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IV. ARGUMENTS PRESENTED BY THIRD PARTIES
A. BRAZIL
1. Introduction
4.1 Brazil explains that the proceeding challenges the WTO-consistency of
France's 1 January 1997 Decree, which bans the manuf acture, processing, sale and possession for sale,
importation, exportation, domestic marketing, offer and transfer of all varieties of asbestos fibres and
products containing them (the Decree or the ban).1  The ban has four narrow exceptions that apply
where no substitutes exist for chrysotile products.  The substitute products that do exist generally are
more expensive than chrysotile products.  Thus, the ban clearly operates to create a commercial
advantage for substitute products.  According to Brazil, a ban is the most trade restrictive of measures.
Therefore, the justification for any ban must be subject to the strictest scrutiny, especially as applied to
a developing country such as Brazil.  The ban has ended Brazilian exports of uncontaminatedchrysotile to France.  In 1994 and 1995, France imported from Brazil 1,100 and 1,500 metric tonnes of
uncontaminated chrysotile, respectively.  Since the ban took effect in 1997, France has not imported
any chrysotile from Brazil.
4.2 According to Brazil, the importance of this proceeding extends far beyond the French ban –
the  proceeding is a test case.  Will other WTO Members be allowed to ban products of developingcountries that can be safely used with appropriate, tested precautions simply to appease the public?
Modern economies use hundreds of products that present health risks if they are misused, but that
present no risks if they are used properly.  Uncontaminated chrysotile is one of them; if properly used,
uncontaminated chrysotile presents no health risk.  Similar products include organic fibres, man-made
fibres, benzene, mercury, ammonia, nearly all forms of pesticide, etc.  Societies regulate theseproducts to ensure they are used safely so as to protect the health of workers handling them directly
and of the general population which is exposed to them indirectly.  The same treatment is appropriate
for uncontaminated chrysotile.  Uncontaminated ch rysotile—the only asbestos fibre Brazil mines and
exports – is the safest by far of all asbestos fibres.  In particular, it is much safer than amphibole, the
asbestos responsible for current health problems from past exposure.  All of the asbestos that Brazilmines, produces and exports is uncontaminated chrysotile.  For this reason, Brazil’s chrysotile
products are among the safest in the world.  The medical explanation for these facts is set forth in
detail in a recent bio-persistence study by Dr. David S. Bernstein, an expert in fibre toxicology
(indeed, the EC often seeks his expertise on this topic).
2
4.3 Brazil asserts that the primary issue in this proceeding is not - as the EC would suggest -
whether asbestos can be hazardous to human health.  It can.  Years of misuse and unsafe utilization of
the most hazardous form of asbestos – amphibole - have caused significant damage to health.  Allcountries, including Brazil, regret the harm to human health caused by decades of exposure earlier this
century to amphibole produced and used worldwide.  Brazil understands well the basis of the public
outcry, experienced in many countries (including Brazil), that led the French Government to
commission the INSERM Report
3 (a study focusing on the health effects of earlier, unsafe uses of
amphibole asbestos) and then to ban asbestos.  France imposed the ban only one day after INSERMreleased its Report.  The Report was commissioned and released to provide a scientific "cover" for a
political decision that had already been taken.  However, as a review of the INSERM Report
demonstrates, the causes of asbestos-related health problems in France are past uses, especially in the
                                                     
1Decree No. 96-1133, dated 24 Decembe r 1996, (J.O. dated 26 December 1996).
2David S. Bernstein, Summary of the Final Reports on the Chrysotile Bio-Persistence Study  (Geneva
Switzerland;  2 October 1998).
3INSERM, Effets sur la santé des princi paux types d’exposition à l’amiante , Les Éditions INSERM,
Paris, 1997 (INSERM Report).WT/DS135/R
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spraying of brittle amphibole on to fireproof buildings and, until quite recently, warships (flocking).
Given the long latency period between exposure to amphibole and the onset of any related diseases,
workers who were victims of heavy exposure with virtually no protection 30 years ago are
experiencing serious health problems today.  The INSERM Report is based on analyses of these
workers' health. The INSERM Report does not focus on data from studies of modern uses ofchrysotile.  Moreover, in the Report, INSERM con cedes that it was unable to produce "scientifically
certain" conclusions, but could present only an "aid to understanding" based on "plausible, though
uncertain, estimates.
4"  Quite simply, the INSERM Report is an inadequate basis for the ban.
4.4 Brazil argues that it has a deep appreciation of the desire - indeed, the need - for the
French Government to address public concern and protect public health.  Brazil also understands the
frustration of being unable to remedy or even mitigate the health consequences of past exposure from
unsafe use of amphibole, and the frustration of bein g unable to take measures to remedy or decrease
exposure from flocked amphibole asbestos that is already in French buildings (because disturbing
flocking increases exposure).  However, when Fr ance approved the WTO Agreement, it agreed not to
restrict trade merely to appease domestic sentiment, no matter how strong.  Brazil cannot accept
France's adoption of a politically motivated measure that will neither (i) make those already sick from
asbestos exposure healthy; nor (ii) reduce risk to the healthy beyond existing levels of protectionguaranteed by modern, controlled uses of chrysotile.  As the European Commission recently stated:
[V]arious national organisations, including the Health and Safety Executive in the United Kingdom,
have made very disturbing projections about the numbers of deaths which are likely to be attributable toasbestos over the next few decades.  However, it is important to note that these figures relate to pastexposures to mixed asbestos types, including the fibres which have already been banned.  It would bewrong to use these statistics alone to justify a ban on the marketing and use of chrysotile because such a
ban would not lead to a lower risk of exposure for workers to asbestos which is already in place, nor
would it reduce the number of deaths which are occurring today as a result of past exposure toasbestos.
5
4.5 Modern uses of asbestos are or should be limited to chrysotile, which most parties, including
INSERM, agree is safer than other forms of asbestos.  Moreover, modern uses are or should be
confined to products in which the fibres are bonded in a finished product and, thus, cannot escape,
e.g., asbestos-cement products.6  For these and other reasons, modern uses are quite safe; they involve
                                                     
4See para. 4.30 below.
5Official Journal of the European Communitie s, C 135/108 (14 May 1999) (30 September 1998 answer
of Mr. Bangemann to Written Question E-2736/98 of Christin e Oddy (PSE)).  See also Official Journal of the
European Communities, C 13/123 (18 January 1999) (24 July 1998 answer of Mr. Bangemann to
Written Question E-1950/98 of Anita Pollack (PSE)) ("[I]t is important to mention that a new ban would notlead to a lower risk of exposure to existing asbestos for workers, nor would it reduce the number of deaths frompast exposure to asbestos.  Possible contamination from asbestos in existing buildings (e.g. in relation tomaintenance activities and asbestos removal operations) will remain an important cause of exposure to workersfor many years.").
6Brazil notes that in the chrysotile-cement industry, the largest present-day use of chrysotile, the
manufacturing process uses a water slurry mixture of chrysotile and cement.  No dust or pollution is createdduring this process.  See also American Lung Association, Asbestos,  pp. 2 and 3
(http://www.lungusa.org/air/envasbestos.html) ("Asbestos is rarely used alone, and it is generally safe whencombined with other materials with strong bonding agents.  As long as the material remains bonded so that
fibers are not released, it poses no health risk."); National Cancer Institute, (1996), p. 
3
(http://www.ncih.nih.gov./clinpdq/risk/Questions_and_Answers_About_Asbestos_Exposure.html)  ("Asbestos
that is bonded into finished products such as walls, tiles, and pipes poses no risk to health as long as it is notdamaged or disturbed (for example, by sawing or drilling) in such a way as to release fibers into the air . . ..
[N]o fiber type can be considered harmless, and prope r safety precautions should always be taken by people
working with asbestos.").WT/DS135/R
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exceedingly low levels of exposure (that often do not exceed even the "natural" levels in ambient air).
Chrysotile is used in a very wide variety of products.  It is used as a flame retardant, to strengthen
friction materials (e.g., truck brakes) and to create cement pipes for carrying water that are far less
subject to corrosion, cracking and breaking than traditional cement pipes.  In most applications,
chrysotile is used because it increases  public safety; thus, using other, less-efficient products in its
place often decreases public safety.  The use of chrysotile as a fire retardant needs no explanation.
However, a discussion of its use in friction materials may be illuminating.  Chrysotile is used
primarily in truck brake pads, drum brakes and brak e blocks to control heat build-up, thus maximizing
friction and stopping power.  It is the preferred product for this application.  As one of the authors of
an American Society of Mechanical Engineers (ASME) study commissione d by the EPA concluded:
(a) The "replacement/substitution of asbestos-based with non-asbestos brake linings will produce
grave risks"; and
(b) "the expected increase of skid-related highway  accidents and resultant traffic deaths would
certainly be expected to overshadow any pot ential health-related benefits of fiber
substitution."7
4.6 Brazil pleads that chrysotile's numerous public safety benefits - the many contributions it
makes to societies around the world - not be ignored in this proceeding, as they were when Francepassed its ban.  In Brazil's view, the primary question in this proceeding is quite narrow - is a
complete ban necessary to protect public health or can public health be ensured by regulating modern,
controlled uses of chrysotile and chrysotile products?   The answer arrived at by those countries in the
Americas that have examined the issue closely, ranging south from Canada, to the United States, to
Brazil, is that public health can be ensured by regulating modern controlled uses.  France may, of
course, take measures that are designed to, and actually do, protect its citizens.  However, the ban does
not meet even this very generous characterization of the general rule set forth in the WTO Agreementon Technical Barriers to Trade (the TBT Agreement).  France must not be allowed to impose a ban on
imports and safe, modern uses of chrysotile as a response to public pressure.  That the ban does not
apply to man-made fibres produced in France, which the available scientific data show present greater
risks when their use is not controlled and which have not been proven safer, confirms that the basis for
the ban may be political and economic, but is not scientific or medical.
4.7 Brazil argues that in many respects, the French reaction is identical to that of the United States
Environmental Protection Agency (the EPA) prom ulgated in 1989, when it banned asbestos under
pressure from panicked U.S. public opinion.  The EPA was unable to justify its ban scientifically to
the United States Court of Appeals for the Fifth Circuit.  After lengthy legal proceedings, the Fifth
Circuit ordered the EPA to reverse its decision and to acknowledge publicly that modern productscontaining chrysotile enclosed in a matrix of cement or resin do not pose any detectable risk to public
health.
8  (Today, although amphiboles are prohibited in the United States, a number of products
containing non-brittle chrysotile are permitted, including the products manufactured by Brazil and
previously manufactured in France from Brazilian chrysotile.)  Unfortunately, France has adopted a
measure that unnecessarily and to no good effect impedes international trade.
4.8 Brazil makes the following claims regarding the ban: (1) the ban is inconsistent with
Article 2.2 of the TBT Agreement because it creates unnecessary obstacles to trade and is more trade
restrictive than necessary; (2) the ban is inconsistent with Article XI of the General Agreement on
                                                                                                                                                                    
In developing countries such as Brazil, the availability of low-cost, high-quality building and piping materials,
such as chrysotile-cement products, is crucial.  Substitu te products are more expensive and thus less available to
those who need them most.
7See Corrosion Proof Fittings v. EPA , 947 F.2d 1201, 1224, n.25 (5th Cir. 1991) ( Corrosion Proof)
(written testimony of Mr. Arnold Anderson, ASME).
8Id.WT/DS135/R
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Tariffs and Trade 1994 (GATT 1994) because it is a quantitative restriction that is not excused by the
exceptions in Article XI:2 or Article XX; (3) the ban is inconsistent with Article 2.8 of the
TBT Agreement because it applies to asbestos but not to man-made fibres or other substitute products
and thus operates as a technical regulation setting forth an unnecessary design or descriptive
characteristic; (4) the ban is inconsistent with Article 2.4 of the TBT Agreement because internationalstandards for producing and using chrysotile and chrysotile products exist and France should have
used them; (5) the ban is inconsistent with Article III:4 of the GATT 1994 and Article 2.1 of the
TBT Agreement (national treatment) because it does not apply to domestic man-made fibres and other
substitute products, which are like products to chrysotile; and (6) the ban is inconsistent with
Article I:1 of the GATT 1994 and Article 2.1 of the TBT Agreement (MFN) because, insofar as it
bans imports of chrysotile and chrysotile products, but not imported like product substitutes, it
improperly discriminates among imports.
2. Factual Aspects
4.9 Brazil concurs with practically all aspects of Canada's presentation, agreeing (i) that the
French ban was passed in response to public outcry in France over the deaths associated with the
intensive exposure to amphibole that had taken place early on in the century;  (ii) with the
circumstances and risks of exposure presented by Canada.  In particular, it agrees with the statementthat exposure, even in asbestos product plants, has decreased significantly and that, apart from existing
flocked amphibole, current exposure is limited, or could be limited, entirely to chrysotile;  in contrast,
past exposure and current exposure from past uses (e.g. flocking) included exposure to amphibole;
(iii) that current levels of exposure to modern uses of chrysotile are not significant and are not
associated with substantial health risks;  (iv) wi th the fact that current controlled-use policies and
standards which are accepted internationally are suffic ient to ensure the health of chrysotile workers
and others exposed to chrysotile and to guarantee their safety;  and, (v) with Canada's argument that
the INSERM Report has many defects and that it was not the reason for France's ban on modern,
controlled uses of chrysotile and chrysotile products.
4.10 Brazil considers that a "battle of experts", with one side presenting experts who support
banning chrysotile and the other presenting experts who oppose banning chrysotile would be, in this
case, both uninformative and unnecessary because the INSERM Report and the Synthesis
9, as a matter
of law, not fact, cannot support the ban.10  This Report and the Synthesis have several defects that
render them utterly incapable of supporting the ban.11  INSERM has not conducted original research,
but merely based itself on existing studies and, furthermore, it has not examined all existing studies as
it has deliberately excluded those that have established a distinction between chrysotile and
amphiboles.  More specifically, the shortcomings of the INSERM Report include the following.  First,the Report completely fails to examine the modern uses of chrysotile and chrysotile products and,
thus, ignores the current state of the industry.  Instead, it focuses on the health effects of exposure to
amphibole that took place in previous decades.  INSERM concedes that it does not have "direct,
certain scientific" data on the health risks associated with current levels of exposure to the modern
uses of any form of asbestos, much less chrysotile.
12  In short, INSERM does not examine current uses
and exposure levels and does not distinguish among the different levels of risk associated with the
                                                     
9INSERM , Rapport sur les effets sur la santé des prin cipaux types d'exposition à l'amiante, Expertise
collective INSERM, Paris, 1997, (hereinafter "INSERM Report");   INSERM , Effets Sur la Sante des Fibres de
Substitution à l’Amiante- Synthèse, Expetise collective INSERM,  Paris, 1998, (hereinafter "Synthesis").
10Brazil concurs with Canada that the weight of all available scientific evidence, including the
INSERM Report, leads to the conclusion that the ba n serves no purpose other than restricting trade.
11Brazil notes that, because it is only the INSERM  Report which preceded the ban, the ban must be
supported by the Report alone.  Brazil has discussed both the Synthesis and the Report because the former
underscores some of the defects of the latter.
12INSERM, (1998), Effets sur la sante des fibres de  substitution à l’amiante-synthèse , Paris, p. 226.WT/DS135/R
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different types of asbestos fibres (chrysotile, the only type produced and exported by Brazil, as well as
used in it, is accepted as being the safest of asbestos fibres, even by INSERM itself).13
4.11 Second, the INSERM Report fails to examine the efficiency of the ways in which worker
exposure has been reduced through the use of air filters in mines and plants14, and employing masks,
laundry services, etc.  Third, it does not even compare the risks of the past to the  risks associated withman-made fibres
15 and substitute products (such as ductile iron or polyvinyl chloride (PVC) pipes).16
By the time INSERM began to examine substitutes, the ban had already been in effect for 1.5 yearsand, in any case, INSERM issued only a synthesis and not a complete report on these substitutes.
INSERM concedes in its Report that it lacked the data required to recommend the banning of
chrysotile and only to allow its substitutes.
17  INSERM emphasizes that because it is the structure (size
and shape) of fibres that makes them toxic when inhaled, any substitute fibre must be viewed as
dangerous to human health.18  Finally, INSERM concedes that, although the health data it applied to
chrysotile are from past, massive and prolonged exposure to amphibole, the data being collected for
substitutes is based on much lower levels of exposu re, replicating modern conditions.  Most telling is
that INSERM states that toxicity levels for "asbestos" as a whole (and not merely for chrysotile)
would yield similar results to those obtained for substitutes if similar testing conditions had been
used.19
4.12 Brazil further argues that INSERM uses a linear risk model to assume illogically and without
any evidence that a threshold does not exist for safe exposure.20  France and INSERM are forced to
commit this methodological error (the assumption) due to the fact that they had data from past
prolonged exposure to amphibole but not to current, much lower exposure to chrysotile.21  To justify
                                                     
13Ibid., p. 409 ("France used asbestos much later and to a much lesser degree than other countries, and
doubtlessly the asbestos used contained a lower proportion of amphibole-type fibres.  Because of these
differences, it is not possible to simply transpose to Fr ance the results of projections concerning mesothelioma
[and cancer] cases prepared recently for Great Britain.").
14Brazil notes that the Cana Brava Mine, in Brazil, for example, has an exceedingly complex and
effective air filtration system.  The mine is the first and only asbestos mine in the world to have been certified ascomplying with ISO 14001.  It was certified by Det Norske Veritas of Rotterdam, the Netherlands.
15See, e.g., Cossette, M., Substitutes for Asbestos , 4 December 1998;  Anderson, A., Fibres in Friction
Materials , December 1998;  Davis, J.M.G., The Biological Effects of Fibr es Proposed as Substitutes for
Chrysotile Asbestos:  Current State of Knowledge  in 1998 , 1998; INSERM  Synthesis .  Brazil notes that these
studies demonstrate that substitute fibres, both when manufactured and used, are likely to present health riskssimilar to those from chrysotile.
16See Corrosion Proof , 947 F.2d pp. 1226-27 (even while banning asbestos, the EPA conceded that
ductile iron pipes and PVC pipes present health (cancer) risks "similar" to those presented by asbestos-cement
pipes).
17INSERM, Effets sur la sante des fibres de  substitution à l’amiante-synthèse , Paris, 1998, pp. 376 and
428.  Brazil notes that the European Commission has also recognized this as an important issue:  "There is a keyscientific issue which Member States and the Commission agree still needs to be clarified.  This is an assessmentof the relative risk posed by the substitutes in comparison to the risk posed by chrysotile."  Official Journal of
the European Communities, C 13/35 (18 January 1999) (11 June 1998, Answer of Mr. Bangemann to Written
Question P-1451/98 of Peter Skinner (PSE)).
18INSERM Synthesis, p. 2.
19Ibid., p. 33.
20According to Brazil, the assumption is contrary to logic because a threshold must exist given that
asbestos is ubiquitous in water and air.  Only those who have suffered intensive, prolonged, exposure have
contracted asbestos-related diseases.
21See also Asbestos in Public and Commercial Buildings:  A Literature Review and Synthesis of
Current Knowledge , Health Effects Institute - Asbestos Research  (1991) at pp. 6-9, para. 6.2.2 (Health hazards
caused by asbestos at levels encountered in buildings today are "on the order of 50,000 times lower thanindustrial exposure levels of the past.");  Report of the Royal Commission on Matters of Health and Safety
Arising from the Use of Asbestos in Ontario  (1984), Background Briefing Notes No.1 - "Health Effects of
Asbestos" (Current exposure of the general public is "thousands of times less" than occupational levels in theWT/DS135/R
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the ban on the modern uses of chrysotile, France /INSERM had to assume that significant risk is
present at all levels of exposure, even at those that are insignificant, out of political self-interest.
INSERM adopted the linear risk model despite the fact that studies cited by the
European Communities (hereinafter "EC") themselves indicate that " bricoleurs " are not at risk.  The
study conducted by Iwatsubo et al.22 indicates that low, sporadic, intermittent and cumulative
exposure of up to 0.5 fibres/ml-years does not present increased risk of mesothelioma.  In commenting
upon the results of an earlier study, the authors note that "no significant risk was observed for those
whose exposure was intermittent".
4.13 Brazil argues that a close examination of the INSERM Report reveals that:  (i) prolonged
exposure to amphibole (its past uses) is associated with severe health problems (a proposition with
which everyone agrees);  (ii) substitute fibres have similar structures and, thus, when subject to
scientific scrutiny, are expected to have similar health effects at similar levels of exposure;(iii) insufficient data exists on the health effect s of current levels of exposure to chrysotile and
substitute fibres, but the available data suggests th at their health effects would be the same;  and
(iv) the Report does not purport to be as conclusive as France would have all believe;  rather, to
overcome (iii) above, INSERM extrapolated from the data used in (i), which as it itself concedes
"does not produce scientifically certain knowledge, but only an aid to understanding the implicationsfor risk management.
23"  Brazil contends that the ban has been based on the irrelevant data described
above.  France employs the linear risk model as a tool to make data on past uses relevant to the
imposition of the ban.  However, INSERM researchers themselves recognize the limitations of this
model and clearly state that it cannot produce "scientifically certain knowledge," but can only serve as
an "aid to understanding," based on "plausible, though uncertain, estimates.24"  These "conclusions"
do not support significant trade restrictions, much less the ban.  Rather, they are merely a call for
further research.
4.14 Brazil argues that recent research focusing on uncontaminated chrysotile demonstrates why it
presents no health risks whatsoever.  According to Dr. David Bernstein's medical explanation25, the
serpentine (braided) structure of chrysotile leads it to unravel in the lungs (whereas the tubular
structure of amphibole and substitute fibres does not allow them to unravel and is unchanging);  and
once unravelled, the smaller and thinner particles are more easily and rapidly enveloped by
macrophages and/or expelled from the lungs.  Dr. Bernstein's research demonstrates that
uncontaminated Brazilian chrysotile of less than 20 microns (the length that has been associated with
pathogenicity for all fibres) is very quickly cleared.  The clearance half-time is 1.3 days (and is
2.4 days for fibres of a length of 5-20 microns).  He concludes that, once in the lung, chrysotile fibres
defibrillate (or unravel), breaking down into shorter fibres.  According to Dr. Bernstein, this result "isin stark contrast to amphibole asbestos where a portion of the fibres longer than 20 [microns] remains
indefinitely or with synthetic mineral fibres where even very soluble fibres are removed by dissolution
in the lung with half-times greater than this."
26  He concludes that uncontaminated chrysotile's lack of
bio-persistence suggests that it has "little if any toxicological effect."27  However, it is of course a fact
                                                                                                                                                                    
three decades during and after World War II (p. 3);  the best estimates are that exposure of current occupants of
asbestos-containing buildings "is 1,000 to 10,000 times lower than the average exposure of insulation workers inthe past" (Volume 2 p. 585).
22Iwatsubo Y. et al ., Pleural Mesothelioma:  Dose-Response Relation at Low Levels of Asbestos
Exposure in a French Population-based Case-Control Study , American Journal of Epidemiology, 1998,
Vol. 148, N° 2.
23INSERM Report, pp. 239 and 414..
24 Ibid.,  pp. 239 and 232.
25Bernstein D., Summary of the Final Report on the Chrysotile Bio-Persistence Study ,
Geneva, 2 October 1998 (document presented by Brazil to the Panel).
26Ibid., p. 4.
27Ibid., p. 10.WT/DS135/R
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that if used improperly, uncontaminated chrysotile could be dangerous, but that would be the case for
virtually all products in existence and not just chrysotile.
4.15 Brazil indicates that it mines, produces and exports only uncontaminated chrysotile and
chrysotile products, and subjects mining, production and use to strict regulations.  In 1990, it signed
the ILO Convention and Recommendation Concerning Safety in the Use of Asbestos (Convention 162and Recommendation 172).  To ensure safety in the mining, manufacture and use of chrysotile and
chrysotile products and to meet its ILO obligations, Brazil passed a primary law
28 and decree29 on
asbestos.  In addition, the production and use of chrysotile and chrysotile products is governed by
"national tripartite (government-industry-workers) agreements".  These set exposure limits, and
processes of production and safety procedures to be used to guarantee worker safety.  Finally, the
Brazilian Asbestos Association (ABRA), a watchd og organization comprised of asbestos producers
and sellers, further regulates the safety of, and trade in, chrysotile and chrysotile products.
4.16 Brazil explains that the ILO Convention and Recommendation are international standards that
establish safety procedures for the handling of chrysotile and chrysotile products.  They follow the
ILO Code of Practice on Safety in the Use of Asbestos.30  The goal of the Code is to prevent the risks
of exposure to asbestos and its harmful effects and to provide practical control procedures for its use.
Convention 162 and Recommendation 172 recommend the controlled and safe use of asbestos.  Theirwording clearly indicates that the replacement of asbestos fibres should only take place when it is
established that this is necessary to protect worker health and when replacement is technically
feasible.  The replacement of chrysotile asbestos fibres contained in modern materials or products (i.e.
where it is sealed in a matrix and cannot be released  into the environment) is not necessary since these
products do not pose any detectable health risks.  International standards, such as Convention 162 andRecommendation 172, recommend the regulation of asbestos on the basis of the type of asbestos fibre
employed, the products in which certain fibres are included, and their planned use.  Thus,
Convention 162 and Recommendation 172 stipulate the prohibition of crocidolite and materials
containing friable asbestos for flocking
31, but permit many uses of chrysotile, including those central
to this dispute (asbestos-cement and friction products).  They allow countries to prohibit other specificuses if national authorities deem this necessary for worker protection, but only on condition that
substitute products be subjected to a thorough scientific examination of their health effects.
32
4.17 In 1995, Brazil passed Law No. 9055 to discipline the extraction, industrialization, use,
commercialization and transportation of asbestos an d of asbestos-containing products, as well as of
natural and synthetic fibres of any source used for the same purpose.  The Law (i) bans the processing
and use of all types of asbestos, except chrysotile and chrysotile-containing products;  (ii) bans the
crushing and spraying (flocking) of all types of asbestos, including chrysotile, and of all substitutefibres;  (iii) provides the framework for the triparti te agreements in that it sets deadlines for the
government's confiscation of the operating licences of companies that do not execute the tripartite
agreements, establishes medical inspection requirements for workers, and sets exposure limits for
those who work with chrysotile and substitute fi bres subject to annual reduction.  (In compliance with
Article 2.4 of the TBT Agreement, the exposure limits are determined based, in part, on therecommendations of "international entities which are scientifically accredited");  (iv) prohibits miners
                                                     
28Brazilian Law No. 9055 of 1 July 1995.
29Brazilian Decree No. 2350 of 15 October 1997.
30Safety in the Use of Asbestos , Code of Practice, International Labour Organization, Geneva, 1990.
31Convention 162, Article 12.
32Article 12 of Recommendation 172 states:
(1) The competent authority, wherever necessary for the protection of the workers, should require the
replacement of asbestos by substitute materials, wherever possible.
(2) Before being  accepted for use in any process, all potential substitute materials should be thoroughly
evaluated  for their possible harmful effects  on health.  The health of workers exposed to such materials should
be continuously supervised, if judged necessary.  (Emphasis added.)WT/DS135/R
Page 201
and wholesalers from supplying chrysotile or substitu te fibres to companies that do not comply with
all provisions of the Law;  (v) applies special restrictions to the use of chrysotile and substitutes in
products currently considered to be the riskiest, such as  textiles;  (vi) calls for research into the health
effects of chrysotile and substitute fibres and provides financing for the effort;  and (vii) provides for
prompt Department of Justice action against infractions.
4.18 Brazilian Decree No. 2350 implements the Law, and (i) requires that prior to marketing, all
products containing chrysotile of imported or national origin bear a "seal of compliance to the
Brazilian System of Certification", and provides for the development of the certification system;
(ii) requires research into and confirmation of the health effects of chrysotile and its substitutes;
(iii) establishes additional requirements for the tripartite agreements which apply to all mines and
companies producing chrysotile and chrysotile products;  (iv) establishes requirements for monitoring
and controlling the use of chrysotile and its substitutes, and ensures that a record is kept of theexposure measurements made by companies while guaranteeing access to them;  and (v) establishes a
permanent National Commission on Amianthus (NCA) to ensure the safety of workers involved in the
chrysotile or substitute fibre industry.  The Decree also establishes certain bodies, such as the NCA,
composed of government  and industry officials as well as workers, to ensure worker safety.
4.19 The tripartite agreements (otherwise known as The National Agreements for the Furtherance
of the Safe Use of Asbestos ) are required by both the Law and Decree.  They are executed by the
Federal Government of Brazil, the industries involved (e.g. the mining or asbestos-cement industry)
and the workers in the industry (through their unions).  They establish mandatory medical procedures
inspection and safety measures, as well as exposure limits.  They also give workers certain rights, both
individual and collective, within their industries.  Their objective is to continuously work towardsimproved worker safety and to decrease exposure limits as well as actual exposure.  First, tripartite
agreements set the maximum permissible exposure limits to 0.30f/cm3, with 50 per cent of all
measurements being below 0.10 f/cm3 (and without there being any constant exposure
above 0.3 f/cm3, even when the workers exposed have special breathing equipment).  Second, they
require the use of specific "collective protection" procedures to protect workers.  The procedures areto include the installation of air filter and exhaust systems, the use of wet processes in the handling of
chrysotile (which reduces dust release and, thus, exposure), the sealing of workspaces and processes to
limit exposure, the demarcation of areas of exposure for warning, the prohibition of dry sandpapering
processes, the implementation of a daily programme for the washing, wetting or vacuum cleaning of
production sites, and provisions for a change of work clothes (which may not be taken off site), of
laundry services and showers for employees.  Third, the agreements require employers to provide
workers with individual protection equipment that complies with relevant standards.  Fourth, they alsorequire them to conduct regular and detailed environmental evaluations of working conditions as well
as to medically inspect their employees.  All results are to be filed with the Control Commission on
the Safe Use of Asbestos and with the Brazil ian Asbestos Association, known as ABRA.  The
Control Commission is comprised of plant workers elected by their peers.  Fifth, they require the
provision of worker education programmes to communi cate the health risks of exposure to chrysotile,
the measures which can be taken to reduce exposure, and the "multiplier effect" which tobacco
smoking has on exposure.  Sixth, they make ABRA  responsible for providing the companies with
technical assistance regarding controls and preventive measures.
4.20 Founded in 1984, ABRA is an industry watchdog group composed of companies from Brazil's
asbestos industry.  Its main goal is to oversee industrial activity in order to ensure that ABRAmembers comply with the Law, the Decree and the tripartite agreements, as well as to educate
workers, wholesalers and end-users of chrysotile asbestos and asbestos products on safe use.  To
accomplish this goal, ABRA has an extensive, independent, monitoring programme.  Biannually, it
conducts spot measurements at the facilities of its members.  It maintains an ISO 9000-certified
laboratory and sends control samples once a year to independent laboratories in Edinburgh (AFRICA)and Paris (LHCF) to ensure the accuracy of its m easurements.  If the company that has been testedWT/DS135/R
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fails to meet the applicable exposure limits, ABRA sends it a letter and informs its suppliers.  It then
provides the company with a maximum number of  days in which to comply, and instructs its
suppliers  to withhold chrysotile and/or chrysotile  products from the company until it is able to notify
its compliance.  The agreement restates the requirements of both the Law and Decree, and develops
certain safety procedures.  In exchange for compliance (and dues), ABRA serves as a low-costrepository for state-of-the-art safe-use technologies, covering areas such as plant, air filter and process
design.  It attempts to encourage as well as facilitate safe use, with its overarching objective being to
regulate the industry in such a manner as to render additional government regulation unnecessary.
The regulatory regime (consisting of the Law, the tripartite agreements and ABRA itself), aligns the
self-interests of the industry with those of its wo rkers.  The industry and the workers individually, as
well as through Safety Commissions and Unions, cooperate to reduce health risks.  The result of this
cooperation has been the creation of an extremely safe workplace with very low exposure levels.  Ingeneral, this system encourages individual plants to exceed applicable requirements in order to
guarantee worker and user safety.  At the Capivari Asbestos Cement Plant, which is the largest
chrysotile-cement plant in South America, the on-site doctor did not report a single case of asbestos-
related disease among the employees whose contact with asbestos had been limited to the plant.
4.21 With respect to regulation of asbestos in the United States, Brazil asserts that, in response to
public outcry based on sensationalist media reports on the dangers of asbestos, the
Environmental Protection Agency (EPA) banned asbestos in 1989.
33  It prohibited "at staged intervals,
the future manufacture, importation, processing, and distribution in commerce of asbestos in almost
all products […]".  In reaction, a United States company that manufactured asbestos pipes, Corrosion
Proof Fittings, filed suit against EPA arguing that the ban was not based on scientific and medicalinformation.  In a 1991 decision, the United States Court of Appeals for the Fifth Circuit called for the
lifting of the ban and ordered EPA to issue new rules grounded in science.
34  The Fifth Circuit
concluded that EPA had presented "insufficient evidence to justify its asbestos ban." 35  Specifically, it
found that the EPA had failed to (i) consider all of the necessary and relevant evidence, and (ii) "give
adequate weight to statutory language requiring it to promulgate the least burdensome, reasonableregulation" that would protect human health.
36  Similarly, France has failed to (i) examine existing
evidence on the modern, controlled uses of chrysotile, (ii) assess the danger associated with substitute
products, and (iii) impose a regulation that is not more restrictive than necessary.  In 1993, EPA lifted
the ban and issued new provisions regulating the production and use of asbestos and asbestos
products.37  Based on a thorough scientific and medical review, EPA then authorized more asbestos
products (18) than it banned (6).  None of the uses that are banned are at issue in this proceeding.  Of
the authorized uses, two are central to Brazil's exports to France and had previously been allowed(they include chrysotile-cement products and chrysotile friction materials).
38  Under existing
regulations, the United States produced 6,890 metric tonnes of chrysotile and
imported 20,900 metric tonnes in 1997.39  In the same year, it consumed nearly 21,000 metric tonnes
of chrysotile, exported unmanufactured fibre for a total value of US$5,690,000 and manufactured
products for a total of US$197,000,000.40  Public health has not suffered in the United States and
public outcry did not resume.  United States regulations ban the dangerous uses of asbestos, and
regulate those that are safe.
                                                     
33EPA Final Rule, 54 Fed. Reg. 29460 (1989).
34Corrosion Proof v. EPA , 947 F.2d 1201 (5th Circuit 1991).
35Ibid., p. 1215.
36Ibid.
37EPA Final Rule, 58 Fed. Reg. 58964 (1993).
38The current US regulations on this topic are set forth at 40 C.F.R. part 763, Sub-Part I (1998).
39United States Government Geological Survey, Minerals Yearbook 1997, Volume I at 4-5.
40Ibid.WT/DS135/R
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3. Legal Aspects
4.22 Brazil argued that, as it turns to Brazil's legal arguments, the Panel should recall Brazil's
complex system of regulation that ensures public safety.  The Panel should serve the same role
regarding France's political decision which the Fifth Circuit served regarding EPA's political decision
- that of a neutral arbitrator.  Brazil understands that the Corrosion Proof  decision does not in the least
bind the Panel - the procedures, legal standards and status of the parties are quite distinct.  However,
the court there faced similar circumstances and issues, and in the face of contrary public sentiment,
issued a very focused, well-reasoned opinion, which is precisely what Brazil seeks here.
(a) The Agreement on Technical Barriers to Trade
(i) Article 12 of the TBT Agreement
4.23 Brazil argues that a prohibition of the trade and use of a product, such as France's ban, is the
most restrictive of all possible trade measures and must be closely scrutinized by the Panel.  Itrequests the Panel to devote particular attention to the ban on imports from Brazil, which is a
developing country (and from Zimbabwe, a least-developed country).  In general, WTO agreements
provide for the special and differential treatment of developing and least-developed country exports.
In the context of the TBT Agreement, special provisions are set forth in Article 12, which obliges
Members that are developing technical regulations and standards to consider the special needs ofdeveloping and least-developed countries and to provide them with differential treatment.  Article 12.2
obliges France to "take into account the special deve lopment, financial and trade needs" of developing
countries and of least-developed countries, when developing its technical regulations.  France did not
meet this obligation.  Rather, it adopted an outright ban that advantages French producers of substitute
fibres and products to the detriment of Brazil's chrysotile and chrysotile product producers (and toZimbabwe's detriment as well).  Moreover, the ban has not contributed to improving public health in
France.
4.24 France violated Article 12.3 which covers the "preparation and application" of technical
regulations and standards.  Article 12.3 requires France to ensure that its technical regulations "do not
create unnecessary obstacles to exports" from developing countries such as Brazil (and fromleast-developed countries such as Zimbabwe).  However, France's ban applies to Brazilian (and
Zimbabwean) exports and creates, to say the least, an "obstacle" to their trade.  The obstacle is
"unnecessary" because it does not contribute to the supposed objective of increasing safety.  The only
trade permissible under the ban is that of chrysotile and chrysotile product substitutes.  The risks
associated with substitute fibres are unknown, but they are suspect.  Meanwhile the risks associated
with the modern, controlled uses of chrysotile, are zero.
(ii) Article 2.2 of the TBT Agreement
4.25 Brazil argues that the ban is inconsistent with Article 2.2 of the TBT Agreement because it is
more trade restrictive than necessary to fulfil a legitimate objective.  Once it is established that the
Decree is a "technical regulation", the EC must demonstrate (and have the burden of proving) that four
different conditions have been met if they are to argue that the ban is in fact consistent with
Article 2.2.
41  To defend the ban, the EC must demonstrate to the satisfaction of the Panel that (i) the
objective of the ban is "legitimate", (ii) that it "fulfils" this legitimate objective, (iii) that it is not
                                                     
41According to Brazil, general rules of pleading, but also Article 2.5 of the TBT Agreement confirm
that France has the burden of justifying its trade restric tive measure.  According to Ar ticle 2.5, a standard shall
be "rebuttably presumed not to create an unnecessary obs tacle to trade" when it pursues a legitimate objective
and is "in accordance with relevant international standard s."  France cannot take advantage of this exception to
normal rules of pleading because, as demonstrated below , the ban is contrary to relevant international standards.WT/DS135/R
Page 204
"more trade restrictive than necessary" to fulfil the legitimate objective, and (iv) that France evaluated
the health effects (i.e. "the risks non-fulfilment would create") on the basis of "available scientific and
technical information".  According to Brazil, the ban meets only the first of these four conditions.
4.26 Brazil argues that the Decree is a "technical regulation" within the meaning of the
TBT Agreement.  The ban sets out certain (i) product characteristics, (ii) process and productionmethods, (iii) administrative provisions, as well as (iv) packaging, marking and labelling requirements
with which compliance is mandatory.  Article 1 of the Decree prohibits the production, importation,
exportation, manufacture, transformation, sale and offer for sale of all types of asbestos fibres and
asbestos-containing products (except those temporarily excepted from the ban by virtue of Article 2.I).
Thus, the ban is explicitly directed at product characteristics (asbestos and asbestos-containing
products) and at process and production method s (all forms of production, manufacture and
transformation of asbestos and asbestos-containi ng products).  Both the prohibition imposed by
Article 1 and the procedures for implementing and re viewing the entitlement to the exceptions set out
in Articles 2.II and 3 of the Decree are "applicable administrative provisions" relating to product
characteristics and process and production methods.  Article 4 of the Decree prescribes certain
marking and labelling requirements for those few asbestos-containing products excepted under
Article 2.  Compliance with the ban is mandatory and violations are penalized under Article 5.  Brazilargues that both France and the EC have conceded that the Decree is a technical regulation.  In WTO
document G/TBT/Notif.97.55, dated 21 February 1997, the French Government notified the ban to the
TBT Committee as a technical regulation.  Paragraph 3 of the Notification indicates that the ban was
being notified under Articles 2.9.2 and 2.10.1 of the TBT Agreement, both of which establish
notification obligations for technical regulations.  The European Commission has also recognized that
the ban is a technical regulation both in a 15 April 1997 document justifying the French ban and
during the 8 July 1998 consultations on this dispute.  Therefore, both France and the EC concede that
the ban falls within the scope of paragraph 1 of Annex 1 of the TBT Agreement and is a technical
regulation.
4.27 Brazil does not contest that the objective of protecting the health of French workers and
consumers is a "legitimate objective" within the meaning of Article 2.2 of the TBT Agreement.
However, it argues that the ban imposed by the Decree creates an unnecessary obstacle to trade.  It
does not in reality fulfil its stated objective, and is more trade-restrictive than necessary to protect the
health of French workers and consumers.  In us ing the word "fulfil" (as in the requirement that
"technical regulations shall not be more trade-restrictive than necessary to fulfil a legitimate
objective"), the text of Article 2.2 requires the existence of a rational link between the regulation and
its stated objective.
42  However, this rational link is absent as the ban does nothing to accomplish its
objective.  It does not make those who are now sick healthy and removing it would not make any of
those now healthy, sick.  The lack of a rational link between the ban and its purported objective is
demonstrated by the following:  (i) that asbestos-related health risks are due to old and already
prohibited uses of asbestos;  (ii) that there are no detectable health risks associated with modern uses
                                                     
42Brazil notes that, while no WTO panel or Appellate Body reports have addressed this issue under the
TBT Agreement, relevant precedents under the SPS Agreement exist:  In Japan - Apples , the Appellate Body
found that an SPS measure was justified only if the Member imposing the measure demonstrated a "rationalrelationship" between the SPS measure and available scientific information.  Japan - Measures Affecting
Agricultural Products  (22 February 1999), WT/DS76/AB/R, para. 84;  similarly, in EC - Hormones , the
Appellate Body required the EC to establish "an objective relationship between two elements, that is to say, anobjective situation that persists and is observable between an SPS measure and a risk assessment."EC - Measures Concerning Meat and Meat Products (Hormones)  (16 January 1998), WT/DS26/AB/R,
para. 189;  the Appellate Body has also held that a finding that an SPS measure is not based on an actualassessment of health risks is "a strong indication" that th e measure does not really protect health but is instead "a
trade-restrictive measure in the guise of an SPS measure."  Australia - Measures Affecting Importation of
Salmon  (20 October 1998), WT/DS18/AB/R, para. 166.  This is precisely the case with the ban.WT/DS135/R
Page 205
of chrysotile;  and (iii) that health risks associated with substitute fibres remain unknown and are
suspect.
4.28 Brazil asserts that the health risks addressed in the INSERM Report are based on past
exposure to high levels of asbestos fibres (largely  amphiboles) and to exposure to old uses of asbestos,
such as flocking.  In prohibiting future importation and sale of chrysotile and modern chrysotile-containing products, the ban does nothing to addre ss the effects (today) of exposure between 1940 and
the early 1960s to extremely high levels of asbestos, mainly amphibole fibres.  It does not cure
workers who now suffer because of long-term exposure in the past to amphibole, the use of which was
banned in France in 1994, or to unregulated concentrations of fibres that are "50,000 times" higher
than the modern-day internationally reco gnized controlled-use level of 1 f/ml.
43  Likewise, prohibiting
the future importation and sale of chrysotile and modern chrysotile-containing products does nothing
to address the effects of exposure to (or the disturbance of) friable asbestos, mainly amphibole, inFrench buildings prior to the 1978 French ban on flocking.  This was recognized by
European Commissioner, Mr. Bangemann, who, in response to a question posed by the European
Parliament, responded that  "[I]t is important to mention that a new ban would not lead to a lower risk
of exposure to existing asbestos for workers, nor would it reduce the number of deaths from past
exposure to asbestos."
44
4.29 Brazil maintains that there are no detectable health risks associated with modern uses of
chrysotile.  There is no rational link between the ban and its purported objective because modern uses
of uncontaminated chrysotile are safe.  Prior to the ban, more than 90 per cent of the chrysotile
imported into France was used in the manufacture of chrysotile-cement products.45 Currently, the
chrysotile is bound to the cement and encapsulated in it, without there being any loose or friablefibres.  Furthermore, most chrysotile-cement products are produced in such a way that sawing or
drilling are unnecessary, and in the few instances when either or both are required, widely recognized
and well-established procedures have been developed for these tasks which prevent fibre release.
46
Similarly, in all other modern uses of chrysotile, the fibres are sealed, bonded or encapsulated in theproduct.  In no instance are loose, friable fibres allowed to be.  Brazil contends that France does nothave credible evidence to suggest that (i) sealed, bonded or encapsulated chrysotile poses a health risk,
(ii) concentrations of chrysotile fibres at or below the internationally-recognized controlled use level
of 1 f/ml present a health risk, and (iii) controls do not eradicate all risk throughout a product's life-
cycle (from mining to manufacture, distribution, sale and use, and eventual disposal).  On the other
hand, much science-based research concludes that the level of chrysotile encountered in the workplace
today, or in buildings, presents no detectable health risk.  After an exhaustive study of the existing
scientific literature, the Health Effects Institute concluded in 1991 that the health hazards created byasbestos at the levels commonly encountered today are "unlikely to be large enough to be actually
                                                     
43Health Effects Institute – Asbestos Research, Asbestos in Public and Commercial Buildings:  A
Literature Review and Synthesis of Current Knowledge , Cambridge, 1991, pp. 6-9 .
44Official Journal of the European Communities, C 13/123 (18 January 1999) (24 July 1998 answer of
Mr.  Bangemann to Written Question E-1950/98 of Anita Pollack (PSE)).
45Le Déaut J.-Y. and Revol H., L’amiante dans l’environnement de l’homme:  ses conséquences
et son avenir , Office parlementaire d'évaluation des choix scientifiques et technologiques,
Assemblée nationale no. 329 / Sénat no. 41, 16 October 1997.
46ISO 7337, §§ 4 and 5 (pp. 2-9):  Brazil notes that th e cutting of plates or tiles for roofing is not a
source of emission if ISO-7337 is followed.  ISO-7337 addresses the use of chains to break pipes throughpressure, low-speed saws, saws equipped with a vacuum dust extractor, and, also, proper wetting of the materialsprior to any action.  The cutting or grinding of all cement pipe (even that which does not contain chrysotile)emits silica in the air, in the absence of proper controls .  The International Association for Research on Cancer
(IARC) rates silica as a Type 1 carcinogen (for man), like asbestos.  The worker who cuts any cement pipe
therefore has an interest in following ISO-7337.WT/DS135/R
Page 206
observed and measured.47" This conclusion (which was reached by an independent United States
health watchdog), confirmed the 1984 findings of the Ontario Royal Commission.48  Similarly, in the
case brought by Corrosion Proof Fittings against the EPA, the Fifth Circuit made the following
comment on the risk of asbestos products relative to toothpicks:
"As the petitioners point out, the EPA regularly rejects, as unjustified, regulations that would
save more lives at less cost.  For example, over the next 13 years, we can expect more than a
dozen deaths from ingested toothpicks  - a death toll more than twice what the EPA predicts will
flow from the quarter-billion-dollar bans of asbestos pipe, shingles, and roof coatings."49
Brazil concludes that, because there are no detectable risks attributable to modern uses of chrysotile,
there is no rational link between the French ban and its purported objective.
4.30 Brazil asserts that the French ban induces consumers to use chrysotile substitutes, whose
health risks are unknown, in place of chrysotile , whose risks are known.  In his 1998 paper on the
biological effects of substitute fibres, Dr. J. M. G. Davis concluded that "replacement [of chrysotile by
substitute fibres] is premature in the present state of our knowledge ....  The need for full toxicology
testing of new fibre products is recommended before these products are marketed."50  This conclusion
was shared by the European Communities Directorate General for Consumer Protection Policies,
which stated that "there is no significant epidemiology base to judge the human health risks [ofsubstitute fibres] … hence the conclusion that [the uses of] specific substitute materials pose a
substantially lower risk to human health, particularly public health, than the current use of chrysotile,
is not well founded … ".
51  The INSERM Report itself acknowledges that the risks associated with
substitute fibres are unknown.  INSERM "urgently"  cautions against their use until further scientific
tests are conducted.  It states that "[T]he absence of epidemiological data concerning the long-term
safety of these substitute products should not obscure the results of experimental systems indicating
the possibility that pathological modifications could result.  It is urgently important that suitableresearch into this area be conducted prior to the widespread use of substitute fibres."
52  Despite this
urgent warning from its own experts, the French Government banned chrysotile and not its substitutes
the day after it received the INSERM Report.  Thus, the French Government knowingly shifted
consumption from chrysotile used in modern ways, and for which there is no detectable health risk, to
substitute fibres for which "experimental systems indicate the possibility that pathologicalmodifications could result".  Brazil concludes, therefore, that the ban does not "fulfil" a legitimate
objective as required by Article 2.2 of the TBT Agreement.  The rational link between the ban and its
stated health objective does not exist because, as demonstrated above, (i) asbestos-related health risks
are due to old, already prohibited, uses of asbestos, and not to the modern uses of chrysotile, (ii) no
detectable health risks are associated with the modern uses of chrysotile, and (iii) substitute fibres,whose health risks are unknown, will replace chrysotile.
4.31 Brazil further argues that even if there were a rational link between the ban and the purported
objective, the French ban would nonetheless be inconsistent with Article 2.2 of the TBT Agreement
                                                     
47Health Effects Institute – Asbestos Research, Asbestos in Public and Commercial Buildings:  A
Literature Review and Synthesis of Current Knowledge , Cambridge, 1991, pp. 6-9 .
48Report of the Royal Commission on Matters of Health and Safety Arising from the Use of Asbestos in
Ontario (1984), vol. 2, p. 585.
49Corrosion Proof v. EPA,  947 F.2d 1201 (5th Circuit 1991.  See also L. Budnick, Toothpick-Related
Injuries in the United States, 1979 Through 1982 , 252 J. Am. Med. Ass’n., 10 Aug. 1984, p. 796 (which shows
that toothpick-related deaths av erage approximately one per year).
50Davis J.M.G., The Biological Effects of Fi bres Proposed as Substitutes for Chrysotile Asbestos:
Current State of Knowledge in 1998 , p. 1 and 5.
51European Commission, DG XXIV, Opinion on a Study Commissioned by Directorate General III on
Recent Assessments of Hazards and Risks Posed by Asbestos and Substitute Fibres (9 February 1998), p. 1.
52INSERM Report, p. 434.WT/DS135/R
Page 207
because it is "more trade-restrictive than necessary to fulfil a legitimate objective, taking account of
the risks non-fulfilment would create.53"  A ban is the most trade-restrictive measure possible.  It
could be justified only if France were able to prove that there was no reasonably available, less trade-
restrictive, alternative.  France cannot do so.  Controlled use policies demonstrably fulfil the objective
of protecting the health and safety of French workers and consumers.  In assessing whether the ban ismore trade-restrictive than necessary, within the meaning of Article 2.2, the Panel should examine
both the risks of non-fulfilment and whether a less trade-restrictive measure is available to fulfil the
objective.
4.32 Brazil argues that available scientific and technical information does not support the
imposition of the ban.  Article 2.2 provides that, in assessing the risk that a technical regulation is
meant to address, Panels should consider, inter alia , relevant scientific and technical information,
related processing technology and intended end uses of products.  The risk to be avoided in the disputeat hand is the risk of illness resulting from exposure to (a) modern uses of chrysotile and chrysotile-
containing products and (b) the disturbance of previously installed friable asbestos (largely
amphibole) in buildings.  Illnesses associated with old, previously banned, uses of asbestos are not
relevant to this analysis.  Moreover, they cannot be addressed through the present ban on trade,
domestic sale and use.  The INSERM Report, which provides the supposed scientific justification forthe ban, does not assess the health effects of current levels of exposure to modern uses of chrysotile.
To determine the health risk associated with exposure to low levels of bonded, sealed and
encapsulated chrysotile in chrysotile-cement and other modern applications, it applies the same risk of
exposure associated in previous decades with higher levels of exposure to friable asbestos (largely
amphibole).  There is no scientific logic for such an extrapolation.  The INSERM Report itselfconcedes that its conclusions are not "scientifically certain"  but are merely "plausible, though
uncertain, estimates".  Several other scientific reports concur that there is no detectable health risk
from modern uses of chrysotile.
54
4.33 Brazil explains that all modern-day uses of chrysotile involve bonding, sealing or
encapsulation.  Such uses, or modern products, do not contain loose, friable chrysotile fibres – whichwere the cause of past asbestos-related illnesses.  The risk associated with modern use is undetectable.
Most modern products are manufactured to specifications well known in the building and public
works trades,  so that sawing or drilling operations are seldom necessary.  When sawing or drilling are
necessary, there are well-established procedures to ensure that workers are not exposed to fibre
release.  Thus, Brazil argues that neither available scientific information, intended end-uses nor
processing technology,  necessitate a ban on chrysotile.  Brazil argues that while the term "necessary"
has not yet been interpreted in the context of Ar ticle 2.2 of the TBT Agreement, the interpretation
provided by the Panel in the case on Section 337 of the Tariff Act of 1930   is instructive:
"[I]t was clear to the Panel that a contracting party cannot justify a measure inconsistent with
another GATT provision as 'necessary' in terms of Article XX:(d) if an alternative measurewhich it could reasonably be expected to employ and which is not inconsistent with otherGATT provisions is available to it.  By the same token, in cases where a measure consistent with
other GATT provisions is not reasonably available, a contracting party is bound to use, among
the measures reasonably available to it, that which entails the least degree of inconsistency withother GATT provisions."
55
                                                     
53Brazil notes that, similarly, under the SPS Agreement, in determining whether an SPS measure is
more trade-restrictive than required, the authorities must evaluate whether an alternative, less trade-restrictive,SPS measure would achieve the importing country’s appropriate level of protection.  See Australia - Measures
Affecting Importation of Salmon  (20 October 1998), WT/DS18/AB/R, paras. 208-210.
54See paragraph 4.29 above, regarding the conclusions of the American Health Effects Institute, the
Royal Commission and the U. S. Court of Appeals for the Fifth Circuit.
55United States – Section 337 of the Tariff Act of 1930,  adopted on 7 November 1989, BISD 36S/345,
pp. 392-93, para. 5.26.WT/DS135/R
Page 208
4.34 Brazil argues that the focus is on the range of measures "reasonably available" to France.  Just
as under Article XX(d), under Article 2.2 of the TBT Agreement, the French ban cannot be justified as
"necessary" since a less trade-restrictive measure that fulfils the legitimate objective is available.
There are numerous examples of controlled use that are both readily available and effective inaddressing the health risks associated with the mode rn uses of chrysotile.  First, the ILO Convention
and Recommendation Concerning Safety in the Use of Asbestos (Convention 162 and
Recommendation 172) establish procedures to ensu re safety in the handling of chrysotile and
chrysotile products.  Second, the ILO's 1990 Code of Practice on Safety in the Use of Asbestos details
appropriate controlled use procedures to ensure worker safety with respect to all chrysotile-containing
products currently in use.  Third, Brazil, the United States and Canada have demonstrated that
controlled-use policy is effective in eliminating th e health risks attributable to the modern uses of
chrysotile.  Controlled use policy is less restrictive than a ban.  Trade and sales are permitted as long
as appropriate safety measures are employed in the manufacture, installation and use of chrysotile-
containing products.  While complying with safety regulations could be expensive for firms, the
decision of whether or not to use chrysotile or substitutes under the safety regulations should be
determined by the marketplace and not by government.  Given the availability of controlled use policyand its effectiveness in addressing the legitimate public health objective which France wishes to
achieve, the ban is inconsistent with Article 2.2 in that it is more trade-restrictive than necessary to
fulfil its objective.
(iii) Article 2.4 of the TBT Agreement
4.35 Brazil contends that the French ban is inconsistent with Article 2.4 of the TBT Agreement
because it ignores appropriate and effective international standards.  Article 2.4 obliges France to base
its technical regulations on existing international standards, or on any "parts of them", that would be
effective and appropriate in any given circumstance.  France violated this obligation when it banned
chrysotile and chrysotile products, ignoring existing international standards that would have been both
appropriate and effective.  To establish that France has not violated Article 2.4, the EC must showthat:  (i) there are no international standards that apply to asbestos;  (ii) if international standards exist,
that the ban is consistent with them;  or (iii) if international standards exist and the ban is inconsistent
with them, that the international standards would not have been an effective or appropriate means of
accomplishing France's stated objective.  The EC cannot make such arguments.
4.36 Brazil argues that a number of international standards apply to  chrysotile and chrysotile
products, including ILO Convention 162 and Recommendation 172, on the types of asbestos that can
be used (only chrysotile) and how, and the International Organization for Standardization's (ISO) 7337standard, entitled Chrysotile Cement Products Guidelines for On-Site Work, regarding the proper
installation and use of chrysotile-cement products.  The fact that the ISO 7337 standard is an
applicable international standard is beyond doubt.  Annexes 1 and 3 to the TBT Agreement expressly
recognize the authority and status of ISO as an international standard-setting body, and the ISO 7337
standard directly governs the primary chrysotile product group.  Each of these documents state thatchrysotile products may be manufactured and used, but only under controlled conditions and in
modern applications.  Each of the standards sets out specific controls to guarantee the safety of
workers and end-users.  They have been incorporated into Brazilian legislation as well as that of many
other countries, including the United States and Canada.  The ban is inconsistent with these
international standards because it bans all imports, manufacture, use, etc., of chrysotile and chrysotileproducts, whereas these permit their use in modern applications.  They only subject them to safety
controls.  Current international standards provide an effective and appropriate means of fulfilling
France's stated objective and the EC cannot argue otherwise.  ILO and ISO standards are "appropriate"
for France's stated objective since they were specifically drafted to protect the health of industrial
workers, the general public and others who may come into contact with asbestos.  ILO and ISOstandards would also be "effective" in achieving France's stated objective since they have successfullyWT/DS135/R
Page 209
protected human health in economies as diverse as those of Brazil, the United States and Canada.  The
EC would be hard pressed to provide evidence of a deterioration in the health of citizens from Brazil,
the United States or Canada due to adherence to ILO or ISO standards.
4.37 Brazil states that a closer examination of the term "ineffective and inappropriate means" is
justified.  The text of Article 2.4 clarifies that this exception is to be quite narrowly construed andapplied.  Were it not to be so, Article 2.4 would be rendered useless.
56  Members would all too easily
claim that the applicable international standard was "inappropriate".  Second, the Article provides
examples of the situations in which exceptions to the use of international standards are allowed.
These include when an international standard would be ineffective or inappropriate due to
fundamental climatic or geographical factors or fundamental technological problems.  Thus, a
Member may ignore an international standard only if the standard will not achieve the results it seeks
because of its unique conditions in terms of climate, geography, or its economy (i.e. level oftechnological development).  No such conditions exist in France.  The EC would be unable to present
any evidence to suggest that different conditions apply to France so as to make the standards followed
by Brazil, the United States and Canada inappropriate or ineffective for it.  France ignored ILO and
ISO standards because it wished to ban chrysotile to appease public opinion and advantage
domestically-produced and substitute products.
(iv) Article 2.8 of the TBT Agreement
4.38 Brazil argues that the French ban is inconsistent with Article 2.8 of the TBT Agreement
because it establishes design requirements for products.  France's ban is inconsistent with this
obligation because, by prohibiting chrysotile and its use in any product, the ban sets out an
impermissible "design or descriptive characteristic". To establish that France has not violatedArticle 2.8, the EC must demonstrate that (i) the ban is a performance requirement;  or, in this case,
(ii) that adopting a performance requirement woul d not have been "appropriate".  The Communities
can demonstrate neither of these points.  The ban sets out an impermissible "design or descriptive
characteristic" because it regulates on the basis of the content and description of a product.  France has
banned chrysotile and products containing it but has not banned competing fibres and products thatcontain them.  Therefore, the ban advantages French-produced substitute fibres, products which are
"like"
57 chrysotile, and chrysotile containing products.  The ban does not contain regulations based on
the performance of a product.  Rather, it states that certain products may be imported and sold only if
they do not contain a certain input, namely chrysotile.  Article 2.8 obliges France to adopt a
performance requirement "whenever possible".  In the case of chrysotile, France could have adopted
any of a number of performance requirements that would have enabled it to achieve its stated
objective.
4.39 According to Brazil, France could have adopte d, for example, detailed regulations regarding
the importation, production, modern use and disposal of chrysotile and substitute fibres and their
products (as France had previously done and as do Br azil, the United States, Canada and many other
countries).  Alternatively, France could have established a single, never-to-be-exceeded exposure level
to apply to the manufacture, use and disposal of chrysotile and substitute fibres, and to their products.France could, and should, have adopted a performance requirement for chrysotile and the products
which contain it.  Instead, it adopted a design or descriptive requirement and violated Article 2.8 of
the TBT Agreement.  Were any other findings to  be reached by the Panel, it would allow Member
countries to take the much easier route of banning, rather than regulating, products which they claim
                                                     
56Brazil notes that interpretations that render a treaty provision null or void, or consign it to "inutility"
are to be avoided whenever possible.  See  United States – Standards for Reformulated and Conventional
Gasoline  (20 May 1996), WT/DS2/AB/R, p. 23.
57Brazil notes that paragraphs 4.42-4.43 below demonstrate that the man-made substitute fibres and
products are like products to chrysotile and chrysotile products.WT/DS135/R
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create health risk.  The TBT Agreement is based on the assumption that certain products present risks
and that those risks are to be managed through standards.  To allow a Member to ban, instead of to
regulate, products due to perceived risks would render the Agreement meaningless.
(b) The General Agreement on Tariffs and Trade
(i) Article XI of the GATT
4.40 Brazil submits that the ban is also inconsistent with GATT Article XI because it is a
quantitative restriction that is not permitted by the WTO.  The ban includes (i) a prohibition of the sale
in France of chrysotile and chrysotile products, which is a violation of GATT Article III:4, and (ii) a
prohibition of the importation of chrysotile and chrysotile products.  In fact, paragraphs I and II of
Article 1 of the ban prohibit "the import […] of all kinds of asbestos fibres […] whether or not these
substances are incorporated into materials, products or devices".  The latter aspect violates Article XI.
In reference to paragraph 1 of Article XI, Brazil argues that the ban on importation is not a "duty, taxor other charge," but is a "prohibition or restriction" that France has instituted and maintained on the
importation of chrysotile from Brazil.  Indeed, the ban is the most restrictive of all quantitative
restrictions in that it sets a quota at the level of zero imports.
58  Therefore, the portion of the Decree
that bans imports is inconsistent with Article XI:1.59  Brazil further argues that none of the three
exceptions contained in paragraph 2 of Article XI apply to the ban.  Simply put, the ban is an outrightprohibition of all imports, supposedly imposed to protect public health.  It is not a "standard or
regulation for the classification, grading or marketing" of chrysotile or chrysotile products.
60
Moreover, whether chrysotile is a "commodity" within the meaning of this exception is questionable.All three exceptions only relate to agricultural products.
(ii) Article III of the GATT and Article 2.1 of the TBT Agreement
4.41 Brazil argues that the ban is inconsistent with France's national treatment obligations under
GATT Article III:4 and Article 2.1 of the TBT Agreement.  The national treatment obligations of
Article III:4 and TBT Article 2.1 are violated when a law, regulation or requirement (or a technical
regulation) that affects the internal sale, offering for sale, purchase, transportation, distribution or use
of any imported product, accords less favourable treatment to the imported product  than that accordedto "like" domestic products.  Each of these criteria are satisfied with respect to the ban.  The ban is
indisputably a law and its three implementing "Arrêtés" are regulations.  For the purpose of Article 2.1
of the TBT Agreement, the ban is a technical regulation.  Article 1 of the Decree bans, among other
things, the manufacture, processing, sale, offer for sale, distribution and use of all varieties of asbestos
fibres and all asbestos-containing products (except for the few temporary exceptions permitted by its
Article 2).  Thus, it indisputably meets the second criterion for the application of GATT Article III:4
                                                     
58The fact that Article XI applies to the ban is further confirmed by Article XI:2(b) which applies to
"import […] prohibitions," among other restrictions.  See also Japan – Trade in Semi-Conductors , L/6309,
adopted 4 May 1988, BISD 35S/126, para. 104 (finding Artic le XI:1 "comprehensive" and applicable to all types
of non-tariff prohibitions).
59The applicability of Article XI:1 to such circumstances has been confirmed by various panels under
the GATT 1947 and GATT 1994.  See, e.g., United States Manufacturing Clause , L/5609, adopted 15/16 May
1984, BISD 31S/74, 88, para. 34;  Japan – Trade in Semi-Conductors , L/6309, adopted 4 May 1988,
BISD 35S/116, 152-53, para. 102;  United States – Import Prohibition of Certain Shrimp and Shrimp Products ,
WT/DS58/R (15 May , 1998), paras. 7.11 to 7.17.
60Brazil notes that a GATT Panel has held that a ban (which, of course, precludes marketing) is not
"related" to marketing under Article XI:2(b).  See Canada - Measures Affecting Exports of Unprocessed Herring
and Salmon , L/6268, adopted 22 March 1988, BISD 35S/98, 1 12, paras. 4.2-4.3 (rejecting Canadian argument
that a ban on exports of certain unprocessed fish was related to marketing, and finding that, to fall under
Exception Two, the regulation in question must apply to "marketing as such," and that Exception Two does not
apply to just any regulation facilitating foreign sales).WT/DS135/R
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and TBT Article 2.1.  It provides less-favourable treatment to chrysotile and chrysotile-containing
products (which, prior to the ban, were imported from Brazil), than that which it does to French
products used as asbestos substitutes (and which are not banned).61
4.42 Finally, the ban itself recognizes that the so-called "substitute fibres", and products
incorporating them, are "like" chrysotile and chrysotile-containing products.  The few exemptionspermitted by Article 2 of the ban apply when no substitute fibre is equivalent in terms of its end-use to
chrysotile.
62  In other words, whenever a French substitute fibre can replace chrysotile, chrysotile is
banned.  There can be no more convincing proof that chrysotile and substitute fibres are "like"
products.  Even if the ban did not by its own terms prove the "likeness" of French substitute fibres to
imported chrysotile, analysis of the precedents set under GATT demonstrate that chrysotile and
substitute fibres are indeed alike, as are chrysotile and substitute fibre-containing products.  Using the
criteria identified by the Appellate Body in the case on Taxes on Alcoholic Beverages  for establishing
"likeness"63, it is self-evident that the end uses of chrysotile and substitute fibres are the same.  The
fibres are used solely because they emulate the desired characteristics of chrysotile in particular
products.  With regard to "consumers' tastes and habits", chrysotile and substitute fibres are not
consumer goods.  They are used solely as inputs in certain products (primarily in various cement
products today).  Industrial consumers purchase substitute fibres rather than chrysotile based onconsiderations of cost and availability.  They can do so because substitute fibres are intended to
emulate chrysotile's characteristics.
4.43 Brazil asserts that the same reasoning applies to the assessment of the products' properties,
nature and quality.  Substitute fibres are "like" chrysotile precisely because they emulate chrysotile's
characteristics.  An additional criterion to determine likeness was added after Border Tax decision –
tariff classification.
64  As previously noted, almost all chrysotile is used as an input into various
cement products.  Chrysotile and other fibre-cement products are classified under the same
Harmonized Tariff System heading (which is number 68.11).  In all instances, the six and eight digit
classification of chrysotile and other fibre-cont aining cement products are the same.  Therefore,
France's conduct violates GATT Article III:4 and the TBT Agreement's Article 2.1, and is inconsistentwith France's national treatment obligation.
(iii) Article I of the GATT and Article 2.1 of the TBT Agreement
4.44 The most-favoured-nation obligations of Articles I:1
65 and 2.1 are violated "with respect to all
matters referred to in paragraphs 2 and 4 of Article III" (or, for purposes of the TBT Agreement,
Article 2.1), whenever any "advantage, favour, privilege or immunity" is granted to a product from
one country and is not "accorded immediately and unconditionally" to a "like product" from other
WTO Members.  This happens to be the case with the French ban.  As previously demonstrated,Brazil argues that the ban violates GATT Article III:4 and, for the purposes of Article 2.1 of the
TBT Agreement, is a technical regulation.  The fact that substitute fibres may be imported into France
                                                     
61According to Brazil, the absence of imports because of the imposition of a ban does not provide a
valid basis for asserting that GATT Article III:4 (and TBT Article 2.1) cannot be applied.  Interpretations thatrender a treaty provision null or void, or consign it to "inutility" are to be avoided whenever possible.  SeeUnited States – Standards for Reformulated and Conventional Gasoline  (20 May 1996), WT/DS2/AB/R, p. 23.
62Brazil notes that the EC acknowledges this when explaining that the French ban does not include
chrysotile diaphragms for use in chlorine environments because substitutes cannot safely be used.
63Japan - Taxes on Alcoholic Beverages  (4 October 1996), WT/DS8/AB/R, p. 20, quoting Report of the
Working Party on  Border Tax Adjustments  (2 December 1970) BISD 18S/87, 102, para. 18.
64Brazil notes that this criterion was first cited in EEC – Measures on Animal Feed Proteins , L/4599,
adopted 14 March 1978, BISD 25S/49, 63, para. 4.2.
65Brazil recognizes that Canada has not alleged a violation of GATT Article I:1.  However, as
demonstrated, the French ban violates the most-favoured-nation obligations of both that Article and of
Article 2.1 of the TBT Agreement.WT/DS135/R
Page 212
while chrysotile imports are banned constitutes an "advantage, favour, privilege or immunity."  This
advantage is accorded to imported substitute fibres but is denied to imported chrysotile, which is
banned.
(iv) Article XX of the GATT
4.45 Brazil argues that the General Exceptions of Article XX do not excuse the Decree.  To obtain
an exception under Article XX, the EC must establish that (i)  the ban does not "constitute a means of
arbitrary or unjustifiable discrimination between countries where the same conditions prevail",
(ii) that it is not a "disguised restriction on international trade", and (iii) that it is "necessary to protect
human life or health."  The EC cannot argue that the ban meets these conditions.  As demonstrated
above, the ban discriminates between like products, without advancing its stated objective.  Therefore,
it is a "means of arbitrary or unjustifiable discrimination".  Also, it disadvantages imports of
chrysotile, but not imports of man-made fibres.  Countries like Brazil (and Canada) produce bothchrysotile and substitute fibres.  Therefore, the criterion of "discrimination between countries where
the same conditions prevail" is obviously satisfied.  Similarly, as previously demonstrated, the ban is a
"disguised restriction on international trade".  Although it masquerades as a measure designed to
protect public health, it is an outright product ban that is designed to quell public outrage and
advantage domestic and European manufacturers of substitute fibres and products.  Moreover, itcannot be argued that the ban is "necessary" to protect human life or health.  For these reasons, the EC
should not be granted recourse to Article XX.
B. U
NITED STATES
1. Introduction
4.46 The United States' submission first discusses the facts concerning the health risks of exposure
to chrysotile asbestos, and reduction of these risks through regulation.  In this connection, the
United States supplies information correcting certain errors and mischaracterizations in Canada’s
description of the United States regulation of asbestos and the former United States ban and
phaseout on asbestos-containing products.  United States regulations are not at issue in this
proceeding.  The United States' submission nevertheless seeks to set the record straight because ofCanada’s assertions concerning United States policy.  Following a factual discussion, it addresses the
legal provisions that the Panel has been asked to interpret.
4.47 In the view of the United States, chrysotile asbestos is a toxic material that presents a serious
risk to human health.  Chrysotile asbestos is no less toxic than other forms of asbestos.  A regulatory
approach that treats all forms of asbestos on a par with each other is scientifically justified.  France,
like all other Members of the WTO, has the right to set its own desired level of protection against risks
arising from exposure to asbestos, and its regulation on asbestos appears neither discriminatory norunnecessarily trade restrictive in ensuring that level of protection.  The United States currently relies
on specified work practices and other controls (including a limited ban) to reduce the risk to human
health from asbestos exposure.  However, the United States does not consider its approach to be the
only appropriate one for regulation of asbestos.  Specification of work practices and other controls
does not avoid all the risks associated with a hazardous material such as chrysotile asbestos.  First,"controlled use" does not eliminate all the risks associ ated with asbestos.  Although it is generally true
that asbestos contained in a cement matrix does not present substantial risks while that product is
intact, the same is not true during the production, installation, maintenance, removal, or disposal of
that product.  Second, in many cases a matrix containing asbestos does not remain intact during its
useful life.   Moreover, while the bulk of Canada’s  submission focuses on cement-matrix applications,
it also acknowledges that chrysotile asbestos is currently used in brake linings and spun fibres for the
production of insulating tissues or cords.  Significant health risks attend the manufacture and repair of
such substances.   Finally, even the best work practice is effective only to the extent that it is followed;WT/DS135/R
Page 213
accidents, use of improper techniques, and intentional non-compliance are virtually inevitable in the
use of these products.   For these reasons, France's ban on the manufacture, processing, distribution in
commerce, export, import and sale of asbestos and its products appears to be a WTO-consistent
response to the risks posed by the use of asbestos.
4.48 As for the legal issues: In the view of the United States, Canada has not met its burden of
proof with respect to any violation by the French Decree of provisions of the GATT or the Agreement
on Technical Barriers to Trade ("TBT Agreement").  In particular, Canada has not shown that
imported asbestos and asbestos-containing products are "like products" with respect to substitute
fibres and products containing them which are of French origin.  As a finding that these products are
not "like products" eliminates any violation of Article III:4, and Article XI:1 is simply irrelevant to the
analysis of this measure, there does not appear to be any violation of the GATT 1994.   With respect
to the TBT Agreement, the United States disagrees with the EC position that the TBT Agreement isinapplicable to the French Decree. The Panel should reject the EC’s position and find that the Decree
is a "technical regulation" within the meaning of Annex 1 of the Agreement;  any other result will
open up a loophole which could entirely nullify the TBT Agreement.  Nevertheless, in the United
States view Canada has not proven any violati on of Articles 2.2, 2.4, 2.8 or 2.1 of the Agreement.
Finally, Canada has not met the particularly high burden of proof for cases of non-violationnullification and impairment.
2. Factual Aspects
4.49 The United States  argues that asbestos - whether chrysotile or in other forms
66 - is a toxic
substance.  In United States lexicography, it is a "Class A carcinogen", meaning a substance whose
carcinogenic properties have been proven conclusively.67  The IPCS has reached the same conclusion:
"[E]xposure to chrysotile asbestos poses increased risks for asbestosis, lung cancer and mesothelioma
in a dose-dependent manner."68  The IPCS Report also concludes:  "[C]ommercial grades of chrysotile
have been associated with an increased risk of pneumoconiosis, lung cancer and mesothelioma in
numerous epidemiological studies of exposed workers."69  In regulating asbestos, the United States
treats chrysotile asbestos the same as any other recognized form of the substance.70  T h e  f i n d i n g s
presented by Stayner et al.71 support the decision not to distinguish between chrysotile and other forms
of asbestos.  This study concluded that it is prudent to treat chrysotile with virtually the same level of
concern as the amphibole forms of asbestos, based on the evidence of a significant lung cancer risk,
the fact that workers are generally exposed to a mixture of fibres, and the lack of conclusive evidence
for the "amphibole hypothesis".72  More recent confirmation of the hazardous nature of chrysotile was
                                                     
66The United States notes that its arguments focus on chrysotile asbestos, as that is the subject of the
Canadian challenge.
67United States Environmental Protection Agency ("EPA"), Integrated Risk Information System (IRIS),
Asbestos Substance File (1993) (www.epa.gov/ngispgm3/iris/subst/0371.htm#II) (includes summary of weight-of evidence classification and human carcinogenicity data, including data showing the carcinogenicity of
chrysotile asbestos).
68IPCS Environmental Health Criteria 203 –  Chrysotile Asbestos , WHO, 1998, p. 144.  (The IPCS
document cites numerous studies supporting this conclusion).
69IPCS Environmental Health Criteria 203 – Chrysotile Asbestos,  WHO, 1998, p. 7.
70Airborne Asbestos Health Assessment Update,  p. 118 (EPA, June 1986) (concluding that "while
differences in pleural mesothelioma risk attributable to fibre type may exist, they are much less than differences
attributable to other factors").
71Stayner, L. T., Dankovic, D. A., and Lemen, R.  A., Occupational Exposure to Chrysotile Asbestos
and Cancer Risk:  A Review of the Amphibole Hypothesis , 86 American Journal of Public Health, 179-186,
1996.
72The United States notes that the "amphibole hypothesis" postulates that the mesotheliomas among the
workers exposed to chrysotile may be explained by confounding exposures to amphiboles, and that chrysotile
may have a lower carcinogenic potency than amphiboles.WT/DS135/R
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provided by Landrigan, concluding on the basis of an epidemiological study undertaken in Quebec
that "chrysotile asbestos is still indisputably a human carcinogen.73"  Concerning exposure to asbestos,
IARC stated in 1976 that "at present it is not possible to assess whether there is a level of exposure in
humans [to asbestos] below which an increased risk of cancer would not occur."74  T h e  I P C S
reaffirmed this conclusion specifically with regard to chrysotile asbestos in 1998, stating:  "[N]o
threshold has been identified for carcinogenic risks" with regard to chrysotile asbestos.75  That means
that it cannot be assumed that any exposure, no matter how small, to asbestos is safe.  Canada
questions France's scientific approach, attacking the use of a "linear risk model".  The United States
takes issue with Canada's criticism of the INSERM Report's use of a linear dose-response model to
estimate cancer risk.  The use of such a model is entirely appropriate when it comes to estimating the
risk of cancer from exposure to asbestos.
4.50 The United States notes that it is not in a pos ition to draw definitive conclusions concerning
the regulatory process in France and the actual factual basis for the French Decree.  However,
generally speaking, regulatory decision-making relating to carcinogens involves two components:
risk assessment and risk management.  Risk assessment defines the adverse health consequences of
exposure to toxic agents.  Risk management combines the risk assessment with the directives of
regulatory legislation, together with socioeconomic , technical, political, and other considerations, to
reach a decision as to whether or how much to control future exposure to the suspected toxic agents.76
Risk assessments are carried out independently from considerations of the consequences of regulatoryaction.
77  A risk assessment involves, among other things, quantitative and/or qualitative estimation of
risks associated with low levels of exposure to carci nogens.  While it is always preferable to rely on
human data, epidemiological studies are often either not available or sufficiently definitive,particularly regarding the specific exposure levels involved, and thus often cannot be relied upon as
the sole basis for a risk assessment.
78  In addition, because testing of thousands of animals would be
necessary in order to have the sensitivity to detect any but large effects, it generally is not practical to
measure risks at low exposure levels directly in animal experiments.79  Accordingly, a number of
mathematical models have been developed to extrapolate from high dose animal studies to low humandoses.
80
4.51 In the United States, models or procedures that incorporate low-dose linearity have been
adopted when data and information are limited and when there is uncertainty regarding the mechanism
of carcinogenic action.81  While low-dose linearity may not be appropriate for all carcinogenic risk
                                                     
73Landrigan, P. L., Asbestos - S till a Carcinogen,  338 New England  Journal of Medicine 1619
(28 May 1998).
74Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man , Vol. 14, IARC,
1976, p. 81.
75IPCS Environmental Health Criteria 203 – Chrysotile Asbestos,  WHO, 1998, p. 144.
76Final Guidelines for Carcinogen Risk Assessment , 51 Federal Register 33992, 33993, col. 3
(EPA, 24 Sept. 1986).
7751 Federal Register 33992, 33993, col.3 (24 September 1986).
78The United States notes that, as the 1986 EPA carcinogen risk assessment guidelines point out:  "It
should be recognized that epidemiologi cal studies are inherently capable of detecting only comparatively large
increases in the relative risk of cancer.  Negative results from such studies cannot prove the absence ofcarcinogenic action … ".  (51 Federal Register 33992 (24 September 1986), pp. 33995-96).  Canada’s statement
that "no epidemiological study to date has detected a hi gher health risk [than the linear risk model] resulting
from low-level exposures" must be viewed in this light.
7951 Federal Register 33992 (24 September 1986), p. 33993, col. 3.
8051 Federal Register 33992 (24 September 1986), p. 33997.  See also EPA Proposed guidelines for
carcinogen risk assessment, 61 Federal Register 17960, 17962 (23 April 1996).  Although these most recentguidelines are not yet final, they demonstrate that EPA’s reassessment of the issues is similar to the approach
taken previously.
8151 Federal Register 33992 (24 September 1986), p. 33997, col.3.WT/DS135/R
Page 215
assessment, it is commonly used in the United States as a default methodology.  This methodology is
supported by scientific studies and is a reasonably protective approach in the face of uncertainty.82
The use of a linear model is appropriate for a quantitative estimation of the risks associated with lowlevels of exposure to asbestos because of the observed linearity of the response in occupational
studies.  The United States has adopted this approach, in addition, because of the incompleteunderstanding of how asbestos causes diseases in humans.
83  In assessing the risk from asbestos, EPA
notes that "[d]irect evidence for linearity of response with asbestos exposure is available from seven
studies (two of the same plant) that compared lung cancer mortality to the cumulative total dust
exposure in asbestos workplaces"[citations omitted].84  Similarly, the limited data that exist for
mesothelioma also indicate a linear relationship.85  The IPCS states:  "there was a clear dose-response
relationship, with crude rates of mesotheliomas (cases/1000 person-years) ranging from 0.15 for those
with cumulative exposures less than 3530 million particles per cubic meter years … to 0.97 for thosewith exposures of more than 10,590 mpcm-years […].
86"  After identifying and defining the adverse
effects of asbestos through the risk assessment process, the next step is to make risk management
decisions.  A risk management decision, while taking into account the scientific findings of the risk
assessment process, also includes a country's choice on whether and how much to regulate a toxic
agent.  It is at this stage that a country selects measures and regulations that will achieve its chosenlevel of protection relating to the health of its people.
4.52 In its arguments, Canada has referred to United States regulations concerning asbestos.
Because its description of the U.S. regulatory approach is substantially inaccurate, the United States
proceeds to set the record straight.  The U.S. regulatory approach at present includes a mix of control
measures, including bans and required work practices.  This approach involves a number of complexstatutes, some of which require the consideration of cost, feasibility and other factors besides human
health.  Almost all control measures are designed to protect workers and building occupants from
exposures resulting from contact with asbestos in installed products.  Although France's approach to
the same problem is different, this different approach is also reasonable under the circumstances.
4.53 Canada references the 1989 rule promulgated by the EPA prohibiting the future manufacture,
importation, processing and distribution in commerce of  asbestos in almost all products ("the Asbestos
Ban and Phase-Out Rule").
87  Several of Canada's statements on this point are factually inaccurate.
According to the United States, the Asbestos Ban and Phase-Out Rule was in large part vacated and
remanded to EPA by the United States Court of Appeals for the Fifth Circuit in a case entitled
Corrosion Proof Fittings vs. Environmental Protection Agency88, based on the court's view that EPA
had not appropriately addressed cost-benefit issues.  Contrary to the claims made by Canada that EPA
was incapable of scientifically justifying its ban, and that the risks posed by asbestos were notsupported by scientific facts, the court specifically agreed with EPA's scientific judgment by
recognizing that "[a]sbestos is a toxic material, and occupational exposure to asbestos dust can result
in mesothelioma, asbestosis, and lung cancer."
89  Indeed, in the record of rulemaking, EPA provided,
among other things, a number of scientific studies and reports on the health risks of asbestos,
including:  Airborne Asbestos Health Assessment Update90,  Report to the United States Consumer
Product Safety Commission by the Chronic Hazard Advisory Panel on Asbestos91,  Asbestiform
                                                     
