Document 8m2DDVJrp3rMBV0X5NZxryKo

/.' NOTICEi Tr.ia w-iter i-il troteotod >'" ' Mortality and Industrial Hygiene Study of Workers Exposed to Polychlorinated Biphenyls DAVID P. BROWN, M.R.H. MARK JONES, M.S. U.S. Department of Health, Education and Welfare Public Health Service Center for Disease Control National Institute for Occupational Safety and Health Division of Surveillance, Hazard Evaluations and Kidd Studies Cinriuniti, Ohio 4S226 ABSTRACT. Because of the demonstrated toxic effects on animals resulting from exposure to polychlorinated bi phenyls (PCBs), the National Institute for Occupational Safety and Health conducted a retrospective cohort mor tality study of 2,567 workers in two plants where PCBs were used in the manufacture of electrical capacitors. All workers included in the study were employed for at least 3 months in areas of the plants where PCBs were used. The viral status of 9SI4 of the two conorts was determined, and 39,018 person-years were accumulated. All-cause mortaliot was lower than expected (163 obs. vs 132.4 exp.) as well as all cancer mortality, (39 obs. vs 43J exp.). Excess mor tality was noted for rectal cancer (4 obs. vs 1.19 exp.) and liver cancer (3 obs. vs 1.07 exp.), although neither excess was statistically significant. In one of the plants the observed mortality due (o cirrhosis of the liver was also elevated. The results of detailed industrial hygiene surveys con ducted in each plant arc also presented. POLYCHLORINATED BIPHENYLS (PCDs) are a class of compounds composed of biphenyl molecules with a varying number of substituted chiurinc atoms. In commer cially p-epjrcd PCS mixtures, the weight-percent of erdorinc has varied from 21 to 6S In some preparations, there has jImj been sonic degree of contamination by ihtnrodibeiuofurans.1 The primary use of PCBs has been as a liquid insulating material in electrical capacitors and transformers, therefore, the greatest potential for occupational exposure has been in the manufacture and repair of these components. Poly chlorinated biphenyls have also been used in heat exchange units, hydraulic systems, vacuum pumps, gas transmission turbines, plasticizers, adhesives, pesticide extenders, paints, and carbonless copying papers. Since 1971, PCBs were sold in the United States only for use in closed systems. According to the Toxic Sub stances Control Act of i975, rules and regulations were promulgated to limit the manufacture and use of PCBs. This Act stipulated that all U.5. production of PCBs end January 1, 1979, and ihti all U.S. sale and distribution of PCBs end July I, 1979. However, continual exposure lo PCBs will occur among workers wno maintain transformers and capacitors, and among the general population via contaminated food. During (iie pasi few years, interest in she health effects among individuals exposed lo PCBs has been stimulated by: (a) the tendency for PCBs to accumulate in tissues and certain organs,il> (b) the stability of PCBs and sheir per sistence in the environment;4'* and (c) the demonstrated long-term toxic effects, including liver tumors and other liter diseases, in exposed laboratory animals.Much of this interest was expressed al the National Conference on Pols chlorinated lli'|i!ienyls in November, 1973,14 and ilic toxicity of PCBs lias been extensively reviewed in she NtOSH Criteria Document on PCBs.11 In comissrknn in 120 Archive! oi Environment*! Health MONS 209814 the accumulated information on acute toxic effects in humans and adverse effects in animals. little is known about the chronic effects from long-term exporuro in man. To determine whether past occupational exposure to commercially produced PCBs has caused any long-term health effects, NIOSH initiated an epidemiologic study among workers in two capacitor manufacturing plants. In conjunction with this study, detailed industrial hygiene surveys were also conducted by NIOSH to document the levels of exposure to PCBs and other chemicals. Dacnptnjn of Fazihiies Both of the plants chosen for study manufacture elec trical capacitors and were selected because: (a) each had a large work force: (b) PCBs had been used for more than 30 yr; (c) there was considerable potential for exposure to PCBs with little potential for exposure to other known toxic contaminants; and (d) the records necessary to iden tify individuals to be included in the Study population were readily available. At the time the study was initiated, both plants wero still using PCBs. Plant 1 is located in New York State and is divided into two manufacturing facilities within close proximity. One facility that has