Mesothelioma Deposition

Below is an affidavit filed in Court by one of the foremost and respected mesothleioma experts in the world concerning asbestos contaning brakes and mesothelioma.

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 Preventive-
Occupational 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 Masters 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 of the development of medical and corporate ethics during the
20th century. I have on two occasions, testified before congressional committees on
the issue of medical 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 of Medical 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 of the art issues at the request of both 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 of the 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 of the 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 of their 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 of the 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 of Brake 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 of brake 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 (Eclipses
largest customer for starter drives). In 1928, through GMs 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 Bendixs
flamboyance. Since GM was Bendixs second largest customer (for the starter drive), they (GM) agreed to
act as Bendixs agent in the transaction.
Bendixs 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 vicepresident
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 60s 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 Citation Findings
Fehnel. “Effects of
inhalation of
asbestos dust on
the lungs of
asbestos workers”
Publ. Health. Rep.
50:1-12
years of employment in the industry” at five plants including one
where molded brake band and clutch friction materials were
manufactured
1935 Fulton, et al.
Asbestosis.
Harrisburg, Penn.:
Dept of Labor and
Industry,
Commonwealth of
Penn.
Report of 25 percent prevalence of asbestosis among selected
workers at four asbestos fabricating plants, including three where
brake linings were manufactured.
1939 George, A.W., R.D
Leonard. “An Xray
study of the
lungs of workmen
in the asbestos
industry covering a
period of ten
years” Radiology
33:196-209
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.
1940 Stone, M.J.
“Clinical Studies in
asbestosis” Amer.
Rev. Tuberc. 41:
12-21
Asbestosis in 148 brake-lining manufacturing workers seen by
Drs. Stone and Hawes.
1940 Stone, MJ.
“Studies in
asbestosis.” Dis.
Chest. 6: 170-171
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
Report of the State
Department of
Health, State of
Conn. Public
Document No. 25,
Hartford, CT. pp.
507-511
Describes the grinding of molded asbestos brake and clutch
parts under varying degrees of local exhaust ventilation. Total
dust counts ranged from 0.6 to 17 MPPCF. The need for dust
sampling and analysis to evaluate these exposures was stressed,
as the visual appearance of the worst grinding exposure was
unremarkable.
1935 Memorandum on
the Industrial
Diseases of Silicosis
and Asbestosis.
London: H.M.
Stationery Ofc.
Lists under “Industries and Processes in which asbestosis
occurs...the sawing, grinding, and turning in the dry state of
articles composed wholly or partly of asbestos such as motor car
brake and clutch linings...”
1939 Case, L.B. “Air
Hygiene Studies.”
General Motors
Use and servicing of brake products produced exposures greatly
exceeding permissible limits.
1940 Brachmann.
“Asbestosis in
grinders and drillers
of brake bands”
Arbeitsschutz 172-
174
Clinical and X-ray examination showed asbestosis in nearly all
workers employed 5 years or more as grinders and drillers of
brake linings.
1941 Brachmann.
Abstract in
“Abstracts”
supplement to J.
Indust. Hyg. Tox.
23:76-77
Clinical and X-ray examination showed asbestosis in nearly all
workers employed 5 years or more as grinders and drillers of
brake linings.
Feb.
1948
Castrop, V.J. “Fume
and dust exposure”
Nat. Safety News.
By General Motors industrial hygienist. Section on asbestos noted
that brake lining grinding and “surfacing” operations were
equipped with local exhaust ventilation Systems.
1957 Thomas, D.L.G.
“Pneumokoniosis in
Victorian Industry”
Med. J. Australia
1:75-77
The following occupations (involve asbestosis hazards)...sawing,
cutting and finishing any product containing asbestos—for
example, brake linings, asbestos sheeting, and various insulating
materials...
1963 Patty, F.A.
Industrial Hygiene
and Toxicology,
New York:
Interscience (2d ed.)
pp. 2243-2244
Written by former director of Industrial Hygiene Dept., General
Motors.
“The sawing, filing, drilling, and grinding of brake linings is
ordinarily well controlled... It is desirable in asbestos exposures
to keep the dust count down to 5 million particles, or less, per
9
Date Citation Findings
cubic foot of air.”
1968 Lynch, J.R.
“Brake Lining
Decomposition
Products” National
Center for Urban
and Industrial
Health Vol. 18 No.
12
“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.”
1969 Hickish, D.E. and
Knight, K.L.
“Exposure to
Asbestos During
Brake
Maintenance”
Ann. Occ. Hyg
Vol. 13 pp.17-21
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 Findings
1965 McVittie, J.C.
“Asbestosis in
Great Britain”
Ann. NY Acad.
Sci. 132:129-138
Describing the occupations of workers diagnosed with asbestosis
(and compensated for disability) in the years 1955-1963, he lists
“brake lining” workers with an average of 14 years’ exposure.
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
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.,
R.O.C. Kaschula,
and R.R.
MacDonald.
“Asbestos as a
Modern Urban
Hazard,” S. Afr.
Med. J. 37:77-81
Expresses fear of public cancer hazard from asbestos released into
the air of cities by brake wear.
1963 “Pulmonary
Asbestosis,” S. Afr.
Med. J. 37:629-630
Editorial expresses similar concerns to Thomson’s
1968 Lynch, J.L. “ Brake
lining
Decomposition
Products,” J. Air.
Pollut. Contr.
Assoc. 18:824-826
Electron micrograph showed no free fibers in accumulated
brake drum dust. Testing was then done on dust released by
braking, using equipment of a brake lining manufacturer. The
apparatus permitted simulation of stopping using complete
brake assemblies.
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 (through 1985)
Date Citation Findings
1961 Hueper, W.C.
“Carcinogens in
the Human
Environment,”
Arch. Path,
71:237-267
Lists brake linings under, “operations and products with contact to
asbestos for producers, processors, users, consumers, residents.”
Lists as a population with occupational and environmental
exposure, in italics, “brake linings producers.”
1965 Hueper, W.C.
“Occupational
and Nonoccupational
Exposures to
Asbestos,” Ann.
N.Y. Acad. Sci.
1.32:184-195
Table lists “garage attendants” under the heading of groups
occupationally exposed to asbestos and lists brake linings as a
source of general environmental asbestos exposure.
July
1968
A Preliminary
Investigation.”
Indust. Hyg.
Foundation—
Report for Johns-
Manville.
Unpublished.
The index card for document no. 3071 at the Institute for
Occupational and Environmental Health, library of the Quebec
Asbestos Mining Association in Montreal, recorded the authors’
summary: “Brake-drum dust has evoked a pulmonary response
which suggests that this dust is biologically ‘inert.’ Brake-drum
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)f the 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 Citation Findings
pp.86-91.
1969 Sullivan, R.J. and
Y.C.
Athanassiadis.
Preliminary Air
Pollution Survey
of Asbestos.
Litton Systems,
Inc. report
prepared for the
National Air
Pollution Control
Administration,
p.32
Refers to Newhouse and Thompson’s report of mesothelioma “in a
mechanic.”
1970 McDonald, A.D.
et al.
“Epidemiology
of Primary
Malignant
Mesothelial
Tumors in
Canada.” Cancer
26:914-919
In a retrospective review of the potential asbestos exposures of
a series of mesothelioma patients in Canada,
“Men employed in... the installation of brake linings...were
responsible for most of the excess of cases over controls.”
In a tabulation of the “occupations classified under definite or
probable exposure to asbestos,” are 21 cases of mesothelioma,
including 2 who did “brake lining installation” and one more
who worked in brake lining manufacture. This study attributes
the main risk of mesothelioma to asbestos exposure in
manufacturing and product use, as opposed to the mining of
chrysotile asbestos. Funded by Quebec Asbestos Mining
Association.
1970 Smither, W.J.
“Asbestos and
Asbestosis.”
Annals of
Occupational
Hygiene. 13: 3-5.
The medical advisor to Cape Asbestos opens with discussion
about the different mineral varieties of asbestos, then notes that all
“current” friction materials contain 50% chrysotile asbestos. This
figure he expected to gradually decline to as little as 30%.
1970 Hickish, D.E. and
K.L. Knight.
“Exposure to
Asbestos During
Brake
Maintenance.”
Annals of
Occupational
Hygiene. 13: 17-
21.
This paper contains data on the asbestos dust exposure of brake
mechanics reported by the Medical Services of Ford of Britain.
The first car servicing tests were done using Cortina and Anglia
vehicles, which presumably had smaller brakes than American
cars of this era. Sampling was done in the dust cloud generated
by blow-out of the accumulated dust in brake drums. This
yielded an average value of 2.55 fibers per cc of air. Other tests
were done beside the car when the repairs were in progress,
yielding somewhat lower values averaging 1.25 f/cc. Personal
samples were also taken, to get the best measure of the workers’
actual exposure to airborne asbestos. The average exposure
during brake servicing was 0.68 f/cc.
14
Date Citation Findings
Truck brakes generated more dust. Sampling was done in an
adjacent bay and two bays away from the service bay where
brake repairs were performed. The values recorded were lower
in these bystander locations. The bystander fiber counts ranged
from 0.17 to 0.49 f/cc in the mornings, during which time only
1.5-2 hours was devoted to brake cleaning. Personal sampling
for mechanics doing truck brake repair showed concentrations
of 7.09 f/cc, declining to 0.08 after cleaning and averaging 1.75
f/cc over the time sampling interval. The duration of this
interval could easily have been adjusted to yield an average
value on either side of the new British asbestos standard, 2 f/cc.
Even clutch repair in the adjacent bay was recorded as 2.25 f/cc
“during cleaning.” Samples from bays adjacent to truck brake
repair showed 0.79 f/cc as a time-averaged exposure (for
cleaning and a post-cleaning combined interval). The authors
conceded, “personal exposures in the vicinity (of truck brake
repair) do exceed the standard.”
Holmes, of Turner & Newall, who found chrysotile asbestos
present at up to 1% in it, analyzed brake drum dust. The
authors advised safeguards during brake repairs:
“It is however recommended that care should be exercised
during brake cleaning to avoid inhalation of dust produced,
and the development of cleaning procedures that would
reduce air contamination is desirable.” [emphasis added]
They also noted that their studies did not include sampling
during such procedures as “filing or grinding brake lining,” but
they assumed that these were hazardous processes “with the
attendant need for strict precautions to prevent the inhalation of
fibers.”
1970 Hatch, D.
“Possible
Alternatives to
Asbestos as a
Friction
Material.” Annals
of Occupational
Hygiene. 13: 25-
29
Representative of Ferodo, a manufacturer. Begins with history
on the development of friction products and the technical role
of asbestos in the products. For brake linings the author said,
“there is no substitute for asbestos which would not result in a
deterioration of performance and strength.” For disc brake pads
the picture was brighter:
“(I)t cannot be said that the use of asbestos in disc brake pads
remains a technical necessity, and it is in this field of friction
materials that some departure from resin-asbestos based
composites could occur in the next few years on technical and
performance grounds.”
15
Date Citation Findings
On the subject of clutches, he said the spider clutch being used
in the U.S. for “heavy duty manual shift gear boxes” could use
asbestos-free materials such as sintered metals or ceramic-metal
composites.
1970 Bentley, M.L.
“Control of the
Use of Asbestos-
Containing
Friction
Materials.”
Annals of
Occupational
Hygiene. 13: 31-
32.
A working group of the ARC’s Environmental Control
Committee was devoted to friction products. Constituent
members were Small and Parkes (now part of Cape Industries),
Ferodo, and Mintex. “The Group (which has been formed
recently) is concerned with the users of friction materials...in
the replacement and service field.”
Bentley also said the ARC work group on friction materials was
preparing “two codes of practice for users of asbestos based
friction materials which will be used by (ARC). One of these is
for ... the guidance of those engaged in servicing brakes and
clutches.”
He called the codes of practice “Notes of Guidance.”
