(Radiographics. 2001;21:1371-1391.)
© RSNA, 2001
Imaging of Occupational Lung Disease1
Kun-Il Kim, MD,
Chang Won Kim, MD,
Min Ki Lee, MD,
Kyung Soo Lee, MD,
Choong-Ki Park, MD,
Seok Jin Choi, MD and
Jong Gi Kim, MD
1 From the Departments of Diagnostic Radiology (K.I.K., C.W.K., J.G.K.) and Internal Medicine (M.K.L.), Pusan National University Hospital, Pusan National University School of Medicine, #1-10, Ami-dong, Seo-gu, Pusan 602-739, Korea; the Department of Radiology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea (K.S.L.); the Department of Diagnostic Radiology, Hanyang University Kuri Hospital, Kyoungki-Do, Korea (C.K.P.); and the Department of Radiology, Pusan Paik Hospital, College of Medicine, Inje University, Pusan, Korea (S.J.C.). Recipient of a Cum Laude award for an education exhibit at the 2000 RSNA scientific assembly. Received April 11, 2001; revision requested May 15 and received July 17; accepted July 17. Address correspondence to K.I.K. (e-mail: kikim@hyowon.pusan.ac.kr).
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Abstract
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Occupational lung disease comprises a wide variety of disorders caused by the inhalation or ingestion of dust particles or noxious chemicals. These disorders include pneumoconiosis, asbestos-related pleural and parenchymal disease, chemical pneumonitis, occupational infection, hypersensitivity pneumonitis, and organic dust toxic syndrome. Most of these disorders produce diffuse lung disease. Although many of the disorders can be detected at chest radiography, high-resolution computed tomography (CT) has been shown to be superior to chest radiography in depicting parenchymal, airway, and pleural abnormalities. Some occupational lung diseases have characteristic radiologic features suggesting the correct diagnosis, whereas in others, a combination of clinical features, related occupational history, radiologic findings, and literature supporting an association between the exposure and the disease process is required for diagnosis. With advances in chest radiology, including high-resolution CT, radiologists play a key role in the clinical evaluation of occupational lung diseases and should continue their involvement in the diagnosis and treatment of these diseases.
Index Terms: Lung, CT, 60.12118 • Lung, diseases, 60.4126, 60.77 • Lung, ground-glass opacification • Pneumoconiosis, 60.772 • Pneumonitis, 60.55 • Pneumonitis, hypersensitivity, 60.55, 60.624 • Silicosis, 60.771
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LEARNING OBJECTIVES FOR TEST 1
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After reading this article and taking the test, the reader will be able to:
- Describe the pathophysiologic background of occupational lung diseases.
- Identify the characteristic radiologic features of a variety of occupational lung diseases.
- Recognize the causative material and related occupation for individual occupational lung diseases.
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Introduction
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Thousands of environmental toxins and commercial chemicals are in use today. These agents may become aerosolized or airborne in the form of fibers, fumes, mists, or dust. Next to injuries, occupational lung disease represents the most frequently diagnosed work-related condition, and knowledge in this area has evolved substantially over the past decade (1,2). Perhaps the greatest increase in pulmonary hazards over this period has been in occupational allergic disorders, asthma, and hypersensitivity pneumonitis, with new sensitizing agents being described frequently (3). Individuals living in major metropolitan areas may inhale more than 2 mg of dust each day, and workers in dusty occupations may inhale up to 100 times that amount. The development of occupational lung disease in an individual worker is dependent on the toxic effects of the inhaled substance, the intensity and duration of the exposure, and the physiologic and biologic susceptibility of the host. The physical state of the inhaled substance (eg, solid, fume, or mixture), its solubility, and its aerodynamic dimensions determine the initial location of disease activity. Depending on the solubility and reactivity of the inhaled substance, acute or chronic reactions occur as particles are deposited in the lower respiratory tract. Acute reactions with associated inflammation and edema, or more chronic reactions characterized by fibrosis or granuloma formation, have been demonstrated following inhalation of many environmental agents (1).
In this article, we briefly discuss the occupational and pathophysiologic characteristics associated with a wide spectrum of occupational lung diseases, including pneumoconiosis, asbestos-related pleural and parenchymal disease, chemical pneumonitis, occupational infection, hypersensitivity pneumonitis, and organic dust toxic syndrome. We also discuss and illustrate the typical radiographic and CT manifestations of these diseases.
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Pneumoconiosis
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Pneumoconiosis is a tissue reaction to the presence of an accumulation of dust in the lungs. One clinicopathologic form of this reaction is fibrosis, which can be focal and nodular (as in silicosis) or diffuse (as in asbestosis). It often results in radiographic abnormalities and, if extensive enough, may lead to significant functional impairment. The other form consists of aggregates of particle-laden macrophages with minimal or no accompanying fibrosis, a reaction that is typically seen with inert dusts such as iron, tin, and barium. Although this reaction is sometimes associated with chronic radiographic abnormalities, it usually results in few, if any, functional or clinical manifestations (4).
Silicosis and Coal Worker Pneumoconiosis
The principal sources of industrial exposure to silica are free silica in mining, quarrying, and tunneling; stonecutting, polishing, and cleaning monumental masonry; sandblasting and glass manufacturing; and, in foundry work, pottery and porcelain manufacturing, brick lining, boiler scaling, and vitreous enameling. Coal miners are exposed to dusts that contain a mixture of coal, mica, kaolin, and silica in varying proportions (5).
Silicosis and coal worker pneumoconiosis (CWP) are distinct diseases, with differing histologic features resulting from the inhalation of different inorganic dusts. However, the radiographic and high-resolution CT appearances of silicosis and CWP are quite similar, so that the two disease entities cannot be easily or reliably distinguished in individual cases (6).
