Document ZnKMv8jrqEg28Lo66QLNrbO1d

ST0030220 A R 30 RN E ASBESTOS A Report; Prepared by Che Committee on Biologic Effects of Atmospheric Pollutants of the Division of Medical Sciences, National Research Council National Academy of Sciences National.Academy of Engineering Washington, D.C. 1971 397379 ST0030221 Committee on Biologic Effects of Atmospheric Pollutants, Division of Medical Sciences, National Research Council: Dr. Arthur B. DuBois, Department of Physiology, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, Chairman Mr. Vinton W. Bacon, College of Applied Science and Engineering, University of Wisconsin, Milwaukee, Wisconsin Dr. Anna M. Baet.jer, Department of Environmental Medicine, School of Hygiene and Public Health, The Johns Hopkins University, Baltimore, Maryland Dr. W. Clark Cooper, School of Public Health, University of California, Berkeley, California Dr. Morton Corn, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania Dr. Bertram D. Dinman, School of Public Health, University of Michigan, Ann Arbor, Michigan Dr. Leon Golberg, Institute of Experimental Pathology and Toxicology, Albany Medical College, Albany, New York Dr. Paul B. Hamnond, Department of Physiology and Pharmacology, College of Veterinary Medicine, University of Minnesota, St. Paul, Minnesota Dr. Samuel P. Hicks, Department of Pathology, University of Michigan Medical Center, Ann Arbor, Michigan Dr. Victor G. Laties, Department of Radiation Biology and Biophysics, University of Rochester Medical Center, Rochester, New York Dr. Abraham M. Lilienfeld, Department of Chronic Diseases, School of Hygiene and Public Health, The Johns Hopkins University, Baltimore, Mary]and 397380 7 7 7 n r.n n i s Committee on Biologic Effects of Atmospheric Pollutants, Division of Medical Sciences, National Research Council (cont'd.): Dr. Paul Meier, Biomedical Computation Facilities, University of Chicago, Chicago, Illinois Dr. James N. Pitts, Jr., Department of Chemistry, University of California, Riverside, California Dr. Gordon J. Stopps, Haskell Laboratory, E. I. duPont de Nemours and Company, Newark, Delaware Dr. 0. Clifton Taylor, Department of Horticulture, University of California, Riverside, California Dr. Jaroslav J. Vostal, Department of Pharmacology and Toxicology, University of Rochester Medical Center, Rochester, New York Executive Director, T. D. Boaz, Jr., M.D. 397381 5 I U U ijU ZZJ Pane! on Asbestos: Dr. V. Clark Cooper, School of Public Health, University of California, Berkeley, California. Chairman Dr. Lewis J. CraLley, Bureau of Occupational Health and Safety, Division of Epidemiology and Special Services, U. S. Public Health Service, Cincinnati, Ohio Dr. Benjamin G. Ferris, Jr., Department of Physiology, Harvard School of Public Health, Boston, Massachusetts Dr. Paul Gross, Industrial Hygiene Foundation, Inc., Pittsburgh Pennsylvania Mr. Duncan A. Holaday, Occupational Health Field Station, Salt Lake C LLy , ui.au Dr. Irving J. Selikoff, Environmental Sciences Laboratory, Mount Sinai Hospital, New York, New York Dr. George W. Wright, Medical Research Department, St. Luke's Hospital, Cleveland, Ohio Dr. Samuel P. Hicks, Department of Pathology, University of Michigan Medical Center, Ann Arbor, Michigan, Associate Editor Dr. i. D. Boaz, Jr., Division of Medical Sciences, National Research Council, Washington, D.C., Staff Officer 397382 PREFACE The naturally occurring fibrous silicates classified as "asbestos" have be cone almost indispensable in modern technology .^ The world's annual production has grown from a few thousand tens in 1900 to over 3 121 million tons in 1968. Annual consumption in the United States averaged nearly 800,000 tons during the period 1965-1969Tke potential of asbestos as a hazard to health has been the subject of a number of reviews 22,1*9,60,131,137,1^6,118,168 in recent years. ' Although it has been known for a half-century that persons who inhaled large amounts of asbestos dust in the course of their work sometimes developed disabling or fatal fibrosis of the lungs, it has been only within the last three decades that other serious effects, such as cancer, have been associated with occupational exposures. Recently, the likelihood of exposure of the public at large to asbestos has been recognized and has led to a demand for more rigorous control of asbestos emissions into the atmosphere. "Asbestos" is a generic term for a number of hydrated silicates that, when"crushed or processed, separate into flexible fibers made up of fibrils.^ Although there are many asbestos minerals, only six are of commercial importance: chrysotile , a tubular serpentine mineral, accounts for 95 % of the world's production; the others, all amphiboles, are amosite, crocidclite, ar.thophyllite , tremolite , and actinolite. The asbestos minerals differ in their metallic elemental content, range of fiber diameters, flexibility or harshness, tensile strength, surface properties, and other vii 397383 5 I U U O U d iO attributes that determine their industrial uses and may affect their respirability, deposition, retention, translocation, and biologic reactivity. This report (l) summarizes the major evidence of the pathogenicity of asbestos in nan and aninals, (2) summarizes the evidence of human nonoccupaticnal exposure to asbestos, (3) evaluates the evidence of a health risk associated with various degrees and types of exposure, (4) identifies sources of environmental contamination by asbestos, and (5) offers recommendations concerning the need for and feasibility of control measures. W. Clark Cooper Chairman vm 397384 CONTENTS Chapter 1 Chapter 2 Chapter 3 Chapter h Chapter 5 Chapter 6 Chapter 7 Pae Pathogenicity of Asbestos.................................. 1 Evidence of Human Nonoccupatior.al Exposures....................................................................... 11 Estimation of Risk in Nonoccupational Exposures...................................................................... l6 Sources of Asbestos Fibers in Ambient Air..................................................................................... 21 Principles of Control............................................... 26 Research Needs................................................................ 30 Conclusions and Recommendations...................... 32 References......................................................................... 3^ ST0030226 397385 ST0030227 CHAPTZH 1 PATHOGENICITY CF ASBESTOS The effects of fibers in biologic systems may result not only from the properties of the fibers themselves, but also from contamination with inorganic or organic substances that occur naturally or are added during mining, milling, processing, shipping, cr use. Contaminants acquired from the atmosphere or in the respiratory tract may be carried on the surface of fibers. Fibers may act as cofactors; conversely, their action may be modified by other cofactors. PATHOGENICITY IN MAN The proven or suspected effects of asbestos minerals on human health include nonmalignar.t changes, such as pulmonary anu pleural fibrosis, and several types of malignancy, notably of the lung, pleura, and peritoneum. Nearly ail the positive evidence of an association between asbestos and human disease has come from occupational groups. With few exceptions, these have consisted of workers engaged in the mining and milling of asbestos , the manufacture of asbestos-containing products (such as textiles and construction materials), and the application and removal of asbestos-centaining insulating materials. Asbestosis Asbestcsis, or asbestotic pneumoconiosis, was the first clearly demon strated adverse effect of asbestos in man. It is characterized by a pattern of roentgenographie changes in the lung consistent with diffuse interstitial fibrosis of variable degree and at times with fibrosis end calcification of the pleura; clinical changes that include fine rale.