Document e72Ee2Q25Mm926RzLyKm45dD4

VRD 0082030253 A To: Interoffice Communication From: Date: Subject: T. Grumbles and Dr. Hamm 0? D. Penney November 2, 1993 Brain tumors and occupational risk factors VISTA Dr. .Mundt has provided what he considers the best review he has found on the epidemiology of brain cancer in general. I think it would be useful for you to look at this review this paper prior to our meeting on November 11. A general conclusion that can be drawn from this review is that not very much is known about the causes of brain cancer. A summary of some of the key points of this review is provided below. The brain and other CNS cancer incidence rate amongst white males in the U.S. is 6.7 per 100,000. The mortality rate is 4.9 per 100,000. These figures are based on 1973-1977 data. . A high percentage of brain tumors reported on death certificates are gliomas, particularly glioblastoma multiforme. Other types of brain tumors reported include astrocytomas and ependymomas. Many death certificates list unspecified brain tumor as the cause of death. . Mortality rates from brain cancers amongst individual over 55 years of age have been steadily increasing since the 1940s. . Diagnostic bias does not seem to explain all of this increase. This suggests that some genetic and/or environmental risk factor(s) may be involved. Brain tumor clusters have been observed in certain occupational groups, including polyvinyl chloride production, oil refining, petrochemical production, pharmaceutical production, use or production of formaldehyde. . Most epidiemilogical studies of brain tumors do not specify the cell type. It is possible that risk factors vary by cell type. . This article reports that gliomas have been induced in animals by inhalation of vinyl chloride. NOU 02 '93 11:18 TO 1 512 331 2387 FROM APPLIED EPIDEMIOLOGY T-430 P.02 REVIEWS_______________________________ Scorut J Work Environ Health ]2 (1986) 1--15 Brain tumors and occupational risk factors A review by Terry L Thomas, MS,1 Richard J Waxweller, PhD2 THOMAS TL, WAXWEILER RJ. Brain tumors and occupational risk factors; A review. ScondJ Work Environ Health 12 (1986) 1--15. Little is known about ih etiology of tumors of the brain and central nervous system (CMS); however, epidemiologic studies have indicated recently that excess brain and CNS tumor risk may be associated with employment In certain occupations or Industries. Some studies have shown that certain white-collar professional groups (eg, artists, laboratory professionals, veterinarians, erabalmers) appear to have an elevated risk of brain tumors, and they raise the issue oft diagnostic sensitivity bias. Some blue-collar occupational groups, including rubber workers, oil refinery workers, chemical plant workers, polyvinyl chloride workers, machinists, and others, have been reported to have an elevated risk .of brain tumors. Most of these workers are potentially exposed to multiple chemicals; nevertheless (hey j have some exposures in common, for example, exposure to organic solvents, lubricating oil, acrylonitrile and vinyl chloride, formaldehyde, polycyclic aromatic hydrocarbons, and phenolic compounds. l Key terms: organic solvents, lubricating oils, acrylonitrile, vinyl chloride, formaldehyde, polycyclic aromatic hydrocarbons, phenolic compounds. The age-adjusted average annual incidence rate for malignancies of the brain and central nervous system (CNS) among white men in the United States (US) dur ing 1973--1977 was 6.7 per 100 000, and the corre sponding mortality rate was 4.9 per 100 000 (104). Mortality rates for malignant brain and CNS tumors among all age groups over 35 years have been steadily increasing since the 1940s (95), Mortality and incidence rates for CNS malignancies ip. the United States are higher among white men than among women and blacks (45,104). About half of the brain tumors (be nign and malignant) diagnbsed among white men of all ages are glioblastoma nniltlforme, but this cell type accounts for a much lower percentage of the brain tumors diagnosed among women and blacks (5). There" is a dramatic peak in mortality due to brain and CNS malignancies among white men between 45 and 65 years of age (45); the peak corresponds with that in the incidence rale for glioblastoma multiforme between the same ages (74). These patterns imply that some genetic and/or environmental risk factors) may be responsible for the elevated rates among white men compared with women and blacks. The age peak and increasing rates over calendar time suggest an environ mental risk factor, possibly occupational. 1 Occupational Studies Section, Environmental Epidemiology Branch. Nitionil Cancer Institute, Bethwda, Maryland 20892, United States. * Special Studies Branch, Chronic Diseases Division, Center for Environmental Health, Centers for Disease Control, At lanta, Georgia 303)3, United States. Reprint requests to: Ms TL Thomas, Occupational Studies Section, Environmental Epidemiology Branch, NCI, Landow Building, Room 4C16, Beihrjda, MD 20892, USA. One of the difficulties in comparing epidemiologic studies of brain and CNS tumors is disease definition and terminology. The term "CNS tumors" Includes tumors of the brain, cranial nerves, and cranial meninges; however, because more than 90 <7* of CNS tumors are brain tumors (104), we have used (he terms brain cancer (malignancies only) and brain tumor to refer to ail CNS tumors throughout our review, regard less of the original author's definition or terminology. More confusing Is the fact that brain tumors con be coded as malignant (International Classification of Diseases, Eighth Revision (ICDA-8) code 191, 192], benign (ICDA-8 code 223), or unspecified as to malignant or benign (ICDA-8 code 238). Unfortu nately, if a physician records just the words "brain tumor" on a death certificate, as U often the case, the unspecified code (ICDA-8 238) will be assigned as (he underlying cause of death. Upon later pathological review, many of these cases may be shown to be primary malignant tumors. In addition, there may be some misclassification on the death certificates between primary brain tumors and those that are metastatic from other cancer sites (62). Thus, If brain tumor risk is to be thoroughly evaluated, it is important to report all 1CD codes for primary brain tumors (ICD 191, 192, 225, and 238) separately and combined. In most in stances investigators have reported mortality or in cidence only for tumors of the brain specified as malignant; however, in the accompanying tables, we have indicated which results also include tumors coded as benign or unspecified. Very little is known about the etiology of brain tumors; however several associations with occupational and other environmental and genetic factors have ap peared in the epidemiologic literature (23). Although 1 A VRD 0002030254 5 iIB E 0 l8 8 B flA> NOY 02 '93 11:19 TO i 512 331 2387 FROM APPLIED EPIDEMIOLOGY T-430 P.03 T*bls 1. Brain tumor* among white-collar and professional occupation* In surveys of mortality by occupation. Occupation or type of work* Study period Observed Measure ol brain association* tumor events' flalio4 Reference Professional A teohnlcel, US 1950 Professional A technical. Canada Accountant* 8 auditors. US Financial workers. MA 1965--1973 1950 1971-1973 Treasurers, financial managers, bank officers. MA Manager*, officials, proprietors, 1971--1973 manufacturing, U8 1950 Managers, officials, proprietors, WA Purchasing agents, buyers, 1950-1079 sales managers, WA 1950--1979 Sales managers (age 85--74 years), UK 1970--1972 Purchasing agents & buyers, sales managers, CA Credit men, WA 1959-1901 1950-1979 Insurance agents, brokers. underwriter*, & appraisers, WA Englnoer*, nec. WA 1950--1079 1960-1079 Engineer*, nec, CA Mechanical engineers, WA Aeronautical engineer*. CA 1959-1961 1950--1979 1959--1961 Eleoirtoal engineers, CA 1969-1961 BectribaJ sriQinears (age 65--74 years), UK 1970-1972 Inspectors, nec, WA \ 1950--1979 Inspectors, neo, CA '> 1959--1961 Checkers, examiners. Inspectors. MA 1971-1973 Public utility supervisor* & officials, WA 1960--1979 Clergymen, WA 1950-1979 Dentists, CA 1959--1951 Teacher*, US 1980 Arttsts & art teachers, CA 1960-1979 Teachers, except music A art, CA 1950-1961 Teachers, elementary 6 secondary, MA 1971-1973 Professor* A Instructors, CA 1059--1961 School professions, MA Lawyers & judges. CA 1871--1073 1959--1061 Lawyers A tudgea, WA Lawyers & judges, MA Postal dark*, CA 1950--1979 1971--1973 1959-1061 Postal clerks, MA Officer*, enlisted men. armed fore**, nec, OA 1071--1073 1959--1961 Armed force* (British & foreign), UK Armed force* (British & foreign), UK 1970--1972 1961 SMR SMR SMR *mor sMOR BMR PMR PMR PMR PMR PMR PMR PMR PMR PMR PMR PMR PMR PMR PMR sMOR PMR PMR PMR SMR PMR PMR SMOR PMR *MOn PMR PMR sMOR PMR sMOR PMR SMR SMR 169 1.34* Qlirelnick (25| 10 1.95 Howe & Lindsey (33) 27 l.93` QuraJnich (2S) 13 2.29* OuDrow & Wegman (IT) 5 3.47* Dubrow & Wegman 07) 43 1.30 Gurainick (25) 64 1.50* Mliham (46) 12 1.78 2.47 Mliham (46) Registrar General (05) 5 2.69 6 2.07' Peterson & Mliham (03) Miinam (40) 21 1.50 Mliham (43) 26 1AT Miinam (4$ 10 Z16* Peterson a Mliham (80) 8 4.23* Mliham (46) 4 2.17 Peterson & Mliham (63) 5 1.55 Peterson & Mliham (63) 2.75 Registrar General (65) 7 2.46 Mliham (48) 10 2.55* Peterson & Mliham (63) 4 5,57* Dubraw 6 wegman (17) 10 1.99 Mliham (48) 14 1.99* Mliham (46) 2 1.52 Peterson A Mliham (63) 21 1.75* Ourelnic* (29) 4 2.96 Peterson & Mliham (03) 8 2.41* Peterson 6 Mllhem (S3) 7 3.71* Dubrow & Wegman (17) 6 2.92* Peterson a Mliham (63) 10 2.54* Dubrow 6 Wegman (17) 5 1.91 Pstsrson & Mliham (63) 13 1.00* Mliham (48) 7 5.56* Dubrow 6 Wegman (17) a 2.7B* Peterson 6 Mliham (83) 6 2.86 Dubraw 6. Wegman (17) 37 1-58* Peterson A Mliham (63) 1-83 Registrar General (65) .. 