DOI: 10.1148/rg.261055070
RadioGraphics 2006;26:59-77
© RSNA, 2006
Pneumoconiosis: Comparison of Imaging and Pathologic Findings1
Semin Chong, MD,
Kyung Soo Lee, MD,
Myung Jin Chung, MD,
Joungho Han, MD,
O Jung Kwon, MD and
Tae Sung Kim, MD
1 From the Department of Radiology and Center for Imaging Science (S.C., K.S.L., M.J.C., T.S.K.), Department of Pathology (J.H.), and Division of Pulmonary and Critical Care Medicine, Department of Medicine (O.J.K.), Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-dong, Kangnam-ku, Seoul 135–710, Korea. Presented as an education exhibit at the 2004 RSNA Annual Meeting. Received March 29, 2005; revision requested April 27 and received May 20; accepted May 23. Supported by the SRC/ERC program of MOST/KOSEF (R11–2002-103). All authors have no financial relationships to disclose.
Address correspondence to K.S.L. (e-mail: kyungs.lee{at}samsung.com).
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Abstract
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Pneumoconiosis may be classified as either fibrotic or nonfibrotic, according to the presence or absence of fibrosis. Silicosis, coal worker pneumoconiosis, asbestosis, berylliosis, and talcosis are examples of fibrotic pneumoconiosis. Siderosis, stannosis, and baritosis are nonfibrotic forms of pneumoconiosis that result from inhalation of iron oxide, tin oxide, and barium sulfate particles, respectively. In an individual who has a history of exposure to silica or coal dust, a finding of nodular or reticulonodular lesions at chest radiography or small nodules with a perilymphatic distribution at thin-section computed tomography (CT), with or without eggshell calcifications, is suggestive of silicosis or coal worker pneumoconiosis. Magnetic resonance imaging is helpful for distinguishing between progressive massive fibrosis and lung cancer. CT and histopathologic findings in asbestosis are similar to those in idiopathic pulmonary fibrosis, but the presence of asbestos bodies in histopathologic specimens is specific for the diagnosis of asbestosis. Giant cell interstitial pneumonia due to exposure to hard metals is classified as a fibrotic form of pneumoconiosis and appears on CT images as mixed ground-glass opacities and reticulation. Berylliosis simulates pulmonary sarcoidosis on CT images. CT findings in talcosis include small centrilobular and subpleural nodules or heterogeneous conglomerate masses that contain foci of high attenuation indicating talc deposition. Siderosis is nonfibrotic and is indicated by a CT finding of poorly defined centrilobular nodules or ground-glass opacities.
© RSNA, 2006
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LEARNING OBJECTIVES FOR TEST 3
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After reading this article and taking the test, the reader will be able to:
- Recognize imaging features that help differentiate pneumoconiosis from other interstitial lung diseases.
- Correlate imaging findings with clinicopathologic findings in the various types of pneumoconiosis.
- Classify cases of pneumoconiosis as fibrotic or nonfibrotic.
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Introduction
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Pneumoconiosis is caused by the accumulation of inhaled particulates and involves a reaction of tissue in the lung (1). The International Labour Organization (ILO) has established a standardized system for classifying radiographic abnormalities in pneumoconiosis on the basis of the presence of the following lung parenchymal and pleural abnormalities: small rounded opacities, small irregular opacities, profusion of opacities, large opacities, zonal distribution of opacities (upper, middle, and/or lower), and pleural thickening (diffuse or circumscribed) (2). Although this standardized system has not helped define the clinical or pathologic entities of pneumoconiosis, it has been useful for epidemiologic purposes. Pneumoconiosis may be clinicopathologically classified as fibrotic (involving focal nodular or diffuse fibrosis) or nonfibrotic (involving particle-laden macrophages, with minimal or no fibrosis) (3). Silicosis, coal worker pneumoconiosis, asbestosis, berylliosis, and talcosis are fibrotic forms of pneumoconiosis. Siderosis (from iron oxide), stannosis (from tin oxide), and baritosis (from barium sulfate) are nonfibrotic forms of the disease. Silicosis, coal worker pneumoconiosis, and asbestosis are the three most common types of pneumoconiosis, whereas berylliosis, siderosis, stannosis, and baritosis are relatively uncommon. The article surveys the imaging findings in common and uncommon types of pneumoconiosis and provides clinicopathologic comparisons.
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Silicosis
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Silicosis is caused by the inhalation of fine particles of crystalline silicon dioxide (silica) (4). Quartz is the most common form of crystalline silica but is less fibrogenic than tridymite or cristbalite. Occupations such as mining, quarrying, and tunneling are associated with silicosis (5). The disease occurs in two clinical forms: acute silicosis, which manifests as alveolar silicoproteinosis; and classic silicosis, which manifests as chronic interstitial reticulonodular disease. Cases of classic silicosis may be classified as either simple or complicated, according to the radiographic findings (4). Simple silicosis is defined by a radiographic pattern of small and round or irregular opacities, whereas complicated silicosis, or progressive massive fibrosis, is characterized by large conglomerate opacities (1).
Carcinoma and tuberculosis are potential serious complications of silicosis (3). The development of carcinoma or tuberculosis is a strong independent predictor of mortality in patients with silicosis (6). Pulmonary symptoms such as dyspnea become increasingly severe as the radiologic abnormalities worsen with carcinoma or tuberculosis (7).
Acute Silicosis (Silicoproteinosis)
Acute exposure to silica dust, an occupational hazard for sandblasters, can result in the filling of the airspace in the lung with proteinaceous material (8). Histopathologic specimens of acute silicosis show severe alveolitis and alveolar filling with a substance that tests positive at periodic acid–Schiff staining, a finding consistent with alveolar lipoproteinosis (Fig 1). In this respect, acute silicosis is quite different from the classic form of the disease.
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Figure 1a. Acute silicosis in a 52-year-old man who worked for 10 years as a crystal craftsman. (a, b) Axial thin-section CT scans (1.0-mm-thick sections) obtained at the levels of the ventricles (a) and the left basal truncal bronchus (b) show ground-glass opacities and mild interlobular septal thickening (arrows) in the middle and lower lobes of the right lung and in the lingular division of the upper lobe of the left lung, respectively. (c) Photomicrograph (original magnification, x40; hematoxylin-eosin stain) of a specimen obtained with video-assisted thoracoscopic biopsy in the lingula shows a fine granular eosin-ophilic material that fills the alveolar space. Note the pigment-laden perivascular and interstitial macrophages and giant cells (arrows).
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Figure 1b. Acute silicosis in a 52-year-old man who worked for 10 years as a crystal craftsman. (a, b) Axial thin-section CT scans (1.0-mm-thick sections) obtained at the levels of the ventricles (a) and the left basal truncal bronchus (b) show ground-glass opacities and mild interlobular septal thickening (arrows) in the middle and lower lobes of the right lung and in the lingular division of the upper lobe of the left lung, respectively. (c) Photomicrograph (original magnification, x40; hematoxylin-eosin stain) of a specimen obtained with video-assisted thoracoscopic biopsy in the lingula shows a fine granular eosin-ophilic material that fills the alveolar space. Note the pigment-laden perivascular and interstitial macrophages and giant cells (arrows).
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Figure 1c. Acute silicosis in a 52-year-old man who worked for 10 years as a crystal craftsman. (a, b) Axial thin-section CT scans (1.0-mm-thick sections) obtained at the levels of the ventricles (a) and the left basal truncal bronchus (b) show ground-glass opacities and mild interlobular septal thickening (arrows) in the middle and lower lobes of the right lung and in the lingular division of the upper lobe of the left lung, respectively. (c) Photomicrograph (original magnification, x40; hematoxylin-eosin stain) of a specimen obtained with video-assisted thoracoscopic biopsy in the lingula shows a fine granular eosin-ophilic material that fills the alveolar space. Note the pigment-laden perivascular and interstitial macrophages and giant cells (arrows).
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Radiographic findings consist of bilateral consolidation and/or ground-glass opacities, which tend to appear in perihilar regions. Findings at thin-section computed tomography (CT) include numerous bilateral centrilobular nodular ground-glass opacities, multifocal patchy ground-glass opacities, and consolidation (8,9) (Fig 1 ), features that indicate the intraalveolar accumulation of proteinaceous material (9). Sometimes, a crazy-paving appearance (airspace filling and interlobular septal thickening) caused by the presence of edematous or fibrous tissue may be seen at thin-section CT (Fig 1).
The clinical course of acute silicosis is usually progressive and ends in death due to cor pulmonale and respiratory failure despite medical therapy with corticosteroids (10).
Classic Silicosis
Histopathologically, silicotic nodules are composed of mature collagen in the central portion, with a peripheral zone of particle-laden macrophages that appears markedly different from the surrounding lung parenchyma. In color, the nodules range from slate gray to dense black, depending on the mineral contents in the silica dust (1,11). A number of birefringent silicate crystals 1–3 µm in length usually can be identified at the cellular level with the use of polarized light microscopy (Fig 2) (12).
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Figure 2a. Classic silicosis in a 53-year-old man who worked for 12 years in sandblasting. Photomicrographs (original magnification, x100; hematoxylin-eosin stain) show a transbronchial lung biopsy specimen. (a) Image obtained with visible light shows intraalveolar aggregation of pigmented macrophages (arrows). (b) Image obtained with polarized light shows scattered interstitial silica particles (arrows).
