Document QRkmgqoY09pJ4Dk6yvV6LGo7

ji yc effects of Atmospheric 'Pollutants TB-- r Hi i^ WMI JMBMWL ||H H H || HM HW f --I llik Biologic Effects o f Atmospheric Pollutants THE NEED FOR AND FEASIBILITY OF AIR POLLUTION CONTROLS Committee on Biologic Effects o f Atmospheric Pollutants DIVISION OF MEDICAL SCIENCES NATIONAL RESEARCH COUNCIL NATIONAL ACADEMY OF SCIENCES WASHINGTON, D.C. T971 NOTICE: The study reported herein was undertaken under the aegis of the National Research Council with the express approval of the Governing Board of the NRC. Such approval indicated that the Board considered that the problem is of national significance, that elucidation of the problem required scientific or technical competence, and that the resources of NRC were particularly suitable to the conduct of the project. The institutional responsibilities of NRC were then discharged in the following manner: The members of the study committee were selected for their individual scholarly com petence and judgment with due consideration for the balance and breadth of disciplines. Responsibility for all aspects of this report rests with the study committee, to whom sincere appreciation is expressed. Although the reports of our study committees are not submitted for approval to the Academy membership nor to the Council, each report is reviewed by a second group of scientists according to procedures established and monitored by the Academy's Report Review Committee. Such reviews are intended to determine, inter alia, whether the major questions and relevant points of view have been addressed and whether the reported find ings, conclusions and recommendations arose from the available data and information. Distribution of the report is permitted only after satisfactory completion of this review process. O The work on which this publication is based was performed pursuant to Contract No. CPA 70-42 with the Environmental Protection Agency. ISBN 0-309-01927-3 Available from Printing and Publishing Office National Academy of Sciences 2101 Constitution Avenue, N.W. Washington, D.C. 20418 First printing, October 1971 Second printing, December 1971 Library of Congress Catalog Card Number 78-172926 Printed in the United States of America PANEL ON ASBESTOS W. C L A R K C O O P E R , School o f Public Health, University o f California, Berkeley, Chairman LEWI S J. CR A L L E Y , Bureau o f Occupational Health and Safety, Division o f Epidemiology and Special Services, U. S. Public Health Service, Cincinnati, Ohio B E N J A M I N G. F E R R I S , J R . , Department o f Physiology, Harvard School o f Public Health, Boston, Massachusetts P A U L g r o s s , Industrial Hygiene Foundation, Inc., Pittsburgh Pennsylvania D U N C A N A. H O L A D A Y , Occupational Health Field Station, Salt Lake City, Utah I R V I N G J. S E L I K O F F , Environmental Sciences Laboratory, Mount Sinai Hospital, New York, New York G E O R G E w. W R I G H T , Medical Research Department, St. Luke's Hospital, Cleveland, Ohio S A M U E L P. H IC K S, Department o f Pathology, University of Michigan Medical Center, Ann Arbor, Associate Editor T. D . B O A Z , J R . , Division o f Medical Sciences, National Research Council, Washington, D.C., Staff Officer COMMITTEE ON BIOLOGIC EFFECTS OF ATMOSPHERIC POLLUTANTS A R T H U R B. D U B O I S , Department o f Physiology, School of Medicine, University o f Pennsylvania, Philadelphia, Chairman V I N T O N W. B A C O N , College o f Applied Science and Engineering, University of Wisconsin, Milwaukee A N N A M. B A E T J E R , Department o f Environmental Medicine, School o f Hygiene and Public Health, The Johns Hopkins University, Baltimore, Maryland W. C L A R K C O O P E R , School o f Public Health, University o f California, Berkeley hi IV ASBESTOS M O R T O N C O R N , Graduate School o f Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania B E R T R A M D . D I N M A N , School o f Public Health, University o f Michigan, Ann Arbor LEON GO LB E R G , Institute o f Experimental Pathology and Toxi cology, Albany Medical College, Albany, New York P AU L B. H A M M O N D , Department o f Physiology and Pharmacology, College o f Veterinary Medicine, University o f Minnesota, St. Paul S A M U E L P. H I C K S , Department o f Pathology, University o f Michigan Medical Center, Ann Arbor v i c t o r G. L A T I E S , Department o f Radiation Biology and Bio physics, University o f Rochester Medical Center, Rochester, New York A B R A H A M M. L I L I E N F E L D , Department o f Chronic Diseases, School o f Hygiene and Public Health, The Johns Hopkins University, Baltimore, Maryland P AU L M E I E R , Biomedical Computation Facilities, University of Chicago, Chicago, Illinois J A M E S N. P IT T S , J R. , Department o f Chemistry, University o f California, Riverside G O R D O N J. S T O P P S , Haskell Laboratory, E. I. du Pont de Nemours and Company, Newark, Delaware O. C L I F T O N T A Y L O R , Department o f Horticulture, University of California, Riverside J A R O S L A V J. V O S T A L , Department o f Pharmacology and Toxi cology, University o f Rochester Medical Center, Rochester, New York T. D. BOAZ, JR., Division o f Medical Sciences, National Research Council, Washington, D. C., Executive Director Preface This document was developed at the request of the National Air _ Pollution Control Administration, which became the Air Pollution Control Office upon the formation o f the Environmental Protection Agency in December 1970. The request was for a report that would set forth in a well-organized fashion the currently available informa tion on asbestos as an air pollutant, with special attention to sources, health effects, measurements, and feasibility of control. It is not a state-of-the-art document and, therefore, does not attempt to cover fully all that is now known about asbestos. The report is the result of the dedicated efforts o f the Panel on Asbestos, chaired by Dr. W. Clark Cooper and formed under the aegis o f the parent Committee on Biologic Effects o f Atmospheric Pollut ants, Division o f Medical Sciences, National Research Council. The Members o f the Panel on Asbestos are to be commended for having produced a report that, although brief, covers the salient points on which the sponsor requested sound scientific opinion. Each item dis cussed in the report is adequately documented in the bibliography. Much credit for the clarity o f expression in this report must be given to the Editor o f the Division o f