Cross-shift changes in blood inflammatory markers occur in the absence of airway obstruction in workers exposed to grain dust.
Grain dust is well known to cause both acute and chronic respiratory disorders, and endotoxins are considered key components in this.
Since endotoxins are known to elicit proinflammatory mediators, we investigated cytokine (tumor necrosis factor [TNF], interleukin-6, interleukin-8) release and a number of proinflammatory and anti-inflammatory proteins (soluble TNF receptors, lipopolysaccharide (LPS) binding protein, bactericidal permeability increasing protein (BPI), C-reactive protein) in plasma of workers exposed to grain dust.
In two surveys during 1 week, lung function was measured daily before and after the shift, using flow-volume curves and/or forced oscillation measurements.
On Monday and Friday, blood samples (30 mL) were drawn and cytokine release was determined by enzyme-linked immunosorbent assay in supernatant of isolated monocytes or whole blood culture, either unstimulated or on the ex vivo stimulation with 3 ng/mL or 1,000 ng/mL endotoxin.
Individual exposures were determined from stationary dust measurements at every workplace combined with personal task analysis during all shifts.
In both surveys, no cross-week change in lung function parameters was observed.
In the first survey (average exposure : 20.2 mg/m3), monocyte spontaneous TNF release was increased sevenfold cross week (p<0.001) and was significantly related both to individual dust exposure (r=0.62) of that week and the increase in soluble TNF receptor 75 kD (r=0.85).
In the seco...
Mots-clés Pascal : Exposition professionnelle, Poussière, Grain, Inflammation, Exploration microbiologique, Marqueur biologique, Cytokine, Récepteur, Facteur soluble, Facteur nécrose tumorale, Modification, Homme, Médecine travail, Poumon pathologie, Appareil respiratoire pathologie
Mots-clés Pascal anglais : Occupational exposure, Dust, Grains, Inflammation, Microbiological investigation, Biological marker, Cytokine, Receiver, Soluble factor, Tumor necrosis factor, Modification, Human, Occupational medicine, Lung disease, Respiratory disease
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Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 96-0227153
Code Inist : 002B06C02. Création : 199608.