Document 6972zzaVajZ0eaBD1q1Q1Bxm

Original Article Mesothelioma Associated With Commercial Use of Vermiculite Containing Libby Amphibole Kari K. Dunning, PhD, Stephen Adjei, MD, MPH, Linda Levin, PhD, Amy M. Rohs, MD, MS, Tim Hilbert, MS, Eric Barton, MS, Vikas Kapil, DO, MPH, Carol Rice, PhD, Grace K. LeMasters, PhD, and James E. Lackey, MD, MS Objectives: To describe asbestos-related mortality among manufacturing workers who expanded and ptocessed Libby vermiculite that contained am phibole fiber. Methods: Standardized mortality ratio was calculated for 465 white male workers 31 years after last Libby vermiculite exposure. Results: 1\vo wotkers died from mesothelioma, resulting in a significantly increased standardized mortality ratio of 10.5 (95% confidence interval, 1.3 to 38.0). These workers were in the upper 10th perccn tile ofcumulative fiberexposure, that is, 43.80 and 47.23 fiber-years/cm3, respectively. One additional wotker with cumulative fiber exposure of 5.73 fiber-years/cm3 developed mesothe lioma but is not deceased. There were no other.significantly increased stan dardized mortality ratios. Conclusions: Workers expanding and processing Libby vermiculite in a manufacturing setting demonstrated an increased risk for the development of mesothelioma following exposure to the amphibole fiber contained within this vermiculite ore source. mtcultte, a 1980 study demonstrated a 2.0% prevalence of localized pleural thickening on chest radiographs.8 Localized pleural thicken ing has historically been associated with commercial asbestos ex posure. A 2004 follow-up of this cohort demonstrated a marked in crease in the rate of pleural changes (28.6% of participants) 25 years after the last Libby amphibole exposure.7 These changes, which were demonstrated in some workers at low lifetime cumulative fiber exposure (CFE) levels, occurred in an exposure-response manner.7 Mortality studies ofLibby miners and millers with historically high exposure to Libby amphibole have demonstrated significantly increased mortality due to lung cancer, mesothelioma, and nonmalignam respiratory diseases (NMRD) including asbesiosis, silicosis, and chron ic obstructive pulmonary disease.8-11 There are indications that malignant and nonmalignani respiratory health risks may not be limited to persons with heavy expos ures.7-9-12-14 Therefore, the pur pose of this analysis was to investigate mortality among workers with relatively low lifetime exposure to asbestiform minerals while ermiculite is a naturally occurring mineral that has been widely processing Libby vermiculite at an Ohio lawn care product manu Vused in consumcrproducts such as insulation, lawn and garden facturing facility: products, and fireproofing material. While vermiculite itself does not pose a known health hazard, the vermiculite mined from Libby, Montana contained 0.1% to 26% naturally occurring asbestiform METHODS minerals,1-2'characterized as winchite, richterite, and tremolite.3 From the 1920s to 1990, the Libby mine produced up to 80% of the worlds vermiculite supply and shipped it to more than 200 US regional processing facilities.'18 After tile occurrence of a cluster of bloody pleural effusions in workers at an Ohio manufacturing facility expanding Libby ver- Study Subjects Subjects comprised a cohort of 513 workers from an Ohio manufacturing facility who participated in an earlier 1980 pulmonary morbidity study.6 Demographic and work history data were obtained from the questionnaires administered in I9S0.6 Because the original cohort was 97% white and 94% men,6 the standardized mortality