Document MvGJY1Dn2GmQarZZw6OVVaKL

372 O. A. SANDEB sharpness of the particles. However, Gardner27 found that no fibrosis was produc by experimental inhalation of aluminum oxide and diamond dusts which are el harder and sharper than silica. Thus, the action is clearly chemical, but the ex' chemicophysiplogical reaction that takes place is still unknown. The mixed reaction sometimes produced by dusts of the inert group in silica is mixed with other minerals emphasizes the possible effect of mixed dusts; the development of silicosis. The probable importance of concomitant exposii has also been indicated by clinical experience. Chapman,28 MacDonald and* associates,28 and Kilgore80 have reported cases of rapidly developing silicif" caused by breathing air with high concentrations of silica and alkali dust. Kett and McCord32 failed to demonstrate such action experimentally. McCord, onj^ basis of extensive investigations of workers in six plants where there was exposii to silica and alkali dusts, found no evidence of an accelerator action by alkali In fact, the absence of silicosis in this group suggested an inhibitor action whi he believes may have resulted from the marked increase in solubility of silica|! the presence of alkali. Peritoneal injection in animals yielded no results to pr< either an accelerator or inhibitor action of alkali in the formation of silica nodu Alkali did, however, cause the silica to spread from the point of injection i increased its primary toxicity. The absence of silicosis in ganister-brick manufacturing was thought at due to an inhibiting effect of accompanying dusts; more recently it has been fp,u, that the concentration of free silica in the work atmosphere was too low to clus fibrosis. Silicosis as found in CQaLminern fanthracosilicoaisI -and-in.-foundcy-:' may be quite different in x-ray appearance and in its course from that obser, in quartz grinders. b. Number oj Particles Inhaled in Relation to Production oj Fibrosis, a apparent that the type of dust may play an important part in determining^ number of particles in the workroom atmosphere. Not only may some componen of admixtures flocculate and thus change the character of a dust, but silica its being a hard material with a tendency to form large particles as compared`;y those formed by softer minerals, may settle out more quickly than other ponents of a mixed dust. However, at this point we are somewhat more concerned with the concent tionsqf_dust thatjije]mrmluLthan ^i1tJh the..factQrs.that.hav.e..prQduced,an:l concentration in the, .air. Determinations of free and total silica in.the luygs patients who have died after fibrosis developed and in those without fibrosis h been made by incinerating the lungs and chemically analyzing the ash for its si content. Although, there have been some variations in published data on.. 'rL. U.Gardner, Am. Rev. Tuberc., 20, 883 (1929) A, M. Chapman, J. Am. Med. Assoc., 98, 9 (1935). * G. MacDonald, A. P. Piggot, and F. W. Gilder, Lancet, 2, 836 (1930). "E. S. Kilgore, J. Am. Med. Assoc., 99, 1414 (1935). "E. H. Kettle, Proc. Inst. Mining Metallurgy (London), Ifird Sess., 1934 MC. P. McCord, 2nd. Med,, 5, 17 (1936), PULMONARY DUST DISEASES 373 count of silica in pulmonary tissue necessary to produce silicosis, Sladden,83 ally,34 Badham and Taylor,35 and Fowweather86 found fairly comparable founts. Drinker and Hatch2 sum up the present knowledge somewhat as follows: lErough guide, a total silica .content as high as 0.2 per cent of dried lung can be glidered normal. A content over 1 per cent is definite evidence of dust exposure, Bthis amount is usually accompanied by fibrosis. There are too much overmifag of data and variation in technique to be sure from published data of the fpficance of quantities between 0.2 and 1 per cent of ashed lung. This fact is of Ulial significance, as pointed out by Cummings.87 Since there is usually no evi||P of silicotic reaction in lungs containing less than 1.5 to 2 g. of silica (1 per jsfef weight of dried lung), it may be inferred that the contraction of silicosis lifhot necessarily follow the inhalation of silica. Silicosis occurs only after the ijllation of amounts in excess of a minimum. Sin any control program we are of course concerned primarily with the amount Hpst in the air that will cause fibrosis. The methods of determining atmospheric mapconcentrations are discussed in Chapter VII. Cummings suggested that Mhpheric concentrations of silica dust should be considered in terms of two ffinolds: the primary threshold, a level at which a healthy man can be employed ||||s lifetime without harm, about 5 million particles per cubic foot (light-field llll); and the secondary threshold, a level at which a healthy man will inevitably H|op silicosis, about 100 million particles per cubic foot ('light-field count). The ijfiphal Silicosis Conference summarizes the situation as follows: "There is eviaE|yfiiaLior_prolonged exposure a concentration of more than 5 million particles rawnibic foot,' of a highly siliceous dust, is dangerous. Therefore it is now con cilia good practice to hold concentrations of highly siliceous dust at 5 million l||cleB per cubic foot, or less," as based bn light-field counting methods. jfflSmce standards of safe atmospheric dust concentration based on medical findjgpjnave been suggested tentatively for only a few industrial dusts, and since j3p|erable study is necessary to form a basis for such standards for other indussraraiists, a tentative arbitrary measure of what is good practice may be used. |||ilhould be within the limits of good engineering practice and yet low enough ||||trol the silicosis hazard for most industrial exposures. The following formula ||||aquently used to express the maximum permissible concentration of silica in Wm;... ............ mi*,. j||l|Multiply the percentage of free silica by the total dust particle count per cubic foot (lightj|l||Ffe<!hnique). If the result is over 5 million, the concentration may be considered too high. ig|||xi;mple: a dust containing 10 per cent free silica with an average total concentration of ulliptn BfijjBBUjB..Sladden, Lancet, 2,.,123 (1933). jgggjjpW; t). McNally, JTAmTMTd. Assoc., IOlT'584~('1933)~ ||||b?.C. Badham and H. B. Taylor, Med. J. Australia, 1, 511 (1933). BEF. S. Fowweather, Chem. Industries, 53, 713 (1934). flffi). E. Cummings, "The Etiology of Silicosis," in B. E. Kuechle, ed., Fourth Saranac MMrMory Symposium on Silicosis. Employers Mutual Liability Insurance, Wausau, Wis., iriDrvSvUU