Pja. Borm et al., CROSS-SHIFT CHANGES IN BLOOD INFLAMMATORY MARKERS OCCUR IN THE ABSENCE OF AIRWAY-OBSTRUCTION IN WORKERS EXPOSED TO GRAIN DUST, Chest, 109(4), 1996, pp. 1078-1085
Grain dust is well known to cause both acute and chronic respiratory d
isorders, and endotoxins are considered key components in this. Since
endotoxins are known to elicit proinflammatory mediators, we investiga
ted cytokine (tumor necrosis factor [TNF], interleukin-6, interleukin-
8) release and a number of proinflammatory and anti-inflammatory prote
ins (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, usi
ng flow-volume curves and/or forced oscillation measurements. On Monda
y and Friday, blood samples (30 mL) were drawn and cytokine release wa
s determined by enzyme-linked immunosorbent assay in supernatant of is
olated 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 b
oth surveys, no cross-week change in lung function parameters was obse
rved. In the first survey (average exposure: 20.2 mg/m(3)), monocyte s
pontaneous TNF release was increased sevenfold cross week (p<0.001) an
d 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/m
(3)), impedance parameters indicated a significant improvement of airw
ay function, and cross-week changes in inflammatory markers were minim
al. Therefore, we conclude that inflammatory events can be used to mon
itor adverse respiratory effects of moderate grain dust exposure.