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Lung diseases, such as asthma, chronic obstructive pulmonary diseases (COPD), and cystic fibrosis (CF), are among the leading causes of mortality and morbidity globally. They contribute to substantial economic burdens on society and individuals. Currently, only a few treatments are available to slow the development and progression of these diseases. Thus, there is an urgent unmet need to develop effective therapies to improve quality of life and limit healthcare costs. An increasing body of clinical and experimental evidence suggests that altered zinc and its regulatory protein levels in the systemic circulation and in the lungs are associated with these disease’s development and progression. Zinc plays a crucial role in human enzyme activity, making it an essential trace element. As a cofactor in metalloenzymes and metalloproteins, zinc involves a wide range of biological processes, such as gene transcription, translation, phagocytosis, and immunoglobulin and cytokine production in both health and disease. Zinc has gained considerable interest in these lung diseases because of its anti-inflammatory, antioxidant, immune, and metabolic modulatory properties. Here we highlight the role and mechanisms of zinc in the pathogenesis of asthma, COPD, CF, acute respiratory distress syndrome, idiopathic pulmonary fibrosis, and pulmonary hypertension.

Maternal iron deficiency occurs in 40–50% of all pregnancies and is associated with an increased risk of respiratory disease and asthma in children. We used murine models to examine the effects of lower iron status during pregnancy on lung function, inflammation and structure, as well as its contribution to increased severity of asthma in the offspring. A low iron diet during pregnancy impairs lung function, increases airway inflammation, and alters lung structure in the absence and presence of experimental asthma. A low iron diet during pregnancy further increases these major disease features in offspring with experimental asthma. Importantly, a low iron diet increases neutrophilic inflammation, which is indicative of more severe disease, in asthma. Together, our data demonstrate that lower dietary iron and systemic deficiency during pregnancy can lead to physiological, immunological and anatomical changes in the lungs and airways of offspring that predispose to greater susceptibility to respiratory disease. These findings suggest that correcting iron deficiency in pregnancy using iron supplements may play an important role in preventing or reducing the severity of respiratory disease in offspring. They also highlight the utility of experimental models for understanding how iron status in pregnancy affects disease outcomes in offspring and provide a means for testing the efficacy of different iron supplements for preventing disease.