Document 0qQyjvvmVROG55BQKpnzznBVk

NOTICE: I1h oatarlxl t ha protected v" '*' "*0 n V Mortality and Industrial Hygiene Study oJ Workers Exposed to Polychlorinated Biphenyls DAVID P. BROWN, M.P.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 DbMon of Surveillance, Hazard Evaluations and Field Studies Onrlnnatl, Ohio 45226 ABSTRACT. Because of the demonstrated toxic effects on aniutah 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 vital status of 9814 of the two cohorts was determined, and 39,019 person-years were accumulated. AH-cause mortality wot lower than expected, (163 obs. vs 182.4 exp.) as well at all cancer mortality. (39 obs. vs 43J exp.). Excess mor tally was noted fur rectal cancer (4 obs. vs 1.19 exp.) and Rver cancer (3 obs. vs 1.07 exp.), although neither excess was statistically significant. In one of the plants the observed mortality due to cirrhosis of die liver was also elevated. The results of detailed industrial hygiene surveys con ducted in each plant are also presented. POLYCHLORINATED BIPHENYLS (PCBs) are a class ofcanpounds composed of biphenyl molecules with a varying number of substituted chlorine atoms. In commer cially prepared PC8 mixtures, the weight-percent of cnlorine has varied from 21 to 68 i. In some preparations, there tos also been some degree of contamination by ihlorodiben tofuraits.' 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 svsterns, 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 i 976, rules and regulations were promulgated to limit the manufacture and use of PCBs. This Act stipulated that all U S. production of PCBs end January 1,1979, and thu all U.S. sale and distribution of PCBs end July I, 1979. However, continual exposure to PCBs will occur among workers wno maintain transformers and capacitors, and among the general population via contaminated food. During the past few years, interest in the health effects among individtulj exposed to PCBs has been stimulated by: (j) the tendency for PCBs to accumulate in tissues and certain organs;2'3 (b) thu stability of PCBs and their per sistence in the environment;4'5 and (c) the demonstrated long-term tonic effects, including liver tumors and other liver diseases, in exposed laboratory animals.4'13 Much of this interest was expressed at the National Conference on Polychlorinated biphenyls in November, 1975,** and the toxicity of PCBs has been extensively reviewed in the NIOSH Criteria Document on PCBs.1* In comnarisnn ns 120 Archives oi Environmental Heiiift HONS 001539 the jccumulitctf information an acute toxic effects in humans and adverse effects in animals, little is known about the chronic effects from long-term exposure in man. To determine whether past occupational exposure to commercially produced PC8s 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. Description of FociIitits 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 were still using PCBs. Plant 1 is located in New York State and is divided into two manufacturing facilities within close proximity. One facility chat 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 "Aroclor" (Monsanto trade name) 1254 (54% chlorine) to 1242 (42% chlorine) to 1016 (41% chlorine). In addition, several other kinds of oils were used, but >n a limited number of capacitor*. 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 power 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 room 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 pre-asscmblcd capacitors were filled or impregnated with the PCBs. Within this area there was potential for exposure to-PCBs, and therefore, those employed in this area were considered "exposed" when choosing the study cohort. Final assembly. The tops of the 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 degreaser 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. (Vol.36 (No. 3)1 Other areas where (here 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. Those em ployed in these jobs were considered "PCS exposed" for purposes of choosing the study cohorts. 