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FILE NAME: Newport News (NN) DATE: 1964 DOC#: NN004 DOCUMENT DESCRIPTION: Government Book Excerpt I OCCUPATIONAL DISEASES ; A Guide To Their Recognition i 3 5 Rewritten and Enlarged Edition of Occupation Hazards and Diagnostic Signs W. M. GAFAFER, D. Sc.f Editor Division of Occupational Health o n <'. >ry NN S-M O R-005759 ! { 4 u V .* *. *>'vv\Y r* tyft <* 50 OCCUPATIONAL DISEASE?; :* ww pulmonary insufficiency or from cor pulmonale secondary to obliteration of the pulmonary vascular bed by fibrous tissue invasion. The roentgenographic characteristics of simple coal workers' pneu. moconiosis include discrete opacities up to 10 mm in diameter, which may be arranged in groups or spread diffusely throughout the lung fields. In the complicated form of the disease, the earliest roentgenographic evidence of PMF is the presence, usually on a background of simple pneumoconiosis, of larger, less well defined opacities, often resembling reinfection-type tuberculosis in both position and appearance. These large shadows tend to increase in size and to coalesce. They later may contract with resultant severe distortion of the lung architecture. References cochbane, a. I_: The attack rate of progressive massive fibrosis. Brit. J. itJust. Mtj. 19:52,1962. doyle, h . N.; flinn, r. H., and dreessen, w. c.: A review of the pneumoconiosis problem in the United States. Am. Indust. Hyg. Assoc. J. 19: 317,1958. FLETCHER, C. M.: Classification of roentgenograms in pneumoconiosis. AM-A. Arrk. Indust. Health 11:17,1955. FLl.NN, R. H.; SEIFERT, H. E.; BRINTOH, H, P.; JONES, J . L., AND FRANKS, R. W.: Soft rest miners health and working environment. Pub. Health BulL No. 270. U.S. Government Printing Office, Washington, D.C., 1941. cilson,' j; c.: Pathology, radiology, and epidemiology of coal workers' pneumoconious in Wales. AM .A. Arch. Indust. Health 15: 468,1957. cilson, j . c. and huch-jo n e s, r . : Lung function in coal workers' pneumoconious Medical Research Council, Special Report Series No. 290. Her Majesty's Stationery Office, London, 1955. cough, j.: Pneumoconiosis in coal workers in Wales. Occup. Med. 4: 86, 1947. heppleston, a. c.: Coal workers' pneumoconiosis. Pathological and etiological con siderations. A M A . Arch. Indust. Hyg. & Occup. Med. 4:270, 1951. holt, p. F.: Pneumoconiosis; Industrial Disease of the Lung Caused by Dust. Ed ward Arnold, London, 1957. kerr, l . e.; Coal workers' pneumoconiosis. Indust. Med. & Surg. 25: 355, 1956. martin, J . E.: Coal miners' pneumoconiosis. Am. J. Pub. Health 44: 581, 1954. SAYERS, R. R.; BLOOMFIELD, J . J.,' DALLAVALLE, J. M.; JONES, R. R.; DREESSEN. W. C.; brundage, d. K., and britten, r. H.: Anthraco-silicosis among hard coal miners. Pub Health Bull. No. 221. U.S. Government Printing Office, Washington, D.C, 1936. (3) Asbestos * Asbestos is a general term used to describe several fibrous mineral silicate which differ in their chemical composition and physical properties The most important types of asbestos are chrysotile, a simple magnesium silicate; amosite and anthophyllite, which are complex magnesium iron silicates; and crocidolite, a complex sodium iron silicate. About 95 percent of the worlJ asbestos production is derived from chrysotile. Deposits of this mineral are found in many countries, but the largest mines are located in Canada. TV-PTM ihpm -- " N N S-M O R-005760 I I . . . -i ~\>um --V i ; PNEUMOCONIOSES 51 Prolonged inhalation of asbestos fibers between 20 and 50 microns long may result in the production of a typical pulmonary fibrosis which may be accompanied by severe respiratory disability. On the basis of experimental studies of asbestosis, it was reported in 1951 that this fibrosis is due to the mechanical action of the asbestos fiber. The fibers, upon being deposited in the terminal bronchioles, initiate a tissue response which results in the coating of the fiber with the. ultimate production of what is known as the i asbestos or asbestosis body. This response appears to be a defense mecha j nism of the lung. If large quantities of the fibers are inhaled over a pro longed period of time, characteristically 10 to 20 years, the tissue reaction progresses until a generalized, diffuse fibrosis becomes evident. This fibrosis is seen first in the lower lobes of the lungs but eventually, if exposure continues, appears in the other lobes as well. Respiratory insufficiency and cardiac failure may supervene. It is of considerable interest and significance that asbestos fibers smaller than about 20 microns in length are thought to be incapable of initiating a fibrogenic response. The roentgenogram of the chest with pulmonary fibrosis resulting from prolonged inhalation of asbestos fibers discloses a typical pattern. In the i early or first stages of the disease, the shadows are fine, diffuse and homo geneous and appear characteristically at the base of both lungs. The typical nodular pattern of silicosis is not seen in asbestosis; rather, the affected lung fields present a ground glass appearance. 