The effects of early low dose exposures to the Environmental Estrogen Bisphenol A on the Development of Childhood Asthma

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. 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