Document a444qep28p4g5eV0ozVXXKZd9

AFFIDAVIT OF DAVID EGILMAN STATE OF MASSACHUSETTS COUNTY OF Before me, the undersigned authority, personally appeared Dr. David Egilman and swore as follows: 1. My name is Dr. David Egilman. I am over the age of twenty-one years old and am otherwise competent to make this affidavit. All of the statements contained in this affidavit are based upon my personal knowledge and are true and correct. 2. I am a medical doctor and Clinical Associate Professor of Community Medicine at Brown University. I am board certified in Internal Medicine and PreventiveOccupational Medicine. My curriculum vita sets forth more fully my qualifications. 3. I received a Bachelor of Science from Brown University in Molecular Biology in 1974. I received a medical degree from Brown University in 1978. I completed a three-year medical residency in Internal Medicine at Strong Memorial Hospital in Rochester, New York, in 1981. I completed a three-year training program in epidemiology, called the National Institutes of Health Epidemiology Training Program, in 1984. As part of this program, I completed a Master's in Public Health at the Harvard School of Public Health. At Harvard, I studied epidemiology, statistics and occupational medicine, industrial hygiene, warnings and occupational and environmental law. I completed a third residency in preventive medicine in 1994. 4. I served two years at the National Institute for Occupational Safety & Health (NIOSH), designing and conducting small and large epidemiologic studies. I was responsible for interpreting and implementing aspects of the OSHA act of 1971. 5. Since 1978, I have published a variety of letters and medical articles on the issues that relate to the manner in which cause-effect determinations are made in medicine (the epistemology of medicine). I have discussed the normal, accepted process of causal determination in medicine in several peer-reviewed articles. In addition, these ideas were accepted for presentation and were presented at the American Public Health Association meetings in 1984. I have also studied, taught, and published articles on the history of medical ethics and the duty to warn. I have taught and done research on the history ofthe development of medical and corporate ethics during the 20th century. I have on two occasions, testified before congressional committees on the issue ofmedical ethics and corporate responsibility. My testimony concerned the history of informed consent. In addition, I have published two papers on the topic of the history of the development of medical ethics. 6. For the past eight years, I have taught a course at Brown University, called the Development ofMedical and Scientific Knowledge in the 20th Century. This course deals specifically with the issues outlined in this report: the history of the development of knowledge of the health effects of asbestos including corporate knowledge, the history of the development of government regulations on occupational and environmental safety, and the history of the development of product warnings. My views on medical epistemology have been cited by the Massachusetts Supreme Court and been adopted by the Wyoming Supreme Court. I have also published on these topics. I served as guest faculty, at the Appellate Judges Seminar Series, on issues related to medical epistemology and Daubert. I have testified on the issues discussed in this report in over sixty cases over the past 16 years. I have also testified twice before Congressional subcommittees. 7. My qualifications and opinions are also based in part on my clinical experience and awareness of the ways that normal physicians in normal medical practice make decisions about causal relationships that affect patients' lives every day. Much of my time is devoted to direct patient care and consulting for corporations. I served as an expert on state ofthe art issues at the request ofboth injured workers and companies. I have retainer agreements to consult on a variety of issues with several asbestos product-manufacturing companies including gasket manufacturers Flexitallic and Crane. 8. In the course of doing research, publishing peer reviewed papers, my corporate consulting in occupational and environmental health and teaching courses, I base my opinions on the following sources of information: Review of medical literature o Medical journal articles o Medical meetings o Medical textbooks o In order to review medical literature, I conducted computer searches of several different databases including: Index Medicus NIOSHtic EPA Cancer Lit MedLine o In addition, my staff or I reviewed each issue of Index Medicus from 1910 through 1966. (Index Medicus was computerized from 1964 forward and was reviewed by computer following this.) Review of corporate documents o I have reviewed corporate documents from several asbestos corporations and their insurers. Most of these documents were exhibits in toxic tort litigation and were supplied as part ofthe discovery process. In addition, I have visited several corporate document repositories to review corporate documents that 2 are available as part of the discovery process, including memoranda. o Company meetings and correspondence o Internal company medical studies o Information from workers' compensation insurance companies o Workers Compensation Claims o Warnings labels and warnings policies Visits and reviews of libraries o General publications o Trade publications o Public libraries' general information o Special research collections in libraries o Organizational and Association Minutes and Documents ACGIH (American Conference of Governmental Industrial Hygienists) Manufacturing Chemists Association (MCA or CMA) American Petroleum Institute (API) Railroads AEC and DOE Health & Safety Policies IHF (Industrial Hygiene Foundation) National Safety Council (NSC) Asbestos Textile Institute (ATI) Friction Materials Standards Institute (FMSI) Quebec Asbestos Mining Association (QAMA) Thermal Insulation Manufacturers Association (TIMA, MIMA or NIMA) Gypsum Products Association o Special libraries and collections Vorwald Archives Saranac Lake Laboratories Drinker Collection at the Harvard School of Public Health Mellon Institute Documents Interviews or deposition reviews of historical figures. o Corporate personnel o Product users o Kenneth Smith o Gerrit Schepers o Harriet Hardy o Clark Cooper o Mort Corn o Bill Burgess o E. Lynn Schall o Thomas Mancuso o Industrial Hygiene Personnel Interviews and/or medical examinations of workers I have been qualified in state and federal court to testify about: o Development and implementation of occupational exposure limits 3 o History of industrial hygienic practices o Occupational health and safety standards throughout the century o Warnings o Comparison between differing corporate approaches to health and safety problems and public health standards relating to these problems 9. I have studied the medical literature pertaining to occupational and non-occupational asbestos exposure and all of the disease inherent to such exposure including pleural abnormalities, asbestosis, lung cancer, gastro-intestinal cancer and mesothelioma. I have also reviewed articles relating to the evolution of medical knowledge of asbestos-related conditions. 10. I have reached the conclusions stated below to a reasonable degree of medical probability based on my review of the medical and scientific literature and based on my years of training and clinical experience. 11. I have performed an evaluation of asbestos brake manufacturing at the GM Inland division, Dayton Ohio. 12. I have served as a consultant to several brake manufacturing companies. Brakes and asbestos: In the United States, companies first developed and sold woven asbestos friction materials around the turn ofthe twentieth century. In the early 1920s companies began to manufacture and promote molded brake linings and by 1940, virtually every automobile was equipped with them. A decade later, companies began to switch to disc (metallic/non-asbestos) brakes, and by 1975 virtually all newly manufactured U.S. cars contained front disc brakes. However, drums continued to be used on rear brakes. Manufacturers used chrysotile asbestos for brake linings almost exclusively because amphibole asbestos tended to score the brake drums, decreasing their useful life. Bendix used amosite asbestos in some products. Asbestos constituted 40 to 50 percent of the brake linings. The health effects of asbestos on human beings are related to the inhalation of asbestos dust. Since 1930 it has been recognized that asbestos dust was a hazard wherever visible dust could be seen. As stated by Merewether in 1930, "If there is visible asbestos dust, then the invisible dust is in dangerous concentration." The protective measures necessary to prevent asbestos induced disease did not differ according to the type of disease asbestos might produce: asbestosis, lung cancer, mesothelioma or other malignancy. A company that protected its work force against any asbestos induced disease would have protected its work force against all asbestos induced diseases. 4 Since the beginning of this century the protective measures that a company should take to protect its workforce from exposures to toxic dust have included: Warning workers of adverse health effects and the means to avoid them Instructing workmen on hazardous substances and giving out warning leaflets Repeating instructions frequently Posting warnings and providing constant supervision of working conditions Maintaining a clean workplace and effective ventilation Arresting dust at place of origin to prevent entrance to the nose and mouth Using less dangerous processes (substituting safer materials for more hazardous materials) Providing showers and separate lockers for street and work clothing, and frequent cleaning of clothing Periodic medical examination of the workers If implemented, these measures would also protect spouses and children from exposure to toxic substances that might be brought home on workers' clothes. It was reasonably foreseeable that this could occur from at least 1930. It was also known at this time that respirators provided workers with a false sense of security and the use of respirators was not a substitute for effective prevention of dust creation and ventilation. In 1934, Gurney and Beyer delivered a paper to the National Safety Council (NSC) addressing this fact; the NSC then published the paper.1 One year later, chemists Brown and Yant presented a paper to the NSC highlighting specific shortcomings of existing respirators.2 "'Household" Exposure Risk In the decades that followed, researchers and asbestos manufacturers began to recognize that the dangers of asbestos extended even beyond manufacturing and servicing facilities. In 1964, Newhouse and Thompson prepared a paper on the health effects of asbestos in people who were exposed in the apparent safety oftheir own houses, from asbestos that was carried home on the clothing of their spouses. The authors presented this paper at a meeting that was sponsored, organized, and run by Dr. Selikoff of Mt. Sinai Hospital in New York City. The knowledge of home risk was so well accepted at Mt. Sinai that physicians at Mt. Sinai wrote about the risk to inform union members ofthe need to shower before they went home. 5 In 1966, Selikoff's views were published in a widely circulated NY Times wire service article written by Jane Brody: Asbestos potential cause of cancer. "The report very strongly suggests that those who work with asbestos have a better than 50% chance of dying of cancer..." Attached article: Brody NY Times Article "The dangers, he said [Dr. Selikoff], extend to workers in `contiguous trades,' such as other construction workers and their families." In his 1967 paper, Lieben (the head of occupational health for the state of Pennsylvania) reported on mesothelioma in three relatives of asbestos workers and in eight individuals who lived or were employed in the vicinity of an asbestos factory. The New Yorker in turn reported on the "household" or bystander exposures reported by Lieben, Newhouse and Thompson on October 12, 1968. The first government regulations to deal specifically with asbestos health effects came into effect in 1972 and specifically required the use of change rooms, shower facilities, and the specific bagging and labeling of asbestos laden clothing. More importantly, once it was recognized in the 1920's that asbestos was toxic, it was known that as a general rule that this dust should not be brought home to contaminate family members. Bendix Knowledge ofBrake Hazards Asbestos-free brakes were used and available as early as 1936. However, in spite of this and despite awareness of the deadly, far-reaching effects of asbestos dust, Bendix did not develop asbestos-free brakes until the 1950s. I have reviewed certain documents produced or otherwise discovered in asbestos litigation for the purpose of assessing the historical knowledge available to Bendix concerning the hazards of exposure to asbestos and how that knowledge compared or related to the information available in the open medical literature. In addition I have interviewed Murray Finkelstein concerning his communications with Bendix that relate to asbestos health hazards. In 1934 Osborn reported that grinding molded asbestos produced exposures above the TLV. 6 By 1939 Bendix knew or should have known that exposures to asbestos during use of brake products resulted in exposures above 10 mppcf because General Motors Company1 conducted and published a study warning of the dangerously high exposures produced during brake installation and routine servicing.3 The study also revealed the inadequacy of ventilation systems to contain the vast quantity of dust generated in these operations, citing measured "concentrations.. .greatly in excess of the permissible limits."4 In 1948 General Motors industrial hygienist V. Castrop published an article that emphasized asbestos health hazards during asbestos product use and control measures.5 "Asbestos used in the formulation ofbrake lining is a potentially harmful compound. This material is the offending agent in the production of the lung ailment known as asbestosis . . . Dust exposures to asbestos and other ingredients of the brake lining exist . . . in the subsequent operations of slitting, grinding, or surfacing." A great quantity of other medical literature on brakes hazards and related issues was also published and available; the following tables summarize the key points from a selection of these articles: Brake lining Manufacture Date Citation Findings 1935 Lanza, McConnell, High prevalence of asbestosis among workers with "more than 3 1 Bendix was controlled to varying degrees by General Motors before and during WWII. Originally, when Bendix purchased Eclipse Machine (1928) they inherited a substantial relationship with GM (Eclipse's largest customer for starter drives). In 1928, through GM's acceptance of 6.8 million dollars in notes, Bendix bought a majority interest in the Eclipse Machine Company. The Eclipse 'Machine Co.' operation was originally the Bijur Motor Appliance Co. of Hoboken, NJ. Bijur was purchased by Eclipse (then in East Orange, NJ) in 1923. Prior to this purchase, Bendix had established a relationship with Eclipse beginning in 1914. Under the agreement, Eclipse (then a struggling motorcycle, bicycle brake and general automotive parts manufacturing firm) was given exclusive rights to manufacture the Bendix starter drive. Eclipse was a stolid conservative operation and was reluctant to deal with Bendix directly because of Vincent Bendix's flamboyance. Since GM was Bendix's second largest customer (for the starter drive), they (GM) agreed to act as Bendix's agent in the transaction. Bendix's formal relationship with GM began in 1929 when GM acquired 25% interest in Bendix Aviation Corp. For this acquisition, GM received 500,000 shares for $15,000,000 in cash. Bendix received the assets of Delco Aviation Corp. and the right to grant licenses for aviation purposes through GM patents and inventions (exclusive for 5 years and non-exclusive for thereafter) together with other licenses. Bendix at that time had about 25% of the world market for brakes. Like many companies before the depression, Bendix was expanding in many automotive directions. This expansion during a period of contracting world markets led GM, which held 25% of Bendix by 1937 to reorganize the company. Vincent Bendix himself was a poor businessman and managed to usher himself into personal bankruptcy. CE Wilson served on the Bendix board while he ran the GM Delco division, which made GM brakes. By 1942, he had to resign from the company chairmanship and Ernest Breech was installed by GM. Breech resigned as a GM vice president and became president of Bendix. Breech overhauled the company after moving it to Detroit (closer to GM), but left as the war closed at a time when defense contracts were plummeting. Malcolm Ferguson (also GM) replaced Breech. By the early 60's Ferguson managed to increase their business through acquisition of Government contracts estimated as approximately 80% of their total. They continued to do other civilian automotive things (primarily through acquisition of companies like Fram and Autolite). 7 Date 1935 1939 1940 1940 Citation Fehnel. "Effects of inhalation of asbestos dust on the lungs of asbestos workers" Publ. Health. Rep. 50:1-12 Fulton, et al. Asbestosis. Harrisburg, Penn.: Dept of Labor and Industry, Commonwealth of Penn. George, A.W., R.D Leonard. "An X- ray study of the lungs of workmen in the asbestos industry covering a period of ten years" Radiology 33:196-209 Stone, M.J. "Clinical Studies in asbestosis" Amer. Rev. Tuberc. 41: 12-21 Stone, MJ. "Studies in asbestosis." Dis. Chest. 6: 170-171 Findings years of employment in the industry" at five plants including one where molded brake band and clutch friction materials were manufactured Report of 25 percent prevalence of asbestosis among selected workers at four asbestos fabricating plants, including three where brake linings were manufactured. Documents asbestosis in brake lining manufacturing workers since 1928, with compensation. Explains that the asbestosis cases seen by Hawes (New Engl. J. Med. 216:162-165, 1937) were brake lining manufacturing workers. Discusses switch from dry to wet methods of processing. Asbestosis in 148 brake-lining manufacturing workers seen by Drs. Stone and Hawes. Asbestosis in 148 brake-lining manufacturing workers seen by Drs. Stone and Hawes. 8 Grinding and Drilling Brake Linings--Early Papers Date Citation Findings 1934 Osborn. Forty-Ninth Describes the grinding of molded asbestos brake and clutch Report of the State parts under varying degrees of local exhaust ventilation. Total Department of dust counts ranged from 0.6 to 17 MPPCF. The need for dust Health, State of sampling and analysis to evaluate these exposures was stressed, Conn. Public as the visual appearance of the worst grinding exposure was Document No. 25, unremarkable. Hartford, CT. pp. 507-511 1935 Memorandum on Lists under "Industries and Processes in which asbestosis the Industrial occurs...the sawing, grinding, and turning in the dry state of Diseases of Silicosis articles composed wholly or partly of asbestos such as motor car and Asbestosis. brake and clutch linings..." London: H.M. Stationery Ofc. 1939 Case, L.B. "Air Use and servicing of brake products produced exposures greatly Hygiene Studies." exceeding permissible limits. General Motors 1940 Brachmann. Clinical and X-ray examination showed asbestosis in nearly all "Asbestosis in workers employed 5 years or more as grinders and drillers of grinders and drillers brake linings. of brake bands" Arbeitsschutz 172 174 1941 Brachmann. Clinical and X-ray examination showed asbestosis in nearly all Abstract in workers employed 5 years or more as grinders and drillers of "Abstracts" brake linings. supplement to J. Indust. Hyg. Tox. 23:76-77 Feb. Castrop, V.J. "Fume By General Motors industrial hygienist. Section on asbestos noted 1948 and dust exposure" that brake lining grinding and "surfacing" operations were Nat. Safety News. equipped with local exhaust ventilation Systems. 1957 Thomas, D.L.G. The following occupations (involve asbestosis hazards)...sawing, "Pneumokoniosis in cutting and finishing any product containing asbestos--for Victorian Industry" example, brake linings, asbestos sheeting, and various insulating Med. J. Australia materials... 1:75-77 1963 Patty, F.A. Written by former director of Industrial Hygiene Dept., General Industrial Hygiene Motors. and Toxicology, New York: "The sawing, filing, drilling, and grinding of brake linings is Interscience (2d ed.) ordinarily well controlled... It is desirable in asbestos exposures pp. 2243-2244 to keep the dust count down to 5 million particles, or less, per 9 Date Citation 1968 1969 Lynch, J.R. "Brake Lining Decomposition Products" National Center for Urban and Industrial Health Vol. 18 No. 12 Hickish, D.E. and Knight, K.L. "Exposure to Asbestos During Brake Maintenance" Ann. Occ. Hyg Vol. 13 pp.17-21 Findings cubic foot of air." "The dust produced by the abrading operations in asbestos friction product factories (figure 1) contains free asbestos fibers that are similar to those in industries where cancer is known to be in excess." Paper presented at conference held at the Central Office of Ford Motor Company. "Our environmental studies have not included maintenance procedures which involve the filing or grinding of brake lining material, and we would envisage that these would give rise to considerably increased air contamination by chrysotile asbestos, with the attendant need for strict precautions to prevent the inhalation of fibres." 10 Compensation Date Citation 1965 McVittie, J.C. "Asbestosis in Great Britain" Ann. NY Acad. Sci. 132:129-138 1979 Smither. "Surveillance of High-Risk Groups - A Survey of Asbestos Workers: The Present Position in the UK" Ann. NY Acad. Sci. 330: 525-532 Findings Describing the occupations ofworkers diagnosed with asbestosis (and compensated for disability) in the years 1955-1963, he lists "brake lining" workers with an average of 14 years' exposure. Updates McVittie's figures through 1969, showing that the four U.K. Pneumoconiosis Panels diagnosed 10 cases of asbestosis in "brake lining" workers in the years 1963-1969. 11 Asbestos Air Pollution Hazard from Brake Wear Date Citation Findings 1963 Thomson, J.G., Expresses fear of public cancer hazard from asbestos released into R.O.C. Kaschula, the air of cities by brake wear. and R.R. MacDonald. "Asbestos as a Modern Urban Hazard," S. Afr. Med. J. 37:77-81 1963 "Pulmonary Editorial expresses similar concerns to Thomson's Asbestosis," S. Afr. Med. J. 37:629-630 1968 Lynch, J.L. " Brake Electron micrograph showed no free fibers in accumulated lining brake drum dust. Testing was then done on dust released by Decomposition braking, using equipment of a brake lining manufacturer. The Products," J. Air. apparatus permitted simulation of stopping using complete Pollut. Contr. brake assemblies. Assoc. 18:824-826 In all but a few tests the automobile drum brake linings showed less than 1% free fiber in the decomposition product... In those tests where a significant mass of free fiber was released, the temperature was in an extremely high range for the lining in question as evidenced by the rapid drop in the coefficient of friction...(under which conditions the brakes would have failed)... Similar results were obtained in the bus and truck drum brake tests... 12 Remaining Chronology of Papers Relating to Asbestos Hazard in Brake Repair (1 hrough 1985) Date Citation Findings 1961 Hueper, W.C. Lists brake linings under, "operations and products with contact to "Carcinogens in asbestos for producers, processors, users, consumers, residents." the Human Lists as a population with occupational and environmental Environment," exposure, in italics, "brake linings producers." Arch. Path, 71:237-267 1965 Hueper, W.C. Table lists "garage attendants" under the heading of groups "Occupational occupationally exposed to asbestos and lists brake linings as a and Non- source of general environmental asbestos exposure. occupational Exposures to Asbestos," Ann. N. Y. Acad. Sci. 1.32:184-195 July A Preliminary The index card for document no. 3071 at the Institute for 1968 Investigation." Occupational and Environmental Health, library of the Quebec Indust. Hyg. Asbestos Mining Association in Montreal, recorded the authors' Foundation-- summary: "Brake-drum dust has evoked a pulmonary response Report for Johns- which suggests that this dust is biologically `inert.' Brake-drum Manville. Unpublished. dust is capable of producing ferruginous bodies in the lungs of hamsters that are indistinguishable from asbestos bodies." Handwritten on the card are the phrases, "Not to circulate!" and "Scientific Committee only." The library is now part of the Asbestos Institute in Montreal. 1969 Gross, P. and R.T.P. de Treville. "Pulmonary Ferruginous bodies/Studies on Their Origin, Pneumoconiosis Proceedings' of the International Conference Johannesburg. H.A. Shapiro, Ed. Cape Town, South Africa: Oxford University Press, 1970, (O)fthe 6 ferruginous bodies isolated from hamster lungs injected with brake drum dust, all gave an electron diffraction pattern characteristic of chrysotile; this, in spite of the relative paucity of fibers in the dust by optical microscopy and the negative X-ray diffraction pattern of the powder. These 6 ferruginous bodies were, therefore, asbestos bodies. 13 Date 1970 1970 1971 April, 1972 Citation Findings would have exceeded 5 MPPCF in brake repair although dailyaverage exposures were unlikely to have been that high in most shops, according to this report. For 5-minute samplesfibers only, "...Asbestos fibers counted on membrane filter samples gave a concentration on the order of 3-5 fibers/cc" Knight, K.L. and D.IE. Hickish. "Investigations into Alternative Forms of Control for Dust Generated During the Cleaning Brake of Assemblies and Drums." Annals of Occupational Hygiene. 