Document ZJ4o96vjv0mxM8yegnwnpV3Z0

FILE NAME: Rogers Corporation (ROG) DATE: 1971 DOC#: ROG038 DOCUMENT DESCRIPTION: Book Excerpt - Asbestos, The Need for and Feasibility of Air Pollution Controls '7 / Biologic Effects of Atmospheric Pollutants ASBESTOS THE NEED FOR AND FEASIBILITY OF AIR POLLUTION CONTROLS NATIONAL ACADEMY OF SCIENCES THKP 0015740 Source: http //industrydocum ents library.ucsf edu/tobacco/docs/grvb0104 Th<* : a Biologic Effects o f Atmospheric Pollutants t ASBESTOS 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. 1971 T H K P 0015741 Source: http://industrydocuments.library ucsf.edu/tobacco/docs/grvb0104 NOTICE: The rtudynqkM tedlM reiii was undertaken under tire ucgb o f lha N ational R e* Council w ith the expteu upt)rorl o f th e G am m ing B aird o f the NRC. Such approval indicated th at th e Board com ideied th at th e problem b o f national rignHVance. that eiu d d ttio n o f th e problem requited id e a tific r technical com peteace, aad th a t the lao tu cet o f NRC were perticidiriy auitable to th e conduct o f the project. The inantntioiial roapomibilitiea o f NRC were then d b ch ei|ed in the foOowIng m am ): The m em benof the study com outtaa were elected fo r th eir iadividual w hotariy com petence and lodgm ent w ith due ccm M enfan fo r the balance and breadth o f dirctpliner. ReiponnbiUty fo r aB upcct of thi* report recta w ith th e rtudy com m ittee, to whom amccrc appreciation la caprened. A lthou|h th e report o f our ttu d y conm uttcei are not subm itted fo r approval to tha Academy membership nor to the Council, etch report u reviewed tqr a reeond group o f fcxntnts according to procedures establislied and m onitored by the Academy's Report Review Com m ittee. Such reviews are intended to determ ine, in ter aiia, w hether the major question and relevant paints o f vinw have been addressed and w hether the reported Andiof, conchinonx and recom m endattoni arose from the arm[table d ata aad iaform ation. D istribution o f tlm report b perm itted only a fte r satisfactory com pletion o f th is review process. The work on which this publication is based was parformed pursuant to Contract No. CPA 70-42 with the Environmental Protection Agency. ISBN 0-WWH927-3 A mikbie from Fnnluii and Fublirlting Office National Academy of Sciences 210L Constitution Avenue, N.W. WuWngton, D.C. 20418 Fini printing, October 1971 Secondpiinting. Decent) ISTI Library o f Congress Catalog Card Number 78-172926 Printed in the United States of America PANEL ON ASBESTOS W. CLARK COOPER. School o f Public Health, University o f California, Berkeley, Chairman LEWIS J. CR ALLEY, Bureau o f Occupational Health and Safety, Division o f Epidemiology and Speeds) Services, U. S. Public Health Service, Cincinnati, Ohio BENIAMIN C. FERRIS, I R,, Department o f Physiology, Harvard School o f Public Health, Boston, Massachusetts PAUL g r o s s , Industrial Hygiene Foundation, Inc., Pittsburgh Pennsylvania DUNCAN A . H O L A D A Y, Occupational Health Field Station, Salt Lake City, Utah IRVING 1. SELIKOFF, Environmental Sciences Laboratory, Mount . Sinai Hospital, New York, New York GEORGE W. WRIGHT, Medical Research Department, SL Luke's Hospital, Cleveland, Ohio SAMUEL P. HICKS. Department o f Pathology, University o f Michigan Medical Center, Ann Arbor, Associate Editor T. D. BOA Z, JR., Division o r Medical Sciences, National Research Council, Washington, D. C , S ta ff Officer COMMITTEE ON BIOLOGIC EFFECTS OF ATMOSPHERIC POLLUTANTS A R T H U R B . D U B O IS , Department o f Physiology, School o f 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 o f 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. CLARK COOPER, School of Public Health, University o f California, Berkeley iii THKP 0015742 Source http //industrydocuments library ucsf edu/tobacco/docs/grvb0104 IV ASBESTOS MORTON CORN. Graduate School o f Public Health, University o f . Pittsburgh, Pittsburgh, Pennsylvania BERTRAM D. DINMAN, School o f Public Health, University o f Michigan. Ann Arbor LE O N C O LB E R G , Institute of Experimental Pathology and Toxi cology, Albany Medical College, Albany, Hew York PAUL B. HAMMOND, Department o f Physiology and Pharmacology, College of Veterinary Medicine, University o f Minnesota, St. Paul SAMUEL P. HICKS, Department of Pathology, University of Michigan Medical Center, Ann Arbor VICTOR G. l a t ie s , Department o f Radiation Biology and Bio physics, University of Rochester Medical Center, Rochester, New York ABRAHAM M. LlLi ENFELD, Department o f Chronic Diseases, School o f Hygiene and Public Health, The Johns Hopkins University, Baltimore, Maryland PAUL m e ie r , Biomedical Computation Facilities, University of Chicago, Chicago, Illinois ia m e s N. PITTS. JR.. Department o f Chemistry. University o f California, Riverside GORDON J. s t o p p s , Haskell Laboratory, E. I. du Pont de Nemours and Company, Newark, Delaware o . c l ift o n TAYLOR. Department o f Horticulture, University of California, Riverside JAROSLAV J. VOSTAL, Department o f Pharmacology and Toxi cology, University of Rochester Medical Center, Rochester, New York t . d . &OAZ, j r .. Division o f Medical Sciences, National Research Council, Washington, D. C., Executive Director Preface This document was developed at the request o f the National Air Pollution Control Administration, which became the Air Pollution Control Office upon the formation of 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 o f 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 o f the dedicated efforts of the Panel on Asbestos, chaired by Dr. W. Clark Cooper and formed under the aegis of the parent Committee on Biologic Effects of Atmospheric Pollut ants, Division of Medical Sciences, National Research Council. The Members of 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 of expression in this report must be given to the Editor of the Division of Medical Sciences, Mr. Norman Grossblatt. THKP 0015743 Source http //industrydocuments library ucsl eau/tobacco/docs/grvb0104 vi ASBESTOS This report (1) summarizes the evidence regarding the pathoge nicity of asbestos in man and animals, (2) summarizes the evidence of human nonoccupational exposure to asbestos, (3) evaluates the evidence regarding a health ride associated with various degrees and types of exposure, (4) identifies sources of environmental contami nation by asbestos, and (3) offers recommendations concerning the need for and feasibility of control measures. Charles L. Dunham Chairman, Division of Medical Sciences Contents THKP 0015744 1 Introduction 1 2 Pathogenicity of Asbestos 3 3 Evidence of Human Nonoecupational 11 Exposures to Asbestos 4 Estimation of Risk in Nonoccupational 16 Exposures to Asbestos 5 Sources of Asbestos Fibers in Ambient Air 20 6 Principles of Control 24 7 Research Needs 28 8 Conclusions and Recommendations 30 References 32 vii Source http //industrydocuments library ucsf edu/tobacco/docs/grvb0104 1 Introduction The naturally occurring fibrous silicates classified as "asbestos" have become almost indispensable in modem technology.47>,i4'141 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 19651969.130 The potential of asbestos as a hazard to health has been the subject of a number of reviews in recent years.M'49,M,li3,1" ''4,,l47,,<* 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 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.4* 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, l THKP 0015745 Source: http://industrydocuments.library ucsf.edu/tobacco/docs/grvb0104 2 ASBESTOS s)] amphiMes, are amo&ite, crocidolite, anthcphyHite, tremotite, and ctinoltU. The asbestos minerals differ in their metallic elemental content, rangeof fiber diameters, flexibility ct harshness, tensile strength.surface properties, and other attributes that determine their mdustrialuscsand may affect their rcspirabiiity, deposition, retention, translocation, and biologic reactivity THKP 0015746 Source http //industrydocuments 2 Pathogenicity of Asbestos The effects of fibers in biologic systems nuy 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 cofactois. p a t h o g e n ic it y m m a n The proven or suspected effects o i asbestos minerals on human health include nonmaiignaitt changes, such as pulmonary and pleural fibrosis, and several types of malignancy, notably of the lung, pleura, and peritoneum. Nearly a31 the positive evidence o f an association between asbestos and human disease has come from occupational groups. With few exceptions, these have consisted o f workers engaged in the raining 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 ibrary ucsTedu/tobacco/docs/grvbO 104 4 ASBESTOS Asbestosis Asbestosis, or asbcstotic 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 ailcification of the pleura; clinical changes th at include fine rales, fin ger dubbing, and shortness of breath, each o f 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 lur 10 years in the carding room o f an asbestos factory, was by H. Montague Murray in 1907.1,0 Cooke reported a second case in 19241and in 1927 provided a more detailed description,11 in which the term "asbestosis" was first used. In 1930, Merewether10* 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 Mcrcwcthcr and Price,,w 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 re ported in the United States in 1 9 3 0 , and guidelines for accept able dust concentrations were proposed by Dreessen el al. in I938.ja 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 llsbestos. '6,4',6J' l07,,, When multiple or bilateral, they arc 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.44 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 ih 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 lust