Document 46GwQJvBL5yKvRLR8jKENyw1

FILE NAME: CERAMICS (CER) DATE: 1950 DOC#: CER041 DOCUMENT DESCRIPTION: Journal Article Excerpt - A Review of Pneumokoniosis and Dust Suppression in Mines CFTAMIC ABSTRACTS 1950 C h a rles S. P ea r c e, Editor M ary J. G ib b , Assistant Editor T helma J. C e c il, Editorial Assistant Committee on Publications: K. C. L yon, Chairman. K arl Schw artzw alder. R. E. B irch, and J. J. C anfield Technical Advisers. L. G. F arber, R alph R o se, and B etty T. O wen Compiled by The American Ceramic Society 2525 North High Street Columbus 2, Ohio / 456 TRANSACTIONS-- THE INSTITUTION OF MININO ENGINEERS [Vol THE INSTITUTION OF MINING ENGINEERS [No. A REVIEW OF PNEUMOKONIOSIS AND DUST SUPPRESS] IN MINES PART J--MEDICAL ASPECTS OF PNEUMOKONIOSIS.* By A. G. HEPPLESTON. M.B., M R.C.P. Department oj Pathology, Welsh National School of Medicine, Cardiff. Introduction.--Chronic respiratory disease is known to have afflicted the wof in dusty trades from prehistoric limes (Rosen, 1943) and the desirability avoiding the inhalation of mine dust was appreciated by the Romans . but it remained for Agricola (De re metallica, 1556) to associate clearly^ inhalation of dust with the occurrence of pulmonary disease in miners, esp where the mines were dry. Following the Roman practice he advocated the; . of a simple respirator as. a preventive measure. Since those early times th e'[ that dust caused pulmonary disease has gradually gained general acceptai more particularly since Zenker (1867) demonstrated beyond doubt that atj spheric dust could be deposited in the depths of the lungs. Miners' sickness, as this respiratory disease was originally called, bore ceii clinical resemblances to pulmonary tuberculosis, such as destruction of the lu and emaciation (Agricola, ibid.). Many of the earlier workers, however,'" careful to distinguish the two conditions. Although detailed studies pathology of miners' lungs are relatively recent, the question of the relation of dust accumulation to tuberculosis was raised in some of the earlier inve" tions (e.g. G raham, 1834; Cox, 1857; Peacock, 1860-61; Begbie, 1866). of such an association was wanting for many years owing to lack of te methods, but with their advent it became clear that tuberculosis, in one fori another, was an important factor in the production of pulmonary disi individuals exposed to certain occupational dust hazards. The magnitude of the problem of pneumokoniosis as it exists today judged from the following facts. In oouth Wales approximately 18,0001 workers have been disabled by pneumokoniosis during the past 17 years (Je 1948), whilst for the years 1941-44 the incidence of new cases of silicosis,'^ and without tuberculosis, in European miners on the Witwatersrand was 9-5" 1,000 examined (Smith, 1941-44). Nevertheless, much has been done to pij the disease, as the corresponding incidence on the Rand for 1917-20 namely 28T1 cases per 1,000 examined (ibid). . Two forms of pneumokoniosis can be distinguished, a simple type due td acting alone and an infected type due to the combined effect of du~* infection, particularly tuberculosis (e.g. Strachan, 1947; G ough, 1947; ' 1947; Craw, 1947). * This review discusses the present state of medical knowledge and has b pared at the request of the Joint Committee of The Institution of Mining and The Institution of Mining and Metallurgy, by whom the Conference on !UD Pneumokoniosis and Dust Suppression in Mines, London, April 1947, was on At a later date it is hoped to publish reviews of the mining and engineering as] the problem. This Review has also been published by "Die Institution of n and Metallurgy, see Bulletin No. 511, June 1949. " / 458 TRANSACTIONS-- THE INSTITUTION OF MINING ENGINEERS 48- 1949) heppleston--pneumokcn also been reproduced experimentally by underground exposure to air-borne iica effect (G ardner, 1934, 193:, in the absence of infection (Heppleston, to be published). Ucosis may well