Document wKXb7jgr9JwY2q928XndX8Y4Q

-;.m^ku JR. . Upecirruzn* ^"JSVE irectur of pnihujqJJ ents. ^.ppoJmed h0noniry iatrJc clinic f ( appointed honorary <*i section of ^ appointed honorary n of the RoyZ tfK . Medical Poliuea Meeting'. I.A.: Ethic* Cob- antJi3otirc. to apply for any first communicated xmcerned, or with dical Association, 7. 13$ Macquarie appointment* la cal Society Ball, services Limited; jFreadliearnalPrudMeuntutiaall Provident Club; or other appointM.A, House, 32$ <bane Associated ndaberg Medical ppointroents and any COUNTRY are advised, in Hr Agreement to try, l?9 North -tents in South neats in South -ary, 20$ Stint al; all Contract a. All govern* ' those of the Journal cannot I articles for* ffered to Tss e contrary he e Editor, Tms louse. Seamer MW 26S1-2.) the Manager. Street, Glebe, ilarity in the >t accept any jf non-receipt within one others sot 1InAsvsiortcuiaetioonf ie Journal by ts and book* nlng of any t rate Is 3 lonwealtb of and foreign PLAINTIFF'S EXHIBIT CSS-546 THE MEDICAL JOURNAL OF ausirml II.--'Vol. 37th Yeah. SYDNEY, SATUKDAY, `NOVEMBER 25, 1050. Table of Contents. (Tbe Whole of the Literary Matter la THE MEDICAL JOURNAL OF AUSTRALIA Is Copyright.} original articles-- - Pass.. Occupational Factors In Pulmonary Dust Disease. by Gordon C. Smith. M.B.. B.S...........................777 The Changing Face of Obstetric Infection, by Arthur M. Hill. M.D., D.G.O., F.R.C.S.E., F.R.C.O.G................................................................. 782 Torsion of the Testis and its Appendages, by S. H. Lovell ................................................................. 78" Hepatitis; Treatment with Brewer's Yeast, toy Neville Davis. M.B., Ch.M.................................. 790 Immunization Against Tuberculosis in Australia and New Guinea, by E. A. North. M.D.. M.R.A.CP.. and D. Jamieson. F.R.F.P.S.. M.R.C.P.. B.fic.. D.T.M. and H........................... 792 REPORTS OF CASKS-- Stiunmous Epithelioma of the Renal Pelvis: A Case Report, by V. S. Howarth....................... 79? REVIEWS-- Pye's Surgical Handicraft ..................................... 798 Paraphitic Portraits .. .. ..................................... 799 Obstetrics and Diagnostic Cynsecology .. .. 799 Diphtheria Prophylaxis............................................ 799 Asthma and Cold Therapy..................................... 900 Autobiography .......................................................... 900 BOOKS RECEIVED.......................................................... 900 LEADING ARTICLES-- A Considered Statement on PAS.............................. 801 CURRENT COMMENT-- Advances in the Field of Cortisone and ACTH .. 802 An Australian Contribution to Genetical Knowledge 803 ABSTRACTS FROjT MISTlCAL LITER A TURK-- Obstetric* and Oynwcology.................................... BRITISH MEDICAL ASSOCIATION NEWS-- Scientific ................................................................ CORRESPONDENCE-- The Australian Tuberculosis Association .. . Acute Myocarditis.................................................. . An Efficient Resuscitator .................................... OBITUARY-- Edward Albert Woodward.............................................. DISEASES NOTIFIED IN EACH STATE AND TBitRITORV OK AUSTRALIA ..................................... POST-GRADUATE WORK-- .. . The Post-Graduate Committee in Medicine in the t . , University of Sydney ..................................... NAVAL, MILITARY AND AIR FORCE-- Appointments .......................................................... MEDICAL PRIZES-- The Australian Orthopaedic Association. Prize, 1952 NOMINATIONS AND ELECTIONS .............................. DIARY FOR THE MONTH.............................. . .. .. MEDICAL APPOINTMENTS! IMPORTANT NOTICE .. EDITORIAL NOTICES ................................................... OCCUPATIONAL FACTORS IN PULMONARY DUST DISEASE.' By Gordon C. Smith, M.B., B.S., JntfRsfriol Health Unit, School of Public Health and Tropical Medicine, Sydney. The Third International Conference of Experts on Pneumonokoniosis, held recently in Sydney under tbe auspices of tbe International Labour Organisation (I960), adopted the following definition of pneumonokoniosis: "a diagnosable disease of the lungs produced by the inhala* tion of dust, the term `dust' being understood to refer to particulate matter in the solid phase, but excluding living organisms" (the term "diagnosable" indicating the presence of signs or symptoms, but not always loss of function). The implications and scope of this definition are very wide. Whilst pneumonokoniosis in the etymological sense deans "dust in the lung" and therefore is applicable to the pulmonary reactions due to all types of dust (and fumes), in practice it has been associated chiefly with silicosis, ashestosis, and in recent years with the lung disease due to coal dust--diseases in which permanent fibrosis occurs and with characteristic radiographic abnormalities. Of late it has become evident that acute, semiacute and ehronic pulmonary conditions may result from inhalation of a variety of dusts, both organic and Inorganic, other than silica, asbestos and coal. Although the nature and severity of tbe tissue reaction vary according to tbe type of dust and conditions of exposure, the term pneumono koniosis can be applied to these conditions. 1 Read at a meeting of the Section of Public Health. Tuberculosis, Tropical Medicine and Industrial Medicine, Aus tralasian Medical Congress (British Medical Association), Seventh Session. Brisbane, May-June, 1960. The Occupational History in Pneumonokoniosis. 