Dust Deposition and Lymphatic Clearance: Radiologic Perspective.—
Rapid turbulent airflow in the large central airways changes to slow laminar flow in the peripheral small airways. This results in predominant deposition of particles 1–5 µm in diameter in and around the respiratory bronchioles, a roughly centrilobular location in the secondary pulmonary lobule.
Regional distribution of pneumoconiotic lesions largely depends on the lymphatic clearance of lung. The main driving force for lymphatic flow is pulmonary arterial pressure. Gravity-dependent gradients exist due to the vertical gradient in pulmonary arterial pressure, with subsequent differences in lymphatic flow between the top and bottom of the lungs. Because the main pulmonary artery is inclined to the left, higher blood flow and lymphatic flow occur in the left upper lobe than in the right. Respiratory excursion increases lymphatic flow. Chest wall motion is thought to milk the lymphatic vessels passively but is not uniform. The outward excursion of the lateral chest wall is less than that of the anterior chest wall but more than that of the posterior chest wall. These regional differences in lymphatic flow result in poor clearance of particles from the posterior part of the right upper lung zone. This superoposterior predilection of dust retention has been described in CT studies (7).
Imaging Features.—
The characteristic radiologic abnormality seen in patients with simple silicosis or CWP consists of small, well-circumscribed nodules that are usually 2–5 mm in diameter but range from 1 to 10 mm, mainly involving the upper and posterior lung zones (Fig 1). Although there is a tendency for the nodules in silicosis to be better defined than those in CWP (Fig 2), this is not always the case (6). These small nodules indicate the presence of simple or uncomplicated silicosis or CWP.
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Figure 1a. Simple silicosis in a 59-year-old man who worked in hard-rock mining for 10 years. (a) Chest radiograph shows diffuse nodular opacities with relative sparing of the basal lung zones. (b) High-resolution CT scan shows numerous micronodules in both upper lungs with posterior zonal predominance. Nodules are more profuse in the right upper lung zone than in the left. Some nodules are centrilobular in location (arrows). Note also the multiple subpleural nodules and the "pseudoplaques," which represent the aggregate of subpleural nodules.
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Figure 1b. Simple silicosis in a 59-year-old man who worked in hard-rock mining for 10 years. (a) Chest radiograph shows diffuse nodular opacities with relative sparing of the basal lung zones. (b) High-resolution CT scan shows numerous micronodules in both upper lungs with posterior zonal predominance. Nodules are more profuse in the right upper lung zone than in the left. Some nodules are centrilobular in location (arrows). Note also the multiple subpleural nodules and the "pseudoplaques," which represent the aggregate of subpleural nodules.
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The appearance of large opacities or hyperattenuating areas over 1 cm in diameter (progressive massive fibrosis) indicates the presence of complicated silicosis or complicated CWP. These masses tend to develop in the midzone or periphery of the upper lung and migrate toward the hila, leaving overinflated emphysematous spaces between the conglomerate mass and the pleura (Figs 3, 4). They are often bilateral, symmetric, and calcified and can demonstrate cavitation (Figs 4, 5). Egg-shell calcifications in hilar and mediastinal lymph nodes are occasionally seen (6,7).
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Figure 3a. Complicated CWP in a 57-year-old man. (a) Chest radiograph shows a conglomeration of small nodules with sparing of the bibasilar area and egg-shell calcifications in both hila. (b) High-resolution CT scan shows conglomerate masses (progressive massive fibrosis) and adjacent small nodules. A thoracostomy tube (arrowhead) was placed in the left hemithorax for a pneumothorax.
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Figure 3b. Complicated CWP in a 57-year-old man. (a) Chest radiograph shows a conglomeration of small nodules with sparing of the bibasilar area and egg-shell calcifications in both hila. (b) High-resolution CT scan shows conglomerate masses (progressive massive fibrosis) and adjacent small nodules. A thoracostomy tube (arrowhead) was placed in the left hemithorax for a pneumothorax.
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Figure 4. Calcified progressive massive fibrosis in a 60-year-old retired coal worker. High-resolution CT scan (mediastinal windowing) shows a densely calcified right parahilar mass.
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Figure 5. Complicated silicosis in a 58-year-old man. High-resolution CT scan shows a cavitary conglomerate mass in the left upper lobe. Note the paracicatricial emphysema between the pleura and the cavitary mass (arrowhead). Although pulmonary tuberculosis may complicate silicosis or CWP, progressive massive fibrosis sometimes demonstrates cavitation due to ischemic necrosis.
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Acute Silicosis
Acute silicosis, also known as silicoproteinosis, is a rare condition related to heavy exposure to respirable free silica in enclosed spaces in which there is minimal or no protection from the silica. Exposure times are frequently as short as 6–8 months. The disease is often rapidly progressive, with death caused by respiratory failure.
Proliferation of type II pneumocytes and profuse surfactant production characterize the process histologically (8,9). The radiologic and pathologic appearances of acute silicosis are quite different from those of classic silicosis and are similar to those of pulmonary alveolar proteinosis (Fig 6). Chest radiographs demonstrate a pattern of diffuse airspace or ground-glass disease in a perihilar distribution with air bronchograms (10). Tuberculosis and infection with atypical mycobacteria are frequent complications (6).
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Figure 6. Silicoproteinosis in a 52-year-old quarry worker. Chest radiography showed bilateral ground-glass opacity and airspace consolidation, predominantly in the lower lung zones. High-resolution CT scan of the right lung shows patchy areas of ground-glass attenuation with fine intralobular reticulation ("crazy paving" pattern) (arrowheads), findings that are common in alveolar proteinosis. No silicotic nodules are seen. Bronchoalveolar lavage and transbronchial lung biopsy confirmed the presence of alveolar proteinosis and silica particles.
