Cytokines in metal fume fever.
Blanc-PD; Boushey-HA; Wong-H; Wintermeyer-SF; Bernstein-MS
Am Rev Respir Dis 1993 Jan; 147(1):134-138
The role of cytokines in the pathogenesis of metal fume fever was examined. The purpose of the study was to test the hypothesis that metal fume fever was caused by zinc-oxide (1314132) fumes stimulating macrophages resident in the lungs to release cytokines known to be associated with fever or inflammation. Twenty three volunteers, 18 males, mean age 32.1 years, performed electric arc welding on galvanized mild steel for 15 to 30 minutes. Subjects wore welding helmets and mimicked standard welding work practices. The welding fumes were analyzed for zinc (7440666). Bronchoalveolar lavage (BAL) was performed 3, 8, or 22 hours after welding. BAL was also performed on 17 referents not exposed to welding fumes. Peripheral blood samples were collected at baseline and at follow up. Lavagate cellularity was determined and the lavage fluid was assayed for albumin, tumor necrosis factor (TNF), interleukin-1 (IL1), interleukin-4 (IL4), interleukin-6 (IL6), and interleukin-8 (IL8). Peripheral blood polymorphonuclear leukocyte (PMN) counts were determined. The welding fumes produced zinc exposures of 0.1 to 5.1 gram minutes per cubic meter. Lavagate albumin, TNF, IL1, IL6, and IL8 concentrations were significantly increased following welding fume exposure. IL4 was not detected in any lavagate samples from exposed subjects or controls. When analyzed by sampling time, TNF concentrations were significantly higher at 3 than at 8 or 22 hours. Albumin concentrations at 22 hours were significantly greater than at 3 hours. Lavagate macrophage and PMN concentrations differed significantly among the 3, 8, and 22 hour follow up groups. Blood PMN counts were significantly increased from baseline at 8 and 22 hours. Zinc fume exposures were significantly correlated with lavagate TNF concentrations at all time points, IL6 concentration at 22 hours, and IL8 concentration at 8 hours. The increase in IL8 concentration at 8 hours was significantly correlated with lavagate PMN concentration. The authors conclude that cytokines are involved in the pathogenesis of metal fume fever and suggest that TNF is a key mediator of this syndrome.
NIOSH-Publication; NIOSH-Grant; Pulmonary-system-disorders; Metal-fume-fever; Arc-welding; Immune-reaction; Physiological-chemistry; Lung-cells; Laboratory-techniques; Occupational-medicine; Inhalation-studies; Humans; Zinc-compounds
Cardiovascular Research Inst University of California PO Box 0924 San Francisco, CA 94143-0924
American Review of Respiratory Disease
University of California San Francisco, San Francisco, California