13: 37 39. Asbestos. Washington, D.C.: National Academy of Sciences, 1971, p.22 Oels, H.C, et al. "Diffuse Malignant Mesothelioma of the Pleura: A Review of 37 Cases," Chest 60: 564-570. Harwood, C.F. "Asbestos Air Pollution A "modified technique" for cleaning brakes used a portable vacuum unit to extract dust raised by brushing out the brake dust with a paintbrush. Damp rag wiping followed. This eliminated visible dust emissions, vastly reduced airborne particle counts, and no fibers were detected in the airborne dust samples. Notes that when the brake dust is blown offwith a compressed air hose, the dust cloud in which the operator works is "proportionate in size to the drum assembly being cleaned." Vacuum funnel and vacuum brush cleaning methods were tested. The peak exposures for both of these were way below that observed for "blow-off'-1.04 f/cc for the funnel, 0.57 f/cc for the brush, and 87 f/cc for blow-off. The vacuum brush method was preferred for its ease ofuse as well as the lowering of exposures. This report on asbestos air pollution notes that "an appreciable percentage (1-3%)" of the asbestos in brake linings survives the heat of friction and remains as fibrous asbestos. One mesothelioma patient with a history of "probable occupational exposure to asbestos" was a "service station operator." "(A)n estimate is presented which indicates that the asbestos emission from brake linings is significant." 17 Date 1976 1976 1977 Citation Watson, and J. Bogg. "Airborne Asbestos in the Vicinity of a Freeway," Atmos. Environ. 10:583-589. Rohl, A.N., A.M. Langer, M.S. Wolff, and J. Weisman. "Asbestos Exposure during Brake Lining Maintenance and Repair," Environ. Research 72:110-128. Lorimer, W.V. et al., "Asbestos Exposure of Brake Repair Workers in the United States," Mount Sinai J. Med. 43:207 218. Findings from the air near a freeway were examined by electron microscopy and electron diffraction. The major effect of braking appears to be in separating bundles of fibers and reducing their average length but not altering their crystal structure. The majority of particles had a maximum linear dimension of 2 microns or less. Unaltered chrysotile asbestos was found in garage air samples and brake drum dust. "(E)xposure of garage mechanics during brake lining maintenance and repair show that fiber concentrations frequently in excess of regulated limits are common." (Optical microscopy) Blowing out automobile brake drum dust yielded exposures of 6.6 to 29.8 f/cc with measurable exposure 50-75 feet away. Some of the other data had been summarized in the NIOSH alert of Aug. 8, 1975. Electron microscopy showed most of the fibers were too small to be seen by optical microscopes. The authors warned that exposure to these very small and numerous asbestos fibers could have adverse effects. Tabulates exposures previously measured by others, includes their own data in great detail for all types of brake work. Clinical study of 90 men with ten or more years of brake repair work and no other history of occupational exposure to asbestos. Most of the general mechanics examined did brake lining more than once weekly. Parenchymal fibrosis was seen on X-ray in 18 (20%) and pleural thickening in 5 (6%). Those who started work before 1946 had twice the prevalence of abnormal X-rays as those starting in 1946-1955. One quarter of the workers had restrictive pulmonary function test findings. Rohl, A.N. et al., "Asbestos Content of Dust Encountered in Brake Maintenance and Repair," Proc. "(T)he findings suggest that asbestos disease will be present among (brake maintenance) workers and that appropriate control measures should be urgently instituted." Another report from the Mt. Sinai group on the presence of chrysotile asbestos in brake drum dust from all over the world, the submicroscopic size of most of the asbestos fibers, and comparison of brake mechanics' asbestos exposure with OSHA standards (optical microscopy.). Authors call for implementation of industrial hygiene practices and for epidemiological mortality _i:-j-- __ i______________ ___________ _______t -- 21 Date 1982 Nov.13, 1982 1983 1983 Citation G. Perkel, and I.J. Selikoff. "Occupational Exposure Asbestos: Population to at Risk and Projected Mortality' 1980 2030," Amer. J. Indust. Med. 3:259-311. Roberts, D.R., and R.D. Zumwalde. "Industrial Hygiene Summary Report of Asbestos Exposure Assessment for Brake Mechanics." NIOSH Report #32.4, Cincinnati. Langer, AM. and W.T.E. McCaughey. "Mesothelioma in a Brake Repair Worker," Lancet 1101 1102. Glickman, L.F., et al. "Mesothelioma in Pet Dogs Associated with Exposure of Their Owners to Asbestos," Environ. Res. 32:305-313. Mancuso, T.F., "Mesothelioma Among Machinists in Findings Time-weighted average exposures for mechanics using various brake repair techniques were generally in the range of 0.1 to 0.3 f/cc. General area air samples were 0.01-0.13 f/cc. Finds asbestos fibers in the lung tissue of a mesothelioma patient whose occupational exposure consisted of many years of brake servicing work. Over a five-year period, 15 pet dogs were diagnosed with mesothelioma at a veterinary hospital. The owners of 2 were car and truck mechanics by occupation, and the hobby of a third was automobile servicing. Two of the other dogs' owners were an automobile body repairer and a used automobile parts supply worker. Report of pleural mesothelioma in an automechanic. 24 Date 1983 Feb. 1985 Citation Railroad and Other Industries," Amer. J. Indust. Med. 4:501-513. Kagan, E., and R.J. Jacobson. "Lymphoid and Plasma Cell Malignancies: Asbestos-related Disorders of Long Latency," Amer. J. Clin. Path. 80:14-20. "Asbestos Fact Book." U.S. Environmental Protection Agency, 11 pp. Findings Reports one case of pleural mesothelioma in a man who had installed automotive brake linings for 25 years. "(P)eople who work directly on brake maintenance are widely exposed to exceptionally high levels of asbestos. This occurs when brakes are cleaned and serviced during routine maintenance activities. EPA is establishing a Brake Mechanics Program to provide information and education on asbestos problems to vocational/technical students, working mechanics, and brake repair and maintenance specialists. The program will alert these specialists to the presence of asbestos in brakes and to methods that will minimize the release of asbestos fiber into the workplace." 25 Patent Number 2118733 2122405 2134512 2134564 2148257 2152017 2152022 2152611 2159935 2163879 2173591 2178527 2187086 2190237 2191460 2198253 2207961 2218615 2239134 2251410 2264192 2277107 2287952 Title ADate PDate Company Inventor Asb Non Asb Ref Mode Vehicle Brake 1937 Friction Surface 1937 Brake 1934 Brake 1936 Brake Shoes 1936 Brake System 1936 Brake 1935 Metallic Element 1936 Brake Lining Brake Brake Drum 1936 1929 1936 Machine Element 1938 Metallic Element 1938 Composite Metal 1937 Structure Article of Mfg. 1936 Metal Bearings 1934 Friction Clutch 1939 Brake Shoe Friction Article 1939 1940 Metal Structure 1939 Friction Clutch 1939 Clutch Facing 1940 Brake Drum 1939 1938 1938 1938 1938 1939 1939 1939 1939 1939 1939 1939 1939 1940 1940 1940 1940 1940 1940 1941 1941 1941 1942 1942 William K. Line, William K. Yes Line Raybestos Bockius, Chris Yes & Batchelor, Clyde S. Bendix Hall, Percy Yes Edgar Bendix Lauer, Leon Yes Nicolas Bendix Budd, Clarence Yes E. Bendix Banning, Yes Thomas A. Bendix Boetto, Jean Yes Charles Cleveland Swartz, Carl E. No Graphite Bronze Co. Stackpole Sanders, Yes Carbon Co. Vernon H. Bendix House, Bryan Yes E. Bendix Miller, Philip M. Yes & Miller, Richard B. S.K. Wellman, No Wellman Samuel K. Co. GM Koehring, No Roland P. GM Koehring, No Roland P. General Fisher, John S. No Metals GM Koehring, No Roland F. S.K. Wellman, No Wellman Samuel K. Co. Bendix McCune, ? Joseph C. S.K. Wellman, S. K. No Wellman Co. GM Koehring, No Roland F. S.K. Wellman, No Wellman Samuel K. P.R. Mallory Imes, Robert H. No & Co., Inc GM Tormyn, No Herman Ben - 3064769 Ben - 3064343 Auto Auto Auto Auto Auto Auto Auto Auto Auto Auto Auto Auto Auto ? Auto Auto Auto Auto Auto Auto Auto Auto Auto 33 Patent Number 2289311 2289689 2299192 2299877 2355419 2369502 2375855 2381393 2381941 2389061 2408430 2410924 2417855 2424655 2428298 2441534 2446892 2457861 2460367 2460367 2464437 2470269 Title ADate PDate Company Inventor Asb Non Asb Ref Mode Comp. Blank 1940 Brake Elements 1940 Sintered Articles 1939 Friction Material 1939 Brake Lining 1942 Friction Material 1940 Disc Brake 1944 Brake Friction App. 1943 1942 Metal Body 1941 Friction Product 1944 Friction Element 1944 Disc Brake 1945 Brake Adjustor 1944 Friction Element 1942 Abrasive Material 1940 Bimetallic Articles 1943 Metal Products 1945 Abrasive Articles 1945 Abrasive Articles 1945 Metallic Structure 1945 Friction Material 1945 1942 1942 1942 1942 1944 1945 1945 1945 1945 1945 1946 1946 1947 1947 1947 1948 1948 1949 1949 1949 1949 1949 S.K. Wellman, No Ben - 3064343 Auto Wellman Samuel K. Co. Wilson, Am. Brake ? Auto Rosser L. Shoe and Foundry Co. GM Tormyn, No Auto Herman Chrysler Calkins, William No Auto G. Johns- Bruce, Donald ? Auto Manville S. Raybestos Walker, Both Auto Frederick S. Lambert Lambert, ? Air/Auto Brake Corp. Homer T. Firestone Brown, Roy W. ? Air S.K. Wellman, S.K. No Wellman & Sawyer, Co. Charles B. Raybestos Kuzmick, No Jerome S.K. Lowey, Francis No Wellman J. & Tower, Charles H. American Blume, William Yes Brake Show A. & Conarton, Co. Edward W. Auto Auto Auto Auto Engineering Barish, Thomas Yes Research Corp. Bendix Goepfrich, Yes Rudolph A. Auto Auto Amer. Spokes, Ray E. Yes Brake Shoe & Keller, Emil C. Babcock & Norton, Charles No Wilcox Co. L. S.K. Wellman, S.K. No Wellman Co. H. A. Herman A. No Brassert Brassert Co. Carborundu Sharpe, Donald No m co. B. Auto Auto ? Auto ? Carborundu Sharpe, Donald No m Company B. Auto Bendix Dasher, Donald Yes Auto Cleveland Schaefer, Graphite Ralph Bronze Co. No Auto 34 Patent Number 2476151 2486140 2516966 2531782 2553828 2554291 2554548 2607245 2628693 2652624 2686140 2724461 2728418 2730199 2731312 2742107 2770325 2770328 2781107 2783529 2784105 2794526 2801714 Title ADate PDate Company Inventor Asb Non Asb Ref Mode Brake Drums 1943 Composition 1952 Brake Block Friction Element 1946 Friction 1947 Assembly Friction Element 1945 Brake Mech. 1945 Brake Lining 1946 Bimetallic Blanks 1945 Brake Shoe 1947 Comp. Metal 1948 Composition Brake Block Brakes 1952 1950 Brake 1948 Brake Adjustor 1954 Brake Assembly 1950 Brakes 1950 Brake 1947 Brake Assembly 1950 Friction Element 1952 Friction Element 1954 Friction Lining 1955 Clutch Device 1953 Friction Shoe 1956 1949 1954 1950 1950 1951 1951 1951 1952 1953 1953 1954 1955 1955 1956 1956 1956 1956 1956 1957 1957 1957 1957 1957 B.F. Le Jeune, No Goodrich Frank H. Johns de Gaugue, Yes Manville Bendix Charles L.E. Du Bois, ? William H. Emmet L. Moore, Emmett Yes Moore L. Westinghou McCune, ? se Air Brake Joseph C. Bendix Bradley, Yes Ronald E. & Fisher, Harold Le Albagnac, Jean ? Carbone- Albangnac Lorraine S.K. Wellman, S.K. No Wellman & Lowey, Co. francis J. Chrysler Rodger, William Yes R. H.A. Wilson Guinee, N Co. Edward Joseph Johns de Gaugue, No Manville Charles L.E. Bendix Goepfrich, Yes Rudolph A. Bendix Dombeck, Yes Edward K. Bendix Britton, Clayton Yes F. Bendix Du Bois, Yes William H. Bendix Du Bois, Yes William H. Bendix Dombeck, Yes Edward K. Bendix Dombeck, Yes Edward K. Am. Brake Smith, Francis ? Shoe Co. H. Am. Brake Huntress, No Shoe Co. Howard B. Bendix Stedman, No Frances E. & Pocock, Robert C. S.K. Canfield, Wade ? Wellman E. Co. Meadville Dotto, John ? Research Ben - 3064769 Ben - 2959254 Ben - 3064343 Ben - 3021592 Ben - 3064769 Auto Rail Auto Auto Rail Auto Auto Auto Auto Auto Rail Auto Auto Auto Auto Auto Auto Auto Auto Auto Air/Auto Auto Auto 35 Patent Number 2806570 2818634 2822892 2824629 2835367 2854098 2856034 2861964 2861964 2863211 2863211 2864468 2871996 2875859 2888105 2892707 2910144 2915145 2930451 2938790 Title ADate PDate Company Inventor Asb Non Asb Ref Mode Friction Facing 1951 Friction Element 1954 Brake Adjustor 1953 Brake Shoe 1953 Friction Button Disc Brake 1955 1955 Fluid Motor Composition Brake Block 1955 1953 Composition Brake Block 1953 Friction Assembly Friction Assembly 1955 1955 Friction Device 1955 Brake Shoe 1955 Brake 1955 Disc and Shoe 1954 Bi-Metallic Article 1956 Shoe and Disc 1955 Kinetic Device 1954 Friction Device 1955 Friction Lining 1955 1957 1958 1958 1958 1958 1958 1958 1958 1958 1958 1958 1958 1959 1959 1959 1959 1959 1959 1960 1960 Products Corp. Bendix Markus, ? Eugene Raybestos Batchelor, No Clyde S. & Steck, Rudolph e. Bendix Clark, Warren Yes G. S.K. Wellman, S.K. No Wellman Co. Raybestos Steck, Rudolph ? Lambert E. Griswold, ? Brakes Frederick D. Corp. Bendix Mossey, ? Joseph Johns de Gaugue, No Manville Charles L.E. & Halstead, Ralph T. Johns de Gaugue, No Manville Charles L.E. & Halstead, Ralph T. S.K. Wellman, S.K. No Wellman S.K. Wellan, S.K. No Wellman Co. Bendix Dombeck, ? Bendix Edward J. Strebinger, ? Bendix Robert L. Strebinger, ? Bendix Robert L. Burnett, ? Richard T. S.K. Biggs, Robert No wellman Co. W. Bendix Burnett, ? Bendix Richard T. Mossey, ? Bendix Joseph L. Burnett, ? Richard T. Bendix Stedman, No Frances E., & Pocock, Robert Ben - 3021592 & 3064769 Ben - 3064769 Auto Auto Auto Auto Auto Air Auto Rail Rail Auto Auto Auto Auto Auto Auto Auto Auto Auto Auto Air/Auto 36 A sample of information available in the general medical literature includes: 1. Annual Report of the Chief Inspector of Factories and Workshops London, 1898. 2. Dangerous Trades, the Historical, Social, and Legal Aspects of Industrial Occupations as Affecting Health, by a Number of Experts, Edited by Dr. Thomas Oliver (1902). 3. Mortality from Respiratory Disease in Dusty Trades, Dept. of Labor, Bureau of Labor Statistics, Frederick L. Hoffman - June 1918 4. Fibrosis of the Lungs Due to the Inhalation of Asbestos Dust, British Medical Journal, Dr. W.E. Cooke - July 26, 1924 5. Pulmonary Asbestosis, Journal of the American Medical Assoc., Vol. 90, No. 2 (January 14, 1928). 6. Report on Effects of Asbestos Dust on the Lungs - Merewether and Price (1930). 7. The Occurrence ofPulmonary Fibrosis and other Pulmonary Affections in Asbestos Workers, The Journal of Industrial Hygiene, E.R.A. Merewether (1930). 8. Compensation Act Extended to Asbestosis - Foreign Letters; London, May 31, 1930. 9. Pulmonary Asbestosis, JAMA, Vol. 95, No. 19, p. 1431 - July/December 1930. 10. Asbestos, Occupation and Health Encyclopedia of Hygiene, Pathology and Social Welfare (1930). 11. Asbestos Bodies in Sputum and Lung, JAMA, Vol. 95: 659-661 - 1930 - Kenneth Lynch And W. Atmar Smith. 12. S. McDonald, Histology of Pulmonary Asbestosis, Brit. Med. J., 2: 1025 1927 - 13. JM Memo regarding excerpts from medical journals - 1930. 14. Bulletin of Hygiene - Gloyne and Woodhouse - Dec. 1928 15. Pulmonary Asbestosis, Radiology, Vol. 17, J.V. Sparks, 1931 16. Asbestosis - Report of Two Cases, Harold L. Stewart, Bucher and Coleman, Archives of Pathology, Vol. 12, 1931. 17. Industrial Commission ofWisconsin, Proceedings of Conference Concerning Effects of Dust Upon the Respiratory System, Nov. 1932. 38 18. Occupational Diseases Are Not Generally Understood, The National Underwriter, Dec. 15, 1932. 19. Journal of Industrial Hygiene, Drs. David L. Edsall and Edgar L. Collins, Editors (Jan. - Nov. 1933). 20. A Memorandum on Asbestosis, Tubercle, Vol. XV, E.R.A. Merewether, Nov. 1933. 21. Asbestos, The Industrial Bulletin, Vol. 13, No.4, April 1934. 22. Pulmonary Asbestosis, A Review of One Hundred Cases, The Lancet, W. Burton Wood and S. Roodhouse Gloyne, Dec. 22, 1934. 23. Pulmonary Asbestosis III: Carcinoma of Lung in Asbestos-Silicosis, American J. Cancer, Vol. 24:56-64; Kenneth Lynch and W. Atmar Smith, 1935. 24. Effects ofthe Inhalation of Asbestos Dust on the Lungs ofAsbestos Workers, Public Health Reports, Vol. 50, Part 1, A.J. Lanza, 1935. 25. Asbestosis: Part II. and Part III., Bureau of Industrial Standards, Commonwealth of Pennsylvania, Dept. of Labor and Industry, Sept. 20, 1935. 26. A Study of Asbestosis in the Asbestos Textile Industry, U.S. Public Health Service, Dressen, Dallavalle, Edwards, Miller and Sayers, Bulletin No. 241 (1938). 27. Asbestosis, Occupation and Health Encyclopedia of Hygiene, Pathology and Social Welfare, Jan. 1938. 28. Great Britain passed Compensation for asbestosis in May 1931 Germany - Dec. 16, 1936 / March 11, 1937; United States North Carolina - March 26, 1935. 29. Occupational Cancer in Asbestos Workers, Abstract of the Literature of Industrial Hygiene, Vol. 20, Jan.-Dec. 1938. 30. Asbestosis, Baader, Deutsche Medizinische Wochenschrift, 65:407-8, 1939. 31. Statistics of Diseases and Injuries in the United States Navy, Annual Report of the Surgeon General, U.S. Navy, 1939. 32. Industrial Welfare and Medicine, Encyclopedia Britannica, Vol. 12, 1940. 33. Asbestosis, W. C. Hueper, Occupational Tumors and Allied Diseases, 1942. 39 34. Bronchogenic Carcinoma in Association with Pulmonary Asbestosis, H.B. Holleb and A. Angrist, American Journal of Pathology, Vol. XVIII, 1942. 35. Bulletin of Hygiene, Bureau of Hygiene and Tropical Diseases, Vol. XVII, Dec. 1942 Kuhn, Illness among Dock Workers at Wihelmshaven (1930 to 1938) [German]. 36. The Occupational Disease Hazard, Industrial Medicine, Volume 11, No. 4 Warren A. Cook, April 1942. 37. Cancer in its Relation to Occupation and Environment. Bulletin ofAmerican Society for the Control of Cancer, Vol. 25, No. 1, pp. 63-69, W. C. Hueper, Jan. 1943. 38. Minimum Requirements for Safety and Industrial Health in Contract Shipyards. Industrial Medicine, 12:249-263, 1943. Philip Drinker served as Health Consultant. 39. Environmental Cancer, JAMA Editorial, 126:836, Nov. 25, 1944 40. Dust as an Industrial Health Hazard. Heating and Ventilating, Vol. 41, No. 6, June F. W. Hutchinson, 1944. 41. Letter from British Chief Inspector of Factories to Thermal Insulation Contractors Assoc., concerning the hazards of asbestos to workers in the shipbuilding and ship repairing and urging precautions to be taken, August 1945. 42. A Health Survey of Pipe Covering Operations in Constructing Naval Vessels. Journal of Industrial Hygiene and Toxicology, Vol. 28, FLEISCHER and DRINKER, 1946. 43. Report of Preliminary Dust Investigation for Asbestos Textile Institute, W.C.L. Hemeon, Industrial Hygiene Foundation of America, Inc., June 1947. 44. A further Study of the Incidence of Cancer in the Lung and Larynx. The British Journal of Cancer, 1:260-298, E.L. and N.M. Kennaway, 1947. 45. Discussion. Diseases of the Chest, Vol. XIV, No. 1, Brahdy, L., Jan-Feb 1948. 46. Cancer and the Environment. Scientific American, Vol. 180, No. 1, Groff Conklin, January 1949. 47. Asbestosis and Cancer of the Lung. JAMA, Vol. 140:1219-20, Morris Fishbien, May-August 1949. 48. Annual Report of the Chief Inspector of Factories for the year 1949. 49. Foundation Facts. Industrial Hygiene Foundation, No. 8, August 1949. 40 50. Pulmonary Asbestosis: Anatomicopathologic Study of A Case. Industrial Hygiene and Occupational Medicine, Vol. 1:362-363, A. Franchini and G. Canepa, 1950. 51. Discussion by Vandiver Brown, Pneumoconiosis, Sixth Saranac Symposium, 1950. 52. Environmental Cancer Hazards Caused by Industrial Air Pollution. Archives of Industrial Hygiene and Occupational Medicine, Vol 2:325-328, W.H.C. Hueper (1950). 53. Abstracts from Current Literature. Archives of Industrial Hygiene and Occupational Medicine, Vol. 1:362-363, Chief Editor - Philip Drinker, 1950. 54. Case Reports - Asbestosis Associated with Bronchogenic Carcinoma. AMA Archives of Internal Medicine, Vol. 88:831-834, Roger Stoll, Richard Bass, Alfred A. Angrist, 1951. 55. 1942, Homburger, Co-Incidence of Primary Carcinoma of Lungs and Pulmonary Asbestosis: Analysis of Literature and Report of 3 Cases. Am. J. Path. 19:797-807 (1943) 56. 1943, Wedler. Asbestose und Lungenkrebs. abstracted in Bull. Hyg. 19:363 (1944). 57. 1947, Merewether, Annual Report ofthe Chief Inspector ofthe Factories in England for 1947. 58. 1948, Lynch and Cannon, Asbestosis VI. Analysis of 40 Necropsied Cases. Dis. Chest 14:874-880 (1948). 59. 1948, R. J. Cureton, Squamous cell carcinoma occurring in asbestosis of the lung. British J. Med. 60. 1949, Wyers, Asbestosis, Post-Grad. M. J., 25:631-638 (1949). 61. Cancer, Encyclopedia Britannica, Vol. 4, p. 731 (1952). 62. Industrial Cancer of the Lungs. Compensation Medicine, Vol. 4:11-18 May R. Mayers, 1952. 63. Asbestosis as Differentiated from Other Pneumoconiosis. AMA Archives of Industrial Health, O.A. Sander, 1953 (read in Symposium on Occupational Disease of the Lungs, sponsored by the Massachusetts Medical Society). 64. Asbestosis and Bronchogenic Carcinoma, report of one autopsied case and review of the available literature. American Journal of Medicine, Vol. XV:721-732, K.J. Isselbacher, H. Klaus, Harriet Hardy, Nov. 1953. 41 65. Mortality from Lung Cancer in Asbestos Workers, Brit. J. Indus. Med., Vol 12:81 Richard Doll, 1955. 66. The Dust Diseases in Great Britain, AMAM Archives of Industrial Health, Vol. 12:83-99, A.I.G. McLaughlin, 1955. 67. Lung Cancer in Asbestosis, The Lancet, June 4, 1955. 68. Editorials - Silicosis, Asbestosis, and Cancer of the Lung, American Journal of Clinical Pathology, Vol. 25:1388-1390, W. C. Hueper, 1955. 69. Industrial Aspects of Bronchogenic Neoplasms, Diseases of the Chest, Vol. XXVIII:421-430, Lester Breslow, October 1955. 70. Chapter 40 - Occupational Pulmonary Disease, Disease ofthe Chest (textbook), pp. 666-68, H. Corwin Hinshaw and L. Henry Garland (1956). 71. Asbestosis with Pleural Calcification Among Insulation Workers, Danish Medical Bulletin, Vol. 3: 202-04, Frost, George, Moller, 1956. 72. Industrial Medicine, Abstracts of World Medicine, Vol. 21, Jan. to June 1957. 73. Bulletin of Hygiene, Occupational Hygiene and Tropical Diseases, Vol 32, No. 12 (December 1957). 74. Industrial Hygiene, The Encyclopedia Americana, Vol. XV, pp. 88-90 (1957). 75. Pneumoconiosis, Encyclopedia Britannica, Vol. 18, pp. 99-100, 1960. 76. Diffuse Pleural Mesothelioma and Asbestos Exposure in the North Western Cape Province, Brit. J. Industr. Med., Vol. 17:260, J.C. Wagner, Sleggs, Merchand, 1960. 42 Johns Manville held a health and safety seminar on asbestos at Bendix headquarters on Aug. 8, 1972. Bendix employees also attended other seminars on the topic. Bendix Attendance at Health & Safety Seminars Given by Johns-Manville Location Date Attended by: Seminar held at Bendix's Corporate Aug. 8, 1972 C. E. Heitman; H. Bobel; H.O. Offices in Southfield, Michigan Stolar; A.C. Joines; N. Saunders; R.B. Hungate; C. Menz; R.B. Burton; J.W. Armstong; J. Tierney; H. Kaplan; A. Raymond Framingham, Mass. Jan. 16, 1974 G. Lovegrove; J. Fountain; D. Stone; B. Brown; A. St. John; R. Hart; J. Jones; F.Jeansonne Manville told the attendees that knowledge of asbestos health hazards dated back to 1924. "THE HEALTH PROBLEM" "For the past 50 years, from the first indications that there were health problems involving workers who inhaled too much asbestos dust, Johns-Manville has led the industry in working to solve these problems." Manville told the attendees about the industry standard for protecting the health ofworkers. "It is our Company's policy to equip our plants for the highest degree of personal safety.. .provided it is technically possible and feasible to do so." "When technology is not available. or when it is not feasible economically from a competitive standpoint to make these installations.. .we will elect to discontinue a particular operation rather than knowingly endanger the health or life expectancy of a single employer." Knowledge of Health Effects Manville told the attendees about asbestos health effects. "ASBESTOS-RELATED DISEASES" Asbestosis Bronchogenic cancer Mesothelioma "Mesothelioma is by far the most serious disease ofthe three diseases because. once diagnosed, it is inevitably fatal - these is no known treatment. Death usually occurs within 18 months after diagnosis." Manville told the attendees about the available engineering controls for protecting the health of workers. 43 "SOME DUST CONTROL PRINCIPLES" "J-M's 30 years of experience in handling asbestos fiber and developing effective dust control systems is available to J-M customers.. "...A good job of industrial housekeeping usually is the first step. An industrial vacuum cleaner should be used in areas where dust may be generated. If a plant already has dust control facilities, it is recommended that a vacuum cleaning system be used as a take-off from the present dust system by installation of a booster fan and a small cyclone. J-M will provide a typical lay-out and schematic of such a system." ."If asbestos fiber is used in an operation and there are no dust control facilities, chances are there is a dust problem - and probably a two fold one. One would be exposure of employees to asbestos dust (OSHA) and the other would be exhausting asbestos dust-laden air out of the building (EPA). "The most appropriate times for an industrial hygiene survey are: If you already have dust control facilities, an industrial hygiene survey will determine how well your facilities meet OSHA standards.. .After installation of dust control facilities, an industrial hygiene survey should be part of the installation agreement to establish the reliability of equipment and compliance with standards." Manville told the attendees that information on health hazards was readily accessible. "An extensive medical library on asbestos-health studies is open to interested parties. To acquire copies of specific medical studies or for more information on additional material available through the Environmental Affairs Department, write or call: Walter A. Cooper Director, Environmental Communications Johns-Manville Corporation" Bendix had access to further knowledge ofthe adverse health effects of asbestos through its membership in the Friction Materials Standards Institute (FMSI); additionally, the Asbestos Study Committee served as FMSI's liaison to the AIA, so that knowledge acquired through either organization was transmitted to the other. Knowledge gained through FMSI included information on the results of a FMSI study on fiber emissions in friction work (produced by the Illinois Institute of Technology and circulated in June 1972). The study concluded that "considerable" amounts of asbestos fibers were released from work on friction materials. The author ofthis report, Dr. Colin Harwood, supported the banning ofthe use of asbestos in friction materials in Illinois, and the members of the Asbestos Study Committee had access to this information. Members ofFMSI (including Bendix) discussed the asbestos "problem" with regards to the 44 use of end products, specifically, the cutting, grooving, drilling, and grinding of end products. They concluded that such operations "can produce airborne concentrations of asbestos fibers in excess of the current exposure limits (5 fibers/cc TWA or 10 fibers/cc ceiling)." In June 1974, Bendix continued to acquire knowledge of dust hazards produced by users of end products. At an FMSI meeting, a paper by Rohl, Anderson, Nicholson and Langer entitled "Asbestos Exposure During Break Lining Maintenance and Repair" was presented. Shortly thereafter this information was circulated at FMSI. The paper describes "deplorable" working conditions in several New York City brake shops. The Asbestos Study Committee concluded that these conditions were probably "common" for end-product users and that the industry must do more to change these conditions. The FMSI also imparted to its members knowledge of safer substitute materials for brakes which they knew to available at least as early as 1972. A report by Dr. Harwood of the Illinois Institute of Technology, distributed to FMSI members in 1972, concluded that, "there is no doubt that substitution of other materials for asbestos is possible," although they would be more expensive. The industry's reluctance to utilize these substitutes indicates a preoccupation with profit that prevailed over concern for consumer and worker safety. Bendix Response to Knowledge Bendix antecedent Marshall Asbestos Corporation was a member ofthe US government sanctioned "Asbestos Industry" as of 1933. The risk of asbestos health hazards was recognized at this meeting and a prohibition of the employment of persons under the age of 18 was implemented. This paralleled the same asbestos health youth protections in England. In 193 6, several asbestos friction product manufacturers hired Dr. Leroy Gardner to perform animal studies of asbestos health effects at the Saranac Laboratory. Gardner discovered three important facts about asbestos. 