Document vVRjQZopbxb4RD5djLOraRXy9

PRELIMINARY AIR POLLUTION SURVEY OF ASBESTOS A LITERATURE REVIEW i i Ralph J. Sullivan Yanis C. Athanassiadis Litton Systems, Incorporated Environmental Systems Division Prepared under Contract No. PH 22-68-25 I U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE Public Health Service Consumer Protection and Environmental Health Service National Air Pollution Control Administration Raleigh, North Carolina October 1969 8000 ]<*{>< SCF-FA-6270 PRODUCED BY FORD ___ / -- 4 The APTD series of reports Is Issued by the National Mr Pollution Control Administration to report technical data of interest to a limited reader ship. Copies of APTO reports may be obtained upon request, as supplies permit, from the Office of Technical Information and Publications, National Air Pollution Control Administration, U.S. Department of Health, Education, and Welfare, 1033 Wade Avenue, Raleigh, North Carolina 27605. National Air Pollution Control Administration Publication No. APTD 69-27 1 I 11 8000 1^05 ' PRODUCED BY FORD FOREWORD As the concern for air quality grows, so does the con cern over the less ubiquitous but potentially harmful contami nants that are in our atmosphere. Thirty such pollutants have been identified, and available information has been summarised in a series of reports describing their sources, distribution, effects, and control technology for their abatement. A total of 27 reports have been prepared covering the 30 pollutants. These reports were developed under contract for the National Air Pollution Control Administration (NAPCA) by Litton Systems, Inc. The complete listing is as follows: Aeroallergens (pollens) Ethylene Aldehydes (includes acrolein Hydrochloric Acid and formaldehyde) Hydrogen Sulfide Ammonia ` Iron and Its Compounds Arsenic and Its Compounds Manganese and Its Compounds Asbestos Mercury and Its Compounds Barium and Its Compounds Nickel and Its Compounds Beryllium and Its Compounds Odorous Compounds Biological Aerosols Organic Carcinogens (microorganisms) Pesticides Boron and Its Compounds Phosphorus and Its Compounds Cadmium and Its Compounds Radioactive Substances Chlorine Gas Selenium and Its Compounds Chromium and Its Compounds Vanadium and Its Compounds (includes chromic acid) Zinc and Its Compounds These reports represent current state-of-the-art literature reviews supplemented by discussions with selected knowledgeable individuals both within and outBide the Federal Government. They do not however presume to be a synthesis of available information but rather a summary without an attempt to interpret or reconcile conflicting data. The reports are 111 6000 1406 PRODUCED BY FORD iririnitfi & mma necessarily limited in their discussion of health effects for some pollutants to descriptions of occupational health expo sures and animal laboratory studies since only a few epidemio logic studies were available. Initially these reports were generally intended as internal documents within NAPCA to provide a basis for sound decision-making on program guidance for future research activities and to allow ranking of future activities relating to the development of criteria and control technology docu ments. However, it is apparent that these reports may also be of significant value to many others in air pollution control, such as State or local air pollution control officials, as a library of information on which to base informed decisions on pollutants to be controlled in their geographic areas. Addi tionally, these reports may stimulate scientific investigators to pursue research in needed areas. They also provide for the interested citizen readily available information about a given pollutant. Therefore, they are being given wide distribution with the assumption that they will be used with full knowledge of their'value and limitations. This series of reports was compiled and prepared by the Litton personnel listed below: Ralph J. Sullivan Quade R. Stahl, Ph.D. Norman L. Durocher Yanis C. Athanassiadis Sydney Miner Harold Finkelstein, Ph.D. Douglas A. Olsen, Ph.D. James L. Haynes iv &.000 1<&7 PRODUCED BY FORD The NAPCA project officer for the contract was Ronald C. ' Campbell, assisted by Dr. Emanuel Landau and Gerald Chapman. ; Appreciation is expressed to the many individuals both outside and within NAPCA who provided information and reviewed draft copies of these reports. Appreciation is also expressed to the NAPCA Office of Technical Information and Publications for their support in providing a significant portion of the I technical literature. i I t . i 6000 1^06 PRODUCED BY FORD ABSTRACT Inhalation of asbestos may cause asbestosis, pleural or peritoneal mesothelioma, or lung cancer. Mesothelioma is a rare form of cancer which occurs frequently in asbestos workers. All .three of these diseases are fatal once they become established. The dose necessary to produce asbestosis has been estimated to be 50 to 60 million particles per cubic foot-years. No information is available on the dose necessary to induce cancer. Random autopsies of lungs have shown "asbestos bodies" in the lungs of one-fourth to one-half of samples from urban populations. Thus, the apparent air pollution by asbestos reaches a large number of people. Animals have been shown to develop asbestosis and cancer after exposure to asbestos. No information has been found on the effectB of asbestos air pollution on plants or materials. The likely sources of asbestos air pollution are uses of the asbestos products in the construction industry and asbestos mines and factories, observations in Finland and Russia indi cate that aebestoB does pollute air near mines and factories. However, no measurements were reported of the concentration of asbestos near likely sources in the United states. A concentra tion in urban air of 600 to 6,000 particles per cubic meter has been estimated. Bag filters have been used in factories to control vl 1 -- V." 8000 1409 PRODUCED BY FORD I j , i '< : asbestos emissions; the cost of this type of control in a British factory was approximately 27.5 percent of the total capital cost and about 7 percent of the operating cost. No information has been found on the costs of damage resulting from asbestos air pollution. No satisfactory analyticalmethod is available to determine asbestosin theatmosphere. ; I < i | j i J | j j * . I i i ij ' -l v t i i l vl 11 8000 1M0 t PRODUCED BY FORD j LIST OF TABLES 1. Deaths of Asbestos Insulation Workers in New York* 1963-67 ......................................................................................................... 16 2. Distribution of "Asbestos (Ferruginous) Bodies" in Lungs in Pittsburgh........................................................................... 20 3. Type and Number of Tumors Induced by Intrapleural Inoculation of S.P.F. Rats with Asbestos.................... 22 4. Dust Counts in Asbestos Mines and Mills in South Africa, 1947 .......................................................................................... 29 5. Cancer of the Lung Among Asbestos Workers l . . . . 62 6. "Asbestos Bodies" in Consecutive or Random Autopsies ......... ....................................................... 64 7. Composition and Properties of Asbestos ...... 66 B. World Production of Asbestos .................................................. 69 9. The Production and Apparent Consumption of Asbestos . in the United States............................................................ .... 71 10. Regional Distribution ofAsbestos Mining and Processing............................................................................................... 72 11. Asbestos Mines in the United States, 1966 .................... 73 12. Apparent Asbestos Consumption, 1965 ................................... 74 13. Proportion of Asbestos in VariousAsbestosProducts 75 14. Quantity and Value of Asbestos Input by Industry, 1963 75 . 15. Population Groups with Occupational and Environmental Exposure to Asbestos.................... ..... ............................................ 76 16. Asbestos Control Equipment .................................................. 77 17. Analysis of Asbestos and Asbestos Products Exports and Imports......................................................................................... 78 18. Selected Statistics for theAsbestosManufacturing Industry ................................................... 79 i iI : ix PRODUCED BY FORD LIST OF TABLES (Continued) 19. Selected Statistics for the Asbestos Products In dustry ................................... .... ............................................. .... 80 20. Asbestos Uses ............. ..................... 81 21. 1967 List of Manufactured Asbestos Products ... 84 22. Asbestos Product Manufacturing Plants, 1963 ... 86 23. Penetration of Fibers Through Nasal Hairs .... 93 24. Particle-Mass Relationship of Asbestos as a- Function of Fiber Length............................................................................... .93 LIST OF FIGURES 1. Comparison of Trends in World Production and U.S. Consumption of Unmanufactured Asbestos ....... 30 X 0600 1M2 PRODUCED BY FORD FOREWORD CONTENTS ABSTRACT 1. INTRODUCTION .......................................................................................... 1 2. EFFECTS.......................................... 3 2.1 Effects on Humans.......................................... 3 2.1.1 Asbesto6is ...... ....................................... 4 2.1.2 Pleural Calcification andPlaques ... 2.1.3 Cancer ........................................................... . . . . 6 7 2.1.3.1 Cancer of theLung.......................... 2.1.3.2 Mesothelioma of the PleUra and 7 Peritoneum................................................ 11 2.1.3.3 other Cancers 15 2.1.3.4 Synergism...................................... .... . 15 2.1.4 "Asbestos Bodies" ...................................... .... . 17 2.2 Effects on Animals .............. 20 2.2.1 Cotwnercial and DomesticAnimals .... 20 2.2.2 Experimental Animals .................................................21 2.3 Effects on Plants........................................................................ 24 2.4 Effects on Materials .......................... ....... 24 2.5 Environmental Air Standards.................................................24 3. SOURCES........................... 26 3.1 Natural Occurrence .............................................................. 26 3.1.1 Mines .................................................................. 26 3.2 Production Sources .............................................................. 29 3.3 Product Sources..................................................... . . 31 3.4 Environmental Air Concentrations..... 33 4. ABATEMENT .................................................................................... 35 5. ECONOMICS............................................................................... 37 6. METHODS OF ANALYSIS.............................................................................33 REFERENCES.................................................................................................... 