-, 1 397386 finger clubbing, and shortness of breath, each of which may be absent in an individual case; and physiologic changes consistent with a restrictive lung disorder. The first published mention cf a case, in a man who had worked for 10 years in the carding room of an asbestos factory', was by H. Montague Murray in 1907.^^ Cooke reported a second case in 192h^ and in 1927 provided a more detailed description,21 in which the term "asbestosis" was first used. In 1930, Merewether^0^ reviewed the salient features of the disease and the environmental exposures of workers, including data derived from an epidemio logic study reported in mere detail by Merewether and Price.This led to the promulgation of regulations for environmental and medical control in the United Kingdom, which became effective in 1932.^ Cases were first reported -i i n t1i*i in the United Ctatcs in 1530 and guidelines for acceptable dust concentrations were proposed by Dreessen et_ al_. in 1938. Industrial experience indicates that pulmonary fibrosis sufficient to interfere with respiratory or cardiovascular function can be prevented by reducing asbestos dust concentrations to levels that are still far above any likely to be encountered in community air. Pleural Calcification Calcified pleural plaques occur frequently in workers exposed to asbestos ^ ,108,130 vfhen multiple or bilateral , they are regarded U 3 71 by some as almost diagnostic of asbestos-related disease. ' In asbestos workers, calcified plaques rarely appear until 20 years after first exposure and do not necessarily correlate with parenchymal fibrosis .91 397387 ST0030229 Calcification appears to differ in frequency in different occupationally exposed groups, but studies are inadequate to verify or explain such differences. Bronchogenic Carcinoma No features of bronchogenic carcinoma associated with asbestos are pathognomonic. Primary sites are more often in the lover lobes, in contrast with the usually higher frequency of upper lobe tumors. Peripheral primary sites are common in asbestos-related lung cancer. All ceil types are represented in most series. The first suggestion that asbestos might be causally related to cancer of the lung was made in 1935 by Lynch and Smith ^ who described squamous cej.1 carcinoma in a South Carolina textile worker with asbestosis. Despite other isolated reports, an association was not firmly supported by epidemiologic evidence until 1947, when Merevether, Chief Inspector of Factories in the United Kingdom, reported 31 instances of cancer of the lung in 235 persons known by his department to have died with asbestosis between 1921* and 1946.^** That constituted an incidence of 13-2?, compared with 1.32? (91/6384) in persons certified as having had silicosis during the same period. Gloyne in 1951"^ reported on the pathologic findings in 1205'lungs from workers whose cases were being evaluated for pneumoconiosis. In 132 asbestos wqrkers, he found 121 with asbestosis, of whom 17, or 14.0/j had cancer of the lung, compared with 55 (6.9?) of 796 persons who had silicosis. The study was done, however, in a hospital to which suspected tumor patients would have been referred; thus, there may have been on overestimate of risk. Doll in 1955,^ after analyzing the enures 3 397388 of death among 105 men vhc i'.ad worked for at least 20 years in areas of asbestos textile plants defined as dusty, concluded that the 18 cases of lung cancer that occurred indicated a risk about 10 times that in the general male copulation. r,.uor . 11,13,15,13,22,21,33,3U.3MO, 59,70 ,7^-76,80-82,87,93,9^, 98, 101,112,u3u,1^9,15^,155,l6l ,169 confirmed an association between occupational exposure to asbestos and a highter-than-expected incidence of bronchogenic cancer. Some studies 13 have demonstrated differences in the degree of risk among different occupationally exposed groups, probably related to dose, as veil as to other factors. 5 IU030230 Mesothelial Tumors Primary malignant turners of the pleura and peritoneum have been regarded as exceedingly rare by most pathologists; until recent years, some even questioned their existence. There are still differences of opinion as to diagnostic criteria. 18 ' TO ' 9 8 ' 1^9 Therefore, statistics on prevalence or incidence in one geographic area cannot be safely compared with those from another. Adherence to strict diagnostic criteria, including an autopsy complete enough to rule out other primary tumors that could metastasize to or involve serosal surfaces, is a difficult constraint on a retrospective series . It was after 1?60 that serious consideration was first given to asbestos as an etiologic factor in mesothelial malignancies. In that year. Wanner et a].'L^ reported 33 cases of pleural mesothelioma in a part of South Africa import-.u'.t for croc idol ite mining. For all but two of the i at ion* .; , the uuth'..T, discover.'a likely ar.bestes contacts two dec-.cos or A 397389 more earlier. However, only if these had had occupational exposure. The remainder had lived near nines or had had household contacts. Although 66 mesothelixa had previously been attributed by some to asbestos exposures, ' ] (51 ' : r-'o no evidence cf a strong association had been developed. Additional information supporting a relationship between asbestos and malignant mesothelioma has accumulated since i960 >75 > 80,66,93,95 ,99,100,102,113-116,132,131.,136 ^ outstandIng feature has been the long period, commonly over 30 years, between the first exposure to asbestos and the appearance of a tumor, as emphasized in reports by 1S3 13U Wagner and Seiikoff et_ al. Other fiecolasia Associations between asbestos exposures and malignancies of the gastro intestinal tract and of other sites have been reported, but the data are still inconclusive 52,59,77,96,13b ST003023I Mutagenic Effects There is no evidence that asbestos is associated with mutagenesis. PATHOGENICITY IN LOWER ANIriALS A comprehensive review of information derived from experimental work in animals entails consideration not only of the variables related to the type and dimensions of the asbestos fibers and of adsorbed or concurrently administered contaminants, but also of the species and strain of animal, the route of administration, and the time and dosage factors. There are at present no satisfactory experimental models to duplicate prolonged in halation cf asbestos by man, but many isolated segments of the problems have been luciv.-'t.-d. The studies are best divided into those dealing with ss''-'.o is :..:d thcr-t: u'-alln*; with .'.eoniasi a. 5 397390 xr"ri~e.ital Ash-estosis Asbescotic pulmonary fitrcsis has been produced experimentally in various srecics of animals, including rats ^ '3 ^ '-'c guinea pigs '11 ^ hamsters,^ rabbits ar.d monkeys .^7 pn many of the studies, the disease resembled earii' asbestotic development in man--e.g., it was multi fecal. Diffuse fibrosis has also been produced,-^7 but to do so it was necessary to use very high concentrations of asbestos dust and long periods of exposure or observation after exposure. (In contrast, experi mental silicosis can be produced with lower cumulative exposure.) In the course of the investigations, it has been asked whether the fibrogenicity of asbestos dust is mostly confined to fibers longer than 5 qUestion is still unanswered. ST0030232 Experimental ifeoplasia Lung cancer from ehrysotile dust has been produced experimentally in ratc'^' and in mouse lung implants.Other investigators who used different methods for introducing the dust^^ did not find lung cancer in the animals they studied. That some asbestos dust has an increased content of trace metals--particularly nickel, chromium, and cobalt-- may explain these differing experiences. Rats whose lung clearance .had been artificially impaired had twice the lung cancer rate of animals with normal clearance! Cancer of the pleural surface (mesothelioma) has been reported in rats and hunsters that received intrapleural injections of the three most ,;i Lynns no 15Q ]60 asbestos. 