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 less homogeneous work force, with two-thirds being female, and reflects the general ethnic make-up of the 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-specific 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 by the companies anti 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. vitil status (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 vehicle 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 nosolog'tt 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 viui 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, were considered to be alive for purposes of analysis. 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)-whichevcr occurred first. Using a modified life tabic computer program similar to that described by Cutler,1* the pcrson-ycjrs for each cohort were combined into 5-yr calendar time periods and S-yr age groups and multiplied by the corresponding U S. white male (for male cohort members) and U.S. while female (for female cohort members) cause-specific mortality rates to yield the expected number of deaths. Person-years were additionally distributed by 5 yr exposure and 5-yr latency (number of years from date first employed in exposed HONS 001540 m Title Y.-Vital Statu* of PCB Workers Males Plant Y Females Total Known io be alive Known io be deceased Unknown vital status Total Person-years 520 SS I 513 7,135 Mi) If 7 MS 3,195 aso 73 15 96* 13,010 Mates 633 28 14 <75 9.229 Plant 2 Females Total <36 62 26 924 16,779 1,469 90 40 1,599 26,008 Grand Total 2,349 163 55 (3%) 2,567 39,018 jobs; categoric*. Observed and expected cause-specific deaths were compared .tnd differences were tested using the Poisson distribution. Industrial hygiene survey. The detailed industrial hygiene surveys included personal time-weighted air sam ples from selected job titles, js well as area air samples. Hi beth plants, samples were taken for PCBs (Aroclor 1016), trichloroethylene, lead, tin, and zinc. In addition, samples for toluene, methyl 'sobutyl ketone (MI8K), alumnum, 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 I where exposures may have been reduced because of new production tech niques recently initiated. RESULTS Mortality study. A total of 2,567 workers met the definition of the study cohort. Table 1 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 assemble the Plant l 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 5tate Department of Health* using method ology similar to that described by Marsh et al.lf 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) not 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 resuits. A similar validity check was not done at Plant 2, as it appeared from our inspection that the personnel file sys tem had been maintained intact. Table 2 shows the distribution of the cohorts by dura tion of employment in iobs 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 amonf Cohort Members in PCB Exposure Jobs Plant 1 Males N (RF)' 3-6 mo 6 mo-i yr 1-2 vr 2-3 yr 3-10 yr 10 yr Total 137 (23.$) 88 (15.1) 93 (16.0) S3 ( M 165 (28.3) 47 ( 8.1) 583 Plant 2 Males N (RF) 34 mo 6 mo-l yr t-2 yr 2-3 yr 3-10 yr 10 yr Total 211 (31.3) 127 (18.8) lit (174) 64 ( 9.5) 123 (18.2) 37 ( 5.7) 675 RF * Relative frequency. Females N (RF) 79 (20.S) 59 (15.3) 92 (23.9) 41 (10.6) 82 (21.3) 32 ( 8.3) 38J Females N (RFT 207 (22.4) 161 (17.4) 175 (18.9) 82 8.9) 188 (20J) m (i2.o) 924 Total N (RF) 216 (22.3) 147 (15.2) 185 (19.1) 94 ( 9.7) 247 (25.5) 79 ( 8.2) 968 Total N (RF) " 418 (26.1) 288 (18.0) 293 (18.3) 146 ( 9.1) 311 (19.4) 143 ( 8.9) 1599 m Archives of Environmental Health Tab* 1,-OtmU hX t CMCTt* DfHtil (Off) Acewrfinf ( MNm Cjuwi ----H fCO Wariitn CMM 90 OmUi (Tin (UvHim ICON*.) ruK i Mata* Mata* r.TMw XU MqptiHM (I40-20J) Nhwi tytttm (JJ01J4. 