arise as a coa^q Disability in simple pneumokoniosis usually presents itself as breathlessi due fundamentally to defective exchange of gases between the inhaled air the blood. According to Simson and Strachan (1935) fibrous tissue overgn is apparent at an early stage in the development of the silicotic nodule and fibrosis steadily extends as the lesion matures. Whilst there is no doubt soi replacement of functioning lung tissue by the nodules, their main effect accori ing to Simson (1935) is to constrict the small air passages around which thi develop. Such focal emphysema as occurs will contribute to the respirato; incapacity. As to the factors underlying the disability in the non-speci pneumokonioses we can as yet speak only of the condition in Welsh coal worke; Here focal emphysema appears to be the primary factor, but its mechanism h; not yet been fully elucidated. Obliteration of small areas of lung tissue by thi (action between the lung tissue an , lelsh coal workers is more readily rx , rt-j lungs with dust irrespective of ect It cannot be denied that free f & disease in coal workers, but its importance than that of the other con C e a r s that as more dust is deposited fizregates which then undergo a n further dispersal of the dust. As a c Bocal emphysema develops (Heppij-s bat pneumokoniosis may arise from f y inert foreign material. dust foci themselves may play a subsidiary role. In both these forms of pneum koniosis general emphysema, apparently occurring as an independent entity, ma; INFECTED i complicate the picture Occasionally simple pneumokoniosis is responsible foi -phis type occurs as a compli'.aiu i I death as a consequence of congestive heart failure. Essentially of pigmented masses ot Several theories have been advanced to explain how dusts as such act on hubstance. In size they vary' fru n lungs. The idea that dust penetrated into the tissues of the lungs by virtue ol located in the upper or middle port its hardness and sharp edges has gradually been discarded since Zenker (186~ tCavitation may occur in massive lesu showed that particles which were neither very hard nor sharp could pass froi ftion due to loss of blood supply o: the atmosphere into the lung substance. G ardner (1923) refuted the belief thal lesions occasionally show other e-ic pulmonary fibrosis was caused by irritation from hard, sharp particles when hi involvement of the whole lung by failed to induce such fibrosis in guinea-pigs by the inhalation of carborundui [ Gardner, 1937a; H ale, 1946; Ckav. dust, the particles of which are nearly as hard as those of the diamond am [severe degree, may occur in relati whose abrasive qualities are well known. Following the work of GyE am emphysema may be present indepen Purdy (1922, 1924) and G ye and Kettle (1922) many people now maintain thal U There is good reason for believl: in silicosis the fibrous tissue over-growth is stimulated by slow " solution ol [tuberculous in origin. They occur free silica particles in the body fluids. Although this view was affirmed by thi j common sites for the development International Conference on Silicosis in 1938 (I.L.O., 1938) the evidence h general population (GARDNp., 1 not conclusive (King, 1938) and has been discussed critically by G ardner (19376)1 bear evidence of a chronic infecti ve For instance G ardner (1934) states, on the basis of his experimental work, that tuberculous. In silicosis, G ardnir "the relatively insoluble quartz particles are definitely more active than the mori readily soluble silicate particles and tissue reactions begin to develop so quickl; that it is hard to conceive of such a solution of silica having occurred in tr1 weakly alkaline body fluids." culosis in 60% of massive lesions, incidence is approximately 30% (-K (1935) isolated tubercle bacilli from Rogers (1946) claims to have demo To meet such objects H effernan (1935, 1944) suggests that the activity Ol from a series of 831 Welsh coal free silica particles on