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Toxicity of Phthalate Esters (PAEs)

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A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Emerging Contaminants".

Deadline for manuscript submissions: 28 August 2026 | Viewed by 6737

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Dr. Zhenxing Chi

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Guest Editor

Department of Environmental Engineering, Harbin Institute of Technology, Weihai, 2# Wenhua West Road, Weihai 264209, China
Interests: environmental chemical pollutants; PAEs; PBDEs; micro-/nanomaterials; hematologic toxicity; oxidative stress; interaction between small molecules and biomolecules

Special Issue Information

Dear Colleagues,

Phthalate esters (PAEs) are commonly used as plasticizers. Due to the weak non-covalent bonding forms between PAEs and the product matrix, PAEs will gradually separate from the matrix into the environment over time. PAEs are commonly found in air, soil, seawater, freshwater, sediment, etc. They have also been detected in food, drinking water, and human body fluids. As one of the most common organic pollutants, their potential environmental and health hazards have attracted widespread international attention. Research has shown that PAEs have estrogen-like effects and are typical endocrine disruptors, which can affect the normal growth, development, and reproduction of organisms. Although their production and use have gradually been restricted, there is still widespread environmental pollution and human exposure to PAEs. The purpose of this Special Issue is to provide a detailed introduction to the toxic effects and mechanisms of PAEs (including their metabolites). For this Special Issue, we cordially invite you to submit reviews and regular research papers focusing on in vitro and in vivo (with animals, plants, or microorganisms) toxicity studies of PAEs, with the aim of enhancing the understanding of the ecological and health risks associated with PAEs.

Dr. Zhenxing Chi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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Keywords

phthalate esters
toxic mechanism
toxic effect
in vivo study
in vitro study

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Published Papers (4 papers)

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Research

17 pages, 12144 KB

Open AccessArticle

Dose-Dependent Hepatotoxicity of Diethyl Phthalate in Female Wistar Rats

by Mehmet Cihan Yavaş, Gül Şahika Gökdemir, Kübra Tuğçe Kalkan, Salih Varol and Fazile Cantürk Tan

Toxics 2026, 14(2), 174; https://doi.org/10.3390/toxics14020174 - 16 Feb 2026

Cited by 1 | Viewed by 1306

Abstract

Phthalates are a class of compounds commonly used as plasticizers in various industrial and consumer products. In line with the increasing environmental and biological exposure concerns regarding these compounds, this study investigated the dose-dependent effects of diethyl phthalate (DEP) on the liver in a subacute rat model. Diethyl phthalate (DEP) was given orally by gavage to female Wistar albino rats at doses of 100, 300, and 600 mg/kg body weight per day for 21 days in order to assess liver tissue and associated function test levels. Liver function was evaluated by analyzing serum biochemical data. Liver tissues were evaluated using histopathological staining (H&E and Masson’s trichrome staining), immunohistochemical analysis of IL-1β and TGF-β, tissue ELISA for IL-6 and TNF-α, and comet assay to determine DNA damage. DEP exposure was found to cause significant, dose-dependent histopathological changes in liver tissue, including hepatocyte necrosis, cytoplasmic vacuolization, sinusoidal dilation, and vascular congestion. AST levels were significantly increased compared to the control group, while no significant changes were observed in other serum biochemical parameters. Compared to the control group, the expression of pro-inflammatory cytokines (IL-6 and TNF-α), IL-1β, and TGF-β was found to be elevated in the DEP-treated groups, and their levels increased with increasing exposure dose. DEP exposure also caused significant DNA damage in liver tissue. These findings indicate that despite an increase in AST levels observed in subacute DEP exposure, there were limited changes in serum biochemical parameters; serum liver enzymes alone may not fully reflect the extent of hepatic damage, and DEP can cause significant inflammatory, histopathological, and genotoxic effects in liver tissue. Full article

(This article belongs to the Special Issue Toxicity of Phthalate Esters (PAEs))

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15 pages, 263 KB

Open AccessArticle

Phthalate Metabolites in Maternal Urine and Breast Milk After Very Preterm Birth: Matrix Concordance

by Esin Okman, Sıddika Songül Yalçın, Deniz Arca Çakır, Fuat Emre Canpolat, Suzan Yalçın and Pınar Erkekoğlu

