title: Cross-shift changes in blood inflammatory markers occur in the absence of airway obstruction in workers exposed to grain dust.
abstract: 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 second survey, where average exposure was much lower (3.67 mg/m3), impedance parameters indicated a significant improvement of airway function, and cross-week changes in inflammatory markers were minimal. Therefore, we conclude that inflammatory events can be used to monitor adverse respiratory effects of moderate grain dust exposure.
authors.affiliation: Department of Health Risk Analysis, University of Limburg, Maastricht, the Netherlands.
authors.forename: P J
authors.initials: PJ
authors.lastname: Borm
authors.forename: R P
authors.initials: RP
authors.lastname: Schins
authors.forename: T J
authors.initials: TJ
authors.lastname: Derhaag
authors.forename: I
authors.initials: I
authors.lastname: Kant
authors.forename: T H
authors.initials: TH
authors.lastname: Jorna
mesh_terms: D000209:Acute-Phase Proteins / Q000032:analysis; D000402:Airway Obstruction; D023181:Antimicrobial Cationic Peptides; D015415:Biomarkers / Q000097:blood; D001770:Blood Bactericidal Activity; D001798:Blood Proteins / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D002352:Carrier Proteins / Q000097:blood; D016207:Cytokines / Q000097:blood*; D004391:Dust; D002523:Edible Grain; D004731:Endotoxins / Q000009:adverse effects; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008448:Maximal Expiratory Flow Rate; D008449:Maximal Expiratory Flow-Volume Curves; D008562:Membrane Glycoproteins; D008565:Membrane Proteins; D009000:Monocytes / Q000276:immunology / Q000378:metabolism; D016273:Occupational Exposure; D018124:Receptors, Tumor Necrosis Factor / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D023181:Antimicrobial Cationic Peptides; D015415:Biomarkers; D001798:Blood Proteins; D002097:C-Reactive Protein; D002352:Carrier Proteins; D016207:Cytokines; D004391:Dust; D004731:Endotoxins; D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D008562:Membrane Glycoproteins; D008565:Membrane Proteins; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000099231:Lipopolysaccharide-Binding Protein; C021623:bactericidal permeability increasing protein