1970 Lee, G.L.
“Removing
Dusts from
Brake
Assemblies
During Vehicle
Servicing
Alternative
Cleaning
Methods.”
Annals of
Occupational
Hygiene. 13: 33-
36.
The author worked for the auto manufacturer British Leland. He
noted that a technique for cleaning brakes that would reduce
dust emissions would also involve an increase in time and effort
involved (hence an increase in cost). He commented:
“When viewed under normal lighting conditions, the result of
applying a compressed-air line to remove brake dusts is very
dramatic.”
Lee provided data (Konimeter sampling) in units one can
convert for comparison with the old asbestos TLV. He showed
that at the beginning of brake blow-out, there were 5000 brake
dust particles per 5 cubic centimeters of air; this declined within
minutes to 580 particles per 5 cc. Converting the units of these
measurements to millions of particles per cubic foot of air:
(1 cu. ft. 28,317 cc),
5000 particles/5cc = 28.3 Million particles/cu. ft. (MPPCF)
580 particles/5cc = 3.3 MPPCF
Though it was only for brief periods of exposure that these high
values were measured, it is still conceivable that the exposures
would be kept high in a shop where numerous and continuous
brake repairs were being done. The old TLV for asbestos
exposure was 5 MPPCF, and it applied to dusts containing
asbestos fibers (i.e., all particles were counted, not just the
asbestos fraction of the particles). So peak exposure levels
16
Date 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 samples fibers only,
“...Asbestos fibers counted on membrane filter samples gave a
concentration on the order of 3-5 fibers/cc.”
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.
1970 Knight, K.L. and
D.IE. Hickish.
“Investigations
into Alternative
Forms of
Control for Dust
Generated
During the
Cleaning of
Brake
Assemblies and
Drums.” Annals
of Occupational
Hygiene. 13: 37-
39.
Notes that when the brake dust is blown off with 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 of use as well as the lowering
of exposures.
1970 Asbestos.
Washington,
D.C.: National
Academy of
Sciences,
1971, p.22
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.
1971 Oels, H.C, et al.
“Diffuse
Malignant
Mesothelioma of
the Pleura: A
Review of 37
Cases,” Chest
60: 564-570.
One mesothelioma patient with a history of “probable
occupational exposure to asbestos” was a “service station
operator.”
April,
1972
Harwood, C.F.
“Asbestos Air
Pollution
R li f
“(A)n estimate is presented which indicates that the asbestos
emission from brake linings is significant.”
17
Date Citation Findings
Resulting from
the Wear of
Brake Linings,”
Supplementary
Notes Supplied
to the Attendees
of Seminar on
Asbestos,
Illinois Institute
of Technology
Research
Institute,
Chicago, pp.65-
74
He assumes that 1% of brake dust is asbestos fiber, that 80% of
this dust is emitted and 20% remains lodged within the brake
system.
This paper contains a several-page discussion, “Alternatives to
Asbestos,” in which sintered metals, ceramic metal, fiberglass,
and sealed systems are discussed.
“At the present time, no alternative to asbestos containing
friction products is developed to the stage of finesse required by
the industry. It is difficult to believe that modern technology
can not overcome the problems presented by the use of
alternates.”
This was a several-day seminar attended by a number of
industry representatives and the author (BC).
June 8,
1972
Newman, B.
“Perilous
Particles,” Wall
Street J.
Article on asbestos begins with description of some mechanics
blowing dust out of brake parts:
“What the mechanics don’t seem to know—like thousands of
other mechanics—is that the brown dust is dangerous. And if a
mechanic breathes in enough dust from worn out linings it
could eventually kill him.”
1972 Moertel, C.G.
“Peritoneal
Mesothelioma,”
Gastroenterolog
y 63:346-350
Explaining that mesothelioma is caused by asbestos, he says,
“particularly vulnerable occupations are ... brake lining
installation...”
Feb.
1973
Control
Techniques for
Asbestos Air
Pollutants.
Research
Triangle Park,
N.C.: U.S.
Environmental
Protection
Agency Office
of Air and Water
Programs, pp. 3-
48 and 3-49.
“In the course of servicing and overhauling motor vehicle brakes
and manual clutches, the accumulated asbestos-containing dust is
frequently dislodged from drums and housings by directing a
compressed air jet against the deposits.” Expressed concern over
environmental air pollution.
1973 Boillat, M.A.
and M. Lob.
“Risk of
Asbestosis
among Workers
Replacing Brake
Linings ”
English summary:
“Thirty-nine workers with the job of replacing automobile
brake linings (asbestos) have been investigated. The working
conditions and clinical findings, including radiology and
spirometric studies, are discussed. In view of the comparatively
18
Date Citation Findings
Linings,”
Schweiz. Med.
Wodi. 103:1354-
1359.
brief exposure during the working day, the maximum
permissible concentration of asbestos fibers, according to the
norms indicated by American health workers, does not appear
to be exceeded. No cases of asbestosis were detected, but in one
instance the diagnosis is open to discussion. Despite the
satisfactory outcome of this study, periodic examinations of
workers in this type of occupation are indicated.”
Subjects of the study averaged only 8 years of brake repair
experience at ½ to 2 hours per day of work. Fiber concentrations
from drilling holes for rivets and grinding ranged up to
29.2 f/cc; four of nine measurements exceeded 5/cc.
May 14-
18, 1973
Jacko, M.G.,
R.T. DuCharme,
and J.I I.
Somers. “Brake
and Clutch
Emissions
Generated
during Vehicle
Operation.”
Society of
Automotive Eng.
meeting, Detroit.
Tests of brake wear emissions from braking showed 14.4 percent
of total car asbestos emissions were “retained in brake” of test
vehicle. The corresponding figure for trucks was 9.2%. The
overall figure for all vehicles in U.S. was 11.2% brake retention.
1973 Davis, J.M., and
S.W. Coniam.
“Experimental
Studies on the
Effects of
Heated
Chrysotile and
Automobile
Brake Lining
Dust Injected
into the Body
Cavities of
Mice,” Exper.
Molec. Pathol.
19:339-353.
Automobile brake lining dust was provided by’ Turner &
Newall from a test vehicle. The dust produced “very small
granulomas and little fibrosis” when injected into the pleural
cavities of mice. So mesotheliomas were induced. 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) The
study was terminated after only one year, and was sponsored by
the Asbestosis Research Council.
1974 Greenberg, M.
and T.A. Lloyd-
Davies.
“Mesothelioma
Register 1967-
68,” Brit, J. Ind.
Med. 31:91-104.
Lists “Industry or Job Title in 167 ‘Definite’ Mesotheliomas with
Definite Occupational Exposure to Asbestos”—includes one
“motor mechanic.”
Aug. 8, Lloyd, J.W. Reports on July 21, 1975 NIOSH meeting with industry, labor,
19
Date Citation Findings
1975 “Dear
Colleague...”
Hazard Alert
letter, National
Institute for
Occupational
Safety and
Health,
Rockville, MD.
and academic attendees to discuss brake repair asbestos
hazards. Data generated by the Mt. Sinai Environmental
Sciences Laboratory included 1) blowout of automobile drum
brakes, 2) grinding used truck brake linings, and 3) beveling
new truck brake linings. “Average peak asbestos air
concentrations for these three activities based on personal
samples taken within 10 feet of the operation were,
respectively, 10.5, 3.75, and 37.3 fibers (greater than 5 microns
in length)” per cc. of air.
“The present findings indicate that enough asbestos is preserved
to produce significant exposures during certain brake servicing
procedures.”
Earlier reports of mesothelioma among persons with jobs
involving automobile brake servicing were cited. NIOSH
estimated that 833,535 auto mechanics, 67,679 garage workers,
and 6,657 (original and rebuilding) manufacturing employees
made up a workforce “potentially exposed to asbestos.”
“Recommended (Interim) Procedures for Asbestos Brake and
Clutch Servicing” were attached. These procedures included: 1)
posting signs in the work area warning people not to stay there
unless their work required it (“ ... May Cause Asbestosis and
Cancer”); 2) use of industrial vacuum cleaners (with high
efficiency filters) for removing dust from brakes; 3) use of
respirators; 4) use of local exhaust ventilation and high
efficiency dust collection on grinding machines; 5) adherence to
OSHA asbestos regulations’ provisions regarding special
clothing and change rooms.
Aug.15,
1975
“HEW Warns of
Asbestos Hazard
in Work with
Brake Linings,
Spackling
Mixtures,” Wall
Street J.
Summarizes the NIOSH alert notice (previous item).
1976 Menck, H.R. and
B.E. Henderson,
“Occupational
Differences in
Rates of Lung
Cancer,” J.
Occup. Med.
78:797-801.
This study on occupation and lung cancer rates in California
shows a statistically significant Standard Mortality Ratio (146,
meaning 46 percent higher than expected) for “Auto Repair”
workers. This figure is based on eight deaths from lung cancer
in the years 1972-1973.
1976 Alste, J., D. Chrysotile asbestos fibers from new and worn brake linings and
20
Date Citation Findings
Watson, and J.
Bogg. “Airborne
Asbestos in the
Vicinity of a
Freeway,”
Atmos. Environ.
10:583-589.
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.
1976 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.
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.
1976 Lorimer, W.V. et
al., “Asbestos
Exposure of
Brake Repair
Workers in the
United States,”
Mount Sinai J.
Med. 43:207-
218.
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.
“(T)he findings suggest that asbestos disease will be present
among (brake maintenance) workers and that appropriate
control measures should be urgently instituted.”
1977 Rohl, A.N. et al.,
“Asbestos
Content of Dust
Encountered in
Brake
Maintenance and
Repair,” Proc.
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
studies of garage mechanics
21
Date Citation Findings
Roy. Soc. Med.
70:32-37.
studies of garage mechanics.
1977 Bruckman, L.,
R.A. Rubine,
and B. Christine.
“Asbestos and
Mesothelioma
Incidence in
Connecticut,” J.
Air Pollut.
Contr. Assoc.
27:121-126.
Reports a case of mesothelioma in a toll booth operator. These
investigators found increased asbestos exposure at toll booths
compared to ambient air of Connecticut cities.
1978 Seshan, K. “On
the utility of
dark-field
electron
microscopy in
the
determination of
the degree of
deformation in
Chrysotile
Asbestos: An
Environmental
Research
Application”
Environ.
Research
16:383-392.
New technique of analysis verifies that “chrysotile asbestos in
various stages of deformation” survives in brake drum dust.
1978 Rohl, A.N.,
A.M. Langer,
and I.J. Selikoff.
“Airborne
Asbestos in the
Vicinity of a
Freeway,”
Atmos.
Environ.12:2030
-2031.
Adds a number of unpublished reports confirming the presence of
chrysotile in disintegrated brake linings from Great Britain (F.
Pooley), France (P. Sebastien), and South Africa (M.S. Kikine).
Refers to findings of asbestosis among automotive maintenance
workers.
Oct.
1978
“Friction
Materials Work
Practices
Guide.” Friction
Materials
Standards
Institute,
Paramus, N.J. 12
pp.
“When removing worn friction materials remove the
accumulated dust in the assembly with an industrial vacuum
cleaner equipped with a high efficiency filter system. If such
equipment is not available, dust can be removed with a damp
cloth. Do not use compressed air or dry brushing for cleaning.
Use a NIOSH approved respirator when removing worn friction
materials, or cleaning brake or clutch assemblies.”
22
Date Citation Findings
Local exhaust ventilation is recommended for machining of
friction materials. Machining and repair areas “should be
isolated from other work areas in a restricted area to prevent
unnecessary exposure of other workers.” Warning signs are
suggested to limit access to brake work areas.
“Work clothing should not be taken home.”
The industry trade group also covers disposal of vacuum
cleaner waste in marked, impermeable bags in this pamphlet.
1979 Kagan, E. et al.
“Asbestos-
Associated
Neoplasms of 13
Cell Lineage,”
Amer. J. Med.
67:325-330.
Reports one case of pleural mesothelioma in a man who had
installed automotive brake linings for 25 years.
1979 de Lajartre, M.
and A.Y. de
Lajartre.
“Mesothelioma
on the Coast of
Brittany,
France,” Ann.
N.Y. Acad. Sci.
330:323-332.
“Certain” occupational exposure to asbestos was identified in 51
cases of mesothelioma, including 4 “mechanics.” Exposure
characterized as “probable” for 6 “construction mechanics.”
1980 McDonald, A.D.
and J.C.
McDonald.
“Malignant
Mesothelioma in
North America,”
Cancer 46:1650-
1656.
A review of mesothelioma cases included 11 with occupational
histories of garage work. A series of matched controls without
mesothelioma included 12 with such histories. Individuals with
histories of asbestos mining and manufacturing, or construction
and shipyard work in addition to garage work were not counted as
garage workers.
June,
1981
Selikoff, I.J. et
al. Disability
Compensation
for Asbestos-
Associated
Disease in the
United States,
U.S. Dept. of
Labor Contract
No. J-9-M-8-
0165.
Projects a risk of asbestos cancer for a number of occupations
compared with insulation work. “Automobile maintenance” is
estimated to carry 4% as much risk as insulation work.
Projected number of deaths from asbestos-related cancer among
automobile maintenance workers estimated to be rising steeply,
from 400/year in 1983 to a peak of 500-600/year during the
years 1990-2015. Quotes Weston as saying that 900,000
workers are continually exposed and 1,070,000 are exposed
occasionally or infrequently.
1982 Nicholson, W.J., Similar to analysis in Selikoff et al (above).
23
Date Citation Findings
G. Perkel, and
I.J. Selikoff.
“Occupational
Exposure to
Asbestos:
Population at
Risk and
Projected
Mortality’ 1980-
2030,” Amer. J.
Indust. Med.
3:259-311.
1982 Roberts, D.R.,
and R.D.
Zumwalde.
“Industrial
Hygiene
Summary Report
of Asbestos
Exposure
Assessment for
Brake
Mechanics.”
NIOSH Report
#32.4,
Cincinnati.
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.
Nov.13,
1982
Langer, AM. and
W.T.E.
McCaughey.
“Mesothelioma
in a Brake
Repair Worker,”
Lancet 1101-
1102.
Finds asbestos fibers in the lung tissue of a mesothelioma patient
whose occupational exposure consisted of many years of brake
servicing work.
1983 Glickman, L.F.,
et al.
“Mesothelioma
in Pet Dogs
Associated with
Exposure of
Their Owners to
Asbestos,”
Environ. Res.
32:305-313.
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.
1983 Mancuso, T.F.,
“Mesothelioma
Among
Machinists in
Report of pleural mesothelioma in an automechanic.
24
Date Citation Findings
Railroad and
Other
Industries,”
Amer. J. Indust.
Med. 4:501-513.
1983 Kagan, E., and
R.J. Jacobson.
“Lymphoid and
Plasma Cell
Malignancies:
Asbestos-related
Disorders of
Long Latency,”
Amer. J. Clin.
Path. 80:14-20.
Reports one case of pleural mesothelioma in a man who had
installed automotive brake linings for 25 years.
Feb.
1985
“Asbestos Fact
Book.” U.S.
Environmental
Protection
Agency, 11 pp.
“(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
Commercial Substitution of Asbestos in Friction Products
Date Citation Findings
Sept.
1976
“ICI Asbestos-
Free Brake
Shoe,”
Asbestos 12-
14.
Announces immediate production and worldwide
marketing of a railroad brake shoe that contains no lead or
asbestos. Called Tiger, the product was developed by
Abex Corporation, subsidiary of IC Industries, Inc.
1976 Kwolek, J.P.
“Friction
Materials for
Small Car
Solid Rotor
Applications,”
SAE
Transactions,
paper
no.750874.
Gives history of development of semi-metallic brakes,
starting with their use in police cars, taxicabs, and “a few
vehicles sold to the general public.” Notes that semimetallic
front disc brakes achieved success in meeting
standards of the Los Angeles Police Department, and
displayed a number of advantages over conventional
asbestos-organic brake compositions by 1970. Increased
cost was a major obstacle to widespread usage at that time.
Author worked for Bendix Corporation.
1976 Annual Report,
Raybestos-
Manhattan,
Inc.
“The escalating costs associated with handling this raw
material and the uncertain consequences of future
government asbestos regulations ... have necessitated our
decision to work toward the elimination of asbestos from all
our friction products and this eventuality has become an
essential part of our long term product and manufacturing
plans.”
1978 Annual Report,
Raybestos-
Manhattan,
Inc.
“Although from a social and political standpoint, publicity
concerning asbestos has not adversely affected our business
nor do we expect it to in the near future ... from a long-range
standpoint, we are planning to eliminate asbestos from our
friction materials products by 1982 in order to minimize the
effect of any further government regulations in this area.”
1980 Castleman, B.I.
and M.J. Vera.
“Impending
Proliferation of
Asbestos,”
Intenat. J.
Health Serv.
10:389-403.
Paraphrases a communication from General Motors to the
U.S. Environmental Protection Agency (Sept. 7, 1979),
called “General Motors Programs on Non-Asbestos Friction
Materials for Brake Systems.” Approximately 60 percent of
all passenger car disc brakes manufactured and used by
G.M. had non-asbestos friction materials in 1979. G.M.
projected that all its 1983-model passenger cars with disc
brakes would have asbestos-free brakes, and all cars with
drum brakes and light trucks would have asbestos-free
brakes by the 1985 model year.
July,
1981
Norman, J.C.
“Synthetic
Fibers Find
Applications in
Transportation,”
Indust.
Research and
DuPont marketing specialist for “Kevlar” aramid fiber
presents test results and describes performance of this
product as an asbestos substitute in brakes. Cost of use
initially higher, but longer service life expected to offset the
25 percent initial cost premium in the life-cycle cost of the
product. Excels in heavy-duty applications, compared with
26
Date Citation Findings
Research and
Development.
conventional asbestos brakes.
27
Control Technology for Brake and Clutch Work
Date Citation Findings
1978 National Loss Control
Service Corp., Long
Grove, IL 60049. Report
of Industrial Hygiene
Study for Ammco Tools,
Inc. North Chicago, IL.
A 15-minute exposure peak of 1.1 f/cc was found with brake
washing using the Ammco Model 1250 brake assembly washer
after use of a hammer. A “poorly maintained” Model 880
created operator exposures during grinding of 1.4 f/cc, but the
“well maintained” Model 880 also created operator exposure
of 1.4 f/cc for grinding brake linings.
This system uses a solvent, which dries into a gel in the
collection tray, trapping the fibers, according to verbal
communication from the manufacturer. Nonetheless, measured
asbestos levels using optical microscopy are excessive and
allow shop contamination to occur.
1980 Asbestos Product Test
Results. GCA Corp.,
Bedford, MA 01730.
Prepared for the U.S.
Environmental Protection
Agency, Office of
Pesticides and Toxic
Substances.
Widespread garage contamination is illustrated by worker
exposure measurements during compressed air use of 0.85 f/cc
with levels of 0.1 f/cc 25 feet away. When the mechanic removed
the brake housing and cleaned it by repeatedly striking it with a
hammer, his 14-minute exposure was measured as 1.29 f/cc. In
these tests, a scanning electron microscope was used to analyze
tile air samples, so this would not be comparable to
measurements using conventional optical techniques.
July
22,
1985
Asbestos Dust Control in
Brake Maintenance. PEI
Associates, Inc., P.O.
Box 46100, Cincinnati,
OH 45246. Prepared for
the U.S. Environmental
Protection Agency,
Office of Pesticides and
Toxic Substances
This report reviews exposures with a variety of improvised
control techniques, which have emerged as alternatives to the
compressed air hose. Their performance was generally poor:
damp rag use permitted peak asbestos exposures up to 2.6 f/cc
with time-weighted averages (TWAs) up to 0.28; a liquid
squirt bottle created a 10-minute peak of 0.54 f/cc with TWA
over five hours of 0.21; the use of stoddard solvent flowing
through an air gun caused peak levels up to 0.68 f/cc and
TWAs slightly under 0.1; dry rag and brush generated peaks up
to 0.81 f/cc with TWAs up to 0.2.
Wetting methods not using a collection system simply disperse
the fibers, and when the liquid dries, fibers remain in the shop
ready to enter the room air with minimal motion. Background
contamination from such methods, therefore, would not
necessarily be less than with the compressed-air cleaning
method.
A wet method system with a collection tray was also evaluated
(Ammco Brake Assembly Washer). Unfortunately, 15-minute
peaks were 1.1 f/cc.
Case Reports of Mesothelioma in Brake Repair Work
28
Date Citation Findings
1982 Langer and McCaughey
(Lancet, 1982).
Case report of mesothelioma in a brake repair worker.
1989 E.S. Hansen, “Mortality
of Auto Mechanics.”
Scand. J. Work Environ.
Health 15.43-46.
Case report of mesothelioma in a brake repair worker.
What A Responsible Brake Manufacturer Did and Should Have Known
About Brakes From 1930-1980
Year Source of
Information
Companies
Involved
Information acquired Action
1930-
1932
Testing of dust levels
during
manufacturing
Raybestos, JM,
Southern:
conducted by
Met Life
Low dose exposures caused
disease. TLV inadequate
None
1930-
1932
Testing for diseases
in production
workers
Raybestos, JM,
Southern:
conducted by
Met Life
Asbestosis often fatal.
May cause heart disease and
obstructive lung disease
Published
Lanza 1935
1937 Worker testing Multibestos Short exposures cause disease Published
(George &
Leonard)
1936 Substitutes available OI, various
German
companies
Various patents;
OI-1936;
Bendix-1955 (ceramic brakes
marketed)
Published
1938-
1946
Animal testing Group of brake
manufacturing
companies
Asbestos causes cancer –
asbestosis not required.
TLV wrong.
New measurement method
for fibers required.
Fibers (not chemical
composition of rock cause of
disease)
Only fiber
information
published
(Vorwald 1951)
1939 Product testing GM Exposures during use above
TLV.
Lead exposure possible
Published
(Castrof 1949)
29
A 1959 study prepared by the Chrysler Corporation reported on the advantages of metallics over
asbestos brakes.6 The study showed that the safer substitutes, metallics, actually outperformed
asbestos brakes on almost every test conducted. Tests proved that, in addition to eliminating
asbestos-associated health risks to brake mechanics and users, metallic brakes could be considered
safer than their asbestos-containing counterparts in many aspects of motor vehicle operation.
Bendix had numerous patents for asbestos free brakes and began commercial sale of such brakes for
trucks in 1956. All Bendix automotive brakes contained asbestos until 1983.
Safety Concerns Metallic Asbestos
Durability and
Effectiveness
• Consistent through extended
use: “With the metallic, fade
is absent…”
• Significantly more durable:
“The police durability
schedule emphasizes the
inadequacy of organic
linings on heat-problem
brakes”
• Tendency to fade (become
less effective) with time
• Develop “considerable
noise, odor, roughness, pulls
and… grabbiness”
• Fail under stress: “Failure
occurred at 396 miles, while
the metallic linings
remained constant
throughout the 1000 mile
schedule.”
Resistance to
high temperature
• Greater heat resistance and
increased efficiency: “…at
each given temperature
reading for both organic and
metallic linings, the metallic
lining pressure is considerably
below the organic. The
metallic lining brakes are
operating more efficiently
with less effort required.”
• “Organic linings are capable
of meeting all the
requirements of safe
stopping…” HOWEVER,
“The test does establish the
superiority of metallic linings
in stopping a vehicle with
ease under severe and
prolonged braking
requirements.”
Performance
under stress (e.g.
descending steep
hills)
• Consistent and effective: “The
car with metallic brake linings
descended Pikes Peak in drive
range…the metallic line
pressure remained practically
constant for the entire
descent.”
