Urinary Concentrations of Bisphenol A and 4-Nonylphenol in a Human Reference Population

By A. Calafat, Z. Kuklenyik, J. Reidy, S. Caudill, John Ekong, L. Needham. Environmental Health Perspectives, 2004

1,039 citations recorded by the source corpus.

Bisphenol A (BPA) is used to manufacture polycarbonate plastic and epoxy resins, which are used in baby bottles, as protective coatings on food containers, and for composites and sealants in dentistry. 4-Nonylphenol (NP) is used to make nonylphenol ethoxylates, nonionic surfactants applied as emulsifying, wetting, dispersing, or stabilizing agents in industrial, agricultural, and domestic consumer products. The potential for human exposure to BPA and NP is high because of their widespread use. We measured BPA and NP in archived urine samples from a reference population of 394 adults in the United States using isotope-dilution gas chromatography/mass spectrometry. The concentration ranges of BPA and NP were similar to those observed in other human populations. BPA was detected in 95% of the samples examined at concentrations ≥0.1 μg/L urine; the geometric mean and median concentrations were 1.33 μg/L (1.36 μg/g creatinine) and 1.28 μg/L (1.32 μg/g creatinine), respectively; the 95th percentile concentration was 5.18 μg/L (7.95 μg/g creatinine). NP was detected in 51% of the samples examined ≥0.1 μg/L. The median and 95th percentile concentrations were < 0.1 μg/L and 1.57 μg/L (1.39 μg/g creatinine), respectively. The frequent detection of BPA suggests widespread exposure to this compound in residents of the United States. The lower frequency of detection of NP than of BPA could be explained by a lower exposure of humans to NP, by different pharmacokinetic factors (i.e., absorption, distribution, metabolism, elimination), by the fact that 4-n-nonylphenol—the measured NP isomer—represents a small percentage of the NP used in commercial mixtures, or a combination of all of the above. Additional research is needed to determine the best urinary biomarker(s) to assess exposure to NP. Despite the sample population’s nonrepresentativeness of the U.S. population (although sample weights were used to improve the extent to which the results represent the U.S. population) and relatively small size, this study provides the first reference range of human internal dose levels of BPA and NP in a demographically diverse human population.

Subfields: Cancer Research, Health, Toxicology and Mutagenesis

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Citations in the corpus

Endocrine disruptors: from endocrine to metabolic disruption. (2011, background): “In a reference study in the United States, as many as 95% of human urine samples contained detectable levels of BPA in a range that is predicted to be biologically active (38, 57).”
Human exposure to bisphenol A (BPA). (2007, background): “With regard to measurable background levels of BPA, there are many other estrogenic environmental contaminants as well as contaminants with other modes of activity that are present in most people examined [31,32].”
Large effects from small exposures. III. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. (2006, background): “The higher-than-predicted tissue levels of parent BPA in human populations in developed countries, including a study as part of the National Health Survey by the Centers for Disease Control and Prevention (CDC) that detected BPA in over 95% of samples (13), suggests that exposure to significant amou”
Urinary, Circulating, and Tissue Biomonitoring Studies Indicate Widespread Exposure to Bisphenol A (2010, neutral): “In the United States, the Centers for Disease Control and Prevention (CDC) is the major source for information on human exposures to a multi tude of environmental contaminants and has developed sensitive assays to reliably measure them (CDC 2008; Kuklenyik et al. 2009).”
Exposure of the U.S. Population to Bisphenol A and 4-tertiary-Octylphenol: 2003–2004 (2007, methodology): “…the last decade, data on the urinary concentrations of BPA in selected populations of various countries have become available (Arakawa et al. 2004; Calafat et al. 2005; Fujimaki et al. 2004; Kim et al. 2003; Liu et al. 2005; Matsumoto et al. 2003; Miyamoto and Kotake 2006; Ouchi and Watanabe…”
A review of dietary and non-dietary exposure to bisphenol-A. (2012, background): “In a study of Calafat et al. (2009), BPA was analysed in urine from 42 low-birth-weight infants in neonatal intensive care Table 4”
Bisphenol A and human health: a review of the literature. (2013, background): “Further, because BPA exposure in humans is likely 4 continuous [10-12] long-term oxidative stress and inflammation, possibly induced by 5”
Endocrine disruptors and reproductive health: the case of bisphenol-A. (2006, methodology): “BPA has been measured in the serum and urine of adult men and women ( Calafat et al., 2005; Takeuchi and Tsutsumi, 2002) and in amniotic fluid, fetal plasma and placental tissue (Ikezuki et al., 2002; Schonfelder et al., 2002).”