C. Pleural plaques
Pleural plaques is a medical condition as a result of exposure to asbestos that lead to accumulated plagues within the pleural cavity(a). Many diseases such as pneumonia, breast cancer, and heart failure can affect the pleural space.,therefore, it is often a secondary effect of another disease process.
1. Dying at a younger age, relatively high ratio of mesothelioma and lung cancer
In the study to review and summarise epidemiological studies, along with other relevant data, and to discuss the potential contribution to environmental risk assessment of Asbestos related diseases from environmental exposure to crocidolite in Da-yao, China, found that dying at a younger age and the relatively high ratio of mesothelioma cases to lung cancer could also be another unique result of lifetime environmental exposure to crocidolite asbestos(10).
Although bleeding is the most serious complication of oral anticoagulant treatment, hemothorax is extremely rare. There is a report of a case with localized pleural plaques and spontaneous hemothorax due to warfarin treatment which was improved with medical treatment is presented because of its rarity. The patients recieving oral anticoagulant treatment should be monitorized for effective anticoagulation and adverse effects, if pleural effusion occurs, hemothorax should be kept in mind in the differential diagnosis. Pleural pathologies such as pleural plaques or thickening may be risk factors for hemothorax(11).
3. Pleural and parenchymal fibrosis
In the data from the County of Uppsala, Sweden, more than 1600 persons with pleural plaques and/or asbestos-related pleural thickening have been seen at the Uppsala University Hospital during a period of about 15 years, showed that during the observation time, 40 patients developed lesions mainly affecting the upper lobes of the lung. They were all men, 41 to 78-years-old, and all had been occupationally exposed to asbestos. The mean latency time from the first exposure was 34 years. The mean width of the apical pleural thickening was 21 mm. In 21 patients the lesions were on the right side, in 15 they were bilateral, and in only four patients was the left side alone affected. Biopsies from the pleura were available in twelve patients and from the lung parenchyma in eight. The biopsies of the lungs all showed varying degrees of asbestosis and of the pleura nonspecific pleuritis. The lesions tended to progress and in all cases except one they were part of a diffuse pleural and parenchymal fibrosis involving the rest of the lung(12).
4. Pulmonary hypertension
In the study to examine whether exposure to amosite asbestos would affect the pulmonary vasculature and produce pulmonary hypertension, by instilling 5 mg amosite asbestor intratracheally into guinea pigs, after 3 months, the animals also showed airflow obstruction, with air trapping and an upward shift of the pressure-volume curve. There was evidence of emphysema, and the animals were moderately hypoxic. We found no consistent increase in inflammatory cells either in lavage or peripheral blood, and the histamine dose-response curves were similar in control and asbestos-exposed animals at 6 months(13).
5. Asbestos-induced airway disease
In the study to determine whether asbestos-induced changes in the structure of the walls of small airways might be associated with abnormalities of pulmonary function with guinea pigs were given 10 mg of amosite asbestos (test group) or saline (control group) by intratracheal instillation, found that pulmonary function tests performed 6 months later revealed significant increases in FRC, RV, and TLC in the test group. Measurement of airway wall thickness showed that both membranous and respiratory bronchioles were significantly thickened in the test group; this group also had airways of smaller internal diameter than the controls. Analysis for lung collagen content as hydroxyproline showed a 50% increase in the asbestos exposed animals. There was, however, only minimal and very focal interstitial fibrosis (asbestosis) in the lung parenchyma(14).
6. Immune disdorder
Silicosis patients (SILs) and patients who have been exposed to asbestos develop not only respiratory diseases but also certain immunological disorders. According to the study by the Department of Hygiene, Kawasaki Medical School, in particular, SIL sometimes complicates autoimmune diseases such as systemic scleroderma, rheumatoid arthritis (known as Caplan syndrome), and systemic lupus erythematoses. In addition, malignant complications such as lung cancer and malignant mesothelioma often occur in patients exposed to asbestos, and may be involved in the reduction of tumor immunity. Although silica-induced disorders of autoimmunity have been explained as adjuvant-type effects of silica, more precise analyses are needed and should reflect the recent progress in immunomolecular findings(15).
7. Cardiovascular disease
Asbestos is an inflammatory agent, and there is evidence that inflammatory processes are involved in the development of cardiovascular disease. According to the study by the Mathematical Sciences Unit, Health and Safety Laboratory, in the analuzing of Cardiovascular disease mortality in a cohort of 98,912 asbestos workers, with median follow-up of 19 years, showed that Altogether 15,557 deaths from all causes, 1053 deaths from cerebrovascular disease and 4185 deaths from ischaemic heart disease (IHD) occurred during follow-up. There was statistically significant excess mortality from cerebrovascular disease (SMR: men 1.63, women 2.04) and IHD (SMR: men 1.39, women 1.89). Job and birth cohort were associated with the risk of cerebrovascular and IHD mortality in the Poisson regression model including sex, age, smoking status, job, cohort and duration of exposure. For IHD only, duration of exposure was also statistically significant in this model(16).
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