suggestion that asbestos might be causally related to cancer o f the lung was made in 1935 by Lynch and Smith,90 who described squamous celt 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 o f Factories in the United Kingdom, re ported 31 instances o f cancer o f the lung in 235 persons known by his department to have died with asbestosis between 1924 and 1946 .KO This constituted an incidence o f 13.2%, compared with 1.32% <91/6,884) in persons certified as having had silicosis during the same period. Gloyne in 1951* 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 o f whom, or 14.0%, had cancer o f the lung, compared with 55 (6.9%) o f 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 o f risk. Doll in 1955,31 after analyzing the causes of death among 105 men who had worked for at least 20 years in areas o f asbestos textile plants de fined as dusty, concluded that the 18 cases of lung cancer th at oc curred indicated a risk about 10 times that in the general male population. Other studies1**3*s>>*>*iaS,34,a*-6<J,S,70,W-75,7*-l 00 , 111,130,140,154,133,i6i,ja9 j,ave confirmed 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 o f risk among different occupationally exposed groups, probably related to dose, as well as to other factors. Mesothelial Tumors Primary malignant tumors o f 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 . THKP 0015747 Source http //mdustrydocuments library ucst edu/tobacco/docs/grvb0104 6 ASBESTOS opinion as to diagnostic criteria.l,,w,,T,M* 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 ou Lather primary tumors, jhat could metastasize to or involve serosal surfaces, is a difficult constraint on a retrospective scries. It was after 1960 that serious consideration was first given to asbestos as an etioiogic factor in mesothelia! malignancies. In that year, Wagner el ai. 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, *.**.**. no evidence of a strong association had been developed. Additional information supporting a relationship between asbestos and malignant mesothelioma has accumulated since ^ e o .7' 13'34'37*41' *,*,'*i,iI2-H3,in,133,133 ^ outstanding feature has been the long period, commonly over 30 years, between the First ex posure to asbestos and the appearance o f a tumor, as emphasized in reports by Wagner144and Selikoff and llammond.113 Other Neoplasia Associations between asbestos exposures and malignancies of the gastrointestinal tract and of other sites have been reported, but the data are still inconclusive.sj,s9,ts, ,i Mutagenic Effects Evidence of a mutagenic effect o f 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 4 } Pathogenicity of Asbestos 7 time and dosage factors. There are at present no satisfactory ex perimental models to duplicate prolonged inhalation o f 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,4S,s**,S6,,S7 guinea pigs,w.,*9,w7 hamsters,14 rabbits,141 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,,$7 but to do so it was necessary to use very high concentrations o f 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 o f the investigations, it has been asked whether the fibrogenicity o f asbestos dust is mostly confined to fibers longer than 5 the question remains un answered. Experimental Neoplasia Lung cancer from chrysotile dust has been produced experimentally in rats5* and in mouse lung implants.137 Other investigators who used different methods for introducing the dust143 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 unpaired had twice the lung cancer rate o f animals with normal clearance.58 Cancer of the pleural surface (mesothelioma) has been reported in rats and hamsters that received intrapleural injections o f the three most common types of asbestos.ua,IH,,M The amounts o f 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 Roc et b/,,**3 which involved pleural and peritoneal mesotheliomas of mice after subcutaneous injections of crocidolite, amosite, or chrysotile, are of particular interest because they yielded evidence of migration of fibers. THKP 0015748 Source http //industrydocuments library ucsf edu/tobacco/docs/grvb(J1U4 8 ASBESTOS Naturally Occurring Effects in Lower Animals There is no evidence that effects o n domestic or wild animats arc 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.111 Webster has demonstrated fibrosis in donkeys, baboons, and wild rodents in South Africa,183 and Kiviluoto has described the finding o f anthophyllite asbestos in the lungs o f a cow in an anthophyllitc-producing area of Finland.78 STUDIES IN VITRO There have been limited studies o f 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.