Occupational agents-mediated asthma: From the perspective of autophagy

Occupational asthma (OA) is a common occupational pulmonary disease that is frequently underdiagnosed and underreported. The complexity of diagnosing and treating OA creates a significant social and economic burden, making it an important public health issue. In addition to avoiding allergens, patients with OA require pharmacotherapy; however, new therapeutic targets and strategies need further investigation. Autophagy may be a promising intervention target, but there is a lack of relevant studies summarizing the role of autophagy in OA. In this review consolidates the current understanding of OA, detailing principal and novel agents responsible for its onset. Additionally, we summarize the mechanisms of autophagy in HMW and LMW agents induced OA, revealing that occupational allergens can induce autophagy disorders in lung epithelial cells, smooth muscle cells, and dendritic cells, ultimately leading to OA through involving inflammatory responses, oxidative stress, and cell death. Finally, we discuss the prospects of targeting autophagy as an effective strategy for managing OA and even steroid-resistant asthma, encompassing autophagy interventions focused on organoids, organ-on-a-chip systems, nanomaterials vehicle, and nanobubbles; developing combined exposure models, and the role of non-classical autophagy in occupational asthma. In briefly, this review summarizes the role of autophagy in occupational asthma, offers a theoretical foundation for OA interventions based on autophagy, and identifies directions and challenges for future research.