BETWEEN : AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) (ACN 000 035 512)

Jurisdiction : SUPREME COURT OF WESTERN AUSTRALIA

Citation : HANNELL -v- AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) [2006] WASC 310

Torts - Negligence - Non-occupational exposure to respirable asbestos fibre - Where exposure was very limited by reason of casual work on asbestos cement products - Causation - Legal principles - Whether causation established - Asbestos-related disease terms: "background exposure" and "background risk" - Whether evidential burden discharged by leading evidence displacing the plaintiff's prima facie case - Evidential burden and burden of proof distinguished - Duty of care - Duty to warn - Whether warnings and cautions were sufficient to discharge duty - Whether risk of contracting mesothelioma was foreseeable

Damages - Assessment of damages - Mesothelioma - Appeal against award for damages

1 Amaca Pty Ltd ("Amaca") appeals from a decision of a judge of this court (Hannell v Amaca Pty Ltd (Formerly James Hardie & Co Pty Ltd) [2006] WASC 310) awarding damages to David Richard Hannell ("Mr Hannell") in respect of the mesothelioma from which he now suffers. On three separate occasions in 1983, 1985 and 1990, Mr Hannell had limited non-occupational exposure to respirable asbestos fibre released as a result of work which he carried out on asbestos cement products manufactured by Amaca. The trial Judge found that by at least 1983, the risk to persons carrying out work of that kind on asbestos cement products for limited times and very occasionally, was sufficiently foreseeable to impose a duty upon Amaca to warn such persons against carrying out work which could expose the worker to respirable fibres. He found that this required the affixation of warnings to its products and the placement of regular advertisements in newspapers. The trial Judge further found that Amaca's breach of that duty caused Mr Hannell to contract mesothelioma. Amaca challenges each of those findings.

2 For the reasons which follow, when regard is had to the very limited exposure to respirable asbestos fibre occasioned by the work carried out by Mr Hannell, the evidence failed to establish that:

(b) the risk of contracting mesothelioma from limited and occasional exposure as a result of work of the kind undertaken was sufficiently foreseeable at the time the asbestos cement products were manufactured to impose a duty upon Amaca to place warning labels upon them;

(c) by the time of Mr Hannell's exposures, it was sufficiently foreseeable to require Amaca to embark upon an advertising campaign directed at those who might undertake work of this kind; and

(d) if Amaca had affixed warning labels to its asbestos cement products, or embarked upon an advertising campaign of that kind, Mr Hannell would not have been exposed to respirable asbestos fibre on the three occasions he has identified.

3 The trial Judge at [30] - [35] made a number of findings in respect of the general nature of the mesothelioma disease, its aetiology and its relationship to the inhalation of asbestos fibre that are not controversial. They provide a convenient context for the issues which were in contest:

"The plaintiff suffers pleural mesothelioma. The pleura is a membrane lining the lungs and separating the lungs from other organs of the chest. Mesothelioma was first reported in 1960 in relation to the inhalation of asbestos. Knowledge as to the nature of mesothelioma has accumulated gradually over the years since 1960.

In Australia, mesothelioma is associated with the inhalation of asbestos. Generally speaking, there are three major issues relating to the connection between mesothelioma and the inhalation of asbestos: the dose issue, the fibre type issues and the lag time issue.

The risk of contracting mesothelioma is related to the dose of the asbestos inhaled. An asbestos fibre must be very small before it can be inhaled and retained in the fine airways of the lung. These tiny fibres are called respirable fibres. A dose may be calculated by counting the concentration of respirable fibres in an atmosphere. This is often expressed in terms of the number of fibres in a millilitre of air and abbreviated to the number of 'fibres/ml'. Calculations of the cumulative dose of asbestos likely to have been inhaled by an individual may be made by multiplying the concentration of asbestos fibres in an atmosphere by the time that an individual was exposed to that atmosphere. The cumulative dose may then be expressed in terms of the numbers of fibres in a millilitre of air over so many years and abbreviated to the number of 'fibres/ml years'.

The risk of contracting mesothelioma is directly related to the type of asbestos fibre which was inhaled by the individual. Studies have demonstrated that each fibre type has a different propensity to induce mesothelioma. Crocidolite or blue asbestos, is the most potent. Amosite or brown asbestos, is the median in terms of potency. Chrysotile or white asbestos is the least potent.

The risk of contracting mesothelioma is greatly increased by the expiry of time since the exposure - the lag time. Mesothelioma has a long latency period. Asbestos inhaled within 10 years of the contraction of mesothelioma is considered by relevant experts to be causally irrelevant to the contraction of the disease.

Medical science cannot explain precisely how asbestos causes mesothelioma. There are different theories. Dr James Leigh, an occupational physician, explained one theory, involving multi-stage carcinogenesis through initiation followed by promotion. Professor Bruce Robinson, a chest physician, considered this theory to be unhelpful and outdated. Professor Robinson advanced an alternative theory based upon a prolonged period of irritation and inflammation arising from the inhaled asbestos fibres. Once an asbestos fibre or fibres have initiated the carcinogenesis it is not known whether the inhalation of additional fibres has any role in the development of mesothelioma."

4 Mr Hannell was born in the United Kingdom in October 1942. He grew up in London. He left school at the age of 15 and worked as a gardener and then as a horticulturist until incapacitated by his disease. For three years, he also worked part-time as a black taxi cab driver in London.

5 In 1981, Mr Hannell emigrated to Western Australia with his family. In approximately May 1982, Mr Hannell and his wife purchased a house situated in Erindale Road, Hamersley. He has lived there ever since. His evidence was that until leaving the United Kingdom, he had only lived at four different houses in that country.

6 The specific incidents of exposure identified by Mr Hannell in the course of his evidence all took place as a result of his contact with asbestos cement products which were used in the construction of his house in Erindale Road, Hamersley and its associated fences. The trial Judge found that the house and relevant fences, which included all the asbestos cement products to which Mr Hannell was exposed in the specific incidents he had identified, were constructed in the late 1970s.

7 The findings made by the trial Judge in respect of Mr Hannell's specific exposure, as a result of the work which he undertook at his house, have not been challenged. The first specific instance of identified exposure occurred in about April or May 1983. Mr Hannell moved a hardiplank fence which had been constructed about half way down the backyard or garden of the house. The work involved taking apart the pieces of the fence and cutting pieces to fit the new fence line. The work was done over a couple of weekends and a couple of nights after work. He pulled the planks off the posts using a claw hammer or screwdriver. Some of the sheets of asbestos cement broke in the process. The process of dismantling the fence gave off dust. Mr Hannell got dust on himself and his clothes. He did not wear a mask. He did not try to keep the dust down or make any effort to avoid the dust. After the sheets came off he stacked them up against the fence. He then handled the sheets again for the purpose of weaving them through the fence posts. Because the required length had changed, he had to cut a number of the sheets, for which he used a handsaw and an old pair of tinsnips. He also had to drill through quite a number of sheets to attach those sheets to the posts. He used an electric drill. The processes of cutting and drilling gave off dust. When he used the drill, it would usually be fairly close to his face, so he breathed in dust as he drilled through the sheets. After the fence had been reconstructed and prior to painting it, Mr Hannell brushed the sheets back with a wire brush. This process also gave off dust and he got dust on himself again.

8 The second specifically identified exposure occurred in or about February or March 1985 when Mr Hannell painted all the underside eaves of the house from back to front because most of the paint was flaking off.

9 In order to undertake the work, Mr Hannell took about a fortnight off work. The first week of that period was taken up with the preparation of sanding and brushing back the eaves, filling holes in timbers and then washing the eaves down to get any last dirt or dust off. As this work was above head height, he used scaffold board and some steps so he could reach the eaves.

10 After his holidays were completed he continued with the job on a part-time basis. The entire job took about a month. He did not wear a mask and while carrying out the work above his head a lot of dust fell on him. He got dust on his face, eyes and mouth as well as over all his clothes.

11 The third occasion of specifically identified exposure occurred in about February 1990 when Mr Hannell painted the corrugated asbestos fence on both sides of his home. Prior to undertaking the painting work, he brushed down the fences and the ridge-capping. One of the fences had a lot of bird droppings on it so Mr Hannell used a fairly hard wire brush. Brushing the corrugated fencing gave off a lot of dust. He was less than an arm's length away from the fence as he was brushing and was often crouching while performing the task. He got dust on his sleeves, hands and clothes and was breathing in dust as he was doing the job. On the fence on the other side of the property there was hard mould or algae on the corrugated fence which needed to be scrubbed back. Again, a hard wire brush was used to undertake that work and the use of the brush gave off dust which got on Mr Hannell's clothes. He breathed it in as he was not wearing a mask. The job took a couple of days.

12 The trial Judge also found that the asbestos cement products on which Mr Hannell worked comprised between 8 and 15 per cent asbestos, which was almost all chrysotile, but about 1 per cent of the material worked on would have been amosite.

13 As the trial Judge found, there are a number of terms in common use by experts working in the field of asbestos-related disease. One of those terms is "background exposure". That expression refers to exposure to asbestos in the general environment. That exposure comes about because of the extensive use of products containing asbestos in almost all urban environments. As a result, there is respirable asbestos fibre in virtually all urban environments, with the result that all residents in those environments are exposed to that fibre to some extent. Although not the subject of a specific finding by the trial Judge, the expert evidence given in the case was consistently to the effect that, with sufficient sensity of analysis, asbestos fibre can be found in the lungs of almost everybody who has lived in an urbanised environment. (See, for example, the report of Dr Leigh dated 12 March 2006 - Exhibit H20).

14 Professor Breslin's evidence was to the effect that, depending upon locality, background environmental exposure in an average urbanised environment is 0.01 fibres per ml years. Therefore, according to the methodology described by the trial Judge, and set out above, a person living in that environment over, say, 50 years, would have a cumulative exposure of 0.5 fibres per ml years.

15 The expression "background risk" is used to describe the risk of contracting mesothelioma as a result of "background exposure". However, as the trial Judge found, and consistent with the expert evidence, the absence of a recalled history of specific exposure to asbestos is not the same as an absence of exposure. All the experts who were questioned on the subject gave evidence to the effect that there is a group of mesothelioma sufferers who are unable to recall a specific exposure to asbestos. The estimates given in the evidence as to the extent of that group varied and it was also observed, that the extent of that group depends upon the quality of the questions put to the patient and to the intensity of the questioning process. However, and subject to those qualifications, the evidence of Professor Musk, accepted by the trial Judge, was to the effect that repeated studies had shown between 15 and 30 per cent of mesothelioma sufferers were unable to recall any specific exposure to asbestos.

16 The expert evidence was consistent in that such a group of patients will be made up of at least two sub-groups: a group who had in fact been specifically exposed to respirable asbestos fibre at levels above those found in the general environment, but who were unaware of that exposure at the time it occurred or unable to later recall it; and another group whose exposure to respirable fibre was limited to that present in the general environment. There are differences of opinion and no conclusive evidence as to whether the group contains a third sub-group of mesothelioma sufferers; being, those who have had no exposure to respirable asbestos fibre whatsoever. A number of experts observed that the difficulty of proving a hypothesis that mesothelioma can be contracted other than through exposure to respirable asbestos fibre, derives from the fact that virtually everybody resident in an urbanised environment has had exposure to respirable asbestos fibre. Therefore the prospect of finding a mesothelioma sufferer who has never had exposure to respirable asbestos fibre is very remote.

17 Having lived his entire life in London and Perth, there is no doubt that Mr Hannell has been exposed to the respirable asbestos fibre which is in the ambient environment in virtually all urbanised areas of the world and this is what the trial Judge found.

18 In the witness statement which comprised the bulk of his evidence-in-chief, Mr Hannell stated that the only exposure to asbestos that he could remember at any time in his life was in the course of the work he had undertaken with asbestos cement products at his house in Erindale Road, Hamersley. He was cross-examined on that assertion. The trial Judge at [44] accurately summarised the substance of that cross-examination in the following terms:

"Senior counsel put to the plaintiff that he was unable to say that he had not been exposed to anything which contained asbestos earlier in his life. The plaintiff agreed but said that as far as he is aware he had never been exposed to asbestos. Senior counsel put to the plaintiff that there may have been asbestos in the houses in which he lived in the United Kingdom but of which he was unaware. The plaintiff said that he did not think there was any asbestos and he was pretty sure he never saw any asbestos. Senior counsel put to the plaintiff that he did not know whether the internal walls at some or all of the places he lived in the United Kingdom were themselves constructed of asbestos-containing material such as fibro. The plaintiff agreed that he would not know and had not looked but said he certainly did not think he ever saw any asbestos. Senior counsel cross-examined the plaintiff about other possible sources of asbestos to which the plaintiff might have been exposed, such as domestic insulation, sheds at his workplace constructed of asbestos and working on car brake linings. The plaintiff did not recall any asbestos insulation in any of the homes in which he lived, was not aware of any of the sheds at his workplace being constructed of asbestos and denied having worked on any car brake linings."

19 As a result of that cross-examination the trial Judge found at [46]:

"... not only that the plaintiff did not recognise or recall any specific asbestos exposure but on the balance of probabilities the plaintiff did not experience any specific asbestos exposure other than the exposure in the course of his handyman activities."

20 This finding was significant to the process of reasoning later adopted by the trial Judge. On the issue of causation, the critical question is whether the evidence establishes, on the balance of probabilities, that the specific exposures identified by Mr Hannell between 1983 and 1990 caused or materially contributed to his contraction of mesothelioma. At trial, both parties addressed that issue on the basis that it required a determination of the extent to which those specific exposures had increased Mr Hannell's risk of contracting mesothelioma on top of the extent to which every person who had lived in an urbanised community was at risk of contracting mesothelioma. This risk was described by the experts as background risk. Both parties called expert occupational hygienists to give evidence on the extent to which the specific exposures identified by Mr Hannell in his evidence increased his risk of contracting mesothelioma over and above the background risk.

21 As all the experts made clear, the background risk includes at least two groups: those who have had no specific exposure to respirable asbestos fibre other than that contained in the ambient environment; and those who had, in addition to that exposure, experienced specific exposures of which they were unaware or which they are now unable to recall. Some of the experts (eg Professor Musk) pointed out that the number of cases included within the background risk category could depend on the manner and extent of the questioning directed at identifying previous specific exposures. Despite that, it is clear that all experts proceeded on the basis that within the background risk group there would always be a group who had experienced specific exposure to respirable asbestos fibre over and above that in the ambient environment but who were either unaware of that exposure at the time it occurred, or unable to recall it when later questioned. Essentially, this is a matter of logic and common sense. By definition, a person who is unaware of a specific exposure to respirable asbestos fibre at the time that it occurs or who has forgotten about that exposure, will necessarily be unable to identify that exposure when questioned about it.

22 Because the trial Judge had found that Mr Hannell had no specific exposure to respirable asbestos fibre, other than the three occasions he had identified in his evidence, he reasoned that the background risk did not apply to Mr Hannell. The reason for this was because he had only been exposed to ambient environmental levels of respirable asbestos fibre, thus his risk of contracting mesothelioma was lower than the background risk. The trial Judge then used that conclusion as one reason for rejecting all the expert evidence led by Amaca and to therefore conclude that Amaca had not discharged an onus of adducing evidence to the effect that Mr Hannell would have contracted mesothelioma even if there had been no breach of duty.

23 In my opinion, this process of reasoning is fundamentally flawed. The trial Judge relied upon the cross-examination of Mr Hannell to conclude that he had experienced no specific exposure to respirable asbestos fibre of which he was not aware or which he could not recall. But, almost by definition, cross-examination could never establish, as a fact, something of which the witness was unaware or had forgotten. Using the classification of knowledge made famous by former US Secretary of Defence Donald Rumsfeld, where he distinguished between known knowns, known unknowns and unknown unknowns, specific exposures to respirable asbestos fibre of which a person was unaware or could not recall would fall within the category of "known unknowns".

24 As Mr Hannell has lived his entire life in urbanised communities in which the use of products containing asbestos is known to be common, his evidence alone is logically incapable of establishing that he had not experienced specific exposures to respirable asbestos fibre of which he was unaware or which he could not recall. As the trial Judge records in the paragraph from his reasons which I have set out above, Mr Hannell conceded in cross-examination, quite properly and reasonably, that he may well have had specific exposure to asbestos products in the houses in which he lived; in the course of his work, of which he was unaware at the time; or which he could not now recall.

25 Presumably, because of the logic which underpins the identification of the background risk and the group who are exposed to that risk during the course of the trial, it was never put to any expert that it was possible to identify and assess the risk of contracting mesothelioma applicable to only those who had experienced ambient environmental exposure and no expert suggested that such an assessment could be made. Nor was it suggested to any expert, nor did any expert express the view that the background risk was irrelevant to Mr Hannell because he was not within the class to which that risk applied, because he had not experienced any specific exposures to respirable asbestos fibre of which he was unaware or could not now recall. Furthermore, at trial, the cases of both parties proceeded on the basis that the background risk was potentially applicable to Mr Hannell and that the critical question was the extent to which the specific exposures he had identified between 1983 and 1990 increased his risk of contracting mesothelioma, on top of the background risk.

26 The trial Judge was wrong to find, as a fact, that Mr Hannell had not experienced any specific exposures to respirable asbestos fibre of which he was unaware or could not now recall and he was therefore wrong to use that as a basis for rejecting all of Amaca's expert evidence. That is one of the reasons why it has been necessary for this Court to undertake its own evaluation of all the evidence given in the case.

27 The trial Judge commenced his consideration of the legal principles applicable to the question of causation with a review of a number of English authorities including McGhee v National Coal Board [1972] UKHL 7; [1973] 1 WLR 1, Wilsher v Essex Area Health Authority [1987] UKHL 11; [1988] AC 1074 and Fairchild v Glenhaven Funeral Services Ltd [2002] UKHL 22; [2003] 1 AC 32. Following that review he observed:

"234 The 'material contribution to risk' principle allows negligent conduct to be treated as a factual cause of harm even though it cannot be proved on the balance of probabilities that there was in fact a causal link between the conduct and the harm. The Fairchild principle accepts that it is appropriate in certain circumstances to bridge the evidentiary gap by allowing proof that negligent conduct materially contributed to the risk of harm to satisfy the requirement of proof of factual causation. The plaintiff did not submit that the Fairchild principle is the law in Australia.

1. Another way in which the problem of evidentiary gaps might be dealt with is by shifting the evidential onus of proof on the issue of factual causation from the plaintiff to the defendant once the plaintiff has established that the defendant's failure to take reasonable care to avoid the risk in question materially contributed to the risk that the plaintiff would contract mesothelioma."

28 The trial Judge then referred to a number of decisions of the High Court, including Bennett v Minister of Community Welfare [1992] HCA 27; (1992) 176 CLR 408; Chappel v Hart (1998) 195 CLR 232; Naxakis v Western General Hospital [1999] HCA 22; (1999) 197 CLR 269 and Rosenberg v Percival [2001] HCA 18; (2001) 205 CLR 434. He also referred to the decision of this Court in City of Stirling v Tremeer [2006] WASCA 73; (2006) 32 WAR 155. He then summarised his review of the Australian cases in the following terms:

"251 The above review of Australian law concerning causation principles demonstrates that the following principles should be applied:

1. Establishing a connection between the plaintiff's injury and the defendant's negligent act or omission is a prerequisite to the recovery of damages.
2. The standard of proof is the balance of probabilities.
3. The legal burden of establishing that the defendant's negligent act or omission caused or contributed to the plaintiff's injury rests on the plaintiff at all times.
4. The evidentiary onus may shift in the sense that where the plaintiff has proved a breach of duty by the defendant and that the breach increased the risk of injury and that risk eventuated then, in the absence of evidence that the breach has no effect or that the injury would have occurred even if the duty had been performed, it will be taken that the breach of the common law duty of care caused or materially contributed to the injury."

29 With respect, that summary of the law could not be faulted. However, it is clear from the reasoning which follows, that his Honour did not apply those principles to the determination of the issues before him.

30 First, having previously acknowledged that the English line of authorities had not been suggested to represent the law in Australia, his Honour then reverted to the English authorities when it came to the assessment of the causative effect of the increased risk occasioned by the specific incidents of exposure identified by Mr Hannell. He observed:

"254 In Fairchild Lord Hutton joined in allowing the appeals but did not consider that the House of Lords had laid down any new principle of law in McGhee. Lord Hutton took the view that an inference of actual causative effect should be drawn where it could be shown that the breach of duty had materially increased the risk of the victim contracting the disease that he had eventually contracted. Lord Hutton considered that the decision of the House of Lords in McGhee was based on an inference from the facts. At [109] of his speech, Lord Hutton said:

'Whilst there is very little practical difference between the two views I prefer, with respect, to take the view that the McGhee approach is based on the drawing of a factual or legal inference leading to the conclusion that the breach of duty was a cause of the disease rather than that the decision in McGhee laid down a new principle that, in cases where medical evidence as to the precise nature of the causation cannot be adduced, the material increase in the risk is taken in law to be a cause of the disease without reliance on a factual or legal inference.'

Lord Hutton said in Fairchild at [104] of his speech that courts in Australia have also taken the view that the decision in McGhee was arrived at on the basis of an inference.

...

1. The plaintiff must prove that the defendant's negligent act or omission materially increased the risk of the plaintiff contracting mesothelioma. In McGhee their Lordships equated materially increasing the risk that the disease will occur and making a material contribution to its occurrence. In Bonnington Castings Ltd v Wardlaw [1956] UKHL 1; [1956] AC 613 at 621 Lord Reid observed:

'A contribution which comes within the exception de minimis non curat lex is not material, but I think that any contribution which does not fall within that exception must be material. I do not see how there can be something too large to come within the de minimis principle but yet too small to be material.' "

31 From the analysis of the evidence which follows those passages, it is clear that his Honour approached the question of causation on the basis that Mr Hannell would discharge his burden of proof if he established on the balance of probabilities that the three incidents of specific exposure already identified had increased the risk of him contracting mesothelioma to any extent above that which would be regarded as falling within the de minimis principle. That may be the law of England, but it is not the law of Australia.

32 This was a case in which both sides called experts who expressed opinions on the extent to which the incidents of specific exposure identified by Mr Hannell had increased his risk of contracting mesothelioma in addition to the background risk in reliance upon epidemiological studies. Indeed, the expert evidence was uniform in that epidemiological studies are currently the only basis upon which an assessment of causative effect can currently be undertaken. This is because the precise aetiology of mesothelioma remains unknown and because science has not evolved to the point where it is possible to say, for example, by lung biopsy, which fibre or fibres from which source or sources caused or materially contributed to the disease,

33 In cases of this kind, I take the law properly applicable in Australia to the issue of causation to be that enunciated by Spigelman CJ in Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; (2000) 49 NSWLR 262. That case concerned the question of whether the inhalation of asbestos fibre had caused the renal cell carcinoma suffered by the plaintiff. The particular issues in the case are conveniently identified in the following passage from the judgment of Spigelman CJ:

"20 His Honour approached the issue of causation, in accordance with the respondent's submissions, by asking two questions:

(i) Is inhalation of asbestos, more probably than not, capable of causing or contributing to the contraction of renal cell carcinoma?

(ii) Was Mr McGuiness' renal cell carcinoma, more probably than not, caused or contributed to by the inhalation of asbestos at the defendants' premises?

1. His Honour answered the first question he posed on the basis of his assessment of the epidemiological evidence. The conflict of expert epidemiological evidence had emerged as a central focus in the course of the trial.
2. The first question - Is the agent capable of causing the disease? - is sometimes referred to by epidemiologists as 'general causation'. The second question - Did the agent cause the disease in this case? - is sometimes referred to as 'specific causation'. Epidemiological evidence - both the statistics and the interpretation - may play a role with respect to both questions. For legal purposes, the relevant question is the second. "

34 After referring to the general nature of epidemiology and a substantial body of literature dealing with the forensic use of epidemiological studies, in the following passage Spigelman CJ identified the use to which epidemiological studies may be put in answering the question of causation under Australian law:

"78 Epidemiology is ... concerned with the study of disease in human populations. It is not, of itself, directed to the circumstances of an individual case. For the purpose of determining whether exposure to a particular substance is the legal cause of a particular disease, epidemiology only provides evidence of possibility.

1. Evidence of possibility, including expert evidence of possibility expressed in opinion form and evidence of possibility from epidemiological research or other statistical indicators, is admissible and must be weighed in the balance with other factors, when determining whether or not, on the balance of probabilities, an inference of causation in a specific case could or should be drawn. Where, however, the whole of the evidence does not rise above the level of possibility, either alone or cumulatively, such an inference is not open to be drawn.
2. The common law test of balance of probabilities is not satisfied by evidence which fails to do more than establish a possibility. See especially the unanimous joint judgment of the High Court in St George Club Ltd v Hines (1961) 35 ALJR 106 at 107; [1962] ALR 39 at 41 where the court referred to Bonnington Castings Ltd v Wardlaw [1956] UKHL 1; [1956] AC 613 as authority for the following proposition: 'In an action at law a plaintiff does not prove his case merely by showing that it was possible that his injury was caused by the defendant's default.'
3. In Tubemakers of Australia Ltd v Fernandez (1976) 50 ALJR 720 at 724; 10 ALR 303 at 310, Mason J referred to:

'... the ordinary onus of proof which rests upon a plaintiff to establish on the probabilities that a medical condition or disability from which he suffers is "caused or materially contributed to" by the defendant's wrongful conduct (Bonnington Castings Ltd v Wardlaw [1956] UKHL 1; [1956] AC 613 at 620, per Lord Reid). Consequently as the decision in that case demonstrates, the plaintiff will fail if all that he can show is that his disability might have been so caused. ...'

