Document 2NrMby68yp4erpn0ZrQ0vMJ5N

ILLEGIBLE L^*. Wi VSSCITa tt i Prevaleuc of disease unions vinyl chloride and polyvinyl clilox*ide workers by Kuth bills, II.P., Henry Anderson, M.D., William J. Nicholson, Ph.D. Susan Daum, M.U., All S. Fischbein,M.ii. and Irving J. Selikoff, K.D. The emei*genco in January 197.4, of vinyl chloride as a new occupational cax-cinogan, producing he-nangiosarcoma of the liver focused new and much enhanced attention on the toxicologic effects of this chlorinated hydro carbon. .` A considerable number of studies had been published on the rather puz zling and unique syndrome of "acroosteolysis" (Table 1) mainly describ ing the bone lesions in the distal phalanges of the fingers, but also the associated scleroderma-like skin lesions and the striking vascular (arterial and arteriolar) changes, pathologically the main lesion, leading to secondary bone and skin changes (Tables 2 and 3). Much less attention had been given to the hepatotoxic effects of vinyl chloride, although convincing experimental evidence had been produced (Torkelson et al., 1961) and scattered reports of ill-defined "liver changes were included in some of the studies of vinyl chloride exposed workers (Table 4). -:V "' ' ' v --- i*i* There was evldenco that liver damage occurred in workers exposed to higher levels of vinyl ^loride. : ^nffseme sft^ies.jtbe liver changes (hepatomegaly," 'tenderness :'oh^j^ph0i^^^h^awirillver'' tes found to to reversible" al^r^^sslItl^^i^'lfe^bsOToil^Oii 'tJi^'o'tlS^jf observe tlons mentioned.; jiessiye.nature of the *> 1Thes*a'" u gthfaowrsa wore alerts ;#i^t^testiimy>leedihg| product , fibrosis of,. 55gt*faa at changes encompassed collagenous ^trahsforraation^of the liver * focal activation of ICupffer cells, ""ificreased collagen deposltibn^n^tlva. portal spaces, portal fibrosis, septal and Intralobular fibrosis. ` v':; There are a few mentions in the literature on.lung changes in FVC workers* One case of pncumonconiosis in a thirty year old worker who had inhaled PVC dust was reported. The lung biopsy showed granulomatous lesions (foreign body type) to be present. Fibrotle changes and altered pul monary function tests were reported in 96 workers exposed to polyvinyl chloride dust; the changes wore jnore pronounced in persons with long,:; exposure (Vortkin et nl. 1970)7^"^" In thu available* litratiu*o on vinyl chloride and polyvinyl chloride ad verse health effects thore were no accurate data on the prevalence of disease in exposed workers, the relative prelnvence of Iho various patho logic changes, their possible association and tine sequence. V.'e have undertaken clinical studies of a number of gx-oups of vinyl chlo ride exposed workers in order to assess the prevalence of vinyl chloride induced changes and to define the natural history of this occupational disease. We ax-e reporting the results of a survey (March 197'!) of 267 workers currently employed in n VC polymerization plant, including vix*tually the entire current production workforce. 