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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: 30 October 2026 | Viewed by 8316

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Special Issue Editors

Dr. Lihua Ren

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Guest Editor

Department of Maternal and Child Nursing, Peking University, Beijing 100191, China
Interests: emerging contaminants; environmental pollution; air pollution; micro-nano plastics; health risk assessment; early life health management; reproductive health

Prof. Dr. Huicai Guo

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Guest Editor

Department of Toxicology, School of Public Health, Hebei Medical University, Shijiazhuang 050017, China
Interests: emerging contaminants; PFAS; cardiovascular toxicity; atherosclerosis; hepatotoxicity; neurotoxicity

Prof. Dr. Minjian Chen

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Guest Editor

Department of Occupational Medicine and Environmental Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China
Interests: metabolomics; exposomics; reproductive and developmental health; exposure science; toxicology; mechanism
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Special Issue Information

Dear Colleagues,

Emerging contaminants (ECs), including pharmaceuticals, personal care products (PPCPs), endocrine-disrupting chemicals (EDCs), per- and polyfluoroalkyl substances (PFAS), microplastics, and plastic additives, are now ubiquitously detected in the environment and human tissues. Due to their persistence, high biological activity, and resistance to conventional treatment, ECs can trigger oxidative stress, immunotoxicity, and metabolic disorders even at trace concentrations. Nevertheless, systematic data on exposure pathways, underlying toxicological mechanisms, and long-term health outcomes remain scarce, impeding evidence-based risk management and policy formulation.

This Special Issue focuses on the toxicological impacts, detection, health risks, and remediation of ECs. It aims to highlight scientific advances in understanding the bioaccumulation and human health risks of ECs.

We welcome original research and reviews on a broad range of topics, including but not limited to the following:

Cellular and molecular mechanisms and health risk assessment of ECs;
Advanced analytical and monitoring techniques for EC detection;
Bioremediation strategies;
Intergenerational toxicity of ECs;
Innovative technologies (high-resolution mass spectrometry, multi-omics, machine learning, etc.) for elucidating exposure–effect relationships.

This Special Issue aims to provide an interdisciplinary platform for researchers to share insights and develop sustainable solutions for EC pollution control.

Dr. Lihua Ren
Prof. Dr. Huicai Guo
Prof. Dr. Minjian Chen
Guest Editors

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

emerging contaminants
health risk assessment
human exposure assessment
toxicological mechanisms
bioremediation strategies
intergenerational toxicity
short-term and long-term toxicity

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Published Papers (5 papers)

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Research

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14 pages, 1036 KB

Open AccessArticle

Early-Life Exposure to the Cooking Oil Fume Component trans,trans-2,4-Decadienal Impairs Ocular Development and Angiogenesis in Zebrafish (Danio rerio) Larvae

by Xiaoli Wu, Xinyue Zhang and Zengliang Ruan

Toxics 2026, 14(5), 388; https://doi.org/10.3390/toxics14050388 - 30 Apr 2026

Abstract

Trans,trans-2,4-decadienal (tt-DDE), the primary aldehyde component found in cooking oil fumes, is a prevalent environmental pollutant. However, its potential adverse effects on ocular development remain largely unexplored. This study evaluated its toxicity on ocular development and angiogenesis in zebrafish larvae, as well as on human retinal vascular endothelial cells (HRECs). Zebrafish (Danio rerio) larvae at 48 h post-fertilization were microinjected intraocularly with various doses of tt-DDE (65.87–521.3 mM) for 24 h. We observed dose-dependent impairments in ocular development following tt-DDE exposure. It significantly reduced eye size and inhibited the intraocular vascular area at concentrations of 128.9 mM and above. Histopathological analysis revealed retinal structural disorganization, eye shrinkage, and a clear dose-dependent increase in acridine orange (AO) fluorescence intensity. Apoptosis assays confirmed a significant escalation in ocular cell death at higher exposure doses. Additionally, our results demonstrated that tt-DDE (5–100 μM) significantly reduced the viability of HRECs in vitro. These findings suggest that early-life exposure to tt-DDE impairs ocular development in zebrafish by inducing histopathological damage, inhibiting angiogenesis, and promoting apoptosis, and also exerts direct cytotoxicity to human retinal cells. This study underscores the potential risk of tt-DDE exposure as an environmental factor contributing to ocular developmental toxicity. Full article

