Document VJnd9E57bbZNJajjyR7rzeLON

Letters RE: Controlled Use of Asbestos A lie can travel halfway around the world while the truth is still putting on its shoes. -- Mark Twain To the Editor:--Castleman's recent article, "Controlled Use of Asbestos" critiques industry's mis representation of the hazards asso ciated with using asbestos.1 We agree with Castleman when he states that, "`Controlled use' of asbestos is the asbestos industry's way of referring to business as usual with a false face." "Controlled use" is but the latest trend in a series of corporate misrepresentations relat ing to asbestos risks. Union Carbide Corporation (UCC) and its consult ants have asserted that asbestos mined from the Coalinga deposit in California and sold by UCC as "Calidria" is innocuous.2 They base these assertions on two arguments: 1) Calidria is unregulated "shortfiber" chrysotile (less than 5 pm) and thus nontoxic, and 2) none of the Calidria mine or mill workers ever developed asbestos-related dis ease. UCC successfully marketed Calidria as short-fiber asbestos, while suppressing evidence that more than 50% of Calidria fibers were actually longer than 5 pm. UCC concealed the results of animal studies, and to give the impression that Calidria was safe, they employed consultants to manipulate Calidria inhalation data from previous studies. As a result of Dr. David Egilman works as a consultant, at the request of both individuals and corpo rations, in environmental and occupational health litigation and research. He has served as a consultant to Union Carbide Corporation on matters relating to Bhopal. Megan Roberts is a researcher for Never Again Consulting. legal actions instigated by injured workers, U.S. courts have forced UCC to divulge some of these secret studies and documents that reveal the perfidious nature of these assertions.*f We report this evidence here. The "Short-fiber" Myth Union Carbide has given customers the impression that Calidria is innocuous because of its short fiber length. However, Kent Pinkerton's 1982 PhD thesis found that 48% of aerosolized Calidria fibers were longer than 5 pm, compared with 25% of Canadian (Jeffrey) and UICC B chrysotile.3 Calidria also had a greater percentage of fibers more than 10 pm long: "At least 92% of the combined fibers and fiber clusters in the Jeffrey and UICC B aerosols were less than 10 pm in length, but only 66% of the combined fibers and fiber clusters in the Coalinga chrysotile aerosol were less than 10 pm."3 Edward Ilgren, a UCC litigation consultant, published selected portions of Pinkerton's thesis but misrepre sented his data on fiber length. Ilgren repeatedly referred to Calidria as a short fiber: "Fibres from . . . Coalinga, Calif., are almost all less than 5 pm in length. . . ."4 In a 1998 deposition, however, Ilgren admitted that he had no data to sup port his conclusion that Coalinga asbestos was a short-fiber asbestos.5 *Many of the documents cited in this letter to the editor were produced in liti gation where one of us (DE) is a consult ant for Kelly Moore: Kelly Moore Paint Com pany vs. Dow Chemical Corporation et al., No. 19785-BHO. fAll Union Carbide Documents referred to in this article may be found at <www.egilman.com/UCC_Corruption>. Union Carbide undertook secret studies that revealed that Calidria fibers were thin, fine, and longer than 5 pm. They realized that Calidria fibers were on average thinner than those of Canadian chrysotile and they therefore were often missed when analyzed by light microscopy (which has a lower limit of detection of 0.25 pm). Three of these studies are high lighted below. In 1975, UCC secretly compared the lengths of Canadian and Calidria fibers released during the use of two, otherwise identical, ceil ing texture paints. The measure ments taken during the dry mixing and spraying of the textures revealed similar exposures to long fibers: "There is clearly no differ ence between these types of asbestos for airborne concentrations of asbestos fibers longer than 5 pm."6 In 1977, some UCC customer and OSHA sampling of Calidria exposures determined that fiber levels were 20-40 times higher than previous UCC counts. In response to these reports, UCC reevaluated its sampling method and found that 20-40 fibers/cc had been missed. UCC noted that: "It has also been our experience in working with ultra-fine fibers that they are very easy to miss completely unless the operator specifically looks for such material."7 UCC did not pass this information on to customers or gov ernment agencies. In 1983, when NIOSH made an undercount error at the UCC mine, UCC again con firmed that fine Coalinga fibers escaped detection: "It would appear that the NIOSH counting lab missed a significant amount of asbestos fiber in some of the samples. . . . Coalinga has a much smaller mean diameter and fiber length distribu 99 tion. Because of this and the fact that most counting laboratories are not familiar with Coalinga asbestos, their fiber counts are often artifi cially low."8 UCC withheld this infor mation from NIOSH. Exposure to "Short-fiber" Asbestos Does Cause Disease: Hidden and Deceptive Studies Ronald Dodson et al. reviewed the pathogenicity of various fiber lengths and concluded that all fiber lengths cause asbestos-related diseases.9 Secret, unpublished, UCCfunded studies performed by the Mellon Institute support these con clusions. The Mellon Institute con ducted at least two animal studies on Coalinga chrysotile, the first in 1966 and the second in 1971. In the 1966 study, Mellon researchers injected Coalinga into the peri toneal cavity in guinea pigs, rats, and rabbits. To mimic the human exposure route, Mellon researchers intratracheally injected a second cohort of rats. The asbestos tested included a Johns Manville Cana dian long-fiber chrysotile and two short-fiber types, including a Coalinga sample (CMS-100). The Mellon researchers concluded that fiber length was unrelated to patho genicity and that Coalinga fiber was potentially more harmful than the Canadian chrysotile: "The results . . . indicate