Document DMqQv8vqm1VbZrQv13JYJOnmn

FILE NAME: Flooring Defense Exhibits (FLDX) DATE: 1969 DOC#: FLDX003 DOCUMENT DESCRIPTION: Pneumoconiosis - Proceedings of the International Conference in Johannesburg 167554851 TITLE Pneumoconiosis; proceedings of the international conference, Johannesburg, 1969. AUTHOR International Conference on Pneumoconiosis, ; Shapiro, H. A. VOLUME ISSUE ARTICLE AUTHOR ARTICLE TITLE NEW ORLEANS PUB LIBR (LNC) DATE PAGES ISBN ISSN PATRON NAME Jillian Brekeen PATRON PHONE PATRON EMAIL jbrekeen@mgmlaw.com PICKUP LOCATION Main , DUE DATE H /% ' i 1$ BORROWER LNC S U P P LIE R AAA PATRON, PLEASE RETURN ITEM TO: Interlibrary Loan New Orleans Public Library 219 Loyola Ave. New Orleans, LA, US 70112-2044 BORROWING LIBRARY, RETURN TO: AUBURN UNIVERSITY LIBRARIES ILL LENDING 231 MELL ST. AUBURN, AL, US 36849-5606 NOTES RMPh BROWn Dt , PNEUMOCONIOSIS Proceedings of the International Conference // Johannesburg 1969 ED ITED BY H. A. SHAPIRO Ph.D., M .B., Ch.B., F.R.S.S.Af. Visiting Professor o f Forensic Medicine University o f Natal, Durban ( p 't'L r M l., CAPE TOWN OXFORD UNIVERSITY PRESS LONDON NEW YORK TORONTO I97O O xford University Press, Ely House, London W. 1 ) GLASGOW NEW YORK CAPE TOWN SALISBURY IBADAN TORONTO MELBOURNE WELLINGTON I NAIROBI DAR ES SALAAM LUSAKA ADDIS ABABAi BOMBAY CALCUTTA MADRAS KARACHI LAHORE DACCA KUALA LUMPUR SINGAPORE HONG KONG TOKYO Oxford University Press, Thibault House, Cape Town PR IN TE D BY CAPE & T R A N SV A A L PR IN TE R S L T D B OiE'N'Otl Preface This Conference (convened in Johannesburg from 24 April to 2 M ay 1969) was the third International Conference on Pneumoconiosis to be held in South Africa. The first one took place in Johannesburg in 1930 and the second (also in Johannesburg) in 1959. The Third Conference was attended by over 250 participants, including some 60 overseas participants among whom were included wellknown scientists in industrial medicine from the United Kingdom, the United States of America, Canada, France, Italy, Belgium, Switzerland, Finland, West Germany, Aus tralia, Japan, Rhodesia, etc. The South African participants included scientists, engineers and administrative officials actively engaged in re search and the administration of compensation legislation, etc. Pneumoconiosis is an important industrial problem which requires the application of con trol and preventive measures, intensive research in the medical and engineering fields and a constant review and reassessment of legisla tive measures. The purpose of the present Conference was, therefore, to bring together recognised experts in the various disciplines in order to pool, on an international basis, knowledge, experience and ideas; to review the present state of research and preventive and control measures; and to determine the further research necessary to deal with the problem effectively. Publication of the Proceedings of this impor tant international survey has been made pos sible by the Department of Mines. We are indebted to the participants for their co-operation in approving their contribu tions for publication. The excellent summaries of the various discussions have been included as a result of the work of the very efficient band of rapporteurs. We also wish to thank Mrs. E. C. Shute for the preparation of the Subject and the Author Index. T o allow the Proceedings to reflect the international character of the authors, a rigid conformity of presentation has not been imposed on their contributions. The lists of References at the ends of articles should often be regarded as bibliographies as well as foot notes applicable to the text. H. A. Shapiro, Ph.D., M.B., C h.B., F.R.S.S.Af., Editor. Johannesburg, 1970. v International Conference on Pneumoconiosis, Johannesburg 1969 Message from the Minister of Mines of the Republic of South Africa It is a great pleasure for me to introduce to you this book, T h e Proceedings of the Inter national Pneumoconiosis Conference held in Johannesburg from 23 April to M ay 2, 1969, under the aegis of my Department. As is well known, the mining industry of this country is large and consists of both mining and processing of a great variety of minerals. Although each of these is associated with specific health hazards, such hazards may vary because of the circumstances in which the mining takes place. The last Pneumoconiosis Conference held in Johannesburg, was in 1959 and it was considered opportune that, after a decade, this subject (so important to my country) should be reviewed by experts from the Western world in conclave with our own South African scientists. Approximately 70 overseas scientists were present at the discussions which covered a wide field including both the medical and the engineering aspects. Lines of research were suggested which could be carried out in our country and which could benefit those who work in dusty occupations in many different countries throughout the world. I am confident that this book, which records the papers and the discussions, will be of interest to a wide field of readers whose work brings them into contact with the pro blem of pneumoconiosis. Minister of Mines, of Planning Pretoria, and of Health. September 1969. Message from the President of the 1969 International Conference on Pneumoconiosis When I was asked by the Minister of Mines, Dr. the Honourable Carel de Wet, M .P., to lead the Organizing Committee and to act as President of another international con ference on pneumoconiosis, my thoughts turned to the last conference which was held in Johannesburg in 1959. At that time the Pneumoconiosis Research Unit had been in existence for only 3 years and scientists from various countries were invited mainly to advise our young but enthu siastic research team on the best evolution of their research projects. Based on the recommendations of the 1959 Conference, the foundation laid by scientists of previous generations such as Pitchford, Irving, Mavrogordato, Simson and Strachan and the activities of the present scientists, the 1969 Conference has paved the way for con tinued progress and for continued intellectual curiosity. With my colleagues of the Organizing Com mittee I considered that every effort should be made to tackle many of the still unresolved problems inherent in exposure to dust. As will be appreciated, we have at our disposal unique facilities and material for purposes of research and we are anxious to repay, through close collaboration, some of the scientific debts we owe to other countries. At the conclusion of the Conference our Organizing Committee and the Vice-Presidents agreed on the best methods by which we in this country can continue to play an active part in assisting to solve problems of universal importance. It is sincerely hoped that the final decisions, which include recommendations about the extension of the terms of reference of the Pneumoconiosis Research Unit and the provision of adequate funds for such purposes, will be speedily put into effect in the interests of all concerned. I regard intellectual contact at the inter national level as an enriching experience, both to the giver and the receiver; the deliberations of the present conference are ample justifi cation of this philosophy. Grateful thanks are extended by myself and the Organizing Committee to all who have made contributions to the success of the Conference. Professor S. F . Oosthuizen, President. ix Officers of the Conference Patron: The Hon. Dr. Carel de Wet, Minister of Mines of the Republic of South Africa. President: Prof. S. F. Oosthuizen, Profes sor of Radiology, University of Pretoria, Pre sident of the South African Medical and Den tal Council and Medical Adviser to the M inis ter of Mines of the Republic of South Africa. Secretary-General: Dr. G. K . Sluis-Cremer, Director of the Miners' Medical Bureau of the Republic of South Africa and Director of the Clinical Sciences Division of the Pneumo coniosis Research Unit of the C.S.l.R . Assistant Secretaries-General: Dr. I. Webster, Director of the Pathology Division of the Pneumoconiosis Research Unit of the C.S.l.R. M r. J. F. Brauckmann, Administrative De puty Director of the Miners' Medical Bureau. Honorary Vice-Presidents: M r. J. J. A. Nel, Dr. S. M . Naude, Dr. A. J. A. Roux, Dr. T . M uller, Prof. J. H. S. Gear, Dr. A . J. Orenstein, Mr. J. G . Mackeurtan, M r. F. G. Hill, Mr. F. Baunach. Vice-Presidents: Dr. M urray C. Brown: United States of America. Dr. J. C. Gilson: United Kingdom. Prof. P. H. Rossier: France. Prof. E. C. Vigliani: Italy Mr. T . L . G ibbs: South Africa. R apporteurs Pathology: Dr. B. Goldstein, Dr. I. Prinsloo, Dr. S. D . Berson. Clinical Sciences: Dr. F. J. Wiles, Dr. H. v. Doom. Dust Physics: Dr. R. S. J. du Toit, M r. L . W. Isserow, Mr. A. F. H. Lombard, M r. P. H. Kitto. Radiation Hazards: Dr. J. K . Basson. Editorial C ommittee Dr. G. K . Sluis-Cremer, Dr. I. Webster and Prof. H. A. Shapiro (Editor). Sponsors The Conference was held under patronage of the M inistry of Mines of the Republic of South Africa and the Hon. the Minister of Mines, Dr. Carel de Wet, the Patron of the Conference. T h e Conference was sponsored financially by the Department of Mines of the Republic of South Africa, the Asbestos M ining Industry of South Africa, the Chamber of Mines of South Africa and the M ining Trade Unions. Accommodation for the Conference and other conference facilities were provided by the South African Institute for Medical Research. O rganizing C ommittee Chairman: Prof. S. F. Oosthuizen. Members: Dr. G. K . Sluis-Cremer, Dr. I. Webster, Dr. J. K . Basson, Prof. J. H. S. Gear, M r. F. A. Snyman, Dr. R. S. J. du Toit, M r. J. F. Brauckmann. L adies C ommittee Convener: Mrs. J. Webster. M em bers: Mrs. E. Oosthuizen, Mrs. J. E. V. Sluis-Cremer, Mrs. J. C. Snyman, Mrs. H. Basson, Mrs. J. Gear, Mrs. N . Brauckmann, Mrs. G. E. F. du Toit. Contents Wednesday, 23 April 1969 Symposium on Asbestos Chairman: T . L . Gibbs, Government Mining Engineer, South Africa Page 1. T he Inhalation o f Fibres. V. T im b r e ll......................................................... 3 2. Dust Sampling Instruments and Dust Standards in the United States o f America for Asbestos. L .J . C r a l l e y ......................................................... 10 3. Dust in South African Asbestos Mines and Fiberizing Plants. R. S. J . du T o i t ............................................................................................................13 4. Hazard Indices, Sampling Strategies in British Asbestos Factories and Standards for Asbestos Dust. C. G. A d d in g le y ...................................... 18 5. D iscu ssio n ...................................................................................................................21 Chairman: I. J. Selikoff, Environmental Sciences Laboratory, Mount Sinai School of Medicine, United States of America 6. The Data Sheets on the Chemical and Physical Properties o f the U IC C Standard Reference Samples. R. E. G. R e n d a ll............................................. 23 7. Characteristics o f the International Union against Cancer Standard Reference Samples o f Asbestos. V. Timbrell....................................................28 8. Dust Problems in the Use o f Asbestos Products.E. Walther . . . . 37 9. Dust Problems in the M ining, M illing and Packaging o f Asbestos. L . N . K u y p e r ................................................................................................... 42 10. D iscu ssio n ................................................................................................................... 51 Chairman: J. C. M cDonald, Department of Epidemiology and Health, M cG ill University, Canada 11. Neutron Activation Techniques in Investigations o f the Composition and Biological Effects o f Asbestos. A . Morgan and A . Holmes . . . . 52 12. Electron Microprobe Analysis o f Asbestos Bodies. A . M . Danger, I. Rubin and I. J . Selikoff...................................................................................................... 57 13. Inhalable Fibrous Materials. L .J . C r a lle y .......................................................... 70 14. T he Suitability o f Conventional Dust Instruments for Sampling Asbestos Dust Clouds. R. E. G. Rendall and G. C. H. van Sittert . . . . 74 15. Discussion . ................................................................................................. 79 Thursday, 24 April 1969 Symposium on Asbestosis Chairman: S. F. Oosthuizen, Adviser to the Minister of Mines of the Republic of South Africa 1. Official Opening o f the Conference by the Honourable the Minister o f Mines, Dr. C.deW e t ........................................................................................... 83 2. Pulmonary Ferruginous Bodies: Studies on their Origin. P. Gross, R. T. P. de Treville and M . Haller . .............................................86 3- Ferruginous Bodies. B . Goldstein and R. E. G. R e n d a l l ..........................92 4. Asbestos Bodies in the N ew York City Population in Tw o Periods o f Tim e. I. J. Selikoff and E.C. Hammond.....................................................................99 5- D iscu ssio n ................................................................................................................. 106 XI xii Contents Chairman: J. C. Gilson, Medical Research Council, Pneumoconiosis Unit, United Kingdom 6. The Detection o f Asbestos in Tissues. F. D. Pooley, P. D. Oldham, ChangHyun Um a n dj. C. W a g n e r ..................................................................... 108 7. T he Pathogenesis o f Asbestosis. I. Webster...................................................117 8. Characteristics o f Respirable Asbestos Fibres. V. Timbrell, F. Pooley and J . C. W a g n e r ............................................................................................ 120 ^9. Problems in the Pathology o f Asbestosis. P. Gross, R. T. P. de Treville, L. J. Crawley and F. L. P u n d s a c k ................................................126 10. D iscu ssio n .................................................................................................. 133 Chairman: E. C. Vigliani, Clinica del Lavoro, " Luigi Devoto" , Italy 11. 12. ^3. 14. T he Synthesis o f Collagen by Newborn Hamster Fibroblasts. J. S. Harington, E. Bey, P. C. King and B. D. Richardson................................135 Pathogenesis o f Pleural Plaques. J. G. T h o m s o n .............................138 Primary Diffuse Malignant Mesothelioma: Problems in its Diagnosis and in its Relation to Asbestos. J . Gluckman and M . Hurwitz . . . . 1 4 2 D iscu ssio n .................................................................................................. 147 Chairman: Murray C. Brown, Public Health Service, United States of America. 15. T he Pathological Diagnosis o f Malignant Mesothelioma o f Pleura and Peritoneum. J. G. T h o m s o n ............................................................ 150 16. Some Observations on Asbestosis in a Factory Population.W .J. Smither 155 17. T he Mortality o f Asbestos Factory Workers. M . L. Newhouse . . . . 