Document MJZzQNZ64eo3Mbk8woOwVgyrM

recruitment meets ASBrSTOS-RM .VTKD Ll'NC DUKASES H)5 /or particles. Short e readily and com- wang fibers are not, h->n gne macrox i (Allison. 7, l particles by these be more than 98 deposited panicles in the case of other fibrogenic dusts, such as sil ica. This difference in clearance attributed to the greater cytotoxic effect of silica, which lends, therefore, to maintain an extracellular position (50). may explain why hilar node enlargement is a more consistent finding in association with silica exposure than in association with asbestos exposure (52). standing of the factors underlying the pathogen esis of mesothelioma. Coated Asbestos Fibers (Asbestos Bodies) The coated asbestos fiber was recognized early in the 1900s, because of its characteristic ap pearance under light microscopy (55). It is usu ally a rod-shaped structure with clubbed ends, Less is known about the penetration of in often bended along its length, is yellow to 1istribution,and Asbestos Particles ung gested fibers through the wall of the gastro intestinal tract, although animal studies suggest that this does not occur (53), except in the face of a heavy load delivered directly into the brown in color, ranges in length from 10 to 30 jun and in thickness front 1 to 6 pm, and has a central, paler core. The coating, consisting of ferritin granules and an amorphous ma ascopy has revealed stomach (40). What relevance this has to human terial, probably protein, varies in thickness from submicroscopic. un disease, such as peritoneal mesothelioma, re very thin to 5 run (55-57). fibrils in the lung , mains to be determined. On the basis of animal studies, coating is now -rker, far more than ' Once it has penetrated the lung, the dust believed to be an intracellular process and fol ; lung fiber popula- appears to remain fixed, but may be remobilued, lows the engulfing of panicles by macrophages microscopy alone apparently even from dust macules or scars, the to which they adhere (56). Several macrophages that the pro- operative mechanism perhaps being episodes of may fuse to engulf large fibers. It is while the ed fibers (i.e., those pulmonary edema and/or infection (48). It is fibers are surrounded by partially fused ma bestos body) is very believed that such remobilization of dust may crophages that coating begins (58). The fiber cent (49), an obser- j result in its excretion, a phenomenon that then becomes incorporated into imracyto- igh penetration and might explain the rare event of apparent re plasmic vacuoles, and the first coating material licroscopic particles j gression of radiologic changes in the worker appears lo be some form of acid mucopolysac environment. Alter- i removed from exposure (Manfretla, Y.: Unpub charide (56). Iron in die form of hemosiderin s and/or particles lished data). Alternatively, it may become re- then accumulates in the cytoplasm of the ma ulown products of | setptesiered and contribute to the extension of crophage. Iron micelles, possibly derived from bers that had pene- disease in the face of no further exposure. breakdown of hemoglobin, become subsequent the lung. A second | iJespite the fact that pleural reactions (effu ly incorporated into the phagosomes, and tend of the amount of as- sion, fibrosis, and/or calcification and neo to concentrate around the fiber; eventually, the difficulty plasm) are common manifestations of asbestos there is clearing of ground substance (57). It is m lungs at nuother pneumoconioschmidt, 5, p. 64). exposure, there is little direct evidence as to of interest that the process appears to be a pro i how the asbestos gains access to the pleura, which gressive one, with the coating increasing with presumably must happen to explain the pleural lime and uncoated fibers becoming coated < applies more to J reactions. Asbestos bodies are rarely seen in the months or years alter instillation (56); how ers, presumably be- , visceral pleura and have never been reported in ever, because the proportion of uncoated to ity (magnesium, in plaques located in the parietal pleura of ex coated fibers in human lungs appears lo remain ted out) and, hence, posed persons, even though they may be readily constant with time (49, 59), there must also be wn chemically and j found in the interstitial tissue of the same lung a parallel process of aging and dissolution of sidence (51). I (54). By contrast, asbestos fragments have been the coated fiber. There is some evidence that the ppears to be a ten- found in mesotheliomas even without evi coating of a fiber renders it nonfibrogenic. Why ilate in the periph- dence of asbestosis or coated fibers in the lung some particles become coated and others do >nes as indicated by | (Hourihane, 5, p. 647). This has led to the not is not understood; however, sire may be ibrotic reactions in suggestion that fibers that become coated in the important, with the typical asbestos body devel l lias been attributed lung are less mobile and less susceptible to oping only on large particles (greater than 5 ns (Thomson, 9, p. ! lymphatic clearance than uncoated fibers. Thus, pm) that cannot be completely engulfed by one hat have penetrated :ly to remain where ey arc intracellular, via lymph channels todes, where coated e seen (Hourihane, pears to be less than | electron microscopic studies may reveal many more uncoated fibers in the pleura than antici pated front the scarcity of coated fibers. Alter natively, any fibers that are cleared to subpleur.il lymphatics may undergo dissolution more readily here than elsewhere in the lung. In any event, information that would sited light on this paradox might well lead to improved under macrophage (58). It must also be emphasized that not all coated fibers seen in the Jung have an asbestos core, and the process of coating is apparently used by the lung in response to a variety of other fibers encountered in the environment. These include glass and cotton fibers, diatomaceous earth, talc, graphite, and carborundum particles (10, 55).