1 Whilst the diagnosis of pulmonary dust disease she never be made without proper consideration of tbe occl tiona! history, medical history, clinical examination i radiographic findings, the first 1b of special imperial Unless there has been exposure to dust of a barm nature there cannot be a pulmonary dust disease, matter what the medical history or clinical examinat: might indicate, and no matter how closely the rad graphic appearances of tbe lungs simulate those pneumonokoniosis. Thorough and detailed inquiries should be made abc any process in which the patient may have been expos to dust--tbe nature and conditions of tbe work, tbe ty of dust and duration of employment at the process. Unfe these particulars are obtained accurately, the industri history may be rendered invalid, with resultant error . diagnosis. Negative evidence as to dust exposure is : important as positive; pneumonokoniosis has been dia nosed in certain individuals with auspicious radiograph signs, evidently on the film appearances alone, for proper inquiry as to the nature of their work would faav revealed uo history of industrial dust exposure in thes cases. Properties of Oust in Relation te its DiseaseProducing Capacity. Although all dusts, if inhaled in sufficient quantitiee may be regarded as being potentially harmful, some ar< known to be considerably more injurious than others Important information concerning tbe potential capacity o: a dusty environment to cause disease of tbe lungs can b( obtained from a study of the following factors: (i) the composition and nature of the dust, (fi) the site of the dust particles, (iii) the intensity of exposure, as determined by (o) the atmospheric concentrations of the dust, (t>) the duration of exposure. 778- thk mi:i)h:a(, journal of Australia. Novkmk *jr>. u>:.i>. The Composition of Dust. tightly cemented typ\ dust high in free silica would he An analysis for the chemical or mineralogical con stituents should be carried out on any dust suspected of j generated, rupture it. because more euergy would be required to causing pneumonokoniosis, and. preferably, the air-borne j dust should be examined. | The Particle Size of Inhaled Dust. The most injurious component of an industrial dust is crystalline free silica (uu. ombined silicon dioxide--SiO,). The pulmonary reactions from amorphous or non-crystal line free silica are less severe, while silicates, that is. silica in a combined form, with the notable exception of asbestos (a hydrated magnesium silicate), are less harmful than free silica. ' Most minerals which contain silicates also contain some proportion of free silica; compounds of other elements, such as iron, aluminium, calcium, magnesium and potassium, may also be present. Because of the possible modifying or inhibitory influence of certain substances on the action of free silica, the analysis should be not only for free and combined silica, but also, where indicated, for other likely The pneumonokoniosis conference concluded that in the case or fibrous dusts, such as asbestos and certain vegetable dusts, the larger sizes appear to he more harmful, whereas in many mineral dusts the smaller sizes seem to be the most injurious. In general, whilst particles of mineral dusts (except asbestos) exceeding five microns in size are of minor importance, tbe lower limit of tbe size of particles causing pneumonokoniosis has not yet been determined. Particles of the harmful size range cannot be seen with the naked eye, and it is well to remember that a dangerous concentration of dust of this particle size may be present in the air without being seen. A visible dust cloud may contain fine harmful particles as well as those of larger innocuous size. constituents, especially if these by themselves are capable The actual number and size distribution of dust particles of producing a lung reaction. depend upon the method by which dust is produced and In regard to metallic dust and fume, even though there may be no question of tbe presence of silica, the con centration and chemical analysts of the atmospheric con taminant should be determined in order that a proper appraisal of the suspected hazard may be made. - the nature of the parent material from which the dust | is derived. Experience in New South Wales, like tbat of | investigations elsewhere, is- that at least 70%, and in some cases over 90%, of dust particles generated in industrial processes are up to three microns in size. About 5% of coal dust particles and only about 1% of sandstone particles In tbe case of siliceous materials, as a general rule and other conditions being similar, the higher the percentage of free silica in a dust, tbe greater is its capacity to produce disease. When pulmonary disease is caused by dusts which contain lower percentages of free silica than, are over five microns in size. Thus not only is there a. relatively small production of the larger particles, but such particles settle out from tbe atmosphere more rapidly than the smaller sizes. Further, it is known that only a portion of inhaled dust is retained permanently in tbe say, sandstone or Quartz, greater exposures due to higher atmospheric concentrations of dust, or to a longer working j lungs, most particles of about five microns and larger being removed by the physiological mechanisms of the nasal and period, or both, are necessary. Thus pneumonokoniosis has upper respiratory passages. been found In men engaged In "dragging" bricks from continuous or pateot kilns. Tests in New South Wales have shown these men to be exposed to very high con centrations of dust containing about 25% of free silica. In a recent review of this subject Hatch (1950) suggests that particles smaller than one micron in size may be the principal contributors to silicosis production. Yorwald (2950) showed in animal experiments that "amorphous" The pulmonary changes in coal miners are out of pro silica of particle size down to 0*005 micron produces pro portion to what one would expect, having regard only to found lung changes, and states that the rate of tissue tbe free silica content of coal dust, which Smith and Whaite reaction to dust is inversely proportional to particle size. <1950) found averaged 1-8% in the under 10 micron fraction of sixteen samples collected from the coal face of five collieries in New South Wales, but a long period of `xposure seems necessary to produce disabling pneumono<oniosis. On tbe other hand, in regard to asbestos, it appears tbat the larger particles are more harmful than the smaller and that in the lungs they act as mechanical rather than as chemical irritants (Gardner, 1938). Wyers (1949) states that dangerous fibres measure about 20 microns. Asbestos, which contains no free silica, produces s severe mlmonary disease, but tbe mode of action of the asbestos ibre differs from that of the silica particle. Oust Exposure, In general, exposure is measured in terms of concentra The pneumonokoniosis conference agreed that an analysis tions of air-borne dust and tbe period of time during which it material from which dust is derived does not of tbe individual is exposed to those concentrations; tbe lecessity represent the composition of the dust Inhaled in higher the average concentration of air-borne dust, and tbe .n industrial process. Tbe free siiica content of air-borne longer the period of exposure, the greater will be tbe risk lust may be similar or may be appreciably increased or of contracting pulmonary dust disease. iecreased. compared with that In tbe parent material, .ccording to tbe nature of the material and type of industrial process. In the case of silicosis and related types of pneumono- koniosis, including asbestosls, the disease is usually of gradual onset and slow development. It does not become Tbe problems associated with exposure to mixed dusts. evident until after exposure for a period of years, the >r example in foundries, are of interest Foundry dusts actual time varying according to the type of dust and my comprise a mixture of carbon, free silica, silicates, industry. on oxide and other metal particles, as well as particles *om carborundum and othet^etbra^ive. materials. Iron Meiklejohn (1949) states that under present conditions in Great Britain silicosis In a diagnosable stage seldom xlde may play some part In -tbe production -of-the nodular ladows seen in radiographs and may influence tbe action f silica in the lungs of certain foundry workers apparently occurs in under fifteen to twenty years' exposure to the risk, and In regard to coal miners,- McVittle (1949) pi* a similar period for the development of pneumonokofliosis- Tected with silicosis. One may also question whether jy of the nodulation seen in films of grinders with jparent pneumonokoniosis is due to particles from metals - synthetic abrasives. I ! My own observations on a group of 416 New South Wales coal miners showed that tbe average period of exposure the men with disabling pneumonokoniosis was thirty-tour The physical nature of substances, whether hard and y or soft and wet, influences their capacity to produce ;at. Thus the fact that work is being done in sandstone -es not necessarily mean that there will be a serious dust ! J j I years, their average age being fifty-four years. Asbestosls apparently occurs after a shorter exposure. Thus Wyers (1949). who investigated 115 fatal cases asbestosls, found the average exposure had been 10*4 years- -zard, despite the high free silica content of the rock. ( Under conditions of intermittent exposure tt Is mors th* -k was wet and soft, little or no dust would be difficult to predict the likely effect on tbe lungs than * " breaking it up. whereas if it was of a dry, ; the exposure was continuous, but the severity of any a baza i howe expos in perio< genev monti instar. TCSCti The "acute expos'. follow In / weeks of his he waFrom fifteen, for twi In the using pick" J His (on tw had let 17 day; the las of "blit. At e silicosis Mlcrosc immatu to nodi; In O Jndustr: in the been en picks a Neverth from 11 Owens's in 193? doubt lb dust inh Occi dust con commone mining o surfacing and mou in iron 1 milling s brick ind lecture ol handling several of specially but still Pneuino other pap to asbest this count It is muc) cessing example, In recei (2949) an of tbe res silica, coa due to vci I propos lung disoi of tbem industries carried ou so w she risks. Till-; MKDICAL JOURNAL OK AUSTRAL) A. OUl(3 ^ tired to t la the tgeuble whereae * be the mineral 1 are oarticiea lined. en with mgeroue Present >ud nay f larger % nartides eed and he dust that of in some dustrla! t 5% of articles there a les, but rapidly t only a In the er being tsal and suggests may be Vorwald rphous" ces pro f tissue t size. ars that smaller tr than ) states ncentrag which os; tbe and tbe the risk mmonetally of become irs, the jst and ldltiODS seldom to the ) gives oniosls. i Wales sure in rty-four posure. ases of i years. s more than if ly dust hazard is usually lessened in such circumstances. This, : Before referring, jo these, however, I wish to make a \ *^eVer. might not apply with very high intermittent | few comments about the lung changes which have been Atposui es. observed in basalt workers and biograph operators in New In the case of metallic and vegetable dusts, the exposure ` South Wales. eriod necessary to produce a pulmonary disturbance is Merally much shorter than with other dusts--sometimes BasaU Work. ' months or weeks, or even less, rather than years. In some Basalt (or "blue metal") is a basic igneous rock, com * jastances a single exposure may be sufficient to cause a posed essentially of a lime-bearing feldspar with smaller action. amounts of one or other of the ferro-magnesian minerals - The literature contains reports of the occurrence of and a little iron oxide. Free silica is typically absent but teste" or "rapidly developing silicosis*' after short may be present up to 2%. Thus basalt is a silicate, with (jposures to high concentrations of silica dust, and the 40% to 50%_oTsTlica in fiproj&jned form (Whitworth, 1947). following notes about a Sydney case are of interest. Badham (1927) described a case of fine fibrosis of tbe " Id April, 1942, a man, aged thirty-eight years, died three i lungs in a man, aged sixty-one years, who for twenty-five - weeks after he had collapsed at work. The significant details ' years bad worked in a blue metal quarry and crusher bouse f his industrial history were as follows: From 1917 to 1919 lie was engaged in coal mining (Cessnock) for two years, from 1931 to 1937 he was with the Water Board, including fteen months on rock work. From 1937 to 1940 he was for two years a builder's labourer, excavating in sandstone and was exposed only "to tbe dust of orthoclase