|
|
||||||||
Guest Access | Sign In via User Name/Password |
|||||||||
1 From the Departments of Health Risk Analysis and Toxicology, University of Limburg, Maastricht, the Netherlands
2 From the Department of Epidemiology, University of Limburg, Maastricht, the Netherlands
3 From the Department of Pulmonology, University of Limburg, Maastricht, the Netherlands
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.
Key Words: BPI CRP cytokines endotoxin grain dust LBP lung function soluble TNF receptor TNF
Submitted on August 21, 1995
Accepted on September 26, 2007
This article has been cited by other articles:
![]() |
I. M Wouters, J. Douwes, P. S Thorne, D. Heederik, and G. Doekes Inter- and intraindividual variation of endotoxin- and {beta}(1 -> 3)-glucan-induced cytokine responses in a whole blood assay Toxicology and Industrial Health, February 1, 2002; 18(1): 15 - 27. [Abstract] [PDF] |
||||
![]() |
E. N. Schachter, E. Zuskin, N. Rienzi, S. Goswami, V. Castranova, M. Whitmer, and P. Siegel Pharmacologic Properties of Brewery Dust Extracts In Vitro Chest, June 1, 2001; 119(6): 1870 - 1877. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |