Document 93D55GjJVLvOE8NdBQgwkOQYq

A REVIEW OF THE INTER-RELATIONSHIP BETWEEN PHYSICAL, BIOLOGICAL 5 ENVIRONMENTAL FACTORS IN THE DIAGNOSIS 6 MANAGEMENT OF ASBESTOSIS BY Hilton C. Lewinsohn, MB., B.Ch., D.I.H., MFCM Corporate Medical Director Raybestos-Manhattan, Inc. 100 Oakview Drive Trumbull, Connecticut 06611 Paper presented at the Association of Clinical Scientists' Sympsoium on "Frontiers of Clinical Science" at the Medical University of South Carolina, Charleston, South Carolina, May 3 - 6, 1979. A0098 1 "'When you come to a patient's home, you should ask him what sort of pains he has, what caused them, how many days he has been ill, whether or not the bowels are working and what sort of food he eats.' So says Hippocrates in his work Affections. I may venture to add one more question: What occupation does he follow?" Bemardini Ramazzini (1700) (Trans. W. C. Wright, 1940) Bemardini Ramazzini, because he suggested inquiring of a patient what his occupation was, is known as the Father of Occupational Medicine. In the practice of occupational medicine the occupational history has become the cornerstone of the medical examination and the facts elicited determine the course and structure of the remainder of the procedure. Asbestos has received, and is receiving, a gTeat deal of attention from all quarters. Much is known about this fibrous mineral; much has yet to be discovered with regard to its biological effects. A small group of scientists have gained international reputations simply because they have maintained their interest in this subject over the course of many years, while the majority of their colleagues have been more concerned with illness and treatment than with prevention of disease. Some workers in this field, more recently arrived on the scene and with little practical experience of industry and occupational health, do not have the same attitude towards the subject or the same approach to its investigation as their older, and perhaps wiser colleagues had. Opinions are no longer solely based upon scientific reason, but are swayed by emotions. Reporters or television commentators who are able to portray the subject most dramatically, using medical and environmental evangelists to preach the gospel, A0030 2 -2- while not necessarily stating all the facts, seem better able to influence politicians and regulatory agencies than the miners, manufacturers and producers of asbestos products. i It is necessary to be specific about such mundane matters as fiber shape and size, minerological differences and geographic variations in disease prevalence and incidence, in order to understand and interpret the clinical situation. Were Bemardini Ramazzini alive today, and had he the instruments and knowledge we have, he would still place as much importance upon occupational history as he did in the year 1700. He would, however, be able to benefit from a much more detailed understanding of occupational hazards, how they create their effects and how such effects can sometime be prevented. A. WHAT IS ASBESTOS? Asbestos is a generic term used to describe naturally occurring durable mineral silicates of filamentary or fibrous nature.^ The varieties of asbestos in commercial use, their chemical description, their physical appearance and their main source of origin are shown in Table 1. Asbestos is used in the construction industry, in floor tiles, asbestos cement, roofing felts, shingles, insulation materials, cement powders, acoustical products, textiles, brake linings, clutch facings, paper, paints, roof coatings, plastics and miscellaneous other products. Asbestos filter pads are used in wine making, spirit distillation, beer production, in filters for blood transfusions, for filtering drugs and for purifying solutions for intravenous infusion. A009 3 -3- It should be appreciated that in the primary and immediate post-primary section of the asbestos industry, i.e., mines and manufacturing industry, relatively few people are involved, whereas millions of people are ultimately exposed to apparently ever decreasing amounts of fiber in the products of the entire industry. Furthermore, asbestos is ubiquitous in the earth's atmosphere and has been since the beginning of recorded time. Fibers below 0.5/m diameter and less than S^um in length are not visible with the optical microscope and need to be identified