The early-life exposome and epigenetic age acceleration in children
Paula de Prado-Bert, Carlos Ruiz-Arenas, Marta Vives-Usano, Sandra Andrušaitytė, Solène Cadiou, Ãngel Carracedo, Maribel Casas, Leda Chatzi, Payam Dadvand, Juan R. González, Regina Gražulevičienė, Kristine B. Gützkow, Line Småstuen Haug, Carles Hernandéz-Ferrer, Hector C. Keun, Johanna Lepeule, Léa Maître, Rosie McEachan, Mark Nieuwenhuijsen, Dolors Pelegrí-Sisó, Oliver Robinson, Rémy Slama, Marina Vafeiadi, Jordi Sunyer, Martine Vrijheid, Mariona Bustamante
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.