1. See also Cole v Commonwealth (1962) 62 SR (NSW) 700 at 708; 79 WN (NSW) 453 at 460. In Roulstone v Ketley [1966] 2 NSWR 389 at 394, Walsh J made a clear distinction between a 'theoretical possibility' and 'future probabilities', as approved on appeal in Ketley v Roulstone (1961) 34 ALJR 495 at 497; and see at 496. Further see Sydney County Council v Furner (1991) 7 NSWCCR 210 at 213-217.
2. The law in Australia is, in my opinion, as stated by Glass JA in this Court in Fernandez v Tubemakers of Australia Ltd [1975] 2 NSWLR 190 at 197:

'... The issue of causation involves a question of fact upon which opinion evidence, provided it is expert, is receivable. But a finding of causal connection may be open without any medical evidence at all to support it: Nicolia v Commissioner for Railways (NSW) (1970) 45 ALJR 465, or when the expert evidence does not rise above the opinion that a causal connection is possible: EMI (Australia) Ltd v Bes [1970] 2 NSWR 238; appeal dismissed (1970) 44 ALJR 360n. The evidence will be sufficient if, but only if, the materials offered justify an inference of probable connection. This is the only principle of law. Whether its requirements are met depends upon the evaluation of the evidence.'

1. It is often difficult to distinguish between permissible inference and conjecture. Characterisation of a reasoning process as one or the other occurs on a continuum in which there is no bright line division. Nevertheless, the distinction exists.

1. The test is whether, on the basis of the primary facts, it is reasonable to draw the inference: see, eg, Luxton v Vines [1952] HCA 19; (1952) 85 CLR 352 at 358.
2. In my opinion, evidence of possibility, including epidemiological studies, should be regarded as circumstantial evidence which may, alone or in combination with other evidence, establish causation in a specific case."

35 In this case, the trial Judge proceeded on the basis that any increase in the risk of contracting mesothelioma was sufficient to constitute a "material contribution" and therefore satisfy the test of causation, unless the increase in risk came within the de minimis principle. He did so in reliance upon the decision of the House of Lords in McGhee (supra) and upon the observations made by McHugh J in Chappel v Hart (supra) at 244 - 245 and which were adopted with approval by Gaudron and Callinan JJ in Naxakis v Western General Hospital (supra). In my opinion, the trial Judge erred in law in taking this approach, for reasons succinctly explained by Spigelman CJ in the following passages from McGuiness (supra):

"102 Some of the epidemiological evidence suggests some increase in risk. On the approach I believe to be appropriate, that evidence and that conclusion are circumstantial facts which may be taken into account as 'strands in the cable' for the purpose of drawing the inference that the particular exposure caused or materially contributed to the injury in the specific case.

1. Mason P has concluded that the law does not regard an increase in risk as satisfying the legal requirements of causing, or materially contributing to, injury: see Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307 especially at 315-316.
2. In that case, Beazley JA said (at 339A) that the onus of proof of causation 'is not discharged by establishing that a particular matter cannot be excluded as a cause of the injury'. The authority to which her Honour referred, Sydney County Council v Furner (1991) 7 NSWCCR 210, stated that proposition as a conclusion from the principle that a mere possibility is not enough. As noted above, authority binding on this Court establishes that principle. Beazley JA does not draw the conclusion that an increase in risk is not capable of establishing causation.
3. The respondent relied on an observation by McHugh J in Chappel v Hart (at 244-245 [27]) where his Honour, noting that 'increases' in this context includes 'creates', said:

'... If a wrongful act or omission results in an increased risk of injury to the plaintiff and that risk eventuates, the defendant's conduct has materially contributed to the injury that the plaintiff suffers whether or not other factors also contribute to that injury occurring. If, however, the defendant's conduct does not increase the risk of injury to the plaintiff, the defendant cannot be said to have materially contributed to the injury suffered by the plaintiff.'

1. Although his Honour's was a dissenting judgment, this passage has subsequently been referred to with approval: see Naxakis v Western General Hospital (1999) 73 ALJR 782 at 787 [31]; [1999] HCA 22; 162 ALR 540 at 547 [31], per Gaudron J and (at 806 [127]; 574 [127]), per Callinan J.
2. The starting point of McHugh J's analysis was that it had been established on the balance of probabilities that the conduct did create or increase the risk of injury, 'and that risk had eventuated'.
3. This starting point is the very matter in issue in the present case. Was there evidence on the basis of which the trial judge could conclude, on the balance of probabilities, that there was an increased risk of injury and that that risk had 'eventuated' in the specific disease of the respondent?"

36 After referring to a number of other cases, Spigelman CJ went on:

"118 The issue in the present case is whether an increased risk did cause or materially contribute to the injury actually suffered.

1. There is a tension between the suggestion that any increased risk is sufficient to constitute a 'material contribution', and the clear line of authority that a mere possibility is not sufficient to establish causation for legal purposes. The latter is too well-established to be qualified by the former. The reconciliation between the two kinds of references is to be found in the fact that, as in Chappel v Hart and in the cases that suggest the former, the actual risk had materialised. The 'possibility' or 'risk' that X might cause Y had in fact eventuated, not in the sense that X happened and Y had also happened, but that it was undisputed that Y had happened because of X.
2. The epidemiological evidence in the present case can be expressed in terms of 'increased risk'. However, in its application to determining causation in the specific case of the respondent that evidence never rises above the level of a possibility. Whether or not the increased risk 'eventuated', is the issue which must be determined. The respondent's reliance on the passage from McHugh J was, in my opinion, misplaced."

37 In this case, as in McGuiness (supra), expert evidence was led relating to the increase in risk occasioned by the specific instances of exposure identified by Mr Hannell by reference to an epidemiological measure known as relative risk. That measure, which is a measure in standard use, was described by Spigelman CJ in these terms:

"67 Most epidemiological studies identify the strength of an association by a measure called relative risk (RR). RR is defined as the ratio of the incidence of disease in exposed individuals compared to the incidence in unexposed individuals. If the relative risk equals 1.0, the risk in exposed individuals is the same as the risk in unexposed individuals. If the relative risk is greater than 1.0 the risk in exposed individuals is greater than the risk in unexposed individuals."

38 Spigelman CJ then considered the extent to which epidemiological assessments of relative risk had been used by American courts for the purposes of inferring causation in an individual case. At [121] he cited the following extract from the Federal Judicial Centre's reference manual on scientific evidence (at 168 - 169):

"The civil burden of proof is described most often as requiring the fact finder to 'believe what is sought to be proved ... is more likely true than not true' ... The relative risk from an epidemiological study can be adapted to this 50 per cent plus standard to yield a probability or likelihood that an agent caused an individual's disease ... The threshold for concluding that an agent was more likely the cause of a disease than not is a relative risk greater than 2.0. Recall that a relative risk of 1.0 means that the agent has no effect on the incidence of disease. When the relative risk reaches 2.0, the agent is responsible for an equal number of cases of disease as all other background causes. Thus, a relative risk of 2.0 implies a 50 per cent likelihood that an exposed individual's disease was caused by the agent. A relative risk greater than 2.0 would permit an inference that an individual plaintiff's disease was more likely than not caused by the implicated agent. A substantial number of courts in a variety of toxic substance cases have accepted this reasoning."

39 Spigelman CJ then went on to consider a number of American cases dealing with the use of assessments of relative risk for the purpose of determining causation. He concluded at [135] that while some of those cases indicated that a relative risk of 2.0 should be applied as a rigid mathematical formula for the purpose of determining whether or not causation had been established, others indicated that it should not be applied in that way.

40 He described the situation in Australian law in the following paragraphs:

"136 The predominant position in Australian case law is that a balance of probabilities test requires a court to reach a level of actual persuasion. This process does not involve a mechanical application of probabilities: see Briginshaw v Briginshaw [1938] HCA 34; (1938) 60 CLR 336 at 361-362; Jones v Dunkel [1959] HCA 8; (1959) 101 CLR 298 at 304-305; West v Government Insurance Office (NSW) [1981] HCA 38; (1981) 148 CLR 62 at 66; State Government Insurance Commission v Laube (1984) 37 SASR 31 at 33; Sir Richard Eggleston, Evidence, Proof and Probability, 2nd ed (1983) especially Chapter 10; The Honourable Mr Justice K J Carruthers, 'Some Observations on the Standard of Proof in Marine Insurance Cases, with Special Reference to the "Popi M" Case' (1988) 62 ALJ 199 especially at 208-209; The Honourable Mr Justice D H Hodgson, 'The Scales of Justice: Probability and Proof in Legal Fact-Finding' (1995) 69 ALJ 731 especially at 732-733; D Hamer, 'The Civil Standard of Proof Uncertainty: Probability, Belief and Justice' [1994] SydLawRw 37; (1994) 16 Syd LR 506 especially at 509-512; D Hodgson, 'Probability: the Logic of the Law' (1993) 13 Oxford Journal of Legal Studies 457; Hodgson, 'Probability: the Logic of the Law - a Response' (1995) 15 Oxford Journal of Legal Studies 51 especially at 58-59; Note (1997) 71 ALJ 33; A Ligertwood, Australian Evidence, 3rd ed (1998) at 14ff; M Redmayne, 'Standards of Proof in Civil Litigation' (1999) 62 Mod LR 167.

1. In Australian law, the test of actual persuasion does not require epidemiological studies to reach the level of a relative risk of 2.0, even where that is the only evidence available to a court. Nevertheless, the closer the ratio approaches 2.0, the greater the significance that can be attached to the studies for the purposes of drawing an inference of causation in an individual case. The 'strands in the cable' must be capable of bearing the weight of the ultimate inference."

41 Spigelman CJ then went on to apply those conclusions as to the legal principles to be applied to the evidence of assessed relative risk in the McGuiness case (supra). After reviewing the evidence of the epidemiological studies, he concluded (at [172]) that they showed that the increased risk of renal carcinoma as a consequence of exposure to respirable asbestos fibre, where detected at all, was generally "low to moderate" and that many studies did not show an increased risk.

42 The following passage from the judgment of Spigelman CJ reveals that the relative risk factors of "low to moderate" to which he was referring were factors in the range of 1.32 to 1.58:

"175 The relative risk factors in the range of 1.32 to 1.58 for four of the six positive studies are well below the level of 2.0 which could satisfy a balance of probability test according to the United States case law. Whilst I do not hold that such a level is required, the fact that the increased risk of most positive studies is only of a low to moderate degree, significantly undermines their importance as a basis for inferring causation in an individual case.

1. One study shows a significant ratio of 1.7 and another a particular significant ratio of 2.758. These studies cannot, on their own sustain an inference of causation, unless the other studies, both positive and negative, are given minimal weight. There is no basis in the evidence for doing so."

43 Accordingly, Spigelman CJ, with whom Davies AJA agreed, concluded that the plaintiff had failed to establish that exposure to respirable asbestos fibre had increased his risk of contracting renal carcinoma to the extent that it could be concluded that such exposure caused that condition.

44 Mr Hannell's claim was advanced on the basis that the three incidents of specific exposure he had identified increased his risk of contracting mesothelioma added to that which he bore as a member of the general population exposed to background risk to such an extent that it could be concluded that those exposures caused or contributed to the mesothelioma from which he suffered. For the reasons enunciated by Spigelman CJ in McGuiness (supra), in this type of case it is necessary for the tribunal of fact to determine the extent of the increase in risk occasioned by the incidents of specific exposure which are said to give rise to liability. Because of the view of the law taken by the trial Judge, he did not make any finding on an issue which was critical to the question of causation; namely, the extent to which those exposures increased Mr Hannell's risk of contracting mesothelioma over and above the background risk. Rather, he approached this case on the basis that any increase in risk above that which would fall within the de minimis principle would be sufficient, unless Amaca discharged the burden of adducing evidence which established that Mr Hannell would have contracted mesothelioma in the absence of the specific exposures he had identified. Since the trial Judge's view of the law caused him to fail to make any findings with respect to the extent of the increase in risk occasioned by the three specific incidents of exposure identified by Mr Hannell, it is necessary for this Court to undertake that task. I will express my views on that subject later in these reasons.

45 The second error of law made by the trial Judge was the view which he took in relation to the nature of the evidential burden imposed upon a defendant once the plaintiff has established that a breach of duty has occurred followed by injury within the area of the foreseeable risk. The trial Judge appears to have taken observations made by McLure JA in Tremeer (supra) as authority for the proposition that the evidentiary onus will only be discharged if the defendant adduces evidence which establishes, on the balance of probabilities, that the risk would have eventuated notwithstanding the breach of duty. That view of the decision in Tremeer (supra) appears at [265] of the trial Judge's reasons and from his analysis of the evidence led on behalf of Amaca. I will deal with that evidence in significantly greater detail below. For present purposes, it is sufficient to observe that Amaca led a significant body of expert evidence from a variety of sources to the effect that it was much more likely than not that Mr Hannell would have suffered mesothelioma irrespective of the three specific exposures to respirable asbestos fibre he had identified. That evidence was adduced without objection to its substance. After reviewing that evidence and expressing views as to its weight, the trial Judge concluded at [307] that Amaca "has not discharged the evidential onus upon it to show that its breach of duty had no effect or that [Mr Hannell] would have contracted mesothelioma even if its duty had been performed".

46 Earlier in the trial Judge's reasons there are passages which accept that the burden of proof remained on Mr Hannell throughout (see: [251] - [252]). However, the approach actually taken by the trial Judge had the effect of imposing upon Amaca not only the burden of adducing evidence to the effect that Mr Hannell would have contracted mesothelioma irrespective of the specific exposures he had identified, but also of proving that proposition on the balance of probabilities.

47 There is, of course, a significant distinction between an evidential burden and the burden of proof. As McLure JA observed in Tremeer (supra) the evidential burden is discharged by leading some evidence which displaces the prima facie case established by the plaintiff. Once that burden is discharged, the burden of proof, which remains on the plaintiff throughout, requires the plaintiff, in this case Mr Hannell, to prove, on the balance of probabilities, that he would not have contracted mesothelioma, or his mesothelioma would not have progressed, unless he had been exposed to respirable asbestos fibre in one or more of the three incidents of specific exposure he had identified.

48 The trial Judge took an alternative approach to the question of causation at [308] - [315] of his reasons. In the course of that passage he referred to the expert evidence adduced by Mr Hannell in the following terms:

"312 I have already referred to the evidence of the principal expert witnesses. Professor Musk opined that the cause of the plaintiff's mesothelioma was asbestos exposure as a result of his handyman activities in 1983, 1985 and 1990. Professor Robinson considered that the plaintiff's mesothelioma is likely to be due to his asbestos exposure in the course of those handyman activities. Professor Henderson said that the plaintiff's handyman exposures were significant for induction of his mesothelioma in that they represented exposures in excess of any background exposure derived from the environment at large. Professor Henderson concluded that the plaintiff's exposure was significant for causation of his mesothelioma. Dr Alvares said that the plaintiff's handyman exposures are clearly powerful etiological factors in causing the plaintiff's mesothelioma. Dr Leigh stated his opinion that the plaintiff's total cumulative asbestos exposure from his handyman activities was significantly greater than background exposure from the environment at large and the plaintiff's handyman exposure made a material contribution to causation of his mesothelioma."

49 He then referred to the reasons he had given for attaching no weight to the evidence given by the experts called by Amaca and concluded at [315] that because he preferred the evidence of the witnesses called by Mr Hannell, he drew the inference that the specific exposures he had identified caused or materially contributed to him contracting mesothelioma.

50 It will be necessary to deal with the evaluation by the trial Judge of the evidence of the various expert witnesses in more detail below. However, for present purposes, it is sufficient to observe that the paragraphs in this portion of his Honour's reasons do not, in themselves, do anything more than reiterate the ultimate conclusions at which the experts arrived and whether or not he accepted those views. Accordingly, whether or not those expert opinions provide a sufficient basis for his conclusion on causation depends upon an analysis of his review of that evidence elsewhere in his reasons.

51 As I have observed, the trial Judge gave no weight to any of the expert evidence led by Amaca. Amaca challenges that conclusion on a number of grounds, which are unnecessary to particularise.

52 Mr Alan Rogers is an occupational hygienist who was President of the Australian Institute of Occupational Hygienists for two years. Since undertaking a course of study in London in the 1970s, Mr Rogers professional activities have focused entirely on the area of asbestos and asbestos-related diseases. He is the author of many articles published in peer review journals on that subject. He was involved in the creation of the Australian Mesothelioma Programme in 1978 and worked on that project until 1996. His work on the assessment of risk relating to asbestos-related disease has been used by the Commonwealth in setting the occupational exposure standards applicable in Australia. He was Chairman of the group which was involved in setting up quality assurance and standards for testing asbestos exposure in Australia.

53 He has also served on a committee of the National Health and Medical Research Council ("NHMRC"), which was involved in the creation of a code of practice for the membrane filter method used to monitor exposure to asbestos fibre. He was also a member of a committee of the National Occupational Health and Safety Commission Standards Committee which sets allowable exposure standards for various toxic agents in Australia. He played a central role in the setting of standards applicable to exposure to respirable asbestos fibre. In Western Australia, he provided advice to the Government of Western Australia in relation to the estimates of risk arising from residence in Wittenoom (where asbestos was mined). He undertakes peer review for papers published in journals relating to risk arising from exposure to respirable asbestos fibre.

54 Mr Rogers produced a report dated 20 March 2006 in which he set out the opinions he had formed in relation to the issues arising in Mr Hannell's case and his reasons for those opinions. In his oral evidence he confirmed that the contents of that report were true and correct on the basis of his understanding of the facts he had assumed at the time of producing that report. His report was then tendered and received in evidence without objection. A supplementary statement made by him and dated 8 May 2006 was also tendered. That statement responded in part to evidence given by Dr Francis in her supplementary report dated 2 May 2006 and also referred to exposure data collected in the files of the New South Wales Dust Diseases Board which Mr Rogers had reviewed. Although objection was initially taken to the tender of that supplementary statement on the grounds of relevance, the objection was withdrawn on the course of argument and the supplementary statement was received.

55 Mr Rogers' report sets out the assumptions he had made in relation to Mr Hannell's specifically identified exposures. Those assumptions accord with the findings made by the trial Judge. He then set out his assumptions with respect to the composition of the asbestos cement materials upon which Mr Hannell worked. Those assumptions also accord with the findings made by the trial Judge.

56 The first appendix to Mr Rogers' report sets out a review of various reports and studies dealing with the amount of respirable asbestos fibre per millilitre of air produced by particular activities. The same appendix refers to procedures generally used in the estimation of time weighted average exposures in relation to particular types of work on asbestos cement products. The appendix identifies the particular reports from which the conclusions set out in the appendix are drawn.

57 Mr Rogers referred to that appendix in the body of his report and then referred to specific studies of the amount of respirable asbestos fibre produced by particular activities which he considered to be relevant to the assessment of the exposures experienced by Mr Hannell in the course of his work.

58 Mr Rogers then calculated the cumulative exposure which he estimates Mr Hannell experienced in each of the three activities he had identified in his evidence. Drawing upon the studies and reports to which he had referred, he estimated that the work done by Mr Hannell in 1983 on the painted fence would have generated fibres at the rate of 0.1 fibre per ml over the period of 20 hours in which he undertook that work. The report then sets out the manner in which Mr Rogers calculated that exposure to be a cumulative exposure of 0.001 fibre per ml years or less.

59 In relation to the work undertaken by Mr Hannell on the eaves of his house, Mr Rogers relied on a report which he identified for his assumption that the work would generate fibre at the rate of 0.007 fibre per ml, and applied that assumption to the hours of work undertaken, to produce an estimate of cumulative exposure of 0.0001 fibre/ml years on the assumption that 27 1/2 hours was spent wire brushing and sanding the eaves or 0.000004 fibre per ml years if, as Mr Rogers thought more likely, only a portion of the work done (1 hour) involved brushing and sanding the eaves.

60 In relation to the third incident of exposure identified by Mr Hannell, Mr Rogers used his estimate that the work would have generated 0.007 fibre per ml or less over a period of 5.5 hours to calculate a cumulative exposure of 0.00002 fibre per ml years.

61 Mr Rogers' report then assesses the increment in risk occasioned by the exposures, using a formula proposed by published researchers in the field and widely adopted and known as the "Peto formulae". Under those formulae, risk is calculated as the product of three factors: cumulative exposure, the potency of the asbestos fibre type and the latency (lag time since first exposure). These are the factors which have been shown, by various studies, to be most significant in elevating the risk of contracting mesothelioma from exposure to respirable asbestos fibre. The formulae were then applied to calculate the risk of contracting mesothelioma as a result of Mr Hannell's specifically identified exposures over the balance of his life time. In respect of the first period of exposure in 1983, the risk was calculated at 0.2 per million persons; for the work on the eaves in 1985, 0.02 or 0.0008 per million persons (depending upon which assumption is made as to the time spent sanding and brushing); and for the work wire brushing and painting the fence in 1990 at 0.004 per million persons. Mr Rogers then adjusted those estimates by reference to the assumptions he had made as to the relevant potency of the asbestos materials contained within the asbestos cement upon which Mr Hannell worked and concluded that the lifetime risk generated by Mr Hannell's cumulative exposure to respirable asbestos fibre in the course of the three specific incidents he identified was 0.002 per million persons or less.

62 Mr Rogers' report then dealt with the extent of the background risk experienced by all members of an urbanised community. He reported that a value of one person per million per year (equating to a lifetime risk of 70 persons per million) is often used internationally, but because Western Australia has a high incidence of asbestos products, the background rate is estimated at 2 - 3 per million adults per year, producing a lifetime risk of 140 to 210 per million persons. Mr Rogers then calculated the percentage increment in risk occasioned by the specific exposures, according to differing assumptions made as to lifetime background risk and concluded that the increased risk of mesothelioma over and above that experienced by the general population, as a result of Mr Hannell's three specifically identified exposures was likely to be less than 0.001 per cent. Put another way, in his view there was more than a 99.999 per cent probability that the mesothelioma suffered by Mr Hannell arose as part of the background risk experienced by the general population.

63 In cross-examination counsel for Mr Hannell put to Mr Rogers that there were many many thousands of reports held by the health authorities of New South Wales relating to observations and testing at sites where asbestos workers were exposed to asbestos. Mr Rogers agreed with that proposition. Those reports identified the fibre levels detected at a wide variety of sites involving work on a wide variety of products over the period between 1970 and 1983. Mr Rogers had reviewed a large number of those reports.

64 Mr Rogers was cross-examined in relation to the estimates he had made of the amount of fibre released by reason of the work undertaken by Mr Hannell. In particular, he was cross-examined about a report of testing undertaken at Amaca's premises. The report of the test was put to him and it was suggested to Mr Rogers that the report might not be impartial. Questions were also directed at the methodology used in the testing process reported upon. During cross-examination, it was also suggested that some reservations might be expressed in applying the values obtained from testing undertaken in occupational settings to domestic settings. It was not put to Mr Rogers that the reports of testing undertaken in occupational settings and upon which he had relied were in themselves unreliable or required verification. It was put to Mr Rogers in cross-examination that some of the tests upon which he had relied provided less than full information, so that assumptions as to the manner of testing had to be made. Mr Rogers agreed with that proposition and indicated that in relation to some tests, he had made assumptions about aspects of them, drawn from what he knew of the circumstances in which they had been carried out. However, those particular studies represented a small sample of the range of studies relied upon by Mr Rogers.

65 Mr Rogers was also cross-examined on the basis that there were other studies which showed exposures deriving from particular activities which were analogous to the work undertaken by Mr Hannell and which he had not taken into account. The cross-examination was directed to the relevance and applicability of the studies, not their integrity or reliability.

66 Mr Rogers also indicated in the course of cross-examination that he relied upon his extensive personal experience of conducting tests monitoring the amount of respirable fibre released by certain activities for his interpretation of the studies and reports and for the opinion he had formed as to the levels of fibre likely to be released by the activities carried out by Mr Hannell.

67 Mr Rogers also conceded in cross-examination that there were limitations upon the accuracy and reliability of the Peto formulae, but observed that the formulae had predicted the outcome of the cohort of people exposed to asbestos in Wittenoom quite accurately.

68 Mr Rogers was also cross-examined at length about the particular figures he had adopted for the purposes of his calculation, it being suggested to him that he should have used higher figures relating to exposure. However, this line of cross-examination has to be viewed in the context that even if the risk assessed by Mr Rogers, as a result of the specifically identified exposures, was multiplied by 100, on his view, the probability that Mr Hannell's mesothelioma was attributable to background risk would still be greater than 99 per cent.

