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The early-life exposome and epigenetic age acceleration in children
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International audience. The early-life exposome influences future health and accelerated biological aging has been proposed as one of theunderlying biological mechanisms. We investigated the association between more than 100 exposures assessedduring 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 ageacceleration 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 byInfinium HumanMethylation450 BeadChips. We performed an exposure-wide association study between prenataland childhood exposome and age acceleration. Maternal tobacco smoking during pregnancy was nominallyassociated 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 theorganic pesticide dimethyl dithiophosphate and the persistent pollutant polychlorinated biphenyl-138 (inverselyassociated with child body mass index) were protective for age acceleration. None of the associations remainedsignificant after multiple-testing correction. Pregnancy and childhood exposure to tobacco smoke and childhoodexposure to indoor PMabs may accelerate epigenetic aging from an early age.
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