1. Asbestos caused cancer in the animals without first producing fibrosis. 2. The "guideline" that had been tentatively implemented to protect workers form asbestosis was too high. 3. The guideline was designed to measure the wrong thing (total dust and not fibers). Gardner had determined that the fibers and not the chemical composition of the dust caused the disease. On November 11, 1948, the sponsoring companies met in Manhattan, to discuss the study report. They had reserved the right under the contract to edit research reports prior to publication. They exercised this right and required the author to strike all information pertaining to cancer and fiber measurement from the published paper.2 2 The industry also employed other strategies to maximize profits; for example, six weeks prior to the meeting where the friction manufacturers agreed to revise Gardner's experiment before 45 The sponsors of this research along with Bendix were members of the BLMI. These sponsors and Bendix were all convicted of violations of federal price fixing statutes with respect to asbestos brake prices. They were convicted in 1948, in New York City a few blocks from the location of the meeting they held eight weeks before at the corporate offices of another brake manufacturer Johns Manville. Both the price fixing and suppression of health information concerning asbestos brake hazards were designed to maximize profits from the sale of asbestos brakes. The fact that all the BLMI companies shared information on the pricing of asbestos brakes and other brake manufacturing and brake component standards indicates that these companies readily shared information that might impact on profits from the sale of these products and the brake companies were aware of the fact that the association of a cancer hazard with the use of asbestos brakes would result in decreased sales and profits. Workers who made asbestos brakes sued Bendix in the mid 1970's. These workers alleged that they had contracted laryngeal cancer from their exposures. 7 Finkelstien studied the Bendix plant and issued a report to Bendix. He determined that two Bendix workers had contracted mesothelioma from their asbestos exposure at Bendix. This information is omitted from Bendix answers to interrogatories. The repeated suppression of scientific information on asbestos health effects by the friction manufacturers represents one of the industry's tactics to increase sales by concealing information from medical, public health and regulatory personnel, as well as workers and consumers. This program to restrict knowledge of asbestos hazards to the senior corporate level and misinform the public was also pursued through the Asbestos Information Association (AIA), a private industry organization to which many friction manufacturers, including Bendix, belonged. The AIA contracted with Dr. Philip Enterline in 1976 to compile a medical literature review, which could be used to fabricate a " State of the Art" defense against asbestos lawsuits. They kept the results ofthe Gardner experiments secret from him and as a result he published misleading and incorrect information in the medical literature. 8 Enterline compiled a report for the AIA, summarizing the state of the art (what was known about asbestos health hazards). The version of the report presented to the AIA for review stated that the fact that asbestos caused mesothelioma was generally accepted by 1953. However, when Enterline published the same report in the American Review of Respiratory Diseases in 1978, this information was omitted and the paper stated that the cancer hazard of asbestos did not become known until 1964. 9 This position was consistent with the AIA's claims and supported the industry's attempt to escape liability for asbestos-related exposures prior to that date. Enterline's paper also omitted all information on the risk of mesothelioma, which had been in the publication, Bendix and other members ofthe Brake Linings Manufacturing Association and most of the sponsors of the Gardner research were found guilty to two felony counts related to price fixing. They also had other ways of communicating health information. They had overlapping boards of directors. For example: Allen M. Harrelson, Bendix vice-president and director (1965 - ) was also a vice-president at H.K. Porter from 1949 to 1965. Edward R. Morgan, Bendix vice-president (1967 )was also a vice-president at H.K. Porter from 1952 yo 1964. Mr. JD Biggers was a Bendix director from 1950 to 1967. His tenure with Manville was 1959 to 1965 or 1966. 46 original paper submitted to the AIA, and failed to mention that the funders had specifically retained him to author a paper that could be used to defend asbestos companies in toxic tort litigation then in progress. Bendix did not follow well-established occupational and public health procedures for protecting worker health. Bendix's expressed policy for protecting workers' health was contrary to the accepted public and occupational health policies for worker protection that have been in existence since Biblical times3, * as is evidenced by the following 1966 letter: "Just to be sure you have a copy, an article that appeared in Chemical Week magazine is enclosed. So that you'll know that Asbestos is not the only contaminant, a second article from O. P. & D. reporter assess a share a share of the blame on trees. My answer to the problem is: if you have enjoyed a good life while working with asbestos products, why not die from it. There's got to be some cause." -Director Of Purchases E. A. Martin"10 [Emphasis added] Bendix's awareness of asbestos-related health problems is reflected in a follow-up to the letter cited above: "A copy of page 7, Chemical Week magazine of October 6 1966, discloses a couple of letters refuting the article appearing in the same periodical on Sept. 10, 1966. This may help to quiet the fear that was aroused by Dr. Selikoffs stigmatic report on `Lung Cancer From Asbestos.' The Purchasing Department has a file on the entire subject including the Canadian Health Department report of May 30, 1949, when the subject was previously incited." -E.A. Martin11 [Emphasis added] While Martin indicates here that the company began compiling a file regarding asbestos health effects in or prior to 1966, the Bendix Corporation stated in their Answers to Interrogatories in Brown vs. AC&S et al that they first acquired knowledge of the dangers of asbestos in 1972. Beginning in 1968 each bag of asbestos Bendix received had a caution label: 3 "When you build a new house, make a parapet around your roof so that you may not bring the guilt of bloodshed on your house if someone falls from the roof." Deuteronomy 22:8 47 CAUTION THIS BAG CONTAINS ASBESTOS FIBER. PERSONS EXPOSED TO THIS MATERIAL SHOULD USE ADEQUATE PROTECTIVE DEVICES AS INHALATION OF THIS MATERIAL OVER LONG PERIODS MAY BE HARMFUL." Bendix removed the asbestos, placed it unchanged into brakes, which were as much as 75% asbestos and sold them with the label removed. Use of asbestos-containing brakes releases friable asbestos that can result in asbestosis and cancer in workers, bystanders and family members. Bendix was a member of the AIA, which lobbied OSHA to remove the word cancer from the asbestos label. Bendix's representative David Stone to the FMSI, on December 10, 1976 voted that the FMSI publish, "Recommended Procedure for Reducing Asbestos Dust During Brake Servicing" and add a page to the FMSI Catalog recommending procedures for reducing asbestos dust during servicing. He correctly noted, "Printing a page in the FMSI catalog does not get procedure into the hands ofthe [unreadable] ?worker. The ideal situation is for rebuilders or other people putting lining sets into individual boxes to include a folded 8 1/2 x 11 sheet on procedures in each box. The downside of course is several pennies cost." [Emphasis added] Apparently the cost was too high, Bendix never followed this sound recommendation. At certain high temperatures, such as those encountered during brake use chrysotile fibers are converted to forsterite. Fibrous forsterite is likely to be a cause of mesothelioma. Forsterite does not lose its fibrous structure until it reaches 2300 degrees Fahrenheit.12 However studies have demonstrated that a significant amount of chrysotile asbestos fiber does not convert to forsterite during brake use, and remains present in the dust generated during brake servicing and use. The same 1974 Rohl paper cited above, which was disseminated among FMSI members in 1976, notes that unaltered chrysotile fibers were found in air and brake drum dust samples following brake servicing. A 1976 letter from Rohl to Eichen (of the Ford Motor Company) states, "Extensive study of both the thermal behavior of chrysotile and brake lining composition and design indicates that chrysotile fiber may survive in the decomposed lining dust."13 I agree with the Manufacturing Chemists Association (MCA) position on warnings as stated in their 1972 letter to OSHA. Largely as a result ofthe AIA's effective lobbying strategy involving industry backed expert testimony, the 1972 OSHA rulings set out weak labeling standards for asbestos and asbestos-containing products. The MCA recognized the inadequacy of the proposed OSHA label and recommended the following warning language:14 48 ASBESTOS WARNING! HARMFUL IF INHALED MAY CAUSE DELAYED LUNG INJURY (ASBESTOSIS, LUNG CANCER) Do not breathe dust. Use only with adequate local exhaust ventilation or approved respiratory protective devices. Remove dust and fibers from clothing only by vacuum cleaning. Clean work areas only with vacuum cleaners or wet cleaning methods. In the same letter to OSHA, the MCA noted that, "This text incorporates all the language proposed by NIOSH, and expands upon it to reflect additional critical information in the criteria which, in our opinion, will strengthen the message."15 However, instead of acceding to the MCA's request to strengthen the label, in response to pressure exerted by the industry, OSHA removed the words "Danger" and "Cancer" from the required label, thus weakening the message. In the end, at the request of the AIA OSHA approved the following, "watered-down" version of the label: 16 CAUTION CONTAINS ASBESTOS FIBERS AVOID BREATHING DUST BREATHING ASBESTOS DUST MAY CAUSE SERIOUS BODILY HARM SMOKING GREATLY INCREASES THE RISK OF SERIOUS BODILY HARM Bendix never placed a warning on their brakes. They may have placed a caution label on some brakes they manufactured beginning in 1974. There is no evidence that they ever placed this caution on exported brakes. I agree with Mr. Swetonic's assessment of the effectiveness of asbestos industry influence over OSHA and the EPA and with his assessment of the "good news" from his 1973 speech to the Asbestos Textile Institute (ATI). Regarding OSHA, Swetonic stated: "I think it is a gauge of effectiveness of the total industry involvement in this most crucial matter that of eleven main requirements in the standards, the industry position was accepted totally by OSHA on nine of eleven, about fifty percent on a tenth, and totally rejected on only one." 49 Swetonic referred to the public health crisis posed by asbestos in terms of a "public relations problem." He openly admitted that, ".. .insulation workers.. .were and still are dying from asbestos related disease at an appalling rate," and cited an estimate based on a review of mortality studies that, ". approximately 25,000 past and present employees in the asbestos industry have died or will eventually die of asbestos-related disease." As for the "mining and manufacturing areas of the industry," Swetonic estimated that "5,000 of our workmen are still going to die of asbestos-related disease and. all things considered, there is absolutely nothing that we can do to prevent it." Nonetheless, Swetonic was cheered by one fact: "And now, having heard the bad side ofthe public relations problem, it's time for the good news. And the good news is. despite all the negative articles on asbestos-health that have appeared in the press over the past half-dozen years, very few people have been paying attention." I believe his speech underestimates the total number of injured workers. I agree with I.H. Weaver's assessments of risk from chrysotile (see below), adequacy of warnings, exposure levels during asbestos brake use, and the corporate responses to these facts, as expressed in his June 27, 1973 speech to the FMSI. Regarding the OSHA-mandated asbestos warning label, Weaver, president of the AIA and of Raybestos Manhattan, and Chairman of the FSMI, stated: "Keep in mind that NIOSH and the OSHA Advisory Committee recommended a much more severe label than the one we are talking about. This subj ect was heatedly debated during the OSHA Advisory Committee deliberations, and their final recommendation called for use of the word `Danger' instead of `Caution' and specifically mentioned that breathing asbestos can cause cancer. Very frankly, I was exceedingly surprised when the final OSHA Standard came out in favor of considerable milder working . . . Many other elements of the OSHA Regulations came out more favorably toward industry than the recommendations that were submitted by NIOSH and the Advisory Committee, and stiff resistance by Industry will be needed to prevent OSHA from strengthening the regulations in months to come."17 In his speech in June of 1973 Weaver also acknowledged that many companies chose to simply ignore rulings requiring labeling: "There has been considerable disregard to a number of provisions mainly in the area of labeling, monitoring, employee education, personal protection, waste disposal, and use of warning signs by segments of asbestos products manufacturing, and I believe this applies to friction material to some extent. One of the most obvious items has to do with industry's reluctance to accept asbestos products labeling as required by OSHA."18 E.J. Killian, ofNational Asbestos Mines Limited, revealed the reason the campaign disregarded the labeling requirement: ". [T]he simple placement of a label on products could cause a degradation of 60% of the business."19 Weaver addressed the fact that use of asbestos end products, specifically friction materials, posed real dangers, which were in need of urgent attention from the industry: 50 "I know of no way any of us can be absolutely sure that his friction products, regardless of whether they are sold as original equipment or on the replacement market, will not be subjected to additional operations or alterations in the field that could result in excessive exposure of workers or bystanders to airborne asbestos fibre. I have been appalled to learn of a number of instances where this problem has occurred, and some ofthese cases involved people that certainly might have been expected to know better... [I]t appears to me there can be no argument about the need for educational measures to reduce chances of unnecessary exposure during grinding, drilling or cutting operations."20 These concerns prompted Weaver to urge the friction materials industry not only to comply with OSHA warning requirements, but also to take even further steps towards consumer and worker education, stressing that the OSHA standards alone were insufficient in this regard: "To me, labeling all containers or packages of asbestos-containing friction materials is the very least the industry can do to fulfill moral obligation to its customers, their employees, and the public and at the same time conform with the minimum requirements of the Occupational Safety and Health Act. I seriously question whether mere labeling is enough to fulfill this requirement. It has been suggested by others as well as myself several times in the past that additional instructions, of a more comprehensive nature than is practical to provide on a label, be inserted inside each package where a possibility exists that the product might be used in such manner that an airborne dust problem could be created. A number of responsible asbestos products manufacturers already are following this procedure, and there is a good possibility that it may be made mandatory in future regulations."21 I agree with the opinions expressed by Mr. Chunko, Honeywell's industrial hygienist, with respect to the ability of all fiber types to cause cancer and the lack of a known threshold for asbestos cancer effects.22 Honeywell sells a CD-rom for asbestos education. I agree with all the opinions expressed in this CD concerning asbestos health effects and controls and particularly the hazard associated with the use of asbestos brakes. This is the kind of educational program Bendix should have provided when they sold asbestos-containing brakes. After my deposition, when I disclosed the fact that Honeywell sold this educational program, the company stopped selling this CD-rom. This is wrong. They should continue to make it available to their workers and customers. Epistemological framework a) Bayesian Analysis For diseases with multiple or unknown causes, Bayesian analysis can be used to judge the role of each suspected cause in influencing the population-level occurrence of disease. Bayesian analysis follows in form and in practice the same basic principles governing Bayesian decision-making.23 Each integrates different forms of medical evidence into a single assessment of causal probability. In short, Bayesian analysis aims to incorporate all the available medical evidence - from case reports to animal studies - into one updated and standardized assessment that measures the overall strength 51 of causal certainty.24 Each type of evidence is hierarchically arranged according to the overall credence the evaluator places on particular types. A summary of all the available evidence is provided in a number usually given on a scale of 0 to 100, where "0" indicates an equally firm level of certainty ofthe lack of a cause-effect relationship, and "100" represents complete and irrefutable certainty of causation (see figure 11). This analysis constitutes an evaluation of the overall level of medical certainty for the likelihood a suspected agent (for example radon gas) is a cause of disease (lung cancer) in the general population. A Bayesian analysis might conclude that in the mind of the evaluator, evidence indicates 20% certainty of a causal relationship buffeted by an 80% certainty of a non-causal relationship. That is to say one central feature of Bayesian analysis is that uncertainty in one conclusion is tantamount to certainty in the opposing conclusion, or the amount of certainty parceled out between two antithetical positions always equals 100%25 All Bayesian assessments of causal relationships are valued somewhere between 0 and 100, since no scientific evidence can sustain intractable and incontrovertible conclusions. In fact, one condition for reaching complete and irrefutable certainty is that even if convincing evidence to the contrary became newly available, the level of certainty would remain unchanged in our assessment.26 This corollary highlights the second key feature ofBayes' theorem: the interpretation of new information depends on one's prior probability of causation.27 At the boundary of 100% certainty, new information becomes less relevant and is incapable of modifying summary values in an important way. Since steadfast conclusions ofthis sort can rarely be made in good scientific conscience, reaching such conclusions is never required for drawing reasonable medical inferences, nor should courts expect such conclusions for reaching valid legal conclusions under a preponderance of the evidence standard. Figure 5: Bayesian the available evidence. model for causation integration of The accepted analysis Suppose we wanted to perform a Bayesian analysis of the available scientific evidence relating the dietary intake of fiber to the reduction of colorectal cancer. We would first analyze each type of medical evidence. We would then order evidence in a manner that reflected the credibility we had for each type of evidence (Figure 5). We would weigh each class of evidence favoring or opposing the proposed association and place the body of evidence on a standard scale of causation from 0 to 100. This value reflects the support for the association internal to each type of medical evidence, without modification from other types of evidence. The second and globally integrative step in this assessment would follow from combining the priors of each type of medical evidence onto the integrated scale of causal certainty. The summary does not classify scientific data according to particular study designs or models but gives the evaluator's overall impression ofthe likelihood of cause-effect relationship. The evaluator expresses her implicit subjectivity through the reasoning and assumptions behind the ordinal weight 52 she gives to each type of evidence.28 Bayesian analysis forces a complete accounting of the epistemologic stance of the evaluator. Causal explanations offered by organizations or individuals should comport with the Bayesian framework of disclosing the subjectivism of their explanations. The sum of all causes has no upper bound (is not 100 percent). That a cause can be deemed with a high degree of certainty to be a specific cause of a disease does not imply that it is the sole or exclusive cause. Some legal defenses seize on the widely-circulated statistic that smoking is responsible for 80% of US lung cancers as ultimate proof that other known causes - radiation and asbestos - are only minor causes between which the remaining 20% of cancers must be split. The second assertion fails to deal with the fact that that a Bayesian analysis evaluates each cause independently, and a finding that one factor is a highly certain cause of disease has no bearing on the presence or importance of other factors. Figure I: Current scientific thought regarding cause-effect relations. Sufficient Cause 1 /eTd\ (a>Cc jy Sufficient Cause 11 Vj3jy Sufficient Cause III /jT'TN \^Kpj V^cjy 50 % 30 % 20 % 53 GENERAL AND SPECIFIC CAUSATION- Methodology 1. In determining cause and effect, physicians and scientific researchers typically look at two distinct issues, general causation and specific causation. General causation focuses on the issue of whether a particular substance is capable of causing a particular injury or condition in the general population. Specific causation, on the other hand, addresses the issue of whether an exposure to a substance or substances has caused or contributed to the development of a particular individual's injury or disease. To determine general causation, researchers evaluate a variety of data sets including animal studies, toxicologic studies, molecular studies, case reports, epidemiologic case-control and cohort studies and general biologic principles. If a review ofthese data sets establishes that there is a general cause and effect relationship, physicians then determine specific causation by ascertaining whether an exposure caused or contributed to a particular individual's disease. This affidavit is limited to a discussion of general causation. HILL'S CONSIDERATIONS FOR DETERMINING CAUSALITY 2. As an overall model for determining causality, the considerations espoused by Sir Austin Bradford Hill are well accepted and have been widely used by epidemiologists.29 They are: temporality, biologic gradient (dose-response), consistency, biologic plausibility, strength of association, analogy, experimental evidence, coherence and specificity. The scope of medical evidence that substantiate these considerations is both comprehensive and widely inclusive of all the available data. The empirical support for the considerations over such a large epistemological landscape represents, in itself, the ultimate merit ofthe considerations. While respected as a framework for determining causation, each ofHill's considerations has been subject to criticism. Accordingly, as Hill noted, "None of my nine view points can bring indisputable evidence for or against the cause-and-effect hypothesis, and none can be required as a sine qua non." Before applying this framework to the issue of whether exposure to chrysotile asbestos causes or contributes to cause mesothelioma, it is important to reflect upon the relative significance of each of these considerations in making such a determination. None of Hill's considerations require epidemiologic data. 3. "Strength of association" is a reflection of the power of a study. Human epidemiologic studies are not the only type of data available to access this consideration. It may also be determined from human, animal or microbiologic studies. The relevance of this consideration is limited by the prevalence of co-factors that may interfere with the measurement of the factor that is being studied. Strength of association is not a measure of the importance of a particular factor in causation.30 It is a gauge of potential errors due to confounding or bias. Studies with large rate ratios are less likely to contain errors attributable to bias or confounding. Causal factors with "relatively low rate ratios" may be equally or more important than strong associations from a public health perspective. In addition, a rate ratio of two is not required to establish that a factor contributed to a disease 54 in a particular individual (specific causation). For example, chronic smoking of less than a pack a day induces less than a two fold increase in the risk of heart disease. Nonetheless, it is a universal opinion of physicians that smoking contributes to a smoker's heart disease if he/she smoked at this rate. In fact smoking is a contributing cause of death for about 400,000 people annually but "only" contributes to fewer than 100,000 cases of lung cancer each year. Most elevations ofblood cholesterol that require medical treatment do not double the risk of heart disease. Furthermore, physicians, when treating a patient for a heart attack, will indicate that previous smoking of a half pack of cigarettes per day for 30 years, family history of heart disease (non-genetic), history of elevated cholesterol of 250 mg/dl are all contributing causes of their patient's heart attack. Considered by themselves, none of these factors have an elevated rate ratio greater than two. Epidemiological studies can, when evaluated together, provide more confidence in an association even in the absence of a "statistically significant" finding from any individual study. Greenland states, ".. .lack of `statistical significance' is not evidence of a lack of hazard... a claim by an expert that `statistical significance' or `nonsignificance' demonstrates presence or absence of causation should serve as a warning to the court that said expert is incompetent in the use of statistics for causal inference." 