Document 0jnGp2e2jbGXXN7bqJjmVrgO

United States Department of the Interior Geological Survey A Survey of Asbestos-related Disease in jy* pors'jr; /4-s t.x. S/*c.-( /'a si-p I W Ju > I ?<PV - p f . S- i - I o / ,'v, "b+V>rtTnnj. /W tt dv\ J re l * if t*j iuv,y 1^* be | J i I 1--c vd/Ne *w , J This report is preliminary and has not been reviewed for conformity with u. S. Geological Survey editorial standards and stratigraphic nomenclature. 1982 UCC 008648 ABSTRACT: A review which is based on thirty six published epidemiological studies is given of the disease patterns that have developed among industrial workers, miners, and millers who were exposed to dusts of one or more of the commercial asbestos minerals or to dusts from minerals perceived to be asbestos-like. Health data is also reviewed for those who were exposed to asbestos dusts in a non-occupational setting. From the published reports it is clear that there are very significant differences in the health effects of the several asbestos or asbestos-like minerals. Of the commercial asbestos utilized in the United States about 95% has been chrysotile or "white" asbestos, about 2% amosite or "brown" asbestos, and about 2% crocldolite or "blue" asbestos. The common white asbestos has had the least effect on those occupationally exposed whereas blue asbestos has had the most effect. Despite the wide dissemination of white asbestos In our environment; In schools, homes, public buildings, brake lining emissions, etc., there is no evidence that the very frequent non occupational exposures to this form of asbestos has caused any harm. On the other hand, nonoccupational exposure to blue asbestos has been conclusively proven to have caused significant mortality. The different health effects of the various forms of asbestos require different regulatory responses and remedial actions. UCC 008649 INTRODUCTION The Problem The widespread use of amphibole and serpentine asbestosl/ by Industrial society for such Items as service In brake and clutch facings, electrical and heat Insulation, fireproofing materials, cement water pipe, tiles, filters, packings, and construction materials, has contributed greatly to human safety and convenience. Yet, while our society was accruing these very tangible benefits, many asbestos workers were dying of asbes tosl s, lung cancer, and mesothelioma. The hazards of certain forms of asbestos under certain conditions have been so great that several countries have taken extraordinary actions to greatly reduce or even ban their use. Recent experiments with animals demonstrate that the commercial asbes:os minerals as well as other fibrous materials can cause tumors to form when the fibrous particles are implanted within the pleura. These experiments have convinced some health specialists that asbestos-related diseases can be caused by many types of elongate particles; the mineral type according to these health specialists, is not the important factor In the etiology of disease, but rather the size and shape of the particles which enter the human body. The question now before the World's health and regulatory establishments Is whether the hazards of asbestos outweigh the benefits. Should the asbestos minerals and perhaps other asbestos-like minerals be banned from use? Minerals belonging to the amphibole group are particularly important In this regard for they are ubiquitous and commonly have cry<talline habits which are considered by some to be asbestos-like. The Dilemma The concern for human health, the great usefulness of many asbestcs products, the appearance of asbestos minerals or asbestos-like minerals In the natural background and In many kinds of mining operations, and the un certainty of the exact health effect? of different kinds of minerals, different mineral particle sizes, and different mineral dust concentrations combine to present a formidable problem to minerals scientists, the 1/At present, the most widely used definition of asbestos in the Unite* States, Is from the not ce of proposed rule-making for "Occupational E posure to Asbestos" published in the Federal Register (Oct. 9, 19?5, p. 4765 47660) by the U.S. Occupational Safety and Health Administr tion {0SHA>. In this notice, the naturally occurring amphibole minerals mosite, crocldollte, anthophyllite, tremolite, and actinolite and tie serpentl le mineral chrysotlle are classified as asbestos If the Individual crysta lites or crystal fragments have the following dimensions: length greater thin 5 micrometers, maximum diameter less than 5 micrometers, and a length-`.odlameter ratio of 3 or greater. Any troduct containing any of these minerals in this size range is also defined as asbestos. 1 UCC 008650 minerals industries, and legal and health professionals. Must the use of all commercial asbestos be stopped? Must all mine dusts containing such particles be controlled to the lowest feasible levels and wastes from those mines be considered toxic and thus isolated from surrounding air and water? Must alj asbestos be eliminated from our drinking water, our schools, and our public buildings? Mjst we cease to use asbestos In brake linings, cement water pipe, and structural building materials? Must even low levels of non-occupatlonal exposure to asbestos or asbestos-like materials be avoided at any cost? In order to obtain an Insight that will enable us to intelligently address these questions I will review the role of asbestos In the world economy, the Important geological occurrences of commercial asbestos, give estimates of asbestos-related mortality In the iJnited States In the recent past, and document the Incidence of asbestos-related disease In the trades occupations, the mining and milling occupations, aid in those non-occupationally exposed to asbestos or asbestos-like minerals. As we will see, the six asbestos minerals used In commerce are not ideitlcal In their crystal structure, chemical composition, abundance, and geologic occurrence; nor do the different asbestos dusts have the same Impact 01 human health. Instead of treating all asbestos minerals as equally poteit carcinogens (apparently the prevailing opinion In the United states) each mlleral should be examined on Its own merits and demerits with regard to Its usefulness to society and Its potential to cause disease. UCC 008651 ASBESTOS IN THE WORLD ECONOMY Early Beginnings Whereas the general use of asbestos In international commerce dates only to the late 19th century, its utility In human culture goes back to at least 2500 B.C. Archeological studies (Europaeus-Xyrapaa, 1930) show that the inhabitants of the Lake Juojarvl region of East Finland knew how to strengthen earthenware pots and cooking utensils with anthophyllite asbestos. This asbestos probably came from the same areas where it has been commercially exploited In recent times. Until recently, however, most other uses of asbestos were trivial; such as Its fabrication Into such curiosities as cremation cloth, tablecloths, lamp wicks, and purses. Even well Inlo the last century, asbestos could not be regarded as a product of commerce unless one Included such endeavors as the small Industry developed In Russia during the rule of Peter the Great where chrysotlle asbestos from the Urals was used for a short period of time in the production of textile?. In the 1860's and 1870's, the market for asbestos products rapidly changed - probably for three reasons; the need for Insulation for the new steam technology, the formation of an international trading company of Italian and English entrepreneurs, and the reopening of the chrysotlle asbestos deposits of northern Italy and simultaneous exploitation of the vast chrysotile resources in Quebec. The supply for the first time was ample, the market was ready. The Modern Industry The reopening of the asbestos deposits of northern Italy, deposit1 which had been worked as far back as Roman times, marked the beginning of the modern asbestos industry. By 1890, the asbestos industry was full blown, with hundreds of applications being introduced (Jones, 1890); by the turn of the century the large South African crocidolite deposits had been opened up and the Russian deposits in the Urals were once again producing in large quantity. Within a few years, the amosite deposits of the Transvaal would be exploited. From the time of the first recorded use of asbestos by Stone Age man to 1900 the total world production of all types of fiber was probably about 200.000 metric tonnes, certainly no more than 300,000 tonnes. Of this 150.000 tonnes came from Quebec. By 1980 more than 100 million tonnes of asbestos had been mined throughout the World; of this more than 90 percent was chrysotlle and more than 5 percent crocidolite and amosite. Nearly 40 million tonnes of this total World production was chrysotile mined in Quebec Province near the towns of Thetford Mines and Asbesti s. Total production of anthophyllite asbestos to date is probably no more than 400.000 tonnes; 350,000 tonnes being produced by Finland alune. Production of tremolite asbestos has been sporadic and it has been mined In various parts of the World for short periods of time. Total production to date for this form of asbestos is probably no more than a few thousand tonnes. Commercial exploitation of actinollte asbestos is practically unknown. UCC 008652 The World asbestos production for 1978 is given in Table 1. Russia leads with 46.1 percent and Canada Is second with 28.9 percent of the world output. Both countries mine only chrysotile asbestos and most of the fiber comes from the Urals and Quebec. The third leading asbestos producer is the Republic of. South Africa (7.1 percent); the asbestos ore consists of amosite, crocldollte, and chrysotile. These three countries furnished 82.1 percent of the World's asbestos In 1978. The other countries listed in Table 1 produce mostly chrysotile. COMMERCIAL ASBESTOS The Asbestos Minerals Standard references published over the past 50 years usually list six forms of commercial asbestos; the amphibole varieties are amosite, crocidollte, anthophylllte, tremolite, and actlnolite, the serpentine variety is chrysotile. A detailed understanding of the chemistry and crystal structures of these asbestos minerals postdate their discoveries; thus some of the older literature can be confusing with regard to mineral identifications. Chrysotile, Mg3S12^5(0H)4, one of the three common polymorphs of serpentine Is generally fibrous although non fibrous varieties are known. About 90 percent of the past and about 95 pe cent of the present World production of asbestos was or Is the chrysot le form. Amosite is the very rare asbestiform va iety of grunerite amphlbole, (Fe,Mg)7S1g022(0H)2; this varietal name is d rived from the word Amosa an acronym for the company "Asbestos lines 0 South Africa" (Hal 1 , 1918, p. 13-14). This valuable commercial isbesto is mined only in the Transvaal Province of South Africa. Crocidolite is the asbesti form variety if riebeckite amphibole, ideally ^(Fe^MgJgFe^Sigt^tOH^, and ha. been mined In only four localities; In the Transvaal and Cape Povinces of South Africa, in the Hammersley Range area of Western Australia, and In the Cochabamba area of Bolivia. Only the South African mines are still active. The only other form of amphibole asbestos that has been mined commer cially on a significant scale is anthophyl 1 i te, (Mg ,Fe) 7Si 8^22(0H)2. from the Paakkila area of East Finland. With the Finnish mines now closed there is now very little anthophylIfte asbestos production anywhere In the World. There are numerous reports of mi lor occurrences of tremolite asbestos, CaoMggSig022(0H)2, and relatively few reports of occurrences of actlnolite asbestos, Cag(Fe,Mg)sSi9O22(0^)2 Tramolite and actlnolite asbestos are now, as they have been in the past, of little economic Importance. The Important Geological Occurrences )f Commercial Asbestos Many minerals, including the ampiiboles and some serpentines, are described variously as fibrous, asbestiform, aclcular, filiform, prismatic; these terms suggest an elongate habit, Alth>ugh such minerals are extremely 4A UCC 008653 Table 1. World asbestos production in 1978 (Clifton, 1 979) Fiber Locality Chrysotile North America Canada United States South America Argentina Brazil Europe Bulgaria Italy U.S.S.R. Yugoslavia Africa Zimbabwe South Africa Swazi 1 and other Asia China Cyprus Indi a Japan Korea Taiwan Turkey Oceania Australia (World chrysotile total; Crocidolite South Africa Amosite South Africa Production (in thousands of metric tonnes) 1620 93 1 100 21 162 2582 10 210 118 48 1 210 37 21 7 7 1 10 6ft 5317 210 71 4B UCC 008654 ! i t common. In only relatively few places do they have physical and chemical properties suitable to be valuable as commercial asbestos. Locally, amphlbole minerals may show an asbestiform habit, for example In vein fillings and In areas of secondary alteration, but usually they do not appear In sufficient quantity to be profitably exploited. Deposits of commercial asbestos are found in four types of rocks: (I) - al pine-type ultramaflc rocks including ophlolltes (chrysotlle, anthophyllite, and tremolite), (II) - stratiform ultramafic intrusions {chrysotile and tremolite), (III) - serpentinlzed limestone (chrysotlle), and (IV) - banded ironstones (amosite and crocidolIte). Type I deposits are by far the most Important and probably account for more than 85 percent of the asbestos ever mined. The most important Type I deposits are those of Quebec and the Urals. Type II deposits are found mostly in South Africa, Swaziland and Zimbabwe. These furnish mostly chrysotile asbestos. Type III deposits are small ; the most notable of these are located in Globe, Arizona and in the Carolina area of the Transvaal Province of South Africa. Type IV deposits are found only In the Precambrian banded Ironstones of the Transvaal and Cape Provinces of South Africa anl of Western Australia. Only the South African deposits are still in production. A complete review of the geological occurrences of commercial asbestos is given by Ross (1981). HEALTH HAZARDS OF ASBESTOS Diseases Related to Asbestos Exposure Three principal diseases are related to exposure to one or more of the commercial asbestos minerals. These are: (1) lung cancer which includes cancer of the trachea, bronchus, and lung proper; (2) mesothelioma, a cancer of the pleural and peritoneal membranes which invest the lung and abdominal cavities, respectively; anr (3) asbestosis, a diffuse interstitial fibrosis of the lung tissue often leading after long exposure to severe loss of lung function and respirator failure. The occurrence of lung cancer in asbestos workers is also complicated by the association with cigarette smoking which leads to considerable difficulty in assigning relative risks of asbestos exposure to smokers. Mesothelioma, a disease which is usually fatal In one to two years after diagnosis, is rare, accounting for less than 300 deaths per year in the United States and Canada. Some epidemiological studies suggest that asbestos workers may suffer excess cancer of the digestive tract (Selikoff and Lee, 1978); other studies do not support this conclusion (McDonald and McDonald, 1980; Meurman et al., 1974; Rublno et al., 1979; Nicholson et al., 1979). Some question still exists then as to the role played by asbestos in the etiology of digestive tract cancers. Recklake (1976), Selikoff and Lee (1978), and Simpson (1979) give a complete review of the subject of asbestos and disease. Particle size and shape appear to be the factors controlling whether mineral particles enter and remain in the lung or are removed from the lung after entering. Particles such as asbestos fibers which have diameters 5 UCC 008655 greater than approximately 5 yn cannot enter the bronchial airways, those having smeller diameters do. Particles having diameters less than 1.5 ym are particularly dangerous for they can penetrate to the smaller bronchioles and even to the alveolar sacs (Davis, 1981). Most particles which enter the upper respiratory tract (the malnstem, bronchi, and bronchioles) are quickly and effectively removed by the mucocllllary escalator. A second lung clearance mechanism operates In the lower respiratory tract (the respiratory bronchioles and alveoli). Here, pulmonary macrophages engulf the foreign particles (phagocytosis) and then: (1) move to the upper respiratory tract to where the mucociliary escalator is operative or (2) move through the alveolar wall into the interstltlum and eventually to the lymph channels. Asbestos fibers which are longer than approximately 10 un are not readily phagocytlzed by the macrophage cells and thus tend to remain In the lower respiratory tract or they ma/ penetrate the pleural membrane and enter the interpleural space. Asbestosls may occur when such fibers remain In the lung parenchyma for lengthy periods of time. The asbestos fibers can stimulate deposition of excess intarstlal collagen and reticulln fibers. This causes the alveolar septa to become thickened with ensuing Impairment of oxygen uptake (Davis, 1981). Long-term residency of fibers In the lung and pleura may also Induce lung cancer and mesothelioma; the mechanisms by which this takes place are far from being understood. As will be described later, pleural cancer seems to be induced by crocidolite asbestos but not by chrysotile or anthophyl1ite asbestos. Lung cancer Is caused by chrysotile, anthyophylllte, amosltf , and crocidolite asbestos; particularly in asbestos workers who smoke cigareites. Two completely different substances, asbestos and cigarette smoke, combine to produce a very significant risk to those who have been heavily exposed to asbestos dusts. Generally, asbestos-related diseases appear in asbestos workers only after many years have elapsed since first exposure. A significant increase in the lung cancer death rate appears 10 to 14 years after first exposure and peaks at 30 to 35 years. The mesothelioma death rate becomes significant 20 years after first exposure but continues to climb even after 45 years have elapsed. The asbestosis death rate becomes significant 15 to 20 years after first exposure and apparently peaks at 40 to 45 years (Sellkoff et al., 1980a). Epidemiol ogy Before considering the mortality studies of the various occupationj1 groups exposed to asbestos, we should )rief1y consider the role the three important types of asbestos (amoslte, :rocido1ite, and chrysotile) played In the commerce of North America and Europe, the areas where the major epidemilogical studies of asbestos wor ers were made. 6 UCC 008656 In North America, chrysotile entered the market In large quantities early In this century. Crocidolite was apparently first used In the United States In 1912 when 9 tonnes were Imported, but It was not until World War 1 that Its use for high temperature Insulation became established - particularly In the ship building industry. By 1930, 35,000 tonnes of crude croci dolite fiber had been imported into the United States. Import statistics for crude crocidolite asbestos from South Africa into the United States are given in Tables 2a and 2b, Large amounts of manufactured goods containing crocido lite were also Imported but tonnage estimates cannot be made. Not until the mid 1930's did amosite asbestos gain a market In North America when it began to replace crocidolite for high temperature insulation. Crocidolite was milled In Bound Brook, New Jersey in 1920 and in 1924 the operation moved to larger facilities In Millington, New Jersey. The many advertisements in the trade journal Asbestos from 1920 to 1945 indicate that crocidolite was used in many products and particularly for insulation of steam boilers, locomotives, and pipes. As an example, a product contain ing crocidolite asbestos and called "85% Magnesian Sectional Pipe Covering" was advertised monthly In Asbestos from 1920 to 1945 {see also, McCullagh, 1980). Amosite, crocidolite, and' chrysotile were almost universally used aboard ship during World War II; amosite for high temperature boilers and pipes, crocidolite for packings exposed to acids or salt water, and chryso tile for low temperature and electric Insulation. The use of asbestos In Europe paralleled that in North America, with one notable exception - the exte ' ' '1 ,J" ` ' sprayed-on coating to fireproof Sprayed-on coatings were also used In the United States after World War II but the coatings contained, with few exceptions, chrysotile rather than crocidolite. Sprayed-on asbestos coatings were not used on U.S. ships; the principal use being to fireproof steel building girders and as acoustical coatings in schools and offices. Asbestos trades workers. Avery significant increased ncidence relative to the general male population, of lung cancer, as>estosis and mesothelioma is found in men who were employed in the "asbestos trades" insulation of steam locomotives, boilers, ships, buildings; fabrication and Installation of asbestos-containing textiles, roofing mater als, cement products, tiles, wall boards, brake linings, clutch facings, filters, packings, gaskets, etc. Those in the "trades" generally us d several types of asbestos minerals during their working careers; most comnonly these were chrysotile, crocidolite and amosite, rarely anthophyllite. Significant exposures by any group < f workers, at least for the past 40 years, to tremolite or actinolite asbestos dusts has probably not occi rred. 1/Mesotbelloma Is prevalent in the shipyard workers of Europe; at Walcheren, Wllhelmshaven, Plymouth, Trieste, Hamburg, Nantes, Rotterdan, Malm# {McDonald and McDonald, 1977). The extensive use of crocidnlite aboard European ships prior to and during World War II Is suggested to be an important factor in the etiology of this disease. UCC 008657 Table 2a. Minimum estimates of Imports of crude crocidolite asbestos from South Africa into the United States (1907-1929),* (1940-1945)**, (1946-1974).*** Year(s) Crocidolite crude (short tons 1907-1908 1909-1910 1911 1912 1913 1914 1915 1916 1917 1918 1919 1920 1921 1922 1923 1924 1925 1926 1927 1928 1929 probably none no data 1 ittle 9 1 no data probably none 1184 . 2081 837 1056 2979 704 1684 2040 1457 606 4873 5587 ? 9952 Total (1907-1929) 35,050 short tons 1940 1941 1942 1943 1944 1945 2708 2976 4213 4808 2946 3100 Total (1940-1945) 20,751 short tons 1946-1974 346,796 short tons Some of the imports were shipped through England. Small amounts of clrysotile may be included in import figures but no amosite. Figures do not include any manufactured asbestos products. Most crocidolite came from the South Cape Prov., some may have come from the Transvaal. Source: Mineral Resources of the United States (1907)...(1929) U.S. Geological Survey, Kashington, D.C. ' **Crocidolite composed 19.4% of the South African crude asbestos Imports Into the U.S. during this period - which totaled 107,039 short tons, over 80,000 tons was amosite asbestos. Sources: Minerals Yearbook (1940).,.(1945), U.S. Bureau of Mines, Washington, O.C. Mineral Trade Notes, Confidential Series, No. 1-31, U.S. Bureau of Mines, U.S. Dept. Interior, Washington, D.C. (1940-1945). Minerals Yearbook (1946)....(1974) U.S. Rureau of Mines, Washington, O.C. 7B UCC 008658 Table 2b. Imports of all crude asbestos from South Africa (1930-1939) Year(s) 1930 1931 1932-33 1934 1935 1936 1937 1938 1939 Asbestos Crude (short tons) 3635 2290 1370 4269 2529 ? 3025 4248 6422 Total 27,788 Import statistics do not differentiate between various forms of asbestos. Little chrysotlle was imported from South Africa thus the figures are for mostly amosite plus crocidolite. Import data for crocidolite during World War II suggests that at least 20% of the 1930-39 imports were crocidolite. The amosite market was just developing in the U.S. in the 1930's. Most of the crocidolite was from the Cape Province. Assuming a ratio of 4:1 of amosite: crocidolite based on IWII import figures, at least 5538 short tons of crocidolite was imported into the U.S. from 1930 to 1939. Sources: Mineral Resources of the United States (1930)(1931 . U.S. Geological Survey/Was lTngton, O.C. Minerals Yearbook ( 932) (1939). U.S. Bureau of Minos, Washington, D.C. 7C UCC 008659 Statistical data for 21 mortality studies of defined cohorts of asbestos trades workers (mostly male) are presented in Tables 3a and 3b. Of those that are continuing prospective studies, the most recent update is given. Twelve of the studies are of asbestos factory workers, eight are of asbestos insulation workers, and one is of asbestos construction workers. In all, 50,143 individuals were followed (1 ,517 were female); of the 7,166 listed deaths 1 ,198 {16.7 percent) were reported as due to lung cancer and 402 (5.61 percent) were reported as due to mesothelioma. In the 21 studies, the lung cancer mortality accounted for 6.1 to 26.6 percent of all deaths; mesothelioma mortality accounted for 0 to 16.1 percent of all deaths (Tables 3a, 3b, Fig. 1). The workers involved in study No. VI worked only with chrysotile, those Involved in Studies X and XXI worked mostly with crocldollte, and those In the remaining studies probably worked with more than one form of asbestos. Estimates of expected cancer mortality are very difficult to predict, for cancer rates are modified by the individual's "lifestyle" as well as by occupation. The "lifestyle" contribution to lung cancer is cigarette use. To better assess the significance of these health studies It Is necessary to examine the cancer-mortality patterns of cigarette smokers who were not exposed to asbestos dusts. Unless prevalence of smoking within the study group Is carefully evaluated it Is Impossible to predict accurately the health effects of occupational exposure to carcinogens such as asbestos, radon gas, and arsenic. Unfortunately, In few of the studies listed in Tables 3a and 3b have adequate assessments been made of the proportion of workers who smoke cigarettes. The contribution of cigarette smoking to the Increased Incidence of disease has been evaluated in several studies and has lead to a consensus that this habit produces a very significant increase in risk of dying of lung cancer as well as of the various cardiovascular diseases. The largest study of cigarette smokers i9kthat of E. Cuyler Hammond and colleagues under the auspices of the American Cancer Society. This study is based on questionnaires and mortality follow-ui accomplished In the United States between July 1960 and June 1971 for approximately 51 ,000 men (Hammond et al., 1978). The proportional mortality of lung cancer (percent lung cancer deaths relative to deaths by a'l causes), based on the Hammond study, is shown graphically in Figure 2. For a group of men who all smoke cigarettes (cohort of 100 percent smokers), lung cancer mortality Is approximately 7 percent at age 45, re ches a maximum of approximately 10 percent at age 70, then decreases sll'htly at older ages. For a cohort of male non-smokers, lung cancer mortalTy Is 2 percent at age 45 and then decreases continuously to approximate y 1 percent at age 95. Smoking Is most prevalent in blut-collar occupations relative to pro fessional and managerial occupations (Sterling and Weinkam, 1978). This prevalence also holds true for the asbestos trades, mining, and milling occupations. In a group of 13,722 asbestos insulation workers, whose smoking habits were recorded, 70 percent had a history of cigarette smoking (Selikoff and Hammond, 1 975; Saraccl, 1977). In a group of 1 ,015 chrysotile asbestos miners and millers 85 perceni were smokers (McDonald et al., 1974). Data given in Figure 2 predicts that fhe lung cancer mortality for a cohort fA UCC 008660 t U K art jlyt o f Atbs&to*; trs d e ; * o c tf* s oxtlw dlr^ a t.ie rt inri tU r* (V s T a b U i)* Hoot r c **t opdato o f prM poctlvo ,,= a s " I 4 --1 u 46 * 8 5 s ~. a Ssa 3 Is <0 * _v _* mN 5 #* 0 A* 4 1.. s _ - PI ff m i; -- i i *-. ss " 11 3! k 8 0 4 -- aa It 5" 35 8 40A - rV .* w stt * 3 a ^ s W p s a a s 2 : % a V5 a S J s= *2 St Oft. w a r s ~ - 0 rat s _ s N f! 8 rt Ml Im i 8S S M l--A M*l M *A ? A- 8 S** 3 A " 5 aa Z fs o" | 5^ S_ mm 2 N v * *" ((** a 2 n m px 5- M 1 pa 4 S N * f* ia : i : V8 4 0* e o 8 Ss S ,, '. 2 fas 3T * -Is w H> *a Cm a 5s 3A IX n Oa & 8 * x St * a nfc dCtp0* 5 -* wS ^ a w s A bfl |J S2 *a a* k 5 It S r C iC 5 ras N *! A a : za S 7 <n X s m* M * t -. o lift O Ad * x. w3 1 O F> ^ 5 5 *? b -- n 3 - -* ss 5 :* a . .t iiti 1 z l'|i 5 _ : - talc a t .. w Aw V --> 4 m 5 SS K v, '1* u4m a . t =2 3 | .| i I it ss|5 i 39 ish Ml A* A* * is 3 32 3 v t 2k S - ||3 Hf s ;? i V & ! 1. V &| ** V & s m M 1 SAW 0b L M W*> ** s t k su :! s ia as *i a 1 2 v? js A V px 00W.54V ft- c m 0--- ---- OSh 0 4 & ft e* v ** oe ivi x- 9m 8* XP # W W * i a iu Mx X0MX4!*wte tmA 0_ 0-w^Www MA0- ^F, b a g*V# S 4 >IU 8UvUb5 S 0 M f4 *2 m 00 a3 0M m 33 t I uv . 3 - .- S S 22 2 *j S. ?8 .-- ^ S' 8 -* * r= SS S . szi A 2! 8 3 352S ; t az ^ r ZZ 1 l *t 5 *8 "s a sf 333 . 0 T i :j 1. a 22 C H2 v * & ir w s 5. s t! ;=st i. as; 5M .. . 8 8 c" JJ, . 8 S8 i c 82 3 & r ft s - |sl 5* * :s i E * 2 2 In !s i U * a .1 ;2 - sj I ~ ~lt i : ih . 3 3 Is 3 2 s 1 5? | | 3 E 8 *s s s * *i n sa . |. || si t / 0_8g Xs 2 i 3s i SJ Mi**** rstj; 22 3 i -'-III 7 I S C 2 p - *> St * iiisstt 2 ^ i V i m s * a s 4 * 7 5? a s o -* x< e s s <X - a #* a ' * *5 s * Ay -I? If 5* Sis 74 1a it* "? ?, > 5 s* _ Ns) ft 9 5 t) * *T C^ o W* M i ^*i -* 0 00 J s i#bsM 3 13 !i * AI i' ** IS ** 't 3Ss a SS 1* *X a A ft V4I V*! 5. s& i +M* 61 S_ i; 1 it} a I* II a i : -7 . * ||f 11 : a 7* | * 1* A a | * a a '' J w, a a - is., ft* l 5 Aj if J* * i i* . i; : ~ 1 r I Iu f f ills> 5- 1 f I Ii|- ocj "c2 * -- 2Sc -- lil* li * ii,3 liia <stt ts v#Si -axSh#lrvffvl f a t f :*s til I.S. . ? sEsst i illiij * Sm* V- * *A S Jr | 3 *9 | t3e 2 VW i! s V S TS i i 1-8 ?0 4*;f* i 1-V hiiin 8 i?i i - & S 'o ?4 0i - aisj |* ci 8* i-S ::5 |eifts| Q4 = Si U`2 8WI I+J '* il H oe i] I I 8 ^3 Z = 1} J , 02 3: s : 4 V* ^ 4 ^4 4 --4?03V*Pe iI 1 1 S! 1 tvVal --4#- oufat I TM i> . Cohort n o r ts llty 8B UCC 008661 U b1 3b. Cohort K t * llt ) r itu d ie t of asfeUo t r i t e f f k t n ; fraelodtng atners nd i m ir * ( i t * I b l* 4 )< * t rcNt vptiat* o* p rtn p a c H ** itu d tM IM - U I tr e g lv t" ( W t - I M ) . | - --* B PH T* se m ' *r "cs Ho * c*as w a r" 5*11 * J5 5j M r Bl Lpl "> --414 1C---- PH ;! ^ ... J *.* i ?- '1I!l .... i i i. _ #sa- .<r LVs..fCfM v". ao^e- H>h. ux^2.-*^ >x4> etrf-1owi. c> -4- -- '-'----- 1---------- ---------- --?-- ii1 4JCfP-tb ef-tf>ac- C-tir -t T11 J5 2S5 , isSrSUhStSC-b I^!4-r. I *aM!P ;--*Pi4 ! ! || ,,I,,t *_S**:fS^-e|'b!U-i Hi 4 Is*5 p> 1 * 5_ *#H 2P-, 4 ** = a s =B -: 2b0 s fp4V-hl i**v. 44 b e b" b a m me- S g,J Sy! nmcv'Sa iPM B= t*1 . #' s fP4bH 4 PPp* PH 4 ja 1 ap i ^ ii W. =e; cj tIpxfifc~i*- V J ^ t^ * 1 5 11 *X sy/w:- 2c; 2!u Ss ft 1 *v Cm t 1 li III a4'b1# 4wi' ll*s;' - *. |r as*i s XB--' R i : 3 H3 *iv. l/H lS 8 t--4 *wfBety# p<Ti **ft 3 *. g*2 |2_e*. *2. 