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Figure 2b. Classic silicosis in a 53-year-old man who worked for 12 years in sandblasting. Photomicrographs (original magnification, x100; hematoxylin-eosin stain) show a transbronchial lung biopsy specimen. (a) Image obtained with visible light shows intraalveolar aggregation of pigmented macrophages (arrows). (b) Image obtained with polarized light shows scattered interstitial silica particles (arrows).
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Simple Form.—
On chest radiographs, simple silicosis is characterized by multiple nodular opacities that are well defined and uniform in shape and attenuation and that range from 1 to 10 mm in diameter (1) (Fig 3). These nodules are distributed throughout both lungs, but they tend to be predominantly located in the upper lobe and posterior portion of the lung (13) (Figs 3, 4). Calcification of nodules is seen on chest radiographs in 10%–20% of patients (1).
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Figure 3a. Silicosis in a 54-year-old man who worked for 20 years as a stonecutter. (a) Chest radiograph shows multiple small nodules in both lungs, predominantly in the upper and middle zones. (b) Axial thin-section CT scan (2.5-mm-thick section) obtained at the level of the aortic arch shows multiple small nodules with similar shape and attenuation throughout the upper lobes of both lungs.
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Figure 3b. Silicosis in a 54-year-old man who worked for 20 years as a stonecutter. (a) Chest radiograph shows multiple small nodules in both lungs, predominantly in the upper and middle zones. (b) Axial thin-section CT scan (2.5-mm-thick section) obtained at the level of the aortic arch shows multiple small nodules with similar shape and attenuation throughout the upper lobes of both lungs.
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Figure 4a. Silicosis in a 56-year-old man who worked for 25 years as a stonecutter. (a) Chest radiograph shows multiple variable-sized nodular lesions in both lungs, predominantly in the upper and middle zones. (b) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the azygos arch shows multiple small nodules with a perilymphatic (centrilobular plus subpleural) distribution in the upper lobe of both lungs. Note the tendency toward coalescence of the nodules in the lung periphery (arrows).
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Figure 4b. Silicosis in a 56-year-old man who worked for 25 years as a stonecutter. (a) Chest radiograph shows multiple variable-sized nodular lesions in both lungs, predominantly in the upper and middle zones. (b) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the azygos arch shows multiple small nodules with a perilymphatic (centrilobular plus subpleural) distribution in the upper lobe of both lungs. Note the tendency toward coalescence of the nodules in the lung periphery (arrows).
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At CT, the most characteristic feature of simple silicosis is the presence of multiple small nodules 2–5 mm in diameter (Figs 3, 4), accompanied by calcifications (14). The nodules in simple silicosis tend to be more sharply defined than those in coal worker pneumoconiosis but are otherwise indistinguishable from the latter at thin-section CT (14). The nodules may be distributed diffusely throughout both lungs, but they tend to be most numerous in the upper lobe, as shown on radiographs. At thin-section CT, nodules are usually observed in centrilobular, paraseptal, and subpleural regions and have a perilymphatic distribution (Figs 3, 4). Subpleural nodules have a rounded or triangular configuration, and if they are confluent, they may resemble pleural plaques (14) (Fig 4).
Hilar and mediastinal lymph node enlargement may precede the appearance of parenchymal nodular lesions. Calcification of lymph nodes is common and typically occurs at the periphery of the node. The so-called eggshell calcification pattern is highly suggestive of silicosis (Fig 5).
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Figure 5. Simple silicosis in a 60-year-old man who worked for 12 years in a tungsten mine. Thin-section CT scan (1.0-mm-thick section) obtained with mediastinal window settings at the level of the bronchus intermedius shows eggshell calcifications (arrows) in the hilar and subcarinal lymph nodes.
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Complicated Form.—
Complicated silicosis, also known as progressive massive fibrosis, develops through the expansion and confluence of individual silicotic nodules. At histopathologic analysis, a large conglomerate lesion, composed of multiple foci of central hyalinized collagen and a surrounding pigmented rim of macrophages, is observed. Focal necrosis is common in the central portions of the lesion and is occasionally associated with granulomatous inflammation (as in tuberculous infection) (1) (Fig 6).
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Figure 6a. Silicotuberculosis in a 52-year-old man who worked for 30 years as a stoneworker. (a) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the great vessels shows an irregular thick-walled cavitary lesion (arrow) in the upper lobe of the left lung, a finding suggestive of pulmonary tuberculosis, as well as subpleural nodular lesions in both lungs. (b) CT scan obtained at the level of the main bronchi depicts bilateral conglomerate masses (arrows), multiple small centrilobular and subpleural nodules, and enlarged mediastinal lymph nodes (arrowheads) in the right lower paratracheal and left peribronchial areas.
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Figure 6b. Silicotuberculosis in a 52-year-old man who worked for 30 years as a stoneworker. (a) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the great vessels shows an irregular thick-walled cavitary lesion (arrow) in the upper lobe of the left lung, a finding suggestive of pulmonary tuberculosis, as well as subpleural nodular lesions in both lungs. (b) CT scan obtained at the level of the main bronchi depicts bilateral conglomerate masses (arrows), multiple small centrilobular and subpleural nodules, and enlarged mediastinal lymph nodes (arrowheads) in the right lower paratracheal and left peribronchial areas.
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On chest radiographs, complicated silicosis usually is indicated by large symmetric bilateral opacities with a diameter of more than 1 cm and with an irregular margin (Figs 7, 8). The large opacities result from nodule coalescence and are observed commonly in the middle lung zone or peripheral one-third of the lung on axial chest images and in the upper lung zone on longitudinal images. The large opacities gradually migrate toward the hilum, leaving emphysematous lung tissue between the fibrotic tissue and the pleural surface (1). The CT features of progressive massive fibrosis are focal soft-tissue masses, often with irregular or ill-defined margins and calcifications, surrounded by areas of emphysematous change (15,16) (Figs 7, 8). The lateral interface of the mass typically parallels the lateral chest wall (17) (Fig 7). Occasionally, cavitation secondary to ischemic necrosis may occur in a mass.
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Figure 7a. Silicosis and progressive massive fibrosis in a 58-year-old man who worked for 30 years as a stoneworker. (a) Chest radiograph shows multiple small nodules and masses in both lungs, predominantly in the upper and middle zones, and eggshell calcifications (arrows) in the lung hilum and the mediastinum. (b) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the aortic arch shows large symmetric bilateral opacities with irregular margins (arrows) indicative of progressive massive fibrosis, as well as numerous small nodules and septal thickening (arrowheads).
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Figure 7b. Silicosis and progressive massive fibrosis in a 58-year-old man who worked for 30 years as a stoneworker. (a) Chest radiograph shows multiple small nodules and masses in both lungs, predominantly in the upper and middle zones, and eggshell calcifications (arrows) in the lung hilum and the mediastinum. (b) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the aortic arch shows large symmetric bilateral opacities with irregular margins (arrows) indicative of progressive massive fibrosis, as well as numerous small nodules and septal thickening (arrowheads).
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Figure 8a. Silicosis and progressive massive fibrosis in a 66-year-old man who worked for 10 years crushing rock with a high quartz content. (a) Chest radiograph shows large bilateral opacities (arrows) in the upper zones of the lung, as well as upward elevation of both hila. (b) Coronal CT scan (2.0-mm-thick section) obtained with mediastinal window settings shows bilateral conglomerate masses with calcifications (arrows), findings that represent progressive massive fibrosis in the upper zone of both lungs.
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Figure 8b. Silicosis and progressive massive fibrosis in a 66-year-old man who worked for 10 years crushing rock with a high quartz content. (a) Chest radiograph shows large bilateral opacities (arrows) in the upper zones of the lung, as well as upward elevation of both hila. (b) Coronal CT scan (2.0-mm-thick section) obtained with mediastinal window settings shows bilateral conglomerate masses with calcifications (arrows), findings that represent progressive massive fibrosis in the upper zone of both lungs.
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Silicotuberculosis
Pulmonary tuberculosis occurs in 25% of patients with acute or classic silicosis, and men with silicosis have a relative risk of tuberculosis that is 2.8 times that for men without silicosis (18). Radiologic features of silicotuberculosis include asymmetric nodules or consolidation, cavitation, and rapid disease progression (Fig 6). Of these features, cavitation is the strongest indicator of probable silicotuberculosis, although cavitation also may be caused by ischemic changes in a silicotic fibrotic mass.
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Coal Worker Pneumoconiosis
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Coal worker pneumoconiosis is caused by exposure to washed coal, which is nearly free of silica, and it has a histologic basis that is very different from that of silicosis. Tissue specimens from patients with coal worker pneumoconiosis demonstrate two characteristic morphologic features: coal macules (Fig 9) and progressive massive fibrosis (Fig 10). The latter is indicated by the presence of a fibrotic mass with a diameter of more than 1 cm and with anthracotic pigmentation. The coal macules range in size from 1 to 5 mm and are characterized by solid anthracotic pigmentation without intervening fibrotic tissue (Fig 9) (19). The macules contain pigment-laden macrophages that surround the bronchioles in the lobular core; thus, the distribution of the macules is primarily centrilobular. Despite these histopathologic differences, the radiologic findings in coal worker pneumoconiosis and those in silicosis are similar, and the two diseases cannot be easily distinguished from one another on images.