by transmission electron microscopy, scanning electron microscopy or combinations of these instruments and various forms of selected area diffraction or microprobe analysis. X-ray diffraction has been used for the quantitative determination of chrysotile and amphiboles in air and water samples. The latter technique has also been used to analyze asbestos in lung tissue. B. WHAT ARE THE PATHOLOGICAL EFFECTS OF EXPOSURE IN MAN? Knowledge of the type of asbestos to which a person has been exposed is of value because it may be an important factor in the appreciation of special risks involved. Differences in the physical characteristics of the various types of asbestos fibers determine their particular commercial usefulness. Chrysotile consists of long, mainly pliable fibers that split progressively into finer fibrils and it may be used in textiles, whereas crocidolite and amosite can be used in marine Insulation because of their acid resistant properties. Certain asbestos cement products may be made from blends of chrysotile and amosite and/or crocidolite. A00904 V 4 Exposure to asbestos at work or elsewhere may result in five conditions: 1. The presence of asbestos in tissues without disease e.g., asbestos bodies in the general population.^ 2. The presence of asbestos in the tissues causing benign 4 changes - e.g., skin warts, pleural plaques. 3. The presence of asbestos in the tissues and the development of malignant mesothelioma of the pleura or peritoneum. 4. Asbestos in the lungs with tissue damage and the development of lung cancer. 5. Asbestos present with potentially fatal damage to the lungs (pulmonary fibrosis or asbestosis), but no cancer. The ranking order of these five situations is intentional and tends to in dicate the diseases associated with the least exposure through the worst exposure. It is, however, easier to discuss the pathological effects in the reverse order. There are two other conditions which have been detected in greater numbers among asbestos workers than would be expected from a similar sample of the general population: a. Cancer of the gastro-intestinal system involving oesophagus, stomach and colon and rectum. A009 b -5- b. Cancer of the larynx. I have listed these two conditions separately, because at the present time, there is insufficient published information regarding the presence or absence of asbestos in human tissue in these cases and the association has been established on purely epidemiological grounds. C. HOW DO PHYSICAL FACTORS RELATE TO CAUSATION OF DISEASE? Whether or not inhaled asbestos fibers will reach the depths of the lung depends on the aerodynamic behavior of the particles, the size of the airways they enter, and the individual's breathing pattern.^ The larger dust particles are trapped in the nose and throat. Smaller fibers get down into the trachea, bronchi and smaller bronchioles, but because of the turbulent airflow in the large airways, fibers are thrown outward and deposit on the sticky lining mucosa. These fibers are carried back out of the lungs on the muco-ciliary escalator by the beating of the cilia. When they reach the larynx, they are swallowed. Thus three factors are involved: 1. deposition Cor inertial forces in large airways), 2. gravitational (settling of fibers in smaller airways), and 3. diffusional forces in alveolar spaces. Other physical factors to consider are itemized: 1. Respirability is dependent upon the size and shape of fibers inhaled. 2. Larger particles are trapped in the upper airways and removed from the lungs by the muco-ciliary escalator. A00986 -6- 3. Fibers with an aerodynamic diameter less than 3are respirable, although their length may be as much as lOO^um - 200^um. 4. Fibers with an aerodynamic diameter less than 3yum and greater than 10 to 20^um in length are thought to be those most likely to cause disease. The shape of inhaled particles, aside from size per se, determines in part their deposition characteristics. Long, irregular particles such as asbestos fibers settle much less than would be expected from their total fiber mass. Other irregularly shaped particles (e.g., quartz, coal) are aerodynamically equivalent to spherical particles one-half to three-quarters of their measured diameters. Most models consider particles in terms of unit density spherical shapes (i.e., as aerosols), to reach a reasonable