• Wear out and fail: “A vehicle
with organic brake linings
making a similar descent
failed at 10.5 miles with
brakes entirely gone.”
Resistance to
wetness
• Consistent performance:
“Metallics are not affected by
wetness”
• Less effective for driving on
wet surfaces: “…organic
surfaces are sensitive to
moisture and contaminants”
Low-speed
driving
• Less effective than at highspeed
travel: “They have
reduced effectiveness at low
• More consistent performance:
“They vary only slightly in
effectiveness with speed.”
30
speeds and temperatures”
Overall
performance
• “Both the police durability
and the Pikes Peak brake
tests are extremely severe
and prove the value of
metallic linings for vehicles
that must withstand
abnormal braking
requirements.”
• “As a result of their superior
performance in heavy-duty
operations, Chevrolet has
released metallic linings as
optional equipment.”
• “Today’s organics are more
equal to the demands of
average daily driving.”
Bendix and other patents for Asbestos and non-asbestos brakes:
Patent
Number
Title ADate PDate Company Inventor Asb Non Asb Ref Mode
542414 Brake Shoe 1895 1895 Kinzer, John F. ? Auto
642295 Brake Shoe 1899 1900 Cardwell,
James R.
? Auto
665298 Brake Shoe 1900 1901 Wolhaupter, B. ? Auto
1082158 Brake Shoe 1912 1913 Am. Brake
Shoe
Jones, Harry No Auto
1532141 Brake Band 1924 1925 Turner
Brothers
Asbestos
Co.
Kenyon, Percy
George
Yes Auto
1539444 Brake Lining 1921 1925 Asbestos
Spinning
and
Weaving
Corp.
Trainor,
Edward
Yes Auto
1687151 Friction Brake 1926 1928 Am. Brake
Materials
Corp.
Thompson,
James S.
? Auto
1756936 Brake Shoe 1927 1930 Bendix Bendix, Vincent Yes Auto
1771594 Friction Brake 1927 1930 Am. Brake
Materials
Corp.
Thompson,
James S.
? Auto
1887981 Brake Lining 1930 1932 Bendix Rosner, Adolph Yes Auto
1899239 Friction Element 1928 1933 De
Lukacsevics,
Charles
No Ben - 3007549 Auto
1902576 Friction Surfaces 1930 1933 Bendix Norton,
Raymond J.
Yes Auto
1919967 Friction Block 1927 1933 Am.
Brakeblok
Corp.
Thompson,
James
? Ben - 3064343 Auto
31
Patent Title ADate PDate Company Inventor Asb Non Asb Ref Mode
Number
1926699 Friction Material 1929 1933 Bendix Norton,
Raymond J.
Yes Auto
1927626 Metallic Material 1929 1933 Chrysler Calkins, William
G.
No Auto
1932912 Brake Lining 1928 1933 Bendix Rosner, Adolph Yes Auto
1947894 Brake Shoe 1929 1934 Bendix Whitworth,
Stanley
Yes Auto
1950262 Brake Shoe 1930 1934 Bendix Norton,
Raymond J.
? Auto
1954521 Brake Shoe 1929 1934 Bendix Cunningham,
Marion M.
Yes Auto
1964177 Brake Lining 1928 1934 Bendix Rosner, Adolph Yes Auto
1964178 Brake Lining 1930 1934 Bendix Rosner, Adolph Both Auto
1971618 Friction Facing 1930 1934 Bendix Norton,
Raymond J.
? Auto
2012259 Friction Lining 1932 1935 Denman, Harry
B.
? Talc - Tremolite Auto
2028621 Brake Apparatus 1931 1936 Bendix Norton,
Raymond J.
Yes Auto
2028625 Brake 1931 1936 Bendix Rosner, Adolph Yes Auto
2038200 Brake 1931 1936 Bendix Rosner, Adolph Yes Auto
2042684 Matrix Materials 1934 1936 Ejner
Schjoth
Schjoth, Ejner No Auto
2044988 Brake 1929 1936 Bendix Rosner, La
Brie, Ludger
Yes Auto
2048468 Brake Shoe 1930 1936 Bendix Rosner, Adolph Yes Auto
2063024 Brake 1933 1936 Bendix Bendix, Vincent Yes Auto
2071297 Brake 1931 1937 Bendix Dodge, Adiel,
McConkey,
Montgomery
? Hycoe Auto
2072070 Friction Article 1933 1937 General
Metals
Powder Co.
Fisher, John S. No Ben - 3064343 Auto
2074723 Brake 1931 1937 Bendix Fowler, Owen
H.
Yes Auto
2077914 Brake 1932 1937 Bendix Axtmann,
Harold G.
Yes Auto
2077955 Brake 1935 1937 Bendix Roberts, Glyn
Pierce
Yes Auto
2080314 Brake 1935 1935 Hoof, Addison
C.
? Ben - 3064343 Auto
2087371 Brake 1935 1937 Bendix Chambers,
Allen C.
Yes Auto
2094065 Brake 1932 1937 Bendix Frank,
Frederick C.
Yes Auto
2102855 Brake Lining 1934 1937 Bendix Rosner, Adolph Yes Auto
2109110 Brake Drum 1935 1938 Bendix Frank,
Frederick C.
? Air
2111297 Brake 1936 1938 Bendix Pontius,
George W.
Yes Auto
32
Patent Title ADate PDate Company Inventor Asb Non Asb Ref Mode
Number
2118733 Vehicle Brake 1937 1938 William K.
Line
Line, William K. Yes Auto
2122405 Friction Surface 1937 1938 Raybestos Bockius, Chris
& Batchelor,
Clyde S.
Yes Auto
2134512 Brake 1934 1938 Bendix Hall, Percy
Edgar
Yes Auto
2134564 Brake 1936 1938 Bendix Lauer, Leon
Nicolas
Yes Auto
2148257 Brake Shoes 1936 1939 Bendix Budd, Clarence
E.
Yes Auto
2152017 Brake System 1936 1939 Bendix Banning,
Thomas A.
Yes Auto
2152022 Brake 1935 1939 Bendix Boetto, Jean
Charles
Yes Auto
2152611 Metallic Element 1936 1939 Cleveland
Graphite
Bronze Co.
Swartz, Carl E. No Auto
2159935 Brake Lining 1936 1939 Stackpole
Carbon Co.
Sanders,
Vernon H.
Yes Auto
2163879 Brake 1929 1939 Bendix House, Bryan
E.
Yes Auto
2173591 Brake Drum 1936 1939 Bendix Miller, Philip M.
& Miller,
Richard B.
Yes Auto
2178527 Machine Element 1938 1939 S.K.
Wellman
Co.
Wellman,
Samuel K.
No Auto
2187086 Metallic Element 1938 1940 GM Koehring,
Roland P.
No Auto
2190237 Composite Metal
Structure
1937 1940 GM Koehring,
Roland P.
No ?
2191460 Article of Mfg. 1936 1940 General
Metals
Fisher, John S. No Auto
2198253 Metal Bearings 1934 1940 GM Koehring,
Roland F.
No Auto
2207961 Friction Clutch 1939 1940 S.K.
Wellman
Co.
Wellman,
Samuel K.
No Auto
2218615 Brake Shoe 1939 1940 Bendix McCune,
Joseph C.
? Ben - 3064769 Auto
2239134 Friction Article 1940 1941 S.K.
Wellman
Co.
Wellman, S. K. No Auto
2251410 Metal Structure 1939 1941 GM Koehring,
Roland F.
No Auto
2264192 Friction Clutch 1939 1941 S.K.
Wellman
Wellman,
Samuel K.
No Auto
2277107 Clutch Facing 1940 1942 P.R. Mallory
& Co., Inc
Imes, Robert H. No Ben - 3064343 Auto
2287952 Brake Drum 1939 1942 GM Tormyn,
Herman
No Auto
33
Patent Title ADate PDate Company Inventor Asb Non Asb Ref Mode
Number
2289311 Comp. Blank 1940 1942 S.K.
Wellman
Co.
Wellman,
Samuel K.
No Ben - 3064343 Auto
2289689 Brake Elements 1940 1942 Wilson,
Rosser L.
Am. Brake
Shoe and
Foundry Co.
? Auto
2299192 Sintered Articles 1939 1942 GM Tormyn,
Herman
No Auto
2299877 Friction Material 1939 1942 Chrysler Calkins, William
G.
No Auto
2355419 Brake Lining 1942 1944 Johns-
Manville
Bruce, Donald
S.
? Auto
2369502 Friction Material 1940 1945 Raybestos Walker,
Frederick S.
Both Auto
2375855 Disc Brake 1944 1945 Lambert
Brake Corp.
Lambert,
Homer T.
? Air/Auto
2381393 Brake 1943 1945 Firestone Brown, Roy W. ? Air
2381941 Friction App. 1942 1945 S.K.
Wellman
Co.
Wellman, S.K.
& Sawyer,
Charles B.
No Auto
2389061 Metal Body 1941 1945 Raybestos Kuzmick,
Jerome
No Auto
2408430 Friction Product 1944 1946 S.K.
Wellman
Lowey, Francis
J. & Tower,
Charles H.
No Auto
2410924 Friction Element 1944 1946 American
Brake Show
Co.
Blume, William
A. & Conarton,
Edward W.
Yes Auto
2417855 Disc Brake 1945 1947 Engineering
Research
Corp.
Barish, Thomas Yes Auto
2424655 Brake Adjustor 1944 1947 Bendix Goepfrich,
Rudolph A.
Yes Auto
2428298 Friction Element 1942 1947 Amer.
Brake Shoe
Spokes, Ray E.
& Keller, Emil
C.
Yes Auto
2441534 Abrasive Material 1940 1948 Babcock &
Wilcox Co.
Norton, Charles
L.
No Auto
2446892 Bimetallic Articles 1943 1948 S.K.
Wellman
Co.
Wellman, S.K. No ?
2457861 Metal Products 1945 1949 H. A.
Brassert
Co.
Herman A.
Brassert
No Auto
2460367 Abrasive Articles 1945 1949 Carborundu
m co.
Sharpe, Donald
B.
No ?
2460367 Abrasive Articles 1945 1949 Carborundu
m Company
Sharpe, Donald
B.
No Auto
2464437 Metallic Structure 1945 1949 Bendix Dasher, Donald Yes Auto
2470269 Friction Material 1945 1949 Cleveland
Graphite
Bronze Co.
Schaefer,
Ralph
No Auto
34
Patent Title ADate PDate Company Inventor Asb Non Asb Ref Mode
Number
2476151 Brake Drums 1943 1949 B.F.
Goodrich
Le Jeune,
Frank H.
No Ben - 3064769 Auto
2486140 Composition
Brake Block
1952 1954 Johns
Manville
de Gaugue,
Charles L.E.
Yes Rail
2516966 Friction Element 1946 1950 Bendix Du Bois,
William H.
? Auto
2531782 Friction
Assembly
1947 1950 Emmet L.
Moore
Moore, Emmett
L.
Yes Auto
2553828 Friction Element 1945 1951 Westinghou
se Air Brake
McCune,
Joseph C.
? Rail
2554291 Brake Mech. 1945 1951 Bendix Bradley,
Ronald E. &
Fisher, Harold
Yes Auto
2554548 Brake Lining 1946 1951 Le
Carbone-
Lorraine
Albagnac, Jean
Albangnac
? Ben - 2959254 Auto
2607245 Bimetallic Blanks 1945 1952 S.K.
Wellman
Co.
Wellman, S.K.
& Lowey,
francis J.
No Auto
2628693 Brake Shoe 1947 1953 Chrysler Rodger, William
R.
Yes Auto
2652624 Comp. Metal 1948 1953 H.A. Wilson
Co.
Guinee,
Edward Joseph
N Auto
2686140 Composition
Brake Block
1952 1954 Johns
Manville
de Gaugue,
Charles L.E.
No Rail
2724461 Brakes 1950 1955 Bendix Goepfrich,
Rudolph A.
