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Inducing-Toxicity in the Neurological System by Environmental Pollutants

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

Deadline for manuscript submissions: closed (15 February 2023) | Viewed by 15166

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Special Issue Editors

Prof. Dr. Irene Camacho

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Guest Editor

Faculty of Life Sciences, Madeira University, Campus Universitário da Penteada, 9020-105 Funchal, Portugal
Interests: air pollution; environmental allergens; air quality; aerobiology

Prof. Dr. Isabel Fragoeiro

E-Mail Website
Co-Guest Editor

Escola Superior de Saúde, Madeira University, Campus Universitário da Penteada, 9020-105 Funchal, Portugal
Interests: mental health; nursing; aging and elderly; community mental health

Dr. Daniel Neto

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Co-Guest Editor

Chronic Diseases Research Center CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, Campo Martires da Patria 130, P-1169056 Lisbon, Portugal
Interests: psychiatry; mental disorders

Special Issue Information

Dear Colleagues,

Despite the recent advances in knowledge, there are still many gaps in the information about pollution and its effects on human health. These gaps include poor knowledge of the toxic effects of many chemicals in common use and the causal link between pollution and dysfunction of the central nervous system.

Exposure to neurotoxic pollutants is widespread as a result of fossil fuel combustion, industrial and agricultural production, and the extensive use of toxic chemicals in consumer products.

Pollutants can be toxic to the developing brain, and several commonly used chemicals, whose neurotoxicity has not yet been described, could be causing damage to children but also the elderly population.

Recent evidence suggests that additional causal associations may exist between particulate matter pollution and several prevalent non-communicable diseases. These include decreased cognitive function, attention-deficit, dyslexia, behavioral disorders and autism in children, and neurodegenerative diseases, including dementia, in adults. Previous epidemiologic studies have identified several neurological diseases associated with air pollution. Air pollution and, especially, traffic-related air pollution seem to increase the risk of Alzheimer’s disease and diverse neurodevelopmental disorders, including autism spectrum disorder, attention deficit hyperreactivity disorder, learning and intellectual disabilities and schizophrenia. Many neurological diseases, such as Alzheimer’s disease and autism spectrum disorder, result from complex interactions between environmental factors and genetic susceptibilities. These conditions exact a tremendous cost on the affected individuals, their families and society, motivating support for research.

The purpose of this Special Issue of Toxics is to increase the insights into underexplored environmental pollutants that are affecting human health. We are pleased to invite you to submit original papers, reviews and short communications that focus on single or complex pollutants and their impacts on neurological systems. The articles may span from epidemiological to molecular aspects of the main theme and propose exposure threshold limits for health surveillance purposes.

The research areas related to novel air pollutants may include (but are not limited to) the following:

Exposomes;
Pollution sources;
Susceptibility profiles;
The mechanisms of the toxic actions of pollutants;
In vivo, in vitro and in silico studies;
Field and laboratory approaches;
Emerging toxicity models;
Health impact assessments;
Short- and long-term effects;
Biomarkers of exposure/effects;
Preventive/mitigation strategies for pollutant exposure.

I look forward to receiving your contributions.

Prof. Dr. Irene Camacho
Prof. Dr. Isabel Fragoeiro
Dr. Daniel Neto
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

cognitive function
environmental pollutants
mental disorders
neurodegenerative disease
neurological disorders
neuropathological risk
neurological system
public health
toxicology

Published Papers (5 papers)

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Research

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14 pages, 1779 KiB

Open AccessArticle

The Influence of Photodynamic Antimicrobial Chemotherapy on the Microbiome, Neuroendocrine and Immune System of Crustacean Post Larvae

by Anas Abdulaziz, Athira Vengalil Pramodh, Vrinda Sukumaran, Devika Raj and Ann Mary Valathuparambil Baby John

Toxics 2023, 11(1), 36; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics11010036 - 30 Dec 2022