'J ' The amounts of asbestos dust introduce; into `he the: cavity i. re very' large, and translation of results l v . r-. I C ur.';' {) 397391 ST0030233 1 2U The studies of Roe et_ al. ," vr.ich involved pleural and peritoneal mesotheliomas of mice after subcutaneous injections of crocidolite, er.csite, or chrysotiie, are of particular interest because they yielded evidence of migrations of fibers. Naturally Occurring Effects in Lover Animals There is no evidence that effects on domestic or wild animals are important as criteria for controlling asbestos emissions. Schuster has described pulmonary asbestosis (without the development of asbestos bodies) in a dog that lived for nearly 10 years as a ratcatcher in a London asbestos factory. Webster has demonstrated fibrosis in donkeys, baboons, and wild rodents in South Africa,and Kiviluoto has described the finding of anthophyliite asbestos in the lungs of a cow in an anthophyllite-producing area of Finland. 79 STUDIES IN VITRO There have been limited studies of the effects of asbestos in biologic systems in vitro. For example, MacNab and Harington^ demonstrated in 1967 that asbestos would hemolyse sheep erythrocytes. This has been I07 129 confirmed by others. " ' Although chrysotiie is markedly hemolytic, amosite, crocidolite, and anthophyliite have little or no activity under similar conditions. Parazzi et al.demonstrated in 1963 that both crocidolite and chryso tiie were cytotoxic for guinea pig macrophages in culture. The activity of the former was. greater; the cytotoxicity of neither was inhibited by 7 397392 pciyvinylpyridine N-oxide, a maeromolecular chemical that is effective in preventing the cytotoxic damage caused by crystalline silica in experi mental conditions. Although the foregoing types of study have no known relationship to fibrcgsr.ic or carcinogenic effects in. vivo, they provide systems that may prove 'useful in determining mechanisms of action and approaches to prophy lactic or therapeutic measures. INFLUENCE OF MAJOR VARIABLES ON PATHOGENICITY when considering the importance of type of asbestos, fiber size, and cofactors on biologic effects, it is necessary to emphasize that a given attribute may influence in differing ways the respirability, deposition, retention, clearance, translocation, and biologic reactivity. Although some in vitro and laboratory studies yield different responses to different types of asbestos, the results do not justify drawing firm conclusions as to the relative pathogenicity of the different types. Nor do epidemiologic studies conclusively support such differences. All the commercially used forms of asbestos can produce asbestosis. In only relatively few studies has the incidence of malignancies been determined in groups with exposures to a single asbestos type. Where there are data that suggest a lower risk, as in the chrysotile-producir.g areas of Canada^-3,100 and Italy, 15^ there are possible explanations for the difference ether than asbestos type. The high incidence of mesotheiial tumors in the North Western Cape area of South Africa has led to the suggestion that crocidolite is unusually har.ardo'is , but mesotheliomas have been rare in the Transvaal, where ocidolitc is also pro: 8 397393 < ( ( < < :r.anv mesotheliomas in insulation workers whose exposures had been largely to chrysotile and anosite, Sluis-Cremer-- ar.d Vebster*0c: have not found the incidence of mesothelioma hig.n in areas where acncsite was mined and milled, and McDonald1 01 did net report an excess in the chrysotile mining ar.d milling areas of Canada. ST0030235 All epidemiologic studies that appear to indicate differences in patho genicity among types of asbestos are flawed by their lack of quantitative cat a on cumulative exposures, fiber characteristics, and the presence of cofactors. Tr.e different types, therefore, cannot be graded as to relative risk with respect to either asbestosis or neoplasia. Fiber size is critically important in determining respirability, deposition, retention, and clearance from the pulmonary tract and is probably an im portant determinant of the site and nature of biologic action. Little is known about the movement of fibers within the body, including their potential for entry through the gastrointestinal tract. The aerodynamic properties of fibers depend largely on their diameter; fibers below 3.5 um in diameter are regarded as being in the respirable range .^2 Fiber length affects deposition, longer fibers apparently having greater fibrogenic effects>156 Until "recently, most work and speculation have involved only fibers detectable by the optical or light microscope (LM), approximately 0.5 mm in diameter and larger. The application of electron microscopic (EM) technique has enlarged our horizons as to the variables that must be considered. Tissues and air samples may contain many EM-sized fibrils for every LM-sized fiber time car. be demonstrated.There is, however, no tody of knowledge that permits the assigning of relative risk factors to fibers in the EM 9 397394 b IU U J U 00 range, compared vith fibers in the LM range. It is possible that the relative risks associated vith fibers cf different sizes are different for nonmalignant and malignant changes. The evidence that bundles of fibrils nay be broken down vithin the body to individual fibrils is important. A namber of investigators have postulated that a probable role of asbestos fibers in producing disease is to carry toxic or oncogenic substances to vulnerable sites . Studies bearing on this have included analysis of various types of asbestos to determine the contaminants present, vith special emphasis on metals2^2? and polycyclic hydrocarbons 61-6*4 studies of the elution of contaminants in biologic materials, and the concurrent exposure of animals to asbestos and to other materials.1^ The present consensus is that contaminants are present, but a special pathogenetic role is still speculative. The work of Selikoff et_ al.-'-35 strongly suggests a synergism of cigarette smoking and asbestos exposure in the increased risk of lung cancer in insulation vcrkers. It is not known vhether this is because of reduced clearance of asbestos, transportation of cigarette-smoke carcinogens by asbestos fibers, or the promotion by one factor of cancer initiated by another-. 10 397395 EVIDENCE OF HUMAN NCNOCCUPATIONAL EXPOSURES SIU030237 Direct and indirect evidence that persons other than those working directly with asbestos minerals are being exposed to asbestos is of several types. For example, asbestos fibers can be demonstrated in the lungs of persons not occupationally exposed. In a few geographic areas, pathologic changes regarded as representing a reaction to asbestos (e.g., pleural calcification) have been found in populations with no history of occupational exposure. Asbestos fibers have been demonstrated in ambient air. FIBERS IN LUNG TISSUE Structures that appear to be fibers coated with a pigmented material were described in lung tissue as early as 1907 by Marchand. 96 These structures To were actually fibers coated with hemosiderin. In 1929, Cooke-' described such "curious bodies" in association with pulmonary fibrosis. Stewart and Haddow^k referred to them as "asbestosis bodies." Because those who work with asbestos exhibit them a few months after starting work, it was recognized that they were evidence of exposure, but not of asbestosis. The term "asbestos body" came to be the preferred designation. As long as the coated fibers were found in persons known to have been occupationally exposed to asbestos, the identity of the central fiber was seldom questioned, although from time to time similar objects were found in persons with no known exposure to asbestos. Meurman^" in 1966 summarized 19 reports published between 1932 and 1962 in which these objects were associated with exposure to graphite, coal, hornblende, rutile, diatomaceous o`.rth, carb-.rundum, and talc (in which case tremolite asbestos might have !