34J CMiMn ifMam (4004**) AttMtntt (100**2) A0*tNr (Mtn ft #.70 y j.h 2*/ 22.31 7/ *.02 10112.M ss/stsf 4/ 7.2* 1/ IJ7 7/ .*3 1/ 1.17 St 5J4 I */ 22.77 V M3 23/ 20.00 21 IJ4 3/ 3X0 14/ 14.1J 13/ 19.64 3/ 7.43 /10.2* IV 40J1 2/ 3.67 19/ 16.19 *2/ *5.10 Tout 39/ 43.79 11/ 12J5 60/ 62.93 >3/ 11.29 40/ 44.79 1*3/1*2.35 (SMX| (09) (M) (9S) (71) (HI lH) 93*! Ci(i4t)M W *22) (44 9979 (73 123) (30 - in) ( mi (7* - 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 in 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 tower than expected in each cohort, with an SMR (Standardized Mortality Ratio (SMR 3 observed deaths/expected 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 SMRs 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 obsorwd and expected number of deaths by specific cancer cause and for cirrhosis of the liver. When both cohorts are 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 s 155, 156A (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 0.50 exp., 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 are 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 oi the liver is shown in Table 5. For "all canter" there is no apparent pattern in either cohort. For cancer of the rectum, there is a slight increase with an increase in the 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 these same causes cf death and length of employment in PCB exposure areas of the plants is given in Table 6. As indicated in tlic fable, 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 (Arcelor 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 1 arc lower than those in Plant 2. In Plant 1, the time-weighted average (TWA) personal air samples ranged from 24 /ig/m* to 393 Mg/m3, and the TWA area air samples ranged from 3 Mg/m3 to 476 Mg/m3. The TWA personal air samples in Plant 2 ranged from 170 pg/m3 to 1200 Mg/m3, and the TWA area air samples ranged from 50 Mg/m3 to 810 Mg,TM3- Trichloroethylene was measured near the dvgreasers in both plants. Of 11 area air samples from Plant I, 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 /me near the soldering operations. There were no delectable levels for tin ji either plant. Of four samples collected tor lead and zinc at Plant 1, lead was detected in one sample at a level of 12 Mg/m3, and zinc was delected on two samples at levels of 8 and 24 Mg/m3. At Plant 2. 15 sam ples were collected for lead and /inc;all but one (41.2 Mg/ m3) of these samples showed no delectable levels for lead. Six of the 15 samples revealed concentrations of zinc ranging from 2.3 to 94.1 Mg/m3. Both personal and area samples were taken in the area | Vot. 36 <No. 3)| HONS 001542 23 I s TaMe 4,-Otanei and Expected Deaths (O/E) According to Sftdfk Cisto Camas and Ckrhesls of the LMr among PCS Werters Causa of Oaatli (7th Revision ICD No.) Plant 1 Males Females Mam 2 Males Females Total (SMR) Ail malignant ntotUsm (140-205) Stomach 051) Intestine exp. rectum 052,153) Rectum (154) Biliary pais liver Liver not specified (155,156A) Pancreas (157) Respiratory system (150-144) Breast 070) ' 9/ 9.70 0/ 0.51 1/ 0J2 1/ 0.31 If 0.23 Of 0J3 SI 3.22 4/ 7.26 0/ 0.22 0/ 0.70 0/ 0.18 0/ 0.18 1/ 0.27 1/ 0.71 1/ 1.86 3/ 6.83 1/ 0.31 0/ 0.54 0/ 0.20 0/ 0.15 0/ 0.35 0/ 2.22 23/ 204)0 39/ 43.79 Of 0.62 3/ 1.97 1/ 1.66 4/ 44)3 3/ OJO* 4/ 1.19 (89) (SOI (99) (3361 2/ 0.51 0/ 0.75 i/ 1.83 6/ 4.98 3/ 14)7 U 1.90 1 V 7.98 V 644 (280) (53) () (102) Lymphatic and hematopoietic (200-205) X o 2 Other Cn Cirrhosis of liver 1511) O o < Ul K.05 * u> 0/ 1.10 1/ 2.98 1/ 1.69 0/ 0.59 1/ 2.55 0/ 0.73 Of 0.94 2f 2.12 2/ 1.26 V 1.71 6/ 7.13 3/ 1.92 21 4.34 10/i 14.78 61 5.60 (46| (61) (107) 95% Confidence Interval (63 - 122] (27 254) (92 * 860) (51 820) (35 - 111) (41 - 211) (32 124) (39 - 233) A n h U ct o f Environments Health Table S.