basalt, which contains no free silica". This man died, but an autopsy was not performed. In recent years I have seen two men, aged forty-nine 1b the sub-basement of a building. Latterly he had been years and fifty-tbree years respectively, wbo, as far as using a "water pick", but earlier had been using a "dry could be ascertained, bad been exposed only to basalt dust. pick" for six months. Bis chest had been examined by X rays in 1937, 1940 (on two occasions, the second being some weeks after he bad left the basement excavation work), and again in 1942, 17 days before his death. It was only in the film from the last examination that the radiologist reported evidence of "bilateral nodular fibrosis". Tbe first man bad been a crusher attendant for fifteen years at tbe same quarry as Badham's patient, and tbe second had worked chiefly on tbe crusher and screens for thirty.five years at another blue metal qnarry. Tbe radio graphs of both men showed a well-marked, generalized, fine type of nodulation throughout the lung fields; in tbe At autopsy, aortitis, congestive cardiac failure, and film of the first man, wbo was totally disabled, there were silicosis of the "rapidly developing" type were found. also large shadows suggesting consolidation. Microscopically the lungs showed generalized, somewhat immature fibrosis, mainly diffuse, but with some tendency to nodular arrangement. In October, 1939, the New South Wales Division of Biograph Operating. Two brothers, whom I first saw in 1947, were aged Industrial Hygiene bad investigated the working conditions forty-one and forty-six years respectively and had both in the basement of the building where this patient had worked in tbe projection booth at the same suburban been employed. Water jets were fitted to the pneumatic cinema--tbe elder for ten years and tbe younger for picks and an exhaust ventilation system was installed. twenty-three years. There was no history of exposure to Nevertheless concentrations of sandstone dust, ranging dust in other employment. Tbe elder man complained of from 1150 to 10,000 particles per cubic centimetre (by shortness of breath and loss of weight; his brother, of Owens's dust counter) were obtained. The dust conditions pains and tightness in tbe chest. Tbe chest radiographs in 1937 were probably worse than in 1939; there is little of both men were similar and showed a generalized fine doubt that this patient contracted silicosis as the result of uodulation throughout both lungs. Films of both men taken dust inhalation during the period 1937 to 1940. In 1949 showed no significant change since 1947. Occupations, Dusts et cetera, Associated with a Pneumonokoniosis Hazard. In 1946 the New South Wales Division of Industrial Hygiene had found that the concentration of dust in the air of the biograph box in the cinema concerned was Tbe most important risks are those where exposure to dust containing free silica is likely to occur. Among tbe commoner processes involved are tunnelling, excavating, mining or quarrying in sandstone or quartz; cutting and surfacing of sandstoue or granite; sandblasting, dressing and moulding in foundries, especially machine moulding approximately 6000 particles per cubic centimetre of air by the Owens dust counter; the dust particles were mostly about half a micron or less in size. The ventilation in the box was faulty. A sample of dust obtained from the biograph room in 1946 on analysis gave tbe following result. in iron foundries if siliceous parting powders are used; milling siliceous ores; certain pottery processes; in tbe brick industry, chiefly "dragging" in patent kilns; manu facture of abrasive soaps and powders; manufacture and handling of refractory materials, and metal mining. In several of these instances, and in a number of others not specially mentioned here, the dusts are of a mixed nature but still coutain significant percentages of free silica. Pneumonokoniosis of coal miners has been discussed in other papers and will not be further considered. In regard to asbesiQsis, which is of very infrequent occurrence in this country, all the evidence from overseas indicates that it is much more common in workers engaged in tbe pro.cessing and fabrication of asbestos in factories (for example, textile work) than in asbestos miners. In recent reviews of the literature. Perry (1947), Doig (1949) and Middleton (1950) have described disturbances of tbe respiratory organs due to mineral dusts other than silica, coal and asbestos, and have discussed the reactions due to vegetable dusts. Total SJOj................ Hare earth oxides .. Al-Oi: Fe*0* .. . CaO ....................... Loss on ignition .. Copper ................ Fluorides ................ PfO* ....................... SO* ....................... 60% 490% 17-0% 6-7% 3-0% Trace Present Present Present Following tbe discovery of the unusual pulmonary con dition in tbe two brothers, seventeen biograph operators from fourteen other theatres were submitted to X ray examination. Their period of employment ranged from seven to thirty-seven years, and some bad worked in badly ventilated bootbs. However, no evidence of a lung reaction resembling pneumonokoniosis was found. Several authorities have investigated gases, fumes and dusts from carbon arcs and the ventilation of motion picture booths. MacQuiddy and others (1939) 6bowed that some of the high-Jntensity carbon arc ashes appear to cause mildly proliferative reactions when injected intraperitoneally in the albino rat. They state that it might be I propose briefly to mention the more important of these lung disorders, because, although to my knowledge most of them have not been reported in this country, the industries or processes involved in their causation are carried out here or may be conducted in tbe future, and so we should be familiar with the possible occupational deduced that, if inhaled in sufficient quantities over long enough periods of time, these ashes might cause a pro liferative type of pneumonokoniosis. On tbe limited evidence at present available, and in the absence of autopsy studies, it is not possible to say wVknd the