Seminars in Roentgenology
Volume 45, Issue 1 , Pages 43-52, January 2010

Occupational Lung Disease: A Radiologic Review

  • Sudhakar N.J. Pipavath, MD

      Affiliations

    • Department of Radiology, University of Washington, Seattle, WA
    • Corresponding Author InformationAddress reprint requests to Sudhakar N.J. Pipavath, MD, Department of Radiology, University of Washington, Box 357115, 1959 NE Pacific St, Seattle, WA 98195
    • ,
  • J. David Godwin, MD

      Affiliations

    • Department of Radiology, University of Washington, Seattle, WA
    • ,
  • Jeffrey P. Kanne, MD

      Affiliations

    • Department of Radiology, University of Wisconsin-Madison, Madison, WI

Article Outline

 

Pneumoconiosis is defined as a lung disease caused by accumulation of inhaled particulates. Occupational lung disease is the number-one work-related illness in the United States. The major substances causing illness include asbestos, coal dust, silica, beryllium, cobalt and tungsten carbide (hard metal), and iron oxide (in arc welders). Additionally, an increasing number of organic and low-molecular weight compounds have been identified as causes of hypersensitivity pneumonitis. We will discuss the diseases caused by these substances, with special emphasis on imaging.

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Asbestos-Related Pulmonary Disease 

Asbestosis is pulmonary fibrosis from inhalation of asbestos fibers. Workers exposed to asbestos include miners, millers, and persons employed in shipyards and building trades. Asbestos-related abnormalities can be nonmalignant, such as asbestosis, pleural plaque or diffuse pleural thickening, and airflow obstruction.1 Asbestos-related malignancies include mesothelioma of the pleura or peritoneum and bronchogenic carcinoma.

Benign Asbestos-Related Pleural Abnormalities 

Pleural plaque is the most common manifestation of asbestos exposure. It is a form of circumscribed pleural thickening, and it almost always involves the parietal pleura. Occasionally, it involves the visceral pleura, sometimes even a fissure between lobes. Plaques typically develop about 15-20 years from initial exposure, and they can calcify with time. In 1 series, the pleural plaques were always bilateral and <1-cm thick, with calcifications in 80% of the cases.2 The pleura in the midchest was involved in all cases; the diaphragmatic pleura in 50% and the upper and lower regions in 60% and 80% of the patients, respectively.2 Although there are many causes of diffuse pleural thickening with or without calcification, including pleurisy, empyema, and hemothorax, bilateral pleural plaques are almost always caused by asbestos exposure.

Pleural plaques may indent the adjacent lung and cause local atelectasis (indentation atelectasis). However, they usually do not lead to fusion between the visceral and parietal pleurae, and thus do not restrict lung motion or cause parenchymal bands or round atelectasis to form in adjacent lung. There is no evidence to suggest that pleural plaques undergo malignant degeneration to mesothelioma.

Diffuse pleural thickening can occur in as many as 22% of patients exposed to asbestos,3 and it is usually the sequela of benign asbestos pleural effusion. It causes the visceral and parietal pleurae to fuse together and, unlike plaque, can cause functional impairment. One study demonstrated a 270-mL reduction in lung volume caused by diffuse pleural thickening. Parenchymal bands4 and round atelectasis are common in the lung adjacent to diffuse pleural thickening. They reflect the contraction and fixation of the overlying visceral pleura, and they may resolve after decortication. Bands and round atelectasis occur with diffuse pleural thickening from any cause, not just that caused by asbestos exposure.

Benign pleural effusion associated with asbestos exposure is exudative. It may develop as early as about 7 years after initial exposure, but may do so even decades later. They usually resolves spontaneously, but may lead to diffuse pleural thickening. Pleural biopsy in a patient with benign effusion shows only nonspecific pleural inflammation and fibrosis. Asbestos bodies or fibers are rarely evident by light microscopy, although sparse fibers, usually chrysotile, may be shown by electron microscopy. Spontaneous resolution of each episode is usual, but the condition may recur with increasing diffuse pleural thickening after each episode. Occasionally, mesothelioma emerges some years after apparently benign effusion.3 Persistent or recurrent effusion raises the concern for malignancy.