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Siderosis
The majority of cases of siderosis are seen in electric arc or oxyacetylene torch workers, who are exposed to iron oxide in fumes during the welding process. Other cases of siderosis or silicosiderosis are seen in individuals involved in the mining and processing of iron ores, workers in iron and steel rolling mills, foundry workers, and silver polishers. Siderosis is believed to be unassociated with fibrosis or functional impairment. When the iron is admixed with a substantial quantity of silica, however, the resulting silicosiderosis (mixed-dust pneumoconiosis) can lead to appreciable pulmonary fibrosis and disability (4).
The radiographic pattern in pure siderosis consists of diffuse fine reticulonodular opacities. Nodular opacities are less dense and less profuse than those in silicosis. In contrast to the majority of cases of pneumoconiosis, the radiographic abnormalities can partially or completely disappear when patients are removed from dust exposure. High-resolution CT findings, which have been described in arc welder pneumoconiosis, include widespread, poorly defined centrilobular micronodules and branching linear structures (Fig 7) or extensive ground-glass attenuation without zonal predominance and fibrosis (Fig 8) (11–13).
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Figure 7. Arc welder pneumoconiosis in a 46-year-old nonsmoker with a 15-year history of employment as a shipyard welder. High-resolution CT scan shows numerous small nodules and branching areas of hyperattenuation that are poorly defined and centrilobular. The diagnosis of siderosis was proved at transbronchial lung biopsy.
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Figure 8. Arc welder pneumoconiosis in a 57-year-old former smoker with a 13-year history of work in shipyards. The patient was asymptomatic, and the results of pulmonary function tests were normal. High-resolution CT scan shows ground-glass attenuation that is diffuse and mainly centrilobular. Follow-up high-resolution CT performed 1 year later showed no change in the parenchymal disease.
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Carbon Black Pneumoconiosis
Carbon black is produced from the burning of natural gas and various petroleum products. It has been used as a filler in rubber, plastics, phonograph records, and inks and in the manufacture of carbon paper and carbon electrodes. The importance of carbon black as a cause of pulmonary disease is unclear. A 1993 survery of carbon black workers in seven European countries, including more than 1,000 workers for whom chest radiographs were available, revealed the presence of reticulonodular abnormalities in 25% of cases (Fig 9) (14). The likelihood of identifying these abnormalities was related to total cumulative dust exposure. However, exposure to pure carbon black was reported to induce little if any clinical or functional impairment (15–17).
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Figure 9a. Carbon pneumoconiosis in a 49-year-old man with a 10-year history of employment in a carbon black factory. (a) Chest radiograph shows a fine reticulonodular pattern with lower zonal predominance. (b) High-resolution CT scan shows diffuse areas of ground-glass attenuation and numerous small centrilobular nodules.
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Figure 9b. Carbon pneumoconiosis in a 49-year-old man with a 10-year history of employment in a carbon black factory. (a) Chest radiograph shows a fine reticulonodular pattern with lower zonal predominance. (b) High-resolution CT scan shows diffuse areas of ground-glass attenuation and numerous small centrilobular nodules.
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Hard Metal Pneumoconiosis
The term hard metal is usually used to refer to an alloy of tungsten, carbon, and cobalt, occasionally with the addition of small amounts of other metals such as titanium, tantalum, nickel, and chromium. The resulting product is extremely hard and resistant to heat and is used extensively in the drilling and polishing of other metals. Exposure to dust can occur during either the manufacture or use of the metal and is well recognized as a cause of interstitial pneumonitis and fibrosis (4). Although hard metal pneumoconiosis may take the form of interstitial pneumonia, desquamative interstitial pneumonia, or giant cell interstitial pneumonia, the finding of giant cell interstitial pneumonia is almost pathognomonic for hard metal pneumoconiosis (18).
Radiographic findings consist of a diffuse micronodular and reticular pattern, sometimes associated with lymph node enlargement. The reticulation may be coarse and in advanced disease may be accompanied by small cystic spaces (Fig 10) (19,20). High-resolution CT findings consist of bilateral areas of ground-glass attenuation, areas of consolidation, and extensive reticular hyperattenuating areas and traction bronchiectasis, findings that are indicative of fibrosis (Figs 10, 11) (13).
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Figure 10a. Giant cell interstitial pneumonia in a 52-year-old man. (a) Chest radiograph shows patchy areas of ground-glass opacity and fine reticulation in both lower lung zones. (b) High-resolution CT scan obtained at the level of the lung base shows bilateral areas with small cysts, ground-glass attenuation, fine reticular hyperattenuation, and traction bronchiectasis, findings that indicate fibrosis. Video-assisted thoracoscopic surgical biopsy revealed giant cell interstitial pneumonia.
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Figure 10b. Giant cell interstitial pneumonia in a 52-year-old man. (a) Chest radiograph shows patchy areas of ground-glass opacity and fine reticulation in both lower lung zones. (b) High-resolution CT scan obtained at the level of the lung base shows bilateral areas with small cysts, ground-glass attenuation, fine reticular hyperattenuation, and traction bronchiectasis, findings that indicate fibrosis. Video-assisted thoracoscopic surgical biopsy revealed giant cell interstitial pneumonia.
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Figure 11. Giant cell interstitial pneumonia in a 45-year-old worker in a saw manufacturing plant. High-resolution CT scan shows patchy areas of ground-glass attenuation and fine linear hyperattenuating areas predominantly involving the lower lung zones. The diagnosis of hard metal pneumoconiosis was proved with occupational history and video-assisted thoracoscopic surgical biopsy.