41 APPENDIX A...........................................................................................................61 APPENDIX B ....... ..................................................................... Xl 8000 1413 * *" PRODUCED BY FORD 1 1. INTRODUCTION . Asbestos is a general name given to a variety of useful fibrous minerals. The value of asbestos ensues from the indestructible nature of products fabricated from the various grades of mineral fibers. The major asbestos minerals are chrysotile, crocidolite, amosite, and anthophyllite,. while . tremolite and actinolite are considerably less important. Over 90 percent of the asbestos is chrysotile. The United States uses about one-fourth of the world production of this substance, practically all imported from Canada and Africa. Inhalation of asbestos dust has long been recognized as 161,165 an industrial hazard. Early in this century, exposure to high concentrations of the fibrous dust was causally associated with asbestosis. In 1935, evidence began to accumulate that cancer of the lung i6 also associated with inhalation of asbestos.55 More recently, certain rare cancers, pleural mesotheliomas and peritoneal mesotheliomas, have been associated with inhalation of asbestos fibers by asbestos workers* 176 Heimann92 states that "The finding of several such rare tumors in any given group makes that group suspect of having special and distinct environmental characteristics, _ in this case, exposure to asbestos duBt." Nonoccupational environmental exposure to asbestos was found as early as 1927 vfoen Haddow81 reported finding 60called "asbestos bodies" in the lungs of a person living near rfifrV --iiPuwiiujJit 8000 19)<< PRODUCED BY FORD HIMIAWI 2 an asbestos factory. Since then, several investiga- have reported finding .neighborhood cases. The subject of nonoccupational environmental exposure to asbestos assumed a new dimension beginning with the re ports of Thomson and his colleagues.213-216 After examining the lungs in consecutive autopsies, they found that approximately one-fourth of the populations in both Capetown, South Africa, and Miami, Fla., have "asbestos bodies" in their lungs. Other investigators have confirmed that one-fourth to one-half of the population in Pittsburgh,^ San Francisco, Milan,^ Glasgow,^ New York,^^ Montreal.^ Jerusalem, # Finland, 167 and Sweden82 have "asbestos bodies" in their lungs. These findings indicate that either these asbeBtos particles or other particles that resemble asbestos in many ways, in- eluding the way in which the body reacts to them, are being inhaled either with the ambient urban air or through direct exposure to asbestos. * , : i ' ! ! t * j j { i 6000 14*5 PRODUCED BY FORD 3 2. EFFECTS 2.1 Effects on Humans Asbestosis (a diffuse pulmonary fibrosis), pleural calcification, pleural plaques, lung cancer, and pleural and peritoneal mesotheliomas can result from exposure to asbestos. Asbestos bodies are commonly found in the lungs of persons exhibiting these complications. Diagnosis of any of these or finding "asbestos bodies" in the lungs signifies the need to review the case history for previous asbestos exposure. Surveys of people living or working near asbestos mines and factories have revealed that many nonoccupational cases of asbestosis and mesothelioma have occurred either from the polluted air or from asbestos carried home on the workers* 175,176,178 clothing. However, in many cases no exposure to asbestos can be established. The fate of the asbestos fiber once it is inhaled* and deposited in the lung is Btill questionable. The 6hort fibers, <0.5 P in length, have been pathologically ignored, probably because they are much too narrow to be visible under a light microscope. The longer fibers which are encrusted in an iron bearing protein (asbestos bodies) become easily visible. Wagner and Skidmore228 and Morris jst al.. 172 have shown that rats which have inhaled asbestos lose the asbestos (probably the short fibers) from their lungs. The biological half-life *A discussion on respirable fibers is presented In Appendix B (page 92). 8060 lil6 PRODUCED BY FORt> r i for asbestOB appears to be 20 to 90 days, depending on the .mineral type. Some of the fibers are removed by phagocytosis to the lymph nodes. 2.1.1 Asbestosis Among asbestos workers, evidence of pulmonary asbestosis is common. This condition results in a diffuse fibrosis, usually in the lower lobes of the lung. Pulmonary asbestosis has been called a monosymptomatic disease, with dyspnea as the main complaint. The British Occupational Hygiene Society1,3" has reported that basal rales are the first symptoms of asbestosis. Asbestosis usually develops after long exposure to high concentrations of asbestos dust. The risk varies directly with the length of exposure and the dust concentration. Following continued exposure to high concentrations of dust, asbestosis may develop fully in 2 to 9 years and may cause death as early as 13 years from onset of exposure. The common exposure period before recognition of asbestosis (as observed among asbestos workers) iB 20 to 40 years, with death following about 2 to 10 years later. Once established, asbestosis progresses even after the exposure to dust ceases: illness or death can occur long after exposure to concentrations not producing immediate effects.19^ The prolonged latency period between exposure and the first signs of asbestosis makes it difficult to establish dosetime relationships. Cooper 4 3 suggested that a time-weighted i | j j | ! | I j ; i I : ^ ! | j ' i i i ! | &00Q 1417 ' PRODUCED BY FORD 5 average concentration of asbestos fibers of 5 mppcf** *is too ' hi.gh. He ci.tes Wells' 234 idea that multiplying average counts by years of exposure provides a rough guide to the total dose allowable. After 50 to 60-mppcf-years, workers began to show evidence of asbestosis. At an average concentration of 5 mppcf, this total allowable dose would be reached in 10 to 12 years. Unfortunately, dust concentrations have been infre quently reported and measurements have been hampered by the varied nature of the sources. Marr1^3 and Selikoff et al.**** have reported that insulation workers are exposed to dust concentrations below 5 mppcf, yet have exhibited a high prevalence of asbestosis. Thus, Cooper's argument is strengthened. In 1946, there were about 700 cases of asbestosis in Germany among a total of approximately 8,000 employees in the 108 235 asbestos industry. Negelius found 125 cases qf;.asbestosis of the lung in X-ray examinations of 476 asbestos workers in a one company in Finland. Of 132 asbestos workers examined by Bohme, 29 percent showed X-ray evidence of asbestosis. The occurrence of asbestosis in members of this worker group rose with the duration of the employment< 5 percent in workers exposed to asbestos for less than 3 years; 56 percent for those employed for 5 to 10 years, and 79 percent for those with over 10 years' exposure. A similar morbidity of 80 percent among *5 million particles per cubic foot based on total dust count and 8-hour-day, 40-hour-week exposure. mmnipjiwi n i ... ........... BbOO 1418 PRODUCED BY FORD mm*Sd ___ .^k... <# 4 English asbestos workers with over 20 years of employment waB reported by Merewether and Price*^ in 1930. Noro*77 noted that the incidence of asbestosis was 65 percent in 167 asbestos workers studi.ed by X-ray. Selikoff t. 197 investigated 1,522 asbestos insulation workers in the New York-New Jersey metropolitan area. Among 392 individuals examined more than 20 years from the onset of exposure, X-ray evidence of asbestosis was found in 339. in half of these, the asbestosis was moderate or extensive. In individuals with less than 20 years of exposure, radiological evidence of asbestosis was less frequent and when present, was much less likely to be extensive. 2.1.2 Pleural Calcification and Plagues Pleural calcification resulting from exposure to asbestos . 120 16 usually bilateral and affects the parietal pleura. 193 Selikoff stated that bilateral pleural calcification involving the diaphragm is diagnostic of asbestosis. Thi6 pleural calcifleetion can be readily identified by X-ray.**7 Kiviluoto120 discovered 499 cases of pleural calcifica tion during a community X-ray survey of 6,312 adults in the Kuu6jari commune in Finland. In Ilomantsi commune he found no such calcification among 7,101 adults. He observed that the Kuusjari commune contained an asbestos mine and suggested that these people had been subject to a localised environmental asbestos exposure. This investigator 121 also observed 77 cases of pleural plaques out of 35,000 routine chest X-rays. The case histories of these 77 revealed that 52 had previous BOOO 1*19 i PRODUCED BY FORD 7 .>vv'-'sure to asbestos either in the home or in their occupations, where they handled asbestos products. Of the Other 25 persons, 16 were questioned and no previous asbestos exposure could be ascertained. Raunioi86 continued the study And found 1,516 adult cases of pleural calcification from 633,201 x-rays taken in 13 Finnish towns and 106 rural communes. In Tuusniemi commune, where an asbestos quarry is- located, pleural calcifi cation was found in 9 percent of the population? in urban populations it was found in 0.7 percent of the people; and in rural areas calcifications were found in only 7 out of 265,273 people examined (0.002 percent). However, Meurman1^ found the pleural plaques were common (39.3 percent of his cases) in all Finland. Approximately 2.B percent of the agricultural workers in Czechoslovakia*^ an(j Bulgarians have also been shown to have appreciable pleural calcification. In Bulgaria the soils worked by the farmers contained asbestos: even stone fences were made of outcrops of anthophyllite mineral. However, in Czechoslovakia no asbestos or known exposure to asbestos was found. After examining children living in the city of Asbest in the Soviet Union, Bobyleva fit jl.^*^ concluded that they were suffering from impaired health caused by air pollution from asbestos plants. ' 2.1.3 Cancer 2.1.3.1 Cancer of the Lung The most common complication of asbestosis is cancer of the lung. However, cancer of the lung apparently induced by PRODUCED BY FORD if'l mmtammm 8 asbestos may appear unaccompanied by a&bestosis. . The association of lung cancer with exposure to asbestos dust has been the subject of many investigations in the second quarter of this century. In 1935, Lynch and Smith in the United States described lung cancer found during autopsy of a patient with asbestosis. According to Homburger' s data,i0i over a 20-year period eight cases of asbestosis were found in 4,137 autopsies at the medical school of Yale University. Of these eight asbestosis cases, four were associated with lung cancer (SO percent). In contrast, lung cancer was found in only two (12 percent) of 17 cases of silicosis. Lynch and Cannon 147 in 1949 found lung cancer in only three cases (7.5 percent) of 40 patients with asbestosis. Gloyne71 in 1951 reported that according to autopsy data for the London Hospital of Chest Diseases, lung cancer was observed in 14 percent of the 121 patients with asbestosis, but in only 6.9 percent of those with silicosis. Usually, the lung cancer incidence in men is four to six times higher than in women, but among patients with asbestosis it is Only twice as high for men. This ha6 been confirmed by Bohlig, Jacob, and Kalliabis. They note that among women working in the asbestos industry, lung cancer is observed at an earlier age than among the rest of the population. In his review, Behrens 19 rep'orted 44 cases of lung cancer (14 percent) in 309 autopsies of patients with asbestosis. After examining . 8000 i42) PRODUCED BY FORD 9 the data of various authors, Xsselbacher gt, al..