1 In moderately advanced or second-stage asbestosis, the infiltration is more in evidence but remains generally confined to the lower lobes. The heart borders may become indistinct or shaggy, a condition which has been irferred to as porcupine heart. In far advanced or third-stage asbestosis, the infiltrate can be seen through out the middle and upper lung fields; however, the apices generally remain clear. There is almost complete obliteration of the cardiac outline, the domes of the diaphragm and the costophrenic sulci. It should be emphasized that the chest roentgenogram cannot accurately he used to estimate the presence or extent of impaired pulmonary function or disability in lung diseases in general, and in asbestosis in particular, since any individuals with radiographic evidence of third-stage asbestosis have been able to carry on their usual work and live fairly comfortable lives for several years. On the other hand, definite disability due to asbestosis has rar,`ly been reported in the absence of a typical radiographic pattern. There is no typical clinical picture for asbestosis. The disease is insidious 1,1 Us onset and is slowly progressive so long as inhalation of the fiber con tinue. There is a 'gradual increase in cough and expectoration, anorexia, and weight loss, all combined with slowly increasing dyspnea. Cyanosis *nd clubbing of the fingers are rare findings. When an acute pneumonitis i f NN S-M O R-005761 1-. % t L: i jy fh,'. \:r- i % \K b y a; 52 OCCUPATIONAL DISEASES i develops in the presence of established asbestosis with fibrosis, recovery U often delayed because healing is slow and relapses are frequent. * ; m.- The primary functional abnormality in pulmonary asbestosis is one of Pr impaired oxygen transfer across the alveolar membrane rather than impair ment of ventilatory capacity. This condition is referred to as an alveolar Hi capillary block. ch Conflicting opinions and differences in reports make it difficult to confirm as or deny conclusively a causal relationship between asbestosis and cancer cti of the lung or extrapulmonary tissues. However, there is increasing evi co dence to suggest that such a relationship exists. With regard to the relationship between asbestosis and tuberculosis, it m is fairly well established that asbestosis does not predispose to the develop r ment of tuberculosis, nor does it aggravate an apparently healed lesion. su References to anderson, j . and campagna, f. a.: Asbestosis and carcinoma of the lung. Case report cc and review of the literature. Arch. Environ. Health 1: 27, 1960. dadollet, M. s.: Asbestos. In Kirk, R. E. and Othmer, D. F. (editors) : Encyclopedia j ei of Chemical Technology. Vol. 2. Interscience Publishers, New York, 1948. doll, R.: Mortality from lung cancer in asbestos workers. Brit. J. Indust. Med. 12: ex 81,1955. n hurwitz, M.: Roentgenologic aspects of asbestosis. Am. J. Roentgenol. 85: 256,1961. isselbacher, K. j.; klaus, h ., and hardy, h.: Asbestosis and bronchogenic.carci m R noma. Am. J. Med. 15; 721,1953. keal, e. .: Asbestosis and abdominal neoplasms. Lancet 2: 1211, 1960. leathart, c. L.! Clinical, bronchographic, radiological and physiological observations in ten cases of asbestosis. Brit. J. Indust. Med. 17 : 213, 1960- St pearl, r. m.: Rocks and Minerals. Bames Si Noble, New York, 1956. S smith, k . w.: Pulmonary disability in asbestos workers. A.M.A. Arch. Indust. Health J 12:198,1955. re vorwald, a. J.; durkan, t. m,, and pratt, p. c.: Experimental studies of asbestosis. IS A.M.A. Arch. Indust. Hyg. <t Occup. Med. 3:1,1951. wacner, j . c.; sleccs, c. a., and marchand, p.: Diffuse pleural mesothelioma and C asbestos exposure in the North Western Cape Province. Brit. J. Indust. Med. 17: 260,1960. WRIGHT, c. w.: Functional abnormalities of industrial pulmonary fibrosis. A M A* ] Arch. Indust. Health 11; 196,1955. t i i (4) Diatomite Pneumoconiosis * c< Diatomite, frequently designated diatomaceous earth, diatomaceous silica, e: or kieselguhr, is composed of the siliceous skeltons of microscopic, unicellular, ft aquatic plants known as diatoms. Because of its remarkable properties, this a. nonmetallic mineral has found many industrial uses, such as in filters, in b sulators, absorbents, and polishes. d Crude diatomite is essentially amorphous silica and contains less than 5 f< percent of quartz and only traces of cristobalite and tridymite; however, n after being processed by high-tcmperature calcining, the cristobalite content si maaBsmmBmamacmmm NN S-M O R-005762