Asbestosis indicates lung fibrosis from exposure to asbestos fibers, typically developing about 20 years or more after initial exposure. Minimal criteria for the pathologic diagnosis of asbestosis include pulmonary fibrosis and the presence of asbestos bodies. Since biopsy is uncommonly performed, clinical diagnostic involves the following: (1) Evidence of structural pathology consistent with asbestos-related disease as documented by imaging or histology, (2) Evidence of causation by asbestos as documented by the occupational and environmental history, markers of exposure (usually pleural plaques), recovery of asbestos bodies, or other means, and (3) Exclusion of alternative plausible causes for the finding.1

Imaging 

Pleural plaques on chest radiography are best seen in profile as focal pleural thickening along the posterolateral chest wall between the 6th and 10th ribs and along the diaphragm (Fig. 1). The costophrenic sulci and the lung apices are typically spared. However, extrapleural fat has a similar distribution and can easily be mistaken for plaque. En face calcified plaque may have the appearance of a holly leaf. On computed tomography (CT), pleural plaques are easily identified along the chest wall (Fig. 2). Sometimes it is difficult to distinguish innermost intercostal muscles from plaque; however, plaques are usually located along the inner surfaces of the ribs and the vertebral bodies, and the innermost intercostal muscles are located between the ribs. Also, noncalcified plaques are usually thicker and have higher attenuation than intercostal muscle. Calcified plaques are easy to identify. Diaphragmatic plaques may be better appreciated on coronal or sagittal reformations. The plaques are usually bilateral, but can be unilateral in up to 30%.5

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  • Figure 1. 

    Posteroanteriorly chest radiograph of a man with asbestos-related pleural disease shows multiple calcified in-profile pleural plaques along the left lateral chest wall and also along the diaphragm (arrows). Enface pleural plaque is also present on the right (arrowheads).

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  • Figure 2. 

    Prone HRCT image of man with asbestos-related pleural disease demonstrates multiple pleural plaques (black arrows), parenchymal bands (white arrowheads), and a mild reticular abnormality with subpleural lines (white arrow) and dots (black arrowheads).

Benign asbestos pleurisy may show features of an exudative effusion on CT with parietal pleural thickening. The presence of pleural plaque suggests the possibility that effusion is asbestos-related.

Diffuse pleural thickening related to asbestos exposure has no specific imaging features. Associated pleural plaques raise the possibility that diffuse thickening is caused by asbestos exposure but do not definitively establish the cause, given the myriad other causes of diffuse thickening. Benign pleural thickening is usually <1-cm thick, and malignant pleural thickening should be considered when thickness >1-cm. Other features of malignant pleural thickening include nodularity, circumferential involvement, and mediastinal pleural involvement (Fig. 3).

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  • Figure 3. 

    Contrast-enhanced CT image of a 67-year-old man with mesothelioma shows circumferential right pleural thickening. The tumor has invaded the chest wall (arrowheads) and mediastinum (arrow).

Imaging features of rounded atelectasis include the rounded peripheral mass adjacent to thickened pleura, curvilinear distortion of the nearby bronchi and the vessels (comet tail sign), and volume loss in the affected lobe (Fig. 4). Recognition of rounded-atelectasis helps prevent unnecessary biopsy or resection.6

Asbestosis on chest radiography is usually indistinguishable from other causes of basal lung fibrosis. On high-resolution computed tomography HRCT (Fig. 5), asbestosis typically has the pattern of usual interstitial pneumonia (UIP).7 The presence of pleural plaques suggests that fibrosis may be asbestosis. Subpleural dots and lines have been suggested to be more characteristic of asbestosis than of other kinds of fibrosis.4 In a study by Akira et al4 of patients with autopsy findings of asbestosis, the HRCT finding of intralobular lines correlated with peribronchiolar fibrosis and involvement of the alveolar ducts. Interlobular lines corresponded to interlobular septal thickening and edema. Subpleural opacities reflected subpleural fibrosis. Parenchymal bands represented fibrosis along the bronchovascular sheath or interlobular septa, with parenchymal distortion. The subpleural curvilinear lines were foci of peribronchiolar fibrotic thickening with and collapse of the alveoli.

