ABSTRACT
Pneumoconiosis was the first reported occupational disease in Korea and was the most common one until 1990. In the past, most pneumoconiosis patients were found among underground workers in various mines. Recently this occupational disease has increasingly affected workers in manufacturing industries such as ship building, briquette, glass, foundry industries, and so on. In order to investigate the scale of pneumoconiosis in manufacturing industries, we evaluated the detailed medical examination records and insurance deliberation data from 1989 until 1994. Information about work history, medical history, and exposure dust type were collected for each member of the study population. All chest X-rays were interpreted and classified using the International Labor Organization(ILO) scale by three radiologist who have had extensive experience evaluation pneumoconiosis. For the calculation of the incidence rate of manufacturing pneumoconiosis, we analyzed the Specific Health Examination data and estimated the population at risk as a denominator of the incidence rate. We divided manufacturing industry into 9 subclasses by industrial classification and estimated the incidence rate of pneumoconiosis per 100,000 workers at risk respectively. The results were as follows, 1. 485 workers were newly diagnosed with pneumoconiosis during 6 years from 1989 to 1994. 482 workers had radiographs consistent with simple pneumoconiosis and three with progressive massive fibrosis. Among those with radiographs consistent with simple pneumoconiosis, 395 workers(81.4%) had category 1 profusion, 76 workers(15.7%) had category 2 profusion and 11 workers(2.3%) had category 3 profusion. 2. Almost all of them were male(97.9%) and their average age was 48.3 uears. Manufacturing pneumoconiosis patients were more common in their forties and fifties. 3. The average duration of dust exposure required for the occurrence of pneumoconiosis was 13.5 years. In the case of metal products manufacturing which is mostly related to welding, the average duration of dust exposure was 12.0 years. It was slightly shorter than other manufacturing industries. The average duration of dust exposure required for the occurrence of pneumoconiosis seemed to be shorter in welding operators, even though the welders lung has a weak tissue reaction and the condition is reversible. 4. According to the Industrial classification, 299 cases(61.6%) were found in workers of non-metal mineral products manufacturing, and 56 cases(11.5%) in basic metals industry. 5. The average annual incidence rate of pneumoconiosis in manufacturing industries from 1990 to 1994 was 56.6 per 100,000 workers at risk. On sub-classification, the average annual incidence rate of pneumoconiosis in non-metal mineral products manufacturing industry was the highest among them, showing 479 per 100,000 workers at risk. 6. Radiologic prevalence rate of tuberculosis in these cases was 6.6%. 7. X-ray category profusion in newly diagnosed manufacturing pneumoconiosis varied according to sub-classification. The proportion of category 1 profusion in metal products manufacturing is higher than that in non-metal mineral products manufacturing. 8. The type pattern of small round opacities varied according to sub-classification in manufacturing industry. In non-metal mineral products manufacturing, the small round opacity were observed 25.9% cases with p type, 72.1% with q type and 2.0% with r type respectively. But in metal products manufacturing, the small round opacity were observed 51.4% cases with p type and 48.6% with q type respectively. The cause might be that the exposed dust is different according to job. 9. The type pattern of small round opacities varied according to dust type. Metal dusts showed similar radiologic shape to the coal dusts, but welding fume showed more frequent p type(60.3%) and less frequent q type(377%). rock dust showed less frequent p types(18.3%) and more frequent q types(75.3%). Since the incidence rate of non-metal manufacturing workers showed higher rate than other manufacturing industry, Preventive measures and health care education should be carefully carried out in these workers.
Subject(s)
Humans , Classification , Coal , Delivery of Health Care , Dust , Education , Fibrosis , Glass , Incidence , Insurance , Korea , Lung , Metals , Occupational Diseases , Pneumoconiosis , Population Characteristics , Prevalence , Ships , Thorax , Tuberculosis , WeldingABSTRACT
No abstract available.