that the asbestos products studied produced fibrotic lesions of the visceral organs . . . regardless of fiber length. Of the 3 products, CMS-100 (Coalinga fiber) produces the most severe reaction."10 After reviewing the results of the 1966 Mellon report, Dr. Dernehl, UCC's associate medical director, remarked that: "The only conclusion we can draw from this crude test is that it is possible that our Coalinga product may be more hazardous to use than long fiber asbestos in that it may induce the disease, asbestosis, at an earlier time after exposure."11 Dernehl also concluded that the 1966 test called into question the adequacy of the threshold limit value to protect employees: "It is probable that the 5 million particles per cubic foot will not be acceptable for the prevention of mesothelioma."11 The 1971 Mellon study tra cheally insufflated rats with a new UCC product, a silica coated asbestos pellet (RG-244). The rats were examined at 30-, 60-, 90-, and 180-day intervals, and the results provided UCC with clear evidence of the hazards associated with expo sure to this double-hazard product: "In general, because of the over whelming preponderance of effect in the asbestos dosed lungs versus in the controls, we have sufficient evidence of damage to warn us to do our best to prevent inhalation of concentrations of asbestos in excess of the Threshold Limit Value pro posed for 1970____ "12 Unfortunately, UCC did not publish either of the Mellon stud ies. In 1982, after passage of the Toxic Substances Control Act (TSCA), which required companies to report toxicologic findings to the EPA, UCC lawyers and manage ment made a decision to hide these findings from the EPA: ". . . the Mellon Institute studies are presently defined as confidential. Since they are more than 10 years old, however, they do not appear to be reportable."13 As mentioned above, between 1997 and 1998, UCC consultants Ilgren and Chatfeld published selected portions of Pinkerton's 1982 PhD thesis (and subsequent abstracts and articles), which com pared the relative fibrogenicities of ground Calidria and Canadian and UICC reference chrysotile.J The consultants claimed that they per formed a "careful review" of Pinker ton's data, and published their con clusion avowing that Coalinga was not fibrogenic: "Exposed animals displayed no fibrosis following exposure to Coalinga chrysotile, JPinkerton refused to co-author these papers. He did not agree that Calidria should be considered a nuisance dust. Personal communication, August 2003. but showed fibrogenic responses with both Canadian fibres."14 How ever, Pinkerton et al., the actual researchers, arrived at the opposite conclusion: "Interstitial fibrosis was seen histologically in all exposed animals [including the Coalinga group] at one year and increased in severity during the year in air [with out exposure]."15 This fibrosis developed even though the Coalinga-exposed rats were exposed to much less asbestos than the other exposed animals.15 Despite the data, Ilgren touted Coalinga chrysotile as "innocuous" and declared that it should be treated as a "nuisance dust."14 Ilgren also claimed that none of the chrysotile fibers tested induced mesotheliomas in any of the rats.4 This "finding" conflicts with other literature, which reveals a direct relationship between exposure to Coalinga asbestos and the develop ment of mesothelioma.16-19 Ilgren's conclusion also conflicts with almost all other animal studies that have examined this question.20 Although Pinkerton did not show that Coalinga asbestos was "innocuous," his experiment did indicate that it was less toxic than comparison chrysotiles. This appar ent conflict with Mellon study find ings is easily explained. Asbestosis is a dose-response disease, and Pinkerton's Coalinga-exposed rats were exposed to 66% less fiber by weight and five times fewer res pirable fibers than rats exposed to the comparison chrysotiles.3 Additionally, the asbestos types were prepared differently prior to testing. The Coalinga asbestos was water processed and ground three times, while the Canadian fiber was passed through a hurricane pulverizer.3 Unlike the Canadian fiber, which was a commercial sample, the Coalinga sample came from the cyclone overflow at the UCC mill.5 The UICC B was untreated.3 Many studies have shown that grinding or manipulating the asbestos structure alters the toxicity and subsequent pathogenicity of asbestos.21,22 100 Letters www.ijoeh.com INT J OCCUP ENVIRON HEALTH Pinkerton confirms this fact, but does not provide any evidence that commercial Calidria is any less toxic than any other asbestos form. Finally, Ilgren stated that Coalinga asbestos was "amphibole-free," but in his 1998 deposition, he admitted he had no data to suggest this assumption.5 Asbestos disease in UCC Calidria mine and mill workers. UCC has denied the presence of asbestos dis ease in any mine or mill workers in sworn testimony and has failed to report any cases to OSHA.23 In the 1960s, UCC implemented a program of periodic surveillance of asbestosexposed workers, including pul monary function tests and chest xrays. Additionally, Dr. Hilton Lewinsohn, their medical director, performed an additional review of the x-rays in 1984. Our review of these medical records and reports reveals that many workers had find ings compatible with asbestosis on chest x-rays, four ofwhom were diag nosed as having asbestosis (see Table 1). Four other employees exhibited possible asbestos-related lung can cers or other chest malignancies, one of whom had "lung cancer" listed on his death certificate.24 Additional Medical Information One worker died in 1991 after working at the King City mill for 28 years. On his original death certifi cate, his treating thoracic surgeon stated that asbestosis was a con tributing cause of death.25 After conferring with UCC corporate lawyers (despite the fact that UCC had sold the mine to a group of investors six years earlier), UCC's mine manager and president of KCAC, the successor corporation, obtained his death certificate, arranged to