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  • Figure 5. 

    Coronal HRCT image of a 76-year-old man with asbestosis shows peripheral-predominant interstitial fibrosis with architectural distortion and traction bronchiectasis. A diaphragmatic pleural plaque is present on the right (arrow).

As with other forms of UIP, prone HRCT imaging is important in evaluation for asbestosis, given that dependent atelectasis can both mimic and disguise subpleural fibrosis.

Silicosis 

Silicosis is caused by inhalation of crystalline silicon dioxide (silica). Abnormalities begin to appear on chest radiographs about 20 years after exposure, mainly in upper and middle lung zones. Silicosis is classified into simple, complicated, acute, and accelerated forms.

Simple Silicosis 

Radiographic and CT abnormalities include small, discrete nodules ranging from 2 to 5-mm in diameter but to a maximum of 10-mm (Figure 6, Figure 7).8 The nodules may cluster in a perilymphatic distribution. Hilar or mediastinal lymphadenopathy with calcification is common, and the calcification may be at the periphery of the nodes. Such “egg-shell” calcification (Fig. 8) can also occur in sarcoidosis, chronic beryllium disease (CBD), and mycobacterial infection. Pleural abnormalities, especially in advanced disease, include pseudoplaques (confluence of nodules along the pleura), pleural effusion, and pleural thickening.9

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  • Figure 7. 

    Maximum intensity projection CT image of a man with simple silicosis shows multiple fine nodules in a random distribution and a solitary larger nodule (arrow), which was determined by biopsy to be the sequela of lipoid pneumonia resulting from inhalation of lubricating oil.

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  • Figure 8. 

    PA chest radiograph of a man with simple silicosis shows multiple calcified hilar lymph nodes, some of which show an “egg-shell” pattern of calcification (arrows). Small nodules are present in the upper lobes (arrowheads).

Complicated Silicosis 

Over time, small nodules in silicosis tend to cluster and coalesce, eventually forming conglomerate masses of size 1-cm or larger. The advanced stage of this conglomeration is termed progressive massive fibrosis (PMF). Conglomerate masses tend to involve the apical and posterior segments of the upper lobes. Associated parenchymal distortion is common, with paracicatricial emphysema (Fig. 9). PMF is typically bilateral and often symmetric. The lesions often contain calcification. Cavitation is unusual, and its occurrence reflects ischemic necrosis or accompanying tuberculosis. PMF can be mistaken for lung cancer or tuberculosis, but can generally be distinguished by symmetry and slow progression. However, positron-emission tomography scanning cannot distinguish PMF from cancer, because both show 18F-deoxyglucose avidity.8 On magnetic resonance imaging, lung cancer has high-signal intensity on T2-weighted images, whereas PMF has isointense signal on T1-weighted images and low-signal intensity on T2-weighted images.10

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  • Figure 9. 

    Contrast-enhanced coronal CT image (A) of a man with complicated silicosis shows bilateral conglomerate masses with associated cicatrization in the upper lobes, hilar retraction, lymph node calcification, bibasilar hyperexpansion, and emphysema. Emphysema and hyperexpansion are best appreciated on the transverse minimum intensity projection image (B).

Accelerated Silicosis 

Accelerated silicosis follows a brief but heavy exposure (usually 4-10 years). Its imaging manifestations are generally similar to those of complicated silicosis.

Acute Silicosis 

Acute silicosis, or silicoproteinosis, may follow intense exposure to silica, even just for months. Radiographic findings are similar to those of pulmonary alveolar proteinosis,8, 11 that is, consolidation and ground-glass opacities, concentrated in perihilar regions (Fig. 10). CT findings include centrilobular nodules, ground-glass opacities, and consolidation.12, 13 However, acute silicosis is progressive and can lead to death from respiratory failure.14

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  • Figure 10. 

    HRCT image of a 28-year old concrete worker with acute silicoproteinosis demonstrates patchy ground-glass opacity with superimposed interlobular septal thickening and intralobular reticulation.

