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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 BMI z-scores slopes between 2 and 5 years of age by prenatal and early-childhood BPA tercile among Cincinnati, Ohio, women and their children. 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 BPA terciles: 1st tercile: 0.4–1.6 μg/g creatinine; 2nd tercile: 1.6–2.6 μg/g creatinine; and 3rd tercile: 2.6–49 μg/g creatinine. Early-childhood BPA terciles: 1st tercile: 2.1–11 μg/g creatinine; 2nd tercile: 11–20 μg/g creatinine; and 3rd tercile: 20–314 μg/g creatinine. Prenatal BPA × age interaction p-values: 2nd vs. 1st tercile: 0.42; 3rd vs. 1st tercile: 0.43. Early-childhood BPA × age interaction p-values: 2nd vs. 1st tercile: 0.51; 3rd vs. 1st tercile: 0.22.
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f3: Adjusted BMI z-scores slopes between 2 and 5 years of age by prenatal and early-childhood BPA tercile among Cincinnati, Ohio, women and their children. 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 BPA terciles: 1st tercile: 0.4–1.6 μg/g creatinine; 2nd tercile: 1.6–2.6 μg/g creatinine; and 3rd tercile: 2.6–49 μg/g creatinine. Early-childhood BPA terciles: 1st tercile: 2.1–11 μg/g creatinine; 2nd tercile: 11–20 μg/g creatinine; and 3rd tercile: 20–314 μg/g creatinine. Prenatal BPA × age interaction p-values: 2nd vs. 1st tercile: 0.42; 3rd vs. 1st tercile: 0.43. Early-childhood BPA × age interaction p-values: 2nd vs. 1st tercile: 0.51; 3rd vs. 1st tercile: 0.22.

Mentions: There was not strong evidence that maternal urinary BPA concentrations were positively associated with rapid growth between 2 and 5 years of age (Figure 3) (age × BPA interaction term p-value = 0.26). There was stronger evidence that BMI slopes increased more rapidly between 2 and 5 years among children in the highest tercile of early-childhood BPA concentrations (BMI increase per year = 0.12; 95% CI: 0.07, 0.18) compared with children in the first (BMI increase per year = 0.07; 95% CI: 0.01, 0.13) or second (BMI increase per year = 0.04; 95% CI: –0.02, 0.11) terciles (age × BPA tercile interaction p-value = 0.14). This increase was coincident with lower BMI at 2 years of age among children in the third tercile compared with children in the first tercile (BMI difference = –0.3; 95% CI: –0.6, 0.0), though BMI differences were not evident at 5 years of age (BMI difference = –0.1; 95% CI: –0.5, 0.2). BMI slopes no longer differed when early-childhood BPA concentrations were not creatinine-normalized (first tercile = 0.04; 95% CI: –0.02, 0.10; second tercile = 0.09; 95% CI: 0.04, 0.15; third tercile = 0.09; 95% CI: 0.03, 0.15; p-value for interaction = 0.42).


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 BMI z-scores slopes between 2 and 5 years of age by prenatal and early-childhood BPA tercile among Cincinnati, Ohio, women and their children. 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 BPA terciles: 1st tercile: 0.4–1.6 μg/g creatinine; 2nd tercile: 1.6–2.6 μg/g creatinine; and 3rd tercile: 2.6–49 μg/g creatinine. Early-childhood BPA terciles: 1st tercile: 2.1–11 μg/g creatinine; 2nd tercile: 11–20 μg/g creatinine; and 3rd tercile: 20–314 μg/g creatinine. Prenatal BPA × age interaction p-values: 2nd vs. 1st tercile: 0.42; 3rd vs. 1st tercile: 0.43. Early-childhood BPA × age interaction p-values: 2nd vs. 1st tercile: 0.51; 3rd vs. 1st tercile: 0.22.
© Copyright Policy - public-domain
Related In: Results  -  Collection

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

f3: Adjusted BMI z-scores slopes between 2 and 5 years of age by prenatal and early-childhood BPA tercile among Cincinnati, Ohio, women and their children. 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 BPA terciles: 1st tercile: 0.4–1.6 μg/g creatinine; 2nd tercile: 1.6–2.6 μg/g creatinine; and 3rd tercile: 2.6–49 μg/g creatinine. Early-childhood BPA terciles: 1st tercile: 2.1–11 μg/g creatinine; 2nd tercile: 11–20 μg/g creatinine; and 3rd tercile: 20–314 μg/g creatinine. Prenatal BPA × age interaction p-values: 2nd vs. 1st tercile: 0.42; 3rd vs. 1st tercile: 0.43. Early-childhood BPA × age interaction p-values: 2nd vs. 1st tercile: 0.51; 3rd vs. 1st tercile: 0.22.
Mentions: There was not strong evidence that maternal urinary BPA concentrations were positively associated with rapid growth between 2 and 5 years of age (Figure 3) (age × BPA interaction term p-value = 0.26). There was stronger evidence that BMI slopes increased more rapidly between 2 and 5 years among children in the highest tercile of early-childhood BPA concentrations (BMI increase per year = 0.12; 95% CI: 0.07, 0.18) compared with children in the first (BMI increase per year = 0.07; 95% CI: 0.01, 0.13) or second (BMI increase per year = 0.04; 95% CI: –0.02, 0.11) terciles (age × BPA tercile interaction p-value = 0.14). This increase was coincident with lower BMI at 2 years of age among children in the third tercile compared with children in the first tercile (BMI difference = –0.3; 95% CI: –0.6, 0.0), though BMI differences were not evident at 5 years of age (BMI difference = –0.1; 95% CI: –0.5, 0.2). BMI slopes no longer differed when early-childhood BPA concentrations were not creatinine-normalized (first tercile = 0.04; 95% CI: –0.02, 0.10; second tercile = 0.09; 95% CI: 0.04, 0.15; third tercile = 0.09; 95% CI: 0.03, 0.15; p-value for interaction = 0.42).

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