87 -former workers were examined as well. In both groups, exposure for some? had stai*ted in 1015, when the plant opened. Altogether 354 men were examined. Table 5 shows the duration of exposure.for the group and Table 6 the age distribution of the men. More than half were under 40 years, 20% were 51 or older. METHODS The medical examination included detailed occupational history, past medi cal history, complete physical examination, with special attention to th skin, hands and feet, arteries accessible.to palpation, liver and spleen. An Allen test for the assessment of the peripheral circulation in th areas supplied by the radial and ulnar arteries was performed. Each examined worker also had the following: ' : , <, ' ' 1 7. '' ""'VY-ii-? ,.X-rays of the chest, hands and feet; pulmonary function tests; counts' including platelets; blood chemistries - SGPT, "alkaline phosphatase, fibriwwgg luscleantibodies * InT^er^tlixidi^f tlfSn of the ^tested'fercarc3 va)tKiUftRgifirbxeIrr>**f,'3iw*.ieCsl" aiSEI es were under RESULTS Unfortunately, appropriate VC measurements Jjad^not been made -in/Jh past. We have ^findings which suggest, howeverCTablo 7), that-Vc^'/^ levels may have been^cohsludrahle at times/ sufficient to produce symptoms of acute overexposure; for example, 14 of the 354 workers had had loss of consciousness at one time or another. In any case, our data Indicate that measured levels would be of limited utility, unless integrated over time, since both total cxposui'c and duration from onset of exposure seem to be of Importance in relation to ...likelihood of abnormality. The influence of these variables may b demonstrated in a humber of areas. This v/a3 so insofar ns abnormal periph ral circulation was concerned (Table S). Numbness and tingling of the fingers, along with increased sensitivity to cold were early symptoms. They were often associated with pain and cyanotic discoloration sometimes also involving the toes. Claslcal Raynaud's syndrome, characterized by cold-induced, marked, sudden and sharply demarcated pallor of the fingers followed by cyanotic dis coloration in the same area, v;as found only in 5,G% of the cases. In general, the effect of vinyl chloride exposure on the peripheral ves sels of hands and Xpet appears to produce a wider range of symptoms . than those characteristic of Raynaud's syndrome. As noted, the prevalence of these, changes rose with duration of ex posure. Typical Raynaud's syndrome was fouhd in aLuost 10% of cases with more than 20 years of exposure. The prevalence of Raynaud's syndrome was significantly higher in workers with wore than 10 years of exposure, than in those with less than 10 years exposure. Symptoms of abnormal peripheral circulation (Table 9)-were more frequent in workers currently exposed than in those with past exposure. An abnormal Allen test indicating delayed arterial circulation in the areas supplied by the ulnar and/or radial arteries, was found in 94 (26.6%) of the examined workers (Table 10). . The percentage of persons with abnormal Allen tests increased with their length of exposure. The prevalence of an abnormal Allen test in workers with more than 5 years- exposure was signixicanfly higher ;,>;tftan in those with less than 5 years exposure ^k*Pseudo-iolubbing of the fingers wag also' found with'increasing quency as the duration of employment increased; the overall preva-> so 'vast 8.7%;. in, the group, with wore than 20 years of exposure, t? o 3^.6()$T|ieaao-clubhu>g. w fatadgt^always associated" fts a more frequent finding .thatT^ical Rayiwnd^l-syndrome ^ Raises,_ especially in persons with past exposure, there was^a i'Si( -'1bl?iS^aud*lSrjs^d,ro^Miii^i had""gradually faded, while * changes (Table 12)t,involving^the fingers, hands,"" forearms lthd,rsoane*5 times face, were found in lZS examined"workers* ^Ttie fingers 'and.' hands -ap*^ peered to be slightly