lung condition present in these basalt w^pulmonary risks. biograpb operators is due to dust. Furthexception) the 780 TIIK MKDH-AL JOURNAL OK AUSTRALIA. Xovkmhku 2.7, l`.C>0. r'esponsible, the question arises whether it has causal fibrosis or is merely present as inert deposits. It seems reasonable to associate the radiographic abnor malities of the basalt workers with inhalation of dust at their employment, but in the case of the hiograph operators, whilst occupational factors cannot be ruled out (indeed, one of these men was compensated for ''silicosis''), as they were brothers, and as examinations of other operators cave negative results a non-industrial etiology has to be considered. Although these cases are incomplete, I mention them In order to emphasise that with present advances in industrial activity and with increasing knowledge of pneumonokoniosis, we must constantly be watching for lung con ditions due to dust, not only from new processes, but also in industries and occupations where previously they have not been suspected. Talc. Until comparatively recently asbestos was considered to be the only harmful silicate. Now, however, there is evidence of several investigators that talc, a hydrated mag nesium silicate which occurs in flaky and fibrous forms and is used in a number of industries, may cause significant lung changes. McLaughlin, Rogers and Dunham (1948) described a case of pneumonokoniosis confirmed at autopsy in a man, aged fifty-one years, who had worked for thirtyseven years in a rubber tire factory, where he had been exposed to a "fair concentration" of talc dust, and who died primarily from rheumatic endocarditis. There was much fibrosis in the lungs and curious bodies similar to absestosis bodies were also present. These authors con clude that tale pneumonokoniosis and asbestosis are similar diseases, and that pneumonokoniosis is probably caused only by the fibrous varieties of talc. Graphite. Doig (1949) and Middleton (1950) refer to recent reports by other authorities in Britain, chiefly Dunner and Gloyne, concerning pulmonary disease in graphite workers. According to Harding and Oliver (1949). graphite (plumbago), which is a crystalline form of carbon, may be mixed with up to 10% of free silica and with other minerals. They point out that grinding of natural graphite produces the greatest dust risk and can lead to a disabling and fatal pneumonokoniosis, which they describe as resembling, both radiologicalJy and histologically, that of South Wales coal workers. Other Silicates. Abnormal reactions is the lungs of animals or man have been described following inhalation of dust from china clay, mica. Billimaoite and fuller's earth. Cement. Cement is mentioned here because of its very widespread use and of questions which periodically arise as to its possible harmfulness. The raw materials from which cement is made are chiefly limestone, which has not more than about 1% of free silica, and shale, which may contain from 20% to 40% of free silica. The finished product has practically so free silica. Gardner and others (1939) examined 2278 employees from 11 cement-making plants in the United States of America. Only eight persons showed evidence of nodul&r fibrosis attributable to dust, and in six of these exposure to silica dust in previous employment was presumably responsible. Baetjer (1947) showed that in rats exposure to high concentrations of cement dust did not lower resistance to lobar pneumonia and did not produce any acute or chronic pathological changes in the lung tissue. Metal Fume Fever. The well-known example of a minor pulmonary reaction, if *'h!. Nme fever, due to fume rather than to dust, mostly r-e exposure to zinc oxide fumes, for example, in xor n Di or jrom welding on galvanized iron. It is said to be caused also by futm% uf other metals. \Vln-n it is due to zinc there is an acute febrile reaction or chill, of short duration, and with no permanent lung damage! If other metallic oxides, such as cadmium or manganese, are involved, a more serious pulmonary condition may ensue. Cadmium. Johnstone (1948) states that "cadmium has probably more lethal potentialities than any other of the metals". The inhalation of dust or fumes from cadmium compounds, especially the oxide (for example in welding on cadmium! plated surfaces, from the ignition of cadmium and from the use of cadmium in-solder) produces *rrUaat effects, which may be severe, in the respiratory tract, perhaps with pulmonary cedema and death. Beryllium. The literature on the pulmonary (and other) lesions affecting workers exposed to beryllium is now extensive, many reports having been published during the past five years. Abstracts of the various papers and articles were recently made in Australia by Taylor (1949). Two prin cipal types of pulmonary lesion have been described: an acute pneumonitis and a chronic diffuse granulomatosis. A number of fatal cases have occurred. It appears tbat the acute form which may follow a single exposure to toxic fumes occurs mainly among workers exposed to compounds in the extraction and refiuing of beryllium from the ore beryl, usually within a few weeks of the first exposure. '. . The chronic or delayed form, which resembles sarcoidosis, is more persistent. A period of from several weeks or years may elapse from the time of the last exposure to the onset and recognition of the disease. This type usually occurs in persons who have been exposed to dust from fluorescent powders containing zinc beryllium silicate, notably in the fluorescent lamp industry. However, eleven cases of the chronic type were recently reported amongst residents in the vicinity of a beryllium-producing plant There was no history of occupational exposure (Eisenbud and others, 1949). Manganese. Doig (1949) mentions that since 1521 a relationship between manganese and pneumonia has been suspected, following reports from Norway and Germany. In England, Lloyd Davies (1946) found tbat men exposed to dust of oxides of manganese experienced a high incidence of a condition which he called "manganese pneumonitis". No permanent lung changes were