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Figure 9a. Coal worker pneumoconiosis in a 62-year-old man who worked for 20 years in a coal mine. (a) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the aortic arch shows numerous small centrilobular (arrows) and subpleural (arrowheads) nodules in both lungs. (b) Photomicrograph (original magnification, x40; hematoxylin-eosin stain) of a pathologic specimen obtained with a transbronchial lung biopsy shows multiple nodules (arrows) and anthracotic pigmentation in the bronchovascular bundles.
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Figure 9b. Coal worker pneumoconiosis in a 62-year-old man who worked for 20 years in a coal mine. (a) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the aortic arch shows numerous small centrilobular (arrows) and subpleural (arrowheads) nodules in both lungs. (b) Photomicrograph (original magnification, x40; hematoxylin-eosin stain) of a pathologic specimen obtained with a transbronchial lung biopsy shows multiple nodules (arrows) and anthracotic pigmentation in the bronchovascular bundles.
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Figure 10a. Progressive massive fibrosis in a 64-year-old man who worked for 25 years as a coal miner. (a) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the aortic arch shows an irregularly marginated mass in the upper lobe of the right lung and multiple small subpleural and fissural nodules (arrows) in both lungs. (b) Contrast material–enhanced CT scan (5.0-mm-thick section) at a level similar to that in a, obtained with mediastinal window settings, shows a central necrotic area of low attenuation (arrows) in the mass. (c) Photograph of lobectomy specimen shows regions of central necrosis (arrows) within the black-pigmented parenchyma.
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Figure 10b. Progressive massive fibrosis in a 64-year-old man who worked for 25 years as a coal miner. (a) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the aortic arch shows an irregularly marginated mass in the upper lobe of the right lung and multiple small subpleural and fissural nodules (arrows) in both lungs. (b) Contrast material–enhanced CT scan (5.0-mm-thick section) at a level similar to that in a, obtained with mediastinal window settings, shows a central necrotic area of low attenuation (arrows) in the mass. (c) Photograph of lobectomy specimen shows regions of central necrosis (arrows) within the black-pigmented parenchyma.
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Figure 10c. Progressive massive fibrosis in a 64-year-old man who worked for 25 years as a coal miner. (a) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the aortic arch shows an irregularly marginated mass in the upper lobe of the right lung and multiple small subpleural and fissural nodules (arrows) in both lungs. (b) Contrast material–enhanced CT scan (5.0-mm-thick section) at a level similar to that in a, obtained with mediastinal window settings, shows a central necrotic area of low attenuation (arrows) in the mass. (c) Photograph of lobectomy specimen shows regions of central necrosis (arrows) within the black-pigmented parenchyma.
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The risk of tuberculosis is increased in individuals with coal worker pneumoconiosis, as it is in those affected by silicosis. Coal dust inhalation also is related to the development of chronic obstructive pulmonary disease, which contributes to increased mortality among patients with coal worker pneumoconiosis (20). Workers with a high degree of progressive massive fibrosis also have a significantly increased mortality rate (21).
Simple Form.—
The radiographic pattern of simple coal worker pneumoconiosis typically consists of small round nodular opacities and occasionally includes reticular or reticulonodular opacities (1). The nodules in coal worker pneumoconiosis have a diameter of 1–5 mm and tend to be less well defined at the margins and more granular in appearance than those found in silicosis (Fig 9). Calcifications are observed on chest radiographs in 10%–20% of patients. Calcification develops as a central nodular dot in coal worker pneumoconiosis, whereas it tends to be more diffuse in silicosis (22,23). Furthermore, the eggshell calcification pattern that is pathognomonic of simple silicosis is uncommon in simple coal worker pneumoconiosis (it is observed in only 1.3% of patients) (22).
The CT features of coal worker pneumoconiosis are similar to those of silicosis. Small nodules may be observed diffusely throughout the lungs, typically with a perilymphatic distribution but sometimes with a centrilobular predominance, but they tend to be most numerous in the upper lung zone (Fig 9). At CT, calcification is observed within the nodules in 30% of patients with the disease. Moreover, hilar or mediastinal lymph node enlargement also is reported in 30% of patients (24).
Complicated Form.—
On chest radiographs, large opacities (progressive massive fibrosis) may be seen in complicated coal worker pneumoconiosis, as in complicated silicosis (Fig 6). However, the histopathologic basis of these features in complicated coal worker pneumoconiosis is different from that in complicated silicosis. In coal worker pneumoconiosis, the fibrotic mass consists of haphazardly arranged collagen with numerous pigment-laden macrophages and with abundant free pigment especially evident in the central region. Foci of frank necrosis, cholesterol clefts, and chronic inflammatory cellular infiltrates also are often present (25) (Fig 10).
Fibrotic masses in complicated coal worker pneumoconiosis are defined according to the regularity of the lesion border and the pattern of the surrounding parenchyma (25). Most such lesions have an irregular border with associated surrounding pericicatricial emphysema (Fig 10). However, some have a regular border without pericicatricial emphysema.
It is clinically and radiologically important to differentiate progressive massive fibrosis from lung cancer. Matsumoto et al (26) reported that magnetic resonance (MR) imaging is potentially useful for this purpose. On MR images, lung cancer appears as a high-signal-intensity lesion on T2-weighted images (Fig 11), whereas progressive massive fibrosis appears as a low-signal-intensity abnormality when compared with the signal intensity of muscle on both T1- and T2-weighted images (Fig 12). Some investigators have suggested that the most common MR characteristics of progressive massive fibrosis are signal isointensity on T1-weighted images and hypointensity on T2-weighted images, in comparison with the signal intensity in skeletal muscle. Moreover, with an intravenously administered MR contrast medium, the lesion in progressive massive fibrosis appears peripherally enhanced more frequently than not (27). Thus, the signal intensity manifested on T2-weighted images provides a clue for the differentiation of lung cancer from progressive massive fibrosis. When a mass lesion is depicted with high signal intensity on T2-weighted MR images, the finding is highly suggestive of lung cancer, and histopathologic analysis should be performed for diagnosis (Fig 11).
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Figure 11a. Lung cancer and coal worker pneumoconiosis in a 68-year-old man who worked for 20 years in a coal mine. (a) Axial CT scan (5.0-mm-thick section) obtained at the level of the left basal truncal bronchus shows a well-defined 2-cm-diameter nodule (arrow) in an upper segment of the lower lobe of the left lung, a finding that represents a combined neuroendocrine large cell carcinoma and adenocarcinoma, as well as multiple smaller nodules (arrowheads). (b) T2-weighted MR image obtained at a level similar to that in b shows the high-signal-intensity nodule (arrow) in the lower lobe. (c) Integrated positron emission tomographic (PET)-CT scan shows a high uptake of fluorine 18 fluorodeoxyglucose (FDG) (arrow) in the nodule, a finding suggestive of malignancy. (d) Photograph of a gross specimen obtained at left lower lobectomy shows the cancer (arrow) and multiple black-pigmented nodules (arrowheads) in the lung parenchyma and pleural surface.
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Figure 11b. Lung cancer and coal worker pneumoconiosis in a 68-year-old man who worked for 20 years in a coal mine. (a) Axial CT scan (5.0-mm-thick section) obtained at the level of the left basal truncal bronchus shows a well-defined 2-cm-diameter nodule (arrow) in an upper segment of the lower lobe of the left lung, a finding that represents a combined neuroendocrine large cell carcinoma and adenocarcinoma, as well as multiple smaller nodules (arrowheads). (b) T2-weighted MR image obtained at a level similar to that in b shows the high-signal-intensity nodule (arrow) in the lower lobe. (c) Integrated positron emission tomographic (PET)-CT scan shows a high uptake of fluorine 18 fluorodeoxyglucose (FDG) (arrow) in the nodule, a finding suggestive of malignancy. (d) Photograph of a gross specimen obtained at left lower lobectomy shows the cancer (arrow) and multiple black-pigmented nodules (arrowheads) in the lung parenchyma and pleural surface.
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Figure 11c. Lung cancer and coal worker pneumoconiosis in a 68-year-old man who worked for 20 years in a coal mine. (a) Axial CT scan (5.0-mm-thick section) obtained at the level of the left basal truncal bronchus shows a well-defined 2-cm-diameter nodule (arrow) in an upper segment of the lower lobe of the left lung, a finding that represents a combined neuroendocrine large cell carcinoma and adenocarcinoma, as well as multiple smaller nodules (arrowheads). (b) T2-weighted MR image obtained at a level similar to that in b shows the high-signal-intensity nodule (arrow) in the lower lobe. (c) Integrated positron emission tomographic (PET)-CT scan shows a high uptake of fluorine 18 fluorodeoxyglucose (FDG) (arrow) in the nodule, a finding suggestive of malignancy. (d) Photograph of a gross specimen obtained at left lower lobectomy shows the cancer (arrow) and multiple black-pigmented nodules (arrowheads) in the lung parenchyma and pleural surface.
