Document wgazMab7NL1RaOqjnvVa7v75E

640 EXPERIMENTAL ASBESTOS18--GROSS A DE TREV1LLE chiole was found in the lungs of guinea pigs disappearance of chryaotite dust from the that had been exposed for three months to lesion, either by dissolution at by transport, an atmosphere containing 20 mg/cu m of is not a sine qua non of healing; but that chrysolite dust. Similar to the appearanoe of healing, at least in the rat, does take place-- such lesions in hamsters, the mural thicken even in the presence of this dust One would ing consisted of proliferated alveolar cells like to think of the formation of the asbestos and their supporting stroma of interconnect body as a protective mechanism by which ing argyrophilic fibers. The lung sections of the asbestos fiber becomes sequestrated and guinea pigs that had inhaled high concentra the tissues safeguarded from further irritant tions (66 mg/cu m) of chrysotile dust for action by the fiber. To what extent this two weeks or longer, manifested similar mechanism may apply is not known; but it minimal mural asbestotic thickening in the does seem that in rats, in which asbestos proximal portion of the raoemus. However, bodies are not demonstrable (with the opti the number of units (raoemi) involved was cal microscope),c healing occurs in the pres much greater than that in the animals ex ence of apparently naked fibers. posed to the lower dust concentration for The diminution, in time, of the amount three months. No evidenoe of healing (sig of dust demonstrable in the tissue and its nificant reduction in oellularity of the lesion apparent disappearance in some of the scars, and collagenization of the stroma) was seen poses an interesting question in regard to in animals examined up to seven months aft the mechanism by which the asbestos fibers er the beginning of the exposure. Following disappear. It is commonly believed that microincineration and treatment with acid, chrysotile fibers have a relatively high solu the amount of ash seen in the guinea pig bility in tissue fluid. This would eeem to ac lung sections was comparable to that noted count for the inability to demonstrate asbes in rats that had inhaled chrysotile dust. As tos fibers in some of the asbestos bodies bestos bodies found in the lung sections found in human asbestotic lungs. However, were few and very small. dissolution of the fibers, particularly of the coarser ones, would require a long time--eo Comment that it would be difficult to explain the fail ure of peripheral alveoli to beoome involved A chronic pulmonary inflammation may be termed progressive if it extends from its original 6ite into adjoining, previously nor mal air spaces, and if it remains active, re taining its argyrophilic precollagenous stro ma and high oellularity. Such a pulmonary inflammation may be considered healed if its argyrophilic stroma has been completely collagenized white its oellularity has become considerably reduced. In the rat that has inhaled high concen trations of chrysotile asbestos fibers for only by inflammation. Furthermore, high solubil ity would not be consistent with the sharp inflammatory localization of the asbestotic lesion in the proximal portion of the racemus in rats. It is much more reasonable to explain this sharp localization of the in flammation on a fairly prompt removal of the inhaled or injected irritant dust from the peripheral alveoli and the subsequent stag nation of the dust in the proximal portions of the raoemus.7 The transport of the chrys otile dust from the peripheral alveoli is ef a few months or has been injected intra- fected by the alveolar clearance mechanism tracheally with this dust, the asbestotic in consisting of a proximally moving film of flammation remains sharply limited to the alveolar fluid.* This transport is dramatical proximal portion of the raoemus and heals 1 ly illustrated by the increase in, and concen by becoming transformed into a hypooellu- tration of dust in the lumen of the alveolar lar collagenous scar. Thus, it would appear duct within 72 hours after the intratracheal proper to classify asbestosis caused by chrys injection of chrysotile dust (cf Fig I and otile dust as nonprogressive in the rat. 2). It may be of interest at this point to It is of basic interest that appreciable note that the localization of the early asbes amounts of asbestos fibers are demonstrable totic lesion to the proximal portion of the within the scars of healed or healing raoemus was first described by Vorwald et inflammation. This would suggest that the al,e and reoently confirmed by Holt et al.' Arch Environ Health--Vol IS, Nov 1967 8005 1466 PRODUCED BY FORD