l-Vom the DepartmenlofEnvironmcntal Health (Dts Dunning, Levin, Rice, LeMaSters, Adiei, Rolls, and Lockey, Mr Borton and Mr Hilbert), University of Cincinnati College of Medicine, Cincinnati, Ohio; the Department ofReha ratio (SMR) analysis was limited to the 465 white men. This mortality study was approved by the University of Cincinnati institutional review board. bilitation Sciences (Dr Dunning), University ofCincinnati College ofAllied Health Sciences, Cincinnati, Ohio; the Department of Internal Medicine, Pul monary Division (Drs Adjei, Rohs, and Lockey), University of Cincinnati College ofMcdfcIne, Cincinnati, Ohio; and National Center for Environmen tal Health and Agency forToxic Substances and Disease Registry (DrKaptl), Centers for Disease Control and Prevention, Atlanta, Ga. This study was supported by funds fiom the Comprehensive Environmental ResponscCompensatlonand LiabilityAct trustfund through a cooperative agree ment with the Agency for Toxic Subsunces and Disease Registry (ATSDR), US Department of Health and Human Services, Centers for Disease Con trol and Prevemion ATSDR grants U50/ATU573006S and 1R0ITS000098-1. In addition, this study was partially supported by the National Institute of Exposure Assessment The manufacturing plant began using vermiculite from South Carolina in 1957, and from Libby, Montana in 1959, until 1980.1S Vermiculite was also obtained from Palabora, South Africa and Louisa County, Virginia starting in 1970 and 1979, respectively.18 On the basis of industrial hygiene measures that began in 1972, ex posure of fiber is defined as particles with a length greater than 5 ftm, a diamejer less than 3 j*m, and an aspect ratio of 3:1 or more.6 Environmental Health Sciences grant ES10957 and by the US Environmental Protection Agency Region 8, as partofthe managementofthe Libby Asbestos Superfund Site Drs Lockey, Dunning, and Levin, Mr Hilbert, and Mr Bonan received partial funding by a grant from ATSDR. Dr Lockey served as a fact and state-of- Therefore, CFE is not specific to asbestiform minerals, as it may also include other mineral or nonmineral fibers. For Libby vermiculite, the concentration of asbestiform minerals has been shown to be as high as 26% in ore ready for expansion.1 Vermiculite from the-art witness for the US Departmen t ofJustice for the District ofMontana, Missoula Division, in the case of United Stales ofAmerica v WR Grace elalThe findings and conclusions in this report are those of the authors and do not necessarily represent the official position ofthe Agency R)r Toxic Su bstances and Disease Registry orthe Centers fa Disease Control and Prevention. Address correspondence to: Ja tries E. Lockey, MD, MS, Departments ofEnviron mental Health, Uitivetsity ofCincinnati College ofMedicine, 3223 Eden Ave, ML 0056, Cincinnati. OH 45267 fjamcs.lockcy@uc.edu). Copyright 2012 by American College of Occupational and Environmental Medicine South Carolina, South Africa, and Louisa County, Virginia has also been shown to include asbestiform minerals but at a concentration less than 1%.16-17 Self-reported work histories collected in 1980 pro vided details regarding all jobs held as well as beginning and end ing dates to calculate CFE estimates in fiber-year/cm3 (f-yr/cc).6-7 Worker smoking history and other commercial asbestos exposure information was also collected. For the analysis reported here, previ ously used CFE estimates6,7 were revised on the basis of additional DOl: 10.1097/JOM.0b013c318250b5f5 exposure data obtained in 2010.18 jOEM Volume 00, Number 00, March 2012 1 Copyright 2012 Uppincott Williams & Wilkins. Unauthorized reproduction of this article Is prohibited. Dunning et al IDEM Volume 00, Number 00, March 2012 Ascertainment of Vital Status All workers in the eoliort were known to be alive in 1980 after the National Death Index (ND1) began eompiling data on all US deaths (January 1, 1979). Vital status follow-up from May 1980 to Deeember 2009 was done using the ND1. Vital status through June 30, 2011 was updated using Soeial Security Administration data through the Internet (RootsWeb.eom). All workers were assumed to be alive unless discovered otherwise. Dead) certificates for deeeased workers were obtained accordingto US andstate requirements and regulations for studies involving human subjeets. Underlying eause of death was determined by death eertifieates as eoded by a single nosologist aeeo rding to International Classification of Disease (ICD), 9th and 10th Revisions (1CD-9 and 1 CD-10),18,19 or by ND1 Plus (for two deaths for whieh obtaining death eertifieates was difficult). The analysis foeused on malignaneies, ineluding lung eaneer and mesothelioma, whieh have been as sociated with oeeupational asbestos exposure, in addition, eaneer of the digestive traet was exam ined. Nonmalignant respiratory diseases were analyzed as separate categories including asbestosis, silieosis, other pneumoeoniosis, ehronie obstructive pulmonary disease, and other respiratory diseases (ineluding interstitial pulmonary disease with fibrosis). Before 1999, a unique ICD eode for mesothelioma did not exist. Starting in 1999, a unique 1CD-10 eode (C45) was established for mesothelioma. Therefore, analyses for mesothelioma were based on deaths from 1999 to June 30,2011, using ICD-10 C45. For deaths from 1980 to 1999, "possible mesothelioma" was categorized for ICD eodes ineluding eaneer of other respiratory sites, eaneer of pleura, and eaneer ofother and unspeeified sites.20 Data Management and Analysis Questionnaire data (1980) were double entered into SAS PROC FSED1T and stored as SAS datasets. Alldeath eeriifieate data were double-entered into a Microsoft 2007 ACCESS database and eompared using SAS PROC COMPARE. A random 10% of the data was verified with hardeopy reeords after identified data entry errors were reetified. For white men, Life Table Analysis System (LIAS, Net Version 3.0),21 developed by the National Institute for Occu pational Safety and Health,22"25 was used to determine expeeted deaths, SMRs, and 95% eonfidenee intervals (Cls). Standardized mortality ratios adjusted for age and ealendaryear were ealeulated to determine whether workers experienced a greater mortality from speeifie eauses than was expeeted on the basis of the US popula tion. For causes of death with larger numbers (all eaneers; eaneer of traehea, bronehus, or lung; eaneer of digestive system and peri toneum), SMRs and standardized rate ratios (SRRs) were ealeulated using tertiles of the CFE distribution among the 465 workers. For nonwhite and female workers, limited sample size did not allow for SMR analysis stratified by raee orgender, and results were deseribed. RESULTS Of the 465 white men from the original cohort, 136 were deeeased as of June 30,2011. Demographie and exposure eharaeteristies for seleeted eauses of deaths are shown in Table 1. Among the 136 deeeased, 16 (11.8%) died of lung eaneer and 2 (1.5%) died of mesothelioma. The mean exposure duration as of 1980 was longer ferrtnose who died of lung eaneer (16.4 years) and mesothelioma (19.0 years) than all workers (11.0 years). Similarly, mean CFE was higher for deaths due to lung eaneer (15.34 f-yi/ee) and