Document rpRyR8qbx59kMMzOar3pyb0er

ENVIRONMENTAL DEFENSE FUND 1525 18th tljfc&btSTREET, N.W., WASHINGTON, D.C. 20036/202 833-1485 June 27, 1973 Honorable Sherman Gardner Acting Commissioner of Food and Department of Health, Education W a s h i n g t o n , D. C. 2 0 204 Drugs and Welfare Dear Sir: The undersigned Petitioners, Center for Science in the Public Interest and Environmental Defense Fund, submit the attached petition pursuant to sections 409, 701(a) and other provisions of the Federal Food, Drug and Cosmetic Act with respect to the issuance of regulations necessary to protect the public health from adulteration of foods and drugs with asbestos particles. The Commissioner's authority to issue the requested regulations is f o u n d in s e c t i o n s 2 0 1 (s), 301(a), 402(a), 409, 501(a) and 701(a) of the Act. Attached hereto in quintuplicate and constituting a part of this petition are the proposed regulations in the form proposed by Petitioners and a statement of the grounds upon which the Petitioners rely for the issuance of the regu lations . Very truly yours Scott H. Lang Attorney for Petitioners 1525 18th Street, N.W. W a s h i n g t o n , D. C. 20036 OFFICES IN EAST SETAUKET, NY (MAIN OFFICE); NEW YORK CITY (PROGRAM SUPPORT OFFICE), WASHINGTON, DC, BERKELEY, CALIF This paper is recycled to protect the environment ASBESTOS AND YOU Barry I. Castleman, M.S.E. and Albert J. Fritsch, Ph.D. Center for Science in the Public Interest 1779 Church Street, Northwest Washington, D. C. 20036 1973 ASBESTOS AND YOU by B a r r y I. C a s t l e m n A l b e r t J. P r i t s c h Center for Science in the Public Interest 1779 Church Street, NW Washington, DC 20036 Second Printing March, 1973 Copyright (c)1973 Center for Science in the Public Interest No part of this publication may be reproduced by any means without the prior written permission of the authors. TABLE OF COHTEHTS Abstract Asbestos, Friend or Foe? I. Health Effects: ' Asbestosis, the First Asbestos Disease Lung Cancer from Asbestos Mesothelioma from Neighbors and Relatives Other Cancers Asbestos Bodies in the Streets II. Environmental Aspects: Urban Air Asbestos in Buildings Asbestos in Personal Items Asbestos in Food, Brinks, and Drugs Conclusion and Recomr.endations Appendix 1 Letters to Environmental Protection Agency on Asbestos in Air Ducts in Buildings Append!:; 2 Letter to Food and Drug Administration on Talc Use Appendix 3 Letter to the Environmental Protection Agency on Air Pollution Standards hAppendix Letter to Labor Department on Occupational Standards Table I Uses of Asbestos Table II Consumption and Production of Asbestos in the U.S. Table III Population Groups with Occupational and Environmental Exposure to Asbestos Table IV Uses of Talc . References 1 3 8 o 10 16 26 27 30 30 31 32 3^ 33 IJx hi UO h9 $0 $1 2 3 5U ABSTRACT 1 Asbestos has become a widely used material in cor industrial society over the last 100 years. Unfortunately, we have found that there are grave hazards attendant upon its use. Severe lung scarring, which can lead to death from heart failure, results from long-term, heavy exposure, (asbestosis). With the implementation of basic dust controls in asbestos processing plants, it was hoped that the workers' hazard would be eliminated. However, as asbestosis became a less severe problem, a startling incidence of lung cancer and stomach cancer appeared among asbestos workers. In the late 1950's an epidemic of an extremely rare cancer was discovered and traced to environ mental asbestos exposure (malignant mesothelioma). As those diseases were associated with successively lower exposures, the populations known to be at risk have increased. Even while this information was being published, new and dangerous applications of asbestos were developed, the worst of which was sprayed fireproofing insulation. This alone exposed millions of American construction workers to high concentrations of asbestos during the I960s, as well as neighbors and passers-by to a lesser extent* It is now established that urban dwellers with no history of occupational exposure to asbestos have asbestos f i b e m and scarring in their lungs. Whether this significantly increases their cancer risk will not likely be known for decades, due to the long latent periods of these diseases and the inability of past studies to define the dose-response relationship. The purpose of this report is to stimulate a greater awareness of asbestos hazards, and generate actions which 'trill reduce and eliminate these hazards. At this time, the many government agencies which should regulate uses of asbestos-- The Labor Department's Occupational Safety and Health Administration, HEW's Environmental Protection Agency and Food and Drug Administration, Interior's Bureau of Mines, and the Federal Trade Commission are all failing to take appropiately strong measures. In many cases, the hazards can be eliminated by substitution of less dangerous materials or reduced by implementing safer tv-ark practices. ACKNCI'JLEBGMEKT The authors gratefully acknowledge the contributions of Hr, Henry Wehman, Dr, Jerome Gavis, and Mrs, Donna Powers in the preparation of this document. Asbestos Friend or Foe? This report deals with the health and environmental effects of asbestos. We Americans have shown far more skill and ingenuity in using asbestos in our consumer products than we have in safeguarding ourselves from this toxic material We know that asbestos is both useful and toxic, but we don't have dose-response information on low levels of environmental asbestos exposure. There is evidence that asbestos exposure in combination with other hazardous substances carries severe risk of cancer. Since surveillance techniques are extremely tedius or primitive, no one has yet defined the concentrations and distribution of asbestos particles within the environment. We show great ingenuity in using asbestos in homes, trains, airplanes, ships, farms and factories. Fortunately, a part of the asbestos used is more or less harmless due to the lower possibility of erosion of the fibers from such items as ceramic products and plastic and tile products. However, other uses are extremely dangerous due to the fact that asbestos is not held tightly in the product or on the applied surface. Examples are asbestos cloth, rope, paper and insulation materials. For ten years we have known that brief and low level exposures to asbestos can cause cancer. Yet this material continues to be incorporated into hundreds of new products, with a blessing and a hope that it is safe. Until recently hazard labeling of asbestos products, such as wallboard sold in hardware stores, was not required. The present situation i3 not much of an improvement, due to the foot-dragging by enforcement agencies, weak regulations and actual loopholes in the law. What is this mysterious substance? Asbestos is an economic term, not a scientific one. It refers to a group of hydrated silicate minerals that seperate readily into fibers. These are divided into two exotic groups: h serpentines (chrysotile) and amphiboles (crocidolite, anosite, tremolite, 9S%actinolite and anth^ophyllite). About of the asbestos that we use is in the form of chrysotile. The major producers of asbestos are the Soviet Union and Canada, which hh%account for and of the world output respectively (all chrysotile)j 6%and the Republic of South Africa, which produces (mostly crocidolite and 3%amosite). The United States produces only of the asbestos but is the largest consumer using about one-fourth (1,2). Asbestos has been known to man for thousands of years. Archeologists k 9S00have found that asbestos was in general use as much as years ago in Finland, as a cementing agent in the preparation of clay pottery (3). Herodotus (10 B.C.) described the Romans mining asbestos in the Italian Alps. He also described a cremation cloth made from it, Pausanias, when speaking about the golden lamps made around i*30 B.C. by Callimaihus mentioned the wicks of Carpasian flax which were incombustible by fire. Strabo, Solinus and Plutarch referred to woven cloths that did not b u m and the "ever-burning lamps" in the Grecian temples. Asbestos is derived from the Greek word meaning inextingui3hable (3a). SO)KLii$r (A.D. referred to difficulties weaving asbestos and the use of respirators to avoid inhalation of its dust. Charlemagne (800 A.D.) had a tablecloth made from asbestos (1|); he would impress his enemy warriors by cleaning it by passing it through a fire. Maybe an investigation of his tomb would reveal that asbestos particles were implanted in his lungs. I-iarco Polo (about 1250 A.D.) wrote that he had seen Tartars using cloth that with stood fire ($) In spite of its long history, it has only been in the last ceatury that asbestos has became more than a mere curiosity. Gradually the heat resistance 5 characteristics have made this substance useful. World production has expanded a thousandfold since 1900, -dth a steep grovrth rate since 19h0, People learned that asbestos had ether characteristics such as a rein forcing binder in such products as Portland cement, rubber and plastics. These expanded uses have resulted in the following consumption figures: 00 metric tons in l p80; 330,000 tons in 192$; hli6,000 tons in 1138; over two million tons in ll8j 3.9 million tons in 1966 (1,5), Both because of its heat resistance and spinnability, asbestos has a use in textiles. Some better-known products of the asbestos textile industry are safety clothing, lagging cloth, woven brake linings, clutch facings and electrical insulation. (See Table I and II on uses) Cement products account for the major us of asbestos (some estimate that 70$ of the world's production of all types of asbestos is used in cement building materials). The cement product is rigid, strong, weather resistant and heat-insulating. The sheet products are such items as shingles, electrical switchboard panels, and laboratory table covers. Asbestos cement is used also in making drain pipes and pressure pipes, water and gas mains, sewage pipes, venting flues, and for electrical cables and mining operations. It is estimated that in some countries 0$ of the drinking water is supplied in asbestos cement pressure pipe (a). The second highest use of asbestos is in vinyl and asphalt floor tile. Likewise, it is used as an inexpensive filler in paints, roof coatings and caulks. Miscellaneous uses include gaskets, sprayed insulation for building construction, undercoating for automobiles, asphalt paving and curbing, welding rod coatings and filter media (6,7). It is estimated that about 8t of the asbestos consumed currently is used in applications in which the fibers are "locked in" or tightly bound 6 1959and not able to beeone airborne to any significant extent (8). In there were over 3,000 industrial applications of asbestos, and the list is rapidly growing (9). Differences among the types of asbestiforra materials are important in terms of their applications as well as in their biological effects. Chrys- otile is flexible, has relatively high tensile strength and has far bettor spinnability than all other types. On the other hand, chrysotile is chemi cally unstable in the presence of dilute acids and even distilled water. An aqueous solution with pH under 10. R will leach magnesium from the fiber (10). Acid resistance of the other major types, crocidolite and amosite, is good. Crocidolite has the greatest tensile strength of the three, but has poor heat resistance (ll). Chrysotile fibers may be curved and can break down into elementary fibrils as small as 200-^00 A in diameter. The unit fibrils are suscep tible to attack by body fluids. Fibers of the amphibole types are straight, and do not break down in similar fashion (12). The smallest amphibole fibers ,,o .. are 800-1,000 A in diameter (13). There is a wide variability in trace metal content of the asbestiform minerals. It is noteworthy that several metal complexes, especially those containing iron, have been shown to induce cancer; and several metals, including chromium, nickel and lead have been proven to be carcinogenic. Special attention has been called to high nickel and chromium content of chrysotile, and the manganese content in crocidolite and amosite (lh,l5). Iron is a major constituent in crocidolite and. amosite. Traces of primary oils occur in crocidolite and amosite (chrysotile has none). Ccmmercial fibers of these amphibole types (i.., after possible contamination by secondary oils) have low levels of polycyclic hydrocarbons in their oils. Jute bags used to transport and store asbestos fiber are a Section I Health Effects There are a number of diseases which have been chcum to have been caused by asbestos exposure. It is noteworthy that by 1913, American life insurance companies routine!;;- declined to insure asbestos workers (3b), This was six years before Cooke reported the first case of asbestos disease to appear in the general medical literature, Asbestosis, The First Asbestos Disease The first recorded case of asbestos disease was reported by hurray in 1906 (U). His patient was the last of a group of ton asbestos cardr00m 35workers to die before the age cf of pulmonary disease, presumed to have been tuberculosis. On the postmortem examination diffuse fibrosis of both lungs was discovered and attributed to asbestos exposure. It was not until 192lj that a second case of asbestosia was reported by Cooke (16), In 1927, Cooke cited "curious bodies" in the lungs of his subject, a female asbestos textile worker who died at age 33 (5), The unique in situ reaction to as bestos fiber was called the "asbestosis body" by Stewart and Iladdow in 1929 (17) That year Cooke wrote that he considered the curious bodies to be pathogneanie of pulmonary asbestosis if found in any numbers (18), In 1930, Iierewether and Price published a report following a thorough investigation of conditions in England's asbestos manufacturing industry. On the basis of 363 workers examined, they concluded that one in eight asbestos workers would have evidence of fibrosis. They made a number of recemendations concerning improved ventilation and dust suppression measures (19), Regulations were drawn up shortly thereafter and became effective March 1, 1932, markedly reducing dust levels in asbestos plants (20), In the United States, Dreessen and co-workers made a Public Health significant source of adsorbed oil contamination, relative to the oils originally present, with all typos of fiber. It is reasonable, in view of the physical and chemical differences of the asbestos types, that there are differences in biological effects-- depending on the type of asbestos and the application. Section I Health Effects There are a number of diseases which have been shcini to have been caused by asbestos exposure# It is noteworthy that by l?l3, American life insurance companies routinely declined to insure asbestos workers (3b) This was six years before Cooke reported the first ease of asbestos disease to appear in the general medical literature. Asbestosis, The Pirst Asbestos Disease The first recorded case of asbestos disease was reported by hurray in 1906 (U), His patient was the last of a group of ten asbestos cordr00m workers to die before the age c 35 of pulmonary disease, presumed to have been tuberculosis. On the postmortem examination diffuse fibrosis of both lungs was discovered and attributed to asbestos exposure. It was not until 192h that a second case of asbestosis was reported by Cooke (16). In 1927* Cooke cited ``curious bodies" in the lungs of his subject, a female asbestos textile worker who died at age 33 (5). The unique in situ reaction to as bestos fiber was called the "asbestosis body" by Stewart and Iladdow in 1929 (17) That year Cooke wrote that he considered the curious bodies to be pathognomic of pulmonary asbestosis if found in any numbers (1$). In 1930, hcrewether and Price published a report following a thorough investigation of conditions in England's asbestos manufacturing industry. On the basis of 363 workers examined, they concluded that one in eight asbestos workers would have evidence of fibrosis# They made a number of recommendations concerning improved ventilation and dust suppression measures (19). Regulations were drawn up shortly thereafter and became effective '-larch. 1, 1932, markedly reducing dust levels in asbestce plants (20). In the United States, Dreessen and co-workers made a Public Health significant source of adsorbed oil contamination, relative to the oils originally present, with all types of fiber. It is reasonable, in view of the physical and chemical differences of the asbestos types, that there are differences in biological, effects-- depending cm the type of asbestos and the application. 9 Service study (21,22) of asbestos textile mill workers* A high incidence of definite clinical and roentgenographic evidence of asbestosis was found in persons who had had 5-10 years of exposure to dust levels in excess of 5 million particles per cubic foot (mppcf). The authors pointed out that methods for controlling dust levels below that threshold existed for most processes. Since only three doubtful cases of fibrosis were found among those with milder exposure, the authors concluded that "5 million particles per cubic foot nay be regarded tentatively as the thrediold value far asbestos dust exposure until better data arc available." A serious flaw inherent in this study was that the average age of the workers was only 32.1, and more than one half were under 30 years old. The British Occupational hygiene Society, in setting its Standards for Chrysotile Asbestos Dust in 1968, spoke in terms of the workers cumu lative lifetime dose. The recommended maximum accumulated exposure (100 $JJ )fibers/ml-years, fibers longer than corresponds to about 15 mppcf- years for asbestos textile mills (23,2ii). This means a maximum of 2f/ml- years far 50 years, 10 f/ml-years for 10 years, etc. This cumulative level of exposure is said to reduce the risk of contracting asbestosis to one percent among those who have a lifetime's exposure. "By 'asbestosis' this committee means the earliest demonstrable effects on the lung due to 7a.asbestos." the final paragraph, the Society admitted that it is not possible at present to specify a safe threshold for asbestos-associated cancers. The threshold limit value (TLV) for time-weighted average 8-hour exposure officially recommended b y the American Conference of Governmental Industrial Ifrgienists in 15>70 was 5 mppcf (25). In 1968, ACGIH published notice of intended change to lower TLV to 12 fibers/millilitor ^ 5 microns 10 $/Xin length or 2 mppcf; and in 1970 they published a limit of 5 f/ml> as anotice of proposed intended change. Cn December 7 1971, the U.3. Department of Labor adopted an emergency standard of 5 f/ml> effective immediately. The Public Health Service recommended in January of 1972 that a standard of 2 f/ml> be effected in rad-1971 (25a). In June of 1972, the Department of labor announced that the 5 f/ml standard would remain in effect until July 1, 1976, at which time a 2 f/nl limit would be in force (29b). Pulmonary asbest.esis is a slowly progressive disease. It nay net be readily apparent on roentgenograms in early stames, and sometimes net even when extensive. Its classical symptom is dyspnea. In addition, finger clubbing, cyanosis, and extensive fine basal rales tend to develop after a long period fitem onset of asbestos exposure (26). Severe fibrosis can ultimately lead to death from cardiac failure. The pathogenesis of the fibrotic lung lesions is still not quantitatively understood (.27). It is known that the disease progresses long after cessation of expo sure, once established. It has occurred in workers with sh ort, heavy expo sures (20,26,28,29). In general, changes indicative of clinical disease are rarely manifested less than 10 to 20 years after onset of asbestos exposure (26,28). Improvements in dust control have resulted in decreased mortality from asbestosis and longer life expectancy for workers in asbestos processing plants. Lung Cancer from Asbestos In 1935, attention was first called to the coincidence of asbestosis and lung cancer (also a rare disease at that time ) in a single case (30 ), There followed a number of clinical reports, but the possibility that asbestos exposure carried an elevated cancer ri3k was not generally taken seriously 11 before 19l>7. Ibrewether found that in Great Britain, of 235 deaths with asbestosis then on record, 31 (13.23) also had limn: cancer. Merewether contrasted this with a frequency of 1.325 lung cancer in 688U cases cert ified at death as having silicosis (31). In 1951 Glcr/ne (32) published a review of 1205 necropsies on persona who had worked in dusty occupations. He found lung cancer in llt.lij of necroosies on subjects with asbestosis (17 out of 121), against 6.9,5 in silicotics (55 out of 796) and 8.3% in 169 with no pneumoconioses. Doll (33) found that among 105 asbestos factory workers examined at necropsy from 1935-53 18 had lung cancer. A follow-up study of 113 men with at least 20 years' exposure showed that 39 deaths had occured (against l5.it expected in the general population). The excess was entirely due to lung cancer (11 against 0.8 expected) and other respiratory and cardiovascular diseases (22 against 7*6 expected). Doll concluded that the average lung cancor risk among men employed 20 years or more was of the order of 10 times that experienced by the general population. He noted that these men had had years of exposure prior to implementation of dust controls in 1932. Including Doll's cases, Hueper (3k) listed a total of 99 cases of asbestosis lung cancer reported in the literature (1955). 