-Observed and Expected Death* According to Latency* among Male and Female PCB Workers ijy (y'l <10 yr 10*<20yr >20 yr <10 yr l0-<20yr >20 yr <10 yr 10*<20 yr >20 yr <10 yr t0-<20 yr >20 yr 1. All Cancers Plant 1 Plant 2 Of $MR a E SMR 6 5.27 3 <41 4 5.07 114 < 7.76 77 45 16 10.91 147 79 4 8.17 49 II. Cancer of Rectum (ICO *154) 0 o.ts 0 0.19 t 0.15 ... 647 0 0.21 3 049 690 0.21 476 I 0.12 0 0.16 0 0.12 1 040 9 141 0 041 III. Liver Cancer (ICO * 155,156A) 833 0.11 356 0.27 370 0 041 ... IV. Cirrhosis of Liver (ICO >581) 125 045 105 ... 1.35 74 ... 3 0.88 341 O 12 19 8 0 2 2 2 1 0 2 1 3 * Latency * number of years from dale first employed In exposed fob. f O a observed deaths. | E expected deaths. Plants e 2 SMR 13.03 17.52 13.24 93 108 60 0.36 0.40 0.36 ... 417 556 040 0.43 043 <67 233 1.75 lit 1.49 114 424 201 of welding operation* for measuring aluminum and iron at Plant 1. The aluminum samples ranged from nondetectable to 233 Mg/m3, and the iron samples ranged from 47 Mg/m3 to 123 Mg/ns3. Twelve personal samples were collected for tolueno and MBK during painting operations at Plant 1. Toluene concentrations ranged from 0.48 to 22 ppm and MIBK ranged from 2 to 5 ppm. Although the exposures to PCBs at the dates of survey (Plant I-April 1977, Plant 2-March 1977), were relatively higher in Ptant 2, the historic levels of exposure may have been more equivalent. The exposures that occurred 20 to 30 yr ago are more relevant when considering the occu pational cancer risk among the study cohorts. The PC8 mixtures used during these time periods were Aroclor 1254 and 1242, whereas Aroclor 1016 was first used in 1971. In addition, several different stabilisers have been added to the PCBs (1% or less by weight) used at Ptant 1 since the early 1960s. These include potential carcinogens such as diglyceride cthcr-disphcnola and, more recently, vinyl cyclehexene dioxide. It is not known which stabilizers have been used at Plant 2. (Vei. M (No. 3)| 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 extern iiwly years after the incident took place in Japan in 1968.1*'* However, the rice oil contaminant also con tained polychlorinated dibenzofurans and other contami nants in higher concentrations than those found in com mercially prepared PCBs. A high prevalence of skin and eyo conditions were noted in the Yusho patients. In odd)ion, there were clinical and laboratory findings that included changes in the microanaeomy of liver cells and a decreased concentration of bilirubin in the scrum of these individuals.5,,M Early reports regarding the health effects from occu pational exposure to PCBs include chtoracnc,25 digestive disturbances, eye irritation, liver injury, and impotence.3*'2* Most of these findings have been reported *s case histories. In a recent study of volunteers conducted by the Mount Sinai School of Medicine,3* 326 workers who were cm* HONS 001544 129 Table 4.-Observed and Expected Ocaths According to Length of Exposure among-Male jnWPemale PCS Workers Length of Employment O* 3 mo -5 yr 5- yr 10-14yr 15-19 rr > 20 yr 11 1 0 1 0 3 mo -5 yr 5-9 yr 10-14 yr 15-19 yr > J0 yr 1 0 0 0 0 3 mo -5 yr J-*yr 10-14 yr 15-19 yr > 20 yr 1 0 0 0 0 Plant 1 Et SMR 12.21 2.95 1.00 0.49 0.11 90 34 145 0.35 0.09 0.03 0.02 0.001 286 0.29 0.04 0.02 0.02 0.002 345 3 mo -5 yr 5-9 yr 10-14 yr 15-19 yr > 20 yr 1 0 0 0 0 *0 observed deaths. f expected deaths. $P<.0l 1.79 56 0.39 0.12 ... 0.10 ... 0.02 Plant 2 O E SMR 1. All Cancers (ICO * 140-205) 20 18.78 106 2 4.10 49 3 2.28 132 1 1.04 96 0 0.63 II. Cancer of Rectum (ICO ~ 154) 1 0.48 208 0 0.11 2 0.06 3333* 0 0.03 0 0.02 lit. Liver Cancer (ICD - 155.156A) 2 0.45 444 O 0.11 0 0.06 0 0.02 0 0.02 O 31 2 0 2 0 2 0 0 3 0 0 0 0 IV. Cirrhosis of the Liver (ICO > 381) 2 2.26 88 1 0.48 208 1 0.24 4)6 1 0.13 769 0 0.08 3 1 I 1 0 Plants 1 2 e SMR 30.99 7.05 3.28 1.73 0.74 100 43 91 !t6 ... 