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Asbestos-related Pleural and Parenchymal Disease
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Exposure to asbestos is an important public health hazard in all industrial societies. Asbestos is the generic term for several fibrous silicate minerals that share the property of heat resistance. These can be classified into two large groups: serpentines and amphiboles. Chrysotile is the only asbestiform mineral in the serpentine group and accounts for more than 90% of the asbestos used in the United States. There are two major sources of exposure to asbestos dust: (a) the primary occupations of asbestos mining and processing, and (b) secondary occupations such as insulation manufacturing, textile manufacturing, construction, shipbuilding, and the manufacture and repair of gaskets and brake linings (21).
The inhaled asbestos fiber is long (up to 100 µm in length), penetrates deeply into the lung and pleura, and has a fibrogenic effect on respiratory bronchioles, alveoli, and pleura. Clinical manifestations typically do not appear until 20 years after initial exposure (4,21). Asbestos-related diseases include benign pleural diseases (plaques, diffuse pleural thickening, effusion, calcification), parenchymal diseases (asbestosis [parenchymal fibrosis caused by asbestos inhalation], rounded atelectasis, benign fibrotic masses, transpulmonary bands), and malignancy (malignant mesothelioma, bronchogenic carcinoma).
Asbestos-related Benign Pleural Disease
Pleural plaques are the most common manifestation of asbestos exposure. They serve as a marker for exposure and are not usually associated with symptoms or functional impairment. Generally, plaques cannot be detected at standard chest radiography until at least 20 years after initial exposure (21,22). At histologic analysis, pleural plaques consist of relatively acellular bundles of collagen in an undulating "basket weave" pattern and may contain large numbers of asbestos fibers (almost exclusively chrysotile) but asbestos bodies are absent (23). They are typically discrete, focal irregular areas of pleural thickening that generally affect the parietal pleura along the posterolateral and diaphragmatic contours of the lower thorax, with sparing of the lung apices and costophrenic angles (Fig 12). Calcification is seen in approximately 5%–15% of patients (Fig 13) (23). Plaques that arise from the visceral pleura are very rare and are usually found in the lower aspects of the interlobar fissures; they may calcify and are usually associated with extensive parietal pleura plaque formation (Fig 12) (24). Asbestosis rarely occurs in the absence of pleural plaques (23).
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Figure 12a. Pleural plaques, diffuse pleural thickening, rounded atelectasis, and asbestosis in a 50-year-old man with asbestos exposure from working in a brake lining production plant. (a) Chest radiograph shows diffuse thickening of the left pleura and curvilinear band opacities in the left lower lung zone. (b) High-resolution CT scan (mediastinal windowing) shows pleural plaques on the right side (small white arrows) and rounded atelectasis (large white arrow) with adjacent diffuse pleural thickening (black arrows) on the left side. (c) High-resolution CT scan obtained at a lower level than b demonstrates pleural plaques along the diaphragmatic contour (black arrows) and an irregular attenuation pattern, which is typical in rounded atelectasis (white arrows). (d) High-resolution CT scan (lung windowing) obtained at the level of the liver dome shows a visceral pleural plaque in the right major fissure (arrow) and curvilinear bands of hyperattenuation in the posterior subpleural area. Note also the rounded atelectasis with posterior displacement of the left major fissure. The diagnosis of asbestosis was proved at open lung biopsy.
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Figure 12b. Pleural plaques, diffuse pleural thickening, rounded atelectasis, and asbestosis in a 50-year-old man with asbestos exposure from working in a brake lining production plant. (a) Chest radiograph shows diffuse thickening of the left pleura and curvilinear band opacities in the left lower lung zone. (b) High-resolution CT scan (mediastinal windowing) shows pleural plaques on the right side (small white arrows) and rounded atelectasis (large white arrow) with adjacent diffuse pleural thickening (black arrows) on the left side. (c) High-resolution CT scan obtained at a lower level than b demonstrates pleural plaques along the diaphragmatic contour (black arrows) and an irregular attenuation pattern, which is typical in rounded atelectasis (white arrows). (d) High-resolution CT scan (lung windowing) obtained at the level of the liver dome shows a visceral pleural plaque in the right major fissure (arrow) and curvilinear bands of hyperattenuation in the posterior subpleural area. Note also the rounded atelectasis with posterior displacement of the left major fissure. The diagnosis of asbestosis was proved at open lung biopsy.
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Figure 12c. Pleural plaques, diffuse pleural thickening, rounded atelectasis, and asbestosis in a 50-year-old man with asbestos exposure from working in a brake lining production plant. (a) Chest radiograph shows diffuse thickening of the left pleura and curvilinear band opacities in the left lower lung zone. (b) High-resolution CT scan (mediastinal windowing) shows pleural plaques on the right side (small white arrows) and rounded atelectasis (large white arrow) with adjacent diffuse pleural thickening (black arrows) on the left side. (c) High-resolution CT scan obtained at a lower level than b demonstrates pleural plaques along the diaphragmatic contour (black arrows) and an irregular attenuation pattern, which is typical in rounded atelectasis (white arrows). (d) High-resolution CT scan (lung windowing) obtained at the level of the liver dome shows a visceral pleural plaque in the right major fissure (arrow) and curvilinear bands of hyperattenuation in the posterior subpleural area. Note also the rounded atelectasis with posterior displacement of the left major fissure. The diagnosis of asbestosis was proved at open lung biopsy.
