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Page 2 Environmental
and Occupational Lung Diseases
Asbestos Lung and Pleural Effects Asbestos exposure may result in asbestosis (pulmonary fibrosis) and in lung cancer in patients with asbestosis. Pleural findings include plaques, calcified plaques, diffuse thickening, effusion, and mesothelioma. The type of asbestos (crocidolite or chrysotile), the duration of exposure, the amount of exposure, and the year the patient was first exposed are related to the type and severity of the asbestos-related condition. Asbestosis is defined as a pneumoconiosis with interstitial fibrosis of the pulmonary parenchyma in which asbestos bodies or fibers may be demonstrated (1). Generally, a large cumulative exposure is necessary for the development of asbestosis, with moderate-to-high levels over several years. Such exposures occurred early in the twentieth century in the weaving industry and later in the ship building and insulation trades in the 1940's and 1950's. In the United States, such high exposures have ceased since the mid 1970's. Considering the latency period, the occurrence of asbestosis should be decreasing in the 1990's. The latency is generally 20 years. A small percentage of asbestos-exposed workers may have clinical features consistent with asbestosis yet have non-asbestos interstitial lung disease (12). Dyspnea is the most common symptom. End-inspiratory fine crackles are heard in more than 60 percent of patients. Finger clubbing, cyanosis, and cor pulmonale are late findings. The chest roentgenogram shows small linear irregular opacities at the lung bases. Honeycombing is seen late. The physiologic findings indicate a decreased vital capacity with no evidence of major airflow obstruction except in smokers. The diffusing capacity is the physiologic hallmark of the disorder and is decreased in virtually all patients with asbestosis. Asbestosis remains static in most patients but progresses in a small percentage of individuals depending fiber type, cumulative exposure, level of exposure, and duration of exposure (13). Asbestos-related lung cancer was described in patients with asbestosis in 1935 (14,15) and was confirmed epidemiologically in 1955 (16). Cigarette smoking is an important factor in asbestos-related lung cancer and acts in a multiplicative synergistic manner; the two combined exposures cause a higher occurrence of cancer than the two exposures separately. Asbestos-related lung cancer is rare among non-smokers. The cancerous lesions may occur centrally or peripherally. Small cell, squamous cell, and adeno-carcinoma occur with equal frequency (17). Pleural effects are the most common asbestos-related findings. Unlike asbestosis, pleural plaques may occur in individuals with peripheral exposure such as working in a shipyard for one or two years during World War II, living next to an asbestos mine, or employment as an electrician, welder, or plumber. Pleural plaques generally have a latency period of 20 years and occur in as many as 60% of shipyard workers (18). Generally single or even multiple plaques are not a cause of symptoms or clinically significant physiologic abnormalities. The chest roentgenogram is distinctive and shows plaques along the lateral pleural surfaces, diaphragmatic surfaces, or along the mediastinal or pericardial surfaces. Plaques may calcify approximately 30 years after first exposure (18). Benign asbestos effusion, unlike other asbestos conditions, can occur within the first 10 years of exposure (18). Approximately 50% of patients with this condition are asymptomatic, but occasionally, a fibrothorax may develop necessitating surgical decortication. Diffuse pleural thickening or blunted costophrenic angles may be the result of a prior effusion (19) and may be associated with volume limitation (14). Mesothelioma usually results from crocidolite asbestos exposure and occurs 30 to 40 years after first exposure (20). Chest pain and effusion develop in 90% of these patients. Long-term survivors have been reported; however, the prognosis remains dismal despite triple therapy including surgery, radiation, and chemotherapy (21). Coal Worker's Pneumoconiosis This disorder has declined during the past 50 years in the United States due to the control of dust levels and improvement of mining techniques but has not been eliminated. Current prevalence rates in working miners are from 5% to 10%, an improvement from historical surveys of 30% to 50% in working miners and 75% in retired miners (22). Chronic cough is the most common symptom. Dyspnea occurs later. Physiologic findings may include airflow obstruction early and decreased diffusing capacity in late stages. Radiographic findings remain the hallmark of this disorder, with small rounded opacities early and large opacities of progressive massive fibrosis in the late stage. No correlation exists between radiographic findings and symptoms or physiologic findings during the initial stages (22). In advanced coal worker's pneumoconiosis with large opacities, symptoms, hypoxemia, and other physiologic abnormalities may be severe (22). In addition, the typical nodular opacities may disappear as the massive fibrosis progresses. Such patients should also be monitored for tuberculosis. Silicosis Although the occurrence of silicosis has declined in the United States, isolated cases continue to bee reported, usually related either to some unusual household situation, such as