Epidemiology

The first well-documented cases of asbestosis were reported in the early 1900s among asbestos textile workers. Through the 1920s and 1930s, reports emerged of asbestosis, pleural thickening, pleural calcification, and right ventricular failure in asbestos-exposed workers. Radiographic studies that began in the 1930s documented an asbestosis prevalence of 25% to 55% in these workers, especially among those with greater cumulative exposure. Early evidence from these studies suggested that exposure to higher concentrations of asbestos over longer periods of time resulted in increased risk for development of pulmonary fibrosis.

Asbestos use increased extensively in the early 1940s, and this mineral substance was used widely in the United States for the next 30 years. Asbestos use began to diminish when the Occupational Safety and Health Administration (OSHA) regulated workplace asbestos exposure in 1972. It is estimated that between 1940 and 1979, more than 27 million people had potential exposure in the United States alone. Data from a study of sheet metal workers examined between 1986 and 2004, reported by Welch and colleagues, found that asbestosis is continuing to occur even 50 years after first exposure. The study also found that the strongest predictor of nonmalignant asbestos-related disease in the workers was the cutoff year in which employment commenced: Prevalence was lowest among those who began working in the sheet metal industry after 1970 and highest among those who began work before 1949. With thousands of commercial applications and the mineral’s resistance to degradation, asbestos remains ubiquitous. Efforts have been made to limit ongoing exposure through abatement programs of asbestos removal from buildings and/or on-site encapsulation. Nevertheless, asbestos-related disability and mortality will continue well into the next decade.

Although the use of asbestos has been curtailed in many developed nations, in less-developed countries this inexpensive but hazardous material continues to be used widely. Many developed countries are now fast replacing the developed ones in the production and use of asbestos. Currently, Russia is the leading producer of asbestos worldwide, followed by China, Brazil, Kazakhstan, and Canada. More than 85% of the world production of asbestos is used to manufacture products in Asia and Eastern Europe. Although asbestos usage in developing countries is increasing, information about asbestos-related disease remains largely obscure. Epidemiologic questions have not been systematically researched.

In keeping with the long latency required before asbestosis becomes clinically apparent, all past and current asbestos workers must be considered to be at risk for development of this fibrosing lung disorder.

Etiology and Risk Factors

The minerals referred to herein as “asbestos” are a family of naturally occurring, flexible, fibrous hydrous silicates found in soil worldwide. Mined asbestos fibers are categorized as either long and curly (serpentine) or straight and rodlike (amphibole). The serpentine fiber, chrysotile, accounts for most of the commercially used asbestos, favored for its properties of heat resistance, flexibility, and ease of spinning for textiles. Five categories of amphiboles are recognized: crocidolite, amosite, anthophyllite, tremolite, and actinolite. These more rigid fibers are less commonly used but are still pathogenic. All major commercial forms have been associated with development of nonmalignant respiratory disorders and of lung cancer and mesothelioma, as discussed in Chapters 47, 65, and 70.

Asbestosis is the result of either direct or “bystander” exposure to asbestos-containing materials. Major sources of exposure are summarized in Table 52-2. During the first half of the 20th century, high-level exposures to asbestos dust occurred in the manufacturing of asbestos textiles and construction materials and in the construction and ship-building trades. Potential exposures still occur in the construction trades and in the process of asbestos abatement. Although the use of asbestos has been curtailed in many developed nations since the 1970s, in less developed countries this inexpensive but hazardous material continues to be used widely. High cumulative, occupational exposures in these settings are still commonplace.

Table 52-2 Major Asbestos Uses and Sources of Exposure

Environmental exposure to asbestiform fibers also is well described as the cause of nonmalignant and malignant asbestos-related lung disease in countries including Turkey, Greece, Japan, and China and the territory of New Caledonia. Exposure in these settings usually occurs when villagers in rural areas disturb natural soil deposits while working in fields or when applying whitewash prepared from these outcrops to their dwellings. In the United States, asbestos-related lung disease caused by nonoccupational exposures is a recently recognized problem, mostly in current and former residents of Libby, Montana. Amphibole asbestos–contaminated vermiculite was mined, milled, and processed near this small town for many years. Personal and commercial use of the contaminated mineral was widespread among residents. During a health screening in 2000 to 2001, nearly 18% of 6668 participants were noted to have pleural thickening on chest radiographs. Less than 1% had findings compatible with asbestosis.

A clear dose-response relationship between asbestos exposure and asbestosis has been recognized, although controversy remains concerning risks at low-level exposure. Risk for asbestosis varies widely among industries, with more disease seen in textile and construction workers than with those in mining. Development of the disease is associated with factors such as respirability of the fiber type, the cumulative dose of exposure, the capacity of the lung to clear the fibers, and the biopersistence of the asbestos. In general, the relative risk for development of asbestosis for asbestos workers increases in proportion to the asbestos exposure levels in the workplace. More severe disease has been associated with higher retention of asbestos fiber in the lungs. Typical asbestos fibers found in the lungs are 20 to 50 µm long and initially are deposited at the bifurcations of conducting airways. Thin fibers, of diameters less than 3 µm, translocate readily into the alveolar space, interstitium, and pleural space. Thicker fibers tend to be incompletely phagocytosed by alveolar macrophages and are retained in the lung, where they can trigger the inflammatory events that lead to fibrosis, as discussed next.

Histopathology and grading

Asbestosis is defined histopathologically as bilateral, diffuse interstitial fibrosis of the lungs caused by the inhalation of asbestos fibers (Figure 52-1). Gray streaks of fibrosis can be seen in the parenchyma along interlobar and interlobular septa. Later, the pleural surface becomes more nodular in appearance, and the parenchyma loses volume and elasticity and forms more fibrotic scars and honeycombing. The gross pathologic changes are most obvious in the lower lung zones bilaterally, with the worst disease nearest to the pleura.

Figure 52-1 Histopathologic features of asbestosis. Disease severity is classified according to a modified grading scheme from the College of American Pathologists, as described in the text. A, In this grade 1 lesion, fibrosis is limited to the peribronchiolar tissue and the walls of the respiratory bronchioles. B, Enlargement of a grade 1 lesion illustrates presence of asbestos bodies. C, In this grade 3 lesion, fibrosis extends into the interstitial space between the respiratory units and into the alveolar ducts. (A to C, Hematoxylin and eosin stain.)

(Courtesy Dr. Val Vallythan, National Institute for Occupational Safety and Health, Morgantown, West Virginia.)

The College of American Pathologists and Pulmonary Pathology Society has modified a 12-point grading scheme that has been shown to be consistently reproducible. The modified grading scheme, based on histologic criteria presented in the 2010 update on the original diagnostic criteria, consists of the following categories of disease severity:

Grade 0—no appreciable peribronchiolar fibrosis, or fibrosis confined to the bronchiolar walls

Grade 1

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