1.57 Logan (39) * US * United States, MA s Massachusetts, WA* Washington, UK * United Kingdom, end nac-not elsewhere classified. PMRa proportionate mortality ratio, 8MR standardized mortality ratio, PIR a praportkxiats incidence ratio, SIR a standardized InoMenoe ratio, 9RRstandardized r*t* ratio, sMOR=standardized mortality odds ratio, and OR" odds ratio. a Ratio s obsarvedsexpeoted ratio or odda ratio. * Statistically significant (Poisson) at the 0.05 level- no causal industrial exposures have been identified, brain tumors seem to cluster in certain occupational groups. Historically, the first occupational association with brain tumors was reported among workers in the rubber industry (42), Since 1968, clusters of brain tumors have been seen among workers involved in polyvinyl chloride production, oil refining, petrochem ical production, pharmaceutical production, uc or production of formaldehyde, and other occupations. This review summarizes the scientific literature on oc cupational risk factors for brain tumors and examines some of the exposures that may be implicated. The measures of association shown in the tables are not directly comparable; thus we have used a test of statistical significance to evaluate the relative impor tance of the results shown. Because the authors of the numerous studies discussed in this review used a va riety of statistical tests to judge the significance of their results, we have ignored the original significance tests, instead, we applied a common lest statistic to each re sult for which the authors supplied an observed num ber of brain tumor events and an expected number of events or an observed:expec(ed (0:E) ratio. If the 0:E ratio was not provided by the original author, we cal culated it from the data published. This calculation in cludes results presented in the form of the propor tionate mortality ratio (PMR), the standardized mor tality ratio (SMR), the standardized incidence ratio (SIR), the proportionate incidence ratio (PIR), the standardized mortality odds ratio (sMOR), and the standardized rate ratio (SRR). The statistical signif icance or each of these results was determined from a table of significance factors for the ratio of a Pois son variable to its expectation ($). Since brain cancer 2 N0Y 02 '93 1U20 TO 1 512 331 2387 FROM RPPL1ED EPIDEMIOLOGY T-430 P.04 accounts for only 2.5 of all cancer deaths (45), the underlying Poisson assumption of a rare event is satisfied In this case. Because our test is inappropriate for case*referent analyses, the statistical significance of the odds ratios from the case-. eferem analyses pre sented in the uhles was determined with the 95 Vs con fidence intervals provided by the authors. Surveys of mortality by occupation Information from death cent)'- ates, registries, or record linkage systems has been used in many surveys to examine disease risks by occupation. Surveys of mortality by industry were not included in tables 1 and 2 because of a lack of specificity with regard to occu pation: however results from some of these surveys are discussed in relationship with specific hypotheses pre sented later in this review. Became an exhaustive list of occupations reported In these surveys would be too lengthy to show in a single table, we decided to limit the faults shown; thus, standardized mortality ratios, standardized incidence ratios, and standardized mor tality odds ratios of less than 1.3 are not shown and proportionate mortality ratios of less than 1.5 arc not shown. Results from the Washington state mortality data (48) were obtained from a table of statistically significant results for brain cancer. The data indicated that certain white-collar and pro fessional groups may have an elevated brain cancer risk (table 1). These groups include financial managers and accountants, sales agents, engineers, teachers, lawyers and judges, postal clerks, and persons in the armed forces. These occupational groups presumably have minimal exposure to chemicals and other potentially carcinogenic agents in their jobs. White-collar and pro fessional groups may receive better than average medical and diagnostic services because of their socio economic status and, thus, may be more likely than the population in general to have a brain tumor diagnosed (24), Mortality was elevated among Cali fornia residents in the armed forces (63) and among British members of the armed forces (39, 65), who typically receive regular medicat surveillance. Tabic 2 shows blue-collar worker groups with ele vated brain cancer mortality in occupational surveys. The most interesting arc the elevated brain cancer mor* taJIcy ratios for electricians and power servicemen in four of the surveys (23,4$, 63. 64). Several of the oc cupations listed in table 2 involve exposure to solvents and organic chemicals, but no prominent patterns of common exposures are evident for particular occupa tions. Several of these surveys obtained the information on occupation from death certificates. Because the "usual occupation" listed on the death certificate may be more representative of last occupation, many of the persons classified in white-collar management occu pations could have begun their employment in bluecollar jobs. Occupations were not cross-classified by industry; thus it is not possible to evaluate whether ele vated risk occurred among white-collar managers in particular industries. Furthermore, relatives of a de ceased Individual may tend to "upgrade" the de ceased's occupation socioeconomically. TeM* a. Brain tumors among,blue-coll*r occupations In surveys ot mortality by occupation. Occupation or typa of work* Study period Measure oi association6 Observed brain tumor events Ratio* Operatives a kindred workers, MA Painters, pepartiangers, olMier*. US Carpenter* (age 80--54 years), MA Brlckmasens, stonemasons, tile sellers, MA Electricians. US Electricians, WA Electricians, Lot Angeles County, CA Unemen & servicemen, telegraph, telephone, power, CA Welders, metal, Sweden Boilermakers, CA Machinist* k Job sellers, US Machtnteta (ape 20--64 year*), MA Airplane mechanlos & repairman, WA Fireman k fire protection workers, WA Crane derrlckmen & holetmen, CA Deliverymen & routamen, CA Class a ceramic makers. UK Glass workers, Sweden Farmer* & farm workers, Canada Railroad clerks, WA 10T1--1973 1960 1971--1073 1871-1973 i960 1950-1979 1979--1077 1959-1961 1961-1973 1959-1961 I960 1971--1973 1950--1979 1950--1979 1059--1961 1959--1961 1970--1072 1961 -- 1973 1965--1973 1950--1979 sMOfl SMR sMOR MOR SMR PMR FIR PMR SRR PMR SMR SMOR PMR PMR PMR PMR SMR SRR SMR PMR 4 3.88 32 1.39 7 2.74* 4 3.14 31 2.21* 43 1.60* 11 1.42 5 2.07 44 1.44* 3 2.16 37 V42 5 3.12* 14 2.or 14 1,77 3 Z.23 6 2.03 1.31 io 2.39* 4 1.77 13 3.40* * Be* table 1 (footnote a] (or a definition of the abbreviations. D Bee table 1 (footnote b) for a definition of the abbreviations. * Ratio m obs*rved:axpectMf ratio or Odd* ratio. ' Statistically significant (Poisson) at (ha 0-03 lavsi. Reference Dubrow & Wegman (1?) GurainlCK (25) Dubrow & Wegman (17) Dubrow & Wegman (17> Guralnick (25) Mltham (40) Praaton-Martln at al (64) Peterson & Milham (63) Engiund et al (10) Peterson k Milham 163) Guralnick (25) DvtilOw k Wegman (17) Milham (48) Milham (48) Paterson & Milham (63) Peterson & Milham (S3) Registrar General (65) Englund et J (10) hows & Undsay (33) Milham (40) 3 VRD 0002030256 A L S W I B W B B AHA** NOU 02 '93 11 s21 TO 1 512 331 2387 FROM APPLIED EPIDEMIOLOGY T-430 P.05 Production of synthetic rubber Table 3 shows results from studies of workers In the production of synthetic rubber. In 1949, an unusual cluster of deaths from CNS tumors was observed among residents of Summit County, Ohio, and a pos sible link with the rubber industry was suggested (42). Subsequently, a cohort mortality study of workers in a rubber plant in the same county Indicated an elevated brain cancer risk among employees in the curing and tire-building department (43). Later studies of the same plant population also implied that men employed in tire assembly and tire building had an elevated brain cancer risk, but brain caocer mortality was less than expected in the entire plant population (31, 32). The elevated risk occurred primarily among men whose at tained age was less than63 years (0:E-8:I.3), those who had worked less than IS years (OiE-, 7:1.4), and those who started working in the industry after 1923 (0:E-- B:l.8). The findings suggested that the elevated r&k may be associated with exposures introduced into the work environment in more recent time periods (51), Exposures in the tire curing, building, and assembly areas included hexamethylenetetramine and drum resins containing coal tar, carbon tetrachloride, and other solvents (51.52). A slightly elevated brain cancer risk was seen among workers in the rubber industry in Sweden (IB), but brain cancer mortality was not elevated among US rubber workers in a 1930 survey by industry (26) nor in other cohort studies of US rub ber plants (46, 83) nor among workers in the rubber and cabiemaking industries in England (19). Polyvinyl chloride production A cohort was assembled from 34 plants to examine the relationship between polyvinyl chloride (PVC) expo sure and risk of cancer (J1,85). Among persons who had worked for at least one year in a Job involving ex posure to vinyl chloride, the total number of brain can cers observed was significantly greater than expected (table 4). The twelve brain cancers observed during the study period included four glioblastoma, two astro cytoma, one ependymoma, and five unspecified. A proportionate mortality ratio study Of deceased workers in two plants using vinyl chloride monomer indicated an increased relative frequency of brain can cer (53). Five deaths were observed, and only 1.2 were expected (table 4). Three of (he five brain cancers were TstJl* 3. Brain tumors among workers In (he production of synthetic rubber. occupation or type of work* Study period Measure of associationB Observed brain tumor events Tire building & curing, Ohio One rubber plant, US Tire building Tire assembly (a 5 years) Rubber Industry, Sweden Rubber product* Industry. US rur US rubber plants -- Men Tire building, US rtre assembly, us Rubber 4 cabiemaking Industry. UK Tire sector 1840--1964 IQ40--1974 >940--1074 1940--1076 1961-1973 1050 1040--1073 1951--t97l 1961-1971 1966--1074 1966--1074 SRfl SMR 8MR SRfl SRR SMR SMR OR OR SMR SMft 4 20 7 7 30 13 14 5 1 20 10 ' See table 1 (footnote a) for a definition or the Abbreviations. See table 1 (footnote b) for a definition of the abbreviations Ratio = observed:expeeled ratio or odds ratio. ' Statlailcally significant (Poisoon) si the 005 level. Ratio4 5.63' 0,80 1.90 4,1* 1.23 0>8 1.10 0.43 0.84 1.08 Reference Maneuso at at (43) MonSOfl & Ntkano (92) Menton & Ntkano (52) Monson a Fine (51) Enalund et al lift) Guralnick 126) MoMichasl et si (46) Symons et *1 (83) Symons et si (83) Fox a Collier (19) Fox ft Collier (19) fable 4. Brain tumors among workers In the production of polyvinyl chloride (PVC). occupation or type of work1 Study period Measure of association* Observed brain tumor vents Ratio5 PVC workers exposed a 1 years, US PVC worker* ever exposed, US PVC worker* exposed 5 years, > 15 year* latency, US Vinyl chloride monomer & PVC ^reduction workers, Sweden PVC workers, Germany ?VC workers ever exposed, UK 1930--1972 1947--1973 1942--1973 1940--1974 < 1959--1974 1940--1974 SMR PM Ft SMR SMR SMR SMR 12 2.03* S 4.17* 3 4.98* 2 6.12 2 1.62 2 0.35 US a United Stales. Germany = Federal Republic ol Germany, UK* Untied KinQdom. "See table 1 (footnote b) for a definition of U> abbreviations. kstio*observed:expected ratio or odds ratio. ' Statistically significant (Poisson) at the 0.0S level. \ Reference Cooper (it) Monson at *< (33) Waxweer et al (97) By'en el ai (0) Weber el a' |98l :Ox & COU'er (20) NOU 02 '93 lit21 TD 1 512 331 2387 FROM APPLIED EPIDEMIOLOGY T-430 P.06 glioblastoma multiforme, and the cell types of the