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Figure 12d. Pleural plaques, diffuse pleural thickening, rounded atelectasis, and asbestosis in a 50-year-old man with asbestos exposure from working in a brake lining production plant. (a) Chest radiograph shows diffuse thickening of the left pleura and curvilinear band opacities in the left lower lung zone. (b) High-resolution CT scan (mediastinal windowing) shows pleural plaques on the right side (small white arrows) and rounded atelectasis (large white arrow) with adjacent diffuse pleural thickening (black arrows) on the left side. (c) High-resolution CT scan obtained at a lower level than b demonstrates pleural plaques along the diaphragmatic contour (black arrows) and an irregular attenuation pattern, which is typical in rounded atelectasis (white arrows). (d) High-resolution CT scan (lung windowing) obtained at the level of the liver dome shows a visceral pleural plaque in the right major fissure (arrow) and curvilinear bands of hyperattenuation in the posterior subpleural area. Note also the rounded atelectasis with posterior displacement of the left major fissure. The diagnosis of asbestosis was proved at open lung biopsy.
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The development of a pleural effusion is probably the earliest manifestation of previous asbestos exposure, usually occurs within 10 years of exposure, and remains the most common complication of asbestos exposure for the succeeding 10 years. At present, there is no definite evidence to suggest a relationship between benign asbestos pleural effusion and the subsequent development of malignant pleural mesothelioma (23).
Diffuse pleural thickening is seen less frequently than pleural plaques following exposure to asbestos. It is defined as a smooth, uninterrupted pleural density extending over at least one-fourth of the chest wall, with or without costo-phrenic angle obliteration (Fig 12). Diffuse pleural thickening is less specific to asbestos exposure than are pleural plaques, given that many causes of exudative pleural effusions can give rise to diffuse pleural fibrosis, including previous inflammatory episodes such as parapneumonic effusion, hemothorax, or connective tissue disease. Diffuse pleural thickening usually results from a benign exudative effusion but may be due to the confluence of plaques or, less commonly, to an extension of parenchymal fibrosis to the pleura. Unlike pleural plaques, diffuse pleural thickening is frequently associated with functional impairment (21–23).
Asbestosis
Most workers in whom pulmonary fibrosis (asbestosis) develops have been exposed to high dust concentrations for a prolonged period. There is a definite dose-effect relationship. Disease usually occurs approximately 20 years following initial exposure. Functional abnormalities consist of progressive reduction of both vital capacity and diffusing capacity. Parenchymal fibrosis begins in and around the respiratory bronchioles in the lower lobes adjacent to the visceral pleura where asbestos fibers tend to accumulate. An intraalveolar reaction that is pathologically similar to desquamative interstitial pneumonitis also occurs. This stage may progress to diffuse interstitial fibrosis and "honeycombing," with complete destruction of the alveolar architecture. Asbestos bodies are frequently observed microscopically in bronchoalveolar lavage fluid or tissue section (21,22).
Radiologic changes consist of small, irregular opacities or hyperattenuating areas in a linear pattern. The fine reticulation eventually progresses to a coarse linear pattern with honeycombing. These abnormalities are usually most severe in the lower lungs, the posterior lungs, and in a subpleural location (Figs 12, 14). These findings are similar to those in idiopathic pulmonary fibrosis. The presence of pleural plaques lends support to the radiologic diagnosis of asbestosis. However, plaques are not invariably present in patients with asbestosis (21,22).
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Figure 14. Asbestosis in a 62-year-old man. Prone high-resolution CT scan shows bilateral subpleural reticular hyperattenuating areas, small cysts, traction bronchiectasis, and areas of ground-glass attenuation. A small left diaphragmatic hernia is incidentally noted. Video-assisted thoracoscopic surgical biopsy revealed asbestosis and discrete pleural plaques.
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High-resolution CT including prone scans is a sensitive, reliable means of detecting thoracic abnormalities in individuals exposed to asbestos (Fig 14). Prone scans allow basal structural abnormalities to be reliably distinguished from gravity-related physiologic phenomena (25).
Major CT findings in early asbestosis include thickened intralobular lines that have been shown at histologic analysis to be due to peribronchiolar fibrosis, thickened interlobular lines, subpleural curvilinear lines, pleura-based nodular irregularities, patchy areas of ground-glass attenuation, small cystic spaces, and small areas of hypoattenuation (Figs 12, 14). Thickened interlobular lines have been shown to be due mainly to interlobular fibrotic or edematous thickening. Areas of ground-glass attenuation are the result of alveolar wall thickening due to fibrosis or edema (26,27). However, these findings can also be seen in a variety of conditions unrelated to asbestosis and are by themselves nonspecific. Their occurrence, even in patients with CT evidence of pleural plaques, does not necessarily indicate the presence of asbestosis (28). In the absence of pathologic proof, the diagnosis of asbestosis must be based on thorough evaluation of the likelihood of asbestosis using all available clinical, physiologic, and radiologic information (29).
Rounded Atelectasis
The most common of the benign masses caused by asbestosis exposure is rounded atelectasis, a form of peripheral lobar collapse that develops in patients with pleural disease. It usually occurs in the subpleural, posterior, or basal region of the lower lobes. Furthermore, pleural thickening is always present and is frequently greatest near the mass (Fig 12). The mass often has a curvilinear tail, frequently referred to as the "comet tail sign." This sign is produced by the crowding together of bronchi and blood vessels that extend from the lower border of the mass to the hilum, creating a whorled appearance of the bronchovascular bundle (22,30). Not all rounded atelectasis is actually round: Atypical features include wedge-shaped, lentiform, or (less often) irregular opacities or attenuation (Fig 12). Volume loss of the affected lobe is uniformly present, often with hyperlucency of the adjacent lung. Serial examination usually shows a stable appearance (30,31).
