Document x5B32O7OD1jybOM3v37GMXaR6
TRANSACTIONS of the
McINTYRE-SARANAC CONFERENCE on
OCCUPATIONAL CHEST DISEASE
Edited by G. W. H. Schepers, M.D., D.Sc.
Town Hall, Saranac Lake, N. Y. Feb. 7, 8, and 9, 19SS
AMERICAN MEDICAL ASSOCIATION PRESS Chicago 10, Illinois 1955
| PLAINTIFFS | PLAINTIFFS |g EXHIBIT 1 |g EXHIBIT
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Acknowledgments
Grateful acknowledgment is made to all the participants who contributed papers this Conference. Appreciation is expressed also to:
American Medical Association for cooperation in printing the Conference transactions
Professor Philip Drinker for editorial advice Thomas M. Durkan for preparing index Edward L. (iockeler for photography
Secretarial Staff of the Saranac Laboratory for preparing manuscripts
Staff of the Saranac Laboratory for preparing Conference halls and exhibits
G. W. H. Schepers, M.D., D.Sc., Editor
FOREWORD
For many years the Saranac Laboratory, of Saranac Lake, N. Y.. and the McIntyre Research Foundation, of Toronto, Canada, have been conducting research along somewhat parallel lines. For the past five years the McIntyre Research Foundation has held its Annual Meeting on Silicosis and Aluminum Therapy in various cities in the United States and Canada, while The Saranac Laboratory, since 1934, has sponsored a series of Symposia on Industrial Pulmonary Diseases at Saranac Lake. These two organizations pooled their knowledge and resources for this conference, and the proceedings are documented in this volume.
Saranac Lake, for many years a center for the study and treatment of pulmonary tuberculosis and other chronic chest diseases and, moreover, a world-renowned recreational resort, provided a unique and attractive setting for the conference. The sessions, which were very well attended, attracted more than 250 persons, including visitors from the United States, Canada, South America, France, Eng land. Scotland, Wales, India, and the Union of South Africa.
The pronouncements in respect of occupational chest diseases, which have been emanating from The Saranac Laboratory and more recently from the McIntyre Research Foundation, have in the past influenced medical, engineering, and legal thinking in terms of these diseases. The views expressed at the preceding con ferences have guided management, labor, compensation courts, physicians, engi neers, lawyers, and educators not only in the United States and Canada but in many other countries. It is hoped that the record of this most recent conference will in equal measure also prove of benefit to those who seek firsthand information and guidance concerning the problem of occupational chest diseases. The prediction that this will be so is strong, because practically every paper presented at the con ference was based on original research.
Anthony J. Lanza, M.D., Conference Chairman Emeritus Professor of Industrial Medicine Yew York University-Bellevue Medical Center
MclNTYRE-SARANAC CONFERENCE PROGRAM COMMITTEE 1955
A. J. Lanza, M.D.............................................................................................Chairman C. P. McCord, M.D.............................................................................Acting Chairman D. A. Irwin, M.D............................................................................................... J. \\ . G. Hannon, M.D.......................................................................... T. L. Shipman, M.D................................................................................. G. W. H. Schepers, M.D.. D.Sc.................................................................. Organizer L' R- Br lXN'....................................................................................................... Secretary
airman airman
amzer retary
Conference Program
Sessions
1. General Chairman: Carey P. McCord, M.D., Consultant in Industrial Medicine, Institute of Industrial Health, University of Michigan, Ann Arbor, Mich.
2. Aluminum in Control of Silicosis Moderator: William A. Sawyer, M.D., Medical Consultant, International Association of Machinists, Rochester, N. Y. Discussant: Paul G. Bovard, M.D., Consulting Roentgenologist, Tarentum, Pa.
2. Epidemiology of Silicosis and Occupational Chest Disease Moderator: Thomas L. Shipman, M.D., Health Division Leader, Los Alamos Scientific Laboratory, Los Alamos, New Mexico Discussant: Philip Drinker, Sc.D., Professor of Industrial Hygiene, Harvard University School of Public Health, Boston, Mass.
4. The Evaluation of Experimental Research on Dust Diseases Moderator : Dudley A. Irwin, M.D., Medical Director, Aluminum Company of America, Pittsburgh, Pa. Discussant: Norton Nelson, Ph.D., Chairman, Institute of Industrial Medicine, New York University-Bellevue Medical Center, New York, N. Y.
5. Medico-Legal and Clinical Aspects of Pulmonary Disability Moderator: Ivan Sabourin, Q.C., Counsel to Quebec Asbestos Producers Association, Montreal, Quebec Discussant: Warren A. Cook, B.A., Associate Professor, Industrial Health and Hygiene, University of Michigan School of Public Health, Ann Arbor, Mich.
b. Experimental and Engineering Aspects of Occupational Chest Diseases Moderator: Angus D. Campbell, Manager, McIntyre Research Foundation, Schumacher, Ontario Epilogue: Carey P. McCord, M.D.
". Conference Banquet Master of Ceremonies: Manfred Bowditch, Director of Health and Safety, Lead Industries Association, New York, N. Y. Leroy U. Gardner Memorial Address: Paul S. Richards, M.D., Senior Consultant, Memorial Medical Center, Salt Lake City, Utah Personal Impressions of Edward Livingston Trudeau and Edward R. Baldwin : Hugh M. Kinghom, M.D., Saranac Lake, N. Y.
Contents
Foreword........................................................................
PACE
111
Program Committee ........................................................................................................................ >v
Conference Program ..........................................
v
Prologue Carey P. McCord, M.D., Ann Arbor, Mich......................................................................... 1
The Objectives and Achievements of the McIntyre Research Foundation Francis B. Trudeau, M.D., Saranac Lake, N. Y.................................................................. 2
The Contribution of the Saranac Laboratory to Research on Chest Diseases E. D. Fox, M.E.,Toronto, Canada........................................................................................ 4
Comparative Vascular Pathology of Occupational Chest Diseases G. W. FI. Schepers, M.D., D.Sc., Saranac Lake, N, Y....................................................... 7
The Value of Lung Biopsy in the Diagnosis of Occupational Pulmonary Diseases H. S. Van Ordstrand, M.D.; Donald B. Efflcr, M.D.; Lawrence J. McCormack, M.D., and John B. Hazard, M.D., Cleveland.................................................................................... 26
Occupational Chest Diseases in Gold Miners G. W. H. Schepers, M.D., D.Sc., Saranac Lake, N. Y......................................................... 33
Accomplishments in the Epidemiologic Study of Silicosis in the United States H. N. Doyle, B.S.; Victoria M. Trasko, A.B.; IV. M. Gafafer, D.Sc., and S. E. Miller, M.D., Washington, D. C.......................................................................................................... 48
Silicosis in Canada N. F. Parkinson, M.E., Toronto, Canada............................................................................. 56
Commentary on References by N. F. Parkinson Concerning the Silicosis Problem in Ontario Andrew R. Riddell, M.B., D.P.H., Toronto, Canada............................................................. 63
Talc Pneumoconiosis Morris Kleinjcld, M.D.; Jacqueline Messite, M.D., and Irving R. Tabershaw, M.D., Netv York ................................................................................................................................. 66
Pneumoconiosis on the Kolar Gold Field, South India Geoffrey E. Fjrcnch, M.A., M.D., F.R.C.P. (C), Oakville, Ont., Canada........................ 73
^The Dust Diseases in Great Britain A. I. G. McLaughlin, M.D., F.R.C.P., London.................................................................... 83
Clearance of Radioactive Dust from the Human Lung Roy E. Albert, M.D., Washington, D. C., and Lawrence C. Arnett, M.D., Brooklyn.... 99
The Antagonistic Biological Action of Quartz and Potassium Carbonate G. W. H. Schepers, M.D., D.Sc., and A. B. Delahant, Saranac Lake, N. Y.................... 107
An Experimental Study of the Effects of Rare Metals on Animal Lungs Anthony B. Delahant, Saranac Lake, N. Y........................................................................... 114
VI
CONTENTS
The Biological Action of Tantalum Oxide
PACE
G. W. H. Schepers, M.D., D.Sc., Saranac Lake, N. Y...................................................... 119
The Biological Action of Cobaltic Oxide G. IV. H. Schepers, M.D., D.Sc., Saranac Lake, N. Y......................................................... I22
The Biological Action of Particulate Cobalt Metal G. IV. H. Schepers, M.D., D.Sc., Saranac Lake, N. Y......................................................... 125
The Biological Action of Particulate Tungsten Metal G. IV. H. Schepers, M.D., D.Sc., Saranac Lake, N. Y................................................... . 132
The Biological Action of Tungsten Carbide and Carbon G. IV. H. Schepers, M.D., D.Sc., Saranac Lake, N. Y......................................................... 135
The Biological Actionjaf Tungsten Carbide and Cobalt G. IV. H. Schepers, M.D., D.Sc., Saranac Lake, N. Y......................................................... 138
The Pulmonary Disability Legislation of South Africa G. IV. H. Schepers. M.D., D.Sc., Saranac Lake, N. Y......................................................... 145
Evaluating Disability in Compensation for Pneumoconiosis Theodore C. Waters, Baltimore.............................................................................................. 157
The Radon Problem in Deep-Level Mining Duncan A. Holaday, B.S., M.A., Salt Lake City................................................................. 161
Current Problems in Dust Control in Metal Mines C. S. Gibson, M.E., Timmins, Ont., Canada........................................................................ 165
The Disability Found in Persons Exposed to Certain Beryllium Compounds Harriet L. Hardy, M.D., Boston.............................................................................................. 172
The Effects of Inhaled Talc-Mining Dust on the Human Lung G. IV. H. Schepers, M.D., D.Sc., and T. M. Durban, M.E., Saranac Lake, N. Y......... 180
Pulmonary Disability in Asbestos Workers Kenneth IV. Smith, M.D., New York................................................................................... 196
Pulmonary Disability Associated with Coal Mining /. IV. G. Hannon, M.D., Washington, Pa............................................................................... 202
Pathological Study of the Effects of Inhaled Gypsum Dust on Human Lungs G. IV. H. Schepers, M.D., D.Sc., and T. M. Durkan, M.E., Saranac Lake, N. Y......... 207
The Demonstration of Aluminum in Animal Tissues Dudley A. Irwin, M.D., Pittsburgh.................... .................................................................. 216
Experiences with the Control of Silicosis in a Foundry Leslie H. Osmond, M.D., Homestead, Pa............................................................................ 219
Prophylaxis and Treatment of Experimental Silicosis by Means of Aluminum M. Dworski, M.P.H., Saranac Lake, N. Y.......................................................................... 224
Experiences with the Control of Silicosis in the Ceramic Industry D. L. Perry, M.D., New Castle, Pa...................................................................................... 242
VII
CONTENTS
Some Experiences with Silicosis Control in Gold Mining
pace
/. K. Godin, M.E., Belleterre, Que., Canada...................................................................... 245
Reaction of Chromium Compounds with Body Tissues and Their Constituents
A. M. Baetjer, Sc.D.; C. M. Damron, Ph.D.; J. H. Clark, Ph.D., and V. Budacz, Ph.D., Baltimore.................................................................................................. 253
Study of Surface Properties of Quartz Dust Lester D. Schccl, Ph.D., Saranac Lake, N. Y...................................................................... 257
Cytobiological Manifestations of the Surface Properties of Quartz G. IK. H. Schepers, M.D., D.Sc., Saranac Lake, N. Y....................................................... 261
An Experimental Study of the Effects of Glass Wool on Animal Lungs G. IV. H. Schepers, M.D., D.Sc., and Anthony B. Delahant, Saranac Lake, N. Y......... 271
The Biological Action of Glass Wool G. IV. H. Schepers, M.D., D.Sc., Saranac Lake, N. Y....................................................... 275
Differential Susceptibility of Animals to Dust IV. R. Franks, M.D., Toronto, Canada............................................................................... 283
An Experimental Study of the Effects of Rare Earths on Animal Lungs
G. W. H. Schepers, M.D., D.Sc.; Anthony B. Delahant, and Andrew J. Rcdlin, Saranac Lake, N. Y............................................................................... 292
The Biological Action of Rare Earths G. IV. H. Schepers, M.D., D.Sc., Saranac Lake, N. Y.
I. The Experimental Pulmonary Histopathology Produced by a Blend Having a Relatively High Oxide Content................................................................................... 296
II. The Experimental Pulmonary Histopathology Produced by a Blend Having a Relatively High Fluoride Content............................................................................... 301
An Experimental Study of the Effects of Talc Dust on Animal Tissue G. IV. H. Schepers, M.D., D.Sc., and T. M. Durkan, M.E., Saranac Lake, N. Y........... 312
The Biological Effects of Calcined Gypsum Dust G. W, H. Schepers, M.D., D.Sc.; T. M. Durkan, M.E., and A. B. Delahant, Saranac Lake, N. Y............................................................................................................ 324
Effect of Inhaled Commercial Hydrous Calcium Silicate Dust on Animal Tissues G. IV. H. Schepers, M.D., D.Sc.; T. M. Durkan, M.E., and A. B. Delahant, Saranac Lake, N. Y............................................................................................................ 343
Relationship of Particle Count. Weight, Shape, and Size of Air-Borne Dusts M. L. Roberts, MS., E.M., Saranac Lake, N. Y.....................................................
356
Personal Impressions of Edward Livingston Trudeau and Edward R. Baldwin Hugh M. Kingharn, M.D.. Saranac I.tike, N. Y.......................................................
365
Memories of Leroy Upson Gardner Paul S. Richards, M.D., F.A.C.S., Salt Lake City..................................................
Annual Report of the McIntyre Research Foundation for Year Ended Dec. 31, 1954
Index ......................................................................................................................... }........
VIII
367 375 379
^Jhe 2W al^idecides in Cjfrecit $3ritciin
A. I. G. McLAUGHLIN, M.D., F.R.C.P., London
markable contributions of the Scottish physi
"i-ilillllillllllillliilllllffill*
cians of the 1800's on the connection between disease of the lungs and coal dust; he also tells
The story of dust diseases in Great Britain how the incidence of anthracosis diminished
.-es back a long way. E. L. Collis, in his with improved ventilation of the mines. The
i>sical Milroy Lectures of 1915, quoted Scottish physicians decided that simple coal
mrbert Spencer as saying that the starting dust was comparatively harmless and that
'int of human progress was the "localization stone dust was the really noxious factor.
industries." There was such a localization
Charles Turner Thackrah, a physician in
prehistoric factories for the making of flint Leeds, played a major part in the study of oc
dements at Grime's Graves, near Brandon cupational diseases (including the dust dis
Suffolk, where the flint knappers still use eases) in Great Britain. In his book "The
Is like the deer-horn picks of their prehis- Effects of Arts, Trades, and Professions," the
ic ancestors. In 1914, Collis showed that second edition of which was published in
use workers have a high mortality from 1832, he crystallized the idea that the inhala
iicnsis. He said that it is probable that "the tion of large quantities of dusts of any kind
acting point of human progress" was asso- can damage the lungs but that some dusts are
nii'd with at least one form of pneumoconi- more harmful than others. His conclusions
is. It has been long known that the dust of were based on first-hand observations of
uit. which is nearly pure Si02, is dangerous workers in hospitals, in their homes, and in
pa health. Over 200 years ago, Thomas Ben- the factories.
nn. of Newcastle under Lyme, was granted a patent for grinding flints by a wet method. At that time it was said that a man who ground the flints dry could not live longer than two years.