other two were not specified. Elevated train cancer risk associated with polyvi nyl chloride production waj observed in a cohort study which combined data from four plants (tabic 4) (97). One major plant was common to this study and those done by Tabenhaw (35), Cooper (11), and Mon* son (S3). Among workers with at least five years' ex posure to polyvinyl chloride and surviving 15 years since first exposure, three brain cancers occurred and less than one was expected. Pour additional brain tumors occurred among employees who had less than five years' exposure to vinyl chloride. Three persons who worked at the plants under study but never in the vinyl chloride-exposed areas also died from brain tumors. No expected numbers were shown for these categories of workers. Nine of the ten brain tumors were histologically confirmed as glioblastoma multiforme. Age at death for these decedents ranged be tween 33 and 65 years. Other exposures that workers might have encountered included acrylates, acrylo nitrile, and chlorinated solvents (96). Studies of polyvinyl chloride workers in Ocrmany and Sweden suggested an excess brain Uncer risk (table 4), but the observed numbers of brain cancer deaths were very small (9, 98). Analyses of mortality among 7 000 men potentially exposed to vinyl chloride monomer in the manufacture of polyvinyl chloride In Great Britain indicated no excess brain cancer risk (20). Petroleum refining and petroohemicei production The first report of elevated brain tumor risk among oil refinery workers appeared in 1979 (table 5). In a cohort study of 1 205 men employed in a Canadian oil refinery for more than five years, three deaths from brain cancer were observed and only 0.77 was expected (87). This excess was confined to workers for whom less than 20 years had elapsed since first employment (0:E --3:0.46). The work histories of the three brain cancer cases were vague with regard to occupational exposures. Two died at 41 years of age and one at age 43. A proportionate mortality ratio study of deceased active and retired members of the Oil, Chemical, and Atomic Workers International Union (OCAW) in Texas indicated an elevated frequency of deaths from brain cancer among white male hourly workers em ployed in petroleum refining and petrochemical plants (90. 92). The increased relative frequency of brain tumors occurred primarily among active employees in Tabi* 5. Brain tumare among workers In petroleum tanneries and patrochemtoal production. Occupation or type of work* Study period Measure o! association* Observed brain tumor events Ratio* Reference Refinery workers {% 5 years), Canada 1028--1978 SMR 3 3.00 All OCAW members in refineries A, B, C, TX 1943-1978 PMR 34" 2.10' Active OCAW members in refineries A, B, C 1943--1976 PM ft 25" 2.291 OCAW members -- refinery A 1943-1978 PMR IS* 2.14' OCAW members -- refinery B 1043--1978 PMR 10* 1.90 OCAW member* -- refinery-C 1943--1978 PMR 7* 2.33 OCAW members in refineries A, B, C Lube on rehnlng 1943-1978 OR s 1.6 Pumping of omduota 1943--1978 OR 7 2.6 Texaco (A) -- salaried & hourly 1047-1977 SMR 31 1.08 Texsao (A) -- research & quality oontrol labs 1947--1977 OR 6 8.9" Texaco (A) -- lube oil refining 1947--1977 OR 3 4.1" Gulf (B) -- all hourly workers 1035--1978 SMR 20* 0 90 Gulf (B) -- hourly workers (% 20 year*) Mobil (C) -- salaried & hourly Ntnieen Tanneries, US 1935-1978 1945--1979 1977--1970 SMR SMR SMR 13 1.40 9B 1.09 1.83 Ninteen refineries, 08 1977--1979 SIR 1.29 Petroleum & coal products, us Eight oil refineries, UK i960 1930--1975 8MR SMR 6163 6ao Oil distribution centers, UK 1950--1873 SMR 30 1.07 Exxon -- operator, mechanic, laborer Union Carbide (NIOSH), TX 1070--1977 1041 -- 1979 SMR SMR 4 1.11 22* 28' Union Carbide (company) -- > 6 months 1941--1977 SMR 10 2.00 Petrochemical operators. LA end TX 1970--1980 PMR 12* 3.40* Dow Chemical, TX 1949-1977 8ampl. 25a 1.26 baaed SMR Theriault & Goulet (87) Thomas at el (9Z) Thomas at *J (92) Thomas at at (92) Tnomaa at af (92) Thomas t el (92) Thomas at at (91) Thomas at ai (91) Olvlna at al (U) Divine et af (15) Divine et at <15) Wen at al (99) Wen el at (99) Morgan A Wong (84) Sehottenfeld at al (79) Schottenfflfd at al (75) Ouralnlek (26) Rushlon & Alderson (70k RuShton 4 Andarson (71) Hanie et al (28) Waxweilor at a) (95) Austin & Schnatter (3) Ntehotson at al (56) Reave at a) (58) * OCAWbOH, Chemical, and Atomic Workers International Union; TX-Texas. US United States; UK a United Kingdom, NtOSH m National Institute lor Occupational Safety and Health; LA s louisane. 6 See table 1 (lootnot* til lor a definition of in abbreviations. 8 Ratio S obaarV0d:expeced ratio or odds ratio. * Observed includes benign and unapecllied brain tumors. * Statistically significant (Poisson) at in* 0.05 level. " Statistically significant at tha 0-05 level using the author's significance lest. 5 VRD 3002030258 A NOU 02 '93 11:22 TO 1 512 331 2387 FROM APPLIED EPIDEMIOLOGY T-430 P.07 65Z0E0Z000 0 8 ^ three oil refineries (A. B, and C) In the Beaumont-Port employees. In one study of refinery workers, investi Arthur area of the Texaj gulf coast (table 5). A nested gators found no association between brain cancer risk case-referent study comparing work histories of the and oil refinery employment (28), and two other groups brain tumor cases with those of persons who died from of investigators did not report (he observed and ex other causes Indicated an elevated brain tumor risk pected values for brain cancer (29, 84). The follow among OCAW members whose Jobs involved the Intra- up period for several studies (28,29,75,84) was very plant pumping and transporting of bulk liquids (crude short (less than 10 years), and risks of fata) disease with oil and products) and the manufacture of lubricating long latency periods may have been underestimated. oil, but the odds ratios were not statistically significant A cluster of primary brain cancer deaths among (91). workers at a Union Carbide petrochemical plant in Industry-sponsored studies of refineries A, B, and Texas City, Texas, was reported In 1980(2). All of the C indicated slightly different results (table 5); however, decedents were less than 66 years of age at death, and the study groups differed substantially in terms of the best medical information available indicated that bourly/salaried status, average duration employed, and 15 of 18 tumors were glioblastoma multiforme. A induction-latency period. A cohort mortality study of cohort mortality study of workers at this plant showed white male Texaco (refinery A in references 90,91,92) a significantly elevated standardized mortality ratio for salaried (white-collar) and hourly (blue-collar) em brain tumors among white male hourly workers (table ployees combined indicated no excess mortality from 5) (95). A similar analysis of the same data by the com brain cancer (15). A nested case-referent analysis in pany also indicated a significantly elevated brain can dicated significantly elevated odds ratios for brain can cer risk among workers who ever held hourly positions cer among persons whose longest job was in research (3), but nested case-referent analyses indicated no Sig and quality control laboratories origin lubricating oil nificantly elevated odds ratios associated with expo refining (15). All male hourly employees of the Gulf sure to any specific chemicals (4, 32). refinery (refinery B in references 90,\91, 92) did not Operating engineers employed in the petrochemical have a significantly elevated standardised mortality ra industry in Texas and Louisiana had an elevated fre tio for brain cancer; however, mortality was slightly quency of brain tumors (observed 18, PMR 1.73) (26). elevated among those who had worked at the plant for This excess was primarily due to a significantly elevated more than 20 years (99). The number of brain cancer proportionate mortality ratio for brain tumors among deaths observed among white male salaried and hourly persons employed as operators in oil refineries and employees of the Mobil refinery (refinery C in references petrochemical plants (table 5). - 90,91, 92) was almost the same as that expected (54). A sample-based cohort mortality study of workers Among white men employed 10 or more years at the at a Dow Chemical petrochemical plant in Freeport, Mobil refinery there were slightly elevated standardized Texas, suggested a slightly increased risk from brain mortality ratios for brain cancer (10--29 years, SMR tumors (table 5) (66). Clinical or pathological infor 142.4; a 30 years, SMR 133.2). mation was obtained for 19 of 22 brain tumors. Based In a mortality study ofoil refinery workers employed on the best medical information available, 12 were glio by 19 US companies (tabic 5), eight deaths from brain blastoma multiforme, and two others were gliomas. A cancer were observed, and 4.9 were expected (SMR nested casc-referent study failed to identify a signif 1.63) (75). The investigators suggested that there may icantly elevated risk associated with employment in any have been underreporting of deaths because of the - parlicuiar department Or with exposure to any specific short study period (two years) and the lag time between chemical or other agent (8). the date of death and receipt of a death certificate. Cancer incidence among actively employed refinery workers during the study period was compared with that for the United States from cancer registry inci Other chemical production dence data. Nine incident cases of brain cancer were Studies of chemical plant workers exposed to formal reported, and about seven were expected. No analyses dehyde showed inconsistent results regarding brain tu by duration of employment or occupation were shown. mor risk. A cohort mortality study of 2 026 workers Brain cancer mortality was not excessive among at a large formaldehyde-producing plant suggested that 35 000 employees of right British oil refineries between workers hired before 1961 had an elevated brain can January 1950 and December 1975 (table 5) (70); how- cer risk (tabic 6) (103). Two of the three persons with ever, about 20 % of the Study subjects had scientific, brain cancer died after a latency period of 10 years. technical, administrative, clerical, or engineering jobs, A proportionate mortality ratio study of workers at most of which axe presumably low-exposure occupa another plant involved in the production of formal tions. The same difficulty occurred in a cohort of dehyde and its use in the production of resins did nut workers at oil distribution centers In England (71), in show an elevated frequency of brain cancer (44); how which supervisors, managers, administrators, and ever only 136 decedents had been exposed to formal clerical workers were included in the analyses. Analyses dehyde. Both of these studies included small numbers were not shown separately for blue-collar (hourly) of exposed workers. No data