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Special Issue Editor

Dr. Michael Caudle

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Guest Editor

Department of Environmental Health, Rollins School of Public Health, Emory University, 1518 Clifton Rd., NE, Claudia Nance Rollins Building, Room 2033, Atlanta, GA 30322, USA
Interests: pesticides; persistent organic pollutants; metals; neurotoxicity; neurotransmitter; synapse; dopamine; Parkinson disease; autism spectrum disorder; attention deficit hyperactivity disorder

Special Issue Information

Dear Colleagues,

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder that comprises a diverse catalogue of cognitive and neurobehavioral phenotypes. Although many genetic contributors to ASD have been identified, the influence of exposure to environmental toxicants—including pesticides, flame retardants, and air pollutants—during vulnerable periods of neurodevelopment has gained considerable attention as an additional risk factor. However, as the human population is routinely exposed to many environmental toxicants, further investigation is needed into specific toxicants that may contribute to ASD risk. Additionally, uncovering neuronal targets and pathways that are disrupted by these exposures is paramount to better understanding ASD as we seek to reduce human exposure to these toxicants and risk for ASD.

This Special Issue focuses on highlighting research studies addressing the contribution of environmental exposures to the risk of autism spectrum disorder. Studies include, but are not limited to, molecular or epigenetic mechanisms of neurodevelopmental toxicity, phenotypic or behavioral outcomes, application of biology systems approaches to toxicant-induced ASD pathogenesis, gut microbiome, population-based assessments, and integration of gene and environmental risk factors. Authors are invited and welcome to submit original research papers, reviews, and short communications.

Dr. Michael Caudle
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 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

air pollution
autism, epidemiology
epigenetics
flame retardants
inflammation
neurodevelopment
neuronal function
pesticides

Published Papers (2 papers)

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Research

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19 pages, 2303 KiB

Open AccessFeature PaperArticle

In Silico Exploration of the Potential Role of Acetaminophen and Pesticides in the Etiology of Autism Spectrum Disorder

by Tristan Furnary, Rolando Garcia-Milian, Zeyan Liew, Shannon Whirledge and Vasilis Vasiliou

Toxics 2021, 9(5), 97; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics9050097 - 27 Apr 2021

Viewed by 3673

Abstract

Recent epidemiological studies suggest that prenatal exposure to acetaminophen (APAP) is associated with increased risk of Autism Spectrum Disorder (ASD), a neurodevelopmental disorder affecting 1 in 59 children in the US. Maternal and prenatal exposure to pesticides from food and environmental sources have also been implicated to affect fetal neurodevelopment. However, the underlying mechanisms for ASD are so far unknown, likely with complex and multifactorial etiology. The aim of this study was to explore the potential effects of APAP and pesticide exposure on development with regards to the etiology of ASD by highlighting common genes and biological pathways. Genes associated with APAP, pesticides, and ASD through human research were retrieved from molecular and biomedical literature databases. The interaction network of overlapping genetic associations was subjected to network topology analysis and functional annotation of the resulting clusters. These genes were over-represented in pathways and biological processes (FDR p < 0.05) related to apoptosis, metabolism of reactive oxygen species (ROS), and carbohydrate metabolism. Since these three biological processes are frequently implicated in ASD, our findings support the hypothesis that cell death processes and specific metabolic pathways, both of which appear to be targeted by APAP and pesticide exposure, may be involved in the etiology of ASD. This novel exposures-gene-disease database mining might inspire future work on understanding the biological underpinnings of various ASD risk factors. Full article

(This article belongs to the Special Issue Prenatal Environmental Exposure and Autism Risk)

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Review

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32 pages, 2164 KiB

Open AccessReview

Polychlorinated Biphenyls (PCBs): Risk Factors for Autism Spectrum Disorder?

by Harmanpreet Kaur Panesar, Conner L. Kennedy, Kimberly P. Keil Stietz and Pamela J. Lein

Toxics 2020, 8(3), 70; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics8030070 - 17 Sep 2020

Cited by 32 | Viewed by 4785

Abstract

Autism spectrum disorder (ASD) includes a group of multifactorial neurodevelopmental disorders defined clinically by core deficits in social reciprocity and communication, restrictive interests and repetitive behaviors. ASD affects one in 54 children in the United States, one in 89 children in Europe, and one in 277 children in Asia, with an estimated worldwide prevalence of 1–2%. While there is increasing consensus that ASD results from complex gene x environment interactions, the identity of specific environmental risk factors and the mechanisms by which environmental and genetic factors interact to determine individual risk remain critical gaps in our understanding of ASD etiology. Polychlorinated biphenyls (PCBs) are ubiquitous environmental contaminants that have been linked to altered neurodevelopment in humans. Preclinical studies demonstrate that PCBs modulate signaling pathways implicated in ASD and phenocopy the effects of ASD risk genes on critical morphometric determinants of neuronal connectivity, such as dendritic arborization. Here, we review human and experimental evidence identifying PCBs as potential risk factors for ASD and discuss the potential for PCBs to influence not only core symptoms of ASD, but also comorbidities commonly associated with ASD, via effects on the central and peripheral nervous systems, and/or peripheral target tissues, using bladder dysfunction as an example. We also discuss critical data gaps in the literature implicating PCBs as ASD risk factors. Unlike genetic factors, which are currently irreversible, environmental factors are modifiable risks. Therefore, data confirming PCBs as risk factors for ASD may suggest rational approaches for the primary prevention of ASD in genetically susceptible individuals. Full article

(This article belongs to the Special Issue Prenatal Environmental Exposure and Autism Risk)

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