used PCBs since 1946 produced small Industrial capacitors and the other facility has produced large pCB-filled power capaci tors since 1951. The type of PCBs used has varied during the years from "Arodor" (Monsanto trade name) 1254 (54% chlorine) to 1242 (42% chlorine) to 1016 (41% chlorine). In addition, several other kinds of oils were used, but in a limited number of capacitors. Plant 2, located in Massachusetts, began to use PCBs to manufacture capacitors in 1938. This plant also changed the type of PCBs used from ''Aroclor'' 1254 to 1242 to 1016. Until 1972, other types of capacitors which did not contain PCBs were made at this plant. Castor oil was used In lieu of PCBs to produce the large puwer capacitors at this plant. Both plants assembled small and large type capacitors using the same general techniques. The following briefly describes the assembly process. Winding and pre-assembly. The inner components of the capacitor were made of paper, foil, and sometimes plastic film; wound together; and subsequently loaded into metal casings. This job was done in an enclosed dust-free roum where there was minimal exposure to PCBs. There fore, the workers in these jobs were not considered "ex posed" when choosing the study cohort. Impregnation. The prc-asscmbled capacitors were filled or impregnated with the PCBs. Within this area there was potential for exposure to PCBs, and therefore, those employed in Ihti area were considered "exposed" when choosing the study cohort. Final assembly. The tups of [he capacitors were closed by crimping, rubber stoppers, or soldering, which involved some exposure to PCBs. The capacitors were washed to remove excess PCBs by running them through a detergent wash or a degreascr such as trichloroethylene. Finally, they were sent through the final operations involving drying, testing, and painting. Those employed in several of these jobs were considered "exposed" when choosing the study cohort. Other areas where there was potential exposure to PCBs in the plants included the laboratory and the area where rejected capacitors were rebuilt. Approximately 10% of the two work forces were employed in areas where there had been potential exposure to PCBs, These em ployed in these iobs were considered "PC9 exposed" for purposes of choosing the study cohoits. Historically, the work force at Plant 1 has been com posed cf approximately 50% white males and 50% white females. Plant 2 has had a loss homogeneous work force, with two-thirds being female, and reflects the general ethnic make-up of ihe area, which is largely Cape Verdean and Portuguese. METHODS Mortality study. A retrospective cohort mortality study was conducted to determine whether individuals occu pationally exposed to PCBs have experienced any increase in cause-spccific mortality. The study cohorts were defined as all workers who accumulated at least 3 months of em ployment at any time in areas of the plants where there was a potential for exposure to PCBs. These '`exposure jobs" were designated ly the companies and verified by the labor unions (at Plant 1), and by the NIOSH industrial hygiene surveys to represent the high-exposure jobs. Tri chloroethylene (TCE) was used as a degreaser in both plants. Therefore, if the work history records indicated that an employee had potential exposure to TCE, the individual was not included in the cohort. This included very few workers. An effort was made to determine the vital statu* (living or deceased) of each individual in the cohorts as of January 1, 1976. Vital status was determined through records maintained by Federal and State agencies, includ ing the Social Security Administration, state motor vcnicle registration, and state vital statistics offices. For those indi viduals who could not be located through these sources, U.S. Postal Mail Correction Services and other follow up searches were used. For all those known to oe deceased, death certificates were requested and causes of death were interpreted by a qualified nosologist according to the International Classification of Diseases (ICDA) in effect at the time of death, and then converted to the 7th Revision of the ICDA. Those who had an unknown vital status were assumed to be alive as of January 1. 