agreement between theoretical predictions and experimental observations. In addition to shape, the density of a particle determines its deposition characteristics. Differences in disease-producing potentials of fibers may arise from the fact that curly, flexible, soft chrysotile fibers are more likely to be caught and filtered out by this system than the straight fibers of the other forms of asbestos in commercial use. To escape this filter mechanism, the fibers must be light enough to remain in suspension and short enough not to be intercepted by the branching of the smaller airways. Examination of human lungs has re vealed straight fibers in the lung up to 200jm. in length and also coils of chrysotile which may be even longer if stretched out. Once a fiber is carried beyond the ciliated part of the airway, i't may still be deposited and stay there or it may be carried out again with the next expiration of air. The A003 7 -7- proportion of fibers trapped at this stage still depends on size - long fibers are caught, small ones breathed out. Because in a typical dust cloud there are millions of very small fibers, more are retained in the lung than larger ones. Many of these very small fibers are too small to be counted with a light microscope and can only be counted by examining the lung or digests of the lung under the electron microscope. Their biological effects, if any, are not yet known. In the tissues of the lung, and elsewhere where the fibers may lodge because of transportation in the body by blood, lymphatics and tissue fluid, the fibers may be coated with a brown iron-pigmented material called ferritin, to form 'asbestos bodies'. Asbestos bodies are thought to be innocuous. Not all asbestos fibers are coated in this way and in humans it has been estimated that for every asbestos body in the lung there are 1,000 uncoated asbestos fibers. It is not known whether this is the case in all types of asbestos or in other tissue. It is known that asbestos bodies form rapidly, reside in tissue many years and gradually degenerate over the years releasing their fiber core. It is not known whether these released fibers, after many years, are still capable of causing disease. It is also known that uncoated fibers are.capable of causing tissue damage when first inhaled, but it is not known whether they retain this potential indefinitely or are dealt with by some unknown defense mechanism other than the ferritin coating process. Chrysotile fibers have been shown to dissolve in tissue fluids so that it may be impossible to confirm that a person has been exposed by looking for these fibers in the tissues thirty or forty years later, unless exposure was continuous throughout the individual's life time up to the tine of retirement. Crocidolite and amosite can be identified in tissue even after as long an interval as this, and it has been claimed by A003S3 -8- one investigator that it is actually possible to identify the geological origin of such fibers by the use of electron microscopic techniques. The physical factors outlined above may be invoked to explain why asbestos miners seem to be less at risk than primary process workers who in turn seem less at hazard than those who use processed asbestos under dusty conditions. It is possible that freshly mined asbestos is still aggregated in bundles and less likely to be respirable or retained in the lung and thus less likely to be damaging. The more processing the asbestos receives, the finer the division of the fiber bundles and the more dangerous it becomes. Dust studies to support this physical characteristic have been reported. Chrysotile fibers collected in the carding area of an asbestos textile plant tended to have smaller diameters than fibers collected in the dryer and bagging areas of an asbestos mill. It should not be forgotten that primary and secondary use of asbestos usually takes place in highly polluted urban environments by people exposed to many additional non-respiratory toxic agents. Cigarette smoking may be a co-factor in the production of occupational disease - it is not usually permitted under ground in mines. There may be a synergy between cigarette smoke and asbestos dust only when they are inhaled simultaneously, but this is unlikely and difficult to deduce from epidemiologic studies. D. WHAT IS THE EVIDENCE FOR STATING THAT ASBESTOS MAY BE PRESENT IN TISSUE WITHOUT DISEASE? Examination of material from random autopsy series in several cities has revealed the presence of asbestos in lung tissue.