>. -'H inw.ri.). The demonstration by Gross that other fibers racy 11 397396 produce such todies in experimental animals indicates that they result from a r.cr.specific reaction to any sparingly soluble fibrous foreign body, as 1Q had first been suggested by Cooke in 1929.There is thus ample justifica tion for abandoning "asbestos body" as a generic term; Gough^ in 1965 suggested the term "mineral fiber-body," and Gross^3 in 1966 recommended "ferruginous body." ST0030238 Thomson et_ al. in 1963, were the first to show that these coated fibers were present in a high proportion of lungs obtained by routine autopsy. They found that 26.of lung smears in 500 consecutive autopsies ir. Cape Town showed what were called "asbestos bodies." Reports from many other areas have confirmed a high prevalence in lungs ^........................... .. , . 3,8,17,30,1*7,107,118,123,150 obtained m similar autopsy series. Utidjian e_t a_1.^3 inferred that, if a sufficient volume of lung tissue were examined in each case, nearly all persons would be found to have such bodies; their study of 100 lungs in Pittsburgh confirmed their suggestion. Identification of the core fibers has proved to be a formidable technical task. 57 ' 8b '1* 19 Without fiber-by-fiber analysis, all that can be said is that coated fibers resembling those in asbestos workers are present in most persons in our urban centers. Stripping the coating and analyzing the cores by various techniques can sometimes demonstrate that the cores are asbestos, but the process is tedious and often inconclusive. Attention is now being directed toward study, not of the ferruginous Lod i tv. 'lo!!'-', but of the total fiber content of the lungs, whether such riia'is are coated or unseated. In a study of 3,000 consecutive autopsies h!i in :.Vw vj:>: ai ty , ban per o_t al. have found thin, ur.coatcd, optically 12 397397 visible fibers in two-thirds of the 1,-19 lung specimens in which coated fibers were demonstrated and in one-fourth of those in which uncoated fibers were demonstrated. Twenty-eight consecutive samples of lung tissue from the sar.e series examined by electron microscopy were found to contain EM-sioed chrysctile fibers.^ Pooley et_ al. have reported similar findings. i>I UU30239 Evidence is therefore strong that most human lungs harbor thousands or millions of fibers. Some of these are chrysotile asbestos, and other types of asbestos minerals are probably there also. In most persons not occupationally exposed to asbestos, the numbers of fibers are relatively small, compared with the numbers found in the occupationally exposed. The systematic application of quantitative techniques, measuring both coated and uncoated fibers, is needed to define a gradient of accumulated fibers for correlation with incidence of disease, on the one hand, and history cf environmental exposure, on the other. Although there appears no doubt that asbestos fibers are present in many human lungs, there are sources of airborne fibers other than asbestos. Some are probably derived from the burning of leaves and plant products, such as paper, wood, and coal. Man-made (mostly vitreous) fibers have also been identified in the sediment isolated from human lungs. Talc, often used generously as a dusting powder, may contain a significant amount of tremolite asbestos fibers. Information is sparse concerning possible increase of fibers in lirnigs with increasing use of asbestos and concerning the existence of significant di fformless between urban and rural populations. Selikoff and Hammond133 mr-.urvd lung c incurs obtained Lr. 193^ and 1967 and found no r. Significant 13 397398 increase in the proportion containing ferruginous bodies. This suggested that, despite increasing 'use of asbestos in ifev fork City betveer. 1951* and 1967, fibers of a type producing ferruginous bodies had not beer. increasing at a corresponding rate. Hovever, Chang-Hyun Un7'J7 reports an increase ever each decade in asbestos bodies in samples of lungs from persons who died in London in 1936, 19^6, 1956, 1966. ST0030240 PLEURAL CALCIFICATION IN THE GENERAL POPULATION *) o ft Meuman* in 1968 reviewed critically the literature related to pleural calcificat ion and asbestos exposure. A number of studies strongly suggested an association between pleural calcification and nonoccupational exposures to asbestos. Kor example, Kiviluoto"f9 in i960 reported calcifications in 9# of the adult population detected during mass roentgenographic survey's in a Finnish commune ir. which there was an asbestos mine ar.d mill: the frequency was low for the remainder of the Finnish population. Raunio-"-^ enlarged on those observations in 1966, reporting that, of 633,201 chest films taker, in Finland between I960 and 1965, 1516 showed pleural calcifi cations; 1232 of the latter were among L3.L83 films taken in 10 communes in which there were anthophyllite mines. Rock and soil in. such areas iisn contain much asbestos, so that the demonstration that airborne uiUiorhy Lli to could be demonstrated over 25 km from the mines is not v sar i 1 y p-levant. Anspach^ reported that, of 2bL subjects with I'leurni c-dciflcation found in a chest roentgenographic survey in hresdon, 17Y nad either worked in or lived near an asbestos factory. Zoiov et_ described a 5 . 1? prevalence of pleural calcification in a rural pciulat.on in Bulgaria and suggested that the most likely cause was i-V.-sta.' ; 1; the soil, hovever, liromek M&rsovfi ^ and Rons and U 397399 Studeny, reporting on a high prevalence cf pleural plaques in a rural district of Czechoslovakia, have been unable to demonstrate a source of asbestos exposure. The consensus at present is that calcification alone may net invariably be considered an index of asbestos exposure in the general population, although it mey prompt a search for an environmental source of asbestos. ST0030Z4I MEASUREMENT Or AIRBORNE AS3E5T0S A more direct method of obtaining evidence on the likelihood cf exposure of the general population would be the sampling of air to determine the presence and amount of respirable asbestos fibers. There are, however, many uncertainties as to the best methods of sampling, identifying, and quantitating airborne asbestos and interpreting data so obtained. 79 ' 90 ' 122 ' 137 Lum leu lu Tu 1'IUclC 1 Oa iiciS L/cca dcriVcu. I i'Om luc 3.5 UT1H flucl'S OH SoJupling 3lt>C; such as that by Laanane.n et_ al_. who showed asbestos fallout diminishing rapidly beyond 1 km from an anthophyllite quarry, but still detectable at 27 km. Counts of asbestos fibers collected on membrane filters by high- voiur.e air sampling and estimated by light microscopic techniques similar to those used in industrial hygiene have shown small numbers of fibers in a few urban sites.Such results, although showing numbers of fibers de tectable by the light microscope that were low by occupational health ex perience, have been too few and variable to be used 'with confidence. Alternative methods that are currently under development, including estima tions of the number and mass cf fibers in the LM and the EM size ranges, have shown measurable concentrations cf asbestos in many samples of ambient ) ' 'i'J edr' ' L'J' Such environmental measurements are in their earliest stages ana provide few -.'lues to the extent or s > gni fi co of the rink from this type ..f to ctr..-r rran-T IS 397400 lC ESTIMATION OF RISK Industrial experience has shewn that prolonged inhalation of asbestos car. in crease the rich of neoplastic disease. Examination of long tissue has made it apparent that a much larger proportion of the general public has inhaled and retained asbestos fibers than had formerly been realized; in fact, most urban dwellers have some such fibers in their lungs. Can these facts be related? Does the general public--as well as persons working near occupational sources , living in the households of asbestos workers, living in the neighborhoods of asbestos plants, or having occasional random exposures--have a detectably increased risk of malignancy or other disease because of airborne asbestos? The limited information we have to unwr the=e.