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Toxics
Special Issues
Neuronal Injury and Disease Induced by Environmental Toxicants
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Neuronal Injury and Disease Induced by Environmental Toxicants

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

Deadline for manuscript submissions: 31 May 2025 | Viewed by 1547

Special Issue Editors

Prof. Dr. Jun Wang

E-Mail Website
Guest Editor
Department of Toxicology, School of Public Health, Nanjing Medical University, Nanjing 211166, China
Interests: neurotoxicology; neurodegenerative diseases; psychiatric disorders; environmental endocrine disruptors
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Guixiang Ji

E-Mail Website
Guest Editor
Nanjing Institute of Environmental Sciences, Ministry of Ecology and Environment, Nanjing 210042, China
Interests: new environmental pollutant exposure and the toxic effects and mechanisms

Special Issue Information

Dear Colleagues,

Exposure to environmental pollutants, metabolic toxins, drugs, and other chemicals can cause damage to the nervous system, leading to a spectrum of neural diseases; however, the mechanisms behind this are unclear. This Special Issue will focus on these harmful factors and explain their direct or indirect toxic effects and potential mechanisms based on various cellular and disease outcomes, such as neurodegenerative diseases, psychiatric disorders, cellular stress, inflammation, death, etc., in human, animals, or cells. Moreover, research on toxicokinetics and the internal exposure levels to toxic substances in humans is also welcomed. These studies will be beneficial for achieving better knowledge of the hazards of these toxic substances, which may lead to novel intervention strategies for the neurological and psychiatric disorders they cause.

Prof. Dr. Jun Wang
Prof. Dr. Guixiang Ji
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 100 words) can be sent to the Editorial Office for announcement on this website.

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

  • neurotoxicology
  • neural injury and mechanisms
  • chemical exposure
  • neurodegenerative diseases
  • psychiatric disorders
  • toxicomics
  • toxic intervention

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (3 papers)