*'*'*58 Chrysotiie differs from amositc. crocidolite, and anthophyllite in th e conditions under which it is hemolytic. Parazzi et of.116 demonstrated in 1968 that both crocidolite and chrysotiie 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 o f 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 o f type of asbestos, fiber site, 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/ 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 o f 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 Canada13'97 and Italy,1*4 there are possible explanations for the difference other than as bestos 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 hazardous, but mesotheliomas have been rare in the Transvaal, where crocidolite is also produced.49'*37 Al though Selikoff e t found many mesotheliomas in insulation workers whose exposures had been largely to chrysotiie and amo- site, Sluis-Cremer137 and Webster181 have not found the incidence of mesothelioma high in areas where amositc was mined and milled, and McDonald et ai. Iw did not report an excess in the chrysotile- mining and -milling areas of Canada. All epidemiologic studies that appear to indicate differences in pathogenicity among types o f asbestos are flawed by their lade 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 th e, gastrointestinal tract. The aerodynamic properties of fibers depend largely on their diameter; fibers below 3.5 fun in diameter are re garded as being in the respirable range.1*1 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 0.5 jutn diameter and larger. The application of electron microscopic (EM) techniques133 has enlarged our hortzons 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 THKP 0015749 i Source http //industrydocuments library ucsf edu/tobacco/docs/grvb0104 to ASBESTOS for noniralignant and malignant changes. The evidence that bundles of fibrils may be broken down within the body to individual fibrils is important.'*4 A number of investigators have postulated that a probable role of asbestos libers 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 metals*4'37 and polycyclic hydrocarbons;41'*1"*4 studies of the elution of contaminants in biologic materials;34 and the concurrent exposure of animals to asbestos and to other materials.14* The present consensus is that contaminants are present, but a special pathogenetic role is still speculative. The work of Sclikoff et a i134 strongly suggests ynerp^in a cigarette smoking and asbestos exposure in the increased risk of lun 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 factorof 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., pleura] 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.91 In 1929, Cooke19 described such "curious bodies" in association with pulmonary fibrosis. Stewart and Haddow'43 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. THKP 0015750 Source http //industrydocuments library ucsf edu/tobacco/docs/grvb0104 12 asbesto s As long as (he coated fibers were round in persons known to hare been occupationally exposed to asbestos, the identity o f the central fiber was seldom questioned, although from time to time similar objects were found in persons with no known exposure to asbestos. Meuman1'* 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-workers*4'** 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.** There is thus ample justification for abandoning L1asbestos body" as a generic term; in 1965, Gough*1 suggested the term "minenl-fiber-body,'1and, in 1966, Gross** recommended " fer ruginous body." Thomson et a/.,150 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% o f tung 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 scries.3,*,,7,3' 4v,i(m,iit,i,14* Utidjian et al.143 inferred that, if a sufficient volume of lung tissue were examined in each case, nearly alt 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.S7*J*,,* 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 o f the ferrugi nous bodies alone, but of 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 at * have found thin, uncoatcd, 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.*4 Poolcy et a/.11* have reported similar findings. Evidence is therefore strong that most human lungs harbor thou sands or millions o f fibers. Some of these are chrysotile asbestos, and other types o f asbestos minerals are probably there also. In most persons not occupationally exposed to asbestos, the numbers o f fibers are relatively small, compared with the numbers found in the occupationally exposed.131 The systematic application o f q uantita 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 on'*. *'> 1, 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 o f airborne Fibers other than asbestos.3*'51 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 o f fibers in lungs with increasing use of asbestos and concerning the existence of signif icant differences between urban and rural populations. SelUcoff and Hammond131 compared lung tissues obtained in 1934 and 1967 and found no significant increase in the proportion containing feiruginous bodies. This