Document 3QZ7ZD494DMnk90Kdv8xnJV0E

SYMPOSIUM MONDIAL SUR L*AMIANTE 24, 25. 26, 27 Mai 1982 MONTREAL Qug., Canada WORLD SYMPOSIUM ON ASBESTOS May 24, 25. 26, 27, 1982 MONTREAL Qud., Canada Stance I - 25 mai L'ami ante; les donnfies midicales Session I * May 25 Asbestos: The Medical Data AS3EST0S-AELATEC DISEASE - AN OVERVIEW, 1932 Irvine j. Selfkoff (UNITED STATES) A ; 774J UCC 007903 Asbestos-related disease - an overview, 1982 Irving J. Selikoff, H.D. Environmental Sciences Laboratory Mount Sinai School of Medicine of the City University of Mew ^or't Introduction This Symposium may prove to be a landmark in the history of asbestos use and asbestos disease. In this respect, it resembles the confer ence held by The Mew York Academy of Sciences in 1964. Unlike that meeting, however, the outcome is not necessarily sanguine nor broadly optimistic. We have come to a decision point, with several directions passible. Which are taken will, in considerable measure, be influ enced by this meeting. The Mew Tork Conference Although the fibrogenic capacity of asbeatos--pocentiaily fatal-- had been increasingly studied since the 1920s and 1930s, it was not 'until the following two decades that the significance of cancer attracted broad attention. This, coupled with the exponential growth of the use of asbestos, spurred scientific inquiry. 3v 1964, accumulating data warranted critical review and in October of that year The Mew Tork Academy of Sciences convened aa International Conference to consider what was known. The prospectives at that meeting were defined by its title "Biological effects of asbestos". The presentations largely focused on observations recently made in defined areas where addi tional scientific data could assist in clarifying scientific ques tions. Many had confidence that, with what was known and what would be studied, the disease hazard would be controlled. Scientific informa tion would allow us to avoid hazard associated with this valuable material. UCC 007904 2 The Montreal 5ymoosiua In che years since 1964, this optimism has been tempered. Asbestos disease has continued, and there is no unanimity that the conditions for its control have been achieved. The fact that this Symposium will address the question "Should the use of asbestos be continued?" is a measure of our past inadequacies, and current uncertainties. -This meeting will again be science-based. But it will, unlike 1964, have the additional responsibility of considering the economic, poli tical, social, administrative, ethical problems associated with the continued and projected uses of asbestos. Perhaps we were remiss in yew Tack in not addressing these problems more vigorously. Science was necessary, but not sufficient. This Symposium, then, has a double responsibility: careful review of the scientific prospectives that have developed since 1964 and their translation into the use of asbestos without significant risk to human health. Scientific perspectives. 1964-1982 8uilding upon and extending the scientific information that had become available by 1964, we have now achieved a useful overview of the scientific background against which the asbestos disease problem may be viewed. At the 1964 meeting, a number of questions were unre solved. Additional data were needed to fully characterise the nature and extent- of the cancer risk, the influence of fiber dose and fiber type on such disease as would occur, the significance of non-occupational exposures, and how standards and controls could best be de veloped. Such information has been obtained, to help understand these critical issues. 1a. addition, problems not predicted in 1364 have also been identified, and useful data obtained. UCC 007905 3 Spectrum of asbestos-associated disease We now have a fairly good 'understanding of the spectrum of asbestosassociated disease, at Least that which obtains with heavier exposure. Two cohort studies illustrate the extent of this knowledge. In the first, 17,300 asbestos insulation workers were registered on January 1, 1967 and followed to December 31, 1976, and included 166,353 manyears of observation. Table 1 summarizes their mortality experience daring that decade. There was significant increased mortality of cancer of the lung, pleural and peritoneal mesothelioma, cancer of the esophagus, stomach, colon-rectum, cancer of the oro-pharynx and larynx, cancer of the kidney, and asbestosis. These data were based upon 3,271 deaths. The experiences of a second cohort confirm this outlook, providing support from another epidemialological direction. On January 1, 1943, there were 632 asbestos insulation workers in the Mew York-Mew Jersey locals of this Union. This group was followed to December 31, 1931, covering 14,547 man-years of observation. In the 39 years, 532 men died; this mortality experience thus covers almost the entire experi ence of this group. Table 2 demonstrates that 4 of tie men died of asbestosis (approximately 8"). Tar greater risks were deaths of cancer. Age, year and sex-specific data indicate that 63.9 deaths of cancer were to have been expected. Two hundred and thirty-sight oc curred (45'',). The major neoplastic risk was lung cancer. 15.7 were expected, 105 occurred (20; of all deaths). There were 50 deaths of mesothelioma (9%) and a modest but statistically significant increased risk of death of gastrointestinal cancer. 3oth Table 1 and Table 2 indicate that the major concerns are lung cancer, mesothelioma, asbestosis and gastrointestinal cancer. UCC 007906 4 Populations at risk 3y 1964, it was already clear that early emphasis on "asbestos work ers" (asbestos miners, millers, asbestos products manufacture) was insufficient. Rather, hazards associated with product use vastly increased the number of people at risk of asbestos-associated disease. The insulation worker experience pointed to the construction industry; the reports by Harries and Stumphius in 1966 added shipyard work as a major concern. Against this background, studies in a variety oi trades expanded both the potential for disease and the necessity for controls--cheoical plants, refineries, power production and utilities, transportation, ship repair and shipboard exposure, etc. Further, utilizing mesothelioma as a marker and "signal" (the work of Cochran and Webster has been particularly telling in this regard), there was further emphasis on the likely importance of disease among family contacts and among those exposed in a number of environmental circumstances. Dr. W.J. Micholson will discuss in this Symposium the results of his analyses concerning occupational populations exposed 1940-1930 in the United States; the number of people involved can only be described as huge. It will be valuable to have analyses made of exposed populations in other countries, to provide a global perspec tive in this regard. Latency Perhaps at the heart of our difficulties concerning asbestos-associ ated disease bas been the long incubation period before important clinical evidence of such disease is noted. The "20 year rule" had been propounded for radiological asbestosis in 1964. It is clear that the same holds true for cancer, as well. Table 3 shows that little lung cancer or mesothelioma occurs in less than 20 years from onset of exposure. This is depicted in Figures 1-3. A corollary of this is that we learned the semantic difference between "duration oi exposure" and "duration from onset o: exposure". The two are by no means synonymous. With asbestos exposure oi sufficient intensity, only short-term exposure is needed to yield long-term risk. UCC 007907 5 We have not yet learned how to loosen this iron grip of latency. In practical terms it means that the disease we are seeing now is the result of past exposure. By the same token, however, and important for this conference, is the fact that present exposure will result in future disease. Low-level exposure I'm not sure that this commonly used phrase is entirely appropriate; perhaps we should employ the more unwieldly "lower level exposure", since there is some contradiction in speaking of exposure as "low" when it produces disease and death, further, we are not