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Clinical Relevance of Cellular Mediators of Inflammation in Workers Exposed to Asbestos

1993; American Thoracic Society; Volume: 148; Issue: 1 Linguagem: Inglês

10.1164/ajrccm/148.1.68

2376-3752

David A. Schwartz, Jeffrey R. Galvin, Kathy L. Frees, Charles S. Dayton, Leon F. Burmeister, James A. Merchant, Gary W. Hunninghake,

Biomarkers in Disease Mechanisms

To identify the clinical relevance of cellular mediators of inflammation in workers exposed to asbestos, we investigated the relationship between inflammatory products primarily released by alveolar macrophages and the clinical expression of asbestos-induced interstitial fibrosis. Our study population consisted of 93 white men who had been occupationally exposed to asbestos and were on average 60 yr of age. Pulmonary function tests, chest radiographs, high-resolution CT scans, and bronchoalveolar lavage (BAL) were performed on almost all study subjects; 11 (11.8%) had restrictive lung function, 22 (23.7%) had abnormal gas exchange, 30 (32.3%) had interstitial fibrosis on chest x-ray, and 24 (25.8%) had interstitial changes on high-resolution CT scan. The cellular markers of parenchymal inflammation that we examined included fibronectin in BAL fluid and alveolar macrophage release of prostaglandin E2 (PGE2), interleukin-1β (IL-1β), and tumor necrosis factor (TNF-α) under unstimulated and endotoxin (LPS)-stimulated culture conditions. Significantly higher concentrations of fibronectin in BAL fluid were observed among those with restrictive lung function. In addition, higher concentrations of PGE2, released from cultured but otherwise unstimulated alveolar macrophages, were associated with restrictive lung function. However, the inverse relationship with PGE2 was observed among subjects with abnormal gas exchange. Interestingly, no consistent changes in these inflammatory mediators were observed in those with interstitial changes identified on either the chest radiograph or the high-resolution CT scan. Moreover, the concentration of IL-1β and TNF-α released by alveolar macrophages under either unstimulated or LPS-stimulated culture conditions were not significantly related to the physiologic or radiographic expression of asbestos-induced interstitial fibrosis. In aggregate, our results suggest that among workers exposed to asbestos, cell products primarily derived from alveolar macrophages do not appear to be associated with mild radiographic manifestations of asbestos-induced interstitial lung disease. However, higher concentrations of fibronectin and PGE2 released from cultured alveolar macrophages appear to be associated with restrictive lung function.