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Figure 11d. Lung cancer and coal worker pneumoconiosis in a 68-year-old man who worked for 20 years in a coal mine. (a) Axial CT scan (5.0-mm-thick section) obtained at the level of the left basal truncal bronchus shows a well-defined 2-cm-diameter nodule (arrow) in an upper segment of the lower lobe of the left lung, a finding that represents a combined neuroendocrine large cell carcinoma and adenocarcinoma, as well as multiple smaller nodules (arrowheads). (b) T2-weighted MR image obtained at a level similar to that in b shows the high-signal-intensity nodule (arrow) in the lower lobe. (c) Integrated positron emission tomographic (PET)-CT scan shows a high uptake of fluorine 18 fluorodeoxyglucose (FDG) (arrow) in the nodule, a finding suggestive of malignancy. (d) Photograph of a gross specimen obtained at left lower lobectomy shows the cancer (arrow) and multiple black-pigmented nodules (arrowheads) in the lung parenchyma and pleural surface.
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Figure 12a. Progressive massive fibrosis in a 59-year-old man who worked for 20 years in a coal mine. (a) Composite of axial thin-section CT scans (1.0-mm-thick sections) obtained at various levels of the distal trachea shows irregularly marginated 20–30-mm nodules (arrows) accompanied by smaller satellite nodules and surrounding reticulation in the upper lobe of both lungs. (b) T1-weighted MR image obtained at a level close to that in a shows the slightly hyperintense lesions (arrows) in both upper lobes. (c) T2-weighted MR image obtained at a similar level shows an absence of signal at the lesion sites and a small pleural effusion (arrowheads) in the right lung. (d) Integrated PET-CT scan shows increased uptake of FDG in both nodules (straight arrows) and in a right paratracheal lymph node (curved arrow).
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Figure 12b. Progressive massive fibrosis in a 59-year-old man who worked for 20 years in a coal mine. (a) Composite of axial thin-section CT scans (1.0-mm-thick sections) obtained at various levels of the distal trachea shows irregularly marginated 20–30-mm nodules (arrows) accompanied by smaller satellite nodules and surrounding reticulation in the upper lobe of both lungs. (b) T1-weighted MR image obtained at a level close to that in a shows the slightly hyperintense lesions (arrows) in both upper lobes. (c) T2-weighted MR image obtained at a similar level shows an absence of signal at the lesion sites and a small pleural effusion (arrowheads) in the right lung. (d) Integrated PET-CT scan shows increased uptake of FDG in both nodules (straight arrows) and in a right paratracheal lymph node (curved arrow).
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Figure 12c. Progressive massive fibrosis in a 59-year-old man who worked for 20 years in a coal mine. (a) Composite of axial thin-section CT scans (1.0-mm-thick sections) obtained at various levels of the distal trachea shows irregularly marginated 20–30-mm nodules (arrows) accompanied by smaller satellite nodules and surrounding reticulation in the upper lobe of both lungs. (b) T1-weighted MR image obtained at a level close to that in a shows the slightly hyperintense lesions (arrows) in both upper lobes. (c) T2-weighted MR image obtained at a similar level shows an absence of signal at the lesion sites and a small pleural effusion (arrowheads) in the right lung. (d) Integrated PET-CT scan shows increased uptake of FDG in both nodules (straight arrows) and in a right paratracheal lymph node (curved arrow).
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Figure 12d. Progressive massive fibrosis in a 59-year-old man who worked for 20 years in a coal mine. (a) Composite of axial thin-section CT scans (1.0-mm-thick sections) obtained at various levels of the distal trachea shows irregularly marginated 20–30-mm nodules (arrows) accompanied by smaller satellite nodules and surrounding reticulation in the upper lobe of both lungs. (b) T1-weighted MR image obtained at a level close to that in a shows the slightly hyperintense lesions (arrows) in both upper lobes. (c) T2-weighted MR image obtained at a similar level shows an absence of signal at the lesion sites and a small pleural effusion (arrowheads) in the right lung. (d) Integrated PET-CT scan shows increased uptake of FDG in both nodules (straight arrows) and in a right paratracheal lymph node (curved arrow).
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PET is useful for distinguishing benign abnormalities from malignancies, but its role in the diagnosis of malignancy in the setting of pneumoconiosis remains unclear. Intensive uptake of FDG may occur in the fibrotic mass in progressive massive fibrosis (Fig 12 ), and the observation of resultant mass enhancement on images may lead to confusion of progressive massive fibrosis with lung cancer (28) (Figs 11, 12).
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Asbestosis
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Asbestosis is diffuse interstitial pulmonary fibrosis that occurs secondary to the inhalation of asbestos fibers (29). It is considered separately from other asbestos-related diseases, such as benign pleural effusion and plaques, malignant mesothelioma, and bronchogenic carcinoma. Asbestos is a term that is used to describe several fibrous silicate minerals that may be classified into two groups: serpentine and amphibole. Materials that contain asbestos (eg, chrysotile, crocidolite, and amosite) are widely used in industry for their tensile strength and heat resistance (11).
At histopathologic analysis, asbestos bodies, which may consist of a single asbestos fiber surrounded by a segmented protein-iron coat, can be identified in intraalveolar macrophages (30) (Fig 13).
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Figure 13. Asbestos body. Photomicrograph (original magnification, x1000; hematoxylin-eosin stain) shows a translucent asbestos fiber (straight arrow) surrounded by a segmented protein-iron coat that is much more prominent around the lower part of the fiber, and an alveolar macrophage (curved arrow).
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Asbestosis manifests with the same clinical, radiologic, and histopathologic features as other forms of diffuse interstitial pulmonary fibrosis. Nevertheless, according to criteria established by the American Thoracic Society (31), asbestosis may be diagnosed without lung biopsy in the presence of three clinical signs (ie, a restrictive pattern of lung impairment, a diffusion capacity below the lower limit of the normal range, and bilateral crackles at the posterior lung base in the latter part of or throughout the respiratory cycle); a history of relevant exposure; and, most important, chest radiographic findings that correspond to ILO classification s, t, or u parenchymal opacities (ie, small irregular opacities with a profusion of 1/1 or greater). Many physicians and epidemiologists have assessed chest radiographic findings in asbestos-exposed individuals according to the ILO classification system (2). However, some reports indicate that a reliance on chest radiography as the sole means of detecting asbestosis may be ill advised: Kipen et al (32) found that 18% of patients with biopsy-proved pulmonary fibrosis had no identifiable radiographic abnormalities and that 80% of patients had chest radiographic findings (according to the ILO classification) that did not correlate with the histopathologic grades.
There are no known radiographic findings that are pathognomonic of asbestosis. Initial chest radiographs show small irregular opacities with a fine reticular pattern, findings that represent peribronchiolar and adjacent alveolar interstitial fibrosis (Fig 14). In addition, pleural thickening or plaques may be seen.
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Figure 14. Asbestosis in a 58-year-old man who worked for 25 years in building construction. Chest radiograph shows small reticular opacities (arrows) at the costophrenic sulcus in the lower zone of both lungs.
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Thin-section CT scans may aid the differentiation of dependent atelectasis from irreversible fibrosis in the dorsal lung region with the depiction of changes indicative of lung fibrosis, especially septal thickening and parenchymal band formation (33). CT scans obtained in a prone position are important for distinguishing between normal increased opacity in the dependent lung regions and mild fibrosis (Fig 15). In the early stage of disease, minimal or no visible abnormalities may be observed on chest radiographs, although thin-section CT scans demonstrate thickened intralobular and interlobular lines, subpleural curvilinear lines, pleura-based irregular small nodules, hazy patches of increased attenuation, and small cystic spaces (34) (Fig 15). Honeycombing is a common finding in advanced-stage disease, predominantly in the lung periphery and the posterior region (35) (Fig 16). Thin-section CT findings in patients with interstitial fibrosis are similar to those in patients with idiopathic pulmonary fibrosis. However, in a comparative CT study of asbestosis and idiopathic pulmonary fibrosis (36), the distribution of fibrosis in the idiopathic pulmonary fibrosis group was more often basal and subpleural than that in the asbestosis group (Fig 16). The presence of parietal pleural thickening in association with lung fibrosis is the most important feature differentiating asbestos-induced pulmonary fibrosis from idiopathic pulmonary fibrosis; this finding is highly suggestive of asbestosis in patients with a history of asbestos exposure. Moreover, the presence of asbestos bodies in bronchoalveolar lavage fluid is highly specific (37).
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Figure 15a. Asbestosis in a 59-year-old man who worked for 30 years at an automobile factory. (a) Axial thin-section CT scan (1.5-mm-thick section) obtained at the level of the liver dome with the patient prone shows small subpleural nodules (straight arrows), patchy ground-glass opacities (curved arrows), and interlobular septal thickening (arrowhead) suggestive of early-stage asbestosis. (b) CT scan obtained with mediastinal window settings at the level of the suprahepatic inferior vena cava shows bandlike pleural thickening (arrowheads) in the lower lobe of both lungs, a finding indicative of pleural plaque. (c) Photomicrograph (original magnification, x12; hematoxylin-eosin stain) of a pathologic specimen obtained with video-assisted thoracoscopic surgical biopsy depicts subpleural and septal fibrous thickening (arrows).
