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Environmental Epigenetics: Implications for Health and Disease

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A special issue of International Journal of Environmental Research and Public Health (ISSN 1660-4601). This special issue belongs to the section "Environmental Health".

Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 17740

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Dr. Jaclyn Goodrich

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Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, Michigan, USA
Interests: epigenetics; toxicology; occupational and environmental epidemiology; children’s health; gene-environment interactions

Special Issue Information

Dear Colleagues,

I am organizing a Special Issue on Environmental Epigenetics: Implications for Health and Disease in the International Journal of Environmental Research and Public Health (IJERPH). The epigenome is the dynamic regulatory framework that controls the use of genetic information to define cellular identify and govern the response of cells and tissues to their environment. Of particular interest to environmental and public health, research has demonstrated that epigenetic profiles are modifiable by the environment, heritable (mitotically and in some cases across generations), and they influence risk for disease development. Environmental factors as diverse as toxicant exposures, diet, and stress have been shown to alter epigenetic programming.

This Special Issue invites papers focusing on the impact of environmental exposures on the epigenome. Environmental exposures considered include not only chemical/toxicant and dietary exposures but also the social environment. Epigenetic modifications include DNA methylation, posttranslational histone tail modifications, chromatin accessibility, and noncoding RNA. Studies that relate epigenetic changes to health outcomes are encouraged. Full-length research articles or brief communications reporting original research results from epidemiological, animal, or in vitro studies are welcome. Critical reviews (systematic reviews or meta-analyses) are also welcome.

Dr. Jaclyn Goodrich
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. International Journal of Environmental Research and Public Health 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 2500 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

Environmental exposures
Toxicants
Nutrition
Developmental origins of health and disease
DNA methylation
Histone code
Noncoding RNA
Epigenomics
Multigenerational
Molecular epidemiology

Published Papers (5 papers)

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Research

15 pages, 847 KiB

Open AccessFeature PaperArticle

Early Life Exposure to Aflatoxin B1 in Rats: Alterations in Lipids, Hormones, and DNA Methylation among the Offspring

by Oluwakemi A. Rotimi, Chinonye D. Onuzulu, Alisa L. Dewald, Jessa Ehlinger, Isaacson B. Adelani, Olutola E. Olasehinde, Solomon O. Rotimi and Jaclyn M. Goodrich

Int. J. Environ. Res. Public Health 2021, 18(2), 589; https://doi.org/10.3390/ijerph18020589 - 12 Jan 2021

Cited by 18 | Viewed by 3596

Abstract

Aflatoxins are toxic compounds produced by molds of the Aspergillus species that contaminate food primarily in tropical countries. The most toxic aflatoxin, aflatoxin B1 (AFB1), is a major cause of hepatocellular carcinoma (HCC) in these countries. In sub-Saharan Africa, aflatoxin contamination is common, and perinatal AFB1 exposure has been linked to the early onset of HCC. Epigenetic programming, including changes to DNA methylation, is one mechanism by which early life exposures can lead to adult disease. This study aims to elucidate whether perinatal AFB1 exposure alters markers of offspring health including weight, lipid, and hormone profiles as well as epigenetic regulation that may later influence cancer risk. Pregnant rats were exposed to two doses of AFB1 (low 0.5 and high 5 mg/kg) before conception, throughout pregnancy, and while weaning and compared to an unexposed group. Offspring from each group were followed to 3 weeks or 3 months of age, and their blood and liver samples were collected. Body weights and lipids were assessed at 3 weeks and 3 months while reproductive, gonadotropic, and thyroid hormones were assessed at 3 months. Prenatal AFB1 (high dose) exposure resulted in significant 16.3%, 31.6%, and 7.5% decreases in weight of the offspring at birth, 3 weeks, and 3 months, respectively. Both doses of exposure altered lipid and hormone profiles. Pyrosequencing was used to quantify percent DNA methylation at tumor suppressor gene Tp53 and growth-regulator H19 in DNA from liver and blood. Results were compared between the control and AFB1 exposure groups in 3-week liver samples and 3-week and 3-month blood samples. Relative to controls, Tp53 DNA methylation in both low- and high-dose exposed rats was significantly decreased in liver samples and increased in the blood (p < 0.05 in linear mixed models). H19 methylation was higher in the liver from low- and high-exposed rats and decreased in 3-month blood samples from the high exposure group (p < 0.05). Further research is warranted to determine whether such hormone, lipid, and epigenetic alterations from AFB1 exposure early in life play a role in the development of early-onset HCC. Full article