Subject(s)
Erythrocyte Membrane , Erythrocytes , Hydroxyl Radical , Lipid Peroxidation , Macrophages, Alveolar , Mineral FibersABSTRACT
Many acute and chronic lung diseased including pneumoconiosis are characterized by the presence of increased numbers of activated macrophages. These macrophages generate several inflammatory cell chemoattractants, by which neutrophil migrate from vascular compartment to the alveolar space. Recruited neutrophils secrete toxic oxygen radicals or proteolytic enzymes and induce inflammatory response. Continuing inflammatory response results in alteration of the pulmonary structure and irreversible fibrosis. Recently, a polypeptide with specific neutrophil chemotactic activity, interleukin-8 (IL-8), has been cloned and isolated from a number of cells such as: monocytes, macrophages and fibroblasts. IL-1 and/or TNF-alpha preceded for the synthesis of IL-8, and we already observed high level of IL-1 and TNF-alpha in vivo experiments. So we hypothesized that IL-8 might play a central role in the pathogenesis of pneumoconiosis. In order to evaluate the clinical utility of IL-1, IL-8, TNF as a biomarker in the early diagnosis of pneumoconiosis, we investigated the increase of IL-1, 8, TNF in the pneumoconiotic patient and the significant (p<0.05) correlation between IL-8 level and progression of pneumoconiosis.
Subject(s)
Humans , Chemotactic Factors , Clone Cells , Diagnosis , Early Diagnosis , Fibroblasts , Fibrosis , Interleukin-1 , Interleukin-8 , Lung , Macrophages , Monocytes , Neutrophils , Peptide Hydrolases , Pneumoconiosis , Reactive Oxygen Species , Tumor Necrosis Factor-alphaABSTRACT
Exposure to various particles and fibers can result in lung inflammation that may progress to fibrosis, even lung cancer for which there is no effective clinical treatment now. The mechanism involved in pulmonary injury has not been well defined ; however, most current evidence implicates a central role for alveolar macrophages (AM) in this process. Also apoptosis or programmed cell death is regarded as a mechanism which is related with the pulmonary fibrosis. We propose that the cytotoxic potential of various particles may be evaluated by measuring lactic dehydrogenase (LDH) from particle co-cultured supernatant and theses particles may induce the characteristics of apoptosis, DNA ladder. We analyzed rat AM culture media which was incubated for 3 days with the same concentration (10 ug/ml) of silica(Si), chrysotile(Ch), crocidolite(Cr), ceramic fiber(CF), rock wool(RW) and glass wool (GW). And each particles (50ug/cm(2)) was incubated with A549 (pneumocyte in tracheal epithelium) cell lines for 24 hours to confirm the DNA ladder. Additionally, silica induced apoptosis in vivo was confirmed by electromicroscopic observation. The results were as follows; 1. Silica, asbestos and man-made mineral fibers (MMMF) co-cultured with AM showed the increase of LDH significantly with the time interval of 24, 48, 72 hours except for ceramic fiber in 48 and 72 hours and crocidolite in 72 hours. 2. Silica, asbestos and man-made mineral fibers (CF, GF) showed the characteristics of apoptosis, DNA ladder, which was induced by incubating A549 cell with each particles for 24 hours in vitro 3. Apoptotic alveolar macrophage was observed the findings of zeiosis (membrane blebbing), condensation of nuclear chromosome and many vacuoles in cytoplasm, electomicroscopically.
Subject(s)
Animals , Rats , Apoptosis , Asbestos , Asbestos, Crocidolite , Cell Death , Cell Line , Ceramics , Culture Media , Cytoplasm , DNA , Fibrosis , Glass , Lung Injury , Lung Neoplasms , Macrophages, Alveolar , Mineral Fibers , Oxidoreductases , Pneumonia , Pulmonary Fibrosis , Silicon Dioxide , Vacuoles , WoolABSTRACT
Exposure to various particles and fibers can result in lung inflammation that may progress to fibrosis, even lung cancer for which there is no effective clinical treatment now. The mechanism involved in pulmonary injury has not been well defined ; however, most current evidence implicates a central role for alveolar macrophages (AM) in this process. Also apoptosis or programmed cell death is regarded as a mechanism which is related with the pulmonary fibrosis. We propose that the cytotoxic potential of various particles may be evaluated by measuring lactic dehydrogenase (LDH) from particle co-cultured supernatant and theses particles may induce the characteristics of apoptosis, DNA ladder. We analyzed rat AM culture media which was incubated for 3 days with the same concentration (10 ug/ml) of silica(Si), chrysotile(Ch), crocidolite(Cr), ceramic fiber(CF), rock wool(RW) and glass wool (GW). And each particles (50ug/cm(2)) was incubated with A549 (pneumocyte in tracheal epithelium) cell lines for 24 hours to confirm the DNA ladder. Additionally, silica induced apoptosis in vivo was confirmed by electromicroscopic observation. The results were as follows; 1. Silica, asbestos and man-made mineral fibers (MMMF) co-cultured with AM showed the increase of LDH significantly with the time interval of 24, 48, 72 hours except for ceramic fiber in 48 and 72 hours and crocidolite in 72 hours. 2. Silica, asbestos and man-made mineral fibers (CF, GF) showed the characteristics of apoptosis, DNA ladder, which was induced by incubating A549 cell with each particles for 24 hours in vitro 3. Apoptotic alveolar macrophage was observed the findings of zeiosis (membrane blebbing), condensation of nuclear chromosome and many vacuoles in cytoplasm, electomicroscopically.