1976, therefore the true risk of mortality was not overestimated. Those who died after January 1, 1976, wore considered to be alive for purposes of analysts. Person-years were accumulated for each worker starting after 1940 when 3 months of employment in exposed jobs were completed, and ending at the date of death or the study end date (1 / l/76)~whichover occurred first. Using a modified life table computer program similar to that described by Cutler,14 the pci son-years for each cohort were combined into 5-yr calendar time periods and 5-yr age groups and multiplied by the corresponding U.S. white male (for male cohort members) and U.S. white female (for fcni-'le cohort members) causc-spccific morulity r.itcs to yield thccxpecied number of deaths. Person-years were additionally distributed by 5-yr exposure and S-vr latency (number of years from djtc first employed in exposed (Vol. 36 lNo.3)| HONS 209815 121 1 Tj&i 1. -- Viui Snfui of PCS WorktM Miles Plant t Ferrule* Total Known to be ttiv* Known ro be deceased Unknown vital surus Total Perwn-years 520 55 I 513 7,125 360 11 7 31S s.ns 110 73 15 96* 13,010 Males 633 21 u 675 9,229 Print 2 females Total 136 62 26 924 16,779 1,669 90 40 1,599 26,001 Grand Total 2J49 163 55 I2S1 2,567 J9,0tl jobs; categoric!. Observed and expected cause-specific dcailis were compared and difference! were tested using the Poisson distribution. Industrial hygiene survey. The detailed industrial hygiene surveys included personal time-weighted air sam ples I'rom selected job titles, as well as area air samples. In both plants, samples were taken for PCBs (Aroclor IOIi'j), trichloroethylene, lead, tin, and tine. In addition, samples for toluene, methyl 'sobutyl ketone (MIBK), alum num, and iron were taken at Plant I. These surveys were designed to characterize the exposures occurring at the time of the survey and may not represent exposures of previous years, especially those of Plant 1 where exposures may have been reduced because of new production tech niques recently initiated. RESULTS Mortality study. A total of 2,367 workers met the definition of the study coiiort. Table I gives a breakdown of the vital status ascertainment and the number of personyears within each sub-cohort. The vital status ascertain ment is 98% complete. The possibility that records might be missing from the personnel files used to assembie the Plant 1 cohort was cited at the beginning of the study- In an effort to deter mine whether eligible workers were missing from the Plant 1 cohort, a validity check was conducted by the New York State Department of Health* using method ology similar to that described by Marsh et al.17 Social Security Administration (SSA) quarterly earning state ments (SSA form 941) from 1945-1965 were obtained and compared to the names appearing on the microfilmed per sonnel records that were used to assemble the cohort- The results of this comparison yielded 35 additional workers (3.5% of cohort) roc included in the Plant 1 study cohort. This small portion of the population at risk that is missing from the study cohort should not seriously bias the results. A similar validity check was not done al Plant 2, as it appeared from our inspection that the personnel file sys tem had been maintained inuct. Table 2 shows the distribution of the cohorts by dura tion of employment in fobs where PCB exposure occurred. The distribution within the two plants is somewhat similar, with the exception of the female workers in Plant 2, where Table 2.--Duration of Employment imortf Cohort Members in PCB Exposure Jobs Punt t Males N (RF)* 3-6 me 6 mo*l yr 1 -2 yr 2-3 yr 1*10 vr 10 yr Tout Plant 2 137 (23.5) 11 (15.1) 43 (160) 53 ( 4.1) 165 (21J) 47 ( i.t) 513 Malei N (RF) 3-6 mo 6 mp-| yr 1-2 yr 2-3 yr 3-10 yr 10 yr Total 21! 131.31 127 (11.1) 1 11 (17.5) 64 ( 9J) 123 (11.2) 32 ( 4.7) 675 *RF * Relative frequency. Females n (RF) 79 ( 20.5) 59 (153) 92 (233) 41 (10.6) 12 (21.3) 32 ( 1.3) 315 Females H (RF> 207 (22.4| I6t (17.4) 175 (ia.9) 12 ( 1.9) 111 (20.3) Ml (12.0) 924 Total N (RF) 216 (72.3) 147 II5.2) 115 (19.1) 94 ( 9.7) 247 (25.5) 79 ( 5.2) 961 Total N (RF) 411 (26.1) 211 (11.0) 293 (11.3) 146 ( 9.1) 311 (19.4) 143 ( 5.9) 1599 12? Archives et Environmental Health HONS 209816 f Tifeit }.-Obvw"Yd Jftd Ei OtCTfd DtilTlf 10/E) AcCafdm* fa Mlwr CvM Cjuvt 0/ 0*i{H (7lft fte*tvioA ICO No.) PUfll 1 Milu Ftftslai AN mjliffunt ncoeUSflV (140-205) NtrvotM lyltrm (330034. J451 CiTCufatory system (*00-46*) Accidents (100*9 6 ?1 Alt other CJUKI 9/ 1.70 3/ 3.14 2*/ 22J1 7/ 4/02 (0/12.10 4/ 7.34 1/ t.*7 7/ 4.13 1/ 1.17 SI SJ4 AN (JUKI 3J/SJJ7 11/22.72 PCI Worhrn PUnt 2 Tlti 3/ 4.43 23/ 20.00 39/ 43.79 2/ U4 sl S0 11/ 12J5 14/ 14.1 J U/ 19.64 60/ 62JJ 3/ 7.43 41 10.24 lit 40-51 It 3.47 19/ 14.19 42/ 65.10 13/ 1*J9 40/ 44.79 141/ 112.35 (SM*1 1*9) ws> If) (9) 1*9) 9J*. Carsl^Jens* InicrsJ IvJ 1231 144 1ST) (73 17t| m - 173) 144 . 