Document rxd98D6J0e8qZpjpYLJX9JXma

In'Mi" /. Srh/mll. ,M/); C,u\ii> 1 Luninmiil, Si I), mill Imnli f.7r//ig. i\ll) Asbestos insulation woikets, as a group. have a high risk of dying of bronchogenic carcinoma (about seven or eight times expected). We have observed 3 70 such work men from Jan 1, 1963 to April 30, 1967. Our findings indicate that asbestos exposure alone is not the entire explanation. Of 87 noncigarette smokers, none died of bronchogenic carcinoma. 01 283 workmen with a history of regular cigarette smoking, 24 died of bronchogenic carcinoma, although only three were expected to die of this disease. Calculations suggest that asbestos workers who smoke have about 92 times the risk of dying of bronchogenic carcinoma as men who neither work with asbestos nor smoke cigarettes. We conclude that asbestos exposure should be minimized, that asbestos workers who do not smoke should nevpr start, and that those now smoking should stop immediately. n 1964, wo repoited rm deaths DiiTrnitfg lii'tuciMi I Jan 1. 19-H. and Dim 31, 1011.1, among I132 members of the International Association <tl Heat and Frost Fnsulafors and Asheslos Winkers.1 All of these men had been occupationally exposed lo asbestos dust for many yea is Then- dentil rale from lung cancer was found f> be (i H limns as high as that reported for Ihe general while male popu lation of the United States dining Ihe saint' veais, with age taken into consideration. Three of the men died of diffuse pleural mesothelioma and one died of a neoplasm histologically suggestive of peri toneal mesothelioma. This was of inloirsl mice mesothelioma is a very rare disease in Ihe general population hut. is repotted to he assoiTiled with exposure to asbestos dust.' In addition, their death rate from cancer of tin* slornaeh. colon, and rectum was higher than expected; hut Ibis may have been I'roni thp IVp.n linen! of f`nnmittnif v Mtmttl Sm it School o( Meiliom* M)rs Sr*liW<*f| itml utitl flu* 1 rnent of Kptrlf*mu>loi*v Klalutirs Atunmn ('.inter Sn< irtv (l)r. I (animomi >, New Ymk Ucnil Iwforr n }nml merhm: of the Vt linn on iv; >f tin* Chest with llio Set lion on l*r*\rniivi* Mrilntite .mil Mi** Amettout Oollrijp of (Tlwsl I'hvsi<ians nl Ihe |Wlh itMiiinl Miiitriilmn of tin* American Motion! Assormlnm, Alinntir I'ilv, N7I. .lime IP, 1 *>f.7 Keprint roipiesl* lo Mounl Nin:u S Imol of Midn me, looih Street anil l iflh Avrmir. No* York (!>r. ScltkniTi. due lo chance, the number of such deaths being small. During the latter part, of the study, we ob tained inhumation on the smoking habits of most of I lie survivors, hut we could not obtain reliable information on Ihe smoking habits of those who had died at an eailier dale. Therefore, we could not at that time investigate death rates in rela tion to smoking habits and exposure to asbestos dust which weie considered both separately and jointly. There is abundant evidence that cigarette smok ing leads to a high rate of death from lung cancer in the absence of occupational exposure to asbestos dust.' ' ()ur findings outlined above suggested (but did mil prove) that exposure to asbestos dust may lead to a high rate of death from--ftfiig-cancer in the absence of cigarette smoking. If the latter be so. Ihi'n the combined effect of both types of ex posure might or might not lie otpial to or greater than the sum of (he two-effects. On (lie other hand, it was possible that exposure to asbestos dust in creases the risk of lung cancer among cigarette smokers hut. does not load to lung cancer among nonsmokei's. The present siudy was undertaken primarily to investigale these possibilities. In addition, we wished to obtain more information on the occur rence of mesothelioma and gastrointestinal cancer among asbestos workers. Material Ftnm records of New York Local 12 and Newark, N l, Local .T2 of the International Association of Heat and Frost. Insulators and Asbestos Workers, a lisl was made ol every man who was a member of either one of these locals on Dee 31, 1942, or who joined between that- date and Dec 31, 1962. No one was omitted vegmdless of his subsequent work history. Personnel data from union records indicated that of the 6.12 on the union rolls on Jan 1. 1943, 339 of Ihe men had first been occupationally exposed to asbestos dust prior to 1922, and an additional 104 JAMA. April 8. 1968 Vol 204. No 2 6113 22343 r> ASBESTOS ExrOSUHE -Sr.UKnn CT AL 107 f).1 men had first been cxiiscd between the he Table l.--Subjects Classified by Ape ,i-, 1i. 196.1, and by Years Freni First Occupational f xpnsiifn to A-.' (lust up to Jan 1. 1963 lming (if 1923 and the nd of 1942. All of these ion were successfully 'need through Dec 31, 062, and 262 of them ere found to- have .died p to that time. Of the 62 deaths, seven ocurred prior to the 20lh nniversary of the man's Af, tf 35 39 40-44 45 49 50 54 55 59 00 04 65 69 70 74 75 79 80 84 Total No of Subfrets 2 13 32 109 (iO 4? 49 1ft ?\ A r70 74 2 12 17 ... No. M 1- nee First Ctpestire to .A..s.bestos 25-29 to 34 35-39 40-44 45-49 1 2 13 .. 1 80 78 1 16 34 ft I \ )n 19 n 1 10 18 ift 3 ir n 5 i\ No. of * Deaths. 50+- 52 Mo 1 2 18 11 16 2 17 17 18 IS 8 23 rst exposure to asbestos Total 370 31 6 m ft 6 59 39 36 94 hist and 256 occurred ftcr the 20th miniveriry. Thus, of the 632 mn, 370 were still living n Jan 1, 1963. These 370 men were `be subjects of the presnt investigation. Table 1 hows their age distribuion as of Jan 1, 1963, old the lapsed time from 1 rst exposure up to that Into. All of them have been traced, and 94 of diem were found to have Tallin ? --Sutijocts Classified by Arn and by Smokmf* Habits on or about Jan 1, 1963 Are. Tr 35 39 40 44 45 49 50 54 55 59 60 r,4 65 69 70 74 75 79 80 84 Total Total No. i U IT j no '0 42 49 3 21 4 370 Nrvnr 9 mn til'd Ronular ly 1 2 ? \? r. 7 (. 7 3 ? IR Pipe. Cir.iie Only 1 r 5 4 R 7 7 1 39 C*cigarette Smokers* i ? 5 76 16 15 i; 12 6 l --101 iCurrent Cigarette Smokers* 19 < Oay 10 19 a O-iv 20-39 a Day 40+^ a Day 54 ,... . 12 12 3 5 33 74 3 20 10 1 11 4 4 95 1 443 i31 -- - ---- S 17 97 63 Includes cigorrtte smok.'rs who also smnkrd pipes or cigar* lied during the four-year hhI four-month interval from Jan 1, 1963, In April 101 were exeigarette smokers, five currently smoked 10. 