Yes Auto
2728418 Brake 1948 1955 Bendix Dombeck,
Edward K.
Yes Auto
2730199 Brake Adjustor 1954 1956 Bendix Britton, Clayton
F.
Yes Auto
2731312 Brake Assembly 1950 1956 Bendix Du Bois,
William H.
Yes Auto
2742107 Brakes 1950 1956 Bendix Du Bois,
William H.
Yes Auto
2770325 Brake 1947 1956 Bendix Dombeck,
Edward K.
Yes Auto
2770328 Brake Assembly 1950 1956 Bendix Dombeck,
Edward K.
Yes Auto
2781107 Friction Element 1952 1957 Am. Brake
Shoe Co.
Smith, Francis
H.
? Ben - 3064343 Auto
2783529 Friction Element 1954 1957 Am. Brake
Shoe Co.
Huntress,
Howard B.
No Ben - 3021592 Auto
2784105 Friction Lining 1955 1957 Bendix Stedman,
Frances E. &
Pocock, Robert
C.
No Ben - 3064769 Air/Auto
2794526 Clutch Device 1953 1957 S.K.
Wellman
Co.
Canfield, Wade
E.
? Auto
2801714 Friction Shoe 1956 1957 Meadville
Research
Dotto, John ? Auto
35
Patent Title ADate PDate Company Inventor Asb Non Asb Ref Mode
Number
Products
Corp.
2806570 Friction Facing 1951 1957 Bendix Markus,
Eugene
? Auto
2818634 Friction Element 1954 1958 Raybestos Batchelor,
Clyde S. &
Steck, Rudolph
e.
No Ben - 3021592
& 3064769
Auto
2822892 Brake Adjustor 1953 1958 Bendix Clark, Warren
G.
Yes Auto
2824629 Brake Shoe 1953 1958 S.K.
Wellman
Co.
Wellman, S.K. No Ben - 3064769 Auto
2835367 Friction Button 1955 1958 Raybestos Steck, Rudolph
E.
? Auto
2854098 Disc Brake 1955 1958 Lambert
Brakes
Corp.
Griswold,
Frederick D.
? Air
2856034 Fluid Motor 1955 1958 Bendix Mossey,
Joseph
? Auto
2861964 Composition
Brake Block
1953 1958 Johns
Manville
de Gaugue,
Charles L.E. &
Halstead,
Ralph T.
No Rail
2861964 Composition
Brake Block
1953 1958 Johns
Manville
de Gaugue,
Charles L.E. &
Halstead,
Ralph T.
No Rail
2863211 Friction
Assembly
1955 1958 S.K.
Wellman
Wellman, S.K. No Auto
2863211 Friction
Assembly
1955 1958 S.K.
Wellman
Co.
Wellan, S.K. No Auto
2864468 Friction Device 1955 1958 Bendix Dombeck,
Edward J.
? Auto
2871996 Brake Shoe 1955 1959 Bendix Strebinger,
Robert L.
? Auto
2875859 Brake 1955 1959 Bendix Strebinger,
Robert L.
? Auto
2888105 Disc and Shoe 1954 1959 Bendix Burnett,
Richard T.
? Auto
2892707 Bi-Metallic Article 1956 1959 S.K.
wellman Co.
Biggs, Robert
W.
No Auto
2910144 Shoe and Disc 1955 1959 Bendix Burnett,
Richard T.
? Auto
2915145 Kinetic Device 1954 1959 Bendix Mossey,
Joseph L.
? Auto
2930451 Friction Device 1955 1960 Bendix Burnett,
Richard T.
? Auto
2938790 Friction Lining 1955 1960 Bendix Stedman,
Frances E., &
Pocock, Robert
No Air/Auto
36
Patent Title ADate PDate Company Inventor Asb Non Asb Ref Mode
Number
C.
2947388 Metal Control 1957 1960 Goodyear Culbertson,
James A.
No Auto
2948955 Friction Article 1957 1960 Bendix Allen, Alfred W.
& Herron,
Robert H.
No Auto
2950783 Friction Device 1955 1960 Bendix Mossey,
Joseph
? Auto
2953220 Brake 1954 1960 Bendix Burnett,
Richard T.
? Auto
2959254 Brake Shoe 1956 1960 Bendix Riggs, James
A.
No Auto
2964142 Brake Shoe 1958 1960 Bendix Goepfrich Yes Auto
2968367 Shoe & Disk 1955 1961 Bendix Burnett,
Richard T.
Yes Auto
2986252 Friction Lining 1957 1961 Bendix Du Bois,
William H.
No Auto
2988176 Vehicle Brake 1956 1961 Bendix Du Bois,
William H.
? Auto
2993578 Friction Segment 1958 1961 Bendix Nordgren,
Arnold W.
No Auto
3007549 Friction Control 1957 1961 Bendix Klein, Bruce W. No Auto
3014884 Friction Element 1957 1961 Dunlop Bray, Horace A No Auto
3017962 Limiting Device 1958 1962 Kelsey-
Hayes Co.
Ingres, Jeannot
G.
Yes Auto
3019514 Friction Lining 1959 1962 Bendix Bickelhaupt,
Roy E.
No Auto
3020634 Friction Segment 1958 1962 Bendix Williamson,
Joseph R.&
Billmeyer,
James g.
No Auto
3021592 Metal Matrix 1959 1962 Bendix Herron, Robert
H.
No Auto
3027979 Brake Structure 1959 1962 Bendix Pocock, Robert
C.
No Auto
3037860 Friction Articles 1957 1962 Bendix Masterson,
James F.
No Auto
3064343 Friction Article 1958 1962 Bendix Baynes, Gene
P.
No Auto
3064769 Fastener 1958 1962 Bendix Billmeyer No Auto
3114197 Brake Element 1960 1963 Bendix Du Bois,
William H.&
Roth, Douglas
J.
No Auto
3139671 Metal-Ceramic 1962 1964 Bendix Heron, Robert
H. & Jannasch,
Norman E.
? Air
3210303 Friction Product 1960 1965 Bendix Biggs, Robert
W.
No Auto
37
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 of Pulmonary 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 of Wisconsin, 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 of the Inhalation of Asbestos Dust on the Lungs of Asbestos 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 of American 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 of the Chief Inspector of the 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 of the 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
Offices in Southfield, Michigan
Aug. 8, 1972 C. E. Heitman; H. Bobel; H.O.
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 of workers.
“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 of the 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 of the 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 of this report, Dr. Colin Harwood, supported the banning of the use of asbestos in
friction materials in Illinois, and the members of the Asbestos Study Committee had access
to this information.
Members of FMSI (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 of the 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 1936, 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
46
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 of the 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 of the 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.
47
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 youll 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. Theres 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. Selikoff’s 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
48
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 of the [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 of the 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
49
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.”
50
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 of the 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 subject 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, of National 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:
51
“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 of these 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
52
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 of the 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 of Bayes’ 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 of this 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 integration of
the available evidence. The accepted
model for causation 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 of the likelihood of cause-effect relationship. The evaluator
expresses her implicit subjectivity through the reasoning and assumptions behind the ordinal weight
53
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.
50 % 30 % 20 %
54
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 individuals 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 of these 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.
HILLS 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 of the considerations.
While respected as a framework for determining causation, each of Hills 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
55
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 of blood 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 patients 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
56
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 of these 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 of the 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 of bias. 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 of whether 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 of biological 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
57
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 Kochs 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
58
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, Hills 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 of the 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] of the 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 of illness 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 of journals 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 of time, 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
59
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 of tremolite, 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 of the 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
60
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
Table 2: Epidemiologic studies
Study (Authors) Year Population
Size Studied
# of
Years
Studied
# of
Meso
Cases
R.R.
>2
(Y/N)
Stat.
Sig.
(Y/N)
Rate
Ratio*
Expected
Cullen, MR and
Baloyi, RS
1991 51 21 3 Yes Yes 2,801 0.001071
Camus, M,
Siemiatycki, J and
Meek, B
1998 11,651 19 7 Yes Yes 32 0.221369
Baloyi 1989 300 9 3 Yes Yes 1,111 0.0027
Enterline, PE,
Hartley, J, and
Henderson, V
1987 1,074 39 6 Yes Yes 143 0.041886
Nokso-Koivisto, P
and Pukkala, E
1994 8,391 38 8 Yes Yes 25 0.318858
Borrow, M et al 1973 600 14 10 Yes Yes 1,190 0.0084
Morinaga et al 1989 50,000 18 6 Yes Yes 2 0.9
Strurm et al 1993 50,000 30 67 Yes Yes 45 1.5
Rogars AJ, et al 1991 50,000 5 2 Yes Yes 2 0.25
Hughes, JM and
Weill, H
1986 5,500 50 12 Yes Yes 44 0.275
Begin R et al 1992 50,000 35 20 Yes Yes 11 1.75
Doll, R and Peto, J 1985 4,022 50 12 Yes Yes 60 0.2011
Feingold, A. citation
from depositions
about mesothelioma
in Quebec workers
10,000 50 38 Yes Yes 76 0.5
Berry 1996 10 #DIV/0!
Stayner, LT,
Dankovic, DA, and
Lemen, RA
1996 45 #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.
61
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 of workers exposed to “pure chrysotile” revealed a SMR or rate
ratio greater than 2 for mesothelioma.6 As Greenland has shown, a rate ratio of two 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
62
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 of workers 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,
Kohtz DS, Kohtz JD,
Johnson EM
chrysotile 1988 chrysotile mediates damage
enabling transfected plasmid to be
replicated.
Bolton RE, Davis JMG,
Donaldson K, Wright A
chrysotile,
amosite
1982 chrysotile samples found to be more
carcinogenic than the amosite
Davis JMG, Beckett ST,
Bolton RE, Collings P,
Middleton AP
chrysotile,
crocidolite,
amosite
1978 chrysotile samples were the most
fibrotic and the most tumorigenic.
Jaurand MC, Kheuang
L, Magne L, Bignon J
chrysotile 1986 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
Article Fiber Type Year
Korkina LG, Durner AD,
Suslova TB,
Cheremisina ZP,
Daugel-Dauge NO,
Afanas’ev IB
chrysotile 1992 mutagenic action probably mediated
by iron-oxygen complexes plus
hydrogen peroxide.
Libbus BL, Craighead JE crocidolite,
chrysotile
1988 rat mesotheliomas induced by
crocidolite or chrysotile. loss of
chromosomes and translocations
observed.
Lund LG, Aust AE crocidolite,
amosite,
chrysotile, or
tremolite
1992 chrysotile induced single strand
breaks in DNA. percent of DNA with
SSB directly related to its iron
content.
Mochaux G, Bichon J,
Jaurand MC, Lafuma J,
Sebastien P, Masse R,
Hirsch A, Goni J
chrysotile,
crocidolite
1981 mesotheliomas in rats, chrysotile
more carcinogenic than crocidolite.
Osgood C, Sterling D 1991 chrysotile and amosite induced sexchromosome
aneuploidy, which is
associated with development and/or
progression of cancers. chrysotile
appeared to be the more effective
agent.
Suzuki Y, Kohyama N amosite,
chrysotile,
and zeolite
1984 chrysotile and amosite had the
highest tumor incidence
Valerio F, de Ferrari M,
Ottagio L, Repetto E,
Santi L
chrysotile,
crocidolite
1983 statistically significant increase in
chromosome and chromatid damage
were present after treatment with
chrysotile fibers.
Anomalies most frequently
chromatid breakage.
Dumas L, Page M chrysotile,
crocidolite,
amosite
1986 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.
63
23. Biologic Plausibility: It is plausible that chrysotile is a cause of mesothelioma because the
64
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*) Most
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).
65
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 of tremolite, 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 of the 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)
66
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
of this 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 of the 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:
Of course, the asbestos people in Canada have advanced that idea for some time as
an explanation of why asbestos seems to be more clinically severe in England than in
this country but I have always had the feeling 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 of some 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 of the 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).
