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Exposure t cancer: a rea British Journal nt Industrial Medicine 1988:45:"/5--82 d the risk of gastrointestinal D A EDELMAN From Medical Research Consultants. Inc. Chapel Hill. .Worth Carolina. CSA abstract In 1964 it was first reported that asbestos workers had a higher risk of gastrointestinal cancer. This notion has persisted despite several studies that have found no increased risk. The risks of gastrointestinal cancer to workers exposed to asbestos were reassessed, based on the results of published studies on 32 independent cohorts of asbestos workers. Not all studies provided risk estimates (SMRs) for all gastrointestinal sites (ICD codes 150-159). No consistent evidence was found to indicate that exposure to asbestos increases the risk of gastrointestinal cancer. Generally, the higher SMRs came from studies conducted in the United States or Canada and might reflect factors not related to exposure to asbestos. In studies in which asbestos exposed and non-asbestos exposed workers were evaluated the SMRs were not consistently higher for the group exposed to asbestos. There was no apparent dose response relation between accumulated asbestos dose and the risk of gastrointestinal cancer. It is concluded that there is no dose response relation between exposure to asbestos and risk of gastrointestinal cancer, and asbestos workers are not at an increased risk of gastrointestinal cancer. -- ~ " " ~~ ~ In 1964 SelikolT and coworkers reported on the mortality experience of 632 asbestos insulation work ers in the New York metropolitan area.' The studyshowed that these workers had an apparent excess of gastrointestinal cancers: there were 12 deaths from gastric cancer compared with 4-3 expected (standar dised mortality ratio (SMR) = 2-79) and 17 deaths from cancer of the colon or rectum compared with 5-2 expected (SMR = 3-27). 1'th SMRs were significantly greater than 1 (p - 05). indicating an increased risk compared with all United States white men. In the 24 years since the publication of this paper the notion of an increased risk of gastrointestinal cancer to asbestos workers has persisted even though several other papers have failed to substantiate it. In 1978 Miller reviewed reports relating to exposure to asbestos and the risk of gastrointestinal cancer and concluded that they were causally related/ Another review was published in 1985 by Morgan et al who found some raised risks of cancer to some parts of the gastrointestinal tract but believed that these rises were not related to exposure to asbestos.' The present paper provides a m^rc Hfija^L^nnii i.";ffWiTii irUrc of gastrointestinal cancer to asbestos workers and is based on data from published studies. Studies that evaluated risks of gastrointestinal cancer from `by stander" expo-tire including exposures from asbestos contaminated drinking water were not included. Study methods Thirty two cohorts of asbestos exposed workers were idcntihcd that pros ided data on their risks of gastroin testinal cancer' . tabic I summarises the types of fable 1 Ot t ufW'ihn t t </ S.- IS .it X .l/lm Is filxlfsi. . XxPc'if' lllsill.l'lfll AO's (m* n.i^K' P.jpct mllhiMjj, rwu.iv* Mtiuiis: .iM mi \lU`v .tv.d PU*d;M *' H........ K.i.ho.iU >*hipv.iid Utxw.iul Woivei-s :fc*pttcsl : '- *' p.uici*. .ippl' "M J * * :..w's ... 'Ms. .: V \ ..( i . * ' - It 0 nKJ o nL/ ,-ir 18--0000626 76 Table 2 Standard ntortu(tt\ ratios S\f R\ lor oncer of various ?astrotnre\imai sites' Rctercmc ICO ISo 0oi/i/weMs 6 I3 l> its IS I SfuntmO /So/'/ Oc'-nphaaio \!uttttnh L mini Sfufv' C '/Ut/U'' ISS { nmn 24 Ill\ 1 25 29 *0 r ft 5 = 2 *2* n 4 2 " a 2 H1 I.X i: * = l 4; i5o io2 4 si:-* < 2 n = | 'u io-2 - j x2" 4 ft 4 4 = o M 4 n * 'ft s 44 1i 12 2 2o - i (HI r 14 .0 :i 25 2ft - 10 14 2S 1 I 41 = n *l '4 2*:-s \ oo ;2 - { ii.h "5 - t) 44 4 5 * i ;o L K otuiiv^ 55 36-1 = 0 41 4ft - i Ih 4 4 5 * 0 45 Studies tntm nf/ier < >u/urit'\ M s 5J = 1 M 1 5* stir v 4 ; = o "o 41 *1 ft = n <* " ft ft* 1 05 x xnx = u se *- I ft (ft * S O 5ft1 ft a u = ( si Gl Gu>(romteMinai *P <lllis. 