Document 5LEXJpaY22yoa57yNwX18N2JN

TURNER. COLLIE TRADEN. INC. CONSULTING ENGINEERS June 19, 1974 General Coble 800 East 2nd Street Bonham, Texes 75418 . " Attention: lir. Dave Richardson Dear Hr. Richardson: In accordance with o request by Union Carbide Corporation, Turner, Collie & Braden Environmental Laboratories ere pleased to submit data on the Industrial Hygiene Survey for Vinyl Chloride Monomer conducted in your plant on June 12, 1974. We would like to thank you for the fine co-operation and assistance , received by our technical representative during his visit to your plant. Turner, Collie 6 Braden Environmental Laboratories welcomes the oppor tunity in being of service to your company in the near future in this .and other areas that are briefly described in brochure's, which are enclosed. If you have any questions concerning the results and/or our services, plea se do not hesitate to call us. Very truly yours. TURNER, COLLIE & BRADEN, INC. Oscar Saenz, Jr. ,, Hded, Environmental Laboratories ^ cc; Mr. M.E. Eisenhour, Union Carbide Corporation Mr. George Tacguard, Union Carbide Corporation' Enclosure < I 23559015 Mailing Address P.O. Bo\ 13039 Houston, Texas 77019 Phono 713 / 528-G301 3203 West Abb.un.i BFG26313 Journal of Occupational Medicine August 1974 Vol. 16 No. 8 >' - V *-$' Mortality Study of Workers in the Manufacture of Vinyl Chloride and its Polymers* Irving R. Tabershaw, M.D. and William R. Gaffey, Ph.D. Animal studies have shown that inhalation of vinyl chloride produces in rats angiosarcoma of the liver as well as cancers of the lung, kidney, skin and other sites. Although workers in occupations involving exposure to vinyl chloride have been found to have an increased risk of hemangiosarcoma, no excess of other cancers has so far been reported. This historical prospective mortality study of 8384 men who had at least one year of occupational ex posure to vinyl chloride before December 31, 1972, demonstrated that cancers of the digestive system (primarily angiosarcoma), respiratory system, brain, and cancers of unknown site, as well as lym phomas, occurred more often than expected in those members of the study population with the greatest estimated exposure. The mortality from other cancers was lower than that of the general male population, with the exception of cancers of the buccal cavity and pharynx. There was an excess of these cancers, which however was inversely related to estimated exposure. The explanation for the latter finding is not apparent. The other major findings of the study are: (1) The overall mortality of the study population was ap proximately 75% of what would be expected in a comparable population of U.S. males; (2) No cause of death showed a statistically significant excess over what would be expected in a comparable U.S. male population; and, (3) No deaths identified as angiosarcoma of the liver were found other than those previously identified. This is the first epidemiological study which suggests that in humans vinyl chloride may also be associated with cancer of multiple sites. < ' I! i T n n n c i e c r 'r Drv Tabershaw and Gaffey are from Tabershaw-Cooper Associates, Inc., Suite 306, 6000 Executive Blvd., Rockville, MD 20852. The research on which this report is based was supported by a group of companies engaged in the syn thesis and/or the polymerUation of vinyl chloride, and administered in their behalf by the Manufacturing Chemists Association. Journal of Occupational Medicine/Vol. 16, No. 8/August 1974 BFG26317 509 V inyl chloride in its manufacture and polymerization has. been identified as a narcotizing agent,1 as a liver toxin,2 3 and as a vasospastic agent producing a specific occupational disease, acroosteolysis.4 Recently, vinyl chloride