Medical Sciences, Mr. Norman Grossblatt. v VI ASBESTOS This report (1) summarizes the evidence regarding the pathoge nicity o f asbestos in man and animals, (2) summarizes the evidence o f human nonoccupational exposure to asbestos, (3) evaluates the evidence regarding a health risk associated with various degrees and types o f exposure, (4) identifies sources o f environmental contami nation by asbestos, and (5) offers recommendations concerning the need for and feasibility o f control measures. Charles L. Dunham Chairman , Division o f Medical Sciences Contents 1 Introduction 2 Pathogenicity of Asbestos 3 Evidence of Human Nonoccupational Exposures to Asbestos 4 Estimation of Risk in Nonoccupational Exposures to Asbestos 5 Sources of Asbestos Fibers in Ambient Air 6 Principles of Control 7 Research Needs 8 Conclusions and Recommendations References vu 1 Introduction The naturally occurring fibrous silicates classified as "asbestos" have become almost indispensable in modern technology.67,124,141 The world's annual production has grown from a few thousand tons in 1900 to over 3 million tons in 1968.120 Annual consumption in the United States averaged nearly 800,000 tons during the period 1965 1969.120 The potential of asbestos as a hazard to health has been the subject o f a number o f reviews in recent years.22,49,60,133,136,145,147,168 Although it has been known for a half-century that persons who inhaled large amounts of asbestos dust in the course o f 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 asbes tos 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.46 Although there are many asbestos minerals, only six ar of commercial importance: Chrysotile, a tubular serpentine mineral, accounts for 95% o f the world's production; the others, 2 ASBESTOS all amphiboles, are amosite, crocidolite, anthophyllite, tremolile, and actinolite. The asbestos minerals differ in their metallic elemental content, range of fiber diameters, flexibility or harshness, tensile strength, surface properties, and other attributes that determine their industrial uses and may affect their respirability, deposition, retention, translocation, and biologic reactivity. 2 Pathogenicity of 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, or use. Contaminants acquired from the atmosphere or in the respiratory tract may be carried on the surface of fibers. Fibers may act as cofactors; con versely, their action may be modified by other cofactors. PATHOGENICITY IN MAN The proven or suspected effects of asbestos minerals on human health include nonmalignant changes, such as pulmonary and pleural fibrosis, and several types of malignancy, notably of the lung, pleura, and peritoneum. Nearly all 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 pro ducts (such as textiles and construction materials), and the application and removal of asbestos-containing insulating materials. 3 4 ASBESTOS Asbestosis Asbestosis, or asbestotic pneumoconiosis, was the first dearly demon strated adverse effect of asbestos in man. It is characterized by a pat tern of roentgenographic changes in the lung consistent with diffuse interstitial fibrosis of variable degree and at times with fibrosis and calcification of the pleura; clinical changes that include fine rales, fin ger clubbing, and shortness of hreath, each of which may be absent in an individual case; and physiologic changes consistent.with.a restric tive lung disorder. The first published mention of 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 1907.110 Cooke reported a second case in V192420 and in 1927 provided a more detailed description,21 in which the term "asbestosis" was first used. In 1930, Merewether104 reviewed the salient features of the disease and the environmental exposures of workers, including data derived from an epidemiologic study reported In more detail by Merewether and Price.105 This led to the promulga tion of regulations for environmental and medical control in the Unit ed Kingdom, which became effective in 1932.7 Cases were first reported in the United States in 1930,109,140 and guidelines for accept able dust concentrations were proposed by Dreessen et al. in 1938.32 ^Industrial experience indicates that pulmonary fibrosis sufficient to interfere with respiratory or cardiovascular function can be pre vented 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.s'6,43'1Q2,l07'l29 When multiple or bilateral, they are re garded by some as almost diagnostic of asbestos-related disease.43'71 In asbestos workers, calcified plaques rarely appear until 20 years after first exposure and do not necessarily correlate with parenchymal fibrosis.90 Calcification appears to differ in frequency in different occupationally exposed groups, but studies are inadequate to verify or explain such differences. 5 Bronchogenic Carcinoma No features of bronchogenic carcinoma associated with asbestos are pathognomonic. Primary sites are more often in the lower lobes, in contrast with the usually higher frequency of upper lobe tumors. Peripheral primary sites are common in asbestos-related lung cancer. All cell 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,90 who described squamous cell 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 Merewether, Chief Inspector of Factories in the United Kingdom, re ported 31 instances of cancer o f the lung in 235 persons known by his department to have died with asbestosis between 1924 and 1946.103 This constituted an incidence of 13.2%, compared with 1.32% (91/6,884) in persons certified as having had silicosis during the same period. Gloyne in 195150 reported on the pathologic find ings in 1,205 lungs from workers whose cases were being evaluated for pneumoconiosis. In 132 asbestos workers, he found 121 with asbestosis, 17 of whom, or 14.0%, 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 an overestimate of risk. Doll in 1955,31 after analyzing the causes o f death among 105 men who had worked for at least 20 years in areas of asbestos textile plants de fined as dusty, concluded that the 18 cases of lung cancer that oc curred indicated a risk about 10 times that in the general male population. Other studies'1'13'15'18'23,24'33'34'38"40,S9'70'73"75'79'S1'86'92'93'97'100' 111,130,148,154,155,161,169 kave co n fu te d an association between occu pational exposure to asbestos and a higher-than-expected incidence of bronchogenic cancer. Some studies13 have demonstrated differ ences in the degree of risk among different