** The frequency of this finding depends upon the diligence of the search. When digested lung tissue is examined, prevalence approaches 1001. These findings can occur in the A0098 3 -9- absence of any asbestos associated diseases. E. DOES A DOSE-RESPONSE RELATIONSHIP EXIST IN ASBESTOS-RELATED DISEASES? The concept of a dose relationship of response to stimulus is a familiar one in pharmacology. This same concept has been invoked in an effort to explain the biologic response to inhaled dust.5 An important question inmediately arises - Why is one person affected and not the person working alongside? A third factor that has to be introduced into the concept is that a given dose-response curve can be developed for a given population (or person), but that it will be applicable only to another population (or person) of the same "susceptibility." Susceptibility may depend upon several biological factors such as the efficiency of pulmonary clearance mechanisms, the anatomic characteristics of the lung/airway system, or the physical fitness of the person. Susceptibility can also be related to immunogenetic factors. Another important variable, not biological, is the differences in work practices and habits of individuals doing essentially the same job. Although asbestos dose-response relationships are evident to a greater or lesser extent for all responses, the degree of correlation is difficult to ascertain precisely because of inadequate records of past exposure in all situations studied. The observed response is usually the result of past, rather than current exposure. This poor correlation has led to the current interest in "susceptibility," i.e., factors accounting for between-subject differences in response. A003 ;G - 10 - F. WHAT ARE THE BENIGN CHANGES IN TISSUES FOUND IN THE PRESENCE OF ASBESTOS AND WHAT ARE THEIR SIGNIFICANCE IN TERMS OF PROGNOSIS? Warts on the fingers and hand, and a discrete reaction involving the parietal pleura, usually in more than one place and referred to as pleural plaques, are often found in people who have been occupationally exposed to asbestos. Pleural plaques are usually a radiographic diagnosis in an otherwise healthy person. Pleural plaques may calcify. Pleural plaques have also been described in people exposed by living in the vicinity of certain mines or tilling soil with 7 a high asbestos fiber content. The above conditions are not in themselves disabling, although the pleural plaques may indicate a level of exposure sufficient to progress to more serious disease. The effect of pleural plaques on pulmonary function, although detectable in population studies, is modest and is mainly seen as small reductions in lung volumes. By contrast, X-ray changes may be very striking, particularly in the presence of calcification. Although the presence of pleural plaques alone does not appear to cause symptoms of disability, there is some evidence that they affect prognosis. - They have been associated by some authorities with increased incidence of lung cancer and malignant mesothelioma has been reported as developing in the cells at the edge of the plaque. G. WHAT IS ASBESTOSIS AND HOW DOES IT AFFECT THE EXPOSED INDIVIDUAL? 1. Asbestosis is a fibrosis or scarring of the lungs and includes the associated thickening of the visceral pleura, but not that of the parietal pleura. A0099 1 - 11 - 2. The lower (dependent) parts of the lungs are affected first progressing as the years go by even after exposure ceases. 3. Asbestosis may be diagnosed using the following criteria: a. Obtaining a history of "adequate" exposure, b. Eliciting fine end-inspiratory crackles at the lung bases on auscultation, c. Finger clubbing (may or may not be present), d. X-ray changes - small irregular and/or rounded Q opacities (ILO U/C Classification), e. Pulmonary function changes indicative of restriction of ventilation or impairment of gas exchange. (Airways obstruction is not usually a feature of asbestosis, but has been reported in some studies.)9,10,11 4. The ILO U/C Classification, developed for epidemiologic purposes, is descriptive, not diagnostic. 12 Serial radiographs over a period of time have to be studied to determine the significance of abnormalities noted. 