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Research

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14 pages, 1804 KiB  
Article
Neurotoxicity and Mechanism in Zebrafish Embryo Induced by Tetrabromobisphenol A bis (2-Hydroxyethyl) Ether (TBBPA-DHEE) Exposure
by Xinyu Zhang, Liguo Guo, Yiwen Luo, Xia Xu, Ying Han, Hui Chen, Haohao Sun, Yingang Xue and Guixiang Ji
Toxics 2025, 13(2), 76; https://doi.org/10.3390/toxics13020076 - 22 Jan 2025
Viewed by 561
Abstract
Tetrabromobisphenol A bis (2-hydroxyethyl) ether (TBBPA-DHEE), a derivative of TBBPA, has been frequently detected in the environment. In this study, the median lethal concentration (LC50) of TBBPA-DHEE at 96 h post-fertilization (hpf) was 1.573 mg/L. Based on the reported environmental concentrations, [...] Read more.
Tetrabromobisphenol A bis (2-hydroxyethyl) ether (TBBPA-DHEE), a derivative of TBBPA, has been frequently detected in the environment. In this study, the median lethal concentration (LC50) of TBBPA-DHEE at 96 h post-fertilization (hpf) was 1.573 mg/L. Based on the reported environmental concentrations, we investigated the effects of TBBPA-DHEE on the nervous system of zebrafish embryos following exposure to varying concentrations (0, 20, 100, and 500 μg/L) for 4 to 144 hpf. Our results indicated that exposure to 100 μg/L at 144 hpf led to behavioral abnormalities in zebrafish. Furthermore, exposure to TBBPA-DHEE inhibited the development of the central nervous system and motor neurons in zebrafish. Real-time polymerase chain reaction (PCR) analysis revealed that exposure to TBBPA-DHEE significantly downregulated the expression levels of neurodevelopmental genes (shha, syn2a, elavl3, gfap, and gap43). Additionally, TBBPA-DHEE increased oxidative stress in zebrafish. Transcriptomic analysis demonstrated that exposure to TBBPA-DHEE affected the signaling pathways involved in neurodevelopment. Overall, this study demonstrated that TBBPA-DHEE may disrupt the early development of the nervous system, leading to abnormal motor behavior in zebrafish larvae, and provided novel insights into the potential mechanisms of TBBPA-DHEE neurotoxicity. Full article
(This article belongs to the Special Issue Neuronal Injury and Disease Induced by Environmental Toxicants)
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16 pages, 293 KiB  
Article
Secondhand Smoke Exposure and Brain Health Indicators in Cuban Preschoolers
by Yaser Ramírez Benítez, Miriela Díaz Bringas, Rodneys Mauricio Jiménez-Morales, Ijang Bih Ngyah-Etchutambe and Linda S. Pagani
Toxics 2025, 13(1), 62; https://doi.org/10.3390/toxics13010062 - 17 Jan 2025
Viewed by 625
Abstract
Secondhand smoke affects nearly 40% of children worldwide, leading to serious health and behavioral problems. Being neurotoxic, it poses potential risks for child health and learning. In Cuba, there is limited research on the association of secondhand smoke with children’s brain health, especially [...] Read more.
Secondhand smoke affects nearly 40% of children worldwide, leading to serious health and behavioral problems. Being neurotoxic, it poses potential risks for child health and learning. In Cuba, there is limited research on the association of secondhand smoke with children’s brain health, especially in vulnerable populations like young children at home. The overall purpose of this study is two-fold. First, we determined the relationship between household smoke exposure and risks to brain health in Cuban children. Second, we analyzed the role of family environment factors, such as socio-economic status, in our estimates. Although this research represents the first investigation of its kind in Cuba, we expect to find evidence of neurotoxic associations with household smoke. We collected data between 2015 and 2018 using the medical records of 627 Cuban preschool children to explore the link between brain health indicators and exposure to tobacco smoke at home. We assessed archival reports on parental smoking, duration and frequency of exposure, and several indicators of brain health, including executive function, language development, sleep quality, and fluid intelligence. The findings indicate that exposure to tobacco smoke at home has a negative association with children’s brain health, affecting both the cognitive (executive and linguistic functions) and non-cognitive aspects (sleep quality) of child development. Continuous exposure (five to seven times per week) and transient exposure (two to three times per week) were found to be more negatively related to sleep quality than in cognitive functions, particularly in children of middle socio-economic status. This highlights the need to implement parental information campaigns in Cuba. Full article
(This article belongs to the Special Issue Neuronal Injury and Disease Induced by Environmental Toxicants)
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Review

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27 pages, 6214 KiB  
Review
The Role of Epigenetic Mechanisms in the Development of PM2.5-Induced Cognitive Impairment
by Lishan Jiang, Mingxia Shao, Chao Song, Li Zhou, Wenke Nie, Hang Yu, Siqi Wang, Yongping Liu and Li Yu
Toxics 2025, 13(2), 119; https://doi.org/10.3390/toxics13020119 - 2 Feb 2025
Viewed by 229
Abstract
PM2.5 is fine particulate matter with a diameter of less than 2.5 μm. Recent evidence has shown that exposure to PM2.5 markedly elevates the risk of neurodegenerative diseases, neurodevelopmental disorders, and cardiovascular diseases, which may culminate in cognitive impairment. Nevertheless, the [...] Read more.
PM2.5 is fine particulate matter with a diameter of less than 2.5 μm. Recent evidence has shown that exposure to PM2.5 markedly elevates the risk of neurodegenerative diseases, neurodevelopmental disorders, and cardiovascular diseases, which may culminate in cognitive impairment. Nevertheless, the precise mechanisms through which PM2.5 affects cognitive function are unclear. Recent studies have demonstrated that PM2.5-induced epigenetic alterations are associated with the development of cognitive impairment. Epigenetic alterations include modifications to DNA methylation, histone modifications, and non-coding RNAs. The underlying mechanisms of epigenetic alterations are related to inflammation, synaptic dysfunction, cardiovascular factors, and alterations in neuronal structure and function. This review reports the latest findings on the relationship between PM2.5-induced epigenetic alterations and the development of cognitive disorders, offering novel insights into the cognitive effects of air pollution. Full article
(This article belongs to the Special Issue Neuronal Injury and Disease Induced by Environmental Toxicants)
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