2t%iie.sS. ;St <;Z5-7 Zii T3 *S<': tis-SS tttSS.sttS- j1 =r -tB- -$--#H * 5--*w CSa!O 2?Si br-i (ann# >(?5S-" BrT) w*4-? Pi 4* Jf SN S* is 2 * m\ ft 4*m m^t W ftp . . I2.2L ss'-ss -aSS.i f1 I S. B t. :^ s ts 1 If`-t*a1- If*t i = X X $ r wPS5BPMI" #B*". S' fPm s#4 24 8p=a1*. s- ^r s5 L4 r 14JH9 2- J*f 3 e i5r 2= eS. 1 * s c e = If If ST 3BS .p"T> 5 s Sft K#u 2a h ^ p* : <- ~IS *c S4 P^c s fH 5^5 _4 a4 s' '3 is-, 2 cl f\ S3 .. 32 2S 2 ' as ?f : * S C1 '1 s 3 I3 III s *f 1. i9 fc * e v N 2ei* S-* Imf.- 8 |r3 !i. 8a S3<C-- 3 sBIf*0-f>ff4Cit*#t^C a CS --cu2.e SK, g4 t S22Z2J s 1 g . . iIf-ic 4-P4s-. ZW0e Cs .. 4b4xsa*04**4SCs-4e5-;5iJtie I1 pA=e#m gfSbtP-1h^-s^bOp2> kiP4S-*sAVS*0--- 3S3ms>"i*-s*.:;' It 5t S Se CS -g - t , =3*.2.2S* K2 SIff hns:*2 ssj: tin a4 . * rs. ' -- ra 1 I" 1- a. a 5t i I 1* e -- 0 ZrJ i| sf b ; s * X 2 2* eel : ij 3C*aJ* 4 " i 1c Bi i;S# mpk g.' 5 __ a o s ^ ?! f kw bM 2 5 i--------<A r 4a+mj baum 4* --' aM Ma X * 4i> MS *-* XM 2* 1 4 X b Z eV ea X h g 6 Z P (S X . F <u:Fp XiS>iitui>i-"*- li s - ij - k. t |WfS tI&*it.,s- iL|- ySsi-sst-T^i-ict-S--i sj5s!rft o * w -- ba *b. a --V is5is* X H H -5 6 ^ % *> 4 *ifSi5r*?ePC- L Ok. PCI B-- 14 j X 2* Z s~ W Pm 2JftfT i c 4xa Ib2w - *2- 0(. y w0 ^# - s?* *> --rrk,s-ft c- f sSi*.* s ;ia " i * a -|#aB Ii^p :0*r- .31. 3j- 44 *l_J *y c. ?; a M0b fts #. '' --t --a a p l. g ft' u 5 5? S * H. b -- t -*. -y at 0sc Is ,= E S! w|SSaa S0^am:PsScw bi2b' .. Si 2 --x9- afi tSailBbt- 4 0 O''^ * i < 4S lit* . ZiV 9 +* * b \ | Cd ijl. --a4v- +f0*mt* x*m# Smu ">* a*** 23gt. eb wa __g a* p w u 4 5-- -- 4 sS.2Is--tS- gsH tS&isS * -- s m b^p# ^#5* ph*4Ibi 8C UCC 008662 -/ % LUNG CANCER MORTALITY ( j / i m e s o t h e l io m a m o r t a lit y i t 1 UCC 008663 i i --t- Figured. Percent of lung cancer deaths in males relative to deaths by all causes (proportional mortality - lung cancer) plotted with respect to age for four groups (cohorts) having different cigarette smoking characteristics and for a cohort of non-smokers. For example, for a cohort of 70-year old males which is composed of 75 percent cigarette smokers, 7.8 percent of all deaths at.age 70 are predicted to he from lung cancer. Graphical presentation based on data from Hammond et al. (1978). 8E UCC 008664 composed of 75 percent smokers would be at least 6 to 7.5 percent, regardless of occupation. In Tables 3a and 3b we see that the lung cancer mortality for the total of 21 cohorts of asbestos "trades" workers was 16.7 percent approximately three times that expected If mortality predictions were based only on the apparent smoking habits. The risk of lung cancer due to asbestos exposure is lower In non-smokers than in smokers (Saraccl , 1977, J. C. McDonald, 1980b). There appears to be no relationship between smoking habits and the Incidence of mesothelioma, the disease Is equally prevalent In smokers and non-smokers alike. Of the studies listed in Tables 3a and 3b, only Study No. VI of chrysotlle factory workers shows a lung cancer mortality that would be expected from the smoking habits alone. Asbestos miners and millers. Men working in the mining and milling of asbestos ore are generally exposed to only one form of fiber. A few exceptions occur in the [lining regions of South Africa where some workers have been employed In crocidolite, amosite, and chrysotlle mines. Anthophylllte and tremollte asbestos miners may have been exposed to some zhrysotlle asbestos, for these minerals can coexist In metamorphosed ultramaflc rocks, for example, those of Paakkila, Finland, Epidemiological studies of asbestos miners and millers vho were exposed to only one form of asbestos are useful to understand how the different asbestos minerals affect human health. Table 4 gives the mortality data for the five major epidemiological studies of asbestos niners and millers. In addition three studies are given of miners exposed to cummingtonite and grunerite amphlbole dusts and one study of tunnel worker; exposed to hornblende amphlbole dust. Some classify these amphiboles as asbestos even though they do not possess the physical properties requisite to be valuable commercially. Such a classification has been made In the ca;e of taconite mining by the courts (United States District Court for M1nnt;ota, 380 F. Supp. 11) and by the U.S. Environmental Protection Agency (Reserve Mining vs. EPA, U.S. Court of Appeals Eighth Circuit, March 14, 1975); the latter has sued to prevent the Reserve Mining Company from dumping taconite tailings into Lake Superior because of the perception that these tailings contain "amosite asbestos" and thus constitute a threat to public health. For a complete review of the case see 514 Federal Reporter, 2d Series, 492-5^2, 1975; 256 North Western Reporter, 2nd Series, 808-852, 1977. Of interest regarding this suit are the health studies of the Reserve iron ore miners exposed to cummlngtonlte and grunerite In the taconite rock (Table 4, Study B) and on the Homestake gold miners exposed to cummlngtonlte In 9A UCC 008665 T o ta ls | e 4. M o rta lity iron selected causes In the p rin c ip a l e p ld e a rlo lo g lc il s t a le s o f commercial asbestos miners and m ille rs o th e r hard rock miners and tunnel workers exposed to rock dust c o n ta ln lh g m inerals sometimes defined as a sb e sto s!/ So. ul M P> 1/1 cn CC 3 ^ pm Pm pi in pp. p <m e cr 4* hm c Pi <v pm a Cm c in <n *7 nc Os -- D p" 1C 4JV cm (C in in) pj 5^ G GO CC --m r e 5-` if cr V CM V! O U4V ^ V> |Q ^ 1> c f 3 C V) C* . p> ^ c -rn*J C & L. VI 4 r t/1 *- Q 4-> V 18 >.& b. .O V OC p o "O -- O' -- C * G U p 4r r-m c 8*2 X 1 * cc o -- U* * a -- Cl an E*.-."i Iftpm LC m *" e m c rm. j 9* l* Id SO2h ^0s m cm an PI e e f"> -- N to cc* ^ no'o P* p o r-- tn e m OlfifiC an O* p- X O Pm PI O' '"iftO'C o epi -- l CM G Gm CSJ O CC * p an 18 O O -9 4V in xo ft c C 30 ou 18 o M e p- *J c & * 18 >m -V -*-9 C*J vi Vi >i kc Xu* V ft 9 a. Bl B >L P p as ip o 4rJ 48 4 s ^ C p 4-> c S. s -- -- *8 VO P VI 18 >1 ( O -5% c O' 6N Vi O' ---- C x* Ua ---- * ft t' 5 ^ O' O-- C ;- X* - pm rm Oh Lb t *7 m Os Oi CD See o l c m O in * -- 09 -- -- n nm n io ' c cn is Pi --i [M** -- 0" Pm. mini na m o i-- an fm. io in *n o * cm *0 e p m p. p "" c O' p PI P PI Pm Ol PI a m en < .-- O Pi <\J an m| e -- p- c CM PI oe e an Pm IS Mt rt*n h U1 O' e in p O CM f\l i-- an e <M * * PP(p pi e O ^- O' ^ wp O G 00 CM 5! K --1 n cm m. in n 0O0' P". tt <ne m c o *" W K c oc Cs5 CM a a a If Pp. **K. *T e ** $ *s a 44 VI i O pi o 1C CM pp. CM a * A'Np cc fm. CM O' P i PI c r P b. an X li p 1/1 X44 35 > 44 UJ tij'T vi & tn 8*2 8 V 0> ,--m VI O ao o u<i --O --o i/i X 44 z* .a Ml P- * w jj v* e >i U P> a. b. - 41^ & u viett pm eg u *-- l* f 4V m IP r- - is . ^ P> c ao e o-- VV L * Op 9tt *VI k ft fc-iC JIZP MO . M a (v VlM AM. * uj i W8 7) -- --' O Ot m- m m C v 1- p p b ID ll 1 k 1 J UO O O *je m an co-- -- (i)p Umw -- VI X4V o .* m p- ft* VI Vi O c -- oo nm E=<i o cm d -* V IS Vtf V V c V4 X VI < Pm c m O' Cm pi pa SC -- ff O Sk OP ev o pl p . SS 48 e OO 4J 'o v 48 V8 13 C d c 48 Obo dp --* -- vi OO v m- 18 *j Ub Uodftd3 g ft tr *j oo O' -- VI Cx* -- *d G X pi i ft op x pU 18 5S u p> pi p* e 44 C 01 c-- m pO v p> 00 *9I'm --Oh -- e 2 ic IE!; 8 : ft O 4-t O 5 O 3 Op MS O' V** Uf 7 X 0 C a> -- V ^fS01 * 44 o U pp Pm "" PI 4* * * 18 p> ^ >-p- ^ m cx e C --U O *j E VI 44 C X I cn 5* c -- w 6 * u p> -- x p* t* r > -- f e i. --a 5 tn -- 84 C C b O 1-- Pm a O VO S pc pi G *- UJC O1 G-- a 18 fc8 -- 4-k * S"! * ? vo p "e 44 -- pl X -- Vsl p 18 P- d V cXe C >- C m-- X c b X G 4. * a u 03 E 44 8 x er m * 4d --oc --Pm Ol viP * 44 a X 48 4/1 cBeG -- X f b p --C B O o b m- +J r e PI P* 01-- C b Pi -- pi ECU Pa 5b3 U O* -- ft -- m C -- O' o -- X Ol u a. fi. -- pj ""8 u U er-- P- 4V S 18 U >4 b 44 JS 4J 0/ --U c --W x-- x Pm an pi if O > an * x-- P>C b-- OtP X IV -- 8b P* E an 9 b X 44 art pm 93 Xpaon o v> V* -- 8 or> p o V* >. 44 G p- an -- in VI IV >1 -- -> v> Or-- 4eu8 0i_ b9> --C Q. o Vi X -- ae tn 0- +J w p- -V ew --X O ac M- <*oo ii ^^ 44 -- -- >| VI xo .44 an X PI X can W eOl % a. -- b c -- TB 44 U 18 3 tn *4 W Co CO* -- E b* -- X * *6 'S'E. ikS -- wo> ULb -- a. -- b vi *s. u b s e -a- C If - ^ d-> PJ " -- ' - U 1/> U 44 C c -o O -- b -t V I41- 5^ i* ! * o i 5 e c c>- -NmK-HtI g^Koh-/ 9B UCC 008666 the gold-beering schists (Table 4, Study D, E)/. Studies B and E show no evidence of asbestos-related diseases appearing in the study groups. Mortality comparisons, trades vs. mines. The cancer mortality pattern for tnose In the asbestos traHes and mining occupations is graphically presented in Figure 1 where percent lung cancer mortality is plotted with respect to percent mortality due to mesothelioma. The studies of the asbestos trades workers (Tables 3a, 3b; Fig. 1, open stars) show a very significant excess of mortality due to mesothelioma relative to that found In the miners (Table 4, Fig. 1 , solid squares) - with one exception, the crocidollte miners of Western Australia (Study F). In regard to high mesothelioma mortality. It Is Important to note two health studies of specialized factory workers who, during World War II, were employed at the task of manufacturing asbestos-bearing filter pads and of placing them Into gas mask canisters. One study (McDonald and McDonald, 1978) was of Canadian workers who, at three factories, were involved with the manufacture or handling of crocldolIte-bearlng filter pads. The maximum duration of exposure during the period 1939-1941 was no more than two and a half years. The cohort studied was composed of 93 men and 83 women (Study X, Table 3a). Of the 56 now dead, 8 died of 1 jng cancer (14.3%) and 9 of mesothelioma (16.1% . The second study (Jones et al., 1976, 980a) was of a cohort of 9 >1 women who worked either at a factory in Not Ingham, England or at a fa tory In Birmingham, England. The Nottingham gro ip worked for only five months in the years 1939-1940 assembling "civilian filter pads'1 that contained chrysotlle asbestos. The Birmingham group vorked for up to four and half years during the period 1940-1944 assembling "military filter pads" that contained crocidollte asbestos. The croclddite was thought to have come from Wlttenoom, Western Australia. The mortality data Is given In Table 5. None of those exposed only to chrysotlle died of lung cancer or mesothelioma whereas there were 11 lung cam er deaths and 16 mesotheli ima deaths among those who worked only with cro<1dolite. None of the womei in either factory, as far as is known, was exposed to asbestos occupationally apart from their wartime work. Dust levels, as with the Canadian gas nask workers, was considered to be very light to moderate. j~/$tudy e (McDonald et al., 1978) discredits Study D (Gillam et al., 1 176). Study D was made on a sub-cohort of the Study E cohort. The latter study is much more complete; satlstically It is based on 631 deaths wh ?reas Study D is based on 71 deaths. In addition. Study D presents an Implausible mortality pattern: (1) No deaths due to silicosis, tuberculosis, or si 11 co tuberculosis were reported despite the fact that the mining company has been coping with a quartz dust problem for a century and (2) a 14*1 percent respiratory cancer mortality (Incorrectly included as respiratory cancer were a sinus and a mediastinal carcinoma) was attributed to "cummlngtonite asbestos" yet no mortality due to asbestosis was reported. The cummingtonite found in the quartz-cummingtonlte schist host rock Is not asbestos; but rather, garden-variety rock-forming amphibole. 10 UCC 008667 Table 5. Mortality Data (Jones et al., 1980a) for a Cohort of 951 Women* (578 traced) who assembled Asbestos-Searing Filter Pads in English Factories (1939-1944). Cause of Death Observed % Mortality Asbestos Exposure All causes -- too Crocidolite and chrysotile G.I. cancer 10 6.0 -- Other cancer 35 21 .1 -- Mesothelioma 16 10.2 Crocidolite only Mesothel1oma 1 Crocido"'ite and chrysotile Lung cancer 11 7.2 Crocldo ite only Lung cancer 1 Crocidolite and chrysotile *727 (139 dead) were exposed to only crocidolite, 102 (10 diad) to only chrysotile, 99 (15 dead) to crocidolite plus chrysotile, ard 23 (2 dead) unknown exposure. To make further comparisons it i s useful to examine tht? mortality with respect to lung cancer and mesothel 1 oia in national populations. In Table 6 Table 6. Cancer mortality in men ove 24 years of <sge for f> nations (McDonald and McDonald, 197') Nation All Deaths (year) Lung cancer No.{%)* Mesothelioma No. (%) * England-Wal es Finland Italy U.S.A. Canada 278,617 (1970) 22,332 (1970) 272,795 (1970) 988,620 (1969) 82,052 (1970) 24913 (8.9) 1586 (7.1 ) 11867 (4.7) 50481 (5.1 ) 4312 (5.3) 15L (0.06) i (0.04) no. reported 250 (0.03) 26 (0.03) Totals 1 ,624 ,41 S' 93159 (5.7) percent of all deaths (proportional mortality) ?T7 (0.03) are given the lung cancer and mesothe ioma mortality of all males over 24 years of age in five nations. These !ata are plotted in Fit ure 1. We find that the average lung cancer mor ality of these five national popula tions Is 5.7 percent, a figure identi<al to the 5.7 percent average mortal ity of the miners and tunnel workers Table 4, excluding crcidolite miners). The mesothelioma mortality of the f1v j national populations is 0.03 percent {Table 6) and is probably significantly underreported because of: (1) the great difficulty in diagnosing this disease, even after aut< psy (McDonald and McDonald, 1977, 1980; Vejlsted an 1 Hansen, 1980; Kanner tein and Churg, 1980; legha and Muggia, 1977) and (2) complications arising in properly and consistently coding this disease for ater information retrieval. It may be more meaningful to compare mesothelioma mortality among asbestos workers and miners. In whom this disease is anticipated, with the mortality in a population where the determinations of the causes of death are based on a large number of autopsies and where a .bestos exposure is minimal. A review 1 UCC 008668 has been made by ROttner (1978) of the deaths in the Ztlrich area of Switzerland where there are no asbestos mines, mills, or industries and where the cause of death is often determined by autopsy. Among the 28,110 male deaths (all autopsied) from 1961 to 1976, 51 deaths were due to meso thelioma (0.18 percent) and 2466 were due to lung cancer (8.8 percent). Among women (22,583 deaths) 23 were caused by mesothelioma (0.10 percent) and 368 caused by lung cancer (1.6 percent). The proportional mesothelioma mortality for hard-rock miners, tunnel workers, and asbestos miners (other than crocidollte) Is 0.17 to 0.20 percent (Table 4). The asbestos trades workers, by contrast, have an average mesothelioma mortality of 5.6 percent (Table 3). Among the asbestos miners and millers there Is no question that those exposed to heavy concentrations of chrysotile and anthophylllte dust over long periods of time have suffered a significant excess mortality due to lung cancer and asbestosls - but not (:o mesothelioma (Studies A, H, Table 4). The most detailed health study of asbestos miners to date is that of the chrysotile asbestos miners of Quebec (Table 4, Study J). Here, McDonald et al . (1980) have carefully documented the relationship between lung cancer incidence and cumulative lust exposure. The average dust concentrations that the miners and millers experienced during the working day were divided into four categories depending on the work tasks performed during their careers In the mines. These are: low level 2.5 to 4.2 mpcfl/, medium level 4.3 to 9.4, high level 11.4 to 23.6, and very high level 46.8 to 82.6 mpcf. The mean within tiese four categories in terms of chrysotile fibers per cm3 is: iow iq ?ibers/cm3. medium 21 fibers/cm3, high 95 f1bers/cm3, and very high 194 fibers/cm3. For the men exposed for over 20 years (see Table 17, colunn A) In the low and medium dust categories (averaging 6.6 mpcf or app'oximately 20 fibers/cm3) total mortality was less than expected (SMR = 0.94). For these m^n there was a slight risk of excess lung cancer (SMR = 1.15) and respiratiry tuberculosis (SMR = 1.14). As exposures of 20 flbsrs/cm3 are an order o' magnitude higher than that experienced now (dust levels for the past *ew years have been maintained at less than 2 fibers/cm**), miners working t lifetime under the present dust levels are not expected to present a iy significant health problems relative to those In other mining Industrie; (Liddell , 1981). McDonald et al. (1980) have also studied the health stitistics of a cohort of 440 women who also worked In the Quebec chrysotil ; asbestos mines and mills. Of the 84 who have died there was one death due to lung cancer and one due to mesothelioma. 