Toxics 2026, 14(2), 141; https://doi.org/10.3390/toxics14020141 - 30 Jan 2026

Cited by 1 | Viewed by 1230

Abstract

Background: Exposure to environmental pollutants, especially endocrine-disrupting chemicals, disproportionately affects vulnerable populations like pregnant women, lactating mothers, and preterm infants. This study aimed to assess the detection patterns of DiNP-, DEP-, and DEHP-related metabolites in maternal urine and breast milk, examine agreement between matrices, and explore maternal factors associated with phthalate exposure. Methods: Fifty-five mothers who delivered at ≤32 gestational weeks and whose infants were hospitalized in the Neonatal Intensive Care Unit (NICU) were enrolled. Breast milk and urine samples were analyzed using a validated isotope-dilution LC–MS/MS method. Urinary phthalate metabolite concentrations were adjusted for specific gravity. Linear mixed-effects models with a random intercept for mother were used to examine associations between urinary and breast milk phthalate metabolite concentrations, assess temporal changes, and evaluate the influence of breast milk lipid content. Results: DEHP and DiNP metabolites were detected in nearly all maternal urine samples. Breast milk contained predominantly primary metabolites (MEHP and MiNP), while secondary oxidative metabolites were rarely detected. Urine concentrations consistently exceeded breast milk concentrations. Urinary and breast milk phthalate concentrations were not correlated across sampling periods, indicating limited matrix concordance. Conclusions: Mothers of very preterm infants experience sustained phthalate exposure in the postpartum period; however, limited metabolite transfer to breast milk indicates that maternal urine remains the preferred biomonitoring matrix for assessing systemic phthalate exposure. Breast milk phthalate profiles exhibit compound-specific temporal changes and appear largely independent of concurrent urinary exposure biomarkers. Full article

(This article belongs to the Special Issue Toxicity of Phthalate Esters (PAEs))

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14 pages, 1358 KB

Open AccessEditor’s ChoiceArticle

Mono(2-ethylhexyl) Phthalate Disrupts Mitochondrial Function, Dynamics and Biogenesis in Human Trophoblast Cells at Human Exposure Range Concentrations

by Luis Daniel Martínez-Razo, Nadia Alejandra Rivero-Segura, Ericka Karol Pamela Almeida-Aguirre, Ismael Mancilla-Herrera, Ruth Rincón-Heredia, Alejandra Martínez-Ibarra and Marco Cerbón

Toxics 2025, 13(9), 770; https://doi.org/10.3390/toxics13090770 - 11 Sep 2025

Cited by 6 | Viewed by 1974

Abstract

Mono(2-ethylhexyl) phthalate (MEHP), a bioactive metabolite of di(2-ethylhexyl) phthalate (DEHP), has been detected in the placenta and urine of pregnant women and is linked to adverse pregnancy outcomes. However, its effects on mitochondrial homeostasis in trophoblast cells remain incompletely understood. This study examined the impact of MEHP (0.5–200 µM) on mitochondrial function, dynamics, and biogenesis in human HTR-8/SVneo trophoblast cells. MEHP (≥5 µM) reduced MTT conversion without compromising membrane integrity, suggesting early metabolic or redox imbalance. A dose-dependent loss of mitochondrial membrane potential was observed, with increased reactive oxygen species (ROS) generation only at 200 µM. MEHP modulated the expression of mitochondrial dynamics genes, with a more pronounced mitofusin 1 (MFN1) induction at low doses and increased mitochondrial DNA content, suggesting a compensatory response to mild stress. Conversely, high doses more strongly induced fission and mitochondrial 1 (FIS1) expression, suggesting mitochondrial fragmentation. Both concentrations induced the expression of the mitochondrial biogenesis regulators peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) and nuclear factor erythroid 2–related factor 2 (Nrf2), while sirtuin 1 (SIRT1) expression and activity declined progressively with dose. These results demonstrate that MEHP disrupts mitochondrial homeostasis in trophoblast cells at concentrations spanning the estimated human exposure range. The dose-dependent effects, from adaptive responses to overt dysfunction, may help explain the associations between MEHP exposure and placental pathology observed in epidemiological studies. Full article

(This article belongs to the Special Issue Toxicity of Phthalate Esters (PAEs))

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14 pages, 1698 KB

Open AccessArticle

Metabolite Monomethyl Phthalate (MMP) Induces Oxidative Damage in Rat Erythrocytes: Role of Vitamins C and E

by Xuxin Zhang, Xu Gao and Zhenxing Chi

Toxics 2025, 13(5), 379; https://doi.org/10.3390/toxics13050379 - 7 May 2025

Cited by 1 | Viewed by 1239

Abstract

Dimethyl phthalate (DMP) can enter the human body and be absorbed into the bloodstream to produce monomethyl phthalate (MMP). MMP in the environment can also enter the bloodstream. However, little is known about the toxicity of the phthalate metabolite MMP in most organisms. In this study, the erythrocyte toxicity of MMP and a preventive approach were investigated using Sprague–Dawley (SD) rats as the model animal under MMP concentrations of 5–250 mg/kg (sub-chronic exposure in vivo) and 1.25–100 μg/mL (acute exposure in vitro). The experimental results indicate that the interaction of MMP with erythrocytes caused oxidative damage, which decreased the number of red blood cells and the hemoglobin content and increased the content of methemoglobin and the iron release of hemoglobin in rat blood. However, the above results were not observed when MMP directly interacted with hemoglobin. The antioxidants vitamin C and vitamin E improved the above blood indicators in rats. The results of this study provide certain theoretical guidance for the evaluation of the potential risks of phthalate metabolites. Full article

(This article belongs to the Special Issue Toxicity of Phthalate Esters (PAEs))

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