make the worker a "coroner's case" and had an autopsy performed on the worker.26 The worker's family was All medical records referred to in this article may be found at <www.egilman. com/UCC_Corruption>. not consulted. The coroner subse quently changed the death certifi cate, replacing "asbestosis" with "non-specific pulmonary fibrosis."27,28 The mine president was a member of the city council at the time (he is now the mayor and has been for 12 years), was a friend of the owner of the funeral parlor (in retirement he currently drives the parlor hearse), and serves on the board of the only hospital in town. The autopsy report listed pleural thickening, diffuse pulmonary fibro sis, and history of asbestos exposure (remote) as diagnoses.30 The text of the report noted the absence of asbestos bodies. The coroner was apparently under the impression that the diagnosis of asbestosis required the finding of asbestos bodies. UCC's secret animal studies indicated, however, that Calidria caused asbestosis but did not induce the formation of asbestos bodies.12 The UCC Lewinsohn Report In 1984, in anticipation of the sale of the King City mill, Union Car bide's medical director, Dr. Lewinsohn, who previously had served as the medical director for the asbestos companies Turner & Newall and Raybestos Manhattan, reviewed all the employees' radiog raphy reports. In his report, Dr. Lewinsohn, stated that ". . . 1/1 is regarded as definite radiographic evidence of the presence of changes consistent with pneumoconiosis."31 Dr. Lewinsohn found that several asbestos millers had x-ray evidence of pneumoconiosis, including evi dence of progression. One worker's x-ray progressed from 0/1 to a 1/1 profusion between 1969 and 1983.32 UCC's medical director noted that this progression could have been related to asbestos exposure, but suggested the possibility that an unidentified asbestos exposure, other than the exposure at the asbestos mill where the worker was employed, might have caused this worker's disease: "Further investiga tion of this case is suggested to determine whether the changes noted are related to asbestos expo sure at King City or elsewhere."32 UCC's records fail to identify any other asbestos exposure for this individual. Even if the worker had other additional exposure, it is indisputable that his 14 year expo sure to Calidria at the King City mine contributed to his asbestosrelated disease. Despite the fact that Dr. Lewinsohn told UCC that informing the employees of their condition was a legal requirement under the OSHA act, we have been unable to find any evidence that UCC, its medical director Dr. Lewinsohn, or any of its consulting physicians ever informed any of the workers that they might have had an asbestosrelated illness. This medical infor mation proves that Calidria causes asbestos-related disease. UCC Successful Marketing: Customers Believed Calidria Was Safe Not only did United Carbide tell employees that Calidria was safe enough to eat, they also expended considerable resources to persuade customers that Calidria was "innocuous."33 After receiving UCC promotional material and/or attending UCC lectures, several UCC customers believed Calidria was safe. After attending a UCC presentation, one Dow employee wrote, "Apparently there are four crystalline structures common to asbestos. Of the four, three are proven bad actors whereas the fourth (which they claim is the Calidria type) is much more innocuous . . . Union Carbide claims they have sufficient toxico logical data that places Calidria in the nuisance dust category. . . ."34 Other customers believed that Calidria was not carcinogenic: "The asbestos we use is a unique type available from just one mine in Cal ifornia. It is produced and processed by the Union Carbide Corporation. The have run exten- VOL 10/NO 1, JAN/MAR 2004 www.ijoeh.com Letters 101 TABLE 1. Disease in King City Mine and Mill Worker 25 Worker 108 Worker 178 Worker 217 Worker 291 Worker 358 Worker 311 Worker 360 Worker 380 Worker 383 Worker 385 Worker 549 Worker 72 Worker 131 Worker 362 Worker 218 Worker 371 Worker 83 Worker 12 "Asbestosis" written on report* ILO section "small irregular opacities" filled in: 0/1 (1969), 1/1 (1983)+ parenchymal abnormalities consistent with pneumoconiosis^ t (1969, 1983); "pi" indicated in comments (1983)p+; "kl" indicated in comments (1983)k+; "the smaller capacities [sic] are more obvious than they were in 1969" (1983)f; "co" indicated in comments (1969)co,t "Shows x-ray evidence of an early pneumoconiosis, must wear respirator in dust." (1970) * "Minimal increase in the interstitial lung markings" (1977) * "Mild obstructive lung disease" (1986)* "There is a mild obstructive lung defect" (198_)* "There is a moderate obstructive lung defect" (1986)* "Mild to moderate obstructive disease" (1983)* parenchymal abnormalities consistent with pneumoconiosis (1966, 1984)++ ILO section "small irregular opacities" filled in: 0/1 (1968), 1/0 (1984)f "Moderate Restrictive pulmonary impairment" (1993)* "There is a moderate obstructive lung defect" (1986)* "Suggestive of asbestosis" (1974)* "May be the first indication of obstructive lung disease" (1970)* "The appearances are consistent with pleural calcified plaques--? Asbestos-related. No definite asbestos seen. Indefinite opacity on [right] lobe above diaphragm--rule out ca." (1984)f; cancer listed as "ca" under "other abnormalities (1984)c,t, "pi" indicated in comments (1972, 1984)pi,t; "co" indicated in comments (1966, 1984)co,t; 0/1 profusion (1972)f; "Contraction of Right lower lobe +pleural thickening in horizontal fissure" (1972)f; "od" indicated in comments (1966)f; Pleural abnormalities consistent with pneumoconiosis (1984)+; parenchymal abnormalities consistent with pneumoconiosis (1972)t-t Cancer listed as "ca" under "other abnormalities" (1984)4,t Death certificate--"lung cancer" and "chronic obstructive pulmonary disease"(1994)* "The chest x-ray does show changes suggestive of chronic pulmonary fibrosis" (1965)*; parenchymal abnormalities consistent with pneumoconiosis (1963)t-t ILO section "small irregular opacities" filled in:1/0 (1963)t; "od" indicated in comments (1984)od,t; 'hi' indicated in comments (1963)hi,t; "cn" indicated in comments (1963)cn,t "Asbestosis" listed on initial death certificate (1991)*; "Rule out [inflammatory changes] before consider ing asbestosis" (1981)t; An 0/1 profusion noted (1981)t; "od" indicated in comments (1963, 1981)t; parenchymal abnormalities consistent with pneumoconiosis (1981)+ ,t Cancer listed as "ca" under "other abnormalities" (1984)4+; "A rounded opacity is present in the left hilium. It appears larger than on 4-30-83, but was probably present on 1981 films. Although unilateral, rule out carcinoma" (1984)+ "This man should not be exposed to further inhalation of asbestos. Dr. Hughes, Radiologist read the file as asbestosis, not even knowing this was a Union Carbide worker, and comparison with films from . . . 