8261 Federal Register 17960 (23 April 1996), p. 17965.
83IPCS Environmental Health Criteria 203 – Chrysotile Asbestos , WHO, 1998, p. 7.
84Airborne Asbestos Health Assessment Update, EPA, June 1986, p. 23.
85Airborne Asbestos Health Assessment Update,  EPA, June 1986, pp. 23-30.
86IPCS Environmental Health Criteria 203 –  Chrysotile Asbestos , WHO, 1998, p. 8.
8754 Federal Register 29460-29513, 12 July 1989.
88Corrosion Proof Fittings v. Environmental Protection Agency,  947 F.2d 1201 (5th Cir. 1991).
89Ibid., p. 1207.
90Airborne Asbestos Health Assessment Update  (EPA, June 1986).
91Chronic Hazard Advisory Panel on Asbestos,  U.S.  Consumer Product Safety Commission, July 1983.WT/DS135/R
Page 216
Fibres:  Non-occupational Health Risks92 and "Short-term asbestos work exposure and long-term
observation.93"  These studies and reports were discussed in the preamble to the Rule.94  The court
based its decision on procedural flaws in the EPA rulemaking process and on the court's own
interpretation of the applicable United States statutory risk/benefit balancing standard for
promulgating such rules, not on any disagreement wi th EPA's findings concerning the health hazards
posed by asbestos.  After the judicial remand, EPA imposed a more limited ban on asbestos-
containing products, including a ban on any new uses of asbestos.95  That ban remains in place.
4.54 The United States notes that Canada makes much of the argument that asbestos entrained in a
cement matrix does not present "detectable risk.96" However, Canada's focus ignores the risks
presented by asbestos products throughout their life-cycle.  The most significant sources of exposure
to asbestos, and therefore risk from asbestos-containing products derive from their manufacture,
installation, repair, removal, and disposal, including disposal of products containing asbestos in acement or resin matrix.  Moreover, while Canada appears to acknowledge France's concern about
protecting health in general terms, it appears to disagree about how protective France should be.  By
arguing that certain small risks are equivalent to  zero risks, the Canadian submission implicitly
questions the sovereign authority of a WTO Member to determine the appropriate level of protection
for its citizens.  What Canada or the United States might consider to be adequate protection in aparticular context is not necessarily what other countries must choose.  To put it another way, Canada
concedes that a ban is acceptable for "certain uses where exposure cannot be controlled to an
acceptable degree".  The United States agrees, but submits that it is up to each Member to determine
what that "acceptable degree" is.  Canada indicates that among the most important commercial
applications of asbestos are as part of brake linings or clutches and in the form of spun fibres for theproduction of insulating tissues or cords.  In connection with its analysis of "friction products", which
include brake linings and clutches, the United States court in the Corrosion Proof Fittings case
recognized that "[w]orkers are exposed to asbestos during the manufacture, use, repair and disposal of
these products" and that, in the asbestos ban and phase-out rule, "EPA demonstrates that the
population exposure to asbestos in this area is great."
97  The court agreed with EPA's determination
that friction products containing asbestos pose a risk to human health.98
4.55 With respect to Canada's argument that a major commercial application for asbestos is as a
reinforcement material for cement, plastic, or rubber, the United States asserts that, in the
Asbestos Ban and Phase-Out Rule, EPA made certain determinations respecting worker exposure to
these products that were not questioned by the Corrosion Proof Fittings court.  EPA determined that
the manufacture, installation, repair, and disposal of flat and corrugated asbestos-cement sheet expose
                                                     
92Asbestiform Fibres:  Non-Occupational Health Risks , NAS, NRC, 1984.
93Seidman, H., Selikoff, I .J., Hammond E. C., Short-Term Asbestos Work Exposure and Long-Term
Observation , 330 Annals of the New York Academy of Sciences 61-89, 1979.
9454 Federal Register 29460 (12 July 1989), p. 29468-70.
9540 Code of Federal Regulations (CFR) 763.165-763.169 (59 FR 33208, 28 June 1994).
96The United States notes that it is not entirely clear what Canada means by the term "undetectable
risk".  The presence of asbestos fibres in the air or ot her media can be detectable or  undetectable.  A risk can be
significant, insignificant, or non-existent.  It appears that Canada uses the term "undetectable risk" to refer to arisk that Canada deems insignificant.  Significance, however, is a judgment call that can only be made by theregulatory authority responsible for public health and safety.  It is up to France to determine what level of risk tothe French people from asbestos (or any other hazard) is significant.
97Corrosion Proof Fittings v. Environmental Protection Agency , 947 F.2d 1201 (5th Cir. 1991), p. 1224.
98Significant damages have been awarded in U.S. courts  with respect to brake applications of asbestos.
In 1985, a retired brake mechanic who was dying of meso thelioma won a verdict of $2 million in a court action
against Raybestos Manhattan.  See  McDonald AD, et al., Dust Exposure and Mortality in an American
Chrysotile Asbestos Friction Products Plant , 41 Br J Ind Med 151-157, 1984;  Newhouse M. L. and
Sullivan K. R., A Mortality Study of Workers Manufacturing Friction Materials:  1941-86 , 46 Br J Ind. Med,
176-179, 1989.WT/DS135/R
Page 217
workers to asbestos.99  Similarly, EPA determined that the manufacture and installation of asbestos-
cement pipe provide "primary routes of exposure"  of workers to asbestos from these products, and
workers may also be exposed during the removal of asbestos-cement pipe.100  The United States
generally agrees with Canada's assertion that as long as asbestos is held within a cement or resin
matrix in an undisturbed state, there is minimal exposure to the fibres - but only while the matrixretains its integrity.  Much asbestos has been installed in United States buildings.  Because of the high
health risk from disturbed building materials and the reduced risk from intact asbestos-containing
materials, EPA has issued guidance recommending management of asbestos-containing materials in
place.
101  Unfortunately, cement and resin matrices do not remain undisturbed.  Putting aside
significant releases that occur during the manufacturing process102, releases of asbestos can occur
when, for example, asbestos-cement pipes are installed (which requires cutting the material), and
when asbestos-containing material (such as cement) deteriorates, as through peeling, cracking, orcrumbling.  Fibre release could also result when the material is dry, has the capacity to be crumbled,
pulverized or reduced to powder by hand pressure, or is subject to sanding, grinding, cutting or
abrading.
103
4.56 The United States asserts that a cement matrix in which asbestos is bound can undergo a
natural process of erosion or degradation resulting in asbestos fibre release:  "[T]he release of fibresfrom external asbestos-cement products [such as siding] due to weathering can be an important
external source of asbestos contamination that can be carried into or can infiltrate into the building
environment".  This has been acknowledged by the 1991 Health Effects Institute-Asbestos Research
(HEI-AR) report, Asbestos in Public and Commercial Buildings:  A Literature Review and Synthesis
of Current Knowledge .
104  As reported in the HEI-AR document, researchers found that weathered
asbestos-cement sheet products washed from gutters and onto walkways were an important source of
chrysotile carried by foot or wind into a classroom.105  The report also cited a research finding of
increased ambient air concentrations in the vicinity of buildings with asbestos-cement products on
their exterior.106  Mere maintenance of some asbestos bound in a matrix may disturb the matrix and
thereby create additional exposures to the asbestos fibres.  For example, in an EPA study107 conducted
at 17 schools in New Jersey involving spray buffing of resilient floor tile containing asbestos, airborne
asbestos concentrations were approximately five times higher during than before spray-buffing with
high-speed machines, whereas spray-buffing with low speed machines showed a two-fold increase.
For school maintenance workers, the maximum estimated eight-hour time-weighted average exposure
concentration was 0.093 f/cc.  Similarly, routine spra y-buffing and wet-stripping as well as ultra-high
speed burnishing and wet-stripping of asbestos-containing resilient floor tile can result in elevated
                                                     
9954 Federal Register 29460-29513 (12 July 1989), p. 29491.
10054 Federal Register 29460-29513 (12 July 1989), pp. 29496-97.
101Managing Asbestos in Place:  A Building Owner’s Guide to Operations and Maintenance Programs
for Asbestos-Containing Materials , EPA, July 1990.
102The United States notes that, for example, a study of mortality among long-term employees of an
Ontario asbestos-cement factory found a substantially increased risk of death from lung cancer andmesothelioma.  Finkelstein, M. M., Mortality Among Long-Term Employees of an Ontario [Canada] Asbestos-
Cement Factory , 40 Br. J. Ind. Med. 138-44, 1983.
103The United States notes that this has been recognized by EPA’s asbestos National Emission Standard
for Hazardous Air Pollutants (NESHAP), promulgated under §112 of the Clean Air Act, 42 U.S.C.  7412.  55
Federal Register 48406, 48408-09 (Nov.  20, 1990), codified at 40 CFR part 61, subpart M.
104Asbestos in Public and Commercial Buildings:  A Literature Review and Synthesis of Current
Knowledge,  Health Effects Institute-Asbestos Research Report, 1991, p. 4-32.
105Ibid., pp. 4-32 and 4-33.
106Ibid., pp. 4-33.
107Project Summary:  Airborne Asbestos Concentr ations During Buffing of Resilient Floor Tile , EPA,
October 1993, p. 4.WT/DS135/R
Page 218
levels of airborne asbestos.108  Part 2 of the Kominsky study demonstrates that the ultra high-speed
burnishing and wet-stripping procedures were associated with a maximum estimated eight-hour time-
weighted average exposure concentration of 0.275 f/cc to operations and maintenance staff.109
Likewise, the HEI-AR Report states that:  "buffing, wax stripping, and other abrasive treatments maycause the release of particulate material from the surface of the floor tile".
110
4.57 The United States' regulatory programme on asbestos is largely aimed at controlling exposure
to asbestos when it is no longer bound in a matrix.  United States regulations address renovation and
demolition of buildings111 and identification and management of asbestos-containing material in
schools.112  Regulations of the Occupational Safety and Health Administration (OSHA) of the
Department of Labor address worker exposures to asbestos including manufacture, installation,
renovation, removal and custodial work where workers come into contact with asbestos-containing
material.  OSHA has established a permissible exposure limit and mandated extensive work practicecontrols, enclosures, hazard communication, training, medical and other industrial hygiene practices to
protect both workers contacting asbestos and other workers who are nearby.  Enforcing and complying
with these regulations entail a significant comm itment of resources by both the public and private
sectors.  Even within a cement or resin matrix, the risk from asbestos is not negligible.  According to
an analysis conducted in 1991 by the Health Effects Institute-Asbestos Research
113, janitors,
custodians and maintenance workers exposed to ambient asbestos fibre levels of 0.1 f/ml (the
permissible exposure limit currently allowed by OSHA regulations) were subject to an estimated
increased risk of death from cancer of 2 in 1,000.  The same analysis estimated that building
occupants (school children and office workers) exposed to airborne asbestos fibres from asbestos-
containing materials (presumably many of which, as building materials, would have been encased incement or resin) have a lifetime cancer risk from such asbestos exposure of 4 to 60 per 1,000,000.
Contrary to Canada's suggestion, such risks are not equivalent to zero.  Each country must determine
for itself what level of protection from risks of exposure to asbestos it wishes to achieve, i.e. what
risks to its population it is willing to accept.  It is not for another country to tell France that certain
risks to its population are not significant.  By way of illustration, the United States regulates risks onthe order of 1 in 100,000 (1 x 10
-5) or 1 in a million (1 x 10-6) in a number of instances.  Canada
concedes that "[t]he principle of controlled use also means that certain uses for which exposure cannot
be controlled to an acceptable degree would be banned". The discussion above demonstrates that
exposure to asbestos even in a cement or resin matrix  cannot be controlled sufficiently to eliminate all
risk.
4.58 The United States argues that both of the pa rties have mischaracterized the substitutes for
asbestos and asbestos-containing products.  Some  products that currently contain asbestos may be
manufactured simply by removing the asbestos, thus eliminating any substitution of risk.
Alternatively, a wide variety of fibrous substances are being used commercially as replacement
materials for asbestos-containing products.  These include the man-made mineral fibres (consisting of
glass fibres, rock wool, slag wool, refractory ceramic fibres), selected organic fibres (e.g., aramid,
carbon/graphite, polyolefin), and several naturally occurring mineral fibres other than asbestos(e.g., wollastonite, sepiolite, palygorskite).  The potential health effects for these non-asbestos fibres
                                                     
108Kominsky J. R., Freyberg R. W., Clark P. J., Edwards A;  Wilmoth, R. C., Brackett, K. A., Asbestos
Exposures During Routine Floor Tile Maintenance.  Part 1:  Spray-Buffing and Wet-Stripping;  Part 2:  UltraHigh Speed Burnishing and Wet-Stripping , 13 Appl. Occup. Environ Hyg. 101-112 (February 1998).
109Ibid., pp. 107-112
110Asbestos in Public and Commercial Buildings:  A Literature Review and Synthesis of Current
Knowledge,  Health Effects Institute-Asbestos Research Report, 1991, pp. 4-70.
111Asbestos NESHAP, 40 CFR 61.145.
112Regulations issued under the Asbestos Hazard Emergency Response Act (AHERA), 15 USC 2641 et
seq.:  40 CFR part 763, subpart E.
113Asbestos in Public and Commercial Buildings:  A Literature Review and Synthesis of Current
Knowledge,  Health Effects Institute-Asbestos Research Report, 1991, pp. 8-9 - 8-10.WT/DS135/R
Page 219
have been evaluated by EPA,114 the IARC115 and the IPCS.116  Although limited health effects
information exists for many of these fibres, available data do not indicate that these fibres are as toxic
as chrysotile asbestos.  For example, none of these fibres have been found to cause either malignant or
non-malignant respiratory diseases similar to those associated with asbestos exposure in humans.
Unlike asbestos fibres, these substitute fibres have not been classified as carcinogenic to humans orknown human carcinogens.  The only fibre that has been shown to be more hazardous than asbestos
fibres is erionite.  Erionite, however, is not known to be available in commerce at this time.
117
4.59 The United States notes that Canada continually urges that "controlled use" will bring the risk
associated with chrysotile asbestos to "undetectable" levels.  It also compares the risk from asbestos to
that of other products and activities, concluding that many are more risky than asbestos.  Canada
overstates the efficacy of "controlled use".  For example, Canada states that where it is necessary to
cut chrysotile-cement materials on site, "the use of t ools that almost entirely eliminate emissions (low-
speed saws, with water injection or equipped with suction units), and the wearing of a mask by the
operator guarantee their safety".  United States regulations recognize, however, that masks may not be
sufficient in some situations and require the use of a supplied-air respirator which is obviously more
cumbersome and costly.118  When a government makes its choice whether to ban a product or to opt
for controlled use, it must necessarily take into account the anticipated effect of the regulations on itspopulation.  Beyond the obvious point that "almost" eliminating emissions of asbestos fibres is not the
same as eliminating them, it must be acknowledged that 100 per cent compliance with "controlled
use" of asbestos is not a realistic expectation due to the burdensome nature of certain work practices
concerned.  Even the best work practice is effective only to the extent that it is followed;  accidents,
use of improper techniques, and international non-compliance are virtually inevitable in the use ofthese products.
119
4.60 The United States argues that Brazil has made a number of unjustified and inaccurate
assertions concerning the U.S. Environmental Protec tion Agency's former ban on all forms of asbestos
and asbestos-containing products in the United States, and a domestic court decision concerning the
EPA ban.  Of course, this U.S. domestic court did not rule on the consistency of the EPA ban with theTBT Agreement or the GATT.  It only dealt with  whether EPA had complied with the risk/benefit
balancing requirements of the U.S. Toxic Substances Control Act (TSCA).  The risk/benefit standard
in this U.S. statute is irrelevant to the Panel's present task of determining whether France's ban on
asbestos is consistent with the WTO Agreement.  France has not adopted such a risk/benefit balancing
standard as the basis for a ban.  First, Brazil misrepresents the domestic court decision and the
situation following, repeating errors made by Canada.  The court in 1991 upheld EPA's determination
that "[a]sbestos is a toxic material, and occupational exposure to asbestos dust can result inmesothelioma, asbestosis, and lung cancer".  The court based its decision not on any disagreement
with EPA's findings concerning the health hazards posed by asbestos, but instead on procedural flaws
in the EPA rulemaking process and on the Court' s own interpretation of the statutory risk/benefit
                                                     
114Health Hazard Assessment of Non-Asbestos Fibres , EPA, 1988.
115Man-Made Mineral Fibres and Radon:  Monographs on the Evaluation of Carcinogenic Risks to
Humans , Volume 43, pp. 39, 148-52, IARC 1988.
116Asbestos and other Natural Mineral Fibres,  IPCS, 1986, Environmental Health Criteria 53,
International Programme on Chemical Safety, World Health Organization, Geneva;  Man-Made Mineral Fibres
(IPCS 1988), Environmental Health Criteria 77, International Programme on Chemical Safety, World Health
Organization, Geneva;  Selected Synthetic Organic Fibres,  (IPCS 1993), Environmental Health Criteria 151,
International Programme on Chemical Safety, World Health Organization, Geneva.
117In addition, see the US answer to question 4 of the EC (contained in Annex II, Section II.A.4).
11840 CFR 763.121(h) (EPA regulations covering employees of certain state and local governments
conducting asbestos abatement projects);  29 CFR 1926.1101(g)(2)(v) (OSHA asbestos regulations forconstruction).
119In addition, see the US answer to question 2 of the EC (contained in Annex II, Section II.A.4).WT/DS135/R
Page 220
balancing required by TSCA.  Because the court agre ed with EPA on the health effects of asbestos,
EPA did not, after the court decision, need to carry out a "thorough review of scientific and medical
data" as a basis to authorize or ban the products Brazil has listed.  All EPA did, pursuant to the court's
instructions, was to determine which product cat egories were no longer manufactured, imported, or
processed when the rule was issued.  For all such products the ban was maintained.  EPA also bannednew uses of asbestos.
120
4.61 Second, contrary to what is alleged by Brazil, the United States has not determined that
controlled-use policy effectively eliminates the he alth risk attributable to modern-day uses of
chrysotile.  Third, Brazil has downplayed the health risk from asbestos by lifting a quotation out of
context from the Health Effects Institute report, in a manner that does not accurately reflect the
discussion of mathematical models found in this section of the HEI report.121  The United States
addressed these issues as described above at para graph 4.40.  Finally, concerning Brazil's discussion
of the French Decree, the United States notes that Brazil concedes that the objective of the Decree -
protection of the health of workers and the public - is a legitimate objective within the meaning of
Article 2.2 of the TBT Agreement.  The United States agrees with Brazil on this point but would also
note that France has a right to set its "legitimate objective" to establish the protection of the health of
French workers and consumers at the level it deems appropriate .  However, when alleging that there is
no "rational link" between the French Decree and health protection, stating that the Decree will not
make those now sick healthy, and removing it woul d not make any of those now healthy sick,  Brazil
conveniently omits the function of the Decree in preventing future  exposure and future disease that
would result from that exposure.
3. Legal Aspects
4.62 For the reasons below, the United States suggests that the Panel should find that Canada has
failed to meet its burden of proof that the French Decree violates any provision of the
WTO Agreement.  The Panel should also find that  Canada has failed to make a showing that the
French Decree gives rise to non-violation nullificati on or impairment of benefits accruing to Canada.
(a) The General Agreement on Tariffs and Trade
(i) Article XI of the GATT
4.63 With respect to Canada's argument that the Decree violates Art. XI:1 because it imposes an
absolute prohibition or restriction on imports, the United States agrees with the EC that Article XI is
simply not relevant to these proceedings, and th e Decree should be analyzed under Article III instead.
The Decree regulates characteristics of asbestos and asbestos-containing products.  It applies to all
asbestos, and is applied to imported products "at the time or point of importation," in the words of the
Note Ad Article III.
(ii) Article III of the GATT
4.64 With respect to Canada's allegation that the Decree violates the national treatment obligations
embodied in GATT Article III:4, the United States argu es that, to show a violation of Article III, there
must be discrimination - that is, unlike treatment of like products.  Yet the relevant domestic and
imported products here are not "like products" for th e purposes of Article III:4.  As the EC has noted,
the classic statement of the factors relevant in determining what constitutes a "like product" is found
                                                     
120For the details, see 40 Code of Federal Regulations 763.160, 763.165-763.169 (59 Federal Register
33208 (28 June 1994).
121Health Effects Institute – Asbestos Research, Asbestos in Public and Commercial Buildings:
A Literature Review and Synthesis of Current Knowledge , Cambridge, 1991, pp. 6-9.WT/DS135/R
Page 221
in the Working Party report on Border Tax Adjustments of 1968, which defined like products in terms
of "the product's end-uses in a given market;  consumers' tastes and habits, which change from country
to country;  the product's properties, nature and quality".122  The United States generally agrees with
the EC's analysis that the properties, nature and quality of asbestos and asbestos-containing products
on the one hand, and substitutes on the other, are not "like".  The substitutes are by definitionsubstitutable for asbestos and asbestos-containing products for certain uses, but that does not mean
that they are "like products".
4.65 According to the United States, Canada has not made the correct product comparison for the
purpose of determining whether the relevant products are "like products" under Article III:4.  In
considering a regulation that bans asbestos and requires the use of substitutes, the relevant products to
compare are the following:  (i) asbestos must be compared to substitute fibres;  and (ii) products
containing asbestos must be compared to products that do not contain asbestos but which perform the
same function.  Where the asbestos elements of a product were inessential, the substitute product may
consist of the same product minus the asbestos element (e.g., a kitchen hot pad with thick cotton
padding but no asbestos);  or the same product redesigned to eliminate the need for asbestos;  or a
similar product which uses different fibres (e.g., a hot pad made of glass fibre);  or a similar product
made of what the EC describes as "classic materials" (e.g., a trivet made of cast iron, ceramic orplastic).  The physical correspondence between the two classes of products is therefore considerably
weaker than Canada has assumed.  Canada has failed to show that asbestos and asbestos-containing
products and the substitutes have the same "properties, nature and quality".  The known severe
adverse human health effects of asbestos are anot her reason why asbestos-containing products are not
"like" the substitutes for which adverse health effects have not been demonstrated.  The substitutefibres differ considerably in physical structure and properties from chrysotile asbestos and thus cannot
be considered "like products."  For example, while chrysotile is a naturally occurring mineral which is
crystalline in nature, the man-made mineral fibres (MMMF) are amorphous (non-crystalline) silicates
which are produced from a liquid melt of different starting materials (e.g., slag, natural rock, glass,
clays).  Furthermore, unlike chrysotile asbestos, MMMF do not split longitudinally into smaller fibrilsof smaller diameter, but may break transversely into shorter segments.
123
(iii) Article XXIII:1(b) of the GATT
4.66 The United States argues that Canada has failed to meet the special burden imposed by
Article 26.1 of the Dispute Settlement Understand ing on parties making claims of non-violation
nullification or impairment.  The United States has been one of the strongest proponents of the non-
violation remedy, as an essential safeguard for bargained-for market access rights against frustration
by government actions.  But the requirements of the non-violation remedy are not satisfied here.  Asthe EC have noted, the text of Article XXIII:1(b) establishes three elements that a complaining party
must demonstrate in order to make a cognisable claim under Article XXIII:1(b):  (i) application of a
measure by a WTO Member;  (ii) a benefit accruing under the relevant agreement;  and (iii)
nullification or impairment of the benefit as a result of the application of the measure.  Canada, as the
complaining party, has the burden of presenting detailed evidence in support of all three elements.  Inthe present case, there is no dispute that the French Decree is a measure of a Member.  The question is
simply whether Canada has a legitimate expectation of benefits accruing to it.  The precedents are
clear that for expectations to be legitimate, they must take into account all measures of the party
making the concession that could reasonably have been anticipated at the time of the concession.
                                                     
122BISD 18S/102, para. 18.
123Man-Made Mineral Fibres , IPCS Environmental Health Criteria 77, 1988, pp. 11-12;  Man-Made
Mineral Fibres and Radon:  Monographs on the Evaluation of Carcinogenic Risks to Humans , Vol. 43, IARC,
1988, pp. 39-53;  Asbestos and Other Natural Mineral Fibres , Environmental Health Criteria 53, IPCS, 1986,
pp. 22-24.WT/DS135/R
Page 222
4.67 The United States considers that, as a matter of principle, the Panel should reject the
possibility of a finding of non-violation nullification or impairment with respect to health and safety
regulations that respond to the development of scientific knowledge concerning health risks.
Members do not have a legitimate expectation that regulatory measures will stay static in the face of
expanding scientific knowledge concerning health risks, and changing societal decisions concerningthe level of acceptable risk.  Canada is also in a poor position to argue that an asbestos ban was
unforeseeable at the time it negotiated the tariff concessions on asbestos.  The dangers posed to human
health by asbestos are notorious and have been so for many years.  Pliny, the ancient Roman author,
described the "diseases of slaves" as including exposure to the textile processes of preparing and
weaving asbestos, and even referred to the use of a transparent bladder skin as a respirator to avoid
inhalation of dusts by slaves.
124  As of the time of the first GATT negotiating round in 1947,
asbestosis had already (in the 1920s) been identified as a distinct condition caused by asbestos.125
By 1935 asbestosis was widely recognized as a mortal threat affecting a large fraction of those who
regularly worked with the material.126  In addition, by the mid-1940s there were indications that
exposure to asbestos in animals and humans was associated with lung tumours.127  Thus Canada
should have reasonably expected subsequent regulatory action (such as a ban) by a GATT contracting
party as a result.  As of the Dillon Round of 1960-61, Canada had even more reason to foresee thepossibility of restrictive regulations of asbestos.  An international symposium of experts on the
pathogenesis of lung cancer in 1953 published its conclusions and recommendations in a journal
which editorialised:  "[I]t seems to be beyond discussion that cancer of the lung is sometimes caused
by occupational exposure to asbestos."
128  In addition, two major studies had been published in 1955
on cancer in the textile industry demonstrating the relationship between asbestosis and lung cancer.129
Since the early 1960s, the hazards posed by asbestos - and particularly chrysotile asbestos - have
become even more widely known and documented.130
(b) The Agreement on Technical Barriers to Trade
4.68 With respect to Canada's arguments that the French ban on asbestos is inconsistent with a
number of provisions in the Agreement on Technical Barriers to Trade (TBT), the United Statesargues that Canada has misread the relevant TBT articles.  The interpretation of the TBT Agreement
on which Canada's arguments are based attempts to read into the Agreement obligations that do not
exist.  The United States urge the Panel to reject that interpretation.  The EC, on the other hand, have
argued that the French Decree is not a "technical regulation" because it is a categorical ban on
asbestos and products containing asbestos.  They have argued that general bans, and specifically this
product ban, are not "technical regulations" because they allegedly do not "lay down product
characteristics or their related processes and production methods" within the meaning of paragraph 1of Annex 1 of the TBT Agreement.  The United States disagree with the EC's view on this point.  In
this instance, the Decree lays down "product characteristics […] with which compliance is
mandatory".  The characteristics in question are that the product may not contain any asbestos if it is
to be marketed, offered for sale, imported, exported, etc. in France.  Compliance with the exclusion of
asbestos is mandatory except if the French Government has accorded a derogation, in which caseadherence to the terms of the derogation is mandatory.  In any event, the French Decree is a technical
                                                     
124Castleman B. I., Asbestos:  Medical and Legal Aspects , 4th ed., 1996, p. 1.
125Lilienfeld, D. E., The Silence:  The Asbestos Industry and Early Occupational Cancer Research - A
Case Study , 81 American Journal of Public Health 791, 792 (1991).
126Castleman B. I., Asbestos:  Medical and Legal Aspects , 4th ed., 1996, p. 39.
127Lilienfield, D. E., The Silence:  The Asbestos Industry and Early Occupational Cancer Research – A
Case-Study , 81 Am. J. Pub. Health 791, 794 (1991);  Castleman B. I., Asbestos:  Medical and Legal Aspects , 4th
ed., 1996 pp. 53-65, 135.
128Castleman B. I., Asbestos:  Medical and Legal Aspects , 4th ed., 1996 pp. 94, 95.
129Ibid. pp. 97, 98.
130See IPCS Environmental Health Criteria 203 – Chrysotile Asbestos, WHO, 1998, and sources cited
therein.WT/DS135/R
Page 223
regulation within the meaning of the TBT Agreement and is subject to the substantive rules of the
TBT Agreement.  The EC's interpretation of Annex 1 would open up a loophole of potentially huge
dimensions in the TBT Agreement.  Measures having a very significant impact on trade - for instance,
regulations limiting the characteristics of spreadable butter or wool - could simply be redefined as
product bans.  Similarly, the EC argument would mean that a regulation on the safety of infant toysthat excluded any parts below a certain size (to prevent choking) would not be a "technical regulation"
nor would regulations excluding water from being added to ham. The provisions of the
TBT Agreement would then be rendered a nullity.  Such a reading of the TBT Agreement is
impermissible as a matter of treaty interpretation, and undesirable as a matter of trade policy.  This
does not mean that the French Decree does not satisfy the requirements of the TBT Agreement,
however.  As discussed below, although the TBT Agreement applies to the French Decree, Canada
has failed to make a case that the French Decree violates any of the provisions it has cited.
(i) Article 2.1 of the TBT Agreement
4.69 The United States argues that, for the reasons discussed in relation to Article III of the GATT,
these products are not "like products."  Furthermore, since the ban is applied without discrimination as
to the source of the product, discrimination between foreign sources is not an issue.
(ii) Article 2.2 of the TBT Agreement
4.70 The United States notes that Article 2.2 provides a key element of the disciplines in the
TBT Agreement.  From the standpoint of the United States, certain aspects of Article 2.2 are
particularly important with respect to health and safety regulation.  The first sentence of Article 2.2 is
important because it recognizes that in certain circumstances, technical regulations may create
necessary obstacles to trade, and the creation of such necessary obstacles is consistent with theTBT Agreement.  We note that the "legitimate objectives" enumerated (non-exhaustively) in
Article 2.2 specifically include protection of human health or safety.  Article 2.2 also recognizes that
in assessing the risks that may arise from non-fulfilment of a legitimate objective, a government may
consider a number of elements, including available scientific and technical information, related
processing technology or the intended end-uses of a product.
4.71 The obligation in Article 2.2 that technical regulations are not to be more trade restrictive than
necessary to fulfill a legitimate objective should be interpreted in a manner similar to Article 5.6 of the
Agreement on Sanitary and Phytosanitary Measures (SPS).
131  Such a reading is supported by the sixth
clause of the Preamble to the TBT Agreement, whic h provides that:  "[R]ecognizing that no country
should be prevented from taking measures necessary … for the protection of human, animal or plant
life or health, [or] of the environment […] at the levels it considers appropriate […]."  The
United States argues that the preamble is part of the context of Article 2.2 in the sense of Article 31 ofthe Vienna Convention on the Law of Treaties, and provides an authoritative indication of the
TBT Agreement's object and purpose for the purposes of treaty interpretation.  Thus, in order for a
Member to show that a government's technical regulation is more trade-restrictive than required, it
would need to show that there is another measure that is reasonably available, fulfils the regulating
Member's legitimate objectives, and is significantly less restrictive to trade.  Accordingly, thecomplaining party should be required to identify a specific alternative measure that is reasonably
available - as a Member is not required to do what is unreasonable.  Furthermore, the alternative
measure must make a significant difference from a trade perspective.  There should be no need to
adopt an alternative measure if it makes only an insignificant difference in terms of trade.  Most
                                                     
131Article 5.6 provides in relevant part "when establishing or maintaining sanitary or phytosanitary
measures to achieve the appropriate level of sanitary or phytosanitary protection, Members shall ensure that such
measures are not more trade-restrictive than required  to achieve their appropriate level of sanitary or
phytosanitary protection, taking into account technical and economic feasibility".WT/DS135/R
Page 224
importantly, the complaining party must demonstrate that the alternative measure fulfils the
government's objectives.  Canada has failed to demonstrate that its preferred alternative to the French
ban –  i.e. "controlled use"  of asbestos and asbestos products – fulfils the French Government's stated
"legitimate objective" of protection of human health.
4.72 Canada alleged that the Decree does not address the "true problem" of asbestos in France
which Canada identifies as the flocking of asbestos.  Yet it is not for Canada to determine what
France's "true problem" is.  It is up to France to determine what level of protection to afford its
citizens.  Second, Canada alleges that the French Decree violates Article 2.2 because it fails to
acknowledge the "scientific reality" that chrysotile encapsulated in a matrix is harmless.  Yet as
discussed above and as demonstrated by the EC, encapsulated asbestos is not harmless at all, as the
encapsulation can easily be breached, and is likely to be breached during the product's life cycle,
resulting in release of fibres and elevated risk to human health.  Canada alleges that the French Decreeviolates Article 2.2 because it replaces use of chrysotile – an allegedly harmless product – with
substitutes whose health risks are unknown.  The Unit ed States fundamentally objects to this reading
of the TBT Agreement.  Canada is implicitly arguing that any regulatory action negatively affecting
trade in a product has to be tested against the hypothetical risks engendered by use of likely alternative
products.  This test has no basis whatsoever in the TBT Agreement.
(iii) Article 2.4 of the TBT Agreement
4.73 Canada has asserted that Article 2.4 requires a panel to determine:  (i) whether a technical
regulation on chrysotile is required;  (ii) whether there are international standards concerning
chrysotile, (iii) whether the international standards are effective and appropriate to achieve the
objective;  and (iv) whether the Decree is based on international standards.  Under this analysis,Canada concludes that France adopted the most restrictive measure possible despite the fact that the
international community has developed standards representing a less restrictive approach
(i.e., controlled use).  This analysis misreads Article 2.4.  First and fundamentally, Article 2.4 does not
contemplate that a panel determine whether a technical regulation is or is not required.  The burden of
proof is on Canada to demonstrate that international standards exist and are relevant.  In regard to theILO standard, both the ILO Convention 162 and Recommendation 172 allow participating countries to
choose the approach they find to be appropriate to protect workers from asbestos hazards.  Indeed, the
Provisional Record to the 72
nd Session of the International Labour Conference, which adopted
Convention 162, states concerning Article 10 of  Convention 162 (which Canada now claims to
condition a ban on a finding concerning the risk posed by product substitutes):  "The Government
member of Canada saw nothing in Article 10 that would prevent any country from doing whatever it
wanted with respect to asbestos." 132
4.74 The United States argues that Brazil's interpretation of Article 2.4 of the TBT Agreement
ignores the fact that climate, geography and fundamental technological problems are listed as
examples, not an exhaustive list, of reasons that an international standard may be an "ineffective and
inappropriate means" of achieving a Member's legitimate objective.
C. ZIMBABWE
1. Introduction
4.75 As an important producer and exporter of chrysotile (white) asbestos fibre and products
containing chrysotile asbestos and also as a developing country in need of foreign exchange,
Zimbabwe argues that it has a substantial interest in the outcome of this proceeding.  In fact, the
                                                     
132International Labour Conference Provisional Record, 72nd Session, Geneva, 1986, 29/1:  Fourth
Item on the Agenda:  Safety in the Use of Asbestos, pp. 29/8.WT/DS135/R
Page 225
present dispute is of such importance to Zimbabwe's asbestos industry and indeed its whole economy
that the Government of Zimbabwe has decided, for the first time ever, to have recourse to the dispute
settlement mechanism of the WTO.  Zimbabwe is of the view that the ban of chrysotile asbestos and
products containing chrysotile asbestos by France is unjustified and contrary to relevant rules of the
World Trade Organization (WTO).  The ban should therefore be lifted without delay.  Zimbabwebelieves that it is not incumbent upon it as a third party to this dispute to set out in full the case against
the responding party, i.e. the EC.  Accordingly, Zimbabwe will limit itself in this submission to the
Panel to addressing a number of factual and legal aspects of this dispute that it feels are of particular
importance to the outcome of this proceeding.  Zi mbabwe argues that the complaining party in this
case, i.e. Canada, has made a compelling case with respect to both the factual and legal issues in
dispute as to why the ban on chrysotile asbestos and products containing chrysotile asbestos is
inconsistent with relevant WTO rules and must be withdrawn immediately.
2. Factual Aspects
4.76 Zimbabwe  asserts that the chrysotile asbestos industry is of great economic importance to its
economy.  Zimbabwe ranks among the world's largest producers of chrysotile asbestos.  In Africa,
Zimbabwe is the number one producer of chrysotile asbestos.  It produces a high-quality chrysotile
asbestos fibre and has sufficient underground reserves for at least another 25 years and infrastructureto continue operations for many more years to come.  Chrysotile asbestos currently accounts for
about 18 per cent of Zimbabwe's mineral production index of volume and value.  Crocidolite (blue)
and amosite (brown) asbestos are not mined in Zimbabwe.  As a developing African country,
Zimbabwe relies primarily on natural resource products and other primary products for much of its
export revenue.  In terms of the revenue it generates, chrysotile asbestos is second only to gold as faras the mining sector is concerned.  As much as 95 per cent of the country's total asbestos fibre
production is exported.  In 1998, for example, 150,000 tonnes of chrysotile asbestos were exported out
of a total production of some 175,000 tonnes, generating foreign exchange in excess of
ZW$1.5 billion.  In addition to the export of chrysotile asbestos fibres, more than 7,500 tonnes of
asbestos-cement products, valued at over ZW$30 million, were exported.  Zimbabwe's sole producerof chrysotile asbestos fibre is African Associated Mines.  The European Union in general, and Spain
and France in particular, have traditionally been important export markets for African Associated
Mines.
4.77 Zimbabwe argues that African Associated Mines suffered a dramatic (more than 50 per cent)
drop in its sales to France in 1996.  The setback suffered by African Associated Mines in the French
market is directly attributable to the French Gove rnment's actions.  It should be pointed out in this
connection that in mid-1996 the French Government announced its intention to ban asbestos.  Beforethat, i.e. towards the end of 1995, the French Government had already announced a programme to
reduce the risks associated with exposure to asbestos.  There is therefore clear evidence that the
French ban on asbestos and products containing as bestos has had a direct and damaging impact on
Zimbabwe's asbestos industry.  The significance of the asbestos industry to Zimbabwe cannot be
overstated.  The country has immensely benefited from its existence.  African Associated Minesdirectly employs about 6,000 people in Zimbabwe, which amounts to about 20 per cent of total
employment in the mining industry.  The industry indirectly sustains more than 70,000 people in and
around the mining towns of Zvishavane and Mashava.  There are no other industries in these towns,
meaning that a decline of the asbestos industry would cause dislocation with all its attendant social
consequences.  It should be borne in mind in this context that the Zimbabwean economy has facedconsiderable difficulties in the past decade and has not been able to create a sufficient number of new
jobs.  Out of a labour force of 5 million people, only 1.4 million people are gainfully employed.  Apart
from generating revenue for the Government of Zimbabwe, the asbestos industry has injected
dynamism into the country's economy.  In addition to the salaries and wages paid by the companies
engaged in the mining and marketing of asbestos and asbestos products, the asbestos industry's morethan 300 suppliers of goods and services receive payments of around ZW$600 million each year,WT/DS135/R
Page 226
including over ZW$150 million for the state-owned Zimbabwe Electricity Supply Authority (ZESA)
and the National Railways of Zimbabwe.
4.78 It is apparent from the foregoing that a ban on asbestos would have severe repercussions for
the Zimbabwean economy.  In fact, as has been demonstrated, the ban on asbestos by France has
already impacted negatively on the Zimbabwean economy.  It must be mentioned in this connectionthat Zimbabwe views with great concern the potentia lly wider implications of the French ban on the
use of chrysotile asbestos.  While it is true that most countries, including the United States, still do not
generally prohibit the use of chrysotile asbestos or products containing chrysotile asbestos, there is the
probability that other governments may be tempted to follow the French example if the French
measure were upheld by the WTO.  Indeed, th e European Union has just announced - without
awaiting the outcome of a WTO ruling - that it will move to ban the use of chrysotile asbestos in all its
member States.
133  Zimbabwe wished the WTO to be aware of the wider implications of the decision it
would render in this dispute.
4.79 Zimbabwe argues that the risks involved in the use of chrysotile asbestos can be adequately
controlled.  It appears that the concerns that governments have with respect to the use of chrysotile
asbestos relate to airborne asbestos dust or respirable asbestos fibres, as they may have an effect on
human health.  For this reason, the United Nations Environment Programme (UNEP), theInternational Labour Organization (ILO), and th e World Health Organization (WHO), within the
Framework of an Inter-Organization Progra mme for the Sound Management of Chemicals,
commissioned a Task Group of international experts to make an evaluation of the risks for human
health from exposure to chrysotile asbestos and to make recommendations for health protection and
further research.  The report of the Task Group was published in 1998.
134  One of the Task Group's
main conclusions was that "[e]xposure to chrysotile asbestos poses increased risks for asbestosis, lung
cancer and mesothelioma in a dose-dependent manner".135  The Group acknowledged, however, that it
was not possible to provide quantitative estimates of risks to humans given the dearth of information
and data.136  Furthermore, the Group cautioned that there was a need for further epidemiological
studies of populations exposed to pure chrysotile so as to clearly and reliably be able to distinguishbetween chrysotile and amphibole exposure.
137  In other words, there is a possibility that the available
data may actually overestimate the risks to humans from exposure to chrysotile asbestos.138  What is
quite clear from the Task Group's conclusion - and this is crucial - is that the risks to humans are
conditional on exposure as well as on doses or concentrations.139  The key objective for any
responsible government must therefore be to reduce exposure.  This said, it should be borne in mind
that chrysotile asbestos is a natural product.  It is present in the air we breathe and in the water we
                                                     
133This information is based on a report by Reuters News Agency, dated 6 May 1999.
134WHO , IPCS Environmental Health Criteria 203 - Chrysotile Asbestos , Geneva, 1998.
135Ibid., p. 144.
136Ibid., pp. 7 and 144.  Zimbabwe notes that, in this regard, it is misleading for the EC to cite the 1998
Task Group report for the proposition that there is an international consensus that no threshold of exposure canbe identified below which no risk to humans exists.  The Task Group in fact merely stated that it could notidentify any such threshold on the basis of the available data.  See WHO, IPCS Environmental Health
Criteria 203 - Chrysotile Asbestos , Geneva, 1998, pp. 7 and 144.
137Ibid., p. 145.
138Zimbabwe notes that this is especially true of applications of chrysotile-containing products in
industries such as construction, on which the EC has placed great emphasis in its Submission, because "studieshave not been in general able to distinguish between chrysotile and amphibole exposure".  See WHO, IPCS
Environmental Health Criteria 203 - Chrysotile Asbestos , Geneva, 1998, pp. 122 and 112.
139According to Zimbabwe, the EC confirms this when stating:  "[L]es principales données qui ont été
présentées illustrent le caractère ubiquitaire de l'amiante en milieu de travail qui peut, à des niveaux d'exposition
suffisamment élévés, entraîner de nombreux cas de maladies mortelles".WT/DS135/R
Page 227
drink.  Exposure is therefore inevitable, and no ban can change that.140 With these facts at hand, the
question arises as to whether the French ban of asbestos is justifiable given the information within the
public domain.  Zimbabwe believes that what is at the heart of this dispute is the risk of occupational
exposure to cement containing chrysotile asbestos.  This is because prior to 1997, i.e. before the
French ban was implemented, around 90 per cent of French imports of chrysotile asbestos fibres wereused for the production of asbestos-cement.
4.80 It is the submission of Zimbabwe that transportation and storage of imported chrysotile
asbestos fibre do not entail a risk of exposure provided that there is proper packaging.  Another
possible activity involving a risk of exposure is the production of chrysotile asbestos-cement itself.  In
Zimbabwe, this risk has been contained, as demonstrated by the monitoring done by a group of
independent experts for Turnall Fibre Cement Company Limited, which is a Zimbabwean company
engaged in the manufacture of chrysotile asbestos-cement.  The focus of the research has been on thehealth hazards related to asbestos during the process of manufacture.  This research has been going on
for more than ten years and so far there have been no reported cases of risks to human life.  It should
be mentioned here that the EC has adduced as relevant evidence a very recent study by the
U.K. Health and Safety Commission which is alleged to demonstrate that notwithstanding the
application of control measures, "primary users" of chrysotile asbestos fibres, i.e. workers in asbestos-cement factories, showed a higher mortality rate in relation to asbestos-related lung cancer and
mesothelioma.  Zimbabwe views this study with consid erable scepticism in view of the fact that there
are long latency periods involved in the above-named diseases and that the current "cases" go a long
way back to a time when the control measures implemented were far less sophisticated than they are
now.
4.81 Zimbabwe asserts that a risk of exposure may also be incurred by workers or any person, for
that matter, during installation, maintenance and repair of asbestos-containing products.  The risks
involved in the use of asbestos-containing products can be adequately controlled, even taking into
account France's high level of protection against health risks, thus making a ban unnecessary.
141  I n
fact, the 1998 Task Group report supports this conclusion when stating that "[n]on-friable productsand appropriate technological controls greatly reduce fibre release.
142"  It can thus be said that the risk
of occupational exposure (i) is a function of the nature of the product and (ii) the risk inherent in that
product can in any event be further reduced through appropriate control measures.  Regarding the
products at issue, i.e. products made from asbestos-cement, the first thing that should be noted is that
asbestos-cement does not contain friable asbestos.  Moreover, and equally importantly, products made
from asbestos-cement are products of high density and thus chrysotile asbestos fibres are firmly
blended into the final product.  This reduces to a minimum the likelihood of fibres being released intothe air and thereby posing a health hazard to human  beings.  The ILO came to the same conclusion in
a report released in 1985:  "[l]a manipulation de produits contentant de l'amiante dans lesquels les
fibres d'amiante sont solidement fixées dans un liant de telle sorte qu'il ne puisse pas se former de
poussières ne présente pas de danger pour la santé.
143"
4.82 It emerges therefore that when products made from asbestos-cement are used and handled
properly, the risks associated with their use are minimal.  The recommendation of the 1998
Task Force was to the same effect.  It recommended that appropriate control measures be
                                                     
140WHO, IPCS Environmental Health Criteria 203 - Chrysotile Asbestos , Geneva, 1998, pp 2 and 129
et seq.
141For a more detailed discussion of this point, see Zimbabwe's arguments with respect to GATT
Article XX .
142WHO, IPCS Environmental Health Criteria 203 - Chrysotile Asbestos , Geneva, 1998, p. 28.
143Bureau International du Travail, La sécurité dans l'utilisation de l'amiante , Conférence internationale
du Travail, Rapport VI (1), 71ème session, 1985, Genève, p. 29.WT/DS135/R
Page 228
implemented wherever occupational exposure might occur.144  Among the control measures which
might be used to minimize exposure to chrysotile asbestos are engineering controls, special work
practices (including workplace hygiene), and protective equipment, such as technical appliances
which eliminate or minimize the formation of asbestos dust, as well as protective respiratory
equipment or special protective clothing.  That risk control is in fact an effective means of dealingwith chrysotile asbestos-related health concerns is borne out by the following passage taken from the
report of the 1998 Task Group:  "[d]ata from industries where control technologies have been applied
have demonstrated the feasibility of controlling exposure to levels generally below 0.5 fibres/ml.
Personal protective equipment can further reduce individual exposure where engineering controls and
work practices prove insufficient."
145  In light of the foregoing, it is the contention of Zimbabwe that
the combined use of high-density products made from asbestos-cement, which inherently are low-risk
products, coupled with adequate risk control measures minimize the risk of exposure to asbestos dust.Whatever residual risk may remain does not, in Zimbabwe's view, justify an outright ban on chrysotile
asbestos.
3. Legal Aspects
4.83 It is the submission of Zimbabwe that the French ban of chrysotile asbestos is contrary to
WTO rules and should be lifted without any delay.  It is the view of Zimbabwe that the French Decreeconstitutes a technical regulation within the meaning of the Agreement on Technical Barriers to Trade.
As such, it must be in accordance with Article 2.2 of the TBT Agreement and hence must not be
"more trade-restrictive than necessary to fulfil a le gitimate objective".  By totally banning the import
of chrysotile asbestos, the French legislation contravenes the express language of this Article.
Furthermore, in the event of the French Decree being found to fall outside the ambit of theTBT Agreement, the Decree contravenes the provisions of GATT Article III:4, as it discriminates
against imported asbestos in favour of other like products which are used in France for the same
purpose.  In the same vein, the French Decree cannot be justified under the terms of
GATT Article XX(b), as claimed by the EC.
(a) The Agreement on Technical Barriers to Trade
4.84 Zimbabwe disagrees with the view of the EC that the Decree does not fall within the scope of
the TBT Agreement.  For a mandatory measure to come within the scope of the TBT Agreement, it
must be a "technical regulation".  The Decree clearly is a mandatory measure.  Notwithstanding the
EC's claim to the contrary, it is the submission of Zimbabwe that the Decree, to the extent that it
applies to products containing chrysotile asbestos, qualifies as a technical regulation within the
meaning of Annex 1 of the TBT Agreement.  The argument of the EC that for the TBT Agreement to
be applicable, the Decree should have specified which particular products were covered by the ban iswithout any merit.  It is the view of Zimbabwe that such an interpretation is overly restrictive.
Annex 1 of the TBT Agreement talks about "product characteristics" in general.  Nowhere does it state
that the national legislator should adopt only product-specific regulations.  Even ignoring this point,
Zimbabwe fails to understand why a Member should be precluded from laying down horizontal rules
applicable to a group or groups of products which call for the same regulatory approach.  In fact, itappears that there would be little merit in forcing Members to specifically enumerate all products
covered by a particular regulation when it is in the nature of things that new products would regularly
have to be added to the list due to, for example, technological developments.  From a public policy
perspective, this would seem to be a rather inefficient and costly approach to adopt.
4.85 Zimbabwe argues that the second reason advanced by the EC in support of its argument that
the TBT Agreement is not applicable in this case is also without any merit.  According to the EC, the
                                                     
144WHO, IPCS Environmental Health Criteria 203 - Chrysotile Asbestos , Geneva, 1998, p. 144.
145Ibid., p. 144.WT/DS135/R
Page 229
ordinary meaning of the noun "characteristic" suppo rts the view that, for the TBT Agreement to be
applicable, product characteristics must be positively defined.  Applying this reading of the
TBT Agreement to the present case, the EC argues that "not containing chrysotile asbestos" should not
be seen as the equivalent of a product characteristic.  Zimbabwe finds this reasoning of the EC very
tenuous.  According to the Shorter Oxford English Dictionary, the noun "characteristic" designates a"distinguishing quality or peculiarity".
146  Zimbabwe believes that, without doing injustice to these
terms, a product's "distinguishing quality or peculiarity" can lie in the fact that it does not contain
asbestos.  The absence of any trace of asbestos clearly sets apart a product in terms of its qualities
from another product which contains asbestos.147  In any event, Annex 1 does not actually require
positive product characteristics.  Zimbabwe submits that its interpretation of Annex 1 is also in
conformity with the relevant context of Annex 1 of the TBT Agreement.  All the Agreements annexed
to the WTO Agreement are part of the relevant context.148  Thus, Article 2(f) of the Agreement on
Rules of Origin obliges Members to ensure that "their rules of origin are based on a positive standard".
From this it follows that where Members wanted to gi ve a special meaning to a term - in this case, to
the term "standard" - they used appropriate language to reflect their intention.  Members did not adopt
that approach as far as Annex 1 of the TBT Agreement is concerned.149
4.86 Given the object and purpose of Annex 1 of  the TBT Agreement, Zimbabwe wonders what
would be the rationale of a rule which compels Members to define product characteristics positively
when all they care about is a negative characteristic.  Why, for example, should France have to
positively define the characteristics of a host of products when its only regulatory concern is with the
asbestos contained in those products?  It is the submission of Zimbabwe that its interpretation is also
in conformity with the jurisprudence of the WTO Appellate Body.  Thus, according to the
Appellate Body, the term "measure" as it appears in various WTO agreements is to be understood to
include a government's failure to act.150  In other words, a "negative" measure, i.e. a failure to act,
counts as a measure no less than a "positive" measure.  By token of the same reasoning, the term
"characteristics" should encompass negative characteristics.  In view of the above reasons, Zimbabwe
joins Canada in believing that the general term  "product characteristics" lends itself to an
interpretation which includes negative characteristics.
4.87 Having demonstrated that the Decree qualifies as a technical regulation under the
TBT Agreement to the extent that it bans products containing chrysotile asbestos, Zimbabwe now
turns to show that the same is true also with respect to the Decree's ban on the use of chrysotile
asbestos fibres as such.  The EC has expressed the view that the French ban on the production and
importation of chrysotile asbestos fibre is not a technical regulation within the meaning of Annex 1 of
the TBT Agreement because, just like the ban on asbestos-containing products, the ban on asbestos
fibres is general (rather than specific) and lays down negative characteristics (rather than positive
ones) or, for that matter, does not lay down any charac teristics.  As the issues of specificity and of
"positive vs. negative standards" have already been discussed, the following submissions will focus on
whether or not the French Decree lays down product characteristics with regard to the ban on asbestos
fibres.  Zimbabwe contends that the matter is more complex than the EC makes it out to be.  To besure, an independent and isolated ban on sales, say, of all cigarettes would not normally be considered
                                                     
146The Shorter Oxford English Dictionary on Historical Principles, Oxford, 1993.
147In this connection, Zimbabwe notes that it is a truism that it is often easier to define objects
negatively than to come up with an exact and exhaustive positive definition.
148Panel Report, Japan – Measures Affecting Agricultural Products , adopted on 19 March 1999,
WT/DS76/R, para. 8.111.
149"A treaty interpreter is not entitled to assume that [the use of different words in different places] was
merely inadvertent on the part of the Members who negotiated and wrote that Agreement".  See EEC - Measures
Concerning Meat and Meat Products (Hormones) , Appellate Body Report, adopted on 13 February 1998,
WT/DS26/AB/R, WT/DS48/AB/R, para. 164.
150See Guatemala – Anti-Dumping Investigation Regarding Portland Cement From Mexico ,
Appellate Body Report, adopted on 25 November 1998, WT/DS60/AB/R, footnote 47.WT/DS135/R
Page 230
a technical regulation.  Yet the situation as it presents itself in this dispute is quite unlike that.  As
Canada rightly pointed out, unlike cigarettes, asbestos fibres per se , i.e. as products in their own right,
serve no useful purpose.  It is the products containing asbestos fibres which have commercial use and
value.  By necessary implication, when it comes to dealing with the health hazards of asbestos, the
concern of policymakers and the law should be with  products containing asbestos fibres, not with
asbestos fibres, per se .  If the products containing asbestos disappear, so will asbestos fibres.
4.88 Zimbabwe considers that the Decree is fully consistent with this straightforward principle.
The EC does not contest this.  On the contrary, the EC sets out the objective of the Decree as follows:
"[l]'interdiction de l'amiante, en France et dans d'autres pays, n'a pas pour objectif de supprimer les
quelques 0,0002 fibres/ml qui existent 'naturellement' dans l'air.  L'interdiction vise simplement à
protéger l'ensemble des travailleurs et des utilisateurs de l'amiante qui sont souvent exposés à des
valeurs très supérieures [...] pour des opérations courantes d'intervention sur des matériaux contenantde l'amiante-ciment."
151 The EC explains the rationale of its asbestos-control policy in the following
terms:  "[l]a politique adoptée en France en 1996 vise en tout premier lieu au remplacement des
matériaux contenant de l'amiante par d'autres matériaux sans danger [...]".152  It clearly emerges from
these two quotes that the Decree aims at asbest os-containing products, not at asbestos fibres per se .
The inference that can be drawn from this is that the import ban - just like the corresponding ban ondomestic production - does not perform an independent function, but a subsidiary one.  Indeed, the EC
expressly states that nothing would change if the import ban - and, by implication, the ban on
domestic production - were lifted.  Imported and domestically produced asbestos fibres could still not
be sold on French territory - because no products containing them could be sold.  The following
sentence pinpoints this underlying logic of the French ban:  "[l]e but est donc bien d'arrêter ladiffusion d'amiante le plus en amont possible".
153 The ban on asbestos fibres is thus based on
considerations of administrative efficiency, which is arguably only a secondary objective pursued by
France.  Again, this is confirmed by the EC:  "[ l]'interdiction d'importation a simplement pour but de
rendre plus efficace, en termes de contrôle, l'in terdiction d'utilisation [which is France's primary
goal]".154
4.89 Zimbabwe asserts that, for the foregoing reasons, it should be readily apparent that the ban on
chrysotile asbestos fibre is very closely related to the ban on asbestos-containing products.  Assuming
the ban on chrysotile asbestos fibres could be viewed in isolation, it could possibly be argued that it
does not, stricto sensu , lay down product characteristics.  As Zimbabwe has demonstrated, however,
such a line of reasoning is unwarranted and misses the point.  The ban on asbestos fibres is an integral
part of the Decree.  In fact, it is part and parcel of the same Article of the same Decree.  Zimbabwe
therefore submits that for purposes of this proceeding there is one single, indivisible regulatorypackage - the Decree - whose consistency the Panel needs to examine with the TBT Agreement.
Zimbabwe is of the view that the Decree falls with in the ambit of the TBT Ag reement.  This view is
buttressed by the reasoning of another Panel which faced a comparable situation.  In the Kodak/Fuji
film case, the Panel had to decide whether a measure that had not been directly brought up under
Article 4 of the DSU could nevertheless be within the Panel's terms of reference.  The Panel foundthat such a measure was not within the Panel's terms of reference, unless it was "subsidiary" or
"closely related" to the measure that was properly before the Panel.
155  By way of analogous
reasoning, Zimbabwe argues that the French ban on asbestos fibres is "subsidiary" and "so closely
related" to the ban on asbestos-containing produ cts - which, as shown, qualifies as a technical
                                                     
151See Section III.B of this Report.
152Ibid.
153See Section III.C of this Report.
154Ibid.
155Japan - Measures Affecting Consumer Photographic Film and Paper , Panel Report, adopted on
22 April 1998, WT/DS44/R, para. 10.8.WT/DS135/R
Page 231
regulation within the meaning of the TBT Agreement - that it can reasonably be found to form an
integral part of the latter, and thus constitute a technical regulation in, and of, itself.156
4.90 Zimbabwe further submits that treating the ban on asbestos fibres and the ban on asbestos-
containing products as separate and "unrelated" could give rise to unreasonable results.  Such a
situation could in fact arise in the present case.  It could be envisaged, for instance, that the ban onasbestos fibres might be found to be consistent with the provisions of the GATT, while the ban on
asbestos-containing products might be found to violate the provisions of the TBT Agreement because
- to use but one example - it is more trade-restrictive than necessary to fulfil a legitimate governmental
objective.  Zimbabwe submits that such an outcome would be unreasonable and could undermine the
practical effectiveness of the TBT Agreement.  Taken to its logical conclusion, such a situation would
imply, on the one hand, that France could not produce asbestos-containing products domestically as a
result of the ban on imported or domestically-produced asbestos fibres.  On the other hand, Francewould be required to lift its ban on imports of asbestos-containing products and adopt instead a less
trade-restrictive measure which, in practice, would mean that a certain quantity of asbestos-containing
products would cross the border into French territory.   France would thus have no choice but to idly sit
and watch as other countries take advantage of the business opportunities offered by the French
domestic market.  Zimbabwe is of the view that the drafters of the TBT Agreement did not and couldnot have intended such a result.
4.91 It is therefore the submission of Zimbabwe that the TBT Agreement applies to the
French Decree in its entirety, i.e. with regard to the ban on asbestos-containing products as well as  the
ban on asbestos fibres.  The French legislation does not meet the requirements of Article 2.2 of the
TBT Agreement, as amply demonstrated by Canada .  Zimbabwe adopts the arguments presented by
Canada in this connection and would like to support the views expressed therein by also relying on the
arguments presented below on whether or not the French measure is necessary within the meaning of
GATT Article XX(b).
(b) The General Agreement on Tariffs and Trade
(i) Article III of the GATT
4.92 Zimbabwe argues that, in the alternative, and in addition to the claimed violations of the
TBT Agreement, the Decree violates GATT Article III:4.  Zimbabwe submits that chrysotile asbestos
fibres and, at a minimum, cellulose fibres, aramid fibres and glass fibres are "like products" within the
meaning of Article III:4.  The EC confirms that cellulose and aramid fibres count among those fibres
which are most frequently used to substitute asbestos fibres in the manufacture of cement.
157
Cellulose, aramid and glass fibres are all produced in France.158  Whereas they may lawfully be sold in
that country, the importation and sale of asbestos fibres is prohibited.  There is thus no doubt that
                                                     
156Zimbabwe believes that its interpretation of the TBT Agreement also finds support in Article 1.6 of
the TBT Agreement.  This Article states that "[a]ll references in this Agreement to technical regulations […]shall be construed to include any amendments thereto and any additions to the rules or the product coverage
thereof, except amendments and additions thereof, except amendments and additions of an insignificant nature".
This provision clearly establishes that the term "technical regulation" as used in the TBT Agreement is not to begiven a narrow reading, but one which promotes the Agreement's effectiveness.
157Zimbabwe notes that, with regard to glass fibres, this follows from the definition of HS tariff
position 68.11.
158In Zimbabwe’s view it does not matter for the purposes of an inquiry under Article III:4 whether
domestic production of the "like product" is substantial or small.  Nowhere does Article III:4 lay down a
requirement that domestic production needs to be substantial.WT/DS135/R
Page 232
asbestos fibres are accorded "less favourable treatment" than cellulose, aramid and glass fibres,
despite the fact that they are "like products".159
4.93 Zimbabwe notes that the EC contests that asbestos fibres, cellulose, aramid and glass fibres
are "like products" within the meaning of Article III:4.  It is well established in WTO jurisprudence
that the determination of whether or not products are "like products" must be made in accordance withsuch criteria as the products' physical characteristics and the products' end-use.
160  It is equally clear
from WTO jurisprudence that any such determination can only be made on a case-by-case basis, i.e.
taking into account the specific and unique circumstances of each case.161  Regarding the first
criterion, i.e. physical characteristics and properties, the EC claims that cellulose, aramid and glass
fibres are not sufficiently similar to asbestos fibres in that their chemical composition is different.  In
this connection, Zimbabwe wishes to recall that the EC has acknowledged that the chemical
composition of all varieties of asbestos fibres is different as well.  This did not preclude the EC,however, from concluding that chrysotile asbestos fibres and amphibole asbestos fibres were "like
products".  Zimbabwe submits that the same logic applies and extends to cellulose, aramid and glass
fibres.
4.94 Even ignoring the inconsistency in the reasoning of the EC, Zimbabwe does not believe that
the differences pointed out by the EC are significant enough to make the relevant products "unlike"within the meaning of Article III:4.  Zimbabwe wishes to recall, first of all, that "likeness" does not
require that products be "identical in all respects".
162  The second thing that should be noted is that the
significance that is attached to differences in physical characteristics depends on the particular
circumstances of each case.  In this case, as has previously been stated, the starting-point of any
analysis must be the fact that chrysotile asbestos fibres, as products in their own right,  serve no usefulpurpose.
163  Chrysotile asbestos fibres are predominantly used as "inputs" in the manufacture of
fibre-cement products.  It follows that substitute fibres like cellulose, aramid or glass fibres, on the one
hand, and asbestos fibres, on the other hand, should not be compared to each other as products in their
own right.  Instead, asbestos fibres and the relevant substitute fibres should be compared to each other
as products incorporated into cement.  It is obvious that if this approach is adopted, as it should be, thedifferences identified by the EC become minor ones and irrelevant.  The EC essentially makes the
point that cellulose and aramid fibres are, on average, less fibrillose and larger in diameter than
asbestos fibres and that only asbestos fibres are internationally recognized as "category I" products,
i.e. as products that have been shown to cause cancer.  With regard to these alleged varying degrees of
health risk associated with the fibres at issue, it should be noted that whatever differences exist
between the relevant products become far less relevant when the fibres are blended with other
materials to produce cement and other related products.
164  As explained by Zimbabwe, any remaining
risks arise from improper handling and manipulation of cement-products and not from the cement-
products themselves.  Beyond that, Zimbabwe is not convinced that much significance should be
                                                     
159Zimbabwe considers that the Decree falls obviously within the scope of Article III:4 inasmuch as it is
a regulation which affects the internal sale of asbestos fibres.
160Japan – Taxes on Alcoholic Beverages , Appellate Body Report, adopted on 1 November 1996,
WT/DS/8/AB/R, WT/DS10/AB/R, WT/DS11/AB/R, p. 20.
161Ibid., p. 20.
162Japan – Taxes on Alcoholic Beverages , Report of the Panel, adopted on 1 November 1996,
WT/DS/8/R, WT/DS10/R, WT/DS11/R, para. 6.21
163This is precisely why, in the view of Zimbabwe, the different tariff classification of chrysotile
asbestos fibres, on the one hand, and of cellulose and aramid fibres, on the other hand, cannot provide any usefulguidance for purposes of determining "likeness" in this case.  The Appellate Body has in fact confirmed in itsreport on Japan – Taxes on Alcoholic Beverages , adopted on 1 November 1996, WT/DS/8/AB/R,
WT/DS10/AB/R, WT/DS11/AB/R, p. 22, that the value of tariff classification as a criterion for establishing
"likeness" must be assessed on a case-by-case basis.
164According to Zimbabwe, it should be borne in mind in this context that diameter and fibrillosity are
in any event relevant only to the extent that these characteristics correlate with health risks to humans.WT/DS135/R
Page 233
attached to the fact that only asbestos fibres are listed by the WHO as a "category I" product.  In fact,
even the EC concedes that there is a lingering uncertainty about the risks involved in the use of
alternative fibres.  Zimbabwe submits that the fact that there are to date no known negative effects on
human health from the use of alternative fibres does not necessarily mean that they are risk-free.165
Zimbabwe notes that the EC shares that view, for it expressly acknowledges that "… un risque
indétectable n'est pas égal à une absence de risque".166
4.95 With regard to the second criterion, i.e. commonality of end-uses, Zimbabwe submits that
asbestos, cellulose, aramid and glass fibres serve "substantially identical end-uses".167  Their chemical
resistance and reinforcing capabilities make them almost perfect substitutes for asbestos fibres.
It is therefore not the case that chrysotile asbestos fibres are unique products, as the EC would have
the Panel believe.  As previously noted, the EC, in fact, acknowledges that cellulose and aramid fibres
are commonly used substitutes for asbestos fibres.168  Moreover, like Canada, Zimbabwe believes that
the structure of the Decree is at least suggestive of the substitutability of asbestos fibres with other
fibres.  This becomes clear if the French Decree is seen in terms of the functioning of the political
process.  If very close substitutes had not been available to the principal  users of asbestos fibres at the
time the Decree was signed into law, it is reasonable to assume that they would have lobbied the
French Government and in all likelihood would have secured a broader exception (allowing the
continued use of asbestos fibres) than the one that is now in the Decree.169  In light of the foregoing
considerations Zimbabwe believes that asbestos fibres and cellulose, aramid and glass fibres should be
regarded as "like products" within the meaning of GATT Article III:4.
(ii) Article XX of the GATT
4.96 Zimbabwe argues that the Decree is not justified under paragraph (b) of Article XX because it
is not "necessary to protect human […] health".170  More particularly, the Decree does not satisfy the
necessity requirement.  GATT 1947 case law has established that a measure qualifies as "necessary"
within the meaning of Article XX if there is "no alternative measure consistent with the
General Agreement, or less inconsistent with it, which [a Member] could reasonably be expected to
employ to achieve its […] policy objectives".171  Zimbabwe believes that it is sufficient for it to
establish that - even assuming that asbestos fibres posed more of a health risk to humans - there are
less trade-restrictive measures available to France to achieve its health objective.  The EC claims that
in order for France to achieve its health policy objective there was no measure reasonably available to
it other than an outright ban on chrysotile asbestos fibres.  In particular, the EC submits that control
measures used to minimize exposure to chrysotile asbestos fibres are not sufficient to ensure that
France reaches its high level of protection.  It also argues that control measures are impracticable in
the case of the large group of "secondary users" of asbestos fibres, i.e. those workers anddo-it-yourself people who, in the absence of control measures, may be exposed to chrysotile asbestos
dust during installation, maintenance and repair of products containing chrysotile asbestos.  The
                                                     
165Zimbabwe notes that this is all the more true in view of the fact that the kind of diseases at issue here
involve long latency periods.
166See Section III.B of this Report.
167United States – Taxes on Petroleum and Certain Imported Substances , adopted on 17 June 1987,
BISD 34S/136, para. 5.1.1.
168According to Zimbabwe, the same is true for glass fibres.
169Zimbabwe notes that the fact that there is an additional and special temporary exemption in Article 7
of the Decree for certain used and agricultural vehicles  precisely suggests that no equivalent and affordable
substitutes existed at the time the Decree was signed into law and that the sectors concerned successfully lobbiedthe Government to provide for a temporary exemption.
170Zimbabwe notes that the question to be answered by the Panel here is whether it was necessary for
France to discriminate between asbestos fibres and "like" domestic fibres in order to protect human health.
171Thailand - Restrictions on Importation of and Internal Taxes on Cigarettes , Panel Report adopted
on 7 November 1990, BISD 37S/200, para. 75.WT/DS135/R
Page 234
problem is compounded, according to the EC, by the fact that in many instances "secondary users" do
not have any information as to whether they are dealing with products that contain asbestos.  The EC
submits that even if they were given that information, control measures are costly and turn what would
otherwise be a simple operation into a costly, complicated and awkward one.  Furthermore, the EC
believes that "une fois mis sur le marché, il n'existe plus aucun moyen raisonnable de contrôler l'usagede l'amiante et, en particulier, de contrôler des opérations banales (découpage, sciage …) que de
nombreuses personnes peuvent être amenées à réaliser".
172
4.97 Zimbabwe is not convinced by the arguments of the EC.  First of all, regarding the
effectiveness of control measures, Zimbabwe believes that the observance of certain work practices
and the use of technical appliances in accordance with the ISO standard 7337, for example, would be
sufficient to meet the maximum exposure level acceptable to France.  The EC argues that, even where
special technical equipment is used when high-ris k activities are undertaken, peak exposure levels to
asbestos would still exceed the French maximum le vel.  What the EC fails to mention, however, is
that, as argued by Canada, the wearing of protective respiratory equipment and humidification of the
materials during those activities could significantly reduce the exposure - so much so, in fact, that the
respect of the French maximum level of exposure would be ensured.  Regarding the argument of the
EC that mandatory control measures are impracticable because they are too costly, Zimbabwe conteststhe relevance of such considerations.  After all, whether or not these costs are too high, is a matter to
be left to the dictates of the market.  If the producers of asbestos-cement face insufficient demand for
their products because of expensive control measures imposed on their customers, they will go out of
business or diversify into the production of cement using alternative fibres.  Likewise, Zimbabwe does
not see any merit in the argument that control measures make certain work procedures complicatedand awkward.  Where certain practices are imposed by law, the question of whether they are
appreciated by those who must follow them becomes meaningless.
173  It certainly does not in itself
provide a rationale for trade-restrictive measures.
4.98 While Zimbabwe recognizes that it may not be readily apparent to an inexperienced person
whether or not he/she is handling a product containing asbestos fibres, it is by no means justificationfor instituting a far-reaching ban on products which might contain asbestos fibres.  It is the contention
of Zimbabwe that it would be possible under the WTO legal framework for Members to impose a
disclosure requirement, which would enable purchas ers to make informed decisions as to whether or
not they purchase products containing asbestos fibres.  Where the materials have already been
installed or incorporated, say, in a building, Zimbabwe does not see why there could not be, for
instance, an asbestos warning message next to the evacuation instructions on a notice board of that
building.  Moreover and specifically with respect to the work of plumbers, electricians and the like,Zimbabwe does not see why the owner of an installation or building could not be required to make
available some sort of map which would document  in which parts of the installation asbestos is
present.
174  With reference to the concern of the EC that the use of asbestos-containing products
cannot sufficiently be controlled, especially when it comes to "secondary users" of such products,
Zimbabwe again does not think that banning all imports of such products would solve the problem.  Infact, it would raise more problems than it would solve.  To begin with, if indeed the French
Government is so concerned about do-it-yourself us ers of asbestos-containing products, it could have
                                                     
172See Section III.C of this Report.
173Zimbabwe notes that, by way of analogy, it might be added here that many people think that the
wearing of seatbelts in cars makes driving more "complicated" and awkward.  Yet many countries made thewearing of seatbelt a legal requirement.
174In this connection, Zimbabwe recalls that a tenant or house owner who wants to drill a hole in a wall
to hang up a painting, for instance, also needs to know  exactly where the electrical wiring and installations are,
lest he/she wants to put his/her life at risk.WT/DS135/R
Page 235
easily banned the sale of such products in all do-it-yourself outlets.175  Furthermore, as a supporting
measure, it could have also restricted the handling of asbestos-made products to certified experts, thus
eliminating contact with asbestos by inexperienced people.176  The protection of workers, such as
electricians and plumbers, could also have been ensured relatively easily.  The French Government
could have, for example, required certification, which would only be bestowed upon an individual
once he/she had successfully followed information and training courses on the use and handling of
asbestos-containing products.  The French Government could also have laid out the precise work
practices and technical appliances that must be used  in all contacts with asbestos-containing products.
To ensure compliance, the regulations could authorize the imposition of heavy fines or a custodial
sentence in the event of a wilful disregard of the government's regulations.  Needless to say, it is also
open to a Member to run information campaigns, so as to raise awareness among workers of the risks
of asbestos fibres and the procedures to be observed in all contacts with such fibres.  It is clear fromthe foregoing that the French Government had a number of alternative measures at its disposal which
would have interfered less with trade and at the same time would have assisted in realizing its
overriding objective of protecting the health and safety of its citizens.
____________________
                                                     