(This article belongs to the Special Issue Environmental Epigenetics: Implications for Health and Disease)

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20 pages, 2503 KiB

Open AccessArticle

Sex-Specific Alterations in Cardiac DNA Methylation in Adult Mice by Perinatal Lead Exposure

by Laurie K. Svoboda, Kai Wang, Tamara R. Jones, Justin A. Colacino, Maureen A. Sartor and Dana C. Dolinoy

Int. J. Environ. Res. Public Health 2021, 18(2), 577; https://doi.org/10.3390/ijerph18020577 - 12 Jan 2021

Cited by 13 | Viewed by 3776

Abstract

Environmental factors play an important role in the etiology of cardiovascular diseases. Cardiovascular diseases exhibit marked sexual dimorphism; however, the sex-specific effects of environmental exposures on cardiac health are incompletely understood. Perinatal and adult exposures to the metal lead (Pb) are linked to several adverse cardiovascular outcomes, but the sex-specific effects of this toxicant on the heart have received little attention. Perinatal environmental exposures can lead to disease through disruption of the normal epigenetic programming that occurs during early development. Using a mouse model of human-relevant perinatal environmental exposure, we investigated the effects of exposure to Pb during gestation and lactation on DNA methylation in the hearts of adult offspring mice (n = 6 per sex). Two weeks prior to mating, dams were assigned to control or Pb acetate (32 ppm) water, and exposure continued until offspring were weaned at three weeks of age. Enhanced reduced-representation bisulfite sequencing was used to measure DNA methylation in the hearts of offspring at five months of age. Although Pb exposure stopped at three weeks of age, we discovered hundreds of differentially methylated cytosines (DMCs) and regions (DMRs) in males and females at five months of age. DMCs/DMRs and their associated genes were sex-specific, with a small, but statistically significant subset overlapping between sexes. Pathway analysis revealed altered methylation of genes important for cardiac and other tissue development in males, and histone demethylation in females. Together, these data demonstrate that perinatal exposure to Pb induces sex-specific changes in cardiac DNA methylation that are present long after cessation of exposure, and highlight the importance of considering sex in environmental epigenetics and mechanistic toxicology studies. Full article

(This article belongs to the Special Issue Environmental Epigenetics: Implications for Health and Disease)

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16 pages, 1349 KiB

Open AccessArticle

Prenatal Multivitamin Use and MTHFR Genotype Are Associated with Newborn Cord Blood DNA Methylation

by Kelly M. Bakulski, John F. Dou, Jason I. Feinberg, Katharine K. Brieger, Lisa A. Croen, Irva Hertz-Picciotto, Craig J. Newschaffer, Rebecca J. Schmidt and M. Daniele Fallin

Int. J. Environ. Res. Public Health 2020, 17(24), 9190; https://doi.org/10.3390/ijerph17249190 - 9 Dec 2020

Cited by 10 | Viewed by 3054

Abstract

Background: Fetal development involves cellular differentiation and epigenetic changes—complex processes that are sensitive to environmental factors. Maternal nutrient levels during pregnancy affect development, and methylene tetrahydrofolate reductase (MTHFR) is important for processing the nutrient folate. Hypothesis: We hypothesize that supplement intake before pregnancy and maternal genotype are associated with DNA methylation in newborns. Methods: In the pregnancy cohort, Early Autism Risk Longitudinal Investigation (EARLI), health history, and genotype information was obtained (n = 249 families). Cord blood DNA methylation (n = 130) was measured using the Illumina HumanMethylation450k array and global DNA methylation levels were computed over 455,698 sites. Supplement use preconception and during pregnancy were surveyed at visits during pregnancy. We evaluated associations between maternal preconception supplement intake and global DNA methylation or DNA methylation density distributions of newborn cord blood, stratified by the presence of a variant maternal MTHFR C677T allele. Results: Maternal preconceptional multivitamin intake was associated with cord blood methylation, dependent on maternal MTHFR genotype (interaction term p = 0.013). For mothers without the MTHFR variant allele, multivitamin intake was associated with 0.96% (95% CI: 0.09, 1.83) higher global cord blood methylation (p = 0.04) and was also associated with the cumulative density distribution of methylation (p = 0.03). For mothers with at least one variant allele, multivitamin intake had a null −0.06% (95% CI: −0.45, 0.33) association with global cord blood DNA methylation, and was not associated with the cumulative density distribution (p = 0.37). Conclusions: We observed that cord blood DNA methylation was associated with maternal supplement exposure preconception and maternal genotype. Genetic context should be considered when assessing DNA methylation effects of modifiable risk factors around the time of pregnancy. Full article