Subject(s)
Animals , Rats , Apoptosis , Asbestos , Asbestos, Crocidolite , Cell Death , Cell Line , Ceramics , Culture Media , Cytoplasm , DNA , Fibrosis , Glass , Lung Injury , Lung Neoplasms , Macrophages, Alveolar , Mineral Fibers , Oxidoreductases , Pneumonia , Pulmonary Fibrosis , Silicon Dioxide , Vacuoles , WoolABSTRACT
The pulmonary recruitment and activation of inflammatory cells, in particular, neutrophils is thought to contribute to lung injury resulting from dust exposure. MIP-2 (macrophage inflammatory protein-2) which is a member of C-X-C chemokine plays a key role in neutrophil recruitment to sites of tissue injury. Especially, mineral fiber induced pulmonary response is as a model for the neutrophil recruitment. Therefore, we evaluated the distribution of MIP-2 expression in lung tissue of mineral fiber exposed rat using immunohistochemical study and the relationship between degree of inflammation of lower respiratory tract and MIP-2 expression. Total cell counts in bronchoalveolar lavage (BAL) fluid in mineral fiber-exposed group were markedly increased compared with each control group even not in ceramic fiber group. Number of neutrophil in BAL fluid in mineral fiber-exposed group were markedly increased compared with each control group until 4th week but except ceramic fiber group. In chrysotile group, number of neutrophil in BAL fluid were markedly increased compared with control group at 8th week. Lung tissue instilled with all kinds of mineral fibers showed remarkable developments of bronchus associated lymphoid tissue (BALT) and small multiple granulomas but not for ceramic fiber group. In chrysotile group, multiple granuloma and inflammatory change were more profuse response compared with other groups. MIP-2 was predominently expresses in epithelial cells of bronchioles and bronchus and was express also found in macrophages with lung section at 1 week after fiber instillation. Small amount of epithelial cell associated MIP-2 was present in chrysotile at 8 week group. But MIP-2 was not seen in epithelial cells and macrophages in the lung tissue instilled with crocidolite, ceramic fiber and glass fiber at 8 weeks. Our finding suggest that MIP-2 is predominantly expressed in bronchial epithelial cells of lung from mineral fiber-exposed rat and correlated with inflammatory cell, especially neutrophil, recruitment and tissue reaction. And we documented that MIP-2 expression and neutrophil recruitment in man-made vitreous fiber-exposed rat, especially glass fiber, less than chrysotile.
Subject(s)
Animals , Rats , Asbestos, Crocidolite , Asbestos, Serpentine , Bronchi , Bronchioles , Bronchoalveolar Lavage , Cell Count , Ceramics , Dust , Epithelial Cells , Glass , Granuloma , Inflammation , Lung , Lung Injury , Lymphoid Tissue , Macrophages , Mineral Fibers , Neutrophil Infiltration , Neutrophils , Respiratory SystemABSTRACT
Pneumoconisosis was the first reported occupational disease in korea and was the most common occupational disease until 1990. Nowadays pneumoconiosis is the second most common occupational disease which accounts for more than at least 40% of all the occupational diseases in Korea. Many studies have been carried out in the prevalence rate, incidence rate, and risk factors assessment of pneumoconiosis. Workers exposed to dust used to take health examination once annually by the Industrial Safety and Health Act(1981). The number of coal workers has steadily decreased due to coal rationalization projects which have been strongly driven by the government since 1988 and the occupational environment has been improving. So, the incidence rate of pneumoconiosis will probably be lower in the future. But a disease control system administed for patient control and compensation, which is not involved in epidemiologic studies may not figure out the prevalence rate, incidence rate, mortality rate and the extent of severity of pneumoconiosis. Several problems and expected solutions are mentioned here as follows: 1. workers exposed to dust and pneumoconiosis patients are under government control, but the retired workers are not. Since we evaluate only visiting retired workers, we don't know exactly the current status and whole scale of the retired workers. If possible, the construction of cohort in all the retired workers is needed. 2. Since most of pneumoconiosis patients retired from the work and had changed their job, it is difficult to figure out the prevalence rate of pneumoconiosis just depending on the annual health exam for those workers at risk. So, systemic control for all pneumoconiosis patients is needed. 3. It is difficult to diagnose the onset of pneumoconiosis. We make a decision the time when the patient is diagnosed with pneumoconiosis on its onset. It is difficult to estimate it, especially in the case of retired workers because we can evaluate only persons with respiratory symptoms. The solution of such a problem is construction of cohort in all of the retired workers. 