1969 shows definitely increased activity in the lungs." (1974) * Parenchymal abnormalities consistent with pneumoconiosis (1966)++; ILO section "small irregular opaci ties" filled in: 1/0 (1966)t; "cn" indicated in comments (1966, 1982)cn,t; "pi" indicated in comments (1966)pi+ Parenchymal (1981, 1982) and pleural(1981) abnormalities consistent with pneumoconiosis+,+; ILO section "small irregular opacities" filled in: 1/0 (1981), 0/1 (1982)t "Mild restrictive pulmonary impairment" (1993)*; "co" indicated in comments (1981, 1982)+ ILO section "small irregular opacities" filled in: 0/1 (1972, 1982)t; parenchymal (1972, 1982) and pleural (1984) abnormalities consistent with pneumoconiosis+,,t; "evidence of obstructive Lung disease" (1980)* "Appears to be developing bi-lateral basal fibrosis" (1973) t parenchymal abnormalities consistent with pneumoconiosis (1973, 1983, 1984)++; "moderate obstructive disease" (1984)*; ILO section "small irregular opacities" filled in: 1/0 (1973, 1983) 0/1 (1984)t; "pi" indi cated in comments (1958, 1961, 1973, 1983, 1984)pi,t; "co" indicated in comments (1983, 1984)"+; "od" indicated in comments (1983, 1984)od-t; "kl" indicated in comments (1983, 1984)kl+ "Calcified opacities" (1982)t; parenchymal abnormalities consistent with pneumoconiosis (1982)++; "small irregular opacities" filled in: 0/1 (1982)t; "od" indicated in comments (1982)od,t Pleural abnormalities consistent with pneumoconiosis (1983),t; "appearances on the left chest wall maybe due to previous trama or pleurisy" (1979)t "[right] upper lobe_ [lung]? Carcinoma" (1982)t; Pleural abnormalities consistent with pneumoconiosis (1982),t; "od" indicated in comments (1982)od,t; "pi" indicated in comments (1982)pi,t * King City Asbestos Mill Surveillance Program. t Lewinsohn Report. + Parenchymal abnormalities consistent with pneumoconiosis ILO box checked on x-ray report. Pleural abnormalities consistent with pneumoconiosis ILO box checked on x-ray report. 4 "ca" is the symbol used to indicate "cancer of lung or pleura." p "pi" is the symbol used to indicate "pleural thickening in the interior fissure or mediastium" k "kl" is the symbol used to indicate "septal (kerley) lines." ""co" is the symbol used to indicate an "abnormality of cardiac size or shape." od"od" is the symbol used to indicate an "other significant abnormality." hi"hi"is the symbol used to indicate an "enlargement of hilar or mediastinal lymph nodes." ""cn" is the symbol used to indicate a "calcification in small pneumoconiotic opacities." 102 Letters www.ijoeh.com INT J OCCUP ENVIRON HEALTH sive medical tests on this asbestos (Calidria RG-144) and we have their assurance it is non-carcinogenic."35 The asbestos industry continues to take advantage of the short-fiber myth to promote the use of chrysotile around the world. For example, the Asbestos Institute, the lobbying arm of the Canadian Asbestos industry, has recently touted a soon-to-be published study that concludes that chrysotile is safe to use.36 This study relies on Ilgen's shortfiber misrepresentations. The evidence presented in this paper illustrates only one example of how corporations have used sci ence to achieve profit growth and escape liability at the expense of dead and injured workers. David Egilman, MD, MPH Never Again Consulting Clinical Associate Professor Department of Community Health at Brown University 8 North Main Street Suite 404 Attleboro, MA 02703-2282 <degilman2@cs.com> Cell: 508-472-2809 Office: 508-226-5091 Fax: 425-699-7033 Megan Roberts, MES Never Again Consulting 8 North Main Street Suite 404 Attleboro, MA 02703-2282 <mroberts@egilman.com> Office: 508-226-5091 x14 References 1. Castleman BI. "Controlled use" of asbestos. Int J Occupl Environ Health. 2003; 9: 294-8. 2. Ilgren E, Chatfield E. Coalinga fibre: a short, amphibole-free chrysotile. Part 3: Lack of biopersistence. Indoor Built Environment. 1998;7:98-109. 3. Pinkerton K. Lung Reaction to Inhala tion of Three Types of Chrysotile Asbestos during the Lifespan of the Fis cher 344 Rat. PhD thesis, Duke Univer sity, Durham, NC, 1982. 4. Ilgren E, Chatfield E. Coalinga fibre: a short, amphibole-free chrysotile. Part 2: Evidence for lack of tumourigenic activity. Indoor Built Environment. 1998;7: 98-109. 5. Conwed Corporation v. Union Carbide Cor poration, Civil Action No. 5-92-88. Depo sition of Edward Ilgren. August 13, 1998. 6. Rhodes HB, Ingalls BL. Comparrison of Airborne Asbestos Concentrations-- Canadian and California Asbestos Based Ceiling Texture Sprays. Union Carbide Corporation Metals Division, New York, June 24, 1975. 7. Rhodes HB, Myers JL, et al. Informal Report 2196-64: The Occurrence of Ultra-Fine Fibers in "Calidria" RG-244 Asbestos Summary and Conclusions. August 24, 1978. 8. Ingalls BL, Kronkhyte RJ,et al. Internal Correspondence: Asbestos Dust Con trol Results of NIOSH Air Monitoring Survey of King City Bagging Room Operations. April 11, 1983. 9. Dodson RF, Atkinson MAL, Levin JL. Asbestos fiber length as related to potential pathogenicity: a critical review. Am J Ind Med. 2003;44:291-7. 