observed. Three years later Lloyd Davies and Harding (1949) reported tbat pneu monitis has continued to affect manganese workers. Firket (1950) states that chemical pneumonia which follows inhalation of dusts of manganese, vanadium, osmium and beryllium resembles virus pneumonia both clinically and histologically, and be questions whether the dusts themselves provoke the disease or whether they activate viruses. Iron Oxide. Doig and McLaughlin (1936) described a fine uodulatlon in the lung fields of welders who were apparently In good health. Later, following further cliuical and radio graphic studies by them and other investigators, it became evident that the pulmonary changes were due to the deposition of iron oxide dust, which is present in welding fume and which is relatively opaque to X rays, and that they were not associated with symptoms, abnormal physic** signs, or lessened capacity for work. A similar condition has been reported in other workers than welders exposefl to iron oxide. Enter and Sander (1938) made an autopsy examination of the lungs of a welder whose chest radiograph ^ fine noduiation and who died following an accident; tber was no fibrosis in the lung tissue. di ca m ex m< sic al> ha tb Alt CO! tbw) UE inwt of di ec ox tu tu EC as to th <f ah Tt Br ab th. mi m; tir c ch rei wc els Tb oil 2 the Oa th! res wo we bre re\ (o: lit: dll! by yet .^ to inc 19. res i* `te.lals- Wbe -ton or chit -u"g "i2 manganew nd`U0n ^ *ta?e proehi compotu *b cad; *od fro ffects, wh srhapa ier) lesions v extensive, a past 8?e rticles were Two pro scribed: an 'tnatosis. a ow a single `K workers refining of few weeks sarcoidosis. weeks or sure to the pe usually dust from n silicate, ver. eleven d amongst -Jng plant (Eisenbud lationship suspected, England, o dust of mce of a ;tia". No ears later lat pneu:ers. ia which anadium. nia both ether the aer they dulatlon sntly in d radio.became to the welding od that >hysical ndltion jxposed ination showed : there .xwsallsufc -"*> is*5il. Till-; M FIJI CAL JOURNAL OF AUSTRALIA. "SI according to Doig and McLaughlin (194S), the changes aye to iron oxide are not necessarily permanent. In one mc described by them the abnormal lung shadows com pletely disappeared some years after cessation of welding. nd in another the shadows became less intense. pusts from compounds of barium and tin, which are nore rodioopaque than iron, are believed to behave fimilariy to the latter in the lungs. Aluminium. Since Penny. Robson and Irwin (1937) showed that experimental animals exposed to quartz dust plus 1% metallic aluminium powder did not develop silicosis, con siderable interest has been taken in the question whethe'r aluminium dust damages the lungs, and conflicting reports btve been published. The recent pneumonokoniosis conference decided that there was no conclusive evidence that the inhalation of aluminium in any form prevents the development of sillcoeis In man, or that aluminium powder is of value as a therapeutic agent in human silicosis or that it is harmful when used for this purpose. There was some evidence that, under certain conditions the inhalation of aluminium in industrial processes may be harmful and further there was experimental evidence that in animals the inhalation of aluminium dust aggravates pulmonary tuberculosis. Pulmonary Carcinoma. Where an occupation, which is associated with an appar ently high incidence of lung cancer, has involved dusi exposure, it is reasonable to consider carcinoma iu a dis cussion of pulmonary dust disease. The problem has been reviewed briefly by both Doig (1949) 8nd Perry (1947). They mention the high incidence of Jung cancer in the Schneeborg miners in Saxony and in miners in the Joachirostal area in Bohemia. Arsenic and radioactive ores are both considered likely causes in these cases. They also refer to reports by various investigators which indicate that workers in chromate factories, and. thrwP exposed to arsenic and asbestos, have a" high incidence of pulmonary cancer. In a personal communication Dr. J. H. Biakemore, of Concord, advises that in a chromate factory in New South Wales, which has been operating since 1944, and which at present employs about 100 persons, all workers engaged in the various stages of production have an X-ray examina tion of the chest before starting work and at three-monthly intervals thereafter. To date, nothing to suggest pulmonary cancer has been found. In its early years this factory bad a number of cases of nasal septal perforation and skin conditions due to chrome, and relatively high concentra tions of chromates were found in the atmosphere. Synthetic Abrasives. Shaver and Riddell (1947) .described an unusual lung disease, with fibrosis, in some cases fatal, in workers engaged in the manufacture of corundum (aluminium oxide). The process involves treating in special electric furnaces a mixture of bauxite, iron and coke at a tempera ture of 2000* C. Dense white fumes are.given off, which, according to Jephcott (1948), consist mainly of alumina and silica. Riddell (1948) states that the lung condition appears to be induced by an irritant of a chemical nature, but that the precise agent has not been determined. These findings are of interest because artificial abrasives (for example, carborundum, that is silicon carbide, and aluminium oxide) have such widespread use in industry. The observations of Smith and Perina (1948) and of Bruusgaard (1948) indicate that dust from synthetic abrasives, when inhaled, may produce nodular shadows in the lungs. Vegetable Duets. A variety of respiratory disturbances, some only of a minor nature, have been attributed to dust from vegetable materials,-such as cotton, flax, hay, grain, bagasse and timbers. Three examples may be cited. Cotton: A condition termed byssinosia (chronic bron chitis and emphysema with a tendency to asthma) has been reported, particularly amongst card-room and blow-room workers, in the cotton-spinning industry in Britain and elsewhere. There are no specific X-ray or autopsy findings. The literature has been well reviewed by Caminita and others (1947). Bapasse: This