edanatous, the akin was thickened, tense and stiff, villi decreased elasticity and sparse folding. Well circumscribed plaque r ' band areas of scleroderma-like skin changes, as described by others, were not found. In 9 of the 23 cases in which skin changes were found, Raynaud's syndrome was also present. `ti Pain in the small joints of the fingers and hands (Table 13\ was a complaint X in 28 (R%) of cases and was found mainly in workers with currcnt .exposaro, even of short duration (Tabic 14). There was no special tren^'^^ard-^' in;; pain in oUicr joints, except for the wrists, where most of the cases v;ere found in workers with more than 5 years of exposure. There were no symptoms suggesting involvement of the sacroiliac joints,,and .. no radiologic evaluation was undertaken. " * '` Hone? changes in the distal phalanges of fingers nnd toes will be separ ately reported in detail. While slight changes, such as marginal cortical defects and slight tuft rcsorbtion wore not scldomly seen, transverse defects and fractures were found in only 4 cases, Vfe were intere.s tcil in the possibility that hypertension (Table 15) might be of importance. V/e did not find this to be so. The overall prevalence of hypertension (as defined by T.'f!0 criteria) was 12%. Ihcrc v.as no correlation with peripheral vascular impairment in the hands and feet. Abnormal urinary findings were not prominent either (Table 10). The liver was found to be slightly or moderately enlarged in 15% of the cases (1 to 2 finger breadth below the_ right costal margin; 11 to 13cm vortical span (Table 17); this finding was more frequent in workers with longer duration of exposure. Only in one case was the liver found to be markedly enlarged. Ihe inferior pole of the spleen was palpable in 12 (3.4%) of cases: Again, only one person had marked splenomegaly. There was a highly significant difference in'the prevalence of enlarged liver in workers with more than 5 years exposure as compared with those with shorter exposure. The same comparison for splenomegaly did not show a statistically significant difference. According to the past medical history, a diagnosis of cirrhosis of the liver had been mad previously in 5 cases. Esophageal varices had been diagnosed, in one patient who had undergone surgery, including portoc&val shunt, 12 years before the present examination, with good clinical result; Abnormal liver function tests (Table 13) were found in small percentages .,.(6% fo.r....b...i.l.i.r. ubin and SGOT, 9% fox' SGPT), except for alkaline phosphatase .which was elevated in 59 (16.6%) of cases). T ? Duration of ^exposure correlated with an increase in the prevalence of alkaline phosphatese. cspecially in workers with more than 5 persons with current or prior exposure. ^ . - The best correlation between clinical findings; of hepatomegaly and/or j ' ^ri^Vsplettojaegaly and abnormal liVer. function tests was. found to be that with ^4?|t^lyated' 'alkaline ^osi>ihat&seV^bdhiit"30)| ' '41%vof TthM^ ^ abnormalities had''increased alkaline phosphatase.'' !' ' Hematologic abnormalities were scant in our study. Thrombocytopenia, a frequent finding In the German studies, was present in only one of the examined workers (Table 21). The possible contx-ibutory effect of significant ethanol intake was care fully considered (Table "2): no trend as related to duration of exposure could be found for ethanol Intake.,. ,, ..av. . X">., In one-third of the cases with