3/mpcf * millions of particles of roc< dust per cubic foot. Conversions of this figure into asbestos fibers per .ublc centimeter, the isual measure ment for industrial hygiene monltorlni, is difficult but an approximate and conservatively small figure is: 1 mpcf = 3 fibers/cm3 (McDmald et al., 1980, p. 21 , 23; see also McDonald and Becklake 1976). 12 UCC 008669 Crocidolite exposure. There are persuasive data, many already surveyed, which show thfS'crocidollte asbestos is much more hazardous than chrysotile, anthophyllite, and amosite. Of the mining populations of the world, only those in the crocldplite mining areas of the Cape Province of South Africa and at Wittenoon Gorge, Western Australia have a statistically significant increase In mortality due to mesothelioma. Also, mesothelioma deaths have been reported among the residents of these areas who are not employed in the mines or mills. For example, Webster (1978) reports that the South African Asbestos Tumour Reference Panel placed 712 cases of mesothelioma on the register, which Included all the known cases since 1956. Of these occupational and environmental background was established for 420 cases. Actual mining exposure accounted for 139 of the 420 cases of which 120 were in connection with Cape crocldollte mining and two with Transvaal crocidolite mining. There were only four mesothelioma cases In those associated with amosite mining and two of these had been exposed to Cape crocidolite as well. In the chrysotile mining industry there was only one case - a miner from Rhodesia. Of the 100 environmental cases (those not employed in any occupation where asbestos is used) 93 had been exposed to Cape crocidolite, two to Transvaal crocidolite, and one possibly to amosite. Additional prevalence studies in the Cape Province (Talent et al ., 1980) discovered 65 active cases of mesothelioma In people who had presented themselves for medical examination. Fifteen of these cases appeared In two groups, numbering 755 and 947 Individuals, who were once employed in the crocidolite mines. An additional thirty eight mesothelioma cases appeared in a survey of certain patients at the St. Michael's Hospital In Kuruman, Cape Province, who were not responding to treatment for suspected pulmonary tuberculosis. Fourteen of these mesothelioma patients were known to have worked in the crocidolite asbestos mines, lastly, 12 of the 65 cases appeared in a medical survey of 53 females who, in the pat, hand-cobbed crocidolite asbestos. In contrast to the prevalence of mesothelioma in the Cape Province, this disease is very rare in the Transvaal where all of the world's amosite is mined. Wagner et al. (1960), in regard to their initial discovery of the association of crocidolite asbestos with mesothelioma, state (p.260) "the tumour (referring to mesothelioma) is rarely encountered elsewhere in South Africa. During the past five years, with the exception of the present series (in Cape Province), no neoplasm of this nature has been diagnosed amongst 10,000 lungs examined at the Pneumoconiosis Bureau in Johannesburg, or in the Pathology Department of the South African Institute for Medical Research." The incidence of mesothelioma in Zimbabwe (Rhodesia), a country which is a major producer of chrysotile but mines no other form of asbestos, is very low. In a communication to Mostert and Meintjes (1979), the Secretary of the Rhodesia Pneumoconiosis Board stated that no cases of mesothelioma were reported in the mining industry. It is of interest to note that two cases of mesothelioma were reported i i the Rhodesian railway industry, a locomotive engineer and a storeman. The locomotives were insulated with crocidolite asbestos to which these tvo men were exposed (Mostert and Meintjes, 1979). Cochrane and Webster (1978) report 12 cases of mesothelioma in men employed as Insulators in the locomotive workshops of the South African Railways. 13 UCC 008670 i The prevalence of mesothelioma among the miners of Wittenoon Gorge has been discussed (Table 4, Study F). The town of Wittenoon, the center of crocldolite mining in Western Australia, reached a peak population of about 1 ,000 in the 1960's. At present the population Is down to about 200 and the West Australian State Government has suggested the closing of the town and evacuation of the residents because of continuing risks of airborne asbestos dust (Chemical Week, December 8 , 1978, p. 26). The risk of mesothelioma among the residents of the town who were not employed by mines is demonstrated by the case of a 27-year-old woman who had an environmental childhood exposure to crocldolite (Langlois et al., 1978). Effects of Non-occupational Exposure to Asbestos It Is difficult to assess the health effects of non-occupational exposure to asbestos, for cohorts are hard to define, exposure levels are usually low, and any excess of lung cancer is disguised by the strong association of this disease with cigarette smoking. To study the nonoccupatlonally exposed, epidemiologists are thus constrained to look far increased Incidence of asbestosis and particularly mesothelioma in two types of cohorts; those who live In neighborhoods surrounding asbestos factories, mills, or mines and those who live within the household of in asbestos worker who presumably carried asbestos dust back to the home tn his or her clothlng. Background incidence of mesothelioma. There appears to be a definite "background1' mortality due to mesothelioma that Is not related to asbestos exposure. McDonald and McDonald (1977), reviewed 4539 fatal mesothelioma cases reported from 22 countries between 1959 and 1976. They found that for 923 of the 2453 cases where a history had been recorded a definite or probable exposure to asbestos could not be shown. More recently, Jones and Silver (1979) report eight cases with no environmental exposure, Brenner et al. (1981 a) report of 25 patients entering Memorial Hospital , N.Y. since 1950 with no exposure history, Brenner et al. (1981b) report of seven children dying of mesothelioma who had no exposure history to asbestos, and Griffiths et al, (1980) report on 10 mesothelioma patients with no history of exposure to asbestos who entered Austin Hospital , Melbourne, Australia. A possible genetic basis for som? mesothelioma incidence is suggested by Risberg et al, (1980) In their repjrt of five deaths due to mesothe ioma within a single family; the father, 3 sons, and a daughter. Four of the five had worked in the building Industry where random exposure to asbestos containing products could have occurred. They lived in a town of 100,000 Inhabitants which had no asbestos Industry In the vicinity. An estimate of mesothelioma mortality not related to exposure to asbestos can be obtained from the data given by McDonald and McDonald (1 980). Ascertainment, through 7 ,400 pathologists, of all fatal malignant mesothelioma tumors in Canada (1960-1975) and in the U.S.A. (1972) was made. The pathology review panel accepted 73 and 65 percent of the U.S. and Canadian cases, respectively. Occupational histories indicate that 50 percent of the male and five percent of the female deaths could be attributed 4 UCC 008671 to asbestos exposure. Thus, in the United States in 1972, there were 245 cases of mesothelioma reported (189 male, 56 female) and of these, 140 male and 39 fwiTe cases are accepted. Assuming a 30 percent underreporting (McDonald and McDonald, 1980, p. 1655), the 1972 incidence in the U.S. is approximately 200 male and 56 female deaths. Of these, about 100 male and 3 female mesothelioma deaths can be attributed to asbestos exposure; the remaining 153 deaths to other causes or background. If these figures are reasonably correct, then the mesothelioma proportional mortality due to "background" In 1972 was 0.008 percent (153 deaths out of 1 ,963,944). The mesothelioma death rate due to background in 1972 is calculated to be 0.7 deaths per million U.S. population. The study of McDonald and McDonald (1980, see also McDonald, 1979) indicate that the Canadian mesothelioma death rates are very similar to those in the U.S. Asbestos-related disease in residential areas. The residents of areas where there are asbestos factories, mines or mills may contract asbestosrelated diseases even though they are not actually employed in the asbestos Industry. The high prevalence of mesothelioma among residents of the crocidolite mining areas of the Cape Province of South Africa has already been discussed. The appearance of 93 mesothelioma deaths among those non-occupatlonally exposed to Cape crocidolite Is in extreme contrast to the rarity of this disease In the amosite mining regions of the Transvaal Province where only one possible case has been reported (Webster, 1978). Asbestos-related disease among residents of chrysotile mining areas Is rare, Theriault and Grand-Bois (1978) report the following mesothelioma mortality in Quebec Province: (1) asbestos-producing regions (observed 2, expected 1.3), (2) areas surrounding the asbestos producing regions (obs. 5, exp. 4.8), (3) other rural regions of Quebec (obs. 12, exp. 32.4), (4) city of Quebec (obs. 7, exp. 4.7), and (5) city of Montreal (obs. 42, ?xp. 24.4). McDonald (1980a) has reviewed all known fatal mesothelioma cases n Quebec Province for the period 1960-1978. Of the total of 254 cases registered, 181 were males, 73 females. Occupational and residential histories were obtained from 91% of the men and 86% of the women. Abo it 40% of the male cases and 5.4% of the female cases were attributed to occupational exposure to some form of asbestos. Twenty one cases were individuals who at some time had been employed in the chrysotile mining and milling industry. But 5 of these 21 had been exposed to crocidolite while manufacturing filter pads for gas masks and 2 more possibly exposed to crocidollfef In one of the mills, which for about two years processed crocidolite fiber for the gas mask filters. In addition to these 21 cases there were four daughters and two sons of chrysotile miners or millers who died of mesothelioma. Apart from these cases McDonald (1 980a) reports of only two persons who died of this disease who lived within 20 miles of the chrysotile mines and mills of Quebec. Pampalon (1980) reported on the mortality patterns of the Quebec asbestos mining towns of Thetford Mines (population approximately 20,000) and Asbestos (population approximately 10,000). Cancer mortality amone the female residents of these towns is particularly informative since very few were employed in the asbestos Industry. However, they lid receive ove 15 UCC 008672 much of their lifetime very heavy non-occupatlonal exposures to chrysotile asbestos conttlned In the rock dusts emitted from the operation of the nearby mines and mills.!/ The mortality data for the female residents of Asbestos and Thetford Mines Is given in Table 7 (see also Tables 8 and 9). Table 7. Mortality Data for Women Living in Quebec Asbestos Mining Towns For the period' Y96'6 to 1977 (Pampaion, 1979). *" Cause of death Observed Expected Excess (Deficiency) all causes all cancer 1ung cancer G.I. cancer resp. disease 1225 292 23 97 35 1356 321 23 91 58 (131) ( 29) 0 6 { 23) Another cancer mortality survey of various regions in Quebec was made by Graham (1981). His data, summarized in Table 8, show the rates for various cancers that may be associated with exposure to asbestos dusts for five regions; asbestos mining counties, counties surrounding the asbestos counties, other rural counties, and the cities of Quebec and Montreal. The rates for the asbestos mining counties, which contain the large semiindustrialized towns of Thetford Mines and Asbestos, are intermediate between the rural counties ("other rural" and "peripheral") and the cities of Quebec and Montreal. This is to be expected for cancer rates are highly correlated with the interrelated factors, (1) degree of urbanization, (2) socioeconomic class, and (3) "lifestyle" (Doll and Peto, 1981; Goldsmith, 1980; Hlgglnson and Muir, 1979; Hlgginson, 1980; Weisberger, 1978; Gori , 1979; Kynder, 1980). Graham (1981) states that the rates for cancers of i/Even in 1974 and 1975, when rock dust levels at the Quebec asbestos mines and mills had been much reduced from levels as high as 200 million particles per cubic foot (ppcf) in the early 1950's to less than 7 million ppcf in the mld-1970's (McDonald and Becklake, 1976), the rock dust in the ambient air over the town of Thetford mines averaged 80,000 ng/m3 when the mines and mills were in operation and 40,000 ng/m3 when the mining operations were shut down during the strike of April to September, 1 975 (Brulotte, 1 976). When the mines were operating, the average weight of dust falling daily over the town was 377 kg/km2. Recent measurements by Gibbs, Rowlands, and Brilotte (Air Pollution Control Assoc., 1980) of dust in the ambient air if the towrs of Thetford Mines and Black Lake show a chrysotile asbestos co itent of U0 to 11 ,000 ng/m3 - a considerable environmental exposure even in these better times. In this regard, it is pertinent to cite the work of Nicholson et al. (1980) who analyzed the chrysotile fiber content in the air in houses located in two chrysotile mining districts (Copperopolls, Cilifornla and Baie Verte, Newfoundland). The 13 air samples taken in hom?s of crysotile miners and millers show the following chrysotile content: 4 (50-100 ng/m3}, 4 (100-200 ng/m3), 2 (200-500 ng/m3), 2 (500-1000 ng/m3), aid 1 (2000-5000 ng/m3). Three samples taken in houses of non-miners in Bai ? Verte gave concentrations of 32, 45, and 65 ng/m3. |6A UCC 008673 Table 8. Cancer m o rta lity rates {deaths per 100,000 residents) fo r various geographic lo c a litie s in Quebec Province and fo r Upper New York S tate. Annual average fo r the period 1969-1973 (Graham, 1981). . 4 5 . 1 1 4 0 . 3 6 3 5 . 5 8 5 1 .17 53.2 1/O nly those cancers known to be associated w ith excess m o rta lity in asbestos trades workers are lis te d . >- * t. to m 4* t. Qa</> CL <j to to o to c 3 o> o rr- a c 0) > CM O O' 0C i- 00 c tn co at r^. CM . ** O' -M c VC mo CM ^r o CM p" c m > c >- QC ^ r-. lf> . Oh r-. o'n}' r- r-- VO f-- 1C CO CO +j o CO O OC co r- 1-- r-- CO Oh z >> 4> *r CO O C f-- vo U0 Oh c IflOOr--CCWVC 910 O 0) .a UO CM VO O lO O CO * * o c O CO CO o c On 00 iO C i-- OOi-- --~ i-- i-- uo CM o CM 3 O to fs r*" o co CO 0C Cn rs rs w tcCl vo vn 00 co O' VC vo CC m (OOONF-CNffiCC o O CM CO cr oo CM ao la n ...a.