occupationally exposed groups, probably related to dose, as well as to other factors. Msothlial Tumors Primary malignant tumors 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 6 ASBESTOS opinion as to diagnostic criteria.18'70'97'148 Therefore, statistics on prev alence or incidence in one geographic area cannot be safely compared with those from another. Adherence to strict diagnostic criteria, in cluding 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 1960 that serious consideration was first given to asbestos as an etiologic factor in mesothelial malignancies. In that year, Wagner et al. 161 reported 33 cases of pleural mesothelioma in a part of South Africa important for crocidolite mining. For all but two of the patients, the authors discovered likely asbestos contacts two decades or more earlier. However, only 17 of these had had oc cupational exposure. The remainder had lived near mines or had had household contacts. Although mesothelioma had previously been attributed by some to asbestos exposures, 85>lft4,i65,i6?> no evidence of a strong association had been developed. Additional information supporting a relationship between asbestos and malignant mesothelioma has accumulated since i 960.9'12'36'37'41' 42,5,74,79,87,92,94,98,99,101,112-115,131,133,135 A n o u t s t a n d i n g f e a t u r e h a S been the long period, commonly over 30 years, between the first ex posure to asbestos and the appearance of a tumor, as emphasized in reports by Wagner158and Selikoff and Hammond.133 Other Neoplasia Associations between asbestos exposures and malignancies o f the gastrointestinal tract and of other sites have been reported, but the data are still inconclusive.52' 59'76'93'133 Mutagenic Effects Evidence of a mutagenic effect of asbestos has not been reported. PATHOGENICITY IN LOWER ANIMALS A comprehensive review of information derived from experimental work in animals entails consideration not only of the variables re lated to the type and dimensions of the asbestos fibers and of ad sorbed or concurrently administered contaminants, but also of the species and strain of animals, the route of administration, and the Pathogenicity o f Asbestos 7 time and dosage factors. There are at present no satisfactory ex perimental models to duplicate prolonged inhalation of asbestos by man, but many isolated segments of the problems have been eluci dated. The studies are best divided into those dealing with asbestosis and those dealing with neoplasia. Experimental Asbestosis Asbestotic pulmonary fibrosis has been produced experimentally in various species of animals, including rats,45'58'156'157 guinea pigs,29'45'69'157 hamsters,55 rabbits,157 and monkeys.157 In many of the studies, the disease resembled early asbestotic development in man, e.g., it was multifocal. Diffuse fibrosis has also been produced,157 but to do so it was necessary to use very high concentrations of asbestos dust and long periods of exposure or observation after ex posure. (In contrast, experimental 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 pm;45'156 the question remains un answered. Experimental Neoplasia Lung cancer from chrysotile dust has been produced experimentally in rats58 and in mouse lung implants.139 Other investigators who used different methods for introducing the dust142 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.58 Cancer of the pleural surface (mesothelioma) has been reported in rats and hamsters that received intrapleural injections of the three most common types of asbestos.138'159'160 The amounts of asbestos dust introduced into the thoracic cavity were very large, and trans lation of results to human inhalation of asbestos is uncertain." The studies of Roe et a/.,123 which involved pleural and peritoneal mesotheliomas of mice after subcutaneous injections of crocidplite, amosite, or chrysotile, are of particular interest because they yielded evidence of migration of fibers. 8 ASBESTOS Naturally Occurring Effects in Lower 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 o f asbestos bodies) in a dog that lived for nearly 10 years as a ratcatcher in a London asbestos factory.127 Webster has demonstrated fibrosis in donkeys, baboons, and wild rodents in South Africa,163 and Kiviluoto has described the finding of anthophyllite asbestos in the lungs of a cow in an anthophyllite-producing area of Finland.78 STUDIES IN VITRO There have been limited studies of the effects of asbestos in biologic systems in vitro. For example, MacNab and Harington91 demonstrated in 1967 that asbestos would hemolyze sheep erythrocytes. This has been confirmed by others.126'128 Chrysotile differs from amosite, crocidolite, and anthophyllite in the conditions under which it is hemolytic. Parazzi et al.116 demonstrated in 1968 that both crocidolite and chrysotile were cytotoxic for guinea pig macrophages in culture. The activity of the former was greater; the cytotoxicity of neither was in hibited by polyvinylpyridine N-oxide, a macromolecular chemical that is effective in preventing the cytotoxic damage caused by crystal line silica in experimental conditions. Although the foregoing types of study have no known relation to fibrogenic or carcinogenic effects in vivo, they provide systems that may prove useful in determining mechanisms of action and approaches to prophylactic or therapeutic measures. INFLUENCE OF MAJOR VARIABLES ON PATHOGENICITY When considering the influence of type of asbestos, fiber size, and cofactors on biologic effects, it is necessary to emphasize that a given attribute may influence respirability, deposition, retention, clearance, translocation, and biologic reactivity in differing ways. 