AMERICAN JOURNAL OF INDUSTRIAL MEDICINE 44:540–557 (2003)
Exposing the ‘‘Myth’’ of ABC, ‘‘Anything But
Chrysotile’’: A Critique of the Canadian
Asbestos Mining Industry and McGill
University Chrysotile Studies
David Egilman,
MD, MPH,1,2 Corey Fehnel, AB,2 and Susanna Rankin Bohme, AM
2
Background
advanced the idea that chrysotile asbestos is safer than asbestos of other fiber types.
Beginning in the 1930s, the Canadian asbestos industry created and
Methods
Asbestos Mining Association (QAMA) and performed by researchers at McGill University.
We critically evaluate published and unpublished studies funded by the Quebec
Results
chrysotile was harmless, and contended that the contamination of chrysotile with
oils, tremolite, or crocidolite was the source of occupational health risk. In addition,
QAMA-funded researchers manipulated data and used unsound sampling and analysis
techniques to back up their contention that chrysotile was ‘‘essentially innocuous.’’
QAMA-funded researchers put forth several myths purporting that Quebecmined
Conclusions
have had a substantial effect on policy and occupational health litigation. Asbestos
manufacturing companies and the Canadian government continue to use them to promote
the use of asbestos in Europe and in developing countries.
2003.
These studies were used to promote the marketing and sales of asbestos, andAm. J. Ind. Med. 44:540–557, 2003 Wiley-Liss, Inc.
KEY WORDS: asbestos; chrysotile; corruption; crocidolite; QAMA; McGill;
tremolite
INTRODUCTION
Chrysotile asbestos was first mined in Canada in the late
1870s. A fierce struggle between the asbestos industry in
Canada, England and South Africa and medical researchers
began in the early 1930s and has been documented in the
professional literature and in the courts and continues to
the present [Hardy and Egilman, 1991; Liddell, 1997;
Nicholson, 1997; Egilman et al., 1998; Egilman and Reinert,
2000].
QAMA’s first efforts to mislead the medical community
about the carcinogenic effects of asbestos exposure were
published in 1958 [Braun and Truan, 1958]. The individually
numbered drafts of the study results circulated to QAMA
members reported, ‘‘[t]he number of lung cancer deaths
combined with asbestosis is larger than would be expected in
each cohort and in the combined cohorts. This difference is
significant at the 95% level using the chi-square test of
significance.’’ At the request of QAMA, the researchers
manipulated the denominator and published, ‘‘On the basis of
what are believed to be complete and reliable data,
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
it seems’’ (emphasis added) [Braun and Truan, 1958].
2003Wiley-Liss,Inc.
1
Rhode Island
Clinical Associate Professor, Brown University, Department of Community Health, Providence,
2
*Correspondence to: David Egilman, NeverAgain Consulting, 8 North Main St., Suite 404,
Attleboro,MA 02703.
Accepted 24 July 2003
DOI10.1002/ajim.10300. Published online inWiley InterScience
(www.interscience.wiley.com)
NeverAgain Consulting, Attleboro,Massachusetts
In 1964, Irving J. Selikoff, who was concerned with the
inadequate response to the public health dangers of asbestos,
organized a New York Academy of Sciences (NYAS)
conference devoted to understanding the physiological
effects of the mineral [Selikoff, 1965]. This conference
firmly established the carcinogenicity and other health
hazards of exposure to asbestos. The information generated
at the conference was widely disseminated in the press,
threatening the industry’s position domestically and in the
global market.
In response, Canadian mining companies, acting
through the Quebec Asbestos Mining Association (QAMA),
renewed their connection with McGill University [Wright,
1926; Asbestos Textile Institute, 1965; Institute of Occupational
and Environmental Health, 1966] to develop contrary
scientific evidence, hoping to sow doubt about the toxicity of
various asbestos fiber types. As a result of the NYAS
conference, the carcinogenicity of asbestos was irrefutable.
QAMA knew that existing research revealed the dangers of
asbestos, and sought to develop ‘‘counter propaganda’’ to the
work of Selikoff and others [QAMA, 1967]. Its members
looked to the tobacco industry as a model for their own
research, noting that that industry ‘‘launched its own program
and it now knows where it stands’’ [QAMA, 1965].
Accordingly, QAMA developed
Anything But Chrysotile
(ABC) arguments in the hope that it could maintain or expand
market share for its form of asbestos and avoid liability. The
ABC argument implicates various substances
Canadian chrysotile as the cause for asbestos’s toxicity.
QAMAhas provided funding to a research unit at McGill
University for the past three decades which has promulgated
several different ABC theories. Most recently these have
been used in an attempt to mislead a variety of international
panels on the true risks of exposure to chrysotile asbestos
[Castleman, 2001, 2002]. The McGill researchers frequently
appear or and sometimes have been hired as ostensibly
objective analysts [U.S. Environmental Protection Agency,
2001; Eastern Research Group, Inc, 2003].
Beyond promoting the marketing and sale of asbestos,
these studies have had a tremendous effect on litigation from
the 1960s onwards. Lawyers for asbestos-manufacturing
corporations have used these studies to assert that the causal
link between asbestos exposure and cancer was unclear and
hypothetical, thus effectively denying injured workers and
their dependents compensation for their illness [Georgia-
Pacific, 2003].
We analyze and discuss three fallacies that underlie the
ABC arguments. The first is that organic and synthetic oil
contamination—and not the chrysotile itself—is the cause of
lung cancer and primary malignant mesothelial tumors in
miners and other people who work with asbestos [Commins
and Gibbs, 1969; Gibbs and Hui, 1971]. The second is that
crocidolite, allegedly imported from Australia and used at
a factory adjacent to one of the mines, caused an increase
in mesothelioma in the mine workers [McDonald and
McDonald, 1978, 1980]. A third fallacy put forth by the
industry is that tremolite was the only culprit, and that current
commercial chrysotile is ‘‘innocuous’’ because contemporary
mining practices either avoid it entirely or remove it
during processing [Case, 2001a]. After examining QAMA’s
‘‘ABC’’construct, we review the methodology that QAMA
funded epidemiologists and scientists used to support various
industry claims. These include ignoring pertinent doseresponse
data and mis-estimating dose through use of
inadequate and out-dated sampling techniques; and ignoring
or misinterpreting worker interview data [McDonald
et al., 1970; Gibbs and LaChance, 1972, 1974; Liddell
et al., 1984].
other than
INDUSTRY MYTHS
Organic and Synthetic
Oil Contamination
In 1965, Harrington and Roe reported that naturally
occurring as well as contaminating organic compounds may
play a key role in the carcinogenic nature of asbestos
[Harrington, 1965; Harrington and Roe, 1965]. From the
industry’s perspective, this was an ideal way to obfuscate the
notion that its product, chrysotile, was deadly. If this
‘‘mystery’’ contaminant could be identified and the chrysotile
‘‘cleaned,’’ the product and profits could be saved.
QAMA supported further studies, both by providing funding
and in helping with the collection of samples and other data
[Gibbs, 1969; Brodeur, 1974].
Further investigating Harrington and Roe’s claims,
Graham Gibbs and others at McGill University examined
the theory of organic contaminants of chrysotile [Commins
and Gibbs, 1969]. Gibbs raised the question of whether the
compounds may: act as carcinogens in and of themselves;
enhance the carcinogenic activity of other substances, such as
trace metals, asbestos itself, or associated oils; inhibit the
action of carcinogens present in the fiber; or have no
influence on the biological action whatsoever [Gibbs, 1969].
Through their studies, the researchers found that the organic
contaminants were implicated in the ‘‘biological action’’ of
chrysotile asbestos products, suggesting that these contaminants,
and not the chrysotile itself, were the cause of cancer in
workers [Gibbs and Hui, 1971].
They determined that the long-chained alkanes found in
asbestos products resulted from three possible sources:
hydrocarbons occurring naturally in the ore body; contamination
from the mining and milling process; and contamination
from shipping, manufacturing, and utilization processes
[Gibbs and Hui, 1971].
Polyethylene bags and asbestos dryers were allegedly
the primary culprits in this oil contamination [Gibbs, 1969].
However, Gibbs recognized the lack of mesotheliomas
Exposing the ‘Myth’ of ABC 541
occurring in animals exposed to organic compounds, and
stressed the need for further investigation into the alleged link
between these compounds and lung cancer. Emphasis was
placed on the importance of assessing the differences in
organic content in the types of asbestos to which workers
were exposed, but in the end there was no evidence that
organic contaminants accounted for increased cancer rates.
Wagner and Berry [1969] published a report demonstrating
that removal of organic contaminants from asbestos did not
decrease, and in fact possibly
fiber to cause mesotheliomas in rats. Therefore, the argument
that oil contaminants were the chief cause of the carcinogenic
effects of chrysotile exposure was no longer plausible, and
had to be rejected in favor of other explanations as to why
chrysotile was supposedly safe.
increased, the ability of the
Crocidolite
Studies published in the late 1970s by J.C. McDonald
and colleagues offered yet another explanation for the noncarcinogenicity
of chrysotile [McDonald and McDonald,
1977, 1978;McDonald, 1978]. They claimed that most of the
mesothelioma cases from the mines in Asbestos, Quebec
occurred as a result of exposure to
also known as
imported from Australia for use in gas mask manufacturing at
the factory located ‘‘adjacent to’’ the Johns Manville Jeffrey
mine during World War II. The McGill researchers
postulated that this use of crocidolite in filter pad manufacturing
from 1939–1941 accounted for increased mesothelioma
and lung cancer rates among miners and millers at the
Jeffrey mine, even though none of them had ever worked in
the factory [McDonald and McDonald, 1980]. It is interesting
to note that there are no citations of interviews with
workers or correspondence that could prove imported
crocidolite
location. The head of shipping and receiving during the
relevant time period was also unaware of any crocidolite used
in the factory (A.R. Carr, unpublished communication).