has been incriminated as a carcinogen producing in a group of workers engaged in the manufacture of polyvinyl chloride a rare fatal liver tumor, hemangiosarcoma.5 Large doses of the chemical in rats reportedly produced cancer of the skin, lung and other organs.6 Unpublished but public in formation7 indicates that inhalation ex periments with rats in doses easily reached in manufacturing operations produces in addition to angiosarcoma of the liver, skin, kidney and other malignant lesions. The present study, however, was not restricted to the conditions and sites suggested by the above investigations, but concerned itself with the entire spec trum of causes of death, to the extent permitted by the size of the study group. The objectives of the study were: (1) To compare the mortality of individuals who have worked in vinyl chloride plants with that of the general population; (2) To compare mortality patterns within the population of vinyl chloride workers, based upon estimated occupational exposure; and (3) To com pare mortality among vinyl chloride workers with the mortality of other oc cupational groups. The study population consisted of in dividuals from 33 plants who had worked for at least one year in a job in volving exposure to vinyl chloride before December 31, 1972, and included retired and terminated as well as active workers. For each such worker the date of birth and an employment history were obtained, and the vital status of the worker as of December 31, 1972, was ascertained. For those found to have died, those death certificates that were available were obtained and the cause of death determined. The observed mor tality was compared with that of the United States male population. particularly those producing the monomer, this determination could be made on the basis of job titles. Usually, however, exposure was a function of both job title and the location of the job in the plant, so that the assessment of exposure had to be made on a case-bycase basis by plant officials. Data were collected for as far back in time as complete records were kept. In most cases this covered the entire history of the plant. In others, records were kept for a fixed period such as a decade. In a few, records were kept for different periods, depending on whether the worker had died on the job or had left employment. In most plants it was impossible to quantify exposure. However, industrial hygiene and safety personnel in each plant were able to identify certain jobs and locations as involving the highest exposures in the plant, and to classify other exposures as medium or low relative to the "high" represented by the jobs with the greatest exposure. Con sequently, each exposed job in a worker's history was scored 1, 2, or 3 to indicate low, medium or high estimated exposure This gross classification has two major failings, as a result of the subjective nature of the estimates. The first is that the scores represent estimated relative exposure within a given plant. It is therefore possible that, in objective terms, a "high" score in one plant corresponds to a "medium" or even "low" score in another. The second is that the scores usually do not take into account changes in exposure over time. A worker with long service may therefore have had jobs in the remote past which involved "low" exposure relative to other jobs at that time, but which might be "high" in comparison with current exposures in the same job. This subjective classification is therefore of questionable validity in characterizing the exposure of a given worker. For epidemiological purposes, however, those who have high scores can reasonably be expected, on the average, to have had the greatest exposure, while those with low scores will have