Document E9OKZ6kzyXKk1e2RyZak7eqg

400 O. A. SANDER asbestosis does not tend to progress after exposure is stopped or markedly reduced; Advanced asbestosis usually is associated with considerable emphysema an, commonly leads to right heart strain and failure. C. BAUXITE PNEUMOCONIOSIS (SHAVER'S DISEASE) A new occupational fibrosis of the lungs was recognized for the first time in 1942 by Dr. Cecil G. Shaver,92 Niagara Peninsula Sanatorium, St. Catherine!, Ontario. It is essentially a diffuse interstitial fibrosis and marked associate emphysema, with a complete absence of any nodular fibrosis. It has been found only in workers exposed to the fumes resulting from the fusion of bauxite in th manufacture of artificial aluminum abrasives. \ Bauxite is a natural hydrated aluminum oxide (Al2Oa) containing small amounts of silica and iron. When it is fused by heating at a high temperature L open electric furnaces, a crystalline artificial corundum results. This process give|j> off dense white fumes containing from 40 to 60 per cent aluminum and 30 to 4& per cent amorphous silica. Particle size ranges of the fume are remarkably small-| from 0.5 p down to .02 p--and can be visualized only with the electron micro scope. Workers with the'heaviest exposures have been the overhead crane opens ators and those who shovel the mix into the furnaces. * In the early stages there are no symptoms or clinical signs. The early x-ray-, pattern is characterized by indefinite granular or lacelike shadows, particularly in the upper lobes, resembling early tuberculous infiltration. As the pathological changes-progressy'involvement-of'theiower'lobes'occursrTlIelKaclbws mayTemam granular or may assume an irregular nodular pattern. The root shadows usualf are enlarged and increased in density. Emphysema usually is present and may. be extreme, with large emphysematous blebs. Spontaneous pneumothorax liar occurred in numerous cases and resulted in the death of several of these workefsl The main symptom of those with advanced disease is shortness of breath. This may be sudden and extreme at the time the pneumothorax occurs. Most cases hav developed in a rather short period of exposure: from two to five years. Approximately 50 cases had been discovered in the Niagara Falls area up t'L about five years ago. No tuberculosis was found in any of them. Since better fume' control measures have been instituted, no new cases have come to light. It is'jjf interest-that-no-pases^of-the-disease-were-recagnmed"mitil"I9427ev8crtlr6u|lS^S fusion'prScess1used since 1914. The only explanatidh ifor this'Is1'tff , tremendous incr&hs!e in production of the artificial abrasives during the war years! The precise causative factor in the fume has not been positively identified? Heretofore, .aluminum and amorphous silica had been- thought to be innnniinn ;- ~AIso, extremely fine particles of any dust, less than 0.5 p in size, had been thought! to have no significance in the development of lung fibrosis. It was believed thal| " C. G. Shaver and A. R. Riddell, Lung changes associated with the manufacture ofS alumina abrasives, J. Ind. Hyg. Toxicol., 29, 145 (1947). PULMONARY DUST DISEASES 401 ph fine particles were not retained in the lungs. However, Hatch98 has calcujad that alveolar retention of particles below 0.5 p is as great as of larger par oles, and may even be greater below 0.1 p because of Brownian motion. If this % atrue, then the fineness-of the particles alone is an adequate explanation for the ,f4pidity of development of this disease. Whether the silica particles alone or the Jvlpminum particles alone are responsible, or whether the combination is necessary, not been determined. German investigators, particularly Goralewski,94 be- Ipyed that aluminum alone was the offender and they still speak of the disease .^.Muminosis. Opinion in this country, however, favors the silica fume as the ^fxic agent, probably modified by the aluminum particles. This seems the most 'logical explanation for the fact that the fibrosis does not assume a nodular char- jigter. Interest in this disease extends well beyond the artificial abrasive industry 'iPliecause of the implications associated with the rapid development of fibrosis due f.ultramicroscopic particles, which are harmless when larger. Is it possible that p|ljer innocuous materials may be harmful in the fume size ranges? This possi&ljty seems unlikely for iron because of the experience with welding fumes, which ntain upwards of 95 per cent iron oxide particles in size ranges below 0.1 p and mtBrownian motion. The evidence is clear, at least for this fume, that no such feaction has occurred, even in welders who had such concentrated exposures that e,:iron collections in their lungs could be seen by x-ray. Such exposures caused i;even a trace of fibrosis in the lungs. This evidence suggests that it is not the j)microscQnia,parti.aIe-Per-S.e that is the toxic factor in Shaver's disease. More ll^nsive research with the fumes of many materials is needed before this filter ing problem can be resolved. D. DLATOMACEOUS EARTH PNEUMOCONIOSIS (DIATOMITE SILICOSIS; DIATOMITE PNEUMOCONIOSIS) The first epidemiological study in the diatomite processing industry in Cali fornia was reported by Legge and Rosencrantz98 in 1932. Of 118 employees who "re x-rayed, 68.5 per cent were said to have shown evidence of pneumoconiosis. ,o correlations were made between the degree of dust exposure and the clinical ..lings. There were no other American reports for the next 20 years, but a Aisstudy-in-Italyrwas-repoFtedibyWigliani-and .Motturafl?:in.-19.48'ijEQr;.the first 'uSi it was shown by way of x-ray diffraction that crude diatomaceous earth 'obtained no crystalline form of free silica, but that after flux calcining at "T. F. Hatch, J. H. Brown, K. M. Cook, and F. G. Ney, Influence of.particle size upon ,.J^etttiaioif-Partic'ilatA:niatter-in- the human lung. Am. J, Pub. Healthr-4,6.450-(1950). f|V'"G. Goralewski, Aluminum lung, Arch. Gewerbepathol. Qewerbehyg., 11, 102-118 (1941), D R. T. Legge and E. Rosencrantz, Observations and studies on silicosis by diatomaceous lica, Am. J. Pub. Health, 22, 1055-1060 (1932). ,. "E. E. Vigliani and G. Mottura, Diatomaceous earth silicosis, Brit. J. Ind. Med., 5, 148,(1948).