31 Consider, for example, five different political polls that indicate that one of the candidates for office is ahead by between two and three points, a finding that is within the "sampling error" of each individual poll (non-statistically significant in each individual poll). It would be reasonable to conclude that the candidate was going to win on a more likely than not basis. 4. "Temporality" considers whether or not the cause precedes the effect. While this is generally relevant to cause effect determination, there will be some cases where strict temporality is not necessary in order to evaluate etiologic relationships. Temporality is most commonly established through non-epidemiological evidence. Tobacco companies argue correctly that the current body of epidemiology literature cannot distinguish temporality from a genetic link between the tendency to smoke and risk factors for cancer. Conclusive support for the temporal relation of smoking and cancer is derived from molecular and animal data. 5. "Biologic gradient" for the cause-effect link in question, asks whether a dose-response relationship, or biologic gradient exists. A common fallacy occurs when scientists limit consideration of dose-response to linear relationships between the proposed cause-effect link. Hemoglobin oxygenation provides a simple example of a common non-linear doseresponse curve. As more oxygen is added to a hemoglobin molecule its affinity for oxygen increases in a non-linear fashion. Hence the dose-response relationship for hemoglobin oxygenation produces a sigmoidal or S-shaped curve. 6. A dose-response relationship is not always necessary in order to establish causation. As Lanes and Poole noted, there are several reasons that a dose-response relationship is not a sin 55 quo non requirement for the establishment of a cause-effect relationship: "First, it is possible for sufficient evidence to be amassed for an association to be considered causal without any form of dose-response relation being observed. As two notable examples, most epidemiologists found persuasive the early evidence of association between vinyl chloride and angiosarcoma of the liver, and between diethylstilbestrol and adenocarcinoma of the vagina, even though no dose-response relations were demonstrated. The acceptance ofthese two cancer-exposure relations was firmly established on case reports only. The presence of a dose-response pattern in epidemiologic data is, after all, partly a function ofthe opportunity to study such a pattern. Second, the interpretation of an apparent dose-response relation in the data must include the possible non-causal reasons for its appearance, such as confounding and other sources ofbias. Hence, one might expect to see a non-causal dose-response relation between alcohol consumption and lung cancer due to a correlation between alcohol and smoking. Third, a dose-response curve reflects complex biological mechanisms and may take any form. For instance, there may be a 'threshold' dose below which there is no effect or a flat portion along which all doses produce the same magnitude of effect ... Finally, estimates of effect made in relative terms (i.e., with the rate ratio) may obscure or present the misleading appearance of a relation of dose to the absolute magnitude of response, which is measured by the rate difference." 32 7. "Consistency" inquires as to whether or not a proposed effect has been or can be observed repeatedly under different circumstances. This consideration is useful, and many different conditions and types of study can meet it. However repetition of findings under similar conditions is not necessarily supportive of this consideration. Similar biases (or confounding) occur under similar conditions. 8. "Specificity" asks if each cause has single or logically related similar effects. This is rarely a useful consideration because many causes have multiple effects. Asbestos causes asbestosis, lung cancer, mesothelioma and other cancers. Smoking causes heart disease, lung cancer, oral cancer, etc. Trauma from a car accident can cause many different injuries. The analysis of specificity can be recast as the exclusion of a group of diseases in which the exposure is not associated with the disease. 9. "Biological plausibility" is an assessment ofwhether or not the theory that explains how an exposure causes a disease is consistent with other known mechanisms of disease causation. Physicians do not usually require a specific understanding of the underlying mechanism of an injury or disease before assessing causation. The contemplation ofbiological plausibly is the most onerous of Hill's considerations to satisfy in that it demands a level of detail of a disease's etiology that is sometimes impractical or unobtainable through existing or possible experimentation. Medical practitioners and etiologists rarely, if ever, hesitate to form conclusions about disease causation for want of more specific knowledge of mechanistic understanding. Scientists do not understand exactly how tobacco smoke causes cancer, yet 56 tobacco smoke is a long-recognized cause of cancer. In the same way, an exposure may be identified as the "sole" cause of a disease, though it is in fact a part of a constellation of causes. A bullet wound to the chest may damage many different organs while causing the death of a person who is shot. Though damage to the heart, lung or pancreas may have been the mechanism of death, no doctor would refrain from concluding that the bullet was the cause of death. 10. "Coherence" addresses the issue of consistency between the causal theory and that which is already known about the exposure or disease. Coherence deals with the known facts, in contrast to the previously mentioned biological plausibility, which deals with theories of disease causation. When little is known about a condition, coherence is easily satisfied. However, in such cases, meeting this aspect of association does not tell much about the association. 11. "Experimental evidence" includes studies of mechanisms of disease causation, which use experimental evidence and observation as the basis for their conclusions. The data may be derived from animal studies, laboratory studies, controlled clinical trials, or observational pathology studies. Animal studies are relevant to human inference. Animal studies are performed for application to human health, not to animal health. Animal studies are not conducted to determine health risks to mice, rats, dogs or cats. They are not conducted out of concern for mouse or rat health. They are conducted because it is generally felt that inferences about human risks can be drawn from animal studies. If scientists argue that animal studies are irrelevant to human inference, they should explain why inferences are not to be drawn since many animal studies indicate that illnesses in humans (especially cancer) can be reproduced in animals. Wilbourn et al. (1986) support this notion from their study of the responses of animals to carcinogens. "Neoplasms of rodents and other animals are, however, fundamentally similar in nature, and there are many examples of chemicals that cause tumors in both humans and animals. It is a fundamental principle of the IARC Monographs evaluations that `in the absence of adequate data on humans, it is biologically plausible and prudent to regard agents and mixtures for which there is sufficient evidence of carcinogenicity in experimental animals as they presented a carcinogenic risk to humans."33 34 Paul Kotin, former medical director for Johns-Manville writes: "...ingestion by human beings of any amounts of a compound shown to be carcinogenic in test animals must be regarded as a threat to human health."35 Companies and government agencies perform the animal studies, which cost as much as five hundred thousand dollars each, because they are valuable. Animal studies are a key component of Koch's postulates and thus have been the fundamental basis for medical epistemology since the 19th century. If negative animal studies are relevant, positive studies must also be relevant. It is for this reason that regulatory agencies including the NIH, FDA, EPA, NIOSH and the National Toxicology Program rely on, conduct, and fund animal studies. Animal models are used to test causation and 57 treatments for a variety of non-cancer effects including drug side effects, teratogenicity, asthma, heart disease, and medical device testing. 12. "Analogy" takes in to consideration epidemiological and other studies to determine if analogous substances caused adverse health effects. 13. After delineating each of his nine points, Hill's final emphasis placed responsibility on scientists for making causal judgments without blind (in fact without any) reliance on "statistical tests." "What they [Hill's nine points] can do, with greater or less strength, is to help us to make up our minds on the fundamental question- is there any other way of explaining the set of facts before us, is there any other answer equally, or more, likely than cause and effect? No formal tests of significance can answer those questions. Such tests can, and should, remind us ofthe effects that the play of chance can create, and they will instruct us in the likely magnitude of these effects. Beyond that they contribute nothing to the `proof of our hypothesis.... The question that I had to answer, by the use of the National Health Insurance records of that time [1930], was this: Do the workers in the cardroom [sic] ofthe spinning mill, who tend the machines that clean the raw cotton, have a sickness experience in any way different from that of other operatives in the same mills who are relatively unexposed to the dust and fibre that were features of the cardroom? The answer was an unqualified `Yes.' From age 30 to age 60 the cardroom workers suffered over three times as much from respiratory causes ofillness whereas from non-respiratory causes their experience was not different from that of the other workers. This pronounced difference with the respiratory causes was derived not from abnormally long periods of sickness but rather from an excessive number of repeated absences from work of the cardroom workers. All this has rightly passed into the limbo of forgotten things. What interests me today is this: My results were set out for men and women separately and for half a dozen age groups in 36 tables. So there were plenty of sums. Yet I cannot find that anywhere I thought it necessary to use a test of significance. The evidence was so clear-cut, the differences between the groups were mainly so large, the contrast between respiratory and non-respiratory causes of illness so specific, that no formal tests could really contribute anything of value to the argument. So why use them? ... Some editors ofjournals will return an article because tests of significance have not been applied. Yet there are innumerable situations in which they are totally unnecessary- because the difference is grotesquely obvious.. .Of course I exaggerate. Yet too often I suspect we waste a deal oftime, we grasp the shadow and lose the substance. We weaken our capacity to interpret data and to take reasonable decisions whatever the value of P. And far too often we deduce `no difference' from `no significant difference.' Like fire, the chi square test an excellent servant and a bad master." 36 58 14. Hill recognized that decisions have to be made in the absence of perfect data noting: "All scientific work is incomplete--whether it be [sic] observational or experimental. All scientific work is liable to be upset or modified by advancing knowledge. That does not confer upon us a freedom to ignore the knowledge we already have, or to postpone the action that it appears to demand at a given time." Applying Hill's Model To The Question Of Whether Or Not Chrysotile As Found In Products Causes Mesothelioma The following analysis of the data according to these aspects of association for determining cause and effect relationships proposed by Sir Austin Bradford Hill clearly shows that chrysotile is a cause or contributing cause of mesothelioma in man. 15. Strength of Association: As shown in Table 1, numerous scientific studies of workers exposed to "chrysotile asbestos" have shown an increased rate ratio > 2 or a Standard Mortality Ratio > 200 demonstrating that the risk of contracting mesothelioma after exposure to chrysotile asbestos is more than double that of individuals who have not had such exposure. While most of these studies are of cohorts of workers who were exposed to chrysotile containing low levels oftremolite, an amphibole form of asbestos, several studies revealed an increased risk of contracting mesothelioma from exposure to chrysotile that did not contain any measurable concentration of tremolite. In a study of Zimbabwean miners exposed to "pure" chrysotile the statistically significant rate ratio was 2801, with a confidence interval of 712 - 7623. 37 Piolatto et al, studied Italian chrysotile production workers at a mine and mill where they could not find tremolite contamination of any ore samples. 38 The statistically significant rate ratio was 37, with a confidence interval of 6.1 121. Rogers et al. performed a case controlled study on mesothelioma cases obtained from the Australian mesothelioma surveillance program. They "recorded a substantial number of mesothelioma patients in home the only detectable type of asbestos was chrysotile (table 9.)"39 The rate ratios for all three studies are statistically significant and well above two. 16. Unfortunately, the companies who present the argument that pure chrysotile does not cause mesothelioma failed to utilize fibers from this region ofthe world as a raw material in the manufacture of their asbestos-containing products. There are no studies of American workers exposed to products made with Zimbabwean chrysotile just as there are no studies of Americans who smoked Zimbabwean cigarettes, neither of which are used in the United States. The absence of such data, however, does not support an argument that Zimbabwean cigarettes do not cause lung cancer nor the argument that chrysotile does not cause mesothelioma. In fact, no one argues that chrysotile is not carcinogenic in man. In addition, studies have shown that chrysotile acts synergistically with other asbestos fiber types including its fellow traveler tremolite. Since there are virtually no worker populations in the United States that have been exposed to "pure" chrysotile fiber, the proper evaluation of their risk for contracting mesothelioma is to look at relative risk rates for mixed asbestos 59 dust exposure, combinations of chrysotile and amphibole asbestos. As Table 2 demonstrates, there are a significant number of well-conducted epidemiologic studies that have found an increased risk of mesothelioma more than two times the rate of mesothelioma in the general population. This is not surprising considering the fact that exposure to asbestos is the predominant cause of mesothelioma in humans. 4,5 4 5 Table 2: Epidemiologic studies Study (Authors) Year Population Size Studied Cullen, MR and 1991 Baloyi, RS Camus, M, 1998 Siemiatycki, J and Meek, B Baloyi 1989 Enterline, PE, 1987 Hartley, J, and Henderson, V Nokso-Koivisto, P 1994 and Pukkala, E Borrow, M et al 1973 Morinaga et al 1989 Strurm et al 1993 Rogars AJ, et al 1991 Hughes, JM and 1986 Weill, H Begin R et al 1992 Doll, R and Peto, J 1985 Feingold, A. citation from depositions about mesothelioma in Quebec workers Berry 1996 Stayner, LT, 1996 Dankovic, DA, and Lemen, RA 51 11,651 300 1,074 8,391 600 50,000 50,000 50,000 5,500 50,000 4,022 10,000 # of Years Studied 21 19 9 39 38 14 18 30 5 50 35 50 50 # of Meso Cases 3 7 3 6 8 10 6 67 2 12 20 12 38 10 45 R.R. >2 (Y/N) Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Stat. Sig. (Y/N) Yes Rate Expected Ratio* 2,801 0.001071 Yes 32 0.221369 Yes 1,111 0.0027 Yes 143 0.041886 Yes 25 0.318858 Yes 1,190 0.0084 Yes 2 0.9 Yes 45 1.5 Yes 2 0.25 Yes 44 0.275 Yes 11 1.75 Yes 60 0.2011 Yes 76 0.5 #DIV/0! #DIV/0! 4 Table 2 in form and data are excerpted from Doll & Peto's 1985 study, "Asbestos, Effects on health of exposure to asbestos."* 5 "Because of its rarity, this tumor [Diffuse Malignant Mesothelioma] is said to be a signal tumor of asbestos exposure. . . . In 1943, Wedler first associated DMM with asbestos exposure, and in 1947 the first case in an asbestos worker in the United States was described in the Case Records of the Massachusetts General Hospital." From Rom, W.N. (ed.), Environmental and Occupational Medicine, Little, Brown, and Company, Boston, 1983. 60 17. Moreover, recent studies indicate that rate ratio of two is not required to establish causation.40 18. Since the Texas Supreme Court's ruling on proof of causation, new medical information has come to light that indicates that the scientific information presented to the court on the establishment of doubling of risk was incorrect. There is unequivocal scientific evidence that chrysotile asbestos is a cause of mesothelioma in human beings and that it doubles the risk of contraction of this disease at very low doses. This would be true whether or not any specific epidemiologic study ofworkers exposed to "pure chrysotile" revealed a SMR or rate ratio greater than 2 for mesothelioma.6 As Greenland has shown, a rate ratio oftwo does not determine whether an exposure is more likely than not to cause a certain disease in an individual. "in legal proceedings one often sees the mathematically incorrect claim that a relative risk (RR) of 2.0 means that there is a 50% chance that a particular case of disease was caused by exposure, and more generally the incorrect equating of the probability of causation to the attributable fraction (RR-1)/RR. ..."41 Epidemiological studies with rate ratios less than two can establish, to a reasonable degree of medical certainty, that there is a doubling of the risk from an exposure in the exposed population. 19. Temporality: In all the studies, the exposure to chrysotile preceded the development of mesothelioma satisfying this consideration. 20. Dose response: A majority of researchers and physicians who have addressed the issue agree that chrysotile as sold and used in the United States, is a cause of mesothelioma, and agree furthermore that the pattern of disease induction has a dose-response relationship.42 Rogers et al., found "evidence of a dose-response effect as reflected in the trend to an increasing odds ratio (OR) at relatively low fiber concentrations..."43 Animal studies have confirmed this dose response relationship. Heintz et al., conducted a tissue culture study of the effects on the expression of two proto-oncogenes of crocidolite and chrysotile asbestos on rat pleural mesothelial cell lines (RPM) and HTE cell lines, progenitor cell types of bronchogenic carcinoma. The researchers found that both fibers increased the expression of these two genes in similar rates in proportion to dosage in grams.44 Every United States government agency that has looked into the issue of chrysotile and mesothelioma, the World Trade Organization,7 and all non-Commonwealth scientists have determined that this dose- 6 In the case of mesothelioma, a rate ratio and a SMR (standardized mortality ratio) can be used almost interchangeably. Since every case of mesothelioma is a death sentence for the individual afflicted with this disease, studies of those who have mesothelioma can be considered mortality studies rather than morbidity studies. Since mesothelioma is invariably fatal, the only question after diagnosis is how long will the individual live. As such, each diagnosed case in a study can count towards determining a SMR for the study. 7 "This carcinogenicity was confirmed by the experts consulted by the Panel, with respect to both lung cancers and mesotheliomas, even though the experts appear to acknowledge that chrysotile is less likely to cause mesotheliomas than amphiboles. We also note that the experts confirmed that the types of cancer concerned had a mortality rate of close to 100 per cent." WTO report, World Trade Organization, WT/DS135/AB/R12, March 2001, (01-1157), European Communities - Measures Affecting Asbestos And Asbestos-Containing Products, AB-2000-11, Report of 61 response relationship has no threshold, that is, there is no level of exposure to chrysotile that does not raise one's risk of developing mesothelioma. 21. Consistency: This consideration has been amply demonstrated with regard to chrysotile and mesothelioma. Animal studies have consistently shown that chrysotile causes mesothelioma in repeated studies various exposure levels, routes of administration and in various species. (See table 3*) Cases of mesothelioma have been observed from chrysotile asbestos in chrysotile miners in Canada,45 46 and in Zimbabwe.47 Workers exposed during the manufacture of chrysotile asbestos cement in Louisiana,48 workers manufacturing textiles containing chrysotile asbestos in North Carolina49 and New Jersey,50 workers who manufactured chrysotile asbestos friction products in Connecticut,51 England52 and Germany,53 mechanics who installed chrysotile asbestos brake linings in Canada54, United States 55 56 57, England 58, and Denmark,59 railroad workers using chrysotile insulation on locomotives in the United States,60 Italy61 and Switzerland,62 an Italian worker in the wine filter industry,63 wives ofworkers who manufactured chrysotile textiles and friction products in New York State,64 and individuals who simply lived in close proximity to a chrysotile asbestos textile and friction products plant have all developed mesothelioma.65 66 Animal Studies of Chrysotile Chrysotile is a proven carcinogen both in animals and humans. It also causes both mesothelioma and lung cancer in both animals and humans. The studies involving human subjects are outlined in the tables 1 and 2 in the appendix and the chart in the text. There are also many experiments involving animal subjects that show that chrysotile causes mesothelioma. These are summarized below in chart format. Table 3: Animal Studies - in vitro studies Article Fiber Type Year Appel JD, Fasy JM, chrysotile 1988 Kohtz DS, Kohtz JD, Johnson EM Bolton RE, Davis JMG, chrysotile, 1982 Donaldson K, Wright A amosite Davis JMG, Beckett ST, chrysotile, 1978 Bolton RE, Collings P, crocidolite, Middleton AP amosite Jaurand MC, Kheuang chrysotile 1986 L, Magne L, Bignon J chrysotile mediates damage enabling transfected plasmid to be replicated. chrysotile samples found to be more carcinogenic than the amosite chrysotile samples were the most fibrotic and the most tumorigenic. in vitro treatment of rat pleural mesothelial cells with chrysotile fibers. At 7 micrograms/ml, induction of 21% abnormal metaphases. Aberrations were primarily of chromatid type, also breaks and fragments. the Appellate Body 62 Article Korkina LG, Durner AD, Suslova TB, Cheremisina ZP, Daugel-Dauge NO, Afanas'ev IB Libbus BL, Craighead JE Fiber Type chrysotile crocidolite, chrysotile Lund LG, Aust AE Mochaux G, Bichon J, Jaurand MC, Lafuma J, Sebastien P, Masse R, Hirsch A, Goni J Osgood C, Sterling D crocidolite, amosite, chrysotile, or tremolite chrysotile, crocidolite Suzuki Y, Kohyama N Valerio F, de Ferrari M, Ottagio L, Repetto E, Santi L amosite, chrysotile, and zeolite chrysotile, crocidolite Dumas L, Page M chrysotile, crocidolite, amosite Year 1992 mutagenic action probably mediated by iron-oxygen complexes plus hydrogen peroxide. 1988 1992 1981 rat mesotheliomas induced by crocidolite or chrysotile. loss of chromosomes and translocations observed. chrysotile induced single strand breaks in DNA. percent of DNA with SSB directly related to its iron content. mesotheliomas in rats, chrysotile more carcinogenic than crocidolite. 