1221 <74 v 104| more employees had worked for 10 or more yr, and in male workers where there was a high frequency of short term (3-6 months) employees. When the two cohorts arc examined by year first em ployed in jobs where PCB exposure occurred, the females m plant 2 are seen to have had an earlier initial date of exposure. In Plant 1.49.4% of the males and 45.1% of the females were first employed in PCB exposure jobs before 1955. In Plant 2, 49-3% of the males and 69.6% of the females were first employed in PCB exposure jobs before 1955, Tables 3 and 4 summarize the number of deaths ob served (obs.) from the study cohorts and the number of deaths expected (exp.). The all-cause mortality is lower than expected in each cohort, with an SMR [Standardized Mortality Ratio (SMR = observed deaths/'cxpectcd deaths X 100)| of 95 (73 obs. vs 76.7 exp,) for Plant 1 and an SMR of 85 (90 obs. vs 105.6 exp,) for Plant 2, These StMRs may be influenced by the "healthy worker effect.There is no increase in observed mortality among the total cohort for any of the major causes of death listed in Table 3. Table 4 lists the observed and expected number of deaths by specific cancer cause and for cirrhosis of the liver. When both cohorts arc combined, the observed num ber of deaths is more than that expected for cancer of the rectum (4 obs. vs 1.19 exp.) and liver cancer-ICDA = 155, T 56A (3 obs. vs 1.07 exp,). The only statistically signifi cant difference \P < .05) in observed versus expected deaths occurred in females from Plant 2 for cancer of the rectum (3 obs. vs 0.50exp.,P <.05). For both cohorts combined, there are 6 deaths due to cirrhosis of the liver, while 5.60 were expected. Five of these cases arc from the Plant 2 cohort, while 3.2 were expected. According to hospital reports, at least 3 of the 6 persons who died of cirrhosis of the liver were known to have consumed alcohol regularly. The relationship between latency and the mortality from all cancer, cancer of the rectum, liver cancer, and cirrhosis ot the liver is shown tn Table 5. For "all Lancer" there is no apparent pattern iri either cohort. For cancer of the rectum, tficre is a slight increase with an increase in [he latency periods. All of the deaths due to liver cancer occur before 20 yr of latency and there is no trend of increasing risk with an increase in the latency period. The risk of mortality due to cirrhosis of the liver docs not show a consistent increase with an increase in the latency periods: there is however, a greater risk after a 20-yr period. The relationship between those same causes of death and length of employment in PCB exposure areas of the plants is given in Tabic 6. As indicated in the Table, there is no increase in mortality with increasing lengths of expo sure, except for cirrhosis of the liver; however, the numbers in this comparison are small. Industrial hygiene survey. The industrial hygiene survey results of area and personal sampling for PCBs (Aroclor 1016) are summarized in Tables 7 and 8. Because of differ ences in the production processes, the results by specific jobs or work areas arc not comparable between the two plants. However, relative comparisons can be made, and the range of concentrations observed in plant I are lower than those in Plant 2. In Plant 1, the time-weighted average (TWA) personal air samples ranged from 24 pg/m3 to 393 pg/m3, and the TWA area air samples ranged from 3 pg/m3 to 476 pg/m3. The TWA personal air samples in Plant 2 ranged from 170 pg/m3to 1200 pg/m3, and the TWA area air samples ranged from 50 pg/m3 to 810 pg/m3. Trichloroethylene was measured near the degreasers in both plants. Of 11 area air samples from Plant T, all were less than 35 ppm, except for two which measured 195 ppm and 321 ppm. At Plant 2, three area air samples were taken which ranged from 53.4 ppm to 77.5 ppm. Area air samples were measured for tin, lead, and zinc near the soldering operations. There were no detectable levels for tin at either plant. Of four samples collected tor lead and zinc at Plant 1, lead was detected In one sample at a level of 12 pg/m3, and zinc was detected un two samples at levels of 8 and 24 pg/m3. At Plant 2, 1 5 sam ples were collected for lead and zinc; all but one (41.2 pg/ mJf of these samples showed no detectable levels for lead. Six of the 1 5 samples revealed concentrations of zinc ranging from 2.3 to 94,1 pg/m3, 1 Both pci sonj! and area samples were taken in the area | Vo!. 3G (no, 3)1 HONS 209817 <23 Table 4--Oburved and Expected Deaths (O/E) According to Specific Cancer Ciuiei and Cirrhosis of lh* Liver among PCB Workers Cause of Death (7lh Revision ICDNo,) Plant 1___________ ___________flam 3 Males Female* Males Females Total (SMAl Alt miti|niAt neoplun (f 40 305) Stomach (151) tnteslinc up. rectum (152,153) Rectum (154) Biliary pan liver Liver not specified (155, 1S6A) Pancreas (157) Respiratory system (160164) Ireast (170) 9/ 9.70 0/ 0.51 1/ 042 1/ 0.31 1/ 0.23 0/ 043 4/ 7,26 0/ 0.22 0/ 0.70 0/ 0.11 0/ 0.1* 1/ 0.27 3/ 643 1/ 0.31 0/ 0.54 0/ 0.20 0/ 0.15 0/ 0,35 23/ 20.00 39/ 43.79 0/ 0.62 1/ 1.66 V 1.97 4/ 4.03 V 0-S0* 6/ 1,19 V 0.51 0/ 0.75 3/ 147 V 1.90 (69) (0) (99) (336) (2*01 153) 5/ 3.22 ............ 