Polycarbonate Bottle Use and Urinary Bisphenol A Concentrations

Department of Epidemiology, Harvard School of Public Health, Harvard University, Cambridge, Massachusetts, USA.
Environmental Health Perspectives (Impact Factor: 7.03). 09/2009; 117(9):1368-72. DOI: 10.1289/ehp.0900604
Source: PubMed

ABSTRACT Bisphenol A (BPA) is a high-production-volume chemical commonly used in the manufacture of polycarbonate plastic. Low-level concentrations of BPA in animals and possibly in humans may cause endocrine disruption. Whether ingestion of food or beverages from polycarbonate containers increases BPA concentrations in humans has not been studied.
We examined the association between use of polycarbonate beverage containers and urinary BPA concentrations in humans.
We conducted a nonrandomized intervention of 77 Harvard College students to compare urinary BPA concentrations collected after a washout phase of 1 week to those taken after an intervention week during which most cold beverages were consumed from polycarbonate drinking bottles. Paired t-tests were used to assess the difference in urinary BPA concentrations before and after polycarbonate bottle use.
The geometric mean urinary BPA concentration at the end of the washout phase was 1.2 microg/g creatinine, increasing to 2.0 microg/g creatinine after 1 week of polycarbonate bottle use. Urinary BPA concentrations increased by 69% after use of polycarbonate bottles (p < 0.0001). The association was stronger among participants who reported > or = 90% compliance (77% increase; p < 0.0001) than among those reporting < 90% compliance (55% increase; p = 0.03), but this difference was not statistically significant (p = 0.54).
One week of polycarbonate bottle use increased urinary BPA concentrations by two-thirds. Regular consumption of cold beverages from polycarbonate bottles is associated with a substantial increase in urinary BPA concentrations irrespective of exposure to BPA from other sources.