British regulations mandated the use of either chrysotile or
crocidolite for World War II gas mask filters. It is unlikely
that QAMA members involved in the production of gas
masks would import crocidolite from Australia, past
Japanese submarines and battleships, past other filter
factories in Ontario that used crocidolite, to fill gas mask
filters at a factory adjacent to the largest chrysotile mine in the
world. Furthermore, Begin et al. [1992] reported that
mesothelioma rates were not as elevated as one would expect
if crocidolite was used in gas-mask manufacturing at the
Jeffrey mine in the town of Asbestos [Begin et al., 1992]. He
revealed his own doubts about the presence of amphiboles at
the factory, stating that amphiboles ‘‘
there and noted that there were no cases of mesothelioma in
other departments that were nearby, such as quality control.
Begin et al. [1992] and Dufresne et al. [1995] reviewed the
detailed job histories of all twenty workers who contracted
mesothelioma and confirmed that
during World War II in the preparation of materials for the
fabrication of gas masks as previously noted by McDonald,
nor had any of them been exposed to crocidolite in the factory
or mill during the 2-year period.
In October 2000, at a presentation to a group of asbestos
defense lawyers, Bruce Case reported that the factory was
located ‘‘immediately adjacent’’ to the mine and mill. He
stated, ‘‘not only had some of the men worked there, but most
has [
areas’’ [Case, 2000]. However, at a deposition a year later,Dr.
Case stated that he did not know where the Jeffrey factory
was located [Case 2001a]. From 1928 to 1972, the factory at
Jeffrey was located across an open pit mine, about a mile
from the entrance to the mine and the mill [Tourist Bureau,
2002]. It is hardly believable that miners would ever walk
through the old factory as a part of their daily routine; it
would include a mile descent, and a 2–3 mile walk.
According to F. Spertini, the mine geologist, there were no
common areas and two separate roads led from the town to
the factory and mine entrances. (F. Spertini, unpublished
communication).
Regardless of its source, the QAMA–McGill scientists
found crocidolite in the lungs of 71% of miners from
Asbestos [Case, 1998]. Initially this finding was only
reported for miners at the Jeffrey mine but later the
researchers found lower concentrations of crocidolite in
13% of miners from Thetford [Nayebzadeh et al., 2001].
Nayebzadeh and colleagues reasserted that the crocidolite in
the lungs of Asbestos miners came from exposure to
imported crocidolite used in the gas mask manufacturing.
However, they overlooked the fact that if crocidolite was
used, it was only during the time from 1939 to 1941, and
about half of the workers in their study began working
after 1941. They offered no explanation for the crocidolite in
the Thetford miners’ lungs. The most likely source of this
crocidolite was the local mine ore, not imported fibers. Two
geological surveys found that mines from both areas
contained blue fibrous riebeckite, otherwise known as
crocidolite [De, 1961; Hebert, 1980].
Howdid the McGill researchers miss this information on
crocidolite contamination of ore? By 1961, QAMA had been
given De’s doctoral thesis showing crocidolite in Quebec
mines. The McGill research team cited that thesis in 1972
[Gibbs and LaChance, 1972]. However, while noting that De
found actinolite in the Canadian mines, they omitted any
mention of his
contamination of the mine ore body. Over two decades
later in 1995, Dufresne and others extracted and published
considerable information from the De’s thesis (See
Appendix, Note 1). However, they failed to mention that
De had written extensively on the location as well as
crocidolite (an amphibolefibrous riebeckite), which was allegedlywas ever used for this purpose at the minemay’’ have been usednone of them had workedsic] to pass through the building as it contains commontwelve-page discussion of the crocidolite
542 Egilman et al.
performed a mineralogic and chemical analysis of the
crocidolite he found in the Eastern Townships asbestos
deposits. It is difficult to believe this omission occurred in
error, especially since De’s study was cited in 1972, 1986,
and 2001 in papers that dealt with the issue of crocidolite in
the miners’ lungs [Gibbs, 1972; Dufresne et al., 1995;
Nayebzadeh et al., 2001]. Moreover, in 2001, some of the
same authors who had cited De’s thesis 6 years earlier
actually make a
confirmed amosite and crocidolite are not present in the rocks
mined in Asbestos region’’ [Nayebzadeh et al., 2001;
Williams-Jones et al., 2001]. Moreover, one of the coauthors
of both of these papers was aware of the presence of
crocidolite in the Asbestos region [Hebert, 1980; C.
Normand, unpublished communicaton].
If the QAMA-funded researchers reported on the
presence of crocidolite in the ore, it would have cast a pall
over any assertion that Canadian asbestos was ‘‘innocuous.’’
Even though crocidolite contamination would have been a
useful scapegoat to cloak the carcinogenicity of chrysotile
asbestos and support the scientific argument that chrysotile
did not cause mesothelioma, it would not have served
QAMA’s need to show that the asbestos they sold was safe.
Crocidolite could not be removed from the ore or final
product and this fact would have completely undermined the
argument that Canadian asbestos was ‘‘innocuous.’’
completely contradictory claim: ‘‘Jones et al.
Tremolite Contamination
More recently, the QAMA-funded researchers have
shifted the onus of increased mesothelioma risk to contamination
of the ore with tremolite. In this instance, they argue
that tremolite contamination of chrysotile—and not exposure
to chrysotile per se—is the cause of asbestos-related cancers
in miners and millers. In 1985, Peto and Doll reviewed this
argument and deemed it to be of academic interest only
because tremolite was found to contaminate commercial
chrysotile fibers, which could be found in the end product
[Doll and Peto, 1995]. In response,QAMAneeded to give the
impression that tremolite-free chrysotile could be safely
mined and sold.
Central-peripheral contention
The ‘‘high-low concentration–central-peripheral mine
location’’ argument was first proposed by J. Corbett
McDonald and Allison McDonald in a 1995 Letter to the
Editor in
and not chrysotile, was the likely cause of mesothelioma
cases present in miners and millers who worked in Thetford
mines in Quebec [McDonald and McDonald, 1995]. It was
the first in a series of articles in which the McDonalds and
other QAMA-funded researchers set forth the argument that
there were central (high tremolite) and peripheral (low
tremolite) mines in Thetford (See Note 2). They have
subsequently presented data showing that all but one of the
mesothelioma cases occurred in miners who had worked in
‘‘central’’ (high tremolite) mines [Liddell et al., 1997, 1998;
McDonald and McDonald, 1997; McDonald et al., 1997,
1999; McDonald, 1998a,b; Vacek, 1998; Nayebzadeh et al.,
2001].
McDonald and McDonald [1995] cited a 1989 article by
Sebastien and colleagues as the source of data indicating a
wide disparity in tremolite contamination levels between
central and peripheral mines in the town of Thetford Mines.
However, the Sebastien study did not include, categorize, or
evaluate the relationship between tremolite lung levels and
mine location [Sebastien et al., 1989]. Dr. Sebastien has
confirmed that his report did not examine this issue, and he
was unaware of any other studies, published or unpublished,
that recorded any lung fiber measurements by mine location
(P. Sebastien, unpublished communication). McDonald and
McDonald failed to specify the exact location or names of the
area A and B mines in any published or unpublished study.
The authors provided no comparative data on age, work
years, date of first exposure, job, underlying disease, or time
spent working in other mines [McDonald and McDonald,
1995]. Any of these variables could explain the comparative
data, and in their 1997 publication, the McDonalds noted that
most of the peripheral mines ‘‘had started so recently that
there were inadequate periods of latency’’ for mesothelioma
to occur in workers at ‘‘peripheral’’ mines [McDonald and
McDonald, 1997]. As chrysotile is cleared from the lung over
time, this fact alone could explain the higher chrysotile/
tremolite ratios in workers from ‘‘peripheral’’ mines
[McDonald, 1994].
If the findings are not confounded by any of these factors,
then the accuracy of the dose estimates used in the entire
series of epidemiologic studies published on the Canadian
miners must be questioned. The study by Sebastien and
his colleagues used comparative chrysotile/tremolite ratios
between mine workers and textile workers to justify their
dose estimates [Sebastien et al., 1989]. If the mine tremolite/
chrysotile ratios used for this comparison came from two
different mine worker exposure categories, then the analysis
is fatally flawed.
In 1997, the McDonalds published a detailed explanation
of the ‘‘tremolite hypothesis,’’ claiming that they had
‘‘re-analyzed’’ the data found in Sebastien et al. [1989].
However, they did not present any data or analysis of lung
tremolite levels [McDonald and McDonald, 1997]. The
authors presented mesothelioma rates in terms of ‘‘central
and peripheral’’ locations, but they again did not provide any
specific information on the exact mine locations [McDonald
and McDonald, 1997]. Gibbs categorized, at most, nine
mines at Thetford Mines, and he did not classify them as
central and peripheral, but McDonald and his colleagues
refer to 15 mines in another paper and 21 mines in still
Science. They proposed that exposure to tremolite,
Exposing the ‘Myth’ of ABC 543
another [Gibbs, 1979; McDonald and McDonald, 1997;
Nayebzadeh et al., 2001]. Of the ten studies that have based
their conclusions on the distinction between central and
peripheral, the 1995 letter to
that provides any foundation for this proposition [McDonald
and McDonald, 1995]. Four other papers, all of which are coauthored
by theMcDonalds, erroneously cited Sebastien et al.