is of interest to Australians because of the sugar industry here. Bagasse (or megaas) is sugar cane after the sugar has been extracted, and is used in the manufacture of wall boards. Since 1941 cases of respiratory disease (bagassosis) have been reported in workers'handling bagasse--in England the persons affected were those engaged on a machine ("shredder") which broke up the hales of bagasse. Hunter and Perry (1946) reviewed the literature fully and described eleven cases (one of the patients subsequently died) of acute bronchio litis and pneumonia, arising from the inhalation of bagasse dust. They considered the disease was most likely caused by fine vegetable dust; however, Its exact etiology has not yet been determined. . Wheat Dust: Investigations have Indicated that exposure to wheat dust may result in asthma (Puke, 1935) and an increased liability to respiratory disease (Smith and others, 1941), The fine hairs of the grain are believed to be responsible, at least in part, for these reactions. Prevention of Pulmonary Oust Disease. The measures to be applied in the suppression aod control of dust, and tor the protection of the workers, are essentially the same, irrespective of the industry and type of dust. Briefly, they include the following: . 1. The abolition of processes creating harmful dust. If that is not possible, the total enclosure of such processes in mechanically ventilated structures, or their segregation from other operations in the factory. Isolation can be applied either geographically or by time, that la, by carrying out a dusty process when no other workers are in its .vicinity. 2. The use of a harmless material in place of one that la dangerous. 3. The removal of dust at its point of origin by local mechanical exhaust ventilation. 4. The use of water or other wetting agent to prevent dust from certain processes becoming air-borne. 5. Electrostatic precipitation. 6. The provision of adequate general ventilation to dilute contaminated air. 7. Maintenance of a high standard of plant cleanliness and housekeeping. 8. Personal respiratory protection of the worker. Respirators should be worn only when other methods of protection are not practicable or for jobs of short duration. They should be well fitting, comfortable and efficient and should be kept clean. 9. Preemployment and periodical medical examinations, including a radiograph of the chest, of workers exposed to a dust hazard. If these control methods, or such of them as are applicable to a particular industry or process, are con scientiously applied and maintained, workers would be protected against hazardous exposures to dust. Summary. The term pneumonokoniosis is defined and its scope briefly outlined; the need for a complete and accurate occupational history in the diagnosis of pulmonary dust disease is stressed. ' The potential capacity of a dust to cause disease Is dis cussed, with special reference to its composition and nature, particle size, and Intensity of exposure. In addition to dusts containing high percentages of free silica, others, In which tree silica ia absent (for example, asbestos and certain metals), are capable of producing severe pulmonary damage. In most dusts (asbestos being an exception) the 782 THE MEDICAL JOURNAL OF AUSTRALIA. .Novemueu 25, 1050. harmful particles are those less than about five microns in LUiyd Davie*. T. A. (1946), "Manganese pneumonitis" Bntttk aise. Intensity of exposure, which varies for different dusts, depends on the atmospheric concentrations ! dust Journal of Industrial Medicine, Volume HI, page 111. ----------- and Harding, It, E. (1949). "Manganese Pneu mentis*: Further Clinical and Experimental Observations" and the duration of exposure. Brief notes of a case of British Journal of Industrial Medicine, Volume VI, page 82 ' "rapidly developing'* silicosis are given. McOuiddy, K. L., Tollman. J. P., La Towsky, L. W.. and Schonberger, S. (1939). "Tissue Reaction to Some Carbon Are The main occupations and dusis associated with a risk Dusts", The Journal of Industrial Hygiene and Tozicoloau of poeumonokoniosis are briefly discussed. In addition to diseases caused by 'silica, coal and asbestos, reference is Volume XXI, page 498 Ul>` McLaughlin. A. 1. G., Rogers, E,, Dunham. K. C. (1949) "Talc Pneumoconiosis". British Journal of Industrial Median/ nude to the radiographic abnormalities of certain basalt Volume VI, page 184. e' workers and biograph operators, and to the pulmonary effects of talc, graphite, cement, zinc, cadmium, beryllium, manganese, iron, aluminium, synthetic abrasives, cotton, McVittie, J. C. (1949), "Pneumoconiosis in Coal Miners" The Post-Graduate Medical Journal, Volume XXV. page 618. * Meiklejohn, A. (1949), "Pneumoconiosis", TAe Tost-Graduai* Medical Journal, Volume XXV, page 699. bagasse and wheat. Middleton. E. L. (1950), "The Etiology and Pathogenesis of The occurrence of pulmonary carcinoma in workers Pneumoconiosis", paper (not yet published) presented to the Third International Conference of Experts on Pneumoconiosis. exposed to chromates, arsenic and asbestos is mentioned. Perry. K. M. A. (1947), "Diseases of the Lung Resulting from Measures for the control of dust and protection of pOacgceup9a1t.ional Dusts - other than Silica", Thorn*. Volume II' workers are stated. Riddell, A. R. (1948), "Pulmonary Changes Encountered in Employees engaged In the Manufacture of Alumina Abrasives: Acknowledgements. Pathologic Aspects", Occupational Medicine. Volume V, page 710 Shaver. C. G., and Riddell, A. R. (1947), "Lung Changes I am grateful to tbe following for permitting me access to clinical records of patients and for the loan of X-ray Associated with the Manufacture of Alumina Abrasives". Tht Journo) of Industrial Hygiene and Toxicology, Volume XXIX page 145. ' films: the Director-General of Public Health. New South Smith, A. R.. Greenburg, L, Siegai, W. (1941), "Respiratory Wales; the Chairman, Workers' Compensation Commission of New South Wales; and the Chairman, Silicosis Com Diseases among Grain Handlers", Industrial Bulletin, Hew York State Department of Labour, Volume XX. page 33. Smith, A. R-, and Perlna, A. E. (1948), "Pneuroonoconiotfs mittee, New South Wales. I am also grateful to Professor S. Ford for helpful criticism and to the Commonwealth Director-General of Health fov permission to publish this paper. .