for observed and cx- 6 NOV 02 *93 11:23 TO 1 512 331 2387 FROM APPLIED EPIDEMIOLOGY T-430 P.08 0 9 0 fli0 0 0 O H k peeled numbers of brain cancer deaths were presented in a report of the mortality experience of 7 680 work ers exposed to formaldehyde In the British chemical Industry (1). An elevated relative frequency of brain cancer was seen among plant employees but not among sales rep resentatives of a large pharmaceutical firm (89). Brain cancer mortality was elevated among white male production workers (0;E~ 8:1.6) and administrative and clerical workers (O:E4:1.0) (table 6). Produc tion workers in this industry ere exposed to multiple chemical and biological agents. Acrylonitrile has been reported to cause brain tu mors in animals (41); however only one epidemiologic study of acrylonitrile-exposed workers has shown an excess of brain cancer (table 6). Two brain cancer deaths were observed among acrylonitrile polymeriza tion workers in the United Kingdom, and only 0.7 was expected (100). In other studies, brain tumor risk was not elevated (57) or not shown 114, 88). $ Nuclear Industry A study of workers at a nuclear fuels fabrication plant indicated elevated brain cancer mortality and incidence among male plant employees (table 7) (27). it was as sumed that all employees had exposure to low levels of gamma radiation; however other exposures in the plant were similar to those in metal working and fab ricating plants and included metal fumes, metal dusts, and oil mists. Seven of the eight incident brain tumors were gliomas, and one was not specified. Ail except one of the men with a brain tumor were between the ages of 40 and 56 years at death. White men employed at the Rocky Rats nuclear weapons fabrication facility for at least two years between 1952 and 1979 (102) had a slight excess mor tality from malignant brain tumors (table 7). and them was a significant excess of benign and unspecified tu mors Of the brain (0:E"6: S 1.48). Exposures in the work environment included plutonium, uranium, beryl lium, other metal dusts, all mists, and other exposures typical of machining operations. Increasing mortality trends by latency were seen for brain tumors; however most of the tumors occurred among persons employed less than IS years. A hospital record review of 16cases in persons who had ever worked at the plant indicated that 14 were gliomas. Age at death ranged from 31 to 77 years, with a median age of 50.5. A nested casereferent study failed to identify any particular jobs or exposures associated with unusually high brain tumor risk (67). A cohort mortality study of white men employed at a Union Carbide nuclear weapons facility showed an excess of brain cancer deaths among workers in departments that did not have exposure to mercury (table 7) (12). The operations in these departments Included TatM* 6. Brain tumor* among workers in other chemical plants. Occupation or type of work* Study period Measure of association6 Observed brain tumor events Formaldehyde producer*, US (hired < I960) Pharmaceutical production, US Pharmaceutical office workers, US Acrylonitrile polymerization, UK Acrylonitrile polymerization. US Chemicals & allied products, US Chemical workers, Italy 1940-1977 1954--197$ 1954-1970 1950-1978 1950-1970 1960 1979--1960 SMR PMR PMR SMR SIR . SMR OR 3 0 4 2 1 22 a * US United Stetee, UKs United Kingdom. 6 See table i (footnote b) tor a definition oi the abbreviations. * Ratio a obeervediexpected ratio or odd* ratio. * Statistically significant (Poisson) at (he 0.03 level. Ratio 2.10 B.00* 4.00* 2.90 ._ 1.00 1.9 Reference Wong (103) Thomas a Oecoufle (89) Thomae a Decoude <39) Werner & Carter (100) O'Bsrg (57) Quralnlck (20) Muelcco el ai (55) Table 7. Brain tumors among workers in we nuclear fuels and weapons fabrication Industry. Occupation or type of work Study period Measure of association1 Observed brain tumor events Ratio6 Nuclear fuels fabrication Rocky flats -- employed a 2 years Malignant brain tumors Benign & unspecified Union Carbide -- nonmercury Haniord plant employees 1950--197B 1951-1877 1951--1977 1963--1970 1955--1974 SMR SMR SMR SMR SMR 4 2.40 6 1.49 5 4.05* 13 2.30* 28 0.99 * $MR b standardized mortality ratio. 6 Rallosobeervd:expected ratio or odds ratio. ` Slai'stioaJly significant (Poisson) at the 0.05 level Reference HSdjimichael et al (27) Wilkinson et al (102) Wilkinson el al (102) Cragie et al (12) Gilbert & Marks (22) 7 I9Z0E01000 ASA*. NCW 02 '93 11 ' 24 TO 1 512 331 2387 FROM AFPLIED EPIDEMIOLOGY T-430 P.09 separation of a uranium isotope through an electro magnetic process and other engineering and manufac turing processes in the fabrication of nuclear weapons. Workers employed in the manufacture, chemical separation, and purification of plutonium at the Han ford plant in Washington state did not have an elevated brain cancer risk (22) overall (table 7) or In any cumulative radiation dose category. Data for men in metalworking and machining occupations were not shown separately. None of the studies at nuclear weapons fabrication facilities showed an association of elevated brain caneer risk in relation to any particular radiation level. One factor common to all of the facilities was the presence of machining operations in which there was an opportunity for exposure to metal dusts and fumes and lubricating all mists. Beryllium was machined at one of the facilities (102). i Other industrial workers \ \ Numerous chemicals, some of which contain formal dehyde, are used in photographic processing opera tions, and high levels of formaldehyde have been mea sured in print laboratories (21). After preliminary stud ies Indicated a possible brain cancer excess among em ployees of an Eastman Kodak plant, a nested case- referent study of brain cancer by exposure category -indicated an elevated risk among photographic pro cessing workers exposed to color developers (24). Risks were slightly elevated among workers exposed to sol vents, animal tissue, and film developers (table 8). None of the results were statistically significant. No deaths from brain cancer were observed among 208 deceased white male press photographers who often developed their own film (49). A study of 47 glioma cases diagnosed in 1979 and 1980 in Milan, Italy, indicated a twofold excess risk of glioma among textile workers (S3). The odds ratio of 2.1 was not statistically significant (table 8). About 20 Vi of the cases had worked In the textile industry, where formaldehyde and other chemicals were used in processing fabrics. In a 1950 survey, US men employed in yarn, thread, and fabric mills had an elevated standardized mortality ratio for brain cancer (26). White male members Of the Pattern Makers League of North America who died between 1972 and 1978 had an increased relative frequency of brain tumor deaths (68). The proportionate mortality ratios were elevated among pattern makers who worked predom inantly with wood and among those who worked predominantly with metal (table 8). A cohort analysis of cancer morbidity among automobile pattern makers who worked with wood found no significant excess of brain cancer (79), Machinists employed at an automobile manufactur ing plant for five years or more in jobs with exposure to cutting oil mists did not have a significantly elevated risk of death due to brain cancer (0:E-5:3.3) (13). Among men who entered the study group after 1948, Table 6. Brain turners among other Industrial workers. Occupation or type of work* Study period Measure of association* Observed brain tumor events R4tta* Kodak workers (age 55--59 years), NY Kodak workers -- solvents Kodak workers -- color developers Kodak workers -- animal tissue Kodak workers -- black & white developers Textile workers, Italy Yarn, thread, fabric mills, us Pattern makers -- wood, US Pattern makers -- metal, Us Automobile wood pattern makers. Ml Automobile machinists (1948 + }, US Aviation electronics workers, US Aluminum reduction workers. US Bua mechanics, UK Railroad oarmen, Canada Railroad -- welding fume*. Canada Railroad workers. US Aebastoa Insulation workers, US Electricians, linemen, serviceman. engineers, MO Qltai tumors Unspecified brain 1904--1975 1956--1975 1956--1975 1966--1875 1958-1975 1979--1980 1950 1972-1978 1972--1978 1070--1976 1937--1967 1950--1980 1946--1976 1967-1975 1995-1977 1965-1977 1967--1979 1967--1970 1969-1962 1069-1982 SIR OR OR OH OR OR 9MR PMR PMR SIR SMR PMR SMR SMR SMR SMR SMR SMR OR OR 14 2.81' 32 1,40 6 Z.16 13 1.32 7 1.31 10 2.1 32 1.46 7* 1.75 5` 2.94 1 1.63 3 3.75 9 3.01* 8 2.25 4 3.20 7 2.78* 10 3.1fl* 5 1.32 21* 1.59 27 2.15' 13* 1.54 * NY = New York, US = Unlld Stale*, Ml s Michigan. UK United Kingdom. MD Maryland. * See table t (footnote b) for a definition Of the abbreviations. 0 Hallo sobserved:expect*d ratio or odd* ratio. d Obaerved Includes benign and unspecified brain tumor*. * Statistically aigniilcant (Poisson) at the 0.05 level. 8 Reference QreenwaJd et ai (24) Greenwaid et al (24) Qreenwald ei al (24) Greenwsld et at (24) Qreenwald at al (24) Mueicco et al (55) Qurolnlck at al (26) Robinson at al 166) Robinson el al 108) Swanson 6 Bells (79) Decoufie (13) Sweeney 6 Ahrenholz (80) Mllhem (47) Rushton et al (72) Howe et al (32) Howe el al (32) SChenker et al (73) Sfttdman at si (76) Lin et al (38) Lin et si (30) NOV 02 '93 11:24 TO 1 512 331 2387 FROM APPLIED EPIDEMIOLOGY T-430 P. 10 .VRD 000 20 30262 however, there was a notable excess of brain cancer elevated brain cancer mortality among electricians and deaths (table 8). power servicemen. Electrical engineers (table 1) also A proportionate mortality ratio analysis indicated had elevated brain cancer mortality. These occupations (hat white male hourly and salaried employees of an have potential exposure to electromagnetic fields, po aviation electronics plant had an elevated frequency lychlorinated biphenyls, solder fluxes, and solvents. of deaths from brain cancer (table 8) (80). Six of the nine brain cancers were glioblastoma multiforme, one was neurilemmoma, and two were unspecified. Poten tial workplace exposures included trichlorethylene, be Professional and other nonindustrial groups ryllium, and a halogenated aromatic hydrocarbon The National Institute for Occupational Safety and balancing fluid. All five hourly employees with brain Health (NIOSH) evaluated the mortality experience of cancer had worked as machinists. white men employed as motor vehicle examiners in A mortality study of aluminum reduction plant New Jersey for at least six months between 1944 and workers (table 8) indicated an elevated risk of benign 1973 (77). The examiners were exposed daily to mo brain tumors (observed 5, SMR. 9.09) but not malig tor vehicle exhaust consisting of aldehydes, carbon di nant tumors (observed 3, SMR 0.99) (47). All five per oxide, carbon monoxide, hydrocarbons, lead com sons with benign brain tumors had worked In "ex pounds, nitrogen, oxides