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Pneumoconiosis refers to any nonmalignant chronic lung disease resulting from inhalation and deposition of mineral, metallic, or dust particles in the pulmonary interstitium. The most common agents responsible for pneumoconioses are asbestos, silica, and coal. The effect of these agents is dependent on the intensity and duration of exposure as well as their clearance after deposition in the lung parenchyma.

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Essentials of Diagnosis

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  • • A careful occupational and environmental history of past inhalational exposures.
  • • Evidence of pleural disease and/or interstitial lung disease (especially bilateral reticular infiltrates).

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General Considerations

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Asbestos is a group of naturally occurring fibrous magnesium silicates that are ubiquitous throughout the world. There are six types of asbestos; one is serpentine (chrysotile) and five are fibrous amphiboles (amosite, crocidolite, anthophyllite, tremolite, and actinolite). Most disease results from direct or indirect exposure to asbestos-containing materials during mining, milling, manufacturing, installation, or removal of asbestos-containing products. Increased risk among workers is not generally observed until at least 20 years following initial exposure. However, patients with particularly high levels of exposure may develop clinically evident disease within 10 years. The three major categories of asbestos-related disease are asbestosis, asbestos-induced pleural disease, and cancer. Asbestosis is parenchymal lung fibrosis that results from asbestos exposure. As with coal workers’ pneumoconiosis and silicosis, the degree of fibrosis is related to the amount and duration of exposure.

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Pathogenesis

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Typical asbestos fibers found in the lungs are 20–50 μm in length. They deposit initially at bifurcations of conducting airways and in alveoli. Fibers greater than 3 μm in diameter generally do not penetrate the distal lung, but those with diameters less than 3 μm readily translocate into the interstitium and pleural space. Fibers greater than 5 μm in length tend to be incompletely phagocytosed and are retained in tissues where they initiate and sustain cellular and molecular events that result in fibrogenesis. Asbestos triggers a chronic inflammatory process promoted by oxidative injury and profibrotic growth factors and cytokines. The principal determinants of the rate of disease progression are cumulative dose, fiber type, and individual susceptibility.

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Prevention

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The most significant preventive intervention in patients with asbestosis is smoking cessation. Cigarette smoking in asbestos workers increases the prevalence of radiographic pleuroparenchymal changes and markedly increases the incidence of lung carcinoma.

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Additional preventive measures include limiting exposure to asbestos. The Occupational Safety and Health Administration (OSHA) has developed regulations to control exposure in the workplace. Similar regulations have also been developed by the Mine Safety and Health Administration (MSHA) regarding exposure of miners. These regulations require use of approved protective equipment, such as respirators, and recommended work practices and safety procedures to limit exposure. Respiratory protection requires that workers be issued the proper size and type of mask, based on respirator fit testing procedures, and that they be trained to recognize the hazards of ...

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