1991 1984 chrysotile and amosite induced sexchromosome aneuploidy, which is associated with development and/or progression of cancers. chrysotile appeared to be the more effective agent. chrysotile and amosite had the highest tumor incidence 1983 1986 statistically significant increase in chromosome and chromatid damage were present after treatment with chrysotile fibers. Anomalies most frequently chromatid breakage. chrysotile was the most cytotoxic of all the fibers tested. chrysotile increased the maximum cell density of fibroblasts, which may be one step in carcinogenesis. 22. Specificity: Like tobacco smoke, other asbestos fiber types, and many other human carcinogens, chrysotile's effects are not specific. Most human environmental carcinogens cause more than one kind of cancer. Therefore, this is not evidence against a cause-effect relationship. 23. Biologic Plausibility: It is plausible that chrysotile is a cause of mesothelioma because the 63 mechanistic and biologic facts concerning chrysotile and mesothelioma are consistent with the known theories of mesothelioma induction accepted in the scientific community. It has been known since the mid-1940s from reports by Gardner and Vorwald that the health effects of asbestos were related to the shape of the fiber and not its chemical composition. Therefore, any argument regarding the chemical constituents of the various asbestos fiber types as a determinant of their capability for causing mesothelioma is not biologically plausible. The shape of the fiber is the key factor in assessing a substance's potential to induce mesothelioma. Chrysotile, like crocidolite, can be found as extremely thin fibers due to longitudinal cleaving.67 It is universally accepted that chrysotile is a cause of cancer in the lung. In addition, chrysotile migrates to and is concentrated in the pleura to a much greater extent than amphibole fibers.68 Since chrysotile is carcinogenic and is present in high concentrations in the pleura where mesothelioma is induced, it is biologically plausible that it causes or contributes to the development of mesothelioma. Many molecular studies indicate how chrysotile induces mesothelioma. (See Table 3*) These studies indicate that chrysotile penetrates the cell, enters the nucleus and induces abnormal chromosome formation in dividing cells. Some of these abnormalities include the deletion of the P53 gene that controls cell growth.69 Finally, no one disputes the fact that tremolite, the type of asbestos that contaminates Canadian chrysotile ore, is a cause of mesothelioma. As Doll noted, this tremolite is not removed in the processing of chrysotile as it moved from mine to product.70 24. Coherence: Chrysotile is a probable cause of mesothelioma according to current known facts about asbestos, mesothelioma, and cancer causation. Chrysotile is found in the pleura during pathological examination, and is found in greater abundance than other forms of asbestos fibers. For example Suzuki analyzed asbestos fibers in the lung and mesothelial tissues taken from 151 human malignant mesothelioma tumors.71 Most commonly they found the lung tissues contained an admixture of chrysotile with amphiboles, followed by amphiboles alone, and also chrysotile alone. However, in the pleura chrysotile alone was found most often, followed by chrysotile plus amphibole and amphibole alone. No consistent relationship was found between fiber types found in the lung and those in the pleura.72 Chrysotile enters cells and disrupts the DNA division in a manner consistent with carcinogenesis. (See Table 3*) Chrysotile causes mesothelioma in animals, and is more potent in doing so than are other forms of asbestos. (See Table 3*) Chrysotile is an undisputed carcinogen in humans, in that it causes lung cancer. All of this evidence indicates that the causal relationship between chrysotile and mesothelioma is coherent with all known facts related to mesothelioma causation and chrysotile pathogenicity. 25. Experimental: Studies of several different animal species who have inhaled or been injected with pure chrysotile fibers show the development of mesothelioma. 8 73 (See table 3 *) Most8 8 Standard "pure" asbestos samples to be used for biomedical research were first prepared by the International Union Against Cancer (UICC) in 1966 in the United States and South Africa. Analysis of these samples shows that the Canadian chrysotile UICC sample does not contain any fibrous impurities like tremolite. Kohyama, Shinohara and Suzuki, "Mineral Phases and Some Reexamined Characteristics of the International Union Against Cancer Standard Asbestos Samples," Am. J. Indus. Med., 30:515-528 (1996). 64 of these animal studies have used UICC reference chrysotile, which has no measurable tremolite contamination.74 Ike Weaver, the Chairman of the Friction Materials Standards Institute, an asbestos brake trade organization, noted the importance of this phenomenon. When advised of a British paper that indicated that mesotheliomas were observed in animals exposed to chrysotile asbestos, he stated this was "bad news for those hoping that chrysotile would be proven not to be associated with mesothelioma."75 26. Analogy: Other asbestos fibers with similar morphologies cause mesothelioma. The presence of tremolite in chrysotile, and the universal acceptance of tremolite's ability to cause mesothelioma further help satisfy this consideration and makes the "chrysotile is safe" argument specious. TREMOLITE CONTAMINATION 27. Chrysotile ore mined in Canada has been found to contain a small percentage oftremolite, a form of amphibole asbestos. Although tremolite is not mined commercially, it is a common contaminant of chrysotile mineral deposits. 76 It is so common that Dr. Bruce Case favors the simple compound phrase "chrysotile/tremolite" to describe chrysotile dust.77 Dr. Case asserts further that, "It is possible that chrysotile is always associated with some degree of tremolite (and often other amphiboles, commercial and non-commercial) if exposure has been long enough and it is looked for (in the lung) hard enough."78 According to Dr. Graham Gibbs, a geologist with extensive experience in the Canadian mines, the manner in which the mined chrysotile ore is "processed" into raw fiber does not remove the naturally occurring tremolite contamination.79 Dr. Thomas Mancuso reached a similar conclusion in his study of railroad machinists.80 The real proof that the tremolite is not removed during the processing of chrysotile ore or in the manufacture of "chrysotile" products can be found in the lungs of exposed workers where tremolite fibers have been found.81 Additionally, Pooley (1976) studied lung tissue samples of American and Swedish textile workers. He found that in many cases considered to be only chrysotile exposures, there were equal, if not greater amounts of amphibole fibers found.82 This indicates not only the presence ofthe amphibole fiber, but also the higher affinity with which amphibole fibers accumulate within the lung. These workers encompassed all types of trades83 and were exposed to a variety of processed chrysotile products, including gaskets.9 28. Furthermore, as Doll and Peto state, the question of whether or not chrysotile alone or chrysotile contaminated with tremolite is the cause of mesothelioma is academic.84 In the 9 A significant number of long tremolite fibers were detected in a man who worked manufacturing chrysotile asbestos blankets and gaskets from 1939 to 1946. Srebro and Roggli, "Asbestos-Related Disease Associated with Exposure to Asbestiform Tremolite," Am J of Ind Med, 26:809 (1994) 65 real world of workers exposed to products, for all intents and purposes, there are no "pure chrysotile" exposures.10 Accordingly, as Doll and Peto note, it is important to look at combined exposures, to chrysotile AND amphiboles, because exposure to a small amount of amphibole added to chrysotile causes a disproportionate mesothelioma risk.85 It is the effect ofthis combined exposure that is being evaluated to determine whether or not the products in question were the cause of the worker's mesothelioma. By way of analogy, placing a lit match alone on a wooden desk may create a risk of fire, but placing a lit match on a gasoline soaked-rag on the same desk transforms that risk into a flame. Evaluating the risk of the match alone is not a measure of the true risk when the lit match is always placed on a gasoline soaked-rag, which is always present on the desk. Corruption of Canadian Research To further the myth regarding the apparent safety of Canadian asbestos and related products, it comes as no surprise that large-scale corruption of scientific literature took place. For over 60 years Canadian asbestos companies successfully repressed and/or modified the state ofthe art to cover-up the hazards of asbestos. The following examples of fraud and distortion by researchers on the payroll of asbestos companies and/or their insurers represent only the tip of the iceberg: 29. Canadian asbestos mine owners created a propaganda program telling buyers who were concerned about the health effects asbestos that their Canadian "chrysotile" asbestos was safe. In a December 13, 1938, Dr. Anthony J. Lanza wrote a letter to M. Bowditch, Director of the Massachusetts Division of Occupational Hygiene, referring to the Canadian theory that some asbestos fibers are more hazardous than others: Ofcourse, the asbestospeople in Canada have advanced that ideafor some time as an explanation ofwhy asbestos seems to be more clinically severe in England than in this country but I have always had thefeeling that their argument was motivated by self-interest rather than to make a scientific contribution. 30. Dr. Lanza knew the chrysotile asbestos being mined in Canada was hazardous because he had refused to allow the publication of a study performed by Dr. Pedley, a researcher at McGill University, of the miners at the Thetford chrysotile mine which showed that of 54 men evaluated 24 were diagnosed with asbestosis. This information is contained in a letter from Pedley to Burnette on October 11, 1932: ...In cooperation with the Metropolitan Life Insurance Company, a survey of two companies mining and milling asbestos, was made in July and September, 1930. Physical examination ofsome 150 men was made, together with chest x-rays, and an interesting state of affairs was disclosed, which was reported to Dr. A.J. Lanza of the Metropolitan Life Insurance Company, but to date permission has not been secured to publish the results ofthe study. [emphasis added] 10The only study of workers exposed to chrysotile without any tremolite contamination is that of Zimbabwean chrysotile miners. Cullen and Baloyi, Chrysotile Asbestos and Health in Zimbabwe, American Journal of Industrial Medicine (1991). 66 31. While in private correspondence Lanza conceded the hazardous nature of chrysotile asbestos, he perpetuated the myth of its safety in his public writings in 1933: Now, I am going to make this a little bit dramatic. So far as we could ascertain, there is no dust hazard or asbestos hazard in connection with the actual mining or quarrying operations.... in the open pit and quarry work there was no apparent pulmonary hazard8 32. He continued his assertions in 1935: In places where asbestos is mined or fabricated in North America there does not appear to be present the clear-cut clinicalpicture which is so unescapable [sic] in communities with a true silicosis hazard..*1 33. He reiterated the same myth in 1940: ...Asbestosis, however, is notfound among asbestos miners, most ofwhom work in open quarries or pits, nor among men engaged in milling operations whereby the asbestos is preparedfor shipment and bagged, but among workers in fabricating plants88 34. Dr. Sparks pointed out the inherent illegitimacy of Lanza's position in his publication in 1931: Of the asbestos imported into England, 80 per cent comesfrom Canada, so that it seems unlikely that you in the United States are dealing with a type of asbestos differentfrom that employed in England*9 35. Dr. Lanza again tried to minimize the effects of exposure to chrysotile at his presentation at the Seventh Saranac Conference in September 22-26, 1952. He indicated that US workers exposed to chrysotile asbestos had not experienced an increased rate of lung cancer in contrast to British workers who he asserted had been exposed to other fiber types. Dr. Merewether, chief inspector of the British factory inspectorate and author of numerous asbestos medical articles, was on hand to point out the fallacy of Dr. Lanza's position: First ofall, I think Dr. Lanza is misinformed about the proportions ofasbestos used and where they are used in England. The original cases ofAsbestosis, fifty years ago, were all Canadian asbestos. The earliest asbestos work in England was either seventy-five or eighty-two and there may have been some crystallinefiber then, but very quickly the asbestos trade concentrated on the white Canadian crystalline 90 36 * 36. This admonition, however, did not prevent Lanza from publishing misstatements with regard to the carcinogenic potential of chrysotile asbestos which were diametrically opposed 67 to the position he took in private correspondence fourteen years earlier and Merewether's specific admonition at the Seventh Saranac conference the very same year: Iwouldalso like topoint out that the experience with asbestosis in England appears to differ sharply with that in Canada and the UnitedStates. The authorities in Great Britain regard asbestosis as a very serious disease, much more so than silicosis, and they seem to be convinced that cancer ofthe lungs is afrequent sequela. This is not the experience in either Canada or in the United States91 37. Despite the efforts ofDr. Merewether, the Canadian plan was successful as the comments of Dr. Lanza were adopted by others and incorporated into their writings. For example, in 1958, H.E. Stokinger, who for 15 years, headed the ACGIH TLV committee (the group that set "safe" exposure levels for asbestos and other hazardous substances), wrote the following: ...Mineral dusts are commonly ofcomplex and inconstant composition, often varying according to locality, and thus are potentially capable of causing a variety of physiologic responses. As a case in point, pulmonary carcinoma is commonly associated with the long-term inhalation of asbestos in England, but not in America92 and ...It is of more than passing interest that the higher rate of cancer in asbestos workers in England is notparalleled in the UnitedStates or in Canada, according to Lanza (6). The causefor this difference may lie in the type ofasbestos; asbestos is a fibrousform ofseveral different species ofminerals, a point often disregarded,93 38. In both cases Stokinger cited Lanza's "authoritative" statements that Canadian asbestos was not harmful as authority for not considering asbestos to be a carcinogen and thus for not lowering the TLV. 39. This pattern of deception that began in the 1930's continued when Carey, Canadian asbestos mining company, considered warnings to be applied to exported asbestos products in 1977 (The domestic products carried a health warning): Confidentially the Kakiuchi staff told me that they have deliberately left out the word cancer from the text because this must not even be mentioned in Japan in connection with asbestos. Altogether they are against a warning label because they do not wish to raise problems with the workers.... I do not believe that we should raiseproblems withpeople who are more primitive than we are or less educated.94 40 * 40. The Canadian mines, through their trade organization the Quebec Asbestos Mining Association (QAMA), further corrupted the literature by forcing the deletion of evidence that 68 Canadian miners suffered from an increased risk of lung cancer. In the mid-1950s, the QAMA retained Drs. Braun and Truan to conduct a study ofthe prevalence of lung cancer in Canadian miners. A secret numbered draft report prepared in 1957 demonstrated a statistically significant (at 95%) increased rate of cancer in the miners. Commenting on the draft, Dr. Kenneth Wallace Smith, the medical director of Johns-Manville, wrote to Ivan Sabourin, the lawyer for the QAMA and head of the Conservative party of Quebec: Hugh Jackson andI have reviewed the condensation ofthe survey which was sent us. We have noted deletion ofall references to the association ofasbestosis and lung cancer in this condensation. While we believe that this information is of great scientific value, we can understand the desire of the Q.A.M.A. to emphasize the exposure of the asbestos miner and not the cases of asbestosis. We also are in agreement with the deletion ofthe reference to smoking and lung cancer. It must be recognized, however, that this report will be subjected to criticism when published because all other authors today correlate lung cancer to cases of asbestosis. [emphasis added]. 41. Incredibly, when the Braun/Truan study was published in 1958, instead of reporting an increased incidence of lung cancer among the Canadian chrysotile asbestos miners, the authors offered the following: On the basis ofwhat are believed to be complete and reliable data, it seemsfair to conclude that the asbestos miners in the province of Quebec do not have a significantly higher death ratefrom lung cancer than do comparable segments ofthe generalpopulation.95 42. Once again the Canadians were successful in influencing the opinions of H.E. Stokinger who, in addition to his powerful role as head of the ACGIH TLV committee, was the editor of the journal to which this paper was submitted. In a letter to Dr. Braun, Stokinger stated: I, myself, was particularly pleased to learn the main conclusion of the paper was against the association of lung cancer with asbestos, for I had come to a similar conclusion on obviouslyfar less information but was afraid to say sofor this reason. I am enclosing a review which contains afew sentences that I have marked in this connection that appears in the AnnualReview ofMedicine, volume 7, 1956. You will recall at this time evidence greatlyfavored thepositive correlation oflung cancer on exposure to asbestos 96 43. The concealment of the true results of the Braun/Truan study influenced other researchers regarding the safety of chrysotile asbestos: In the United States, particularly since the studies of Braun and Truan, there is considerable conviction that asbestosis does not predispose to the development of lung cancer91 69 44. The QAMA's activities in corrupting the medical literature continued in the 1960s. Despite the attempts to convince the world that lung cancer was not associated with exposure to asbestos, they could not prevent the world medical community from discovering the truth about the hazards of asbestos. In October of 1964, Dr. Irving J. Selikoff and his colleagues held a conference on the biological effects of asbestos in New York. At that conference, Dr. Selikoff revealed the results of his study of some 1,500 asbestos insulation workers in the New York-New Jersey metropolitan area, which found a significant number of lung cancer deaths and cases of mesothelioma. At the conference, Dr. W.J. Smithers from England reported an increasing incidence oflung cancer in certain factory workers located in London. In addition, Dr. Thomas reported that, in a survey of urban dwellers in Cape Town, South Africa and Miami, Florida, the results showed an increase in the occurrence of cancer ofthe pleura, mesothelioma, likely due to the inhalation of asbestos dust. 45. At a meeting ofthe Asbestos Textile Institute on June 4, 1965 at Thetford Mines in Canada, Ivan Sabourin explained his plan to again enlist McGill University to combat this "adverse" information on asbestos carcinogenicity. He explained that the QAMA will: ...seek alliance with some university, such as McGill, for example, so that authoritative backgroundforpublicity can be had. Theprogram will start modestly, with competent men coming into it - men with a vast background of actual experience. They recognize the need to consolidate experiences, and also having traveled widely in other countries, theyfind that research units are usually located adjacent to a large, well equipped hospital. Frequently, the worker has a condition that is not attributable to association with asbestos, discovered through cooperation with the hospital staff.98 46. In addition to associating with McGill University, the QAMA created the Institute of Occupational and Environmental Health patterned after the British Asbestosis Research Council, a council appointed by three major British asbestos factories in 1958. In forming the Institute, the QAMA recorded that: Another long discussion was devoted to the question ofwhether or not we should publicize some of the activities ofour Committee. In this respect there was a very strongfeeling that this should be very restricted. All ofus are mindful ofthe rather poor reception given to the efforts ofthe tobacco industry to set up a council and a scientific committee to deal with the problem oftobacco and its effect on health. A good bit ofthis stemsfrom thefact that they erroneously over-publicized the council and its committee anddid it in a too wide-spreadfashion. Therefore, our Committee emphasized the absolute necessity of existence of a vote power of our Committee over any publicized statements concerning the existence of the Committee and the Institute and its activities. 99 47. The main item on the agenda ofthe first meeting of Occupational and Environmental Health 70 Committee was to review a proposal by Dr. J.C. McDonald ofMcGill University to conduct an epidemologic survey of Canadian miners and millers. At the time, the Committee was trying to combat the adverse publicity about asbestos generated by Dr. Selikoff's study. The Committee reported that: Appropriate material, it wasfelt by many, should be collected to counter some ofthe recent badpublicity suffered by the asbestos industry in the USA; after a review of information available, it was concluded that nothing newsworthy could be released at this time.100 48. A year later, the QAMA, still suffering from the revelations of Dr. Selikoff, reported: We continue to receive an extremely badpress concerning the question ofasbestos and health. Not only has Dr. Selikoff's latestpaper been given wide publicity across Canada concerning the alleged relationship between smoking, asbestos and lung cancer, but the Financial Post recently had an article on asbestos insulation in British railway coaches which seems almost actionable. The Public Relations Committee is strongly ofthe opinion that the time has comefor us to produce some rebuttal ourselves, either in a general way or medically substantiated to the extentpossible at this time, and we are anxious to meet with the Scientific Committee with a view to discussing the possibilities ofproviding some counter propaganda, as agreed at the Jasper meeting last summer.101 49. To formulate this propaganda and counter the claims made by Dr. Selikoff, the Scientific Committee needed "reliable" data other than that provided by a study of insulation workers. The Committee found what it was looking for in the studies of Dr. McDonald: The epidemiological survey ofDr. McDonald is a good case with chrysotile fibre, and the kind of study required with well defined exposures. Dr. McDonald also proposes to study the incidence ofmesothelioma in Canada.102 50. In furtherance of his study of the incidence of mesothelioma in Canadian miners and millers, Dr. McDonald, with substantial financial assistance from the QAMA, recruited his wife, Dr. Alison McDonald, and fellow McGill University colleagues, Drs. Graham Gibbs and Bruce Case. To date, Dr. McDonald has published dozens of papers, each of which attempts to exonerate chrysotile fibers as a cause of mesothelioma. Significantly, QAMA sought to fool the medical community, regulators, potential jurors, judges and members of the public. Its own scientist Dr. George Wright, the Chairman of the Institute of Occupational and Environmental Health, the man who approved the funding for Dr. McDonald's research, like Dr. Lanza before him, was: convinced that there is strong evidence that all types ofasbestosfibres are a cause of Mesothelioma... particularly when mixed with another material. Proofis positive 71 thatfibres cause other lung ailments besides cancer. This statement is intended to disclaim that only South African blue fibres [crocidolite] are the culprit.103 51. Similarly, Ike Weaver, the Chairman of the Friction Materials Standards Institute, a trade organization for the manufacturers of chrysotile asbestos brake products, declared in a speech before the Asbestos Textile Institute in 1973: Probably the single most significant event that occurred during the pastyear on the subject ofasbestos hazards was the meeting ofthe InternationalAgencyfor Research on Cancer that was heldat Lyon, France last October. This meeting was attended by more than a hundred and thirty medical researchers and representatives of government, industry and laborfrom virtually every major asbestos consuming or producing country in the world.... I think the followingfive items summarize their most important conclusions: (1) All major commercial types of asbestos cause cancer... (3) Evidence has been greatly strengthened that all commercial types of asbestos except Anthophyllite may be responsible for mesothelioma.... The most important item here is the incrimination of all major types of asbestos as causal agents for carcinoma, particularly mesothelioma. Most of the other items only confirm or substantiate previous conclusions. Since most of us use substantial amounts ofChrysotile asbestos in ourformulations, association ofthis material with mesothelioma and other types ofcancer is ofserious concern.104 52. The corruption of the medical literature continued into the 1990s. Paul J. Hanly, Jr. an attorney for Turner & Newell described the relationship of Dr. J. C. Wagner, another scientific "authority" in the asbestos field, with Owens-Illinois (O-I). ... O-I had beenpayingDr. Wagner $6,000.00per monthfor some time irrespective ofwhether Dr. Wagner did any workfor O-I, andfurther that the money waspaid by O-I to a bank account in the U.S. in the name ofa thirdparty. Hanly continued by demonstrating how the O-I payments effectively altered Dr. Wagner's published findings: ..Mr. Shaw [O-I's lawyer] privately confirmed to me after the meeting that he was trying to persuade Dr. Wagner to say or write publicly that only crocidolite asbestos was an undeniable cause ofmesothelioma, and that the role ofamosite asbestos was non-existent or at most minimal. At the time my own lay view was that thisposition was scientifically unsupportable. For that reason I also believed that Mr. Shaw would not be able to persuade Dr. Wagner to espouse a position that downplayed the role of amosite. I was therefore quite surprised when in a paper written two years later, Dr. Wagner wrote in a published paper that the evidence was overwhelming that the main cause ofmesothelioma was crocidolite asbestos- afiber type that O-I apparently never used- and that amosite asbestos was implicated in just a "few " cases. The paper fails to mention any financial 72 supportfrom O-I.105 53. Despite the efforts ofthe QAMA and Dr. McDonald and the other Canadian scientists, there is overwhelming evidence to support the conclusion that chrysotile asbestos fibers can cause mesothelioma. Universally, it is agreed that the predominant cause of mesothelioma in humans is exposure to asbestos. Outside of the Canadian community, it is widely accepted that chrysotile exposure is a significant contributing factor to mesotheliomas. The timing of the McDonald's research is significant. In the majority of articles discussing lung cancer and mesothelioma before 1965, there was no differentiation between different asbestos fiber types. As can be seen in the following chart, however, when chrysotile was mentioned, it was mentioned in the context of being associated with mesothelioma. 