Objective
In the prospective study all miners previously investigated in several cross sectional studies were screened for chest radiograph, exposure history (cumulative dust), lung function, high resolution computed tomography (nested study), and several biological markers (tumor necrosis factor-alpha (TNF), procollagen type III peptide, anti-oxidant enzymes). Data analysis concentrated on the relation between prospective individual changes in standardized chest radiographs and the biological markers.
In the cross sectional study biological markers (eg TNF, sputum cellularity, fibronectin, leucocyte elastase, neutral metalloendopeptidase, elastin peptides) were determined in relation to regional differences in prevalence of both simple and massive coal workers pneumoconiosis. Apart from specific interests, both studies concentrated on the role of the cytokine TNF in both cross-sectional (exposure) and prospective way (risk). Furthermore, a quality control on the TNF assay and on intra-reader variations in ILO chest radiograph readings have been used to cross-link our data and optimalize validity of our studies. The results of this collaborative study on coal workers pneumoconiosis have put many new insights with respect to disease mechanisms into the right perspective.
Coal workers pneumoconiosis (CWP) is a lung disorder that becomes manifest after several decades of exposure to coal mine dust and is commonly detected and classified using chest radiograms. Experimental animal and clinical research continue to find new immunological, biochemical and molecular biology based factors involved in interstitial lung diseases and generate new methods to measure early adverse effects of inorganic dust exposure.
Several years ago the two labs involved in this study set out to investigate the applicability of these new insights into research on CWP. In fact, the Maastricht group was the first one to show that Tumor Necrosis Factor (TNF) played a role in CWP in humans. The main objective of this type of study is not to determine the causative agent, but to appraise and use mechanisms in order to design more specific studies, eg directed to individual susceptibility and biological effects of cumulative exposure. The biological entities (enzymes, degradation products, DNA damage etc) that are used are called 'biological markers', since they 'mark' the (effect of) cumulative exposure, a cascade leading to early disease or disease itself.
If our biological markers are valid, it would improve industrial hygiene surveys of coal mine workers. Moreover, they can be easily applied to other types of occupational lung diseases occurring in the mining and steel industry.
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Programme(s)
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Coordinator
60550 Verneuil-en-Halatte
France
The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.