W V 9 f W W if , ll| i i PUji wupB U m An Information Resource U.S. Department of Health, Education, and Welfare ; -,V.:NI <, f':fi«AR0U. !?;c. SHORTHAND REPORTERS Public Health Service National Institutes of Health I DU 035374 • DUP 0931637 BMaSawaaM,lali&i asbestos: An Information Resource Prevention Branch Division of Cancer Control and Rehabilitation Richard "J. Levine, M.D. Editor National Cancer Institute Bethesda, Maryland .. u.'s. Department of Health, Education, and Welfare Public Health Service National Institutes of Health DHEW Publication Number (NIH) 79-1681 May 1978 DU 035375 DUP 0931638 "■■ypusaitim flaijwwp' ’ awSsiEsgigr- ACKNOWLEDGMENTS SRI International (formerly Stanford Research Institute) acknowledges the invaluable advice and assistance of the following individuals during the preparation of this monograph on asbestos: Henry Anderson, M.D. Department of Environmental Medicine Mount Sinai School of Medicine New -York, New York Robert E. Baumann, Ph.D. Professor of Engineering Iowa State University Ames, Iowa Arnold Brown, M.D., Chairman Department of Pathology and Anatomy The Mayo Clinic Rochester, Minnesota Jean Spencer Felton, M.D. Long Beach Naval Shipyard Long Beach, California Graham W. Gibbs, Ph.D., Director Occupational Health and Safety Unit Institute for Mineral Industry Research McGill University Montreal, Quebec, Canada Philippe Shubik, M.D., Director Eppley Institute for Research in Cancer Omaha, Nebraska Acknowledged also are the many contributions from the staffs of SRI's Center for Occupational and Environmental Safety and Health, Center for Resource and Environmental Systems Studies, Biorganic Chemical Department, Minerals and Metals Center, and Center for Research on Stress and Health. DU 035376 DUP 0931639 ■tr.' A iUMiaiMliiMH Mm CONTENTS LIST OF ILLUSTRATIONS..................................................................................................... ix LIST OF TABLES.................................................................................................................... ix FOREWORD.................................................................................................................................. xi ACKNOWLEDGMENTS.................................................................................................................... xiii I INTRODUCTION ............................................................................................................... 1 II PRODUCTION AND USE OF ASBESTOS FIBERS AND PRODUCTS 9 U.S. Consumption of Asbestos Fibers ..................................................... U.S. Production and Producers of Asbestos Fibers ......................... End Uses of Asbestos.............................................................................. Handling of Fiber and Products During Their Production ... 9 11 13 15 Mining.......................................................................................... 13 Milling.................................................................................. 17 Transportation ....................................... ........... Manufacture of Asbestos-Containing Products ...... III BIOLOGICAL EFFECTS OF ASBESTOSFIBERS ...................................... Disposition of Fibers in the Body................................................ ............................. 21 21 Inhaled Asbestos ............................................ ......... Ingested Asbestos ................................. Injected Asbestos ....... ...................................................... "Asbestos Bodies".............................................................. Carcinogenic Effects--Human Studies 18 19 21 22 23 23 ..... 23 Evidence of Lung Cancer......................................................................... Evidence of Mesothelioma.................................................................... Laryngeal Cancer.............................................................. Digestive System Cancer................................. Other Cancers................................................................................................. Association of Effects with Fiber Type........................ . . Dose-Response Relationship ............................................................... The Cancer Latency Period ..................................................... ... Incidence of Cancer and Age at First Exposure to Asbestos ............ ....................................... Smoking and Asbestos-Related Cancer ............................................ Cancer from Incidental Occupational Exposure .................... Disease in Workers' Households ...................................................... Cancer in the Neighborhood of Asbestos Facilities . . . 24 25 25 26 26 iii DUP 0931640 DU 035377 Ill BIOLOGICAL EFFECTS OF ASBESTOS FIBERS (Continued) Carcinogenic Effects--Animal Studies ..................................................... Noncarcinogenic Effects of Asbestos ..................................................... Asbestosis............................................................................................................ Asbestos Pleural Effusion ......................... . .................................. Pleural Calcification, Diffuse Fibrosis, and Plaques....................................................................................................... Asbestos Warts............................................................................................. Animal Studies—Evidence of Noncarcinogenic Effects . . 32 34 34 37 37 38 38 IV OCCUPATIONAL EXPOSURES ........................................................................................... Exposures in Mining and Milling................................................ .... Exposures in the Asbestos Products Industries .............................. Friction Products ........................................... • Asbestos Paper.......................................................................... Asbestos-Reinforced Plastics ........................ . ......................... Asbestos-Cement Pipe and Sheet.................................................... Floor Tile.................................................................................................. Asbestos Textiles . ......................................................................................... Exposures in the Utilization of Asbestos-Containing Products Insulation Trades............................................................................... Brake and Clutch Repair .......... ............................... Installation of Floor Tile, Roofing, and Siding .... Use of Spackling, Patching, and Taping Compounds .... Wearing Asbestos Garments ......... ............................... V NONOCCUPATIONAL EMISSIONS AND EXPOSURES 41 42 42 43 45 45 45 46 46 47 47 48 48 49 49 .................................................. 51 Asbestos Emissions from Natural Sources .................................................. Asbestos Emissions from Human-Created Sources .................................... Redistribution and Fate of Asbestos in the Environment ... 51 51 52 Redistribution by Air ................................................................ Redistribution by Water ............................................................................... The Ultimate Fate of Asbestos Fibers.............................................. Exposure to Airborne Asbestos ............................................ ..... Exposure from Ambient Air........................................................... Exposures from Asbestos Mining, Milling, and Product Manufacture ..... ........................ .... Exposure from Transportation of Materials Containing Asbestos .......................................................... .... Exposure from Asbestos Manufactured Products ..... Exposures from Disposal of Asbestos Products and Wastes............................................................................ Exposures of Asbestos Workers' Families ......................... •• Exposure to Asbestos in Drinking Water ..... ......................... Exposure to Asbestos in Foods and Drugs ............................................ iv 52 54 54 55 55 56 57 58 61 52 52 64 DUP 0931641 DU 035378 VI CONTROL OF THE ASBESTOS HAZARD—PHYSICAL CONTROL ..................... 67 Engineering Measures ....................................................................................... 67 Enclosure...................................................................................................... Exhaust Ventilation .............................................................................. Isolation...................................................................................................... Plant Design............................................................................................ Treatment of Asbestos ......................................................................... Substitution ............................................................................................ 68 68 69 70 72 72 Administrative Measures .............................................................................. 75 Limiting the Number of Employees Exposed ......................... Limiting the Duration of Exposure for Any Given Person...................................................................................................... Restrictions on Smoking and Eating ....................................... Smoking Cessation Programs .......................................................... 75 75 76 77 Work Practices, Including Housekeeping and Use of Personal Protective Equipment .................................................................................. 77 Housekeeping ............................................................................................ Personal Protective Equipment ..................................................... 78 78 Control in Specific Manufacturing and Consuming Indus­ tries .................................................................................................................... Asbestos Textile Production .......................................................... Asbestos Paper ....................................................................................... Asbestos-Cement Pipe and Sheet................................................. Automotive Brake and Clutch Repair ....................................... Construction............................................................................................ ' Demolition and Rip-out of Asbestos-Containing Insulation............................................................................................ Control of Emissions to the General Environment 80 80 81 81 81 81 82 .................... 83 Air Pollution Control ......................................................................... Water Pollution Control .................................................................... Waste Water Treatment Processes ................................................. Control of Asbestos Fibers in Potable Water Supplies................................................................................................. Waste Disposal............................................................................. ..... • Identification ....................................................................................... Separation................................................................................................. Secure Transport .................................................................................. Secure Ultimate Disposal ............................................................... 83 83 84 85 86 86 87 87 87 Control During Transportation DUP 0931642 DU 035379 ymwiiiMiaiw atiinfc ;■ tfd3 VII CONTROL OF THE ASBESTOS HAZARD—MEDICAL MANAGEMENT .... 89 Composition of the Workforce.................................................................... 89 Lung Cancer................................................................................................. Mesothelioma ............................................................................................ Asbestos is................................................................................................. 90 90 92 Early Detection and Treatment of Asbestos-Related Diseases............................................................................................................... 92 Lung Cancer................................................................................................. Laryngeal Cancer .................................................................................. Mesothelioma ............................................................................................ Cancers of the Alimentary Tract ................................................. Asbestos is................................................................................................. 92 96 96 96 97 CONTROL OF THE ASBESTOSHAZARD—EDUCATION.................................... 99 VIII Goals of Education ............................................................................................ Modes of Education—The Written and the Spoken Word . . . The Educators ...................................................................................................... Physicians................................................................................................. Nurses.......................................................................................................... Health Educators (Communication Specialists) .... Industrial Hygienists ......................................................................... Union Health and Safety Specialists ....................................... Industrial Safety and Other Training Specialists . . Science/Medical Writers .................................................................... Target Groups for Education ... ............................. ..... 101 101 102 102 102 102 103 103 Managerial and Supervisory Personnel ................................... 103 Workers in the Asbestos, as Well as Other, Trades . . 104 Retirees and Other Former Workers ............................................ 104 Workers' Families .............................................................................. 104 Occupational Health Professionals.......................................................104 Assessment of Education's Value .......................................................... 105 APPENDICES A ASBESTOS-RELATED AND -ASSOCIATED MINERALS ....................................... B FEDERAL REGULATIONS OF OCCUPATIONAL EXPOSURE C MONITORING AND MEASURING ASBESTOS CONTAMINATION ......................... D ANIMAL STUDIES RELATED TO CARCINOGENIC EFFECTS OF FIBERS ............................................................................................................... E AIR AND DRINKING WATER ASBESTOS CONCENTRATIONS FROM SOME PUBLISHED SOURCES .................................................................... vi A-l .............................. DUP 0931643 DU 035380 iaMHMls• Httr,-iittggife^vgviAi*- - 'A-mm--* i It-.fqivBgjjap -1;.--.^:-l?iimmmmm '^'dastc ,,KV V *** M •." B*tam F SMOKING CESSATION PROGRAMS . . G SOURCES OF EDUCATIONAL MATERIALS H REFERENCES ............................................ : r .; > I : vii DU 035381 DUP 0931644 iil__ ■.. >-i»asai. i£zmvmiM.±kmi ami « « ; * *v'f t *■ > \\.V„ ** wAlhliilftl hitom&ttttSkkmkiiA ILLUSTRATIONS 1 2 3 Distribution of Ultrabasic and Metamorphic Rock Formations in the United States ............................................................... 4 Disposals and Emissions of Asbestos from Asbestos Production, Manufacturing, and Consumption in the United States .......................................................................................................... 53 Locker Room, Shower Arrangement ............................................................... 71 TABLES 1 Apparent U.S. Consumption of Asbestos Fiber .................................. 10 2 Operating and Nonoperating Asbestos Mines and Mills in the United States....................................................................................... 12 3 Selected Asbestos Products and Their End Uses .............................. 14 4 Major U.S. End Uses of Asbestos Fiber, By Type &Grade . 16 5 Deaths from Respiratory Cancer by Cumulative Dust Exposure.................................................................................................................... 28 Exposure to Airborne Asbestos in Selected Asbestos Product Manufacturing Industries .......................................................... 44 Medical Examinations for Asbestos-Exposed Workers .................... 93 6 7 . DU 035382 ix DUP 0931645 FOREWORD There is increasing realization that asbestos may be present across the entire spectrum of human exposure--in our air, water, food, drugs, cosmetics; in our homes and, most importantly, in our workplaces. There is also developing awareness that several types of cancer may be the con­ sequence of exposure to this material, especially for certain segments of the population. Recognizing our responsibility to transfer information to the scien­ tific community and the public, the Division of Cancer Control and Rehabil­ itation, National Cancer Institute, is making available this document on asbestos and cancer. Several of the more important objectives of the document are to: (1) present both current and historical evidence of the carcinogenic potential of asbestos; (2) examine potential exposure of the public; (3) describe current intervention and control technology; and (4) discuss the possible prevention roles of various individuals and groups in the community. Dissemination of information is a fundamental prerequisite to the formulation and implementation of action programs for effective cancer control and prevention at the federal, state, and local levels. This document represents work of individuals in many different research fields, and the contributions of all these individuals are acknowledged. The comments of many scientists in the federal government and private sector are greatly appreciated. Particular thanks must be given to Dr. Herman Kraybill and the Interagency Collaborative Group on Environmental Carcinogenesis for their comments and to Drs. Irving Selikoff, Mearl Stanton, Paul Kotin, Elizabeth K. Weisburger, and Kenneth Bridbord for their review and suggestions. Dr. Winfred F. Cancer Institute. Malone served as Project Officer for the National f\ A /up Diane J. Fink, M.D., Director Division of Cancer Control and Rehabilitation National Cancer Institute X)\3 035383 xi DUP 0931646 :HwSa»s%fc:?...^.. sa-ijjgg ACKNOWLEDGMENTS SRI International (formerly Stanford Research Institute) acknowledges the invaluable advice and assistance of the following individuals during the preparation of this monograph on asbestos: Henry Anderson, M.D. - Department of Environmental Medicine Mount Sinai School of Medicine New York, New York Robert E. Baumann, Ph.D. Professor of Engineering Iowa State University Ames, Iowa Arnold Brown, M.D., Chairman Department of Pathology and Anatomy The Mayo Clinic Rochester, Minnesota Jean Spencer Felton, M.D. Long Beach Naval Shipyard Long Beach, California Graham W. Gibbs, Ph.D., Director Occupational Health and Safety Unit Institute for Mineral Industry Research McGill University Montreal, Quebec, Canada Philippe Shubik, M.D., Director Eppley Institute for Research in Cancer Omaha, Nebraska Acknowledged also are the many contributions from the staffs of SRI's Center for Occupational and Environmental Safety and Health, Center for Resource and Environmental Systems Studies, Biorganic Chemical Department, Minerals and Metals Center, and Center for Research on Stress and Health. DU 035384 xiii DUP 0931647 ..areaaiiau ..awjafei -^WtiaiBftiljMgi Chapter I INTRODUCTION Because of their unique combination of resistance to heat and chem­ ical attack, high tensile strength, and flexibility, fibrous asbestos minerals have long been used by man. The early Greek geographer, Pausanias, speaks of golden lamps made about 430 B.C. with incombust­ ible wicks of "Carpathian flax." The Romans used asbestos as cremation clothes to conserve the ashes of deceased persons of rank. The French emperor, Charlemagne, had a tablecloth of asbestos and is reputed to have impressed his enemies by passing it through fire to clean it. . Today, asbestos is found in thousands of commercial products including heat-resistant textiles, reinforced cement, special filters for industrial chemicals, thermal insulation, floor tiles, gaskets, and brake linings. More than 725,000 metric tons (800,000 short tons) of asbestos have been consumed in the United States alone in producing these products in each of.:sever^l recent years. As a consequence of man’s utilization of asbestos, coupled with the natural occurrence of the min­ eral, asbestos fibers are found in the air we breathe, the food we eat, and the water we drink. A Hazard to Human Health The fact that asbestos is a hazard to man’s health was recognized quite early. In the first century, both Pliny the Elder, the Roman naturalist, and Strabo, the Greek geographer, wrote of a sickness of the lungs in slaves whose occupation was the weaving of asbestos into cloth. However, the association of asbestos with chronic respiratory disease had to be rediscovered in the modern era. A series of case reports was followed by an epidemiologic study published in London in 1930,1- 52 years after large-scale raining of asbestos had begun with the opening of a mine at Thetford, Quebec, Canada. The cancer-producing potential of asbestos was not established until 1949, when a report was published describing an excess of cancer of the lung and pleura among individuals dying from asbestosis.^ It is now clear that among asbestos workers, there is, in addition to the risk of asbestos is, a greatly increased risk of death from lung cancer and from pleural and peritoneal mesothelioma, malignancies that are seldom found in the general population.^Moreover, asbestos has been linked with gastro-intestinal, oropharyngeal, and laryngeal cancer According to the U.S. Public Health Service, one million persons now living in the United States either work or have worked in the DUP 0931648 DU 035385 l • ■jy8M'g'»aBL asbestos product manufacturing industry. This figure does not include those employed in mining and milling asbestos; those whose work may involve installation, modification, or repair of asbestos products; persons exposed indirectly to asbestos in the course of their work such as at shipyards or in the construction industry; persons living in the neighborhood of an asbestos product factory; or consumer users of asbestos materials. What is "Asbestos?" To the mineralogist, asbestos is the generic name for a group of naturally occurring hydrated mineral silicates of the amphibole or serpentine series that are characterized by fibers or bundles of fine single crystal fibrils. Naturally occurring asbestos fibers typically have length-to-width ratios of the order of 100 and higher. Included in this definition are the following minerals: • Chrysotile • Crocidolite • Amos ice, and • The fibrous varieties of anthophyllite, tremolite, and actinolite.* All of these minerals may occur in a nonfibrous form, in which case they are not classified as asbestos. Commercially, chrysotile is the form of asbestos used most. Crocidolite, amosite, and anthophyllite also have some commercial significance. It is important to note that identification of asbestos fibers is relatively simple with macroscopic samples that clearly show the fibrous nature and other unique characteristics of these minerals. Positive identification is based on morphology, crystallographic structure, color, hardness, optical properties, and appearance. However, in the case of microscopic samples, positive identification becomes increasingly difficult, even when special microanalytical techniques are used." The identification of asbestos is complex because many of the min­ erals that are chemically almost identical to different varieties of asbestos (e.g., grunerite to amosite, serpentine to chrysotile) exhibit Crocidolite, amosite, anthophyllite, tremolite, and actinolite are derived from the amphibole series and may be referred to as "amphiboles." 2 DUP 0931649 DU 035386 WMWBI;-• IF :i—WiaaiiRt«fTi. ■■ ■ atBafrn»Cr~i -Ltsiriga—HMLiMKaswiaiBsam.:' perfect prismatic cleavage (the ability to break along well-defined crystallographic planes), so that physical degradation often leads to the formation of minute cleavage fragments that are chemically as well as physically indistinguishable from asbestos fibers. Recent compre­ hensive studies at the U.S. Bureau of Mines have concluded that there is currently no absolute way to distinguish between finely divided asbestos and certain other minerals of similar composition.6 Some minerals other than asbestos chat may exhibit fibrous structure are listed in Appen­ dix A. On the other hand, recent biological studies suggest that, in terms of carcinogenic activity, mineral shape and size may be more important than chemical nature.^ The question of asbestos carcino­ genicity can, therefore, be viewed as part of a broader issue—i.e., tissue modification caused by mineral fibers. Occurrence of Asbestos All forms of asbestos develop through several stages of geologic processes (paragenesis) from parent rocks that are transformed into asbestos. Parent rocks of asbestos minerals include basic constituents normally found in ultramafic, dolomitic, or limestone rocks. Transfor­ mation may occur under localized conditions of temperature and pressure which lead to recrystallization of other in-situ minerals (metamorphism). It may occur as a result of the action of hot mineral solutions that can dissolve or otherwise alter some minerals to'form others (hydrother­ mal processes). In all of the commercial asbestos deposits, the geologic conditions have been favorable to the development of fibers of sufficient quality and concentration to warrant their extraction. (The same conditions may operate in other mineral deposits but yield asbestos fibers that are too disseminated or scarce to be of commercial interest.) Minerals and rocks that can contain asbestos are listed in Appen­ dix A. A favorable mineral association is not a sufficient condition for the formation of asbestos—it will form only if special structural and other geologic conditions are met. If asbestos presence is, in fact, established, the minerals and rocks listed in Appendix A would be significant sources of contamination for humans, since they include important raw materials for industry and are rained in commercial quan­ tities, worldwide. The areas of the United Stated having basic geologic constituents associated with the formation of asbestos are shown in Figure 1. Again, this graphic does not necessarily depict actual asbestos occurrence but, 3 DUP 0931650 X>\J 035387 CO UJ I< hCO Q UJ H UJ X z co z o i- < S oc o u. * o o co g x 0. CE o 2 < IUJ 5 Q Z < CO < < cr H CD D CO CO Q UJ CE X a DUP 0931651 WMtBfc -MEtr ■ ji'Sti la—BMM. ~ Wl’iWpp. ■ ^3-1 liiSI' ■ u n rm u uuui<. fU H M A [ lUNb IN THfc UNITED STATES rather, is an overview of the areas that are more Likely than others to provide the geologic setting associated with formation of asbestos. : i i ! 1 Although deposits of asbestos may be found throughout the United States, asbestos is commercially mined and milled at only five loca­ tions, in the states of California, Arizona, and Vermont. (Most of the asbestos consumed in the United States is imported, nearly all of it from Canada.) In addition to commercial mining and milling of asbestos, human-created occurrences of asbestos fiber may result from the mining and milling of mineral ores associated with asbestos; from the inadver­ tent disturbance of asbestos deposits by activities such as farming and road building; from the transportation of asbestos ore, milled fiber, products, and wastes; from the manufacture, use, repair, and demolition of asbestos-containing products; and from the disposal of asbestos wastes. All are discussed in succeeding chapters of this monograph. Regulation of Asbestos-Fiber Emissions A recommendation for limiting exposure to asbestos in U.S. industry was made in 1938 by the U.S. Public Health Service.^ The recommended limit, an airborne concentration of less than 5 million particles per cubic foot, was formally recognized in 1964—as a guideline issued by the Bureau of Labor Standards. No legal regulations were established until passage of the Occupational Safety and Health Act of 1970 and establishment of the Occupational Safety and Health Administration (OSHA). Occupational Exposure OSHA regulations apply directly to all private employers, including federal government contractors, but not to federal, state, or local government agencies. Federal agencies are required to establish their own occupational safety and health programs consistent with the stand­ ards of the Act and subsequent OSHA regulations. States are encouraged by the Act to develop programs and regulations, for private employers, chat are at lease as effective as OSHA regulations and can, under these conditions, assume responsibility for enforcing standards—at the time of this writing, 24 states have programs of their own.9 The current OSHA limit on occupational exposure to asbestos fibers is an 8-hour time-weighted average of 2 fibers per milliliter, no longer than 5 micrometers, with a length-to-width ratio of at least 3:1, detected by a method using phase-contrast (optical) microscopy. The permissible levels of occupational exposure to asbestos con­ tained in all federal regulations (and one proposal) are summarized in tabular form in Appendix B. Also, the provisions of these regula­ tions for method of compliance, monitoring, medical surveillance, edu­ cation, and the keeping of records are summarized there. DU 035389 5 DUP 0931652 Emissions to Air and Water, Disposal of Solid Waste, Transportation Anational air emission standard for asbestos, first published in 1-973, requires either the institution of specified air-cleaning meth­ ods or else no visible emissions (except water) to be released to the outside air. The standard applies to the milling of asbestos (but not to adjacent storage depots); manufacturing or processing of specified products; renovating or demolishing certain buildings (but not ships) containing more than a specified amount of friable asbestos insulation; and to wastes containing commercial asbestos or products of asbestos mining and milling. Friable or spray-on insulating materials, except when applied to equipment or machinery, must contain no commercial asbestos; however, spray-on paints, decorative materials, and weather­ proofing are not regulated. Under the terms of guidelines and standards promulgated in 1974 and 1975, certain asbestos-manufacturing operations were to achieve, by July 1, 1977, wastewater effluent limitations requiring application of the best practicable control technology currently available; and by July 1, 1983, except for operations involving solvent recovery, there is to be no discharge of wastewater pollutants to navigable waters.H Federal agencies are directed by two Executive Orders to monitor, evaluate, and control their activities so as to protect and enhance the quality of the environment and to conform to air and water quality standards of the Clean Air Act and the Federal Water Pollution Control Act. Food, Drugs, Consumer Products The Food and Drug Administration (FDA) has reviewed several com­ mercial practices that may result in asbestos contamination of food and drugs and, in January of 1976, revoked approval for use in foods of (sodium chloride (salt) produced by the electrolytic diaphragm process.^ In the absence of more-reliable data on background concentrations of asbestos in water and the contribution of asbestos filters to levels of asbestos found in ingestible products, the FDA has not regulated the use of asbestos filters for filtering edible foods, beverages, and nonparenteral drugs.^3 The agency has, however, enacted regulations to limit asbestos and other fibrous materials in parenteral drugs.^ The FDA has approved (1) the use of asbestos as a component of various types of food-contact articles in which contamination of food is not DU 035390 6 DUP 0931653 m '■ t ■• - j- •- **4*»*i-4 * t=- s-iSI181i;Hat r - '» at a&BE3W—w. ~9mnwattawali*: likely co occur, and (2) the use of talc, in which asbestos is a possible impurity, in cosmetics.* The Consumer Product Safety Commission has banned general-use garments containing asbestos. The use of asbestos in special garments such as fire-fighting suits is permitted, but only if they are con­ structed so that asbestos fibers will not become airborne under normal conditions of use. 161" Constraints on Monitoring and Measuring Asbestos Levels As will be brought out later in this monograph, it is simply not known what attributes of asbestos it is that constitute a health hazard—size, shape, mass, type etc.—nor is it known what amount is hazardous or over what period of time. The U.S. federal occupational standards are, perforce, an attempt to optimize what is known about the health hazard with the technical and economic practicalities of measuring the substance. For example, by using phase-contrast optical microscopy, rather than the higher resolution electron microscopy, it is not possible to count all the fibers and not always possible to even distinguish between asbestos and other fibers (as noted previously); electron microscopy, on the other hand, is time-consuming and expen­ sive. The difficulties of measuring and identifying are of such pro­ portions that there are extreme variations in the measurement of a sample, both within a laboratory and among laboratories. As a consequence, the reader should always bear in mind the pos­ sible grossness of measurements referred to throughout this document, even when they are expressed in terms that bespeak of precision—e.g., the decimal point. At the same time, the fact remains that asbestos is a human carcinogen and that, as such, is a suitable subject for treat­ ment in this document, the prime purpose of which is helping man control cancer. The constraint on monitoring and measuring asbestos is such, nevertheless, that it is the subject of more extensive treatment in Appendix C of this- document. Talc is listed as a "generally recognized as safe" (GRAS) substance for use in paper, paperboard, and cotton food packaging materials; as an anticaking agent for forms used in molding various food shapes and in chewing gum base; and to coat polished nonenriched rice, as a free­ flow agent, and as a vehicle for enrichment formulas.^ An FDA ruling on talc as a direct food or drug additive has been deferred until an acceptable analytic method can be developed.^ Full attainment of the desired result of regulation inevitably requires adequate means of enforcement. Legal powers of enforcement as well as de facto enforcement practices differ widely among the various govern­ ment agencies having statutory authority. See Reference 17 for an ex­ ample of divergence of enforcement practice in just one regulatory agency from what is required by law. DUP 0931654 7 DU 035391 ■■ • • ~i^^:#'-s~~-i - s ' • js:w^ -—-• ? * *•«*■*'* ** -'WWWHWI.:ig3i?7*^ MBBk •kirfrkk Summarized in the next four chapters are: production and uses of asbestos fiber and fiber-containing products; the biological effects, carcinogenic and noncarcinogenic, of exposure to asbestos; occupational and nonoccupational exposures and exposure levels. In the final three chapters, strategies and programs for the control of the health hazard represented by human exposure to asbestos are set forth. DU 035392 8 DUP 0931655 Chapter II PRODUCTION AND USE OF ASBESTOS FIBERS AND PRODUCTS Although some exposure of humans to asbestos fibers in air and water is always possible as a result of the weathering of asbestoscontaining rock, it is man's large-scale commercialization of the mineral that has engendered greater health risk. In this chapter, the major facets of such commercialization in the United States are reviewed— consumption and production volumes; categories of manufactured goods; and processes for mining, milling, transporting, and manufacturing asbestos and asbestos-containing produces.* U.S. Consumption of Asbestos Fibers During the five years ending in 1975 the amount of asbestos fiber apparently consumed'*' in the United States averaged some 800,000 tons annually, although between 1974 and 1975 apparent consumption declined 27% from 856,000 to 629,000 tons.f It is expected that consumption will have recovered to about 820,000 tons in 1976. The sharp decline between 1974 and 1975 reflects not only a market affected by a sharp recession, but also a substantial interruption of supply associated with work stoppages, a landslide at a major mine, and a serious fire at an asbestos mill in Quebec, Canada. The estimated U.S. apparent consumption of asbestos fiber for the 1971-75 period is shown in Table 1. It can be seen in Table 1 that most of the asbestos fiber used in the United States is imported (about 90%). Nearly all of this imported asbestos is chrysotile fiber that comes from Canada (96.5% in 1974). The This chapter includes information obtained through a special survey of industry carried out in the Fall of 1976 by the Mineral and Metals Center, SRI International. ^""Apparent" consumption—i.e., production plus imports, plus net ship­ ments from government stockpiles if any, less exports. Apparent con­ sumption figures do not take into account any changes in inventory levels of manufacturers and therefore differ from "actual" consumption figures (an example of which is found in Table 4 in this chapter). Volumes in this chapter are expressed in short tons (2,000 pounds) in accordance with industry practice. DU 035393 9 DUP 0931656 Table 1 APPARENT U.S. CONSUMPTION OF ASBESTOS FIBER (Thousands of Short Tons) 1971 19 72 1973 1974 1975 Production 131 132 150 113 100 Imports 681 736 792 776 575 S tockpile releases 10 13 7 29 4 Exports 54 59 66 62 50 768 822 883 856 629 Apparent consumption Source: U.S. Bureau of Mines, Commodity Data Summaries, 1976. Republic of South Africa accounted for some 3Z of the U.S. imports in 1974 (crocidolite and amosite fibers), and a number of countries sup­ plied the remainder. A substantial portion of Canadian output is pro­ duced there by U.S. companies that manufacture asbestos products. It should be noted that in addition to importing both crude and milled fibers, the United States imports products manufactured from asbestos. In 1974, for example, the value of products exported from Canada to the United States was as shown below:^ Canadian Dollars (millions) Brake linings and clutch facings $0.9 Building materials 3.7 Other products 3.2 Total $7.8 However, the value of imported products is not large compared with U.S. domestic shipments, which, for example, totalled $742.6 million in 1972.2 The U.S. Bureau of Mines has estimated that U.S. demand for asbes­ tos in the year 2000 will range between 1.0 million and 1.8 million cons.^ It is also possible, however, that substitution of other DU 035394 10 DUP 0931657 wm mmtMWKt '3 MBiiagHm materials for asbestos could result in a lower level of demand. substitution could occur for a number of reasons such as: • More rapid price increases for asbestos than for its competitive products. • Health and safety considerations. • Lack of availability (an industry expert has estimated that by 1980 supply could fall short of potential world demand by about 500,000 tons, or about 10% of world demand). * IrWBW 1 This U.S. Production and Producers of Asbestos Fibers The volume" and value at the mines of asbestos fiber production in the United States during recent years is shown in the tabulation that follows: Production (Thousands of Short Tons) Value Per Ton 1971 131 $ 93 $12.2 1972 132 102 13.5 1973 150 121 18.2 1974 113 158 17.9 1975 100 182 18.2 Total Value (Millions of Dollars) decline in production volume from the all-time peak of 150,1 in 1973 resulted primarily from the closing or reduction in output of several mines such as GAF Corporation's Lowell Vermont mine (acquired by the Vermont Asbestos Group), Pacific Asbestos Corporation's mine near Copperopolis, California (later reopened by Calaveras Asbestos Limited), and the Christie mine of' Coalinga Asbestos Company, Inc., at Coalinga, California (a 15,000-ton-per-year mine that has remained closed). The average domestic production of only 125,000 tons annually during the 1971-75 period is a relatively small fraction of the nearly 800,000 tons consumed annually in the United States during those years. As a result of an increase in the production volume and average value per ton in 1976, the value of U.S. asbestos fiber production could be in the range of $25-30 million in 1976 (11-13% of the mine/mill value of all asbestos likely to be consumed during the year). U.S. asbestos mines and mills, their locations, output, and employ­ ment are shown in Table 2. The current total mill capacity is on the DU 035395 11 DUP 0931658 4 suwwafltjaitjL .fPi'OT stm,t order of 143,000 cons per year (all in the form of chrysoeile fibers). California mines and mills account for about 70% of total U.S. output. It is difficult to predict changes in U.S. asbestos output because such changes will be a function of costs, including environmental costs, in the United States as compared with costs in Canada and other sources of supply. Neither current nor projected costs are published. End Uses of Asbestos The high tensile strength, flexibility, heat and chemical resis­ tance, and favorable frictional properties of asbestos fiber make it adaptable to a large number of uses. Depending on the length of fibers and other characteristics, asbestos can be: Carded, spun, or woven Used as structural reinforcement of materials such as cement, plastic and asphalt Laid and pressed to form paper. Some authorities, such as the U.S. Bureau of Mines, state that there are more than 2,000 discrete uses of asbestos; others, such as the Asbestos Information Association and Canada's Department of Energy, Mines and Resources, suggest that there are upwards of 3,000 uses. A selected few of the many applications are shown in Table 3. The properties of asbestos fibers determine the uses to which the fibers are put. Properties of major importance are length distribution, bundle diameter distribution, harshness, tensile strength, and surface activity. Other considerations include color and content of iron and dust. The relative-strength standard developed for chrysotile asbestos by the raining industry in Quebec is a convenient basis for delineating some major uses. For example: • • * Long fibers (Groups 1 and 2 and 3) are used in textiles, electrical insulation, filtration media, and maximumstrength asbestos cement products. Medium length fibers (Groups 4, 5, 6) are used as rein­ forcing fillers in asbestos cement products, in friction materials such as brake linings and clutch facings, in paper, and in pipe covering. No. 1 crude is 3/4 inch staple and longer (to nearly 6 inches). No. 2 crude is 3/8 to 3/4 inch staple. Other groups are milled fibers. 