Iron is an element essential for the survival of most aerobic organisms. However, when its availability is not adequately controlled, iron, can catalyze the formation of a range of aggressive and damaging reactive oxygen species, and act as a microbial growth promoter. Depending on the concentrations formed such species can cause molecular damage or influence redox signaling mechanisms. This review describes recent knowledge concerning iron metabolism in the lung, during both health and disease. In the lower part of the lung a small redox active pool of iron is required for reasons that are at present unclear, but may be related to antimicrobial functions. When the concentration of iron is increased in the lung (usually because of environmental exposure), iron is deleterious and contributes to a range of chronic and acute respiratory diseases. Moreover, aberrant regulation of iron metabolism, and/or deficient antioxidant protection, is also associated with acute lung diseases, such as the acute respiratory distress syndrome (ARDS). Iron, with the consequent production of reactive oxygen species (ROS), microbial growth promotion, and adverse signaling is strongly implicated as a major contributor to the pathogenesis of numerous disease processes involving the lung. Heme oxgenase, an enzyme that produces reactive iron from heme catabolism, is also briefly discussed in relation to lung disease.