had the least, even though the true exposure in each group may vary considerably from person to person. The estimated exposure history of each worker was summarized by calculating an Exposure Index (El). This was done by multiplying the number of months on each job by the exposure score, totalling these overall exposed jobs, and dividing by the total number of months of ex posure. Follow-up of Study Population A follow-up procedure was instituted for those who had left employment and whose vital status could not be deter mined at the local plant, using direct mail follow-up and retail credit bureau investigations. Table 1 shows the vital status of the population as of December 31, 1972. Follow-up is 85% complete. Those who were not found were born (and began their exposure) about ten years before the group on which follow up was complete, and had about half the duration of employment in exposed jobs with a slightly higher El. Although there appears to be nothing very unusual about this group in terms of work history and exposure, it is nevertheless true that their exposures took place further back in time than that of the group suc cessfully traced. It is therefore possible that their mortality, after a substantial latent period, might show a somewhat different pattern from that of the traced group. All of the subsequent analysis is con cerned with the 7128 workers on whom follow-up was complete. Table 2 shows their distribution by duration of exposed employment and the year in which that employment began. Although almost half the study group first entered ex posed employment in 1960 or later, there are nevertheless 854 workers with 20 years or more exposure, and 1640 with 15 years or more. Table 3 shows the relationship between duration of ex posure and El. There does not appear to be a close relationship between the El Data Collection In each plant, data were collected for each worker stated by the plant management to have been employed for at least one year in a job involving ex posure to vinyl chloride. In some plants, 510 ' Nufflbar ir'Pra* TiWt L -- FaHae-a* Stain at S3S4 VkqTQIhrUa Barkan. 1 far 1 1 Tatal Mk OtWcataa tocU IW tac'l ;83S4 100.0 677* Ml " ~ U32Sr ~ r 24 7J Mortality Study of Workers in Manufacture of Vinyl Chloride/Tabershaw, Gaffey BFG26318 and the duration of exposure, that is workers with a higher El do not differ substantially in duration of exposure from those with a lower El. One im plication is that in assessing the relation ship between mortality and exposure, both duration and level of exposure can be examined separately, as well as in combination. Calculation of Risk of Death The risk of death is expressed as a Standardized Mortality Ratio (SMR), which is the ratio of the number of observed deaths in the study population to the number of deaths to be expected in a comparable population of U S. males. SMR's were calculated for overall mortality and for 33 major cause groups. Table 4 shows observed and expected deaths, and the SMR, for each of these causes for the total study group. In calculating the SMR's for specific causes, the 24 deaths for which no certificates were found were assumed to have the same cause distribution as those for which certificates were available. In the standard population, each SMR would be equal to 100. Therefore, the statistical significance of the deviation of each SMR in the study population from the expected value of 100 was tested.