10. Mellon Institute Special Report. The Fibrotic Potential of Asbestos Products via Intraperitoneal Injection in Guinea Pigs, Rats and Rabbits and by the Intra tracheal Route in the Rat. Confidential Report 29-55, July 8, 1966. 11. Dernehl CU to TJ Hall. Internal memo, Re: "Asbestos as a Health Hazard in the United Kingdom," June 7, 1967. 12. Mellon Institute Special Report 34-70. Calidria Asbestos-Resin Grade RG 244 Tracheal Insufflation of Rat Lungs with Interpretation of Pathology after 30, 60, 90, and 180 Days. Confidential Report 34-70, September 3, 1971. 13. Rhodes HB to DL Haywood. Reporting of "Health and Safety Studies to EPA" under TSCA Section 8(d) (4.3.12.2.2). November 29, 1982. 14. Ilgren E, Chatfield E. Coalinga fibre: a short, amphibole-free chrysotile. Part 1: Evidence for a lack of fibrogenic activity. Indoor Built Environment. 1997; 6:264-109. 15. O'Neil J, Pinkerton K, Crapo C. Lung Volume Changes in Rats Exposed to Chrysotile Asbestos (abstract). Am Rev Resp Dis 1981;123:146. 16. Suzuki Y, Kohyama N., Malignant mesothelioma induced by asbestos and zeolite in the mouse peritoneal cavity. Environ Res. 1984;35:277-92. 17. Suzuki Y. Carcinogenic and fibrogenic effects of zeolites: preliminary observa tions. Environ Res. 1982;27:433-45. 18. Rittinghausen S, Ernst H, Muhle H, Mohr U. Atypical malignant mesothe liomas with osseous and cartilaginous differentialtion after intraperitoneal injection of various types of mineral fibres on Rats. Exp Toxicol Pathol. 1992; 44:55-58. 19. Maltoni C, Minardi F.Recent results of carcinogenicity bioassays of fibres and other particulate materials. IARC Sci Publ. 1989; 90:46-53. 20. Maltoni C, Minardi F, Morisi L. The rel evance of the experimental approach in the assessment of the oncogenic risks from fibrous and non-fibrous par ticles. Med Lav. 1982; 4:394-407. 21. Langer AM, et al. Variation of proper ties of chrysotile asbestos subjected to milling. Jf Toxicol Environ Health. 1978 4:173-88. 22. Vorwald AJ, Durkan T, Pratt P. Experi mental Studies of Asbestosis. Archives of Industrial Hygiene and Occupa tional Medicine. 1931; 3: 1-28. 23. Charles R. Latham, et al vs. Garlock, Inc. et al. In the District Court Brazoria County, Texas 23rd Judicial District. Union Carbide Corporation's Responses to Plaintiffs' First Set of Interrogatories and Requests for Pro duction, 2001. 24. Worker #360, UCASB07005868. 25. Original death certificate of Paul Whit lock. 1/3/91.UCASB07006991. 26. Myers JL. Internal correspondence. UCASB07008154-UCASB07008160. 27. Revised death Certificate of Paul Whit lock. June 14, 1991 (date issued). UCASB07006994. 28. Coroner's amendment to revised death certificate. June 14, 1991 (date issued). UCASB07006995. 29. Cause No. 19785-BH02; Kelly-Moore Paint Company, Inc. v. Dow Chemical Com pany, et al.; in the 23rd Judicial District Court of Brazoria County. Deposition ofJohn L. Myers taken July 29, 2003. 30. County of Santa Clara Office of the Medical Examiner-Coroner. Report of Autopsy completed by Angelo K. Ozoa, MD, at the Santa Clara County Morgue. January 9, 1991. UCASB07006996- UCASB07007000 31. Lewinsohn HC. A Review of Chest Radiographs of Calidria Corporation Employees on 12/12/84. Full Report: UCASB07100000-UCASB07100329. Specific Reference: UCASB07100009, p. 10. 32. Lewinsohn HC. A Review of Chest Radiographs of Calidria Corporation Employees on 12/12/84. Full Report: UCASB07100000-UCASB07100329. Specific Reference: UCASB07100011, p. 12. 33. Kelly Moore Paint Company, Inc., vs. Dow Chemical Company et al, No. 19785- BH02 Deposition of George Navarro, December 9, 2003. 34. Dow Chemical. The Use of Asbestos as a Thixotrope in Derakane Applica tions. October 16, 1974. 35. Smith M (Manager of Technical Divi sion, Castor Oil Co.) to J Gallagher, Dupont. July 5, 1972. 36. Asbestos Institute. Conclusive results from a study by international scientists-- Quebec chrysotile proven to be far less hazardous. Canada NewsWire: Sept.9, 2003. <http://www.finance.lycos.com/ qc/news/story.aspx?symbols=CCN:100 &story=35624326>. VOL 10/NO 1, JAN/MAR 2004 www.ijoeh.com Letters 103 Occupational Histories of Cancer Patients in a Canadian Treatment Center and the Generated Hypothesis Regarding Breast Cancer and Farming To the Editor.--We commend Mr. Brophy and his colleagues for their recent article examining the rela tionship between farming and breast cancer.1 The article focuses attention on occupationally related cancer, an area of research that is relatively understudied. Although the proportion of cancer attributable to occupational exposure is much smaller than those attributable to other known risk factors for cancer (e.g., smok ing and diet), knowledge regard ing the relationships between exposures to hazardous agents at the workplace and their roles in the carcinogenic process is invalu able to many workers in Ontario. Unfortunately, the scientific evi dence available to date, particu larly in relation to farming and cancer, remains inconclusive. A recent study conducted by Brophy and colleagues reported an increased risk of breast cancer in women associated with a previous history of farming for more than a year before age 56 compared with women with no previous farming history (OR = 9.05, 95% CI, 1.06 77.43). This estimate is based on a convenience sample of cancer patients from the Windsor Regional Cancer Centre. While the article suggests a number of interesting hypotheses, dependence on the convenience sample, small sample size, and the inadequate control of potential confounders limits the interpretability of study conclusions. Duell and colleagues2 conducted a large population-based study of farming and breast cancer in North Carolina, comparing 862 cases with 790 population controls. Unlike the Brophy study, the Duell study did not observe an increased risk for breast cancer associated with farming in general. The risk esti mates obtained from the Duell study had been adjusted for poten tial confounders such as age at diagnosis, age at menarche, race, education, smoking, family history of breast cancer, and body mass index, among others. Recently, an agriculture job-exposure matrix was developed for British Columbia