Two other great Englishmen in the history of pneumoconiosis about the middle of the 19th century were T. B. Peacock and E. H. Greenhow. Peacock first established miners' disease as an entity and distinguished it clin
Our greatest localization of industries took ically from pulmonary tuberculosis before
place during the Industrial Revolution, and little was known about bacteriology and noth this was really the starting point of our in ing about x-rays. Greenhow carried out the
tensive knowledge about the effects of dust on first large field investigations into the dusty
the lung.
industries of England and Wales, including
The first notable contribution was that of the heavy-metal industries, the potteries, coal,
Pearson (1813), who, after many autopsies, copper, and lead mining, and even agriculture.
decided that the black pigment in the bron In the Transactions of the Pathological So
chial nodes and the lungs was due to the in halation of small particles resulting from the burning of coal, wood, and other inflammable materials. The German pathologists, on the other hand, thought that the pigment came from inside the body. Meiklejohn (1951) has described the hitherto little-known and re
ciety of London (1860-1866) there are to be found excellent descriptions by both of these physicians of the disease, which was later to be called silicosis by Visconti, in 1870. They even found the dust of free silica in the lungs and examined it under polarized light.
For a long time after this excellent work
recorded for publication April 7, 1955.
nothing much was done about the dust dis
H. M. Medical Inspector of Factories.
eases, but about the beginning of the 20th
83
McLaughlin
century a new interest began to be taken in the problem not only in England but also in other parts of the world. About the same time the tempo of life in general began to in crease, and there was an urge for increased speed of production--an urge which has grad ually gathered momentum. With the replace ment of hand labor by the machine, dusty processes have become more dusty and meth ods of dust control have lagged behind output. The result has been a remarkable increase of the incidence of the dust diseases.
A noteworthy contribution in 1892 was Arlidge's book on the occupational diseases, which was only the second to be published in England.
In 1904, J. S. Haldane and his colleagues ascribed the high mortality among tin miners to the inhalation of rock dust. A little earlier, dust phthisis among slate workers was shown to be related to the dust of slate, particularly when it had a high quartz content.
E. L. Collis (1915) pinpointed the dust of free silica as the main cause of most of the dust diseases. He also drew attention to the role that dust inhalation plays in determining the mortality from lung diseases experienced by the general population. Long ago he showed the influence of air pollution on the mortality from lung diseases in general. Though Collis did this work 40 years ago, he is always up-to-date. He had, and still has, an uncanny knack of seeing to the heart of any problem. Just now in England there is controversy about chronic bronchitis and emphysema and whether they can be held to be caused by the inhalation of dust. It is true that the incidence of chronic bronchitis and emphysema is high among the general popula tion, and the possible causes are legion. It is difficult to decide (in Arlidge's words) how much of the malady is "town-made" or "trademade." But as Collis showed years ago, an agent which irritates the lung parenchyma can also irritate the bronchial mucous membrane. At present there is one industrial pulmonary disease of which the diagnosis is made largely on the presence of chronic bronchitis and emphysema, and that is byssinosis.
84
In the last 50 years in Great Britain (as elsewhere), there has been intensive research into all aspects of the dust diseases, such as causation, pathology, incidence in various in dustries, and prevention. For the first 25 years or so, much of the impetus came from H. M. Medical Inspectors of Factories, and prominent in the study of the chest diseases were Collis, Middleton, and Merewether. It might be said that they played almost a lone hand, with meager facilities for investigation. However, they were helped greatly by hospi tal physicians, general practitioners, radiolo gists, and pathologists, notably Hall, Robertshaw, Kettle, Gloyne, and Cooke. During this period much attention was paid to silicosis, and it, with tuberculosis, was established as being the cause of disability and death in most of the industries where there is exposure to the dust of free silica. Pari passu, regulations laying down dust-control measures were is sued bv the Factory Department for most of the major industries. Notable contributions were Collis's work, already mentioned, on the role of free silica and Middleton's field in vestigation (with E. L. Macklin) into the grinding industry in 1923. In the late '2CTsj a series of brilliant observations by Cooke, Gloyne, Burton Wood, Stuart McDonald, and! M. J. Stewart on the clinical, radiological,1 and pathological features of a new disease, which Cooke named asbestosis, led to field in vestigations by Merewether and Price (1930). These firmly established that the dust of as bestos was dangerous to health, and it was the first time that the dust of combined silica, as opposed to free silica, was found to damage the lungs. The condition, as Legge points out, was first seen in 1906 by Murray at Charing Cross Hospital, but little or no notice of it was taken at that time.
An important landmark was the passing of the Workmen's Compensation (Silicosis) Act of 1918, which came into force in 1919. For the first time compensation for disable ment or death was given in respect of an in dustrial pulmonary disease. The Act pro vided initial and periodical medical examina tion of all workers in the refractories industry
Dl'ST DISEASES IN GREAT BRITAIN
.mkI suspension from the industry on a diag nosis of simple silicosis as well as silicosis .ith tuberculosis. The medical officers re-ponsihle for the examinations were the Tu berculosis Officers of the Local Authority ad ministering sanatorium benefit under the National Health Insurance Act. The scheme
as revised in 1925, and again in 1931, to mvide for examinations by a medical board. 1 his was the beginning of the whole-time dicosis and Asbestosis Medical Board under - first (and only) Chief Medical Officer, . 1.. Sutherland.
A close association began between the Medical Inspectorate of Factories and the
ilicosis and Asbestosis Medical Board, both : roups working under the Home Office. In neral, the Medical Inspectorate made the Md investigations which established the risk : silicosis (or asbestosis) in an industry or i vocess and which led to the establishment of he various compensation schemes. But the members of the Board (stationed at Sheffield, Manchester, Stoke on Trent, and Cardiff) also carried out field investigations into vari ous industries, such as sandstone (Sutherland and Bryson, 1929), granite (Sutherland and Bryson, 1929), and potteries (Meiklejohn, 1949). But perhaps the most significant re sult of the formation of the Board was that there was begun a systematic and valuable collection of case histories with x-ray films, together with occupational details and post mortem findings.
At first the Board was limited to a few in dustries. but gradually its scope has increased and more and more dusty industries have come under examination. Workers in the re fractories industry first came under a com pensation scheme in 1925, metal grinders in 1927, and sandstone workers in 1929. In 1928, the Various Industries Scheme included the processes of mining, quarrying, drilling, and blasting in silica rock, the crushing and grind ing of siliceous materials, and also isolated processes in steel foundries (not iron foun dries) and metal works, in potteries, and in tin mines. In 1934 the Various Industries Scheme was amended to include coal miners
with silicosis; in 1935 hematite ore miners were included, and in 1939 slate miners. Workers with asbestosis were first compen sated in 1931 ; compensation for byssinosis was introduced in 1941 and was dealt with by a specially constituted board. Pneu moconiosis, as opposed to classical silicosis, in coal miners was brought under the compensa tion schemes in 1943 and in coal trimmers in 1946. The Various Industries Scheme was again amended in 1946 to include-molders of iron castings who used siliceous parting pow ders and also blasters of any type of metal castings to free them from adherent sand, even if the blasting abrasive was nonsiliceous. The National Insurance (Industrial Injuries) Act was passed in 1946 and altered the whole basis of compensation in that it became the re sponsibility of the Government but with con tributions from employers and workers. Ber yllium "poisoning" became compensable in 1949. In 1954 all foundry workers (iron, steel, and nonferrous) became entitled to com pensation under the Industrial Injuries Act. A fuller account of the development of com pensation in Great Britain has recently been written by Meiklejohn ( 1954). The Silicosis and Asbestosis Medical Board was trans ferred from the Home Office in 1946 to the Ministry of National Insurance (later com bined with the Ministry of Pensions). The Board was divided into a series of Pneu moconiosis Panels, but they work in much the same way as the Board did, except that there is now no Chief Medical Officer.
The various compensation schemes men tioned above reflect the evolution of the study of the industrial lung diseases in Great Brit ain. There are comparable legal enactments and regulations designed to control the risks in each industry, but they are too numerous to mention in detail.
To "flash back" a little, in 1936 Middleton, in his Milrov Lectures, reviewed the position of the dust diseases in Great Britain. He covered all the dusty trades, including coal mining, but at that time only cases of silicosis in coal miners were recognized as being eligi ble for compensation. Most of the miners,
85
McLaughlin
such as hardheaders, drifters, or rippers, had been exposed to stone dust, but Middleton also showed that there was a high incidence of a lung disease among coal miners, particularly in South Wales, which was not classical sili cosis. Much of his evidence was drawn from the findings of the Silicosis and Asbestosis Medical Board. Following his paper, there began a series of intensive investigations by the Medical Research Council into the health risks of coal mining, which covered all as pects, such as clinical, radiographic, and en vironmental (Medical Research Council Spe cial Reports I [1943], II [1943], and III [1945]). The important fact emerging from this work was that coal dust by itself could cause pneumoconiosis, and this was followed, as previously mentioned, by the extension of compensation to coal miners and coal trim mers. In 1945, the Pneumoconiosis Research Unit of the Medical Research Council was set up in Cardiff, and an impressive body of work has emerged on various aspects of coal miners' pneumoconiosis. This work is well known, and I propose, therefore, to limit my remain ing observations mainly to the dust diseases resulting from work in places which come under the Factories Acts, with only inciden tal references to coal mining.
3. Stone quarrying, crushing, and dressing. This group includes workers with sandstone, millstone, gritstone, slate, granite, and other igneous rocks. The risk varies with the amount of free silica in the rock and, of course, with the protective measures adopted. 1 Recently some limestone quarrymen have contracted silicosis, but the limestone con tained a fairly high proportion of free silica.* In this group could be included rock tunnelers, in whom the onset of silicosis may be very rapid. As regards' slate workers, a bil liard-table maker has recently received com pensation for silicosis.
DEATHS FROM SILICOSIS IN METAL GRINDERS
1930-1951
40
30
20
10
o
SILICOSIS
Silicosis has been found to be a cause of disability in the following broad groups of in dustries as well as in coal mining and other forms of mining, such as tin, hematite, copper, barites, and fire clay.
1. Refractories industry. This group in cludes the making of silica bricks, furnace dismantling and rebuilding, and retort setting and. repairing.
2. Pottery industry. Workers in this group have been engaged in the manufacture of both earthenware and china with their various subdivisions and as flint millers and polishers. The substitution of ground flint by alumina for the placing of biscuit ware has resulted in a diminution of deaths from silicosis among workers in that process.
86
Fig. 1.--Chart showing diminishing numbers of deaths among metal grinders during the period 1930-1951, inclusive.
4. Metal grinding. The silicosis risk in the grinding of metals has greatly diminished, owing to the replacement of the sandstone grinding wheels with artificial ones composed of Carborundum, alumina, or emery. Apart from the lower "toxicity'' of the dusts from these substances, the wheels are much harder than sandstone, and less dust is created. But the grinders of castings (iron, steel, and nonferrous) are still exposed to a silicosis risk on account of the presence of burned-on sand on the castings. The diminishing number of deaths among grinders is shown in the chart
(Fig- 1).
* Dotg, A. T.: Unpublished data.
DUST DISEASES IN GREAT BRITAIN
5. Sandblasting. This job, as Merewether (1936) showed, had a high silicosis risk. The position has altered materially after sand be gan to be replaced by other nonsiliceous abra sives, such as steel shot, and since the use of sand as an abrasive was prohibited in 1949 by ;he Blasting of Castings (and other Articles) Regulations. The process of wet sandblasting ! if ships' hulls does not come under the Regu lations (because legally a ship is not an arti cle), but it is thought that there is also a risk of silicosis in the job. Sandblasting is still used in the open air on works of engineering construction, e. g., in order to prepare large metal surfaces for the application of paint.
6. Manufacture of abrasive soap. Middleton showed in 1936 that the manufacture of abrasive soaps carried with it a risk of acute or subacute silicosis, accompanied by tubercu losis. There was a disastrous experience at one factory in London between 1921 and 1928, when there were 13 deaths among 81 workers. This experience led to rigorous dust control in the processes, but between 1941 and 1952 there were nine deaths from silicosis among this type of worker. It is not possible to state the incidence of disease and disability, because there is a rapid turnover of labor (mostly young women) in the job. Silica flour is still being used as an abrasive, though efforts are being made to find a less harmful substitute which will be acceptable to the manufacturers and the users. There were no new cases of silicosis in this trade in 1953.
7. Foundry industry. The iron and steel foundry industry has been investigated in great detail during the past 10 years or so, and the results were published in 1950 in bookform by McLaughlin and others ("Industrial Lung Diseases of Iron and Steel Foundry Workers"). Pathological studies of 64 cases, as well as clinical and x-ray examinations of some 3000 workers, showed that there was a varying risk of silicosis and mixed dust pneu moconiosis (to which reference is made be low) in the various categories of foundry workers.
Steel fettlers (dressers or castings clean ers) had a severe risk, largely owing to the
fact that the dust from the pneumatic hammer is not controlled. The main pathological lesion was classical silicosis, with or without tuber culosis. Among iron fettlers, the risk was not so great as among steel fettlers, and the main pathological lesion found was mixed dust pneumoconiosis, though classical silicosis did occur. Steel molders were less affected by dis ease and disability than iron molders, though statistically the incidence of x-ray abnormal ities was greater among steel workers. More deaths occurred among iron molders, and this fact appeared to be related to the use of siliceous parting powders. The use of siliceous parting powders has now been prohibited by the Foundries (Parting Materials) Regula tions, 1950. Silicosis still occurs among shot blasters of both iron and steel castings, but the risk is controlled by ventilation and per sonal protective devices, and the numbers of cases and deaths, in contrast with the experi ence among steel fettlers, are not increasing. Other categories of iron and steel foundry workers are subject to much less risk than the above groups of workers. New and strin gent regulations (Iron and Steel Foundry Regulations) were issued in 1953. They re quire strict dust control in the dusty proc esses.
The question of pneumoconiosis among nonferrous foundry workers is now being ex amined in detail. Isolated cases of silicosis and mixed dust pneumoconiosis have occurred among both casters and dressers of nonferrous metals, but an extensive survey has not yet been carried out. Harding and McLaughlin f have described the pathological, clinical, ra diological, and environmental details of six fatal cases.
Table 1 shows the number of new cases of pneumoconiosis (i. e., silicosis and mixed dust pneumoconiosis) in foundry workers diag nosed by the Pneumoconiosis Panels in 1953.
These figures can be regarded as an under statement of the real position. More than half
t Harding, H. 1L, and McLaughlin, A. I. G.: To be published.
87
McLaughlin
Table 1.--New Cases of Pneumoconiosis--1953 Foundries
Occupation
Iron molding-................................................................ Iron dressing....................... Iron foundry knockout............................................ Steel molding................................................................ Steel dressing...................................... ........................ Nonferrous dressing................................................... Welders and burners (in castings cleaning
shops) ........................................................................ General foundry work...............................................
Total 57 21 1 4 45 2
10 52*
Total..................................................................... 192
* Twenty-seven of these workers had also been exposed to coal dust for varying periods.
of the cases in iron molders came from one area where there had been an x-ray survey of three foundries. If more iron foundries had been similarly surveyed, more cases would have been found. In certain steel foundries the dressers (chippers or castings cleaners) are x-rayed each year, but a complete picture of the true position will not be obtained until all workers undergo periodical medical examina tion. This statement also applies to other dusty industries.
In Table 2 details are given of fatal cases of silicosis and asbestosis investigated fully by the Medical Inspectorate of Factories between 1930 and 1953. The average ages at death and the length of employment in the dusty indus tries are also given.
It is seen that as regards silicosis the manu facture of scouring powders and sandblasting were the most dangerous industries, with the lowest average age at death and the shortest average period of employment. Another in teresting point is that' tuberculosis occurred in about half of the cases of silicosis, whereas it was found in only about two-fifths of the cases of asbestosis. The average age at death and the length of exposure in the cases of as bestosis were much lower than in the silicotic group as a whole but more on the level of sandblasters and makers of scouring powders.c
The connection between asbestosis and cancer of the lung is becoming clearer, and in one series of 100 autopsies on asbestosis cases there were 25 cases of cancer of the lunge Wyers (1949) has pointed out that the x-ray
Table 2.--Fatal Cases of Silicosis and Asbestosis Investigated by Factory Department, 1930-1953
Silicosis Pottery Silicosis............................................................... Silicosis with tuberculosis.............................
Sandstone Silicosis............................................................... Silicosis with tuberculosis.............................
Grinding of Metals Silicosis............................................................... Silicosis with tuberculosis.............................
Sandblasting Silicosis ............................................................... Silicosis with tuberculosis............................. .................
Manufacture of scouring powders Silicosis............................................. Silicosis with tuberculosis.............................
Miscellaneous Silicosis.................................... Silicosis with tuberculosis.............................
Total Silicosis.................................... Silicosis with tuberculosis...............................
Asbestosis Asbestosis..................................................... Asbestosis wjth tuberculosis..................
Deaths, No.
99
Average
Age at Death,
Yr.
Duration of Employment
r ,--
A
______ _
Longest, Shortest, Average, Yr. Yr. Yr.
61.7 62.0 56.2 67.0
60.9 62.0 57.5 58.0
59.5 54.0
61.0 56.0
50.4 42.0 46.2 46.0
40.3 37.0 40.8 11.2
55.4 57.0 51.6 50.0
59.4 54.4
J49.5
40.2
62.0 67.0
48.0 33.0
2.8 5.0
9.0 5.0
14.0 2.8
1.7 2.0
2.3 2.0
1.5 0.7
1.5 0.7
0.5 0.3
38.4 34.7
39,0 37.4
35.9 33.0
13.4 13.1
8.3 7.0
24.3 24.8
34.1 31.2
11.4
DUST DISEASES IN GREAT BRITAIN
appearances of asbestosis are undergoing some change in that nodular as opposed to ground-glass shadows are beginning to ap pear. He thinks it probable that this is because of the lessened exposure to dust over a longer period, owing to the rigorous application of exhaust ventilation to the dusty processes and the use of personal protective devices. Cases \ of asbestosis, however, are now appearing in \ workers who do asbestos lagging of pipes and j boilers. In this process, particularly if as! bestos is being sprayed, it is difficult to apply adequate protective measures, more especially because the workers are usually peripatetic.
PRESENT POSITION
How many cases of pneumoconiosis (sili cosis. asbestosis, coal miners' pneumoconiosis,
In all industries there were 8789 deaths from occupational fibrosis of the lung in the 12-year period, and it will be seen that the total yearly figures are going up. Over the same period there were 6907 deaths from nonoccupational fibrosis of the lungs. About twothirds of the total number of deaths in the occupational group occurred in coal miners, who form the largest group (about 700,000) exposed to dust inhalation. The figures rose steeply from 232 in 1940 to 937 in 1951 (in 1952 the figure dropped slightly, to 912). It may well be that part of the increase is due to more accurate diagnosis, or at least to greater interest in the pneumoconiosis problem, among coal miners. In Figure 2 is shown a comparison, based on the crude figures of Table 3, between the coal miners and factory
Table 3.--Deaths from All Types of Pneumoconiosis in England and Wales, 1940-1951
Industry
retteries ..................................................... Sandstone .................................................. ................ Grinding of metuls, etc......................... ................ Itefractories............................................... ................. Miscellaneous ............................................ ................ Goa! mining............................................... ................ other mining............................................. ................ Asbestos ..................................................... ................ Got ton (byssinosis).................................
1940
109 41 16 7 232 64 11
1941
45 82 26 12 5 196 40 17
1942
47 54 26 7
7 230
46 11 6
1943
41 77 21 7 5 276 43 8
7
1944
32 57 24 6 13 311 39 10
1
1945
41 65 22
9 19 387 40 11 10
1946
49 61 32
8 14 421 51 16 3
1947
54 55 27 10 26 577 50 15
4
1948
48 68 26 13 27 639 49 15 8
1949
63 51 37 13 25 756 64 17
7
1950
73 29 2 S 70 &16 42 12 11
1951
62 71 21 S 129 937 51 18 8
Total
608 779 325 117 347 5,808 579 161 65
Total........................................................
423 434 485 493 604 655 818 893 1,033 1,113 1,305 8,789
Xonoccupational ......................................
461 443 493 531 529 568 616 651 554 679 732 6,907
etc.) occur in Great Britain? It should be mentioned that at the present time it is im possible to give accurate figures of the popu lations at risk in the various trades and proc esses. Both the Registrar-General and the Ministry of Labour classify occupations in groups too broad to give specific figures of the populations in the dusty industries, and those in the possession of employers' asso ciations and trades unions are not complete. It may be possible in several years' time to give more accurate information. All that can be done now is to state the numbers of deaths reported to the Registrar-General and to give the figures for one year of the new cases diag nosed by the Pneumoconiosis Panels.
The deaths from all forms of pneumoconi osis between 1940 and 1951, inclusive, in England and Wales are given in Table 3.
workers. In the factory processes, the yearly number of deaths was going down until 1943, but there has been a slight rise in the later years.
In both groups, it should be emphasized that the deaths in each year are related to conditions which obtained in mines and fac tories some years previously, possibly 10 to 20 years or even longer.
Nczv Cases in Factory Occupations.--The following Table 4 gives the numbers of new cases of pneumoconiosis diagnosed by the Pneumoconiosis Panels in 1953. These fig ures have been kindly supplied by the Minis try of Pensions and National Insurance, but it should be noted that they differ slightly as regards the numbers in each occupation from the figures originally supplied. The Ministry usually classifies the cases as falling into the
89
McL.ll'CHLlX
OEATHS FROM All TYPES Of PNEUMOCONIOSIS,
CNglAfO AMO WlCi IW-Nfl
CsOioAcLo- MstlsNtNtCpnCumocomio^.
S7T
19*0 J<Mt 1742 {94J 19*4 lJ l*6 IW >941 19*9 19SO 19/1
fAcrooy processes.
9*0 19*1 >H2 19*3 194* l**S 19*4 I9*J 19*9 19*9 /**} i*Jt
Fig. 2.--Chart showing trends of deaths from fibrosis of the lungs among coal miners and factory workers during the period 1940-1951, inclusive. category of the last jobs done by the workers, whereas Dr. G. O. Williams, of the Factory Department, has reclassified some of the cases on the basis of all occupations done by each worker in order to determine the most likely cause of the pneumoconiosis.
There were 896 cases of pneumoconiosis diagnosed, and this figure includes 54 cases of byssinosis. The cases with an uncomplicated occupational history numbered 665, and in the
remainder there was exposure for varying pe riods to other dusts, mainly coal dust. Addi tional exposure to coal dust occurred mainlyin those industries situated in coal-mining areas, such as refractories, stone (sandstone and granite), pottery, slate, and foundry in dustries. The pottery industry contributed the greatest number of cases (353, mainly sili cosis), and the foundry industry came next w'ith 190 cases. There are roughly 25.000 pot tery and about 220.000 foundry workers (iron, steel, and nonferrous) ; so it is probable that the pottery industry has a higher pneu moconiosis risk than foundries. Such general statements are not of much value, because the risk varies from process to process within the same industry. The substitution of ground flint by calcined alumina has reduced the sili cosis risk among placers of biscuit ware in potteries, whereas the fettling of steel castings is still a dangerous job.
Nezv Cases in Mining.--Table 5 gives the numbers of new cases of pneumoconiosis oc curring in all mining operations in 1953.
These figures show clearly the tremendous problem which faces the coal-mining industry. There is no space to give in detail the varying degrees of severity of pneumoconiosis found in the 4048 cases, but the figures are given in the "Digest of Pneumoconiosis Statistics
Table 4.--Xeiv Coses of Pneumoconiosis--1953 Factory Occupations
Industry
(1) Refractories ..................................................... (2) Stone workers (sandstone, granite)......... (3) Pottery ............................................................. (4) Slate workers Ojuarrying and splitting) (.') Foundries .......................................................... (6) Metal grinding (other than foundries)... (7) Sandblasting ..................................................... (8) Shot blasting.................................................... (9) Furnace dismantling, etc.............................. (10) Boiler sealing.................................................... 01) Abrasive wheel manufacture........................ (12) Asbestos ............................................................ (13) Abrasive soap powders................................. (14) (Graphite and carbon electrodes.................. (15) Tin smelting...................................................... (lfi) Cotton (byssinosis)......................................... (17) Coal trimming.................................................... (18) Miscellaneous ....................................................
Totul...............................................................
No Other Dust
Exposure 15 55
254 62 154 5 5 2 17 4 3 14
1 40 10
--24
065
Other Dust Exposure
Coa
10 10 S6 39 27 o
4
Other
1 13
9
7 1
53
14
----
205 26
Total 25 06
353 101 190
7 9 o 24 5
OO3
1 54 10
_24
S96
90
OUST DISEASES IN GREAT BRITAIN
Table 5.--Nciv Cases of Pneumoconiosis--1953
Mining *
Industry
('uses, No.
11 > Coal mining'........................................................ 4,018
f'2) Tin mining.........................................................
3
m Barites mining..................................................
1
(4) Fire clay mining t............................................
16
i'> Other clay mining...........................................
2
r<j Hematite mining..............................................
4
(7) Lead mining......................................................
2
i8) Tunneling ..........................................................
3
Total.............................................................. 4,079
No cases in chert, oil shale, or stratified ironstone iiuning.
> Fourteen fire clay miners were also exposed to coal
Mist.
lor 1953," issued by the Ministry of Fuel and Power (1954). It can be said, however, that more than 50% of the cases had only slight disability, and only about 3% were totally disabled.
The number of cases in hematite mining is diminishing, but the small numbers found in tunneling are usually instances of rapid and severe silicosis.
DUSTS OTHER THAN SILICA, ASBESTOS,
AND COAL
About the middle 1930's the Factory De partment began to turn its attention to other dusts. Middleton, in his 1936 review, referred to dusts, such as tripoli, sillimanite, kieselguhr, talc, china clay, and fullers' earth. In the same year Doig and McLaughlin pub lished a paper on the x-ray appearances of the lungs of electric-arc welders. From this has arisen a world-wide study of the inert and radiopaque dusts, and notable American contributors have been Sander, Enzer, Pen dergrass, Vorwaid, and Hamlin. Perhaps the most interesting outcome of this study has been the alteration of the approach to the interpretation of x-ray films of the chest, because the x-ray features of siderosis, baritosis, and stannosis, in the absence of occu pational histories and clinical examinations, can be mistaken for fibrotic changes in the lungs. In fact, an alarming x-ray picture is often found in a worker who has little or no disability. The study of siderosis was helped by the excellent work of Stewart and Faulds (1934) and later Craw (1937) on the hema
tite miners, in which group the lesion was found to be siderosilicosis, often accompanied by tuberculosis. Craw's later work (1947) in eliminating tuberculosis from the hematite mines and in improved dust control methods is of major importance.
Other occupations and dusts which have been studied include those of boiler scalers, graphite workers, grain dockers, and workers exposed to beryllium and its oxides, to the dust of leather mixed with other dusts, and to bagasse. Attention has also been given to exposures to the dusts of aluminum, man ganese, and vanadium and to asthma occur ring in workers exposed to the double salts of platinum and also to various wood dusts, such as western red cedar.
Pathology.--A great deal of work has been done on the pathology (gross, histological, and experimental) of coal miners' lungs by Gough, Harding, King, Heppleston, Wright, Gloyne, Nagelschmidt, and others. I might, however, state some conclusions about pa thology which Harding and I (with our late colleague, S. Roodhouse Gloyne) have ar rived at after studying the lungs of workers in many diverse industries.
Until about 10 years ago, the pathology of the dust diseases was dominated by the class ical silicotic nodule (Fig. 3). In the same way, before a diagnosis could be made, the patient had to have x-ray nodulation, or the classical "snowstorm" effect. Classical sili cosis usually occurs after the worker has been exposed to dust containing a high proportion of free silica. It is becoming increasingly clear, in our opinion, that even small propor tions of free silica in a dust can cause a fibro sis which is composed of nodules not of the classical type (Fig. 4). The arrangement of the fibers is linear and radial, and the outline of the whole nodule is stellate. It looks like a black star. Harding, Gloyne, and I have applied the term mixed dust pneumoconiosis, or mixed dust fibrosis, to this nodule. It has been found in foundry workers, especially in cleaners of iron castings, in persons exposed to the dust of graphite containing about 10%
free silica, and in boiler scalers who are ex-
91
Me!.. ICl.llLIX
Fig. 3.-- Classical silicotic nodule from lung of a gold miner (30 years old) ; hematoxvlin and eosin ; X 24.
mixed dust pneumoconiosis nodule. Indeed, there are also nodules which show a transi tion stage between the mixed dust nodule and the classical one (Fig. 5). It should be men tioned that the x-ray appearances of the lungs of a worker with mixed dust pneumoconiosis differ little, if at all, from those of one with silicosis, and the disease is just as disabling and as fatal.
Boiler Sealers' Pneumoconiosis.-- Experi ence of pulmonary diseases in ships' boiler scalers illustrates well the etiology of mixed dust pneumoconiosis. These men are exposed to a mixed dust which varies according to the type of fuel used to heat the boilers and also according to the source of the water used
posed to a mixed dust with a low proportion
of SiCL. The coal nodule of coal miners'
pneumoconiosis has much the same appear
ance as our mixed dust pneumoconiosis
nodule. Coal contains varying proportions
of free silica. In any case, the common de
nominator in those cases and occupations in which this type of nodule is found appears to
be the presence of a small proportion of free
silica in the dust. Where there is a high pro
portion, as stated above, the classical silicotic
nodule is found. But in the same case, there
may be both the classical nodule and the
Fig. 4.--Mixed dust pneumoconiosis nodule from a steel fettler's lung; hematoxylin and eosin; X 24.
