Asbestos is a family of naturally occurring silicates whose heat-resistant and structural properties made it useful for inclusion in construction and shipbuilding materials, automobile brakes, and some textiles. Chrysotile (a serpentine fiber), crocidolite, and amosite (amphibole, or straight fibers) are the 3 main types of asbestos that cause disease.
Asbestosis is a much more common consequence of asbestos exposure than cancer (eg, mesothelioma).
Many workers are at risk of exposure to asbestos, particularly shipbuilders, textile and construction workers, home remodelers, workers who do asbestos abatement, and miners who are exposed to asbestos fibers. Secondhand exposure may occur among family members of exposed workers and among people who live close to mines.
Specific occupations at highest risk of exposure include welders, auto mechanics, tile setters, boilermakers, U.S. Navy personnel, shipyard workers, merchant marines, sheet metal workers, bricklayers, building inspectors, carpenters, roofers, plumbers, plasterers, refinery workers, pipefitters, painters, demolition workers, drywall workers, electricians, floor covering workers, furnace workers, glaziers, millwrights, insulators, ironworkers, laborers, Libby vermiculite exfoliation plant workers, longshoremen, maintenance workers.
Alveolar macrophages attempting to engulf inhaled fibers release cytokines and growth factors that stimulate inflammation, oxidative injury, collagen deposition, and ultimately fibrosis. Asbestos fibers may also be directly toxic to lung tissue. Risk of disease is generally related to the duration and intensity of exposure and the type, length, and thickness of inhaled fibers. Recent advances suggest there may be a common genetic predisposition between asbestosis and other fibrosing lung diseases, specifically idiopathic pulmonary fibrosis (1).
1. Platenburg MGJP, Wiertz IA, van der Vis JJ, et al: The MUC5B promoter risk allele for idiopathic pulmonary fibrosis predisposes to asbestosis. Eur Respir J Jan 16, 2020. pii: 1902361. doi: 10.1183/13993003.02361-2019 [Epub ahead of print]
Asbestosis is initially asymptomatic but can cause progressive dyspnea, nonproductive cough, and fatigue. The disorder progresses in > 10% of patients even after cessation of exposure. Advanced asbestosis may cause clubbing, dry bibasilar crackles, and, in severe cases, symptoms and signs of right ventricular failure (cor pulmonale).
Diagnosis of asbestosis is based on history of exposure to asbestos and chest x-ray or high-resolution CT and only rarely requires lung biopsy for confirmation. Chest x-ray shows linear reticular opacities signifying fibrosis, usually in the peripheral lower lobes. Opacities are often bilateral and are often accompanied by pleural changes—pleural plaques are virtually pathognomonic of a previous exposure to asbestos. Honeycombing signifies more advanced disease, which may involve the mid and lower lung fields. As with silicosis, severity is graded on the International Labor Organization scale (International Classification of Radiographs of Pneumoconioses) based on size, shape, location, and profusion of opacities. In contrast to silicosis, asbestosis produces reticular opacities with a lower lobe predominance. Hilar and mediastinal adenopathy and nodular opacities are uncharacteristic and suggest a different diagnosis. Chest x-ray is insensitive; high-resolution (thin-section) chest CT is useful when asbestosis is a likely diagnosis. CT is also superior to chest x-ray in identifying pleural abnormalities.
Pulmonary function tests, which may show reduced lung volumes and diffusing capacity for carbon monoxide (DLCO), are nonspecific but help characterize changes in lung function over time. Pulse oximetry done at rest and during exertion is nonspecific but sensitive for detecting asbestos-induced impairment.
Bronchoalveolar lavage or lung biopsy is indicated only when noninvasive measures fail to provide conclusive diagnosis; demonstration of asbestos fibers indicates asbestosis in patients with pulmonary fibrosis, although such fibers can occasionally be found in lungs of exposed people without disease and may not be present in specimens from patients with asbestosis. Thus, demonstration of asbestos fibers may be helpful but is not necessary for diagnosis.
Lung cancer (usually non–small cell lung carcinoma) develops in patients with asbestosis at 8 to 10 times the rate of those without asbestosis and is especially common among workers exposed to amphibole fibers, although all forms of inhaled asbestos have been associated with an elevated cancer risk. Asbestos and smoking have a synergistic effect on lung cancer risk.
No specific treatment exists. Early detection of hypoxemia and right ventricular failure leads to use of supplemental oxygen and treatment of heart failure. Pulmonary rehabilitation can be helpful for patients with impairment.
Preventive measures include eliminating exposure, asbestos abatement in occupational and nonoccupational settings, smoking cessation, and vaccination with pneumococcal vaccine and influenza vaccine. Smoking cessation is particularly important in light of the multiplicative risk of lung cancer in patients who have both tobacco smoke and asbestos exposures. Annual lung cancer screening should be considered for patients 55 to 80 yr with a history of asbestos exposure and a smoking history of ≥ 30 pack-years who are currently smoking or have quit within the past 15 years.