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Figure 15b. Asbestosis in a 59-year-old man who worked for 30 years at an automobile factory. (a) Axial thin-section CT scan (1.5-mm-thick section) obtained at the level of the liver dome with the patient prone shows small subpleural nodules (straight arrows), patchy ground-glass opacities (curved arrows), and interlobular septal thickening (arrowhead) suggestive of early-stage asbestosis. (b) CT scan obtained with mediastinal window settings at the level of the suprahepatic inferior vena cava shows bandlike pleural thickening (arrowheads) in the lower lobe of both lungs, a finding indicative of pleural plaque. (c) Photomicrograph (original magnification, x12; hematoxylin-eosin stain) of a pathologic specimen obtained with video-assisted thoracoscopic surgical biopsy depicts subpleural and septal fibrous thickening (arrows).
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Figure 15c. Asbestosis in a 59-year-old man who worked for 30 years at an automobile factory. (a) Axial thin-section CT scan (1.5-mm-thick section) obtained at the level of the liver dome with the patient prone shows small subpleural nodules (straight arrows), patchy ground-glass opacities (curved arrows), and interlobular septal thickening (arrowhead) suggestive of early-stage asbestosis. (b) CT scan obtained with mediastinal window settings at the level of the suprahepatic inferior vena cava shows bandlike pleural thickening (arrowheads) in the lower lobe of both lungs, a finding indicative of pleural plaque. (c) Photomicrograph (original magnification, x12; hematoxylin-eosin stain) of a pathologic specimen obtained with video-assisted thoracoscopic surgical biopsy depicts subpleural and septal fibrous thickening (arrows).
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Figure 16a. Asbestosis in a 70-year-old man who worked for 30 years in a shipyard. (a, b) Axial thin-section CT scans (1.0-mm-thick sections) at the level of the suprahepatic inferior vena cava. (a) Scan obtained with lung window settings shows subpleural consolidation (arrow) in the lower lobe of the left lung, with reticulation, ground-glass opacities, and honeycombing. (b) Scan obtained with mediastinal window settings shows subpleural consolidation (arrow), pleural thickening (arrowheads) and effusion. (c, d) Photomicrographs of pathologic specimens obtained with video-assisted thoracic surgical biopsy. (c) Low-power micrograph (original magnification, x40; hematoxylin-eosin stain) shows dense collagen fibers in the pleura (arrows). (d) High-power micrograph (original magnification, x200; iron stain) shows asbestos bodies in the parenchyma (arrows).
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Figure 16b. Asbestosis in a 70-year-old man who worked for 30 years in a shipyard. (a, b) Axial thin-section CT scans (1.0-mm-thick sections) at the level of the suprahepatic inferior vena cava. (a) Scan obtained with lung window settings shows subpleural consolidation (arrow) in the lower lobe of the left lung, with reticulation, ground-glass opacities, and honeycombing. (b) Scan obtained with mediastinal window settings shows subpleural consolidation (arrow), pleural thickening (arrowheads) and effusion. (c, d) Photomicrographs of pathologic specimens obtained with video-assisted thoracic surgical biopsy. (c) Low-power micrograph (original magnification, x40; hematoxylin-eosin stain) shows dense collagen fibers in the pleura (arrows). (d) High-power micrograph (original magnification, x200; iron stain) shows asbestos bodies in the parenchyma (arrows).
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Figure 16c. Asbestosis in a 70-year-old man who worked for 30 years in a shipyard. (a, b) Axial thin-section CT scans (1.0-mm-thick sections) at the level of the suprahepatic inferior vena cava. (a) Scan obtained with lung window settings shows subpleural consolidation (arrow) in the lower lobe of the left lung, with reticulation, ground-glass opacities, and honeycombing. (b) Scan obtained with mediastinal window settings shows subpleural consolidation (arrow), pleural thickening (arrowheads) and effusion. (c, d) Photomicrographs of pathologic specimens obtained with video-assisted thoracic surgical biopsy. (c) Low-power micrograph (original magnification, x40; hematoxylin-eosin stain) shows dense collagen fibers in the pleura (arrows). (d) High-power micrograph (original magnification, x200; iron stain) shows asbestos bodies in the parenchyma (arrows).
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Figure 16d. Asbestosis in a 70-year-old man who worked for 30 years in a shipyard. (a, b) Axial thin-section CT scans (1.0-mm-thick sections) at the level of the suprahepatic inferior vena cava. (a) Scan obtained with lung window settings shows subpleural consolidation (arrow) in the lower lobe of the left lung, with reticulation, ground-glass opacities, and honeycombing. (b) Scan obtained with mediastinal window settings shows subpleural consolidation (arrow), pleural thickening (arrowheads) and effusion. (c, d) Photomicrographs of pathologic specimens obtained with video-assisted thoracic surgical biopsy. (c) Low-power micrograph (original magnification, x40; hematoxylin-eosin stain) shows dense collagen fibers in the pleura (arrows). (d) High-power micrograph (original magnification, x200; iron stain) shows asbestos bodies in the parenchyma (arrows).
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The two most important complications of asbestosis are pulmonary fibrosis and pleuropulmonary malignancy (3). The individual risk of death from asbestosis increases significantly with the increasing severity of underlying pulmonary fibrosis (38). With regard to pleuropulmonary malignancy, there is a period of latency of at least 20 years between the initial exposure to asbestos and the development of a pulmonary carcinoma or pleural mesothelioma (39). Apart from the potential pulmonary complications, various extrathoracic neoplasms also are reported to be associated with asbestos exposure, a group that includes peritoneal mesothelioma and gastrointestinal, renal, oropharyngeal, and laryngeal carcinoma, as well as leukemia (3).
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Berylliosis
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Berylliosis, a chronic granulomatous lung disease caused by exposure to beryllium dust or fumes, is characterized by the accumulation of CD4+ T cells and macrophages in the lower respiratory tract (40). Exposure to beryllium may occur in ceramics manufacture, nuclear weapon production, and aerospace industry. Acute beryllium disease is rare today because of industrial control measures. The potential for developing beryllium sensitization or chronic beryllium disease is increasingly recognized (41). Chronic beryllium disease develops in up to 16% of exposed workers, depending on individual genetic susceptibility and the extent and type of exposure. Symptoms usually include dyspnea, cough, fever, anorexia, and weight loss (42). Skin lesions are the most common extrathoracic manifestation, but granulomatous hepatitis, hypercalcemia, and kidney stones also may occur (43).
Depending on the severity of the histopathologic response to beryllium inhalation, noncaseating granulomas may form and, eventually, fibrosis may occur in the lungs (44) (Fig 17). Granulomas in berylliosis are histopathologically indistinguishable from those in other granulomatous disorders, such as sarcoidosis (44). However, the granulomatous reaction derives from an immunopathologic process due to beryllium-specific CD4+ T lymphocytes in lung tissue (44). In the early stages of chronic beryllium disease, sensitivity to beryllium can be detected by testing a sample of blood or bronchoalveolar lavage fluid for lymphocyte transformation and proliferation (45). Therefore, granulomatous inflammation proved at lung biopsy and evidence of sensitivity to beryllium demonstrated at testing of blood or bronchoalveolar lavage fluid (lymphocyte transformation or lymphocyte proliferation testing) are required to confirm a diagnosis of chronic beryllium disease.
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Figure 17a. Berylliosis in a 49-year-old man who worked for 7 years in metal polishing. (a) Chest radiograph shows bilateral mediastinal and hilar lymph node enlargement, as well as internal fixation of a right clavicular fracture. (b, c) Axial thin-section CT scans (1.0-mm-thick-sections) obtained at the levels of the bronchus intermedius (b) and the basal segmental bronchus (c) show multiple small nodules along the bronchovascular bundles (straight arrows) and in subfissural regions (arrowheads) and enlarged hilar lymph nodes (curved arrows). (d) Photomicrograph (original magnification, x100; hematoxylin-eosin stain) of a pathologic specimen obtained with mediastinoscopic lymph node biopsy shows multiple noncaseating granulomas (arrows).
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Figure 17b. Berylliosis in a 49-year-old man who worked for 7 years in metal polishing. (a) Chest radiograph shows bilateral mediastinal and hilar lymph node enlargement, as well as internal fixation of a right clavicular fracture. (b, c) Axial thin-section CT scans (1.0-mm-thick-sections) obtained at the levels of the bronchus intermedius (b) and the basal segmental bronchus (c) show multiple small nodules along the bronchovascular bundles (straight arrows) and in subfissural regions (arrowheads) and enlarged hilar lymph nodes (curved arrows). (d) Photomicrograph (original magnification, x100; hematoxylin-eosin stain) of a pathologic specimen obtained with mediastinoscopic lymph node biopsy shows multiple noncaseating granulomas (arrows).
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Figure 17c. Berylliosis in a 49-year-old man who worked for 7 years in metal polishing. (a) Chest radiograph shows bilateral mediastinal and hilar lymph node enlargement, as well as internal fixation of a right clavicular fracture. (b, c) Axial thin-section CT scans (1.0-mm-thick-sections) obtained at the levels of the bronchus intermedius (b) and the basal segmental bronchus (c) show multiple small nodules along the bronchovascular bundles (straight arrows) and in subfissural regions (arrowheads) and enlarged hilar lymph nodes (curved arrows). (d) Photomicrograph (original magnification, x100; hematoxylin-eosin stain) of a pathologic specimen obtained with mediastinoscopic lymph node biopsy shows multiple noncaseating granulomas (arrows).
