title: Early-life bisphenol a exposure and child body mass index: a prospective cohort study.
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.
authors: Department of Epidemiology, Brown University School of Public Health, Brown University, Providence, Rhode Island, USA.
authors: Joseph M
authors: JM
authors: Braun
authors: Bruce P
authors: BP
authors: Lanphear
authors: Antonia M
authors: AM
authors: Calafat
authors: Sirad
authors: S
authors: Deria
authors: Jane
authors: J
authors: Khoury
authors: Chanelle J
authors: CJ
authors: Howe
authors: Scott A
authors: SA
authors: Venners
mesh_terms: D000328:Adult; D001559:Benzhydryl Compounds / Q000633:toxicity / Q000652:urine*; D015992:Body Mass Index; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D052244:Endocrine Disruptors / Q000633:toxicity / Q000652:urine*; D005260:Female; D006130:Growth Disorders / Q000453:epidemiology; D006801:Humans; D008297:Male; D018811:Maternal Exposure / Q000009:adverse effects* / Q000706:statistics & numerical data; D009820:Ohio; D010636:Phenols / Q000633:toxicity / Q000652:urine*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011446:Prospective Studies; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D052244:Endocrine Disruptors; D010636:Phenols; C006780:bisphenol A; D000098826:Bisphenol A Compounds