69 On Mr Rogers' evidence, the increased risk of contracting mesothelioma as a result of Mr Hannell's specifically identified exposures was many magnitudes away from producing the conclusion that those exposures were more likely than not to have caused or contributed to his mesothelioma. The same observation can be made in relation to the concession made by Mr Rogers during cross-examination that his figures were calculated on the assumption that the asbestos contained within the products worked upon by Mr Hannell were entirely chrysotile; whereas, by the time he gave evidence he had learnt of evidence to the effect that those products contained 1 per cent amosite, which would have slightly increased the potency factor. Mr Rogers also observed that his estimates might err by plus or minus 50 per cent, but again, that evidence must be viewed in the context of the orders of magnitude to which I have referred. An error of 50 per cent or 100 per cent or even 1000 per cent would make no material difference to Mr Rogers' general assessment of the relative risks.

70 In his evaluation of Mr Rogers' evidence, the trial Judge accurately observed that the view formed by Mr Rogers as to the amount of respirable fibre released in the course of the activities undertaken by Mr Hannell was critical to the calculations he had performed. He then observed that those views were based upon "tests of which Mr Rogers has no personal knowledge or upon estimates made by other people". That observation is also accurate, although it does omit to refer to Mr Rogers' extensive personal experience in the testing of amounts of respirable fibre produced by particular activities.

71 The trial Judge then posed the question of whether the opinions expressed by Mr Rogers were admissible, given that the tests and studies upon which Mr Rogers relied had not been independently proven. The trial Judge took this course notwithstanding that no objection had been raised to the tender of Mr Rogers' statement or to his evidence generally, nor had any line been pursued in cross-examination to the effect that the tests upon which Mr Rogers relied were unreliable or lacked authenticity. If that line had been taken during cross-examination or if objection had been taken to the tender of Mr Rogers' statement, it would have been open to Amaca to lead evidence to prove the studies and reports upon which Mr Rogers had relied.

72 Because that evidence was not led, the trial Judge concluded that the opinions expressed by Mr Rogers lacked foundation, with the result that his views carried no weight. Although he did not expressly enunciate the view that his opinions were, for that reason inadmissible, the authorities to which he referred (including Makita (Australia) Pty Ltd v Sprowles [2001] NSWCA 305; (2001) 52 NSWLR 705) support a strong inference that he was, in effect, ruling the opinions inadmissible.

73 The trial Judge erred in taking a point as to the admissibility of the opinion evidence of Mr Rogers, which was not taken by Mr Hannell or otherwise adverted to at trial, and then used that as a basis for entirely rejecting his evidence. (see Hughes v National Trustees, Executors & Agency Co of Australasia Ltd [1979] HCA 2; (1979) 143 CLR 134, 153; Jones v Sutherland Shire Council [1979] 2 NSWLR 206, 219; Cross on Evidence (7th Aust ed, [1645], et seq)).

74 Further, even if the reasons for decision are to be construed as only going to the weight of the opinions expressed, the course of reasoning adopted denied Amaca procedural fairness, because the trial Judge has taken a point which was not taken in either objection or in cross-examination and which could, if taken, have been addressed by Amaca in the course of its evidence.

75 The trial Judge expressed another reason for placing no weight upon Mr Rogers' evidence, which he described as an independent reason. He expressed it in these terms:

"286 I have referred to only parts of the evidence of Mr Rodgers [sic] concerning how he assessed and calculated the cumulative exposure of the plaintiff in the course of carrying out the handyman activities he described. On considering the whole of the Mr Rodgers' [sic] evidence I am not satisfied that his calculation or assessment of the cumulative exposure of the plaintiff from the handyman activities is sufficiently reliable or accurate to provide a proper basis for calculating the relative risk of contracting mesothelioma from the handyman activities compared to 'background exposure'. There are simply too many assumptions, estimates and variables involved in Mr Rodgers' [sic] calculations."

76 With respect to the trial Judge, this paragraph constitutes the expression of a conclusion, rather than the elucidation of a process of reasoning. A scientific assessment of the increment in risk occasioned by the specific exposures identified by Mr Hannell must inevitably involve assumptions, estimates and variables. No basis is provided for the view expressed by the trial Judge to the effect that Mr Rogers' opinion depended upon "too many" such assumptions, estimates and variables, nor is that conclusion more fully enunciated or explained in any other portion of his reasons. Nor do his reasons identify which assumptions, estimates or variables the trial Judge considered to be unreliable or inappropriate, or why.

77 But perhaps most significantly of all, no where in his reasons does the trial Judge acknowledge or refer to the fact that even if the assumptions made by Mr Rogers were altered to produce an assessment of risk which was ten times, or even one hundred times, greater than his calculated estimate, the increment in risk attributable to the specific exposures identified by Mr Hannell would still fall manifestly short of sustaining the conclusion that those exposures were more likely than not to have caused or contributed to his mesothelioma.

78 The trial Judge expressed a third reason for rejecting Mr Rogers' opinion. That was because Mr Rogers had relied upon estimates of background risk which included both those who had only been exposed to ambient or environmental respirable fibre, and those who had specific exposures of which they were unaware or had forgotten. Because the trial Judge had concluded that Mr Hannell had only been exposed to ambient or environmental respirable fibre, other than on the three specific occasions he had identified, he concluded that the background risk estimates were not applicable to him.

79 I have already expressed the view that the trial Judge was wrong to find that Mr Hannell had not experienced any specific exposures to respirable fibre of which he was unaware or had forgotten. It follows that the process of reasoning adopted by the trial Judge in relation to the evidence of Mr Rogers in this respect was also flawed.

80 In my opinion, none of the three reasons given by the trial Judge for rejecting the evidence of Mr Rogers can be sustained. While there is obviously scope for argument and differing views as to the precise values adopted by Mr Rogers for the purposes of his calculations, the important point to emerge from his evidence, and which is not referred to by the trial Judge, is that even if different figures are used, so that his calculation of risk is increased by ten, or even one hundred times, the increment in the risk of contracting mesothelioma occasioned by the specific exposures identified by Mr Hannell would still fall manifestly short of sustaining the conclusion that those exposures were more likely than not to have caused or contributed to his mesothelioma.

81 Mr Hannell led evidence from Dr Eva Francis. Dr Francis is a retired occupational hygienist. She obtained the degree of Doctor of Philosophy in Pharmaceutical Chemistry in 1970. After obtaining her doctorate she became a scientific officer at the Division of Occupational Health within the Health Department of New South Wales. She worked in that capacity between 1971 and 1999. Her duties primarily focused upon the investigation of workplaces where employees were exposed to respirable fibres. Her particular speciality focused on respirable asbestos fibres. She has written a number of papers in the field and served on a number of committees of the NHMRC which produced guidelines relating to acceptable levels of exposure to respirable asbestos fibre. She has also served as a member of the International Standards Organisation Expert Working Group relating to the analysis of asbestos in air and water. She was also a member of the National Occupational Health and Safety Commission Expert Working Party which compiled a number of guidance notes relating to the methodology to be used in the estimation of airborne synthetic fibres.

82 Dr Francis produced two reports containing her opinions on issues relevant to Mr Hannell's case. They were each tendered without objection.

83 In her first report, dated 15 March 2006, Dr Francis sets out her experience and the assumptions that she had made with respect to Mr Hannell's specific exposures to asbestos fibre between 1983 and 1990.

84 Dr Francis estimated that when Mr Hannell cut the hardiplank fence with a handsaw in 1983 he would have been exposed to airborne asbestos levels of about 3 fibres per ml, or about 300 times greater than the general environmental background levels. I digress to observe that if Mr Hannell had performed, say, 30 hours work producing respirable fibre at the levels of 3 fibres per ml, his cumulative exposure over that period of 30 hours would be approximately equal to the cumulative exposure of each and every member of an urbanised community over the course of one year. Put another way, as Mr Hannell was 41 years of age at the time of his first specifically identified exposure in Western Australia, by the time of that exposure, on the assumptions referred to, he had already received cumulative exposure 41 times greater than that which he experienced in the course of the work he identified in 1983, without allowing for any previous specific exposures of which he was unaware or had forgotten. Further, it seems unlikely that Mr Hannell would have been actually cutting the asbestos fencing for anything like a period of 30 hours while he was working on the fence; rather, the period of time when he was actually cutting the fence would have been a small portion of the total time engaged in the work.

85 Dr Francis estimated that when Mr Hannell was drilling the hardiplank with an electric drill, or cutting it with asbestos fibres or handling the asbestos sheets during the period he was working on the fence, he would have been exposed to average daily airborne asbestos levels of about 0.3 fibres per ml, or about 30 times general environmental background levels or levels 10 times less than those he would have experienced while cutting the fence.

86 Dr Francis also estimated that during the time in 1985 when Mr Hannell sanded and wire brushed the overhead asbestos cement eaves for a total period of between three and four days, he would have been exposed to average airborne asbestos levels of about 4 fibres per ml, or about 400 times general environmental background levels. She multiplied that estimate by a factor of two for overhead work, which generates dust which is easily inhaled.

87 Dr Francis estimated that when Mr Hannell brushed the corrugated asbestos cement fence in 1990 for about one and a half days, he would have been exposed to average airborne asbestos levels of about 2 fibres per ml, or about 200 times general environmental background levels.

88 Dr Francis identified the reports upon which she relied for the purposes of forming her views about the levels of respirable fibre to which Mr Hannell would have been exposed in the course of the work he had identified.

89 In a supplementary report dated 2 May 2006 Dr Francis repeats virtually everything contained in her original report, but includes an estimate of total cumulative asbestos exposure as a result of the specific exposures identified by Mr Hannell of 0.2 fibres per ml years. Given that Dr Francis estimated ambient background environmental levels at 0.01 fibres per ml, this means that Dr Francis estimated the total cumulative exposure to respirable fibre experienced by Mr Hannell during the three periods he had identified as being the equivalent of the cumulative exposure experienced by every member of the community over the course of 20 years.

90 In the course of cross examination, a number of propositions were put to Dr Francis to the effect that she had over estimated the exposure experienced by Mr Hannell in the course of the work he had identified. Dr Francis agreed that asbestos insulation boards contain between 40 and 80 per cent asbestos, whereas asbestos cement contains 8 to 15 per cent asbestos. Dr Francis also accepted that work on asbestos insulation board was generally much dustier than work on asbestos cement, because the cement bound the fibre. She also acknowledged that many of the studies upon which she had relied for the formation of her opinion involved work on asbestos insulation board, not asbestos cement.

91 Dr Francis also acknowledged that when estimating the amount of fibre released by the work done by Mr Hannell on the eaves, she had not made any allowance for the fact that the eaves were painted, even though the paint would have adhered to the fibre.

92 Dr Francis also acknowledged that she had relied upon a study from the United Kingdom reporting the amount of fibre released from the activity of hand sawing asbestos cement published in 1976, when a later report published by the same authority in the 1990s had reduced the estimate from 3 fibres per ml to below 1 fibre per ml. However, she had relied only upon the 1976 report.

93 Further, Dr Francis agreed that the use of a circular saw to cut asbestos cement created a lot of dust which included asbestos. She agreed that studies showed that 10 to 20 fibres per ml were released by that activity. In that context, it was put to her that her estimate of 8 fibres per ml for the sanding and brushing of painted eaves was a significant over estimate. However, she maintained her view.

94 The general effect of the cross-examination was to establish that if Dr Francis had made any error in her estimate of the exposure to the respirable fibre experienced by Mr Hannell in the course of the specific incidents he had identified, it was to over estimate that exposure.

95 The trial Judge took the same approach to his evaluation of the evidence of Dr Francis as he had taken in relation to the evidence of Mr Rogers. He expressed the view that he found her calculations and conclusions to be no more reliable than those of Mr Rogers. In his evaluation of the evidence of Dr Francis, he observed that the tests and data relied upon by her had not been proved so as to form a proper basis for her opinion, notwithstanding that no objection was taken to the tender of her report on behalf of Mr Hannell, nor was any cross-examination directed to the issue of the authenticity or reliability of the reports upon which she had relied.

96 Further, the trial Judge stated that the cross-examination of Dr Francis by counsel for Amaca caused him to lack confidence in her calculations. However, as I have observed, the effect of that cross-examination was to suggest quite strongly that to the extent that Dr Francis had made errors, those errors resulted in an over estimate of Mr Hannell's cumulative exposure to respirable asbestos fibre in the course of the specific incidents he had identified.

97 Notwithstanding the tenor and effect of the cross-examination, the trial Judge expressed his conclusions in relation to the evidence of Dr Francis in the following terms at [294]:

"I do not accept that the likely or probable cumulative exposure resulting from the plaintiff's handyman activities would have been no greater than the calculations made by Dr Francis. As with Mr Rodgers [sic] there are too many assumptions, estimates and variables involved in Dr Francis' calculations and they are based to too great a degree upon unpublished results of tests where there is no evidence of the scientific reliability of those tests."

98 The finding that the likely or probable cumulative exposure would have been no greater than the calculations made by Dr Francis was against the evidence. The evidence plainly established that her assessments would, if anything, have resulted in an over estimate of exposure. The comments I have made above with respect to the trial Judge's general disparagement of Mr Rogers' evidence as being based on "too many assumptions" and his reliance upon the lack of direct evidence in relation to the tests and reports relied upon, apply with equal force to the approach he took to the evaluation of the evidence of Dr Francis.

99 Amaca led evidence from Professor Geoffrey Berry, who is a biostatistician and epidemiologist. He is currently Emeritus Professor in the School of Public Health at the University of Sydney. He has worked in the area of dust related diseases since 1966. He is the author of numerous articles and chapters in books related to lung diseases, especially occupational diseases. A large number of his published papers are devoted to the specific area of asbestos-related lung diseases. Professor Berry's opinions were reduced to writing in a report dated 21 March 2006 which was tendered in evidence without objection from counsel for Mr Hannell.

100 In his report Professor Berry set out the assumptions of fact he had made in relation to the incidents of specific exposure identified by Mr Hannell. Those assumptions correspond with the findings of fact made by the trial Judge.

101 Professor Berry then dealt with a number of factors which bear upon the level of risk of contracting mesothelioma. The first factor he addressed was the relationship between risk and time. He observed that it is well established that the risk of mesothelioma as a consequence of a period of exposure to asbestos increases as time passes since exposure. Only a minority of cases occur earlier than 20 years since first exposure - the majority occurring more than 30 years since first exposure.

102 The relationship between the time of exposure and the risk of mesothelioma has, according to Professor Berry, been investigated in a number of studies. Those studies lead to the conclusion that exposure 20 years ago carries a risk which is eight times greater than exposure 10 years ago; whereas, exposure 30 years ago in turn has a risk three and a half times greater than exposure 20 years ago.

103 The next factor assessed by Professor Berry was the relationship between fibre type and risk of contracting mesothelioma. He referred to the general effect of studies in the area. The studies suggest that the risk of contracting mesothelioma as a result of crocidolite is 15 times greater than the risk arising from exposure to chrysotile. The risk associated with exposure to amosite is about six times that associated with exposure to only chrysotile.

104 Further, because of the association between risk and delay following exposure, Professor Berry expresses the view that studies suggest that the risk associated with exposure at the age of 40 is 0.4 times the risk associated with exposure at the age of 30. Mr Hannell was 41 years of age at the time of his specific exposure in 1983.

105 Professor Berry then calculated the increase of risk as a result of Mr Hannell's specifically identified exposures, accepting Mr Rogers calculation of the cumulative effect of those exposures as about 0.001 fibres per ml years. Professor Berry estimated that if the fibre to which Mr Hannell was exposed was crocidolite, his increased risk would be about 14 per cent of the background risk and about three per cent of the background risk if the asbestos was amosite. The asbestos was in fact largely chrysotile with only a very small proportion of amosite. Further, in his evidence-in-chief, Professor Berry observed that if he had used the levels of background risk for the Western Australian population calculated by Professor Musk, which were higher than the levels he had used, the increment in risk due to Mr Hannell's specifically identified exposures would have been significantly less, relative to the background risk.

106 During his evidence-in-chief Professor Berry was also asked if he had undertaken calculations of the increment in risk experienced by Mr Hannell as a result of his specifically identified exposures on the assumption that the cumulative effect of those exposures was as assessed by Dr Francis. Professor Berry stated that he had undertaken such a calculation on the assumption that half the fibre to which Mr Hannell was exposed was chrysotile and half amosite (being a significant over estimate of the amount of amosite in the material to which Mr Hannell was exposed). Professor Berry calculated that the relative risk as a result of exposure at that level would be 1.4, taking background risk as 14 persons per 100,000 or 1.3 taking background risk as 21 persons per 100,000. Accordingly, he assessed the relative risk occasioned by the specific exposures identified by Mr Hannell on the basis that those exposures were of the level calculated by Dr Francis, at 1.3 to 1.4.

107 I digress to observe that this calculated relative risk is of the same order of magnitude as that described by Spigelman CJ as low to moderate in McGuiness (supra) and, in that case, was found to be manifestly insufficient to establish the conclusion that there was a causal connection on the balance of probabilities.

108 Despite this, the trial Judge referred to Professor Berry's evidence in these terms at [296]:

"Professor Berry's evidence, if accepted, is not sufficient to discharge the evidential burden on the defendant of adducing evidence that the plaintiff's handyman exposure had no effect or that the plaintiff would have suffered mesothelioma even if he had not experienced the handyman exposure. Professor Berry is not able to say that the asbestos fibre or fibres that caused the plaintiff's mesothelioma were not inhaled by the plaintiff in the course of his handyman activities. Professor Berry's evidence, if accepted, is that on a population basis the risk of contracting mesothelioma as a result of 'background exposure' is greater, or many times greater, than the risk of contracting mesothelioma from asbestos exposure in the order of the plaintiff's handyman exposure. Professor Berry does not go so far, and his calculations do not permit him to go so far, as to say that the plaintiff's handyman exposure did not materially increase the risk of contracting mesothelioma."

109 The first point to make about these observations is that they reinforce the views I have expressed earlier as to the erroneous approach taken by the trial Judge with respect to the evidential burden. The evidence of Professor Berry, if accepted, was sufficient to displace any prima facie case set up by Mr Hannell.

110 They also reinforce the views I have expressed as to the erroneous approach taken by the Judge in relation to the applicable test for causation, in that they reflect an adoption of the test for causation adopted in the English cases, rather than that applicable in Australia. It is clear from the paragraph set out above that the trial Judge took the approach that any increase in risk as a result of the three identified exposures, which was not de minimis, was sufficient to establish causation. He did not pose or answer the specific question of whether, on the evidence, it was more likely than not that Mr Hannell's mesothelioma was caused or materially contributed to by the specific exposures he had identified, as compared to the background risk.

111 The trial Judge also observed that Professor Berry's views were dependent upon the assessments performed by Mr Rogers and Dr Francis and they had been rejected. He gave that as an additional reason for rejecting Professor Berry's evidence. In my view, because the trial Judge's rejection of the evidence given by Mr Rogers and Dr Francis was erroneous, it follows that his rejection of Professor Berry's evidence on these grounds was also erroneous.

112 The final reason given by the trial Judge for rejecting the evidence of Professor Berry was that Professor Berry used the background risk applicable to persons who had been exposed to respirable fibre in the ambient environment some of whom may have experienced specific exposures of which they were not aware or had forgotten; whereas, the trial Judge had found that Mr Hannell was not in that group because he had not experienced any specific exposures of which he was unaware or had forgotten. Because of my view that the trial Judge's finding in that regard was flawed, it follows that his rejection of Professor Berry's evidence on that ground was also flawed.

113 Accordingly, the various reasons given by the trial Judge for rejecting the evidence of Professor Berry cannot be sustained.

114 Amaca led evidence from Professor Antony Breslin, a consultant thoracic physician and Clinical Associate Professor of Medicine at the University of Sydney. His field of particular interest is respiratory medicine, including in particular diseases of the lung and pleura. Professor Breslin's opinions were reduced to writing in a report dated 15 April 2006, which was received in evidence over objections taken to two particular passages.

115 In his report Professor Breslin set out the assumptions he had made with respect to Mr Hannell's specifically identified exposures. Those assumptions accord generally with the findings made by the trial Judge.

116 Professor Breslin stated in his report that he has no reason to doubt the estimates of cumulative exposure made by Mr Rogers.

117 Based upon the low level of cumulative exposure from the specific incidents identified by Mr Hannell, the fact that his exposure was predominantly to chrysotile, although with some exposure to amosite; and the relatively short latency period (23 years); and the fact that all exposure was outdoor (thus reducing the risk of inhalation), Professor Breslin said that it is unlikely that the specific exposures made a significant contribution to the development of his mesothelioma and that it is more probable than not that his mesothelioma is attributable to background risk.

118 In cross-examination Professor Breslin corroborated the evidence given by Dr Francis effectively being that ambient environmental exposure is generally taken to be 0.01 fibres per ml. The estimates of Mr Hannell's cumulative exposure made by Dr Francis were also put to Professor Breslin in cross-examination. His view was that there was no doubt that Mr Hannell's specifically identified exposures were very, very low. Whether the cumulative exposure from the specific incidents was 0.25, 0.025 or 0.0025 was a matter Professor Breslin would leave to the occupational hygienists.

119 I digress to observe that this evidence reinforces the fundamental proposition which emerged from the evidence of Mr Rogers and Dr Francis. The proposition being that the total cumulative exposure of Mr Hannell in the course of the three incidents he had identified was, on any view of the mathematics involved and on any basis of calculation, of a very low order of magnitude. This basic proposition does not appear to have been recognised or acknowledged by the trial Judge.

120 Professor Breslin reinforced that proposition with his evidence that even if he accepted the assessments of cumulative exposure made by Dr Francis (which were 100 times greater than those of Mr Rogers), it would not alter his opinion as to the probable cause of Mr Hannell's mesothelioma.

121 The trial Judge gave two reasons for not accepting the opinions expressed by Professor Breslin. The first was the trial Judge's view that Professor Breslin had erroneously placed Mr Hannell in the group exposed to background risk, because of his finding that Mr Hannell had not experienced any specific exposures of which he was unaware or had forgotten. As I have observed, that process of reasoning starts from a flawed finding of fact.

122 The second reason given by the trial Judge for rejecting Professor Breslin's evidence is his reliance upon Mr Rogers' estimates. With respect, this approach misconstrues the evidence given by Professor Breslin and in particular, overlooks the fact that his opinion was based upon what he took to be a very very low cumulative exposure in the specific incidents which Mr Hannell had identified and of which Professor Breslin was certain. It also overlooks the evidence given by Professor Breslin that his opinion would not change even if he assumed the estimates of exposure made by Dr Francis.

123 Accordingly, the reasons given by the trial Judge for giving no weight to the evidence of Professor Breslin cannot be sustained.

124 I turn now to the evidence of the witnesses called on behalf of Mr Hannell (other than Dr Francis) whose evidence the trial Judge relied upon for his conclusions as to causation.

125 Professor Musk is an eminent respiratory physician who has specialised in the field of asbestos-related lung disease. He is a clinical professor of medicine at the University of Western Australia. He also holds a chair in public health at the same university. He has conducted research in relation to the cohort of people exposed to asbestos at Wittenoom for at least 30 years. His opinions relevant to Mr Hannell's case were provided in the form of two reports dated 20 March 2006 and 23 April 2006 respectively and a further statement setting out the substance of the evidence to be given by him.

126 Professor Musk's first report relating to Mr Hannell deals with his diagnosis of mesothelioma, the clinical history provided by Mr Hannell and the likely future costs of treatment.

127 The report also contains a summary of the specific incidents of asbestos exposure related by Mr Hannell to Professor Musk and which correspond with the findings of fact made by the trial Judge. The report contains Professor Musk's opinion that the cause of Mr Hannell's mesothelioma was the specific incidents of asbestos exposure, but contains no process of reasoning supporting that view.

128 Professor Musk's second report relating to Mr Hannell is concerned entirely with foreseeability. It need not be addressed at this point.

129 The document setting out the substance of the evidence to be given by Professor Musk, and which was tendered in evidence, deals with anatomy, the pathological effect of exposure to the inhalation of asbestos fibre, the symptoms of the conditions contracted through the inhalation of asbestos fibre, diagnosis, treatment and prognosis.

130 Under the heading "Dose Response" Professor Musk states that there is no safe level of exposure to any carcinogen and that there are clear dose-response relationships for mesothelioma and lung cancer. He observes that for both malignant mesothelioma and lung cancer, risks increase with time since first exposure, especially mesothelioma where the risk increases exponentially (to the power of 3.6) with years from first exposure after the first 10 years.

131 The rest of the statement is concerned with the development of knowledge in relation to asbestos-related lung disease. In the first portion of that section of the statement, Professor Musk reviews 72 publications dealing with the subject in chronological order between 1898 and 1964. The second portion is concerned with the development of knowledge after 1964 and the third portion is concerned with standards, regulations and legislation in various jurisdictions.

132 It can thus be seen that there was nothing in the three items of written evidence presented by Professor Musk dealing with the question of causation specifically by reference to Mr Hannell, other than the unreasoned assertion that the specific incidents of exposure were the cause of his mesothelioma.