158 18. Asbestos Fibre Contamination by Storage in Polyethylene Bags. G. W. G ibbs......................................................................................... 165 19. D iscu ssio n .........................................................................................................168 Friday, 25 April 1969 Symposium on Asbestosis (Continued) Chairman: S. Forssman, National Institute of Occupational Health, Sweden. 1. Asbestos Health Hazards: Recent Observations in the United Kingdom. J. C. G ils o n ................................................................................................173 2. Mesothelioma and Asbestos on Tyneside: A Pathological and Social ' Study. T. Ashcroft and A. G. Heppleston...................................................177 3. Mortality Experiences o f Asbestos Insulation Workers 1943-1968. I. J . Selikojf, E. C. Hammond a n d j. C h u r g ................................................180 4. Results o f Asbestos Exposure in France. J. Avril a n d j. Champeix . . 187 5. Results o f Asbestos Exposure in Finland. R. Kiviluoto and L.Meurman 190 6. Asbestos Exposure and its Results in Italy. E. C. Vigliani...................... 192 7. Epidemiology o f Primary Malignant Mesothelial Tumours in Canada. A . D. McDonald, A. Harper, O. A . E l Attar a n d j. C. McDonald. . 197 8. Asbestos Exposure in Australia. J. C. M c N u l t y . ................................... 201 9. Asbestosis in Rhodesia. M . Gelfand and S. A . Morton. . . . . . 204 10. Asbestos Exposure in South Africa. I. Webster......................................... 209 Chairman: J. F. Murray, South African Institute for Medical Research, Johannesburg, South Africa 11. D iscu ssio n ........................................................................................................ 213 12. Mesotheliomas in Rats Following the Intra-Pleural Inoculation o f Asbestos. J. C. Wagner, G. Berry and V. T im b r e ll................................216 Contents xiu 13. Studies on the Carcinogenic Effects o f Asbestos Dust. P. Gross, R. T. P. De Treville and L. J . Cralley ...................................................................... 220 14. Mesothelioma, Including Peripheral Lung Malignancy and Tuberculosis in the North West Cape. C. A . Sleggs........................................................ 225 15. Lung Function in Relation to, Radiographic Changes in Quebec Asbestos Workers. M . R. Becklake, G. G. Fournier-Massey, J . C. McDonald, J . Siemiatycki and C. E. R o s s ite r ............................................................... 233 16. D iscu ssio n ............................................................................................................237 Symposium on the Radiology of Asbestosis Chairman: E. P. Pendergrass, Department of Radiology, University of Pennsylvania, United States of America 17. Radiology o f Asbestosis. A . Solomon......................................................... . 243 18. T he Problem o f Asbestosis in Relation to the International Classification o f Radiographs in Pneumoconiosis. H. B o h l i g .................................... 248 19. Asbestosis: Aspects o f its Radiological Features. R.Kiviluoto . . . 253 20. D iscu ssio n ..........................................................................................................256 Symposium on the Radiology of Pneumoconiosis Chairman: G. Worth, Krankenhauses Bethanien, Germany 21. Radiological Features o f Diffuse Mesothelioma. A .Solomon . . . . 261 22. Some Aspects o f the Electronic X-ray Image Manipulation Particularly in Connexion with Disseminated Pulmonary Changes. H. Blaha and J . Nrnberger.......................................................................................................... 266 23. The Reduction o f Observer Variation in Categorizing Coal Workers' Pneumoconiosis. S.Rae . ............................................................................. 268 24. Is Coal Mine Dust Visible in X-rays o f the Lungs ? G. Worth . . . 273 25. D iscu ssio n ................................................................................................................ 278 Monday, 28 April 1969 Symposium on Coal Workers' Pneumoconiosis Chairman: F. M . Engelbrecht, Department of Physiology, University of Stellenbosch, South Africa 1. Dust Sampling and Dust Control on South African Collieries. G. H .J . Kitson.................................................................................................................. 283 2. Cumulative Dust Exposures and Pneumoconiosis Responses in German Coal Mines. M . T. R. Reisner...................................................................... 286 3. Progress o f the 25-Pit Scheme. W. H. W alton............................................ 292 4. The Relation between Physiological Changes and Pathology in Coal Workers' Pneumoconiosis. E. F r i t z e ......................................................... 295 5. The Influence o f Dust Elimination and the Effects on the Development o f Pneumoconiosis. H .J . Einbrodt............................................................... 299 6. D iscu ssio n ............................................................................................................ 305 Chairman: P. H. Rossier, Medical Clinic, University of Zurich, Switzerland 7. Complicated Coal Workers' Pneumoconiosis. J . C. Wagner . . . . 306 8. Coal Workers' Pneumoconiosis in the United States: Radiographic Considerations with Special Reference to Large Opacities. E. P. Pendergrass ............................................................................ . . . 309 9. Emphysema in Relation to Dust Exposure. A . G. Heppleston. . . . 312 10. D iscu ssio n ..........................................................................................................315 xiv Contents Chairman: J. H. S. Gear, South African Institute for Medical Research, Johannesburg, South Africa n . Dust and Chronic Bronchitis. J . C. G ils o n ...................................................317 12. Epidemiological Evidence on the Relationship Between Lung Function and Coal Dust Exposure. G. W o r t h ......................................................... 322 13. T h e Relationship Between Dust Exposure and Chronic Bronchitis and Emphysema. W. T. Ulm er................................................................................ 328 14. D is c u ss io n .................................................................................................................337 Symposium on Chronic Bronchitis and Emphysema Chairman: G . Wright, Department of Medical Research, Saint Luke's Hospital, United States of America 15. T he Bronchi in the South African Bantu. 5 . D. Berson and N . F. Laubscher.................................................................................................................341 16. Chronic Bronchitis in Bantu Mine Workers. G.K . Sluis-Cremer. . . 345 17. A Cohort o f White Gold Miners. F. J . Wiles, M . H. Faure, G. K . Sluis- Cremer, H . T. van Doom andW. de K . K r u g e r .............................................350 18. D is c u ss io n .................................................................................................................352 19. Simson Memorial Lecture: Silicosis in South Africa. I. Webster . . . 354 Tuesday, 29 April 1969 Chairman: W . T . Ulmer, Medical Division o f the Silicosis Research Institute of Bergbau-Berufsgenosschenshaft, West Germany 1. An Evaluation o f Some Methods Used for the Assessment o f Chronic Respiratory Disease. B . van L i n g e n .............................................................. 362 2. T h e Effects o f A ir Pollution-- Epidemiological Evidence. E. C. Hammond and I .J . Selikoff.................................... 368 3. Experimental Emphysema as a Tool in the Study o f Pneumoconiosis. P. Gross and R. T. P. de T r e v ille ............................................................... 374 4. Emphysema in South African G old Miners. I. Prinsloo andN. F . Laubscher 380 5. Relationship between Chronic Bronchitis and Pneumoconiosis in Coal- Miners. A . Minette and F . L a v e n n e .............................................................. 386 6. Discussion ........................................................................................ 393 Chairman: M . Gelfand, University College of Rhodesia and the Pneumoconiosis Medical Bureau, Rhodesia 7. T he Mechanism o f Silica in Fibrogenesis. F . M . Engelbrecht. . . . 396 8. Asbestos Bodies in the Lungs o f a Series o f Finnish Lung Cancer Patients. L. O. Meurman, M . Hormia, M . Isomdki and S. Sutinen . . . . 404 9. Pneumoconiosis Induced by Vegetable Dust. J . R. Riittner.............................408 10. Byssinosis in Textile Workers. A . Bouhuys........................................................412 11. Pulmonary Disability and Pulmonary Function in Gold Miners on the Witwatersrand, Related to Duration o f Service. L . D . Erasmus and Helen van Doom .................................................................................................... 417 12. Fibrosis in Rats' Lungs Produced by Radioactive Dust. F . M . Engelbrecht and B . F. Thiart.................................................................................................... 422 13. D iscu ssio n .................................................................................................................425 Contents xv Symposium on Mixed Dust Pneumoconiosis Chairman: J. R. Rttner, Histopathologiscken Institut, Universitt, Zurich, Switzerland 14. The Relative Toxicities o f the Main Classes o f Minerals. B . Goldstein and R. E. G. Rendall.................................................................................................... 429 15. Lung Clearance: Silicosis and Anthracosis. H. Jammet, J . Lafuma, J . C. Nenot, M . Chameaud, M . Perreau, M . Le Bouffant, M . Lefevre and M . M a r t i n ........................................................................................................435 16. Dust Index Versus Period o f Service on South African Mines Before Certification for Pneumoconiosis. R. S .J . du T o i t .....................................438 17. D iscu ssio n .................................................................................................................442 Chairman: A. G . Heppleston, Department of Pathology, University of Newcastle Upon Tyne 18. A Study o f Respiratory Responses to Duration o f Foundry Work. J . C. Gilson, T. A . Lloyd Davies and P. D. O l d h a m ...................................... 445 19. Silicosis and Silico-Tuberculosis in Industry in West Germany. R. W a g n e r .................................................................................................................450 20. D iscu ssio n .................................................................................................................453 Thursday, 1 May 1969 Symposium on Silicosis Chairman: F. G. Hill, Rand Mines Limited, South Africa 1. South African Methods for the Assessment o f Dust in Gold and Coal Mines. P. H.K i t t o ............................................................................................... 457 2. T h e Composition o f Airborne Dust in South African Gold Mines. D. G. Beadle and A . A . B r a d le y ................................................................................. 462 3. Recorded Dust Conditions and Possible New Sampling Strategies on South AfricanGold Mines. W. L . le R o u x ................................................... 467 4. Period o f Service Before Certification for Pneumoconiosis on South African Gold Mines. R. S. J . du T o it.........................................................470 5. The Relationship Between the Amount o f Dust Breathed and the Incidence o f Silicosis: An Epidemiological Study o f South African European Gold Miners. D. G. Beadle, G. K . Sluis-Cremer and E. Harris 473 6. D iscu ssio n .................................................................................................................478 Chairman: F. Lavenne, Institute of Mining Hygiene, Belgium 7. Recent Progress in Dust Control in South African Gold Mines. D. G. B e a d l e .................................................................................................................486 8. Protein Biosynthesis and Fibrogenesis after Silica Administration. W. F its c h e n .................................................................................................................489 9. Cell Membranes in the Pathogenesis o f Silicosis. T. A .Kilroe-Smith . 492 xo. The Pathogenesis o f Silicosis. A . G. H e p p le s to n ........................................... 496 x i. D is cu ss io n .................................................................................................................499 Chairman: L . Noro, Institute of Occupational Health, Finland 12. Aspects o f Silicosis Prophylaxis. W. T. Ulmer and W. Weller - 503 13. Aspects o f Pulmonary Function in Silicosis in South African Gold Miners. C. M . Prowse . 508 14. Silicosis and Lung Cancer in Switzerland. J . R.R ttn e r ................................ 512 15. Lung Diffusing Capacity for Carbon Monoxide and Alveolar-Arterial XVI Contents Tension Differences for Oxygen and Carbon Dioxide in Coalminers Still at Work. A . Frans, N . Portier, C. Veriter, L. Brasseur and F. L a v e n n e ............................................................................................................514 16. D is cu ss io n ..........................................................................................................519 Symposium on Aspects of Pneumoconiosis Compensation Chairman: G . K . Sluis-Cremer, Miners' Medical Bureau, South Africa 17. What in Pneumoconiosis Should be Compensated ? F. A . Snyman . . 525 18. What in Pneumoconiosis Should be Compensated? R. Wagner . . . 529 19. D is c u s s io n ........................................................................................................... 531 Friday, 2 May 1969 Symposium on Radio-Activity in Mining Chairman: A. J. A. Roux, Atomic Energy Board, South Africa 1. Uranium Mining in South Africa. S. L. S. S w a rt...................................... 537 2. Physical Behaviour o f Radon and its Daughters with Particular Reference to Monitoring Methods. A. M o r g a n ............................................................. 540 3. Radiation Levels in Gold Mines in South Africa with Special Reference to Radon and Radon Daughters. J . D. Greig and R. Rolle . . . . 544 4. Uranium Toxicity with Specific Reference to its Radiation Hazards. H. Jammet, D. Mechali and M . D o u s s e t ............................................... 547 5. On an (M PC)a for the Short-Lived Daughters o f Rn-222, -1969. C. G. Stewart and S. D. S i m p s o n ...........................................................................551 6. D is c u s s io n ................................................................................................................ 555 Chairman: S. F. Oosthuizen, Adviser to the Minister of Mines of the Republic of South Africa 7. Radiation Hazards in Uranium Mining in Australia. J . R. Stewart . . 558 8. Radiation Hazards o f Uranium Processing in South Africa. J. K . Basson 561 9. Personnel Monitoring o f Uranium Workers with Specific Reference to Urine Analysis. J . D. Greig and C. C. F r e e d ............................................ 565 10. American Uranium Miners and Lung Cancer. V. E. Archer and Murray C. B r o w n ..................................................................................................... 569 11. Bronchogenic Carcinoma in South African Gold Mines. I. Webster . . 572 12. D is c u s s io n ........................................................................................................... 575 Symposium on the Engineering Aspects of Pneumoconiosis Monday, 28 April 1969 Chairman: P. H. Kitto, Chamber of Mines of South Africa 1. Measurement o f Dusts Containing Asbestos for Assessing Asbestos Hazards. D. Hasenclever and A . S c h t i t z ................................................... 581 2. Conversion Factors Between Particle Numbers, Surface Area and Mass Concentrations for Coal Dust. W. H. W a l t o n ...................................... 584 3. Calculation o f the Relationship Between Photoelectric Readings and Particle Number, Area and Weight Concentrations in South African Coal M ine Dust Clouds. G. H. J . K i t s o n ............................................ 587 4. D is c u s s io n ........................................................................................................... 593 Contei ats xvu Chairman: V. Tim brell, Medical Research Council, Pneumoconiosis Unit, United Kingdom 5. Dust Sampling Instruments to Collect the Respirable Fraction o f Coal Dust for Compositional Analysis and Animal Experiments. H. Breuer and M . T. R. R e i s n e r ......................................................................... 595 6. Hazard Indices in West German Mines. K . S c h i d t e ......................................600 7. Dust Sampling Instruments and Hazard Indices in Coal Dust in the United Kingdom. W.H. W a lto n ..................................................................... 603 8. D is c u ss io n .................................................................................................................607 Tuesday, 29 April 1969 Chairman: W . H. Walton, Institute of Occupational Medicine, United Kingdom X. Suggestions on Criteria for Sampling Asbestos Dust. V. Timbrell and S. H o l m e s ........................................................................................................610 2. The Measurement o f Airborne Dust Concentration in U .K . Iron Found ries. R. I. H i g g i n s ..............................................................................................613 3. Production o f Dust Clouds o f Steady Concentration for Animal Experi ments and Dust Sampling Calibration. H. Polley, K . Schulte and J . S t u k e .................................................................................................................617 4. A Method for Assessing Dusts Containing Free Crystalline Silica in Industries Other than the Mining Industry. D. Hasenclever . . . 620 5. Environmental Dust Survey o f Bituminous Coal Mines in the United States. M . Jacobson..............................................................................................623 6. D is c u ss io n .................................................................................................................628 Chairman: C. T . Hardy, Government Mining Engineer's Division, Department of Mines, South Africa 7. A New Sampling Instrument and an Automatic Method o f Assessment o f Dust Samples from South African Gold Mines. J . H. Talbot . . 631 8. The Labour Involved in Computing Cumulative Dust Exposures for Individual Miners: T he Reaction o f Miners to being Removed from One Working Area to Another to Lim it their Cumulative Exposures. K . S c h u l t e .......................................................................................................... 634 9. Infrared Methods o f Dust Compositional Analyses. M . Gade and M . T. R. R e i s n e r .......................................................................................................... 636 10. Testing o f Dust Masks in Germany. D. H asenclever..................................... 640 11. Automation o f X-ray Diffraction Meters to Increase the Number of Samples Analysed per Unit o f Tim e. R. W. Schliephake and K . Schulte 643 12. D is c u ss io n ................................................................................................................ 645 Index o f A u t h o r s .......................................................................................................... 649 Index o f S u b j e c t s ..........................................................................................................651 m rnm m m m m m Symposium on Asbestos 36 Timt,Te|] T able 13: d Spacings (A) from Selected A rea D iffraction P atterns d u st problem s in th e u se o f asbesto s pr o d u cts Amosite 3-88 3'45 3-00 2 64 1-74 1 -6i 1-55 1 32 1 05 0-89 o-88 0-755 Anthophyllite 4-58 M 2 65 S 2-27 1-75 S 1-55 S i -33 M 1-28 1 23 1-14 1 06 1-005 o -93 0-895 Crocidolite 3-41 2-57 2-24 2* 13 1-78 1*70 I *6i 1-49 1-30 1-27 i *o6 0-985 0-89 Rhodesian Chrysotile 7-27 4-58 367 S 2-6i 2-14 1-76 M i -55 S i -34 S 1-29 1-20 1-065 I -00 M 0-89 S Canadian Chrysotile 7-60 4-58 3-67 2'55 2-09 i '73 i -54 1-33 1-28 1-20 1-05 I -00 o -8q<: S = strong rings. M = medium strength. T able 14: Principal L attice Spacings C u K a R adiation A = 1 45 A Asbestos Type Amosite Anthophyllite Crocidolite Rhodesian Chrysotile Canadian Chrysotile Peak No. 2 d I. 10-7 2. 27-3 3- 29-1 4- 32-3 I. 9 -3 2. io -6 3- 19-4 4- 27-5 5- 28-5 6. 29-2 d 8-26 A 3-27 A 3 07 A 2 '77 A 9 ' 5 A 8-40 A 4-58 A 3 '25 A 3 13 A 3-06 A I/Ii 100 *0 36-4 52-3 43-2 100*0 361 55'5 47-2 58'3 63-9 I. io-5 8-43 A 100*0 2. 19-7 4 ' 5 i A 3- 26-0 3-43 A 2 5 '7 25-7 4- 28-7 3 - 1 1 A 41-4 5- 32-9 2-72 A 50*0 6. 3 4 -4 2 -6 i A 20*0 7- 35 -3 2-54 A 35'7 I. 12-0 7-38 A 100*0 2. 19-5 4'55 A 28-8 3- 2 4 ' 3 3-66 A 50-8 4- 36-5 2-46 A 5- 60-2 1-54 A 27-1 20*3 I. 12-0 7-38 A 100*0 2. 19-5 4 ' 55 A 3- 24-3 3 -66 A 27*0 57-1 4- 36-5 2-46 A 5- 60-2 j 1-54 A 23-8 20-6 The electron diffraction studies have indicated that the grinding involved in the preparation of the reference samples did not 1 affect the crystalline structure of the fibres. Electron D iffraction The X-ray diffraction patterns of the sample] have been prepared and from these pattern] the principal lattice spacings determined, These lattice spacings are listed in Table 14, By comparing these figures with equivalent figures obtained from material extracted from lungs it would be possible to detect changes in the crystal structure due to biological activity or other causes. P u b lic at io n s Data sheets are distributed periodically tol recipients of the reference samples giving brief information on their characteristics, and details of the analysis methods are being published in the literature. I wish to acknowledge on behalf of the UICC the assistance given by all those who have con tributed to this work. R eferences Tim brell, V. and Rendall, R, E. G . (1969): In tli( press. Report and Recommendations of the Working Group on Asbestos and Cancer (1965 a): Ann N .Y. Acad. Sci., 132, 706-721. (1965 b): Arch, environm. Hlth., 11, 221-225. (1965 c): Brit. J. Industr. M ed., 22, 165-17'- Tim brell, V., Gilson, J. C. and Webster, I. (1968): Int. J. Cancer, 3, 406-408. Tim brell, V ., Hyett, A. W . and Skidmore, J. $ (1968): Ann. Occup. H yg., 11, 273-281. Timbrell, V, (1954): Brit. J. appl. Phys. Suppi 3, 586 E rnst W alther Former Member of the Research Advisory Committee (Engineering) Asbestosis Research Project of the Pneumoconiosis Research Unit, Council for Scientific and Industrial Research i Introduction. According to the preamble in the invitation to this conference, its purpose has been defined as the pooling of knowledge, experience and ideas, to reviewing the present state of research and preventive or control measures, with a view to determining further research which is necessary to deal with the problem effectively. x.2. Many statements have been made in recent years stressing the hazards associated with mining, milling and handling of asbestos (ores and fibres) and the uses of asbestos (occupationally) and asbestos products by the general public. Some of these have been sen sationally exploited by the press and other news media, often taking facts out of context and creating an atmosphere of fear, not only in occupational circles but also amongst the general public, out of proportion to any possible real hazard. 1.3. After years of extensive research and deliberation by world authorities on Asbestosis, Mesothelioma and Talcosis, we shall, in the course of the next few days, be brought up to date by their contributions on these subjects, and the objective analysis of the facts gathered so far, should allow industries and government bodies to plan future research programmes and campaigns to eliminate health hazards, where such should exist and are attributable to the products manufactured from asbestos and like fibres. 2. When discussing the dust problems attri buted to asbestos, there are 2 main con siderations : 2.1. The first has to do with the precise nature of exposure to asbestos fibre by workers actually handling the products, or occupa tional exposure, which has been studied extensively, and on which legislation has been passed in many countries.1- 2 There is little doubt that excessive quantities of asbestos dust, or any dust for that matter, are harmful to health. Dust prevention in plants, factories and building sites, introduced in recent years, has reduced and eliminated health hazards and in most cases led to fairly satisfactory conditions. It can be expected that such improvements would also reflect in a greatly reduced aerial pollution in the immediate surroundings of the operations, thus removing hazards to the general public from this source. 2.2. The second aspect falls within the definition of this paper, namely the exposure to asbestos dust, which might be incurred by the general public using asbestos products, where exposure will be of an infinitely lower intensity. 2.3. Asbestos products could conceivably release asbestos dust into the ambient air as a result of environmental influences upon the products. Unfortunately, there is a paucity of factual information pertinent to this question. 3. Before commenting on the specific dust hazards, I wish to refer briefly to the main diseases attributed to exposure of asbestos in recent years. 3.1. Asbestosis and Bronchogenic Cancer. These have been strongly linked with occupa tional exposure to asbestos fibre where the exposure to fibre was intense, over lengthy periods, and the number of fibres in the ambient air, very great. 3.2. L . J. Cralley et al.3 pointed out, that `all coated fibres resembling golden yellow fibrous bodies found in the lungs of asbestos workers, had been termed " asbestos bodies" , even though the nature of these fibres had never been identified'. These scientists attri bute the presence of these bodies, comprising fibres coated with protein and iron pigment, subsequently termed `ferruginous' bodies, to a variety of respirable fibres. Besides asbestos, rock wool, gypsum, talc, magnesite, mica, etc., as well as certain synthetic products such as ceramic fibres, glass fibres, slag fibres and metal whiskers, etc., are listed as respirable fibres, together with those of vegetable and animal origin. 3.3. Mesothelioma has been linked in a similar way, but is thought to be associated with exposure of a lower order of intensity. Despite all the attention focused upon it in recent years, this rare tumour still constitutes a problem because of the difficulties of 37 3 E- Waith p u s t Problems in the Use o f Asbestos Products diagnosis. T he matter is further complicated as `these tumours have occurred in people on whom no evidence of exposure to asbestos dust was established'.1 On the occasion of the Annual General Meeting in August 1968, Dr. I. Webster, Chief Pathologist of the Pneumoconiosis Research Unit of the C.S.I.R. South Africa, stated that the `explosion of mesothelioma feared some years ago, had not taken place'. M uch of the campaign against Crocidolite could therefore, no doubt, be attributed to a `statistical explosion', extra polation of clinical observations in earlier years, or, that other unidentified causative agents were at work. T o place the problem of mesothelioma in its proper perspective, it has been pointed out that the total number of cases known at present in the entire world is less than 1,000:5 according to some authorities, possibly even less than 500:6 and this, after 10 years of research and focusing of attention upon it. It constitutes an insignificant problem compared with the death rate of about 29,000 in 1967 in the U .K . alone, from various forms of lung cancer. 3.4. Talcosis: Another occupational disease with symptoms similar to asbestosis should be mentioned in this context. In their work presented to the American Industrial Hygiene Conference in M ay 1968, L . J. Cralley et aV reported `that talcum powder contained a significant percentage of respirable fibres, and was a potential source of " feiruginous" bodies observed in the lungs of humans'. 3.5. These diseases are considered to be dose-related in respect of asbestos fibre (or talc). It is, however, unlikely (even under adverse conditions) that exposure of a general nature in the normal use of asbestos products could, in any way, reach the critical levels of intensity, determined or accepted in the occupational environment. Such exposure will be of a very low order, but we lack knowledge on the tolerable limits. We cannot transfer experience in one kind of exposure, namely industry, into the very different exposure sphere affecting the gen eral public. 3.6. T o reach clarity in these matters, a number of questions must be answered by research where we lack factual knowledge: i. We need to know accurately, the expo sure levels in terms of dust concentrations, frequency and duration of such exposure to start or induce the alleged disease processes. ii. T o which degree or concentration 4 asbestos fibres actually exist in the ambient air of our city streets? , iii. W e need factual information concerning the kinds and numbers of all types of fibrebs (not only asbestos fibres) in rooms where asbestos products could conceivably release some fibres either from walls, ceilings, insula tion linings, air ducts, or from floors. iv. T o which degree might asbestos cement products weather and release fibres into the ambient air directly or indirectly by subse quent re-dispersion? v. Is asbestos fibre as indestructible as t is made out to be, or to what degree, and will it retain its identity in the process of destruc tion? vi. How much real asbestos fibre is dis seminated during the use of brake linings, clutch linings, in the normal operation of the automobile in built-up areas? vii. W e need to obtain a factual picture the general pattern of living of suspect! cases, in investigating their exposure levels, not only to asbestos fibres, but to other fibroi bodies in the ambient air; their individual ways and habits of living (smoking, drinking, drug addiction, nutrition), the overall patho logical picture (tuberculosis), nervous tension associated with modern living, factors of general air pollution from industry and trans port in combination with the weather pattern, radiation etc., all of which might lead, in their combined effect, towards a possibli predisposition to trigger off the diseasi by reducing the individual's protectivi mechanism. 