13 DUP 0931660 DU 035397 • Show fibers (Croups 7, 8) are used as reinforcing filters in plastics, floor die, and asphalt and in paints and oil-well drilling muds. The consumption pattern for asbestos fiber in the United States is shown in Table 4. The construction industry—including new building, renova­ tion, and maintenance-accounts for an estimated 70%-80X of total U.S. consumption. The first four uses showa in Table 4, which are constructionindustry relsted, account for only 65% of ths total use, but a portion of some of the other uses is assoclsted in vsrlous ways with ths con­ struction industry. Several ocher aspects of Tsble 4 axe noteworthy: e Chrysotile fiber accouncs for a very high proportion of total asbeacos use (94% in 1974). e About 98% of the crocidollte is used in the production of asbestos cement pipe, because of (1) its hardness, brittleness, and high tensile strength, which add to the rigidity of the end product, and (2) its superior fil­ tration qualities, which enhance the drainage of water, permitting the cement to dry more rapidly. • Asbestos cemenc pipe end sheets account for a large pro­ portion of total use (38% in 1974). • A very large proportion of total asbestos use is accounted for by the shorcer-lengch fibers (Quebse Grade 7 chrysotile alone accounted for nearly 40% of the total use in 1974). , The transportation industry uses aboue 14% of ell ths asbestos coaThe sppllcance Industry uses soma 5Z-6X of Che total.5 euaad. Handling of Fiber and Products During Their Production Producing che many asbestos-containing products chat are used involves mining asbeacos ore; milling, or hand-separating, che fibers from che ore and from each other; transporting both ore end fiber; and msnufsecuring che products cheaiselves. These four genmral processes are reviewed briefly in che sections that follow. Mining Most ssbsstoe ore is mined in surface operations. Of che five U.S. mines in operation, four are surface mines and one is underground.* Each operating mine is associated with e mill that processes the ors. For a description of each mine and a discussion of the mining, milling, and dust-concrol procedures, see National Environmental Rasesrch Canter, Characterization and Control of Asbestos Emissions from Open Sources, North Carolina, Sepcembsr, 1974. 13 DU* 0931^62 DU 035399 .fliii. JjUSUlLi DU 035400 ■aS*1' »tr"" r jgf; In three cases, chs mine and mills are at the same location, but two mines send their ore by truck co mills 32 and 55 miles away. (See Table 2.) The methods used co mine asbescos ore in the United States are described below. Area scrip mining, as practiced in the California operations, entails removal of the ore by earth-moving equipment from shallow deposits—in one instance without even the need far blasting. Generally, a shallow overburden with low concentrations of asbestos fiber must be removed. Open pic mining, as practiced in the Vermont operation, is similar co area scrip mining operations except that to follow the fiber veins, the workings are much deeper. Blasting and removal of ore occur primarily on the sides of the pic along terraces chat spiral down around the-sides of the pic coward the bottom. Underground mining, as practiced in the Arizona operation, entails following the veins of ore with shafts, galleries, and drifts, using blasting and earth-moving equipment. This operation is followed by transporting ore co che surface, where it is processed further. At che typical asbestos mine, coarse ore is crushed by a Jaw or gyratory crusher co e size thee esn be accomodated by che mill. Oversize rock is ssparacsd by rotating cylindrical trommel screens and is crushed in e secondary crusher, usually of a conical type. The ore screams are conveyed to driers—rotary kilns in larger installations— where moiaeure la the ore (up co 30X by weight) la removed. The dried ore la than scored, wteh larga amounts bains held co allow far varia­ tions la flbar demand and mins production over time. Prior to milling, dried ore is conveyed co an additional crushing step. Milling Milling, dons primarily by hsamsr mills (fiberizers) or crushers, serves co frts ths fibers from the rock and separata chs fibsrs from’ each other. In ganeral, longsr-lsngth fibsrs in chs final mix bring, higher prices. Hanes, it is desirable co hold che mechanical working or fibars to a minimum sines, although chs fibers have very high cantile strength, they are so fine thee they ere eeally broken. The most expensive grades of fiber ere not mechanically milled at all; rather, they are head-separated ("cobbed") from che surrounding rock into bundles of relatively long fibers with lengths of 3/1" or more. Such fiber is valued for manufacturing asbestos textiles. The solution to the problem of maximizing the recovery of fibers ocher then hand-cobbed, in all but one of the asbestos mills in che United States, is co use mechanical means co fras chs fibss bundles from che rock, but co use sir aspiration lyscsms co separata and convey the 00? 0931664 W 035401 fiber*. la these systems, the ore is shaken on progressively finer screens through which small rocks and fiber bundles pass for further treatment while larger rocks are retained for further crushing or for conveyance to tailing dumps. The fibers freed are removed by the flow of ait through powerful suction hoods. Separated fibers are caught in dry cyclones and conveyed to screens that separate them according to size. After sizing, the fibers art sent to bins for storsge. Subse­ quent operations include removing the fibers from the storage bins, blending in fibers of different sizes to produce the desired flnel shipping specificttlon, and bagging for shipment. The one exception to the air-aspiration milling system is found in a California mill that procassss ths loots fibsr ore by a vetseparation systsa. Transportation Conveyors and trucks art used at mine and mill sites to move ore from mines to mills. , Asbestos flbsrs typically are shipped from the mills in 100-pound, mulclvall, paper or plastic bags.* (One producer reports the use of a stronger, woven, polyvinyl beg for some shipments.) Begs ere pressurepecked to reduce bulk, damage, and duet. It la customary to tape rip­ ped or punctured begs when the deaege it discovered; yet Che fact chat the fibers ere tightly pecked may often prevent them from escaping even if the damaged area Is noc rapalrad. The technology is now available to peck aebeecoe even more tightly—i.e., to form blocks with evict Che density of fiber shipped in conventional bags, s 100-pound block having a volume of about one cubic foot. Pelletizing is used almost universally, with the bags glua-lockad to aaeh ocher or shrink-wrapped to the pellet (wrapped with s film of plastic which is then shrunk) to stabilize the load. Much of the asbes­ tos shipped is further unitized by being loaded into seeled railroad boxcars or shipping containers. Sometimes the aabeaeoa is made into pellets, which, racher chan being pecked in begs, are loaded on and off railroad boxcars by gravity flow through pipes. The majority of Canadian chrysoclla fiber la shipped Into the United Scares In conventional scaled railroad boxcars In which the con­ tents are protected by inflated-rubber begs. The modern damage-free bulkhead cere ere being used as they becone available. The cars are routed directly from the Canadian mills to the U.S. manufacturing planes. Smaller proportions of chrysotlle imports from Canada are received in containers, either by rail or by ship vie the Atlantic *Soae manufacturers can add the begs, along with the fibers, to their product mix without even opening them. 13 DUJ 0931665 D\] 035402 Slipiir ;:iS4~ : -I .mu&mm; Oc«»n. All fiber from South Africa, the source of all U.S. import* of crocidolite, arrive* by ship in containerized bag* at Gulf Coast porta. U.S. export* of fiber, virtually all of which are from California and destined for Mexico, Central America, and the Far East, leave the mills by both rail and truck. Containerized ocean shipments leave from ports such as Stockton, Sacramento, Oakland, and San Francisco. Although 100-pound bag* are by far the most widely used in the industry, one of the California mill*, for the convenience of it* customer*, ships all of its fibers in bag* weighing from 10 to 50 pound*. On* company plan* to shrink-wrap each paper bag individually, for added protection, since some user* buy in le**-than-pallec lot*. A representative of on* of the world's largest shippers of asbestos reports that about 2Z of the bags shipped sustain some damage. Manufacture of Asbestos-Containing Products Production processes used in thj consumption of asbestos are high­ lighted below for selected products. Asbestos cement product* us* the largest amount of asbestos of any product category (about 317,000 eons, or 38Z in 1974). Specific products include wallboard, pipe, shingles, and blocks. Advantages of the products over their nonasbestos counterparts are better tensile strength, strength-to-wcight ratio, strength under heat stress, resis­ tance to acid, and smoothness of finished surface (critical to ensure laminar flow in pip* used for transport of liquids). Asbestos fiber (primarily chrysotlle, but also others te a limited extent) is mixed, either wet or dry, with Portland cement and silica In proportions ranging from 10Z to 70X of the total material. If the mixing is don* dry, the mixture is generally metered in a flat layer onto an open surface, where the requisite water la applied by over­ head spray. The resulting layer, much thinner than the final product, is then wound onto mandrels in a spiral mac (for pipe) until the requi­ site thickness is built up, or is layered flee (for wallboard or shingle forms). The same winding or layering process may be used for wet-mixed products, or the mixture may be cast. Finishing processes for eh* dried cement products vary with performance requirements and type, and may include grinding, drilling, sawing, or cuttingr Asbestos can be made into the full rang* of textile products— from nenwerea lap and felt, chrough yarn and cord, to woven doth, rope, and tube. The asbestos fibers required for textiles are significantly different from those used for oeher asbestos products; they must be quite For a more detailed discussion of the manufacture of asbestos-containing products, see U.S. Environmental Protection Agency, "Development Docu­ ment for Effluent Limitations, Guidelines and Standards of Performance: Asbestos Manufacturing," Washington, D.C., 1973. 19 DUP 0931666 DU 035403 long co be splnnabla. Spinnable fiber is sometimes obtained by textile producers in hand-cobbed, "crude," form—l.e., as unopened, roc!c-£rae fiber blocks or bundles—since, as noted previously, It Is difficult to protect fiber length during milling operations. If the fibers are received as crude, they ere opened In edge (knife) mills into smell bundles and then milled into extremely fine flexible fibers. The resultant fibers, as well as being more delicate and breakable, are also more "floatable," leading to a greater emission potential per unit weight. Once che fibers have been adequately opened and fluffed, they may be blended with up co 20% of a celluloslc fiber such aa cotton, eha specific material chosen depending upon che appli­ cation of che final product. The subsequent processes, such as csrding, lapping, roving, spinning, and weaving or braiding (aa required) are all performed on equipment essentially identical to standard textile machinery. Asbestoe is used In vinyl and asphalt floor tiles as s filler and reinforcement co provide scrsngch and stability without reducing flexibility and compressibility. Very shore fibers srs used, compris­ ing 8-30% of che cocsl weight. In che esse of vinyl tile, for example, ' polyvinyl chloride resin serves as ehs binder, limestone and other materials are used as fillers, snd pigments and chemical scabillzara make up the rest of the typical mix. The manufacturing procaaa la typically a 24-hour operation chat includes weighing, mixing, heating to about 150°C, decorating, calandarlng, cooling, waxing, stamping, inspec­ ting and packaging. Friction produces and gaaktea typically contain 30-80% asbes­ tos, gtnarally in soma tore of organic binder. In friction products, cha aabescoa la usad for lea uniqua combination of serangch, compaction characteristics, friction propareias, and stability at high eamparaeurts. Aabescoa Is used In chase produces in-two diffaranc ways: (1) eha asbestos, as loose fiber, la mixed with ehs binder; or (2) cha aabaatoa, aa either matted or woven eexeila, is impregnated with eha binder. The low eoeal volume of the latter process is because it is used only in special situations, generally in gaskets, where dimensional stability and elasticity are of significance. Asbestos paper has sssaneislly ehs same properties as the usual calluiose-based paper, except thee it has superior thermal insula­ tion properties end firs resistance. It is used primarily aa building paper (roofing sad flooring) although it has been reporttd chat cha above-mentioned qualities also find use in high-quality-bond document papers. Asbestos paper is made using eha same proeassaa aa chose used for standard woodpulp papers, but the raw materials mix, by weight, might be 7Q-90Z asbestos flbscs (typically shore in length), chins clay and starch (or sodium silicate) aa the binders, plus ocher constituents that provide special properties. 20 OOP 0931667 DU 035404 Chapcer III BIOLOGICAL EFFECTS OF ASBESTOS FIBERS Aa noted in the Introduction co chit monograph, asbestos fibers are known co cause cancer. In this chapcer, (1) a summary of whac is known abouc the disposition of these fibers in the body is followed by (2) e description of the carcinogenic effaces of the fibers, based on human studies as well as animal experimentation; also included is (3) a dis­ cussion of the noncarcinogenic effects of asbestos fibers. Disposition of Fibers in the Body Technical difficulties associated with the assay of biological tissues for asbestos have limited the amount of information available abouc the disposition of asbestos. Almost all data have come from animal experiments in which asbestos was monitored by electron micro­ scopy or radiotracers. Asbestos fibers typically enter the body by Inhalation or ingestion. Inhaled Asbeseos The disposition of asbestos fibers entering the respiratory tract is not fully understood. Certainly some fibers are ultimately deposited in the airways and lung tissue. Some could also be expectorated or con­ veyed co the gastrointestinal tract by airway clearance mechanisms and possibly some co the pleural and peritoneal cavities via lymphatic drainage. Of asbestos fibers found at autopsy in human lungs, a majority are less Chan 5 urn in length;1*2 seldom do they exceed lengths of 200 ua or diameters of 3.3 urn.3 One autopsy study of persons with occupational exposure demonstrated that all asbestos fibers examined in the lung were less than 0.3 urn la dlasMter.2 This preponderance of small fibers in part reflects their ability to remain 'suspended In air for longer per­ iods them larger fibers, but it is also a function of their deposition and clearance characteristics once they enter the respiratory tract. It is also possible that some fibers may be fragmented as the result of biological activity vlthln pulmonary tissues. Longer fibers are screened more effectively by the nasal hairs. Inside the upper respiratory tract, fibers are deposited through the forces of gravitational sedimentation and impaction at points where the air stream changes direction; and these depositions depend largely on DU* 09316«8 DU 035405 fiber diameters.3,4 In che small airways, especially at airway branch points, che collision cross-seccional area, which is a function of fiber length, is of greater importance.3 as a result of these obstacles, a greater proportion of fibers reaching the gas-exchange surface of che alveoli may be small, compared with fibers entering che upper respira­ tory tract. Studies with mammalian cells in culture indicate thae these shorter fibers (usually less chan 5 pm) may be engulfed by alveolar macrophages and transported to lymphatic channels or che mucociliary blanket for excretion. Longer fibers may be only partially engulfed or may be engulfed by several macrophages at once.*7 Data from autopsies of humans have suggested that some flbsrs may enter alveolar lymphatic channels and be carried to hilar and mediastinal lymph nodes.8 Numerous fibers can be found In che pleura, a seroua membrane which covers the surface of the lungs, thoracic diaphragm, and chest wall; how they gain access to che pleura Is not known. Generally, che concentration of fibers in che pleura is leas chan in che lung lcself, buc In some areas of cha plaura, fiber concentrations similar to chose within the lung tissue have been observed.9 * Ingested Aabaacoa Most asbascos fibers entering cha gastrointestinal tract art prob­ ably excraead with che faces. Although it has bean reported In one study that there is little evidence of asbestos fibers") peneeraeins the walls of the gastrointestinal trace, chars have been animal studies showing such penetration. In a study reported In 1965, chrysotile fibers were found in the lining of the colon la rats fad a disc contain­ ing a massive amount (6X) of chrysotile asbestos.^ xn another study, fibers of amosite asbestos suspended in saline, whan placed into an Isolated segment of rat jejunum in vivo, were found penetrating end within cha Jejunal wall.3-2 One recant study of rata fed 250-300 mg of asbsatos par week for a year did Indicate thae If penetration of the gastrointestinal tract lining does indeed occur, cha number of Za an experiment with rata, about one-chlrd of inhaled aabescos (crocidolice) was deposited on cha surface of the respiratory tract. Half tha amount deposited at Inhalation was found immediately afterward in the gastrointestinal tract, noaa, pharynx, and larynx; clearance from these latter respiratory tissues to tha gastrointestinal tract was practically complete within an hour. Of cha remaining crocidolica deposited In che lungs, one-quarter had been evacuated at tha and of tha month.3 in another study of rsts exposed to amphibole aabaatoa for six months, 412-74X of cha asbestos found In che lungs isxiediecely after expoaure had been removed within 13 months.8 22 DU? 0931669 DU 035406 penetrating fibers would be very snail (90Z probability of leas than 1500 fibers). 13 n“ Injected Asbestos Asbestos Injected into the bloodstream is rapidly removed anddeposited in various tissues, with highest concentrations observed in lungs, liver, and spleen.l^.iS Limited evidence suggests thac asbestos in Che blood may be transported across the placenta of rats.16 In mice, asbestos injected subcutaneously migrates along lymphatic pathways from the injection sices. Fibers accumulate in lymphoid tis­ sues, particularly in regional lymph nodas, and art usually contained within macrophages. Small numbers of fibers may ba found in cha splsen, pleura, liver, kidneys, and brain.13 "Asbestos Bodies" Approximately 10X to 30Z of the fibers rscalned by human lungs (usually longsr than 5 urn) btcome coscsd with mucopolysaccharide and hemosiderin to form yellow-co-brown rod-shaped structures with clubbed ends, of can beaded along thsir length.1-8 These structures were first called "asbestos bodies," but not' they are frequently referred to by the more general term, "ferruginous bodies," sines identical structures may result from the costing of fibers ocher chan asbestos. It has bean hypothesized chat this coating, laid down by engulfing macrophages, render* the fibers biologically less eceive. It is thought chat a certain balance is achieved between the forma­ tion of asbestos bodies and thsir dissolution or excretion.1-8'30 Asbestos bodies found in the sputum are strong presumptive evidence of asbescoe exposure. Occupational exposure as brief as one day and as long ago as esa years has been shown co produce sputa containing asbes­ tos bodies.30 Asbestos bodies In lung sneers or tissue (unlike chose la sputum) era cotmwaly found among residents of urban arses who may never have been exposed to asbestos in the workplace.21-23 Asbestos bodies or fibers have been detected in extra-pulmonary tissues of parsons occupationally exposed to asbsaeoa: la tonsils, thoracic and abdominal lymph nodes, pleura, peritoneum, liver, spleen, pancreas, kidney, adrenals, and small intestine. The numbers found appear to ba far fewer chan in cha lung.8*24 Carcinogenic Effects—Hunan Studies The many observations, both case reports and epidemiologic studies, of cancerous effects among humans exposed co asbescoe fibers could be23 23 OOP 0931670 DU 035407 A looked ac from a number of points of view, but the ones used here are: types of cancer; fiber type; dose-response relationship; latency; age at first exposure; smoking; indirect occupational exposure; household expo­ sure; and residential exposure. The section on human carcinogenic affects is followed by a summary discussion of animal experiments and asbestosrelated cancer. High races of lung cancer have been observed in asbestos workers exposed to all commercial asbestos cypes. Among some groups of asbestos workers, approximately 201 of all deaths are caused by lung cancer where the proportion of deaths expected from this cause would be only about 5Z.25 Pleural and peritoneal mesotheliomas* art a frequent occurrence among occupational groups exposed to chrysocile, croctdolite, and amoslte. Estimates for certain occupational groups suggest that as many as 3Z-11Z of deaths may be due to mesothelioma, e relatively rare cauea of death in the general population.Some occupational groups exposed to asbestos have, furthermore, demonstrated an excess of ocher cancers, especially of the larynx and gastrointestinal tract. Asbestos exposure leading to an excess of cancer may occur among groups axposed indirectly, as in shipyard workers or in groups mining * other minerals chat may contain asbestos as a contaminant. Mesothelioma also has occurred among persona living in cha hoaas of asbascos workars or in the vicinity of aabestos facilities. Both cigarette smoking and occupational asbestos exposure individ­ ually lnereeae the risk of lung cancer but, together, they act to pro­ duce a risk of lung cancer chat exceeds the sum of chair saparaca risks. Evidence of Lung Cancer The evidence chat asbestos Is a causa of lung cancer is over­ whelming. Lung cancer wee first linked with exposure to aabestos In 1933, when three cease of aebescosia and carcinoma of the lungs wars found at autopsy in asbestos textile workers.27>23 other case reports followed. In 1949 the Chief Inspector of Factories of England and Wales examined 223 deaths from esbescosis or in which asbestos is had been proved at autopsy. Cancer of the lung or pleura was found in 31, or 13.2Z. This vss not characteristic of ocher pneumoconioses; among 6,384 deaths with silicosis ac autopsy, for exsmpla, only 91, or 1.32Z had cancar of cha lung or pleura.29 Further evidence implicating aabestos in the etiology of lung can­ cer cam* from a matched-pair cast-control scudy published in 19S4. Upon claealfying by 5 yeets or more employment in occupations ^Mesothelioma is a tarm usad to refar to a tumor raada up of calls from cha pleura or peritoneum. OOF 09316^1 035408 jgif rr aagjin ImsIT ,;-uafli Involving asbestos exposure (sceaa fitters, bollenukers and asbestos workers), 10 patients with lung cancer but only one control had been so employed.30 In a study reported one year Later, 11 of 113 workers employed in an asbestos textile factory in the United Kingdom for at least 20 years were found to have died from lung cancer, by applying to this group age-specific mortality rates for lung cancer In the general population, 0.8 deaths would have been expected. The ratio of observed to expected deaths, therefore, was greater than 13.33- Continued study of workers at this factory Has shown a reduced risk of lung cancer, although scill two- to three-fold in excess, among workara first employed after 1933, when regulations for control of asbestos exposure in the United Kingdom had gone Into effect.32,33 Numerous other studies heve independently confirmed an increased risk of lung cancer In various occupational groups exposed to asbestos.25,34-39 Evidence of Mesothelioma There is also overwhelming evidence ehet asbestos Is a cause of pleural and peritoneal mesothelioma. Cases have been described in per­ sona with occupational and nonoccupational expoaurea. The first case report of a pleural neoplasm related to asbestos exposura appeared In 1933.40 Additional cases were noced In the 1940s,41-43 an(j ia 1934 4 peritoneal tumor was reported.44 However, it wes not uncil I960, with the publication of a series of cases from South Africa, chat the asso­ ciation between mesothelioma and asbestos exposure was gsnsrslly rscogniatd. Of 33 South African patients with mesothelioma, 32 gave a history of occupational exposura to asbestos or residence la a crocldolita min­ ing araa.45 Subsequently, a plethora of individual case reports, case series, case-control studies, and studies of the mortality of occupa­ tional groups have related the occurrence of mesothelioma to a history of exposure to aebe*coa.26*39,46-53 xha ratio of plaural to peritoneal tumors varies considerably in different studies, but peritoneal tumors seem to be associated with heavier exposures and with asbescosis.34-56 Laryngeal Cancer The evidence casually linking asbestos and laryngeal cancer is highly suggestive. In a study of 119 patients with squamous carcinoma of ths larynx and age- and sax-matched controls, 33 with laryngeal can­ cer, but only 3 controls, gave a history of occupational exposura to asbestos.57.38 This difference was striking, and the suggested increased risk has sines been confirmed by similar case-control studies,59 and studies of occupational cohorts.60»61 DU» 0931672 DU 035409 -«SWi'.f8 Digestive System Cancer Aa excess risk of cancers of the digestive system eccrlbucsble to occupational asbestos exposure has been suggested by a number of epide­ miological scudies.25,34,35,60,62-69 A Mjor probl#a wich ch.M studies has been the inclusion of peritoneal mesothelioma cases among all observed cases, asking it difficult to document an Increased risk of any one digestive system cancer independent of that for mesothelioma. In occupetionel cohort mortality studlee whara paritonaal mesothe­ liomas vara saparatad from other cancera of tha digaativa ayatas, excass cancers of some sites hevt been observed. Among 933 amoslte esbeetoe factory workers who were first employed between 1941 and 1945, there were 11 deaths from stomach cancer by 1971 (va. 4.58 expected): 13 deaths from csncar of tha colon or rectum (vs. 7.05 expected), and none from cancer of the esophagua (va. only 1.23 expected).25 of 1.779 deaths through 1974 among a cohort of 17,800 Insulation workers there ware observed 15 deaths from orophsryngsal csncsr (vs. 7.87 expsetsd); 14 deaths from cancer of the esophagus (vs. S.3S expsetsd); 18 from stoosch cancer (vs. 11.23 expected), and 47 from cancer of the colon or , rectum (vs. 28.63 expsetsd).25,60 other studies of groups exposed to asbestos examining the risk of these specific cancers efeer excluding mesotheliomas art needed to further elucidate the role of aebeetoe in cancers of the digestive system. Other Cancers Studies of women asbestos worksrs have suggested possible inereeeee in cancers of the ovary and uterine cervix. Among a group of female English asbestos worker, 4 and possibly 6 deaths from ovarian csncar were observed while only 2.1 had bean expected.35 Investigators from the Soviec Union have reported significantly increased races of cervical cancer among older female asbeseos workers: however, the numbers of per­ sons in the study populations were not indicated.3* Findings in these reports need confirmation elsewhere. Association of Effects with Fiber Type There ere few studies of persons exposed to e single type of esbeetoe, end the studies that are available often leek information on potential confounding factors such as cumulative exposure, smoking history, end physical characteristics of airborne fibers. It is there­ fore exceedingly difficult to assign a scale of relative pathogenicity to different types of aebeetoe. For example: e Croeidollta mined in the Northern Cape Province of South Africa and In Wastarn Australia is frequently aeaociatad with pleural mesotheliomas, whereas fewer cases have been reported for crocidolite from the South African Transvaal. OUT 0931673 DU 035410 It has been proposed that this apparent difference in risk may relace co a difference in physical characteristics of fibers from these areas—crocidolice fibers from the Transvaal are thicker and longer.7,7 • As asbestos proceeds from mine to mill to manufacturing plant, it can become subdivided (and fractured), pro­ ducing fibers of smaller diameter and length, with pos­ sibly greacer or smaller attendant biological risk. e Asbestos thought to be of one type may be "contaminated'' with asbestos of another type. Lung tissue from men employed In Canadian chrysotlle mining has been observed co contain cremolite and ocher amphlboles, often more chan che amount of ehrysocile.71 All types of commercial asbestos have been related co high races of lung cancer in asbestos workers, and in occupational groups exposed co chrysotlle, crocidolice, and amoslee, pleural and peritoneal mesothe­ liomas have been observed.7? Studies of anchophyllice miners in Finland have shown a slight excess of lung cancer, but no mesotheliomas.36,37 The lack of mesotheliomas may be due co che small size of the cohort studied; however, none has been reported from che cosssunltles in the mining area.7' There is some information suggesting chat chrysotlle may not be as hazardous as ocher types of asbescos.38,47,74-78 The mortality experi­ ence of a cohort of workers employed at an asbestos paper and millboard manufacturing plane ehae used only chrysoelle aabeeeoa would seem to bear this out.7* Pleural and peritoneal tumors, as well as excess lung cancer, have been found in che mortality experience of workers who had mined and milled New York State calc.80,81 This tale may contain large quanti­ ties of cremolite asbestos as well as smaller amounts of anthophyllite and ehrysocile. In Italy, where che calc is reportedly uncontaminaead, mining and milling has noe been associated with mesothelioma or excess lung cancer.82 Dose-Response Relationship Evidence that the risk of developing cancer is related co che degree of exposure to asbestos by sons quantitative estimate strengthens the basis for assuming asbestos to be of causal importance. A precise dose-response relationship is difficult co establish for any environ­ mental exposure and no less so for asbestos. However, attempts have been made for asbestos and there is some evidence suggesting that dose DU? 0931674 27 DU 035411 mrv-wmmmm ax measured by severicy of exposure and duration of employment relates to rates of cancer in groups occupacicnally exposed to asbestos. One study concluded that within an age cohort for which data were most accurate there was an increasing mortality due to lung cancer with increasing duration of employment.®3 However, races for individuals employed che longest were lower than those in the category of next greatest duration of employment; persons employed longest might more likely be chose whose occupational exposure to asbestos was less incense or who were themselves less susceptible to cancer and respiratory dis­ eases (for example, persons who do not smoke). An investigation of mortality among workers at an asbestos textile factory in England found markedly reduced mortality from lung cancer, and from other diseases in the presence of asbescosls, with reduction in length of exposure before 1933.32 Moreover, che risk of lung cancer and mcaochelioma among workers at a Londom asbestos textile and insulat­ ing materials factory was independently found to be related to the severicy and duration of exposure.39,55,83 The respiratory cancer mortality (includes deaths due to pleural mesothelioma in addition to cancars of cha lung and larynx) of a group of retired asbestos workers was categorized according to cumulative dust exposure. "Exposure" was the product of job-characteristic dust levels in millions of psrticles per cubic fooe (rappef) and number of yeers on the Job, summed across all Jobs held (thus giving cumulative exposure in mppef-years). The result is shown In Table 3. It can be seen that chare la a clear gradient of increasing Standard Moreality Ratio (SHR), or ratio of observed to expaccad deaths x 100, with increasing cuuwlatlva dust exposure. Table S DEATHS FROM RESPIRATORS CAHCER 3Y CUMULATIVE DUST EXPOSURE local Oust Exposure (mppef-yr) ((umber Men Respiratory Cancer Deaths SHR Expected Observed Under 125 533 15 9.0 166.7 125-249 305 12 4.8 250.0 230-499 328 17 5.2 326.9 300-749 126 9 1.8 500.0 750 end over 56 5 0.9 533.6 Source: Chapter Reference 78. DUP 0931675 DU 035412 Th« Cancer Latency Period from all available evidence, the period beeveen fine exposure to asbeaeoa and deach from lung cancer appears eo be relaeed eo Intensity of exposure.3* Among workers at an English asbestos textile and Insu­ lating materials factory, an excess mortality from lung cancer was demonstrated following a latency of IS years for those with heavier exposures, whereas an excess did not appear undl 23 years from onset of exposure for chose whose exposures were lass incense.39,61,83 Fifteen years is probably the minimum latency period for asbestosrelated lung cancer. An excess of lung cancer deecha first appeared among a group of haavily exposed amoslrs asbestos workers IS yeers aftsr onset of exposure,85 end in e large cohort of insulation workers fol­ lowed from 1967 through 1974 (135,000 person-years of observsclon), no applicable increase In mortality from lung cancer was observed before IS years had eLapsad from onset of exposure. The peak increasa occurred about 30-35 yeara after onset of exposure.25 In 35X of one series of mesothelioma caaaa, death oceusrad more chan 25 yaars after first exposure to asbestos, with a ranga of 3.5 to 53 years.36 Another investigator reported a mean latancy period of 37. yaars,87 and among a larga cohort of aabeaeos workers, most deaths from pleural and peritoneal mesotheliomas occurred 30-35 years after first exposure.25 ' Incidence of Cencer and Age at First Exposure eo Asbestos A characteristic of many cancers is a marked increase in incidence with advancing age. It is generally acknowledged that the higher inci­ dence of cancer in older persona la not neceaaerlly btcauae their tis­ sues are more predisposed to cancer, but because of the usually long period between initial exposure and the appearance of diagnoaable tum­ ors.38 In face, with regard eo susceptibility of body tissue to cancer, it haa been hypothesized, from experimental animal evidence, chat the tissues of younger people mey be more susceptible to carcinogens but that, conversely, older people mey be more susceptible to cencer because of a laas efficient lmuna surveillance system.8* In a study of the relative incidence of lung cancer according to age at first exposure to eebeetos, date were obtained on 117 men who ware exposed for more then 20 years and who were followed for an average of 13 additional yeers. A greeter incidence of lung cancer was observed among man first exposed at older ages. For those first exposed under age 25, the annual lung cencer incidence wee 26Z of the race for all ages) for first exposure between ages 25 and 29 it was 165Z; at age 3Ot­ ic vea 195X. These Incidence rates were corrected to account for varia­ tion in the duration of exposure, duration of survival after first exposure, and for cha fact that some lung cancers may have been due to DO* 0931676 DU 035413 ■immi LiUBaiL. nonoceupational causes mors common among older men. The decs suggested that susceptibility to asbestos-related cancer may increase with age.”' It seeoe unlikely, however, that age £*r s* is a principal factor in determining frequency of cancer, and it is not clear whether age itself plays a part that is independent of exposure duration and time elapsed since first exposure. Smoking and Asbestos-Related Cancer Thera Is strong evidence chat cigarette smoking alone is sufficient to cause lung cancer. Many studies attempting to examine the effect of cigarette smoking on the increased risk of lung cancer observed in groups exposed to asbestos have been deficient in one or more of these respects: e Follow-up periods have been too short to allow accurate computation of risk after the necessary 15-20 year latency. e Nonsmoking asbestos-exposed groups hsvs bssn very email. e Smoking habits have not been completely ascertained. e Smoking-adjusted mortality raeas from the ganaral population have not been uaed for comparison. A few studies have found that dgarstta smoking was insufficient to account for tha ineraaaad risk of lung cancer among asbestos workers. This has bssn gsnarally accaptad as avldanca that asbeetoe can set independently to cause lung cancer, a view thee has been corroborated by animal axparimants and by soma avldanca auggaaelng an ineraaaad risk among nonsmoking asbaaeoa workers.*2 An invaseigation of two groups of asbestos worksrs—ons with s high dust exposure and s high respiratory cancer mortality, the othar with a lover dust sxpoaura and a lower respiratory eancar mortality—found that thalr smoking habits wars similar.7* This implies thee high doses of asbestos can account for higher mortality among smokers. Another inves­ tigation, a caaa-control study of lung cancer patients, revealed an anhancad risk of lung eancar with asbestos exposure, whatever the number of cigarettes smoked.*2 Is e study of tha combined effects of asbestos exposure and smoking, tha smoking habits of 1,334 mala and 482 faaala asbastos factory vorkars warm axamlnad la rslstloa to mortality from lung eancar ovar a 10-yasr period. Among 933 smokers with savers asbastos exposure, 41 lung cancer deaths vara observed, while only 11.3 vers expected for smokers from the general population. Among 161 never-saoklag asbestos worksrs with 30 OOP 0931677 DU 035414 severe asbestos exposure, 1.7 lung cancers deaths were observed, while only 0.2 were expected for nonsmokers la the general population. There were approximately five times as many person-years of observation in the smoking group compared with the nonsmoking group, but about 24 times as many lung cancer deaths among the smokers.90 In another study, smoking histories were obtained from 11,657 of a cohort of 17,800 insulators. In 9,591 workers with a history of ciga­ rette smoking, 248 lung cancer deaths were observed, compared with 59.5 expected. Among 609 workers who had smoked pipes and/or cigars, two lung cancer deaths were observed and 1.24 were expected. Of 1,457 workers who never smoked regularly, four lung cancer deaths were observed, while 1.08 were expected.25 Expected deethe were besed on approximate smoking-specific U.S. death ratea. Further analyses of group data have been performed to examine how cigarette smoking and asbestos might be seeing together.91,92 On e statistical basis it appears ehse these two independent causae of lung cancer Interact positively. In the general population, cigarette smokers have e 10-15-fold excese risk of lung cancer. One study observed an 8-foLd exeees of lung cancer among smoking asbestos workers compered with smokers in the gsneral population, but the excsss wee 92-fold when coo­ pered to the general population of nonsaokers.^* This suggests that the combined effect of smoking and asbtseoa exposure is greater than the simple sum of their separate effects. The relation of this statistical Interaction to the pathogenesis of lung cancer is uncertain. However, it seems clssr that, due to the important enchancement of risk by one cause complementing the other, the increased risk of lung cancer in groups exposed to esbeatoa may be concentrated among thosa who also smoke. , There is very little evidence that cigarette smoking increases the frequency of developing pleural mesothelioma after asbestos exposure, and no evidence exists that smoking increases the risk of peritoneal mesothelioma. Of 9,951 insulation workers with a history of cigarattt smoking, chars wars 23 deaths froa pleural mesothelioma and 47 deaths from peritoneal mesothelioma, with none expected. Among 1,457 workers who never smoked.regularly, there were two deaths froa pleural meso­ thelioma, eight deaths from peritoneal mseothelioma, and none expeceed.2^ Cancer from Incidental Occupational Exposure Persons who do not work with asbestos directly, but who may be incidentally exposed to asbestos while working, may suffer excesses of cancer. A 102 random ssapls of shipyard workers, widely distributed *This is an adjusted figure to compensate for missing smoking infor­ mation for the deceased. j i POP 0931678 J 035415 throughout the various trades, revealed chat some had pleural plaques and some had pulmonary fibrosis, and retrospective and prospective cohort mortality studies have revealed a 2.5-fold excess risk of lung cancer as well as a number of mesotheliomas among workers with pleural plaques. Sven those without X-ray evidence of exposure to asbcstoshada slightly increased risk of lung cancer and a few mesocheliomas. A study of sheecmecal workers also revealed a small excess of lung cancer and one mesothelioma.93-95 Disease in Workers' Households There are presently 37 reported cases of mesothelioma in parsons whose presumed exposure to asbestos wes limited to living in the homes of asbsstos workers.9^ However, no comprehensive studies of ths dis­ tribution of mssothelioma by aga and sex among contacts of asbsstos workers in their homes have been conducted. The majority of reported mesotheliomas related to household exposure have been in women, perhaps because they are more likely to be exposed to asbestos by washing ths garments of asbsstos workers.96,97 Thirty-five percent of examined family contacts of asbestos workers vers found to have radiological abnormalities characteristic of asbestotle disease.72,96 Cancer in ths neighborhood of Asbestos Facilities On ths basis of numerous snoedotal reports, indirect assessments, and case-control studies, there seems little doubt thst both pleural and peritoneal mesotheliomas may rasult from some types of rteldental expo­ sure to asbestos.45,44-50,74,86,98-103 However, there have been no adequate populaelon-based studies, and an accurate eatimet# of risk, where occupational and household exposure are definitely excluded, cannot be made. On the basis of one case-control study of mesothelioma patients, relative risk of mesa the ilosia wes estimated at 2.1 for rtaidentially exposed, and 4.3 for occupational exposed, persons.49 Two studies have bean made of tha possible effects of increased asbestos contamination of drinking water in Duluth, Minnesota, due to tha disposal of taconite tailings into Lake Superior. Mo carcinogenic effects have been noted, but the period of observation waa short rela­ tive to the probable latency period of environmentally-induced can­ cer. 104,105 Carcinogenic Effects—Animal Studies All commercial types of asbestos—chrysotlle, crocidolite, amosite, anthophyllite—have been found to be carcinogenic when eeetad in mice, rats, hamsters, and rabbits. A brief review of evidence derived from 32 OOP 0931679 DU 035416 experimental observations is presented below for its value in corrobo­ rating known human cancer risks, predicting ocher effects, and Increas­ ing the plausibility of certain hypotheses on causal mechanisms. A. more detailed treatment of these and other relevant studies in animals can be round in Appendix 0. Intrapleural or ineraperitoneal injecdon of asbestos has produced sarcomas'* and mesotheliomas. Laboratory animals have not been known to develop mesotheliomas spontaneously, so that finding even a single such tumor in an experiment may be significant. Rats and rabbits receiving intrapleural Injections of crocidollta developed pleural mesotheliomas, as did rats receiving chrysotile. J-06 For both these fiber types the carcinogenic response appeared to be dose-related in another study with rats. 10' Mesotheliomas have also been induced in racs by Russian chrysotlle^-08 and in hamsters by various types of asbestos fibers.