1 sit. ISl. IJ1-IJ4. 151-154 a:n(cMinai ' 150-- 15X: digestive. probuMv l.'D-t?" occupational exposure. Data on some ot` the cohorts hate heen published numerous times auBi the illusion that there is considerably more evidence on the risks of gastrointestinal and other cancers to .-.shesios workers thtm actuallv exists. For each cohort the most up to dale data have been used. Studies were included in the review if ihcv provided data on the risks of cancer to anv gastrointestinal site i International Clas sification of Diseases (IC'D) codes Ifu L'di. Studies that gave P\1 Rs (proportional mortahtv ratiosi or odds ratios were not included. If causes o( death according to death certificate information and the be'i evidence ofdeath based on medical and oilier ev idcmc were given onlv the death certificate data were used The statistical significance of the SMRs was mes sed assuming, the observed mini her of deaths I'ollowco a Poisson distribution. Statistical tests of'igmiicaucc (two sided) were performed using the procedure described hv Bailur and Ederer. The risks of gastrointestinal cancer i IC'D codes 1 *n If"-)) to asbestos workers were evaluated bv consider ing the following: (I) The SMRs lor gastrointestinal ca comparison of.SMRs lor gastrointestinal ... asbestos exposed and non-exposed worker evaluation of the dose-response relation be risk of gastrointestinal cancer and some m asbestos dose, SVtRS FOR (.(ASTRO! S TESTIN' A L CANCER Table 2 shows the SMRs for cancers o gastrointestinal sites for each of the 32 eor table separates the studies into those conduv United States, the United Kingdom, and ot tries. Not all studies gave SMRs for all gastro sites Some studies identified the cancers "gastrointestinal" (GIi without further ina to which IC'D codes were included. Table 2 shows that, except for one studv e Utiucti States Canadian studies were anv of; 'ignmcanilv ip < iM)5i greater than I. Fori1 for which there were data from the Unite Canada and other countries, the larges i regardless of whether or not thev dtffercd sig Exposure to asbestos and the risk /1tasiromtestmalcancer' a reassessment - 1 onnnued tH (,thm rt>t turn ISO /// Ot.v>Ptoutu\ i ohm. \mail tnie\UtU' rectum If Pam rcu.\ 4 101 .' - 1) 'X*a 5 2 - : i:* yi JO 5 * i " 16 :96 i) 54* 30 X1 0 XX 10 ' A = i j: 47 = 0 4A 4 * Ai - :4A: i 0 : oo ;o.'' = i \n as = l *9* 4<J ftj _ n -aj **o 5: S 1 U4 19 1 1 = 1 II IX 19 A 1)92 1X = 4A 15 5 ' 4?* 3 J 1 = 0-46 '4 51 A 1 14 :a r i _ i **, 54 47 4 * 1 13 2"A r: i ~ l 01 50-1 * 0 50* NN J9 9 s 1 JS* xj '.x: -= 1 OA 101 A9-3 = 1 4A*" u: 134 A = l) 4X ,*: iw X * tT. 1 nj 11 5-9 1 XA* :o JO-3 9 0-AA so 'OX = 1 41 IS 1 5 IA - 1 19- \ 2 45 1 n: - (141) r 15J a i n i) 1 >K - 0*00 14 19-3 -= 0*4X' 14-9 - 0-4-* til II) 9 5 = i 05 4 : *: - 1 i5 11 X" s i :a 10 :o = (| 44* 63 Xj 8 II **A* N l - i 55 from I) occurred in the United States Canadian studies and the smallest occurred in studies conducted in other countries. This was true for all ICD codes except for the GI category. Since m most studies the expected number of deaths was calculated from national death rates, it might be hypothesised that in countries other than the United States and Canada the workers exposed to asbestos and national populations are more homogeneous and less subject to factors that might confound the relation between asbestos exposure and the risk of gastrointestinal cancer. The data in table 3 summarises the SMRs given in table 2. Ten were significantly greater than I (p < t)-05) and nine were significantly less than I (p < 0 05). sxirs fur xsiusros fxposfd and no\VSItf-N ros F\ Pc JXFD WORKERS Six studies provided gastrointestinal cancer SMRs lor non-asbestos expired workers I table 4). No consistent pattern in the relative m/c of ihc pairs of SMRs is seen for the asbestos exposed and non-ashestox exposed workers n \ of the 12 SMRs shown in the table were lower loi -itc asbestos exposed workers. The data presentee ; table 4 do not indicate any increased risk ol gastrointestinal cancer for asbestos exposed com