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Shin-ichiro Narita,¹ Randall M. Goldblum,¹ Cheryl S. Watson,² Edward G. Brooks,¹ D. Mark Estes,¹ Edward M. Curran,¹ and Terumi Midoro-Horiuti¹

¹Department of Pediatrics, Child Health Research Center; and ²Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas, USA

Abstract
Background: Prevalence and morbidity of allergic diseases have increased over the last decades. Based on the recently recognized differences in asthma prevalence between the sexes, we have examined the effect of endogenous estrogens on a key element of the allergic response. Some lipophilic pollutants have estrogen-like activities and are termed environmental estrogens. These pollutants tend to degrade slowly in the environment and to bioaccumulate and bioconcentrate in the food chain ; they also have long biological half-lives.

Objectives: Our goal in this study was to identify possible pathogenic roles for environmental estrogens in the development of allergic diseases.

Methods: We screened a number of environmental estrogens for their ability to modulate the release of allergic mediators from mast cells. We incubated a human mast cell line and primary mast cell cultures derived from bone marrow of wild type and estrogen receptor (ER-) –deficient mice with environmental estrogens with and without estradiol or IgE and allergens. We assessed degranulation of mast cells by quantifying the release of ?-hexosaminidase.

Results: All of the environmental estrogens tested caused rapid, dose-related release of ?-hexosaminidase from mast cells and enhanced IgE-mediated release. The combination of physiologic concentrations of 17?-estradiol and several concentrations of environmental estrogens had additive effects on mast cell degranulation. Comparison of bone marrow mast cells from ER-–sufficient and ER-–deficient mice indicated that much of the effect of environmental estrogens was mediated by ER-.

Conclusions: Our findings suggest that estrogenic environmental pollutants might promote allergic diseases by inducing and enhancing mast cell degranulation by physiologic estrogens and exposure to allergens.

Key words: allergy, asthma, ?-hexosaminidase, environmental estrogen, estradiol, estrogen receptor , IgE, mast cells. Environ Health Perspect 115:48–52 (2007) . doi:10.1289/ehp.9378 available via http://dx.doi.org/ [Online 3 October 2006]

Address correspondence to T. Midoro-Horiuti, Child Health Research Center, University of Texas Medical Branch, 2.300 Children's Hospital, 301 University Blvd., Galveston, TX 77555-0366 USA. Telephone: (409) 772-3832. Fax: (409) 772-1761. E-mail: tmidoro@utmb.edu

This work was a pilot project supported by the NIEHS (National Institute of Environmental Health Sciences) Center for Environmental Science at the University of Texas Medical Branch (pilot project grant P30 E06676 to T.M.H.) and by grants R01 AI052428 (R.M.G.) and K08 AI055792 (T.M.H.) from the National Institute of Allergy and Infectious Diseases.

The authors declare they have no competing financial interests.

Received 25 May 2006 ; accepted 3 October 2006.