^09 Peritoneal mesotheliomas were ooserved in racs following lntrapericoneal injections of chrysodle and crocidollta but not aaoslce.^06 Racs chet received lncraperlconeelly chrysoclle milled to 992 <3 urn also developed peritoneal tumors.Mesotheliomas wera Induced in racs inoculated with crocidollta^}- and in mice inoculated with chrysodle, crocidolite, or glass fiber.^ Lung carcinomas and pleural mesotheliomas have followed from the inhalation of asbestos. Racs exposed to various doses of chrysodle, crocidolite, and amoaica have developed mallgnanc tumors of the lung and of the mesocheliuo.^'^-llS Among these studies, adenocarcinoma, squamous cell carcinoma, and fibrosarcoma were reported. Among groups of racs chat ware exposed with varying durations to five different types of asbcscos fibers, all of which produce aabsscosis, a dose-respons* relationship for malignancies was suggested.6 la this study it was observed that as little as one-day exposure was sufficient to produce tumors. few data exist about the effects of asbestos administered orally. One study found that oral administration of asbestos filter material to rats led to an incraased incidence of malignant tumors.116 Car­ cinomas of the lung, kidney, and liver, as well as ratlculum-cell sarcomas, were found. The available evidence from animal studies relating aabeecos type to differences in carcinogenic potency is limited and inconsistent. This may be due to the predominant influence of size and shape of fibers, which may vary from ona study to anothar for each aabestoa type. Min­ eral fibers ocher chan asbestos, but of similar size, can produce mesocheliomee in racs after intrapleural or ineraperitoneal Injection.10'• 117,118 Alehough the carcinogenic mechanism involving fibers has not * A sarcoma is a malignant tumor derived from mesodermal tissue. 33 DUS 0931680 DU 035417 be«n entirely elucidated, a reasonable hypothesis is that it may be relaced co morphologic characteristics. There are few studies in which fiber 3ize alone has been varied and adequately recorded (diameter as well as lengch). Furthermore, the preparation^ fibers for experimental purposes may alter mineral properties.However, smaller fibers are choughc co be more active in producing tumors. Noacarcinogenic Effects of Asbestos Noncarcinogenlc effects of asbestos exposure were noted several decades before the asaoclatlon bwcween asbestos and cancer was recog­ nized. In 1906, deaths among asbestos textile workers from penumoconiosis were reported in England and France.121,122 these were the first reports in modern times of the diffuse incerstitial fibrosis of the Lung associated with asbestos exposure—"asbescosls AsbestosIs Asbestos is, which is characterized by e diffuse interstitial fibro­ sis of the Lung, is one of the many dust-related lung diseases chat are terminal pneumoconioses. However, unlike some of the ocher pneumo­ conioses, asbescosls does not predispose to the development of pulmon­ ary tuberculosis, nor does evidence suggest thee it is causally related co emphysema and chronic bronchitis.123 Clinical Findings The signs and symptoms of asbescosls, listad below, are no different froa chose for ocher forme of diffuse Incerstitial fibrosis; there are no pathognomonic features. Symptoms: e Breathlessness on exertion e Cough, usually dry, but may be productive e Chest tightness or pain* * Bell milling of chrysotlle, for example, can result la decreased crystallinity and changes in interlayer branching and surface hydroxyl configuration. These alterations have been accompanied by decreaaed hemolytic activity.120 34 DU? 0931681 DU 035418 iialiiiiQLaiMuifiMissfc- Signal • Decrements in lung function (decrease in Lung volume and flows) • Radiographic abnormalities (chesc) • Rales, basilar • Restricted chesc motion e Clubbing of fingers • Cyanosis • Cor pulmonale (right ventricle hypertrophy) • Pleural effusion. The earliest and most prominent clinical finding—breathless­ ness on exertion—rarely becomes apparent until after at least a decade of exposure. Thus, by the time this "early" clinical finding appears, the underlying disease process is veil under way. As the disease pro­ gresses, breathlessness may be present even at rest. The most characteristic physical sign exhibited by the patient with asbestos is is the presence of dry, crackling sounds (rales), heard on auscultation at the lung bases and in the axillae during inspiration. As fibrosis progressas, rales become more widespread and occupy a greater pert of the Inspiratory cycla. Clubbing of tha fingers is usually a lata feature of asbestoaia and la not found conalatantly. Cyanoata of the skin and mucous membranes of the mouth and tongue may also occur in tha later stages of the disease. Radiographic Abnormalities Radiographic features of asbeatosia are similar to chose of ocher fores of diffusa intarselcial fibrosis of tha lung, except for the frequency of pleural changes, expecially pleural plaques (which should always signal the possibility of eabeetos exposure). Radiographic diagnosis of asbeatosia is based on the presence of small, irregular, or round opacities distributed prominently in eha lower lung fields. The earliest changes often occur bilaterally la the cosophrenlc angles. Short, horisoneal, linear septal lints (Kerlay B-lines), which are believed to represent lymphatic obstruction,12* may also ba present. With time, the abnormal shadows gradually spread upward into the middle and upper zones of the lung fields and become increasingly coarse and blotchy. In more advanced caaaa, a "honeycomb" pattern may ba present. 33 DOF 0931682 °V 03*419 and the outline of the diaphragm and heart nay become blurred and "shaggy." Pleural changes are likely to be present as well, perhaps in as many as 502 of the cases. Pulmonary Function Changes The interstitial fibrosis associated with asbestos exposure is accompanied by changes in pulmonary function characteristically observed with interstitial fibrosis from ocher causes as well. Thus, while these changes are not unique to pulmonary asbestosis, they provide useful diagnostic information when interpreted together with ocher evidence such as exposure history, signs and 3ympcoms, and chase radiographic findings. Changes in pulmonary function conslderad moat characcarls tie of asbtscoais are: e General reduction of lung volume, especially of vital capacity (VC) • Decrease in pulmonery flow races such as indicated by forced expiratory volume in one second (FEV^ Q) e Impaired alveolar-capillary diffusing capacity, raflactad by raducsd oxygtnscion of the arterial blood and increased alveolar-arterial PO2 gradient (alveolar-capillary block syndrome). Although it is usually claimad that airway obstruction Is rarely a major faacura of asbaetosie, 123-125 one inveatigecor has poinced out that epidemiologic studies of lung function have been unable to clarify ehe ralacionahip between obstructive airway diaease and aabaacos exposure. She advised chat, until further evidence becomes available, "an open mind should be kept in this regard."54 Aabeseoala and Cancer On the basis of csss rspores, an association between asbes­ tosis and lung esaeer wss suspected as asrly aa tha 1930s. More than a decade later, two authors^1127 reported that, among British asbestos workers, carcinoma of the lung and plsura had been found in about 1SX of deaths elehsr caused by asbestosis or in which asbestosis had been proved present at autopsy.* By tha period 1961-1963, figures from the British Ministry of Labour showed that approximately SOX of patients certified as auffaring from asbestosis (in contrast to exposed to It remained for another investigator * to show that the actual risk of dying from lung cancer wee Increased on the order of 10-fold over the general population for male asbestos workers employed for 20 years or more between 1922 and 1953. 36 DUI 0931683 t)\] 035420 . 123* asbeaeo«) died of (or with) lung cancer. Although carcinoma of the lung is ofcan found In cha presanca of asbascosis. chars appaars co ba no scitnelflc avldanca chat the cvo lesions are interrelated, escape chat they both nay ba classifiad as dlsaaaes that ara causally associ­ ated with exposura to asbestos. With regard co another asbaacos-ralaced cancer, two reviewers of cha subject have nocad that mesochelioua of cha pleura and periconeun has of tan bean associated with avan low levels of asbestos exposure for brief periods in the resioce past.54> 123 There appears to be no regular correlation between severity of asbescosis and occurrence of mesothe­ lioma. In fact, it is unusual to find significant pulmonary interstitial fibrosis (asbescosis) with pleural mesochelioua. However, proainenc asbascosis is frequently observed in association with tumors of the peritoneum,34,123 and peritoneal tumors generally appear to be associ­ ated with heavier asbestos exposure.45,130 One reviewer noted that this appears co support the nbclbn of retrograde lyaphatie spread of asbestos fibers from the lung co the abdominal lymphatics resulting from thoracle Lymphatic obstruction due co advanced pulmonary fibrosis.34 Asbestos Pleural Effusion Benign pleural effusion, which usually occurs in cha presence of soma degree of parenchymal asbescosis. is another clinical manifesta­ tion of disease due co asbestos exposura. Among a serias of 57 patients with asbescosis or asbestos exposure, 12, or 21Z, ware found to have "as bee cos pleural effusion"—1. a., a pleural effusion in an individual with a history of occupational exposure co asbestos in the absence of any other disease known co cause pleural effusion.131 a number of individuals diagnosed as having had asbestos pleural effusion have sub­ sequently developed mesothelioma.132,133 Pleural Calcification, Diffuse Fibrosis, and Plaques Asbestos-related plaques occur as discrete, elevated, grey-white lesions on the inner surface of the rib cage and on the diaphragm. The reason for this apparent increase in the percentage of deaths in which asbestosis and lung cancer were found on autopsy is not clear. One explanation nay be chat the cases described by earlier authors^® • 127 received much of their asbestos exposure in the eerly quarter of the cencruy, when it was likely that airborne concentra­ tions of asbestos were high. As a result, many of these cases nay have succumbed to asbestosis at an early age—before lung cancer, with its long latent period, could develop.l28,129 37 OUP 0931684 DU 035421 Microscopically, eh* plaque* consist primarily of eonnsetivs tiaau*, o£e«n containing deposits of calcium. Th«y do noe interfere vith pulaonary function to any significant extent, nor do they neceaaarily indicate the presence of pulaonary fibroaia. An aaaociation between pleural abnoraalitiea and exposure to asbestos—both occupational and nonoccupational—has been elearly deaonscracad.54,123,134-139 Accordingly, their presence should always alert the exaainer to the possibility of asbestos exposure. In this regard, it aay be 20 to 40 years after exposure to asbestos that pleural calcifications appear radiographically. 135 fil of fe< i-to ev« Although pleural plaques do not, themselves, appear to be precursort of malignant disease, a retrospective death-certificate study of 408 shipyard workers vith pleural plaques shoved that the risk of developing bronchial carcinomas was increased by a faecor of 2.4.93 Three cases of mesothelioma also occurred in this series. In e prospectlvs study from the same shipyard, 235 men with radiographic evtdenes of pleural plaques were found to have a 2.4-fold increased risk of bronchial carcinoma. Among 70 deaths, 13 were due to mesothelioma, an excess of obvious significance.34 tax rat * In fli (at Lir gri ant Aebeetoe Wart* Asbestos verts, or corns, are of minor hsslth significant, but thty art sn indication of axposure to asbestos. They are caused when asbestos fibers penetrate the skin and are most ofeea found on tha heads and forearms.140 the wares may have e pinpoint, black center and ara often tender to pressure. Unless rasioved by excision, they aay persist for years. obf chc phj be* Animal Studies—Cvidance of Honcsrcinogsnlc Effects Exposure by Inhalation to any of the four commercial aabeacos cvpes may result in fibroaia of the lungs in animals as wall as in human*.1*1 Under experimental conditions a fibrogenic response to inhaled asbeaeoe has been reported in rata, hamster*, guinea pigs, rabbits, end moak eye. 142-14* Outsld* Cbm laboratory, pulmonary fibrosis la tha presents of fibers end asbestos bodies has bean demonstrated in baboons, donkeys, and wild rodents living in the vicinity of croeidolite mines or mills.145 Pulmonary asbeatosis has also been reported in s dog kspe as s ret catcher in a London aabaseo* factory.146 Thera are marked Incarspeelas differences in susceptibility to asbeseosls. Tissue reaction in rets, rabbits, end monkeys la typically laas severe then in hemseers end guinea pig*.142,14/ Su it pb iy se me 38 out 0931685 DU 035422 •wimiailry F?.S4l^-;lnt-+si;saii3 Subeutaneoua injection of asbestos or injection into the pleural or peritoneal cavities produces a fibrocic reaction, thickening of the pleural, pericardial, and peritoneal membranes has been reported, with formation of adhesions and granulomas as veil as pulmonary and media­ stinal abscesses.17-148-149 Neither shape nor chemical composition is sufficient to explain the fibrosing effects of asbestos. Fibrosis has been Induced with a variety of fibrosis as veil as nonfibrosis mineral dusts. Some Investigators feel that fibers are more fibrogenic than nonfibrous particulates and chat fibrogenic reaction Increases vlth increasing fiber length. How­ ever, the role of fiber length is difficult to evaluate without simul­ taneously caking into account possible effects of diameter end aspect ratio (lengch/diamecer). On injection, chrysocile heated to 400°C caused fibrotic reaction in the pleura of mice equivalent to that of unheated chrysotile, but fibrosis production diminished as temperatures Increased above 40Q°C (at 600 C, 800°C, 1000°C). Asbestos in dust from automobile brake linings, which are subjected both to high temperature end mechanical grinding, resembled chrysocile chat had been heated to 800°C or more and then ground. Effects of asbestos chat may ba ralatad to fibroganesia have been observed in vivo In mammalian tlssuaa as vail aa in cell culture. Bio­ chemical changes, including stimulation of anasroblc matabolism, and physical sffacts such ss damage to cell membranee and chromosome# have been noced. l50~138 Such observations may shad light on the mechanisms by which asbestos Induces fibrosis. For example. It has baen poatulatad that during phegocytoels, eebeecoe cauaes damage to the membranee of macrophage lyaosomes, which are cell orgenellea that contain lytic enzymes. Sub­ sequent Intracellular release of these ensymea may injure or kill the macrophages, resulting la release of e fibrogenesia-stisailatlng factor.0* 39 DO? 093168$ DU 035423 Chapter IV OCCUPATIONAL EXPOSURES There Is little recent date in the published literature on expo­ sures to asbeacoa, and it ia difficult to aaaeaa whether vhac haa been published is typical. Furthermore: e Occupational asbeacoa concentrations are commonly reported aa optlcal-nicroscope-vlsible fibers per milliliter greater than 5 um long, and these may account for only a small fraction of che total electron-microacopa-viaible fibers • It is not known whether small differences in fiber counts actually reflect differences in fiber levels or, if they do, whether they indicate a change in the risk of incurring asbestos-related diseases (see Appendix C). Nevertheless, quantitative air sampling data from representative occupa­ tions is provided in this chapter la aa attempt to indicate the range of exposures found in three workplace situations: asbestos mining and milling, production and processing of asbeseos produces, and utiliza­ tion of asbeseos-containing products. Fever then 600 parsons in che United States ere employed in mining and milling asbestos.* However, industries thee manufacture asbeseos products or chat make use of them provide jobs for millions. These industries may be categorised aa primary, secondary, or consumer accord­ ing to whether thay produce manufactured goods from raw asbestos fiber, process asbestos manufactured products to make other products, or utilize a finished produce containing asbeseos wlthoue additional modi­ fication. Over 37,000 persons ere employed ia the manufacture of primary asbestos produces; 300,000 sre employed in secondary ssbestos industries; and mllliona more work la the eebeetoa consumer induetries—over 183,000 a Many more may ba exposad to asbestos as a contaminant during tha mining and milling of other minerals. 41 OOP 0931687 DU 035424 of them in shipyards and almost 2 million in automotive sales, service and repair.i’ *o Exposures in Mining and Milling at Soureaa of asbestos axpoaure in mining and milling includa blaating, cruahing, transporting, and drying ora; air-aapiracion milling; and diapoaing of waste. Tima-weighted-average (TWA) lavala of fibar in mining repotted in 1973 rang ad from 0.3 to 2.3opeical-microacopa-vtaibla (o-m-v)* fibara par millilitar, with an avaraga of 0.9. Much highar concancraclona vara found in milling, vhara expoauraa rangad from 6.0 to 12.1 fibara par millilitar.J ch of ce ba 22 ni di In addition to mining and milling of aabaatoa, tha mining and mill­ ing of oehar mineral oraa that may contain aabaatoa aa an impurity la a potantlal aourca of aabaatoa axpoaura. For example, coneantrationa of aabeatlform fibar la ona hard-rock gold mina vara reported in 1976 to avaraga 0.25 o-a-v fibara par millilitar, ranging up to 2.1,3 and fiber counce of 3 to 260 par millilitar vara recorded in a calc mining and milling operation, according to a 1973 report.* , to gr lm ba ha sh gei thi dui lit Expoauraa in tha Aabaatoa Products Induetriaa For all tegmenta of tha primary induetry, manufacturing bagina with fiber receiving and varehoualng. Lavala of airborne fibar in thaaa areas have rangad from 0.2 to 2.3 o-m-v fibara par millilitar and are typically aboue 1.0.+ Lavala ae tha upper limit of tha range raflace damaged shipments, earalaaa unloading or ineffective housekeeping. The moat important factor Influencing aabaatoa exposure at this step of production la tha condition of tha bags in which aabaatoa la shipped. Tat Next, aabaatoa fibara arc lntroducad into tha procaaa. Baga of aabaatoa era usually cut open and dumped manually, either into open hoppers or Into bag opening enclosures. This activity can result la relatively high expoauraa if hooding is inadequate or lacking. Disposal of tha emptied baga may also add to airborne fiber levels. In four of tha seven major primary Industriaa, highest TWA expoauraa occur la fibar introduction sad have rangad from 0.3 to 10.0 o-m-v fibara par milli­ liter, typically aommhat above 2 fibers. in avi trt fit elt hat mat see pr* Exposures in mixing and blending depend upon haw dry the materials are chat are being mixed, the intensity of agitation, and tha effective­ ness of vent list ion. Typical TWA values in tha peat have bean c tnt * ing Greater than S micro: tears in length. ape +Data in this section are from Chapter Reference 1 (published in March 1976). 42 DOS 0931688 DU 035425 exa taastfe e. .n approximacely 2.2 fibers per raiUiliter, with a rang* of 0.2 co 10.0 fibers par milliliter. Sometimes asbeseos is dumped directly from tha bags into mixing or blanding tanks, augmenting tha usual exposures found at this step. Onca the asbestos fibers are engulfed by a medium that prevents them froa bacoaing airborne, exposures drop. This may oeeur at tha step of nixing and blending—as in the production of floor tile, paper, and ceaenc pipe—or in a subsequent step. it co Exposure levels in formulation operations have ranged froa 0.2 to 22.0 fibers per milliliter, with an average level of 1.3 fibers per milliliter. This vide variety of exposures is due co the nuifcer of different processes represented by that stage. l- Finishing operations vary significantly froa one type of industry to another, but usually include machining (i.a., cutting, drilling, grinding) che rough produce co specification. The mechanical energy imparted during machining causes asbestos fibers to break loose and become airborne. Average TVA levels of-exposure in these operations have ranged froa 0.1 co 8.0 fibers per ailliliter, with a mean of 1.6. tn the last two production seeps—inspection, and storage and shipping—asbestos exposures are usually the result of airborne dust generated by ocher operations, which may drift through che plane to these areas or adhere to che products themselves< becoming airborne during handling. Exposures are typically leas chan 1 fiber per milli­ liter. Exposure levels in the major asbestos industries sre summarized in Table 6 and are discussed below.1 Friction Products friction produces may contain 30J! to 80S asbestos, and TVA exposures in tha industry vary widely (0.1 to 13.0 o-s-v fibers par milliliter), averaging 2 fibers per milliliter for most operations. Grsstsr concen­ trations may occur la preforming operations, ranging from 0.3 to 22.0 fibers per milliliter and typically about 4 fibers par milliliter. The elevated exposure levels found la these operations result from manual handling of tha dry preform mix (asbestos fibers and metal reinforcing materials in en organic matrix), which is conveyed in open certs, scooped by hand, weighed, and pourad into a block mold for mechanical presting Into the shape of the finished produce. Other operations thee may yield high aabsstoa levels include fiber Introduction, mixing of the dry preform, and finishing. During finish­ ing, the produces are trlsssed, drilled, sanded, ground, and sawed to specification. Exposures vsry with work practices and equipment. For example, exposures ae ventilated radial grinders are below 2 flbera per 43 DUF 0931689 J DU 035426 -■n- ' Tikli i tXMSUW TO tllKIH ASIUTOI [, StUCTID liitroi rnx'xr wuwncrottHc tKOwtiu >n«tH Csncaaeratlaii. tTlaa-WtlttiraK Avar... In H.aca/«L)* laiai Ubm TiHea i >>mi l 0.1-13.0 * 0.5-22. 0 Miaa at 0p«raeion(p) Productlaa tarlttra F«nU| «p tolUflf *,W0 ' flk*r tttn* duceiM 1,100 Ftfetr liter** 4<«celM 300 ftlccioA froduett Frlury SecMdjry Frlaary iteaaaary Aaka.tae uufareW Kniiii Jrtmry 2.S-4.J l 0.7S-2.7 2 0.0-2.4 1.0-3.5 1 0.2-2.J 2 0.3*3.0 0.3-2.0 Cmmmmt Ftp* 7.M0 34,300 4.300 L9I,OOQ 2.(00 11.000 l.S 0.23O.S 2 0.4-4.} riituhtiif 1,400 2 0.1-4.7 2 0.9-4.4 9ry HUU|. 3«4in« <00 2.400 ClM !k(t( FrlMfy S«eon4«ry ria«r til« Fflury t.0-4.0 l 0.3-*.} 4 0.4-4.2 Fl4«r Caeroduceta* 2,W0 4,;oo 4 0.20-10 4 2.0-19 cirtui 2.400 2.700 U«M4iry fllMIt Clltlltt i«4 tuUiu 1,3(30 24.000 2.0-4.0 i 1.0*2.3 7,300 2.S 1.5-4.0 FUar l«et** 4ucclt» 3S0 3,000 *anU»l««ltmt»)i»iri»lH« Mkara, ) ua loaf #f lonm. Sautaai 3*Lay UU layka AJ, Sak* JU TaakaaU(i«aI faaaiklltcy la «ia-lt 1«m*( if 0*M .rayaa.4 ravialaa ta rka ukaacaa itaUarl. lay r, Vaataa bivLraaaancal Caa*aLciat«-Oaait»«Tat Kara* 1*7, (.rayarao (act AlUlCH tnLorutlaa AaaacUUan at Karen UMflia). 44 DO? 0931690 DU 035427 mlllilicar, but chamfers and backgrindars may cause exposures of 3-3 fibers per miliillcer.3 If the finished products have not been cleaned of adherent particulates, exposures may be high during Inspection (4-7 fibers per milliliter). Asbestos Paper Exposure levels In the asbestos paper Industry vary with the asbestos content of the manufactured product, which can range from 5Z to virtually 100Z. Typical TWA concentrations in the primary industry average 1 o-m-v fiber per milliliter (range 1-3 fibers per milliliter) except In fiber introduction and scock preparation (vet blending), where concentrations typically average 1-3 fibers per milliliter and range up to 10. The lever concentrations are achieved in plants which use disintegrating, puipable bags, thus obviating bag opening, dumping, and disposal. Since papermaking is a wee process, little asbestos dust exposure is realized after fiber introduction until the product Is dried. Expo­ sure concentrations may than be elevated somevhec by the manual handling and mechanical modification (slitting, calendering, converting, etc.) needed to prepare paper sheet according to specifications. , Asbestos-Reinforced Plastics The asbestos conttnt of reinforced plestlc is relatively small,1 and reportad exposures in boeh primary and secondary industries are lower chan in most ocher segments of the asbestos industry. TWA concen­ trations during most opsraelons range from 1.0 to 2.5 o-m-v fibers per milliliter. Fiber introduction, dry blending, and handling of the blended mixture and preform are sources of moderate levels of exposure. After the preform has been reaelted, the asbeeeoe Is bound tightly in the polymer matrix, reducing the potential for airborne raleaae. Fibers may still break free, however, during finishing. Asbestos-Cement Pipe and Sheet Asbestoe-cement products may contain 10Z to 70Z asbeatos. Although tnora aabastoe ia used In manufacturing aabeetoe-cement pipe end sheet then any other primary aabascos products, relatively few workers are employed in these branches of cht Industry (3,600 total, 2,200 in pro­ duction) .1 (n asbestos-cement pipe factories, TWA fiber Levels range from 0.5 to 4.5 o-m-v fibers per milliliter, averaging about 1.5. In the 45 DOS 0931691 035428 * * a«1;lfii8gS« ill • -» manufacture of asbestos-cement sheet, some fiber-introduction and drymixin* operation* may yield higher exposure level* (0.3 to 8.7 fiber* per aillilicer) than in the manufacture of aabeatos-ceaent pipe, because fiber may be introduced directly into the dry mixer. Onca fiber* are engulfed by the cement mortar during wet mixing, there l* little oppor­ tunity for them to become airborne until finishing. Higher level* (averaging above 2 fiber* per milliliter) may be found during cutting and machining in cement pipe factories; and sheet trimming and sanding present the highest levels of exposure in the asbestos-cement-sheet process, generally about 2.S and 3.0 fibers per milliliter, respectively. Floor Til* Asphalt or vlnyL asbestos floor til* contains 8X to 302 asbestos. Airborne TWA asbestos concentration ranges from 0.S to S o-m-v fibers per'milliliter. Typical concentrations are approximately I fiber per milliliter, except for fiber introduction, where concentrations of 4 fibers per milliliter are conon. Once the asbestos is engulfed by the agglomerated plastic during the later phases of mixing, the potential for exposure is reduced significantly. Asbestos Textiles levels of exposure in primary and secondary production of asbestos textiles vary directly with the asbestos content of the manufactured products but generally ere higher than in any other asbestoe industry besides milling. A typical TWA concentration of airborne fiber—i.s., for most operations—in the primary textile industry is 4 o-m-v fibers per aillllicer (rang* 0.1 to 22.3 fibers per milliliter) except in the carding operation, where the typical concentration exceeds 5 fibers per milliliter (range 6.1 to 27.3). High asbestos exposures in the asbestos textile Industry result from ehe processing of dry—or, at base, par­ tially damp—fibers, which are easily dispersed into the atmosphere. During carding, the vigorous manipulation of the dry fibers to asperate and align them accounts for the particularly high concentrations observed at this step—even in the face of intensive efforts to achieve effective ventilation. The liquid dispersion method of asbestoe textile manufacture, in which asbestos fibers are mixed in veter with chemical dispersing agents, results la much lover exposure levels (less chan 1 fiber per milliliter) them in conventional plants.& Moreover, the use of asbeseos textiles I 46 DOT 0931692 DU 035429 imi. iSjrjil!,";-naBfc.ihUii ajflBllfc i iud« from dispersed yarn* result* in. significantly lower asbestos exposures to the user than from conventionally manufactured products.7 Exposures in the Utilization of Asbestos-Containing Products Vlth two notable exceptions, the insulation trades and clutch and brake Installation and repair, levels of exposures to workers in the consumer Industries are generally very low. But although exposure levels are low, the vast majority of workers in the asbestos consumer industries, it is surmised, are less aware of the health hazards of asbestos chan are workers in the production industries and may not utilize basic control methods to minimize risk. Insulation Trades ’Exposures in the insulation trades vary widely, but they include the highest occupational exposures and control la difficult, tn the early 1970's, there were approximately 36,000 Insulation installers8 employed largely in insulating industrial equipment, commercial buildings,, and ships. It is difficult to obtain characteristic exposure levels for these workers due to the many different Insulating materials and condi­ tions of work. The asbestos content of materials In use ranges from 10Z to almost L00Z. Asbestos substitutes 4fk gaining in use as regulations over the use of asbestos become increasingly more restrictive. Jobs performed by insulation workers can be classified into six categories: e Prefabrication: materials are precuc and shaped using hand or power save either on the job or at the con­ tractor's shop (10Z of time). e Application: Materials ere fitted, heanered, or carved and aetachad to surfaces by wiring or gluing (40Z of time). Some materials used to be sprayed applied, but this practice has been virtually eliminated in raeene years. e Finishing: Materials are coated with asbestos-containing cameac, resin, asbestos or cotton doth, or petroleum based sealer (30Z of time). "Rip-out": Removal of old or unusable materials la the process of rsinsuleting (10Z of tlma). a • Mixing: Mineral wool, asbestos, fiber glass, and cement or glue are mixed in buckets or troughs saperetely or In combination (5Z of time). • Miscellaneous: (SZ if time). Cleaning up, transporting materials 47 DU? 0931693 DU 035430 at Percent of time at each cult is highly variable, of courts, and incandad only aa a rough guide.9 Highest concentrations encounterad by insulation workers hava occurred during "rip-ouc" or removal of old aabescoa insulations. In a 1968 report on air saaplaa collected on a ehip during removal of sprayed aabeacoa coatings, removal of IQOX-aabeatoa lagging, and subse­ quent cleanup ware said to average 248 o-m-v fibers par milliliter, 62-159 fibers par milliliter, and 353 fibers per milliliter, respec­ tively; in comparison, the application of pipe lagging containing 1SX asbestos resulted in exposures of 5-60 fibers per milliliter, and cut­ ting and drilling incombustible board prior to installation yielded exposures of 0.7-4.5 fibers per milliliter.10 levels of 30-100 o-m-v fibers per milliliter have been reported ruing application of spray asbestos insulation.11 Nearby workers may be exposed to elevated levels of asbestos as the result of the activities of insulators— especially in shipbuilding, where work often goes on in enclosed poorly ventilated spaces. Brake and Clutch Repeir There are almost 2 million persons employed in automotive sales, service and repair, of whom 900,000 are said to be frequently exposed to asbeetos from automotive brake and dutch repair.1- (Kota that this figure does not Include persons who repair ocher kinds of brakes and dutches.) Asbestos exposures were determined for specific brake servicing operations including blowing-out automobile brake drum assemblies, grinding used truck brake linings, and bevelling new truck brake linings. Average peak o-m-v asbestos air concentrations for these activities based on sampling within 10 feee of the ooeracor were 10.5, 3.75, and 37.3 fibers per milliliter, respectively.^ In s similar study, mean eoncaatraclons found 3-5 fast, 5-10 fatt, and 10-20 feae from aa operator blowing dust out of brake drums were 16.0, 3.3, and 2.6 fibers per milliliter. Grinding truck brske shoes gave average concentrations of 4 fibers per milliter, and bevelling produced an average count of 37 fibers per milliliter. Measurable con­ centrations (0,1 fibers per milliliter) were found sc distances up to 75 feet from the blowing-out oparetlon (14 minutes after), 60 feet from grinding, end 30 feet from bevelling, indicating that other garage employees besides those directly Involved in brake and dutch repeir are ae risk.13 Another study estimated the else-weighted average exposure for brake mechanics to be 0.8 o-m-v fibers per milliliter.14 Installation of Floor Tile, Roofing, and Siding There la limited Information relating to levels of exposurs during Installation of asphalt or vinyl eebeetoe floor tile. Because asbestos 48 DU» 0931694 DU 035431 ~MM£ it fibers art firmly ‘imbedded in cha riles, installation per se is unlikely to be a source of important asbestos exposure. It is accepted practice, however, to sand old asphalt or vinyl tile floors before installing new* covering. Conventional belt senders with coarse grit are used to sand che tiles, and, normally, 240 to 250 square feet of tile can be sanded per hour. One report states that levels of 1.2 and 1.3 o-a-v fibers occurred during a simulation of normal sanding activities over a short­ term sampling period.15 It is likely chat fiber levels fluctuate slgnificancly depending on the age and condition of the tile being sanded, grade of sandpaper, speed of the sender, size of the workspace, ambient humidity, and quality of ventilation. Installing asbescoa roofing and siding should result in exposures of lesser magnitude sines chase operations are performed outside. Use of Spackllng, Patching, and Taping Compounds Asbescos may be a primary component of speckling, patching, and caplng compounds used in wallboard construction to finish joints and repair damage, or it may be a contaminant of calc, limestone, or other rock used as rav material. Used mostly in the construction induscry, che compounds are also used by persons doing their own construction and repair, and intermittent exposure to asbescos may occur during nixing, application, and sanding (finishing). To determine possible exposure during application, air samples were collected at various jobs and sites. Peak airborne asbestos concen­ trations measured during such operations as hand sanding, poie sanding, mixing of dry spsckle with vatsr, and svssplng-up averaged 2.3 to 47.2 opclcal-mlcroscope-vlslble fibers par milliliter.1* All exceed che current OSHA oecupationsl stenderd for an 8-hour tlrae-uelghted-everagt (2 fibers per milliliter), end many exceed the permissible ceiling (10 fibers per milliliter). Wssring Asbestos Garments Tests of wearing asbsatoa garments hsvs indicated that breathing zone concentration esn exceed 2 o-m-v fibers per milliliter. At one plant where hoods, coats, mittens, and leggings were worn, concentra­ tions of airborne asbescos fibers ranged from 9.9-26.2 fibers per milli­ liter, sad the 8-hour cise-weighted-sverage concsncrsclon was 4.7 fibers per milliliter.17 Exposures from wssring flrs-flghtlng helmets also have been mea­ sured. A new helmet with an unllned asbestos cover, an identical older helmet, and a helmet covered with sluainizsd asbestos cloth produced breeching zone concentrations of 2.3, 1.4 and 0.0 o-«*-v fibers per milliliter, respectively.13 DU? 093169S DU 035432 ' jit i.wnwagi- ..nrr.i-pai.. Chapter V SONOCCUPATIOHAL EMISSIONS AND EXPOSURES Persona noc employed in asbestos-related occupations are exposed co asbescos fibers chac originate from natural sources or from mancreaced sources such as che manufacture and use of asbescos produces. Such asbescos may be Inhaled—is, for example, in an office building in which che air is contaminated by asbestos insulation—or it may be ingested with water, food, and drugs. As would be expected, che further one gets from the occupational environment, the fever data there are on such exposures—termed "nonoccup-tional" exposures. However, the avail­ able data are reviewed here co provide at least some indication of possible general environmental contamination. (See Appendix C for a discussion of che difficulties in measuring asbestos contamination.) Asbestos Emissions from Natural Sources Rock chat contains asbestos can be disturbed by natural means, such as weathering or landslides, or inadvertently by such human interven­ tions as road building, construction, and tilling of che soil. In such cases, free asbestos fiber may be deposited onto soil or enter air and water,1- thereby contributing co levels of contamination in the ambient air and in water as discussed la this chapter. The occurrence of rock formations that could possibly contain asbestos was discussed la Chapter I of this monograph, and che geograph­ ical distribution of such rock formations in the United Stated is shown in Figure 1. If the primary areas of source rock are looked at in conjunction with high population density, che most critical areas for emissions from natural sources appear co be eastern Pennsylvania, south­ eastern New York, southwestern Connecticut, and greater Los Angeles and San Francisco. Aabeatoe Emissions from Human-Created Sources Human-created sources of nonoccupational exposures co asbescos Include the mining and milling of asbescos; Che transportation of asbes­ tos materials and products; che manufacture, installation, use, and demolition of asbestos products; and che disposal of wastes. Some gross estimates of annual emissions in che United States from asbescos mining and milling, manufacturing, use of asbescos 51 DUP 0931696 DU 035433 •eagrem* product*, and disposal of vast** hav* been made and art shown in Fig­ ure 2. Although the*e estimate* are uncertain, by at least an order of magnitude, several important conclusion* are indicated: • Asbestos is preponderantly disposed to land, least to water. • Most of che asbestos disposed to land is consumer waste, which is more likely to be disposed to uncontrolled waste dumps and handled by persons unaware of che hazards. • Disposal to land is an important source of atmospheric asbestos and, because of proximity to urban popula­ tions, may be even more significant to health chan the emissions to air chat come from mining and milling. Redistribution and Fate of Asbestos in the Environment Because asbestos is exceptionally resistant to thermal and chemical degradation, it persists in the environment and can be widely redis­ tributed by both natural forces and human means. The magnitude of this redistribution is governed by an extraordinarily complex see of factors which Include che height of the emission souree, che races of air and waeer flow, fiber diameter, rain, thermal air inversions,, electrostatic forces, agglomeration of particles, and the density of vehicular traffic on asbestos-containing landfill, to name only a few. Redistribution by Air If, for example, asbeatos is emitted to air aa part of a "large" egglomarated particle, it will settle to earth relatively quickly and thereby have a limited potential for environmental contamination; thus, concern over che relatively large quantities of asbestos emitted co air from mines is somewhat attenuated by knowledge that the mining processes tend to produce relatively large particles. At che same time, however, an appreciable fraction of che large maas of asbestos dis­ charged by mills is in che form of free fibers that may remain in the atmosphere for long periods of time, travel great distances, and expose many people. Studies of atmospheric pollution in che area surrounding asbestos mines and mills in Finland showed small astounts of asbestos dust as far sway as 27 kilometers.2 K simplified calculation of "drift discance" for two sizes of 3 asbestos fibers was made for this monograph using che method of Cowherd and a terminal settling velocity as determined according to Harris. Fibers were presumed to be injected ac a height of 50 feet (15.2 mecers) 52 DOF 0931697 DU 035434 disposals a n d e m is s io n s o f a s b e s t o s f r o m asbesto s raooucTiOM. MANUFACTURING. AND CONSUMPTION M THE UNITED STATES" ( h u e Torn! „ jig £.■ f ig u r e 2 . g-ijP Hi*: iA. OUF 0931698 DU 035435 —::jilftjftralMlMiaii Igat «■ ?; into * constant crosswind of 10 mph (4.5 mecara/sacond) vleh no ntt efface of turbuienea. The locality was assumad to be rural with a "roughness height" equivalent co chat of a wheat field. A small fiber« one with a diameter of 0.1 mlcrooetera and length of 10.0 alcromecera, under such conditions would drift 1120 kilometers; a large fiber, 1.0 mlcromacar in diameter and 50 micrometers long, would drift 13.3 kilom­ eters . Redistribution by Water Asbestos borne by water can alao travel considerable distances. Studies of Lake Superior, reported in 1974, indicate that asbestos particles can move several hundred miles or more.5 Another report, made In 1976, shows chat high river flows in surrounding regions have resulted in unusually high fiber counts in the Philadelphia and Atlanta water supplies.& Water samples taken from wells located in areas containing asbestos rock have shown elevated concentrations of asbestos. A well at Malvern, Pennsylvania, drilled in a belt of serpentine rock, had an asbestos concent of up co 0.157 nicrograns per liter, in contrast with a well at Glendale, Arizona, In an area known not co have such rock, which had an asbestos content of 0.023 nicrograns per liter or less.? The Ultimate Pate of Asbestos Fibers Very little has been reported on the ultimate fate of asbestos fibers once they are released to the environment. While it is known chat fibers can be readily subdivided by mechanical means into fibrils of submicron diameter, it has not been established if fibers are sub­ divided by natural means. It does seem Likely, however, chat natural forces such as erosion, grinding, abrasion, moisture, and temperature gradients would cause their eventual subdivision. All types of asbestos resist prolonged attack by strong alkalis. However, it has long been known chat hydroxyl groups of chrysoclle, in contrast with other asbestos types, will react with weak acids and even waeer, causing magnesium and silicon to be released from the crystal lattice.8-10 Generally, despite some degradation, it is felt that the fibrous morphology is retained.8 Thus, to a limited extsnt, ebryeotile may undergo decomposition through reeceion with water and add present in the environment. Temperatures required for thermal decomposition of asbestos are seldom attained in the natural environmanc. With chrysoclla, dehydra­ tion occurs at about 100°C, and full dehydroxylation is achieved at DUf 0931699 DU 035436 hlgher temperatures. Exposure to Airborne Asbestos As one would expect, airborne asbestos csn be found in the vicinity of asbestos mines, mills, manufacturing facilities, and waste dumps. But elevated levels of fibers also may be found near concentrations of braking vehicles, in buildings in which asbestos spray products have been used, and in cars and homes of asbescos workers who have contamin­ ated them with dust brought from the work area on clothing, body, or equipment. Asbestos may ba inhaled by persona who inatall their own aabestoa roofing or flooring, or who repair such items as automobile brakes and clutches, home heating and plumbing systems, wiras for toastara and waffle irons, or cha valla of thalr homes. Other situations with possible exposures to airborne aabtstos include the use of roads and driveways surfaced with asbestos-Peering gravel or paving, humidifiers charged with water containing high levels of asbescos, talcum powders, paints containing asbestos, and cigareecaa with asbescos filters (reportedly no longer used in 17.S. cigarettes). Even powdered pipier machd mixes, which are widely used in claaantary schools, have been found to contain 50Z or more asbestos.