175Zimbabwe notes that, after all, in most countries,  drugs cannot be bought in supermarkets, but only in
pharmacies upon production of a doctor's prescription.
176To give another analogous example, Zimbabwe notes that in many countries the installation of
ceiling lamps and other electrical appliances may only be carried out by certified electricians.WT/DS135/R
Page 236
V. PANEL'S CONSULTATION WITH SCIENTIFIC EXPERTS
A. DETERMINATION OF THE PROCEDURE
5.1 The Panel  noted that the dispute before it raised scientific and technical issues.  At the first
substantive meeting, the Panel informed the parties of its intention to seek the opinion of individualscientific experts except where, in the light of th e parties' written rebuttals, it concluded that such a
procedure was not necessary.  The areas in which the Panel wished to obtain information included the
circumstances of exposure to chrysotile asbestos and the associated risks, as well as the effectiveness
of the controlled use of chrysotile.  The Panel in vited the parties to submit their comments to it in
writing, particularly regarding the areas on which the experts were to be consulted, the possible
approaches to such a procedure and the international or other bodies that could usefully be consulted
in order to identify suitable experts.
5.2 In a letter to the Panel dated 14 June 1999, Canada  proposed, in regard to the possible
approaches to a procedure for consultation with indi vidual experts, that five requirements should be
met, each one intended to ensure observance of the right of the parties to be heard at all stages of the
procedure:  (i) the Panel should consult the parties on the choice of scientific experts;  (ii) the Panelshould seek the opinion of the parties concerning the formulation of the questions to be put to the
experts;  (iii) the Panel should provide the parties with an opportunity to make written comments on a
draft report by each of the experts;  (iv) the parties should be able to question each of the experts on
the content of his final report at a meeting with the Panel;  (v) the parties should be given the
possibility to make written comments on the conclusions set out in the final report of each expert andtheir legal implications.  Like the Panel, Canada also believes that the areas on which the scientific
experts should be consulted ought to include the circumstances of exposure to chrysotile asbestos and
the risks associated with present applications as well as risk management by the controlled use of
chrysotile asbestos.  The experts should also be consulted in two other areas, namely the comparative
toxicity of the different types of asbestos fibres and substitute fibres, and risk assessment methods,including the question of whether there are exposure thresholds below which the risk is undetectable
in practice.  In Canada's opinion, there are four specializations that in one way or another cover the
above-mentioned areas and from which the experts should be drawn.  These are toxicology,
epidemiology, risk analysis and occupational health.  Given the scientific characteristics of the
dispute, Canada would wish that each question be submitted to more than one expert, and that each
expert submit an individual report.  As regards the international institutions that could usefully be
approached in order to identify suitable experts, Canada believes that they should be consulted inorder to come up with a sampling of experts in the above-mentioned domains.  The main selection
criteria and hence the best guarantee of impartiality should be that experts must have conducted
recognized and independent research into chrysotile asbestos.  The international organizations that
could be approached included the World Health Or ganization, the International Labour Office and the
International Organization for Standardization.  Once a list of prospective candidates has been drawnup with the help of the international organizations, the parties should then be able to submit their own
list of names of specialists who could act as scientific experts in the areas mentioned above.
5.3 In a letter dated 14 June 1999, the European Communities were of the opinion that the
scientific issues raised in this dispute were simple and clear.  The DSU rules on the burden of proofalso provided the Panel with sufficient guidance in dealing with the factual and scientific issues raised
by the parties to the dispute.  With respect to the general selection procedures and criteria, the
European Communities believed that the Panel's use of experts for obtaining scientific and technical
advice should respect the general principles of law.  In particular, it should be transparent, avoid
conflicts of interest, reinforce the integrity of the dispute settlement mechanism and foster publicconfidence in the outcome of the dispute.  In the view of the European Communities, the Panel can in
this case establish only an expert review group under the terms of Appendix 4 to the DisputeWT/DS135/R
Page 237
Settlement Understanding.  Indeed, the measure at issue in the present dispute is one that must be
examined strictly in terms of the GATT 1994, to the exclusion of the Agreement on Technical Barriers
to Trade.  Article 13:2 of the DSU provides as fo llows: "… With respect to a factual issue concerning
a scientific or other technical matter raised by a party to a dispute, a Panel may request an advisory
report in writing from an expert review group.  Rules for the establishment of such a group and itsprocedures are set forth in Appendix 4".  The esta blishment of an expert review group is the only
option provided under the DSU for panels wishing to obtain information on scientific matters.  The
first sentence of Article 13:2 applies only to situations in which a Panel wishes to obtain factual or
technical but not scientific information.  In their co ntext, the ordinary meaning of the terms, as well as
the object and purpose of Article 13:2, first and second sentences, clearly lead to the conclusion that
panels are not authorized to deviate from the procedure laid down by Appendix 4 to the Dispute
Settlement Understanding.  Whether the request come s from a party or arises at the initiative of the
Panel itself makes no difference.  Strictly scientific matters cannot be resolved by means and/or
procedures other than those envisaged in Appendix  4 to the Dispute Settlement Understanding.  The
chapeau  to Appendix 4 to the Dispute Settlement Understanding also confirms this interpretation by
providing that the rules and procedures set forth in the Appendix "… shall apply to expert review
groups established in accordance with the provisions of paragraph 2 of Article 13", that is, regardlessof whether the Panel bases itself on the first or second sentence of that Article.  This interpretation is
supported by the fact that, if the Agreement on Technical Barriers to Trade (TBT) should be
applicable (which is not the case), Article 14:2 of that Agreement explicitly prescribes that panels
establish only a technical expert group (which is equi valent to an expert review group).  In such a
case, the procedural rules set forth in Annex 2 to  the TBT Agreement must apply.  Annex 2 to this
latter agreement and Appendix 4 to the Dispute Settlement Understanding are almost identical.
Moreover, by virtue of Article 1:2 and Appendix  2 to the DSU, only Article 14:2 of the TBT
Agreement is applicable.
5.4 The European Communities also point out that the previous cases in which panels requested
the opinion of scientific experts all came under the Agreement on the application of Sanitary and
Phytosanitary Measures, which is not applicable in this case.  Those previous cases are therefore
irrelevant to the present dispute.  The dispute concerning Shrimp  is the only other case for which the
opinion of scientific experts was requested under the GATT 1994.  But this example per se  is not
enough to set a valid precedent applicable to all cases, especially because the parties to the Shrimp
dispute apparently did not request the exclusive ap plication of Appendix 4 to the Dispute Settlement
Understanding.  The result is that, in the present cas e, should the Panel decide to seek the scientific
opinion of external experts, it can do so only under Article 13:2, second sentence of the Dispute
Settlement Understanding or under Article 14:2 of the TBT Agreement.
5.5 According to the European Communities, Appendix 4 to the DSU and/or Annex 2 to the
TBT Agreement lay down almost identical rules on  the establishment of an expert review group.
These rules must all be observed in this disput e.  Moreover, to ensure that the aforementioned
principles are respected, the European Communities believe that the Panel should observe the
following specific criteria when choosing scientific experts:  (i) the experts should not be citizens of
the parties to the Dispute;  (ii) the Panel should select scientific experts in different areas of
specialization in order to ensure coverage of all the areas identified by it.  These areas are:  the humanhealth hazards posed by asbestos, especially chrysotile asbestos;  the inapplicability of a threshold;
the circumstances of exposure and the question as to whether what is known as "controlled use" can
eliminate the potential hazards to human health;  (iii) the European Communities believe that if the
Panel decides to request information, it should consult at least five experts so that more than one
expert will have the requisite expertise and provide answers to the questions in the various areasidentified by the Panel.  In the light of the number of experts that the Panel should consult, only
scientists with proven expertise in the realm of asbestos should be selected;  (iv) the experts should be
drawn mainly if not exclusively from the Intern ational Agency for Research on Cancer (IARC), a
specialized agency of the WHO.  The IARC has studied asbestos from all possible angles and shouldWT/DS135/R
Page 238
therefore be well placed to propose experts covering all the areas in which questions could be posed.
The Panel should also explore the possibility of consulting the International Labour Office (ILO) in
the event that the IARC is unable to cover all the areas in question; (v) the experts chosen must have
no link whatsoever, present or past, with the industry producing asbestos or substitute products.  They
must furthermore clearly demonstrate the lack of any conflict of interest.  The parties should receive atthe outset the Curricula Vitae of all the candidates proposed and should have at least ten working days
in which to verify the skills, expertise and possible conflicts of interest of the candidates;  (vi) the
Panel should also request the opinion of the parties as to the aim of the consultation with experts, the
type and nature of the questions to be put to them;  (vii) the aim of the consultation should be to
further the knowledge of the scientific considerations germane to this dispute.  Therefore, and in
accordance with the provisions of the Dispute Settlement Understanding, the questions to be put by
the Panel must have a direct and strict bearing only on the scientific aspects of the case.  The questionsmay not relate to legal problems nor to any problem of interpretation of any WTO Agreement under
examination.
5.6 Having taken cognizance of the comments from the parties, the Panel  decided to consult the
experts on an individual basis, pursuant to paragraphs 1 and 2, first sentence, of Article 13 of theUnderstanding on Rules and Procedures Governing the Settlement of Disputes.  The Panel convened
the parties to a meeting on 10 July 1999 to acquaint them  with the procedure it intended to follow and
to give them the opportunity to state their opinions on the matter.  The Panel recalled Article 13 of the
Dispute Settlement Understanding which, among other things, provides that:
"Each panel shall have the right to seek information and technical advice from any individual or
technical body which it deems appropriate." [ … ]
"Panels may seek information from any relevant so urce and may consult experts to obtain their opinion
on certain aspects of the matter."
5.7 At that meeting, the Panel told the parties that, in its opinion, Article 13 of the Dispute
Settlement Understanding empowered it to seek such  information and technical advice as it deemed fit
in a given matter;  in particular, a panel was free to determine whether it was necessary or appropriate
to establish an expert review group.  In the case at hand, the consultation of experts acting in their own
right seemed to it to be the most appropriate form of consultation.  The Panel intended to seekinformation concerning the circumstances of chrysotile exposure and the attendant hazards.  In the
circumstances, the Panel indicated that it would structure its questions around the following main
topics:  the pathogenicity of chrysotile, the relative pathogenicity of amphiboles, chrysotile and
substitute products;  the assessment and management of risks associated with the use of chrysotile;
the effectiveness of controlled use of chrysotile.
5.8 The Panel then presented to the parties the procedure that it intended to follow, which is the
same used by previous panels that had consulted experts selected on an individual basis:
• The experts will be placed under the authority of the Panel.  They will be consulted on
a personal basis and not as representatives of a government or organization.  Their
opinion will be strictly in the nature of advice;  it will not be binding on the Panel;
• the number of experts to be chosen by the Panel will be decided depending on the
number of matters on which an opinion will be sought, as well as the number of
matters on which each expert can give an opinion;
• the Panel intends to request names from the World Health Organization (WHO), the
International Labour Organization (ILO), the International Programme on ChemicalWT/DS135/R
Page 239
Safety (IPCS), the International Agency for Research on Cancer (IARC), the
International Organization for Standardization (ISO), and from the parties;
• the Panel does not intend to appoint experts who are citizens of one or other of the
parties to the dispute, unless the parties consent to their appointment or the Panelbelieves that it would otherwise be impossible for it to secure the specialized
scientific advice needed;
• the Secretariat will request the persons suggested to submit a curriculum vitae .  The
curricula vitae  will be transmitted to the parties. The parties may not establish contact
with the experts suggested;
• the parties will have an opportunity to make comments and to state any major
objections they may have to any expert under consideration.  The Panel will informthe parties of the experts it chooses;
• the experts will receive all the relevant elements of the communications on a
confidential basis;
• the Panel will prepare draft questions for the experts.  They will be communicated to
the parties.  The parties will have the opportunity to comment on the questionsproposed or to suggest additional questions before they are sent to the experts.  The
Panel will then draw up a definitive list of questions which will be sent to the experts
and simultaneously to the parties;
• each expert will receive all the questions.  He will be requested to reply to the
questions falling within his sphere of competence and, if necessary, to indicate the
areas on which he does not feel competent to reply.  The experts will be invited to
provide written answers;  copies of those answers will be transmitted to the parties.
The parties will have an opportunity to make written comments on the replies from
the experts and the replies will be included in the Panel's final report;
• should the Panel deem it fitting, either on its own initiative or at the request of a party,
a meeting may be held with the experts immediately before the second substantivemeeting.  Before the meeting, the Panel will ensure that:  (i) experts are made privy to
the parties' comments on their replies;  (ii) the experts each receive the replies of theother experts to the Panel's questions;
• the minutes of the meeting with the experts will be submitted to the parties and to the
experts so that they may make corrections.  The corrected version will be attached to
the Panel's final report.
5.9 The Panel gave the parties the opportunity to transmit their written comments to it.
5.10 In a letter dated 19 July 1999, Canada  recalled all the points that it had notified to the Panel
in its letter of 14 June 1999.  Canada agrees with the Panel as to the nature of the information and
advice that it intends to seek from the scientific experts.  It nevertheless believes that the experts best
qualified to reply to the Panel's questions concerning the circumstances of exposure to chrysotile and
the associated hazards are to be found in the area s of toxicology, epidemiology, risk assessment and
occupational safety.  In addition to the opportunity given to the parties to make written comments on
the experts' replies, the Panel should also provide for the possibility of a final written submission by
the parties following the second substantive meeting.   As regards the stipulation that the scientific
experts may not be citizens of any of the parties to the dispute, Canada believes that this proceduralWT/DS135/R
Page 240
rule, established in Appendix 4 to the Dispute Settlement Understanding, normally applies only to the
establishment of an expert review group.  In the Hormones  case, the Appellate Body stated in that
connection:  " … once the Panel has decided to request the opinion of individual scientific experts,
there [was] no legal obstacle to the Panel drawing up, in consultation with the parties to the dispute, ad
hoc rules for those particular proceedings".1  As the agreement of the two parties to the dispute is
required if the selection of citizens of one of the parties is to be allowed, Canada is surprised at the
refusal of the European Communities to allow the selection of their citizens.  Canada is prepared to
consider the selection of experts who are citizens of the European Communities despite the refusal of
the European Communities to consider experts from Canada.  In this dispute, if the citizens of the
parties are automatically excluded, the Panel risks facing a situation in which it will be unable to
select the experts with the best scientific knowledge considering the nature of the advice being sought.
Canada therefore requests the European Communities and the Panel to reconsider their decision withregard to the non-participation of citizens of the parties.
5.11 Moreover, Canada cannot accept that, as demanded by the European Communities, the
experts must clearly demonstrate the absence of any conflict of interest.  It is not incumbent upon a
prospective expert to prove his impartiality, instead he is merely required to fill out a disclosure formconcerning his interests, relationships and any matters that may affect his independence.  This form is
provided for in the document entitled Rules of Conduct for the Understanding on Rules and
Procedures Governing the Settlement of Disputes .
2  Once the persons approached as potential experts
have filled out their disclosure forms, the parties to the dispute may oppose any candidate who has
disclosed an interest, relationship or matter that may place him in a situation of conflict of interest.The Panel is empowered to decide whether the information disclosed in the form really places a
candidate expert in a situation of conflict of interest and to uphold a party's objection to an expert's
candidature.  The approach taken by the Panel in the Shrimp  case should be followed in this instance.
Having noted that in their disclosure forms three of the experts approached had disclosed what might
be considered as potential conflicts of interest, the Panel nevertheless decided to confirm theirappointments "being of the view that the disclosed information was not of such a nature as to prevent
the individuals concerned from being impartial in providing the scientific information expected of
them.  The Panel has also taken into account the disclosed information when evaluating the answers
provided.  The Panel underlined that, in making its choice, it had been guided primarily by the need to
gather expertise of the best quality and covering as wide a field as possible.  In [the circumstances
specific to this case], it was difficult – if not impossible – to reconcile this need with an agreement by
all the parties to the dispute on each and every individual concerned".
3  Canada is surprised at the
European Communities' insistence on the absence of any link between the experts and producers of
chrysotile asbestos but not between the experts and anti-asbestos pressure groups.  No one opposes
the principles of independence and impartiality of experts or the observance of the rules on conflicts
of interest.  The single pertinent consideration re mains the way in which these principles should be
applied in this particular instance.
5.12 In a letter dated 19 July 1999, the European Communities  took note of the Panel's decision
to consult individual scientific experts pursuant to Article 13:1 of the Dispute Settlement
Understanding.  The European Communities contest th e legal basis of the Panel's decision.  Under the
international customary principles of treaty interpretation, a systematic interpretation of Articles 13:1and 13:2 of the Dispute Settlement Understanding suggests that as far as scientific matters are
concerned, the preferred option in the Dispute Settlement Understanding is the establishment of an
expert review group.  The term "scientific matter" appears only in the second sentence of Article 13:2
                                                     
1 EC Measures Concerning Meat and Meat Products (Hormones) Report of the Appellate Body,
WT/DS26/DS48/AB/R, adopted on 13 February 1998, para. 148.
2 WT/DSB/RC/1, of 11 December 1996.
3 United States – Import Prohibition of Certain Shrimp and Shrimp Products,  Report of the Panel,
WT/DS58/R, adopted on 6 November 1998, para. 5.7.WT/DS135/R
Page 241
of the Dispute Settlement Understanding, which envisages only the constitution of an expert review
group.  The drafting history of the WTO Agreements also confirms this interpretation.4  T h e
three previous cases in which panels sought the opinion of scientists in their own right all had to do
with matters arising under the SPS Agreement, Article 11:2 of which expressly mentions "scientific"
matters and envisages the possibility of consulting experts individually.5  Canada furthermore requests
that the TBT Agreement be applied to the measure at issue here.  It is worth noting that Article 14.2 of
the TBT Agreement provides only for the possibility of consulting a technical expert group.  This
Agreement contains no provision equivalent to Article 13:1 of the Dispute Settlement Understanding
or to Article 11:2 (first sentence) of the SPS Agreement.  The very terms of Article 14.2 of the
TBT Agreement are therefore different from Articles 13:1 and 13:2 (first sentence) of the Dispute
Settlement Understanding and from Article 11:2 of the SPS Agreement.  This difference is not
accidental.6  It denotes the clear intention of the WTO Members to settle scientific or technical matters
in the framework of the TBT Agreement only by establishing an expert review group.  The decision of
the Panel to consult experts on a personal basis is also contrary to Article 1:2 of the Dispute
Settlement Understanding, which provides as follows:
"To the extent that there is a difference between the rules and procedures of this Understanding and the
special or additional rules and procedures set forth in Appendix 2, the special and additional rules and
procedures in Appendix 2 shall prevail."
5.13 As explained above, there is a clear difference between Article 13:1 and 13:2 (first sentence)
of the DSU, invoked in this case by the Panel, and Article 14:2 of the TBT Agreement.  The special
rules and procedures mentioned in Appendix 2 to the DSU, namely Article 14:2 of the
TBT Agreement, which provides for the establishment of a technical expert group, should thus beapplied in the present case, should the Panel judge the TBT Agreement to be applicable.
7  Therefore,
the European Communities consider the Panel's decision contrary to the letter, object and purpose of
Article 14:2 of the TBT Agreement (if the latter is applicable), in conjunction with Article 1:2 of the
DSU, and to Article 13:2 (second sentence) of the DSU.  Besides, from a systematic point of view,
the Panel's decision renders useless and obsolete the provisions of the Dispute Settlement
Understanding and of the TBT Agreement regarding expert review groups, which are clearly the
option preferred by WTO Members and the only one fo r which rules of procedure have been drawn up
in the WTO for the settlement of "scientific" questions.8  At this stage, the European Communities are
therefore obliged to reserve all their rights on this issue.  They would also request the Panel, in
keeping with current WTO practice and for the sake  of transparency and due process, to state in
writing the criteria and the reasons for its decision to call on individual scientific experts and the
reasons for which is has not entertained the arguments put forward by the European Communities, andto communicate this information to the parties to the dispute.
                                                     
4 According to the European Communities, confirmation can also be found in the chapeau  to
Appendix 4 to the Dispute Settlement Understanding which provides that "[the following rules and procedures]shall apply to expert review groups established in acco rdance with the provisions of paragraph 13", that is,
regardless of whether it is the first or the second sentence of this Article that is being used by the Panel.
5 That also explains the Appellate Body's reasons for its finding on that matter in the Hormones  case.
See the report AB/1997-4, para. 147.
6 As the Appellate Body found in Hormones  (para. 164), "a treaty interpreter is not entitled to assume
that such usage was merely inadvertent on the part of the Members who negotiated and wrote that Agreement".
7 The third sentence of Article 1:2 of the Dispute Settlement Understanding is not applicable in this
case, as the GATT 1994 does not contain contradictory rules and procedures on this matter.
8 The Panel's interpretation is also contrary to one of the corollaries of the general rule of interpretation
set out in the 1969 Vienna Convention, which is that the interpretation must give meaning and effect to all theterms of a treaty.  As held by the Appellate Body in the Gasoline  case "an interpreter is not free to adopt a
reading that would result in reducing whole clauses or paragraphs of a treaty to redundancy or inutility"
(AB-1996-1, page 22).  Specifically, the Panel has so far refrained from providing explicit substantive reasons
for its choice of consultation with individual experts over the establishment of an expert review group.WT/DS135/R
Page 242
5.14 As regards the type of scientific background and specializations, the European Communities
take the view that the experts should be cancer specialists, in particular in lung cancer and
mesothelioma.  They should also be epidemiologi sts experienced in the area of asbestos and cancer.
The European Communities are not clear as to what type of scientific discipline would encompassthose persons who would be required to provide advice regarding "risk evaluation and management in
the use of chrysotile" and "the effectiveness of th e controlled use of chrysotile", nor what type of
technical expertise they should have.  If such expert s exist, they should be able to provide information
about all the categories of persons who could come into contact with asbestos and asbestos-containing
products, such as those working in maintenance, repair and construction (for example, carpenters,
plumbers, heat repairers, workers in insulating materials, do-it-yourself enthusiasts, etc.).  The
European Communities believe that the scientists chosen should also have expertise in the inspectionof houses, buildings and factories for the presence and possible removal of asbestos.  Obviously, such
experts cannot be allowed to have any link, whether direct or indirect, with the industries producing
asbestos or those producing the equipment for reducing the risk of asbestos fibre inhalation.  Such a
link would seem particularly possible if the experts were to be designated by the ISO.  The European
Communities consider that at least two experts should be designated for each scientific domain andeach area of questions.  That is a minimum prerequisite for a balanced view and for not being entirely
dependent on the views of just one person.  At all events, the overall number of experts should not be
less than six.
5.15 The European Communities have expressed their wish to receive copies of the letters to be
sent by the Panel to the aforementioned institutions under this point and of their replies.  The experts
appointed should not be nationals or residents of the parties to the dispute.  The European
Communities consider that all the candidates must submit a detailed  curriculum vitae  in time so as to
enable the parties to verify their scientific credentials, experience and independence.  The candidates
must therefore clearly indicate in their curriculum vitae  whether in the course of their professional life
they have worked for or provided advice, in whatever form, to the industries producing asbestos,
asbestos-containing products and substitute products or to the industry producing "controlled use"
equipment.  In addition, the selected experts must complete a disclosure form concerning potential
conflict of interest, pursuant to the Rules of Conduct for the Understanding on Rules and Procedures
Governing the Settlement of Disputes  adopted (WT/AB/WP/3, Annex II, page 16, 28 February 1997).
The disclosure form must contain all the informa tion indicated in the illustrative list appearing in
Annex II to the Rules of Conduct  mentioned above.  It should also explicitly contain  information as to
whether the expert has done any type of paid or unpaid work (scientific research, consulting, expert
advice, participation in the board of directors or board of management, etc.) for the enterprises
engaged in the extraction, production, processing of or trade in asbestos, asbestos-containing products
or substitute products, or for enterprises producing the equipment intended for "controlled use".
5.16 It is the opinion of the European Communities, that the Panel should, for example, request
that the disclosure form further indicate:  (i) the expert's professional situation (job in an enterprise or
institute connected to the asbestos, substitute products or "controlled use" equipment industries);
(ii) whether the expert is a member of the board of directors, board of management or any other
supervisory body within an enterprise, associati on, institution or interest group linked with the
industries producing asbestos, substitute products or equipment for "controlled use";  (iii) whether he
has conducted scientific research or provided expert advice at the request of or under contract to an
enterprise, association, institution or interest group connected with the industries producing asbestos,
substitute products or a "controlled use" equipment.
9  If the aforementioned clarifications and
                                                     
9 As far as the European Communities are concer ned, additional support for the proposition that the
term conflict of "interest" should be interpreted as broadly as possible may be drawn from Article III.1 of the
Rules of Conduct  mentioned above, and in a systematic interpretation (by analogy) of the following provisions:WT/DS135/R
Page 243
information are not given in the curriculum vitae  and in the disclosure form, the parties will not be in
a position to exercise their rights and make the type of comments being requested of them by the
Panel.  Therefore, the European Communities consid er that the issue of the scientific credentials,
experience and, in particular, that of the independence and impartiality of the experts, are of
paramount importance and that they need to be reflected in the Panel's decision on the selection andconsultation of scientific experts.  They therefore wish to reserve their rights until completion of the
selection procedures.  The parties should be allowed sufficient time to enable them to make effectively
known to the Panel their views on the above issues.  Specifically, they should be given sufficient time
to make known their views on the list of potential  experts to be chosen by the Panel and to submit
their comments on the written replies from the experts to the questions put to them by the Panel.
5.17 In a letter to the parties dated 2 August 1999, the Panel  confirmed its intention to consult
experts individually, in application of Article 13 of the DSU.  The Panel carefully examined the
arguments advanced by the parties concerning the expert consultation procedures, in particular, the
European Community argument that Article 13.2 of the DSU Agreement requires the constitution of a
technical expert group as envisaged in Appendix 4 to the DSU for the purposes of consultation with
experts on scientific matters.  Article 13 of the DSU provides, among other things, that "each Panelshall have the right to seek information and take advice from any individual or body which it deems
appropriate" and that "Panels may seek information from any relevant source and may consult experts
to obtain their opinion on certain aspects of the matter".  In addition, Article 13.2 prescribes that
panels "may" request an advisory report in writin g from an expert review group specifically though
not exclusively to examine a factual issue concerning a scientific matter.  The Panel deems this text toallow for the establishment of such an expert group, while not ruling out consultation of experts on an
individual basis, both with regard to a scientific matter "or other technical matter".  This interpretation
of Article 13:2 of the DSU seems to the Panel to be perfectly in line with the text of this provision,
interpreted in accordance with Article 31 of the Vienna Convention on the Law of Treaties, and with
the interpretation given by the Appellate Body that Article 13 of the DSU does not prevent panelsfrom consulting with individual experts and leaves to the sound discretion of a panel the determination
of whether the establishment of an expert review group is necessary or appropriate.
10
5.18 The Panel also considered the European Community's argument that, if the measure at issue
should be deemed to fall under the TBT Agreement, which the Communities contest, Article 14.2 of
that Agreement would require the establishment of  an expert review group for any scientific or
technical matter, and the EC position that pursuant to Article 1:2 of the DSU, that provision wouldprevail over those of Article 13 to the DSU.  Article 14:2 of the TBT Agreement is among the
provisions mentioned in Appendix 2 to the DSU and which, under Article 1:2 of that Understanding,
will prevail over the provisions of the Understandin g to the extent that there is a difference between
the two.  The Panel notes, however, that it is only "to the extent that there is a difference" between the
rules and procedures of the Understanding and a special or additional rule or procedure in Appendix 2to the DSU that the latter will prevail.  Yet, as stated by the Appellate Body, it is only where the
provisions of the DSU and the special or additional rules of Appendix 2 cannot be read as
complementing each other that the special or additional provisions will prevail over those of the DSU,
                                                                                                                                                                    
Articles 8:2, 8:3 and 17:3 of the DSU, paras. 2 and 3 of Appendix 4 to the DSU, as well as paras. 2 and 3 of
Annex 2 to the TBT Agreement.
10 See the Reports of the Appellate Body in European Communities – Measures Concerning Meat
Products (Hormones)  (WT/DS26/26-DS48/AB/R), para. 147 (" … in disputes involving scientific or technical
issues, neither Article 11.2 of the SPS Agreement, nor Article 13 of the DSU prevents panels from consultingwith individual experts.  Rather, both the SPS Agreement and the DSU leave to the sound discretion of a panelthe determination of whether the establishment of an expert review group is necessary or appropriate") andArgentina – Measures Affecti ng Imports of Footwear, Tex tiles, Apparel and Other Items  (WT/DS56/AB/R)
para. 84 ("Article 13 of the DSU enables a panel to seek information and technical advice as it deems
appropriate in a particular case, and ( … ) the DSU leaves  'to the sound discretion of a panel the determination of
whether the establishment of an expert review group is necessary or appropriate'.").WT/DS135/R
Page 244
that is, in a situation where the two provisions would be mutually incompatible.11  In the present case,
Article 14:2 of the TBT Agreement provides that a panel "may" establish a technical expert group.
Like Article 13:2 of the DSU, this text envisages the possibility of establishing a technical expert
group and lays down the procedures that would be applicable in the event.  Nevertheless, it does not
exclusively prescribe the establishment of a technical expert group, and this possibility, in our opinion,is not incompatible with the general authorization given under Article 13 of the DSU to consult with
individual experts.  The two provisions can be read as complementing each other.
5.19 The Panel believes that in this case the consultation of experts on an individual basis is the
more appropriate form of consultation, inasmuch as it is the one that will better enable the panel
usefully to gather opinions and information on the scientific or technical issues raised by this dispute.
Considering in particular the range of areas of competence that might be required, it is appropriate inthis case to gather information and different individual opinions rather than asking for a collective
report on the various scientific or technical matters in question.  In the light of the foregoing, the Panel
wishes to underline that its decision to consult experts on an individual basis is without prejudice to
the applicability of the TBT Agreement to the measure in question, on which the parties disagree.
B. S
ELECTION OF EXPERTS
5.20 The Panel has requested the assistance of five institutions in identifying experts.  The
institutions concerned are the World Health Organization (WHO), the International Labour
Organization (ILO), the International Programme on Chemical Safety (IPCS), the International
Agency for Research on Cancer (IARC) and the International Organization for Standardization (ISO).The parties have also submitted names to the Panel.  The Secretariat then requested those of the
proposed experts who were prepared to participate to submit to it a detailed curriculum vitae .  Those
curricula vitae  were forwarded to the parties, who were able to convey to the panel their comments
concerning the potential experts and to indicate, where appropriate, whether they had any major
objections to any of them.  Upon careful examination of the curricula vitae  and the comments of the
parties, the Panel accepted the following four ex perts, whose nominations were not opposed by the
parties:
• Dr. Nicholas H. de Klerk, Senior Resear ch Fellow, Department of Public Health,
University of Western Australia, Australia;
• Dr. Douglas W. Henderson, Professor of Pathology, Head of the Department of
Anatomical Pathology, Flinders Medical Center and The Flinders University of South
Australia, Australia;
• Dr. Peter F. Infante, Director, Office of Standards Review, Health Standards
Programme, Occupational Safety and Health Administration, Washington D.C.,
United States;
• Dr. Arthur W. Musk, Clinical Professor of Medicine and Public Health, University of
Western Australia, and Physician, Department of Respiratory Medicine, Sir Charles
Gairdner Hospital, Nedlands, Australia.
5.21 The experts were asked to acquaint themselves with the Rules of Conduct for the
Understanding on Rules and Procedures Go verning the Settlement of Disputes
12, paying special
                                                     
11 See the Report of the Appellate Body in Guatemala – Anti-Dumping Investigation Regarding
Portland Cement from Mexico  (WT/DS60/AB/R), paras. 65 and 66.
12 WT/AB/WP/3, of 28 February 1997.WT/DS135/R
Page 245
attention to Annex 2 (Illustrative list of information to be disclosed).  No expert has disclosed any
circumstance that could be considered as the potential source of a conflict of interest.
5.22 In consultation with the parties, the Panel prepared precise questions which it submitted to
each expert individually.  The experts were requested to answer only those questions that theyconsidered to be within their domain(s) of competence.  Written communications by the parties,
transcriptions of their oral statements, as well as the references they submitted to the Panel were
transmitted to the experts for their information.  The written answers from the experts have been
forwarded to the parties, who have had a chance to comment on them.  The questions posed by the
Panel and the answers given by the experts are contained in section V.C.  The observations of the
parties are reproduced in section V.D.
5.23 On 17 January 2000, the experts were invited to discuss with the Panel and the parties their
written answers to the questions and to provide additional information.  Annex VI to this report
contains the minutes of the meeting.
C. 
QUESTIONS BY THE PANEL AND COMMENTS BY THE SCIENTIFIC EXPERTS
5.24 The Panel requested the experts to comment on the areas of difference between the parties
highlighted in the first paragraph of each question, as well as to address the specific points listed.  The
Panel encouraged the experts to indicate, to the extent possible, key points on which they considered
that (i) there is scientific proof, (ii) there is broad agreement among experts, (iii) there is uncertainty
and/or a range of divergent opinions among experts.
1. Introductory Comments by Dr. Henderson
(a) Introduction
5.25 This introduction sets out a general summary of prevailing knowledge and uncertainties on
asbestos-related disorders, with emphasis on mesothelioma and lung cancer, together with discussionof both the amphiboles and commercial chrysotile, patterns of exposure, and some brief details of
in vivo  and in vitro  experimental studies.
5.26 This introduction has two purposes:  (i) to provide a general background and broad
perspective to the questions and answers that follow;  and (ii) to correct some inaccuracies and errors
in the documentation supplied already to the WTO.  In so doing, I have tried to broaden the
perspective beyond the classical Canadian studies on the Quebec chrysotile miners and millers, and
beyond the INSERM Report.  A number of the general discussions in this introduction have beentruncated after the issue has been put into context, and some of these discussions are then continued
and amplified in my specific responses to the questions.  This has produced some iteration of some
points, but I believe that the advantages - avoidance of the potential for distortion created by answers
without adequate background information - outweigh any disadvantages.  The division of my report
into these sections also provides an opportunity to  indicate the relative importance of epidemiological
studies versus in vivo  or in vitro  experimental models in the form ulation of my opinions and answers.
5.27 At the outset, I emphasize that Australia (including Western Australia) is no longer an
asbestos producer.  Production of crocidolite at th e Wittenoom blue asbestos industry stopped in 1966.
None has been produced or exported since.  Crocidolite was used in asbestos-cement products in
Australia until 1966 when its use was discontinued, but imported amosite was used in these productsuntil 1984 [NICNAS 99]
13.  The use of chrysotile in fibro-cement products was discontinued in 1987.
                                                     
13For complete references, see Annex III to the Panel Report.WT/DS135/R
Page 246
5.28 As stated repeatedly in the documentation provided to the WTO, asbestos has the capacity to
induce at least five benign pleuropulmonary disorders, and two cancers:  parietal pleural fibrous
plaques;  benign asbestos pleuritis with effusion;  diffuse pleural fibrosis;  rounded atelectasis;
asbestosis;  primary lung cancer;  malignant mesothelioma.  The essential characteristics of these
disorders are discussed in the documentation submitted to the WTO and lie beyond the scope of thisreport;  if further details are required, standard texts should be consulted [26-30].  There is no
persuasive or compelling evidence that asbestos of any type causes cancers other than lung cancer and
mesothelioma, with the arguable exception of cancer of the larynx.  At this stage, it is sufficient to
point out that:  " ... there is an exposure-response relationship for all chrysotile-related diseases.
Reduction of exposure through introduction of control measures should significantly reduce risks.
Construction and demolition operations may pres ent special control problems".  [EHC 203, p 141].
(b) Malignant mesothelioma – Introduction and general observations on asbestos and
mesothelioma
5.29 Malignant mesothelioma is a cancer of the meso thelial cells that line the serosal membranes
of the major body cavities, namely the pleura, the peritoneum, the pericardium and the tunica
vaginalis testis;  the constituent neoplastic cells characteristically express the phenotype of a
recognized pattern of differentiation of the mesothelium, whether epithelioid, sarcomatoid or both(biphasic), as revealed by conventional light microscopy, mucin immunohistochemistry,
immunohistochemistry or electron microscopy, or a combination of these techniques [31-33].  Like
other forms of cancer, mesothelioma has the capacity for local invasion of tissues such as the chest
wall or lung, with confluent serosal spread in most cases but not all, and in some instances distant
metastasis [31], with an almost invariably fatal ou tcome.  Mesothelioma is resistant to conventional
cancer therapies (e.g. radiotherapy or chemotherapy), but some long-term survivals have been
recorded following radical surgery (pleuropneumonectomy) in patients in good physical condition and
with early-stage disease [34-43];  radical surgery of this type is not a treatment option for the majority
of mesothelioma patients.
5.30 Most mesotheliomas encountered in the 1990s are a consequence of prior occupational
exposure to asbestos [24], including bystander exposure.  The relationship between asbestos -
especially one or more of the amphibole varieties - and mesothelioma is accepted by virtually all
authorities as causal.  In this respect, asbestos fulfils all The Bradford Hill Criteria  for the
establishment of causality (e.g. please see Stolley and Lasky [44]).
5.31 The following points about asbestos and mesothelioma are worth emphasis:
(i) Inhalation of asbestos fibres represents the overwhelming cause of mesothelioma in
industrialized societies, so much so that the incide nce of mesothelioma is usually considered to be an
index of those societies' past usage of asbestos.
According to Peto et al.  [24]:
"The great majority of mesotheliomas are caused by asbestos, and the much higher incidence in men
indicates that most are due to occupational rather than environmental exposure.  The incidencecontinues to rise approximately as the third power of time since first exposure to asbestos for many
decades after exposure has ceased (Peto et al. , 1982), and most patients are men first exposed 30 or
more years ago.  A country's mesothelioma rate is therefore a quantitative indicator of its population'spast exposure — mainly occupational — to asbestos."  [p 666].
5.32 Boffetta [15] claims that:WT/DS135/R
Page 247
"Asbestos is the only established risk factor of mesothelioma.  Because of the rarity of the disease and
the specificity of the causal association, all cases occurring among asbestos-exposed workers areattributed to this exposure."  [p 476;  please see following discussion].
4.33 The asbestos exposure may take the following forms:  (i) direct or indirect occupational
exposure (including bystander exposure);  (ii) domestic exposure:  e.g. household contacts of asbestos
workers, such as wives who washed the asbestos -contaminated work clothes of their husbands [45-
47];  (iii) environmental exposure:  this catego ry includes those who lived downwind of asbestos
industries or in townships contaminated by asbestos [45-47].  For example, ≥ 27 mesotheliomas have
been recorded among those who lived at Wittenoom as children (the roads, airstrip and school yardswere surfaced with crocidolite tailings from the mine, and children often played in the mine tailings).
"The tumor [mesothelioma] is more often seen in workers who have only moderate or small amount of
asbestos in their lungs, and who show little, if any, clinical or radiologic evidence of pulmonaryfibrosis.  This amount of asbestos may be inhaled not only by professional asbestos workers, but alsoby those who handle products containing only a small proportion of asbestos, those who do not handleasbestos at all but merely work alongside asbestos workers such as craftsmen employed in the building
industry — carpenters, electricians, etc. — those who have relatives who carry asbestos home in their
workclothes and those who live close to asbestos plants."  [47] [p 295].
5.34 No history of asbestos exposure is obtainable in about 15-25 per cent of mesothelioma cases
[31, 48].  Nonetheless, absence of a history of exposure does not equate to absence of exposure, andevidence indicates that many of these mesotheliomas are in reality attributable to asbestos inhalation
— e.g. remote, brief or forgotten exposure, or alternatively, the individual may be unaware that he (the
male:female ratio is about 8:1) was in fact exposed to asbestos:  (i) from my own series of
mesotheliomas, 79 per cent of the request forms that accompanied the biopsies on which the diagnosis
was made gave a positive history of past asbestos exposure;  clinical review of the remaining 21 percent yielded a history of asbestos exposure in a substantial proportion, including some for whom the
original history stated that there was no exposure, so that my estimate of the proportion for whom a
positive history of exposure was eventually obtained is ≥ 85-90 per cent.  This estimate is in
reasonable agreement with figures in the 1999 Report for the Australian Mesothelioma Register
[AMR 99], where 85 per cent of mesotheliomas had a history of asbestos exposure;  (ii) Leigh et al.
[49] found measurable asbestos fibre levels (> 200,000 fibres per gram dry lung tissue) in 81 per cent
of the 28 per cent of Australian mesothelioma cases that had no history of occupational or
environmental exposure to asbestos.
(ii) Putative or possible factors other than asbestos implicated in the induction of mesothelioma
5.35 In the reply to Question 3 from the European Communities, Canada makes the following
statements:
"... Canada wishes to inform the European Communities of the considerable body of evidence
contradicting their statement that asbestos in all forms (amphiboles and chrysotile) is the only knownfactor that can cause mesothelioma or pleural cancer.  ...  A number of studies suggest other potentialrisk factors that may have been under-estimated in  epidemiological studies in industrialized countries.
...  A number of artificial fibres cause mesothelioma when they are injected into the pleura and
peritoneum of laboratory animals.  Note also that the International Agency for Research on Cancer
(IARC) has classified refractory ceramic fibres as probable carcinogens, partly because of instances of
mesothelioma induced by inhalation and injection in animal experiments.  The SV40 virus readilyinduces mesothelioma when injected into animals;  studies suggest that the virus contaminated anti-
polio (poliomyelitis) vaccines from 1955 to about 1963 and may induce mesothelioma with or withoutthe help of asbestos fibres.  Some studies of humans report the presence of the simian SV40 virus in the
biological tissue of mesothelioma victims.  Ionizi ng radiation used in cancer therapy and perhaps
occupational exposure to radiation have induced me sothelioma.  ...  [E]rionite has been shown to be
even more toxic than crocidolite in causing mesothelioma;  it has killed large numbers of villagers inWT/DS135/R
Page 248
Turkey.  Erionite is a mineral fibre but does not belong to the asbestos family."
5.36 Possible factors other than asbestos implicated as contributory or causative for rare
mesotheliomas are tabulated below:
TABLE 1:  PUTATIVE OR POSSIBLE RISK FACTORS AND MEDIATORS OF RISK OF MESOTHELIOMA
OTHER THAN ASBESTOS
Factor Comments
Erionite Very high incidence of mesothelioma due to environmental exposure in
Turkey (restricted geographic localization only).
Chronic inflammation Pleural scars (tuberculosis,  pleurisy, therapeutic pneumothorax, familial
Mediterranean fever);  see following discussion.
Radiation Single cases after Thorotrast injection or radiotherapy;  causality unproven.
One case in atomic bomb survivor.
Beryllium Two doubtful cases described.
Vegetable fibres No proof in humans.
Hereditary factors Familial cases (explicable by common asbestos exposure ± unidentified
genetic susceptibility factors, including association with other cancers infirst-degree relatives).
Immunological factors Rapidly progressive cases in patients with HIV infection;  very rare —
single case(s) only.
Dietary factors Provitamin A, β-carotene may decrease the risk (unproven).
Viruses Mesotheliomas in animals.  Simian virus 40 (SV40) DNA sequences
reported in mesotheliomas;  see following discussion
Modified from Hillerdal [20].
5.37 There are anecdotal reports of mesothelioma following radiation, including radiotherapy for
childhood cancer such as Wilms' tumour [50-56].  In addition, excess rates of mesothelioma have been
reported among both Danish and German patients e xposed to radioactive thorium dioxide (Thorotrast)
for radiological procedures [57, 58], although a similar but smaller Japanese study found no such
excess [59].  Neugut et al.  [60] investigated women with breast cancer and patients with Hodgkin's
disease, many of whom had been treated by radiotherapy (RT):
"The authors performed a retrospective cohort study utilizing 251,750 women registered with breast
carcinoma in the Surveillance, Epidemiology, and End Results Program of the U.S. National Cancer
Institute from 1973-1993, 24.8% of whom received RT as part of their initial management, and 13,743
people with Hodgkin's disease, 50. 6% of whom received RT as part of their initial management.
RESULTS:  Six cases of malignant pleural mesothelioma were found:  two in breast carcinoma patientstreated with RT and four found in women not treated with RT.  No cases occurred in the patients withHodgkin's disease.  The overall estimated relative risk for malignant pleural mesothelioma after RT was1.56 (95% confidence interval, 0.18-5.63).  CONCLUSIONS:  To the authors' knowledge, this is the
first controlled study to investigate thoracic radiation exposure and malignant pleural mesothelioma,
and no association was found."  [abstract].
5.38 I am also aware of at least one mesothelioma in a patient with HIV infection (AIDS) [61].
Other mesotheliomas have occurred many years afte r chronic inflammatory lesions of the pleura —
e.g. chronic empyema or packing of the pleura l cavity with leucite spheres as treatment for
tuberculosis [62, 63], and there are a few reports of an association between familial Mediterranean
fever (FMF) and mesothelioma (about eight cases only;  possibly related to recurrent FMF serositis
[64-67]).  However, cases of this type are exceptional and most cases of "post-inflammatory"
mesothelioma with a short interval between inflammation and tumour (e.g. ≤ 2-3 years by analogy
with the criteria for the diagnosis of benign asbestos pleuritis [33, 68, 69]), are probablyWT/DS135/R
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mesotheliomas that presented with a burst of inflammatory activity, followed by a period of
quiescence [70].
5.39 In addition, background asbestos exposure represents a confounding factor for some cases
associated with radiation and immunodeficiency:  (i) in one report on mortality among 260 plutonium
workers, all six mesotheliomas occurred in individuals who had also sustained asbestos exposure [71]:"... no apparently elevated causes of death except for six cases of mesothelioma and six cases of
astrocytoma glioblastoma multiforme. The mesothelioma cases had a documented occupational
exposure to asbestos ..." [extract from abstract];  (ii) in one of my own cases, the patient had been
treated for Hodgkin's disease by mantle radiotherapy 10 years before the diagnosis of his primary
pericardial mesothelioma, but he also had a background of occupational exposure to asbestos;  (iii) in
another case — a pleural mesothelioma in a renal transplant recipient — the patient had also sustained
earlier occupational exposure to asbestos.
(iii) Erionite and mesothelioma in Turkey
5.40 Erionite (a fibrous zeolite) represents a naturally occurring fibrous mineral implicated in the
induction of mesothelioma in certain villages (notably Karain and Tuskoy) in the Cappadocian region
of Turkey [72, 7 3], and in Turkish emigrants [74].  So far as I am aware this represents a restricted
geographic pocket of mesothelioma cases induced by erionite used as stucco or whitewash inbuildings, so that the inhabitants were exposed to high concentrations of erionite fibres from birth.
Erionite has no relevance to the broader mesothelioma problem in Western Europe, North America,
and Australia.  Nonetheless, in its physical properties erionite has similarities to the amphibole
varieties of asbestos and it has been suggested that  its greater mesotheliomagenicity is related to a
greater surface area (200 m
2 per gram) than crocidolite (8-10 m2 per gram), due to the presence of
pores in the crystal lattice (see Roggli and Brody [75]);  such differences in surface topography might
correlate with differences in free radical generation at the surface of fibres.
(iv) Simian virus 40 (SV40) and mesothelioma
5.41 Recently, a voluminous literature has grown rapidly on the detection of SV40 DNA in up
to 60 per cent of human mesotheliomas [76-87] and some other tumours, such as papillary carcinomaof the thyroid [88], osteosarcomas and brain tumours [83, 89-91].  These observations followed an
initial finding that SV40 could induce mesothelioma in  hamsters when injected into the pleural cavity
[92], and the later demonstration that SV40 could in activate the tumour suppressor genes p53 and the
retinoblastoma gene (Rb) via the large T antigen (TAG) [80, 82, 93, 94].  For humans, early
poliomyelitis vaccines contaminated with SV40 were a potential source for the SV40 DNA [82-84].
The following points on this interesting association are also worth emphasis:
• It has been suggested that the presence of SV40 might explain:  (i) why mesothelioma
only develops in a relatively small proportion of asbestos-exposed individuals
(usually < 10 per cent);  and (ii) why no history of asbestos exposure is obtainable on
a sizeable minority of mesotheliomas [95].  However, almost all the mesotheliomas in
which SV40 DNA has been found were asbestos-associated;  to the best of my
knowledge, there is no reported case-control analysis of SV40-associated
mesotheliomas where asbestos fibre counts were not elevated above reference values,with the exception of a recent study by Mayall et al.  [96] (please see following
discussion).  Therefore, the existing data do not adequately address either (i) or
(ii): there are many other possible explanations for these observations.
• In other studies, SV40 or TAG could not be detected within mesotheliomatous tissue
[97-99].  Galateau-Sallé et al.  [100] found that SV40 was present not only in
mesotheliomas but also in benign inflammatory disorders of the pleura and non-WT/DS135/R
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neoplastic lung tissue.  In an as yet unpublished investigation carried out in
collaboration with Prof. Alec Morley in the Department of Haematology-Oncology at
the Flinders University, we have also identified SV40 in mesotheliomas, and in non-
neoplastic pleural lesions, normal tissues and colon cancers, casting doubt on the
specificity of the association.
• Two epidemiological studies have shown no increase in the incidence of bone or brain
tumours — or mesotheliomas — 30 years after the use of polio vaccines contaminatedwith SV40 [101, 102], although in a later study using SEER data
14, Fisher et al.  [103]
reported an increased frequency of these tumours in subjects who had received SV40-
contaminated poliomyelitis vaccines.
• The evidence so far only points to SV40 as a possible co-factor for asbestos in the
genesis of mesothelioma [96].  For example, Mayall et al.  [96] detected SV40
sequences in five of seven asbestos-associated mesotheliomas, but none of four
mesotheliomas that were not asbestos-related (investigated by fibre burden analysis oflung tissue, using electron microscopy).  However, the evidence in favour of SV40 as
a co-factor for mesothelioma induction is still inconclusive and non-persuasive, and in
humans the SV40 may represent an innocent bystander or passenger:  the criteria for
causality  [44] have not been fulfilled.
"It remains to be shown whether the presence of SV40 contributes significantly to malignant
transformation or whether certain human neoplasms provide a microenvironment that favorsviral replication in humans with latent SV40 infection."  [91] [last sentence of abstract].
5.42 The point of these comments is that the evidence for a role of SV40 in the development of
mesothelioma is inconclusive, and most of SV40-associated cases still represent asbestos-associated
mesotheliomas.  Although the literature contai ns anecdotal reports of mesothelioma following
radiation, some of these cases (e.g. among plutonium  workers) are complicated by coexistent asbestos
exposure and it is worth emphasizing that these cases are rare:  together they add up to only a small
fraction of 1 per cent of the total burden of meso theliomas in industrialized societies, for which
asbestos remains the overwhelming cause.  As emphasized already, there is general agreement that the
incidence of mesothelioma in various nations is a reflection of the past usage of asbestos by those
societies.
5.43 Hillerdal [20] comments along similar lines:
"... SV40 might be a cofactor to asbestos in some patients with mesothelioma, but the [findings] have
not been confirmed and are still disputed.  ...  In summary, then, as far as is known today, factors other
than mineral fibres can only explain a very small proportion of mesotheliomas, and can for practical
purposes be disregarded [i.e. when approaching the causation of mesothelioma among large cohorts orpopulations].  Thus, a malignant mesothelioma can be regarded either as caused by asbestos orbelonging to a normal background level — that is a spontaneously occurring tumour."  [p 506].
(v) Male: female ratio for mesothelioma
5.44 Asbestos-induced mesothelioma affects males more often than females in a ratio of about 8:1,
as a reflection of occupational exposure.
(vi) Anatomical distribution of mesothelioma
5.45 With the exception of one series in which 44 per cent of mesotheliomas were peritoneal [104],
                                                     
14The National Cancer Institute's Surveillance Epidemiology and End Results program.WT/DS135/R
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there is general agreement that primary asbestos-induced mesothelioma affects the pleura more often
than the peritoneum, in a ratio of at least 3:1 or even up to ≥ 11:1 [31, 33] (see also AMR 99).  In
Australia, ≥ 91 per cent of mesotheliomas arise in the pleural cavities, whereas about 7 per cent
represent primary peritoneal mesotheliomas and ≤ 1 per cent affect the pericardium or tunica vaginalis
testis [33].  This predominance of pleural mesothel iomas in comparison to the peritoneum appears to
correlate with gender differences in the frequency of occupational exposure to asbestos (the same high
ratio of pleural to peritoneal tumours is also encount ered in the United States).  In females, a smaller
proportion of mesotheliomas arises in the pleura, and in one study of Swedish insulation workers, all
seven mesotheliomas arose in the peritoneum [105] (please see following discussion).
5.46 One report [106] that included cases notifi ed to the Australian Mesothelioma Register
from 1986 through 1988 gave figures for the anatomical sites affected in men and women:  676 of 723
men had a pleural mesothelioma (93 per cent), whereas 38 were peritoneal tumours (5 per cent) andnine occurred in other sites (1 per cent).  In contrast, 84 mesotheliomas in 101 women were pleural in
location, whereas 17 per cent had a peritoneal mesothelioma.
5.47 Presumably, this difference in anatomical distribution between sexes is a reflection of
different rates of occupational exposure to asbestos.  On theoretical grounds, one would expect
mesotheliomas entirely unrelated to asbestos to o ccur with about equal frequency in the pleura and
peritoneum, or more often in the peritoneum because of the greater surface area of the peritoneal
cavity.
5.48 A partial list of the factors that might explain the higher proportion of peritoneal
mesotheliomas in some series and in  women includes the following [33]:
• The high proportion of pleural mesotheliomas in men is presumably a reflection of
asbestos exposure, with deposition of asbestos fibres in lung tissue, followed by
translocation of the fibres to the pleura;  on this basis, asbestos inhalation appears to
skew the proportional distribution of mesoth elioma towards the pleura in comparison
to other sites.  In contrast, fibres presumab ly follow a more circuitous route from the
lung to the pleura, across the diaphragm and into the peritoneal cavity, to induce
peritoneal mesothelioma;  higher inhaled doses of asbestos might be necessary for therequisite number of fibres (whatever that is) to reach the peritoneum via the pleura, in
order to induce peritoneal mesothelioma.
• The high proportion of peritoneal tumours in some series may be a consequence of
patterns of referral for cases that constitute problems in diagnosis, because thediagnosis of peritoneal mesothelioma is, in general, more difficult than for pleural
mesotheliomas.  This may explain the higher proportion of peritoneal mesotheliomasamong cases referred to the US-Canadian Mesothelioma Panel [107], because many
of these represented problems in diagnosis, whereas the Australian Mesothelioma
Surveillance Program (AMSP) captured all mesotheliomas throughout Australia [48].
• Genuine biological differences in the inhaled dose, deposition or transport of different
asbestos fibre types in some groups of workers, notably insulation workers [108] and
former Wittenoom workers [109] — as a consequence of heavy occupational
exposure — and in women [106, 110].
5.49 In answer to questions posed by the European Communities (Question 3, see Annex II), the
following comment is made:WT/DS135/R
Page 252
"... malignant diffuse mesothelioma is a cancer of the mesothelial cells of the pleura, the pericardium
and the peritoneum.  Furthermore, peritoneal mesothelioma is an even more typical result of exposureto amphiboles than pleural mesothelioma."
5.50 From the preceding discussion on the proportions of mesotheliomas arising in the pleural
cavities versus the peritoneum, it is evident that this proposition is not correct:  use of the term typical
in this context is inappropriate.  In reality, pleural mesothelioma is a more typical or usual outcome of
asbestos exposure, whereas asbestos-induced peritoneal mesotheliomas are usually associated with
more prolonged and heavier exposures than pleural mesotheliomas, so that the proportion of patients
with asbestosis is higher than for pleural mesothelio ma [111].  It has also been claimed that peritoneal
mesotheliomas are almost always a consequence of amphibole exposure (as opposed to chrysotile
only) [112].  Nonetheless, although some of the pe ritoneal mesotheliomas in my own series of cases
followed high-dose exposures to asbestos that included one or more of the amphiboles, a few followed
lower cumulative exposures, and Neumann et al.  [111] have reported peritoneal mesotheliomas as a
consequence of exposure in the building trades and metal industries, in addition to asbestos industries;Rogers et al.  [3] recorded peritoneal mesotheliomas in whom only chrysotile fibres were detected on
lung fibre analysis (see Table 9, paragraph 5.137).
(vii) Latency intervals (lag-times)
5.51 In all reported studies, mesothelioma is a disease of long latency between exposure to asbestos
and the subsequent diagnosis of the mesothelioma.  In the AMSP [48], the mean latency interval (lag-time) was 37 years, with a reported range of 4-75 years;  the lag-time was reported to be < 10 years in
only four of 499 asbestos-associated mesotheliomas (0.8 per cent).  Many authorities set a minimum
lag-time of 10 years (e.g. The Helsinki Criteria [113]), and for most patients the lag-time is in the
range of 20-40 years,  When the lag-time is < 10 years, it is likely that the proximate exposure was
coincidental, and that there were one or more earlier exposures.
(c) Spontaneous or background mesothelioma:  does it exist?
4.52 The rare occurrence of mesothelioma in childhood and even as a congenital malignancy
supports the existence of a background of spontaneous mesotheliomas unrelated to asbestos (in
addition, mesothelioma has been reported in fish (t rout) [114], where inhalation of airborne asbestos
fibres cannot be invoked).  However, in epidemiological studies on adult populations, it is virtually
impossible to separate spontaneous mesotheliomas from those that are arguably attributable to
environmental exposure to asbestos [70, 115].  The incidence of mesothelioma in women issometimes used as an index of the background or spontaneous rate:  the crude incidence rate for
women in Western Australia is about 2.6 per million person-years at age ≥ 15 years [115].  The
incidence rate in other populations is listed in Table 2 (following page).
5.53 In the answer to the WTO Panel's questions to Canada (Question 9, see Annex II), the
following statement is made:
"Recent analyses of Canadian data on mesothelioma in Canada, British Columbia and Quebec all agree
that the incidence rate of mesothelioma has been stable among women of all age groups since 1984.
The rates are 70% higher in Quebec than in the rest of Canada, presumably as a result of more frequent
and more intense exposure in the workplace."
5.54 The statistics for Australia differ on this point (Table 2):  mathematical modelling of
Western Australian data suggests that the incidence rate in women has risen about two-fold from the
1970s until the 1980s, which might be explicable by increased general environmental exposure to
asbestos, plus some occupational exposures among women [70, 115] (please see also AMR 99 —i.e. the graph for the Age Specific-Incidence Rate s of Malignant Mesothelioma in Australia Women,
1986-1995, especially for ages 50-64 and 65-79).  This increased incidence among womenWT/DS135/R
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presumably reflects direct or indirect occupational exposure, domestic exposure or environmental
exposure [115];  in this respect, it is worth emphasizing that domestic (household contact) exposure to
asbestos — e.g. among wives laundering the dust-laden workclothes of an asbestos-exposed husband
— is not necessarily low-level exposure, and analysis of the asbestos fibre content of the lungs in a
small number of such patients indicates that this type of exposure can approach occupational levels[116].
TABLE 2:  INCIDENCE OF MORTALITY OF MESOTHELIOMA IN VARIOUS COUNTRIES AND AREAS
OVER TIME , 1960 S TO 1994 ( PER MILLION INHABITANTS PER YEAR )
Country or area Year Males Females
United States 1968-81 2.1 0.8
North America 1972 2.8 0.7
Texas 1976-80 5.8 2.1
Selected cities, United States 1970s 4.4-11.1 1.2-3.8
United States 1986 7-13 1-2
Nantes-Saint-Nazaire, France 1956-74 5.2 0.2
Nantes-Saint-Nazaire, France 1975-84 17.2 0.8
Nantes-Saint-Nazaire, France 1985-92 19.4 4.0
Great Britain 1968-71 8.4 2.3
Great Britain 1972-76 12.6 2.8
United Kingdom 1983 17.5 3.2
Great Britain 1968-71 20.7 4.3
Great Britain 1982-86 30.5 4.9
Great Britain 1987-91 44.0 6.4
Australia 1982-88 28.3 3.3
Australia 1994 49.9 4.8
Denmark 1978-80 14.7 7.0
Barcelona, Spain 1983-90 8.3 4.7
Finland 1990-94 10 2.9
Modified from Hillerdal [20].
5.55 The often-cited background or spontaneous rate of mesothelioma of 1-2 per million person-
years [10, 117], has in part also been derived fr om backward extrapolation of the incidence rates in
men, to the point where the estimated incidence rates for men and women diverged from each other
(i.e. linear extrapolation to the point where the sex ratio = 1:1) [117] .  Hillerdal [20] suggests that thisincidence probably represents a high estimate and comments in the following terms:
"... there seems to be a small spontaneous basal or background incidence of the tumour [mesothelioma]
... However, it is of course possible that some of these background cases might in fact be due to
occupational, domestic, or even environmental exposure, unknown to (or forgotten by) the patients
themselves.  ... There are authors who claim that th e presumed background levels must be very low,
and retrospective searches for the tumour in the medical literature reveal no convincing cases ofmesothelioma before 1946, although such negative evidence is of questionable value.
15  McDonald and
                                                     
15Mark and Yokoi [118]  have called into question the existence of mesothelioma in the absence of
asbestos exposure, pointing out that the early descriptions of pleural tumours may have dealt with localizedfibrous tumours of the pleura (four of the five tumours reported by Klemperer and Rabin [119]) or secondarycarcinoma.  Thus, mesothelioma might represent a new disease consequent upon the industrial use of asbestos(analogous to AIDS) and it may disappear upon withdrawal of the causative asbestos from the environment(analogous to smallpox).  In support of this propositio n, these authors cited the records of the Massachusetts
General Hospital, where no examples of mesothelioma were diagnosed before 1946, in contrast to 100 autopsy
cases thereafter, in a total of 47,000 autopsies.  They also referred to the Henke-Lubarsch Handbuch derWT/DS135/R
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McDonald, in a recent review, estimated the background level to be 1-2/million per year;  they came to
this figure by extrapolating backwa rds from epidemiological studies from various countries.  ... It is
nevertheless possible that there is a background level of mesothelioma, — that is, that the tumour can
occur even in the complete absence of asbestos (or erionite) fibres.  However, the data reviewed here
indicate that if so, this background level must be very low — probably much < 1 case/millionpeople/year.  This figure comes from studies of industrialized countries, where background exposure toasbestos is unavoidable.  What the true figure is can only be guessed ... ". [p 507].
5.56 De Klerk [115] and Comin et al.  [70] have commented that in the absence of specific
exposure to asbestos, the final estimated rate for both men and women in Australia is 2.6 per million
person-years — higher than the equivalent figure of 1.6 for Los Angeles [115].  This difference maylend some support to the proposition that general environmental exposure to asbestos may have
produced an increase in the mesothelioma rate in Western Australia [115].  However, it is difficult or
impossible in general to draw firm conclusions from  differences between different studies, because of
variation in the accuracy of diagnosis and differences in the ways that data are collected.
5.57 In response to questions from the WTO Panel (Question 9, see Annex II) the Canadian
document also observes that:
"The incidence of [mesothelioma] among men levelled off after 1984 in British Columbia ... and seems
to have levelled off in Quebec after 1990 ...  Finally, analysis of Canadian rates between 1973 and 1992... estimates that the risk is four times greater for men born before 1940 than for men born between1951 and 1955.  Those analyses therefore suggest that the incidence of mesothelioma has levelled off inCanada, is declining in British Colombia, and has levelled off in Quebec ..." .
5.58 In response to these observations, I emphasize the following:  (i) the incidence of
mesothelioma among Australian males shows little evidence of levelling off, and has continued to rise
until 1994-1995 and thereafter (please see Table 2 and the 1998 and 1999 Reports for the Australian
Mesothelioma Register);  (ii) from the recent report by Peto et al.  [24], it is also evident that the
incidence of mesothelioma in Western Europe continues to rise, with particular emphasis on males
born between 1945 and 1950 who used asbestos-contai ning products in the 1960s and the 1970s (and
the early 1980s).
(d) Magnitude of the mesothelioma problem
5.59 Malignant mesothelioma continues to represen t a major health problem within industrialized
societies, and together with lung cancer it repr esents the most important occupational cancer among
so-called blue-collar workers [121-124].
5.60 It has been estimated that across Western Eu rope, North America a nd Australia (combined
population ~ 800,000,000), around 10,000 mesotheliomas and 20,000 asbestos-induced lung cancersoccur annually, related mainly to occupational exposure (about one mesothelioma for every 200 tons
of asbestos produced, taking into account the prolonged lag-times) [125].  Steenland et al.  [126]
estimate that approximately 9000-10,000 men and 900-1900  women develop lung cancer each year in
                                                                                                                                                                    
speziellen pathologischen Anatomie und Histologie,  wherein the four pages devoted to tumours of the pleura did
not specifically acknowledge the existence of mesothelioma;  the Henke-Lubarsch authors concluded that many
cases described in the literature as primary pleural neoplasms were cases of lung cancer with spread to the
pleura.  I find the evidence for Mark and Yokoi's proposition to be underwhelming and unconvincing.  The casereported in the 1920 paper by Du Bray and Rosson [120] is, I believe, a clear example of a mesothelioma, as isthe fifth case of Klemperer and Rabin [119].  Failure to diagnose a tumour is hardly synonymous with its non-existence, and the pathological features of many tumours have been delineated in quite recent times.Pathological diagnoses follow prevailing evidence and fashions, and because the groundwork for modern
concepts of mesothelioma was laid down in 1931 by Klemperer and Rabin, it is hardly surprising that the
diagnosis became more widespread only after this time.WT/DS135/R
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the United States because of past exposure to occupational carcinogens, and more than half of these
lung cancers are related to asbestos (this overall estimate is considered probably to be conservative).
Predictions of asbestos-related diseases in Au stralia (population ~ 18,000,000) indicate that about
13,000 cases of mesothelioma (range 8000-20,000), about 40,000 cases of lung cancer (range 30,000-
76,000) and 1000 cases of asbestosis are likely to occur between the years 1987 and 2020 [70, 127].
5.61 More recently, Peto et al.  [24] have predicted that about 190,000 mesothelioma deaths are
likely to occur throughout Western Europe (Britain, France, Germany, Italy, the Netherlands and
Switzerland) over the next 35 years.  If one adds in lung cancer at a ratio of one lung cancer for every
mesothelioma death, this figure would rise to 380,000 deaths, and if the ratio of lung cancers to
mesotheliomas is 2:1 the figure rises to 570,000 deaths.
5.62 Overall, asbestos may have caused approximately 5,000,000 deaths across industrialized
societies so far.  When future deaths in so-called developing nations are added, the final toll is almostcertain to be substantially higher, especially because occupational exposures in those countries are
likely to be heavier (e.g. China).  Estimates of this magnitude are likely to engender alarm among
those who set social policy.  Even so, it is important  that this problem, like others (e.g. atomic energy),
is approached with common sense, rationality and prudence, taking into account population-based risk
estimates:  it would be irrational to swap one risk  for another higher risk if the two risks were equally
serious.
(e) Some general observations on approaches to risk assessment on society and on
epidemiological studies of asbestos-related cancers
5.63 The documentation supplied to the WTO includes  estimates of risks from low-level exposure
to chrysotile in proportion to various other risk factors in society:  in fact, the relative risk ofmesothelioma from low-level exposure to asbestos in  place is the focus of considerable controversy.
Clearly, detailed analysis of this issue is beyond the scope of this report, but the excess risk of
mesothelioma from very low-level exposure to asbestos — e.g. simple occupancy of public buildings
or schoolrooms where average asbestos fibre concentrations are about < 0.001-0.02 fibres per litre —
appears to be very slight:  about ≤ 5.5 mesotheliomas per million lifetimes of 80 years, or < 1 case
per 10,000,000 per year.
5.64 The estimated mesothelioma risk for a 10-year exposure to low levels of airborne asbestos in
schools (age start 7-8 years;  fibre concentration 0.00065-0.001 fibre per ml
16 is in the range 6.6-20
per million lifetimes (0.0825-0.25 per million person-years).  Estimates of this type are predicated on
linear dose-response models with no threshold, and these have been the subject of argument and
criticism.  The occupational groups from which they were derived were exposed to mixtures of
asbestos types, but one might expect the risk to be even less or "undetectably low" in nations whereonly chrysotile was used.  At this point, it is sufficient to emphasize that -  even if one accepts for a
moment the no-threshold linear dose-response relationship - calculations indicate that a single
asbestos fibre (the so-called "one fibre" hypothe sis) would only have a 50-50 chance of producing a
single excess mesothelioma among all the humans who have ever inhabited Planet Earth.
5.65 These observations on mesothelioma risk estimates for very low-level exposure to asbestos in
buildings do not contradict the earlier suggestion in this report that Western Australian and Australian
increases in mesothelioma incidence among females were a possible consequence of general
environmental exposure to asbestos:  the two-fold rise in incidence in Western Australia could be due
to environmental fibre levels higher than those recorded in public buildings elsewhere.
                                                     
16Given in various publications as fibres/ml, fb/ml, f/ml, f/mL and fibres/cm3.WT/DS135/R
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5.66 If it exists, the risk of mesothelioma from very low-level environmental exposure to asbestos
needs to be considered in proportion to other risks of death in society.  The lowest death-risk at any
age occurs in girls aged 4-14 years and is ~ 100 per million per year, but the risk in late teenage
increases by 300-400 per million per year — attributable largely to increased travel by motor vehicle.
A 40-year-old man at risk of mesothelioma from low-level exposure to asbestos during childhood(excess mesothelioma risk < 1 per million person-years) has an annual risk of death from all causes of
about 2000 per million.  In 1990, de Klerk [128] had this to say on the subject:
"In the US the acceptable (or possible litigation-proof) lifetime risk seems to be one per million.  The
FDA have this as a set policy;  the EPA approximates to it, and other agencies seem to employ similar
figures.  In the UK the Royal Society has set a higher range with an annual risk of one per million
considered negligible, with any form of control unjus tified;  one per 100,000 considered low ("very few
would consider action necessary" — e.g. 16,000 km air or rail travel);  one per 10,000 moderate (fewwould commit their own resources to reduce risk" — e.g. 16,000 km car driving, working as acoalminer);  one per 1,000 high (e.g. age 30-39, 16,000 km motor cycling);  and one per hundred
unacceptable (e.g. age 55-59, smoking 20 cigarettes per day, heavy exposure to crocidolite)."
5.67 Within this context, one might ask what constitutes a negligible as opposed to an acceptable
(or unacceptable) risk?  In the context of the foregoing discussion, one might argue that a negligible
risk is a statistical and scientific concept:  a risk so slight that it does not require preventive or
remedial steps in comparison to other risks in society (although some might argue about the dividing
line between negligibility and unacceptability in this context).  With acceptability or unacceptability
other factors come into play:  they include, for ex ample, social, political and industrial considerations
— and the likelihood of litigation over any situation wherein the theoretical or estimated risk is
elevated to a background level, no matter how slight ly.  Accordingly, a risk, though slight or even
negligible, might still be considered unacceptable in legal or sociopolitical terms.
5.68 Others may dissent from the acceptability of the Royal Society approach to low, moderate and
high risks discussed above.  Conclusions about the acceptability or unacceptability of risk will alsovary according to the seriousness of the risk (e.g. th e approach to a lethal risk such as mesothelioma
would be quite different from a factor that caused a large proportion of the population to sneeze once
or twice);  these assessments will also vary according to the avoidability of the risk, the individuals
making the assessment, and the question of informed consent by those at risk.
5.69 Furthermore, society abounds with inconsistencies and contradictions over the relativity of
various risks.  For example, some societies that regulate or propose a ban on chrysotile asbestos make
extensive use of radioactive materials — e.g. in nuclear power stations and the production of
radioactive isotopes for medical purposes.  Even so, the use of fissionable materials for these purposes
may be justified and justifiable within those societies, because:  (i) the risk of morbidity or death from
well-publicized mishaps at nuclear reactors is still substantially less than the risk of death fromalternative energy sources (e.g. higher mortality rates among coalminers); and (ii) because the
materials in question can be regulated and controlled so that they are accessible to only a small
fraction of society (i.e. workers who can be trained in the controlled use of radioactive substances);
and (iii) nuclear power does not contribute significantly to air pollution or greenhouse gas emissions
in comparison to the burning of fossil fuels.
5.70 In addition, Nicholson [129] places the problem into the perspective of voluntary versus
involuntary risks:
"Rather than compare asbestos risks with voluntary ri sks (smoking, school football) or risks that remain
high despite expenditures of substantial public and private money (aircraft and highway accidents), it is
worthwhile to compare them with other involuntary environmental risks that are controlled by
regulatory agencies (pesticide exposures, drinking water contamination).  In a review of regulatoryactions taken by the FDA ... and the EPA it was found that for estimated population risks exceeding oneWT/DS135/R
Page 257
death/year, the individual lifetime risks were usually regulated if they exceed 1/1,000,000 for a lifetime
exposure.  Only eight of 31 carcinogenic exposure circumstances that exceeded this level were notregulated.  They involved saccharin, aflatoxin, formaldehyde and polycyclic organic matter ... " [p 81].
5.71 In fact, it is my view that over-reaction to the low risks produced by asbestos in place may
lead to a greater risk — i.e. the carcinogenic risks imposed by asbestos removal programmes.  Two
mesotheliomas encountered in my own practice during 1999 occurred not in asbestos removal
workers, but in others who sustained bystander exposure as a result of this activity:  (i) pleural
mesothelioma in a lecturer who had walked to and from her classroom at an Australian university each
day over a period of weeks, through a building where an asbestos insulation removal programme wasbeing carried out;  (ii) pleural mesothelioma in  a fireman who attended fires in buildings that
contained asbestos-cement products and who participated in clean-up operations thereafter;  about
once a month for some years, he also attended and examined buildings where fire alarms had been
activated by high atmospheric concentrations of asbestos fibres produced by removal programmes.
(In addition, a recent survey in Finland found "occasional high fibre concentrations even insidepersonal protectors during asbestos removal work" [130]).
5.72 Two other important points are worth emphasis.  First, because they usually focus on specific
cohorts or groups of workers, epidemiological studies may fail to identify a small but real risk,
because of low statistical power.  In this respect, the documents submitted to the WTO state that it
may be impossible to prove a negative (absence of risk), but one can also state that absence of proofdoes not constitute proof of absence.  For example, a number of investigations have failed to identify a
statistically significant increase in the relative risk (RR) of cancer among individuals with parietal
pleural fibrous plaques.  In an extensive review of asbestos and lung cancer, Henderson et al.  [131]
commented along the following lines in relation to pleural plaques and lung cancer:
"Nurminen and Tossavainen [132] also emphasized the issue of statistical power;  they calculated the
RR for plaque-associated lung cancer in the general population to be as low as 1.1, given the prevalence
of 4.6% among unlikely exposed and 13.0% among probably exposed men with an estimated twofoldrisk of lung cancer.  Detection of this RR at a level of statistical significance would require a populationsample of about 300 000."  [p 102].
5.73 In a discussion of the Hughes-Weill study [133 ] on radiological asbestosis and lung cancer in
New Orleans asbestos-cement factory workers — one of the three key investigations that proposed an
obligate intermediary step of pulmonary fibrosis for the induction of lung cancer by asbestos —Henderson et al.  [131] also commented in the same review:
" ... the number of lung cancer cases [in the Hughes-Weill investigation] was small.  What number of
workers would be required in such a study to detect an increase in risk of, say 1.4, 1.56 or 2.0, asopposed to the risk in workers with chest x-ray opacities?  ... person-years of follow-up equivalentto 20-50 expected cases would be required to have an y reasonable chance of detecting RRs of 1.4 to 1.6
at a level of significance of 0.05.  ...  The power level for the actual sample of 420 ... to detect a risk of
1.5 would be about 40%.  That is, a true effect would be falsely declared 'non-significant' 60% of the
time.  ...  The low power of the Hughes-Weill study is exemplified by the fact that ... lung cancer riskwas not significantly associated with duration of employment or cumulative exposure (there was afairly restricted range of employme nt periods) and even the association of lung cancer with fibrosis was
only marginally significant."  [pp 93-94].
5.74 The point is that a low, non-significant or undetectable risk in a small cohort may nonetheless
translate into a substantial body of disease when sp read over a large population:  e.g. an RR of 1.1
representing an increase in risk of 10 per cent may require a population size of 300,000 to bedetectable at a level of statistical significance of 0.05, whereas this 10 per cent increase in a common
disease such as lung cancer may amount to a substantial burden of disease when spread across aWT/DS135/R
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population of, say, 1,000,000, 10,000,000, or 100,000,000.  (Please see also later discussion on
mesothelioma among brake mechanics:  answer to Question 2.)
5.75 Another point is that a high frequency of a cancer such as mesothelioma in a small population
may be overshadowed in absolute numbers by a lower occurrence rate for the same disorder spread
over a large population.  For example, among non-smoking former Wittenoom workers, mesotheliomais now the most common cause of death [70] (in most cohorts exposed to amphibole asbestos, < 10
per cent will develop mesothelioma).  Nonetheless, mesotheliomas among the Wittenoom cohort
contribute only 5-6 per cent of the total burden of mesothelioma across the Australian population
[AMR 99].  For example, the 1999 Report for th e Register records 189 mesotheliomas among the
former Wittenoom population with only a single exposure to asbestos, in comparison to 187
mesotheliomas among carpenters/joiners with only a single exposure to asbestos;  the point is that the
lower risk of mesothelioma from asbestos exposure among carpenters has produced almost the samenumber of cases, because carpenters among the Australian workforce constitute a much larger
occupational group than the entire Wittenoom cohort of about 6000.
5.76 This observation also applies to the numbers of mesotheliomas among chrysotile miners and
millers in Quebec, in proportion to other cases among the general population of Quebec.  Bégin et al.
[134] divided Quebec mesotheliomas into thr ee groups, as shown in the following Table:
TABLE 3:  MESOTHELIOMAS IN QUEBEC , 1967-1990
  GroupType of asbestos exposureNumber of
casesAverage age Average duration of
exposure
1 Chrysotile miners and millers,
Thetford and Asbestos, Quebec49 62  ± 8.1 yrs 30.5 ± 13.7 yrs
2 Manufacturing, industrial insulation,
shipbuilding yards of Quebec50 56.7 ± 8.6 yrs 21.4 ± 14 .5 yrs
3 General construction/ building
maintenance industries of Quebec21 57.7  ± 7.2 yrs 27.7 ± 7.2 yrs
From Bégin et al.  [134].
5.77 In this study, Bégin et al. [134] also commented that "the incidence of pleural mesothelioma in
chrysotile miners and millers, although not as high as in the crocidolite workers, is well above the
North American male rate".  They also observed that "asbestos exposures in Group 3, although
difficult to quantify on the basis of the record, appear to be often very low intensity".  Bégin et al. also
commented in the following terms:
"The present study documents an increasing incidence of malignant mesothelioma in chrysotile miners
and millers of the eastern townships of Québec, with 49 cases in the last 23 years and a rate of 2.5 casesper year in the last 10 years in the primary industry, as compared with a rate of 0.3 per year in the yearsprior to 1969  ...  To put these rates into perspective, a comparison of the incidence for the combinedpopulation of the Asbestos and Thetford townships of Québec of some 40,000 adult males or themaximal estimated workforce of 10,00-15,000 men [sic;  surely this is a typographic error in the
original, and it should be 10,000-15,000], 20 years ago and currently at risk, reveals that the incidence
of mesothelioma in the chrysotile mining townships of Québec would give an annual incidence rateof 62.5 cases per million per year for the 1980-1990 period, or in chrysotile miners and millers ofQuébec, would give an incidence rate of 150-250 cases per million per year for the 1980-1990 period.These values are well below the annual incidence rate of the crocidolite mining townships of SouthAfrica, estimated at 542 cases per million per year, and well above the rate for the North American
population, estimated at between 2.5 to 13 cases per year per million adult males for the 1970-1980
period, and 14.1 cases per year per million adult males in 1984 and 15 cases per million for 1980 andprojected to increase for the 1990s.  ...WT/DS135/R
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Thus, our observations add information of interest to the on-going debate regarding the relative
carcinogenicity of different types of asbestos fibers.  Our data suggest that some of the cases ofmalignant mesothelioma in Québec chrysotile miners and millers may not be necessarily attributable to
amphibole and could be chrysotile-induced.  Lung tissue burden analyses, a better indication of
exposure than tumour tissue burden, will be done on these cases to further investigate this point.  ....
Finally, our data strengthen the view that a substantial number of malignant mesothelioma cases have a
relatively short asbestos exposure, particularly seen in Group 3.  In our study, 25% of all cases are insuch a category"  ... [pp 539-541].
5.78 In one of the documents submitted to the WTO, it is argued that evaluation of, and actions on,
risks should be based on probability rather than mere possibility.  This proposition is open to dispute.
For example, action is often taken to avoid the possibility of harm — by regulation or prohibition —
even though the likelihood of injury is remote, because of the seriousness of the potential outcome.  In
medical ethics, this is the principle of first, do no harm ( primum non nocere ).  Two examples follow:
(i) the antibiotic chloramphenicol was known to be highly effective in the treatment of various
infections, including typhoid fever, but on rare occa sions it induced bone marrow aplasia;  despite the
low likelihood of this side-effect — about 1 in 250,000 — the use of chloramphenicol was restrictedto only a few life-threatening infections (e.g. typhoid fever), and it is now almost never used because
safer effective alternatives are available;  (ii) over recent years, there has been a flood of publicity
over global warming and greenhouse gas emissions.  A causal or direct relationship between
greenhouse gases (such as CO
2 and methane) and climate change is open to argument, and Earth
undergoes repeated cycles of natural cooling and warming;  in this respect, there is also evidence thatmelting of the Antarctic ice cap has been going on for some thousands of years, and global warming
for over 100 years.  Nonetheless, the consequences of inaction over greenhouse gas emissions are
potentially so serious that strategies to reduce the release of these gases into the atmosphere are
entirely appropriate, despite uncertainty over the link between them and global warming.
(f) General observations on induction of mesothelioma by asbestos, especially the amphibole
varieties of asbestos such as crocidolite and amosite
(i) The linkage between the amphibole varieties of asbestos, and commercial chrysotile, and the
subsequent development of malignant mesothelioma is well established and is not in dispute.
5.79 This link is generally accepted as causal;  in this respect, asbestos fulfils all  The Bradford Hill
Criteria  for the establishment of causality [44].
(ii) There is a dose-response relationship between cumulative exposure to asbestos and the
subsequent incidence of mesothelioma in asbestos-exposed cohorts or populations;  the incidence is
also related to time since exposure, so that early exposures are more significant for mesothelioma
induction than later exposures, other factors being equal.
5.80 This relationship is expressed by the Peto model and its various modifications:
I = K*F*(T
p – [T – D]p)
where I = incidence;  K depends on fibre type, mix, size and other site-specific variables;
F = intensity of exposure in f/ml;  and D = years of exposure.  For the purposes of modelling, T can be
replaced by (T – 10) to build in a minimum 10-year lag-time, and the cubic power of time (T3) is often
used, so that:
I = K*F*([T – 10]3 – [T – 10 – D]3)WT/DS135/R
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An important aspect of this model is that early exposures are more significant for mesothelioma
induction than later equivalent doses.
5.81 Of the variables D, F and K, it is D that is the most accurately measurable, whereas the values
for K and F are often unknown, though some estimates of F can be made from the type of workactivity.  When there are multiple periods of employment for which the type of work is similar for
each, one can assume that the value for each of F
1, F2, F3 ... F n remains constant, which also applies to
K1, K 2, K 3 ... K n, so that:
I ∝ ([T – 10]3 – [T – 10 – D]3)
In practice, a simpler equation can be used: I = ctk
where the constant c is dependent on exposure, usually taken as proportional to the intensity of
exposure multiplied by its duration (i.e. cumulative exposure), with weightings for different fibre
types;  the power k remains about 3.5, or 3 for short periods of exposure.  As de Klerk and Armstrong[135] state:
"The model predicts that risk is increased after each increment of exposure by an amount proportional
to the level of exposure and the cube of time after that.  In terms of the multistage model of cancer, it
implies that asbestos acts at the first stage of a 4-st age process. ...  The model predicts that incidence is
much more dependent on early or low levels of exposure and increases less rapidly as exposurecontinues to increase, depending mainly on time since first exposed."   [p 232].
5.82 When one is faced with multiple exposures to asbestos, the following points emerge,
specifically for mesothelioma induction, provided that the characteristics and time for each exposure
are appropriate for a biological effect:  (i) it is not valid to point to one exposure among the others and
incriminate it as the sole cause of a mesothelioma, with exoneration of the other exposures;  (ii) it is
not valid to point to one exposure among the others and exonerate it from a causative role in thedevelopment of a mesothelioma, and to incriminat e all the others;  (iii) when there are multiple
episodes of exposure as a background to a mesothelioma, it is often the case that each exposure in
isolation would be sufficient for attribution of the mesothelioma to asbestos, with the provisos
mentioned above (characteristics and times of exposures).  When each exposure among others is
appropriate for mesothelioma induction if the particular exposure occurred alone, it is not logical tostate that this exposure — which could have a biological effect in isolation — has no effect when in
combination.  In such circumstances, it is not the presence or absence of an effect that is in question,
but the magnitude of each effect in proportion to the others.
5.83 A dose-response relationship has been observed with both estimates of airborne exposure to
asbestos [136], and quantitative and qualitative fibre burden analysis of the asbestos content in human
lung tissue of mesothelioma patients [3, 25, 137, 138]:  e.g. see Rogers et al.  [3], and, more recently,
Williams et al.  [138], who noted in 1997 that:
"It was shown there that while the relative risk of all three diseases [i.e. asbestosis, mesothelioma and
lung cancer] increased with increasing exposure, the relative risk of malignant mesothelioma is greater
at low levels of exposure when compared with the risk of asbestosis but is lower at very high levels of
exposure."  [p. 39].
5.84 In their study on the relationship between lung asbestos fibre type and the lung tissue
concentration of asbestos versus the relative risk of mesothelioma, Rogers et al.  [3] made the
following comment:
"Fiber content in the lung depends on both the amount of fiber deposited and the amount cleared.  The
amount deposited depends on duration and intensity of exposure in the occupational or generalWT/DS135/R
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environment.  Clearance rate is thought to be dependent on the amount deposited at any point in time,
i.e, clearance is exponential.  Thus, the same fiber content in the lung at death or time of resection maybe achieved from a high initial deposition, followed by absence of deposition and absence of clearance
over a long period of time, or by a continuous deposition at a lower level, with or without clearance.
Since detailed mechanisms of mesothelioma initiation and progression are not known, 'dose' asestimated by final lung fiber content may not relate to the 'dose' required to produce mesothelioma.  Itis thus possible that a high lung fiber conten t in a mesothelioma case may represent continuing
accumulation of fibers after a lower level of fibers had produced malignant change.  It is more likely,
however, that the malignant change did not occur until the fiber content reached a sufficiently high
level."  [p 1913].
(iii) The dose-response relationship between the amphiboles and mixtures of asbestos types is
linear at high exposures [15]
5.85 For example, please see EHC 203 and Table 4.
(iv) This dose-response relationship between asbestos exposure and the risk of mesothelioma has
also been detected at low levels of exposure, which overlap with environmental exposures.
TABLE 4:  INCIDENCE OF MESOTHELIOMA IN OCCUPATIONALLY EXPOSED GROUPS BY FIBRE TYPE AND
TIME SINCE FIRST EMPLOYED
Fibre type Industry Years since first
employedRate per million
person–years
Mixed: crocidolite, amosite andchrysotileManufacture textiles
and insulation20-24
25-30
30+1520
17103180
Mixed, mainly amosite Insulation workers 20-24
25-2930-34
35-39
40-44
45+290
15502760
6300
63308110
Mixed:  crocidolite andchrysotileFibrous cement manufacture 20-24
25-2930-342700
63009600
Chrysotile, some crocidolite Textile manufacture 20-24
25-2930-34
35-39
40+108
143
1156
493
1774
Amosite Insulation manufacture 20-24
25-2930-34
35+744
262350781842
Mixed Dockyards 20-24
25-29
30-34
35-4040-4445-49120
410
220
370
12401510
Crocidolite Mining and milling 20-24
25-2930-34
35-39900
22003000
7000
From de Klerk and Armstrong [135].WT/DS135/R
Page 262
5.86 A recent case-control study [136] from France on the dose-response relationship between low
levels of asbestos exposure and the odds ratio (O R) for mesothelioma showed a clear dose-response
relationship between estimated cumulative asbestos exposure and the OR for pleural mesothelioma.
In the final paragraph of the article, the authors stated:
"We found a clear dose-response relation between cumulative exposure to asbestos and pleural
mesothelioma in a population-based control study, with retrospective assessment of exposure.  Asignificant excess of mesothelioma was observed for levels of cumulative exposure that were probably far
below the limits adopted in many industrial countries during the 1980s."  [last sentence of abstract].
Although some concerns have been expressed about this type of investigation [139], it is my opinion
that these points were addressed in the original paper [136], and they are common and intrinsic to
epidemiological studies of this type — e.g. see Camus et al.  [140, 141].  This study [136] found an
OR for mesothelioma of 4.2 [95 per cent CI 2.0-8.8] at estimated cumulative exposures of 0.5-0.99
fibre-year,17 with elevation of the OR at about 0.5 fibre-year.
5.87 In a fibre burden study on mesothelioma patients, Rödelsperger [137] observed that:
"A significantly increased OR [for mesothelioma] is obtained even within the very low concentration
range of 0.1-0.2 F/µg [i.e. concentrations in the range of 100,000-200,000 fibres per gram dry lungtissue], which may be expected for about 5% of the population."  [p lll] (which also corresponds to an
estimated cumulative exposure in the range of about 1-2 fibre-years).
5.88 In a more recent study on mesothelioma cases (N = 66) and controls (N = 66), Rödelsperger et
al. [25] found an OR for mesothelioma of 4.5 at fibre concentrations of 100,000 to < 200,000 per
gram dry lung tissue  (for fibres > 5 µm in length;  95 per cent CI 1.1-17.9).  These authors also
recorded an OR = 2.4 at concentrations of 50,000 to < 100,000 fibres per gram dry lung tissue (95 per
cent CI 0.8-7.6).  The controls for this study — surgical lung resections mainly for lung cancer —would be expected to bias the OR towards 1.0 (i.e . underestimate the effect) [25], and hence the OR of
2.4 probably represents a genuine doubling of risk or more at these low fibre concentrations.
"Even within the concentration interval of 0.1-0.2 f/µg dry weight [i.e. 100,000 to 200,000 fibres per
gram dry weight], a significantly increased odds ratio of 4.5 was obtained.  Previously, the same
method of tissue analysis was used to estimate a 95 percentile of the amphibole fibre concentration of0.1 f/µg dry weight for persons without detectable exposure to asbestos at the workplace.  Therefore,
within the range of the normal background level [up to 300,000 fibres per gram dry lung in Germany],a positive dose response is observed."  [p 191].
This study did not detect an increase in the OR for chrysotile or for other mineral fibres.
5.89 The risk detected by Rödelsperger et al.  [25] appears to correlate reasonably well with the
French case-control study reported by Iwatsubo et al.  [136], which found an OR for mesothelioma
of 4.2 at estimated cumulative exposures of 0.5-0.99 fibre-year, with elevation of the OR at
about 0.5 fibre-year.
(v) No lower threshold (minimum) level of asbestos exposure has been delineated, below which
there is demonstrably no increase in the risk of mesothelioma.
5.90 This observation is expressed by Hillerdal [20] in the following terms:
"There is no proof of a threshold value — that is, a minimal lower limit below which asbestos fibres
cannot cause the tumour [i.e. mesothelioma] — and thus it is plausible that even such low exposure can
                                                     