- n nsst.i onr. comes either from direct, epidemiologic studies of groups with various levels of nonoccupational exposure or by extrapolation from the experience of industrial populations with direct or indirect asbestos exposures. EPIDEMIOLOGIC STUDIES RELATED TO HOHPCCl NATIONAL EXPOSURES Two general indices of asbestos exposure are available for use in direct 'pidemiclogic studies of groups not known to be occupationally exposed to asbestos. The first is based on knowledge of each member's place of work and place of residence; because of the long latent periods of asbestosrelated disease, this knowledge must cover each person's whole lifetime. Thu second is a quantitative estimate of each member's lung content of 'tr.b-'-s tos fibers. There are few such direct epidemiologic studies, and t.ls-y ''.re i nab' `quote to answer the questions at issue. 16 397401 S IU U J U 4 0 The only studies that appear to implicate asbestos in the development cf malignancies in persons not occupationally exposed are those involving diffuse mesothelioma, a tumor that is uncommon and that has beer, the subject of special attention in recent years. Many of the mesotheliomas reported by Wagner e_t a-U11 in South Africa vere attributed to household and neighborhood exposures in a crocidolite-producing area. Although r.onoccupational, these exposures have been described as substantial.1 Nevhouse-1 studied 76 patients with mesothelioma diagnosed in London Hospital from 1917 to 196b. Of these 31 (1*0.8$) had occupational exposures to asbestos, 9 (11.8/5) had a relative who worked 'with asbestos, 11 (ll*.5$) had neither of those backgrounds but had lived within a half-mile of an asbestos factory, and 25 (32.9/5) had no known contacts. Corresponding percentages for a group of matched control subjects (patients in the same hospital for other diseases) were 10.5$, 1-3$, 6.6$, and 8l.6$. Stumpnius and Me ye 5 reported no mesotheliomas in the community near the shipyard in Flushing (Holland), although 17 of 21 mesotheliomas reported in the province of Iceland in if)01*-19b7 had been in workers in that yard. RaunioJ-`'u found no excess of pulmonary, pleural, or peritoneal malignancies in the areas of Finland where pleural calcifications attributed to anthophyilite were pres'ent in o%~9% of routine chest survey films. In a series of 17 1p mesotheliomas collected by Bo row et_ al_. , all but two vere in persons who had worked in an-asbestos mill, although the autopsy series from which the cases were drawn came from an area that included inhabitants of the mill's Qer environs. Lichen and Pistawka0 found that cf 1*2 persons with mesotheliomas r"pm-tod in Pennsylvania, 10 had worked in asbestos plants, 8 lived or v cies'' to an asbestos industry, and 3 were members of fardlLes ti'.'t 17 397402 S-3 oc~t.cs w'ork.c rs , --- :r.e remaining riaci 'ocf nr-' a - :; expos xre coll^o oe rt ' t- eu n random exposures. i-icLonal .x' cc.. ea.t q_,i 1. 00 lected inf "mat i on on Icq fatal malignant me sethe licnas known t< pathologists in Canada between 1959 and l?bc. They confirmed an association with occupational expos'ore to asbestos but concluded that the excess was in tr.e manufacture and industrial application cf asbestos, rather than in raining or milling. It is apparent that no quantitative conclusions were ers.-ible from these studies, which present serious methodoiogic problems to tr.e epidemiologist . They suggest a risk in household contacts and in residence in the immediate neighborhood of asbestos plants. There appear to be different levels of risk in different tepees cf occupational exposures, and scme of these may be reflected in corresponding household and neighborhood experience. C c < < ( r In no analysis cf causes of death in a large population has there been quantitative estimation of the lung content of ferruginous bodies and bare asbestos fibers, to determine whether a detectable gradient of disease can l-e correlated with asbestos content . The series so far studied have been loo small, and methods have been too variable, to permit any conclusions nr, to the importance of small numbers of fibers in the iur.g. KXTK/vT0LATIPN FROM OCCUPATIONAL EXPTPJluiCI-I Another source of evidence of the relative risks associate! with inhaling moderate or small numbers of asbestos fibers is the experience of persons wiio have had occupational exposures below those known, to be definitely r. .carious . TV: maximal airborne fiber concent rat: ons recommended for pre vail: j\\ cf ar: - si os is are much higher la-ui an y lively to Le or. counts red in 1 397403 ncncceunationai situation exano:e * o v~ m ' irrjr.s r. ae d s t ar. a a r the average concentration of airborne cnrysctiis tc 2CC0 fibers per liter 14 determined by light-field count.' anc that has been trccosed would o limit average concentrations of fibers to 5000 fibers per liter.^ Occupation-related asbestcsis can be effectively controlled with airborne fiber concentrations much higher than are likely to be encountered in ncn- occupational situations. It is important to determine whether workers whose exposures have been reduced to levels that prevent or greatly delay asbestcsis, as well as others whose exposures are indirect, have a lower risk of lung cancer than those with higher and more direct exposures. ST0030245 workers who began employment in a British textile mill after 1933, when implementation of the Asbestos Industry Regulations of 1931 reduced (but did not abolish) dust exposures , were reported in 1963 to show no excess of neoplasms. 82 The long latent periods of asbestos-related lung cancer and mesothelioma, which would probably be even longer at lower dose levels, are such that it is too soor. tc draw final conclusions as to the eventual incidence of these malignancies. Nevertheless, reduced exposure seems to ue having an effect. Another indication of reduced incidence or delayed 111 onset cf disease with lower exposure is in the observations of Ilewhouse, who found that, although there were more deaths from lung cancer and chronic respiratory disease among those who had heavy exposures many years previously in a London asbestos-products plant, this was net true ancr.g those who had 101 low or moderate exposures. McDonald et_ al_. recently reported tne mortality experience cf men who worked in ciirysctile mines and mills of ."..uebec . there was a slight ^xces.: of I'.tng cancer : uttar. r. the m57 deaths !v :v '. rn i'QG-15D0, hut all could be explained by the excess that 19 397404 recurred in those who had seen maximally exposed. This suggests that, insofar as chrysotile miners and millers are concerned, the risk drops off rapidly with decreasing accumulated dosage. ST0030246 Most series of case retorts of mesothelioma include some persons vho have worked in the construction or shipbuilding industries, but in trades not involving direct contact with asbestos. Such persons els plumbers, electricians, and metal workers often have more ferruginous bodies in their lungs than do white-collar workers Although Dunn and Weir,^ in a study of occupational groups in California that revealed an excess of deaths from lung cancer in insulation workers , found no excess lungcancer deaths in other construction trades, the groups they studied were diluted with many persons who were unlikely to have had exposures. Nevertheless, there may be a definable gradient of effect within the construction trades. More thorough studies of groups with indirect exposures are certainly needed. We cannot extrapolate from the mortality experience of those who are directly and indirectly exposed to asbestos in their employment to the general public who have had moderate or slight exposures from embient air. There is evidence to suggest a gradient of effect from direct occupational, to indirect occupational, to family and neighborhood situations, in all of which dust concentrations are probably high by comparison with most community air. This suggests that there are levels of asbestos exposure that will not be associated with any detectable risk. 