*-1 These exposures may be of a one-time or intermittent nature, but, because of the cumulative permaaencm of a small portion of inhaled aabeacoa, they contribute to a person's total risk. Asbestos is also found as a contaminant in the ambient air, and this source is created first in the review of exposure sources that follows. Exposure from Ambient Air The large majority of the U.S. population doss not live in areas that have alavacad levels of atmospheric aabeacoa due to aabeacoa min­ ing, milling, manufacturing, or construction. Nor are most people Involved la pare-cinm installation or repair of aabeacoa products. Ambiaae air, therefore, conaeleutee the basic source of atmospheric exposure for chm population ac large. There la a paucity of atmospheric asbestos-concentration data, due, in part, to cha coat and difficulty of obtaining it. Moreover: data have sometimes bean reported as mass of aabestoa per volume of air (nose often cha case)* while sometimes as concentration of fibers; *Appendix E contains data from several studies. 55 ou, osmoo DU 035437 ■> usually only chrysocile asbestos has been measured; and the procedures for measuring, and hence the precision of the measurements, have varied widely. The Environmental Protection Agency is currently developing standardized measurement procedures, but until these are implemented and substantially more data are accumulated, atmospheric asbestos levels will be largely unknown for most geographical areas. The scant data available for ambient levels of asbestos in rural air include a reported range of 0.01-0.1 nanograms per cubic meter,12 and levels of 40-100 elactron-microscope-visible fibers per cubic meter found in a remote area of California.Id Average reported concentrations of asbestos in urban air vary between 0.09 and 70 nanograms per cubic meter^>12 and, from one study, between 0 and 2,400 electron-microscope-visible (2.4 o-m-v) fibers per cubic meter.t3 Fiber readings in one study of air at Silver Bay, Minnesota—readings that are not typical, since the locale is near a taconite milling operation—ranged up to 130,000 electron-miseroacopevisible fibers per cubic mater.16 Exposures from Asbestos Minina, Milling, and Product Manufacture Asbestos fibers are released in mining and milling during removal of overburden and preparation of ore bodies for serlp and open-pit min­ ing, as well as during drilling blasting to remove ore. Other emissions occur from ore piles and wests dumps that are exposed to wind due to dis­ turbance by bulldozers. Drying, crushing, grinding, and screening of the ore result in the release of fibers. In this connection, the large volume of air required for alr-esplratlon milling (seven to tea tons of process air for every ton of fiber produced),17 together with the length of time chat asbescoa fibers can ramain suspended in air, generates a significant potential for emissions. Baghouaes ara tha predominant anglnaarlng control maasurs used to remove airborne dust from sffluent air streams st mills ind manufac­ turing plants. A study la 1974 shoved that baghousos using spselfie filter materials, and when properly designed, operated, and maintained, have a collection efficiency of over 99.99% for fibers greeter then l.S micrometers in length.18 However, the collection efficiency for fibers less than 1.3 microns in length was approxiaatsly 982. Since generally thsrs era an snoraous number of short fibers, s considerable quantity of fibers can be released to the atmosphere even after passage through the best available baghousas. Fibers removed that ere not reintro­ duced into tha production process must be disposed of outside the plant and may result in emissions to air. A 1974 field survey on the air concentrations of aabeatoa fibers in the vicinity of an asbestos mill at Coalings, California, shoved 100 million electron-microscope-visible fibers per cubic meter within 300 meters from the mill-tailings pile.18 No data for farthar distances 56 DU* 0931701 DU 035438 jMtMS*. from cha source are reported. A 1974 EPA report showed atmospheric concantraeion* of 2 to 106 micrograms per cubic meter within about ona kilometer of the. Vermont mine-mill complex.19 Average reading! ware about 30 micrograaa par cubic meter. Ac another alta, about 1.5 kilom­ eters from the plant, the readings ware .012 to 0.130 micrograms par cubic meter, with an average of about .096 micrograms par cubic mater. In 1972, soma atmospheric sampling was conducted at cha asbestos mill located near King City, California.20 one sampling station locaced 100 maters downwind of the sourca showed concentrations on the ordar of 100 million fibers per cubic mater, and, due to unusual wind conditions, concentrations on cha ordar of 10 million e-m-v fibers par cubic aatar ware recorded at a station located 500 meters upwind from cha sourca. Anocher atmospheric sampling, conduccad within 3 milometers of the mill during August and November of 1974, showed concentrations of up to 1 million fibers per cubic merer downwind and 10,000 fibara per cubic merer upwind.21 Elevated concentrations (4,500 fibers per cubic meter) were found out to the farthest station (3 km). These samoles were obtained with an 0.8 micron-pore-sized Nuclepore filter, whereas the 1972 samples were collected with a Milllpors filter. Hence, it would appear that the Nuclepore filter failed to collect a substantial number of fibers smaller chan one micron and that the 1974 data may have under­ estimated the total number of fibers present. The King City mill is unique in that it uses a vac proeass; hanca, it la balltvad that most of the fibara in the atmosphere comm from the ore pile and tailings dump. Disparalon of asbaatos emitted to the atmosphere depends upon fiber length, topography, meteorological conditions, and the emission source Itself. Wind speed and taatperature stratification are importane factors. Aa asbeecos travels in the etmosphere, gravity and rain remove le from the atmosphere, and the procaas of agglomeration can be a significant decarmlnanc of how many fibers will be present. Because moat of these factors are different at each site, detailed estimates of asbestos con­ centration in the atmosphere ae each sits require individual, special­ ized, calculations. Exposure from Transportation of Materials Containing Asbestos Movement of asbestos ore from mine to mill in open trucks, often over roads paved with mill tailings, may contribute to cha overall con­ tamination of tha environment.* However, three of five mills operating ^ 22 The national asbeacoa air emission standard prohibits tha surfacing of roadvaya with wastes containing commercial asbestos or tailings from asbestos mining and milling, except for temporary roadways in the area of an ore deposit. The use of wascas that may contain noncommercial asbestos aa a contaminant has not been regulated. 57 DU? 0931702 DU 035439 r, -f. FW-iffc .£1 la the United States ere located at the minest che remaining evo ere separated by shore, rurel, dlseancas (32 and 33 miles). Shipment of milled asbestos fiber, usually in bags, can result in emissions when begs are broken, but such emissions era minimized by pressure packing and unitization as described in Chapter II of this monograph. If begs are reused, either in che asbestos industry or elsewhere, they may become a source of contamination.23 When milled asbestos is pelletized end transported in seeled railroad cars (see Chapter II) che potential for emission is no doubt reduced considerably. Emissions of fibers could occur during che shipment of manufac­ tured products, but they would be negligible, since most manufactured products contain asbestos tightly bound in a matrix. A more important emission source, perhaps, would be che transporting of asbestoscontaining solid wastes in open vehicles through urban areas. Also, the transportation of ocher asbeseos-bearing ores, such as calc and caconlce, and their products may result In environmental emissions. Exposure from Asbestos Manufactured Products Most asbestos is incorporated into finished products where che fibers are bound in a matrix (e.g., asbestos-cement pipe and sheet, flooring and roofing products, and friction products), and this reduces the possibilities for air contamination. Yet, by the application of sufficient energy, fibers may be dislodged from even tightly bound materials; automobile brake linings are an example. Clearly, there era opportunities for human nonoeeupatlonal atmos­ pheric exposure during installation, use, and rapeir of asbestos pro­ duces. However, sines there ere so many produces thee use eebeseos or materials that may be contaminated with asbestos, it would be nexe to impossible to eetiaete human exposure for each produce type. In the paragraphs thee follow, some date end information era presented for automotive friction materials and aprey asbestos. Automotive Friction Materials Friction materials used In automotive brake linings, disk pads, ,mt clutch facings contain an average concentration of 30Z chrysocile asbestos by weight.24 It has been estimated that about 118 million pounds of asbestos art ussd annually to product brakes in the U.3. and, assuming « 13Z grinding and milling loss, approximataly 103 million pounds of asbastos are actually incorporated into brakes; similarly, it has baan tatimatad that 4.5 million pounds are incorporated annually into automotive clutch facings.23 However, since brakes end clutches are usually repaired before they ere completely worn out, and since aome working automobiles are scrapped, not ell this automotive asbestos DOF 0931703 DU 035440 w*:i.jejatj Matg-aimat. ■: d - Oil -jaHiiatfc: will b« released to the atmosphere. Hence, the estimate of how much actually la worn away annually is 74 million pounda, but only a small amount of which la- released as fibrous material.^ Testa performed on brake linings have indicated that under con­ ditions of normal usage, considerable alteration of the asbestos occurs. One study has reported that most of the dust collected from brake drums is nonfib roue and la similar in appearance to thermally degraded asbes­ tos, and it was suggested that the temperature at the points of contact of brake linings and drum actually reaches levels at which thermal daeraj..,_-_i______ ._____ • dation of asbestos can_____ occur.24 Three research studies of asbestos emissions from brake linings give estimated percentages of free fiber at IX or less, 0.3Z, and less than 0.Q2Z, respectively.25,26,27 in t^e first of these studies, it was estimated that annually in the United States there are 239,340 pounda of asbestos fiber emissions Irom cars, buses, and trucks and that, of this amount, 204,952 pounds drop out on the roadway; 7,633 pounda become airborne, and 26,733 pounds are retained within the brake and clutch housings.*25 These atmospheric emissions are of greatest concern in ubran areas near traffic routes with high volumss of braking vehlclss. Electron end light microscopy were used in e recent study to analyze the number and size of asbaatos fibars collactad from air at four los Angeles fresvay loop sites and from upwind ambient air controls within 200 fast of the freeway.13 Concantrationa of chryaoeila asbastos at the four freeway sices were low, generally in the range of 0 to 12,000 electron-microscope-vlslble fibers per cubic meeer, and thsy did not differ significantly from concentrations of chrytotile In the matched upwind ambient air samples (0 to 9,000 fibers psr cubic mstsr). Concen­ trations of amphlbole asbestos did not dlffar between freeway or controls (1200 fibsrs per cubic meter). There was no correlation of aabestos fiber concentrations in the freeway samples with number or spaed of motor vehicles psssing by during the sampling periods, nor was there a correlation with wind direction or velocity. Measurements were also mads of chrysotils and amphlbole asbestos at the Sea Francisco Bay Bridge coll pleee, end the concentrations chars *There is apparently an error in date used in this study from "Brake Emissions: Emission Measurement from Brake end Clutch Linings from Selected Mobile Sources," March 1973 EPA (HT1S #68-04-0020). Toeal emissions should have been 239,340 pounds and, therefore, the other amission figures have bean scaled up accordingly la this monograph. L 39 eat osnio* DU 035441 were found Co be 1,400 electron-microscope-vislble fibers of boch types per cubic oarer. This coopered with an average San Francisco Bay Area acaospherie chrysoeile concentration of 500 fibers per cubic meter.^ Spray Asbestos From 1958 through 1973, spray materials containing 10X to 30Z asbestos by veight were used extensively to fireproof girders, spandrels, and decking of high-rise office buildings, and use of spray asbestos for decorative and acouscical purposes dates from the mid-1930s. Erosion of such spray materials alone may cause asbestos fibers to enter building air, but the materials might also be damaged and dislodged—as, for example, by workmen repairing fixtures inside the space between a ceiling and~ the floor above. In large office buildings, air is often returned to the ventilation system through these spaces. A recent study of public buildings in which asbestos sprays had been used showed that there were elevated levels of asbestos within the buildings, as compared with the air outside. Also, the difference between inside and outside air was greater in the case of fibroussprayed buildings than in the case of buildings sprayed with cementi­ tious asbestos.'* • Flaking of sprayed asbestos from ceilings has been reported inside schools, libraries, dormitories, and warehouses.19•29»30 •31 Air conceneraeions may range from 0.02 optical-microscope-visible fibers per milliliter under quiet conditions to 4.0 per milliliter during dry dusting.31 Prior to implementation of federal regulations on asbestoscontaining fireproofing materials,* data were obtained ae various building sites in lower Manhattan where such materials were being sprayed.32 Generally, average atmospheric concentrations within onequarter mile of a construction site were at lease ewica the background level. Current spray materials that contain IX asbestos or less may be Spray-on materials used to insulate or fireproof structures, pipes, and conduits must contain less than IX asbestos on a dry-weight basis, and, for ths spray application of matarial containing morn than IX aabeaeoa uaed to insulate or fireproof machinary or aquipmant, no viaibla eaiaaiona are permittad.22 spray-on painea, decorative mate­ rial#, and weatherproofing are not regulated. 60 DUP 0931705 DU 035442 hi nws*Ftft "g. WteTiSib expected to result la no more than ons-tenth of the elevated asbestos air concentrations that occurred previously. Exposures from Dispoaal of Asbestos Products and Wastes* Solid wastes produced from the manufacture and use of asbestoscontaining products and from demolition^ can be emission sources, and in the past, these waste materials were often disposed of without regard to their emission potential. Moreover, their disposal may result in the mingling of asbestos-containing wastes with municipal wastes in open dumps, thus creating a long-term emission source. Industrial asbestos wastes include process wastes such as dust, slurries, waste from overspraying, and mill tailings; waste collected by air control equipment (e,g., the dust from sawing, grinding, drilling, etc. that Is vented to control devices); scrap; and emptied asbestos shipping bags. This latcer item, the bags in which the milled fiber is received, is an asbestos-containing waste common to almost all manu­ facturers of asbestos products. If the bags are not shredded and Incor­ porated directly into the product mix, they are incinerated or disposed to landfill, sometimes sealed in plastic bags. Occasionally, they may be treated like nonasbestos wastes and result in exposures to unknowing handlers.23 * Water may become polluted with asbestos fibers in manufacturing, particularly in the paper and cement product industries, and during use in wee cyclones for cleaning exheuee geses from factories. Ths slurry waste from such processes msy be directed either into settling ponds end the water recirculated (ths drisd wests disposed to lend), or it msy bs dumped directly into convenient severs, rivers, or lakes.*3 ia either case, but especially In the latter, it can contribute to contamination of the environment with asbestos. The results of a survey of waste disposal methods used by asbestos products manufacturers show that 3 75S of 97 plants surveyed used dumps for wastes and that 13.4Z used landfills. (Ths remainder reuse. I *Sea also taferenca 19. i +For years, asbestos has been Incorporated into material such as insula­ tion, cement sheet, roofing, and floor tilas and ustd in constructing Industrial and commercial buildings and ships. (For ths most part, single-family residences contain only small amounts of ssbsscos insula­ tion.) When such buildings and ships ara demolished, areas of loosened asbestos, especially from Insulating mattrlals, are open to ths ambient air and can emit fibers. Obviously, demolition will continue to bs s source of emissions in ths future, requiring control measures. 61 DU? 0931706 DU 035443 3«11, score or wet-slurry their vutu.) Of grtscsse concern from the standpoint of emissions are those wastes that are disposed to uncovered dumps. Asbestos mills generate vast quantities of waste. Whereas a large manufacturing waste disposal sice may have a surface area of 12,000 square meters (abouc 3 acres), a large mill tailings disposal sice may be 400,000 square meters (about 100 acres). Mill waste may contain from less than IX asbestos by weight, as In the case of the Vermont mill, to over 30Z asbestos, in some California operations. Obviously, there also are opportunities for asbestos emissions from che disposal of nonindustrial wastes, which constitute the majority of asbestos wastes disposed to land (Figure 3). Moat notable of these wastes are chose generated by the renovation and demolition of ships and buildings, which may contain large amounts of friable asbestos insula­ tion as well as many other asbestos products. Three studies of asbestos concentrations in air near asbestos waste dumps, all conducted prior to the establishment of EfA standards in the fall of 1973, have been published.13.19.3* it is apparent from these studies that atmospheric asbestos concentrations la che vicinity of waste disposal sices, often la urban areas, are considerably higher chan background concentrations—perhaps 10 to 1,000 tiaas higher—and may even approach occupational levels. (The revised EFA asbestos standard that went into effect after these data were recorded may help reduce amissions.)33 Exposures of Asbestos Workers* Families Families of persons employed in che asbestos Industry may be sub­ jected to asbestos contamination chat augments their exposures from ocher sources. Workers may bring asbestos fibers home on their skin or clothing or on equipment such as lunch boxes and automobiles. Atmos­ pheric concentrations of asbestos in che homes of asbestos workman have been reported to be 100-500 nanograms per cubic meter,3# concentrations similar to estimated concentrations in the vincinity of asbestos mines and mills and much higher than the 0.09 to 70 nanograms per cubie meter reported in some U.S. cities.*3.4,13 Exposure to Asbestos la Drinkina Water Drinking water is one of the possible routes by which humans are exposed to asbestos. Contamination of drinking water may be due partly *lc is known that occupants of households of asbestos workers have elevated rates of asbestosls and mesothelioma. 62 DUf 0931707 DU 035444 '• fri^l i;sj:mbum... ilMLSZ jjjjjjgH ajm. co erosion from natural deposits of sarpanclna and ochar asbeatoscontaining materials found throughout tha United Statas, as nocad pre­ viously in this chapter ("Redistribution and Face of Asbestos in the Environment"). Substantial contamination may also result from improper disposal of asbestos vestas. Thesa vestas may be effluents chat are directly discharged into vacer systems, or they may be released to the atmosphere or disposed of on land and subsequently join the vacer system. Another potential contaminacpr of drinking water is the piping and pumping of municipal vacer distribution systems. About 200,000 alias of asbeacoa-ceaenc pipes are used co carry water co U.S. consumers, and tha pipes provide a source of asbestos fibers from leaching and erosion.'>33 .Caskets and insulation used in treatment and in pumps are ocher possible contaminacors.*^ The major difficulties in determining the asbestos content of water ara discussed in Appendix C. Furthermore, most of the analyses that are available arc for "grab" samples—samples of a few liters of vacer chat are taken from one source at one time. The degree to which grab sam­ ples represent the characteristics of an entire municipality's water supply over location and time could be questioned—soma municipalities receive their vacer from several sources, and seasonal and climatologi­ cal variations can change the asbestos content of vacer.* For this monograph, data on the concentration of asbestos in drink­ ing waeer vara axeraccad from 9 different published studies, raprssancing 105 water supplies in Che United States,6,7,39-45 (Sea also Appen­ dix £.) An effort was made to select data only for finished drinking * A study of asbestos concentrations In tvo water syatese using asbestoscement pipes ravealsd svsrsge increases of 0.074 end 0.004 mlcrograma of aabastoa respectively par liter of water at tha eap.7 Laboratory casts conducted by the EFA37 and Johns-Manvilla7 on sactions of asbestos-esmaac pipe also have shown increased concentrations of fiber in water. However, a recant (February 1978) report showed no signifi­ cant release of chrysotlle aabastoa from asbasCos-cement pips exposed co the actios of "moderately egreaeive" water.3* l’ln San Francisco, water from other sources la supplemented by water from e reservoir that is located in a chrysotlle rock area. (Recall also the study mentioned previously chat showed higher aabastoa fiber counts in Philadelphia and Atlanta water supplies during periods of high river flows in the surrounding regions.) Further, s study pub­ lished In 1974 found Chet Che amount and mineralogical nature of sus­ pended solids In the Duluth water supply is moat evident when heavy rainfalls ara followed by an increase in tha amount of suspended solids resulting from river runoff and shore erosion.39 DUP 0931708 DU 035445 __£*£iiiaL vatar—some of the samples were taken from caps In the water supply system; others vers taken at municipal water stations. Also, only studies in which electron-microscope measurements were made are included. The cities in the studies were not selected to be representative of U.S. cities; Indeed, some were selected because asbestos was suspected to be in thalr drinking water. Chrysotlle fibers, amphibole fibers, or both were found to be present la 56 of the 105 water supplies. Fiber concentrations In indi­ vidual samples varied between the lower Holt of detection and 130 mil­ lion electron-microscope-vislbIs fibers per liter (for only two cities did che samples range over 40). Mass asbestos concentrations in indi­ vidual samples varied between bslow-detectable and 800 aicrograms per liter (for only three cities did the samples range over 60). Exposure to Asbestos in Foods and Drugs Asbestos contents of food and drugs have not been well-established to dace, and che FDA has no regulations concerning the content of asbestos in foods and nonparenteral drugs. Foods may be contaminated during their agricultural phase from asbestos in air and soil and from asbestos impurities in talc used as a pesticide vehicle. Uptake of contaminated water by plant roots, as well as deposition of contaminated water directly onto leafy surfaces by sprinkler irrigation, ars possibilities, but no published litera­ ture has been found to substantiate them. One instance of accidental contamination of food in tha coursa of transportation has bean docu­ mented.*^ Processed foods may bscoma contaminatad with asbestos sithsr from watsr used in their preparation or from tha usa of aabaatos filters, adheslvas, rubber, end resins in procssslng end packaging.Fooda for which asbestos filtsrs are used may include beer, wine, liquors, fruit julcss, sugar, lard, and vegetable oil.^ Aabaatos filters have also basn employed to process cidar, condimsnts, drinking watsr, mouehwaahss, syrups, tonics, and vinegar.49 The authors of oam aeudy found between 1.1 and 6.6 million eleetron-microseope-vlslbls flbars per liter in U.S. end Canadian baar, and between 1.7 and 12.2 million fibers per liter in Canedlan soft drinks. They else reported between 1.8 end 11.7 million fibers par liesr in wins# from various pares of tbs world.'® In another study, between 13.1 sod 24.0 Billion fibers per liter were found in one *Sone authors reported thsir data as fibers per liter, soma reported aicrograms per liter, and soma reported both. 64 00» 0931709 DU 035446 manufacturer's gin; cha water uaad In cha processing of gin contained between 3.3 and 3.7 million fibers per Liter.51 Any eseiaate of the quantity of asbestos consuaed with food must be purely speculative since virtually no concentration data have been reported. The FDA has reported that under test and market conditions certain foods contained less chan 10 ppb asbestos.52 Asbestos filters also have been used In the processing of drugs and blood plasoa. But since April 1975, as noted in Chapter l, the FDA has disapproved their use in preparing parenteral drugs and bio­ logies . Asbestos filters may be used, however, in the aanufacture of nonparenteral drugs and their ingredients. Talc, which may contain asbestos as an impurity, has been used in the manufacture of medicinal capsules and tablets and has found various ocher uses in medicine and dentistry.53-55 Also, talc may be added to processed foods, either directly as an ingredient or indirectly as a fora release agent or as a constituent of packaging materials.^6-66 65 OW 0931710 DU 035447 usmn .-.ml- ..ajas .iL* Chapter VI CONTROL OF THE ASBESTOS HAZARDPHYSICAL CONTROL Three program approachee for controlling the adverse health effects of asbestos fibers in man's environment are presented in this and the following two chapters. These approaches are: e Physical control of human exposure to asbestos fibers—i.e., reducing the coneace between man and the fibers • Medical surveillance—measures taken by physicians and other health-care personnel in behalf of asbestosexposed persons e Education—ultimately, of course, of persons exposed to asbestos fibers so that physical and medical con­ trol measures will be of maxima effectiveness, but also education of persons who are in a position to motivate those who are exposed, and other persons with responsibilities for asbestos-control measures. Reducing the extent of contact between asbestos fibers and man can be accomplished by actions dlscussad In this chaptar. Such actions include: (1) engineering of the materials, processes, and facllitlas for utilizing asbastoa commercially; (2) administrative measures that ralata to the persons who might be exposed; (3) improvement of work practices; (4) control of omissions and asbestos wsstss; and (5) con­ trol during transportation of asbestos raw materials and products. The chspter includes a section on the epplicatlon of control measures la several specific manufacturing and consumer Industrias. Engineering Measuras Control of alrborna asbestos fiber by engineering methods is not greatly different from the control of ocher solid particulate matter having a similar aerodynasrt.c slza, chough some special problems and technologist may ba involvad. Engineering control methods include: e Enclosure e Exhaust ventilation # Isolation 67 nut 0931111 035448 j* *n,k • Plane dealga • Trsatasneof aabeacoa • Substitution of alternative material*. Enclosur* Units* borne by vlnd, dust particle*, even when impelled ac extremely high velocities, travel only a ahore distance in air—a lev Inches ac the most. This behavior Is particularly true of asbescos fibers, due to their low mass and aerodynamic characteristics. Because of the shore travel distance, a good scare toward control of asbescos duse generated by machine operations Is enclosure or hooding. However, enclosures must often have openings, to permit manual operation of a machine or so that the machine may otherwise carry out Its function. Hence, there muse be a continual inflow of air into the unit at suf­ ficient velocity to prevent the escape of asbescos duse. For many operations, an intake velocity of 200 feet per minute ac the face of an enclosure is adequate. Enclosures for high-velocity wheels or operations involving very large pares require special cars In design. Exhaust Ventilation Adequate exhaust ventilation, with negative pressure, muse be pro­ vided for enclosed areas to reaove airborne fibers. The design of a proper exhaust system is critical and should be accomplished by persons who sre expert.snesd in the principlee of eir movement sad oehsr important aspeecs of ventilation-system design. ' Duses for asbestos operation carry air at veloeitiaa ranging from 3.000 to 3,500 feet per minute. The lover velocities are used where relatively smell concentrations of well-divided fiber* must be carried, such as in the dust-control systsms ac tsxtila plants. The higher velocities era used where apace is restrtetsd snd where larger pieces of material must be carried, as In dust systems for mschinss chst cut and shape brake shoes or aabastoe-cement pip*. Most systsms, including lovprtssur* psnumstic conveying systsms, function well at velocities of 4.000 to 4,300 feet per minute. All parts of asbestos control systems should bs maintained under negative prsssurs to prsvsnt leakage of duet into the plane from loose joints and opts seams, as wall as eo ansurs adequate collection at hood faces. Another major consideration in a plant's ventilation system is the provision of maka-up air—the amount of makt-up air introducad should slightly exetad ths amount of sir txhauatad. A mschanicsl air 68 out 0931712 DU 035449 ftipply syaca,. rather than "natural" rooa ventilation, i* preferred and, in most'cases, necessary to achieve the neceaaary ventilation per­ formance. Many specifications for duct contruction design may be found in Industrial Ventilation issued by the American Conference of Governmental Industrial Hygienists.1 Even with a ventilation system chat is designed and built according to good engineering principles, periodic measurements muse be made to determine that the system is adequately balanced and performing accord­ ing to design. Such measurement include: e Static pressure • - Air flow e Supply, capture, and conveying velocities e Pan performance. Frequent measurements are essential, since plugging and wear can cause variations in the balance and, hence, efficiency of the system. • Isolation "Dirty" operations in che asbestos Industry ere frequently Isolated to minimize human exposure to asbestos fibers. For ease operations, particularly vibrating screens and bagging at asbestos mills, such engineering measures as venellaeion and enclosure have not been able to reduce airborne asbestos levels below the two-fiber time-weightedaverage limit, thereby necessitating isolation. In addition to raducing fiber levels through e plane, chare are ocher advsntsges in Isolating asbestos-flber-ealetlng operations and rastrieting access eo them: (1) in employee working at a dusty opera­ tion la not eo likely to relax his sdhsrence to rastriccivs work prac­ tices if he is sepsrstsd from fellow employees who ere working freely at operations thst present no exposure hasard; also, isolation can (2) reduce costa for local exhaust venellaeion, and (3) nake for more efficient housekeeping. Unloading and storage of aabeatoe is another candidate for isolation becauam of dust from bags thst art inevitably perforated by in-transit shifting or careless loading. Such bags should be repaired—or che asbestos rebagged—and vacuum-cleaned within the boxcar before being 69 DO? 0931713 035450 transferred to the warehouse. Also, of course, careful unloading Is required to alnlnize bag breakage. Bag-opening 8cations, as veil as being enclosed and ventilated, should be isolated from other operations In the mixing or compounding area. The emptied bags themselves should be "Isolated" by being rolled up within the opening station's ventilation hood and put into either a clean, sealed bag, a shredder, or a cube that conveys eopcled bags to an isolated, enclosed, central collection point from which they are ulti­ mately disposed of In sealed containers. (In some industries, bags esn be mixed with other material and submersed into the manufacturing pro­ cess.) Plane Design Not often is industry afforded the opportunity of designing and constructing a plane to specifications that place such hazard control measures as isolation and dust conerol at the forefront of priority. As a rule, process flow efficiency, quality control, and cost factors receive higher priority. But enlightened management is aware thee efficiency, product quality, and cose savings do not necessarily con­ flict with design for health and safety. An ideal design for isolating a dusty work area is one in which entry can be made only through locker and dothea-change rooms. Two locker rooms, separated by a shower room should be provided—one for street cloches, the other for work clothes and protective equipment. Interposing a shower bath between the two locker rooms makes taking a shower ae the end of a shift more likely. (See Figure 3.) The contaminated change room should be under negative pressure, with the exhaust air directed to a suitable collecting system. Air flow between the two locker rooms should be toward the contaminated room. If connecting doors between change rooms and shower are self-closing and well sealed, it say be possible to use the separating shower room as an air lock. Some other important considerations in designing for asbestos fiber control aret • Engineering a dusty operation so chat it can be handled by as few employees as possible. o Including a protected observation area next to an Isolated work area so that entry of supervisory personnel and visitors can be kept to a minimum. DU? 0931714 DU 035451 C , oi ; o □ D auu □ 0 0 0 oi 0 D 0 01 H n nn 71 DU» 0931715 DU 035452 • Pluming the layout so chat airflow Into hoods. •nclosurej, and other exhaust equipment Is not disturbed by drafts from fans, windows, and doors. Off-sec doors with Indirect, right-angle entries help to deflect ' and diffuse Incoming air currents. e Constructing interiors such that beams, pipes, and ledges do not serve as areas whers airborne asbestos can settle. Treatment of Asbestos There are various methods of creating loose asbestos to reduce fiber emissions. One of the most effective is wetting. Although not applicable to operations that will not tolerate moisture, such as the manufacture of friction products, wetting can be used in mining and milling and in the construction industry. AC present there is one asbestos mill in che Uniced States chat utilizes wet processing. Ac this mill, asbestos Is separated from heavier rock through a scries of flotation devices. It is then col­ lected between pillow filters and extruded and dried in pellet fora, or it is fluff-dried and packaged as loose fibrous material. Dust control is needed only for pelletising and bagging the finished product. Use of pelletized asbestos, which can be pumped pneumatically into enclosed railroad cars and unloaded through gravity releeee at lea destination, has bssn triad in ths manufacture of friction products and taxtilaa but with little success. Thssa products require long fibers, but pelletizing brisks fibers into shorter, unusable, lengths. The shorter fiber length of pelletized eabestoa should present less of a problem in ths msnuficturs of other asbestos-containing products. A recent method of treatment to reduce airborne fibers in ths ssbsstos textile industry is the application of polymer to asbestos yarn.2 Such a costing, however, is not useful where the inherent sur­ face characteristics of ssbsstos fibers srs required, particularly when the fibers ere to be bound la e matrix with other materials. Trtatmant of asbestos with anti-dusting agents may ba helpful. These agents era viscous liquids that ere applied to dry asbestos by spraying or mixing. Ths fibsrs srs then drlad sc room tempsreturs. This proetdura retains ths performance criteria of untreated eebeatos. Substitution Although the use of eabestoa is well entrenched in many important applications, it i« likely that substitution will play soma future role In reducing the health hazards from esbeatoe. For example, one o. 72 0931116 DU* DV°354S3 n i i'in -ft'l' rr iri-tr mi i '"WW— che largest asbestos users, che U.S. Navy, has Issued an "Instruction" chac asbe*cos not be used in construction, overhaul, repair, and mainte­ nance where suitable alternative materials have been dasignsced. Materials that hava bean investigated as possible alternatives to asbestos Include: Fibrous glass oceea wool AWWft WOOi Kaolin wool Slag wool Exfoliated vermiculita Silica Cellulose Potassium citanata Ceramics Sintered metals Carbon fibers Few alternative materials have proved as satisfactory as asbestos due to lack of strength, heat resistance, flexibility, or durability, or because of cost. Moreover, since attention has been drawn to the possibility chac Inhaled fibers ocher chan asbestos may be carcinogenic,4 it is essential that the toxicity of proposed asbestos substitutes be evalu­ ated. In certain industrial processes where asbestos is used as a binder, less coxie materials have been substituted with little effect on the quality of cha product. This has been the esse in the manufacture of rubber, plaseics, and various adhesives and cements. Similarly, less asbestos might bs used in paints, coatings, caulks, sealants, and joint fillers. Satisfactory asbestos substitutes have been developed for a variety of reinforced plasties and resins and for insulating materials. ?or critical insulating applications, however, che strength and heat resistance of asbestos cannot be duplicated economically. Mot many replacements have been found for eabeatos In paper pro­ ducts in which the heat resistance, chemical lnartaaee, and alectrlcal and insulating propsrtias of aabastos art highly valusd—products such as mill board, roofing fairs, pip* coverings, fin* quality elsetriesl and insulating papers, sod asbestos-lstex flooring felts. Glass doth, felt, and thread hav* found limitsd application In roofing and floor­ ing undsrlsymsnes, but la tha majority of ehas* paper products, aabsatos fibers srs still ussd. Two of tha mors sueesssful sabeatos substitutes, sods-liae-silie* and high silica glass fibsrs, srs vlawtd brlafly balow. Sods-Ums-Sillca Glass Fibers Soda-lims-silica glass filaments, mad* by highly rsfinsd processes involving tha us* of platinum dias, art of high quality and 73 DUP 0931717 DU 035454 ■dBUSSBL'JiE..MSjfiiiBff aftwa uniform size. Some are leas chan one-half micron in diameter and are adaptable to highly specialized uses, such as veavlng into fabrics. Glass fibers will nat burn, but they will soften and coalesce at temperatures which vary according to the composition of the glass. Their heat and moisture resistance is limited by Che organic film applied to them during manufacture to improve processing and to reduce breakage during subsequent plying and weaving operations. (Without such a coating, the fibers are more brittle and self-abrasive.) Highccmperacure properties are impaired to some extant, but the fibers will withstand temperatures up to 1,2Q0°F. Exposure of very fine glass fibers to water vapor results in relatively rapid deterioration, making them less reelstane than asbestos to the effects of steam and moisture. Attempts to use them in place of asbestos in asbestos-caaant products have been unsuccessful because of a chemical reaction, between the glass and cement, chat decomposes Che fibers. Glass fibers are efficient thermal insulators in types of equip- ' raene, such as scovas and refrigerators, whara conditions are not corrosivef Their high tensile strength, greeter thermal stability compared with organic fibers, and electrical resistance make them suitable for elec­ trical insulation. Glass fiber is used in conjunction with asbestos, or as an optical alternative materiel in Navy shipboard cable.* A glaaa-aabeseoa cloth designed during World War II to exceed the supply of asbestos textile fibers has continued in use as a covering on thermal insulation applied to piping on naval vessels. It is woven with a plied yarn, having one strand each of glass and asbestos. Glass fabrics or combined glsee-eebeetos fabrics have some advantage over asbestos textile produces because they are lighter and stronger, but they era generally less resistant to flexure, abrasion, and chemical action. Fabrics mads of interwoven glass and aabsacos yarns are being made in many weights and colors for use as theater curtains and fireproof draperies. As a substitute for asbestos in friction equipment, gless fiber hsa, in general, given unsatisfactory results, chiefly because of the poor abrasive characteristics of glass. Hlgh-Sillca Glaas Fibers Glass fibers approximating vitreous silica in composition arc superior to soda-lima-slllcs glass fibers in resistance to the 009 093171S X)U 035455 action of watar vapor and high tsmperaeure. They art difficult to menu factura, however, bacausa fused silica is extremely viscous at its melting point (1,725°F). Administraclva Measures Administrative oaasuras are a complement to engineering control of the hazard in the workplace. Possible administrative measures include (a) limiting the number of employees exposed, (b) limiting the duration of exposure for any given parson, (c) restricting smoking and eating in the workplace, and (d) smoking cessation programs.