In silicosis, there is only weak correlation between pulmonary function tests and the profusion of nodules on radiographs or CT scans. CT scoring of emphysema correlates well with some pulmonary function tests, forced expiratory volume, and diffusing capacity. Emphysema in patients with silicosis is typically more common in smokers, in which paracicatricial emphysema and centrilobular emphysema are combined. However, silicosis is an independent risk factor for emphysema, even in nonsmokers.15, 16, 17 Recently, Arakawa et al18 reported that the extent of air trapping by expiratory CT was the best CT index of the degree of obstruction.

Silicosis predisposes to pulmonary tuberculosis; in men the relative risk is 2.8.19 Radiologic features of silicotuberculosis include asymmetric nodules or consolidation, cavitation of conglomerate masses, and rapid progression. Of these features, cavitation is the most strongly associated with silicotuberculosis, although uninfected conglomerate masses can cavitate.20

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Coal Workers' Pneumoconiosis 

Chronic exposure to coal dust can cause pneumoconiosis. Coal mining often exposes workers simultaneously to silica, which is more fibrogenic than coal, but workers who are exposed to coal that has been washed nearly free of silica can still develop pneumoconiosis. Like silicosis, coal workers' pneumoconiosis (CWP) has simple and complicated forms, but only a small percentage of patients advance to complicated CWP, because of the coal's low fibrogenicity. Significant CWP generally requires at least 20 years of exposure. A shorter exposure to coal dust is more likely to cause chronic bronchitis than CWP.

In CWP the 2 characteristic pathologic features are coal macules and PMF. A coal macule contains centrilobular anthracotic pigment without fibrosis, and typically measures <0.5 cm. PMF consists of a fibrotic, pigmented mass of >1-cm diameter.21

On imaging, distinguishing CWP from silicosis is often difficult. The radiographic pattern of simple CWP includes small, round, poorly defined 1-5-mm nodules. In CWP, calcification in lung nodules, seen in a maximum of 30% patients, is typically central (vs diffuse) in silicotic nodules.22, 23 “Eggshell” calcification is uncommon in CWP.22

CT features of simple CWP include small nodules with a perilymphatic or centrilobular distribution with some concentration in upper lung. Hilar or mediastinal lymph node enlargement is present in 30% of patients.24 The fibrotic masses in CWP and silicosis at CT are similar, although their histology is different (Fig. 11). Conglomerate masses may or may not be surrounded by paracicatricial emphysema.

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  • Figure 11. 

    PA chest radiograph (A) of a 45-year-old miner with CWP shows bilateral upper lobe large opacities surrounded by small nodules. The hila are retracted cephalad, and the lower lobes are hyperinflated. HRCT images (B, C) demonstrate cavitation of the large mass in the left upper lobe. Calcium is present in both upper lobe masses as well as in hilar and mediastinal lymph nodes. Small nodules and paracicatricial emphysema are present.

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Berylliosis 

Berylliosis is a multisystem disorder with acute and chronic forms. The acute form, which is now rare, is a kind of chemical pneumonitis resembling adult respiratory distress syndrome caused by exposure to dust, fumes, or aerosols of beryllium metal or its salts. The chronic form, which is called chronic granulomatous beryllium disease (CBD), develops months or years after exposure in a maximum of 16% of exposed workers.25 There is generally a dose–response relationship, but even minimal exposure can sometimes cause CBD.

Patients may be asymptomatic with an abnormal chest radiograph, or may have restrictive or obstructive lung disease. Dyspnea, cough, fever, anorexia, and weight loss are some typical symptoms.25 Extrathoracic manifestations include skin lesions, granulomatous hepatitis, hypercalcemia, and kidney stones.26 CBD can be misdiagnosed as sarcoidosis. Therefore, the beryllium registry has developed detailed clinical and pathologic criteria for diagnosis of CBD (Table 1).27

Table 1. Criteria to Establish a Diagnosis of Chronic Beryllium Disease
Documented exposure, preferably including air samples in the workplace
Objective evidence of lower respiratory disease and clinical course consistent with berylliosis
Chest radiograph showing fibronodular opacities
Functional evidence of restriction, obstruction, or decreased diffusing capacity
Pathology consistent with berylliosis in lung or thoracic lymph nodes
Beryllium in lung lymph nodes or in urine

Beryllium case registry review requires at least 4 of the 6 criteria mentioned to establish a diagnosis of chronic beryllium disease (CBD).

