Occupational Lung Diseases and Pneumoconiosis
Factors influencing effects of inhaled agents
Physical properties: size (<1 micron are the most destructive to lung parenchyma) and density of particles, shape and penetrability, solubility, hygroscopicity (will it pick up water?), and electric charge
Chemical properties: acidity and alkalinity, combining capacity, fibrogenicity, and antigenicity.
Host factors: lung defenses (genetic and acquired), anatomic and physiologic factors, immunologic state (allergies).
Mechanisms of deposition: sedimentation (due to gravity), inertial impaction (deposit lodges itself in parenchyma when being inhaled), and diffusion.
Normal lung clearance mechanism (see figure below):
Caused by inhalation of free crystalline silica (SiO2).
Three types of silicosis: acute, accelerated, and chronic.
- Other types of silica include: amorphous and microcrystalline.
- Occupational exposure to silica: mining, quarrying, stone cutting, masonry, abrasive blasting, and foundry work.
Pathogenesis: Silica is taken up by macrophages Þ lysosome inside macrophage tries to degrade, however silica is toxic to lysosomal membranes Þ leakage of tissue damaging enzymes and silica particles injure cells Þ silica can be released, and injured macrophage can release oxidants and cytokines Þ pulmonary fibrosis. Impaired phagocytosis of surfactant and cellular debris probably plays a role in the accumulation of alveolar proteinosis in accelerated silicosis. Silica particles may also stimulate type II pneumocytes to proliferate and release phospholipids.
Caplan’s Syndrome (Rheumatoid Pneumoconiosis): patients with rheumatoid arthritis show a more rapid evolution and progression of conglomerate lesions. Nodular lesions of Caplan’s syndrome resemble rheumatoid nodules (central necrosis and peripheral palisaded, epithelioid cells). Silicosis may lead to an autoimmune process in the lung.
- (1) Chronic Silicosis – Most common form; long latency and slow progression.
- Simple: early stage in development of conglomerate.
- Hallmark lesion is the hyalinized nodule (< 1cm). Microscopically, the nodule is made of laminated acellular hyaline tissue, a few chronic inflammatory cells, and doubly refractive particles of silica within nodule and periphery.
- Macroscopically, lesions are palpably hard and may be heavily pigmented. Hilar lymph nodes are enlarged by hyalinized silicotic nodules which may calcify in a peripheral fashion (egg-shell calcification).
- Conglomerate: as simple nodules enlarge and coalesce (> 1cm), lung tissue is replaced and obliterated.
- Associated with tuberculous infection: if TB, caseation necrosis and cavitation may occur. Cavitation can also occur as a result of a massive conglomerate lesion which causes ischemia.
- Complications include breathlessness and physiologic alterations of obstructive lung disease, panlobular emphysema, cor pulmonale, and clinical heart failure.
- (2) Accelerated Silicosis: Much more rapid evolution due to inhalation of large quantities of fine dust. Simple lesions appear within 5-6 years of exposure and rapidly progress to conglomerate lesions. Diffuse interstitial fibrosis may be seen in addition to nodular fibrosis.
- (3) Acute Silicosis: Evolves over a brief (< 1 year) period of massive inhalation of fine dust. CXR is characterized by diffuse, rather than nodular, infiltrates. Pathologically diffuse interstitial fibrosis and silcotic nodules are present.
- Alveolar spaces are also filled with lipoproteinaceous material resembling pulmonary alveolar proteinosis.
Describes the pulmonary manifestations of worker’s exposed from the dust in coal mines
Mine environment (not all the worker’s have the same exposure): Face workers, transporters, maintenance personnel, and surface workers.
Lung has deep black pigmentation on the pleural surface. Black dust foci (> 0.5 mm in diameter) are located in the vicinity of the terminal and respiratory bronchioles. Non-palpable pigmented lesions surrounding the alveoli are called coal macules. A macule can turn into a small fibrotic lesion (micronodule) if silica is inhaled. Microscopically, the dust appears to be contained within macrophages which are enmeshed in a collection of reticulin fibers.
