Article

Exposure to Bisphenol A and Other Phenols in Neonatal Intensive Care Unit Premature Infants

Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia 30341, USA.
Environmental Health Perspectives (Impact Factor: 7.98). 05/2009; 117(4):639-44. DOI: 10.1289/ehp.0800265
Source: PubMed

ABSTRACT

We previously demonstrated that exposure to polyvinyl chloride plastic medical devices containing di(2-ethylhexyl) phthalate (DEHP) was associated with higher urinary concentrations of several DEHP metabolites in 54 premature infants in two neonatal intensive care units than in the general population. For 42 of these infants, we evaluated urinary concentrations of several phenols, including bisphenol A (BPA), in association with the use of the same medical devices.
We measured the urinary concentrations of free and total (free plus conjugated) species of BPA, triclosan, benzophenone-3, methyl paraben, and propyl paraben.
The percentage of BPA present as its conjugated species was > 90% in more than three-quarters of the premature infants. Intensity of use of products containing DEHP was strongly associated with BPA total concentrations but not with any other phenol. Adjusting for institution and sex, BPA total concentrations among infants in the group of high use of DEHP-containing products were 8.75 times as high as among infants in the low use group (p < 0.0001). Similarly, after adjusting for sex and DEHP-containing product use category, BPA total concentrations among infants in Institution A were 16.6 times as high as those among infants in Institution B (p < 0.0001).
BPA geometric mean urinary concentration (30.3 microg/L) among premature infants undergoing intensive therapeutic medical interventions was one order of magnitude higher than that among the general population. Conjugated species were the primary urinary metabolites of BPA, suggesting that premature infants have some capacity to metabolize BPA. The differences in exposure to BPA by intensity of use of DEHP-containing medical products highlight the need for further studies to determine the specific source(s) of exposure to BPA.

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Available from: Jennifer Weuve, May 17, 2014
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    • "Bisphenol A (BPA) is an endocrine disrupting chemical (EDC) released from polycarbonate plastics and linings of food and beverage containers that contaminates the consumed contents of the container [1] [2] [3]. Consumption of BPA-contaminated foods and beverages is the major route of exposure in humans, with additional exposure occurring through handling of thermal receipt paper, application of dental sealants, and transfer from medical equipment [4] [5] [6]. Supporting widespread and prolonged human exposure to BPA, measurable levels of BPA metabolites were found in over 93% of human urine samples in the 2003–2004 National Abbreviations: EE, 17-ethinyl estradiol; E2, 17-estradiol; BPA, bisphenol A; DES, diethylstilbestrol; EDC, endocrine disrupting chemical; EPF, endometrial periglandular fibrosis; ECM, extracellular matrix; MMP, matrix metalloproteinase; NOAEL, no observed adverse effect level; TIMPs, tissue inhibitors of metallopro- teinases. "
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    ABSTRACT: Bisphenol A (BPA) is an endocrine disrupting chemical (EDC) with known estrogenic activity. Exposure to BPA in adult mice was shown previously to increase uterine pathology with associated alterations in the immune response and fibrosis. Reported here are uterine histopathology findings from CD1 mice exposed to BPA or 17α-ethinyl estradiol at multiple doses from conception through postnatal day 90. Along with uterine pathology, impacts of exposure on collagen accumulation and F4/80 positive macrophage numbers, as an indicator of immune response in the endometrium and myometrium, are presented. These companion data are from offspring (F1) of the dams analyzed for effects of adult exposures published in the Reproductive Toxicology manuscript titled “Strain-Specific Induction of Endometrial Periglandular Fibrosis in Mice Exposed during Adulthood to the Endocrine Disrupting Chemical Bisphenol A” (doi: 10.1016/j.reprotox.2015.08.001).
    Full-text · Article · Nov 2015
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    • "In 2003, more than 6 billion pounds of BPA were produced worldwide [5], and production is expected to exceed 5.4 million tons this year (for detailed international market analysis, see Bisphenol A (BPA): 2015 World Market Outlook and Forecast up to 2019 from mcgroup.co.uk). The United States Environmental Protection Agency (EPA) estimates that over 1 million pounds of BPA leaches into the environment each year and over 90% of tested humans have detectable BPA in their systems with the highest levels found in infants and children [6] [7] [8] [9] [10] [11]. BPA is an estrogenic compound [12]. "
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    ABSTRACT: The estrogenic properties of bisphenol A (BPA), a ubiquitous synthetic monomer that can leach into the food and water supply, have prompted considerable research into exposure-associated health risks in humans. Endocrine-disrupting properties of BPA suggest it may impact developmental plasticity during early life, predisposing individuals to disease at doses below the oral reference dose (RfD) established by the Environmental Protection Agency in 1982. Herein, we review the current in vivo literature evaluating the carcinogenic properties of BPA. We conclude that there is substantial evidence from rodent studies indicating that early-life BPA exposures below the RfD lead to increased susceptibility to mammary and prostate cancer. Based on the definitions of "carcinogen" put forth by the International Agency for Research on Cancer and the National Toxicology Program, we propose that BPA may be reasonably anticipated to be a human carcinogen in the breast and prostate due to its tumor promoting properties.
    Full-text · Article · Oct 2015 · Reproductive Toxicology
  • Source
    • "Bisphenol A (BPA) is an endocrine disrupting chemical (EDC) released from polycarbonate plastics and linings of food and beverage containers that contaminates the consumed contents of the container [1] [2] [3]. Consumption of BPA-contaminated foods and beverages is the major route of exposure in humans, with additional exposure occurring through handling of thermal receipt paper, application of dental sealants, and transfer from medical equipment [4] [5] [6]. Supporting widespread and prolonged human exposure to BPA, measurable levels of BPA metabolites were found in over 93% of human urine samples in the 2003–2004 National Abbreviations: EE, 17-ethinyl estradiol; E2, 17-estradiol; BPA, bisphenol A; DES, diethylstilbestrol; EDC, endocrine disrupting chemical; EPF, endometrial periglandular fibrosis; ECM, extracellular matrix; MMP, matrix metalloproteinase; NOAEL, no observed adverse effect level; TIMPs, tissue inhibitors of metallopro- teinases. "
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    ABSTRACT: The aim of this study was to compare effects of bisphenol A (BPA) on collagen accumulation in uteri of two mouse strains. Adult C57Bl/6N and CD-1 mice were exposed to dietary BPA (0.004-40mg/kg/day) or 17α-ethinyl estradiol (0.00002-0.001mg/kg/day) as effect control. An equine endometrosis-like phenotype with increased gland nesting and periglandular collagen accumulation was characteristic of unexposed C57Bl/6N, but not CD-1, endometrium. BPA non-monotonically increased gland nest density and periglandular collagen accumulation in both strains. Increased collagen I and III expression, decreased matrix metalloproteinase 2 (MMP2) and MMP14 expression, and increased immune response were associated with the endometrosis phenotype in the C57Bl/6N strain and the 30ppm BPA CD-1 group. The association between the pro-collagen shift in increased collagen expression and decreased MMP2 expression and activity implies that strain differences and BPA exposures alter regulation of endometrial remodeling and contributes to increased fibrosis, a component of several human uterine diseases. Copyright © 2015. Published by Elsevier Inc.
    Full-text · Article · Aug 2015 · Reproductive Toxicology
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