mesothe lioma (45.51) than for all workers (9.00). Table2 shows SMR results. The SMR for mesothelioma based on two deaths that oeeurred after 1998 was significantly increased at 10.5 (95% Cl, 1.3 to 38.0). There were no deaths due to eaneer of pleura, peritoneum, or pericardium. There were also no deaths due to silieosis or other pneumoeoniosis. The two deaths in the NMRD eategory "other respiratory diseases" were Speeifiealty "interstitial pulmonary diseases with fibrosis" (J84.1). The 13 eaneers of the digestive system and peritoneum eonsisted of the following: 3 of esophagus (C15.9), 4 of panereas (C25.9), an d 6 ofintestine (C18.9). For eauses of death with larger numbers (all eaneers; eaneer of traehea, bronehus, or lung; eaneer of digestive system and peri toneum), SRRs and SMRs were ealeulated using tertiles of the CFE distribution among the 465 workers (Table 3). There were no signif icant SRRs or SMRs for these diagnoses. Although not significant, SRRs increasedwith increasing CFE eategory for eaneer ofdigestive system and peritoneum. Ofthe original eohort of 513 workers, 16 were nonwhite men and 32 were women. The 16 nonwhite men had an average CFE of 2.50 (SD, 7.48)f-yr/ee. Of those 16 nonwhites, 4 were deceased by June 30,2011. Amongthe 12 living nonwhite workers, average age as ofJune 30,2011,was 59.9 (SD, 6.5) years. Causes of death among the four deeeased nonwhite workers were eaneer ofthe intestine (C18.9), eerebrovaseular disease (161.9), isebemie heart disease (121.9), and pneumonia (J18.9). The worker who died of eaneer of the intestine (C18.9) was hired in 1977, was 61 years old at death (2002), and had a CFE level of2.75 f-yr/ee. The 32 female workers had an average CFE of 0.98 (SD, 2.36) f-yr/ee. Of these, 7 were deeeased by June 30, 2011. Among the 25 living women, average age as ofJune 30,2011 was 61.1 (SD, 10.6) years. Causes of death amongthe seven deeeased women were eaneer of the intestine (C18.9), otherrespirato ry eaneer (C38.9), dis ease ofthe eireulatory system (171.3), leukemia (C92.0), pneumonia (JI8.9), dementia (F03), and isehemie heart disease (125.1). The fe male worker who died of eaneer of the intestine (C18.9) was hired in 1974, was 82 years old at death, and had a CFE level ofO. 10 f-yr/ee. The female woikerwho died of other respiratory eaneer (C38.9) was hired in 1969, was 66 years old at death, and had a CFE level of6.93 f-yr/ee. DISCUSSION This study found a significantly elevated SMR for mesothe lioma. The two mesothelioma deaths were in the top-tenth CFE pereentile, speeifieally 43.80 and 47.23 f-yr/ee. There were no sig nificantly elevated SMRs for other malignant orNMRDs, consistent with asbestos exposure. One reason for nonelevated asbestos-related malignant and NMRD SMRs may be due to relatively low fiber ex posure (CFE mean, 9.0; median, 0.63; range, 0.0 to 106.31 f-yr/ee). Previous studies ofLibby vermieulite miners and millers with higher CFE levels have shown significantly inereased mortality due to lung eaneer, mesothelioma, andNMRD.8"11 In a 1987 study of 575 Libby mine workers with an average exposure of 200 f-yr/ee, SMRs for lung eaneer andNMRD was 2.2 (95% Cl, 1.4 to 3.4) and 2.4 (95% Cl, 1.5 to 3.8), respectively.8 In a 2004 study of 406 Libby mine workers, SMRs for respiratory eaneer andNMRD was 2.4 (95% Cl, 1.7 to 3.2) and 3.1 (95% Cl, 2.3 to 4.1), respectively.10 In a.2007 study of 1672 Libby vermieulite mine workers with a median fiber exposure of 8.7 f-yr/ee (ranging from 0 to >250 f yr/ee), SMRs were as follows: lung eaneer, 1.7 (95% Cl, 1.4 to 2.1); mesothelioma, 15.1 (95% Cl, 