Compensation and Diagnosis of Asbestos Related Disease / 가정의학회지

Asbestos is a fibrous silicate that was widely used because of its heat resistance properties. Asbestos exposure affects workers involved in mining or processing asbestos or those involved in the use of asbestos in the shipbuilding, construction, and textile- and insulation-manufacturing industries. There are three commonly available types of asbestos; chrysotile (white asbestos), amosite (brown asbestos), and crocidolite (blue asbestos). All three have been associated with cancerous and non-cancerous lung disease. Asbestos-related diseases includes benign pleural effusion, pleural plaques, diffuse pleural thickening (a non-malignant disease affecting the lung lining), rounded atelectasis, asbestosis (a scarring of the lung tissue caused by asbestos), mesothelioma and lung cancer. Mesothelioma is a malignant pleural or peritoneal tumor that rarely occurs in patients who have not been exposed to asbestos. The latency period of most asbestos-related disease is 10 years or longer, asbestos-related disease remains an important public health issue. The clinical diagnosis of asbestos related diseases should be based on a detailed interview of the patient and occupational data on asbestos exposure, signs and symptoms, radiological and lung physiological findings and selected cytological, histological and other laboratory studies. Radiological imaging plays a pivotal role in the diagnosis and management of asbestos-related disease.

A Case of Lung Cancer Caused by Long-Term Asbestos Exposure / 대한산업의학회지

OBJECTIVES: To report a case of lung cancer caused by long-term asbestos exposure in a shipyard. METHODS: We evaluated chest X-ray, pulmonary function test, and chest CT and analyzed asbestos concentration in the lung tissue and bulk sample from the workplace. We also performed a workplace survey. RESULTS: The patient had worked at the shipyard for 31 years. The biopsy samples were processed to determine the asbestos content in the lung tissue and bulk sample using a transmission electron microscope (TEM) equipped with an energy dispersive X-ray analyzer (EDX). The TEM-EDX analysis revealed many asbestos fibers, the majority of which were amosite. In addition, the concentration asbestos fibers in the workplace exceeded the occupational exposure limits of asbestos. CONCLUSIONS: Our findings strongly suggest that this patient's lung cancer was related to the long-term asbestos exposure.

Effect of Asbestos on Fibroblast Proliferation of Rat / 대한산업의학회지

Asbestosis is a chronic inflammatory disorder of lower respiratory tract in which alveolar wall are progressively thickened by a fibrotic process. Fibrotic process characterized by an expansion of fibroblast and collagenous extracellular matrix secreted from this fibroblast. Alveolar macrophage is believed to be a primary target cell and major participant in the evolution of lung fibrosis after asbestos inhalation. Alveolar macrophage are known to release a variety of substance that induce tissue damage and stimulate inflammatory cells and fibroblast. Macrophage also release a variety of metabolite of arachidonic acid. Of these, PGE(2) is known to suppress fibroblast proliferation. Asbestos may be a very effective stimulus for fibroblasts without triggering the relase of PGE(2). To assess the fibrogenic properties of asbestos according to kind and dosage of asbestos and the ability of PGE(2) to suppress the proliferation of fibroblast, alveolar macrophages cultured with crocidolite, amosite and chrysotile in presence or absence of PGE(2)10(-5)M. At 24 hours after alveolar macrophage cultured with various stimuli, the released fibronectin and TNF-alpha was measured. Viability of alveolar macrophages was observed and growth promoting activity of macrphage supernatant to fibroblasts was quantified. The results were as follows; 1. The viability of alveoair macrophages stimulated with asbestos fiber was markedly decreased compared with control group except chrysotile 10 microgram group. Crocidolite and amosite were more cytotoxic than chrysotile. 2. All of asbestos augmented fibronectin production in concentration dependent fashion. 3. There was a significant positive correlation between TNF-alpha production in supernatant and fiber concentration. 4. Supernatant from alveolar macrophages cultured with asbestos were inducible a significant increase in fibroblast proliferation. 5. Incubation of avieolar macrophages with asbestos in the presence of PGE(2) resulted in significant decrease of TNF-alpha production in supernant. 6. Supernatant from alveolar macrophages cultured with asbestos were inducible a: sig nificnat decrease in fibroblast proliferation when PGE(2) was added. The result of this study strongly suggested that crocidolite and amosite were more cytotoxic and fibrogenic and exogenous PGE(2) suppressed fibroblast proliferation following exposed to asbestos.