4. Because the patients who died outside of hospital don't seem to be reported, the mortality rate of pneumoconiosis is underestimated. So, systemic control and follow-up observation for all pneumoconiosis patients is needed. 5. A definite severity classification criteria for pneumoconiosis hasn't been established in Korea. We should try to make one. 6. Since workers who had exposed to dust in various mines at least 1 yr are subject to pneumoconiosis laws, workers easily don't report their full dust exposure history. Therefore we can't obtain the exact lifetime dust exposure from administrative data. We should try to make basic raw data of whole dust exposure in workers. It's concluded that the construction of cohort in workers who are or were exposed to dust in various mines is required and epidemiologic study of pneumoconiosis should be carried out with the administrative control of pneumoconiosis side by side. With the database of these materials, we can speculate and devise the measure for the further affecting subjects who are presumed to be most common in manufacturing industries.
Subject(s)
Humans , Classification , Coal , Cohort Studies , Compensation and Redress , Dust , Epidemiologic Studies , Follow-Up Studies , Incidence , Jurisprudence , Korea , Mortality , Occupational Diseases , Pneumoconiosis , Prevalence , Rationalization , Risk FactorsABSTRACT
Early recognition of coalescence in pneumoconiotic lesions is important because such coalescence is associated with the respiratory symptoms and deterioration of lung function. This complicated form of pneumoconiosis also has worse prognosis than does simple pneumoconiosis. High resolution computerized tomography(HRCT) provides significant additional information on the stage of the pneumoconiosis because it easily detects coalescence of nodules and emphysema that may not be apparent on the simple radiograph. The Purpose of this study is to clarify the role of HRCT in detection of large opacity and the relationship of change between the coalescence of nodules or emphysema and lung function in dust exposed workers. 1. There was good correlation between the HRCT grade of pneumoconiosis and ILO category of profusion. 5(9.09%) in 55 study population had confluent nodule extending over two or more cuts on HRCT. HRCT could identify the pneumoconiotic nodules which was not found by simple radiography in 6 workers with category 0/0. 2. No significant difference was observed coalescence of nodules and emphysema by dust type. 3. There was no significant difference in pulmonary function according to ILO and HRCT classification. 4. HRCT could detect the significant reduction in FEV1, FEV1/FVC, PEER, FEF25, FEF50, and FEF75 and remarkable increase in RV and TLC in study persons with emphysema compared with non-emphysema group. 5. Emphysema was found more often in nodules-coalescence group than small opacity group by HRCT. We found that HRCT could easily detect areas of coalescence and complicated emphysema compared to plain chest X-ray. Also our data suggest that it is primarily the degree of emphysema rather than the degree of pneumoconiosis that determines the level of pulmonary function.
Subject(s)
Humans , Classification , Dust , Emphysema , Lung , Pneumoconiosis , Prognosis , Radiography , ThoraxABSTRACT
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.
Subject(s)
Animals , Rats , Arachidonic Acid , Asbestos , Asbestos, Amosite , Asbestos, Crocidolite , Asbestos, Serpentine , Asbestosis , Collagen , Extracellular Matrix , Fibroblasts , Fibronectins , Fibrosis , Inhalation , Lung , Macrophages , Macrophages, Alveolar , Respiratory System , Tumor Necrosis Factor-alphaABSTRACT
Occupational lung diseases caused by metal oxide are classified as follows, metal fume fever, chemical pneumonitis, hypersensitivity pneumonitis, and occupational asthma. Even though it's well known the immunologic mechanism is involved in metal fume fever, the exact cause is unkown yet. Some authors have speculated that metal fume fever is a form of hypersensitivity pneumonitis. A smelter exposed to metal oxide fumes was hospitalized with some complaints such as severe cough, dyspnea and fever. Chest radiographs on admission showed ill-defined reticulonodular density especially prominent in the base of the both lower lobe. HRCT of chest was observed diffuse fine granolar and reticular involvement with multiple small honeycomb cystic lesion. Bronchoalveolar lavage showed a lymphocyte predominant alveolitis and TBLB had the finding of noncaseating granuloma infiltrating with giant cells, lymphocytes and macrophages. This is a case of alveolitis caused by metal oxide fume which has the characteristics of hypersensitivity pneumonitis in clinical picture and the finding of BAL and TBLB.