Focal (or centrilobular) emphysema (enlargement of the air spaces surrounding collections of dust) may occur. It may be caused by shrinkage of reticulin tissue in the coal focus and dilation of the surrounded air space or bronchiole.
Simple coalworker’s pneumoconiosis: Minimal or no physiological abnormalities unless there is associated disease. Minute opacities on CXR which correspond to coal macules. Patients may present with cough and black sputum.
Complicated coalworker’s pneumoconiosus (progressive massive fibrosis): Characterized by large confluent zones of dense fibrosis, usually presenting in one or both upper lobes. Masses are darkly pigmented and rubbery. Microscopically, they are dense acellular fibrous tissue which contain much pigment. Lung parenchyma has been completely replaced and vessels show an obliterative end arteritis. A few chronic inflammatory cells may be present. Patients present with dyspnea, cough, sputum, melanoptysis (large amounts of black crap expectorated), and lobar collapse.
Theory: PMF may be a result of the combination of TB on simple coalworker’s pneumoconiosus. Caseous necrosis and ischemic cavitation may also contribute to the lesions. In PMF, right heart enlargement and ultimately failure commonly cause death. Pulmonary embolism or thrombosis is another terminal complication.
Asbestosis-Related Pleuropulmonary Disease
Asbestos is a fibrous silicate. Individuals in insulation and construction businesses are exposed to high levels of airborne asbestos upon removing insulation or demolishing buildings.
Marked by a diffuse pulmonary interstitial fibrosis characterized by the presence of asbestos bodies and interstitial fibrosis in close proximity. The lung may be contracted and small. Alternatively, a honeycomb pattern in which large airspaces rimmed by fibrous walls indicate longstanding interstitial fibrosis can also occur. Both forms of fibrosis are frequently seen in the lower lobes.
Early lesions occur at the level of the respiratory bronchioles. Asbestos fibers are deposited at this site Þ macrophages and neutrophils are attracted to site Þ asbestos fibers ingested by macrophages. Macrophages also release oxidants and proteases that are injurious to the tissue and polypeptide growth factors that stimulate proliferation of mesenchymal cells.
Asbestos body – alveolar macrophages coat ingested fibers with protein and iron, forming the classical, beaded, asbestos body. They are non-injurious and only a small amount form. They appear as a golden brown, fusiform or beaded rod with a translucent center and consist of asbestos fibers coated with an iron-containing proteinaceous material. Majority of asbestos bodies are formed on amphiboles rather than crysotile fibers. Observance of asbestos bodies in lung tissue is diagnostic for asbestosis.
Asbestosis is a disease of long latency (>20 years) in persons with heavy exposure to asbestos. Fibrotic lesions extend from the respiratory bronchiole to involve a greater portion in length. Injurious fibers are > 5 microns.
Clinically, the patient will present with dyspnea and cough as well as crepitations, clubbing, and rhonchi. All lung volumes will be reduced.
Pleural lesions – major abnormalities include effusion, diffuse visceral pleural fibrosis, and pleural plaques. Malignant mesothelioma, a primary malignant tumor of the pleura is also strongly associated with asbestosis. Possible mechanisms involve small fibers reaching the periphery of the lung directly penetrate the visceral pleura and irritate serosal membranes.
- (1) Crysotile – most commercially important; wavy fiber subject to fragmentation and chemical degradation in lung.
- (2) Amphibole – shorter, more rigid fibers; highly correlated with malignant mesothelioma.
Ý asbestos in lung tissue, precursor for diffuse fibrosis.
Diffuse pleural fibrosis: lung encased by a ring of fibrous tissue involving the visceral pleura and adherent to the parietal pleura. Histologically dense, acellular fibrous tissue is seen. Asbestos fibers are increased in lung.
Pleural plaques: clinically innocuous; raised, firm, opaque, often symmetrical lesions which may be calcified. Histologically they are composed of sparsely cellular bands of collagen in a "basketweave pattern." Concentration of asbestos fibers in lung tissue is less in patients with pleural plaques than in those with asbestosis.
- Pleural effusions: may occur unilaterally, early event,