3h 1958 Braun and Truan (35) published a study of lung cancer among Canadian chrysotile miners. In their opening remarks thev reviewed critically the case for a casual relation between asbestos and lung cancer. They first cited studies by Saupe (no lung cancer among 620 cases of asbestosis) and Hegelins (no lung cancer in 126 radiologicallv diagnosed cases of asbestosis in Finland, among kl6 workers examined) (36,3 7 ), They claimed that a series of clinical (not epidemiological), reports had led to the belief that the relationship was mroved. Thev cited the frequent absence of information on smoking habits, length of time in the industry, and dust exposure levels# Gloyne's cases were criticized as earning from a select group of cases which were brought to his attention fen* their unusual or complicated pathology# They suggested that Hueper's 99 cases contained some duplication among British authors? and finally, only 17 were in the United States and Canada (the other 82 were in Great Britain)# The cohort studied consisted of nearly 6,000 miners with at least 5 years employment as of the start of the study (1950)# They were followed for the next six years and a careful search m s made for possible lung cancer deaths. Only 9 proven and 3 questionable cases of primary lung cancer were found. All 12 were known to have smoked at least 5 cigarettes per day. This rate is not significantly higher than the age-standardized male mortality for the province of Quebec in those same years. Major weaknesses of the Canadian study were the short period it covered (66%)and the large dilution factor of men aged 20-hit in the original cohort. It should be borne in mind that the miners in the original cohort were healthy in 1950 and themselves represented a "survivor group". Their chances of living another six years were undoubtedly greater than those of age-standardized counterparts in the general population. The only epidemiological study of lung cancer in asbestos factory workers to result in negative findings was done in Dresden in the late 1950 (38) In subsequent years, a sharp rise in lung cancer among these same workers was found, however. The later report (39) concluded that lung cancer had replaced right heart failure (cor pulmonale, usually the result of severe asbestosis) as the most common cause of death among Dresden asbestos workers* Jacob and Anspach noted that the average lapsed oeriod from onset of exposure to death from cor pulmonale (25.7 years) was consid erably shorter than the corresponding lapsed period for lung cancer associ- 13 ated with asbestos exposure (30.7 years). The implementation of improved industrial hygiene methods and the great reduction of tuberculosis since (19h2the advent of antibiotics ) were given as the reasons for asbestos (39jkO).workers surviving long enough to die of lung cancer In a study of workers employed in an asbestos products plant as of 1938 followed through i960, I'uncuso and Coulter found an excess of deaths from lung cancer (19 vs. 5.6 expected;. The authors considered this a conser vative figure because: the whole plant population was used, not just production line employees at risk; and events of the war affected employ 3kment patterns of 2/3 of the cohort aged 15 to in 1938 (hi). By the end of 1963, the British Ministry of Labour had knowledge of 58Lt persons in whose death certification asbestos is had been cited. The proportion with lung cancer as a complication had risen steadily from 13.2/ in liererjether1s 19h7 report to 255 in 1963 (h2). Building trades insulation workers in the Hew fork area who had entered the trade before 19h3 were traced b y Selilcoff and co-workers through 1962 (h3 ) Of 255 deaths, lj.5 died of cancer of the lung and pleura, where only 6.6 such deaths were expected. These men have relatively light, inter mittent exposure to asbestos. Their practices have changed little over the years. Recent measurements have shown that their 6-hour time-weighted average exposure to asbestos i3 3 f/ral, with occasional peaks about ten (kk,times that level hJj.a). This study has been extended through December 31, 1971 (U5, 1*6), by which time 123 men who had lived for 20 years after their 8kfirst exposure had died (against 288.5 expected). Of these, (one in five) died of lung cancer (11.U expected); the average lapsed period was 230-2*0 years; of ij cases of lung cancer found through 1971 and for which smoking histories were known, hi had histories of cigarette smoking. This indicates that an asbestos worker who smokes cigarettes has 92 tines Xk the risk of crying of lung cancer compared Tilth a nan who neither works with asbestos notr smokes cigarettes. This is an order of magnitude above the risk attributed to cigarette smoking alone; in other words, 9 out of 10 cases of lung cancer among cigarette-smoking insulation workers are attributable to occupational hazard. On the other hand, no increased lung cancer incidence was found among the non-smoking workers. It is striking that the separate effects of cigarette smoking and the asbestos work are negligible compared to their combined effect in causing lung cancer. Tragically, most lung cancers detected among insulation workers are inoper able because the men have seme degree of asbestosis and cannot support ary further loss of lung function. Newhouse (4.7) found no excess mortality from lung cancer in asbestos factory workers first exposed less than 17 years before her study (1969). There was significant excess among those with longer lapsed periods. There was little difference in lung cancer mortality between those with under two years on the payroll (8 against 1.6 expected) and those with over two years on payroll (11 against 1.5 expected) among men working heavily exposed areas. In areas with low to moderate dust exposure, no excess mortality occurred 2,h(3 lung cancer deaths in I46I4 men with over 16 years lapsed time, expected.) K i v U u o t o and Meurmau (U8) found threefold excess of lung cancer deaths (8 cases) among anthTopbyllite mine and mill workers in Finland, all of whom had asbestosis. This was a small study and the exposure times observed were short; but it indicates that occupational exposure to this type of asbestos carries a lung cancer hazard also. Isselbacher and co-workers (h9), in reviewing published autopsy reports, noted that in 71 cases of asbestosis lung cancer in which the patients* sex was given, 21 (29.6$) were females, in contrast to ii.O to 10.3I in the 15 general population. In IJresden (39), where females made up less than half 21% 9%of the work force studied, they incurred of the lung cancer against in the general population. Keal (50), reporting 15 deaths of females with asbestosis, listed It as having lung cancer, all of whom were non-smokers. Of 15 males with asbestosis, 10 died of lung cancer. In a recent study of mortality in chrysotile mines and mills of Quebec (5l) IfcDonald and co-workers found only a small excess lung cancer mortality (97 against about 82 expected). However, the "heavily exposed" workers had a rate of lung cancer 5 times as great as that of the "lightly exposed" workers. The study group was composed of all the individuals employed between the years 1891 and 1920 (11,788). Of the 9981 (88) who were traced 2U57 had died. This provides evidence that miners and mill workers incurred a lower excess of lung cancer than other types of asbestos workers. The reason for the carcinogenicity of asbestos is not known, and it ha 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, the number of susceptible cells, the concentration of carcinogens on the fibers, and the time from exposure (52). In conclusion, it is now established that excess lung cancer mortality occurs among asbestos workers. Asbestos workers who smoke cigarettes have a much higher incidence of lung cancer than groups of workers whose smoking histories were not obtained, indicating a strong cocarcinogenic effect. There are no epidemiologic data, such as available for cigarette smokers, which indicate that cessation of exposure to asbestos is associated with subsequent decreased risk of lung cancer (26). The cases reported in recent years are a reflection of conditions decades earlier. Continuous and substantial improvements have subsequently been made in asbestos processing plants. The 16 hazards have not been long realized in trades where asbestos-containing materials are handled (and exposures are milder), Newhouse's recent study indicates that lung cancer risk may be normal among those with light exposure, even in cases of long exposure. Selikoff has found that virtually all recent lung cancer deaths in a group of insulators were among those who smoked cigarettes. It remains for more quantitative studies of lightlyexposed workers to define the dose-response relationship, both for workers who smoke cigarettes and those who do not. Mesothelioma for Neighbors and Relatives The existence of primary mesothelial tumors of the pleura, peritoneum, and pericardium has been a matter of dispute until very recent times. These tumors are rare, and in almost all cases death follows within months of development of symptoms. Campbell (53) reported finding U pleural mesoth eliomas in 3533 consecutive autopsies. The possibility that mesothelial tumors were metastatic from undetected primary sites was suggested by Willis (5U) and by Hinson (55) and maintained as recently as the I960 edition of Willis* pathology text (56). Others, however, observed cases of mesothelial tumors with no detectable primary tumors in other organs (53,57-6 1). The first report of pleural mesothelioma with asbestosis was made in 19h3 b y Wedler in Germany (62). In 1952 Cartier (63) reported 2 cases of pleural mesothelioma among Canadian chrysotile miners. Two years later Leicher (6U) reported finding a primary peritoneal tumor in an asbestos worker. By use of X-ray diffraction techniques he detected the presence of asbestos within the tumor. Bonser and co-workers (65), reporting 72 cases of asbestosis (in factory workers examined post-mortem), found 2 pleural and 1; peritoneal cancers, "the primary site not being found in any organ". Nearly 20 years after the British asbestos industry was ordered to control 17 dust exposures in domestic processing plantSjthere were still no dust controls in South Africa where the asbestos was mined. Schepers gave the following account of a 19il9 survey of ti c Transvaal asbestos mining district (reportedly less dusty than the Cape District) (69a). "At that time industrial hygiene in one of those mines and asbestos works was simply deplorable. Exposures were crude and unchecked. I found young children completely enclosed within large shipping bags, trampling down fluffy amosite asbestos, which all day long came cascading dorm over their heads. They were kept stepping lively by a burly supervisor with a hefty whip. T believe these children to have had the ultimate of asbestos dust exposure. X-ray revealed several to have radiologic asbestosis with cor pulmonale (right heart failure) before the age of 12.... "in the valley where the mill was located, asbestos dust rolled through like the morning dust, and I had a hard time keeping m y staff in working trim because of itching skins caused by asbestos adhering to our clothes. Even food at the local hotel was gritty with dust." Progress in dust control has been substantial but production has also increased tenfold in the Cape restrict in the last 20 years (69a,69b) In 1996, the first South African case of pleural mesothelioma was diagnosed. Within a year, SLeggs and Karchand had 16 cases in Kimberly and Johannesburg with histologically proven pleural mesotheliomas. They sug gested that asbestos might play seme part in the etiology, since asbestos bodies had been found in the lungs of the first case and large crocidolite asbestos deposits were located 200 miles west of Kimberly. Hone of the original cases admitted to mining asbestos* Detailed histories were ob tained from patients and surviving relatives. By 1999, an association with the Cape asbestos fields or the use of asbestos was established in 32 out of 33 cases with histologically proven pleural mesothelioma (66), m As an example of environmental exposure, bapier mentioned a woman born on the asbestos fields in 1900. oho left there at the age of 5 , and m s in 55good health until she developed a pleural effusion at Ghe died 18 months later of pleural mesothelioma. Detailed questioning revealed that she had attended an inf.ants' school near .an asbestos dump. The children used to slide dorm the dump on their way home. Two of her playmates at this school have subsequently died of the same condition, (67) The only type of asbestos mined in the Cape province is crocidolite. In Transvaal province (330 miles axrayj, m e r e amosite is the principal type mined (with some crocidolite), no mesotheliomas were found as late as I96H, despite intensive search. As of the end of I960, 179 cases of "definite" mesothelioma had been found in Couth Africa. (60) Of the II18 in which the history was known, 3 were listed a3 having exposure in the Transvaal amosite mines, against 51 who worked in the nines of the Cape. In 2k there was no evidence of environmental or occupational exposure to asbestos. It is still unexplained how such a disproportionate fraction of cases had exposure in the Cape fields as compared with exposure in the Transvaal amosite and crocidolite areas. Levels of dustiness and numbers of per3 ons-at-risk indicate that more cases should have been found in the Cape area, but not as many more as were observed (69). Recently, however, it has been reported that analysis of samples of airborne dust from Transvaal mines show that the average fiber diameter for amosite and crocidolite is three times that found in samples frem Cape mines (70). If the very small fibers cause mesothelioma, as many observers feel, this alone could explain the discrep ancy. In 1962, McNulty reported a case of pleural mesothelioma in an asbestos miner in Australia, one of the few other places in the world where crocido- 19 lite is mined (71)* In their study of asbestos workers in the United States (hi) 1'ancuso and Coulter found 5 cases of peritoneal mesothelioma, and suspected others. Enticknap and Slither (72) reported 9 primary peritoneal tumors among 52 cases of asbestosis seen at necropsy. All 52 worked in an asbestos factory where all three major types of asbestos were handled (Essex, England). Outside of these cases, the writers had not encountered a mesothelioma in several thousand necropsies. "A remarkable feature of the cases is the minimal fibrosis of the lungs." Hourihane (73) reviewed all cases of primary diffuse tumors of the pleura and peritoneum in the necropsy files at London Hospital from 1917-1962. He found asbestos bodies or fibers in the lungs, usually accompanied by fibrosis of the lungs, in 15 of 30 ("certain" and "probable") mesothelioma cases. He found no cases with fibrosis and only 3 with asbestos bodies or fibers in 100 controls at necropsy. More recently, Hourihane detected amphibole asbestos within nesothelial tumors of one quarter of the cases (7h). Newhouse and Thompson made a careful study of London Hospital mesothel ioma cases for histories of exposure to asbestos (75). Eighty-three cases were confirmed by necropsy or biopsy through 1961*$ in 76 of these full occupational and residential histories were obtained (73 died in 1950 or later). Forty (52.6*) had a history of occupational or domestic (living in the house with an asbestos worker) exposure. In comparison, only 9 out of (11,6%)76 control patients from the same hospital suffering from other diseases had such exposure (P^O.OOl). Among those with no evidence of occupational or domestic exposures, 11 of the mesothelioma patients lived within half a mile of an asbestos factory, compared with 5 of the control series (P^O.Ol). Mean interval between first exposure and death varied from 29*1* years among 23 factory workers to 1*8.6 years among the 11 neigh- 20 borhood cases. In Belfast, KeCaughey and co-workers reported finding asbestos bodies in the lungs of 12 out of 15 patients who died of pleural mesothelioma (76). Three years later there was a total of U5 cases (77). A highly significant k2difference in histories of exposure to asbestos was found between the 9most recent cases and matched controls (32 against 1 P c 0,001). Asbestos 2hbodies were observed in 21 (88$) of the mesothelioma cases where lung tissue was available. In 2l| matched controls and 5 other comparison groups lh%(totaling ij.00 cases) the prevalence of asbestos bodies varied from to 27:"'. Host of the mesothelioma patients had "light" exposures, such as indirect occupational exposure in the shipyards. No attempt was made to classify exposure by asbestos type since all three major types are used in shipbuilding and repair. Similar reports of mesothelioma in shipyards in the Netherlands (78) and Great Britain (79,80) followed. In 2500 consecutive autopsies in Hew York (1953-196^) Selikoff and co workers found h pleural and 3 peritoneal mesotheliomas (81). All were associated with asbestosis (found only in 26 of the autopsies). One of the men with mesothelioma was a carpenter, who had denied ever having seen, used, or handled any asbestos product. This may have been a case of indirect occupational exposure in the construction industry. In a survey of 152 hospitals (Pennsylvania), Lieben and Pistawka (82) found U2 mesothelioma cases in the years 1958-1963. Ten worked in asbestos plants, 8 lived or worked close to an asbestos plant, 3 were family members of asbestos workers. In 10 others a history of questionable exposure to asbestos was obtained after prolonged questioning. In the other 11, no history of exposure could be found. The "most striking finding" was the clustering of 6 of the lj.2 cases around one insulation plant (only 2 worked there) in the geographical area of approximately 30,000 square miles 21 covered by this study. Borow and co-workers (83) reported a concentration of mesothelioma cases (17 in 3 years) at a hospital 2 miles from a huge asbestos plant in Kanville, 5%New Jersey in which 7 of all asbestos mined in North America is converted to commercial use. Tiro patients there had only environmental exposure} i.e. they lived near the plant. liore recently, the total reported number of cases from this town of 1>,000 reached 52 (83a). Hamburg,: Germany is a center for asbestos factories, as well as a major port. Between 1958 and 1968, 319 cases of pleural mesothelioma wore found in Ij. medical institutions there (8U). "There may be many more in other hospitals." The prevailing wind in Hamburg is from the west, and most of the cases resided to the east of the shipyards and in a residential district around the largest asbestos plant. In this district alone there were 5l cases of mesothelioma among 53,000 inhabitants. Of the 119 of these cases which could be fully investigated, "definite" or "likely" histories 6%),of asbestos exposure were established in 55 (U Average lapsed time from onset of exposure to tumor development was 35*2 years (85). The first use of dust suppression techniques within the Hamburg asbestos