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Prenatal Bisphenol A Urine Concentrations and Early Rapid Growth and Overweight Risk in the Offspring

Valvi, Damaskini; Casas, Maribel; Mendez, Michelle A.; Ballesteros-Gómez, Ana; Luque, Noelia; Rubio, Soledad; Sunyer, Jordi; Vrijheid, Martine

doi: 10.1097/EDE.0b013e3182a67822

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.

Supplemental Digital Content is available in the text.

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.

This study was funded by grants from the RecerCaixa (Register number: 2010ACUP 00349), the “Instituto Carlos III” (Red INMA G03/176, CB06/02/0041, and predoctoral grant PFIS 2010, Register number: FI10/00399), the Spanish Ministry of Health (FIS-PI041436, FIS-PI081151), the Generalitat de Catalunya-CIRIT (1999SGR 00241), and the Fundació Roger Torné.

The authors declare they have no competing financial interests.

Supplemental digital content is available through direct URL citations in the HTML and PDF versions of this article ( This content is not peer-reviewed or copy-edited; it is the sole responsibility of the author.

Correspondence: Damaskini Valvi, Centre for Research in Environmental Epidemiology (CREAL), 88 Dr.Aiguader St, 08003 Barcelona, Spain. E-mail:

Received February 20, 2013

Accepted May 21, 2013

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