V. Vallyathan et al., Changes in bronchoalveolar lavage indices associated with radiographic classification in coal miners, AM J R CRIT, 162(3), 2000, pp. 958-965
Previous studies on symptomatic coal miners have shown that alveolar macrop
hages, recovered by bronchoalveolar lavage (BAL), release excessive amounts
of reactive oxygen species (ROS) and inflammatory cytokines. It has been p
roposed that these secretions may mediate cell injury and initiate the dise
ase process. We hypothesized that acellular bronchoalveolar lavage fluid (B
ALF) indices in coal miners chronically exposed to coal dust may reflect th
e status of important homeostatic modulations in the lung that lead to the
development of coal workers' pneumoconiosis (CWP). To test this hypothesis,
we measured inflammatory status, oxidant burden, antioxidant defenses, cyt
okines, growth factors, fibronectin, and alpha(1)-antitrypsin (alpha(1)-AT)
in the BALF of healthy never-smoker control subjects, never-smoker undergr
ound coal miners with negative radiographs (ILO 0/0-1/0), and two miners wi
th moderate changes in the chest radiographs (ILO 2/2). Interestingly, indi
ces of injury and inflammation increased with the progression of disease in
coal miners. Antioxidant enzymes, such as catalase, glutathione peroxidase
, and superoxide dismutase, showed a 19-fold, 22-fold, and 6-fold increase
above control, respectively, in coal miners with category 2/2 CWP. Signific
ant increases in the secretion of IL-1, IL-6, TNF-alpha, TGF-beta, fibronec
tin, and alpha(1)-AT also were evident in coal miners with disease. This up
-regulation of antioxidant defenses and cytokines was not evident in coal m
iners in the absence of clinically evident radiographic disease. In additio
n, the concentration of lipid peroxidation by products in the BALF of coal
miners without evidence of radiographic disease showed a moderate 3-fold in
crease, whereas, in coal miners with category 2/2 CWP it showed a 59-fold i
ncrease compared to control subjects. These results are in good agreement w
ith our hypothesis that development of CWP and its progression may be corre
lated with an oxidative stress and up-regulation of cytokines and mediators
of growth.