Cell injury and repair.
Occupational lung disease results from a remarkably complex interaction of the inhaled material with the lung parenchyma and the worker's immune and inflammatory mechanism, (Fig 1). The past decade has seen a marked increase in our understanding of individual events involved in the pathogenesis of occupational lung disease, and has seen increased appreciation of the prominent role of lung inflammation in the production of lung disease following inhalation of a potentially injurious agent. Further work with isolated cells and tissue in culture and with experimental animal models will be required to assess the contribution of individual pathogenetic events to the total disease picture, and to better understand the ability of the lung parenchyma to repair itself following injury.
D002630:Chemotactic Factors / Q000276:immunology; D003165:Complement System Proteins / Q000276:immunology; D006099:Granuloma / Q000473:pathology; D006801:Humans; D008168:Lung / Q000166:cytology / Q000276:immunology / Q000473:pathology; D008171:Lung Diseases / Q000139:chemically induced / Q000473:pathology*; D008214:Lymphocytes / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D009784:Occupational Diseases / Q000473:pathology*; D010586:Phagocytes / Q000276:immunology; D011014:Pneumonia / Q000473:pathology
D002630:Chemotactic Factors; D003165:Complement System Proteins