Urinary Free Bisphenol a and Bisphenol a Glucuronide Concentrations in a Sample of Neonates in Baltimore, Maryland

Abstract

Background: Bisphenol A (BPA) exposure is widespread in the general population. Public health concerns stem from its estrogenic properties. Poor glucuronidation capacity at birth may impede its conjugation to BPA glucuronide, a biologically inert form. Aim: To determine the impact of poor glucuronidation capacity on BPA toxicokinetics in healthy full-term neonates. Methods: Mothers and healthy full-term neonates were recruited at the Johns Hopkins Hospital in Baltimore, Maryland from December 2012 to July 2013. Urine samples were collected and a questionnaire administered at ages 3-6 and 7-28 days. A quality control protocol was implemented to reduce contamination of samples with BPA from field and laboratory sources. Free BPA and BPA glucuronide concentrations were quantified by high performance liquid chromatography, tandem mass spectrometry with dansyl chloride derivatization (LOQ=0.1 ug/L). BPA glucuronide concentrations were adjusted for the difference in the molecular weights of free BPA and BPA glucuronide. Results: BPA glucuronide was quantified in 71% of 78 urine samples from 44 neonates. No free BPA concentrations exceeded the LOQ in any sample. BPA glucuronide concentrations were higher at age 3-6 days (geometric mean: 0.25 ug BPA/L) than at age 7-28 days (geometric mean: 0.11 ug BPA/L). In a linear regression analysis that accounted for within-person correlation of BPA glucuronide concentrations (?=0.46), age group (ß=-0.5 [95% CI: -0.94, -0.06]) and breastfeeding (ß=-0.72 [95% CI: -1.4, -0.06]) were significantly associated with a decrease in urinary BPA glucuronide. Conclusions: Quantification of BPA glucuronide in these samples demonstrates exposure to and efficient glucuronidation of BPA during the neonatal period among healthy full-term neonates aged 3-6 and 7-28 days. These data include the first urinary BPA measurements in healthy full-term neonates in the first week of life. Formula intake may be a risk factor for BPA exposure.