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 Pathogenicity of Asbestos 9 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-producing areas of Canada13'99 and Italy,154 there are possible explanations for the difference other than as bestos type. The high incidence of mesothelial tumors in the North Western Cape area of South Africa has led to the suggestion that crocidolite is unusually hazardous, but mesotheliomas have been rare in the Transvaal, where crocidolite is also produced.49'137 Al though Selikoff et al. 131 found many mesotheliomas in insulation workers whose exposures had been largely to chrysotile and amosite, Sluis-Cremer137 and Webster162 have not found the incidence of mesothelioma high in areas where amosite was mined and milled, and McDonald et al. 100 did not report an excess in the chrysotilemining and -milling areas of Canada. All epidemiologic studies that appear to indicate differences in pathogenicity among types of asbestos are flawed by their lack of quantitative data on cumulative exposures, fiber characteristics, and the presence of cofactors. The 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, de position, retention, and clearance from the-pulmonary tract and; is probably an important determinant of the site and nature of bio logic action. Little is known about the movement of fibers within the human body, including their potential for entry through the gastrointestinal tract. The aerodynamic properties of fibers depend largely on their diameter; fibers below 3.5 fim in diameter are re garded as being in the respirable range.151 Fiber length affects de position, longer fibers apparently having greater fibrogenic effects.44 156 Until recently, most work and speculation have involved only fibers detectable by the optical or light microscope (LM), approxi mately 0.5jam diameter and larger. The application of electron microscopic (EM) techniques133 has enlarged ourdiorizons as to the variables that must be considered. Tissues and air samples may contain many EM-sized fibrils for every LM-sized fiber that can be demonstrated.83'133 There is, however, no body of knowledge that permits the assigning of relative risk factors to fibers in the EM range, compared with fibers in the LM range. It is possible that the relative risks associated with fibers of different sizes are different 10 ASBESTOS for nonmalignant and malignant changes. The evidence that bundles of fibrils may be broken down within the body to individual fibrils is important.146 A number 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, with special emphasis on metals26'27 and polycyclic hydrocarbons;45'61' 64 studies of the elution of contaminants in biologic materials;26 and the concurrent exposure of animals to asbestos and to other materials.108 The present consensus is that contaminants are present, but a special pathogenetic role is still speculative. The work of Selikoff et al. 134 strongly suggests a synergism of cigarette smoking and asbestos exposure in the increased risk of lung cancer in insulation workers. It is not known whether 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. 3 Evidence of Human Nonoccupational Exposures to Asbestos Direct and indirect evidence that persons other than those work ing directly with asbestos minerals are being exposed to asbestos is of several types. For example, asbestos fibers can be demon strated in the lungs of persons not occupationally exposed. In a few geographic areas, pathologic changes regarded as represent ing 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 ma terial were described in lung tissue as early as 1907 by Marchand.95 In 1929, Cooke19 described such "curious bodies" in association with pulmonary fibrosis. Stewart and Haddow143 referred to them as "asbestosis bodies." Because those who work with asbestos ex hibit them a few months after starting work, it was recognized that they were evidence of exposure, but not o f asbestosis. The term "asbestos body" came to be the preferred designation. 11 1 2 ASBESTOS 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. Mcurman106 in 1966 summarized 19 reports published between 1932 and 1962 in which these objects were associated with ex posure to graphite, coal, hornblende, rutile, diatomaceous earth, carborundum, and talc (in which case tremolite asbestos might have been involved). The demonstration by Gross and co-workerss4'56 that other fibers may produce such bodies in experimental animals .indicates that they result from a nonspecific reaction to any sparingly soluble fibrous foreign body, as had first been suggested by Cooke in 1929.19 There is thus ample justification for abandoning "asbestos body" as a generic term; in 1965, Gough51 suggested the term "mineral-fiber-body," and, in 1966, Gross53 recommended "fer ruginous body." Thomson et al.,,5 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 26.4% of lung smears in 500 consecutive autopsies in Cape Town showed what were called "asbestos bodies." Reports from many other areas have confirmed a high prevalence in lungs obtained in similar autopsy series.3'8'17'30' 4 7 ,io 6 , in,m.149 utidjian et al.153 inferred that, if a sufficient volume o f lung tissue were examined in each case, nearly all persons would be found to have such bodies; their study of 100 lungs in Pittsburgh con firmed their suggestion. Identification of the core fibers has proved to be a formidable technical task.57'83'118 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 urban centers. Stripping the coating and analyzing the cores by various techniques can sometimes demon strate that the cores are asbestos, but the process is tedious and often inconclusive. Attention is now being directed toward study, not of the ferrugi nous bodies alone, but o f the total fiber content of the lungs, whether such fibers are coated or uncoated. In a study of 3,000 consecutive autopsies in New York City, Langer et al.S3 have found thin, un coated, optically visible fibers in two thirds of the 1,449 lung speci mens in which coated fibers were demonstrated and in one fourth of those in which coated fibers were not demonstrated. Twenty-eight consecutive samples of lung tissue from the same series examined Evidence o f Human Nonoccupational Exposures to Asbestos 13 by electron microscopy were found to contain EM-sized chrysotile fibers.84 Pooley et al.lis have reported similar findings. Evidence is therefore strong that most human lungs harbor thou sands 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.132 The systematic application of quantita tive techniques, measuring both coated and uncoated fibers, is needed to define a gradient of accumulated fibers for correlation with inci dence of disease, on the one '-f l, and history of 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.28'57 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 lungs with increasing use of asbestos and concerning the existence of signif icant differences between urban and rural populations. Selikoff and Hammond132 compared lung tissues obtained in 1934 and 1967 and found no significant increase in the proportion containing ferruginous bodies. This suggested that, despite increasing use of asbestos in New York City between 1934 and 1967, fibers of a type producing ferrugi nous bodies had