133 Professor Musk was cross-examined in relation to background risk and confirmed that repeated studies over the years have demonstrated that between 15 and 30 per cent of mesothelioma suffers are unable to recall any particular exposure to asbestos. Thus, the group may include those who have had no specific exposure other than the respirable fibre present in the ambient environment and those who have had specific exposure of which they were unaware or cannot now recall.

134 Professor Musk was also cross-examined on the relationship between risk and the factors known to affect risk; namely: dose, fibre type and lag time. He confirmed the views expressed by all experts called in the case; namely, that crocidolite had the greatest propensity to cause mesothelioma, chrysotile the least propensity and amosite somewhere in between. He confirmed that even a small dose of crocidolite can be much more dangerous than relatively large doses of chrysotile. He further confirmed that lag time increases the risk exponentially by a factor of three and that mesothelioma is not seen within 10 years of exposure. Accordingly, if there are two periods of specific exposure identified by a patient, the earlier exposure can safely be regarded as much more causally potent.

135 Professor Musk was also cross-examined in relation to the relative contributions made to the risk of Mr Hannell contracting mesothelioma by his membership of the background risk group and the specific exposures he had identified. In the course of that cross-examination the following exchange occurred:

"That's really what we are examining in terms of each of Mr Moss and Mr Hannell - is the risk of them contracting mesothelioma due to the exposures which they describe?---Yes.

Medical science in relation to mesothelioma doesn't permit us to know, at least as yet, by looking at an individual patient as to which exposure was the causative exposure?---That's correct.

And because we know that there is a background risk, it could be said in relation to any patient who described a very slight exposure that we would not know whether the slight described exposure was causative as compared to the background risk. Do you agree?---Yes, once the disease is there we don't know which exposure caused it.

And if we go to the specifics, if we talk about the case of Mr Hannell, for example, we ask the question: but for that home handyman exposure that he described, would he have got the disease?---Yes.

The answer would have to be: 'We can't say'?---That's correct."

136 In cross-examination, Professor Musk was then taken through the procedures relating to the calculation of relative risk by biostatisticians. In that context, he confirmed that he and Dr de Klerk had calculated the background risk for mesothelioma in Western Australia at between two and three persons per million persons per annum. This equates to a lifetime risk of between 140 persons per million to 210 persons per million.

137 Professor Musk was then taken through Professor Berry's calculation of relative risk, based upon the estimates of exposure made by Mr Rogers. It will be recalled that based on those estimates, Professor Berry calculated a relative risk of 1.04. Counsel for Amaca put to him the proposition that in medical or scientific terms that reflected an increment in risk that was tiny, to which Professor Musk responded:

"It depends on the perspective you have and what is tiny to some people isn't tiny to other people but I am comfortable with [Professor] Berry's calculations. I think they come out reasonable."

138 In the course of re-examination, Professor Musk was asked about causation in the context of statements he had made in his report relating to Mr Alan Moss, whose claim against Amaca was being heard simultaneously with the claim by Mr Hannell. Professor Musk's reports relating to the two claimants were in almost identical terms and accordingly, the views he expressed when asked about his statements in the report relating to Mr Moss shed light on the approach he had taken to the expression of his opinion relating to Mr Hannell. In that context he gave the following evidence:

"Yes. I don't think I've said it very well here. I mean, I believe the cause of his mesothelioma is asbestos. I think there's probably enough background asbestos exposure although it's never been directly studied, and in fact it's a study that we've just recently been funded, I believe, by the [NHMRC] to carry out. The cause of his mesothelioma I think was asbestos exposure, but not simply the handyman jobs he did, the background as well, but that - in the second sentence: the episodes of exposure, albeit small, I believe, would have increased that risk, so the first sentence would include background exposure and I'm sorry that it doesn't say that explicitly."

139 Following the completion of re-examination, the trial Judge asked Professor Musk if that evidence was applicable also to the statement in his report relating to Mr Hannell. Professor Musk stated in that report: "It is my opinion that the cause of your client's mesothelioma was asbestos exposure as described". He then confirmed that the evidence I have set out above was equally applicable to both men.

140 It is a fair inference from that evidence, taken with Professor Musk's acceptance of Professor Berry's calculations showing a very low increase in risk as a result of the specifically identified exposures, that when Professor Musk refers to causation in his written evidence, he uses that term to embrace and include any event which increases risk, however slight.

141 The evidence I have set out above is the only evidence given by Professor Musk on the question of the issue of causation as it relates to Mr Hannell. Apart from the extent to which Professor Musk's views might be inferred from those passages, he gave no direct testimony on the relative contributions to risk presented by the specific incidents of exposure as compared to the background risk. It is difficult to see how he could have formed a view as to the causative effect of the specific incidents of exposure without undertaking that exercise. If he has undertaken that exercise, he gave no evidence of it.

142 The trial Judge dealt with Professor Musk's evidence in that portion of his reasons relating to foreseeability. Not surprisingly, the six paragraphs of his reasons dealing with Professor Musk's evidence in that context deal only with his evidence relating to the development of knowledge with respect to the risks attending the inhalation of asbestos.

143 The only references to Professor Musk's evidence in the portion of the reasons of the trial Judge dealing with causation are as follows:

"259 In his report of 20 March 2006 Professor Musk stated his opinion that the cause of the plaintiff's mesothelioma was asbestos exposure 'as described' that is, the plaintiff's handyman activities in 1983, 1985 and 1990.

...

1. ... Professor Musk opined that the cause of the plaintiff's mesothelioma was asbestos exposure as a result of his handyman activities in 1983, 1985 and 1990 ...

1. I prefer the evidence of the medical experts - Professor Musk, Professor Robinson, Professor Henderson, Dr Alvares and Dr Leigh - to that of the industrial hygienists - Mr Rodgers [sic] and Dr Francis - on the issue of the contribution of the plaintiff's handyman asbestos exposures to the plaintiff contracting mesothelioma and the risk of the plaintiff contracting mesothelioma from his handyman exposures compared with the background risk."

144 I have already observed that Professor Musk provided no process of reasoning or elaboration for the conclusion that he had expressed on the subject of causation. His evidence on the subject of specific causation is analogous to "the bare ipse dixit of a scientist" referred to by Lord President Cooper in Davie v Magistrates of Edinburgh [1953] SC 34, cited with approval by Heydon JA in Makita v Sprowles (supra). The trial Judge has provided no process of reasoning or elaboration upon his preference for Professor Musk's unexplained conclusion. It was of course the obligation of the trial Judge to make findings of fact, including findings drawn from the expert evidence, and then to enunciate in his reasons the way in which he had applied those findings to the legal question of causation (Makita v Sprowles (supra); Mount Lawley Pty Ltd v Western Australian Planning Commission [2004] WASCA 149; (2004) 29 WAR 273, 282 - 283; Soulemezis v Dudley (Holdings) Pty Ltd (1987) 10 NSWLR 247, 269 - 270; Beale v Government Insurance Office (NSW) (1997) 48 NSWLR 430, 441). At least in the case of the evidence of Professor Musk, he seems, with respect, to have abdicated that responsibility in favour of accepting an unexplained conclusion drawn by the witness and which, for the reasons I have given, appears to proceed upon an entirely different basis of causation to that required by law.

145 Professor Musk's evidence provides no basis for a conclusion that the specific instances of exposure identified by Mr Hannell were more likely than not to have caused or contributed to him contracting or developing mesothelioma.

146 Professor Bruce Robinson is a consultant physician at the Department of Respiratory Medicine at Sir Charles Gairdner Hospital. He has spent a significant part of his career dealing with asbestos-related disease, has published 162 papers dealing with the subject and has been the editor of a number of books, including the text "Mesothelioma".

147 Professor Robinson prepared a report dated 13 February 2006 setting out a number of opinions he had formed in relation to Mr Hannell. That report was tendered in evidence without objection. It contains the following paragraph:

"Aetiology:

The patient's mesothelioma is likely to be due to his asbestos exposure. He had no exposure in his occupation but he has incidental exposure about twenty years ago whilst working on fences where he [sic] cutting and drilling asbestos fences. This represents a short incubation period but I have not been able to identify any prior asbestos exposure in his history to this point."

148 Professor Robinson also verified a written statement setting out the substance of the evidence to be given by him in each of the cases concerning Mr Hannell and Mr Moss. That statement was tendered without objection. It included the following statements:

"(a) that the cause and effect relationship between asbestos and mesothelioma is one of the strongest associations known to medical science. This powerful association is supported by the growth in mesothelioma paralleling the growth in the use of asbestos last century, the incidence in exposed cohorts and the fact that if you implant asbestos fibres into mice you get mesothelioma;

(b) no threshold dose below which no risk of mesothelioma exists has been demonstrated. Consequently all asbestos inhalation increases the risk of mesothelioma. If a mesothelioma occurs after a period of latency after inhalation then the exposure must be presumed to have had significance in the aetiology of the disease. And each exposure contributing to the cumulative total dose will have significance.

(c) low risks calculated from comparatively low doses of asbestos may state the chance of a particular individual contracting mesothelioma, but once the mesothelioma occurs the risk is realised and the chance means nothing. It is like having tickets in a lottery; a Wittenoom worker exposed to millions of fibres has millions of tickets and a high chance; someone such as Mr Hannell or Mr Moss may only have tens of thousands of tickets and a relatively low chance of the ticket coming up; but there are a lot of people with the same number of tickets and inevitably some will win, or in the case of mesothelioma, lose. Or as in the case of uv and melanoma, another cause and effect with a strong association, everyone will get sunburnt, but only some people will be unfortunate to contract a melanoma.

(d) 'background risk' of asbestos disease other than the 1 in a million incidence in non asbestos-exposed populations is something of a misnomer. Nearly everyone in Australia has had some significant level of exposure and each time they are further exposed the total cumulative dose increases, increasing their chance of mesothelioma; of 'winning the lottery'. We are seeing more cases of so-called low dose exposure such as these cases. It may just be that the ability to identify relevant causative exposure is getting better, and our understanding of the effects of such exposures is better, so that the percentage of 'background' or 'no known exposures' will continue to lessen.

(e) In these cases we have a clear history of asbestos exposure and a subsequent mesothelioma after a sufficient, albeit short latency. The exposure is the likely cause of the disease in each case.

(f) Although the latency periods from first exposure are short in each case (about 20 years in Mr Hannell's case and about 15-17 years in the case of Mr Moss) each is a sufficient period of latency. I have seen a clear history of an 11 year latency described and I have had four patients who developed mesothelioma in their 20's; one a Wittenoom child, one who did an apprenticeship at the Midland Railway workshops, one a fitter-and-turner with no identifiable exposure and one a student at Belmont High School, one of the schools identified as having asbestos hazards. Other latencies less than 20 years are described in the literature. In my opinion these cases cannot be excluded as having been caused by the exposures described on the basis of the periods of latency."

149 Professor Robinson also gave oral evidence-in-chief, the substance of which was accurately set out by the trial Judge in the following paragraphs of his reasons:

"192 In his oral evidence Professor Robinson was asked and gave the following opinion on how mesothelioma tumours develop:

'Whilst it's not absolutely certain, I can tell you, ... current concepts of what is most likely. The types of asbestos that cause mesothelioma or are most likely to cause it are shaped like a spear, are long and narrow, and when they're inhaled they work their way through the lungs and find themselves on the outside of the lungs where they irritate the sac in which the lung sits known as the pleura ... It is thought that over a period of time the damage caused by that fibre, which is probably made worse by breathing - if you can imagine the lung rubbing up against the pleura every time you take a breath and you've got fibres sticking out, it's always scratching the pleura causing damage and it's those repeated cycles over many years of damage and repair, damage and repair and production of molecules like oxidants that damage the DNA that allow pleura mesothelial cells to accumulate DNA damage. Now, most of the time damage does not cause mesothelioma but it is thought that in everybody that has been exposed to asbestos there is probably some DNA damage. How much DNA damage do you need to get mesothelioma? Well, the answer is every cancer cell probably has tens of thousands of mutations but most of them occur in non-dangerous genes. It's when you get a set, may be two, three, four, five, six genes, that cause cancer in that, let's say 15,000 or 11,000 mutations - call it 11,000. You need 11,000 and you get six maybe that are the dangerous ones. They are the ones that unfortunately trigger the mesothelioma but it takes a long time to accumulate that much DNA damage. When the cancer is finally triggered, it has disordered growth. Cells of course normally grow. That's how we grow from childhood to adulthood and that's how when we have a wound the skin will grow and cover it over. So growth is normal but cancer is when that growth has lost its controls. I guess like a mob out of control. That happens because of a number of reasons but the simplest way to think about it is that the cell growth is driven by an accelerator, which are growth factors and by brakes which stop growth, so that when your skin has healed from a wound the body realises that and the skin stops growing. So there's an accelerator and a brake and cancer is when there's too much accelerator and no brake. The things that are accelerators are ... things called oncogenes and the things that are the brakes are things called tumour suppressor genes and mesothelioma clearly has disorders in both of those two things. So it grows. It takes a while to kick off but once it has kicked off it grows relentlessly unfortunately ...'

1. Professor Robinson was asked what is meant by the terms initiation and promotion with respect to asbestos and mesothelioma. The Professor replied:

'I'm not sure they're actually that helpful those sorts of terms, because initiation is something that will cause initial DNA damage and promotion is something that takes the cells from that point to becoming a cancer. In the case of asbestos which probably does the whole lot, causing DNA damage right through to - I mean, it doesn't need help from anything else. It can get help, for example, in lung cancer, from smoking, but it doesn't need help, if you like. So I don't actually find those terms - those terms are a little bit outdated I think in science. It's better to think of cancer and exactly what is going on in terms of DNA. So, for example, you can get DNA damage and then you can get a disorder of growth that causes those cells to then become more dominant in that pool of cells.'

Professor Robinson then further referred to initiation and promotion in this context:

' ... there's initiation which by itself won't cause cancer and they [sic: then] you get subsequent molecular events that take the cancer from its damaged state to a ... growth advantage state.'

1. Professor Robinson was asked whether, after asbestos fibres have caused initial DNA damage, it required further asbestos fibres to cause the subsequent development of the tumour. Professor Robinson replied:

' ... it's impossible to answer because the asbestos stays there. ... the asbestos stays in the lung. But why it's interesting is that the other thing that asbestos does is to cause chronic inflammation and chronic inflammation is thought to promote cancer, not only in the lung but also, for example, in the gut, so that anti-inflammatory drugs can marginally reduce the risk of cancer, bowel cancer. So the capacity of asbestos to induce inflammation is another reason why it takes such a long time. So no-one knows whether it's ongoing damage from DNA or the inflammation that's associated with it over that period of incubation or both.' "

150 In cross-examination, Professor Robinson agreed that the estimate of background risk varied between one per million per annum (which equated to a lifetime risk of 70 per million) and two to three persons per million per annum (equating to a lifetime risk of 140 to 210 per million), depending upon the community. He agreed that in Western Australia the appropriate figure was two to three persons per million per annum.

151 In cross-examination, he also agreed that when, in his evidence, he was referring to the aetiological factors, he was referring to the combination of the background risk and the additional risk caused by specific home handyman exposures.

152 In his report of 13 February 2006, Professor Robinson asserts that Mr Hannell's mesothelioma "is likely to be due to his asbestos exposure". This is entirely unsupported by any enunciated process of reasoning. However, the process of reasoning that led to that conclusion is relatively clear from the further statement of evidence and his cross-examination. It is a clear inference from that evidence, that Professor Robinson has approached the question of causation by reference to his lottery ticket analogy. He has taken the view that because it is impossible to say which lottery ticket has won the prize (or in the case of mesothelioma, caused the injury), he proceeds on the assumption that every ticket is causative because once mesothelioma has been contracted, the risk has come home so that notions of risk and chance are irrelevant.

153 For the reasons which I have set out above, this process of reasoning does not accord with the legal test of causation. Pursuing Professor Robinson's lottery ticket analogy and assuming that each fibre or group of fibres inhaled creates the prospect of contracting or developing mesothelioma, Mr Hannell's claim could only succeed if he establishes that it is more likely than not that the fibres or group of fibres which he inhaled during the specific incidents of exposure he identified between 1983 and 1990 caused or contributed to him contracting or developing mesothelioma (or were the ticket that won the lottery in the analogy).

154 Pursuing the analogy further, in a case such as this where Mr Hannell has acquired his "tickets" from two sources: one source being background risk and the other source being the specifically identified exposures; any evaluation of the likelihood of the "ticket" having been acquired from the home handyman exposures, necessarily requires an assessment of the number of "tickets" obtained from each source. Thus, if the background risk is equivalent to, say, 100 tickets in a lottery and the risk occasioned by the home handyman exposures is equivalent to four tickets or even 40 tickets, it could be said that it is more likely than not that the mesothelioma came from the background risk than from the home handyman exposures. This is precisely the form of analysis which Professor Robinson has eschewed. In his view, once the lottery has been drawn and the risk has come home, it does not matter which tickets came from which source. While this may be an understandable view, it does not correspond with the relevant legal test.

155 As I have observed, the trial judge referred at length to Professor Robinson's evidence in those portions of his reasons dealing with the aetiology of mesothelioma. In the portion of his reasons dealing with the causation of Mr Hannell's mesothelioma, the references made by the trial Judge to Professor Robinson's evidence were limited to the following:

"260 Professor Robinson said in his report of 13 February 2006 that the plaintiff's mesothelioma is likely to be due to his asbestos exposure about 20 years ago whilst working on fences where he was cutting and drilling asbestos fences.

1. ... Professor Robinson considered that the plaintiff's mesothelioma is likely to be due to his asbestos exposure in the course of those handyman activities"

along with [314], which I have set out above, where the trial Judge records his preference for the evidence of Mr Hannell's experts to those called by Amaca.

156 Nowhere in his reasons does the trial Judge evaluate the process of reasoning which caused Professor Robinson to express the views on specific causation which the trial Judge has recorded and adopted. As I have already observed, a trial Judge is under such an obligation when contentious expert evidence is given. Analysis of Professor Robinson's reasoning to the extent that it is enunciated in his evidence, makes clear that it does not correspond to the applicable legal test of causation. Professor Robinson's expressed conclusions provide insufficient support for Mr Hannell's claim. That is because Professor Robinson has declined to attempt any assessment of the relative contributions to the risk of Mr Hannell contracting or developing mesothelioma made by background risk on the one hand and the specifically identified exposures on the other.

157 Professor Douglas Henderson is a pathologist. He holds the chair in pathology at Flinders University. He has had a particular professional interest in asbestos-related lung disease since he practised in Perth in the mid-1970s. He served on the Australian Mesothelioma Surveillance Programme Pathology Panel ("the Panel") between 1979 and approximately 1986; during which time, the Panel analysed between 800 and 1000 cases to validate the diagnosis of mesothelioma or to exclude the diagnosis in some instances. He was a substantial contributor to a book entitled "Malignant Mesothelioma" published in 1992.

158 The opinions formed by Professor Henderson in relation to Mr Hannell's case were provided in the form of a written report dated 17 April 2006 and a statement of the further substance of the evidence to be given by him. That report and statement were both tendered. In his report, Professor Henderson sets out the assumptions he had made in relation to the specific exposures experienced by Mr Hannell between 1983 and 1990. Those assumptions generally correspond to the findings of fact made by the trial Judge, save that Professor Henderson had assumed that the fence upon which Mr Hannell worked in 1983 contained only chrysotile; whereas, in fact, a sample taken from the fence showed that it contained both amosite and chrysotile (about 1 per cent amosite).

159 Professor Henderson noted in his report that he had assumed that Mr Hannell did not sustain any other significant occupational or non-occupational exposure to asbestos. Accordingly, Professor Henderson has proceeded on the same basis as the trial Judge in that respect. For the reasons I have given above, in my opinion, that approach is flawed.

160 On the subject of the causes of mesothelioma, Professor Henderson observed that while it was generally accepted that some types of asbestos were substantially more potent in causing mesothelioma than others, the exact ratios of potency remained uncertain. While all commentators agreed that crocidolite was by far the most potent and chrysotile the least potent, with amosite somewhere in between, estimates of potency have ranged from a ratio of 500:100:1 to about 30:15:1.

161 In common with the other experts, Professor Henderson agreed with the propositions inherent in the Peto model and formulae to the effect that risk varied with fibre type, dose and latency period. He also observed that one factor which emerges from that model, is that when there are multiple exposures, each contributes to cumulative exposure "and hence to the risk and causation of mesothelioma". It seems clear that at least in this context, Professor Henderson is not using the word "causation" in the legal sense, but is proceeding on the assumption that any increment in risk, however small, is causative.

162 From the Peto model, Professor Henderson draws the deduction that:

"When there are multiple episodes of exposure, each increment of exposure within an acceptable latency interval produces a corresponding increment in the risk/incidence of mesothelioma, dependent upon the time of the exposure, its magnitude and the types of asbestos fibre involved."

163 I digress to observe that this proposition appears to be common ground amongst all the experts called to give evidence in Mr Hannell's case.

164 Professor Henderson also adheres to the view (which is not universally shared) that there is no minimum threshold dose of inhaled asbestos that has been delineated below which there is no increase in the risk of mesothelioma. Of course, academic debate on this topic is of limited utility and the proposition of limited relevance to this case. That is because it is accepted that all residents in developed urban communities will experience exposure to respirable asbestos fibre which is present in the ambient atmosphere.

165 Professor Henderson then referred to a number of studies dealing with relative risk calculations based upon relatively low level exposures. Amongst the studies to which he referred was a study by Hodgson and Darnton. They estimated that for a cumulative exposure of 0.01 fibres per ml years in the case of crocidolite, deaths could be estimated at 20 deaths per 100,000 persons; for amosite three deaths per 100,000 persons; and for chrysotile the risk was described as "probably insignificant" with a highest arguable estimate of one death per 100,000 persons. I digress to observe that these figures should be compared to Professor Berry's estimate of background risk in Western Australia of 14 to 21 deaths per 100,000 persons.

166 Professor Henderson also refers in his report to the studies which have shown particular levels of increase in respirable asbestos fibre as a consequence of different types of home handyman work undertaken on asbestos cement materials. In this section of his report, the following sentence appears:

"My own consultation and referral files include many cases of pleural malignant mesothelioma related to brief and transient 'handyman'-type asbestos exposures similar to those recorded for Mr Hannell."

167 However, that observation of itself, would not appear to sustain the conclusion that there is a causal relationship between brief and transient asbestos exposure and mesothelioma. Rather, as a matter of logic, all that can be said without epidemiological analysis of the kind carried out in the studies to which reference has been made, is that amongst people who suffer from mesothelioma, there is a group who have had brief and transient exposure to respirable asbestos fibre. Because there are a very large number of people within the community who have had brief and transient exposure to respirable asbestos fibre and who have not contracted mesothelioma, at the level of generality expressed by Professor Henderson, his observation does not appear to significantly advance consideration of the issues of causation.

168 In the portion of his report dealing specifically with the causation of Mr Hannell's mesothelioma, Professor Henderson expresses the view, drawn from preceding sections of his report, that two essential criteria must be met before mesothelioma could be attributed to specific asbestos exposure. The first was the performance of work or another activity that would have resulted in elevated concentrations of airborne respirable asbestos fibres in the breathing zone of the individual concerned, having a cumulative exposure in excess of any exposure derived from the general environment. The second is that there be an appropriate latency interval between exposure and diagnosis (that is, greater than 10 years).

169 It is obvious that these criteria are essential conditions which would have to be met before it could be concluded that any particular exposure was causative of mesothelioma. But if these criteria are regarded as sufficient to establish a causal link, it would have the effect that any specific exposure, no matter how slight, more than 10 years earlier than diagnosis, would be assumed causative of the diagnosis. Such an approach would not accord with the test of causation in law.

170 Professor Henderson summarised his views in relation to the causation of Mr Hannell's mesothelioma in the following terms:

"To summarise: I would assess Mr Hannell's cumulative asbestos exposures in 1983, 1985 and 1990 to have represented only light asbestos exposure in the form of chrysotile-only exposure (1983), followed by chrysotile + likely amosite exposure in 1985 and then chrysotile + amosite exposure in 1990. Given the fact that at least Mr Hannell's last exposure in 1990 involved amosite asbestos, it is my assessment that his cumulative exposures were significant for induction of his mesothelioma in that they represented exposures in excess of any 'background' exposure derived from the 'environment at large' for a control/reference urban or rural population with no identifiable occupational, domestic or environmental exposure to asbestos. Therefore, it is my assessment that his exposure was significant for causation of his mesothelioma, 'on the balance of probabilities'." (footnote omitted)

171 It is clear from this paragraph that Professor Henderson has proceeded on the basis that satisfaction of the two criteria he identified is sufficient in itself to establish causation on the balance of probabilities. Thus, Professor Henderson has approached that question on the basis that any exposure to respirable asbestos fibre in excess of ambient environmental levels more than 10 years prior to diagnosis will be regarded as causative. An opinion on the subject of causation expressed on that basis does not correspond to the relevant legal test.