1967. one to nine cigatclles a day, 17 smoked If) to 19 Beginning in October 1962, we made arrange rigarelics a day, 97 smoked 20 to 39 cigarettes a ments to examine these men periodically, once day, and 63 smoked 40 or more cigarettes a day. very six to twelve months: the interval depended The smoking hnhits of the 370 subjects were upon age and physical condition. The examinations compared with the smoking habits of a large num melude chest x-ray films as well as physical ex- ber of men selected from the general population.1 irnination and cover past and present smoking There wore proportionally more cigarette smokers habits, occupational history, medical history, and among the 370 subjects than were found in the urrent physical complaints. Altogether, we have genet a I population sample; age was taken into "xamined 338 (91.4i:) of the men at least once rnnsidern I ion. \nd have repeatedly examined most of those who ('a uses of Death.--A copy of the death certificate are still living. was obtained for each of the 94 deaths. In addi Information on smoking habits was obtained by tion, we examined hospital records, postmortem personal interview with the .338 men who were ex findings (41 cases), as well as the surgical and amined. Of the 32 men who were not examined, pathologic reports whet! surgery was performed (39 six told us their smoking habits by lelephmie and cases). We also reexamined histologic specimens. five gave us the informalion by mail. The local It was found that the death certificate was inac union secretaries (who personally knew these men curate in 14 instances. However, this did not alter .veil) ascertained the smoking habits of 18 men, tln> picture as much as might have been expected and family members supplied the informalion on since Ilieri' weie several compensating errors. For the remaining three men. This aceotmts for all of example, in one instance the death certificate in I tie 370 men. Tabic 2 shows their smoking habits dicated luonciiogenie. carcinoma as the cause of on or about Jan 1, 1963, the men being classified death while a review of the histologic specimen hy their ages on that date, even 'though some showed that death was due to pleural mesothe hanged I heir smoking habits between 1963 and lioma; hut in another instance exactly the reverse 1967. was found. Likewise, review in one instance re Of the 370 men, 48 never smoked regularly, 39 sulted in changing the reported cause of death smoked or had smoked pipes or cigats hut never from bronchogenic carcinoma to cancer of the smoked cigaretles regularly, and 283 had smoked stomach with metastasis to the lungs while review cigarettes regularly. Some of those wilh history of in aniiilier instance resulted in exactly the oposite cigarette smoking also smoked pipes or cigars. Of change The 94 deaths were asetibed to the follow the 283 with a history of regular cigarette smoking, ing causes: bronchogenic carcinoma, 24; pleural JAMA, April 8, 1968 Vol 204, No 2 6113 22344 ior ' 11 1 i11 i ti 1 ,i i i'll I ' , i Hi I 1 i (. j ;ii t. i, *99 , 108 /vsmstos f ' iuni-SLUKOir u al Table 3.--Observer) ainl Fxiwtril Numl.n el PimHix * 370 Asbestos Workers Huong the sj Month Porn i r. Can** of Death Total, ranee* tall sues) Cancer of tun*. pleura, bronchus. and trachea SronchoJtenic carcinoma Pleural mesothelioma Peritoneal mesothelioma Cancer of stomach Cancer of colon and rectum Cancer of ah other site* combined Asbestosis Heart and circulatory disease mrltidme strode AM other cancel of death Ohsnved Deaths .10 ,7 n 3 7 ? ; 15 p I r* '! `i . 1 t t t 06 I7 VS s in a Total, ait cans*** hi t/,5 * Based nnon US mortality d-<t. !. r sool.ii'H h.ibrl 1 United State* data not av.nl.bh\ but I'jnrre hcmr| hr r*ily OicMIy less than tUmled Slates data not available, hut Xbsi ae rare causes nt death in genera! peculation. mesothelioma, three: peiiloiu al mesothelioma, sevon; cancer of tlie colon, four; cancer of the rectum. one; cancer of the slomach. three; cancer of the pancreas, two: cancer of buccal cavily and pharynx, two; cancer of bladder. one; cancer of undeter mined primary site, two: ;vd>estnsis, 15; cur pul monale, one; cornary heart disease, 17: congestive heart failure, one; cerebral vascular lesion, two; aortic aneurysm, one; cirrhosis of the liver, three: bronchopneumonia, one: encephalopathy, one; acute pancreatitis, one; Wegener's granulomatosis, one: and accidental fall. one. Expected Deaths.-I'm piuposrs of comparison, we wished to ascertain how many of the '70 sub jects- would have died durinj: the rrl-monlh period (Jan 1, 19<5J, to April JO. int`>7) if their ace-specific death rales hail been exactly the same ns for the general white male population of the t toiled Slates. For this purpose, we made use of the I tailed Stales 19(54 life table for white males; this provided the most stable basis for comparison. It should he noted that for while males total death rates and death rates from respiialorv cancer were slightly higher in the industrial slates of New York and New Jersey than in the United Stales as a whole.'" On the other hand, respiratory cancer death rates in white men aged 20 to til are reported to he a trifle lower than average among lahmers. not elsewhere classified employed in const ruction work." From the life table we determined for each of the 370 men the probability of his dying within a pe riod of 52 months, considering his age on Jan 1, 19(53. and assuming that the life table probability applied to him. Summing these probabilities for the 370 men yielded an estimate of the "expected" number of deaths under the null hypothesis that the age-specitic death rail's of these asbestos work ers are the same as for United States while males in general. The compulation indicated that 47.5 deaths would have been expected. Next, we wished to estimate the expected num ber of deaths from each of several causes. For this, we made use of lire percentage distribution of deaths by cause of deatlr among United Slates white m ites of various ages during the. year 19(54 as reported by the National Center for Health Sta tistics. These percentages were IIrerr standardized for age according to lire age distribution at time of the 17.5 expected deaths. Tire results are shown in Table 3. Expeeted is Observed Deaths.--An shown in Table 3, there were 91 observed deaths (ic, 94 of the 370 asbestos workers died) as compared with 47.5 deaths expected on the basis of the agc-spccifrc death rates of all while males in (lie United States in 19(54. Thus, there were 94 minus 47.5 * 46.5 excess deaths. The excess deaths were line to bron chogenic carcinoma, mesothelioma of the pleura and peritoneum, nshestnsis, and cancer of tire stomach, colon, and reel run. Cancer nf Lung, I'leura-, and Tiachea.