not been increasing at a corresponding rate. However, Chang-Hyun UmIS2 reports an increase over each decade in asbestos bodies in samples of lungs from persons who died in London in 1936, 1946,1956,1966. PLEURAL CALCIFICATION IN THE GENERAL POPULATION Meurman,107 in 1968, reviewed critically the literature related to pleural calcification and asbestos exposure. A number of studies strongly suggested an association between pleural calcification and nonoccupational exposures to asbestos. For example, in 1960, Kiviluoto78 reported calcifications in 9% of the adult population detected during mass roentgenographic surveys in a Finnish commune 14 ASBESTOS in which there was an asbestos mine and mill; the frequency was low for the remainder of the Finnish population. Raunio119 enlarged on these observations in 1966, reporting that, of 633,201 chest films taken in Finland between 1960 and 1965, 1,516 showed pleural cal cification; 1,232 of the latter were among 43,483 films taken in 10 communes in which there were anthophyllite mines. Rock and soil in such areas also contain much asbestos, so that the demonstration that airborne anthophyllite could be demonstrated over 25 km from the mines is not necessarily relevant. Anspach4 reported that, of 244 subjects with pleural calcification found in a chest roentgenographic survey in Dresden, 177 had either worked in or lived near an asbestos factory. Zolov et ol. 110 described a 5.1 % prevalence of pleural calci fication in a rural population in Bulgaria and suggested that the most likely cause was asbestos in the soil. However, Hromek,72 Marsova,96 and Rous and Studeny,125 reporting on a high prevalence of 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 not invariably be considered an index of asbestos exposure in the general population, although it may prompt a search for an environmental source of asbestos. MEASUREMENT OF AIRBORNE ASBESTOS A more direct method of obtaining evidence on the likelihood of 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 inter preting data so obtained.77,89'12,=136 Limited information has been derived from measuring fibers on sampling sites; for example, Laamanen et ai 82 showed asbestos fallout diminishing rapidly be yond 1 km from an anthophyllite quarry, but still detectable at 27 km. Counts of asbestos fibers collected on membrane, filters by high-volume air sampling and estimated by light microscopic tech niques similar to those used in industrial hygiene have shown small numbers of fibers in a few urban sites.10'16 Such results, although showing numbers of fibers detectable by the light microscope that were low by occupational health experience, have been too few and variable to be used with confidence. Alternative methods that are .... Evidence of Human Nonoccupational Exposures to Asbestos 15 currently under development, including estimations of the number and mass of fibers in the LM and the EM size ranges, have shown measurable concentrations of asbestos in many samples of ambient ajj-1,66,136 such environmental measurements are in their earliest stages and provide few clues to the extent or significance of the risk from this type of exposure to asbestos or to other mineral fibers. 4 Estimation of Risk in Nonoccupational Exposures to Asbestos Industrial experience has shown that prolonged inhalation of asbestos can increase the risk of neoplastic disease. Examination of lung tissue has made it apparent that a much larger proportion of the general pub lic 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 available to answer these questions 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 NONOCCUPATIONAL EXPOSURES Two genera] indices of asbestos exposure are available for use in direct epidemiologic studies of groups not known to be occupa- 16 .............. ^ H p lJ BWBBm m I Estimation o f Risk in Nonoccupational Exposures to Asbestos 17 tionally 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 asbestos-related disease, this knowledge must cover each person's whole lifetime. The second is a quantitative estimate of each member's lung content of asbestos fibers. There are few such direct epidemiologic studies, and they are inadequate to answer the questions at issue. The only studies that appear to implicate asbestos in the develop ment of malignancies in persons not occupationally exposed are those involving diffuse mesothelioma, a tumor that is uncommon and that has been the subject of special attention in recent years. Many of the mesotheliomas reported by Wagner et al. 161 in South Africa were attributed to household and neighborhood exposures in a crocidoliteproducing area. Although nonoccupational, these exposures have been described as substantial.168 Newhouse and Thompson113 studied 76 patients with mesothelioma diagnosed in London Hospital from 1917 to 1964. Of these, 31 (40.8%) had occupational exposures to asbestos, 9 (11.8%) had a relative who worked with asbestos, 11 (14.5%) had neither of those backgrounds but had Jived within a halfmile of an asbestos factory, and 25 (32.9%) had no known contacts. Corresponding percentages for a group of matched control subjects (patients in the same hospital for other dieases) were 10.5, 1.3, 6.6, and 81.6%. Stumphius and Meyer14 reported no mesotheliomas in the community near the shipyard in Flushing (Holland), although 17 of 21 mesotheliomas reported in the province of Zeeland in 19641967 had been in workers in that yard, but not in insulation or asbes tos workers. Raunio119 found no excess of pulmonary, pleural, or peritoneal malignancies in the areas of Finland where pleural calcifi cations attributed to anthophyllite were present in 6-9% of routine chest survey films. In a series of 17 mesotheliomas collected by Borow et al.,12 all but two were 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 en virons. Lieben and Pistawka87 found that, of 42 persons with meso theliomas reported in Pennsylvania, 10 had worked in asbestos plants, 8 lived or worked close to an asbestos industry, and 3 were mem bers of families that included asbestos workers; in 11, no history of exposure could be obtained, and the remaining 10 had question able random exposures. McDonald et al.99 collected information on 165 fatal malignant mesotheliomas known to pathologists in Canada between 1959 and 1968. They confirmed an association 1 8 ASBESTOS with occupational exposure to asbestos but concluded that the ex cess was in the manufacture and industrial application of