[1989], and not the
different tremolite levels, while five other papers failed to
provide any basis for this conclusion [McDonald and
McDonald, 1995, 1997; Liddell et al., 1997, 1998; McDonald
et al., 1997, 1999; McDonald, 1998a,b; Vacek, 1998;
Nayebzadeh et al., 2001].
The assertion that the Thetford mines have varying
tremolite contamination levels conflicts with other published
data on this topic. McDonald et al. [1997] cited Sebastien
et al. [1989] and Gibbs [1979] as support for the centralperipheral
theory. However, Gibbs, a McGill colleague,
published contrary and confusing information on this intermine
difference [Gibbs, 1979]. He concluded that differences
in tremolite concentration, if they existed, could not explain
differing disease rates [Gibbs, 1972, 1979]. He also noted that
the mines were all part of the ‘‘same ore body’’ and there was
no geological evidence showing any difference between the
mines in Thetford Mines [Gibbs, 1979].
In pursuit of the missing data, we contacted J.C.
McDonald and Janet Hughes (co-author of a post-1995
study). Dr. Hughes did not know which mines were central
and which were peripheral (J.M. Hughes, unpublished
communication) and McDonald has yet to respond to our
inquiries. Case, a co-author of another paper with the
McDonalds that relied on the distinction between high and
low tremolite mines, also stated that he did not know
which mines were central and which were peripheral [Case,
2001b].
It is hoped that it is only the citation that needs to be
rectified. However, this incorrect citation, which was overlooked
by the reviewers of ten separate articles in five
different journals, is further evidence of shortcomings in and
the importance of the peer review process [Egilman and
Reinert, 2000]. The perpetuation of this error has cast the
mantle of sound science upon the tremolite hypothesis. In
1997, McDonald and colleagues contended that, based on the
low disease rates in peripheral mines, ‘‘the explanation [for
the high rate of mesothelioma] is mineralogical’’ [McDonald
et al., 1997]. Liddell implied that the medical community
had ‘‘generally accepted’’ this high-low distinction when he
asserted, without citation, that ‘‘
chrysotile by fibrous tremolite
in the central than in the peripheral area,’’ going on to
conclude that ‘‘
that [the excess incidence of mesothelioma] was confined to
the central area there (Emphasis added)’’ [Liddell et al.,
1998]. More recently, the Canadian researchers have used
this evidence before the World Trade Organization and in
U.S. tort litigation to buttress the proposition that chrysotile
is not a cause of mesothelioma [World Trade Organization,
2000]. Medical literature based on the central-peripheral
tremolite distinction continues to be used as an argument to
promote the sale of Canadian chrysotile in the developing
world [Browne, 2000].
Science is the only publicationScience letter, as the source for the data on. . .contamination of thewas known to be much greater. . .it is now clear for all practical purposes
Tremolite-free argument
The second theory put forth by the QAMA-funded
McGill researchers is that there are mere trace amounts of
tremolite in the asbestos mined today because it is avoided
during mining or removed during the milling process. Kevin
Browne presented these arguments at the International
Seminar on Safety in the Use of Chrysotile Asbestos held
in Havana, Cuba; the transcript bears the Asbestos Institute
logo and is available at http://www.chrysotile.com/en/
hltsfty/browne.htm (See Note 3). He states that all Canadian
mine-related cases of mesothelioma were related to tremolite
contamination. However in 2001, when one of the authors
(DE) asked, Browne did not knowwhether or not Black Lake,
the only operating mine at the time, was a central or
peripheral mine. After ‘‘checking’’ a few days later, he
reported that it was a peripheral Thetford mine and therefore
had low tremolite contamination (K. Browne, unpublished
communication). The Black Lake mine is not even in
Thetford; it is 6 miles away in the Town of Black Lake.
The McGill researchers use four pieces of evidence to
support the ‘‘Tremolite-Free Argument’’ for Canadian
chrysotile production. A description of the mining process
and the route tremolite travels to get into the final product will
highlight each argument used by the researchers, and
demonstrate the inherent flaws of each. In reality, the mining
and milling process actually
process is described by Spertini (See Note 4).
While it is clear from this process that most of the
tremolite is bagged with the short fibers, the Canadian
asbestos industry has presented several arguments in the
attempt to show that current chrysotile product is tremolitefree.
For example, industry advocates note that Frank and
colleagues were unable to find tremolite in any UICC-sample
chrysotile, which was prepared in the late 1960s [Frank et al.,
1998]. However, at that time, it was undisputed that the
chrysotile product contained tremolite—as it has been found
in the mines, as well as in the lungs of miners and textile
workers who used Canadian chrysotile [Dufresne et al.,
1995]. The most likely explanation for Frank’s tremolite-free
samples is that the samples were taken from crude 1 and 2 ore.
Historically, the highest-grade chrysotile, crude 1 and 2, did
not go through the usual milling process. Miners hand-picked
this product from veins of pure chrysotile and it was not
milled at the mine (F. Spertini, unpublished communication).
adds tremolite to chrysotile. The
544 Egilman et al.
Another myth is that tremolite is removed from the
chrysotile in ‘‘processing.’’ Bruce Case has claimed that this
process takes place at Canada’s last and largest operating
mine, Black Lake [Case, 2001a]. In fact, Case himself has
admitted that he ‘‘do[es] not know how the milling process
[works]’’ or, indeed, the basis for claiming that tremolite can
somehow be separated from the chrysotile fibers:
I don’t know why it is that the miners’ lungs, for
example, contained so much tremolite whereas
the end product users’ lungs contained so much
less tremolite. Something happens in the processing
to remove the tremolite. [W]e can talk about
water filtration, we can talk about screening, we
can talk about milling but the exact mechanism
by which it happens or it occurs I don’t know
[Case, 2001a].
Contrary to Case’s testimony, we cannot ‘‘talk about’’
water filtration at Black Lake. That is because the mine is
located at the bottom of a waterless lake. It took 4 years to
drain the lake and at the time it was viewed as an engineering
marvel. There is no water in the milling process, either. No
one who has ever visited or reviewed the mine or milling
process at Black Lake would ever make this mistake. Case’s
testimony makes it clear that neither QAMA nor its
researchers had sufficient evidence or knowledge to make
their claim that tremolite could be removed from the
supposed less-dangerous chrysotile.
McGill researchers continue to insist in the literature that
there is no tremolite in today’s chrysotile. For example,
Williams-Jones and colleagues claim that ‘‘Amphibole-free
chrysotile can be produced from the Jeffrey mine, and other
chrysotile mines, provided that appropriate measures are
taken to avoid contamination of the ores’’ [Williams-Jones
et al., 2001]. While this may be true, any inference that
current or past production has utilized these ‘‘appropriate
measures’’ is incorrect and misleading. Despite the results of
this study, the newest shaft at the Jeffrey mine is located in
one of the most heavily tremolite-contaminated parts of the
mine (C. Normand, unpublished communication).
As discussed earlier, tremolite and other fibers released
during the mining process end up in the bags of end product.
Therefore, it is likely that current and past shipments from the
Jeffrey mine, as well as from all other Quebec mines, were
contaminated with tremolite, crocidolite, and amosite
[De, 1961; Gibbs, 1972]. This conflicts with information
dispensed to the public under The Asbestos Institute logo
[Browne, 2000]. The Asbestos Institute does not mention the
fact that crocidolite and amosite are also present in the mine
ore, and claims that tremolite is removed through various
mining and milling processes [De, 1961; Browne, 2000].
This is simply untrue. In fact, other McGill researchers have
shown that a substantial quantity of the mined tremolite ends
up in the lungs of textile workers [Gibbs, 1972; Sebastien
et al., 1989]. Clearly, the idea that current shipments of
asbestos are amphibole-free is absolutely false, and one that
continues to pose a grave threat to the health of mine workers.
It remains to be seen whether the mine operators will
implementWilliams-Jones and colleagues’ suggested survey
techniques in the future.
QAMA’S FLAWED METHODOLOGY
The Textile Mystery: Another ABC
The QAMA-funded McGill researchers have claimed
that, even if fiber mined from Canada causes mesothelioma
and lung cancer, studies showthat the dose required to induce
these diseases is so high that there is no practical risk to
current workers. Yet studies of textile workers exposed to
the same fiber have revealed that the ‘‘slope of the exposure
response lines for lung cancer in the textile industry was
some fifty times steeper than that observed in Quebec
chrysotile miners and millers
have dubbed this variation the ‘‘textile mystery’’ and have
failed to provide any kind of explanation for it [McDonald,
1998b]. Ignoring the textile dose response data, the McGill
researchers have vociferously opposed the French chrysotile
ban before the WTO. In testimony at the WTO hearings,
chrysotile asbestos product manufacturers have claimed
that their chrysotile products did not in any way contribute
to workers’ asbestos-caused mesotheliomas and lung
cancers (B.I. Castleman, unpublished communication).
J.C. McDonald sat with the Canadian legal team, separate
from all other experts, and presented part of Canada’s
argument at the appeal of the WTO ruling on the French ban
(B.I. Castleman, unpublished communication).
McDonald summarily dismissed a number of possible
explanations for this apparent disparity between mining and
textile dose responses, including miscalculations in dose
measurement or errors that occurred when the Canadian
researchers converted particle to fiber counts. He asserted,
‘‘There is
exposures in the relevant cohorts were seriously in error
although questions of peak exposures and fibre size distributions
in ambient air have not been examined (Emphasis
added)’’ [McDonald, 1998b]. However, the McGill researchers
evaluated the quality of the dose estimates quite differently
when they first reported them [Gibbs and LaChance,
1972, 1974]. While McDonald flatly stated that errors in
measurement or actual differences between these populations
could not explain more than a tenfold difference in the
dose-response slope, Gibbs [1972] and Gibbs and LaChance
[1972] reported that dose estimates alone differ by more than
one-hundred-fold for the same job, both within the same
mine and between mines. Gibbs and LaChance [1974] noted
‘‘If membrane filter and midget impinger counts were
. . .’’ [McDonald, 1998b]. Theynothing to suggest that the estimates of cumulative
Exposing the ‘Myth’ of ABC 545
considered by work area, it was clear that the ratios of the two
in some mines were of a different order [of magnitude] from
those in others where the
. .