tissues depends upon the electrically unsatisfied oxyg' bacteriological evidence of tube.cul atoms of the freshly produced silicon-oxygen tetrahedra. Silicate particles on the nical methods are inadequate, that other hand are electrochemically inert even when fresh. G ardner (1938), how y healed lesion, or that the massise ever, points out that, whilst freshly fractured free silica may be more potent., tuberculous inflammatory process s than silica which has aged, the ageing process is not progressive since silica periTients show that tuberculous remains active for long periods, even when it is suspended in dilute aqueous inhalation of various dusts, mdud sodium chloride solution. In coal workers' pneumokoniosis free silica has again (Gardner, 19376, 1938) but nor-t been incriminated since coal-dust contains a small amount of this substance rabbits failed to do so (Vorwaxd, (G ardner, 1934, 1935, 19376, 1939; Sayers et a!., 1935; Cummins and SlMideN, i the view that tuberculosis is the nr, 1930; Belt and Ferris, 1942). The adherents of this view explain the different koniosis we must admit that the ti pathological appearances of classical silicosis and coal workers' pneumokoniosis one which suggests a retardation c as being due to modification of the action of the free silica by the other com ponents of the coal-dust. The results of in vitro and in vivo experiments ba , extent. ll is comparatively easy to appr on this idea have not provided completely satisfactory support (King and N ag lung tissue by massive fibrosis v.il schmidt, 1945; King, 1945; Belt and King, 1945), and the direct effect ot in duce disability, especially wher.^ ig major portion of the dust has received insufficient attention (BadhaM and . a consequence of the fibrosis v v< 1936). The disease in haematite workers has also been explained as a modi two factors and congestive hear! f 460 TRANSACTIONS-- THE INSTITUTION OF MININO ENGINEERS [Voi. 108 issue. This termination appears to be commoner than active tuberculosis in Welsh coal workers (G ough, 1947), whereas the reverse obtains in classical silicosis (Strachan, 1947). Death is sometimes due to causes other than pneumo- koniosis. ASSESSMENT OF THE DEGREE OF DISABILITY. This assessment provides the basis for compensation and also for recommenda tions as to suitable alternative employment. Conditions simulating pneumokoniosis must first be excluded. Simple Pneumokoniosis. The clinical history and examination may be quite misleading owing to the subjective factor and the absence of diagnostic features. The degree of clinical disability in silicosis cannot be correlated accurately with the extent of the radiological changes (George, 1938; Irvine, 1938; Crombie, Blaisdell and MacPherson, 1944), and the same is true for Welsh coal workers. In the latter Gough (1947 and to be published) has demonstrated that the X-ray appearance of " reticulation" (Hart and Aslett, 1942) is produced by the superimposition of the shadows of the dust foci, no matter whether these are accompanied by focal emphysema or not, yet it is precisely the focal emphysema which is believed to be mainly responsible for the disability. The physiological tests so far applied to this problem have not proved very satisfactory. Many of them are open to subjective errors, are time consuming, lack delicacy and seem incap able of distinguishing incapacity due to pneumokoniosis from that due to associated but not necessarily related pulmonary or cardiac conditions (Irvine, 1938; McM ichael, H art and Aslett, 1942; Crombie, Blaisdell and MacPherson, 1944). For practical purposes a simple and reliable objective test has still to be found. . Infected Pneumokoniosis. Similar considerations apply here. Whilst there is perhaps a closer correlation between the degree of clinical disability and the extent of the radiological opacities in the infected than in the simnle form of pneumokoniosis, this is by no means absolute and there may even - ro