asbestos, rather than in mining or milling. It is apparent that no quantitative conclusions were possible from these studies, which present serious methodologic problems to the epidemiologist. They suggest a risk in household contacts and in residence in the immediate neighborhood of an asbestos plant. There appear to be different levels of risk in dif ferent types of occupational exposures, and some of these may be re flected in corresponding household and neighborhood experience. In no analysis of 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 be correlated with asbestos content. The series so far studied have been too small, and methods too variable, to permit any conclusions as to the importance of small fiber numbers in the lung. EXTRAPOLATION FROM OCCUPATIONAL EXPERIENCE Another source of evidence of the relative risks associated with in haling moderate or small numbers of asbestos fibers is the experience of persons who have had occupational exposures below those known to be definitely hazardous. The maximal airborne fiber concentra tions recommended for prevention of asbestosis are much higher than any likely to be encountered in nonoccupational situations. For ex ample, one recommended standard would limit the average concen tration of airborne chrysotile to 2,000 fibers per liter as determined by light-field count.14 Another that has been proposed would limit average concentrations of fibers to 5,000 fibers per liter.2 Occupationrelated asbestosis can be effectively controlled with airborne fiber con centrations much higher than are likely to be encountered in non occupational situations. It is important to determine whether workers whose exposures have been reduced to levels that prevent or greatly delay asbestosis, as well as others whose exposures are indirect, have a lower risk of lung cancer than those with higher and more direct exposures. 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 1968 to show no excess of neoplasms.81 The long latent periods of asbestos-related lung cancer and mesothelioma, which would prob- HHB Estimation of Risk in Nonoccupational Exposures to Asbestos 19 ably be even longer at lower dose levels, are such that it is too soon to draw final conclusions as to the eventual incidence of these malignan cies. Nevertheless, reduced exposure seems to be having an effect. Another indication of reduced incidence or delayed onset of disease with lower exposure is in the observations of Newhouse,111 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 not true among those who had low or moderate exposures. McDonald et al. 100 recently reported the mortality experience of men who worked in chrysotile mines and mills of Quebec. There was a slight excess of lung cancer among the 2,457 deaths in workers bom 1890-1920, but all could be explained by the excess that occurred in those who had been maximally exposed. This suggests that, insofar as chrysotile miners and millers are concerned, the risk drops off rapidly with de creasing accumulated dosage. Most series of case reports of mesothelioma include some persons who have worked in the construction or shipbuilding industries, but in trades not involving direct contact with asbestos.101 Such persons as plumbers, electricians, and metal workers often have more ferru ginous bodies in their lungs than do white-collar workers.133 Although Dunn and Weir,33 in a study of occupational groups in California that revealed an excess of deaths from lung cancer in insulation workers, found no excess lung cancer deaths in other construction trades, the groups they studied were diluted with many persons who were un likely 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. One cannot extrapolate from the mortality experience of, on the one hand, those who are directly and indirectly exposed to asbestos in their employment to, on the other hand, the general public, who have had moderate or slight exposures from ambient 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 o f 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 there may be ferruginous bodies or fibers in their lungs. Sources of Asbestos Fibers in Ambient Air Precise information is not available on tonnages, numbers o f 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 occu pational exposure experience, information regarding actual and po tential sources of emissions of asbestos fibers is of value both for directing future studies and for understanding the steps that might be taken now to safeguard the health of the public. NATURAL SOURCES OF AIRBORNE 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, con struction, 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 dissem- Sources o f Asbestos Fibers in Ambient Air 21 mating forces. Such naturally occurring talc, as well as the large quantities used as a diluent and carrier for pesticides, can add to the background fiber concentration in the ambient air.166'167 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 contribu tions of natural and industrial sources. MINING AND MILLING OF ASBESTOS Mining and milling of asbestos constitute another source of asbestos emissions. In the United States, such activity is presently confined to a few mines in California, Vermont, Arizona, and North Carolina. Fibers are emitted during removal of overburden and preparation of the ore body for open-pit mining. Further release occurs during drill ing and ore-breaking. Waste dumps from mining and milling are ex posed 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 or elsewhere, they will become a source of fibers. Occasionally, bags are broken and asbestos is spilled during handling. Similar emissions occur during the shipment of products. Transporting asbestos-containing solid wastes in open vehicles through urban areas can be a more important emission source. MANUFACTURE OF PRODUCTS CONTAINING ASBESTOS Industries that must provide ventilation and other dust-control measures for the protection of workers may emit asbestos fibers 2 2 ASBESTOS into the surrounding environment unless effective air cleaning is applied to effluents. Fibers removed by ventilation and filtering de vices and not reintroduced into the production process and asbestoscontaining waste products of the manufacturing process ultimately are disposed of outside the plant. USE OF PRODUCTS CONTAINING ASBESTOS Many products, at times unknown to the user, contain asbestos of one kind or another. There are great variations among such products with respect