Background: The pathogenesis of chronic inflammatory diseases in the upper and lower airways is common and mutually influential and should be managed systematically. Disorders of iron metabolism and redox homeostasis imbalance, which lead to the accumulation of reactive oxygen species (ROS) and lipid peroxidation, are considered key common characteristics linking ferroptosis to chronic inflammatory diseases of the upper and lower airways. Recognizing the mechanism of ferroptosis and how it contributes to chronic inflammatory diseases of the upper and lower airways enables a more comprehensive understanding of the pathogenesis of these conditions and offers novel avenues for therapeutic intervention. Summary: Ferroptosis is a novel form of iron-dependent, regulated cell death that is regulated by integrated oxidative and antioxidant systems and is typified by the accumulation of ROS. The Excessive iron can induce the Fenton reaction, leading to the generation of large amounts of ROS. Under the catalytic action of iron-containing enzymes, ROS promotes the formation of lipid hydroperoxides, which is a key mechanism underlying ferroptosis. In contrast, the antioxidant system centered on glutathione peroxidase 4 serves as the primary regulatory pathway for inhibiting ferroptosis. Inflammation promotes the excessive production of ROS and Fe2+ within cells, thereby inducing ferroptosis in airway epithelial cells and inflammatory cells. This, in turn, triggers the release of damage-associated molecular patterns, further amplifying the inflammatory response. Key Messages: In this review, we explore the bidirectional interactions between ferroptosis and chronic inflammatory diseases of the upper and lower airways, as well as the potential role and complex effects of ferroptosis in the pathological processes of these diseases.