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Epidemiology. 2013 Nov;24(6):791-9. doi: 10.1097/EDE.0b013e3182a67822.

Prenatal bisphenol a urine concentrations and early rapid growth and overweight risk in the offspring.

Author information

1
From the aCentre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain; bHospital del Mar Research Institute (IMIM), Barcelona, Spain; cCIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain; dPompeu Fabra University, Barcelona, Spain; eDepartment of Nutrition, Gillings School of Public Health, University of North Carolina, Chapel Hill, NC; and fDepartment of Analytical Chemistry, University of Cordoba, Cordoba, Spain.

Abstract

BACKGROUND:

Increasing experimental evidence suggests that prenatal bisphenol A (BPA) exposure induces offspring weight gain, but these effects remain largely unexplored in humans. We examined the effects of prenatal BPA exposure on postnatal growth and obesity.

METHODS:

BPA concentrations were measured in two spot-urine samples collected in the 1st and 3rd trimesters of pregnancy from mothers in a Spanish birth cohort study (n = 402). We used the average of the two creatinine-adjusted BPA concentrations as the exposure variable. Rapid child growth was defined as a weight gain Z score >0.67 in the first 6 months of life. Age- and sex-specific Z scores for body mass index (BMI) were calculated at age 14 months and 4 years, based on the World Health Organization referent; overweight was defined as a BMI Z score greater than or equal to the 85th percentile. Age- and sex-specific waist circumference Z scores were calculated at age 14 months and 4 years using the analysis population mean.

RESULTS:

Twenty-six percent of children were rapid growers; 25% were overweight at 14 months and 21% at 4 years. Geometric mean BPA concentrations were 2.6 μg/g creatinine (standard deviation = 2.3) in 1st trimester and 2.0 (2.3) in 3rd trimester samples (Pearson r = 0.13). At 4 years, BPA exposure was associated with increased waist circumference (β per log10 μg/g = 0.28 [95% confidence interval = 0.01 to 0.57]) and BMI (β = 0.28 [-0.06 to 0.63]). BPA was not associated with obesity-related outcomes at earlier ages.

CONCLUSIONS:

This study provides some evidence for an association between prenatal BPA exposure and obesity-related outcomes in childhood, although not in infancy. The large uncertainties in BPA exposure assessment require that findings be interpreted with caution.

PMID:
24036610
DOI:
10.1097/EDE.0b013e3182a67822
[Indexed for MEDLINE]
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