*** reported that of 603 persons vith asbestosis, lung cancer was found in 83 (13.8 percent) at autopsy. Hueper*^ and Doll^ record an even higher percentage (15 percent). Doll emphasizes that the majority of those who died had worked under conditions of high dust content in the air. 33 Braun and Truan found lung cancer in 12 (three cases were not conclusive) of 1B7 workers in the Canadian asbe6toB industry who had died. Boehme reported 74 patients with asbestosis; lung cancer was found in six of these. The average age of the patients was 53; the average period from the beginning of work to death was 28 years. Keal 114; points out that of 30 patients with asbestosis, 14 (47 percent) died of lung cancer and 10 from carcinoma of the peritoneum or ovaries. Some additional statistics on the association of lung cancer with asbestos workers are listed in Table 5 in the Appendix. Cancer of the lung produced by asbestos needs further study. The latent period between exposure and evidence of carcinoma may be even longer than for asbestosis. Hothing is known about the dose-time relationship. Cases of lung cancer have been observed when only a very short exposure or no exposure to asbestos was known. Furthermore, the low number of "asbestos bodies" observed in one-fourth to one-half of the urban population may be sufficient to cause cancer. Because 8000 PRODUCED BY FORD 10 the long "asbestos bodies" remain in the lungs, a person who has inhaled asbestos may carry the potential (for the rest of his life) to develop carcinoma of the lung. Moreover, it has not been determined whether more than one fiber is necessary to induce a malignant tumor. Cox^ has suggested that the probability of cancer induction is proportional to the number of asbestos fibers, number of susceptible cells, the concen tration of carcinogens on the fibers, and the time from exposure. Why asbestos is carcinogenic is not clearly understood. At least three hypotheses have been advanced* . (1) That the fibers act as a physical irritant vhich after 20 to 30 years of constant irritation induces a tumor. (2) That the fibers contain small amounts of carcinogens-- such as bento (a) pyrene, nickel, and chromium--vAtich are eluted from the fibers by the serum in the lungs. These carcinogens then produce the cancer. Harington and Roe80 have shown that (a) chrysotlle contains little or no benzo(a)pyrene, but about 100 M9 of chromium per g of fiber and 5,000 ug of nickel per g of fiber? (b) croeidolite contains 0.2 to 24 ug of bento(a)pyrene per 100 g of fiber and negligible amounts of nickel and chromium; and (c) amosite contains 0.2 to 2.4 ug of bentota)pyrene per 100 g of fiber, 100 wg of nickel per g of fiber and 15 ug of chromium per g of fiber (see Appendix B, page 92). The authors have not only shown that these agents can be dissolved in the lung serum, but also that airborne fibers can adsorb 8000 i<*23 PRODUCED BY FORD 1 11 ituitions present in the air. In studies of the adsorption of benzo(aJpyrene by asbestos, chrysotile adsorbed 100 percent of benzo(a)pyrene from solution after 48 hours at 37C, compared with 40 percent for crocidolite and 10 percent for amosite. Harington and Roe suggest that these carcinogens can be adsorbed on airborne fibers. Thu6, the fibers become a transporting vehicle to carry a concentrated quantity of carcinogens into the lung. (3) That the fibers accumulate in the lung and are immobilized as "asbestos bodies" which disintegrate after 20 to 40 years. The resulting free particles cause asbestosis or carcinoma of the lung. In addition, Hammond . has suggested that asbestos is a cocarcinogen; i.e., it increases the cancer-producing poten tial of 6mall amounts of some other agent. In a study of asbestos workers, he and his colleagues 199 found cancer of the lung only in cigarette 6mokers. The number of deaths attributed to cancer of the lung was eight times higher in asbestos workers who smoked cigarettes than in smokers who were not exposed to asbestos (see Section 2.1.3.4). 2.1.3.2 Mesothelioma of the Pleura and Peritoneum Primary tvonors of the pleura and peritoneum are so rare that for years they were considered to be pathologic curiosi ties. In 1960 the first large series of cases of diffuse mesothelioma were reported by Wagner et. 229 in South Africa. ' 8000 ia?4 PRODUCED BY FORD 12 . * 226 In trying to explain this mysterious epidemic, Wagner, * noting that "asbestos bodies" were found in the lungs of some of their patients, obtained detailed life histories of these patients. By 1960, he was able to establish an association with exposure to the Cape of Good Hope asbestos fields, or the industrial use of asbestos, in 32 of 33 patients with histolog ically proved pleural mesothelioma. The majority of these patients had not actually worked with asbestos but had lived in the vicinity of the mines and mills, and some had left these areas of exposure as young children. The average period between exposure and development of the tumor was 20 to 40 years. By 556 1962, Wagner had diagnosed a total of 87 pleural and two peritoneal mesotheliomas. In only two cases was it impossible to establish a history of exposure to asbestos dust. Of these B7 cases, 12 had been industrially exposed and the remainder had been environmentally exposed from living in the vicinity of the mills and dumps. This association between mesothelioma and asbestosis became even more intriguing when in 1955, Bonser et al. 30 described a series of 72 autopsies on patients with asbestosis in which four cases of peritoneal mesothelioma were 152 found. Subsequently, Mancuso and Coulter found five peritoneal mesotheliomas in 1,495 asbestos workers, and Hourihane, 102 upon reviewing the necropsy files of the London Hospital from 1917 to 1962, found 34 cases of mesothelioma, half of the pleura and the other half of the peritoneum. All i Ii I i \I i 8006 PRODUCED BY FORD I 13 of these patients had pulmonary asbestosis, even though in a few there was no history of exposure to the asbestos dust. In 103 a subsequent study Hourihane found 74 cases of mesothelioma in a London hospital over a 10-year period. Borow et, o. 31 report that in two years they observed 11 cases of mesothelioma during surgery in New Jersey. These cases, added to six others previously diagnosed by them, totaled 17 cases of mesothelioma, eight of which were peritoneal and nine pleural. They suggest that the high prevalence of these rare tumors in New Jersey can be explained by its close proxim ity to a major asbestos mill, where a large percentage of all the asbestos fiber mined in North America is converted to commercial use. In an attempt to determine whether mesotheliqma of the serosal surfaces was related in any way to asbestos exposure in the United States, Selikoff e_t a 1. 198 studied 307, consecutive deaths among asbestos insulation workers in the Northeastern United States. They found 10 deaths caused by four pleural and six peritoneal mesotheliomas. In addition, these workers had a high death rate attributed to cancer of the stomach, colon, and rectum. Of the 307 deaths, 40.4 percent were attributed to cancer, 5.5 percent to asbestosis, and 54.1 percent to other causes. In a second study, the investigators reviewed 26 consecutive autopsies of patients with asbestosis, and found four mesotheliomas of the pleura and three of the peritoneum.' ^fjinjuMii|iki|i.i .. . 8000 1426 ...... ........ ' PRODUCED BY POR n iViliiiiiiiiirf Mwiiiktliaa rtvAitiia 14 A series of B3 patients from the London Hospital with 6 diagnosis of mesothelioma (confirmed by necropsy or biopsy) were studied by Newhouse and Thompson^^ for possible exposure to asbestos. The series consisted of 41 men and 42 women; 27 of the patients had peritoneal and 56 pleural tumors. Although the earliest death recorded from this group was in 1917, only 10 patients died before 1950, while 40 (48 percent) died between 1960 and 1964. In 76 of the 83 cases, full occupational and residential histories were obtained. Porty patients (52.6 percent) had a history of occupational exposure to asbestos or of domestic exposure (living in the house with an asbestos worker). In comparison, only 11.8 percent (9 of 76) of the patients from the same hospital suffering from other diseases had previous exposure to asbestos. There was also evidence that neighborhood exposures may be important. Among those in this study with no history of occupational or domestic expo sures to asbestos, 30.6 percent of the mesothelioma patients and 7.6 percent of the inpatients with other diseases lived within half a mile of an asbestos factory, of the 31 patients with occupational exposures to asbestos, only 10 held jobs scheduled under the British Asbestos Regulations of 1931. The interval between first exposure .and the development of the terminal illness from mesothelioma ranged between 16 and 55 years. The duration of exposure varied widely, ranging from two months to over 50 years. In 47 patients in this mesothelioma aOOO 1927 PRODUCED BY FORD 15 series, lung tissue or sputum was available for examination. In 30 (62.5 percent), either asbestosis or the presence of asbestos bodies was noted. Mesothelioma is now-considered a frequent cause of death among asbestos workers. No attempt has been made to summarize the reports of mesothelioma, since they appear almost weekly in the current literature. So far, however, there appear to be few cases among the general population. Selikoff 198 reviewed 31,652 deaths among the general popula tion of over 1,048,183 in the United States and found only three cases of mesothelioma. Moreover, he 195 points; out that asbestos is not the only cause of mesothelioma; it has also been produced by silica224 and polyurethane.107 2.1.3.3 Other Cancers Extrapulmonary cancer has also been noted as a cauBe of death among asbestos workers. Kogan et. al_.172 in 1966 reported 14 cases (31.1 percent), 11 women and 3 mep. Pour of the women died of uterine cancer, two of intestinal cancer, two Of breast cancer, and one of liver cancer. Among the men, one died of stomach cancer, another of cancer of the urinary bladder, and a third of cancer of the prostate* Other cases of extrapulmonary cancer have been cited in Section 2.1.3.2. 2.1.3.4 Synergism While the exact cause of lung cancer or pleural peritoneal mesothelioma Induced by asbestos is not known, air pollution by 8000 1928 ' PRODUCED BY FORD 16 other pollutants may accelerate the morbidity. One form of air pollution which is easily studied in individuals is smoking. . Selikoff t al_.199 recently studied the mortality of 370 asbestos insulation workers. in this group 24 men died of lung cancer and all had a history of smoking. (See Table 1 below.) This rate was eight times greater than the expected mortality rate, with age and smoking habits taken into account. TABLE 1 DEATHS OP ASBESTOS INSULATION WORKERS 1H NEW YORK, 1963-67199 (By Smoking Habits) Smokina Habits Never smoked regularly History of pipe, cigarsmoking only History of regular . cigarette smoking Total No. of Cases 48 39 283 370 Observed Deaths O 0 . 24 24 Expected Deaths O.OS 0.13 2.98 3.16 aAll with more than 20 years from onset of exposure. blncludes cigarette smokers who also smoked pipes or cigars. The blue asbestos. crocidolite, from South Africa is believed by many53'79'136' 140,209 to jje muCh more carcinogenic than the other .minerals of asbestos. Studies in Finl,and.167 2 26 Indicate that anthophyllite also produces cancer. Wagner, 8000 1429 L PRODUCED BY FORD 17 Smith et. al.. and recently Godwin and Jagati'c?^ reported that they had induced mesothelioma in mice using chrysotile. Moreover, animal experiments 76,78,98-100,113,172,225,228 have demonstrated that pulmonary complications occur with crocidolite, chrysotile, amosite, and anthophyllite. Some investigators believe that the fiber is not the carcinogenic agent, but rather the vehicle on which the carcinogens are carried to the target tissue. As Btated earlier, chrysotile contains the most nickel and chromium of all asbestos minerals, while crocidolite contains the most benzo(a)pyrene.^9 three of these impurities in asbestos are suspected'of being carcinogenic. This knowledge, together with results which indicate carcinogens can be adsorbed from urban air or tobacco smoke, indicate that there may be no necessity to distinguish urban asbestos dust by mineral types. 2.1.4 "Asbestos Bodies" as stated earlier, the recent finding of "asbestos bodies" in one-fourth to one-half of the urban population (see Table 6 in the Appendix) has added new impetus to the examination of asbestos as a general air pollutant. An "asbestos body" has been defined as "an elongated golden or reddish-brown structure usually with clubbed ends; . the shaft, vftiich often shows a segmented or beaded appearance, is usually straight, but sometimes curvilinear with a tendency toward symmetry} usually it is from 3 to 5 u in diameter and 8000 1^30 ' PRODUCED BY FOR n mmm iiA. U IB 20 to 100 M In length. The coating contains iron demonstrable by Perle's stain (Prussian blue reaction}, and probably composed of ferritin or ferritin-like material; it may cover the structure completely, masking the central fiber from direct view, or may be incomplete in the central portion of the 6haft or in the interstices of the body, revealing an expanse of naked fiber.220 There is no doubt that the "asbestos bodies" formed in the lungs of the asbestos workers contain asbestos. Stumphius and Meyer 210 have investigated the composition of the "kernel" in the "asbestos bodies" removed from deceased shipyard workers (an occupational group with only indirect exposure). They found by electron microscopy and X-ray microanalyses that the "asbestos bodies" did indeed contain Borne minerals of asbestos. Out of 27 fibers, 17 were classified as serpentine (possibly chrysotile) and 10 as amphibole (possibly crocidolite) But what about the so-called "asbestos bodies" in the lungs of the general population? While these "asbestos bodies" probably contain some asbestos, there is no experimental evidence to date which shows vdiat fractions contain asbestos or whether they contain any asbestos at all.