very confi dent about quantitation of "lower level exposure" since it was pre cisely in such circumstances chat, in the past, few measurements were made. This has been the case for family contact disease. When this phenom enon, heralded by Wagner's description of environmental mesothelioma in 1960, was documented by Mewhouse In 1965, we had no information on what level of exposures might have been responsible for what was seen. Hicholson and Kohl in our Laboratory have made some measurements in recent years, but I believe that a valuable opportunity was lost after the Hew York meeting when extensive household asbestos exposure studies were not done. We would now know something at least about the lower limits of exposures associated with asbestos-associated disease. Low-level exposure is sometimes used to characterize what has happened in occupational situations where exposure has been Intermittent and indirect. These may not be the same as exposures in family contact circumstances, since the intensity of exposure on occasion can be more or less severe, albeit for short periods. It might well be that three hours in the hold of a ship where asbestos was being extracted could provide a much heavier lung burden than 10 years of residence in an asbestos worker's home! Too, the general use of the phrase "low-level exposure" may not be at all pertinent to the levels of exposure that exist in ambient air and UCC 007908 6 experience of brake repair and brake maintenance workers, or sheet metal workers in the construction industry provide no necessary guide to evaluation of risk of the general population. Selection within high risk grouns When it is said that one in five asbestos insulation workers dies of lung cancer, it is also implied that four in five don't. Similarly if .one in 15 dies of mesothelioma, Id do not. The reasons for such selection within groups at high risk have begun to be explored. One factor that has been identified has been the importance of tobacco smoking, primarily cigarettes. Asbestos exposure by itself increases the risk of lung cancer, by about five times. However, since the risk of non-smokers is low, even such increase does not produce a very large number of cases of lung cancer. Cn the other hand, the same five times increase among cigarette smokers results in sharp multipli cation of an already very high risk, resulting in a devastating lung cancer incidence. In one study (the 17,300 asbestos insulation work ers mentioned above) in which the experience of more than 73,000 like men were used as a control, the rate for men who neither smoked cigar ettes nor worked with asbestos was 11 per 100,000 per year. For noa-smokers who worked with asbestos, it was 53. Among those who smoked, but were not asbestos-exposed, the risk was 112 per 100,000 per year and for those who had both exposures, asbestos and cigarette smoking, it was 601. The multiple factor interaction of asbestos and cigarette smoking pertains as well to cancer of the esophagus, cancer of the oropahrynx and buccal cavity, cancer of the larynx but not to mesothelioma, cancer of the stomach or colon-rectum or cancer of the kidney. There may well be multiple factor interaction with other in fluences for a variety of asbestos cancers, but this has been little studied. One set of circumstances that can turn out to be of con siderable importance is iamunomodification; this is a subject of in tense research at this time in our Laboratory. UCC 007909 7 Reversal of risk During the cigarette smoking-asbestos exposure investigations, an im portant observation was made. Those asbestos workers with a history of cigarette smoking who stopped smoking, within 5-10 years had only one-half to two-thirds the lung cancer risk of those who continued to smoke. Data are not yet available concerning whether risk of oro pharyngeal and buccal cavity cancer, laryngeal cancer, and esophageal cancer will show the same happy effect, but I anticipate that it will be so. Cigarette smoking was also found to increase the risk of death of asbestosis, presumably by adding the