0.83 0.20 0.09 0.05 0.02 241 22221 0.74 0.19 0.08 0.04 0.02 405 4.05 0.87 0.36 0.23 0.10 74 IIS 278 435 ployed at Plant 1 wort examined. The most prevalent symp tom* noted were dermatological and those of the central nervous system. There was a low prevalence of abnormal Hver findings on physical examination. However, a sub group exposed to PCBs were found to have liver enzyme changes different from those of a normal, non-exposed group. In addition, abnormal scrum glutamic oxaiacctic transaminase (SGOT) levels were associated with plasma levels of PCBs. There was a relatively high prevalence of decreased lung capacity among a subgroup of 243 workers tested.27 In a preliminary report. Bahn2* reported an increase in deaths due to malignant melanoma (2 obs. vs 0.04 exp.) and cancer of the pancreas among 51 research and devel( opmvnt employees and 41 refinery plant employees at a , New Jersey petrochemical facility. These individuals were ** exposed to Aroclor 12S4 during various periods between 1949 and 1957, along with exposure to other toxic and potentially carcinogenic compounds. ^ In a summary of case histories among approximately ~ 300 workers employed in the manufacturing of PCBs,2* no malignant melanomas or pancreatic cancers were observed. However, among the death certificates of 50 former workers at this manufacturing facility, 7 cases of lung cancer were observed whereas 2.7 eases were expected. The findings were preliminary and were not adjusted for "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 the present study. There are no observed deaths due to malignant melanoma and only 1 obscivcd death from pancreatic cancer while 1.89 are expected. There are 7 observed deaths from rcsoiratorv 121 Archives of environmental Health 3- HONS 001545 L system cancer, whereas 7.69 are expected. The only cate goric* of cancar in which the number of observed deaths are freatcr than expected are 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 ara statistically significant at P < .OS. Howavar, the excess in liver cancer is noteworthy because it is consistent with the toxicology data observed in labor atory animals exposed to PCBs, where effects have been noted in the liver.**'1 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 C2ncer 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 PC8 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 ofTfie excesses occur in Want 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 siae 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.-Cencentrations of PCBs (Aroclor 1016) at Plant 1 (April 1977) A. Power Capacitor Manufacturing Facility Personal Air Samples Area Air Samples Job Titles No. of Samples Toul Sampling Time (min) TWA* lWM3) Location No. of Samples Total Sampling Time (min) TWA* imm'i Recovery Repair Salvage Operator CMP operator Treat helper Treat operator Rapalr 3 340 293 Test and 2 340 Paint 1 426 155 Assembly 2 31 1 431 115 Shipping 1 426 2 67 30 Storage 1 427 2 731 66 Winding 1 420 1 422 50 B. Small Capacitor Manufacturing Facility Mo reman (Staling area) Mowman (Testing and soldering area) Testing Packer Treat operator Rework and final uumkiy 2 2 3 3 2 2 639 1306 1220 12*7 45 324 393 220 213 199 160 152 Maintenance Rework tester Rework packer Rework tester solder 1 404 150 1 433 140 1 435 132 1 271 24 *TWA is calculated during the total sampling time period. Soldering 2 Assembly 2 Shipping 2 Winding 2 Can 2 Manufacturing Cover 2 Manufacturing 732 127 333 123 136 34 41 29 16 T4 3 476 115 56 54 51 45 (Vol. 36 (No. 3)) MQNS 001546 127 Table 8.