5. A diagnosis of asbestosis can only be made by examining the worker, all the available x-ray films, the pulmonary function test made over a period of time and the couplete occupational history. A 00 O C - 12 - 6. Other respiratory diseases such as chronic bronchitis, emphysema, asthma and certain chronic lung diseases can be mistaken for asbestosis. 7. The severity and progression of asbestosis depends on the amount of asbestos retained in the lung. This can be related to dust con centrations in the work place and length of exposure.^ 8. From the time symptoms are first noted, most workers can continue with light work for 10 to 15 years and may live another 5 to 10 years after finishing such work. 9. Asbestosis is unusual under the age of 50. Other conditions leading to the necessity for light work and retirement may precede it in this age group. 10. Improving industrial conditions over the past 20 years have resulted in a type of asbestosis less severe than in the 1930's, 1940's and 1950's. At the present time life expectancy may not be appreciably shortened by this disease. * 11. The effects of improvements in industry on the incidence of excess deaths appears to have reduced this complication of exposure in parallel with the reduction in asbestosis, but further evidence is still needed to prove this observation conclusively. A00933 - 13 - H. WHAT ARE TOE FEATURES OF ASBESTOS-ASSOCIATED MALIGNANT DISEASE OF TOE LUNGS? 1. The risk of premature death from malignant chest disease seems to be con fined to those with high dust exposure, though sanetimes of brief duration. 2. Asbestosis is no longer an inevitably fatal condition because improved dust conditions have resulted in a nmilder,, form of disease, or in fact a sub-clinical entity which is not always recognized. Less mortality from asbestosis occurring after longer periods of exposure to lower concentrations of dust than in past years has resulted in survival of workers through the long latent period of lung cancer. 13 * 14 3. The interaction of cigarettes and asbestos exposure as risk factors is of great importance. Non-smoking asbestos workers rarely get lung cancer. 14 * 15 4. The primary lung cancers in smoking asbestos workers do not differ in their effects from primary lung cancers in other people, and the results of treatment do not differ either.^ * 5. Although lung cancer is usually associated with asbestosis, some authorities believe that this is not necessarily so. I. WHAT ARE THE CURRENT VIEWS REGARDING MALIGNANT MESOTHELICMA? 1. Epidemiologic evidence indicates a gradation of effect related to fiber type.* Crocidolite, particularly fiber from the North West Cape Province of South Africa and from Western Australia, is con sidered to be the type of fiber most frequently associated with A00994 - 14 - mesothelioma. Chrysotile is considered to be least likely to cause it and amosite has been allocated an Intermediate status. Although anthophyllite has been associated with asbestosis, pleural plaques and lung cancer, no cases of mesothelioma have been attributed to it. 17 2. Cigarette smoking does not seem to be a causative factor. 3. Exposure may be of brief duration and there is a long lapsed period (latent interval] between first exposure and diagnosis or death. This lapsed period may be from 20 to 40 years or more - disease diagnosed today had its causation in working conditions between 20 to 40 years ago or longer. 4. The tumor affects the pleura, gTows slowly, doesn't spread readily and kills by slowly compressing first the lung on one side and then the vital structures in the center of the chest or the lung on the other side. Peritoneal tumor is less cannon and is similar in its effects. 5. The tumor can occur from about the age of 35 onwards, but more than 50% do not develop until over the age of 60. 6. Domestic or neighborhood exposure has resulted in the development of this disease. 18 7. Mesothelioma is not uniquely associated with asbestos exposure and in most reported series a small proportion (151-301) cannot be related to asbestos. A0093b - 15 - In 1978, the suspicion that other materials could be partly responsible for mesothelioma cases without known exposure to asbestos, was apparently verified by the finding in Turkey that asbestos related diseases, mainly calcified pleural plaques, chronic fibrosing pleuritis and malignant pleural mesothelioma are endemic in some villages without asbestos deposits. 