of nitrogen, oxygen, and sul posed" jobs in the carbon plant, rodding, potlining, fur dioxide. Four deaths from brain cancer were ob potrookis, or quality control. Exposures included fluo served, and only 1.7 were expected (table 9). All four rides, particulate alumina, polycyclic aromatic hydro brain cancers were malignant gliomas. carbons, and sulfur dioxide. An excess of benign neo A proportionate mortality ratio study of profes plasms was found In another study of workers em sional artists indicated a significant threefold excess ployed in 14 aluminum reduction plants (69); however frequency of brain cancer deaths among white male no details were given regarding the primary site of these artists (table 9) (50). The excess deaths were not linked tumors. to any particular art specialty. Artists may be exposed Maintenance workers exposed to hydrocarbons in to numerous potentially carcinogenic substances in the form of diesel exhaust in London bus garages had cluding components of pigments, dyes, solvents, metal a slightly elevated standardized mortality ratio for fumes, .and dust. brain cancer (SMR 1.21) (72). This excess was prima Professional chemists are exposed to numerous ' rily due to the elevated standardized mortality ratio chemical agents In the laboratory setting. An elevated for brain cancer among bus mechanics, who were also standardized mortality ratio for brain cancer was seen exposed to oils, greases, and solvents (table 8). tnvotvg Sib chemists who had been educated at one A study of Canadian railroad workers exposed to school in Sweden (38) between 1930 and 1949. No brain diesel fumes and coal dust showed an elevated brain cancer deaths occurred among 331 men educated at cancer risk among carmen (table 8) (32). Railroad a second Swedish school (58). Further follow-up of the workers exposed to welding fumes had a threefold ex first cohort indicated a significantly elevated mortality cess of brain cancer mortality. A survey of mortality from brain cancer (table 9) (59). Other studies of by occupation in Sweden also showed excess brain can chemists have not reported elevated brain cancer mor cer among welders (tabled) (18). US railroad workers had a slightly elevated standardized mortality ratio for brain cancer (table 8), but no data were shown for tality (31, 37). Members of the Royal College of Pathologists in 1973 were followed for vital statu* in 1981 (30). Among those with high levels of exposure to diesel or welding 2 300 men, six deaths from brain cancer occurred and fumes (73). less than two were expected (table 9). Hematology was A slightly elevated brain tumor risk was reported In a common subspecialty among the decedents with a cohort study of asbestos insulation workers (table brain cancer. Pathologists are exposed to formalde B) (76). These workers were employed primarily in the hyde and other laboratory chemicals. Anatomists, who building construction trades, but they also could have are exposed to similar chemicals, had a significantly worked in shipyards, chemical plants, and oil refin elevated brain cancer risk (78) compared with the US eries, where there are exposures to numerous sub general population (table 9). When another profes stances. sional group was used Tor a comparison, the stan A case-referent study using the occupation listed on dardized mortality ratio was 6.00. Risk appeared to death certificates suggested an elevated risk of glioma increase by duration of employment, but was also and unspecified brain tumors among a category of elevated among those employed less than 20 years. Risk workers which included electric and telephone com was elevated regardless of presumed level of exposure pany servicemen, linemen, foremen, and engineers; to formaldehyde. Four of the 10 brain cancers were railroad and telecommunication engineers; electricians; listed as "astrocytoma" on the death certificate, while and electric and electronic engineers (table 8) (38). the remaining six were listed as "glioblastoma." These findings are consistent with those seen In four Proportionate mortality raiio analyses of deaths surveys of mortality by occupation (table 2) that found among embalmers and funeral directors in New York 9 NCW 02 '93 11:25 TO 1 512 331 2387 FROM APPLIED EPIDEMIOLOGY T-430 P.11 ? 9 m 0 l0 0 0 a a * Tibia 9. Brain tumors among professional and other nonlnduatrtai workara. Occupation or type of work1 Study period Measure of association k Observ'd brain tumor event's Ratio6 Reference Moto vehicle examiners, NJ Professional anlata, US Chamiatt -- ona school. Sweden DuPont ehamlale, U8 Pathologists, UK Anatomists, U8 Embaimers, NY Embaimers, CA Embaimers, Ontario Peruala cosmetologists. OT Rsglstersd female nurses, Wi Veterinarian*, US Farmers attar I960, Italy Agricultural Industry, Canada Agricultural workers, Sweden 1944--1973 1940--1969 1930--1977 1984--1977 1974--1081 1924--1679 1923--1680 1923-1980 1950--1977 1935--1978 1963-1977 1947--1977 1979--1980 1985--1973 1981--1973 SMR PM Ft SMR SIR 8MR SMR PMR PMR SMR SIR PMR PMR on SMR SMR 4 2.3$ S 2.90* 5 4.17* 2 0.67 S > 3.00* 10 2.71* 8 2-34 9 1.94 3 1.19 16 1.68 21 1.61 28 1.63* 13 3.9* 4 2.68 744 1.08* Stern at al {77) Millar at al (90) Olin & Ahlbom (59) Hoar 8 Pell <3t) Harrington & Oakes (30) Stroup ei ai (76) Walrath & Fraument (93) Walrath & Fraumeni (94) Levine et al (36) Tata et i (66) Katz (34) Blair A Hayes (7) Musicco et et ($5) Howe & Lindsay (33) WlklunO (101) * NJsNaw Jarsey, US United Statea, UK "United Kingdom. NY-New York, CA California. CT Connecticut. Wl Wisconsin. * See table 1 {footnote b) lor definition of the abbreviation*. 6 Ratio *obeerved:expected ratio or odds ratio, * Statistically significant (Poieson) at the 0.03 level. (93) and California (94) Indicated elevated frequencies of brain cancer death* (table 9). Amorig white men in New York licensed only as embaimers, there was a 2.5-fold excess (93). A cohort mortality study of On tario embaimers did not show an excess brain cancer risk, but the study group was small, and no data were shown by latency or duration of exposure (36). Em balming fluids consist primarily of formaldehyde, but also contain phenol and methanol. Professional cosmetologists are occupationally ex posed to numerous chemical substances, including for maldehyde solutions, hair dyes, permanent wave solu tions, and other cosmetic preparations. Female cos metologists in Connecticut had an elevated Incidence of brain cancer (table 9) (86). This excess was more prominent among those who began hairdressing school between 1925 and 1934 (observed 6, SIR 2.02). Ten of the 16 cases observed were histologically confirmed glioblastoma multiforme. A significantly elevated frequency of nervous sys tem cancers was seen among registered nurses in Wis consin In a comparison with other gainfully employed women (table 9) (34). The observed number of deaths was also greater than the number expected on the basis of mortality among other female professional workers (PMR 1.47). An analysis of mortality among veterinarians indi cated an excess frequency of deaths from brain can cer (table 9) (7). The increased relative frequency was not confined to any particular veterinary specialty group. Four studies have shown an elevated brain cancer risk among farmers (table 9). Odds ratios for gliomas were statistically significant among Italian farmers who had been farming for more than 10 years and among those who had been engaged in farming since I960, when the use of phosphoric acid and organochlorine compounds became very common as pesticides In Ita ly (55). A study of primary CNS neoplasms in Minne sota indicated a slightly higher than expected propor tion of farm residents among the brain tumor cases (10). The authors speculated that there may be an as sociation with toxoplasmosis gondii infection. Elevated brain cancer risk was also found in a study of Swed ish agricultural workers (101) and among agricultural workers in Canada (33). Discussion There were several limitations in (he presented epide miologic studies. First, there is a paucity of casereferent studies of brain tumors; thus most of the in formation was obtained from mortality studies that lacked sufficient statistical power to evaluate specific occupational risk factors adequately for brain tumors. The observed and expected numbers of brain tumor cases in most of the studies were very small. Exposure information was ascertained from work histories in some of the studies and from interview data in some, but, in others, no specific information on workplace exposures was available. In the nested case-referent studies the numbers were very small, and there were difficulties in relating exposures to specific jobs. In most instances workers had multiple exposures, and risks due to any single exposure could not be ade quately evaluated. Brain tumor diagnosis was ascertained from death certificates in most of the studies; therefore the accu racy of the diagnoses may be questionable. The diag nosis "brain tumor" listed on a death certificate would be necologically coded as a primary tumor of the brain, unspecified as to whether malignant or benign. Many 10 m B E B IB flfl UNA* NQU 02 '93 11:26 TO 1 512 331 2387 FROM APPLIED EPIDEMIOLOGY T-430 P.12 of these tumors may actually have been primary me* tignancic* of the brain. Alternatively, since the brain U a common site for metaiuuea of other primary can cers, some death certiHeat* diagnoses may not reflect the actual primary site. A study of deceased persons in the Third National Cancer Survey areas indicated that about 97 ft of deaths from malignant brain tu mors would be ascertained from death certificates (62), whereas only 89 ft of all primary brain cancer diag noses on death certificates were confirmed by hospital records. This finding indicates that about 10 ft of the brain cancer cases ascertained from death certificates may be misdiagnosed. The issue of misdiagnosis is not considered a major problem, particularly if the general population Is used to calculate expected numbers of death in studies that ascertain cause of death from death certificates. In 1981 Grecnwald et al (24) concluded that an ex cess of brain tumors noted among Kodak employees may have resulted from a '`diagnostic sensitivity bias." This conclusion was drawn because none of the results of the hasted case-referent study were statistically sig nificant and because Kodak employees had brain tu mor diagnoses that were histologically confirmed more often than did other brain tumor patients in New York. This explanation might appear plausible in light of the excess risk noted in several professional and whitecollar groups: however, all of the workers reported to have elevated brain tumor risk in this review were probably not enrolled in comprehensive medical sur veillance programs. Furthermore excess brain tumors were seen only among certain