Conversion from particle to fiber counts compounded
the dose estimate problem: ‘‘Though only 87 pairs of samples
were collected in this pilot investigation, these were sufficient
to demonstrate that no single conversion factor could be
applied to all mines or to all work areas
same process was employed.(Emphasis added)’’ [Gibbs and LaChance, 1974].within a mine
(Emphasis added)’’ [Gibbs and LaChance, 1974]. In low
fiber specimens, which accounted for nearly one-third of the
samples, the QAMA–McGill researchers found that particle
counts were
the higher the particle counts, the lower the fiber exposure
[Gibbs and LaChance, 1974]. They concluded, ‘‘Thus, the
conversion of dust-disease relationships for the Quebec
mining and milling industry to fiber-disease relationships
does not seem possible at the present time’’ [Gibbs and
LaChance, 1974]. However, later ignoring their own data and
recommendations, McDonald et al. [1980b] converted from
particle to fiber dose estimates. It appears that incorrect dose
estimates and a systematic bias against diagnosing asbestosrelated
disease in the Canadian asbestos mining region may
explain the textile mystery.
inversely correlated with fiber counts. That is,
Mis-Estimating the Dose: Particles
Are Not Fibers
Gibbs and Hui [1971] used available dose measurements
from 1949 to 1966, which were measures of ‘‘total’’ particles
collected by midget impinger. This method cannot distinguish
fibers from other dust particles, such as silica and other
‘‘non-toxic’’ dusts [Egilman and Reinert, 1996]. Only
which may or may not be captured in the total particle
measurements, cause disease. In reality, it is difficult to make
accurate estimates of the actual exposure of the Canadian
miners and millers during that period. However, the estimates
that have been made indicate that the miners were, in all
likelihood, exposed to fewer fibers than were the South
Carolina textile workers—rather than the other way around.
The dose estimates from the QAMA–McGill mine studies
are wholly inaccurate. Based on the comparative mine/textile
risk ratio, it seems clear that they have systematically
overestimated the actual exposures.
As early as 1951, QAMA researchers realized that the
accurate calculation of dose estimates for Quebec miners was
impossible. While the problem of dose conversion exists in
all studies that are based on historical particle count data, this
problem was exacerbated in the mine studies due to the large
number of locations and jobs involved. As Vorwald, a
consultant to the QAMA, wrote to Cartier, the director of the
QAMA industrial disease clinic in Thetford mines, the data
did not exist (See Note 5). Cartier later served as a consultant
to the QAMA.
What was clearly ‘‘impossible’’ in 1951 became the dose
reconstruction of 1971 [Gibbs and Hui, 1971]. Dr. McDonald
was aware of this problem by no later than April 23, 1969.
During the discussion period following his chairing of a
session on asbestos measurement techniques, which was
highly critical of the midget impinger method, he asked,
‘‘Can an
(MI), give an accurate result?’’ [Shapiro, 1970]. Despite the
MI’s drawbacks, the QAMA researchers have continued to
use MI data to estimate exposures through the 1990s, a
quarter of a century after the mines converted to fiber
counting. Dose-response relationships based on a completely
inaccurate, but
a false sense of statistical security to these results.
fibers,inaccurate instrument like the midget impingerapparently large set of exposure data, provide
Measuring Visible Fibers:
The Iceberg Effect
The measurement of fibers by light microscopy and any
conversion from particle to fiber count rests on the
assumption that the visible fibers measured constitute some
fraction of the total number of fibers present in the air. This is
because most fibers present in the air are not visible under
light microscopy. In addition, by convention, light microscopy
does not measure fibers measuring less than 5 microns
in length [Sebastien et al., 1989]. Therefore, for QAMA–
McGill exposure estimates to be considered valid, two
requirements must be met. First, there must have been a
consistent proportional relationship between visible fibers
and total fibers. This also necessitates a consistent relationship
between visible fibers and fibers less than 5 microns
in length in various processes (i.e., mining, milling, and
maintenance). These relationships needed to be maintained
over a 60-year time period during which many processes
changed dramatically.
Second, in order to compare exposures between two
completely different processes like mining and textiles, the
ratio of visible to invisible and uncounted fibers must be
similar. There are more invisible fibers per visible fiber in
textile manufacturing than in mining. Therefore, each textile
fiber counted represents more invisible fibers than each mine
fiber counted. An examination of the mining, milling, and
textile processes and the history of fiber measurement
techniques indicates that neither of these two requirements
was ever met in the context of the QAMA–McGill research.
Nicholson [1986] summarized the main technical problems
in establishing asbestos exposure-disease relationships:
Even with the advances in fiber counting techniques,
significant errors may be introduced into
attempts to formulate general fiber exposureresponse
relationships. The convention now in
use, that only fibers longer than 5
was chosen solely for the convenience of optical
mm be counted,
546 Egilman et al.
microscopic evaluation (since surveillance agencies
are generally limited to such instrumentation).
It does not necessarily correspond to any
sharp demarcation of effect for asbestosis, lung
cancer, or mesothelioma. While it is readily conceded
that counting only fibers longer than 5
enumerates just a fraction of the total number of
fibers present, there is incomplete awareness that
the fraction counted is highly variable, depending
upon the fiber type, the process or products
used, and even the past history of the asbestos
material (e.g., old vs. new insulation material),
among other factors. For example, the fraction of
chrysotile fibers longer than 5
can vary by a factor of 10 (from as little as
0.5% of the total number to more than 5%).
When amosite aerosols are counted, the fraction
longer than 5
variability of the fraction counted to two orders
of magnitude [Nicholson, 1986].
mmmm in an aerosolmm may be 30%, extending the
Fiber length is not the only consideration relevant to fiber
counting. Nicholson also notes that as many as half of the
fibers may have been missed using optical microscopy that
cannot measure fibers of the smallest diameters (See Note 6).
Asbestos fiber-counting is a ‘‘tip of the iceberg’’
phenomenon because fibers are counted by light microscopy.
Since chrysotile fibers split longitudinally, some of the
fibers are too narrow to be seen and are not counted. The first
steps of the textile process are specifically designed to split
fiber bundles; therefore, textile exposures involve a higher
percentage of thin (invisible) fibers than mill or mine
exposures [Dement and Harris, 1979]. As a result of increased
fiber splitting in the textile process, each fiber counted
represents many more uncounted fibers than those in the
mining and milling process [Nicholson, 1986; See Note 7].
Mesotheliogenic Potential
of Thin Fibers
Fiber width is clinically important to carcinogenic
potency. Thinner fibers (generally less than 0.1
are invisible under light microscopy and therefore
uncounted, are far more mesotheliogenic than wider (visible)
fibers [Pott et al., 1972; Stanton et al., 1981; Lippmann,
1988]. Lippmann first noted this explanation for the ‘‘textile
mystery’’ in 1988:
mm), which
‘‘The origin of this lower risk [for miners] is not
fully understood, but part of the difference may
lie in the different fiber size distributions between
the mining and milling of chrysotile and its
use in a textile plant or other production facility
(See Note 8).’’
Critique of McGill Dose Estimates:
Sampling Methods
The McGill researchers based their dose estimates on
midget impinger measurements taken between 1948 and
1966.
before 1946. In fact, the QAMA began the exposure
measurement program to help control dust levels. Case
[2001a] claimed that the exposure sampling, because it relied
on 4,152 individual samples, reflected real exposure levels
and was of high quality, stating that ‘‘
than you’re ever going to get in the average epidemiological
study, this was a monumental task,’’ and ‘‘
data base was of a quality better than most.’’ Gibbs
asserted, ‘‘Measurements from other sources such as
government reports, insurance companies, mining companies,
and others were consulted and data gathered when
necessary using surveys by the research team. The distribution
of measurements was such that it was possible to obtain a
reasonable estimate of the concentrations associated with
most jobs and work areas on an annual basis’’ [Gibbs, 1994].
However, Gibbs and LaChance [1972] admitted the poor
quality of sampling from the factory in the town of Asbestos,
noting, ‘‘A total of 3,096 dust measurements, made periodically
since 1944, was used as a guide to the exposure in the
factory. Since they were made by several different persons
using various methods, including the Greenberg Smith
impinger, midget-impinger, and Owens jet sampler, these
measurements were less satisfactory than those for the mills.’’
Nonetheless, the QAMA–McGill researchers based several
publications on these data [Liddell et al., 1997, 1998; Liddell
and McDonald, 1980; McDonald, 1980; McDonald and
McDonald, 1980; McDonald et al., 1980b, 1993, 1997, 2001].
In 1984, they asserted, ‘‘We cannot claim precision or
certainty for our estimates, only that the available data—
more plentiful in this industry than most others—were used
to the best of our ability’’ [Liddell et al., 1984]. Despite the
fact that these researchers recognized that the MI samples
were of no practical value, they acknowledged that ‘‘No
attempt was made to extend work histories beyond 1966
because exposure levels in the period 1967–75 were much
lower than in the past, and exposure in a short period before
death could not be expected to contribute to risk’’ [Liddell
et al., 1984]. However, the QAMA–McGill researchers
followed the cohort until 1992, finding that about one-quarter
of the cohort had significant post-1966 exposures long before
they died [Liddell et al., 1998]. Incredibly, although they had
access to the cohort and could have prospectively determined
exposure levels from 1966 forward, the QAMA–McGill
researchers merely projected the previous 18 years of exposure
data measurements forward to 1992 [Liddell et al., 1998].