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Figure 17d. Berylliosis in a 49-year-old man who worked for 7 years in metal polishing. (a) Chest radiograph shows bilateral mediastinal and hilar lymph node enlargement, as well as internal fixation of a right clavicular fracture. (b, c) Axial thin-section CT scans (1.0-mm-thick-sections) obtained at the levels of the bronchus intermedius (b) and the basal segmental bronchus (c) show multiple small nodules along the bronchovascular bundles (straight arrows) and in subfissural regions (arrowheads) and enlarged hilar lymph nodes (curved arrows). (d) Photomicrograph (original magnification, x100; hematoxylin-eosin stain) of a pathologic specimen obtained with mediastinoscopic lymph node biopsy shows multiple noncaseating granulomas (arrows).
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Chest radiographs are often normal in early-stage disease but are abnormal in 54% of patients (46). With disease progression, radiographs usually show reticulonodular opacities that predominate in the middle and upper zones of the lungs (47). In more advanced disease, interstitial fibrosis with honeycombing or mass lesions may be apparent; the mass lesions likely are caused by the coalescence of granulomatous lesions (48). Hilar lymph node enlargement also is frequently present (Fig 17), but it is moderate, compared with that observed in sarcoidosis (48).
Thin-section CT findings of berylliosis are similar to those of granulomatous lung diseases such as sarcoidosis. The most common findings are parenchymal small nodules, which are observed in 57% of cases and are predominantly distributed along bronchovascular bundles or interlobular septa. Interlobular septal thickening is observed in 50% of cases (46). Other findings include ground-glass opacities (32%), honeycombing (7%), conglomerate mass (7%), and bronchial wall thickening (46%) (46). Hilar or mediastinal lymphadenopathy is observed in 39% of cases (46,47) (Fig 17).
Prolonged treatment with corticosteroids is usually necessary in patients with significant symptoms or physiologic derangements (43). Although response to corticosteroid therapy is usually excellent, oxygen therapy is occasionally required. In a few patients, progression to end-stage lung disease occurs (45,49). The prognosis is poor for patients with symptomatic chronic disease, especially when it is complicated by cor pulmonale (50). Like silica and asbestos, beryllium is well recognized as a cause of pulmonary carcinoma, particularly in patients with acute berylliosis (51).
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Hard-Metal Pneumoconiosis
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Hard-metal lung disease is caused by exposure to dust produced in hard-metal industry (eg, during the processing of tungsten carbide and cobalt, sometimes with the admixture of other metals) (52). Cobalt, which acts as a cytotoxic or allergenic agent, is generally considered the main cause of hard-metal lung disease. Excessive exposure to hard metals may result in various respiratory disease manifestations, including upper respiratory tract irritation, asthma, and a specific form of interstitial lung disease that previously was called hard-metal pneumoconiosis (53). However, most patients with hard-metal lung disease manifest a chronic cough or dyspnea, have either diffuse interstitial fibrosis or asthma, and show a pattern of restricted or obstructed pulmonary function at pulmonary function testing (54).
The diagnostic criteria of hard-metal lung disease include the following: (a) a history of exposure to metal dust; (b) characteristic clinical features, including shortness of breath, cough, and dyspnea on exertion over a prolonged period; (c) radiologic findings of interstitial lung disease; (d) histologic findings of interstitial lung disease or a giant cell interstitial pneumonia pattern (presence of a large number of giant cells filling the airspace), with thickening of the interstitium and alveolar walls by mononuclear cells; and (e) a histopathologic finding of metallic content in lung tissue (55).
The histopathologic manifestations of hard-metal disease range from bronchitis to subacute fibrosing alveolitis to interstitial fibrosis. Obliterative bronchiolitis is reported to be the earliest manifestation of hard-metal disease. Subacute fibrosing alveolitis is characterized by the desquamation of epithelial cells and the accumulation of macrophages and multinuclear giant cells in the alveolar spaces (as in giant cell insterstitial pneumonia) (Fig 18) within a few years of initial exposure, whereas chronic diffuse mural fibrosis with honeycombing occurs several years or more after initial exposure (56). Although the histopathologic pattern of giant cell interstitial pneumonia is pathognomonic of hard-metal lung disease (57), diffuse mural fibrosis with honeycombing may predominate, accompanied by a small area of subacute fibrosing alveolitis, especially at an advanced stage of disease (58,59).
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Figure 18a. Giant cell interstitial pneumonia in a 47-year-old man who worked for 13 years as an iron driller. (a) Chest radiograph shows multiple ill-defined small nodules and reticular opacities in the upper and middle zones of both lungs. (b) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the liver dome shows bilateral patchy subpleural ground-glass opacities (arrows) and reticulation. (c) Photomicrograph (original magnification, x100; hematoxylin-eosin stain) of a pathologic specimen obtained with video-assisted thoracoscopic surgical biopsy in the lower lobe of the right lung shows intraalveolar macrophages with occasional giant cells (arrows).
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Figure 18b. Giant cell interstitial pneumonia in a 47-year-old man who worked for 13 years as an iron driller. (a) Chest radiograph shows multiple ill-defined small nodules and reticular opacities in the upper and middle zones of both lungs. (b) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the liver dome shows bilateral patchy subpleural ground-glass opacities (arrows) and reticulation. (c) Photomicrograph (original magnification, x100; hematoxylin-eosin stain) of a pathologic specimen obtained with video-assisted thoracoscopic surgical biopsy in the lower lobe of the right lung shows intraalveolar macrophages with occasional giant cells (arrows).
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Figure 18c. Giant cell interstitial pneumonia in a 47-year-old man who worked for 13 years as an iron driller. (a) Chest radiograph shows multiple ill-defined small nodules and reticular opacities in the upper and middle zones of both lungs. (b) Axial thin-section CT scan (1.0-mm-thick section) obtained at the level of the liver dome shows bilateral patchy subpleural ground-glass opacities (arrows) and reticulation. (c) Photomicrograph (original magnification, x100; hematoxylin-eosin stain) of a pathologic specimen obtained with video-assisted thoracoscopic surgical biopsy in the lower lobe of the right lung shows intraalveolar macrophages with occasional giant cells (arrows).
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Radiographic findings include diffuse small nodular and reticular patterns and small cystic spaces, especially in advanced disease (Fig 18). Thin-section CT findings consist of bilateral ground-glass opacities or consolidation on a panlobular or multilobular scale, extensive reticular opacities, and traction bronchiectasis (Fig 18 ). In advanced disease, parenchymal distortion and honeycombing may be seen (52,59). In a CT and histopathologic study of hard-metal pneumoconiosis, Akira (52) found that consolidation corresponds to areas of marked intraalveolar desquamation of multinuclear giant cells mixed with macrophages and areas of intramural mononuclear cellular infiltration and multinuclear giant cell infiltration. However, in a recent study of CT images with pathologic correlation, Choi et al (59) found that the main patterns of parenchymal abnormalities were ground-glass opacities and reticulation, which were noted in all patients; consolidation was not observed in their patient series, but honeycombing was found in one patient. Because these patterns are similar to those of other idiopathic interstitial pneumonias, including idiopathic pulmonary fibrosis and non-specific interstitial pneumonia, a diagnosis of hard-metal lung disease should be based on combined occupational, clinical, radiologic, and pathologic findings (60,61).
Early-stage hard-metal pneumoconiosis is reversible, whereas interstitial fibrosis leads inevitably to end-stage lung disease (56). However, patients with hard-metal pneumoconiosis tend to develop lung cancer (62).
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Talcosis
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Talc is a hydrated magnesium silicate used in the manufacture of leather, rubber, paper, textiles, and ceramic tiles (1,63). It is usually incorporated into such products with other elements, such as iron and nickel, and it is often found in association with minerals such as quartz, mica, kaolin, and asbestos (1,63,64). The recognized causes of pulmonary talcosis, each of which results in a different form of disease, are the following: inhalation of pure talc; inhalation of talc in association with silica (talcosilicosis); inhalation of talc in association with asbestos fibers (talcoasbestosis); and intravenous ingestion of talc, which occurs most often during recreational drug use (65,66).
The pathologic conditions that are caused by the ingestion of asbestos or silica with talc, rather than by talc alone, include pleural, parenchymal, and interstitial fibrosis and peribronchiolar and perivascular macrophage infiltration (64). Whether inhaled or injected, talc causes nonnecrotizing granulomatous inflammation that leads to progressive fibrosis (67).
Radiographic findings may include generalized haziness, nodulation, and reticulation similar to those observed in asbestosis, but the apices and costophrenic sulci typically are spared (1). As in other forms of pneumoconiosis, nodule confluence results in large opacities that resemble those in progressive massive fibrosis (1). In some patients, hilar lymphadenopathy develops (1).
CT findings in talcosis from injected talc consist of diffuse small nodules, perihilar conglomerate masses, ground-glass opacities, and emphysema (68,69) (Fig 19). Thin-section CT findings in patients with talcosis caused by inhaled particulates include small centrilobular and subpleural nodules and heterogeneous conglomerate masses with internal foci of high attenuation that are consistent with talc deposition (65) (Fig 19).
