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Early-life bisphenol a exposure and child body mass index: a prospective cohort study.

Braun JM, Lanphear BP, Calafat AM, Deria S, Khoury J, Howe CJ, Venners SA - Environ. Health Perspect. (2014)

Bottom Line: 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.All associations were attenuated without creatinine normalization.

View Article: PubMed Central - PubMed

Affiliation: Department of Epidemiology, Brown University School of Public Health, Brown University, Providence, Rhode Island, USA.

ABSTRACT

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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Related in: MedlinePlus

Urinary BPA concentrations during pregnancy at 16 and 26 weeks and the first 2 years of life among Cincinnati, Ohio, women and their children. Whiskers represent the minimum and maximum, box edges represent the 25th and 75th percentiles, the line in the box represents the median, and the diamond represents the arithmetic mean. The number of mothers/children for the average concentrations is greater than the individual concentrations because not all the same participants returned at the both visits.
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f1: Urinary BPA concentrations during pregnancy at 16 and 26 weeks and the first 2 years of life among Cincinnati, Ohio, women and their children. Whiskers represent the minimum and maximum, box edges represent the 25th and 75th percentiles, the line in the box represents the median, and the diamond represents the arithmetic mean. The number of mothers/children for the average concentrations is greater than the individual concentrations because not all the same participants returned at the both visits.

Mentions: Median urinary BPA concentrations were lower in women than in their children (Figure 1, Table 1; see also Supplemental Material, Table S2). Creatinine-normalized BPA concentrations at 16 and 26 weeks (Pearson r = 0.09) or 1 and 2 years (Pearson r = 0.10) were not correlated; however non-normalized concentrations were weakly correlated (Pearson r ≤ 0.3; see Supplemental Material, Table S3). Averaged creatinine-normalized maternal urinary BPA concentrations were not correlated with averaged children’s concentrations (Pearson r = 0.03, p = 0.67), but non-normalized concentrations were weakly correlated (Pearson r = 0.17, p < 0.01).


Early-life bisphenol a exposure and child body mass index: a prospective cohort study.

Braun JM, Lanphear BP, Calafat AM, Deria S, Khoury J, Howe CJ, Venners SA - Environ. Health Perspect. (2014)

Urinary BPA concentrations during pregnancy at 16 and 26 weeks and the first 2 years of life among Cincinnati, Ohio, women and their children. Whiskers represent the minimum and maximum, box edges represent the 25th and 75th percentiles, the line in the box represents the median, and the diamond represents the arithmetic mean. The number of mothers/children for the average concentrations is greater than the individual concentrations because not all the same participants returned at the both visits.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4216170&req=5

f1: Urinary BPA concentrations during pregnancy at 16 and 26 weeks and the first 2 years of life among Cincinnati, Ohio, women and their children. Whiskers represent the minimum and maximum, box edges represent the 25th and 75th percentiles, the line in the box represents the median, and the diamond represents the arithmetic mean. The number of mothers/children for the average concentrations is greater than the individual concentrations because not all the same participants returned at the both visits.
Mentions: Median urinary BPA concentrations were lower in women than in their children (Figure 1, Table 1; see also Supplemental Material, Table S2). Creatinine-normalized BPA concentrations at 16 and 26 weeks (Pearson r = 0.09) or 1 and 2 years (Pearson r = 0.10) were not correlated; however non-normalized concentrations were weakly correlated (Pearson r ≤ 0.3; see Supplemental Material, Table S3). Averaged creatinine-normalized maternal urinary BPA concentrations were not correlated with averaged children’s concentrations (Pearson r = 0.03, p = 0.67), but non-normalized concentrations were weakly correlated (Pearson r = 0.17, p < 0.01).

Bottom Line: 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.All associations were attenuated without creatinine normalization.

View Article: PubMed Central - PubMed

Affiliation: Department of Epidemiology, Brown University School of Public Health, Brown University, Providence, Rhode Island, USA.

ABSTRACT

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.

Show MeSH
Related in: MedlinePlus