Bisphenol A (BPA) is used in various areas of daily life as a major component of
plastic products. However, it is also known as a strong
endocrine disruptor that affects the human immune system. Studies have indicated that BPA possibly exacerbates allergic diseases such as
atopic dermatitis and
asthma. The main aim of this study was to elucidate whether BPA is directly involved in the exacerbation of allergic
inflammation. Initially, in vivo experiments with mouse models of allergic
inflammation induced by Th2 type
hapten toluene-2, 4-diisocyanate (TDI) was performed. Mice were subjected to
oral administration of BPA 48, 24, and 4 h before challenge with TDI. Dermal challenge of TDI onto the ear auricle was performed for the allergic
dermatitis model, and intratracheal challenge of TDI was performed for the allergic airway
inflammation model. In the allergic
dermatitis model, ear-swelling response was significantly downregulated by high doses of BPA. The opposite reaction was observed in the allergic airway
inflammation model, including significant exacerbation of red coloration in the lung, local
cytokine levels, and total
IgE levels in serum by BPA administration. To confirm the in vivo results, in vitro experiments with human epidermal keratinocytes (HEKs) and bronchial epithelial (BEAS-2B) cells were carried out. Significant enhancement of
cytokine release from BEAS-2B cells but not HEKs in the BPA-treated group supported the in vivo observations. Our results imply that exposure to BPA directly exacerbates allergic airway
inflammation but not allergic
dermatitis.