Early Life Exposure to Persistent Organic Pollutants, a Particularly Sensitive Period

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Reproductive and Developmental Toxicity".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 15778

Special Issue Editors


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Guest Editor
1. Biological Monitoring Laboratory, Department of Toxicology and Biological Monitorin, Institut National de Recherche et de Sécurité - INRS, 1, rue du Morvan - CS 60027, 54519 Vandoeuvre Cede, France
2. CALBINOTOX, Faculté des Sciences et Technologies, Université de Lorraine, Campus Aiguillettes BP70239, 54506 Nancy, France
Interests: environmental toxicology; Persistent Organic Pollutants (POPs); Polycyclic Aromatic Hydrocarbons (PAH); neuro-developmental disorders; biomarkers

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Guest Editor
Principal Investigator, Immune Endocrine and Epigenetics Research Group, Luxembourg Institute of Health, Esch-sur-Alzette, Luxembourg
Interests: behavioural epigenetics; molecular consequences of early life adversity; DNA methylation; HPA axis; glucocorticoid receptor; genetics and epigenetics of the stress response
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Special Issue Information

Dear Colleagues,

 

Accumulating evidence suggests that exposure to persistent organic pollutants (POP) during critical periods of development may be a major risk factor in the occurrence of chronic diseases later in life. An increase in the incidence of asthma, cancer, birth defects and developmental and neurodevelopmental disabilities has been pointed out in children over the last two decades. For some of these diseases, an environmental origin has been clearly established; for others, it is still at the level of assumption. This underlines the importance of the mode and period of exposure as a critical window for development and suggests that epigenetic modifications may play a key role in the onset of these disorders. The toxicity of early exposure to low levels of POP remains, therefore, to be elucidated and needs to be studied further, especially regarding the long-term effects of such cocktail exposure and its role in the incidence of disease later in life. In this context, we are pleased to invite you to participate in this Special Issue, which aims to assess the impact of POP exposure across the developmental period on the occurrence of later life phenotypes.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • Environmental medicine and public health
  • Environmental epidemiology
  • Health risk assessment
  • Early developmental toxicity
  • Neurodevelopmental toxicity
  • Neurodevelopmental disorders
  • Endocrine disruptions
  • Immune toxicity
  • Immune-aging
  • DOHAD (Developmental Origins of Health and Disease).

We look forward to receiving your contributions.

Dr. Nathalie Grova
Dr. Jonathan Turne
Guest Editors

Manuscript Submission Information

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Keywords

  • early life adversity
  • perinatal exposure
  • persistent organic pollutants
  • DOHAD
  • environmental epidemiology
  • epigenetics
  • neurodevelopmental toxicity
  • overall life trajectories

Published Papers (3 papers)

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Research

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17 pages, 2005 KiB  
Article
Head-to-Head Study of Developmental Neurotoxicity and Resultant Phenotype in Rats: α-Hexabromocyclododecane versus Valproic Acid, a Recognized Model of Reference for Autism Spectrum Disorders
by Chloé Morel, Armelle Christophe, Katy Maguin-Gaté, Justine Paoli, Jonathan David Turner, Henri Schroeder and Nathalie Grova
Toxics 2022, 10(4), 180; https://doi.org/10.3390/toxics10040180 - 6 Apr 2022
Cited by 5 | Viewed by 3116
Abstract
Evidence is now growing that exposure to environmental pollutants during the critical early-life period of brain development may contribute to the emergence of Autism Spectrum Disorders (ASD). This study seeks to compare the developmental neurotoxicity of the α-isomer of hexabromocyclododecane (α-HBCDD), a persistent [...] Read more.
Evidence is now growing that exposure to environmental pollutants during the critical early-life period of brain development may contribute to the emergence of Autism Spectrum Disorders (ASD). This study seeks to compare the developmental neurotoxicity of the α-isomer of hexabromocyclododecane (α-HBCDD), a persistent brominated flame retardant, to the valproic acid (VPA) model of ASD in rodents. Pregnant Wistar rats were divided into three groups: control, α-HBCDD (100 ng/kg/day p.o., GD0-PND21) and VPA (600 mg/kg i.p., GD12). Male offspring were tested for their neuromotor development from PND2-21. At PND21, brain functionality was assessed by measuring cytochrome oxidase activity (CO). Modifications in neuroglia and synaptic plasticity were evaluated in the cortex. Similar subtle behavioural changes related to neuromotor maturation and noise reaction were observed in both treated groups. At PND21, a reduction in CO activity was measured in the VPA group only, in specific areas including auditory nuclei, visual cortex, cingulate and frontal cortices. At the same age, α-HBCDD pointed out significant overexpression of cortical markers of synaptic plasticity while both treated groups showed a significant under expression of astrocyte proteins (S100-β and GFAP). Early-life exposure to a low dose of α-HBCDD may trigger neurobehavioural alterations in line with ASD. Full article
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Review

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22 pages, 15449 KiB  
Review
Inflammation and Autophagy: A Convergent Point between Autism Spectrum Disorder (ASD)-Related Genetic and Environmental Factors: Focus on Aluminum Adjuvants
by Loïc Angrand, Jean-Daniel Masson, Alberto Rubio-Casillas, Marika Nosten-Bertrand and Guillemette Crépeaux
Toxics 2022, 10(9), 518; https://doi.org/10.3390/toxics10090518 - 31 Aug 2022
Cited by 5 | Viewed by 11125 | Correction
Abstract
Autism spectrum disorder (ASD), schizophrenia, and bipolar disorder are genetically complex and heterogeneous neurodevelopmental disorders (NDDs) resulting from genetic factors and gene-environment (GxE) interactions for which onset occurs in early brain development. Recent progress highlights the link between ASD and (i) immunogenetics, neurodevelopment, [...] Read more.
Autism spectrum disorder (ASD), schizophrenia, and bipolar disorder are genetically complex and heterogeneous neurodevelopmental disorders (NDDs) resulting from genetic factors and gene-environment (GxE) interactions for which onset occurs in early brain development. Recent progress highlights the link between ASD and (i) immunogenetics, neurodevelopment, and inflammation, and (ii) impairments of autophagy, a crucial neurodevelopmental process involved in synaptic pruning. Among various environmental factors causing risk for ASD, aluminum (Al)-containing vaccines injected during critical periods have received special attention and triggered relevant scientific questions. The aim of this review is to discuss the current knowledge on the role of early inflammation, immune and autophagy dysfunction in ASD as well as preclinical studies which question Al adjuvant impacts on brain and immune maturation. We highlight the most recent breakthroughs and the lack of epidemiological, pharmacokinetic and pharmacodynamic data constituting a “scientific gap”. We propose additional research, such as genetic studies that could contribute to identify populations at genetic risk, improving diagnosis, and potentially the development of new therapeutic tools. Full article
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1 pages, 200 KiB  
Correction
Correction: Angrand et al. Inflammation and Autophagy: A Convergent Point between Autism Spectrum Disorder (ASD)-Related Genetic and Environmental Factors: Focus on Aluminum Adjuvants. Toxics 2022, 10, 518
by Loïc Angrand, Jean-Daniel Masson, Alberto Rubio-Casillas, Marika Nosten-Bertrand and Guillemette Crépeaux
Toxics 2023, 11(2), 95; https://doi.org/10.3390/toxics11020095 - 19 Jan 2023
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Abstract
There was an error in the original publication [...] Full article
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