pared will! non-asbesios exposed workers DOSE RESPOs.SK RELATION' BE TWEEN EXPOSURE TO XSBFSTOS AND GASTROtNTI STtN AL (AMTR Dose response data were given in nine studies. The relation between the risk of death from gastrointes tinal cancer, lung cancer, and in some eases other diseases, and the accumulated dose of asbestos is shown in the figure ra gt. No attempt was made to convert accumulated asbestos dose to common units. Deaths from lung cancer are also shown since many investigators have reported a dose response relation between the risk of lung cancer and asbestos dose.1' None of the studies listed in the figure computed dose response relation for lung cancer for workers with different lifetime smoking habits. Failure to do this could obscure a dose response relation, especially if the 002047 18-0000628 "8 Table 5 Summary at SMRs divert m tuble - ta> 150 151 150-151 155 154 155-154 150-154 15* 15iM54 Gastrointestinal Studies 0 4 s 4 t lo in - ii 6 Median S'\f R 1u 1 00 i:: 1 44 1 09 1 IS 1 08 0-49 1 06 1 05 Runze of SUR* 0-64-2 62 o-r-:o4 091-1 82 0-56-::: 0-^-1 24 0 74_; M> 0*4-: 46 0-00-2 97 047-| 52 0 49-1 55 SWR* < t p < n it* 0 1 0 1 0 2 1 0X X Edelman SUR* >1 p< l 0 2 n 0 2 2 1 2 0 smoking habits of the asbestos workers differ from those of the populations with whom the asbestos workers are compared. The figure shows no consistent dose response rela tion for gastrointestinal cancers. Although the data from some studies suggest dose response relations, they are most probably an artifact of the way in which accumulated dose was measured. For example. .McDonald et al in their study of miners and millers show that the SMR for colon and rectal cancer increases with accumulated asbestos dose/4 They also show that the same relation exists for deaths from respiratory tuberculosis and cerebrovascular disease. In another study of miners and millers death rates from lung cancer, gastrointestinal cancer (ICD 151159). tuberculosis of the lung, and cardiovascular disease increased with increasing accumulated dose of asbestos. " Since diseases such as cardiovascular dis ease and respiratory tuberculosis have not been associated with asbestos exposure, it appears that the reported "dose response" relation are in fact a measure of other factors unrelated to accumulated asbestos dose. Discussion In evaluating the risks of gastrointestinal cancer to workers exposed to asbestos several problems were encountered. (I) The studies reviewed made no attempt to evaluate gastrointestinal tract death rates in terms of any of the known risk factors. 12) Some studies identified the site of the gastrointes tinal cancer by an ICD code, others did not. The different ways in which the ICD codes were combined precluded comparisons of cancer risks among the 52 cohorts. Table 4 Comparison ot SMRs lor gastrointestinal tamers /root studies that included a group of Markers not exposed to asbestos Rcrcrcm r Oi t upattomu st'oup C'jtu cr \iie 4*he\nt* worker* Other workert ft Shipsard workerst Oesophagus, stomacn. v.olon. rectum 45 47 s n-96 i: Insulation board manufacturing Stomacn Colon Rectum " "s h 44 4 t2 = 044 = ir - 1 24 15 Asbestos cement factors GI i IC'D 1 i-- 1541 4 \ r5 = : 46* :s Shipsard workerst Oesopnaeus 1 ! -M = 0 "l Stomach h f-i" - i 05 Colon ' 4 <4 s 1 M Rectum t 2 '4 ) 114 Pancreas 1 ; - i) no *4 Anthophviltte miners* GI i ICD i .'11-1591 14 a - U 4~* 55 Asbestos production (building products, melton materials, textile products) GI i IC'D 150-1*91 V < *': - Hh IS 25-6 - 0-70 4 ' 5 - 1-59 2 1 4 = 1 4i 0 11 -- 0 00 1 1 64 = 0 61 1 x_^s = 0-18 51 :i 54 * l 45 14 10-49 = 1 si5 * 72 = 0 68 \ 4 2a = 0 '1 4 144 - 0-60 22 x = 0 96 GI = Gastrointestinal. *p < u 5 fNonexpos<d worker* included workers who had no or ai most minimal likelihood .i a-mesi.ix exposure ^Separation into asbestos reposed and non*exposcd was nude on tne basis ot Jcv.r.r".ou% i ovwjpjtiort' and whether they brought the workers into contact with asbestos. ;Non-e\pose\l group consisted of subjects selected imm an agricultural area *m no mines *r other :ndu>ir:al plants This croup was matched to the asbe>to> workers by age and and lor date oi death tor those worker *no nad J.cd Nonex posed group consisted of workers irom cotton textile plants 4 For the exposed group the SMRs were >imilur lor JiiTcrcni l.itencs intervals i*-w 2i-2g s -.car' srom tirst cmplosutcnt i and durations oi exposure t 15. ? 