identified 59 overlapping genes between 157 putative PET-MPs targets and 1693 liver injury-associated genes. Protein–protein interaction analysis revealed six hub genes (AKT1, PIK3CA, PIK3CB, PIK3CD, PIK3R1, and SRC), all components of the PI3K/AKT signaling pathway. Gene ontology analysis showed that PET-MPs affect cellular stress responses and kinase activities, while pathway enrichment analysis identified PI3K-Akt, Ras, and reactive oxygen species pathways as primary targets. Molecular docking demonstrated strong binding affinity between PET-MPs and these core targets (binding free energies <−5 kcal/mol). In vitro, PET-MPs induced mitochondrial depolarization, oxidative stress, upregulation of TNF-α and IL-6, and decreased p-AKT/AKT ratio, accompanied by increased apoptosis; the apoptotic effect was reversed by the AKT agonist SC79. In vivo experiments confirmed that AKT activation reduced PET-MP-induced liver injury, evidenced by decreased inflammation, lower serum transaminases, and restored oxidative balance. These protective effects were abolished by PI3K/AKT pathway inhibitors. Our study identifies potential therapeutic targets and strategies for PET-MP-induced liver injury. Full article
(This article belongs to the Special Issue Emerging Plastic-Related Toxicity: From Environmental Exposure to Human Health)
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22 pages, 12944 KB  
Article
Network Toxicology and Molecular Docking Reveal the Toxicological Mechanisms of DEHP in Bone Diseases
by Zhonghao Fan, Haitao Du, Xinyi Zhou, Cheng Wang, Mengru Zhang, Tiefeng Sun, Yi Wang and Ping Wang
Int. J. Mol. Sci. 2025, 26(22), 10895; https://doi.org/10.3390/ijms262210895 - 10 Nov 2025
Cited by 3 | Viewed by 2222
Abstract
Di(2-ethylhexyl) phthalate (DEHP), a widely employed exogenous plasticizer, has become pervasive in the environment and living organisms due to its extensive use in food packaging, medical devices, and daily consumer products, and is established as a typical endocrine-disrupting chemical. Growing evidence indicates a [...] Read more.
Di(2-ethylhexyl) phthalate (DEHP), a widely employed exogenous plasticizer, has become pervasive in the environment and living organisms due to its extensive use in food packaging, medical devices, and daily consumer products, and is established as a typical endocrine-disrupting chemical. Growing evidence indicates a strong association between DEHP exposure and the incidence of chronic bone disorders, including osteoporosis (OP), osteoarthritis (OA), and osteonecrosis of the femoral head (ONFH). However, the molecular mechanisms underlying its pathogenic effects across these diseases remain poorly defined. In this study, we applied an environmental network toxicology approach to integrate predicted protein targets of DEHP with known disease-associated targets of the three bone disorders using multiple databases. Through Venn analysis, protein–protein interaction (PPI) network construction, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, we identified core targets and key signaling pathways. Molecular docking and molecular dynamics (MD) simulations were further employed to validate the binding modes and stability between DEHP and the core targets, thereby elucidating common and distinct mechanisms of DEHP across these bone diseases. A total of 109 overlapping targets of DEHP and the three bone diseases were identified, among which 7 core targets—AKT1, SRC, ESR1, CASP3, MMP9, BCL2, and BCL2L1—were common to all three disorders. These are implicated in critical biological processes such as apoptosis regulation, inflammation, extracellular matrix degradation, and estrogen signaling. KEGG enrichment analysis revealed significant involvement of the PI3K-Akt, MAPK, Ras, TNF, and estrogen signaling pathways across all three diseases. Molecular docking and MD simulations confirmed stable binding of DEHP to key targets including AKT1, ESR1, and MMP9, supporting its potential to disrupt bone metabolic homeostasis via multi-target and multi-pathway mechanisms. Further analysis indicated that DEHP exerts both shared and disease-specific effects: it disrupts osteoblast/osteoclast balance in OP, amplifies inflammatory responses and matrix degradation in OA, and contributes to impaired angiogenesis and osteocyte necrosis in ONFH. This study systematically reveals how DEHP disrupts bone homeostasis through a multi-target and multi-pathway network, constructing a cross-disease osteotoxicity framework. It is the first to delineate the common and distinct molecular mechanisms of DEHP in OP, OA, and ONFH. Although these insights are derived from computational models and require further experimental validation, they provide a novel theoretical basis for combined intervention strategies targeting multiple bone diseases and for environmental health risk assessment. Full article
(This article belongs to the Special Issue Emerging Plastic-Related Toxicity: From Environmental Exposure to Human Health)
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Review

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27 pages, 876 KB  
Review
Micro- and Nanoplastics as Disruptors of Digestive and Hepatopancreatic Homeostasis: Insights into the Plastic-Gut-Liver Axis
by Nicoletta Capuano, Martina Lombardi, Noemi Cafà, Marianna Marino, Flora Salzano, Federica Scalia, Raffaele Marfella, Giovanni Villone, Francesco Cappello, Marta Anna Szychlinska, Gianluigi Franci, Antonietta Santoro and Luca Rinaldi
Int. J. Mol. Sci. 2026, 27(7), 3272; https://doi.org/10.3390/ijms27073272 - 4 Apr 2026
Viewed by 1033
Abstract
Micro- and nanoplastics (MPs/NPs) have emerged as pervasive environmental contaminants with increasing implications for human health, particularly within the digestive system. This review critically examines the role of MPs/NPs as disruptors of gastrointestinal and liver homeostasis through the lens of the plastic–gut–liver axis. [...] Read more.
Micro- and nanoplastics (MPs/NPs) have emerged as pervasive environmental contaminants with increasing implications for human health, particularly within the digestive system. This review critically examines the role of MPs/NPs as disruptors of gastrointestinal and liver homeostasis through the lens of the plastic–gut–liver axis. We synthesize current evidence on primary exposure routes—including ingestion, inhalation, dermal contact, and transplacental transfer—and highlight their intestinal uptake, systemic dissemination, and tissue accumulation. Mechanistically, MPs/NPs compromise intestinal barrier integrity, promote oxidative stress, and induce microbiota dysbiosis, facilitating the translocation of microbial-derived signals to the liver via the portal circulation. This process triggers inflammatory signaling cascades, metabolic reprogramming, and immune dysregulation, contributing to hepatic steatosis, insulin resistance, and potential carcinogenic processes. Emerging evidence also implicates pancreatic dysfunction and β-cell stress within a broader gut–liver axis context. We further discuss the systemic propagation of MPs/NPs-induced dysbiosis along multi-organ axes, including gut–lung and gut–brain interactions. Despite robust preclinical data, human evidence remains limited due to methodological heterogeneity and the lack of standardized biomarkers. This review underscores critical knowledge gaps and emphasizes the need for integrative, translational approaches to clarify long-term health risks and inform regulatory strategies within the environmental exposome framework. Full article
(This article belongs to the Special Issue Emerging Plastic-Related Toxicity: From Environmental Exposure to Human Health)
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