Iron Homeostasis in the Lung Following Asbestos Exposure

Abstract

Human exposure to asbestos can cause a wide variety of pulmonary diseases, including pneumoconiosis (i.e., asbestosis). This lung injury is mediated by oxidant generation which increases with the concentration of iron associated with the asbestos. Iron from host sources is complexed by the surface of these fibrous silicates following introduction into the lower respiratory tract. Using bronchoalveolar lavage from unexposed and exposed workers, we demonstrate that asbestos disrupts the normal iron homeostasis in the lungs. Based on these findings, we propose a model of oxidative stress and human lung injury after asbestos exposure.