3.7. M ost of the controversy of recent years, no doubt, stems from lack of factual knowledge on these points or from the extra polation of observation from one field to another. There are many essential materials and processes in modern industry which involve an element of risk. This should he recognised, understood, and steps need be taken to reduce it to a tolerable level. In this connection the progress made in the asbestos mining fields in South Africa, is worth men tioning, as we shall hear in detail from the next speaker. By studying problems con fronting the industry a few years ago, in co operation with the Government Mining Engineer, the Department of Mines and tbs C.S.I.R., a step by step programme />' improvement was implemented, so reducing exposures and, in many cases, complete elimination of hazards was achieved. In the Annual Report 1967/68/ C.S.I.R . Department of Mines, we read: `Considerable progress continues to be made in dust-control, but as research in the medical field is by its very nature, a long term undertaking, only limited progress has been achieved so far in this field.' . . , , 4. Turning to various asbestos products which have been under scrutiny for some time, I wish to offer the following comments: 4.x. Asbestos cement products absorb a large portion of the world's asbestos producdon, particularly Chrysotile, Crocidolite and to a lesser degree Amosite, in combination with Portland Cement. Asbestos fibre and cement, form a homogeneous union, extremely inert to the action of the elements. 4.1.1. It has been implied that small quan tities of fibres are released through the weathering of asbestos cement. Under extreme climatic conditions like heavy hail, certain frost conditions, or, through aggressive chemical actions, small quantities might con ceivably be released, but `there is no evidence that such small doses are harmful'.5 nor will this occur with normal usage. Roofings, ceilings, partitions, etc., used in dwellings and halls often receive a decorative finish, thus further eliminating any hazard of exposure. 4.1.2. The Asbestosis Research Council in the U .K .'a has reached the conclusion, and emphasizes the fact, that there is no hazard in the handling, working and fixing of asbestos cement products, provided certain simple precautions, outlined in their Code of Practice, are followed. There is, therefore, no reason to assume or to expect any health hazard to the general public in using such products once they are fixed and installed. 4.1.3. In support of this, I present the following information made available by Dr. Lepoutre of Belgium : 11 `Professor Van de Voorde and Professor Meulepas of the University of Louvain, at the request of the Belgium Eternit, have done a survey (published in Acta Tuberc. et Pneumologica Belgica No. 6 Nov.-Dee. 1967) in respect of the death causes among the inhabitants of 13 communities situated in a radius of 7 k.m. around the Eternit plants of Kapelle-op-den-Bos and Tisselt and a similar survey in 13 communities in the district of Westhoek, an agricultural area devoid of industries. In comparing the frequency rate of certain affec tions witnessed between 1959 and 1963 in the 2 *he following conclusions were reached: The populations living within the radius of 7 k.m. of a transformative plant of asbestos, did not present for the period 1959-63 a higher degree 39 of mortality caused by malignant tumours than the average for the agricultural area of Westhoek.' 4.1.4. If we consider that the population of the area surveyed by Professors Van de Voorde and Meulepas, is not only living within close proximity of an extensive asbestos product operation (one of the largest single units in Europe), and that a great number of asbestos products were used in the construc tion of roofing, ceiling, piping, partitioning and decorating of their homes, and further, that an undisclosed but presumably large percentage of this population has been em ployed over a number of years by the manu facturing concern, it would appear that a health hazard to the general public from the environmental exposure of a modern, well protected operation, or from the normal use of asbestos cement products, could be ruled out. It is noteworthy that the above operation, in 1954 introduced an annual clinical and radiological examination of all its workers including clerical staff. 4.2. Brake Linings. It has been suggested that the braking of countless vehicles fitted with brake linings containing a large per centage of asbestos fibre (30-50%) mostly Chrysotile, in combination with resins, polymers, oxides, pigments, metals, carbon black and graphite, would produce hazardous dust. 4.2.1. Investigators have found no substance in these allegations. Their theory of what happens to the asbestos in brake linings is explained by J. R. Lynch12 that `Wear occurs not by abrasion of the lining by the drum, but by the production of minute areas of intense heat at the point of contact between drum and lining. Decomposition not only of the binder, but also of the asbestos occurs at these locations, as the breakdown temperature of Chrysotile asbestos of about 9ooF, is exceeded. T h e decom position products will thus include no free asbestos fibres, but a different mineral resulting from the thermal metamorphosis of the asbestos'. 4.2.2. J. R. Lynch reaches the following conclusions: `Only a very small proportion of the asbestos worn from brake linings is released as free fibre, the remainder is converted into some other mineral as a result of the extreme temperature generated at small spots on the surfaces. Thus, although urban air contains a few free fibres as a result of brake lining wear, they represent a very small proportion of the total asbestos used in the manufacture of brakes, and many sources of respirable fibres not associated with asbestos products have been identified to be present in urban air and the free fibres from brake lining 40 E- WalthC[ I wear appear to be an inconsequential health factor in urban air pollution.'3 4.3. Floor Tiles. These have been men tioned as potential dust hazards. In the floor tiles, asbestos (Chrysotile) is intimately em bedded in thermo-plastic resins. T he wear resistance is, however, extremely high, and the liberation of asbestos fibre in normal usage must be termed infinitesimal. We have no scientific evidence of anyone having contracted a disease from exposure to floor tiles in normal use. In most instances, such tiles, which have a high decorative value, receive a good wax covering which acts as an additional sealer. 4.4. Insulations. T he occupational hazards in this field have been extensively investigated, occupational exposures are controlled through regulations1 and Codes of Practices5*10i.*3 regard ing industrial hygiene, both in the new equipment, maintenance, and break-up fields. Fibre-based insulation products, having little resistance of their own to abrasion or shock, are provided with protective coverings of varying degrees of mechanical resistance, such as metal sleeves and covers, bandages, panels, or sealers, adhesives, tough decorative coatings or other hard setting renderings. There is no factual evidence of a health hazard from these products once they are installed and properly maintained. 4.5. Asbestos Textiles. These are used for very special and limited applications and the general public will not normally be associated with their use. T he undisputed life saving properties of these products will far outweigh any imaginary health hazards. 4.5.1. There is, further, no health hazard to the general public arising from the use of asbestos based jointings and packings. 4.6. Battery Boxes. A field of application for considerable tonnages of Crocidolite in thermo-setting compounds, these do not con stitute any health hazard in normal use. 5. C onclusion i. We should not lose our sense of propor tion when numerically evaluating available facts and indications and keep them in proper perspective vis--vis the global hazards and diseases affecting the general public. ii. Any industrial occupation presents cer tain hazards, but we cannot transfer experience gained in industrial exposure into the very different exposure sphere affecting the general public. iii. In these days, when all substances jn I the air, water and in food are constantly under scrutiny as to their effect on public health there should be no surprise that asbestos is among the subjects of intense investigation.*1 iv. On the strength of present knowledge we may conclude that the normal use 0f asbestos products does not give rise to abnor mal health hazards. v. There is a strong belief that health hazards previously attributed to asbestos fibre might in fact be associated with exposure to other respirable fibres or causative agents. vi. Additional detailed research is required to answer the question in paragraph 3.6. R eferences 1. D raft Statutory Instrument. The Asbestos Regulations 1968-U .K . The Threshold Limit Values for Asbestos. H .M . Stationery Office -- 1968. 2. H . Schlegel. Silikatosen (Asbestos, Talkose) SU V A -M erkblatt 1-- Nov. 1968. 3. L . J. Cralley, R. G. Keenan, J. R. Lynch and W . S. Lainhart. Sources and Identification of Respirable Fibre. American Industrial Hygiene Ass. J. 29:129 (M arch/April 1968). 4. J. C. Wagner and Gilson. Asbestos in tin Lungs. Nature, Nov. 25 '67-- 170. 5. G . K . Sluis-Cremer and I. Webster. Asbestos the Lethal Dust. 1967, S. Afr. M ed. J., 41, 1204. 6. J. Gluckman. Asbestos, Asbestosis, Mesothe lioma. Letter to Executive Comm. Asb. Res. Project, Oct. 23, 1968. 7. L . j . Cralley, M . M . K ey, D. H. Groth, W. S. Lainhart and R. M . Ligo. Fibrous and Mineral Content of Cosmetic Talcum Powder. American Ind. Hygiene Assoc. June-Aug. 1968: 300. 8. I. J. Selikoff, J. Churg and E. C. Hammond. | Asbestos Exposure and Neoplasia. J.A.M.A. 188:22 (1964). 9. Asbestosis Research Project. Annual Report C .S.I.R . (S.A.) 67/68, p. 11/6. 10a. Asbestosis Research Council. Asbestos Cement. U .K . Recom. Code of Practice, 6.67: 1. 10b Asbestosis Research Council. Thermal Insu lation. U .K . Recom. Code of Practice, Dec, 1966. 11. J. Lepoutre, Belgium. Personal communication | M arch 1969. 12. J. R. Lynch. Brakelining Decomposition Pro ducts. U .S. P u b .: H. S. O ccup .: Health Pro gramme Cincinnati, Ohio. Comm. Dr. G. W right, February 1969. 13. J. C. Wagner. L 'Amiante et le Cancer. Abbotempo L iv. 3, 1968. 14. J. C . Wagner, C. A. Sleggs, P. Marchand and I. Webster. D if. pi. Mesothelioma and Asb. | exp. in the N .W . Cape Province. Br. J. Ind, M ed., 1 7 : 260. 15. J. G . Thompson, R. O. C. Kaschula and P. B M cDonald. Asbestos as a Modern Urban I Hazard. S.A. Med. J., Jan. 19, 1963. Arch. 0* Path. 81-- 1966. p ust Problems in the Use o f Asbestos Products 16. I. Webster. Annual Rep. P.R.U . 1965. 17 P. G- Harries. Asb. Hazards in Naval D ock ' yards. Ann. Occup. Hy. Vol. 11:13 5 / 14 5 , 1968. ,8. J. L . Balzar and W . C. Cooper. The Work Envir. of Insulating Workers. Am. Ind. Hyg. Ass. Journal, May-June '68. I9. Ministry of Labour. Problems arising from tht use of Asbestos. Her M ajesty's Stationery Office-- 1967 20. Asb. Inform. Com m .: London. Asbestos Safety and Control 3/68. 4i 21. R. Hackney. Asbestos Safety Reaffirmed. Chemical Week, Oct. 66. 22. G . W . H. Scheepers and T . M . Durkan. Effects of inhaled Talc-Mining D ust on the Human Lung. A M A Arch. Ind. Hlth, 12:182 (1955). 23. T . F. B. Collins. Asbestos the Lethal Dust. 1968, S. Afr. Med. J., 42, 218. 24. T . L . Gibbs. The Health Hazard of Asbestos: What are the Facts? Rep. to P.R .U . 12.2.68. 25. J. Stumphius. Asbest in een bedrifsbevolking Assen, 1969. 98 B. Goldstein and R. E. G. Rei It would appear that there may be an optimal range in the diameter of fibres neces sary for the production of ferruginous bodies. Summary The morphology of asbestos bodies was studied by means of the Cambridge Stereoscan scanning electron microscope and this revealed the characteristic dumb-bell shape with seg mentation of the shaft and expanded ends. The incidence of ferruginous bodies in the lungs of deceased mine-workers was 4 4 % and most of the cases occurred in asbestos workers. In addition, the incidence of different types of malignant lung neoplasms was signi ficantly higher in the cases with ferruginous bodies. Experimental work is in progress to attempt to produce ferruginous bodies by administering various fibrous materials of mineral, vegetable and animal origin but so far typical bodies have only been produced with the various asbestos dusts and fibre-glass, while the material of vegetable and animal origin pro duced foreign body granulomas. It is suggested that there may be an optimal diameter neces sary for the formation of ferruginous bodies. We would like to thank Dr. N. F. Laubscher, Head, Statistics Division, National Research Insti tute for Mathematical Sciences of the Council for Scientific and Industrial Research for the statis tical analysis; M r. R. E. Greasley of the Department of Physics, University of the Witwatersrand, for the use of, and assistance with, the Stereoscan electron microscope; and Dr. I. Webster, Head of the Division, for the helpful suggestions in the preparation of this paper. R eferences 1. Cralley, L . J., Keenan, R. G ., Lynch, J. R. and Lainhart, W. S. (1968): Source and identifi cation of respirable fibres. Amer. Industr. Hyg. Ass. J., 29, pp. 129-135. 2. Gross, P., Cralley, L . J. and D e Trevill ,, T . P.. (1967): Asbestos bodies: their 1 specificity. Amer. Industr. Hyg. Ass T Alt J pp. 541-544- ' 1^ 3. Blount, M ., Holt, P. F. and Leach, A (1966): The protein coating of asbestos knit' Biochem. J., 101, pp. 204-207. ASBESTOS BODIES IN THE NEW YORK CITY POPULATION IN TWO PERIODS OF TIME* I. J. S e l ik o f f , M .D . and E. C u yler H am mond, S c .D . Environmental Sciences Laboratory, Mount Sinai School of Medicine, New York, N .Y. 4. Davis, J. M . G . (1965): Electron microscot studies of asbestos in man and animals. M i d. Lavoro, 56, pp. 521-529. 5. Gross, P., D e Treville, R. T . P., Cralley T 1 and Davis, J. M . G . (1968): Pulmonary 3 ruginous bodies: development in response 1 filamentous dusts and a method of isolation and concentration. Arch. Path., 85, pp. 539-345 " 6. Beattie, J. (1961): The asbestos body. In: pro ceedings of an international symposium on inhaled particles and vapours (1), Oxford 20 March-1 April, i960. C. N. Davies, Editor Oxford, Pergamon, pp. 434-441. 7. Thomson, J. G ., Kaschula, P. R. an(j MacDonald, R. IC. (1963): Asbestos as a mod ern urban hazard. S. Afr. Med. J., 37, pp, 7, 81. 1 the demonstration by Thomson, K aschula and MacDonald in 19631 that ,bestos bodies (or, particles seemingly identical with those seen in asbestos workers) ere frequently found in the lungs of urban residents at autopsy, in Cape Town, similar findings have been reported from many Sties- New York City is no different-- asbestos bodies are found in approximately half of those individuals now examined at autopsy- asbestos body could be found in almost every one.13 In our current studies, we use 2 techniques: basal smear and ashed sections. The latter technique may be briefly described: Sections measuring 25 /* X 1.0 cm2 are taken from each of the 7 sites in the lung recommended by the U I C C Working Group14 (Fig. 1). T he 7 sections are stacked one upon another making a pile 175 /i thick; and this is ashed by activated oxygen.15 T h e ashed material is examined by phase 8. Polliack, A. and Sacks, M . I. (1968): Pre valence of asbestos bodies in basal lung smears. Israel J. Med. Sci., 4, pp. 223-226. 