15 yearsi For the non*c\poscd group the SMRs were similar tor dolerem Gtctu.* intervals 002048 l8_0000629 Exposure to asbestos unit tin- risk ot gastrointestinal cancer: a reassessment 00204:j Cohorts 1 Frtrhon products manufacturing 2 Textile manufacturing 3 textile rt)d friction products manufacturing 79 O CO CO o o o o / CO !<(> Edvbnun (.') Although mesotheliomas were identified in most studies, in some it was not clear whether these cancers were included or e\cluded from the croup of gastroin testinal cancers, including the group of cancers under GI and ICD codes 150-159. (4) Since there is a high likelihood of misdiagnosing mesotheliomas as gastrointestinal cancers and since some studies mas have included mesotheliomas among the gastrointestinal cancers, the reported SMR' mat overestimate the true SMRs for gastroin testinal cancers Numerous articles have identified factors that might place an individual at an increased risk of cancer to anv gastrointestinal site ilCD codes 150 159). These risk factors include smoking; diet including alcohol, beer, and beef, familial inheritance factors--for exam ple. adenomatosis, history of ulcerative colitis; and place vif residence. Small but significantly increased relative risks (relative risks less than 2. for example) may occur because of spurious associations or failure to account for the effects of other risk factors, such as diet or smoking, that might affect the relative risk. For relative risks that lie between I and 2 it is extremely difficult to disentangle the various contributions of biased information, confounding of two or more factors, and cause and effect. Doll and Peto note that the simplest and most likely explanation of the excess mortality of gastrointestinal cancer reported for asbes tos workers in some studies is from the misdiagnosis of cancer of the lung and mesothelioma of the pleura or peritoneum. ' In studies that seek out moderate risks considerable care must be taken both in the analytical methods used and in the interpretation of the results, since the biases inherent in poorly controlled and designed epidemiological studies may exceed the mag nitude of the effects that could be observed. Doll and Pcto noted that unless local death specific rates are used. ratiostSMRsi under 1-5 nia> bo largely or wholly artifactual. ' The importance of using local death rates is illustrated hv the study of brewery workers reported by Dean ci al. ' These investigators found a higher SMR for colonic cancer based on all Ireland death rates 11 -65. p < 005) than the SMR based on death rates in Dublin county borough (1 Iff p > O-IOl. One major difficult} with the dose response data provided in most studies is that the accumulated asbestos dose (either in terms of the quantii} ofdusi or asbestos fibres) is computed for workers in terms of their average exposure in different jobs multiplied h} the duration of exposure. This procedure does not differentiate between workers with high exposures of short duration or low exposures of long duration. In addition, if there are no major differences in level of exposure between workers in different |oh categories the procedure will result in people with longer dura tions of exposure being placed in the higher exposure groups. These higher exposure groups will tend to include the older workers who are at an increased risk of death, regardless of their exposure to asbestos. One approach to the evaluation of dose response relations that would not suffer from the above defietenc} woulu be to compute mortality risks (SMRs. mortalit} rates, odds ratiosi for cohorts of workers who experienced relative!