*.* C p-- r-- Oh CJ o vo Ul LU _J < L. VI 3 to L 4-> L. C O3 /= o 4J <J d co CM pp- CM CM Oh CM r- ro vo o> CO Oh Oh t* C C CM e o cr CM r-- r-- CM m * co vo r- o n c 00 a-- in fv rr lCOO <\1 * n c o lc c c LT> CC 9 r-- *0 L. 3 U (7) r- <D ns -rL. OJ c 3 Cl o r- O fc. 01 a. f-- OC r-^ ^ 00 00 PO OC C- CNj CO IT CO un * in * CO c O CM C CO o CM p-- 1-- p- oc CM VC al'CCO^fCOO'fCC ^..co.i.^caor^.-.o.o o c >^> c 6 VI 1 OJ V) *rO +J c V 3 01 O AO V) < c o p CT5 0) a: Oh CM o CM to 00 vn c VO c *-** o e * * co -- vc CM f-- to r^. CO r" pco ET 3 lA *> 4-> 4> 3 c c c -c ai ^-1 o O to E 4-J TO 1 (-- a> 3 cn 3 r- r CL 1-- 014-1 C <D t_ c o m t_ O 3 01 4 ' in E m a> --t CL. a. c/) LU <n --i OC O' in co in id MM MCMISCO * .C a a a . Tf O O' r-- C' 00 O E3 UMJ+J OS 3 C C C JC O'I-- t~t US O O rtJ E coimt3- c4J>.-oUeS o-oC.nr>----scnc0+)J.i3j j3ar.--a0.i)/4)JU</jyEinjaSm 16B UCC 008674 the pleura!*/, peritoneum!*/, lip, tongue, sail very gland and small intestine!*/ in males and of the pleura|/ 11pJ*/, kidney, sallvery gland and melanoma in females, are In excessj/ in the asbestos mining counties, Graham (1981 , p. 40) further states that cancer of the colon, stomach, and lung were "at a level so low as to be unimpressive," These are cancers known to be excess in many cohorts of asbestos trades workers (Table 3a, 3b). The low c?ncer rates found in the asbestos mining localities are not surprising for McDonald et al. (1980, p. 12) report that during the five decades, 1926-1975, 4350 male Quebec asbestos miners and millers died compared to 4107 expected on the basis of Quebec age-and-year specific death rates, giving a standardized mortality ratio (SMR) of 1.06. It should also be noted that the residents of Thetford Mines and Asbestos, Quebec used drinking water that contained very high concentrations of chrysotile asbestos, ranging from 172 million to 1.3 billion fibers per liter (Wigle, 1977). No evidence of excess cancer mortality could be attributed to asbestos in the drinking water of these towns (Wigle, 1977J.J*/ Toft et al. (1931) expanded on the study of Wigle (1977) by comparing mortality data from 71 municipalities to the amount of asbestos in the drinking water. Particularly informative are the death rates of the female residents of Thetford Mines relative to the rates found in women who lived in 52 other localities that had very little asbestos in the drinking water. Most of the women of Thetford Mines did not work In the asbestos industry, but they did receive heavy non-occupatlonal exposure to chrysotile asbestos carried in the air and water. Death-rate comparisons (Table 9) indicate that the women of Thetford Mines have not been effected by exposure to chrysotile asbestos. 1/A total of 1 to 3 deaths for these cancers were reported for the five year period 1969-1973. The statistical significance of such small numbers is questioned. 1/ln regard to ingestion of asbestos and cancer incidence, a number of animal studies are now complete (Donham et a' ., 1980); Hallenbeck et al., 1981 ; Hlldlng et al., 1981; Smith et al., 1980; DHHS, 1981a; DHHS, 1981b). None of these studies show any evidence that ingestion of asbestos causes tumors in animals. Hallenbeck et al. (1981, p. 349) state, "the results of this study (a baboon gavaged with commercial asbestos) indicate that asbestos fibers do not penetrate the gastrointestinal tract of the baboon and migrate to various tissue." 17 UCC 008675 Table 9. Age-adjusted Mortality Rates (per 100,000 Residents) for Female's "(age 'gS-ffiTToTrTfar (V9BTT------------------ ------- Cause of Death Thetford Mines]/ 52 Comparison all causes all cancer 1ung cancer G.I. tract cancer respiratory system!/ 420 138 8.5 42.2 8.9 433 158 13.A 41 .5 16.9 VTreated water, 110-150 million chrysotlle fibers per Viter. All localities contained less than 5 million fibers per liter of water, i/non-neoplastic Hammond et al. (1979) have given mortality statistics for the residents in the neighborhood of Riverside which surrounds the Patterson, New Jersey amoslte asbestos factory. The mortality experience of the workers in this factory is given in Table 3b, Study XIX. The mortality data of Riverside is statistically indistinguishable from that of the control community of Totowa , N.J., situated several miles from the amoslte factory (Table 10). One mesothelioma death occurred in Riverside in 1966 but none since. Table 10. Cancer Mortality Data for Riverside and Totowa, New Jersey for t'fteTeTi oTTgg2-l375 (Hammond et al., -------------------------- Cause of Death Riverside!/ No. t Mortality Totowa!/ No. % Mortality all causes all cancer lung cancer colon-rectal cancer stomach cancer esophageal cancer 780 163 41 24 9 4 100.00 20.90 5.26 3.07 1 .15 0.51 1735 353 98 74 22 12 100.00 20.35 5.65 4.27 1 .27 0.69 ^/Neighborhood near amosite asbestos factory f/Control neighborhood _______________ Asbestos-related diseases in households of asbestos workers. There are a numb'er'of reports of mesothelioma occurring In indlviduals who, though not occupationally exposed to jsbestos, lived in hou eholds which included an asbestos worker. Epler et al. (1980, p. 236) stmmarizes 14 published reports of 43 such mesothelioma cases plus four m< re found in their own study. Antman et al ., (1980) mention 3 more and Vianna and Polen (1978) report on 10 female patients who lived with husbands or fat lers employed in asbestos-utilizing occupations. It is difficult, perhap; Impossible, to define retrospectively what kinds of asbestos was causing tne mesothelioma 18 UCC 008676 In these household contacts, but It Is most probable that the workers handled more than one kind of asbestos. The report of Newhouse (1981 , see also Newhouse and Thompson, 1965) may enlighten us on this subject. She reports that 11 individuals who died of mesothelioma and had neither worked with asbestos nor had a relative who worked with asbestos all had lived In the immediate vicinity of a factory that was a heavy user of crocldolite asbestos. ESTIMATES OF MORTALITY IN THE UNITEO STATES DUE TO EXPOSURE TO ASBESTOS Previous Estimates On September 11 , 1978, Joseph A. Califano, then Secretiry of the U. S. Department of Health, Education and Welfare, gave a major soeech at the AFLCIO National Conference on Occupational Safety and Health ii which he described how the Federal Government was assisting in discovering and preventing occupational disease. One of his statements was that 17 percent of all cancer deaths in the United States each year for the next 30 to 35 years will be associated with previous exposure to asbestos. This translated into 67,000 cancer deaths per year due to asbestos (NCI, NIEHS Press Release, Draft Summary, Sept. 11 , 1978). The Califano speech was based upon an unpub11 shed document (Bridbord et al., 1978) prepared by several medical scientists at three of the National Institutes of Health (NCI, NIOSH, NIEHS). Doll and Peto (1981) have reviewed this document and state (p. 1240) "However, these estimates of total risk were so grossly in error that no arguments based even loosely on them should be taken seriously;" see also, Doll and Peto (1981 , p, 1241 , 1305-1308). On January 15, 1980, Dr. Irving Selikoff of the Mt. Sinai School of Medicine, New York City, stated at a press conference in conjunction with the annual AMA meeting in Chicago, that 20,000 U.S. asbestos workers will die each year for the next 40 years of "excess disease" (see 0. Am. Med. Assoc., vol. 243, p. 211, Jan. 18, 1980). On September 27, 1981 , through a press release to Robert Locke (Associated Press Wire Service), Dr. Selikoff stated that 10,000 American workers are dying each year because of asbestos exposure. Dr. Selikoff doe; not state upon what data he bases these two estimates. 1 Hogan and Hoel (1981) estimate (p. 74) that future excess cancer deaths among U.S. workers exposed to asbestos could constitute as nuch as 3.0 percent (range 1.4-4.41S) of an estimated annual cancer death toll of 400,000 persons - or 12,000 asbestos-related cancer deaths per year. These authors based their estimates on an analysis of the number <>f people possibly exposed to asbestos, possible exposure levels, and estimate' exposureassociated cancer risk. In the above paragraphs, future mortality projections of 67,000, 20,000, 10,000 and 12,000 deaths per year due to asbestos exposure are quoted. Are any of these predictions correct? In the following, a method is proposed of estimating past asbestos-related mortality which can be used to predict future mortality. 19 UCC 008677 Past Mortality Based on Asbestoses incidence The number of deaths due to asbestosis reported in the Vital Statistics of the United States {vol. II - Mortality, U.S. Oept. of Health and Human ITervTces', National Center for Health Statistics) for the whole nation for the 11 year period 1967-1977 Is: 1967(36 deaths), 1968(29), 1969(34), 1970(26), 1971(33), 1972(58), 1973(42), 1974(35), 1975(45), 1976 (54), and 1977 (55). The average number of asbestosis deaths per year for the period 1967-1977 Is 41 with a high of 58 In 1972 and a low of 26 in 1970. If It Is known how many die from asbestosis each year :hen the total yearly asbestos-related deaths can be estimated from major )pidem1ological studies of asbestos workers. One of the largest such studl js Is of the 17,800 North American insulation workers (Sellkoff et al., 979a). This group, of which 2271 are now dead is one of the most severely effected by asbestos dusts. The mortality data and estimates of "exces;" death due to asbestos Is given in Table 11 (see also Table 3b, Study XVI 0* Mortality Among 17 ,800 Insulation Workers (Sellkoff et al., 1979a juse of death Expected Observed(BE)* Excess all causes all cancer mesothelioma lung cancer G.I. cancer other cancer Asbestosis Non-In feetious Respiratory disease 1659 320 - 106 59 155 59 2271 995 175 486 99 235 168 212 612 675 175 380 40 80 168 153 *BE-Best Estimate If the asbestosis deaths given in the Vital Statistics are underreported by the same amount as observed by Selikoff et al, (T9T9, p. 103, Best Estimate (168)/Death Certificate (78) = 2.15), the average number of asbestosis deaths each year during the period 1967 to 1977 is 41x2.15 or 88. Using diseas# ratios taken from Table 11 (asbestosls/excess cancer, asbestosis/excess respiratory disease), the average annual asbestos-related mortality In the United States for the period 1967 to 1977 Is estimated to be 522 deaths, including 354 cancer deaths (Table 12). 20 UCC 008678 Table 12. Average Yearly Mortality due to Asbestos (1967-1977) Based on u.5. Recorded Asbestosis deaths Mesothelioma Lung cancer G.I. cancer Other cancer Asbestosis Non-infectlous resp. disease 92 199 21 42 88 80 Total asbestos-related deaths per year 522 Past Mortality Based on the 1972 Mesothelioma Incidence It is not possible to obtain accurate mortality data for mesothelioma from the Vital Statistics of the United States for this disease is coded (ICO.8) with a number of other neopYasms under the headings: malignant neoplasms of peritoneum and retroperitoneal tissue (158.0, l5873) and malignant neoplasms of other and imspeel fled respiratory organs; pleura (163.6), mediastinum (163.1), and site unspecified (163.9). Afso, as pointed out previously, mesothelioma is a difficult disease to diagnose. These difficulties in coding and diagnosis make it necessar/ that national mortality estimates be made on decisions of mesothelioma re/lew panels such as those described by McDonald (1979), Kannerstein et il. (1979), McDonald and McDonald (1980), and Jones et al . (1980b). The mesothelioma study of McDonald and McDonald (1980) can be used to estimate the excess asbestos-related mortality. Their cita, as described above, indicates that approximately 103 mesothelioma deaths in the United States in 1972 can be attributed to exposure to asbestos, \gain, using the mortality data of Sellkoff et al. (1979a) listed in Tabie 11 to calculate disease ratios (mesothelioma/excess other cancers, mesothelioma/ asbestosis, mesothelioma/excess respiratory disease), the n imber of asbestosrelated deaths in the United States in 1972 Is estimated to be 587 of which 398 are due to cancer (Table 13). Table 13. Mortality due toAsbestos in 1972 Based on Estimated Mesothelioma Deathj of HcDonaid and McDonaId, 1966 Mesothelioma Lung cancer G.I. cancer Other cancer Asbestosis Non-Infectlous resp. disease 103 224 24 47 99 90 Total asbestos-related deaths in 1972 587 21 UCC 008679 In order to obtain a sense of perspective, it is useful to compare the death estimates obtained above for asbestos-related disease (522 and 587 deaths per year) to mortality from other types of industrial dusts, such as those of silica and coal. The Vital Statistics of the U.S. report that there were 215 silicosis deaths (ICO.ft,UT5.6) and 92 sllicotuberculosls deaths (ICO.8, 010) in 1976. If it is assumed that mortality due to silicosis and asbestosis are equally underreported by a factor of 2.15 (Selikoff et al., 1979a, p. 103) and that the ratio of silicosis to excess non-infectious respiratory disease mortality Is the same as the ratio of asbestosis to excess non-infectious respiratory disease, then the silica-related mortality for the United States in 1976 is estimated to total 975 deaths (Table 14). Table 14. Estimated Mortality in 1176 due to Silica Dust Silicosis 462 Silicotuberculosis 92 Non-infectious resp. disease 421 Total silica-related deaths in 1976 975 In 1976, there were 879 reported deaths due to anthracosilicosis (ICD.8, 515.1 , Vital Statistics of the U.S.). Underreporting and other excess respiratory disease may have also occurred in coal miners who have suffered the "black lung" diseases. These estimates of past asbesto -related mortality indicate that there will be nowhere near 10,000 deiths per year in the future. Asbestosrelated mortality should peak betwee 1980 and 1985, 35 to 40 years after the large World War II shipyard employment. Linear regression analysis of past mortality (Vital Statistics of he U.S.) due to asbestosis (515.2, males and females, 1967-1977) and "pleural neoplasms" (163.0, malesl/, 1968-1977) suggests that there has been an Increase in the number of deaths with time. Calculated mortality for various years is given In Table 15. The variance (r^) of the regression line Is 0.49 'or asbestosis and 0.31 for "pleural neoplasms." If this apparent Increae in mortality is real and continues, then the calculated mortality for asbestosis given in Table 15 predicts that a total of 1337 asbestos-related deaths will occur in the year 2000 (calculation by the method given previously). Hopefully, asbestos-related mortality Is now peaking and will soon decline. UA significant number of male mesothelioma cases will jrobably be reported under this code (163.0) thus a trend in thi= mortality may reflect a trend In total asbestos-related mortality. 22 UCC 008680 Table 15. Calculated mortality based on linear regression analysis of past reported mortality - asbestos!s (males + females, 1967-1977) and "pleural neoplasms" [males. 