plants was in the mid-1930's, but only after World War II did the asbestos factories, for economic reasons, begin to filter the asbestos dust from air $0%exhausted from the factories. The fact that ever of these cases had had no other known asbestos exposure led the authors to conclude that neighbor hood exposure to pollution from these plants was a major cause of death in the Hamburg cases (85)* At first, it was hoped that mesotheliomas were caused only by exposure to crocidolite asbestos, the type mined in South Africa's Cape Province. The insulation workers studied by Selikoff and co-workers had extremely high incidence of mesothelioma: 6 pleural and 16 peritoneal tumors in 380 22 workers who had died by the end of 1968 (U$). The mean lapsed period from onset of exposure was 3k. 8 years for pleural mesothelioma and k3.0 for oeritoncal. The only types of asbestos known to have been used in insulation materials are c'nrysotile and amosite. The largest asbestos manufacturer in the United States has never used crocidolite for the manufacture of insula tion. Only small amounts of crocidolite were imported into the U.3, before 19li.O (crocidolite is not mined in the U.3.). In other words, even if croc idolite exposure occurred, it could not account for the pattern of mesothe liomas seen among these insulation workers. Selikoff and co-workers did a prospective study of local units of the international Association of Heat and Frost Insulators and Asbestos Workers where all insulation work is done in shipyards. The purpose of their study, which included two comparison groups of workers with little and no shipyard employment, was to compare the health hazards of insulation work which in cluded amosite asbestos exposure (shipyard insulation) with insulation work much more limited to chrysotile (general construction work). All three groups were found to suffer similar, severe mortality primarily from lung cancer, mesothelioma, and asbestosis (Ska). These researchers also followed 230 men who began work in an amosite insulation factory between 19kl and 19k$, worked there for a year or more, and were alive on January 1, I960, Total deaths in this group through June 30, 1971 was 10$, against U6.U expected. The excess was limited to the categories of cancer of various sites and asbestosis, including $ cases of mesothelioma (8kb). Gilson attempted to register all mesothelioma cases in the United Kingdom (86). In 1969, he reported that $$0 cases had been found. From the distribution of cases by year when known (8/year from 19$$-19$9, 27/ year from I96O-I96I1, Ub/year from 196$-1963) he concluded that, "Although some of the increase is undoubtedly due to more widespread recognition of 23 the tumour, it seems highly probable that there has been a real increase in incidence as well," He went on to say that it is likely that the totals are under- rather than over-estimates. In checking the validity of death certificates of 301 asbestos workers, IJcwhouse and Hagner examined necropsy reports for 158 and histological material for 8H of those. The additional information gathered led to a number of revisions in the stated causes of death. Mesothelioma was the certified cause of death of U; another 15 mesotheliomas were identified upon review of histological material. Most of these workers died between 1955-196h, a period of ascending prominence of mesothelial tumors. In contrast, the revised number of lung cancer deaths was 28 against 29 cert ified (87). Thomson (88), writing in 196?, pointed out that the criteria for diag nosing mesothelioma put forth by Churg and co-workers in 1965 are too restrictive for diagnosing pleural tumors. The criteria are (89): (a) there is no other primary tumor that can conceivably cause serosal spread} (b) the gross appearance of the tumor is that of a superficial growth with only shallow invasion of the underlying organs; and (c) metastases, if any, are by and large limited to regional lymph nodes. Thomson remarked that while most cases have no secondary tumors, there are examples of extensive spread. He based his conclusions on a series of 17 recently autopsied cases and more than 50 positive biopsies. Included were examples of direct spread as well as blood and lymphatic spread to a wide variety of organs. Referring to the confusion in the standard texts and the medical literature, he noted that the histopathologist tjho is not familiar with mesotheliomas and wishes to diagnose them is presented with severe difficulties. ill deaths from mesothelial tumors known to pathologists in Canada 16$between 195? and nid-1968 were registered. They numbered (2/3 in males), or about one per million persons per annum. Occupational and residential histories wore obtained from survivors of 91/ of the cases and two matched control series. An association with definite or probable contact with asbestos was clearly demonstrated (P<0.001), but only 20/ of the male cases and one female case had any such contact. There was increase in rate of occurrence in the final few years of the period, but the authors attributed this to record-keeping differences and to .greater interest in these tumors. The mortality was appreciably higher in Quebec (1.//million) than in Ontario (0.8/million) or the rest of Canada (0.9/million). The "most noteworthy finding" was that all excess deaths occurred in workers engaged in manufac ture and industrial applications rather than in mining or milling (5l,90) . Two reasons for the relatively low cancer risk of mining chrysotile were offered: either chrysotile is less likely to cause mesothelioma and lung cancer than other types of asbestos, or something in addition to asbestos is necessary (90). It is certain that people living along the serpentine belt in eastern Quebec have a lower incidence of mesothelioma than those . living in the Cape province of South Africa. Likewise, there has been no excess incidence of mesothelioma in the anthTophyllite mining region of east Finland (91) Wagner and co-workers (92) have produced mesotheliomas in 1/3 to 2/3 of the rats they injected intrapleurally with the three major types of asbestos. There was no difference in effect between the natural and oil- extracted forms of crocidolite. The risk of developing a mesothelioma was proportional to the dose applied. Wagner suggested that although chrysotile 25 is biologically active, the spiral shape of nary of its fibers nay inhibit their inhalation, rendering then less hazardous. This may be one reason for the comparatively low mesothelioma mortality of chrysotile miners and mill workers. Earlier, Wagner reported induction of mesotheliomas in rats injected with silica (53). Huepor reported producing mesotheliomas in rats by peritoneal injection of polyurethane foams (raising concern over the use of polymeric foams in surgery) (9U). This leads to the question: what normally encountered agents besides asbestos fibers can lead to development of raesothelial tumors in man? Cocarcinogenie agents have been sought for mesothelioma as well as for lung cancer. Iron and manganese are mined in the Cape province but not in Transvaal province. Felders and other men employed in shipyards are exposed to iron o3d.de dust as well as asbestos. Several authors have suggested.that there may be a combined effect which enhances the likelihood of development of mesothelioma (68 , 82). So far, the association between mesothelioma and the suspected cocarcinogens named is only casual, however. Assertions of family or neighborhood exposure should be viewed with caution, according to Selikoff (95), as often there is a short but forgotten period of employment in an asbestos plant. Relatives of workers and those who live near asbestos plants would know when openings escLsted and may have worked a month or so when their own trade was slow. Selikoff and Hammond (96) concluded that no quantitive conclusions regarding the dose-response relationship will be available without epidemiological studies with indirect occupational exposure and environmental exposure. Kesothelioma is still a rare tumor in the United States. In a prospective study of cancer in the general population, Hammond (97) found that only 3 out of 31,652 deaths (in over a million people between 30 and 89 years of 26 age) were caused by mesothelioma. The previous studies lead to the following conclusions, Hesotholioma is caused by exposure to airborne asbestos fibers. Though there is nrobably a difference in the mesothelioma hazard posed by different types of fibers in different applications, it is prudent to regard all asbestiform materials a3 hazardous. There is indication that the laosed tine from exposure is longer for loti levels of exposure (76,86). At low levels or(where there is little or no competing risk of asbestosis lung cancer) the likelihood of contracting mesothelioma must be a monotone increasing function of dosage. The large proportion of cases of mesothelioma with light exposure to asbestos (occupational, indirect occupational, neighbor hood, and domestic) indicates that the safe exposure threshold level is substantially lower for mesothelioma that for asbestosis or lung cancer. Other Cancers There is evidence that gastrointestinal cancer occurs in excess among those exposed to asbestos: the insulation workers studied by Selikoff and co-workers (U6) have had more than 3 times the expected number of deaths from this cause, liL, against 12.6 expected. The authors considered the number sufficient to be conclusive proof of relationship, taken together with similar findings among insulation workers in Belfast (100). Asbestos has also been suspected in increased incidence of ovarian cancer. Graham and Graham (98) reported that 6 out of 12 patients with early ovarian malignant changes had birfringent crystalline material in the ovaries. The main point of the authors is that there was a similarity in the histological appearances of ovarian carcinoma and mesothelioma. To date, epidemiological evidence to sunport the hypothesis that asbestos ex posure carries an excess risk of ovarian cancer does not exist. 21 Asbestos Bodies in the Streets As mentioned earlier, Cooke fj rst referred to "curious bodies" in asbostosis, noting that the lung characteristically reacted by coating entrapped asbestos fibers () These ijere first called "asbestosis bodies" in 1929 (17). The designation was shortened to "asbestos bodies" when it was realized that people without asbestosis were found to have the in their lungs. The first report of non-occupational asbestos bodies was made in 1929 by Stewart and liacldow (18), who examined lur>/- tissue of a oerson who lived across the road from an asbestos plant. Shortlv afterward Identical "bodies" were reported in the lungs of coal miners (101). Subsequently, thev have been reported in graphite workers and diatcmaceous earth workers (102). Until recently, however, these "bodies" have generally been associated with occupational exposure to asbestos. In 1963, Thomson and co-workers (1 0 3 ) reported what appeared to be asbestos bodies in the lungs of a large oroportion of urban dwellers who had no recorded occupational exposure to asbestos. .Analysis of lung tissue sections and expressed lung fluid all over tho world (99, 10)4-1 1 2 ) sub stantiated Thomson's findings. In most studies where sex was noted, pre valence of "asbestos bodies" was higher in males than in females. The percentage of cases in which "bodies" were found varied with the technique used in the investigation, the amount of lung tissue examined, and the diligence and persistence with which they were sought. The percentage of positive findings has been reported as high as 97% (99) and 100# (112). A question arose whether the "bodies" found in the lungs of urban dwellers with no occupational exposure to asbestos were asbestos bocU.es or nseudoasbestos bodies; that is, did they have asbestos fiber cores or not? Gross and co-workers produced what they called "ferruginous bodies" (llij.) by injecting intratacheally aluminara silicate fibers, silicon carbide whiskers, glass fibers, and cosmetic talc (commercial talc may contain as much as 52# tremolite asbestos) (115) into the lungs of hamsters. These were identical to asbestos bodies. Still the question remained, is as bestos present in the lungs of urban dwellers, either enclosed in ferritin or as free fiber? Numerous technical difficulties impeded the quantitive analyses of cores of "bodies" found in lung samples. The main problem was that chrysotile, the only asbestos type with an unristakeable morphology (and by far the most abundant type), tends to split into unit fibrils 200 to ItOO Angstroms in diameter. It is also altered chemically and physically in vivo (12). Langer and co-workers (116) finally overcame these obstacles, employing electron-microprobe and high magnification (up to 217,000 X) electon microscopic techniques. They found that 15 of 16 electron micro probe analyses of asbestos bodies found in lungs of urban dwellers were consistent with magnesium-leached chrysotile, and one was consistent wdth amosite. Furthermore, analyses of samples (conservatively estimated at one millionth of the total lung burden) of lung unequivocally showed chryso tile in 2h of 25 consecutive ife-vvYork City autopsied cases (117). Similar observations have been made in London; Pooley and co-workers (117) not only found chrysotile asbestos in almost 50# of their cases, but also noted it to be the most c a m n and abundant of all fibers detected. Eight hundred fifty-six New York City autopsy cases were examined for asbestos bodies in lungs and lifetime occupational histories were obtained (115). The results suggested that asbestos bodies are not randomly dis tributed among the general population. Forty percent of housewives showed asbestos bodies, 50# of males in clerical or professional work, 50$ of males in manual ironic effusive of those who had a history, hoi-rover brief, of shipyard or construction work. The last mentioned group had asbestos bodies in 90 of 129, or 7Of' of the cases. One hundred consecutive Ifew York City autopsy cases in each of two years, 193k and 1967, were examined for asbestos bodies in ashed 175/* lung sec tions by Selikoff and Hammond (118). Ho significant difference in the percentage of positives occurred in the two years (93$ and 60$, respectively). A similar study of secular changes in asbestos body prevalence was carried out by Pooley (119) in London, examined 30^c lung sections (not a3hed) in 123 cases autopsiod in 1936, and 100 each in 19.U6, 19.96, and 1966. He found no asbestos bodies in those who died in 1936 or in females who died in 19'i.6. The overall percentages of positive cases rose steadily to 20$ in i 960, a figure idlieh Pooley noted is in accord with that found in London in a recent siolticcntor survey using the same techniorue of analysis. Do such preliminary studies reflect real differences in prevalence trends between Heir York and London? If further study can establish that the prevalence of asbestos bodies in the general population was the same 30 years ago as it is today, and if pathological studies can demonstrate that mesothelioma was indeed uncommon until recently, there trill be less reason to suspect that the finding of asbestos bodies in the lungs of the general population is a harbinger of an incipient epidemic of mesothelicma. 30 Section II Environmental Aspects Having considered in detail the various diseases which can be caused by breathing and coming in contact -with asbestos fibers, let us now look at the various parts of the human environment where the danger of asbestos contamination exists. Urban Air lynch and Ayer (121), compared light macroscopic samples with the same material studied by electron microscopsyj they reported that only 1 in 100 fibers present in air could be seen by light microscopic methods. This meant that dust-counting instruments used in making measurements in asbestos factories could not be used for environmental asbestos measurement. Preliminary electron microscopic analysis (122) suggested that chrysotile levels were greater in Manhattan than elsewhere in Hew York. Nicholson and his co-workers attributed this to the extensive use of asbestos in construction in Manhattan. Tihile values ranging from approximately 10 to 200 X 10"9 grams per cubic meter of sampled air is a snail quantity of asbestos (total urban particulate loading is on the order of 100 X 10"^ grams per cubic meter (1 2 3 )), 10** grams of chrysotile could represent a million fibrils. "For the past 10 years, during which spray fire-proofing came to be exten sively used, it was not uncommon to see extensive snowfalls of asbestoscontaining material over widespread areas of New York and other metropolitan cities. In sene cases, the fireproofing was even done with no attempt to enclose the spray area b y tarpaulins or other means." (.122) Sampling around construction sites where extensive spraying of asbestos fireproofing was in progress demonstrated a significant contribution of this material to air pollution. In some instances chrysotile asbestos levels approximately 31 10 tines ''background" were observed. A few months after this report was made, the use of sprayed asbestos insulation was totally banned in Boston and Chicago and severely restricted in Hew York, Los Angeles, Detroit, and Fxiiladelphia (12lt). Tho U.3. Environmental Protection Agency has proposed to ban it nation-wide (I2l;a). toother suspected significant source of asbestos Pollution is abrasion and erosion of brake lining .and clutch facings in motor vehicles. The brake linings are generally fabrics woven from asbestos yarn only or from asbestos yarns and notal threads. The linings are made to adhere to drums or plates by means of themosetting resins. Lynch examined the emissions from automobile brake wear and found that most, but not all the fiber was destroyed by heat of friction (12?). Mechanics typically use air hoses to blot; the dust from brake parts and thus contaminate garage areas with asbes tos dust. Vacuuming or wet washing with a paintbrush and kerosene would be much safer. Asbestos in Buildings It is evident from Table 1 that the major use of asbestos is in mate rials used in building construction. These include cement products of which 70/o of the world's production of asbestos is used. The cement product is rigid, strong, weather resistant and heat insulating. Cement sheet products include fireproof shingles, electrical switchboard panels and laboratory table covers. Asbestos cement is also used in malting drain pines, water and gas mains, sewage venting flues and for coverings to electrical cables. Though this use is not dangerous in itself, in the process of installation of cement products, the fitter must often cut, smoothe, and work the materi als, often allowing considerable dust to accumulate in the working areas. One building practice may result in serious contamination of asbestos in interiors of public structures. This is the practive of designing ceiling 32 spaces as return air plenums. Instead of running metal ducting across the ceiling and connecting exhaust with return ducts, air is allowed to move through ceiling spaces sprayed, with asbestos for fire protection and thermal control. The asbestos coating can easily erode through the stead;/ current of air passing over it.s surface, and the nartlcles of asbestos can find them selves in the rcheatad or cooled air. The degree of tlr'.s contamination i3 dependent upon a number of factors: rate of air flow, tyne of asbestos used, method of application to building surface, length of space traversed by returned air. No one knows tho degree of asbestos contamination by thi3 source, but Ir. William Puckelshaus of the Environmental Protection Agency promised that the Agency would look into this problem of potential contamination of indoor air (126). However, after a 20 month lapse the Environmental Protection Agency still has not initiated a monitoring program. (See Appendix: l) A school built in Lander, Wyoming in 1961 had sprayed on asbestos ceil ings in classrooms. Public Health Service investigators found that "asbestos falls intermittently in both large and small quantities, and one is able to wipe up asbestos dust at random from the surfaces of the schoolroom furniture. The ventilation system recirculates room air, and the intake filters are clogged with asbestos fibers." Though airborne asbestos levels were below 5 f/ml, these investigators