to the chances of fiber release during the use o f the pro duct. The likelihood depends predominantly on the ease with which the fibers can be dislodged by the application of energy and on the de degree to which the application of energy actually destroys the fibers during the use of the product. Almost all the asbestos fiber used in the United States for manufacturing products becomes tightly bound within the products and usually 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 files are in this category. Some asbestos-containing products, such as brakelinings, are subjected to great friction; their rate of wear is con siderable, and at times they are almost completely worn away. In the case of brakelinings, the application of energy is so intense and the heat created so great that most ehrysotile fibers are destroyed by be ing converted to another substance, which is nonfibrous.65'68'88 Nevertheless, an appreciable percentage (1 - 3%) remains as fibrous asbestos. In some products-for example, asbestos cloth, paper, and sprayed fireproofing materials--asbestos fibers are not tightly bound or mixed with another material that holds them in place. Fiber release from these products occurs primarily during application and removal. The spray fireproofing of buildings with asbestos-containing materi als is a case in point This operation can be a serious source of emis sion, in that it usually occurs in densely populated areas. Talc is mined and milled and used in greater quantities than is as bestos in the United States. Because it contains asbestos fibers, its uses will add 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. m b Sources of Asbestos Fibers in Ambient Air 23 DEMOLITION For years, asbestos has been incorporated in building materials. In some forms of insulation and wallboard, the amount present is less than 20% of the total; but other materials consist mostly or entirely of asbestos. When a building is demolished, areas of loosened asbestos are open to the ambient air and fibers are emitted. In general, singlefamily residential structures contain only small amounts of asbestos insulation. Demolition of industrial and commercial buildings that have been fireproofed with asbestos-containing materials will prove to be an emission source in the future, requiting control measures. SOLID-WASTE DISPOSAL Solid wastes produced during manufacture of asbestos-containing products, use of such products, and demolition can be emission sources. These waste materials are usually disposed of without re gard to their potential as emission sources. Alternate methods of dis posal often result in commingling of asbestos-containing wastes with municipal wastes in open dumps and thus create a long-term emission source. 6 Principles of Control The natural background level of asbestos fibers is difficult to quantify or modify. The major sources of local ambient-air contamination with asbestos are industrial processing and use of products containing asbestos. It is feasible to identify the sources of emission, select those to which presently available control procedures can be applied, and point out areas that need further study and development of new methods of control. NATURAL SOURCES OF 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 o f the contamination from natural sources, geographic variation, 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 contamina tion that might be achieved in different areas of the country. 24 25 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. Road ways in open pits should be treated with dust-suppressive agents; truckloads of ore should be covered with tarpaulins while being trans ported; handling of ore should be minimized; ore storage piles should be moistened to reduce wind erosion; and waste dumps should be treated with dust-suppressive agents. MILLING OF ASBESTOS An in-plant dust-control program for protecting workers in asbestos mills includes exhaust ventilation with efficient dust-collecting and air-cleaning equipment, isolation, enclosure, wet methods, and good housekeeping and maintenance. MANUFACTURE OF PRODUCTS CONTAINING ASBESTOS The elements of dust control recommended for the milling of asbestos ore 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. USE OF PRODUCTS CONTAINING ASBESTOS An important emission source is the use of insulating materials con taining asbestos. This constitutes only a small fraction of the asbestos used. But the asbestos in some insulating materials is not bound as it is in cementitious products or tiles; construction activities usually are carried on in urban areas, where many people are exposed to contam inated air; and control of dust during construction, although feasible, is difficult. The most effective approach in reducing exposures of the general public to asbestos from this source involves controlling dust produc tion and release at its origin during construction work. The generation 2 6 ASBESTOS of dust should be reduced by changing material-handling methods, work practices, and cleanup procedures. Local exhaust systems should be used for dust collection at points of generation; for example, dust collectors for band saws are available, and hand-powered tools sup plied with exhaust systems are being made. Much developmental work is needed to produce portable air-moving and air-cleaning systems for use in tunnels, crawl spaces, and other confined areas. This subject has been neglected by industrial hygienists and ventilation engineers, and no satisfactory-equipment is available. DEMOLITION AND WASTE DISPOSAL Demolition and waste disposal are likely to be emission sources if appreciable amounts of asbestos are used in construction, unless opera tional procedures are strictly controlled. Isolation, enclosure, and wetting down are useful. Caution must be observed not 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. MEASUREMENT OF AIRBORNE ASBESTOS An important consideration in the development of a strategy for con trol is whether there are methods for measuring airborne concentra tions of asbestos that are sufficiently sensitive, specific, and reproduc ible. Present methods of sampling, identifying, and measuring airborne asbestos are not entirely satisfactory, especially if one is dealing with low concentrations and unidentified or mixed sources. Only within recent years have methods for determining concentrations of fibers for industrial hygiene purposes been standardized ;14,3S they use samples collected