73 Article Wedler Wedler Mallory et al. Chief Inspector of Factories Wyers Doig Smith Cartier Weiss Leicher Bonser et al. Doll Bohlig and Jacob Francia and Monarca Braun and Truan Konig Keal Eisenstadt and Wilson Wagner et al. Schepers Sleggs Frenkel and Jager Heard and Williams McCaughey et al. Eisenstadt Thompson Wagner Smither et al. Enticknap Mancuso and Coulter Thomson et al. Thomson Enticknap and Smither Year 1943 1944 1947 1949 1949 1949 1952 1953 1953 1954 1955 1955 1955 1956 1958 1960 1960 1960 1960 1960 1961 1961 1961 1962 1962 1962 1962 1962 1962 1963 1963 1963 1963 Fiber Type Mentioned No No No No No No Yes Chrysotile [Data from Cartier] No No No No No No No No No No No Yes Crocidolite and chrysotile No No No No No No No Yes Crocidolite and chrysotile No No Yes Chrysotile No No Yes Crocidolite and chrysotile 74 Article Hourihane Owen Gafafer Elwood and Cochrane Year 1964 1964 1964 1964 Fiber Type Mentioned No No No No 75 54. Two recent publications highlight the fact that the maj ority ofthe world medical community considers chrysotile to be a cause ofmesothelioma. In 1997, a multidisciplinary gathering of nineteen pathologists, radiologists, occupational and pulmonary physicians, epidemiologists, toxicologists, industrial hygienists, and clinical and laboratory scientists held a meeting in Helsinki, Finland to agree upon criteria for attributing disorders of the lung and pleura in association with asbestos. Collectively, the group had published over 1000 articles on asbestos and asbestos-associated disorders. The consensus ofthe group was that all types of malignant mesothelioma can be induced by asbestos, with the amphiboles showing greater carcinogenic potency than chrysotile.106 55. The second publication was a monograph devoted specifically to chrysotile asbestos that was prepared by the International Programme on Chemical Safety in conjunction with the World Health Organization. After an extensive review of the world's literature, this body concluded that "commercial grades of chrysotile have been associated with an increased risk ofpneumonoconiosis, lung cancer and mesothelioma in numerous epidemiological studies of exposed workers."107 WTO Report On Chrysotile 56. Much ofthe information and language used by companies to try and show that chrysotile does not cause mesothelioma was developed by the Canadian asbestos mining industry and the Canadian government. This information was used to oppose the EEU's ban on all asbestos, including chrysotile. The WTO recently ruled on this ban, and in deciding the case in favor of France and the European Union, and against Canada, the WTO rejected the two main Canadian arguments; that chrysotile can be used in a safe manner, and that chrysotile doesn't cause mesothelioma. The language used in the decision was quite clear, as shown in this extensive excerpt. 76 i. We note that the carcinogenicity ofchrysotilefibers has been acknowledged for some time by international bodies.108 This carcinogenicity was confirmed by the experts consulted by the Panel, with respect to both lung cancers and mesotheliomas, even though the experts appear to acknowledge that chrysotile is less likely to cause mesotheliomas than amphiboles. We also note that the experts confirmed that the types of cancer concerned had a mortality rate ofclose to 100 per cent. We therefore consider that we have sufficient evidence that there is in fact a serious carcinogenic risk associatedwith the inhalation ofchrysotilefibres. Moreover, in the light ofthe comments made by one ofthe experts, the doubts expressed by Canada with respect to the direct effects of chrysotile on mesotheliomas and lung cancers are not sufficient to conclude that an official responsibleforpublic healthpolicy would find that there was not enough evidence ofthe existence ofapublic health risk. 57.The WTO also made it clear that Canada had failed to overcome their burden of proof in regards to showing that chrysotile didn't pose a unique health risk by causing mesothelioma. ii. The EC has made a prima facie case for the existence of a health risk in connection with the use ofchrysotile, in particular as regards lung cancer and mesothelioma in the occupational sectors downstream ofproduction and processing and for the public in general in relation to chrysotile-cementproducts. Thisprimafacie case has not been rebutted by Canada. Moreover, the Panel considers that the comments by the experts confirm the health risk associated with exposure to chrysotile in its various uses. The Panel therefore considers that the EC have shown that the policy of prohibiting chrysotile asbestos implemented by the Decree falls within the range of policies designed to protect human life or health.109 58. All of the experts consulted with by the WTO determined that chrysotile did indeed pose a health risk to those exposed to it in general, with one of those risks being mesothelioma. "The pathologies which the Panel identified as being associated with chrysotile are of a very serious nature, namely lung cancer and mesothelioma, which is also a form of cancer."110 It becomes clear through examining this decision, that the argument that chrysotile doesn't cause mesothelioma is one based not in health, medicine or science, but rather a decision based on financial motives for a small group of individuals. 59. The INSERM report, a report by experts in France, found that "As regards the risk of mesothelioma, the effect of chrysotile fibres is incontestable, even though less serious than 77 that of certain amphiboles."111 60. The EC point out that any doubts with regard to the carcinogenicity of chrysotile asbestos have been removed by the joint report: Chrysotile is carcinogenic, just as much as amphiboles when it comes to lung cancer but less than amphiboles when it comes to mesothelioma (ratio of1 to 3 but same order of magnitude). As regards mesothelioma, this information has been largely confirmed by the study published by Camus et al.112 on cancer mortality among women living in close proximity to chrysotile asbestos mines in Quebec. This study shows a net excess of mesothelioma cases (the risk is at least seven times higher than among women living elsewhere in Quebec).113 61. The report of the Panel on European Communities - Measures Affecting Asbestos and Asbestos - Containing Products114, made several relevant conclusions: 3.104 The European Communities affirm that the carcinogenic character ofasbestos for humans is internationally recognized. Since 1977, the WHO has recognized that all varieties of asbestos, including chrysotile, are carcinogenic, causing cancer of the lung or mesothelioma.115 In 1986, the ILO advised lawmakers, through Convention No. 162116, to have asbestos replaced by less harmful materials or technologies as soon as possible. In 1996, the WHO recommended that asbestos, including chrysotile asbestos, be replaced by harmless substitutes, whereverpossible. In 1998, WHO reaffirmed the carcinogenic effect of chrysotile asbestos, particularly with respect to mesothelioma, continued to promote substitution and noted that the risk was very widespread among numerous categories ofworkers. 3.105 According to the EC, asbestos is at the root of a public health problem and chrysotile is the cause of most asbestos-related diseases. In 1998117, the WHO reaffirmed that chrysotile "has been associated with an increased risk ofpneumoconiosis, lung cancer and mesothelioma in numerous epidemiological studies ofexposed workers", which confirms the conclusions of the 1996 INSERM report. Since asbestos began to be usedfor industrial purposes, chrysotile has accounted for about 95 percent of world asbestos consumption. Between 1945 and 1980, about 97 percent of the asbestos consumed in France was chrysotile asbestos. Since 1988, chrysotile has accountedfor all the asbestos consumedin France.118 According to the EC, thesefigures show that most asbestos-related diseases are caused by chrysotile and not amphiboles, as Canada would have the Panel believe. This is confirmed by recent 78 publications. Thus, according to the study by Stayner et al.: iii. Our review of both the toxicologic and epidemiologic literature strongly supports the view that occupational exposure to chrysotile asbestos is associatedwith an increased risk ofboth lung cancer and mesothelioma.119 (a) The EC note that the study coordinated by J. Peto120 andpublished in 1999found that in six European countries (France, Germany, Italy, Netherlands, Switzerland, UnitedKingdom) nearly 10,000people died ofmesothelioma between 1990 and 1994. Moreover, it estimated that during the period 1995-2029 about 200,000 people would die of mesothelioma. Ifthesefigures are extrapolated to all the countries of Western Europe and deaths due to lung cancer are included, then the results show that exposure to asbestos could lead to about 500,000 deaths by cancer between now and 2029. In France, the number of deaths due to mesothelioma is increasing steadily. A recently published study,121 similar to that made by Peto et al., predicts that the annual number ofdeaths due to mesothelioma in France will go on increasing up to 2020. It is estimated that in France over the entire period 1996-2020 a total of20,000 men and 2,900 women will die ofmesothelioma. 62. The EC note that "safe" use is not a guarantee even when it is practised. Safe use is contested in two quite official publications: (b) A study conducted by the Quebec Workers' Health and Safety Commission (CSTT). This study shows that the risk ofmesothelioma increasedsteadily in Canada between 1967 and 1990, principally among servicing and maintenance workers. Ofthe 120 cases ofmesothelioma identified in the study, 49 were miners and mill workers, 50 were workers in the asbestos industry and 21 were servicing and maintenance workers. Ofthe 25 percent ofthese cases which involved short exposure, the most affected group were the servicing and maintenance workers. The study shows that the occurrence of mesothelioma is indeed due to chrysotile asbestos and that the incidence of the disease is growing more rapidly in the servicing and maintenance sector. This shows that, even in Canada, which specializes in safe use, the efficacy ofthe method remains to be proved. The EC note that, despite the existence ofthis CSTT study, the Canadian party declared during the consultation meeting held on July 8th, 1998 that it did not have any study at its disposal which covered the servicing and maintenance sector.122 (pp) an HSE study123, mentioned in the annex to the reportproducedfor Canada's Royal Academy in 1996following the publication ofthe INSERMreport. It shows that despite strictly controlled use - itfocuses exclusively onproduction workers -, there was still a 1.28 percent excess of mesothelioma cases, as opposed to 4.61 79 percent among people who had worked prior to 1969, when legislation was introduced in Great Britain. From this it can be concluded that controlled use does not prevent deaths from mesothelioma, even in specific sectors of industry employing limited numbers which are easy to regulate and control. The scientificfindings available to France when it took its decision to ban asbestos were unambiguous. It has been scientifically established that: (i) chrysotile is a toxic material which has a dramatic effect on health (mesothelioma, cancer ofthe lung, asbestosis) and is no less toxic than other varieties ofasbestos124 86. As I have outlined in this affidavit, the WTO panel found that "Much of the data relied upon by these companies and by Canada to maintain that chrysotile does not cause mesothelioma is largely erroneous and purposefully confusing and misleading." The European Communities (EC) also recognized this about Canada's WTO submission: According to the EC, Canada's case is based on incomplete and largely erroneous data. In its arguments, Canada relies heavily on assertions, which have no scientific foundation and, more often than not, are based on old or partial reports that are scientifically obsolete or of very debatable value. Canada makes many erroneous statements in support of its case and seeks to obscure well-established facts by creating confusion or omitting important data. The EC contend that many of Canada's assertions are unfounded or erroneous. For example: The failure to make a distinction between the risk ofmesothelioma and the risk of cancer of the lung: Canada regularly omits to point out that, whereas the risk of mesothelioma is lowerfor chrysotile thanfor amphiboles, this is not truefor cancer ofthe lung;* Additionally, The assertion that the risk due to chrysotile is "undetectable", whereas many scientific studies show that its effects are indisputable .125 87. The fallacy of the assertion that chrysotile is a safe fiber was demonstrated by the Asbestos Advisory Board for the State of New York in 1990 when they reported that the: [c]laim that various types ofasbestos differ in their hazard isparticularly insidious. It is putforth by the manufacturers ofCanadian asbestos (chrysotile asbestos), the type of asbestos most widely used in New York and throughout the United States. The central claim here is that the Canadianproduct, termed "chrysotile asbestos " is relatively harmless. However, that claim is not based onfact, and it is not supported by the results ofepidemiological and toxicological studies conducted in the United States and overseas. These studies show that all types of asbestos, including Canadian asbestos, are fully capable ofproducing the full spectrum of asbestosrelateddiseases including asbestosis, mesothelioma, lung cancer, laryngeal cancer, cancer ofthe pharynx and cancer of the gastrointestinal tract.* 80 88. Furthermore, a Congressional Statute posits that: "medical science has not established any minimum level of exposure to asbestos fibers which is considered to be safe to individuals exposed to the fibers;"126 As a result, there is not any basis for further debate over TLV's because the issue has been preempted federally. 89. The preponderance of evidence implicating asbestos in a multitude of health risks still has not deterred the Canadian government from "protecting] the Canadian interests." Sebastien Theberge, spokesperson for Canada's International Trade Minister states: "Canada still believes, that is, the government of Canada still believes, that chrysotile asbestos can be used safely and legitimately, as long as the exposure levels are closely monitored,"127 Over 95 percent of asbestos mined in Canada is exported. The Canadian government and Canadian scientists continue to tout the "asbestos is safe" argument when they themselves have largely discontinued its use. 90. Governmental entities within the US charged with protecting the health of workers, consumers, and members of the public agree that mesothelioma is caused by exposure to chrysotile asbestos. These governmental entities include NIOSH, OSHA, the EPA, and the CPSC. In addition, international organizations whose purpose and function is to determine harmfulness of substances to which people are exposed, and to protect the health of people, have accepted that chrysotile causes mesothelioma. These international organizations include the ILO, the WHO, the IPCS, the Collegium Ramazzini and the IARC. Virtually every nonCanadian governmental or public health organization that has considered the matter has concluded that chrysotile causes mesothelioma. 91. Finally in February 2001, Henderson reviewed this issue for the WTO and reported on his cohort study of brake mechanics: Nonetheless, the 1999 Reportfor the Australian Mesothelioma Register11 (AMR 99) records 58 mesotheliomas among brake mechanics with no other exposures to asbestos, during the almost 13-year period between 01 January 1986 and 31 October 1999 (total cases with a stated history ofasbestos exposure = 2585). Mechanics whofrequently or consistently work on brake linings and brake blocks represent only a sub-fraction of the total workforce ofmechanics in Australia. If one takes the 1996 censusfigure of82,827for male mechanic12, this amounts to 58 mesotheliomas in 1,062,946person-years (= 54.6 mesotheliomas per million person-years). Ifone rounds offthe workforce to 100,000 male mechanics, the figure becomes 45 mesotheliomas per million person-years. Ifone then doubles the workforce population to take into account retirees and other workers who moved on to other occupations (although afigure of200,000 is almost certainly an overestimate because it would include all mechanics, whereas brake 11The Register is a compilation of all and unselected mesotheliomas throughout Australia. 12This over-estimates the number of brake mechanics, because the figure includes all automotive mechanics, engine mechanics, apprentices, and supervisors: Australian Bureau of Statistics, 12 October 1999. 81 mechanics constitute a smaller sub-class), the mesothelioma rate becomes 22.6 per million person-years -- well under the rate of337 mesotheliomas per million person-yearsfor the Quebec chrysotile miners and millers but still substantially above the upper limit ofthe estimated background rate of 1-2 mesotheliomas per million person-years (about 10-fold). One might suspect that mesotheliomas in brake mechanics will cluster in those involved in the grinding, bevelling and other operations on new brake blocks and brake linings (i.e. brake materials unaltered by heat).128 Using an earlier set of data for Australia, NICNAS 99 came to a similar conclusion: "Out of2119 mesothelioma cases registered (with a response to history) for the period 1986-1995, 46 cases were listedfor the category 'brake lining manufacture/repair', 40 ofwhich were recorded in car mechanics, ofwhich 37 were exposed to asbestos in this occupation only... Overall the numbers indicate a slight increase ofaround 1-2 cases per year, which is roughly proportional to the growth rate ofall mesothelioma cases in Australia"... [p 66].* It is apparent that these considerations apply to occupational circumstances. Evidence indicates that the general population is exposed to only very low levels of asbestos derived from the braking of passing automobiles, and that most of these fibres represent shortlength fibres and heat-altered chrysotile. NICNAS 99 has this to say on the subject: "It is claimed that the amount ofasbestosfound in the dust arisingfrom braking is rarely more than 1% of the wear product (Asbestos Information Committee, 1975). It is not known what quantity ofchrysotile is imported in brake linings and otherfriction materials, but ABS [Australian Bureau of Statistics] data indicates in excess of 750,000 articles (brake linings, pads and clutchfacings) being imported in 1997 containing asbestos and therefore possibly containing chrysotile. Assuming each unit weighs 200 g and contains 50% chrysotile, this equates to around 150 tonnes ofchrysotile per annum. Assuming afurther 1000 tonnes ofchrysotile present infriction products manufactured in Australia, it is estimated that (assuming a worst case scenario of 1% release per annum, i.e. allproducts are completely worn in one year), around 11.5 tonnes of chrysotile will be releasedper annum countrywide or 32 kgper day spread all around the country. It is acknowledged that thisfigure may be an overestimate, as studies have shown that some ofthe chrysotile is degraded to magnesium silicates andforsterite ... In addition, some of the debris will be retained in the brake system and removed and disposed ofunder controlled conditions." [p 78]. Even if the break down brake exposure is 1% asbestos this quantity has long been known to be sufficient to cause asbestosis. What was the state of the art in 1947 concerning the toxicity of this amount of fibrous asbestos in a dust cloud? 82 "Thus, an inhalation experiment was carried out with ball-milled asbestos in which an attempt was made to eliminate allfibersfrom the material. It was found to be impossible to break up all ofthe fibers and about one percent ofthe air suspended dust consisted offibers. The characteristicperibronchiolarfibrosis developed in the exposed animals after forty months. Thus, it appears that very small numbers of fibers are capable ofproducing asbestosis, although the development ofthe lesions is delayed." Vorwald to OI, October 30, 1948 Epistemology of Brake Exposures: General Causation issues: General causation is established when it is agreed that a particular substance can cause a particular disease in general. Specific causation is established when it is agreed that an exposure to a substance that can cause the disease in general has cause of the disease in a particular individual. The determination of whether or not a particular job or exposure has caused or can cause disease in individuals who are exposed in this manner is a question of specific causation and must be dealt with as explained below on an individual basis. Conflation of general and specific causation issues. Some asbestos lawyers have argued that specific epidemiologic studies of brake workers are required to show that exposures to asbestos brakes (which are composed of 50-75% nonencapsulated asbestos) can result in asbestos disease. First of all as described above, there are numerous epidemiologic studies that show that brake workers not only have increased risk of asbestos induced cancers but also have increased risk of the development of nonmalignant asbestos disease. The exposures required to induce nonmalignant disease are well above those that cause increases in malignant disease rates. More importantly however the requirement that an epidemiologic study is necessary to establish causation for each and every occupational group, race, and gender is ridiculous. Scientists have never established this rigid requirement to establish cause effect relationships. There are no epidemiologic studies that show that any ofthe cigarettes currently marketed cause increases in any smoking-related disease. Currently marketed cigarettes are different from historically marketed cigarettes, which were the subject of epidemiologic studies, and the latent time since first exposure and likely disease incidence is insufficient for an effect to be found even if such epidemiologic studies were performed. However no regulatory agency, scientist, physician student or layman would ever argue that cigarettes like Virginia Slims, which are new to the market, do not carry the same risks as previously marketed cigarettes. Nonetheless going boldly forward where no other reasonable individuals would venture to go, some asbestos defense lawyers have argued that an epidemiologic study is necessary to establish causation for each and every occupational group. 83 While this may be good advocacy is not good science. This argument also overlooks the difference in the requirements for proof of causation for toxins that leave a signature disease (mesothelioma) or a real fingerprint (measurable asbestos fiber in the cancer tissue) at the scene of the crime and those that don't. The need to rely on epidemiologic proof to determine the health effects of for Agent Orange and silicone from breast implants may be different from epistemological methods used by doctors to determine that asbestos causes a variety of diseases. Neither Agent Orange nor silicone cause signature diseases nor can pathologists detect either at the disease site.13 But the visualization of asbestos fibers or a specific unique disease histopathology is precisely the method doctors use to determine the cause of asbestos induced disease. When a murder occurs the medical examiner does not call for an epidemiologist or check the epidemiological literature. He/she calls for the pathologist, the radiologist, and or the toxicologist. The determination of causation for asbestos disease utilizes the same specialists. Pathologists actually see the fibers at the "site of the crime." In a similar sense, doctors determine that a bullet found in the chest is the reason that a person has died. They find a bullet hole and a bullet. Similarly, this is how doctors determined that asbestos exposure caused lung fibrosis, lung cancer (which was a rare disease like mesothelioma in the 1930s) and mesothelioma. The fibers were found in the site of the crime. This is how Cook "discovered" asbestosis based on only one case, Nelly Kershaw, in 1927, how Wood and Gloyne established that asbestos caused lung cancer in 1934, in another single case and how Wedler determined that asbestos caused mesothelioma in 1940. There was no need for epidemiology to determine causation for rare or unusual diseases that only occurred in the presence of asbestos fibers like asbestosis and mesothelioma. In fact, there was no such thing as epidemiology as we know it, at the time physicians made these cause effect determinations. This epistemologic framework is unchanged. The requirement that an epidemiologic study to exist before it can be stated that particular exposure increases the risk or can cause a disease in exposed individuals implies that the only exposure a worker has occurs during work with a particular product. Unless it can be proven that there no or trivial asbestos exposure with the use of the particular product, the possibility that an exposure which might in an of itselfbe insufficient to cause disease (and thus not reveal a measurable effect in epidemiologic studies) can contribute to cause disease when added to other exposures in a particular individual cannot be excluded in a general way. Similarly exposures that may not result in excess disease rates in populations of exposed individuals may still contribute to disease occurrence in particular individuals who are uniquely susceptible due to concomitant exposures to other synergistic substances like cigarette smoke or radiation. 