--In pub lished moitalit y data for I lie United Stales show ing deaths each year from various causes by age, sex. and race, the following diseases are combined: cancer of the lung (including sarcoma of tiie lung), cancer of the bronchus, earner of the pleura, and cancer of the trachea. For this group of diseases, theie were 27 observed deaths and only 2.3 ex pelled deaths, a ratio of nearly 12 to 1. It is well known that, for the United Stales as a whole, all except a very lew of the deaths re ported in the combined category are due to bron chogenic carcinoma. Thus, it may he assurped that there were close to 2.3 expected deaths from this cause as compared with 24 observed deatiis, a ratio of over 10 to 1. Mesnthelioma.-Ten of lire 94 observed deaths were due to mesothelioma, three were duo to plemal mesothelioma, and seven were due to peri toneal mesotheliomas. This is such a rare disease that if lire 370 subjects had been selected as a random sample from the general population, one would not have expected any of them to die of mesothelioma within a period of 52 months. A ll I lu ce of the men who died of pleural meso thelioma had a history of regular cigarette smoking. Of Hie seven who died of peritoneal mesothelioma, one never smoked regularly, one smoked only pipes and cigars, and live Irad a history of regular ciga rette smoking. ('ancer of Stomach, Colon, and Rectum.--In our earlier study of asbestos workers,' there were more deaths than expected from cancer of the stomach, colon, and rectum (9.4 expected, 29 observed). As compared with a total of 1.8 expected deaths from these causes, there were eight observed deaths in litis study, due to carreer of the following sites: stomach, three: colon, four; and rectum, one. Al though this heats out our earlier findings, the num ber of deaths from these causes was so small that we still refrain from drawing any conclusion at this time. Ashestosis. -- Ashestosis accounted for 15 of the 91 deallrs. While it is not srtrprisitrg that deaths front this disease occur among men exposed to asbestos dust, attention must he called to the fact 106 ' JAMA, April 8. 1968 Vol 204. No 2 6113 22345 1* t Asnrsios rxrosuRF-- si mki- r f.i ai. 109 that- these subjects were primarily insula lion work ers. While all of them were occupationally ex posed to asbestos dust, their degree of exposure was light as compared with, the dcprhe of ex posure of asbesios miners, processors, and weavers in earlier times. lironchnznruc Care i- nama.--Bronchogenic car cinoma accounted for 21 deaths while only about 2.3 were expected on the Tnljltt A.--FMiinrAtvl Nnm|.nr of 1 i r 1 'nror On-illis Fxprctpd to Occur Dunnn A Period of Months |>ot in.OpO Men l tvi"i* *' '*"* ShlM of fVnocI; by A|*o nncl by Smoking (Mbits* 1A*e. {Jan , 1V0r63) 35 39 40 44 45 19 5051 55 59 60 G4 65 GO 70 74 75 n HO f*4 Never Smoked 0 2 7 1 G li 14 1? 79 ro rne. Ct *r Only .. t 7 17 IS 31 37 57 51 17 f _ Current CiR>re(le Smokers! .. . ........ _ F *or.'ctte i <> 10*19 70-39 Smokerst 5 a Day a Day a Oay 76 15 !0 ?B a4*4-- 30 f,9 51 91 117 n B0 100 nt 157 305 i no 1P1 206 788 In0 185 .311 ItK 40 f a Oay 15 46 , 00 , 185 756 350* 450* 379 1 0.i'.rl i*fwti frnMi i |tro*,|i(*< live shifty ^ilti ,i'l|ii^lini>i>| (nr US mri'i.ilily osprncnce H Up*,r<; Me ( Ihn T.ihlelor ill^iif.ps villi no sublets m Mwtly See 2 1 inrifl***> ,,i'tvrrs wi*n ,u*.n vu*rd po<* or c'r.^r Men w*i> a btMoty of only C'ft^relts inmhinfr h.vr holier lunf; c merr Ih.sn shown here, rd>M'ned tw Muraitnof the iI.Ma basis of general United States mortality data for divided into many five-year age groups, some of the white males. However, as previously mentioned, subgroups contained only a small number of men. evidence at hand suggests that them were propor In consequence, the lung cancer death rail' was tionally somewhat more eigarette smokers among" statistically unstable in some of Ihe very small sub- the 370 subjects than among white males iu the gioups. In (luce instances where the observed rate United States ns a whole, age being taken inlo in a small subgroup appeared to he badly out of consideration. This might have partial!v arcmmtrd line, we aibilrnrilv made an adjustment to bring it for the high bronchogenic carcinoma death rate of more into line with adjacent figures in the table. the subjects. For this and other reasons we made These adjusted figures which are indicated with estimates of the expected number of brumhogmic symbols in 'Fable 1 can y very til tic weight in the carcinoma deaths, I he smoking habits of the men final calculation. All of the rates were then ad being taken into consideration. This was done as juster! as follows: follows: Lung cancer death rates in the United States Data are available on lung cancer deaths in re have risen steadily year by year and weie higher lation to the smoking habits of t Hl.nno own en in 1904 than during the period 1900 to 1964 ns a rolled by American Cancer Society vohmh'eis in whole. Furthermore, in the study described above, a prospective epidemiological study between Or- we avoided enrolling seriously ill people and, as of tober 1950 and March 1960 and trared through Ihe cut-oil rlate for preparing the computer tape, Sept 30,1964. Causes of death were ascertained fmm we had not. yet leceived death certificates for nil death certificates, but whenever cancer was men of (he men now known to have died during lho tioned on a death certificate inquiry was made of specified period of lime. For I hose reasons, lung the physician who signed the cerlificale. fn ea-.c cancer death rales in the study population were of disagreement between the two sou ices of infor appreciably lower Ilian those icporlcd for while mation, the physician's statement was accepted. males in the United Stales in 1904. To compensate For the puiqiose at band, we only made use of data for this, we raised the rate of each individual smok covering the 52-month period beginning on .lime 1, ing category so that the total lung cancer death 1960, and ending on Sept 30, .1961. The number of late (disregarding smoking habits) in each five- lung cancer deaths occurring during the fVJ-mnnth year age gioup would be the same as lhat. of all period was divided try the number of men alive at United Stales while males (based upon flu* 1964 the beginning of the period. This was done by live- life fable and (he 1901 distribution of deaths by year age groups for men in each of the following causes of death). The results of these computations smoking categories: (1) never smoked regulailv are shown in 'Fable -I. (It should he noted that fnonsmokers and occasional smokris being com 'I'alile I shows