suggested that, despite increasing use o f 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 Um,5i 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 I960, Kiviluoto7* reported calcifications in 9% of the adult population detected during mass roentgenographic surveys in a Finnish commune THKP 0015751 Source http //industrydocuments library ucs1.edu/tobacco/docs/grvb0104 14 ASBESTOS in which there was an asbestos mine and mill; the frequency was low for the remainder of the Finnish population. R aunio"' enlarged on these observations in 196$. reporting that, of 633.201 chest films taken in Finland between 1960 and 196S, 1,516 showed pleural cal cification; 1,232 of the latter were among 43,483 films taken in 10 communes in which there were anthophylllte mines. Rock and soil in such areas also contain much asbestos, so that the demonstration that airborne anthophytlite could be demonstrated over 25 km from the mines is not necessarily relevant. Anspach* 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. Zolmr et a l 110 described a 5.1% prevalence o f pleural calci fication in a rural population in Bulgaria and suggested that the most likely cause was asbestos in the soil. However, Hromek,12 Marsova,** and Rous and Studeny,'3* 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 serch for an environmental source of asbestos. MEASUREMENT OF AIRBORNE ASBESTOS A more direct method o f obtaining evidence on the likelihood of exposure of the general population would be the sampling of air to determine the presence and amount o f respirable asbestos fibers. There are, however, many uncertainties as to the best methods o f sampling, identifying, and quantitating airborne asbestos and inter preting data so o b t a i n e d . 34 Limited information has been derived from measuring fibers on sampling sites; for example, Laamanen *t ai. " 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.10,14 Such results, although showing numbers of Tibers 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 THKP 0015752 Evidence o f Human Nonoccupatonal Exposures to Asbestos IS currently underdevelopment, including estimations o f the number and mass of fibers in the LM and the EM size ranges, have shown measurable concentrations o f asbestos in many samples o f ambient air.l'M>m Such environmental measurements are in their earliest stages and provide few clues to the extent or significance o f the risk from this type of exposure to asbestos or to other mineral libers. Source http //industrydocuments library ucsl edu/tobacco/docs/grvb0104 4 Estim ation of R isk in N on occu p ation al Exposures to Asbestos Industrial experience has shown that prolonged inhalation o f asbestos can increase the risk of neoplastic disease. Examination o f 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 detcctably increased risk of malignancy or other disease because of airborne asbestos? The limited information available to answer these questions comes cither 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 general indices of asbestos exposure are available for use in direct epidemiologic studies of groups not known to be occupa 16 Estim ation o f Risk in Nonoccupational Exposures to Asbestos 17 tionally exposed to asbestos. The first is based on knowledge o f each member's place o f work and place o f residence; because o f the long latent periods of asbestos-related disease, this knowledge must cover each person's whole lifetime. The second is a quantitative estimate o f i each member's lung content o f asbestos fibers. There are few such direct epidemiologic studies, and they are inadequate to answer the i 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 o f the mesotheliomas reported by Wagner e ta l.161 in South Africa were attributed to household and neighborhood exposures in a crocidoliteproducing area. Although nonoccupational, these exposures have been described as substantial.1** Newhouse and Thompson113 studied 76 patients with mesothelioma diagnosed in London Hospital from 1917 to 1964. O f these, 31 (40.8%) had occupational exposures to asbestos, 9(11.8%) had a relative who worked with asbestos, 11 (14.5%) had neither o f those backgrounds but had lived within a halfmile o f an asbestos factory, and 25 (32.9%) had no known contacts. Corresponding percentages for a group o f matched control subjects (patients in the same hospital for other dieases) were (0.5, 1.3, 6.6, and 81.6%. Stumphius and Meyer14 reported no mesotheliomas in the community near the shipyard in Flushing (Holland), although 17 o f 2 1 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 o f Finland where pleural calcifi cations attributed to anthophyllite were present in 6-9% of routine chest survey films. In a series o f 17 mesotheliomas collected by Borow et at.,11 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 o f the mill's en virons. Lieben