1968-1977) - Vital Statistics of the U.S., 1967-1977. Year Asbestos!s (males & females) "Pleural Neoplasms"(males) 1967 1977 1982 2000 27 deaths 52 64 105 184 deaths 222 241 308 In regard to mesothelioma incidence, it Is pertinent to note the number of deaths from this disease in the four hospitals of the New York University Medical Center. The reported deaths for the period 1967 to 1976 are (Demopoulos, 1980a): 1967(3 deaths), 1968(2), 1969(3), 1970(4), 1971(1 ), 1972(2), 1973(1 ), 1974(3), 1975(4), and 1976(3). No significant trend with time is noted (r? = 0.01). Sprayed-on chrysotile asbestos was extensively used in building construction in New York City until recently. Also, chrysotile asbestos emissions from brake linings give measurable fiber counts in the ambient air of the New York City streets. For example, Nicholson et al, (1980) report that 43 of the 89 air samples collected In New York City exceeded 50 ng of chrysotile asbestos per Samples taken In New York City public schools ranged from 9 to 1950 ng/nw with 15 out of 27 samples exceeding 100 ng of chrysotile per m3. Despite the long presence of chrysotile asbestos In the New York City air, Demopoulos (1980b) found no evidence of an Increase in the number of mesotheliom<i deaths in this city over the past 12 years (1967-1978). Vi anna et al . (1981) in a study of malignant mesothelioma in New York State (excluding New York City) found that there was no increase in the Incidence of disease from 1973 through 1978. 23 UCC 008681 SUMMARY Asbestos Pnx&itlon Of the six forms of asbestos, only four have been used to any significant extent in commerce. These are amoslte, crocidollte, anthophyllIte, and chrysotlie. Although asbestos was used by Stone Age man it was not until the latter part of the 19th century that It came into widespread use in the industrialized world. The modern Industry began in Italy and England after 1860, with Quebec being the main supplier of the crude fiber. By 1980, more than 100 million tonnes of asbestos had been mined worldwide of which more than 90 million tonnes was the chrysotlie variety, about 2.7 million tonnes the crocidolite variety, about 2.2 million tonnes the amosite variety, and about 0,4 million tonnes the anthophyllite variety. Approximately 75 percent of all asbestos ever mined has come from just three chrysotlie mining localities, Quebec, Canada and the central and southern Urals of the Soviet Union. The chrysotile-produclng countries in order of importance are: the Soviet Union (46.1 percent of the world's total asbestos production In 1978), Canada (28.9*), Zimbabwe (3.8*), China (3.8%), Italy (2.9%), South Africa (2.1%), Brazil (1.8%), U.S.A. (1.7%), and Australia (1.0%). Comparative Epidemiology The three principal diseases which are related to asbestos exposure are: (1) lung cancer, (2) cancer of the pleural and peritoneal membranes (mesothelioma), and (3) asbestosls, a condition in which the lung tissue becomes fibrous and thus loses its ability to function. These diseases, however, are not equally prevalent in the various groups of asbestos workers that have been studied; the amount and type of disease depends on the duration of exposure, on the Intensity of e<posure, and particularly >n the type or types of asbestos to which the individual was In contact. Chrysotlie or "white" asbestos. Chrysotile asbestos, sometimes referred to in the trade as "white" asbestos, is the form that is usually used in the United States - as wall coatings, in brake linings, as pipe insulation, etc. About 95 percent of the asbestos in place in the U.S. is the chrysotile variety and a large percentage of this was mined and milled in Quebec. Epidemiological studies of the chrysotile asbestos miners and millers of Quebec undertaken by medical researchers in Canada show that for men exposed for more than 20 years to chrysotile dust averaging 20 fibers/cm3 the total mortality was less than expected (62*observed deaths, 659 expected deaths). Risk to lung cancer was slightly tftcreased; 48 deaths observed, 42 deaths expected (Table 17, column A). Exposures to 20 fibers/cm^ are an order of magnitude greater than those experienced now (generally less than 2 fibers/cm^); thus chrysotile miners working a lifetime under these present dust levels .hould not be ex pected to suffer any measurable excess cancer. A similar Mortality picture is reported for Italian chrysotile miners and millers (Study g, Table 4). The results of only one epidemiological study of a cosort of trades workers known to be exposed only to chrysotile asbestos be ;n published (Study VI, Table 3a). This study reports 2 deaths due to isbestosls nut no excess of any cancer was detected. 24 UCC 008682 Mesothelioma Incidence among those working only with chrysotile asbestos is very low. Thus far, about 16 deaths due to this disease have been reported among chrysotile asbestos miners and millers and none among chrysotile trades workers.8/ In addition, 6 deaths among sons and daughters of chrysotile miners and millers and two among others living in chrysotile asbestos mining localities have been reported as being due to mesothelioma. Four epidemiological studies of the female residents of the Quebec chrysotile mining localities show no statistically significant evidence that their life-long exposure to asbestos dust from the nearby mines and mills has caused excess disease. Crocldolite or "blue11 asbestos. Crocldolite, usually referred to in the trade as "blue" asbestos, was first Imported Into the United States in 1911 or 1912. By 1930, 35,000 short tons of crude blue fiber had entered the country and by 1946 an additional 21 ,000 tons were imported. In addition to these Imports, much crocldolite came into the United States as manufactured products such as yarns, tapes, and pipe coverings. Almost all of the imported crocldolite came from South Africa. Epidemiological studies of groups who worked only with crocldolite asbestos show that rather short periods of exposure, or even relatively light exposure, causes a large excess of mortality due to lung cancer, mesothelioma, and asbestosis. This is evident not only In those exposed to crocldolite during gas mask fabrication and building construction but in those employed In the crocidolite mines. There are only two mining regions in the world where mesothelioma is a statistically significant cause of death. These are the crocidolite mining districts of the Cape Province, South Africa and at Wlttenoom, Western Australia. Prevalence studies In the Cape Province report that at least 278 people have died of mesothelioma as a result of exposure to crocidolite; 161 of these people worked In the mines and mills and 117 others lived In the vicinity of the mines. Thirty-one men who worked in the crocidolite industry at Wlttenoom, Western Australia have died of mesothelioma. Of these, 13 had worked for less than 12 months and 9 had light to medium exposure to blue asbestos. Sixty miners and millers at Wlttenoom have died of lung cancer; 34 of these men had worked 1n the industry for less than 12 months and 19 had light to medium exposure to the crocldolite dust. In addition to this occupationally related mortality, 6 others who lived near but did not work in the mires or mills have died of mesothelloma. Amoslte or "brown'1 asbestos. All amosite asbestos comes from the Transvaal Province of South Africa where between 1917 and 1979 approximately 8/Acheson et al. (1981 , p. 1405) cite two new studies (in press) of asbestos trades workers thought to have been exposed to only chrysotfl e which confirm the rarity of mesothelioma associated with chrysotile. 25 UCC 008683 2.2 million tonnes have been mined. Importation of amoslte into the U.S. started In th# 1930's. One complete epidemiological study of trades workers exposed mainly to amoslte asbestos has been published. The Incidence of asbestos-associated disease In this group of men formerly employed at a factory in Patterson, N.J. was excessive; there being a 19.7% lung cancer mortality (60 cases), a 4.6% mesothelioma mortality (14 cases), and a 5.9% asbestosls mortality (18 cases). An additional study, only partially published, reports on a group of workers exposed mostly to amoslte in a London Insulation board factory. Here 5 men have thus far died of mesothelioma (Acheson et al., 1981). Only prevalence studies have been made of amosite miners and millers. Two have died of mesothelioma. One resident of an amoslte mining district has been reported as having died of this disease. The rock-forming amphibole minerals grunerlte and cummingtonlte, which are Isostructural and chemically similar to amoslte, are considered (incorrectly) by some to be forms of asbestos. Health studies of miners working ores which contain these minerals as gangue do not show any Indication of asbest)srelated mortality (studies B,E, Table 4). Anthophyl11te asbestos. This form of asbestos has been mined sporadically In many localities but the only major production was at Paakklla, Finland where approximately 350,000 tonnes was mined between 1918 and 1975. The only health study of Individuals exposed predominantly to anthophylllte asbestos Is that of the Paakkila miners (Study A, Table 4). This group showed a 67% excess of lung cancer and a large mortality due to tuberculosis and asbestosls. Hone died of mesothelioma. Because anthophyllite was and Is used so little In commerce no additional health studies appear possible except for follow-up of the Paakklla miners. Comparison of health effects of white, blue, and browi asbestos. There Is a large contrast In the Incidence of mesothelioma among those who were exposed to only one form of the three commonly used a bestos mineralschrysotile, crocldolite, and amoslte. This Is demonstrate by comparing the total asbestos production to the number of mesothelioma deaths reported in the literature for miners, millers, and residents of four major asbestos mining localities. The pertinent data are given in Table 16. The difference between mesothelioma mortality reported in the chrysotile lining district and that reported In the crocldolite and amoslte mining districts may be even greater then Indicated In Table 16. This Is because csbestos-related mortality Is probably much underreported in Western Australia and South Africa due to the transient nature of the mining population where many are lost from view. Quebec, on the other hand, has a very statle mining <nd residential population, the medical surveillance of which has been excellent. 26 UCC 008684 Table 1(5. MHothelloma Mortal!tyl/in Four Asbestos Mining Districts Relative toAsbestos Production Asbestos type Tonnes mined Years mined No. deaths (mesothelloma) deaths/100,000 tonnes mined Quebec Canada chrysotlle 40,000,000 1878-Pres. 221/ 0.06 Western Australia crocldollte 155,000 1938-1966 37 23.9 Cape Province South Africa crocldoYl tie 2,700,000 1893-Pres. 278 10.3 Transvaal Prov. South Africa amoslte 2,200,000 1917-Pres. 31/ 0.14 1/Reported In the scientific literature up to 1979 for miners, millers and other residents of the mining districts 2/Excludes 7 mesothelioma cases that were exposed to crocidolite. J/Excludes 4 mesothelioma cases that were exposed to crocidolite. Several studies (Jones et al., 1980a, 1980b; McDonald, 1980b; Mclonald, 1980c) have been made on the types and amounts of asbestos fiber in tie lung tissue of asbestos workers who died of mesothelioma and in "controls" who died of other diseases and who were not occupationally exposed to asbestos. For example, Jones et al. (1980b) found that chrysotlle was present no more frequently nor In greater amounts, in the mesothelioma cases than In the control cases. They further state (p. 197) that "this study therefore provides no evidence to Indict chrysotlle in the etiology of mesothelioma." Similar findings are reported by McDonald (1980b) and McDonald (1980c). The above cited studies also show that amphibole fibers (crocidolite and amoslte) were more prevalent In the lung tissues of the mesothelioma cases than in the controls. The constrast in mortality holds also for lung cancer and asbestosis. All three forms cause significant excess of these two diseases in those exposed for long periods of time to high dust levels. However, short term exposure to moderate levels of crocidolite dust appears to be more dangerous than long term exposure to high levels of chrysotlle dust. This can be seen by compering the mortality data for the Quebec chrysotile asbestos miners and millers who were exposed to high to very high di st levels for 20 or more years (Table 17, column B) to the data for the Can<dian gas mask assemblers who were exposed to moderate levels of crocidolite dust for no more than 2.5 years (Table 17, column C). For further comfarlson, mortality data Is given for Quebec miners and millers who were exposfJ to low to medium dust levels (column A). 27 UCC 008685 Table 17. Mortality Data for Quebec Chrysotile Miners and Millers (columns A,B) with 20 or more years service and Tor Canadian Gas' Mask Assemblers (column C). a!./ &l/ cy Exposure Low-medium (10-21 f./cmi) High-V.high(95-194 f./cml) Moderate Cause of death Al1 causes All cancer Lung cancer G.I. cancer Asbestosis Other Resp. Mesothel 1oma Ohs. 620 147 48 47 11 28 Exp. 658.8 150.6 41 .6 58.7 0.7 34.3 %3/ 100 23.7 7.7 7.6 1.8 4.5 Obs. 478 132 56 45 25 31 - Exp. 367.7 82.8 23 32.6 0.4 18.4 %3/ 100 27.6 11 .7 9.4 5.2 6.5 Obs. *2/ 56 100 23 41 .1 8 14.3 3 5.4 2 3.6 4 7.1 9 16.1 VData from McDonald et al. (1980, Table 7d). / Ex posed to moderate levels of crocldollte dust for no more than 2.5 years (McDonald and McDonald, 1978). See also Study X, Table 3a. 3/Percent of all observed deaths. The contrast between cancer mortality in the mining-milling cohorts (Table 4) and the trades cohorts (Table 3a ,b) is clearly seen in Figure 1 where the proportional mortality due to lung cancer is plotted with respect to mesothelioma proportional mortality. The average mortality for the 8 mining-milling cohorts (excluding the crocldollte miners. Study F, Table 4) is: mesothelioma (0.2%), lung cancer (5.7%). For the 21 trades cohorts, the average mortality Is: mesothelioma (5.6%), lung cancer (16.7%). The cancer mortality pattern of the crocidolite mining cohort is very similar to that of the trades cohorts; 3.3% of this group having died of mesothelioma and 11.6% of lung cancer. Many of the men in the trades cohorts were probably exposed to crocidolite asbestos at some time during their working career. They also were probably often exposed to very high concentrations of asbestos dust, particularly during Installation or removal of asbestos In closed spaces such as heating conduits, ship compartments, etc. Peto (1978, 1980) ind Peto et al. (1982) suggest that chrysotile asbestos contributes significantly to mesothelioma mortality. Peto bases his conclusions on a study of workers in an asbestos textile factory in the UK (Peto et al., lc77; Peto 1978, Peto 1980). Exposure was mainly to chrysotile asbestos but crocidolite fiber was processed in this factory at various times since 1933 (Peto, 1978, p. 487). Peto does not cite the work of Jones et al. (1980a) and McDonald and McDonald (1978) on the gas mask assemblers, nor the work of Hilt et al , (1981) on construction workers; studies which clearly show the extreme hazard of crocidolite. Only brief exposure to crocldollte can set up a disease pattern very similar to that 28 UCC -008686- found In trades workers heavily exposed to asbestos for many years. From this we can conclude that mortality studies of asbestos workers who are exposed to crocldbllte, even for short periods of time, are not valid In predicting the health effects of other forms of asbestos. Estimates of Asbestos-related Mortality in the United States In various press releases and scientific publications, it has been suggested that asbestos exposure in the United States will cause from 10,000 to 67,000 deaths per year for the next 20 to 30 years. These estimates do not appear to be valid when compared to estimates of past mortality that are based on reported asbestos-related death due to mesothelioma or asbestosls. For example: (1) utilizing the mortality pattern of excess disease In 17,800 North American asbestos Insulation workers and the incidence of mesothelioma in 1972 given by a pathology review panel, it is estimated that 587 individuals died In that year because of exposure to asbestos; or (2) taking the reported number of asbestosls deaths as given In the Vital Statistics of the United States and again utilizing the mortality data of the North American insulation workers, It Is estimated that the average yearly asbestos-related mortality in the United States during the period 1967-1977 was 522 deaths. There Is some suggestion from the mortality data given in the Vital Statistics that the Incidence of asbestos-related disease has 1ncreased somewhat during this same period. 