declared the condition a hazard to health, and renovation to replace the asbestos material began in June, 1972 (127). A similar situation is being repaired in dormitories at UCIA. Asbestos in Personal Items With over 3,000 uses of asbestos, little wonder each and every American should become concerned. Prom ironing board covers to drapes, asbestos items find their way into the homes of our people. It is thought that one of the 33 nost dangerous areas where asbestos contamination would cause untold h a m is when used as additives in tobacco products, i-lany patents exist for such practices. Investigation has revealed that none are being used today, but one of the first American cigarette filters was almost pure asbestos. An investigation of Buroooan cigarette filters is being conducted at this moment. Those of us who use gas masks should be pleased to lcnow that the llaval Research Laboratory has develowed a fiberglass filter said to be "superior" to Bolivian crocidolite asbestos, the Bureau of Mines reported in 1970 (128), Attempts arc being made to find out whether the Bureau has taken steps to assure that this hazardous use of crocidolite has been discontinued. One can buy asbestos dust in many hardware stores. One of the uses made y' of this dangerous commodity was a Practice among art teachers until recently. They would mix asbestos dust Trith modeling clay for consistency and ease at working the material. However, the presence of the dust and use by children was declared a ma.ior hazard, and warnings were given by the Food and Drug Administration under pressure from public interest groups. One use of asbestos can be a source of danger for persons of special occupations: protective clothing. Firemen use suits (129) and other equip ment made of asbestos; asbestos gloves are found in places where ovens are operated and around scientific laboratories. Continual use over a period of time may be a source of asbestos insult. In laboratories are also asbestos heating tapes, asbestos insulation nads, filtering materials and asbestos paper for making insulated coatings around heated glassware. Many of these items are subject to wear and flaking. The atmosphere of the working space can easily be contaminated b?;- asbestos. For other croups, see Table III. One unsuspected source of asbestos is in talcs which contain varying amounts of trenolite asbestos. Talcs are soft and can be reduced to small 3k particle size* they are cheap and are good t h e m a l and electrical conductors and, like asbestos, are resistant to attack by acids and bases* These prop erties alio;-; for a multiplicity of uses (see Table IV) ranging from fillers in scouring soaps to solid lubricants. Blejer (130) has called attention to the potential cancer hazard posed by the strong chemical similarity between talc and asbestos, and has also written to one of the authors that nany mineralogists doubt if such a thing as an asbestos-free talc deposit o;d.sts* This latter complication has so far prevented the appearance of a study of cancer incidence of workers exposed to pure talc* Talc miners who work ;-rith a talc containing about 30% tremolite risk developing a talc fibrosis similar to a3bestosis and incur four times as much cancer of the lung and pleura as their counterparts in the general popu lation (131). A few mineralorical analyses have been made on talcs used in these many items* A study by Schulz and Williams on 3l coaaaercial talcs indicated a range of 0 to 82% tremolite with greater than trace amounts in 1 7 , or or third (113). This alarming report beckons a thorough analysis of all uses of talcs# Some of the area which requires immediate investigation should be in talcum powders and vaginal, deodorants. Here large quantities of talc which could contain different amounts of asbestos can be easily administered to prime cancer sites. Among talc uses which should be strictly controlled include the use as lubricants in the interior walls of balloons, where children naturally inhale and exhale the air used to inflate the item, kecent analyses of a limited number of brand by the Food and Drug Administration revealed no asbestos in the talc. However, strict regulations on talc use are still needed with an active program of surveillance. A recently discovered serious contamination problem is in the area of 3? coats imported fro.:. Italy -which contain asbestos mixed with wool. This was detected because the coats were declared to contain asbestos in order to escape the wool duty. Before the public was alerted in 1971* there wa3 an estimated 100,000 coats sold to women in this country. A measurement of air concentrations near lightly brushed coats were 10,000 times more asbestos than normal background (132). Asbestos in Food, Prinks, and Brags Though asbestos is not directly added to human foods, still it is able to contaminate them through careless and thoughtless practices. One such practice is the polishing of rice by the use of talcs. Talc is also used as a dusting powder for salami and a polishing medium for peanuts (128). Kerliss believes that since much of the polished rice eventually is exported to Japan, this might be a reason why there is a very high incidence of stomach cancer in that country (133) While this inference was highly questioned in recent months, kerliss1 report eventually led the Food and Drug Administration to propose a ban on asbestos-containing talc as a polishing agent (see Appendix 2). A use of asbestos which causes considerable worry is the use of asbestos filters for beer, wine, and hard liquors. This allows for small fibers to be washed into the final product and find their way into the stomachs of drinkers. One of the authors spoke with the chief engineer at a Carling brewery and informed him of the hazardous potential of asbestos to workers and the public. The company immediately procured a cellulose substitute from Grcfco, Incorporated, 'pilch had also furnished the asbestos-containing filter material. Asbestos filter media are widely used in united States breweries, and at this time a number of companies are switching to substitutes voluntarily in order to preempt government regulation and adverse publicity. 36 The above experience supports the clair. that the resistant properties and low cost of asbestos load to -ridesoread, nonessential uses which can be readily substituted and eliminated. Asbestos-containing filter's are also used by sons manufacturers of pin. Representatives of Seagrams, one of ''hose products is Calvert pin, maintain that asbestos has unique filtration properties and the company is seeking other materials which can produce satisfactory claritjr in their product. Electron microscopist Henry Eehman found yrcater concentrations of asbestos fibers in Calvert gin than wore proseiit as background levels in the water from which it was made (133a)# Asbestos filters are also used in processing fruit juices, sugar, lard, and vegetable oils, and the listing here is by no means all-inclusive, Nicholson and co-workers found that asbestos filters contaminate drug solutions used to intravenous, intramuscular, ana intraperitoneal injections (133b). This last form of "therapy" is particularly alarming in view of the fact that the peritoneum is a urine site for development of mesothelioma. The Food and Drug Administration has said it is conducting analyses to determine if asbestos is entrained in certain products filtered Tilth asbestos. However, the FDA spokesman claims they are having trouble adapting their chosen techniques, optical microscopy, and X-rav diffraction, to perform the analyses. This is because optical microscopy is incapable of detecting most of the tiny fibers, and X-rav diffraction depends upon the crystal structure remaining intact (as mentioned earlier, even water will leach magnesium from chrysotile). A leading New York asbestos researcher has not only told FDA officials that their methods won't work, but has also demonstrated this claim for then# This deliberate subterfuge of studying a problem to death shows the FDA's contempt for its stated mission of protecting the public health'. Asbestos cement pipe carrying potable water requires periodic drilling 37 and tapping for maintenance purposes* In addition, asbestos may be slowly eroded by crater flowing through these pipes. Analyses are being undertaken to determine the degree of contamination of water from these causes, where this pipe is used. Jn Baltimore, asbestos cenent nine is prohibited for metropolitan water because cast iron and prostressed non-asbestos cement pipe have better physical properties (l33c). However, word did not travel far. % In neighboring Harford County, bO percent of the trater supply is carried in asbestos cement pipe. The Environmental Protection Agency has proponed no regulations for the discharge of asbestos into waterways. Conclusion and Recommendations The widespread contamination of asbestos throughout tho United States is knrnm but has not been publicised. The public is simply unaware of how dangerous this toxic material is. The work of good research scientists over the past few decades which shows the cancer-causing potential of this mater ial has not been coupled by a socially responsible education of the great mass of citizens who eerie in contact with asbestos. It is time that public interest scientists broadcast the simnlc proven truth and demand that unanswered questions as to extent of contamination and types of use be addressed. The leading cause of death among asbestos workers today is lung cancer. Asbestosis, formerly the leading cause of death of these -orkers, is declining. The reason is that asbestosis is caused by relatively severe occupational exposure, characteristic of prc-19ii0 asbestos plant conditions. Continuous improvements made since then and implementation of recently adopted standards should virtually eliminate asbestosis as an occupational hazard, in the meantime, incidence of lung cancer in asbestos workers has increased drama tically. The recent discovery that insulators who smoko cigarettes have 92 times as gre-vt a chance of developing lung cancer as men who neither handle asbestos nor smoko is particularly alarming. Lung cancer in urban areas is twice as high as in rural areas, and the national Academy of Sciences attributes the difference largely to air pollution (I3I4). It is also known that urban dwellers yjith no history of occupational exposure to asbestos commonly have numerous asbestos fibers in their lungs. kJhat role do low levels of asbestos exposure play in urban lung cancer, particularly amonm the millions of cigarette smokers? Ilesothelioma i3 another na.ior cause of death among asbestos workers. Others who receive neighborhood and inlinect occupational exposure are also 39 subjected to increased mortality fron mesothelioma, which occurs mostly in workers with light exposure. Because it i3 caused by lower level exposure, me3othelioma has become the disease of greatest concern to those who 3tudy the health hazards of asbestos exoosure. Gastrointestinal cancer is two to throe times as prevalent among asbestos workers than in the general population. It might be considerably more com mon if not for the competing risks of other asbestos cancers and asbestosis. This finding has grave imnlication3 for the presence of asbestos fibers in foods and drinks consumed by the public. That excess mortality in the above categories claims hop of insulators and asbestos processing plant workers has led same to call asbestos work the worst occupational health problem in the U.3. decent Labor Ttepartment stand ards are demonstrably insufficient to protect workers against asbestos cancer. Selikoff and co-workers (13$) estimated that there are fewer than 100,000 workers regularly using asbestos in construction trades in the United States, let more than 3,000,000 other building trade employees work in the same structures. A large number of workmen have similar indirect occupational exposure in shipyards (136). In addition to the plight of those workers, there are many Americans subject to family and neighborhood exoosures to asbestos. Everything from talcum powder to playing and living near construction and demolition sites open about half of all Americans to serious confrontation with asbestos. The knowledge we now have about the carcinogenic effects of asbestos cane as a result of retrospective epidemiological studies. Because of the inherent incompleteness of these studies and the difficulty in compiling accurate information on causes of deaths, wo have obtained an inconclusive picture about dose-response relationships for mesothelioma and lung cancer. Studies now undertalcen will hot yield results for many shears owing to the long latent periods of those diseases. Since the threshold concentration that humans can safely tolerate for continuous exposure has not been determined, it is impossible to evaluate the health hazards posed by present ambient concentrations. Likewise, it is not possible to determine the hazard posed by nonoccupational use of asbestoscontaining items at thi3 moment. The effect of asbestos as an environmental carcinogen zrill bo more fully determined in future studies on mesothelioma mortality trends. Asbestos is one of the major environmental contaminantsj it was declared so by the Environmental Protection Agency in the spring of 1971. However, this declaration has not been fortified as of this moment by Standards. The original proposed regulations (Federal Register, Dec. 7 1971) have not yet been implemented. In fact, an intermediate draft document was found to be weakened (see Appendix 3). yhile more scientific research is necessary, the need should not retard us from demanding stricter regulations on the manufacture, advertisement, distribution and use of asbestos products. Both collective and individual action is necessary. Among collective citizen actions should be the following a) demand a zero fiber tine-weighed average for all occupational exposure to asbestos by July, 197& (see Appendix U); b) provide that all hand-operated and power-operated tools for asbestos have local exhaust ventilation systems including fabric filter dust dust collections; c) require personal protective equipment for work places where asbestos concentrations exceed the level of 2 f/ml; d) ban the use of friable asbestos materials in building construction, except where no substitutes can be found; e) implement strict control of asbestos use in shipyards in order to eliminate indirect occupational exposure; f) inform all brake servicing mechanics, people who wear asbestos protective clothing and others who are exposed to asbestos in their work of the hazards ,and recommend safe practices; g) affix caution labels to all raw materials, mixtures, scrap, waste, debris and other products containing asbestos fibers; h) halt tho use of asbest.os in the making of ary friable consumer product and remove these materials from the store shelves; i) discontinue the use of asbestos filter materials in the preparati r of foods, drugs, and alcoholic drinks; 1) stop the use of talc containing even trace amounts of asbestos in any product where fibers could become airborne; lc) forbid the use of talc in foods and some consumer products including vaginal deodorant sprays; l) require public buildings, which allow return air to cross sprayed asbestos areas, to have air plenums surfaced with metal ductwork; m) require all buildings with exposed asbestos ceiling surfaces to undergo renovation for removing or covering the asbestos; n) require adequate wetting to lay dust in demolition of buildinrcobtaining asbestos; o) prohibit the use of asbestos cement pipe in metropolitan water supply systems. Tfnat can you do as an individual concerned citizen? How that you know that asbestos is used in a multitude of products, map-/ of which are not labeled, beware of any product which could conceivably contain friable as bestos fibers. If you suspect that a product in a hardware store contains asbestos, read the label, ask the salesman, and (if necessary) write to the manufacturer. Ask your local hardware dealer to remove asbestos dust from the shelf Check pipe and boiler insulation in your home and see that the surfae is not broken. You can buy resin-inpremated cloth to rrao the mire iiigi-'1 =. tion. Replace torn ironinfrboard covers and bur;'- them (asbestos waste can c-thor'rise find its way into the air via a municipal incinerator). Like'-dsc, bury anv imnorted coats purchased in 1970-71 which contains asbestos as in dicated on the label. -*akc sure that you neighborhood elementary school no longer has tx.. . oowder for making punnet3 and masks. P'ind out whether the buildino vou work in has uncovered asbestos firenroofing in the recirculation air plenum or on ceilings. Ask local breweries and distillers if they use asbestos filters. If there is an asbestos mine, mill or manufacturin''' plant near you, kkvi out what it discharges into the air and water. Arc ore-carrying trucks cov ered with tarpaulins? Before 1895, when Johnson and Johnson began talc manufacture, babies were commonly dusted with corn starch; this safe substitute is still available, and at one-fourth the cost of talc. lie recommend it. Don't use feminine hymiene sprays which contain talc. Avoid talc dusted balloons, rice, pro phylactics and chewing rum. If you suspect a product, write to the mar.. . turer-- and let us know if you discover another use of asbestos. 