clinical liver and/or spleen changes sig nificant ethanol intake could have been a /actor (Table 23), and in 25^> of the cases with increased alkaline phosphatase was there a history of significant intake (Table 24). Further, the prevalence of tin enlarged liver nnd/or spleen in.persons with and without significant ethanol intake vas compared (Tallin 23). While there was no statistically signifleant (li fXercncc in workers with less than 10 years of exposure, In those with iiora than 10 years exposure, there was a higher prevalence of enlarged liver and/or spleen in persons with a significant ethanol intake. A multiple factor additive interaction may be considered. Liver function tests were also analyzed in relation to ethanol intake (Table 26). There was no significantly higher prevalence of elevated alkaline phosphatase, bilirubin or LDH in the group with significant ethanol intake. However, high SGOT or SGFf values were significantly more frequent in this' group| It is of interest that .elevated alkaline phosphatase, the most frequent biochemical ronomality found, did not correlate with ethanol intake,, while there was a significant correlation with duration of vinyl chloride exposure. Many of the' examined workers (Table 27) gave a past medical history of "gastritis," ulcer (gastric and duodenal), upper gastrointestinal bleed ing (most often attributed to ulcer) and gallbladder disease. However, it is difficult to know whether such symptoms were morn common than might be expected in a similar group without VC exposure. Out of the 112 workers with such past medical history, there we.re 28 (25%) '-ho were found to have enlarge liver and/or spleen (Table 28); the percent age was 38% for those with past upper gastrointestinal bleeding and 38.4% . for those with a history of gallbladder disease. In the other 242 workers without such a past medical history, 29 (12%)Ywere found to have an en-`V*i , larged liver and/or spleen. Cuihceasti x---rraays orf 142 evxjoaumuinemd..sprlcers were available at the time . thatthis report was prepared.., lrt;sonie^'^^^ nodular Changes w^re' ^dutidr reticular lower 'lpg Ko relationship was observed[''with smoking oF chronic bronchitis' rylnyl cbldrlde tresih*as^^(jf^^^^^^^^^...p...r..^...p...i.t.'.-.'i.V.',,.%...^>ce'~'; ^^^^kbnoraal. nes 'io^^r'ioAa' Fang." between/chcst x-ray chan Sift' of!^peripheraiVascular" impaiS^ntjC^yna^^^yhdraae*, 'cyahcfrp^ ^bbiigVj^itiye-Allen tcst)^Ta^leIn^uoro^^ (53%) '' '' '* Discussion and Conclusions Our findings confilm the broad outlines of tho clinical syndromes reported by other investigators. In the examined group relatively high VC exposure had occurred in the past, and symptoms of acute prcnarcotic effects were reported by more than half of the examined workers. ': ' i' rL; && ffjoti-a. t6 Clinical signs and symptoms of abnormal peripheral circulation in the fingers anti toes were quite frequent, with cyanosis present in in per cent, excessive sensitivity to cold in IS percent and numbness and lingling of the fingers in 24 percent of cases. A typical Raynaud's syndrome was present in 0.7% of cases. An abnormal Allen test, indicat ing delayed arterial circulation in the areas supplied by the ulnar and/or radial arteries was found in 94 (26.6%) of the examined workers. The prevalence of all these abnormalities increased with length of VC exposure. Hepatomegaly was a finding in 15% of the examined workers, while splen omegaly was