^'*^ This subject is currently being debated by several investigators.53,79,209 ln fact, some object to the use of the term "asbestos bodies" end prefer to call them "ferruginous bodies." htoreover, Gross 79 et al.. have shown that "ferruginous bodies"--which appear identical under the microscope to those formed from asbestos-- ebOOO H31 l i i l I PRODUCED BY FORD 19 can be produced from ceramic aluminium eilicate, glace fibers, and silicon carbide fibers. However, Thomson claims that a skilled pathologist can tell the difference. This cont.roc5 194 versy should soon be resolved, since both Gros6JJ and Selikoff are investigating the composition of the central fiber with the electron microprobe. Generalized contamination with fibrous material is evidenced by the figures in Table 6 in the Appendix. Two other obvious conclusions are that "asbestos bodies" are found more frequently in older people than in younger, and more frequently in men than in women. In none of the aforementioned studies has there been any quantitative count of "asbestos bodies" in the lungs of the general public. In most studies, "asbestos-bodies" found were scanty, although in some instances the bodies were numerous. 214 214 In most of the investigations, the method of Thomson was used (smears taken from basal lobes of the lung were examined and the asbestos bodies counted). Since only about one-half millionth of a lung is examined, the finding of only one asbestos particle may be extrapolated to mean that perhaps a half-million fibers are present in the lung. 214 In one recent study in - Pittsburgh, Utldjian t fil.. 220 made an attempt to quantify their results. In thiB study 98 percent of the 100 lungs examined contained "asbestos bodies" ("ferruginous bodies"). The results are given in Table 2. Por comparison they suggested that if those cases with only one "asbestos body" were ignored, then 6000 U3? PRODUCED BY FORD y mm 20 42 percent of the lungB examined contained two or more bodies, (20.5 percent of the women and 60.7 percent of the men). This 47 percent is in substantial agreement with the compar able 41 percent reported by Cauna^ (see Table 6 in the Appendix) for residents of Pittsburgh. table 2 DISTRIBUTIOtt OP "ASBESTOS (FERRUGINOUS) BODIES" IN LUNGS IN PITTSBURGH220 Sex Men Total Women Total No. of Caaea 1 21 15 19 56 2 29 B 5 44 Mean Ape 89 62 64 70 65 29 57 68 64 60 Fibers/Unit of Luno 0 1 2-5 >5 0 1 2-5 >5 Distribution (Percent) 2 37 27 34 100 5 66 16 11 100 2.2 Effects on Animals 2.2.1 Commercial and Domestic Animal a Krviluoto 121 reported finding some asbestos bodies in 201 a cow near an asbestos mine. In 1931, Shuster reported finding extensive pulmonary fibrosis in a dog kept for ratting in an asbestos factory. The lungs of the dog also contained some asbestos fiberB but no asbestos bodies were found. 8000 1433 i) \ r< i ) t * PRODUCED BY FORD 21 Peacock and Peacock 182 have studied the effect of asbestos on white leghorn fowl. They tried dusting the birds with asbestos but found that the fibers did not penetrate far into the lung. When the fibers were injected into the lumen of the air sac, an immediate inflammatory reaction occurred, macrophages appeared and engulfed the fibers, and giant cell formation was observed. Four of the 17 chickens examined developed tumors: of the six injected with crocidolite, two developed tumors; of the 10 injected with amosite, only one developed a tumor; and one chicken injected with an unidenti fied variety of asbestos also developed a tumor. 2.2.2 Experimental Animals Studies with experimental animals have shown that asbestos can induce fibrosis (asbestosis), cancer of the lung, and mesothelioma and can form 'asbestos bodies." Wagner 234 described experiments with rats in >A:ich 600 animals were exposed to various minerals of asbestos. The results are given in Table 3. Gross and De Treville"^ made the following observations in studies on rats, hamsters, and guinea pigs. In rats that have inhaled high concentrations (86,000 pg/ma) of chrysotile asbestos fibers for only a few months, minimal fibrotic lesions can be observed in the lungs of all animals. However, this form of asbestosis in rats is nonprogressive. In hamsters that have inhaled chrysotile dust, a fibrosis develops *dtich is WSP*pi.!!8y!!W!5 WS& 8000 1*34 PRODUCED BY FORD i; TABLE 3 TYPE AND NUMBER OP TUMORS INEUCED BY INTRAPLEURAL INOCULATION OP S.P.F. RATS WITH ASBESTOS234 f Asbestos ' minerals 1 Croc. Ia Croc. IIb Amosite Chrysotile Silica Saline Total Animals Exposed 100 100 100 100 100 100 600 Animals Died 19 10 4 25 11 5 74 Mi sc. Nonmalio. 5 4 1 5 1 2 18 Misc. Tumors 1 1 1 3 Reticulum-cell Sarcomas 1 1 2 2 2 8 Mesotheliomas 12 6 2 18 7' 45 &. Crocidolite from Northwest Cape, South Africa. bCrocidolite with oil extracted from it. i vn i ft N> PRODUCED BY FORD 23 progressive; "asbestos bodies" are also formed. In guinea pig8, the inhalation of chryeotile dust produces fibrotic lesions similar to those observed in rats. The data indicate that the minimum time to produce asbestosis in rats and guinea pigs is 60 to 120 hours at an asbestos dust concentration of 86,000 ug/mS. The investigators thinX the time required is shorter for hamsters. 228 Wagner and Skidmore have shown that asbestos dust tends to accumulate in the alveoli arising directly from the respiratory bronchioles of rats. They also investigated the elimination of asbestos from the lungs as discussed in Section 2.1. Gross and be Treville76 also observed a decrease in fiber content as the time from end of exposure increased. Ho' lt et al_. 98 suggest from their observations on rats that fibrotic lesions in the lungs are caused by asbestos fibers (chryeotile) which are less than 3 u long. Longer fibers are stored in the lungs as "asbestos bodies;" shorter fibers are removed from the lungs by phagocytosis. After some years, the larger fibers disintegrate, producing a- large - number of small particles. These small particles are then phagocytosed and produce fibrosis. They also suggest that asbestos is only fibrogenic when it is ingested by phagocytes. Holt et al.*^ exposed guinea pigs to asbestos du6t. After 14 days of exposure to dust, bronchiolitis was observed; after 21 days the damage was very severe, and "asbestos bodies" 8000 i<*36 PRODUCED BY FORD tfrtNrtM lit* ! 24 were observed along with asbestos fibers. After 226 days the lungs of animals dusted for more than 1,000 hours over a 76day period developed a wide-spread, progressive fibrosis with only a few asbestos fibers and "asbestos bodies" present in the lung tissue. The experimenters concluded that asbestos fibers too small to be seen under the microscope will produce asbestosis. - In order to evaluate the possible distribution of 194,195 asbestos within New York City, Selikoff ' is now examining ' the lungs of rats found in the city for asbestos fibers. In a similar investigation carried out in South Africa. wild animals captured near an asbestos mine were examined. However, the small nuntoer of "asbestos bodies" found in them precluded any conclusions. ^4 * 2.3 Effects on Plants No information has been found in the literature on the effects of asbestos air pollution on plants. . 2.4 Effects on Materials No information has been found in the literature on the effectB ofasbestos airpollutionon materials. 2.5 Environmental Standards Both theAmerican Conference ofGovernmental Industrial 21B Hygienists and the American Industrial Hygiene Associa tion110 have recommended an industrial threshold limit value for asbestos dust of 5,000,000 particles per cubic foot 6000 )437 V i ; I j j , t 1 [ I ' j I | i j ! ' ' PRODUCED BY FORD 25 (5 mppcf), based on total dust count and on an 8~hour day, 40I hour week. This value was recommended by Dreessen et al.^ after a study of 541 employees in three textile plants using chrysotile. Only three doubtful cases of asbestosis were found in those exposed to dust concentrations of less than 5 mppcf, whereas numerous cases were found above 5 mppcf. 136 Recently, the British Occupational Hygiene Society published its standards for chrysotile. The Society has I recommended a maximum accumulated exposure of 2.8 mppcf-years i (108 particle-year6 per m3). For example, maximum doses of 0.056 mppcf-years (2 x 106 particle-years/m3) for 50 years, 0.112 mppcf-years (4 x 10 particle-years/m ) for 25 yearB, or 0.28 mppcf-years (107 particle-years/m^) for 10 years are recommended. They have also recommended that dustiness be designated by categories according to the following schemei Concentration Averaged Over 3 Months I Dust Category {Million Particles/ro3) i Negligible 0-0.4 Low .5-1.9 Medium i High 2.0-10 Over 10.0 Only fibers longer than 5.0 u in length with a 3*1 length-to-breadth ratio are counted. With these standards the risk of asbestosis may be reduced to 1 percent; that is, 1 percent of the workers exposed to a dose of 10 particle-years/m3 would contract asbestosis. a00 0 U38 ' PRODUCED BY FORD tttM Mi mm HimMMtUUaM 26 ( ... ' : | I ' j. | j , 3. SOURCES . 3.1 Natural Occurrence Asbestos is a broad term embracing several fibrous minerals. The minerals are divided into two groups* (l) ' Pyroxenes--chrysotile; (2) Amphiboles--crocidolite, amosite, tremolite, actinolite, and anthophyllite. Properties of these minerals are listed in Table 7 of the Appendix. Asbestos probably occurs in nearly every country in the world, but only a few of the deposits are commercially valuable. Over 90 percent of the world asbestos production is Chrysotile, and Canada is the major source of this mineral for 93 the United States. Table 8 in the Appendix lists the world production. Prom these figures an estimate of known free- world deposits is possible. It is noteworthy that some soils near asbestos mines contain considerable quantities of asbestos. In Finland, farmers working these high-asbestos-content soils have been 120 observed to suffer from asbestosis. ' . 3.1.1 Mines The mining of asbestos in the United StateB has in- creased 180 percent in the last 10 years. (See Table 9 in the Appendix.) This mining may constitutea source of air pollution. A high percentage of the increase in domestic production has been credited to California producers, who accounted for 65 percent of the total output in 1966. Four x : 8000 H39 L. PRODUCED BY FORD t i I 27 companies produced chrysotile asbestos fiber: Atlas Minerals Corp. and Coalinga Asbestos Co., Fresno County; Pacific Asbestos Corp., Calaveras County; and Union Carbide Corp., San Benito County. The latter company processed the crude material in a plant at King City, Monterey County, whereas the other producers operated plants near the mine sites. 171 Amphibole asbestos was mined by Powhatan Mining Co. near Burnsville, Yancey County, N.C. Their output increased 66 percent during 1966.171 . There are four chrysotile mine6 in Arizona in the Salt River Valley near Globe. Since these mines are underground, only the waste needs to be considered in connection with air pollution (other than the possible pollution from transporting the mineral). Nearly all of the output from these mines was used in the cement industry to manufacture asbestos cement and building products: 28 percent was classified as filter fiber and 2 percent as spinning grade; the rest consisted of sand and waste, floats, or other short fibers. Jacquays Mining Corp. operated the Regal and Chrysotile Mines and shipped the ore to a company mill at Globe after hand-sorting the chrysotile. Western Asbestos Manufacturing Co. operated the Phillips Mine, and the Metal Asbestos Corp. the tucVy Seven Mine.