Abstract
The early-life exposome influences future health and accelerated biological aging has been proposed as one of the underlying biological mechanisms. We investigated the association between more than 100 exposures assessed during pregnancy and in childhood (including indoor and outdoor air pollutants, built environment, green environments, tobacco smoking, lifestyle exposures, and biomarkers of chemical pollutants), and epigenetic age acceleration in 1,173 children aged 7 years old from the Human Early-Life Exposome project. Age acceleration was calculated based on Horvath’s Skin and Blood clock using child blood DNA methylation measured by Infinium HumanMethylation450 BeadChips. We performed an exposure-wide association study between prenatal and childhood exposome and age acceleration. Maternal tobacco smoking during pregnancy was nominally associated with increased age acceleration. For childhood exposures, indoor particulate matter absorbance (PMabs) and parental smoking were nominally associated with an increase in age acceleration. Exposure to the organic pesticide dimethyl dithiophosphate and the persistent pollutant polychlorinated biphenyl-138 (inversely associated with child body mass index) were protective for age acceleration. None of the associations remained significant after multiple-testing correction. Pregnancy and childhood exposure to tobacco smoke and childhood exposure to indoor PMabs may accelerate epigenetic aging from an early age.
Highlights
Current evidence shows that early-life, including prenatal and early postnatal periods, could be considered as an important window of sus ceptibility to environmental exposures (Wright, 2017)
This study aimed to investigate the association between the early life exposome and epigenetic age acceleration in children from the Human Early-Life Exposome (HELIX) project
This study was conducted in the context of the HELIX project, which was based on six on-going longitudinal population-based birth cohorts established in six countries across different parts of Europe (Born in Bradford [BiB; UK], Etude des Determinants Pre et Postnatals du Developpement et de la Sante de l’Enfant [EDEN; France], Infancia y Medio Ambiente [INMA; Spain], Kaunas Cohort [KANC; Lithuania], Norwegian Mother, Father and Child Cohort Study [MoBa; Norway], and Mother-Child Cohort in Crete [RHEA; Greece]) (Magnus et al, 2016; Maitre et al, 2018; Vrijheid et al, 2014)
Summary
Current evidence shows that early-life, including prenatal and early postnatal periods, could be considered as an important window of sus ceptibility to environmental exposures (Wright, 2017). Being exposed during these stages might permanently change the body’s structure, metabolism, and physiology, and promote health or diseases in later stages of life (Barouki et al, 2012). Biological aging is reported to be a risk factor for the development of age-related diseases such as cancer, diabetes, cardiovascular, and neurodegenerative diseases as well as increased mortality (Kumar et al, 2017) In this context, aging could be considered as a continuous process already starting in early-life. Evaluating aging during this period might provide new evidence to slow down this process from the beginning and, prevent or delay the development of adverse health outcomes during adulthood and elderly (Benetos et al, 2013; Martens et al, 2019)
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