found'in 3.4%. Cirrhosis'of the liver-had been previously diagnosed in 5 workers, and in. one esophageal varices with upper gastro intestinal bleeding had led-to surgery including.portocaval shunt. Alkaline phosphatase was the test which was most frequently found to be abnormal and showed the best correlation with clinical findings-. Hepatomegaly and elevated alkaline phosphatase were significantly more frequent in workers with longer VC exposure. . Radiologic pulmonary changes, linear reticular and nodular opacities in the lower and middle lung fields-were found in a number of cases; the prevalence of these changes was higher with longer duration of exposure, and. there was a significant association with peripheral circulation abnormalities. The evaluation of these pulmonary changes is still in .progress. """/v/ _ Our results indicate that liver ^involvement and probably lung involve-- V`||>t?went in PVC workers are significant and.should be given,ull attention /i-v^in the medical surveillance of'workers with past "a Future exposure to..vinyl chloride should be controled in order to pre- .5/ * ii . ^^'-g-^^yent development ofalladverse effects, including the carcinogenic ' - ' ' '"''A- -ty-uSL; '* fS Table 1 Acroosteolysis 1957 Filatova and Grorisberg 1963 Suciu et al 1 1966 Cordier 1967 Harris and Adams 1967 Wilson et al :'U" 1971 Winman et al ''Angioneurosis of spastic character" Raynaud's syndrome - (hands and feet) 6% of 168 exposed workers Scleroderma-like skin changes - (hands, feet, face, neck, thorax)' 3.6!* of examined Raynaud's syndrome Scleroderma-like skin changes Lytic lesions of terminal phalanges in -hands and feet - The same changes and -'pseudoclubbing of fingers *- Involvement of sacro-iliac joints and V patella * Table 2 Ac'roosteolysls Bone Changes / - Marginal and/or cortical detects in distal phalanges - loss of cortex in tufts of the distal phalanges -- "Half-moon" defects or cuts -- Transverse defects or fractures - Complete resorbtion of tufts and part of shafts * -- Involvement of the larger bones Cystic lesions and, increased radlolucency (ulna, radius,fhumerus, os calcis, patella) i'; - Erosive and sclerotic changes In sarcorllke joints *. .. Suffer-?' vj, Vi-*4~-f^i44^,1 fi44'V: r- ->/. vft .fe '"; #'r' ,, - Jrv- - '*vy?', - .a^ Table 3 Acroosteolysls Skin biopsy pathology * - Thickening of dermis - Nonfibrillary homogenization of collagen and thickened collagen bundles I - Disorganization of elastic fibers, which are split and broken , , , .. - Inflammatory infiltrates, predominantly perivascular (lymphocytes, few histiocytes) j-Mst:-., - Intersitital edema. . - 4^Jife 44 - . / '4'""" v ^>J>il&tation .of ly|^tica-444v4'Hg& ; ' > 'r4y,Y;.V' &\4- Table 4 Evidence-of liver damage in PVC exposed workers 1949 "Hepatitis-lilie liver changes" Tribuch et al. (Russia) 1963 "Chronic epithelial hepatitis" in 15% of cases; hepatomegaly, in- .creased bilirubin and prothrombin time, abnormal Takata-Ara test. j 1963 Hepatomegaly in 30% of 168 ex amined workers, splenomegaly (6%). Liver biopsy in 2 cases: "chronic hepatitis." ` . 