(This article belongs to the Special Issue Health Risks and Toxicity of Emerging Contaminants)

19 pages, 1213 KB

Open AccessArticle

Exposure to Urinary and Dust Parabens: Compound-Specific Risks for Pediatric Respiratory Allergic Phenotypes

by Yangyang Zhu, Shuang Du, Zhiqi Lin, Qingshuang Li, Hao Tang, Zhiping Niu, Dan Norbäck, Tippawan Prapamontol, Chanjuan Sun, Jiufeng Li and Zhuohui Zhao

Toxics 2026, 14(4), 281; https://doi.org/10.3390/toxics14040281 - 26 Mar 2026

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Abstract

Parabens, a prevalent class of endocrine-disrupting chemicals (EDCs), are ubiquitous in consumer products; however, their role in linking pediatric allergic phenotypes remains poorly understood. This case-control study analyzed paraben levels in urine and indoor dust as proxies for internal and external exposures and investigated their associations with allergic rhinitis only (AR Only), asthma only (AS Only), and comorbidities (AR&AS) among children in Shanghai. The concentrations for each of four paraben compounds were quantitatively measured, and multi-pollutant frameworks—including Bayesian Kernel Machine Regression (BKMR) and Weighted Quantile Sum (WQS) regression—were employed to characterize the mixture exposure and risk. Propylparaben (PrP) was detectable in 100% of urine samples and over 90% of dust samples, and the concentrations ranked the highest out of the four compounds in both samples. Benzylparaben (BzP) was detected in >70% of urine samples and over 50% of dust samples at relatively lower levels. Urinary PrP exhibited significantly positive associations with all phenotypes (OR in 2.18–2.92) and BzP with the AR&AS Comorbidity (OR = 3.55, 95% CI: 1.32–9.55). Dust-borne PrP was associated with AR Only (OR = 2.26, 95% CI: 1.16–4.43), indicating a potential “Portal of Entry” effect via direct nasal deposition. According to BKMR and WQS analyses, urinary PrP and BzP emerged as two primary risk drivers. Using interaction analysis, an additive synergistic effect was observed between urinary PrP and BzP with parental history of allergy, suggesting heightened vulnerability to paraben exposure in genetically predisposed subgroups. In conclusion, children with respiratory allergies were associated with higher exposure to PrP and BzP and exhibited higher susceptibility in those with a parental history of allergy. Full article

(This article belongs to the Special Issue Health Risks and Toxicity of Emerging Contaminants)

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16 pages, 3708 KB

Open AccessArticle

Co-Exposure to Bisphenol A and a High-Fat Diet Induces Insulin Resistance via Suppression of Insulin Signaling Molecule Expression and GLUT4 Translocation

by Zeqi Lu, Min Cao, Jiaoxiang Zhang, Congzheng Qi, Bing Huang, Wenxue Li, Juntao Li, Guangyu Yang, Yan Zhang, Jinyin Wu, Weiwen Liu and Wei Zhu

Toxics 2026, 14(2), 146; https://doi.org/10.3390/toxics14020146 - 1 Feb 2026

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Abstract

While the adverse health effects of bisphenol A (BPA) or high-fat diet (HFD) exposure alone have been relatively well documented, the mechanisms underlying their combined impact on insulin resistance and type 2 diabetes remain poorly understood. In this study, we observed the effects of 90 days of treatment with BPA and an HFD on insulin resistance in mouse gastrocnemius muscle, as well as the expression of signaling molecules and proteins potentially associated with glucose transporter type 4 (GLUT4) translocation. Additionally, C2C12 myotubes were co-treated with BPA and palmitic acid (PA) to observe the effects on insulin signaling molecules, GLUT4 translocation, and insulin resistance. Specifically, in vitro cellular experiments further demonstrated that BPA and PA inhibited GLUT4 translocation from the nucleus to the cell membrane. Taken together, co-exposure to BPA and an HFD (or PA) treatment significantly altered the expression of insulin signaling molecules in both gastrocnemius muscle and C2C12 cells, suggesting a potential link to their impacts on insulin resistance and GLUT4 translocation. Full article

(This article belongs to the Special Issue Health Risks and Toxicity of Emerging Contaminants)