disability at all. The discrepancy probably depends upon the coexistence of bullous emphysema, generalized emphysema, simple pneumokoniosis or active infection, singly or in any combination. The separation of disability due to pneumokoniosis from that due to associated diseases may again prove difficult. The presence of active tuberculosis in massive lesions is often revealed as " fluffy " shadows on the X-ray film, but clinical evidence of such infection may not be apparent until the later stages. Occasionally bacteriologicai examination demonstrates tubercle bacilli in the sputum. . Although the assessment of disability on the basis of clinical or X-ray examina tion leaves much to be desired, the current practice of combining the two methods does achieve a reasonable degree of accuracy in experienced hands. If such examinations are carried out prior to and at intervals during the occupational exposure to dust a continuous record is provided for each man and, from the South African experience of silicosis, it appears that many errors of assessment can thereby be reduced (Orenstein, 1938). The supplement of a simple objec tive physiological test would provide a measure of disability instead of relying on personal judgement. Because a miner is physically disabled by pneumokoniosis it does not necessarily mean that he is incapable of any other work. If he can work it is most desirable that he should do so in his own as well as in the national interest. The rehabilitation of disabled men entails a complete know ledge of their physical capacities together with the type and maximum physical requirements of the alternative occupation. These factors must be equated in each case. ' 1948-1949] HEPPLESTON- TKE i There are two main aspe> Engineering. The basic requirement f< preferably at its source, c* that dusts of very different be to eliminate all forms of Apparently more attenUon Orenstein (1947) suggests i particles from the air. Medical. Short of prevention the removal from the dust haz ideal is removal at the earth necessitate a modification i The eradication of infecti ance. Ideally, tuberculosis with a dust hazard, and a must be removed from his avoid the possibility of infe These objects can only b medical examinations for al include a full industrial hit when practicable, physiolof certain cases. To interpre essential to correlate them cl Much has already been dor (Irvine, 1935-1938; Smith, Poucard, 1938), and Gou< Welsh coal workers. In So British industries clinical an cally with appreciable succe tion may prove to be the rr men whose physical feature pneumokoniosis or tubercul Initial and periodical met hazard provide information koniosis in the population between the incidence of remainder of the working f in the fact that the value of ing or medical, must ultima the disease in both its fo supervision will be necessar coming. It is desirable th continue after exposure to d silicosis shows that this form 1938; Smith, 1947), as migh Welsh coal workers, where in the simple form of the d but this contention requiri continued supervision of c. employment is the detection Infected pneumokonios.s, v. transactions- the institution of minino engineers (Vol. 108 462 a rr'zrs; h'sr<s*.*^ accordingly men sufferingJrom U -- . member . Z P^ao. pneumokoniosis is far from settled TTi ; d DelaHANT (1944) leaves and Irwin (1937, 1939) and of G a in e r ^ ^ d " " rrested by the inhalation no doubt that silicosis in animals c ^ P ^ nevertheless believe that alumina of aluminium or alumina dust. G abon h c l i , clinical trials in Canada, ,, y irtfluccc unf^vouy.bly " bicc.i.c t o . . 