1967 Hepatomegaly; persistent raised bilirubin. . i'-ii, Pushin (Russia) Suclu et al (Romania) Harris (England) 1 .'tyr- 'T " icreased CSP retention, raised *..............s...l.ated to degree 'sb exposure. \4m |P'; - ......3*DQ'.. ,-g-. bj.;; *ith scleroderma-like skin changes). , '`'2,^1 ^ ` i V>K - 1 I^.V, v , ,, 4#* Table 5 Duration of vinyl chloride.exposure among 354 workers in Niagara Falls Duration of exposure (years) Currently employed Formerly employed Total ) Duration of Exposure (years) Table 7 ./ Symptoms of acute overexposure ' among 354T vinyl clilorido workers Symptoms Lightheadedness Dizziness 21 9 30 30 25 20 40 44 26 32 Loss of Consciousness 3 3 0 7 1 | Total I 2S 1 43 1 33 j 35 j 36 _% 46 57 53 53 69 135 (38%) 14 (4%) 1S6 55% ! ??*& \W.' v :',r V '' " '` v 1 i- `5 - ..i^r'5-!-: s\ 1 - -. - . >-* * Table S t-y^ ' * 4 VVV % Vi (ii- j ''k'si; v*ff^crV- ^1S' ^ ' i ^ o*1 k . ,, -linical signs and symptoms of abnormal peripheral circulation among 3S4 vinyl chloride exposed workers Ilayna synd: ,'if*eS*f. - M?r *j ,-fiL-v-y 'Prevalence in workers with more than 10 years exposure significantly higher than in these with less than 10 years exposure, &-:*&p <P."oa .. V'-iMfci-. - ' Table Raynaud's Syndrome among 354 vinyl chloride workers Exposure ` Raynaud* s Humber . Number % Active Prior 267 17 6.4 87 3 3.4 354 20 5.6 ' t. + , \ 1 1 ' iv ;' I r: ***$#% Tabic 10 Abnormal Allen Tost among 3S4 vinyl chloride workers - .Abnormal Test Results Current Exposure Prior Exposure Total* *' 5,1-10.-'^" ao.i-20 w-:aaw r p;f Mi; 7/36 11/62 16/47 ,22/77 12/40 68/267(255%),. 2/25 9/6i (14.7%) 18/73 (24.0%) 23/62 (37.1%) 27/104(26.0%) 17/52 (32.7%) 26/87(29.9%) 94/354(26.6%) bf-S., W-S.-. ...... ' abnormal, Allen Test in workers with more than 6 years - moxpogixtmm^tic^tly' higher than in those with less than 5 years exposure.^ %a. # QS4 002<p< 0.05 -illfw?' Table 11 Psuetlo-clubbing of fingers among 354 vinyl chloride workers Duration of exposure (years) Pseudo-clubbing of fingers Current exposure Past exposure Total t2 2.1-5 ,5.1-10 10.1-20 20+ 2/36 3/62 3/47 7/77 7/45 *I 2/25 0/13 3/15 2/27 2/7 4/61 (6.0%) 3/75 (4.0%) 6/62 C9.7%) . . 9/104 <S.6%) 9/52 (17.3%) 31/354 (8.75%) In 25 cases - signs/symptoms of peripheral vascular disease In 8 cases - typical Raynaud's syndrome. , '^/y. ` \ ^ ^ ' 1 : '^ ' ' m- 1 * v',-. 1 . ' ' *; v , >js H -CxW Table 12 Skin changes in 354 vinyl chloride exposed workers Tabl 13 Pain in joints of fingers and hands Duration of exposure (years) Total number examined Fingers, Hands No. % Wrists No. % >2 G1 5 8.1 1 1.6 2.1-5 75 5 6.7 5.1-10 10.1-20 62 104 2 3.2 1 1.6 ......*4 8 7.7 3 2.9 20* 52, 8 15.4 1 2.0 J. Total Koto: 354 28 8.0 6 1.7 r.` -.^T -V. $;;,4 Difference in prevalence not significant for workers with less than 10 years or wore than 10 years of ', ' 0g?p! v. jVVfrfy,-* k- ****?? *. >' ,' ^ A*' , * ^ . . .>' . ',>, * ?&(!>-' jRaKsfit?1' j,, ^Sx*?' VV -' * :-v^ V) Table 14 Pain in the joints of fingers and hands I1 i < 5 i <SBf CO* r -I I j. J g iL S2I' :[ S~ O- j ,1s ,% *. - -`^-v Table 17 Hcpatosplbnoncgaly among 354 vinyl chloride workers Enlarged spleen** W h^ ^Wv`- ':;' . ;$,& J9teV 53 15.0 in^prevalenoe of enlarged liver in workers less-than 5 'years as compared to those eac-'moap'than 5 years. .2 , ,, .._ * ' *' ' ' ' p <0,001 , .*- ' ^ f&t'W**fi*rS9(i .spleen yCm 0.S48 rflS:`>`ta &J EH*??vI>.V-SC^' : -'. - - n s * 1 y^:"?; >v V;w- Tablo 18 , Abnormal LPT among 354 Vinyl chloride workers Duration of exposure (years) K2 Total; nt&bQr OTcanin^d s&u-rvr : 2.1-5 \r< 75r' . . Bilirubin >1.1 SG0T >50 SGPT >36 LDH >225 2 3 50 5 470 Aik. Phos.,> >86 9 12,6% 7 9.3% 5.1-10 10.1-20 62 ;xhr 1 v-f' ./1J>0,,4` - 7 2 3 54 683 11 17.7% 19 18.2% 20+ ' : 5 461 13 25. C% Total '^#y , "mv- 354 -T, 21?6%) 20(6%) 31(9%) 8(2.3%) 59 (16.6%) Prevalence of elevated alkaline phosphntaso significantly higher In workers with more than'5 yeors exposure than In those with less than 5 years exposure. -?. :2 \) Ipgj . ^C'- 3!84 p*0.05 , ;' ' S' . VV V V r;j*Ufit^SSf '-i* .': ; - ' :if ' -*'' &' ^!fMr '* - + iM* -i-co; "S3* >.'