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Figure 19. Talcosis in a 52-year-old man who worked for 8 years in magnesium silicate processing. Axial thin-section CT scan (1.5-mm-thick section) obtained at the level of the main bronchi shows dense consolidation, with dilated bronchi, pericicatricial emphysematous changes (arrows), ground-glass opacities, and interlobular septal thickening (arrowheads) in the upper lobe of both lungs. (Courtesy of Nestor Müller, MD, PhD, Vancouver Hospital and Health Sciences Center, Vancouver, Canada.)
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Siderosis
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Siderosis is caused by the accumulation of iron oxide in macrophages within the lung. It is observed most commonly in workers exposed to metal fumes during welding and thus is known as welder siderosis or arc welder pneumoconiosis. In general, siderosis is not associated with fibrosis or functional impairment. However, when the iron inhaled is admixed with a substantial quantity of silica, the result is silicosiderosis, which may be associated with pulmonary fibrosis (70).
Typical radiographic findings include small nodules, which are most prominent in the middle third of the lungs, in perihilar regions. The nodules do not indicate reactive fibrosis but, rather, radiopaque accumulations of iron particles in macrophages aggregated along perivascular and peribronchial lymphatic vessels (71). The pathologic changes are reversible, and complete resolution is possible after the cessation of exposure (52).
In a thin-section CT–histopathologic study of 21 arc welders, Akira (52) reported that CT scans showed small ill-defined centrilobular nodules (71% of subjects) with or without fine branching structures indicating the deposition of minute iron oxide particles along perivascular and peribronchial lymphatic vessels; emphysematous changes (33% of subjects) likely related to smoking; and honeycombing resembling that in usual interstitial pneumonia (14%) (Fig 20). Other findings included ground-glass opacities, reticulation, pleural irregularity suggestive of exposure to asbestos, and conglomerate masses with areas of high attenuation indicating organizing pneumonia with siderosis. These CT findings are further supported by Han et al (72), who reported that the most frequent thin-section CT findings in patients with arc welder pneumoconiosis are poorly defined small centrilobular nodules and branching linear structures and, less commonly, extensive ground-glass attenuation without zonal predominance. All of these findings represent macrophage accumulations in the alveolar space.
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Figure 20. Siderosis in a 49-year-old man who worked for 8 years in a shipyard. Thin-section CT scan (1.5-mm-thick section) obtained at the level of the aortic arch shows multiple small and poorly defined centrilobular nodules (arrows) in the upper lobe of both lungs. (Courtesy of Yeon Joo Jeong, MD, Pusan National University Hospital, Pusan, Korea.)
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Siderosis usually does not cause any symptoms, but silicosiderosis may manifest with respiratory symptoms such as cough and dyspnea (3). Like other types of pneumoconiosis, siderosis and silicosiderosis are associated with the development of pulmonary carcinoma, although there is no direct evidence of a link between iron oxide accumulation and the development of carcinoma (73).
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Summary
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Pneumoconiosis is an occupational lung disease. The most common forms of the disease are silicosis, coal worker pneumoconiosis, and asbestosis; siderosis and hard-metal pneumoconiosis also are relatively common. Pneumoconiosis may occur with or without fibrosis. In fibrotic forms of pneumoconiosis, histopathologic and radiologic findings are suggestive of fibrosis. Silicosis, coal worker pneumoconiosis, asbestosis, berylliosis, and talcosis are fibrotic forms of pneumoconiosis. Siderosis (from iron oxide), stannosis (from tin oxide), and baritosis (from barium sulfate) are nonfibrotic forms of pneumoconiosis. A diagnosis of pneumoconiosis should be made by integrating a history of occupational exposure to inorganic dusts or fumes with the pathologic and radiologic findings.
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Footnotes
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Abbreviations: FDG = fluorine 18 fluorodeoxyglucose, ILO = International Labour Organization
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References
|
|---|
- Fourth International Pneumoconiosis Conference. Report of the Working Party on the Definition of Pneumoconiosis. Geneva, Switzerland: International Labour Organization, 1971.
- International Labour Organization (ILO). Guidelines for the use of ILO International Classification of Radiographs of Pneumoconioses. Geneva, Switzerland: ILO, 1980.
- Fraser R, Müller NL, Colman N. Inhalation of inorganic dust (pneumoconiosis). In: Fraser R, Müller N, Colman N, eds. Diagnosis of diseases of the chest. 4th ed. Philadelphia, Pa: Saunders, 1999; 2386–2484.
- Weil I, Jones R, Parkes W. Silicosis and related diseases. In: Parkes W, ed. Occupational lung disorders. 3rd ed. London, England: Butterworths, 1994; 285–339.
- McLoud TC. Occupational lung disease. Radiol Clin North Am 1991;29:931–941.[Medline]
- Ng TP, Chan SL, Lee J. Predictors of mortality in silicosis. Respir Med 1992;86:115–119.[Medline]
- Infante-Rivard C, Armstrong B, Ernst P, Petitclerc M, Cloutier LG, Theriault G. Descriptive study of prognostic factors influencing survival of compensated silicotic patients. Am Rev Respir Dis 1991; 144:1070–1074.[Medline]
- Dee P, Suratt P, Winn W. The radiographic findings in acute silicosis. Radiology 1978;126:359–363.[Abstract]
- Marchiori E, Ferreira A, Müller NL. Silicoproteinosis: high-resolution CT and histologic findings. J Thorac Imaging 2001;16:127–129.[CrossRef][Medline]
- Goodman GB, Kaplan PD, Stachura I, Castranova V, Pailes WH, Lapp NL. Acute silicosis responding to corticosteroid therapy. Chest 1992; 101:366–370.[Abstract/Free Full Text]
- Fujimura N. Pathology and pathophysiology of pneumoconiosis. Curr Opin Pulm Med 2000;6: 140–144.[CrossRef][Medline]
- Curran RC. Observations on the formation of collagen in quartz lesions. J Pathol Bacteriol 1953;66: 271–282.[CrossRef][Medline]
- Bergin CJ, Müller NL, Vedal S, Chan-Yeung M. CT in silicosis: correlation with plain films and pulmonary function tests. AJR Am J Roentgenol 1986;146:477–483.[Abstract/Free Full Text]
- Oikonomou A, Müller NL. Imaging of pneumoconiosis. Imaging 2003;15:11–22.[Abstract/Free Full Text]
- Begin R, Bergeron D, Samson L, Boctor M, Cantin A. CT assessment of silicosis in exposed workers. AJR Am J Roentgenol 1987;148:509–514.[Abstract/Free Full Text]
- Begin R, Ostiguy G, Fillion R, Colman N. Computed tomography scan in the early detection of silicosis. Am Rev Respir Dis 1991;144:697–705.[Medline]
- Stark P, Jacobson F, Shaffer K. Standard imaging in silicosis and coal worker’s pneumoconiosis. Radiol Clin North Am 1992;30:1147–1154.[Medline]
- Cowie RL. The epidemiology of tuberculosis in gold miners with silicosis. Am J Respir Crit Care Med 1994;150:1460–1462.[Abstract]
- Green FH, Laqueur WA. Coal workers’ pneumoconiosis. Pathol Annu 1980;15:333–410.[Medline]
- Cochrane AL, Moore F, Moncrieff CB. Are coalminers, with low "risk factors" for ischaemic heart disease at greater risk of developing progressive massive fibrosis? Br J Ind Med 1982;39:265–268.[Medline]
- Sadler RL, Roy TJ. Smoking and mortality from coalworkers’ pneumoconiosis. Br J Ind Med 1990; 47:141–142.[Medline]
- Williams JL, Moller GA. Solitary mass in the lungs of coal miners. Am J Roentgenol Radium Ther Nucl Med 1973;117:765–770.[Medline]
- Young RC Jr, Rachal RE, Carr PG, Press HC. Patterns of coal workers’ pneumoconiosis in Appalachian former coal miners. J Natl Med Assoc 1992;84:41–48.[Medline]
- Remy-Jardin M, Degreef JM, Beuscart R, Voisin C, Remy J. Coal worker’s pneumoconiosis: CT assessment in exposed workers and correlation with radiographic findings. Radiology 1990;177: 363–371.[Abstract/Free Full Text]
- Remy-Jardin M, Remy J, Farre I, Marquette CH. Computed tomographic evaluation of silicosis and coal workers’ pneumoconiosis. Radiol Clin North Am 1992;30:1155–1176.[Medline]
- Matsumoto S, Miyake H, Oga M, Takaki H, Mori H. Diagnosis of lung cancer in a patient with pneumoconiosis and progressive massive fibrosis using MRI. Eur Radiol 1998;8:615–617.[CrossRef][Medline]
- Matsumoto S, Mori H, Miyake H, et al. MRI signal characteristics of progressive massive fibrosis in silicosis. Clin Radiol 1998;53:510–514.[CrossRef][Medline]
- O’Connell M, Kennedy M. Progressive massive fibrosis secondary to pulmonary silicosis appearance on F-18 fluorodeoxyglucose PET/CT. Clin Nucl Med 2004;29:754–755.[CrossRef][Medline]
- Ross RM. The clinical diagnosis of asbestosis in this century requires more than a chest radiograph. Chest 2003;124:1120–1128.[Abstract/Free Full Text]
- Müller NL, Fraser RS, Lee KS, Johkoh T. Occupational lung disease. In: Müller NL, Fraser RS, Lee KS, Johkoh T, eds. Diseases of the lung: radiologic and pathologic correlations. Philadelphia, Pa: Lippincott Williams & Wilkins, 2003; 183–207.