farmers.3 This approach can pro vide more accurate historical esti mates of specific exposures, thereby reducing misclassification and subsequent bias in estimates of cancer risks. It is likely that the het erogeneity of study results in the lit erature can be attributed in part to variations in sampling methods, measurements, and adjustments of potential confounders. With the limited current body of evidence, it is difficult to determine whether farming activities are asso ciated with breast cancer. With appropriate study design and analy ses, these hypotheses could poten tially translate into scientific knowl edge invaluable to all stakeholders. Minh T. Do, MSc Division ofPreventive Oncology Cancer Care Ontario 620 University Avenue Toronto, ONM5G 2L7 Canada Telephone: (416) 971-5800 Fax: (416) 971-6888 E-mail: <minh.do@cancercare.on.ca> and Members of the Occupational Cancer Research and Surveillance Project References 1. Brophy JT, Keith MM, Gorey KM, et al. Occupational histories of cancer patients in a Canadian cancer treatment center and the generated hypothesis regarding breast cancer and farming. Int J Occup Environ Health. 2002; 8:346-53. 2. Duell EJ, Millikan RC, Savitz DA, et al. A population-based case-control study of farming and breast cancer in North Car olina. Epidemiology. 2000; 11:523-31. 3. Wood D, Astrakianakis G, Lang B, Le N, Bert J. Development of an agriculture job-exposure matrix for British Colum bia, Canada. J Occup Environ Med. 2002; 44:865-73. In reply:--Do and colleagues at the Occupational Cancer Research and of the Surveillance Project of Cancer Care Ontario raise several issues regarding our study of breast cancer and farming,1 including some of the acknowledged limita tions of the study and our interpre tation of the study by Duell et al.2 Because the incidence of female breast cancer has been rising steadily by about 1% annu ally over the last 30 years through out the industrialized world, including Canada, this disease should be regarded as an unsolved public health crisis. The crisis is made more profound not only because the majority of breast cancer cases cannot be explained by known risk factors,3,4 but also because relatively few epidemio logic studies have scrutinized the potential occupational breast cancer risks in general and for farming in particular,5 and few new hypotheses have been proposed and incorporated into studies. For example, animal bioassays have identified over 200 chemical sub stances that trigger breast carcinogenesis6-8 but although such agents exist in high concentrations in many workplace environments, their influences on breast cancer incidences among exposed workers remain largely unstudied. Traditional toxicology and epi demiology are being challenged by 104 Letters www.ijoeh.com INT J OCCUP ENVIRON HEALTH a new synthesis leading to new hypotheses, particularly regarding possible associations between pre natal exposures to agricultural chemicals and predisposition to cancer.9 Increasing evidence is emerging from epidemiologic investigations and from laboratory research of an association between breast cancer and xenoestrogens; i.e., endocrine disruptors.10 Some organochlorine pesticides, which "mimic" estrogens, are hypothe sized to contribute to the prolifera tion of damaged cells, thus promot ing the neoplastic process.11 The herbicide atrazine is one of the most widely used agricultural pesti cides. In animal studies, exposure to atrazine in utero delays mam mary gland development and "may also confer an extended window of sensitivity to potential carcinogens after sexual maturity."10 The Windsor Regional Cancer Centre was the first local cancer treatment center in Ontario to par ticipate in a program to track the occupational histories of its patients. Our original intention was not to study breast cancer and occupation, but rather to collect data on the occupational histories of all cancer patients. The breast cancer cases made up the largest proportion of the participating cohort, providing an adequate sample size with which to conduct data analysis. As this study was designed to capture limited data from a wide range of cancer patients, data regarding a few of the risk factors specifically identified with breast cancer were unavail able. We therefore suggested, based on our findings, that a more focused study was necessary, and funding was secured for a subse quent case-control study that did control for such risk factors. The Duell et al. study2 pre sented a complex picture of the associations between farming and breast cancer risk in women with and without pesticide exposure that supports our conclusions. The odds ratio was below that expected for farming women when analyzed without controlling for pesticide exposure or the use of protective equipment. However, women who reported being present in the fields during or shortly after pesticide application had an 80% increased risk of developing breast cancer (OR 1.8, 95% CI 1.1-2.8). Among those who reported using pesti cides without protective clothing, there was a twofold excess breast cancer risk (OR = 2.0, 95% CI 1.0-4.3), while women with protec tive clothing had a lower-thanexpected risk (OR = 0.8, 95% CI 0.4-1.8). Duell et al. conclude that while farming may not present an elevated risk per se, farming women exposed to pesticides may have an elevated breast cancer risk (p. 329). This reaffirms the weak ness in using occupation as a surro gate for exposure, since misclassification of exposure occurs when subjects with less exposure are aggregated with the more highly exposed. Such non-differential misclassification decreases the proba bility of detecting associations12,13 and tends to underestimate the actual risks. In addition, Band and col leagues have recently reported the findings of a possible elevated breast cancer risk among farmers through a comprehensive popula tion-based case-control study utiliz ing the British Columbia Cancer Registry.14 The authors sought to investigate occupations while con trolling for known or suspected hormonal risk