} constant doses of asbestos over time. The data in the figure show no consistent dose response relation between accumulated asbestos dose and lung cancer. This certain!} raised questions con cerning the validity of this reported dose response relation. One problem with the lung cancer dose response data is that the lifetime smoking habits of the asbestos workers were not taken into consideration. Even if the smoking habits of the asbestos workers were known similar information was not available on the comparison populations. Since rates of lung cancer generally increase with the duration of smoking, one may expect to find higher SMRs for higher accumulated asbestos doses, especially if the accumulated asbestos dose is computed as a product of the average concentration of asbestos and duration of employment. Since in most of the studies the accumulated asbestos dose was a function of the duration of employment, the dose response relation between lung-cancer and accumulated asbestos dose might more correctly reflect a dO'C response relation between lung cancer and duration oiNmoking. If asbestos has a carcinogenic effect on the gastroin testinal tract it should be possible to show this effect through lifetime ingestion studies in laboratory annuals. Selikolf and Lee noted that "attempts to inuuce carcinoma in the intestinal epithelium or me'vuhelioma in the peritoneum by feeding asbestos have been uniformly disappointing . . . In a later review of published studies of asbestos administered by mouth Condie concluded, "the bulk of the experimental evidence indicates that the long-term, high-level ingestion exposure to various types of asbestos fibres laded to produce any definite, reproducible, organ-specific carcinogenic effect."'1 Condie cued the evidence from 12 studies that had evaluated the carcinogenic effects of ingesting asbes tos. In two Mibv.'quent life lime -tuuies of asbestos ingesiion hv K'44 rats and Syrian golden hamsters McConnell i; M reported no increase in the incidence of gustroiniesiin.tl cancers''' and rea(firmed the con clusions ofCondie.' 'A ard i (ul evaluated the effects of intrugu'iically administered ashc'lO' in F.'J4 rats a Some group' of rais ai'o received -uheutuneous injection' of a/oxymethane (AOM). a known gas trointestinal carcinogen. The proportions of rais ihai developed mic'imol tumours were 77-1 and 002050 /man ad os ,,T.\ ICC n- .11 id Exposure in asbestos am/ tlw risk nl casirointestinal cane cr- a reassessment 81 32-6 o in the AOM (48 rats). AOM plus amosite asbestos (48 rats), and amosite asbestos (49 rats) treated groups, respectively The authors noted that F344 rats at the same laboratory "rarely develop intestinal tumours." Several investigators have sug gested that the feed of the rats who received amosite might have been.contaminated by AOM. thus giving an erroneously high rate of intestinal tumours.41 The criteria that should be met to establish cause and effect relation have been stated in many different ways bv numerous investigators. These criteria as restated bv Sehkoff and Lee* are that: (1) a statistically significant association be establi shed between exposures of subjects to the agent (asbestos) and the subsequent development of the v ndrome: 12) some degree of dose response relation should be demonstrable: (3) in the event that the agent or its metabolic product can be shown in tissue, the concentration in exposed subjects should be greater than in unexposed subjects: (4) the demonstration of pathological changes in animals after exposure to the agent, similar to those seen in man. would strengthen the evidence for causation, but the failure to obtain such changes would not negate other evidence supporting a causative relation: and (51 the role of numerous attendant circumstances capable of influencing the appearance of manifesta tions of the disease initiated by the agent should be evaluated. The present evaluation found no consistent statis tical association between exposure to asbestos and gastrointestinal cancer, a dose response relation was not apparent, and results of ingestion studies in laboratory animals were