Longitudinal Studies on Prenatal or Early Life Exposures, Their Associated Epigenetics, and Population Health

A special issue of Epigenomes (ISSN 2075-4655).

Deadline for manuscript submissions: 31 August 2025 | Viewed by 1311

Special Issue Editors


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Guest Editor
Division of Epidemiology, Biostatistics, and Environmental Health, School of Public Health, University of Memphis, Memphis, TN 38152, USA
Interests: epigenetic marker detection; variable selection; clustering; gaussian direct and undirected networks

E-Mail Website
Guest Editor
Division of Epidemiology, Biostatistics, and Environmental Health, School of Public Health, University of Memphis, Memphis, TN 38152, USA
Interests: Bayesian statistics; latent variable modeling; structural equation model; genomics and epigenetics
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Special Issue Information

Dear Colleagues,

Background: Earlier environmental exposures (e.g., mother's smoking during pregnancy, second-hand smoking, etc.), comorbidities (e.g., allergy), and substantial changes in life (e.g., adolescence) leave marks on DNA without changing the DNA sequence. Many studies have examined and demonstrated concurrent connections between epigenetics and population health. Epigenetics marks earlier exposures and thus has a potential to serve as a predictive biomarker for later life health conditions and related outcomes. Hence, assessing such associations in the context of longitudinal studies is critical and valuable in disease prediction, prevention and intervention or treatment. However, such studies, including longitudinal association studies and predictive modeling, are limited. Objective: Most epigenetic studies have been focusing on DNA methylation and will be the focus of this special issue as well, but other epigenetic mechanisms, e.g., histone modification, are welcome. Through this special issue, we aim at attracting longitudinal studies in the following areas: (1) prenatal epigenetics and postnatal health, (2) early life epigenetics and later life health conditions, and (3) epigenetics before disease treatment and response to the treatment. Longitudinal association studies for epigenetic markers or studies utilizing predictive modeling for predicting markers are strongly encouraged.

Prof. Dr. Hongmei Zhang
Dr. Yu (Joyce) Jiang
Guest Editors

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Keywords

  • earlier environmental exposures
  • early life epigenetic
  • postnatal health
  • epigenetic marker detection

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Published Papers (1 paper)

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Research

14 pages, 1099 KiB  
Article
The Association of Childhood Allergic Diseases with Prenatal Exposure to Pollen Grains Through At-Birth DNA Methylation
by Rajesh Melaram, Hongmei Zhang, James Adefisoye and Hasan Arshad
Epigenomes 2025, 9(1), 9; https://doi.org/10.3390/epigenomes9010009 - 11 Mar 2025
Viewed by 801
Abstract
Background: Pollen exposure in early life is shown to be associated with allergy and asthma. DNA methylation (DNAm), an epigenetic marker, potentially reacts to pollen. However, the role of at-birth DNAm between prenatal pollen grain (PPG) exposure and childhood asthma and allergic rhinitis [...] Read more.
Background: Pollen exposure in early life is shown to be associated with allergy and asthma. DNA methylation (DNAm), an epigenetic marker, potentially reacts to pollen. However, the role of at-birth DNAm between prenatal pollen grain (PPG) exposure and childhood asthma and allergic rhinitis is unknown. Methods: Data in a birth cohort study on the Isle of Wight, UK, were analyzed (n = 236). Newborn DNAm was measured in cord blood or blood spots on Guthrie cards and screened for potential association with PPG exposure using the R package ttScreening. CpGs that passed screening were further assessed for such associations via linear regressions with adjusting covariates included. Finally, DNAm at PPG-associated CpGs were evaluated for their association with asthma and allergic rhinitis using logistic regressions, adjusting for covariates. The impact of cell heterogeneity on the findings was assessed. Statistical significance was set at p < 0.05. Results: In total, 42 CpGs passed screening, with 41 remaining statistically significant after adjusting for covariates and cell types (p < 0.05). High PPG exposure was associated with lower DNAm at cg12318501 (ZNF99, β = −0.029, p = 0.032) and cg00929606 (ADM2, β = −0.023, p = 0.008), which subsequently was associated with decreased odds of asthma (OR = 0.11, 95% CI 0.02–0.53, p = 0.006; OR = 0.14, 95% CI 0.02–1.00, p = 0.049). For rhinitis, cg15790214 (HCG11) was shown to play such a role as a mediator (β = −0.027, p ≤ 0.0001; OR = 0.22, 95% CI 0.07–0.72, p = 0.01). Conclusions: The association of PPG exposure with childhood asthma and allergic rhinitis incidence is potentially mediated by DNAm at birth. Full article
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