Transgenerational effects of bisphenol S exposure on the development of experimental asthma.

Abstract

Early exposure to bisphenol A (BPA) is associated with increased asthma prevalence. To examine the effects of the most widely used BPA substitute, bisphenol S (BPS), on the development of childhood asthma, we conducted the study using the mouse model of early exposure. To simulate the burden from the human chronic exposure, we used a short-term exposure with 10 µg/ml BPS in the drinking water of female BALB/c mice (F0) from one week before pregnancy until the weaning of F1 pups. The pups were sensitized with low doses of ovalbumin (OVA) injection on postnatal day 4 and inhalation of OVA two weeks later. Twenty-four hours after the last inhalation, allergen-specific IgE and IgG1 levels, airway inflammation, and hyperresponsiveness were assessed. Non-OVA-sensitized females were mated with non-exposed male mice for the next generation at eight weeks of age. 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 sensitization. We observed enhanced asthma phenotype in the F1-F4 derived from BPS-exposed F0 females compared to those derived from non-exposed females. Maternal exposure to BPS caused the multigenerational effects on the development of experimental asthma.