Oxidants such as
superoxide anion,
hydrogen peroxide, and
myeloperoxidase from activated inflammatory cells in the lower respiratory tract contribute to
inflammation and injury. Etiologic agents include inorganic particulates such as
asbestos,
silica, or
coal mine dust or mixtures of inorganic dust and combustion materials found in World Trade Center dust and
smoke. These etiologic agents are phagocytosed by alveolar macrophages or bronchial epithelial cells and release
chemotactic factors that recruit inflammatory cells to the lung.
Chemotactic factors attract and activate neutrophils, eosinophils, mast cells, and lymphocytes and further activate macrophages to release more
oxidants. Inorganic dusts target alveolar macrophages, World Trade Center dust targets bronchial epithelial cells, and eosinophils characterize tropical
pulmonary eosinophilia (TPE) caused by filarial organisms. The technique of bronchoalveolar lavage in humans has recovered alveolar macrophages (AMs) in dust diseases and eosinophils in TPE that release increased amounts of
oxidants in vitro. Interestingly, TPE has massively increased eosinophils in the acute form and
after treatment can still have ongoing eosinophilic
inflammation. A course of
prednisone for one week can reduce the
oxidant burden and attendant
inflammation and may be a strategy to prevent chronic TPE and
interstitial lung disease.