Archives of Asthma, Allergy and Immunology Open Access HTTPS://WWW.HEIGHPUBS.ORG 015 ISSN 2639-3182 Review Article The effects of early low dose exposures to the Environmental Estrogen Bisphenol A on the Development of Childhood Asthma Terumi Midoro-Horiuti* and Randall M Goldblum University of Texas Medical Branch, Department of Pediatrics, 301 University Blvd. Galveston, Galveston, USA *Address for Correspondence: Terumi Midoro- Horiuti, University of Texas Medical Branch, Department of Pediatrics, 301 University Blvd, Galveston, USA, TX 77555-0366; Email: tmidoro@ utmb.edu Submitted: 25 May 2017 Approved: 07 July 2017 Published: 10 July 2017 Copyright: 2017 Horiuti TM, et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited Abbreviations: BALF: Broncho Alveolar Lavage Fluid; BBzP, di-n-butyl phthalate and butylbenzyl phthalate; BPA: Bisphenol A; BW: Body Weight; ER: Estrogen Receptor; IP: Intraperitoneal; FEV1: Forced Expiratory Volume in the first second of expiration; Intraperitoneal; MBzP, Monobenzyl phthalate; NHANES: National Health and Nutrition Examination Survey; OVA: Ovalbumin; PN: Post Natal; PND: Post Natal Day How to cite this article: Horiuti TM, Goldblum RM. The effects of early low dose exposures to the Environmental Estrogen Bisphenol A on the development of Childhood Asthma. Arch Asthma Allergy Immunol. 2017; 1: 015-027. https://doi.org/10.29328/journal.haard.1001003. INTRODUCTION Allergic diseases, including asthma are often considered to be related to our genes and/or environment. However, changes of the genetic code in a population typically take a long period of time, suggesting that the recent, rapid increase in the prevalence of allergic diseases is more likely to be due to the changes in our environment, which may alter gene expression (gene/environment interaction [1]). Further, during the last few decades, campaigns to promote smoking cessation in the US and elsewhere have reduced exposure to direct and second hand smoke in pregnant women and their children. The concentrations of the six other common air pollutants (ozone, carbon monoxide, nitrogen dioxide, particulate matter, sulfur dioxide and lead) have also decreased by 60% during these decades (EPA, http://www.epa.gov/ airtrends/aqtrends.html), yet the overall prevalence of asthma has increased during this period. Another important consideration is that the increasing prevalence of allergic rhinitis and asthma is seen predominantly in women after adolescent, while prevalence of allergic rhinitis and asthma in boys and young men decrease during and after adolescent. These observations coupled with an increase in the incidence of new or recurrent asthma in women who took hormone replacement therapy after SUMMARY Exposure to environmental chemicals is a potential cause for the rapid increase in the prevalence of allergic asthma over the last few decades. The production of the environmental estrogen bisphenol A, the monomer of polycarbonate plastics, has increased rapidly over the last 50 years, such that bisphenol A is one of the most highly produced chemicals. It is detectable in the urine of the vast majority of the human population. While the relationship between the increase of bisphenol A in our environment and the prevalence of asthma does not prove a cause and effect relationship, it provides a strong rationale for experiments that have tested the hypothesis. Because of its small molecular size and hydrophobicity, bisphenol A is easily transferred from the mother to the fetus, via the placenta and in breast milk. We have reviewed all the publications available on medline on the human epidemiological studies of the early bisphenol A exposure on the development of allergic asthma and experimental studies using mouse model of the effects of early bisphenol A exposure on the development of asthma. There are eight human epidemiological studies and five mouse model studies currently published. The human studies suggest that bisphenol A exposure in early life enhances the likelihood of developing asthma on at least one of the study groups. The effects of early bisphenol A exposure were observed as an enhanced development of asthma before adolescent in the animal model.