Bronchogenic Carcinoma and Asbestos Exposure
The association between asbestos exposure and bronchogenic carcinoma is accepted as being causal in nature. Bronchogenic carcinoma is estimated to develop in 20%–25% of workers who are heavily exposed to asbestos. The risk is increased in asbestos workers who smoke because smoking and asbestos exposure interact in a multiplicative manner (22). The risk of bronchogenic carcinoma in asbestos workers who smoke may be as much as 80–100 times that in the nonsmoking, nonexposed population. Asbestos-related tumors frequently occur in the periphery of the lungs with a lower lobe distribution, which correlates with the usual distribution of asbestosis (32).
Malignant Mesothelioma
Diffuse malignant mesothelioma is an uncommon and fatal neoplasm of the serosal lining of the pleural cavity, peritoneum, or both. The risk of mesothelioma in an asbestos worker is approximately 10% over his or her lifetime. Persons at risk include not only the worker but other household members as well as persons who reside near asbestos mines and plants. Usually, a latency period of approximately 20–40 years occurs between exposure and tumor detection. The tumor commences as nodules on the visceral or parietal pleura that progress to a thick rind encasing and constricting the lung. Unilateral pleural effusion is the most frequent manifestation of malignant mesothelioma at initial chest radiography (22,33). At CT, the combination of mediastinal pleural involvement and thick (>1 cm), nodular, circumferential pleural thickening is highly suggestive of diffuse mesothelioma (Fig 15) rather than benign pleural disease (34). Mesothelioma may also manifest as a single, discrete pleural mass (Fig 16). The tumor may extend into the interlobar fissures and interlobular septa, with superficial invasion of the underlying lung. Findings in patients with advanced tumor consist of invasion of the chest wall, pericardium, diaphragm, and abdomen (Figs 15, 16).
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Figure 15a. Malignant mesothelioma in a 51-year-old man. (a) Chest radiograph shows irregular nodular pleural thickening in the right hemithorax. (b) Intravenous contrast-enhanced CT scan helps confirm an irregular thick rind along the right pleural surface. (c) CT scan shows tumor invasion of the abdomen (arrow).
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Figure 15b. Malignant mesothelioma in a 51-year-old man. (a) Chest radiograph shows irregular nodular pleural thickening in the right hemithorax. (b) Intravenous contrast-enhanced CT scan helps confirm an irregular thick rind along the right pleural surface. (c) CT scan shows tumor invasion of the abdomen (arrow).
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Figure 15c. Malignant mesothelioma in a 51-year-old man. (a) Chest radiograph shows irregular nodular pleural thickening in the right hemithorax. (b) Intravenous contrast-enhanced CT scan helps confirm an irregular thick rind along the right pleural surface. (c) CT scan shows tumor invasion of the abdomen (arrow).
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Figure 16. Malignant mesothelioma in a 66-year-old man. Intravenously administered contrast material-enhanced CT scan shows a focally enhancing pleura-based mass invading the chest wall with destruction of the adjacent ribs (black arrow). Note the calcified plaque in the paravertebral area (white arrow).
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Chemical Pneumonitis
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The inhalation of noxious chemical substances is a comparatively uncommon but significant cause of occupational lung disease. The mechanism of pulmonary toxicity caused by different agents varies considerably. Noxious chemicals include organic (eg, organophosphates, paraquat, polyvinyl chloride, polymer fumes, smoke), nonorganic (eg, ammonia, hydrogen sulfide, nitrogen oxide, sulfur dioxide), and metal (eg, cadmium, mercury, nickel, vanadium) compounds.
Inhalation of the toxic agent may cause direct irritation and inflammation of the tracheobronchial tree. In general, more soluble gases (eg, ammonia) cause greater irritation of the upper respiratory tract and result in death before the gas reaches the alveoli. Exposed patients may be spared lower respiratory tract involvement, but high concentrations of soluble gases may cause pulmonary edema. Less soluble gases (eg, nitrogen dioxide) reach the distal airways in sufficient quantities to cause immediate or delayed pulmonary edema. Toxic agents can be absorbed through the respiratory tract, gastrointestinal tract, mucous membranes, or skin. The absorbed compound can affect the lung directly or through its metabolites. Toxic agents in high concentrations can displace oxygen from the airways and cause asphyxia (35).
Carbamates
Carbamate insecticides are agricultural insecticides that are commonly used in the United States and throughout the world. These are cholinesterase inhibitors and function similar to organophosphates except that they do not penetrate the central nervous system as effectively as the organophosphates, producing only limited central nervous system toxicity (36). The major cause of morbidity and mortality in acute carbamate poisoning is respiratory failure associated with pulmonary edema. Rarely, carbamate poisoning can cause interstitial pneumonitis and fibrosis (37).
Paraquat
Paraquat is an herbicide that is used in agriculture in many countries. It is inactivated by materials in the soil and leaves no toxic residue. Paraquat poisoning may be occupational but is often intentional. Most instances of paraquat toxicity result from ingestion of the agent, although a fatality resulting from cutaneous exposure has been reported (35). Paraquat accumulates rapidly in the lungs and is thought to be responsible for the production of superoxide radicals, which indirectly damage pulmonary cellular structure. Ingestion of a large quantity of paraquat leads to the rapid onset of pulmonary edema. Ingestion of smaller doses results in delayed onset of pulmonary abnormalities, which may progress to respiratory failure (35).
The radiographic appearance of paraquat pneumonitis varies widely. There may be no abnormality, increased interstitial or granular opacities, or confluent bilateral opacities indicative of pulmonary edema depending on the level of exposure. Pneumomediastinum occurs frequently (Figs 17, 18). Consolidation or diffuse haziness on initial radiographs evolves into a pattern of fibrosis (Fig 18) (38).