- American Thoracic Society. Medical Section of the American Lung Association. The diagnosis of nonmalignant diseases related to asbestos. Am Rev Respir Dis 1986;134:363–368.[Medline]
- Kipen HM, Lilis R, Suzuki Y, Valciukas JA, Selikoff IJ. Pulmonary fibrosis in asbestos insulation workers with lung cancer: a radiological and histopathological evaluation. Br J Ind Med 1987;44: 96–100.[Medline]
- Oksa P, Suoranta H, Koskinen H, Zitting A, Nordman H. High-resolution computed tomography in the early detection of asbestosis. Int Arch Occup Environ Health 1994;65:299–304.[CrossRef][Medline]
- Akira M, Yokoyama K, Yamamoto S, et al. Early asbestosis: evaluation with high-resolution CT. Radiology 1991;178:409–416.[Abstract/Free Full Text]
- Primack SL, Hartman TE, Hansell DM, Müller NL. End-stage lung disease: CT findings in 61 patients. Radiology 1993;189:681–686.[Abstract/Free Full Text]
- Copley SJ, Wells AU, Sivakumaran P, et al. Asbestosis and idiopathic pulmonary fibrosis: comparison of thin-section CT features. Radiology 2003; 229:731–736.[Abstract/Free Full Text]
- Vathesatogkit P, Harkin TJ, Addrizzo-Harris DJ, Bodkin M, Crane M, Rom WN. Clinical correlation of asbestos bodies in BAL fluid. Chest 2004; 126:966–971.[Abstract/Free Full Text]
- Markowitz SB, Morabia A, Lilis R, Miller A, Nicholson WJ, Levin S. Clinical predictors of mortality from asbestosis in the North American Insulator Cohort, 1981 to 1991. Am J Respir Crit Care Med 1997;156:101–108.[Abstract/Free Full Text]
- Selikoff IJ, Bader RA, Bader ME, Churg J, Hammond EC. Asbestosis and neoplasia. Am J Med 1967;42:487–496.[CrossRef][Medline]
- Fontenot AP, Canavera SJ, Gharavi L, Newman LS, Kotzin BL. Target organ localization of memory CD4(+) T cells in patients with chronic beryllium disease. J Clin Invest 2002;110:1473–1482.[CrossRef][Medline]
- Eisenbud M. Origins of the standards for control of beryllium disease (1947–1949). Environ Res 1982;27:79–88.[Medline]
- Sprince NL, Kanarek DJ, Weber AL, Chamberlin RI, Kazemi H. Reversible respiratory disease in beryllium workers. Am Rev Respir Dis 1978;117: 1011–1017.[Medline]
- Stoeckle JD, Hardy HL, Weber AL. Chronic beryllium disease: long-term follow-up of sixty cases and selective review of the literature. Am J Med 1969;46:545–561.[CrossRef][Medline]
- Freiman DG, Hardy HL. Beryllium disease: the relation of pulmonary pathology to clinical course and prognosis based on a study of 130 cases from the U.S. beryllium case registry. Hum Pathol 1970;1:25–44.[Medline]
- Barna BP, Culver DA, Yen-Lieberman B, Dweik RA, Thomassen MJ. Clinical application of beryllium lymphocyte proliferation testing. Clin Diagn Lab Immunol 2003;10:990–994.[Free Full Text]
- Newman LS, Buschman DL, Newell JD Jr, Lynch DA. Beryllium disease: assessment with CT. Radiology 1994;190:835–840.[Abstract/Free Full Text]
- Harris KM, McConnochie K, Adams H. The computed tomographic appearances in chronic berylliosis. Clin Radiol 1993;47:26–31.[CrossRef][Medline]
- Maier LA. Clinical approach to chronic beryllium disease and other nonpneumoconiotic interstitial lung diseases. J Thorac Imaging 2002;17:273–284.[CrossRef][Medline]
- Sood A, Beckett WS, Cullen MR. Variable response to long-term corticosteroid therapy in chronic beryllium disease. Chest 2004;126:2000–2007.[Abstract/Free Full Text]
- Andrews JL, Kazemi H, Hardy HL. Patterns of lung dysfunction in chronic beryllium disease. Am Rev Respir Dis 1969;100:791–800.[Medline]
- Steenland K, Ward E. Lung cancer incidence among patients with beryllium disease: a cohort mortality study. J Natl Cancer Inst 1991;83:1380–1385.[Abstract/Free Full Text]
- Akira M. Uncommon pneumoconioses: CT and pathologic findings. Radiology 1995;197:403–409.[Abstract/Free Full Text]
- Fischbein A, Luo JC, Solomon SJ, Horowitz S, Hailoo W, Miller A. Clinical findings among hard metal workers. Br J Ind Med 1992;49:17–24.[Medline]
- Davison AG, Haslam PL, Corrin B, et al. Interstitial lung disease and asthma in hard-metal workers: bronchoalveolar lavage, ultrastructural, and analytical findings and results of bronchial provocation tests. Thorax 1983;38:119–128.[Abstract/Free Full Text]
- Coates EO Jr, Watson JH. Diffuse interstitial lung disease in tungsten carbide workers. Ann Intern Med 1971;75:709–716.[Abstract/Free Full Text]
- Pakes WR. Cobalt. In: Pakes WR, ed. Occupational lung disease. London, England: Butterworths, 1982; 464–467.
- Liebow AA. New concepts and entities in pulmonary disease. In: Liebow AA, Smith DE, eds. The lung. Baltimore, Md: Williams & Wilkins, 1968; 332–365.
- Ohori NP, Sciurba FC, Owens GR, Hodgson MJ, Yousem SA. Giant-cell interstitial pneumonia and hard-metal pneumoconiosis: a clinicopathologic study of four cases and review of the literature. Am J Surg Pathol 1989;13:581–587.[Medline]
- Choi JW, Lee KS, Chung MP, Han J, Chung MJ, Park JS. Giant-cell interstitial pneumonia: high-resolution CT and pathologic findings in four adult patients. AJR Am J Roentgenol 2005;184: 268–272.[Abstract/Free Full Text]
- Rizzato G, Fraioli P, Sabbioni E, Pietra R, Barberis M. The differential diagnosis of hard metal lung disease. Sci Total Environ 1994;150:77–83.[CrossRef][Medline]
- Kinoshita M, Sueyasu Y, Watanabe H, et al. Giant cell interstitial pneumonia in two hard metal workers: the role of bronchoalveolar lavage in diagnosis. Respirology 1999;4:263–266.[CrossRef][Medline]
- Moulin JJ, Wild P, Romazini S, et al. Lung cancer risk in hard-metal workers. Am J Epidemiol 1998; 148:241–248.[Abstract/Free Full Text]
- Hildick-Smith GY. The biology of talc. Br J Ind Med 1976;33:217–229.[Medline]
- Gibbs AE, Pooley FD, Griffiths DM, Mitha R, Craighead JE, Ruttner JR. Talc pneumoconiosis: a pathologic and mineralogic study. Hum Pathol 1992;23:1344–1354.[CrossRef][Medline]
- Marchiori E, Souza Junior AS, Müller NL. Inhalational pulmonary talcosis: high-resolution CT findings in 3 patients. J Thorac Imaging 2004;19: 41–44.[CrossRef][Medline]
- Feigin DS. Talc: understanding its manifestations in the chest. AJR Am J Roentgenol 1986;146:295–301.[Abstract/Free Full Text]
- Pare JP, Cote G, Fraser RS. Long-term follow-up of drug abusers with intravenous talcosis. Am Rev Respir Dis 1989;139:233–241.[Medline]
- Ward S, Heyneman LE, Reittner P, Kazerooni EA, Godwin JD, Müller NL. Talcosis associated with IV abuse of oral medications: CT findings. AJR Am J Roentgenol 2000;174:789–793.[Abstract/Free Full Text]
- Padley SP, Adler BD, Staples CA, Miller RR, Müller NL. Pulmonary talcosis: CT findings in three cases. Radiology 1993;186:125–127.[Abstract/Free Full Text]
- Billings CG, Howard P. Occupational siderosis and welders’ lung: a review. Monaldi Arch Chest Dis 1993;48:304–314.[Medline]
- Guidotti TL, Abraham JL, DeNee PB, Smith JR. Arc welders’ pneumoconiosis: application of advanced scanning electron microscopy. Arch Environ Health 1978;33:117–124.[Medline]
- Han D, Goo JM, Im JG, Lee KS, Paek DM, Park SH. Thin-section CT findings of arc-welders’ pneumoconiosis. Korean J Radiol 2000;1:79–83.[Medline]
- Mur JM, Meyer-Bisch C, Pham QT, et al. Risk of lung cancer among iron ore miners: a proportional mortality study of 1,075 deceased miners in Lorraine, France. J Occup Med 1987;29:762–768.[Medline]
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LEARNING OBJECTIVES FOR TEST...