subgroups of some plant populations (C8. workers in the tire building sector of rubber production, refinery workers in lubricating oil manufacture). In addition other groups with medical surveillance programs, for example, Du Pom em ployees, do not show an elevated brain tumor risk (61). Despite limitations in study methodology, some si milarities are seen between the findings of these stud ies with respect to age and cell type diagnoses. Ages at death for most of the brain tumor cases ranged between 40 and 62 years. It is not dear whether this pattern reflects the age distribution of the populations studied or a biological phenomenon related to the origin of brain tumors. Age-specific mortality rates for U$ white males indicate a peak between the ages of 45 and 65 years (42). Very few studies included diagnostic information from sources other than death certificates. Since death certificates do not often indicate the cell type of these tumors, most studies grouped all brain tumors without distinction by cell type, it Is possible that risk factors vary by cell type. In the studies that had diagnostic information from medical records, a high percentage of the diagnoses were gliomas, particularly glioblas toma raultifOrme; however, no expected numbers could be calculated for this type. Table 10 shows selected categories of exposures com mon to the work environments of the occupational groups that appear to have an elevated brain tumor risk. This list is by no means all-inclusive, and one must keep in mind that most of the occupational groups listed are exposed to multiple agents. Numerous groups with elevated brain tumor risk are likely to be exposed Tabla 10. Common ocupaUooal exposures among groups with elevated brain tumor risk. Occupational group potentially exposed Acrylonitrile polymerization workers Airplane mechanic* and repairmen Aluminum reduction plant workers Anatomists Artists Bus mechanics Chemists Cosmetologists Etactrioians Embeimers Fanners and agricultural workers Formaldehyde production workers Machinists Motor vehlole examiner* Nuclear fuel* & weapons fabrication Nurses Oil refinery workers Pathologists Pattern makers -- metal Pelrochemleel plant workers Pharmaceutical workers Photographic process workers Polyvinyl chloride production workers Rubber workers Textile workers Veterinarians Organic solvents X X x X X X X X X X X X X X X X X X Lubrl"catlng oils X, t X tt X X X X X Exposure Acryloni trile or vinyl chloride Formalde hyde X X X X X X Polycyclic aromatic hydro carbons Phenols and phenolic compounds X X X 11 NOU 02 'S3 11:27 TO 1 512 331 2387 FROM APPLIED EPIDEMIOLOGY T-430 P.13 to organic solvent*. This broad category of compounds tumors in laboratory animals. These include certain includes aliphatic hydrocarbons and aliphatic ha* polycyclic aromatic hydrocarbons, vinyl chloride, and Jognated hydrocarbons like methylene chloride, car* acrylonitrile. However, several of the substances, spe bon tetrachloride, tetrachloroethylene, and others. It cifically, formaldehyde, certain solvents, and some also includes aromatic hydrocarbon solvents like ben* phenolic compounds, are known to cause neurotoxic zene and toluene. One of the common acute effects effects after acute high-level exposure. Thus, the brain of exposure to many of these compounds is CNS de U obviously a target organ for the toxic effects of these pression (16); however solvents are not known to cause materials. brain tumors experimentally. Oil refinery workers, Clearly, further epidemiologic studies are necessa chemical plant workers, rubber workers, and many ry to evaluate the relationship between brain tumors other occupational groups are exposed to organic and occupational exposures. These studies should in solvents. clude large numbers of cases and diagnostic confirma Exposure to polycyclic aromatic hydrocarbons oc tions so that data may be analyzed by celt type. Suffi curs in the rubber manufacturing, petroleum refining, cient care should be used in selecting referents so that and aluminum reduction industries. Motor vehicle ex the diagnostic sensitivity problem, if it exists, is mini aminers and bus mechanics may also be exposed to mized. Finally, and most importantly, an attempt these hydrocarbons In motor vehicle exhaust. Certain should be made to develop detailed occupational ex polycyclic aromatic hydrocarbons have induced brain posure Indices. tumors in animals by direct implantation and trans* placcntally, but not by inhalation exposure (81). NOTE: Use of trade names is for identification only Lubricating oils produced by oil refineries are used for maintaining mechanical equipment and machines and Tor lubricating cutting edges'. Thus several of the and does not constitute endorsement by the Public Health Service or by the United States Department Of Health and Human Services. groups with elevated brain cancer mortality are ex* posed to various types of lubricating oils. Gliomas have been experimentally Induced in ani* mals by inhalation exposure to acrylonitrile and vinyl chloride (40, 41). These compounds are similar in chemical structure and are found in plastics depart* menu in the rubber industry, in polyvinyl chloride production, and in acrylonitrile polymerization. Formaldehyde has recently been shown to induce nasal cancer in rats (82), a finding implying that it may also be carcinogenic in humans. Several of the groups with elevated mortality from brain cancer were occu* pationally exposed to formaldehyde. These groups in* elude blue-collar workers involved in formaldehyde production, photographic processing and textile production, professionals who use formaldehyde in the laboratory setting, and embalmers. * Phenols and phenolic compounds are used widely in manufacturing industries, and many of the com* pounds have commercial uses. These include phenol, chlorophenoia, cresol, resorcinol, hydroqulnooe. and quinone. Phenolic compounds arc used in the produc tion of explosives, fertilizers, textiles, paints and paint removers, rubber, wood preservatives, synthetic resins, pharmaceuticals, photographic chemicals, rubber, and organic chemicals. Commercial uses include fungicides and herbicides, disinfectants, laboratory reagams, and photographic processing (60). Acute Intoxication of these compounds causes severe CNS effects. Including tremors, convulsions, vertigo, and mental disturbances. None of these compounds have induced brain tumors experimentally; however some phenols arc known to be tumor promoters and cocarctnogens in certain tis sues (16). Of the broad categories of aforementioned sub stances, only a few have been shown to cause brain Relarenoes 1. Acheson ED, Gardner MJ. Pannetl B. Barnes HR, Os mond C, Taylor CP. Formaldehyde In the British chem ical Industry. Lancet 1 (1984) 611--616. 2. Alexander V, Ltffingwcll SS, Lloyd JW, 'Waxweiter RJ, Miller RL. Brain cancer In petrochemical workers: A case series report. Am J IndMed 1 (1980) 115--123. 3. Austin SG, Schnatter AR. A cohort mortality study of petrochemical workers. J Oecup Med 25 (1983) 304--312, 4. Austin SG, Schnatter AR. 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Mor tality from primary central nervous system neoplasms In Minnesota. Am J Epidemiol 91 (1970) 238--259. 11. Cooper WC. Epidemiologic study of vinyl chloride workers: Mortality through December 31,1972. Envi. ron Health Persptct 41 11981) 101 -- 106. 12. Cragte Dt. Hollis DR, Qualters JR, Tankersley WG, Fry 5A. A mortality study of min exposed to elemental mercury. J Occup Med 26 (1984) 817--821. 13. Decoufle P. Further analysis of cancer mortality pat. 12 A VRD 000 20 36265 NOU 02 '93 11:27 TO 1 512 331 2387 FROM APPLIED EPIDEMIOLOGY T-430 P.14 VRD 0002030266 term Among workers exposed to cutting oil mists. J Natl Cancer Jn 61 (1975) J0g5-I030. 14. Delzdl E, Monson RR. Mortality Among rubber work ers: VI Men with potential exposure to Acrylonitrile. J Occup Med 24 (1982) 767--769. 13. Divine BJ, Barton V, Kaplan $D. Texaco mortality study. Texaco, Inc, Houston, Tx, 1983. 16. Douil J, Kla&sxen CD, Amdur MO, cd. Cantrell and Doull's toxicology. Macmillan Publishing Company, lac. 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In: Lilienfeld AM, ed. Reviews in epidemiology. Elsevier/North Holland, New York, NY 1980, pp 243--292. 24. Grecnwald P, Fricdiander BR, Lawrence CE, Hearne T, Earle K. Diagnostic sensitivity bias -- An epidemio logic explanation for an apparent brain tumor excess. J Occup Med 23 (1981) 690--694. 23. Guralnick L. Mortality by occupation and cause of death among men 20 to 64 years ofage: United States, 1950. US Government Printing Office, Washington, DC 1963. (Vital statistics special reports, vol 33, no 3). 26. OuralnidcL. Mortality by industry and cause of death among men 20 to 64 years of age: United States, 1950. US Government Printing Office, Washington. DC 1963. (Vital statistics special reports, vo) 53. no 4). 27. Hidjtariehad OC, Ostfeld AM, D'Atri DA, Brubaker RE. Mortality and cancer incidence experience of em ployees in a nuclear fuels fabrication plant. J Occup Med 25 (1983)48--61. 28. Hanis NM, Holmes TM, Shallenbeiger LG, Jones KE. 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Case-control study of gliomas of the brain among workers employed by a Texas City, Texas chemical plant. Neurocpidetniology 2 (1983) 179--195. 36. Levine RJ, Andjelkovkh DA, Shaw LK. The mortality of Ontario undertakers and a review of formalde hyde-related studies. J Occup Med 26(1984)740--746. 37. Li FP, Fraumeni )F, Mantel N, Miller RW. Cancer mortality among chemists. J Natl Cancer Irut 43 (1969) 1159--1164. 38. Lin RS, Dischinger PC, Conde J, Farrell KP. Occu pational exposure to electromagnetic fields and (he oc currence of brain tumors. J Occup Med 27 (1985)413-- 419. 39. Logan WPD. Cancer mortality by occupation and social cUt, 1851--1971. international Agency for Research on Cancer, Lyon 1983, (IARC scientific pub lications no 36, studies on mtdleid and population sub jects no 44). 40. Maltoni C, CQlbertl A, Cafreui D. Experimental con tributions in identifying brain potential carcinogens in the petrochemical industry. Ann NY Acad Scs 381 (1982) 216--249. 41. 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En viron Res 22 (1980) 154--161. 60. Panneggiani L, ed. Encyclopedia of occupational health and safety. Third (revised) edition. International Labour Office, Geneva 1983. 61. PeQ S, O'BefgMT, Karrii BW. Cancer epidemiologic surveillance in the DuPont company. J Occup Med 20 (1978) 725--740. 62. Percy C, Stuck E. Olocdder L. Accuracy of cancer death certificates and it) effect on cancer mortality statistic*- Am J Public Health 71 (1981) 242--250. S3. Peterson OR, MilhamS. Occupational mortality in the state of California, 1939--61. US Government Print- Jug Office, Washington, DC 1980. (DHEW (NIQSH) ) publication no 104). \ 64. Preston-Martin S, Handersoo B& Peters JM. Descrip tive epidemiology of centra] nervous system neoplasms ' .In Los Angeles County. Ann NY1 Adid Sci 381 (1982) 202--208. 