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The human lung represents a functionally essential and structurally sophisticated organ composed of over 40 distinct cell types, predominantly including epithelial cells, immune cells, endothelial cells, and stromal cells. As a vital organ continuously exposed to airborne pollutants, cigarette smoke, pathogenic bacteria, viruses, and various toxic stimuli, the lung is highly susceptible to persistent tissue injury, which ultimately drives the progression of multiple pulmonary disorders, such as asthma, chronic obstructive pulmonary disease (COPD), lung cancer, and diverse respiratory infections. Immortalized cell lines and primary human lung cells have long served as conventional research models for investigating lung development and disease pathogenesis due to their accessibility and low experimental cost. However, primary cells exhibit restricted proliferation and passaging ability, limiting their application in long-term experimental studies, whereas immortalized cell lines display significant genetic and phenotypic deviations from authentic in vivo lung tissues. In addition, animal models are hampered by inherent interspecies differences and fail to recapitulate the intricate cellular heterogeneity of the human lung, resulting in unavoidable experimental limitations. Possessing robust self-renewal capacity and multilineage differentiation potential, lung organoids have emerged as an advanced and versatile model for elucidating the molecular mechanisms underlying smoking-related pulmonary diseases and facilitating therapeutic screening. Accumulating evidence has confirmed that lung organoids faithfully recapitulate human lung developmental processes, three-dimensional tissue architecture, and physiological functions. Accordingly, they provide a powerful experimental platform for exploring lung development, injury repair, and pathological mechanisms, holding great promise for broad biomedical applications.