Abstract

It has been hypothesized that environmental exposures at key development periods such as in utero play a role in childhood growth and obesity. To investigate whether in utero exposure to endocrine-disrupting chemicals, dichlorodiphenyltrichloroethane (DDT) and its metabolite, dichlorodiphenyldichloroethane (DDE), is associated with childhood physical growth, we took a novel statistical approach to analyze data from the CHAMACOS cohort study. To model heterogeneity in the growth patterns, we used a finite mixture model in combination with a data transformation to characterize body mass index (BMI) with four groups and estimated the association between exposure and group membership. In boys, higher maternal concentrations of DDT and DDE during pregnancy are associated with a BMI growth pattern that is stable until about age five followed by increased growth through age nine. In contrast, higher maternal DDT exposure during pregnancy is associated with a flat, relatively stable growth pattern in girls. This study suggests that in utero exposure to DDT and DDE may be associated with childhood BMI growth patterns, not just BMI level, and both the magnitude of exposure and sex may impact the relationship.

Highlights

  • The number of obese individuals has drastically increased recently worldwide [1]

  • A solution that we propose is to first transform the outcome by subtracting individualspecific means prior to using existing mixture model methods in order to temporarily remove the level in order to focus on growth [32]

  • We present a novel statistical analysis of the association of a well-known endocrine disruptor, the pesticide DDT and its metabolite DDE, with trajectories of childhood body mass index (BMI) in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) study, a longitudinal birth cohort study in an agricultural community in California

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Summary

Introduction

The number of obese individuals has drastically increased recently worldwide [1]. Obesity is likely caused by a complex combination of genetic, behavioral, and environmental factors. While much attention has been placed on curtailing overeating and encouraging physical activity, there have been many attempts to understand the biological mechanism behind the disease. Researchers have attempted to quantify the role of heredity using twin studies [2] and more recently, it has been suggested that early environmental factors may play a role. Prenatal exposure to endocrine-disrupting compounds (EDCs) is hypothesized to deregulate the metabolic system, disrupt growth regulation, and increase the risk of childhood obesity.

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