9. Cauna, D ., Totten, R. S. and Gross, P. (1965): > Asbestos bodies in human lungs at autopsy. J. Amer. Med. Ass., 192, pp. 371-373. ' 10. Anjilvel, L . and Thurlbeck, W. M. (1966): The incidence of asbestos bodies in the lungs at random necropsies in Montreal. Canad. Med. Ass. J., 95, pp. 1179-1182. 11. Ghezzi, I., Molteni, G . and Puccetti, U. (1967): Asbestos bodies in the lungs of inhabitants of Milan. M ed. d. Lavoro, 53, pp. 223-227. 12. Meurman, L . (1966): Asbestos bodies and pleural plaques in a Finnish series of autopsy cases. Acta. path, microbiol. Scand., suppl, 181, pp. 1-107. 13. Pneumoconiosis Research U n it: Council for scientific and industrial research. 8th annual report, 1963/64. P R U report No. 2/64, Johan nesburg P.R.U ., 1964, p. 20. > T echniques The method used to search for asbestos bodies affects the readiness with which they are found.12 For example, it is more difficult to see and correctly identify asbestos bodies in stained sections than in ashed sections; and the volume of tissue examined is obviously i important. It is even conceivable that if enough lung tissue is processed, at least one microscopy at 440 X . T h e presence or absence of asbestos bodies (and the number if any are present) is recorded as well as presence or absence of uncoated inorganic fibers and nonfibrous mineral particles. Tables 1 and 2 show what may be called the `stability' of each of the 2 methods. After the first several hundred consecutive cases were * This study was supported by the USPH S grant # U I 00440. 99 100 I. J. Selikoff and E. Cuyler Hanu studied from each of 3 hospitals, we divided them into several sequential groups and recorded the percent of `positive' cases in each group. There is no reason to suppose that subjects from the 3 hospitals should be exactly alike; and the size of each group within each Table 3 shows the findings in the first 1 j, subjects studied by both methods. prJ| studying basal smears, 84.7% of the subject! would be called `negative' for asbestos bodie and 15.3% would be called `positive'. From studying ashed sections, 53.9% would be T able i : `Stability' of Smear T echnique Hospital `A ' Hospital `B ' Hospital `C ' Group 1 20/98 = 20% 8/91 = 9% 18/98 = 18% Hospital `A ' H ospital`B' Hospital `C ' 2 15/98 = 15% 11/92 = 11% 15/98 = 15% 3 17/98 = 12/97 = 22/98 = 17% 12% 22% . . . 67/392 = 17% . . . 41/369 = 11% . . . 70/388 = 19% 4 15/98 = !5% 10/89 = 15/94 = T able 2: ` Sta bility' of A shed Section T echnique Positive Sections per 100 Cases Hospital `A ' . . . . 53 52 49 50 59 50 Hospital `B ' . . . . 39 32 42 42 51 34 Hospital `C ' . . . . 43 46 51 47 52 53 Hospital `A ' . . Hospital `B' . . Hospital `C ' . . 358/700 = 5 1% 289/700 = 4 1% 342/700 = 49% hospital was such that the percent positive is subject to considerable sampling variation. (` Stability' depends on sampling of subjects, sampling of material and accuracy of technical procedure.) The `stability' was not unreason able; but the magnitude of the variation from called `negative' and 46.0% would be called `positive'. Furthermore, 5 or more asbestos bodies were found in only 2.0% of the smears but in 7.9% of the ashed sections. However, 23 (2.0%) of the subjects had `positive' smears but `negative' ashed sections. Thus the T able 3: D istribution of F irst 1,149 Subjects in R espect to N umber of A sbestos B odies (A.B.) Found in A shed Sections and in Basal Smears Ashed Sections 0 A .B ................................................... 1-4 A .B ............................................... 5 + A .B .............................................. Total N u m b e r ................................ % ................................................... 0 A.B. 596 330 47 973 84-7 Basal Smears 1-4 A.B. 20 105 28 153 13-3 5 + A.B. 3 4 l6 23 2-0 Total Number 619 439 91 1,149 -- % 539 38-2 7'9 -- 100*0 Note: In an additional 51 cases, basal smears were not obtained. Ashed sections in these 51 cases indicated 35 with no asbestos bodies, 13 with 1 to 4 asbestos bodies and 3 with 5 + asbestos bodies. group to group illustrates the necessity for including large numbers of subjects in studies of this type. use of both methods reveals slightly more `positive' cases than the use of ashed sections done. Asbestos Bodies in the N ew York City Population A sb e s t o s B o d ie s in N .Y .C . 1966-1968 are studying 3,000 consecutive autopsies Jro66-r968) in 3 large N .Y .C . hospitals Mount Sinai, Manhattan; Elmhurst, Queens; d the Veterans Administration Hospital in Bronx). Concomitantly with the asbestos bodies studies, we are collecting much ersonal, clinical, pathological, residence and occupational information. 101 40% of housewives showed asbestos bodies, 50% of `white collar' males (clerical and professional work), 50% of `blue collar' males (manual work), except those `blue collar' males who had any history, however brief, of ever having done shipyard or construction work (all trades-- carpenters, electricians, plumbers, laborers, etc.)-- they showed asbestos bodies in 70 of 129 cases or 70% (Table 5). T able 4: D istribution of A sbestos B odies in G eneral P opulation-- in 1,975 C ases --------- Age .---- ----- - ' 0-1 . . . . 20-29 . . . . 40-49 50-59 60-69 70-79 80-89 90+ .... .... .... .... .... .... Total . . Male Total Cases 40 2 4 22 50 178 280 359 32I 105 7 1,368 Total + O I 0 4 14 83 149 2O5 180 62 4 7O2 % + -- -- -- 1 8% 28% 47% 53% 57% 56% 59% 57% 5i% Age 0- 1 2-9 IO-I9 2O-29 30-39 40-49 50-59 60-69 70-79 80-89 90+ Total Female Total Cases Total + 34 0 2 0 8 3 12 4 18 7 58 18 85 38 147 57 151 65 80 40 12 8 607 24O % + -- -- 38% 33% 39% 3i% 45% 39% 43% 50% 66% 39% We have analyzed the results in our first 1,975 cases (Table 4); asbestos bodies were found in 942 (47.7% ). In 772, they were few in number (1-4); in 170, they were more numerous (5 or more). Moreover, when housewives or white collar males were positive, they generally had few asbestos bodies; when men who had worked in the construction industry were positive, often many bodies were present (Table 6). T able 5: A sbestos B odies in 856 A utopsies in N Y C , C orrelated w ith O ccupation F e m a le s ............................................................................ Male `white collar' employment...................................... Male `blue collar' employment (no construction nor s h ip y a r d ) ...................................................................... Male-- construction or shipyard employment . . . Total ................................................................ Number Examined 275 206 246 I29 856 Number with Asbestos Bodies 108 97 121 90 416 Percentage with Asbestos Bodies 39% 47% 50% 70% We have so far completed the investigation of the lifetime occupational history of 856 oases. The data obtained suggests that asbestos bodies are not randomly distributed among the general population of N .Y .C . In addition to variations with sex and age (Table 4), there was significant variation by occupational category. Broadly considered, Parenthetically, there is evidence that examina tion by smear tends to demonstrate highly positive cases more readily; smears are negative much more frequently when few bodies are seen in the sections (Table 3). These data warrant the following tentative conclusions: First, that while asbestos bodies are 102 I. J. Selikoff and E. Cuyler Hamuio^ commonly present in the lungs of adults in N .Y .C ., their occurrence is not a random event but, to an important extent, occupationally related. Second, that the construction and ship building industries are rich potential sources of direct and indirect occupational asbestos exposure16-20 and, especially if possible neigh borhood and family contacts are considered, could be responsible for a large proportion of the asbestos bodies found in routine autopsies. the 719,700 tons of asbestos consumed in ti, United States, were used in construction. 6 Secular C hanges in A sb e sto s Bodies in N ew Y ork C ity, 1934-1967: Preliminary O bservations We have investigated the incidence of asbestos bodies in the lungs of individuals examined at autopsy at the Mount Sinai Hospital in years: 1934 and 1967. T able 6 : A sbestos B odies b y O ccupation: Q uantitative R esults Examined 0 `White collar' m a le s ......................................................... 206 109 `Blue collar' males (no construction nor shipyard) 246 125 Construction or s h i p y a r d ............................................. 129 39 / + 2+j 3+ 87 IOI 10 (5% T 20 (8%) 61 2 9 (23%) T able 7: E stimated U .S . A sbestos C onsumption construction industries vs non-construction industries (short tons) I 9 2 O ......................................................... 1 9 2 5 ......................................................... 1 9 3 0 ......................................................... 1935 ......................................................... 1 9 4 0 ......................................................... 1945 ......................................................... 1 9 5 0 ......................................................... 1955 .......................................................... i 9 6 0 ......................................................... 1 9 6 5 .......................................................... Construction Industry Tons 63,600 141,600 136,200 101,700 160,200 214,500 354,300 444,300 437,400 532,300 % 40.8 69-1 66 0 58-2 6l I 56-7 48 6 60 0 65-3 7 4 -o Non-Construction Industry Tons 92,400 63,200 70,300 73,000 102,000 163,500 374,400 296,100 232,100 187,400 % 59-2 3'9 340 41-8 389 43-3 51-4 40-0 347 26-0 Total 156,000 204,800 206,500 174,700 262,200 378,000 728,700 740,400 669,500 719,700 These conclusions are consistent with com mercial data concerning asbestos use. In the past 40 years from one-half to three-quarters of all asbestos consumed in the United States was used in the construction industry (Table 7, Fig. 2).21 In 1965, 532,300 tons (74% ) of M ethod: 100 consecutive cases were selected from the autopsy files of our hospital in each of 2 years, 1934 and 1967. We did not use our 7-site procedure, since these were not available for 1934. Instead, from both years we prepared 175 X 1 cm2 sections from the routine block taken by the prosector. T he sections were ashed and examined as described. T able 8 : Secular C hanges: A sbestos B odies in A shed T issue Sections (N Y C ) 0 - 9 ................................................... 10-29 ............................................. 30-59 ............................................. 6 0 + ................................................... A ge U n k n o w n ................................ Male 1/4 0/4 17/29 16/22 2/5 36/64 1934 Female 0/4 2/7 8/11 6/9 1/5 17/36 Total 1/8 2/11 25/40 23/31 3/10 53/100 Male 0/0 0/1 9/16 23/37 32/54 1967 Female 0/0 3/6 15/25 10/15 28/46 Total 0/0 3/7 24/41 33/52 60/100 Asbestos Bodies in the N ew York C ity Population Source identification was removed from all slides; oU WaSs ggliVvCeUn aa rlaanned.oTMm* .n..u..m...b..e.r.. Tahe sequence^ Cf xamination ensured thorough admixture of both t e` ^]i readings were the responsibility of one dividual, using criteria previously established and Jested.12 There was no significant difference in the ercentage of cases having asbestos bodies in 1067 or 1934- While 53 of 100 were positive in 1934 compared with 60 of 100 in 1967 (Table 8), this may be attributed to sampling variation or differences in age distribution in 103 spect. W e examined such routine stained, unashed sections in the 200 cases. In only 3 of 335 slides were asbestos bodies found; none in the 100 1934 cases although we knew 53 of the 100 showed bodies in ashed 175 /i sections (Table 10). D iscu ssio n The 1934 findings are not inconsistent with the hypothesis developed from the current 600.000, Fig. 2A. Estimated U .S. asbestos consumption. 1915 Fig. 2B. Estimated U .S. asbestos consumption. the two groups. For individuals 30 or over, 50 of 81 (62% ) were positive in 1934, as against 57 of 93 in 1967 (61% ). Nor were there qualitative differences; 13 were positive, 54- asbestos bodies in 1934, against 12 in 1967 Table 9: Secular C hanges: A sbestos B odies in A shed T issue Sections (N Y C ) Number of Asbestos Bodies 0 1-4 s-14 15+ 1934 47 40 10 3 100 1967 40 48 10 2 100 (Table 9). Incidentally, the failure to have found asbestos bodies in the past is easily explained-- it is very difficult to find these ln routine 5 ,u H & E sections even in retro- (1966-1968) study: that the construction industry is a major source of occupational T able 10: A sbestos B odies: A shed Section and R outine H & E Sections 1934 Total Sections . IOO + O Ashed Section* 53 47 H & E Section** . . . 4 0 1967 IOO + O 60 40 3 0 *200 blocks o f 200 cases. **335 blocks o f 200 cases. asbestos exposure and may be responsible for a large proportion of asbestos bodies in routine autopsies. In 1935, for example, almost 60% of asbestos used in the U .S. was used in this industry. But even more germane is the fact that building materials in which asbestos fibers were not firmly bonded, and 104 I. J. Selikoff and E. Cuyler Hamm0 Bodies in the New York City Population Asbesfs thus potentially free to contaminate the atmosphere when worked, have not changed very much in total quantity used, in the past 40 years (Table xi). T he growth in asbestos consumption, 1920-1965, has been largely in products in which asbestos is `locked-in,' as floor tiles, roofing felts, asbestos cement products. Although airborne fibers may occasionally be derived from these, this is far ' SS with risk. If it will be confirmed that c urban asbestos neoplasia risk in the general future aSD The rjs^ to more intimately populations 35-45 years ago had asbest0s P ^ T n o P u la tio n s will remain for definition bodies in their lungs as often as such PPula. exposed P U .g .g question enough, but the tions do now, and if appropriate patholo;, and wjii be a manageable one and within studies will demonstrate that mesothelioi problem . resources which could be was indeed uncommon until recently,,2255 ttylJa [he scope anu will perhaps be less reason to expect that tti' available. gest that specific asbestos current finding of asbestos bodies in the lun 5 We fU and u se? in the construction and of the general population is a harbinger of Pr S ld in p industries have an important T able i i : U se of A sbestos in the U .S . C onstruction Industry ( T ons) 1920-1965 sblpb n to occupational and community disrela-` tlon of asbestos; focus of control Firmly Bonded Friable or Powder pleasures here are strongly indicated. MC Tile Other Total Insulation Cement Total R eferences 1 9 2 0 .......................... 1 9 2 5 .......................... 1 9 3 0 ......................... 1 9 3 5 .......................... 1 9 4 0 .......................... 