172 Professor Henderson's report also contains the following paragraphs:

"Given Mr Hannell's development of pleural mesothelioma with a relatively short latency interval and only light asbestos exposure (and provided that he did not sustain any exposure to asbestos apart from those exposures recorded in your letter of 07 April), there appears to be a reasonable likelihood that he has an underlying innate/acquired susceptibility to carcinogenesis - specifically mesothelioma induction - by asbestos. Even so, it would be highly unlikely that any such predisposition to the carcinogenicity of asbestos would find expression as mesothelioma, in the absence of the asbestos exposure (in other words, if no exposure, then no mesothelioma, at a good order of probability).

Therefore, although Mr Hannell's first 'handyman'-type exposure in 1983 was apparently chrysotile-only exposure, it is worth pointing out that the risk of mesothelioma from chrysotile only exposure although substantially less on a fibre-for-fibre basis than for the amphibole forms of asbestos, it is not a zero risk. Therefore, it is my assessment at a reasonable order of confidence and a level of reasonable medical certainty that Mr Hannell's pleural malignant mesothelioma is attributable by way of causal-contributory relationship to his total cumulative 'handyman'-type asbestos exposures sustained in 1983, 1985 and 1990 as set forth in your letter of 07 April 2006. I suspect that the 1990 exposure may have made a somewhat (but unquantifiably) greater causal contribution towards the development of Mr Hannell's mesothelioma than the earlier 1983 chrysotile-only exposure, but the effect of the lower potency of chrysotile-only exposure for mesothelioma induction is offset to some degree in this case by the earlier timing of that 1983 chrysotile-only exposure. The point is that it is my assessment that the combined and cumulative effects of the 1983 + 1985 + 1990 exposures was significant for causation of Mr Hannell's mesothelioma.

It is also my assessment that the causal relationship between Mr Hannell's 1983 + 1985 + 1990 exposure took the form of a causal-contributory relationship, whereby his total cumulative 'handyman'-type exposure imposed a significant increase in the risk of developing mesothelioma, by way of an incremental risk on top of any underlying background risk of mesothelioma in Mr Hannell's case." (not my emphasis)

173 Although in the last portion of these observations, Professor Henderson acknowledges the underlying background risk of mesothelioma, the first paragraph of the quotation appears to presume that there was no exposure to respirable asbestos fibre in Mr Hannell's case other than the specific exposures he had identified. Further, nowhere in this passage, or indeed anywhere in Professor Henderson's report, is any attempt made to assess the magnitude of the risk to which Mr Hannell was subjected by way of background risk and the extent of the increment to that risk occasioned by his specifically identified exposures. When the passages immediately above are read in context of the report as a whole, it is a fair inference that Professor Henderson has proceeded upon the basis that any increment in risk, however small, occasioned by way of the specific exposures, is sufficient to lead to a conclusion of causation. That approach does not correspond with the position at law.

174 The document containing the further substance of the evidence to be given by Professor Henderson and which was tendered, refers to the information received after the provision of his earlier report to the effect that the hardiplank asbestos fence upon which Mr Hannell worked in 1983 included both amosite and chrysotile. Based on that modification to the factual assumptions made, Professor Henderson asserts that:

"My assessment is that to a good order of confidence, and a level of reasonable medical certainty, Mr Hannell's pleural malignant mesothelioma is attributable by a causal contributory relationship to his total cumulative handyman type exposures to asbestos.

In other words, the causal contributory relationship between Mr Hannell's mesothelioma and his prior 'handyman-type' asbestos exposures takes the form of a significant causal contribution incremental upon and on top of any underlying 'background' risk of mesothelioma."

175 However, the comments I have made above in relation to the processes of reasoning and the general approach taken by Professor Henderson remain equally applicable to those assertions.

176 In cross-examination, Professor Henderson agreed that studies of groups of mesothelioma sufferers will always reveal a proportion of persons who are unable to recall a specific exposure of asbestos. This does not necessarily mean that they have not had such an exposure. He expressed the view that it is impossible to ascertain scientifically that mesothelioma can be contracted without being exposed to respirable asbestos fibre, because it is impossible to assemble a group of humans with absolutely no asbestos fibres in their lung tissue. However, he believes that there may be such cases, although they would be very, very rare.

177 Professor Henderson confirmed that asbestos products had been widely used in the United Kingdom in a variety of different settings and circumstances. He confirmed that it had been estimated that asbestos had been used in about 3000 different industrial products across industrialised societies. Accordingly, Professor Henderson agreed that the atmosphere in London would likely include respirable asbestos fibre of all types. Professor Henderson agreed that Mr Hannell would have been inhaling low doses of respirable asbestos fibre in the ambient environment for 53 years which could have caused or contributed to his mesothelioma (given that his age at diagnosis was 63 years and the minimum latency period is 10 years).

178 Professor Henderson also accepted in cross-examination that Mr Hannell may have had some specific exposure to asbestos which he did not recognise or could not recall.

179 Professor Henderson was also asked about Professor Robinson's lottery ticket analogy in cross-examination. His attention was then directed to the question of the extent by which the risk of Mr Hannell contracting mesothelioma had been increased by his home handyman exposure, to which he gave the following answer:

"I would not attempt to put a figure, a numerical figure, on it. All I would say is that his risk was increased, that it was in my opinion a significant increase in risk but a small risk, and it would be a risk incremental on any background risk, and if one goes back to the analogy with lottery tickets, if one says that for example his background exposure has given him, say, three lottery tickets out of 100,000 towards winning the prize, then his home handyman exposure may have given him an additional two or three tickets, but the point is that the prize is not for any one ticket, but in this case the analogy breaks down. The prize of mesothelioma is for all the tickets."

180 When that answer is read in the context of his evidence as a whole, it is clear that the numbers of lottery tickets chosen by Professor Henderson were for the purposes of example only and were not intended by him to be indicative of the relative degrees of risk. For example, shortly after giving that answer Professor Henderson stated in answer to another question:

"I shy away from trying to make numerical estimates of increase in risk because they are necessarily based upon a whole series of assumptions about quanta of exposure, fibre types and the circumstances and the like. As the exposure is very low, as in these cases, the errors implicit in this sort of exercise become proportionately very large and therefore I shy away. All I would say is that I think that Mr Moss's and Mr Hannell's exposures have increased each of their risk of developing mesothelioma by way of increment in risk on top of background."

181 Later in Professor Henderson's evidence this exchange took place:

"To put it another way, in the case of Mr Hannell you couldn't say that except for his home handyman exposure he would never have got mesothelioma, can you?---No, I can't. All I can say is that the chance of his developing it would have been less if he had not sustained that handyman exposure."

182 In re-examination Professor Henderson was asked about the causal contribution made by the specific asbestos exposures in the case before the court. He replied:

"I suppose what I was trying to say was that we know that there is a relationship, or a dose response relationship between asbestos exposure and the likelihood of the development of mesothelioma and that when there are multiple exposures each exposure is considered to add to the overall risk of the development of mesothelioma, so that each exposure will exert an incremental increase in risk on top of background and on top of exposures that have gone before. In terms of the causation, again it comes down to probabilities and I really couldn't do better than to quote from page 4 of Dr James Leigh's report where in dealing with the development of mesothelioma he comments, 'All of these processes at cellular level are stochastic in that the probabilities of fibre cell interaction depend on the number of fibres and the number of cells present at any point in time, hence simplistically the more fibres the more free radicals and the greater probability of initiated, promoted or proliferated cells at any given point, at any given time point.' So there is a theoretical basis to explain the increase in risk in terms of the numbers of fibres inhaled and the more fibres that you have the greater the probability that these fibres will interact with mesothelia cells and eventually leave [sic - lead] by a multistage process to mesothelia."

183 On this view of the aetiology of mesothelioma, it is quite possible that Mr Hannell may have contracted the disease irrespective of whether or not he had experienced the specific exposures to respirable fibre which he identified between 1983 and 1990. That possibility is confirmed by the significant number of background risk cases that are identified each year. That possibility having been identified by the evidence, Mr Hannell bore the onus of proving that it was more likely than not that the specific exposures he had identified caused or materially contributed to his contraction of mesothelioma. If, as Professor Henderson and Dr Leigh assert, the processes leading to the development of the disease are stochastic, it follows that an assessment of whether Mr Hannell would, on the balance of probabilities, have suffered mesothelioma irrespective of the specific exposure he identified must turn upon an assessment of the extent of the incremental risk occasioned by those exposures. Nevertheless, Professor Henderson has eschewed any attempt to assess the extent of that incremental risk. Rather, his approach appears to be similar to that taken by Professor Robinson; namely, to the effect that because the risk has eventuated, any increment in risk - however small - can be properly characterised as causative. This approach is revealed by his answer to another question he was asked in re-examination:

"In these cases, did any background exposure that each of the plaintiffs have play a role in the aetiology of their mesothelioma?---Again, as I mentioned before, I think that's an unanswerable question in that it's not really known whether background mesotheliomas represent pre background or spontaneous cases unrelated to the low levels of asbestos fibres in lung tissue or whether they are a reflection of those low levels. I incline to the latter explanation and I believe that background exposures do play a role in the risk of mesothelioma, but that identifiable exposures in excess of and incremental on top of background will play an additional causal role and this is what I talk about, causal contribution, in terms of contributing to the overall risk of mesothelioma."

184 His approach was further exemplified in the answer he gave when asked by the trial Judge to explain his earlier evidence, which I have set out above, to the effect that, in the lottery ticket analogy, the prize of mesothelioma was for all the tickets and not just one ticket. He explained that answer as follows:

"What that is in terms of the analogy, your Honour, was trying to indicate that the outcome mesothelioma in terms of the total cumulative risk is related to the summation of all of the risks imposed by the prior exposures. So, as I gave an analogy, if in a lottery of 100,000 tickets background risk gives you three tickets and a small handyman type exposure gives you an extra two or three tickets, then the person wins the prize but the prize mesothelioma, if it is a prize, is not due to a single winning ticket but due to all of the tickets. So that all of the tickets have contributed to the overall winning, if you like. So what I was trying to say is that each identified episode of exposure will impose an increased risk of mesothelioma by way of an incremental effect on top of background and on top of any others that have gone before."

185 The trial Judge referred to Professor Henderson's evidence in the context of that portion of his reasons relating to foreseeability. The only references in his reasons to Professor Henderson's views on the subject of the causation of Mr Hannell's mesothelioma are as follows:

"261 Professor Henderson said in his report of 17 April 2006 that the plaintiff's 'handyman' exposures were significant for induction of his mesothelioma in that they represented exposures in excess of any background exposure derived from the environment at large for a control/reference urban or rural population with no identifiable occupational, domestic or environmental exposure to asbestos. Professor Henderson concluded therefore that the plaintiff's handyman exposure was significant for causation of his mesothelioma.

...

1. ... Professor Henderson said that the plaintiff's handyman exposures were significant for induction of his mesothelioma in that they represented exposures in excess of any background exposure derived from the environment at large. Professor Henderson concluded that the plaintiff's exposure was significant for causation of his mesothelioma ..."

and at [314] of his reasons, which I have set out above, in which the trial Judge expressed his preference for the opinions expressed by Mr Hannell's experts to those expressed by those called by Amaca.

186 The reasons of the trial Judge do not disclose any process of analysis of the opinions expressed by Professor Henderson on this topic. As I have observed, in a case of competing expert testimony, a trial judge is obliged to explain the process of reasoning which has caused the acceptance of one view over another. The reasons for decision in this case do not reveal that process. Further, as the evidence to which I have referred reveals, it is clear that Professor Henderson's views with respect to causation were based upon a quite different approach to that required by law and are explained by his view that any increment in risk, however small, is properly regarded as causative if the risk has eventuated. Professor Henderson's evidence is not capable of discharging Mr Hannell's burden of proving that it was more likely than not that the specific exposures to asbestos he had identified had caused or materially contributed to his mesothelioma. At its highest, Professor Henderson's evidence was to the effect that those specifically identified exposures had increased the risk of Mr Hannell contracting mesothelioma to an unspecified and indeterminate extent. Given that Professor Henderson accepted that there was another source of the risk of Mr Hannell contracting mesothelioma; namely, background risk, it could not be concluded on the balance of probabilities that Mr Hannell would not have contracted mesothelioma in any event, irrespective of the specifically identified exposures, unless and until an assessment of the relative magnitudes of the respective risks was undertaken.

187 Dr James Leigh is a consultant occupational physician. Between 1988 and 1996 he was head of the Epidemiology and Surveillance Unit and coordinator of the Australian Mesothelioma Register ("the Register") maintained by the National Occupational Health Safety Commission. Between 1996 and 2001 he was head of the research unit and coordinator for that Register. He has published some 79 refereed publications in various journals including many publications relating to asbestos-related disease.

188 Dr Leigh's opinions in relation to Mr Hannell's case were provided in the form of a report dated 12 March 2006 which was tendered in evidence.

189 Dr Leigh set out the assumptions of fact he had made in relation to Mr Hannell's specific exposures to asbestos. The terms of those assumptions, albeit general, correspond with the findings of fact made by the trial Judge. That is, with the exception that Dr Leigh has allowed for the possibility of exposure to crocidolite, which was not established by the evidence. Dr Leigh observed:

"All exposure, recalled and unrecalled or unrecognised, would have contributed cumulatively to the risk of mesothelioma. The detail provided is insufficient to make any reliable quantitative estimate of exposure. I suggest if possible that you obtain approximate quantified estimates of the cumulative exposure from other independent expert hygienists or engineers, familiar with the products and practices of the relevant periods. However, I am aware that such levels of exposure as in Mr Hannell's case have been associated with mesotheliomas in Australia and elsewhere. In the Australian Mesothelioma Register cases 1/1/86-31/12/2001, 71/3956 gave only exposure as built asbestos fence or dwelling."

190 It is clear that inclusion in the Register of a small number of cases of people who cite their own exposure as minimal home handyman work cannot, of itself, establish any causal connection between that work and the mesothelioma any more than Mr Hannell's inclusion in the Register would support a conclusion as to causation in another similar case. Many people in Australia will have experienced specific exposure to respirable asbestos fibre. The fact that a very small number of those persons later contract mesothelioma does not, on its own, tell one anything of the causal connection, if any, between those particular exposures and the disease.

191 I would also observe that Dr Leigh recommended that quantified estimates of cumulative exposure be undertaken by independent expert hygienists, which is precisely what Mr Rogers and Dr Francis have done.

192 Dr Leigh also expressed the following view in his report:

"In view of the capacity of asbestos fibres to be involved at several stages of tumour development, all cumulative exposure to asbestos in an individual case must be considered to play some part in causation. In an individual case current understanding suggests that cells are being initiated, initiated cells promoted and altered cells proliferating at different times. DNA repair process are occurring, and oncogenes and suppressor genes being activated and inactivated. Altered cells are being removed by apoptosis, necrosis and immunological means. Fibres are being cleared at differing rates and, if exposure is continuing, being deposited in the lung. All these processes at cellular level are stochastic in that probabilities of fibre/cell interaction depend on the number of fibres and number of cells present at any point in time. Hence, simplistically, the more fibres, the more free radicals and greater probability of initiated, promoted or proliferated cells at any given time point."

I do not construe this passage as suggesting that every asbestos fibre inhaled by a patient causes or contributes to the development of mesothelioma in the event that the patient later contracts that disease. Rather, I take Dr Leigh to be saying that every inhaled asbestos fibre increases the risk of mesothelioma being contracted or developed. He takes the view that every increment in risk is to be considered causative. In other words, he takes the same approach to causation as Professors Robinson and Henderson. That approach does not accord with the legal criterion in cases where the effect of incremental exposure is limited to incremental risk.

193 Dr Leigh also reports that mesothelioma has been recorded after exposures as short as one day. He refers also to records of cases in which exposures of one week and other exposures less than those of Mr Hannell's case have been recorded. However, as I have already observed, the mere fact that a very small number of mesothelioma patients can recall specific incidents in which they had small and limited exposure to respirable fibre does not, of itself, establish a causal connection between that exposure and the disease. Dr Leigh describes these cases as being the subject of "scattered case reports", from which it is clear that they are not sufficient in number to enable any conclusion of causation to be drawn, at least without further epidemiological study and analysis.

194 In his report Dr Leigh also refers to a number of published studies reporting increased relative risks of contracting mesothelioma associated with varying degrees of involvement in asbestos and asbestos cement plants, including those who did nothing more than reside nearby. However, unless the cumulative exposure of the persons the subject of those studies is quantified and compared to the cumulative exposure experienced by Mr Hannell as a consequence of the specific incidents he has identified, those studies cannot, of themselves, support any conclusion as to causation in Mr Hannell's case.

195 Dr Leigh expressed his conclusion on the question of causation in the following terms:

"1. Mr Hannell's total cumulative asbestos exposure during the period 1983-1990 was significantly greater than background exposure from the environment at large (the background exposure would be included in the total exposure) and Mr Hannell's exposure to asbestos in 1983-1990 made a material contribution to causation of his mesothelioma."

196 However, it is apparent from the passages in his report that Dr Leigh expresses this view not because of a view that every asbestos fibre inhaled by Mr Hannell contributed to either the initiation or development of his disease, but rather because of his view that every asbestos fibre inhaled by Mr Hannell increased the risk of mesothelioma being initiated or developed. Dr Leigh has not made any estimate of the magnitude of the increase in risk likely to have been caused by the specific exposures identified by Mr Hannell, but has suggested that task be referred to expert industrial hygienists (such as Mr Rogers and Dr Francis).

197 In his examination-in-chief, Dr Leigh expanded upon the passage of his report in which he refers to the stochastic processes at cellular level. The following passage from his oral testimony confirms the construction which I have put on that passage:

"Well, simplistically, the more fibres - I have used the analogy in court cases, including here in this jurisdiction, that it's like sperm and ova. I mean, only one sperm actually fertilises the ova but there's millions sent out to do the deed, so the more there are the more chance of one being hit.

You referred to number of fibres acting on cells. Referring again to the analogy you just made with sperm cells, is one fibre sufficient or is it possible that one fibre could initiate the changes in the cells?---Ultimately one fibre does initiate the change in the cell, but it's because it's been given a big chance by being one of a huge force.

Yes?---It's a bit like the army, if you have a lot of soldiers you've got more chance of hitting somebody."

198 It is therefore clear that Dr Leigh's opinion as to causation is based upon the proposition that every asbestos fibre inhaled increases risk. Accordingly, in order to apply the legal test of causation, it is necessary to assess the increment in risk occasioned by the inhalation of asbestos fibres during the specific exposures identified by Mr Hannell, as compared to the level of background risk.

199 The following evidence, given by Dr Leigh in the course of cross-examination, confirms the approach which he had taken:

"You see, medical science doesn't permit us now to say that in the case of Mr Hannell he would not have got mesothelioma except for the specific period of home handyman exposure he has described. Do you agree?---What I say is that the specific periods of home handyman exposure added to his overall risk. I'm not necessarily saying that that tipped him over the line but it certainly added to his risk.

...

Even if one accepts that asbestos fibres have a capacity to be involved at several stages of tumour development it still remains the case in relation to Mr Hannell that medical science doesn't permit us to say that in the absence of his home handyman exposure he would not have got mesothelioma?---No.

Again it's all a matter of risk and increase of risk?---Well, it's a matter of the fact that he's got it and he had this exposure, so that you have to assume, you know, from the end point that all the exposure must have had something to do with it, whatever the risk creating-potential was. You have to assume that some of those fibres had something to do with it."

200 The general approach taken by Dr Leigh was further confirmed in his responses to the following questions asked by the trial Judge after he had completed his re-examination:

"Can I ask you whether, from those last few comments you made, Dr Leigh - you were asked about the effect of the specific exposure in the case of each of Mr Moss and Mr Hannell. That involved what we might loosely call handyman work. Then you went on and made a statement something to the effect that they got mesothelioma, therefore the exposure must have had something to do with it?---Yes.

What exposure are you referring to there?---The additional exposure, the handyman exposure.

Why must it have had something to do with it?---Well, you can't say that it didn't because they were additional fibres. As I said, the whole process is probabilistic. There must have been some probability that those additional fibres had something to do with it. You can't exclude that possibility. You can't exclude that.

If a single fibre may initiate the - I'm struggling for the right words - cell change is it necessary that there be further fibres to promote the process?---That's a good question. I would say yes. Certainly there needs to be some more - some agents acting to further the process. Whether they are further fibres or something else I don't know but I would say yes.

And if one or more fibres have initiated the process commencing with the cell change will the inhalation of further fibres necessarily play some part in the promotion or further promotion of that process?---You can't exclude the possibility that they do. You can't exclude it."

201 The trial Judge referred to Dr Leigh's evidence in that part of his reasons dealing with foreseeability. In that part of his reasons dealing with causation, the trial Judge set out a number of substantial passages from the report and oral evidence of Dr Leigh dealing with the processes involved in the development of the disease, including a number of the passages I have set out above.

202 On the topic of specific causation; that is, the causation of Mr Hannell's mesothelioma, the trial Judge's references to Dr Leigh's evidence in his reasons are limited to the following:

"In his report of 12 March 2006 Dr Leigh stated his opinion that the plaintiff's total cumulative asbestos exposure during the period 1983 - 1990 was significantly greater than background exposure from the environment at large and the plaintiff's exposure to asbestos in 1983 - 1990 made a material contribution to causation of the plaintiff's mesothelioma.

...

Dr Leigh stated his opinion that the plaintiff's total cumulative asbestos exposure from his handyman activities was significantly greater than background exposure from the environment at large and the plaintiff's handyman exposure made a material contribution to causation of his mesothelioma".

203 Further at [314], which I have set out above, the trial Judge expresses his general preference for the experts called by Mr Hannell as compared to the experts called by Amaca.

204 Accordingly, as with the other experts called by Mr Hannell on the subject of specific causation, in his reasons, the trial Judge has gone no further than to repeat the conclusions at which Dr Leigh arrived. No process of analysis or reasoning leading to the acceptance of those conclusions is enunciated in the reasons for decision.

205 Upon analysis and for the reasons I have given, it is clear that Dr Leigh's opinion that Mr Hannell's specifically identified exposures "made a material contribution to causation of his mesothelioma" derives from an approach in which every increment in risk, however small, is taken to be causative if the risk has come home. Dr Leigh has made no attempt to estimate or quantify the respective contributions to the risk of Mr Hannell contracting mesothelioma made by his specifically identified exposures on the one hand, and the background risk on the other. Rather, he has suggested that industrial hygienists, such as Mr Rogers and Dr Francis should be consulted for the purposes of making that estimate. Accordingly, his evidence alone is not capable of discharging Mr Hannell's burden of proving that it is more likely than not that the exposures to asbestos which he specifically identified caused or materially contributed to his mesothelioma.

206 The only other expert witness called by Mr Hannell was Mr Alvarez, who is his practising thoracic surgeon. His report was tendered in evidence. It is mainly concerned with diagnosis, treatment and prognosis. It also contains the following statement:

"Mr Hannell's exposure to the asbestos fibres of Hardieplank in 1982, 1983 and early 1990's [sic] and the method of exposure, in my mind, are clearly powerful aetiological factors in causing this man's mesothelioma. A single such exposure, let alone several, will trigger the malignant process."

207 This conclusion is unsupported by any enunciated process of reasoning or analysis. As Heydon JA observed in Makita v Sprowles (supra), expert opinions expressed in this way tend to usurp the function of the court and deprive it of the capacity to form its own view after reviewing the process of analysis and reasoning that has led to the formation of the opinion.

208 The conclusion expressed by Mr Alvarez was not explored during his oral examination-in-chief, his cross-examination or re-examination. However, at the conclusion of his evidence, the trial Judge asked him to elaborate on the view he had expressed. He gave the following answer:

"I don't have my personal notes here but from reading that report and the other reports, as best as I could put together for this patient there did not seem to be any familial factors, his father working in a shipyard or a mine or whatever. His occupational factors didn't add up to an exposure to asbestos. However, what occurred in 82, 83 and the early 90s was his method of exposure, sawing, cutting, sanding, grinding, particularly when he was doing the roof work on the eaves, which means dusts were coming straight down on top of him - with [sic without] him having any protective clothing - so we're talking about a period of, depending on the estimates here from Dr Breslin or Dr Musk that I have here, of 11 to 13 days, six, seven, eight hours a day, so we're talking about 60-odd hours perhaps, 50, 60-odd hours of exposure to particulate matter and I would say to you that in my view that is a substantial exposure when no other factors I could find or discuss with my colleagues that he was exposed to anything else in his either occupational or work habits or even the family history; was there anyone that was possibly bringing in asbestos fibres? As best as this patient could recollect, he did not. But those three episodes of continued exposure, highly concentrated, I'm afraid to say in my mind that's a powerful aetiological factor. Or the converse, your Honour; I don't think you would find anybody at this stage doing that sort of a work like that without considering they're going to be at risk of getting mesothelioma."

209 After giving that evidence, Mr Alvarez was again cross-examined by counsel for Amaca. It was clear from the answer he gave that he had made no specific assessment of the increment in risk occasioned by the specific exposures identified by Mr Hannell, as compared to background risk, and doubted that any such estimate could be made.