on membrane filters in which fibers are counted with phase-contrast illumination. Electron microscopic methods give a much more complete indication o f the total fiber content of the air; but when the need for fiber identification is included, they are tedi ous and expensive for routine use.1'66136 The relative biologic signi ficance of different sizes of fibers is not known, nor is the relative importance of fiber numbers and fiber mass. There appear to be no published data on the efficiency of air-cleaning equipment as related to fibers of different sizes. Principles of Control 27 In spite of the difficulties, it is possible to sample air, determine the approximate concentration of airborne fibers, and identify the major types of 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 health. Because of methodologic and other uncertainties, it is not yet feasible to base control on numerical ambient air quality standards. Research Needs Two recent reports25'167 have discussed in some detail the many kinds of research needed to answer pressing questions concerning the effects of asbestos on health and the degree and nature of necessary controls. Investigations along the following lines should be given high priority. Study of the mechanism of action of the asbestos minerals should continue, with particular attention to carcinogenic effects. It is impor tant to learn more about the influence of asbestos type and fiber size on respirability, 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 smaller than the LM size range be clarified. Methods of sampling, identifying, and quantitating airborne asbes tos need continued development. Coordination with studiesdn ani mals and man is essential to ensure that environmental data will be biologically relevant. Similarly, methods for identifying and quanti tating asbestos in biologic tissue need development and application. Quantitative methods for measuring airborne asbestos should be applied widely to determine the natural background and the concen tration and distribution of fibers in the air near various sources. 28 Research Needs 29 Conventional LM and EM methods should be applied simultaneously in selected occupational and community situations. More epidemiologic studies are needed. Populations in several different exposure ranges should be studied, including occupational, household, and neighborhood exposures. Special studies of meso thelioma are needed to determine whether the incidence has been increasing and to determine the current pattern of distribution. 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. Conclusions and Recommendations PATHOGENICITY OF ASBESTOS MINERALS Any of the commercially used asbestos minerals, when inhaled in suf ficient numbers, as in uncontrolled occupational exposures, can cause disabling fibrosis of the lungs. An association between occupational ex posures to asbestos and bronchogenic carcinoma has been established, but the dose-response relation and the role of cofactors have not been defined. Evidence of a causal association between some but not all ex posures to asbestos fibers and diffuse malignant mesotheliomas of the pleura and peritoneum is substantial, but evidence of such a relation with other tumors is inconclusive. Although the different types of as bestos differ in some of their biologic effects, no type can be regarded as free of hazard. The hypothesis that asbestos fibers act as cofactors or carriers of carcinogens is attractive, but as yet unproved. EVIDENCE OF HUMAN NONOCCUPATIONAL EXPOSURES TO ASBESTOS The demonstration of ferruginous bodies, 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 Conclusions and Recommendations 31 persons with no occupational contact may have inhaled and retained asbestos. Proof has come in some areas with positive identification of chrysotile asbestos fibers. Analyses of community air for asbestos have been too limited to define the sources, concentrations, and distri bution of fibers in the environment. The fiber concentrations that have been demonstrated in ambient air are small, compared with those in industry, but data are inadequate for definitive comparisons. ESTIMATION OF RISK IN HUMAN NONOCCUPATIONAL EXPOSURES TO ASBESTOS The most important question in the case of persons with nonoccupa tional exposures to asbestos is whether there is an increased risk of malignancies. Industrial experience indicates that there is no likeli hood of significant asbestosis in nonoccupational exposures. The major potential for risk appears to lie in those with indirect occupa tional contacts, household contacts, or residence in the immediate neighborhood of an asbestos source; and even there, the actual risk Is poorly defined. The appearance of a gradient of effect in such groups, however, suggests that there are levels of inhaled asbestos without detectable risk. It is not known what range of respirable airborne asbestos fibers will ultimately be found to have no measur able 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 OF CONTROLS Asbestos is too important in our technology and economy for its essen tial use to be stopped. But, because of the known serious effects of uncontrolled inhalation of asbestos minerals in industry and uncer tainty as to the shape and character of the dose-response curve in man, it would be highly imprudent to permit 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 emis sion into the atmosphere be defined and controlled. In the absence of such controls, local fiber concentrations might at times approach those in occupational sites. Analytic methods and epidemiologic data are not yet adequate for the development of an ambient air standard, but emission controls are needed and appear to be feasible. References 1. Alcocer, A. E., J, Murchio, and P. K. Mueller. Asbestos Content of Some Urban Air Samples. AIHL Report 90 (revised). Berkeley: State of California Department of Public Health, 1970. 12 pp. 2. American Conference of Governmental Industrial Hygienists. Threshold Limit Values o f Airborne Contaminants and Intended Changes Adopted by ACGIH for 1970. Cincinnati: American Conference of Governmental Industrial Hygienists, 1970. 27 pp. 3. Anvilvel, L., and W. M. Thurlbeck. The incidence of asbestos bodies in the lungs at random necrospsies in Montreal. Can. Med. Assoc. J. 95:11791182, 1966. 4. Anspach, M. Sind Pleuraverkalkungen pathognomonisch fur eine Asbestose? Int. Arch. Gewerbepath. 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