factors. Women were stratified by pre- and post menopausal status as well as by both combined. Among the com bined pre- and post-menopausal group, there was a threefold ele vated breast cancer risk among women ever employed in fruit and other vegetable farming (OR = 3.11, 90% CI 1.24-7.81); there was a sevenfold elevated breast cancer risk among women ever employed in other vegetable farming (OR = 7.33, 90% CI 1.16-46.2). The authors conclude: Several significant associations observed only in the combined group of pre- and post menopausal women (in part owing to larger numbers) are of substantial interest, particularly those in crop farming and in the fruit and vegetable, publishing and printing, and motor vehicle repair industries. Farmers are exposed to pesticides, com pounds suspected of being associ ated with an increased breast cancer risk, whereas the other occupations and industries entail exposure to various solvents and to carcinogenic substances such as aromatic amines in the print ing and polycyclic aromatic hydrocarbons in the motor vehi cle repair industries (p. 309). While Do and colleagues acknowledge that understanding the etiology of occupationally related cancer is "invaluable" to Ontario workers, they somewhat arbitrarily assign the attributable risk of occupational exposures to a much less prominent place than such personal "lifestyle" causes as smoking and diet. Confidence in this hypothesized hierarchy of cancer causality may be misplaced, since no Canadian Cancer Agency, including Cancer Care Ontario, has begun to systematically collect or analyze the occupational histories of cancer patients. Given the parsi mony of epidemiologic studies regarding occupational cancer risk factors, I believe that, as Doll and Peto15 suggested more than 20 years ago, it is "impossible to make precise estimates of the proportion of the cancers today that are attrib utable to hazards at work." It might be more useful to acknowledge that our current state of knowledge does not allow us to confidently link cancer incidence to any one specific factor; it is more likely, given the current evidence, that it is related to a variety or combina tion of factors, including environ mental, occupational, genetic, lifestyle, and socioeconomic16 fac tors that should all be included in future epidemiologic studies. VOL 10/NO 1, JAN/MAR 2004 www.ijoeh.com Letters 105 This lack of scientific consensus about the causes of breast cancer has profound implications for this crisis in public health and for for mulating comprehensive preventive strategies that could include protec tion from occupational and environ mental exposures to carcinogenic and hormonally disrupting agents. Researchers, cancer agencies, and public health institutions with the goal of cancer prevention are urged to use their influence to actively sup port research efforts designed to explore links between environmen tal exposures and breast cancer risk. James T. Brophy Adjunct Lecturer Department of Sociology and Anthro pology University of Windsor 401 Sunset Avenue Windsor N9B 3P4 Ontario Canada <jimbrophy@sympatico.ca> References 1. Brophy JT, Keith MM, Gorey KM, et al. Occupational histories of cancer patients in a Canadian cancer treatment center and the generated hypothesis regarding breast cancer and farming. Int J Occup Environ Health. 2002; 8:346-53. 2. Duell EJ, Millikan RC, Savitz DA, et al. A population-based case-control study of farming and breast cancer in North Caro lina. Epidemiology. 2000; 11:523-31. 3. Health Canada. Summary Report: Review of Lifestyle and Environmental Risk Factors for Breast Cancer. Minister of Public Works and Government Ser vices, Canada, 2001. 4. Madigan MP, Siegler RG, Benichou J, Byrne C, Hoover RN. Proportion of breast cancer cases in the United States explained by well-established risk fac tors. J Natl Cancer Inst. 1995; 87:1681-5. 5. Aronson KJ, Howe GR. Utility of a sur veillance system to detect associations between work and cancer among women in Canada, 1965-1991. J Occup Med. 1994; 36:1174-9. 6. Brody JG, Rudel RA. Environmental pollutants and breast cancer. Environ Health Perspect. 2003; 111:1107-19. 7. Brown NM, Lamartiniere CA Xenoestrogens alter mammary gland differentia tion and cell proliferation in the rat. Env iron Health Perspect. 1995; 103:708-13. 8. Stevens JT, Breckenridge CB, Wetzerl LT, GillisJH, Luempert LG, EldridgeJC. Hypothesis for mammary tumourigenesis in Sprague-Dawley rats exposed to certain triazine herbicides. J Toxicol Environ Health. 1994; 43:139-53. 9. Colborn T, Short P, Gilbertson M. Health effects of contemporary-use pes ticides: the wildlife/human connection. Toxicol Ind Health. 1999; 15(1-2):1-257. 10. Birnbaum LS, Fenton SE. Cancer and developmental exposure to endocrine disrupters. Environ Health Perspect. 2003; 111:389-94. 11. Degen GH, Bolt HM. Endocrine dis rupters: update on xenoestrogens. Int Arch Occup Environ Health. 2000; 73:433-41. 12. Blair A, Linos A, Stewart PA, et al. Eval uation of risks for non-Hodgkin's lym- phoma by occupation and industry exposures from a case-control study. Am J Ind Med. 1993; 23:301-12. 13. Checkoway H, Pearce NE, CrawfordBrown DJ. Research Methods in Occu pational Epidemiology. New York: Oxford University Press, 1989. 14. Band PR, Spinelli JJ, Threlfall WJ, Fang R, Le ND, Gallagher RP. Identification of occupational cancer risks in British Columbia. Part I. J Occup Environ Med. 1999; 41:224-32. 15. Doll R, Peto R. Avoidable Causes of Cancer. Oxford, U.K.: Oxford Univer sity Press, 1981. 