1.8 to 54.4); NMRD, 2.4 (95% Cl, 2.0 to 2.9); asbestosis, 165.8 (95% Cl, 103.9 to 251.1); and ehronie ob structive pu Imonary disease, 2.4 (95% Cl, 2.0 to 2.9).9 Other studies of Libby vermieulite mine workers have shown decreased SMRs for eaneer of the digestive system and peritoneum: 0.7 (95% Cl, 0.3 to 1.6) * and 0.8 (95% Cl 0.6 to l.l).11 In the eurrent analysis, ean eer of the digestive system and peritoneum demonstrated inereased SRRs with i nereasing CFE categories. These SRRs were not statisti cally significant, and this finding should be interpreted with eaution beeause of small sample size. Several other studies of higher CFE levels among the Libby mine worker cohort showed an exposure-response relation ship of inereased mortality with increasing CFE categories,3-11 Nevertheless, only one study9 ealeulated SMRs for workers with `2 2012 American College ofOccupational and Environmental Medicine Copyright 2012 Lippincotf Williams & Wilkins. Unauthorized reproduction of this article is prohibited. jOEM Volume 00, Number 00, March 2012 Occupational Mesothelioma From Libby Vermkulite TABLE 1. Demographic and Exposure Characteristics of White Male Workers (N = 465): Deaths From 1980 to June 30,2011 Characteristic All Workers All Deaths Lung Cancer* Mesothcllomaf No. workers 1 Mean age in 19S0 (range) Mean year of birth Mean year ofhire Mean age at first exposure (range) Mean year of death Mean age at death (range) Mean time in years (SD.) and (range) from first exposure to date of death Mean exposure durations in years (range) Mean CFE (fiber-years/cin3) (SD) and (range) Pack-years 1980 (SD) and (range) (ex- and current smokers) Smoke ever 1980, % (n) Smoke status 1980, % (n) Never Ex Current 465 37.8(19.2-66.1) 1942 1969 26.8(15.3-54.2) i i t 11.0(0.3-23.7) 9.00 (20.84) (<0.01-106.31) 17.8 (16.5) (0.3-96.0) 64.1 (298) 35.9(167) 25.6(119) 38.5 (179) 136 49.1 (21.0-66.1) 1931 1964 33.5 (18.0-53.2) 2001 70.4 (29.1-92.4) 36.9 (10.6) (2.0-54.0) 15.6 (0.8-23.7) 16.76(28.44)0.02-106.29 29.0 (19.2) (0.5-96,0) 71.3 (97) 28.7 (39) 31.6(43) 39.7 (54) 16 51.3 (39.7-633) 1929 1964 34.9 (18.0-51.8) 2001 72.6 (60.0-85.5) 37.7 (9.8) (18.6-52.1) 16.4 (2.0-23.4) 15.34 (30.35) 0.03-106.29 43.2 (16.2) (28.0-74.0) 93,8(15) 6.3 (1) 18.8 (3) 75.0(12) 2 53.9(45.6-62.1) 1926 1961 35.1 (30.9-39.3) 2006 80.7 (75.1-86.2) 45.6 (1.9) (44.3-46:9) 19.0(15.0-23.0) 45.51 (2.43) (43.8-47.23) 20.5 (12.02) (12.0-29.0) 100(2) 0 100(2) 0 *lCD-10 C33-34. tlCD-lOOIS fTlicsc numbers are not applicable to "all workers'' because only 136 oftbe-465 all workers worn deceased. See "all deaths'' column fbr data regarding 136 deaths. Cumula11ve fiber exposure estimates begin In I9S7. The manufacturing plant began using vermiculitc from South Carol] [la ill 19S7 and Horn Libby, Montana, In 1959. For those workers hired before 19S7. exposure began in 19S7. Bar those workers hired after 1957, exposure began at the date ofhire. Exposure duration Is the year exposure began up to 1980. TABLE 2. Standardized Mortality Ratios for Selected Cancers and Diseases Among White Male Workers (N = 465) by Underlying Cause of Death (From 1980 to June 30,2011) Cause of Death ICD-9 Codes 1CD-10 Codes Obs Deaths US Exp Deaths US SMRa (95% Cl) All causes , All cancers Cancer of trachea, bronchus,or lung Mesothelioma'1 Nonmalignant respiratory disease0 Asbestosis Chronic obstructive pulmonary disease Other respiratory diseases'1 Cancerofthe digestive system and peritoneum0 140-239,273.1,273.3 162 b 501 490-492,496 470-478,494-95, 504,506-519 150-159 COO-C99 C33-34 C45 J61 J40-J44 J30-33, J34.I-J34.8, J35-J39, J47, J66-J95, J98-J99 