^7^ In Vermont, the Vermont Asbestos Mines Division of the Ruberoid Co. quarried and processed chrysotile near Lowell in Orleans County. Twenty-four grades were produced for spinning, cement stock, paper stock, and other uses. Some waste rock 8000 1440 PRODUCED BY FORD mrnU i \ ' -- MMMMU iMfiM ' 28 ' was used for roadstone. , Data on these mines are summarized in Tables 10 and 11 in the Appendix. . Other deposits of asbestos have been found in Georgia and Maryland. Although no measurements have been made of the asbestos air pollution from mining in the United States, some evidence of the extent of pollution can be drawn from measurements and observations in foreign countries. The extent of air pollution from an asbestos mine in Finland was studied by Laamanen, Noro, 133 and Raunio. They found asbestos dust at distances up to 50 km from the mines, including dust-fall rates ranging from 1.52 g/100 nr/month at 4 km to 34.6 g/100 m /month at 0.5 km. They concluded that asbestos dust is disseminated from mining and milling areas rather extensively and that the degree of pollution varies according to thedistance from themine or mill and the prevailing winds. Schepers 234 described the dust from asbestos mines and mills in South Africa ae duBt which "rolled through like a morning mist," producing "itching skins caused by asbestos adhering to our clothes. Erven the food at the local hotel was gritty with dust." Sluis-Cremer20* reports dust counts inasbestos mines and mill6 of South Africa as listed in Table 4. He pointed out that living quarters near the mines were polluted with asbestos </o that the main source of pollution was airborne asbestos eooo im ' 1 I I ' j i 1 1 . ; ( I . ! I ' i I ' i i ' PRODUCED BY FORD 29 blown off dumps and roads made from the mine tailings. TABLE 4 DUST COUNTS IN ASBESTOS MINES AND MILLS IN SOUTH AFRICA, 1947202 Location Dust Count, mppcf (mppm2) Mines Mill Northwest Cape Province 2.8-24 (100-840) 10-55 (360-1920) Transvaal 2.3-6.5 (80-228) 4.6-20 (162-720) 3.2 Production Sources World production of asbestos during the period 1956 to 1967 increased at the average rate of approximately 13 percent per year. Figure 1 shows that the world production nearly tripled during the period 1945 to 1965, while United States consumption only doubled during the same period. However, during the period 1956 to 1967, domestic apparent consumption fluctuated between 665,000 and 813,000 short tons per year and may be leveling off as substitute materials (such as fiberglass and plastics) provide competition. The relative importance of the various industrial uses of asbestos is given in Table 12 in the Appendix. It is seen that the highest input of asbestos occurs in the asbestos cement,.floor tile, asbestos paper products, and asbestos textile industries. The proportions of asbestos used in various products are shown in Tables 13 and 14 in the Appendix. 6000 1442 PRODUCED BY FORD Thousands of Short Tons U. S. WORLD CONS. PROD. 30 FIGURE 1 Comparison of Trends in World Production and U.S. Consumption of Unmanufactured Asbestos170'171_ 6000 1443 PRODUCED BY FORD 31 Of the 78,056 short tons of domestic production in 1965, 66 percent were produced in California and 31 percent* in Vermont, amounting to 97 percent of the total production. This 97 percent was produced and processed in five counties.^ More than 50 percent of the 124 plants comprising the asbestos products industry were located (in 1963) in the States of California, New Jersey, Illinois, Pennsylvania, and TexaB, in decreasing order.^ Bobyleva a 1 24 25 have shown that the air can be polluted by asbestos from plants manufacturing asbestos products. This asbestos may be carried in the air for distances of 25 to 50 miles. In a study of asbestos air pollution from three plants in the U.S.S.R., they found that at a distance of 3 km from the plant, the dust concentration ranged from 0 to 6,000 ug/m*. at 1.0-1.5 km it was 3,000-33,000 ug/m*; and at 0.5 km it was 6,000 to 34,000 ug/m*. In the United States some' attempts have been made to determine the concentration of asbestos near asbestos factories, but the asbestOB content of the atmosphere was masked by the Other dusts. Asbestos fibers were detected, but a quantitative count was not possible. 3.3 Product Sources The uses of asbestos are numerous. Some products which use asbestos are the following! asbestos cement which may be Extrapolated.* 8ooo PRODUCED BY FORD r 32 applied as mortar or plaster, or sprayed on walls; insulating materials for the covering of pipes, ducts, boilers, cables, and conduitB; siding shingles, roofing shingies, tiles, flat and corrugated sheets, wallboard, clapboard, and automobile undercoating; threads, yarns, wicks, cords, tapes, cloths, sheets, and blankets; friction materials, brake linings, clutch facings, gaskets, and lagging cloths; and asphalt tiles, plastics, and similar materials. 108 Abrasion of brake linings and clutch facings has been suggested as a primary source of asbestos air pollution. Ayer13 and Lynch145 have examined the emissions from brakes on automobiles and found that the fiber is destroyed by the heat of friction. Asbestos crystalline structures are also destroyed and are recognizable only by the chemical composition. Newhouse and Thompson175 have reported one case of mesothelioma in a mechanic. .. The existence of a wide potential for direct or in direct occupational exposure has been cited^' ^4 'as a possible explanation for the frequent occurrence of "asbestos bodies" in the general public. Asbestos is now used in more than 3,000 products. Most people working in the construction and demolition of buildings come into contact with asbestos. Electricians and homeowners strip asbestos insulation off wires; the carpenter saws asbestos boards and often pounds the asbestos insulated furnace ducts to make them fit. As a result, the air around a construction site is contaminated with asbestos fibers. i 1 8000 la&S PRODUCED BY FORD 33 and the foreman, carpenter, painter, plumber, or new occupants all breathe this dust. In most homes, the owner will at some time handle these asbestos products during normal home main tenance. A large number of workers in other industries are similarly exposed. Some of these are listed in Table 15 in the Appendix. Although only a few of these people work in the asbestos industry, all may have inhaled sufficient asbestos to show "asbestos bodies" upon autopsy. The hazard is there, but how great is the hazard? It will be necessary to obtain quantita tive concentration data to delineate its seriousness. Prom the above discussion it may be concluded- that approximately 100,000 asbestos workers in the United States have a high exposure to asbestos.195 An additional 3.5 million construction workers--carpenters, welders, electricians, masons, plumbers, steamfitters, tile setters, etc.--are indirectly exposed,either by themselves handling asbestos products or by worki.ng on the job with people handling asbestos. 195 3.4 Environmental Air Concentrations Only one estimate of the environmental air concentrations of asbestos in the United States was found. Smith and Tabor206 have roughly estimated that urban air in the vicinity of heavily 3 traveled streets contains 600 to 6,000 particles/m . They indicate that the validity of these values is highly suspect because the methods available for the determination of asbestos w gijyi jimiuwi 8006 1^46 PRODUCED BY FORD 34 are Inadequate at the concentrations found in the urban air. / 6000 l**4*? PRODUCED BY FORD 35 4. ABATEMENT The asbestos industries in the United States have developed elaborate ventilation systems to prevent high dust concentrati.ons wh.ich m.ight be i.nhaled by the workers. 13,95 This dusty air is passed from the ventilators through fabric sleeve filters and then discharged to the atmosphere. The asbestos fibers are easily filtered out since the fibers form a mat which becomes an absolute filter.*^ In addition to the ventilation system, it has been necessary to carry out some operations (such as spinning and weaving) as wet processes to eliminate duBt. As a result, the pollution from factories is minimal. Attempts to measure concentrations in the vicinity of an asbestos plant have proved futile with present analytical methods. Pollution during the transportation of asbestos has been controlled by enclosing the material in plastic-coated bags. Although the most common procedure used to suppress - dust emission is wetting of the material, it is unfortunately not desirable to wet a large number of asbestos products. In New York, insulators are required to enclose the area vhen asbestos fireproofing is blown onto steel frames, but even this does not prevent pollution. Asbestos fibers are reported to be a common occurrence in the air around construe* ti,on s.ites. 34 . wi'j-.i .ji'.!.r.,ij,u WJ4JWM 6<M)0 1A4B PRODUCED BY FORD I I i * ; \ -*., 36 No information has been found on the abatement methods used in United States asbestos mines"and in asbestos mills near the mines. S. t c i i .0 00 ]449 ' PRODUCED BY FORD 37 5. ECONOMICS No information has been found in the literature on the damage costs or economic losses due to the effects of asbestos air pollution on humans, animals, plants, or materials. However, a large fraction of the people in the United States have been . exposed to asbestos, including the following: (1) approximately 100,000 workers using asbestos in their occupations, (2) approximately 3,500,000 construction workers ex posed indirectly to asbestos as they work with asbestos products or near those who handle asbestos products, (3) approximately 50,000,000 Americans who possibly have "asbestos bodies" in their lungs. No attempt has been made to assess the cost of health impairment for these people. Workmen's compensation laws for dust di.seases are in effect -in most States. 234 No information has been found on the cost of the present and future abatement of air pollution by asbestos in this country. The data in Table 16 in the Appendix, which refer to the asbestos industry in Britain, show that the dust extraction equipment cost alone, for a given size and type of plant, amounts to 27.5 percent of the total capital cost and approximately 7 percent of the operating cost of that plant. The type of control equipment used is primarily designed to meet government speci fications relating to occupational health standards. Data on the production and consumption of asbestos are presented in Section 3. - 8000 1450 PRODUCED BY FOPn aMsi 38 6. METHODS OP ANALYSIS Of the methods presently being used 1,2,206 to count dust samples in the asbestos industry,* none is applicable to atmospheric asbestos air pollution. There are at present no proven satisfactory methods for the collection, detection, and identification of asbestos fibers in the 0.1 to 5.0 u range in ambient air. Satisfactory sampling can probably be accomplished by use of a membrane filter-pump system. The major difficulty lies in the problem of identifying a very few asbestos fibers in the presence of relatively large num bers of a wide variety of other inorganic particulate matter found in the same air. Attempts to determine the asbestos content of urban air have revealed the need for development of new methods. Battelle Memorial Institute is currently developing one such method for the National Air Pollution 20S Control Administration. Mn all the asbestos monitoring methods used, microscopic counting of th'e fibrous particles is necessary to determine the proportion of fibrous material, and even then it i6 not known what fraction of the fibers are asbestos. Counting of fibers by eye under the microscope is tedious and difficult. If the number of fibers is less than 1 percent (<5 wt*) of total dust, the other dust masks the fibers, and quantitative results cannot be obtained. In parts of the asbestos industry where the asbestos-todust ratio is high (>5 wt%), it is often possible to determine the asbestos content indirectly.136 For example, if the pro portion of asbestos in the airborne dust was known by microscopic count for a given sampling location, the concentration (at least the order of magnitude) could then be inferred from a simple measurement of the concentration of the total dust. 8006 1S1 PRODUCED BY FORD 39 Modern analytical methods and instrumentation used in. the asbestos industry are listed below: ' Microscopic particle counting of samples on membrane filters1'2*14,15*57'97,136'187 Thermal precipitators1 Impingers12#1415*136,187 Royco particle counter1'2*136,187 Mass concentration methods1'1^'136'187 Microsieving116 Digestion116 ` Column chromatography of organics adsorbed on the surface116 X-ray diffraction14'46,47'116 Low-temperature ashing116 Atomic adsorption spectrophotometry14,116 Electron microprobe116 Neutron activation116 Owens jet counter12 Konimeter12 PPPifRpp 8600 1452 PRODUCED BY FORD 41 REFERENCES 1. 