emphysema-bronchitis burden of smoking to the pneumoconiotic effect of the dust. Here, again, it is likely that cessation of smoking will have an important beneficial effect. This raises some very practical--and ethical--questions. It has been demonstrated that we can, at least in part, reverse the risk of lung cancer among individuals previously exposed to asbestos by cessation of smoking. Is it incumbent upon us to notify all those who we know have been exposed to asbestos to tell them of the added risk they have of death of lung cancer, compared to smokers in general, and of the potential of reversing that risk by smoking cessation? Dose-response Ample evidence has now been accumulated to indicate that an important dose-disease response gradient exists for asbestos, as for many other carcinogens. We will hear about this, I am sure, in some detail at this symposium. While the exact projections may be debated, it is clear that the less asbestos inhaled, the less the disease risk and, conversely, the more asbestos inhaled, the greater the risk. A cor ollary will be that avoidable exposure translates into avoidable disease. UCC 007910 3 An addendum to this subject has been added in recent years. W knew in 1964, and this has been confirmed since, that different exposed populations had variable disease outcome, as measured by mortality experience. One possible explanation was that different fiber types had different pathogenicity and after the Sew York. Conference, the experience of populations exposed uniquely to one or another fiber type was sought. This was not easily come by in industrial circum stances, due to mixed exposures. In our laboratory, we have been able to obtain information on two fiber varieties. First, we have been investigating the experience of 1,663 men who were employed in an asbestos products factory in Pater son, Hew Jersey 1941-1954. A great deal of information demonstrated that amosite was the sole fiber used in this plant, apart from some minor amounts of ehrysotile. Table 4 summarizes the experience of 332 men who began work 1941-1945 aad were still alive 20 years later, and were followed prospectively from that point to 1973. It will be seen that their mortality experience was very much like that of asbestos insulation workers. Amosite, apparently, did not have a unique poten tial to result in ocher than the anticipated asbestos-associated diseases. We have had the opportunity of investigating the experience of asbes tos insulation wockers in the Xew Yorx-^ew Jersey ares for two periods of time; one, in which employment began and continued when only chrysotile was used (before World War II) and a second group of men in the same union locals, in the same cities, doing the same work, employing the same work practices but exposed not only to ehrysotile but poten tially to amosite as well, which had by then been added to asbestos insulation materials. Tables 5-3 show that, for equivalent times from onset of exposure, no difference could be seen in the mortality exper ience of those exposed only to ehrysotile or to ehrysotile and amo site. Unfortunately, we have no experience with crocidolite exposed popula tions in our laboratory. UCC 007911 9 It may well be thac the question posed in 1964 was ouch too restric ted. The assumption was made that fiber type would be the major dif ference in explaining observed variations in the disease risk of various groups. It is now realized that exposure intensity certainly plays a very important role, perhaps a critical one. However, other factors may be of equal or even greater importance. I would go even further than Dr. McDonald (this Symposium) when he states that "While it is clear that, in experimental animals, fibres of different type but similar dimensions have much the same pathogenicity, various in dustrial processes could have a major effect on fibre size...." focus ing, as he did, on the size of the inhaled fibers as a determinant of pathogenicity. Other changes besides those in size can occur in the fiber during its journey from the time it is extracted