negative. In terms of these criteria the findings of the present evaluation do not support a cause and effect relation between exposure to asbestos and gastrointestinal cancer. The third criterion was not evaluated since studies have not been conducted to evaluate the concentration of asbestos fibres or bodies in the gastrointestinal tissues of asbestos exposed and non-exposed subjects. Although various factors associated with an increased risk of gastrointestinal cancer have been identified, none of the 32 studies made any adjustments to the risk estimates for gastrointestinal cancer for any of these factors. Based on the epidemiological, clinical, and experimental studies evaluated, there is no evidence to support a cause and effect relation between exposure to asbestos and cancer of any gastrointestinal sue. Requests for reprints to Dr D A Fdelman. Medical Research Consultants. Inc. 6 Windine Creek Lane. Chapel Hill. \C 2"514. References 1 SehkofT IJ. Churg J. Hammond EC Asbestos exposure and neoplasia JAMA 1964.188 142-6 2 Milter A 8. Asbestos fibre dust and gastrointestinal mjlicnancics Review of literature with regard to a cause effect relationship J Chnmtt Ots 197X.3I.23-?? ? Morgan RW. Fohuri DE. WongO. Asbestos and gastrointestinal cancer A review of the literature. H/J Met! I9X5.M3'W*-5 4 Hodgson JT. Jones RD Mortality of asbestos workerxin England and Wales I97I-XL Br J hut Med 19X6:43 I5K-64. 5 W'onowttz HJ. Lange HJ. Beierl L. et at. Mortality rate** in the Federal Republic of Germany following previoub occupational exposure to asbestos dust, tnt Areh On up Environ Health 19X6:57 I6l-?l 6 Kolonei LN. Yoshizawa CN. Hirohata T. Myers BC Cancer occurrence in shtpyard workers exposed to asbestos in Hawaii. Cant fr Res 19X5:45:3924-8 * Ohlson C-G. Hogbtedt C. Lung cancer among abbesios cement workers. A Swedish cohort study and a review dr J Inti Med 19X5.42.397-102. x Hilt B. Langard S. Andersen A. Robenberg J Asbestos exposure, smoking habits. and cancer incidence among production and maintenance workers m jn electrochemical plant. Am J ind Med !9K5:8-565-77 9 Pcto J. Doll R. Hermon C. Binns W. Clayton R. GofTe T. Relationship of mortality to measures of environmental asbes tos pollution in an asbestos textile factory Ann Oteup Med NX5.29 305-55. 10 Cookson WOC. Mubk AW Glancv JJ. ei at Compensation. radiographic changes, and survival in applicants for asbestosis compensation BrJ hut Utti 19x5.42.461 -X 11 New house ML. Berry G Vagner Jt\ Mortality of factory workers incjsi London l9?3-xu Br J hut Wo/19x5,42 4-11. 12 Acheson CD. Gardner MJ Winter PD. Bennett C Cancer in a factory using amosite asbestos Ini J Eputenuot 19X4:13:3-10 13 McDonald AD. Fry JS. Woolley AJ. McDonald JC Dust exposure jnd mortality in an American chrysolite asbestos iricnon products plant Br J hut Wo/l9x44l 15I-7 14 OhlsonC-G. Klaesson B. Hogstedt ( Mortality among asbestos* exposed workers m a railroad workshop Stand J U ork Enurtui Health I9.x4.l0 2X3-91 I* Fmkelstem MM Mortality among employees of an Ontario jsPesios*vcmcni Ijctorx Am Re\ Re\ptr /)/ I9X4.I29 **?4-ft| 16 McDonald AD. Fry JS. Woolley AJ. McDonald J Dusi exposure and mortality in an American chrysolite tcxiite plant. Br J hut W. ,/|9.xt.4(Mx|.` I* Berrv G. Newhou>e ML Mort.iliiy oi worker*, manulactunnc inctu>n materials using jshestos Hr J hut W/ 19X3.40 I 15 Mi.Donald AD. Fry JS. Woollcv AJ. McDonald JC Dust exposure and moriaht' man American luctory jsingchry sonic, amosite. and cri*vidolitc in mainly textile manuiuciuring. Br J hut \tvd Wx;.?9 hx "4 Thomas HF Bcnumin IT. Elwnnd PC. Sweetnam PM Further ttdlow*upstudv oi worker* trom an ashesuw^ement laciory Br J hut Mt,119X2.39 2"-o 20 AthcMin ED. Gardner MJ. Pippjrd EC. Grime LP Mortality of twii croups oi women wno nunuiuctured gas musxs Irom .hrxMillie and crocidoluc asbestos jaiuccursollow-up Br J hut Med 19x2.39 144 \ 21 Berry u Mortalitv ol workers wC-micd by pneumoconiosis medical panels a* having j*pc>U'sis 5?