-Concentrations of PCB* (Arotlor 1016) at Plant 2 (March 1977) fob Titlas No. of Samples Personal Air Samples Total Sampling Time (min) TWA* (fig/m3) Area Air Samples No. of Location Samples Total Sampling Time (min) TWA* U*/m3) Degreaser Solder Tanker Moveman (soldering area) Ileal soak operator Taster Pump Mechanic Ftoorman (pre-assembly) 1 3 9 3 3 3 1 6 311 184 2120 7J2 172 917 377 1683 1,260 1,060 ISO Impregnation Pump room Testing 2 3 5 720 Pre-assembly 4 630 290 280 Shipping 2 Winding 4 Cover 3 manufacturing 170 Office 2 176 1079 1424 810 490 320 7213 741 637 7019 740 90 70 60 741 50 The TWA Is calculated during the toui sampling time period. A potential confounding variable or interaction variable in this study is 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 is known about the ingestion of alcohol among the entire study cohort. 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 were examined. Among the cancer causes, there was increased cancer of the liver and rectum. Cirrhosis of the liver was also elevated in one of the plants. The slight exersses for liver cancer and cirrhosis of the liver are con sists m with previously reported findings on experimental animals exposed to PCBs, and suggest that there may be an association between these causes of death and occu pational exposure to PCB* (i.o., Arocioi 1254 and 1242). However, the findings for liver cancer do not reflect a rtlj'.iomhtp with latency that has been observed for other carcinogens found in the workplace. The observed excess in cancer of the rectum rcljtcd to PCB workers was un expected and requires further investigation. the authors would like to express (heir ipprcji'afion for tire *etk of many injiidu.)l who helped to siKwtstully complete this tludy, including llu guidance ol Joseph Wifantr, Richard 171 Lemcn, end Richard Waxweltcr; the assistance of the clerical and secretarial staff in the Biometry Section, Industry-wide Studies -Bunch of NIOSH; the dm entry and analysis provided by the Southwest Ohio Regional Computer Center; the cooperation of the companies and labor unions chosen for the studv; and for the information provided by the New York State Department of Health. Mr. loncs Is now employed at Kaiser Aluminum and Chemical Corp., Ravenswood, West Virginia, 26164. Submitted for publication March 27,1911; accepted for publication April 20, 1911. Requests for reprints should be sent to: David P. Brown, I.W.S.B., NIOSH, 4676 Columbia Parkway, Cincinnati, OH 45226. REFERENCES 1. Hutzinger, O.; Safe, Zitko. V. 1974. The chemistry of PCB's, pp. 3-23. Cleveland, Ohio: The Chemical Rubber Co. Press. 2. Yobs, A. R. 1972. Levels of polvchorinated biphenyls in adipose tissue of the general population of the nation. Environ Health Penpeel, (Experimental issue No. 1)1: 79-11. 3. Price, H. A., and Welch, R. L. 1972. Occurrence of polychorinated biphenyls in humans. Environ Health Ptnpect, (Experimental issue No. I) 1:73-78. 4. Jensen, 5.; Johnels, A. G.; Oisson, M.;Otterllnd,C. 1969. ODT and PCB in marine animals from Swedish waters. h'attire 224: 247-50. 5. Jensen, S. 1972. fhe PCB story. Ambio 1: 123-31. 6. VonWedel, H.; Holla. W. A.; Denton, J. 1932. Observations on the toxic effects resulting from exposures to chlorinated naphthalene and chlorinated phenyl* with suggestion* for prevention. Rubber A<je 54: 419-26. 7. Miller, J. W 1944. Pathologic changes in jnlmih exposed to a commercial chlorinated diphenvl. Public Health Ren S9: 1015-93. Archives of Enrlienmuitd Health HONS 0015*7 8. brwtknvt, J. V.; Klinn( K. LiCamWi, M. H. 1974. Flychlorinated biphenyl-induced alteration of biologic para* mtttrt kn the rat. Toxicol Aop! Pharmacol 38: 189-99. 9. Kimbrough, R. 0.: Under, R. E.; Glint*, T. B. 1972. Morphological changes in livers of rats fed polychlorinated biphenyls. Arch Environ Health 25: 354-64. 10. Kimbrough, R. 0.: Under, R. E.; Burse, V. W.; Jennings, R. W. 1973. Adenofibrosis in the rat Jiver-with persistence of polychlorinated biphenyls in adipose tissue. Arch Environ Health 77; 390-93. 