.* - , i >rtp Liver function tost Bilirubin SCOT SGPT ZJDB All:,.Phos. >1 >50 >36 >225 >86 Current Prior employment (2C7>.w.^alrln^seaTHoywont (87) 18. <6.7%>JOggtf|l:: <3,6%) 17 t<3,0%) 26 "<2.4%jplf^ 6 <5.7%) <2,3%) 1. sol'/-.: <18.0%) i Hcpatosplcnonesaly, Hepatic tenderness (66) 6/20 <30.0%) ^ 8/31 <26.9%) - 27/59 <45.S%) ile 20 - - ^gr %>tO. :j9apit >jg|^iunoJsgf ..no phosphatase rjr^ilprjU|e1 workers ' 4^ -IT Duration of exposure (years) K2 2.1-3 -' 5.1-10 . .10 1-20 20+ .pod liver, and/or ipp|efc^ . hepatic Elevated ^iftrodernessV '&* ` alkaline phosphatase i'<, V:- ='.'.> v1S..:. j;: '*' :-i fj - .i<js4i; VJ . j#t f ' -'vk ` TV , ' f " 1 ^r,y vt, *f 's. J%i '.f&'-Z'i : 1- t 3 1 4 43%' 14%. 40% .... 20 - , 10 45% . '_ 0 45% 27 41% *4 ' I-?-;' -Vfc .Mfo'iffe- , i * i ',"^1 - Heaatologie .haage#iin 354 chloride workersif; 'r * ^4J-l ,' Total number Thrllinkrb! o'Vc^iy1' ^to'' p* enift^ ; -. Loueoponin > examined # t-inXiso'iooo^^ <1,000 4,000-5;000 Hemoglobin <14 gr; *2. . . 2.1-5 ; 5.1-10 61 v,^ 75 , k-M^MM ''2* 3-:. Ji5U?-' &k> . -,t4-- ' ..---'-v*/v 10.1-20 104; ,8 ' ^ ,'ir'- 6 '& . . \.q: 2 .-- -"^,-*j6S!*; 6'.^% ;; 1 :1 : n"' -. "' s ,,;. 4+ '.v> 20+ 52 Total 354 ' , 4 f*<i ,-: +persons with past history.of 0; 't- ''t `i' - 6 ft. *jg 'm ,:fi (1.4%) 28 (7.8%) -*Xv.. ' 2++ -,/ 8 (2,2%) ` *; /' / *tf" IJA .JD O ];; o il! JO IJ O /O itfl'in n n i rrr Table 22 Alcohol intake in 354 vinyl chloride exposed workers Alcohol Intake Duration of exposure (years) Total number examined ++ (1-2 qusrts/vreok) +++ (2-3 quarts/week) S J. 61 'V 10 5 ++++ Known alcoholic 0 Total ~Sb. %' 15 24.6 v1 414 : 2.1-s; -\J. 75 \V; 5.1-10 62 ' f -, v, < < . It -,'.44 ;;; "5'Y"" *7 f , o 44-' '>; , S-, "':'k. * ''.''4 16 ' 21.2 '* 13 21 it; io;i-20 Tf 104 ''-5' '& jgmMffifa:; ?,;,r tr-- - :*4 /.Vf-fXi , 4a,' if. ^ ':4 13 12.5 ` ' * yV*4" ,.V-? 2o.i-> vi&f' ' % -v ' V, 10 ' '' : ~ . 'V ' 1 12 23 , 4":'' T-Vrj fC^V-: . . ; Total 354 53 15% 14 3.9% V 4 ,/ 2 0.6% 6> 19.5fi t V/ith UrjovircKjil cind di t'cl IhfPP l> r* T * f.i. fm Jr :-r T*-r J*. t i - . Significant alcohol intoki|s*&jliv*r. chans* (clinical) V-t-lWCSfekttfjr^ r , &iir: ' 'V Duration of. exposure (years) *------------- ' ----------M S _ ** Cases with significant alcohol, intake :i&.- Table 24 ''-v `L'-;' Klevated alkaline phosphatase , ;y,-., ,. .-. . ; manud bsiiugan^ixfi^ccaaniiit. Bajliccooih] ol intake <v'. -.-v y.r? v.-v >".......:........... ' `P-- -v!; ,." ;:. * a AAllhkaline Significant , . Duration, of: Total ' 1 phhoossiphatase alcohol intake exposure (years) examined Mo. % No. . * % -* * T"1 ^ *4? Vt- r^1' < ^ ^1A04A1' " 52 *i4,4V-J w * 19 13 12.6 ,:^l':v;^1.6 -, - v,**'1 17*7 '*>' 0 r*;j&f.7 18.2 ' >2 3'"' ,1.9 25 4 7.7 Total 354 59 16 14 3.9 /' HI f Jl Sl \r:- "Table ' ' /A- fir'.:i0r. *;w,*3*+`i .V,'* V# i**:A V'*,*'?&* **?., - sC ., ,i! Hopato- aod signifl ^*noragaly4~ ` ol intake Significant alcohol .; No significant alcohol *2 V ^n^argQ4, Total number :^pllvepg and/or oxaminod ' , '^Kaaanmm- I^^A;eie6n'V"' 'Jjaffis*'-. i, aStssk wftniWo'T^tf "~H %-s 61 4^, r Total number ,40 Sniurged liver and/or -* spleen No. % 47 13.0% 2.1-5 5.1-10 10.1-20 20+ Total 73 ... <w.v, t - -.tn. 