* A single dagger indicates those SMR's which differed significantly from 100 at the 5% level, that is, which had a probability of .05 or less of occurring by chance. A double dagger indicates those which were significant at the 1% level. SMR's based on fewer than five ob served cases were not tested for significance. Table 5 shows the same SMR's for workers with an Exposure Index below 1.5 versus those at 1.5 or above. The dividing point of 1.5 represents a level hallway between "low" and "medium." Table 6 shows similar results for workers with less than five years ex posure versus those with five years or more. In order to examine the possible in teraction between duration and level of exposure, the study population was divided into four groups on the basis of both El (low vs high) and duration of ex posure (short vs long) using the same dichotomization as Tables 5 and 6. Table 7 shows the results for short ver sus long exposure in the low El group, and Table 8 shows the same comparison in the high El group. In each of the above tables, deaths for which certificates had not been received were assumed to be distributed as a uniform percentage of all causes. The cause specific SMR's were therefore ad justed upward by a percentage which varied in each subgroup. Results of Analysis The overall mortality of the study population is statistically significantly lower than that of the U.S. male population. There were 352 observed deaths compared with 467 exptected, for an SMR of 75. Table 4 shows that no specific cause of death was statistically significantly greater than expected Several, par ticularly heart disease, accidents and "other diseases" not detailed in the tables, were significantly below their ex ported values. When the study population is divided according to intensity and duration of exposure (Tables 5 and 6) and com binations of these measurements (Tables 7. and 8) three major patterns emerge. For malignant neoplasms as a whole, the SMR increases with increasing ex posure, whether measured by level, duration, or both. In the high exposure group with 5 years or more exposure (Table 8) there are 36 observed cases and 26.11 exported. For cardiovascular -- renal diseases as a group, there are also increases in the SMR with increasing exposure, but the numbers of observed cases remain less than expected, the differences being statistically significant in all groups ex cept the high exposure, long duration group in Table 8. For all other causes, there are no con sistent relationships with exposure. Within the malignant neoplasms, the largest (although not statistically) significant SMR is in cancers of the buc cal cavity and pharynx, with five ob served, 2.84 exported, and an SMR of 189. However, Tables 5 to 8 show that all these cases have Exposure Indexes below 1.5 and four out of the five have less than five years exposure. Table 10 is a listing of these deaths with age at death, duration of exposure, and cause as stated on the death certificate. Cancer of the digestive system shows UtXi3S 3 Up--M Mat m.4 1.5+ Llnlwof Tat* TlMt 1 -- Ifa Mi % f 7US Mail CMarM* fatal by UmDu if Cm--4 Cmflfymmt ItaMi 0 fetal u% 4032 (100) 3057 (100) 9 719(100) it* 1715(41) 12* (41) * 113(9) *71 (22) fa* 402 (10) 295 (10) fa* 4 (If) 39 (12) : jjfrr 2*5(4!) 17* (9) *7(10) 29 <W ' Journal of Occupational Medicine/Vol. 16, No. 8/August 1974 kirn. ' '' .......... ' - -C"-"' .< ' BFG26319 511 * SMR's adjusted for deaths with cause unknown. tSicnifiCMt it 5% level. *Sipifieant at 1% level. no excess in the study population as a whole. However, in those workers with an El of 1.5 or higher, there are 12 ob served cases where 9.14 are expected (Table 5). In the subgroup of the above workers with five years or more ex posure, there are 11 observed cases and 7.47 expected. Respiratory cancer shows a slight ex cess in the total group, and a similar pat tern for different exposure categories, with 13 observed versus 10.28 expected when the Exposure Index is 1.5 or higher, and 12 observed versus 8.50 ex pected when, in addition, the