Pulmonary Alveolar Proteinosis Secondary to Occupational Exposure

Purpose of Review Occupational exposures are associated with a wide array of respiratory disorders that include asbestosis, coal workers' pneumoconiosis and silicosis, asthma, COPD, bronchiolitis, hypersensitivity pneumonitis, pulmonary fibrosis, sarcoidosis, and certain infections. Pulmonary alveolar proteinosis (PAP) is characterized by accumulation of lipoproteinaceous material in the alveoli and alveolar macrophages. Autoimmunity is the most common etiology for PAP and involves autoantibodies targeting GM-CSF signaling. However, certain occupational and environmental inhalational exposures have been considered causative for PAP, although this constitutes a relative minority of the patients. The review article sheds light on the current knowledge of occupational/environmental respiratory exposures that can cause PAP. Recent Findings There is increased recognition of occupational respiratory exposures implicated in PAP. The role of silica exposure in causing PAP is well recognized and constitutes the most common etiology for occupational PAP. However, since its original description, several other agents have been identified that can trigger PAP in those exposed. Most recently, PAP has been described in a cohort of indium workers who produce indium-tin oxide (ITO), used to manufacture transparent conductive coating for flat panel displays such as liquid crystal displays (LCDs), touch screens, and solar cells. Some exposed workers with PAP have been found to have autoantibodies to GM-CSF. Besides silica, PAP is associated with a wide variety of vapors, gases, dusts, and fumes. In some patients with occupational exposure, it is possible that the offending agent may trigger autoimmunity against GM-CSF that can induce PAP. Patients with occupational PAP may have concomitant emphysema and/or pulmonary fibrosis. Depending on the degree of manifestations, treatment approach ranges from watchful monitoring to invasive modalities like whole lung lavage. Recognition of an occupational etiology for PAP has implication both for the patient and for co-workers, who may also be at risk. Physician reporting to regulatory and public health authorities can ensure that existing exposure limits and medical surveillance requirements, such as are in place for silica, are enforced and that novel or unregulated exposures are characterized.