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Original Articles

Age-Related Trends in Urinary Excretion of Bisphenol A in Australian Children and Adults: Evidence from a Pooled Sample Study Using Samples of Convenience

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Pages 1039-1055 | Received 23 Jun 2013, Accepted 12 Aug 2013, Published online: 04 Nov 2013
 

Abstract

Bisphenol A (BPA or 4,4′-(propane-2,2-diyl)diphenol) is a chemical intermediate in the production of polycarbonate and epoxy resins, and is used in a wide range of applications. BPA has attracted significant attention in the past decade due to its frequency of detection in human populations worldwide, and has demonstrated animal toxicity and potential impact on human health, particularly during critical periods of development. The aim of this study was to perform a preliminary assessment of age-related trends in urinary concentration and to estimate daily excretion of BPA in Australian children (aged >0 to <5 yr) and adults (≥15 to <75 yr). This was achieved using 79 samples pooled by age and gender, created from 868 individual samples of convenience collected as part of routine, community-based pathology testing. Total BPA was analyzed using online solid phase extraction (SPE)–liquid chromatography tandem mass spectrometry (LC-MS/MS) and detected in all samples with a range of 0.65–265 ng/ml. No significant differences were observed between males and females. A urine flow model was constructed from published values and was used to provide an estimate of daily excretion per unit body weight for each pooled sample. The daily excretion estimates ranged from 26.2 to 18,200 ng/kg-d for children, and from 20.1 to 165 ng/kg-d for adults. Urinary concentrations and estimated excretion rates were inversely associated with age, and estimated daily excretion in infants and young children was significantly higher than in adults (geometric mean: 107 and 47.0 ng/kg-d, respectively). Higher excretion of BPA in children may be explained by their higher food consumption relative to body weight compared to adults and adolescents, and may also reflect alternative exposure pathways and sources.

Acknowledgments

The authors thank Nathaniel Price and the laboratory staff at Sullivan Nicolaides Pathology Taringa for their assistance with sample collection, and James Milton for technical support.

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