Silicosis is an irreversible, chronic, progressive respiratory disease. No therapy has been proven to effectively modify the progression of silicosis. Whole lung lavage (WLL) is used in treating Pulmonary Alveolar Proteinosis but reported only once in the Western literature treatment for dust-induced lung disease. Recently physicians in China have used this therapy for pneumoconiosis in coal miners. The rationale for WLL in dust-induced lung disease is removal of activated cells, cytokines and dust-containing cells, all of which are likely contributing to the fibrosis. We performed WLL on a 53 year old motorman and roof bolter with significant silica exposure, ILO category 2 with coalescence chest radiograph, and normal pulmonary function. We also performed a segmental bronchoalveolar lavage (BAL) prior to and 10 days after the WLL on each side. WLL on the right lung consisted of 8 liters of saline, at which time he suffered a hydropneumothorax which led to premature termination of the procedure. A small catheter was inserted, the pneumothorax evacuated, and he was discharged the following day. Six weeks later, he underwent WLL on the left with 13 liters of saline without incident. Total cells recovered during WLL were 5.22 x 108 on the right and 3.91 x 108 on the left. Total macrophages recovered were 4.71 x 108 on the right (90% of total cells) and 3.70 x 108 on the left (94.6% of total cells). WLL removed 1.82 gm of mineral dust (non-coal) on the right and 1.64 gm on the left. Cytokine analysis paralleled the dust and radiographic findings of more disease on the right. Cultured alveolar macrophages from pre-WLL lavage released higher basal TNFa values on the right (213 pg/ml) versus left (28 pg/ml). With zymosan stimulation the levels increased to 331 pg/ml (right) and 213 pg/ml (left). Similar values were obtained for basal I1-lB, 322 pg/ml (right) and 18 pg/ml (left). Zymosan stimulated cells yielded 396 pg/ml from the right versus 115 pg/ml from the left lung. WLL appears to be a feasible means of removing dust, cytokines, and dust-laden cells that may reflect differential disease activity and allow modification of the progressive fibrosis that is associated with silica exposure.
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