1/ 0.71 1/ 1.16 0/ 2.22 ............ V 143 6/ 44* V 7.9* V 644 (*S) (102) Lymphatic and hematopoietic (200-205) Other Cirrhosis of liver (5*1) 0/ 1.10 1/ 2.9* 1/ 1.69 0/ 0,59 1/ 2.55 0/ 0.73 0/ 0,94 2/ 2,12 2/ 1.26 2/ 1.71 6/ 7.13 3/ 1.92 2/ 4.34 10/ 14.7* 6/ 5.60 (46) (6*1 (107) mf < .05 95% Confidence Interval (63 - 1221 (27 - 254] (92 - *60) (5* *20) (35 1*1] (41 . 211) (32 124) (39 233) HONS 209816 inuam uom u j u v iip jyj n- i Table 5.-Ot,sarvfd and Expected Otitht Aeeurdlnt to Latency* amone Malt and Femele PCS Woikiri Latency (yr) <10 yr !0-<20yr >20 yr <10 yr 10-<20 yr >20 yr <10 yr 10-<20 yr >20 yr <10 yr 10-<20 yr >20 yr 1. All Cancers Plant 1 Plant 2 Of Et SMR 0 E $MR 6 5.27 3 6.61 4 5.07 0 0,15 0 0.19 1 0,15 114 6 7.76 77 45 16 10.91 147 79 4 8,17 49 It. Cancer of Rectum (ICO * 154) V t 0 0.21 . , , ... 2 0.29 690 667 1 0.21 476 III, Liver Cancer (ICO - 155, 1J6A1 1 0.12 833 0 0,16 ... 0 0.12 ... 1 0.18 556 1 0.27 370 0 0J1 -- IV. Cirrhosis of Liver (ICD * 581) t 0.80 0 1.01 0 0,61 125 ... ... 1 035 105 1 1,35 74 3 0.88 341 O 12 19 8 0 2 2 2 1 0 2 I 3 * Latency " nutnbtr of yean from date first employed In exposed job. | O observed deaths, t E * expected deaths. Plants 1 2 E SMR 13.03 17.52 13.24 93 108 60 0.36 0.48 0.36 ... 417 556 0.30 0.43 0.33 667 233 ... 1.75 2.36 1.49 114 424 201 of welding operations for measuring aluminum and iron at Plant 1 .The aluminum samples ranged from nondetectable to 233 jug/m1, and the iron samples ringed from 47 pg/m* to 123jug/ms. Twelve personal samples were collected for toluene and M1BK during painting operations at Plant 1. Toluene concentrations ranged fiom 0.48 to 22 ppm and MI8K ranged from 2 to 5 ppm. Although the exposures to PCBs at the dates of survey (plant 1--April 1977, Plant 2-March 19771, were relatively higher in Plant 2, the historic lewis of exposure may have been more.equivj(cnt, The exposures that occurred 20 to 30 yr ago are more relevant when considering the occu pational cancer risk among the study cohorts. The PCB mixtures used during these time periods were Aroclor 1254 and 1242, whereas Arodof 1016 was first used in 1971. in addition, several different stabilisers hive been added to the PCBs (llior less by weight) used at plant I since the early 1960s. These include potential carcinogens such as digiyccride cthcrdisphcnol-a and, more recently, vinyl cyclohcxcnc dioxide, it is not known which stabilisers have been used Jl Plant 2. [Vol. 36 (No. 3)1 DISCUSSION There are few previous epidemiologic studies that have examined the long-term health effects on humans exposed to PCBs. Individuals poisoned by rice oil heavily contam inated with PCBs (Yusho Disease) have been studied exten sively years alter the incident took place in Japan in 1968,t'1 However, the rice oil contaminant also con tained polychlorinated dibenzofurans and other contami, nants in higher concentrations chan those found in com mercially prepared PCBs. A high prevalence of skin and eye conditions were noted in the Yusho patients. In addlion, there were clinical and laboratory findings that included changes in the microanatomy of liver cells and a decreased concentration of bilirubin in the scrum of these individuals.:l,!1 Early reports regarding the health effects from occu pational exposure to PCBs include ehloraeno,13 digestive disturbances, eye irritation, liver injury, and impotence.'4'1* Most of these findings have been reported vs case histories. In a recent study of volunteers conducted by the Mount Sinai School of Medicine,14 326 workers who were cm- HONS 209819 125 Table and C*0td Oeath* Acro'dif'f I Len^h of r*onf Male jnd Female PCB Worker* Length 0/ Employment O' 3 mo *5 yr 5-9 yr 10-14 yr 13-19 yr > 20 yr It t 0 1 0 3 mo '5 yr 5*9 yr 10-14 yr 15-19 yr > 20 yr t 0 0 0 0 3 mo -5 yr 5-9 yr 10-M yr 15-19 yr > 20 yr 1 0 0 0 0 3 mo *S yr J-9 yr 10-14 yr 13-1* yr > 20 yr t 0 0 0 0 *0 QbMnrcd deaths. 16 " expected deaths. P> c.ot Plane 1 Et SMR 12.21 90 2.95 34 1.00 0.69 145 0.11 ... 0.JJ 2(6 0.09 ... 0.03 ... 0.02 ... 0-001 ... 0.29 345 0.01 ... 0X12 ... 0.02 0.002 ... 1.79 SC 0.39 ... 