Special Issue "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 "Toxicology".

Deadline for manuscript submissions: 15 November 2022 | Viewed by 1452

Special Issue Editors

Dr. Nathalie Grova
E-Mail Website
Guest Editor
1. Immune Endocrine and Epigenetics Research Unit, Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, L-4354 Esch-sur-Alzette, Luxembourg
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
Dr. Jonathan Turner
E-Mail Website
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

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 1800 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

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

Published Papers (1 paper)

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Research

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
Toxics 2022, 10(4), 180; https://doi.org/10.3390/toxics10040180 - 06 Apr 2022
Viewed by 1210
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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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

1. Title: Individual genetic susceptibility on autophagy, immune dysfunction and early exposure to Al-containing vaccines: a deleterious gene x environment combination?

Abstract: Neurodevelopmental disorders such as schizophrenia or Autism Spectrum Disorders (ASD), are increasingly viewed as paradigmatic of “gene x environment” interaction-based diseases. They are also associated with sustained inflammatory states and described as closely linked to autophagy-dependent synaptic pruning defect, leading to consider neurodevelopmental disorders as neuro-inflammatory and autophagy-related diseases.
Among the variety of environmental factors suspected to play a role in ASD pathophysiology, the strong and growing exposure to aluminum-containing vaccines injected in very early life, i.e. during key developmental periods of both nervous and immune systems, deserves special attention.
Indeed, although benefits of pediatric vaccination are unquestionably huge, recent studies, conducted in both humans and animals, have turned upside down old reassuring dogmas about vaccine adjuvants, such as rapid elimination and absolute innocuity of aluminum (Al) salts. For example, Al oxyhydroxide is a pro-inflammatory particulate compound that is very slowly cleared out from the body since it is promptly phagocytosed after injection and then persists for long in phagocytic cells, migrating within monocyte/macrophage lineage cells from the injection site to distant organs, including brain.

2. Title: Study of the early neurobehavioral toxicity induced by a perinatal exposure to hexabromocyclododecane to that of valproic acid used as a model of reference for Autism Spectrum Disorders in rodents

Abstract: Evidence is now growing that exposure to environmental pollutants during the critical period of early-life brain development may be a strong risk factor, contributing to the emergence of Autism Spectrum Disorders (ASD). This study seeks to compare the developmental neurotoxicity induced by early-life exposure to hexabromocyclododecane (α-isomer, α-HBCDD), a persistent organobromine flame retardant to that observed in the valproic acidexposed rat model (VPA) used as a model of reference for ASD in rodents. Pregnant Wistar rats were divided in three treated groups: control, α-HBCDD (100 ng/kg/day p.o., GD0-PND21) and VPA (600 mg/kg i.p., GD12). The males were tested for their neuromotor development from PND2 to PND21. At PND21, changes in brain functionality were assessed by measuring cytochrome oxidase activity (CO) in cortices, cerebellum and specific brain regions involved in the sensory systems. Modifications in neuroglia and synaptic plasticity were evaluated in cortex as well. Similar subtle behavioral changes related to neuromotor maturation and noise reaction were observed in both treated groups. At PN21, a reduction in CO activity was observed in the VPA group only, in specific areas including most of the auditory system, 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 neurobehavioral alterations in line with ASD-like phenotypes.

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