Diversity of occupational pathologies
Exposure to various workplace agents creates unique patterns of lung tissue damage that are clearly visible on high-resolution computed tomography (HRCT):
- Flock worker's lung (Flock worker’s lung): manifested by lymphocytic bronchiolitis. Scans show centrilobular nodules and areas of ground-glass opacities.
- Food processing worker's lung (due to flavorings): causes obliterating bronchiolitis with mosaic attenuation and air trapping.
- Berylliosis: radiologically almost indistinguishable from sarcoidosis. Characterized by the formation of non-caseating granulomas, lymphatic distribution of nodules, and septal thickening.
- Hard metal pneumoconiosis (titanium, cobalt, tungsten): leads to giant cell interstitial pneumonia with areas of consolidation.
Silicosis and coal worker's pneumoconiosis (CWP)
Inhalation of silicon dioxide (Silica) or coal dust causes identical early changes. Well-defined centrilobular and subpleural micronodules (1–3 mm) appear in the posterior regions of the upper lobes. Subpleural lesions can coalesce into pseudoplaques. Enlargement of intrathoracic lymph nodes with eggshell calcification is characteristic.
The most formidable complication is progressive massive fibrosis (PMF). This is the confluence of large nodules into massive opacities, usually in the upper lobes. These formations cause volume loss of the lobe due to cicatricial retraction, upward traction of the lung hilar structures, and the formation of compensatory peripheral traction emphysema. If cavities develop within the masses (cavitation), tuberculosis must be ruled out.
Asbestos-related diseases
Asbestos is a group of heat-resistant fibrous silicates (chrysotile and amphiboles). Pathologies can affect both the pleura and the lung parenchyma itself.
- Benign effusions: hemorrhagic exudate that can appear as early as 5 years after exposure (an exception to the long-latency rule). Asbestos bodies are usually absent in the fluid.
- Pleural plaques: discrete foci of fibrosis on the parietal pleura (often under the anterior ends of the ribs and on the diaphragm).
- Diffuse pleural thickening: fibrosis of the visceral pleura with symphysis of the pleural layers. Often arises as a sequela of effusion.
- Round atelectasis ("folded lung"): collapse of the parenchyma adjacent to the thickened visceral pleura. CT shows the comettail sign—arcuate convergence of bronchi and vessels toward the hilum. Unlike cancer, atelectasis shows intense contrast enhancement and is stable on follow-up imaging.
CT appearance and diagnosis of asbestosis
Asbestosis is parenchymal fibrosis. It begins in the interstitium of the respiratory bronchioles of the lower lobes.
Early HRCT signs: subpleural curvilinear lines, dots, parenchymal bands, and fine reticular opacities. These changes are better visualized in the prone patient position.
Late stages: coarse reticulation and the formation of honeycombing (honeycombing). The picture becomes indistinguishable from usual interstitial pneumonia (UIP).
The diagnosis of asbestosis is based on a confirmed history of asbestos exposure and the presence of classic features of fibrosis. The key differential diagnostic criterion distinguishing asbestosis from idiopathic pulmonary fibrosis (IPF) is concurrent pleural involvement (plaques or thickening are detected in 83% of patients with asbestosis).
Briefly: answers to topical questions
What malignancies develop with prolonged asbestos exposure?
Malignant pleural mesothelioma develops with prolonged asbestos exposure.
- Malignant mesothelioma (Malignant Mesothelioma) is a rare primary neoplasm of the pleura strictly associated with asbestos exposure.
- On imaging, mesothelioma is often indistinguishable from metastatic disease.
What complications and associated syndromes can occur in silicosis?
Cardiovascular, inflammatory, and structural complications of the lung tissue can occur in silicosis.
- Cor pulmonale develops as a result of diffuse sclerotic processes in the lungs and pulmonary hypertension.
- Inflammatory processes — include pleurisy, interstitial pneumonia, and bronchopneumonia.
- Pulmonary emphysema is a structural alteration of the lung parenchyma.
- Spontaneous pneumothorax is possible against the background of emphysema, but occurs rarely due to pronounced adhesions in the pleural cavity.
- Progressive massive fibrosis (Progressive Massive Fibrosis) is the confluence of large nodules accompanied by shrinkage of the upper lobes.
"Silicosis in the upper zones, asbestosis in the lower zones." In silicosis, nodules and masses (PMF) predominantly affect the posterior segments of the upper lobes, whereas asbestosis fibrosis manifests in the basal (lower) and subpleural regions of the lungs.
Class and exam questions
How to distinguish progressive massive fibrosis (PMF) from lung cancer?
Features favoring PMF include concurrent lobar volume loss, marked peripheral traction emphysema adjacent to the lesion, and outer contours of the masses running parallel to the chest wall.
What is the difference between pleural plaques and diffuse pleural thickening?
Plaques are localized on the parietal pleura, do not impair respiratory function, and are the most frequent sign of asbestos exposure. Diffuse thickening affects the visceral pleura, causes its fusion with the parietal pleura, and often forms following previous effusion.
Why perform prone CT when suspecting early asbestosis?
This helps distinguish true early fibrotic changes (subpleural lines, fine reticulation) from gravitational blood pooling in the posterobasal lung regions, which disappears when the patient is turned.
What else to study on this topic
- Principles of pneumoconiosis classification according to the International Labour Organization (ILO) system.
- Pathomorphology and differential diagnosis of round atelectasis ("folded lung").
- Cavitation in progressive massive fibrosis: criteria for ruling out tuberculosis.
- Features of hard metal-induced giant cell interstitial pneumonia.
- Radiological differential diagnosis of berylliosis and pulmonary sarcoidosis.
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