'What those levels are is not known, but there is no evidence that persons in the general population--without occupational, household, or neighborhood exposures--have any increased risk of neoplasm, even though ther- may be fer-aginour todies of fibers in their 1 units. op 397405 / n z n c n o is Q Precise information is not available on tonnages , numbers cf fibers , fiber sizes and varieties, atmospheric dispersion, and 'ultimate fate of the asbestos emitted into ambient air. Although there are no reliable data to justify extrapolation from the more completely studied occupational exposure experience, information regarding actual and potential sources of emissions of asbestos fibers is of value both for directing future studies and for understanding the steps that might be taken new to safe guard the health of the public. NATURAL SOURCES OF AIR30RN5 ASBESTOS FIBERS Several varieties of asbestos ore and counterpart rock (containing EM-sized asbestos fibers) occur as outcroppings or are just below the surface of the earth throughout the world. Asbestos fibers can become airborne from these formations during road-building, construction, and tilling of the soil, as well as by landslides, erosion, and weathering. Talc, mined and used extensively in the United States, exists in fibrous, as well as platy, form. Like asbestos ore and rock, talc exists on or close to the earth's surface and is subject to disseminating forces. Such naturally occurring talc, as well as the large quantities -used as a diluent and carrier for pesticides, gg _ gY can add to the background fiber concentration in the ambient air. ' It is thought that studies of fibers in glacial and polar ice now under way will permit comparisons of recent deposition with those in the past and thereby provide definite information on the relative contributions of natural ;md industrial sources. 397406 n 7nr nn i c MINING AI.'2 `TILING CF ASBESTOS Mining and milling of asbestos provides another source of asbestos emissions. In she Ir.ited States , such activity is presently confined to a few nines in California, Vermont, Arizona, and North Carolina. Fibers are emitted during removal of overburden and preparation of the ore body for cpen-pit mining. Further release occurs during drilling and ore-breaking. Waste dumps fraa mining and milling are exposed to wind and to disturbance by bulldozing. Fibers are emitted during drying, crushing, grinding, and screening of the ore. If dust collectors and air-cleaning devices are used, disposal of the collected dust provides a potential source of fiber emission. TRANSPORTATION OF MATERIALS CONTAINING ASBESTOS Transportation of asbestos ore, milled asbestos fiber, and asbestoscontaining products and wastes is an emission source of varying importance. Movement of asbestos ore from mine to mill in open trucks contributes to the overall emission. The shipment of milled asbestos fiber, usually in bags, can result in emissions. If bags are reused, either in the asbestos industry cr elsewhere, they will become a source of fibers. Occasionally, bags are broken and asbestos is spilled during handling. Similar emissions 397407 c h ^ n c n n 1c occur during the shipment of products. Transport i.-.g asbestos-containing solid vastes in open vehicles through urban areas can be a core important emission source. MAIF/FATTUr-E hF FPCIUCTS CCtITAINIh'G AGEZSTCS Industries that must provide ventilation and other dust-oontrol measures for the protection of workers may emit asbestos fibers into the surrounding environment unless effective air cleaning is applied to effluents. Fibers removed by ventilation and filtering devices and not reintroduced into the production process and asbestos-containing waste products of the manufacturing process ultimately are disposed of outside the plant. USE OF FRODUCTS CONTAINING ASBESTOS Many products, at times unknown to the user, contain asbestos of one kind or another. There ere great variations among such products with resDect to the chances of fiber release during the use of the product. The likeli hood depends predominantly cn the ease with which the fibers can be dis lodged by the application of energy and on the degree to which the appli cation of energy actually destroys the fibers during the use of the product. Almost all the asbestos fibers used in the United States for manufacturing products becomes tightly bound within the products and undergoes little actual abrasion or wear before being discarded. Asbestos cement products (accounting for most of the asbestos used in the United States), shingles, and floor tiles are in this category. Some asbestos-containing products, sue!', as brokolir.ings, are subjected to high energy, and their rate of wear is considerable and at times almost complete. In the case of brakelinings, the application of energy is so intense and the heat created so great that 23 397408 n c 7 n e n n is mcs t SUDS -.settle fibers are destrcyed by being converted to another b = UA -q .. ,, :e , which is r.cnfibrous .~ .<evertheiess , an appreciable cercentsge (2 :X-- 3/S) remains as fibrous asbestos. In seme products -- for oxur.ole. asbestos cloth, paper, and sprayed fireproofing materials -- asoestos fibers are not tightly bound or mixed with ether material that r.cids tr.em in dace. Fiber release from these products occurs primarily during application and removal. The sprat' fireproofing of buildings with asbestos-containing materials is a case in point. This operation can be a serious source of emission, in that it usually occurs in densely populated areas. The total amount of asbestos fiber used in such procedures, how ever, is relatively small. T.aJ c is mined ar.d milled and used in greater quantities than is asbestos in tin. United States. Because it contains asbestos fibers, its uses will ado to the total number of fibers (including nonasbestos fibers) emitted. The use of talc in dispensing pesticides over wide areas of the country and its use in cosmetics are two examples of how this material may act as a source of asbestos and other fibers. DEMOLITION For years, asbestos has been incorporated in building materials.- In .vino forms of insulation and wallboard, the amount present is less than ;'C"t of the total; but other materials consist mostly or entirely of 'isb'-rtos . When a building is demolished, areas of loosened asbestos are '.per. to the ambient air and fibers are emitted. In general, single-f ami ly r*s i ic-nti nl r Structures contain only small amounts of asbestos insulation. ! `TT-.d i r. i of induct rial and commercial buildings that have been fireproofe p); 397409 vith asbestcs-ccntainir.g materials will prove :: be ar. emission scarce ir. the future, requiring centre! measures. wastes produced during manufacture cf asbestcs-cont air.ir.g product j > f such crcducts, and demolition can be emission sources. Tb.ese Vac e materials are usually disposed cf without regard to their potent! as en issicn sources. Alternate methods cf disposal often result in jgiing of asbestos-containing wastes with municipal wastes in open and thus create a long-term emission source. i 2> 397410 ST0030252 as'cestcs are industrial processing and use of products containing asbestos. It is feasible to identify the sources of emission, select these to which presently available control procedures can be applied, and point cut areas that need further study and development of new methods of control. NATURAL IURGES 0" AIRBORNE ASBESTOS FIBERS Natural sources of asbestos fibers have been identified in many areas of the United States. It is assumed that emissions of fibers from these reservoirs through'erosion and wind make up a natural background of asbestos in ambient air. Few data are available on the magnitude cf the contamination from natural sources, variation with geographic location, and seasonal variation. It is desirable to have information on the natural background, because it would assist in evaluating the effects of control measures and permit some estimates of the lower limits of con tamination that might be achieved in different areas of the country. MINING OF ASBESTOS The standard techniques for dust control in underground or open-pit mines, if not already in use, can be applied in asbestos mines. Roadways in open pits should be treated with dust-suppressive agents; truckloads of ore should be covered with, tarpaulins while being transported; handling of ere s ho'lid be minimized; ore sterng- piles sh.r.rid be mcister.ei to r 'd'.jce wind erosion ; 'vnd waste dumps -:ho"id be treated with, dust-cuprresr * ve \gv;: t . . 