17Fibre-year = concentration of airborne asbestos fibres (f/ml) x years of exposure.WT/DS135/R
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cause mesothelioma (even if the risk is extremely low).  Patients with mesothelioma whose lungs show
fibre concentrations within the normal range cannot be dismissed as background cases, — that is, notdue to asbestos.  ...  The only way to prove such a hypothesis would be to compare the incidence of
mesothelioma in a group with such background exposure with the incidence in a truly non-exposed
group.  This is not possible, as no such group can be found."  [i.e. the lung tissue of virtually allmammals contains some asbestos fibres derived from natural, environmental or occupational sources][p 510].
5.91 Points worth emphasis in Hillerdal's review [20] include reports of mesothelioma among
school teachers (9/487 patients with mesothelioma in one reference), in jewellers, and in individuals
exposed to asbestos insulation at home (6/262 patients with mesothelioma according to one reference).Hillerdal [20] also makes the point that low-level asbestos exposure "more often than not contains
peak concentrations which can be very high for short periods" (e.g. airborne asbestos fibre
concentrations of up to 78 f/ml from sweepin g asbestos from the floor [New Caledonia]).
(vi) The dose-response relationship for commercial Canadian chrysotile and mesothelioma
incidence is also linear at high levels of exposure.
5.92 For example, among the Quebec chrysotile miners and millers it has been noted that:
"All the observed 38 cases were pleural with the exception of one of low diagnostic probability, which
was pleuro-peritoneal.  None occurred in workers exposed for less than two years.  There was a cleardose-response relationship, with crude rates of mesotheliomas (cases/thousand person-years) rangingfrom 0.15 with cumulative exposure < 3530 million particles per m
3 (mpcm)-years (< 100 million
particles per cubic foot (mpcf)-years) to 0.97 for those with exposures of more than 10 590 mpcm-years
(> 300 mpcf-years)."  [EHC 203, p 8].
(vii) So far as I am aware, there are no observational data on dose-response relationships between
chrysotile only at low exposure levels and mesothelioma  incidence;  in this respect, estimates are
based on extrapolation of a linear dose-response line from high exposures down to low exposures.
"Overall, the available toxicological data provide clear evidence that chrysotile fibres can cause
fibrogenic and carcinogenic hazard to humans.  Th e data, however, are not adequate for providing
quantitative estimates of the risk to humans.  This is because there are inadequate exposure-responsedata from inhalation studies, and there are uncer tainties concerning the sensitivities of the animal
studies for predicting human risk."  [EHC 203, p 7].
5.93 Because of the lack of such data, no definite threshold for chrysotile in relation to
mesothelioma and lung cancer has been de lineated:  According to EHC 203 (p 144):
"(a) Exposure to chrysotile asbestos poses incr eased risks for asbestosis, lung cancer and
mesothelioma in a dose-dependent manner.  No threshold has been identified for carcinogenic risks."
5.94 In summary:
TABLE 5:  ASBESTOS -RELATED DOSE -RESPONSE RELATIONSHIPS FOR MESOTHELIOMA
Amphiboles Chrysotile
Heavy exposure Dose-response effect;  linear Dose-response effect;  linear
Low-level exposure Dose-response effect No data
Threshold No threshold delineated No threshold delineated
(viii) To the best of my knowledge, there are no observational data on the interactive effect of low
(or for that matter, high) concentrations of inhaled chrysotile fibres only, when these areWT/DS135/R
Page 264
superimposed later and separately upon a pre-existing amphibole ± chrysotile burden within lung
tissue (?superimpositional additive or multiplicative effect).
5.95 For example, it has been estimated that up to 15-20 per cent of men in industrialized societies
may have sustained occupational exposure to asbestos (chrysotile/amphiboles).  Rödelsperger et al.
[137] indicate that fibre concentrations of 1 00,000-200,000 amphibole fibres per gram dry weight lung
tissue may be expected for about 5 per cent of the population in Germany.  We do not know what the
effect of subsequent chrysotile fibre inhalation on top of this type of amphibole burden might be.
"Data were analysed on a case-referent basis, to relate relative risks of mesothelioma to dose of fibre, as
measured both by lung content and estimated airborne exposure.  Multivariate analysis of cases found a
dose response relationship for lung fibre content of crocidolite, amosite and chrysotile and the
development of mesothelioma.  Either a multiplicative or additive model could be used to fit therelative risk/dose coefficients for the various asbestos types.  A progressive increase in relative riskwith increasing fibre content was reported for all fibres ... .  Tests for trend were highly significant in allcases."  [NICNAS 99, p 61].
(ix) There is a long lag-time between asbestos exposure and the subsequent diagnosis of
mesothelioma (10 years as a minimum;  usually in the range of 20-40 years).  It follows that the
mesotheliomas encountered in the 1990s and the incidence of mesothelioma in various nations are a
consequence of exposures, especially occupational exposures, sustained from the 1940s through to the
1970s and even beyond.
5.96 Exposures from the 1940s through to the 1980s usually involved one or more of the
amphibole varieties of asbestos.  For example, asbestos-cement building products used in Australia
usually contained one or more of the amphibole varieties of asbestos, namely crocidolite or amosite,or both, at different times;  in this respect, the use of crocidolite in the products was discontinued
in 1966, and amosite in 1984.
5.97 Peto et al.  [24] make this point in the following terms:
"The extraordinarily high mesothelioma inci dence throughout Western Europe in men born
around 1945-50 reflects the extent of asbestos use in the 1960s and 1970s at the beginning of theirworking lives.  Annual raw asbestos imports to European Union countries peaked in the early to
mid 1970s and remained above 800 000 tonnes per year until 1980, falling to about 100 000 tonnes
by 1993 (European Commission, 1996).  Increasingly stringent exposure limits were enforced in themanufacture of asbestos-containing products over this period, but exposure to users of such materials,particularly in the building industry, remained virtually uncontrolled in many countries.  Chrysotileasbestos products are still widely used in several European countries, and maintenance or demolitionwork on older buildings may result in substantial exposure to amphiboles as well as to chrysotile.  We
have not included men born after 1955 in our projections, but the effects of asbestos exposure during
the 1980s and 1990s, although not yet apparent, may prove considerable."  [p 670].
(x) Properties of asbestos fibres that determine carcinogenicity
5.98 As indicated in the documents submitted to the WTO Panel, the properties of asbestos fibres
implicated for mesothelioma induction (and, possibly, lung cancer and other disorders), can be
summarized as the three Ds :
5.99 Dose :  this issue is covered in the preceding sections [(f)(ii)to (vi)].
5.100  Dimensions :  according to The Stanton Hypothesis , the carcinogenicity of asbestos fibres
appears to reside primarily in long thin fibres (length > 5 µm and especially > 8 µm, and in the range
of 10-20 µm, and diameters < 0.25 µm) — e.g. see Pott [142].  On the other hand, shorter fibres
appear to be less carcinogenic, although data indicate that tremolite fibres > 4 µm in lengthWT/DS135/R
Page 265
and < 1.5 µm in diameter produce malignant mesenchymal tumours when implanted into the pleural
cavities of rats [2].  On the other hand, very short-length fibres appear to have little carcinogenic
activity, although Churg [143] comments on fibre dimensions in the following terms:
"There has been extensive investigation of the relation of mesothelioma induction and fiber size in
experimental models.  Using intrapleural inoculation of different types of fibers with different sizedistributions, Stanton et al.  concluded that long, thin (i.e., high aspect ratio) fibres were much more
powerful mesothelial carcinogens than were short, thick fibers and that fiber type was less important.
The exact size of fiber that qualifies as long and th in is unclear:  fibers ... longer than 8 µm and widths
narrower than 1.5 µm are usually cited from Stanton's work, but the same experiments show that fiberswith lengths greater 4 µm and widths less than 0.25 µm were also effective carcinogens.  The Stantonhypothesis has been supported by animal inhalation experiments using size-separated fibers:  fewmesotheliomas were found with either amosite or chrysotile prepared to contain few fibers longerthan 5 µm.
Human data on the question of fiber length and mesothelioma are equivocal.  The tremolite found as a
natural constituent of chrysotile ore is a relatively short, thick fiber compared with commercial amositeor crocidolite, and if one attributes 'chrysotile-induced' mesotheliomas in man to the tremolitecomponent, the differences in mesothelioma do correlate with fiber size.  However, attempts to provethis proposition directly have produced  equivocal results  ...  McDonald et al . concluded that the
number of fibers longer than 8 µm explained most mesotheliomas and that chrysotile played no role.
However, Rogers et al . found that fibers both longer and shorter than 10 µm, including chrysotile
fibers, played a role, although long fibers were generally more important.  The problem with both ofthese studies is that most patients with mesothelioma have had occupational asbestos exposure, andfibers in lungs from those with occupational exposure are always longer than fibers in the generalpopulation;  thus the same result would have been obtained if the test group were exposed but had no
disease or some disease other than mesothelioma.  My colleagues and I have attempted to circumvent
this problem by comparing fiber sizes in a chrysotile mining and milling cohort and a cohort with heavyamosite exposure, using exposed workers with no disease as the control group.  In neither cohort couldwe show that fibers in mesothelioma cases were significantly longer and thinner than those in the otherdisease categories or even in the disease-free workers."  [p 353].
5.101  In other words, it is possibly the bio-persistence of amphibole fibres that is important for
mesothelioma induction, rather than precise fibre dimensions.
5.102  Durability  (bio-persistence):  the greater mesotheliomagenic (mesothelioma-producing)
potency of the amphiboles in comparison to chrysotile is widely ascribed to greater persistence of the
amphiboles in tissues, with significantly longer half-lives than chrysotile (please see later discussion,
Section (g)(v)).  On the other hand, it is conceivable that the same effect might be achieved by
sustained inhalation of chrysotile over a prolonged time interval or, possibly, shorter, but more intense
exposures so that the chrysotile fibres persist despite shorter half-lives than the amphiboles.
(xi) There is general though not universal agreement of a differential potency between the
amphiboles versus chrysotile for mesothelioma induction
5.103  In this respect, the amphiboles are substantially more potent, with estimates ranging from
2-4X, to 10X, to 12X on a fibre-for-fibre basis, to 30X, to a 30-60X greater potency, or more
(e.g. please see EHC 203).  A minority view that the amphiboles in chrysotile have roughly equalmesotheliomagenicity is not supported by th e prevailing evidence for humans.  Although
acknowledging the greater potency of the amphiboles for mesothelioma induction, some argue that
chrysotile is of equal or greater importance overall, because chrysotile accounts for > 95 per cent of
world asbestos production.  According to this perspective, commercial chrysotile is a weaker
carcinogen on a fibre-for-fibre basis, but this lesser potency is multiplied across a much greatertonnage, leading to an overall equivalent or greater effect [144].WT/DS135/R
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(xii) Tobacco smoke plays no role in the development of mesothelioma at any anatomical site —
unlike the synergy between asbestos and tobacco sm oke for the causation of asbestos-related lung
cancer (see section (i)(i) below).
(g) Commercial Chrysotile and Mesothelioma Induction
(i) There is general agreement that commercial chrysotile has the capacity to induce
mesothelioma in experimental animals and humans
5.104  There is dispute, however, over which fibres in commercial chrysotile are implicated (i.e. the
predominant chrysotile or the trace quantities of fibrous tremolite).
(ii) Canadian chrysotile contains trace amounts of tremolite, including fibrous tremolite, as a
contaminant [2, 10, 13, 14, 145-148]
5.105  The amount of tremolite appears to vary from one sample to another, but is generally < 1 per
cent (please see EHC 203).
(iii) It has been argued that the occurrence of mesotheliomas among the Quebec chrysotile miners
and millers is a consequence — not of the chrysotile  per se — but of the coexistent trace quantities of
tremolite (a non-commercial amphibole).
5.106  Analysis of the asbestos fibre content of lung tissue from this cohort demonstrates
disproportionately high concentrations of tremolite in comparison to chrysotile;  this appears torepresent a bio-accumulation phenomenon whereby chrysotile is cleared from lung tissue more rapidly
than the tremolite, so that the tremolite not only persists but increases in proportional concentration.
In this respect, the tremolite content of the lung tissue can be used as an index on the past chrysotile
exposure and some claim that the incidence of mesotheliomas in the same cohort can be related
directly to the tremolite content [13, 14].
(iv) It is known that fibrous tremolite has the capacity for mesothelioma induction
5.107  Mesotheliomas related to the use of tremolite in whitewash or stucco have been reported in
Turkey, Greece, Cyprus and Corsica [149-152] (for additional references, see Hillerdal [20]).
"Tremolite asbestos, a minor component mineral of commercial chrysotile, has also been shown to be
carcinogenic and fibrogenic in a single inhalation ex periment and an intraperitoneal injection study in
rats.  Exposure/dose-response data are not available to allow direct comparison of the cancer potency oftremolite and chrysotile."  [EHC 203, p 6].
5.108  Tremolite has also been implicated in lung cancer and  mesothelioma induction in a group of
vermiculite miners in Montana [2, 16, 153, 154].  It appears that these miners were exposed only to
tremolite-actinolite fibres.  The group was shown to have a:
" ... very high lung cancer incidence (standard mortality ratio [SMR] 285 ...), as well as four cases of
mesothelioma and eight of pneumoconiosis.  Examination of sputum samples from all but three
(170/173) current workers demonstrated asbestos bodies (AB) in 75%, the numbers showing a closeparallel with cumulative exposures in fibre-years."  [2] [p 493].
5.109  Case [2] has extensively reviewed the biohazards of tremolite, including epidemiological
investigations in humans and experimental data on animal models.  In his review, he emphasized the
pathogenicity of the tremolite found in Quebec chrysotile samples, especially at Asbestos and in the
Thetford mine:WT/DS135/R
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"Tremolite was not identified in Montreal air, was just detectable (0.2 fibres/l) in Asbestos, and was
one order of magnitude higher in Thetford mines (still only 1.5 fibres/l or 0. 0015 fibres/cc ...)."  [pp
496-497].
5.110  He also favoured the expression "chrysotile/tremolite" for Quebec chrysotile:
"As to the separate issue of 'chrysotile vs. tremolite', few would dispute the abilities of both to produce
lung cancer and asbestosis, again in sufficient exposure dose.  The weight of epidemiological, animal,
and, especially, lung internal-dose biomarker studies leads to the inevitable conclusion that it is the
tremolite 'component' of Quebec chrysotile which causes mesothelioma [but please see later discussionin this report].  It is unfortunate that adequate terminology for tremolite-contaminated chrysotile has notbeen introduced:  I for one would favour the simple  compound phrase 'chrysotile/tremolite'."  [p 500].
5.111  Case [2] also states:
" ... it becomes important to know to what degree 'chrysotile-in-place' is really 'chrysotile/tremolite-in-
place'.  No easy answer can be expected:  both bulk analyses and air sampling, even with analyticalelectron microscopy, can miss very low levels of tremolite.   Studies in the Quebec mining districtindicate that, at the very least, such low levels (roughly 0.0015 fibres/cc) can induce biological effects
(i.e., pleural plaques).  Unfortunately, only expensive in vivo  animal bioaccumulation assay systems
can truly answer the question:  the alternative is to wait 40 to 50 years for the next wave of asbestosdisease — which is likely to occur mainly among present-day asbestos abatement workers and to somedegree in custodial personnel and other tradesmen" …. [p. 500].
(v) Clearance of chrysotile from lung tissue
5.112  It is well known that chrysotile fibres are cleared more rapidly than amphiboles, especially in
long-term studies [145].  Clearance of amphibole  fibres does occur and the clearance mechanisms
appear to be more effective for short fibres (for both chrysotile and the amphiboles) so that the mean
length of retained fibres increases over time.  Churg and Vedal [155] calculated a half-life in lungtissue of about 20 years for amosite.  Estimates of the tissue half-life for crocidolite fibres have been
somewhat shorter (in the order of 5-10 years) [156-158], and de Klerk et al.  [158] could find no
difference between the clearance rates for long and short fibres.  Oberdörster [159] estimates human
clearance half-times to be about 90-110 days for chrysotile and 200-1500 days for crocidolite
fibres > 16 µm in length, based on extrapolated rat and primate inhalation data.
5.113  It has been claimed that chrysotile is cleared from lung tissue within 28-48 hours of
inhalation.  This claim seems extraordinary and begs the question:  why, if chrysotile is cleared from
lung tissue so rapidly, is it still demonstrable in human lung tissue many years or decades after
cessation of inhalation of commercial chrysotile (or mixtures of asbestos types)?  For example, in one
of my recent referral cases — an elderly man with lung cancer who sustained exposure from mixingloose asbestos and sweeping up dried insulation materials — an asbestos fibre analysis carried out on
lung tissue resected 16 years after his exposure stopped showed a total asbestos fibre count of
8,440,000 fibres/gram dry lung (> 1 µm in length; aspect ratio ≥ 3:1), made up by 6,250,000 chrysotile
fibres + 940,000 tremolite fibres + 940,000 anthophyllite fibres + 310,000 crocidolite fibres (the 24
year lag-time is enough for a carcinogenic effect).
(vi) The Quebec chrysotile cohort
4.114  In an analysis of mesotheliomas among the Qu ebec chrysotile miners and millers, up to 1997,
McDonald et al.  [13, 14]  reported 38 mesotheliomas, and most of these occurred after prolonged and
heavy exposure, especially at the mine where the greatest concentrations of trace tremolite occurred
(Thetford).  For example, these authors [13] r ecorded the breakdown of the mesotheliomas shown in
Table 6 (below).WT/DS135/R
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5.115  McDonald et al.  [13] identify two main reasons for the low mesothelioma rate from the five
smallest mines (1 case only among 6010 person-years, equivalent to 166 cases per million person-
years):  firstly, workers within this sub-group were younger than the remainder of the cohort;
secondly, these mines had been opened recently so that "there were inadequate periods of latency".  A
single additional mesothelioma shortly after comp letion of the study would erase the difference in
incidence rates between the five smallest mines and the main complex.  McDonald et al.  [13] go on to
indicate that the other rates are "reasonably comparable".  In comparison to the Thetford main
complex, there were relatively few mesotheliomas among workers at the asbestos mine and mill
(23 versus 8), despite nearly equivalent person-y ears of observation;  in addition, asbestos fibre
analysis on lung tissue demonstrated crocidolite and amosite in five out of the eight cases from the
mine and mill at Asbestos and in two out of the five mesotheliomas from the Asbestos factory
(Table 7, below).  In focussing on the Thetford mines group, it was noted that most of themesotheliomas came from the five central mines (Area A; Group C) as opposed to the 10 peripheral
mines (Area B;  Group P), so that the odds ratio for mesothelioma for Group C plus employees who
had jobs in both Area A and Area B (Group M) was 2.50 (based on net service;  20 adjusted years), in
comparison to an odds ratio of 0.80 for Group P.
TABLE 6:  MESOTHELIOMAS AMONG QUEBEC CHRYSOTILE MINERS AND MILLERS , 1997
Number of
mesothelioma deathsSubject-years
(000s)Rate
(per 100,000 subject-years)
23 65.14 35.3Thetford Mines:
Main complex and theoldest of the smaller mines
The five smallest mines 1 6.01 26.6
8 60.64 13.2Asbestos:
Mine and millFactory 5 10.84 46.2
From McDonald et al.  [13].
5.116  The clear implication of this complex and sophisticated study is that the risk of mesothelioma
was related strongly to years of service in the central area at Thetford where geological factors "in
Area A would probably result in tremolite, some in fibrous form, being mined with the ore".  In
addition, the mesothelioma rate for miners and millers was > 2.5 times higher at Thetford mines
(excluding the smallest mines) than at Asbestos, and this difference was also attributed to differencesin the amount of fibrous tremolite in the ores.  Despite these differences within the cohort for the
distribution of mesothelioma related to chrysotile and tremolite (and also to crocidolite and amosite at
the Asbestos factory and the Asbestos mine and mill), the results indicate that Quebec chrysotile — on
average contaminated by fibrous tremolite in sm all amounts — is capable of mesothelioma induction:
the Abstract describes 25 mesotheliomas from the Thetford mines, representing a mesothelioma rateof 337 per million person-years, which is substantially (almost 20X) higher than the mesothelioma
incidence rate of about 17 per million per person-years for men in British Colombia and the USA in
1982 and 1973-1984 respectively, and well above the background rate for spontaneous mesotheliomas
of 1-2 per million person-years.WT/DS135/R
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TABLE 7:  ASBESTOS FIBRE CONCENTRATIONS IN LUNGS AT AUTOPSY FROM 21 MESOTHELIOMA
CASES AMONG QUEBEC CHRYSOTILE MINERS AND MILLERS
(FIBRES PER µg:  GEOMETRIC MEANS )
Place of employment No. of cases Chrysotile Tremolite Crocidolite Amosite
Mines and mills
   Thetford Mines 14 12.8 104.1 0 0
   Asbestos 5 4.3 7.5 1.7 0.3
Factory   Asbestos 2 2.1 0.5 6.4 0.3
Table from McDonald et al.  (1997):  Table 2 in the original reference.  See also Table 1 in the original.
In calculating geometric means, a zero count ha s been replaced by half the detectable limit.
For crocidolite and amosite, all counts were zero:  i.e. below the detectable limit.For fibre counts/g lung tissue, multiply the figures by 106.
5.117  In the final two paragraphs of the paper, McDonald et al. [13] comment as follows:
"The tremolite hypothesis, if correct, has several important implications.  First, it supports the widely
but not universally held view that most, if not all, asbestos-related mesotheliomas are caused byamphibole fibres.  This in turn points to fibre durability and biopersistence as critical factors in
aetiology ... a point of even greater relevance in assessing the safety of man-made mineral fibres.
Second, it implies that uncontaminated chrysotile carries very little risk of mesothelioma.  In Asbestos,
exposures were not to uncontaminated chrysotile, but also to some tremolite and crocidolite, yet amongthe miners and millers only five deaths from a total of over 3,300 can be confidently attributed to theirwork.
At present-day levels of dust control the mesothelioma risk must be vanishingly small.  Even so, it
remains desirable to minimise, perhaps by screening, the contamination of commercial chrysotile by
amphibole fibres, however difficult this may be."  [p 718].
5.118  Despite the importance of this study by McDonald et al.  [13], the following comments can
also be made:
• The number of mesotheliomas in all groups except for the Thetford main complex
was small (1, 8 and 5 mesotheliomas respectively;  please see Table 6 above).  In this
respect, misdiagnosis or misclassification of the mesotheliomas according to theplaces worked could significantly affect the results, although there is no evidence that
this happened; however, the probability for th e diagnosis of mesothelioma also varied,
with a high probability in 19 cases, moderate probability in 14, and a low probability
(though considered more likely than not) in five;  of these 38 cases, only 18 had been
coded on the death certificate to ICD 163, and the rest to a variety of other diagnosticcodes.  Furthermore, in analysing the mesotheliomas according to Area A versus
Area B at the Thetford mines (groups C, M and P), the numbers were 104 for group
C, 69 for group P and 35 for group M;  McDonald et al.  noted that the odds ratio for
group P was unstable as shown by the "very wide confidence intervals, and as the
point estimate is well below unity it is quite unrealistic ".
• The low incidence of mesotheliomas in th e Quebec chrysotile cohort appears to
parallel similar low incidence rates for asbestosis and lung cancer for the same cohortWT/DS135/R
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[160, 161];  the incidence rates for lung cancer and mesothelioma appear to be
different in other chrysotile-exposed cohorts.
5.119  For these reasons and because of the different rates of various asbestos diseases (asbestosis,
lung cancer and mesothelioma) between the Quebec cohort and other groups of workers, I would be
reluctant to recommend national policies from the find ings in this cohort in isolation, and I would look
for coherence of the evidence across different cohorts and studies.
5.120  In relation to the Quebec cohort, there is an important error in the Canadian reply to
Question 4 (see Annex II) from the European Communities, where the following statement is made:
"Regarding asbestos-related mesothelioma, a number of studies have demonstrated cogently that this
type of cancer is almost exclusively linked to exposure to amphiboles.  Cases of mesothelioma inchrysotile asbestos miners in Quebec are quite rare — in a cohort of 11,000 workers who were verycarefully tracked (in the McDonald study), there were no more than 50 or so cases over several
decades.  Exhaustive research on their employment history revealed that most of the cases were related
to short-term exposure to commercial amphiboles.  For example, during World War II, some of theminers with mesothelioma had worked in plants manufacturing products for the Allied Forces andamphiboles imported into Canada had been used to make a variety of products, including gas masks, toassist in the War effort."
5.121  The statement that "most of the cases were related to short-term exposure to commercial
amphiboles" is incorrect and misleading.  As  demonstrated in the study by McDonald et al.  [13], most
of the mesotheliomas occurred among chrysotile mi ners who worked at the Thetford main complex,
without exposure to commercial amphiboles such as crocidolite or amosite.  This is clearly shown in
Table 7 (above), slightly modified from the paper by McDonald et al.  [13] where fibre burden analysis
on lung tissue from 14 mesothelioma cases from the Thetford mines showed both chrysotile and a
high concentration of tremolite, with a zero count for the commercial amphiboles crocidolite and
amosite.  The point to be emphasized is that the mesotheliomas from the Thetford mines were notrelated to commercial amphiboles such as crocidolite or amosite, but to chrysotile with its content of
fibrous tremolite.
(vii) As discussed earlier, a dose-response relationship between the incidence of mesothelioma and
cumulative asbestos exposure has been demonstrated for commercial chrysotile.
5.122  Mesotheliomas have also been produced in experimental animals by implantation and
inhalation of chrysotile (presumably also containi ng trace amounts of tremolite).  Mesotheliomas can
also be induced in rats by intraperitoneal injection of chrysotile, with evidence of a dose-response
effect [1] (see also bibliography for EHC 203).
"In non-inhalation experiments (intrapleural and intraperitoneal injection studies), dose-response
relationships for mesothelioma have been demonstrated for chrysotile fibres."   [EHC 203, p 5].
(viii) Chrysotile is also known to be toxic to a variety of cell lines in vitro, with induction of a
variety of chromosomal alterations (e.g. please see EHC 203, pp 69-102).
(h) Other Chrysotile-Exposed Cohorts and Studies
5.123  In addition to the Quebec chrysotile miners and millers, mesotheliomas have also been
reported among other workforces apparently exposed only to chrysotile, with no significant tremolite.WT/DS135/R
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(i) Russia
5.124  Chrysotile from the Urals region (Uralasbest) in  Russia [162, 163] is said to represent pure
chrysotile.  Although precise figures for the mesothelioma incidence in this area are difficult to
procure, Kogan [164] makes the following comment in a recently-published textbook on occupational
lung diseases:
"In the Middle Ural mountains, the main asbestos mining region in Russia, only chrysotile asbestos is
produced.  In the 50 districts of this region, the mortality from mesothelioma over a 10-year period wassix-fold higher than the average rate in the Sverdlovsk region, an area of negligible asbestos mining.
Most with mesothelioma had worked at the asbestos mining and milling plants, or had lived in an
adjacent town near old and very 'dusty' mills."  ... . [p 251].
5.125  Because it is difficult to equate exposure levels in the Russian chrysotile industry with other
industries (e.g. the airborne fibre concentrations at Uralasbest are usually expressed as gravimetricmeasurements), and I have been unable to ascertain the numbers of cases relative to exposure levels, I
consider this evidence to be weak in comparison to other studies.
5.126  One might expect data on mesothelioma incidence in Central and Eastern European nations to
be of interest, from an assumption that some of these countries would have imported mainly chrysotile
from Russia until the breakup of the Soviet Union.  Unfortunately, it is difficult to evaluate nationalmesothelioma statistics, because a number of these nations also imported amphibole asbestos.  For
example, in Slovenia, the total consumption of  asbestos (1947-1995) was 580,000 tonnes, of which
crocidolite accounted for 37,133 tons, until its use was stopped in 1992 [165].  Similarly, the annual
usage of asbestos in Bulgaria during the 1970s and 1980s reached approximately 32,000 tons of
chrysotile (mainly from Russia and Canada), together with about 1000 tons of crocidolite from Africa
and 6000-7000 tons of Bulgarian amphibole material (anthophyllite and tremolite) [166].  In Poland,
total consumption of asbestos for the manufacture of asbestos-cement products between the end of theSecond World War until 1993 was about 1.4 million metric tons which included about 8500 metric
tons of amosite and approximately 86,000 metric tons of crocidolite [167].
(ii) Germany
5.127  The former German Democratic Republic (GDR):  Sturm et al.  [5, 7] have published data on
asbestos-related diseases and asbestos types in the German State of Saxony-Anhalt.  These authorspointed out that:
"All asbestos-based products were made from raw asbestos which was primarily imported from the
former Soviet Union, particularly from the Kiembay mining area in the Ural mountains (said torepresent pure chrysotile).  Small quantities of long-fibred grades came from Canada (2,990 tonnesin 1989) and were mainly used for the manufacture of asbestos-cement pressure pipes free of
amphibole asbestos.  This was a share of approximately 7% in total imports.  We never obtained any
information about the Canadian mines from which the asbestos processed in the former GDRoriginated.  ... However, several analyses carried out by the GDR Central Institute for IndustrialMedicine confirmed that both the Canadian and the Russian asbestos were pure chrysotile.  In additionto these imports of chrysotile asbestos, smaller quantities of amphibole asbestos were imported.  Forexample, in the period from 1980 to 1985, some 90 tonnes of anthophyllite were imported annually
from Mozambique.  This anthophyllite was used exclusively by a Berlin manufacturer and was of acid-
proof products, similar to the way crocidolite had been used in previous years to produce filters, sealsand acid and lye-proof plastic materials.  In Saxony-Anhalt, our region of work, these amphiboleimports did not have any significance from the point  of view of industrial medicine" ... [p 318/173].
5.128  Between 1960 and 1990, a total of 1082 mesotheliomas was recorded in Saxony-Anhalt, and
these included 843 "proven asbestos-accepted mesotheliomas";  Table 8 from Sturm et al.  [5, 7] givesWT/DS135/R
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a breakdown of 812 cases for which adequate data were available:  67 were said to follow exposure to
chrysotile only, and 331 were associated with "chrysotile;  possible amphiboles".
(iii) Italy
5.129  Two mesotheliomas have now been recorded am ong more than 900 workers employed at the
Balangero mine and mill in Italy [168, 169].  EHC 203 gives the following summary:
"The cohort of chrysotile production workers empl oyed at the Balangero mine and mill ... was almost
exactly one tenth the size of the Quebec cohort.  At the end of 1987, when 427 (45%) of the cohort haddied, there were two deaths from pleural mesothelioma, both in men employed for more than 20 yearswith cumulative exposure estimated respectively at 100-400 and > 400 f/ml years.  One diagnosis wasconfirmed histopathologically, and one was based on radiological findings and examination of pleural
fluid.  Fibrous tremolite was not detected in samples of chrysotile from this mine, but another fibrous
silicate (balangeroite), the biological effects of which are not known, was identified in low proportionsby mass (0.2-0.5%).  At a comparable stage in  the evolution of the Quebec cohort, mesothelioma
accounted for 10 of 4547 deaths, a lower but not dissimilar proportion."  [p 112].
TABLE 8:  MESOTHELIOMAS ACCORDING TO TYPES OF EXPOSURES
TO ASBESTOS IN SAXONY -ANHALT
Amphiboles Amphiboles
and chrysotileChrysotile;
possible
amphibolesChrysotile Mean values
Age at beginning of
exposure25 28 28 34 28
Duration of exposure 16 21 19 14 19
Lethal period (years) 40 40 41 31 38
Age of person dying
of mesothelioma65 68 69 65 66
Number of
mesotheliomas135 279 331 67 N = 812
Note:   All types of application of asbestos with common addition of chrysotile fall under the heading "Chrysotile.
Amphiboles possible" when previous admixture of amphiboles cannot be definitely excluded.  From Sturm et al.  [5, 7] .
(iv) China
5.130  At the XV International Scientific Meeting of the International Epidemiological Association
(Florence, September 1999), Yano et al.  [170] presented a paper on lung cancer incidence in a cohort
of 515 male asbestos workers heavily exposed to chrysotile containing < 0.001 per cent tremolite, inChongqin;  two mesotheliomas over 11,850 person-years of observation occurred in this cohort
(discussion to the paper;  assuming this rate to be representative, it would amount
to 170 mesotheliomas per million person-years).
5.131  In a retrospective cohort mortality study of 1227 men employed at a chrysotile mine in Hebei
Province of China before 1972, Zou et al.   found three deaths from mesothelioma (please see
EHC 203, p 120).
(v) United States
5.132  Two mesotheliomas have also been observed among the cohort of South Carolina chrysotile
textile workers — who used Canadian chrysotile — studied by Dement et al.  [171, 172] (please see
EHC 203, p 115).WT/DS135/R
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(vi) Australia
5.133  There is also some indication of an increased frequency of mesothelioma among Australian
brake mechanics who were potentially exposed only to chrysotile from grinding of brake blocks that
contained Canadian chrysotile (please see later discussion on friction products, and NICNAS 99 and
AMR 99).
(vii) Zimbabwe
5.134  One pathologically confirmed case of mesothelioma has been recorded in association with
occupational exposures to asbestos in the Zimbabwe mines and/or mills, with one other case said to
resemble mesothelioma radiologically (EHC 203, p 121).
(viii) Fibre burden studies on human lung tissue from mesothelioma patients
5.135  Fibre burden analyses also support the notion that some mesotheliomas occur in association
with, or as a consequence of, inhalation of pure chrysotile.
5.136  Morinaga et al.  [173] detected asbestos fibres in 19 of 23 mesothelioma studied;  amphibole
fibres were found in 13 cases, but six were found to have only chrysotile fibres (five pleural
mesotheliomas and one peritoneal mesothelioma).  Nonetheless, the methodology for this study seems
unimpressive, with relatively small numbers of fibres analysed.
4.137  The 1991 paper by Rogers et al.  [3] recorded a substantial number of mesothelioma patients
in whom the only detectable type of asbestos was chrysotile (Table 9), with evidence of a
dose-response effect as reflected in a trend to an increasing odds ratio (OR) at a relatively low fibre
concentration of ≤ 106 fibres per gram dry lung tissue (log 10 = 5.5–6;  OR = 8.67).
TABLE 9:  DISTRIBUTION OF FIBRE CONCENTRATION :  TRANSMISSION ELECTRON
MICROSCOPIC ANALYSIS , CHRYSOTILE ONLY (ALL LENGTHS )
Mesothelioma cases Controls Odds ratio
No. Percent No. Percent 95% Cornfield
Cl
f/g 0-200.000
1248.0
2683.9
log 10 (f/g) 5.3-5.5
14.0
26.5 1.08 (0-17.95)
5.5-6
728.0
39.7 8.67(1.77-
48.14)
6-6.5
312.0
6.5-7
14.0
7-8
14.0  Χ2 1 = 9.80
(P<0.0005)(trend)
From Rogers et al.  [3].  Cl:  confidence interval;  f/g: fibres per gram of dried lung tissue.
5.138  Finally, fibre burden studies have demonstrated that both chrysotile fibres and amphibole
fibres can translocate from lung parenchyma to reach the pleura;  EHC 203 summarizes these findings
in the following way:
"In a study of asbestos fibres in the lung parenchyma and the parietal pleura of 29 asbestos workers,WT/DS135/R
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Sebastien et al.  (1980) found that chrysotile fibres predomin ated in the pleura and that amphibole fibres
could not be detected.  A similar result was reported by Dodson et al.  (1990).  Kohyama & Suzuki
(1991) found short chrysotile fibres in pleural plaques and in mesothelial tumours.  In contrast, Boutin
et al. (1993) found 0.21 x 106 fibres per g of parietal pleura and 1.96 x 106 in samples of lung
parenchyma.  Fibre concentrations were higher in subjects with a history of asbestos exposure and mostof the fibres were amphiboles.  Churg (1994) reported  detection of chrysotile fibres in the subpleural
parenchyma in chrysotile miners and millers."  [pp 64-65].
(ix) Other Observations
5.139  Nicholson and Raffn [8] analysed mesothelioma risk over 40 studies for which little or no
exposure information was available, using the excess numbers of lung cancers as a measure ofexposure and comparing the ratios of mesotheliomas to excess lung cancers across these studies.
They suggested that:
" ... the ratio of mesothelioma to excess lung cancer is the same for exposures to 100% chrysotile
(presumably Canadian chrysotile), 97%+ chrysotile, 100% amosite, and mixtures of chrysotile, amosite
and crocidolite, within statistical uncertainty.  On ly 100% crocidolite exposures appear to have a
greater ratio, about two to four times that of predominantly chrysotile.  This relatively small differencein the potential for crocidolite to produce mesotheliomas compared with other fibre exposure cannotexplain the high risk seen in chrysotile exposures accompanied by a very small crocidolite exposure.The data speak strongly that much of the mesothelioma risk in predominantly chrysotile exposures is
from the chrysotile."  [p 402].
5.140  In other words, these authors appear to argue, like Smith and Wright [144], Stayner et al. [11],
and Landrigan et al.  [21] that although chrysotile may be cleared more rapidly from lung tissue than
tremolite — and that tremolite can be used as an indicator of past chrysotile — it may not be valid to
ascribe all the mesothelioma risk to the tremo lite and to ignore the far more numerous chrysotile
fibres.  Nonetheless, I do not find Nicholson and Raffn's argument to be persuasive, taking into
account  the K values for different industries.
5.141  Therefore, it is my perception that epidemiological and experimental evidence clearly
demonstrates that Canadian chrysotile with its trace amounts of fibrous tremolite has the capacity for
mesothelioma induction.  Although the tremolite may have a disproportionately large effect, it is my
perception that the evidence does not allow one to conclude that the chrysotile has no effect on
mesothelioma induction:  there is evidence from other cohorts and studies that chrysotile per se canalso induce mesothelioma, even when tremolite is undetectable, and in experimental models in
animals, chrysotile is as carcinogenic as, and more toxic than, the amphiboles.  However, there is also
general agreement that in humans, chrysotile is su bstantially less carcinogenic for the mesothelium
than the amphiboles, and my estimate is that it has a potency 1/10
th – 1/30th the carcinogenicity of
crocidolite, with amosite being less mesotheliomage nic than crocidolite but more carcinogenic than
chrysotile on a fibre-for-fibre basis.  Amosite is an  important factor in the incidence of mesothelioma
in the United States, because of its widespread use in insulation materials from the 1960s [155, 174-
176].
(i) Abestos and Lung Cancer
5.142  Still the focus of some controversy, this subject has been reviewed by Henderson et al. :
(i) Henderson DW, Roggli VL, Shilkin KB et al. , Is Asbestosis an Obligate Precursor for Asbestos-
Induced Lung Cancer?   I n:  Pete rs GA, Pe te rs B J, eds.  Sourcebook on Asbestos Diseases, vol 11 .
Charlottesville:  Michie; 1995;11:97-168  [177];   (ii) Henderson DW, de Klerk NH, Hammar SP, et
al.,  Asbestos and Lung Cancer:  Is it Attributable to Asbestosis, or to Asbestos Fiber Burden?   In:
Corrin B, ed.  Pathology of Lung Tumors ,  New York:  Churchill Livingstone; 1997:83-118 [131];
(iii) Leigh J, Berry G, de Klerk NH, Henderson DW.,  Asbestos-Related Lung Cancer:  ApportionmentWT/DS135/R
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of Causation and Damages to Asbestos and Tobacco Smoke,  I n :   P e t e r s  G A ,  P e t e r s  B J ,  e d s .
Sourcebook on Asbestos Diseases, vol 13 ,  Charlottesville:  Michie; 1996:141-66 [178];  (iv) Multiple
authors.  Consensus Report:  Asbestos, Asbestosis, and Cancer:  the Helsinki Criteria for Diagnosis
and Attribution,  Scand. J. Work Environ. Health  1997;23:311-6 [113].
5.143  Some salient features of asbestos-associated lung cancer include the following:
(i) Synergy between asbestos and tobacco smoke
5.144  Historically, most asbestos workers have also been cigarette smokers, and the lung cancer rate
in virtually all cohorts is an outcome of the combined and synergistic effects of tobacco smoke and
asbestos.  Vainio and Boffetta [179] emphasize that asbestos and tobacco smoke are complex
carcinogens that can affect multiple steps in the multistage process of cancer evolution, and that the
combined effects will depend on the relative magnitude of each carcinogen at each stage;  the
interactive effect ranges from less than additive to  supramultiplicative, but the model for insulation
workers approximates a multiplicative effect (reviewed in Henderson et al.  [131]).  If the multistage
model of carcinogenesis holds, and asbestos and smoking act at different stages, then a multiplicative
relationship follows [180].  Leigh et al.  [178] have reviewed various models for the apportionment of
fractional contributions from cigarette smoke and asbestos towards the development of lung cancer.
(ii) Lung cancer incidence rates for asbestos-associated lung cancer vary greatly from one cohort
to another
5.145  Please see following discussion.
(iii) Asbestos fibre type and lung cancer risk
5.146  The greater carcinogenicity of the amphiboles for the mesothelium in comparison to
chrysotile appears not to  extend to the induction of  lung cancer [11].  In this respect, chrysotile is
implicated in one of the lowest rates of asbestos -associated lung cancer (in Quebec chrysotile miners
and millers), but also the highest rate (in South Carolina asbestos textile workers who used Canadian
chrysotile) [171].  The reasons underlying this ≥ 30-fold difference in lung cancer risk remain
unknown (reviewed recently by McDona ld [161];  please see also EHC 203).  The risk of lung cancer
in other asbestos-exposed cohorts is interm ediate between these two extremes [15].
(iv) Dose-response relationship
5.147  In most studies, there is a direct and linear relationship between the relative risk of lung
cancer and cumulative exposure to asbestos, including chrysotile and the amphiboles.
5.148  Accordingly, EHC 203 gives the following account:
"The slopes of the relationship between cumulative exposure to chrysotile and the relative risk of lung
cancer are summarized in Table 23 for those studies that reported this information.  These studies all
expressed this relationship using the following linear relative risk (RR) model:
RR = 1 + B x Ewhere B is the slope and E is the cumulative exposure to chrysotile asbestos expressed in f/ml-years.The slopes from the studies of the mining and milling industries (0.0006 to 0.0017), the latter having
been estimated on a subset of the cohort on which the former was based, and the friction production
industries (0.0005 to 0.0006) are reasonably similar.  Hughes et al. (1987) in a study of cement workers
(section 7.1.2.1b) reported a similar slope (0.0003) in one plant (plant 1) that only used chrysotile, andWT/DS135/R
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a nearly 20-fold higher slope (0.007) among workers only exposed to chrysotile in another plant
(plant 2).
The slopes of 0.01 and 0.03 reported for the two studies of the chrysotile-exposed textile workers
conducted on overlapping populations, as well as the slope of 0.007 from one of the two plants (plant 2)
of cement workers in the study of Hughes et al.  (1987), were an order of magnitude greater than those
reported for the other cohorts.  It should be noted that the two textile cohorts were identified from thesame textile facility, but were based on different cohort definitions.  Hence, it is not surprising that theslopes from these two studies were similar.  The slopes in the studies of chrysotile-exposed textile
workers are also remarkably similar to those reported in other studies of textile workers with mixed
fibre exposures (Peto, 1980;  McDonald et al. , 1983b;  Peto et al., 1985).  This similarity in findings
provides some support for the validity of the slopes reported in the chrysotile-exposed textile cohorts.
The reason for the much higher slopes observed in studies of textile workers is unknown, although
several possible explanations have been suggested.  The first is that these differences might beattributed to errors in the classification of exposures in these studies.  Particular concern has been raised
about errors in the exposure assessment related to conversions from mpcm (mpcf) to fibres/ml that were
performed, particularly in the mining and milling studies (Peto, 1989).  Sebastien et al.  (1989)
conducted a lung burden study specifically designed to examine whether the differences in lung cancerslopes observed in the Charleston chrysotile textile cohort and the Quebec mining industries could beexplained by differences in errors in exposure estimates.  Lung fibre concentrations were measured in:(a) 32 paired subjects that were matched on duration of exposure and time since last exposure;  and
(b) 136 subjects stratified on the same time variables.  Both analyses indicated that the
Quebec/Charleston ratios of chrysotile fibres in the lungs were even higher than the correspondingratios of estimated exposures.  This finding was interpreted by the author as being clearly inconsistentwith the hypothesis that exposure misclassification could explain the large discrepancy in the lungexposure-response relationships observed in the two cohorts."  [pp 118-119].
5.149  Boffetta [15] expresses the relationship in the following terms:
"A large number of studies have been conducted on lung cancer risk following asbestos exposure.  The
interpretation of their results is complicated by severa l factors:  (i) dose, geological type of fibres and
industry are all important determinants of risk and are strictly correlated;  (ii) the biologically relevant
exposures occur 20 or more years before appearance of the disease, and their quantitative assessment is
imprecise;  and (iii) the role of potential confounders, in particular, tobacco smoking, can hardly beevaluated.  In general, the risk of lung cancer is smaller in studies of miners and friction productmanufacturers, is intermediate in studies of asbestos-cement and asbestos product manufacturers, and ishighest in studies of asbestos textile workers.  This likely reflects a stronger carcinogenic effect ofindividual, long and thin fibres, like those occurring in the textile industry, as compared to grouped,
short and coarse fibres, like those occurring in mining.
Several cohort studies provide sufficient details to allow a quantitative evaluation of the risk of lung
cancer from cumulative asbestos exposure.  In all cohorts, the empirical relationship fits well a linearcorrelation with no threshold, which can be expressed as:
RR
1 = 1 + K 1*CE,
where RR 1 is the relative risk of lung, CE represents cumulative asbestos exposure, expressed as fb/ml-
yrs, and K 1 is the industry-specific slope of the relationship (RR for the increase in 1 fb/ml-year of
exposure) for lung cancer and varies across cohorts.  Similarly, the risk difference (RD 1) can be
expressed as
RD 1 = K 1*CE*Exp,
where Exp is the number of expected cases of lung cancer.  In other words, the number of cases of (or
deaths from) lung cancer attributable to asbestos exposure depends on the number of expected cases
(deaths), the cumulative exposure, and the intrinsic carcinogenic potential of the exposureWT/DS135/R
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circumstance.  The value K 1 varies from 0.05-0.01 in cohorts of insulation and asbestos textile workers
to 0.001-0.0005 in friction manufacturers and miners, while cohorts with mixed exposure have, in mostcases, intermediate values. ... While all estimated values of K
1 are positive, the type of asbestos does
not seem to be correlated to lung cancer risk.
In the interpretation of these results, however, one should consider several limitations.  Most studies are
based on a small number of cases or deaths:  for example, the risk estimate of 100 fb/ml-yrs for thecohort of asbestos textile workers presented by McDonald and colleagues (RR 2.4) has a 95%confidence interval from 1.7 to 3.8.  Another source of uncertainty, and possibly bias, relates to the
estimate of cumulative exposure:  in the same cohort of asbestos textile workers, the range of RRs
based on the extremes of the distribution of possible exposure values is 1.3-6.7.  For these reasons,several governmental and scientific committees have suggested to adopt an 'average' value of K
1,
independent from fibre type and circumstance of exposure ...:  the most widely accepted value is 0.01which corresponds to an increase of 1% of the risk of lung cancer for each fb/ml-yr of exposure.  ...
Tobacco smoking is the main cause of lung cancer, an d this applies also to the cohorts of asbestos-
exposed workers.  Despite the limitations of the available studies, which limit the precision of the
estimates of the combined effect of the two carcinogens, the risk from tobacco smoking seems to actsynergistically with that of asbestos exposure, acco rding to a multiplicative model.  ... The available
data are consistent with the most widely accepted model of quantitative dose-response betweencumulative exposure to asbestos and lung cancer risk, which assumes a linear relationship with nothreshold.  Alternative models, however, would also be consistent with the data.  In particular, as no
precise data are available for cumulative exposures below 1 fb/ml, a model with a threshold at low
exposure cannot be rejected."  [pp 473-475].
(v) Histological types of lung cancer
5.150  Although some studies have shown a relative excess of adenocarcinomas in proportion to
other histological types of lung cancer, all of the major histological types occur among asbestos
workers in proportions equivalent to, or only slightly different from, those in the general population
[112].  Therefore, the histological type of a lung cancer has no value in ascertaining whether or not
asbestos has contributed significantly to the genesis of the cancer (reviewed by Henderson et al.
[131]).
(vi) Lobar distribution and the central versus peripheral distribution of asbestos-related lung
cancer
5.151  Some studies have reported a reversal of the upper lobe:lower lobe ratio for lung cancers in
asbestos workers, in comparison to a reference non-exposed population.  Recently, Lee et al.  [181]
addressed the lobar distribution of lung cancer in  asbestos-exposed individuals and found that the
tumours were predominantly located in the upper lobe (i.e. they did not find a reversal of the upper
lobe to lower lobe ratio).  The lobe of origin for a cancer has no value in ascertaining whether thecancer is likely to be asbestos-related.  The distribution of lung cancer between the central versus the
peripheral airways does not differ significantly in asbestos workers from a control non-exposed
population (please see Henderson et al.  [131]).
(vii) Asbestos and lung cancer risk
5.152  Cumulative exposure versus fibrosis (asbestosis):  as discussed already, most epidemiological
studies dealing with lung cancer risk in asbestos workers have reported a direct correlation between
the relative risk of lung cancer and cumulative asbestos exposure, although the slope of the
dose-response line varies from one cohort to another.  Most of the documents submitted to the WTO
appear to agree on this relationship, the main area of uncertainty or dispute being the question of
whether a threshold exists or not.WT/DS135/R
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5.153  However, Canada's answers to questions from the Panel and the European Communities
appear to resurrect the fibrosis-cancer hypothesis, which postulates that asbestos does not induce lung
cancer per se, but only through an obligate intermediary step of pulmonary fibrosis (asbestosis), so
that fibrosis becomes the determinator of lung cancer risk,  not cumulative exposure:
"1. Canada does not disagree that chrysotile causes lung cancer.  However, the way in which
exposure to chrysotile asbestos may increase the risk of lung cancer has not yet been fully explained;  it
could be just an indirect cause.  ...
2. The risk may become detectable in cases of long-term exposure to high levels, but it is by no
means certain that chrysotile acts as a direct carcinogen or that it acts in the form of pulmonary fibrosis,which would be a precursor to neoplasia.  In other words, exposure must be intense and long enough to
induce pulmonary fibrosis, which predisposes the pulmonary parenchyma to a high risk of cancer."
5.154  It is my perception that the fibrosis →cancer hypothesis represents a minority opinion: with
some prominent exceptions, most authorities in this area reject the fibrosis →cancer theory and focus
instead on the asbestos fibre burden in lung tissue as the main determinator for lung cancer risk, as
discussed earlier in this report.
5.155  The fibrosis →cancer hypothesis is predicated upon three key but flawed studies:
• In the investigation reported by Kipen et al.  [182], there was major problem with case
selection (only 138 cases out 450 — 31 per cent — had a tissue specimen with
sufficient non-malignant tissue for assessment of fibrosis);  in addition, the
histological criteria used for the diagnosis of asbestosis are unacceptable to most
pathologists — i.e. no asbestos bodies in some cases;  fibrosis restricted to the
subpleural zone considered to be asbestosis — so that this study seems to have
suffered from an over-diagnosis of asbestosis [183, 184].
• As discussed in Section (e) above, the Hughes-Weill study [133] on chest X-ray
opacities related to lung cancer mortality in New Orleans asbestos-cement workershad low statistical power, so that it had only a 40 per cent chance of detecting a
significant lung cancer standardized mortality ratio (SMR) of 1.5.  Other studies
based on X-rays have shown an increase in risk or mortality for lung cancer in the
absence of radiological asbestosis (e.g. Wilkinson et al.  [185], Finkelstein [186] and
de Klerk et al.  [187]).
• The autopsy study on South African crocidolit e miners reported by Sluis-Cremer and
Bezuidenhout [188] was also bedevilled by problems of selection (black people
excluded;  autopsies on 36.7 per cent of deaths only;  autopsies on cases for which
compensation was sought).  Analysis of the findings indicates that the effect of
duration of exposure (the most accurately measurable of the exposure variables) wasstill significant even after adjustment for the grade of asbestosis and other variables.
This indicates that exposure to asbestos still had an independent effect on lung cancer
mortality even after adjustment for the grade of asbestosis, as in the study reported by
Wilkinson et al.  [185].  In subsequent correspondence, Sluis-Cremer and
Bezuidenhout [189] conceded that when they carried out a logistic regressionanalysis, allowing for the grade of asbestosis, years of exposure accounted for most of
the variation, but the degree of asbestosis still emerged as a highly significant risk
factor.
5.156  Recently, Case and Dufresne [190] have commented as follows:WT/DS135/R
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" ... Hughes and Weill go much further in stating that asbestosis is a prerequisite for lung cancer
attribution in those with asbestos exposure.  This statement goes beyond the known facts and relies onmechanistic speculation.  The authors believe that asbestosis is produced by a mechanism or
mechanisms that will also lead to lung cancer.  Their hypothesis requires that the mechanism(s) always
be intermediate in that lung cancer always follows asbestosis.  Finally, the speculation requires thatlung cancer occurring without asbestosis can never be caused by asbestos exposure alone (or in synergywith cigarette smoking) regardless of the level of that exposure, and that no mechanism can occur thatdoes not involve intermediate fibrosis.  The biological fallacy of this argument has been well
documented  ...  one must remember that lung cancer originates in the large airways, while asbestosis is
a disease of the lung parenchyma at and beyond th e respiratory bronchioles.  ...  To ignore our
knowledge of indices of exposure other than the simple presence or absence of asbestosis is simplisticand biologically naïve."  [p 1118].
5.157  The case-control studies carried out on South Carolina asbestos textile workers by Dement et
al. [171] clearly undermine the fibrosis →cancer hypothesis and, in this respect, they constitute
Popper's Black Swan  factor:18  Dement and his colleagues clearly identified a lung cancer SMR > 2.5
at 2.7-6.8 fibre-years of exposure (well below the exposure level necessary for histological asbestosis
in the same cohort [191]).
(viii) Non-occupational asbestos exposure in Quebec and lung cancer risk
5.158  The first written submission from Canada also refers to the study reported by Camus et al.
[140] on non-occupational exposure to chrysotile asbestos in Quebec and the risk of lung cancer:
"It is also interesting to note the work of Dr Camus et al.  (see Camus, M., Siemiatycki, J. Meek, B.,
Nonoccupational Exposure to Chrysotile As bestos and the Risk of Lung Cancer , (1998) 338, New
England Journal of Medicine 1565).  They published a vast study on women in chrysotile miningcommunities in Quebec, many of whom were exposed to very high levels of fibres between 1920 and
1975.  These women were subjected to exposure of 0.0107 f/ml,
19 higher than the current exposure
limits in France, and literally thousands of times higher than the levels measured in public buildings.Nonetheless, no excess in lung cancer was detected in this population.  According to the study'sauthors, this is particularly important in the light of the current French situation.  In fact, applying therisk model adopted by France for the exposure studied, results in a forecast of approximately 100 lung
cancer deaths, while in reality there are none.  Likewise, use of the French risk model would have
resulted in estimates of approximately 250 and, at any rate, no less than 50 deaths from mesothelioma,while the preliminary results of the study in question show only 10 cases, some of which may beassociated with exposure to amphiboles.  Research continues, particularly with an analysis of the workhistory of each individual in order to determine the exact link, if any, between these cases ofmesothelioma and on-the-job exposure, as well as exposure to amphiboles."
                                                     
18"The philosopher of science, Sir Karl Popper ...  coined the term 'falsification' to express the concept
that scientific theories are not proven by repetition of results but rather survive because they successfully
withstand refutation (falsification).  His example of the black swan makes this point clearly.  Suppose you have
a hypothesis that all swans are white ... you observe, say, 10,000 swans and they are all white.  Another scientistrepeats your efforts and observes another 10,000 swans:  th ey too are all white.  So far the theory is standing up
well.  The repetition helped to strengthen it — but if only a single black swan is sighted, this falsifies the theory:it is no longer tenable.  Popper asserted that scientific statements have to be formulated in a manner that subjects
them to the possibility of falsification.  One of the important demarcating criteria between science and
nonscience, according to Popper, is this formulation of statements in a manner permitting falsification" [pp 18-
19] [44].
19This figure is inconsistent with the former limit of 0.1 f/ml in France, and contradicts Case's claim
that the Quebec women were exposed at up to 1 f/ml [192];  at a level of 0.0107 f/ml (a figure two orders ofmagnitude less than 1f/ml), a cumulative exposure of 5 fibre-years would require residence of > 150 years
(adjusted for equivalence to an 8-hour working day) and > 750 years to reach 25.0 fibre-years (using the same
adjustment).WT/DS135/R
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4.159  In fact, Camus et al.  [140] investigated the relative risk of death from lung cancer among
2242 deaths between 1970 and 1989 among women ≥ 30 years of age who lived in two chrysotile
asbestos-mining areas that comprised eight towns of which three (Thetford mines, Black Lake and
Asbestos) contained nearly all the asbestos mines and mills.  Eighty percent of the women lived within
4 km of a mine or mill, and all lived within 10 km.
5.160  The estimated average cumulative level of exposure was 25 fibre-years (range 5-125
fibre-years) made up by neighbourhood exposure (1 6.0 fibre-years), household exposure of 7.8 fibre-
years and occupational exposure of 1.2 fibre-years, making a total of 25.0.  The authors of this study
pointed out that:
" ... The lower limit of 5 fibre-years per ml corresponds, for example, to 50 years of exposure to
asbestos at a level of 0.1 fibre per ml (the actual mean ambient airborne asbestos level in the area in
1974);  the upper limit of 125 corresponds for example, to 50 years of exposure to 2.5 fibres per ml — arelatively low exposure level in local asbestos-mining and asbestos-milling industries before 1960." [p1568].
5.161  This investigation found a standardized mortality ratio of 1.0 in comparison to the reference
population (i.e. no observed excess of lung cancer mo rtality).  However, seven deaths from "pleural
cancer" were observed (RR = 7.64; p < 0.05).
5.162  A few points about this study are worth emphasis:
• The Quebec chrysotile miners and millers have a low risk of lung cancer in
comparison to other cohorts, such as the South Carolina chrysotile textile workers, for
whom the frequency of lung cancer is at least 30 times higher.  Therefore, it is not
surprising that the low risk of lung cancer in the chrysotile miners and millers of
Quebec extends across residents exposed environmentally to the same ore.  In otherwords, the absence of a detectable increase in lung cancer mortality in female
residents of this region of Quebec may not apply to other groups exposed
environmentally to asbestos from other asbestos industries.
• The study reported by Camus et al.  [140] stimulated considerable correspondence in
the columns of the same journal (NEJM), and at least two of the correspondents
(Churg [193] and Case [192]) emphasized that the seven-fold increase in
mesothelioma mortality (seven cases) among the women was probably explicable by
occupational exposure to amphiboles from manufacture of gas masks, repair of bagsthat contained imported asbestos, and, possibly in one case, domestic exposure to
"tremolite brought home on  miners' clothes".
In his letter to the editor, Case [192] also pointed out that "[T]hese women were
exposed to levels of chrysotile as high as 1 fibre per ml of air as recently as one
month in 1984."
• I have some misgivings over the exposure estimates for this female population, and
the figure of 25 fibre-years from environmental exposure in the general
neighbourhood or vicinity of the Quebec chrysotile industry seems high in
comparison to neighbourhood or environmental exposures from other industries.  For
example, ECH 203 (p 35) reproduces a Table of asbestos fibre concentrations inQuebec chrysotile mining towns, where the fibre concentration in 1984 is in the
vicinity of 0.005 fibre/ml and the concentrations in 1973 and 1974 are given
as 0.08 fibre/ml.  In other words, Case's figure of 1 fibre/ml for one month in 1984
[192] may be doubtful, unless there were some catastrophic event in the industry, withWT/DS135/R
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a burst of asbestos into the general environment.  Unless earlier environmental
airborne fibre concentrations were substantially above the 1973/1974 concentrations,
it is difficult to see how a cumulative exposure of 25 fibre-years would come about;
e.g. Camus et al.  [140] state that residence in the area for 50 years at a mean fibre
concentration of 0.1 fibre/ml would lead to the lower estimate of 5 fibre-years.
In addition, the estimate of 25 fibre-years seems high in comparison to data on
environmental airborne fibre levels related to the Zimbabwean and Russian chrysotile
industries.  For example, EHC (p 47) states:
"There are some data concerning fibre levels in the air close to chrysotile mines.
Baloyi (1989) found fibre levels around the Shabani mine (Zimbabwe) to range frombelow the limit of detection of the method" (less than 0.01 f/ml) to 0.02 f/ml of air,
assayed by PCOM.  [PCOM = phase contrast optical microscopy].
Scherbakov et al.  [163] also give a comparable environmental airborne fibre
concentration in Asbest City of 0.1 mg/m3 (comparative data for the same industry
[194] suggest that the gravimetric measurement of mg/m3 is very roughly equivalent
to the same number of fibres/ml).
The point is that if the estimate of cumulative asbestos exposure in the Quebec female
population is high, this would lead to underestimation of lung cancer risk or mortality.
For example, no detectable increase in lung cancer mortality among the 2242 deaths
would be expected at the low cumulative estimate of ≤ 5 fibre-years.
• In addition, in their reply to the Letters to the Editor, Camus and Siemiatycki [141]
state that "[W]e agree ... that the study had low statistical power to detect small risks;this was conveyed by the wide confidence intervals for our risk estimates ...",
although they go on to indicate that the Quebec study should have detected a risk of
the magnitude predicted by the Environmental Protection Agency [EPA].
(ix) The Helsinki Criteria
5.163  This set of criteria deals with attribution of lung cancer to asbestos for the individual patient
[113]:
"Because of the high incidence of lung cancer in the general population, it is not possible to prove in
precise deterministic terms that asbestos is the causative factor for an individual  patient, even when
asbestosis is present.  However, attribution of causation requires reasonable  medical certainty on a
probability basis that the agent (asbestos) has caused or contributed materially to the disease.  Thelikelihood that asbestos exposure has made a substantial contribution increases when the exposureincreases.  Cumulative exposure, on a probability basis, should thus be considered the main criterionfor the attribution of a substantial contribution by asbestos to lung cancer risk."  [p 314;  emphasis in
original].
5.164  The Helsinki Criteria set an exposure level of ≥ 25 fibre-years of exposure;  however, it
should be emphasized that this level of cumulative exposure is required for the individual patient as an
index for an asbestos-attributable relative risk of lung cancer of ≥ 2.0 (which, in the individual patient,
equates to a probability of causation or material contribution of ≥ 50 per cent — the civil standard of
proof).  Intended as a criterion for individual compensation, this exercise is clearly different from
population-based relative risks relevant to the dispute before the WTO.WT/DS135/R
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5.165  In summary:
TABLE 10:  ASBESTOS -RELATED DOSE -RESPONSE RELATIONSHIPS FOR LUNG CANCER
Chrysotile or Amphiboles
Heavy exposure Dose-response effect;  linear
Low-level exposure Dose-response effect for South Carolina textile workers (chrysotile)
Threshold No threshold delineated
(j) Some General Observations on Experimental M odels of Asbestos Carcinogenesis, including
in vivo  and in vitro  Systems
(i) In vivo experimental models
5.166  Although animal models of asbestos carcinogen esis - especially induction of mesotheliomas
in animals such as rats - are of value to demonstrate the capacity of different fibres to induce tumours
and to elucidate the mechanisms underlying carcinogenesis, they are not strictly comparable to
carcinogenesis in humans, for a number of reasons:
• The airborne fibre concentrations to which experimental animals are exposed for
inhalation experiments are substantially high er than in workplace or environmental
situations for humans.
• The routes of administration of asbestos or other fibres - e.g. injection or direct
implantation into the pleura or peritoneum - are not comparable to the human
situation, with the exception of inhalation experiments.
• High concentrations of asbestos or other fibres are necessary to reduce latency
intervals so that a reasonable yield of mesotheliomas or other cancers is obtainable
within the life span of the animal used.  In other words, the latency intervals are notcomparable to the human model.
• There are known to be marked differences in the susceptibility of different species to
asbestos carcinogenesis.
5.167  For example, in a review of asbestos and lung cancer, Henderson et al.  [131] state the
following:
"The dose of asbestos delivered by inhalation or installation over a short time interval in experimental
animals, the lag-times, and the histological spectru m of the tumors also make it difficult or impossible
to extrapolate the findings from such models to humans.  The exposure to asbestos in positiveinhalation experiments seems to have been so high that fibrosis was an unavoidable association with anincreased cancer risk (exposure to at least 100 f/ml, > 1,000 f/ml for some groups, 5 x 7 hours perweek, up to 12 months or more).  Wagner et al. remarked on a number of 'surprising' results in their
study (e.g. no differences in carcinogenicity or fibrogenicity between chrysotile and the amphiboles). ...
The sensitivity of humans to the carcinogenic effects of asbestos is about 100-fold greater than that of
rats.  ...
... Experimental studies of this type address asbestos inhalation in isolation, instead of asbestos
combined with tobacco smoke [for the study of lung cancer].  Hence, they are of questionable relevanceto most lung cancers in asbestos workers, for which tobacco smoke is an important co-factor.WT/DS135/R
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For the reasons stated above, we consider that the existing literature on tumorigenesis by inhalation of
asbestos in laboratory animals allows no conclusions on the asbestos-asbestosis-lung cancercontroversy in humans."    [p 96].
5.168  Davis [195] comments in the following terms:
"In experimental inhalation and injection studies, however, chrysotile has repeatedly produced as many
mesotheliomas as other asbestos types.  This finding probably indicates that the carcinogenic potential
of chrysotile to cells is as high as the other asbestos types, and it is just sufficiently durable to exert its
maximum effect in rats, although it is unable to survive long enough to do so in humans."  [p 201;  butsee discussion in this report on chrysotile clearance from lung tissue, Section A.(g)(v)].
(ii) In vitro systems
5.169  It is obvious that the effects of asbestos and other fibre types on isolated cell lines used for
in vitro  studies are not comparable to the induction of mesothelioma or lung cancer in humans.  In
vitro  studies of this type are of most value in showing that asbestos and other fibres can induce
chromosomal injury, oncogene expression or mutations similar to those induced by other known
carcinogens.
5.170  Detailed discussion of the voluminous literature on this topic lies beyond the scope of this
report.  Henderson et al.  [131] give some details of the effects of asbestos on cell lines in vitro ;  more
extensive reviews are given in EHC 203 (pp 69-102), Both et al.  [196], and Mossman et al.  [197-202],
and Bielefeldt-Ohlmann [203].  Only a fe w recent studies on chrysotile follow:
• "In the study by Haugen et al.  [204], chrysotile was about 10 times more cytotoxic
than amosite or crocidolite (as assayed by inhibition of clonal growth rate) and > 100-
fold more toxic than glass fibres;  epithelial cells were 10-15 times more sensitive tothe cytotoxic effects of asbestos fibres than bronchial fibroblasts from the same
human.  We can find no comparison with mesothelial cells in this paper [204], despite
at least one claim to this effect [197] ... " [p 97].
• "Harrison et al . demonstrated synergy between the lung carcinogen
N-nitrosoheptamethyleneimine (NHMI) and chrysotile in the production of
hyperplastic epithelial lesions in the lungs of rats, with a dose-response relationshipfor NHMI, augmented by chrysotile.  Neoplastic lesions (adenoma and
adenocarcinoma) were found only in animal s treated with both NHMI and asbestos,
but the number of such tumours was small (N = 6 among 115 rats studied)"  [p. 118;
see Henderson et al.  [131] for references].
• "Hei and Piao reported on malignant transformation of a human papillomavirus-
immortalized human bronchial epithelial cell line (BEP2D) by a single 7-day
treatment with chrysotile:  the cells so treated evolved through a series of sequential
steps to become tumorigenic, with the formation of progressively growing tumours in
nude mice"  [p. 118;  see Henderson et al.  [131] for references].
• In an investigation of the capacity of different asbestos fibre types to induce loss of
heterozygosity [L OH] mutations in lymphocytes and diploid mesothelioma cells that
were heterozygous for the HLA A2/A3 histocompatibility complex studied (incollaboration with Dr David Turner at the Department of Haematology-Oncology at
the Flinders University), it was found that chrysotile was more toxic to the cell lines
used so that few viable cells remained, making it difficult to evaluate LOH mutations,
in contrast to UICC South African crocidolite.WT/DS135/R
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• More recently, Dr. Turner and I have investigated the effects of UICC South African
crocidolite injected into the peritoneal cav ity of mice, for the investigation of somatic
intrachromosomal recombinational events in mice that are transgenic for the gene that
encodes the enzyme β-galactosidase;  using PCR [the polymerase chain reaction], we
detected a 5-fold reduction in SIR within only a few days of administration of the
crocidolite.  This finding parallels the results obtained with other carcinogens(e.g. cytotoxic drugs used for cancer chemotherapy) and may be explicable by a
reduction of SIR because the asbestos produces an increase in other classes of
mutation (e.g. point mutations or deletions), or because of impairment of DNA repair
mechanisms.
5.171  The picture now emerging on asbestos carcinogenesis is a prolonged multistage parametric
process [205], in which asbestos fibres may participate in both the initiation and promotion phases
[196].  Some classes of mutation potentially inducible by asbestos - e.g. loss of heterozygositymutations - are implicated in the initiation or progression phases of cancer development in humans,
thought to be related to loss of tumour suppressor genes (e.g. retinoblastoma, astrocytoma, and
colonic, gastric, prostatic and breast cancer) [206-211].
5.172  Free radicals — generated either from the surface of the fibres themselves [205, 212-215] or
via macrophages [213, 216-218] — have been shown to have genotoxic or clastogenic properties[205, 212-214, 217, 219, 220],  and are also implicated in asbestos carcinogenesis.
2. Questions by the Panel and Comments by the Scientific Experts
Question 1:
High-density chrysotile products (i.e. products where chrysotile fibres are bound in a
matrix, such as chrysotile-cement, as opposed to "friable" products, such as flocking and heat
insulation) represent the main use of chrysotile asbestos. The parties to this dispute disagree as to
the circumstances of exposure to chrysotile and the risks to human health associated with such
products. In this context, various questions arise with respect to the risks to human health
associated with the use of high-density chrysotile products, in particular chrysotile-cement (ofparticular concern are installation, modification, repair, maintenance, demolition and disposal).
1.(a) Canada argues that workers who are at greatest  risk of exposure to chrysotile asbestos are,
in descending order: (i) chrysotile miners and workers employed in the processing (milling)
industry; (ii) workers in the chrysotile textile industry;  (iii) workers involved in the production of
friction materials (such as brakes, clutches);  (iv) workers involved in the manufacturing ofchrysotile-cement products;  (v) workers involved in the removal of asbestos from buildings;  and
(vi) workers involved in construction, renovation, maintenance and the heat insulation of buildings.
Furthermore, according to Canada, the last two categories are likely to be exposed to amphiboles.
On the other hand, the European Communities argu es that, in France, the secondary users, which
includes installation, maintenance, repair, insulation, waste management and "handyman" type
persons, etc. are at the greatest risk of exposu re and that they are mainly exposed to chrysotile
asbestos, since, for some fifty years, chrysotile has represented about 97 per cent of asbestosconsumption in that country.  Could you comment on these contrasting views, with a special focus
on current uses and products?
Dr. de Klerk :
5.173  This question is rather curious and is either irrelevant or the wrong words have been used:
trying to elucidate an ordering of working groups according to their "risk of exposure to chrysotile
asbestos".  The risk of an event is the probability that  it will occur.  The event in question here is that aWT/DS135/R
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worker will come into contact with chrysotile asbestos. It is certain that the workers in groups (i) to (v)
are exposed to chrysotile so their risks are all the same and equal to 1.0.  Workers in group (vi) may
not come into contact with chrysotile so their risk of exposure is less.  The more relevant question here
is: who is likely to receive the most exposure and therefore have the greatest risk of disease?  In
general, workers in well-regulated industries, where government inspection is mandatory, where thereis a long history of efficient industrial hygiene practi ces, will have less risk of disease than those in the
smaller less well-regulated industries. A good example can be found with silicosis: the majority of
cases now occurring in both the USA and Australia arising from small unregulated industries with no
awareness of risks or hygiene practices.  Similar examples from own experience are: witnessing (in
1992) use of Russian asbestos in an asbestos-cement factory in Czechoslovakia (as it was then) where
all the warnings on the bags of asbestos were in English;  passing by demolition in progress of an old
asbestos cement factory building in Sydney last m onth where no observable precautions of any kind
were being taken.  (Note added later: It has struck me that the misunderstanding with this question
could be due to the relative imprecision of the French language, where "de" means both "of" and
"from", words with quite different meanings, especially in this context!)
Dr. Henderson:5.174  In past historical terms, the Canadian proposition about the classes of workers at risk of
exposure to chrysotile is correct — provided that this risk is expressed in terms of a numerical value
for the risk per person-years of observation (e.g. per 100,000 or 1 million person-years).  However,
this situation has changed over recent years, as airborne fibre concentrations have been reduced in the
mining and milling industries and during the production of friction products.  As one example,NICNAS 99 points out that manufacture of friction products (brake linings and gaskets) in Australia is
a completely closed operation, with low airborne fibre concentrations.
5.175  EHC 203 refers to this reduction in airborne fibre concentrations:
"Based on data mainly from North America, Europe and Japan, in most production sectors workplace
exposures in the early 1930s were very high.  Levels dropped considerably to the late 1970s and havedeclined substantially to present day values.  In the mining and milling industry in Quebec, the averagefibre concentration in air often exceeded 20 fibres/m l (f/ml) in the 1970s, while they are now generally
well below 1 f/ml.  In the production of asbestos-cement in Japan, typical mean concentrations
were 2.5-9.5 f/ml in 1970s, while mean concentration of 0.05-0.45 f/ml were reported in 1992.  Inasbestos textile manufacture in Japan, mean concentrations were between 2.6 and 12.8 f/ml in theperiod between 1970 and 1975, and 0.1-0.2 f/ml in the period between 1984 and 1986.  Trends havebeen similar in the production of friction materials:  based on data available from the same country,
mean concentrations of 10-35 f/ml were measured in the period between 1970 and 1975, while
levels 0.2-5.5 f/ml were reported in the period between 1984 and 1986.  In a plant in theUnited Kingdom in which a large mortality study was conducted, concentrations were generally above20 f/ml in the period before 1931 and generally below 1 f/ml during 1970-1979."  [pp 2-3].
5.176  In contrast, the risk per million person-years of observation may be less in building
construction, renovation and maintenance workers, but this smaller risk is spread across a substantially
larger workforce (i.e. there are many more carpenters/joiners, builder's labourers, electricians,
plumbers and other tradespeople in Western societies than the numbers of workers engaged in the
mining, milling or production of high-density asbestos-containing materials such as asbestos-cementsheets and pipes or brake blocks).
5.177  According to EHC 203:
"It should be recognized that al though the epidemiological studies of chrysotile-exposed workers have
been primarily limited to the mining and milling, and manufacturing sector, there is evidence, based on
the historic pattern of disease associated with exposure to mixed fibre types in western countries, thatWT/DS135/R
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risks are likely to be greater among workers in construction and possibly other user industries."
[EHC 203, p 9].
"Past uncontrolled mixed exposure to chrysotile and amphiboles has caused considerable disease and
mortality in Europe and North America.  Moreover ,  historical experience to mixed fibre types in
European countries has clearly indicated that a larger proportion of mesotheliomas occurs in theconstruction trades than in production.  Far larger quantities of chrysotile than of other types of asbestoswere used in most construction applications.  Epidemiological studies that contribute to ourunderstanding of the health effects of chrysotile conducted to date and reviewed in this monograph
have been on  populations mainly in the mining or manufacturing sectors and not in construction or
other user industries.  This should be borne in mi nd when considering potential risks associated with
exposure to chrysotile."  [EHC 203, p 137].
"Few data on concentrations of fibres associated with the installation and use of chrysotile-containing
products were available to the Task Group, although this is easily the most likely place for workers tobe exposed."  [EHC 203, p 138].
"There is potential for widespread exposure of maintenance personnel to mixed asbestos fibre types due
to the large quantities of friable asbestos materials still in place.  In buildings where there are controlplans, personal exposure of building maintenance personnel in the USA, expressed as 8-h time-weighted averages, was between 0.002 and 0.02 f/ml.  These values are the same order of magnitude asexposures reported during telecommunication switch work (0.009 f/ml) and above-ceiling work(0.037 f/ml), although higher concentrations have been reported in utility space work (0.5 f/ml).
Concentrations may be considerably higher wher e control plans have not been introduced.  For
example, in one case, short-term episodic concentrations ranged from 1.6 f/ml during sweepingto 15.5 f/ml during cleaning (dusting off) of library books in a building with a very friable chrysotile-containing surface formulation.  Most other values, presented as 8-h timed-weighted averages, areabout two order of magnitude less."  [EHC 203, p 139].
5.178  These points are also borne out by the 1999 Report for the Australian Mesothelioma Register
[AMR 99], where the broad spread of prior occupa tions among mesothelioma victims is plain.  For
example, the number of mesotheliomas from the former Wittenoom blue asbestos industry
(189 mesotheliomas related to a single exposure only;  25 additional mesotheliomas as a consequence
of multiple exposures;  total = 214) is less than the numbers of mesotheliomas as a consequence of
asbestos exposure in different occupations (e.g. carpenters/joiners:  187 mesotheliomas from a single
exposure;  33 additional mesotheliomas due to multiple exposures;  total = 220;  for builders/builders'
labourers the corresponding numbers are 150 + 27 = 177).  In other words, mesotheliomas among theformer Wittenoom cohort constitute a relatively small number (214) in comparison to the aggregate
numbers of mesotheliomas from asbestos exposures in other occupations (2585 – 214 = 2371 other
asbestos-associated mesotheliomas;  no exposure data for 717 cases, and no apparent exposure
for 443;  aggregate total = 3745).
5.179  NICNAS 99 makes the same point (p 59):
"Occupation/industry classification of the mesothelioma cases on the register are based on the
Australian Bureau of Statistics 'Industry and Occupation Codes'.  The percentage of overall cases of
mesothelioma (January 1986 to March 1995) according to exposure category are: repair and
maintenance of asbestos material (13%), shipbuilding (3%), asbestos cement production (4%), railways(3%), power stations (3%), boilermaking (3%), mining (Wittenoom) (5%), wharf labour (2%), para-occupational, hobby, environmental (4%) carpentry (4%), building (6%) navy (3%), plumbing (2%)brake linings (manufacture/repair) (2%) and combinations of the above (multiple) (12%) (Leigh et al.,
1997).  Leigh (1994) reported that the pattern of exposure is shifting away from the older traditional
industries towards product, domestic and environmental exposure.  An analysis of 16 years data in 1996
by Yeung et al.  (1997) showed more cases (on a number of cases basis) in more recent years in the
asbestos user industries and from occupations such as plumbers, carpenters, machinists and carmechanics."WT/DS135/R
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5.180  Similar patterns of exposure — and resultant diseases (lung cancer;  mesothelioma) — have
been recorded in the United Kingdom (EHC 203, pp 123-124):
"Based on analyses of mortality of workers with mixed exposures to chrysotile and amphiboles in the
United Kingdom, by far the greatest proportion of mesotheliomas occurs in users of asbestos-
containing products, rather than those involved in their production. ...
1. Asbestos exposure caused approximately equal numbers of excess deaths from lung cancer
(749 observed, 549 expected) and mesothelioma (183 deaths) within the occupations covered by the1969 and 1984 Regulations ...
2. Only a few (5%) of British mesothelioma deaths were among workers in regulated
occupations (Peto et al. , 1995).  The majority of deaths occurred in unregulated occupations in which
asbestos-containing products are used, particularly in the construction industry.  The risk wasparticularly high among electricians plumbers an d carpenters as well as among building workers."
5.181  As shown by the literature cited in this discussion, it is my perception that there is broad
agreement among experts on these patterns of exposure.
Dr. Infante:
5.182  The relative exposure categorization of the six job situations mentioned in the question
depends on the nature of controls being used in each situation.  In general, exposures are more easily
controlled in manufacturing and more difficult to control in construction, maintenance, repair,demolition and disposal activities.  Today, exposures would be more easily controlled in mining and
milling because of awareness of the hazard and the clear identification of the operations as sources of
asbestos exposure.  Quite often workers involved in maintenance, repair and handyman type activities
do not know whether asbestos is present or not.  In the absence of such knowledge, workers usually do
little, or nothing to protect themselves from exposures to asbestos in these situations. As a result,workers involved in these activities are most likely to be the most heavily exposed in the occupational
setting today.  These types of activities often result in asbestos being carried home on the workers'
clothing.  A typical scenario that comes to mind is a situation whereby a worker is in a crawl space
and encounters asbestos insulation.  There is no active supervision in this situation and the asbestos
most likely is not labelled.  Thus, the worker cuts through the insulation to get to the area needing tobe repaired without knowledge of the hazard and without having the appropriate personal protective
equipment.  In the latter scenario, even when workers do wear respirators, they are often dust masks,
which do not provide a proper face seal and the filter medium is not adequate i.e., HEPA filters are not
part of the filtration material on these masks. In the repair trades particularly, it is common practice for
workers to use dust masks that do not provide HEPA filtration.   As a result, the respirator isinadequate for filtering out the fibres of dimensi ons that are thought to lead to cancer and other
asbestos related diseases.  Furthermore, even in situations where the appropriate respirators may be
worn, comprehensive respiratory fit-testing programmes may not be included as part of the industrial
hygiene programme and as a result, the respirators leak because of the inability to achieve a proper
face seal.   In situations where workers may be drilling, sawing, crushing, or sanding asbestos cement
products the only appropriate respirator may be a supplied air respirator, but it may not be used
because it is too cumbersome for the job situation.  In my opinion, scenarios (v) and (vi) are usuallythe most dangerous in current times because the workers are not aware of the presence of asbestos and
they are more likely not to have received training and education about the hazards of asbestos
exposure.
5.183  The risk of exposure should be considered not only by level of exposure, but also by the
extent of the populations exposed to chrysotile asbestos.  The large number of mesotheliomasassociated with secondary and tertiary users of chrysotile asbestos (maintenance workers, electricians,
bystanders, etc.) is a reflection of the large number of individuals in the population exposed in theseWT/DS135/R
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situations.  Thus, in terms of the risk of disease from chrysotile exposure, one must consider not only
the intensity of exposure in the various work situations, but also the extent of the population exposed.
One study (Begin et al. , 1992) reports that 33 per cent of mesothelioma cases identified among
maintenance workers, electricians, bystanders, etc. were the result of exposure for less than five years,
and that the incidence of these occasionally exposed cases was increasing more rapidly than in theprimary industries (mines and mills), or in the secondary industries (manufacturing, daily handling of
asbestos).
Dr. Musk:
5.184  The term "risk of exposure" is taken to mean who is most likely to receive the most exposure
and therefore be at the greatest risk of developing asbestos-related disease.  This would depend on the
nature of the industry in the locality and the type of asbestos being produced or used or otherwiseencountered.  Those workers likely to receive the most exposure would be those in industries where
regulations are most permissive or compliance with them is poorest from absence of supervision or
means of personal protection.  It would also depend on the conditions of work such as indoor versus
outdoor etc.  Canada's "argument" could be settled by monitoring of exposure!  The "arguments" do
not seem to be incompatible.
1.(b) Should we consider that the risk to human health associated with the various uses of
chrysotile throughout its life-cycle is a workplace issue or does this risk affect a larger part of the
population?
Dr. de Klerk:
5.185  The risk of disease from chrysotile affects everyone.  The risk of disease depends on intensity
of exposure, the duration of exposure and the time since exposure.  The population who do not work
with asbestos will still come into contact with it, albeit at a much lower intensity, however this
population is much larger and hence the burden of disease may be greater.  There are numerous
examples of asbestos-related disease arising in people living in the vicinity of asbestos works or livingwith asbestos workers.
Dr. Henderson:
5.186  From my perspective, this is overwhelmingly a workplace issue (e.g. construction workers).
The risk of cancer for the larger general population from exposure to asbestos in place has been
discussed in an earlier part of this report (see abov e section C.1.(e)).  Please see also my answer to the
preceding question.
5.187  For example, asbestos-cement roofs are common in Germany where corrosion by acid rain
represents a potential problem.  Measurements carried out by Spurny et al.  [221-224] on airborne
asbestos fibre concentrations in the vicinity of such buildings consistently reveal levels in the order of
0.0002-0.0012 f/ml, in comparison to fibre concentration in other urban environments that range up
to 0.1 f/ml (but generally ≤ 0.001 f/ml).
5.188  Measurements have also been made on airborne fibre levels related to asbestos-cement
roofing in schools in Western Australia [128] , with only one asbestos fibre detected in each of two
schools (air monitoring at 9 sites over 720 hours).  Based on the findings, it was estimated that
airborne fibre concentrations would be unlikely to exceed 0.002 f/ml and were likely to
be < 0.0002 f/ml.  These levels were considered to represent a negligible risk to health;  theWestern Australia Advisory Committee on Hazardous Substances that carried out this investigation
considered that a greater risk to health would arise from:  (i) unskilled attempts to clean up theWT/DS135/R
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asbestos-cement roofs before application of protective coating;  and (ii) trauma to the workers —
e.g. falling from or through the roofs.
5.189  It is my perception that there is little or no dispute among experts on this issue.
Dr. Infante:5.190  In general, workers are at relatively greater risk of exposure to chrysotile and disease,
particularly those involved in maintenance, modification, demolition, repair and disposal activities as
compared to those exposed in non-occupational situations.  A large number of people from the general
population, however,  also will be exposed to chrysotile and elevated risk of disease when they engage
in home repairs that involve manipulating or disturbing asbestos-containing products.  (The latter
individuals usually have little or no education about the hazards of asbestos, nor of the most
appropriate means to handle it with the least amount of exposure.)  These types of operations will alsocreate some standby exposures (Ascoli et al.  1996).  If appropriate controls are not used when
handling asbestos insulation in buildings, the building can become contaminated and the occupants
will become exposed.  Therefore, the major problem with asbestos exposure is related to occupational
situations though a much larger population is exposed beyond the occupational setting to relatively
lower levels.  Reports of cases of mesothelioma among non-occupationally exposed individualsdocument non-occupational exposures to asbestos causing disease.  Family members of workers
involved in the asbestos cement industry (Magnani et al.  1993) as well as children of miners and
millers (McDonald and McDonald 1980) have been diagnosed with mesothelioma.
Dr. Musk:5.191  It is my opinion that the risks resulting from exposure affects all exposed people and depends
on the cumulative level of exposure.  It is also my opinion that there is not an exposure threshold
below which there is no risk.  The risks to people not occupationally exposed to asbestos are likely to
be much less than the risks to those with occupational exposure because the degree of exposure is
likely to be less (though not necessarily always so).  However, while the individual risks may be muchless the total burden of disease in the community ma y not be because it is likely that there are many
more people experiencing these risks (albeit lower).  For example the burden of disease in the
residents of the town of Wittenoom, Western Australia has been significant albeit less than that of the
workers.  The WA Mesothelioma Registry contains subjects whose only exposure was from
neighbourhood industries.  Similar cases have been documented in the Quebec areas.
1.(c) Can chrysotile-cement products (for inst ance in buildings) release fibres, through
weathering, corrosion or general degradation, thus  presenting a possible risk to human health?
Can you quantify this risk?
Dr. de Klerk:
5.192  There is good evidence that both wind and rain cause the release of fibres even from new
asbestos cement sheeting.  Other possibilities are fires and unwanted demolition.  It is hard to quantify
the risk which again depends on intensity and duration, but measurements have been made in the
vicinity of such buildings which are detectable but low.
Dr. Henderson:5.193  Please see the preceding answer, and section C.1.1(e).  Quantitation of the risk is based on
backward extrapolation according to the linear no-threshold model because there are no observational
data on the dose-response effects from low-level exposure to chrysotile, and the estimates are,WT/DS135/R
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therefore, open to question and dispute, but the risks to health from very low-level environmental
exposure appear to be minuscule or negligible.
Dr. Infante:
5.194  Yes, weathered and corroded asbestos cement products are capable of releasing chrysotile
fibres into the environment, and most of the fibr e is transported by rainwater though some will be
released into the ambient air in low concentrations .  One study indicates that chrysotile exposure in
such circumstances will generally be less than 1,000 fibres longer than 5 microns per cubic meter of
air.  The fibres released were shown to have the same carcinogenic potency as "standard" chrysotile
fibres (Spurny, 1989).  Asbestos fibres also will be released into water from cement water pipes.
I have not seen any estimates of risk from this type of asbestos exposure.  Although the relative risk of
disease is considerably less than that from occupational exposures, the population at risk isconsiderably larger.
Dr. Musk:
5.195  I understand that asbestos-cement products do release fibres as they weather.  Release of
fibres occurs from both old and new products.  Asbest os fibres can also be released when asbestos-
cement products are involved in fires. Quantitative estimates of the risks are theoretically possible as
airborne concentrations can be measured and dose-response relationships are known.
1.(d) Can interventions on chrysotile-cement and other high-density chrysotile products release
fibres, thus presenting a possible risk to the health of the individual making such interventions or to
the public in general? Can you quantify this risk?
Dr. de Klerk:
5.196  It is during interventions such as drilling, sawing, sanding, moving in stacks, loading onto
transport etc, that concentrations of fibres are greatest, both for the operators and bystanders.  The
concentrations associated with such operations have been extensively tabulated in the literature.Exposure response relationships can be used to estimate the risk for any combinations of intensity,
duration and time after exposure, as shown in the Table below.
5.197  Lifetime risks (to age 85 years) of mesothelioma after exposure to chrysotile,
assuming 0.1 f/ml for 10 years from age 20 with competing causes of death at 1992
Western Australian death rates.
Assumptions Expected cases per million lifetimes
Health Effects Institute equation 724
Wittenoom crocidolite equation 1/12th potency 210
Wittenoom crocidolite equation , 1/80th potency 32
Background risk (Peto study of "unexposed"
Los Angeles population)112
Dr. Henderson:
5.198  My answer to the first question is YES.  Operations such as drilling or sawing asbestos-
cement products release fibres and produce elevated airborne fibre concentrations.  (i) asbestos-
cement sheets can release respirable fibres in the absence of manipulation, even when new (up
to 0.001 f/ml;  for references, see de Klerk and Armstrong [135]);  (ii) a 1938 report inWT/DS135/R
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New South Wales indicated that cutting asbestos-cement products with a power saw could
generate 4-5 million particles/cubic foot (roughly eq uivalent to 12-15 f/ml);  cutting with hand saws
produced lower concentrations;  (iii) as shown in the following Table 11, Sturm et al.  [5, 7] reported
measurable fibre concentrations from various oper ations on asbestos-containing materials, including
asbestos-cement in the former East Germany, as measured by occupational inspectors.
TABLE 11:  ASBESTOS FIBRE CONCENTRATIONS AT WORKPLACES , WITHOUT SUCTION DEVICES ,
DETERMINED BY KONIMETRY (FROM UNPUBLISHED REPORTS
PREPARED BY OCCUPATIONAL INSPECTORATES )
Type of Work Fibre Concentration (f/ml)
Scratching and crushing of asbestos-cement 0.03 to 0.3
Abrasive cutting of asbestos-cement without dust removal by suction 0.3 to 10.0 approx.
Drilling asbestos-cement without dust removal by suction 0.5 to 3.4
Machining of brake linings 0.1 to 13.0
Replacement of gaskets 0.02 to 0.5
Punching of gaskets (rubber asbestos) 0.02 to 1.9
Use of asbestos gloves 0.02 to 0.6
Replacement of clearing layers 0.06 to 0.5
Use of talcum for powdering gloves 0.6 to 20.0
Level limit value (over a whole working day) 1.0
5.199  In 1993, Kumagai et al.  [4] in Japan reported on dust levels generated by repair work on
asbestos-cement pipes, including use of a high-speed  disc cutter both inside holes dug in the ground to
gain access to the pipes and outside the holes.  The concentration of asbestos fibres > 5 µm in length
ranged from 48-170 f/ml inside the hole (average = 92 f/ml) and ranged from 1.7-15 f/ml outside the
hole.  The Abstract for this paper follows:
"Asbestos cement pipes (ACPs) containing 15 to 20% chrysotile or crocidolite have been used for
underground conduits.  Even today 16.2% of all conduits in Japan are ACPs, though the production ofACPs was suspended in 1985.  When such a conduit is accidentally damaged the workers belonging to
the Waterworks Bureau of a local government cut off the damaged conduit using a high-speed disk
cutter and replace it with a new conduit.  This operation develops a cloud of dust and the workersinvolved run the risk of asbestos exposure.  It was the aim of the present study to estimate asbestosexposure levels among these workers.  First, in the experiment, we established the typical workingconditions and requested an experienced worker to cut an ACP using a high-speed disc cutter in a holedug in the ground as he routinely does.  The experiment was repeated three times.  During a bout of
each experiment, dust was sampled at several points both inside and outside the hole.  Second, a self-
administered questionnaire survey was conducted to  obtain information from the workers regarding
their working conditions in cutting ACPs.  The subjects of the survey were 1,048 men belonging toconduit repair sections of the Waterworks Bureau of 119 local governments.  The results obtained canbe summarized as follows.  (1) Each bout of cutting ACPs required about five minutes.  Theconcentration of asbestos fibers longer than 5 microns with 3:1 aspect ratio ranged from 48
to 170  fibers/ml (92 fibers/ml on an average) inside and 1.7 to 15 fibers/ml outside the hole.  The
concentration inside the hole exceed ed the ceiling limit (10 fibers/ml) recommended for asbestos by the
Japanese Association of Industrial Health.  A concentration of 92 fibers/ml is equivalentto 0.96 fibers/ml as 8-h time-weighted average.  (2)  The number of subjects with experience of cuttingACPs was 849 (81.0%).  The average length of service in conduit repair section was 14.2 yr.  Based on
the information obtained from each subject regarding the average working days per yr for each decade
from 1946, the cumulative days to date expended in cutting ACPs was estimated to average 235 d, thatis, 17 d per yr.  Only 18.1% of the subjects used a protective respiratory device."WT/DS135/R
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5.200  EHC 203 also gives the following data (p 40):
"Weiner et al.  (1994) reported concentrations in a South African workshop in which chrysotile
asbestos-cement sheets were cut into components for insulation.  The sheets were cut manually, sandedand subsequently assembled.  Initial sampling showed personal sample mean concentration of 1.9 f/mlfor assembling, 5.7 f/ml for sweeping, 8.6 f/ml for drilling and 27.5 f/ml for sanding.  Afterimprovements and clean-up of the work environment, the concentrations were 0.5-1.7 f/ml.
Nicholson (1978) reported concentrations of 0.33-1.47 f/ml in a room during and after sawing and
hammering of an asbestos-cement panel."
5.201  It is my perception that there is no dispute among experts on this issue.
5.202  In relation to the second part of this question, apart from stating that there is a risk because of
the generation of airborne asbestos fibres from interventions on asbestos-cement and other high-
density asbestos products, it is not possible to quantify the risk in a way that would meet with
universal agreement or a broad consensus, because few data are available for the risks for this type of
operation on chrysotile-cement products:  the risk would be related to cumulative exposure, which
would vary according to the types of operation carried out, and their frequency.  In addition, riskestimates would be dependent on extrapolation from the linear dose-response model that has been
called into question by Canada.  Therefore, I woul d expect disagreement among authorities on the
magnitude of the risk.
5.203  Table 12 derived from NICNAS 99 gives risk esti mates for lung cancer at airborne chrysotile
concentrations of 0.1-1.0 f/ml, according to the National Occupational Health and Safety Commission
in Australia (NOHSC) and two US occupational health and safety bodies (OSHA and NIOSH).
TABLE 12:  ESTIMATED RISK OF LUNG CANCER AT VARIOUS LEVELS OF EXPOSURE TO CHRYSOTILE
Exposure(yearly average fibre/ml) Excess risk (per 100,000 persons exposed)
NOHSC US OSHA US NIOSH
1 173 2880 5760
0.5 86 1440 2880
0.1 17 288 576
Excess risk = Risk coefficient x lifetime exposure (yrs) x average exposure level (f/ml) background risk.*
*A cumulative background risk for lung cancer in the male population was used in these calculations
(i.e. 7200/100,000 assuming mixed smoking habits).
5.204  However, NICNAS 99 goes on to discuss uncertainties concerning these risk estimates:
"There are several other reasons why there is consid erable uncertainty regarding these risk estimates,
which include:
1. Past occupational exposures have generally involved exposure to a mixture of asbestos fibres.  As it
appears likely that different types of asbestos have different degrees of hazard, it is difficult todetermine the risk attributable to chrysotile  per se.  In addition, commercial chrysotile often has
low levels of tremolite contamination.
2. Fibre size, such as difference in fibre size between different chrysotile industries, probably
influences the degree of hazard and/or potency.
3. There is a long latency between exposure to asbestos and development of lung cancer.  Hence, it is
not possible to state definitively what fibre type and level of exposure caused the disease.Consequently, risk estimates are related more to duration of employment rather than intensity of
exposure.WT/DS135/R
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4. A linear, non-threshold model may not be an appropriate model as there is some evidence
suggesting that lung cancer due to chrysotile exposure may have a threshold for effect.
5. Past exposure estimates (both quantitative and qua litative) are subject to considerable error.  For
example, conversion of historical results in mpcf units to fibres/mL has inherent uncertainties.
6. There is a high background level of lung cancer in the general population due to smoking.  Cases of
lung cancer attributable to asbestos cannot be distinguished from those due to smoking.  Attributioncan only be assessed in terms of excess of lung cancers above a control population, hence the choiceof control population is critical.
7. The identification of the disease is dependent on  medical diagnosis, however autopsies are not
always conducted.
The impact of some of these uncertainties can be accounted for to some extent.  For example, it is
considered that (1) and (2) are largely accounted for by  basing risk estimates on epidemiological studies
where exposure was only to chrysotile in the most relevant industry.  For the remainder of the aboveuncertainties it is unclear what influence they have on the risk estimates and how they should be
accounted for.  For example, recently there has been some debate in the literature as to whether a
threshold or non-threshold model should be used when predicting risk due to chrysotile exposure.Meldrum (1996) states that based on balance of toxicological evidence, the linear no-threshold modelfor chrysotile-induced lung cancer may not be appropria te.  ...  Epidemiological data alone are not able
to clearly distinguish between the possibility of a threshold or a non-threshold model due to therelatively high background rate of lung cancer in the human population.  There is at present no
consensus with respect to a threshold level of exposure for chrysotile below which there is no risk of
disease" [pp 70-71].
5.205  Table 13 gives an estimate of lifetime mesothelioma risk from exposure to low levels of
chrysotile (1.0 f/ml and 0.1 f/ml), based on dose-response data for the Wittenoom cohort, andassuming lower potencies for chrysotile than crocidolite (i.e. 1/12
th, 1/30th and 1/80th).20
TABLE 13:  ESTIMATES OF LIKELY MESOTHELIOMAS RELATED TO CHRYSOTILE INHALATION AT
AIRBORNE CONCENTRATIONS OF 1.0 AND 0.1 F/ML, ASSUMING A CARCINOGENIC
POTENCY 1/12TH, 1/30TH OR 1/80TH THAT OF CROCIDOLITE
Numbers to age 85
Mesotheliomas/million persons
Airborne fibre concentr ation;  Potency Duration of exposure* (years)
1 yr 10 yrs 40 yrs
1.0 f/ml -1/12th282 2101 3530
1.0 f/ml - 1/30th113 840 1412
0.1 f/ml - 1/12th28 210 353
0.1 f/ml - 1/30th11 84 141
0.1 f/ml - 1/80th43 2 5 3
*Starting at age 20 yrs.
                                                     
