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Journals
Toxics
Special Issues
Toxicity of Phthalate Esters (PAEs)
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Toxicity of Phthalate Esters (PAEs)

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

Deadline for manuscript submissions: closed (16 January 2026) | Viewed by 2814

Special Issue Editor

Dr. Zhenxing Chi

E-Mail Website
Guest Editor
Department of Environmental Engineering, School of Marine Science and Technology, Harbin Institute of Technology, Weihai 264209, China
Interests: environmental chemical pollutants; PAEs; PBDEs; micromicro-/nano materials; 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.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxics is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

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Published Papers (3 papers)

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Research

15 pages, 378 KB  
Article
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
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 [...] Read more.
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  
Article
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 1 | Viewed by 1259
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 [...] Read more.
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  
Article
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
Viewed by 909
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. [...] Read more.
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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