only such rales as were required for bined); (2) history of regular pipe or cigar smok further calculations.) ing, past or present, but never smoked cigarettes 'Flu* talcs shown in 'Fable 4 were then applied In regularly; (3) exeigaretle smokers fine hiding those Ihe number of asbestos workers shown in each of who had smoked or currently smoked pipes or (he cmlespoiuiing internal cells of 'Fable 2. This cigars): and (4) current regular cigarette smokers yielded an estimate of the number of lung cancer (including those who also had smoked or currently deaths expected to occur during a 52-month period smoked pipes or cigars). The last, of these cate among the 370 asbestos workers classified by their gories was further divided by current number of smoking habils. Ily "expected" number, we here cigarettes smoked per day: (4a) one to nine ciga mean an estimate of Ihe number of lung cancer rettes a day; (4b) 10 to 19 cigarettes a day; < tc) deaths which would have occurred under the null 20 to 39 cigarettes a day; and ( Id) 10 or more hypothesis that asbestos workers do not difTer from cigarettes a day. Since the men were divided into oilier men in respect lo (heir lung cancer death seven groups by smoking habits and further sub rales, both age and smoking habils being taken JAMA, April 8. 1968 Vol 204, No 2 6113 22346 107 110 ASHI SIOS I : ' :.UHI -Sll IK(I1 F Er AL Tabte 5 --Ob*cvrcl nn<l r*piv;trft HirMirliruv'ntr: "IP Deaths bv SmnUnif: M.ibiK fo* .1/0 Ashi'MilS Wort-* * Smokmp; Habits Never smoked rrfltd.irly History nt pipe. c'C-v smnkmg only History qI regular cigarette imnkmgi Obsrwnd Depths n 0 ?a f ` -1 lv .n "i :w Tool 74 1.16 "Sated upon data m Table ? and rahle A. t Includes cigarette smokers who alto vno^Aci pipf* nr cigar Table 6 --Expected and Observed 0>',ill's Amnnr. 63? Asbes tos Workers Exposed to AsbeslO t)ust 70 yi'.its or I oiipei Tot it depths: all causes Erprctcd Observed Tot.il cancer: all sites Etorcted Observed Canerr ol lung. trachea, pleura E*pected Observed Cancer of stomach, colon, rectum E*oected Observed Cancer all other sites combined Expected Observed Asbcstosis Expected Ohserved AM other causes E*oec!ed Observed 19111962 7n t 5 7r*Ti lot-il i9fit in*/ 1913 n<7 t; 6 7SI in V. 5 95 a6 49 4S 1 HI 6 6 7 .1 4*i 77 89 72 n 4 1 ft 11.2 79 a 37 , 70 5 a > ?5 ?! M 3S 00 0 1? IS 77 k.; in a 70S.9 H8 to 17B into consideration. The results are sniiniiamed in Table 5 which shows t he expected and observed number of lung cancer deaths in each of three smoking categories. Taking smoking hnlrits ns well as age into con sideration (Table 5) a total of 3.2 Immeliogeuie carcinoma deaths were exported whereas taking only ape into consideration 2..T deaths were ex pected from this cause (Tal'le 3). Thus, peihaps otic of the excess bronchogenic carcinoma deaths might be attributed to the fad that there appear to have been proportionally somewhat more ciga rette smokers among the 371) subjects than among men of the same ages in the general population. The following sfalemenls arc* baser) upon the data shown in Table fi. Twenty-four deaths from bronchogenic carcinoma occurred among the .'170 subjects compared with only It.Hi expected, a ratio of about 7.0 to 1. This is slightly higher than found in our earlier study which indicated a ratio of (i.8 to 1 (not taking smoking habits into condderation). It should lie noted in this i onneelion that the 370 subjects in this study hart been exposed (o asbestos dust somewhat longer than the snhjeds of our previous study (the present- 370 subjects are survivors as of Jan 1, 11)03, of subjects in the previous study). Of the subjeels who never smoked regularly and those who smoked only pipes or cigars, none died of bronchogenic carcinoma whereas 0.18 of these men wore expected to die of lung cancer. This sug gests that exposure to asbestos dust, does not. in crease the risk of bronchogenic carcinoma among men who never smoked rigniet/es regu/nr/v. How ever. r misidering the small number of such subjects in this study, we only conclude that exposure to ashesios dust floes nut greatly incieaso the risk of bronchogenic carcinoma among men who never ' smoked cigarettes regularly. Twenfy-fnur of the men with a history of regular J cigarette smoking died of bronchogenic carcinoma ` whereas only 2.98 were expected to die of it, a ratio of 8.03 to t. From this it appears that exposure to. asbestos dust greatly increases the risk of lung , cancer among cigaiel le smokers. Now we may ask how greatly is the risk of bron- ' 1 ehogeuic carcinoma increased hv tin* combined ef- . j feels of cigarette smoking and exposure to asbestos ; dust. To answer this question, we applied rates ' shown in Table I for nonashcslos workers who ' never smoked regiilailv to Hie number of subjects ' with a history of regular cigarette smoking as shown in Table 2. This indicated that only 0.26 of the subjeels with a history of regular cigarette smoking ; would have been expected to die of bronchogenic j carcinoma if they had never smoked regularly and ! had never been occupationally exposed to asbestos . dust. Since 21 of them actually died of this cause, the ratio of observed to expected deaths is 92 to 1 (ie. 2't divided by 0.26 = 92). This appears to in dicate that cigarette smoking plus occupational ' exposure to asbestos dust increases the risk of . bronchogenic carcinoma by a factor in t.he' order of magnitude of 92 to 1. It should he noted that this estimate does not take current amount of cigarette i smoking into consideration. ('nmfiansan With Earlier Findinpst.--As explained, we started with a cohort of 632 asbestos insulation workers, (he entire membership of the union locals on Jan 1. 19.(3. We have now traced each man through April 30, 1967..Table 8 shows the observed and expected number of deaths for each of two , periods (the first, 1943 to 1962, being previously reported') and for the entire period. In respect to respiratory cancer (lung, trachea, and pleura) and in respect to cancer of the stomach, colon, and ' rectum, the findings in the two periods are in close ^ agreement. . ,j( Comment The increased risk of neoplasia (mainly broncho genic carcinoma and mesothelioma) among insula tion workers reported here should he evaluated in , the knowledge that these men have comparatively light exposure as asbestos trades go. Primarily em ployed in const ruction work, many of the materials they use contain little or no asbestos and olhers have only 5% to I.r>%. Conditions of work vary; these men often work outdoors unlike asbestos ..; operators in factory work. Comparatively few dust- j1 exposure surveys have been made in this trade but V their results have generally been within the 5 mil-* lion particles per cubic foot permissible limits cur-' rentiy accepted hv the American Conference of Governmental Industrial Hygienists.""' Nor have 108 JAMA. April 8. 