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648 EXPERIMENTAL ASBESTOS18--GROSS A 1>E TREV1LLE rat or of the hamatpr unit whether tissue exposed to the different dust concentrations reactivity of the rat or of the hamster more is too small, and the time allowed for matu closely resemble that of mnn. ration of the lesion too short to permit A study of the ash-pattern (microindn- definitive conclusions. eration) of a number of lungG from asbestos The results of this investigation also have workers (exclusive of cases of ailiooasbcsto- given some insight into the relative patho sis) has disclosed no instance in which the genicity of chrysotile asbestos dust far rats amount of mineral dust in the lung sections insofar as a single intratracheal injection of has been more than scanty.12-1* Other in 8.5 mg of this dust has produced minimal vestigators have found upon chemical analy asbestotic lesions in rats. This result may be sis that the silicate content of manifestly as- compared with that of King, et al1* who bestotic lungs was surprisingly low.14-1* found that a quantity of more than 2 mg and These observations approximate the findings lees than 5 mg of quartz dust injected intra- in the rat. Another similarity of human tracheally into rats was the smallest amount chrysotile asbestosis to findings in asbestotic of ailica capable of producing demonstrable rat lungs is the complete oollagenization silicosis in this animal. Thus, it seems that with associated aoellidarity that may be for the rat, chrysotile has about the same or found in "burned-out" cases of human as der of pathogenicity as quartz du6t. bestosis.18 Nevertheless, in 6pite of the simi For the hamster, the smallest amount of larity of the oollagenization in man and intratracheal!)- injected chrysotile dust ca rat, there is an important and significant pable of producing minimal lesions has not difference. The early disease in rats is multi been determined. This dose will apparently focal, affecting the proximal portion of the be smaller than that found for rats. raoemus; whereas in man such multifocal By the inhalation technique, using a very distribution has not been described--only high concentration of respirable cluysotile diffuse involvement. A possible explanation dust (86 mg/cu m), the exposure time re of the diffuseness of asbestotic involvement quired to produoe minimal asbestosis in rats in human lungs could be that the inflamma and guinea pigs seems to be somewhere be tion, initially confined to the proximal por tween 60 and 120 hours. tion of the racemus because of continued The hyperplasia of smooth muscle ob exposure, spreads peripherally, thereby be served in the asbestotic rats is very similar coming confluent with that of neighboring to such hyperplasia observed in human as raoemi. The fact that an asbestotic inflam bestosis cases studied in this laboratory and mation may "burn out" in man, does not is also similar to that found in bronchiolar rule out the possibility that this inflamma emphysema of the lung.11 Although the ex tion remained active and progressive for same years alter exposure had ceased before finally attaining the terminal healed stage. There is, unfortunately, no information on the activity of the asbestotic inflammatory act origin of the muscle was not determined, its location made it appear most likely that it was derived from the circular muscle in the alveolar ducts that regulate the openings of the evaginating alveoli. process in human lungs at various intervals following removal from further exposure to Summary and Conclusions the specific dust. Rats, hamsters, and guinea pigs were giv In guinea pigs, the results of the inhala en various lung dust burdens of chrysotile tion of chrysotile dust are very similar to asbestos; some, by inhalation and others, by those observed in rets with respect to the intratracheal injection. An attempt was site and extent of the lesion, but conversion made to determine the smallest amount of of argyrophilic stroma to collagen is not en chryBotile dust that would produce a recog countered in the sections of guinea pigs that nizable minimal asbestotic lesion. The time had been killed up to seven months after the lapse between the imposition of the lung initiation of the dust exposure. The amount dust burden and the death of the animal of dust found in the lung sections is scanty varied from zero to 24 months. and is limited to the proximal portion of the The following conclusions have been racemus. However, the number of animals reached: Arch Environ Health--Vol IS. Nov 1967 8005 1468 PRODUCED BY FORD