1 9 4 5 .......................... 1 9 5 0 ......................... 1 9 5 5 .......................... i 9 6 0 .......................... 1 9 6 5 .......................... 5,000 3 5 ,3 0 0 17,600 14,000 28,500 43,800 99,600 139,200 136,200 180,800 15,500 41,300 45,500 38,500 5,500 60,000 70,000 121,500 127,400 137,500 12,300 25,800 28,900 24,600 36,900 65,700 147,400 150,000 133,500 172,000 32,800 102,400 92,000 77,100 120,400 169,500 317,000 410,700 397,100 490,300 12,300 19,200 16,600 7,400 13,600 14,800 12,700 12,200 13,000 16,100 18,500 20,000 27,600 17,200 26,200 30,200 24,600 21,400 27,300 25,900 3 0 , 8oo 3 9 2oo 44 )2oo 24,600 39>8oo 45)000 37)300 3 3 )6 oo 40,300 42,000 ,, t Ct Kaschula, R. O. C. and f e a k J ' R . R. 0 9 6 3 ): S. Afr. M ed. J., j.S d eV so n , W. A. (1966): Am. J. Clin. Path., 3 Hrfo' u3n;hBaanne, DD.g6O)';B.^, LesMsoef,d L J. ;anj d 1R06ic9h. ardAmivei L . and Thurlbeck, W . M . (1966): 6. G h e z z if 'u ! Molteni, G . and Puccetti, V. more unlikely than from more friable sub stances, as insulation materials, asbestos cement powder or acoustical products; and these, as noted, were used in the same quantities in 1935 as 1965. T o summarize: if the construction industry is the major source for the asbestos fibers in asbestos bodies found in urban areas, we could expect 1934 findings to be similar to 1967, since the amount of friable asbestos products used then was the same as now. Much more extensive data are needed to see whether the findings in these first 200 cases will be confirmed. Too, findings in other cities should be sought: New York might be unusual in some way. It would seem impor tant to obtain this additional information since it will surely assist in efforts to define those populations at risk to asbestos associated disease. We now appreciate the significant hazard associated with direct occupational exposure and we are aware that other intimate environmental contact, as with indirect occupational,18-20 neighbourhood22-2* or family exposure,23'24 may also be associated with risk, although the extent of this risk awaits more exact characterization. What is not known is whether that level of exposure which results in scant asbestos bodies in the lungs of individuals other than those in the above categories-- `asbestos bodies in the lungs of the general population'-- is also associated future disaster, that we face a widespread epidemic of mesothelioma. Such definition of the problem will allow appropriate focus of public health control measures. Our data suggest that among these, construction and shipyard work must be prominently considered. In doing so, not only will hazardous direct and indirect occupational . exposure be limited, but a major source of the I asbestos bodies in the general population will j be simultaneously minimized. Thomson, in 1963,1 posed an important problem. Close contact with asbestos (of vary ing intimacy and duration, as with direct or indirect occupational, neighbourhood or family exposure) could be associated with significant neoplasia risk. But was there also a risk associated with general community dissemination of the fibers, presumably in scant numbers and marked by his frequent discovery of occasional asbestos bodies at routine autopsies? Because of the long lapsed period between initial exposure and evidence of disease,26 future risk attached to the current presence of asbestos bodies could not be denied, although such risk was not evident at this time.19 Our observations, preliminary and still to be extended and confirmed, suggest that asbestos bodies were as frequently present 35 years ago as now. If this is true, then scant asbestos bodies may not be associated with 7. (Me6urmaiJeL. (1966)' Acia^path. et microbiol. 8 I t a e i T ' C.8andUWPade, O. L. (1965): Ann. N.Y. Acad. Sc., 132, 549. 105 9. Anspach, M . (1968): Intern. Conf. Biol. Effects Asbestos, Dresden. 10. Gibson, A. A. M ., M cEwen, J., F r a y s ' . Angela and M air, A. (1968): Internat. Conf. Biolog. Effects Asbestos, Dresden. 11. Smith, P. (1968): Ibid. , 12 Baden, V., Schwartz, Jo Ann, Churg, J. and Selikoff, I. J. (1968): Ibid 13 Utidjian, M . D ., Gross, P. and de [reville, 3 p -p p (1968) : Arch. Envir. Health, 17, 327. 14. Working Group on Asbestos and Cancer. (1965) : Ann. N .Y . Acad. Sc., 132, 706. 15. Berkley, C ,, Churg, J., Selikoff, I. L and Sm.th, W E (1965) : Ann. N .Y . Acad. Sc., 132j 48. 16. Selikoff, I. J., Churg, J. and Hammond, E. C. (1964): J.A.M .A., 188, 22. 17. Harries, P. G . (1968) : Ann. Occup. Hyg., 11, 18. Stumphius, J. and Meyer, P. B. (1968): Ibid., 19. Selikoff! I. J. and Hammond, E.C. (1968): Amer. J. Pub. Health, 58, 1658 20. Selikoff, I. J., Hammond, E. C. and Churg, J. (1968): J.A.M .A., 204, 106. . 21. Pundsack, F. L . (1969): Personal commumca- 22. Wagner, J. C., Sleggs C. A. and Marchand, P. (i960): Brit. J. Industr. M ed., 17, 26; 23. Newhouse, M . L . and Thompson, H. (19 5) ` Brit. J. Industr. M ed., 22, 261. 24. Lieben, J. and Pistawka, H. (1967): Arch. Envir. Health, 14, 559. T 25. Selikoff, I. J., Hammond, E. C., Churg, j . . This conference. . c 26. Selikoff, I. J., Bader, R. A., Bader, M . E., Churg, J. and Hammond, E. C. (1967): Amer. J. Med., 42, 487- M ORTALITY EXPERIENCES OF ASBESTOS INSULATION WORKERS 1943 - 1968* Irving J. Se lik o ff, E. C uyler H ammond and Jacob C hurg Environmental Sciences Laboratory, Mount Sinai School of Medicine and the Department of Epidemiology and Biostatistics, American Cancer Society On December 31, 1942, there were 632 members of the Asbestos Workers Union in the New York area (New York and Newark, New Jersey locals of the International Associa tion of Heat and Frost Insulators and Asbestos Workers, I.A.H.F.I.A.W .). From January 1, 1943, to December 31, 1962, another 890 men joined the union. We have followed each of these 1,522 men prospectively to the present. Four hundred and four died by December 31, 1968. Analyses of these deaths demonstrate that serious risks have been associated with work in this trade. own observations and those of others3-45 indicate that trade practices are essentially uniform throuBk the country, the data which follow may be taken to represent mortality experience in this trade fot the United States and Canada; direct study of all United States union insulation worker deaths 1967-1968, supports this.6 Exposure: There is scattered information re corded concerning variation in insulation materials used in the United States, 1870-19691. 7; it would appear that some materials (as, hair-felt, cork mineral wool) have sharply decreased while others (as, fibrous glass, plastics) have increased.1 Table 1 lists material currently used. T able i : Insulation M aterials (U .S.)-i9698 Minerals Containing Asbestos Product Asbestos Content B la n k e ts...................................................................... 100%-amosite M o ulded...................................................................... 9 5% -amosite (5% filler) Insulation b lo c k ..........................................................{a) 85% magnesia: 10 -15% amosite + chrysotile (b) 85% cal. silicate: 10 -15% amosite (c) 85% cal. silicate: 10 -15% amosite + chrysotile (d) 85% calcined diatomaceous silica 10-15% amosite + chrysotile Finishing `cements' . 85% calcium silicate: 10-15% chrysotile (a) 100% chrysotile (.b) 50% chrysotile, 50% cement Sprayed asbestos 10-15% asbestos-variable 2. Fibrous Glass and/or Mineral Wool Block, rolls, prefabricates, high temperature insulation, finishing cements, mineral wool and cement, 3. Plastics Polystyrenes and polyurethanes: prefabricated, powdered and foamed in place. 4. Other Cork, glass flakes, adhesives (epoxy and solvents; asphalt base and solvent, wheat paste, silicones, magnesia, Portland cement). M aterials and M ethods T h e procedures followed in this study have been described.1' 2 Briefly, these men install insulation in the construction and (to a limited extent) in the shipbuilding industries. Approximately 10% of United States union insulation workers are in the N ew York-N ew Jersey locals and since our T he quantity of asbestos used annually in insula tion materials has not changed very much in the I past fifty years-- 12,300 tons in 1920 and 16,000 \ tons in 1965 (Table 2).8 There are currently, how- | ever, more insulation workers than previously; pre- * This study was supported by the Health Re- ( search Council of the City of N ew York. 180 jylortabty Experiences o f Asbestos Insulation Workers 1943-1968 181 ,,hly less asbestos per workman is now the * * Asbestos exposure varies by type of instalC1S'on (Table 3); about 40% of an insulation TinrE 2: A sbestos U sed in Insulation M aterials in the U .S ., 1920-1965 Year 1920 1925 1930 1935 1940 1945 1950 1955 i960 1965 Short Tons 12,300 19,200 16,600 7,400 13,600 14,800 12,700 12,200 13,000 16,100 OBSERVATIONS 632 M em bers of th e U nion on D ecember 31, 1942 Three hundred and eighty of these men were dead by December 31, 1968. Age, year and sex specific expected death rates were avail able to mid-1967;1' 10 observed rates by cause are compared in Table 5. All deaths to December 31, 1968 are tabulated in Table 6, by cause. T able 5: Expected and O bserved D eaths A mong 632 N Y -N J Insulation W orkers, January i , 1943 to A pril 30, 1967* Expected** Observed Table 3: U se of A sbestos I nsulation (% ) V aria tion b y C onstruction T ype, 1969 Construction Commercial (Schools, factories) . . . . Power process (Power plants, boiler rooms) M a r in e .......................... Fibrous Glass Asbestos Other 75 10 U 20 60 20 20 70 10 worker's time is spent in work using asbestos mate rials (Table 4). T able 4: U se of A sbestos b y Insulation W orkmen in the U .S ., 1969 Material Asbestos . Fibrous glass. Other Volume % o f Total 35 45 20 Application % o f Time 43 40 U Exposure of insulation workers in the United States cannot necessarily be equated with that of similar workmen in other countries. For one thing, besides variations in working conditions, the type of fiber and materials used may be different. U ntil 1930, chrysotile was almost the only asbestos used, amosite making its appearance later and crocidolite practically not at all (see below). Second, spraying of insulation has not been, until recently, widely used in this country, in contrast to some other areas and, in so far as this affects exposure, would not be reflected in our mortality observations. Finally, because of union jurisdictional agreements, the men we have studied are restricted to insula tion against temperature change; acoustical insula tion and fireproofing are the work of men in other trades and variables peculiar to such work would not be demonstrated by our data. A ll c a u s e s .......................... 25I-0 349 Lung Cancer . . . . 89 66 G .I. Cancer . . . . Pleural Mesothelioma II -2 *** 37 6 Peritoneal Mesothelioma *** 14 A ll other Neoplasms . 25-0 21 A sb estosis.......................... *** 27 * O f workmen reaching 20 years from first exposure. In addition seven men died before reaching this point. ** Based on United States Mortality data.1' 10 *** U nited States data not available, but these are rare causes o f death in general population. T able 6: C auses of 380 C onsecutive D eaths A mong 632 Insulation W orkers, January i , 1943 to D ecember 31, 1968 Lung cancer . . . . Pleural Mesothelioma . Peritoneal Mesothelioma . Gastrointestinal Cancer Oropharynx Larynx Cancer Cancer o f Pancreas . All other Neoplasms . A s b e s t o s is .......................... A ll other causes. . . . Before 20 Years from First Exposure After 20 Years from First Exposure O 72 0 6 0 l6 0 37 I 5 0 3 0 19 0 30 6 185 7 373 LUNG CANCER One in five deaths was caused by lung cancer. Despite the recent rise in prominence of meso thelioma, this remains the most important asbestos-associated neoplasm among insula tion workers. It is of interest, therefore, that there appears to be a special relationship to 182 I. J. Selikoff, E. Cuyler Hammond and J. T able 7 : P leural and P eritoneal M esothelioma A mong N Y C A sbestos I nsulation W orkr8, January i , 1943 to D ecember 31, 1968 Number Age at Onset (Years) M e a n ................................................... M e d i a n ............................................. S .D ......................................................... Range ................................................... Age at Death (Years) Mean . Median S.D. . Range . Lapsed Period (Years) Mean . Median S.D. . Range Mesotfidioma Pleural 6 Peritoneal l6 Bronchogenic Carcinoma 72 Asbestosis 30 25-2 21 5-4 17-25 20-0 19 4'3 16-30 25'4 25 6-36 16-54 24 24-5 5*6 14-36 560 55 2 -4 54-60 34'8 34'5 2'3 32-38 62 7 60 10-2 50-83 43-0 40-5 8-9 32-61 63-8 64 7'25 39-83 38-7 39 8-5 22-60 66-7 66 8-02 53-79 42'8 44 7-69 30-59 *In addition, we have observed 2 peritoneal mesotheliomas found at autopsy, in men who had died of broncho genic carcinoma. cigarette smoking among asbestos insulation workers10 (see below). Overall lung cancer death rates were seven times expected.* MESOTHELIOMA Twenty-two of the 380 deaths were due to mesothelioma, 6 pleural and 16 peritoneal. Tw o occurred 1943-1954; 20, 1955-1968; average lapsed period from onset of exposure was longer and average age at death was greater for peritoneal than for pleural meso thelioma. Peritoneal mesothelioma does not seem to be related to cigarette smoking-- we have seen 4 such cases in men who never smoked cigarettes. In the 3 cases of pleural meso thelioma for which we personally recorded smoking histories, all had smoked cigarettes. T he preponderance of peritoneal meso thelioma among our cases, as in the series of Enticknap and Smither,11 is not necessarily contradictory to the observations of Wagner,12 Hourihane13 and others in which pleural neoplasms were largely seen. It may, rather, reflect the derivation of the cases-- consecu tive series with regular occupational exposure on the one hand, against random cases, many with non-occupational environmental ex *There are, in addition, three men found to have lung cancer during our survey, and who are now alive following therapy. posure, on the other. It may be that in those people who develop mesothelioma in associa tion with asbestos exposure, the site of the mesothelioma tends to vary to some extent with the intimacy and duration of exposure pleural with lesser exposure and peritoneal with greater. GASTROINTESTINAL CANCER As in our first observations,1 we have con tinued to see more deaths due to cancer of the stomach and colon than expected. However, the ratio is only 3 times expected and, with so few deaths, we are not yet certain of the relationship. CANCER OF PANCREAS; OROPHARYNGEAL CANCER T h e same insecurity noted with gastro intestinal cancer is associated with these as well. We are, however, concerned that the incidence of both of these neoplasms will be increased among asbestos workers. As a practical measure, we now inspect the oral cavity during all clinical examinations of asbestos workers; one cancer of the lip has been discovered and successfully excised. It is of interest that 2 of the 3 recent deaths of tongue cancer, were in men who never smoked cigarettes. Experiences o f Asbestos Insulation Workers Mott'ality ASBESTOSIS deaths of the 380 were due to T jjg to r y insufficiency with cor pulmonale. ggo m e n e n t e r i n g u n io n a f t e r J DECEMBER 31, I 942 f eSK *srass l flJ four of these men had prior insulation Fifttlyy-1t"ou" *r p before entering this union work expe By and large, Pnd of serious risk of neoplastic death. This theoretical Consideration has so far Ibeen con firmed by our experience (Table 8). ,, ,, R- Onset of Exposure and D eaths of TABn Poplasm A mong 890 M en W ho Joined ^Insulation W orkers' U nion, 1943-1962 Year Onset of Asbestos Insulation Exposure 1 ^1929 2 1930-1942 3 1943-1947 4 1948-1952 5 1953-1957 6 1958-1962 . Number 8 46 164 250 186 236 890 Deaths 1943-1968 Total Neoplasm 3 3 2 i 9 4 5 0 5 0 0 0 24 8 i 83 1943-1968 canc_er among asbestos insulation workers On Tanuarv 1, 1963, there were 370 men still alive of our original 632 cohort (all now with long-lapsed periods from onset of exposure and very much at risk). Eighty-seven never smoked cigarettes: one died of lung cancer by December 31, i 968- T w o hundred and eighty three had a history of cigarette smoking _ 21 have died of lung cancer (Table 9)- T able 9 C igarette Smoking and L ung C ancer in I No History of Cigarette Smoking Number of men . 