16. Davis DL, Pongsiri M, Wolff M. Recent developments on the avoidable causes of breast cancer. Ann NYAcad Sci. 1997; 837:513-23. Is Sleep a Priority for Yourself or Your Research? To the Editor:---Just how effective is a daytime nap or siesta in improving work performance? Should a nap be requiredfor the night shift worker? How does chronotype affect work productiv ity? Can sleeping longer on weekends eliminate weekly sleep debt? If you cannot answer these few simple questions, you can relax-- we actually know very little about sleep and how it impacts health and safety. If you ever worked a night shift, or missed a night of sleep for any reason, you would be well aware of how it can affect your judgment, your daytime function ing, and your quality of life. The public's health and safety are also at risk from those who drive trucks and automobiles while drowsy and deprived of adequate sleep. To a certain extent, medication errors and work-related injuries can also be blamed on sleep debt. The 2003 Sleep Research Plan, recently approved by the National Center on Sleep Disorders Research, contains priorities for sleep research that would be of interest to researchers in occupa tional health and safety. This Center, located within the Heart, Lung and Blood Institute (NHLBI) at the National Institutes of Health (NIH) in the United States, released its original research plan in 1996. A task force of interdisci plinary sleep experts recently updated research priorities for the next five years, and the plan is avail able at the following NIH Web site: <http://www.nhlbisupport.com/ sleep/research/research-a.htm>. The 2003 Sleep Research Plan specifies ten priority areas, all of equal importance, for research during the next five years. One pri ority is the need for more training in sleep medicine, but other priori ties are detailed for both basic and clinical research. Occupational health researchers will be interested in reading more about the priority for understanding the impact of sleep deprivation on work perform ance and safety (see pages 55-58 of the document). Sleep debt, defined as sleeping less than six hours a day, has become a major health concern in the United States1 and in other industrialized nations.2 Concerns include cumulative sleep debt and its detrimental effects on cognitive functioning over time,3 accidents 106 Letters www.ijoeh.com INT J OCCUP ENVIRON HEALTH and errors in the workplace, and alterations in metabolic and endocrine function.4 The best prescription for ade quate amounts of sleep at different stages of life remains unknown, effects of chronic sleep debt are poorly understood, and the timing and effectiveness of naps or siestas during the day require further study. If you are not accounting for all the variance in your outcome of interest, perhaps it is time to con sider adding sleep quality and quantity measures to your occupa tional research endeavors. A visit to the NIH Web site will help you learn more about the need for research in this area. Kathryn A. Lee, RN, PhD, FAAN Research Advisory Board Member National Center on Sleep Disorders Research, Heart, Lung, and Blood Institute Department of Family Health Care Nursing Box 0606, N411Y University of California, San Francisco San Francisco, CA 94143-0606 Telephone: (415) 476-4442 E-mail: <kathy.lee@nursing.ucsfedu> References 1. National Sleep Foundation. Sleep Survey. Washington, DC, 2001. <www. sleepfoundation.org>. 2. Bjorkelund C, Bengtsson C, Lissner L, Rodstrom K. Women's sleep: longitudi nal changes and secular trends in a 24year perspective. Results of the popula tion study of women in Gothenburg, Sweden. Sleep. 2003; 25:894-6. 3. Doi Y, Minowa M, Tango T. Impact and correlates of poor sleep quality in Japan ese white-collar employees. Sleep. 2003; 26:467-71. 4. Spiegel K, Leproult R, Van Cauter E. Impact of sleep debt on metabolic and endocrine function. Lancet. 1999; 23: 1435-9. Bhopal Priorities To the Editor.--One of the argu ments that Carlsten1 makes for giving priority to the prevention of Bhopal-type accidents over further research on its victims is that too much time has passed and that con founding factors and recall bias may limit the validity of any research studies. While this is certainly true, we do not believe that it is an insur mountable barrier. Very large num bers of people in Bhopal (probably over 200,000) continue to experi ence persistent symptoms; this alone should warrant further popu lation-based research. Further more, and crucially, there has been no research focusing on those who were children at the time of the dis aster. Studies conducted in 1994 by the International Medical Commis sion on Bhopal addressed a number of the epidemiologic issues raised by Carlsten. For example, using a cross-sectional method, we found that by stratifying the cur rent adult population by distance of residence from the Union Car bide plant to estimate exposure to the gas cloud, we could also control satisfactorily for confounding by various environmental factors such as air pollution and for socioeco nomic factors.2 We were also able to develop individual exposure esti mates associated with subjective and objective measures of ill health.3 These methods were rapid, cheap, and effective. A large cohort of exposed and unexposed persons is still being examined periodically by the local government. Limitations of this effort include the relatively few health end points being studied, and that the results are not being widely disseminated. However, we believe that this effort can be expanded given the resources and commitment of personnel. In a recent meeting, Dr. N. K. Ganguly, Director General of the Indian Council of Medical Research, indi cated that enough funds are avail able for research projects in Bhopal. While prevention of industrial accidents is certainly paramount, we believe that valid research can and should continue to be done for the Bhopal gas victims. V. Ramana Dhara, MD, ScD 3200 Hampton Ridge Way Snellville, GA 30078 E-mail: <rdhara@aol.com> Paul Cullinan, MD International Medical Commission on Bhopal References 1. Carlsten C. The Bhopal disaster: pre vention should have priority now. Int J Occup Environ Health. 2003; 9:93-4. 2. Cullinan P, Dhara VR, Acquilla SD. Res piratory morbidity 10 years after the Union Carbide gas leak at Bhopal. BMJ. 1997; 314:338-43. 3. Dhara VR, Dhara R, Cullinan P, Acquilla SD. Personal exposure and long-term health effects in survivors of the Union Carbide disaster in Bhopal. Environ Health Perspect. 2002; 110:487-500. VOL 10/NO 1, JAN/MAR 2004 www.ijoeh.com Letters 107