* Limiting the Humber of Employees Exposed The number of employees exposed to excessive airborne concentra­ tions of asbestos may be Limited by: a Restricting access to contaminated areas (this swasure can also Involve engineering design; hence, also see "Isolation" and "Plant Design" further on in this chapter) e Reducing to a minimum the number of persons handling asbestos e Conducting particularly dusty operations during shifts where the number of persons in the plant is at a minimum. Smaller numbers of continuously exposed employees are more easily and effaccivaly trained, controlled, and proeactad than a largar group that is only casuslly and occasionally axpoaad. Limiting tha Duration of Expoauta for Any Given Person As noted previously, ths OSHA standard for aabeseos la an 8-hour time-weighted average of no more than 2 flbars, graatar than 5 Another administrative measure, which has been used In the British dye­ stuffs Industry la connection with cancer control,° would be to give preference to job applicants who are of an advancad age end who have not prevloualy beam occupationally exposed to aabestos. The seasoning here la chat the risk of developing aebeetos-releted cancer during the em­ ployees' lifetimes will be somewhat reduced. However, while this meas­ ure may have some baals in theory with regard to lung cancer, it does not taka into account other asbsstos-ralatsd diseases or even tha pos­ sible aggravation of adverse health conditions not normally considered to be asbaatos-relatad. Moreover, thara ara other ethical and economic considerations that would need to be explored. Still another possible administrative measure-giving praftrance to job applicants who do not smoke (because of tha graatar risk to smokers)—would appear to be sub­ ject to tha asms considerations. 75 Dtw 0931719 DU 035456 micrometers in length per milliliter of air; also concentration* ouat never exceed 10 fiber* per milliliter. This mean* that during any single shift, employee* may be exposed to airborne asbestos levels above 2 fibers per milliliter so long as such excursions are compensated for by equivalent reductions in exposure, except that in no instance can the exposure exceed 10 fibers per milliliter. As an example: employees on a shift can be exposed for 4 hours to an airborne asbescos level of 4 fibers per milliliter, which is equivalent to a 2-fiber exposure for 3 hours, as long as they are subject to zero exposure for the remainder of the day. The remaining four hours of the shift would be covered by employees who had received zero exposure during the first half of the 8hour day. Or, for example, a worker could be exposed to an air­ borne level of 9 fibers per milliliter for 1 hour, as long as he vas“exposed to a level of no more chan 1 fiber per milliliter for the remaining 7 hours of the shift. Control of exposure using averaging is deficient in a number of respects since, in effect, it is assumed that: (1) exposure levels will remain constant, not fluctuate; (2) the worker receives no asbescos exposures, on or off shift, other chan chose associated with his work; (3) 2 fibers per milliliter greater than S microns in length is that level at which, for practical purposes, there is zero physiological response; and (4) the submicron fibers present but not counted are unimporeant fora a toxicity standpoint. Other assumptions are that a sufficient work force is available for required alternation of person­ nel, and that aconomica (increased payroll) is not a factor. Restrictions on Smoking and Eating For any toxic materials, a strong corporate stand should be estab­ lished against the practice of eating, drinking, or smoking on the job. These activities should be restricted to a designated, clean location visited only after established decontamination procedures have been followed. If such action represents a change in policy, the change should be clearly and frankly explained as a step being taken to pro­ vide a safe work environment. It is noted in a recent publication that asbestos fibers longer than 5 um having a langth-to-diamater ratio greater than 3 (using 430x phasecontrast light microscopy) account for approximately 2X of all asbestos fibers present in Industrial settings and chat, hence, every fiber greater than 5 um in length corresponds roughly to an actual fiber count of 50.^ 76 OOP 0931720 DU 035457 aitfc Juia,-*. . .^../HSL-la riBmdg. Smoking Caaaatlon Programs Because of che interaction of tobacco smoking and working around asbestos in producing lung cancer, and since smoking is s health hazard in its own right, a smoking cessation program might be undertaken as a cancer control measure. Unfortunately, however, the various programs that have been tried have rarely brought about significant long-term cessation, although smoking rates have been reduced. It is possible that recent moves of federal and stats governments to restrict smoking in public places* and public-service media campaigns to educate the pub­ lic on che hazards of smoking could improve the efficacy of cessation programs. Various approaches to smoking cessation are discussed in Appendix E of this monograph with a view to providing a broad perspective of the available options. If it is decided that a smoking cessation program should be undertaken, the discussion should be of help to che health­ care worker in selecting an appropriate program. Work Practices, Including Housekeeping and Use of Personal Protective Equipment Changes in work practices often may be the most cost-effective way of reducing occupational exposure to asbestos. Some of the ways in which work practices may be modified Include: • Mixing asbestos mortar in closed polyethylene bags rather chan in mortar boxes or buckets. s Maintaining central fabrication shops from which insulation matarial is sene eo che field for inscallaeion with minimal on-site cutting or sawing. • Permitting power tools to be used only in central shops. e Using single-point cutting and chipping cools, rather than saws or cutting equipment using abrasion. • Jettisoning polyethylene begs into the product mix whan possible. • Substituting vacuuming for che blowing off of aachinea and equipment with compressed air. e Good housekeeping (as discussed in mors detail balov). e Use of personal protective equipment (also discussed balov). f Since 1976, 19 states have passed e total of 23 anciamoking ordinances chat restrict smoking in public places of recreation, waiting rooms of health facilities, and restaurants. 77 DU? 0931721 DU 035458 Housekeeping Good housekeeping is essential co reducing level* of eirborne asbestos. Waste materials such as rejects, scrap, shavings, or other debris should be picked up and placed In plastic bags. At the end of a shift, these bags should be taped shut, labeled as to the hazard con­ tained therein, and disposed of. Asbestos dust on floors, ledges, equipment, overheads, and other plant surfaces can become alrborna when disturbed by drafts or work activity, and it should be removed. Sweeping is not the way to remove it, however, because the fine fibers are entrained into the air and deposited on remote ledges, pipes, and ocher inaccessible surfaces. Nor is wet mopping a satisfactory way of cleaning, sines it tends only to spread the dust around. Vacuum cleaning is the recommended method— preferably a central vacuum system. Personal Protective Equipment The control measures previously discussed in this chapter can sig­ nificantly reduce exposure to asbestos fibers, and they muse be employed first. If, however, these measures are not sufficient, or if an unex­ pected event creates a potential for exposure greater than the maximum permitted, personal protective equipment will be necessary. To reiter­ ate, respirators and protective clothing must always be available, but they should never serve as a replacement for engineering control mea­ sures . Respirators Respirators may always ba necessary during tha cleaning or repair of exhaust ductwork or during manual shakadown of collection bags in baghouats. Also, this fora of protection cay ba tha only faaaibla method of controlling aabastos exposures during tha removal of thermal insulation or the application of some eebestoe products. The use of reeplrecors le not to be taken lightly, however. Since the devices place a burden on the raepirecion of the wearer—end, at beat, ere e nuisance—a determination must ba made as to whether an Individual can uaa the equipment and perform whatever work It is that he le assigned to do. Factors thee muse be considered in such e deter­ mination include: physlologic/phyeicel ones such as oxygen needs for the teak, heir, beards, end glasses; medical conditions thee may be present such as pulmonary or cardiovascular disease; and psychological disposition toward wearing a respirator. The type of reeplretor needed—for example, powered versus man-powered—will be dictated by the preceding feetore ee well as by the 78 DU* 0931722 ptJ 035459 - ygp;f1 i«i-_ - ~i at ■ h mmmi»r N *r--gr^t^-. • * rffgfg- concentration of airborne asbestos fiber.® (The concentration of fiber should always be rtcheeked whenever there are significant changes in process, control, worksite, or climate.) Respirators require proper fitting, maintenance, and cleaning to be effective. The elements of an acceptable respirator program are see forth by the American National Standards Institute (New York) in ANSI Standard Z88.2-1969 "American National Standards Practices for Respiratory Protection." Protective Clothina Special clothing, not to be worn outside the workplace, should be worn by all asbestos workers—not only to protect them, but to curtail exposure of ocher persons. The most satisfactory basic protection is afforded by coveralls, preferably made of cotton-polyester material—cotton alone cannot be used, because static build-up causes fibers to adhere to the cloth tenaciously. Disposable paper coveralls, although they are compara­ tively inexpensive and they eliminate the potential for exposure of ' laundry workers, are easily torn or perforated by body movement, chemi­ cal action, or sparks. Moreover, some types of paper suits are hardfinished and nonporous, almost airtight, and they can lead to heat stress if worn over street clothes. The coverall garment should be onepiece, without pockets, cuffs, or rolled edges, and with adequate clo­ sures for necessary openings. Coveralls should be clean each day and must never be worn away from the plant. A head covering is also required, and lightvalght paper surgical-type caps ars satisfactory. Hard hats do not prtvant the accu­ mulation of fibers in the hair, and, where the hats are required, a paper cap should ba worn under them. Foot coverings, in ths fora of canvas booties, rubber geloshea, or safety shoes, are also needed. Either form is satisfactory as long as they are not worn away from the plane. Street clothes and personal effaces should bs kspt in s "dean conditions" rooa, and work clothes and protsetive aquipmsnt should be kept in e "contaminated locker" room. (See Figure VII-1.) When personnel leave e restricted work ares thsy should enesr the "contaminated locker" room and remove clinging asbestos fibers by using s vacuum equipped with a filtered exhaust systsa. Proctcclve equipment should be removed DU* 0931723 035460 (respirators late) and deposited In the "contaminated locker" room lockers. The vorker should then shower and put on his personal outer clothing in the "clean conditions" room. If laundering of work clothing is done by an outside laundering service, rather than in the plant, the laundry service should be advised in writing of the asbestos hazard. When collected for laundering, the clothing should be vecuua-cleaned, dampened, packed in plastic bags, sealed, and clearly marked "Asbestos Contaminated Clothing—Vet Before Handling." Control la Specific Manufacturing and Consuming Industries Following are some observations on exposure control as it relates specifically to several major asbestos manufacturing and using indus­ tries and to demolition and rip-out. Generally speaking, control of asbestos exposure outside of mining, milling and manufacturing indus­ tries is difficult—persons at risk are less aware of the hazard and of proper work practices, and, moreover, engineering controls and personal protective equipment may be lacking. Asbestos Textile Production Control of asbestos exposure during production of asbestos textiles has presented a greater problem than during the manufacture of other asbestos products. In part, this may bs due to the use of machlner chat was originally designed for processing other, less toxic, fibrous materials. Fiber preparation—which involves fluffing, grading, beating, and combing and which generates heavy concentrations of dust—is followed by the mixing of asbestos with another material such as cotton or rayon. Dust from these operations must be controlled by enclosures and venti­ lation. Carding, twisting, spinning, weaving, and braiding of fibers are dry processes which, by their physical arrangement, ace very difficult to enclose and ventilate, and it appears that current technology cannot eliminate excessive exposure from these operations. Control of tempera­ ture and hualdlty and general room ventilation have been used to reduce exposures. It is usual practice to keep the ventilated room at a slightly positive pressure to help maintain proper temperature and humidity, and since the rate of air change is often as frequent as 30 DU* 0931724 DU 035461 one complete change every 6 minutes, it is necessary to recycle the air before cleaning. Asbestos Paper Since much of the paper-making process involves wet materials, little dust is created. Drying is usually accomplished by passing the wet sheec over steamheated rollers, vhich gradually remove the moisture. The lov-pressure, high-exhaust-volume hoods that are used to collect the water vapor and to transport it avay from the drying paper also serve to remove any asbestos dust that may be released during che dry­ ing operation. 3ulk packaging of paper products by winding them on spools, reels, or beams is a dry operation, but local exhausts and vented area hoods are effective dust-control measures for this operation. In general, the use of hydropulpers with pulpable bags; proper ventilation rates; and the control measures mentioned previously will serve to maintain asbestos exposure in paper making at acceptable levels. Asbestos-Cement Pipe and Sheec The prime point for application of control procedures in che manufacture of asbestos-cement pip* and sheec are ae che mixing vac into vhich dry asbescoa is introduced and in which the asbestos is agitated and at che final stage where the finished product is cut, machined, buffed, and packaged. (The addition of water, sand, and cement curtails dust exposure in the interim stages.) Local exhaust ventilation with carefully designed enclosures are essential for proper dust control at che critical exposure points. Automotive Brake and Clutch Repair The greatest exposure to aabestoe during repair of automotive brakes and clutches occurs when brake drums are cleaned by blowing them with compressed air and when brake linings are ground and beveled. Brake drtas should be vacuumed instead of blown out. Grinding and beveling operations will have to be controlled by enclosure and exhaust ventilation. Construction Control of exposure to asbestos fibers in building construction is difficult since few operators are sufficiently localized to permit che 81 DUP 0931725 DU 035462 * mum* ■aJtSaiBB& use of enclosures or exhaust ventilation. General room vancilacion couplad ulch respiratory protection are the only means of preventing excessive exposure to fibers chat may occur during necessary on-site sawing or shaping of asbestos products such as Insulation; mixing and application of asbestos patching, taping, or spaclcling compounds; and sanding and finishing of spackllng, tape, or floor tile. Generally, the application of floor tile, roofing, and siding does not require extraordinary control procedures, since asbestos fibers are securely embedded in the product and little or no dust is created. A vacuum device Installed on the periphery of a sanding wheel to evacu­ ate dust and fibers would help maintain low levels of exposure and recharging of fibers into the air from the work area can be controlled by careful housekeeping. Much of the exposure in the building Industry has been reduced by substltltulons for asbestos-containing materials, and further emphasis on using alternative materials is anticipated as awareness of the health hazard of asbestos fibers Increases. Demolition and Rip-out of Asbestos-Containing Insulation The potential for exposure to asbeseos fibers during demolition of ships and buildings and during rip-out of asbestos thermal insulation is high. Insulating materials that contain asbestos have been used less and less in recent years but, because there is so much asbestos material already in place and because dust control during deawlition and rip-out is difficult, these operations will remain potentially hazardous for years to come. The following measures will help to reduce the hazard: s Airborne dust can be reduced eonsldersbly by soaking the insulation—nonabsorbent surfaces punctured to permit water to be introduced, and absorbent surfaces soaked by a fine, low-pressure water spray so chat dust does not arise from the impingement of the water upon the surface. e Insulation should be removed, if possible, by sawing or cutting with tools fitted with dust collecting devices rather then by tearing away. e Materials removed should not be allowed to fall to the ground but should instead be placed in bags for disposal. e Slurries of waste chat fall must not be allowed to dry— they should be removed while still vet. e If possible, a high-capacity exhaust system should be employed at Che work site. e Where vetting and exhaust ventilation are not possible, control efforts should be directed toward isolating che hazardous operations. 32 DUP 0931726 DU 035463 Control of Emissions eo the General Environment Air Pollution Control Methods for controlling asbestos emissions to coaaiunity air are similar to those for controlling any perticulete matter, with some variations due to the special characteristics of asbestos. Since oper­ ations that generate asbestos fibers are usually conducted under nega­ tive pressure, careful cleaning of the air in the ventilating system will adequately control general air pollution. Hovever, while the air-cleaning methods mentioned below may be adequate for many asbestosrelated activities, they are not practical for use in demolition or rip-out. Control of general air pollution in this case is limited to use of water sprays. The most useful control method is fabric filtration, and design parameters for successful systems have been published.9-12 The effi­ ciency of fabric filter units used to collect asbestos fibers ranges from 95X to 99.9X on the basis of weight. These units operate dry, and removing the filters and packaging them for disposal can be a dusty operation, requiring the use of personal protective equipment. Wet collectors—wee dynamic scrubbers and Venturi-type collectors— range in efficiency from 50Z to 90Z. The fibers collected are in a slurry and may pose a water pollution problem. Usually, the slurry is filtered and the wet fibers disposed of in a suitable container. Mechanical collectors (cyclones) generally operate.with the same efficiency range as wet scrubbers, the actual efficiency depending on the size, design, and enargy expended. Although the fibers colltcted ere dry, many of them ere fractured, thereby limiting their further use. Because the fibers are dry, personal protective equipment may be required when they are removed from the collectors for disposal. Because they require no power other than to move air and they have no pares eo wear out other than chs collector shell,2 mechanical collectors are econom­ ical to operate end maintain. Elactrostatic precipitation has provad to be lass sffactive then other alr-polluelon-control means for asbestos fibsrs—yialding, at ths best, 70Z efficiency. Water Pollution Control Until recently, little attention was directed toward ths vasts waters sssociatsd with asbestos manufacturing, and there is virtually no published information on such waters, Ths number of planes Is not Large, and ths volumes of vsstas have been relatively small. Further­ more: a significant amount of procsss wstsr in manufacturing operations Is recirculaced, most plants have some form of vases treatment, and many planes are situated vhere they can discharge the process waste 83 DUP 0931727 DU 035464 ^maisasji1, j; j:MHI lifejll-i'-M t"'_^ waters to municipal sewers. Recently, however, increased concern over asbestos fibers in the air has resulted in (1) conversion of some dry processes into wet ones and (2) use of water sprays to control dust from mining and from piles of tailings or gob (low-grade ore), thereby increasing the potential for water pollution. Waste Water Treatment Processes The standard processes for removing suspended-solid wastes from water have been found to be satisfactory for removing asbestos fibers: e Precraatmene—removal of oil, grease, and the larger aggregates of solid matter. • Primary treatment—sedimentation and chlorination • Secondary treatment—biological processes such as aerated lagoons • Tertiary treatment^ Tertiary treatment—sometimes referred to as "advanced *:ne water treatment" or "physical-chemical treatment”—is required ifeffluent from secondary treatment Is not considered satisfactory.** The several means of removing suspended solids in tertiary treatment including microscralnlng, diacomaceous earth filtration, chemical clarification, and deep-bed, granular media filtration.' In microstraining, the waste water is scrainsd through a woven mesh screen on che surface of a rotary drum that revolves on its hori­ zontal axis. As che drum rotates, Cht solids are strained out of the water and to a position from which they are removed from the drum. Diacomaceous eerth filtration is s fora of mechanical separa­ tion that utilizes diatoaactous earch, a finely powdered filter-aid that is built up (coated) on a supporting medium, to trap solid material. The fibers removed are mixed in with che filter medium, and both must be disposed of. In che chemical clarification process, chemicals such as aluminum, iron, or calcium oxides are added to the water to coagulate fine solids. Coagulation is followed by a flocculation phaat, in which particulates are aggregated into larger dumps that will settle. This process if followed by sedimentation, in which the floes that have been previously formed are allowed to settle to che bottom of a settling tank. While some of the solid material will have been removed by sedimentation, the material remaining must be removed by filtration, usually carried 84 093l728 DU 035465 : -i Tiigff wSiM..i;;i5 ii J :&Ig.T.:' ouc In bads of a porous medium such aa sand or coal, or a combination of ~acia such aa sand and coal, or sand, coal, and garnat. Control of Asbeatoa Fibers in Potable Water Supplies Tha extent of asbestos in tha nation's water supplies has not been established conclusively, and it has not been established to what extent ingested asbestos might be harmful to humans. In the meantime, it is the opinion of some researchers that oral intake of asbestos should be reduced as much as possible. ^ One method of reducing asbeatoa concantrationa in potable water involves minor modification of standard coagulation/filtration techniques as practiced in mose water-treatment plants. Preliminary results show chat the number of asbestos fibers could be consistently reduced to belov-deeectsble limits (<20,000 fibera par liter). Even simple filtra­ tion systems have been shown to be partially effective and could prove' useful as a low-cost interim measure in areas of high fiber concentra­ tion. ^ the results of one study indicate that both alum and polyelecerolyce coagulation optimize fiber removal and that they can be used with sand filters. This is a definite advantage, since sand filters are used in che majority of filtration plants in North America, and Europe as well.^ During 1974, two diatomite-fliter pilot plants operating at 10 gallons per minute removed over 80X of amphlbolc asbestos fiber from a drinking water source. The turbidity of the finished water was 0.05 or 0.06 FTU (Fortnazin Turbidity Units), with over 95Z of the fiber removed. Removal of amphibole fiber seemed to be significantly better than that of chrysotlle fiber.17 The pilot plant study suggests the following conclusions applicable to the filtration of Lake Superior Water at Duluth:• • Several filter operating conditions esn result in 9SZ to 98X removal of asbestlfora fibers. Conditions pro­ viding the best filtered water would Involve the use of either alum-coated Hyflow Super Cel (or equivalent grade) as body feed and precoae, or alum-coated C-512 filter aid (or equivalent grade) as precoat plus a continuous coagulant feed of Cat-Floe 8 polymer to che filter influent water. e The operating data indicaca chat vacuum diacomite filcars are significantly more expensive as a means of producing filtered water and chat they would be very difficult to operate under conditions of high turbidity. 85 DUP 0931729 • A laasc-cosc-desiga analysis of several alternative plants suggests that a plant designed for a 20-year Life and for a turbidity of 1.9 FTU equalled or ex­ ceeded only 51 of the time could produce 30,000,000 gallons of water per day at a cost of 5.56c per 1000 gal. It is suggested In che study chat the best pro­ tection against price increases for filter-aid would occur if the filtration plant were designed for a water turbidity of about 2.5-3.5 FTU. Waste Disposal The greatest hazard associated with asbestos solid waste is che potential.for air emissions arising from improper handling and from improper final disposal. At each step in the handling of che solid wasce material—whether the waste is to be concentrated, isolated, dis­ posed of, reused, or otherwise treated—hazards to the waste handlers may arise. Hence, asbestos-containing wastes must be treated with che same respect accorded asbestos products and their production. The most desirable general waste management options, in order of priority, are:^ • Waste reduction—by reducing che amount of asbestos used, substituting less-hazardous material, and making the process more efficient. e Wasce separation and concentration—segregating hazardous and nonhazardous wastes. e Waste recovery—reusing the material. • Secure ultimate disposal—disposal to landfill in a way that precludes future reencralnment. The most important aspects of controlling asbestos solid waste are discussed in che paragraphs that follow: (a) identification, (b) sep­ aration, (c) secure transport, and (d) secure ultimate disposal. Identification Obviously, there can be no control measures directed at asbestos solid waste if asbestos has not been identified as part of che solid wasce stream Issuing from a plant—identification and then cracking asbestos-containing materials as necessary. 86 PUP 0931730 * DU 035467 WIWiSrglWSBatrMlBagBMS: Separation* The source of asbestos-containing waste having been Identified, that vasce should be separated from nonhazardaus wastes, taking care to prevent exposures to workers during separation. For holding small quan­ tities of dry asbestos wastes, the most generally satisfactory containers are heavy-gauge, impervious plastic bags. Asbestos may also be disposed of as a slurry, provided the slurry does not dry between collection and disposal. Secure Transport Waste must be transported to the ultimate disposal site with­ out producing emissions. In practice, this means that community (public or private) disposal services cannot be relied upon unless they are aware of the hazard and of proper handling procedures, and unless they can provide closed conveyance to the ultimate disposal sice. If waste Is disposed of on the premises of a plant, employees of the facility will likely be familiar with handling precautions. The integrity of the vasce contsiner must be maintained. Care muet be taken not to rip or tear plastic bags, and mors-permancnt waste containers such as cans or bins must have tight-fitting lids that will not coma off during transit. Secure Ultimate Disposal The only disposal of asbestos waste thst can be considered "secure ultimate disposal" Is depositing it in a site that Is covered with a layer of nonasbestos-contalnlng waste or earth that is at least 15 centintters deap If an adtquata vegetativa cover Is also establishad and maintainad, or 60 centimaters deep if there is no such vegetative cover. Emissions from waste may also be controlled by (1) maintaining a resinous or petroleum-bated dust-suppression cover at the site, or (2) by vetting the waste with wacer and saaling it in an lmparmeable container before disposal.^ Covering weete with soil and planting vegetation does not require as much care as is needed for maintaining a disposal siea with dust-suppresalon aganca; hanca, lc Is ehs more desirable control machod In most cases. Control During Transportation The transportation of asbestos ore from mine to mill is generally not a significant sourca of airborne asbestos fibers, although private *See Chapter TV, Occupational Exposure, for additional datails and applications. 87 DUP 0931731 DU 035468 nine-mill roads nay be paved wich tailings from which fibers can be liberated when trucks pass by.. Some of these emissions can be reduced by tarring, sprinkling, or creating the roads with dust-suppressing chemicals. SPA regulations permit no visible emissions from mine or mill roadbeds. Manufactured asbestos products not firmly embedded in a matrix,* such as asbestos cextilas or spray asbestos materials, should be either: e Transported and scored in enclosed, impermeable, sealed areas e Wetted and covered with tarpaulin or similar material to prevent drying e Appropriately packaged—packaging chae is leakproof and durable enough to withstand abrasion or puncture during normal handling, and chat bears easily visible labels that warn persons about the hazard. Areas used to transport or store asbestos not appropriately pack­ aged should not be used at the same time to transport or store other goods. Such areas should be posted with signs warning of the asbestos hazard. Before the areas are used to transport or score goods, accum­ ulations of asbestos fiber should be removed thoroughly, preferably with a vacuum cleaner having a high-efficiency filter. Personnel working in or near areas used to transport or score regulated asbestos that is not appropriately packaged should follow the procacclva procedures outlined earlier in this chapter. Manufactured products containing asbestos firmly embedded in a matrix asbestos cement, asphalt, plastics, and the like—may not reasonably be expected to result in asbestos air concentrations that are high enough to warrant packaging. DUF 0931732 DU 035469 ......=.r mmmSj* .iliiilg ailtijflU. U-iliwi; MUM iiaiiiHilit Chapter VII CONTROL OF THE ASBESTOS HAZARD— MEDICAL MANAGEMENT A means of Limiting, in the industrial population, diseases that tan be somehow related to asbestos is to recognize during a preemploy­ ment examination persons who have increased risk for these diseases by virtue of ocher attributes they possess and to recommend chat they not be hired for jobs involving asbestos exposure. Those workers necessarily exposed to asbestos should be enrolled in a medical monitoring program. In this way, hopefully, asbestos-related diseases, disorders predispos­ ing to these diseases, and conditions likely to be aggravated by asbes­ tos exposure can be decected early enough so that removal from exposure or medical intervention may successfully limit their course. Neverthe­ less, asbestosls may progress even after removal from asbestos expo­ sure, and screening programs for the early detection and treatment of lung cancer have not yet proved to be more than marginally beneficial. Composition of the Workforce The extent to which discovering and not hiring certain high-risk persons for jobs involving asbestos exposure can be put into effect in any particular situation will be limited, inevitably, by social and political considerations. Each industrial physician must develop his own program for dealing with these matters in relation to preemploymenc examination policy. The deaired nee effect of the employment screening approach is to assemble and malnealn a workforce whose combined average risk of devel­ oping disease, with exposure to asbestos, is lest than what it would be were it eo include persons whose individual risks, even without occupa­ tional asbestos exposure, ere relatively higher. The approach would be expected to be most affccclva in ralaeion to choaa diseases for which evidence of a causal role of asbestos is most convincing and the magni­ tude of the problem is greatest—lung cancer, mesothelioma, and asbestosis. Suaurlzad below are some considerations for applying control 89 00? DU 035470 33 R an ovar tha industrially exposed population by excluding from employment certain Individuals on medical grounds. Lung Cancer Lung cancer is the most frequent of cancers related to asbestos exposure and today exacts the heaviest mortality of any asbestosrelated disease. Several risk factors for lung cancer have been identified: e Cigarette smoking greatly increases the mortality from lung cancer, and, based on present knovledge, it is the moat impor­ tant single risk factor. • A history of lung cancer in a first-degree relative—parents, siblings, offspring—has been shown to confer almost the same magnitude of risk of lung cancer for the general population as cigarette smoking, and, together, both factors are synergistic. • Prior occupational exposure to carclnosena affecting the lung also may reasonably be expected to enhance the risk of lung cancer in an asbestos worker. Such carcinogens include arsenic; chloromsthyl ethers; chromium; eoal tar, petroleum, and by­ products; creosote; mustard gas; nickel; radium; and uranium. • Nonmalignant respiratory disease may increase the risk of lung cancer. Pulmonary fibrosis has been noted in association with lung cancer in persona with scleroderma^•* and certain rare hereditary diseases of tha lung such as fibrocystic pulmonary dysplasia'*6 and congenital cystic disease of the lung.7 Several reports have associated an excess risk of lung cancer with chronic bronchitis, after taking into account differences in smoking habits.3”11 However, such studies have often employed broad smoking categories and have neglected such important vari­ ables as duration of smoking and extant of inhalation.1* Perhaps most convincing was the finding of a substantial excess mortality attributed to nonmalignant respiratory diseases among nonsmoking blood relatives of lung cancer cases that was not present among case spouses.1^ And significantly higher rates of impaired forced expiration have recently been found among never-smoking relatives of patients with lung cancer or chronic obstructive pulmonary disease when compared with neighborhood controls.14 Experiments with animals indicate that individuals with asbes­ tos is may be at increased risk of lung cancer, regardless of level and duration of asbestos exposure. ^ Possible laboratory measures of lung-cancer risk Include inducible levels of aryl hydrocarbon hydroxylase and tha condition of exfoliated cells in sputum. Aryl hydrocarbon hydroxylase (AHH) is an inducible DUP 0931134 DU 035471 amyoe thought to be responsible for converting hydrocarbon carcinogens such as are found in tobacco 3moke to an active form. One team of investigators has reported that levels of inducible AHH activity in human tissues appear to be genetically regulated and chat patients with bronchogenic carcinoma have higher levels of inducible activity than controls.17 Inducible enzyme levels, therefore, might indicate among cigarette smokers those individuals at greatest risk of develop­ ing lung cancer, At present, however, there are numerous difficulties with the assay technique even in the most experienced laboratories, and the mechod is not ready for general use.18 Furthermore, the associa­ tion between levels of inducible AHH activity and cancer has not yec been firmiy established.^ Examination of exfoliated cells found in sputum has been used to assess che scats of the human tracheobronchial tree. Cancer has been observed to develop after a series of gradual cytological changes occur­ ring over several years. These changes have been categorized into stages of regular squamous cell metaplasia, various degrees of a typical squamous cell metaplasia, carcinoma in situ, and invasive carcinoma. The more severe the cellular changes, the greater is the likelihood of developing lung cancer.21' Cytological examination of sputum can be used to complement che use of risk factors listed above since, at any one time, che condition of exfoliaced cells must reflect the interrelated effects of all operating risk factors, age, and latency. A great limi­ tation to the widespread use of this technique at present is the paucity of laboratories capable of accurate cytologic interpretation of sputum • samples.22 Persons with any of che risk factors for lung cancer or whose sputum examination reveala cytopachology of severity equel to or greeter chan moderate atypical squaaioua cell metaplaela would beat not be hired for jobs involving asbestos exposure.* Mesothelioma Little la known about susceptibility to mesothelioma, an Important cause of mortality in aabeatoa workers. Persona who have hed en The evidence that asbestos la causally related to laryngeal cancer is highly suggestive, but not as overwhelming ss it is for lung cancer and mesothelioma. Therefore, the exclusion from employment of individuals with other risk factors for this disease would probably be leea bene­ ficial. It should be noted, however, that except for family history, the risk factors identified for lung cancer generally apply to cancer of the larynx. Risk of laryngeal cancer has, in addition, been corre­ lated with alcohol consumption.22"2* This cancer is rare, and moat susceptible persons will have been screened from employment in efforts to excluds persons with elevstsd risk of lung cancer. 91 uUP 0931735 DU 035472 asbestos-related pleural effusion may be ac great risk,2^ and further asbestoe exposure should be prevented. Asbestos Is Exclusion from employment of those persons mosc susceptible to disease would likely prove more efficient for asbescosis, for which exposure to asbestos is a necessary factor, than for lung cancer or mesothelioma, for which it is noc. However, despite suggested effects of cigarette smoking,27 immunological response,2®*2^ and specific HL-A antigens,30 risk factors for asbescosis have noc been established,31 and there is to date no method for identifying from medical testing or questioning those individuals who are more susceptible to asbescosis. Because of the potential adverse effects of further respiratory disability from asbescosis in individuals with existing chronic res­ piratory disease, it would be prudent not to hire such persons for jobs involving asbestos exposure. Early Detection and Treatment of Asbestos-Related Diseases In general, treatment of asbestos-related diseases, even when detected early, is far from satisfactory. Curs is rarely possible, and oftentimes death or severe disability supervenes despite the best of efforts. Furthermore, programs for early detection and treatment run che risk of instilling a false sense of security, which may detract from more primary efforts to prevent disease by controlling exposures. This must be kept in mind during che subsequent discussion. A suggested protocol for preemployment and follow-up medical exaainations of asbes­ tos workers is given in Table 7. Lung Cancer Screening programs, which rely on roetgenograns and symptom ques­ tionnaires ac intervals of six months have been notably unsuccessful in improving the changes of survival from lung cancer.32, 33 The Phila­ delphia Pulmonary Neoplasm Research Project reported a 5-year survival rate of only 12Z of individuals whose tumors were detected within 6 months of a negative roentgenogram, as against 4X in those whose tumors were detected more chan 6 months afterward. A semiannual screening program conducted among residents of Veterans Administration doaiciliaries and consisting of stereoroentgen films, questionnaires, and sputum cytology slides reported a 3-year P°etoperative survival of only 12Z.22- This study documented a considerable DUP 0931736 DU 035473 Table 7 MEDICAL EXAMINATIONS FOR AS8ESTOJ-EXJOSED WORKERS Prisonlovaant Questionnaire: medical history, family history, history of snoking* and consumption af alcoholic beverages, occupational history Physical Examination: concentrating on the oral cavity, chaat, and abdoaaa aad Including a digital examination of tha rectum Splraaatry: Including ocasurtaanta af vital capacity, forced vital capacity, and faread expiratory volume at one aeeond Cheat X-ray: poateroancerior and lateral views (14 x 17 lachaa) Sputum Cytology _FollowJJg Monaaokara-, Ex-Saoktrs. and Smokers Who do not Inhale e No Kore Than HIId Atypical Sputum Cytopathologyr ometry, cheat i-ray, and apucurn cytology a yearly questionnaire, epir- • More Than Mild Atypical Sputum Cytepathology■ a yearly quaacionnaire aad aplromatry; cheat X-ray and aputum cytology every 4 months a 40 Yeara Old and Older, At Laaat 20 Yeara from Onaec of Aabeetee Expoaura: add facal occult-blood tearing aad aa examination of tha oral canty every & aoathe Sankara Who Inhale e laaa then IS yeara froa Onaec af Aabeatoa Expoaura: -No more chan mild atypical aputum cytopathology—a yearly queeclonnalra, epit­ ome try, cheat X-ray, aad aputimi cytology -Mora than aild atypical aputum cytopathology—a yearly questionnaire and aplroaatry, cheat x-ray and aputum cytology every 4 eonthe a 11-20 Yeara from Onaec of Asbeecoa Expoaura: -No more then aild atypical aputum cytopathology—a yearly queeclonnalra and aplroaaery; eheat X-ray and apucurn cytology every & aontha -Mara ehaa aild atypical aputum cytopathology— a yearly questionnaire aad spiroaatry; chaat X-ray and aputum cytology tvary 4 aontha • Mora Than 20 Years from Onset of Aabaatoa Expoaura: -Laaa chaa 40 years old—a yearly questionnaire and aplroaaery; chase X-ray aad aputum cytology every 4 aontha -40 years old and older-add fatal occult-blood tasting aad aa axamlaaeloa of tha oral cavity every < aoathe. Since eaokiag le euch an important risk factor, breath should be sniffed for tobacco odor; aad la aleusclons vhare the reliability of lacking histories la In doubt, levels of expired air carbon monoxide or aerum thiocyanate aay be used to distinguish cigarette lookers froa aonsmokars.^Sources: Protocol modified froa tha Mt. Sinai School of Madidna, Environmental Science* Laboratory Pulmonary Surveillance Program for Aabeatoa Exposed Workers. 93 DUf 0931737 035474 may, l»aSlffl5i ;.afiiaa- XPS^-m- '■ :f Mj’1» kt*?