Abstract Text: We have reported the effects of maternal exposures to bisphenol A (BPA) on the development of experimental asthma. BPS has been used as a BPA substitute, but the effects on immune development have not been examined. The purpose of this study was to test the hypothesis that maternal exposure to environmental estrogens (EEs), including BPS, enhances the allergic sensitization that underlies childhood asthma. Female BALB/c mice (F0) received 10 g/ml BPS in their drinking water from one week before pregnancy to the end of the study. The pups were sensitized with low doses of ovalbumin (OVA) or PBS control on a postnatal day (PND) 4. On PND 22, serum IgE anti-OVA levels were quantified, and airway inflammation and hyperresponsiveness were assessed by enumerating eosinophils in bronchoalveolar lavage fluid and response to methacholine. Non-sensitized female pups were saved and mated with non-exposed male mice at eight weeks of age for the next generation. The resulting pups were sensitized, and the asthma phenotype was examined up to F4. Pups exposed to BPS displayed an asthma phenotype in response to their “suboptimal” sensitization. OVA-specific IgE, eosinophilic airway inflammation, and airway hyperresponsiveness were significantly increased in the F1-F3 pups derived from BPS-exposed F0 dams than in the pups derived from non-exposed dams. Maternal exposure to EE, including BPS, promotes the development of experimental asthma. The immune alterations may be epigenetically perpetuated, causing multigenerational effects.
