ABSTRACT
Recent advancements in immunological technology have allowed occupational lung diseases to be studied from a new and different aspect. The application of immunological testing to workers with occupational asthma, hypersensitivity pneumonitis, and fibrotic pulmonary disease secondary to silica and asbestos exposure have allowed immunological mechanisms to be suggested in the pathogenesis of these diseases. Modern techniques have identified several types of allergic tissue injury [1] which are important in the pathogenesis of occupational lung disease. For example, in many types of occupational asthma, immediate type hypersensitivity responses (type I) mediated by IgE antibodies which produce the release of mediators from tissue basophils and mast cells may be the immunological event that is important. However, the mechanisms operative in other types of occupational asthma such as that secondary to toluene diisocyanate (TDI) vapor inhalation are still not clear and may involve altered (3 adrenergic activity in the absence of an underlying primary immunological aberration. It has been suggested that immune complex (type III) and cell-mediated (type IV) responses may be the most important types of allergic tissue 126injury in patients with hypersensitivity pneumonitis due to inhalation of biological dust such as that observed in farmer's lung and pigeon-breeder's disease. Finally, the pulmonary fibrosis seen in patients with silicosis and asbestosis may be in part the end of a smoldering inflammatory response caused by activation of certain serum proteins such as the complement system to produce tissue injury or by mediators released from macrophages through immunological means which ultimately affect the function of fibroblast and produce collagen deposition. It is possible that the inflammatory response could be the result of the direct effects of the particles on various alveolar cell types. Therefore, the data of most studies of patients with occupational lung disease indicate there are several types of immune mechanisms which ultimately result in tissue injury.