210 It is clear from the cross-examination of Mr Alvarez, a practising thoracic surgeon, that, as might be expected, he did not have anything approaching the degree of research experience or familiarity with the research relating to the causation of mesothelioma as the other experts who had given evidence. For example, he had never heard of Julian Peto, whose formula for assessing risk was referred to by all other experts, nor of Chris Wagner, whose pioneering work in relation to mesothelioma in the 1960s has resulted in a medal being given in his honour for work in the field of mesothelioma. Nor had he heard of Professors Berry and Henderson, who are acknowledged world-renowned experts in the field. He had never seen Professor Henderson's book entitled "Malignant Mesothelioma", nor was he aware of any material relating to the relative risks occasioned by the inhalation of crocidolite as compared to chrysotile. He said that he did not read journals relating to industrial hygiene often, if at all, and had never read an article in any industrial hygiene journal relating to the cause of mesothelioma, nor in the Journal of Industrial Medicine. He had not undertaken any studies in relation to the causes of mesothelioma. He was not aware of the measure of the background incidence of mesothelioma in an urban population. He was not aware of the way in which occupational hygienists measured the amount of respirable fibre produced by particular activities, nor of the way in which those results are used by clinicians and biostatisticians in assessing the likely causes of mesothelioma.

211 Construed in that context, Mr Alvarez's oral evidence, in answer to the question posed by the trial Judge, does not go any further than an unexplained assertion that because the three specific incidents of exposure identified by Mr Hannell were the only specific exposures he could identify and because of his assumption that those episodes gave rise to "continued exposure, highly concentrated" (which assumption is not borne out by the evidence), were "powerful aetiological factors" in causing Mr Hannell's mesothelioma. Expressed at this level of generality and in the context of the limitations upon his particular expertise in the field of mesothelioma, the evidence of Mr Alvarez cannot be given any significant weight, especially when compared to the evidence of the other experts called who are all world-renowned experts in the field of mesothelioma.

212 The only reference made by the trial Judge to the evidence of Mr Alvarez (other than in the portion of his reasons dealing with the assessment of the quantum of damages), is the following:

"Dr Alvares [sic Mr Alvarez] said that the plaintiff's handyman exposures are clearly powerful etiological factors in causing the plaintiff's mesothelioma."

Moreover at [314] of his reasons, he expresses his general preference for the experts called on behalf of Mr Hannell.

213 Given that Mr Alvarez did not enunciate in any meaningful way the process of reasoning or analysis which caused him to arrive at that conclusion, it is hardly surprising that the trial Judge did not himself undertake any evaluation of the conclusion he had expressed. For the reasons I have given above, given the generality of the terms in which the conclusion is expressed, the dubious factual assumptions as to the extent of exposure which appear to underpin it, the limited expertise of Mr Alvarez in the particular field of mesothelioma and his failure to undertake any attempt to estimate the extent of the increment in risk occasioned by the specific identified exposures identified by Mr Hannell as compared to background risk, the conclusory opinion expressed by Mr Alvarez cannot be given any significant weight.

Summary of the expert evidence on causation

214 The expert evidence was consistently to the effect that the most that could be said about Mr Hannell's exposure to respirable asbestos fibre in the three specific incidents he identified was that it increased the risk of him contracting mesothelioma. No witness advanced the proposition that all asbestos fibre inhaled by a mesothelioma sufferer caused or contributed to that disease. All witnesses were of the view that the larger the number of asbestos fibres inhaled, the greater the risk of disease being caused by one or more small number of those fibres.

215 I have had the advantage of reading the reasons to be published by Steytler P and McLure JA. I think the essential difference between us on the subject of causation is that unlike their Honours, in my opinion, the expert evidence did not establish that asbestos fibres from all sources make a cumulative contribution to the contraction of the disease. In my respectful opinion, the expert evidence went no further than to suggest that increased exposure to respirable asbestos fibre, increased the risk that mesothelioma or some other lung disease would be contracted. The adoption of the "lottery ticket" analogy by many of the experts is only consistent with this view of the connection between exposure and initiation of the disease. And Dr Leigh's use of the analogy to sperm and ova seems to me to compel the conclusion that he was not proposing that each asbestos fibre in the pleura cumulatively contributed to the disease because, of course, except in the case of multiple births, spermatozoa do not cumulatively contribute to fertilisation of the ovum. Nor does his description of the cellular processes involved as "stochastic" - which I take to mean as having a random and variable pattern which cannot be predicted, support the view that he was suggesting all fibres inhaled made a cumulative contribution to the disease, as compared to the increasing risk of contracting the disease.

216 Nor, in my respectful opinion, was the case fought or decided at first instance on the basis that each asbestos fibre inhaled made a cumulative contribution to the contraction or development of the disease. It follows that the approach taken in Bonnington Castings Ltd v Wardlaw [1956] UKHL 1; [1956] AC 613 has no application to the facts of this case. Rather, because the evidence established that the effect of increased exposure was an increment in risk, rather than a cumulative contribution to initiation or promotion of the disease, in my opinion, the epidemiological assessment of the extent of the increased risk as a result of the specifically identified exposures, and the principles enunciated by Spigelman CJ in Seltsam Pty Ltd v McGuiness (supra) are applicable in this case.

217 Professor Berry's assessment of the relative risk occasioned by the specific exposures identified by Mr Hannell as being 1.3 to 1.4 is, as I would understand it, expressly predicated on the assumption that each of background risk and the specific exposures are alternative sufficient causes of the disease. So, with respect to the other members of the Court, it does not seem to me that such an assessment can be used as an empirical assessment of the extent to which those exposures materially contributed to the contraction of the disease on the hypothesis that the process of initiation of the disease was one in which all fibres inhaled made a cumulative contribution. Inherent in the notion of "Relative Risk" is a comparison between two alternative sources of risk, and by definition therefore, the concept can have no direct application to a hypothesis in which all fibres inhaled cumulatively contribute to inhalation and promotion of the disease.

218 Further, all witnesses accepted that every resident of an urbanised community will be exposed to respirable asbestos fibre in the ambient atmosphere of that community and may also be exposed to higher than ambient levels of fibre by reason of specific exposures which they did not recognise or have forgotten. Those exposures create a risk of contracting mesothelioma which has been variously estimated, but perhaps most reliably estimated for the Western Australian community by Professor Musk and Dr de Klerk (and also Mr Rogers) at between 140 and 210 persons per million per lifetime.

219 It is possible that Mr Hannell is, or would have been, one of those persons irrespective of the specific exposures to respirable asbestos fibre which he has identified. Therefore, in order to succeed in his claim, it is necessary for Mr Hannell to establish on the balance of probabilities that it is more likely than not that his mesothelioma was caused or its development was promoted by one or more of the fibres which he inhaled in the course of those specific exposures. Because the effect of the inhalation of those fibres was to increase the risk of contracting mesothelioma, Mr Hannell's burden of proof could only be discharged by ascertaining the extent of the additional risk created by the inhalation of those fibres and comparing it to the level of background risk experienced by Mr Hannell in common with all other members of the community.

220 None of the expert witnesses called on behalf of Mr Hannell, other than Dr Francis, approached the case on this basis. In particular, to the extent that their processes of analysis and reasoning were revealed, all proceeded on the basis that once mesothelioma had been diagnosed, the risk had come home and therefore any increment in risk, however small, should be taken to be causative. Whatever else might be said about that approach, it does not accord with the legal test to be applied.

221 Conversely, Mr Rogers and Dr Francis each undertook the task of attempting to estimate the cumulative exposure experienced by Mr Hannell in the course of the incidents he had specifically indentified, and to relate that to the cumulative exposure he experienced as a result of breathing the ambient atmosphere in London and Perth. Although their assessments differ numerically, by a factor of 100, both estimates show that the cumulative exposure to respirable fibre experienced by Mr Hannell in the course of the specific incidents he identified was very low compared to the exposure he experienced from the ambient atmosphere. Because the evidence strongly suggested that the estimate made by Dr Francis was, if anything, an over-estimate, on the evidence adduced at trial, it may safely be assumed that her estimate represented the outer limit of the respirable fibres to which Mr Hannell was exposed in the course of the specific incidents he identified. The only experts to specifically apply the estimates performed by Mr Rogers and Dr Francis to a comparative evaluation of the risks created by the specific exposures identified by Mr Hannell and the background risk, were Professors Berry and Breslin; although Professor Musk observed that he "was comfortable" with Professor Berry's calculations. Both Professors Berry and Breslin gave clear and rational reasons for their view that it was much more likely than not that Mr Hannell would have suffered mesothelioma irrespective of the specific exposures to respirable fibre which he identified.

222 The reasons given by the trial Judge for rejecting the evidence of Mr Rogers, Dr Francis, Professor Berry and Professor Breslin cannot be sustained. The evidence adduced from the experts called by Mr Hannell was, by its nature, incapable of discharging the burden of proof. In the case of Mr Alvarez the evidence was expressed in such general and conclusory terms as to be of little or no weight. Amaca adduced clear and coherent evidence which should have been accepted that it was more likely than not that the specific exposures identified by Mr Hannell played no role in causing or contributing to his mesothelioma. The trial Judge should have found that Mr Hannell had failed to establish that the specific exposures he had identified caused or contributed to his mesothelioma.

223 That conclusion is sufficient to dispose of this appeal. However, because a number of other matters of significance were argued, I will provide reasons for the views that I have formed in relation to those issues, although in rather less detail.

Causation - failure to warn by signage on the products and advertising

224 Mr Hannell's case was that Amaca had breached a duty owed to him as a member of a class of persons who might deal with asbestos cement products, to warn of the dangers of dealing with those products by affixing suitable warning notices to the product and by advertising the dangers involved.

225 Mr Hannell did not purchase any asbestos cement products manufactured by Amaca himself. Those products were installed "in the late 1970s". Assuming for present purposes that the state of knowledge of the risks of dealing with asbestos cement products was such as to impose upon Amaca a duty to warn at the time it manufactured and supplied the products installed into Mr Hannell's house in the late 1970s, the evidence did not enable the trial Judge to conclude that the affixation of such labels would have had any effect in preventing or discouraging Mr Hannell from working on those products between 1983 and 1990. That is because there is no evidence that would enable the trial Judge to have concluded that those labels would have remained in place and be visible to a later purchaser of the house, such as Mr Hannell.

226 Mr Hannell worked on two types of asbestos cement product manufactured and supplied by Amaca. One was fencing product and the other was sheeting used on the eaves of his house. The evidence was that when warning labels were affixed to asbestos cement fencing panels produced by Amaca, they were adhered to the end of each sheet, so that when the sheets were overlapped, the labels were not visible. Obviously, it would have been unsightly for each panel in a domestic fence to bear a visible warning label and it could be reasonably assumed that whatever Amaca did in relation to such labels, they would be removed or obscured by owners or occupiers after construction of the relevant fence.

227 In the case of asbestos cement sheeting, the evidence was to the effect that when warning labels were affixed, they were affixed to the rough rear surface of the product, rather than the smooth surface which would be presented to view and which would very often be painted in any event. Again, it is reasonable to assume that whatever steps were taken by Amaca, any warning label affixed to its asbestos sheet products would, at or after installation, have been removed or obscured so as to not be visible to subsequent occupiers of the premises in which the products are installed.

228 For these reasons, it could not be concluded that if Amaca had affixed warning labels to its fencing or sheeting products prior to their installation in the house later acquired by Mr Hannell, those labels would have been visible to Mr Hannell. Rather, it is significantly more likely than not that if such labels had been affixed, they would not have been visible to Mr Hannell at the time he commenced working on the asbestos cement products in 1983. Accordingly, it could not be concluded that any breach of duty by Amaca in failing to affix warning labels had any effect in relation to the work later done by Mr Hannell in relation to those products.

229 The witness statement adopted by Mr Hannell contains the following paragraph:

"I watch the news. I am not an avid news watcher but I watch it if it is on. The only newspaper I get is the Sunday paper. Most of the time I would listen to the radio at work but mainly classic FM."

230 In cross-examination, Mr Hannell referred to having got a Wednesday paper for a time, "but that was some years ago now". It is not clear from that evidence whether or not he was getting the Wednesday paper between 1983 and 1990.

231 Mr Hannell was shown a number of articles relating to asbestos risks published in newspapers including The Sunday Times from 1983 onwards. He did not recall seeing any of them. He was shown an article published in The Sunday Times on 31 July 1983 regarding the threat of asbestos halting building work. He replied that it was probably not the sort of article that would have caught his eye back in 1983. He was also taken to advertisements published in The Sunday Times in 1989, including an advertisement for an asbestos product (a roof sealant) which referred to the dangers involved in use of the product. Mr Hannell stated that he did not think it was the sort of advertisement he would have read. When asked why not, he replied:

"I wasn't aware that I had come into contact with any asbestos. I don't think asbestos would have meant anything to me at the time."

232 It is clear from this evidence that at the time Mr Hannell was working on the fences and eaves, he was not aware that the asbestos cement products of which they were constructed contained asbestos or of the possible significance of that fact. In light of that evidence, it is a fair inference that the only advertising programme that would have altered his level of consciousness in such a way as to have prevented or discouraged him from undertaking the work which he carried out on the asbestos cement products between 1983 and 1990 would have had to have been extremely extensive - to the point of saturation, and would also have had to clearly identify all the products in the community which contained asbestos fibre.

233 The findings made by the trial Judge in this regard are contained in the following of his reasons at [327]:

"It may be inferred, and I do infer, that if in or before 1983 the defendant had made public announcements or placed advertisements in a Perth daily or weekly newspaper monthly or more frequently saying that a handyman or casual user of asbestos cement building products ran a risk of contracting mesothelioma and that the risk could be minimised by the taking of certain steps then that information is likely to have come to the attention of a person such as the plaintiff who watched the news, listened to the radio and regularly read a newspaper, even if only weekly. It may be inferred, and I do infer, that it is likely that the information would have come to the attention of the plaintiff either directly or through republication or repetition by other media sources or family, friends, work colleagues or other acquaintances."

234 The evidence given by Mr Hannell does not sustain the conclusion that the placement of monthly or more frequent advertisements in a daily or weekly newspaper saying that a handyman user of asbestos cement building products ran a risk of contracting mesothelioma would have discouraged Mr Hannell from undertaking the work he did. Mr Hannell was not aware that the products upon which he was working contained asbestos. That is not surprising because they were products mainly composed of cement, using other materials, including a relatively small amount of asbestos, for binding. Of course, if the reference to the placement of advertisements "more frequently" than monthly is taken to connote a saturation advertising programme in both printed and electronic media and which would enable viewers and readers to differentiate between products which contained asbestos and those which did not, there is a reasonable prospect that such a campaign would have come to Mr Hannell's attention and affected his conduct in such a way as to make it more likely than not that he would not have worked upon the asbestos cement products.

235 Yet, the question of whether Amaca was under a duty to undertake an extensive advertising programme of that kind, at considerable expense, turns upon the magnitude of the risk to persons in the class of Mr Hannell which was reasonably foreseeable between the time he acquired his house in 1982 and his last specifically identified exposure in 1990. I turn, therefore, to the issue of foreseeability.

236 The issues which arise in the area of foreseeability of harm are related to the medical issues which I have addressed above in relation to causation. Central to both issues, is the question of the risk of harm created by exposure to relatively small quantities of respirable asbestos fibre released as a result of carrying out work on asbestos cement products very occasionally in a non-occupational or domestic environment. The significant distinction between the issues is, of course, that in the context of causation, the question is to be determined by reference to the state of knowledge at the time of trial; whereas in the context of foreseeability, the question is to be determined by reference to the state of knowledge at the time of the alleged breach or breaches of duty: in this case, during the 1970s and the 1980s. As the review of the evidence led on the subject of causation reveals, factors relevant to the magnitude of the risk of harm consequent upon exposure in the course of work of the kind carried out by Mr Hannell, which was foreseeable over the relevant period include:

(a) the relatively low proportion of asbestos contained within asbestos cement products (8 to 15 per cent);

(b) the fact that, in asbestos cement products, the asbestos fibres are bound in with the cement, which reduces the extent to which they are liberated in respirable form when the product is cut, drilled, sanded or otherwise worked upon;

(c) the fact that the asbestos component of the asbestos cement products manufactured during the relevant period, and to which Mr Hannell was exposed, did not include any crocidolite, it included a small amount of amosite (about 1 per cent of the total product) and otherwise comprised chrysotile, which is the least harmful of the types of asbestos; and

(d) the fact that exposure to respirable asbestos fibre in a non-occupational or domestic environment will be occasional and sporadic, with the consequence that cumulative exposure to respirable fibre will be substantially less than that experienced by workers who are regularly exposed occupationally.

237 The magnitude of the reasonably foreseeable risk of harm to those who undertook work of the kind undertaken by Mr Hannell over the period Amaca is said to have breached its duty is critical to the resolution of the question of whether Amaca owed a duty to take steps to warn those such as Mr Hannell who might be exposed to that risk, and if so, as to the extent of that duty - see Wyong Shire Council v Shirt [1980] HCA 12; (1980) 146 CLR 40, 47 - 48; Graham Barclay Oysters Pty Ltd v Ryan [2002] HCA 54; (2002) 211 CLR 540 at [107, 113, 202 - 203].

238 The evidence clearly established that by the commencement of the relevant period in the late 1970s, it was well known that inhalation of substantial amounts of asbestos fibre posed a serious threat to health. The disease most frequently associated with exposure to respirable asbestos fibre was asbestosis: a condition only acquired after exposure to substantial amounts of asbestos over lengthy periods of time. Lung cancer and mesothelioma were also known to be associated with exposure to smaller amounts of asbestos. The critical issue on the topic of foreseeability was the extent of the risk known or thought to be associated with non-occupational activities involving asbestos cement products. That question is critical because the magnitude of the risk thought to be associated with activities of the kind undertaken by Mr Hannell will strongly influence determination of the question of whether a reasonable person in the position of Amaca would or should have embarked upon an extensive advertising campaign of the kind necessary to alert people like Mr Hannell to the risks of doing any work on asbestos cement products which would release respirable fibres.

239 The trial Judge approached this question from two perspectives: first, from the perspective of the knowledge generally available; and second, from the perspective of the knowledge available to Amaca.

240 The trial Judge relied substantially upon the evidence given by the experts called by Mr Hannell on the extent of the knowledge of the association between exposure to asbestos fibre and mesothelioma during the relevant period.

241 The trial Judge recited Professor Musk's reference to the pioneering work of J C Wagner in South Africa. This was presented to a conference in Johannesburg in 1959 and later published in the British Journal of Industrial Medicine. Professor Musk relied upon that work for the assertion that it was thereafter known that exposure to small amounts of asbestos could cause mesothelioma. The trial Judge also referred to Professor Musk's reliance upon the work of Dr Newhouse in 1965 among the relatives of asbestos workers in London. The trial Judge cited with approval, Professor Musk's opinion drawn primarily from these studies to the effect that:

"By 1961 the serious dangers to health occasioned by even small exposures should have been known by persons responsible for exposing other persons to asbestos and appropriate warnings and safeguards should have been implemented. By the mid 1960s no person should have been exposed to asbestos, especially blue asbestos, without exposure being reduced to a minimum, together with appropriate warnings of the risks to those exposed."

242 However, it is significant to the circumstances of this case that all the reports relied upon by Professor Musk involved reviews of populations who were exposed to asbestos fibre on a continual basis either by reason of occupation, residence near an asbestos factory, or association with asbestos workers who carried fibre home on their clothes. None of the studies cited by the trial Judge involved persons who were only exposed to small doses of chrysotile on a few occasions.

243 The only reference made by the trial Judge to the cross-examination of Professor Musk on this subject was the following:

"66 Professor Musk was cross-examined about a publication of the Australian National Health and Medical Research Council [NHMRC] described as being the 'Code for the Handling of Asbestos by Small Users' and to a report on the health hazards of asbestos published by the [NHMRC] in mid-1981 and other publications. None of the matters put to Professor Musk, nor his response to them, caused him to qualify his opinions nor did they undermine those opinions. I accept the opinions expressed by Professor Musk."

This appears to be the only reference by the trial Judge to a code published by a reputable Australian authority at a very relevant time for the purposes of these proceedings. Given that that code may be taken to provide strong evidence of the state of knowledge among reputable scientists at the time of its publication, it merits particular attention. It should also be considered in the context of other regulatory instruments and recommendations of reputable authorities which preceded and followed it.

244 As Professor Musk pointed out in his evidence, in the United States in 1969, a limit of 12 fibres per ml over an eight hour time weighted average was given legal force. It will be recalled that 12 fibres per ml is a concentration significantly in excess of anything experienced by Mr Hannell. It should also be noted that this standard relates to occupational exposure and therefore contemplates exposure of up to 12 fibres per ml every hour of every working day over a working lifetime. This would permit a cumulative exposure many magnitudes greater than that experienced by Mr Hannell in the course of the specific incidents he had identified.

245 In 1976, a standard of 2 fibres longer than 5 µm per ml, with a 15 minute ceiling of 10 fibres per ml was adopted in the United States. Again, given that this represents a standard applicable to occupational exposure for every working day, it also represents a permissible exposure many magnitudes greater than that experienced by Mr Hannell in the course of the specific incidents he identified.

246 In the United Kingdom in 1970, employers were required to provide breathing protection to employees who were exposed to more than 2 fibres of chrysotile per ml in the absence of exhaust ventilation. This standard would also permit exposure many magnitudes greater than that experienced by Mr Hannell in the specific incidents he had identified.

247 In Australia in 1969 the NHMRC recommended a maximum exposure of 4 fibres per ml over an eight hour time weighted average. As this applies to occupational exposure on a continuous basis, this would also permit cumulative exposure many magnitudes greater than that experienced by Mr Hannell in the specific incidents he identified.

248 It was in this context that in 1978 the NHMRC published a document entitled "Code for the Handling of Asbestos by Small Users". The introductory paragraph of that code provided:

"In some Australian States, the use of asbestos and asbestos containing products is controlled by statutory regulations. While the need for health precautions in large scale operations involving asbestos is undisputed, this may not be so in the case of small users such as construction firms and insulation contractors who use less than, say, 5 tonnes of raw asbestos per annum, or regularly use products containing asbestos such as those shown in Section 4 below [including asbestos cement]. Such limited usage might be considered insufficient to cause harm to health of those exposed. Asbestos hazard is related to the dose of respirable dust, that is to say, very small particles inhaled by an individual. The actual amount of asbestos processed may therefore be of much less importance than the methods of handling and use which give rise to dust."

Under the heading "Asbestos Cement Products" the code provided:

"Asbestos cement ('fibro') is a hard surfaced material, in which the asbestos fibres are reasonably bonded by cement. Work with this material can be carried out safely with hand saws and other hand tools and also with power drills.

Occasional power sawing does not present a problem if limited to an operation of, say, 15 minutes in a shift, and if carried out in the open air. For longer periods dust extraction equipment should be used, or the dust should be suppressed by the use of water, or an approved respirator should be used. Where water is used for dust suppression, care should be taken to ensure that power tools are electrically safe."

249 Thus, in a code published by a reputable Australian authority a few years prior to Mr Hannell's first exposure, it was stipulated that work of the kind which he carried out could be performed safely. It also contemplated significantly greater exposures than those experienced by Mr Hannell, through the use of power saws for up to 15 minutes per shift. The only reference to this code in the reasons of the trial Judge is in the paragraph I have set out above.

250 In 1981 the NHMRC published a document entitled "Report on the Health Hazards of Asbestos". The committee responsible for the preparation of that report included Dr McNulty, of the Western Australian Department of Health and Medical Services, who is widely acknowledged as having been a leading authority in the development of knowledge of the risks of exposure to asbestos. The NHMRC committee also included Dr J Milne, of the Health Commission of Victoria, who is also acknowledged as a leading expert in the field and was chaired by Professor Davidson of the Commonwealth Institute of Health.

251 The first paragraph of that report contains the recommendation that:

"exposure to asbestos should, in all phases of the asbestos industry, be reduced to the lowest practicable level by the most efficient technology currently available."

252 Significantly, the NHMRC committee did not recommend that all exposure be eliminated. Rather, it recommended that:

"The average fibre concentration of the air breathed by the worker throughout a working shift, as calculated from measurements made by the [NHMRC] Membrane Filter Method for Estimating Airborne Asbestos Dust, over a sampling period of not less than four hours, during which one or more samples may be taken, should not exceed:

• Chrysotile and amosite asbestos - 1.0 fibres per millilitre
• Crocidolite - 0.1 fibres per millilitre

The [NHMRC] recommends the adoption of the standard by industry as soon as practicable and not later than 31 December 1982."

253 Given that this standard relates to continuous occupational exposure, assuming a working life of 25 years, the standard contemplates a permissible cumulative exposure of 25 fibres per ml years. It is to be recalled that Dr Francis, whose estimate of Mr Hannell's cumulative exposure in the specific incidents he had identified was 100 times greater than that of Mr Rogers, estimated his total cumulative exposure in the course of those incidents at 0.2 fibres per ml years, which is more than 100 times less than the cumulative exposure permitted under the NHMRC standard.

254 In August 1990 the Western Australian Advisory Committee on Hazardous Substances ("the Committee") published a report dealing with asbestos cement products. The chairman of the Committee which was responsible for the preparation of that report was Dr Bruce Armstrong, Commissioner of Health. The Committee included Professor Musk, Dr de Klerk and Dr Psaila-Savona.

