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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

Adjusted change in child BMI z-score between 2 and 5 years of age with a 10-fold increase in maternal or early-childhood urinary BPA concentrations among Cincinnati, Ohio, women and their children, stratified by child sex. Adjusted for maternal race (white, black, and other), marital status (married living together, unmarried living together, and unmarried living alone), parity (0, 1, ≥ 2), age at delivery (continuous, years), household income (continuous, $10,000 increments), education (< high school, high school, some college, and ≥ bachelor’s degree), employment (any and none), insurance (private and public/none), BMI at 16 weeks (continuous, kg/m2), depressive symptoms at baseline (continuous), and prenatal serum cotinine (continuous, log10-transformed). Prenatal effect-measure modification p-values: with creatinine: 0.30; no creatinine: 0.39. Early-childhood effect-measure modification p-values: with creatinine: 0.05; no creatinine: 0.06. Error bars represent 95% CIs.
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f2: Adjusted change in child BMI z-score between 2 and 5 years of age with a 10-fold increase in maternal or early-childhood urinary BPA concentrations among Cincinnati, Ohio, women and their children, stratified by child sex. Adjusted for maternal race (white, black, and other), marital status (married living together, unmarried living together, and unmarried living alone), parity (0, 1, ≥ 2), age at delivery (continuous, years), household income (continuous, $10,000 increments), education (< high school, high school, some college, and ≥ bachelor’s degree), employment (any and none), insurance (private and public/none), BMI at 16 weeks (continuous, kg/m2), depressive symptoms at baseline (continuous), and prenatal serum cotinine (continuous, log10-transformed). Prenatal effect-measure modification p-values: with creatinine: 0.30; no creatinine: 0.39. Early-childhood effect-measure modification p-values: with creatinine: 0.05; no creatinine: 0.06. Error bars represent 95% CIs.

Mentions: Inverse associations between maternal urinary BPA concentrations and child BMI were slightly stronger among girls (β = –0.4; 95% CI: –0.9, 0.2; n = 165) compared with boys (β = 0.0; 95% CI: –0.5, 0.6; n = 132), although the EMM p-value did not reach conventional levels of significance (p = 0.30) (Figure 2). The evidence for EMM was stronger for early-childhood urinary BPA concentrations (p = 0.05), where higher concentrations were associated with lower child BMI among girls (β = –0.6; 95% CI: –1.1, –0.1; n = 155) than among boys (β = 0.1; 95% CI: –0.4, 0.5; n = 130). The magnitude of the differences between the sexes was attenuated when BPA concentrations were not creatinine-normalized (see Supplemental Material, Table S7).


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)

Adjusted change in child BMI z-score between 2 and 5 years of age with a 10-fold increase in maternal or early-childhood urinary BPA concentrations among Cincinnati, Ohio, women and their children, stratified by child sex. Adjusted for maternal race (white, black, and other), marital status (married living together, unmarried living together, and unmarried living alone), parity (0, 1, ≥ 2), age at delivery (continuous, years), household income (continuous, $10,000 increments), education (< high school, high school, some college, and ≥ bachelor’s degree), employment (any and none), insurance (private and public/none), BMI at 16 weeks (continuous, kg/m2), depressive symptoms at baseline (continuous), and prenatal serum cotinine (continuous, log10-transformed). Prenatal effect-measure modification p-values: with creatinine: 0.30; no creatinine: 0.39. Early-childhood effect-measure modification p-values: with creatinine: 0.05; no creatinine: 0.06. Error bars represent 95% CIs.
© Copyright Policy - public-domain
Related In: Results  -  Collection

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

f2: Adjusted change in child BMI z-score between 2 and 5 years of age with a 10-fold increase in maternal or early-childhood urinary BPA concentrations among Cincinnati, Ohio, women and their children, stratified by child sex. Adjusted for maternal race (white, black, and other), marital status (married living together, unmarried living together, and unmarried living alone), parity (0, 1, ≥ 2), age at delivery (continuous, years), household income (continuous, $10,000 increments), education (< high school, high school, some college, and ≥ bachelor’s degree), employment (any and none), insurance (private and public/none), BMI at 16 weeks (continuous, kg/m2), depressive symptoms at baseline (continuous), and prenatal serum cotinine (continuous, log10-transformed). Prenatal effect-measure modification p-values: with creatinine: 0.30; no creatinine: 0.39. Early-childhood effect-measure modification p-values: with creatinine: 0.05; no creatinine: 0.06. Error bars represent 95% CIs.
Mentions: Inverse associations between maternal urinary BPA concentrations and child BMI were slightly stronger among girls (β = –0.4; 95% CI: –0.9, 0.2; n = 165) compared with boys (β = 0.0; 95% CI: –0.5, 0.6; n = 132), although the EMM p-value did not reach conventional levels of significance (p = 0.30) (Figure 2). The evidence for EMM was stronger for early-childhood urinary BPA concentrations (p = 0.05), where higher concentrations were associated with lower child BMI among girls (β = –0.6; 95% CI: –1.1, –0.1; n = 155) than among boys (β = 0.1; 95% CI: –0.4, 0.5; n = 130). The magnitude of the differences between the sexes was attenuated when BPA concentrations were not creatinine-normalized (see Supplemental Material, Table S7).

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