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Available from: Xiaoyun Ye, Mar 25, 2015
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    • "It is widely used to line metal cans, water pipes [2], baby bottles, drinking cups [3], dental sealants [4] [5], and many other household appliances. Studies have shown that for incomplete polymerization and for degradation of the polymer, bisphenol A can leach out from food and beverage containers [6], as well as from dental sealants and composites under normal conditions of use. Bisphenol A has been found not only in environmental samples, including air, water, sewage sludge, soil, and dust [7] [8] [9], but also in specimens of human body fluids, such as plasma, umbilical cord blood, placental tissue, amniotic fluid, follicular fluid, and breast milk. "
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    ABSTRACT: The present investigation was an attempt to elucidate oxidative stress induced by bisphenol A on erythrocytes and its amelioration by green tea extract. For this, venous blood samples from healthy human adults were collected in EDTA vials and used for preparation of erythrocytes suspension. When erythrocyte suspensions were treated with different concentrations of BPA/H2O2, a dose-dependent increase in hemolysis occurred. Similarly, when erythrocytes suspensions were treated with either different concentrations of H2O2 (0.05–0.25 mM) along with BPA (50 μg/mL) or 0.05 mM H2O2 along with different concentrations of BPA (50–250 μg/mL), dose-dependent significant increase in hemolysis occurred. The effect of BPA and H2O2 was found to be additive. For the confirmation, binding capacity of bisphenol A with erythrocyte proteins (hemoglobin, catalase, and glutathione peroxidase) was inspected using molecular docking tool, which showed presence of various hydrogen bonds of BPA with the proteins. The present data clearly indicates that BPA causes oxidative stress in a similar way as H2O2 . Concurrent addition of different concentrations (10–50 μg/mL) of green tea extract to reaction mixture containing high dose of bisphenol A (250 μg/mL) caused concentration-dependent amelioration in bisphenol A-induced hemolysis. The effect was significant (P < 0.05). It is concluded that BPA-induced oxidative stress could be significantly mitigated by green tea extract.
    08/2014; 2014:259763. DOI:10.1155/2014/259763
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    • "Recently, BPA has been widely detected in various human tissues such as blood, fetal serum during pregnancy, amniotic fluid, follicular fluid, placental tissue, umbilical cord blood, and urine (Lee et al., 2008; Vandenberg et al., 2010; Wan et al., 2010). For example, BPA has been detected in 100% of urine samples from Chinese children with a mean concentration of 3.00 ng/mL (Li et al., 2013), and in 96% of urine samples from American college students with a mean concentration of 1.3 ng/mL (Carwile et al., 2009). BPA has been implicated as a potential endocrine disrupting chemical (EDC), primarily as a weak estrogen receptor ␣/␤ (ER␣/␤) agonist (Vandenberg et al., 2009). "
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    ABSTRACT: Sertoli cells play a pivotal role in supporting proliferation of germ cells and differentiation during spermatogenesis in mammals. Nanomolar concentrations of Bisphenol A (BPA) can significantly stimulate the proliferation of mouse immature Sertoli (TM4) cells. However, mechanisms by which BPA caused these effects were still unclear. In the present study, an inverse U-shaped curve was observed when treating TM4 cells with increasing doses of BPA: 1 to 10 nM BPA significantly stimulated the proliferation of TM4 cells and increased the proportion of cells in S phase; > 1 μM BPA caused lesser proliferation of cells. Exposure of TM4 cells to G15 or ICI 182,780, which are specific antagonists of GPR30 and estrogen receptor α/β (ERα/β), respectively, abolished BPA-induced proliferation of cells, which suggests that both GPR30 and ERα/β were involved in the observed effects of BPA. Furthermore, exposure to BPA caused rapid (5 min) activation of ERK1/2 via both GPR30 and ERα/β. Blocking the GPR30/EGFR signal transduction pathway by antagonists suppressed both phosphorylation of ERK and BPA-induced cell proliferation. BPA up-regulated mRNA and protein expression of GPR30 in a concentration-dependent manner. In summary, the results reported here indicated that activating ERK1/2 through GPR30 and ERα/β is involved in low doses of BPA that promoted growth of Sertoli TM4 cells. The GPR30/EGFR/ERK signal is the downstream transduction pathway in BPA-induced proliferation of TM4 Sertoli cells.
    Toxicology Letters 04/2014; 226(1). DOI:10.1016/j.toxlet.2014.01.035 · 3.36 Impact Factor
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    • "It leaches during heating from microwave containers into the food, into beverages and in polycarbonate bottles from repeated usage and contact with acidic and alkaline content (Brotons et al., 1995). In recent years, there has been an increase in the frequency of human exposure due to increasing use of polycarbonate plastics and epoxy resins (Carwile et al., 2009; Olea et al., 1996; Vandenberg et al., 2007, 2010). Although BPA have reduced affinity to bind to estrogen receptors as compared to 17␤-estradiol, it possesses equivalent activational capacity of the nonclassical estrogen receptors (Krishnan et al., 1993). "
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    ABSTRACT: Bisphenol A (BPA) is used in the production of polycarbonate plastics and epoxy resins. Our previous studies have demonstrated that neonatal exposure of male rats to BPA causes decrease in sperm count and motility, increase in postimplantation loss (POL), ultimately leading to subfertility during adulthood. Epigenetic mechanisms such as DNA methylation play an important role in embryo development. DNA methyltransferases (Dnmts) are the key players involved in regulating DNA methylation marks. The objective of the present study was to determine the mechanism involved in resorption of embryo as a result of BPA exposure. The results of the present study demonstrate that neonatal exposure of male rats to BPA down regulates the gene expression of Dnmts and related transcription factors in resorbed embryos as compared with the viable embryo. Thereby, suggesting that BPA may have altered the sperm epigenome, which might have affected the embryo development and leading to an increase in the POL. © 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:337-343, 2012; View this article online at DOI 10:1002/jbt.21425.
    Journal of Biochemical and Molecular Toxicology 09/2012; 26(9):337-43. DOI:10.1002/jbt.21425 · 1.32 Impact Factor
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