65. Registrar General. Occupational mortality; The reg istrar general's decennial supplement for England and Wales, 1970--72. Her Majesty's Stationery Office, London 1972. 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Ann NY Acad Sci 381 (1982) 160-171. 77. Stern FB,.Lemen RA, Curtis RA. Exposure of motor vehicle examiners to carbon monoxide: A historical prospective mortality study. Arch Environ Health 36 (1980) 59--46. 75. Stroup NE, Blair A, Erikson GE. Brain cancer and other causes of death in anatomist*. Am J Epidemiol 120 (1984) 500. 79. Swanson GM. Belle SH. Cancer morbidity among woodworkers in the US automotive industry. J Occup Med 24 (1982) 315--319. 80. Sweeney MH, AhrenhoU SH. NiOSH health hazard evaluation report HETA 80-250-1529. National Insti tute for Occupational Safety and Health, Cincinnati, OH 1984. 81. Swenberg 3A. Chemical induction of brain tumor*. Adv Neurol 15 (1976)85--99. 82. Swenberg JA, Kerns WD, Mitchell RJ, Induction of squamous ceil carcinoma of the rat nasal cavity by in halation exposure to formaldehyde vapor. Cancer Ret 40(1980) 3398-3402. 83. Symons MJ, Andjelkovteh DA, Spinas R, Herman DR. Brain and central nervous system cancer mortality in US rubber workers. Ann NY Acad Sci 381 (1982) 146-159. 84. Tabershaw |R. a mortality study of petroleum refinery workers. Project OH-1 prepared for the American Pet roleum institute, Tabershaw/Cooper Associates. Wash ington, DC 1974. 85. Tabershaw JR, Caffey WR. Mortality study of work ers In the manufacture of vinyl chloride and its poly mers. J Occup Med 16 (1974) 509--318. 86. Tcia MJ, Walrath J, Meigs JW, Flannery IT. Cancer incidence among cosmetologist*, j Natl Cancer Inst 72 (1984) 1051--1057. 87. Theriault G, Goulet L. A mortality study of oil refinery worker*, J Occup Med 21 (1979) 367--370. 88. Thleu AM, Frentzel-Beyme R. Link R, Wild H. Mortallutsstudle bef chcmSeficharbeitern versehledener produkdonsbetriebe mit exposition auch gegenuber ac- ryloitril. Zaiuralbl Arbdtuned Arbeitssch Prophyl Ergonomic 30 (1980) 259--267. 89. Thomas TL, Decouflc P. Mortality among workers employed in the pharmaceutical industry: A preliminary investigation. J Occup Med 21 (1979) 619--423. 90. Thomas TL. Decoufie P, Moure-Eraso R. Mortality among workers employed in petroleum refining and petrochemical plant*. J Occup Med 22(1980) 97--103. 91. Thomas TL, Waxweiter RJ, Crandall MS, White DW, Mouro-Eraso R, Fraumeni JF. Cancer mortality pat terns by work category in three Texas oil refineries. Am J lnd Med 6 (1984) 3--16. 92. Thomas TL. Waxweiler RJ, Crandall MS. White DW. Moure-Eraso R. Itaya S, Fraumeni JF. Brain cancer among OCAW members in three Texas oil refineries. Ann NY Acad Sci 381 (1982) 120-129. 93. . Walrath J. Fraumeni JF. Mortality patterns among embatmen. Int J Cancer 31 (1983) 407--411. 94. Walrath J, Fraumeni JF, Cancer and other causes of death among embalmer*. Cancer Res 44 (1984) 4638-- 4641. 95. Waxweiler RJ, Alexander V. Leffingwell 55, Haring M, Lloyd JW. Mortality from brain tumor and other causes in a cohort of petrochemical workers. J Natl Cancer liut 70 (1983) 75--81. 96. Waxweiler RJ. Smith AH. Falk H, Tyroler HA. Ex cess lung cancer risk in a synthetic chemicals plant. En viron Health Penpecl 41 (1981) 159-16). 97. Waxweiler RJ, Stringer W, Wagoner JK, Jones J. Falk H, Carter C. Neoplastic riik among workers exposed 14 VRD 0002 0 30 267 A NOU 02 ' 93 11:29 TO 1 512 331 238? FROM APPLIED EPIDEMIOLOGY T-430 P.16 torinyl chloride. Ann NT Acad Sd 271 <1976)40--48. tional Technical Information Service. Epidemiology $). Weber H, Relnl W, Ortuer E. Citidu invtMi)llioiii applied to health physics: Proceedings of the sixteenth on morbidity end mortality of workers exposed to vinyl midyear topical meeting of the Health Physics Society. chloride. Environ Health Pertpect 41 (1981) 9S--99. Springfield, VA 1983, pp 328--337. (CONF-830101). 99. WenCP, Tsai SP, WUs NS, McClellan WA, Oibion 103. Wong O. An epidemiologic mortality study of a cohort RL. 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Cancer 51 (1983) 566--568. 103. - Wilkinson OS. Vodz GL, Acquavella JP, TiMjcn GL, Reyes M, BrackbUl R, Wtggs L. Mortality among plu tonium and other workers at a nuclear facility. In: Na Received for publication: 1 July 1985 i \ A : - w.;, 15 VRI) 000 2 0 30269 -COMM. JOURNAL- ******** DATE CeC-01-1993 ***** TIME 12:48 ****** P.l MODE-TRANSMISSION FILE NO.- 005 NO. COM ABBR.NO. 01 OK STATION NAME'' TELEPHONE NO. 912018907029 START-DEC-01 12:46 END-DEC-01 12548 PAGES PRO.NO. PROGRAM NAME 003/003 -UISTA RID ***owc***#*********###**^^ viaiH kbjj 512 331 2594- *********** ` -rf-YMr U4T 3$fif" 'r&w Tvti o&otfrrjirciv ` W VXVtWVi-- * *-------< !i Ketchum I,i!l!l,lr lilll.ATIDNS HO: Thomas Barfliecht David McAllister James G. Bryant draig H. Farr SsNWDaUvUide POewnennesy Jdhn L. Festa hinxda Hardy Kerry Peters Robert Strierko Sjewan E. Holm Don Townsend Robert G. Kaley, in Florence Kinoshita Phil Watanabe John Wilkinson Robert Ku > ifROM: ; IjlzTait > Ketchum *ubllc Relations bATE: November 23,1993 PAGES; ; 2j(two) SUBJECT) Jc : Answers About "Sources" for the IGCCA Dioxin Q&A Document i ijrad Lienhart .rut Mason Uzabeth Brooks . As most of yo'u know from the last Dioxin Work Group meeting. Bob Ku and I have been workingin tandem on a first draft of the IGCCA dioxin Q&A document. We've met in person and by telephone in the last couple of weeks, and Bob U Completing a draft which I am editing for lay comprehensibility and suitable tone, content and structure. I will distribute It to each of you on December 1,1993, as planned.! ' iI Bob's answer 'to the question "What are the sources of dioxin in the environment to. which I may tye exposed?" is general, which may be enough for a document as modest in scope as tills one. In any case, he is reluctant to answer In greater detail on behalf of your respective industries, and suggested that some of you draft a oneto one-arid'orie-half page (double*$paced) response to the issue of source emissions based on your knowledge and experience. He suggested the following assignments: i: : f i Pulp and paper mills - Vinyl manufacturing - Incineration 4- Stewart Holm and John Festa Dave Penney Phil Watanabe Manufacture pf chlorinated pesticides - j Phil Watanabe and Bob Kaley Manufacture jof chlorine and chlorinated compounds Bob Smerko ? J , UJUjhaa '--A 77 Qk*W -/A^t i-w VRD 0002030270 CHEMICAL MANUFACTURERS ASSOCIATION CHLORINE CHEMISTRY COUNCIL SCIENCE TASK GROUP DIOXIN WORK GROUP MINUTES OF MEETING NOVEMBER 9, 1993 M Street Conference "Room CMA, Washington, D.C. PARTICIPANTS AFFILIATION R. G. Kaley, Chair S. E' Holm F. Kinoshita D.^Penny R.jStnerko P. Watanabe J. Wilkinson Monsanto Company Georgia Pacific Hercules, Inc. Vista Chemical Chlorine Institute Dow Chemical Vulcan Chemicals CMA Staff A. M. Mason, Staff Executive D. B, Fischer M. Gallant* R. B. Lienhart* CMA CMA CMA CMA By Invitation E. Tait* Ketchum * Indicates Part-Time Attendance The following business items were discussed. Action items are underlined. 1.0 Administration 1.1 Minutes: The minutes of the October 1, 1993, meeting were approved without changes. 1.2 Meeting Expectations: The work group identified the following meeting expectations: a. Agree on Mission Statement b. Concur with direction of sub-group c. Identify new challenges 1.3 Meeting/Conference Call Schedule: Conference Call: Thursday, Dec. 16,1993 1:00-3:00 p.m. Dioxin Work Group--Page 2 Minutes (#3--FY 93/94) VRD 0002030271 Topic: Next Meeting: Discuss dioxin Q/A document Tuesday, Jan. 11, 1994 9:00a.m.-3:30p.m. I.4 Work Group Mission Statement The work group discussed and revised the draft mission and goal statements. A. Mason will make the changes. 2.0 International Joint Commission B. Lienhart presented a summary of the IJC Meeting. He discussed the groups on which additional industry representatives could serve, including the IJC Science Advisory Board. During his presentation, he discussed several issues including the: j Virtual Elimination Task Force's final report and the recommendations that call for a thorough evaluation of chlorine chemistry - specifically recommendation 22. Weight-of-evidence workshop which was a series of case studies but not a process for determining the weight-of-evidence. Formation of an IJC ad-hoc group to address weight-ofevidence. The group discussed the IJC weight-of-evidence group, identified the key players, and discussed alternatives. J. Wilkinson reminded the group that an understanding of the IJC process will be important for U.S. legislative efforts. The work group suggested a joint meeting with the Federal Advocacy Task Group to discussion scope and direction of the dioxin issues and to agree on a joint strategy. A. Mason and M. Gallant will work on setting up this joint meeting. 3.0 American Public Health Association (APHA) During a discussion on the APHA resolution, B. Lienhart discussed the process and indicated that CCC will be sending a follow up letter to APHA. R. Kaley will send A. Mason a copy of Dr. Frank's speech for distribution to the work group. 4.0 Sub-group Reports: 4.1 Dioxin Q/A Subgroup E. Tait, Ketchum Associates, presented the status of the Q/A document and passed out two documents: one prepared by Ketchum and the other by R. Ku. Dioxin Work Group--Page 3 Minuses (03--FY 93/94) She lead a discussion about the scope and audience for the document. The Work Group agreed that the primary audience is the public and the answers would be two-tiered: the first part of the answer should be targeted to the general public and then followed by more detailed fact-based answers. The Work Group was asked to send third party quotes to A. Mason and E. Talt on key issues. The Work Group agreed that the primer will have references. The work group discussed and agreed to the following schedule. E. Tait will send out a revised draft by 12/1/93. Each member will send comments back to E. Tait for receipt by 12/9/93. E.Tait, R. Ku, and CMA staff will meet on 12/9/93 to revise the document. The Work Group will have a conference call on 12/16/93 to look.at the revised document. E. Tait will send another draft out by 12/15/93 for a second conference call on 1/3/94 that will approve the document. The work group reminded the group that these drafts should not be distributed publicly. Each member was asked to work with their own attorney during their internal review process. The work group emphatically stated that NO document should go to the European partners for broad distribution until after the revised draft is prepared from the 12/16/93 conference call. 4.2 Dioxin Science Subgroup: P. Watanabe presented a summary of the conference calls and discussed the key scientific issue areas* P. Watanabe outlined the plans for a group meeting at L. Birnbaum's EPA laboratory in January and a co-sponsored ILSI workshop to discuss immunotoxicologic tests and their interpretation. The outcome of the ILSI conference is a published paper outlining the issues/controversy around the different models and interpretation around toxicology and immunotoxicology. F. Kinoshita presented an overview of the current EPA work on host resistant model. The group discussed the importance of getting NOEL's. The sub group urged a joint meeting with the endocrine sub group of the Science and Health Work Group. P. Watanabe and A. Mason will work out these details. VRD 0002830272 A fcXZ0E0Z008 QUA` Dioxin Work Group--Page 4 Minutes (//3--FY 93/94) The work group approved the concept of the ILSI workshop and recommended $20K for its funding. P. Watanabe and A. Mason will take this recommendation to the Science Task Group. R. Ku Is asked to coordinate with R. Kalev on the Toxicity Equivalence Factors to ensure consistency with previous CMA comments to EPA (re: PCB panel). The group discussed meeting with Linda Birnbaum in Washington but the work group recommended waiting until after the Dioxin Science Subgroup visit in January. 