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Noro, L., Occupational and "Non-Occupational" Asbestosis in Finland, Am. Ind.- Hyg. Assoc. J. jg9.:196 (1968). 179. Nutt, A., and J. S. Harington, The Reaction of Reduced Glutathione with Quartz Powder and with Associated Iron and Copper, Med. Lavoro (Milan) !55(3):176 (1964). 180. 181. Owen, W. G., Mesothelial Tumors and Exposure to Asbestos Dust, Ann. N.Y. Acad. Sci. 132:674 (1965). Parkersburg, Wost Virginia--Marietta Ohio, Air Pollution Abatement Activity, U.S. Public Health Serv. (March 1967). 182. 183. Peacock, P. R., and A. Peacock, Asbestos-Induced Tumors in White Leghorn Fowls, Ann. N.Y. Acad. Sci. 132:501 (1965). Perni6, E. C., C. Vigliani, and I. J. Selikoff. Rheumatoid Factor in Serum of Individuals Exposed to Asbestos, Ann. N.Y. Acad. Sci. 132:112 (1965). 184. 185. Polliack, A., and M. J. Sacks, Prevalence of Asbestos Bodies in Basal Lung Smears, Israel J. Of Med. Sciences 4(2) U96B). Radczewski, O. 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Stevens & Co., Synthetic Industrial Fabric Dept., 1966). . 193. Selikoff, I. J., The Occurrence of Pleural Calcification Among Asbestos Insulation Workers, Ann. N.Y. Acad. Sci. 132:351 (1965). 194. Selikoff, 1. J., personal communication (Oct. 1968). 195. Selikoff, I. J., and E. C. Hammond, Community Effects of Non-Occupational Environmental Asbestos Exposure.Am. J. Public Health 5B(9):16S8 (1968). 196. Selikoff, I. J., J. Churg, and E. C. Hammond, Asbestos Exposure and Neoplasia, J. Am. Med. Assoc. 188:22 (1964). 197. Selikoff, X. J., J. Churg, and E. C. Hammond, The Occurrence of Asbestosis Among Insulation Workers in the United States, Ann. N.Y. Acad. Sci. 132:139 (1965). 198. Selikoff, I. j., j. Churg, and E. C. Hammond, Relation Between Exposure to Asbestos and Mesothelioma, New Engl. 3. Med. 272:560 (1965). . 199. Selikoff, X. J., E. C. Hammond, and J. Churg, Asbestos Exposure, Smoking, and Neoplasia, J. Am. Med. Assoc. 204: 106 (1968). 200. Selikoff, X. J., R. A. Bader, M. E. Bader, 3. Churg, and E. C. Hammond, Asbestosis and Neoplasia, Am. J. Med. 42: 487 (1967). 201. ShU6ter, N. H., Pulmonary Asbestosis in a Dog, J. Pathol._ Bacteriol. 34:751 (1931). ' ' --'.r 8000 1467 ' PRODUCED BY FORD ( \ 7 -V;7 II II I 202. Siuie-Cremer, G. K., Asbestos in South Africa*--Cfertain Geographical and Environmental Considerations, Ann. N.Y. Acad. Sci. 132:215 (1965); 203. Sluis-Cremer, G. K., and C. PI. Theron, A Proposed Radiological Classification of Asbestosis (Part I of Radiological and Pathological Correlations in Asbestosis in the Republic of South Africa and the United Kingdom), Ann. N.Y. Acad. Sci. 132:373 (1965). 204. Smith, K. W. , "Pulmonary Disability in Asbestos Workers," in Transactions of the Mclntvre Saranac Conference on Occupational Chest Disease. G. W. H. Schepers, Ed". (Chicago: A.M.A. p. 196, 1955). - 205. Smith, K. W., Trends in the Health of the Asbestos Worker, Ann. N.Y. Acad. Sci. 112:685 (1965). 206. Smith, R., and E. Tabor, personal comnunication (Sept. 1968). 207. Smith, W. E., L. Miller, R. E. Elsasser, and D. D. Hubert, Tests for Carcinogenicity of Asbestos, Ann. N.Y. Acad. Sci. 132:456 (1965). 208. Smither, W. J., Secular Changes in Asbestosis in an Asbestos Factory, Ann. N.Y. Acad. Sci. 132166 (1965). 209. Smither, W. J., Asbestos Bodies, Brit. Med. J. 2:51 (1968). 210. Stumphius, J., and P. B. Meyer, Asbestos Bodies and . Mesothelioma, Ann. Occup. Hvg. 21.: 283 (1968). 211. Szymczykievict, K., The Mesenteric Test as a Method of Evaluation of Harmful Effects of Indbstrial Dust, Med. Pracy (Lodz, Poland) 15(4):221 (1964). 212. Tanaka, S., and J. Lieben, Community Chest X-rays for Pneumoconiosis Prevention, Arch. Environ. Health 12: 10 (1966). 213. Thomson, J. G., Exposure to Asbestos Dust and Diffuse Pleural Mesotheliomas, Brit. Med. J. 1:123 (1963). 214. Thomson, J. G., Asbestos and the Urban Dweller, Ann. N.Y. Acad. Sci. 132:196 (1965). | j ; ; ; : 1 \ 8000 1468 PRODUCED BY FORD 57 215. Thomson, J. G., and W. M. Graves, Asbestos An an Urban Air Contaminant, Arch. Pathol. 81(S):4S8 (1066). 216. Thomson, >J. C., R. 0. C. Kasthula, and R. R. MacDonald, Asbestos as a Modern Urban Hazard, S. African Med. J. 37:77 (1963). 217. Thomson, M. L., A. M. Pelzer, and W. J. Smither, The Discriminant Value of Pulmonary Function Tests in Asbestosis, Ann. N.Y. Acad. Sci. 132:421 (1965). 216. 219. Threshold Limit Values for 1967. Adopted at the 29th Annual Meeting of the American Conference of Governmental Industrial Hygienists, Chicago, 111. (May 1-2, 1967). * Timbrell, V., The Inhalation of Fibrous Dusts, Ann. N.Y. Acad. Sci. .132:421 (1965). ' ' 220. Utidjian, M. D., P. Gross, and R. T. P. deTreville, Ferruginous Bodies in Human Lungs, Arch. Environ. Health 12*327 (1968). 221. Vasil'eva, A. A., and M. D. Manita, Carboxyhemoglobin in the Blood of Persons Directing City Traffic, Gigiena i .Sanit. 25(12):77 (1960), Translated by B. S. Levine, U.S.S.R. Literature on Air Pollution and Related Occupational * diseases 7:290 (1962). 222. Vigliani, E. C., G. Mottura, and P. Marazana, Association of Pulmonary Tumors with Asbestosis in Piedmont and Lombardy, Ann. N.Y. Acad. Sci. 132:558 (1965). 223. Vorwald, A. J., T. M. Durkam, and P. C. Pratt, Experimental Studies of Asbestosis, Arch. Ind. Hyg. Occup. Med. J:1 (1951). 224. Wagner, 3. C., Experimental Production of Mesothelial Tumors of the Pleura by Implantation of Dusts in Laboratory Animals, Nature 196(4850)tlBO (1962). 225. Wagner, J. C., Asbestosis in Experimental Animals, Brit. 3. Ind. Med. 20tl (1963). . 226. : Wagner, 3. C., Epidemiology of Diffuse Mesothelial Tumors, Evidence of an Association from Studies in South Africa and the United Kingdom, Ann. N.Y. Acad. Sci. -13257S (1965). \ 8000 1469 ---------- PRODUCED BY FORD k /-" 'x ( -.1 6-:>!^ jgfiiii* :M I WlMlM 58 227. Wagner. J. C., The Sequelae of Exposure to Asbestos Dust.. Ann. N. Y\ Acad. Scl. 132:691 (1965). 228. Wagner. J. C.. and J. W. Skidmore, Asbestos Dust Deposition and Retention in Rats, Ann. N.Y. Acad. Sci. 132:77 (1965). 229. Wagner, J. C., C. A. Sleggs, and P. Marchand, Diffuse Pleural Mesothelioma and Asbestos Exposure in North Western Cape Province, Brit. J. Ind. Med. 3^2.:260 (I960). 230. Walter, E., Evaluation and Assessment of Dust Measure ments in Asbestos Plants of the Textile Industry, Staub (English Transl.) (Dusseldorf) 2(10):16 (1966). 231. Warren, S., Survey of Some Current British and European Studies of Occupational Tumor Problems, Occup. Med. 5:249 (1948). 232. Webster, I., Mesotheliomatous Tumors in south Africa: Pathology and ExperimentalPathology, Ann. N.Y. Acad. Sci. 222:623 (1965). 233. WegeliuB, C., Changes in the Lungs in 126 Cases of Asbestosis Observed in Finland, Acta Radiol. 28:139 (1947). 234. Whipple, H. E., Biological Effects of Asbestos, Ann. N.Y. Acad. Scl. 132 (1965). 235. Wickert, K., SO3 Determination in Dust-Laden and DustFree Combustion Gases, Text in German. Erdoel Kohle (Hamburg) 20(8)56B (1967). 236. Windom, H., J. Griffin, and E. D. Goldbert, Talc in Atmospheric Dusts, Environ. Sci. Tech. 1(11):923 (1967). 237. Wbod, W. B., and S. R. Gloyne, Pulmonary Asbestosis, Lancet 1:445 (1930). 238. Zolov, c., T. Bourilikov, and L. Baladjoa, Pleural Asbestos in Agricultural Workers, Environ. Res. 2(3): 287 (1967). ' | ! ! i l ; ' i } : j ' j \ ; i I I . 1 | ! 8>00 H?o PRODUCED BY FORD OTHER REFERENCES Asbestos (Philadelphia: Secretarial Service, 1968). A-S'restcs. Ce-er.t Quarterly (New York: Asbestos Cement Products Assoc., 1968). The Asbestos Mining industry (Ottawa* Bureau of Statistics, 1968). The. Asbestos Products Industry (Ottawa: Bureau of Statistics, 1966). Bankoff, E., The Canadian. Asbestos Industry (Toronto: General Research Associates, p. 41, 1958). Berger, H., Asbestos Fundamentals. Translated from the German (New York: Chemical Publishing Company, 1963). Berger, H., Asbestos with Plastics and Rubber (New York: Chemical Publishing Company, 1966). Bowles, 0., The Asbestos Industry, D.B. Bur. Mines Bulletin_.5_S2 V (1959). Monthly Report--Asbestos Production, in Canada (Ottawa: Bureau of Statistics, 1968). " 6000 rr:.~r~ --------V" y ' PRODUCED BY FORD "\ APPENDIX A I 8000 jPIPPi iMMmppgMp mm PRODUCED BY FORD J APPENDIX A TABLE 5 CANCER OF THE LUNG AMONG ASBESTOS 43 WORKERS ft Place United Kingdom United Kingdom Population Studied Reported deaths from asbestos Cases of asbestosis in 1,247 autopsies with pneumoconiosis No. of Years Workers Followed 235 1924-1947 121 No. With Lung Cancer 31/235 <13.1*) 17/121 Comparison Groups Silicotics (1.32*) Silicotics (6.9*) United Kingdom Asbestos textile workers, industry areas, 20 years' or more exposure 113 1922-1953 11/39 deaths 0.8 Expected United Kingdom Quebec Reported deaths from asbestosis Chrysotile miners and mill workers with over 5 years' enployment 365 5,958 1924-1955 1950-195$ 65/365 (17.8*) 9/187 deaths 6+ Expected T Pennsylvania <o37 New York & New Jersey Workers in asbestos products plant employed in 1938-39, aged 25-64 Insulating workers, over 20 years' union membership 1,495 632 1940-1960 1932-1962 19/186 deaths 45/255 deaths 5.61 Expected 6.6 * Expected 1*1 (continued} ros*j PRODUCED BY FORD ' \1 1 < 1 - l.;z' ' . ^ ^. i ' >& -) : ' *..?*0J 1 ,f ** ' ;V , ft r* i; * ! J >i f 3 i3 3 00 o o o & v P3 8 mcn o 3J A oa 3 APPENDIX A TABLE 5 CANCER OF THE LUNG AMONG ASBESTOS WORKERS (Con titlued) Place California Dresden Population Studied Insulating workers. mixed, 15 years in trade, aged 35-64 All asbestos trade mixed exposures No. of Years workers Followed 529 1954-1957 2,636 1924-1963 No. With Lung Cancer 10/41 deaths ' 34/150 deaths Comparison Groups 2.8 Expected 11.4 Expected United States Asbestos textile workers employed in 1948-1951, aged 15-64 2,833 1951-1963 24/285 deaths 11.9 Expected United Kingdom Reported deaths from asbestosis 584 1924-1963 146/584 (25%) Bulgaria Agricultural workers near 3,325 an asbestos mine 1962 155/3325 asbestosis New York Asbestos insulators employed more than 15 years, aged 40-80 152 1945-1965 18/46 deaths 3.1 Expected Pennsylvania Asbestos textile and friction workers - - --- ------- 68 1957-J.962 13/68 deaths w J APPENDIX A TABLE 6 "ASBESTOS BODIES IN CONSECUTIVE OR RANDOM AUTOPSIES T.nrtion Capetown Miami Pittsburgh Milan Tyneside Jerusalem Glasgow Finland Sweden % Total PosiCases tive <24 ,, Positive bv Aoe* 25-34 35-44 45-54 55-64 65-74 500 26.4 .5 2.4 4.4 4.6 7.4 7.4 (4.3) (25.6) (28.4) (22.4) (31.6) (28.0) >75 Sex Year % Positive* of Refer- Female Male Study ence 7.8 18.6 1960 214,216 (20) (30.4) 500 27.2 0 0 1 3.4 5.6 9 8 19.2 1961 214,216 (16.1) (23) (27.2) (3o!6) (31.9) (20.4) (31.6) 100 41 0 5 5 3 13 8 6 16 25 (0) (83) (46) (38) (54) (40) (30) (34) (47) 1964 40 100 51 ------- 3 (14) ------r*) 30 (60) 18 (66) 16 (44) 35 (54) 1966 67 311 20.3 0 0.3 1.6 2.9 4.8 7.7 2.9 4.2 16.1 1967 (0) (25) (19.2) (17.3) (18.5) (28.9) (15) (13) (25.5) 11 100 26 (14) 7 Trtf- -1 o (21) (30) 10 16 1967 (29.1) (22.2) 184 100 23 0 0 01 4 11 7 0 23 1967 188 (12) (22) (32) (19) (0) (37) 264 57.6 1.5 (57) 3.0 3.8 8.7 20.0 16.7 3.8 23.9 33.7 (57) (71) (55) (64) (58.7) (34.5) (54.3) (60) 1966 167 34 35.3 0 0 0 0 11.7 14.7 18.8 14.7 20.6 1966 82 (80) (25) (43) (38) (33) $L*)\ 0009 ) (continued) Oi Iv;. . APPENDIX A TABLE 6 "ASBESTOS BODIES" IN CONSECUTIVE OR RANDOM AUTOPSIES (Continued) Location % Total Posi- % Positive bv Aoe* Cases tive <24 25-34 35-44 45-54 1 55-64 65-74 Johannesburg 39.2 San Francisco 42 Belfast 200 20 London Montreal 50 6 100 48 (30)* (50) - -7 (50) New York 355 50.5 Year % Positive* of Refer- >75 Female Male Study ence 1965 234 1966 43 1965 60 16 (36) 3.9 (29.8) 32 (57) 1964 102 1966 % y 46.5 1966 (53.7) 195 Numbers in parenthesis represent percentage of group-age or sex. X* av\ PRODUCED BY FORD V, s APPENDIX A TABLE 7 COMPOSITION AND PROPERTIES OF ASBESTOS MINERALS66 Approximate Formula Percentaoe of Maior Comoonents Silica Si02 Alumina AI2O3 Ferrous Oxide FeO Ferric Oxide Fe203 Manganous Oxide MnO Calcium Oxide CaO Magnesium Oxide MgO Sodium Oxide Na20 Potassium Oxide KjO Carbon Dioxide C02 Water of Crystallization HjO Chrvsotile 3MgO-2SiO2-2H20 40.3 0.7 1.0 .. 