20Estimates calculated at my request by Dr. N.H de Klerk.WT/DS135/R
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Dr. Infante:
5.206  Interventions on chrysotile cement products can result in extremely high atmospheric fibre
concentrations (Rodelsperger et al.,  1980) and studies of roofers have demonstrated asbestosis from
such exposures (Stauder et al. , 1982).   A study of workers involved in inside finishing work with
concrete asbestos containing 30 per cent chrysotile asbestos has also shown that airflow obstruction
among workers can be caused by such exposure (Harless et al.  1978).  Open-air cutting such as that
involved in roofing and inside finishing operations also will result in exposure to other workers not
directly involved in the manipulation of the asbestos, e.g., standby exposure.  Such manipulation of
asbestos cement will also expose the general population.
5.207  A study of 404 roofers with long term exposure to cement dust indicated that 14 per cent had
significantly increased small irregular opacities with profusion in 13 per cent (Stauder et al. , 1982).
The prevalence of these abnormalities was significantly greater than that observed in the control
group.  The study by Harless et al.  (1978) indicated that approximately 50 per cent of workers
exposed for about six months to dust from asbestos cement developed airflow obstruction.  The risk of
developing lung pathology per unit of asbestos fibre exposure cannot be determined from these studies
because of lack of exposure data.  The studies do indicate, however, that uncontrolled manipulation ofchrysotile cement products can result in a high rate of lung pathology.  Lung function can be adversely
affected as a result of exposure over a very short period of time.
5.208  A large number of reports indicate mesothelioma related to car mechanics involved in brake
repair.  General population exposures from such wo rk would be minimal except for those situations
where individuals would engage in their own brake repair work.
Dr. Musk:
5.209  Interventions on asbestos-cement products can release fibres therefore a risk of disease exists
as in 1(c).
1.(e) Can occasional interventions on high-densi ty chrysotile products, either in occupational
circumstances (such as electricians, plumbers, repairers, insulation workers, etc.) or by private
individuals ("handyman" type) release fibres, thus presenting a possible risk to the individual
making such interventions or to the public in general?  Can you quantify this risk?
Dr. de Klerk:
5.210  Yes of course, see (c) and (d).
Dr. Henderson:
5.211  To answer the second question first, I am unable to quantify potential risk, because there are
no systematic observational data available for this type of work, to the best of my knowledge (but
please see Tables 12 and 13 above in my answer to Question 1(d)
5.212  The first part of the question has been covere d in the preceding answer, with the observation
that occasional interventions of this type would pr edictably produce low cumulative exposures, with a
lower risk, for the reasons discussed earlier.  Please also refer to AMR 99, for data on mesotheliomas
among electricians, carpenters, plumbers, insulation workers and so forth (it is acknowledged that
most if not all these mesotheliomas are a consequence of exposure to asbestos-containing materials
that included a mixture of asbestos types, including chrysotile and one or more of the amphiboles);  indrawing attention to AMR 99, my purpose is simply to use mesothelioma rates as a reflection of past
exposures and hence evidence that airborne fibre concentrations were produced by these types ofWT/DS135/R
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operation, without regard to the fibre types.  My own cases of mesothelioma also include a number of
individuals whose only exposure to asbestos took  the form of maintenance work and renovations
carried out on the patient's  home, where there were asbestos-cement building materials.  Again, in
drawing attention to this type of background, it is not my intention to address fibre type, but simply to
indicate that mesothelioma as an outcome of this type of exposure indicates that elevatedconcentrations of respirable airborne fibres were produced.
5.213  EHC 203 gives the following account (pp 122-123):
"Although the odds ratio for l ung cancer associated with exposure to "asbestos" has been estimated in
many case-control studies, the studies have not been in general able to distinguish between chrysotile
and amphibole exposure, and are therefore less info rmative for the present ev aluation ...  In a multisite
case-control study from Montreal, Canada, however, exposures to chrysotile and to amphiboles wereseparated, although exposure to amphiboles was not controlled for in the analysis for exposure tochrysotile (Siemiatycki, 1991).  In this study, the occupational history of male cases (age 35-70) ofcancer at 20 sites and of 533 population controls was evaluated by a team of industrial hygienists andchemists to assess exposure to 293 agents.  Overall, the lifetime prevalence of exposure to chrysotile
was 17% and that of exposure to amphiboles 6%.  The main occupations involving exposure to
chrysotile that were considered were motor vehicle mechanics, welders and flame cutters, andstationary engineers.  When lung cancer cases (N = 857) were compared with cases of all other types ofcancer, the odds ratio (OR) of any exposure to chrysotile was 1.2 (90% CI = 1.0-1.5;  175 exposedcases), and that of 10 or more years of exposure with at least 5 years of latency ('substantial exposure')
was 1.9 (90% CI = 1.1-3.2;  30 exposed cases).  Corresponding ORs of exposure to amphiboles were
1.0 and 0.9.  The OR of exposure to chrysotile was higher for oat cell carcinoma than for other types oflung cancer. Twelve cases of mesothelioma were included in this study.  The OR of any exposure tochrysotile was 4.4 (90% CI = 1.6-11.9;  5 exposed cases) and that of substantial exposure was 14.6(90% CI = 3.5-60.5;  2 cases).  Corresponding ORs of exposure to amphiboles were 7.2 (90% CI = 2.6-19.9;  4 cases) and 51.6 (90% CI = 12.3-99.9;  2 cases). "
5.214  Please see also Tables 5, 9, 10, 11, 12, 13, in EHC 203.
5.215  It is my perception that there is no dispute among experts that such interventions release
fibres;  disagreement is likely over the magnitude of the risk.
Dr. Infante:
5.216  The worker making the intervention would be the most highly exposed and presented with the
greatest risk of asbestos related diseases.  The extent of exposure to the worker as well as to those in
the surrounding area would depend on the nature of the intervention, e.g., the circumstances under
which the chrysotile asbestos product is manipulated in terms of work practices, the controls, or lack
of controls in place and the type of personal protective equipment provided to the worker.  While data
on fibre exposure levels in these situations are sparse, data on mesothelioma indicates association withworkers who have jobs that result in occasional interventions to asbestos products.  Because these
exposures are not routine and the hazard often goes unrecognized, these operations are unlikely to be
well controlled, i.e., they are not anticipated so proper training and education about these types of
exposures is often lacking.
5.217  It is difficult to quantify this risk because atmospheric measurements are usually not made
during these interventions.  However, the identifi cation of cases of mesothelioma associated with
these interventions in the literature indicate th at they are perhaps the most detrimental to human
health.  Mesothelioma has been identified from these exposure situations because it is a marker cancer
related to asbestos exposure.  What goes unidentified and unmeasured from these situations is the
much larger burden of disease and death from pneumoconiosis and lung cancer.  The attributable
burden from these latter diseases will be much greater than that from mesothelioma, but they are not
usually recognized because lung cancer has a high background rate in the general population andWT/DS135/R
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asbestosis may be diagnosed as another type of pneumoconiosis unrelated to asbestos exposure.
Mesothelioma has also been documented among the wives of construction workers, indicating that the
family member portion of the public in general is also at risk.  These latter cases of mesothelioma are
most likely the result of carry-home exposure from contaminated clothing.
5.218  If one considers that the handyman types of exposures are considered as exposures to the
general public, then this segment of the general population would also be at an elevated risk of
developing asbestos related diseases.  Exposures to family members that might result from
interventions by home owners would depend on the nature and location of the removal or
manipulation of the asbestos.  The general public is  also exposed through manipulation of asbestos in
residential buildings that is not carried out with appropriate controls in place and by carry home
exposures from contaminated work clothing.
Dr. Musk:
5.219  Occasional interventions on asbestos-cement products by anyone can release airborne fibres,
therefore there is some risk as in Question 1(c).
1.(f) Are chrysotile fibres from chrysotile-cement dust released during interventions (cutting,
sawing, etc.) on chrysotile-cement products as dange rous as pure chrysotile fibres? Is the physical
and chemical composition of asbestos-cement dust different from pure asbestos dust?
Dr. de Klerk:
5.220  Risk from fibres depends on size, shape and durability (and their quantity).  Asbestos cement
contains about 10-20 per cent asbestos, so that the dust concentration is going to be less than if thesheets were pure asbestos.  However, cement doe s not form fibres, so that any airborne fibre
measurements made would only reflect the asbestos concentration in the air.
Dr. Henderson:
5.221  To answer the second part first, the physico-chemical composition of asbestos-cement dust
does differ from pure asbestos dust, because the asbestos in asbestos-cement products is diluted by the
cement (asbestos = 10-15 per cent by weight);  this being so, one expects the asbestos fibres to be
diluted by cement dust, in comparison to equivalent operations on pure asbestos materials.
5.222  To return to the first part of this question:  the claim may be made that chrysotile fibres
released from asbestos-cement products by high-speed cutting are altered physically or chemically,
with a predominance of short-length fibres not implic ated in carcinogenesis.  For example, in Canada's
first oral submission, the following comments are made:
"The European Community has also advanced the thesis that the ban is necessary because France has
no control over trade persons or the 'handyman' who will cut into chrysotile-cement and, in so doing,
free some of the chrysotile that was locked into it.  Canada is puzzled by France's assertion that la
République Française is unable to regulate its handymen.  In any event, there are three technical
reasons why France's concern is misplaced.
First, this thesis is based on the misconception that cutting high-density locked-in non-friable asbestos-
containing materials releases substantial amounts of chrysotile.  In fact, even if improper tools such ashigh-speed saws are used to cut chrysotile-cement, the dust released from such an operation contains
only a very small amount of pure, respirable-size chrysotile fibres, if any at all.
Second, science tells us that most of the chrysotile fibres released during high-speed cutting have been
chemically altered:  the resulting entity is chemically and structurally different, and has a biologicalWT/DS135/R
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potential to induce harmful effects, which is different, and less than amphiboles.  Similarly, the dust
that results from abrading chrysotile-containing resin or plastic reinforced products contains very smallamounts of chrysotile fibres.  The same is also true of the dust that comes from wear and abrasion of
friction materials:  analysis of brake shoes shows that almost all of the chrysotile fraction of the
finished product is found to be transformed into a totally different, biologically-inactive material calledforsterite ...."
5.223  The first paragraph of the Canadian statement is  dealt with in later discussion in this report
(my answers to Question 5).  For the second and third paragraphs of this statement, one can state that
in other situations, only a small fraction of airborne asbestos fibres are of respirable size:  as one
example, about 0.67 per cent of airborne asbestos fibres within indoor air of buildings were longer
than 5 µm in length.  However, in the Japanese study reported by Kumagai et al.  [4] on cutting
asbestos-cement pipes with a high-speed disc cutter, where airborne fibre concentrations within the
hole used to gain access to the pipes averaged 92 fibres/ml (range 48-170 fibres/ml), the study dealt
with fibres longer than 5 µm (i.e. dimensions in the range for which carcinogenicity has been
reported).  Please see also Table 11 in EHC 203 where Rödelsperger et al.  recorded airborne fibre
concentrations of 4-5 f/ml and 5-10 f/ml for fibr es longer than 5 µm, from blowing off and grinding
brake blocks, including truck brakes.  (Please see also Table 11 and my answer to Question 2.)
5.224  Clearly, there is disagreement between the parties to the dispute and their respective experts
over the issue of whether chrysotile fibres released from high-density products are dangerous.  For the
reasons outlined above and in later discussion, it is my perception that at least a small proportion of
the fibres has dimensions that are associated with carcinogenicity.
Dr. Infante:5.225  As long as the interventions result in the release of chrysotile fibres, the exposures should be
considered as dangerous as pure chrysotile fibres because respirable-sized asbestos fibres will be
released.  The study by  Spurny (1989) indicates that the fibres released from weathered and corroded
chrysotile asbestos cement products have the same carcinogenic potency as "standard" chrysotile
fibres.  Although fibres released by weathering ma y be somewhat different from fibres released from
cutting or drilling asbestos cement products, the former fibres show a potency similar to that of pure
chrysotile fibres.  Moreover, because of the potential for cleavage during interventions on asbestos
cement products, the dust resulting from cutting, drilling, etc. on asbestos cement may actually contain
a greater portion of the asbestos fibres being thinner and more respirable than those that were initially
mixed into the cement during the manufacturing process.  Therefore, the fibres released from cementduring interventions should be considered at least as dangerous as "pure chrysotile fibres."   I can find
no data to support an opinion that fibres released from interventions on chrysotile asbestos cement
products would be less carcinogenic, or less danger ous.  Further, asbestos related pathology has
resulted from such situations.
5.226  The asbestos cement dust would be somewhat di fferent in physical and chemical composition
from pure chrysotile asbestos because the cement dust would contain respirable asbestos fibres,
crystalline silica plus other substances added to the cement.
Dr. Musk:
5.227  It is my opinion that in general airborne fibres released from asbestos-cement products pose a
risk.  This may differ from other sources of chrysotile depending on the characteristics of the fibres.
The area of fibre characteristics and their relationship to different sources is not within my area of
expertise.WT/DS135/R
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1.(g) What is the risk to human health associat ed with demolition and removal of high-density
chrysotile products, such as chrysotile-cem ent products?  Can you quantify this risk?
Dr. de Klerk:
5.228  See my answers to Questions 1(c) and (d).
Dr. Henderson:
5.229  I am not aware of any studies that have specifically focussed on either of these situations:
therefore, no firm data are available, but one would expect the biohazards to be related to cumulative
doses of respirable fibres (i.e. airborne fibre concentrations and the frequency of exposure from these
types of work).  This being so, one would expect the risks to be equivalent to other operations of like
frequency that generated similar airborne fibre levels (Tables 12 and 13).
Dr. Infante:
5.230  Exposure to high density chrysotile products through demolition carries with it the potential
risk of lung cancer, asbestosis and mesothelioma.  Testimony presented at the OSHA hearings related
to its Final Asbestos Standard that was promulgated in 1994 indicated that removal of intact chrysotileasbestos "transite" panels that were held in place by screws can result in airborne fibre concentrations
that exceeded 1 f/cc.  In this situation, the exposed surfaces were wet prior to removal and the
operation was done within a negative pressure enclosure.  Many transite panels used in interior wall
construction consist of rough inner surfaces from which asbestos fibre is readily released into the air.
Other testimony (OSHA, 1994) presented evidence that transite panels can be removed in a mannerthat results in exposure well below 0.1 f/cc when appropriate work practices are followed.  Because of
concern for the potential release of asbestos fibres into the air from such demolition, the OSHA
standard requires that a "competent person" supervise such activities, e.g., make an assessment and
determine that the type of controls being used ar e appropriate for the removal situation and that the
required work practices are being followed.   Therefore, the extent of the risk during demolition ofchrysotile cement products depends upon the compliance with mandated requirements.   (See my
answer to Question 5(c) regarding compliance with procedures to reduce risk of disease from asbestos
exposure.)
Dr. Musk:
5.231  In so much as demolition activities may result in airborne fibres there is a risk (as above).
1.(h) What is the risk to human health associat ed with high-density chrysotile wastes, such as
chrysotile-cement waste?  Can you quantify this risk?
Dr. de Klerk:
5.232  This depends on how the waste is treated and stored, depending of course on the chance of
any fibres becoming airborne and hence respirable.  Otherwise, see my answers to Questions 1(c)and (d).
Dr. Henderson:
5.233  See my response to Question 1(g).WT/DS135/R
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Dr. Infante:
5.234  I have not researched this issue, but I am inclined to believe that there would not be much
potential for fibre exposure from the handling of such waste unless a person at a waste site was
hauling asbestos cement and not aware of the product he/she was moving.
Dr. Musk:
5.235  The risk posed by waste products will also be dependent on the chances of fibres becoming
airborne as above.
1.(i) Can high-density chrysotile products wastes, such as chrysotile-cement wastes, be dealt with
so as to eliminate risks to human health?
Dr. de Klerk:
5.236  They can, by following approved methods for disposal which ensure that fibres are sealed
from airborne release.  There is of course the chance that subsequent work (for example, waste
removal) may disturb the waste and release fibres.
Dr. Henderson:
5.237  In theory, YES — once the asbestos-cement or other high-density product has been removed
from its in-place location (though few data are available on exposure levels produced by the actual
removal).  For example, in Australia, imported chrysotile is delivered to production facilities in sealed
plastic bags, so that the same procedure for bagging or encapsulation of high-density wastes shouldalso be applicable, and should prevent release of  asbestos fibres once the encapsulation or bagging
exercise is complete, unless the bags are ruptured for one reason or another.
5.238  According to NICNAS 99 (p 74), in Australia:
"Waste chrysotile, the polyethylene bags in which it is supplied, and chrysotile containing materials
from the manufacturing process, are disposed to landfill by licensed disposal contractors.  As chrysotilefibres are unlikely to be mobile in the soil or water table, landfill is not inappropriate from a publichealth perspective."
Dr. Infante:
5.239  I have not researched this issue.
Dr. Musk:
5.240  These risks may be eliminated if the fibres could be successfully sealed so that they cannot
become airborne.
Question 2:
What is the risk to human health associated  with other current applications of chrysotile
asbestos (in particular, friction materials and text iles)?  In occupational circumstances?  In non-
occupational circumstances?WT/DS135/R
Page 300
Dr. de Klerk:
5.241  While the industries themselves may be well regulated, controlled and compliant with
standards, the major problem again could occur in "downstream" users: boilermakers, plumbers, brake
mechanics etc.  Fibres released from friction produc ts have a higher proportion of shorter fibres than
those from textiles, which release the highest proportion of longer fibres.
Dr. Henderson:
(i) Friction Products (e.g. brake linings)
5.242  Automotive mechanics and garage workers constitute a large population of workers
potentially exposed to chrysotile derived from brake linings.  For example, brake blocks and linings
used in Australia have contained only Canadian chrysotile for many years, and the materials are eitherimported as pre-formed brake blocks and linings, or chrysotile is imported into Australia for
subsequent manufacture of these products.  It has been estimated that this group of mechanics
amounts to at least 900,000 workers in the US, and the figure may be even higher if one adds in all
those who have ever worked in the automotive repair industry but then moved into other
employments, and those who have retired.
5.243  For Australia, the number of persons employed as mechanics in 1991 amounted to 85,155
(84,293 males);  for 1996, the corresponding figures are 83,647 (82,827 males), out of a total
population of 16,852,256 in 1991 (8,363,677 males);  for 1996, the total population was 17,892,423
(8,849,224 males).  These figures for Australia include all mechanics, including automotive, brake and
engine mechanics, together with supervisors and apprentices;  the figures for 1996 also includemechanics' assistants (not included for the 1991 figures).
21  Taking into account the fact that the
Australian population is less than 1/10th that of the United States population, these statistics appear to
be roughly comparable.
5.244  The literature contains anecdotal reports of  malignant mesothelioma among automotive and
brake mechanics.  However, the question that arises is whether these anecdotal reports are explicableas the chance occurrence of spontaneous or background mesotheliomas among a large population of
mechanics, or whether this group of workers has sustained other significant exposures to asbestos,
including one or more amphiboles.  In other words, the question is whether there is a general increase
in the incidence of mesothelioma among automotive and brake mechanics with no other exposures to
asbestos.
5.245  Brake repair workers are potentially exposed to asbestos during a number of procedures,
which include removal of dust from bakes by air hoses, and a variety of other manipulations that
include bevelling, grinding and drilling.  Clearance of dust from brakes by use of an air hose can
create a cloud of visible dust, and airborne fibre concentrations of 2.0 to 29.4 f/ml have been recorded
in the immediate vicinity [225, 226].  Plea se see also Table 11 in EHC 203 (pp 42-43).
5.246  In North America, chrysotile has been used almost exclusively in brake linings since
the 1940s;  chrysotile is also the type of asbestos used in brake linings in Europe (and also Australia).As I mentioned previously, commercial chrysotile  (e.g. Canadian chrysotile) contains on average
small quantities of contaminant amphiboles in the form of tremolite (usually ≤ 1%).
5.247  However, the significance of this type of potential exposure among brake repair workers is
complicated by a number of factors:
                                                     
21Statistics supplied by the Australian Bureau of Statistics on 12 October 1999.WT/DS135/R
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• During moderate braking of automobiles, temperatures as high as ≥ 500oC can be
reached within the brakes, and at this temperature a proportion of the chrysotileundergoes dehydroxylation and recrystallization to form the mineral forsterite, which
is not implicated in mesothelioma induction.
"Heating of chrysotile at 700°C for an hour converts it to an amorphous, anhydrous
magnesium silicate material ...  Intensive dry grinding also destroys the structure ofchrysotile.  Analysis of wear debris from brake linings made with asbestos has shownthat virtually all of the chrysotile fibre is converted to amorphous material, in
association with the mineral forsterite (a recrystallization product).  The conversion is
explained by localized temperatures above 1000°C at the point of contact between thebrake lining and the drum" ... . [EHC 203, p 14].
• Most chrysotile fibres released from brakes comprise short-length fibres < 0.4 µm in
length (> 80 per cent of all chrysotile fibres from brakes).  However, some fibres > 5µm in length and even > 10 µm in length appear to survive (e.g. please see Table 11
in EHC 203).  The short-length fibres appear to have only questionable or limited
carcinogenicity, and this property is thought to reside primarily in fibres > 5 µm in
length.  In addition, limited fibre burden studies on brake repair workers have showna low pulmonary asbestos content.
"The fibres found in the brake wear debris are predominantly (99%) less than 0.4 µm
in length … Rödelsperger et al.,  (1986) found less than 1% of fibres longer than
5 µm." [EHC 203, p 14]
• One also needs to remember that assessment of mesothelioma risk among brake repair
workers can be confounded by other occupational exposures to asbestos  [227].
5.248  In a review of changing risk groups for malig nant mesothelioma, Huncharek [228] gives the
follow account for brake mechanics:
"A major problem with epidemiologic studies of this workforce is the difficulty in tracing a large, non-
unionized group of workers.  Estimation of disease risk has been impeded by lack of quantitative dataon exposure levels among individuals with long-term exposure.  ...
In 1976, investigators at the Mount Sinai School of Medicine studied asbestos exposure among brake
repair workers in New York city.  Both clinical examinations and fibre counts produced by variousoperations in brake maintenance workers were analyzed.  Samples taken at a distance of 3-5 feet frombrake drums during periods of blowing dust showed fibre concentrations of 6.6 to 29.4 fibres/ml, with amean of 15.9 fibres/ml.  In addition, ten samples of brake drum dust were analyzed by phase contrast,optical microscopic examination and transmission electron microscopic examination to determine the
percentage of short fibres (i.e., 25-500 angstroms x 760 to 3750 angstroms
22).  Eighty-three percent of
all chrysotile fibres were in this category, and almost 20% of the total mass of 10 samples waschrysotile (determined by electron diffraction).  'Throughout the examination by electron microscopy,attention was given to the morphology of the fibres.  A majority of fibres showed little alteration in thetypical chrysotile fibre'.
In an additional report from Mount Sinai, Rohl et al.  analyzed residual dust recovered from brake
linings and made direct measurements of the free asbestos fiber content of 'workroom air' in areas in
which brake lining maintenance and brake shoe installation occurred.  Airborne asbestos dustconcentrations were similar to those cited by Lori mer et al. (i.e., mean airborne fiber concentrations
during compressed air blowing of brake drums ranged from 2.6 fibers/ml at a distance of 10-20 feet to16.0 fibers/ml at 3-5 feet).  Samples of brake drum dust showed that the proportion of chrysotile in this
material averaged 3% to 6% (both as free fibr e and as particulates in pulverized binder).
                                                     
2210,000 Ångstroms = 1.0 µm.WT/DS135/R
Page 302
Regarding the health effects resulting from the exposures described, Langer and McCaughey published
... a case of mesothelioma in a brake repair worker ... a 55-year-old man who had worked in the usedcar, tire and car repair business since the age of 19 y ears.  He reported routinely servicing automobiles,
including the replacement of brake linings.  No other source of asbestos exposure was found.
Analysis of lung tissue showed the presence of chrysotile fibres (no amphibole was found) confirmed
by electron diffraction techniques.  Ten percent of the fibers found were longer than 10 microns.
23  The
authors point out that 'Controversy over the potential of chrysotile to cause mesothelioma has continueddespite evidence from asbestos textile fabricators, thought to have used only chrysotile, from workers
making brake pads, from chrysotile miners and millers, and from animal studies'.  They also state 'The
risk of malignant asbestos disease among these workers seems to be low but mortality data have yet tobe thoroughly evaluated.'
The most recent report of mesothelioma in a brake mechanic reviews a pleural mesothelioma occurring
in a 47-year-old male automobile mechanic whose only known exposure to asbestos was from clutchand brake repair work during an 11-year period.  ...
Another case of mesothelioma in a brake repair worker was recently published.  In this report, a
56-year-old male elevator mechanic ... reported working as an elevator mechanic for 30 years.  Hereported exposure primarily from elevator brake linings that he routinely cut, fitted, and removedduring elevator installation and maintenance.
Several recent studies from Scandinavia on this topic also deserve mention.  Hansen, from the Institute
of Community Medicine in Denmark, completed a hi storical cohort study examining the mortality of
car mechanics from ischaemic heart disease and malignant neoplasms.  The study cohort was identified
using records of a nation-wide census carried out in Denmark in November 1970.  Comparison wasmade with another cohort of skilled male workers who were not exposed to asbestos or 'petrochemicalsubstances'.  Of 583 observed deaths, one case of pleural mesothelioma was found.
Likewise, Jarvholm and Brisman, in a 1998 report, used the Swedish death register and the census of
1960 to study the occurrence of asbestos-associated tumors in car mechanics.  One hundred and eighty-
seven deaths attributable to cancer were observed, whereas 154 were expected.  Thirty-nine were
caused by lung cancer, whereas only 23 were expected.  Again, one death from pleural mesotheliomawas found.  ...
It has been estimated that 20,000 deaths from asbe stos-related cancer will occur during the next 40
years among automotive maintenance workers in the United States.  With the many difficulties faced
by epidemiologists studying this workforce, it is unclear how accurate this estimate will prove to be.
Clearly, what is needed is better information on duration and intensity of exposure to respirableasbestos fibers in this occupational group.  Additional study is needed to accurately determine theincidence of mesothelioma among members of this workforce."  [pp 2704-2705].
5.249  The situation is further complicated by other reports on garage mechanics and workers
involved in friction products manufacture  [229, 230].  These studies have been reviewed briefly by
Wong [231]:  three found no increase in the RR for mesothelioma among garage mechanics (RR =
0.9, 0.65 and 1.0 respectively).
5.250  An analysis of > 13,000 workers at a UK friction products factory showed no detectable
excess mortality due to lung cancer or other canc ers;  13 mesotheliomas were found but 11 had known
exposure to crocidolite [229, 232].
                                                     
23This relatively high proportion (10 per cent) in comparison to the smaller fraction of airborne fibres of
the same size is presumably explicable by preferenti al clearance of short fibres from lung tissue, with a
proportional increase of long fibres over time.WT/DS135/R
Page 303
5.251  McDonald et al.  [230] identified excess mortality from lung cancer among friction products
workers, but there were no mesotheliomas:
"A study by McDonald et al . (1984) investigated mortality due to lung cancer, mesothelioma and
asbestosis in three US factories manufacturing fr iction products and packings.  The cohort comprised
3641 men employed between 1938-1958.  During the 1930s exposures for most processes were 1-5
mpcf (millions of particles per cubic foot) and > 10 mpcf during dry mould mixing.  By the 1960s most
exposures were < 0.5 mpcf.  A significant excess of deaths (reference was to mortality rates forConnecticut) due to respiratory cancer was observed however this was not related to duration ofemployment.  No cases of mesothelioma were reported.  There was limited evidence of an increase in
risk of lung cancer with increasing exposure.  However the SMR for lung cancer was noted in workers
with less than one year of service.
A study by Finkelstein, (1989) investigated mortality rates among 1657 employees at two Ontario
factories manufacturing chrysotile friction materials.  The study population consisted of workersemployed for at least 12 months after 1 January 1950.  The study showed a significant increase inmortality from laryngeal cancer and lung cancer.  No increase in mortality was noted from
gastrointestinal cancer or from non-malignant respiratory disease.  One or two deaths may have been
due to pleural mesothelioma.  Case-control analysis demonstrated a lack of association between the riskof death from laryngeal or lung cancer and the duration of employment or employment in departmentswhere chrysotile had been used.  The author also noted that cigarette smoking is a risk factor forlaryngeal cancer and lung cancer, and therefore, increas ed risk may be in part attributable to differences
in smoking habits."  [NICNAS 99, p 65].
5.252  Similarly, Woitowitz and Rödelsperger [227, 233] found that:
"There is no evidence that car mechanics are exposed to an increased risk of mesothelioma even if they
do brake repairs, but asbestos exposure in other employment is an important confounding factor, so that
if there is a mesothelioma risk for car mechanics but it was small, it would not be detectable."
5.253  Nonetheless, the 1999 Report for the Australian Mesothelioma Register24 (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 Oc tober 1999 (total cases with a stated history
of asbestos exposure = 2585).  Mechanics who frequently or consistently work on brake linings andbrake 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 mechanic
25, 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 mechanics constitute a smaller sub-class), themesothelioma 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 brakelinings (i.e. brake materials unaltered by heat).
5.254  Using an earlier set of data for Australia, NICNAS 99 came to a similar conclusion:
                                                     
24The Register is a compilation of all and unselected mesotheliomas throughout Australia.
25This 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.WT/DS135/R
Page 304
"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].
5.255  It is apparent that these considerations apply to occupational circumstances.
5.256  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 short-length
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 ofStatistics] data indicates in excess of 750,000 articles (brake linings, pads and clutch facings) beingimported in 1997 containing asbestos and therefore possibly containing chrysotile.  Assuming each unitweighs 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 countrywideor 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 andforsterite  ...  In addition, some of the debris will be retained in the brake system and removed anddisposed of under controlled conditions." [p 78].
(ii) Exposure from chrysotile textile materials
5.257  Table 14 represents a reproduction of Table 7 in EHC 203 for exposure estimates in the South
Carolina chrysotile textile plant (1930-1975) before and after controls on exposure levels.  As can be
seen from this Table, the application of controls on exposure levels produced a significant reduction of
exposure, and currently available control technology allows even lower levels to be attained
(EHC 203).
5.258  EHC 203 refers to a study in Japan which reported a geometric mean concentration
of 0.1-0.2 f/ml in the period 1984-1986, for asbestos spinning.  From published studies, it seems clear
that asbestos textile workers are at greater risk for asbestosis (historically) and lung cancer than
mesothelioma.  EHC 203 also gives the following comments:
TABLE 14:  EXPOSURE ESTIMATES IN A CHRYSOTILE TEXTILE PLANT (1930-1975)
(ESTIMATED MEAN EXPOSURE TO FIBRES LONGER THAN 5 µM IN F /ML)
Operation Without cont rols With controls
Fibre preparation 26.2-78.0 5.8-17.2
Carding 10.8-22.1 4.3-9.0
Spinning 4.8-8.2 4.8-6.7
Twisting 24.6-376.0 5.4-7.9
Winding 4.1-20.9 4.1-8.4
Weaving 5.3-30.6 1.4-8.2
From Dement et al.  (1983)WT/DS135/R
Page 305
"Studies that correlate disease prevalence or symptoms with cumulative exposure can under-estimate
disease risk due to progression of disease after employment ceases.  Although workers were exposed to
both chrysotile and crocidolite (the latter being approximate 5% of all asbestos used), results
for 379 men employed at least 10 years in the Rochdale asbestos textile plant are informative ...
Exposure estimated from work histories range from an average of 2.9 to 14.5 f/ml.  Overall, smallopacities (> 1/0) were reported in 88/379 (23%) of chest radiographs, with evidence of a gradientseriously confounded by date of first employment and transfer of subjects with suspected asbestosis toless dusty conditions.  On the basis of data on incidence, the authors drew conclusions on exposure-
response between cumulative exposure and prevalence or incidence of crepitations, possible asbestosis
and certified asbestosis - all three depending on clinical opinion and judgement.  The authors state thatpossible asbestosis occurs in no more than 1% of men after 40 years of exposure to concentrationsbetween 0.3 and 1.1 f/ml" [EHC 203, p 105].
5.259  On p. 114, EHC 203 goes on to discuss other consequences of exposures sustained during
textile manufacture:
"The health of employees has been studied in any detail in only three asbestos textile plants.  These
comprise a factory at Rochdale, England, originally studied by Doll (1955) and more recently by Peto
et al.  (1985), another located in Mannheim, Pennsylvania, USA, studied by McDonald et al. (1983b)
and a plant in Charleston, South Carolina, USA.  Only the study in South Carolina is consideredprimarily relevant for assessment of the health effects of chrysotile.  Although the SMRs for lungcancer in these plants were broadly equivalent, the rates of mesothelioma varied considerably, which
may reflect the greater proportions of amphiboles in the Mannheim and Rochdale cohorts.
The textile workers in South Carolina plant have been studied in two separate but overlapping cohorts
... .  The only amphibole used in this plant was a pproximately one tonne of imported crocidolite from
the early 1950s until 1972, plus a very small quantity of amosite for experimental purposes briefly in
the late 1950s.  The crocidolite yarn was processed at a single location only, so Charleston can beconsidered an almost pure chrysotile operation.  Exposure levels for workers at this plant wereestimated by Dement et al.  (1983a) using nearly 6000 exposure measurements covering the period
1930-1975 and taking into account changes in plant processes and engineering controls (Table 7).  Theconversion of past exposures measured in mpcm (mpcf) to f/ml was based on both paired sample data
(100 pairs) and concurrent samples (986 samples) by these two methods collected in plant operations
during 1968-1971.
The most recent update of the Charleston study by Dement et al.  (1994) demonstrated an overall lung
cancer SMR of 1.97 (126 observed) and an overall SMR for non-malignant respiratory diseases ... of3.11 (69 observed).  The data for white males, for which data were more complete, demonstrated anoverall lung cancer SMR of 2.34 for those achieving at least 15 years of latency.  The risk of lung
cancer was found to increase rapidly in relation to cumulative exposure.  Data for the entire cohort
demonstrated an increase in the lung cancer risk of 2-3% for each fibre/ml-year of cumulativechrysotile exposure.  Two mesotheliomas were observed among this cohort and an additionalmesothelioma was identified among plant workers, occurred after the study follow-up period.  Analysesof an overlapping cohort from the same factory ... provided similar results.
... the regression line slopes for relative risks of lung cancer in relation to accumulated exposure in the
Charleston plant are all some 30 times steeper th an those observed in chrysotile mining and cement
product manufacture."
5.260  From the foregoing discussion, it is plain that these risks apply to occupational circumstances,
and not to non-occupational situations.  It is my perception that there is debate among experts over thecarcinogenicity of chrysotile released from or associated with friction products and textiles
respectively.WT/DS135/R
Page 306
Dr. Infante:
5.261  Exposure to chrysotile asbestos through the manufacturing and downstream manipulation of
friction products and textiles carries with it the risks associated with exposure to asbestos, most
notably, lung cancer, asbestosis and mesothelioma.  This is mostly an occupational issue except forconsumers, who do their own brake replacement whic h would put them at risk of developing these
diseases.
5.262  Epidemiological studies of workers involved in the manufacturing of friction products
demonstrate an elevated risk of lung cancer (McDonald et al.  1994).  Other investigators have not
observed an excess of lung cancer in the manufacturing of chrysotile and cricidolite containing
friction products, but have identified cases of mesothelioma related to both types of asbestos used to
produce these products (Berry and Newhouse, 1983).  Cases of mesothelioma also have been reportedamong car mechanics who serviced brakes containing chrysotile fibres only and were exposed to
levels estimated to be below 1 f/cc-year cumulative exposure (Woitowitz and Rodelsperger, 1991).
Epidemiological study results indicate a high risk of disease related to chrysotile textiles. See my
responses to Questions 4(a)-4(c).
Dr. Musk:
5.263  It is my opinion that there is a risk of disease from the release of chrysotile fibres from friction
materials (as in brakes and clutches) or textiles (as in asbestos blankets and suits).  In general the risk
will be dependent on the degree of exposure (as above) and is therefore likely to be greater in people
with occupational rather than non-occupational exposur e.  Fibres released from friction materials may
be shorter than from other sources.  These fibres may clear more rapidly from the lungs and possibly
be related to lower risks but I am not aware of any direct data on this.
Question 3:
The parties disagree as to the relative pathogenicity of amphibole and chrysotile asbestos.
Canada argues that, due to chemical and physical differences, a crucial distinction is to be made
between amphibole and chrysotile asbestos: the latter is less pathogenic than the former.  The
European Communities, on the other hand, argues th at chrysotile is as dangerous as amphiboles.
In answering the four sub- questions below, please specify to what extent your opinion is based on
epidemiological data, in vivo or in vitro evidence.
3.(a) For the purpose of assessing the risk to hu man health arising from exposure to asbestos
fibres, should a distinction be made be tween chrysotile and amphibole asbestos?
Dr. de Klerk:
5.264  In terms of risks to human health, epidemiological evidence is clear that, for a given quantity
(intensity and duration) of exposure, chrysotile imparts less risk than amphibole fibres.
Dr. Henderson:
5.265  YES — a clear distinction should be made between chrysotile and the amphibole forms of
asbestos.  On a fibre-for-fibre basis, amphiboles such as crocidolite and amosite are substantially more
carcinogenic for the mesothelium than chrysotile.  This potency differential is to some extent
confounded by the far greater usage of chrysotile both now and historically (> 95 per cent of world
asbestos production).  In addition, it is worth reiterating that Canadian chrysotile on average contains
trace quantities of fibrous tremolite (an amphibole).WT/DS135/R
Page 307
5.266  It is my perception that there is broad agreement among experts that the amphiboles are more
potent carcinogens for the me sothelium than chrysotile.
Dr. Infante:
5.267  For purposes of assessing disease risk from exposure to asbestos fibres, I see no basis for
making a distinction between chrysotile and amphibole asbestos.  Several high quality
epidemiological studies of workers exposed to chrysotile asbestos demonstrate an elevated risk of
death from lung cancer, asbestosis and mesothelioma.  The risk of death from lung cancer and
asbestosis related to chrysotile exposure appears to be similar to that from exposure to other forms of
asbestos.  Although epidemiological study suggests that the risk of death from mesothelioma from
chrysotile exposure may be less than the mesothelioma risk from amphibole asbestos, it is somewhat
difficult to make this comparison.  Many of the studies of workers exposed to amphibole asbestos goback further in time and less information is available on the quantitative aspects of exposure.  Thus,
the role of error in exposure estimation on the perceived difference is difficult to determine.  On the
other hand, some experimental inhalation studies demonstrate that chrysotile asbestos may be more
potent than other forms of asbestos in the induction of mesothelioma (and lung cancer) in relation to
the amount of dust deposited in the lungs (Wagner et al.,  1974).  In any event, the attributable risk of
respiratory diseases from exposure to asbestos is going to be heavily weighted by lung cancer and
asbestosis.  So, even if  exposure to chrysotile asbestos would result in a slightly lower relative risk of
death from mesothelioma, the overall risk of the asbestos related diseases combined, i.e., lung cancer,
asbestosis, mesothelioma, decrements in pulmonary function, will not be perceptively different for
chrysotile as compared to the amphiboles.  Thus, a distinction should not be made between chrysotile
asbestos and amphibole asbestos.  In my opinion, exposure to all forms of asbestos results in a
significant disease burden to society.
5.268  I believe that there is a need to distinguish chrysotile asbestos from amphiboles based on the
epidemiological data at least.
3.(b) What are the key properties which cause pathogenicity of, respectively, amphiboles and
chrysotile fibres for (i) asbestosis, (ii) lung cancer, (iii) mesothelioma, and (iv) other asbestos-
related pathologies?
Dr. de Klerk:
5.269  The properties are the same: size, shape and durability in the lung, that is fibres have to be of
certain size and shape to be deposited in the lungs and have to stay there long enough to produce a
response.  Since most of the body's responses to fibres appear to be stochastic in nature, the additionalfeatures are of course the intensity and duration of exposure as outlined above.  All the types of
asbestos differ according to these properties, the ma in difference with chrysotile is that it is less
durable in lung tissue than amphibole fibres: it is more soluble and the fibres tend to break more
readily into smaller fibrils, it also tends to be more curly rather than dead straight in shape.
Dr. Henderson:
5.270  As discussed already, the pathogenicity of asbestos appears to reside in the physical properties
and biopersistence of the fibres, summarized as the 3 Ds — namely dose, fibre dimensions and
durability (bio-persistence).  All commercial asbestos has the capacity to induce asbestosis, lung
cancer, mesothelioma and other pleural abnormalities (e.g., parietal pleural fibrous plaques, benignasbestos pleuritis with effusion, and diffuse pleural fibrosis).  Chrysotile and the amphiboles have
different potencies in generating these disorders:  for example, the amphibole varieties of asbestos
appear to be substantially more pathogenic than chrysotile for the induction of asbestosis and
mesothelioma, whereas the differential is not sustained for the induction of lung cancer, for whichWT/DS135/R
Page 308
chrysotile is associated with one of the lowest lung cancer rates (in Quebec chrysotile miners and
millers) and the highest rate of lung cancer (South Carolina asbestos textile workers, who used
Canadian chrysotile).
5.271  Asbestosis:  There is good evidence that asbestosis is a dose-dependent disorder with a
threshold effect.  There is widespread agreement that asbestosis in general is a consequence of highintensity exposure (or lower intensity but more prolonged exposure) than mesothelioma not associated
with asbestosis, so that the concentration of asbestos bodies and uncoated asbestos fibres within the
lung tissue of asbestotics is considerably higher than the concentrations encountered in mesothelioma
patients without asbestosis and in individuals with parietal pleural plaques.  In addition, some studies
have shown that the severity of asbestosis and its liability to progression are related to the asbestos
body and fibre concentration in lung tissue.  In the past, asbestosis as a consequence of high-dose
exposure was a progressive disorder leading to progressive respiratory insufficiency and death,whereas many cases of asbestosis encountered during the 1980s and 1990s represent milder and static
forms of the disease.
5.272  Churg [234] points out that:
" ... a considerably greater burden of chrysotile (with its accompanying tremolite) than of amosite or
crocidolite is required to produce any particular diseases.  ...  For exampl e, the mean burden of
chrysotile plus tremolite in the lungs of [Quebec chrysotile] miners and millers with asbestosis is 17
times the amosite burden in the lungs of shipyard workers with asbestosis."  [p 294].
5.273  To some extent, this differential in potency may reflect fibre dimensions and the generation of
oxidants, but a more likely explanation is the faster clearance of chrysotile from lung tissue than any
of the amphiboles.  However, Churg's comments seem to apply to Quebec chrysotile miners and
millers in particular;  in contrast, the study reported by Green et al. [191], which reported histological
asbestosis at relatively low cumulative exposures was carried out on South Carolina asbestos textile
workers who also worked with Canadian ch rysotile (please see following discussion).
5.274  There is also evidence that long fibres are implicated in the development of asbestosis, but
this may reflect in part the anatomical distribution of long versus short fibres in lung tissue.  For
example, some studies have shown that short fibres in the vicinity of 1 µm in length have a biological
potency similar to that of the longer fibres for initiation of the inflammatory changes implicated in the
development of asbestosis, but they do not penetrate the walls of bronchi or bronchioles to the sameextent as the longer fibres, to reach the alveolar interstitium.  Another study related the development
of asbestosis to the total surface area of deposited fibres, rather than to particular lengths of fibres.
5.275  The effect of dose:  There is good evidence that the inhaled dose of asbestos affects:  (i) the
development of the disease itself;  (ii) the latency period between exposure and the onset of the
disease;  and (iii) the severity and progression of disease.
5.276  Fibre burden studies on human lung tissues show that patients with asbestosis in general have
higher tissue burdens than patients with asbestos-related diseases other than asbestosis.  Accordingly,
Mossman and Churg [202] state that:
" ... asbestosis is clearly a fiber-dose driven disease but, nonetheless, only a fraction of any cohort
exposed to a fibrogenic dose of asbestos develops asbestosis.  It has been proposed that person-to-person variations in either fiber deposition or  fiber clearance may account for this phenomenon."
[p 1671].
5.277  The Ontario Royal Commission [235] noted that asbestos exposures < 25 fibre-years would
be unlikely to produce clinical asbestosis (about ≤ 1 per cent of individuals exposed at this level mayWT/DS135/R
Page 309
develop clinical or radiological asbestosis), wher eas Browne [236] considered that the minimum dose
required to produce clinical asbestosis was in the range of 25-100 fibre-years.
"Chest X-ray changes among textile and friction product workers in China were reported by Huang
(1990).  A total of 824 workers employed for at leas t 3 years in a chrysotile products factory from the
start-up of the factory in 1958 until 1980, with follow-through to September 1982, were studied.  Chest
X-ray changes compatible with asbestosis were assessed using the Chinese standard system forinterpretation of X-rays.  Cases were defined as Grade I asbestosis (approximately equivalent toILO ≥ 1/1).  Overall, 277 workers were diagnosed with asbestosis during the follow-up period,
corresponding to a period prevalence of 31%.  Exposure-response analysis, based on gravimetric data
converted to fibre counts, predicted a 1% prevalen ce of Grade I asbestosis at a cumulative exposure
of 22 f/ml-years."  [EHC 203, p 106]
5.278  In an autopsy study of South Carolina asbestos textile workers who used Canadian chrysotile
— the same group studied by Dement et al. [171, 172, 237-241] and McDonald et al. [161, 242] —
Green et al. [191] showed that histological asbestosis was usually present at ≥ 20 fibre-years of
exposure, and a few cases were observed at 10-20 fibre-years.  Thimpont and de Vuyst [243] reportedthat around 50 per cent of specimens of lung tissue removed because of lung cancer showed low-grade
airway and interstitial fibrosis with asbestos bodies, when the asbestos body concentration was ≥ 5000
per gram dry lung tissue.
5.279  These different threshold doses are not inconsistent with each other, because they deal with
identification of asbestosis by different modalities (i.e. clinical/radiological asbestosis versushistological asbestosis).  In this respect, histolog ical examination is generally considered to represent
the most sensitive and specific technique for the diagnosis of asbestosis, followed in descending order
by high-resolution CT scanning, conventional CT s cans and chest X-rays (which will fail to detect
asbestosis in about 20 per cent of cases, especially low-grade asbestosis).  In other words, early
(grade I) asbestosis may be undetectable by clinical investigations.
5.280  Latency interval:  there is also evidence that the latency period between first exposure to
asbestos and the subsequent diagnosis of asbestosis is roughly inversely proportional to the exposure
level, so that short latencies are encountered with high exposures (e.g. the Wittenoom cohort).
5.281  Mossman and Churg [202] also state that:
"Fibre burden studies also indicate that there is a correlation between pathologic severity of asbestosis
and increasing burden of asbestos bodies (which are largely markers of amphibole exposure) oruncoated amosite and crocidolite fibres" ... . [p 1670].
5.282  There are two additional points that are worth emphasis:
• There appears to be considerable variation among individuals in their propensity to
develop asbestosis (or variation in the latency intervals for equivalent exposures).  For
example, I have seen cases where there was a high content of amphibole asbestos in
lung tissue (up to 100 million fibres per gram dry lung tissue or more), in the absence
of histological asbestosis — at the time when the fibre burden analysis was carried
out — whereas other cases had clinical asbestosis with much lower tissue fibre
burdens.  Of course, one caveat about this situation concerns latency, whereas another
relates to the time when the fibre burden analysis was carried out, which is different
from the time when the disease was developing.
• In addition to high fibre burdens, the severity and progression of asbestosis can beWT/DS135/R
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influenced by other factors, such as cigarette smoke (though tobacco smoke by itself
cannot cause asbestosis, of course).
5.283  Mesothelioma:  Please see discussion in Section C.1.(f) to(h).
5.284  Lung cancer:  Please see discussion in Section C.1.(i).
5.285  Other asbestos-related pathology:  The effect of dose is less clear for the induction of parietal
pleural fibrous plaques than for other asbestos-related  disorders.  There is evidence that the frequency
and extent of plaques are dose-related, so that plaques tend to be more extensive with higher
exposures.  However, plaques can also follow trivial exposures to asbestos and asbestos-like minerals,
so that the frequency of asbestos-related pleural plaques appears to correlate more closely with
duration since exposure than the level of exposure.  Plaques are known to be endemic in Finland,
apparently as a consequence of very low-level exposure to asbestos-like fibres in the generalenvironment;  on the other hand, in societies where plaques are not endemic — e.g. North America,
Western Europe and Australia — about 80-90 per cent of radiologically well-defined plaques are a
consequence of occupational exposure to asbestos.  In such societies, pleural plaques also represent a
useful tissue marker for prior asbestos exposure.  At the same time, it is also worth emphasising that
parietal pleural plaques by themselves do not predispose to any other asbestos-related disorder, theliability being related to inhaled dose and fibre types.
Dr. Infante:
5.286  The key properties of the pathogenicity of amphiboles and chrysotile fibres, although not
known for certain, are thought to be related to the physical characteristics of the fibres, namely thediameter, length, aspect ratio of length to diameter, surface area and perhaps surface charge of the
fibres.  Toxicological data suggest that long thin asbestos fibres may be relatively more potent than
other asbestos fibres in their ability to induce asbestos related diseases.  There is also experimental
evidence, however, that shorter fibres can produce asbestos related diseases, though not in as great a
magnitude.  Any manipulation of these fibres that results in their diameter becoming thinner mayprovide a relatively greater contribution to the associated pathology and a greater toxic response than
if the fibres were not manipulated in any way.   The issue of solubility has been raised in terms of
asbestos fibres and their capability to cause disease.  The role of solubility with asbestos fibres and
disease potential, however, is not so clear because chrysotile asbestos seems to have the same overall
potency as other forms of asbestos, yet chrysotile fibres appear to be relatively more soluble than
amphibole fibres.
Dr. Musk:
5.287  It is my opinion that the key characteristics determining the pathogenicity of asbestos for
asbestosis, lung cancer, mesothelioma and other diseases are determined by the physical and chemical
characteristics of the asbestos.  The physical characteristics include length, diameter and
"straightness" of the fibres.  The chemical properties determine the durability of the fibres.
3.(c) What is the respective capacity of amphiboles and chrysotile to induce (i) asbestosis,
(ii) lung cancer, (iii) mesothelioma, and (iv)other asbestos-related pathologies?
Dr. de Klerk:
5.288  Comparisons between chrysotile and the amphiboles in their capacity to produce
mesothelioma and lung cancer have been extensive, for the other diseases, much less so.  There is
some in vitro  and in vivo  evidence that amphiboles, particularly crocidolite, are more fibrogenic than
chrysotile, but there is no clear epidemiological evid ence on this.  Pleural plaques appear to be moreWT/DS135/R
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common among anthophyllite workers than others while crocidolite workers have more diffuse pleural
thickening, and benign asbestos pleurisy also seems to be more common after crocidolite exposure.
Historically, asbestosis occurred commonly after heavy exposure to all types of asbestos.  For
mesothelioma, it is thought that for a given cumulative exposure, chrysotile is between one tenth and
one hundredth as potent as crocidolite.  There is some controversy over the relative capacity ofamosite and crocidolite, but amosite seems to carry about one tenth of the risk of crocidolite.  For lung
cancer, amosite and crocidolite seem to have similar capacities, with chrysotile weighing in around
one tenth to one fiftieth of this.
Dr. Henderson:
5.289  See my response to Question 3(b).
Dr. Infante:
5.290  The quantitative risk of dying from lung cancer as a result of  exposure to chrysotile asbestos
is at least as great as that from exposure to other forms of asbestos.  Quantitative risk assessments
based on several epidemiological studies indicate a very high risk of lung cancer (potency) among
workers exposed to chrysotile asbestos.  The cohort study by Dement et al., first published in 1983and updated in 1994 contains one of the best estimates of worker exposure to chrysotile accompanied
by the estimates of relative risk (RR) for lung cancer and asbestosis.  In this study, the investigators
determined conversion ratios from the available industrial hygiene data by evaluating sampling results
from surveys that used the impinger method to measure dust in million particles per cubic foot
(MPPCF), and membrane filter samples that allowed for the counting of fibre concentrations.  Forearly exposure periods, the investigators converted one MPPCF to the equivalent of 3 f/cc > 5 um in
length for all areas except for preparation where a conversion factor of 8 fibres for every MPPCF was
used.  In my opinion, this study is the strongest in its methodology for estimating asbestos exposure
among cohort members.  Quantitative risk assessment based on data for the entire cohort estimates an
increase in the RR of lung cancer ranging from 2-3 per cent for each fibre/cc-year of cumulativechrysotile exposure.  To my knowledge, this is the highest estimated risk of lung cancer among
asbestos exposed workers that has been corroborated by other investigators, i.e., the same population
was also studied by McDonald et al., (1983) and the results are remarkably similar.  Studies of lung
cancer risk among chrysotile asbestos textile workers from two additional occupational cohorts by
McDonald et al., (1982) and Peto et al., (1985) also provide similar results.  Using data from the
McDonald et al., (1983) study and a conversion fact or of 6 fibres per MPPCF, Peto et al., (1985)
estimated an increase in the RR of lung cancer among chrysotile textile workers to be 1.25 per centper fibre/cc-year of exposure.  From their own study of Rochdale textile workers, Peto et al., (1985)
estimated the excess lung cancer risk to range from 0.5-1.5 per cent per f/cc-year of cumulative
exposure depending upon whether the estimate was based on the entire cohort or on those employed in
1951 or later, respectively.  These estimates are of surprisingly similar magnitude given that they are
from epidemiological studies that incorporated retrospective exposure estimation that had to rely upon
the conversion of measurements from particles to fibres per cc.  Thus, three separate populations of
chrysotile asbestos textile workers demonstrate remarkably similar elevated risks of lung cancer and
therefore add to the confidence of the estimates of excess lung cancer risk per unit of fibre exposure
that these studies demonstrate.
5.291  Studies of workers exposed to chrysotile in several industries demonstrate a significantly
elevated risk of lung cancer.  Studies of workers exposed to a combination of chrysotile and
cricidolite, or to chrysotile only in cement production (Hughes et al., 1987) indicate a virtually
identical excess risk of mortality from lung cancer.  In a study of workers exposed to crocidolite in
mining, de Klerk et al., (1989) estimate an elevated relative risk of lung cancer of 1 per cent per f/cc-
year of exposure.  Essentially, the excess relative risk for lung cancer indicated in all of these studiesis close to about 1 per cent per fibre per cc-year of exposure (Stayner et al., 1997). The risk of lungWT/DS135/R
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cancer from chrysotile asbestos exposure is at least as great as the risk of lung cancer associated with
amphibole asbestos exposure.
5.292  Analyses based on the study by McDonald et al. (1993) indicates a much lower dose response
for lung cancer in relation to chrysotile asbestos  in mining and milling as compared to the risk
estimates from other studies, particularly chrysotile textile workers.  I suspect, however, that the fibreexposure from this study may be overestimated, particularly among the portion of the cohort that is
comprised of miners and that a fair amount of misclassification took place in the amount of fibre
exposure estimated for individual cohort members.
5.293  Gibbs and Lachance (1972) who published the initial exposure estimates for this population of
workers stated that their cumulative dust concentrations for the cohort members may have been far
from their actual experience.   Subsequent dose response analysis of this cohort applied only a single
conversion factor to estimate fibre exposures from the dust count data for the entire cohort.  In thestudy of Siberian chrysotile miners and millers (Tossavainen et al., 1999), those involved in mining
experienced average exposures of 0.08 f/cc, while those involved in two separate mills experienced
average exposures of 3.62 f/cc (ranges of average exposures for different milling
operations 0.37-6.21 f/cc) and 0.65 f/cc (range of average exposures 0.20-1.26 f/cc).  The gravimetric
sampling results indicate a 5-fold difference in average exposure for miners versus millers, while thesampling results for fibre exposures (the exposure of concern) indicate a 45-fold difference in average
exposure concentrations between miners and millers.  Taking into consideration the variation within
mining and milling jobs, the difference between exposures to workers involved in these jobs would be
even greater.  The large difference in the fibre exposures between miners and millers that was
observed in the Tossavainen et al. (1999) study adds further support to my concern that applying asingle conversion factor from dust samples in estimating chrysotile fibre exposures for miners and
millers is the most likely explanation for the slope of the dose response for lung cancer in the
McDonald et al. study being so different from the slope for lung cancer based on the studies of
chrysotile textile workers.  Stayner et al. (1996) provide a summary of data indicating that the lung
cancer risk from exposure to chrysotile in either experimental animals or in humans is similar to therisk from exposure to amphibole asbestos in these species.
5.294  With regard to asbestosis, Stayner et al. (1997) published a dose response analysis based upon
the updated study of chrysotile textile workers by Dement et al. (1994).  Their analysis indicates an
excess risk of 2 deaths from asbestosis per 1000 employees exposed to 0.1 f/cc for an occupational
lifetime exposure of 45 years, or 0.2 per cent from a cumulative exposure of 4.5f/cc-years.  Two
additional studies estimate similar risks of death from asbestosis in relation to cumulative chrysotile
exposure.  The study by Berry et al. (1979) estimates a risk of 1 per cent for those categorized as"probably having asbestosis" among chrysotile textile workers who were exposed to an estimated
range of 0.3 f/cc to 1.1 f/cc for 40 years, or a cumulative  exposure of 12-44 f/cc-years.  For those
categorized as "certified asbestosis" a 1 per cent excess risk of death was associated with 63 f/cc-years
of exposure.  Huang (1990) estimates a risk of asbestosis of 1 per cent associated with 22 f/cc-years of
exposure during the manufacturing of chrysotile textile and friction products.  Data from Dement et al.(1994) allow for an estimate of 2 per cent asbestosis associated with 22.5 f/cc-years of exposure.
Studies of workers exposed to a mixture of chrysotile and crocidolite asbestos in the manufacture of
cement products have demonstrated an elevated the risk of "certified asbestosis" of 1 per cent
associated with 10 f/cc-years of exposure (Finkelstein 1982).  Finkelstein was of the opinion that he
identified a 1 per cent excess risk of asbestosis related to a lower cumulative dose of asbestosexposures than Berry et al. (1979) because of the l onger period of follow-up of the cohort which gave
more time for the asbestosis to clinically manifest itself.
5.295  I am not aware of evidence that similar cumulative exposures to amphibole forms of asbestos
will result in a greater risk of asbestosis.  Thus, it is difficult to make any distinction in potency
between the amphiboles and chrysotile asbestos in relation to asbestosis.WT/DS135/R
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5.296  Chrysotile exposures related to numerous jobs and occupations has been associated with
mesothelioma through epidemiological studies and case reports.  In  some situations, standby exposure
only was associated with mesothelioma.  Based on epidemiological studies, the potency of chrysotile
to induce mesothelioma may be less than that from other forms of asbestos.  However, the rarity of
mesothelioma in the general population and the difficulty in determining asbestos exposure levelsexperienced by cohort members decades before measurements were taken, coupled with conversion of
dust counts in particles to fibres per cc, make it di fficult to determine differences in potency estimates
with regard to the various forms of asbestos and mesothelioma.  Based on toxicological study results,
in terms of the quantity of dust deposited and retained in the lungs, chrysotile may be more potent than
other forms of asbestos in the induction mesothelioma and fibrosis (Wagner et al., 1974).  The
population attributable risk of contracting mesothelio ma from chrysotile, however, will be greater than
from other forms of asbestos because of the much greater potential for exposure to chrysotile.
5.297  I have not seen any quantitative data related to decrements in lung function for either
chrysotile and amphibole asbestos.  On the basis of mortality from asbestosis, I assume there is little
difference in lung function related to the various forms of asbestos.
5.298  In summary to this question, in evaluating th e epidemiological evidence, I see no basis for
concluding that the overall disease potential from exposure to the amphiboles is any different than thatfrom exposure to chrysotile asbestos with the possible exception that amphiboles may be more potent
in causing mesothelioma and chrysotile may be more potent in causing lung cancer.  Studies in
experimental animals demonstrate the ability of chrysotile asbestos as well as the amphiboles to
induce fibrosis, lung cancer and mesothelioma.  From a public health standpoint, in terms of
quantification of disease, it would be extremely diff icult to make any distinction between exposure to
the amphiboles and chrysotile asbestos fibres.
Dr. Musk:
5.299  Broadly it is my understanding that the relative pathogenicity of the different fibres for the
various diseases is different (see Table)
CROCIDOLITE AMOSITE ANT HOPHYLLITE CHRYSOTILE
Asbestosis 1 1 1 1
Lung cancer 10 10 10 <1
Mesothelioma 100 10 5 1
Benign asbestos
pleural effusion/
diffuse pleural
thickening100 10 10 1
Pleural plaques 1 1 10 1
Question 4:
The parties in this dispute disagree as to the risk to human health associated with chrysotile
asbestos fibres at low levels of exposure, i.e. either prolonged exposure to low concentrations of
fibres or occasional peaks of exposure. The Eu ropean Communities considers that, because of a
lack of data at low levels of exposure, it is appropriate to endorse the linear relationship model to
assess risks associated with such low levels of e xposure.  On the other hand, Canada is of the view
that, at such low levels of exposure, empirical evi dence suggests that there is a practical threshold
below which chrysotile asbestos fibres present no measurable effects on health.WT/DS135/R
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4.(a) Are epidemiological data available for low levels of exposure to chrysotile fibres and what
do they show?
Dr. de Klerk:
5.300  There have been several epidemiological studie s that have shown no increased risk for low
levels of exposure to chrysotile, particularly in friction products industries.
Dr. Henderson:
5.301  So far as I am aware, there are no exposure-response data for such levels of exposure.
5.302  For example, EHC 203 states the following:
"Few data on concentrations of fibres associated with the installation and use of chrysotile-containing
products are available, although this is easily the most likely place for workers to be exposed"[EHC 203, p 3.].
"Overall, the available toxicological data provide clear evidence that chrysotile fibres can cause
fibrogenic and carcinogenic hazards to humans.  The data, however, are not adequate for providing
quantitative estimates of the risk to humans.  This is because there are inadequate exposure-response
data from inhalation studies, and there are uncer tainties concerning the sensitivities of the animal
studies for predicting human risk" [EHC 203, p.7].
"There is evidence that fibrous tremolite causes mesothelioma in humans.  Since commercial chrysotile
may contain fibrous tremolite, it has been hypothesized that the latter may contribute to the induction ofmesotheliomas in some populations exposed primarily to chrysotile.  The extent to which the observed
excesses of mesothelioma might be attributed to the fibrous tremolite content has not been resolved"
[EHC 203, p 8-9].
"Epidemiological studies that contribute to our understanding of the health effects of chrysotile
conducted to date and reviewed in this monograph have been on populations mainly in the mining ormanufacturing sectors and not in construction or other user industries.  This should be borne in mindwhen considering potential risks associated with exposure to chrysotile" [EHC 203 , p 137].
Dr. Infante:
5.303  One means of determining the risk from low exposure levels for carcinogens is to estimate the
risk from studies where exposure information is of reasonably good quality and the estimates of risk
were made using sound epidemiological principles and methodology.  Once these studies have been
identified, an appropriate way to determine quantitative risk from low exposure levels is to use all ofthe available data in a particular study and to estimate dose response.  As mentioned in my response to
Question 3(c) above, several studies of workers exposed to chrysotile asbestos can be used to estimate
risk from low levels of exposure.  The studies mentioned above, which represent three separate
populations of chrysotile textile workers demonstrate an excess relative risk of lung cancer ranging
from 0.5-3 per cent for each fibre/cc-year of exposure.  Risk assessment based on the study ofSouth Carolina chrysotile textile workers (Stayner et al., 1997) indicates that individuals exposed
to 0.1 f/cc-year for an occupational lifetime of 45 years, e.g., 4.5 f/cc-years cumulative exposure to
chrysotile, have an elevated risk of  5 extra deaths from lung cancer and 2 extra deaths from asbestosis
per 1000 workers.  Dose response for mesothelioma could not be estimated because there were too
few deaths from this cause in the study.
5.304  Epidemiological study results and case reports indicate that a large number of jobs which
entail occasional peak exposures to chrysotile asbestos have resulted in workers being diagnosed withWT/DS135/R
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mesothelioma.  Furthermore, mesothelioma has been diagnosed among household contacts of asbestos
cement workers (Magnani et al., 1992; Ascoli et al., 1996), among individuals living near chrysotile
mining and milling operations (Began et al., 1992), or living in houses constructed with asbestos
cement (Ascoli et al., 1996), or who were expose d to low cumulative amounts of chrysotile asbestos
from brake lining work (Woitowitz and Rodelsperger, 1991), or from standby exposure as bakers(Ascoli et al., 1996). This information contributes to  the evidence that very low exposure to all forms
of asbestos can induce cancer.  These observations of mesothelioma should be considered as sentinel
events for the pathologies other than mesothelioma that are more difficult to identify among large
populations that experience relatively more remote exposure to chrysotile asbestos. In my opinion,
these studies constitute high level risk from low levels of exposure to chrysotile asbestos.
Dr. Musk:5.305  It my understanding there are epidemiological studies which do not show a statistically
increased risk of disease from low levels of exposure to chrysotile.  However, the absence of
demonstrating an increased risk does not mean that there is not some risk as it is not possible to prove
a negative and a threshold has not been demonstrated for any carcinogen (nor in my opinion is it
biologically likely that one exists).
4.(b) Is there a threshold below which exposure to chrysotile fibres does not induce (i) asbestosis,
(ii) lung cancer, (iii) mesothelioma, and (iv) ot her asbestos-related pathologies, such as pleural
plaques?  If there is such a threshold, is it a practical one or is it scientifically established?
Dr. de Klerk:
5.306  It is extraordinarily difficult to demonstrate lack of an effect, or a threshold effect, in
epidemiological studies because of the ubiquitous problems of bias, confounding and chance.  In
particular, the smaller effect that needs to be demonstrated, the larger the study needs to be, both in
population size and follow-up time and such studies can rarely be done, even with animals.
Dr. Henderson:
(i) Asbestosis
5.307  Please see my answer to Question 3(b).
(ii) Lung Cancer
5.308  Please see discussion in Section C.1.(i).  Please see also the statement from EHC 203 below
on the question of a threshold for carcinogenesis by asbestos.  Some authorities favour a linear no-
threshold model, whereas others argue that a threshold probably exists;  nonetheless, there is nogeneral agreement on a numerical threshold for asbestos-induced lung cancer.  Dement et al. [171]
observed odds ratios of > 2.5 at 2.7-6.8 fibre-years of  exposure among South Carolina asbestos textile
workers.
(iii) Mesothelioma
5.309  As indicated in previous discussion in this report, a linear dose-response model has been
identified for mesothelioma induction by the amphiboles, and the dose-response relationship is
maintained at low occupational levels of exposure that overlap with environmental exposures:
e.g. definite dose-response relationship reported by Rödelsperger et al. [25, 137] at asbestos fibre
concentrations in lung tissue of 100,000-200,000 fibres per gram dry lung tissue, with an indication
that this relationship is maintained at lower levels of 50,000-100,000 fibres per gram dry lung (theWT/DS135/R
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level of 100,000-200,000 fibres corresponds to a cumulativ e dose of 1-2 fibre-years).  Iwatsubo et al.
[136] identified an increase in the relative risk at 0.5-0.99 fibre-year.  No threshold has been identified
for amphibole-related mesothelioma.  For chrysotile exposures, a dose-response relationship has also
been identified at high exposures, but to the best of my knowledge, there are no dose-response data for
low-level exposures to chrysotile.
5.310  On this point, EHC 203 states that "No threshold has been identified for carcinogenic risks"
[for chrysotile;  p 144].  At the same time, no increa se in risk for mesothelioma has been identified at
very low-levels of exposure, of the type associated with well-maintained asbestos in place, in public
buildings.  However, it is impossible to ascertain whether or not there is an increase in risk at this
order of exposure, because no control or reference group can be assembled where there is no asbestos
content in lung tissue.  If a threshold exists, it must lie somewhere in this area, between no exposure,
low-level environmental exposure, and low-level occupational exposure.
5.311  De Klerk [115] has also commented on the difficulty or impossibility of distinguishing
between background versus environmental mesotheliomas:
"There have been increases in the incidence rates of malignant mesothelioma in women, in those
without identified exposure to asbestos and, possibly, those younger than 35 years of age in Australia
and Western Australia.  Although part of the first two in creases, at least, may be attributable to specific
exposure to asbestos, mathematical modelling of the Western Australia data suggests that there hasbeen about a twofold increase in incidence rates from the 1970s to the 1980s that may be due toincreased general environmental exposure to asbestos.  ...  The excess of 1 per million person yearsover this presumed 'background' rate is also, coinci dentally, the amount that was estimated as possibly
caused by exposure of school children to 1 fiber per liter ... , a level that might result from use of
asbestos-based insulation or other general contamination of the environment with asbestos.
A final consideration in the use of national trend data for estimating environmental effects is the
comparison of the likely extrapolated risk from o ccupational data with the background risk estimated
here or from Peto's Los Angeles data.  From the Peto paper ... , the incidence of mesothelioma is related
to age in the following way:
Incidence = 1.7 • 10
-12 • (age)3.5
which translates to a lifetime risk to age 80 of just over 100 per million people, which is much greater
than any of the estimated environmental risks described earlier.  An equivalent risk from the adjusted
Western Australian data is about 160 per million lifetimes.  The question remains as to how these
background risks and environmental risks interact.  Is the postulated environmental incidence already
included in the background incidence, or should the risks be added or even multiplied together?  Thisquestion is almost certainly unanswerable using epidemiological methods. ...
It is doubtful whether epidemiological methods ... coul d ever be definitive in deciding whether there is
an appreciable hazard from general environmental exposure to asbestos ... or, more importantly,
whether the hazard is large enough to justify specific remedial action ..." [pp 29-31].
5.312  Clearly, this issue is one major focus of dispute between experts;  from the preceding
discussions, it is my perception that — with the exception of asbestosis — no threshold has been
delineated, and that even those who claim that a practical threshold must exist cannot delineate such a
threshold in precise numerical terms (in this respect, I do not know what the expression "practicalthreshold" really means).
Dr. Infante:
5.313  Thresholds have not been demonstrated for any substance known to cause cancer and there is
no theoretical basis to assume a threshold for the diseases related to chrysotile, or other forms ofWT/DS135/R
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asbestos, particularly when the mechanisms involved in the pathology are not fully understood.
Furthermore, it is not possible to determine thresholds from epidemiological studies because of lack of
statistical power to distinguish that the risk is virtua lly zero.  [Note:  At times, some investigators state
that a single point estimate from the lowest dose evaluated in an epidemiological study that does not
demonstrate a significant elevation in cancer risk constitutes a threshold level for the carcinogen.Such a conclusion is scientifically invalid.  When estimating dose-response, one has more confidence
in the risk related to a particular dose level by using all of the data available in the study.  Using only a
single point estimate results in more instability in the estimate of risk for that data point in contrast to
using all of the available data in the study.]
5.314  Dose response analyses and modeling specifically for chrysotile asbestos exposure and lung
cancer and asbestosis have been conducted recently by Stayner et al. (1997) using data from the
Dement et al. (1994) study.  Alternative exposure-response models were evaluated as part of thestudy.   A model designed to evaluate evidence of a threshold also was fitted for asbestos exposure in
relation to lung cancer and asbestosis.  There was no significant evidence for a threshold in models
pertaining to either lung cancer or asbestosis.
5.315  With regard to mesothelioma, and other asbestos-related diseases, I am not aware of any
evidence of a threshold pertaining to either chrysotile, or other forms of asbestos.  Furthermore, from apractical standpoint, even if there were a threshold for the chrysotile related diseases, the exposures
that workers will routinely encounter in the future  through continued use of chrysotile in commerce,
will expose them to concentrations of asbestos that  have already been related to pathology in humans.
In other words, continued use of asbestos will continue to expose individuals to levels and exposure
circumstances that have already been related to disease.  The threshold question, therefore, seemsmoot.
Dr. Musk:
5.316  It is my understanding that a threshold for disease has not been scientifically established.
4.(c) Is the linear relationship model an appropriate method for assessing the risk to human
health posed by exposure to chrysotile asbestos at low levels of exposure?
Dr. de Klerk:
5.317  The linear relationship model is generally used as a so-called "conservative" estimate, that is,
if it is incorrect, it is more likely to err on the side of safety.  In some ways, how one extrapolates risk
assessment outside the range of available data is more of a societal decision than a scientific one.Biological plausibility could probably be given to any model.
Dr. Henderson:
5.318  In the absence of alternatives because of unavailability of data on exposure-response
relationships at low levels of exposure to chrysotile, the linear relationship model is widely employed.Under these circumstances, this may be an appropriate method for risk assessment at low levels of
exposure.  Whether or not it is a valid method is unknown.
5.319  NICNAS 99 (p. 72) observes that:
"There are many problems associated with low-dose risk extrapolation, such as the assumption of a
linear relationship.  However, as insufficient data exist to indicate a threshold exposure for effect, thelinear extrapolation methodology provides a conservative worst-case scenario estimate of risk.  OtherWT/DS135/R
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confounding factors in estimating risks from epidem iological data are possible contamination by other
fibre types and inaccurate estimates of historical exposures."
5.320  Clearly, this too is one major focus of dispute between experts.
Dr. Infante:5.321  A linear relationship model is appropriate for determining dose response for chrysotile
exposure and lung cancer, and perhaps asbestosis and mesothelioma as well, but the most reasonable
model for the latter two diseases are less clear than fo r lung cancer.  With regard to this issue, Stayner
et al. (1997) evaluated exposure-response relationships for chrysotile asbestos, and lung cancer and
asbestosis by applying several alternate models.  The exposure-response relation for asbestos and lungcancer gave the best fit when using a linear model.  This observation is consistent with the conclusions
of other investigators, who have evaluated dose response for chrysotile asbestos textile workers, or
other asbestos workers and mortality from lung can cer (McDonald et al., 1983; Peto et al., 1985;
Enterline, Hartley & Henderson, 1987).   Furthermore, there appears to be a linear relationship
between asbestos exposure and lung cancer over a wide range of exposures where such data are
available.  Therefore, it seems reasonable to accept a linear relationship for lung cancer when
extrapolating risks to exposures below the ranges th at have been evaluated in epidemiological studies.
Moreover, I am not aware of any literature that convincingly proves that the dose response for
asbestos and lung cancer is non-linear.  Thus, in my opinion, the linear model is the most appropriate
model for estimating dose-response for chrysotile exposure and lung cancer.
5.322  A linear relationship might also be used for chrysotile asbestos exposure and asbestosis
although one might make the argument that a non-linear model is also appropriate for asbestosis.
Stayner et al. (1997) evaluated this issue using data from the Dement et al. (1994) study and
concluded that the association between chrysotile exposure and asbestosis appeared to be non-linear.
Stayner et al. (1997) used a non-threshold, non-linear model and  the estimates of asbestosis predictedfrom the model seem to fit very closely with point estimates for asbestosis from other studies of
chrysotile exposed populations as mentioned in my responses to Questions 3(c) and 4(a).
5.323  An analysis by Peto et al. (1985) of chrysotile asbestos textile workers shows that a linear
model fits the data for mesothelioma with the cube of time since first exposure.  In this non-threshold
model, the response is linear with dose of asbestos, but exponential with time since initial exposure.
The predicted number of mesotheliomas by dose and time since first exposure was in reasonable
agreement with the observed number.  According to the authors, however, there were too few cases to
test the model stringently and they did not attempt to fit other models to their data.  Nevertheless,
given the consistent observations of the long latency period between initial exposure to various forms
of asbestos and the clinical manifestation of mesothelioma, it seems reasonable to use a model that is
linear with exposure and exponential with time from initial exposure for chrysotile asbestos and
mesothelioma.
Dr. Musk:
5.324  It is my opinion that the linear relationship model is the most appropriate one.
4.(d) Are there scientifically acceptable methods other than the linear relationship model which
could be used to assess the risk to human health at low levels of exposure?  What results do theysuggest?WT/DS135/R
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Dr. de Klerk:
5.325  While a threshold model suggests a lack of risk below a fixed level, it is unlikely that this risk
would be completely zero, so that if applied to a much larger population, such a risk could lead to
cases of disease.
Dr. Henderson:
5.326  I am not aware of any other methods that have met with broad scientific acceptance or a
consensus.  It has been suggested that an S-shaped curve might be more appropriate, but I have not
seen any data on what the form of the S-curve migh t be;  in other words, the S-shaped model appears
to presuppose the existence of a threshold, but no such threshold has been established to the best of
my knowledge.
5.327  The problem with arguing that there exists a practical threshold level for lung cancer and
mesothelioma induction is that it is impossible to delineate such a threshold in numerical terms,
because of a lack of observational data.  (Please see also my answer to Q.5(c)).
Dr. Infante:5.328  From the public health perspective, it has been the convention to use non-threshold linear
models for estimating cancer risk to humans.  This is particularly the case for substances known to
cause cancer in humans.  One might deviate from this concept if the mechanism(s) by which the
substance causes the cancer were known.  This is not the case with chrysotile, or any other form of
asbestos.  In the particular case of chrysotile asbestos, Stayner et al. (1997) selected several Poissonregression models to explore the shape of the exposure-response relationship between chrysotile
asbestos exposure and risk of death from lung cance r.  The models were capable of reflecting a wide
range of exposure response patterns, including linear, sublinear and supralinear relationships.   They
also considered a threshold model to determine whether there was evidence that exposures below a
certain exposure concentration were equivalent to zero, i.e., that a threshold was present.  Asmentioned above, for lung cancer, a linear model gave the best fit; for asbestosis, the response
preferred was that based on a non-linear, non-threshold model.  In both cases, the models did not
provide any support for the existence of a threshold.  Thus, in my opinion, these models are
appropriate to assess risk for these diseases as a result of occupational exposure to chrysotile asbestos.
With regard to lung cancer and asbestos, I am not aware of any public health organization, or
governmental agency that has ever used a non-linear model to estimate risk.  During the hearings held
by the U.S. Occupational Safety and Health Administ ration (OSHA) as part of its rulemaking related
to the standard promulgated for asbestos in 1994, numerous scientists were of the opinion that a non-
threshold linear model was the preferred model to use for estimating the relationship between asbestos
exposure and lung cancer.  It is my opinion that a non-linear model is not an acceptable model to use
in estimating dose response for asbestos exposure and risk of death from lung cancer.  Formesothelioma, I would favor a non-threshold model that incorporates a linear relationship withexposure.
Dr. Musk:
5.329  I believe that there is no reason to discard the linear model as no threshold for any carcinogen
is known to exist.
4.(e) To what concentration of chrysotile fibres and for how long must a person be exposed in
order to be considered at risk of developing a chrysotile asbestos-related disease (lung cancer,
mesothelioma or other asbestos-related pathology)?WT/DS135/R
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Dr. de Klerk:
5.330  A person is "at risk" of developing a chrysotile asbestos-related disease after any exposure to
chrysotile asbestos, the lower the amount of exposure, the lower the risk.  For example, it could be
estimated that there was a 50-50 chance that exposure to 1 fibre of crocidolite could cause 1 case ofmesothelioma among the whole population of the wo rld (including all those who have ever lived),
i.e. a very small probability, but still greater than zero.
Dr. Henderson:
5.331  This question iterates the issue of a threshold exposure.  The answer is essentially the same as
for Questions 4(a)-4(d) in the absence of exposure-response data at low levels of exposure.
Dr. Infante:
5.332  The answer to this question depends upon the amount of risk that is considered unacceptable
by a particular country.  It is a matter of health policy.  In the United States, the Environmental
Protection Agency (EPA) regulates risk to a level below one extra death in a  population of 100,000
people over its entire lifetime.  I have already provided estimates for excess risk of death from lungcancer and asbestosis from chrysotile exposure.  These risk estimates, however, are average risks to a
group of individuals that are based on maximum likelihood estimates (MLEs) and they do not
incorporate statistical uncertainty in terms of variability, e.g., they are not based on upper 95 per cent
confidence limits as is usually the health policy when estimating adverse health effects to a group of
individuals at risk from exposure to an environmental insult.  In addition, the risk estimates may onlybe appropriate to workers' health risks.  They are derived from a group of healthy adults, who were
able to pass a physical in order to gain  employment. They are not representative of  individuals in the
general population who may be exposed to asbestos and have a compromised immune system, or be
exposed to other conditions which may exacerbate their risk of contracting the various diseases related
to chrysotile asbestos as estimated from a healthy worker population.  There will always be some riskfrom exposure to asbestos and the degree of that risk will depend upon the amount of asbestos
exposure in relation to the susceptibility of the individuals exposed in terms of their health status and
other factors that interact to produce clinical manifestation of disease.
5.333  It is noteworthy, as mentioned in my response to Question 1(a) above, that the population
surrounding the Quebec mining and milling operation (Begin et al., 1992) that was exposed to
background levels of chrysotile asbestos, developed mesothelioma at an incidence of 62.5 cases per
million population per year, or 0.625 per 10,000 per year. This risk level translates to 0.5 per cent ofthe population developing mesothelioma over an 80-year lifetime from this background exposure.
This estimate may well represent an underestimate of risk since the identification of cases was based
on a workman's compensation board review, and additionally, out-migration of inhabitants would also
result in loss of some cases.  In the same report, it was pointed out that the largest increase in the
mesothelioma rate in Quebec was among individuals that had occupations where their exposure wouldbe occasional only, and that 33 per cent of these cases were exposed for less than a 5-year period.
When one adds to this information to additional case s of mesothelioma reported in the literature that
are associated with standby exposure to chrysotile, it leads one to the conclusion that occasional
exposure for a short period of time, or constant low level exposure to chrysotile asbestos leads to
death from mesothelioma (and lung cancer and asbestos is).  [Note: while an excess of lung cancer was
not identified in the Camus et al. (1998) study of women in the same Quebec population, the study
had limited power to detect an excess of lung cancer; it did, however, demonstrate an excess of
asbestosis and mesothelioma even though out-migration may have resulted  in the loss of all three of
these diseases in the study.]WT/DS135/R
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Dr. Musk:
5.334  In my opinion any level of exposure to chrysotile (or other form of asbestos) constitutes some
risk and that the level of "acceptable risk" is not a scientific issue but an issue for society to debate and
determine at different times according to the evidence as they perceive it.
Question 5:
Canada states that, with controlled use, "health risks associated with occupational
exposure throughout the life-cycle of chrysotile asbestos can be reduced to acceptable levels already
recognized as such by competent international organizations.  The European Communities
questions this assertion and says that "les données scientifiques disponibles montrent que
l'utilisation dite "sécuritaire" de l'amiante chrysotile ne permet pas d'empêcher un grand nombrede cas d'exposition entraînant des pathologies mort elles".  ["available scientific evidence shows
that so-called "controlled" use of chrysotile asbestos does not make it possible to prevent many
cases of exposure causing fatal pathologies"]
5.(a) Is there a generally agreed methodology applicable to any use of chrysotile-cement products
and other high-density chrysotile products throughout their life-cycle that can be referred to as
"controlled use"?  Is it embodied  in international standards?
5.335  This is rather outside my areas of expertise.  It does however appear theoretically feasible but
practically very unlikely given the problems with "downstream" use described above.
Dr. Henderson:
5.336  In principle, regulation and control of chrysotile and high-density chrysotile products is
feasible at some points of the life-cycle (manufacture and disposal), but in reality not others (please
see following discussion).
5.337  The manufacture of high-density products is usually carried out under closed conditions with
dust extraction.  As one example, the manufacture of chrysotile friction materials in Australia involves
the following processes:  following transfer of  other ingredients required for the product mix,
unopened 50 kg plastic bags of raw chrysotile are placed in the mixer and opened under dust
extraction.  The empty bag is then delivered into a second plastic bag attached to the mixer.  When
full, this second bag is sealed and taken to a controlled disposal site.  Mixing is a closed process.
After mixing, the material is emptied under dust extraction before decanting into smaller buckets forweighing and use in moulding and finishing processes.  The moulding is a hot process and when
complete, the moulded product undergoes finishing processes that include grinding, grooving and
drilling — all carried out under dust extraction.  The finished disc pads and commercial vehicle brake
blocks and linings are then wrapped and packed into sealed containers.
4.338  The potential for exposure includes opening and emptying chrysotile bags into the mixer, the
moulding and finishing processes, and handling of  damaged bags containing raw chrysotile.  The
workforce amounts to a few hundred workers, and the maximum exposures per employee vary from
minimal, to the largest group involved in the processing operations.  Airborne asbestos fibre levels are
assessed by personal monitoring.  About 84 per cent of 461 samples between 1992 and 1997
were < 0.1 f/ml;  10 per cent ≥ 0.01–≤ 0.2 f/ml;  6 per cent were ≥ 0.02–< 0.5 f/ml, and < 1 per cent
were ≥ 0.5 f/ml.  The manufacture of compressed asbestos fibre sheeting — most for export and the
remainder processed into finished cut gaskets for industrial applications is also a closed process
carried out under similar conditions to the manufacture of friction products (please see NICNAS 99,
pp 32-34).  A total of 232 personal samples between 1991 and 1996 showed similar low airborne fibreWT/DS135/R
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concentration (58 per cent < 0.1 f/ml and only one sample ≥ 0.5 f/ml).  Static samples recorded during
guillotine and trimming activities were all ≤ 0.05 f/ml.
5.339  Although controlled use of this type is feasible for these manufacturing processes, and for
disposal of materials left over (e.g. empty polythene bags), it is my perception that, historically and in
reality, it is almost impossible to extend analogous controlled and regulated use to the end-users of
asbestos products such as workers involved in building construction and demolition (e.g. builders'
labourers, carpenters, electricians, painters, plasterers and plumbers), or to individuals who carry out
maintenance or renovation work on their own homes, or to brake mechanics (please see AMR 99).
This is because these groups add up to a large population of disparate and varied workers;  many such
individuals work for small businesses or are self-employed, so that it is difficult or impossible to
extend controlled use or training to all of them.
5.340  Some of the supporting documentation submitted to the WTO refers to ILO recommendations,
but it is also worth emphasizing that prohibition or  regulation of asbestos-containing products varies
from one nation to another, with different upper limits of airborne fibre concentrations (e.g. < 1 f/ml
or < 0.1 f/ml).  These are summarized in Tables 27 and 28 and Appendix 7  in NICNAS 99.
5.341  From the literature cited throughout this report and the reasons discussed, it is my perception
that broad agreement exists among experts that controlled use of chrysotile (or other varieties of
asbestos) is not a feasible option in the real world for certain worker groups, notably those involved in
construction trades (e.g. see EHC 203).
Dr. Infante:5.342  I am not familiar with any "agreed upon" methodology applicable to chrysotile-cement
products and other high-density chrysotile products related to "controlled use"  in the sense that these
products could be used without harm to human health.  Perhaps the consensus is that when using
asbestos, the exposure should be controlled, and various countries have developed programmes or
standards that recommended, or require, specific engineering controls, work practices, training andeducation and personal protective equipment to control exposures to asbestos to the extent feasible.
This, to me, is different from the concept of "controlled use"  in the dialogue being used by Canada,
which seems to imply that using or manipulating asbe stos or asbestos containing products can be done
in such a manner that people are not exposed, or that the risk from such exposure is de minimus .
5.343  I also am not aware of international standards related to "controlled use" of asbestos products.
What you may be referring to here are recommendations from international organizations, or
recommendations or regulations (in the context of being enforceable by law) from various countries.These documents, however, should not be consider ed as international standards that lead to the
"controlled use" of asbestos.  For example, in 19 94, the United States, promulgated a new standard for
occupational exposure to asbestos which required the permissible exposure limit (PEL) to be no
higher than 0.1 f/cc as an 8-hour time-weighted- average (TWA).  In the opinion of OSHA, workers
exposed to this PEL over an occupational lifetime (45 years) are still at a significant risk of developing
asbestos related diseases.  Therefore, the Agency included in the standard several provisions ancillary
to the PEL.  One could argue that the PEL plus the ancillary provisions constitutes one of the best
examples of the concept of "controlled use" of asbestos as I understand it in the concept being brought
forward by Canada.  Yet, in the United States, the PEL for asbestos as well as the ancillary provisions
that include training and education about the health hazards of exposure, work practices, requirementsfor personal protective equipment, medical surveillance, etc. are not complied with for various reasons
in a large number of workplaces.  Based on the observations of violations of several provisions of the
asbestos standard in the United States, discussions with occupational safety and health personnel from
other countries and my review of the literature, it is my opinion that a controlled use concept for
chrysotile asbestos is not realistic in workplace situations.  It would be much less realistic as appliedWT/DS135/R
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to non-occupational situations where individuals would make repairs involving the manipulation of
asbestos products in their homes.
5.344  I am not aware of any international standard that embodies "controlled use" of asbestos in the
context that the manipulation of asbestos, or asbestos containing products will result in exposures that
will not result in harm to many of those exposed.  Furthermore, it should be recognized thatprogrammes to control asbestos in many countries are "agreements" and as such, they are not
enforceable by law.  Even more disconcerting is the observation that countries like the United States
that promulgated stringent requirements to control asbestos find that their standards are often violated.
A general downfall with the concept of  "controlled use" is that it relies upon human behaviour, which
cannot be controlled in too many situations.  Hence, it is unreliable.
Dr. Musk:5.345  In my opinion "controlled use" of asbestos is theoretically possible but not practically
feasible.  The second half of the question is not within my area of expertise.
5.(b) To what extent is controlled use feasible in terms of the training of those involved in such
use, implementing process changes, monitoring, etc.? Have there been studies conducted in this
regard and what do they show?
Dr. de Klerk:
5.346  This is definitely outside my area of expertise.
Dr. Henderson:
5.347  In theory, training of specific workers (e.g. products manufacture) and some other personnel
in the controlled use of chrysotile ought to be feasible (as for other potentially hazardous materials
such as radioactive materials used in nuclear reactors).  As a matter of common sense, training is most
likely to be effective when there is a small and cohesive workforce using materials that are notaccessible to most other workers who have limited or no training, and when the workers have a clear
understanding of the hazards and risks of the materials handled.
5.348  However, training of this type becomes less feasible or impossible in practice when there is a
large and non-cohesive workforce and when there is general accessibility to the materials in question
(e.g. builders' labourers, carpenters, electricians, plumbers and so forth at building sites, and brake
mechanics).
5.349  Even so, I am sceptical about the consistent and universal effectiveness of training
programmes in the real world, even when the work force is small and cohesive, and involved in the
handling of materials that present a clear hazard (e .g. radioactive isotopes).  For example, following
the recent mishap at a nuclear reactor in Japan, a BBC report broadcast by ABC News Radio on
Sunday 31 October 1999 pointed out that the workers at the Japanese nuclear plant had been poorly
trained, with a poor understanding of the risks.
5.350  An analogous report was printed in The Guardian Weekly  (October 28-03 November 1999,
p. 9):
"Britain's key nuclear warheads factory this week admitted to more than 100 breaches of safety in the
past year but ... the Director of Communicati ons at the Atomic Weapons Establishment in
Aldermarston ... branded claims that only luck had prevented an accident worse than that in Japan as
'irresponsible scaremongering'.  ... The Plant's emphatic denials came after The Observer newspaperWT/DS135/R
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published details of a leaked report highlighting more than 100 dangerous incidents since September
last year.  ... Among these were eight breaches of the 'criticality' rules ... and eight instances ofenvironmental contamination outside the site.  There were also eight occasions when materials —
including plutonium — were incorrect ly packaged or labelled, and 19 highly serious health and safety
incidents, including all fire-fighting pumping appliances being unfit to service.  ... The lead-in of thecatalogue of breaches comes as the environment agen cy prepares to decide whether to prosecute the
privatised Aldermarston for dumping tritium, a radioactive substance, in a stream from which Reading'sdrinking water is sourced ... it also follows the imposition of a £22,000 fine on the company after two
workers breathed in radioactive particles from plut onium that had escaped from a laboratory in August
last year.  ... The establishment insisted it was 'regul ated up to the eyeballs' by external agencies and
said it was penalised for its 'openness and transparency' in reporting breaches ...".
Dr. Infante:
5.351  Training is beneficial in reducing worker exposure to toxic substances in some circumstances,
but minimizing exposure to asbestos to the extent that a significant amount of disease will not occur,
is not one of these circumstances because of the extent of the training provisions necessary to reduce
exposures, the lack of ability to reach all of the potentially exposed populations, and the wide-spread
use of chrysotile asbestos.  Training would be relatively better achieved in the manufacturing sectorwhere the employed population is relatively more stable as compared to the construction sector
wherein many workers are transient employees.  Because of the transient nature of the workforce and
the cost involved to train workers, there is a tende ncy to not train those who will only be employed for
short periods of time.
5.352  In terms of studies related to the feasibility of using chrysotile asbestos in a "controlled
manner" OSHA health compliance data may offer some insight.  The United States has an asbestos
standard that includes training requirements that are enforceable by law, and violations of which are
punishable by monetary penalties.  Yet, improper work practices (presumably a reflection of lack of
training) and violations of the permissible exposure limit continue to be identified.  Since 1980,
OSHA compliance officers have identified almost 14,000 violations among establishments for failureto comply with provisions of its asbestos standard.  During the recent 3-year period of 1996-98,
over 4,000 violations have been cited.  Because of the small number of OSHA compliance staff in
relation to the number of facilities in the United States, it has been estimated that compliance officers
are able to visit industrial workplaces an estimated one time in every 84 years.  Thus, the non-
compliance with provisions of the United States as bestos standard as identified by its compliance
officers, represents a "tip of the iceberg" in identifying non-compliance with provisions of the
standard that are thought necessary to control asbestos exposure in the workplace.   As difficult as thissituation is in the occupational setting, I am inclined  to believe that training leading to "controlled use"
of chrysotile would be even more difficult to achieve outside of the occupational setting.
Dr. Musk:
5.353  As above in my opinion controlled use of chrysotile is theoretically feasible but probably not
practically possible.  The second question part of the question is not in my area of expertise.
5.(c) Can controlled use, when properly applied, reduce exposure levels to chrysotile fibres to
below 0,1 f/ml
26?  Can controlled use provide the assurance that there will be no peaks above this
figure for any type of use of high-density chrysotile products?  For workers or other persons
exposed to chrysotile asbestos at this level, can you quantify the risk?
                                                     