7/hile many of the applications of asbestos products cannot be judged at this moment due to lack of sufficient evidence of hazardous use, still we should err on the side of prudence; we should remove a suspected product until the manufacturer proves that the item is not harmful. It is not the duty of the public interest scientist to prove whether each and every item is harmful or safe. The public has the right to demand this scientific evidence from the manufacturers of the consumer products which will otherwise simply be means to further profits at the expense of the health and safety of the American people. h3 bcononics should not be the major determinant as to A e t h e r to remove an asbestos-containing product. Building plans nay have to be modified and construction and demolition costs increased, but these are small when com pared to the risk of health involved. The application of insulation in sheet or other solid form, although less convenient than sprav application, still provides adequate insulation and fireproofing. Furthermore, a3bestos-free sprays have been developed. It is t:'me for the American people to vie:; asbestos as neither friend nor foe. The far ud.ser position is to treat this potentially toxic material srith utmost resroct, ana onlr use it where absolutely necessary. If ue did so, the volume o? asbestos mined and orocossed would undoubtedly decrease, but the life and health of many people would be prolonged and improved. It is time the citizen oiakes his views knoum on this environmental pollutant Appendix !l March 29, 1971 44 Mr. William D. Ruckelshaus, Administrator Environmental Protection Agency 1626 K Street, N.W. Washington, DC. 20,l60 Dear Mr. Ruckelshaus: Some time ago our attention was called to the new building practice of designing ceiling spaces, especially in large public buildings, as return air plenums. Many plenum tareas have been sprayed with asbestos fiber for fire protection and thermal control. The connection of these closed ceilings with the duct system must result in some erosion of the asbestos coating and varying amounts of asbestos contamination of the air most surely occur. The degree of this dreaded contamination is dependent upon many factors including the rate of air flow and the type of asbestos fiber used. This letter is a request that you initiate federal monitoring of the asbestos content of indoor air. We have brought this potential asbestos pollution problem to the attention of sheet metal contractors, unions and various interested parties. Presidents A.E. Hutchinson of the Inter national Association of Heat and Frost Insulators and Asbestos Workers Union and E.J. Carlough of the Sheet Metal Workers International Association have expressed concern and encourage us in this request for government monitoring of indoor ambient air. Further investigation by a staff member of the Center for Study of Responsive Lav; showed that no government agency was doing systematic monitoring of interior air systems of residen tial or business establishments, although several agencies, including the Bureau of Mines and the National Bureau of Standards, have the sophisticated equipment necessary for such studies. The National Bureau of Standards is presently conduc ting a study on indoor pollution, but does not intend to look Appendix lb 45 JUN 1 1971 Mr. Ralph Nader Dr. Albert Fritsch Bor. 19367 Washington, D.C. 20036 Gentlemen: lhie is in reply to your March 29 letter cal ling attention to the practice of sing ceiling spaces in new buildings as return air plenums and the consequent potential hazard of introducing asbestos fire-protection fibers into the air. This Agency is concerned about airborne asbestos fibers. On March 31 of tnir year we Included asbestos ir the initial lift of hazardous air pollutants. Under section 112 of the Clean Air Act, as -- nndefl. Federal regulations controlling emi sions into the aablent air of any hazardous pollutant so listed must be prou!gated by March 31, 1972. During the past year -'e hare carried out a field saapling program for asbestos in some fifty urban and nonurban areas. These sample^ are being analyzed at a rate of ab-^ut 20 to 30 simpler per month. X note that your letter questions vhether the Environmental Protection Agency has authority to require modifications in building design in order to control potential contamination of indoor air. nevertheless, exploratory isearurements have already been made inside buildings in Columbus, Ohio, in Tew York City, and in Berkeley, San Diego and Santa Clara, California. Our present plans are to initiate a pilot study to mcarure asbestos concentrations inside and outside public buildings as soon as a competent contractor can be found. Let me again say that we welcome the continued efforts of the Center for Study of Responsive law to help us identify problems of the environment and develop effective programs to deal with such problems. Sincerely yours. william D. Ruckeishaus Administrator Appendix la Mr. William D. Ruckelshaus page two March 29 , 1 Protection Agency is charged with protecting our people f m n different types of air contaminants, this problem seems to enter under its jurisdiction. EPA may not be able to require modifications in building design, but it has the authority to take air samples, analyse them and fine known polluters. The hazards of continual breathing of asbestos pa cles over a period of time are well known. Prolonged inhala tion of asbestos dust is known to cause cancer of the 1unr', pleura and peritoneum. The `dangers of asbestos pollution arc well documented by medical authorities. These experts tell us that asbestos contamination can cause an epidemic wnen growing numbers of people spend large amounts of their work, study, recreational and shopping time in public buildings with such duct systems. If the clear warning of these men is valid, then some monitoring of the dust is necessary. Gener ally several decades elapse between initial asbestos exposure and noticeable detrimental health effects. Americans can :\'~ afford to wait until these effects are observed; we must clearly see how serious are the asbestos and inorganic pa a- culate levels of our buildings, so that steps be taken to correct faulty designs in ventilation and heating systems. It is incredible that such a large number of people can be subjected to such pollution dangers all for construction savings of a few hundred feet of sheet metal duct work. We trust you will give this matter your urgent consideration. Sincerely /cjs Albert Fritsch [Refer questions] 833-3^0 h (202) 332-6000 CENTER )R SCIENCE IN THE PUBLIC INTER 1779 Church Street, N.W. Washington, D.C. 20036 T December 15, 1972 45a Mr. William Ruckelshaus Administrator Environmental Protection Agency 401 M Street, S.W. Washington, DC 20460 Dear Mr. Ruckelshaus: I sent a letter to you on March 24, 1971 to call your attention to asbestos hazards arising from circulation of air in buildings through areas with exposed asbestos on interior surfaces. It was requested that you embark upon a program to determine to what extent these plenums are contaminated by asbestos. In your reply of June 1, 1971 you mentioned having plans to initiate a pilot study to measure asbestos concentrations inside and outside public buildings. After an 18 month lapse we are seriously concerned about your findings. It is evident from your letter that your agency has the authority to require modifications in building design in order to control potential contamination in indoor air. I would like to know what corrective actions have been initiated as the result of the above study. One final request. May I have permission to use our correspondence in an appendix to a report on asbestos which is to be published in January, 1973. A prompt reply would be deeply appreciated. ' Thank you for considering these requests. Sincerely yours Albert J. Fritsch, Ph.D. cc American Institute of Architects Environmental Defense Fund Attorney Scott Lang; Dr. Lucile Adamson Appendix Id ENVIRONMENTAL PROTECTION AGENCY Office of Air Quality Planning and Standards Research Triangle Park, North Carolina 27711 January 17, 1973 46 Dr. Albert J. Fritsch Center for Science in the Public Interest 1779 Church Street, N.W. Washington, D.C. 20036 Dear Dr. Fritsch: This is to confirm our telephone conversation today on the problem of asbestos concentrations in indoor a ir of selected commercial buildings. I t w ill also respond to your lette r of December 15 to Mr. Ruckelshaus. In our discussion, I believe I covered f u lly the points raised in your letter. In summary: 1. Our emission standards for hazardous pollutants, soon to be promulgated, w ill contain a ban on spraying of materials contain ing over 1% asbestos during construction of buildings. This should eliminate future situations. 2. The existence or magnitude of the problem of asbestos in indoor a ir is unknown; the measurements ju st don't exist. Contrary to our e a rlie r indications to you, EPA's sampling program has been limited to outdoor air. 3. Erosion from asbestos-lined plenum chambers in buildings is a potential problem. With the successful promulgation of the regulations to reduce emissions of asbestos into the outdoor a ir, i t seems appropriate at th is time to s h ift some of our resources into programs to define the magnitude of indoor exposures. This is also in keeping with a recent formalization of concern in my group for indoor pollutants. We w ill in itia te a modest sampling program to develop a data base on asbestos in indoor a ir and attempt to relate it to past construction practices. 4. The question of the need for and a d v isa b ility of control, regulations, and legal authority are a ll ambiguous at th is time. However, such considerations are premature until we determine whether we have a problem and we w ill postpone further discussion on them until a later date. Appendix le 46a 2 We w ill begin to develop a monitoring study and keep you informed of progress and schedules. Mr. Robert Neligan, Director, Monitoring and Data Analysis D ivision, Office of Air Quality Plan ning and Standards, w ill be responsible for the program. I have presumed on your knowledge and interest and assured Bob that you would be w illin g to make recommendations to him and our contractor on selection of sampling site s and be available for additional discussions on the problem. I enjoyed talking with you and hope we can continue the exchange. Sincerely yours cc: W. D. Ruckelshaus R. L. Sansom R. Neligan Director Air Quality Planning and Standards (202)3326000 CENTER FOR SCIENCE IN THE PUBLIC INTEREST 1W77as9hCinhgutorcnh, DS.iCre. d2,0N0.3W6. October 4, 1972 HDeeaprairntmg eCnlterokf H ealth; Education and W elfare LaneRood 6-88 5600 Fishers Rockville, Maryland 20852 Dear Sir or Madam: We a r e w r i t i n g t o c o m m e n t o n t h e p r o p o s e d n e w r e g u l a t i o n s (F e d e r a l R e g i s t e r , August 12, 1972) r e l a t i n g to pri o r - s a n c t i o n e d food i ngredients and a change in the prior sanction for talc. It has long bee n known that m a n y talcs contain substantial fractions o f tremolite asbestos. Schulz and h'illiars4 analyz ed SI different samples of commercial talc and found tremolite asbestos present in greater than trace arounts of 17. K l e infeld et a l z p e r f o r m e d a m o r t a l i t y s t u d y o n ta l c miners in Kew York and found a substantial excess of lung cancer. The talc these workers handled contained 25 to 35% tremolite.3 Among asbestos w o r k e r s e v e n more severe hazards were exposed in Sclikoff's investigations4 of mortality of insulation workers. Among these men, who handled chrysotile and amosite containing materials, 40% of the observed deaths were attributable to occupational asbestos exposure. G a s t r o i n t e s t i n a l canc'er w as t he ca u s e o f d e a t h in 37 c a s e s ( v e r s u s 11. 2 expected based on U.S. Mortality data), and malignant mesothelioma of the p e r i t o n e u m was the cause of d e a t h in an a d d itional 14. T h i s latt e r is an extremely rare cause of death in the general population. There certainly would have been larger numbers of cases in the above categories were it not for competing risks o f lung cancer (66 versus .9 expected), pleural m e s o t h e l i o m a (6 v e r s u s n o n e e x p e c t e d ) , 3 n d a s b e s t o s i s ( 27 v e r s u s n o n e e x pected) . In a review o f the literature for the National A i r Pollution Control Administration, it was stated by the authors that, "it has not been det e r mined whether nore than one [asbestos], fiber is necessary to induce a malignant tumor. We are concerned that talc will continue to enjoy the status, "generally recognized as safe." Th e r e is a strong s i milarity in the c o m positions of the asbestiforn silicates and talc. Talc particles have been found deeply embedded within tumor tissue taken from a n umber of patio-.vs PPargioer 2Sanction for Talc in Food* with ovarian and cervical cancer.* No asbestos particles were found in these tumors. We know of no epidemiological studies of workers with pure talc e x posure. H o w e v e r , at this time there is p l e n t y o f r e a s o n to s u s p e c t t h a t talc is not "safe" for use in foods, perfumed vaginal sprays, etc. In view of the above reports, vc conclude that a ban o f asbestifona minerals In foods is long overdue. The p r e s ently p roposed b a n on asbestosc o n t a i n i n g t a l c s is a b e g i n n i n g , a n d w e f a v o r i t s a d o p t i o n . Vie u r g e t h e Tood and Drug Administration to extend its activities to assure that a s bestos is not used in filtering of such items as beer, w hiskey and parenteral drugs. Sincerely yours, A* (Adto Appendix Page S Prior Sanction for Talc in Foods |r o References: 1. S c h u l z , R . Z . a n d C . R . W i l l i a m s , J. I n d u s t r i a l H y g i e n e . 2 , 7 S ( 1 9 4 2 ) . 2. K l e i n f e l d , M . e t al_., A r c h . E n v i r o n . H e a l t h 14_, 6 6 3 ( 1 9 6 ? ) 3. P r i v a t e C o m m u n i c a t i o n , M. K l e i n f e l d t o B. C a s t l e m a n . A u g u s t 1, 1 9 7 2 . 4. S e l i k o f f , I. J . et_ al_., P n e u m o c o n i o s i s . P r o c e e d i n g s o f t h e I n t e r n a t i o n a l Conference, Johannesburg, 1969, Capetown Oxford UnivorsTty' Press, p.180. 5. Sullivan, R.J. and Y.C. A t h a n a s s i a d i s , P r e l i m i n a r y A i r P o l l u t i o n S u r v e y of A s b estos, NAPCA Publication APTD 69-27, Releigh, National Air P o l l u t i o n C o n t r o l A d m i n i s t r a t i o n (1969), p. 10. 6. H e n d e r s o n , W . J . et^ a U , J . O b s t e t . G y n . 7 8, 2 6 6 ( 1 9 7 1 ) . ( )202 332-6000 CENTER FOR SCIENCE IN THE PUBLIC INTEREST 1W77as9hCinhgutorcnh, DS.tCre.et2,0N0.3W6. November 9, 1972 Mr. Wm. D. Ruckelshaus Administrator Environmental Protection Agency 401 M Street, SW Washington, DC 20460 Dear Mr. Ruckelshaus: We have been following for some tine your agency*s progress toward National Emission Standards for hazardous air pollutants. We are particularly concerned about proposed standards for asbestos, which is a m a j o r contaminant in our environment. Our center has received copies of the proposed"StandaTd for Hazardous Air Pollutants: Asbestos, Beryllium and Mercury" as sent to you for final approval. Further, we have seen the comments of the Baltimore County Health Department on this document. There is no need to repeat the deficiencies referred to in their letter of November 6th. We concur with all the contents o f that letter and think it should be given immediate c o n sideration. Overall, our impression is that the w a t e r e d - d o w n v e r s i o n o f the S t a n d a r d s e n t to y o u fo r a p p r o v a l is n o t r e a l l y a r e y u l a t i o n - - i t is a p e r m i t to o p e r a t e "business as usual." All six sections of the Standard,as originally proposed i n t h e F c d c r a l R e g i s t e r o f D e c e m b e r 7, 1 9 7 1 , h a v e b e e n w e a k e n e d o r d i s c a r d e d completely. Ve remind you that u n d e r the law, the emis s i o n of h a z a r d o u s air pollutants must be regulated by the Environmental Protection A g e n c y so as to provide "an ample margin of safety to protect the public health." As the Baltimore County letter makes clear, you will be put in an embarrassing position if called upon to explain how the sanctioning of visible emissions of asbestos dust from demolition (or any .source) is protective of the p u b l i c health. There is little need to remind you of the voluminous medical literature on asbestos. We are all familiar with many reported cases of malignant m e s o thelioma of the pleura and peritoneum, a disease extremely rare in the general population, but quite common among asbestos workers. Also a number of persons have this disease whose only known exposure to asbestos was environmental, that is, they have lived or worked near a mine, mill, m a n u f acturing plant, or fabrication area where asbestos was handled. Lung cancer among men who are occupationally exposed to asbestos and smoke cigarettes is n early 100 times as common as among m en w ho neither smoke n o r handle asbestos, and is ten times as common as among men who smoke but do not work with asbestos. T h e s e figures would undoubtedly be considered higher if asbestos workers were not simultaneously subjected to competing risks of mesothelioma, gastrointestinal cancer, and asbestosis. It is nea r l y impossible to e s t i m a t e the level o f a s b e s t o s e x p o s u r e to w h i c h the general population can be continuously exposed with no increased risk of m e s o thelioma, or to which the cigarette-smoking population can bo exposed with no i n creased risk of lung cancer. The National Institute of Occupational Safety and Health, in its recently published criteria document on "Occupational Exposure to Asbestos Standard Page 2 Asbestos'* says: "there is insufficient information to establish a standard to prevent such diseases including asbestos-induced neoplasms by any all-inclusive limit other than one o f zero." In the P r e l i m i n a r y A i r Pollution S u r v e y o f A s b e s t o s , it is stated that "...it has not been determined whe t h e r m o r e than o n e fiber is necessary to induce a malignant tumor." Obviously, it was a ppropriate to designate asbestos as a h a z a r d o u s a i r pollutant, and make it the subject of a regulation whose only criterion for acceptance is the prot e c t i o n of the public health. The Labor Depa r t m e n t has gore through the ritual of promulgating a standard foT occupational exposure which is insufficient to protect the health of asbestos workers and m a n y o thers w o r k i n g i n t h e v i c i n i t y o f a s b e s t o s c o n s t r u c t i o n m a t e r i a l s , h'e s t r o n g l y u r g e the L'nvironncntal Protection Agency to adopt a much tougher position on asbestos contamination, and to do so at the earliest possible date. Sincerely yours, Director, C m t e r for Science Merest lja r\,vy l Barry Castleran, M.S.E. Appendix Appendix: Letter to Mr. E.C. Guenther, Occupational Safety and Health Administration. ( )202 833-3721 CENTER FOR SCIENCE IN THE PUBLIC INTEREST 1346 Connecticut Avenue, N.W., Room 812 Washington, D.C. 20036 J u ly 1 7 , 1972 Mr. E.C. Guenther, Assistant secretary of Labor Occupational Safety and Health Administration Constitution Washington, Avenue D.C. 2 a0n0d0 k l^th Street Dear Sir: We deplore your recently promulgated Standard for Exposure to Asbestos Dust (Federal Register. Vol. 37, No. 110-- June 7, 1972) It Is well established In the medical literature that workers ex posed to the conditions prescribed face a greatly enhanced risk of developing fatal asbestos diseases. Your action followed pleas by the AFL-CIG for a one fiber per cubic centimeter (1 f/cc) limit and by the Oil, Chemical and Atomic Workers Union for a zero ex posure limit, as well as statements by recognized authorities of the Fount Sinai Environmental Sciences Laboratory to the effect that ko% of deaths of Insulation workers In this country, whose time-weighted exposure to asbestos Is 3 f/cc, are attributable to occupational asbestos exposure. This fact was revealed at the Karch 1972 Hearings. The Criteria document prepared by the National Institute for Occupational Safety and Health, "Occupational Exposure to Asbestos," makes It clear that while a 2 f/cc level cannot be de clared safe. It is undoubtedly less hazardous than 5 f/cc and all haste should be made to reach that level Industrywide. Tabershaw, reviewing the literature on asbestos In 19 6 7 , compared asbestos to radiation. If there is a safe threshold above natural background to which large human populations can be exposed with no enhanced risk to developing certain diseases, this thres hold Is not known. It will not soon be known, and It appears to be quite low. We are perplexed and alarmed by the government's In consistency In Imposing severe restrictions on occupational exposure to radiation while historically treating asbestos as a typical work room air contaminant. The following Is the standard we seek: a) Permlssable exposure to airborne asbestos fibers-- a 2 f/cc maximum time-weighed average (TWA) to become effective July 1, 1973, followed by a 1 f/cc (TWA) to become effective on July 1, 1975 and a zero fiber TWA effective on July 1, 1976. Celling concentrations-- 5 f/cc effective January 1, 197^. to be reduced to 2 f/cc by July 1, 1976. 