Abstract

BackgroundObesity and type-2 diabetes are on the rise and in utero exposure to environmental contaminants is a suspected contributing factor. Our objective was to examine associations between prenatal exposure to potential endocrine disrupting chemicals and markers of fetal metabolic dysfunction.MethodsThe Maternal-Infant Research on Environmental Chemicals Study (MIREC) recruited 2001 women during the first trimester of pregnancy from 10 Canadian sites. First trimester maternal urine was measured for 11 phthalate metabolites and bisphenol A (BPA). Leptin and adioponectin measured in 1,363 available umbilical cord blood samples served as markers of metabolic function. Restricted cubic spline curves were used to assess the relationship between continuous measures of phthalate and BPA levels and cord blood adipokines. Polytomous logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (CI) for the association between phthalates and BPA and both high (≥90th percentile) and low (≤10th percentile) fetal adiponectin and leptin, adjusting for confounding factors. Analyses were conducted for all subjects, overall, and separately by fetal sex.ResultsLeptin was significantly higher in female than male infants. We observed an inverse, non-linear relationship between BPA and adiponectin among males in the restricted cubic spline and linear regression analysis. Mono-(3-carboxypropyl) (MCPP) was associated with increased odds of high leptin among males in the polytomous logistic regression models (4th quartile OR = 3.5 95% CI: 1.1-11.6).ConclusionOur findings contribute to the growing body of evidence examining the influence of early life exposure on metabolic regulation and function. Associations between maternal exposure to chemicals and markers of metabolic function appear to be potentially sex specific. However, further investigation is required to determine whether in utero and childhood exposure to BPA and phthalates are associated with metabolic dysfunctions later in life.

Highlights

  • Obesity and type-2 diabetes are on the rise and in utero exposure to environmental contaminants is a suspected contributing factor

  • The objective of the present study was to assess the association between prenatal exposure to phthalates and bisphenol A (BPA) and fetal levels of adiponectin and leptin using data collected in the Maternal-Infant Research on Environmental Chemicals (MIREC) study, a multisite Canadian cohort study

  • Pre-pregnancy body mass index (BMI), parity, and cord blood adiponectin levels were associated with leptin

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Summary

Introduction

Obesity and type-2 diabetes are on the rise and in utero exposure to environmental contaminants is a suspected contributing factor. Diabetes, and metabolic syndrome are on the rise globally and within Canada. Between the years of 1980 and 2008, the global prevalence of obesity doubled from 6.4% to 12.0% [1]. In Canada, nearly 20% of girls and boys between 12–17 years of age were reportedly majority of the US and Canadian population [4,5], and have received recent attention for their potential obesogenic properties [6]. Experimental data has demonstrated that exposure to phthalates and BPA alters normal lipid metabolism and adipogenesis [7]. By binding to PPAR-γ receptors, a critical regulatory component of lipid metabolism and adipogenesis, phthalate exposure has the potential to promote weight gain [7,8]. BPA exhibits its effects on metabolic function by inducing adipocyte formation, promoting insulin resistance, and inhibiting adiponectin [9,10]

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