* from Synthetic Abrasive -Materials", Occupational Medicine, Volume V, page 396. Smith, G. C-, and Whalte, H. M. (195(0. "An Investigation into the Incidence of Pneumocontosie in New South Wales Coal Miners, and its Relation to Dust Exposure at Selected Collieries", paper (not yet published) presented to the Third References. International Conference of Experts on Pneumoconiosis. Taylor, C. R. (1949), "The Toxicity of Beryllium", Informa Badham, C. (1927), "Notes on a Fine Type of Fibrou* Fneumonokonloals produced by Silicates and other Minerals". "Report ot the Director-General of Public Health, New South Wales, for the Year ended 31st December, 1927", page 102, Baetjer, A. M. (1947), "The Effect of Portland Cement Dust *> the Lungs, with Special Reference to Susceptibility to Lobar Pneumonia: Animal Experiments", The Journal of industrial Hygiene and Toxicology, Volume XXIX, page 250. tion Circular 15, Defence Research Laboratories, Maribyrnong, Victoria. ' Vorwald, A. J. (1950), "Problems in Pneumoconiology", paper (not yet published) presented to the Third International Con ference of Experts on Pneumoconiosis. Whitworth, H. F. (1947), personal communication. Wyers, H. (1949), "Asbestosis", TAe Post-Graduate Medical Journal, Volume XXV, page $31. Bruuagaard, A. (1949), "Pneumoconiosis in Silicon Carbide Workers", Proceeding* of the Hiftth International Congress on Industrial Medicine, London (1948), page 77. Caminlta, B. H-, Baum, tv. F.. Neal, P. A., and Schneiter. R. <1947), "A Review of the Literature Relating to Affections of tbe Respiratory Tract In Individuals Exposed to Cotton Dust", THE CHANGING FACE OF OBSTETRIC INFECTION.1 Public Health Bulletin, Number 297. _ Denny. J. J.. Robson. W. D., and Irwin, D. A. (1937). 'The Prevention of Silicosis by Metallic Aluminium", The Canadian Medical Association Journal, Volume XXLXV12, page 1. Dole, A, T. (1949), "Other Lung Diseases due to Dust", The By Akthks M. Hjli,, M.D., D.G.O. (Melbourne), F.R.C.S.E., F.R.C.O.G., Post-Graduate Medical Journal, Volume XXV, page $39. Gyntrcologist to In-Patients, The Women's ----------- and McLaughlin. A. 1. G. (1936), "X-Ray Appear ances of the Lungs of Electric Are Welders", TAe Lancet, Hospital, Melbourne. Volume L page 771. ,, " (1948), "Clearing of X-Ray Shadows in Welders' Slderosis", ibidem. Volume I, page 789. Tut last fifteen years of the half-century now ending Duke, W. W. (193$), "Wheat Hairs and Dust as a Common have seen the greatest advances of all time in the pre Cause of Asthma among Workers in Wheat Flour Mills", The Jpoaguern9a9l7.of the American Medical Aeeociation, Volume CV, vention and treatment of obstetric infection. This is due predominantly to the Introduction and development of Elsenbud, M., Wanta. R. C., Dustan. C.. Steadman, L. T.. modem chemotherapy and antibiotic therapy; but impoi* Harris.W. B.. Wolf, B. S. (1949), "Non-Occupatfona! Berylli tant contributory factors are improved bacteriological osis , The Journal of Industrie) Hygiene and Toxicology, Volume XXXI. page 282. . Enter. N.. and Sander, A. O. (1938). "Chronic Lung Changes knowledge and methods of investigation and a clearer appreciation of the place of maternal resistance in com* to Electric Arc Welders", TAe Journal of Industrial Hygiene bating Infection. and Toxicology, Volume XX, page 333. . Flrket, J. (1950), "Industrial Pneumopathies", conference In It is proposed to review the major effects of th** Belgium, December, 1949, The Lancet, Volume I, page 225. advances on puerperal morbidity, on the death rate ot tbs Gardner. L. U. (1938). "Experimental Pathology", Section V of Silicosis and Asbestosis". edited by A. J. Lanza (Oxford 1 University Press. New York), page 257. 1 - - -- Durkan, T. M., Brumfield, D. M., and Sampson, main bacterial types ot puerperal and abortional infection, and on modern obstetric practice, at the Women's Hospital' Melbourne, over the past ten years. During that period H. L. (1939), "Survey In Seventeen Cement Plants of Atmos 41,643 women, 80% of whom had attended our own *j* pheric Dusts and their Effects upon the Lungs of Twenty-Two Hundred Employee*", 7ke`Journal of Industrial Hygiene and Toxtcology, Volume XXI. pocC^t* ' - Harding. H. E., and Oliver. G. B. USWr "Changes in the natal clinics, were confined; and 18,285 cases of abortion, of which 5175 were diagnosed as septic'*, were " with. The annual morbidity following the confinement* Lungs Producejl by Natural Graphite", British Journal oj Industrial Medicine, Volume Vf, page 91. Hatch, T. F. (1950), "Analytical Requirements for Appraisal of Dust Exposure", paper (not yet published) presented to the is shown in Figure I. - Suiphonamides were in use in the earliest of these although tbe compounds employed were, in general Third International Conference of Experts on Pneumoconiosis. toxic and less efficient than those now available- Hunter, D., and Perry, X M. A. (194$), "Bronchiolitis Result ing from the Handling of Bagasse", British Journal of Industrial Medicine, Volume 111, page $4. addition, they were not always given in adequate ao****: and their use was largely restricted to the therapy International Labour Organisation (1950), "Third Inter established infection. However, when it is reme""%*j national Conference of Experts on Pneumoconiosis", Thr Msdjcal Journal or Australia, Volume I, page 514. Jephcott. C. M. (1948), "Fume Exposure in the Manufacture that leas than 10% of all cases of obstetric infection likely to be of a bacterial type responsive to sulpMg" __ of Alumina Abrasives: Review of Associated Physical and Chemical Factors", Occupotionai Medicine, Volume V. page 701. Johnstone. R. T. (1948). "Occupational Medicine and Indus trial Hygiene", page 263. The C. V. Mosby Company, St Loulw. 4 Read at a meeting of the Section ot Gynwcology, Australasian Medical Congress * 930. Association). Seventh Session, Brisbane, May-lunc.