Relationship of inflammatory cell cytokines to disease severity in individuals with occupational inorganic dust exposure.
The pneumoconioses due to chronic occupational exposure to asbestos, coal, or silica are characterized by an alveolar macrophage-dominated alveolitis with exaggerated spontaneous release of mediators: oxidants, chemotaxins for neutrophils, and fibroblast growth factors. Bronchoalveolar lavage was performed on 66 non-smoking inorganic dust-exposed individuals with a chest x-ray greater than or equal to 1/0 stratified by presence or absence of restrictive respiratory impairment, and 28 unexposed non-smoking controls. Both dust-exposed groups stratified by presence or not of impairment had increased numbers of total cells recovered by lavage compared to normals, and those with respiratory impairment (n = 40) had a significant increase in percent and number of neutrophils recovered. Similarly, only those with respiratory impairment had macrophages that spontaneously released significant amounts of the oxidants superoxide anion and hydrogen peroxide. There was a significant trend for the release of fibronectin by macrophages from controls to dust-exposed without impairment to those with impairment. Both dust-exposed groups also had increased release of alveolar macrophage-derived progression growth factor, but this was significantly less than macrophages from patients with idiopathic pulmonary fibrosis. Since occupational exposure was virtually identical in inorganic dust-exposed individuals with versus without respiratory impairment, the quantitative differences in the release of macrophage mediators may be due to factors in host susceptibility.
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Department of Medicine Bellevue Hospital, New York University Medical Center, NY 10016.
D001194:Asbestos; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D003031:Coal; D003430:Cross-Sectional Studies; D016207:Cytokines / Q000378:metabolism*; D005069:Evaluation Studies as Topic; D006801:Humans; D008264:Macrophages / Q000378:metabolism*; D011009:Pneumoconiosis / Q000453:epidemiology / Q000209:etiology* / Q000378:metabolism; D011650:Pulmonary Alveoli / Q000166:cytology; D011658:Pulmonary Fibrosis / Q000453:epidemiology / Q000209:etiology* / Q000378:metabolism; D012720:Severity of Illness Index; D012822:Silicon Dioxide
D003031:Coal; D016207:Cytokines; D001194:Asbestos; D012822:Silicon Dioxide