67
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 hazard.86
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 clinical picture which is so unescapable [sic] in
communities with a true silicosis hazard...87
33. He reiterated the same myth in 1940:
...Asbestosis, however, is not found among asbestos miners, most of whom work in
open quarries or pits, nor among men engaged in milling operations whereby the
asbestos is prepared for shipment and bagged, but among workers in fabricating
plants.88
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 comes from Canada, so that it
seems unlikely that you in the United States are dealing with a type of asbestos
different from that employed in England.89
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 of all, I think Dr. Lanza is misinformed about the proportions of asbestos used
and where they are used in England. The original cases of Asbestosis, 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 crystalline fiber then, but
very quickly the asbestos trade concentrated on the white Canadian crystalline.90
36. This admonition, however, did not prevent Lanza from publishing misstatements with
regard to the carcinogenic potential of chrysotile asbestos which were diametrically opposed
68
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:
I would also like to point out that the experience with asbestosis in England appears
to differ sharply with that in Canada and the United States. 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 of the lungs is a frequent sequela. This is not
the experience in either Canada or in the United States.91
37. Despite the efforts of Dr. 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 of complex 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
America.92
and
...It is of more than passing interest that the higher rate of cancer in asbestos
workers in England is not paralleled in the United States or in Canada, according to
Lanza (6). The cause for this difference may lie in the type of asbestos; asbestos is a
fibrous form of several different species of minerals, 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 raise problems with people who are more primitive
than we are or less educated.94
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
69
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 of the 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 and I have reviewed the condensation of the survey which was sent us.
We have noted deletion of all references to the association of asbestosis 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 of the 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 of what are believed to be complete and reliable data, it seems fair to
conclude that the asbestos miners in the province of Quebec do not have a
significantly higher death rate from lung cancer than do comparable segments of the
general population.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 obviously far less information but was afraid to say so for this reason.
I am enclosing a review which contains a few sentences that I have marked in this
connection that appears in the Annual Review of Medicine, volume 7, 1956. You will
recall at this time evidence greatly favored the positive correlation of lung 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 cancer.97
70
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 of lung 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 of the
pleura, mesothelioma, likely due to the inhalation of asbestos dust.
45. At a meeting of the 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 background for publicity can be had. The program 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, they find 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 of whether or not we should
publicize some of the activities of our Committee. In this respect there was a very
strong feeling that this should be very restricted. All of us are mindful of the rather
poor reception given to the efforts of the tobacco industry to set up a council and a
scientific committee to deal with the problem of tobacco and its effect on health. A
good bit of this stems from the fact that they erroneously over-publicized the council
and its committee and did it in a too wide-spread fashion. 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 of the first meeting of Occupational and Environmental Health
71
Committee was to review a proposal by Dr. J.C. McDonald of McGill 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 was felt by many, should be collected to counter some of the
recent bad publicity 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 bad press concerning the question of asbestos
and health. Not only has Dr. Selikoff’s latest paper 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 of the opinion that the time has come for
us to produce some rebuttal ourselves, either in a general way or medically
substantiated to the extent possible at this time, and we are anxious to meet with the
Scientific Committee with a view to discussing the possibilities of providing 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 of Dr. 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 of mesothelioma 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 of asbestos fibres are a cause of
Mesothelioma... particularly when mixed with another material. Proof is positive
72
that fibres 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 past year on the
subject of asbestos hazards was the meeting of the International Agency for Research
on Cancer that was held at Lyon, France last October. This meeting was attended by
more than a hundred and thirty medical researchers and representatives of
government, industry and labor from virtually every major asbestos consuming or
producing country in the world.... I think the following five 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 of Chrysotile asbestos in our formulations, association of this material with
mesothelioma and other types of cancer is of serious 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 been paying Dr. Wagner $6,000.00 per month for some time irrespective
of whether Dr. Wagner did any work for O-I, and further that the money was paid
by O-I to a bank account in the U.S. in the name of a third party.
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 of mesothelioma, and that the role of amosite
asbestos was non-existent or at most minimal. At the time my own lay view was
that this position 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 of mesothelioma was crocidolite
asbestos- a fiber 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
73
support from O-I.105
53. Despite the efforts of the 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.
74
Article Year Fiber Type Mentioned
Wedler 1943 No
Wedler 1944 No
Mallory et al. 1947 No
Chief Inspector of
Factories
1949 No
Wyers 1949 No
Doig 1949 No
Smith 1952 Yes Chrysotile [Data from Cartier]
Cartier 1953 No
Weiss 1953 No
Leicher 1954 No
Bonser et al. 1955 No
Doll 1955 No
Bohlig and Jacob 1955 No
Francia and Monarca 1956 No
Braun and Truan 1958 No
Konig 1960 No
Keal 1960 No
Eisenstadt and Wilson 1960 No
Wagner et al. 1960 Yes Crocidolite and chrysotile
Schepers 1960 No
Sleggs 1961 No
Frenkel and Jager 1961 No
Heard and Williams 1961 No
McCaughey et al. 1962 No
Eisenstadt 1962 No
Thompson 1962 No
Wagner 1962 Yes Crocidolite and chrysotile
Smither et al. 1962 No
Enticknap 1962 No
Mancuso and Coulter 1963 Yes Chrysotile
Thomson et al. 1963 No
Thomson 1963 No
Enticknap and Smither 1963 Yes Crocidolite and chrysotile
Article Year Fiber Type Mentioned
Hourihane 1964 No
Owen 1964 No
Gafafer 1964 No
Elwood and Cochrane 1964 No
75
76
54. Two recent publications highlight the fact that the majority of the world medical community
considers chrysotile to be a cause of mesothelioma. 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 of the 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
of pneumonoconiosis, lung cancer and mesothelioma in numerous epidemiological studies of
exposed workers.”107
WTO Report On Chrysotile
56. Much of the 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.
77
i. We note that the carcinogenicity of chrysotile fibers 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 of close to 100 per cent. We therefore consider that
we have sufficient evidence that there is in fact a serious
carcinogenic risk associated with the inhalation of chrysotile fibres.
Moreover, in the light of the comments made by one of the 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 responsible for public health policy would
find that there was not enough evidence of the existence of a public
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 of chrysotile, in particular as
regards lung cancer and mesothelioma in the occupational sectors
downstream of production and processing and for the public in
general in relation to chrysotile-cement products. This prima facie
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
78
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 of 1 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
of asbestos 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, wherever possible. 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 of workers.
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 of pneumoconiosis, lung cancer
and mesothelioma in numerous epidemiological studies of exposed
workers, which confirms the conclusions of the 1996 INSERM
report. Since asbestos began to be used for 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 accounted for all the asbestos consumed in France.118
According to the EC, these figures 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
79
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 associated with an increased risk of both lung
cancer and mesothelioma.119
(a) The EC note that the study coordinated by J. Peto120 and published in
1999 found that in six European countries (France, Germany, Italy,
Netherlands, Switzerland, United Kingdom) nearly 10,000 people died
of mesothelioma between 1990 and 1994. Moreover, it estimated that
during the period 1995-2029 about 200,000 people would die of
mesothelioma. If these figures 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 of deaths 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 of 20,000 men and 2,900 women will
die of mesothelioma.
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 of mesothelioma increased steadily in Canada between
1967 and 1990, principally among servicing and maintenance workers. Of the 120
cases of mesothelioma identified in the study, 49 were miners and mill workers, 50
were workers in the asbestos industry and 21 were servicing and maintenance
workers. Of the 25 percent of these 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
of the method remains to be proved. The EC note that, despite the existence of this
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 report produced for Canadas
Royal Academy in 1996 following the publication of the INSERM report. It shows
that despite strictly controlled use - it focuses exclusively on production workers -,
there was still a 1.28 percent excess of mesothelioma cases, as opposed to 4.61
80
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 scientific findings 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 of the
lung, asbestosis) and is no less toxic than other varieties of asbestos124
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, Canadas 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 Canadas assertions are unfounded or erroneous. For example:
The failure to make a distinction between the risk of mesothelioma and the risk of
cancer of the lung: Canada regularly omits to point out that, whereas the risk of
mesothelioma is lower for chrysotile than for amphiboles, this is not true for cancer
of the 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 of asbestos differ in their hazard is particularly insidious.
It is put forth by the manufacturers of Canadian 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 Canadian product, termed “chrysotile asbestos” is
relatively harmless. However, that claim is not based on fact, and it is not supported
by the results of epidemiological and toxicological studies conducted in the United
States and overseas. These studies show that all types of asbestos, including
Canadian asbestos, are fully capable of producing the full spectrum of asbestosrelated
diseases including asbestosis, mesothelioma, lung cancer, laryngeal cancer,
cancer of the pharynx and cancer of the gastrointestinal tract.*
81
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 “protect[ing] the Canadian interests.” Sébastien
Théberge, 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 non-
Canadian 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 Report for 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 of asbestos exposure = 2585).
Mechanics who frequently or consistently work on brake linings and brake blocks
represent only a sub-fraction of the total workforce of mechanics in Australia. If
one takes the 1996 census figure of 82,827 for male mechanic12, this amounts to
58 mesotheliomas in 1,062,946 person-years (≡ 54.6 mesotheliomas per million
person-years). If one rounds off the workforce to 100,000 male mechanics, the
figure becomes 45 mesotheliomas per million person-years. If one then doubles
the workforce population to take into account retirees and other workers who
moved on to other occupations (although a figure of 200,000 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.
82
mechanics constitute a smaller sub-class), the mesothelioma rate becomes 22.6
per million person-years — well under the rate of 337 mesotheliomas per million
person-years for the Quebec chrysotile miners and millers but still substantially
above the upper limit of the 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 of 2119 mesothelioma cases registered (with a response to history) for the
period 1986-1995, 46 cases were listed for the category brake lining -
manufacture/repair, 40 of which were recorded in car mechanics, of which 37
were exposed to asbestos in this occupation only ... Overall the numbers indicate
a slight increase of around 1-2 cases per year, which is roughly proportional to
the growth rate of all 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 of asbestos found in the dust arising from
braking is rarely more than 1% of the wear product (Asbestos Information
Committee, 1975). It is not known what quantity of chrysotile is imported in
brake linings and other friction materials, but ABS [Australian Bureau of
Statistics] data indicates in excess of 750,000 articles (brake linings, pads and
clutch facings) 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 of chrysotile per annum. Assuming
a further 1000 tonnes of chrysotile present in friction products manufactured in
Australia, it is estimated that (assuming a worst case scenario of 1% release per
annum, i.e. all products are completely worn in one year), around 11.5 tonnes of
chrysotile will be released per annum countrywide or 32 kg per day spread all
around the country. It is acknowledged that this figure may be an overestimate,
as studies have shown that some of the chrysotile is degraded to magnesium
silicates and forsterite ... In addition, some of the debris will be retained in the
brake system and removed and disposed of under 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?
83
Thus, an inhalation experiment was carried out with ball-milled asbestos in which
an attempt was made to eliminate all fibers from the material. It was found to be
impossible to break up all of the fibers and about one percent of the air suspended
dust consisted of fibers. The characteristic peribronchiolar fibrosis developed in the
exposed animals after forty months. Thus, it appears that very small numbers of
fibers are capable of producing asbestosis, although the development of the 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 of the 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.
84
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 itself be 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.
85
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 of the 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. If you 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 of the 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
86
comparable to exposures in well-controlled trials where individuals have had excesses in
mesothelioma rates. The question of individual exposure and contribution of brake 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-bycase
basis.
2) Rate ratio of two requirements:
Some have argued that a rate ratio of two 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 of Bradford 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 of the 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
87
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 of these 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
88
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 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 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 of the 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
sales. 145
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 of the 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.
89
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 proof test 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
90
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 of the
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 of brake 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 of the 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.”
91
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 What They are Doing Level/Finding
J.L. Lee 1970150 Blow out of brake drums Peek concentration 3-5
fibers/cm3
Knight and Hickish 1970151 Blow off personal sample 5.35 fibers/cm3 and peek
sample 87 fibers/cm3
Hatch 1970152 Brake cleaning by
compressed air jet
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
Longo studies14 Bendix brakes 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.