C15-C26, C48 136 46 16 2 1 8 2i 13 182.1 48.9 16.9 0.2 0.1 8,4 2.4 11.8 0.8 (0.6-0.9)* 0.9(0.7-1.3) 0.9 (0.5-1.5) 10.5(1.3-38.0)** 15.4 (0.4-85.9) 1.0 (0.4-1.9) 0.8 (0.1-3.0) 1.1 (0.6-1.9) *7'<0.0l;"/3<0.0S. "Comparison ofSMR Tor deaths in the US population ofsame age category, race, and sex during thesomo calendar year. bSMRs for mesothelioma include only deaths from 1999 to June 30,2011. There is no 1CD-9 code for mesothelioma- In 1999, a unique ICD'10 code was assigned to mesothelioma. There were no "possible mesothelioma'1 deaths before 1999 (1CD-9): cancer ofother respiratory sites (160,164-165): cancerofpleura (163): or cancer ofother and unspecified sites (187.194-199). "There were no deatlts due to silicosis (J62) orolher pneumoconiosis (J60, J63-J64). dThe 2 deaths in (lie-category "other respiratory diseases'1 were specifically "interstitial pulmonary diseases with fibrosis (J84.1).M "There were no deatlis due to cancerofthe peritoneum. SMR indicates standardized mortality ratio; Cl, confidence Interval. 2012 American College ofOccupational and Environmental Medicine Copyright 2012 Uppincott Williams & Wilkins. Unauthorized reproduction ol this article is prohibited. 3 Dunning et oi IOEM * Volume 00, Number 00, March 2012 TABLE 3. Standardized Rate Ratios and Standardized Mortality Ratios Among Workers (N = 465) by Underlying Cause of Death (From 1980 to June 30,2011) Based on Tertiies of the Cumulative Fiber Distribution* Cause of Death Cu mutative Exposure Category* (flber-years/cm3) Person-years Obs Exp SRR (95% Cl) SMR (95% Cl) All cancers Cancer o f trachea, bronchus. or lung Cancer ofdigestive system and peritoneum 0.00-0.31 >0.31-1.40 >1.40-106.31 0.00-0,31 >0.31-1.40 >1.40-106.31 0.00-0.31 >0.31-1.40 >1.40-106.31 5,342 6300 6,436 5,342 6,300 6,436 5,342 6,300 6,436 5 7.5 (reference) 21 19.4 1.1 (03-4.1) 20 21.9 1.1 (0.3-4.0) 2 2.4 (reference) 7 6.8 1.0 (02-4.9) 7 7.7 0.9 (03-4.6) 2 1.9 (reference) 6 4.7 3.4 (0.7-17.6) 5 5.2 4.2 (0.8-23.7) 0.7 (0.2-1.6) 1.1 {0.7--3.7) 0.9 (0.6-1.4) 0.8(0.1-3.0) 1.0{0.4-2.1) 0.9 (0.4-1.9) 1.1 (0.1--3.8) 1.3 (0.5-2.8) 1.0(03-2.2) CoinpaIison ofSMR for joollm in llic US populnlion ofsame npc category, race, and sex during the some calendar Umo period. Categories based on tetliles of the cumulative Bberdislribulion among while men (N = 465) followed in this cohort (fibcr-ycars/cm1). SMR indicates standardized mortality rolio; SRR,standardized role ratio; Cl, confidence interval. lower CFE estimates. Among workers with less than 4.5 f-yr/cc, lung cancer SMR was elevated at 1.5 (95% Cl, 0.9 to 2.3).9 Among workers with 4.5 to 22.9 f-yr/cc, lung cancer SMR was significantly elevated at 1,6 (95% CIt i. I to 2.5). Among workers with less than 4.5 f-yr/cc and 4.5 to [9.9 f-yr/cc, NMRD SMR was significantly elevated at 1.8 (95% Cl, 1.1 to 2.8) and 2.0 (95% Cl, 1.3 to 3.0), respectively.9 A recent case series also reported mesothelioma due to oc cupational exposure or potential environmental exposure or both to Libby vermicuiite ore.1'" Of 15 mesothelioma cases, 4 were reported for Libby mine workers and the remaining 11 reported potential nonoccupationa! exposures: 9 from environmental exposure and 2 from home contamination by family employed at the mine/niill facil ity. On the basis of interviews with patients or next of kin, latencies ranged fi'om 13 to 67 years from first known potential exposure to Libby vermicuiite. in the formal SMR analysis, there were two deaths due to mesothelioma. One workerbegan employment at the facility in 1943, was first exposed to vermicuiite in 