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

Abstract

BACKGROUND: Chemical and nonchemical environmental exposures are increasingly suspected to influence the development of obesity, especially during early life, but studies mostly consider single exposure groups. OBJECTIVES: Our study aimed to systematically assess the association between a wide array of early-life environmental exposures and childhood obesity, using an exposome-wide approach. METHODS: The HELIX (Human Early Life Exposome) study measured child body mass index (BMI), waist circumference, skinfold thickness, and body fat mass in 1,301 children from six European birth cohorts age 6-11 y. We estimated 77 prenatal exposures and 96 childhood exposures (crosssectionally), including indoor and outdoor air pollutants, built environment, green spaces, tobacco smoking, and biomarkers of chemical pollutants (persistent organic pollutants, metals, phthalates, phenols, and pesticides). We used an exposure-wide association study (ExWAS) to screen all exposure-outcome associations independently and used the deletion-substitution-addition (DSA) variable selection algorithm to build a final multiexposure model. RESULTS: The prevalence of overweight and obesity combined was 28.8%. Maternal smoking was the only prenatal exposure variable associated with higher child BMI (z-score increase of 0.28, 95% confidence interval: 0.09, 0.48, for active vs. no smoking). For childhood exposures, the multiexposure model identified particulate and nitrogen dioxide air pollution inside the home, urine cotinine levels indicative of secondhand smoke exposure, and residence in more densely populated areas and in areas with fewer facilities to be associated with increased child BMI. Child blood levels of copper and cesium were associated with higher BMI, and levels of organochlorine pollutants, cobalt, and molybdenum were associated with lower BMI. Similar results were found for the other adiposity outcomes. DISCUSSION: This first comprehensive and systematic analysis of many suspected environmental obesogens strengthens evidence for an association of smoking, air pollution exposure, and characteristics of the built environment with childhood obesity risk. Cross-sectional biomarker results may suffer from reverse causality bias, whereby obesity status influenced the biomarker concentration.

When Pandemics Collide: The Impact of COVID-19 on Childhood Obesity

“…With children spending more time inside due to COVID-19 restrictions, indoor pollution especially from parental smoking, fine particulate matter, and nitrogen dioxide increase the likelihood of the child having overweight or obesity (Vrijheid et al, 2020). Children exposed to primary care giver"s smoking showed an increase in odds ratios for obesity at age three and five years, and it is hypothesized that tobacco smoke"s chemicals may lead to impaired metabolic and immune functions of the child increasing susceptibility to obesity (Sunday & Kabir, 2019).…”

Unravelling the chemical exposome in cohort studies: routes explored and steps to become comprehensive

“…HELIX undertook a variety of outcome assessments starting with one-exposure-one-outcome assessments to elaborate benefit-harm scenarios in order to cover different complexities of exposure scenarios [104]. These results were documented in various publications on blood pressure during pregnancy and in children [105,106], birth weight [68], fetal growth [2], lung function in children [3], and childhood obesity [103]. For this, HELIX used data of six European birth cohort studies with a total of 32,000 mother-child pairs with initial recruitments ranging from 1999 to 2007 and a representative gender ratio [104].…”

“…We found it useful to separate the exposure categories lifestyle, air pollution, integrative exposome groups and defined chemicals. Out of the 25 publications that were identified for the EU projects in relation to health outcomes, most associations established considered only a single or few exposures, while five HELIX publications explicitly covered exposome-based groupings; namely the pregnancy exposome [ 2 ], the early-life exposome [ 3 , 103 , 106 ], and the urban exposome [ 68 ]. HELIX so far published on health outcomes and their relations to integrative exposome groupings and to individual chemicals, while HEALS addressed defined chemicals and single lifestyle factors (as simple correlations and not as part of a specific, more comprehensive exposome concept).…”

Exposure to PM2.5 and Obesity Prevalence in the Greater Mexico City Area

“…Nevertheless, results from human studies on the association between PM 2.5 exposure and obesity remain mixed [ 12 ]. Some have found null associations [ 13 , 14 ], while several others point to an increased risk of obesity from PM 2.5 exposure at different life stages [ 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 ]. Therefore, the aim of this study was to analyze the association between past-year exposure to PM 2.5 with the prevalence of obesity in two representative samples (ENSANUT 2006 and 2012) of children, adolescents, and adults from the GMCA.…”