26Maximum exposure limit which was authorized in France before the ban.WT/DS135/R
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Dr. de Klerk:
5.354  See Table in paragraph 5.197 above.
Dr. Henderson:5.355  When properly applied, controlled use in specific situations (e.g. friction products
manufacture) can reduce airborne chrysotile concentrations to < 0.1 f/ml for most of the time:  e.g. as
mentioned in my answer to Question 5(a), at the Australian friction products factory in Victoria,
84 per cent of 461 samples (1992-1997) showed an airborne fibre concentration < 0.1 f/ml;  however,
the remainder showed airborne fibre levels above this figure, although the concentrations were still
low.  This also demonstrates that one cannot always guarantee that fibre concentrations will never
exceed 0.1 f/ml, even in highly regulated circumstances such as the manufacture of high-densitychrysotile products.  For the reasons discussed in preceding sections of this report, it is not possible to
quantify the risks (e.g. lung cancer or mesothelioma) from occasional peak exposures > 0.1 f/ml,
because these risks necessarily depend upon fibre type, the intensity of the exposure, and the
frequency and duration of exposure;  in addition, quantification of the risk necessarily involves
extrapolation from a linear dose-response model, which is the subject of dispute, because there are noobservational data on risks from low-level chrysotile exposure.
5.356  Tables 12 and 13 above (see my response to Question 1(d)) give some estimates of lung
cancer and mesothelioma risk at various levels of exposure to chrysotile.
5.357  Finally, occasional bursts or peak concentrations of fibres can be released from buildings by
catastrophic and uncontrollable events that include, for example, destruction by fire [244-247],earthquake, or explosions [246], including war (e.g. bombing of cities).  Although disasters like these
are infrequent — and the fall-out from fires is probably of little consequence to nearby residents or the
public in general [247] — they pose a potential health risk for some occupational groups likely to
encounter asbestos fall-out and debris more often, such as fire fighters and those involved in clean-up
operations.
Dr. Infante:
5.358  Since I believe that "controlled use" is a misnomer in relation to potential for exposure to
asbestos, I prefer to answer this question in the context of whether a stringent standard for the control
of asbestos in the workplace can reduce exposures to below 0.1 f/cc.  In many situations, when
standards are properly applied, or adhered to, it is possible to maintain exposures below 0.1 f/cc.
However, in many situations today, even in the presence of a stringent standard to control exposure,the 0.1 f/cc level for asbestos is exceeded, specified work practices and housekeeping provisions that
are required to reduce exposures are not adhered to, communication of hazards is not provided, and
appropriate personal protective equipment is not used.  As a result,  both  average exposures and peak
exposures above 0.1 f/cc will occur.  With regard to high density chrysotile products specifically,
over 2,000 violations of the OSHA asbestos standard  have been identified in standard industrial
classification (SIC) sectors where potential for exposure to chrysotile asbestos would occur, namely:
wrecking and demolition work, asbestos products manufacturing, roofing, siding and sheet metal
work, manufacturing of gasket, packing and sealing devices and automotive repair shops.
5.359  In addition to the above examples, in my opi nion, many work practices are simply not good
enough in some situations to reduce exposures below 0.1 f/cc.  For example, even though asbestoscement products may be "pre-sized" in manufacturing, cement sheets need to be modified, drilled, cut
and ground to fit them into specific areas.  Although wetting may be used in some of these situations
for cutting asbestos cement, the material dries and the dust becomes airborne resulting in uncontrolled
asbestos dust being released into the work environment.  Even in such situations where workers areWT/DS135/R
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provided with respirators to prevent exposure, the respirators supplied for the situation are often the
wrong ones.  In addition, respirator effectiveness depends upon how well the masks fit the face, how
often they are replaced, cleaned and repaired and how well the employees are trained to select, clean
and repair their respirators. In spite of rules requiring good respirator practices, employers often
simply do not comply with the regulations.
5.360  In a more general sense, non-compliance with re gulations that could assist in the control of
asbestos to exposure levels below 0.1 f/cc is often the result of human error, (not recognizing that
asbestos is present, not understanding the requirements to protect workers from exposure in specific
situations), wilful non-compliance, poor judgemen t, accidents, inability to adequately reach the
potentially exposed population with proper training and education of the health hazard, etc.  Based on
my experience in occupational health and the results of OSHA compliance data and the literature, it is
my opinion that it is impossible to use asbestos and assure that exposures can be kept below 0.1 f/cc ina great number of situations.
5.361  Regarding health risks from chrysotile exposure to 0.1 f/cc, as mentioned in my answer to
Question 3, the risk assessment conducted by Stayner et  al. (1997) based on the study by Dement et al.
(1994) provides a good estimates of disease risks from exposure to chrysotile asbestos which are not
much different from those provided from other studies.  The analyses estimate that exposureto 0.1 f/cc of chrysotile asbestos for an occupational lifetime of 45 years, e.g., 4.5 f/cc-years of
cumulative exposure, results in five extra deaths from lung cancer and two extra deaths from
asbestosis per 1000 workers.  The analysis did not include mesothelioma because there were too few
deaths from this cause in the study to provide estimates of risk.  I have not seen risk assessments for
mesothelioma based on chrysotile exposure.  Thus, I cannot provide a quantitative estimate of risk forthis cause of death.
5.362  Of these diseases, the risk of developing asbestosis is most likely underestimated.  This
underestimation is a reflection of the fact that most risk assessments are based on mortality studies and
individuals diagnosed with asbestosis often die from other causes. For example, in the study by
Finkelstein (1982), of 24 individuals with certifi ed asbestosis, who had died, 14 (58 per cent) died
from lung cancer or mesothelioma and three (12.5 per cent) died from ischemic heart disease.  Thus,
70 per cent of the individuals with asbestosis who died would not have been identified from a
mortality study of this population of exposed workers.   Asbestosis may also be underestimated in a
study because it may be confused  clinically with other non-malignant lung diseases. Therefore, the
risk of death from asbestosis based on mortality studies may usually be underestimated.  I am not
familiar with quantitative estimates of risk from other pathologies related to chrysotile asbestos.
Dr. Musk:
5.363  The question is not within my area of expertise except that risks from exposure could be
calculated if exposure levels are known.
5.(d) Is it possible to control the risks to human health presented by exposure to high-density
chrysotile products, in particular chrysotile-cem ent, throughout the life-cycle of the product? Is
controlled use a feasible and practicable option in everyday life for workers who are exposed
occasionally to potentially high levels ("peaks of exposure") of chrysotile asbestos (such as
plumbers, electricians, maintenance, repair, insulation, demolition, waste management and
"handyman" type persons)?
Dr. de Klerk:
5.364  See my response to Question 5(a).WT/DS135/R
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Dr. Henderson:
5.365  From my perspective, these questions are crucial to the dispute before the WTO.  In my
opinion, the answer to both questions is NO.  I do not see how asbestos in place — or existing
chrysotile products — can be controlled at every point of end-use.  For example, EHC 203 indicates
repeatedly that exposure is most likely to affect workers involved in building construction or
demolition;  this is because of the large number of these workers involved in myriad different tasks;
in addition, these various workers represent a non-cohesive workforce, many self-employed or
working as part of "small business".
5.366  My perception is also based on studies such as that reported by Kumagai et al. [4] on Japanese
workers involved in the repair of asbestos-cement  pipes, where fibre concentration for fibres > 5 µm
in length ranged from 92 f/ml inside the hole where this work took place (range 48-170 f/ml) and up to15 f/ml outside the hole;  the final sentence of the Abstract for this Report indicates that only about 18
per cent of the workers used a protective respirat ory device.  In addition, a survey in Finland found
occasional high fibre concentrations inside personal protectors during asbestos removal work,
suggesting that these devices are not always effective.
5.367  Another factor that merits consideration in some societies such as Australia, is poor worker
compliance with controls.  For example, I am aware of non-compliance in the use of protective
equipment (despite penalties), because respiratory protective devices may be cumbersome and
uncomfortable — especially in hot climates like Australia — with skin irritation from sweat
accumulating within them.
5.368  From the literature cited throughout this report and the reasons discussed, it seems clear that
there is a broad consensus among experts that controlled use of chrysotile (or other varieties of
asbestos) is not feasible in practice for certain worker groups, notably those involved in construction
trades (e.g. see EHC 203).
Dr. Infante:5.369  As mentioned in my responses to several previous questions, in my opinion, it is not possible
to control the risk to human health posed by exposure to chrysotile asbestos throughout its life cycle.
"Controlled use" is not a feasible and practical option in everyday life for workers.  While "controlled
use" is relatively more achievable in the manufacturing sector, violations of  regulations enforceable
by monetary fines still occur.  In the construction sector, control of  exposure to asbestos is much
more difficult to achieve as compared to manufacturing.  Workers who have jobs as plumbers,
electricians, maintenance personnel, repairmen, insulators, demolition, waste management andhandymen will most likely experience intermittent peak exposures to asbestos.  These exposures result
from lack of awareness of the hazard, lack of reco gnition of the hazard, lack of personal protective
equipment, lack of training on the maintenance of the protective equipment, etc. as mentioned in
responses to other questions above.
Dr. Musk:
5.370  In my opinion controlled use is probably not practically possible but this is not an area of my
expertise.
5.(e) Is it possible to control the risks to human health presented by exposure to high-density
chrysotile products, in particular chrysotile-cem ent, in non-occupational circumstances, such as
intervention on these products by private individual s (cutting, sawing, removal, etc.)?  Is controlled
use a feasible and practicable option for this category of the population?WT/DS135/R
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Dr. de Klerk:
5.371  See my response to Question 5(a).
Dr. Henderson:5.372  As a follow-on to my answer to the preceding question, my answer to both of these questions
is also NO.  However, the risks from occasional or infrequent interventions on chrysotile-only
products (e.g. by home "handymen") - although not quantifiable because of absence of data - must be
very small for lung cancer and mesothelioma, and non-existent for asbestosis.
Dr. Infante:
5.373  As difficult as it is to control exposure to chrysotile asbestos during intervention with cement
products in the occupational setting, it is much more so in non-occupational circumstances because
there is no effective means of identifying the potential population at risk.  As a result, there is a lack of
awareness of the hazard, lack of recognition of the hazard, lack of personal protective equipment, lack
of training on the maintenance of the protective equipment, etc. as mentioned in responses to other
questions above.  Therefore, in my opinion, it is not possible to limit exposure in such circumstances.
Dr. Musk:
5.374  Controlled use is probably not practically possible, in my inexpert opinion.
Question 6:
The parties disagree as to the relative pathogenicity of chrysotile fibres vs. substitute fibres,
in particular cellulose fibres, para-aramid fibres, glass fibres and polyvinyl alcohol (PVA) fibres.
Canada considers that, overall, substitute fibres have not been demonstrated to be less toxic than
chrysotile fibres, and that, by banning chrysotile, France has replaced the "much studied but
nonetheless undetectable risk associated with m odern uses of chrysotile with the unknown, and
perhaps greater risk associated with the use of substitute fibres" [Premier exposé oral du Canada,
paragraph 90]. On the other hand, the European Co mmunities argues that none of the substitute
products -fibrous or non-fibrous- for chrysotile, and in particular none of the substitutes for
chrysotile-cement, has been classified as a proven  carcinogen to humans; hence, overall, substitute
products present less of a risk to human health th an chrysotile asbestos [see Deuxième soumission
écrite, pp. 10-15].
6.(a) Is it correct to argue that non-fibrous substitutes are safe or less hazardous than chrysotile
and that concern over potential health risks shou ld be focused on fibrous ones? In this context,
could you elaborate upon the "effet fibre" ["fibr e effect"] of substitute fibres? What general
conclusions can be drawn as to the respirability and biopersistence of substitute fibres?
Dr. de Klerk:
5.375  As outlined above, the pathogenicity of fibres is related to their size, shape, durability and
quantity.  Thus, all the parts to this question can be answered in the same way.  The argument here is
whether it is safer to stick with the well-studied chrysotile that has a semi-quantifiable and definitecarcinogenic risk, than to use other substances which have the potential to increase risk in an
unquantifiable way, ie. the "better the devil you know" principle.  For example, para-amid fibres have
recently been classified by IARC in Group 3, that is, 'not classifiable as to its carcinogenicity'.WT/DS135/R
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5.376  Substitutes need to be compared to chrysotile in terms of the parameters listed above, namely,
size, shape, durability and quantity.  These are all properties of fibres and therefore "concern should
be focused on fibrous substitutes".  Substitute fibres can then be compared with chrysotile on the
four parameters.  I am inexpert in commenting on the "extent to which hazardous concentrations can
be controlled" but it is my understanding that all four substitutes mentioned involve less dusty
operations than equivalent ones involving chrysoti le.  As far as the other three parameters are
concerned:  all four substitutes except glass fibre produce a larger proportion of non-respirable fibres
than chrysotile does, but respirable fibres are similar for all substances and glass fibre is the least
durable; all four except cellulose are less durable than  chrysotile, but cellulose is much less dusty and
has also been in use for a long while without evidence of ill effect.
5.377  On balance, the substitute fibres appear less li kely to cause adverse effects (from their fibres)
than chrysotile.
Dr. Henderson:
5.378  Current thinking on this issue indicates that the bio-hazards — specifically the carcinogenic
risks - of all fibres are determined by the three Ds:  dose, fibre dimensions and durability (bio-
persistence) [248-250].  Therefore, substitute materials that have engendered most concern are fibrousmaterials as opposed to non-fibrous substances (non- fibrous materials may or may not show different
effects in terms of toxicology, but this discussion focusses on carcinogenic risks).  For example,
refractory ceramic fibres (RCF) are a cause for concern [251] because they may have dimensions
similar to those of the amphibole varieties of asbestos and RCF have been reported to induce
mesothelioma in experimental animals.
5.379  In a 1995 review, de Vuyst et al. [248] concluded that:
"The group of man-made mineral or vitreous fibres (MMMFs or MMVFs) includes glass wool, rock
wool, slag wool, glass filaments and microfibres, and refractory ceramic fibres (RCFs). Experimentalobservations have provided evidence that some ty pes of MMVF are bioactive under certain conditions.
The critical role of size parameters has been demonstrated in cellular and animal experiments, whenintact fibres are in direct contact with the target cells. It is, however, difficult to extrapolate the results
from these studies to humans since they bypass inhalation, deposition, clearance and translocation
mechanisms. Inhalation studies are more realistic, but show differences between animal speciesregarding their sensibility to tumour induction by fibres. Fibre biopersistence is an important factor, assuggested by recent inhalation studies, which demonstrate positive results with RCF for fibrosis, lungtumours and mesothelioma. There is no firm evidence that exposure to glass-, rock- and slag wool isassociated with lung fibrosis, pleural lesions, or nonspecific respiratory disease in humans. Exposure to
RCF could enhance the effects of smoking in causing airways obstruction. An elevated standard
mortality ratio for lung cancer has been demons trated in cohorts of workers exposed to MMVF,
especially in the early technological phase of mine ral (rock slag) wool production. During that period,
several carcinogenic agents (arsenic, asbestos, polycyclic aromatic hydrocarbons (PAH)) were alsopresent at the workplace and quantitative data about smoking and fibre levels are lacking. It is not
possible from these data to determine whether the risk of lung cancer is due to the MMVFs themselves.
No increased risk of mesothelioma has been demonstr ated in the cohorts of workers exposed to glass-,
slag- or rock wool. There are in fact insufficient  epidemiological data available concerning neoplastic
diseases in RCF production workers because of the small size of the workforce and the relatively recentindustrial production" [abstract].
5.380  In a 1999 review published in French, Boillat et al. [250] came to similar conclusions:
"The group of man-made mineral fibres includes slagwool, glasswool, rockwool, glass filaments and
microfibres, as well as refractory ceramic fibres. The toxicity of mineral fibres is determined by severalfactors such as the diameter (< or = 3-3.5 microns) and the length of the fibres (< 100 microns), their
biopersistence, which is much shorter for man-made mineral fibres than for asbestos fibres, theirWT/DS135/R
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physicochemical structure and surface properties, and the exposure level. The chemical composition of
the various types of man-made mineral fibres depends directly on the raw material used to manufacturethem. While naturally occurring fibres are crystalline in structure, most man-made mineral fibres are
amorphous silicates combined with various metal oxides and additives. Observations using
intracavitary administration have pr ovided evidence that some types of man-made mineral fibres are
bioactive in cellular and animal experiments and may induce lung tumours and mesothelioma. It isdifficult to extrapolate these results to humans since they bypass inhalation, deposition, clearance andtranslocation mechanisms. Inhalation studies show mo re realistic results but differences are observed
between animal species regarding their sensibility to tumours. There is no firm evidence that exposure
to various wools is associated with lung fibrosis, pleural lesions or nonspecific respiratory disease inhumans. A possible exception may be mentioned for refractory ceramic fibres. A slightly elevatedstandard mortality ratio for lung cancer has been documented in large cohorts of workers (USA, Europeand Canada) exposed to man-made mineral fibres, especially in the early technological phase. It is notpossible to determine from these data whether the risk of lung cancer is due to the man-made mineral
fibres themselves, in particular due to the lack of data on smoking habits. No increased risk of
mesothelioma has been demonstrated in these cohorts.  Epidemiological data are insufficient at this time
concerning neoplastic diseases in refractory ceramic fibres" [abstract].
5.381  In one study on RCF, Glass et  al. [252] reported that:
"In recent inhalation experiments conducted with both rats and hamsters ... at the highest dose tested ...
there was an increased incidence of tumours in both species. Lower doses were only examined in therat and at these doses there was no significant excess of lung tumours. Epidemiological investigationsof workers engaged in the manufacture of ceramic fibres have shown a small excess of pleural plaques.This phenomenon is being further investigated but could be due to confounding exposures. The
populations available for study are small and their exposures fairly short, but it is considered prudent
that they should remain under surveillance for some time to come. This is despite the fact that presentexposures in the ceramic fibre industry are low (< 1 f/ml) and are being reduced" [abstract].
5.382  Okayasu et al. [253] also found that RCF-1 fi bres were less cytotoxic and mutagenic than
chrysotile:
"Cytotoxicity and mutagenicity of tremolite, erionite and the man-made ceramic (RCF-1) fibre were
studied using the human-hamster hybrid A(L) cells. Results from these fibres were compared with
those of UICC Rhodesian chrysotile fibres. The A(L) cell mutation assay, based on the S1 gene marker
located on human chromosome 11, the only human chromosome contained in the hybrid cell, has beenshown to be more sensitive than conventional assays in detecting deletion mutations. Tremolite,erionite and RCF-1 fibres were significantly less cytotoxic to A(L) cells than chrysotile. Mutagenesisstudies at the HPRT locus revealed no significant mutant yield with any of these fibres. In contrast,both erionite and tremolite induced dose-dependent S1- mutations in fibre-exposed cells, with the
former inducing a significantly higher mutant yield than the latter fibre type. On the other hand, RCF-1
fibres were largely non-mutagenic. At equitoxic doses (cell survival at approximately 0.7), erionite wasfound to be the most potent mutagen among the three fi bres tested and at a level comparable to that of
chrysotile fibres. These results indicate that RCF-1 fibres are non-genotoxic under the conditions usedin the studies and suggest that the high mesothelioma incidence previously observed in hamster may
either be a result of selective sensitivity of hamster pleura to fibre-induced chronic irritation or as a
result of prolonged fibre treatment. Furthermore, the relatively high mutagenic potential for erionite isconsistent with its documented carcinogenicity" [abstract].
5.383  An important consideration is that fibre dimensions for some substitute materials
(e.g. fibreglass) can be varied according to the manufacturing processes employed, so that they can bedesigned to have fibre characteristics and dimensions different from asbestos, or similar to asbestos:
as one example, the dimensions of fibreglass can be varied and when implanted into experimental
animals, fibres of the "right" size can induce mesothelioma.
5.384  For this reason, testing of substitute materials with fibre dimensions similar to those of
asbestos should be carried out before these materials are used in products available to the generalWT/DS135/R
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public (e.g. testing for toxicology,  clastogenicity, DNA strand breaks, mutagenicity and free radical
generation using in vitro  systems and/or testing in vivo  — such as the intraperitoneal test in rats) [248,
249, 251-256].
5.385  Nonetheless, it is my perception that lumping all substitute fibres together is as erroneous as
lumping amphibole and chrysotile fibres into the same category.  For example, RCF are the subject ofcontinuing concern, but other substitute fibres such as cellulose fibres, para-aramid fibres and
polyvinyl alcohol (PVA) fibres appear to be different from chrysotile, in terms of fibre dimensions
and especially bio-persistence.
5.386  NICNAS 99 summarizes these considerations in the following terms:
"Any substitution of chrysotile should be with a less hazardous substance.  There has been ongoing
debate regarding the health effects of alternatives, such as synthetic mineral fibres (SMF), natural
organic fibres and synthetic organic fibres.
In general, less data on health effects of alternative materials (in comparison to asbestiform fibres) are
available and because of this, it is difficult to make an assessment of the pathogenicity and potentialcarcinogenicity of many substitutes.
Although not the only determinant of potential pathogenicity, fibre dimensions (length, width and
aspect ratio) are considered to be [some] of the most important factors associated with carcinogenic
(lung cancer and mesothelioma) potential  ...  The commonly accepted 'peak hazard' dimensions ...are > 5 µm long (length) and < 3 µm wide (diameter).
The most commonly used alternatives in Australia (and overseas) for friction materials are aramid
fibres, attapulgite, fibreglass, refractory ceramic fibres (RCF), semi-metallics, mineral wool, steel wool,
cellulose, titanate fibres and wollastonite, and for gaskets are glass fibre, carbon fibre and aramid fibre.
... It should also be noted that ...  differences in  fibre length, diameter and surface properties may lead
to entirely different toxicological profiles.
A recent report by EC concludes that the available data are generally supportive of the conclusion that
PVA, cellulose, p-aramid, glass wool and slag wool are likely to be safer in use than chrysotile.However, RCFs are the subject of ongoing concern ..." [p 125].
Dr. Infante:
5.387  I have not seen any information that indicates that non-fibrous substitutes for chrysotile are
carcinogenic, or cause non-malignant lung diseases.  I would focus attention on the fibrous substitutes
in terms of their ability to reach lung tissue (respirability) and their known toxicity.  Clearly, if the
substitute fibres are not respirable, there is little concern for their "potential" to cause lung diseases.(Attention would then focus on adverse effects from expos ure to the skin and eyes.)   If the substitute
fibres are respirable, then attention needs to focus on their toxicity relative to that of chrysotile in their
ability to cause lung cancer, non-malignant lung diseases and mesothelioma.
5.388  The data I have reviewed in this area of investigation appear to indicate that polyvinyl alcohol
fibres (PVA) are mostly in the range of 10-16 microns in diameter and hence are too large torespirable and thus cause lung disease.  In terms of biopersistence, if they were respirable, they would
degrade very slowly.  Para-aramid fibres are also generally 10-12 microns in diameter and they also
would have little chance of being respired.  These fibres, however, contain fibrils of about 0.2 microns
in diameter that can be liberated with high energy input and they would be respirable.  P-aramid fibrils
greater than 5 microns in length are less biopersistent than chrysotile fibres greater than 5 microns in
length (Searl, 1997).  Data for dimensions of cell ulose fibres show a median length and diameter of
about 7.5 and 1.50 microns, respectively, which indicates that they are in the respirable range (MuhleWT/DS135/R
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et al. 1997).  In terms of biopersistence, cellulose fibres had a mass half time in the rat lung of 72 days
and bioaccumulated in the lungs.  Data on the distribution of glass fibres indicates that the majority
are in the respirable range, but the fibre size distribution of glass filaments indicates that a small
portion are in the respirable range.  Glass fibres are less biopersistent than chrysotile fibres.  In
general, in terms of the combination of respirability and biopersistence, with the exception of cellulosefibres, it appears that the substitute fibres would have less bioaccumulation in the lung than chrysotile
fibres because they are either less respirable, or they are not as biopersistent.
5.389  The role of biopersistence in relation to toxicity is complicated.  Chrysotile fibres are less
biopersistent than amphibole fibres, yet experimental data demonstrate a similar potency for lung
cancer, mesothelioma and fibrosis.
Dr. Musk:5.390  I agree with the Canadian argument philosophically.  However there is no evidence that I
know of carcinogenicity of substitutes in animal studies and only rockwool has been associated with
increased lung cancer risk in epidemiological studies.
6.(b) To what extent do physical characteristics and chemical properties of substitute fibres
determine their toxicity?  Is it correct to say that man-made fibre substitutes are superior to naturalfibre ones in terms of the extent to which exposu re to hazardous concentrations can be controlled
during the various stages of production?  Is your  opinion based on one or more of the following
evidence:  (i) chemical/physical characteristics of the substitute fibres, (ii) epidemiological data, (ii)
in vitro evidence, (iv) in vivo evidence?
Dr. de Klerk:
5.391  See my response to Question 6(a).
Dr. Henderson:5.392  These questions are covered to a large extent in my answer to the preceding question.  Again,
dose, fibre dimensions (including surface chemistry) and bio-persistence appear to represent the
properties that determine the toxicity and carcinogenicity of fibres of any type.  The issue of
controllability during various stages of production is an engineering and industrial question, and falls
outside my expertise.
5.393  My opinions concerning the potential bio-hazards of these fibres are based on the physical
characteristics of the substitute fibres, in vivo  evidence (tumour induction in experimental animals)
and in vitro  studies (mutagenicity analogous that reported for other known carcinogens).   To the best
of my knowledge, there are no large-scale epidemiological studies on cellulose fibres, para-aramid
fibres or PVA fibres;  two large epidemiological investigations on slag wool fibres in both Europe and
the United States did show an increase in the relative risk for lung cancer among the production
workers, but this effect may have been explicable by other confounding factors involved in themanufacture of these materials.
Dr. Infante:
5.394  As a matter of general toxicology, I would focus concern on the "potential" for adverse health
effects from any fibrous material of dimensions and aerodynamic diameter that will result in its beingrespirable.  This is discussed in my response to Question 6(a) above.  The toxicity of the substitute
fibres and whether that information was determined on the basis of epidemiological or toxicological
evidence is discussed in Question 6(c).  The role of the chemical properties of fibres to induce cancerWT/DS135/R
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is not clear to me.  The nature of the production process makes the substitute fibres more amenable to
control than asbestos fibres.
Dr. Musk:
5.395  I do not know: but it is my broad understanding  that the physical and chemical properties of
the substitute fibres suggests less risk of disease.
6.(c) The parties focus part of their arguments on cellulose fibres, para-aramid fibres, glass
fibres and polyvinyl alcohol (PVA) fibres. What ev idence exists with respect to the toxicity and
health risks of these substitutes? Does the existing evidence suggest that these products are
less/equally/more toxic than chrysotile asbestos fibres?
Dr. de Klerk:
5.396  See my response to Question 6(a).
Dr. Henderson:
5.397  In experimental studies on para-aramid fibres in comparison to chrysotile, Warheit et al. [12,
257] found that p-aramid is bio-degradable in the lungs of exposed rats, with faster clearance than
long chrysotile fibres which showed greater bio-persistence.  In their 1996 study, these authors [12]
found that:
" ... p-aramid is biodegradable in the lungs of exposed rats; in contrast, the clearance of long chrysotile
fibres was slow or insignificant, resulting in a pulmonary retention of long chrysotile asbestos fibres.The dimensional changes of asbestos fibres as well as the pulmonary cell labelling data indicate thatchrysotile asbestos fibres may produce greater long-term pulmonary effects when compared to inhaled
para-aramid fibrils" [abstract].
5.398  The present status of knowledge has been summarized by Harrison et al. [19] in a recent
review of the comparative hazards of chrysotile and its substitutes:
"There are now practicable substitutes for the major remaining uses of chrysotile.  Although lack of a
full health and toxicological data set precludes a comprehensive assessment of the safety of substitutefibers, the application of basic principles of fiber toxicology enables a pragmatic decision to be made
on the relative safety of potential substitutes.  Our judgement is based on relative considerations of the
intrinsic properties of fibers, on the pathogenicity of chrysotile in comparison with that of substitutefibers, and on the potential for uncontrollable exposures.  The three parameters of dose, dimension(especially diameter), and durability are key to determining the differential hazards.  Due considerationof these factors leads us to the following conclusions regarding chrysotile and its main substitutes.
Chrysotile per se can cause lung cancer and asbestosis;  it is less clear that chrysotile alone can cause
mesothelioma in humans, and indeed it may not, whereas tremolite and other amphiboles certainly can
do so.  There is no definitive evidence for a threshold exposure level for lung cancer induction,although some studies suggest that a threshold does exist.
The intrinsic hazardous properties of chrysotile can never be 'engineered out', and the potential for harm
will always remain.  Prevention of ill health will thus always rely on the control of exposure, somethingthat history has shown cannot be guaranteed.
Unlike chrysotile, substitute fibres can often be design ed or selected to have particular characteristics.
Criteria for the substitution of asbestos by other fibers include a) the substitute fibers are not in therespirable range, do not readily fibrillate, and/or are less durable than chrysotile;  b) other materials that
must be incorporated into the replacement product  do not, in combination with the replacement fiber,WT/DS135/R
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produce more harm overall than chrysotile alone;  c) the replacement product has an equivalent or
acceptable performance;  and d) substitution would result in overall lower fiber exposures duringmanufacture and use and disposal, taking into account likely exposures.  The same general principle
can be applied to substitute fibers others than those considered here.
We judge that PVA fibers will pose less risk than chrysotile because they are generally too large to be
respirable, do not fibrillate, and the parent material causes little or no tissue reaction.  Aramid fibershave a reduced potential for exposure when compared to chrysotile because they are generally of highdiameter and the production of respirable fibrils is  energy intensive.  The fibrils are less pathogenic
than chrysotile, are less biopersistent, and are biodegradable.  Cellulose has the benefit of long
experience of use in a variety of industries without having raised significant concern.  The potential forthe generation of respirable fibers seems to be less than is the case for chrysotile, although fibrillation ispossible.  Cellulose is durable in the lung, and its biological properties should therefore be investigatedfurther.  However, exposure levels for current uses are low, and it is biodegradable in the environment.
We believe that the continued use of chrysotile in asbestos-cement products is not justifiable in the face
of available and technically adequate substitutes.  Li kewise, there seems to be no justification for the
continued residual use of chrysotile in friction materials" [pp 610-611].
5.399  From known past uses of asbestos and surveys of current uses in Australia, it is evident that
alternatives have replaced chrysotile to a larg e extent for the following products [NICNAS 99, p 111]:
"Products where chrysotile use has been completely replaced:
• Cement sheeting, tubes and piping.
• Roofing tiles.
• Textiles.
• Fibre insulation.
• Railway brake blocks.
• Brake disc pads in new automotive vehicles (only 1 new vehicle model was identified
as being supplied with asbestos pads in  Australia).
Products where a major proportion of chrysotile use has been replaced:
• Clutch facings (in automotive vehicles and industrial machinery e.g. tractors,
centrifuge drives).
• Brake disc pads (in older taxi and cour ier vehicles, and industrial machinery).
• Gaskets, such as spiral wound and head gaskets.
• Washers.
• Packing material.
• Rotor blades (e.g. in high vacuum pumps)".
5.400  It is notable that chrysotile is no longer used for brake linings in new passenger cars produced
in Australia by most manufacturers, having been replaced by substitute materials:  NICNAS 99
comments that:
"Out of 26 companies, 25 stated that they are using non-asbestos original equipment in all current
models.  One company (Ford Motor Australia) reported that they are still using asbestos parts in twocurrent models:  asbestos head gaskets for the Econovan and asbestos rear brake linings for the Fordutility.  Ford Australia introduced non-asbestos components for their most popular models (e.g. Laser,
Falcon and Fairlane) between 1989 and 1995.  Other current models manufactured by Ford have been
asbestos-free since their introduction.  ... Asbestos parts are imported by 6 of the 26 companies (BMW,Ford, Mazda, Mitsubishi, Nissan and Toyota) with five companies using asbestos parts for supersededvehicles and one company (Ford Australia) using asbestos parts in superseded and current models ... themajority of the vehicle manufacturing companies stated that they have had policies in place in regard to
not using asbestos components in new vehicles for the last 5 to 10 years" [p 22].WT/DS135/R
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5.401  This trend to use of brake linings free of asbestos is shown in the following Table 15 — in
comparison to the usage of asbestos brake li nings — between 1994 and 1998 (asbestos-containing
brake linings appear to be used primarily on older and superseded vehicle models).
TABLE 15:  IMPORTS OF ASBESTOS AND NON -ASBESTOS BRAKE LININGS INTO AUSTRALIA , 1994-1998
Number of Articles
Import 1994 1995 1996 1997 1998 (Jan-Aug)
Asbestos
brake linings,passenger cars492,295 47,735 43,087 771,182 (548,692)
Non-asbestos
brake linings,
passenger cars70,109 321,472 485,812 2,084,963 (4,057,143)
Source:  NICNAS 99.
Dr. Infante:
5.402  There is no information to my knowledge that cellulose fibres, para-aramid fibres or ployvinyl
alcohol (PVA) fibres are carcinogenic.  Cellulose fibres have not been studied experimentally for
carcinogenicity.  It is noteworthy, however, that cellulose has been used in the paper industry for
hundreds of years and to date an elevated risk of death from lung cancer and mesothelioma has not
been observed.  Excess incidences of pharyngeal and/or laryngeal cancers were reported in two
studies, but these observations have not been corroborated in other studies (IARC, 1987).  Wood dust
is associated with sino-nasal cancer, but not with  lung cancer or mesothelioma.  A relatively greater
risk appears to be associated with hard woods as  compared to soft woods, which suggests that the
cellulose may not be the primary factor in the induction of these cancers.  Workers exposed to cotton
dust also do not demonstrate an excess of lung cancer or mesothelioma even though they develop
byssinosis.  The debate as to whether this disease is due to cotton dust per se, or to contaminants of the
cotton fibre, however, is not resolved.
5.403  Para-aramid fibrils have been studied for carcinogenicity in experimental animals by
inhalation and by intra-peritoneal injection.  No cancer response was observed.  As concluded by
IARC (1997), there is inadequate evidence for the carcinogenicity of para-aramid fibrils in
experimental animals.  The carcinogenicity of para-aramid fibrils has not been evaluated in humans.
Likewise, IARC (1987) concl uded on the basis of its review of animal cancer tests that there is no
evidence for the carcinogenicity of  PVA fibres.  PVA fibres have not been evaluated for
carcinogenicity in humans.  It is also my opinion that there is no evidence that these fibres present any
risk of cancer to humans.
5.404  With regard to glass fibres, IARC (1988) concluded there was sufficient evidence for the
carcinogenicity of glass wool in experimental animals and that there was inadequate evidence for thecarcinogenicity of glass wool to humans.  Subseque nt to the IARC (1988) review, my colleagues and I
have reviewed the toxicological and epidemiological studies related to exposure to glass fibres.  In our
opinion, there is conclusive evidence from implantation and inhalation studies that glass fibres are
carcinogenic in experimental animals (Infante et al . 1994).  Studies of workers exposed to glass fibres
also demonstrate a significantly elevated risk of death from lung cancer.  It is our interpretation ofthese studies that employment in the manufacturing of glass fibres carries with it an elevated risk of
death from lung cancer.  Is it proven beyond a doubt through epidemiological study that fibrous glass
is a human carcinogen?  In my opinion, it is not. However, given the positive animal cancer test
results, knowledge that these fibres can be inhaled and retained in the lungs, evidence that workersWT/DS135/R
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employed in the manufacturing of these fibres die at a significantly elevated rate of lung cancer, it is
my opinion that it is more likely than not that glass fibres are carcinogenic to humans and that
employment in this industry carries with it an elevated risk of death from lung cancer.
5.405  It is also my opinion that glass fibres are not as potent as chrysotile asbestos in causing
disease.  With regard to the capability of glass fibres to cause lung cancer, I have previously published
the opinion that on a fibre-per-fibre basis, glass fibres may be as potent or even more potent than
asbestos in causing lung cancer.  This opinion was based on epidemiological studies which generally
demonstrated 10 per cent to 20 per cent elevation in the relative risk of lung cancer (the 1987 study of
Canadian workers by Shannon demonstrated a 2-fold risk) as a result of exposures to glass fibres that
were reported to be fairly low. Within the past year, however, I have had the opportunity to discuss
occupational exposures during glass fibre manufactu ring with workers formerly employed at the
Canadian facility that manufactured fibrous glass.  According to several workers, they were alsoexposed to crystalline silica many times over the permissible limit through the dumping of sand into
the hopper that was used to feed the furnace for melt down.  They were exposed to asbestos that lined
the furnace when they removed the insulation from the oven doors by hand, or chiselled it away in the
absence of respiratory protection; they would then add water to asbestos fibre to make "asbestos mud"
that was applied to the oven doors by hand, or by trowel.  Workers were so uninformed of the hazardthat they sometimes would throw  "asbestos mud balls" at each other. The workers at this facility were
also exposed to phenol formaldehyde resin that was used as a binder for the glass fibres; they were
also exposed to tar that was applied to paper that was then applied to the glass fibre pack.  Exposures
to glass fibres only is mentioned in the study of these workers that was published by Shannon (1987).
5.406  Furthermore, there is less evidence from epidemiological studies that exposure to glass fibres
is associated with a pneumoconiosis as compared to the data for chrysotile asbestos exposure and
asbestosis.  There is no evidence that exposure to glass fibres is associated with mesothelioma.  For
the few cases of mesothelioma that have been identified among workers exposed to glass fibres to
date, there is claim that they also had been exposed to asbestos fibres.  Therefore, it is difficult to
attribute these cases of mesothelioma to the glass fibre exposures. Therefore, the totality of diseaserelated to chrysotile asbestos exposure would be greater than that related to a similar amount of
exposure to glass fibres.
5.407  In conclusion, only one of the fibres (glass fibres) that may play any significant role in
substitution for chrysotile asbestos demonstrates evidence of  being carcinogenic.  Data for the total
toxicity related to these fibres, however, is less than that for chrysotile asbestos fibres.   Cellulose
fibres have not been tested for carcinogenicity in experimental animals, but epidemiological studies of
workers exposed to cellulose in three separate industries, i.e., furniture manufacturing, cotton textilemanufacturing and the paper products industry, have not  demonstrated an elevated risk of contracting
lung cancer or mesothelioma.  Regarding non-malignant lung disease among cotton dust exposed
workers, it is not known whether the cotton dust per se, or contaminants of the cotton fibre, are
responsible for the byssinosis observed in these workers.
Dr. Musk:
5.408  I understand that substitutes have been shown to be less toxic in animals.
3. Summary Comments by Dr. Henderson
5.409  In-place asbestos is widely distributed in industrialized societies and much includes mixtures
of chrysotile and amphiboles — although chrysotile has been the predominant type of asbestos usedthroughout Western Europe for many years (about 94-97%).WT/DS135/R
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5.410  Lung cancer and mesothelioma are the most important bio-hazards from asbestos in place and
the continued use of asbestos.
5.411  Because of the prolonged lag-time between exposure and the subsequent development of
either lung cancer or mesothelioma, most mesothel iomas in the 1990s and beyond can be attributed to
exposures sustained decades before;  the mesothelioma "epidemic" predicted for Europe over the nextthree decades can be attributed to exposures before, during and after the 1960s and 1970s, especially
to one or more of the amphibole varieties.
5.412  For the amphibole forms of asbestos and mixtures of asbestos types, a linear dose-response
relationship has been found at high levels of exposure;  a dose-response relationship with an increase
of the relative risk of mesothelioma to > 2.0 has also  been observed at low levels of exposure, in the
order of 0.5-1.0 fibre-year (which overlaps with non-occupational environmental exposures).  No
lower threshold dose for mesothelioma induction has been delineated for the amphiboles.
5.413  Chrysotile also has the capacity to induce mesothelioma, although it is less
mesotheliomagenic than the amphiboles (my estimate is 1/10
th-1/30th).
5.414  Commercial Canadian chrysotile on average contains trace quantities of tremolite, including
fibrous tremolite (< 1%).
5.415  Tremolite — a non-commercial amphibole — also has the capacity to induce mesothelioma.
5.416  The carcinogenicity of Canadian chrysotile may be attributable to the trace tremolite content,
but it is not possible to separate the dose-response effects for the chrysotile and the tremolite.
5.417  At high levels of exposure to Canadian chrysotile, a linear dose-response relationship has
been observed.
5.418  To the best of my knowledge, there are no epidemiological or observational data on dose-
response effects of chrysotile only at low levels of exposure.
5.419  No lower threshold dose for the carcinogenic ef fects of chrysotile has been identified (EHC
203).
5.420  To the best of my knowledge, there are no observational data on the potential carcinogenic
effects of inhaled chrysotile when superimposed upon a pre-existing burden of amphiboles ±chrysotile in lung tissue.
5.421  Although the amphiboles are far more potent than  chrysotile for mesothelioma induction, this
differential in carcinogenicity may be less obvious or absent for lung cancer induction, but this is still
the subject of some dispute;  chrysotile is associated with a low risk of lung cancer among Canadian
chrysotile miners and millers, but the highest risk for lung cancer induction has been observed for
South Carolina asbestos textile workers who used Canadian chrysotile almost exclusively.
5.422  A linear dose-response relationship has also been observed for the risk of lung cancer versus
cumulative asbestos exposure.  Although some authorities favour a linear no-threshold model for lung
cancer induction, others suggest that a threshold may exist, but this has not been delineated in
numerical terms.
5.423  In contrast, asbestosis is a dose-dependent non-cancerous disorder, with clear evidence of a
threshold effect, although the threshold may be lower than previously supposed, at least forWT/DS135/R
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histological asbestosis;  there is no risk of asbestosis at low levels of chrysotile exposure.
5.424  Although reduction of airborne asbestos fibre co ncentrations in the mining and manufacturing
industries has been achieved, it is too early to evaluate the effects of these reduced exposures, because
no epidemiological data are available;  however, with reduction of cumulative exposures, a reduction
in the incidence of both asbestos-related mesothelioma and asbestos-related lung cancer can beexpected.
5.425  The risks from low-level occupational exposure to chrysotile, or from occasional peak
concentrations, have not been delineated but are predictably small.
5.426  Carcinogenic hazards from ultra-low levels of atmospheric chrysotile fibres (e.g. simple
occupancy of public buildings) appear to be minuscule, negligible or undetectable.
5.427  Therefore, health concerns over chrysotile dust exposure narrow down to a workplace issue.
5.428  There is evidence of an increased incidence of mesothelioma among, say, brake mechanics in
Australia exposed to chrysotile derived from brake blocks and lining.
5.429  With the reductions of airborne fibre concentrations in the asbestos mining, milling and
manufacturing industries, construction trades workers constitute the group of workers at greatest risk
from exposure to asbestos-cement products (e.g. builders, builders' labourers, carpenters, electricians,
plumbers and roofing workers).  This group constitutes a large, disparate and non-cohesive workforcefor which controlled use of asbestos is not achievable, for the reasons discussed earlier in this report.
5.430  Therefore, chrysotile asbestos should not be used in building materials, because of the hazards
imposed by installation, maintenance and remo val operations (EHC 203);  these risks may be
compounded for some groups by catastrophic events affecting buildings — e.g. fires (with a burst of
asbestos fibres into the atmosphere and the necessity for clean-up operations), and other disasters.
5.431  Substitutes for chrysotile are available for many applications (e.g. cellulose fibres, para-
aramid fibres and polyvinyl alcohol);  evidence indicates that these fibres are less bio-persistent than
chrysotile and, therefore, national health authorities (EHC 203, NICNAS 99) have recommended
phasing out or prohibition of chrysotile whenever safer substitute materials are available.
5.432  Therefore, from a perspective of caution and prudence for occupational health and safety, it
follows that chrysotile should either:
(a) Be restricted to only a few and well-defined applications so that it is inaccessible to
the great majority of workers and is available for use by only small and cohesive
specialized worker groups that can be trained effectively in its controlled use
(e.g. analogous to nuclear fuels);  in effect, this means that chrysotile should not be
used in building products (e.g. high-density fibro-cement materials such as asbestos-
cement sheets) or friction products.
OR
(b) It should be made inaccessible to everyone, by prohibition, unless the alternatives
pose equal or greater hazards and equal or greater problems with control.
5.433  These views are also expressed in EHC 203, wherein it is stated:WT/DS135/R
Page 339
"a) Exposure to chrysotile asbestos poses increased risks for asbestosis, lung cancer and
mesothelioma in a dose-dependent manner.  No threshold has been identified for carcinogenic risks.b) Where safer substitute materials for chrysotile are available, they should be considered for use.
c) Some asbestos-containing products pose particular concern and chrysotile use in these
circumstances is not recommended  These uses include friable products with high exposure potential.Construction materials are of particular concern for several reasons.  The construction industryworkforce is large and measures to control asbestos ar e difficult to institute.  In-place building materials
may also pose risk to those carrying out alterations, maintenance and demolition" …  [p 144]
d) The combined effects of chrysotile and other insoluble respirable particles needs further study.
e) More epidemiological data are needed concerning cancer risks for populations exposed to fibrelevels below 1 f/ml, as well as continued surveillance of asbestos-populations" …  [p 145]
5.434  NICNAS 99 sets out a similar set of recommendations:
• "Chrysotile is a known human carcinogen.
• Prudent OHS [occupational health & safety] policy and public health policy favours
the elimination of chrysotile wherever possible and practicable.
• The main exposure to Australian workers arises from manufacture, processing and
removal of friction products and gaskets.  Home mechanics are also exposed during
'do-it-yourself' replacement of brake pads/shoes.  ... .  In Australia, chrysotile is no
longer used in high density materials such as chrysotile-cement.
• Current overseas experience with the phasing out of chrysotile products indicates that
a range of alternatives is available to suit the majority of uses.  Good OHS practice
dictates that use of chrysotile products should be restricted to those uses where
suitable substitutes are not available, and alternatives should continue to be sought for
remaining uses".
5.435  Whether the objective of removal of chrysotile from the workplace and the general
environment is achievable by enforcement of controlled use for a few restricted applications — or byprohibition — is essentially a societal question and a public health policy issue.  For the reasons
discussed in this report, a complete ban is more certain to accomplish this objective
(paragraph 5.432(b)).  Therefore, as a cautious and prudent approach to national occupational health
policy, a complete ban is neither unreasoned nor unreasonable;  on the balance of prevailing scientific
evidence and uncertainties discussed in this report, such a policy seems defensible and, arguably,justifiable as a national health measure.  Perhaps it is best to let Bradford Hill have the last words:
"All scientific work is incomplete — whether it be observational or experimental.  All scientific work is
liable to be upset or modified by advancing knowledge.  That does not confer upon us a freedom toignore the knowledge we already have, or to postpone action that it appears to demand at a given time."
4. Endnote by Dr. Henderson
5.436  Wishing to add two further pertinent references after completing his Report, Dr. Henderson
attached the following Endnote.  These references27 deal with the following:
5.437  Clearance of chrysotile fibres from human lung tissue:   In the past, the kinetics of chrysotile
clearance from lung tissue have been investigated main ly in experimental models using rodents.  In an
autopsy study published in 1999, Finkelstein and Dufresne [1] investigated clearance of chrysotile
                                                     