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17 pages, 2240 KB

Open AccessArticle

Gut Microbiota Dysbiosis and Toxic Metabolite Pathways Linked to Childhood Obesity in Eastern China

by Ruijing Zhou, Mengyuan Zhu and Minjian Chen

Toxics 2025, 13(11), 929; https://doi.org/10.3390/toxics13110929 - 30 Oct 2025

Viewed by 1251

Abstract

Childhood obesity is a newly emerging public health and an emerging concern in environmental health in rapidly urbanized areas of China. This preliminary study investigated the gut microbiome composition and toxic metabolite pathways of school-aged children in Nanjing. Using 16S rRNA sequencing and PICRUSt2-based functional predictions, we observed significant microbial structural changes between the normal weight group and the overweight/obese group, although α diversity was similar. Overweight and obese children exhibited a markedly higher Firmicutes/Bacteroidetes ratio as well as an enrichment of genera such as Subdoligranulum, Ruminococcus, and Lachnospira, indicating increased energy harvesting and inflammation. Functionally, the downregulation of tryptophan metabolism in obese children suggests a reduction in anti-inflammatory indole and an increase in the production of pro-inflammatory kynurenine. In contrast, the upregulation of thiamine metabolism may be linked to enhanced carbohydrate utilization and lipid biosynthetic activity. Our toxicology network analysis and molecular docking experiments suggest that AhR and thiamine-related metabolic enzymes are targets of tryptophan and thiamine metabolism, respectively, and that PPARG is also a potential molecular target mediating thiamine metabolism in childhood obesity. These findings highlight the environment–microbiome–host axis as a potential pathway for metabolic toxicity in childhood obesity. Further studies are needed to validate these toxicological mechanisms and identify microbial biomarkers for early intervention. Full article

(This article belongs to the Special Issue Health Risks and Toxicity of Emerging Contaminants)

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22 pages, 1371 KB

Open AccessEditor’s ChoiceReview

Environmental and Human Health Risks of 6PPD and 6PPDQ: Assessment and Implications

by Sainan Zhang, Jiayue Tang, Zhiying Qiu, Xia Huo, Dongling Liu and Xiang Zeng

Toxics 2025, 13(10), 873; https://doi.org/10.3390/toxics13100873 - 14 Oct 2025

Cited by 6 | Viewed by 5028

Abstract

This review aims to synthesize current knowledge on the environmental contaminants N-(1,3-dimethylbutyl)-N′-phenyl-p-phenylenediamine (6PPD) and its quinone derivative (6PPDQ) derived from tire wear particles (TWPs), focusing on their environmental distribution, transformation, human exposure pathways, toxicological effects, and health risks to ecological and human health. A comprehensive literature review was conducted, compiling and analyzing data from environmental monitoring studies, toxicological assessments on aquatic and mammalian models, and emerging human biomonitoring research. Key findings on concentrations, toxicological endpoints (e.g., LC50, oxidative stress, genotoxicity), and exposure pathways were evaluated. 6PPD and its transformation product 6PPDQ are ubiquitous environmental pollutants found in air, water, soil, sediment, and dust. 6PPDQ is notably highly toxic to aquatic organisms, with an acute LC50 of 790 ng/L for coho salmon. Human exposure to these compounds occurs through inhalation, ingestion, and dermal contact, and their presence has been confirmed in human matrices including blood, urine, and cerebrospinal fluid. Toxicological studies, primarily on model organisms, indicate that 6PPD and 6PPDQ can induce oxidative stress, cause DNA damage, and disrupt metabolic and neurological functions. Adverse outcomes such as intestinal toxicity, reproductive impairment, neurobehavioral changes, and potential carcinogenicity have been observed. However, direct evidence of their health impacts on humans remains limited. 6PPD and 6PPDQ pose significant and widespread ecological risks, with 6PPDQ representing a particularly potent aquatic toxicant. While human exposure is confirmed, the full scope of human health implications is not yet well understood. The review highlights the need for longitudinal environmental tracking, mechanistic studies, and refined exposure models to inform regulatory actions and mitigate risks. Addressing these challenges is essential to mitigate the ecological and health burdens posed by 6PPD and 6PPDQ. This study underscores the global societal importance of addressing 6PPD-related pollution—a pervasive and transboundary environmental challenge stemming from universal tire wear. Full article

(This article belongs to the Special Issue Health Risks and Toxicity of Emerging Contaminants)

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