duration of exposure is five years or more. 512 Malignant neoplasms of other and un specified sites show an excess in the total group, and an increase with both level and duration of exposure (Tables 5 and 6). The relationship with exposure is more pronounced, since those with ex posures of less than five years have fewer cases than expected. The lymphomas, although occurring at about the expected rate when the whole group is considered, are concentrated almost entirely in the high exposure, long duration group. In that category there are four cases observed and 1.84 expected. Cancers of the genital and urinary organs, and leukemia, have fewer cases than expected. The number of cases is too small to examine any trends Discussion The favorable overall mortality of the study population is a phenomenon com monly observed in working populations. Standardized Mortality Ratios in the low 80's and below have been found.' ,0 Even in occupations with well defined hazards which cause an increased risk from a specific cause, the overall mor tality may still be favorable because of the low risk from other major causes of death, frequently in the cardiovascular -- renal category.11 Mortality Study of Workers in Manufacture of Vinyl Chloride/Tabershaw, Gaffey BFG26320 23560004 I ~1 "'f (B HtgSgH * fioo-wwlf - 'SM -yk'ggB glrnmumm Tiiiil'wjH^.^ - . ' Ifajor mwwto ito, nut dtoaou (330-334, 400454. 592-594X - "*' Vacate Mat'lfhctef CMS (330334) ' ; . 'll-'? ^ ` 'afcyjjf Rtematic tote I ckrak rtemtoie teat dh/(400-402. (10411) AitetowteoWr kart (teat (420) [/; Narkaiatk atfaxCte (421, 42Z) ' llpsrtatek kart dtoaa (440443) Otter kjpsrtatoa dbaa (444447) - drak t atpuciM aokritto 4 tad ictoretos (592594) _S|/7144V. .07420 1/5.40 1/1.52 0050 Mma ad lanwmdi (4(0413) 5AJ0- - liar id toandi ad dadoar (540 541) 1/2.21 Xwadkitto (550553) > 07039 E75# -i 2/110- j$ |201 '~i ?a*ffi.07U7- - -S .o ^511 S^IITOU'^-'-. -- .% iiu it -. "^ ^Smoo*'.- ' ?'* - m :|r4).0L27 " Q *' S Hrrm ad Moteto utetnctia (500 5(1, 570) . 07001 ; .-*98* ' - -3, 14153 171 tetritto. dtedattto, ateltit ad ctotel (543, 571. 572) Cirrkotos to kvur (501) HwoMi to krattos (010) Sitetew, saflKy ad illdtokiid cadOiat (700795) 90.70 2/090 07025 07422 <4 it'' r ,3J i--.% *N#r 1/095 . V ,, . 1/0(4 .;V-wo.i4 \y 1/109 - -f <- .190 ' -fi 14 34 M otter disniis (ntodal) 14/21.90 .r,~ " (if- 5/15.89 41 Mote vskieto scoterB (110435) Otter ocddats (800407. B409S2) 1/19.01 11/17.(3 -'V li.'dS " i (O.t 9/13.40 0/12.57 72 - * 50* Stoddt (903, 970979) 9/9.73 ' .91- 7/7.02 107 Hadddr (9(4, 9(0905) 07098 - 0- . 174.94 21 Ite to Mrten Piria >ar 4032 45350 3(57 mm - 'SMR's adjusted tor deiths arrtti cause unknown tSigiiOcMt at 5% level. tSieiificaet at 1% level. In view of these facts, SMR's which are higher than expected may be worthy of attention even if they are not statistically significant. This is especially true in the present study since the num ber of deaths from many causes is quite small, and even a relatively high SMR may not reach statistical significance. If, in addition, a particular cause shows a consistent pattern of increase with exposure or estimated exposure, the findings are particularly interesting. By these criteria, mortality from digestive cancer, respiratory cancer, can cer of other and unspecified sites, and lymphomas, appear to be related to ex posure as defined in this study. In view of the association between vinyl chloride exposure and angiosar coma of the liver, the digestive cancers were examined further to see what con tribution angiosarcoma made to the ob served mortality pattern. Of the 19 digestive cancers, seven were liver cancers, of which two were angiosarcomas according to the death certificate. However, among angiosar coma deaths in vinyl