19 In one village, where 11 mesothelioma deaths occurred in 1974, there are no deposits of asbestos in the area, nor has there been any processing of such material brought in from elsewhere. Research has shown many fibers in the respirable size range in rock samples, samples from streets and fields of the village, but not from control villages 4 and 7 km further up the valley. These fibers were shown to be erionite type zeolite. Thus, it would seem that fiber-shape and size is important in the eitology of malignant mesothelioma and fibrous minerals from sources other than asbestos mining or processing may be implicated in the epidemiology of this disease. J. DOES ASBESTOS HAVE OTHER CARCINOGENIC PROPERTIES? 1. Cancer of the gastro-intestinal tract involving oesophagus, stomach, colon and rectum, has been reported in excess in asbestos insulation workers and other asbestos workers.^ 2. An association has been found in seme reported studies between an excess incidence of cancer of the larynx and asbestos exposure. 20 3. At present there is insufficient published information regarding the presence or absence of asbestos in human tissue in these conditions and the association has been established purely on epidemiologic grounds. A00933 i - 16 - K. WHAT ARE THE CLINICAL TESTS WHICH CAN BE USED IN THE DIAGNOSIS OF ASBESTOSIS IN LIGHT OF THE BACKGROUND INFORMATION IN THE PREVIOUS SECTIONS? Asbestosis is a clinical diagnosis in the living patient and reliance is placed upon radiographs, corroborated by an occupational exposure history and con firmatory findings on examination and after performing tests of lung function. Asbestos bodies in the sputum are an index to exposure and not diagnostic of disease. The post-mortem diagnosis of asbestosis is also improved by finding of asbestos bodies and fibers in the lung tissue. The features of pulmonary fibrosis found in asbestosis are well described in the paper of Becklake.^ TurnerWarwick has proposed that anti-nuclear antibody (ANA) acts as an accelerator once fibrosis has been initiated by a separate agent and this may explain why asbestosis may appear for the first time and progress long after exposure to dust has ceased. Turner-Warwick found that non-organspecif ic autoantibodies (ANA), occur with only slightly greater frequency in exposed, compared to nonexposed persons in the general population, and within exposed populations, with greater frequency in those with clinical disease than those without. * Thus, the finding of clinical relevance is that a positive ANA test (or rheumatoid factor test) occurs frequently in asbestosis, and therefore, in the patient with asbestos exposure, in the absence of any features of underlying collagen disease, could be regarded as a confirmatory diagnostic sign. When pleural effusion develops in a patient with known asbestos exposure, it is usually in the form of an exudate. Exfoliative cytology should be performed on the exudate to exclude an underlying malignancy, especially bronchogenic A0099? - 17 - carcinoma or mesothelioma. Butler, in 2 of t patients found to have atypical macrophage-13 cells, similar to cells found in proven mesothelioma, describes their eventual diagnosis as mesotheliomata. Butler was able from appropriate aspirates to correctly diagnose by exfoliative cytological techniques 25 of 26 mesotheliomata, 28 of 30 metastatic pulmonary carcinomas and 19 of 21 cases of mesothelial reaction. Sputum exfoliative cytology has been suggested as a screening examination for asbestos workers over the age of 45 or with more than 10 years of exposure to the dust. Studies for evaluating this, technique are in progress, but do not to date indicate a high yield of treatable early disease. In my opinion, this is not as yet a satisfactory screening tool. Furthermore, the finding of suspicious cells in a worker with a normal x-Tay and no abnormal physical findings forces invasive techniques to be used such as fiber-optic bronchoscopy. If no tumor is found, but sputum cytology remains positive, there is no option other than to repeat all the investigations at frequent intervals, with the likelihood that many years may elapse before a positive diagnosis can be made. The psychological traumas to the patient hardly seems worth it in view of the poor prognosis after treatment. L. IS 'MERE A SAFE STANDARD TO PROTECT AGAINST THESE DISEASES? There is a scarcity of adequate data from which to derive a safety standard which would give a 1001 assurance of preventing the diseases associated with asbestos. The present standard is based upon evidence presented in a 1968 report published by the British Occupational Hygiene Society. 