92
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 of 20-25ft.”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 adjacent 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
93
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 of vehicle 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
94
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
95
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 ½ 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 of x-ray abnormalities is in accord with estimates of asbestos
96
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).
Estimated that 20,000 deaths from asbestos-related
cancer will occur during the next 40 years among
automotive maintenance workers in the United States
Hueper, Carcinogens in the Human
Environment, ARCHIVES OF
PATHOLOGY, 71(3):237-267 (1961).
Risk of cancer fro brake exposures
Menck et al., Occupational
Differences in Rates of Lung
Cancer, JOURNAL OF OCCUPATIONAL
MEDICINE, 18(12) 797-801 (1976).
Standard Mortality Ratio (SMR) for lung cancer of
146 for automobile repair
McDonald et al., Dust Exposure and
Mortality in an American Chrysotile
Asbestos Friction Products Plant,
BRIT J INDUS MED, 41:151-157
(1984).
49 observed, 35.7 expected for an SMR of 137.
Jarvholm, Asbestos associated
tumours in car mechanics, BRIT. J.
INDUST. MED., 45:645-646 (1988).
Lung cancer: 39 observed, 23 expected, SMR 170.
Levin et al., Asbestosis and small
cell lung cancer in a clutch
Asbestosis and small cell lung cancer caused by
asbestos in a clutch refabricator
97
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 of Pleura 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 and Mesothelioma,
JAMA, 204(11):151 (1968
43 year-old who wove brake
linings for three years and later
died of mesothelioma
McDonald et al., Epidemiology of Primary
Malignant Mesothelial Tumors in Canada,
CANCER, 914-918 (1970)
Mesothelioma in two workers
who installed brake linings
Oels et al., Diffusae malignant
mesothelioma of the pleura: A review of 37
cases, CHEST, 60(6):564, December 1971
Mesothelioma in a service
station operator
Rubino et al., Epidemiology of pleural
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 and Malignant 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
98
McDonald et al., Malignant Mesothelioma
in North America, CANCER 46:1650-1656
(1980)
Mesothelioma in eleven garage
mechanics
Langer et al., Mesothelioma in a Brake
Repair Worker, THE LANCET, November 13,
1982
Mesothelioma in a man whose
sole exposure to asbestos was to
chrysotile during brake repair
and maintenance
Kagan et al., Lymphoid and Plasma Cell
Malignancies: Asbestos-Related Disorders of
Long Latencey, AMER. J. CLIN. PATH.
80(1):14-15 (1983)
Mesothelioma in brake lining
machinist
Guillon et al., A Case of Association 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)
Mesothelioma in man who
worked in automobile workshop
for many years
Castleman, Asbestos: Medical and Legal
Aspects, Harcourt Brace Jaovanovich (1984)
Ziem reported 4 cases of
mesothelioma in mechanics and
one in a mechanic’s wife
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)
Four cases of mesothelioma in
men exposed to asbestos dust
from friction products
Environmental Protection Agency,
Guidance for Preventing Asbestos Disease
Among Auto Mechanics, p. 2 (1986)
Mesothelioma in a ten-year old
son of a brake mechanic
Huncharek, Chrysotile Asbestos Exposure
and Mesothelioma, BRIT. J. INDUS. MED.
Three cases of mesothelioma
among friction product workers
99
44:287-288 (1987) 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.
Huncharek et al., Pleural Mesothelioma in
a Brake Mechanic, BRIT. J. INDUS. MED,
46:69-71 (1989)
Mesothelioma in man whose
only asbestos exposure was from
clutch and brake products
Newhouse et al., A mortality study of
workers manufacturing friction materials:
1941-86, BRIT. J. INDUST. MED., 46:176-179
(1989)
Two cases of mesothelioma in a
friction materials manufacturing
facility
Huncharek et al., Pleural Mesothelioma in a
Lift Mechanic, BRIT. J. INDUS. MED, 46:500-
501 (1989)
Mesothelioma in patient whose
primary exposure was to
chrysotile asbestos from lift pad
brakes
Jarvholm et al., Asbestos Associated Tumors
in Car Mechanics, BR. J. INDUS. MED.,
45:645-646 (1988)
Mesothelioma in a Swedish car
mechanic
Hansen et al. Mortality of Auto Mechanics,
Scand. J. WORK AND ENVIORN. HEALTH
15:43-46 (1989)
Mesothelioma in Danish garage
mechanic
Animal evidence
Study Findings
Hardy Egilman Chrysotile asbestos exposure causes lung cancer in mice
without first inducing asbestosis
.
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 of the 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: Misrepresentation Actual findings:
Jarvholm et al., Asbestos
Associated Tumors in Car
Mechanics, BR. J. INDUS.
MED., 45:645-646 (1988) and
Hansen et al. Mortality of
“no increased risk of
mesothelioma in car
mechanics”
The other half of the sentence
which is omitted states, “but
possibly and increased risk of
lung cancer”
101
102
Auto Mechanics, Scand. J.
WORK AND ENVIRON. HEALTH
15:43-46 (1989)
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.
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. “
The coding system did not
code for mesothelioma!! A
nosologist used the ICD 7 to
code causes of death.
”
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
Lining Repair and Maintenance
Workers Occupationally
Exposed to Asbestos,
Environmental Sciences
Laboratory, Mount Sinai
School of Medicine of the City
University of New York
(1983).
“…garage mechanics who did
brake repairs were at no greater
risk for x-ray abnormalities
than garage mechanics who did
not repair brakes.”
“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.”
Marcus et al., Asbestos- “..no respiratory impairment or Fail to mention that the authors
103
associated lung effects in car
mechanics, SCAND J WORK
ENVIRON HEALTH, 13(3):252-4
(1987)
asbestosis was found” 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., Lung function and exposure
to asbestos among vehicle
mechanics, AM J IND MED,
22(1):59-68 (1992).
McDonald et al., Malignant
Mesothelioma in North
America, CANCER 46:1650-
1656 (1980),
Cited as negative study 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.
Teta et al., Mesothelioma in
Connecticut,1959-1977, J
OCCUP MED, 25: 749-755
(1983)
Cited as negative study 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.
Teschke et al., Mesothelioma
Surveillance to Locate
Sources of Exposure to
Asbestos, CANADIAN J. PUB.
HEALTH 88:163-167
Cited as negative study 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

105
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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. Vol 1-4 Beginning March 7.*
23 See e.g. the use of Bayesian analysis in medical decision-making and for probabilistic medical
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58Greenberg and Davies, “Mesothelioma Register 1967-68,” Brit. J. Indus. Med., 31:91-104 (1974)
59Hansen, Mortality of auto mechanics, a ten year follow-up, Scand. J. Work Environ. Health,
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60Mancuso, “Relative Risk of Mesothelioma Among Railroad Machinists Exposed to Chrysotile,”
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61Maltoni, Pinto and Mobiglia, “Mesotheliomas due to Asbestos Used in Railroads in Italy,” The
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62 Discussion: Part II, Annals of the New York Academy of Sciences, 643:415 (1991).
63Scansetti, Mollo, Tiberi, Andrion, and Piolatto, Pleural Mesothelioma After a Short Interval From
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64Vianna and Polan, Non-Occupational Exposure to Asbestos and Malignant Mesothelioma in
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65Lieben and Pistawka, Mesothelioma and Asbestos Exposure, Arch. Environ. Health 14:559-566
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66Wolf, Piotrowski, Engel, Bekeris, Palacios and Fisher, Malignant Mesothelioma With
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67 Bellmann, B., Muhle, H., Pott, F., Konig, H., Kloppel, H., Spurny, K. “Persistance of man-made
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68 Suzuki and Kohyama, “Translocation of Inhaled Asbestos Fibers from the Lung to Other
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108
69Levresse, Renier, Fleury-Feith, Levy, Moritz, Vivo, Pilatte, Jaurand, “Analysis of Cell Cycle
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70 Doll, Peto Report to British Health and Safety Commission. (chapt. 6) 1985.
71Suzuki Y; Yuen SR, Asbestos tissue burden study on human malignant mesothelioma, Ind.
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72Suzuki Y; Yuen SR, Asbestos tissue burden study on human malignant mesothelioma, Ind. Health
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73 Mochaux, Bignon, Jaurand, Lafuma, Sebastien, Masse, Hirsh, Goni, “Mesotheliomas in rats
following inoculation with acid-leached chrysotile asbestos and mineral fibres,” Carcinogenesis,
2:229-236 (1981); Bolton, Davis, Donaldson, Wright, “Variations in the carcinogenicity of mineral
fibres,” Ann. Occup. Hyg., 26:569-582 (1982); Minardi, Maltoni, “Results of recent experimental
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74 Frank AL, Dodson RF, Williams MG., Carcinogenic implications of the lack of tremolite in
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75 Letter of E.W. Drislane, Executive Director of the FMSI to Asbestos Study Committee members
dated March 10, 1975.
76 McDonald, Armstrong, Case, Doell, McCaughey, McDonald Sebastien, “Mesothelioma and
asbestos fiber types: Evidence from lung tissue analyses,” Cancer 63:1544-1547 (1989)
77 Case, BW Health Effects of Tremolite, Now and in the Future, NYAS 643:491-504 (1991)
78 Case, BW “Biological Indicators of Chrysotile Exposure” Ann Occ Hyg 38:503 (1994).
79 See Deposition of Dr. Graham Gibbs taken on December 16, 2000 in King v. Allied Signal,
24242-C03, pp. 14-22.
80 Mancuso, “Relative Risk of Mesothelioma Among Railroad Machinists Exposed to Chrysotile,”
Am. J. Ind. Med., 13:639-657 (1988) at page 649.
81 Churg, “Chrysotile, tremolite, and malignant mesothelioma in man,” Chest, 93:621-628 (1988).
82 Pooley, F. D., Mitha, R. “Fiber types, concentrations and characteristics found in lung tissues of
chrysotile-exposed cases and controls.” Mineralogy and Dust Physics (1976)
83 Roggli, Pratt, Brody, “Asbestos Fiber Type in Malignant Mesothelioma: An Analytical Scanning
Electron Microscopic Study of 94 Cases,” Am J Ind Med, 23:605-614 (1993) (shipyard workers,
chemical maintenance workers, construction workers, carpenters, painters, spacklers, and power
plant workers were studied)
84 Doll, Peto, “Asbestos, Effects on health of exposure to asbestos,” Report to the British Health and
Safety Commission pp. 15-17 (1985).
85Acheson & Gardner, “Mesothelioma and exposure to mixtures of chrysotile and amphibole
asbestos.,” Arch. Environ. Health, 34:240-242 (1979).
86Lanza, AJ, Proceedings of The Home Office Life Underwriters Association, p. 396 (Nov. 1933).
87Lanza, A. J. et. al. Effects of the Inhalation of Asbestos Dust on the Lungs of Asbestos
Workers, Public Health Reports, Vol. 50, Number 1, January 1935
109
88Lanza and Vane, Underwriting Aspects -Dust Hazard, Proceedings of the thirtieth annual
meeting of the medical section of the American Life Convention (1940)
89Sparks, Pulmonary Asbestosis, Radiology, Vol. 17, p. 1249 (1931)
90Merewether, in transcript of the Seventh Saranac Symposium, p. 419 Vorwald Archives, Armed
Forces Institute of Pathology (July, 1952)
91Lanza, AJ, “Asbestosis,” McIntyre-Saranac (1952)
92Stokinger, H.E. Standards for safeguarding the health of the industrial worker, Public Health
Reports (January 1955) 70(1):1-11.
93Stokinger, H.E. Toxicologic aspects of occupational hazards, Annual Rev. Med., (1956) 7:
178.
94 Letter from Peter Reiser to M. Prus regarding “Asbestos Warning Labels” April 14, 1977.
95 Braun, Truan “Lung cancer in asbestos miners” A.M.A. Archives of Industrial Health Vol. 17
(1958).
