Molecular Epidemiology of Coal Worker's Pneumoconiosis: Application to Risk Assessment of Oxidant and Monokine Generation by Mineral Dusts
- 1 January 1990
- journal article
- research article
- Published by Taylor & Francis in Experimental Lung Research
- Vol. 16 (1), 57-71
- https://doi.org/10.3109/01902149009064699
Abstract
It is generally accepted that fibrotis lung diseases are mediated by macrophagederived cytokines and growth factors. Basic research continues to find new factors involved in these disease processes to incorporate into new hypotheses. Two hypotheses implicitly generated by recent findings were tested in an epidemiologic approach among workers in coal mines. This approach is described as molecular epidemiology and is exemplified by two studies focused on different mechanistic aspects of coal workers' pneumoconiosis (CWP): antioxidants in red blood cells of miners with CWP and generation of tumor necrosis factor (TNF) by blood monocytes of miners with CWP. Most findings in the antioxidant study may merely be reflections of pulmonary inflammatory processes. Some data in the TNF study indicate, however, that TNF release is a risk factor for the development of lung fibrosis after prolonged exposure to coal mine dust.Keywords
This publication has 21 references indexed in Scilit:
- Generation of Free Radicals from Freshly Fractured Silica Dust: Potential Role in Acute Silica-induced Lung InjuryAmerican Review of Respiratory Disease, 1988
- Alveolar macrophages release an insulin-like growth factor I-type molecule.Journal of Clinical Investigation, 1988
- ESR evidence for the hydroxyl radical formation in aqueous suspension of quartz particles and its possible significance to lipid peroxidation in silicosisJournal of Toxicology and Environmental Health, 1988
- Interstitial Pulmonary FibrosisAmerican Review of Respiratory Disease, 1987
- Implication of Active Oxygen Species as Second Messengers of Asbestos ToxicityDrug and Chemical Toxicology, 1987
- Macrophages, Dust, and Pulmonary DiseasesExperimental Lung Research, 1987
- Some aspects of the problem of individual predisposition to silicosis.Environmental Health Perspectives, 1986
- Silica-stimulated monocytes release fibroblast proliferation factors identical to interleukin 1. A potential role for interleukin 1 in the pathogenesis of silicosis.Journal of Clinical Investigation, 1984
- Individual susceptibility to inhaled particles. A methodological essay.Scandinavian Journal of Work, Environment & Health, 1983
- Production of fibronectin by the human alveolar macrophage: mechanism for the recruitment of fibroblasts to sites of tissue injury in interstitial lung diseases.Proceedings of the National Academy of Sciences, 1981