Prenatal chemical exposures and the methylome: current evidence and opportunities for environmental epigenetics DOI Creative Commons
Anne K. Bozack, Leonardo Trasande

Epigenomics, Journal Year: 2024, Volume and Issue: unknown, P. 1 - 9

Published: Nov. 14, 2024

Exposure to pollutants and chemicals during critical developmental periods in early life can impact health disease risk across the course. Research environmental epigenetics has provided increasing evidence that prenatal exposures affect epigenetic markers, particularly DNA methylation. In this article, we discuss role of methylation programming review linking intrauterine environment modifications, with a focus on exposure tobacco smoke, metals, endocrine-disrupting chemicals. We also challenges novel approaches research explore potential biomarkers studies pediatric populations as indicators risk. Overall, aim highlight how advancements may transform our understanding early-life inform new for supporting long-term health.

Language: Английский

Prenatal Exposure to Metals Is Associated with Placental Decelerated Epigenetic Gestational Age in a Sex-Dependent Manner in Infants Born Extremely Preterm DOI Creative Commons

Katelyn Huff,

Kyle R. Roell, Lauren A. Eaves

et al.

Cells, Journal Year: 2025, Volume and Issue: 14(4), P. 306 - 306

Published: Feb. 18, 2025

Prenatal exposure to metals can influence fetal programming via DNA methylation and has been linked adverse birth outcomes long-term consequences. Epigenetic clocks estimate the biological age of a given tissue based on are potential health biomarkers. This study leveraged Extremely Low Gestational Age Newborn (ELGAN) (n = 265) evaluate associations between umbilical cord concentrations 11 as single exposures well mixtures in relation (1) placental epigenetic gestational acceleration (eGAA) (2) status Robust Placental Clock (RPC) CpGs. Linear mixed effect regression models were stratified by infant sex. Both copper (Cu) manganese (Mn) significantly associated with decelerated eGA -0.98 (95% confidence interval (CI): -1.89, -0.07) -0.90 weeks CI: -1.78, -0.01), respectively, male infants. Cu Mn levels also at RPC CpGs within genes related processes including energy homeostasis inflammatory response placenta. Overall, these findings suggest that prenatal impact eGAA sex-dependent manner ELGANs, future work could examine mechanism mediating utero metal later life

Language: Английский

Citations

1
Chemical and Climatic Environmental Exposures and Epigenetic Aging: a Systematic Review DOI Creative Commons
Raj P. Fadadu, Anne K. Bozack, Andrés Cárdenas

et al.

Environmental Research, Journal Year: 2025, Volume and Issue: unknown, P. 121347 - 121347

Published: March 1, 2025

Language: Английский

Citations

1
Causal effects of denture wearing on epigenetic age acceleration and the mediating pathways: a mendelian randomization study DOI Creative Commons
Xin Chen, Cheng Zheng,

Junyu Xu

et al.

BMC Oral Health, Journal Year: 2024, Volume and Issue: 24(1)

Published: July 13, 2024

Abstract Background The epigenetic-age acceleration (EAA) represents the difference between chronological age and epigenetic age, reflecting accelerated biological aging. Observational studies suggested that oral disorders may impact DNA methylation patterns aging, but their causal relationship remains largely unexplored. This study aimed to investigate potential associations dental traits EAA, as well identify possible mediators. Methods Using summary statistics of genome-wide association predominantly European ancestry, we conducted univariable multivariable Mendelian randomization (MR) estimate overall independent effects ten (dentures, bleeding gums, painful loose teeth, toothache, ulcers, periodontitis, number two measures caries) on four EAA subtypes (GrimAge [GrimAA], PhenoAge [PhenoAA], HannumAge [HannumAA] intrinsic [IEAA]), used two-step evaluate twelve mediators associations. Comprehensive sensitivity analyses were verity robustness, heterogeneity, pleiotropy. Results Univariable inverse variance weighted MR revealed a effect dentures greater GrimAA (β: 2.47, 95% CI: 0.93–4.01, p = 0.002), PhenoAA 3.00, 1.15–4.85, 0.001), HannumAA 1.96, 0.58–3.33, 0.005). In MR, remained significant after adjusting for caries, teeth gums. Three out 12 aging risk factors identified including body mass index, fat percentage, waist circumference. No evidence reverse causality pleiotropy detected ( > 0.05). Conclusions Our findings supported genetic liability denture wearing with partial mediation by obesity. More attention should be paid obesity-monitoring management slowing among wearers.

Language: Английский

Citations

1
Prenatal chemical exposures and the methylome: current evidence and opportunities for environmental epigenetics DOI Creative Commons
Anne K. Bozack, Leonardo Trasande

Epigenomics, Journal Year: 2024, Volume and Issue: unknown, P. 1 - 9

Published: Nov. 14, 2024

Exposure to pollutants and chemicals during critical developmental periods in early life can impact health disease risk across the course. Research environmental epigenetics has provided increasing evidence that prenatal exposures affect epigenetic markers, particularly DNA methylation. In this article, we discuss role of methylation programming review linking intrauterine environment modifications, with a focus on exposure tobacco smoke, metals, endocrine-disrupting chemicals. We also challenges novel approaches research explore potential biomarkers studies pediatric populations as indicators risk. Overall, aim highlight how advancements may transform our understanding early-life inform new for supporting long-term health.

Language: Английский

Citations

0