chloride workers identified by other investigators, there were six which occurred in the present study population during the study period. They were all found in the course of the study. Table 11 shows these cases with the cause of death as given on the death certificate. Note that one case was certified as cirrhosis, and was so considered throughout this study, since the validity of comparisons with population data required that cause of death be determined only from in formation on the death certificate. The other five were correctly classified as Journal of Occupational Medicine/Voi. 16. No. 8/August 1974 513 BFG26321 23560005 ZZ9Z0i% Aajjeg MEi|Sjaqe]yap!Jom3 |Au;a jo ajnpejnue^ ui sja^iOM jo Apnjs Ajfiejjo^ US |M9t 11 le lurajiuJis* Pl IS P tunjiuaiSi uaounuft kito iw* stjpap jgj pajsnlpe s.nh$. mat Kit IKK ' 6662 tmi --j *m* P *U 0 tot 4*s *E> + ts 0 - c;, r~. '`" 0 ' OZ'VO 9201/01 2921/01 S9'91/2 K9Z/9I 60V0 : '9/0 invz 260/0 02 >11 4 52 Ofr es 0 92 toe 095/1 wm 2in >1'91/0I 2G*ll/> 927/1 200/0 *>>/] Ot'O/I (596-096 '>96) (626626 `96) SOW'S (296*099 209-009) *>> I10 (5(9-019) *W* *pup *VW (ttnptsu) sastasip jaqio |y (562-092) owwure pupM? pot (pirns -suMui/s (019) W4l P ***PVu (195) 11 WM0 (225 '125 ') *Wira P #M*1 *wMPonp 'MW '01*1/1 0 2>'6/0 (025 '195 795) "WV PW P PH W i'i\. / 'orz/i 0 -ni >27/0 201/1 (55-055) BP<9 (IK 'OK) wwpoiip P" vnmp r> JUKI i- .,602/2 21 ES2/E (69099) *9*"* > *91 7 i'trvt Itrui *rtfl - -9 trsoi/oo . tSVt sSr.-;.^raii 0 6> 0 4*2 ICI I* . >S9 ... `., " 9 ssi/o *21/0 2>2/l 621/0 K2E/12 ft'2/2 ~ 265/9 S> Isni ; (965 265) swaps PJ 9 *us|ds WRarfsm f 5WJ90 - (2>> "*#> w4i( *00 (o> > *W9 Wll (22> 72>) ifflpiooom spnimmoN (02>) *s 4*l PPSW> (9IH)t> *20M0 * WH SBHWV XU(P *H >0<11I . 3J"' .-T " <>> 690 *JWK nopaj pma ^ .`<>65265''09009 'K-0) 9 FJ m m*>**W*`A'm z,Itl.'1' cgnbjma'-. '.r; . ,>: (092) MI.o)o s.jxitrm ; `i' ^*--;t07/t (502 `02-002) wniWl^. *4.. * K : W: r~nn 3 .^aas*H . >, - 7* CiE i * * "38 gjglSgflftlrttt,. - :-g Jr <2) *!W > . '<661661) * *<P `**f*|dcw.-|iwPitp| /*/ i ' (191-091) Kjo (ww Bi|6oMjpM||i||'iy. ' ^-.4622tj W PP| W?-W IS rafagawjRg!ff>>sw3^ HMKT' TBg^WjBa'^p^wgiCTWiBewi^^ifv^ry 'ycs-ReBi/jLjWfcyfij .. lagfe > j)dfeiSfe^Pepoatflo^M>t6iwlwi Mfcrmiiiii Mvl" CTgfe-^T^'^^-;;ii^^|p^^-K6I0-l0ffl^W>Wl Ipp;.: r Dutto&ppctad Duth* art $tMb*^lNWR|f 1 : V'V-r.'..- Eintm tartlets Balm hr Dmflu. Cam d tMtk ah UA Ha - ,. M Cams - -. Tahorcafcais (001-014) TaberaHos) <d respiratory system (001-400) Ma/ipum noop/asm (140-205) MaUanat aeoplams, heccal cajp and pheryna (140-140) Makaant neoeiesms, ditestiyt erpas and peritomim (150159) HaUpnat Montana, raspintory system (160164) Mali0Uttt Moptasata^cenital orpas (170179) MaHcnant neoplasms, snnary urpas (160161) MaUpuat asepiasms. ether and oaspadtad sitae (190199) Laakaaaa and aleukemia (204) lymphoma (200203. 205) Diabetai mallitaa (260) Major cardmaacalar aid raui ddaaaat (330334, 400460, 592-594) Vascular teams sftsctief CMS (330334) Menmatic km 0 daaaic rtwamatic haart die. (400402. 410416) Ortariasdaratk kaart *lease (420) Hoarhaematic eadocardltii (421,422) Hypartaasiat kaart diseas (440443) Otksr kypsrtaasha disaasa (444447) Chaotic 6 vespacitied ntphribs 6 renal sclerosis (592-594) InPuerua and pneumonia (400493) Ulcar erf stomach aarf duodtotim (540, S41) Appendicitis (550553) Hvmi md intestinal obstruction (560, 561. 570) Gastritis, doodaaitis, entarttis and coffin (543, 571, 572) Cirrhosis ol Km (501) Hyperpiasu of prostata (610) Symptoms, senility and iK-deOned conditions (700795) W other disaasa (residual) Motor vehicle accidents (010035) Other eeddents (000002, 040962) Soode (963. 970979) Homicide (964. 