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Figure 17a. Paraquat poisoning in a 43-year-old farmer. The patient had taken a mouthful of paraquat and spat it out in a drunken state. (a) Chest radiograph obtained 3 days after the accident shows a large right pneumothorax, pneumomediastinum (arrows), and diffuse haziness in the left lung. (b) High-resolution CT scan obtained following thoracostomy shows ground-glass attenuation throughout both lungs, a right pneumothorax, interstitial pulmonary emphysema (arrowheads), and pneumomediastinum (arrow).
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Figure 17b. Paraquat poisoning in a 43-year-old farmer. The patient had taken a mouthful of paraquat and spat it out in a drunken state. (a) Chest radiograph obtained 3 days after the accident shows a large right pneumothorax, pneumomediastinum (arrows), and diffuse haziness in the left lung. (b) High-resolution CT scan obtained following thoracostomy shows ground-glass attenuation throughout both lungs, a right pneumothorax, interstitial pulmonary emphysema (arrowheads), and pneumomediastinum (arrow).
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Figure 18a. Paraquat poisoning in a 19-year-old man. Initial chest radiography showed peripheral areas of consolidation and ground-glass opacity in both lungs. (a) Follow-up chest radiograph obtained on the 30th day of hospitalization shows diffuse reticular opacities in both lungs with decreased lung volume. Note the pneumomediastinum and subcutaneous emphysema. (b) Initial high-resolution CT scan shows areas of ground-glass attenuation and consolidation predominantly involving the peripheral lungs. (c) High-resolution CT scan obtained on the 39th day of hospitalization shows reticular hyperattenuating areas, small cysts, and traction bronchiectasis corresponding to the affected areas in b, indicating progression to interstitial fibrosis. (Fig 18a-c courtesy of Mi Jeong Shin, MD, Wallace Memorial Baptist Hospital, Pusan, Korea.)
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Figure 18b. Paraquat poisoning in a 19-year-old man. Initial chest radiography showed peripheral areas of consolidation and ground-glass opacity in both lungs. (a) Follow-up chest radiograph obtained on the 30th day of hospitalization shows diffuse reticular opacities in both lungs with decreased lung volume. Note the pneumomediastinum and subcutaneous emphysema. (b) Initial high-resolution CT scan shows areas of ground-glass attenuation and consolidation predominantly involving the peripheral lungs. (c) High-resolution CT scan obtained on the 39th day of hospitalization shows reticular hyperattenuating areas, small cysts, and traction bronchiectasis corresponding to the affected areas in b, indicating progression to interstitial fibrosis. (Fig 18a-c courtesy of Mi Jeong Shin, MD, Wallace Memorial Baptist Hospital, Pusan, Korea.)
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Figure 18c. Paraquat poisoning in a 19-year-old man. Initial chest radiography showed peripheral areas of consolidation and ground-glass opacity in both lungs. (a) Follow-up chest radiograph obtained on the 30th day of hospitalization shows diffuse reticular opacities in both lungs with decreased lung volume. Note the pneumomediastinum and subcutaneous emphysema. (b) Initial high-resolution CT scan shows areas of ground-glass attenuation and consolidation predominantly involving the peripheral lungs. (c) High-resolution CT scan obtained on the 39th day of hospitalization shows reticular hyperattenuating areas, small cysts, and traction bronchiectasis corresponding to the affected areas in b, indicating progression to interstitial fibrosis. (Fig 18a-c courtesy of Mi Jeong Shin, MD, Wallace Memorial Baptist Hospital, Pusan, Korea.)
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The most common pattern at initial high-resolution CT is bilateral and diffuse areas of ground-glass attenuation (Figs 17, 18). The ground-glass attenuation evolves into consolidation with bronchiectasis, irregular lines, and traction bronchiectasis (Fig 18). At pathologic analysis, an exudative phase of diffuse alveolar damage is often initially seen in individuals who survive for several days, followed by interstitial fibrosis in the later phase (39).
Hydrogen Sulfide
Hydrogen sulfide is an irritant and chemical asphyxiant gas that exerts its primary toxic effects on the respiratory and neurologic systems (40). It has a characteristic smell of rotten eggs. Industrial exposures occur in coal mines, tanneries, petroleum manufacturing plants, geothermal power plants, aircraft factories, sewer works, and rubber works (35,41,42). When inhaled acutely in large quantities, hydrogen sulfide causes death from inhibition of the medullary respiratory center. Inhalation of smaller quantities or more prolonged exposure may lead to pulmonary edema (Fig 19). Although pulmonary edema is a common consequence of poisoning, some affected workers reported having experienced a "knockdown" (ie, a brief loss of consciousness from which they recovered) due to bronchial hyperresponsiveness (40,42). Buick et al (43) recently showed that isolated reduction in residual volume on pulmonary function tests could represent a subacute and subclinical manifestation of hydrogen sulfide intoxication. Determination of urine thiosulfate levels can be useful for monitoring occupational exposure. Determination of sulfide ion concentrations in the blood or major organs can be useful in corroborating a diagnosis of fatal toxicity; however, there are many pitfalls in collecting, storing, and analyzing tissue and fluid samples (40).
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Figure 19a. Hydrogen sulfide gas poisoning in a 45-year-old man who was found unconscious in a storage tank of salted radish in rice bran (Danmuji). A major component of the gas examined at chromatography was hydrogen sulfide. (a) Chest radiograph shows diffuse bilateral opacities. (b) Thin-section CT scan shows areas of airspace consolidation and ground-glass attenuation in the dependent portion of both lungs. Follow-up chest radiography performed 1 month later demonstrated resolution of the parenchymal infiltrates.