The chest radiographic features range from normal findings to extensive nodules, reticulation, and masses.28, 29, 30 The radiographic and CT appearance of CBD is similar to that of sarcoidosis, although mediastinal and hilar lymphadenopathy is less common in CBD. On CT, lung nodules are present in a perilymphatic distribution (peribronchovascular, centrilobular, and subpleural) with either smooth or nodular septal thickening. Nodules are concentrated in the mid and upper lungs (Fig. 12).31 Other findings include ground-glass opacities (32%) (Fig. 13), honeycombing (7%), conglomerate masses (7%), and bronchial wall thickening (46%).28 Hilar or mediastinal lymphadenopathy occurs in 32%-39% of cases.28, 29, 31

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  • Figure 13. 

    HRCT images (A, B) of a 34-year-old man with chronic berylliosis demonstrate patchy ground-glass opacity, especially along bronchovascular bundles. A few low-attenuation lobules are present, suggesting air trapping.

CBD has a variable clinical course, with some cases regressing spontaneously, and some responding to corticosteroid therapy. A minority of patients progress to respiratory failure. The prognosis is poor when disease is symptomatic, especially when complicated by cor pulmonale.32, 33 Like silica and asbestos, beryllium is thought to promote lung cancer, particularly in patients with acute berylliosis.33

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Hard Metal Lung Disease 

Hard metal is a generic term for matrix that consists of cobalt and tungsten carbide. It has great strength, heat resistance, and resistance to oxidation. Exposure occurs during drilling, grinding, cutting, and polishing operations. Cobalt is the primary offender.34 The lung disorder ranges from reactive airway disease to obliterative bronchiolitis to giant cell interstitial pneumonia (GIP), now known as hard metal pneumoconiosis.

The criteria for diagnosis of hard metal lung disease are as follows: (a) History of exposure to metal dust, (b) shortness of breath, cough, and dyspnea on exertion over a prolonged period, (c) radiologic findings of interstitial lung disease, and (d) histologic findings of interstitial lung disease or a GIP pattern with thickening of the interstitium and alveolar walls by mononuclear cells, and (e) demonstration of metal in lung tissue.35, 36

Radiographic findings are bilateral ground-glass opacities and reticulation, particularly in the bases. HRCT findings in hard metal pneumoconiosis are ground-glass opacities, consolidation, and reticulation; honeycombing is rare. Reticulation and honeycombing are concentrated in the bases and periphery. Emphysema was noted in 1 patient with hard metal pneumoconiosis, possibly from cigarette smoking.37 Obliterative bronchiolitis can occur early in hard metal lung disease, with air trapping as the dominant finding on expiratory CT. In early stages, fine nodules, centrilobular nodules, and ground-glass opacities are found (Fig. 14). Abnormalities suggesting nonspecific interstitial pneumonia, UIP, and sarcoidosis have also been described in hard metal pneumoconiosis.38

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  • Figure 14. 

    HRCT images (A, B) of the right lung of a 27-year-old male grinder with hard metal pneumoconiosis show ground-glass nodules, especially in upper lobes. Mild bronchial dilation is present (arrow).

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Hypersensitivity Pneumonitis 

Hypersensitivity pneumonitis (HP), also referred to as extrinsic allergic alveolitis, is a diffuse granulomatous interstitial lung disease involving the interstitium and distal airways. HP is caused by the repeated inhalation of antigenic organic and low-molecular weight inorganic particles.9, 39, 40, 41, 42 HP is common in farmers and bird breeders. Other causes are a multitude of animal and microbial antigens and some inorganic compounds, including plastic vapors, paints, and metal-working fluids.