2 b) Kethod s of Compliance i all hand-operated and power operated tools which may produce or free asbestos fibers, shall be provided with local exhaust ventilation systems In accordance with the American National Standard Fundamentals Governing the Design and Operation of Local Exhaust Systems, ANSI Z9.2-1971. c) Personal Protective Equipment: for exposures above the permlssable levels but single-use respirator must bleessusetdh;anbe1t0w.efe/cnc,10aanrdeus 0ablfe/ccora full facepiece powered air purifying respirator must be used; above 50 f/cc a type "C" supplied air respirator must be used. The use of respirators would not be an acceptable substitute for applica tion of the best available technology. d) Caution Tabels; these shall be affixed to all raw materials, mixtures, scrap, waste, debris and other products con taining asbestos fibers, or to their containers where, during any foreseeable use, handling, storage, disposal, processing or tran: portatlon, airborne asbestos fibers will be released. "Foresee able use" will not be limited to directions printed on product labels (for Instance, recently reported cases of mesothelioma from floor tile sanding, an operation not specified by the manu facturer). Appendix 4 We are in general agreement with other aspects of your recently promulgated standard not alluded to above (monitoring, housekeeping practices, etc.) The asbestos Industry has stated that It would be hard pressed to comply with such strict standards as those mentioned here. We believe that what is needed Is a complete review of all possible exposure of the labor force to airborne asbestos, as well as a careful examination of the many unnecessary exposure of the general population to asbestos fibers In consumer products foods and beverages, and drugs. After comprehensive review, it must be decided which are necessary and essential uses and which are not- Exceptions might be granted but the burden of proof would be on the manufacturer to show that a product could give rise to no hazard before marketing. We believe that this action Is necessary for the health and safety of Americans,both workers and the general public. We can hardly afford another decade of asbestos exposure while academicians and governmental agencies quibble over how much cancer the market can bear. Please give this matter your urgent consideration. Sincerely yours, ObdiuJt *1. Albert jJJ Frltsch, Ph.D. Center for Science In the Public Interest ^ Table I So Uses of Asbestos (1) a p r o n s (2) a r m p r o t e c t o r s (3) b a g s (4) b e l t i n g (5) b l a n k e t s (6) b l o c k s (7) b o a r d s & s h i n g l e s (8) b o n d e d p i p e (9) b r a i d (10) b r a k e l i n i n g (11) C ciV")s (12) c a r d s (13) c e m e n t b o a r d s (14) 11 c l a y , (15) " m a c h y (16) !i p a r t i t i o n s (17) " roofing (18) " tile (19) sewer pipe (20) c e m e n t s (21) cloth) (22) c l o t h i n g (23) c o a t i n g (24) c o r d s (25) c o r r u g a t e d r o o f i n g (26) " sheets (27) c o v e r e d c a b l e s (28) " hose (29) " wire (30) c o v e r i n g (31) c u r t a i n s (theatre) (32) c o v e r s (33) d i s c s (34) f a b r i c s (35) f e l t (36) f i b r e & c e m e n t p i p e (37) f i l l e r s (38) f i l t e r i n g m a t e r i a l s (39) f i l t e r s (40) f l o o r i n g (41) g a s k e t s (42) g l o v e s (43) h a t s (44) h e l m e t s (45) h o o d s (46) i n s u l a t e d c a b l e s (47) i n s u l a t i o n (48) l a g g i n g (49) l e g g i n g (50) l i n i n g (51) l u m b e r (52) m a t s (53) m e t a l l i c c l o t h (54) m i l l b o a r d s (55) m i t t e n s (56) o v e r g a i t e r s (57) p a c k e d c o r r u g a t e d m e t a l (58) p a c k i n g (59) p a d s a n d c o v e r s (60) p a i n t s (61) p a n e l s (62) p a p e r p a s t e (63) p i p e & b o i l e r c o v e r i n g s (64) p l a s t i c s h i n g l e s (65) p o t & p a n h o l d e r s (66) p o w d e r (67) p r o t e c t e d m e t a l s (68) p r o t e c t i n g r o o f i n g (69) r i b b o n s (70) r i n g s . (71) r o o f c o a t i n g s (7 2 y r o o f v e n t i l a t o r s (73) r o p e (74) s c r a p (75) s h e e t i n g (76) s h e a t h i n g (77) s h e e t s (78) s i d i n g (79) s l e e v e s (80) s l e e v i n g (81) s t o v e l i n i n g s (82) s t o v e m a t s (83) s u i t s (84) t a b l e p a d d i n g <85) tapes (86) t e x t i l e s (87) t h r e a d (88) t u b i n g a n d t u b e s (89) t w i n e (90) w a l l b o a r d (91) w a s h e s (92) w i c k i n g (93) w i r e (94) w o o d (95) w o o l (96) w o r k i n g m a c h y (97) y a m s gaskets Reference; "Thomas Register of American Manufacturers'; 1971, Vol. 8 $1 Table I (Continued) a) C e m e n t p r o d u c t s : Uses of Asbestos U .S . C o n s u m p t i o n in short t o n s (1968) siding shingles, roofing shingles, interior wall siding, pipe (flat and corrugated) 410,000 b) F l o o r t i l e s : lineoleum, epoxy, asphalt and vinyl asbestos 200,000 c) M i l l b o a r d p r o d u c t s a n d p a p e r 30,000 d) F r i c t i o n p r o d u c t s : brake linings, clutch facings, packings 104,000 e) G a s k e t s - f) E l e c t r i c a l a n d h e a t i n s u l a t i o n g) T e x t i l e s 18,000 h) F e l t s a n d h o m e i n s u l a t i o n i) M i s c e l l a n e o u s - 55,363 Table II 817,363 Consumption & Production of Asbestos in U.S. in Recent Years 1964 813,306 (short tons) Production 1965 794,708 118,275 1966 805,391 125,928 1967 720,583 123,189 1968 817,363 120,690 1969 784,321 125,936 R e f e r e n c e : " M i n e r a l s Handbook',' 1968, Voi. 2, p. 179 ff. I \ TABLE I H POPULATION GROUPS WITH OCCUPATIONAL AND EF/IRCI'irEITAL EXPOSURE TO ASBESTOS (6) Occupational Groups asbestos rock miners asbestos truckers asbestos loaders asbestos crushers asbestos millers asbestos Tireavers masons heating equipment workers shingle and tile manufacturers asbestos spinners electrical appliance and wire manufacturers carpenters rubber workers filtering material manufacturers molders of asbestos products asbestos-asphalt makers putty manufacturers asbestos paper workers asbestos cement makers cardboard and brake-lining producers asbestos felt insulation workers asbestos insulators asbestos tube wrappers construction workers garage attendants asbestos sound insulation workers pipe coverers asbestos cork insulation workers automobile makers Wonoccupational Groups Hssidents in vicinity of asbestos processing and textile mills inhaling plant effluents polluted with asbestos dust, and individuals living and working along roads on which asbestos is trucked; residents in the vicinity of build ing construction and demolition, inhabitants of homes or offices with asbestos acoustical tile. Table IV Uses of Talc 53 1. A s p h a l t f i l l e r 2. C a r v i n g 3. C e r a m i c s 4. C h e w i n g g u m 5. D r e s s i n g t e x t i l e s 6. D u s t i n g f o u n d r y f a c i n g s 7. D u s t i n g r u b b e r to p r e v e n t s t i c k i n g 8. F i l l e r s f o r a s b e s t o s p a p e r 9. F i l l e r s f or s c o u r i n g s o a p s 10. Fillers for rubber products 11. Gasburner tips 12. Glazes 13.Insecticide carrier 1 4 . Non-transparent glass 15. Plaster Products 16. Polish 17. Porcelain 18. Refractory Brick 19. Roofing 20. Solid lubricants 21. T a i l o r 's c h a l k 22. Toilet preparations: t alcum powder, vaginal deodorants. 23. Toy balloons 24. Surgical gloves (discontinued in most hospitals). $k RSFSHSECES 1. Spell, S., and J.P. Loinewebor. Environ. Res. 2, 166 (196?). 2. May, T. "Asbestos" in Ilineral Facts and Problems, U.5. Dept of interior, Bull. Ho. 630 (1965). 3. Kiviluoto, R. Ann. H.Y. Acad. Sci. 132, 235 (1965). 3a. 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Mineral Facts and Problema, U.S. Dept, of the Interior, 1970, pp. 853, 1272. Byg129* Bamber, H.A., et al. Ann. Occup. 13, 77 (1970). 130. 131. ELejer, H.P. Personal comraunication to B. Castleman, October, 1972. l h tKLeinfeld, M. et al. Arch. Environ. Health 663 (196?). 132. Nicholson, W. Personal communication* 133 Morliss, R.R. Science 173 Hill (1971). 133a. Wehman, H. Personal communication to authors, January, 1973* 133b. Hicholson, W.J., C.J. Haggiore, and I.J. Selikoff. Science 177. 171 (1972). 133c. Lenger, H. F, Personal communication. 13U. Particulate Polyclic Organic Matter. National Academy of Science*} Wash ington, D.C., 1972, p. 2U6. 135. Selikoff, I.J., E.C. Hainmind, N. Heinann. Paper presented at Second International Air Pollution Conference, Washington, D.C. (1970). Byg.136. Harries, P.G. Ann. Occup. 11, 135 (1968). BOLOi ,CAL K noi Instiu'.' c Health PeLriiary i. iChA-r.sr--3;;:LnC'.ViroAri..f.-'r!t'sf!.ii.-Pn.Ycn L`nviron-v:v,',l Mount Sine tis City U Ch.iTJr t.'.'j. F.. C. i i s v - , , / ; ! A:.U. A. Lruy/jy ; .1' VV J, HLiiohC'i, ` C. Y /^ : i J y *1 Program , ,,:n Cl*'.' i'i.,,;/ '.rncer l`;u r, and pori tono el Tnesothelio.no 0 :r;io-in*e iral nfogl nome Oi. ;j' nuop!.S'it.'j > :-} jh! p ioiij-al chances 1.i, . u c OJ* nter .et1 Oilb I ! .... i' ooit! ar.nr?1 :oti i- , lij' ( ?t'^')o.- e >'Lai ionsiti p~ t-,.' - : of c>'<-'.'ji:ceLai coni arm-nnfon i" rto ' j ].1 iULi')il ^ 1 .s ... 1er o. 'vi.den 4 , i ,,, iaV.i-20 0 K\> ;/ lu)v^.~ j`jY ( d i.'i b111s el.ri (ii^ciisso'na i. J. Sellkof f , M A. M. Langer, rh ,! I. .1. Selj kofi , M E. C. Hammond, C-. J. Chu rg, fv.il. Y. Suzuki, M.U H. j. Mi choiro.i, ' A. M. Langer, Ph.) 1 . J. Selikofi t ^ E. C. Hammond, Ce i -, M ;>! a r e b e i n g 11 or r.1 I li :: i.1 i i'.tc o a Lh 0<y/`.'2 a n d n.c ])'/iiUd bv loaearch progra iOitl.U-ni ?j Peo U: Soi oncee !'< c \ c e e r Scierei ist A",<.rd Parti ci m-nts Mount S i m :,i S c h o o l o f M e d i c i n e o f t h e Ci f;y Uni von;- 1 1 v o f No'V t o r i 1. J a c o b CHU' , M. D. E. C u y i e r Huiortond , Sc.D. A rth ur M Lar or, IV. b. Y,'i] 1 1 or, j . jvj r;] o'.' eo n , Ph . b , I r e inc J. S oli...off, M.D. P rofessor of Pathology and Prof essor o Cop'iHi i l y Modi c m r . Di i e c t o r o f Labo" a f o r i e s , E n v i r o n n e n t a3 S c ie n c e s Laboratory. A d ju n ct P r o f e s s o r o f Community Modi c 11. ( E p id c o i o l o ? ; y ) , yj c c - P r e s i d c n t , Amor i ( 'a n e w Son: err, : " f D i r e c t o r , boprtnnr, o f i . j - i d w i oli. g y -tid St . l i s l e s . A s s o e t i D c P r o :'r-rr . o i Com ,nr iM y '-rc J ' c (K ivu i i l c j y ) . H e a d , P h y s i c : ; ] Hemov; i. Section, Environnent;:.] Sciences Laco.r A s s o . 'i r - t e P r o f e s s o r o f Commer-i t y i ! _ ;i c (B iopbj hi of) . Head, P h y sic s Lalrm ; 1r\r Envi roomer ial Sciences LaboratoryProw .m or of M ed:cine and P rofesso r o r Community M edicine. D irector, Lnvi To'iiiiout a S c ie n c e s Labourite.;;, . A s s o c i e to P r o f e s s o r o f f o r .rnuni t y Med:,.. (Envi r>..mental Pathology ) and A ssocit P r o f on c.o r o f P,.t ho] o j y . M O V f Out 1ine of Asb.:s1os Miliei u 1ogy 1. Asbestos defined; Asbestos is a generic term for o varieties of fibrous, hydrated, silicate mi nor a] s \*hich possess the fol lowing common properties arc si.curable into thin fibers: are electrical and thermal insulators; may be woven and fabricated into forms easily: are chemically resistant. Mineral Group Serpentine asbestos (1) Amphibole asbestos (4) Mineral Species Chryso i.ile Avosi to C'rocidolite An Lhophyi lite Tremoli to 2. Structure: (A) Ciirysolile: (sheer silicato) Sheet:;: silica (tridymite) , brucilo Curva Lure Spiral; coree"fric growth Fibril unit Bund le (D) Anphibolcs (chain silicate) Si li <a totrulii-hru (units) QLinking; of sta,gg~ered double Cation ,,it1,;.. i.u.40 - 1.40 A chains accomodatici ) Ani or. coni igiv .'iron Chem i.ca 1 v iation Natura ] occu e:vnee Order ~Iriso: dc1 of cations Chomi;t r y : (struetur a l f. (A) CL.rjsoli 1e a) c<`^t (2.4 Q 1 0 } (0 ,0 H , t*S6Si i10 (0H)S (B) A 'iphi bole s Range of Supe: (V,,x Y) 7 (V.0 -1X 2 .-A8 ( ' / ;,0 o 1 ;2 }2 ' (o;OH, F) 2 (0 ,oii,r)2 for WVO O' Chenjc a1 An ]yscs rnr As!)C^1 os Mineira Is Chi'ysot iI Amo ^)tC C v oc i((O \ 1 ( AiiVhop'-yJi 17e Tr-..moli tV cH s T\ io2 F Cr2 0 o 1'eO NiO i'1nO A;gO c aO Na,,0 KvO li;0 41 .8 -42.0 0- 0.1 0 .1- 0.5 0 .2 - .3 0 - Tr 0 .1- 1.6 0 - Tr 0 - Tr 41 .4-12 . 8 0- 0.L 0 Tr 0 - 0.1 ]3 .0 i i.0 40 '11 0 .25 0 .03 4 .15 0 35 .03 0, 0 .6 ! 6 .57 0 A2 0 .02 0 .20 2 .22 47 .6 -3**.] 0 - .t9 0 .2 - 3 ,r; 9. S~ 20 .i 02 .3- 2 4 ./] 0- 0 - 1 .5 0 -15 .8 0 - 4. 9 5- . 8 0 - 2 .1 0 - 3 .3 fN>0 .!-58 .9 0 12 0 ,c,~ 8 .1 c - 4.15 Tr - 0 2 0 .3 Ti-- 03 j?i .6 -30 .8 0. J~ 3 . 0 - 0 .8 0 - 0 .2 L.G- <!a 54 .9-59. 0 - 0 .3 0 - 4. 6 0 - 0 .5 00 - 0 .4 0- 0- 0 . 2 1 .7-25 ,,'y 11 .9- 13 .i 0 - 1 .3 0 - 0 .0 0 - 2 .'< O u t l i n e o f Asir; t os Mi n r .r al oyv Associated Truco Yni'cr..l Phaser: (A) Chry ,=oti >?: S erp en tin e phases (1 j z ardi te ; antiiToie Magnet j t e Chrer.it v Bi uC.it e (fibr oes-nuwnixte) nT e le Magnesi t ''otalgie pitases (av-arri tei Calci io Olivino, 1; rosones , er.piu boi es O D Amplia bojes : Amo site (qrnrlz, Fe or idos 1 hydr ssol Croci do !i1 o (i'0 aracxite 4: copilibe s55) An tliophy?lite (t03 c, chi ysolilo , 4 arnf Tremoli te (t , SPrpen ti.rey," d a1ard'i A s soci eteri T r a c e LI oriolts (A') Chrysoli ]o : (IT Atr;phjbo e.* Ki ,Cv ,Co,Cu ,Aln,Ca (-T.- mi il op'iyl Iilo : Ar ,Ra ,Co,Cr,C1u j Sr, V/ / . " pros;ent in > ]0 pp'i) (cu , Ci'.'Oido!ii o : Z r,Ab ,Tii,Co ,Y , La,ita As SOC La*-cJ 0 v,('nrn c Oc -d jri rats : (A) Ciiry. e1 ; Sinai 1 ru*el Ilice pf )ds and v/cjxrs (B) Ariai-;bu1vs: Up te o.s b~ Olila, v.sx po, nasino nei. Jn c?iiior>11o riad eroe iciol ilo fiorii So. Atrio --fac;e pv-Opal i,..f^_ CA) Chr.v so`l ?.io. (FO Ani.!,i!Ol 0 " SI gh ri y (e) il X?S:P surf soo lyci ..si chong es i 1h ph and ovbed '.e-t.-ri p A!adelSiisiy (-), chas gos vote s(-cr'oif' sti111 *OI- o I eai iom : aini aorbed ;n1.:I u; ma teiial . A jso ci.:f :crei! e!'arpe i<l i11 . situi- Generai ];rIc-roneos X r W .A ., Howie, R. A. fiT;ei / ,U'' -.an, a. , 19i!.2, The ROl't. Roirurg- Pinec mi n ; v. oe filain Si1 1cr:tC.-, C29p.: V ...!, The Sho( -i Si]icat es , yVp, J. \ r L (-y c.p SIS , y. St , V.'.(j- j 30`3-S, Ar-T''i)xjOI* - Cry.n al Chi i,.1 riiiy , Phnr-.-e Rei a(ioi.s. rMit: Ol.;c\ \ ' x c-nco: \'. J of ' ri IH.'; .e-, H o c lo; r,rd ino; ani c Aiats-rr.Is , 1 yy?i Si^rinyor-Vf.-i-!a;'. N V \sJ-a _ OS f Ss 1, il Ja. l'rJ ':*J1 ii`r> (. (a a-b --ai :a V , ! n p . , < V ti I , r-.d Se;-n> i1' * .1 j- , ' i i.ei ne' j " .p . 9 , isber;ios el u i . - : . 1 ii. ,'t'-.1-'i-u rj!t eliin.> A Asbestos Disease 1 . Asbestosis .This is confined to ooeupati ore 1 c::jv.,.-:urc . .There is connidnrcbJe iindividual variation in response. Some workers nay be or,ployed in 'li-iv.sto'i troies for more titan 40 years and still have normal chest, f-rays. In others, as little as ] day of factory es porur; (inndi liu.t.cly coni roiled) will result in par euebyraa1 Oi' pleural, disease dec.sU s later. .Asbestos! s, sui ficieutlp sever; to i;e fatal Ins been seen in our studies in run little as eight yt.u iter on.n 't oi exposure, but this is most unusual. Death, oi ,,s. csi.osis, when it occurs, usually is observed twenty, thirty, forty or moie years after onset of work Three facto generally mist be considered in any analysis: Intensity of exposure Duration oi exposure Duration iron onset, of exposure (Kesid nee time ot citibV in Lungs) .By and large, signi fie nut asbee lOvJ s is not scon until at ler.ut SO year's from onset have elapr-ed ~ the' "?0 yen.'" rule." .All varieties of asbestos can. produce disease'; vheihor m s typo is wore fibre,.,_o c than anojier is iuu:ertair. Ci i11IcD.1 ft atin cs of note a- e , For onyr ]PCO-"at c di lienee HfU: I r criv<' Y\ .-KF i VI' u on dys pile:ly a pat :orn; diffuri os: *1wloeis T i n r aTV e FCionr ;noi1r ch; ;'I>'i L M rg :putii;i nO I yrcmir'cc:4 except v,itll o rr 1CoOIr:tipeune1VV.UJc0Li:r-o7ri>i~ ii ni-TctoiJ lTt o Stage's J PC 1ur " Inc onpy';o rT: r !CU i.-X-ray-tur Ct'on coto Ip.j j a* yCSptyueloulanrir1npj.1oSosLtrO.iraiarpiyrny''CoI>OrPpfOrUi-obCi.1C1it'1l"tV>'11' 1S^1 ri-.<cijor'r'ln,orGeOoniiiogaGtJfj;nsoduin'sva:ei):eVi.1's1..f1iit1oir cereu:atrlbloecyrcaror mdcJieoy:Vft1]eCYc(yjV 1 r j .n ct i\ c: d y.iCsTio tec}' :iapnosi s , l1dico;nnto. f di Ai Sld/'O!' Se ni qties do il X- ea p'Ci js cay, and tut enSca a'O*C; ; cXI st. CcPBai.i7iislekl!; tiijnf.iCreo-,`daaTTnoih1oicpira)oisinnteitvqoi oupnj1")eoe/n. C' 1lOSt ' c st hcr\r ;T- j ; jo-r ai i'M tu' ;r"tro!e-nre\*il1i' Urc1oc.is-c;tu>-ilrp]Ts.ii.f?.Cririiiax.cfInoi ': ; J ' n f'>1 i. c '1 afniiog'pCiir.f.'btcpj,uai`crJ.t,oe>J,1;,y(Si.-t!oTi;yeyeLafVs'iiipVsah'iebayoreen,,soilchuaiocn1)isu.1-tr\.ciay.IVo:i. reay,errCaidIaTcJJ*ft*-n\o<y'r;!1 Onset of osuro fyrs.) X-ray cimu igea tf r/l to !.- t'torsi ve affer I'ici e than 20 j fr>;n onset ol V.ork. Fjhd lnt>s ir 1 ,1.17 a.sbe.st op illRIIii. ifeoi wori t'.'s. Asbesto 3 3 (grade: cA C' No. Norn:a1 Abnorme- 1 ] 2 3 40; 30-3 0 P0 -7 0 }0 -10 0-9 10.1 194 77 37 9 3-ri .....1 ijr/ 5.8 12.9 27.2 rri n 8 0,0 0 J .8 94.2 87.1 72.8 4 4 .i 1 .1 4S .5 35 51 28 102 49 1835 17 4 118 9 0 30 0 0 360 126 50 Vc ar in i o.nc,e t oi' C.'.jlii/'Vc 40-r 30-89 20 -8 9 10-] G 0-9 xairriet;Sinriofentsacebhtl eanefg:eecsv*:oe roknt-1uain-'20v also years Nu' i-b- :1 cxa.T;rn.c' N Ol'ii'a i plein * bin a n i pleura Fibrs. s Cu le ilication 121 28 ]94 96 77 47 37 9 340 346 34 8 65 62 25 30 4 70 67 8 5 0 Ct.' Asbestos Disenso Tlio cardinal clinical symptom - dyspnea generally obeys !he "20 year rule." Onset of osujs- (yrs r) No. C;~u> Rru r si % byspnea Dys'noa (de<n 1ee) -- 1o5 40+ so-;:p 20-29 I'd-IS 0-2 121 194 77 37 9 346 52.1 70. C 70 .0 92 ,,6 9S .6 4? .0 79.4 23.4 7 .4 1.4 26 17 35 14 12 3 27 1 50 to 8 '> 0 0 ng enneor . ' , : Jj;;po'i ;,i ; b'-v,:ns as carly u ~ 10-14 yeurs fvom orset of expu.sure, but rc--u] ts m signi fi cant nrmber ci exc. .;s deaths only after 20 years fro.r. or.:.et of ex posar e . Doperei ing upon 1he nature oi th cohor t under studi, ve Lave iur.od a 5X - 7N itici caca in Lung cancor . This j s the uor-i :impoi M i t <t t+vi of death among asbestos rockers ~~ 207 oi rii (ic"t!i;S t i l O C U S OQ b> the tumor A 1 1 cell tj pes n r e s c ' .i (sec Vohol o g a: . Hov.evov, 1ho cancer lias ceie unusual features in tisbeslsr < a posse 2 / ;i o n 1over lobe rat her than upper lobe; thoj tend to be path].h ;rrl (nai u hrtrehus tu.uors are infrequoti 1.; so bi'oncho seoyy tords to b:nve le S ;s U 1 . lily); tin pi ourn is often involved early. Diminis hod rospi ratory rcsb rv e makes open-ation less available, and conce1. ' - :; 1 1 ai.beSt OS i s nay r ita:; rut loica.j cal diagnosis difficult. The cliitic aJ course rp.d orc rosi s art; very ;ricl. like thuSi. in non-asbestocnses . b"ng carift-;' as a >*esu `t oi fc'U:Lra >.;`j4al asbestos exposure lias not yc t L- n e \plored; j Inuy turn t'*!t. t"> be even trioit; important, i.r 1c n : i s i> IHP'be.r o eaes, than CM 1 ronjacr ial me.-.-otlr'l i<si a. It should be not <.J ihlit ad;1 1 in nrb ! an o s teir! to have asbestos iilors in the i J13ugs (a1boit many fcV0i in ;rj.,,bci titan ;n Krugs of ashes l<n v,oi'j;:r...) The *b r i. .1canco oi th p m 'ur-e oi these fibers among cibare iie .ir.okera , n uh geni i'a1 1)0pula tion is not now known. Studies are la, a:e v,ay to de l r vnitie if lung cancer rates arc increased anting i'ar'ii"1y Gor i.r.c 1s Oi a.,b a Los Co*rbe , ."nong residents of net ghborboods abc i.t be:-LOS rac to :es , and ah>'>ng workers indirectly exposed to aSG>Jr. LO> 3I:. 1Jr Co>r ini rtion iIlotirt .y. Rates yjl] be correlated with ashest o aup b rd cr at indivit.au 1 S In t'nose pope 1r Li one . If rates j the C 'i"tripe oro eJo ted ::dd1 L.j o p u j apur > ' chey y.'*i1 be necessary to eva ili 1' a.In-the V o;',bes(op 1an h. 1l.Sl ti.nl J.u the u amoral pubJli < i'''tl1"S 1 0 it" 1ur.g canee > V ia!: b Asbestos Diseas; - b 4 , Cast ro-i nt i'oiina! c .o t .o (s 1 ovach , colon, rectum, esophagus) There is a modest jncren ;,o of giislro-intc.- t.-.nal tract cancer among asbesi os i-crkei's ("y _ ;>y!. Whether it also occurs as the result of environ! ".Hita1 ashes Ins -vposure ha s not been studied. Ivo o!*i.ervt<*ions may he relevant . 1) Amon;; asbestos workers, asbes tos liber.- arc- prov" f is the h /...1 wa LI ii'm;: ;iter occupational ex posure has ccased. 7) Thore may so oppov'umiy ion acbostos cont.im- ina liei of toed and iiu.bs (lx itraLion through asbestos fil fur throuyh aslustos cel ext pipe's; talc: a; food auditive.;. 7'he signifi cance of 1hose ebseivai ions is not known. Mortality Data In g en eral, deaths m the asb esto s worker cohorts studied may he b r o r - K \ i a t . xo> i ucci a s f o l l o w s : Total cancer ........................ ,. ..... ............... M;t' isnog t hr.ea1nicere....n.....a ......................... .7%...... . 20% G. I . c a n c e r .......................................................................... 8% A sow si c':i 40% *7* The dire' l occupai id inn 1 i1 sk is associated with current or prior regular ter!: wi uh urbe !os . j-f lias boon est ima ted that 1 ,0 0 0 , 0 0 0 in the Dui ted States have or have had such expciicuce, IWhile ft.'- aumbel of individuals prt uwcci to have indirect occupational exposure (or ami 3y co,itaci, or u>.lgbborhooo exposure) is very much larger, the magnitude of their risk of ashe .-tos-a ssocia ted disease: h.c- not yet been dot; rm i'.u.d nun i t itatjvejy . The data in the iirst six: tables win ch follow are derived from th-' experiences of cohorts o L workers with diruct occupai ional ex.-posm e and rotor only to suedi groups. Tailles 7 and 8 provide some infor mation from 2 series ti.ri. r n r p the proponile.n of environment.? 11 vinduced musothe Jioiri, j-c>!afive to Those occupationally derived. Tcbl o 1 El'p r> cecl anc observed nirn'cer of Q ^11S among 6 ?"*New York-New Jcese y asbesto. insol iLion wor'-'ors, J an . ;, 19A3-Occ. 31, 1971, twenty or more VO '1vs a itor o'-.of of [;,'ct (.; p i-o asbe stos. Total Cancer: all sites Lung cancer P1cural m csofh(11icma T er :tone a1 mo sn t;he 1iom a C-u'cer oi stomach, caln, rectum., esophagus Cancer all ether sites / sLcs tjsi s A l i c'ti. 'v causos rrut.i ill causes HJ.-V/IW"1^r.* 1 ici:2_" rn i IPG 2-1071 Total 1943-1971 Exp. Ohs:crv . it.p. 0 );o rv . Exp. Observ. fix'' Cose'"7 11.0 1.5 no r 2 18.3 i'' i 3 ,5 V>; .* 57 17 .6 104 23 tftJ1i. 48 25 o yc-if 20 47.2 10.1 +>- 139 84 S 24 4.1 5.7 6:5.i 76.4 7 5.0 6 Oc X >* 44 o r . 