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Figure 19b. Hydrogen sulfide gas poisoning in a 45-year-old man who was found unconscious in a storage tank of salted radish in rice bran (Danmuji). A major component of the gas examined at chromatography was hydrogen sulfide. (a) Chest radiograph shows diffuse bilateral opacities. (b) Thin-section CT scan shows areas of airspace consolidation and ground-glass attenuation in the dependent portion of both lungs. Follow-up chest radiography performed 1 month later demonstrated resolution of the parenchymal infiltrates.
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Ammonia
Ammonia is a corrosive gas widely used in the production of explosives, petroleum, agricultural fertilizers, and plastics. It is also used in refrigeration. Occupational exposure results from damage to storage containers and pipes. This highly soluble gas acts as a severe mucosal irritant and primarily damages the upper airways (35).
The radiographic appearance of ammonia inhalation varies with the severity of the exposure. In mild exposure, chest radiographic findings are normal. After more severe exposure, radiographs may demonstrate a pulmonary edema pattern. Patients who survive the initial insult usually recover completely. Bronchiectasis or bronchiolitis obliterans may develop (Fig 20) (44,45).
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Figure 20. Bronchiolitis obliterans due to ammonia inhalation in a 56-year-old woman who had survived the explosion of an industrial refrigerator 15 years earlier. The patient was treated at that time with mechanical ventilation due to prolonged pulmonary injury. Chest radiography showed overinflation of both lungs with diffuse bronchiectasis in both lower lung zones. High-resolution CT scan shows bronchiectasis and areas of hypoattenuation with hyperattenuating vessels throughout both lungs.
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Hydrocarbon
Acute pneumonitis following ingestion or aspiration of petroleum products is usually related to accidental poisoning in children. Accidental aspiration of petroleum in performers demonstrating the art of fire-eating can cause a distinct type of chemical pneumonitis known as fire-eater pneumonia (46,47).
Radiologic findings include unilateral or bilateral consolidation, well-defined nodules, and pneumatoceles (Fig 21). At histopathologic analysis, the acute phase is characterized by the intraalveolar, intrabronchial, peribronchial, and interstitial accumulation of inflammatory cells with edema. The chronic or "proliferative" phase occurring within 1 to 2 weeks after the initial onset of symptoms is characterized by proliferative bronchiolitis and eventually by parenchymal fibrosis or pneumatocele formation. Pneumatoceles are thought to result from coalescing areas of bronchiolar necrosis or partial obstruction of the bronchial lumen, thereby creating a check-valve mechanism (46,47).
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Figure 21a. Hydrocarbon pneumonitis in a 54-year-old man who accidentally aspirated liquid petroleum while repairing an obstructed pipe. The patient presented with fever, dyspnea, and hemoptysis 1 day after aspiration. (a) Chest radiograph shows airspace consolidation in both lower lung zones. (b) High-resolution CT scan obtained on the 2nd day of hospitalization shows areas of ground-glass attenuation and areas of patchy or nodular consolidation (arrows) in both lower lung zones. (c) CT scan (mediastinal windowing) shows hypoattenuating areas of consolidation, a finding that suggests necrosis. Bloody secretions were obtained at bronchoscopy. Transbronchial lung biopsy and bronchoalveolar lavage showed necrotic tissue with degenerated inflammatory cells and many red blood cells.
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Figure 21b. Hydrocarbon pneumonitis in a 54-year-old man who accidentally aspirated liquid petroleum while repairing an obstructed pipe. The patient presented with fever, dyspnea, and hemoptysis 1 day after aspiration. (a) Chest radiograph shows airspace consolidation in both lower lung zones. (b) High-resolution CT scan obtained on the 2nd day of hospitalization shows areas of ground-glass attenuation and areas of patchy or nodular consolidation (arrows) in both lower lung zones. (c) CT scan (mediastinal windowing) shows hypoattenuating areas of consolidation, a finding that suggests necrosis. Bloody secretions were obtained at bronchoscopy. Transbronchial lung biopsy and bronchoalveolar lavage showed necrotic tissue with degenerated inflammatory cells and many red blood cells.
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Figure 21c. Hydrocarbon pneumonitis in a 54-year-old man who accidentally aspirated liquid petroleum while repairing an obstructed pipe. The patient presented with fever, dyspnea, and hemoptysis 1 day after aspiration. (a) Chest radiograph shows airspace consolidation in both lower lung zones. (b) High-resolution CT scan obtained on the 2nd day of hospitalization shows areas of ground-glass attenuation and areas of patchy or nodular consolidation (arrows) in both lower lung zones. (c) CT scan (mediastinal windowing) shows hypoattenuating areas of consolidation, a finding that suggests necrosis. Bloody secretions were obtained at bronchoscopy. Transbronchial lung biopsy and bronchoalveolar lavage showed necrotic tissue with degenerated inflammatory cells and many red blood cells.
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Mercury
Mercury contamination is a serious environmental problem worldwide. However, exposure to mercury vapor is an uncommon cause of occupational lung disease. Two primary sources of contamination are dumping of large quantities of inorganic mercury and exposure in the mining industry. Mercury is used in industry in electrolysis, the manufacture of thermometers, and the cleaning of boilers (35,48). Exposure to mercury vapor has been shown to occur while smelting silver from dental amalgam containing mercury (49).
Exposure to more than 1–2 mg/m3 of elemental mercury vapor for a few hours causes acute chemical bronchiolitis and pneumonitis (Fig 22). This is followed by diffuse alveolar damage with hyaline membrane formation. Acute mercury inhalation poisoning is usually fatal owing to progressive pulmonary failure (49,50). Although most workers who survive the acute episode recover completely, pulmonary interstitial fibrosis may progress, and pulmonary function impairment may be persiste
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Abstract
LEARNING OBJECTIVES FOR TEST...
