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  • Pneumoconioses refer to a family of respiratory diseases caused by chronic inhalation of organic or inorganic dust particles.
  • A wide variety of organic and inorganic dusts can result in pneumoconiosis and exposure is often associated with an occupational activity. For example, long-term inhalation of coal dust can result in a pneumoconiosis and is observed most frequently in coal miners. Alternatively, long-term inhalation of silica dust can result in a pneumoconiosis and is observed most frequently in workers in the mining, sand-blasting, or stone cutting industries. A comprehensive list of the different subtypes of pneumoconioses is beyond the scope of this work; rather, we focus on a few prototypical examples caused by inorganic dusts. It should be pointed out that, pneumoconioses caused by inhalation of organic dusts may also result in a component of hypersensitivity pneumonitis.
  • Despite their diverse etiological sources, pneumoconioses are thought to share a common pathogenic sequence although unique features of disease development exist for each type of dust. These unique features likely depend on the physical characteristics of the dust, such as its size and shape, as well as its chemical identity and whether it can dysregulate biological processes
  • In general, most inhaled dust are trapped within the mucous lining of the conducting airways and are slowly moved out of the lung by the mucociliary elevator.
  • However, dusts that cause pneumoconioses are typically small enough to reach the alveoli but large enough not to cross the alveolar membrane. These dusts deposit within the alveoli and are thus engulfed by alveolar macrophages. Some dust-laden alveolar macrophages will travel up local lymphatics while others move onto the mucociliary elevator and are thus out of the lung. However, when exposure to dust is large, frequent, and chronic, dust-laden alveolar macrophages remain within the pulmonary interstitium. On its own, this is rarely a problem; however, certain dusts are biologically active and can induce the alveolar macrophage to initiate an inflammatory response. Because these dust-laden macrophages remain within the lung, they generate a chronically-activated inflammatory milieu that can yield progressive fibrosis of the lung and thus development of restrictive lung disease.