in the mine to its use in a variety of industrial processes. Dr. Danger will address this question here later. Dose response, then, may reflect oot only the number of fibers inhaled, but various attributes such as fiber type, dimension, surface, structural alteration, etc. Conclusion When a death of asbestosis was observed in 1900 and recorded in 1906, it could not have been widely known. But it would have been difficult to overlook the serious potential of the dust when the careful clini cal studies and surveys in the decade after 1924 found that asbestosis was common among exposed workers, and that deaths could occur. De spite this understanding, the 1930s, 1940s, L950s went by with few precautions in trades in which there was asbestos exposure. Mor did accumulating scientific knowledge concerning the cancer potential of asbestos increase protective measures until the 1960s and 1970s. This Symposium again, as the meeting in Hew Tcrx in 1964, will still be science-based. However, it will also have the task of identifica tion and resolution of industrial, economic, social, political and ethical questions. Thus, there will be debate concerning the dimen sions of the disease legacy we now face as the result of our years UCC 007912 10 of failure--'exactly how much lung cancer or mesothelioma or gastroin testinal cancer or cancer of the larynx or other cancers or asbestosis--in shipyards, Che construction industry, transport, nines, fac tories, chemical facilities and refineries, power plants, insulation work or other trades. We will be asked whether levels of 10,000 or 2 million f/m^ of air (0.01-2.0 f/ml) will protect people in the future and we will not be able to answer confidently because few measurements were nude years ago to correlate with subsequent cancer experience. Still, we'll be able to give the key answer--that there is a "doseresponse" for all asbestos disease--the more asbestos, the more risk, the less asbestos, the less risk. But this discussion will not be able to answer the critical ques tion-should the use of asbestos be continued--if evidence will not be available that it can be safety used, that there will be vigorous insistence on all feasible safety measures; noc minimal controls but maximum capabilities. Would this prevent all asbestos disease? No--but it would avoid all that can be avoided, at least with what is presently known. It may well be that to do less than we can will prove unacceptable. Therefore, one perspective by which to judge this Symposium is that it has as its task the unique opportunity of decid ing who will live, and who will die. It is this decision which will answer the question of whether or not asbestos should continue to be used. UCC 007913 Deaths of mesothelioma Wwww if run 5wjih4m* ii Ofliai if Ciwun Deaths of lung tanner **** s* 'tv. IwO'.eiMS-f '3 a: ^ Deaths of asbestosls UCC 007914 A ; 77SC Table 1 Oca(A> .:mnn 17.31)1* A*nMua [ftMiiatiurt VVoi*.iir ert !htf Cntccvl Stales .ifivi Canada Jamaf\ :. I^AT-QccCfnnuf 31. 19*6 l:mJ*rty>n$ eauac of death rtAvirvftj BF; if!C Balm w* BKj 1 OCl Tool death*. ill cauin Total cancer, ill Cancer of tune P!*tiral fflcaoihcliuflu Peritoneal Mcaotnctnvnu. f.o.. Cirtetf or CiUCtff Jt Cancer r colon%-c:um Cancer in' larvtu Cirtcof of pharyn*. C.i/icw? of `iiJn* s\+l `ler cancer N,iiv.rtic\!iiWi v ii-iwu .-> l.-Mi ail . ittcr s..ii'^i l*5V9 319.* 105.6 * , . 7.1 u: }! ! a7 iO.I i; ..`i i * i:30.: t - :ri *+< 63 ill 0 \t zz <y [1 zin 1 55 \i is * ^ l .}* i E1 a *j 1 <A 1 ,f< :..'j 1.3? 13* a f* 153 l.is 1 <: T.*l :r :6 in* 1 :* 3 11! 'JZ : \M 1 *a ', a *;i -- -- 1 :m iM? 1 ;i NumPef oi Tten -- J 7 >00- Mutt-w,* 1 V k>l 1 'Hn.1 s ..lum1 -- 11^1 ' Eatneticd death) art ?acd aeon aAllii ^.UC new :irc L' S dciitn ntr fr*nn 'he Lj. 5. N,;tiue1ui Cenitff \ir i'JA*- ij?a -l..:.' iHt .iv. n aciiJMiwi. . .!v,:.i-" i . lie a-.lwrjl * m1ui.iI i< irt In L--I v' : 1I1. . .V ... . > i^,ini< flftH M.iiiiifl ..:it<>r`i 1)1 VmhiVf n( siknilii .:> .bi.i 11.mu ,.* ;. ...; i;.-... .1- UCC 007915 A ; 776 Tab!