Fig. 5.--Transition nodule, from mixed dust pneu moconiosis nodule to silicotic nodule in an iron dresser's lung; hematoxylin and cosin: X 24.
in them. It contains carbonates, silicates, iron, and carbon. There is usually under ol free silica, but there is often a high pro
portion of iron and its oxides. Flue dust
contains more iron than docs the scale on the
water tubes, sometimes as much as 48W-
In the first case of boiler scalers' pneumo
coniosis the worker had been scaling boilers
for over 40 years (Harding. Tod. and
McLaughlin. 1944), In 1938 an x-rav film
of his chest showed Modulation in the upper
and outer lung fields, and in the lower zones
reticulation (or micronodulation). At that
time we made a tentative diagnosis of sili
cosis in the upper zones, with siderosis in the
lower zones. Seven years later the patient
92
,///./.v udeed, ' ransi-
and meninngs " iosis
with ;:Iing
WltCS, /Or "> r> produst :l I he
"Icrs and him `Per
lies
hi,it i.'i: (l;e '"nt
f 'ST DISEASES IN GREAT BRITAIN
d oi cancer of the lung, and histological animation of the lungs showed (apart from : r cancer) the presence of classical silicotic dules in the upper and outer zones, and in lower zones (where there was x-ray u alation) there were mainly deposits of :! on and iron dust in the lungs, with no : -osis. In all other parts of the lung there : e nodules of mixed dust pneumoconiosis.
:o the present time we have had autopsies nne boiler scalers, and all showed this : of fibrosis. Only one scaler had classical coric nodules in addition. But five of them died of cancer of the lung, and this may 1 have been partly caused by carcinogenic -tances present in the soot,
lie change from coal to oil as a fuel for ips' boilers has brought with it another >hlem. The dust from oil-fired boilers uses symptoms of bronchospasm or asthma : a high proportion of cases, and it is likely at this is due to the presence of vanadium :: the oil soot. Williams (1952) has published ;i interesting series of cases illustrating this ,<int. My colleagues and I are at present xamining (with clinical, radiographic, and nvironmental details) the boiler scalers i .'ome 300 of them) in the port of South ampton, where the boilers of ocean-going and large passenger liners are cleaned. The inves tigation has not been completed, but up to the present we have not found as much lung damage as was shown in a previous inquiry m the port of Hull, where the boilers of fishing trawlers are mainly scaled. So far we have found three cases of compensable pneumoconiosis among 50 workers and one case of cancer of the lung, together with a proportion of cases with lower degrees of pneumoconiosis and disability.
Talc Pneumoconiosis.--A great deal of work on talc pneumoconiosis has been done in the United States and Canada (Dreessen, 1933; Dreessen and Dalla Valle, 1935; Riddell, 1940; Siegal, Smith, and Greenburg, 1943, etc.). Merewether (1933-1934), in England, studied the x-ray and clinical features of rubber workers exposed to talc dust. But it was not until 1949 that we were
able to study the histological appearances of a proved case of talc pneumoconiosis (Mc Laughlin, Rogers, and Dunham, 1949). A man, 51 years of age, had worked for 37 years in a rubber-tire factory, where he had been exposed to a fairly high concentra tion of talc dust. Moderately advanced pneu moconiosis of both lungs was found at au topsy (in addition to incompetence of the aortic valve). Throughout the lung substance were scattered small gray nodules, more numerous in the lower lobes. In some areas the nodules had coalesced to form small masses. The fibers appeared to be arranged concentrically around small vessels, giving the impression of whorling, but not like the appearance of silicosis. There were, in addi tion, many "curious" or talc bodies, resem bling, but easily distinguishable from, asbes tos bodies. Much dust, which proved to be talc, appeared in the sections, and it was thought at the time that the particles were all fibers. More recent work on the lung by Nagelschmidt i has shown that the bulk of the dust is in the form of plates with only a few fibers.
At least three other autopsies on cases of talc pneumoconiosis (all from rubber works) have been made, and they show similar fea tures to the first published case. Small sur veys have been made on workers exposed to talc dust in various industries, hut larger ones have been planned to take place shortly. It is clear that talc dust, though fibrogenic. is not so active as asbestos in damaging the lungs.
Leather Dressers' Pneumoconiosis.--Co operation between the directors of chest clin ics, the mass radiography units, and the Medical Inspectorate of Factories has been instrumental in bringing to light hitherto unsuspected causes of pneumoconiosis. Since the mass radiography campaign was begun in 1948 for the early detection of cases of pulmonary tuberculosis, some 13.000,000 per sons have undergone examination. Many factory populations have been surveved, and
t Nagelschmidt, G. : Personal communication to the author.
93
1
M cl. A UGH UN
included among them have been factories mental details of five nonfatal cases, one of
where there is a dust risk. The workers at whom is now very ill. The other four cases
one leather factory were examined by Dr. are either recovering, or their condition is
Hugh Ramsay, of the Wanstead Mass Radi stationary. It is also remarkable that five out
ography Unit. He drew our attention to the of six affected workers were chemists en
fact that in one department a high proportion gaged in the development of the beryllium
of the workers showed abnormal x-ray lamp powders. At the factory where the fatal
changes, whereas in- other departments, case of beryllium granulomatosis occurred,
where there was no dust, no abnormalities 150 of the other workers were examined
were seen. In the department with the high clinically and radiographically and no more
proportion of x-ray abnormalities, skins cases were found, though there had been con
loaded with china clay and calcium carbonate siderable exposure to the dust of the lamp
are dressed on rapidly revolving felt wheels powders in the early days. It is undeniable
covered with a layer of fine Carborundum that beryllium oxide is toxic, but examina
powder. The job is very dusty, though it is tion of the histology of the lungs of the one
done under exhaust ventilation. The dust is fatal case has led me to hold the unorthodox
composed of much fine leather dust, with view that beryllium was not the sole cause of
smaller proportions of china clay (kaolin), the condition. There were two types of le
calcium carbonate, and Carborundum. It was sion : one of a granulomatous type, in which
found that the dust contained about 5% of there were giant and epithelioid cells, and the
free silica. The x-ray films showed all stages other in which were many fibrotic nodules
of abnormality, varying from early reticula indistinguishable from silicosis. Under polar
tion (micronodulation) through nodulation ized light many doubly refractile particles
to massive shadows. In a few cases there was were seen in the nodules, and an eminent
clinical evidence of disability. One man with crystallographer stated that these were cristo-
an x-ray film showing massive shadows had balite, one of the most active forms of free
died from "asthma and pneumonia" a year silica. This is not surprising, because one of
before the investigation began, and there was the ingredients of the lamp powder is silica
no autopsy. In spite of the fact that up to gel (25%), which in the preparation of the
the present time no pathological evidence has powder is heated up to about 1100C. The
been available, it is likely that the condition changed methods of preparing the lamp pow
will fall into the group of the mixed dust der have eliminated both the beryllium oxide
pneumoconioses. The dust of china clay, and the free silica, so that the risks both of
which for years has been thought to be com beryllium granulomatosis and of silicosis have
paratively harmless, is becoming more and also been eliminated.'
more suspect. Even apart from china clay, the presence of a small proportion of free silica is prima facie evidence that the dressing of such skins is a hazardous occupation.
