Asbestosis 

Pneumoconiosis is the general term for lung disease caused by inhalation and deposition of mineral dust.

Pneumoconiosis caused by asbestos inhalation is called asbestosis. The word asbestos is derived from Greek and means inextinguishable, and asbestos is a group of naturally occurring, heat-resistant fibrous silicates. Asbestos fibers are long and thin (length-to-diameter ratio >3) and may be either curved or straight. The curved fibers are called serpentine (chrysotile is the prime example), and the straight fibers are amphiboles. Several different types of amphiboles (ie, amosite, anthophyllite, tremolite, actinolite, crocidolite) have been recognized. Chrysotile is by far the most common type of asbestos fiber produced in the world and accounts for virtually all asbestos used commercially in the United States.

Production and use of asbestos increased greatly between 1877 and 1967. In the 1930s and 1940s, scientists recognized a causal link between asbestos exposure and asbestosis. In the 1950s and 1960s, researchers established asbestos as a predisposing factor for bronchogenic carcinoma and malignant mesothelioma.

Also see Asbestos-Related Disease and Asbestosis for a radiological focus. Note the image below.

The cumulative dose of fibers inhaled over a period of time and the type, durability, and dimensions of the fiber influence carcinogenicity and fibrogenicity. The incidence of asbestosis varies with the cumulative dose of inhaled fibers; the greater the cumulative dose, the higher the incidence of asbestosis. All types of asbestos fibers are fibrogenic to the lungs. Amphiboles, particularly crocidolite fibers, are markedly more carcinogenic to the pleura. Fibers with diameters smaller than 3 micrometers are fibrogenic because they penetrate cell membranes. Long fibers (ie, >5 micrometers) are incompletely phagocytosed and stay in the lungs, setting up cycles of cellular events and the release of cytokines.

The initial inflammation occurs in the alveolar bifurcations and is characterized by the influx of alveolar macrophages. Asbestos-activated macrophages produce a variety of growth factors, including fibronectin, platelet-derived growth factor, insulinlike growth factor, and fibroblast growth factor, which interact to induce fibroblast proliferation. Oxygen free radicals (eg, superoxide anion, hydrogen peroxide, hydroxy radicals) that are released by the macrophages damage proteins and lipid membranes and sustain the inflammatory process. A plasminogen activator, which is also released by macrophages, further damages the interstitium of the lung by degrading matrix glycoproteins.

Individuals probably differ in their susceptibility to asbestosis based on respiratory clearance and other unidentified host factors. People who smoke have an increased rate of asbestosis progression, likely due to impaired mucociliary clearance of asbestos fibers.^[1]

Frequency

United States

Asbestos consumption (per capita) peaked in 1951, declined gradually until 1971, and declined rapidly thereafter.

No reliable information exists regarding the number of people presently at risk in the United States and in other countries. Since the early 1940s, as many as 10 million workers in the United States may have been exposed to asbestos. In 1972, reports estimated that 250,000 persons were at risk. By the 1980s, the number of active asbestos miners and millers had fallen to a few hundred. Strict regulation (eg, prohibition of asbestos sprays in buildings, controls in the level of asbestos fibers in the air) has drastically reduced the risk of developing asbestosis. However, those who have been previously exposed continue to be at risk for asbestosis and other asbestos-related diseases.^[2]

International

Trends in usage of asbestos and observational studies suggest that asbestosis and other asbestos-related diseases are likely to be continuing problems in developing countries.

Mortality/Morbidity

Study of mortality trends in the United States show that while deaths from other pneumoconioses are declining, deaths from asbestosis are increasing. Further, they are not expected to decrease in the next 15 years. One model predicts 29,667 deaths from 2005 to 2027.^[3]

Estimated annual years of potential life lost before age 65 years attributable to asbestosis totaled 7267 in the years 2001-2005 and represented a significant increase from 1968-1972.^[4]

People who smoke are likely to develop chronic bronchitis and obstructive airway disease and are prone to respiratory tract infections. People who smoke are at high risk for the development of bronchogenic carcinoma because asbestos and tobacco smoke are synergistic in carcinogenicity. Individuals who both smoke and are exposed to asbestos are several times more susceptible to developing lung carcinoma than individuals who have neither exposure.^[5]

Some studies show that asbestos exposure alone, without a smoking history, increases the risk of lung carcinoma 6-fold. Asbestos exposure increases the risk of developing malignant mesothelioma and cancers of upper respiratory tract, esophagus, kidney, and biliary system. Asbestosis may coexist with other asbestos-related diseases, including calcified and noncalcified pleural plaques, pleural thickening, benign exudative pleural effusion, rounded atelectasis, and malignant mesothelioma of the pleura.

Ameille et al found no causal relationship between airway obstruction and asbestos exposure. Their study evaluated lung function in persons (n=3660) with previous occupational exposure to asbestos.^[6] No significant correlation was shown between pulmonary function parameters and cumulative asbestos exposure.