980985) tit tf Warfcms firm ymi ' ` ;r ' SM"I ' - 07131 Wt ' WF- ia43 2/3.56 070.66 070.55 170.97 079.79 0/176 2/1.15 21/33.30 2/3.93 2/1.50 16/21.14 0/1.10 171.50 0/0.50 0/0.97 3/1.96 070.61 070.15 0/0.27 0/0.26 1/7.90 0/0.05 0/1.43 4/7.45 3/9.07 3/7.90 3/4.00 0/3.55 "f-'i ' - -0 0 120 0 0 203 . 73 * 59 155 80 t 74 0 0 100 0 0 0 0 42 0 0 63 35 44 16 0 1715 21411 - .V- **WSSwj 9fltt00 mst 1/4.43 1/140 1/223' 3/250 63/0832 5/1051 1/2.40 525737 mm 0/3.90 1/132 0/1.53 2/3.95 1/153 0/024 05.61 070.51 1/6.09 0/9.20 0/2.79 10A2.92 5/922 8/9.15 6/5.66 0/3.43 *>' - ,,. 12T 67 107^ . 73 46 r ' : 7g^ ' *#*, 41 93 0 0 101 0 53 67 0 0 0 16 0 0 79 56 S3 109 0 2317 23224 * SMR s adjusted hr deaths with cause unknown tSifniiicant at 5% level. uSitnificant at It level. 23560007 Journal of Occupational Medicine/Vol. 16, No. 8/August 1974 BFG26323 515 /&Mktedttfiiii poooetari (480493) . .. >Widlcttv (5M-B3y: J 561. 570) Castro* duudawitldSaterite ad tatts (543. 571. 577) 1. _ HffvpMrof patt* <610) SdahuM. tmm mt iOdeOaed tadMoa (780-755) . ote dtaaa (latfni) Motor vehicle acodewts (110435) 0tar.iet*ttts (800802. 840962) y Mdde ~- ^ 'HadSP^MkMS) ; **e ' Rn Mn- hum Toon * Shot's adjusted tor deaths with cause unknown. tSipilicant at SI level tSifnifieant at 1% level. 516 0095 1/135 04)06 M14 iaic 0/1.56 0/031 1/030 0/4.02 7/5.0$ 4/4.73 3/2.40 1 1AM 1240 ua 0 362 0 0 004 0 0 156 0 144 107 158 58 0/3.13 0US MU9 1A.49 0/0.41 1/5.06 0/0.13 0/7.30 6/11.88 2/7.43 2/736 4/4.62 0/2.76 107 19305 0 0 0 209 0 20 0 0 51 + 28 26 88 0 N> 0* cn CD Mortality Study of Workers in Manufacture of Vinyl Chloride/Tabershaw, Gaffey BFG26324 7300 4 7371 7300 S7SS 5246 2050 4779 44 58 S3 52 67 M 4788 61 5713 69 7101 55 211 Onto taaot, A 249 Brai* bnor, 216 TkyroM arcmom ijfl 239 CvdMMlaate' Cnimi iMM 201 Utente trite '&> 193 Cardaomteris, ptUnry nteorteC * ^ M< i .,>* ' * ' .\'v*. (Past histey, rtmaataU rtriT^ tnitel WMhi) ' . '''. 300 Itffan (2 4>n) viiovsQOH mow* fiftwi^ . (2 KM.) '.,'? 31S GmntinO MUteSB .Miter- owotel Swum. <aU onimm, ?tew* st. utetenaM n> , 166 Matastabc anmm at iMaw r.g^ Critical si* udinriail^ : vr ..*.; ~ (Mmmit iion--)- .' 133 Carcnomatam (4 am.) Primary sat* uattarotinad .a^. - . MW., 23560009 Journal of Occupational Medicine/Vol. 16, No. 8/August 1974 BFG26325 517 liver cancer, but only two were specified as angiosarcoma. If there had been no angiosarcomas, the number of deaths classified as cirrhosis in this study would have decreased by one, and the number classified as digestive cancer would have decreased by five. The pattern of duration and intensity of exposure in these five cases was such that if they had not been present there would have been no relationship between exposure and digestive cancer. The mortality pattern in this cause group is therefore attributable to angiosarcomas of the liver. The other cause group worth further investigation is cancer of other and un specified sites, both because it is a heterogeneous category and because it seems, unlike the other cancers, to be more related to duration than to level of exposures. Table 9 shows a list of the sp>ecific causes included in this category, which is essentially brain cancer and generalized cancer with primary site unknown. About 40% of the observed deaths were due to brain cancer. In the general male population, about 22% of this category is due to brain cancer, so that not only is the mortality from cancer of other and unspecified sites excessive, but brain cancer is overrepresented within the category. The possibility exists based on the lack of specificity of some of the listed causes that some of the brain cancers were not primary, but metastases from another unidentified site such as the lung. The cancers of the buccal cavity and pharynx are difficult to explain because of their occurrence in the low exposure, short exposure group. It is