1 However, cohort workers were most heavily exposed. . .this is far more data. . .this environmental
1
1949.
Some of the studies say the dose estimates began in 1948 and others report
Exposing the ‘Myth’ of ABC 547
In addition to attempting to equate the
measurements with
presentation of the quantity of samples is also misleading. In
fact, a very small percentage of samples were taken, given the
number of mines and mills, job classifications, variability of
exposures in the same process within and between mines, and
the 80-year follow-up period. The QAMA mine owners
sampled 44 mines. Each mill and mine had at least eight
major processes, each of which resulted in variable particle
counts and particle/fiber ratios taken over an 18-year period
[Gibbs and LaChance, 1972, 1974]. In actuality, the QAMA
sampled each of the major mine processes an average of
less than once every 3 years for between 5 and 30 min.
Furthermore, QAMA
workers, miners, and maintenance workers who comprised
20–30% of the entire study population [Gibbs, 1972].
Gibbs based his dose estimates for these groups on
interviews with workers, which depended on remembered
visual estimations of dust levels. In his PhD thesis he noted,
‘‘Visibility, which was affected by fog and lighting, as well as
dust, probably played a part in the workers’ assessment in
underground mines and mills and may have led to an
quantity ofquality, theQAMA–McGill researchers’never monitored two large cohorts of
overestimation of dust levels
1972]. It should be noted that lighting and distance variables
alone could result in particle estimate differences of onehundred-
fold [Hemeon, 1963]. This problem is compounded
by the fact that visibility is a function of total particles and not
fiber counts. The researchers stated that their ‘‘historical
analysis,’’ based on interviews, indicated that the maintenance
workers had high exposures compared to the miners
[Gibbs and LaChance, 1972]. This may be true, but Gibbs
later reported that miners had twice as much pleural disease
as millers or rock crushers in the same mines and the
maintenance workers who generally worked in the mill or
other process buildings [Gibbs, 1979].
In 1971, Gibbs noted that there was ‘‘general
among the workers questioned on remembered
dust conditions [Gibbs and LaChance, 1972]. However, in
another paper published 12 years later, Liddell et al. [1984]
noted that the occupational histories often conflicted with
written records. TheQAMA–McGill researchers applied the
dose estimates based on worker interviews to particular types
of jobs, which included 13,346 different job descriptions
[McDonald et al., 1971]. Gibbs ‘‘reduced’’ these to 5,783
different jobs in thirteen general exposure categories, and
then applied these individual exposure categories to
individual work histories based on written records. It should
be noted that on the average, each worker had ten different
jobs [Gibbs and LaChance, 1972].
Gibbs claimed the QAMA samples were taken to assess
both industrial dust control effectiveness and individual
exposures. In the same paper, he also noted that the midget
impinger is ‘‘a relatively short-term instrument, is difficult to
use for personal monitoring and is not specific for fibers’’
[Gibbs, 1994]. Gibbs reported that QAMA knew which
samples were recorded for control purposes and which were
collected to be ‘‘representative’’ of actual exposures.
However, no breakdown of the relative proportion of samples
in each category has ever been provided and there is no
indication that any personal sampling was ever done [Gibbs,
1994]. Interestingly, in the same paper, Gibbs criticized
Dement’s textile exposure estimates for failing to provide
‘‘information on whether or not samples were personal
samples’’ or any information on ‘‘the distribution of locations
at which side by side samples were taken’’ [Gibbs, 1994].
Each midget impinger sampling lasted between 5 and 30 min
and thus, could not possibly reflect average daily—let alone
yearly—exposures. QAMA did not record counts below
the supposed ‘‘exposure limit’’ and the QAMA–McGill
researchers never indicated what the ‘‘exposure limit or
limits were during the relevant time period or how they dealt
with these ‘unrecorded’ measurements in their dose
estimates’’ [Gibbs, 1994].
(Emphasis added)’’ [Gibbs,. . .agreeagreement’’
Missing Data Points
In 1972, Gibbs and Lachance hinted at the inadequacy of
the sampling locations when they reported the results of new
samples taken ‘‘to obtain information in areas where no dust
measurements had previously been made’’ during the
preceding 60 years [Gibbs and LaChance, 1972]. These
areas included most of the job categories involving
exposures. While they reported that this data was missing
for only three mines, these actually represented ten mines,
which had either previously merged or whose exposures the
authors felt were comparable. Another five mines were
closed at the time of the study and no data of any sort appears
to be available for the workers at these mines [Gibbs, 1972].
Gibbs collected some samples for each of the job categories,
but he created and used an entirely new method for measurement,
one which is not completely described and does not
appear to have been validated in any way [Gibbs, 1972].
Gibbs made no attempt to compare these results to the midget
impinger total particle counts that were available for the rest
of the workers. Although ‘‘median’’values are reported in the
published paper, many of these values correspond to only
single sample results [Gibbs, 1972].
Gibbs and Lachance [1972] based much of their dose
reconstruction on the aforementioned biased results. They
reported that maintenance workers had higher exposures than
millers, but the range of exposures for maintenance workers
was 1.1–61.8 (personal samples). The range for mill workers
was 0.3–159 (area samples). Moreover, the exposure
measurements varied widely. Gibbs published the data on
between-mine variance, but omitted data on the variation of
doses at the same mine for the same job. In fact, Gibbs found
that exposures at the same mine for the same job had a range
of as much as 200% [Gibbs, 1972].
548 Egilman et al.
Particle-Fiber Conversion Issues
QAMA has long known both the impossibility of
estimating asbestos fiber exposures for every job class, and
the irrelevance of particle counts in determining toxicity. In
1953, the QAMA executive board meeting minutes noted,
‘‘The industrial hygiene surveys that have been made in the
past, and in which only dust particles were measured, are
practically without value’’ [Jackson, 1953].
QAMA waited 20 years to change to membrane filter
measurement after receiving this information. The McGill
researchers were left with only particle counts, but if the
particle counts could not be correlated with fiber counts or
were inversely related to fiber levels, then the particle counts
were useless as indices of exposure to determine asbestos
toxicity. Gibbs and Lachance tested this hypothesis by
performing 87 matched pairs of tests utilizing light microscopy
and membrane filters to count fibers and comparing
these with midget impinger particle counts [Gibbs and
LaChance, 1974]. They found that, overall, the relationship
between particle counts and fiber counts were 13% better
than
count exposures, the particle counts were
fiber exposures. This inverse relationship occurred in more
than one-third of the samples (31/87). Therefore, for at least
one-third of the particle counts, it was determined that the
higher the count, the lower the workers’ exposure to asbestos.
Gibbs and Lachance note:
random number generation. Incredibly, for low fiberinversely related to
For thirty-one samples with less than one fiber
per field, the linear correlation was very close to
zero, 0.03, and the correlation of log rhythmically
transformed data was 0.25. However,
these correlations suggest that for all mines the
regression lines are unsatisfactory for the prediction
of fiber counts from impinger counts, as
the improvement and prediction for the best
correlation, 0.45, is only 13% better than a conversion
obtained at random. Thus the conversion
of dust disease relationships to fiber disease
relationships does not seem possible [Gibbs and
LaChance, 1974].
Gibbs and Lachance acknowledge the poor correlation
of side-by-side midget impinger samples and recommend
that safety standards, at least in this industry,
should continue to be based on dust counts for
which there is considerable epidemiologic support
rather on fiber counts, for which there is no
direct evidence [Gibbs and LaChance, 1974].
They concluded, ‘‘The conversion of dust disease
relationships for the Quebec Mining and Milling Industry
to fiber disease relationships
present time.’’ Gibbs and Lachance suggest that even though
we now know that the fiber and not the particle causes
disease, and most of the particles counted are not asbestos,
that safety standards should continue to be based on particle
counts.
The lack of scientific validity of these dose estimates did
not stop the QAMA-funded McGill research team. They
selected a single conversion factor for all processes and
henceforth all subsequent publications have relied on this
single value (although minor adjustments to the value have
been made from time to time). McDonald states in a 1973
IARC conference publication that dust-sampling methods, in
addition to unreliable particle-fiber conversions, produced
data too variable to be considered a reliable basis for
estimating exposure [McDonald, 1973].
does not seem possible at the
Attempted Corrections
By 1989, the QAMA-funded McGill researchers
realized that they needed to provide better justification for
their high dose estimates. Since the chrysotile came from
the same mine, the most obvious and simple explanation
for this ‘‘mystery’’ appeared to them to be the inadequacy or
non-comparability of the dose estimates from these two
operations. After all, they had already shown that there was,
at best, no correlation between particle and fiber counts in the
QAMAsampling. At worst, there was an inverse relationship
between particle and fiber counts [Gibbs and LaChance,
1974].Onthe other hand, the textile particle counts correlated
with fiber counts because each textile process produces a
narrow range of particle/fiber ratios. The researchers tried to
‘‘fix’’ this clearly irreparable problem with the dose estimates
by comparing particle counts to retained fiber levels in the
lung [Sebastien et al., 1989]. This could only add another
level of error since, as they noted, lung fiber counts depend on
retention, clearance, and dissolution (See Note 9).
Sebastien reasserted the inadequacy of the original
QAMA–McGill exposure data, stating:
Initially we thought it might be appropriate to
use regression analysis to relate exposure, intensity
(mpcf) to lung fibre concentrations in the
two series and to compare observed values in one
with those expected by application of the regression
equations from the other. Although the
results obtained by this approach were similar to
those from the matched pair and stratification
analyses, we have not quoted them here because
the underlying assumptions as to linearity did
not seem justified [Sebastien et al., 1989].