1968 Vol 204, No 2 > 6113 22347 ASBCSTOS F.xrOSUrtE- Sf.1 IKHI r I r Al. ill ditiona! potentially carcinogenic substances been 10 yea is Youngsters who start smoking now "ntificrl among the other materials vised. have' a m a h greater chance of hav ng both ex Heavier or even lighter exposure may result in posure ''iltaneouslv. Ifcrent degrees of risk of neoplasia. Heavy fnctmy Stuwii- "nr al b'imhnpii fur Ashrstns Wnrkrrs.-- posure in the past has in some instances resulted The impoit of the data reported here seems clear. considerable lung cancer risk." In others, para* Tht-re is an extraordinary risk of developing and ixically, little lung,cancer was seen because n* dying from lung cancer for asbestos workers who stosis was so eqmmon and so severe as to cause smoke cigarette's regularly. In the group studied, ath of the exposed xtorkers before they cmdd live the eomhinalion of asbestos exposure and cigarette ng enough to develop lung cancer. Once exposure smoking increased (be risk approximately 90 times as reduced bv improved industrial hygiene prae- compared with men who neither work with asbestos es, early death from asbestosis sharply dimin* nor smoke! bed and lung cancer became common.''' Of 285 asbestos workers who bad a history of In any case, heavy exposure is not likely to he _ cigarette smoking, 78 died within a period of 52 '0 most important problem in the future, unless months wheiens onlv 82.t would have been ex ere he sheer carelessness nr unconcern. Rather, pected to die within that length of time if their age :ht exposure, similar to that in insulation work, specific death rates had been the same as for tire ill be much more common, both in direct asbestos general white male* population of the United States. orking trades and as the result of imlim t neeupa- Of live 78 deaths, 2 t (81%) were due to broncho onal exposure, ns in the construction and slup- genic carcinoma. It is estimated ttint if these men lilding industries. had smoked cigavcttcs hut had not been exposed to There is another type of "light exposure-' uhi> h asbestos dust, only 2.98 would have died of brem- 'ay affect many more people than those industrial- - < Itogenie carcinoma within the same' length of time. exposed. In the past several years, it has been If they had neither smoked nor been exposed to. monstrated that asbestos bodies can be found in asbestos dust, only 0.2b would have been expected mo lungs of 25% to 50% of adults examined al to die of the disease within a period of 52 months. ttopsy in large cities, such as Belfast. Northern Of 87 asbestos workers who never smoked ciga eland, Capetown, Republic of South Africa, rettes regularly, none died of lung cancer within the liami, Fla, Pittsburgh, and Montreal. This is 52-montlr period (although three died of asbestosis resumably due to "asbestos air pollution" by and one died of peritoneal mesothelioma). This hers derived from industrial "spillover" (as dust finding, being based upon the experience of only um construction sites or factory wastes) (>r from 87 men. docs not prove that exposure to asbestos ud-product use. Such community asbestos rvir dust has no influence on the risk of lung cancer ullution may bo important since llieie is already among nonsmokevs. However, it suggests that ex idcncc that in certain circumstances, as living posure to asbestos dust does trot lead to an ex ithin half mile of an asbestos plant or in the tremely high risk of lung cancer among nonsmokers. ouseliold of an asbestos worker, intimate environ- The conclusions me evident: lontal contamination can bo associated with some* 1. Occupational exposure to asbestos dust, should sk of mesothelioma."1 What is not now known is .he reduced to as low a level as possible; hut tlrpre .hether the minimal amounts inhaled by the gen in.-iv he an irreducible minimum level if asbestos, a ial public carry a similar risk." very useful material, is to he used at all. Such Nor do we know whether inhalation of the very reduetioit irt exposure will benefit asbestos workers nail amounts of asbestos present in tin- air of some of Hie frit net*. However, we are also concerned vvitlr immunities is associated with a special lung _woikeis who have already been exposed at signifi nicer risk in cigarette smokers (or, innversrlv. cant levels tor many years. Asbestos libers will re hether cigarette smoking makes the inhalation of main in their tissues for the remainder of their lives. cry small amounts of asbestos particularly hazard- 2. All people incur a great increase in risk of lung us). It will he important to ascertain whether such cancer if they smoke cigarettes; for asbestos work ocarcinogenic or potentiating or precipitating rein- ers the increase in risk is tremendous. Asbestos innships exist because, with the rapid growth o'f workeis who do not now smoke cigarettes should diestos use (500,000 tons per year woild produe- never begin. Those wlvo do smoke, should stop nn in 1050 has risen to over .1,000.(100 tons per immediately. We may hope (hat the decrease in ear now), it may be diflicult for cigarette smokers li.' l; which results Imm icssalion of smoking among n avoid inhaling air contaminated with asbestos. 'the geneial public1 will be the good fortune of the It may not be easy to unravel the interrelation* asbestos workers as well. hips which might exist between community a- I Ini um \%:is Mippni trtl lv I hr 1 !<:! fit Resruirh Cntin* stos air pollution and cigarette smoking. Built til if lh* t*tl\ **l New Yti lx sbestos exposure and cigarette smoking have a Reference* ing-lapsed period between unset of exposuie and 1 S*lktWf I .1 ; Chtiifj, .1 , rimI Mninmnnrl, I T.f Ashrsfn* Kx* ccurrcnce of neoplasia, yet for current smokers hese two exposures may trot have begun simulta neously; there was much less asbestos used 20 to |wi .imt* .Iiol N# ttpln-.r*. ,1AM \ l`*M */ S* hl *f, I J , f'hiiiif. .1 ; mill Ihimm'Mul, I* (* : Uclnlmtt llr* (Kern to A'.hr* Ins :iitH Mrsolltrlimn;i, Afell' Hit/! /If erf 272:M*n iMnrrh 18) I AMA, April 8. 1968 Vo( 204, No 2 6113 22348 109 112 ASBEStOF. i I'OSURE--SEIIKOTF ET AL 3 \ 1nu)ntnn<|, I'*. C! ` "Smnkinf? in In llw I I-* 1.000.<K10 Mrn nml Womm." in / '/*##*-m Iff Sttnfv */ * and Other (.'