21 The data upon which this A003Q8 - 18 - report was founded was obtained from an asbestos textile factory which had personnel and medical records available for study, as well as dust measurements, from 1951 onwards. The standard assumed that a combination of two variables, namely length of exposure and concentration of fibers during the exposure period, could be statistically analyzed and correlated with the earliest signs of the effects of asbestos exposure recognizable by the plant physician. As a result, it was postulated on this evidence that a cumulative exposure of 100 fibers per cubic centimeter would result in only 1% of persons exposed developing these early signs of asbestosis. The committee speculated that a worker could work for 50 years in dust concentrations of 2 fibers/cc and only run a 1% risk of developing asbestosis. The committee did not propose the standard for protection against lung cancer or mesothelioma. The crucial issue at stake is whether exposure to dust levels of 2'fibers/cc will also prevent lung cancer and mesothelioma. Furthermore, should the same standard apply to all types of asbestos fibers or should there be an even tighter control on the use of crocidolite. There is circumstantial evidence from the same factory that the high excess incidence of lung cancer deaths in the heavily exposed groups of workers who were employed before the regulations were introduced in 1931 and became effective in 1933 has been much reduced in the more recently exposed groups, i.e., the post 1933 cohort, although a slight excess may still be detected even in the cohort first exposed after 1950. 22 This slight excess is not highly statistically significant and might be drastically influenced in the future by increasing the follow-up population. Furtheimore, it can be explained by the fact that conditions in the factory were by no means all A00 39 9 - 19 - in compliance with' the standard requirements of today and not until this is achieved will this small excess number of deaths abate. There is no numerical data with regard to mesothelioma upon which to build a dose-response curve, although some authorities do believe that a dose-response has been demonstrated based upon historical descriptions of conditions allowing jobs to be classified as severe, moderate, light and negligible exposures.^ The present situation is that in the United States no data is available for study, which enables asbestos fiber counts to be correlated with morbidity or mortality. The best data still comes from the factory in the U.K. mentioned previously and it is currently under review by the BCHS. Cancer is an emotional word. NIOSH and OSHA, both under criticism and charged with being inefficient, respond to pressure groups readily and over-react regularly. Nobody seems to know what to do. Time will tell. Even if the uses of asbestos decline, the deposits in the earth's crust will be there to exploit again when the dust of past misuse settles and the dose-response can be more clearly determined based upon adequate dust measurement records now being compiled and better record keeping of morbidity and mortality statistics. AO 1 0 REFERENCES 1. Campbell, W. J., Blake, R. L., Brown, L. L. et al: Selected Silicate Minerals and their Asbestiform Varieties. Mineralogical Definitions and Identification - Characterization. U. S. Dept, of the Interior, Bureau of Mines, Information Circular, 1977. 2. Hendry, N. W. The Geology, Occurrences, and Major Uses of Asbestos. Ann. N. Y. Acad. Sci. 132: 12-22, 1965. 3. Thomson, J. G. Asbestos and the Urban Dweller. Ann. N. Y. Acad. Sci. 132: 196-214, 1965. 4. Leathart, G. L. Pulmonary Function Tests in Asbestos Workers. Trans. Soc. Occup. Med., 18_: 49, 1968. 5. Becklake, M. R. Asbestos-Related Diseases of the Lung and Other Organs: Their Epidemiology and Implications for Clinical Practice. Lung Disease. State of the Art, 1975-1976 (Ed. John F. Murray) American Lung Association, New York, N. Y., 1977, pp. 55-95. 