Early-Life Environmental Exposures and Childhood Obesity: An Exposome-Wide Approach

Title	Early-Life Environmental Exposures and Childhood Obesity: An Exposome-Wide Approach
Authors	Martine Vrijheid, Serena Fossati, Léa Maitre, Sandra Márquez, Theano Roumeliotaki, Lydiane Agier, Sandra Andrusaityte, Solène Cadiou, Maribel Casas, Montserrat de Castro, Audrius Dedele, David Donaire-Gonzalez, Regina Grazuleviciene, Line S. Haug, Rosemary McEachan, Helle Margrete Meltzer, Eleni Papadopouplou, Oliver Robinson, Amrit K. Sakhi, Valerie Siroux, Jordi Sunyer, Per E. Schwarze, Ibon Tamayo-Uria, Jose Urquiza, Marina Vafeiadi, Antonia Valentin, Charline Warembourg, John Wright, Mark J.
Magazine	Environmental Health Perspectives
Date	06/24/2020
DOI	https://doi.org/10.1289/EHP5975
Introduction	The influence of chemical and non-chemical environmental factors on obesity development, particularly during early life, is a growing area of concern, with most prior investigations focusing on isolated exposure types. This study undertakes a systematic evaluation of the relationship between a broad spectrum of early-life environmental exposures and childhood obesity, employing an exposome-wide methodology. The Human Early Life Exposome (HELIX) study collected data on body mass index (BMI), waist circumference, skinfold thickness, and body fat mass from 1,301 children aged 6–11 years across six European birth cohorts. Researchers quantified 77 prenatal and 96 childhood exposures cross-sectionally, encompassing indoor and outdoor air pollutants, characteristics of the built environment, green spaces, tobacco smoking, and biomarkers of chemical agents such as persistent organic pollutants, metals, phthalates, phenols, and pesticides. An exposure-wide association study (ExWAS) was utilised to independently screen all exposure-outcome associations, followed by the deletion-substitution-addition (DSA) variable selection algorithm to construct a multiexposure model. The combined prevalence of overweight and obesity was observed to be 28.8%. Maternal smoking emerged as the sole prenatal exposure linked to a higher child BMI. For childhood exposures, the multiexposure model indicated that indoor particulate and nitrogen dioxide air pollution, urine cotinine levels signifying secondhand smoke exposure, and residence in more densely populated areas with fewer facilities were associated with increased child BMI. Furthermore, elevated child blood levels of copper and cesium correlated with higher BMI, while levels of organochlorine pollutants, cobalt, and molybdenum were associated with lower BMI. Consistent patterns were observed for other measures of adiposity. This initial extensive and systematic examination of numerous suspected environmental obesogens reinforces the evidence connecting smoking, air pollution exposure, and features of the built environment to childhood obesity risk. It is acknowledged that cross-sectional biomarker results may be subject to reverse causality, where existing obesity status could influence biomarker concentrations.
Quote	Martine Vrijheid, Serena Fossati and Léa Maitre et al. Early-Life Environmental Exposures and Childhood Obesity: An Exposome-Wide Approach. Environ. Health Perspect. 2020. Vol. 128(6). DOI: 10.1289/EHP5975
Element	Copper (Cu) , Cobalt (Co) , Molybdenum (Mo) , Nitrogen (N)
Materials	Chemical Compounds
Topics	Environmental and Green Materials
Industry	Research & Laboratory , Chemical & Pharmacy