1 5 5 * . using aluminium powder, on 34 silicotic p cptiombie Blaispell, and and832% showed objective evidence ^ ^ w i t h ^um inium MacPherson, 1944). These authors b e t o e t o t * * TM o{ powder of respirable size offers every prospect of p r e v e n t ^ ^ human silicosis. Other workers, however, whether aluminium therapy in the treatment of the disease. f 11 "J i L ^ e sycosis as judged by X-rays, has ever caused the regression of established^simpl ^ ^ mu$t there. and as a preventive measure the method r" " fore be subjected to the strictest medica silicosis aluminium is believed to act by ovPer a prolonged period. In . . _jjjca particles with an 8 so preventing " solution " insoluble and impermeable layer 0 a theory, however, aluminium of the silica in the body fluids. On "nica tetrahedra to form a combines with the unsatisfied oxygen (Denny, Robson, and surface layer of alumina, so Irwin, 1937). It has been suggestedl that th _ b e n e den ^ aluminium ^ of i treatment may depend on quite a diff cedhjn ^ o{ this contention. bronchial spasm. No evidence has be . . , the Simple pneumokonioses which must therefore be regarded as sp chemical or physico-chemical due to dusts with a low free s.hca-con ent the cJ e^ 1CalminiuPrnymay havc no ssslse sl '~ r H r i r -- wrirf"* tooric. of 1, action n , not be *PP" " ''l " "" " . to t o t altodv substitute for the accepted methods of dust control. PRIMARY CARCER OF THE LUNO IN RELATION TO PNEUMOKONIOSIS. south Africa to r e is no c i d c n c to..uE Sct t o . frequent in silicotic miners than in non-silicotic min VorwalD and Karr adult males in the general population (1938) from America state that there is no r 6 .P or experie recognized 2 3 S , s t o S S radium'and ^ ^ -5 and coal workers' pneumokoniosis. REFERENCES. Agricola (1556). See Rosen pp^ 59 and 60- industrial Hygiene, No. 19 " Begbie, I. W. (1866), C l a s g m e d . A, 3rd senes, 1, 13 and 169 Coun,, No. 243. Belt T. H.. and F erris. A. A. (1942), Spec. Rep. er. mea p. 203. (London, H.M5.0.) N 25o, p. 29 Belt-, T. H,, and Kino, E. J. (1945), Spec. Rep. Ser. med. Res. Coun., no (London, H.M.S.O.) 1948-1949] h eppl esto n --fntu Capian, A. (1947). Proc. Coni, o Mines, Instn. Mm. Engrs. Cox. W. I. (1857), Bril. med. K P raw J. (1947). Proc. Conf. or *Mines, Instn. Min. En^rs, Croizier. L., Martin, E., and Poi (Paris, Masson et Cic.) Crombie, D. w ,, Blaisdell, 1. I 50, 318. Cummins, S. L., and Sladden, A. Denny, J. 3-, Robson, W. D-, anc Denny, J. J.. Robson, W. D , am Drinker, P. (1925), J. industr. H: F enn, W. O. (1920-21). J. get. 1 Fenn, W. O. (1922-23), J. gen l G ardner. L. U. (1923), Amer. R G ardner, L. U. (1932. J. indust G ardner. L. U. (1934). J. Amer. G ardner, L. U. (1935), Int. Clir G ardner, L. V. (1937a). J. Instr. G ardner, L. U. (19376), Third S G ardner, L. U. (1938). See Un. G ardner. L. U. (1939), Fourth i G ardner, L. U. (1940), J. Amer. G ardner, L. U., and Cummings G ardner, L. U., D worski, M.. G eorge, W. E. (1938). I.L.O., G ough, J. (1944), Rep. Adv. Cor Wales Region suflenng Ii G ough, J. (1947). Proc. Conf. Mines, Instn. Min. Engrs. G raham, T. (1834), Edinb. med. G ye, W. E., and K ettle, E. h . C ye, W. E., and Purdy, W. 3. ( G ye, W. E., and Purdy, W. 3. ( H ale, L. W. (1946). Thorax. 1, H art, P. D 'A., and Aslett, E p 48. (London, H.M.S.( HEFFERNAN, P. (1935), Tubercle H effernan, P. (1944), Brit, med H eppleston, / G. (1947), J. P> International Labour Office, Prt No. 17, p. 96. Irvine, L. G. (1935-38). Trienn. Irvine, L. G. (1938), I.L.O., Se lENKINS, T. H. (1948), Proc. S Kino, E. I. (1938), I.L.O.. Serif K ing, E. 3. (1945), Spec. Rep. S K ing, E. 3., and N agejjchmid p. 1. (London, H.M i.O Lanza, A. J. (1938), Silicosis a Lehmann, G. (1933), Arbcitsph, Mavrogordato, A. (1926), Pul McCrae, J. (1913), Publ. S .A) McM ichael, 3-, Hart, P. D A p. 120. O renstein, A. 3. (1938), 1 L.C Orenstein, v4. 3. (1947), First Peacock, T. B. (1860-61), Tra VOL. 10S-I9M -I949  1948-1949] HEPPLESTGN--PNEUMOKONIOSIS AND DUST SUPPRESSION 463 , ENGINEERS IVol. 108 ip indefinitely after their rtPLAN A (1947) Proc. Conf. on Silicosis. Pneumokoniosis, and Dust Suppression in Min, Instn. Min. Engrs. and Instn. Min. Metall.. London. oes develop, the members fection in them, id treatment of human g * Wi \ l 9AT) ! Pw!'