Asbestosis Tuberculosis And Alimentary Cancer

One interesting study is called, Insulation workers in Belfast. A further study of mortality due to asbestos exposure (1940-75). - Br J Ind Med 1977;34:174-180 by P C Elmes, M J Simpson. Here is an excerpt: Abstract - A follow-up study of 162 men already working as insulators (laggers) in 1940 has been extended from 1965 to 1975. By the end of 1975 there were 40 survivors when 108 had been expected. Until 1965 there had been an overall excess of deaths; these were due to asbestosis with or without tuberculosis and to alimentary cancer, as well as to bronchial carcinoma and mesothelioma. From 1965 onwards the overall death rate among survivors is not so excessive but there is still a marked excess of deaths from bronchial cancer and mesothelioma. The continued risk of death attributable to malignancy after asbestosis had ceased to contribute directly, does not appear to be caused by any changes which occurred before 1940 in the conditions at work.

Another interesting study is called, Frequency of sister chromatid exchange and chromosomal aberrations in asbestos cement workers. - Br J Ind Med 1991;48:103-105 by N Fatma, A K Jain, Q Rahman Abstract Exposure to asbestos minerals has been associated with a wide variety of adverse health effects including lung cancer, pleural mesothelioma, and cancer of other organs. It was shown previously that asbestos samples collected from a local asbestos factory enhanced sister chromatid exchanges (SCEs) and chromosomal aberrations in vitro using human lymphocytes. In the present study, 22 workers from the same factory and 12 controls were further investigated. Controls were matched for age, sex, and socioeconomic state. The peripheral blood lymphocytes were cultured and harvested at 48 hours for studies of chromosomal aberrations and at 72 hours for SCE frequency determinations. Asbestos workers had a raised mean SCE rate and increased numbers of chromosomal aberrations compared with a control population. Most of the chromosomal aberrations were chromatid gap and break types.

Another interesting study is called, Asbestos-Induced Pleural Disease - Clinics in Chest Medicine, Volume 19, Issue 2, Pages 311-329 by S.Nishimura, V.Broaddus. Here is an excerpt: Abstract - Asbestos, for unknown reasons, has an unusual affinity for the pleura. The manifestations of asbestos-induced pleural disease are multiple and varied, from effusion to fibrosis to malignancy. Certain types of pleural disease, such as pleural plaques, are nearly specific for asbestos exposure, whereas others, such as asbestos-induced pleural effusion, are difficult to identify unequivocally as asbestos-related. Although much progress on the basic mechanisms of asbestos-cellular interactions has been achieved, the origin of pleural disorders remains unknown. Furthermore, the relationship of the different pleural conditions with each other and with the pulmonary manifestations of asbestosis and lung cancer are not understood. In this article, we attempt to concentrate on the newer studies that offer answers to some of the questions above. We refer readers to recent reviews on asbestos-related pleural disease.26, 32, 43 and 52

Another study is called, Pulmonary fibrogenesis after three consecutive inhalation exposures to chrysotile asbestos by PG Coin, AR Osornio-Vargas, VL Roggli and AR Brody - Am. J. Respir. Crit. Care Med., Vol 154, No. 5, 11 1996, 1511-1519. Here is an excerpt: Previously, this laboratory developed a model of asbestos-induced pulmonary fibrogenesis in rats and mice after a brief (1 to 3-h) inhalation exposure. However, typical human environmental exposures would be repeated, although at lower concentrations than those used in our animal model. Here we have extended this model to encompass repeated exposures and consequent long-term effects. Groups of rats were exposed to chrysotile aerosol (10 mg/m3) for 3- to 5-h periods over 3 consecutive days. Lung fiber burden and pathologic features were studied for as long as 6 mo after exposure. We found that many of the longest (> or = 8 microm) fibers were retained in the lung for at least 6 mo, whereas shorter fibers were cleared more rapidly. The three exposures to chrysotile caused a large increase in DNA synthesis in the epithelium of terminal bronchioles and more proximal airways. When compared with a single exposure, the triple exposure caused an enhanced inflammatory response as well as a prolonged period of increased DNA synthesis in the proximal alveolar region. Hyperplastic, fibrotic lesions subsequently developed in the same region and persisted for at least 6 mo after exposure. These findings will be valuable in directing future studies of the mechanisms of pulmonary fibrosis in this model.

If you found any of these excerpts interesting, please read the studies in their entirety. We all owe a debt of gratitude to these fine researchers.

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