164
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

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

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Objective

          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.

          Measurements

          We measured the urinary concentrations of free and total (free plus conjugated) species of BPA, triclosan, benzophenone-3, methyl paraben, and propyl paraben.

          Results

          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).

          Conclusion

          BPA geometric mean urinary concentration (30.3 μg/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.

          Related collections

          Most cited references48

          • Record: found
          • Abstract: found
          • Article: not found

          Exposure of the U.S. Population to Bisphenol A and 4-tertiary-Octylphenol: 2003–2004

          Background Bisphenol A (BPA) and 4-tertiary-octylphenol (tOP) are industrial chemicals used in the manufacture of polycarbonate plastics and epoxy resins (BPA) and nonionic surfactants (tOP). These products are in widespread use in the United States. Objectives We aimed to assess exposure to BPA and tOP in the U.S. general population. Methods We measured the total (free plus conjugated) urinary concentrations of BPA and tOP in 2,517 participants ≥ 6 years of age in the 2003–2004 National Health and Nutrition Examination Survey using automated solid-phase extraction coupled to isotope dilution–high-performance liquid chromatography–tandem mass spectrometry. Results BPA and tOP were detected in 92.6% and 57.4% of the persons, respectively. Least square geometric mean (LSGM) concentrations of BPA were significantly lower in Mexican Americans than in non-Hispanic blacks (p = 0.006) and non-Hispanic whites (p = 0.007); LSGM concentrations for non-Hispanic blacks and non-Hispanic whites were not statistically different (p = 0.21). Females had statistically higher BPA LSGM concentrations than males (p = 0.043). Children had higher concentrations than adolescents (p $45,000/year). Conclusions Urine concentrations of total BPA differed by race/ethnicity, age, sex, and household income. These first U.S. population representative concentration data for urinary BPA and tOP should help guide public health research priorities, including studies of exposure pathways, potential health effects, and risk assessment.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Human exposure to bisphenol A.

            Bisphenol A (BPA), 2,2-bis(4-hydroxyphenyl)propane, is made by combining acetone and phenol. It has estrogenic activity and is acutely toxic to aquatic organisms. BPA is used mainly as a material for the production of epoxy resins and polycarbonate plastics. Due to an increase in products based on epoxy resins and polycarbonate plastics, human exposure to BPA has increased. The environment (aquatic environment, air and soil) can be one source of human BPA exposure, but the primary route of human exposure is foods. The daily human intake of BPA is <1 microg/kg body weight/day on the basis of several studies, and whether these doses can have an adverse endocrine disruptive effect on humans, especially fetuses, needs to be studied carefully.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Developmental exposure to estradiol and bisphenol A increases susceptibility to prostate carcinogenesis and epigenetically regulates phosphodiesterase type 4 variant 4.

              Early developmental perturbations have been linked to adult-onset prostate pathology, including excessive exposure to estrogenic compounds; however, the molecular basis for this imprinting event is not known. An important and controversial health concern is whether low-dose exposures to hormonally active environmental estrogens, such as bisphenol A, can promote human diseases, including prostate cancer. Here, we show that transient developmental exposure of rats to low, environmentally relevant doses of bisphenol A or estradiol increases prostate gland susceptibility to adult-onset precancerous lesions and hormonal carcinogenesis. We found permanent alterations in the DNA methylation patterns of multiple cell signaling genes, suggesting an epigenetic basis for estrogen imprinting. For phosphodiesterase type 4 variant 4 (PDE4D4), an enzyme responsible for cyclic AMP breakdown, a specific methylation cluster was identified in the 5'-flanking CpG island that was gradually hypermethylated with aging in normal prostates, resulting in loss of gene expression. Early and prolonged hypomethylation at this site following neonatal estradiol or bisphenol A exposure resulted in continued, elevated PDE4D4 expression. Cell line studies confirmed that site-specific methylation is involved in transcriptional silencing of the PDE4D4 gene and showed hypomethylation of this gene in prostate cancer cells. Importantly, the PDE4D4 alterations in the estrogen-exposed prostates were distinguishable before histopathologic changes of the gland, making PDE4D4 a candidate molecular marker for prostate cancer risk assessment as a result of endocrine disruptors. In total, these findings indicate that low-dose exposures to ubiquitous environmental estrogens affect the prostate epigenome during development and, in so doing, promote prostate disease with aging.
                Bookmark

                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                1552-9924
                April 2009
                10 December 2008
                : 117
                : 4
                : 639-644
                Affiliations
                [1 ] Centers for Disease Control and Prevention, Atlanta, Georgia, USA;
                [2 ] Rush Institute for Healthy Aging, Rush University Medical Center, Chicago, Illinois, USA;
                [3 ] Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA;
                [4 ] Schools of Public Health and Medicine, University of Michigan, Ann Arbor, Michigan, USA;
                [5 ] Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA;
                [6 ] Neonatology Unit and
                [7 ] Vincent Memorial Obstetrics and Gynecology Service, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
                Author notes
                Address correspondence to A.M. Calafat, Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, 4770 Buford Hwy., Mailstop F53, Atlanta, GA 30341 USA. Telephone: (770) 488-7891. Fax: (770) 488-4371. E-mail: acalafat@ 123456cdc.gov

                The authors declare they have no competing financial interests.

                Article
                ehp-117-639
                10.1289/ehp.0800265
                2679610
                19440505
                4b53d021-aacf-4a88-8f65-38b44920c023
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.
                History
                : 8 October 2008
                : 10 December 2008
                Categories
                Research
                Children's Health

                Public health
                nicu,glucuronidation,bpa,paraben,triclosan,biomonitoring,neonate,benzophenone
                Public health
                nicu, glucuronidation, bpa, paraben, triclosan, biomonitoring, neonate, benzophenone

                Comments

                Comment on this article