—M^taatauaBi -pf*~* amount of inter- and intra-observer variability in the interpretation of sputum smears and chest X-ray films, but noted chat Che addition of positive and suspect sputum cycopathology increased the sensitivity of the screening method by about SOX without significantly compromising its specificity.21,34,35 Currently, large detection and follow-up programs are under way at the Mayo Foundation, Johns Hopkins University, and Memorial SloanKeccering Cancer Center to evaluate the efficacy of sputum cytologic examinations, chest X-rays, and questionnaires administered every four months. At the Mayo Lung Project each chest X-ray is reviewed by three physicians individually; and check roentgenography for patients having follow-up examinations at the Mayo Clinic Itself consists of postaroantsrior (PA) stereoroentgenograms and 350-kV PA views, as opposed to conventional PA and lateral films.36*37 In the presence of normal chest X-rays, if a single sputum speci­ men t contains frankly cancerous cells or if repeated specimens from the same individual contain markedly atypical cells, procedures to localize a tumor are set into motion. Detailed radiologic and radioIsotope studies are undertaken, and a thorough otolaryngologic examina­ tion is made to rule out cancer of the upper respiratory tract. If localization is not achieved, a meticulous endoscopic investigation follows utilizing fiberoptic bronchoscopy, succeeded if necessary by b ronchographic s tudies.3o , Initial results from the Mayo Lung Project suggest that no more chan a third of detected cases of lung cancer may be expected co sur­ vive five years or more. However, more observation is needed in order co determine actual rates of survival. Roentgenographically occult tumors, which are likely to be centrally placed, were generally smaller and had a bettar postoperative prognosis. Most newly diagnosed lung cancers (64%) were detectable by chest X-ray alone, and only 13% of cancers detected after an initially negative screen were first noted as the result of clinical sympeoma.36.37 I i. f Whatever the outcome of the currant detection and follow-up programs, certain limitations will apply: e ! i I Some Individuals should be ineligible for screening because of inability co tolerate pulmonary resection or unwillingness to undergo operation if it becomes necessary.38-40 To screen such persons not only would be wasteful, but also might ultimately contribute co lowering the morale of ocher parcicipants in Che screening program—chat is, whether or not the death of a screening participant was due co inability or unwillingness co be operated on, it might be regarded by others as a failure of che program. DO? 0931738 DU 035475 _ _ _ _ —'■ ....... . . . . .r-f,ii:l;iaaaaH>,r^i ■inirimni.S'iai • A considerable number of persons may discontinue participation in the screening program because at retirement, termination of employment, or other reasons. Since the Incidence of lung cancer increases with age^1 and has been found in one study to be higher among screening dropouts,38 there is reason to believe that persons who discontinue participation in a screening pro­ gram may in fact be at greater risk. • A certain proportion of screening examinations will be found to be incomplete or technically unsatisfactory. e Ones a cancer haa been detected, there will inevitably be a delay until localization and operative resection. The greeter this delay, the less the potential benefit chet can accrue from the screening program. a It will be difficult to extrapolate from results obtained at premier centers of medical care to likely results in an average industry program. (The difficulty in finding laborstoriae cap­ able of accurate sputum cytologic diagnosla has already been mentioned.) e The considerable financial expense of a screening program and the drain on available time of medical care personnel should not be overlooked. e Despite screening, some cancers will not be detected early; and despite early detection, certain cancers will be inoperable or have a poor prognosis. e A not-inconsiderable percentage of persons who will have been successfully operated on to remove e lung cancer will develop a second tumor.38 Despite these limitations, medical screening remains the only means of assisting the unfortunate individuals destined to develop asbestos-related diseases and should not be abandoned. The use of spucum cytology to distinguish persons of heightened susceptibility to lung cancer for removal from asbestos exposure or for motivation to quit smoking deserves to be tested. Screening examinations remind the workers of the health hazards of his Job and may be used to enlist his cooperation in Improving work practices as well as in changing detrimental personal habits. It is suggasted that programs for early detection of lung cancer In asbescos.workers consist of periodic spucum cytologic examinations, chest X-rays, and symptom questionnaires administered according to a schedule which varies with sga, risk of lung cancer, and time elapsed since first exposure to asbestos (see Table 7). Available medicel facilities chet are competent In localizing and resecting lung cancer should be identified In advance of the program to minimize time taken from detection of cancer to operation. Emphasis muee be placed on proper check roentgenography, since chest X-rsys alone should detect 95 OOP 0931739 DU 035476 kaiiSkiMJ&Miib. -isUHii 21 m&k 37 the majority of lung tumors; sputum cytology is more effective in detecting centrally placed tumors36 whereas asbestos workers may mors likely develop peripheral lung cancers (adenocarcinomas).4^ Each chest film must be read independently by more chan one physician especially trained to detect early lung cancer and qualified in the ILO/U/C classification of radiographs of pneumoconioses.4^ Laryngeal Cancer Asbestos workers with clinical symptoms of hoarseness or pain or soreness of the throat should be referred to an ear, nose, and throat specialist for a detailed otolaryngologic examination of the upper respiratory- tract. Kesochelioma At present, mesotheliomas are uniformly fatal. Neither radical surgery, radiation, nor chemotherapy prolongs survival; in fact, these modes of treatment may be harmful. Since no useful therapy is avail­ able, screening for early detection beyond what may be done to detect lung cancer is of no clinical value. Invasive diagnostic procedures should be kept to a minimum and.management restricted to the relief of pain and breathlessness.4^44 Cancers of the Alimentary Trace Fecal occult-blood testing has been used an an annual screening device to detect colorectal cancer in asymptomatic men and women 40 years old and older.45 Positive tests have been obtained from persons with cancer of the stomach, small intestine, colon and rectum, and, to a lesser extent, from persons with benign gastrointestinal lesions.4° Persons with positive results should be referred to a gastroenter­ ologist for further studies, which may Include endoscopy, cytology, biopsy, and radiology. Early detection and excision of a colorectal and gastric cancer, it has bean noted, may result in 5-year survival races as high as 902, compared with overall national averages of 40Z and 10Z, respectively.49,50 *False poeitivee can be reduced considerably by using guaiac-impregnated filter paper slides in conjunction with a diet high in residue (to stimulate bleeding from existing lesions) and free of red meat and high peroxidase foods (e.g., horseradish and beets). Vitamins and aspirincontaining medications should also be avoided.4‘»4', 8 96 DUP 0931740 ^ 035477 Asbescosis Periodic comparative chest X-rays and pulmonary function tests (see table 7) will Lnprove the chances of detecting early asbescosis. Many abnormalities, however, are nonspecific, and it will be difficult to determine if these reflect early asbescosis or are merely related to smoking or aging.31 Pleural thickening or plaques in an asbestos worker must always be suspected as evidence of a biological effect related to Inhaled asbestos.5* Persons vich early asbescosis or with pleural chickening should be removed from asbestos exposure and referred to a chest physician for careful follow up. 97 out DU 035478 Chapter VIII CONTROL OF THE ASBESTOS HAZARD—EDUCATION Asbestos was tha subject of cha first occupational safety and health standard issued by tha Department of Labor, following passage of tha OSHA Ace of 1970. But although cha standard has bean amended since (to change the allowable airborne exposure concentration), no specific directive has been included regarding education or training of super­ visors or employees. However, in standards subsequently promulgated for a mnfcer of carcinogens—including vinyl chloride, che subject of another control monograph by che National Cancer Institute*—there are particular requirements specified for employee training and indoctrination in, for example, the following: nature of che carcinogenic haaard, nature of che operation involving the carcinogenic agent; recognition of conditions chat may release the agent; purpose and application of decontamination practices; emergency practices and procedures and che employee's specific role in then; and purpose and application of che medical surveillance program.1 It would appear that a comparable mandate should exist for work with asbestos. Goals of Education Implicit in the fundamental goal of controlling the human carcino­ genic hazard from asbestos are several goals of education—increased knowledge of: e Work processes involving asbestos end the potential for fiber emissions e The physical characteristics of asbestos, so as to understand its dispersion and potential for inhalation e Diseases that may result from exposure to aabeetoe fibers and how these diseases are manifested The reader is advised to read the section on "Educational Control" in the cancer control monograph Vinyl Chlorida, sinca soma of tha infor­ mation pcesancad thara complements the materiel presented here with regard to Che esbestoe-concrol situation. Among tha copies discusssd there are "Understanding 'Risk;'" raview of a National Academy of Sciences study on Informing workers and employers about occupational cancsr; and an outline of an on-going vinyl chloride education program that embodies soma of cha approaehas dlscussad hers with ragard to asbestos. 99 DUP 0931742 DU 035479 • The concept of "risk" • Reasons far, and methods of, environmental monitoring e The purpose and nature of engineering and work practice control methods as discussed in the previous chapter (exhaust ventilatlon, personal protective devices and clothing, personal hygiene, etc.) e The elements of medical surveillance and the reasons for It • The role of related factors in disease production, such at smoking. Modes of Education—The Written and the Spoken Word Of the two modalities employed In delivering health messages, the written word and the spoken word, the written word is far less effective. lc lacks the elements of concern, warmth, dedication, and personal in­ terest of the instructor, and there is no opportunity for question and discussion. Furthermore, the efficacy of the written word depends on the reading skills of the reader. However, if one must reach hundreds ' of employees ec once the written word might have to be used but, even then, it should be as a reinforcement to the oral mode of communication. One good opportunity for oral communication Is when the physician and an employee review the results of the employee's periodic medical examination. Attention is then focused on one lndividuel—one who is, at the same time, full of foreboding end apprehensivenees. nurtured by misunderstanding, folk beliefs, Inadequate information, and rumor. The physician at this time can clarify medical terms, give meaning to test results, and suggest changes In work habits and life styles. Most oral communication will take place at group education sessions. In some employment jurisdictions, such sessions may be required by labor-management contracts or by lew.2 The subjects for presentation may be mandated; selected solely by the occupational health staff; or, perhaps most effective, chosen through joint consultation of health personnel with department heads, plant manager, and trade union offi­ cials. Education oust go beyond a pro forma attempt to meet mandated raquiremaned. Aa recommended by a special committee of the National Research Council,2 provision must be made for the worker to acquire more information than is provided by the "package" of educational material. Ha, the worker, must be assured that hie questions will be answered, if not during the information session, then later by telephone. 100 DUP 0931743 DU 035480 - jaiggalji'lr letter, or consultation with a member of che occupational haalth staff or someone equally knowledgeable. An excellent forum for group health education la during the orlencation of nev employees. The occupational health staff should use the occasion co discuss che purposes of che preplacemenc medical examina­ tion recently completed, co describe available health services, and co explain engineering controls, work practices, and use of personal pro­ tective equipment. Pursuit of a health problem in che future will be facilitated by chls initial introduction. The Educators Persons from a variety of backgrounds may be Involved in the educa­ tion effort—physcians, nurses, health educators, industrial hygienists, safety specialists, and others. Physicians Physicians chat teach usually do so in institutions of higher learning, where they can remain comfortable with a technical lexicon and oral shorthand. It takes greater effort and more time to describe medical disorders and risk factors co a layman in terms he can under­ stand, yet this must be che charge of the physician, particularly che specialists In occupational raadlcine pulmonary disease. Pulmonary disease specialists, in particular, aa they become more knowledgeable about asbestos-related diseases, must inform their col­ leagues in che medical community of diseases. For in spite of a growing body of pertinent literature, many physicians remain uninformed about, and unsuspecting of, asbestos-related diseases. Many cheat physicians are members of lung associations, and such membership can provide many opportunities for ths education of fallow medical practitioners as well as lay community leaders. Also, when neceaeary, ths pulmonary disease specialist could assist che occupational physician in educational pro­ grams for industry. Hurees Health education has long besn recognized as a primary function of the occupational health nurse and an area in which she can make « considerable contribution. The nurae often hes a closer relationship with the employee than does the physician and therefore may have greeter influence on changing the employee-patient's behavior. Whereas the advice of the medical director might be interpreted as the biased word 101 DUP 0931744 atMiUtti i&m mrnmsi of management, a skilled nurse utilizes every patient visit as an opportunity for presenting material relevant to health behavior. Health Educators (Communication Specialists) Professionally trained health communicators may be found in tha larger occupational health programs of industry. As full-time personnel In Che medical facility, they have been able to learn the mission of the organization, to become acquainted with work processes, to identify problems or concerns peculiar to the work population, and to absorb the "shop patois." This background puts the health educator in an excellent position to eossaunicate successfully with the employee. Industrial Hygienists The industrial hygienist is an integral part of the occupational health staff. Whereas the occupational physician has expertise in the recognition, evaluation, and control of diseases relating to environ­ mental hazards in chc workplace, the industrial hyglsnise is trained to recognize, evaluate, and control Che environmental hazards themselves. One aspect of this responsibility is the education of the working communlcy. The industrial hygienist informs workers about measures to control physical hazards and motivates them to do what they can to min­ imize personal exposure and to assise in improving the work environment. Union Health and Safety Specialists In recent years, a sasll but increasing number of trade unions have appointed full-time staff persons in the aree of occupational safety and health. These individuals may be extremely lnfluentlel, because they know the Issues and supporting data wall and can communicate information to their.locals by means of periodic lactars, memoranda, newsletters, or reprinted presentations. Industrial Safety and Other Training Specialists Ever sines the birth of the aefety movement in the United States, specialists in accident prsvancion have conducted educational programs for employees. Although moat of chess efforts have ralscad to physical trauas, soma alight redirection could channel th«a toward the preven­ tion of asbestos-caused disease. In addition to training in safety, chert may be company training programs In ocher subject matter, from management skills to technical 102 DUP 0931745 DU 035482 craft apprenticeship information. Training specialises who conduct such program* might also assist in health-hazard education. Science/Medical Writers Medical writers on the staffs of large daily newspapers and other periodicals might be asked to e plant to be made familiar with the con­ tent of a medical surveillance program, to be apprised of health survey result*, and to be updated on general occupational health activities. If a good working relationship evolves, chances will be improved thee reports are ln-dapth and accurate, and the result could be yee another avenue for education of the worker. Target Croups for Education As indicated, there are many target groups within industry for whom instruction in prevention of asbestos disease is needed. The language in the OSHA occupational safety and health act of 1970 direct training toward both the employer end the employed end, in addition, there ere trade union officials, retirees and other former workers, workers' families, and miscellaneous persons in the community at large. Managerial and Supervisory Personnel Managers should be as fsmiliar, or even more familiar, with the risks of the materials they ask their workers to handle and with preven­ tive measures, medical surveillance, and the other areas of knowledge lisced at Che beginning of this chapter under "Goals of Education." Thera is often an unusual climate in which to educate managers about asbestos-related disease. That is, e number of executives end line managers have risen from the ranks, so that ae the inception of their careers they, themselves, worked with asbestos fiber. Hence, any occupational health proeadura draws special attention because such managers know of the latency period before manifestation of disease. Their concern la aa graac as chat of newly employed mechanics' helpers, while, ae the seme time, their literacy level la probably highar. However, while they may know that the fiber la hazardous, they might not ba aa familiar with eapecta of the problem ae they should be, and they should receive as much medical and industrial hygiene information aa they cam absorb. Because ha is at the level of management closest to the worker, a well-informed supervisor should be particularly effective in OOP 0931746 103 DU 035483 -:=‘* modifying the behavior of workers sinct ha will be la a position to motivate rather chan commanding or invoking the sanction of regula­ tions . Workers in the Asbestos, aa Well aa Other, Trades While workers in the asbeseos trades are obvious targets of educational efforts, there are other workers who may be exposed to asbestos and who, therefore, should be informed of the asbestos hazard and how to minimize it. Thesa workers include those who dismantle ships and buildings, welders, painters, electricians, carpenters, marine machinists, shipfltters, machinists, and automotive brake and clutch repairman. Retirees and Other Former Workers Because of the long delay in manifestation of asbestos-related disease, it is necessary to maintain contact with rstirsss and with persona who have lefe work with ssbeaeoa to obtain employment else­ where. The asbestos workar cannot be permitted to depart with ehe misapprehension that if ha no longar hsa contact with that matarlal ha is no longer at risk of davalopaent asbastos-reiatad distasas. Exit lntarvlews provide an opportunity to emphasise ehe need, for life-cime contact and to streaa the need for continued medical surveil­ lance. Wherever possible, former asbestos workers should be included in plant programs of health education, smoking csssstlon, and medical surveillance. Workers' Families In addition to learning about asbestos-related disease, the families of asbestos worksrs should bs informed aboue the importance of smoking cessation and about tha potential contamination by fibers _ brought horn on clothing, equipment, lunchboxas, and automobiles, snd' in the form of souvenir ore samples. Also, ifhaa bssn observ^ thst wives who visit with thsir employee-spouses ac tha plant physician's' office often aak more astute, more penetrating questions than thsir metes. Communication is good with mixtd audiences, and tha program of prevention will be acrongly reinforced by informed families. Occupational Health Professionals Bscauss thara art so many substances, combinations of substances, induatriaa, lavela of industry (raw materials, intermediate manufac­ turing, finished product manufacturing and distribution), occupational L04 DU? 0931747 DU 035484 health personnel are noe all-knowing shout all hazardous substances cur­ rently in use. For example, with the poasibility of asbestos insulation In innumerable buildings being removed during renovation or demolition, it is possible that the health personnel of a company or institution not in the asbestos Industry may suddenly be faced with Che inauguration of a project to protect personnel against the untoward effects of fiber inhalation. Finally, the ubiquity of asbestos is such that it could be present in a plant without a company's health personnel's knowledge— i.e., through the reworking of asbescos-containing parts or raw materials manufactured elsewhere. Information on the asbestos hazard will sharpen the health profesalonal's index of suspicion, and ha will seek out the material’s presence throughout the workpiece. Assessment of Education's Value Every health education program should bs validated ss to its worth. Uhlls a rigorous evslustlon may not be possible, there art means by which the effectiveness of an education program might be judged. Although for a work fores es e whole, some workers ere retiring end some workers are leaving for other employment, small groups can be tested informally before and after various education segments in which they participated es follows: s Compliance in engineering controls and safe work practices— without giving greec visibility Co the check-off procedure, workers could be observed prior to and after the educational program to determine if there la a change in their use of engineering control devices or in their complience with sefe work practices. e Compliance in medical surveillance programs—workers often report for chest rsdiogrsphy or pulmonary function tasting only after innumerable telephone calls and notices, and im­ proved complience rata would indicate some success In education. e Basle knowledge appropriate to target group—groups can be preend post-tested for retention of common knowledge expected of workers In deily contact with asbestos. Differences in rsadlng ability, cultural differences sad anxiety levels will Influence test results, but there should be et least some rough indication of added information or altered behavior. 105 DUP 0931748 ^03S4ss ■waaiaitBIflA mum Appendix A ASBESTOS-RELATED AND -ASSOCIATED MINERALS Minerals Other Than Asbestos that Hey Exhibit Flbroue Structure Mineral Species4 Morphological Characteristics Pyrophyllite Sometimes occurs as radiating needlelike crystals in feldspars, kyaniee, and in quarts veins from reef mines. Vemiculite Normally exhibits a flaky structure, but fibrous varieties have been reported. AttapulgiCe (a clay) Commonly crystallizes in well-defined fibrous forms. l.epldolite (a mica) Normally fibrous or granular when present as overgrowths on muscovite micas. Mlnneaocalte (a talc) Commonly fibrous rather than piety. Chamosite Sometimes occurs in the form of minute flbroue crystals, associated with sedi­ mentary iron formations (ironstones) Halloysita (a clay) Frequently occurs with kaoUnite and is characterized by elongated tubular crys­ tals, similar to needles. Holaquietite (an aaphlbole) Commonly occurs in aggregates and someclass displays an asbestlform texture. Rlchterlte (am amphlbole) Commonly exhibits a fibrous crystallo­ graphic habit similar to asbestos. t The first three have important Industrial applications; the others ere found in connection with coenarelal mineral operations, where they are normally considered an impurity, . . DUP 0931750 DU 035487 —■- tivilli'nfr-il, liiit ifiA mam mi DU9 0931751 DU 035488 Minerals and Rack* Possibly Associated With Aabaseaa Mineral or Rock Talc a I'ssa Ceramic applications (vhitevare, wall tiles, electrical porcelain}; extender for paints and pigments; lubricant and filler for cosmetics, and in the preparation and packaging of foods. Phlogopita A member of the mica family, used in a number of electric and electronic applications, such as insulation in air­ craft sparkplugs, and as a thermal insulator.& Chlorite A common conetitvant of matamorphie rocks; due to its green coloration, is used in construction for aesthetic purposes. Kaollnicie clay* Used la ceramics (whitewares, thermal insulators); as a filler or extender in the rubber, paint, and plastics industries; la the paper Industry to impart gloss, opacity,' brightness, and prlntability; and in medications. • Bentonitic clay* (Montmorillonite, Fuller'a earch) Drilling muds; as a binder for iron ore pelletizing; in filtering applications; and a filler for paints, cosmetics, pharmaceuticals, and ceramics. Ventieulice Used primarily in the construction industry as an Insulator but la also employed la the agricultural and horticultural industries as a soil conditioner. Tacanlte and timilar metamorphic iron deposits A primary source of iron for the steel industry. Magnesite and Used as a raw material for magnesia-containing refractories, fluxes, and miscellaneous chemicals and can be used la the production of magnesium metal. Brucite is often associated with magnesite and, as such, is used as a source of magnesia. 3rucite Marble6 Matamorphie carbonate rock used for polished stone and other applications la construction and for sculpture ‘Also know as steatite or soapstone. bHose phlogoplte is imported into the United States. Its occurrence in this countty is restlctsd mostly to small, noacoasMrcial deposits and as an impurity in certain marbles. cThe term "marble" is scentimes used lndlscriminataly to describe other rocks that can be polished snd that here e pleasing appearance; such rocks include the so-called verde antique or serta grean, soae onyxs, and slatas. Verde antiqua (aarta green) is commonly s ssrpsntlne and is therefore likely to include chrysotlls contaminants. Sourcss: W.A. Dear, st al. "Bock-Forming Minerals," Longmans Green 4 Co., 1961 N.U. Hendry, "The Geology, Occurrences snd Major User of Asbestos, New York Academy of Sciences, 132, Dec. 31, 1963. Malcolm Ross, "Geology, Asbestoe and Health," Environmental Health Psrspsctivss, 9, 1974, pp. 123-4. Robert L. Bates, "Ceology of the Industrial Rocks snd Minerals, Dover Publications, Inc., K.T., 1969. . „ DUF 0931752 DU 035489 I 3=2 O un —»w to a 44 0 w3 ^X« s *^i -4 « U v4 ji x A* 9\ <33 <7» «N Q 4 La. . * -3 OJ -J « W • V o « U <2 i . <* S u * kA O *J 4 r* 4 • u §•* 2 U ^ W 3 83 :P u us — - a > . w jS 36 23 w fi a •* o • O'** 2# 4 w 5 <4 4u •H e •« w a. 2 33a B-t M 1* 4 ♦ 3 •«4 W ^ -t a e»i w9 ww 0 4e ft w *3 * C 0 ft* ft ftft <*ft • ft y a• > U 0 y 32 <*4 w a 44 «4 ft 44 .2 ft 3 Ift u o a. ft o q ft* 3 ■o a 1 2? S33 3 a U 1* 3b f o u 0 *4 u d o y 1 M *4 ■g » ft 0 a if w J © ft W ft I 44 s 3 S-2 3 3 3S 3 S ftft u01 b . _ 3 !> So ft* 33 u ft «4 ft ft ft *9 11 b SSi d* • 3 • i iiil 3 3b ^ «t --•a i’ 3 3 5 3 2 3£ *37 3 * i 33 3 <3 M > 532 ft M ft 73 14 «* « ! 0 1 DU* 0931754 DU 035491 3 a o (j w a w -j a y aw 0 cu u a •s K « ^ m •* o i *h w a *» 0 o a 2» a +4 W Q 35 | °1 I 2 S 8 k a p-f w ^ a ^ 3 3 • « 8 I • >1 u a o • s 13 « J5 + k u •• o ■o i> m u o u A w 9 0S K 6 ■5 3 a1 a *9* 3 a a it u a> a * * ■o 0 a e u a ►% 8 a (44 a a« o •* u o u a 3 u 3 U 11 i2 § 3 *4 U *S m O 3 a •8 a U V b 13 W A •A Z S ■ 3 A u u u M SI O I? 3 I'lis 9 l u «3 u II Is, 3 K W O CU& «* S ai E i a. fn «u 3a si * v * S t U 0 a • w u JS • *4 m v u « «s •3 0 3. h •* <4* 4* Hu a q)j:v >4 u « on-* W A 'm m 3 •Wg u i o 3 3 3 n a. j3 J ry o f P ro v is io n s fo r C onpllanc' a 3 a 3 a *4 1*8 US 8 I« 8■h a S* 3 ? 1 OKS W n I 3 A S O « 1 I* 3. si 3 9l!« Q •* 3 m ai ° u h « • .*81 &2 2 *. <* •H M 3 1* o K* 3 at o o « o u I a «3 t* w *•»! a**: Jj 2 3 & ** U *4 1 m w I 2 I? It u k* u Hiu o j a a “ a A* w » o u u 3 3 <4 er 1-3 DUf 0931755 DU 035492 Appendix C MONITORING AND MEASURING ASBESTOS CONTAMINATION Although the role of asbestos as a cause of cancer and other diseases is clear, the mechanisms underlying disease causation arc nor well understood, and this impedes efforts to measure and, control human exposures to the substance. ■subsequently, As if the technical and economic difficuitic: of measuring asbestos concentrations—the subject of this chapter—were not enough, two other facets of the hazard are murky: (1) Which a<-trihute(s) of asbestos it is that actually causes disease and which therefore must be measured accurately; and (2) the amount of asbestos that is hazardous, and over what period of time. The attributes of asbestos that have been implicated in various •k hypotheses on asbestos carcinogenesis include: • Size and shape of individual fibers • Number of fibers • • Total mass of asbestos 2 Type of asbestos • Trace metal content • • Trace organic content 6 Surface charge • Surface adsorptive characteristics 2 3 4 6 Because of the inordinate difficulties of separating the last four attributes from nonasbestos "background", these four are not suitable indices of exposure for routine monitoring situations. In addition, hypotheses based on trace metal or organic content have fallen out of favor. Because there is no consensus on the attribute(s) that cause cancer and, therefore, no consensus on the appropriate indicator of risk from environmental exposure to asbestos, the "best" monitoring and measuring method will be that which permits the most detailed character­ ization of exposure through measurement of the first four variables—size and shape of individual fibers; number of fibers; total mass of asbestos; and type of asbestos. DU 035493 References will be found at the end of this Appendix. C-l DUP 0931756 In addition to the limitations just mentioned, it has not yet been established whether the time-course of exposure, or dose rate, is significant in determining carcinogenic risk. This leaves open the possibility that it may be just as important to determine peak exposures as to determine time-weighted average exposures. Because of these limitations, and because of the technical difficulties and costs of measurement discussed below, the method of measuring must be chosen judiciously to fit the circumstances: occupational versus general environment; measurement of asbestos concentrations in water versus chose in air; monitoring the environment at large versus determining exposures to certain individuals. Also, the methods chosen may differ according to che fiber type that is of concern. * Monitoring Devices and Methods The most desirable means of monitoring in general, would be one in which a device could measure directly the asbestos concentration in air, water, or In a bulk sample of material. Such a device, which might be used for continuous monitoring, is not available for most situations, however. Some Limited-Application Monitoring Devices Some devices for measuring general parcieulata contamination of 8 9 fluids—based upon che piezoelectric balance, Beta-ettenuation, or light-scattering principles^—may be suitable for monitoring applica­ tions where the asbeatos concentration is a known, constant, and relatively large fraction of the general particulate contamination. They are not appropriate for such purposas as asbestos-pollution monitoring in comunlty sir, where the total particulate loading will be several orders of magnitude greater chan the asbestos loading. 12 Nor are they appropriate in survey* of industrial sitaa, whara tha asbaatos/total loading ratio and che size of airborne asbmstos fibers may fluctuate markedly. Thus, continuous monitoring is generally not practicable, and sampling will almost always be necessary. C-2 DUP 0931757 DU 035494 Monitoring by Membrane Filtration The major method of monitoring in use for environmental media is membrane filtration. The membrane filter method is directly applicable to air, stack gases, -.ater, food liquids, and other fluid media. With solid media, it can be used as a final concentration step for fibers that remain after some preliminary digestion procedure. The procedure most commonly used is a single-step filtration, in which all suspended particulate material in the medium is entrapped, together with the suspended asbestos. It is also possible, however, to utilize a dual-filter set-up in which the first (coarser) filter entraps the larger material while allowing much of the smaller material (including most of the asbestos) to pass through to be collected on the second (finer) filter for analysis. 12 Although this dual-filter method has some advantages for applications in which the asbestos concentration is low and concentrations of other particulate material are high, the method cannot be generally recommended because as filter loading increases, the collection characteristics change causing an increasing amount of asbestos fibers to be trapped on the first filter. The filter beat-suited for use in most environmental sampling for asbestos is a mixed cellulose-ester membrane filter (similar to those manufactured by the Millipore Corporation), with a mean nominal pore size of 0.4S or 0.8 um. These filters will remove, from water, 13 and are estimated to be "...almost 14 100Z efficient..." for removal of asbestos fibers from air. 99.92 of asbestos fibers present For some applications, the "Nuclepore" membrane filters manufactured by Ceneral Electric are most appropriate. 12 They are more suitable for scanning electron microscopy of collected samples because of their relatively flat surface and their relative stability in an electron beam. However, they are difficult to use in direct environmental monitoring, because they have a high pressure drop at nnrmi sampling races and a C-3 DU 035495 DUP 0931750 :andency to develop static charges,which makes them difficult to handle * after sampling. Measuring Asbestos in Air It is most probable that inhalation of airborne asbestos is attended by greater carcinogenic risk chan is ingescion (as discussed in Chapter III). Hence, it is most important that present knowledge of | exposure to airborne asbestos, as a function of time for various popula- j tion groups, be refined so that chose groups at greatest risk can be ascer­ tained. I The biologically effective concentration and deposition characteris­ tics of the particles available for inhalation (in the breaching zone of the individual) are the critical parameters to be measured. The biologically effective concentration will be sons complex function of • fiber number, size, shape, mass, and type of asbestos best correlated with disease. Deposition characteristics (deposition in the airways of of man) are complex and are diacuseed elsewhere in this monograph (Chapter III). Suffice it to say chat the diameter of the Individual fiber Is the principal controlling variabla in deposition, but langth is important enough that both should be measured, although thia is difficult in practice. Measuring Asbestos in Water The sampling of water to determine asbestos concant requires special care if the results are to be representative of potential human exposures. As with air, there ere seasonal effects on sources of asbestos and on the distribution of ssbestoa in a given body of water. Stream flow rates, thermal stratification, sedimentation, and differing source flow rates may all have an effect, as may (for drinking water) the characteristics of ths distribution system. The Environmental Measurements Advisory Committee of the EPA hai recently been studying the question of measuring asbestos in drinking water. As part of this effort, the Athena (Georgia) Environmental Research Laboratory has developed a preliminary method for such assessment.* *For discussions of membrane filtering that are much more thorough, see References 14, 20, 24, 23, and 26. DUP 0931759 DU 035496 In pare, the guidelines given there include: "It is beyond the scope of this procedure to furnish detailed instruction for field sampling; the general principle* of sampling waters are applicable. There are some considerations that apply to asbestos fibers, a special type of particulate matter. are snail, and in water range from .1 vs or more. These fibers Because of the rang* of size there may be a vertical distribution of particle sizes. This distribution will vary with depth depending upon the vertical distribution of temperature as wall aa tha local oataorological conditions. Sampling should take place according to the objective of the analysis. If a representative sample of a water supply is required a carefully designed set of samples should be taken, representing the vertical aa well aa tha horizontal distribution, and thaaa samples composited for analysis. The sampling containar shall be a dean polyethylene, screw-capped bottle capable of holding at leaat one liter. The bottle should be rinsed at Isaac two elmaa with the water chat ia being sampled prior to sampling. (Note: sampling containers.) Glass vaaaels are not suitable aa A minimum of approximately one liter of water is required end the sampling container should not be filled. It is desirable to obtain two samples from on* location."^ Whan tha bulk water sample has been collectad, it'la filtered through a membrane filter and the filter prepared further for analysis. Measuring Asbaatoa in Food Tha most critical, and yet unresolved issue in measuring asbestos in food is a method to be used la preparing solid or ssmi-soild food for separation of any asbestos that may be contained. such generally suitable method exists. At present, no Surface contamination (e.g. on rice) may ba measured relatively easily by straightforward washing and filtration techniques. For liquid foods and beverages, almpl* filtration, with membrane f11tars, is often appropriate, followed by treatment to 16 remove organic co-contamination of tha filter surface. C-5 D\j 035497 Analysis of Simples—Some Technical and Economic Constraints The most valid analytical methods for complete assessment of asbestos contamination are those methods based upon electron microscopy. -his is particularly true for assessment of general community exposure from air or water. In some cases, where the fiber-slae distributions of asbestos exposures are constant and already known from electron microscopy, the use of optical microscopy, or the methods of continuous monitoring referred to earlier, may be justified for routine surveillance. Technical Constraints Individual asbestos fibers can be identified by phase-contrast optical microscopy. However, without using electron microscopy it is not always possible to distinguish asbestos fibers from amorphous inorganic (fibrous glsss or mineral wool), natural organic (plant or animal), or synthetic organic (nylon, orion, aee.) fibers. ' Moreover, in moat monitoring situations the majority of fibers will be belov the resolu­ tion of the phase-contrast microscope. Complete characterisation and identification of such fibers requires the following information: 17’ ^ • Dimensions and morphology • Electron diffraction pattern • Elemental composition For samples such ea community sir end water, for which more chan one fiber type cannot be ruled out a priori, obtaining this information ia no simple matter. Each fiber muse ba identified separately by using electron microscopes,^ equipped with E-ray fluorescence and selected area electron diffraction capabilities, for the determination of elemental composition and crystallographic characteristics. With any of the analytical methods, compromises are necessary because of the relatively "heroic" sampla-praparation methods required, especially for transmission electronic microscopy. Many of these methods--Involving suen techniques as ashing, multiple transfers of liquid rsauspenslsns, and filtrationa—tend to subdivide fibers into fibrils. Thus, it is often difficult to reconstruct the original slse distribution. C-6 nn» 0931761 DU 035498 For samples in which che concentration of asbestos fibers is low and the size distribution small, size distribution analysis may be unreliable because only a few fibers will be seen. Economic Constraints The equipment needed for complete analyses in a continuous monitoring program will require a highly skilled and experienced operator and extensive technical support. The minimum initial capital investment required for new equipment will be in the range of $100,000-$250,000, and an annuel operating budget of nearly $100,000 will be required. This will cover che expense of purchasing and installing a scanning/trans­ mission electron microscope, and che salaries, fringe benefits, and overhead expenses for a microscopist and two or three ceehnlciens. For an uncomplicated membrane filter sample—when only one type of fiber is present, and ocher perciculece meterial Is not excessive— the number and mass of fibers and their size distributions may be obcalned for a cose of a few hundred dollars per sample. If the sample is more complex, the costs may run to several thousand dollars, and the sample 19 may require several weeks for analysis. Some progress has been mads in automating the counting and sizing of fibers, from photomicrographs,20,21 but these automated methods are based only upon recognition of fibrous morphology end see therefore unsuitable for evaluation of "mixed" exposure by fiber type. Haproduclbiilty of Measurements Because of the difficulties of measuring asbestos-fiber contaaination, there ere large variations in the measurement of asbestos In samples of sir end water, both within end among laboratories. Several replicability and duplicability studies are suanerlzed below. Asbestos in Water Although che attainment of an intraleborscory precision of *302 in analysis of water has been reposted,1* it is not uncommon for results 0-7 OUP 09317*5 DU 035499 from duplicate samples anaLyzed by competent workers in independent laboratories to vary by more than an order of magnitude. In a reproducibility study reported in 1975, seven "competent" laboratories showed readings of below-detection-'imit to 9 million fibers per liter for a water sample known to contain 7.5 million fibers per liter. In another case where five replicate analyses were made in each of two laboratories on an identical sample, one laboratory showed readings of CK79 to 4.0 million fibers per liter, while the other showed readings of 8. to 29. million fibers per liter.^ In another study, reported in 1976, investigators evaluated variation among and within nine laboratories that analyzed samples of water from five different sites on Lake Superior. The averages for the nine laboratories varied from 1.6 million to 78.7 million fibers per liter. The within-laboratory coefficient of variation (standard deviation divided by the average) ranged from about 50% to 100%. 