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Maternal bisphenol A exposure and experimental asthma in mouse pups.

It has been proposed that the increasing prevalence of childhood asthma in developing countries may be related to immunologic effects of environmental contaminants, including exposure to environmental estrogens recently shown to induce mast cell degranulation and enhance allergic responses in animal models. Midoro-Horiuti et al. (p. 273) evaluated airway hyperresponsiveness (AHR) in the offspring of female BALB/c mice that received 10 [micro]g/mL bisphenol A (BPA; a dose designed to produce body burdens similar to those of humans) in their drinking water from 1 week before conception through pregnancy and lactation. A subset of pups was also exposed to ovalbumin (OVA) at a dose below that normally required to cause allergic sensitization. The authors report that OVA-sensitized pups born to BPA-treated mothers had increased numbers of eosinophils in broncho alveolar lavage fluid, increased airway responsiveness (based on whole-body barometric plethysmography following a methacholine challenge), and higher anti-OVA serum IgE concentrations than pups born to BPA-unexposed mothers. The authors conclude that perinatal exposure to BPA enhanced allergic sensitization and bronchial inflammation and responsiveness in their animal model of asthma, but note that additional research is needed to determine cellular and molecular mechanisms for these effects.

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Title Annotation:Research
Publication:Environmental Health Perspectives
Article Type:Brief article
Date:Feb 1, 2010
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