27For complete references, see Annex III to this Panel Report.WT/DS135/R
Page 340
from the lung tissue of 72 Quebec chrysotile miners and millers in comparison to 49 control subjects,
using regression analyses, with the following findings:
• There was a significant association between the duration of occupational exposure
and the tissue burdens of chrysotile and tremolite.
• The concentration of chrysotile decreased with time after exposure ceased but the
concentration of tremolite did not.
• The clearance rate varied inversely with the length of chrysotile fibres.  For fibres
> 10 µm in length - i.e. fibre lengths in the reported range for carcinogenicity - the
clearance half-time was estimated to be eight years.  In other words, the tissue
bio-persistence of chrysotile fibres in this study seems substantially more prolonged
than in rodent experiments, and presumably corresponds to persistent high chrysotile
fibre concentrations for many years after cessation of occupational exposure in
humans, as discussed in paragraphs 5.112 - 5.113.  It is also notable that theconcentration of 6,250,000 chrysotile fibres mentioned in those paragraphs (for an
individual but by no means unusual patient) is probably above the level at which
Rogers et al. [2] identified an odds ratio for mesothelioma of > 8.5 (even allowing for
differences in fibre size between the two different laboratories), and even the duration
of 16 years after exposure stopped (as opposed to its commencement:  24 years) falls
into the lag-time range lung cancer induction by asbestos.
• Studies like this suggest that clearance mechanisms can be overwhelmed and break
down at occupational levels of exposure in humans, with the existence of a long-term
sequestered fraction of chrysotile fibres.
5.438  Mesothelioma rates in men and women in Sweden:   attached to this Endnote is a recent paper
by Jarvholm et al. [3] on trends in mesothelioma incidence in Sweden, which re-emphasizes some of
the points made earlier in this report.
D. 
COMMENTS BY THE PARTIES ON THE RESPONSES FROM THE EXPERTS
1. Canada
5.439  Canada is pleased that the experts agree with Canada on certain crucial aspects of the debate
in this case.  Most importantly they opine that:
• Chrysotile is significantly safer than amphibole asbestos (three of the four experts
agree);
• there is no risk to the public from low-level environmental exposure to chrysotile or
from exposure in buildings that contain chrysotile (all of the experts agree);
• there is no risk to workers in mines or factories where use of chrysotile is controlled
(three of the four experts agree);  and
• there is no risk to "handymen" or "do-it-yourselfers" who disturb chrysotile products,
because their exposure is intermittent and thus inconsequential (three of the four
experts appear to agree).
5.440  In short, although the experts agree on the inadequacy of a data (statistical limitation to
support a threshold), their findings are consistent with the view that low levels of exposure toWT/DS135/R
Page 341
chrysotile asbestos create no detectable health risks.  Indeed, the only population that the experts view
as having problematic exposure is tradesmen, e.g., plumbers, electricians and mechanics, who disturb
or modify chrysotile cement and friction products.  At this point, the experts and Canada diverge; also,
at this point, the experts stray beyond their specialities (as several admit).  Canada maintains that
adequate controls for these exposures can be developed and applied and has set forth such controls inComments to Experts' Answers to Question 5.
5.441  Several other aspects of the experts' answers require comment.  Some of the responses of the
experts appear not to distinguish between chry sotile and amphibole exposure, and between modern
uses (e.g., chrysotile friction and cement products) and historical uses (e.g., insulation containing
amphiboles).  In many places, for example, the experts appear to draw conclusions regarding
chrysotile based in part or in whole on data from individuals exposed to amphiboles and/or
amphiboles and chrysotile.  This is of greatest concern to Canada regarding the experts' conclusionson tradesmen; as the experts no doubt agree, the greatest risk to tradesmen is not exposure to modern
chrysotile products, but the disturbance of flocki ng or insulation containing amphiboles.  Similarly,
the experts do not always distinguish peak and cumulative exposures.  For the purposes of defining
health risks, the cumulative measure, not the peak measure, is key.
5.442  It is crucial that this proceeding forms on the pertinent issues.  The key issue is whether
exposure to modern uses of chrysotile can be controlled to ensure worker safety or if a total ban is
required to achieve an equivalent level of safety.  The experts' answers help to focus the proceeding on
tradesmen exposure.
Question 1(a)
5.443  Canada believes that the Panel should take note of the clarifications to this question proposed
by Drs. de Klerk and Musk.  The former writes that "the more relevant question here is: who is likely
to receive the most exposure and therefore have the greatest risk of disease".  Dr. Musk rephrases the
question in almost identical terms, taking the expression "risk of exposure" to mean "who is most
likely to receive the most exposure and therefore be at the greatest risk of developing asbestos-relateddisease".  In Canada's view, because the evidence suggests different risk per unit fibre exposure in
different sectors, it is the combination of level of exposure, duration of exposure and risk per unit fibre
exposure that is important.
5.444  The experts have confirmed that any risk from exposure to chrysotile will depend on the
nature of an individual's specific occupational setting and the risk per unit fibre exposure in that
setting, certain sectors being the subject of more stringent controls than others.  For example, the
experts echo the Parties' agreement to the effect that the mining and manufacturing sectors havesuccessfully controlled the risks to which their workers had previously been exposed.  Certain settings
pose lower risk per unit fibre exposure than others do.
5.445  Canada does not disagree with the statement that the so-called secondary user sector is the
most diverse.  Canada nevertheless understands that the experts do not believe that the diversity of this
particular workforce is to be considered the only factor that may contribute to a greater likelihood ofexposure;  rather, as Dr. Musk puts it, "the risk of developing asbestos-related disease [...] (also)
depend(s) on [...] the type of asbestos being produced  or used or otherwise encountered.   It would
also depend on the conditions of work such as ind oors versus outdoor etc."  As the Panel also knows,
the specific uses or products also entail more or less risk.
5.446  Canada does not believe that the diversity of this workforce precludes effective control.  The
diversity of a specific workforce is not indicative of the quality of the work practices actually
observed by the members of that workforce.  A ty pical construction site offers numerous examples of
sound safety practices: from hard hats to proper fo otwear, from the use of common sense to followingWT/DS135/R
Page 342
trade-specific work practises, measures are taken to insure safety and avoid trauma.
5.447  Canada notes that the experts have not commented on the assertion by the
European Communities that there is a correlation between the amount of chrysotile used by France
and the incidence of asbestos-related disease.  Clearly no such correlation can be made, in logic or in
fact.  The logic on which the European Communities purports to base this assertion is a sophism, andshould be dismissed accordingly.  From a factual poi nt of view, the following factors suggest that the
correlation is false: the relative difference in potency and in biopersistence of amphiboles and
chrysotile, the historical uses of each fibre type, and the differences in risk per unit fibre exposure in
different sectors.
5.448  Canada notes that Dr. Infante assimilates friable amphibole or mixed fibre type exposure
circumstances to those of high-density chrysotile  products, thereby answering the wrong question.  He
correctly identifies worker contact with insulation as being the "typical scenario" in which exposure toasbestos will occur.  But most insulation is friable, as opposed to high-density, and most friable
insulation products contained amphiboles or mixed fibr e types.  It is not clear how this answer based
on friable mixed asbestos products responds to a question relating solely to safety of high-density
chrysotile products.
Question 1(b)
5.449  Canada takes note that the experts have indicated that the risk of human health associated with
the various uses of chrysotile throughout its life cycle is overwhelmingly a workplace issue, and
therefore not related to the "handyman".28
Question 1(c)
5.450  The answers given by the experts indicate th at, on their own, chrysotile cement products do
not pose a health risk because of their normal weathering, erosion or general degradation, and that
"there is little or no dispute among experts on this issue".29
5.451  Canada wishes to draw the attention of the Panel to the results of the investigation carried out
by the Western Australia Advisory Committee on Hazardous Substances (WAACHS), cited by
Dr. Henderson.30 This report contains different sections describing asbestos cement products, their
production and use and their health effects, as well as surveys of schools and other relevant
measurements of asbestos concentrations.  In addition to pertinent recommendations, the report
contains several appendices, including one on the Effects of Asbestos Cement Products – A Review of
the Literature and another on Acceptable Air Concentrations of Asbestos Fibres in the General
Environment , both prepared by one of the experts to this Panel, Dr. de Klerk.
5.452  On low level air concentrations, Dr. de Klerk writes:  "[M]ost of these estimates are on or
below the level of what the Royal Society would consider acceptable [...] The 1986 IPCS report did
not even bother to estimate such risks and summarised the risk exposure unrelated to occupation as
being undetectably low".31 Indeed, the executive summary of the WAACHS report indicates: "[...]
[T]he level of risk is low enough to be considered to be negligible relative to these other risks in our
                                                     
28Canada notes that, according to Dr. Henderson: "[ f]rom my perspective, this is overwhelmingly a
workplace issue […]".
29Henderson, answer to Question 1(d).
30Henderson, p. 54, citing Multiple Authors, Asbestos Cement Products.  Report by the
Western Australia Advisory Committee on Hazardous Substances , Perth, 1990, hereinafter the WAACHS
Report.
31De Klerk, N., Acceptable Air Concentrations of Asbestos Fibres in the General Environment.  A
Review of Scientific Evidence and Opinion  in the WAACHS Report, Appendix 3, p. 10.WT/DS135/R
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society".32 Similarly, in his report to the Panel, Dr. Henderson underlines that compared to the fibre
concentrations observed in the vicinity of asbestos-cement roofing, "a greater risk to health would
arise from [workers ] falling from or through the roofs".33
5.453  High-density chrysotile on buildings has been extensively studied.  Indeed Teichert found the
following: "the study of emission conducted on coated and uncoated roofing materials revealed lowasbestos fibre concentrations, even though severe corrosion was observed on uncoated asbestos
cement roofs and a considerable quantity of material containing asbestos could be removed by
blowing or suction.  The asbestos fibre concentrations that were measured in populated areas are well
below the level considered acceptable by the Health Authorities of the Federal Republic of Germany,
i.e. clearly below 1000 fibres/m
3 (or 0.001 f/ml)".34 Felbermayer and Ussar, for their part, write: "a
comparison of the asbestos fibre concentrations in those areas with and without asbestos-cement
roofing (...) lead to the conclusion that there is no statistical significant connection between the use of
asbestos-cement materials and the asbestos fibre concentrations found in the various measurement
areas."35
5.454  Finally, Canada would like to bring to the Pa nel's attention the following recommendation of
the WAACHS report, which is: "[A]n asbestos cement roof, which has not deteriorated to an extent
where physical safety or structural integrity is of concern, should not be replaced.  In addition, an
asbestos cement roof should not be treated with a coating on the basis of risk to health.  Other asbestos
cement products are generally less prone to deterioration and do not require attention for health
purposes".36 Nonetheless, many chrysotile-cement products  are coated with protective sealant agents.
Question 1(d)
5.455  The experts agree that the degree of risk to the health of workers intervening on high-density
chrysotile cement products will depend on the manner in which an intervention is carried out.  As
noted by Dr. Infante in his response to question 1(e) , "the extent of the exposure to the worker (...)
would depend on the nature of the intervention, e.g., the circumstances under which the chrysotile
asbestos product is manipulated in terms of work practices, the controls, or lack of controls in placeand the type of personal protective equipment provided to the worker".  Dr. Henderson illustrates this
proposition when he writes that "cutting (chr ysotile-cement) with hand saws produced lower
concentrations."
5.456  Canada accepts that abrasion and cutting of high-density chrysotile products can release
materials.  However, the degree of exposure, if any, will depend on the methods and controls used.
Canada notes that the experts disagree as to the exact composition of the materials that would be
released by such interventions (see question 1 (f)), although there is apparent agreement that cutting
chrysotile cement releases crystalline silica, an IARC Class 1 carcinogen.
37 Cutting chrysotile cement
using simple work practices such as those outlined in ISO Standard 7337 will therefore provide
protection from any potentially harmful material contained in such a product.  Wetting the productbefore cutting and/or using commonly found suction attachments when sawing are techniques that can
be used as added, but perhaps unnecessary, precautions.  A final safety barrier would be for the
worker to wear a facemask: this step would render it virtually impossible for the worker to inhale dust.
                                                     
32WAACHS Report, p. 2.
33Henderson, answer to Question 1(b).
34Teichert, U., Immissionen durch Asbestzement-Produkte, (1986) Teil 1 Stub Reinhaltung der Luft,
Vol. 46, No. 10, pp. 432-434.
35Felbermayer, W., Ussar, M. B., Research Report: Airborne Asbestos Fibres Eroded from Asbestos
Cement Sheets , (1980) Institut für Umweltschutz und Emissionesfragen, Leoben, Austria.
36WAACHS Report, p. 4.
37Infante, answer to Question 1(f).WT/DS135/R
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5.457  Neither the European Communities nor the experts have demonstrated that such practices
would subject workers to cumulative exposures presenting health risks.  An American survey
estimated that a worker would spend less than 1/16th of his work time on tasks that would involve
aggressive interventions on chrysotile-cement of th e type susceptible of releasing any substantial
amount of dust.38  Canada submits that the European Communities have not identified any population
of workers that would be subject to a detectable risk because of professional contact with high-density
chrysotile cement.  The European Communities' contentions vis-à-vis  the "handyman" are therefore
even less convincing (see next answer).
Question 1(e)
5.458  Canada agrees with Dr. Henderson's conclusion that "occasional interventions (...) would
predictably produce low cumulative exposures, with a lower risk (...)". Dr. Henderson also affirms thatfor "electricians, carpenters, plumbers, insulation workers and so forth", "it is acknowledged that most
if not all these mesotheliomas are a consequence of exposure to (...) a mixture of asbestos types,
including chrysotile and one or more of the amphiboles."
5.459  The Panel has not been presented with evidence that contradicts Canada's assertion that
occasional interventions do not pose a risk that is significantly different from zero (statistically).Therefore, the experts have not validated the EC's claim that an alleged risk for workers or the
"handyman" is something more than undetectable.
5.460  Nor has the Panel been presented with evidence or expert opinion that supports the
European Communities' claim with respect to the "handyman".  Given that cohorts exposed to
relatively high concentrations of chrysotile over entire occupational lifetimes show no increase ofdisease, it is unlikely that occasional interven tions by a "handyman" would produce more than an
equally undetectable risk.  Obviously the "handyman" or bricoleur du dimanche  will not encounter
high-density chrysotile-cement products on a daily basis, nor devote his "handiwork" exclusively or
principally to cutting such products.  Rather, the typical "handyman" will rarely, if ever, come into
contact with chrysotile cement products, let alone be sawing them.
5.461  The Panel should note that no evidence has been presented that shows any fatality in workers,
let alone in "handymen", who would have been subj ect to any form of exposure, high or low, from
contact with chrysotile cement products;  the argument presented by the European Communities has
been based entirely on hypothetical scenarios.
39
Question 1(f)
5.462  There is debate in the scientific community and among the experts appointed by the Panel as
to the exact physical and chemical composition of what is contained in dust from certain interventions
on chrysotile cement products.  Dr. Infante writes, however, that this dust (indeed, all cement dust)
will contain "crystalline silica", a known IARC Class 1 carcinogen found in all cement.
5.463  A 1992 IARC publication determined that "in asbestos-cement products, the asbestos fibres
usually represent 10-15 per cent of the total weight and are embedded in the cement.  Therefore, it isnot certain a priori that dust generated from asbestos-cement products will have the same effect as
dust from pure chrysotile.  [I]n asbestos-cement dust most of the asbestos fibres form aggregates with
cement particles ...  [t]hose which do not form aggregates ... appear to be coated with a calcium-
containing layer.  In absorption experiments, the asbestos-cement dust behaves more like cement dust
                                                     
38CONSAD Research Corporation, 1990, No. 8282.
39See Canada's Comments to Questions 5(c) and (e).WT/DS135/R
Page 345
than like asbestos dust."40 Because the surface properties of asbestos fibres are altered by certain
heating, pH, and abrasion conditions41, it can be deduced that the composition and effect of the final
aerosol would be different than that suggested by st udies of concentrations of fibres alone.  And again,
controlled use procedures limit release, and proper breathing equipment precludes exposure.
Question 1(g)
5.464  Canada believes that the Panel was not presented with any quantification of this risk, or
indeed its existence.  Dr. Infante describes how the removal of chrysotile cement panels can be
accomplished with negligible release of respirable fibres.  Most other chrysotile cement products are
found in the form of underground water pipes.  Studies show that these products remain intact for
decades after installation.42  Hence, very little of this product will need to be disturbed.  Moreover, the
excavation and removal of pipes is not executed by manual labour, the bulk of any removal beingdone by heavy machinery.
5.465  The Panel should also note that the removal of chrysotile cement products does not generally
entail crushing.  Rather, if and when necessary, chrysotile cement products can be removed,
transported, and disposed of by means that do not constitute a detectable risk to human health.  The
French Circulaire 97-15 accomplishes this goal for the high-density products at issue in thisproceeding.
43  Also, if France is ensuring the safe removal and disposal of friable asbestos materials44
known to contain amphiboles or mixed fibre types, the Panel should conclude that the removal and
disposal of high-density chrysotile cement products can be accomplished even more safely,
since high-density materials are indisputably recognised, even by France, as much easier to manage
than anything in friable form.45
                                                     
40Characterization and Proprieties of Asbestos-Cement Dust,  in Biological Effects of Mineral Fibres,
Vol. 1, IARC Scientific Publications No. 30, Lyon, 1980, pp. 43, 49 and 50.
41Henderson, answer to Question 2.
42Canada notes that a study of 15 water supply systems in the State of Illinois U.S.A., where some
asbestos-cement pipes were up to 40 years old, and where the water was non-aggressive to moderatelyaggressive, shows no significant differences in the water before and after passing through the asbestos-cementpipe network: Hallenbeck, W. H., et al., Is Chrysotile Asbestos Released from Asbestos Cement Pipe into
Drinking Water , (1978) Journal of the American Water Works Association 70 (2): 97-102.
43Circulaire no. 97-15 du 9 janvier 1997 relative à l'élimination des déchets d'amiante-ciment générés
lors des travaux de réhabilitation et de démolition du bâtim ent et des travaux publics, des produits d'amiante-
ciment retirés de la vente et provenant des industries de fabrication d'amiante-ciment et des points de vente ainsique tous autres stock .
44Circulaire no. 96-60 du 19 juillet 1996 relative à l'élimination des déchets générés lors des travaux
relatifs aux flocages et aux calorifugeages contenant de l'amiante dans le bâtiment .
45Canada notes that French regulations indeed reco gnize a difference in disposal proscriptions between
"les matériaux friables" and "l'amiante liée" – see Note DPPR/SDPD/BGTD/LT/LT no. 97-320 du 12 mars 1997
relative aux conséquences de l'interdiction de l'amiante et à l'élimination des déchets, which is as follows:
"III. – Quelles sont les fillières d'élimina tion des déchets cont enant de l'amiante?
"Deux circulaires ont été diffusées, l'une le 19 juillet 1996 pour les déchets issus des travaux relatifs
aux flocages et aux calorifugeages, l'autre le 9 janvier 1997 pour les déchets d'amiante-ciment.
"Les fillières d'élimination des déchets contenant de l'amiante autres que ceux qui ont fait l'objet des
deux cricularies précitées peuvent être déterminées par analogie aux prescriptions de ces deuxcirculaires:
- Les matériaux friables, c'est-à-dire les matériaux  susceptibles d'émettre des fibres sous l'effet
de chocs, de vibrations ou de mouvements d'air, sont assimilables aux flocages et auxcalorifugeages.  Ils devront être éliminés dans des installations de stockage des déchets
industriels spéciaux ou dans l'unité de vitrification;
- pour les déchets contenant de l'amiante liée, trois cas sont envisageables:WT/DS135/R
Page 346
Question 1(h)
5.466  See comments on previous question.
Question 1(i)
5.467  Canada wishes to add the following comments on the answers to this question.  Once removed
from a building, a chrysotile cement panel, even if broken into several pieces, remains as intact as
when it formed part of that building.  Studies refe rred to above indicate that chrysotile cement roofing
does not contribute ( < 0.001 f/ml) to the levels of chrysotile occurring naturally in the environment.
Likewise, chrysotile cement piping is generally found below ground, and therefore does not contributeto the levels of chrysotile naturally occurring in the atmosphere.  If removed from roofing, or if
excavated and removed from a water system, chrysotile cement products are transported to a landfill
and buried anew beneath a layer of earth.  Conseque ntly, Canada is of the view that used chrysotile
cement products can be eliminated safely.
5.468  Canada also notes that recent technology has enabled safe (in some cases, on-site) disposal of
chrysotile products.  For example, chrysotile can be treated with chemicals and/or subjected to high
temperatures so as to render the end product entirely harmless and, in fact, suitable for enhancing the
quality of soils.  For example, in the United States, a foam has been developed that eliminates the risk
associated with removing asbestos from buildings;  when this product is sprayed onto asbestos
fireproofing, the fibres turn into harmless globs of magnesium silica.  A U.S. building contractor
recycles asbestos by subjecting it to a chemical bath and high temperatures resulting in a totally inert
end-product suitable for soil improvement.  A Japanese company, responding to a government lawmandating pollution-free disposal of asbestos, melts asbestos into harmless glass.
46
Question 2
5.469  Canada has advocated the use of chrysotile in high-density products only;  textiles are not of
that category, and had been banned in France prior to the adoption of the measure that is the subject ofthis dispute.  Friction materials using chrysotile ha ve not been shown to constitute a risk to human
health.
47  Indeed, the contrary is probably true:  lesser braking action of linings manufactured without
                                                                                                                                                                    
- Si les déchets sont composés d' amiante associée uniquement avec des  matériaux
inertes, ceux-ci pourront être éliminés conformément à la circulaire du 9 janvier
1997 relativement à l'élimination des déchets d'amiante-ciment;
- si l'amiante est associée avec des matériaux , qui lorsqu'ils deviennent des déchets,
sont classés déchets ménagers et assimilés,  c'est par exemple le cas des dalles vinyl-
amiante, ils pourront être éliminés dans des installations de stockage de déchetsménagers et assimilés;
- si l'amiante est associée avec des matériaux , qui lorsqu'ils deviennent des déchets,
sont classés déchets industriels spéciaux, ils devront être éliminés soit dans desinstallations de stockage de déchets industriels spéciaux, soit dans l'unité devitrification.
"Dans tous les cas, l'industriel ou l'entreprise devra fournir des éléments permettant
de caractériser les déchets afin de dé terminer les filières d'élimination adaptées."
46Acid v. Asbestos , Discover, Information Access Company, No. 7, Vol. 20, July 1, 1999, p. 102.;
Contractor Recycles Asbestos for Re-Use in Construction , Air Conditioning, Heating & Refrigeration News,
Business News Publishing Company, Vol. 194, No. 2, January 9, 1995, p.1 ; Kent Firm Fires up New Asbestos-
Disposal System , Puget Sound Business Journal, Vol. 13, No. 14, August 21, 1992, p. 9; Japanese Plant Turns
Asbestos into Glass , American Metal Market, Vol. 100, No. 145, July 28, 1992, p. 4.
47Appendix A on Control Use in the Friction Industry, Canada's Comments to Question 5(a), contained
in Annex IV to this Report.WT/DS135/R
Page 347
chrysotile is cited by France as the safety concern for which it exempted certain military vehicles from
the purview of the Decree.48
Question 3(a)
5.470  Three of the four experts concur with the position of Canada and the WHO that a clear
distinction must be made between chrysotile and amphiboles.  Dr. Musk believes that "there is a need
to distinguish chrysotile asbestos from amphiboles based on the epidemiological data at least" and that
the relative pathogenicity of some amphiboles to chry sotile may, in some cases such as mesothelioma,
be 100 to 1.  Dr. de Klerk affirms that the "epidemiological evidence is clear that, for a given quantity
(intensity and duration) of exposure, chrysotile imparts less risk than amphibole fibres." The
difference in pathogenicity is, according to Dr. de Klerk, up to 50-fold in the case of lung cancer and
up to 100-fold for mesothelioma.  Dr. Henderson concludes that:  "a clear distinction should be madebetween chrysotile and the amphibole forms of asbestos."
5.471  Domestic legislation and international standards have long recognized the relative
pathogenicity of different asbestos fibre types by permitting higher exposures to chrysotile than to
amphiboles.  In the European Communities in 1998, for example, the maximum exposure level for
amphiboles was 0.3 f/ml, whereas it was 0.6 f/ml for chrysotile.  In Canada (Quebec), it is 0.2 f/ml forcrocidolite and 1 f/ml for chrysotile.  Similarl y, international instruments such as the ILO's
Convention 162  and Recommendation 172 advocate an outright ban on crocidolite, while
recommending replacing chrysotile if and only if  safer substitutes exist.
5.472  Dr. Infante acknowledges epidemiological data to the effect that chrysotile is less dangerous
than amphiboles, but sees no basis for distinguishing between asbestos fibre types.  Dr. Infante'sdissident view to the question of relative pathogenicity between asbestos fibres – one which echoes
the European Communities' argument but simply begs the question – is that because amphiboles and
chrysotile are both classified as carcinogens, no distinction should be made.
5.473  In 1998, the WHO affirmed that a distinction should be made between chrysotile and
amphiboles because using data from exposures to amphiboles "contribute[s] less to our understandingof the effects of chrysotile, due to concomitant exposure to amphiboles."
49  The distinction between
chrysotile and amphiboles is crucial in this instance since the current problem of asbestos in France is
due to past uses of friable materials, high-level exposures, and the use of amphibole fibres.  The
distinction between chrysotile and amphibole asbestos is also important because the extrapolations
made by INSERM to assess the risks associated with chrysotile are based on exposures to amphibole
fibres in proportions of up to 100 per cent in circumstances which have nothing to do with the current
uses of chrysotile.50
Question 3(b)
5.474  Physical properties, as well as chemical properties that determine biopersistence, are
identified as relevant factors of pathogenicity by Drs. Musk, Henderson and de Klerk and by the
WHO.51
5.475  Dr. de Klerk, for example, has written that:
                                                     
48Article Ier 2a) Arrêté du 17 mars 1998 relatif aux exceptions à l'interdiction de l'amiante .
49WHO,  IPCS Health Criteria 203 on Chrysotile , WHO, Geneva, 1998, p. 107.
50See notably INSERM Report, p. 213.
51WHO,  IPCS Health Criteria 203 on Chrysotile , WHO, Geneva, 1998, p. 51: "[I]t is considered that
the potential respiratory health effects related to [...] ai rborne concentrations, patterns of exposure, fibre shape,
diameter and length (which affect lung deposition and clearance) and biopersistence."WT/DS135/R
Page 348
"[T]he important carcinogenic properties of asbestos are related to the physical properties of size and
shape of the fibers, and to their quantity.  To cause any harm, fibers must be able to reach the targetorgans [...].
"  […]
"[I]n all occupationally exposed series of mesotheliomas, none have occurred in cohorts whereamphibole asbestos has never been used or detected.  Chrysotile asbestos has not been directlyimplicated in any case of peritoneal mesothelioma .  [...] The main differences between the effects of
chrysotile and amphibole fibers are
:
1. Industries using a mixture of asbestos types have higher rates of disease than similar industries
using only chrysotile.
2. Chrysotile fibers are eliminated more readily from the lungs than are amphibole fibers.3. Much smaller doses of amphibole fibers than chrysotile fibers can induce mesothelioma."
52
5.476  All four experts recognize the lower biopersistence of chrysotile.  INSERM, citing numerous
studies, also acknowledges the lower biopersistence of chrysotile:
"Les études expérimentales ont montré que la biopers istance des fibres de chrysotile était inférieure à
celle des amphiboles (Wagner et al., 1974;  Davis et al.;  Davis and Jones, 1988, Churg et al., 1989;
Churg, 1994)."53
5.477  Dr. Infante identifies the physical characteristics as also relevant to the relative pathogenicity
of asbestos fibre types, but, unlike the three other experts and the WHO, believes that the role ofbiopersistence, through the element of solubility, "is not so clear."
5.478  Chrysotile fibres are "curly" and downy while amphibole fibres are straight and rigid like
needles.
54  Drs. de Klerk and Musk both specifically address the "straightness" element.  The WHO
has observed that:
"Inhalation of respirable straight fibres [amphi boles] is reported to be associated with greater
penetration to the terminal bronchioles than in the case of 'curly' fibres [chrysotile]."55
5.479  Once they have entered the respiratory tract, chrysotile asbestos fibres, because of their curly
shape, are more easily cleared by the mucociliary process than are straight and rigid amphibole
fibres.56 Dr. Henderson writes:  "[I]t is well known that chrysotile fibres are cleared more rapidly than
amphiboles, especially in long-term studies (Churg, 1994)."57  This is confirmed by a 1994 European
study by Dr. Albin:  "[A]dverse effects are associated rather with the fibres retained (amphiboles),
than with the ones being cleared (largely chrysotile)."58
5.480  For chrysotile fibres that do nonetheless manage to become lodged in the lungs, the solubility
of the fibres and the action of macrophages come into play to make chrysotile a much less potent
fibre.  First, as the WHO recognizes, chrysotile has a lower resistance than amphiboles in acidic
                                                     
52de Klerk, N.H. and Armstrong, B.K., The Epidemiology of Asbestos and Mesothelioma  in Malignant
Mesothelioma, Henderson, D.W. et al., eds. Hemisphere Publishing, New York, 1992, 223 at p. 230.
53INSERM Report, p. 92.
54WHO, IPCS Health Criteria 203 on Chrysotile, WHO, Geneva, 1998, p. 11.
55WHO, IPCS Health Criteria 203 on Chrysotile, WHO, Geneva, 1998, p. 11.
56Kumar, V., Cotran, R. and Robbins, S., Basic Pathology , 6th Ed., London, Saunders Co., 1997,
p. 228.
57Henderson, see above para. 5.112.
58Albin, M., et al., Retention Patterns of Asbestos Fibres in Lung Tissue Among Asbestos Cement
Workers  (1994) 51 J. of Occupational Environmental Medicine 205.WT/DS135/R
Page 349
environments such as the lungs.59 Second, the macrophages responsible for eliminating fibres from the
lungs are able to deal more easily with chrysotile fibres than with amphibole fibres.  A 1997 report of
the French Government (G2SAT) referred to by the European Communities, recognizes that as a
result of the chemical dissolution process that takes place in the lungs, carcinogen activity is
subsequently practically nil:
"Il a été démontré que le chrysotile est nettement plus facilement éliminé du poumon humain que les
autres formes [amphiboles].  Par ailleurs, il ne présente pratiquement plus d'activité cancérogène (parinjection intra-cavitaire) après attaque acide, laquelle dissout la majorité du magnésium."
60
5.481  Dr. Wagner, in his 1988 study of asbestos-related diseases, concluded:
"Chrysotile is the least harmful form of asbestos in every respect and [...] more emphasis should be laid
on the different biological effects of amphibole and serpentine asbestos fibre."61
5.482  It should also be noted that gravimetric comparisons between amphiboles and chrysotile –
widely used in the past in experimental work – tend to grossly misrepresent the relative pathogenicity
of the fibres.  According to the WHO, chrysotile "may contain more than 10 times more fibres per unit
weight."62 Recent studies that use both the fibre mass and the number of fibres as dose units confirm
that, on a per fibre basis, amphiboles are far more pathogenic than chrysotile.63
Question 3(c)
(i) Asbestosis
5.483  Dr. Henderson asserts that:  "[T]he amphibole varieties of asbestos appear to be substantially
more pathogenic than chrysotile for the induction of asbestosis and mesothelioma."  According to
Dr. Henderson, "[A]sbestosis is a dose-dependent disorder with a threshold effect [...] There is
widespread agreement that asbestosis in general is a consequence of high intensity exposure (or lower
intensity but more prolonged exposure)."
5.484  INSERM also supports the existence of a threshold for asbestosis,64 and according to
INSERM, current low-level exposures to chrysotile pose no threat of asbestosis:  "les expositions
actuellement relevées dans les industries directement utilisatrices d'amiante devraient conduire à la
disparition des cas d'asbestose confirmée (Doll et Peto, 1985)."65  It is clear, therefore, that asbestosis
is not relevant to this dispute.
(ii) Lung Cancer
5.485  Dr. Musk believes that lung cancer risks are more than ten times greater in the case of
amphiboles than in the case of chrysotile asbestos.  Dr. de Klerk suggests the difference may be up
to 50-fold.
                                                     
59WHO,  IPCS Health Criteria 203 on Chrysotile , WHO, Geneva, 1998, p. 4.  Kumar, V., Cotran, R.
and Robbins, S., Basic Pathology , 6th ed., London, Saunders Co., 1997, pp. 227; INSERM Report, p. 396.
60INRS, Rapport du Groupe scientifique pour la surveillance des atmosphères de travail (G2SAT) ,
1997, p. 47.
61Wagner, J.C. et al. , Correlation between Fibre Content of the Lung and Disease in East London
Asbestos Factory Workers , (1988) 45 British Journal of Industrial Medicine 305.
62WHO, IPCS Health Criteria 203 on Chrysotile, WHO, Geneva, 1998, p. 69.
63See WHO,  IPCS Health Criteria 203 on Chrysotile , WHO, Geneva, 1998, p. 69 and 81; INSERM
Report, Table 2, p. 196; EPA, Integrated Risk Information System, Asbestos , Document No. CASRN 1332-21-
4 on-line: EPA, <http://www.epa.gov/ngispgm3/ir is/subst/0371.htm> (access date: June 10, 1999).
64INSERM Report, p. 327.
65INSERM Report, p. 327.WT/DS135/R
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5.486  Dr. Henderson states that the "greater carcinog enicity of the amphiboles [...] appears not to
extend to the induction of lung cancer"66 but he admits that "chrysotile is implicated in one of the
lowest rates of asbestos-associated lung cancer (in Quebec chrysotile miners and millers)."67
Dr. Henderson's reluctance to conclude the greater carcinogenicity of amphiboles seems to be causedby the results of Dr. Dement's study of the Ch arleston, South Carolina asbestos textile industry.
68
5.487  The Charleston data has recently been revisited by Bruce Case, André Dufresne,
A.D. McDonald, J.C. McDonald and Patrick Sébastien in a study released in Maastricht in
October 1999 at the VIIth International Symposium on Inhaled Particles , a symposium attended by
some of the world's leading experts.  This study shows that a significant amount of crocidolite and
amosite fibres was found in the textile workers' lungs.  This analysis sheds new light on the issue and
explains the extreme results of the original study by Dr. Dement69 and the subsequent study by
Dr. Stayner.70 These studies of textile workers exposed to crocidolite and amosite can thereby no
longer be used to demonstrate the risks associated with chrysotile fibres.
5.488  The seminal findings of Case et al . may cause Dr. Infante to reconsider his view – based
principally on the studies by Dement and by Stayne r – that "chrysotile may be more potent in causing
lung cancer."
(iii) Mesothelioma
5.489  On the relative risks of mesothelioma, Dr. Henderson observes that:  "[T]here is general
though not universal agreement of a differential potency between the amphiboles versus [chrysotile]
for mesothelioma induction."  He believes amphiboles may be greater than 60 times more likely than
chrysotile to induce mesothelioma.71  Drs. Musk and de Klerk estimate that the potency of amphiboles
may be 100 times greater.  And although Dr. Infante also concedes that "amphiboles may be morepotent in causing mesothelioma", he fails to conc lude from this that a distinction exists between
chrysotile and amphibole fibres.
5.490  This distinction is also emphasized in pathology medical reference books:
"It is important to make the distinction between various forms of amphiboles and serpentines, because
amphiboles, even though less prevalent, are more pathogenic than the serpentine chrysotile, particularlywith respect to induction of malignant pleural tumors (mesotheliomas).  Indeed, some studies haveshown the link is almost invariably to amphibole exposure."
72
(iv) Other Diseases
5.491  Dr. de Klerk links other asbestos-related diseases such as pleural plaques and pleural
thickening more with amphiboles than with chrysotile:  "[P]leural plaques appear to be more common
among anthophyllite workers than others while crocidolite workers have more diffuse pleural
                                                     
66Henderson, see above paragraph 5.146.
67Ibid.
68Ibid.
69Dement, J.M., Brown, D.P. and Okun, A. , Follow-Up Study of Chrysotile Asbestos Textile Workers:
Cohort Mortality and Case-Control Analyses,  (1994)  26 American J. of Industrial Medicine 431.
70Stayner, L., Smith, R., Bailer, J., Gilbert, S., Steenland, K., Dement, J., Brown, D., Lemen, R.,
Exposure-Response Analysis of Risk of Respiratory Disease Associated with Occupational Exposure toChrysotile Asbestos,  (1997) 54 Occupational Environmental Medicine 646.
71Henderson, see above para.5.103.
72See Kumar, V., Cotran, R. et Robbins, S., Basic Pathology , 6th Ed., London, Saunders Co., 1997 at
pp. 227-28.WT/DS135/R
Page 351
thickening, and benign asbestos pleurisy also seems to be more common after crocidolite exposure."
Dr. Henderson also raises the issue of types of fibres in dealing with parietal pleural plaques.
Question 4(a)
5.492  Drs. de Klerk and Musk agree that the existing epidemiological data show no excess health
risks at low-level chrysotile exposures.  Dr. Henderson is not aware of exposure-response data for
low-level exposures.  Dr. Infante again relies heav ily on Stayner's study, a study on one single cohort
of textile workers now known to be based on textile workers exposed to amphiboles as well as to
chrysotile.73  Newhouse and Sullivan studied exposures to chrysotile in the manufacturing setting:
"[I]t is concluded that with good environmental control, chrysotile asbestos may be used in
manufacture without excess mortality."74
5.493  Thomas et al. concluded similarly for an asbestos cement factory:  "[T]hus the general results
of this mortality survey suggest that the population of the chrysotile-cement factory studied are not at
any excess risk in terms of total mortality, all cancer mortality, cancers of the lung and bronchus, or
gastrointestinal cancers."75
5.494  There is clearly no increased risk of lung cancer in the friction products manufacturing
industry at levels below 356 f/ml-years.  This means that there was no chrysotile-related increase inlung cancer risk for persons exposed to the equivalent of up to 8.9 f/ml for 40 years.  Even if we
allowed a 10-fold protection factor this would be 0.9 f/ml for 40 years for lung cancer.
76  M o r e
recently in 1997, McDonald et al. concluded from th e analysis of a cohort of 10,000 asbestos workers
with average exposures to 45 f/ml over 20 years  that:  "[...] from the point of view of mortality [...]
exposure in this industry to less than 300 mpcf.years [approximately 45 f/ml over 20 years] has beenessentially innocuous."
77 This unequivocal data comes from the longest term study of the largest group
of chrysotile workers ever conducted.  A review of eight studies of cohorts exposed to chrysotile only
led its authors to conclude:  "[T]he evidence for chrysotile shows that for lung cancer and
mesothelioma there exist levels of exposure below which risks are for practical purposes zero."78
Question 4(b)
5.495  According to Dr. Henderson, whether a threshold exists generally is a much-debated issue.
For the case at hand, i.e . low-level exposure to chrysotile, Dr. Henderson states that:  "[I]f a threshold
exists, it must lie somewhere in this area, betw een no exposure, low-level environmental exposure,
and low-level occupational exposure."  He also points out that, although no threshold has been
identified, " [a]t the same time, no increase in risk of meso thelioma has been identified at very low-
levels of exposures."  Drs. Musk and de Klerk agree that the epidemiological data show an absence of
risk at low exposure levels, but are unwilling to commit to the existence of a threshold.  If there is
                                                     
73See Canada's Comments to Question 3.
74Newhouse, M.L. and Sullivan, K.R., A Mortality Study of Workers Manufacturing Friction Materials,
(1989) 46:3 British Journal of Industrial Medicine 176, p. 176.
75Thomas, H.F., Benjamin, I.T., Elwood, P.C. and Sweetnam, P.M., Further Follow-Up Study of
Workers From an Asbestos Cement Factory,  (1982) 39:3 British J. of Industrial Medicine 273, p. 275.
76Berry, G. and Newhouse, M.I., Mortality of Workers Manufactu ring Friction Materials Using
Asbestos , (1983) 40 British Journal of Industrial Medicine 1 at 6, p. 6.
77Liddell, F.D.K., McDonald, A.D. and McDonald, J.C., The 1891-1920 Birth Cohort of Quebec
Chrysotile Miners and Millers: Development from 1904 and Mortality to 1992 , (1997) 41 Annals of
Occupational Hygiene 13, p. 13.
78Browne, K. and Gibbs, G., "Chrysotile Asbestos – Thresholds of Risk" in Chiotany, K., Hosoda, Y.,
Aizawa, Y., eds., Advances in the Prevention of O ccupational Respiratory Diseases , Elsevier, Amsterdam, 1998
at p. 306.WT/DS135/R
Page 352
agreement that low level exposures show no increased health risk, admitting the existence of a
threshold is academic.
5.496  The extreme difficulty of proving a threshold scientifically is echoed by the
European Communities' DG XXIV Report:
"In fact, a threshold implies the demonstration that an effect does not occur at or under a given dose
level.  The unequivocal demonstration (i.e. identification) of a 'negative' is tantamount to impossible."79
5.497  The corollary to the proof of a threshold is the proof of the absence of a threshold.  The proof
that no threshold exists would need to explain the absence of an excess risk of lung cancer or
mesothelioma in chrysotile-only cohorts, as well as the lack of any chrysotile-related increase in lung
cancer mortality in workers exposed to less than 900 f/ml-years in the 10,000 miners and millersstudied in Quebec.
80   Dr. Henderson does acknowledge the existence of a threshold for asbestosis in
his answer to Question 3:  "Asbestosis is a lung de pendent disorder with a threshold effect [...] There
is widespread agreement that asbestosis in general is a consequence of high intensity exposure (or
lower intensity but more prolonged exposure)."  INSERM also supports the existence of a threshold
for asbestosis:
"La plupart des données épidémiologiques recueillies dans des populations professionnelles exposées
suggèrent que l'asbestose cliniquement et/ou radiologiquement caractérisée n'apparaît qu'à partir
d'expositions suffisamment élevées [...] un seuil minimal de 25 f/ml-années a ainsi été avancé (Doll et
Peto, 1985)."81
5.498  Why could there not be a threshold for other asbestos-related diseases?  Dr. de Klerk asserts
that:
"[I]t is now widely believed that the risk for chrysotile workers in fibrous cement and friction product
manufacturing is so slight as to be undetectable.  It is widely held that this kind of negligible risk level'threshold' exists at different levels for all types of asbestos for all relevant diseases."
82
5.499  Some experts advising the EC believe there is a threshold for diseases other than asbestosis:
"It is very likely that there is a practical level of exposure below which it will be impossible to detect
any excess mortality or morbidity due to asbestos.  [...] Thus, it is possible that there is a level of
exposure (perhaps already achieved in the general public) where the risk is negligibly small."83
5.500  This links to Dr. de Klerk's observation that:  "[T]he smaller the effect that needs to be
demonstrated, the larger the study needs to be."  Dr. Infante, who dismisses the Panel's question as
"moot", points out that "it is not possible to determine thresholds from epidemiological studies
because of the lack of statistical power to distinguish that the risk is virtually zero."  Canada argues –
                                                     
79DG XXIV, Opinion on a Study Commissioned by Dir ectorate General III (Industry) of the
European Commission on "Recent Assessments of the Hazards and Risks Posed by Asbestos and Substitute
Fibres, and Recent Regulation on Fibres World-Wide" , Environmental Resources Management, Oxford (opinion
expressed on 9 February 1998).
80Liddell, F.D.K., McDonald, A.D. and McDonald, J.C., The 1891-1920 Birth Cohort of Quebec
Chrysotile Miners and Millers: Development from 1904 and Mortality to 1992, (1997) 41 Annals of
Occupational Hygiene 13.
81INSERM Report, p. 327.
82de Klerk, N.H. and Armstrong, B.K., The Epidemiology of Asbestos and Mesothelioma,  in Malignant
Mesothelioma, Henderson, D.W. et al., eds. Hemisphere Publishing, New York, 1992, 223 at pp. 230-31.
83CEC, Report of the Working Group of Experts to the Commission of the European Communities:
Public Health Risks of Exposure to Asbestos , Oxford, Pergamon Press, 1977 cited in: WHO, Environmental
Health Criteria 53 for Asbestos and Other Mineral Fibres , WHO, Geneva, 1986, p. 43.WT/DS135/R
Page 353
epidemiological data in hand – just that low-level e xposures to chrysotile pose a risk that is "virtually
zero":  "un risque indétectable".  Dr. Infante uses Stayner's data once again to claim that the chrysotile
data fit with a linear no-threshold model.  With the new analysis on the Charleston cohort data
discussed above, this argument does not hold.84
Question 4(c)
5.501  Drs. de Klerk and Musk agree that there is epidemiological data indicating no increased risk at
low-level exposures, but the experts believe the linear model may be appropriate.  However,
"[W]hether or not it is a valid method is unknown."85  According to international experts from the
Health Effects Institute-Asbestos Review (HEI -AR), such as Julian Peto, David G. Hoel and
W. Nicholson, the linear model is not used for its validity, but precisely because it tends to
overestimate risk.86  Dr. de Klerk shares this view and states that the model provides a "conservative
estimate."
5.502  The limits of the linear model and the conditions under which extrapolations are made must
be clearly set out.  Extrapolations from high-level exposures and exposures to amphiboles should not
be taken at face value to ban chrysotile in today's context of low-level chrysotile-only exposures.
Canada's critical view of the linear model is supported by a 1999 report by the Australian NationalIndustrial Chemicals Notifications and Assessments Scheme (NICNAS) cited by Dr. Henderson:
"There are many problems associated with low-dose risk extrapolation, such as the assumption of a
linear relationship.  However, as insufficient data exist to indicate threshold exposure for effect, thelinear extrapolation methodology provides a conservative worst-case scenario estimate of risk.  Otherconfounding factors in estimating risks from epidem iological data are possible contamination by other
fibre types and inaccurate estimates of historical exposures."
87
5.503  Not only does the linear model provide a worst-case scenario, it provides a grossly
exaggerated estimate of risk when "confounding factors", as Dr. Henderson calls them, are so clearly
present.  INSERM made extrapolations from hi gh-level amphibole exposures to mixed fibre type
exposures, as well as from exposures in the textile industry and during the installation of low-density
products such as flocking.88  Amphiboles are much more potent than chrysotile, and the risks in the
textile industry cannot be compared with the risks in the high-density chrysotile products, asDr. Henderson points out in citing Boffetta:  "[I]n general, the risk of lung cancer ...  is highest in
studies of asbestos textile workers."
89
5.504  Another important consideration is the human biological defence mechanisms that are
naturally much more effective at low-levels of exposure, i.e . clearance, biopersistence and DNA repair
mechanisms.90 Given these mechanisms, the reasoning behind the threshold model is both intuitively
                                                     
84See Canada's comments to Question 3.
85Henderson, answer to question 4(c).
86Health Effects Institute-Asbestos Research, Asbestos in Public and Commercial Buildings:
A Literature Review and Synthesis of Current Knowledge (Executive Summary), Cambridge, 1991, p. 6-62.
87Australia National Industrial Chemicals Notifications and Assessments Scheme (NICNAS),
Chrysotile Asbestos:  Priority Existi ng Chemical No. 9 (Full Public Report) , February 1999 at p. 72, cited by
Henderson in his answer to question 4(c).
88INSERM Report, p. 213.
89Henderson, paragraph 5.149 above, citing: Boffetta, P ., Health Effects of Asbestos Exposure in
Humans: A Quantitative Assessment,  (1998) 89 Med. Lav. 471.
90Voir Holland CD, Sielken RLJ., Quantitative Cancer Modeling and Risk Assessment . Englewood
Cliffs, New Jersey: Prentice Hall, 1993;  Sielken RL, Jr., Bretzlaff RS, Stevenson DE., Incorporating Additional
Biological Phenomena into Two-Stage Cancer Models  in: Spitzer HL, Slaga TJ, Greenlee WF, McClain M, eds.
Receptor-Mediated Biological Processes: Implications for Evaluating Carcinogenesis . New York: Wiley-Liss,
1994;237-60. Stevenson DE, Sielken Jr. RL, Bretzlaff RS., Challenges to Low-Dose Linearity in CarcinogenesisWT/DS135/R
Page 354
and scientifically sound, as well as epidemiologically validated.  To illustrate this, consider the
following illustration:  the effect of 50 fibres in the lungs will be more than five times the effect of ten
fibres.
5.505  According to Sir Richard Doll, who first dem onstrated the link between asbestos and lung
cancer (as well as between smoking and lung cancer), "[W]e have no real ground for postulating that alinear relationship for lung cancer can be extrapolated  back to the levels of dose with which we are
concerned in non-occupational settings."
91  Ames and Gold are of the same view:  "[l]inear
extrapolation from the maximum tolerated dose in rodents to low-level exposure in humans has led to
grossly exaggerated forecasts in mortality." 92  Fournier and Efthymiou are even more categorical:
"[L]inear extrapolation to zero is an unscientific methodology whose social consequences are so
immense that it warrants unconditional elimination."93  INSERM acknowledges the limits of the linear
model's application when it states that it provid es nothing more than food for thought:  "cette
extrapolation ne crée pas une information scientifiquement certaine, elle représente une aide à la
réflexion en matière de maîtrise de risque."94
5.506  As Dr. de Klerk points out, " how one extrapolates risk assessment outside the range of
available data is more of a societal decision than a scientific one."
Question 4(d)
5.507  Situations where there is no increased risk at low levels of exposure have been used by
Stayner et al. to establish NOAELs [i.e.  no observable adverse effect levels] for silica.  A similar
model is used for asbestosis.  Canada believes that the use of such a model is warranted for other
asbestos-related diseases, particularly since it ha s been acknowledged by Dr. Musk and Dr. de Klerk
that epidemiological data exists to justify such an approach.
Question 4(e)
5.508  We concur with Dr. Henderson's view that "[t]his question iterates the issue of a threshold
exposure."  Canada nonetheless notes the use by Dr. Infante of a 1992 study by Bégin et al . to
demonstrate the risks related to "background levels" is erroneous.  As has been pointed out by Canada
in its factual arguments,95 this study is based on exposures to a mix of chrysotile and amphiboles in
the manufacturing and construction industry, and therefore is not relevant to exposures from the
current uses of chrysotile.
                                                                                                                                                                    
from Interactions among Mechanistic Components as Exemplified by the C oncept of 'Invaders' and 'Defenders' .
BELLE Newsletter 1994;3(2):1-8.  Stevenson DE., Dose-Response Studies of Genotoxic Rodent Carcinogens:
Thresholds, Hockey Sticks, Hormesis or Straight Lines? - Comment on the Kitchin and Brown paper , BELLE
Newsletter 1995;3(3):14-15.
91Doll, R., Mineral Fibres in the Non-Occupational Environment:  Concluding Remarks,  in Bignon, J.,
Peto, J. and  Saracci R., eds., Non-Occupational Exposur e to Mineral Fibres, IARC Scientific Publication No 90,
1989,  pp. 516-17.
92Ames, B.N. et Swirsky Gold, L., Causes and Prevention of Cancer: Gaining Perspectives on the
Management of Risk,  in Risks, Costs, and Lives Saved: Gettin g Better Results From Regulation?, New York,
OUP, 1996, p.6.
93Fournier, E. and Efthymiou, M.-L ., Problems with Very Low Dose Risk Evaluation:  The Case of
Asbestos,  in What Risk?, p.49.
94INSERM Report, p. 239 and 414.
95 See above Section III.A.5.WT/DS135/R
Page 355
Question 5(a)
5.509  Clearly the answers given by the four experts are based on their concept of what is meant by
controlled use.  It is also evident that the controlled use concept as espoused by Canada was not the
approach that resulted in their answers.  We must  therefore respectfully disagree with the answers
given by the experts in respect of controlled use of chrysotile and high-density chrysotile containing
products.  The fact that they agreed that controlled use of chrysotile and high-density chrysotile
products is feasible at some points of the life cycle, but not in others, suggests that they are not far
from the view of Canada.  The only difference is that Canada believes that the experts misunderstand
the controlled use principle and that, as properly understood and implemented, use can be controlled
throughout the full life cycle of high-density chrysotile containing products.  The basis for our view,
with supporting evidence, is set out below.96
(i) Canada's understanding of the "Controlled use" principle
5.510  The Canadian government's review of the experts' reports and answers to the questions posed
by the Panel reveals that there is one crucial issue, which seems to override all other issues.  This is
the question of whether the application of the controlled use principle is feasible and credible in all
stages in the life cycle of a product.  While there is a reasonably high degree of agreement amongexperts that controlled use can be a reality in the mining and manufacturing sectors, serious doubts are
expressed that controlled use can be applied in a few sectors of use − installation, maintenance and
demolition.  However, the basis for this view is not documented, except by Dr. Infante and
Dr. Henderson.
5.511  By "controlled use", the Canadian government means "stewardship" based on the total life
cycle.  This is outlined in the document The Mineral and Metals Policy of the Government of Canada:
Partnerships for Sustainable Development .
97  With regard to asbestos, this "controlled use" is based
on the following general principles:
• Only the chrysotile variety is used;
• only a limited number of well-defined product applications, where it has been
demonstrated that they can be handled safely, are allowed (i.e.  where the fibres are
encapsulated in a matrix such as cement, bitumen, plastic, resin, etc.);98 and
• new product applications may be introduced only after a strict evaluation to ensure
that a certain level of fibre release is not exceeded during its life cycle.
                                                     
96Canada notes that the "controlled-use" approach has been endorsed by the WHO in its 1998
Environmental Health Criteria 203: Chrysotile Asbestos , p. 144.  "Control measures, including engineering
controls and work practices, should be used in circumstances where occupational exposure to chrysotile canoccur.  Data from industries where control technologies  have been applied have demonstrated the feasibility of
controlling exposure to levels generally below 0.5 fibres/ml.  Personal protective equipment can further reduce
individual exposure where engineering controls and work practices prove insufficient."
97NRCAN, The Minerals and Metals Policy of the Government of Canada:  Partnership for Sustainable
Development , Public Works Canada, 1996. Canada notes that the "controlled-use" approach to regulating
chrysotile asbestos is well researched as evidenced in the studies and conclusions referred to by Canada in itsfactual arguments (see above Section III.A.6).
98To illustrate this point, examples of  "controlled use" of friction products and asbestos-cement are
detailed in Appendices A and B respectively to these comments.  (These Appendices can be found in Annex IV
to this Report).WT/DS135/R
Page 356
5.512  With regard to the downstream use sectors, "controlled use" implies that all
distributors/manufacturers of asbestos will be required to have an import permit.  This permit will be
withdrawn if the company does not meet the following commitments:
• To distribute its products only to companies (users) licensed to purchase these
products.  Those companies must have workers trained and licensed to install
products, and must be in compliance with regulations.  Approved users shall not resellto third parties, and any unused materials must be returned to the manufacturer;
• to provide a list of users of products to the responsible government agency;
• to provide products cut to specification and to establish centres equipped to cut the
products to size, and where persons cutting the products are trained and are licensed
to work with asbestos;  and
• to police the downstream users in co-operation with the government.  The product
manufacturer visits, monitors and reports on the performance of the downstream users
at regular intervals.  There are penalties for failing to provide this productstewardship.
5.513  While high-density products in most countries are not considered to pose any occupational or
environmental health risk, disposal should only be undertaken by approved and appropriately trained
persons.
5.514  Dr. Infante's description of the permissible exposure limit for chrysotile asbestos, as well as
programmes or standards that recommend or require specific engineering control, work practices,
training and education and personal protective equipment to control exposures to asbestoscorresponds, to some extent, to Canada's approach.  Dr. Infante seems to suggest that because some
workers do not comply with standards and regulations on controlled use in the United States,
controlled use is not feasible.  As explained in Appendix A on friction material and Appendix B on
asbestos cement, the controlled use approach can minimize, if not eliminate, workers' non-
compliance.
99
5.515  Canada does not propose that any chrysotile products produced, sold or used without the
implementation and enforcement of very stringent control procedures.  Taking into account the types
of products being manufactured and used in France at the time of the ban, Canada does not advocate
re-introducing any product that cannot be handled according to the safety criteria outlined above.
Canada is not advocating the introduction anywhere in the world of manufacturing facilities ofproducts for which the technology does not exist to protect workers from exposure to chrysotile at
levels where risks would be above epidemiologically based practical thresholds.
5.516  The experts have indicated that the level of exposure is such that they are not concerned about
asbestos-related disease for persons living in buildings containing chrysotile asbestos products,
including friable insulation.  As none of the chrysotile products that will be used in the future arefriable, this conclusion would be further reinforced.  If the procedures envisaged under the "controlled
use" policy are followed by licensed practitioners, the public will not be placed under any practically
determinable increased risk of disease as a result of the manufacture and use of chrysotile containing
products.  Unlike friable insulation products where janitorial staff, electricians, carpenters, and others
may be required to work regularly in an environment where exposures to asbestos would occur, thenature of the high-density products will ensure that exposures are a much rarer event.
                                                     
99Appendices A and B can be found in Annex IV to this Report.WT/DS135/R
Page 357
5.517  Canada recognizes that the clock cannot be turned back.  Friable mixed products produced in
the past are now in place, and trades such as electricians or telephone engineers face situations where
the potential health risk from exposure is considerably greater than any additional risk that new high-
density chrysotile products would present.  It is evident that the protection of workers who come into
contact with friable products must be assured by the responsible jurisdictions through training in tradeschools, appropriate information programmes by unions, and by governments and employers ensuring
that the appropriate equipment and tools are made available to workers.
100
5.518  Regarding high-density products, Canada believes that no less stringent measures should be
required, even though the evidence shows that th e risk from exposure to high-density chrysotile
products is minuscule compared to the risk from fr iable products, in many cases containing mixtures
of chrysotile and amphibole fibres.  Furthermore, in the absence of sound scientific data to the
contrary, the same criteria should be applied to the handling of all products in which respirable fibres,including asbestos substitutes, may be released.
(ii) International Standards
5.519  None of the experts acknowledges that controll ed-use of chrysotile asbestos cement products
and other high-density chrysotile products stems from international standards.  Dr. Infante even denies
the existence of international standards on controlled-use of high-density chrysotile products.  Canadawishes to remind the Panel that international standa rds, as the term is defined in the Agreement on
Technical Barriers to Trade, do exist.  Regulatory developments on asbestos fibres have been guided
by ILO Convention 162 concerning Safety in the Use of Asbestos.
101 ILO convention 162 provides
for:  (i) the prescription of adequate engineering c ontrols and work practices;  (ii) the prescription of
special rules and procedures for the use of asbestos or certain types of asbestos or products containingasbestos or for certain work processes;  (iii) where necessary to protect the health of workers and
technically practicable, the replacement of asbestos or of certain types of asbestos by other materials
or the use of alternative technology scientifically evaluated by the competent authorities as harmless
or less harmful;  and (iv) total or partial prohibition of the use of asbestos or of certain types of
asbestos in certain work processes.
102
5.520  The Code of Practice on Safety in the Use of Asbestos of the International Labour Office
referred to by Canada in all its submissions is another international standard on controlled-use.103 The
objects of the Code are:  (i) to prevent the risk of exposure to asbestos dust at work;  (ii) to prevent
harmful effects on the health of workers arising from exposure to asbestos dust;  and (iii) to provide
reasonably practicable control procedures and practices for minimising occupational exposure to
asbestos dust.  To do so, the Code gives detailed guidance on the limitation of exposure in respect of
asbestos cement and friction materials.  Finally, Canada has referred the Panel to International
Standard ISO 7337:  Asbestos Reinforced Cement Products − Guidelines for On-Site Work
Practices.104 This international standard gives guidelines for tools and working methods to be used on
site with a view to maintaining the dust emission at the lowest practicable level.  It applies to asbestos-
cement products.
                                                     
100See Section III.A.5 of this Report and Camus M., L'amiante et les risques pour la santé , April 1999.
101Conférence internationale du travail, Convention concer nant la sécurité dans l'utilisation de l'amiante
(Convention 162), adoptée le 24 juin 1986, and Recommand ation concernant la sécurité dans l'utilisation de
l'amiante (Recommandation 172), adoptée le 24 juin 1986.
102According to Canada, the emphasis of ILO Convention 162 is on controlled-use and not on product
prohibitions. The Convention calls for two specific prohibitions: crocidolite and all products containingcrocidolite, and sprayed-on applications of asbestos.
103Recueil de directives pratiques du BIT sur la sécu rité dans l'utilisation de l'amiante, Organisation
internationale du travail, Genève, 1984.
104ISO, standard ISO-7337 1984.WT/DS135/R
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5.521  The ILO Convention 162 and the Code of Practice on Safety in the use of chrysotile should be
supplemented by a national policy on responsible use based on the recognition and acceptance of the
principles that both international standards set forth.105 As explained above, the objective of
responsible use is to limit the handling of chrysoti le to companies that comply with the national
regulations or that have submitted action plans and formal commitments in writing with a view tobringing their activities into line with these regulations.
Question 5(b)
5.522  The experts recognize that training could be achieved in the manufacturing sector, where there
is a small and cohesive workforce, but assert without support that it cannot be achieved in the
construction sector, where there is a large and non-cohesive workforce.  Dr. Infante wrongly equates
non-compliance with regulated training requirements to non-feasibility of training for controlled-useof chrysotile asbestos.
106
5.523  In Europe, as in other countries, there are now requirements for training workers.  In Canada,
both levels of government require training at all workplaces.  It is possible for training to be made
available by industry.  In fact, information and training is one of the most important elements of a
company's preventive control programme.  In line with the controls suggested at paragraphs 5.511and 5.512, France could require through legislation that all construction workers handling asbestos
products attend training sessions.  France could also require that only designated, properly trained
workers be allowed to work with those asbestos products that need to fall under a controlled regime.
5.524  During manufacture, controls such as wet processes and exhaust ventilation, essentially
eliminate all exposure.  On the work site, process changes are reduced by the industry manufacturingproducts requiring no, or virtually no, modifications on site.  The controlled use approach includes the
use of pre-cut and pre-drilled asbestos cement products, and provides for designated locations where
chrysotile asbestos cement sheets or pipes are cut and drilled and where the appropriate controls are in
place.  The monitoring process is similar to that for other workplaces:  all complaints are submitted to
governmental inspectors for evaluation.  The supplier has the responsibility for ensuring that allcompanies to which they supply have in place the proper equipment and training to ensure safe use of
the product throughout its life cycle.  Finally, the removal of high-density chrysotile products is
carried out in accordance with government codes.
Question 5(c)
5.525  Both Dr. Henderson and Dr. Infante agree that, in many situations, when standards are
properly applied, it is possible to maintain e xposure below 0.1 f/ml.  Also, as explained in
Appendix A on the friction industry and Appendix B107 on the asbestos cement industry, experience
shows that a level below 0.1 f/ml can be achieved because the technology and work practices exist to
control exposure during manufacture.  No guarantee can be offered that there would never be a
situation in which 0.1 f/ml might be exceeded as a peak exposure.  However, there is no evidence that
occasional peak exposures increase the risk of l ung cancer or mesothelioma in chrysotile exposed
workers.  For example, the health experience of brak e mechanics, i.e. no evidence of an increased risk
of mesothelioma or lung cancer, is based on exposures that involved peak exposures, such as occurred
during the blowing out of brake wear debris and th e occasional grinding of brake linings.  These
operations involved short exposures above 0.1 f /ml.  The actual concentrations associated with various
                                                     
105Memorandum of Understanding between the Government of Canada and the Asbestos Industry on
Responsible-Use of Chrysotile Asbestos , 1997.
106Canada notes that it should be recalled that his basis for risk assessment is based on the textile
industry.
107See Annex IV to this Report.WT/DS135/R
Page 359
tasks have been reported by Kauppinen and Korhonen,108 and by Rödelsperger.109 I n  s p i t e  o f  t h e s e
short-term peak exposures, the average exposure of auto mechanics was less than 0.05 f /ml.
5.526  A person repairing their own brakes periodically nowadays (using disc brake pads mainly)
would have extremely low cumulative exposures compared to full time auto mechanics and there is no
reason for them to have any, even short term, exposures exceeding 0.1 f /ml.  The risks associated with
cumulative exposure to chrysotile at these levels  would not be epidemiologically detectable for
handymen handling friction or asbestos cement products.
5.527  Rödelsperger110 made dust measurements on about 40 buildings sites in Germany.  He
reported peak exposures of more than 100 f /ml in the vicinity of a grinding machine used to cut
asbestos cement sheets.  However, when he used the standardized work histories of 61 roofers, who
had a mean duration of exposure of 16 years, he found that their mean cumulative exposure
was 1.6 fibre-years /ml.  These measurements were made 20 or more years ago, with the products and
technology available then and for regular constructio n workers.  It is evident that even under these
circumstances, lifetime cumulative exposures were low.  Thus, a handyman, even if he did not take
proper precautions would still have a low cumulative fibre exposure because peak exposures are of
short duration and he would be at a very low, undetectable risk of health effects.
5.528  It is generally agreed that at the levels of exposure associated with the use of the modern high-
density products, they would not even put a full-time worker at increased risk of asbestosis and,therefore, this would not be of concern for a handyman working occasionally with the product.  It has
been amply demonstrated that the risk of lung cancer increases with increasing cumulative lifetime
exposure that combines duration and level of exposure.  A person exposed at 0.1 f /ml for 40 years has
a cumulative lifetime exposure of 4 f /ml-years.  If that person worked on a project only once each
week for four hours for 40 years, he would not achieve the same lifetime exposure unless he was
exposed to 1 f /ml continuously for the four hours of exposure every time he was exposed for 40 years.
Thus occasional peak exposures of a few minutes contribute very little to cumulative lifetime
exposure which is important in evaluating the risk of chronic diseases such as lung cancer or
mesothelioma.
5.529  Gardner
111 found no increased risk of lung cancer or other asbestos-related disease in a
chrysotile asbestos cement plant where exposures were less than 1 f /ml.  This was in a cohort of
workers employed between 1941 and 1983.  It is eviden t that any risk would have been well below the
detection limit at 0.1 f /ml.  A study of chrysotile cement production workers by Thomas112 and
Neuberger & Kundi113 identified no chrysotile-related increased risk of lung cancer and Weill,114 while
reporting an increased risk of lung cancer in asbestos cement workers, found the increased risk only in
                                                     
108Kauppinen, T. and Korhonen, K., Exposure to Asbestos During Brake Maintenance Of Automotive
Vehicles by Different Methods , (1987) 48 Am. Industr. Hyg. Assoc. J, pp. 499-504.
109Rödelsperger, K. et al., Asbestos Dust Exposure During Brake Repair , (1986) 10 American Journal
of Industrial Medicine, pp. 63-72.
110Rödelsperger, K., Woitowitz, H.J. and Krieger, H.G., Estimation of Exposure to Asbestos-Cement
Dust on Building Sites , in Biological Effects of Mineral Fibres, Vol. 2, J.C. Wagner Editor,  1980, International
Agency for Research on Cancer: Lyon, pp. 845-853.
111Gardner, M.J., Winter, P.D., Pannett, B. and Powell, C.A., Follow-Up Study of Workers
Manufacturing Chrysotile Asbestos Cement Products , (1986) 43 British J. of Industrial Medicine, pp. 726-732.
112Thomas, H.F., Benjamin, I.T., Elwood, P.C. and Sweetman, P.M., Further Follow-Up Study of
Workers from an Asbestos-Cement Factory , (1982) 39 British Journal of Industrial Medicine, pp. 273-276.
113Neuberger, M. and Kundi, M ., Individual Asbestos Exposure: Smoking and Mortality − A Cohort
Study in the Asbestos-Cement Industry , (1990) 47 British Journal of Industrial Medicine, pp. 615-620.
114Weill, H., Biological Effects:  Asbestos-Cement Manufacturing , (1994) 41 Ann. Occup. Hyg.,
pp. 533-538.WT/DS135/R
Page 360
those with asbestosis.  In this study, there was little evidence of asbestosis below 30-40 f /ml-years of
exposure.  This is about 0,75-1 f /ml continuous exposure for 40 years.  Thus, there is little evidence to
support a detectable increase in risk of lung cancer in workers with a 40 years cumulative lifetime
exposure at 4 f /ml-years.
5.530  Any risk estimates obtained by linear extrapolation from high exposures to such low
exposures are somewhat hypothetical and both Lash115 and Camus116 have shown that the risk
estimates made by the U.S. Government have overestimated lung cancer risks.
Question 5(d)
5.531  Canada disagrees with the views of Dr. Henderson117 and Dr. Infante that controlled use of
chrysotile asbestos is not feasible for workers invo lved in the construction trade and that service and
maintenance workers such as carpenters, plumbers, and electricians will experience peaks of
exposures to asbestos that place them at risk.  The nature of high-density chrysotile asbestos productsis such that few of the trades listed above will ever need to work on the products, with the possible
exception of demolition workers.  Again, there is evidence that during demolition exposure
concentrations associated with chrysotile asbestos cement products is very low.
118  Today, with
chrysotile cement products and controlled use procedures, health risks become insignificant.
5.532  Recommended installation methods can eliminate th e need to cut or drill into chrysotile-based
products at construction sites, since those products  are distributed in a variety of pre-cut and pre-
drilled sizes, according to buyers' specifications.  In fact, many asbestos cement products are pre-
formed ready for use.  They are factory-made to th e correct size and shape including holes so that a
minimum of on-site preparations is needed.  Once installed, chrysotile asbestos cement pipes are
below ground and pose no risk to workers.  Even if dug up, they pose no risks unless comminuted,
ground or sawed, and, when this is necessary, the use of appropriate tools and controls will keep the
release of dust and exposure well within the level considered safe by the WHO.  Chrysotile asbestoscement sheets are used for roofing and exterior bu ilding walls.  Once installed, there is no need to
modify the roof until the life of the product is over.  Similarly, there is no need to modify chrysotile
asbestos sheets used as walls once they have been installed.  The product can be painted without fibre
release.
5.533  Chrysotile cement products are unlikely to release fibres into the environment or breathing
zones of workers such as janitors, plumbers, electricians, repair men, etc., unless these workers have
to actually cut or drill the product.  Unlike insulation products, there will rarely be a need for anyone
to perforate, saw, or grind installed chrysotile cement products.  Where cutting or drilling is required,
hand tools and low speed power tools are recommended in combination with wetting to keep dust
levels to a minimum.  Dust levels for various types of on-site working have been measured both inlaboratories and in the field and these facts showed that risks could be maintained below detection
limit.
                                                     
115Lash, T.L., Crouch, E.A.C. and Green, L.C., A Meta-Analysis of the Relation between Cumulative
Exposure to Asbestos and Relative Risk of Lung Cancer , (1997) 54 Occupational and Environmental Medicine,
pp. 254-263.
116Camus, M., Siemiatycki, J. and Meek, B ., Nonoccupational Exposure to Chrysotile Asbestos and the
Risk of Lung Cancer , (1998) 338 N. Eng. J. Med., 1565.
117Henderson, answers to Questions 5(a) to (d).
118Hoskins J.A., Chrysotile in the 21st Century , UK, 1999, p.12.WT/DS135/R
Page 361
Question 5(e)
5.534  Dr. de Klerk and Dr. Musk wrote that efficiency of controlled-use in the case of home
handymen is outside their area of expertise.  However, both Dr. Henderson and Dr. Infante have
concluded that it is not possible to control exposure to chrysotile asbestos high-density products innon-occupational circumstances (occasional interventions by home handymen).  Neither bases his
conclusion on data.  Dr. Henderson adds to his answer that although such risks are not quantifiable
because of absence of data, these risks must be very small for lung cancer and mesothelioma, and non-
existent for asbestosis.
5.535  Controlled use will reduce and even eliminate risks.  The risk of chrysotile-related health
effects is tied to cumulative exposure, that is, duration and level of exposure.  Rarely will an
individual under non-occupational circumstances achieve the exposure of a full-time worker.
Occasional uncontrolled exposures for a handyman would not result in appreciable cumulative
exposure.  Data published by Brown
119 showed time-weighted average (TWA) levels during
demolition of weathered asbestos-cement roofing between 0.3 and 0.6 f/ml.  One can likely guess that
a handyman would not practice such an activity more than 40 hours in 25 years.  This would average
out to a TWA of 0.015 f/ml for the year of this activity, and a TWA of 0.0006 f/ml each year of theworker's adult life.  This is 1 million times less than past asbestos workers are.  It is equivalent to
exposure levels in schools containing ACM.
120
5.536  Based on INSERM121 and HEI-AR risk tables, which are based on mixed asbestos exposures,
the resulting lifetime cancer risk would be betw een 10 and 20 in a million depending on the time
occurrence of this exposure scenario.  More accurately however, the lifetime risk would be near zeroper million, based on chrysotile friction workers who were exposed to similar fibres (species and
dimension wise), and about 1 in a million, based on the risks of past chrysotile miners and millers.
The casual user of a high density product, even if the product were weathered, is not likely to be at
any increased risk of an asbestos related disease.  If the supplier follows through on the requirements
of controlled use, the casual purchase of chrysotile asbestos-cement products by the handyman willnot be possible.  However, there is probably no wa y of stopping any individual from doing something
to any product if they can obtain it.  This is a problem that exists for any product many of which pose
serious health risks if abused.
Question 6(a)
5.537  Canada respectfully disputes the conclusions of the experts regarding the risk from substitute
fibres, and with respect to one expert, the ability of substitutes to serve as suitable replacements tochrysotile.  Canada notes that the treatment of the issue by two of the experts is terse, comprising only
several sentences.  To their credit, Drs. de Klerk and Musk indicate that the use and control of
substitute fibres is not within their areas of special expertise.  They offer some responses nonetheless.
Canada is concerned, in particular, by their lack of familiarity with the relevant studies and actual
modes of production, use and disposal of substitute fibres.  For example, they apparently are unawareof research conclusively demonstrating the significant health risks from exposure to refractory
ceramic fibres (RCF), which are discussed below.
5.538  This concern applies to Dr. Infante as well.  Dr. Infante further appears unaware of (or
ignores) recent research demonstrating that chrysotile is less biopersistent than many substitute fibres.
                                                     
119Brown, S.K ., Asbestos Exposure During Renovation and Demolition of Asbestos-Cement Clad
Buildings , (1987) 48 Amer. Ind. Hyg. J., pp. 478-486.
120Health Effects Institute − Asbestos Research, Asbestos in Public and Commercial Buildings:  A
Literature Review and Synthesis of Current Knowledge (Executive Summary) , Cambridge, 1991, pp. 1-11.
121INSERM Report.WT/DS135/R
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Dr. Infante also ignores the population the experts agree are most at risk from exposure to any fibre –
tradesmen – when he concludes (without support or, even, explanation, Canada notes) that the "nature
of the production process makes substitutes more amenable to control than asbestos fibres."
Assuming he is not again conflating chrysotile w ith amphiboles when referring to "asbestos," his
point, were it true, would be irrelevant.  The experts agree that chrysotile and chrysotile products canbe safely mined and produced.  The key is exposure to tradesmen.  And, for that exposure, no
rationale exists suggesting that the ability to impose effective controls differs based on the type of the
fibre.
5.539  Dr. Henderson, for his part, recognises that, as with all fibres, the pathogenicity of substitutes
is defined by the "3Ds" (dimension, dose, durability).  He seems also to understand that, due to the
(lack of) historical use of substitutes, we cannot fully know the risks of using them.
122  However, he
then seems to ignore the importance of these facts.
5.540  All of the experts fail to take into account several very important factors.  First, the chrysotile
products at issue in this proceeding are quite few.  Second, the exposure levels during the
manufacture, use and disposal of these products are extremely low.  Third, the data demonstrate that
these few products have been and can be used without detectable health effects in humans.  Moreover,
in order to assess whether a substitute is safer to use than chrysotile in a product:  (i) it is fundamentalthat the characteristics of the fibres being compared  be those of the fibres as they are used in the
product or as they are released from the product throughout the product's lifecycle;  (ii) it is essential
that data on at least the key parameters (exposure, biopersistence and dimensions) be available to
make this assessment.  Unfortunately, the experts have not addressed these topics.  In short, the
experts have based their opinions on very limited, if any, data.  While the experts reach conclusionsthat various substitutes (PVA fibres, glass fibres, cellulose and para-aramid fibres) are safer to use
than chrysotile, they provide no systematic comparison of risks and very limited, questionable
scientific data in support of their opinions.
5.541  Canada presents below a survey of the studies and concepts that the experts ignored.  These
studies give a picture of risks from substitute fibres starkly different from that suggested by the Panel'sexperts.  As demonstrated below, the situation concerning risk from substitute materials is as Canada
set out in its factual arguments.
123
(i) The Fibres to Compare
5.542  Experimental data for a wide range of fibres have shown that the physical characteristics
(diameters, lengths, density) of fibres are important  in determining their respirability, when they are
deposited in the respiratory system, and their capacity to induce fibrosis and cancers.  Further, the risk
of effects also depends on dose (exposure).  Thus, differences in the risk of disease in variousindustrial sectors would be expected to occur because of differences in these, as well as other factors.
As the characteristics of chrysotile and any substitute fibres are likely to be dictated by the product in
which they are used, it is not appropriate to assess the risks associated with friction products or
asbestos cement products using data from other industrial sectors.  The data that should be available
and used for the purpose of comparing risks should be those for the fibres as used in the specificproducts under review.  Canada's presentation proceeds on this basis.
5.543  Davis
124 pointed out that while materials like wool, cellulose and other fibres have in some
cases been used for many years, they are now being used in quite different applications, about which
                                                     
122Henderson, response to Question 6(b).
123See above Section III.A.6.
124Davis, J.M.G., The Toxicity of Wool and Cellulose , (1996) 12 J. Occ. Health and Safety Australia and
New Zealand, pp. 341-344.WT/DS135/R
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knowledge is very limited.  As a consequence, the characteristics of the fibres used in the newer
applications may not be the same as those in the conventional products manufactured in the past.
Such changes can modify the respirability and biological activity of the materials.  There is a further
complication for substitutes that is not addressed by the experts.  This is the fact that substitution does
not always involve replacement of chrysotile by a single fibre, but often by several different materialsor substitute fibres.  For example, cocktails of fi bres are needed to meet technical requirements in
friction products.  In addition, when substituting for chrysotile, other materials such as silica or other
fibres, fire retardants or biocides must often be added.  These agents may themselves be toxic or
carcinogenic, and may act synergistically.
(ii) The Outcomes to be Measured
5.544  While it is reasonable to compare the risks of lung cancer and mesothelioma between the
various fibre types, it must be remembered that di fferent sized fibres may lead to fibre deposition at
different locations in the respiratory system.  For example, if more fibres of one material than another
are likely to be deposited in the nasal passages, one should consider the possibility of an increased
frequency of nasal cancer in evaluating the substitute.  Dr. Infante mentioned the increased risk of
nasal cancer in woodworkers, which has been well established.
125 This might raise a question
concerning the sources of the cellulose used as a substitute and whether controls are in place to avoidexposure to cellulose from woods that have caused such cancers.  Also, some materials may cause
dangerous allergic responses.  Certain glass fibres cause skin irritation.  Harrison
126 notes that there
are indications of an accumulation of oligomers in th e kidney in some circumstances, so that attention
should be given to the molecular weight of PVA used "especially if a smaller diameter material were
to be produced."
5.545  In considering risks, the composition of the dusts and fibres to which workers are exposed
when handling the "raw substitute" materials, manufacturing the product, cutting, grinding,
manipulating or disposing of the product also must be considered.  For example, it is important to
know whether the fibres of para-aramid, PVA or cellulose are opened (fibrillised) or comminuted
during preparation or manufacture of the product?  Does manipulation, sawing or drilling of the
product give rise to narrower diameter respirable "fibres" such as result with polyester fibres during
weaving?  Do these fibre fragments have biological significance?  What are actual use concentrations?
It must be remembered throughout that there exists a substantial body of information concerning
chrysotile.  Unfortunately, in the case of substitute s, there are rarely any human epidemiological data
available and even experimental data are limited.   Perhaps this fact led Dr. de Klerk to conclude that
"[G]iven the comparative lack of knowledge about the health effects of substitute materials, the
continued use of chrysotile under [controlled] circumstances seems sensible .127
(iii) The Essential Data
5.546  The data that need to be compared in an evaluation of the relative safety of chrysotile and
substitutes include the following:
• Epidemiological data that provide direct evidence of the risks associated with the
products.
                                                     
125Infante, answer to Question 6(c).
126Harrison, T.W., Levy, W.S., Patrick, G., Pigott, G.H. and Smith, L.L., Comparative Hazards of
Chrysotile Asbestos and its Substitutes: A European perspective , (1999) Environmental Health Perspective, 107.
127de Klerk, N.H. and Armstrong, B.K., The Epidemiology of Asbestos and Mesothelioma", in
Malignant Mesothelioma , Henderson, D.W. et al., eds Hemisphere Publishing, New York, 1982, p. 231.WT/DS135/R
Page 364
• Experimental data by inoculation of fibres or by inhalation experiments in
experimental animals.
• Dimensions of fibres in the respirable airborne dust during the manufacture of the
product.
• Dimensions of fibres in the respirable airborne dust during the use of products
containing the fibre.
• Dimensions of fibres in the lungs of wo rkers engaged in the manufacture of products
containing the fibre.
• Dimensions of fibres in the lungs of persons exposed during the use of products
containing the fibre.
• Dimensions of fibres in the respirable airborne dust and in the lungs following
exposure during the disposal of the fibre or products.
• The biopersistence of the fibres in humans and animals.
• The cumulative exposure (i.e.:  concentration x time) of workers engaged in all phases
of manufacture, use and disposal of the product.
• Data on alterations or modification of the fibres chemically, physically and
biologically during their life cycle that might affect their potential to cause healtheffects.
5.547  Even if one were to narrow the requirements to a smaller number of key parameters such as
fibre dimensions, biopersistence and exposure-response, the available data are still inadequate to
provide a credible basis for an adequate comparison.  Thus, the unqualified wholesale affirmation that
"substitutes are safer than chrysotile" is not well founded and potentially very dangerous.  For
example, prior to the finding of a very high risk of mesothelioma for persons exposed to very low
concentrations of fibrous zeolite erionite in Turkey, there had been no indications world-wide thatsuch fibres might after 30 years from first exposure at such very low levels produce such a high rate of
mesotheliomas in humans.  In South Africa, crocidolite had been used for about 60 years before
Wagner
128 reported that mesotheliomas were associated with crocidolite exposure.  In humans,
mesotheliomas do not occur until 40-60 years after first exposure.  Thus, caution is needed in the
absence of data regarding substitute fibres.  As one expert stated:  "better the devil you know" than thedevil you do not know.
129
Question 6(b)
(i) Dimensions
5.548  The experts present no data that show that the dimensions of all fibrous substitutes are outside
the respirable size range during the substitute product's lifecycle.  This is because no such data exist.
                                                     
128Wagner, J.C., Newhouse, M.L., Corrin, B., Possister, C.E. and Griffiths, D.M., Correlation between
Fibre Content of the Lung and Disease in East London Asbestos Factory Workers , (1988) 45 British J. of
industrial Medicine, 305.
129de Klerk, answer to Question 6(a).WT/DS135/R
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(ii) PVA & Aramid Fibres
5.549  Views from the experts appear to be mixed.  Dr. Henderson quotes Harrison's review stating
that PVA and aramid fibres are too large to be respirable.  Dr. de Klerk states that all substitutes
except glass (cellulose, aramid, PVA) produce a larger proportion of non-respirable fibres than
chrysotile but respirable fibres are similar for all substances.   Dr. Musk offers no opinion.  Dr. Infantestates that PVA fibres are "mostly" in the size range 10-16 µm and aramid fibres 10-12 µm.  However,
he notes, quite correctly, that, as mentioned below, the aramid fibres can and do split into fibrils of
about 0.2 µm in diameter.
5.550  In assessing fibre respirability, none of the experts accounts for the fact that respirability
depends on density as well as fibre diameter.  The densities of PVA and para-aramid fibres are both
considerably less that that of chrysotile.  This means that much larger diameter substitute fibres would
be respirable.  In fact, the upper limits of diameters that are respirable for these fibres, as reported byHarrison
130, are approximately 7 µm and 6-7 µm respectively.  The equivalent upper level diameter for
chrysotile is about 3-3.5 µm.  Thus, fibres of much greater diameter can penetrate into the alveolar
region of the lung.  A review of the available information in the literature is that there is a general
opinion without data that the respirable fraction of PVA fibres is small.  However, there do not appear
to be any data on the dimensions of airborne fibres during mixing with cement or other materials, or as
released from the products during processing and use.
(iii) Glass and Cellulose Fibres
5.551  As far as cellulose and glass fibres are concerned, none of the experts provided any actual
measurement data on the sizes or respirability of the fibres.  Also, the dimensions of fibres at various
stages of the processing, use and disposal of cellulose have not been reported.  The actual dimensionsof fibres in the airborne dust will depend on the specific glass fibres used and how they were prepared.
(iv) Biopersistence
5.552  It is well known that biopersistence is a key parameter.  Indeed, the human evidence for
chrysotile indicates that it is likely to be one of the main reasons why chrysotile is less dangerous than
the amphiboles in respect to mesothelioma risk.  This is clearly recognized by three of the four
experts, as well as by INSERM.
131
(v) Cellulose
5.553  Drs. Infante, Henderson and de Klerk recognise that cellulose is durable in the lung.   In fact,
the data show that some cellulose fibres have half lives of about 1000 days in the lung, which are
many times longer than even those published data for amphibole fibres, much less chrysotile fibres.132
(vi) PVA
5.554  Dr. Musk and Dr. Henderson had no comment on PVA durability.  Dr. de Klerk presented no
data, but expressed the view that PVA was less durable than chrysotile.  Davis, in a review in 1998,
found no published data on the biopersistence of PVA fibres.  Data was not published until 1999,
                                                     