The researchers compared the ratio of chrysotile exposure
in millions of particles per cubic foot in miners and
Exposing the ‘Myth’ of ABC 549
millers, with the exposure data from textile workers in South
Carolina with the amount of retained chrysotile and tremolite
in the worker’s lungs [Sebastien et al., 1989]. However, the
QAMA–McGill researchers selected lung cancer cases for
8% of the Charleston workers but 25% of the Quebec miners.
This introduced another systematic bias, since it is likely that
workers with lung cancer had higher exposures to asbestos.
The selected cases from Thetford were not even representative
of the Thetford cohort, as Sebastien noted, ‘‘high
[exposure] values were over-represented in necropsied
cases’’ [Sebastien et al., 1989]. Ironically, they concluded
that tremolite was not responsible for the ‘‘higher risk of lung
cancer in Charleston. In fact,
reverse.’’
The QAMA–McGill researchers did not count fibers
less than 5
seen.’’ Not surprisingly, the mean diameters and fiber lengths
were similar. Unfortunately, the comparison of mean ratios
did not comport with their theory because the mean ratio of
the particle counts between Thetford and Charleston was
11.8 and the mean chrysotile/tremolite lung fiber count ratio
was 18. The QAMA–McGill researchers did not report this
comparison of means; they simply calculated geometric
means to minimize the impact of outlier data points. These
outliers, however, comprised precisely the type of information
the QAMA–McGill researchers claimed to be evaluating
in the first place.
ratios to determine if exposure measurements are accurate
does not call for an evaluation of geometric means. If any
statistical test is appropriate, it is the comparison of
arithmetic means. This comparison again showed that the
QAMA–McGill exposure measurements were inaccurate
and that their research methods were fatally flawed. Of
course, knowledge of this shortcoming was already firmly
established in 1974 from Gibbs’ original analysis [Gibbs and
LaChance, 1974].
. . . The analyses indicate themm and they only analyzed ‘‘the first five fibers2 Clearly, comparing the averages of
Worker interviews
Since the QAMA exposure data did not measure
exposures for most of the workers in the relevant cohort,
the McGill researchers relied on company records to
reconstruct exposures. Their reports on this ‘‘check’’ of the
validity of the work records are wholly contradictory.
As mentioned earlier, Gibbs first reported in 1971, ‘‘Men
were asked to relate dust conditions they remembered to
those in areas where measurements had been made recently.
In general, there was agreement among thosewe questioned’’
[Gibbs and LaChance, 1974]. However, in 1984, Liddell
reported:
Over the years, we had come across several inconsistencies
and other evidence of errors in work
histories. We took this opportunity to attempt
correction where appropriate, but for reasons
outlined elsewhere, we were unable to make use
of this effort.
elicited by ‘blind’ field inquiry and checked
against company files, were certainly justified,
but we have not made them, and so allowed
errors to remain
1984].
Many of the changes in work history,(Emphasis added) [Liddell et al.,
Even after recognizing their errors, they consistently and
continually ignored them. They even attempted to justify
their decision not to correct the errors, stating, ‘‘However,
this type of error appears to have been distributed unevenly,
and so like might not have been compared to like. In casereferent
comparisons, minor random unbiased exposure
errors are probably less serious than bias; we therefore
returned to the situation that existed before the field work was
instituted’’ [Liddell et al., 1984]. They provided no analysis
of the magnitude or randomness of the errors. No effort was
made to compare the interviews with the written record to
determine whether or not the written records contained a
systematic bias.
Conversion factors
First Gibbs and LaChance [1974] and later Liddell et al.
[1984, 1998] evaluated the merits of converting particle
counts to fiber counts [Gibbs and LaChance, 1974; Liddell
et al., 1984, 1998]. In addition to their realization that worker
interviews indicated that the original dose estimates were
even less accurate than previously assumed, they again
recognized that particle/fiber ratios were ‘‘virtually independent
of the level of exposure’’ [Liddell et al., 1984].
Furthermore, it was clear that if a conversion factor were to
be used, it needed to be specific for each job category [Gibbs,
1994]. Disregarding their own findings, they used
particle/fiber ratio standard for all years in all job categories
They based this standard on the worker histories, which they
then proceeded to ignore in calculating the actual particle
counts because they postulated that the histories would
introduce a ‘‘systemic bias’’ into their analysis (See Note 10).
Liddell et al. [1998] again recognized the inadequacy of
their dose estimates concluding that:
a single.
the classification of jobs by dust category would
not be a reliable classification by fibre count
[Liddell et al., 1998; See Note 11].
2
example, they can be used to determine what an average interest rate
would be if $100,000 was invested in the bank in 1990 and had variable
interest rates each year of 2, 5, 7, and 10 over the next 4 years.
Geometric means are utilized to calculate power function averages. For
550 Egilman et al.
They also understood why the dose estimates were so
inaccurate. Fiber/dust ratios necessarily differed by
orders of magnitude for different types of work and for
the same work process at different points in time. Liddell
et al. [1998] noted that, ‘‘The two important reports by
Gibbs and Lachance [1972, 1974] give some indication of
the inherent complexity; a simple example is that work
on the tailings dump in 1968 was extremely dusty but,
as most of the fibre would have been extracted the
fibre:dust ratio must have been quite low.’’ The exposure
data was so inaccurate that, ‘‘taken at face value,’’
exposures even appeared
other words, unmanipulated, the exposure data indicated that
chrysotile exposure actually prevented workers from developing
pneumoconiosis, lung cancer, or mesothelioma
[Liddell et al., 1998]. Their original findings would be
plausible if one considered an alternative hypothesis in which
workers who had the highest exposures died from nonmalignant
disease before the latent period for the induction of
cancer had been attained. Instead, since they believed an
inverse exposure relationship was ludicrous, they manipulated
the exposure estimates until the dose-response curve fit
their a priori understanding of the proper form for the doseresponse
relationship. The researchers discarded all of the
exposure levels that were inversely related to disease. They
described this manipulation in an appendix titled ‘‘Elimination
of negative regression coefficients,’’ and proceeded to
‘‘revise’’ the exposure data to create results that would
allow them to argue that chrysotile exposure was ‘‘innocuous’’
(See Note 12).
protective for the workers. In
Years of exposure ‘‘correction’’
In 1980, McDonald commented on the exposure data
and noted:
Relative risks of lung cancer were considered in
detail by Liddell et al. and it appeared that there
was little to suggest that the way in which dust
exposure had been accumulated played any part
in determining the risk
1980a; See Note 13].
. . .[McDonald et al.,
Even after this ‘‘validation’’ of the dose estimates,
they unequivocally concluded that the dose estimates
were worthless when Gibbs wrote, ‘‘thus it is clear that
there is no single overall conversion factor that can be
applied to the mine and mill data’’ [Gibbs, 1994].
Manipulation of the cohort to achieve
desired results
In his 1980 paper, McDonald justified the age 45 cut-off,
stating that ‘‘by this time most of the men had completed their
service’’ [McDonald et al., 1980b]. This was simply not true.
In 1997, Lidell et al. revealed that over 2,400 men in the
1890–1920 study cohort were still employed in 1967, and
the
longer produced the linear dose-response curve they sought,
in 1997 they calculated exposures up to age 55. Rather
than using exposure data obtained after 1966, the year the
QAMA–McGill studies began, they used the
youngest of these was 47. Since the age 45 cut-off noalreadydiscredited
pre-1966 data to estimate these exposures. They
also altered the dose calculation methodology, asserting that
‘‘it did not prove feasible to use the same methods as
previously’’ [Liddell et al., 1997]. They do not provide any
rationale for this change (except perhaps for large computer
file size), nor do they provide a comparative analysis of
results using the ‘‘old’’ and ‘‘new’’ dose estimate methods
(See Note 14).
Despite these manipulations, the McGill researchers
themselves have cast doubt on the reliability of the exposure
estimates for pneumoconiosis and mesothelioma, stating:
‘‘Pneumoconiosis death rates per 100,000 subject-
years were clearly associated with exposure
at the two main places of employment, but the
exclusions from this table [early deaths: 12 from
pneumoconiosis and 1 from mesothelioma] may
have distorted these associations, and certainly
make comparison between the Asbestos mine
and mill and Company 3 particularly difficult.
There is little sign of corresponding associations
with mesothelioma’’ [Liddell et al., 1997].
Misleading Conclusions
In 1998, Liddell delineated the pre-determined conclusion
that the QAMA–McGill researchers planned to
expound in the last paper of the series, namely, that the
health effects of chrysotile were ‘‘essentially innocuous’’
(See Note 15).
The QAMA–McGill researchers thus concluded that
nearly half (72) of the deaths that they attributed to asbestos
exposure were inconsequential because these deaths did not
significantly alter overall mortality rates. Since their conclusion
is a political one, perhaps a current political analogy
will help shed light on this analysis. If one were to apply the
same standard to the World Trade Center destruction, one
could similarly conclude that this act of terrorism, that has
changed the world for years to come, was ‘‘innocuous’’
because it did not significantly impact the US SMR for 2001.
