Assessment of air pollutant O pulmonary exposure using a bronchus-on-chip model coupling with atmospheric simulation chamber.

Heavy air pollution is now a serious public health issue. Many studies have shown strong connections between ozone (O) with the occurrence and development of various respiratory diseases. However, the exact mechanism is still a matter of debate. In this work, we developed a human bronchial epithelial cells (HBECs) chip that differentiates different functional cell groups of ciliated, goblet, and club cells to model the pulmonary bronchial barrier function. Concurrently, we designed an Atmospheric-Biochemical-Chip reactor (ABC-reactor), a system that could simulate different levels of O and particle matter. Coupling the HBECs-on-chip model with ABC-reactor, we investigated the effects of O at 400 ppbv and 200 ppbv on the pulmonary bronchial barrier. Our results showed that O at 400 ppbv severely disrupted the bronchial barrier and upregulated the expression of pro-inflammatory cytokines. However, 200 ppbv of O did not cause severe barrier impairment but induced cellular dysfunction, apoptosis, and reduced immune response. These suggest that bronchial trauma does exist at 200 ppbv of O but is not easily detected by the body due to the reduced inflammatory response. However, more research is needed to understand if the trauma induced by 200 ppbv of O is reversible and the interaction mechanism between O and PM.