255 In the introduction to that report, the Committee referred to asbestos cement products in the following terms:

"[A]n asbestos cement product was defined as a product manufactured from a mixture of asbestos fibre, portland cement and water (with or without other additives) which is formed to a specific shape. The content of asbestos, by weight, in asbestos cement products has commonly been of the order of 10 - 15%. During manufacture asbestos fibres are firmly bound into the cement matrix."

256 In its report, the Committee referred to the expression of concern by parents, teachers and members of the public regarding possible adverse effects on the health of children as a result of the release of asbestos fibres from weathered asbestos cement products in schools and other buildings.

257 In the section of its report dealing with the effects of asbestos cement products on health, the Committee referred to the differing potencies of different types of asbestos fibre. In that context, the Committee referred to chrysotile in these terms:

"Chrysotile fibres are eliminated more readily from the lungs than are amphibole fibres.

The general consensus is that chrysotile does not appear to produce significant levels of mesothelioma. There is a difference in potency between the various types of fibres with crocidolite being the most potent and chrysotile the least.

There is no reliable evidence for or against a threshold dose requirement for disease causation, but many people now believe that for chrysotile workers in cement and friction product manufacturing the risk is so slight as to be undetectable. It is generally assumed that this kind of negligible risk level of exposure exits at different airborne fibre concentrations for all types of asbestos for all the relevant diseases.

Industries using a mixture of asbestos types have higher rates of disease than similar industries using only chrysotile."

258 In relation to the particular qualities of asbestos cement products, the Committee reported in the following terms:

"There are very few data available that are directly relevant to the effects on health of exposure to asbestos cement products. This is probably a consequence of the commonly held opinion that under most circumstances asbestos cement products are unlikely to be hazardous because the fibres are bound together in a solid matrix from which individual fibres are 'not expected to be released under normal circumstances'. It has been accepted, however, that fibres 'may be emitted during manipulation or renovation of such materials or products' as, for example, by cutting, grinding, drilling or extensive breakage, but under these circumstances would be a potential hazard to few people on few occasions (World Health Organisation, 1986)."

259 In relation to the risk arising from low levels of exposure, the Committee reported in these terms:

"While mesothelioma can occur in association with quite low levels of exposure to asbestos, and it has been argued that 'even one fibre can cause cancer' (although no one can ever know whether or not this statement is true), the risk of mesothelioma (and lung cancer) is quite clearly related to the amount of exposure to asbestos and it is reasonable to suggest that there exists a level of exposure below which there is a negligible risk of harm."

260 In the result, the Committee did not recommend that significant remedial action be taken in relation to asbestos cement products, such as roofs, in schools.

261 An appendix to the report contained a review of the literature relating to the effects on health of asbestos cement products undertaken by Dr Nicholas de Klerk. He expressed his summary and conclusions from the literature review in the following terms:

"There is no direct evidence of any ill-effects arising from use of AC [asbestos cement] products, only the results from animal studies. Predictions of the consequences of environmental exposure to asbestos appear to be unfulfilled. AC products containing only chrysotile pose no measurable threat to health. ... Removal of asbestos building products can increase the environmental levels of pollution as well as being potentially dangerous to those during the removal."

262 Although Professor Musk was cross-examined at some length in relation to this report, the trial Judge makes no reference to it in his reasons.

263 In May 1995, Worksafe Australia published a standard setting out maximum acceptable exposures to atmospheric contaminates in an occupational environment. The standards are expressed to cover long term exposure to a substance over an eight hour day for a five day working week over an entire working life. The standard is said to provide:

"An airborne concentration of a particular substance in the worker's breathing zone, exposure to which, according to current knowledge, should not cause adverse health effects nor cause undue discomfort to nearly all workers."

264 In the case of asbestos, the standards specified in 1995 were 0.1 fibres per ml in relation to amosite and 1.0 fibre per ml in relation to chrysotile. Because these standards apply to continuous exposure over an eight hour day for a five day week for an entire working life, adherence to those standards would permit workers to be cumulatively exposed to respirable asbestos fibre at levels which are many magnitudes greater than the exposure experienced by Mr Hannell in the course of the specific incidents he identified. In the case of chrysotile, which constituted almost all of the cement component of the products on which he worked, under that standard, cumulative exposure of 25 fibre per ml years, according to its terms, should not cause adverse health effects to nearly all workers, according to knowledge current in 1995. As I have already observed, this exposure is more than 100 times greater than the total cumulative exposure which Dr Francis estimated Mr Hannell had experienced in the course of the specific incidents he had identified, which is in turn 100 times greater than that estimated by Mr Rogers.

265 The trial Judge made no reference to this standard in his reasons for decision.

266 In the course of cross-examination, Professor Musk confirmed that the Committee on which he served in 1990 had undertaken the monitoring of air at several schools and discovered that the levels of respirable asbestos fibre in the environment of schools, which were constructed using asbestos cement as a significant component, was about double that of the general environment. Nevertheless, the Committee recommended against any specific action being taken to reduce those levels because it considered that the risk of disease resulting from those exposures was lower than the risks which would be associated with removal and replacement. This evidence should again be considered in the context of the evidence to the effect that the cumulative exposure to respirable fibre experienced by Mr Hannell during his lifetime was significantly greater than cumulative exposure experienced by him in the course of the three incidents he had identified. The eminent Committee recommended the continuation of a situation in which students and teachers continued to be exposed to double environmental levels on a continuing basis. This provides a potent indication of the levels of risk, which in 1990, an expert committee thought to be associated with slight increases in levels of exposure to respirable asbestos fibre.

267 In cross-examination Professor Musk also confirmed that in 1990 there was debate about whether pure chrysotile did in fact cause any disease. The suggestion was that disease associated with chrysotile might be due only to a contaminant such as tremolite.

268 Professor Musk was taken in cross-examination to Dr de Klerk's literature review, which was an appendix to the report of the Committee. He accepted that it was a reliable source of the state of knowledge as at 1990. It is to be recalled that the summary to the report contained the assertion that asbestos cement products containing only chrysotile posed no measurable threat to health.

269 Professor Musk was also cross-examined in relation to the other reports and standards to which I have referred. They provide cogent contemporaneous evidence of the perception of the magnitude of the risk associated with low levels of exposure to respirable asbestos fibre by reputable bodies charged with the responsibility for protecting the health of workers. Those bodies included reputable scientists with specialist knowledge in the field. Evidence in that form was of significantly greater probative value than generalised assertions made by Professor Musk 16 years after Mr Hannell's exposures.

270 As I have observed, the trial Judge has undertaken no analysis of these reports in his reasons for decision. They were plainly a key component of Amaca's case. In my opinion, the trial Judge was obliged to set out the reasons why he did not consider that those reports sustained the conclusions for which Amaca contended. In the absence of any such reasoning, it is not possible to accept the trial Judge's assertion that these reports did not undermine the opinions expressed by Professor Musk.

271 The trial Judge relied also upon Dr Leigh's evidence. Dr Leigh referred to materials published before and up to 1976, where reference is made to the possibility of mesothelioma being caused by low level exposures. However, the difficulty with evidence expressed at that level of generality is that it is not at all clear what is meant to be conveyed by the notion of "low level" exposures. It is a fair inference that the best guide to the levels of exposure that were considered to pose an acceptable level of risk were those specified in the reports and standards, to which I have referred, and upon which Dr Leigh was cross-examined. In the course of cross-examination Dr Leigh confirmed that in 1979 the applicable standard in Australia permitted occupational exposure at levels up to 2 fibres per ml for amosite and chrysotile. This would have allowed a cumulative exposure of 50 fibre per ml years over a working life. This is of course, many magnitudes greater than the cumulative exposure experienced by Mr Hannell in the course of the three incidents he has identified.

272 Dr Leigh confirmed that in 1984 the Australian standard applicable to chrysotile was reduced to 1 fibre per ml and for amosite to 0.1 fibre per ml. As I have observed, this standard would also permit cumulative lifetime exposure many times greater than that experienced by Mr Hannell in the specific incidents he identified.

273 In his reasons for decision, the trial Judge does refer to the standard recommended in the 1981 NHMRC report. His only observation in relation to that recommended standard was as follows at [73]:

"However, that recommendation follows the following statements:

'Expert evidence suggests that it is not possible to establish a threshold value below which a carcinogenic effect of asbestos cannot be identified, although some recent evidence suggests that such a threshold may exist. The Subcommittee recommends that exposure to asbestos should, in all phases of the asbestos industry, be reduced to the lowest practicable level by the most efficient technology currently available and enforced through ...'"

Two observations may be made about the portion of the report cited by the trial Judge. First, the proposition that there is no minimum threshold value below which there is no carcinogenic effect, does not shed any light on the magnitude of the risk arising from low levels of exposure. Second, the recommendation to reduce exposure to asbestos to the lowest practicable levels, was directed at those engaged in the asbestos industry - not in respect of persons like Mr Hannell, who are only occasionally exposed.

274 Because the trial Judge did not undertake any other analysis of the reports and standards that were put to Dr Leigh in the course of cross-examination, it is not possible to accept his conclusion that those matters did not undermine Dr Leigh's opinions.

275 At [76] the trial Judge referred to Professor Henderson's evidence in the following terms:

"In his report (Exhibit H18) Professor Henderson said:

'The causal relationship between asbestos and mesothelioma had been well established by the late 1980s and early 1990s, and at that time I was aware that no threshold level of asbestos exposure had been delineated below which there is no risk of mesothelioma above background risk: in other words, I and other authorities were aware by that time that mesothelioma could follow exposures to asbestos that were non-occupational in character - brief and transient and low-"dose" - including, for example, the development of mesothelioma from asbestos exposures related to "handyman" - type work on A-C sheeting material: the development of mesothelioma from bystander, environmental and neighbourhood-type exposures had been recorded even earlier.' "

276 Given that Mr Hannells' case was based on breaches of duties, which he says Amaca owed to him in the late 1970s and through the 1980s, it is not surprising that Amaca did not cross-examine Professor Henderson about the evidence he gave in relation to the state of knowledge in the late 1980s and early 1990s. The only exposure Mr Hannell experienced, to which that evidence would be relevant, is his exposure in 1990. This was accepted by all experts to be his least causally relevant exposure because of the relationship between latency and causation to which I have referred.

277 At [78] the trial Judge referred to the evidence that Dr Francis gave in relation to the state of knowledge in the following terms:

"Dr Francis provided an opinion as to the availability of information as to knowledge in relation to hazards to health associated with exposure to asbestos. She was not cross-examined in relation to that opinion. Her opinion, which I accept, is accurately summarised by the plaintiff as follows:

'(a) From the early 1980s to 1990, and by 1983, asbestos was recognised among occupational health specialists as a carcinogen, with the association of asbestos exposure and lung cancer being reported in medical literature as far back as 1935.

(b) From the early 1980s to 1990, and by 1983, it was recognised among occupational health specialists that there was no threshold of safe exposure to airborne asbestos for mesothelioma induction.

(c) From the early 1980s to 1990, and by 1983, it was recognised among occupational health specialists that each dose of asbestos inhaled by a person increased the risk of that person contracting an asbestos related disease, including mesothelioma.' "

278 Again, it is not surprising that Dr Francis was not cross-examined in relation to the views which the trial Judge has set out. As I have already observed, this is because the suggestion that there is no minimum threshold of safe exposure tells one nothing about the magnitude of the risks associated with low level exposure. The perceived magnitude of those risks is the central issue in relation to foreseeability in this case. Nor does the observation that each dose of asbestos inhaled increases the risk of contracting an asbestos-related disease tell one anything of the magnitude of that risk. It is clear from the reports and standards to which I have referred, that reputable scientists and regulatory authorities were, throughout this period, of the view that the levels of risk associated with inhalation of quantities of fibres significantly greater than those inhaled by Mr Hannell, in the course of the three incidents he has specified, were acceptable and posed no appreciable risk to health.

279 The opinions expressed by the expert witnesses called by Amaca do not outweigh the clear and cogent inference to be drawn from the reports, regulations and standards to which I have referred. That inference that the exposures to respirable asbestos fibre, at the levels experienced by Mr Hannell and which would presumably be experienced by others carrying on work of the type he carried out, were, during the relevant period, considered to be within the scope of an acceptable level of risk.

280 The trial Judge relied upon a written statement from Mr Peter Russell which was tendered in evidence. Mr Russell worked for Amaca between 1948 and 1970. He held a position as a safety engineer between 1961 and 1964. In that capacity, he read a number of published materials relating to the dangers associated with the inhalation of asbestos. In 1963, Mr Russell urged that a written warning should be placed on products produced by Amaca. In 1964, he prepared a memorandum which outlined the development of knowledge concerning the health hazard of asbestos dust exposure. Later in the 1960s, he recalled reading papers published in various medical journals dealing with the relationship between asbestos exposure and mesothelioma. One such paper was that by Newhouse and Thompson which was referred to by Professor Musk.

281 Mr Russell lacks the specialist qualifications and training of the experts who were called on behalf of Mr Hannell. At its highest, his evidence involves a non-expert perception of the research materials that were being produced during the 1960s. His evidence was not, of its nature, of a kind that could diminish the force of the reports that were produced and the standards that were imposed by expert committees and responsible authorities during the relevant period and to which I have already referred.

282 The trial Judge also relied upon the evidence given by Mr James Lawless, who was called by Amaca. Mr Lawless served as an assistant occupational hygienist at Amaca's factory in Welshpool, Western Australia, between 1973 and 1988. His evidence was to the effect that warnings were applied to Amaca's products in the 1970s and that Amaca ceased using asbestos in its products during the 1980s.

283 Mr Lawless confirmed that concerns had been raised with Amaca over the years in relation to the use of its products. Those concerns were not generally expressed in relation to consumers of the end products, but rather in relation to the trades people regularly engaged in the installation of the products. He confirmed that there were discussions within Amaca about how information relating to possible risks might be communicated, including visits to hardware stores and demonstrations of the safe methods of dealing with asbestos sheeting. Brochures were prepared and distributed to hardware stores showing the correct tools and equipment to be used to minimise the production of dust when the materials were being worked on. Further, he said that there were no concerns within Amaca about exposures to persons in the community. However, Amaca was concerned to ensure that working methods were used which would minimise the quantity of respirable fibre produced when their products were being worked on.

284 Amaca admitted, in answers to interrogatories, that during the relevant period, it was aware that home handymen might use its asbestos cement products and that cutting those products could release asbestos fibres or dust into the atmosphere. However, that fairly obvious admission tells one nothing about Amaca's knowledge of the magnitude of the risk created by such exposures. Amaca's other answers to interrogatories, which were tendered in evidence, were to the effect that it was, at all relevant times, of the view that only inhalation of substantial quantities of fibre over extensive periods of time caused significant levels of risk.

285 The trial Judge also referred to a letter from Alco Hardware to Dr McNulty, Commissioner of Public Health, in 1983. The letter enquires as to whether there is any present or potential health risk to either customers or staff arising from the range of asbestos products manufactured by Amaca which it was distributing. Dr McNulty replied to that letter by a letter dated 6 September 1983, in which he advised that:

"Unless the asbestos products are cut, drilled or smoothened by sanding in an enclosed space with high dust levels generated, these products do not present any health risk when they are stored or fixed in position." (underlining removed)

286 None of the work undertaken by Mr Hannell was undertaken in an enclosed space - all was undertaken outdoors.

287 This letter provides particularly cogent evidence of the state of knowledge of responsible authorities and scientific experts at a time which is particularly relevant to Mr Hannell's case; namely, 1983. Although the trial Judge referred to Alco's inquiry, he did not refer anywhere in his reasons to Dr McNulty's response. Dr McNulty is generally recognised as having been one of the leading pioneers in the recognition of the association between respirable asbestos fibre and mesothelioma and other lung disease, and is widely regarded as expert in these fields.

288 The trial Judge referred to a large number of documents discovered by Amaca. It is not necessary to review those documents in detail. It is sufficient for present purposes to observe that the documents record, and in some cases respond to, assertions made in respect of the dangers of exposure to respirable asbestos fibre. However, none of the documents contain any admission by Amaca of a knowledge or belief that occasional exposure to low levels of fibres produced by working on asbestos cement products, which contained mainly chrysotile fibre, posed any significant or unacceptable risk to health.

289 The findings of the trial Judge based upon this evidence are set out in the following paragraphs of his reasons:

"139 The evidence of Mr Russell and Mr Lawless shows that senior managers within the defendant were aware of medical and scientific literature to the effect that small doses of asbestos could lead to mesothelioma and respirable fibres could be released from the sort of handyman activities the plaintiff engaged in. That conclusion is confirmed by the documents discovered by the defendant to which I have referred. Senior managers within the defendant were aware of medical and scientific literature as well as popular literature that said that even low-dose exposure could lead to mesothelioma or other lung diseases and that handymen or non-occupational users of the asbestos cement products might inhale respirable asbestos fibres in the course of activities such as cutting or drilling the products.

1. The defendant knew that a brief and slight exposure to asbestos dust might result in mesothelioma. There was no known safe level of exposure below which there was no risk of mesothelioma. The defendant knew that there was concern amongst various people, including public health authorities, and unions, about the hazards of asbestos to people cutting or drilling asbestos in the course of using asbestos products. The defendant knew that even sawing asbestos cement products for a quarter of an hour could reach or exceed the permitted standard for asbestos exposure in a day. The defendant knew that handymen drilling or cutting asbestos should take precautions to keep dust levels down.
2. The defendant knew that asbestos exposure could cause mesothelioma. The defendant knew that cutting or demolishing or brushing or sanding asbestos cement products would release asbestos fibres into the air and be inhaled and could cause mesothelioma. The defendant knew that handymen used asbestos cement products and that cutting them releases fibres into the atmosphere that could be inhaled. The defendant knew that many of the users of asbestos cement products were not aware of the risk of mesothelioma or cancer from inhaling asbestos dust as a result of using asbestos cement products."

290 With respect to the trial Judge, neither Mr Russell nor Mr Lawless said or suggested that senior managers within Amaca were aware of medical and scientific literature to the effect that small doses of asbestos could lead to mesothelioma and that those fibres could be released from the sort of handyman activities in which Mr Hannell engaged.

291 Nor did any of the evidence, to which the trial Judge referred, sustain a finding that Amaca knew that brief and slight exposure to asbestos dust might result in mesothelioma. The terminology used by the trial Judge suggests that he may have been considering a letter dated 29 March 1966 from Dr McCullagh, who later became Amaca's chief medical officer. However, as the trial Judge observes at [106] that in that letter, Dr McCullagh was merely noting a suggestion that had been made, he was not endorsing or accepting it.

292 Contrary to the findings of the trial Judge, none of the evidence he referred to sustained the conclusion that Amaca was aware or believed, during the relevant period, that occasional exposure to low levels of asbestos fibre (as a consequence of carrying out work on asbestos cement products which contained mainly chrysotile) posed a significant or unacceptable level of risk to health.

293 When regard is had to the reports of the expert committees and the standards imposed by regulatory authorities over the period relevant to Mr Hannell's case, the finding of the trial Judge that it was reasonably foreseeable to a person in Amaca's position that an occasional and casual user of asbestos cement building products would suffer mesothelioma, or other lung disease as a result of undertaking casual work on those products, cannot be sustained. Considering those reports and standards, it should be concluded that the balance of scientific opinion and the opinion of those responsible for the imposition of safety standards throughout the relevant period, was that the levels of exposure likely to be experienced by those undertaking casual work on asbestos cement products; being, mainly chrysotile asbestos, would not pose a significant or unacceptable risk to health.

294 It follows from this conclusion that on the evidence adduced in this case, it should be concluded that Amaca did not owe a duty to warn those who, like Mr Hannell, might undertake occasional work on asbestos cement products which comprised mainly chrysotile cement. The perception of the level of risk created by such work was not of such a magnitude to impose a duty to warn, let alone a duty to embark upon an advertising programme which would have been sufficiently extensive to come to Mr Hannell's attention.

295 In my opinion, Amaca's appeal should be allowed and Mr Hannell's judgment set aside. Judgment should instead be entered in favour of Amaca and Mr Hannell's claim dismissed.

296 STEYTLER P & McLURE JA: We agree with the Chief Justice that the appeal should be allowed but for different reasons. The respondent claims against the appellant in negligence. In order to succeed he had to establish that the appellant owed him a duty of care, had breached that duty and that there was a causal connection between the damage sustained and the breach of duty. The appellant claims the learned trial Judge made

material errors of fact or law in relation to each element of the claim in negligence.

297 The respondent suffered personal injury in the form of mesothelioma which he claims was physically caused by asbestos fibres released during work done on in situ asbestos cement building products in or around his home, which products were manufactured by the appellant. The asbestos cement building products in question were present when the respondent purchased his home.

298 The respondent contends that the appellant breached its duty of care by failing to advise (1) that the products contained asbestos; (2) that asbestos was extremely injurious to human health; and (3) as to the measures to be taken when handling and working with the products to prevent or minimise the release of asbestos fibre or dust. In particular, the respondent claimed that the appellant should have provided the advice on labels attached to the product and by advertising in the mass media.

299 Foreseeability is relevant to, inter alia, the existence and scope of a duty of care and breach of that duty. A necessary, although not sufficient, condition of the existence of a duty of care is reasonable foreseeability of the kind of injury that has been suffered by the person to whom the duty is owed: Tame v New South Wales [2002] HCA 35; (2002) 211 CLR 317 at [12] per Gleeson CJ. The "kind of injury" is a reference to the different categories of injury such as, for example, personal injury, property damage, or pure economic loss. The particular injury suffered need not be foreseeable: Mount Isa Mines Ltd v Pusey [1970] HCA 60; (1970) 125 CLR 383 at 402.

300 A risk is foreseeable if it is real, not far-fetched or fanciful; it can be a real risk even if it is extremely unlikely to occur: Wyong Shire Council v Shirt [1980] HCA 12; (1980) 146 CLR 40 at 48 per Mason J; Rosenberg v Percival [2001] HCA 18; (2001) 205 CLR 434 at [64]; Dovuro Pty Ltd v Wilkins [2003] HCA 51; (2003) 215 CLR 317 at [60]. Mason J said in Wyong Shire Council v Shirt (at 47) that "when we speak of a risk of injury as being 'foreseeable' we are not making any statement as to the probability or improbability of its occurrence, save that we are implicitly asserting that the risk is not one that is far-fetched or fanciful".

301 Reasonable foreseeability must be determined at the time of the alleged breach. The asbestos cement products were installed at the time of construction of the respondent's house in the late 1970s. It appears to have been common cause that a product label should have been attached to the products before they were sold by the appellant. We will proceed on the basis that the appellant sold the product in 1979. The respondent's case was that advertising should have commenced prior to the first of three incidents when the respondent was exposed to asbestos fibres. Those incidents are as follows.

(a) In April or May 1983 the respondent removed a Hardiplank fence in his backyard using a hammer or screwdriver; some planks broke; he stacked and later reassembled the planks, cutting and drilling some; he then brushed and painted the planks. The process took a couple of weekends and a couple of nights.

(b) In about February or March 1985 the respondent brushed, sanded, washed and painted the eaves of his house. This work was above his head; the preparation took about one week.

(c) In about February 1990 the respondent brushed fences and ridge cappings to remove bird droppings and algae in preparation for painting. The task took a couple of days.

The respondent took no precautions to minimise the generation of asbestos dust and fibres.

302 The contraction of mesothelioma (and other forms of cancer) from inhaling asbestos fibres relates to three issues: dose, fibre type and lag time. Asbestos is the name given to naturally occurring fibrous silicates. There are two main groups of asbestos: serpentines, which include chrysotile and amphiboles, which include crocidolite and amosite. The risk of contracting mesothelioma varies according to the fibre type. In descending level of risk they are crocidolite, amosite and chrysotile. As to the lag time issue, the risk of contracting mesothelioma is greatly increased by the expiry of time since first exposure. Asbestos inhaled within 10 years of the contraction of the disease was accepted to be causally irrelevant. The respondent was born in the UK in October 1942. He first noticed symptoms of the disease in October 2005.

303 Asbestos cement is a hard mixture of cement, silica and asbestos, where the asbestos comprises 8 to 15 per cent of the total mix. Of the asbestos component, the amosite content was likely to be approximately 1 per cent in this case. Asbestos cement is to be distinguished from asbestos in its raw form which is not bound by cement or other binding agents. The risk of mesothelioma associated with asbestos in its raw form is greater than that connected with asbestos cement products.

304 It was accepted that the dose of respirable asbestos fibres generated by the respondent's activities in 1983, 1985 and 1990, both individually and cumulatively, would have been very low. It was also accepted by the appellant at the time of trial in 2006 that a very low dose of respirable asbestos fibres from its asbestos cement products is capable of causing mesothelioma. However, the appellant's case on foreseeability at trial was that at all material times between 1979 and 1990 the appellant did not know, and had no reasonable grounds for knowing, that a very low dose of asbestos fibres from its asbestos cement products (a combination of chrysotile and amosite) was capable of causing mesothelioma. It has been held elsewhere that a plaintiff does not have to show that the particular disease (mesothelioma) was foreseeable or that the particular fibre type (chrysotile) was known to be dangerous: Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307 at 332. However, the respondent did not challenge the correctness of the appellant's formulation of the foreseeability requirement, perhaps because of the nature of the breach relied on: see Rosenberg v Percival at 453 - 460 per Gummow J.