/ironic 7)itca lU llw.il. Mil Nnlinn:i 'hislitulr, P*. |>p I'.!7 *.'01__ . . .f *rr n rr 4. Samhtna and Health. IK-finrl nf flu* Al\i`.mv (\>ni. . . lo f ?(* SlifKroti Urncriil of flic I'uhlic | !*. I fit KVr\ ire. |l' **im 1103, US Urpt of Umltli, Krln* iilinn, nnfl Willur, If**.! 5. I lamtitoitrl, IvC. nml fJ.irfirtkrl. !#. t'li.infrc* in I t-Me Smoking lOrrfMWW. Amcr ./ Vuhtte Health 53:30 If. Mn 1*108 0. Vital Slattttir* of tht* f Uuted State* IWU), pm t A. US Urpt of HcflHh. Kfhirntiin. nmt W<*lf:n\ IWl.'i, vnl 2 7. /tenth Hate* From Muhvnnnt 7.9/JO,- I'nUIic ,#l|rllh Service. publication 1113. US 1)rpt of llrnlllt, Kilurnttnn. unci -Wrlfnio, I?NV1. 3, Mortality hv Occupation amt ('mu** nf lhnth, I'uMi* llntlih Service. US Dept of llrnllh. I,'ilui Minn. ml Welfnrc. Vihil Sin- hvlim Ihvt-nnn. ViJ.il Sljlnliri-S/>rcinl Hcj*orts, 53:323 (Sept) **. 1 I'M** 1n*r. W lv, rt nl A Health Survey of Pipe-Covering Opcr.iinms m fniivfturtinj* Naval Vrswls, J /ntluttr l/vg Toxtc 28:** Pi <.Inn) 10 Kruno. W. I', ami Zavon. M II,: (Vmpnlionnl Tln/nrtla of Pipe 1tw,,l.Urr Arch Fnunnn Health 13:171-178 (Aug) PHUJ, 11 I kill. If; Mortality from f.unc Cancer in Aaltcatna Workers, flnf./ fm/iMfr A frit 12:81-80 I April) 1055. 12. .lamb, (, nml Ait|inrlit M.: Pulmimnry Ncnplnain Among UrcMlm Asl>c*lo* Workers, Ann NY Acad Sc 132:5n6T>4JI (Dec ni) hhw. 13 NesUnmse. MU. nmi *nmtpan. H.: Mraolhcltouta of PlfMita ami IVrihmenm Kolbming KxpnMire (o Aaltcalo* in fht IrfMutitn Atc;v flnf ./ /mfnafr Afnf 22:201 -2IH1 (Oct) i'.MS5. 11. Sf'hkoff. I 3 . el nl: Ashratmia `ami Nroplaaia. Amcr J Med 42:487-4W5 I April I 11Hi7. VS J\1.S t\ M:mv, possihlv most. of tin- words in tin- dictionary stand there .is representatives of ;i wlicilr- family of forms. No! even I ho limidesl of tlu- linguislii ally timid will run Words}, to tin- dictionary for encouragement when, for instance, they won I to refer to a spell of "hiccupinc." provided they me eerlniii that Webster does know "to hiceiip.'' All the tense founs. the participles, the gerunds are assumed to he authorized hv implication the moment tlu- infinitive is known to exist. The plurals of nouns are similmlv token for (.'ranted, and the forms of comparison and the adverbial foims of :|(I jrrl i\es. _ This phenomenon is generally eovered hv the assertion that a dictionary is not a grammar and that each individual entry in a dictionary stands simultaneously for all its grammatically possible forms. (For details, consul I your erammar.) Huf is a gerund a i.-iammalieal form? Or is il a suHix-derived noun? f am not really looking for an answer. I ask those questions to suggest that the dividim: line between grammatical form and derived neolocism is troth hard to de fine and artificial If I distimmish amone men Ihr "himtinc" from (he "hunted." I have done no mme than form (prnmmnlicnllyl two nouns from two adjectives which are foims ' iaanimalically I implied in Ihe existence of "to hunt." I3lit if "Inmline" is implied, why not "hunter"? Why not "huntee" and "luinlahle" and "Inml.ahiliVc"? _------- -- 'Hie i|iieslioii of when a new wort I is a new word and when il is merely an "im plied" form of a eonvent ional term is indeed more complex than is crossly ap parent. Take "flehaiiahility" as an example. Can I claim Ihe word is implied in Ihe existence nf "hair." or must 1 assume the resj)onsibility for having spawned a monster? Or lake "mie>|iii\oealily." which indeed was tin- slartini: point of all this rea soning arid wondeiini:. for it was spotted as a hold ni-ologism in 'IAM A in the sentence. "Rescan h at the Public Health Service Hospital at l.exinglon, Kv, has uneqidvocablv pi oven that methadone has all of the euphoric properties of mmphiue. . . Now, clearly, the adverb "uncquivocably" is grammatically implied in Ihe ad jective "imeqtiivnrnhle." and this in loro is implied grammatically of semi-gram- mat ically or otherwise in "cquivncnhlc." If we grant further that formations in "-alilr" of " ible" ate likewise, legitimate without special dispensation, we shall conclude that `'imequivocablv" is in no sense a hold departure since "to equivo cate" is a firmly established, standard Knglish word. Mul llieie is a liilcli and a (law ill Ihe argument. "To equivocate" means "to use aiiiliigiiMiis language" and I hv extension l "to render ambiguous." Hence, "equixocahte" can only suggest the trail, of "being apt or able to he made ambig uous," and that. I fear, was not intended. Which means, by (nongrammalical) implication, that the discrepancy between the obviously intended meaning of "un- equivoeahlv" and its structurally suppmted significance was the cause of the un pleasant jolt experienced I'V the spotting reader. I'S II is of comse possible, and even likely, that "unequivocalily" was just a typo for "equivocally." Ai.i:xanoki< (Ioiik, PhD ltO JAMA, April 8. 1968 Vol 204, No 2 6113 22349 ARCHIVUM IMMUNOLOGIAE ET THERAP1AE EXPERIMENTAXIS 1978, 25, 899 c NOTICE {THIS MATERIAL MAY BE l PROTECTED BY COPYRIGHT ; l.'V.V iTITLE 17U.S. CODE.) CELLULAR IMMUNITY IN ASBESTOSIS* by Andrzej Lange, Roman Smolik, Wiktor Chmielarczyk, Dorota Garncarek and Zdzislawa Gielgier Department of Occupational Diseases, Institute of Internal Diseases, Medical School, 50-367 Wroclaw A highly statistically significant correlation was found between asbestosis and impaired responsiveness in skin reaction to intermediate and second strength tuberculin and SK* SD. Considering ANA incidence these antibodies were found with higher frequency in asbestos workers who lacked a cutaneous response to the recall antigens. In asbestosis cases peripheral blood lymphocyte profiles are also abnormal demonstrating low propor tions of E-RFC. Moreover, MIF test results showed the impairment of this cytokine generation when lymphocytes were stimulated with SK-SD, PPD and PHA in asbestosis cases. The lymphocyte transformation study documents an impaired response mainly to a lower dose ofPHA and ConA in asbestosis cases and in asbestos workers with ANA. The occurence of rheumatoid factor and antinuclear antibodies (ANA) in asbe stosis is well documented6* *X1. Furthemore, it was shown that abnormalites in humoral immunity are accompanied by changes in immunological cell-mediated reactions in asbestosis namely low proportions and absolute numbers of T-lymphocytes were found1*3* *. Moreover, skin reactions to recall antigens were also impaired in these patients as well as abnormal responses to PHA1. The problem to what extent lymphocyte malfunction is involved in the patho genesis of asbestosis has become the most challenging problem in view of the data documenting the high incidence of neoplasmas in asbestos workers10. * This work was supported by the Polish Academy of Sciences (Grant No. 10.5). 