29 UCC 008687 COMMENTARY The Relative ttWards of the Asbestos Minerals It is pertinent to repeat one of the questions asked in the introduction of this review: Must the use of all commercial asbestos be stopped? The answer is an emphatic no - but with qualifications presented below. Non-occupational exposure to chrysotile asbestos, despite its wide dissemination in urban environments throughout the world, has been shown by epidemiological studies to be of no health significance whatsoever. If it were, the women of Thetford Mines, Quebec, where over 20 million tonnes of chrysotile asbestos has beer mined, would be dying of asbestosrelated diseases. They are not. The health studies accomplished in Canada show that populations can safely breath air and drink water that contain significant amounts of chrysotile fiber. These studies also show that there is a "threshold" value for chrysotile asbestos exposure below which no measurable health effect will occur. The same fiber dose-disease response relationships observed for chyrsotlle asbestos do not hold for crocldollte asbestos. Health studies of those exposed to only crocldollte show It to be much more hazardous than chrysotile; with respect to mesothelioma perhaps 100 to 200 times more hazardous. No study has been reported comparable to that made for chrysotile which Indicate what a safe level of exposure to crocldollte would be. The danger of crocldollte dust Is particularly emphasized by the many mesothelioma deaths occurring among the residents of the crocidolite mining districts of the Cape Province, South Africa whose only exposure was in a non-occupational setting. Such mortality Is practically unknown among residents of the chrysotile mining localities of Quebec. Control of crocidolite dust, particularly in the mines and mills, presents a considerable engineering problem in that dust levels at or below the 1969 British Standard of 0.2 flbers/cnr can be achieved hardly anywhere (Simpson, 1979, p. 74). The hazards of amosite asbestos are more difficult to access. The amoslte factory employees of Patterson N.J., who worked under very dusty conditions during World War II, have experienced a great deal excess mortality due to lung cancer, asbestosis, and mesothelioma. In contrast to these factory workers, amoslte miners and millers, at least with regard to mesothellomt, do not appear to be at much risk. This suggests that dust controls are possible which can much reduce or prevent the occurrence of asbestos-related diseases In amoslte workers. The fear caused by heavy handed statements such as "one fiber can kill you" and by the much exaggerated predictions of the amount of asbestosrelated mortality expected in the next 20 or 30 years has generated great political pressure to remove asbestos from our environment and to greatly reduce or even stop its use. An example of this is the concerted effort in several industrial nations including the United States to remove asbestos from schools, public buildings, homes, ships, appliances, etc. This is being done, even though most asbestos in the U.S. Is of the chrysotile variety, and even though asbestos dust levels in chools, public 30 UCC 008688 buildings and city streets Is much lower than found In chrysotlle asbestos mining conmmttles where no asbestos-related disease appears In the nonoccupatlonally exposed residents. The Impetus for these costly removals and appliance recalls (hair dryers, for example) apparently comes from propagandizing the "one fiber can kill you" concept. Not only Is this program costly - It could be dangerous If the removal of blue asbestos Is not accomplished with great care. In most cases, asbestos coatings and Insulation, where necessary, can be repaired at no risk and at a fraction of the cost of complete removal. Substitutes for Asbestos If all use of asbestos were to be discontinued, substitutes would have to be developed to meet many diverse requirements such as non flammability, high strength, flexibility, reasonable cost, and safety. With respect to safety, the substitutes must not Induce disease In those exposed to them and also must not endanger lives In other ways because of Inferior strength and durability, Increased flammability, etc. A high cost for a good substitute must not force Instead the use of an Inadequate replacement. Possible problems with substitutes may occur, for example, with the replacement of chrysotlle asbestos In drum brake linings. The chance of increased automobile accidents due to a possibly Inferior substitute material must be weighed against the probability of anyone being harmed by the small amounts of chrysotlle asbestos that are emitted from drum brakes. Also, the health effects of emissions from substitute brake linings must be considered. The requirements of strength and flexibility necessitate that asbestos substitutes be fibrous. Generally, the thinner and longer the fibers, the stronger, more flexible, and useful they are. However, fibers longer than 4 microns and less than 1,5 microns in diameter are capable of producing malignant neoplasms when Implanted Into the pleura of rats (Stanton et al., 1981). The test fibers In these studies included aluminum oxide, fiber glass, wollastonlte (CaSi03), silicon carbide, dawsonlte (NaAlCO^OK), and potassium octatltanate. Lee et al. (1981a, 1981b) studied the effects on rats, hamsters, and guinea pigs of Inhalation of different concentrations of "Fybex", a commercially made potassium octatltanate fiber used to strengthen materials. They found that In addition to the development of pulmonary Fibrosts In many animals, 3 hamsters developed pleural mesothelioma, a rire disease In the control animals. In the report of the Advisory Committee on Asbestos, Health and Safety Commission of Great Britain, the following statement is made In regard to substitutes for asbestos (Simpson, 1979, vol. 1, p. 69). "As a general principle we take the view that control of any useful but hazardous material is preferable to the ultimate sanction of prohibition. It is very easy to say that a dangerous substance or process should be banned and to hope that that will solve the problem. In our view this Is a gross 31 UCC 008689 over-simplification of a complex equation of inter linked factors. It Ignores the possibility that prohibition of a particular substance may directly result In an Increase In health or safety risks, for example from fire, which the use of that substance currently prevents or reduces. It also Ignores the Implications of statutorily enforcing substitution by materials or substances which at present appear to be suitable but may at a later date be found to constitute a risk to health. The social and economic consequences of the possible closure of factories using the original material or process need to be taken Into account." The recent animals experiments such as those cited above make the Advisory Committee's statement particularly meaningful. The cost of asbestos substitutes is of particular Importance to the "Third World" countries whose developing ecoromles are very dependent upon making the maximum use of cheap, domestically produced materials whereever possible. Asbestos cement is such a material and large quantities of it are vital to the Industrialization of these nations. Importation of possible substitutes, for example, plastic and metal water pipe and construction materials, Is not an economic choice for many nations. It Is significant that several courtrles are greatly expanding their chrysotlle mining and milling operation; the U.S.S.R., Zimbabwe, Greece, Mexico, Yugoslavia (Asbestos, vol. 6~, January 1982). The Ubiquitous Fibrous Minerals and Future Health and Regulatory Policy Those outside the mining and geoscience professions probably do not appreciate how common fibrous minerals are. 'lost hard rock mines contain some gangue minerals that are considered by ome to be asbestos or asbestos like. For example, the common rock-forming mineral cummingtonite found in the Reserve Mining Company's Iron ore deposits near Lake Superior, Minnesota Is considered to be asbestos by the U.S. Environmental Protection Agency and the Courts of Minnesota, although I know of no geologist who would call this mineral asbestos. However, be It as It may. If cummingtonite and other amphlboles are considered to be asbestos for regulatory purposes then a great many mining operations will alsc be considered asbestos mining operations. The mining and milling oi gold and iron ere, talc, vermlcullte, and crushed stone have already t>en effected by asbestos regulations. In addition to the fibrous minerals four 1 in numerous o>e deposits, they are also found in many water supplies, ii soils and sed ments, In certain sand and gravel deposits, In drilling muds, In portend cement. In ceramic materials, and In large areas overlain by volcanlt ash. Shoild the public be told that even low doses of these mineral fibers can possibly cause cancer? Should human exposure to these fibers be regulated to the lowest feasible limit? Should extreme measures be taken sucf as moving people out of regions where fibrous minerals are endemic? Sich action 32 UCC 008690 was proposed by P. C. Elmes, Director of the MRC Pneumoconiosis Unit, Llandough Hospital, Penarth, Wales. He writes (Elmes, 1980, p. 529), "Populations living on soils contaminated with the fibers under dry climatic conditions need to be moved." In regard to his proposal, it Is noted that fibrous zeolite minerals occur In many areas of the southwestern United States and that fibrous clay minerals are common In the coastal plane sediments of the eastern United States. One does not have to consider the above questions very long before coming to realize that If answered In the affirmative they would present a regulatory, legal, and economic nightmare. Instead of overreacting to every perceived health risk (this seems to occur particularly In regard to suspected carcinogens) we must allocate our scientific and economic resources to our environmental health problems In proportion to their seriousness. Billions of dollars have been spent directly and Indirectly, In understanding anc mitigating asbestos-related cancers. Many billions more may be awarded to those filing clafms against asbestos companies. In contrast, relatively little has been spent on understanding and mitigating the more serious non-neoplastlc lung diseases such as the pneumoconioses caused by Inhalation of crystalline silica and coal dusts. A great deal has been accomplished In urderstandlng the relationships between the Intensity of exposure to the several forms of commercial asbestos and the Incidence of the asbestos-retated diseases. Epidemiological studies have shown that modern dust control nethods now In effect can prevent most morbidity and mortality related to exposure to chrysotlle asbestos. Similar studies should be completed In order to set dust levels to protect the anthophyl1ite and amoslte asbestos workers (in this regard see the Simpson Report, Simpson, 1979). 33 UCC 008691 References Acheson, E.D., Gardner, M.J., Bennett, C. and Winter, P.D. (1981) Mesothelioma in a factory using amoslte and chrysotile asbestos. Lancet, Dec 19/26, 1403-1406. Antman, K.H., Blum, R.H., Greenberger, J.S., Flowerdew, fi., Skarln, A.T., and Canellos, G.P. (1980) Multimodality therapy for malignant mesothelioma based on a study of natural history. Am. J. Med., 68, 356-362. Becklake, M. R. (1976) Asbestos-related diseases of the lung and other organs: Their epidemiology and Implications for clinical practice. Am. Rev. Resp. Disease, 114, 187-227. Brenner, J., Sordillo, P.P., and Mag 11, G.B. (1981a) Malignant mesothelioma in children: Report of seven case, and review of the literature. Med. Pediatr. Oncol., 9 , 367-373. Brenner, J., Sordillo, P,P., Magi 11 , G.B., and Golbey , R.B., (1981b) MaiIgnant peritoneal mesothelioma. Am. J. Gastroenterol., 75, 311-313. Bridbord, K., DecoufI e, P., Fraumeni , J .F., dr., Hoel , D.G., Hoover, R.N., Rail, D.P., Saffiotti , U., School derman, M.A., and Upton, A.C. (1978) Estimates of the fraction of cancer in the United States related to occupational factors. Unpublished document from the NCI, NIESH, and NIOSH, Sept. 15, 1978, 49 p. Brulotte, R. (1976) Study of atompshorlc pollution in the Thetford Mines area, cradle of Quebec's asbest is industry. Atmospheric Pol 1utlon. Proc. 12th International Colloq., Paris, France, May 1 $7(5, M.M. Benarie, Ed., 447-458. Clemmesen, J., and Hjalgrim-Jensen, (1981) Cancer incidence among 5686 asbestos-cement workers foil owe! from 1943 through 1976. Ecotoxicology Env. Safety,5,15-23. Clifton, R. A. (1979) Asbestos. MCP mineral commodity profiles, U. S. Bureau of Mines, July 1979, 19 pp. Cochrane, J. C. and Webster, I. (1971) Mesothelioma in relation to asbestos fibre enpasure - a review of 70 serial cases. S. African Med. J., 54, 279-281. Davis, 0. M. G. (1981) The biological effects of mineral fibers. Ann, Occup. Hyg., 24, 227-234. Demopoulos, H.B., M.D. (1980a) Personnal communication. Demopoulos, H.B. (1980b) A scientist's viewpoint on the issue of environment and health. Bulletin, L'Assoc. des Mines D'Amiante Ju Quebec, 4, 1-7. 