Document MJRrVx46D381j00yJNoyY9yJV

398 0. A. SANDER bined with cotton and woven as a textile for fireproof and heat-resistanf and other substances. Lanza82 estimates that there are about lO.OOO'geLu posed to asbestos in the United States. Most observers feel that .theuiir|pje asbestosis in American asbestos workers is quite low. Asbestosis been reported more frequently in England and Canada. Lanza, McConnell, and Fehnel83 concluded from their study that prolonged exposure to asbestos dust causes pulmonary fibrosis,difieg that produced in silicosis and demonstrable by roentgenogram. ClinK sembles silicosis in that it is not disabling in the early stages, '.but^ markedly disabling when advanced, and frequently leads to death, byg^g failure. Although tuberculosis has been shown to be no more prevalently; with asbestosis than in the general population, lung cancer is undervsut occurring more frequently with asbestosis, especially in England. Symptoms. The onset of symptoms of asbestosis, as of although symptoms in advanced cases are apt to be somewhat more mil, in silicosis. As in silicosis, dyspnea is the cardinal symptom. AnorSx! frequently in advanced stages, and cyanosis and clubbing of the to appear with greater constancy in asbestosis. Pathology. The fibrosis in asbestosis is diffuse and tends to ; the basal portions of the lungs in contrast to the generalized nod,.,,,^ silicosis with a predominance in the upper portions of the lung. Brondffi| bronchiolectasis are frequent, especially in the more fibrous portions.#?) proliferation of fibrous tissue is caused bv chemical_ac.tionJ.n-silica,^-iv^ induced by mechanical action in asbestos exposures. Gardner?4vfouip fibrosis-producing character of asbestos could be almost eliminateSlfl the fibers so that no particles more than 20 y in length were present. mentioned, asbestos is classified among the inert dusts. Vorwaldfslfi Pratt88 report that the typical bronchiolar fibrosis is best produce^ ranging from 20 to 50 y in length but not by fibers shorter than 20?/uf cance of this finding on prevention of the disease will be discussed belof, Microscopic anatomy. Johnstone88 described the microscopib#fjL, the lungs somewhat as follows: In the early phases of the disease tKerajl ing of the alveolar septa which results from fibroblastic proliferation?!!* spaces contain numerous phagocytes. With progression of the, disease comes more matked; the Alveolar struct^ gradually disappealij|$nf|p there is;nqw,deuse.;fibrpus tissue. The few alveoli that remain in`tKe^l^ are lined with low cuboidal epithelium giving them an almost glandbM| ance. ""A, J. .Lanza, J. Am. Med. Assoc., )06, 368 (1936). "A. J. Lanza, W. J. McConnell, and J. W. Fehnel, V. S. Pub. Health Repts$ *L. U. Gardner, Jnd. Med., 9, 45 (1940). "A. J. Vorwald, Experimental studies of asbestosis, Arch. Ind. Hy'g. and- Med., 3,1 (1951). % m R. T. Johnstone, Occupational Diseases. Saunders, Philadelphia, 1942 :';i PULMONARY DUST DISEASES 399 Ired throughout the lung in both the diseased and healthy parts are J!j|qd structures described first by McDonald.87 These bodies are . 20 to iS|th and are bulbous on one or both ends so that they appear club- or llhaped. They are brownish in color, do-not stain, and give a Prussian- jon.for iron. Simson88 has produced these bodies in guinea pigs by extffltecposure to atmosphere containing asbestos. Lynch89 concludes that Pspjj^bodies" signify exposure to asbestos dust but do not necessarily *|j|||t,osis. In other words, they are more properly referred to as "asbestos not "asbestosis bodies." `ej}x^a7'mination. For an excellent review of roentgenographic findings in |j||!and asbestosis the reader might well refer to Pendergrass.90 Char^|ei;qnce8 in the roentgenographic findings in silicosis and asbestosis H&elow: Asbestosis jse (film may have ground glass ffi!om pleural involvement), either bilateral or uair Silicosis Fibrosis nodular. Findings characteristically bilateral. the lower one half or two ng fields. .^gripper portion of lung fields. [Iffgfeev difficult to recognize. Lesions predominantly in the upper twothirds of the lung fields. Emphysema in lower portion of lung fields. Borderline degree more easily recognized. .i^TrjEn.tkm-oL.aabes.to.a.is^RejidsJ.argelx^!LPXeLenting e_xposure to %gh concentrations of long fibers to produce the characteristic reac- ittly long fibers cause, the disease, fine dust respirators are not neces- |jre comfortable gauze respirators appear to be perfectly adequate or^-ijilong fibers. Up to this time, however, they have not. been approved a88pS&te8 Bureau of Mines for this purpose.' wMpConcentrations. Dreessen, Dal1aValle,Edwards, Miller, and ^Mmund evidence to indicate that 5 million particles per cubic foot of iSfaMdiy figure for the maximum permissible , atmospheric .copcentra- ^Mos.to which workers may be exposed. Howeyer, in setting 'up this tillers dess than 10 y in length were counted and the longer ones were IknsLRDPeaPsJihatJbe^ to fbe:;disrega,rded bussiKltponcentrations of long fibers established, which has not been dope. SjBmfprbghqsis with early to moderately advanced asbestosis is good, pro- lation of asbestos fibers is materially .decreased.^nljKf silicosis, figgj&aateBaaaaBK!!fca02B-ft98-:........... ............ , MBBHBiHM. Brit. Med. J., 1, 885 (1928). iljknch, J. Am. Med. Assoc., 109, 1947 (1936). ntlergraas, "Roentgen-Ray Diagnosis in Silicosis and Asbestosis," in A. J. Lanza, ISS^Sl^i'pi'l'rUbestosis. Oxford Univ. Press, New York, 1938. ,< rDreessen, J. M. DallaValle, T. I. Edwards, J. W. Miller, and R. R. Sayers, U. S. No. 241, 1938. S?5-'1 1 irtyr?" '>: r -