0.12 ... 0.10 ... 0.02 ... Plant 2 0 E SMR 1. All Cancers (ICO 140-205] 20 11.71 106 2 4.IO 49 3 2.2* 132 1 1.04 96 0 0.63 ... II. Cancer of Rectum (ICO = 154) 1 0.4* 201 0 0.11 2 0.06 33331 0 0.03 ... 0 0.02 ... III. Liver Cancer (ICO - I55. 156A) 2 0.4S 444 0 0-M ... 0 0.06 ... 0 0.02 0 0.02 ... IV. Grrfcosts of the Liver (ICO * 511) 2 2.26 U 1 0.41 20* 1 0.24 416 1 0.1J T69 0 0.01 O 31 3 3 2 0 2 0 2 0 0 3 O 0 0 0 3 1 1 1 0 Mams 1 2 E SMR 30.99 100 7.05 43 3.2* 91 1.73 116 0.74 ... 0.13 241 0.20 ... 0.09 2222 f 0.05 ... 0.02 ... 0.74 405 0.19 ... 0.01 ... 0.04 ... ` 0.02 ... 4.05 74 0.(7 115 0.36 271 0.23 435 0.10 ... ployed at Plant 1 wort examined. The molt prevalent symp toms noted were dermatological and those of the central nervous system. There was a low prevalence of abnormal liver findings on physical examination. However, a sub group exposed to PCBs were found to have liver enryme changes different from those of a normal, non-ex posed group. In addition, abnormal scrum glutamic oxalacciic transaminase (SGOT) levels were associated with plasma levels of PCBs. There was a relatively high prevalence of detrcased lung capacity among a subgroup of 243 workers tested." In a preliminary report. Bahn1* reported an increase in deaths due to malignant melanoma (2 obs. vs 0.04 exp.) and cancer of the pancreas among 5 t research and devel opment employees and 41 refinery plant employees at a New |crscy petrochemical facility. These individuals wcie excused to Arodor 1254 during various periods between 1949 and 1957, along with exposure to other toxic and potentially carcinogenic compounds. ^ In a summary of case hisiorm among approximately " 300 workers employed in the manufacturing of PCBs," no malignant melanomas or pancreatic cancers ware observed. However, among the death certificates of 50 former workers at this manufacturing facility, 7 cases of lung cancer were observed whereas 2.7 cases were expected. The findings were preliminary and were not adjusted fur age or smoking. These previously reported findings of an increased risk of mortality due to malignant melanoma, cancer of the pancreas, and lung cancer among workers exposed to PCBs are not corroborated in ill* present study. There are no observed deaths due to malignant melanoma and only 1 ubscivcd death from imiKi vatic cancer while 1.89 arc expected. There are 7 observed deaths from rcsoiratorv 126 Archivesol environmental itrillh HONS 209820 system cancer, whereas 7.69 are expected. The only cate gories of cancer in which the number of observed deaths are greater than expected arc for cancer of the rectum and cancer of the liver and only a slight increase for breast cancer. When both cohorts and sex groups are combined, none of the excesses are statistically significant at P < .OS. However, the excess in liver cancer is noteworthy because it is consistent with the toxicology data observed in labor atory animats exposed to PCBs, where effects have been noted in the liver.4'15 The slight increase in deaths due to cirrhosis of the liver in the Plant 2 cohort is also consistent with the notion that PCBs have a toxic effect on the liver. In most occupational health studies where cancer mortality is being assessed, latency is an important variable; the hypothesis being that there is an increased risk of mortality once a certain time period has elapsed after initial exposure. In this study, this hypothesis is difficult to examine because of the small number of deaths. None of the causes of death analyzed according to latency clearly demonstrates this association. Rectal cancer shows a slight increase with an increase in latency, and cirrhosis of the liver shows an increase in risk with an increase in latency after 20 yr. There is no relationship between increasing durations of employment in jobs involving PCB exposure and the risk of mortality due to cancer or cirrhosis of the liver. When cancer mortality is examined by Plant, it is evi dent that most of the excesses occur in Plant 2-especially among the female group. This finding may be related to more exposures to PCBs at Plant 2, as indicated by the industrial hygiene results. In addition, there was an oppor tunity for earlier exposures at Plant 2, potentially allowing for a longer latency period. However, this difference in mortality may be a function of the size of the cohorts (Plant 1 only has half the number of person-years as Plant 2), and thus, simply be a statistical quirk. Table 7.