Cited by 1 | Viewed by 1978

Abstract

Photodynamic antimicrobial chemotherapy (PACT), employing a combination of light and natural photosensitizer molecules such as curcumin, has been accepted as a safe modality for removing aquatic pathogens which cause diseases such as cholera in humans and vibriosis in aquatic animals. Curcumin and its photodegradation products are generally considered as safe to animals, but the impact of reactive oxygen species (ROS) generated by these products on the growth and survival of organisms at a cellular level has not been studied in detail. The ROS generated by curcumin on photoexcitation using blue light (λ_max 405 nm, 10 mW cm⁻²) disinfects more than 80% of free-living Vibrio spp. in the rearing water of Penaeus monodon. However, it is less effective against Vibrio spp. colonized inside P. monodon because the carapace of the animal prevents the transmission of more than 70% of light at the 400–450 nm range and thus reduces the formation of ROS. The influence of curcumin and photoexcited curcumin on the microbiome of P. monodon were revealed by nanopore sequencing. The photoexcited curcumin induced irregular expression of genes coding the moult-inhibiting hormone (MIH), Crustacean hyperglycaemic hormone (CHH)), prophenoloxidase (ProPO), and crustin, which indicates toxic effects of ROS generated by photoexcited curcumin on the neuroendocrine and immune systems of crustaceans, which could alter their growth and survival in aquaculture settings. The study proposed the cautious use of photodynamic therapy in aquaculture systems, and care must be taken to avoid photoexcitation when animals are experiencing moulting or environmental stress. Full article

(This article belongs to the Special Issue Inducing-Toxicity in the Neurological System by Environmental Pollutants)

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14 pages, 1957 KiB

Open AccessArticle

Lung-Based, Exosome Inhibition Mediates Systemic Impacts Following Particulate Matter Exposure

by Keegan Lopez, Alexandra Camacho, Quiteria Jacquez, Mary Kay Amistadi, Sebastian Medina and Katherine Zychowski

Toxics 2022, 10(8), 457; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics10080457 - 7 Aug 2022

Cited by 4 | Viewed by 1788

Abstract

Particulate matter (PM) exposure is a global health issue that impacts both urban and rural communities. Residential communities in the Southwestern United States have expressed concerns regarding the health impacts of fugitive PM from rural, legacy mine-sites. In addition, the recent literature suggests that exosomes may play a role in driving toxicological phenotypes following inhaled exposures. In this study, we assessed exosome-driven mechanisms and systemic health impacts following inhaled dust exposure, using a rodent model. Using an exosome inhibitor, GW4869 (10 μM), we inhibited exosome generation in the lungs of mice via oropharyngeal aspiration. We then exposed mice to previously characterized inhaled particulate matter (PM) from a legacy mine-site and subsequently assessed downstream behavioral, cellular, and molecular biomarkers in lung, serum, and brain tissue. Results indicated that CCL-2 was significantly upregulated in the lung tissue and downregulated in the brain (p < 0.05) following PM exposure. Additional experiments revealed cerebrovascular barrier integrity deficits and increased glial fibrillary acidic protein (GFAP) staining in the mine-PM exposure group, mechanistically dependent on exosome inhibition. An increased stress and anxiety response, based on the open-field test, was noted in the mine-PM exposure group, and subsequently mitigated with GW4869 intervention. Exosome lipidomics revealed 240 and eight significantly altered positive-ion lipids and negative-ion lipids, respectively, across the three treatment groups. Generally, phosphatidylethanolamine (PE) and phosphatidylcholine (PC) lipids were significantly downregulated in the PM group, compared to FA. In conclusion, these data suggest that systemic, toxic impacts of inhaled PM may be mechanistically dependent on lung-derived, circulating exosomes, thereby driving a systemic, proinflammatory phenotype. Full article

(This article belongs to the Special Issue Inducing-Toxicity in the Neurological System by Environmental Pollutants)

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23 pages, 5395 KiB

Open AccessEditor’s ChoiceArticle

Environmentally Toxic Solid Nanoparticles in Noradrenergic and Dopaminergic Nuclei and Cerebellum of Metropolitan Mexico City Children and Young Adults with Neural Quadruple Misfolded Protein Pathologies and High Exposures to Nano Particulate Matter

by Lilian Calderón-Garcidueñas, Angélica González-Maciel, Rafael Reynoso-Robles, Héctor G. Silva-Pereyra, Ricardo Torres-Jardón, Rafael Brito-Aguilar, Alberto Ayala, Elijah W. Stommel and Ricardo Delgado-Chávez

Toxics 2022, 10(4), 164; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics10040164 - 29 Mar 2022