4 18 3.9 8.6 10 +* S4 78.3 13 12.0 4] 15 24.1 32 ** 232.3 33 ,, 41 >1 73 107.7 161 S3.9 187 230.0 <cT.lW7.S years ei O b s e rv a tio n : 3,726 4,403 :,8 98 11,030 632 members were on the Union's rolls on January 1, 1943. Seven died before reaching 20 J - rs from first employment. .All others entered these calculations upon reaching the 20 year-fron-Onset of first exposure point. Expected rates are based upon age-specific death rate data of U.S. National Office of Vital Statistics from 2949-1937. Kates wore extrapolated 1943-1948 from rates fo-*'* 1049 1953 aru for 1968-1971 from rates liar 1961-1967. ceatn rates rol available but these are rn?'e causes of death in the general lotion. o M i i. Expected* arc! o b s c rvcd deaths among 1 7 ,8 0 '. a -bo ' t o - '.r'u.l a t : ors w o r k e r s - n ^ -e Onitec! 5 i a c c s ; ..a.ua'-, 1, 136 7-December 31, 1971 OistriLi'tior. by duration ir o n ; o r . s o t o i t.xposuro Totn I Loss than 20 _vcar 20 voors ;nd nor '""'tni deaths Career: all sites cancer PI c-":a1 j:iq sotholiorr.a 1'ci'1 .cnea1 niosot1e 1ion a O nc -v- oj stonach C; near oi colon, reevum Cnear ol esophagus AIL o Or r cancer.-: Asbestoai s Ail other causes in.rib'?2 o;[ rir,n .5-l-con-yrers cl observation Ih:pec tec! Observed 803 .63 I ,OS'2 1 11 .09 /i4 ^;;; ;,-a '59 Ow. ns 6.63 17.51 6 O1 72,1:2 vj lo 2S 13 1" 4 ** 78 661 .00 oj5 17 -00 or. ^^ ^r^'n n'' 6xpec tec! Ob =erv 173.3 i *;;1 36.3 1 51 7.93 22 1 >0 0.97 3.51 e .i-I 15.36 5 * .i J 3 J. 19 5 152.63 155 12,6 S1 62,673 Expec ted o'- <:cr,a 326 .6 3 ? '7.78 SSI 40s p7 p9 -- AA 5.05 15,0 C 2,77 5`5.07 -A 1 oo op 08 ir, 12 95 / 5CS .91 400 5,119 23.627 * Expected d e a t h s arc based upon ngc spool Tic death rate data ol the I'.S. National Ol !:re ol Vit a 1 Stat isii cs . Ra ics ter 1968-1371 were ex tra.no] ated I v o r ? r >tes lor 1931-1967. 54^ u ,2 r{v p b _;p r*p b pc; not. P V P,1 1 p< o 1 n , but those ar o rare cause a of death in th ^oncrol * 'bu, 1(1 1,1 Oil a r Asbestos Disease 8 Table 4 Expected and observed deaths Kong 089 asbestos prod ut 11 or. and textile w o r k e r s , Tan ], 1CO9 - Dec. 31, 1971 Total cancer (all sites) Cancer of lung, pleura,trachea,bronchus Lung cancer Pleural resoihc-l 1or.-,a Peritone-'] esci c l iova Cancel' of si owner., coloii andi*c.tun Cancer all othoi sit.'.'.Asbcstosis All other causes Total deaths Observed deaths 72 35 27 8 7 13 17 24 103 199 Expected desilo, 27.8 8.4 + + + 5.0 14.4 + 106.5 134.3 United' -,a ics data noe a v H Icblu but ligure should be onlj slightly loss tin n 8 . i T Uni Ieri Siate., fiata noi avalladle but `hese arc rare causes of death in the vivrai population. -r o 3 Expected* and observed deaths among 933* amosite asbe stos factery workers first ct.ployed 1941-1315 fi>y{ cb.c-Orved to Dec. 31, 1971 Before 1352 Expcc ted Observed Total deaths 6 9.98 68 Total career: all sites 9.51 15 Lung cancer Pleura 1 mesothelioma Peritoneal mesothelioma Oncer of stomach Canaar ox color, resturn Career of esophagus .All other cancers 1.4 S *** * ?}c 1.45 1.05 C .27 5.04 Asbestosi s * +* All other causes 60.17 3 1 0 3 o 0 6 o 70 1352-1 331 1962-197 1 Expected Cv -.e-rved Expected ObS erved IOC 146 121.24 250 13 .72 4-1 21.63 84 3.71 'Jr 23 0 6.21 *+sfc 47 2 *So\ * -oA GA fX jrfc* 1.29 4 4 2 .C 1 5 2. SS Q n * ~ 9 0,51 0 1 0.11 12 10.74 19 7 *** 17 89.55 95 99.61 149 Total, 1941-1971 Expected Observed 299.19 484 50.16 143 11.41 * 4.58 7.05 1.23 25 .89 73 3 4 11 15 0 37 27 249.33 314 *Expected rates are based upon age-specific death rate data of U.S. Na tional Office of Vital Statistics from 1949-1967 Rates were extrapalated 1941-1948 from ra tes for 1949-1955 and for 1968-197i iron ;'ate& for 1961-1367. **933 m e n were employed. In 5 cases, )2GS were not known and these men have been excluded and frcm the: ulatjons. S7r ".en were traced to death or to Dec. 31, 1371. 51 men were par tially traced and remain in the calculations until being lost to observation. ***U.S. death rates are not available, but these are rare causes of death in the general population. sbestos Disease o Asbestos Disease - 10 Table 5 Deaths of lung cancer and pleural mesothelioma among 17,800 asbestos insulation workers in the U.S. and Canada, Jan. 1, 1067-Dec. 31, 1971: relation to elapsed period from -inset of work exposure. Lung cancer Pleural Mesothelioma Years from onset Expected deaths* Observed dea ths Ratio Observed deaths < 10 10-11 15-19 20-21 25-2 9 30-37 35-3 9 40-4-1 45-4 9 50i 0.48 1.69 4.86 7 .55 8.50 6.24 3.53 4.04 3.72 3.81 0 4 18 25 41 44 23 24 17 17 -- 2.4 3,7 3 .3 4.8 7.1 C .5 5.9 4.6 4.5 0 0 2 4 7 4 1 3 4 ]. Tot a1 44 .42 213 4.8 26 Expeeled deaths are based upon a g e .specific death rate data of the U.S. National Office of Vital Statistics. Rates for 1908JS71 v.erc exirapulated from d a m lor JUui-1967. Asbestos Disease Tabic 6 Expect*. d and observed deaths of lung cancer among 876 aiRosite asbestos factory workers, first employed 1941-1945, and observed to Dec. 91, 1971. Distribution by duration of employment. Duration of Person-years Deaths ol lung cancel' employment Number of Mon of observation Exp. ** Observ. Ratio < 3 iiiontn:; 3-11 Mon las 1+ V'. P.V S Total 256 291 32G 87C 5,869 6,158 G ,91 2 18,93 9 3.5a 13 3 .6G 3.58 ]5 4.19 4.03 d a 1 1 . 0 0 11.22 73 6.51 *Th is tabic excludes 57 men. 10 died during first year of employ nei'.t, 39 could not be trace! alter the first year. 7 had prior occuj ,'tj<mai t..posure It; asbestos and 1 had employment of uncer i duialioo. 17 men of the 876 v m e partially traced and remained the calculations only until Jo=t to observation. **E>.p'U- ted rates are based upon age -sped fie rate dats o U.S. National Office of Vital Statistics, 1919-1937. Rates vere extrapolated 3Oil-191 from rates for 1919-1955 and for 19681971 Ira. rates for 1961-1967. 17 Asbestos Disease - 12 Table _7 lieS'-'theli one in London hospital (Newhouse and Thomson, I9G5) Total patients.,............ . .... ....... . 7G Occupa L1on.1 asbestos oxposui c ... . 31 Family contact.... ............... 9 Neighborhood residence........... 11 No known contact ...... . 25 Table 8 Pleural liesol he J3 orna : 232, cases in South Africa Me sot he liorna Regi sury* Exposure hi s1ory not avaj lab.1e ..... . . .22 Exposure ascertained...................... .210 Occrp.h lonai asbestos exposure .... 102 (48.6b) Environmental asbestos e x p o s u r e . . . 7G (36.2;!) No asiiP.l.o:, expo -uro........ . 32 (15.2%) *A iua1 He por t 1371. National Rt search Institute ior Occupational Disc.iscb of the Sou .a African Medical Research Council, .Johannesburg, 1972 fC Asbestos Psense - 13 Bibliographical Landmarks in Asbestos Disease 1924 19 31 1935 .1953 19 34 19 5o 19 55 1900 First case report of pulmonary asbestosis (Cooke, 19241. Not fully accepted at iirst, reported again in 1927 (Cooke, 1927) when case reports elsewhere confirmed the existence of the disc as In re trosp-jet , Parliament had been notified of the hazard in 1906 when Montague Murray testified concern up fatal pulmonary fibrosj among asbestos textile workers. (Departmental Committee on Com pensation for 1ndust ri ;.l Disease, 1907). Industrial survey showed high prevalence of asbestosis in osiiratos textile tact Giles in Great Britain (Merewether, 1931). Similar prevalence in bS. asbestos textile industry was found in PHS study (Dreessen, et al, 1938). A case of lung cancer with nsbostosi s was reported and et iol ogi c:.I associ at ion .suggested (Lynch and Smith, 1935). Despite numerous similar case reports, !h? possibility of a chare associ a t ion could not b e avoided and the question remained open. An instance 01 pleural mesothelioma, aaid one of perit oneal me-soi be 11 om a. i21 ass0c1aLion \vith r.sbc stasis, were repor red (Weiss, 1953; Lei cliner , 1354) . Again, ihemi -ardomi ci ses, ana oil:.0 ri.. reported id sewhere in ^ho next sovu al years, did not prove .1 etiological rcl ati onship; the- possi iij]1i y 0 f ri 0}1r-11crj ertoci it'on reiiiiiud, nit hough the frequml linking wii.h asbestos of inis otherwise rare tumor (see '/.'uglier, et al , 1960) was striking. Lung cryncer _iink of asbestos factory workers clearly established 'ey epidcmiolcy, I cal st udy (Do] 1 , 19 55) . Careful epidemiologicnl study, going beyond, lung cancer, showed U.S. f a c t o r y hazard as veil (dcncuso ;nd Coulter, 1963). Pleural calc.Jfication ontphnsj zed as jrad iological accompaniment of asbesi osj s (J b and liohl ig , 1955). Fxtraordlnary incidence in asbestos workers later demonstrated (Sclikof f , 196 5; ,, Pleural calcification may occur m nO'f of experienced asbestos workers against. 1 in 1,000 general hospital admissions. Knvi ronmcnl a] asbestos disease sugf.e-tod by tv-'o brilliant studies. KcJCh^tjaok advantage of clinical asbestos ^marker.'' Pleural c 1 cifiention was found io be common in neighborhood about an nsbosro.s mine and nill (499 oi 6,312 x-rayed). (Kivlluoto, i960.) Kuiirnms cas.es oi pleural n.esot hcJ iowe imported in asbostos~ rich area of .South Ainca, On inquiry, many had had no occu pational expo- ure but. lather, potential er.viro.uncut nl contact (V/ngncr, .Siege..-, and Va rebuild, 1360). This study also die! much to est eh mrmsloi-iemoi noli owa rciul 7 ^uship. 1961 196?, 1963 19; 1 193 4 19Sf, 1965 1963 Asbestos Disease - 14 Physiological defect m asbestos is clari fied as re? Lrictive dis ease wi thout important ob^ (.motive airway component (Bader , Bad or ncT ScTi~aTf7~T'^~r. ' Experimental mesot ltd joi.m produced by int r,pleural instillation of asbestos (Wagner, 1 9 6 9 ), More recently, tine ut'cl has been well used i o investigate iiapoi taut vai'i al les (Sta.it on and Wrench., 1972), Lung cancer has also been induced (Gross, 19G7). V.'ide environmental eon t.a.nin 'l 4on suggest by frocuent preseiK c of ""asbestos both c in lungs o i ioa !jno an, psics yineyason, Ka.~,chula and" MacDonald, 90377 ~~~ Tbi s v/as soon con 1irneb in many ciu Ja1a of the world. The con- cep t derived dv/cilexs arc ir oiu L.ilfa? observation ? Vas tna1 lungs of regu Iarly contaminated 1.)y sues l o s . This urban. was cli o. put cd. It had It!mg been i;no\ui thru a ni-r.bee of fibers other than asbestos cou Id also be coated to gi\G Sip.il nr appearanee It was pi'ojir:-.t.c Lhat , unless one wa s CCI tai n of the na turc of the core, nun,-spc cii'icily lie "ft;rrup- inous bod ies ir (Gross, signal Cralle cd y UT and ca1 ling these de TreviIf e , sL rue 1957). iitres The matter wa S liebe r(.solved until 197 1 (See Larger, ct al) . Asb 'if -S disfrse de; al i b j :` cowman ur.iOl): i asuJ. 1or. vo''];er s , nru*iI\', i: tien i,i oa, to tne f.cuuatrac fif: j nr;V Si ry , which uses 2/6 of asIk ,st-s I'.S.'. xid tn }ji> l t-iikiaJ i<j 1'"m110 11 v%\ (;er oovjrihilent a L coni U\ j coon tha n eh at dn "o! frc'1' 1 M or'J! ' (Sc ii hofi, Cnurg and Haim,!ond . it 14). Ga sI7-0-ii.tc st jna ! oanCCi` found three tj'os as froquent as expectod dn coho? 1, Con / jr:nou of 3 )i .Jaas;l.c.r-StOss. livevO1desa,.n s (oeliKOj iJ Cn0 T'f.; ancl Hammond , 1930 , Epi d OCC11 OU Jological iuves tip;a1 \ ( jonal ns!; (Sr ii heii, Pci itonea 3 no SOI be] iora. s t u d i e s ( r n t L l h e a p and ,S 115' esiauii sh."il Hieso t.hoi jo.;ia as naiinondi ana (Jrutj- il i 1 9 63 i. e vixs ithe now r, lP ec'' 'i')b.has \ zed iii these a cone,on arid olh e i Potential .xigin fie.once of cnyi remuer,la 1 asbestos disease hi -hiif: btea by report of ! icie is urong jh.mi :y eoniss is and residents about an asbestos pj.nf (N'ev house and Ibo.ipson, l9o-i). . c Lguiu or arli;r1 o r di s e a r )L 'C C 'I'uiea::opnoesia::r?e sdia9i6py;,a;rrb'_!>Cirr.,O, n.. A } ' ain, ui el, ce a e 1ur a' raat da a. ai used t i k he' U ti wide`ned by ' O T wk?T lieior a "wa(TKCr *" 1 v ik ii ;*,ehr ijspttoiroyn x e .r r ' T G a T , T1io problem of oi eX ri 1: 1 rVdcL.<eua0ir3rs'"hiogWnasscsI r;, ia1a ctSl.c1csdHoro`naa>sa*t"-r.a]*-av' s'u,,\!,en<iL.ieare?\,t'e:.car-.u",()jrd;I:.MrGUnysi(.yofbiei"101bst-(eatp1.Oe";-'.:.'('m>>ccr:..r.ou-i^mjv-j'iel'ueaeyp*i1,nbbaU*\e.*,b':biiiaOoo' ijnVlo'et'lo-Lfejsvidil,.dse.-cpoenotr(frisF.iiiarceatutit,Cca,VW1tt1jiis:' Asbestos Disease; - 15 190S 1970 1971 1972 197 2 Multiple factor effect demonstrated. In addition to direct card no gent c and potenti al o1ljbrcioggaerneitcteactsimoonk,ingasb(ebs'teoliskoi.iiluJ,LKiapmlaieoidid the and lung cancer Churg, 196b) . sbesTT"ivorFcrs"v110 smoko cigarettes have eight times greater risk ol dying oi lung cancer, as cigarette smokers who do not work with asbestos, and ninety times the risk oi men who neither smoke nor work with asbestos. Soils naturally conta: n n itcd v-ith arbestos-boa ing geological forma tions may <spose ag ri cul n u ' o 1 pupu lut ions ( B i t i1 kov and ic h a d ova , 1970) and uroaide so. .o n'.easure of 'nr;turn 1 bsc.ground1 of environnental asbestos cunt rmi n;.t io:i. Chrysotile asbastos in lunga of Xc.v Yorkers deinonstrated by electron microscopy (,anger, hclikoii and Suatro. 19/1). Biologi cal polenti a] of sudi contamination not now known. A 'DosLos avi pollnlion i-my be responsible, ut least in part, for Jung coni amin a i un of ure.au dr.veliers (.'cholson, Joa' and Ferrami, 19)2; Sclikol f, hicJioiuon and La.nger, 1979). Air samplcs, stuc'ied by electron microscopi', uniformly shov/cd asbesios present in osch oi -17 U.S. cilics. l.evels u.rc well helow thoec of pj'oesuos Works! 1es, owevrr. Fnvironmc n t?1 caimcs o f icotb. Iieia btres.s*.-'! by analysis of cases m houli) .tirici (houli; Ajrican Medicai icaseari ti Coun.cj 1, 1972), 3t',c oi bit; cuses vere causi dered tho resu.lt of environr.ientnl e.vposili'c. io ascesios, -9g a c occupati ona 1 in origin and 15d had no :n .hot y ad asbesto^ c>:posare . Bibli ogrnphicc References 1 . Badar , M.id, 13mclt_s', R .A . and SeliLo fi, l.J, Pu Imonary function in asb'.'r t.Oslo oi tilu lung; an utreOl .m'-cepi llar v block syt:droiie. Amer. J, Mad. 20:23 5 , J9G 1. 2 , Bur i.1 or , I . , M lena i1 ova , ! . . : Asbestos content of the soil and ende,.lic pleur a] ashes tools. Fnvir on. Res. 3 :-14.- '51, 11.V0 . Oo Cooke: , W. K. lb lo osi s Of th. Jungs da.' so the juba !iibo:i of astir:Stosi S. Brit. Med. J . 2 :67b-5 1929. 4 . Cooke , V/.b. Du 1me.lie!y ns!1 slosis. Lin t . Med, J . 2:1024-1023, J927 . 5 . Dej) r tmenia1 Co: sitto " on C o sinana , 1 ion j .-'i' Indurir ial Di K'.oane . Pond en. 11.M. S . 0 . , 1907 . pp. i 1- . 13 o i sonati.,-, o f oviden.r. 0 . b'ol I , K. Mor i. 1 ! ty jroru 1mi g cuncar in astiaste-, v.orkars. Biot. J , .( hd1 cc o Asbestos Disease - ir Dreossen, W.GV, DallavuIle, J.M., Iliwards, T.I., Miller, J.VV, and Sayers, R . R . A Studj of Asbestos ju the Asbestos Textile Industry. (Public Heal tit bulletin No. 241) Washington: U.S. Govcrra.,r:nt Printing Office, 1938. 126 pp. EntickiK'p, J.B. and Slither, V/..J, Peritoneal tumours in asbe.s tosis. Brit. ,3. Industr. lieti. 21:29-31, Flo telici-, D. A mortality .study of shipyard workers with pleural plaques. IP'T. J, Ina. Fed. 29:1 12-145 , 1:672. 1 0 . Gm,. s, . doTrevi tic , n .t .p., Totic-r, E.B Kxp-.-r1 ivit a ! asbe: tos i s. 1 he r.;onar y' deposits uf ciirj'sotilo asbestos du 15:3-13 -5;;5, 1967, --1 > n Gross, P,, , Grali'-y, B.J, and dcTrtvilte, R.T.P. "Asbestos" bodies: their nonspeci fici Iy . Ai.er. tidustr . K/g. Au. J . 28:511-31?, 1937. 12. Harri es, lie'. Asbestos Hazards in Favai Dockyards. Ann. Occiip. Ilyg. l ; 135-115, 1938. 33. Jacob, C and Bohlig, H. Roentgonoj <my ca i conpl- cations in pulmonary asbestos!-- , For tsehr . Rc>: u tgoast r . 8.3:515-323, 1955. 3-3. Fir, is rc;. U . I-'JCUJ'fiJ c..j( jfree `:n.' as a roentgens log i^ aign 0f nor- occup : ' O 1'' '-if ;jviLcphylli tc-asbos tosis, Acta. Radi ol. Suppl. 1 9 ':1 "` 3 If 15 , larg -, A .1'., 9OJjelOf 1 , 1,4. an-' Sasire, A. Chrysolite es bestes in the 1ong .> Oi 0o:/ -(-ii 3 11 7b-w Yo; a City. Arch . Environ, health 22:348-361, Marcii J971 16 . lx iohe i'. Y\ Privi. ' r e r bacio-el Ienturor- dr-s Bauchfells boi A.bostose . Arch . Gcvi(- r iirp.Tl h10 u . Gove rboiiyc . 13 :58 2 -39?, 1954. 17. bync'i, i<; %; M:d JUi, V.A. lung in I3CbO Si 'a- ;lict.-j.:,. Pulmonary ypbesLouis III: Carejnona Aver, J. Cancer 2-1:56-6 1, 3935 of 18. liancnso. T .P . ai < Ct.uLie , J:.J . Methode logy in induott ial health studies. The colici t approach, wi ili special reference to on asbesto company. Arch. Environ. !h.alti'. 6,210-226, IP-'ig. 39. M e r c \ . ;the r, 3J.J.A. Tb >j occurrenc t o i p ii j o n . ' . r y fibrosis and other pul ir,on. y aiiictions in asbo- tos v.'orlxrr . I. Industr. Hvg. 12:198-222, 239- 257, 1930. 20 hcvdieaee, i : , L . sad Thompson, II. K the Hone of pleura and peritoneum folio m g c.Xj sure to as6 -s:,os in Tendon arca. Brit. J. Industr. Maui. 2:2:261 -239, 1205. 21 . 7 ierai-on . V .4 ., Fa-IF, A. 3Ii [< : Un -b (`: In: Pj T.;-;g Paa , j; ! ' , mir![ Barry, !'-j l'<'a.a,.nii . 8< c o n s J u t ' ! Ac:d. Prt t, Asbestos air ullutiou Cjcan Air Congress, Lcl. Nav Yuk, 197] pp. 3oG--13u. Asbestos Disease - 17 2 2 . Seliko, I.-i. The occurrenc e o pii uval c;<le f j (ation amona; asbestos insu latto u V, orkcrs, Ann. N.Y. Acari. Se. 13?1:25 i-367 , 1965, 23 , Se 1i!;oi, I..!., Churg, J. and liara:ond , E .C . Asbos tos Exposure and Neo p]asia . J.A..i.A. 188:22-26, 196'i. 21 . Se 1i k 11 i , 1 .J ,, Churc, ,1 . and narrinomi , 71.C. Re 1a tion between ex pensi:ce to asbtstos and ciesotlicljema. New Kii" , J. Mod, 272:560-563, J965 , 25 . Sc 1ikujf , I -J ., Kanimond, E.C. ami (bury, J, A sb'-slos exposure, smohlnp J11ci n* 'opl -i^ a . J.A.tl.A. 20-1 (2) :10C-.I 12 , Apri 1 1968 . 26 . South Air ic,aa Medicai Re:-.caroli Council. Annua 1 Report 197i of the Nation.: 1 Irsi ilute lei Occupa iion a1 Da m ase .s. Jobannesbur , 1972. 27 . Si au Lon , :.i.r. end: Wrench, C. Meelwui] sus o Ile-notile 1ionia Indue It on with Asbes tos and Fi Eroe- Gl as s. ,T,, Nat. Cancer 3nst. 18:707-821, 1972. 28 . Th .'SO,! , .G ,,, Kse.'lnils, R.O.C., MasDoneid, R. N.: Asbestos as a modera uri:n ti'o/Citi, S. Air, M<-d . d. 7:77 81, 1963. 2 6 , V,'a,l c v j J.( ' , Slepys, (Mi ., .Vsvciaru' , P. : Dili rsi. p1cural ;icso!v lit-1a end 'C'1, V .polvi: in North te o..ern C.-pc. Province. rir.it. 1 . ndu.-sn, Ned . 17 :2GO .G7 1, 196 0. 30 . banei', J .0 Ex per lev ii1 pr cidnc ta on oi rat:set,hel.ial tur, out--- i.f the ulmar by .iplan liti on rf dusts in laboratory animals . Naturi 196:180-181, .1962 31 ,, V,eiss, A. PI ea'-airebs ine i .miueivihcstose, in v^ vo n orpbo 1op isc h -e.-,iclient . Il evii 7,iisiscb'> 3:93-9-1, 1 0 5 3 , Multiple Factor Effect In 196 3, workers, deed,333 a studyeach of had reoc was i ".horn h'sl t n itia te d of a co had begun h irty yeai -s.vn.frrkccji ht-oorr1. esf of ase et) . 376 as twenty Prev besto year j o '.o s s a insula before nalysis t ion (m of t h e e xp er .fence o f members oi t i n `o UPiO u .18 !3 -1 36 2 ]-,ad shown l ung c a n - ce wi wi rd Lh th e a t h U-. growi r lung, c t e a o a n s c be on, e l '' . 6 . t 8 h a l t i me th s e s a e s j 37 i a. t.'-UMu; mvfC. Vi Ol`<'\lob e x h pec ave t e a d n . u n I h t s p wa py s e a x ss pt um ri ed, < n e e It was soon fo u n d , however, that t h e r e ai e a s b e s to s workers and a s b e s t o s w o r k e r s . Tims, among th e 370 s e n , ihi r e were 87 who had no h i s t o r y oofc c c u i r gar red e t a te s mong moking them. . By P p r i l 3 0, 1067, no d-_a ch o f lu.ng c a n c e r had On t h e o t h e r h a r d , among t h e /!3 v.jtli a h i s t o r y of re g u la r c i g a r e t t e smoking 24 died of lung cancer, although only 2.98 such deaths had been exp ected, given the i.r smoking h a b its. I t was n o t th e sntoki r.t al o ne ; only t h r e e d e a t h s or so would have occur! o d . I t was not the asb esto s alone - - the 87 non-smoker., had no lung canccy d e a t h s . ho combi ns 1i on of th e two had a s h a r p , m u l t i p l y i n g e f f e c t . I t has been c a l c u l a t e d t h a t an a s b e s t o s worker who omokps c i g a r e t t e s has eight times the smokers of the same risk age wohfo dying of lurg cancer compared to similar do not work w ith a s b e s t o s , ; nd 92 times the risk, compared to a i d l e r nun who n e i t h e r v o ik s with, a s b e s t o s nor smokes c ig a r o tte s . lids cohort has been followed an a d d i t i o n a l 36 months; the f in d in g s r e main v e r y much t h e s a n e . By Dce.cirhcr 21, 1971, o f t h e 283 men who had smoked c i g a r e t i . e s r e g u l a r l y 41 d i e d of lung cancel' w h il e of 87 men who never smoked c ig n r e tto:-' r e g u l a r l y , only one die d oi lung c a n c e r . We have o b t a i n e d d a t a i n a s ec on d f a r l a r g e ; s t u d y . On J a r m r y 1, 1967, we r e g i s t e r e d a l l inembers o f t h e i n s u l a t i o n wcu kei s u n i o n i n t he U n it e d S t a t e s arc! Canada ( 1 7 , 8 0 0 m e n) . 