-Corcentraiionl of PCBs (Aroctor 10161 it Plant 1 (April 1977) A. Power Capacitor Manufacturing Facility Personal Air Samples Area Air Samples Job Titles No. of Samples Total $*mplin| Time (min) TWA* UK/m3) Location NO. of Samples Total Sampling Time (min) TWA* (fK/m3) Recovery Repair Salvage Operator EMF operator Treat helper Treat operator Repair 2 140 291 Test and 2 (40 Palm 1 426 1SS Assembly 2 S51 1 431 IIS Shipping 1 426 2 S67 SO Storage 1 427 2 73V 66 Winding 1 420 1 422 50 B. Small Capacitor Manufacturing Facility Move man (Sealing area) Moveman (Testfng and soldering area) Testing ' Packer Treat operator Rework and final uxmbly 2 3 3 3 2 2 619 393 1306 1290 12(7 I4S 124 220 211 199 160 1S2 Maintenance Rework tester Rework packer Rework tester solder 1 404 ISO 1 433 140 1 43S 132 1 271 24 TWA It calculated during the total lampling lime period. Soldering 2 Assembly 2 Shipping Winding 2 2 Can 2 Manuftciurlng Cover 2 Manufacturing 712 127 S3S I2( 136 134 41 29 16 14 3 476 US 56 S4 si 45 (Voi.JS (No. J)| HONS 209821 127 Tjb<c Concentrations of PC8f (Arorlor 1016) it Plant 2 (March 1977) fob Titles DcgTeaicr Solder Tanker Movtffltn (soldering area) Heat soak operator Tester Pump Mechanic Floorman (pre-atsembly) No. of Sample* 1 3 9 3 3 3 1 6 Personal Air Samples Total Sampling Tim* (min) TWA* (s^/m*) Location No. of Sample* Area Air Samples Total Sampling Tim* (min) Twa* Unfit!5) 311 414 2120 1,260 1,060 ISO Impregnation Pump room Testing 2 3 3 176 1079 1424 *10 490 370 7S2 720 Pre-assembly 4 1213 140 *72 630 Shipping 2 741 90 917 290 Winding 4 637 70 377 2*0 Cover 3 1019 60 manufacturing 1613 170 Office 2 741 SO The TWA It calculated durtnt ;he total sampling time period. A potential confounding variable or interaction variable in this study it the possible effect of alcohol ingestion on the observed increase {at Plant 2) in mortality from cir rhosis of the liver. However, this cannot be properly assessed in the present study, since not enough il known about the ingestion of alcohol among the entire study coh.rft. CONCLUSIONS because a relatively small number of deaths were observed, conclusions drawn from the results of this study are tentative. . All-cause mortality is lower than expected, and there was no increase in mortality for the major causes of death that svtre examined. Among the cancer causes, there was incr-;.ised cancer of the liver and rectum. Cirrhosis of the liver was also elevated in one of the plants. The slight excesses for liver cancer and cirrhosis of the liver arc con sistent with previously reported findings on experimental animals txposed to PC0s, and suggest that there may be an association between these causes of death and occu pational exposure to PCBs {i.c,, Aroclor 1254 and 1242). However, the findings for liver cancer do not reflect a relationship with latency that has been observed for other carcinogens found in the workplace. The observed excess in unccr of the rectum related to PCS workers was un expected and requires further investigation. i he authors would lika 14 r.xpreye their appreciation tor ilia voi k jf mans inditidual who hdued to tucvvn'ullv complete *'"i .:udy, mclud.tig tt-k guidance ol Juv-ph Wjfoncr, kiehard lit Lrmtn.and Richard Waxweiler; the aaaitlanca of th clerical and secretarial staff In the Biometry Section, Industry -wide Studies Branch of NIOSH-. the data entry and analysis prnvrded by tha Southwest Ohio Regional Computer Center; the cooperation of the companies and labor unioni chosen for the iludv; and Tor tha Information provided by the New York State Department of Health. Mr. I ones Is raw employed at Kaiser Aluminum and Chemical Carp., Raven(wood, West Virginia, 26164. Submitted for publication March 27,19*1; accepted for publication April 20, 1911. Requests for reprints should be sent to; David P. Brown, I.W.S.8., NiOSH,4S76 Columbia Parkway, Cincinnati, OH 4S22C, REFERENCES 1. Hutalnger, O.; Safe, s.: Zitko. V. 1974. The Chemistry Of PCB's, pp. 3-2S. Cleveland, Ohio; The Chemical Rubber Co, Press. 2. Yobs, A. R. 1972. Levels of polvchorinated biphenyls In adipose tiuue of the general population of the nation. Environ Health Pcnectl. (Experimental Issue No. 1)1: 7941, 3. Price, H. A., and Welch. R. L. 1972. Occurrence of polvchorlnated biphenyls in humans. Environ Hcuith Ptnotci, {Experimental issue No. I) 1:73-7*. 4. lenten. S.; Johnets, A. G.; OliSon. M.I Otterlind, G. 1969. DDT and PCS in marine animals from Swedish waters. Aur.-me 224: 247.JO. 5. lensen, S. 1972. The PCB storv-Ambio 1: I2J-J1. 6. Von Wedel.H.; Holla, W. A.: Denton. |. 1932. Observations on the toxic effects resulting from exposures to chlorinated naphthalene and chlorin.uid phenyls wills suggestions for prevention. Rubber Am 54: 419-26. 