1-5 0.2 42.4 0.2 13.7 Crocidolite Na20-3FeOFe2O8Si02*H2O 51.4 20.3 17.5 0.1 0.8 1.4 6.2 0.4 1.9 Amosite 1.5 MgO-5.5FeO8Si02 *H20 49.3 40.9 0.4 0.7 0.4 5.7 0.2 0.3 0.2 1.9 (continued) t l: o\ ft O' ft PRODUCED BY FORD ) \ APPENDIX A , TABLE 7 COMPOSITION AND PROPERTIES OF ASBESTOS MINERALS (Continued) y Approximate Formula Chrysotile 3Mg0-2SiO2*2H20 Crocidolite Na20-3FeOFe2O8Si02*H20 Arosite 1.5 MgO-5.5Fe08Si02*H2O Trace Organic Impurities .. Oil^ax (mg/100 g fiber) Benso (a )pyrene (uo/100 a fiber) Trace Inoraanic Impurities (ug/g fiber) 4-7.6 none detected * 4-200 0.2-24 .. " 4-20 0.2-2.4 Pb Sn Ga Bi V Mo Cu Ti Ag Ni <0 Zv o Co . o Mn i> Cr w oo ' ..... ,, " 2 <5 <2 <5 50 <2 35 50 <0.2 5.000 (1.000-14,000) <200 <5 (<100) 130 (400-500) 1,000 (400-900) 5 <5 <2 <5 <2 <2 7 50 0.2 <10 (<100) 700 <5 (<100) 180 (200) 20 (<100) 20 <5 2 <5 <2 <2 7 300 0.2 1,000 (<100) 1,000 <5 (<100) 7,000 (7,900) 150 (<100) (continued) PRODUCED BY FORD 1 J APPENDIX A TABLE 7 COMPOSITION AND PROPERTIES OF ASBESTOS MINERALS (Continued) Approximate Formula Radioactive Contaminants (uuc/g fiber) *40 Th238 Ra226 Phvsical Properties Flexibility Length \ Texture Tensile strength Acid resistance Heat resistance Ob Spinnability % xs> Chrvsotile 0.14 0.07 Crocidolite 0.02 <0.01 Amosite 0.55 0.05 0.15 Very flexible Short to 3* Harsh to silky Very high Fairly soluble Good Very good Fair to good Short to 3" Harsh to soft Very high Very good Poor Fair Good h" to 6" Coarse but plial Fair Good Good Fair CD PRODUCED BY FORD I / v-- V \ / .: > i .> APPENDIX A TABLE 8 WORLD PRODUCTION OF ASBESTOS170 {Short Tons) M Location 1962 *? North America Canada (sales) . . . . 1,215,814 United States (shipments) . . . . 53,190 1963 1964 1,275,530 66,396 1.420,769 101,092 1965 1966b'e 1,387,555 1,479,281 118,275 125,928 South America Argentina ...... 203 Bolivia (exports) . . 56 > Brasil ... .................. 4,900* 365 10 l,440f 542 7 1,430''f 243 3 1,204 240* 4 1,820 Europe Austria . ....................... Bulgaria ....... Finland? ....... France ................................ Greece ........ Italy ... .................. Portugal ........................... U.5.S.R............................ Yugoslavia ....................... 503 l323c 10,869 28,034c 60,860 710,000*'c 7,401 638 l,323c 10,201 26,094 74 63,016 29 755,000*' 9,074 1,433 11,611 24,289 65* 75,573 810,000*' 9,280 ' l,433c 13,307 7,506 85* 79,214 53 865,000 10,585 1,430* 13,250 7,720* 85* 90,464 10 925,000 8,411 Africa 00 Botswana ........................... 2,375 o o o Kenya ........ Mozambique ...... 212 370 2,368 78 2.161 204 888 136 880 73 3 O C7 Rhodesia, Southern . . 142,195 Oco o South Africa .................. Swaziland . ~.................. 221,302 32,830 United Arab Republic . 606 142,254 205,744 33,350 192 153,450 215,592 39,862 1,739 176,149 240,752 40,884 3,225 175,000 276,597 36.142 2,057 C 8 o (continued) w < o (O APPENDIX A . i. TABLE 8 WORLD PRODUCTION OF ASBESTOS (Continued) (Short Tons) Location 1962 Asia China ........ Cyprus ....... Japan ............................... Korea, South .... Philippines ..... Taiwan ....... TurXey ..;.... 100,000 22,391 1,865 15,407 1,333 1,037 525 * 709 Oceania Australia ...................... New Zealand ..... a World Total * . * 18,416 457 2,655OOOc 1963 1964 110,000 19,962 3,038c 18,210 2,120 421 604 408 130,000 13,755 3,710c 17,979 1,402 586 526 1,291 ' 13,374 439 2,760,000c 13,545 3,050,000 1965 1966. b, e 140,000 17,622c 4,989 16,451c 1,710 883 1,376 140,000 24,449 7,646 17,067 687 721 1,258 11,647 13,472 3,140,000 3,350,000 wo J"h Estimated. ^ bPreliminary. * cRevised. ^Asbestos also is produced in CzechoslovaXia, Eritrea, Malagasy, North Korea, and Rumania. No estimates for these countries are included in the total because production is believed to be negligible. eCompiled from data available May 1967. ^Bahia only. ^Includes asbestos flour. ` PRODUCED BY m O APPENDIX A TABLE 9 THE PRODUCTION AND APPARENT CONSUMPTION OF ASBESTOS IN THE UNITED STATES41,170,171 71 ^ar 1967 1966 1965 1964 1963 1962 1961 1960 1959 1958 1957 1956 1955 1950 1945 1940 1935 _ Quantities in Short Tons Product!on 123,190 ;; 125,928 118,275 101,092 66,396 53,190 52,814 45,223 45,459 43,979 43,653 41,312 50,431 Imports 645,110 726,459 719,559 739,361 667,860 675,953 616,529 669,945 713,047 644,331 682.732 689,910 716,480 . Exports 47,710 46,996 43,126 27,147 10,044 2,949 3,799 5,525 4,461 3,026 2,893 2,950 7,001 Consumption 720,580 805,391 794,708 813,306 . 7241212 726,194 (665,440) 709,193 754,045 685,284 723,492 782,272 759,910 727,002 378,030 270,000 170,000 year .Production_ 1967 1966 1965 1964 1963 1962 1961 1960 1959 1958 1957 1956 811,100 11,056 10,162 6,143 5,108 4,677 4,347 4,231 4,391 5,127 4,918 4,742 4,534 . values. _(X X.-O0OJ Imports Asbestos . _ Asbestos Products _ 866,000 73,100 70,457 72,973 61,739 64,112 (63,000) 63,345 65,006 58,314 60,104 61,939 59,339 86,030 5,763 5,294 3,199 1,304 598 759 857 793 424 350 375 1,497 . 621,963 19,139 16,288 16,267 14,274 13,233 15,223 14,181 12,464 6000 ^62 PRODUCED BY FORD /: f \' \ J * --- APPENDIX A * TABLE 10 REGIONAL DISTRIBUTION OF ASBESTOS MINING AND PROCESSING170'171 (Ranging and Production) Ranh I960 1 Vt. 2 Arir. 3 N .C. 4 Calif. State 1964 Cf.lif. Vt. Arir. N.C. 1966 Calif. Vt. Aris. N.C. Ouantitv (Short Tons) 1964 1965 1966 55.041 74,587 * 81,671 * 3,469 * *# * (55.041) (78,056) (81,671) Value (X 1.000) 1964 1965 1966 54,419 $6,177 ** $6,945 * * 441 #* * (4,419) (6,177) (6.945) Data withheld to avoid disclosure of producer's confidential information to the Bureau of Mines. PRODUCED BY o09 o Sao' w 3 iv V-V J ' APPENDIX A \ r.` \ TABLE II ASBESTOS MINES IN THE UNITED STATES, 1966 170 State California 4 3 \% \ Mineral Chrysotile Chrysotile Chrysotile Production Rank* ' Name of Producer 1 Atlas Minerals Corp. 2 Coalinga Asbestos Co. 3 Pacific Asbestos Corp. Chrysotile 4 Union Carbide Corp. b Ash Bonding Co. Location--Coun' v or City of Mine Processina Plant Fresno County Near Mine Fresno County Near Mine Calaveras County Near Mine San Benito County Monterey County (King City) Napa Vermont Chrysotile 1 Vermont Asbestos Mines Div. of Ruberoid Co. Orleans County (Lowell) Arizona Chrysotile Chrysotile 1 Jacquays Mining Corp. Salt River Valley (North of 2 Western Asbestos Mfg. Co. Globe) o<oP Chrysotile 3 Metate Asbestos Corp. o Kyle Asbestos Mines Of `AYiz? * CD * LeTourneau Asbestos Corp.a | North Carolina Crocidolite l Povhatan Mining Co. aRanked by production only within the State. Tlot in operation during previous years. Yancey County (Burnsville) wNJ PRODUCED BY FORD APPENDIX A TABLE 12 APPARENT ASBESTOS CONSUMPTION, 1965170 (In Thousands of Short Tons) 74 Use Asbestos Industry Production Mining and Processing Asbestos in Products Textiles Cement Friction Materials Asbestos Paper Floor Tile Paints, Roof Coating, Caulks Plastics Miscellaneous Total Products World97 66 2,190 111 220 307 85 21 221 3,221 "Based on 25% of world consumption. United States* 78 17 548 28 55 77 21 5 55 806 i l 6000 1485 i PRODUCED BY FORD APPENDIX A TABLE 13 PROPORTION OF ASBESTOS IN VARIOUS ASBESTOS PRODUCTS170 7S Product Asbestos textiles ' Asbestos cement Friction materials and gaskets Asbestos paper and products Floor tile Other asbestos products Percenta Asbestos B0-100 15-90b 30-80 80-90 10-30 c U.D. Chrysotile asbestos is used unless otherwise stated. ^594 to 9 OX chrysotile, with some materials containing as much as 85# amosite and small amounts of crocidolite and antho- phyllite. ' cThese products contain undetermined quantities of chrysotile. tremolite, actinolite. and anfhophyllite. TABLE 14 QUANTITY AND VALUE OF ASBESTOS INPUT BY INDUSTRY 1963170 Product . Quantity Value Short Fraction Fraction Tons(000) of Total 5(000,000J of Total. Asbestos textiles Asbestos cement Friction materials and gaskets Paper and products Floor tile Paint and coating fillers Plastics Other 66 2,190 111 220 307 es 21 220.7 0.02 0.68 0.04 0.07 0.09 0.02 0.01 0.07 26.4 328.5 11.1 19.8 13.2 3.7 9.2 19.7 0.06 0.78 0.03 0.05 0.03 0.01 0.04 Total 3,220.7 1.00 423.3 1.00 e*oo met> r -i * PRODUCED BY FOPD i y :.y i mmm . -w- L. *v. *****< APPENDIX A TABLE 15 POPULATION GROUPS WITH OCCUPATIONAL AND ENVIRONMENTAL EXPOSURE TO ASBESTOS108 Occupational Groups Asbestos rock miners, loaders, truckers, crushers, millers, asbestos spinners, weavers, electrical appli ance and wire manufacturers, masons, carpenters, heating equipment workers, rubber workers, shingle and tile manufacturers, building material manufacturers, filtering material manufac turers, molders of asbestos products,, asbestos-asphalt makers, putty manufacturers, asbestos cement makers, asbestos paper, cardboard and brake-lining producers, asbestos felt insulation workers, asbestos sound insu lation workers, asbestos insu lators, pipe coverers, asbes tos tube wrappers, asbestos cork insulation workers, con struction workers, automobile makers, garage attendants Nonoccupational Groups Residents in vicinity of asbestos processing and tex tile mills inhaling plant effluents polluted with asbestos dust, and indivi duals living and working along roads on which asbestos is trucked: residents in the vicinity of asbestos mines; residents in vicinity of building construction and demolition, inhabitants of homes or offices with asbes tos acoustical tile i ! PRODUCED BY FORD APPENDIX A TABLE 16 ASBESTOS CONTROL EQUIPMENT95 Cost Data Asbestos Textile Industry Dust extraction equipment Total capital cost (fixed) Operating cost per year Operating cost/labor cost Operating cost/total cost conversion Asbestos Mines'3 ' Dust extraction equipment Total capital cost (TCC) (TCC/TCC of plant) x 100 Operating cost (per year) , ~ $1,500,000 ~ $ 250,000 ~ 7. % ~ 2.7* ~ $ 360,000 ~ 27.5* ~ $ 195,00Q 77 Specifications Asbestos Textile Industry Volume of dust-containing air extracted from textile machines Quantity of asbestos dust filtered per year (at above rate) Asbestos Mines Total installed horsepower Part used to generate air for dust removal Total air needed (for aspiration and dust removal) per pound of fiber produced 1,000,000 ft3/min or 700 ft3/min/operative 700 tons or 2.B tons/working day 796 230 (29*) 1,350 ft3 ^Figures apply to the Turner Bros. Asbestos Co. plant at Rochdale. England. ^Figures apply to the Cape Asbestos Co. at Penge in the Transvaal. The most modern mill (in Canada), which is 10 times larger, needs only about half the quantity of air stated (using gravity instead of air-swept mills and horizontal transportation of ore). ' m ~ sVy?, -I.Vf - 6000 1488 PRODUCED BY FORD /. V' APPENDIX A TABLE 17 ANALYSIS OF ASBESTOS AND ASBESTOS PRODUCTS EXPORTS AND IMPORTS170 Exports Short Tons . 1965 1966 Dollars (000) 1965 1966 Re-exports Short Tons ,Dollars(000) 1965 1966 1965 1966 Crude and spinning fibers Nonspinning fibers Waste and refuse 1 ,251 24 ,221 17 ,523 1,455 326 28,017 3,622 17,218 1,323 325 3,973 1,414 50 176 10 30 81 130 13 21 Total 42 ,995 46,690 5,271 5,712 131 306 23 51 Gaskets and packing Brake lining Clutch lining (number) Textiles and yarn Shingles and clapboard Asbestos-cement Sub total Other products. 