* 2 Sxpecced and observed deaths anong 632 Mew York-Mew Jersey asbestos insulation workers January 1, 1943-Deceaber 31, 1331 (14,547 Man-years of Observation) i'r.derlvia* Cause of Death Total deaths, all causes Total cancer, all sites Cancer of lung Pleural seso chelioaa Peritoneal tiescthelloma Cancer of esophagus Cancer of stonach Cancer of colon-rectum Cancer of laryroc, pharynx, Cancer of kidney All ocher cancer buccal cavity Mcninfectious pulmonary diseases, total ' Asbestesis All ac.'.er caus xn. ' 333 .2 63.9 L5.7 4* 1.6 5.6 9.2 3.1 1.4 27.3 11.0 333.3 Cbs. 532 238 105 14 36 1 13 26 6 2 29 50 s*6 Cii * expected deaths are based user, white rele age-specific :J.S. death races c: the 'J.5. Macicnal Center far health Statistics, 1343-1373 rates for specific C3use of deach for 1943-1343 were excrercleced from rates tor 1943-19;:. hates far 1379-1931 were extrapolated from rates for 1373-1373. * " Sates ere not eveilabie, but these have been rare causes of death In the general peculation. UCC 007916 A ; 7762 lafil* 3 Ovuih* dinony 17.400 Aaaentin instillation Worker* m United Stain and Cinmia. iaminry i, !967-0eesmeer 31, 19*6: Anaiym by Durumin fmm Qniei a( Oyraimn from t*n*ei - vm N. uf men yn of observe* (ion Eifl.' Lung cancer 0b*pre4 Au*m ore OEi I DC) i BKl iDC) P!tumr mewtftefioma No. ai > OCi Nq./l000 jenon- yean '8EJ ?emonai meseinetiema No, (BE) iOG Noj 1000 jenon- n'jri (SE) < to JO- 14 13-19 :o-n 2j _ *o-.w nJ.aj i*. - i. I'#0 9.043 9.904 1J4t 4JV4 .'..'-17 :,o i.:ott I.144 16.393 a M3 34.064 3I.3M 30.637 MJ94 3,403 J.IW JJdJ 0,7 :.7 i.s f7 0 :i.o rs.4 II-J s.r I7.J 0 0_ 7 J :.!} 13 r 3.40 39 <7 ? 103 M 5 00 n: 103 6 04 4J J7 3.64 *0 31 * 93 69 .*1 1 yy SJam* ire baaed niton white mflie afd-*'pv,.::<,'s L if -fis u' . S. NlliOfUl Center Tor nttaiin .^l.il r -s. i , <' ** y** ^.iTiuine lahii* nw lancn into eceount. H> 'Us--; Numeer of denifts eatejunrud jr'fwr r--v:Wj, t.tf J.lT 3..-4 *; J.J9 * 94 3 J2 :.m 0 a 1 A 13 9 tj 4 U 0 0 2 4 < 3 i 3 4 0 0 7.06 o.:9 0.43 0.71 :.*i ' .J7 :.w 00 00 30 3 19 J 13 6 19 c 16 3 :s f 0 0 3.09 0. :0 o.n ! 99 \ i 36 < if Scm ivuupiv fii'iwM*m-f)on autonsv. iurffiCat. 1 OCi. Number >f jcm n* i reearuec fmm gemn uttVifmairon jfliy. csfr:ncr-ie UCC 007917 A ; 7763 Tibi* i Oaach aaar.g 532 sac si; a asbascas factory workers 1961-1977, evaney or nor# yaars from ansae of aanloyxanc All causas Cancar, all aleas lung cancar ?laural easechalices ?rlsanaal aesochalices Gastr a-in c as claal LarytHC, oral, pharynx Xidnay Ochar Asbascasla .411 a char causas Oaatha ZXDtCZtd Obsarrftd 133.6 30A 33.4 116 10.1 - 3.0 1.6 0.3 12.9 60 7 7 16 5 l 19 * y < n 13 170 * 3asea an data an 0.5. N'aci anal Cancar for Haalrr. acacijsics far 7e'J Jarsay vhica zaLu . UCC 007918 A 7 / 76 Table 5 Onsat af asployaanc, Jt.Y.-S.J. asbestos issulaeion vor'itars ^uiabcr 0 0 Year of onset 1953-1962 1943-1952 Ilusber 421 412 Asbestos (Cbrysotile Chrysocila-aaosits) 40 1934-1943 145 1929-1934 140 1924-1929 108 1919-1924 199 3e/ore-1919 652 0 0 0 (Chryaoeila) 0 0 833 UCC 007919 k i 776b Tibi* 6 Mortality experience of 1,153 M.T.~X.J. asbestos insulation voricers, Jan. 1, 1943-Dec. 31, 1981 Less than 10 wears fron onset Chrysocll* 3eiora 1943 325 1,970 # Sxnected Observed 9.0 9 1.1 2 Exposure Onset number Man-wears Causa of daath Total, all causes Total, all cancer ! Chrysocile; chrysosAle-anosite 1943-1962 333 16,414 Exs toted Observed 42.5 24 3.5 5 0.2 0 tuns 1.2 2 ---- 0 Pleural neso. ---- 0 ---- 0 Peritoneal neso. 0.3 0 G.Z. cancer 0.3 1 0.6 2 All ocher cancsr 3.5 2 ---- 0 Asbescosis ---- 0 7.9 7 j All ocher causes 37 19 * Expected races based upon voice nala age-specific L'.S, death races of che 2.3. national Cancer cor Health statistics. UCC 007920 ft ; 776 Table 7 Jiorcalicy experience a 1,300 M.Y.-N.J. asbestos insulation workers, Jan. 1, 1943-Dec. 31, 19SL 20-34 years from onset Chrysociia Bafor* 1943 361 6,366 # Sxneeted Observed Exposure Onset timber han-vaars Causes of death Chrysotile chrysocile-anosit# 1943-1962 739 6,135 Extectad Observed 30.4 13.5 119 53 Total, all causes 1 Total, all cancer 1 -3.7 11.2 63 23 3.0 3.3 -- 66.9 26(22") ^ (52) 13 j 3! 