7. Miller. |. W. '.944. Pathologic changes in animals exposed to a commercial chlorinated diphenyl. Public r/eo/rn Rep S9: IOfS-93. Archives of Environmental Health HONS 209822 >. Bfutkn.r, V., Kh.nrt, K. L-. C^rniih, H. H. 1974. Poly chlorinated biphenyl-induced alteration of biologic para meter! in me rat. Pipxicol Appi Pharmacol 28: 189-99. 9. Kimbrough, ft. 0.; Linder, ft, E.; Gaines, T. B. 1992. Morphological change! in liven of ran fed polychlorinated biphenyl*. Arch Environ Health 25: 354-64. 10. Kimbrough, ft, 0.; Linder, R. E.; Bunt, V. W.; Jenningj, R. W. 1973. Adcnofibrosis in the rat livef-wuh persistence of polychlorinated biphenyl* in adipose tissue. Arch Environ Health 27: 390-95. 11. Kimbrough, R. D., and Under, R. E- 1974. Induction of ad.nofibfoiit and hepatomas of the liver in BALB/oj mice by polychlorinated biphenyls (Arcelor 1254)./ Had Cancer Inst 33: 547-52. 12. Allen, |- R,; Abrahamson, L- Norback, 0. H. 1973. Biological effects of polychlorinated biphenyl! and triphenyls on the subhuman primate. Environ fits 6; 344-54, 13. Vos,), G,, and Notenboom-Ram, E. 1972. Comparative tonicity study of 2, 4,5,2', 4', j'-hexachlorobiph*nyl and a polychlorinated biphenyl mixture in rabbits. Toxicol Appi Pharmacol 23:563-71, 14. Environmental Proteelion Agency. 1976. Proceeding! Of the National Conference on Polychlorinated Biphenyls, EPA 560/6 - 75 - 004. Washington, 0. C.: Office of Toxic Substancei, 15. NJOSH, COG, PNS, 0HEW. 1977, Criteria for a recommended standard: Occupational exposure to polychlorinated biphenyls (PCB'i). Publication No. 77 225. 16. Cutler, 5. J., and Edcrer, f. 1958. .Maximum utilisation of the life table methods in analyzing survival. / Chronic Dis S: 699-709, 17. Marsh, G. M,, and Enterline, P. E. 1979. A method for verifying the completeness of cohorts used In occupational -- mortality studies. / Occup ,Med II:665-70. 1*. McMlchatl, A.Haynes. S. G.; Tyroter, H. A. 1977. Observations on th evaluation of occupational mortality dan./Occur, ,t/ed 17: 128-31. 19. Kuratsune, M.; Masuda. Y.: Nagayama. [. 1976. Some of the recent findings concerning Yusho. In Proceedings of rhe Hatienal Conft'cnct on Polychlorinated 8iphemis, EPA560/6-75-004, pp. 14-29. Washington,0. C.: U S. Environ mental Protection Agency, Office of Toxic Substances. 20. Urabe, M. 1974. [foreward. The fourth reports ol the study of ''Yusho" and PC3.J Fukuoka Acta hied |/jp) 65: 1-4. 21. Hlrayama, C.| Irisa, T.f Yamamoto, T. 1969. Fine structural Changes of the liver In a patient with chlorobtphenyls Intoxi cation. Fukuoka Acto Atrd (Jan1 60: 45 5-56. 22. Hirayama, C.| Okumura, M.; Nigal, JMasuda, Y. 1974, Hypobiiirubln In patients with polychlorinated biphenyls poisoning, Gin Cftfm Acta 55: 97-100. 23. Meigs, J. W-; Albom, J. J.; Karlin. B. L. 1954. Chtoricne from an unusual exposure to Aroclor. JAM A 154: 1417-18. 24. Schwartz, L. 1936. Otrmatitis from synthetic resins and waxes. Am / Public Health 26: 586-92. 25. Drinker, C. K.; Warren, M. F.: Bennett, G. A. 19 87. The problem of possible systemic effects from certain chlorinated hydrocarbons. / ind Hyg Toxicol 19: 283-99. 26. Flschbeln, A.; Wolff, M. S.; Lilli, R.; Thornton, l,;Se(lkoff, I. J. 1979. Clinical rinding! among PCB-exposed capacitor manufacturing workers, Ann MY Acad Sci 320: 703-15. 27. Warihaw, R.; Flschbeln, A.,- Thornton, 1.: Miller, A.: Sellkoff, I. J. 1979. Decrease in vital capacity In PCB-expoied workers In a capacitor manufacturing facility. Ann NY Acad 5c, 320 277-84. 28. Bahn, A. K.; Rosenwaifce, l.| Herrmann, N.; Grover, P.; Stallman,].; O'Leary, K. 1976. Melanoma after exposure to PCB'i, N Eng! J Mtd 29S: 450, -->29. Roush, G, September, 1976. Written communication toNloSH. 30, Taylor, Philip, ft. April, 1980. (Personal Communication). N. Y.: New York Sut* Departmcntof Health. Ihfces IbaasMSSS siia*sss caass Ihii&h Stress on thejob is a real problem for most of us. Many people think high-pressurejobs cause high blood pressure. m ~:>.L Scientists and doctors aren't sure if stress causes high blood pressure. But one thing is forsure: anybody, no matter how they react to stress, can have high blood pressure, r If you have high blood pressure, you can control it--with medication, weight control, less salt, and wliatever else your doctor tells you to do. every day. . -> . Mr 'v^' ,, \ / f sT ' 1 > /AJalL / "*3 i) No mal ter what >ou do lor a living... keep on living. High blood pressure. Treat it and live. Nhiioru! rtgh Booa Fhessure (-audition Program. NtHnyuu Hoan Lurq ;,n0 GlCCO Institute. (J S Deoanmeni o! Hcailh and Human Services [Vol. 36 (No. 3)) HONS 209823 179