6. Thomson, J. G., Graves, W. M. Asbestos as an Urban Air Contaminant . Arch. Pathol., 81: 458, 1966. 7. Navratil, M. Pleural Calcification due to Asbestos Exposure Compared with Relevant Findings in the Non-Exposed Population. Inhaled Particles and Vapors III. Walton, W. H. (ed.): ProceWings of the British Occupational Hygiene Society Symposium, London 1970. Old Woking, 1970, pp. 695-701. 8. Becklake, M. R. Pneumoconioses, in Handbook of Physiology, Sec. 3, Respiration, Vol. II, W. 0. Fenn and H. Rahn, ed., American Physiological Society, Washington, D.C., 1965. 9. Murphy, R. L. H., Ferris, B. G., Burgess, W. et al. Effects of Low Concentrations of Asbestos: Clinical Environmental, Radiologic and Epidemiologic Observations in Shipyard Pipe Coverers and Controls. N. Engl. J. Med., 285: 1271, 1971. AO 1 00 1 10. Morphy, R. L. H., Gaensler, E. A., Redding, R. A., et al. Low Exposure to Asbestos: Gas Exchange in Ship Pipe Covcers and Controls. Arch. Environ. Health, 25: 253, 1972. 11. Foumier-Massey, G., Becklake, M. R. Pulmonary Function Profiles in Quebec Asbestos Workers, Bull Physiopathol Respir. (Nancy), li: 429, 1975. 12. International Labor Office, ILO U/C Classification of Radiographs of the Pneumoconioses, 1971, Occupational Health and Safety Series No. 22, International Labor Office, Geneva, 1972. 13. Doll, R. Mortality from Lung Cancer in Asbestos Workers. Brit. J. industr. Med. 12, 81, 1955. 14. Selikoff, I. J., Bader, R. A., Bader, M. E., et al. Asbestosis and Neoplasia, Am. J. Med., 42^: 487, 1967. 15. Berry, G., Newhouse, M. L., Turok, M. Combined Effects of Asbestos Exposure and Stacking on Mortality from Lung Cancer in Factory Workers. Lancet, 2: 476, 1972. 16. Report of the Advisory Committee on Asbestos Cancers to the Director of the International Agency for Research on Cancer in: Biological Effects of Asbestos, P. Bogovski, J. C. Gilson, V. Timbrell and J. C. Wagner, eds. IARC Scientific Publication No. 8, Lyon 1973 - pp. 346. 17. Meurman, L. 0., Kiviluoto, R., Hakama, M. Mortality and Morbidity Among Miners in Finland, Brit. J. industr. Med., 31: 105, 1974. 18. Wagner, J. C., Sleggs, C. A., Marchand, P. Diffuse Pleural Mesothelioma and Asbestos Exposure in the North-West Cape Province. Brit. J. industr. Med., 17: 260, 1960. 19. Baris, Y. I., Sakin, A. A., Ozesmi, M., et al. An Outbreak of Pleural Mesothelioma and Chronic Fibrosing Pleurisy in the Village of KarainUrgup in Anatolia. Thorax, 33, 181-192, 1978. A01002 20. Stell, P. M., -McGill, T. Asbestos and Laryngeal Carcinoma, Lancet, 2: 615, 1973. 21. British Occupational Hygiene Society: Committee on Hygiene Standards: Hygiene Standards for Chrysotile Asbestos Dust, Ann. Occup. Hyg., 11: 45, 1968. -- 22. Peto, J., Doll, R., Howard, S., et al. A Mortality Study Among Workers in an English Asbestos Factory, Brit. J. industr. Med., 34: 169, 1977. AO 1 003 TABLE 1 CHARACTERISTICS OF MAIN TYPES OF ASBESTOS FIBER Qiaracteristic Theoretical Fomila Colour Qirysotile Crocidolite Anosite Antfaophyllite Treaolite Actinolite Mgr (Si|0sKCH)4 ^FellsFelll, (ft. Mg) 7 (Mg, ft)7 Ca2Mgs Ca2(Mg,Fe)s (SiB022]ICH)2 [Sig0223(CH)2 [SijOal(OHJ2 [Sl|022l(CH)2 lSi8022](CH)2 Usually white Blue to pale green yellow1, pink1 Light grey to White to grey, White to grey Pale to dark pale brown pale brown green Decomposition Tanperature* CC) Fusion Temperature of residual material (C) Density g/aa3 Resistance to acids Resistance to alkalis Mechanical properties of fiber as taken from rock samples: Tensile strength 103 kg/an2 (Average)(103 psi) Young's Modulus 103 kg/as* (Average)(106 psi) Texture Producing countries 450-700 1S00 2-S5 Undergoes fairly rapid attack Very good 400-600 1200 3*3-3*4 Good Good 31 (440) 35 (495) 1,620 1,860 (23) (27) Usually Flexible to flexible, silky brittle and and tough tough USSR Canada Qiina Rhodesia USA Italy South Africa Swaziland South Africa 600-800 1400 3-4-3-S Attacked slowly Good 600-850 1450 2*85-3*1 Very Good Very good 17 (2S0) (-C7) (-cl00) 1,620 (23) Usually brittle -- Usually brittle South Africa Finland USA Mozambique 950-1040 1315 2-9-3-1 Very Good Good 5 (-*70) -- *- Usually brittle USA 620-960 1400 3-0-3.2 Attacked slowly Good S 70) -- NOTES: -Dehydroxylatian or dehydrogenation iccompanicd by disruption of crystal lattice and major loss of strength. ^Froo serpentinised dolomite deposits. A0 1 004