^Coin f /o n Psmcosis, P?eu^ ^ ? s 0adn0,, DuSt SuPPression m ' Mines Instn Min. Engrs. and instn. Min. Metall.. London O . o . i t 't E,, and POLICARD, A. (1938). Lo Fibrose Pulmona.re des M,neurs. vork of D enny, Robson, t D elahant (1944) leaves Crombie* !)! w ! SBw is d ^ , , J. L., and M acPherson, G. (1944), Canad. med. Ass. J.. irrested by the inhalation eless believe that alumina Clinical trials in Canada, ubjective benefit in 55%, Crombie, Blaispell, and ratment with aluminium nting the development of ;hieved the same success icther aluminium therapy osis as judged by X-rays, iven. Its use must therea prolonged period. In silica particles with an so preventing " solution " CUMMINS s ' L,, and Sladden, A. F. S. (1930), J. Path. Bad.. 33, 1095 n r t Z 1 J Robson W. D., and Irwin, D. A. (1937), Canad. med. Ass. J.. 37, 1 K ' ! : w. D.; and irw ,n. d. a. 0939). canad. ,,/. /.. 40,2.3. DRINKER, P. (1925), J. industr. Hyg.. 7, 305. Fenn, W. O. (1920-21), J. gen. Physiol.. 3, 575. Fenn, W. O. (1922-23),./. gen. Physiol.. 5, 311 G ardner, L. U. (1923), Amer. Rev. Tuberc.. 7. 344. Gardner. L. U. (1932, /. industr. Hyg.. 14, 18. Gardner, L. U. (1934), /. Amer. med. Ass 103,, 743. Gardner, L. U. (1935), Int. Clin, senes 45, 2, 15. G ardner. L. U. (1937a), J. Instr. Hyg.. 19, 111. . _ G ardner, L. U. (19376), Third Saranac Laboratory Symposium on Silicosis, p. 70. G ardner L U. (1938), See Lanza, A. J., pp. 285, 331. G ardner', L. U. (1939), Fourth Saranac Laboratory Symposium on Silicosis, p. 3 . ory, however, aluminium ica tetrahedra to form a rt (Denny, R obson, and G ardner! L.' U. (1940), /. Amer. med. ^ ..1 1 4 , 535. G ardner L U. and Cummings, D. E. (1933), Amer. J. Path.. 9, 751. G ardner' L.' U., D worski, M.. and D elahant, A. B. (1944), /. Industr. Hyg.. 26, 211. derived from aluminium m, namely, the relief of A f tiS on' "Deatment* and Rehabilitation of Miners in the jpport of this contention, ic simple pneumokonioses lical or physico-chemical aluminium may have no ore dust to that already account be regarded as a GouoH^j!e(lM7),'Proc.^Coiff. ^on"SH icos^^e^okon'm sis and Dust Suppression in Mines, Instn. Min. Engrs. and Instn. Min. Metall., London. . G raham, T. (1834), Edinb. med. /.. 42, 323. G ye, W. E.. and K ettle, E. H. (1922), But. J exp. Path.. 3, 241. - G ye, W. E., and Purdy, W. J. (1922), Br,t. J. exp. Path 3, 75 and 86. Gye, W. E,, and Purdy, W. J. (1924), Brit. J. exp. Path.. 5, 238. Hale, L. W. (1946), Thorax. 1, 71. ,_ _ *. , , , HART P. D'A , and ASLET", E. A. (1942), Spec. Rep. Ser.med. Res. Conn.. No. 243, ) PNEUMOKONIOSIS. pulmonary cancer is more or in a similar body of 8). Vorwald and K arr , post mortem or experi dust (except recognized an increased incidence of Wales, although not yet n regard to both silicosis ' p. 48. (London, H.M.S.O.) H effernan, P. (1935), Tubercle, 16, 397. Heffernan, P. (1944), Brit. med. /., 2, 706. Heppleston, A. G. (1947), /. Path. Bad.. 59, 453. International U bour Office, Proc. Internal. Conf. onSilicosis, _ Geneva. iq ,,, cprl, , c 1938. Series F. Irvine^L . g !'(1*935-38), Trienn. Rep. Miners' Phthisis Med. Bureau, Johannesburg. Irvine, L. G. (1938), I.L.O., Series F, No. 17, pp. 66 and 151. Jenkins, T. H. (1948), Proc. S. Wales Inst. Engrs.. 64, 39. K E I S 's ^ R S ^ r ^ R d . l o l l . No. 250, p. 69. (London, H M S > 1 2 I L and Nagelschmidt, G. (1945). Spec. Rep. S e , med. Res. Coun.. No. 250, p. 1. (London, H.M.S.O.) Lanza, A. J. (1938); Silicosis and Asbestosis. O.U.P. Lehmann, G. (1933). Arbeitsphysiologie. 7, 167. M avrogordato, A. (1926), Publ. S. Afr. In, med 3, No. 19, p. 1. McCrae. J (1913). Publ. S .Afr. Inst. med. Res.. 1, No. 3, 11/. dustrial Hygiene, No. 19." 'ales. McMichaeL, J., Hart, P. D'A., and Aslett, A. E. (1942), See Hart and Aslett (1942), p. 120. !t 69. med. Res. Coun.. No. 243, S ^ ^ ^ K ' ^ r ^ ^ ^ I n s t n . Min. M etal, London. Peacock, T. B. (1860-61), Trans, path. Soc. Lond.. 12, 36. Res. Coun.. No. 250, p. 29 VOL. 108--1948-1949 I