(This article belongs to the Special Issue Environmental Epigenetics: Implications for Health and Disease)

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13 pages, 2864 KiB

Open AccessArticle

Environmental Epigenetics of Diesel Particulate Matter Toxicogenomics

by Stephanie M. Bilinovich, Kristy Lewis, Barbara L. Thompson, Jeremy W. Prokop and Daniel B. Campbell

Int. J. Environ. Res. Public Health 2020, 17(20), 7386; https://doi.org/10.3390/ijerph17207386 - 10 Oct 2020

Viewed by 3081

Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by disruptions in social communication and behavioral flexibility. Both genetic and environmental factors contribute to ASD risk. Epidemiologic studies indicate that roadway vehicle exhaust and in utero exposure to diesel particulate matter (DPM) are associated with ASD. Using the Comparative Toxicogenomics Database (CTD), we identified genes connected to DPM exposure and ASD, extracted the known enhancers/promoters of the identified genes, and integrated this with Assay for Transposase Accessible Chromatin (ATAC-seq) data from DPM-exposed human neural progenitor cells. Enhancer/promoter elements with significantly different chromosome accessibility revealed enriched DNA sequence motifs with transcription factor binding sites for EGR1. Variant extraction for linkage disequilibrium blocks of these regions followed by analysis through Genome Wide Association Studies (GWAS) revealed multiple neurological trait associations including exploratory eye movement and brain volume measurement. This approach highlights the effects of pollution on the regulatory regions of genes implicated in ASD by genetic studies, indicating convergence of genetic and environmental factors on molecular networks that contribute to ASD. Integration of publicly available data from the CTD, cell culture exposure studies, and phenotypic genetics synergize extensive evidence of chemical exposures on gene regulation for altered brain development. Full article

(This article belongs to the Special Issue Environmental Epigenetics: Implications for Health and Disease)

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17 pages, 532 KiB

Open AccessArticle

Neonatal Lead (Pb) Exposure and DNA Methylation Profiles in Dried Bloodspots

by Luke Montrose, Jaclyn M. Goodrich, Masako Morishita, Joseph Kochmanski, Zachary Klaver, Raymond Cavalcante, Julie C. Lumeng, Karen E. Peterson and Dana C. Dolinoy

Int. J. Environ. Res. Public Health 2020, 17(18), 6775; https://doi.org/10.3390/ijerph17186775 - 17 Sep 2020

Cited by 24 | Viewed by 3497

Abstract

Lead (Pb) exposure remains a major concern in the United States (US) and around the world, even following the removal of Pb from gasoline and other products. Environmental Pb exposures from aging infrastructure and housing stock are of particular concern to pregnant women, children, and other vulnerable populations. Exposures during sensitive periods of development are known to influence epigenetic modifications which are thought to be one mechanism of the Developmental Origins of Health and Disease (DOHaD) paradigm. To gain insights into early life Pb exposure-induced health risks, we leveraged neonatal dried bloodspots in a cohort of children from Michigan, US to examine associations between blood Pb levels and concomitant DNA methylation profiles (n = 96). DNA methylation analysis was conducted via the Infinium MethylationEPIC array and Pb levels were assessed via high resolution inductively coupled plasma mass spectrometry (HR-ICP-MS). While at-birth Pb exposure levels were relatively low (average 0.78 µg/dL, maximum of 5.27 ug/dL), we identified associations between DNA methylation and Pb at 33 CpG sites, with the majority (82%) exhibiting reduced methylation with increasing Pb exposure (q < 0.2). Biological pathways related to development and neurological function were enriched amongst top differentially methylated genes by p-value. In addition to increases/decreases in methylation, we also demonstrate that Pb exposure is related to increased variability in DNA methylation at 16 CpG sites. More work is needed to assess the accuracy and precision of metals assessment using bloodspots, but this study highlights the utility of this unique resource to enhance environmental epigenetics research around the world. Full article

(This article belongs to the Special Issue Environmental Epigenetics: Implications for Health and Disease)

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