In farmers, the inciting antigens are typically Aspergillus and thermophilic actinomyces, but in many occupational settings there are multiple potentially culpable antigens; the antigen is not identified in up to one-third of histologically proven cases of HP.43

HP is characterized histologically by the triad of cellular bronchiolitis, poorly-formed, non-necrotizing granulomata, and lymphoplasmocytic interstitial pneumonitis. Organizing pneumonia and giant cells may be present.44 Patients with HP can develop lung fibrosis similar to nonspecific interstitial pneumonia or to UIP.

HP is often grouped both clinically and radiographically into acute, subacute, and chronic forms.11, 39, 42 However, extensive overlap of imaging findings is frequent, and only the presence of lung fibrosis confirms chronicity.

Acute HP is very uncommon. Patients present with fever, cough, and dyspnea 4-6 hours after heavy exposure to antigen. CT findings include diffuse ground-glass opacity, reticulation, and basal-predominant, tiny, poorly-defined nodules.45, 46

Subacute HP occurs with recurrent low-level exposure to the antigen. CT findings consist of patchy or diffuse ground-glass opacity, small (<5-mm), poorly defined centrilobular nodules, and patchy lobular air trapping (Fig. 15). Scattered thin-walled cysts are present in about 10% of patients, and about 50% have mediastinal lymphadenopathy. The prognosis of subacute HP is favorable with early detection and removal from exposure.39

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  • Figure 15. 

    HRCT images (A, B) of a 73-year-old male farmer demonstrate extensive ground-glass opacity with sparing of secondary lobules. Mild fibrosis is present in the right upper lobe, characterized by mild reticulation and traction bronchiolectasis (arrowhead).

The CT findings of chronic HP on CT vary. As with subacute HP, poorly defined centrilobular nodules and lobular air trapping may be present. Reticulation, traction bronchiectasis, and volume loss reflect fibrosis (Fig. 16). Honeycombing occurs as fibrosis progresses. There is no consistent zonal predominance. Emphysema and obstructive lung disease develop occasionally.39, 40, 42, 46

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  • Figure 16. 

    Transverse (A) and coronal (B) HRCT images of a 65-year-old female quail breeder show diffuse ground-glass opacity with lobular sparing. Peripheral and central reticulation is present, and there is subpleural traction bronchiectasis and bronchiolectasis.

Chronic HP may progress to respiratory failure; 5-year mortality approaches 61% when fibrosis is present.40 Fibrosis on CT, marked by abnormal pulmonary function tests, and crackles on physical examination indicate poor prognosis.

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Siderosis 

Arc welders are exposed to iron oxide in fumes generated by consumable electrodes. The inhaled iron oxide is consumed by macrophages, which accumulate around the small airways and vessels and form siderotic nodules, giving the term siderosis. At this stage, the clinical significance is limited, with only radiologic and pathologic findings, and removing the worker from exposure may allow the nodules to resolve.47 However, a few cases may progress to peribronchiolar fibrosis with surrounding paracicatricial emphysema.

On CT, the most common findings include centrilobular or peribronchial lung nodules (Fig. 17). Most of these are poorly defined, similar to those in HP.48, 49 Other findings in arc welders include perinodular and paracicatricial emphysema (with cigarette smoking as a confounding factor) and UIP.47 Other uncommon findings reported are ground-glass opacities, reticulation, and conglomerate masses with high-attenuation.

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  • Figure 17. 

    HRCT image of a 39-year-old male welder shows diffuse, poorly-defined centrilobular nodules in both lungs. These are similar to those occurring in hypersensitivity pneumonitis and in respiratory bronchiolitis-interstitial lung disease.

There is a dearth of longitudinal analyses that systematically examine the direct and long-term effects of welding. Thus, the clinical consequences of siderosis are uncertain.50

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Conclusion 

In summary, increased use of CT has lead to clearer description of known, and insight into newer, occupational lung diseases. Imaging features of many of these diseases overlap with those of other pneumoconioses and nonoccupational diseases as well. Thus, a thorough history of occupational exposure is invaluable in the diagnosis of these conditions.

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PII: S0037-198X(09)00072-8

doi:10.1053/j.ro.2009.07.008

Seminars in Roentgenology
Volume 45, Issue 1 , Pages 43-52, January 2010

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