the inhalation of domestic scouring powder, (23) or by ignoring or not taking effective preventive measures as regulated by governmental agencies (24). A small group of stone masons cutting and shaping hard sandstone to replace the tracery in the in the windows of a ruined medieval cathedral were exposed to levels of respirable quartz up to 130 times the workplace standard over a period of up to 6 years. Two of these workers died of acute silicosis, one had an early stage of accelerated silicosis, and two others had early silicosis. Dyspnea and wheezing may be early symptoms. The chest roentgenogram shows rounded opacities in the mid and upper part of the lungs. As in coal worker's pneumoconiosis, the chest radiograph in early stages often does not correlate with the degree of symptoms and physiologic findings (25). This is in contrast to radiographs in patients with pulmonary fibrosis in whom moderately involved lung bases may reflect severe physiologic dysfunction. One explanation for the discrepancy is that in disorders showing rounded opacities (coal worker's pneumoconiosis or silicosis) or reticular nodular opacities (granulomatous disorders), the lung is normal between the opacities, whereas in disorders with linear opacities (asbestosis), the scarring is diffuse. Chest CT identifies more opacities and confluences than standard radiography, and high-resolution CT can increase the number of cases diagnosed by 10% (26). Bronchoalveolar lavage and transbronchial lung biopsy combined with energy dispersive x-ray analysis may be able to confirm the diagnosis of silicosis (27). Vigorous adherence to dust control regulations and dust count monitoring can eliminate this disorder. "Inert Metal" Pneumoconiosis Metal dusts, such as iron, tin and barium can cause the so-called "benign" pneumoconiosis (29). The chest radiograph may show rounded or reticular nodular opacities, but these are not associated with symptoms, chest physical findings, or pulmonary function abnormalities. Iron dust exposures occur during mining, milling, metal cutting, and with the use of a jeweler's rouge. Exposures to tin and barium occur during crushing or bagging operations. It is possible that in susceptible individuals or in individuals with high exposures, symptoms and physiologic abnormalities may occur, i.e., it is not a benign process. Some epidemiologic studies confirm such findings whereas others do not (30). Cadmium effects Cadmium, which is used for antifriction coatings and in metal alloys, can cause lung injury. Bronchitis (30) and pneumonitis (31) may result from cadmium fumes released during the welding of cadmium-plated metals or the burning of scrap that contains cadmium-plated metals. Aluminum effects Aluminum has been implicated as the cause of pulmonary fibrosis in workers exposed to bauxite smelting fumes (30). Pulmonary fibrosis has been reported in workers exposed to aluminum oxide in the production of abrasives from alundum ore (32). Berylliosis Beryllium was used as an agent to prolong the life of fluorescent light bulbs in the 1930s but was found to be a cause of acute and chronic berylliosis in the mid 1940s. An investigation by Hardy (33) of a large number of cases of sarcoidosis in Salem, Massachusetts resulted in establishing the cause and effect relationship. Beryllium exposure from fluorescent light bulb production has ceased, but copper-beryllium alloy exposures occur during the production and grinding of springs and electrical switches and in work on beryllium oxide ceramic materials in jet and rocket engines and nose cones, Table 8. Workers in dental laboratories are exposed to the fine powder that may be produced while finishing and polishing beryllium metal alloys. For the most part, the acute form of beryllium lung disease has been eliminated by strict environmental controls. It is almost always responsive to cessation of exposure or corticosteroid therapy. Chronic berylliosis is a granulomatous disorder caused by a cell-mediated immune reaction to beryllium (34). Generally, a direct relationship exists between airborne beryllium levels and acute berylliosis but not for chronic berylliosis. The reason for this remained puzzling until the development of bronchoalveolar lavage in the late 1980s, which demonstrated that lung cells from patients with chronic beryllium disease would proliferate in the presence of beryllium salts (34). Excessive production and accumulation of helper T-lymphocytes in the lungs occurs in the cell-mediated immune granulomatous process (35). Dyspnea is the most common symptoms, and crackles occur in 20% of patients. The vital capacity and diffusing capacity are decreased, and the radiograph shows small reticular-nodular opacities throughout the lungs and occasional hilar lymphadenopathy. The illness is indistinguishable from sarcoidosis. Chronic beryllium disease can be confirmed by testing of the peripheral blood or lung cell proliferative response to beryllium (34). The lowest dose of corticosteroid therapy should be used. Beryllium is eliminated from the lungs slowly; thus, patients may have to take corticosteroids indefinitely. Corticosteroid therapy may reduce inflammation, possibly by suppressing the immune response to beryllium, but has no effect on the scarring. Prevention of exposure and continual education of individuals using beryllium products remain essential for elimination of the disorder.
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