Document EdJzVKZJ8mob4B1MdMOJBpM6g

374 0. A. SANDEK 30 million particles per cubic foot would give 0.10 times 30 million, which equals 3 mil]i|i (good practice); a dust containing 30 per cent with an average total concentration of 50 milj&f particles per cubic foot would equal 0.3 times 50, or 15 million (unsatisfactory). This formula! not applicable to any dust containing less than 5 per cent free silica. The Division of Occupational Health, U. S. Public Health Service,38 has suf gested that an attempt should be made to have highly siliceous dusts kept atl|g concentration below 4 million particles per cubic foot since considerable silicoail occurred in the pottery industry even with low dust concentrations. Dust may also be simply a nuisance. It is considered good practice to control even relatively harmless dust sufficiently to prevent concentrations in excess, 50 million particles per cubic foot (by light-field count) in the workroom air. c. Particle Size in Relation to Development oj Fibrosis. We have already mentioned the fact that large particles settle more rapidly than small ones an? that particle size is important as a determining factor in the actual amount of dtifl in air. Particle size is even more important in determining the chemical activity,^ the dust and physiological responses to it. Chemical activity is, of course, increase in small particles because of the increased surface area. McCrae89 found thatJT per cent of the particles in silicotic lungs were less than 1 y. in diameter and thaf the largest were not greater than 10.5 y. An upper limit of 10 /i as the maximuf size that will produce silicosis has been suggested because larger particles;J| probably collected by mucus in the upper respiratory tract and moved out ofjT lungs by ciliary action. The importance of small particles in the production^ fibrosis has been well demonstrated by Tebbens, Schulz, and Drinker,40 These,at vestigators produced liver fibrosis in experimental animals by intravenous 'inj|t tions of suspended silica and found that particles less than 0.6 y in diame|f caused much more fibrosis than larger particles. Briefly, silicosis is caused by the inhalation of silica particles less than l|f in diameter. Recent work suggests that particles of less than 0.6 y may bejg greatest importance in this respect. d. Individual Predisposition. Detailed discussion of the role of indpvidi|l predisposition in the etiology of silicosis is hardly necessary. Race and sex stpn to play little part, although race may be a factor in the development of tubel culosis just as financial status may be a factor. Certainly it is known that of-sW persons working in the same dusty exposure one may contract silicosis in.ayiffj years while the other, may require many years. We have already mentionripfl possible influence of 'differences in nasal ,filtration as a factor in causatilifS silicosis. It is likely that there are sound explanations for the many variations individual susceptibility, but clarification is lacking. Many of these variatj||| -undoubtedly-are-related-to-difTerences-in-adrenal-cortical-'-hormone-activit " R- H. Flinn, W. C. Dreeaaen, T. I. Edwards, E. C. Riley, J. J. Bloomfield, and R:| Sayers, XJ. S. Pub. Health Bull. No. 244, 1939. "J. McCrae, Pub. S. African Inst. Med. Research, Report No. 3 (1913). "B. D. Tebbens, R. Z. Schulz, and P. Drinker, J. Ind. Hyg. Toxicol., 27, 199 (1945). J PULMONABY DUST DISEASES 375 4. Pathological Anatomy and X-ray Findings So. Benign Pneumoconiosis. All dust other than that containing free silica and gsfos generally is inert and produces little or no fibrosis in the lungs. W-mu examination. There is simply an accentuation of the normal, branching, fe|lce shadows cast chiefly by the pulmonary blood vessels. As an occasional ^if%on in this picture there may be superimposed fine reticulations. These :retic"||j|qns are thought to be caused by thickening of the sheaths of the pulmonary flfies and thickening of the interlobular septa (see Figures 4 and 5). ` Vail ''<> ' WjfEH) re 4. Normal adult chest. Note that fows and vascular markings are not -Underexposed films may cause agjpr&tion of the vascular pattern and '|||n of dust retention. Figure 5. Increased linear markings. These usually are due to increased vascularity of the lungs for one -reason or another and are not diagnostic of ^silicosis or other fibrosis. They may, however, fcedue to early inert dust retention in the lymphatics of the lungs. jjjjfegte.with higher atomic weights, such^as. irpn ,.(5), ,ttn .(119):,, and .barium fmSr.p at times retained in the lungs to such' a degree that the perivascular and gmpjgnchiolar collections of the dust actually cast nodular shadows on chest Sfilms. This was first shown by Enzer and Sander41 in 193 in the post, fps'tissue studies of an electric arc welder, and was subsequently confirmed jltEnzer and"0.^ Sander, Chronic lung changes in electric arc welders. J. Ind, Hyg. TM>xicbit*20i 333-350 (May, 1938). Hamlin and A. J. Vorwald, SideroBis: a benign pneumoconiosis due to the inhaifl- 'innifiomron dust, Ind. Med. and Surg., 19, 151--180 (April, 1950).