and Pistawka*1 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 o f 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 z/99 collected information on 165 fatal malignant mesotheliomas known to pathologists in Canada between 1959 and 1968. They confirmed an association THKP 0015753 Source http //industrydocumenls library uest edu/tobacco/docs/grvb014 18 a sb esto s 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 mthodologie 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 o f these may be re flected in corresponding household and neighborhood experience. In no analysis o f causes of death in a large population has there been quantitative estimation of the lung content o f fenuginous 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 chrysotilc to 2,000 fibers per liter as determined by light-field count.14 Another that has been proposed would limit average concentrations or fibers to 5,000 fibers per liter.1 Occupation- related 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 j a lower risk of lung cancer than those with higher and more direct J exposures. i Workers who began employment in a British textile mill after 1933, when implementation of the Asbeitos Industry Regulations of 1931 reduced (but did not abolish) dust exposures, were reported in 1968 to show no excess of neoplasms.11 The tong latent periods of asbestos-related lung cancer and mesothelioma, which would prob- 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 o f these malignan cies. Nevertheless, reduced exposure seems to be having an effect. Another indication o f reduced incidence or delayed onset o f disease with lower exposure is in the observations o f Newhouse,*11 who found that, although there were more deaths from lung cancer and chronic respiratory disease among those who had heavy exposures many yean previously in a London asbestos-products plant, this was not true among those who had low or moderate exposures. McDonald ei al. 100 recently reported the mortality experience of men who worked in chrysotile mines and mills o f Quebec. There was a slight excess o f 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 o f case reports o f mesothelioma include some persons who have worked in the construction or shipbuilding industries, but in trades not involving direct contact with asbestos.>M 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 o f 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 arc 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 o f effect from direct occupational, to indirect occupational, to family and neighborhood situations--in all o f 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. THKP 0015754 \ Source http //industrydocumenls library ucst edu/tobacco/docs/grvb0104 5 Sources of Asbestos Fibers in Ambient Air Precise information is not available on tonnages, numbers of fibers, fiber sues 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 o f the public. I NATURAL SOURCES OF AIRBORNE ASBESTOS FIBERS i 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- 20 Sources o f Asbestos Fibers in Ambient Air 21 inating 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.IM,1*T It is thought that studies o f 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 o f asbestos constitute another source o f 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 ate 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 liber, and asbestoscontaining products and wastes is an emission source o f varying importance. Movement of asbestos ore from mine to mill in open trucks contributes to the overall emission. The shipment o f 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 o f 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 THKP 0015755 Source http //industrydocumerits library ucsf edu/tobacco/docs/grvb0104 22 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 arc 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 Ihe 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 tiles 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 chrysotile fibers are destroyed by be ing converted to another substance, which is nonfibrous.6*-**-** 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 mined with another material that holds them in place. Fiberrelease 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 o f 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. Sources o f Asbestos Fibers In Ambient Air 23 DEMOLITION For years, asbestos has been incorporated in building materials. In some forms o f insulation and wallboard, the amount present in less than 20% of the total; but other materials consist mostly or entirely of asbestos. When a building is demolished, areas o f loosened asbestos are open to the ambient air and fibers are emitted. In general, anglefamily residential structures contain only small amounts o f 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, requiring