13 There is a slight parallel between localized silicone disease and asbestos-related disease. In both of these cases, the silicone and asbestos are located at the site of the disease. In contrast to the way that the courts have dealt with silicone breast implants systemic disease, the MDL and courts have determined that doctors are able to determine causation of localized silicone inflammation, pain and suffering at the site of silicone spills into the body where the doctors can actually see the silicone in the body at the site of the injury. Epidemiology is not required. 84 Additive and contributing cause considerations It is agreed that: 1) Asbestos is the major cause of mesothelioma, and a contributing cause of mesothelioma in individuals who have a history of any asbestos exposure. 2) Even "brief' or "trivial" exposures to asbestos can cause mesothelioma in some individuals. Even if there is some threshold dose that is required for mesothelioma to be induced in an individual, exposure to brake linings can, in an additive way, contribute to this total dose even if brake linings themselves can never produce a sufficient exposure. 3) Many individuals have worked with asbestos in a variety of locations and have been exposed to a variety of forms of asbestos fiber. i. Let us say hypothetically that a hundred fiber years of exposure is required before asbestos induces mesothelioma. ii. Let us say that an individual has been exposed to 99 fiber years of asbestos from non-brake exposures and one fiber year of asbestos from brake exposures since it is generally agreed that there is some asbestos exposure in working with brakes. iii. From a scientific standpoint, the asbestos exposure from brake work not only contributed to causing a mesothelioma that occurred in such an individual but was essential to the development of the individual's mesothelioma and therefore, is a significant contributing factor in the development ofthe mesothelioma. This is true not withstanding anything else that may be said about epidemiologic studies in brake workers because none of these studies would be sensitive enough to pick up the contribution of asbestos exposure from brake work in the face of the other exposures. iv. Consider a glass nearly full of water. Ifyou add one grape at a time until the water spills over the edge (water spilling being the induction of cancer), there is no way you can attribute one grape as being more important than another, in causing the water to spill. Moreover with respect to asbestos and cancer induction most physicians believe or a few grapes (asbestos fibers) in some unlucky individuals can theoretically cause water to spill over the lip of the glass (i.e.- induce mesothelioma). This argument is theoretical because all brake workers who work with asbestos brakes, have been exposed to more than a single or a few fibers. The law in Texas may require a comparison of exposures comparable to a group of individuals who have been part of an epidemiologic study, once it has been established that the exposure can cause the disease in question. Of course, this would requirement is quite burdensome for workers. The companies never told workers or their employers to monitor levels of exposure even after the companies were well aware ofthe fact that the asbestos could kill them. But nonetheless, reasonable estimates of brake exposures can be made and these reasonable estimates of brake exposures are 85 comparable to exposures in well-controlled trials where individuals have had excesses in mesothelioma rates. The question of individual exposure and contribution ofbrake asbestos to other asbestos exposures must be decided patient by patient on an individual basis. It is not contested that asbestos causes mesothelioma. If there is a threshold for induction of mesothelioma, then one must calculate that threshold for each and every individual on a case-by case basis. 2) Rate ratio of two requirements: Some have argued that a rate ratio oftwo is required to establish causation. It is important to note at the onset that even the proponents of this incorrect argument state that it only rigidly applies in the absence of non-epidemiologic evidence. This criterion is not mentioned in any standard epidemiologic literature. It is not part ofBradford Hill's analysis or the Surgeon General's causation analysis. In 1999 Sander Greenland, one of the foremost authorities in epidemiology authored a paper published in the American Journal of Public Health analyzing the mathematical errors that lead to the RR two criterion. He clearly states that, "The probability of causation cannot be computed solely from the relative risk." He states that it is "unscientific" to equate probability of cause (PC) to rate fraction (RF), or attributable risk. He continues that, "some experts will stand by the PC=RF assertion on the grounds that society (or the court) needs a probability of causation formula immediately." The designated need for a formula plays no relevance in the strength current epidemiologic evidence. Dr. Greenland concludes that, equating probability of cause to attributable risk is beyond the power and scope of modern epidemiology, and therefore an incorrect translation of science into law which is used as key-pass for gaining access to this nation's courtrooms. Analysis of literature on brake risk applying standard epistemologic criteria: Exposures: The relevant question is are exposures to asbestos from brake use high enough o induce disease by themselves or can they significantly contribute to disease when added to other asbestos exposures or when they occur in combination with other synergistic exposures? Asbestos friction products, brake linings, and clutch facings, are composed of anywhere between 30% and 60% asbestos fibers. It is also undisputed that the inhalation of asbestos fibers can result in a variety of different diseases. As aptly summarized by a Ford Motor Company document entitled Carcinogenic Substances, Asbestos: During the past several years, positive evidence has established the link between the inhalation of asbestos-containing dust and chronic respiratory disease (asbestosis), as well as several forms of cancer. These include lung cancer, mesothelioma (cancer ofthe membranes lining the chest and abdominal cavities), and gastro-intestinal cancer. Asbestos is found in a variety of automotive components, and thus many occupational exposures are possible. The most critical exposure occurs during brake and clutch 86 repair. Brake workers are exposed from the time the friction products are removed from their boxes, then again when the surface of the friction product is disturbed by sanding, filing, beveling, drilling, or grinding the surface, and again, when the debris from these processes is swept up or blown off during the clean up process, and then finally once again during repair or replacement when the brake and clutch housings are cleaned and blown out with compressed air. In the succeeding sections I have divided these into two categories: installation and removal. Governmental agencies, international health organizations, respected researchers and most importantly the asbestos "friction materials" manufacturers and their trade organizations, outside of the litigation context, have all recognized that "[t]here are frequent asbestos exposures during brake repair in the vehicle maintenance work force." 129 While most asbestos pre-formed thermal insulation contained only 8-12% asbestos, asbestos friction products were at least 50% asbestos by weight and, at times, contained as much as 75% asbestos. As has been noted, "[a]sbestos concentrations in these materials are sizable, ranging from 30-80%".130 In the early 1980's, the National Institute of Occupational Safety and Health (NIOSH) reported that 128 million pounds of asbestos were used annually in the United States for the production of brake friction materials.131 Admittedly the medical community did not come to recognize this hazard until 1930 when Merewether noted, "...(d) Brake and Clutch Linings...The amount [of dust] is considerable at sawing and grinding machines and localized exhaust draught, to remove it, has been applied-in some cases with much success-and is always necessary."132 In the 1930's, GM was aware ofthese asbestos exposures from machining and specifically provided exhaust ventilation at the grinding machines in its Inland Manufacturing Division where asbestos brake linings were manufactured and closely monitored asbestos dust levels at those operations. 133 Bendix and GM had overlapping boards and as noted above a GM vice-president Mr. Breech became president of Bendix in the early 1940s. By the mid-1930s even the medical community became aware of the hazard of asbestos brakes and with the publication of papers by Hawes and George and Leonard.134 As early as 1940, articles reporting asbestos disease in "grinders and drillers" of asbestos brakes began appearing in the medical literature.135 This paper, which was published in Germany during WWII, was circulated by the IHF. In 1948, the Assistant Head of the GM Industrial Hygiene Department, published an article noting that "[a]sbestos used in the formulation of brake lining is a potentially harmful compound... [and that] [d]ust exposures to asbestos... exist when the dry materials are handled and emptied into the mixers and in the subsequent operations of slitting, grinding or surfacing." 136 This was mailed to all members of the national Safety council. In 1968, a United States Public Health Service researcher published that, "[t]he dust produced by the abrading operations in asbestos friction product factories. contains free asbestos fibers that are similar to those in industries where cancer is known to be in excess."137 87 One year later, at a major friction materials conference in England, Ford Industrial Hygiene Specialists reported that they had specifically analyzed the dust produced by sanding asbestos brake linings and found 28% of the dust was asbestos fibers.138 These Ford hygienists noted, "[o]ur environmental studies have not included maintenance procedures which involve the filing and grinding ofbrake lining material, and we would envisage that these would give rise to considerably increased air contamination by chrysotile asbestos, with the attendant need for strict precautions to prevent the inhalation of fiber's." Dr. Rohl measured asbestos dust levels for various brake repair activities on trucks. Fiber concentrations were as follows: beveling new linings, 87.3 fiber/ml; riveting linings, 1.5 fibers/ml; sweeping floors around the grinding area, 3.6 fibers/ml.139 Automotive brake lining application also results in significant fiber levels. For example, light grinding of new linings yielded 4.8 fibers/ml and grinding new linings before installation yielded 2.7 fibers/ml.140 Chrysler manufactured asbestos friction material products at their Trenton chemical plant since 1959.141 Records indicate that the company was measuring airborne asbestos concentrations as early as May 27, 1963. 142 Many ofthe operations conducted at the Trenton plant were admittedly similar to those that a mechanic would perform if he ground asbestos brake parts before putting them on a car. 143 Servicing: The friction companies were also well aware that, when servicing brake assemblies, brake workers were sanding, grinding or cleaning their parts. In fact, for that very reason, Chrysler placed a caution in their service manual in 1973.144 Interestingly though, Chrysler chose to remove that warning from their service manual after the 1973 version and never included it again. Despite being questioned on the issue, no explanation was offered for the deletion, except perhaps that Chrysler was the only company that included the warning in their manual and its inclusion must have affected The major brake manufacturers' trade association, The Friction Materials Standards Institute ("FMSI") supported Chrysler's understanding that brake workers were drilling, cutting, beveling and grinding linings. The FMSI was a trade association of most of the leading friction materials manufacturers including GM, Chrysler, Bendix, Abex, JM, Raybestos and others. In a November 28, 1972 letter from Ed Drislane, Executive Director of FMSI to J. H. Kelly of Bendix Corporation Mr. Drislane states in no uncertain terms "[w]hen customers of yours drill linings, chamfer linings, cut linings, or grind linings, they may very well raise the asbestos concentrations in the atmosphere to above the OSHA standard" [FMSI 20]. Mr. Drislane goes on to state "[s]ome members have indicated that the drilling and grinding operations are problem areas in brake lining factories with existing exhaust systems. Therefore, if a customer of yours started drilling or grinding without having proper dust collectors, he would probably be in violation ofthe OSHA standard. It therefore becomes your responsibility, as a supplier of the brake lining, to warn the customer of this possibility." At that time, the TLV was 5 fibers/cc. Since 1990's, the TLV standard has been reduced 50-fold, to 0.1 fibers/cc. 88 At the Chrysler plant in Trenton, various dust counts were taken into the 1980s, which showed levels that exceeded the . 1 fiber/cc level in numerous operations. The levels reported at the Chrysler plant were high even though ventilation systems were installed in the mid-1960s and were in place in the grinding and sawing areas where these tests were taken.146 As Mr. Drislane of FMSI stated above, customers generally did not have these elaborate ventilation systems in place when they were installing asbestos brake products in the field. I provide a few example of the exposure levels measured by Chrysler. Breathing zone of a saw operator removing linings from the forming machine and stacking them 6.7 million particles per cubic foot of air (May 1965); Breathing zone sample #2 disc pad flat grinder, operator 1 fiber/cc (November 1972); Breathing zone brake shoe edge grinder .6 fibers/cc (November 1972); Personal air sample, packing drum brakes into cardboard boxes on the Mopar line 2.8 fibers/cc (May 1976); Personal air sample, pad only inspection time weighted average 2.1 fibers/cc (June 1977); Personal air sample, pad only inspection, after Besly rough grinder operation, time weighted average 37.8 fibers/cc (August 1977); Personal air sample, south prooftest and slot grinder operator, time weighted average 1.0 fibers/cc (December 1977); Personal air sample, Leone, #2 slot grind and flat finish operator 1.4 fibers/cc (June 1982); Personal air sample G. Dickens Besly grinder operator 3.4 fibers/cc (June 1982); And; Friction Products Building OEM grinder, time weighted average 1.7 fibers/cc (November 4, 1983). All of these tests at the Chrysler plant were measuring only fibers greater than five microns in length. The findings of Chrysler's above were the same as those measured throughout the industry in the 60s, 70s and 80s. In the minutes for the August 17, 1982 meeting of The Friction Materials Standards Institute, the FMSI reported "[i]n an inspection at one member's plant, the OSHA people set up five stations and while four of them sampled below the 5 fibers/cc TWA, one station read 18 fibers/cc TWA. This member was cited (in averaging the readings)." "One member indicated that 89 when pallets of brake linings were shipped there apparently is additional dust created during transportation." The issue of asbestos exposure from friction products was a regular concern for FMSI. For example, toward the end of 1972, FMSI told its membership that a problem existed when brake linings and clutch facings were cut, grooved, drilled or ground after shipment, because these operations produced high concentrations of airborne asbestos fibers.147 In the February 16, 1973 minutes ofthe FMSI's Asbestos Study Committee meeting noted "[i]n many drilling and grinding operations without dust collectors, Committee members indicated that the 10 fibers/cc ceiling concentration has been exceeded." During the meeting, the Committees Chair called to the Committee's attention a survey (conducted in the Metropolitan area by an individual affiliated with Mount Sinai Hospital) concerning the relining of brakes on bakery trucks. The survey "indicated that during radius grinding and drilling ofbrake linings, the airborne concentrations of asbestos fibers exceeded the 10 fibers/cc ceiling value." Most members of the Committee believed that, where no adequate dust collection machinery was employed, "the 5 fibers/cc (TWA) is exceeded in many areas such as inspection, drilling, and grinding." The Committee acknowledged that such exposure might be particularly likely in garages where subsequent drilling and grinding is often necessary and adequate dust collection equipment is not present. On this point, the Committee noted: While the members of the OEM accounts are dealing with manufacturers who should understand the OSHA regulations, the biggest problem may be with the small shops that are exempt from the requirements of the OSHA regulations." The Committee also acknowledged that exposures may occur just from opening boxes containing new friction products. On this point, the Committee stated "with undusted linings from a manufacturer [,] it is likely that customer inspection, or possibly opening of cartons, could show airborne fiber concentrations of excess of the 5 fiber/cc (TWA)." The Asbestos Study Committee expressed concern regarding asbestos exposure from friction products once again in their June 1973 minutes. In those minutes, Mr. Weaver suggested that the possibility of additional cutting, drilling, or grinding is always present and that he felt the OSHA label should be used here also. His point was that, in these subsequent operations, asbestos can be increased to levels more than the 5 fiber/cc limit in the OSHA standards. Mr. Weaver's concern was clear in 1973, when he said that this will be even more of a problem when the standards drop to 2 fibers/cc." (Again, the current level is 0.1 fibers/cc.) Later in 1973, the Chair ofthe FMSI Asbestos Study Committee delivered a speech to the annual meeting, acknowledging asbestos exposures result from working with brakes and clutch materials. In his speech, he informed the assembled group that the claim by some of the other asbestos product manufacturers that the asbestos in these other companies' products was "locked in" and could not become airborne during use, was not "at all applicable to friction materials". Weaver, I.H., Asbestos and the Friction Material Industry, June 27, 1973. Chairman Weaver further stated that operations and alterations of asbestos friction materials in the field "could result in excessive exposures of workers or bystanders to airborne asbestos fiber."148 And, again, in December 1979, GM confirmed that brake work creates exposure in an article in Business Week entitled, The Growing Need or Asbestos Substitutes. The article discusses the brake repair worker practice of sanding asbestos brake linings whenever a customer brought a brake problem to their attention, and quotes a GM engineer's response: "This puts all sorts of harmful fibers in the air." 90 Exposures To Asbestos Dust From removal of Friction Materials. The published literature with regard to the blowout of brakes has numerous references to levels that violate the present 0.1 fiber/cc level. In a study performed by the Medical Services Department of Ford, Hickish and Knight took samples during the blow out procedure of car brakes. Results indicated that the time-weighted average by car was 1.25 fiber/cm3. Cleaning of truck brakes yielded a TWA of 1.75 fiber/cm3. These levels exceed the present PEL/TLV of 0.1 fibers/cc. 149 Author/Date J.L. Lee 1970150 Knight and Hickish 1970151 Hatch 1970152 Longo studies14 What They are Doing Blow out of brake drums Blow off personal sample Brake cleaning compressed air jet by Bendix brakes Level/Finding Peek concentration 3-5 fibers/cm3 5.35 fibers/cm3 and peek sample 87 fibers/cm3 Ten minute average for fiber counts from two to five microns - 5 fiber/cc. Ten minute average for fibers above five microns - .8 fibers/cc. Peek concentration 43 fibers/cc Tremolite in the brakes by digestion; exposures over the TLV Dr. Rohl reported in 1976 that average concentrations from blowing the dust out of brake drums with compressed air jets gave a mean fiber concentration of 16 fiber/ml and that measurable concentrations of asbestos fiber were measured fifteen minutes after the brake blow out stopped 75 feet away.153 Lorimer confirmed this finding in 1976. The table above provides a summary of the various results in either peek concentration or time-weighted average received by the tests set forth above.154 Dr. Rohl once again published on this topic and in 1977 and he indicated while forsterite "might be expected to form as a result of recrystalization during the braking process [it] was not unambiguously detected in any sample. Moreover, both free chrysotile fiber bundles and fibrils were observed in all 39 samples." Data presented by Dr. Rohl in the second table once again confirmed his prior findings with regard to fibers concentrations.155 Kauppinen and Korhonen found concentrations of <1 to 8.2 fiber/cc during brake dust blow out studies, while two independent laboratories found concentrations of a 11.0 to 16.5 fiber/cc and 1.6 to 12.2 fibers/cc respectively.156 14 In addition there is crocidolite contamination in the Canadian asbestos mines. It is likely that this like tremolite has also has been incorporated into brakes. 