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It is generally accepted that to cause pulmonary disease, mineral fibers must be relatively long and thin but also able to remain in the lung for long periods. This "biopersistence" of fibers is limited by two main mechanisms of fiber clearance: removal by macrophages after phagocytosis and, for some fibers, by actual dissolution. The relative importance of these mechanisms has not been properly evaluated for any type of fiber and will certainly vary with mineral type. The efficiency of macrophage clearance is greatest with short fibers (&lt; 5 microns long) and is reduced as fibers get longer. Fibers &gt; 50 microns long cannot be cleared by macrophages and for some mineral types they may remain in the lung permanently. Others may fracture into shorter lengths, perhaps aided by chemical dissolution, and thus become susceptible to macrophage clearance. However, for a number of areas relating to fiber removal from the lung parenchyma detailed information is still needed: Do dusts differ in their ability to attract macrophages and stimulate these cells to phagocytosis? Following dust uptake what controls the movement of macrophages? Some may penetrate to the interstitium, some phagocytosing fibers in interstitial sites may migrate back to the alveolar space. Some move to the mucociliary escalator and some to the lymphatics. Some, most importantly, move to the pleura. Fibers are found and phagocytosed in the interstitium during the early stages of disease development, but with time many fibers appear isolated in areas of fibrous tissue. Are such fibers subsequently ignored or can they reenter the disease process after years of isolation? Finally, can phagocytosis by macrophages effect dissolution of fibers?(ABSTRACT TRUNCATED AT 250 WORDS)

The role of clearance and dissolution in determining the durability or biopersistence of mineral fibers.