1 ,732 3 ,065 2, 020 ,864 794 5 ,465 6 ,101 * 2,678 4,528 3,630 4,728 2,246,986 1.691 900 1,067 10,010 1,096 4,742 1,588 14,698 4,389 5,261 5,236 1,897 1,326 1,797 1,332 16,849 5,058 11 5,000 5,000 113 231 5,114 5,232 * 1 2 4 37 44 8 1 2 1 41 45 11 Total . ^ 19,087 21.907 Imports Short Tons Dollars (000) 1965 1966 1965 1966 52 56 Chrysolite Crude Spinning/ Textiles All Other 12,496 17,339 643,149 6 ,596 16 ,839 642 ,894 6,245 55,077 6 ,319 56 ,308 Total 672,984 666 ,329 Crocidolite Amosite Total Not available 21,165 17,042 711,191 26 ,995 23 ,934 716 .258 70,454 73 ,100 6000 U 8 9 79 APPENDIX A TABLE IB SELECTED STATISTICS FOR THE ASBESTOS MANUFACTURING INDUSTRY41 (Employment Size) Number of Employees* 1-49 50-99 100-2,499 over 2,500 Total Number of Companies 39 6 10 18 73 Number of Plants 39 6 17 62 124 Number of Production , Workers 308 231 2,445 12,754 Value of Shipment* $ (000) B, 264 4,827 89,131 407,014 15.73B .509,236 *The employment size cla6B is determined by the total company employment in all manufacturing activities in the U.S., including central offices and auxiliaries serving manufacturing establishments. All establishments of a company are therefore included in the same employments size column regardless of establishment size. i 6000 1490 PRODUCED BY FORD APPENDIX A ` TABLE 19 SELECTED STATISTICS FOR THE ASBESTOS PRODUCTS INDUSTRY41 BO Expenditures (in $000) New plant and equipment New structures New machinery and equipment Total Used plant and equipment Total 1958 2,419 10,418 12,837 ^ 428 13,265 1963 2,613 9,768 12,381 1.289 13,670 I i i l i / ii i % i I> 6000 1991 PRODUCED BY FORD APPENDIX A 81 TABLE 20 ASBESTOS USES85 Textiles: Varieties used: Yarns and Cords: Chrysotile, crocidolite, and in part amosite Processes: Weaving of yarns and cords Braiding (interlacing) Classification of chrysotile fabrics: Class 1 2 3 4 5 Quality Code AAAA AAA AA A Underwriters Commercial Asbestos Content (K) 75-79.9 80-84.9 85-89.9 90-94.9 95-100 Sealing and Packing Materials: ( Packing (woven fabrics.) stuffing for boxes and sleeves manhole rings, boiler covers Flat Packing: Gaskets, flanges (on pipes) and containers 1. Without metal: high pressure gasket sheets (rubber) 2. With metal material for sealing cylinder heads and exhausts in motors and combustion engines, and for sealing compressors and turbines Asbestos Boards and Papers: Boards Filtering and clarifying Coverings, coatings, casings, and jacketings for all kinds of surfaces ............... Manufacturing of welders' and melters' shields Slideways in the glass industry Handles and fire-doors Auto Parts Safes Protective walls Curtains, etc. I 1 . ipww?^w>!|^iwggggpwgggg^ . (continued) 6000 PRODUCED BY FORD  APPENDIX a . > WUttii'- iii TABLE 20 (Continued) ASBESTOS USES85 Sheets Inner/outer linings of furnaces and heating vessels drying ovens, incubators, heaters, climatecontrolled spaces, etc. Plates Insulating buildings against vibrations (aluminumasbestos) solar-heat reflecting surfaces (70% of Bolar heat) Special Asbestos Papers Filters Asbestos Cement (10 to 25% asbestos): Slabs Corrugated sheets Pipes Corrugated tiles for roofs in industry, agriculture, and dwellings Planks for platforms in buildings under construction Balcony canopies . Rain gutters Interior walls Ventilating shafts - Air conditioning assemblies Pressure piping (for underground drinking water distribution systems, fuel gas, and sewage) Cooling towers (electricity-generating stations) . Thermal Insulants and Fire-Proofing: Sprayed asbestos (insulant in both heating and refrigeration\ sound absorbent (eliminates booming and improves acoustical properties' of walls and ceilings) Magnesia asbestos (85S magnesia, 15% asbestos) as thermal insulant for covering pipes - Friction Material: woven: Brake lining Nonwoven: Clutch lining Transmission lining (continued) 8000 1493 appendix A B3 TABLE 20 (Continued) ASBESTOS USES85 Asbestos Plastics Flooring tiles (asbestos-asphalt tiles and, increasingly, asbestos-polymers of vinyl) Pressed or molded (thermal insulation and in electrical machinery) Resinated asbestos felt (manufacturing of wings and firing of missiles and expansion cones for nozzles of boost motors). Other uses in aircraft industry: nozzles for motor tubes, missile tailpipes, and missile-heat barriers; fuselages for guided missiles, fuel tanks for fighter bombers, cabin floors, etc. Radar (large molded reflectors and scanners) Asbestos Acid-Resistant Compositionsj Used mostly in chemical industry **' / 8000 )494 MP PRODUCED BY FORD 'Hitimmk MMHia APPENDIX A TABLE 21 1967 LIST OF MANUFACTURED ASBESTOS PRODUCTS85 84 Industry and Product Description Quantity Measure Miscellaneous Nonmetallie Mineral Products Asbestos Products Asbestos Friction Materials Brake Linings Woven, containing asbestos yarn, tape, or cloth Molded, including all nonwoven types Clutch facing Woven, containing asbestos yarn, tape, or cloth Molded,; including all nonwoven types Linear feet Cubic feet Thousand pieces Thousand pieces Asbestos-Cement Shingles and Clapboard Siding shingles and clapboard, including accessories Roofing shingles Squares Squares Asphalt Floor Tile Asphalt floor tile Thousand square yards Vinyl Asbestos Floor Tile Vinyl asbestos floor tile ' Thousand Bquare yards ' Asbestos Textiles and Other AsbestosCement Products Asbestos textiles Yarn, cord, and thread Cloth Other asbestos textiles, including roving, lap, wick, rope, tape, carded fibers, etc. Pounds Pounds . Pounds ; Asbestos-cement products Flat sheets and wallboard, all : thicknesses converted to basis Corrugated sheets Pipe, conduits, and ducts, including pressure pipe .100 square feet 100 square feet Short tons * (continued) 6000 1h95 PRODUCED BY FORD APPENDIX A tl TABLE 21 (Continued) B5 1967 LIST OP MANUFACTURED ASBESTOS PRODUCTS85 I i Industry and Product Description Quantity Measure Asbestos felts Roofing-asphalt or tar saturated Other Other asbestos and asbestos-cement products, including millboard and prefabricated housing components Short Tons Short Tons Gaskets and Insulation Gaskets, All TypcB Gaskets (for Booling nonmoving parts') Asbestos, asbestos-metallic, and asbestos-rubber ' Packing (except leather, rubber, and metal) and Asbestos Insulations A6be6t08 compressed sheet Pounds Packing (for sealing moving parts) ( Asbestos, asbestos-metallic, and asbestos-rubber Thousand pounds ' Insulation materials containing asbestos pipe insulation Cellular and laminated Linear feet i 85 percent magnesia Linear feet Diatomaceous silica, calcium, silicate, expanded 6ilica, and asbestos fiber Linear feet Other pipe insulation Linear feet Block insulation, including sheet and lagging Thousand i 85 percent magnesia board feet i Diatomaceous silica, calcium i silicate, expanded silica, and Thousand asbestos fiber board feet Other block insulation, including celluar and laminated Thousand board feet All other asbestos insulation 6909 1496 ' PRODUCED BY FORD APPENDIX A 86 TABLE 22 ASBESTOS PRODUCT MANUFACTURING PLANTS, 196341 vocation Jew Hampshire Belknap ^ Hillsborough Total Massachusetts Essex Franklin Middlesex Suffolk Worcester Total Connecticut Fairfield Hartford Middlesex Total lew York Albany Kings Orange Suffolk Total Jew Jersey Bergen Essex Hudson Mercer Morris Passaic Somerset Union Total No. of Plants with Emplo'/ment of Total 2 20 50 100 250 500 1,000 Plants 19 49 99 249 499 999 or more 11 11 2 11 1 11 21 22 1 74 1 1 1 3 3 11 11 11 5 1111 1 1 1 3 11 1 11 6 21 1 1 ,2 1 1 11 3 21 1 2 1 32 4 1 16 5 2 1 2 il 1 211 3 51 (continued) 8000 169? PRODUCED BY FORD i APPENDIX A 87 TABLE 22 (Continued) ASBESTOS PRODUCT MANUFACTURING PLANTS, 196341 --------------------------- ---.---- No . of Plants with Employment of Location Total 1 20 S0- 1 DO- 250 500 1,000 Plants 19 49 99 249 499 999 or more Pennsylvania Elk Lancaster Montgomery Northampton Philadelphia Cit) Potter 1 1. 2 l 3 1 2 1 1 2 1 1 1 Total Ohio Cuyahoga Paulding Portage Ross Total Indiana Henry Huntington Kosciusko Lagrange Lake Rush 93 13 1 11 1 1 1 41 1 1 1 3 1 1 1 11 1 1 1 1 1 1 1 l Y Total Illinois Cook Kankakee Lake Will Total 6 11 8 S1 1 4 1 14 s 1 22 2 1 21l 1 3 4l Michigan Wayne 11 Total 11 (continued) 8000 1498 .... mmmmmm wua** PRODUCED RY POn APPENDIX A / 88 TABLE 22 (Continued) ASBESTOS PRODUCT MANUFACTURING PLANTS, 19634* Location Total Plants Wisconsin Milwaukee 1 Total 1 Missouri St. Louis St. Louis City 2 3 Total 5 Kansas Barton 1 Total 1 Virginia Essex Frederick-, Norfolk City 1 1 1 Total 3 forth Carolina Mecklenburg Union 2 1 Total 3 south Carolina Charleston Marlboro 1 1 Total 2 leorgia DeKalb Talbot Troup 1 1 1 Total 3 1 19 1 1 1 1 1 1 1 1 2 1 1 2 No. 20 of PI ints with EmDlovrnent 50 1 DO- 250 500 of 1,000 49 99 249 499 999 2 2 22 1 1 1 1 1 1 1 1 J // i 1 1 1 1 1 1 1 1 (continued) 8000 r<*99 PRODUCED BY FORD APPENDIX A i * TABLE 22 (Continued) ASBESTOS PRODUCT MANUFACTURING PLANTS, 196341 69 Location Total Plants 119 Florida Dade 11 Total 1' 1 Alabama Mobile 1 Total 1 Mississippi Hinds Union 1 11 Total 21 Louisiana Jefferson Orleans 3 3 Total 6 Texas Dallas Ector Grayson Harris Hill 22 11 1 3 1 Total 83 California A1 ameda Contra Costa Los Angeles Orange Sacramento San Benito San Joaquin San Mateo Santa Clara Total 2 1 9 1 1 1 1 1 1 18 1 1 '1 1 1 S JN1TED STATES TOTAL 124 ---------------------------- 1------------------- 40 No of Plants with Employment of 2 b- 50- 100- 250- 500- ~ 1,000 49 99 249 499 999 or more 1 1 1 1 2 -1 1 1 ^3 1 1 2 1 21 1 41 11 1 214 1 ." 1 1 336 1 10 13 34 21 4 2 wmzmpm iwwuwwiimmmmim 6000 1500 PRODUCED BY FORD I iI APPENDIX B t! Y eooo> 1501 PRODUCED BY FORD riMWAHMIilMklfel >i 'I i (. 92 RESPIRABLE ASBESTOS PIBERS A number of question* arise regarding respirable asbestos fibers. What length of fiber is respirable? What is the particle-to-mass ratio? Should all fibers, whatever their length or diameter, be counted? if not, can any instrument be designed to select the right size distribution in the atmosphere? Timbrell2.19 has Btudied the deposition of fibrous material in the respiratory system. Fibers 50 or even 200 u long are found in the lungs because the free-falling speed depends largely on the diameter. Thus, particles less than 3.5 u (moBt asbestos particles are less than 0.5 p) in diameter can possibly penetrate deeply into the lung. The more symmetrical a fiber is, the greater its chance of pene trating. The largest compact particles normally found in the lung are about 10 M in diameter. Limitation on the lengths of the fibers which reach pulmonary air spaces is imposed by the nasal hairs and the small diameters of the respiratory bronchioles. These limitations are summarized in Table 23. Respirable fibers have been defined by the British Occupational Hygiene Society^^ as fibers less than 200 u long, less than 3.5 U in diameter, and having a length-tobreadth ratio of 3 si. Only the fiberB longer than 5 m in length are counted. / <sfi t j j . j ; I - I . 8000 1502 PRODUCED BY FORD 93 TABLE 23 PENETRATION OF FIBERS THROUGH NASAL HAIRS2*1*9' Length of Fiber (microns) % Penetration throuqh Nasal Hairs . 1st Staqe 2nd Stacie 3rd Staqe 0.5 ' 100 100 100 50 75 57 42 100 . 53 24 11 150 31 10 3 200 26 5 1 250 20 3 300 17 2 350 14 1 Walter23 has investigated the mass of average particles in the asbestos textile industry (see Table 24). He found that respirable duet contains approximately SO percent asbestos and that 10 particles of dust per ug contain 5 x 105 particles of asbestos per Mg. Prom this conversion factor the threshold limit value for asbestos can be calculated* as approximately 350 pg/m^ (5 mppcf). TABLE 24 PARTICLE-MASS RELATIONSHIP OP ASBESTOS AS A FUNCTION OF FIBER LENGTH229 Total Concentration , Mg/nr Particles*/cnr (approx) 100 200 400 600 100 400 1,000 2,500 Incineration Residue ug/nr (aoorox) 50--60 200-300 700-000 1,800-2,000 . Fiber Length in Microns (approx) < 150 < 500 < 700 <10,000 . ^Particles counted with a Ronimeter. *5 mppcfl?7 x 106 p/m3*350 Mg/m3. The concentration estimated in air is 600-6,000 p/m3*1.2 - 12 x 10 9 wg/nr. 8006 1603 ' PRODUCED BY FORD f.Lm 1 lUm mmimSim 94 Finally, there remains the problem of counting respirable fibers in ambient air. It appears that a fairly sophisticated instrument will be required which can (1) separate the other particles from fibers, (2) identify the asbestos fibers in a host of other fibers, and (3) count only those fibers longer than 5 m and shorter than 200 p with diameters less than 3S m ] I I 8000 1504 iI I PRODUCED BY FORD