'A 62 :Mdmm SSwft: i*.; - Jr. 104 52 *'c 354 -. o*" ".A ; e#|Sl^i 29** 59 49 91 40 285 U4 5 . , 17 .12 , 45 6.8% **>10.2% IS.7% 30.0% 16.0% Difference .in prevalence of on] 'lif' f-u rand/or spleen between the group with alcohol Intake and thoso .without ft! i^tako^aon-signifleant for workers with less than 10 years of "life 'Sf A ..........^.i.'A...'.US105' 1k:' ' 4-; '). ' ' .1 . !'s <t-, - . ..1$-,- . -4" -Y:- < Significant for workers with more than 10 years, exposure. *)t2 7.243 p< OiOl > "*#. j if""' "'^1^ &A?m hr <3P *wS'V.-- * - f1 ! ' KV& ...t f g!S, ?' *1 '-V /IV*, ' ' Table 29 t ' sg .. :v.U \ - -vi! ' - -i i <9 Alcohol intoko and abnormal llvor function tosts -jfe. Total number ---------------------------------------1 examined Ko.J. AXStL^Jib.; , ' Significant alcohol intake I jjjl- ^ 20* 69 j SCOT so?r -So, -J', .% Tfol % No. % i ,;,9 13.0% 11 16.0% 2 2.9% Non-significant alcohol Intake Total .' j 285 354 ,'*6 .- ^ . 45 V, 15*i|^ I^aoii- Ti^ 11 3,9% 20 7,6% [frM - - , -u -> a>- 59 ; 16.0%^ teii'0.0%^ ,20 6,0% -w ;&8* 2 r>.i_ 33***;0t88*T,^^'VE;S:- >V-7^ 8,790 ^siSMI`.ff;Pf O.01 31 9.0% 7&i 5,337 P <5.01 6 2.1% 8 2.3% n.s. v "mmM - ;'Ss':-IVA V:X. I ''Oft* * -9 *3 ' ;.i Sv-Kk'.K SIS*-- iv.i SHlIsS??' ,V-fe- GastrointestJUwl diseasp (|y I*f*tory) in 354 vinyldhlorido exposodwjrkers *&** * ' "Gastritis"#'; *.; ^.iijTf-:i --*- ,E; id fV.' -.? KS , Ulcer (gastric ' 3*\ 9* or duodenal) ; . . ) 52 -i. tlS Ulcer and upper 2%) , G.I,<bleedin^ zfc.;\ 1 *.- k . f. Gall.bladder; -"; jja&r ^9fc=- disoase ^,V,.-- .v - !:- ' s^'-- *- Total . ,&' | ; 112 l.W'- '>I1. r ;. <s> ,'.-Aasv;- is step&-'? ' '-:/ -;': SV i* .iir *i ' -:'%y * -` '"'HQ -"'* :*': 0 ''if" ' ^ ^ *` t > 'jH ty%jT'f -f 0 ^ I------------ V-Vfe' i '' ^ ' j' ' t^trotntoptina|^L^|^by h.istory). and enlarged^ "Gastritis" '-Enlarged liver i-Mmi Mo ;**-- % |iJ* * l7-* Ulcer (gastrio or duodenal) 7 22.6% Ulcer and upper G,I, bleeding; .. Gall bladder disease , j {Vi..- >/ 13 .' ` " * j*>i ` ' ~ ;8 38.0% UvW'.,"- * *- /j-. 5 38.4% * ID- |Aj 1 4 li Duration of Exposure (years) ^2 142 vinyl chlori' .- = P Current MT.;; Exposure^" V' 1 ........ \ ^ 13 Current; ; 6 Prior 2.1-5 5.1-10 10.0-20 -- 3 Prior *i 19 Current,^:-:- 8 Prior ' '- '' 32 Current '5 Prior ! Ar } 204- . 23 Current 3 ^ !6 ,3t ? ng 5-2* r0,-^- r-?.. ,'?ii.o >, -;'ig -I1' '^15 ; 3O-: %VvK^">:'i' 33.3% Total Data incomplete --.in --j m '.-V.iS-.gr. 'T%' 'fvS '' 38 *.. 27,0% ~Sfe - -i ,;f ; i : [ * lltej " J:y' ^i/s^-v'-X kiP-1 .kft' '-. Cfte. - -H Chost x-ray | To*al B number Normal | 104 : ' Smokors -: /So, ` Ex smokers '' % sVk, 53 "v |51'lllf^i 22 Non-smokers So. % 26 27 Abnormal | 38 ! i 'r- w?. '^Tf, * '' r so /`l k '0.;, ts&f&rc llfe?k .- i-/I ; 7 IS Prevalence of abnormaMflifceat :,.x-S ^persons with history of smoking - hotp|pn.ifiS(atly. different from that in non-snok.e...i.. 'A.^-s^sfee*`wS^^,0^8&3?V t . - >- ''' >'>3v<' * r" *- 'e tt** ,-= fttffiflHBlfc? .f>r%*`irr.tih.(Tt -c . - - . --5>r -.*J- L-;':.:-'f-' If1'' -J. -1' 'i f; >vr V * If? *-,.; .V'.^avf- . >3 1 \? : 4^ \ " '-tf'if'' ^'. > tfffef *i;: -1: O'flWb't tilA/, ^ * -it . ' -.fc fy Abnormal cheat x-rayond Raynaud'8 syndrome J '-,sc'v''>< , .. >,) ' X '*%* L ': -- ' Pseudo-clubbing Xomal Abnormal 5 4,3#t *4% -Jl'#:' I'''"" , *8-4' *^2 6.667>; p <b.oi;f: ^W^-C - :^.;V ,'$f 4Jyh, *H'h' J-V'* } ' -r 4 --` '*- .:--: - . . I ] ' 'J Abnormal Alien test 20 19 13 34 f?m 3.501 n.s. / CD >D I Q - - 'tlv'" - - ' Si-.' i