87 Expected lung cancer deaths to 4.30-67 Observed deaths to 4.30.67 0 Observed deaths to 12.31.08 I Total cases to 12.31.68 . . History of Cigarette Smoking 283 2-98 24 27 30* *3 men still alive (all cigarette smokers). C o m p u ta tio n s su ggest tthhaatt aann asbestos worker who smokes cigarettes has 90 times the risk of d yin g o f lu n g cancer com pared w ith a m an w ho neither works w ith asbestos nor smokes cigarettes. age at onset of exposure ,! v PA Lung (31), Pancreatitis, CA Lung (21), Asbestosis, Peptic ^ lce r, C A\ 3' Pancreas S(20), C A Tongue (20), C A Colon (17), Pulm. embolism, Cirrhosis, Coronary. 4: Accident, Coronary, Cong. Heart Failure, Coronary, Coronary. ,, rjr_ 5: Pneumonia, Rheumatic H .D ., Coronary, Cir rhosis, S.B.E. 6: ,, ( ) = years from onset of exposure. MULTIPLE NEOPLASMS Table 10 records the mortality experience of the 632 men, by age category at onset of exposure. FIBER VARIETY AND MESOTHELIOMA,EVIDENCE FROM PRESENT OBSERVATIONS Crocidolite seemed initially to be unique among asbestos varieties in having * sP f ^ relationship to mesothe iomas lt ha been considered desirable to obtain We have seen several instances of mow than one primary neoplasm in the sam em d (lung-lung; lung-larynx, etc.). T h been too infrequent to warrant more than brief recording except perhaps for two men who died of bronchogenic carcinoma and were found, at autopsy, to also have peritonea mesothelioma. EFFECTS OF CIGARETTE SMOKING on this S e r i e s . 14-15 It may be therefore, to evaluate the experiences of N Y -N T insulation workers in this regard, of N .Y . N .j. msu CROCIDOLITE EXPOSURE OF INSULATION WORKERS IN THE UNITED STATES There is no crocidolite mined in the United all must be imported either from South :a m U " b" v V A u s a l i hasbeen to S S f e y c L u S e e crocidolite use. ' 184 T able -- I- J. Selikoff, E. Cuyler Hammond and I- Ch, M0RTALITY EXPERIENCE F 632 N Y C ^ sulatxon W orkers, B v A ge at O nset Cancer of Lung . . Pleural Mesothelioma Peritoneal Mesothelioma Gastrointestinal Cancer A ll other neoplasms . Asbestosis . . . . A ll other causes . Deceased 12.31.68 Alive 12.31.68 Total Age at Onset of Exposure g|20 !4 (5 -7%) 10J 5 ' 2 % ) la6 (4 -9 % ) 11 (4 -5% ) 45 IOI 21-30 52 (17-3 % ) 5/ ( 2 '7%) *7 (5 ' 7%) 15 !5 (5 ' 0 % ) 92 199 30+ 6 (7 - i% ) ?}(l-2 % ) 8 (9 -4 %) 7 4 (4 -7%) 54 80 145 102 5 246 301 ___________ 1 85 Total j ~~ 72 6 16 37 28 30 191 380 " j 252 632 " j Mortality Experiences o f Asbestos Insulation Workers 1943-1968 185 extent aaunud.> as seen in Table 1, is still a very minor affair. i m esoth eliom a am ong u n ited s t a t e s in su la tio n w orkers The first mesothelioma reported in which ccupational asbestos exposure was described, C.,,rred in an insulation worker, a member " tie I.A.H.F.I.A.W., in 1946.17 It is not known whether cases occurred before then, but they have been noted since.18 W e have seen 22 cases, 1947-1968, in our group of men as detailed above. Every one has occurred in an insulation worker who began work before 1930 (Table I2)- The mean lapsed period from onset of exposure to death of mesotheliomas among the 836 men in our study who began work in 1943 or later (Table 8). These considerations are relevant only to conditions in the United States, among insula tion workmen. They do not disprove a special role for crocidolite elsewhere, in other circum stances. They should, however, engender caution in relying on other asbestos varieties always to be significantly less likely to cause mesothelioma. The relative mesothelioma hazard for each fiber variety is still to be defined in humans. A t this time our data suggest that it would be prudent to regard all fiber varieties as potentially hazardous, and to utilize appropriate industrial hygiene measures for all. tarle 12- L apsed Period from Onset of E xposure to D eath of 22 C ases of M esothelioma, 1947-1968, ' A mong 632 Insulation W orkers F ollowed Prospectively from January i , 1943 1920 1925 1930 1935 1940 1945 1950 1955 i960 1965 8,700 8,500 1 1,700 19,600 17,100 4)5o 5,400 18,000 19,500 21,400 152,000 200,700 198.200 154.200 225,900 355. 800 687,400 699.100 605.800 661.100 4.000 4,100 8,500 20,500 36,300 9.000 27,400 11.600 24.600 20,100 156.000 204,800 208,407 175,201 270,268 378.000 728.700 740,400 669,580 719.700 Total Amosite and Crocidolite* 1930 1931 1932 1933 1934 1935 1936 1937 1938 1939 1,907 823 212 233 152 SOI 1,432 2,928 3,282 6,129 Source: U.S. Department of Commerce crocidolite entered this country untd World War II (Table 11). Asbestos used here was almost entirely chrysotile. The la rg e r aabestos manufacturer in the United States first used crocidolite in 1929 (for sheet packing, not insulation). This company never used crocidolite for the manufacture of insulation at any time (1929-1968), employing it only in two product lines (asbestos cement pipe, and packings).18 These data are consis tent with an analysis of insulation materials used in past decades on the United States west coast where only chrysotile and amosite were ound. During these same years, 1920-1940, more than 2 6 7 ,0 0 0 tons of chrysotile were used tor insulation purposes. This is not to say that it can be proven at crocidolite was never used before 1930 tor insulation in the United States. Rather, if any was so utilized, it could only have been in very small amounts. Therefore, crocidolite exposure of United States insulation workers etore 19 3 0 and probably before 19 4 0 is un1 e y to have occurred to any significant Patient 2 A .M ............................................ 3 A .S............................................. 4. J.B.............................................. 4 F .C ............................................. 6. T .C ............................................. 7. E .M ............................................ 8. F.S............................................. 9. M .C ............................................ 10. H.H............................................ I I . J.B.............................................. 12. H .D ............................................ 13. W .N ........................................... 14. A .C ............................................. 15. J.D............................................. 16. J.LaG ......................................... 17. J.O'C .......................................... 18. G .V ............................................ 19. H .C............................................ 20. J.P.............................................. 21. R.B............................................. 22. H .T ............................................ Site Pleural Pleural Pleural Pleural Pleural Pleural Peritoneal Peritoneal Peritoneal Peritoneal Peritoneal Peritoneal Peritoneal Peritoneal Peritoneal Peritoneal Peritoneal Peritoneal Peritoneal Peritoneal Peritoneal Peritoneal Year Onset Employment 1922 1923 1929 1929 1927 1928 1910 1923 1924 1918 1905 1925 1919 1918 1924 1929 1917 1924 1929 1929 1907 1929 Year of Death 1947 1956 1961 1963 1964 1966 1949 1956 1956 1959 1963 1963 1964 1964 1965 1965 1966 1967 1967 1968 1968 1968 Age at Death 60 58 54 54 53 56 6l 50 52 60 86 66 63 68 58 53 79 59 57 58 83 56 Years from Onset 25 33 32 34 37 38 39 33 32 41 58 38 45 46 41 36 49 43 38 39 6l 39 was 34.8 years for pleural mesothelioma and 43.0 years for peritoneal. As detailed, crocidolite exposure of United States insulation workers, to the extent that it occurred, could not have been very exten sive be;ore 1940. Therefore, if a long lapsed period is required for asbestos-induced mesothelioma, crocidolite exposure alone cannot easily explain the mesotheliomas seen among insulation workers in the United States. O f course, it may be that crocidolite's virulence makes for shorter lapsed periods between onset of exposure and death. But if this is so, it is difficult to explain the absence R eferences 1. Selikoff, I. J., Churg, J. and Hammond, E. C. (1964) : J. Amer. Med. Assoc., 188, 22. 2. Selikoff, I. J., Churg, J. and Hammond, E. C. (1965) : Ann. N .Y . Acad. Sc., 132, 139. 3. Fleischer, W. E., Viles, F. J., Gade, R. L . and Drinker, P. (1946) : J. Indust. H yg., 28, 9. 4. Keane, W . T . and Zavon, M . R. (1966) : Arch. Envir. Health, 13, 171. 5. Cooper, W . C. (1968) : Internat. Conf. Biol. Effects Asbestos, Dresden. 6. Selikoff, I. J., Hammond, E. C. and Churg, J. (1969): Unpublished data. 7. Marr, W. T . (1964): Amer. Indust. Hyg. Assoc. J., 25, 264. i 86 8' S X " ** F - L - (I969): Personal communi- 10. Selikoff f r ('iq (58') . rr F,, f ' t(I9^9) ' PersonaI communication. if ?" w-' <** a ^ arn?l0 j0*' p ' C. and Churg, mCr- M ed' Assoc-> 204, I06. .T L S * ' ?? ',ef5~ M'"7Ms h" d- 1 5 S " 'B- <*> A * N Y . A,,d. ' 4- S i f S ; . *1' C- < * > ' Ann. N.y. ^ ,3 g f " - J' C- " ` S , Ann. N .Y .A M .& , ' >6. F. L. (,, 68): Pm on,, ^ RESULTS OF ASBESTOS EXPOSURE IN FRANCE Jean A v r il and Jean C h am peix Paris and Clermont Ferrand ' 7 Jf-l Mf e' dl .l,236,) 400?7. & l8' Jn7 " ,," NnegwE'n^ The asbestos industry in France employed bout 14,000 persons in 1968 of whom there E. c ?*ere 5,0 m manufactured asbestos, 1,000 the production of the textile and 8,000 in asbestos cement. Chrysotile represents 95% of the tonnage 0{ crude asbestos consumed in France. in the Rouen and in the Clermont Ferrand districts because the great textile plants are located near Rouen in Conde sur Noireau and in Clermont Ferrand. In Conde sur Noireau, Ferodo S.A.F. has 2 plants. One for textiles employs about 600 persons and another for brake linings employs T able i : C onsumption r -------- I All p r o d u c t io n ......................................................................................... Asbestos cem ent and floor t i l e s ....................................................... , Manufactured asbestos and o t h e r s ................................................ 1938 i"j3ioo 11,700 5,400 1950 ^2,400 25,300 7,100 1957 61,800 11,300 1967 120^300 101,900 18,400 The consumption in 1967 is almost the , double of that in 1957 and 4 times that in 1950 (Table 1). In France the law recognizes asbestos 1 fibrosis as an occupational disease but not tuberculosis or carcinoma of the lungs or mesothelioma of the pleura. about 1,200. At present there is an increase of fibrosis disease because 1968 is just 20 years after the production increase at the end of the last war. Table 3 shows, year by year, between i960 and 1968, the number of workers pensioned in the textile plant (Ferodo S.A.F.). T able 2 : Statistics of A sbestosis D iseases NUM BER O F COM PEN SATION S Com pensation Bordeaux D ijo n C lerm ont F erra n d L ille M a rseille N a n tes 150%% -- - i -- --i - i _ -- 15% 20% -- i 1 1 -- -- -- i i 25% 27% -- -- -- -- i -- -- -- -- 30% 35% i - ---- 1 -- --i i -- --2 40% 45% -- -- --I 2 -- --3 50% 55% -- -- -- --1 -- -- -- i -- 60% -- -- 1 -- -- -- 65% - 67% -- -- -- -- -- -- 70% 75% --i ---- -1 ---- ---- --- 80% 90% -- -- -- -- -- -- -- -- __ _ _ !0% - - - - - - 2 2 7 5 2 8 P a ris -- i I i I 2 --I --2 -- I --2 -- _ I - 13 R ouen Strasbourg L im oges - - - i i -- 2 4 --i -- --4 -- -- 3 -- -- -- -- 38 - - i 12 -- -- -- -- i 2 ---- -- i - - - 23 -- -- -- -- 2 I -- -- -- _ -- _ _ 3 - - 52 2 i T o ta l i 4 58 6 I 10 5 13 163 i 4i 5 24 i i 3 94 Asbestosis is mainly observed in asbestos textile plants. We have much asbestosis because of the unsatisfactory working condi tions in asbestos textiles after the war. The statistics of Securit Sociale for all France in 1962 are shown in Table 2. The great majority of pensioned persons are T h e number for the whole textile factory is 89 workers pensioned in January 1969. Pleural Plaques Pleural plaques are observed among workers in textile plants. There is no parallelism between fibrosis and pleural plaques. 187 196 E. C. Vigliatlj cant difference in the incidence of tumours of the lung was seen between workers with con tinuous and intermittent exposure to asbestos. T o the workers with continuous exposure, 16 insulation workers working for other com panies should be added. Among these, 5 available. A ll counts were made with phase contrast microscopy at a magnification of 500 diameters, after dissolution of the millip0te membrane filter with methylcellosolve. Table 12 gives the range of dust concentration in the different work places. T able 13: Result of C ounts of A irborne A sbestos F ibres (On M illipore M embrane F ilter) B a la n g e r o M i l l s ................................................................................ T e x t i l e s ................................................................................................ F r i c t i o n p r o d u c t s ................................................................................ O n b o a r d `L a u r a C ' ........................................................................ N o. o f Counts with < 1 2 Fibres/cm3 No. % 29 25*0 63 57-3 106 94-6 33 673 No. > of 12 3 Counts with Fibres/cm No. % 87 750 47 4 6 -7 6 5 `4 9 32-7 Total I 16 HO 112 49 cancers of the lung and 1 mesothelioma of the pleura occurred. Our study of asbestosis in Italy also includes the measurement of airborne dust concentration in the working places. U p to date the results of 380 measurements are Table 13 gives the percentage of counts with less than 12 fibres/cm.3 air as com pared with the percentage of the counts with more than 12 fibres/cm.3 It is planned to carry out approximately 1,000 counts per year. EPIDEMIOLOGY OF PRIMARY MALIGNANT MESOTHELIAL TUMOURS IN CANADA A. D. M c D o n a l d , A. H a r p e r , O. A. E l A t t a r and J. C . M c D o n a l d Department of Epidemiology and Health, M cG ill University, Montreal Evidence for an association between malig nant mesothelioma and asbestos exposure rests mainly on the remarkable concentration of cases reported by Wagner et al. (i960) in the crocidolite mining areas of South Africa, the case-control studies of Elmes et al. (1965) in Belfast and Newhouse and Thompson (1965) in London, and the considerable excess mortality due to this disease observed by Selikoff et al. (1965) in American insulation workers. The survey described here was undertaken to obtain a more generally repre sentative view of the problem in one of the two major chrysotile-producing countries of the world. Our aim has been to study all fatal cases known to have occurred in Canada since JC959- M ethod At th e e n d o f 1 9 6 7 w e w r o t e to t h e 4 2 3 m e m b e r s of either the C a n ad ia n A sso ciatio n o f P a th o lo g ists or the Q u eb e c A sso c ia tio n o f L a b o r a to r y P h y sic ia n s inquiring w h eth e r o r n o t sin ce 1959 th e y h ad seen w ere fou n d ; 113 w ere pleural, 45 periton eal, 3 pleural and periton eal and 4 pericardial. T h e d iag nosis w as su ppo rted b y au to p sy in th ree-qu arters o f the cases an d b y b io p sy in th e rem ain d er. L a te r w e plan to h ave m aterial from as m an y as possible review ed b y a pan el o f pathologists. D u rin g the v isit to the p ath ologist 2 fa tal con trol cases (one prim ary and one secon dary lu n g cancer) w ere selected from th e au to p sy o r b io p sy record s, m atch ed for sex and as clo sely as possible for age and date of death. In 2 instances no adequ ately m atch ing case o f prim ary lu n g cancer cou ld be foun d. T h e cases of secon d ary lu n g cancer are referred to h ereafter as con trol gro u p A and o f prim ary lu n g cancer as con trol gro u p B. A field su rvey w as th en arranged in w h ich in vestigators (doctors, p u b lic h ealth n urses and p u b lic health inspectors) sought ou t the relatives and frien d s o f th e deceased and com pleted a d etailed questionn aire relatin g to occu pation , residence, in d irect h ou sehold exposure to dust, fa m ily h istory and sm okin g habits. N o in terview er k n ew to w h ich gro up th e case un der in vestigation belon ged and the in form ation record ed in the questionn aires has also b een co d ed b lin d . Q u estio n n aires h ave been com p leted so far fo r 433 (8 8 % ) o f the 493 cases and controls. T h e fo llo w -u p is still in progress and in form ation for perhaps h alf the rem ain d er m ay even tu ally be obtained. T able i : D istribution of C ases b y Y ear of D eath and Province Year i 9 6 0 ................................................................ 1 9 6 1 ................................................................ 1 9 6 2 ................................................................ 1 9 6 3 ............................................................... 1 9 6 4 ................................................................ 1 9 6 5 ................................................................ 1 9 6 6 ................................................................ 1 9 6 7 ................................................................ 1968 ( 1 s t h a l f ) ........................................ Incidence per million per year 1960-1962 ................................................ O ntario -- 4 9 6 7 8 6 5 46 Quebec 6 6 4 3 8 7 13 14 8 70 1-5 O th er Provinces 10 2 5 7 3 5 10 6 2 49 0-9 Canada l6 9 13 19 17 19 31 26 15 165 1*0 any cases o f fatal p rim ary m alignan t tum ours of the p leu ra o r p e rito n e u m d ia g n o sed b y a u to p s y o r biopsy. In d u e co u rse w e o b tain e d re p lies fro m them all an d , if th is w as in th e affirm ative, a personal visit w as m ad e b y one o f us to review the reco rd s an d to e x c lu d e cases w h ic h d id n o t meet the criteria m en tion ed above or abou t w h ich the p ath ologist h ad seriou s d o u b t. In all, 165 cases F in d in g s The distribution of cases by province and year of death is shown in Table 1 and by age, sex and site in Table 2. More cases were found in 1966 and 1967 than in previous years. Recent interest in these tumours may 197 198 A . D. M cDonald, A . Harper, O. A. El Attar and J. C . M cD o n T able 2: D istribution of M sothlial T umours by A ge, Sex and Site Age (Years) A ll Total Pleura M F "" -- 2 I 4 7 4 9 7 18 3 26 5 15 5 3 4 80 33 113 Peritoneum M F -- I -- -- I I 4 I II 4 2 5 7 6 I I 26 19 45 Pleura and Peritoneum M F Pericardium M F Total M i 2 108 57 165 have contributed to this and, as the records in some hospitals were poorer for the earlier years, memory may also have been a factor. j ,se P*nts hi mind the rate of increase is difficult to assess. During the 8 complete years, 1960-67, the average annual incidence was 1.0 per million of population. The rate was appreciably higher in Quebec (1.5) than in Ontario (0.8) or in the rest of Canada (0.9) . I,? 6 6 .a d 1967 again accounting for much of the difference. There was no difference in the sex distribution under the age of 50 but hereafter males were in considerable excess. The case and two control series were very similar in age distribution and in the propor tion of each for which the questionnaire was mpleted (Table 3). In this prelimary report T able 3: A ge and only the more immediately important ques tions relating to asbestos exposure and tn cigarette smoking have been examined Table 4 summarizes the occupational exposure for males aged 15 years or more at death, exclu ding the 10 years preceding death. There was a substantial excess of `definite' and `probable' exposures over both control groups ( P < noil but virtually no difference in the frequency f jobs m which exposure was classified as `pos sib le. In 61% of the cases, however, occupa- `uunnhliikeellvy?.P On nTly ttw0o aswboemstoesn winasalcl onhsaidderaendy occupational exposure; one was classified as definite and she was a case. The occupations involving definite or prob able exposure to asbestos are listed in Table 5. Sex D istribution Age (Years) A ll M ales Cases 2 8 13 2371 234 !8 (97) 58-7 139 Controls Group A I 26 14 223056 4 108 (92) I 2 24 24 35 17 4 108 (94) 59 ' i 59' i 133 12-5 Pernales Cases Controls Group A Group B 57 (51) 558 193 57 (52) 57-4 17-3 56 (47) 58-8 15-5 No. o f questionnaires completed shown in parenthesis (). Total: 433/493 = 88% ' o f P rim ary M align an t M sothlial T u m o u rs in Canada 199 ti n employed in asbestos textile manuIfeture, the installation of brake-linings or as ulators were responsible for most of the *cess of cases over controls. Mine or mill 6orkers made little contribution to the differ^ and only one person, a hardware store man had worked with asbestos-cement pro ducts. The time between first exposure and death for the 21 cases in the definite or probable class ranged from 16 to 50 years; 5 persons who worked on the job for less than \ years had intervals of between 18 and 33 years. Residential histories have been analysed only as regards proximity to an asbestos mining area. Excluding 5 cases (3 mine or mill workers and 2 textile workers) and one mine and mill worker in each control group who lived in mining towns, only 3 men and 2 women had ever lived within 20 miles of an asbestos mine. One of the 5 was a case, T able 4: Occupational Exposure to A sbestos M ales: N o .Cases% Controls Group A Group B No. % No. % D efin ite P robable P o s s ib le U n likely A ll* F em ales: D efinite P robable P ossible U n lik ely A ll* " } 20-8 1} 3-3 3} 4-3 17 59 61 17 -- 47 20 68 22-0 74-7 15 74 161 79-6 96 100 91 100 93 100 I2 -- -- 49 98 50 100 -- --2 i 50 98 51 100 -- -- -- 46 100 46 100 ` O n e ch ild in each gro u p d yin g u n der th e age o f 15 has been exclud ed . Males. D is tr ib u tio n o f d e fin ite a n d p r o b a b le g ro u p s co m p a red w ith p o ssib le and u n lik e ly : x 2 = *4 '9> 2 d .f, P < 0 001. T able 5: D istribution of Occupations C lassified under D efinite or Probable Exposure to A sbestos A sb e sto s m in e o r m i l l ................................................................................ A sb e sto s t e x t il e m a n u f a c t u r e ................................................................ B ra k e -lin in g i n s t a l l a t i o n ................................................................................ I n s u l a t i o n ............................................................................................................... Other occupations in vo lvin g co n tact w ith in su lation m aterials Hardware store (han dling asbestos sh eet and pipe) . .. T o t a l ........................................................................................ Cases 3 5* 2 6 4 i 21 ` Includes on e person w h o w ork ed in `b rake-lin in g m an u factu re'. Control Group A 1 0 0 0 2 0 3 Control Group B 1 0 0 0 3 0 4 Males: Cp eigr aDr eatyte s N il 10 o r less H -29 30 o r m o re Total* T able 6 : Average D aily N umber of C igarettes Smoked Case Group 20 22 18 19 35 19 2308 93 100 C o n tro l Group A 19 19 2211 36 40 16 18 90 100 C on tro l Group B 140 115 46 50 32 35 92 100 Cases with Asbestos Exposure 2 4 1200 13 I 6 55 20 w o Females: Cigarettes per Day N il 10 or less n -29 30 or m o re Total* Case Group 29 58 9 li 2128 I 2 50 100 C on tro l Group A 3558 611806 3 6 51 100 C o n tro l Group B 21 46 8 17 134 / 298 46 100 ` E x clu d in g 6 persons u n d er 15 years o f age and 5 m ales w h ose sm okin g h isto ry w as n o t record ed . 200 A. D. McDonald, A. Harper, O. A. El Attar and J. C. McD, naij g r ip b" C0"tr0' grUP A " d "e iD The possibility of contact as a result of some other member of the family brinain? clearly demonstrated by onl,, raseTiad anvTnrh CaSeS a n d T nly one fen^ TMl 7 ch exPosure- Lesser degrees ,, ASBESTOS EXPOSURE IN AUSTRALIA home dusty clothes from an occupation in- " I T * h USehold con. J. C . M cN u l t y AAgaaaintoVexrcfluSdin' g* 6J *men" "(4ca*ses anadmi1,,eidn. each control group) already themselves occu pationally exposed (definitely or probably) there was one case in a female with `definite' home exp...o..s..u..r.e....a..n..d....o..n..e....m.. .a.l..e min conttrol group B With i-irnkokln,' ______ T ,R. . E probable' home exposure. In addition there were 26 persons with a `possible' home exposure: 10 cases, 9 in control group and 7 in control group B. An analysis of cigarette smoking habits A shown in Table 6. In both males'and females' SSS mcZST/ `" fccaS either the case or secondary lung cancer groups The latter 2 groups had almost an identical distribution of smoking habits. The 20 men with definite or probable occupational exposure to asbestos showed no great differ ence in smoking habits from cases without occupational exposure. C onclusion The findings from this national survey indi cate that primary malignant mesothelial tu mours are very rare in Canada and it is some what doubtful whether there has been any true increase in incidence since 1959. An association between these tumours and defi nite or probable occupational exposure to wweere nTMo mS oSreTfrLeqSuedntSly Tre!p?ort"edf *fo*r areas than controls Probably our most n o t e w S j finding was that almost all the excess in S pational exposure was in the manufactur, industrial application of asbestos rather ^ w itTM X S m stfitf^ f' in-,con,unction - reSuIts of other em dem inl^M a f a d d h io n a l^ S r " n^ " " - " " S aTy- If the* * This survey was made possible by the erear l,i agnivdeno ustby hpatheolorgist"s andd miemsbersc o v e firmalS mUch ^ eb te d to all those who^HH the deceased^ ^ h ' the fricnds and latiVe/if of^'bccupatiotSl"and EnvironmUarH?ahhInt T Quebec Asbestos Mining Association. * f I R eferences Elmes, o. L- & ei r ; 7 .,E35r Erb8"'! ^ L ' and Thompson, 3H (i96j). Selikoff r f M rd-' 22' 261- ' fiofi-cV Nr C nUrg' r l and Hammond, E. C. Wagne? l ` C v * ' J ^ M ed" 272> 50. ((.i1a9k0o0);.. BRr;iitr.SIJT.ggITnSCduCs-tr.A -Maendd., M17a,rc2h6a0n. d, P1. 1 Physician, Occupational Health Section, Department of Public Health, 57 Murray Street, Perth, Western Australia, 6000. Asbestos exposure in Australia has predictbly produced asbestosis in many workers, particularly in the asbestos-cement and insulation industries, and pleural meso thelioma has been reported in every State, frequently with evidence of asbestos exposure. The pattern is familiar. The exception to the pattern has been the effects of exposure to crocidolite at the blue asbestos mine in Wittenoom, Western Australia. In 1939, large crocidolite deposits were r e d at Wittenoom, which is about b5 miles north of Perth' in latitude 22-19s. Significant production of fibre commenced in 1942, and the amount produced per annum haS VaHed gratly' fr0m 3 feW hundred tons initially to (between 1958 and 1966) a maximum of 15,000 tons of fibre per annum. The number of men employed has also varied considerably and rose to between 300 and 400 during this latter period. There were very considerable fluctuations in the production figures, and in the number of men employed. The very high tempera tures, the barrenness of the terrain, the lack of amenities, the dust itself, and a main From the outset, all the asbestos miners had an initial clinical examination, with a chest X-ray and annual periodical chest X-rays, supplemented after 1957 by an annual clinical examination. Pulmonary function tests were not done routinely, but only where there was other suggestive evidence of disease. The first patient was a migrant, aged 33 years, an underground scraper driver, who developed pulmonary tuberculosis, and in 1958 had a lobectomy. An examination of the resected specimen showed asbestosis. Subsequent enquiries have shown that there might have been two other asbestos miners diagnosed in earlier years as suffering from pneumoconiosis, but these were recorded simply as `silicosis' and both had had exten sive previous exposure to quartz in other industries. T able i : A nalysis of M en A ffected Since June 1958, 103 men who worked at Witte noom have developed pneumoconiosis: Mill W o r k e r s ................................. 41 Underground W orkers..................... 29 Mixed Underground and Mill Workers (5) (4) 6 (1) labour force consisting almost entirely of new migrants to Australia, led to an exceedingly high labour turnover. Men with other significant mining . . Men excluded because of lack of clinical d e t a i l .............................................. 3 24 (2) (2) In 1966, poor fibre return, labour problems, transport and production costs, etc., forced the mine's closure. Probably fewer than 20% of the men employed at the mine at any one time had been there for as long as three years, and this would include tradesmen, supervisory and office staff. From the beginning, it was obvious that the mine and mill were too dusty and the Health Department first became concerned about the health of the men in 1948. Despite this concern, and despite earnest attempts at dust suppression and improved ventilation, the situation was always far from satisfactory. Costly attempts at dust suppression were defeated by lack of maintenance, lack of skilled tradesmen and the economic necessity f continuing production, at all costs. Table 1 is an analysis of the men affected until December 1967. T h e figures in brackets are additional cases which have been diagnosed since this initial analysis. O f the original 103, 33 have been excluded from further analysis because of previous dust exposure, mixed mine and mill history or insufficient clinical data. Table 2 shows the year the men commenced work at the mine and mill, and the year diagnosed. It would appear that, although working conditions were poor and dusty from the beginning, these did not cause significant lung disease while the production of fibre remained low.