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CLARITY-BPA: Effects of Chronic Bisphenol A Exposure on the Immune System: Part 1 - Quantification of the Relative Number and Proportion of Leukocyte Populations in the Spleen and Thymus

Overview
Journal Toxicology
Publisher Elsevier
Specialty Toxicology
Date 2018 Feb 12
PMID 29428349
Citations 9
Authors
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Abstract

Bisphenol A (BPA) is extensively used in manufacturing of a broad range of consumer products worldwide. Due to its widespread use, human exposure to BPA is virtually ubiquitous. Broad human exposure coupled with a large scientific literature describing estrogenic activity of BPA in animals has raised public health concerns. To comprehensively evaluate the health effects of BPA exposure, a chronic toxicity study using a wide-range of BPA doses (2.5-25000 μg/kg bw/day) was conducted jointly by the NTP, thirteen NIEHS-supported grantees, and the FDA, which is called the Consortium Linking Academic and Regulatory Insights on Toxicity of BPA (CLARITY-BPA). As a participant in the CLARITY-BPA project, the objective of the current study was to evaluate the effects of chronic BPA exposure in Sprague-Dawley rats on the relative number and proportion of defined leukocyte populations in the spleen and the thymus. Toward this end, lymphoid tissues from a total of 641 rats were assayed after being continuously dosed with BPA or controls for up to one year. To comprehensively evaluate the effects of BPA on leukocyte compositions, extensive endpoints that cover major populations of leukocytes were assessed, including B cells, T cells, NK cells, granulocytes, monocytes, macrophages and dendritic cells. In total, of the 530 measurements in BPA-treated rats, 10 measurements were statistically different from vehicle controls and were mainly associated with either the macrophage or dendritic cell populations. Most, if not all, of these alterations were found to be transient with no persistent trend over the one-year time period. In addition, the observed BPA-associated alterations were mostly moderate in magnitude and not dose-dependent. Due to the aforementioned, it is unlikely that the observed BPA-mediated changes alone would adversely affect immune competence.

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References
1.
Vanacker J, Pettersson K, Gustafsson J, Laudet V . Transcriptional targets shared by estrogen receptor- related receptors (ERRs) and estrogen receptor (ER) alpha, but not by ERbeta. EMBO J. 1999; 18(15):4270-9. PMC: 1171503. DOI: 10.1093/emboj/18.15.4270. View

2.
Khan D, Ahmed S . The Immune System Is a Natural Target for Estrogen Action: Opposing Effects of Estrogen in Two Prototypical Autoimmune Diseases. Front Immunol. 2016; 6:635. PMC: 4701921. DOI: 10.3389/fimmu.2015.00635. View

3.
Medina K, Garrett K, Thompson L, Rossi M, Payne K, Kincade P . Identification of very early lymphoid precursors in bone marrow and their regulation by estrogen. Nat Immunol. 2001; 2(8):718-24. DOI: 10.1038/90659. View

4.
Carreras E, Turner S, Frank M, Knowlton N, Osban J, Centola M . Estrogen receptor signaling promotes dendritic cell differentiation by increasing expression of the transcription factor IRF4. Blood. 2009; 115(2):238-46. PMC: 2808152. DOI: 10.1182/blood-2009-08-236935. View

5.
Kuiper G, Lemmen J, Carlsson B, Corton J, Safe S, van der Saag P . Interaction of estrogenic chemicals and phytoestrogens with estrogen receptor beta. Endocrinology. 1998; 139(10):4252-63. DOI: 10.1210/endo.139.10.6216. View