control measures. SOLID-WASTE DISPOSAL Solid wastes produced during manufacture o f 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 o f dis posal often result in commingling of asbestos-containing wastes with municipal wastes in open dumps and thus create a long-term emission source. THKP 0015756 Source http //industrydocumerits library ucst edu/tobacco/docs/grvb0104 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 o f 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 of 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 o f contamina tion that might be achieved in different areas o f 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 waysin open pits should be treated with dust-suppressive agents; trackloads o f ore should be covered with tarpaulins while being trans ported; handling o f 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 o f asbestos ore also apply to the manufacture o f 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 o f 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 o f 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 THKP 0015757 Source http //industrydocuments library ucsf edu/tobacco/docs/grvbO 104 26 ASBESTOS of dust should be reduced by changing material-handling methods, work practices, and cleanup procedures. Local exhaust systems should be used Tor dust collection at points or 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-clcaning 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. Principles o f Control 27 In spite o f 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. 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 mensu ring 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;1*''5 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.1'64*13* 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-cieaning equipment as related lo fibers of different sizes. THKP 0015758 \ Source http //industrydocuments library ucst edu/tobacco/docs/grvb0104 7 Research Needs 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- j thelioma are needed to determine whether the incidence has been i increasing and to determine the current pattern o f distribution. A large series of routine autopsies should be studied to determine whether causes of death can be related to amounts o f asbestos in the lungs and other organs. All the above are urgent if a range o f safe exposure is to be established with confidence. Two recent reports15'" 7 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 o f necessary controls. Investigations along the following lines should be given high priority. Study of the mechanism of action o f 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. El is especially important that the role o f fibers smaller than the LM size range be clarified. Methods of sampling, identifying, and quantitating airborne asbes tos need continued development. Coordination with studies in 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 THKP 0015759 Source htlp //industrydocuments library ucst edu/tobacco/docs/grvbO 104 Conclusions and Recommendations n * 8 C onclusions and Recom mendations 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 flbrosis o f 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 fibera and diffuse malignant mcsotheliomasof the~ pleura and peritoneum is substantial, but evidence o f such a relation^"* with other tumors is inconclusive. Although tho different types o f asbestos differ in some of their biologic effects, no type can be regarded as free of hazard. The hypothesis that asbestos fibers act as co factors 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 30 persons with no occupational contact may have inhaled and retained asbestos. Proof has come in some areas with positive identification of chrysolite asbestos fibers. Analyses of community air for asbestos have been to o limited to detine the sources, concentrations, and distri bution o f 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 im portant question in the case o f persons with nonoccupational exposures to asbestos is whether there is an increased risk o f malignancies. Industrial experience indicates that there is no likeli hood o f 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 o f an asbestos source; and even there, the actual risk is poorly defined. The appearance o f a gradient o f effect in such groups, however, suggests that there are levels o f inhaled asbestos without detectable risk. It is not known what range o f 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 o f 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 inhatation o f 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. THKP 0015760 I Souice hUp //industrydocuments library ucsf edu/tobacco/docs/grvb0104 I R eferences 33 t < | \ References 1. Alcocer, A. E., J. Murchio. and P. K. Mueller. Asbestos Content of Some Urban Air Samples. AKIIL Report 90 (revised). Berkeley State of California Department of Public Health, 1970. 