"Pneumoconiosis'' from Vegetable Dusts. --Apart from cotton, not a great deal of work has been done on the vegetable dusts. The illnesses noted among cotton workers
Beryllium Pneumonitis and Granulomato include mill fever, a transitory illness which
sis.--It is remarkable that British experience affects nearly all new workers in cotton, flax,
of beryllium pneumonitis and granulomatosis and hemp mills and also in malt houses;
is not as extensive as that in the United "Monday fever" (or feeling) ; weavers'
States, though many workers have been ex cough, and byssinosis.
posed to the dust of fluorescent lamp powders containing beryllium oxide and also the dust and fumes from the alloys. Only one death has occurred, and the Factory Department
Byssinosis develops after about 20 years as a natural progression from "Monday fever" and in its final stage has the characteristics of chronic bronchitis and emphysema. As
has collected clinical, x-ray, and environ Schilling (1954) says, though it was de-
94
'/ '('.HUN
-es. one of lour cases ndition is u live out mists en'ryllium
e fatal vurred,
nined more : conlamp liable mina one '"dox -e of i lehich d the Liles
i11 1K
>% R
fI
&F TI I
B v 8 *x<< 888B &
VI %1
rsT DISEASES IN GREAT BRITAIN
., ribed by Greenhow nearly 100 years ago, . , tiology is still obscure. It presents an odd :i characteristic history of chest tightness i breathlessness on Mondays, which grad'v extends to other working days as the a-e progresses. "In its later stages these upturns are very distressing, but usually lain worse on Monday than on any other v. It causes no specific x-ray changes in lung fields." In the main, the workers he cotton card and blowing rooms suffer -t from the disease. Strippers and grindwho clean the carding engines are especiaffected. As mentioned previously, workwith hyssinosis are compensated under a . ial scheme.
agassosis.--Only one factory in the coun. handles bagasse (or sugar cane without - sugar), and bagassosis has occurred inly in those workers who were grinding gasse in a drv state. The condition is an ate bronchiolitis, with high temperature, ere dyspnea, and x-ray picture of the lungs owing generalized miliary shadows. Fiton cases of this acute disease have come to he notice of the Factory Department; some f these have been described by Castleden and Hamilton-Paterson (1942), Gillison and Taylor (1942), and Hunter and Perry ( 1946). The last case occurred in 1948. Since we got the firm to grind the bagasse under water, there have been no further cases.
Farmers Lung.--Farmers', or threshers', lung was first described by Campbell (1932), and after that Fawcitt (1936 and 1938) did a great deal of work on the condition. It has features similar to bagassosis, but, since it occurs mainly among workers who have been handling moldy hay during a wet summer, it is regarded as being caused by a fungus. Fawcitt was firmly of this opinion. Single cases of the condition are described from time to time by physicians in the agricultural districts.
Pneumoconiosis in Grain Dockers.--Dunner, Hermon, and Bagnall described in 1946 the clinical features and abnormal x-ray ap pearances in a group of 55 grain dockers.
Thirty of these men had pulmonary tubercu losis, but 11 others had x-ray changes sug gestive of the presence of pneumoconiosis. Fourteen had normal x-ray films. Analysis of the dusts from various grains showed small percentages of free silica; oat dust, for instance, had 5%. No autopsies have been carried out. but it seems that a case has been made out for an extended investigation of larger groups of grain dockers. `
Graphite Pneumoconiosis.--It has been found by some observers in England (Dunner. 1945, 1948, and 1949; Gloyne. Marshall, and Hoyle, 1949, and Harding and Oliver, 1949) that workers exposed to the dust of natural graphite develop radiographic changes in the lungs and disability. The range of x-ray abnormalities closely resembles that seen in coal miners. Pathological and experi mental studies (Gloyne and others, 1949. Harding and Oliver, 1949) show that the condition falls into the group of the mixed dust fibroses, the fibrotic nodules having a linear and radial pattern as opposed to the whorled fibrosis of the classical silicotic nodule. Natural graphite contains small per centages (of the order of 5%-10%) of free silica. There is as yet no evidence that pure graphite will produce a similar condition.
Manganese Pneumonitis.--A few cases of manganese poisoning affecting the nervous system occurred in the middle 1930's in workers grinding manganese dioxide for use in lamp batteries. In 1946, Lloyd Davies re ported a high incidence of pneumonia in a group of workers exposed to manganese di oxide dust in the manufacture of potassium permanganate. Animal experiments by Lloyd Davies and Harding (1949) confirmed that manganese dioxide irritated the lung tissue and caused intense infiltration of the alveolar walls and alveoli. Later granulomatous changes developed in some instances. These results are in line with those described byworkers in other countries.
Vanadium Pneumonitis.--Wyers (1946) recorded his observations on workers exposed to vanadium pentoxide dust, and his results
95
McLaughlin
are similar to those described by Sjoberg which make a dusty process more dusty and
(1949) in Sweden. The effects are a combi cause a lag in dust-control methods.
nation of systemic poisoning and irritation of the pulmonary tissue, leading in some cases to bronchospasm and pneumonia. Doig and Williams (1952) have described the marked bronchospasm occurring in workers exposed to the soot of oil fuel, which is thought to be caused by the high percent age of vanadium in the soot.
3. Compensation for industrial pulmonary disease began soon after 1918, and gradually most of the processes and industries which damage the lungs are being brought under the provisions of the various Acts of Parlia ment. The Industrial Injuries Act of 1946 removed the responsibility for compensation from employers and insurance companies to
the Government. Since then cases taken
SUMMARY
under Common Law against the employers
The position as regards the dust diseases have increased rapidly.
in Great Britain may be summarized as fol 4. Numerous legal provisions, contained
lows :
both in Acts of Parliament and in Regula
1. During the past 50 years, the risk of sili cosis in most of the major industries has been firmly established. Until the late 1920's, free silica was the only dust which was thought
tions, have been brought into force. Routine inspection by inspectors of factories and mines has been instrumental in limiting the numbers of cases of disability and death
to damage the lungs. Asbestosis, caused by brought about by inhalation of the dangerous
the dust of a combined silica mineral, came dusts.
into prominence about that time. In the mid dle 1930's, attention was given to the effects of other dusts on the lungs, such as iron and its oxides, and of radiopaque dusts, china clay, sillimanite, kieselguhr, talc, and mixed dusts containing free silica.
5. It is expected that more accurate infor mation about the incidence of the dust dis eases will be obtained in the near future, when statistical studies of the information obtained by the Pneumoconiosis Panels have been carried out, and when the report of the
During the middle 1930's also, the effects Registrar-General about the occupational
of coal dusts on the lungs were given increas incidence of disease at the time of the 1951
ing attention, and extensive surveys were Census becomes available. At the present
carried out, culminating in the formation of time no reliable information exists about
the Pneumoconiosis Research Unit of the the populations at risk in each industry and
Medical Research Council in 1945. The coal process.
miners numerically constitute the greatest 6. Surveys of the population by mass radi
problem of dust disease in Great Britain.
ography to detect early tuberculosis are
2. Despite the combined efforts of inspec bringing to light information about the ef
tors of factories and mines, physicians, chem- fects of dust in some hitherto unsuspected
sists, engineers, and research workers, the occupations.
deaths from pneumoconiosis have continued to rise yearly. The reasons for this increase may be found in more accurate diagnosis of the condition and in the publicity given to occupational diseases of the lungs, leading to more frequent mention of pneumoconiosis by physicians on death certificates. But a more likely cause is the urge for increased speed of
7. Many problems about dusts and the lungs are still unsolved, and some would say that we have only just begun to attack the fringes of the problem. Nevertheless, a great deal has already been accomplished.
Assistance in compiling the information con tained in this paper was rendered by Dr. P. K. Walker and the members of the Pneumoconiosis
production, and the introduction of machines Doig, A. T.: Unpublished data.
Panels of the Ministry of Pensions and National Insurance; Drs. E. R. A. Merewether, A. T. Doig, and G. 0. Williams, of the Factory Department,
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ers
ic-d : ia :ne nid i .he iin HiS
:oriis;re, :ion ave the nal 51 ant 'lit ad
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DUST DISEASES IN GREAT BRITAIN
Ministry of Labour and National Service; Dr. H. E. Harding, lately of Sheffield University, and Dr.
Nagelschmidt, of the Safety in Mines Research Laboratories, Sheffield.
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