96Letter from Stokinger to Braun 1/20/58 re: Braun/Truan paper 1958 An Epidemiological
Study of Lung Cancer
97Johnston, RT. and Miller, Seward. (1960) Occupational Diseases and Industrial Medicine (W. B.
Saunders Company: Philadelphia).
98Minutes, General Meeting, Asbestos Textile Institute, June 4, 1965.
99Minutes of the First Meeting of the Scientific Committee of the Institute of Occupational
Environmental Health in Montreal, July 25 and 26, 1966.
100Minutes, Special Summer Meeting of the Quebec Asbestos Mining Association, August 3-6,
1966.
101Minutes, Special Summer Meeting of the Quebec Asbestos Mining Association, August 8-11,
1967
102Minutes, Special Meeting of the Quebec Asbestos Mining Association, August 10, 1967.
103Minutes, Meeting of the Quebec Asbestos Mining Association, “Asbestos Fibres vs.
Environmental Health.”
104Address of I. W. Weaver, “Asbestos and the Friction Material Industry,” given at the Annual
Membership of the Asbestos Textile Institute on Wednesday morning, June 27, 1973.
105 Affidavit of Paul J. Hanly, Jr. in support of Defendant’s Motion for Relief From Default
Judgment in Owens-Illinois, Inc. v. T&N, LTD. 2-99-CV01117-DF para. 23-24. January 24, 2000.
106Consensus Report, “Asbestos, asbestosis, and cancer: the Helsinki criteria for diagnosis and
attribution,” Scand. J. Work Environ. Health,23:311-6 (1997).
107Environmental Health Criteria 203: Chrysotile Asbestos, International Programme on Chemical
Safety (IPCS).
108 Since 1977 by the IARC (see List of Agents Carcinogenic to Humans, Overall Evaluations of
Carcinogenicity to Humans, Monographs of the International Agency for Research on Cancer,
Volumes 1-63), see also WHO, IPCS Environmental Health Criteria (203) on Chrysotile, Geneva
(1998), cited in para. 5.584 above. On the development of knowledge of the risks associated with
asbestos, see Dr. Henderson, para. 5.595.
110
109Panel Report, para. 8.194.
110Panel Report, para. 8.188. See Panel Report, para. 5.29, for a description of mesothelioma given
by Dr. Henderson.
111 INSERM, Effets sur la santé des principaux types d’exposition à l’amiante, INSERM joint
report, Paris, INSERM publications, 1997. as cited in translation by the WTO in WT/DS135/R.
112 Camus M. et al., Non-occupational Exposure to Chrysotile Asbestos and the Risk of Lung
Cancer, New England Journal of Medicine, 1998, vol.338, no. 22: pp.1566-71.
113 Para 3.236, WTO report WT/DS135/R.
114 World Trade Organization WT/DS135/R, 18, September 2000, (00-3353), European
Communities – Measures Affecting Asbestos and Asbestos – Containing Products, Report of the
Panel.
115 According to the EC, it is estimated that asbestos causes twice as many cancers of the lung as
cancers of the pleura (mesotheliomas), see Stayner et al. Exposure to Chrysotile Asbestos and
Cancer Risk: a Review of the Amphibole Hypothesis, American Journal of Occupational Health,
1996, 86:179-186.
116 International Labour Organization, Geneva, Convention concerning Safety in the Use of
Asbestos (Convention 162, adopted on 24 June 1986), International Labour Conference, Geneva.
See, in particular, Article 10.
117 IPCS Environmental Health Criteria (203) on Chrysotile, WHO, Geneva, 1998.
118 See para. 3.22 above.
119 Stayner, L.T. et al., Occupational Exposure to Chrysotile Asbestos and Cancer Risk: a Review of
the Amphibole Hypothesis, American Journal of Public Health. 1996, 86:179-186. Smith et al.,
Chrysotile Asbestos, the Main Cause of Pleural Mesothelioma, American Journal of Industrial
Medicine, 1996, 30:252-266.
120 Peto et al., The European Mesothelioma Epidemic, British Journal of Cancer (1999), 79 (3/4),
666-672.
121 Gilg Soit Ilg, A., Bignon, J., Valleron, A-J., Estimation of the Past and Future Burden of
Mortality from Mesothelioma in France. Occupational Environmental Medicine, 1998; 55:760-765.
122 Bégin, R. et al., Work-Related Mesothelioma in Quebec, 1967-1990, American Journal of
Industrial Medicine, vol.22, 1992, pp.531-542.
123 Hutchings, S. et al., Asbestos-Related Diseases, Occupational Health Decennial Supplement,
London, Health and Safety Executive, 1996, pp.127-152.
124 WTO report, para 3.110
125 WTO report, para 3.114
126 20th US Congress, Title 20 – Education, Chapter 49 – Asbestos School Hazard Detection and
Control. Sec. 3601
127 Schiller, B. “Chilean ban to boost asbestos woes” Toronto Star July 8, 2001.
128
B.E. Henderson, “Occupational Differences in Rates of Lung Cancer,” J. Occup. Med. 78:797-
801
129 In-Depth Survey Report: Evaluation of Brake Drum Service Controls at United States Postal
Service Vehicle Maintenance Facility, Nashville, Tennessee, Report No. ECTB 152-20b, Godbey, et
al., NIOSH, August 1987
111
130 Pathology of Asbestos-Associated Diseases, Roggli et al., Little, Brown and Company, 1992, at
page 23.
131 . Industrial Hygiene Report, Assessment of Asbestos Exposure to Mechanics Performing Brake
Service Operations, Report No. 32.4, Roberts, et al., April 27, 1981
132 Merewether and Price, Report on the Effects of Asbestos Dust on the Lungs and Dust
Suppression in the Asbestos Industry, His Majesty’s Stationery Office, 1930 pages28-29.
133 Case L.B. Air Hygiene Studies, Inland Manufacturing Division, Dayton, Ohio, October 31 and
November 1, 1939.
134
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.*
135 Brachmann, Arbeitschutz, Abstract of Asbestosis in Grinders and Drillers of Brake Bands, Digest
of Industrial Hygiene (1940) pages172-4.
136 Castrop, V.J., Recognition and Control of Fume and Dust Exposure, National Safety News,
February, 1948
137 Lynch, J., Brake Lining Decomposition Products, Journal of the Air Pollution Control
Association, Vol. 18, No. 12, December, 1968 page 824
138 .Hickish and Knight, Exposure to Asbestos During Brake Maintenance, Ann. Occup. Hyg. Vol.
13, pp.17-21, Pergamon Press, 1970.
139
Rohl, A.N. Langer, A.M., Wolff, M.S., Weisman, I., “Asbestos Exposure During Brake Lining
Maintenance and Repair”, Environmental Research 12, pp. 110-128 (1976).
140 Lorimer, W.V., Rohl, A.N., Miller, A., Nicholson, W.J., Selikoff, I.J., “Asbestos Exposure or
Brake Repair Workers in the United States,” The Mount Sinai Journal of Medicine, Vol. 43, No. 3,
May-June 1976, pp. 207-217.
141 Deposition of James Noll p. 21
142 Plaintiff’s Exhibit 2 at deposition of Gerald Sattelmeier, March 9, 1989
143 Deposition of James Knoll p. 30-31.
144 Deposition of Jack Koblin p. 90-91
145 Jack Koblin p. 90-92
146 Deposition of James Noll p. 51-52
147Drislane , E.W., Executive Director, FMSI, Memorandum Re: Interpretative of OSHA Labeling
Requirements, November 6, 1972.
148 FMSI Minutes of Annual Meeting, June 27 and 28, 1973.
149 Hickish, D.E., Knight, K.L., “Exposure to asbestos during brake maintenance” Ann. Occup.
Hyg., Vol. 13, pp. 17-19 (1970).
150 Lee, G.L. “Removing Dust From Brake Assemblies During Vehicle Servicing-Alternative
Cleaning Methods”, Ann. Occup. Hyg. Vol. 13, pp. 33-36. (1970).
151 Knight, K.L., Hickish, D.E., “Investigations Into Alternative Forms of Control For Dust
Generated During the Cleaning of Brake Assemblies and Drums,” Ann. Occup. Hyg. Vol. 13,
pp. 37-39 (1970).
112
152 Hatch, D. “Possible Alternatives to Asbestos as a Friction Material,” Ann. Occup. Hyg. Vol.
13, pp. 25-29 (1970).
153 Rohl, A.N., Langer, A.M., Wolff, M.S., Weisman, I. “asbestos exposure during brake lining
maintenance and repair”, Environmental Research, Vol. 12, pp. 110-128 (1976).
154 Lorimer, W.V., Rohl, A.N., Miller, A., Nicholson, W.J., Selikoff, I.J., “Asbestos Exposure or
Brake Repair Workers in the United States,” The Mount Sinai Journal of Medicine, Vol. 43, No.
3, May-June 1976, pp. 207-217.
155 Rohl, A.N., Langer, A.M., Klimentids, R., Wolff, M.S., Selikoff, I.J., “Asbestos Content of
Dust Encountered in Brake Maintenance and Repair,” Proc. Roy. Soc. Med. Vol. 70, pp. 32-36
(1977).
156 Kauppinen, T. and Korhonen, K., “Exposure to Asbestos During Brake Maintenance, Brake
Maintenance of Automotive Vehicles by Different Methods,” Am. Ind. Hyg. Assoc. J., Vol. 48,
No. 5, pp. 499-504.
157 Hickish, D.E., Report 52/68, Exposure to Asbestos Dust During Brake Maintenance Operations
on Commercial Vehicles, Fleet Repair Garage, Dagenham, October 1968.
158 Toth, P.E. Memorandum Re: Vehicle Brake Rebuilding, August 3, 1973.
159 Williams, J.B. Memorandum Re: Vehicle Brake Rebuilding, August 23, 1973.
160 Knauss, J.R. Memorandum Re: Controlling Asbestos Exposure, November 16, 1973; See
also, Product Engineering Evaluation, Rotunda Ford, July 1975 (describes the product as “ a
brake service vacuum cleaner designed for recovery of dry dust containing asbestos fibers”);
General Field Bulletin No. 1469, Ford Parts and Service Division, Re: Rotunda Shop Safety
Equipment Promotion, July 8, 1976 (“Rotunda has just added a special vacuum cleaner to its
equipment line, which is designed to remove hazardous asbestos dust fibers which result from
certain brake and clutch operations.”); Rotunda Ford 1977 Dealer Catalog.
161 Deposition Gerald Sattelmeier p. 106
162 Trenton dust studies November 1972
163 Guidance for Preventing Asbestos Disease Among Auto Mechanics, Asbestos Action Program,
EPA, June 1986.
164 Environmental Health Criteria 203, Chrysotile Asbestos, World Health Organization, Geneva,
1998, page 41.
165 Fulton et al., Special Bulletin, Commonwealth of Pennsylvania, Department of Labor and
Industry, No. 42, Sept. 20, 1935
166 Hamlin, Industrial Dust – The Pneumoconiosis, Industrial Medicine, March 1944.
167 George et al., An X-ray Study of the Lungs of Workmen in Asbestos Industry Covering a Period
of Ten Years, Radiology, 33:196-202 (1939).
168 Stone, Studies in Asbestosis, Disease of the Chest, 6:170-171 (1940).
169 Brackman, Asbestosis in Grinders and Drillers of Brake Bands, Arbeitzschutz (1940) asbstract
printed Journal of Industrial Hygiene and Toxicology, 23(4):76-77(1941) distributed by the IHF.
170 Thomas, Pneumonokoniosis in Victorian Industry, Medical Journal of Australia, January 19,
1957, pp. 75-77
171 NOISH Investigation, Friction Division Products, Trenton, New Jersey, September 1986.
172 McVittie, Asbestosis in Great Britian, Ann NY Acad Sci 132:128-138 (1965).