ptossible that this is a chance occurrence, that ex posures to other substances were in volved, or that the mouth and pharynx may be peculiarly susceptible because of the gaseous nature of the chemical. Possible Biases in the Calculation of Risk There are two major potential sources of bias in the study. The first is that the follow-up rate is lower than is desirable. The second is that observations of workers with long exposures followed by a long latent period are not adequately represented, so that the power of the study to detect causes of death associated with long exposure and long latency is impaired. Populations with such characteristics exist and 518 TaMa It -- MMfaaat WiipliwH at (Hl<. Ltt) ia Ml EpMaMMap SppMHM^//; Stady Hw Mk -- Mm. Opal t, 3003 31 3431 56 3001 5? 7365 54 3354 63 49 Clnilia|i d-M> MM t ****** 30 PMgf'4<M* (Kifci, 71 40 Mat M 6 Mta (1 yy.) AdMMwdMM of nasal ptwyu (2 m.) 26 Mmm htmarrfcap iato tradHO-fftt Statu* port `rymrt^Tfurrlfy. toft radlat Mck tisudfea "IN* "I OIIWM.O. K. M. aR--m---t-M--U---m--f sqnaiMM call cardnoma of left pyilorw stats (moa.> m .X at 'i 1 m ,j m } yu TaMa 11. -- Oaitaarcaan Daitk* ia KM EpMtaiMoo Stady hgwIatiM. Stady 0 4250 4255 5765 7303 7376 7305 Aft at MU 54 60 45 36 52 43 Mm. EaaM Cant at Qvaa 203 CirrlMsis of Ihar (s. watk!) 281 BtMOtNf fron hapatma (3 days) (Uanaacs drrtnas) 157 AifWMfBWM rt fata of (war (10 not.) 174 Lhnr Myra (1 mo.) Caacar of Ihar. priawy <15 ana.) 230 Cardiac tatapanada and maoha Ml htmotfcxix (min.) WkMy mataditic Mfknaroxiia of lhar (4 moo.) 214 Hapatic Mura Primary carcinoma tivar Autapaf yes m m yw should be investigated References 1. Lester D, Greenberg LA, Adams WR: Ef fects of single and repeated exposures of humans and rats to vinyl chloride. Am Ind Hyg Assrtc / 24:265-75, 1963. 2. Marsteller HI, Lelbach WK, Muller R, et al: [Chronic toxic liver lesions in the PVC (polyvinyl chloride) -- producing workers ! Dtsch Med Wochenschr 98:2311-14, 1973. 3 Kramer CG. Mulchler IE: The correlation of clinical and environmental measurements for workers exposed to vinyl chloride. Am Ind Hyg Assoc / 33:19-30, 1972. 4. Dodson VN, Dinman BD. Whitehouse WM, et al: Occupational acroosteolysis III. A clinical study. Arch Environ Hllh 22:83-91, 1971. 5. Creech IL, lohnson MN: Angiosarcoma of liver in the manufacture of polyvinyl chloride. I Occup Med 16:150-51 1974 6. Viola PL, Bigotli A, Cuputo A: Onceogenic response of rat skin, lungs, and bones to vinyl chloride. Cancer Res 31:516-22, 1971. 7. Occupational Safety and Health Ad ministration: Occupational Safety and Health Standards. Emergency Temporary Standard for Exposure to Vinyl Chloride. Federal Register 39 (67) 12342-44, April 5, 1974. 8. Chiang CL: Standard error of the ageadjusted death rate. Vital Statistics Special Reports, 47 (1961) pp 275-285. 9 Lloyd |W. Ciocco A: Long-term mortality study of steelworkers: I Methodology I Oc cup Med 11:229-310, 1969 10. Tabershaw/Cooper Associates, Inc , un published. 11 Redmond CK, Ciocco A, Lloyd |W, Rush HW: Long-term mortality study of steelworkers: IV. Mortality from malignant neoplasms among coke oven workers. / Oc cup Med 14621-629, 1972. Mortality Study of Workers in Manufacture of Vinyl Chloride/Tabershaw, Gaffey GT009Qr2 BFG26326 INDUSTRIAL HYGIENE SURVEY FOR VINYL CHLORIDE Company: General Cable 800 East 2nd :Street Bonham, Texas 75418 Date of Sampling: June 12, 1974 Operation Time at Start (hours) Mixer Operator Pelletizer Operator Swiss Extruder, Operator Right Line, Machines 7-12 . Swiss Extruder, Operator-Machines 23-28 ' 4 1/2 Final Jecketting line 1133 . 1135 1141 1145 1154 Duration of Exposure (minutes) 120 . 120 120 120 126 Vinyl Chloride Concentration Found (ppm) <1.0 <1.0 <1.0 <1.0 1.5 ' 4 \ i 23559016 / BFG26314