Accumulating literature supports a bidirectional relationship of obstructive sleep apnea (OSA) with chronic lung disease (CLD), such as asthma, chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis. OSA is more common in CLD and apart from traditional risks, a unique set of characteristics related to CLD may predispose. In asthma, for example, these appear related to complex dynamic physiology between upper and lower airway during sleep, asthma-related inflammation, and additional effects of corticosteroids. Once established, OSA aggravates CLD. Patients with overlap of OSA and COPD or pulmonary fibrosis have higher morbidity and mortality. Likewise, in asthma, OSA relates to worse control, quality of life and more health care use. Mechanistically, OSA features appear intricately linked with modulating the lower airway caliber, inflammatory milieu and remodeling. For example, in rodents with allergen-induced inflammation, chronic intermittent hypoxia (CIH) caused airflow limitation, a monocyte-predominant Th-1 inflammation, and collagen deposition in more proximal airways, coincident with matrix degradation in the distal airways and parenchyma. Furthermore, following bleomycin-induced lung injury, CIH augmented the total lung collagen content and led to impaired gas exchange. These changes are concerning, since none are responsive to current standard therapies for example, for asthma. Although the Sleep field has been dominated by pulmonologists, much work is needed to understand this interaction. This talk will review the pathophysiology of OSA in the context of lung disease, describing available clinical data on the effects of OSA on CLD, and mechanisms emerging from human and animal studies. Further research directions will also be outlined.