34 UCC 008692 DHHS (1981a) Carcinogenesis bioassay of amoslte asbestos in Syrian Golden Hamsters. DHHS pub. no. (NIH) 81- , 23 June 1981, NTP-81-58. Public Health Service, Dept, of Health and Human Services, pp. 1-87. DHHS (1981b) Carcinogenesis bioassay of chrysotile asbestos in Syrian Golden Hamsters. DHHS pub. no. (NIH) 81- , 23 June 1981, NTP-81-51. Public Health Service, Dept, of Health and Human Services, pp. 1-191. Doll , R. and Peto, R. (1981) The causes of cancer: Quantitative estimates of avoidable risks of cancer in the United States today. J. Nat. Cancer Inst., 66, 1193-1308. Donham, K.J., Berg, J.W., Will, L.A., and Leinlnger, J.R. (1980) The effects of long-term ingestion of asbestos on the colon of F344 rats. Cancer, 45, 1073-1084. Elmes, P. C. (1980) Fibrous minerals and health. J. Geol. Soc. London, 137, 525-535. Elmes, P.C. and Simpson, J.C. (1977) Insulation workers in Belfast. A further study of mortality due to asbestos exposure (1940-75). Brit. J. Ind. Med,, 34, 174-180. El wood, P. C. and Cochrane, A. L. (1964) A follow-up of workers from an asbestos factory. Brit. J. Ind. Med. 21, 304-307, Epler, G.R., Fitz Gerald, M.X., Gaensler, E.A., and Carrington, C.B. (1980) Asbestos-related disease from household exposure. Respiration, 39, 229-240. uropaeus-J(yrapaa, A. (1930) Die relative Chronologie der steinzeitlichen Keramlk In Finland. Acta Archaeol., 1, 169-190. Gil lam, J. 0., Dement, J. M., Lemen, R. A., Wagoner, J. K., Archer, V. E. and Blejer, H. P. (1976) Mortality patterns among hard rock gold miners exposed to an asbestlform mineral. Annals N. Y. Acad. Sc., 271 , 336-344. Goldsmith, J.R. (1980) The "urban factor" in cancer: Smoking, industrial exposures, and air pollution as possible explanations. J. Env. Pathol. Toxicol., 3, 205-217. Gori , G.B. (1979) Dietary and nutritional implications in the multi factorial etiology of certain prevalent human cancers. Cancer, 43, 2151-2161. Graham, S. (1981) Methodological problems in ecologic studies of the asbestos-cancer relationship. Env. Res., 25, 35-49. Griffiths, M.H., Riddell, R.J., and Xipell, J.M. (1980) Malignant mesothelioma A review of 35 cases with diagnosis and prognosis. Pathology, 12, 591 603. 35 UCC 008693 Hall , A. L. (1918) Asbestos in the Uni on of South Africa. Mem. no. 12, Geol. $urv% of South ATrica, 1$2 pp. Hallenback, W.H., Markey, D.R., and Dolan, D.G. (1981) Analyses of tissue, blood, and urine samples from a baboon gavaged with chrysotlle and crocldolite asbestos. Env. Res., 25, 349-360. Hammond, E. C. Garflnkel , L. and Lew, E. A. (1978) Longevity, selective mortality, and competitive risks In relation to chemical carcinogenesis. Env. Res., 16, 153-173. Hammond, E.C., Garfinkel , L., Selikoff, I.J., and Nicholson, W.J. (1979) Mortality experience of residents in the neighborhood of an asbestos factory. Annals. NY Acad, Sci., 330, 417-422. Henderson, V.L. and Enterline, P.E. (1979) Asbestos exposure: Factors associated with excess cancer and respiratory disease mortality. Annals. NY Acad. Sci., 330, 117-126. Higgins, I. (1981) Mortality study of employees of the Reserve Mining Company. Personal communication, May 12, 1981, from Ian T. T. Higgins, M. 0. , Professor at Epidemiology, School of Public Health, The University of Michigan. Higginson, J. (1980) Multiplicity of factors involved in cancer patterns and trends. J. Env. Pathol. Toxicol., 3, 113-125. Higginson, J. and Muir, C.S. (1979) Environmental carcinogenesis: Misconceptions and limitations to cancer control. J. Nat. Cancer Inst., 63, 1291-1298. Hllding, A.C., Hildlng, D.A., Larson, D.M., and Aufderheide, A.C. (1981) Biological effects of ingested amosite asbestos, taconite tailings, diatomaceous earth and Lake Superior water in rats. Arch. Env. Health, 36, 298-303. Hilt, B,, Rosenberg, J., and Langard, S. (1981) Occurrence of cancer in a small cohort of asbestos-exposed workers. Sand. J. Work Env. Health, 7, 185-189. Hobbs, M. S. T., Woodward, S., Murphy, B., Musk, A. W. and Elder, J, E. (1980) The incidence of pneumoconiosis, mesothelioma and other respiratory cancer In men engaged in mining and milling crocidolite in Western Australia. Biological Effects of Mineral Fibres, vol. 2, J. C. Wagner, Ed., No. 30. Lyon, 615-625. Hogan, M.D. and Hoel, D.G. (1981) Estimated cancer risk associated with occupational asbestos exposure. Risk Analysis, 1, 67-76. Jones, C.D.F. and Silver, 0. (1979) Peritoneal mesotheliomas. Surgery, 86, 556-560. 36 UCC 008694 Jones, J.S.P., Pooley, F.O., Clark, N.J., Owen, W.G., Roberts, G.H., Smith, P.G., Wilier, J.C., Berry, G. and Pollock, D.J. (1980b) The pathology and mineral content of lungs in cases of mesothelioma in the United Kingdom In 1976. Biological Effects of Mineral Fibres, vol. 1 , J.C. Wagner, Ed., Lyon, 1 aScS s'cI . Pub. No."70, T87-199. Jones, J.S.P., Pooley, F.D., Sawle, G.W., Madeley, R.J., Smith, P.G., Berry, G., Wignall , B.K. and Aggarwal , A. (1980a) The consequences of exposure to asbestos dust in a war time gas-mask factory. Biological Effects of Mineral Fibres, vol. 2, J.C. Wagner, Ed., Lyon, lARC 5cT. Pub."No. Iff, 637-653. Jones, J. S. P., Pooley, F. 0. and Smith, p. G. (1976) Factory populations exposed to crocidolite asbestos - a continuing survey. IARC Scl. Pub. No. 13, 1NSERM Sym. Series Vol. 52, 117-120. Jones, R. H. (1890) Asbestos, its Properties, Occurrence and Uses. Crosby, Lockwood and Son, London, 236 pp. Kannerstein, M. and Churg, J. (1980) Mesothelioma in man and experimental animals. Env. Health Perspect., 34, 31-36. Kannerstein, M., Churg, J, and McCaughey, W.T.E. (1979) Functions of mesothelioma panels. Annals. NY Acad. Sc., 330, 433-439. Kleinfeld, M., Messite, J. and Kooyman, 0. (1967) Mortality experience in a group of asbestos workers. Arch. Environ. Health, 16, 177-180. Langlois, S. Le P., Glancy, J. J. and Henderson, D. W. (1978) The radiology of malignant pleural mesothelioma in Western Australia. Aust. Radiol. 22, 305-314. Lee, K.P., Barras, C.E., Griffith, F.D., and Waritz, R.S. (1981a) Pulmonary response and transmigration of inorganic fibers by inhalation exposure Am. J. Pathol.. 102, 314-323. Lee, K.F., Barras, C.E., Griffith, F.D., Waritz, R.S., and Lapin, C.A. (1981b) Comparative pulmonary responses to inhaled inorganic fibers with asbestos and fiberglass. Env. Res., 24, 167-191 . Legha, S. S. and Muggia, F. M. (1977) Pleural mesothelioma: Clinical fea tures and therapeutic applications. Ann. Internal Med., 87, 613-621. Liddell, F. D. K. (1981) Asbestos and Public Health. Can. Med. Assoc. J., 125, 237-239. Mancuso, T. F. and El-Attar, A.A. (1967) Mortality pattern in a cohort of asbestos workers. J. Qccup. Med. 9, 147-162. McCullagh, S. F. (1980) Amosite as a cause of lung cancer and mesothelioma in humans. J. Soc. Occup. Med., 30, 153-156. McDonald, A.D. (1979) Mesothelioma registries in identifying asbestos hazards. Annals. NY Acad. Sc., 330, 441-454. 37 UCC 008695 McDonald, A.D. (1980a) Malignant mesothelioma in Quebec. Biological Effects of Mlneraf FIbres, vol. 2, J.C. Wagner, Ed., Lyon, I ARC Sci, Pub. No. 30, 673-690.---------- McDonald, A.D. (1980c) Mineral fibre content of lung in mesothelioma tumours: Preliminary report. Biological Effects of Mineral Fibres, vol . 2, J.C. Wagner, Ed., Lyon, IARt Sci Pub, NoT30, 681 -685. McDonald, A. D. and McDonald, J. C. (1978) Mesothelioma after crocidolite exposure during gas mask manufacture, Env. Res., 17, 340-346. McDonald, A. D. and McDonald, J. C. (1980) Malignant mesothelioma in North America. Cancer, 46, 1650-1656. McDonald, J.C. (1980b) Asbestos-related disease: An epidemiological review. Biological Effects of Mineral Fibres, vol. 2, J.C. Wagner, Ed., Lyon IARC l&TFet.' "No. 10,"587^01"-------- McDonald, J. C., and Becklake, M. R. (1976) Asbestos-related disease In Canada, Hefte z. Unfallheilkunde, 126, 2. Deutsch-OsterreichischSchweizeische Unfalltagung in Berlin 1975, Springer-Verlag , Berlin, 521-535. McDonald, J, C., Becklake, M. R., Gibbs, G. W., McDonald, A. 0. and Rosslter, C. E. (1974) The health of chrysotile asbestos mine and mill workers of Quebec, Arch. Env. Health, 28, 61-68. McDonald, J. C., Gibbs, G. W., Liddell , F. D. K. and McDonald, A.D. (1978) Mortality after long exposure to cummingtonite-grunerite. Am. Rev. Resp. Disease, 118, 271-277. McDonald, J. C., Liddell, F.D. K,, Gibbs, G. W., Eyssen, G. E. and McDonald, A. D. (1980) Dust exposure and mortality in chrysotile mining, 1910-75. Brit. J. Ind. Med., 37, 11-24. McDonald, J. C. and McDonald, A. D. .1977) Epidemiology of mesothelioma from estimated incidence. Preventive Med., 6, 426-446. Meurman, L. 0., Kiviluoto, R. and Ha%ama, M. (1974) Mortality and morbidity among the working population of anthophyl1ite asbestos miners in Finland. Brit. J. Ind. Med., 31, 105-112, Mostert, C. and Meintjes, R. (1979) Asbestos and mesothelioma on the Rhodesia railways. Central African J. Med., 25, 72-74. Newhouse, M, (1981) Epidemology of asbestos-related tumors. Sem. Oncol. 8, 250-257. Newhouse, M.L. and Berry, G. (1979) Patterns of mortality in asbestos factory workers in London. Annals. NY Acad. Sc., 330, 53-60. 38 UCC 008696 Newhouse, M.l, and Thompson, H, (1965) Mesothelioma of pleura and peritoneum foil owl (i^txposure to asbestos In the London area. Br. J. Ind. Med., 22, 261-f9. Nicholson, W. J., Lanyer, A, M. and Selikoff, 1. J. (1978) Epidemiological evidence on asbestos. In C. C. Gravitt, P. D. Lafleur, and K. F. J. Helnrich, Eds., National Bureau of Standards Speelal Publication 506. Proc. Workshop on AsbesFo?: PefTnl tt oris' and Measurement Method?, "71-93. Nicholson, W.J., Rohl , A.N., Weisman, I,, and Selikoff, I.J. (1980) Environ mental asbestos concentrations in the United States. Biological Effects of Mineral Fibres, vol. 2, J.C. Wagner, Ed., Lyon, IARC Scl. T*ul>rNb. 70, -------------- Nicholson, W. J., Selikoff, I. J,, Seidman, H., Lllls, R. and Formby, P. (1979) Long-term mortality experience of chrysotile miners and millers In Thetford Mines, Quebec. Annals N. Y. Acad. Sc., 330, 11-21. Pampalon, R, (1979) A comparative analysis of mortality in asbestos-mining and other towns of Quebec, Unpublished work document (Doc. No. 5596/79c), Asbestos-health project. Division of Epidemiological Studies, Ministry of Social Affairs, Quebec, P.Q, Peto, J. (1978) The hygiene standard for chrysotile asbestos. Lancet, 4 Mar, 1978, 484-489. , Peto, J. (1980) The Incidence of pleural mesothelioma in chrysotile asbestos textile workers. Biological Effects of Mineral Fibers, vol. 2, J.C. Wagner, Ed,, Lyon, lAtfc. c. Pub, "No.-Jo',' 7o3-711. Peto, J., Doll, R., Howard, S. V., Kinlen, L. J. and Lewinsohn, H. C. (1977) A mortality study among workers in an English asbestos factory. Brit. J. Ind. Med., 34, 169-173, Peto, J., Seidman, H., and Selikoff, 1.J. (1982) Mesothelioma mortality in asbestos workers: Implications for models of carcinogenesis and risk assessment. Br. J. Cancer, 45, 124-135. Puntonl , R., Vercelli , M., Merlo, F ., Valerio, F ., and Santi, L. (1979) Mortality among shipyard workers In Genoa, Italy. Annals. NY Acad. Sc., 330, 353-377. Risberg, B., Nickels, J., and Wagermark , J. (1980) Familial clustering of malignant mesothelioma. Cancer, 45, 2422-2427. Ross, M. (1981) The geological occurrences and health hazards of amphfbole and serpentine asbestos. Reviews in Mineralogy, vol. 9A, Amphlboles and other Hydrous Pyriboles-MfrieraTogy, O. vebien , EcTTT Min. Joe. Am., Hashffigton, DG, p .279 Rubino, G, F.,P1o1atto, G., Newhouse, M. L., Scansetti , G., Aresini , G. A. and Murray, R, (1979) Mortality of chrysotile asbestos workers at the Balangero mine, northern Italy, Brit. J. Ind. Med., 36, 187-194. 39 UCC 008697 Riittner, J. R,. (1978) Comments. In H. H. Glen, Ed., Proceedings of Asbestos Symposium, Johannesburg, South Africa, October 3-7, 1977, Dept, of Mlnes , 5. Africa, p. #8-837 Saracci , R. (1977) Asbestos and lung cancer: An analysis of the epidemio logical evidence on the asbestos-smoking Interaction. Int. J. Cancer, 20, 323-331. Sellkoff, I. J. (1978) Carcinogenic potential of silica compounds. In G. Bendz and I. Lindquist, Eds., Biochemistry of Silicon and Related Problems , PIeunum Pub. Corp., 311-335. Sellkoff, I. J. and Hammond, E. 0. (1975) Multiple risk factors in environ mental cancer. In Persons at High Risk of Cancer, J. Fraumeni Ed., Aca demic Press , N. Y. ~ Selikoff, I. J., Hammond, E. C. and Seidman, H. (1973) Cancer risk of insu lation workers in the United States. In Biological Effects of Asbestos, I ARC Scientific Publication No. 8, 209-2167 WHO, Lyon. Selikoff, I.J., Hammond, E.C., and Seidman, H. (1979a) Mortality experience of insulation workers in the United States and Canada, 1943-1976. Annals. NY Acad. Sc., 330, 91-116. Selikoff, I. J., Hammond, E. C. and leidman, H. (1980a) Latency of asbestos disease among insulation worker; in the United States and Canada, Cancer, 46, 2736-2740. Selikoff, I. J. and Lee, D. H. K. (1978) Asbestos and Disease, Academic Press , N. Y., 549 p. Selikoff, I.J., Lilis, R., and Nicholson, W.J. (1979b) Asbestos disease in United States shipyards. Annals NY Acad. Sc., 330, 295-311 . Selikoff, I. J., Seidman, H. and Ham lond, E. C. (1980b) Mortality effects of cigarette smoking among amos te asbestos factory workers. J. Nat. Cancer Inst., 65, 507-513. Simpson, W. (1979) Asbestos, vol. 1: Final report of the advisory committee; vol. 2: Papers commissioned Fy the committee. HeaTth and Safety Com missi on, Great Britai n , ?03"pp. Smith, W.E., Hubert, D.D., Sobel , H. 1., Peters , E.T. and Doerfler, T.E. (1980) Health of experimental animals Jrinking water with and without amosite asbestos and other mineral particles. J. Env. Pathol. Toxicol., 3, 277-300. Stanton, M.F., Layard, M., Tegeris, \., Miller, E., May, M., Morgan, E., and Smith, A. (1981) Relation of particle dimension to carcinogenicity in amphibole asbestos and other fibrous minerals. J. Nat. Cancer Inst., 67, 965-975. 40 UCC 008698 Sterling, T. D. and Weinkam, J. J. (1978) Smoking patterns by occupation, industry, sex, and race. Arch. Env. Health, Nov./Dec., 313-317. Talent, J. M,r Hirrlson, W. 0., Solomon, A. and Webster, I. (1980) A survey of black mine workers of the Cape crocldollte mines. Biological Effects of Mineral Fibres, vol. 2, J.C. Wagner, Ed., Lyon, I ARC, Sc. Pub. No" iff, -------- Theriault, (i.P. and Grand-Bols, L. (1978) Mesothelioma and asbestos in the Province of Quebec, 1969-1972. Arch, Env. Health, 33, 15-19. Thomas, H.F., Benjamin, I.f., El wood, P.C., and Sweetnam, P.M. (1982) Further follow-up study of workers from an asbestos cement factory. Brit. J. Ind. Med., 39, 273-276 (see also El wood and Cochrane, 1964). Toft, P., Wlgle, D., Meranger, J.C., and Mao, Y. (1981) Asbestos and drinking water in Canada. Sc. Total Environ. 18, 77-89. Vejlsted, H. and Hansen, B. F. (1980) Pleural mesothelioma. Scand. J. Thor. Cardlovasc. Surg., 14, 119-122. Vianna, N.J., Maslowsky, J., Roberts, S., Spellman, G., and Patton, R.B. (1981) Malignant mesothelioma-epidemiologic patterns in New York State. NY State J. Med., April 1981, 735-738. Vianna, N.J. and Pol an, A.K. (1978) Non-occupatlonal exposure to asbestos and malignant mesothalioma in females. Lancet, May 20, 1978, 1061-1063. Wagner, J.C., Berry, G., Skidmore, J.W., and Timbrel 1 J. (1974). The effects of the inhalation of asbestos in rats. Br. J. Cancer, 29, 252-269. Wagner, J. C., SI eggs, C. A. and Marchand, P. (1960) Diffuse pleural meso thelioma and asbestos exposure in the northwestern Cape Province. Brit. J. Ind. Med., 17, 260-271. Webster, I. (1978) Discussion. In H. W. Glen, Ed., Proceedings of Asbestos Symposium, Johannesburg South Africa, Oct. 3-7, 1977 ,"beptY"M1nes, S. Africa p. 7ffT Weill, H., Hughes, J., and Waggenspack, C. (1979) Influence of dose and fiber type on respiratory malignancy risk in asbestos cement manufacturing. Am. Rev* Resp. Disease, 120, 345-354. Welsberger, J.H. (1978) Environmental cancer: On the causes of the main human cancers. Texas Rpts. Biol. Med., 37, 1-18. Weiss, W. (1977) Mortality of a cohort exposed to chrysotile asbestos. J. Occup. Med., 19, 737-740. Wigle, D.T. (1977) Cancer mortality in relation to asbestos in municipal water supplies. Arch. Env. Health, 32, 185-190. Wynder, E.L. (1980) The environment and cancer prevention. J. Env. Pathol, Toxicol3, 171-192. 1 UCC 008699