4.3 Dioxin Reassessment Subgroup D. Penney presented the subgroup's work plan and identified the key tasks for the subgroup. The work group discussed the pros and cons of advocating for an EPA stakeholder meeting to discuss the Risk Characterization chapter. The subgroup scheduled a conference call Friday, Nov. 12, 1993, 9:00am to noon eastern time to set the agenda for the meeting with Bill Farland. D. Penney identified the opportunities and constraints about jointly funding work to evaluate the science issues in the Risk Characterization chapter. The subgroup recommended jointly funding the scientific panel and/or review of the Risk Characterization chapter. The subgroup agreed that CMA/CCC will develop and submit separate interpretative analysis and comments. D. Penney and J. Festa will explore how best to fund a joint scientific evaluation of the Risk Characterization chapter. D. Penney and A. Mason will prepare the 1st draft requesting additional funds for the subgroup review. D. Penney and A. Mason will communicate with M. Ferris and L. Smith about the need for additional funds and will transmit the request for additional funding to the Science Task Group and Operating Committee. The work group endorsed having a joint meeting with AFPA to review the tasks of covering all aspects of the dioxin reassessment process. A. Mason will work with J. Festa to coordinate a joint meeting. 4.4 NRDC Petition: J. Wilkinson briefed the group about a meeting with outside counsel discussing a long term strategy around the NRDC petition, the pulp and paper cluster rule, and the dioxin reassessment process. VRD 000203021* Dioxin Work Group--Page 5 Minuses (#3--FY 93/94) These lawyers indicated that the industry may want to begin building factual basis to challenge EPA if it becomes necessary or-to file an amicus to support EPA vs. other litigants. J. Wilkinson identified a timeline for future conversations with outside legal advisors and D. Fischer discussed some of the key aspects underlying future basis for discussion. EPA will take no action on the NRDC petition until the dioxin reassessment is completed. 5.0 Pulp and Paper Cluster Rule: S. Holm identified the AFPA actions on the pulp and paper cluster rule. He indicated that there was a reg-neg on the land part of the rule. S. Holm discussed some of the proposed tests that AFPA is considering; including a chemical characterization of dioxin and chlorinated phenol compounds. 6.0 NIOSH: R. Kaley presented an overview of a conversation with E. Delzell on the examination of the NIOSH dioxin study. She indicated that there was one plant driving the conclusions. J. Collings, G. Bond, R. Kaley plan to meet on Dec. 20, 1993. R Kaley will summarize these discussions at the next Work Group meeting. 7.0 CanTox Incineration: 8.0 B. Lienhart said that CanTox is about to release the chapter to the work group for review. A. Mason will send the document to the Work Group and to the RCRA Combustion Work Group for its quick review. 1 Adjourn f The meeting adjourned at 3:30 p.m. Eastern. MINUTES SUBJECT TO APPROVAL November 10, 1993 AMM/DF Regulatory Affairs StJ0Sf)l008 liP I The ' Vinyl Institute The Campaign Against Vinyl -- The Facts A Division of The Society of The Plastics industry, Inc. In recent years, certain environmental groups have pushed for the elimination of various chlorine-containing products, claiming that their manufacture represents a threat to human health and the environment. But the evidence these groups present to support their campaign against chlorine rely either on bad science or emotional rhetoric. One product singled out for attack is PVC (polyvinyl chloride, or vinyl), the world's second largest selling plastic material. What's vinyl's crime? Apparently, nothing more that its use of chlorine as a feedstock. In fact, Greenpeace has admitted in public meetings that vinyl is merely a piece in its "chess game" against the entire petrochemical industry. One result of this chess game campaign can be seen in the April 1992 report issued by the International Joint Commission of the United States and Canada. That report, the IJC's sixth biennial report on Great Lakes water quality, deals with those lake contaminants known as persistent toxic substances. However, one of the specific recommendations in the report (Recommendation Seven) suggests that the IJC develop timetables to sunset the use of chlorine and chlorine-containing compounds used as industrial feedstocks. Vinyl is the largest such use for chlorine and is not a persistent toxic substance. Why the vinyl industry vigorously objects to the IJC's recommendations, especially Recommendation Seven: The report treats all chemicals within a class the same, regardless of the safe performance history of individual products within the class. Vinyl is one of those products with a demonstrated record of safe production and use. The report acknowledges, but deliberately chooses to ignore, that harmful effects have not been established for many of the substances it examines. Vinyl is one of those substances for which the IJC does not establish, with any scientific validity, harmful effects. The report erroneously concludes that chlorine-based manufacturing is an uncontrollable process and that the environmental impact of that process is unknown and unpredictable. To the contrary, the manufacture of vinyl chloride and polyvinyl chloride is a sophisticated and well-understood process that is entirely predictable and controllable. All of the by-products are known and quantifiable. In fact, one independent consultant, ICF Incorporated, characterized Recommendation Seven as "overly broad and not supported by analysis of risk and costs, including net environmental costs." In essence, through business and payroll taxes, the vinyl industry is being forced to underwrite an effort that will put it out of business -- without justification! More facts about vinyl's environmental performance: The overall vinyl production process has a 99+ percent conversion rate. By-products are either contained, neutralized, recycled or incinerated, or disposed of in an environmentally approved manner. -more Wayne Interchange Plaza II 155 Route 46 West Wayne, NJ 07470 (207; 890-9299 Fax # (201) 890-7029 VRD 000 20 30 ? Vinyl is a highly efficient user of energy and feedstocks. For instance, it takes about half the energy to make PVC sewer pipe as it does to make other plastic pipe, and about a third the amount it takes to make cast iron pipe. In its 1992 lifecycle comparison of various packaging materials, Chem Systems found vinyl to be the material with "the lowest production energy and carbon dioxide emissions, and the lowest fossil fuel and raw material requirements of the plastics studied" Vinyl chloride, the raw material used to make vinyl plastics, is one of the most studied and carefully regulated chemical substances in use today. There are strict controls in place to measure and limit all environmental emissions. Those controls, along with voluntary efforts undertaken by industry, have virtually eliminated any health hazards to workers and plant-site communities. Since the 1970s, the industry has reduced its VCM emissions in the U.S. more than 95%. What are the consequences of eliminating the production and use of vinyl? In April 1993, the consulting firm of Charles River Associates, Boston, looked at the cost to replace vinyl with alternative materials in fourteen major applications and markets. The study calculated the amount of material needed to maintain the same market share currently held by vinyl in each application. It also estimated, where appropriate, the capital cost to build new capacity or convert existing capacity to produce that material or fabricate end-products from it, and considered any incremented or additional costs to install the material compared to the current cost to install the vinyl product The study found that the cost to replace vinyl in these markets would require an additional investment of $974 million in new equipment and cost consumers 56.7 billion more per year to purchase substitute materials. The vinyl industry contributes $4 billion to the U.S. economy each year and operates 1,008 plants in the Great Lakes states alone, where approximately 60% of its employment is concentrated. Eliminating vinyl would shut down this business, and have serious implications for customers in hundreds of markets, including health care, communications, aerospace, automotive, retailing, textiles, construction, durable goods and agriculture. Even more important are the societal benefits at risk by eliminating the use of vinyl. A few examples: % Pipe made from it economically delivers pure water to places that have never had this basic necessity; PVC irrigation pipe helps increase crop yields, and studies have shown that PVC pipe is less expensive to install and maintain than competitive materials. Medical goods and pharmaceutical packaging made from vinyl help provide a higher, safer standard of health care. Wiring made from it makes electrical service safer and more dependable. Construction products made from it make housing more affordable. % Packaging made from it reduces food spoilage and waste, and helps package designers create innovative "downsized" packaging that reduces landfill waste. The industry's position The vinyl industry is proud of its environmental performance and welcomes an examination of its record. Any such review, however, should be based on sound science and conducted in the public interest. The current campaign against vinyl does neither and does society a misservice by potentially restricting the use of products that have demonstrated their value for years. July 1993