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

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. 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. 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. 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.