Subject(s)
Alveolitis, Extrinsic Allergic , Asthma, Occupational , Bronchoalveolar Lavage , Cough , Dyspnea , Fever , Giant Cells , Granuloma , Hypersensitivity , Lung Diseases , Lymphocytes , Macrophages , Pneumonia , Radiography, Thoracic , ThoraxABSTRACT
BACKGROUND: Pleural abnormality is the the most common respiratory change caused by asbestos dust inhalation and also develp other asbestos related disease after cessation of asbestos exposure. So we conducted epidemiologic study to investigate if the pleural abnormality is associated with pulmonary function change and what factors are influenced on pulmonary function impairement. METHODS: Two hundred and twenty two asbestos workers from 9 industries using asbestos in Korea were selected to measure the concentration of sectional asbestos fiber. Questionnaire, chest X-ray, PFT were also performed. All the data were analyzed by student t-test and chi-square test using SAS. Regressional analysis was performed to evaluate importent factors, for example smoking, exposure concentration, period and the existence of pleural thickening, affecting to the change of pulmonary function. RESULTS: 1) All nine industries except two, airborn asbestos fiber concentration was less than an average permissible concentration. PFT was performed on 222 workers and the percentage of male was 88.3%, their mean age was 41+/-9 years old, and the duration of asbestos exposure was 10.6+/-7.8 yrs. 2) The chest X-ray showed normal(89.19%), pulmonary Tb(inactive)(2.7%), pleral thickening (7.66%), suspected reticulonodular shadow(0.9%). 3) The mean values of height, smoking status, concentration of asbestos fiberwere not different between the subjects with pleural thickening and others, but age, cumulative pack-years, the dura-tion of asbestos exposure were higher in subjects with pleural thickening. 4) All the PFT indices were lower in the subjects with pleural thickening than in the subjects without pleural thickening. 5) Simple regression analysis showed there was a significant correlation between FEF75 which is sensitive in small airway obstruction and cumulative smoking pack-years, the duration of asbestos exposure and the concentration of asbestos fiber. 6) Multiple regression analysis showed all the pulmonary function indices were decreased as the increase of cumulative smoking pack-years and especially in the indices those are sensitive in small airway obstruction. Pleural thickening was associated with reduction in FVC,FEV1, PEFR and FEF25. CONCLUSION: The more concentration of asbestos fiber and the more duration of asbestos exposure, the greater reduction in FEF50,FEF75. Therefore PFT was important in the evaluation of early detection for small airway obstuction. Furthermore pleural thickening without asbesto-related parenchymal lung disease is associated with reduction in pulmonary function.
Subject(s)
Humans , Male , Airway Obstruction , Asbestos , Dust , Epidemiologic Studies , Inhalation , Korea , Lung Diseases , Peak Expiratory Flow Rate , Smoke , Smoking , ThoraxABSTRACT
Asbestos is widely used in the textile, asbestos cement, construction products, friction material, paper products, insulation products, chemical and plastic products because of its heat resistance, flexibility, tensile strength, and texturability. It is now generally recognized that longterm and excessive inhalation of asbestos dust causes asbestosis, lung cancer, malignant mesothelioma and malignancies in other organs such as cancer of gastrointestinal tract, leukemia, lymphoma. Although eighty thousand tons of asbestos has been annually consumed since 1979 in korea, it has not been reported asbestos and lung cancer by asbestos dust so far, while a case of mesothelioma was officially diagnosis as a occupational disease at 1993. We experienced firstly a case of asbestosis and lung cancer caused simultanously by occupational asbestos exposure 11 years, which was confirmed by chest x-ray, pulmonary function test, chest CT and HRCT, bronchoalveolar lavage, and gallium scan. And so We present a case of asbestosis, pleural effusion and lung cancer with a review literature.