6113 22350 900 AUTOIMMUNITY PHENOMENA I MATERIAL AND METHODS All people investigated except the controls came from asbestos textile plant. They underwent a thorough medical examinations when blood was collected for immunological studies. The groups of people which were compared to each other were matched for age and sex. Details about these people are given in the tables. Hospital staff who were in apparent good health served as controls for lymphocyte studies. Autoantibodies in sera were detected with the use of the immunofluorescence method. Delayed hypersensitivity skin testing. As recall antigens tuberculin and streptokinase-streptodornase (SK-SD), (Serum and Vaccine Factory, Warsaw) were used. Intermediate test strength were 2 U and 5 U for tuberculin and SK-SD, respectively. The second strength was 5 U for tuberculin and 40 U for SK-SD. The results were read 48 hrs after injections. Induration at least 5 mm in dia meters was regarded as positive. Erythrocyte (-) and complement (EAC-) rosettes forming cells (RFC) study. Lymphocytes were obtained from peripheral blood by centrifugation at a density gradient Ficoll (Pharmacia-Uppsala) -- Uropolinum (Polfa, Poland). To determine E-RFC 0.25 ml of 1% SRBC suspension in Hanks' balanced salt solution (HBSS) was mixed with 0.4 ml previously absorbed with SRBC heat inactivated calf serum and with 0.5--l.Ox 10 lymphocytes suspended in 0.1 ml HBSS and with 0.4 ml HBSS. EAC-rosettes were measured using IgM antibody sensitized SRBC and fresh mouse serum. Details of the method are given elsewhere ' 12. Direct migration inhibitoryfactor (M1F) assay. This test was performed according to the method given by Rocklin*. The following stimulants were used: PHA (Wellcome) 2 (ig and 8 [tg/ml of medium, PPD (Serum and Vaccine Factory, Warsaw) 1 (jtg and 10 (ig/ml of medium and SK-SD (Serum and Vaccine Factory, Warsaw) 100 U and 200 U/ml of medium. Inhibition of macrophage migration was never observed with cells obtained from guinea pig peritoneal exudate with addition of only stimulants without human lymphocytes. Mitogen-induced lymphocyte transformation test. This test was performed with the use of micro assay of DNA synthesis. In general the method given by Oppinheim and Schecter7 was followed with some modifications. The following mitogens were used (in brackets are given the intermediate and the higher concentrations of mitogens which were used): PHA (Wellcome; 5 (ig/ml and 20 ftg/ml), ConA (Sigma; 2 jrg/ml and 10 (xg/ml), PWM (Gibco, Grand Island; 0.01 ml/ml). Titriated thymidyne (0.5 p.Ci/well, specific activity 28 Ci/mmole) was purchased from Institute for Research Production and Application of Radioisotopes, Prague. Statistical analysis was made with the chi3 test with Yates modification. I I I / i . ( RESULTS Skin testing. 271 asbestos workers were examined with SK-SD and tuberculin. 48 of them did not respond to any of the antigens when they were used in intermediate strength. In this group of people, asbestosis was found more frequently when com pared to workers responding at least to one antigen (19% versus 4%; chi2 = 11.0, p < 0.001). ANA positive cases regardless of the presence or absence of asbestosis, were also more frequently found in this group of non-responding asbestos workers when compared to responders (31% versus 11%; chi2 = 11.0, p < 0.001). However, when asbestosis patients were excluded from the calculation this difference became weaker and statistically non-significant (18% versus 7%; chi2 = 3.2, p<0.1). 44 of the non-responders to both antigens intermediate strength were retested with second strength antigens. 29 of them failed to respond again. Asbestosis cases were | found in 17., an 5% and 12% fo E-and EAC-i proportions of I pared to asbest p < 0.05). How to absolute nun: tions of cells lac cases (32%;z7 v lute number of In ANA pos percentage but i lacking ANA (4 gnificant when MIF study. PPD, SK-SD a generate MIF pstimulants were with ANA but 4 AN me dur: me All results with first strength of stimulants All results without se cond strength of stimulants *' Number o with impaired Ml of impaired respc = 5.11; p < 0.05 P < 0.05). ANA, and in > ate considered follows: 42%, fc w*~ *-- -------- jSSBst?fe!5 ` autoimmunity phenomena 901 i it. They underwent :tudies. The groups details about these rved as controls for :ence method, okinase-streptodor- test strength were 5 U for tuberculin : least 5 mm in dia- Lymphocytes were rmacia-Uppsala) pension in Hanks' SRBC heat inacti* iS and with 0.4 ml resh mouse serum. ding to the method g and 8 (xg/'ml of edium and SK-SO on of macrophage .date with addition I found in 17% and ANA in 28% of this group. The percentage for responders equaled i 5% and 12% for asbestosis and ANA occurence, respectively. ' E-and EAC-RFC study. This work confirmed our previous work* showing that 1 proportions of E-RPC were significantly lower in asbestosis cases (n = 14) as com pared to asbestos workers without lung fibrosis (n = 51; 46%7 versus 5210, p < 0.05). However, no statistically significant difference was found in respect to absolute number of E-RFC. On the other hand, in asbestosis cases higher propor tions of cells lacking E-and C-receptors were found when compared to non-asbestosis cases (32%7 versus 25%11; p < 0.05). No difference in the proportion and abso lute number of EAC-RFC was found. In ANA positive cases regardless of the presence or absence of asbestosis a lower percentage but not absolute number of E-RFC were found when compared to people lacking ANA (47%8 versus 529; p < 0.05). However, this difference became insi gnificant when patients with asbestosis were excluded from the calculation. MJF study. A majority of patients with asbestosis lacked responsiveness to PPD, SK-SD and PHA, when these stimulants were used at their first strength to ! generate MIF production. The percentage of people who did not respond to any of the stimulants were 67%, 30% 35%, 33% for asbestosis cases with ANA, asbestos workers with ANA but lacking asbestosis, asbestos workers cases without asbestosis and Table 1. Summary of migration inhibition test results a the use of micro-TER7 was followed a the intermediate me; 5 jig/ml and ad; 0.01 ml/ml), ised from Institute analysis was made t Asbestosis with Without asbestosis Without asbestosis ANA it = 12 (9/3)* with ANA n = 10 and without ANA mean age = 52 yrs (8/2) mean age -- 47 n =*17 (13/4) mean duration of employ- yrs, duration of em- age -- 46 yrs, dura- Contrl group n = (14/2) ment from 13 to ployment from 7 to tion of employment mean age ^ 26 yrs 25 yrs from 4 to 30 yrs All results with first strength of stimulants 30/36*b** (83%) 19/25 (65%) 29/50* (58%) 26/45b (57%) All results and tuberculin. : in intermediate without setend strength of stimulants 23/26 (64%) 16/29 (55%) 24/49 (50%) 22/45 (48%) ntly when com* v,,; chi* = 11-0. :e of asbestosis. sbestos workers .001). However. > * Number of people investigated (in brackets female/male); ** ratio of the numbers 6f tests with impaired MIF generation to numbers of all test performed (in brackets are given percentages of impaired responses); * the difference statistically significant between groups labeled a (chi2 -- * Ml; p < 0.05); b the difference statistically significant between groups labeled b (chi2 * 4.98; j P < 0.05). Terence became = 3.2, p < 0.li ANA, and in controls, respectively. When the results of second strength stimulants , re retested with j are considered, the differences were less pronounced and these percentages were as :osis cases were follows: 42%, 30%, 24% and 27% for asbestosis, asbestos workers without asbestosis 6113 22352 sr tf c S&t- rH pii i4f i m Hn U\ i 902 AUTOIMMUNITY PHENOMENA but with ANA, asbestos workers without ANA and asbestosis, control group. 'Summary of MIF results are presented in Table 1. When MIF results obtained with the first strength stimulants were taken together within the groups, it showed that asbestosis cases differed significantly from the controls in the number of test results demonstrating a lack of significant macrophage migration inhibition. Lymphocyte transformation study. Lymphocyte transformation test results are considerably scattered in all groups investigated but mainly in asbestosis cases. To evaluate the results expressed in counts per minute it was judged that all results below the mean value of the control group minus one SD were considered as abnor mal. Table 2 shows the number of patients test results below this value. This clearly Table 2. Frequency of impaired response of lymphocyte microcultures in vitro to mitogens Without asbestosis Without asbestosis Asbestosis with with ANA u = 5 and without ANA ANA it - 12 (9/3)* (3/2) mean age -- 50 n -* 11 (9/2) mean mean age -- 52 yrs yrs age 44 yrs PHA (20 fig/mi) PHA (5 (ig/ml) ConA (10 (ig/ml) ConA (2 (ig/ml) PWM (0.01 ml/ml) 6/12 (50%)** 8/12 (67%) 8/11 (73%) 8/11 (73%) 8/11 (73%) 3/5 (60%) 3/5 (60%) 4/5 (80%) 3/5 (60%) 4/5 (80%) 2/11 (18%) 3/11 (27%) 5/9 (55%) 3/9 (33%) 3/9 (33%) Results ofthe test were expressed as mean counts per minute of tritiated thymidine incorporated by quadruplicate microcultures. Impaired response means those results below mean value of control group minus SD; * number of people investigated (in brackets femaie/male); ** ratio of numbers ofimpaired response results to ail number of patients tested (in brackets are given percentages of impaired responses). demonstrates that in asbestosis cases 67% and 73% of cases are in the abnormal range when PHA and ConA were used in the intermediate concentration. Similar results were also found in the asbestosis negative but ANA positive group. Only 27% and 33% of asbestos workers with prolonged employment but lacking asbestosis and ANA were in the abnormal range with the same concentration of PHA and ConA. When indices of stimulation were considered the percentages of abnormal results in the asbestosis group and in asbestos workers without asbestosis and ANA were comparable. The highest percentages of abnormal results were found in groups oi asbestos workers using the intermediate concentration of PHA (73% to 100%) and ConA (40% to 64%). Interestingly stimulation indices of PWM activated cultures in asbestos groups of people were in almost all cases within normal range. This is a p: abnormalites i different techn asbestosis case ANA. The abi relationship tx workers. How fibrosis. This i the disease pr 1. Kagan E.,S Clin. exp. I ' 2. Kagan E., S . noL 1977, 2t 3. Kang K. Y 4. Langs A., : 5. Langs A., 6. Lange A., S 7. Oppenhhm of clinical i 8. Pernxs B., ' 9. Rocklin R H. FriedMi p. 95-100. 10. Seutoff I. 11. Turner-W, 12. Zwounski Received in M 6113 22353 xol group. :ained with -.owed that rest results results are : cases. To ail results i as abnorTiis clearly '0 to cosis -NA nean udine suits id (in mber rmal range This is a preliminary report of our work on the Tange of lymphocyte functional abnormalites in asbestos workers. It was clearly documented with the use of four different technics that cell-mediated immunity is impaired to the greatest extent in asbestosis cases and to lesser extent in asbestos workers without asbestosis but with ANA. The abnormalites found in the group of people with ANA points to the close relationship between humoral and cell-mediated immunity abnormalites in asbestos workers. However, the most pronounced abnormalites are found in cases with lung fibrosis. This implies that impairment of cell-mediated immunity is closely linked to the disease process in asbestosis, which is connected with a high risk of cancer. REFERENCES 1. Kagan E., Solomon A., Cochrans J. C., Beissner E. I., Gluckman J., Rocks P. H., Webster I.: Clin. exp. Immunol. 1977, 28, 261--267. 2. Kagan E., Solomon A., Cochrans J. G, Kuba P., Rocks P. H., Webster L: Clin. exp. Immu nol. 1977, 28, 268-275. 3. Kang K. Y., Sera Y., Okochi T., Yamamura Y.: N. EngL I. Med. 1974, 291, 735. 4. Lange A., SiaBtNSia G.: Scand. J. Immunol. 1977, 6, 720. 5. Lange A., Skibinski G., Garncarek D.: in preparation. 6. Lange A., Smouk R., Zatonski W., Szymanska J.: Int. Arch. Arbeitsmed. 1974,32,513 --325. 7. Oppenhhm J. J., Schecter B.: Lymphocyte transformation in N. R. Rose, H. Friedman: Manual of clinical immunology. Am. Soc. Microbiology, Washington 1976, p. 81--94. 8. Perms B., Vigliani E. C., Seukoff I. J.: Ann. N. Y. Acad. Sd. 1965, 132, 112--120. 9. Rocklin R. E.: Production and assay of human migration inhibitory factor in N. R. Ross, H. Friedman: Manual of clinical immunology. Am. Soc. Microbiology, Washington, 1976, p. 95-100. 10. Seukoff L J.: Rev. fir. Mai. Resp. 1976, SuppL 1, 4, 7--24. 11. Turner-Warwick M., Parkes W. R.: Br. Med. J. 1970, 2, 492--495. 12. ZwouNsn J., Wieczorek Z., Skibinski G.: Arch. Immunol. Ther. Exp. 1976, 24, 689--695. Received in May 1978 The author's address: uL Pasteura 4, 50-367 Wroclaw 4 ^*