22 Asbestos in Air There is also considerable variability in measurements of atmospheric asbestos concentrations, especially of ambient air, both within and among laboratories. Data on duplicate analyses of ten ambient air samples from measurements by the Mount Sinai Department of Environmental Medicine and the California Department of Health are given in Table C-l Differences between the two laboratories may be two orders of magnitude or more. No one laboratory's readings were consistently higher. The Mount Sinai group also conducted replicate analyses of four samples. These results, shown in Table C-2, order of magnitude. show differences of less than an The authors of the study in which these findings were reported state that an individual value may be accurate within a 23 factor of two or three of a sample mean. The inaccuracy in values obtained from a specific analysis can result from several circumstances: (1) statistical variation in the number of fibrils found in given grid squares, (2) a much greater varia­ tion in volume of these fibrils, bundles, (3) incomplete dispersal of chrysotile (4) variability in the amount of material lost during processing, and (5) low-level contamination of the sample at various points during its preparation and analysis. DUP 0931763 DU 035500 Table c-l DUPLICATE ANALYSIS OF TEN AMBIENT AIR SAMPLES Sample Number Aabescos Concentration (nanograms/mecer^) Mounc Sinai Calir.Depe. ot Health 74-000-003 0.6 120.0 74-000-012 44.0 0.4 74-000-023 0.0 13.0 0.0 74-000-032 2.7 73-003-038 2.6 73-003-046 7.3* 0.0 <800.0 73-003-054 7.3 0.0 73-003-064 21.0 0.0 74-000-110 46.0 14.0 74-000-119 1.4 2.2 “With an annotation: Source: "Disregard, only 2 fibers observed.” Reference 23 (end of this Appendix). BU? 0931764 DU 035501 Tabla C-2 REPLICATE ANALYSIS OF FOUR AMBIENT AIR SAMPLES Samolft Nutnbtr Asbestos Concentration (nanograms/meter^) Isc Analysis 2nd Analysis Average 73-003-038 0.0 73-003-046 7.6 7.1 7.3 73-003-054 3.2 11.4 7.3 7 3-00 ■'-064 12.0 30.0 21.0 Source: 5.3 2.6 Reference 23 (end of this Appendix). Although cha phase-contrast microscopic method has bean demonstrated to ba useful for evaluation of occupational asbestos exposures, and a coefficient of variation (for stapling and analysis) of 22Z has bean 24 reported for trained technicians, it should be recognized that there may be a two-fold variation between results (for reference staples) from experienced and novice aicroscopists for aaosite, and a four-fold 25 variation for chrysotile. It is also Important to recognize chat the fraction of fibers in a staple of airborne asbestos that will be visible In using this oechod will vary by type of asbestos and also (within each type) by the particular industrial process being evaluated. Conversions Between Counts hr Different Methods and Between Nusber of Fibers M*TfBeeauae of the large variations in measurements, it is generally not possible to convert counts by the phase-contrast optical method eo equivalent electron microscopic counts, excepc witnin very wide margins of error. Indications of the error that may be introduced by uncritical acceptance of any constant factor for conversion may be found in (a) a study of size distributions for airborne asbestos exposures in C-10 DUP 0931765 DU 035502 • 2 various asbestos process*# and (2) a comparison of optical and electron microscopic methods applied to samples of air taken from Inside public buildings. In the latter study, variations by factors of 20-30, and no apparent correlation, were found. Kor can counts of visible dust particles by the midget iapinger method be equated with fiber levels determined by phase-contrast microscopy, as illustrated in another study which gives measurements of both methods for 26 Within a plane, asbestos levels one job at four asbestos textile plants increased with midget impinger counts; but if comparisons are made across plants, it is clear chat the limits of uncertainty are approximately an order of magnitude. In a 1974 study, chars wars differences of several orders of magni­ tude between fiber/mass ratios in emission streams of asbestos processing plants and sills, making any attempt to apply a constant conversion factor between number and fibers and ness uncertain at best.2* Some important conclusions can be drawn: a The ratios of alactron-microaeope-vialbla to optlcai-microecopevislble fibars vary among plant amissions, ths workplace, and the general environment, aa well as within eeeh of these categories. • No universal ratios or factors for convarsion of optical microscopa results to elactron microscope results exist. In this monogreoh, when needed, e factor of 50 has bean used to convert occupational fiber levels from optleai-mleroseope-vlsibls to elactron-microscope-viaibla fibers. The factor is based on a conservative uciaici that 2X of total fibars are opclcal-microscopavialble. • No single factor for conversion of mass emissions to fiber emissions exists. e Fiber/mass ratios diffar markedly from the occupational to the general environments, and they also diffar markedly within each environment. The number of electron-microecope-visible fibers per nanogram might well range from 100-10,000. Baaed on the observed dace available and for convenience sake, 1000 fibers per nanogram C-ll mr» 33.lV.li.i- DU 035503 • has been used in this monograph for atmospheric levels nsar planes, ! and 230 fibsrs per nanogran for ambient urban air. j The aonieoring method chosen will be different for each application i j but must depend upon electron microscopy as a reference nathod. e Because mass of asbestos can be directly calculated from asbestos type and electron-microscope-visible fiber size and number, it is recosmended that these indices be recorded whenever possible. The fiber size distribution can be completely stated by the geometric means and standard deviations of fiber length and diameter, assum■ ing that fiber length and disaster vary independently of each other. REFERENCES L. Stanton MF, at al: Carcinogendty of fibrous glass: pleural response in the rat in relation to fiber dimension. J Nat Cancer Inst 58(3}: 587-603, 1977. 2. Gibbs GW, Hwang CT: Physical parameters of airborne asbeseos fibers in various work environments—preliminary findings. Am Ind Hyg Assn J 36(6):459-466, 1975. 3. SRI International: 1976. 4. Cralley U, Keenan RG, Lynch JR: Exposure to metals in the manufacture of asbeseos textile produces. Am Ind Hyg Assn J 28(3):452-461, 1967. 5. Harrison JS, Roe FLC: Studies of carcinogenesis of asbestos fibers and their natural oils. Ana NY And Sci 132:439-450, 1963. 6. Gorski CH, Stattler LS: The surface energetics of asbeseos minerals. Am lad Hyg Assn J 33(6):345-333, 1974. 7. Cooper WC (Ed.): The Need for and Feasibility of Controls of Asbeseos Air Pollution. National Academy of Sciences, Washington, O.C., 1971. 8. Sea CJ, Teurubayaaki Kf A new mass sensor for respirable dust measure­ ment. Aa Ind Hyg Assn J 3(11):791-800, 1975. 9. Ataieh B, Solomaa M, Carson GA: A theoretical and laboratory evaluation of a portable direct-reading particulate mass concentration inserwsent. U.S. Dept. Health, Education and Welfare, Public Health Service, CDC, NI0SH, July 1975. Personal communication with Nicholson WJ, October ntl» 0031767 DU 035504 l ( - 10. Mercer, TT: Aerosol Technology in Hatard Evaluation, Academic Press, New York, 1973. 11. Harwood CF: Asbestos Air Pollution Control. Chicago, State of Institute for Environmental Quality, 11 E0 Document 12. Spumey KR, et al: The sampling and electron microscopy of asbestos aerosol in ambient air by means of Nuclepore filters. J Air Pol’ut Control Assoc 26(5): 496-498, 1976. 13. Manalan DA: Asbestos removal by membrane filter. Presented ae the Spring meeting of the Parenteral Drug Aasociation, Inc., Dorado Beach, Puerto Rico, April 5, 1974. 14. - Lynch JR, Ayer HE: Measurement of asbestos exposure. 10(1): 21-24, 1968. J Occup Med 15. Anderson CH: A Preliminary Interim Procedure for Determining Fibrous Asbestos. Athens, CA, U.S. Environmental Protection Agency, . Environmencel Reseerch Laboratory, July 28, 1976. 16. McGrath PP, Ewell J8: Application of electron microscopy to the problem of particulate contaminants in food, drugs and biological!. Scanning Electron Microscopy 1976 (Part III). Proceedings of the Workshop on Techniques for Particulate Matter Studies in SEM. Chicago, ITT Research Inscicute, April 1976. 17. Pooley FD: The identification of asbestos dust with electron microscop microprobe enalysis. Ann Occup Hyg 13(3): 181-186, 1975. 18. 3easua DR, File DM: Quantlatlvs determination of aabeatoa fiber concentration. Anal Cham 48(1): 101-110, 1976. 19. Langer AM: Approaches and constraints to identification and quanti­ fication of aabaacos fiber. Environ Health Parapect 9: 133-136, 1974. 20. Harness I: Airborne asbestoe dust evaluation. 397-404, 1973. 21. Pavlidis T, Steiglitx K: The automatic counting of asbestos fibers in air samplsa. Presented ae the 3rd Joine Conf on Pattern Recog­ nition, IEEE Computer Society, Nov. 8-11, 1976. 22. Brown, Jr. AL, Taylor WF, Carter RE: The reliability of measures of amphibols fiber coneaneration in water. Environ Res 12(2): 150-160, October 1976. 23. Nicholson WJ, at al: Aabeatoa Contamination of the Air in Public Buildings. Research Triangle Park, NC, U.S. Environmental Protection Agency Pub. 0450/3-76/004, Oct. 1975. Ann Occup Hyg 16(4): C-13 qq» O931760 DU 035505 24. Leidel NA, Bayer SG, Zunvalde RD: Membrane Filter Method for Evaluating Airborne Asbestos Fibers. U.S. Public Health Service, NIOSH, TM 84, 1973. 25. 3eckett ST, Attfield MD: Znter-laboratory comparisons of the counting of asbestos fibers. Ann Occup Hyg 17(2):85—96, 1974. 26. Ayer HE, Lynch JF, Fanney JH: A comparison of impinger and membrane filter techniques for evaluating air samples in asbestos plants. Ann NY Acad Sci 132:274-287, 1965. 27. Harvood CF, Siabert P, Blazsak TP: Assessment of Particle Control Technology for Enclosed Asbestos Sources. Research Triangle Park, NC, U.S. Environmental Protection Agency Pub 0650/2-74/008, Oct 1974. i i I C-14 DUP_09J17^9__, DU 035506 Appendix D ANIMAL STUDIES RELATED TO CARCINOGENIC EFFECTS OF FIBERS Inhalation Mice Hybrid mica (AC/F^) were exposed to a commercial preparation o£ chryaoeile duet at a concentration of 150-500 mppcf 40-60 houra per weeic for 17 months and were sacrificed after exposure. A high incidence of aultiple pulmonary adenomas* was observed in the exposed group (45.7X, or 58/127), than in controls (36.OZ, or 80/222).160+ Rata Whits rata, some of whoa had received an intratracheal application of caustic, (reportedly to impede mucociliary clearance), were exposed to chrysotile dust 30 hours per week for 62 weeks at a mean concentration of 86 rag/. Of 72 rats surviving 16 months or more, 25 developed malignanae thoracic tumors (adenocarcinomas, squamous cell carcinomas, fibrosarcomas, and a mesothelioma). The incidence of animals with cancer was twice as great among caustic-treated survivors (15/31 or 48Z) as among those who had not been treated (10/41 or 24Z). There were no tumors in 39 csuseie-trastad and untrsated control animals.1^ Squamous carcinoses of the lung vers found in 2 of 31 Charles River CD race surviving exposure to croeldolite ee a concentration of 49 ng/s»3 16 hours a week for two years. No malignant tumors wars obssrvsd among rats sxposed to ehrysotila or aaosita, but 5 of 40 sxposad to chrysotile developed multiple pulmonary adenomas. ‘Benign tumors of the lung. ♦Chapter III references—see Apendlx H. D-l DU 035507 I Group* of 69 Charles River CD rats were exposed to crocidolite, aaosite, or chrysotile at mean concentrations of about 60 mg/m per week for two years. 16 hours Among the group exposed to crocidolite, four developed malignant lung tumors (squamous cell carcinomas and an adeno­ carcinoma). Three of the group exposed to aaosita developed thoracic caneers (a broneoalveolar carcinoma, a fibrosarcoma, and a pleural meso­ thelioma). Two pulmonary carcinomas (a squamous cell and a papillary carcinoma) and one pleural mesothelioma developed in the animals exposed to chrysotile. In a similar experiment, exposure for six months to two years produced a SZ Incidence of thoracic malignancies among groups exposed to chrysotile and amosite, but a 14Z incidence among the group exposed to crocidolite. While mass concentrations of the three types of asbestos were all about SO mg/m3, counts of optically visible fibers were 54, 364, and 1105 million per cubic meter, respectively. 114 In another study, C/D Wisear rats vara exposed to amosita, anthophylllte, crocidolite, and chrysotile (Canadian or Rhodesian) at a con­ centration of 12 mg/m3 respirable dust 7 hours per day for varying lengths of exposure. All fiber types produced asbestosls, which progressed efter removal of the rats from tht dust. Lung carcinomas and pleural meso­ thelioma* were found in groups exposed to each of the four fiber types, and a single peritoneal oeaothalloma vaa observed among animals exposed to crocidolite. Forty percent of animals exposed for two years developed malignant tumors of tht lung and pleura. Ho such cancers were found among control animals A dose-responsa relationahip between aebeetoa end cancer waa noted— with increasing duration of exposure there wee an increasing incidtnce of obsarved malignancies. As little as one-day exposure vaa sufficient to produce lung carcinomas and pleural mesotheliomas. There was significant­ ly more asbestosls (caking severity of asbestosls and length of survival into account) among animals with lung tumor* than among chose without tumors. In addition, among groups txpostd for only one day, thsra ware D-2 DU? 0931771 i DU 035508 significantly more lung tumors among animals with asbestosis than among those without asbestosis.^ Intratracheal Injection Rats White rats received 1, 2, 3, 4, or 6 intratrachael injections of 3.5 mg chrysotile in aqueous suspension. Among 16-month survivors, 3 of 19 developed pulmonary adenocarcinomas. Two of these had received 113 4 intratracheal injections, and one had received 6 injections. After administration of 3 injections of 2 mg chrysotile containing 0.14 mg benzo(a)pyrene (a carcinogen in cigarette smoke) at monthly intervals, or a single injection of 2 mg chrysotile and 5 mg benzo(a)pyrene, lung papillomas, epidermoid carcinomas, reticulosarcomas, and pleural mesotheliomas were noted in 6/21 and 6/11 animals, respectively, within 28 months. No tumors occured in 49 rats given 3 monthly injections of 2 mg chrysotile alone or in 19 rats administered a single dose of . , % 108 5 rag benzo (a) pyrene. Hamsters Eight pulmonary adenomas, 9 tracheobronchial papillomas, and 6 pulmonary carcinomas developed among 31 LVG/LAK hamsters receiving a dose of 4.5 benzo(a)pyrene and 12 mg chrysotile over a period of 12 weeks. No tumors were observed in 17 animals administered chrysotile alone. Among 34 receiving benzo(a)pyrene alone, 9 tracheobronchial papillomas and 1 pulmonary carcinoma were reported. The effect of intratracheal instillation of asbestos with oral or subcutaneous administration of nitrosodiethylamine (NDEA) was studied in Syrian golden hamsters. Aqueous NDEA was administered per gastric tube twice weekly for 20 weeks (total dose 60 mg), or 3.5 rag aqueous NDEA was injected subcutaneously once a week for 12 weeks (total dose, 42 rag). One mg chrysotile asbestos in polyglucin suspension was injected intratracheally once weekly for 6 weeks (total dose, 6 mg), beginning one month after the start of NDEA treatment. After 8-10 months of 21/52 D-3 DUP 0931772 DU 035509 jaigai -MfcL and 14/51 animals developed beniga and malignant pulmonary tumors among the groups receiving asbestos and oral NDEA or subcutaneous NDEA, respec­ tively. Among control groups receiving oral NDEA, subcutaneous NDEA, or asbestos alone, only 1/50, 5/47, and 0/50 developed pulmonary tumors.16^ Intrapleural Injection Mice Two of 75 BALS/c mice receiving Intrapleural Inoculations of 10 mg crocidolite in aqueous suspension developed pleural tumors, but no tumors were observed among 75 mice injected with 10 mg chryeotile. 163 Rate A single dose of 20 mg of crocidolite, svelte, anthophyllite, or • chrysoeile from varioue sources administered to CD Ulster rets produced an incidence of pleural mesothelioma ranging from 19X to 70S. Yet ma Little ea 0.5 mg chrysotile or crocidoliea was sufficisnt to Indues u ,, 107 mesotheliomas. Various asbestos types heve induced mesotheliomas following intra­ pleural injection in Osborna-Mendtl, Sprsgue-Dswley, CFY and Uiatar/Aldsrly ICI ratg#^7,108,161,163 carcinogenic response to chryeotile and crocidolite appeared to be doee-related.107’11^ Oil-extracted aabeetoa gave results similar to untreated samples,107,1'64 165 thus casting doubt upon the hypothesis that natural oils and waxes, 166,167 contaminant oils fro* the milling process or organic materials 168 originating fro* storage in plastic or juts bags eonerlbuta to the carcinogenicity of asbestos. It has also been suggested thst metal contaminants added during processing of fiber play a role in asbestos carcinogenesis.^^ Subsequent experiments using rate^^ »^-70 I d*aonstraced that (1) treat­ ment with acid, base, and ethylene diamine tetra-aacetic acid to remove metal contaminants; (2) selecting asbeetos saaplas fro* among Interior fibers not exposed to contsinminating haxmrmills; or (3) using different D—4 DUP 0931773 DU 035510 samples of che seat asbestos type containing different quantities of trace metals did not produce different tumor yields. By way of contrast, heating samples for wo hours at 900-1000°C resulted in a substantial 169 loss of carcinogenic activity in rats. Fiber diameter and length, in addition to shape, may be Important determinants of carcinogenic potency. Eight subsaaples of U.I.C.C. (Union Internationale Contre le Cancer) standard reference chrysotile vers milled Individually to a finer powder than the standard mixture. Injection of each subsaaple intrapleurally resulted in a higher yield of mesotheliomas in Ulster rats chan did the pooled refer­ ence material. The highest tumor yield of all was produced by a separate superfine chrysotile prepared by water sedimentation of Grade 7 commer­ cial asbestos. Carcinogenicity was correlated with number of fibers less than 0.5pm in diameter and greater than 10pm long.107 ' On the other hand, pulverizing aabestos before applying it to the pleura of Oaborns-Msndel rata by maana of a coated glass plsdget reduced carcinogenicity. Fibers of disaster less then 0.2um end length 5-lOpm, which were present in greeter numbers la pulverized specimens, vers considered to be less effective carcinogens then fibers of greater size. 118 By contrast, after lntraperltonesl injection (see "Intraperlconeal Injection" below), fibers less then 5pm long were fully potent in inducing tumors. It muse be kept in mind thee prolonged milling may alter the crystalline structure of asbestos end thus influence biological effects. Hamsters. Guinea Pigs, and Rabbits Pleural mesotheliomas developed In Golden Syrian hamsters after intrapleural injection of 10 mg chrysotile, aaosite, anthophyllite, or crocldollte. An apparent dose-response relationship was observed for chrysolite, with 0, 4, and 9 mesothallooas induced among 50 animals by Injection of 1, 10, Or 25 mg, respectively. Prolonged milling, which reduced the majority of fibers to submicroacopie dimensions, eliminated 109 carcinogenic effects and greatly reduced fibrogenlc activity. D-5 DUP 0931774 DU 035511 On* pleural tumor was observed among 50 guinea pig* inoculatad with 10 mg crocidolite in an aqueous suspension, but non* were observed in a similar group inoculated with chrysotila. Of 3 rabbits surviving at least 12 months following injection with 16 mg crocidolite, 2 developed pleural mesotheliomas, one at 22 and on* at 24 months . Intraperitoneal Injection (Mice and Rats) Peritoneal mesotheliomas occured in 20 of 60 BALB/c mice within 18 months of injection with 10 mg crocidolite. Peritoneal mesotheliomas were reported in Charles River CD, Sprague Dawley, and Wistar rats following intraperitoneal injection of crocico^it•^,^'2,^•^2 and in Charles River CD and Wistar rats following injection of chryeotil*.106,110,122 Although the incidence of peritoneal tumors among groups of 40 animals was virtually identical, the time from injection to observation of the earliest tumor was 276 days for 25 mg chrysoelle as opposed to 343 for 6 mg chrysotila.173 Tumors were produced by four 25 mg injections of powdered chrysotlle (99.8Z) of the fibers less chan 5|jia long), although tha incidence was somewhat less than for standard chrysotil* (12/37, or 32X, vs. 18/33, or 55X).112 Subcutaneous Injection (Mice and Rats) CBA mica developed injection-site sarcoma* and pleural and peritoneal mesotheliomas (2+5/17, 2+2/13, 1+1/12) after three sets of bilateral inguinal injections of 10 mg crocidolite, amosite, or chrysotila at inter­ vals of 5 weeks. No tumors were observed among 15 controls injected with 174 saline. The investigators, however, have bean unable to duplicate their findings and believe chat, in chair experiments, asbestos either was in­ jected directly into the pleural or peritoneal cavities or ulcerated into these cavities through the overlying tissues.^ A single local tumor was observed following injection of 75 mg 112 chrysotil* to 33 Wistar rats. D-6 DUP 0931775 DU 035512 Oral Administration (Rats and Hamsters) One gastric leiomyosarcoma developed among 32 Wistar SP? rats fed 100 rng/day chrysotile 5 days per week for 100 days in a 6-month period. Mo tumor occurred among 16 controls.^ Among 42 animals examined after an average of 441 days on a diet containing 50 mg/kg body weight per day asbestos filter material (52.62 chrysotile asbestos), 12 malignant tumors were observed: 4 kidney carcinomas, 1 lung carcinoma, 3 reticulum cell sarcomas, and 4 liver cell carcinomas. Seven benign tumors including 1 lung adenoma, 2 cholangiomas, 2 stomach papillomas, and 2 mammary fibroadenomas were also noted. Among 49 untreated controls surviving an average of 702 days, 2 liver cell carcinomas and 5 mammary fibroadenomas occurrsd. The increased incidence of malignant tumors is ths group fad asbestos filter material was statistically significant (p <0.01) however, the meaning of this study as regards asbestos is uncertain since asbcatos comprised only half of the filter material administered. Ten rats fed a diet containing chrysotile, 5Z by weight, for 21 months did not develop malignancies. Groups of 28-35 rats fad 10 mg chrysotile or crocidoLite in butter once weekly for 16 or 18 veeke de­ veloped no oelignent lesions which, when compered with a control group, could be related to the ingested asbestos.10 No tumors of the gastrointestinal tract were observed in groups of 45 hamsters fed a diet containing IX chrysotile or amoslte by weight for their lifespans.1^ Carcinogenicity of Other Mineral Fibers Mineral fibers othsr then aebeatoa have been shown to be carcino­ genic by the Intrapleural or lncraperitoneal routes of administration— but only when of e diameter similar to that of asbeatos fibers (less then Sun)• In groups of 32 rats, mesotheliomas occurred In 18 of those injected intrepleurelly with fibrous brucite or "nemalita,'’ which may be contam­ inated with chrysotile, in 3 of those injected with e ceramic fiber, n_7 DU? 0931776 DU 035513 and la 1 each of chose injected with fibers of barium sulfate, glass ’ 07 powder, and aluminum oxide.'" In studies by another teaa of Investiga­ tors, the following results were noted: intraperitoneel injection of palygorscite (attapulglte) and neoaiita--3 doses of 23 mg and 4 doses of 25 mg, respectively-resulted In tumors In about 75Z of Wistar rats (26/34, 25/34). Gypsum, although fibrous, gave a low tumor yield (3/35), perhaps because it dissolves in tissue. Non-fibrous dusts (pectolite, 3anidine, talc, blocite, hematite) produced few or no tumors, k dose- response relationship was observed for glass fibers—intraperitoneel injection of 2 mg, 10 mg, and 2 doses of 25 mg results in tumors in 27Z (21/73), 53Z (44/77), and 71Z (55/77), respectively. Mo tumors appeared among 72 control animals. 147,118 D-8 DUP 0931777 pu 035514 Appendix E AIR AND DRINKING WATER ASBESTOS CONCENTRATIONS FROM SOME PUBLISHED STUDIES Table E-l Atmospheric Con centre cion* of Aebeetoe In Some U.S. Urban Areas - Concentration _ (Nanoarama/ia^) Average Ranee Berkeley, CA 6.3 3oston, MA 5.0 Chicago, IL Source (Chapter 7 Reference) 2.1-12 67 67 24 9.5-200 Dayton, OH 6 0.4-11 14 Frankfort, KT 0.09 0.02-0.15 14 Houston, TX 5 4-6 14 67 Los Angeles (freeway) 27* Los Angeles (control) 43* New fork City, NT 13.2 8.2-41 67 Manhattan, NT 30* 8-65 32 Brooklyn, NT 19* 6-39 32 Bronx, NT 12* 2-25 32 Queens, NT 9* 3-18 32 Staten Island, NT 8* 5-14 32 Pittsburgh, PA 4 2-8 14 Philadelphia, PA 70* 45-100 15 Port Allegany, PA 15* 10-20 15 Ridgewood, PA 20* 15 15 San Francisco, CA 25 8.7-68 67 Washington, DC 21 1.6-40 14 13 13 identified as chrysotlle asbestos by the authors. DUP 0931778 E-l Bt/0355,5 <2 u u > u 3S3SSr"^SS53333r'33353Sr"°333!5S'0 3 U O 4 W S4 jS u A f> O © d i a ca © © Q ^ ©© CN Ui j3 « H rs Nt o cn oo • • o o &6 e c «*a £ c 3 V U e 5 <2 I I * w a ps O ".A0. d m d d "* >-t 9 > 2 3 a a a »h 3 5 q •« in -rt c a a 3 « * * a 9 o a ■ tPfc^aoxi j>^o jjJ hMdMM«M«n 3 «a 0 * Araphlbole o >r V5 E-2 POP 0931779 DU 035516 A 3 o n • • o o « w N NO U4 o c2 2i © CJ IO r* 099 w N u U/s w© <0 w w rs HMN *50 * O • » • Q«Q a ^ 90 (9 O'O ^ 9 * — S.(X • • •a 288 O **4 *4 ¥< WOO 2 2 « *4 • ot fl U • 9 m o w S ^ w 3 8 S &M ^ fldb* 2> 3 > 23S a a q sr MUM to t/i Vi 3 • lim it (le s s than 50,000 flb e rs /1 .) t o d O * Hot e ig n lfle a n t (le a s than 5 fib e rs in 20 fie ld s ) . C - C h ry a o tlla A * A m p h lb o le NO NSS o ^ O «-4 • % oo BEL ■ Below d e te c tio n A sbestos C o n c e n tra tio n s in D rin k in g W ater o r Some U.S. C om m unities s< 6 E-2 DUP 0931779 DU 035517 A * A n p h ib o le - Below d e te c tio n U n it (le a s than 50,000 flb e ra /1 .) - Not s ig n ific a n t (la s s than 5 fib e rs In 20 fie ld s ) . C - C h ry s o tlle MSS BDL V cc u > u 3 U 0 V 71 W 333333S333SSS3SSS,°:?SS35SSSS,'"<,S a <1 Ph PH o\ CO O 09 i tn *■4 • 5 8? d d ( c o n c lu d e d ) ft -t w o Q0 tn d i 1 44 O V* .o C“ -5 ° 0 93 X — . SS5 . «t2 u * 4S • m a* J --o a — — u U 0 • fi • H «4 <— X X 52 X 09 X u n e s X °32 »• s « ^o.nwTJn-. _ u u x <* i n o>2«>.00—000 — < «4 i i x « .5S52!3g**{f5afti9flq <5—3 »"4 -2oooa5 m4 0 u w 5£3 9 fi CO **5, E-4 o 0 1 u b5JS iH O J3 9 ' 01 « *4 •o tOw O 3 « 5*4 fi Sc5 ■ * i to o < 2 OUP 0931781 1)17 035519 E -2 *4 *T T a h it i _____ C o n c e n tra tio n T a b le E-2 (c o n tin u e d ) oi u V or^ooo^o^ooo'a^ooooooooo'o ^ ^ sf s/ >f 'f 't'f't'^sT'tsT^^sr a u o u w $ a ay U 3> u cr » >T >* M os • • CO os 4>A • H M °sa O 09 O * i S1 «i-l» U<« > < S3* 3 51 « So So ag . x-t as a » o e/o a 8 8 d .jj • o* H * JQ g «4 I a •* T a m el a > - >■* g -< * e «j ,h £■ 0 *9 O a 31 s « > - 3 « u u U B..S 113 3* sM^isIii*! S3 & 09 01 g w g * 0 2| r O *-4 « <• m U Q *9-0 Z66 uxz * -a v « a| s ililsSaa°4*a6* 8. S' 3 0 0 9 M 4 A asa C h ry a o tlle u i -•a * 3 ft • Aaphlbole u iT o lis le (la s s than 50,000 flb e r s /i.) u w u >■* KSS C ■ 0 BDL « Below d e te c tio n U - Hat s ig n ific a n t (le s s than 5 fib e rs in 20 fie ld s ). O E-5 DU? 0931782 p\J 035520 Appendix F SMOKING CESSATION PROGRAMS Although a number of different program strategies nay reduce smoking rates, significant long-term cessation of smoking is rare. Most reviews Indicate that the greatest rate of recidivism occurs between 1 and 3 weeks following treatment, when only 30Z of those who had been abstinent at the and of treatment report continued abstinence. Follow-up at 3-13 months indicates approximate cessation races of 20X-30X. cessation at 5 years after treatment.1 One report noted 18X Most smoking cessation programa have enrolled volunteers, who may have been motivated to quit on their own. Since 16X of persona who quit by themselves have been reported to remain abstinent one year, the 20Z to 30X rates of abstinence achieved 3 to 18 months after smoking cessation programs suggest that formal cessation programs may be only of tsodase benefit. Such programs, however, cay be substantially beneficial for persons who might not have been able to quit on their own. The discussion in this Appendix is intended to provide e broad per­ spective of the available options. Thera ere several published works chat providt a more comprshertiive review of the subject.3»^»3»6t7 Counseling by Health Professionals When they advise patients to quit or reduce smoking, health profes­ sionals, particularly physicians, serve as agents of bahavior change. One report described the results of e physician counseling program in which 100 surgical patients were seen far e brief Interview during which che health haserds and financial burdens of smoking wars discussed. one year, 30Z of males and 11X of females had stopped smoking. After Following another such program, which Included medical lectures, physical examinations, group discussions and films, the quit rate ves 58X, and 29X were still 8 9 abstinent a year laear. ’ DU? 0931783 P-1 DU 035521 Mi i . A. number of health organizations hava developed visual aide—pamphlets, films and posters—to assist physicians and others in counseling patients •.•ho smoke. These organizations include the American Lung Association, American Cancer Society, National Clearinghouse for Smoking and Health, and the American Heart Association. Titles of a number of the visual aids offered by these organizations are given in the National Cancer Institute's Self-Help Program A recent Gallup poll (1974) Indicated that only 34X of smokers expressing a desire to quit were interested in attending cessation clinics. The majority of smokers who became abstinent quit without the use of formal. smoklng-cesaadon interventions. 10 There appears, however, to be a great deal of interest in self-help manuals and kits as judged by the amount of such materials requested during interpretation of smoking, e general explanation of the principles of behavior change, and specific instructions for Implementing self-control be instructed to: a Lise positive reasons for quieting • Rscord the time each eigaraeta ia amoked • Note feelings and behavior prior to and during each smoke a Seduce gradually the number of cigarettes smoked • la^osa circumstantial barriers to smoking, such as not carrying matches • Change brands twice weakly, choosing each time a bread lower in tar and nicotine • Inertaaa physical activity • Refrain from smoking for 48 hours a Avoid situations moat closely associated with smoking a Find substitute behaviors for smoking The effectiveness of self-help program* has not bean established. r-2 DU 035522 ■ Table F-I POTENTIAL SOURCES OF ADDITIONAL INFORMATION Action on Snoking and Health (ASH) 2000 H Street, NW Washington, D.C. 20006 (202) 659-4310 American Cancer Society 777 Third Avenue New York, New York 10017 (212) 371-2900 American Health Foundation Deparcnenc of Behavioral Sciences 1370 Avenue of the Americas New York, New York 10019 (212) 489-8700 American Heart Association 7320 Greenville Avenue Dallas, Texas 7S231 (214) 750-5300 Aaerlcan Lung Association 1740 Broadway New York, New York 10019 (212) 245-8000 Canadian Council on Smoking and Health 343 O'Connor Ottawa, Ontario K-2P-1V9 (613) 236-6033 Cancer Information Clearinghouse 7910 Woodaont Avenue Suite 1320 Sethasda, Maryland 20014 (301) 565-3955 General Headquarters S Day Plan to Stop Soaking Seventh Day Adventist Church Narcotics Education Division 6840 Eastern Avenue, N.V. Washington, D.C. 20012 (202) 723-0800 Kslser Foundation Reaeareh Institute 1956 Webatar Street, Rooe 310B Oakland, California 94612 (415) 645-5000 National Association on Smoking and Health 4155 Eaat Jewel Avenue Denver, Colorado 80237 (303) 753-0777 • (Continued, next page) - * DU» 0931785 DU 035523 mam aafcal Table F-l (continued) !j. i National Clearinghousa for Smoking and Health Public Health Service U.S. Department of Health, Education & Welfare Center for Disease Control Atlanta, Georgia 30333 (404) 633-3311 X 3235 - Tech. Info. X 3143 - Public Info National Interagency Council on Smoking and Health 419 Park Avenue South New York, New York (212) S32-6035 Occupational Health and Safety Administration U.S. Department of Labor Constitution Avenue and Third Street, N.W. Washington, D.C. 20210 (202) 523-7081 Schick Center 4101 Frawley Drive Fort Worth, Texas 76118 (817) 268-1157 Smoking and Health Information Program P.O. Box 2003 Tyler, Texas 73710 (214) 877-3011 SmokEnders Memorial Parkway Phillipsburg, New Jersey (201) 454-HELP 08863 The Tobacco Institute 1776 K Street, N.W. Washington, D.C. 20006 (202) 457-4800 Tyler Asbestos Workers Program P.O. Box 2003 Tyler, Texas 73710 (214) 877-3011 Source: Adopted from The Smoking Digest. National Cancer Institute (in press). 7-4 DUP 0931786 DU 035524 Ti;i! Croup Therapy and Flve-Dav Plan Various health organizations have sponsored community group 3tio!cing cessation clinics, which provide health information, encourage­ fo. nfo. ment, and group therapy. Groups typically involve 8-18 persons and a group leader, seating once or twice weekly for a month. Participants in Che group are informed of smoking risks, asked to describe why they smoke and to detail their smoking habits, and are then encouraged to follow one of several procedures for quitting. Estimates of the effec­ tiveness of these programs after one year range from 18Z-25X.13,i^ Higher succesa rates result from programs stressing formal long-term naintenance support. One variant of group therapy is the Five-Day Plan, which consists ■jc five daily meetings, 1-1/2 to 2 hours each. Up to several hundred volunteer participants may be treated at these aeaelona. Intervention strategies range from lectures and inspirational meaaeges to fear-arousing stimuli and behavior modification procedures. One such program—a liva-in clinic including lectures, exercise, and individual as wall as group therapy— 7 reported 212-40* quit races at a three-month follow-up. Isolated use of the nonspecific treatment factors characteristic of the smoking clinic approach (e.g., suggestion, high expectation of success In quitting) result in posc-treatmenc caseation races similar to those of 3 13 clinics chat use specific planned intervention strategies. ’ K follow­ up of a group of 559 volunteers who had attended such a smoking clinic (pharmacologic agents, health education, and brief suggestions to use certain techniques for quitting) indicated that only 18Z remained abstinent at five years.3. Behavior Therapies The behavior therapy approach assumes that problematic behavior Is a function of a person's learned pattern of interacting with the environment. The goal la to teach mora adaptive meant of responding. The initial step Is a "behavioral assessment," an evaluation that in­ cludes identification of antecedent events that trigger smoking; determin­ ation of thoughts and feelings that influence smoking behavior; analysis of DU? 0931787 DU 035525 personal smoking behavior (frequency, situation*) • and identification of the psychological consequences of smoking. A number of techniques may then be used to teach the individual new patterns of interacting with environmental smoking stimuli. These techniques can be grouped into five major categories; systematic desensitization, punishment and aversive conditioning, stimulus control, reinforcement of nonsmoking, and multicomponent Interventions. Assuming that it is anxiety that elicits the urge to smoke, attempts have been made using relaxation techniques to desensitize smokers system­ atically to anxiety-evoking stimuli.^»17tl8 However, no substantial effect on smoking behavior has been reported. A number of aversive conditioning techniques have been employed to modify smoking behavior. Loud noises or electric shocks have been coupled to smoking or to the urge to smoke, generally with little effect. 12 Two techniques incorporate cigarette smoke as the aversive stimulus: * Rapid smoking, which requires the individual to smoke rapidly end continuously, somaclass in conjunction with drafts of warm smoky air • Satiation, which requires increasing eigarstts consumption over a certain parlod of tins (a.g., smoking double or triple the usual amount for a weak) In the context of a persuasive interpersonal relationship between patient and therapist, the rapid smoking technique appears to result in about SOX abstinence three to six months following termination. 12 While one report of a satiation program indicated 62Z cassation four months 19 12 following treatment, other programs have not bean aa successful. Bafors isgjlementing the rapid sinking method, e medical scraanlng should be required of participants due to the possible deleterious effects of increased carbon monoxide levels. 20 Another behavioral technique is stimulus control. This may involve forbidding smoking in situations where smoking would habitually occur (e.g., no smoking whila drinking coffee, watching TV, or following a meal) aa well as gradually restricting the number of situations where smoking is permitted. While (a) thare appears to be no deer cessation F_a DUP 0931788 DU 035526 efface from using this tnechod and (b) a high attrition has been reported frequently, reduction in the rate of cigarette consumption does result.4 "he reinforcement of abstinence through the use of social or monetary incentives has been relatively successful. An example of a technique incorporating a monetary incentive is the use of a deposit made prior to Initiation of the program. The money is returned in portions made con­ tingent upon progressively longer periods of abstinence. Fifty percent cessation has been reported at six months as opposed to 24Z in a group 21 22 or ’ not employing the incentive. Multicomponent interventions have been designed by combining these techniques. A number of reports indicate that this approach may yield high abstinence rates (65Z to 100Z immediately; 55% to 65% after one ,..r).22'27 . Miscellaneous Individualized Techniques There are a series of cigarette filters designed to assist smoking cessation by gradually reducing levels of inhalad tar and nicotine. The extene to which this method hee been effective hae not been evaluated.10 A diverse array of medlcatione—including stimulants as well as tranquilizers, nicotine substitutes as wall as antagonists, and anti­ cholinergics—havs been prescribed to eeelet smokers in overcoming withdrawal symptoms. With regard to actual cassation, hovavsr, none of 28 these pharmacologic agents has shown any sore prosiee then placebos. In feet, several studies have suggested that placebo groups may have higher quit rates.* Very little research is available on the effects of acupuncture as a sacking cessation cool. In one study, 50X of subjects were reported abstinent six weeks following auricular acupuncture. This caseation race is similar to those obtained using less invasive techniques, and, at tht present time, the use of acupuncture does not appear to be just. -isd. Hypnotic techniques hsve included attempts to reveal personality conflicts assumed to be major underlying causes of the smoking hsblt as wall as direct suggeaclone to quit.^0’^1 While certain inveatlgetors DUP 0931789 F-7 DU 035527 have reported positive initial results,32’33 there have been few controlled studies. follow-up. Furthermore, initial successes have not been maintained at One report of the results of a single session self-hypnotic creataent noted a cassation rate at one year of 20X.^ Using this approach, another investigator has observed significantly higher rates of recidivism 35 chan with group counseling. Three issues related to smoking cessation—monitoring of smoking behavior, the "successful quitter," and gain of weight—ere summarized briefly in Tahle F-2. Smoking Cassation Programs in Industry Industry provides an ideal secelng for smoking cessation programs. Industrial programs often have the advantages of; • An existing system of occupational health care, which affords s means of careful health surveillance end follov-up • An established network of coammieatiana, which permits the rapid dissemination of health information • Peer and management interaction,which provides for social Incentives e Readily perceived benefits in terms of diminished illness and absenteeism, which csa be assessed against program costa. While the plane physician may wish to refar workers to sacking cessselon programs outside the workplace, on-site programs rsduce lose time and inconvenience. The local chapter of the American Cancer Society would be an excellent resource for information on available outside programs, (See also other information resources is Table P-1.) A number of issginaelve industry-based smoking cessation programs have bean established, but as yet there have been no published reports of their effectiveness. Several programs have been describeds10 Intermatic Incorporated (Detroit) haa a no-smoking "parimutuel" window where employees can bet up to $100 on their ability to stop smoking for s year. The company has contributed $1,000 to be divided among suceesaful participants. Persons not remaining abstinent donate their bee to the American Cancer Society. DO? 0931790 F-8 DU 035528 Tabla F-2 MONITORING SMOKING BEHAVIOR, THE SUCCESSFUL QUITTER, AND WEIGHT GAIN • Monitoring Smoking Behavior A* with any intervention, monitoring of treatment effectiveness is critical. Although self-support has been the major measure used to date, it lacks precision for a variety of reasons which include the desire to please, denial of shortcomings, or inconsistent motivation to maintain accurate records over reporting intervals. Such objective measures as serum thiocyanate or explred-air carbon monoxide, along with self-support, might be useful for monitoring.36 • The Successful Quitter The successful quitter is likely to be a man, to be concerned about his health, to be older, to report fewer neurotic or psychosomatic symptoms, to smoke lees and to have begun smoking at a later age, to have a supportive social milieu, and to have tried to quit on several 1 37 previous occasions. ’ The behavior of-spouses appears to be a significant factor. Smokers with nonsmoking spouses, spouses who also quit, or spouses who "made it easier to quit" were more likely to remain abstinent at 5-year follow-up.1 e Weight Gain A frequent concern expressed by those planning to stop smoking Is whethsr or not they will gain weight. Indeed, three out of four 38 persons in one study gained weight after giving up cigarettes. Specific attention to the possibility of weight gain—i.e., s special dietary or behavioral weight management program—might pos­ sibly be used to good advantage in ceeaatioa programs. Source: Appendix References cited. DUP 0931791 F-9 DU 035529 The Alumineire Standard Class Company (Phoenix) ha* established a program In vhich a dollar amount equivalent to what abstinent sac iters would have spent for cigarettes is deducted fvoti paychecks. At che end of one year the company matches the total deductions and pays the entire sum to the worker providing he has remained abstinent. Sears Roebuck and Company (New York) encourages employees to take outside smoking cessation courses by rebating a portion of course feet to those remaining abstinent for tlx monthe or more. An Interesting program package including education and social monetary incentives uaa implemented at the Dow Chemieel Company (Fraaport, Texas) in collaboration with the American Cancer Society. Abstinence was rtvardad by s dollar each week, and abstinent workers were enrolled in monthly end quarterly lotteriee for prizes that included a boat and motor as well as cash awards. Ex-smoksrs wars used to recruit program participants. For each recruited participant who remained abstinent for one month, the recruiter was avmrdtd s chanca in a lottery. (Recruiter Incentive la thought to provide a useful souree of social mobilization.)^ Of 395 participants, only 15 (less than 42) continued to stsoke at program termination; however, the lack of adequate follow-up precludes sa assessment of long-term effects. While these progrsms ere useful in providing rstionsle and moti­ vation for smoking abstinancs, sons persons do not possess ths skills needed to quit. It would be ueeful eo assist such persons through ths use of behavior therapies. REFERENCES 1. West DW, ec al: Five yeer follow-up of e smoking withdrawal clinic population. Public Health 67:536-344, 1977. 