Special Issue "Developmental Environmental Exposures, Epigenetics and Long-Term Health"

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

Deadline for manuscript submissions: closed (30 April 2021).

Special Issue Editor

Dr. Laurie Svoboda
E-Mail Website
Guest Editor
Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, MI 48109-2029, USA
Interests: toxicology; developmental origins of health and disease; toxicoepigenetics; sex differences; metabolomics; stem cells; cardiovascular disease; nutrient–toxicant interactions

Special Issue Information

Dear Colleagues,

It is increasingly evident that environmental exposures during critical windows of development can impact human health across one’s lifespan. Developmental exposures linked to adverse health effects include heavy metals (lead, cadmium, arsenic), endocrine disruptors (phthalates, bisphenols, per- and polyfluoroalkyl substances (PFAS)), air pollutants (tobacco smoke, ozone, particulate matter) and radiation. Normal development is governed by widespread epigenomic reprogramming in the somatic cells and primordial germ cells of the developing embryo. This reprogramming includes changes in DNA methylation, DNA hydroxymethylation, chromatin modification/structure, and expression/function of noncoding RNAs. Epigenetic changes continue during the postnatal period, early childhood, and adolescence. An important mechanism by which early environmental exposures may affect long-term health is through interfering with these critical developmental processes. The effects of environmental agents on epigenomic programming during critical periods of development, and the implications these changes have for health across the lifespan, are incompletely understood.

In this Special Issue, we invite contributions (original articles, reviews, and communications) that address these important research questions. These include mechanistic studies conducted in a variety of models (animal, cell culture, human tissues), as well as human epidemiologic studies. Of particular interest are studies that address the sex-specific effects of develomental environmental exposures on the epigenome and health.

Dr. Laurie Svoboda
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 papers will be 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 1600 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

  • developmental origins of health and disease (DOHaD)
  • epigenetics
  • toxicoepigenetics
  • DNA methylation
  • DNA hydroxymethylation
  • chromatin
  • environmental health

Published Papers (2 papers)

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Research

Open AccessArticle
Elimination of Intravenous Di-2-Ethylhexyl Phthalate Exposure Abrogates Most Neonatal Hypertension in Premature Infants with Bronchopulmonary Dysplasia
Toxics 2021, 9(4), 75; https://doi.org/10.3390/toxics9040075 - 02 Apr 2021
Viewed by 367
Abstract
(1) Background: The incidence of hypertension in very low birthweight (VLBW) infants in a single neonatal intensive care unit (NICU) dropped markedly during a 2-year period when the IV fluid (IVF) in both the antenatal unit and the NICU temporarily changed to a [...] Read more.
(1) Background: The incidence of hypertension in very low birthweight (VLBW) infants in a single neonatal intensive care unit (NICU) dropped markedly during a 2-year period when the IV fluid (IVF) in both the antenatal unit and the NICU temporarily changed to a di-2-ethylhexyl phthalate (DEHP)-free formulation. The objective of the current report is to document this observation and demonstrate the changes in incidence of hypertension were not associated with the variation in risk factors for hypertension; (2) Methods: The charts of all VLBW infants born in a single NICU during a 7-year span were reviewed. This time includes 32 months of baseline, 20 months of DEHP-free IVF, 20 months of IVF DEHP re-exposure, and two 4-month washout intervals. The group of interest was limited to VLBW infants with bronchopulmonary dysplasia (BPD). Chi-square analysis was used to compare incidence of hypertension among periods. Vermont Oxford NICU Registry data were examined for variation in maternal and neonatal risk factors for hypertension; Results: Incidence of hypertension in VLBW infants with BPD decreased from 7.7% (baseline) to 1.4% when IVF was DEHP-free, rising back to 10.1% when DEHP-containing IVF returned to use. Risk factors for neonatal hypertension were stable across the 3 study periods in the NICU’s group of VLBW infants; (3) Conclusions: Serendipitous removal of IVF containing DEHP resulted in near elimination of hypertension in one NICU—an effect entirely reversed after the same brand of DEHP-containing IVF returned to clinical use. These results suggest that DEHP exposure from IVF plays a major role in neonatal hypertension. Full article
Open AccessArticle
Paternal Biomass Smoke Exposure in Rats Produces Behavioral and Cognitive Alterations in the Offspring
Toxics 2021, 9(1), 3; https://doi.org/10.3390/toxics9010003 - 31 Dec 2020
Viewed by 554
Abstract
Particular concern at the present stage is the health effects of wildfires’ smoke. The aim of the study was to determine the impact of paternal biomass-smoke exposure on offspring’s behavior and cognitive abilities. Male rats were exposed to biomass smoke for four hours/day, five [...] Read more.
Particular concern at the present stage is the health effects of wildfires’ smoke. The aim of the study was to determine the impact of paternal biomass-smoke exposure on offspring’s behavior and cognitive abilities. Male rats were exposed to biomass smoke for four hours/day, five days/week, for four weeks. Average concentration of carbon monoxide and particulate matter of 2.5 μm PM2.5 in the chamber during exposure were 28.7 ± 5.3 mg/m3 and 1.9 ± 0.5 mg/m3, respectively. At the same time, high concentrations of furfural and acetaldehyde were detected in the air environment of the exposure chambers. Offspring was obtained by mating of experimental males with untreated females, immediately after the end of the exposure and after 60 days (long-term period). Offspring were tested by using the Morris water maze and open field at three months of age. Male and female offspring born by mating immediately after exposure demonstrated decreased exploratory behavior, locomotor activity, and spatial navigation, as well as increased anxiety levels. Locomotor and exploratory activity in rats of both sexes from progeny obtained after long-term exposure to smoke had no statistically significant differences when compared to the control; however, the females showed a high level of anxiety and impaired cognitive functions. The recovery period after biomass-smoke intoxication, comparable in duration of spermatogenesis in rats, was an important factor in reducing the risk of developing central nervous system (CNS) disorders in offspring. Full article
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