11,656 comp.1etc d a cue s r l o a n s :i r e p r o v i d i n g , imong o t h e r d e t a i l s , i nlorirat ion concern j r.g t h e i r smoking h a b i t s . Ohsorvat i on of lue.^e men th ro u g h December 31, 1571, c o n fi rm s and e x te n d s our o r i g i n a l o b ue r va t i o n s . Of 2,056 men v.itu no h i s t o r y of c i g a r e l tc smoking, on J y two dca whs 9,590 cigarette smokers, (of ]34 73) were dm.- t o death,- (n( 583) lung wore can the cer. re& u l .Among t of l utnhge cancer. Lung cancel' i s uncommon among a e b o s t o s w o rk ers who have no h i s t o r y o f C i g a r e t t e smoking; i f t h e n r i s k i s am r e u s e d , suet) i n c r e a s e in not. gr irseka ta. s s oOcni at ht eed owt hiet hr h.-amnodk,ingi i i nt h egseen eer xa pl o issedmiunldt ii vp il di euda l smadnoy tsimnoioke, t h e Table 1 Expected* and observed deaths among 370 hew YorkXcw Jcrsev asbestos _rsuIat3 on workers, Jan. 1 f 1963-Pee . 31, 1971 Lumber of men Jan, 1, 1963 Per-.on-years of observation Tot a1 370 2,320 y<o hli ten'y of cic 'rOtt.e smoking*'1' 87 C08 Hi story of cigarette smoking 283 1,912 Cancer all sites L/jng\ cancer Picur a1 mesothelioma Per 11o ea1 mesothelioma Cancer of stomach' Career of colon, rectum Career of e :op::ac,us Asbestosis All oilier causes 7c U I deaths Expected deaths 13 .74 4,57 *'<* 0.94 2 .15 C ,,27 * M- 62.22 84.96 O b served deaths 91 42 5 20 6 G - 21 53 168 Ilspec ted Cbs ervod dcct hs u- aths 4.75 15 i .26 f> 0.30 0.69 C.il ^S: ^ 1 7 2 2 - 5 22.28 15 27,03 55 Expected deaths 10.99 3.31 -1** 5$:* >fc 0.64 1.4S 0 .26 -4.>jf 46.94 3 7 .93 Observed deaths 79 41 5 13 4 4 - 16 38 133 mExpecI ed deaths based upon age specific u ,S, mortality for white males, disregarding t'moking habits o Lung cancer estimate s based upon U .S. rate s lor cancer of lung, pleura, bronchus and trachea, categories 162 and 163. **Including 30 non who smoked pipe or cigars. *!''in* --.ed States data not available, but these .are rare causes of death in tht general population. Multiple Factor Effect *% i"" Number of men Jan. 1, 1967 Person-years of observation Tab lo Expected and observed deaths among 17,800 U.S. and Canada asbestos insulation workers, Jan. 1, 1937-Dec. 31, 1971* Total No history oi cigarette smoking** Hi story | of cigarette j smoking 17,800 83,300 2, US 3 10,1S3 1 9,590 | 46,615 Smoking habits not known 6,144 29,522 Cancer all sites Lurg cancer PPo1reiurt ai m eso the 1iom a one a1 me sothelioma Cancer of stomach Cancer of colon, rectum Cancer ox esophagus Asbestosis Expected Observed deaths deaths 544 .09 45 9 44.42 > ** 6.62 17.51 3.21 i>, iff iU3 26 51 IS 26 13 78 Expected Observed deaths deaths 19.92 33 5.98 "lpjji?fc 'k>k>k 0.95 o co C. , yj/ 0.44 >j<5k 2 2 9 JL 4 0 4 Expected Observed deaths deaths 7 9.58 255 Expected Observed deaths deaths 44.5 9 161 25.>jc0"M.9 ** -fr 3.60 S .53 1.80 iJ.\r_ititTi 17 29 8 14 7 ' 13 .35 ** 2.07 5 .46 0.97 77 7 13 7 8 6 ^^V 45 *** 29 All other causes 631,54 555 92.67 36 356.67 283 212.20 233 focal deaths 805.63 .1,092 112.59 73 436.25 59G 256.7 9 423 "Expected deaths based upon age specific U.S mortality rates for white males disre garding smoking. E n g cancer estimates based upon U. S. rates for cancer of lung, pleura t bronchus and trachea > categories 162 and 163. ^Included 609 men. who smoked pipes o? cigarettes. ***United States data not available, but these are rare causes of death in the general population. \ Multiple Factor Effect I CO PathoJogy of Asbestos-Associated Disease Asbestos enters the human body via two principal routes: the respiratory tract and the gastrointestinal tract. Respiratory tract Asbestos dust consists mainly of fine, noedle-like fibers, ranging in length from a few hundred microns fro consider July less than one micron. The dust is easily inhaled and smaller fibers are carried to the most distant segments of the lung -- respiratory bronchioles and alveoli -- where they become trapped. Some of the fibers remain in situ; others are taken up by macrophages and carried into the alveolar septa ami the lymphatic vessels, and from there to the regional lymph nodes and to the subpleura1 lymphatics. Asbestos fibers are able to penetrate into the pleural space; either because they have sharp ends and are quite rigLd, or because they are carried by ntcrophages. Fate of asbestos fiber's: Some fibers slowly dissolve at. a rate dependent upon the type of asbestos. Some are coated by iron-protein compound and thus probably neutralized. Both of the se are very slow processes. In other instances, fiber's remain in situ apparently little altered. In cither case, asbestos has time to exert in iurinus effect on the cells of the lung. Its toxicity prob ably depends not only upon its chemical composition but also upon its physical properties (e.g. size and shape of fibers, piezoc1octric prop erties) and its ability to concentrate various, often toxic, substances on its highly adsorbent surfaces. Pulmonary fibrosis (asbeslosis); Minor degrees of injury can be rope i r e d . Considorab)e concentration of asbestos is needed to pioduce widespread irreversible d a m a g e . Injury and death of cells and their replacement by connective tissue leads to pulmonary fibrosi s . This at firs! is limited to the septa, but eventually destroys the alveoli and bronchioles while some of the remaining air spaces become d i l a t e d . Within the fibrosed areas variable numbers of asbestos libers and bodies can be found. The function of the lung;, gas exchange, is much reduced. Pneumonia is a frcqi'enl and sometimes fatal complication, because of poor ventilation and poo1" clearance oi the affected lung tissue. ' Plaques represent localized areas of pleura] thickening;. Though they can occur in various pulmonary diseases, they are particularly frequent in asbeslosis and are more often i oui'd on the parietal than on the visceral pleura. Right sidt'd iica^'t Ca ilure is another frequent conpJ ication of severe asbcstosls.. IC is caused by obliteration of a lingo part of 1he pulmonaj y vascular tree, leading to pulmonary hyper tensi on .amt to cardiac o v o r s t m u. Malignant tumors: Pathology - 2 Pulmonary nsbestosis is relatively less frequent now than it was 30 years ago, when the danger of inhaling asbestos was less widely appre ciated. However, another serious complication appears many years after asbestos exposure, namely, malignant tumors. The exposure is very often light and limited in time causing only slight or moderate pulmonary fibrosis. However, 20 or 30 years later a large proportion of exposed people develop either pulmonary carcinoma cr pleural or peri tuneal mesoth e l i o m a . Pulmonary carcinoma associated with asbestos exposure has a predilection for the lower lobes (in contrdistinotion to the general population where it is more common in the upper lobes), but otherwise it is similar in its rate of g r o w t h , metastases and histologic structure. Pulmonary fibrosis, ii present, may mask early lesions and make recognition dif fieult. It can be demonstrated experimentally that asbestos is a carcinogen, though in the lung its carcinogenic potential is very weak. Of the people exposed to asbestos, only those tend to develop carcinoma who also smoke cigarettes, but the combination of asbestos and smoking pro duces strikingly high incidence of malignancy. (See multiple factor effect data.) Plevr.il r..esolho) ioma arises from the Hiring cells of the pleura, the inesothei in L cel'is. It is less common Liian carcinoma, but in those exposed to asbestos it is at: least ICO limes as common as in the general population, fmoking apparently has no effect upon its incidence. Mesothelioma tends to grow along the pleural, surfaces encasing the lung in a thick layer ci tumor tissue, but it may also invade the lung and produce distent motnstases. It comes in a variety of histolcgic patterns, the most characteristic of which combines features of carcinoma and sar coma (bi phasic: tumor). Cells of mesothelioma, as well as the normal D-csoLhelial cells, secrete material rich in acid mucopolysaccharides, Expcr jmerit a 1ly mesotheli cm a can be produced by intrapleural injection of asbestos. Gastroi sites 11 nu J tr act Part of inhaled asbestos m ay be expectorated and .swallowed, or asbestos may be carried into the mouth by contaminated lood on fingers. It can be demonstrated experimentally that asb-stos libers lodge In the walls of the stomach and intestine and may penetrate into the peri tonea3 cavity. In limited studies to clnto., no c>xcess oi tumors has been observed in the gastrointestinal tract of animats fed asbestos, but in man carcin oma of stomach and largo intestine is snore frequent In those exposed to asbestos than in the general populetion. The incidence of mesothelioma of tin: per itone u a Is strike i\-..ly increasco after asbestos exposure. M e s o thelioma can be produced in animal. by jutrapoi itores 1 injection of asbestos. Peritoneal mesothelioma tends 1o grow along the peritoneal surfaces, but it also produces large soljd or iioluhr masses. Histo logically, it is very similar t o pleural wesot hoi io: :a. Asbestos Dose-Disease Relationships Only 1 imi ted data are available on asbestos dose-disease rela tionships'" Few" dust counts were "'taken 20, 30, or 40 years ago and those1 done usually reflected the presence of other dusts, silica, Laic, mica, etc., along with asbestos, Materials, pro duction techniques, and control equipment have changed signifi cantly and current conditions cannot bo used to evaluate past exposures. Some d at a , albeit scant y , are aval 1abl o_ on the asbestos oxpo- sure of insulation workmen and a group of workpeop] e in an integrated asbestos manufacturing complex. These exposure data, which are only semiquantitative, can be related to ex cellent mortality information (Table 1 and Table 4 of Asbestos Disease section'' As a result ol past occupational exposures of about 10 to 20 fiber's (longer than 5jj) per milliliter of air nearly 40% of the deaths of these workpeople can be attributed to their work environment. No data are available on the asbestos dose-disease relationship at lover exposure levels. While any asbestos disease present in other Iban occupational circumstances will bo at a signifi cantly reduced intensity, the 3urge number of people at risk give rise to serious concern. In addition to the 250,000 work people directly exposed to asbestos by virtue of their job, 5,000,000 are exposed indirectly in their occupations. Their asbestos exposure may bo 30 to 1000 rimes less thru the expo sures which produced the current catastrophic occupational asbestos disease experience. At these lower exposures, if the percentage oi deaths related to asbestos is, hypothetically, even 100 times less than direct occupational, 40,000 individuals may be affected. In environmental circumsi aliens with 200,000,000 people potentially exposed, an additional tenfold reduction in asbestos associated disease would still leave 80,000 individuals affected. Dose-response data are, urgently required for other than direct, occupntione! asbestos exposures. Analysis of the mortality expedience and ashes Ios exposure of workpeople indirectly ex posed is important. Indirect methods of assessing past air levels, such as the analysis of settled dust, can be helpful in the studj of populations environmentally exposed. Autopsy lung tissue burdens of asbestos provide an especially useful method of assessing past exposures. Analytic mot hods will require electron mi croscopic techniques. Most asbestos iihers present in the' a i r , even in occiput i on a 1 c irour.si ai'Cc's , are not visible by ligir1 microscopy. In many circumstances, positive jdent ifica I,ion of single as bostos fi bers can only be accompj ished by e] ec tron mic roprobo techniques. ZA Sources of Environmental Contamination Indirect occupational exposures to asbestos have been documented as causative of disease in a wide variety of trades in the shipbuilding and ship repair industry. Mesothelioma is now observed, at an increasing rate, in other than asbestos workers -- in plumbers, welders, electricians, carpenters, pipe fitters, etc. The exposures of those other workmen rav come from simply working in the vicinity of asbestos application or from brief periods when asbestos must be removed from pipes or fittings before their own work can be done. Similar exposures are common throughout the construction industry, especially during the past ten years. Since; i960 spray fireproofing of steelwork with asbestos eontnj ring matciials has produced extensive contamination throughout construction sites with men of all trades ex p o s e d . Over 4,000,000 workmen are employed in the building industry. Their number's alone create serious concern for their potential risk, A variety of indirect occupational exposui es can occur whenever asbestos is widely used. Many electric utility employees are exposed during repairs of boilers or turbines. Chemical plants make extensive use of asbestos insulation material on high temperature pipes and vessels as well as incorporating the fiber .into sore or their products. For example', in one chemical plant we have seen, the transport oi asbestos from a warehouse a r e a , .through the plant, to the point of use exposed unnecessarily every production employee. Famjly exposures court alute an insidious form of asbestos exposure. The dust on w o r k m e n 's clothing (see Figure le) serves as a ready source of contamination o f. the employee's home. V.e readily find fibers of asbestos and other insulation material ir. the settled dust of asbestos clothes have been implicated in the deaths of wives of lnctory workmen. Moreover, children's play clothes washed with a 1alia r '& asbestos laden overalls are likely to be come: contaminated with fiber and prov.ido n continuing asbestos exposure to the child. (Tims cross con tamination of garments has been found to occur during the dry cleaning of a woman's coat containing asbestos fiber.) The magnitude of average asbestos air levels in these family exposures is not known. In fact the variability of ihe exposure precludes accurate definition. However, these family exposures can be virtually; eliminated by proper use of change rooms, shower iacilitics, and laundry facilities which should be avail able to all asbestos workpeople. At the present time only a limited number of work sites have adequate change rooms and few, if any, special laundry facili ties exist j>) the asbestos industry. Such laundry iacilitics must, oi course, be well coni,rolled as mesothelioma has been found among dj y cleaning and laundry employees. Environmonta1 exposures range from ubiquitous virtually continuous, low level concentrai ions derived ircr a wide variety of commonly us-.c! products to those iro.ii .short term pathological uses of asbestos with ex irc-j.elv high concentra tions oi l i m .ied d u r a t i o n . Exampiles oi the ioimrr arc airborne asbestos from the erosion products oi di a..c linings, I'esic ice near a a ,ory with inadequate omis.si on couti'cls, asbestos jn water systems, and asbestos j bovei neos nrd food products. ' Environmental Centaminntion - 2 It is estimated that 40,000,000 pounds of asbestos is incorporated into brake linings each year. Mille high temperatures may alter much of the fiber during use, hundreds of thousands of pounds of asbestos can enter the en vironment annually from this source. Definitive data on the asbestos air concentrations from motor vehicle brake usage are Jacking. However, in some very lira ted studies, asbestos levels two or three times background were observed at sites of extensive broking. Water systems have been found to contain concentrtionsof asbestos in excess of 10 micrograms per gallon. The source of this Water contamination is ill defined but it could arise from geological erosion, rain cleansing of the air, or pollution from human use of asbestos. Asbestos filters have often been u: ed in the food, beverage, and drug industry Studies in our laboratory have demonstrated that erosion of the fibers from the filters occurs and the products can become contaminated. Rome very questionable uses of arbe.stos that have given rise to significant environmental exposures include the open transport and dumping of asbestos waste, the use of asbestos in paper macho and cement act material which is rnixc'-1 dry by children, the incorporation of asbestos into consumer fabrics, and a m - procedure which can generate uncontrolled asbestos aerosols (such as spray fireproofing). Of ter, e-bestes exposures occur as a result of fiber contamination of other products laic often coexists with varieties of asbestos and the use of cosmetic talcum powders car. produce a significant ashes tos exposure. In some foreign "talcum powders" the material may contain subs 1antial amount- of anthophyllite a s b estos. Industrial talcs, especially, are liable to be ccrilaminated as a major source of such talc coexists with extensive deposits of asbestos. Indivi duals doing home repairs nay occasionally have short terra exposures, oiten unsuspected. Gypsum spackie compounds used to seal wallboard joints or patch pilaster often contain asbestos in amount:.- up to a few percent bv weigh; . The sanding of such 'materiel, when dried, can generate high con centrations of asbestos. An insidious such exposure is that to irdividuals in urban areas whose apartments have been rehabiLite fed under lead control p r o g r a m s . Here, 'sailboard is typically install led over the lead contaminated paint. Spackie is applied to the joints and sanded with the result that asbestos dust rather than lead may con Laminate the household. Over 3000 uses of asbec os have been documented. Many rf these products are produced safely and can be used s a f e l y . 'ihn product .1 >n an' use of others, however, c.>n easily give rise to si gni r1can t human exposu! es . Only constant vigilance by indus lry, by government, by research, sci antis I s , and by consumers v ill assoie their eventual safe u s e , t Asbestos Air Pollution Ambient air levels of asbestos range from approximately 10 gm/m" to over 10 gm/m' . Thus, asbestos may constitute only 0.0001 per cent to 0.1 percent of the particulate matter present in a given air sample. Moreover, the asbestos found in the ambient air in cludes both micron-size fibers and numerous individual fibrils which may be; agglomerated with a variety of other material present in the- air sample. These considerations preclude the possibility of quantitative analysis of such ambient air samples by light microscopy, bulk spectroscopic techniques, or X-ray diffraction. The agglomeration of the asbestos wj th other mat eri als and the presence of many sub light microscopic fibers render light microscopy ineffective. M o r e o v e r , the unique identificali:;:' of small optically visible fibers is not always possible, ever, using u petrographic mic r o scope. Any bulk analysis method attempted to date has failed be cause of the presence of the much greater quantity of other inor ganic and itiinora 1 m.a tev ia 1. The only effective analysis method has required the use of election microscopic tc clini ques and involves the following .steps: 1. collection of the air samp It s on merib?u.r.c filter paper, 2. low temperature ashing of the collected material to remove' the filter material and other organic matter, 3. dispersion of the residue by grinding or use of ultrasonic energy, 4 . fixation of the dispersed residue in a nitrocellulose film which, is mounted on an electron microscope grid, and 5. scanning at 40,000 X magnification using cLectror microscopy to determine the mass of asbe `-tos 'or igl nat Lug from a prescribed fraction of the initial sample. The di sponsion procedure has hoc n found necessary as large frag ments of oiher inorganic materia] obscure the presence oi asbestos which often exist;; in fibril form at 1ached to other par! icles. Un fortunately, this procedure allows only the mast concentration to be deterrii r.rd and ini m-mat ion on the s-.iz a cUstribut ion of the fiber is lost. One hundred eighty s'-ven samples from 4 9 United States cities, collected by the ' r ] e-r;a.1 Air Pol 1r.tion Control Administration during 1909 ..nd 1970, were ana 1 vs* d at the Ur-"i'-oicfeatai Selene-a.