2. Guilford 3: Factors Ralatad to Successful Abstinence from Smoking: Pinal Report. Los Angelas, American Inatituta for Rasaareh, 1966. 3. Sernatain DA; Modification of amoking behavior: review. Psychol Bull 71:418-440, 1969. 4. Bernstein DA, McAlister A: The Modification of Smoking Bshtvior: Progress and problsms. Addict Bshav 1:89-102, 1976. 5. Hunt WA, Matsrssso JD: Thrte years lstsr: rscsnt developmsnts in the experimental modifications of smoking behavior. Abnorma Psychol 81:107-114, 1973. 6. Schwartz JL: A critical review and evaluation of smoking control methods. Public Health Rep 34:489-506, 1969. F-10 An evaluative DUP 0931792 DU 035530 7. Schwarts JL, Rider C: Smoking cessation cathode la the United Statu and Canada; 1969-1974. In: Steinfeld J, Griffiths W, 3all K, Taylor Ra, (ads.) Proceedings of the 3rd World Conference on Suiting and Health. DHEW Publication Ho. (MIH) 77-1413, 1977. 8. Handel S: Change In suiting habits in general practice. Med J 49:479-681, 1973. 9. Belarus NC: A study In suiting withdrawal: the Toronto suiting withdrawal study centre: description of activities. Can J Public Health 64:2,5-19, 1973. 10. national Cancer Institute. The Suiting Oigese: a Hatlon Kicking the Habit (in press). 11. Dubren R: Evaluation of a televised scop-suklng clinic. Rep 92:81-34, 1977. 12. Lichtenstein E, Danaher SC: Modification of suiting behavior: A ' critical analysis of theory, ruearch and practice, _In Hersan M, Elslar RM, Miller PM, (eds.) Progress In behavior udificaelon (vol 3) Sew York: Academic Prus, 1976. 13.. national Clearinghouse for Suklng and Health. L97S. HEW Public Health Service, 1976. 14. Schwarts JL. Oubltzky M: One-year follow-up raaulta of a suklng csasaclon program. Can Public Health 59:161-165, 1968. 15. Lichtenstain E, et al: Comparison of rapid smoking, wan, saoky air, and aeeaneion placebo in the udifleetlon of suklng behavior. J Consult Clin Psychol 40:92-98, 1973. 16. Koenig KP, Masters J: Experimental traataane of habitual suklng. Behav Rase Thar 3:235-243, 1965. 17. Fyke S, McK Agnaw N, Kopperud J: Modification of an overlssrned mslsdsptivs rasponas through a relearning prograa: A pilot study on suklng. Behav Rasa Thar 4:197-203. 1966. 18. Wagner JK, Bragg 8A> Comparing behavior aodificaeion approaches to heble decreaaae-eukiag. J Consult Clin Psychol 34:258-263, 1970. 19. Rasalek JH: Effaces of stimulus satiation on the overlearned maladaptive response of clgerecte suiting. J Consult Clin Psychol 32:501-503, 1968. 20. Miller LC, at al: Potential haxarda of rapid suklng am a techni­ que for cha udifleetlon of suiting behavior. H Engl J Mad 297:590-592, 1977. 21. Tlche TJ, Elliott t: Breaking the cigarette habit: affects of the technique involving threatened loss of money. Paper presented at the annual meeting of the American Psychological Association, 1967. 22. uiaect RA: Parameters of deposit contracts in the udlflceeion of suklng. Psychol lee 23:49-60, 1973. Postgrad Progress Repore on Pub Health Adult use of tobacco: DUP 0931793 Du 035531 —adTM!«L»J—’ X ilMi j HWW W'Sft 23. Harris HB.'Rochberg C: A self-control approach to reduced smoking. Psychol Rap 31:L65—L66, 1372. 24. Chapman RF, Saleh JW, Laydan TA: Ellminaelon of clgaracea looking by punishment and self-msnageaenc training. 3ahav Res Thar 9:253-264, 1971. 25. Morrow J, ee al: Elimination of cigarette looking behavior by itlaulus satiation, self-control techniques, and group therapy. Paper presented to the meeting of the Western Psychological Asso­ ciation, Los Angeles, April 1973. 26. Pomerleau OF, Ciccone P: Preliminary results of a treatment pro­ gram for smoking cessation using multiple behavior and modification techniques. Paper presented to the meeting of the Association for Advancement of Behavior Therapy, Chicago, November 1974. 27. Tooley JT, Pratt S: Ah experimental procedure for the extinction of smoking behavior. Psychol Rac 17:209-218, 1967. 28. Cries ER, Jarvlk HZ: Pharmacological aids for the cessation of smoking. In Steinfeld J, Criffitha W, Sell K, Taylor RM. (ads.) Proceedings of the 3rd World Conference on Saoklng and Health, DHEW Publication No. (NIH) 77-1413, 1974. .. Globglee A: Auricular acupuncture and the smoking hable. Presse Had p. 980, 1974. 30. Bryan WJ: 31. Johnston E, Donoghue Jl: Hypnosis and saoklng: A review of the literature. Am J of Clin Kypn 13:268-272, 1971. 32. Korger WS: Clinical and Experimental Hypnosis. Thomas, L9f3. 33. von Dedenroeh TEA: The use of hypnosis la 1000 cases of "tobaccomaniacs." Am J Clin Hypo 10:194-197, 1968. 34. Spiegel H: A single-treatment method to aeop smoking using ancillary lalf-hypnoals. Iat J Clin Exp Hypn 18:235-249, 1970. 33. Shevchuk LA: A comparison of smoking cessation techniques: Initisl success and eventual recidivism. Submitted to Public Health Reports, Hypnosis and smoking. Nouv J Am Inst Hypo 5:17-37, 1964. Soringfisld: 1976. 36. Vogt TM, at el: Expired air carbon monoxide end terua thiocyanate as objective measures of cigarette exposure. Am J Public Health 67:545-349, 1977. 37. Pederson LL, Lefcoe MM: A psychological and behavioral comparison of ax-smokers end smokers. J Chronic Die 29:431-434, 1976. 38. Hammond EC, Percy C: 39. Janie IL, Hoffman 0: Paciliteting effects on daily contact between partners who make a decision to cut down on smoking. J Pars and Soc Psychol 17:25-35, 1970. Ex-Smokere. NT Scats J Med 58:2956-2959, 1958. . , DU? 0931794 DU 035532 Appendix G SOURCES OF EDUCATIONAL MATERIALS Sources of Published Educational Materiel* Asbestos Information Aaaociation/NA Materials: Brochures on work practices, fact books, reprints of scientific articles, conference proceedings, and films Address: reference library. 1835 "K" Street, N.W. Washington, D.C. 20006 Asbestos Information Counittee Materials: Brochures on work practices, health effects, and control procedures. Address: 10 Wardour Street London, W1V 3HG England Asbestos Research Council Materials: Brochures on work practices, ventilation, control procedures, protective devices, and disposal methods. Address: P.0. Box 13 Clsckhsston Wsst Yorkshire, BD19 3UJ, England Conaress of the United States Materials: Pertinent Public Leva Address: Docuaene Room, Congress of the United States, Washington, D.C, Johns-Manvtlle Corporation Materials: Brochures on work practices, health effects, filaa, slide* with sound, slides with script, video tapes, newspaper, bulletins, letters, reports, and reprints of scientific articles. DU? 0911195 G-l DtJ 035533 Himma.aawi:a:seilsasiaiWim::.. ^adugsiMSKa Address: Health, Safety and Environment Department Ken-Caryl Ranch Denver, Colorado 30217 National Institute of Occupational Safety and Health. U.S. Department of Health, Education and Welfare Materials: "Criteria Document" on Asbestos: reports of occupational disease research and epidemiologic investigations. Address: Robert A. Taft Laboratories 4676 Columbia Parkway Cincinnati, Ohio 45226 National Safety Council Materials: Reprints of articles, safety data sheets; reference library. Address: 425 Morth Michigan Avenue Chicago, Illinois 60611 Occupational Safety and Health Administration. U.S. Department of Labor Materials: Occupational Safety and Health Standard: Subpare 2, Sec. 1910.1001, Asbeseos Brochures on 0SHA 1970 Address: Occupational Safety and Health Administration U.S. Department of Labor Washington, D.C. 20210 Oil. Chemical and Atomic Workers International Union. AFI-CIO Materials: Foster, slide-tape casaette presentation Address: Citizenship-Legislative Department 1126-16th Street, N.W. Washington, D.C. 20036 Quebec Asbestos Mining Association Haterials: Brochures on work practices, health effects, and control procedures. Address: 5 Place Villa Marie Montreal 113, Quebec, Canada G-2 DUP 0931796 DU 035534 Possible Sources of Published Educational Materials American Association of Potion Contra! Canters c/a Academy of Medicine of Cleveland Poison Information Center 10525 Carnegie Avenue Cleveland. Ohio 44105 American Medical Association 535 North Dearborn Street Chicago, Illinois 60610 American Public Health Association 1015-lSth Street, N.W. Washington, D.C. 20036 Center for Science in the Public Interest 1757 "S" Street, H.W. Washington, D.C. 20009 Companies mining asbestos ore Consumer Federation of America 1012-14ch Street, H.V., Suite 901 Washington, D.C. 20005 Consumers Union 256 Washington Streee Mount Vernon, Hev Tork 10530 Health Research group 2000 "P" Street, H.V., Suits 708 Washington, D.C. 20036 Insulation Industry Hygiene Research Proeram Environmental Sciences Laboratory Mount Sinai School of Medieine of the City University of Hev Tork Fifth Avenue end 100th Street Hsu Tork, Hev Tork 10029 03 DU? 0931797 DU 035535 Appendix H REFERENCES Chapter I 1. Marewecher ERA, Price CW: Effect of Aebeecoa Duet on Lunge and Data Suppression in the Aebeecoa Induetry. London, H.M. Stationery Office, 1.9 30. 2. Merewether ERA: Aabeecoaie and carcinoma of the lung. In Annuel Report of the Chief Inepeetor of Factories for the Tear 1747. London, H.M. Stationery Office, 1949, p. 77. 3. Selikoff IJ: Cancer risk of asbestos exposure. In Symposium on the Origins of Human Cancer. Cold Spring Harbor,“Sew York, Cold Spring Harbor Laboratory, September 7-14, 1976. 4. Nevhouae, ML, Berry G: Predictiona of mortality from mesochelial tumours in asbestos factory workers. Br J Ind Med 33:147-131, 1976. 5. Wagoner JX: 6. Minerals and their nonaabeaeos analogs. In Electron Microscopy of Microfibers, Mineral Fibers Session. University Park, Pennsylvania, Pennsylvania State University, August 23-25, 1976. 7. Stanton MF, Wrench C: Mechanisms of mesothelioma induction with asbestos and fibrous glass. J. Had Cancer Inst 48(3):797-821, 1972. 8. Draessen WC, at al: A Study of Aabestoala in the Asbestos Textile Industry. U.3. Treasury Department, Publie Health Service. Public Health Bulletin HO. 241, Aug 1938. 9. SIX International. Personal communication. Attorney John Hynan, Occupational Safety and Health Administration, November 18, 1976. 10. U.S. Code of Federal Regulations, Title 40, Part 61.22. 11. U.S. Code of Federal Regulations, Title 40, Part 427. 12. Federal Register 41(15):3286-3287, January 22, 1976. 13. Federal Sagiscar 40(51):11865-11869, March 14, 1975. 14. Coda of Fedaral Regulations, Title 21, Perce 133.8 end 133.9. ' Occupational carcinogenesis--The 200 years since Percivall Pott. Ann NT Acad Scl 271:1-4, 1976. DUP 0931799 DU 035536 (I) (II) (III) 15. U.S. Code of Federal Regulation*, Title 21, Parts 121.101; and personal communication, Donald Miller, Food end Drug Administration, October 24, 1976. 16. U.S. Code of Federal Regulations, Title 16, Part 1500.17(7). 17. Nicholson WJ: Case study 1: asbestos—the TLV approach. NY Acad Sci 271:152-169, 1976. Ann Chapter II 1. Canadian Mineral Yearbook. Dept, of Energy, Mines and Resources, Mineral Resources Branch, 1974. 2. U.S. Census of Manufactures, U.S. Dept, of Commerce, Bureau of the Census, 1972. 3. Mineral Facts and Probleas. Mines, 1975. 4. Commodity Data Suaaariss. Mines, 1976. 5. Asbestos Information Association of North Anarice: general Information. Washington, D.C., 1973. U.S. Dept, of Interior, Bureau of U.S. Dept of Interior, Bureau of Asbestos- Chapter III 1. Davis JMG, Conlaa SWt Experimental studies on tha effects of heated chrysotile asbestos and automobile brake lining dust injected into the body cavities of alee. Exp Mol Pathol 19:339-353, 1973. 2. Fondiaare A, at al: Quantitative study of the deposition of asbestos In the lung and pleura of subjects with diverse exposures. Proceedings of the Syaposlua on the Pathology of Asbestos. Rouen, France, Oct 28, 1975. 3. Tlrtrell V: Inhalation and biological effects of asbestos. In Assessment of Airborne Particles (Mercer TT, Morrov PS, Strober W, ads.). Proceedings of the Third Rochester International Conference on Environmental Toxicity. Springfield, Illinois, CC Thomas, 1972, pp 429-445. 4. Gross P, DeTreville RTF: The lung as an eabattlad domain against inanimate pollutants. Am Rev Sespir Dis 106:684-691, 1972. 5. Evans JC, et el: Studies on the deposition of inhaled fibrous material in the respiratory tract of the rat and its subsequent clearance using radioactive trace techniques. Environ Res 6:180-201, 1973. H-2 DUP 0931600 DU 035537 6. Vagner JC, ac *1.: the effects of inhalation of asbestos in rata. Br J Cancer 29:252-269, 1974. Allison AC: Experimental methods——cell and tissue culture* effects of asbestos particles on macrophages, aesothelial cells and fibro­ blasts. In Biological Effects of Asbestos (Bogoyski, et al., ads.). Lyon, France, International Agency for Research on Cancer,*Scientific Pub. Ho. 8, 1973, pp 89-93. 8. Godwin ML, Jagatic J: (5-6):391-416, 1970. Aabestos and mesotheliomas. Environ Res 3 9. Sabaatlen P, et al: Topographic distribution of asbestos fibres in human lungs in relation with occupational and nonoccupational exposure. 4th International Symposium on Inhaled Particles and Vapors. Edinburgh, - 1976. 10. Cross P, et al: Ingested mineral fibers: do they penetrate tlseue or cause cancer? Arch Envlrotuaan Health 29:341-347, 1974. « Vastlake GE, Spjut HP, Smith Iff: Penetration of colonic mueose by asbestos particlss, an alseeron microscopic study la rats fad asbestos dust, lab Invest 14(11):2029-2033, 1965. 11. 12. Storeygard AR, Brown AL: Psnetratlon of the smell intestinal mucosa by ssbsstos fibers. Mayo Clinic Procaediags 52:809-812, 1977. 13. Bolton RIZ, Davis JMC: The short-term effects of chronic asbestos Ingestion in rats. Ann Occup Ryg 19:121-128, 1976. 14. Cunningham HM, Pontefract RD: Asbsatos fibers la beverages, drinking wsesrs and tlssuas: thalr passage through the intestinal wall and movemant through the body. J Aeeoc Offlc Anal Chea 56:976-981, 1973. 15. Pontefract SO: Penetration of asbeatoa through the digestive wall in rata. Environ Health Perspecc 9:213-224, 1974. 16. Cunningham HM, Pontefract SO: 249:117-118, 1974. 17. Kanazawa K, at al: Migration of aabeatoa fibers from injection aitee in alee. Br J Cancer 24:96-106, 1970. 18. Becklaks MR, et al: Lung function profiles In the chryeotile aabeatos fibers from injection eltes in mice. Br J Cancer 24:96-106, 1970. 19. Aehcrofe T, Reppleston AG: The optical and electron microscopic determination of pulmonary ssbsstos fibre concentration and its rslstion to the human pathological raaction. J Clin Pathol 26:224234, 1973. 20. Parity ML, et si: Farraginous bodiss in spues of former asbestos workers. Tylsr, Tsxss, Taxes Chest Foundation (unpublished), 1976. Placental transfar of asbaatos. Nature DUP 0931801 DU 035538 (Ill) 21. Gro*« ?, deTreville RTP, Haller, MN: Pulmonary ferruginous bodiea In city dweller* (a ecudy of their central fiber). Arch Environ Health 19:186-188, 1969. 22. Slgnon J, et al: Incidents of pulmonary ferruginous bodies in France. Environ Rea 3:430-442, 1970. 23. Selikoff IJ, Hammond EC, Churg J: Carcinogenicity of amosite aabescoa. Environ Health 25:183-186, 1972. 24. Langer AM, Mackler AD, Pooley FD: Electron aieroocopial investiga­ tion of asbestos fibres. Environ Health Perspect 9:63-80, 1974. 25. Selikoff IJ: Cancer risk of asbestos exposure. In Origins of Human Cancer (Hiatt HH, Watson JD, Wins ten JA, eds.). Cold Spring Harbor, Hew York, Cold Spring Harbor Laboratory, 1977, pp. 1765-1284. 26. Hewhouse ML, et al: Predictions of mortality from mesothelial tumours in asbestos factory workers. Br J Ind Med 33: 147-151, 1976. 27. Cloyne, SR: asbestosis. 28. Lynch KM, Smith WA: Pulmonary asbestosls. III. Carcinoma of lung in asbestos-silicosis. Am J Cancer 24: 56-64, 1935. 29. Merevether ERA: Annual Reoore of the Chief Inspector of Factories for the Year 1947, London HMSO, 15-17, 1949. 30. Brealow L, at al: Occupations and cigarette smoking as factors in lung cancer. Aa J Public Health 44: 171-181, 1954. 31. Doll R: Mortality from lung cancer in asbestos workers. Med 12:81-86, 1955. 32. Knox JT, et al: Mortality from lung cancer and other causes among workers in an asbestos textile factory. Br J Ind Med 25: 292-303, 1968. 33. Howard S, et al: A mortality study among workers in an English asbestos factory. (Submitted to Br J Ind Hyg) 1977. 34. Elms* PC, Simpson MJC: Insulation workers in Belfast, III, Mortality 1940-1966. Br J Ind Med 28: 226-236, 1971. 35. Kogan FM, Gulsenikova NA, Gulevskaya MR: The cancer mortality rate among workers in the asbestos industry of the Urals. Gig Sanit 37: 29-32, 1972. 36. Meuraan LO, Kiviluoto R, Hakama M: Mortality and morbidity among the working population of anthophyllite asbestos miners in Finland. Br J Ind Med 31: 105-112, 1974. • Two cases of squamous carcinoma of the lung occurring in Tubercle 17: 5-10-, 1935. Br J Ind DUP 0931802 Du 035S39 (III) 37, Nurminen M: A study of the mortality at worker* in en snthophyllits asbestos factory in Finland. Work Environ Health 9: 112-118, 1972. 38. McDonald JC, et al: The health of chryaotila asbestos min* and mill workers of Quebec. Arch Environ Hlth 28: 61-68, 1974. 39. Mewhousa ML: Asbestos in the work place sad the community. Occup Hyg 16: 97-107, 1973. Ann 40. Gloyne SR: The morbid anatomy and histology of asbestosis. 14: 530-538, 1933. Tubercle 41. Wedler KW: 1943. 42. Wedler HW: Uber den Lungenkrebs bei Asbestos*. 191: 189-209, 1943. 43. Wyers H: That Legislative Measures Have Proved Generally Effective in the Control of Asbestosis, M.D. Thesis, University of Glasgow, U.K., 1946. 44. Leisher F: Primarer Deckzellentunor des Bauchfslls bei Asbestose. Arch Geverbepath Gewerbahyg 13: 382-392, 1954. 43. Wagner JC, Sleggs CA, Marchand P: Diffuse pleural mesothelioma and asbestos exposure in the North Western Cap* Province. Br J Ind Med 17: 260-271, 1960. 46. Selikoff IJ, Churg J, Hammond EC: Relation between exposure to asbestos and mesothelioma. Hew Eng J Mad 272: 360-563, 1965. 47. McDonald AD, McDonald JC: Etudes epldeadLologique* aur lee maladies dues a l'anisata au Cands. Raw Franc Hal Rsap 4, Supp 2: 23-38, 1976. 48. Hewhousa ML, Thompson H: Mesothelioma of plaura and parltonsum follow­ ing exposure to asbestos In the London area. Br J Ind Med 22: 261269, 1965. 49. Mdwea J, at el: 50. Dalquea P, Dabbart AP, Hint ft The epidemiology of mesothelioma: A preliminary report on 119 cases from the Hamburg ares. Ger Med 13: 89-95, 1970. 51. Hein E, at al: Retrospective study of 130 cases of meeothelioms in the Hamburg area. Int Arch Arbaeiamed 33: 13-37, 1974. 32. Rubino GF, at al: Epidemiology of pltural mesothelioma in. KorthWeatarn Italy (Piedmont). Br J Mad 29: 436-442, 1972. Asbestos* uad Lungenkrebs. Dtach mad Wachr 69:575-576, Dtach Arch Klin Med f Mesothelioma in Scotland. Br Med J 4: 575-573. 1970. DUP 0931003 H-3 DU 035540 (Ill) 53. Zialhuia RL, at si: Pleura aasoehelloaa and exposure to asbestos; a retrospective case-control study in tha Netherlands. Int Arch Occup HIth 36: L-18, 1975. 54. 3ecklake M: Asbestos-related diseases of tha lung and othar organs. Thair epidaniology and implications for clinical pracelca. Aa Rav Raspir Dis, 114: 187, 1976. 55. Newhoust ML, ac al: A study of tha uortality of faaala asbestos workars. Br J lad Mad 29: 134*141, 1972. 56. Selikoff IJ, Haanond EC, Churg J: Mortality expsrlaneas of asbestos insulation workers, 1943*1968. In Pnauaoconloala.(Shapiro EA. ed.). Proceedings of tha International Conference, Johannesburg, 1969. Capa town, Oxford University Press: 180*186. 57. Stall PM, McGill T: 417, 1973. 58. Stall PM, McGill T: Exposure to asbestos and laryngeal carcinoaa. J Laryngol Otol 89:513*517, 1975. 59. Morgan RSf, Shettlgara PT: Occupational aabeetoe expoeure, smoking, and laryngeal carcinoaa. Ann NT Acad Sel 271: 309*310, 1976. 60. Oaua SM, Seldaaa H, Selikoff IJ: Laryngeal and hucco-pharyugaal cancers in asbestos workers. In Proceedings of Third International Symposium on the Detection sad Prevention of Cancer. Mew York, 1976. 61. Newhouae ML, Berry G: 615, 1973. 62. Martlschnig KM, at al: Unauspacead exposure to asbestos and bronchogenie carcinoaa. Br Mad J (6063): 746*749, 1977. 63. Kancuso Tf, El-Attar AA: Mortality pattern in a cohort of sabeetos workere. A atudy based on eaployaent experience. J Oecup Med 9: 147-162, 1967. 64. Kewhouee ML: Cancer saong workers in the asbestos taxella industry. In Biological Effects of Asbestos (Bogovskl P, st si., ads.). Lyon, Francs, Iatsrnstionsl Agency for kesearch on Cancer, Scientific Pub. Mo. 8, 1973, pp. 203-208. 65. Selikoff IJ: Zpideaiology of gastrointestinal cancer. Perspact 9: 299-305, 1974. Asbestos and laryngeal carcinoma* Lancet 2: 416* Asbestos and laryngeal carcinoaa. Hp4 Lancet 2: Environ Health _ DUS 0931®°4 p\J 035541 i i ! (Ill) Sslikoff IJ: Epidtmiology of gsatroincsatiaal cancer. Perspect 9: 299-305, 1974. Environ Hsalth Sslikoff IJ, Hammond ZC, and Churg J: Carcinogenicity of aaoslta aabaatoa. Arch Environ Health 25! 183-136, 1972. Hasnond EC, Selikoff LI, and.Churg J: Neoplasia among inaulaelon workera in the United Statee with apecial reference to intraabdominal neoplaaia. Ann NT Acad Sd 132: 519-525, 1965. Bradahtv E, Schonland H: Oesophageal and lung cancers In Natal African sales in relation to certain socioeconomic factors. Br J Cancer 23(2): 275-284, 1969. Tinbrell 7: Inhalation and biological effects of asbestos. In Assessment of Airborne Particles. Pundaaantals, Applications and Implications to Inhalation Toxicity (Mdreer IT, Morrow PE, Stober W, ads.). Springfield, Illinois, CC Thomas, 429, 1972. * Pooley FD: An examination of the fibrous mineral contant of asbestos lung tissue from the Canadian ehryaotlle mining induatry. Environ Ras 12: 1281-1298, 1976. IAXC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Man, Aabeseos. 14: Lyon, Prance, International Agency for Research on Cancer, 1977. Nurmlnen M: The epidemiologic relationship between pleural meso­ thelioma and asbestos exposure. Scand J Work Environ & Health 1: 128-137, 1975. Vagner JC, at al: 71-76, 1971. Epidemiology of asbestos cancers. Br Mad Bull 27: Enterline PI, Henderson 7: Type of asbestos sad respiratory cancer in the asbestos induatry. Arch Environ Haalth 27: 312-317, 1973. McDonald JC: Caacar in chrysotlla mines and mills. In Biological Effaces of Aabescos (Bogovskl P, at al., eds.). Lyon, France, International Agney for Raaeareh on Cancar, Sciantific Pub. No. 8, 1973, pp 189-194. McDonald JC, et al: Mortality in the chxysotile aaheatoe mines and mills of Quebec. Arch Environ Hlth. 22: 677-686, 1971. Enterline PE, De Coufle P, Henderson V: Mortality in relation to occupational exposuras among ratlrsd asbsseoa workers. Br J Ind Mid 30: 162-166, 1973. 8-7 OOP 0931805 DU 035542 (Ill) 79. Weiss Ws Mortality of a cohort exposed to chryaoeile aabeatoa. Occup Mad 19: 737-740, 1977. J 80. Kleinfald K, at: Mortality among calc miner* and miller* in New York State. Arch Environ Health 14: 663-667, 1967. 31. Kleinfeld M, Mea*it* J, Zaki K: Mortality experience among calc miner* and miller*. J Occup Mad 16: 345-349, 1974. 82. Rubino G, at al: Mortality study of talc miners and miliars. J Occup Med 18: 186-193, 1976. 83. Newhouse ML: A study of mortality of workers in an asbestos factory. 8r J Ind Mad 26: 294-301, 1969. 84. Jones H3, Grendon A: Environmental factors in cha origin of cancer and estimation of tha possible hazards to man. Food Cosmat Toxicol 18: 251-268, 1975. » 85. Seldman.H, Lilis R, Selikoff IJ: In Short-tarn asbestos exposure and delayed caacar risk. Proceedings of Third International Symposium on cha Detection of Cancer, New York, 1976. 86. Greenberg M, Lloyd Davies TA: J lad Med 31: 91-104, 1974. 87. Lualey KPS: A proportional study of cancer registrations of dockyard workers. Br J Ind Med 33:108-114, 1976. 88. Doll R: Susceptibility to carcinogenesis at different ages. Clin 4: 211-221, 1962. 89. Doll R: Cancer in aging: the epidemiological evidence. Dorn Memorial Lecture, 10th International Conference of the International Union Agalnae Cancer. Houston, Tsxss, May, 1970. 90. Barry G, Newhouse ML, Turok M: Combined efface of sabaseos exposure and smoking on mortality from lung cancer in factory workers. Lancae ii: 476-479, 1972. 91. Saracei Rj Asbestos and lung cancer: an analysis of tha epidemiological evidence on the asbestos-smoking interaction. Int J Cancer 20: 323331, 1977. 92. Selikoff LI, Humaond SC, Cburg J: plasia. JAMA 204: 106-112, 1968. 93. Cooper WC, at al: Study of Sheet Metal Workers—Pinal Raport, Contract KSM-099-71-55, Washington, DC, US Dept Health, Education and Welfare, National Institute for Occupational Safety and Health, 197S. Mesothelioma Register 1967-1968. 3r Gerontol Asbestos sxposure, smoking and neo­ H-8 DUP 0931806 D\J 035543 I :) i 94. Edge JR: Asbestos related disease la Barrow-in-Furness 11: 244-247, 1976. 95. Fleccher DE: A mortality study of shipwsrd workers with pleural plaques. Br. J Ind Med 29: 142, 1972. 96. Anderson HA, at al: Household-contact asbestos neoplastic risk. NY Acad Sci 271: 311-323, 1976. 97. Lillington GA, Jaaplie SW, Differding JR: Conjugal malignant meso­ thelioma. N Eng J Med 291(11): 583-584, 1974. 98. Selikoff IJ, Churg J, Hammond EC: JAKA 188: 22-26-, 1964. 99. McDonald AD, McDonald JC: Epidemiologic surveillance of mesothelioma in Canada. Can Med J 109: 356-362, 1973. 100. Bohllg H, Haln £: Cancer in relation to environmental exposure In 81ological Effects of Asbestos (Bogovski P, at el., eds.). Lyon,, France, International Agency for Research, on Cancer, Scientific Pub.* No. 8, 1973, pp. 217-221. 101. Yazlcloglu S, et al: Asbestosis ve solunua sisteminin primer malign tumorlerl arasindaki iliskller uaerinde arastlrma: 162 vak'anln dosyasl uzerlnde retrospektif inceleme. Tuberkoloz ve Toraak, Derglsinin 23: Kayls-Kasarlti, Seyl 2-3, Ayrl Baskl, 1976. 102. Blot WJ, Frauaeni J?: Geographic pattarns of lung cancer: correlations. Amar J Epidaadol 103(6): 539-550, 1976. 103. Bohllg H, et al: Epidemiology of malignant mesothelioma in Hamburg. Environ Res 3: 365-372, 1970. 104. Masson TJ, McKay EV, Miller RSf: Asbestos-like fibers in Duluth water supply. JAHA 228(8): 1019-1020, 1974. 105. Levy 33, et el: Investigating poealble effects of asbestos in city witer: surveillance of gastrointestinal cancer incidence In Duluth, Minnesota. Am J Epidemiol 103(4): 362-368, 1976. 106. Reeves AL, et el: 4i 496-511, 1971. 107. Wagner JC, Berry G, Timbrell V: Mesoehelioaata In rats after inocula­ tion with asbestos and other materials. Br J Cancer 23: 173-185, 1973. 108. Shabad LM, at al: Exparlmental studias on aebaatoa carcinogenicity. J Natl Cancer Inat 52: 1175-1187, 1974. 109. Smith WE: Experimental studies on biological effaces of eermolies talc on hamsters. U.S. Bur. Mines Inf Clr (IC8639):43-48, 1974. i i ii Environ Res Ann Asbestos exposure and neoplasia. Experimental asbestos careinogtnesis. H-9 industrial Environ Res OUP 0931807 __ DU 035544 (Ill) 110. Pott F, Friedrich* KH: Tumoren der Ratten nech l.p. Injektion faserfortalger Setubs. Haturvlssenachafdn 59 s 318, 1972. 111. Melconi C, Aanoacia C: Mesotheliomas la rad following che iatraperitonaal injection of croeldollea. In Characdrlzatlon of human cunor* (Melton! C, Davla W, eda.) Proceeding* of ch* Fifth.:Intemacional Sympoaiua oa th* Biological Charact*rization of Human Tumors. Bologna, 4-6 April, 1973, 1:115 112. Pott F, Friedrich* KH, Huth F: Ergebnisae aus Tlerversuehen zur kanzerogenen Wlrklng faaerforalgar Staub* und thr* Deutuag la Hlablick auf die Tumorentatehung balm Men*chan. Zentralbl Bakterlol Hr* 162: 467-505, 1976. * 113. Gross P, ee al: Experimental aebeseoals: The development of lung cancer In rats with pulmonary deposits of chrysotll* asbestos dust. Arch Environ Health 15: 343-355, 1967. 114. Reeves AL: The carcinogenic effect of inhaled asbestos fibers. Ann Clin Lab Sel 6: 459-466, 1976. 115. Reeves AL, Puro HE, Smith EG: Inhalation carcinogenesis from various forme of asbestos. Environ Res 8> 178-202, 1974. 116. Glbel W, ee al: Tlerexperlmentelle Uatexsuchungen uber elne kanserogene Vorkung nach Aabestfllter Material nach oraler Aufnahme. Arch Pathol 96: 245-250, 1973. 117. Stanton MF, Wrench C: Mechanisms of mesothelioma induction with asbestos and fibrous glass. J Mad Cancer Inst 48(3): 797-821, 1972. 118. Stanton MF: Sobs etiological considerations of flbrs carcinogenesis. In Biological Effects of Aabeetoe (Bogovski P, ee el., eds.) Lyon, France, International Agency for Research on Cancer, Scientific Pub. Ho. 8, 1973, pp. 289-294. 119. Occslls g, Meddeloa G: X-rsy diffraction cherecteriatice of tome types of asbestos in relation to different techniques of ccanunication. Med Lav 54(10): 628-636, 1963. 120. Laager AM, ee el: Variation of some physical, chemical and biological properties of chrysotll* asbestos subjected to prolonged milling. J Toxicol Environ Health (in prase), 1977. 121. Murray M: In Report of the Departmental Committee on Compensation for Industrial Diseases. London, H3S0, 1907, pp. 127-128. H-10 DUF 0931008 DU 035545 122. Auribaulc M: Bulletin de I'Inepeetion du Travail, 1906, p 126. 123. Rarkes WR: Asbestos related disorder*. Br J Die Cheat, 67(4): 260 124. Murphy, Jr. RJ, et el: Low exposure to asbestos gas exchange in ship pipe coverers and controls. Arch Environ Health 25:253-264, 1972. 125. - 3ad*r ME, et al: Pulmonary function and radiographic changes in 598 workers with varying duration of exposure to asbestos. Mt Sinai J Med 37(4): 492-500, 1970. 126. Merawether ERA: Asbescosis and carcinoma of the lung. In Annual Report of the Chief Inspector of Factories for the Tear 1947. London, HUSO, p. 77, 1949. » Gloyne.SR: Pneuaoconiosia. A historical survey of necropsy material in 1205 cases. Lancet 1:810-814, 1951. 127. 128. Buchanan WD: Asbestosls and primary intrathoracic neoplasms. Acad Sci 132(1): 507+, 1965. 129. Selikoff IB, «c el: Aebescosis and neoplasia. Ann MT Am J Med 42(4): 487-496, 1967. 130. Davis JM: Histogenesis and fine structure of perltonesl tumors produced in animals by injections of asbestos. J Natl Cancer Inst 52: 1823, 1974. 131. Gaensler EA, Kaplan AX: 74: 178-191, 1971. 132. Elder JL: A study of 16 cases of pleurisy vith effusions in ex-miners from Wittenoon Gorge. NZ J Med 2(3): 328-329, 1972. 123. SRX International. 134. Navratil M., Trippe F: Prevalence of pleural calcification in person* exposed to asbestos dust, and in the general population in the seas district. Environ Ran 5: 210-216, 1972. 135. Selikoff IJ: The occurrence of pleural calcification among asbestos insulation workers. Ann NT Acad Sci 132(1): 351-367, 1965. 136. Kiviluoto, R: Pleural calcification as a roentgenologic sign of nonoceupational endemlx aathophyllite-asbestoeis. Acte Radiol Supp 194, 1-67, 1960. Asbestos pleural effusion. Ann Intern Med Personal communication, EA Gaensler, October 1976. H-ll OUP 0931309 DU 035546 Fill SasKStf (ill) 137. Burllkov T, Michailova L: Asbestos concaat of the soil and endemic pleural aabestosis. Environ Res 3: 443-451, 1970. 138. Zolov C, Burllkov T, Babodjov L: Pleural aabestosis in agricultural workers. Environ Res Is 287-292, 1967. 139. Yaaieioglu, S: Pleural calcification associated with exposure to chrysotile asbestos in southeast Turkey. Chest 70: 43-47, 1976. 140. Aldan HS, Howell WM: 312,. 1944. 141. Vigliani EC: The fibrogenic response to asbestos. 401-410, 1968. 142. Vagner JC: Aabestosis in experimental animals. 3r J Ind Med 20(1): 1-12, 1963. 143. Vehner AP, at al: Chronic inhalation of asbestos and cigarette smoke by haaseers. Environ Res 10(3): 368-383, 1975. 144. Holt PF, Hills J, Young DC: The early effects of chrysotile asbestos dust on Che rat lung. J Pathol Bacteriol 87(1): 15-23. 1964. 145. Webster I: Aabestosis in noa-experiaental animals in South Africa. Nature (London) 197(4866): 506, 1963. 146. Schuster NH: Pulmonary asbestos in a dog. 751-757, 1931. 147. Holt PF: Experimental aabestosis with four types of fibers: of ssall particles. Ana NY Acad Scl 132: 87-97, 1965. 148. Burger BP, Eagelbreeht PM: The biological effects of long and ahort fibers of crocidolits and chrysotile after intrapleural injection into rata. S Am Air Med J 44(44): 1268-1270, 1970. 149. Davis JUG, Cross ?: Are ferruginous bodies an indication of atmospheric pollution by asbestos? In Biological Effects of Asbestos (Bogoveld ?, at si., eds.). Lyon, Francs, International Agency for Research on Cancer, Scientific Pub. Ho. 8, 1973, pp. 238-242. 150. Rahman a materials survey. Circular 7880, Washington, D.C., 6. Engineering Equipment Users Association Handbook if33: for Handling Asbestos, London, 1969. 7. Bruckamn L, Rublno RA: Asbestos: rationale behind a proposed air quality standard. J Air Pollut Control Assoc 25(12): 1207-1215, 1975. 8. ' Federal Register 40(197), October 9, 1975, p 47662. 9. U.S. Environmental Protection Agency: Control Techniques for Asbestos Air Pollutants. U3EPA Publ lAP-117, Research Triangle Perk, HC, 27711, Feb. 1973. H-20 Information Recommendations DUP 0931818 DU 035555 t (VI) evil) 10. Harwood CF, Siabart P, Blaszak TP: Asstsaaanc of Particle Control Technology for Enclosed Asbestos Source*. EPA Publ #EPA 650/2-74088, USEPA, Research Triangle Parle, NC. October 1974. (Alao available aa NTIS Publ 0PH239926). 11. Harvood CP, et al: Asbestos emission* fro* baghouae controlled sources. J Am Ind Hyg Assoc 36(8): 595-603, Aug. 1975. 12. Seibert PC, Ripley TC, Harwood CP: Assessment of Particle Control Technology for Enclosed Asbestos Sourcee-Phase II. EPA Publ PEPA 600/ 2-7-6-065, USKPA, Research Triangle Park, NC, 27711, March 1976. 13. Krenkel PA:. Waste treatment maehodology. (Sam, ed.), 1974. 14. Levy BS, et al: Investigating poasibl* effaces of asbestos in city watsr: surveillance of gastrointestinal cancer incidence in Duluth, * Minnesota. Aa J Epidemiol 103: 362-366, 1976. 15. Lawrence J, et al: Asbestos: Res Dev Nov/Dec: 29-30, 1973. 16. Lawrence J, «e al: In Industrial Pollution ““ its rsaoval from potable water. Can Renovel of asbestos fibers from potable water by coagulation and filtration. Water Research 9: 397-400, 1975. 17. Baumann 8£: Diatoadte Filters for Asbestifom Fiber Removal from Water. Proc of Aa Water Works Assoc, 95th Annual conf, Minneapolis, 1975. 18. Federal Register 40(6): 1873-1878, 1975. 19. U.S. Environmental Protection Agency: National emissions standards for hazardous sir pollutants: Amendments to standards for ssbsseos end mercury. Federal Redaear 40(199): 48292-48302, Oct. 14, 1975. 20. Harvood CF, Aas P, and Selnson Mt Study of eh* Effect of Asbestos Waste Piles on Aaftlene Air. .In Proc of Symp on Fugitive Emission Measurement sad Control. Washington D.C., Environmental Protaetion Agancy, EPA Publ FEPA-600/2-76-246, p. 183-202, Sapt. 1976. Chapter VII 1. Tokuhata CK: Cancer of the lung: host and environmental interaction In Cancar Genetics (Lynch HT, Thomas CC, ed.), Springfield, Illinois, 1976. 2. Cole P, Goldman MB: Occupation. In Pereone at High Risk of Cancer (Fraumeni Jr., F, ad.) New Tork, Acadamie Presa, 1975, pp. 167-183. dU7 O931019 H-21 DU 035556 evil) 3. Montgomery RD, Stirling GA, Hamer NAs Bronchiolar carcinoma la progreeaive ayatenic aclaroaia. Lancac 1: 486-487, 1964. 4. Godeau P, at al: Carcinoma bronehioloalveolaira ae aelerodaraie. San Hop Paria SO: 1161-1168, 1974. 5. Koch BL: Fanilial fibrocyatie pulmonary dyaplaaia: In ona family. Can Mad Aaaoe J 92: 801-808, 1963. 6. Svaya P, at al: Pasilial. Hannan-Rich Syndroaa: caaaa. Diaeaaea Qiaat 55: 7-12, 1969. 7. McKuaick VA, Piahar AM: Congenital cyaeie diaaaaa of eha lung with progreaaiva pulmonary fibroaia and careinoaatoaia. Ann Int Mad 48: 774-790, 1958. 8. Boucoc KR, «c al: Cigarattaa, cough, and cancer of the lung. 196: 985-990, 1966. 9. Campbell AH, Lea BJ: The ralationahip batwean lung cancar and chronic bronchieia. Br J Dis Cheat 57: 113-119, 1963. 10. Dean G: Lung cancer and bronchitla in Northern Ireland, 1960-2. Br Med J 1: 1506-1514, 1966. 11. Van dar Wal AM, at al: Cancar and chronic non-epecific lung diaaaaa. Scand J Reap Die 47: 161-172, 1966. 12. Wyndar EL, Fairchild, Jr. EP: The role of a hiatory of peraiacanc cough in'the epidanlology of lung aancar. An Rev Reap Die 94: 709-720, 1966. 13. Tokuhata GJC, Lilianfald AM: Fanilial aggregation of lung cancer in huaana. J Natl Cancer Inat 30(2): 289-312, 1963. 14. Cohen BH, at al: A cornea fanilial co^onant In lung cancar and chronic obatructlve pulnonary diaaaaa. Lancet il: 523-526, 1977. 15. Vagner JC, at al: The affacta of inhalation of aabeetoa in rata. Br J Cancar 29: 252-269, 1974. 16. Kelleraann C, Luytan-Kellarnan M, Shaw CR: Genetic variation of aryl hydrocarbon hydroxylaaa in human lyaphocytaa. An J Hun Genet 25: 327-331, 1973. 17. Kelleraan G, Shaw CR, Luytan-Kallerme&n H: Aryl hydrocarbon hydroxylaae lnducibility and bronchogenic carcinone. N Engl J Mad 289(18): 934-937, 1973. obearvationa raport of eight H—22 JAMA DUP 0931820 DU 035557 «<* (VII) 13. Shaw CR: The microeomal mixed function oxidases and chemical carcinogens. In Isozymes III Developmental Biology. San Francisco, Academic Press, Inc., 1975. 19. Paigen 3, ee al: Questionable relation of aryl hydrocarbon hydroxylase to lung cancer risk. N Eng J Med 297(7): 346-350, 1977. 20. Saccomanno G, at al: In exfoliated cells. 21. Lllienfeld A (Chairman), at al: Aa evaluation of radiological and cycologlcai screening for early detection of lung cancer. A co­ operative pilot study of the American Cancer Society and the Veterans Administration. Cancer Res 26: 2033-2147, 1966. 22. SRI International. 23. Hammond EC: Tobacco. In Persona at High Risk of Cancer. (Prauaeni Jr., JP, ed.) Hew York, Academic Press, 1975. 24. Rothman KJ: Alcohol. In Persona at High Risk of Cancer. (Fraumenl, Jr., J?, ed.) New York, Academic Press, 1975. 23. Lynch KT: Miscellaneous problems, cancer, and genetics. Genetics. Springfield, Illinois, CC Thornes, 1976. Development of carcinoma of the lung aa reflected Cancer 33(1): 256-270, 1974, Personal communication with G Saccomanno, November 1976. In Cancer 26. 3RZ International. Personal coamamlcatlon, EA Geenelcr, October 1976. 27. Velas V: Cigarette smoking, asbestos, and pulsunary fibroaia. Rev Resplr Die 104: 223-227, 1971. 28. Tumar-Wanrlck K: Immunology and aebeetosla. In Biological Effacta of Asbestoe (Bogovskl P, et al., ads.). Lyon, France, International Agency for Research on Cancer, Scientific Pub, Ho. 8, 1973, pp. 258-263. 29. Rang M, at al: 735-736, 1974. 30. Merchant JA, ee ml: 1: 189-191, 1975. 31 Beeklaka KR: Aabea cos-related diseases of Che lung and ocher organs, their epidemiology and implications for clinical practice. Am Rev Reepir Die 114: 187-227, 1976. 32. Brett GZ: The value of lung cancer detection by sir-monthly chase radiographs. Thorax 23: 414-420, 1968. T-lymphoeytaa in aabeacoals. Aa N Engl J Had: 291: The HL-A system in asbestoe workers. H-23 DU 035558 Br Mad J (VII) 33. Boucot KR, Weiss V: la curable lung cancar detected by semiannual screening? JAMA 224(10): 1361-1365, 1973. 34. Lilienfeld AM, Kordan B: A study of variability in cha interpretation of cheat X-raya in the detection of lung cancer. Cancer Rea 26: 2145-2147, 1966. 35. Archer PG,~ et al: A acudy of variability in the interpretation of sputua cytology slidea. Cancer Rea 26: 2122-2144, 1966. 36. Fontana RS, et al: The Mayo lung project for early detection and Localization of bronchogenic carcinosa, a acacua report. Chest 67: 511-512, 1975. 37. Fontana RS: Early diagnoaia of lung cancar. 399-402, 1977. 33. Welsa W, Saldana H, Boucot KR: The Philadelphia pulmonary neoplaaa research project: thwarting factors in period screening for lung cancer. Aa Rev Reap Dla 111: 289-297, 1975. 39. Baker RB, et al: The detection and treatment of eerly lung cancer. Ann Surg 179(5): 813-318, 1974. 40. Grzybowskl S, Coy ?: Eerly diagnoaia of carcinoma of the lung: simultaneous screening with cheat X-ray and sputua cytology. Cancar 23: 113-120, 1970. 41. Whitvell F, Newhouae ML, Bennatt DR: A study of the histological types of lung cancer in workers suffering froa aabeatoala in tha United Kingdom. Sr J Ind Mad 31: 298-303, 1974. 42. International Labour Office: ILO-U/C classification of radiographs of pneyaoconiosea. Geneva, Switzerland, 1971. 43. Elaae PC: The natural history of diffuse mesothelioma. In Biological Effaces of Asbestos CBogoveki ?, at al., ads.). Lyon, Franca, International Agency for Research on Cancer, Scientific Pub. tto. 8, 1973, pp. 267-272. 44. Rises PC, Sispson MJC: The clinical aspects of meaothallone. Mad, Maw Series, XLV (179): 427-449, 1976. 45. Viaever SJ, at al: Feasibility of fecal occult-blood eeseing for detection of colorectal neoplasia: debits and credits. Cancer 40 (Sup 5): 2616-2619, 1977. 46. Stephens F0, Lawreaaou 10: The pathologic significance of occult blood In faces. Die Colon Rectus 13(6): 425-428, 1970, Aa Rev Reap Dla 116(3): Quart J vat o’318” H-24 DU 035559 (yin (yin) ^7. Gresgor DH: Occult blood casting for detection of asymptomatic colon cancer. Cancsr 28(1): 131-134, 1971. 48. Ostros JD, et al: Sensitivity and reproducibility of chemical testa for fecal occult blood with an emphasis on false-positive reactions. Aa J Dig Die 1801): 930-940, 1973. 49. Sherlock P, Winavar SJ: Modern approaches to early identification of large-bowel cancer. Aa J Dig Die. 19(10): 939-9.64, 1974. 50. Prolla JC, Kobayaahi S, Kirsner JB: Mad 124: 239-246, 1969. 51. Selikoff IJ: The occurrence of pleural calcification aaong asbestos insulation workers. Ann NY Acad Sci 132: 331-367, 1965. 52. Vogt TM, et al: Expired air carbon monoxide and serua thiocyanate as objective measures of cigarette exposure. Aa J Public Health 67: * 545-549, 1977. Gastric cancer. Arch Intern Chapter VIII 1. Code of Federal Regulations. Title 29. Chap. XVTI, Subpare z. Section 1910.1003-1910.1029. 2. Committee on Public Iafonutlon In the Prevention of Occupstionsl Cancer, Division of Medical Sciences, Asseably of Life Sciences, National Research Council: Informing Workers and Employers about Occupstionsl Cancer. Washington, D.C., National Academy of Sciences, 1977, p. 26. 3. Felton.JS: Health education--s responsibility of the occupational health professional. J Ocepp Mad 19: 346-350, May 1977. 4. Felton JS: Orltneiag the new employes in the services of the industrial medical department. Indust Med 16: 319-525, November 1947. 5. Felton JS: Orientation of the new employee by the health divieion of an atomic energy research laboratory—a four-year review. Induet Mad add Surg 21: 107-110, March 1952. 6. Expert Committee on Health Education of the Public—First Report, Geneva, World Health Organization, October 1974, p. 22. 7. Scope, Objectives, and Functions of Occupstionsl Health Programs (Revised December 1971). Chicago, American Medical Association, 1971. 8. Moser RH: Psychossnanelcs (On Spsakiag to Patients). Medical Progress: A Study of Iatrogenic Disease, Ed. 3. ad.). Springfield, Illinois, CC Thomas, 1969, p. 812. Dissssss of Otossr RH, DUP 0931823 S-25 DU 035560 n_' jaaiaift, jeMiM-t is< ^aE.i,£3BgiBm.fl (VIII) •: 9. Council on Occupational Health, American Medical Aasociacion: The Sola of Medicine Within a Buainaaa Organization. JAMA 210t (Nov 24) 1969. 10. Joint Statenant of tha Role of tha Raglaterad Nuraa in Employe* Health Prograaa—California Madical Aaaoelation, California Nuraaa' Aaaociatlon, California Hoapltal Aaaoelation, in Joint Stataoanta (of tha Aaaociatlona). Sacramento California Nuraaa* Aaaociatlon, 1972, p 27. U. Sanuala 3: I Cancer. In Public Information In tha Pravanelen of Occupational Proceeding* of a Sjnnposiua held in Waahington, O.C. Deceaser 2-3, 1976. Waahington, D.C., National ttaaaarch Council, National Academy of Sdancaa, 1977, p. 147. 12. Mancuao, Tf: Halp for tha Working Wounded. Waahington, D.C., National Aaaociatlon of Maehiniata and Aaroapaca Worker*, 1976. #U.J. SOVeNJMNT MMTINO 0*»Wi 1*7* C— iM-Ott-mS IMION >1 DO? 0931S24 H-26 DU 035561 AC/ NMana Cancar MMara OhEW Puolication Numear (NIH) 79-1681 DUP 0931825 DU 035562