1957, and had a CFE level of47.23 f-yr/cc. He died in 2004 atthe age of86 years, 47 years after his initial exposure. In 1980, he had reported no known commercial asbestos exposure. He worked in multiple work areas including maintenance, warehousing, and production areas using vermicuiite. The second death was reported for a worker who began employment at the facility in 1965 and had a CFE level of 43.80 f-yr/cc. He died in 2009 at the age of 75 years, 44 years afler'his initial exposure. He worked in areas using vermicuiite and reported no known commercial asbestos exposure. . Through continued follow-up of this cohort, it is known that another worker had a diagnosis of mesothelioma in 2010 at the age of 66 years. He began employment in 1966 and had a CFE level of 5.73 f-yr/cc. In 1980, he reported no known commercial asbestos exposure. This worker is not deceased but the case has been described here to offer a glimpse at the future possibility of mortality among this cohort This cohort offered a unique perspective because of its rela tively low cumulative exposure to Libby vermicuiite compared with most studies that involve more heavily exposed Libby mining and milling workers. An ample latency period had occurred, with a mean of44 (range, 31 to 54) years since initial exposure to vermicuiite. In addition, industrial hygiene records, workerjob histories, and respi ratory health histories were available to recreate CFE estimates and historical smoking status. The number of deaths in this cohort was relatively low, re ducing the power to detect mortality potentially related to Libby vermicuiite exposure. Another limitation was the potential misclassification of exposure estimates as derived from previous historic industrial hygiene records available. This analysis, however, used updated CFE estimates based on additional quantitative and qual itative exposure information obtained in 2010.15 The SMR for all causes of death (0:8; 95% Cl, 0.6 to 0.9) was significantly lower in our analyses than in the national population, suggesting a healthy worker effect Furthermore, SMRs by CFE exposure should be in terpreted with caution. Limitations ofthis approach include possible different person-year distributions by exposure category due to dif ferences in worker ages (older workers have higher fiber exposure). Standardized rate ratios do not have this limitation. Finally, among the original cohort of 513 workers, 16 were nonwhite men and 32 women. The limited sample size of these groups did not allow for SMR analysis stratified by race or gender. In conclusion, the results of this study demonstrate an in creased risk of malignant mesothelioma mortality in a worker pop ulation involved with expanding and using Libby vermicuiite as a carrier for lawn care products. Further follow-up ofthis aging cohort will provide additional data and statistical power to determine po tential association between relatively low CFE in workers exposed to Libby vermicuiite that contained amphibole fiber and malignant and NMRDs. ACKNOWLEDGMENTS The authors thank the workers andfamilies who volunteered their timefor this study and express their appreciationJar the coop eration ofthe companypersonnel REFERENCES 1. Atkinson GR,RoseD,Thomas K,JonesD,ChatfiddEJ, Going JE.Collection, Analysts and Characterisation of Vermicuiite Samplesfir Fiber Content and Asbestos Contamination. Kansas City, MO: Midwest Research Institute EPA Office ofPesiicides and Toxic Substances; 1982. EPA Report No. 68-01-5915. 2. Moaiamed F, Lockey JE, Parry WT. 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