<w ~ J hut Mat lvxt.38 22 Fmxelsiem \l Kumjc R. Suranv (i Moriainv among worker* receiving compensation lor jshestoos m tlntano ( ,/n \te%l it,,.. / 19x| 125 259-h2 2* lones JSP Ponlev FD. Sawle CiW , * ,u The ..onsequences ol exposure io asbestos Just in a wartime ga**niask factory In Wagner JC . cd Bio/n^ua. / mnnr,u tthn Gencvj. International Acency lor Research on Cancer. Wxiih**-?? ^a-0000632 x; v, py^l N* *n i M MJ),.n,nJ Jt L.JJell FDK.GiM'nG'V Ev-xn GE. M^Don^J \D Duvt exposure and mortality in*hryotiIemtmng. I 19-'. BrJ hul UiJ lx37 I 1-24 _ < Sci'k.'ir IJ. SciJmjfi H. Hammond EC Morialnv 1,1 .iCareiii .mming amonj amoMie jheuv. uuor> "orker> J i nu.' lu-i lxxil.*S 507-1J ,, ......... (. E. Coles RM H' Kkvard. Desunport: 1X47 mor- uln/xudv In Wagner JC. =U ../ rife. o / mweral cents j Inlcrnationai Agents for Rexardi on Canter, laxii'p 31 i Sei publ No 30 I - HuenesJ Weill H Lung cancer risk associated xnh manufacture ..pc,,os .emem product.. In. Wagner JC. ed. Bint,.total ,./ mater,it tthrei Genesa. Inlernalional Agents lor Research on Cancer. IVKOor-35. (Sci publ No 30.1 :s Pumom R. Vercelh M. Merlo F. Valeiro F. Sami L. Mortality among shipyard ssorkers in Genoa. Ilal> Inn \ I" -tiui/ Sit 10'U 330-353-" 39 Henderson V. Enierlme PE. Asbestos esposure. factors associated *uh exceed cancer and respiratory Ut^ca^e mortality I/m VY wsm 19-9 330 i t-:a tp Hammond EC. Selikotf IJ. Seidman H. AsbeMos exposure, cigarette smoking and death rates. Ann V) lead Su 19-9.330 473-90 " M Rubino GF. Piolalto G. New house ML. Scansetti G. Are>im GA. Murrav R- Mortality oi chr>sotile asbestos workers at the Balangero Mine. Northern Italy BrJ /mi Uni l9**9.36 I.S`r-94 >3 Nicholson WJ. Sehkoff IJ. Seidman H. Lilts R. Formby P Long* term mortaiuv experience of chrwmle miners and mtllers in Thettbrd Mines. Quebec. Ann \ > AuitiSu 19-9.330 11-21 Edelman n Weiss W Mortality of a cohort exposed to chrysotile asbestos J Oitup Med |9^.|9 '?7-W U Meurman LO. Kiviluoto R. Hjkamu M Mortaiuv and morhijnv among the working population of anthophy Hite Jshesios miner* ,n Finland. BrJ hit Med I9U3! 105-12. 35 Enteriine PE. Kendrick MA Asbestos-dust exposures at various levels and mortaiuv An h En\iron Health \'k>1 15'I.M-b '6 Bailar JC. Ederer F Sigmncanve factors r*r the ratio oi a Poiwn variable to its expectation 8onetni \ l9M.20`b59-43 J7 Browne K A threshold for jsbestos related lung cancer. 8r J hut Med I9KP.43 55ft-X 3X Doll R. Peto J J /*%/% Ellei t* ntt heuith >n exposure to a\he\tns London HMSO. 19*5 39 Dean G. MjcLennjn R. McLoughlm H Shelley E Cause ot'Jeath of blue-collar worker* at a Dublin Brewerv. 1954-.'^ 8r J Cumrr 1979;40 5X1-9 40 Seiikotf IJ. Lee DH K Asbestos ximldixs use New ^ork. Academic Press. 19-9 41 Condte LW Review of published studies of orallv administered asbestos Environ Health Perspeet l9h3.53.3-9 12 McConnell EE. Shefner AM. Rust JH. Moore JA Chrome effect* ofdietary exposure to amosite and chrysotile asbestos in Syr-jn golden hamsters Environ Health Pcrvpcti 19X1.53 11-25 43 McConnell EE. Rutter HA. Llland 8M. Moore JA Chronu. effects ot dietary exposure to amosite asbestos and iremome n F544 rats. Em iron Health Pervpeet l9X3.53.2",-44 ( 44 Ward JM. Frank AL. Wenk M. Devor D. Tarone RE. Invested asbestos and intestinal carcinogenesis in FUa rats. J Em mm Pathol T\aol 19X0.3 301-12. ' Correspondence and editorials The British Journal of Industrial Medicine wel comes correspondence relating to any of the material appearing in the journal. Results from preliminary or small scale studies may also be published in the correspondence column if this seems appropriate. Letters should be not more than 500 words in length and contain a minimum of references. Tables and figures should be kept to an absolute minimum. Letters arc accepted on the understanding that they may be subject to editorial revision and shortening. The journal now also publishes editorials which are normally specially commissioned. The Editor welcomes suggestions regarding suitable topics: those wishing to submit an editorial, how ever. should do so only after discussion with the Editor ! 1 j . 0n 7n^ O ^ KJ U. 18-0000633