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Published on: March 6, 2018
Early-life bisphenol a exposure and child body mass index: a prospective cohort study
Joseph M Braun1, Bruce P Lanphear, Antonia M Calafat
1Department of Epidemiology, Brown University School of Public Health, Brown University, Providence, Rhode Island, USA.
Insights
Early exposure to bisphenol A (BPA) did not increase childhood obesity risk. However, higher early-childhood BPA levels were linked to accelerated growth trajectories in children aged 2-5 years.
Area of Science:
- Environmental Health
- Pediatric Endocrinology
- Epidemiology
Background:
- Early-life exposure to bisphenol A (BPA) is a potential risk factor for childhood obesity.
- Prospective epidemiological data on this association are limited.
Purpose of the Study:
- To investigate the association between early-life BPA exposure and body mass index (BMI) from ages 2-5 years.
- To analyze BPA exposure during pregnancy and early childhood in relation to child BMI trajectories.
Main Methods:
- Urinary BPA concentrations were measured in pregnant women and children at ages 1 and 2.
- Child BMI z-scores were calculated annually from ages 2-5.
- Linear mixed models were used to assess associations between BPA levels and BMI outcomes.
Main Results:
- No significant association was found between prenatal or early-childhood BPA and child BMI at ages 2-5.
- A suggestive inverse association was observed, particularly in girls.
- Higher early-childhood BPA was associated with lower BMI at age 2 and accelerated BMI growth from ages 2-5.
Conclusions:
- Prenatal and early-childhood BPA exposure were not linked to increased BMI in early childhood.
- Elevated early-childhood BPA exposure correlated with accelerated growth during ages 2-5.
Background:
Early-life exposure to bisphenol A (BPA) may increase childhood obesity risk, but few prospective epidemiological studies have investigated this relationship.
Objective:
We sought to determine whether early-life exposure to BPA was associated with increased body mass index (BMI) at 2-5 years of age in 297 mother-child pairs from Cincinnati, Ohio (HOME Study).
Methods:
Urinary BPA concentrations were measured in samples collected from pregnant women during the second and third trimesters and their children at 1 and 2 years of age. BMI z-scores were calculated from weight/height measures conducted annually from 2 through 5 years of age. We used linear mixed models to estimate BMI differences or trajectories with increasing creatinine-normalized BPA concentrations.
Results:
After confounder adjustment, each 10-fold increase in prenatal (β = -0.1; 95% CI: -0.5, 0.3) or early-childhood (β = -0.2; 95% CI: -0.6, 0.1) BPA concentrations was associated with a modest and nonsignificant reduction in child BMI. These inverse associations were suggestively stronger in girls than in boys [prenatal effect measure modification (EMM) p-value = 0.30, early-childhood EMM p-value = 0.05], but sex-specific associations were imprecise. Children in the highest early-childhood BPA tercile had lower BMI at 2 years (difference = -0.3; 95% CI: -0.6, 0.0) and larger increases in their BMI slope from 2 through 5 years (BMI increase per year = 0.12; 95% CI: 0.07, 0.18) than children in the lowest tercile (BMI increase per year = 0.07; 95% CI: 0.01, 0.13). All associations were attenuated without creatinine normalization.
Conclusions:
Prenatal and early-childhood BPA exposures were not associated with increased BMI at 2-5 years of age, but higher early-childhood BPA exposures were associated with accelerated growth during this period.
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