130Harrison, T.W., Levy, W.S., Patrick, G., Pigott, G.H. and Smith, L.L., Comparative Hazards of
Chrysotile Asbestos and its Substitutes: A European perspective , (1999) Environmental Health Perspective, 107.
131See Canada's comments on Question 3.
132Muhle, H., Ernst, H. and Bellman, B ., Investigation of the Durability of Cellulose Fibres in the Rat
Lungs , (1997) 41 Ann. Occup. Hyg., pp. 184-188.WT/DS135/R
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when Harrison [1999] reported that  PVA "will degrade very slowly, if at all in the lung."133  There do
not appear to have been any systematic studies of the biopersistence of PVA fibres, a crucial
parameter in assessing the hazard associated with PVA fibres.
(vii) Para-aramid Fibres
5.555  Based on a study by Searl,134 who compared chrysotile and para-aramid fibres, the general
view of the experts is that para-aramid fibres are less biopersistent.  However, Searl failed to check the
lung tissue to confirm that the retained fibres were chrysotile.  Based on studies using a standard
protocol, Dr. David Bernstein has found that the biopersi stence of chrysotile is in fact less than that of
para-aramid fibres.135
(viii) Glass Fibres
5.556  Drs. Musk, de Klerk and Henderson presented no data on the biopersistence of glass fibres.
Dr. Infante, without identifying the specific glass fibres, reports that glass fibres are less biopersistentthan chrysotile.  In fact, the recent work by Dr. Bernstein, in which the same protocol was used as for
synthetic fibres, found that long [i.e.:  > 20um] pure chrysotile fibres are removed from the lung faster
than most, if not all, of the glass fibres reported in the published literature.
136
(ix) Chrysotile
5.557  As far as chrysotile is concerned, it is well accepted that chrysotile is readily removed from
the lung.  This is why the lungs of chrysotile millers and miners, exposed to chrysotile, have been
found at autopsy to contain more tremolite (an amphibole asbestos mineral) than chrysotile.137 The
chrysotile cleared, but the tremolite fibres remained in the lung because of their much greater
biopersistence.  There are various estimates of the half time for chrysotile clearance.  Oberdöerster138
studied baboons and estimated a 90-110 day half time for chrysotile fibres.  The study by Searl was
mentioned above.  The estimates by Dr. Bernstein are even shorter (< 10 days).139  For direct
comparison purposes, the clearance rates for fibres in the same ranges of dimensions must be studied.
In addition, it is crucial that the fibres be tested using the same methodology.  The studies by
Bernstein best fit these criteria and show that, size for size, chrysotile has a very short half-life.
Question 6(c)
(i) Exposure-Response
5.558  In the absence of exposure-response data, it is not possible to quantify the risks associated
with the various fibres.  The question to be addressed is not:  is one material more dusty than another?
Nor is it:  is the concentration higher when working with one material compared to another?  Rather,
                                                     
133Davis, J.M.G., The Biological Effects of Fi bres Proposed as Substitutes for Chrysotile Asbestos:
Current State of Knowledge , 1998.
134Searl, A., Clearance of Respirable Para-Aramid from Rat Lungs: Possible Role of Enzymatic
Degradation of Para-Aramid Fibrils , (1997) 41 Ann. Occup. Hyg., pp. 148-153.
135Bernstein, D.M., Graph on Biopersistence of p-Aramid Fibres.
136Bernstein, D.M., Summary of the Final Reports on the Chrysotile Biopersistence Study , Geneva,
1998, document submitted to the Panel by Brazil as a Third Party (see above Section IV).
137Rowlands, N., Gibbs, G.W. and McDonald, A.D., Asbestos Fibres in the Lungs of Chrysotile Miners
and Millers − A Preliminary Report , (1982) 26 Ann. Occup. Hyg., pp. 411-415.
138Oberdörster, G., Macrophage-Associated Responses to Chrysotile , (1994), 38 Ann. Occup. Hyg.,
pp. 601-615.
139Bernstein, D.M., Summary of the Final Reports on the Chrysotile Biopersistence Study , Geneva,
1998, document submitted to the Panel by Brazil as a Third Party (see above Section IV).WT/DS135/R
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the question that must be asked is:  what is the risk for workers manufacturing or using the product?
The decision on which fibre is safer has to be made on the basis of an assessment of the risk of disease
for workers when manufacturing and using a product containing chrysotile compared to that when
manufacturing and using the same product containing the substitute when subjected to the same or
equivalent handling.
5.559  Three sources of data might be considered:  experimental animal studies;  human
(epidemiological) studies;  and in vitro  studies.  The latter ( in vitro ) are of little value for estimating
risk as they only involve tests of, for example, biological activity in cells isolated from the processes
which occur in a complete organism.  Thus, they are an inadequate basis of comparison to the effects
of inhalation on animals, much less humans.
(ii) Animal Studies
5.560  The first approach involves the exposure of animals to fibres of well-defined characteristics
and concentrations by inhalation and following them for their lifetimes.   Such studies have been done
for a wide range of synthetic mineral fibres.  Problems with this approach are many, as has been
demonstrated in the considerable work done in recent years on synthetic mineral fibres.  First, the
animal species may have a limit on the size of fibre that it can inspire.  Second, there are marked
differences in the sensitivity of different animal species.  For example, a refractory ceramic fibre(RCF) which produced one or two mesotheliomas in rats, produced mesotheliomas in 40 per cent of
the hamsters exposed.  Third, the lifetime of rats is about two years.  In order to produce an effect
within the lifetime of the animals they are subj ect to enormous exposures.  Such exposures can
produce the abnormal situation of lung overload so that  the real reason for any biological effect is not
clear.  Fourth, an animal must produce an effect within two years (before it dies of natural causes).  Ifbiopersistence is important, fibres that are readily removed in humans over the course of a human's
life are not removed from the lung of an experimental animal because of the high exposures and
shorter life.  Fifth, the interpretation of much of the experimental work must be done with caution,
because until recently, fibre exposures were reported on mass not number basis.  As the materials
tested can have quite different dimensions, the same mass can lead to exposures involvingconsiderably different concentrations of fibres on a number basis.
(iii) PVA
5.561  There are no studies relating the long-term effects of exposure to PVA fibres.
(iv) Cellulose
5.562  Studies that have been done with cellulose have shown that it initiates a severe inflammatory
response
140 and fibrosis.141  Unfortunately, no chronic exposure data have been published.
(v) Glass Fibres
5.563  While there have been many studies of glass fibres, the only study in which the same
methodology was applied to the study of synthetic mi neral fibres and chrysotile asbestos is that of
Hesterberg.142 He found that while there is an increased risk of lung cancer identified at high
                                                     
140Hadley, J.G., Kotin, P. and Bernstein, D.M., Subacute (28 Day) Repeated Dose Inhalation of
Cellulose Building Insulation in the Rat , (1992) The Toxicologist, 225 (abstract).
141Muhle, H., Ernst, H. and Bellman, B ., Investigation of the Durability of Cellulose Fibres in the Rat
Lungs , (1997) 41 Ann. Occup. Hyg., pp. 184-188.
142Hesterberg, T.W., Miller, W.C., Theveney, Ph. and Anderson, R., Comparative Inhalation Studies of
Man-Made Vitreous Fibres:  Characterization of Fibres in the Exposure Aerosol and Lungs , (1995) 39 Ann.
Occup. Hyg., pp. 637-653. Hesterberg exposed rats to a concentration of 10,000 WHO fibres/ml of chrysotile,WT/DS135/R
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concentrations (as for glass and other fibres) the animal data suggest that at low level exposure, the
risk associated with the chrysotile exposure is cons iderably less than that associated with the synthetic
mineral fibres tested.
(vi) Para-aramid Fibres
5.564  While in recent years the information base concerning aramid fibres has increased greatly,
there remain several issues.  The only data are those derived from experimental studies in animals.
While studies of biopersistence suggest that long fibres are shortened by enzymes in the lungs of
animal experiments (Searl) and hence removed from  the lung, the situation in humans is not known.
Two researchers (Davis143 and Pott144) have produced mesotheliomas by intra-peritoneal injection of
these fibres, so their potential to produce mesotheliomas cannot be dismissed.  The interpretation of
"proliferative keratin cysts" observed during inhalation experiments remains unclear.145 Minty et al., in
a criteria document for an occupational exposure limit (OEL) in the UK, summarized what was knownabout the para-aramid fibres at that time and drew several parallels with chrysotile.  For example they
state that "[T]he balance of evidence suggests that respirable aramid fibres possess a low potential to
produce mesothelioma which is likely to be at least as low as with chrysotile
.146
5.565  Referring to chrysotile, they conclude that mesothelioma "would only be detectable following
very heavy and prolonged exposures."  The recent ev idence that the mesothelioma risk for chrysotile
miners and millers is associated with tremolite, will render the threshold of mesothelioma for
downstream workers even more remote.  These authors considered a clear no-effect level of 2.5 f/ml
for pulmonary toxicity and a recommended OEL of 0.5 f/ml to allow for "uncertainties in interspecies
differences."
(vii) Epidemiological Data
(i) PVA
5.566  Drs. Musk, de Klerk, Henderson and Infante did not identify any epidemiological studies of
PVA fibre workers.  In fact, there is one study involving a small number of PVA fibre production
workers (about 400 exposed employees).147 Even though the length of exposure thus far is quite short,
already two lung cancer deaths have occurred in the cohort to date.  Clearly a much longer follow-upis needed.  Regarding mesothelioma, it must be noted that with such a small population, even if half
were dead and there were one mesothelioma, the risk would be 0.5 per cent which is more than the
risk of mesothelioma found in Quebec miners and millers exposed to tremolite contaminated
                                                                                                                                                                    
which resulted in 18.9 per cent lung tumours. Rats exposed to 232 f/ml of one type of glass fibre resulted in
5.9 per cent lung tumours, with 4.4 per cent lung tumours reported with other man-made vitreous fibres and13 per cent with a RCF sample. The air control resulted in 1-3 per cent tumours (At 1000 f/ml, the risk of lungtumours would be just under 2 per cent which is well within the rate of tumours in the control animals).
143Davis, J.M.G., Carcinogenicity of Kevlar Aramid Pulp Following Intraperitoneal Injection into Rats ,
(1987) Technical Memorandum No. TM/87/12 Published by the Institute of Occupational Medicine, Edinburgh,Scotland.
144Pott, F., Roller, M., Ziem, U., Reiffer, F.J., Bellman, B., Rosenbruch, M. and Huth, F.,
Carcinogenicity Studies on Natural and Man-Made Fibres with Intraperitoneal Tests in Rats,  (1989) In: Non-
Occupational Exposure to Mineral Fibres. J. Bignon, J. Pe to, K. Saracci eds. IARC Scientific Publication No. 90
Publ. International Agency for Research on Cancer, Lyon, pp. 173-179.
145IARC International Agency for Research on Cancer (1997), Monographs on the Evaluation of
Carcinogenic Risks to Humans. Vol. 68.
146Minty, C.A., Meldrum, M., Phillips, A.M. and Ogden, T.L., P-aramid Respirable Fibres Criteria
Documents for an Occupational Exposure Limit , HMSO (1995).
147Morinaga, K., Nakamura, K., Koyama, N. and Kishimoto, T., A Retrospective Cohort Study of Male
Workers Exposed to PVA Fibres , (1999) 37 J. Industr. Health, pp. 18-21.WT/DS135/R
Page 369
chrysotile.  (Also, the Panel should note that there were no mesotheliomas among 1267 deaths in
chrysotile exposed friction product manufacturing workers exposed to chrysotile.)  Thus, this study
cannot detect either mesothelioma or lung cancer risks as low as at that already known for chrysotile.
Clearly, there are no human data on which to assess risk to conclude that the risk is less than it is for
chrysotile either per f/ml of exposure or globally from work with products manufactured using PVAfibres.
(ii) Cellulose
5.567  Dr. Infante states that there are three studies in which cellulose exposures have been
investigated, but he does not identify them.  The other two experts do not suggest any epidemiological
data.  Studies in which there is no overall increase in mortality from lung cancer are not adequate to
investigate the risk of exposure.  To assess this risk, the relationship between lung cancer and
cellulose fibre exposures on a per fibre basis must be, but has not been, examined.
(iii) Para-aramid Fibres
5.568  None of the experts reported any epidemiological data.  Clearly, para-aramid fibres can be
inhaled, as experimental animals inhaled them.  However, because para-aramid fibres have been used
for such a short time, there are no data on the relationship between levels of fibre exposure and the
risks of lung cancer, mesothelioma or other adverse effects for persons working with this substitute orproducts manufactured using it.
(iv) Glass Fibres
5.569  There have been several studies of workers exposed to glass fibres during fibre manufacture.
Studies have also included rock [stone] and slag wool exposures.  The latter were associated with an
increased risk of lung cancer even at very low levels of exposure.  Doll
148 concluded that the risks
from such exposures were greater than those associated with chrysotile asbestos.  Doll summarized the
situation as follows:  "an occupational hazard of lung cancer has been demonstrated in the rock and
slag wool section of the industry and possibly the glass wool section."  The human evidence since that
time has not dispelled concern about the risks associated with these fibres.  This question is still not
resolved.
5.570  Dr. Infante149 and co-workers once reached the same conclusion for glass fibre (although he
has changed his opinion in his current report).  In his report, Dr. Infante mentions that after speaking
with workers, he now thinks that there was as bestos exposure at the plant studied by Shannon in
Ontario, Canada, where a high level of risk of lung  cancer was found in glass fibre workers.  A recent
discussion with Dr. Harry Shannon about his study of glass fibre workers reveals that to his
recollection, no one had raised the question of asbestos as a potential confounder in his study.  He
noted that, as the study was published many years ago, it seems unlikely that this issue – if it actuallyexisted – would not have been raised and studied, especially by the glass fibre industry.
150  Clearly, no
new analyses have been done, so the impact of supposed asbestos exposure, if it took place, is not
known.  Dr. Infante's reversal of opinion does not seem justified, as no new data are presented.  For
example, it is not known whether the "asbestos exposed workers" had high or low glass fibre
exposure.  If they had low glass fibre exposure, then the risk associated with the glass fibre exposures
                                                     
148Doll, R., Mineral Fibres in the Non-Occupational Environment:  Concluding Remarks,  in Bignon, J.,
Peto, J. and Saracci, R., eds., Non-Occupational Expos ure to Mineral Fibres, IARC Scientific Publication
No. 90, 1989, pp. 511-518.
149Infante, P.F. et al., Fibrous Glass and Cancer , (1994) 26 Am. J. Industrl. Med., pp. 559-584.
150Gibbs, G., Phone Communication.WT/DS135/R
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might increase.  Thus, without additional analyses, the best estimates at present are the original
analyses by Shannon.151
5.571  It was noted earlier that exposure levels during production may not be the same as those
during product use.  While it has not been possible to find data on the use of glass fibres in chrysotile
cement or friction products, there has been an estimate of the risk associated with glass fibres asinstalled in homes.  In this study, Wilson
152 used animal data to derive lung cancer risk estimates for
glass fibre exposure.  They assumed an exposure of 1f/ml for one year based on available data and
estimated that the lung cancer risk in smokers associated with blown glass wool without binder in a
smoker without a respirator would be 2.4 x 10-4.  If one uses the same methodology as applied by
them to derive a chrysotile estimate (based on epidemiological data), but for friction product
manufacture, the risk would be very much lower:  0.12 x 0.00058 = 0.00007 or 7 x 10-5.  This is a
lower risk than calculated for glass fibres.  In fact, there is no demonstrated increased risk of lungcancer in the friction industry, so even this chrysotile risk is hypothetical and certainly an
overestimate.  Wilson acknowledges this in their paper.
5.572  In this light, it is safer to work with chrysoti le in friction products than to work with glass
fibres.  While it might be argued that there has been no report of an increased risk of mesothelioma in
humans as a result of manufacturing glass fibres, in the case of chrysotile, there is greater confidenceconcerning this lack of risk because there is no evidence of an increased risk of mesothelioma
associated with friction products throughout their lifecycle, and the studies are far more voluminous
and varied in approach.  There are no systematically gathered data available concerning downstream
risks for glass fibres as used as a substitute in cement or friction products.  Similarly, with regard to
the asbestos cement industry, Harrison
153 reports that most studies have not found an increase in
mesothelioma;  certainly this is true for chrysotile  asbestos cement plants.  Thus, it is evident that
there are clear no epidemiological or experimental data to conclude that "glass fibres" are safer than
chrysotile, indeed, there is evid ence to suggest the contrary.
5.573  In summary, the experts have based their opinions on very limited, if any, data.   The data that
do exist suggest that the conclusions of the Panel's experts concerning the relative safety of thesubstitutes and chrysotile at low concentrations are incorrect.
2. The European Communities
(i) Introduction
5.574  Each of the four scientific experts appointed by the Panel has recently responded to the points
which the Panel wished to clarify.  The European Communities note that the four experts consulted
unanimously and unambiguously corroborate the analysis that led France to adopt the Decree 96-1133
banning asbestos.  This analysis was communicated to  the Panel in the two written submissions of the
European Communities of 21 May and 30 June 1999 and is based on the following points:
(a) All forms of asbestos, including chrysotile asbestos, are carcinogens, and there is no
scientifically established threshold below which exposure to asbestos would be
without risk for humans;
                                                     
151Shannon, H.S. et al., Mortality Experience of Ontario Glass Fibre Workers − Extended Follow-Up ,
(1987) 31 Ann. Occup. Hyg., pp. 657-662.
152Wilson, R., Langer, A.M. and Nolan, R.P., A Risk Assessment for Exposure to Glass Wool , 30
Regulatory Toxicology and Pharmacology, pp. 96-109.
153Harrison, T.W., Levy, W.S., Patrick, G., Pigott, G.H. and Smith, L.L., Comparative Hazards of
Chrysotile Asbestos and its Substitutes: A European Perspective , (1999), Environmental Health
Perspective, 107.WT/DS135/R
Page 371
(b) exposure to asbestos, including chrysotile asbestos, is the cause of many cancers, the
vast majority of which affect secondary users, particularly workers coming into
contact with materials containing asbestos, including asbestos cement;
(c) so-called "controlled" use of asbestos is in fact impossible in practice;
(d) there are asbestos substitutes which are far less dangerous for human health.
5.575  In this document, the European Communities do not wish to make systematic and detailed
comments on all the replies by the four experts consulted, but will simply refer to the main
conclusions and give a summary of their replies in the annex.154
(ii) The four experts consulted agree that all types of asbestos, including chrysotile, are
carcinogens and that there is no established threshold under which exposure to asbestos is without
risk for humans
5.576  The four scientific experts unanimously consider that chrysotile asbestos, as well as
amphiboles, can cause mesothelioma and lung cancer inter alia .
5.577  The four experts also unanimously agree that there is no scientifically established threshold
below which exposure would not pose any risk of cancer for humans.  All the experts state that the
risk of cancer is proportional to the cumulative level of exposure and all consider that the
non-threshold linear model is the most scientifically appropriate model for guaranteeing the level ofhealth protection decided upon by France in this particular case.  This explains and confirms that the
non-threshold linear model has always been used, without exception, by the authorities in all those
countries that have so far carried out scientific assessment of the cancer risk.
(iii) The four experts consider that exposure to asbestos, including chrysotile asbestos, is the cause
of many cancers that mainly affect secondary users, particularly workers in contact with materialscontaining asbestos, including asbestos cement
5.578  The four experts consider that the vast majority of the risks concern so-called "secondary"
users
155, in other words, workers making intervention s (building workers, electricians, plumbers,
maintenance workers, handymen, etc.) because of their large number and the nature of their activities,
even if the individual risks are sometimes lower.
5.579  For example, most cases of mesothelioma now affect this category of workers in all the
industrialized countries, including Canada (Quebec) and Australia, countries which produce asbestos.
The four experts point out that the levels of exposure in the course of occasional contacts with
asbestos cement products are very high, much higher than the levels at which a risk of cancer has been
definitely and scientifically established.
(iv) The four experts consider that the so-called "controlled" use of asbestos is not practically
possible
5.580  The four experts unanimously agree that so-called "controlled" use aimed at ensuring a
constantly low level of release of the fibres into the atmosphere is absolutely impracticable in the vast
majority of work situations where workers have to deal with friable or non-friable materials
containing asbestos.
                                                     
154See Annex V to this Report.
155 See factual arguments by the EC, Section III.A.4.WT/DS135/R
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5.581  The four experts consider that it might be possible in very special situations where a small
number of workers carry out a very precise task.  They also indicate that interventions on materials
such as asbestos cement can release very large quantities of asbestos fibres;  that protective equipment
is not or not always effective and not always used;  that the recommended procedures are rarely or
incorrectly followed in small enterprises such as those in the building sector;  that it is quiteimpossible to apply them to non-professionals (for example, handymen, etc.).
E. S
UPPLEMENTARY REMARKS FROM DR . HENDERSON156
1. Concerning the comments from  the European Communities
5.582  The comments from the European Communities are very brief, occupying only four pages in
English translation, so that only a short comment is needed.  The tabular summary of the four experts'
reports appears to represent a fair précis  of my conclusions and opinions, if an oversimplification.  In
para. 5.579, the European response refers to Canada (Quebec) and Australia as countries that produceasbestos.  As pointed out in para 5.27, Australia is no longer an asbestos producer.
2. Concerning the comments from Canada
5.583  At 62 pages and with over 50 Annexes, the comments from Canada are far lengthier than the
response from the European Communities;  the Canadian documents include new information,
necessitating more extensive discussion.  Some general comments follow;  other issues are discussedlater under specific sub-headings.
5.584  In para. 5.441, the comment is made that some of the answers from the experts "appear not to
distinguish between chrysotile and amphibole expo sure" or between "modern uses ... and historical
uses ... ."  Throughout my own Report, I tried to make this distinction wherever appropriate, and my
answers to the Panel's questions deal almost excl usively with chrysotile (like EHC 203 [1]) -e.g. my
discussion of the risks to brake mechanics
157 and the tabulation of risk estimates for lung cancer and
mesothelioma (Tables 12 and 13 in paras. 5.203 and 5.205.  At the same time, it seems worth
reiterating that commercial chrysotile from Canada on average contains variable trace amounts (about
<1 per cent) of tremolite (fibrous tremolite is a non-commercial amphibole;  e. g. please see EHC 203).
In relation to Canada's concerns about the "experts' conclusions on tradesmen" (e.g. buildingconstruction workers), my perspective seems to concur with the IPCS/WHO monograph on chrysotile
(EHC 203):
"... (c)  Some asbestos-containing products pose particular concern and chrysotile use in these
circumstances is not recommended  These uses include friable products with high exposure potential.
Construction materials are of particular concern for several reasons.  The construction industry
workforce is large and measures to control asbestos ar e difficult to institute.  In-place building materials
may also pose risk to those carrying out alterations, maintenance and demolition" ...  [p 144].
5.585  My recognition that chrysotile is substantially less potent than the amphiboles on a fibre-for-
fibre basis for mesothelioma induction - and that present exposures overall are substantially less than
in the past - explains why my Report dwelt mainly on workplace exposures (e.g. to building materials
and friction products).  Non-workplace exposures (e.g. non-occupational exposures including
household contact or neighbourhood exposures [2-4]) - and exposures to friable insulation materials -received less attention and were included mainly to put the present situation into historical
perspective.
                                                     
156For complete references of the documents quoted in  this Section, see Annex III to this Panel Report.
157For decades, brake blocks and brake linings used in Australia have contained Canadian chrysotile
asbestos only, with no added amphiboles.WT/DS135/R
Page 373
5.586  In para. 5.489, the Canadian comments state th at:  "... He [Henderson] believes amphiboles
may be greater than 60 times more likely than chrysotile to induce mesothelioma ... ."  In fact, in
para. 5.103, I had stated that:
"There is general though not universal agreement of a differential potency between the amphiboles
versus chrysotile for mesothelioma induction;  in this respect, the amphiboles are substantially morepotent, with estimates ranging from 2-4X, to 10X, to 12X on a fibre-for-fibre basis, to 30X, to a 30-60Xgreater potency, or more (e.g. please see EHC 203)."
5.587  Later in my Report (paras. 5.141 and 5.413), I gave my estimate that chrysotile has a
potency 1/10th-1/30th the carcinogenicity of crocidolite  for the mesothelium.   This estimate has not
changed.
5.588  Some clarification of my answer to Question 1(b)158 from the Panel seems necessary, taking
into account Canada's quotation of my view and the comment that:  "Canada takes note that ... [this is]
... overwhelmingly a workplace issue, and therefore not related to the 'handyman'."  In my answer, Itook "workplace" to refer to any situation where work  of any type is carried out (e.g. cutting, sawing,
drilling, grinding, rasping or sanding of asbestos -cement building products), whereas I interpreted the
expression "a larger part of the population" to refer to general environmental exposure to asbestos
(e.g. simple occupancy of buildings, or potential exposure of urban dwellers in general to asbestos
derived from the brakes of passing vehicles).  Obviously, any risks to handymen who carry outmaintenance on homes only occasionally will be much less than the risks to professional tradesmen
such as carpenters, who work day in, day out at building construction sites - because the frequency
and duration of exposures for the handyman will be less (with lower cumulative exposures), assuming
the types of asbestos to be the same.  However, this may not always be so.  For example, I know that
some "handymen" in Australia specialize in buying and living in dilapidated houses, to carry out
extensive renovations on these dwellings (e.g. throughout each weekend or more often) before selling
them a year or more later;  because the house qualifies as a principal place of residence, the profit isnot taxable.  The handyman then repeats this exercise on another "handyman  special" house, and so
on.  Many such handymen also regularly carry out maintenance and renovation work on other homes,
so that their exposures may approach those of pr ofessional tradesmen, but they style themselves as
"home handymen" .  The activities of such handymen are virtually unregulated because they are
self-employed and a number work on a "strictly cash" basis.
5.589  In commenting on the experts' responses to Questions 1(b), Canada reiterates the proposition
that "chrysotile is readily removed from the lung", and estimates of the half-life of chrysotile are given
as 90-110 days, and even a shorter estimate of < 10 days from Dr. David Bernstein.  Canada goes on
to state that "size for size, chrysotile has a very short half-life."  I again draw attention to the 1999
study by Finkelstein and Dufresne [5], who found a l ung tissue half-life of eight years for chrysotile
fibres > 10 µm in length;  this investigation was discussed briefly in the Endnote to my report (see
Section V.C.4):
" ... in the past, the kinetics of chrysotile clearance from lung tissue have been investigated mainly in
experimental models using rodents.  In an autopsy study published in 1999, Finkelstein and Dufresne
[5] ... investigated clearance of chrysotile from the lung tissue of 72 Quebec chrysotile miners andmillers in comparison to 49 control subjects, using regression analyses, with the following findings:
There was a significant association between the duration of occupational exposure and the tissue
burdens of chrysotile and tremolite.
The concentration of chrysotile decreased with time after exposure ceased but the concentration of
tremolite did not.
                                                     
158Please see also my answers to Questions 1(e) and 5(a).WT/DS135/R
Page 374
The clearance rate varied inversely with the length of chrysotile fibres.  For fibres > 10 µm in length -
i.e. fibre lengths in the reported range for carcinogenicity - the clearance half-time was estimated to beeight years.  In other words, the tissue bio-persistence of chrysotile fibres in this study seems
substantially more prolonged than in rodent experiments, and presumably corresponds to persistent
high chrysotile fibre concentrations for many years after cessation of occupational exposure in humans,as discussed on p 31.  It is also notable that th e concentration of 6,250,000 chrysotile fibres mentioned
on p 31 (for an individual but by no means unusual patient) is probably above the level at which Rogerset al. [6] identified an odds ratio for mesothelioma of > 8.5 (even allowing for differences in fibre size
in the counts by the two different laboratories), and even the duration of 16 years after exposure
stopped (as opposed to its commencement:  24 years) falls into the lag-time range for lung cancerinduction by asbestos.
Studies like this suggest that clearance mechanisms can be overwhelmed and break down at
occupational levels of exposure in humans, with the existence of a long-term sequestered fraction ofchrysotile fibres."
5.590  This study seems to be of particular significance for the tissue bio-persistence of chrysotile
fibres in comparison to substitute materials (please see below, paras. 5.642 to 5.652).
5.591  I also emphasize that some of the estimates given in my Report were conservative, with
potential under-estimation of effects.  For example, after discussing the incidence rate for spontaneous
mesothelioma unrelated to asbestos as being in the range of 1-2 mesotheliomas per million person-
years - whereas the likely true figure is probably less than one [4] - I nonetheless used the upper figureof two cases/million for comparison with mesoth elioma incidence in some occupational groups
(e.g. the incidence of mesothelioma among male automobile/brake mechanics in Australia;  please see
para. 5.253).  In a similar way, I referred to a 30-fold differential rate for lung cancer among the
South Carolina (Charleston) chrysotile textile work ers in comparison to the Quebec chrysotile miners
and millers, whereas others give the differential as up to "about 50 times higher in Charleston" [7].
5.592  I also draw attention to the occurrence of mesothelioma among various cohorts and studies
other than the Quebec chrysotile miners/millers, as set out in paragraphs 5.124-5.141, and to the
incidence of mesothelioma among mechanics in Australia as shown in the 1999 Report for the
Australian Mesothelioma Register [AMR 99] an d in NICNAS 99 (see my answer to Question 2).
5.593  In my Report, I discussed the limitations or deficiencies of those studies which reported an
increased risk of lung cancer only among workers with pre-existing asbestosis (e.g. the Hughes-Weill
study [8]) - and the uncertainties of the study by Camus et al. [9] on lung cancer risk from non-occupational exposure to chrysotile among females in Quebec
159 - but the comments from Canada
(para. 5.529) reiterate the Hughes-Weill conclusion that an increased risk of lung cancer occurs "only
in those with asbestosis."  (Please see paras. 5.73-5.74 and 5.152-5.162 above;  this subject was
reviewed extensively by Henderson et al. [13] in 1997.  Lung cancer risk among the South Carolina
chrysotile textile workers versus  the Quebec chrysotile miners/millers is also discussed in paras. 5.596
to 5.620 below).
                                                     
159Canada's comments also refer to the meta-analysis of  lung cancer risk reported by Lash et al., [10],
which identified a low risk.  Meta-analysis is a field that lies outside my expertise, but I understand that there are
various models for meta-analysis and problems with this appr oach (e.g. see Blettner et al. [11] who state that "...
Meta-analyses from published data are in general insufficient to calculate a pooled estimate since publishedestimates are based on heterogeneous populations, different study designs and mainly different statistical models[Abstract] ... Meta-analyses using published data are, ther efore, restricted and seldom useful to produce a valid
quantitative estimate or to investigate exposure relations such as dose-response [p 8] ...").  In a meta-analysis
of 69 asbestos-exposed occupational cohorts, Goodman et al. [12] identified "... meta-SMRs of 163 and 148 [for
lung cancer]  with and without latency, with significant heterogeneity of results ..."WT/DS135/R
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5.594  At various points (paragraphs 5.475, 5.498 a nd 5.545), the comments from Canada quote
de Klerk and Armstrong [14], in a chapter on The Epidemiology of Asbestos and Mesothelioma , in the
book Malignant Mesothelioma,  for which I was the senior editor and a co-author.  I shall leave it to
Dr. de Klerk to respond.
5.595  In passing, I point out that Malignant Mesothelioma  was published in 1992;  the text for those
chapters which I wrote was current up to September 1990, and the manuscript was sent to the
publisher shortly thereafter.  Much new information on asbestos-related diseases has accumulated
since that time (e.g. references 15, 16, 113, 125, 126, 131-133, 140, 141, 170-172, 177-179, 181,
185-187, and 190-194 in my Report, to list but a few).  My views on many aspects of asbestos-related
disorders have changed very substantially since Malignant Mesothelioma  was published (e.g. my
views on asbestos and lung cancer - please see references [13, 15-18] in these Supplementary
Remarks).
(a) Lung cancer rate among South Carolina (Charles ton) chrysotile textile workers versus the
Quebec chrysotile miners/millers
5.596  With respect to this question, Canada states (see paras. 5.485-5.486):
"Dr Henderson states that the "greater carcinogenicity  of the amphiboles [...] appears not to extend to
the induction of lung cancer [p 40], but he admits that 'chrysotile is implicated in one of the lowest ratesof asbestos-associated lung cancer (in Quebec chrysotile miners and millers)' [where I also stated that
chrysotile is also implicated in the highest lung cancer rate].  Dr Henderson's reluctance to conclude the
greater carcinogenicity of amphiboles seems to be caused by the results of Dr Dement's study of theCharleston, South Carolina asbestos textile industry [...]".
"The Charleston data has [ sic] recently been revisited by Bruce Case, André Dufresne, A.D. McDonald,
J.C. McDonald and Patrick Sébastien in a study released in Maastricht in October 1999 at the VIIth
International Symposium on Inhaled Particles, a symposium attended by some of the world's leading
experts.  This study shows that a significant amount of crocidolite and amosite fibres was found in the
textile workers' lungs.  This analysis sheds new light on the issue and explains the extreme results of theoriginal study by Dr Dement [...] and the subsequent  study by Dr Stayner [...].  These studies of textile
workers exposed to crocidolite and amosite can thereby no longer be used to demonstrate the risksassociated with chrysotile fibres."
5.597  Subsequently, the manuscript for a paper by Case et al. [19]  entitled Asbestos Fibre Type and
Length in Lungs of Chrysotile Textile and Production Workers:  A Preliminary Report  arrived by
facsimile transmission.  I offer the following comments on this document (and, later, on the Abstractfor the corresponding presentation at the Maastricht meeting [20]):
5.598  A disclaimer beneath the title [19] indicates that this is a "
DRAFT DOCUMENT :  SUBJECT TO
REVISION - NOT TO BE CITED ".  It is cited nonetheless.  There is no indication that this document has
gone through a process of peer review and been accepted for publication.
5.599  This study revisits the study reported in 1989 by Sébastien et al. [7], and the draft manuscript
indicates that the same grids were examined (but fewer cases).  The main difference between this
investigation and the earlier study by Sébastien et al. [7] is that Case et al. [19, 20] analysed long
fibres > 18 µm in length, whereas Sébastien et al. [7 ] studied fibres > 5 µm in length, with an aspect
ratio > 3:1.  (It is common practice for fibre burden analyses to focus on fibres ≥ 5 µm in length and
there is no evidence that the carcinogenicity of asbe stos fibres - in terms of lung cancer induction - is
restricted only to fibres about 20 µm in length or more.)
5.600  Another study on the lung fibre content of the Charleston chrysotile textile workers was
reported in 1997 by Green et al. [21];  this investigation studied all fibres resolvable by electronWT/DS135/R
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microscopy and with an aspect ratio > 3:1.  For this study, lung tissue was analysed from 39 textile
workers versus 31 comparable controls matched closely for age (median age at death for the asbestos
workers was 56.0 years, versus 59.0 years for the controls).
5.601  In the Green et al. [21] study, the Charleston chrysotile workers had a higher lung content of
chrysotile in comparison to the controls (geometric mean = 33,450,000 versus   6,710,000 f/g dry
lung), with a higher content of tremolite (3,560,000 vs. 260,000);  the asbestos workers also had a
slightly elevated mean amosite/crocidolite content of 470,000 fibres vs. 210,000 for the controls
(please see Table 1).
TABLE 1: MINERAL FIBRE CONTENT OF LUNG TISSUE , SOUTH CAROLINA ASBESTOS
TEXTILE WORKERS VS. CONTROLS (ALL COUNTS = FIBRES X 106 / G DRY LUNG )*
Textile workers Controls
Age at death (median;  years) 56.0 (M );  57.0 (F) 59.0 (M);  62.5 (F)
Year of death (median) 1971 (M and F) 1972 (M);  1971 (F)
Chrysotile (fibres x 106/ g dry lung) 33.45 6.71
Tremolite 3.56 0.26
Amosite/crocidolite 0.47 0.21
Anthophyllite 0.16 0.13
Mullite 1.63 4.01
Other 1.02 1.9
All fibres 52.46 16.02
*Modified from Tables 1 and 3 in Green et al. [21];  M = men;  F= females.
5.602  In the discussion section, Green et al. [21] commented that:
"The population was exposed almost exclusively to chrysotile asbestos from Quebec.  The native ore
contained about 1% tremolite asbestos.  The high concentrations of chrysotile and tremolite asbestosfound in the lungs of the asbestos textile workers are also consistent with their exposure histories.  Ourfinding on enrichment of tremolite relative to chrysotile in the lungs of asbestos workers is consistent
with previous reports.  The presence of crocidolite in some of the lungs of the asbestos workers is in
keeping with the use of small quantities of crocidolite between 1950 and 1975, but the values were onlyslightly greater than those found in the control population .  ... The increased risk of lung cancer in the
asbestos textile workers is also unlikely to be due to differences in exposure to tremolite asbestos, asSebastien et al. have shown that the textile workers had less tremolite asbestos in their lungs thanminers and millers of the original ore after matching for exposure intensity.  Differences in exposure to
other commercial amphiboles (crocidolite and amosite) may have played a small part based on our own
data ... and on the data of Sebastien et al., which showed a small excess of these amphiboles in thelungs of the textile workers compared with the miners;  however, it is very unlikely that this is thewhole explanation as commercial amphiboles formed a very small proportion of the total amphiboles inboth studies.  Moreover, review of the 10 cases with lung cancer in this study on whom lung fibre
analyses were made, showed only one case with substantially increased (> 1 x 10
6 fibre/g dry lung)
crocidolite or amosite".
5.603  In this study, it is also notable that the lung cancer cases on which fibre burden analysis was
carried out were not representative of the cohort as a whole:  e.g. autopsies were carried out on only
about 10 per cent of all deaths in the cohort, and the mean lifetime cumulative exposure for the ten
lung cancer cases was 94.6 fibre-years in comparison to 67 fibre-years for male lung cancer casesacross the whole cohort [21, 22].WT/DS135/R
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5.604  There are even greater concerns about the representativeness of the cases on which fibre
burden analysis was carried out by Sébastien et al. [7 ].  For example, this study was confined to tissue
from 72 autopsies among 857 deaths (8.4 per cent) among the Charleston cohort, and there were only
seven lung cancer cases out of 66, whereas Case et al. [19] list 126 lung cancers, so that the fibre
burden data reported by Case et al. [19] appear to deal with no more than 5.56 per cent of theCharleston lung cancers.  It is also notable that the mean age at death in the Charleston group was
about a decade younger than the age at death for the Thetford group which formed the basis for
comparison in the 1989 study by Sébastien et al. [7]
160
5.605  In addition, as reported by Sébastien et al. (see Table 3 in reference [7]), those cases from the
Thetford group that came to autopsy showed an over-representation of asbestos-related diseases (lung
cancer, mesothelioma and pneumoconiosis) than the Thetford cohort overall - so that cases of lung
cancer + mesothelioma + pneumoconiosis added up to 37 out of 89 autopsies (42 per cent), incomparison to 306 out of 4463 deaths across the whole cohort (7 per cent) [7].  For the Charleston
cohort, the figures were more comparable, so that lung cancer + mesothelioma + pneumoconiosis
cases added up to 13 out of 72 autopsies (18 per cent) in comparison to 10 per cent across the
cohort [7].
5.606  In the more recent study from Case et al. [19], there is a further point on which the two study
groups (Thetford versus Charleston) are not comparable:  the time following cessation of exposure
was a median of eight years for the Thetford group, in comparison to 20 years for the Charleston
cohort (please see Table 2).  Therefore, it is clear that those lung cancer cases on which fibre burden
analysis was carried out from each cohort were not representative of each cohort, and that there were
also substantial differences between the two coho rts for the same types of case.  Finally, the
manuscript from Case et al. [19] does not include a control group against which the two cohorts can be
compared (the only one of the three investigations that does is the Green study [21]).
TABLE 2: COMPARISON OF THE SOUTH CAROLINA AND QUEBEC CHRYSOTILE WORKER COHORTS *
South Carolina textile workers Quebec miners/millers
Cohort number 3022 10,918
Cohort deaths 1258 8009
Age at death (years) 67 ± 10 (??)** 56 ± 6 (??)**
Lung cancers in cohort 126 [SMR 197] 657 [SMR 137]
Mesotheliomas in cohort 2 38
Years since cessation of exposure
(median)20 8
Geometric mean exposure (mpcfy)*** 3.63 186
Subjects studied 64 43
Lung cancer cases studied ?
(7/72 autopsies in ref [7])?
("random" selection of 43 cases
from 89 original cases that
included 22 lung cancer cases -
ref [7])
Chrysotile (fibres x 106/ g dry lung) 0.054 0.231
Tremolite 0.027 0.325
                                                     
160There is a discrepancy between the ages at death in the original paper by Sébastien et al. [7]
(i.e. mean = 55.8 ± 9.7 for the Charleston cohort vs 67.5 ± 9.7 for the Thetford group) and the follow-up study
by Case et al. [19] (Table 1A, where the ages are reversed:  67 ± 10 for the Charleston group vs 56 ± 6 for
Thetford).  Clearly, one or the other must be wrong.WT/DS135/R
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South Carolina textile workers Quebec miners/millers
Amosite/crocidolite 0.037 0.024
Total amphibole (tremolite +
amosite/crocidolite)  0.064    0.349
*Modified from Case et al. [19].  Fibre counts repres ent geometric means;  all expressed as fibres x 106/ g dry
lung;   **see footnote 160;  ***mpcfy = mi llions of particles per cubic foot-years.
5.607  From the above Table, it is evident that the amosite/crocidolite content of lung tissue from the
textile workers is slightly (< 2-fold) higher than  the amosite/crocidolite in the lung tissue from the
Quebec miners and millers (37,000 fibres > 18 µm in length versus  24,000).  This difference in
concentration seems to be insufficient to explain th e "huge" [19] risk difference (about 30-fold) in the
slope of the lung cancer dose-response line between the two groups.  In addition, it is noteworthy that
the tremolite content of lung tissue was higher in the Quebec miners and millers than the Charleston
textile workers (325,000  versus  27,000 for fibres with a mean fibre length of 21.7 versus  21.9 µm).
The point is that the total amphibole content (tremolite + amosite + crocidolite) is higher in the
Quebec miners and millers at 349,000 f/g dry lung in comparison to a total amphibole content
of 64,000 among the Charleston textile workers.  In this respect, there is no evidence that tremolite issubstantially less potent than the other amphiboles for lung cancer induction, as shown by the high
lung cancer incidence (SMR = 285) among Montana vermiculite miners exposed only to
tremolite/actinolite (please see paragraph 5.107-5.111).
5.608  From these studies, it appears that the amosite/crocidolite content of lung tissue among the
Charleston textile workers may in part be a reflection of low level exposure to the small amount ofcrocidolite (< 1000 kg total) used in the plant from 1950-1975 to make an asbestos tape or braided
packing.  The material was received at the plant as a yarn ready for weaving, and no fibre preparation,
carding, spinning or twisting was done using croc idolite.  Packing workers were not included among
the textile worker cohort, and analysis of lung cancer risk by operation in the plant shows all
operations to be at about the same lung cancer risk after controlling for chrysotile exposure in alogistic model (Dement, personal communication, 1999).
5.609  A portion of the amosite/crocidolite content may also be explicable by general environmental
(non-occupational) exposure, taking into account the small differences between the amphibole content
in the textile workers versus  the controls in the study reported by Green et al. [21].  In this respect,
amphibole concentrations of up to 100,000-200,000 fibres per gram (f/g) dry lung tissue can be
expected for about 5 per cent of the population in Germany [23].  Therefore, it seems that the
amosite/crocidolite cannot explain the risk of lung cancer in the Charleston cohort in comparison toeither matched controls (also matched for smoking) versus the Thetford miners and millers.
5.610  If major significance is to be assigned to the small difference in amosite/crocidolite content of
lung tissue between the Charleston workers versus the Thetford miners/millers for lung cancer
induction, a question that immediately arises is:  where are the mesotheliomas among the Charleston
workers?   Case et al. [19] suggest that misclassification of mesotheliomas as lung cancers among the
Charleston workers could have produced under-estimation of the true number of mesotheliomas
"while having virtually no effect on the lung cancer excess or lung cancer exposure-disease slope of
risk."  No evidence in support of this proposition is adduced, and Case et al. [19] state that this is
"speculation."  The larger number of mesotheliomas in the Quebec cohort may be explicable in part by
the higher mean total amphibole content for this group, but this still leaves unexplained thedisproportionately larger numbers of lung cancers in the Charleston group (e.g. the ratio of lung
cancers to mesotheliomas in the Thetford group is 657/38 = about 17:1, whereas the ratio for the
Charleston group is 126/2 = 63:1).WT/DS135/R
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5.611  Case et al. [19] are also rather more cautious in their interpretation than the propositions put
forward in Canada's responses to the reports from the experts. For example, on the last page of text
they state:
"... comparison of groups of individuals using this technique is valid only insofar as those studied are
representative of the larger groups ... from which they are derived.  We cannot be certain to whatdegree our groups of chrysotile miners/millers and textile workers are representative of the cohortsfrom which they are derived
161 ...  the two groups are not directly comparable in some ways:  not only
was exposure much higher in the miners/millers, but the interval between cessation of employment and
death was shorter .... .  Our results closely parallel th ose reported by Sebastien et al..  Any other result
would be surprising since the subjects were drawn from the latter study.  ...  Caution remains ininterpretation.  ...  One continuing mystery, given the apparent non-trivial long-fibre commercialamphibole exposures is the low level of reported mesotheliomas in this cohort ...".
5.612  Given the data on fibre lengths across the cohorts, in comparison to the data in Sébastien et al.
[7], the difference in lung cancer rates between th e two groups cannot be explained by differences in
fibre length.  This is stated explicitly by Case et al. [19].
5.613  However, on looking at the data, it seems that the differences between the two cohorts might
be explicable in part by the exposure estimates.  Differences in exposure assessment are not refuted by
the "new" study reported in draft form by Case et al. [19] or by the earlier study reported by Sébastien
et al. [7]:  e.g. the difference between 20 years (Charleston) and eight years (Quebec) for clearance
after exposure ceased could have a large effect.  One can calculate the final exposure (end ofexposure) (N
0) from the final fibre content in lung tissue at death (N), from the equation
N/N 0 = e-λt
where λ represents a clearance coefficient ( λ = 0.693 ÷ T 1/2 ) and t = half-life in tissue (T 1/2).  For T 1/2 =
8 years [5], λ = 0.693/8, so that for the chrysotile miners/millers, where N = 0.231, N 0 = 0.462.  For the
Charleston textile workers, where N = 0.054, N 0 = 0.306.
5.614  If T 1/2 is shorter (e.g. one year), then N 0 for the miners/millers = 59.2 and the corresponding
N0 for the textile workers = 56456.
5.615  Therefore, for a half-life of eight years, one would expect the ratios of exposure (exposure
miners/millers ÷ exposure textile workers) to be 0.462/0.306 = 1.5.  For a half-life of one year the
ratio becomes (exposure miners/millers ÷ exposure textile workers) 59.2/56465 = 0.001.  (For tissue
half-lives of 90-110 days or < 10 days, the differences would be even more drastic.)  However, the
ratio of the estimated exposures (mpcfy Quebec /mpcfy Charleston ) is 186/3.63 = 50, suggesting that one or
other particle count estimate is incorrect.
5.616  In this respect, it might be argued that the exposure estimates for the Charleston cohort
represented an under-estimation of exposure, but this suggestion is not supported by the low tremolite
content in the lung tissue of the Charleston workers, and is explicitly rejected by Sébastien et al. [7],
who state (p. 187):
"The hypothesis of a systematic underestimation of exposures to asbestos in Charleston, which would
have accounted for the difference in risk, must ther efore be rejected and other explanations sought."
5.617  Given that contamination of the Charleston chrysotile by mineral oils has now been excluded,
one possibility that remains is over-estimation of the exposures for the Quebec chrysotile
                                                     
161Clearly, from the data in Table 2 and the discussion in paras. 5.604 to 5.609, they are not
representative.WT/DS135/R
Page 380
miners/millers (with under-estimation of risk).  If this  explanation is unsustainable, it follows that the
paradox remains, it remains unexplained, and seems likely to remain so.
5.618  Finally, I draw to the attention of the Panel th e following comment by Case and Dufresne [20]
in the Abstract for their presentation at the Maastricht meeting:
"Risk assessment for asbestos exposure is based on lung cancer risk for textile workers, rather than
miners/millers."
5.619  In the draft manuscript, Case et al. [19] state only that:
"... suggestions that the textile worker mortality data [are] suitable for chrysotile risk assessment [for
lung cancer] should be re-evaluated ... ."
5.620  Therefore, even if one accepts this proposition for the moment, the claim that the
South Carolina cohort can "thereby no longer be used to demonstrate the risks associated with
chrysotile fibres" goes beyond the data in this study.  For the reasons discussed in this section, I
conclude that the data in Sébastien et al. [7] and in Case et al. [19] do not detract from the conclusionsdrawn by myself and other authorities from the investigations carried out the South Carolina cohort by
Dr. Dement and his colleagues [22, 24].
(b) The question of a threshold for the carcinogenicity of chrysotile (lung cancer and
mesothelioma
5.621  On this question, I simply reiterate EHC 203:
"Exposure to chrysotile asbestos poses increased risks for asbestosis, lung cancer and mesothelioma in
a dose-dependent manner.  No threshold has been  identified for carcinogenic risks" [p. 144].
5.622  In the absence of a threshold or an agreed alternative (non-linear) exposure-response model,
the linear relationship model is widely employed for risk assessment at low levels of exposure.
5.623  As indicated, the precision or validity of this model is not known at low levels of exposure
and, as stated by Dr. de Klerk, the model provides a "conservative estimate".  This is the point:  in the
absence of direct observational data or credible alternative models, the linear model errs - if it does err
- on the side of safety, which is appropriate for risk assessment as a prelude to the formulation of
occupational health and safety and public health policy.  The principle is:  if there is doubt, play safe
(i.e. first, do no harm;   primum non nocere).
5.624  In relation to prudent approaches to occupational and public health policy, The Minerals and
Metals Policy of the Government of Canada162 states the following (p 7):
"The precautionary principle is an important factor when the Government needs to make a decision in
the face of scientific uncertainties about cause and effect, and when the potential environmental
consequences are generally considered to be seriou s or irreversible.  This principle was enunciated
clearly as Principle 15 in the 1992 Rio Declaration on Envi ronment and Development
(the Rio Declaration) of the United Nations Conference on Environment and Development (UNCED),to which Canada is a signatory:
'Where there are threats of serious or irreversible damage, lack of full scientific certainty shall not be
used as a reason for postponing cost-effective measures to prevent environmental degradation.'
                                                     
162NRCAN, The Minerals and Metals Policy of the Government of Canada:  Partnership for
Sustainable Development , Public Works of Canada, 1996.WT/DS135/R
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The principle complements science-based approaches for the management of risks.  Its use is premised
on the recognition that our scientific understanding of the potential magnitude and consequence ofimpacts on human health and the environment of the production and uses of some minerals and metals
may be incomplete.  While there is a need to work toward closing such gaps in our understanding, there
is also a requirement, where potential impacts are 'ser ious or irreversible', to consider a cost-effective
precautionary approach."
5.625  Later, on page 12, the same Minerals and Metals Policy  document states:
"...  It is generally accepted that, in some cases, the risks associated with certain products or product
uses cannot be properly controlled or managed.  Consequently, where such a situation exists, theGovernment [of Canada] will either discontinue or prohibit the specific product or product use."
5.626  Three additional points are worth iteration:
• Exposure to commercial Canadian chrysotile is not "chrysotile-only", but usually
chrysotile + trace tremolite exposure, although evidence indicates that chrysotile
when uncontaminated by tremolite also has the capacity for the induction of lungcancer and mesothelioma.
• Risk estimates for lung cancer and mesothelioma for low levels of chrysotile exposure
were set out in Tables 12 and 13 (see my response to Question 1(d)).
• As stated in section C.1(f)(viii) and in paragraph 5.95, there are no observational data
on the interactive effects of inhaled commercial chrysotile fibres when these aresuperimposed separately and later upon a pre-existing amphibole ± chrysotile burden
within lung tissue (?superimpositional additive or multiplicative carcinogenic effect).
In my Report, I emphasized that it has been estimated that up to 15-20 per cent of
men in industrialized societies may have sustained occupational exposures to asbestos(chrysotile/amphiboles), and Rödelsperger et al. [23] indicate that fibre concentrations
of 100,000-200,000 amphibole f/g dry lung tissue may be expected for about 5 per
cent of the population in Germany.  Rödelsperger et al. [23] have also identified a
dose-response relationship for mesothelioma induction at these low fibre
concentrations.  We do not know what the effect of subsequent chrysotile fibreinhalation superimposed upon an existing amphibole burden of this order might be,
but NICNAS 99 states the following (p. 61):
"... multivariate analysis of cases found a dose-response relationship for lung fibre content of
crocidolite, amosite and chrysotile and the development of mesothelioma.  Either a multiplicative or
additive model could be used to fit the relative risk/dose coefficients for the various asbestos types.  Aprogressive increase in relative risk with increasing fibre content was reported for all fibres ... ."
5.627  Because the risks of both lung cancer and mesothelioma show a dose-response effect related
to total cumulative exposure levels, it may be expected that later superimpositional inhalation of
chrysotile ± tremolite fibres would aggravate the overall consequences of a pre-existing asbestos
burden (i.e. increase the risk further).
(c) The feasibility in practice  of "controlled use" of chrysotile asbestos
5.628  In para. 5.510, Canada identifies the feasibility in practice of "controlled use" of chrysotile
asbestos as "one crucial issue, which seems to over ride all other issues" (i.e. the question of whether
the application of the "controlled use principle" is feasible and credible at all stages in the life cycle of
chrysotile asbestos).WT/DS135/R
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5.629  As already indicated (see my reply to Question 5), I agree that this proposition is crucial to the
dispute before the WTO.  However, for the reasons discussed in my Report, I see no requirement to
resile from my perception that - although regulation and control of chrysotile and high-density
chrysotile products may be achievable at some points of the life-cycle (e.g. the manufacture of friction
and high-density products) - "controlled use" of this type is not feasible in reality or in practice atothers (e.g. in building construction and other points of end-use).
5.630  No airborne fibre measurements are available for the overwhelming majority of asbestos-
related diseases encountered in my everyday practice, even for exposures throughout the 1970s and in
some cases extending into the late 1980s.  Among my series of asbestos-associated lung cancers and
mesotheliomas, I cannot recollect ever seeing actual airborne dust and fibre measurements at points of
end-use (e.g. at building construction sites or shipyards).
5.631  The concentration of total asbestos fibres in lung tissue from one of my cases of asbestos-
associated lung cancer was up to 125,000,000 f/g dry lung (up to 108,000,000 amosite + crocidolite
fibres), for a worker who had been employed at a major asbestos-cement manufacturing facility for
about 2-3 years (lag-time = 28 years) [15].  I also  note Dr. de Klerk's comment about demolition of an
old asbestos-cement factory in Sydney in the latter half of 1999 (probably the same factory) "where no
observable precautions of any kind were being taken"
163 (Dr. de Klerk, response to Question 1(a)).
5.632  Other interventions on high-density asbestos-cement materials that can lead to high fibre
concentrations are discussed in my first Report (e.g. Kumagai et al. [25];  my answer to question 1(d);
please see also the 1980 report by Rödelsperger et al. [26] on exposure to asbestos-cement dust at
building sites, which refers to a daily mean airborne fibre concentration of 0.6 f/ml for fibres > 5µm in
length, and "peak concentrations of more than 100 fibres/ml").
5.633  In para. 5.532, the comments from Canada include the statement that chrysotile "can be
painted without fibre release" (presumably including building products).  However, painting of such
products can cover warning notices and disguise the true nature of the product, so that workers who
later carry out maintenance or renovation work on the same product - and those who recycle the same
material - may be unaware of its true nature.  In my own series of mesotheliomas, it is not uncommonto encounter cases for which the patient was unaware or unsure that he (or less often she) had worked
in the past with an asbestos-containing product.
5.634  In one recent case, the patient worked (1973-1988) at a factory where tins and pails were
produced.  In about 1979 she had worked for several months at a conveyor belt that carried the tins
and pails into a fan-forced oven, which appears in retrospect  to have been lined by asbestos-
containing insulation.  The patient was present when maintenance work on the oven was carried out,
and she recalled hot air continually blowing from the oven into her face as she worked on theconveyor.  After diagnosis of her mesothelioma and its treatment in the late 1990s by radical
pneuropneumonectomy, an asbestos body and fibre analysis on her lung tissue revealed a count of
1640 asbestos bodies per gram dry lung, and a to tal asbestos fibre count of 34,120,000 f/g dry lung
(30,770,000 chrysotile fibres
164 + 3,350,000 crocidolite fibres).  This was the only history of exposure
that was obtainable on exhaustive questioning.
                                                     
163The potential for misuse of asbestos-containing materials remains, as shown by some prosecutions
(e.g. please see the UK Health & Safety Executive (HSE) press releases E198:98 and E079:99;http://www.hse.gov.uk/press/e98198.htm and http://www.hse.gov.uk/press/e99079.htm), but cases that comebefore the courts almost certainly represent only a sm all fraction of the misuses, most passing unnoticed by
regulatory agencies.
164Please note the high chrysotile count almost a decade after the patient's employment ended.WT/DS135/R
Page 383
5.635  A similar history was also obtained in another mesothelioma case seen on referral in 1999,
where a radio assembly worker had used asbestos-c ontaining cloths used to clean soldering irons,
together with a history of about one fibre-hour of exposure to four asbestos-cement building sheets
used for maintenance work on his home;  only later di d I discover that during his work at the radio
factory, he often entered a walk-in fan-forced oven apparently lined by insulation bricks.
5.636  Again, please see the spread of occupations in AMR 99 attached to my Report;  a similar
spread of occupations is listed by Hodgson et al. [27] in a 1997 report on mesothelioma mortality in
Britain165 - e.g. see Table 1 and Fig 1 in the original reference.  In footnote 96 to the comments from
Canada, it is stated that:
"The 'controlled use' approach has been endorsed by the WHO in its 1998 Environmental Health
Criteria 203:  Chrysotile Asbestos, p. 144.  'Control measures, including engineering controls and work
practices, should be used in circumstances where the occupational exposure to chrysotile can occur.Data from industries where control technologies have been applied have demonstrated the feasibility ofcontrolling exposure to levels generally below 0.5 fibres/ml.  Personal protective equipment can furtherreduce individual exposure where engineering controls and work practices prove insufficient'."
5.637  I interpret this passage from EHC 203 differently when it is taken in the context of the
preceding paragraphs;  apart from the heading, the complete text on page 144 of EHC 203 is:
a) Exposure to chrysotile asbestos poses incr eased risks for asbestosis, lung cancer and
mesothelioma in a dose-dependent manner.  No threshold has been identified for carcinogenicrisks.
b) Where safer substitute materials for chrysotile are available, they should be considered for use.c) Some asbestos-containing products pose particular concern and chrysotile use in these
circumstances is not recommended.  These uses include friable products with high exposure
potential.  Construction materials are of par ticular concern for several reasons.  The
construction industry workforce is large and measures to control asbestos are difficult to
institute.  In-place building materials may also pose risk to those carrying out alterations,maintenance and demolition.  Minerals in place have the potential to deteriorate and createexposures.
d) Control measures, including engineering cont rols and work practices, should be used in
circumstances where occupational exposure to chrysotile can occur.  Data from industrieswhere control technologies have been applied have demonstrated the feasibility of controllingexposure to levels generally below 0.5 fibres/ml.  Personal protective equipment can furtherreduce individual exposure where engineering controls and work practices proveinsufficient.
166
e) Asbestos exposure and cigarette smoking have been shown to interact to increase greatly the
risk of lung cancer.  Those who have been exposed to asbestos can substantially reduce theirlung cancer risk by avoiding smoking."
5.638  When seen in the context of para. c), I take d) to mean that in those situations where exposure
is likely or unavoidable, exposure can be reduced or minimized by certain procedures appropriate to
the circumstances (e.g. engineering controls in manufacture/production or best work practices), but
EHC 203 has already identified friable products and building products as materials of "particularconcern" and their use is "not recommended", in part because of difficulties of control in the
construction industry.  I do not see paragraph d) as an endorsement of on-going "controlled use".
5.639  A similar sentiment is expressed in NICNAS 99:
                                                     
165Hodgson, J.T., Peto, J., Jones, J.R., and Matthews, F.E., Mesothelioma Mortality in Britain:  Patterns
by Birth Cohort and Occupation, (1997), 41 Ann. Occup. Hyg., 129-133.
166Omitted from my original Report because I did not - and do not - take this to be an endorsement of
"controlled use", and also because the figure of up to 0.5 f/ml is up to five times higher than the level of 0.1 f/ml
mentioned in Question 5(c) from the WTO Panel.WT/DS135/R
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"Prudent OHS [occupational health and safety] policy and public health policy favours the elimination
of chrysotile wherever possible and practicable [p 139] ...Best practice must be implemented to minimise occupational and public exposure, and to minimise
environmental impact, over the remaining period(s) of use [p 140].
A risk reduction strategy using all available and appropriate measures is required to  ensure that therisks posed by chrysotile are continually reduced and eliminated wherever possible" [p 140].
5.640  NICNAS 99 also goes on to state (p 140):
"In achieving this it is further recommended that:
a) Specific phase-out periods should be set, with stages (over the shortest possible period of time)
to encourage and reflect the availability and suitability of alternatives [to chrysotile].
b) Action is taken in the immediate future to prohibit the replacement of worn non-chrysotile
original equipment with chrysotile products, as alternatives are now available.
c) No new uses of chrysotile or chrysotile products should be introduced (i.e., an immediate
prohibition on new uses).
d) Occupational health and safety authorities take the lead role in considering this
recommendation and specific strategies to implemen t it as worker health is identified as the
major concern."
5.641  As stated in the paper by Jarvholm et al. [28] attached to the Endnote (Section V.C.4) for my
report:
"... The first regulation of asbestos [in Sweden] was introduced in the early 1960s and subjects who
started their occupational career in the 1960s should have been exposed to lower doses on average, thanthose who started earlier.  On the other hand, by the 1960s asbestos was being used more extensively sothe number of people exposed to asbestos may have increased.  ...  More stringent regulations of
asbestos were introduced in the mid-1970s, which led to the sharp decrease in its use.  People who have
only worked under such conditions were born from 1955 onwards.  They have not yet reached asufficient latency time for possible mesotheliomas to have developed so the number of cases [is] few.However, the first indication is that they may have a decreased risk compared with earlier birth cohorts.
A more certain conclusion can probably not be drawn for another ten years.  Thus, the preventivemeasures of the mid-1970s can probably not be evaluated with reasonable precision until around 2005,
30 years later.
The present situation in Sweden, that mortality from mesothelioma due to early use of asbestos is of a
similar size to the total number of fatal occupationa l accidents, is caused by a situation in which at
least 90% of the asbestos used was chrysotile.  However, we have no information about the type ofexposure to asbestos among the cases of mesothelioma - whether they had an exposure to crocidolite oramosite.  There is some pressure from the asbestos industry world-wide to change the asbestos
regulations to allow the use of chrysotile.  To evaluate such an experiment would take at least another
30 years.  Even if the major cause of mesothelioma in Sweden was from types of asbestos other thanchrysotile, it is difficult to see how the benefits from an increased use of asbestos in Sweden couldoutweigh the uncertainty of the risks.  A similar pr udent approach would also be appropriate in other
European countries ..."
(d) Are substitute fibres safer than chrysotile?
5.642  In para. 5.539, Canada states:
"Dr. Henderson, for his part, recognises that, as with all fibres, the pathogenicity of substitutes is
defined by the "3 Ds" (dimension, dose, durability).  He seems also to understand that, due to the (lackof) historical use of substitutes, we cannot fully know the risks of using them.  However, he then seemsto ignore the importance of these facts."WT/DS135/R
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5.643  My comments on the safety or potential biohazards of substitute fibres were based on the
following:
• The dimensions and respirability of substitute fibres.  For example, it appears that
synthetic fibres can be engineered to be either shorter than the lengths of asbestosfibres that have been associated particularly with carcinogenicity, or to be
predominantly non-respirable.  In contrast, according to Harrison et al. [29]:
"The intrinsic hazardous properties of chrysotile can never be "engineered out", and the potential for
harm will always remain.  Prevention of ill-health will thus always rely on the control of exposure,something that history has shown cannot be guaranteed.  ... Unlike chrysotile, substitute fibers can often
be designed or selected to have particular characteristics."
• Dose:  reported airborne fibre concentrations from the manufacture or use of
substitute (e.g. synthetic) fibres are low - comparable to or lower than the airborne
fibre concentrations produced by the manufacture or subsequent use of chrysotile-
containing materials.  This being so, my conclusions about the relative safety of
chrysotile versus  substitute fibres are based primarily on fibre dimensions (discussed
above) and biopersistence (discussed below).
• Durability (biopersistence):  in para. 5.552, Canada states the following:
"It is well known that biopersistence is a key parameter.  Indeed, the human evidence for chrysotile
indicates that it is likely to be one of the main reasons why chrysotile is less dangerous than theamphiboles in respect to mesothelioma risk.  This is clearly recognised by three of the four experts, aswell as by INSERM."
Canada then emphasizes the rapidity of clearance of chrysotile from lung tissue, with
reference to a 90-110 day half-life for chrysotile in lung tissue, and an even shorter estimate of
< 10 days.  Again, I draw attention to the recen t study from Finkelstein and Dufresne [5] who
estimated a lung tissue half-life of eight years for chrysotile fibres > 10 µm in length in
Quebec chrysotile miners and millers.  Accordingly, in my survey of the literature, I placed
particular emphasis on the biopersistence of substitute fibres in comparison to chrysotile.
• The relative potency of substitute fibres or chrysotile fibres to produce pathological
changes (e.g. genotoxicity/mutagenicity and the capacity for tumour induction).
5.644  Warheit et al. [30]  claim that p-aramid fibres are biodegradable in the lungs of exposed rats,
with faster clearance times than long chrysotile fibres, which showed greater biopersistence.
" ... p-aramid is biodegradable in the lungs of exposed rats;  in contrast, the clearance of long chrysotile
fibres was slow or insignificant, resulting in a pulmonary retention of long chrysotile asbestos fibres.The dimensional changes of asbestos fibres as well as the pulmonary cell labelling data indicate thatchrysotile asbestos fibres may produce greater long-term pulmonary effects when compared to inhaled
para-aramid fibrils" [Abstract].
5.645  In 1993, Hesterberg et al. [31] compared the effects of size-separated respirable fractions of
fibrous glass (FG) with refractory ceramic fibres (RCF) and chrysotile fibres.  They found that:
"Exposure to chrysotile asbestos (10 mg/m3) and to a lesser extent RCF (30 mg/m3) resulted in
pulmonary fibrosis as well as mesothelioma and sign ificant increases in lung tumours.  FG [fibreglass
designated MMVF10 and MMVD11] exposure was as sociated with a non-specific inflammatory
response (macrophage response) in the lungs that did not appear to progress after 6-12 months of
exposure.  The cellular changes are reversible and are similar to the effects observed after inhalation of
an inert dust.  No lung fibrosis was observed in the FG-exposed animals.  Further, FG exposure resultedWT/DS135/R
Page 386
in no mesotheliomas and no statistically significant increase in lung tumour incidence when compared
to that of the negative control group.  These findings, along with previous inhalation studies, suggestthat respirable fibrous glass does not represent a significant hazard for fibrotic or neoplastic lung
disease in humans" [Abstract].
5.646  In a later (1995) study, Hesterberg et al. [32] found that exposure of rats to crocidolite and
chrysotile asbestos and to RCF by inhalation induced pulmonary fibrosis, lung tumours and
mesotheliomas (41 per cent of hamsters exposed to RCF developed mesothelioma167);  fibreglasses
MMVF10 and MMVF11, slagwool (MMVF22) a nd stonewool (MMVF21) did not produce a
significant increase in lung tumours or mesotheliomas168
5.647  In a further study published in 1998, Hesterberg et al. [33]  investigated the biopersistence of
synthetic vitreous fibres and amosite in the rat lung, together with refractory ceramic fibres (RCF1A).
They found that "the very biopersistent fibres were  carcinogenic" (amosite, crocidolite, RCF1 and two
relatively durable special application fibreglasses designated MMVF32 and MMVF33), whereas "themore rapidly clearing fibres were not" (including rock [stone] wool designated MMVF21,
HT stonewool designated MMVF34, slag wool, and insulation fibreglasses designated MMVF10 and
MMVF11).
169
5.648  An Annex from Canada170 also includes a 1995 document on p-aramid fibres from the Health
& Safety Executive (HSE) in the United Kingdom.  In a summary statement (p. 22) the HSEdocument states that:
"The balance of evidence suggests that aramid fibr es possess a low potential to produce mesothelioma,
which is likely to be at least as low as for chrysotile asbestos.  While chrysotile is thought to present ahazard with respect to mesothelioma development, current knowledge indicates that the risks for humanexposure are low, and would only be detectable following very heavy and prolonged exposure.  Thus, ifin terms of mesothelioma production, aramid fibres  are equally, or less hazardous than chrysotile, it can
be concluded that the risks at occupationally relevant levels of exposure would be extremely low."
5.649  The HSE then set an exposure limit of 2.5 f/ml, but in a subsequent document on Substitutes
for Chrysotile (White) Asbestos,  the HSE171 commented that:
"There are many long-established alternatives to chrysotile which do not rely on fibre technology.  For
example, corrugated polyvinylchloride (PVC) and steel sheeting can be used instead of asbestos cement
sheets.
                                                     
167The hamster seems to show a propensity for mesothelioma induction in some circumstances
(e.g. SV40 inoculation) but not others;  in some studies (Research and Consulting Company) chrysotile did notinduce mesothelioma or lung in hamsters but in rats it produced pulmonary fibrosis, lung tumours andmesotheliomas, so that the rat has been advocated as the most appropriate model for assessment of the humanrisk from fibre inhalation [32].
168Hesterberg, T.W., Miller, W.C., Thevenez, Ph. and Anderson, R., Chronic Inhalation of Man-made
Vitreous Fibres:  Characterization of Fibres in the Exposure Aerosol and Lungs , (1995) 39 Ann. Occup. Health,
pp. 637-653.
169Wilson et al. [34] estimate that fibreglass is 5-10 times less "risky" than chrysotile and they state that
"... no one has found any cancer attributable to the manufacture or installation of glass wool fibers ... ."  In theirestimates of lung cancer risk from chrysotile, they use the unit carcinogenicity factor of 0.01 (K;  used before
them by the US EPA), and they calculate an absolute excess lung cancer risk of 1.2 x 10
-3 for smokers,  and 1.4 x
10-4  for non-smokers;  for 40 yrs exposure at 1.0 f/ml, these estimates equate to 4.8  x 10-2 (smokers) and 5.6
x10-3 (non-smokers) - i.e. about 5 per cent and 0.5 per cent respectively, both of which can be considered quite
"high".  (Wilson, R., Langer, A.M. and Nolan, R.O., A Risk Assessment for Exposure to Glass Wool , (1999) 30
Regulatory Toxicology and Pharmacology, pp. 96-109.
170Minty, C.A., Meldrum M., Phillips, A.M., and Ogden, T.L., P-aramid Respirable Fibres Criteria
Documents for an Occupational Exposure Limit , HMSO (1995).
171HSE document:  http://www.hse.gov.uk/pubns/misc155.htm.WT/DS135/R
Page 387
Several types of non-asbestos fibres can also be substituted for asbestos;  they have been developed for
use in a wide range of products.  The main non-asbestos fibres in current use are polyvinyl alcohol(PVA), aramid and cellulose.  A considered scie ntific view on their safety has recently become
available. In July 1998, the UK's Department of Health Committee on Carcinogenicity (CoC)
concluded that these three asbestos substitutes (PVA, cellulose and aramid) are safer than chrysotile.This view was endorsed by the European Commission Scientific Committee on Toxicity, Ecotoxicityand the Environment in September 1998."
5.650  More recently, a press release172 from the UK Health and Safety Commission (HSC/HSE)
announced a prohibition on the importation, supply or use of chrysotile in Great Britain, effective
from 24 November 1999.
5.651  I also re-emphasize the comments in the reviews quoted in my original Report (answer to
Question 6), including the review by Harrison et al. [29] who comment along the following lines:
"The diameter of PVA [polyvinyl alcohol] fibres, as manufactured, is well above the respirable limit
and most of them are not inhalable.  ... the fibres are mostly in the range of 10-16 µm diameter.  There
is evidence that they do not fibrillate (split lengthwise).  Many of the particles seen in the atmosphere
are non-fibrous.  ... Although the published toxicolo gic information on PVA is relatively sparse, the
parent material has been used extensively in surgery and has food contact clearance, presumably basedon unpublished studies.  Indications of an accumulation of oligomers in the kidney in somecircumstance
173 ... mean that the spectrum of molecular weight of material in the fibres as used should
be considered, especially if a smaller diameter mate rial were to be produced.  The material will degrade
only slowly, if at all, in the lungs.  ... Thus, substitution of PVA for asbestos fibers in products such asasbestos-cement should result in reduced exposures.  This prediction has been confirmed in industrialapplications where very low fibre counts have been experienced.  Misuse of installed material would
not result in significant exposure.
... On balance, the use of aramid fibers should result in reduced levels of fiber exposure as compared to
chrysotile asbestos and the fibrils released will be no more toxic and will be less biopersistent.  The
predicted reduction in absolute exposure levels has been achieved in industrial practice.  Misuse ofinstalled material would not be expected to give significant exposures.
... On balance, the coarse fiber structure and the long experience in use indicate that substitution of
cellulose fiber for chrysotile asbestos should result in reduced occupational exposures to fiber andlower levels of deposition in the lung.  The apparent biopersistence of cellulose in the lung would be a
possible cause for concern if the potential for limited lung damage is confirmed.
... We believe that the continued use of chrysotile in  asbestos-cement products is not justifiable in the
face of available and technically and adequate substitu tes.  Likewise, there seems to be no justification
for the continued residual use of chrysotile in friction materials."
5.652  These comments also coincide with one of the recommendations in NICNAS 99:
"... Current overseas experience with the phasing out of chrysotile products indicates that a range of
alternatives is available to suit the majority of us es.  Good OHS practice dictates that use of chrysotile
should be restricted to those uses where suitable su bstitutes are not available, and alternatives should
continue to be sought for remaining uses" [p 139].
                                                     
172HSC press Release C054:99:  http://www.hse.gov.uk/press/c99054.htm.
173Referred to in the comments from Canada.WT/DS135/R
Page 388
(e) Summary
5.653  It is my perception that the conclusions in my Report submitted already to the WTO concur
with mainstream thinking and approaches to occupational and public health policy from national and
international health authorities;  these include, inter alia:
• The National Occupational Health & Safety Commission in Australia (WorkSafe
Australia).  (Please see NICNAS 99.)
• The World Health Organization (EHC 203).
• INSERM (France).
• The National Health & Safety Commission/Health & Safety Executive (HSC/HSE) in
Great Britain.
• Medical Research Council (MRC) Institute for Environment and Health at the
University of Leicester (UK).
• National health authorities in other European Nations.
• The Collegium Ramazzini.
5.654  This being so, it is my perception that the disp ute before the WTO is, to some extent, focused
upon inappropriate issues.  There has been on-going argument among scientists on the health hazardsof chrysotile asbestos (the chrysotilophiles versus the chrysotilophobes).   Given the extent and
complexity of the scientific literature - with contradictory observations on some important issues and
with uncertainties related to gaps in observatio nal data - it is almost inconceivable that this
controversy can be resolved by the WTO Panel, or, indeed, that it will be resolved in the foreseeable
future (partly because no control group free from asbestos exposure can be assembled to ascertain thetrue spontaneous mesothelioma rate).
5.655  The point to be emphasized is that there exists a substantial body of independent scientific and
medical opinion - embodied in national and international health authorities - that chrysotile is
carcinogenic with no delineated threshold;  that it cannot be controlled at all points of end use;  and
that existing scientific evidence indicates that safer substitute materials are available.
5.656  To me, this body of opinion is no tendentious artifice designed only to secure a commercial
advantage.  From my perspective, this is perhaps the crucial issue, from the so-called precautionaryprinciple , given that neither side is likely to concede that the other has proven its case at a high order
of scientific probability.  In other words, the question is not so much whether there exists a proven
health risk or virtually no risk  from the continued use of chrysotile, but whether there exists a body of
independent and reputable opinion that the possible risks or uncertainties about risk justify a policy of
highly restricted use or non-use.
5.657  From this perspective, restriction of chrysotile to only a very few special applications - or its
prohibition - is a reasonable and defensible measure designed as a cautious and prudent approach to
public and occupational health policy.
5.658  Therefore, I re-affirm the conclusions set out in my original Report (paragraph 5.431) that
chrysotile should either:WT/DS135/R
Page 389
(a) Be restricted to only a few and well-defined applications174 so that it is inaccessible to
the great majority of workers and is available for use by only small and cohesive
specialized worker groups that can be trained effectively  in its controlled use
(e.g. analogous to nuclear fuels);  this means that chrysotile should not be used in
building products (e.g. high-density fibro-cement materials such as asbestos-cementsheets) or friction products.
OR
(b) It should be made inaccessible to everyone, by prohibition, unless the alternatives
pose equal or greater hazards and equal or greater problems with control.
5.659  In this latter circumstance, the principle is that minimization of exposure is more certain when
no new chrysotile-containing products are introduced into the workplace or the general environment,
so that the total amount of asbestos in-place will diminish over time;  the problem then becomes
primarily one of minimization of exposure to existing asbestos products during maintenance, repair,
removal, demolition and disposal.
____________________
                                                     
174In the UK HSC Press Release C054:99 announcing implementation of a policy of prohibition of
chrysotile from 24 November 1999, the following specific uses are allowable until 2001-2005:
• The use of compressed asbestos fibre (CAF) in gaskets for use with saturated and superheated
steam, and with certain flammable, toxic and corrosive chemicals until 1 January 2001;
• The use of CAF in gaskets for use with chlorine until 1 January 2003;
• The use of any sheet which, when in a dry state, has a density greater than 1900 kilograms per
cubic metre and is used at temperatures at or above 500°C until 1 January 2003;
• The use of asbestos components in aeroplanes and helicopters where this is crucial for their
safe operation until 1 January 2004;
• The use of any product consisting of a mixture of asbestos with a phenol formaldehyde or with
a cresylic formaldehyde resin in vanes for rotary vacuum pumps, vanes for rotary
compressors, any bearing or its housing or for split-face seals used to prevent water leakage
from hydro-electric power generation turbines or from cooling water pumps in power stationsuntil 1 January 2004;
• The use of asbestos in pre-formed joints made from proofed asbestos cloth for sealing the
doors of steam boilers until 1 January 2004;
The use of asbestos in personal protective clothing when used in very high temperatures (500°C or
more) until 1 January 2005.WT/DS135/R
Page 390
VI. SUBMISSIONS FROM NON-GOVERNMENTAL ORGANIZATIONS
6.1 The Panel received four amicus briefs  from the following non-governmental organizations:
- Collegium Ramazzini , dated 7 May 1999
- Ban Asbestos Network , dated 22 July 1999
- Instituto Mexicano de Fibro-Industrias A.C. , dated 26 July 1999
- American Federation of Labor and Congress of Industrial Organizations , dated
28 July 1999
6.2 These amicus briefs  were transmitted to the parties for their information.  In their written
rebuttals of 30 June 1999, the EC incorporated by reference the submission of the Collegium
Ramazzini .  In a letter dated 18 August 1999, Canada notified the Panel that, bearing in mind the
general nature of the opinions expressed by the non-governmental organizations in those submissions,
they would not be useful to the Panel at this advanced stage of the proceedings.  Should the Panel
nonetheless accept the submissions as amicus briefs , Canada believed that the parties should be given
the possibility to respond to the factual and legal arguments set out in them.  In a letter dated3 November 1999, the EC informed the Panel that it was incorporating by reference the amicus brief
submitted by the American Federation of Labor and Congress of Industrial Organizations , as that
body supported the EC's scientific and legal arguments in this dispute.  The EC also proposed to the
Panel that it reject the submissions from the Ban Asbestos Network  and the Insituto Mexicano de
Fibro-Industrias A.C. , as those documents contained no information of relevance to the dispute.  In a
letter dated 10 November 1999, Canada again urged the Panel to reject the four amicus briefs  as it was
inappropriate to admit them at this stage in the proceedings.  Should the Panel nevertheless consider
these submissions, Canada considered that, for the sake of procedural fairness, the parties should have
an opportunity to comment on their content.
6.3 In a letter dated 12 November 1999, the Panel informed the parties that, in the light of the
EC's decision to incorporate into its own submissions the amicus briefs  submitted by the Collegium
Ramazzini  and the American Federation of Labor and Congress of Industrial Organizations , the Panel
would consider these two documents on the same basi s as the other documents furnished by the EC in
this dispute.  It was also on that basis that the Panel submitted those two submissions to the scientific
experts for their information.  At the second substantive meeting of the Panel with the parties, the
Panel gave Canada the opportunity to reply, in writing or orally, to the arguments set forth in thesetwo amicus briefs .  At that same meeting, the Panel also informed the parties that it had decided not to
take into consideration the amcius briefs  submitted by the Ban Asbestos Network  and by the Instituto
Mexicano de Fibro-Industrias A.C.
6.4 On 27 June 2000, the Panel received a written brief from the non-governmental organization
ONE ("Only Nature Endures")  situated in Mumbai, India.  The Panel considered that this brief had
been submitted at a stage in the procedure when it could no longer be taken into account.  It therefore
decided not to accept the request of ONE  and informed the organization accordingly.  The Panel
transmitted a copy of the documents received from ONE  to the parties for information and notified
them of the decision it had taken.  At the same time, it also informed the parties that the same decision
would apply to any briefs received from non-govern mental organizations between that point and the
end of the procedure.
_______________