Cited by 14 | Viewed by 4978

Abstract

Quadruple aberrant hyperphosphorylated tau, beta-amyloid, α-synuclein and TDP-43 neuropathology and metal solid nanoparticles (NPs) are documented in the brains of children and young adults exposed to Metropolitan Mexico City (MMC) pollution. We investigated environmental NPs reaching noradrenergic and dopaminergic nuclei and the cerebellum and their associated ultrastructural alterations. Here, we identify NPs in the locus coeruleus (LC), substantia nigrae (SN) and cerebellum by transmission electron microscopy (TEM) and energy-dispersive X-ray spectrometry (EDX) in 197 samples from 179 MMC residents, aged 25.9 ± 9.2 years and seven older adults aged 63 ± 14.5 years. Fe, Ti, Hg, W, Al and Zn spherical and acicular NPs were identified in the SN, LC and cerebellar neural and vascular mitochondria, endoplasmic reticulum, Golgi, neuromelanin, heterochromatin and nuclear pore complexes (NPCs) along with early and progressive neurovascular damage and cerebellar endothelial erythrophagocytosis. Strikingly, FeNPs 4 ± 1 nm and Hg NPs 8 ± 2 nm were seen predominantly in the LC and SN. Nanoparticles could serve as a common denominator for misfolded proteins and could play a role in altering and obstructing NPCs. The NPs/carbon monoxide correlation is potentially useful for evaluating early neurodegeneration risk in urbanites. Early life NP exposures pose high risk to brains for development of lethal neurologic outcomes. NP emissions sources ought to be clearly recognized, regulated, and monitored; future generations are at stake. Full article

(This article belongs to the Special Issue Inducing-Toxicity in the Neurological System by Environmental Pollutants)

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Review

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23 pages, 1444 KiB

Open AccessReview

Neuroinflammation and Neurodegeneration of the Central Nervous System from Air Pollutants: A Scoping Review

by Frances Vivienne Armas and Amedeo D’Angiulli

Toxics 2022, 10(11), 666; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics10110666 - 6 Nov 2022

Cited by 5 | Viewed by 2904

Abstract

In this scoping review, we provide a selective mapping of the global literature on the effects of air pollution on the life-span development of the central nervous system. Our synthesis first defines developmental neurotoxicants and the model effects of particulate matter. We then discuss air pollution as a test bench for neurotoxicants, including animal models, the framework of systemic inflammation in all affected organs of the body, and the cascade effects on the developing brain, with the most prevalent neurological structural and functional outcomes. Specifically, we focus on evidence on magnetic resonance imaging and neurodegenerative diseases, and the links between neuronal apoptosis and inflammation. There is evidence of a developmental continuity of outcomes and effects that can be observed from utero to aging due to severe or significant exposure to neurotoxicants. These substances alter the normal trajectory of neurological aging in a propulsive way towards a significantly higher rate of acceleration than what is expected if our atmosphere were less polluted. The major aggravating role of this neurodegenerative process is linked with the complex action of neuroinflammation. However, most recent evidence learned from research on the effects of COVID-19 lockdowns around the world suggests that a short-term drastic improvement in the air we breathe is still possible. Moreover, the study of mitohormesis and vitagenes is an emerging area of research interest in anti-inflammatory and antidegenerative therapeutics, which may have enormous promise in combatting the deleterious effects of air pollution through pharmacological and dietary interventions. Full article

(This article belongs to the Special Issue Inducing-Toxicity in the Neurological System by Environmental Pollutants)

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24 pages, 1833 KiB

Open AccessReview

Neurotoxicity of Polycyclic Aromatic Hydrocarbons: A Systematic Mapping and Review of Neuropathological Mechanisms

by Tosin A. Olasehinde and Ademola O. Olaniran

Toxics 2022, 10(8), 417; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics10080417 - 25 Jul 2022

Cited by 20 | Viewed by 2689

Abstract

Several studies present the neurotoxic effects of polycyclic aromatic hydrocarbons (PAHs), a class of environmental pollutants capable of causing neurological deficits. However, a collective review approach to this research topic is scarce. This study presents the effect of PAHs on the central nervous system using a bibliometric approach. The neuropathological mechanisms of PAHs are also highlighted. Published articles were searched for in the Scopus and Web of Science databases from January 1979 to December 2020 using the keywords ‘polycyclic aromatic hydrocarbons’ and ‘neurotoxicity’. The total number of documents retrieved from both databases was 338. Duplicated documents (80) were excluded and 258 articles were used for the final analysis. Our findings revealed that there has been a significant increase in research outputs on this topic in the last ten years. The countries with the highest scientific productivity in this area are USA, China, France and Italy. The result also showed that, in the past few years, global scientific output in research relating to PAH neurotoxicity focused on neurodegeneration, cholinergic function, neurodevelopmental toxicity, behavioural studies, oxidative stress, neuroprotection and therapeutic intervention using different experimental models, including zebrafish, neuronal cell lines, Caenorhabditis elegans and rats. Recent studies also revealed the neuroprotective roles of some natural products against PAH-induced neurotoxicity. However, more investigation involving clinical trials is required to emphasize the observed neurotoxic effects. Full article

(This article belongs to the Special Issue Inducing-Toxicity in the Neurological System by Environmental Pollutants)

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