397411 MILLING CF Ac An in-plant dust-control program for protecting workers cn asbestos nulls includes exhaust ventilation veto effucuer.t oust-ccuceettng ar.a air-cleaning ec'i_cr.ent, isolation, enclosure, vet ms :is, and good housekeeping and maintenance . MANUFACTUF * -p ^ The elements of dust control reccrxended for the milling of asbestos ere also apply to the manufacture of asbestos-containing products. It is important that a dust-control system be specific to the operation for which it is used and that it be tested to ensure its effectiveness. Only persons especially trained and experienced in dust control should be used to develop and institute dust-control procedures. -- ^ -nAr r< r\M m a t : * " * * '* \ C -- Z" ^ '"'.'"'iC UCL Jl` ri'i'Jt'-'Wi. .J k, iAai' -- <j r-w ww An important emission source is the use of insulating materials containing asbestos. This constitutes only a small fraction of the asbestos used. But the asbestos in some insulating materials is net bound as it is in cementitious products or tiles', construction activities usually are carried on in 'urban areas where many people are exposed to contaminated air: and control of dust during construction, although feasible, is difficult. The most effective app roach in reducing exposures of the general public to asbestos from__this source involves controlling dust production and release at its origin during construction work. The generation cf dust should be reduced by cdianging material-handling methods, work practices and cleanup procedures Local aust syclems shoull be used for dust col lection '-t point ': o f generation: fer ample, due. col .'.actors for or. 397412 ST0030254 saws are available, and hand-severed reels rumpire a wrtr. exr.a'rst systems are being made. Mucr.- develcsnental wcrx is needed to produce rentable air-ucvir.g and air-c leaning systems for use in vmsls, crawl spaces, and caber confined seaces. This subject has beer, neglected by industrial, hygienists and ventilation engineers, and no satisfactory equipment is available. DEMOLITION AND VAEEE DISPOSAL Demolition and waste disposal are likely to be emission sources if aooreciable amounts of asbestos are used in construction, -unless operational procedures are strictly controlled. Isolation, enclosure, and wetting down are useful. Caution must be observed net to demolish during high winds and to keep sludge from drying out and becoming airborne later through natural forces and from being introduced into sources of drinking water. MEASURE!SLIT OF AIRBORNE AEEEET05 .An imrortar.t consideration in the development of a strategy for control is whether there are methods for measuring airborne concentrations of asbestos that are sufficiently sensitive, specific, and reproducible. Present methods of sampling, identifying, and measuring airborne asbestos are net entirely satisfactory, especially if one is dealing with low concentrati" and unidentified or mixed sources. Only within recent years .'save methods ('or determining concentrations of fibers for industrial hygiene purposes been Stand-indited; 1` U "3^ they 'use samples collected or. .Memorar.e filters in which filers are counted with phase-contrast illuminrtion. Electron microscopic met hr Is give r. much more ccmvlote indication ; f the total fiber cent art 397413 cf the air; but vhen the .tees for fiser t tert.fi cation is included, they are tedicus and expensive for routine use . - 1 --te relative tiOxOjtc significance of different sites ef fitu-rs is net xr.cvn , r.cr is tr.o relative 3.3. 3 3. or er ea c c v> .-i . a o e r.o published :ers sues sr;i:e of the di ' r ? I O s , it as oc: t- u o a., u . , l ^ x i: c approximate concentration cf airborne fibers, and identify the major types cf asbestos. It is not desirable to limit environmental measurements to a single method until there is a clearer definition of the critical variables in terms of hhee;alth. Because cf methodologic and other un- certainties, it is net yet feasible to base control cn numerical ambient air quality standards. S 5 7 n rn n ic ,i 397414 9 Q ? n rn n ic two rece ire: cLi s cuss some d= tail tie mar.v k ^scsr^r 213i 1 to a tress ins cue steers ::: e ots c f asbestos or. health a ;e ani o:^ >* co me s. It at along tr.e fo,,cw: she u^L d :e i:iven high priority. Study cf the mechanism cf action of the asbestos minerals should continue , with particular attention to carcinogenic effects. It is important to iearr. .tore about the influence of asbestos type and fiber sice on respirabidity, deposition, retention, translocation, and effects at the tissue, cellular, and molecular levels, with and without cofactors. It is especially important that the role of fibers below the LM range be clarified. Methods of sampling, identifying, and quantitating airborne asbestos need continued development . Coordination with studies in animals and man is essential to ensure that environmental data will be biologically relevant. Similarly, methods for identifying and quantitating asbestos in biologic tissue need development and application. Quantitative methods for measuring airborne asbest os should be applied widely to determine the natural background and the concentration and distribution of fibers in the air near various sou.roes. Conventional LM methe.is and EM methods should be applied simult anecusly in selected occupational ;un 1 community situations. 30 397415 / C7 fir n n i c Mere ecidemioiogic studies are needed. Populations in several different exposure ranges should be studied, including occupational, household, and neighborhood exposures. Special studies cf mesothelioma are needed to determine whether the incidence has been increasing and to determine the current pattern of distrib'ution. A large series of routine autopsies should be studied to determine whether causes of death can be related to amounts of asbestos in the lungs and other organs. All the above are urgent if a range of safe exposure is to be established with confidence. 397416 QCPnonn i Any cf the commercially used asbestos minerals , when inhaled in sufficient numbers, as in uncontrolled occupational exposures, can cause disabling fibrosis of the lungs. An association between occupational exposures to asbestos and bronchogenic carcinoma has been established, but the dose relationship and the role of cofactors have net been defined. Evidence of a causa! association between some but not all exposures to asbestos fibers and duff'use malignant mesotheliomas cf the pleura and peritoneum is substantial, but evidence of such a relationship with other tumors is inconclusive. Although the different types cf asbestos differ in some of their biologic effects, no type can be regarded as free of hazard. The hypothesis that asbestos fibers act as cofactcrs or carriers of carcinogens is attractive, but as yet unproved. tv/1 IE.'.' CE OF HU MAT? hCNCCCbPATlOUAl ZXPCu'TFES TO A5EESTCS The demonstration cf ferruginous todies, similar to those found in asbestos workers, in a large proportion of randomly selected lung specimens in many parts of the world is presumptive evidence that persons with no occupational contact may have inhaled and retained asbestos. Proof has come in seme areas with positive identification cf chrys-utile asbestos fibers. Analyses of community air for asbestos have beep, too limited to define the sources, concentrations, and distribution of fibers :n the environment . The fiber concentration:; that have been durcnui. rated i r. .ambient air arc sm.ili, compared with those ir: industry, b r '`a or - ".'i'.!:. yu.'ic f " " f i n i. L ! ' e mi. 397417 6S3QC00J S The .