Inadequate Case Ascertainment
In addition to the overestimating of dose, systemic
underestimates of asbestos-associated diseases may have
Exposing the ‘Myth’ of ABC 551
also contributed to the apparent ‘‘low risk’’ of chrysotile
exposure. In 1950, in a meeting with QAMA officials,
Dr. Lanza noted that this was a likely explanation: ‘‘It was
pointed out that in the Province [Que´bec] it is the practice not
to list cancer as a cause of death even when it is, so that
information on this may not be of much help to us’’[Trudeau
Institute, 1950]. Metropolitan Life provided group life insurance
to the mine workers, and began collecting mortality
data and death certificates on the workers in the 1920s. Begin
and colleagues provided further support for this diagnostic
and/or reporting bias when he documented ‘‘an increasing
incidence of cases of malignant mesothelioma in chrysotile
miners and millers of the Eastern Townships of Que´bec, with
49 cases in the last 23 years, and a rate of 2.5 cases per year in
the last 10 years in the primary industry, as compared with a
rate of 0.3 per year in the years prior to 1969 ‘‘(McDonald
et al., 1979 as cited by Begin et al. [1992]).’’Asimilar eightyfold
undercount of lung cancer case finding can easily
account for the fifty-fold ‘‘textile mystery.’’
There is clear evidence that this under-count occurred
and was, in fact, organized by the main financial sponsor of
the studies, QAMA. In 1995, Schepers reported that Ivan
Sabourin, head of the Conservative Party of Quebec and legal
counsel to QAMA, had systematically removed stored
pathological specimens—the removed lungs—of deceased
Quebec miners diagnosed with lung cancer and sequestered
them at the Trudeau Institute at Saranac Lake New York
[Schepers, 1995]. By 1946, at least 17 cancer cases had
been removed and are still currently missing from the
QAMA–McGill analysis. While unprecedented, this
‘‘organ-snatching’’ clearly had a differential impact on the
number of cancer cases attributable to the QAMA mine
operations and those reported from the control group.
Because the cohort workers were born between 1890 and
1920, some mesothelioma deaths are likely to have occurred
before the disease was widely recognized by most physicians
in the mid- to late-1960s. Until the eighth revision of the
International Classification of Diseases
in the US in 1968, mesothelioma of the pleura was classified
as a benign neoplasm of the respiratory system [U.S.
Department of Health, Education andWelfare, 1975]. By this
time, much of the cohort was over 65 years of age and had
accumulated more than 40 years of latency. It is likely that
this diagnostic bias is also a cause of the apparently low
mesothelioma rate.
, which was adopted
Influence of Political Considerations
Under-reporting by Quebec physicians must also be
considered as a likely explanation of the fallacious results.
No less an authority than Pierre Elliott Trudeau noted that the
QAMA mines have been the absolute center of Canadian
politics during this century. In the foreword to
Strike
event in Canadian politics in the twentieth century [Trudeau,
1974]. The political importance, power, and influence of
QAMA during this century cannot be overestimated. This is
particularly true with respect to QAMA’s recognition of the
potential impact of asbestos-related health problems on
profits. At the suggestion of Wade Wright, the medical
director of their insurer, Metropolitan Life, the mine owners
began undertaking projects to influence the medical literature
and individual physicians in Quebec in the 1920s when they
took a ‘‘mortgage out on McGill’’ [Wright, 1926; See Note
16]. Initially, the QAMA was concerned with the potential
financial impact of workers’ compensation claims. By the
mid-1930s, they had already developed programs to deal
with the adverse consequences of the fear of asbestos-related
diseases on sales [Lanza, 1937; Lilienfeld, 1991].
The Asbestosof 1949, Trudeau called the strike the most important
CONCLUSION
The Canadian asbestos mining industry has a long
history of manipulating scientific data to generate results that
support claims that their product is ‘‘innocuous’’ [Liddell
et al., 1998]. Researchers complicit in this manipulation
seem to be motivated by a variety of interests, including a
desire to support an important national industry and a preexisting
ideological commitment to support corporate
interests over worker or community interests. Conducting
industry-friendly research can also anchor an academic
career by guaranteeing the steady stream of funding necessary
to stay afloat in the ‘‘publish or perish’’ environment of
the university. Yet, as industry’s scientists must know, their
research has implications extending far beyond their offices
or laboratories.
Today, the impact ofQAMA’s policies is most dire in the
developing world. Almost all of Canada’s asbestos is
exported to the developing world, and corrupt medical
literature continues to be used in arguments to promote the
sale of Canadian chrysotile there [Castleman, 2002]. While
there are few studies on the extent of asbestos-related disease
and death in the developing world the death toll there
is likely to be staggering. QAMA–McGill researchers
interested in preserving this key market have argued
before the World Trade Organization to buttress the proposition
that chrysotile is not a cause of mesothelioma and
should therefore not be subject to national bans [B.I. Castleman,
unpublished communication; Browne, 2000 http://
www.chrysotile.com/en/hltsfty/browne.htm; World Trade
Organization, 2000].
In the United States, QAMA-supported researchers are
currently influencing federal policy on asbestos. A recent
report to the Environmental Protection Agency by the
Eastern Research Group, Inc. [2003] was based on the
QAMA-funded research we have reviewed here. The report
was reviewed by Bruce Case and other scientists who have
been retained by QAMA member companies [Eastern
552 Egilman et al.
Research Group, Inc., 2003]. The legitimacy that has been
granted to QAMA’s ‘‘anything but chrysotile’’ theories is
evidence of the success of QAMA’s more than three decade
campaign of ‘‘propaganda’’ [QAMA, 1967]. QAMA has
been even more successful than the tobacco industry they
emulated. It would be politically impossible for the FDA
to depend on the opinions of tobacco industry-funded
researchers who stated that tobacco was ‘‘innocuous.’’ Yet
that is exactly what has happened with EPA’s designation
of Bruce Case and others as ‘‘experts’’ on asbestos risk.
QAMA’s unsound science does not deserve such credibility.
Until their spurious nature of their data and conclusions are
exposed, injured workers and bystanders will go uncompensated
and chrysotile will produce yet another generation of
victims.
APPENDIX: NOTES
1. De’s PhD thesis entitled, ‘Petrology of dikes emplaced in the
ultramafic rocks of South Eastern Quebec’ was deposited in
1961 at Princeton University. The objective of the thesis was to
study the dike rocks and their relation to the ultramafic rock in
the Eastern Townships. The concentration of amphiboles in the
rocks are variable and can be substantially high in some dikes
of granitic and dioritic composition. For instance, he reported
the presence of fibrous actinolite in concentrations as high
as 14% in granitic dikes and suggested that the granitic
pegmatite from the Jeffrey mines in the town of Asbestos
would even contain anthophyllite. Thus as suggested by lung
burden analyses and mineralogical data, the concentrations of
amphibole fibers (especially tremolite and actinolite) contaminating
the chrysotile mineral ore from Asbestos or Thetford-
Mines are at about the same level, although this may not be
reflected in sporadic air samples. These mineral matters were
likely constituents in the final product. There is a need to
clarify how high were the concentrations of amphibole fibers
in the host dunite rock especially tremolite and actinolite
[Dufresne et al., 1995].
2. McDonald and McDonald state, ‘‘The possibility that this
distribution [fewer mesothelioma cases in peripheral mines]
might be related to the concentration of fibrous tremolite in the
two areas was then tested with data on asbestos fiber concentrations
in lung tissue from 83 cohort members from Thetford
mines who had died from causes other than mesothelioma and
had been examined by electron microscopy in 1988. The
number of lungs examined was 58 from area A (central-high
tremolite mines) and 25 from area B (peripheral-low tremolite
mines); the groups were similar in duration of employment
(36 and 37 years) and time from termination to death (8 years
in both), but estimated accumulative dust exposure was about
30% higher in group B. The geometric mean concentrations of
fibers equal to or greater than 5
dried lung were as follows: chrysotile, area A, 7; area B, 13
(not significant); tremolite, area A, 32; area B, 7 (
[McDonald and McDonald, 1995].
3. Browne stated, ‘‘The main tremolite-contaminated mines are
now closed.’’ He also said, ‘‘But in the past, the percentage of
tremolite in the fibre could be as high as 1%, whereas the high
tremolite-contaminated mines in the central Thetford area
have closed, and in any case the high geological research has
shown that tremolite is not uniformly mixed with the
chrysotile, but occurs in separate seams which can be
identified and avoided. And lastly, there is evidence that much
of the tremolite is lost in the milling, so that what is delivered
to the manufacturer will have an even lower content. So
present and future supplies from these sources have and will
have minimal tremolite’’ [Browne, 2000 http://www.chrysotile.
com/en/hltsfty/browne.htm].
4. A. Chrysotile composes about 5% of the ore deposit. It forms
in layers or sheets between serpentine rocks. Tremolite and
crocidolite are present in the adjacent rock alongside the
100% pure chrysotile vein. The adjacent rock is compressed
in rock crushers, a process that is repeated three
times. The rock is left to dry for 48 hr after the first
crushing. This initial process releases tremolite from the
serpentine, and it is mixed in with the chrysotile.
B. The crushed ore is moved to a conveyer where all fibers on
the belt, including the released tremolite and crocidolite,
are vacuumed off and carried into the mill As a result, the
end product is contaminated with tremolite and crocidolite.
C. The fiber is transported to the sorting mill. The sorting mill
then separates the fiber by size. This is a two-part process.
The fiber is shaken and rocked from side to side on a
‘‘sifter,’’ which slopes down towards a cyclone vacuum. A
five-foot-long by two-inch-wide cyclone at the end of the
sifter vacuums the fiber into a tube and it is carried by the
force of air to the bagging area. This is how fiber sizing is
achieved. The suction is set to pull short fibers, of any
chemical composition, off first. The remaining longer fibers
are dropped onto another conveyer and the process is repeated
until the longestfibers are cyclone-vacuumed off. It is
clear that the tremolite is sized along with the chrysotile.
D. The fiber is blown from the sifting area and transported to
the bagging area where it is blown into bags ready for
shipment.
5. Vorward wrote, ‘‘Last week, while in Washington, I had the
opportunity to discuss our program concerning the epidemiology
of pulmonary cancer in subjects exposed to asbestos dust
and to present the problem which you posed regarding job classification.