11. Kimbrough, R. 0.,and Under, R. E. 1974. Induction of adenofibrosis and hepatomas of the liver in BALB/cf mice by polychlorinated biphenyls (Arocior 1254). / Mad Cancer Inst 33: 547-52. 12. Allen, J. R.; Abrahamson, l. |.;Norbach, O. H. 1973. Biological effects of polychlorinated biphenyls and triphenyis on the subhuman primate. Environ Res 6: 344-54. 13. Vos, J.G.,and Notenboom-Ram, E. 1972. Comparative tonicity study of 2, 4, 5,2', 4',5'-hexachlorobiphenyl and a polychlorinated biphenyl mixture in rabbits. Toxicol Appi Pharmacol 23:563*78. 14. Environmental Protection Agency. 1976. Proceedings of the Notional Conference on Polychlorinated Biphtnyis, EPA 560/6 75 004. Washington, 0. C.: Office of Toxic Substances. 15. NIOSH, C0C, PHS, DHEW. 1977. Criteria for a recommended Standard: Occupational exposure to polychlorinated biphenyls (PCS'*). Publication No. 77 225. 16. Cutler, S. J., and Ederer, F. 1958. Maximum utilization of the life table methods in analyzing survival. / Chronic Dis 1:699-709. 17. Marsh, C. M.,and Enceriine, P. E. 1979. A method for verifying the completeness of cohorts used in occupational _ mortality studies. I Occup Med 21 `.665-70. 18. McMichael, A. J.; Haynes, S. G.; Tyroler, H. A. 1977. Observations on the evaluation of usupsilsnal n cmIts, data. / Occup Med 17: 128-31. 19. Kuratsunt, M.; Masuda. Y.; Nagayama. |. 1976. Some of the recent findings concerning Yusho. In Proceedings of mo National Conference on Polychlorinated Biphenyts, ERA560/6-75-004, pp. 14-29. Washington, 0. C.: U.S. Environ mental Protection Agency, Office of Toxic Substances. 20. Urabc, H. 1974. (Foreward, The fourth reports of the study of "Yusho" and PC9.| Fukuoka Acta Med {Jap) 65: 1-4. 21. Hirayama, C.; Iriu, T.; Yamamoto, T. 1999. Fin* umcn/al changes of the liver In a patient with chlorobiphenyis intoxi cation. Fukuoka Acta M*d [Jap) 60: 435-36. 22. Hirayama, C.; Okumura, M.; Nagai, |.; Masuda, Y. 1974. Hypobillrubin in patients with polychlorinated biphenyls poisoning. Qin Cham Acta 55: 97-100. 23. Meigs, J. W.; Albom. J. |.; Kartin. B. L. 1954. CMoracne from an unusuaJ exposure to Arocior. jAMA 154: 1417-18. 24. Schwartz, L. 1936. Oernutitit from synthetic reside and waxes. Am J Public Health 26: 586-92. 25. Drinker, C. K.; Warren, M. F.; Bennett, G. A. 1937. The problem of possible systemic effects from certain ddorinaotO hydrocarbons. / Ind Hvg Toxicol 19: 283*99. 26. Fischbein, A.; Wolff, M. S ; Lilts, R.; Thornton, SeMwff, I. j. 1979. Clinical findings among PCS-exposed capacitor manufacturing workers. Ann .V Y Acod Sci 320: 703-1S. 27. Warshaw, R,; Fischbein, A.; Thornton, J.; Milter, A.;SHboff, 1.1.1979. Decrease in vital capacity in PCB-exposad woeIw* in a capacitor manufacturing facility. Ann iV Y Acad Sci 320: 277-84. 28. Bahn, A. K.; Roscnwaike, I.; Herrmann, N.; Grover, P.; Stellman, J.; O'Levy, K. 1976. Melanoma after exposure to PCB's. N Engl / Med 295: 450. --> 29. Roush, G. September, >976. Written communication to NIOSH. 30. Taylor,Philip. R. April, 1980. (Personal Commumtatten). N. Y.: New York State Department of Health. ES teSKESS S&-25S CSKSC hagh fllO Stress on thejob is a real problem for moot of u*. Many people think high-pressurejobscause high blood pressure. Scientists and doctors aren't sure ifstress causes high blood pressure. But one thing is for suit; anybody, no matter how they react to stress, can have high blood pressure. Ifyou have high blood pressure, youcan control it--with medication, weight control less salt, and whatever else your doctor tdlsybu to do. everyday. No matter what you do Cora living... keep on living. High blood pressure. Treat it and Ihe. Nohonal High Booo Pressure Education Program. National Hoar! Lung and Qkxxi institute. (J S Deonnmmt of Health and Human Services (Vol. 36 (No. 3|| HONS 00154S 129