Document nmvQgqKR9Jper8xjZ6ExXDb26

E.KKtTTJVE ()fK!CK Johns -Maxvii.le Corporation twentv-t^'o east FOiiriETii street N i;w YORK. X Y Dece er 14, 193S UHABCO document OU> At. L. J. Silverman Secretary-Treasurer Union Asbestos 4 Rubber Company 10 South Michigan Avenue hicago, Illinois Re: Dr. Gardner Asbestos Hast Experiments Dear Lew: I am enclosing he re wit:' a copy of a further progress report from Dr. Gardner, dated December 9, 1938. With kindest regards, I am Sincerely yours, Enclosure VB: k C^7 vanaiver Brown, General Attorney 01 056 0218 !ir. C. hosier December 19, 1938 !.!r. R. J. Cryor DOCUMENT .ittachec hereto please find the report and correspondence which you recently 'landed ne rofarrin^* to the asbssncs duni experiment heinr oonduoted by Dr. Gardner at Garunac Lolco. in the present report I find most of the information la farther in confirmation of previous reeult3 C3 reported in :*pril of this year. hen this axrarimontol -or!: started In march of 1C37, Tr. Gardner outlined tha objectives ns bain? two-fold: 1. To observe b** x-rerr examination any tendency towards devoi jpmant of fibrosis in the luii.mj of experimental animals subjoctod tc high concentrations of asoostos dust over prolonged time i:rt arvols. f. To determine if pcsaiblo another the irritation that develo's iron nsuos.oe Gust in the lur.r tissues is a reeu.lt of chemical affects, cr mechanical action* To date the xc suits seon to point definitely to mechanical action as being the cause of fibrosis* This means s imply that the shape and size of the part idea that accumulate in the lunrs arrears to be of more importance as o source of Irritation than the chemioal composition of the particloa. Dr* Gardner has fourn^ contrary to what, was expeoted, that the finer particles oauee less irritation than the coarser particles. Animals exposed to high concentrations of very fine dust for twenty months have not developed fibrosis of lung tissues, whereas In previous experiments with coarser part id C3 of asbestos dust, fibrosis developed in IP months exposure. This appears to be an important point and something heretofore not known. most of the experimental results seen to indicate that asbestos dust la probably loss likely to prouuoe fibrosis of the lunrs than other forms of silica or silloate dust. There is some ovidence to show that crysotile fiber may be more harmful than other varieties of asbeetos that have boon tested Including Anosite. uhla la not conclusive at this time however. iO further oheoh the nechanloal theory as the souroe of Irritation Injections of ooarse dust are being made . 01 056 0219 Progress Report on Asbestos Experiments December 9, 1938 In reply to your letter of the 6th, I may say that any progress report of experiments on asbestos dust will necessarily be extremely brief. In the original experiment, undertaken with the grant from the asbestos industry, animals have now been exposed to the very finely ground asbestos fiber for a period of 20 months. Concentrations of atmospheric dust ranging from 125 to 160 million particles per cubic foot of air have been maintained in the dusting room. Animals killed at intervals throughout this period have failed to exhibit any gross evidence of fibrosis. Minute asbestosis bodies have been observed since the second month but cellular reaction is still limited to widely scattered microscopic foci of early fibrous tissue. This is at variance with the experience in a previous experiment where concentrations of only 39.5 to 55.6 million particles per cu.ft. of air had already produced gross evidence of fibrosis in the lungs after 15 months exposure. As previously reported, the assumption that grinding asbestos fiber to an extremely fine state of subdivision would accelerate the development of reaction in the tissues has not been justified. On the contrary such treatment seems to have had the opposite effect and almost destroyed their capacity to irritate the lungs. This has led to the hypothesis that the 01 056 0220 'VsEr'.T irritation iron asbestos dust is not of chemical but is more probably of a mechanical nature. Several collateral observations appear to support this view. In a series of intravenous injection experiments with four different varieties of asbestos, ground so that none of the particles exceeded 3yi in diameter, one gram doses failed to produce fibrous changes in any organ of the body after one years time. Since free silica introduced in tnis manner in variably does cause fibrosis of a characteristic nature and since such reaction is inversely proportional to the size of the injected particles, it seems logical to infer that the re action to asbestos is of a different nature. Chrysotile asbestos continues to give trouble, we have never been able to inject the full dose nor to xeep an animal alive for more than 7 days thereafter. Either the physical or the chemical properties of this mineral render it unsuitable for injection into the veins. Three other forms, crocidolite, amosite and amphibole have produced no ill effects. The reaction to inhaled asbestos, unlike that to crystalline silica, is not a progressive one in experimental animals. In a previous experiment 3 months exposure followed by removal of the animals to a normal atmosphere for 2 or 3 years resulted in retrogression rather than progression of pul monary changes. The asbestos fibers were present in the lungs in very appreciable numbers and they became coated with the 01 056 0221 -3- UNARGO DOCUMENT material responsible for the formation of the asbestos body. They were still present at the ena of the observation period but no fibrosis haa appeared. Perhaps one might agree with Dr. Leary that the coating on the fibers is protective and that because of it they lose their capacity to irritate the tissues. These observations continue to suggest a mechanical form of irritation which is manifested only in the lungs because only this organ moves enough in normal function to be so irritated. Ve are attempting to Chech these hypotheses by a new inhalation experiment with long-fibered crysotile. Another dust room has been assigned to asbestos and a suitable apparatus has been perfected for breaking up this material and generating a dust containing a high percentage of fibers. Concentrations of 120 million per cubic foot of air are being maintained in the dust room. A group of 100 guinea pigs, 20 rats, 20 mice and 6 cats have now been exposed a little over one month. The time of course is much too short to anticipate results of any hind. We are also making further checks by injecting short and long fibered asbestos directly into both lungs of a group of animals. To ascertain the influence of active motility on the part of the lung, we have induced an artificial pneumothorax on one side to put the organ at rest; the other lung continues to move normally with respiration. If our assumption is correct, we may expect that the long fiber material will produce fibrosis only on the side where active motion occurs; in the collapsed lung the long fiber should have little effect. The finely ground 01 056 0222 -4material should produce no'reaction in either lung. If, as anticipated, the long fiber inhalation experi ment gives rise to pulmonary fibrosis we shall follow the development of the changes in x-ray films as originally proposed when the short fiber inhalation test was undertaken. However there is little point in undertaxing this phase of the work until the monthly autopsy samples begin to reveal definite evidence of pulmonary change. (signed) LEROY U. GARDNER 01 056 0223