63 lung Pleural rase. Peritoneal neso. 0.1. car.car .All other cancer Asbestosis All ocher tausas ! ! ! i.3 "" -- 37.5 15(242) ;C62) 7 31 bettered ratas based upon white rale age-specific J.3. death 'anas or zr.t U.S. .'Jacionai Canter for rlealch Statistics. A ;7767 UCC 007921 Tabl* 3 Mortality expariancs of 571 JT.T.-K.J. asbestos insulation vorkers, Jan. 1, 1943-Dec. 51, 1932 35 or more veers frog onset Chrysoeil* 3fort 1943 504 3,311 * txsectsd Observed 253.7 404 49.3 133 Exposure 0ns at Xumbar Mar.-v*ars Causes of daacb To cal, all causes Total, all caccsr Chrysoeila chrysacile-amosic* 1943-1962 67 43 Exgeeced 0.9 0.2 Observed 3 2 12.5 12.3 24.J -- 79(20*3 1303('158=)' 33 23 43 Luag Pleural aaso. Peritoneal nasc. 0.2. cancer All ether cancer Asbestoses 0.1 0.04 0.1 ---- 0 0 2 0 219. - 178 All achar causes 0.7 1 * EaTpsccsd :i:ts based icon vftisa sals s^s-sceciiic . 3, itash racsi 3: ;.i "a. cicnal 2 an car zz r Healer. Scariscirs. A .'7768 UCC 007922 * '7763 UCC 007923 AbJtSJtiSTOS IXN lbKiNAiiUiNAJL AbbOUiAJL iUiN (Limited by Guarantee) 68 GLOUCESTER PLACE, LONDON WiH 3HL -"T ' ' memorandum Qj TO: All Member Associations Members of Executive Committee FROM: Sir Neville Stack RECEIVED APR Z 6 1979 UCC-CALIDRIA NIAQAftA FALL". y. AIA/20/1/10/HAS 11 April 1979 ESTIMATES OF THE FRACTION OF CANCER IN THE UNITED STATES RELATED TO OCCUPATIONAL FACTORS (THE "ESTIMATES" PAPER),' (The following deliberately over-simplified comments on the above paper are provided as background material for laymen) A;805J The quality of scientific publications often used as a basis for ' regulatory action by the United States Departments of Health, Education and Welfare (HEW), and of Labor, had been sternly criticised by a wide range of academics and others well before the publication of the HEW paper "Estimates of the Fraction of Cancer in United States Related to Occupational Factors", often referred to more briefly as the Estimates Paper. ' The Estimates Paper has received much detailed criticism, not only from spokesmen for the various industries alluded to in that paper but also from academia, the scientific press and even from other US Government agencies. The Estimates Paper has been criticised on many grounds but the three most fundamental are:- Using misleadingly high estimates of the number of people in a work force exposed to different occupational carcinogens. Using further misleadingly high estimates when predicting the number of this exposed workforce which will develop cancer from their exposures. Frequently assuming that all those who are in any way exposed to potential carcinogens are exposed to equally heavy concentrations; this ignores the fact that most published studies are based upon the experience, of those most heavily exposed. Critics have further observed that, were the predictions of the Estimates Paper sound, the "epidemic" of occupationally related cancer in the United States expected by the authors of that document would already be occurring - and it is clear, on the basis of data published by the US National Cancer Institute, that it is not. The authors of the Estimates Paper have asserted that they believe its reasoning to be sound and its conclusions justified but have not, so far, replied to their critics with any rigor or precision. The authors of the Estimates Paper note that asbestos is a "well-studied example" of an occupational carcinogen and, in developing their predictions, devote much attention to the asbestos exposed workforces of the World War II ere. U(X All Member Associations Member of Executive Committee 2- - AIA/20/1/10/HAS 11 April 1979 The Paper, and the furore it has engendered, are of concern to AIA. The AIA does not wish to enter the dispute, already involving so many authorities from so many different sources, but is resolutely of the view that it would be most improper for the Paper to influence Government policy, in the US or elsewhere, until it can be subjected to adequate peer review. Sir Neville Stack cc Chairman, Medical Advisory Panel Dr. H.C. Lewinsohn Dr. P. Kotin 4 `go UCC 007925