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Iron is an essential micronutrient, but its redox reactivity also renders it potentially toxic. The lungs are particularly vulnerable to iron-dependent oxidative injury due to continuous exposure to high oxygen tension, environmental particles, and microbial pathogens. Pulmonary iron homeostasis is therefore tightly regulated at systemic, cellular, and local levels through coordinated actions of transferrin, ferritin, ferroportin, hepcidin, and the iron responsive element/iron regulatory protein system. Disruption of these pathways contributes to a broad spectrum of pulmonary diseases. In COPD, asthma, idiopathic pulmonary fibrosis, pulmonary arterial hypertension, infectious lung diseases, and lung cancer, iron dysregulation promotes oxidative stress, ferroptosis, inflammation, aberrant repair, vascular remodelling, or pathogen persistence. Notably, systemic iron deficiency may coexist with local pulmonary iron overload, highlighting the compartmentalised nature of lung iron metabolism. Emerging experimental and clinical evidence suggests that therapeutic manipulation of iron availability through supplementation, chelation or targeting iron-dependent pathways may be beneficial in selected contexts. A deeper mechanistic understanding and improved biomarkers will be essential for developing disease-specific iron-modulating strategies.