I agree with your views. Certainly it is an
mm in length per microgram ofP¼0.0002)’’impossible
task to tabulate the various jobs on comparable scientific data,
since such data does not exist. Therefore the code suggested by
both you and Ken [Smith, medical director of Johns-Manville]
should be used (Emphasis added)’’ [Vorwald, 1951].
6. As Nicholson noted, ‘‘Using electron microscopy, Rendall and
Skikne [1980] measured the percentage of fibers with a
diameter less than 0.4
of an optical microscope) in various asbestos dust samples.
mm (the approximate limit of resolution
Exposing the ‘Myth’ of ABC 553
In general, they found that more than 50% of the 5
longer fibers are less than 0.4
visible using a standard phase contrast optical microscope’’
[Nicholson, 1986].
7. Nicholson continued, ‘‘Moreover, as with length distribution,
diameter distribution varies with activity and fiber types. As a
result, the fraction of fibers longer than 5
microscopy varies from about 22% in chrysotile and
crocidolite mining and amosite/chrysotile insulation manufacturing
to 53% in amosite mining. Intermediate values of
40% are measured in chrysotile brake lining manufacturing
and 33% in amosite mill operations. Thus, even perfect
measurement of workplace air, with accurate enumeration of
fibers according to currently accepted methods, would be
expected to lead to different exposure-response relationships
for any specific asbestos disease when different work
environments are studied’’ [Nicholson, 1986].
8. Lippman continued, ‘‘Animal experiments
fibers most likely to produce cancer are too thin to be observed
by a light microscope. In the mine and mill the chrysotile fiber
bundles have only been partially broken apart. Many of the
fibers are large and easily counted: some of those counted
are curly and non-respirable. When shipped to a chrysotile
textile mill the fibers are further broken apart during carding.
In the high-speed spinning and weaving processes, thin fibers
may split off from the threads most of which are not visible in a
light microscope. Thus in the air of a textile plant the
percentage of thin, uncounted, but highly carcinogenic fibers
can be greater than in the mine and mill air and a greater
cancer risk observed for the same measured cumulative fiber
exposure’’ [Lippmann, 1988].
9. Sebastien writes, ‘‘In the absence of an accepted model for
lung retention of asbestos fibres comparison between the two
groups was restricted to cases having similar time characteristics
of exposure (duration and cessation). In these circumstances
it was assumed that retention would be proportional to
mean intensity of exposure. This assumption, impossible to
test without good environmental data, may be questioned,
especially for chrysotile’’ [Sebastien et al., 1989].
10. Liddell et. al. argue, ‘‘The conversion factor should be
amended because many more histories have led to more reliable
estimates. We have made four other estimates: the fibre
and dust slopes for pneumoconiosis and for lung cancer were
in the ratios 3.67 and 3.57 (f/ml)/mpcf; while, based on mean
exposures for all subjects, the ratio was 3.46 (f/ml)/mpcf in this
report, and was 3.44 in a study of elderly male workers in
Thetford Mines. These factors, all based on substantial groups
of persons, show little variation. However, the ratios calculated
for each of the 2,535 non-zero pairs of exposures in this study
ranged between 0.32 and 30 (f/ml)/mpcf, while the correlation
of the fibre/dust ratio and its denominator, in the 2,535 sets,
was so small that the ratio could be thought of
independent of the level of exposure.
‘average’ must depend on each specific group of workers,
and on the method of obtaining it. Further, all the above
estimates are for workers at Asbestos and Thetford Mines in
the period from 1904–66; there is no assurance that they might
apply in different circumstances. We would add that there is
great assurance that the particle/fiber ratio applied in the
circumstance under investigation’’ (Emphasis added) [Liddell
et al., 1984].
11. The full passage reads, ‘‘Liddell et al
factor to convert dust counts to fibre counts as about 3.5
(fibres/ml), mpcf but stated this would be
mm ormm in diameter and, thus, are notmm visible by light. . .indicate that theas virtuallyNevertheless, any. [1984] estimated aquite unreliable
except applied to mean dust levels for substantial groups of
Quebec asbestos workers. For the many jobs in which the 2217
men included in their study had worked, the fibre:dust ratios
had ranged from 0.3 to 30 (fibres:ml):mpcf virtually independently
of the dust level; in the current study ratios job by
job must have varied similarly so that the classification of jobs
by dust category would not be a reliable classification by fibre
count (Emphasis added)’’ [Liddell et al., 1998].
12. They wrote, ‘‘In all the conditional regression analyses of
the full model, i.e., with 13 exposure measures, there was at
least one negative regression coefficient, which taken at face
value would imply a protective effect of exposure. Years in
the highest relevant dust category were pooled with those in
the adjacent category and the analysis was repeated. This
process was iterated until either all coefficients had become
positive, when it was terminated, or until the only negative
coefficient was for category 1; in that circumstance, category 1
was eliminated from the model, which was equivalent to
setting the coefficient to zero and the odds ratio to unity
. . .
Admittedly,
pooling carried out
‘significant’ effects’’ (Emphasis added) [Liddell et al., 1998].
13. McDonald et al. continue, ‘‘It therefore seemed appropriate to
base a second series of analyses on dust exposure accumulated
to a certain age, arbitrarily taken as 45 years, at which age
most men had completed their service. After the cohort had
been divided by exposure to age 45, two further, but separate,
subdivisions were made by mining area (Asbestos and
Thetford Mines) and by smoking habit; those whose smoking
habit was unknown being added to the largest group—that is,
moderate smokers. The study interval started at age 45’’
(Emphasis added) [McDonald et al., 1980a].
14. Liddell et al. state, ‘‘As over 2,400 men in the cohort were still
employed in 1967, attempts were made to estimate exposures
yearly up to 1985, when the last man had retired. It did not
prove feasible to use the same methods as previously. Instead,
each man was allocated dust levels as follows: for 1967, the
same level as in 1966; for each subsequent year, a proportion
of that level in accordance with the average trend of fibre
concentration for his specific mine or mill. From these levels,
we estimated yearly exposures from 1967 to 1985 [McDonald
et al., 1993], and extended each man’s exposure record by a
further 19 years. To give much-needed greater flexibility for
the calculation of exposures to the age of 55, for instance, or,
there was a degree of arbitrariness in some of thebut every effort was made to retain any
554 Egilman et al.
for case-referent analyses, in relation to the age at death of the
case the exposure file was re-organized: first, the annual record
of exposure, incorporating the adjustment for length of the
working week, was changed to the dust level, with an indicator
of the work-week adjustment; second, each man’s work
history was recorded annually from the year in which he
started to the year in which he finished, thus reducing the
maximum number of years from 82 to 59; and thirdly, the
format was changed slightly.With these changes, the complete
file was reduced in size by over one-quarter, but remained
enormous (5.9 MB)’’ [Liddell et al., 1997].
15. The researchers contended, ‘‘For men first employed in
Asbestos, mine or factory, they [the SMRs] were very much
what might have been expected for a blue collar population
without any hazardous exposure. SMRs in the Thetford Mines
area were almost 8% higher, but in line with anecdotal
evidence concerning socio-economic status. At exposures
below 300 (million particles per cubic foot)
equivalent to roughly 1,000 (fibres/ml)
in the 1940s at 80 (fibres/ml)—findings were as follows. There
were no discernible associations of degree of exposure and
SMRs, whether for all causes of death or for all the specific
cancer sites examined. The average SMRs were 1.07 (all
causes), and 1.16, 0.93, 1.03, and 1.21, respectively, for
gastric, other abdominal, laryngeal and lung cancer. Men
whose exposures were less than 300 mpcf/y suffered almost
one-half of the 146 deaths from pneumoconiosis or mesothelioma;
the elimination of these two causes would have reduced
these men’s SMR (all causes) from 1.07 to approximately
1.06. Thus it is concluded from the viewpoint of mortality that
exposure in this industry to less than 300 mpcf/y has been
years, (mpcf.y),years—or, say, 10 years
essentially innocuous
pneumoconiosis or mesothelioma’’ (Emphasis added) [Liddell
et al., 1997].
16. Wright wrote, ‘‘It is suggested that we approach the Dean of
the faculty of Medicine of McGill University with a proposal
that upon the establishment of an adequate Department of
Industrial Hygiene in the McGill Medical School the
Metropolitan enter into an agreement with McGill to secure
for the Company certain services and information relating to
the health of industrial workers in Canada.
, although there was a small risk or
‘‘
specific information regarding such matters as:
‘‘1. The distribution of industrial establishments, mines
and lumbering operations with data concerning the number
of employees in each establishment and district
. . .It would be of great value to the Company to have. . .
‘‘
difficult and very expensive. If it could be obtained from a
department of industrial hygiene in Canada’s leading
university in return for a moderate annual for the Company
would undoubtedly benefit
. . .To secure such information directly would be. . .
‘‘
payments specifically conditioned upon a commensurate
return, the adequacy of such return to be determined by the
President, or those to whom he may delegate the decision
. . .Such a plan involves a definite quid pro quo,. . .
‘‘
mortgage on McGill
matters affecting community or individual health—such as,
aid in preparation of publicity, occasional research matters
not involving great outlays of money, field investigations as
of sanitation, water, or milk supplies, or industrial hazards.
‘‘
add that Martin should not only be prepared to render certain
types of service but certain services, more or less routine
perhaps, should be specified. Unless there is a definite,
tangible quid pro quo the interest of a financial supporter may
well languish after a few years’’ (Emphasis added) [Wright,
1926].
. . .The Sun Life might well ask—if it secured a. . .Technical guidance in regard to. . .Observations of our scheme at Harvard leads me to
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