12 pp. 2. American Conference of Governmental Industrial Hygienists. Threshold Until Values of Airborne Contaminants and Intended Changes Adopted by ACGfH for 1970. Cincinnati: American Conference of Governmental Industrial Hygienist*, 1970.27 pp. 3. Anvilvel, U, and W. M. Thuribeck. The incidence of asbestos bodies in the limp at random necroepsfes in Montreal. Can. Med. Assoc. J. 95:11791182. 1966. 4. AllSpach, M, Sind Pleuravcikalkungcn pathognoraoni*ch fur eine Asbestos? Int. Arch. Gewerbepath. Gewerbchyg. 19.108-120, 1962. 5. Anton, H. C. Multiple pleural plaques. Brit, j . Radiol 40:685-490, 1967. 6. Anton, H, C. Multiple pleural plaques. Part II. Brit. J. Radiol. 41;341-348, 1969. 7. Asbestos Industry Regulations, 1931, Statutory Rules and Orders, 1931, No. 1140. London: H. M. Stationery Office, 1931.4 pp. 8. Ashcroft, T. Asbestos bodies in routine necropsies on Tyneside: A patho logical and social study. Brit. Med 1.1:614-618,1966. 9. Ashcroft, T., and A. G. Htppleston. Mesothelioma and asbestos on Tyneside: A pathological and social study, pp, 177-179. In H. A. Shapiro, Ed. Pneumoconiosis. Proceedings of the International Conference Johannes burg. Cape Town; Oxford University Press, 1970* 10. Biker, J. L., WTC, Cooper, and D, F. Fowler. Fibrous lined air transmission 32 systems: An assessment of their environmental effects. Arch. Esviron. Health, (in press) I I . Bonier G. M., J. S. Fauldi, end M. J. Stewart. Occupational cancer of the urinary bladder in dyestuffs operatives and of the lung in aabeat* textile worker and iron-ore miners. A n n . J, Clin. Path. 25:126-134, 1935. 12. Boraw, M., A. Conston, L. L. Urornese, and N. Schalet. Mesothdloms and its association with asbestosia. JA .M A . 201:587-591,1967. 13. Braun, D. C,, and T. D. Truan. An epidemiological study of lung cancer in asbestos miners. A.M.A. Arch. Ind. Health 17:634-653,1958. 14. British Occupational Hygiene Society. Hygiene standards for ctnyaotile asbestos dust. Ann. Occup. Hyg. 11:47-69, 1968. 15. Buchanan, W. D. Asbestosia and primary intxathoraeje neoplasia*. Ann. K Y. Acad. Sci. 132:507-518, 1965. 16. Byrom, J. C., A. A. Hodgson, and S. Holmes. A dust survey carded out in buildings incorporating asbestos-based material in their construction. Ann. Occup, Hyg. 12:141-145.1969. 17. Cauna, D,, R. S. Totten, and P. Gross. Asbestos bodies in human lungs at autopsy. J.A.M-A. 192:371-373, I96S. 18. Churg, J., S. H. Rosen and S. Moolten. Histological characteristics o f mesothelioma associated with asbestos. Ann. N. Y. Acad. Set. 132:614-622, 1965. 19. Cooke, W. E. Asbestos dust and the curious bodies found in ashestoais. Brit. Med. J. 2:578-580, 1929. 20. Cooke, V. B. Fibrosis of the lungs dee to (he inhalation of asbestos dust. Brit. Med. J. 2:147, 1924. 21. Cooke, W.B. Pulmonary asbestos. Bnt. Med. J. 2:1024-1025, 1927, 22. Cooper, W. C. Asbestos as a hazard to health. Arch. Environ. Health 15:285-290,1967. 23. Cooper, W. C., and i. L. Balzer. Evaluation and control of asbestos ex posures in the insulating trade. Presented a t the 2nd International Con ference on Biological Effects of Asbestos, Dresden, April 22-25,196$. 24. Cordova, J, F,, H. Tetluk. and K. P. Xnudtion. Asbestos and carcinoma of the Lung. Cancer 15:1181-1187,1962. 25. Crallcy, L. J., V. C. Cooper, W. S. Lainhart, and M. C. Brown. Research on herith effects of asbestos. J. Occup, Med, 10:38-4!, 1968, 26. Cfalley, L. J., R, G. Keenan, R. E. Kupel, R, E. Kinser, and J. R, Lynch. Characterization and solubility of metals associated with asbestos fiber*. Amer. Ind. Hyg. Assoc. J. 29:569-573, 1968. 27. Cralley, L. J., R.C. Keenan, and J. R. Lynch. Exposure to metals in the manufacture of asbestos textile products, Amer. Ind. Hyg. 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Environ. * Health 17:71-76, 1968. 34* Duon, 1, C., Jr,, and 1. M. Weir. Cancer experience of several occupational groups followed prospectively- Amer. J. Public Health 55:1367*1375, 1968. 35. Edwards, G* H.t and 7. R, Lynch. The method used by the (J. S. Public Health Service for enumeration of asbestos dust on membrane filters. Ann, Occup.Hyg. 11:1-6, 1968. 36. Elmes, P. C., W, T . E. McCaughcy, and O. L. Wade. Diffuse mesothelioma | of the pleura and asbestos. Brit. Med. J. 1;350-353,1965. j 37. Elmei, P. C., and O. L. Wade. Relationship between exposure to asbestos I and pleural malignancy in Belfast. Ann. N. Y. Acd. Sci 132:549-557, j 1965. { 38. Elwood, P. C-, and A. L. Cochrane. A follow-up study of workers from an 8 asbestos factory. Brit. J. Ind. Med. 21:304-307,1964. j 39. Enlcriine.F. E. Mortality among asbestos products workers in the United | States. Ann. N. Y. Acad. Sci. 132:156-165.196$. 40. Enleriine, P, E., and M. A. Kendrick. 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