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 (cross-sectionally), 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. https://doi.org/10.1289/EHP5975

中文翻译：

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早期环境暴露和儿童肥胖：一种暴露体范围的方法。

摘要

背景：

越来越多的人怀疑化学和非化学环境暴露会影响肥胖的发展，尤其是在生命早期，但研究大多考虑单一暴露组。

目标：

我们的研究旨在使用暴露组范围的方法系统地评估各种早期环境暴露与儿童肥胖之间的关联。

方法：

HELIX（人类早期生活暴露组）研究测量了来自 6 个 6-11 岁欧洲出生队列的 1,301 名儿童的儿童体重指数 (BMI)、腰围、皮褶厚度和体脂肪量。我们估计了 77 次产前暴露和 96 次儿童暴露（横截面），包括室内和室外空气污染物、建筑环境、绿地、吸烟和化学污染物的生物标志物（持久性有机污染物、金属、邻苯二甲酸盐、苯酚和杀虫剂） . 我们使用暴露范围关联研究 (ExWAS) 来独立筛选所有暴露-结果关联，并使用删除-替换-添加 (DSA) 变量选择算法来构建最终的多重暴露模型。

结果：

超重和肥胖的患病率为28.8%。母亲吸烟是唯一与较高儿童 BMI 相关的产前暴露变量（z分数增加 0.28，95% 置信区间：0.09，0.48，主动与不吸烟）。对于儿童暴露，多重暴露模型确定了家中的颗粒物和二氧化氮空气污染，表明二手烟暴露的尿可替宁水平，以及居住在人口稠密地区和设施较少的地区与儿童 BMI 增加有关。儿童血液中铜和铯的水平与较高的 BMI 相关，而有机氯污染物、钴和钼的水平与较低的 BMI 相关。对于其他肥胖结果也发现了类似的结果。

讨论：

这是对许多疑似环境致肥胖因素的首次全面和系统分析，加强了吸烟、空气污染暴露和建筑环境特征与儿童肥胖风险之间关联的证据。横断面生物标志物结果可能存在反向因果偏倚，即肥胖状况影响生物标志物浓度。https://doi.org/10.1289/EHP5975