91 In addition to the published literature corporate documents also shed additional light on the issue of "blowout". Dr. Hickish, in a secret unpublished paper in 1968, examined asbestos brake "blowout" exposures. He reported that the "generation of a dust cloud by blowing off dust from commercial vehicle brakes results in increased background contamination of 3 to 4 times the background level at any point within a radius of20-25ft"157 He further noted that, not only was the asbestos exposure of the mechanic engaged in "the blowing off task" nearly 4 times the Threshold Limit Value, but also the asbestos measured in the breathing zone of a different mechanic in an adj acent work bay, during the blow off period, exceeded the Threshold Limit Value. In the early 1970's, the Ford Industrial Hygiene Section began monitoring asbestos dust levels during brake repair operations. In a May 29, 1973 letter from Harry Lick to Ford's J.A. Keller, Mr. Lick discussed air samples taken during blow off of truck brake drums and assemblies, and states "results of the air sample.... indicated an over exposure to the 10 fibers greater than five microns in length per millimeter of air ceiling concentration limit prescribed by OSHA." In August 1973, Mr. Toth, the Supervisor of that Section, circulated a memorandum reporting that " [r]ecent industrial hygiene studies have demonstrated overexposure to asbestos fiber in air during certain vehicle brake rebuilding and inspection operations. Overexposure occurred when brakes and brake drums were cleaned using compressed air blow off."158 Shortly thereafter, Ford secretly banned the use of compressed air to clean brakes and brake linings during servicing of any automobile, truck, trailer, hilo and any other unit having asbestos brake linings.159 In that same month, Ford issued Maintenance Bulletin No. 137, warning Ford employees that "[o]verexposure to asbestos fiber in the air can occur during inspection and repair operations on brakes, brake drums, clutches, and associated components of these units when compressed air is used to blow off asbestos laden dust." In place of compressed air blow out, Ford ordered its employees to use specially designed vacuums, which its Rotunda Equipment Division later marketed to Ford dealerships.160 Until those vacuums were available, Ford ordered its employees to wear approved dust respirators should it become necessary to "dust" or clean brakes, "regardless of length of exposure to asbestos dust." Clearly Ford sold this special equipment and required respirators because they knew a hazard existed. By late 1975, Ford issued Technical Service Bulletin No. 99, which contained a section entitled, "Brake Asbestos Dust Fiber Removal." The Bulletin read: "CAUTION: Dust and dirt conditions present on wheel brake assemblies and rotors and drums, may contain asbestos fibers that can represent a potential health hazard when made airborne by cleaning with compressed air." Ford reaffirmed its position on blow out exposure in an April 23, 1975 internal letter, where Ford stated "for the most part, whenever air hoses were used to clean dust out of brake drums, we found exposures in excess of limits established in OSHA standards on asbestos dust." In 1977, the FMSI Brake Lining and Clutch Facing Automotive Data Book contained a page entitled, "Recommended Procedures For Reducing Asbestos Dust During Brake Servicing." These procedures advised that an air purifying respirator should be worn "during all procedures starting with the removal of the wheels and including re-assembly." Furthermore, "[o]f extreme importance are the precautions which must be taken during machining of friction material. This is the operation in brake servicing when exposure to asbestos dust is at its highest." In 1977, the FMSI, for the first time, included in its publication, the Brake Lining and Clutch Facing Automotive Data Book, a page entitled, "Recommended Procedures For Reducing Asbestos Dust During Brake Servicing". These procedures advised that an air purifying respirator should be worn "during all procedures starting with the removal of the 92 wheels and including reassembly." Furthermore, "[o]f extreme importance are the precautions which must be taken during machining of friction material. This is the operation in brake servicing when exposure to asbestos dust is at its highest." In October 1978, FMSI issued its, Friction Materials Work Practice Guide, which reported that "[p]otentially hazardous airborne concentrations of asbestos dust can be created by improper cleaning and handling of worn brake and clutch assemblies, uncontrolled machining operations and poor housekeeping." Good housekeeping was stressed to avoid exposures during cleanups. Only special vacuums were to be used to remove "accumulations of asbestos dust and waste." Compressed air and dry sweeping were "never" to be used for cleanup. In May 1980, Ford's Carcinogens in the Workplace Task Force Report was issued. The section on asbestos concluded that "[a]sbestos is found in a variety of automotive components, and thus many occupational exposures are possible. The most critical exposure occurs during brake and clutch repair." In August 1983, Ford issued its Industrial Relations Bulletin No. 4 on Asbestos. Ford noted that asbestos exposures "can cause asbestosis, cancer of the lungs and digestive tract, and mesothelioma." Under the section entitled "Employee Exposure," the Ford Employee Health Services Department wrote: "... Employee exposure can generally occur during material handling and maintenance of asbestos-containing friction materials. Exposure can occur during grinding, sawing, sanding, drilling or otherwise disturbing or finishing asbestos-containing products." In addition to Ford, Chrysler studied exposures to garage mechanics brushing dust out of brake drums on vehicles. In a November 1972 test, Chrysler found .2 fibers/cc during that operation. In addition to the preceding test, Chrysler performed dynamometer testing at its plant where disk brake pads were made. A dynamometer creates energy that severely tests brake linings to determine how they hold up under the most severe punishment.161 This stress test for brake linings subjects the brakes to the highest temperature and pressure; even higher then they would be subject to under normal conditions. Even under these conditions, with high temperatures and pressures that allegedly convert the asbestos to forsterite, Chrysler found 1.0 fibers/cc in the air.162 NIOSH has concluded that asbestos exposures occur during work involving the use of asbestos friction materials. In addition to NIOSH, the United States Environmental Protection Agency (EPA) has recognized this hazard: "Millions of asbestos fibers can be released during brake and clutch servicing. Grinding and beveling friction products can cause even higher exposures. .Asbestos released into the air lingers around a garage after a brake job is done and can be breathed in by everyone inside a garage, including customers."163 Additionally, the World Health Organization (WHO) has reviewed this subject and concluded that "[a] considerable number of reports have included airborne asbestos concentrations during maintenance and replacement ofvehicle brakes. In the early period, poor or no engineering control measures were utilized, resulting in high total dust exposures. 164 Evidence of asbestos disease in workers exposed to dust from asbestos brake use Asbestosis: In 1935, researchers reported a 25% prevalence of asbestosis in four asbestos manufacturing 93 plants, three of which manufactured friction products, including brake linings.165 Brake lining manufacturers were well aware of these hazards. In 1944, while discussing asbestosis, L.E. Hamlin, the Medical Director of American Brake Shoe Company wrote that:166 The greatest occupational hazard exists in mining, handling and crushing crude asbestos, making insulation and the carding and weaving of asbestos. In other industries such as the compounding of materials for automobile brake linings, the hazard is recognized but the disease is uncommon. He went on to note that: In one of our plants where considerable asbestos is used in the manufacture of automobile brake linings, a recent survey of 189 employees exposed to variable amounts of dust, revealed no actual cases of fibrosis. A few men's films showed haziness which suggested evidence of disease, but they were not sufficiently typical to warrant a diagnosis of asbestosis. However, it should be stated that the hazard in this particular plant is well controlled by adequate exhaust ventilation. The recognition that the asbestos incorporated into friction products was capable of producing disease was supported by other investigations of the friction product manufacturing facilities. For example, out of 90 workmen examined from a Massachusetts brake lining manufacturing plant, researchers made a positive diagnosis of asbestosis in 12 and a questionable diagnosis in three others.167 Another study of the same plant yielded astounding results, 82% of the 180 workers examined had symptoms and chest x-ray evidence of pulmonary asbestosis, 78 patients with Stage I, early asbestosis, 54 patients with Stage II, moderate asbestosis, and 16 patients with Stage III, advanced asbestosis. 168 Similar studies were replicated all over the world with similar results. In Germany, Brackman reported on the machining of brake bands. These brake bands were composed of asbestos remnants that were impregnated by an artificial resin. The resulting band was then ground to obtain the correct thickness and drilled to create rivet holes to attach the brake lining to the metal brake shoe. Researchers found that after two years of grinding and drilling with these brake bands, a few isolated cases of slight asbestosis occurred. After five years, however, definite changes of asbestosis on clinical and x-ray examinations were found in all workers.169 In Australia, chest x-rays of 300 asbestos workers were examined and 47 demonstrated positive evidence of asbestosis. The occupations of the group diagnosed with asbestosis involved, among 94 others, the "sawing, cutting and finishing any product containing asbestos - for example brake linings."170 Finally, in a National Institute of Occupational Safety and Health investigation of a friction products plant in New Jersey, government officials reviewed x-rays of 20 long- term employees. Of these 20 workers, 7 showed changes consistent with the effects of asbestos exposure, 2 with asbestosis and 5 with asbestos-related pleural abnormalities.171 2. Workers who Repair and Replace Brakes Develop Asbestosis. The incidence of asbestosis has not been limited to only those workers engaged in the manufacturing of asbestos brake linings. All over the world, researchers have reported the incidence of asbestosis in automobile mechanics engaged in the repair and replacement of brake linings. In England, McVittie published an analysis of cases of asbestosis approved by the Pneumoconiosis Medical Panel of the Ministry of Pensions and National Insurance. From 1955 through 1963, four cases of asbestosis were approved in brake lining workers, and workers engaged in the repairs to brake and clutch parts.172 An additional ten cases of asbestosis in brake repair workers were approved from 1963 through 1969.173 In Germany, two cases of asbestosis were found among 39 vehicular maintenance workers who had performed brake lining service for about U to 2 hours a day for eight years. 174 In the United States, Lorimer and his colleagues at Mount Sinai School of Medicine in New York published the results of their examination of 104 members of a union of vehicular maintenance workers. Many of these workers showed signs of asbestosis, 29% had a decreased vital capacity on pulmonary function testing and 27% had chest x-ray abnormalities. The authors noted, "the prevalence both of chest x-ray changes and restrictive function results was significantly higher after 20 years exposure than before, a result expected after occupational exposure to asbestos."175 The authors "suggest that asbestos disease will be present among such workers and that appropriate control measures should be urgently instituted." At the request of the National Institute for Occupational Health and Safety, the Mount Sinai group expanded the study to compare more than 900 garage mechanics, those that performed brake work and those that had not, to a control population of blue collar workers without any exposure to asbestos. The authors concluded: A greater prevalence of x-ray abnormalities is found among garage mechanics who repaired brakes than among blue collar controls or garage workers who do not engage in brake or auto body work. . . a significant excess is seen in workers who had occasion to grind and machine brake linings prior to installation on larger vehicles. The prevalence ofx-ray abnormalities is in accord with estimates ofasbestos 95 exposure in the different circumstances. 176 Finally, in Finland, six verified cases of asbestosis have been reported to the Finnish Register of Occupational Diseases during the period of 1964 to 1984.177 The disease occurred in four car mechanics, one turner, and one garage supervisor. Swedish researchers discovered asbestos-related pleural plaques in 41 of the car mechanics and that the authors concluded, "asbestos exposure can generally cause pleural plaques in car mechanics."178 A subsequent Swedish study showed that Swedish car mechanics had a respiratory impairment in the form of a reduced oxygen transfer factor on spirometry.179 These are particularly noteworthy since worker protection was and I much better in Sweden than the United States. Analysis of arguments and studies presented by Bendix as evidence that Brake asbestos exposures are innocuous. Studies have shown that Exposure to Friction Products has caused or contributed to Lung Cancer in exposed individuals. Study Finding Huncharek, Brake Mechanics, Asbestos, and Disease Risk, Amer J Forensic Med and Path, 11(3):236-240 (1990). Hueper, Carcinogens in the Human Environment, Archives of Pathology, 71(3):237-267 (1961). Estimated that 20,000 deaths from asbestos-related cancer will occur during the next 40 years among automotive maintenance workers in the United States Risk of cancer fro brake exposures Menck et al., Occupational Differences in Rates ofLung Cancer, Journal of Occupational Medicine, 18(12) 797-801 (1976). McDonald et al., Dust Exposure and Mortality in an American Chrysotile Asbestos Friction Products Plant, Brit J Indus Med, 41:151-157 (1984). Jarvholm, Asbestos associated tumours in car mechanics, BRIT. J. INDUST. med., 45:645-646 (1988). Levin et al., Asbestosis and small cell lung cancer in a clutch Standard Mortality Ratio (SMR) for lung cancer of 146 for automobile repair 49 observed, 35.7 expected for an SMR of 137. Lung cancer: 39 observed, 23 expected, SMR 170. Asbestosis and small cell lung cancer caused by asbestos in a clutch refabricator 96 refrabricator, Occup Environ Med, 56(9):602-605 (1999).______________ Exposure to Asbestos from Friction Products has been shown to cause or contribute to mesothelioma in exposed individuals Newhouse et al., Mesothelioma ofPleura and Peritoneum Following Exposure to Asbestos in the London Area, Brit. J. Indus. Med. 22:261 69 (1965) Mesothelioma in man who was garage hand, chauffeur, and mechanic Godwin et al., Asbestos andMesothelioma, jama, 204(11):151 (1968 43 year-old who wove brake linings for three years and later died of mesothelioma McDonald et al., Epidemiology ofPrimary Malignant Mesothelial Tumors in Canada, Cancer, 914-918 (1970) Mesothelioma in two workers who installed brake linings Oels et al., Diffusae malignant mesothelioma ofthe pleura: A review of37 cases, chest, 60(6):564, December 1971 Mesothelioma in a service station operator Rubino et al., Epidemiology ofpleural mesothelioma in North-western Italy (Piedmont), Brit J Industr Med, 29:436 442 (1972) Mesothelioma in 3 car assemblers and 1 mould maintenance technician in a friction material factory Greenberg et al., Mesothelioma Register 1967-68, Brit. J. Indus. Med. 31:91-104 (1974) Mesothelioma in motor mechanic Vianna et al., Non-Occupational Exposure to Asbestos andMalignant Mesothelioma in Females, The Lancet, May 20, 1978, pp. 1061-63 Mesothelioma in two house wives whose husbands worked with brake linings Robinson et al., Mortality Patterns, 1940 1975 Among Workers Employed in an Asbestos Textile Friction and Packing Products Manufacturing Facility, Dust AND Disease, Pathotox Publishers, pp. 131-143 (1979) Fifteen mesothelioma cases in a factory that made textile and friction products 97 McDonald et al., Malignant Mesothelioma in North America, CANCER 46:1650-1656 (1980) Langer et al., Mesothelioma in a Brake Repair Worker, The Lancet, November 13, 1982 Kagan et al., Lymphoid and Plasma Cell Malignancies: Asbestos-Related Disorders of Long Latencey, Amer. J. Clin. Path. 80(1):14-15 (1983) Guillon et al., A Case ofAssociation of Myeloproliferative Syndrome and Pleural Mesothelioma After an Asbestos Exposure, Archives Des Maladies Professionnelles De Medecine Du Travail Et De Securite Sociale 45(2):119 (1984) Castleman, Asbestos: Medical and Legal Aspects, Harcourt Brace Jaovanovich (1984) Woitowitz et al., Pleuramesothelioma After Asbestos Dust Exposure in Brake Repair Work in Automobile Repair Workshop: Case Observation, Praxis Und Klinik Der Pneumologie 39(10):362 (1985) Environmental Protection Agency, Guidance for Preventing Asbestos Disease Among Auto Mechanics, p. 2 (1986) Huncharek, Chrysotile Asbestos Exposure andMesothelioma, Brit. J. Indus. Med. Mesothelioma in eleven garage mechanics Mesothelioma in a man whose sole exposure to asbestos was to chrysotile during brake repair and maintenance Mesothelioma in brake lining machinist Mesothelioma in man who worked in automobile workshop for many years Ziem reported 4 cases of mesothelioma in mechanics and one in a mechanic's wife Four cases of mesothelioma in men exposed to asbestos dust from friction products Mesothelioma in a ten-year old son of a brake mechanic Three cases of mesothelioma among friction product workers 98 44:287-288 (1987) Huncharek et al., Pleural Mesothelioma in a Brake Mechanic, BRIT. J. INDUS. Med, 46:69-71 (1989) Newhouse et al., A mortality study of workers manufacturingfriction materials: 1941-86, Brit. J. indust. med., 46:176-179 (1989) Huncharek et al., Pleural Mesothelioma in a Lift Mechanic, BRIT. J. INDUS. Med, 46:500501(1989) Jarvholm et al., Asbestos Associated Tumors in Car Mechanics, Br. J. INDUS. MED., 45:645-646 (1988) Hansen et al. Mortality ofAuto Mechanics, Scand. J. Work and Enviorn. Health 15:43-46 (1989) Tissue samples taken from the lining of the lung of an automobile mechanic who died as a result of mesothelioma. An analysis of three such specimens revealed 51 million to 266 million asbestos fibers per gram of wet tissue, 99% of which were chrysotile asbestos. Mesothelioma in man whose only asbestos exposure was from clutch and brake products Two cases of mesothelioma in a friction materials manufacturing facility Mesothelioma in patient whose primary exposure was to chrysotile asbestos from lift pad brakes Mesothelioma in a Swedish car mechanic Mesothelioma in Danish garage mechanic Animal evidence Study Hardy Egilman Findings Chrysotile asbestos exposure causes lung cancer in mice without first inducing asbestosis 99 Davis,J.M.; Coniam,S.W, Experimental studies on the effects of heated chrysotile asbestos and automobile brake lining dust injected into the body cavities of mice, Exp.Mol.Pathol., Volume:19, 3 1973,339-369 Mesotheliomas induced. Study funded by Asbestosis Research Counsel (Industry group). Designed to be a three-year study. Mice "lost" after initial findings reported and never completed. Repeat study that was recommended was never conducted. (Personal communication JMG Davis) Wozniak,H.; Wiecek,E.; Bielichowska-Cybula,G., The fibrogenic activity and neurotoxicity of heat-treated chrysotile, Pol.J.Occup.Med Volume: 4,1991 pages 21-31 Thermal degradation of heated chrysotile results in dehydration and changes in its crystalline structure. The impact of heat treatment at 150-1200 degrees C on the biological activity of chrysotile was tested in rats. Heating the chrysotile produced an increase in its biological aggressiveness measured in terms of animal survival rate and fibrogenic activity after intratracheal administration of the dust. The highest death rate (100% of the animals) was noted after administration of chrysotile heated at 600 degrees C. Moreover, increased fibrogenic activity of chrysotile heated at 150 degrees C up to 800 degrees C was found. The biological effect of chrysotile heated at 1200 degrees C did not differ from the effect exerted by unheated chrysotile. After intraperitoneal administration of the dust, the most violent reaction could be observed when chrysotile dust was heated at 600 degrees C, which resulted in symptoms of nervous system impairment (of the hind legs, no reaction to nociceptive stimuli, drop of internal body temperature) and death of the test animals. In male rats, the period between dust administration and the manifestation of symptoms and death was found to be longer than in females 100 (Wozniak and Wiecek 345-53), [Biological effect of fibrous mineral dust. I. Fibrogenic properties of the products of the thermal degradation of chrysotile, Med. Pr 1985, 36, 6, pages 345-353 Chrysotile asbestos samples, on comminution, were exposed to temperatures typical for asbestos products exploitation. Subsequently, in an experiment on white rats the effects of temperature upon asbestos fibrous effects were evaluated. The highest aggressiveness was that of the sample heated at 600 degrees C. All the animals died as soon as 50 or 25 mg of dust had been administered intratracheally. Only 3 samples could be administered intratracheally at a dose of 50 mg: non-heated. heated at 400 degrees C and heated at 800 degrees C samples. The doses heated at 400 and 800 degrees C had be reduced by half. Samples heated at 150 to 800 degrees C induced higher hydroxyproline increases than the non-heated sample. The fibrogenic activity ofthe dust heated at 1200 degrees C was very similar to the fibrogenic activity of the non- heated dust Pathologic Evidence Churg et al., Fiber Size and Number in Workers Exposed to Processed Chrysotile Asbestos, Chrysotile Miners, and the General Population, Am J Ind Med, 9:143-152 (1986). Two brake mechanics and one brake lining factory worker workers with lung cancer. In comparison to the general population, the authors found that the mean concentration of asbestos in brake workers exceeded the controls Roggli (deposition), Hammar, Abraham have reported or are aware of more than 150 mesothelioma cases in brake mechanics often with elevated fiber counts. (Personal communication) This is more than the expected number based on estimates of the total number of brake mechanics in the US during the past forty years accounting for turn over and competing causes of death. The following is an analysis of studies presented by Bendix attorneys in support of a motion that there is no evidence that brake exposures can cause asbestos disease. Lies and misrepresentations in the Bendix motion Study: Jarvholm et al., Asbestos Associated Tumors in Car Mechanics, Br. j. INDUS. MED., 45:645-646 (1988) and Hansen et al. Mortality of Mi srepresentation "no increased mesothelioma mechanics" risk in Actual findings: of The other half of the sentence car which is omitted states, "but possibly and increased risk of lung cancer" 101 Auto Mechanics, Scand. J. Work and Environ. Health 15:43-46 (1989) AD McDonald, JS Fry, AJ Woolley, JC McDonald (1984) Br. J. Ind. Med. 41 "Dust Exposure and mortality in an American chrysotile asbestos friction products plant" "...not a single case of asbestosis was found in a study of 3,641 men employed at the plant. " 1 Mesothelioma, 0 expected in car mechanics. The RR is infinity. Lung cancer rate was doubled. Sweden had real worker protection and lower exposures than the US for the past 40 years. The disease is preventable; that is the point. The coding system did not code for mesothelioma!! A nosologist used the ICD 7 to code causes of death. 55 There were, in fact, 12 deaths coded as pneumoconiosis but none of the death certificates listed asbestosis. These were probably asbestosis deaths. A study that the defendants actually cite for something else, found two cases of mesothelioma that the McDonald's failed to report. See Teta et al., Mesothelioma in Connecticut, 1959-1977, J Occup Med, 25: 749-755 (1983) AT P. 755. Nicholson, et al., Investigation of Health Hazards in Brake LiningRepair andMaintenance Workers Occupationally Exposed to Asbestos, Environmental Sciences Laboratory, Mount Sinai School of Medicine of the City University of New York (1983). Marcus et al., Asbestos- ".garage mechanics who did brake repairs were at no greater risk for x-ray abnormalities than garage mechanics who did not repair brakes." "..no respiratory impairment or "A greater prevalence of x-ray abnormalities is found among garage mechanics who repaired brakes than among blue collar controls or garage workers who do not engage in brake or auto body work. . . a significant excess is seen in workers who had occasion to grind and machine brake linings prior to installation on larger vehicles. The prevalence of x-ray abnormalities is in accord with estimates of asbestos exposure in the different circumstances." Fail to mention that the authors 102 associated lung effects in car mechanics, SCAND J WORK Environ Health, 13(3):252-4 (1987) asbestosis was found" McDonald et al., Malignant Mesothelioma in North America, Cancer 46:1650 1656 (1980), Cited as negative study Teta et al., Mesothelioma in Connecticut,1959-1977, J Occup Med, 25: 749-755 (1983) Cited as negative study Teschke et al., Mesothelioma Surveillance to Locate Sources ofExposure to Asbestos, CANADIAN J. PUB. health 88:163-167 Cited as negative study 103 discovered asbestos-related pleural plaques in 41 of the car mechanics and that the authors concluded, "asbestos exposure can generally cause pleural plaques in car mechanics." They also omit a subsequent study that showed that Swedish car mechanics had a respiratory impairment in the form of a reduced oxygen transfer factor on spirometry. See Dahlqvist et al., Lungfunction and exposure to asbestos among vehicle mechanics, Am J IND Med, 22(1):59-68 (1992). No calculation of any relative risk or provide any information by which to assess the power of the study to detect the risk of disease or assess the statistical significance of their findings. Relative risk of 0.65 for garage workers with a 95% confidence interval ranging from .08 to 5.83. This study is consistent with a finding of a five fold excess relative risk. If the point estimate is used as the Bendix lawyers suggest than brake work reduces the risk of mesothelioma by 40%. This proposition is so ridiculous it makes the entire study questionable. This is no surprise since the authors themselves question the validity of the job categorizations. Odds Ratio for vehicle mechanics of 0.8 with a 95% confidence interval of 0.2 and 2.3. The finding is consistent with a doubling of the risk. If the point estimate is used as the Bendix lawyers suggest than brake work reduces the risk of mesothelioma by 20%. This proposition is so ridiculous it makes the entire study questionable. I render the opinions expressed in this affidavit with a reasonable degree of medical or scientific certainty. Further, Affiant sayeth not. Norfolk, ss SUBSCRIBED AND SWORN TO BEFORE ME, on this the day of ___________ , 2001, to certify which witness my hand and official seal of office. NOTARY PUBLIC IN AND FOR THE STATE OF MASSACHUSETTS My Commission Expires_____________ 104 References: 1 Gurney, Stuart and Beyer, David. "Respiratory Protective Devices." Transactions of the National Safety Congress. Published by the National Safety Council. 1934 2 Brown, Carlton and Yant, William. "Respiratory Protective Devices." Transactions of the National Safety Congress. Published by the National Safety Council. 1935. 3 Case, L.B. "Air Hygiene Studies." General Motors Inland Manufacturing Division. Dayton, OH: October 31-November 1, 1939. 4 Ibid. 5 V.J. Castrop, Safety Director of GM, National Safety News, "Recognition and Control of Fume and Dust Exposure" February 1948 6 "What's New in Brake Linings." SAE 1959 7 Finkelstein to Egilman, personal communication, 2001 8 Hardy, HL., Egilman, D.: Corruption of Occupational Medical Literature: The Asbestos Example (letter). Am. J. Ind. Med. 20(1):127-129.1991 9 Ibid. 10 Martin, E.A. to Noel Hendry. September 12, 1966. 11 Martin, E.A. to Stolar, et al. Oct. 16, 1966. 12 McNallan trial testimony, Baltimore City, In The Personal Injury And Wrongful Death For Asbestos Cases Baltimore City Abate, et al, Plaintiffs vs. ACandS, INC., et al Defendants CROSS CLAIM PROCEEDINGS 8/11/1984 page 88 lines 8-10. 13 Rohl, A. to Erwin, Eichen. 1976 14 Best, George E. of MCA to G.F. Scannell of OSHA. March 15, 1972 15 Ibid. 16 Swetonic Speech to the ATI June 7, 1973. 17Ibid., p. 4-5. 18 Speech by I.H. Weaver to the Friction Materials Standards Institute, June 27, 1973, p. 3. 19 Minutes of 119th Meeting of the Directors of the AIA/NA, January 24, 1972, p. 6. 20 Ibid. 21 See e.g. the use of Bayesian analysis in medical decision-making and for probabilistic medical determinations of individual causation in "probability of causation" section, sub. * 22 Deposition by Aaron DeLuca. Gutshall v. A-Best Products et al. 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