~ost importsr.- ques::cn os. me cam c: persons w::n r.enoccupaticnel exposures to asbestos is whether there is an increased risk, cf malignancies. In ius t ri a_ e:rserieace indicates tr.-at there is no lineiir.scd of significant asbestmis in asr.occupational expos'ures. The major potential for risk arrears to lie in those vith indirect occupational contacts, household contacts, cr residence in the immediate neighborhood of asbestos sources ; and even there, the actual risk is poorly defined. But the fact that there appears to be a gradient of effect in such groups suggests that there are levels of inhaled asbestos without detectable risk. It is net known what range of respirable airborne asbestos fibers will ultimately be found to have no measurable effects on health. At present, there is no evidence that the small numbers of fibers found in most members of the general population affect health or longevity. NEED FOR AND FEASIBILITY CF CONTROLS Asbestos is too important in our technology and economy for its essential use to be stopped. But, because of the known serious effects of uncon trolled inhalation of asbestos minerals in industry and 'uncertainty as to the shape and character of the dose-respense curve in man, it would be highly imprudent to permit 'unrestricted additional contamination of the public environment with asbestos. Continued use at minimal risk to the public requires that the major sources of man-made asbestos emission into the atmosphere be defined and controlled. In the absence of such controls, local fiber concentrations might at times approach these in occupational sites. Ar.aiyci c methods mu epidemiologic data are inadequate for toe do V'-lemon t of amt ten: air n t;ir. cards , but emission controls ire 397418 iIU U O U d O U American Conference of Governmental Industrial Hygienists. Threshold Limit Values cf Airborne Contaminants and Intended Changes Accepted by ACGIH for 1970. Cincinnati: American Conference of Governmental Industrial Hygienists, 1970. 27 pp. 3. Ar.jilvel, L., and V.'. M. Thurlbeck. The incidence cf asbesfts bodies in the lungs at rar.dc." necropsies in Montreal. Car.ad. Med. Ass. J. 95:1179-1132, 1966. ). ' aI, \jf W.., .4. Q 1 ^ <( W-.44W4 * - ~ -- - -- * *-- ----- .--.4^3^44 ^ V-, /* --^ *w"> ti -I e-t ------- tf 4.-4. i na N 'r m. m *" ^ t. 'P W 4. . 4 W . ,, W X. W W W w , Int. Arch. Gewerbepath. u. Gewerbehyg. 19:108-120, 1962. 5. Antcn, K. C. Multiple ple-ural plaques. 3rit. J. Radiol. 10:635-690, 196-7 . n. Anton, H. C. jMultiple pleural plaques: Part II. Brit. J. Radiol. 11:311-313, 1969. 7. Asbestos Industry Regulations, 1931. Statutory Rules and Criers, 1931, No. lllO. London: H. M. Stationery Office, 3931. 1 pp. P. Ashcroft, T. Asbestos bodies in routine nocropsi.es on Tyn-'-sido: a pathological and social study. Brit. Med. J. l:6ll-6la, 193 3. 397419 y 2 -- \'CV J. , -- - r 0 ^ . J. L., '. C. Coccer, and 1. F. Fcvler. Fibrc-us line; air trsr.s.;icr. systems: an assessment o:' their envirernre.rtai effects. Arch iron. Heaith (in cress) . G. M. , J. G. Faulis, and M. J. Stevart. Occupational cancer the urinary bladder in dyestuffs operatives and of the lung in estos textile vcrxers and ircn-ere miners. Aner. J. Clin. Path. 126-lii, 1955 . M. , A. Constcr. , L. L. Livomese , and . S chalet. Mesothelioma its asscciaticn with asbestosis. J.A.M.A. 201:587-591, 1967. . 0. C., and T. D. Truan. An epidemiological study of lung cancer asbestos miners. A.M.A. Arch. Industr. Health 17:63^-653, 1958. u Occupatianal Hygiene Society. Hygiene standards for chrysotile sstos d'ust . Ann. Occup. Hyg. 11:^7-69, 1968. .an, W. D. Asbestosis and primary intrathoracic neoplasms. . ,'i . V. Acad. Cei . 132:507-513, 1965- . J. C. , A. A. hodmen, and S. Holmes. A dust survey carried cut : millings : .rrr.wrutinc acbestcs-c.n.c-d rr.at-ri ;1 in their cor.- uran -1 --; r~' -3.c" tenstics d uO asbestosis . asbestos -5, 1927. l. Ke al th C < < < < I < isbestos international 'l. OO ~ rr d carcinoma . Research 96b. S IU U J U 4 D ns. L. iz autcpsy. J.A.M.A. = 0^ CS luzan lungs 'S f*r : resot.ra-icr.a ri5:oc:i:?c vat.n as52 :c,1u-g22 , 1565. Lstclcgical characteristics . Ann. j. .. Acad, Eci . 19. Cache, V. E. Asbestos dust ar.d the curious bodies found in asbestosis. Brit. `fed. J. 2:578-560, i?29. 20. Cache, . E. Fibrosis of the lur.gs due to the inhalation of asbestos dust. Brit. Med. J. 2:1^7, 152 k. 21. Cocke, W. E. Puir.onary asbestosis. Brit. Med. J. 2:102^-1025, 1927. 22. Coorer. W. C. Asbestos as a hazard to health. .Arch. Environ. Health 15:265-200, 1967. 23- Cooper, W. C., ar.d J. L. Baiter. Evaluation and control of asbestos exposures in the insulating trade. Presented at the 2nd International Conference on Biological Effects of A.sbestos, Dresden, April 22-25, 1963. Ccrdova, J. F., H. Tesluk, of the lung. Cancer 15: r'r.ud: son. Asbestosis and carcinc.ru. T, ,T cn hot:*:: feet:: of at: t, ~nd M. C. Ercvn. research . Ml. 10 : 33-hI , ICfS I*. 397420 Craiiey, 1. J., P . 3. Keenan, .3. '. E-pel, E . I. ilir.ser, and J. R. lyn Character!cation and sclub illtv of ret ala associated with asbestos fibers. Arer. Industr. Kys. ,^s. J. 29:3'L9-,73, 1963. r.xtcsure to neta^s m Ass. J. 23:152-161, 196?. 23. Cralley, L. J., R. G. Keenan, J. R. Lynch, and V. S. Lainhart. Source and identification of respirable fibers. Amer. Industr. Hyg. Ass. J. 29:129-135, 1968. 29- Davis, J. M. G. Electron-microscope studies of asbestosis in man and animals. . Ann. N. Y. Acad. Sci. 132:98-111, 1965. 30. Diche, T. 2., and B. Naylor. Prevalence of ''asbestos" bodies in humor. lungs at necropsy. Dis. Chest 56:122-125, 1969. 31. Doll, ?.. Mortality from lung cancer in asbestos workers. 3rit. J. Industr. Med. 12:31-36, 1955- 32. Dreessen , W. C., J. M. Dadlavalle, T. I. Edwards, J. W. Miller, and R. R. Sayers. A Study of Asbestos Lr. the Asbestos Textile Industry. (Public Health Bulletin No. 2ll) Washington: fJ. S. Government Printing Office, 1938. 126 pp. 33. Dunn, J. E., Jr., and J. M. V/eir. A prospective stub,.' of mortality of several occupational groups. Special emphasis on. lung cancer. Arc).. Environ. !'ealth 17 ; rl -- T'o , iyGS. 397421 * id J. X. <:_ir ^3 55 19c: several * iq ? n rn n i q 3c. Elmes , P. C., W. T. E. McCaughey, and C. L. Wade. Diffuse mesothelioma of the pleura and asbestos. Brit. Med. J. 1:350-253, 1965- 37- Elmes, P. C., and 0. L. Wade. Pe laticr.ship betveen exposure to asbestos and pleural maiigr.ar.cy in Belfast. Ann. N. Y. Acad. Sci. 132:5^9-557, 1965. 35. Elwocd, ?. C., and A. L. Cochrane, A fcllov-up study of workers from an asbestos factor;,'. Brit. J. Ir.dustr. Med. 21:301-307, 1961. 33. Enterline, ?. E. Mortality among asbestos products workers in the 'United States. .Ann. '1. Y. Acad. Sci. 132:156-165, 1965. l0. Enterline, P. E., and M. A. Kendrick. Asbestos-dust exposures at -various levels and mortality. Arch. Environ. Health I5:l2l-l86, 1967. Enticknap, J. B-.-, and W. J. Smither. Peri tcaeai tumours in asbestos: Brit. '. Indus tr. lied. Fowler, P. P. 3., J. 7. SD.r.er, and Z. 7. Warner. Etc t enure or!'! v y "> *1 he 1 i' .r.s. of t'.c : Ivorr.. 5r;.y., 'yd. J. 2 * 2d ] -- 0.0 _> .Cb 397422 D I U U O U C .U J calcif csticr. a 195c. Gardner, 1. "J. Chrysctile ccs as an indicate of scbcile differences in animal tissues. Aner. Rev. Tubers. -5;~c2-766, 19*1. **5. Gardner, L. :J. , and D. I. Cunnings . Studies on experimental pneumo coniosis . VI. Inhalation of asbestos dust: its effect upon primary tuberculous infection. J. Ir.dustr. Kyg. 13:65-81, 97-11*+, 1931. 46. Gaze, R. The physical and molecular structure of asbestos. Ann. N. Y. 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