Occupational Lung Diseases: Spectrum of Common Imaging Manifestations

Abstract

Occupational lung diseases (OLD) are a group of preventable conditions caused by noxious inhalation exposure in the workplace. Workers in various industries are at a higher risk of developing OLD. Despite regulations contributing to a decreased incidence, OLD remain among the most frequently diagnosed work-related conditions, contributing to significant morbidity and mortality. A multidisciplinary discussion (MDD) is necessary for a timely diagnosis. Imaging, particularly computed tomography, plays a central role in diagnosing OLD and excluding other inhalational lung diseases. OLD can be broadly classified into fibrotic and non-fibrotic forms. Imaging reflects variable degrees of inflammation and fibrosis involving the airways, parenchyma, and pleura. Common manifestations include classical pneumoconioses, chronic granulomatous diseases (CGD), and small and large airway diseases. Imaging is influenced by the type of inciting exposure. The findings of airway disease may be subtle or solely uncovered upon expiration. High-resolution chest CT, including expiratory-phase imaging, should be performed in all patients with suspected OLD. Radiologists should familiarize themselves with these imaging features to improve diagnostic accuracy.

Keywords: Asbestosis; Asthma; Chronic beryllium disease; Coal worker's pneumoconiosis; Hypersensitivity pneumonitis; Obliterative bronchiolitis; Occupational lung disease; Silicosis.

Fig. 1. Frontal (A) and lateral (B) chest radiographs showing ill-defined calcific densities along the posterior and diaphragmatic pleural surfaces (arrows) and sparing the costophrenic sulci and the apices of the lungs.

Fig. 2. Frontal chest radiograph (A) and corresponding dual energy subtraction image (B) show improved visualization of pleural plaques (arrows) provided by dual energy technique.

Fig. 3. Cropped down frontal chest radiograph (A) shows an asbestos-related plaque resembling a holly leaf appearance on radiography. Picture of a holly leaf (B) is provided for comparison.

Fig. 4. Round atelectasis and asbestos related pleural disease. Non-contrast axial computed tomography (CT) image in soft tissue window (A) shows bilateral pleural thickening reflective of non-calcified pleural plaques (white arrows). Axial CT image in lung window (B) showing right lower lobe rounded consolidation with broad base attachment to adjacent pleural thickening. Associated volume loss is evidenced by posterior fissural displacement and convergence of adjacent bronchovascular structures (hurricane sign or comet tail sign). Findings are compatible with round atelectasis.

Fig. 5. Asbestos related pleural disease and asbestosis. Non-contrast chest computed tomography (CT) images in lung (A) and bone (B) windows show subpleural reticulation with subtle traction bronchiolectasis and architectural distortion (circle) and subpleural dot-like opacities (arrowheads) compatible with asbestosis. Concurrent posterolateral calcified pleural plaques are compatible with asbestos related pleural disease (white arrows in B). Non-contrast chest CT images at a lower level in lung (C) and bone (D) windows show peripheral reticulation with subtle bronchiolectasis (black arrows) and subpleural dot-like opacities (arrowheads). Calcified pleural plaques are also present (white arrows in D) indicating asbestos exposure.

Fig. 6. Severe asbestosis. Axial chest computed tomography images in lung windows (A-D) show peripheral posterobasilar fibrosis with subpleural honeycombing compatible with a usual interstitial pneumonia pattern. Subpleural curvilinear opacities are present bilaterally (arrowheads in A). Bilateral calcified pleural plaques are present indicating asbestos exposure. Findings are compatible with asbestosis.

Fig. 7. Mild asbestosis in the absence of asbestos-related pleural disease. Non-contrast axial chest computed tomography images in lung window (A, B) showing mild multifocal subpleural reticulation indicative of mild pulmonary fibrosis. Pleural plaques were not identified.

Fig. 8. Patient with simple silicosis. Frontal chest radiograph (A) showing extensive upper to mid lung nodularity with relative basilar sparing. Non-contrast computed tomography scans from upper (B) to lower (C) aspect of thorax demonstrating nodules throughout, but more numerous throughout the upper and mid lung zones. Nodules demonstrate clustering in the centrilobular and subpleural portions of the lungs.

Fig. 9. Silicotic pseudo-plaques (arrows). Cropped down non-contrast coronal chest computed tomography images (A, B) in soft tissue windows demonstrating biapical focal calcified plaque like nodularity.

Fig. 10. A 55-year-old male with complicated coal worker pneumoconiosis. Non-contrast axial computed tomography images of the upper lung in lung (A) and soft tissue (B) windows show mass like opacities with subtle relative hyperattenuation relative to the aortic blood pool (black arrows in A) and internal coarse calcification (white arrows in B), consistent with progressive massive fibrosis. There is associated architectural distortion (C). Findings are consistent with progressive massive fibrosis. Small nodules are also present in continuity and adjacent to the upper lung masses. There are calcified mediastinal and left hilar lymph nodes (white arrows in D).

Fig. 11. Acute silicosis (silicoproteinosis) acquired from sandblasting. Axial non-contrast chest computed tomography images (A, B) in lung window show multifocal ground glass opacities with interlobular and intralobular septal thickening resulting in a “crazy paving” appearance and with geographical margination.

Fig. 12. Chronic beryllium disease. Coronal non-contrast chest computed tomography (CT) image in lung window (A) demonstrating upper lung preponderant perilymphatic nodularity, with nodules extending along interlobular septa and in a subpleural and peribronchovascular distribution. The lung bases are relatively preserved. Non-contrast axial chest CT in lung window (B, C) show diffuse micronodularity extending in a perifissural, subpleural and peribronchovascular distribution.

Fig. 13. A 75-year-old male with history of woodworking and mold exposure demonstrating non-fibrotic hypersensitivity pneumonitis. Non-contrast axial (A, B) and coronal (C) chest computed tomography images show diffuse centrilobular ground-glass nodularity with inspiratory mosaicism. Non-contrast expiratory axial (D), coronal (E), and minimum intensity projection (F) images show air trapping.

Fig. 14. Fibrotic hypersensitivity pneumonitis in a farmer. Fibrotic non-contrast expiratory axial (A, B) and coronal (C) images in lung windows show mid to lower-lobe-predominant fibrosis with reticulation, cystic change, patchy ground-glass opacities, and lobular regions of air trapping. All arrows are pointing towards lobular air trapping.

Fig. 15. Obliterative bronchiolitis. Non-contrast axial (A-D) images in lung windows show geographic areas of hypodensity representing air trapping associated with bronchial wall thickening, mild scattered bronchiectasis and pruning of smaller vessels due to hypoxia.

Fig. 16. Differences in imaging appearance of obliterative bronchiolitis (A, B) and asthma (C, D). Non-contrast axial in lung windows in inspiration (A, C) and expiration (B, D) demonstrating geographic air trapping appearing more confluent in obliterative bronchiolitis.