305 Thus, we proceed on the basis that it was necessary for the respondent to establish that, having regard to the medical and scientific evidence at the time, the appellant knew or ought to have known that very small doses of asbestos cement in which the primary asbestos component is chrysotile in combination with amosite was capable of causing mesothelioma. Much of the medical and scientific evidence adduced on the known risks of small doses refers to asbestos generally without reference to whether the asbestos was in its raw form or in asbestos cement products, or the type of asbestos fibre involved.

306 The trial Judge found that the person against whom reasonable foreseeability of risk must be considered is a home handyman or other casual user of asbestos cement building products who does not encounter the product in industrial or occupational situations. There is no challenge to that identification of the class.

307 The trial Judge accepted the evidence of medical experts called by the respondent, Dr Leigh, Professor Henderson and Professor Musk, and found that the appellant knew (1) from the 1950s that asbestos inhalation was dangerous and that fibre released from its products could cause respiratory illness; (2) by the mid-1970s that product purchasers should be warned of such risks; (3) that a brief and slight exposure to asbestos dust might result in mesothelioma, there being "no known safe level of exposure below which there was no risk of mesothelioma"; and (4) that cutting or demolishing or brushing or sanding asbestos cement products would release asbestos fibres into the air and they would be inhaled and could cause mesothelioma.

308 Based on those findings, the trial Judge made the further finding on foreseeability as follows (at [143]):

"I find that in 1983 it was reasonably foreseeable to a person in the position of the [appellant] that a home handyman or other casual user of asbestos cement building products would suffer mesothelioma as a result of inhaling asbestos dust released from the asbestos cement products by the home handyman or casual user cutting, sanding, drilling or demolishing the asbestos cement products."

309 The primary challenge to the trial Judge's finding on foreseeability is that he reached it without considering, or giving reasoned consideration to, the evidence on which the appellant relied and without analysis or explanation for preferring the evidence of the respondent's medical experts.

310 On the issue of foreseeability, the appellant relied primarily on the following reports and correspondence:

1. Code for the Handling of Asbestos by Small Users, National Health and Medical Research Council ("NH&MRC"), June 1978;
2. Report on the Health Hazards of Asbestos, Report of Subcommittee of NH&MRC, June 1981;
3. Asbestos Cement Products, Report of Western Australian Advisory Committee on Hazardous Substances, August 1990;
4. Exposure Standards for Atmospheric Contaminants in the Occupational Environment, Worksafe Australia, May 1995;
5. Letter dated 13 August 1981 from an officer of the Western Australian Public Health Department to the Electrical Trades Union ("ETU");
6. Letter dated 16 December 1980 from the Minister for Health to Mr T Herzfeld MLA;
7. Memorandum dated 12 September 1983 from the WA Department of Mines to the Public Health Department.

311 The principles relating to the adequacy of reasons were considered in Mount Lawley Pty Ltd v Western Australian Planning Commission [2004] WASCA 149; (2004) 29 WAR 273 at [26] - [30]. Those principles include a requirement that relevant evidence should be referred to and, where there is conflicting evidence of significance to the outcome, both sets of evidence should be referred to. Where one set of significant evidence is preferred over another, the trial Judge should set out findings sufficient to explain why. However, inadequacy of reasons does not necessarily amount to an appealable error. An appeal court will only intervene when no reasons have been given in circumstances in which they were required or when the inadequacy is such as to give rise to a miscarriage of justice. Nor does an appealable error arising from inadequate reasons necessarily result in a new trial. The appeal court is entitled to consider the matter and, if it can do so (where, for example, only one conclusion is reasonably open on the available evidence), it may decide the matter.

312 We agree with the Chief Justice that the trial Judge erred in failing to adequately refer to the substance of the evidence on which the appellant relied and to provide any, or any adequate, explanation as to why he preferred the evidence of the experts called by the respondent. However, the parties agree that this Court is in a position to decide the issue of foreseeability.

313 The appellant also claimed that there was no evidentiary basis for the foreseeability finding together with other incidental challenges that fall away in light of this Court having to determine the question of foreseeability.

314 We propose to confine the review to evidence that is most closely referable to asbestos cement products comprising predominantly chrysotile in combination with amosite. The following references to the evidence are taken largely from the trial Judge's reasons.

315 Dr Leigh said in his report (exhibit H20) that in 1969 the well-known text Hunter's "The Diseases of Occupations" stated the following, in relation to the then draft Asbestos Regulations 1968 (UK):

"The new regulations apply to factories, some warehouses, ships under construction or in the course of repair. But the Factories Act cannot protect private users. we [sic] know that inhalation of dust from such activities as sawing or sanding material containing asbestos presents the hazard of malignant mesothelioma outside as well as inside industrial situations. It seems not unreasonable, therefore, to insist that materials containing asbestos should be clearly marked to show this, so that adequate precautions can be taken by the users. For instance, amateur handymen sawing materials containing asbestos could easily wear a lightweight dust mask, and either work out of doors or in a well ventilated room."

"[I]n 1974, the first major report of the UK Mesothelioma Register (relating to cases diagnosed in 1967-68) described several cases of mesothelioma in insulation workers, building workers, dockers, workers handling asbestos cement products and following hobby exposure incurred when sawing asbestos sheets and drew attention to the possibility of mesothelioma occurring at low dose ... No fibre type distinctions were made. Anderson et al ... drew attention to the risk of asbestos related disease, including mesothelioma, from household contact."

317 According to Dr Leigh, the appellant ought to have foreseen the risks of handyman exposure from 1983 onwards.

318 In his report (exhibit H18) Professor Henderson said:

"The causal relationship between asbestos and mesothelioma had been well established by the late 1980s and early 1990s, and at that time I was aware that no threshold level of asbestos exposure had been delineated below which there is no risk of mesothelioma above background risk: in other words, I and other authorities were aware by that time that mesothelioma could follow exposures to asbestos that were non-occupational in character - brief and transient and low-'dose' - including, for example, the development of mesothelioma from asbestos exposures related to 'handyman'-type work on A-C [asbestos cement] sheeting material: the development of mesothelioma from bystander, environmental and neighbourhood-type exposures had been recorded even earlier."

319 Professor Henderson was not cross-examined about these matters and the trial Judge accepted his opinion. Later in his reasons (at [145]) the trial Judge stated that Professor Henderson referred to "well before the late 1980s and early 1990s" (emphasis added) and that he was specifically addressing the dates on which he had been informed the respondent had experienced the handyman exposure (1983, 1985 and 1990) and was referring to the state of knowledge well before those times. The trial Judge clearly erred in his restatement of Professor Henderson's evidence which undermines the inference that he was speaking of a time well before 1983.

320 Dr Francis provided an opinion as to the availability of information as to knowledge of health hazards associated with exposure to asbestos. She was not cross-examined in relation to that opinion. Her opinion, which the trial Judge accepted, was summarised as follows (at [78]):

"(a) ...

(b) From the early 1980s to 1990, and by 1983, it was recognised among occupational health specialists that there was no threshold of safe exposure to airborne asbestos for mesothelioma induction.

(c) From the early 1980s to 1990, and by 1983, it was recognised among occupational health specialists that each dose of asbestos inhaled by a person increased the risk of that person contracting an asbestos related disease, including mesothelioma."

321 In May 1976 the appellant conducted trials to determine the extent of exposure to airborne asbestos from cutting asbestos cement products (exhibit P2366). The memorandum states that:

"Yesterday three short A.C. [asbestos cement] Sheet cutting trials were carried out. Breathing zone samples were taken during three cutting periods ... These tests were carried out in the open air ... The exposure to airborne asbestos is specified in terms of 8 hour time weighted average and is then a maximum of 4 fibres/ml in N.S.W."

"These results show that about a quarter of an hour of sawing A.C. sheet is all that could be allowed in a day in well ventilated surroundings, such as were used in these trials."

323 Exhibit P439 is an exchange of correspondence between the appellant and Dr Vianna and Ms Polan who had published an article in The Lancet of 2 September 1978. Vianna and Polan advised that there had been 37 case reports suggesting an association between non-occupational asbestos exposure and malignant mesothelioma.

324 Exhibit P1483 is a handwritten note indicating that the attached report entitled "Criteria Document for Swedish Occupational Standards: Asbestos and Inorganic Fibers" by William J Nicholson had been circulated at James Hardie in or about April 1982. The report is a lengthy one. Four conclusions are set out. The first is to the effect that three studies indicated that "excess mortality" may result from exposures as low as 0.5 fibres per ml for a working lifetime which was below the then current national standards. The second conclusion is that no data existed in any study that would indicate a threshold below which there is no risk of asbestos cancers. The third conclusion is that all fibre types carry significant cancer risk, although differences in exposure may result in variations in the distribution of types of neoplasms. The fourth conclusion is that exposure control to the lowest level possible is required not only for the usual asbestos worker trades, but for the vastly larger number of exposure circumstances associated with the use of asbestos products or their maintenance and repair.

325 Professor Musk gave evidence that by 1961 the serious dangers to health occasioned by even small exposures should have been known by persons responsible for exposing other persons to asbestos and appropriate warnings and safeguards should have been implemented. His evidence failed to differentiate between different forms of product and types of fibre which on the evidence affected the level of the risk. The trial Judge accepted the opinion of Professor Musk that well before 1983 a reasonable product supplier had means of being aware of the necessity to minimise the risk of inhalation of asbestos and to warn of the potential dangers.

326 The evidence to which we have referred, in particular that of Dr Leigh, Dr Francis, and the Criteria Document for Swedish Occupational Standards, support the conclusion that the appellant knew or ought to have known that low doses of asbestos fibres from its asbestos cement products were, or may be, capable of causing a life threatening injury including mesothelioma.

327 As to the documents relied on by the appellant, much of the material relates to an assessment and value judgment as to what was an acceptable level of risk of injury. That is relevant to, but not conclusive of, whether a defendant has breached its duty of care: Sibley v Kais [1967] HCA 43; (1967) 118 CLR 424; Aerospace Engineering Services Pty Ltd v Ibrahim [2007] WASCA 33 at [25]; Thompson v Johnson and Johnson Pty Ltd [1991] VicRp 84; [1991] 2 VR 449. We propose to identify those aspects of the documents that refer to the existence and extent of the risk as well as the reasonable response thereto.

328 The June 1978 NH&MRC report is directed to health precautions for workers regularly using products containing asbestos such as asbestos cement building products. Notwithstanding the reference to regular use of such products, the report states "[s]uch limited usage might be considered insufficient to cause harm to health of those exposed". Clause 7.2(a) provides:

"Asbestos cement ('fibro') is a hard surfaced material, in which the asbestos fibres are reasonably bonded by cement. Work with this material can be carried out safely with hand saws and other hand tools and also with power drills.

Occasional power sawing does not present a problem if limited to an operation of, say, 15 minutes in a shift, and if carried out in the open air. For longer periods dust extraction equipment should be used, or the dust should be suppressed by the use of water, or an approved respirator should be used."

329 The June 1981 NH&MRC Subcommittee report recommended that the entry for asbestos in the approved occupational health guide be amended to read:

"The average fibre concentration of the air breathed by the worker throughout a working shift ... over a sampling period of not less than four hours, during which one or more samples may be taken, should not exceed:

• chrysotile and amosite asbestos - 1.0 fibres per millilitre
• crocidolite - 0.1 fibres per millilitre."

330 The Subcommittee also recommended that all products containing asbestos be labelled by the manufacturer so as to alert the user to potential hazards giving an example:

• Contains asbestos fibre
• Avoid creating dust
• Breathing asbestos dust may cause serious damage to health, including cancer
• Smoking greatly increases the risk".

331 The trial Judge noted the Subcommittee recommendation as to the average fibre concentration of air breathed by workers throughout a working shift. However, he emphasised the following statement in the June 1981 report:

"Expert evidence suggests that it is not possible to establish a threshold value below which a carcinogenic effect of asbestos cannot be identified, although some recent evidence suggests that such a threshold may exist. The Subcommittee recommends that exposure to asbestos should, in all phases of the asbestos industry, be reduced to the lowest practicable level by the most efficient technology currently available and enforced through ... "

332 The occupational standard permitted an exposure many times higher than that to which the respondent was exposed whilst at the same time noting that there was no known threshold level below which a carcinogenic effect could not be identified and recommending product warnings. It is implicit that the Subcommittee made a value judgment as to what it deemed to be an acceptable level of risk of cancer without stating what the level was.

333 Dr Musk (as he then was) was on the Western Australian Advisory Committee that reported in August 1990. Its task was to assess the risk of release of asbestos fibres from weathered asbestos cement products. An Expert Working Party, which reported to the Committee, was established in response to extensive community concern as a result of the widespread use of asbestos cement products in schools in Western Australia. The report notes that between 1955 and 1966 crocidolite was used in asbestos cement products but, before and after that period (until the use of amosite was phased out in 1984), chrysotile with amosite was used. The report notes that asbestos in its raw form was well-known to cause a range of adverse effects on health in humans including benign pleural effusion and fibrosis, asbestosis, mesothelioma of the pleura and peritoneum and cancer of the lung. The report continues (at 6.2):

"All of the adverse effects listed above, except mesothelioma of the pleura and peritoneum, appear to be caused to about the same degree by the different forms of asbestos. Mesothelioma is much less frequent in persons exposed only to serpentine asbestos (ie chrysotile) than it is in those exposed also, or only, to amphibole asbestos. Indeed, it has been argued that cases of mesothelioma in persons believed to have been exposed only to chrysotile ... may have been due to low level contamination of the chrysotile with an amphibole."

334 Amosite is an amphibole. The report also states there is no reliable evidence for or against a threshold dose requirement for disease causation.

"There are very few data available that are directly relevant to the effects on health of exposure to asbestos cement products. This is probably a consequence of the commonly held opinion that under most circumstances asbestos cement products are unlikely to be hazardous because the fibres are bound together in a solid matrix from which individual fibres are 'not expected to be released under normal circumstances'. It has been accepted, however, that fibres 'may be emitted during manipulation or renovation of such materials or products' as, for example, by cutting, grinding, drilling or extensive breakage, but under these circumstances would be a potential hazard to few people on few occasions (World Health Organisation, 1986)." (emphasis added)

336 The first half of that extract is addressing the risk associated with the mere presence of asbestos products in the community. The conclusion (at 7.1) is that while mesothelioma can occur in association with quite low levels of exposure to asbestos, the risk of mesothelioma and lung cancer is related to the amount of exposure to asbestos and it is reasonable to suggest that there exists a level of exposure below which there is a "negligible risk of harm". The Committee considered that it would be reasonable to consider mixed asbestos fibre concentrations in ambient air of less than 0.001 fibres per millilitre to be associated with a negligible risk of harm to human populations. That is a constant background level. Its assessment was that a death rate of one person per 100,000 per year was negligible. The evaluative process in determining whether to characterise a risk as negligible is clear from the discussion in the report on death rates. The report states (at 7.7 and 7.8):

"To gain some understanding of what an annual risk of death of 1 per million per year means, it is worth noting that the lowest risk of death at any age is experienced by girls aged 4 to 14 years and is 1 per 10,000 per year (ie 100 per million per year). As such a girl moves into late teenage, her annual risk of death increases by 300-400 per million per year mainly due to her use of motor vehicles and her association with the opposite sex in so doing. By way of further comparison, it may be noted that a 40 year old male who could be at risk of developing a mesothelioma because of exposure to asbestos in childhood has an annual risk of death from all causes of about 2 in a thousand, or 2,000 per million. The addition of an increment in risk of death of 1 in a million per year would, therefore, be only a very small fraction of the total risk of death at this age.

These considerations suggest that it would be reasonable to consider mixed asbestos fibre concentrations in ambient air of less than 0.001 fibres per millilitre to be associated with a negligible risk of harm to human populations."

337 An annexure to the report contains a review of the literature conducted by an epidemiologist. It is noted that:

"Asbestos-related diseases among asbestos-cement producers has been clearly shown in several reviews of numerous studies to be consistently low or undetectable when only chrysotile is used ... [but] when amphiboles have also been used the rates are much higher."

338 The 1995 Worksafe exposure standards applied to occupational environments and reflect exposures which "should neither impair the health of nor cause undue discomfort to nearly all workers". The exposure standards do not represent "no-effect" levels that guarantee protection to every worker.

339 The exposure standards for airborne contaminants are expressed as a time-weighted average ("TWA") concentration of that substance over an eight-hour working day, for a five-day working week. The average fibre concentration of the air breathed by a worker throughout a working shift over a sampling period of not less than four hours should not exceed a TWA exposure standard of 0.1 fibres per ml of air for crocidolite and amosite and 1.0 fibre per ml of air for chrysotile.

340 In the December 1980 letter the WA Minister for Health advised that a person cutting asbestos cement with power tools was at risk of developing an asbestos related disease and the risk was dependent upon the total amount of dust to which the user was exposed and would vary therefore "from negligible for the handy man cutting asbestos cement sheets once or twice in a life time to considerable for the person who regularly cuts sheets in the course of his work". In the August 1981 letter from the Health Department officer to the ETU, the officer advised that asbestos cement products posed no health threat unless large volumes of dust were created by sawing or other such operation and that even in such cases it is only after long over-exposure that asbestos disease is a possibility. The statements in these letters are not supported by the scientific evidence at the relevant time.

341 The memorandum of September 1983 from the Mines Department reports on the analysis of paint scrapings from a State Housing Commission asbestos-clad house. It was said to be unlikely that any respirable size fibres were present or that a significant amount of airborne fibre relative to the then current NH&MRC occupational hygiene standard of 1 fibre per ml had been generated by removal of the paint.

342 Regard should also be had to the appellant's conduct in the relevant period. Warnings were placed on the appellant's asbestos cement products from 1978. The early version stated that asbestos dust "can damage health" and to keep dust down by following safety rules as follows:

"1. When sawing, drilling, etc. work in a well ventilated space, preferably outdoors.

1. Use hand tools designed for cutting asbestos-cement sheets such as fibro cutters or a score and snap knife - or use an old hand saw. If cutting by power saw use one which has a dust suppression attachment.
2. Avoid drilling overhead where possible by pre-drilling before fixing.
3. Damp down waste dust and dispose of it in a sealed bag."

343 The 1982 version of the product label (which appears to have followed the 1981 NH&MRC Subcommittee report) contained a warning that breathing dust "may cause serious damage to health including cancer" and repeated the safety rules.

344 As from the late 1970s, literature about the appellant's asbestos cement products was supplied to point of sale outlets such as hardware stores which literature included the warnings. The appellant also conducted road shows to hardware stores to advise of the risk of its products and to demonstrate safe methods of use.

345 In April 1983 the Board of the appellant resolved to "cease within the next few months the production and sale in Australia of those building products which have not already been converted and still contain asbestos fibre". The phase out of use of asbestos in those products occurred between 1981 and 1987. Most uses of amosite ceased in May 1984 and use of chrysotile ceased in 1987. The use of crocidolite had ceased many years earlier.

346 The evidence establishes that the appellant knew or ought to have known in 1979 and thereafter that:

(a) asbestos cement products containing chrysotile and amosite would release respirable asbestos fibres upon cutting, sawing, sanding or drilling;

(b) science was unable to determine whether or not there was a threshold dose below which there was no risk of a life threatening injury;

(c) even if there was a safe threshold dose, very small doses of respirable asbestos fibres from its asbestos cement products were, or may be, capable of causing a life threatening illness, including mesothelioma, but the risk of that occurring was extremely low.

347 In circumstances where the appellant was the manufacturer of the product, the risk of members of the relevant class contracting a life threatening disease was real, not far-fetched or fanciful, even though the risk of it occurring was extremely low. Although the primary Judge erred in failing to give reasoned consideration to the determination of foreseeability issues, he came to the correct result in which event we would dismiss the appellant's grounds of appeal challenging the finding of foreseeability.

348 Where the existence and scope of a duty of care is settled by authority, it is unnecessary to identify and apply the legal principles that govern the determination of those questions. The existence and scope of the duty of care owed by the appellant to the respondent were in issue in this case.

349 There has been a return to the words of Lord Atkin in Donoghue v Stevenson [1932] AC 562 as the foundation for all modern considerations of duty of care. Reasonableness is the test for the imposition of a duty of care (Tame at [35] per Gleeson CJ; [109] per McHugh J; [185] per Gummow and Kirby JJ; [272] per Hayne J; [331] per Callinan J). Gleeson CJ said in Tame, that it is the reasonableness of a requirement that a person should have certain persons or interests in contemplation that determines the existence of a duty of care. Further, reasonable foreseeability is to be understood and applied with due regard to whether it is reasonable to require a person to have in contemplation a risk of the injury that eventuated.

350 It is an error to formulate the duty of care with such particularity as to in effect circumvent the requirement of reasonableness at the breach stage of the analysis: Graham Barclay Oysters Pty Ltd v Ryan [2002] HCA 54; (2002) 211 CLR 540 at [191] - [192] per Gummow and Hayne JJ. On the other hand, to formulate a duty at too high a level of abstraction may provide an inadequate legal mean by which to determine the issues in a particular case; it will be too abstract if it is divorced from the facts said to enliven the duty: Cole v South Tweed Heads Rugby League Football Club Ltd [2004] HCA 29; (2004) 217 CLR 469 at [56] and [81] per Gummow and Hayne JJ.

351 The appellant contended that it was necessary at the duty stage of the analysis to determine the existence and scope of the duty by reference to the particular breach relied on; that is, the trial Judge was required to determine whether the appellant owed to the respondent a duty to warn.

352 That approach is certainly used in novel situations where it is otherwise only possible to formulate a duty of care at such a high level of abstraction as to be of no practical assistance. A good illustration of this is in Cole v South Tweed Heads. When faced with that situation, the duty analysis brings to account the same considerations as are relevant in determining whether the specific breaches relied on would constitute a breach of any duty however formulated.

353 Save in medical negligence cases where it has been authoritatively determined that a medical practitioner owes to his or her patient a duty to warn, ordinarily the question whether the provision of a warning is within the scope of the duty in a particular case is determined at the breach stage of the analysis by assessing whether a failure to warn constitutes a breach of duty: Thompson v Johnson and Johnson at 488 - 489; Seltsam Pty Ltd v McNeill [2006] NSWCA 158 at [104]; Modbury Triangle Shopping Centre Pty Ltd v Anzil (2000) 205 CLR 254 at [105] per Hayne J; Vairy v Wyong Shire Council [2005] HCA 62; (2005) 223 CLR 422; Mulligan v Coffs Harbour City Council [2005] HCA 63; (2005) 223 CLR 486. However, the result should be the same regardless of the approach.

354 The trial Judge found that the appellant owed a duty of care to the respondent as a member of the class of persons who cut, saw, sand or drill the appellant's asbestos cement products occasionally, intermittently or from time to time, the duty being to take reasonable care to avoid injury being suffered by members of that class using the product as intended or in a way in which the product was normally used. The duty is formulated at an appropriate level of generality and does not circumvent the requirement of reasonableness at the breach stage of the analysis. We would dismiss the appellant's challenge to the trial Judge's formulation of the duty of care.

355 Having concluded that a reasonable person in the appellant's position would have foreseen that its conduct involved a risk of injury to the respondent, it is then for the court to determine what a reasonable person would do by way of response to the risk. As stated by Mason J in Wyong Shire Council v Shirt at 47 - 48:

"The perception of the reasonable man's response calls for a consideration of the magnitude of the risk and the degree of the probability of its occurrence, along with the expense, difficulty and inconvenience of taking alleviating action and any other conflicting responsibilities which the defendant may have."

356 A failure to eliminate a risk that is reasonably foreseeable does not establish negligence. Proper inquiry at the breach stage involves identifying with some precision what a reasonable person would do by way of response to a foreseeable risk: Graham Barclay at [192]. It is incumbent upon the respondent to demonstrate that there was something the appellant could have done which would eliminate or reduce the risk complained of and which was practicable: Roman Catholic Church Trustees for the Diocese of Canberra and Goulburn v Hadba [2005] HCA 31; (2005) 221 CLR 161 at [13].

357 We are here concerned with an extremely low risk of very significant harm, being death from mesothelioma. By 1987 all of the appellant's cement building products were free of asbestos. However, by 1987 there was, and remains to this day, a widespread and substantial incidence of asbestos cement building products in residential and other properties throughout Western Australia and beyond. There was no claim that the appellant should have ceased manufacturing and selling asbestos cement products at some time before they were used in or on the respondent's property. That provides a practical illustration and acceptance of the fact there was a very small risk of harm from the products once they were (and remained) installed.

358 The documents on which the appellant relies demonstrate that bodies responsible for the assessment of public and occupational health characterised the risk of handyman-type exposure as "negligible" and, in an occupational setting, permitted exposure which was significantly higher than that to which the respondent was exposed. However, as already pointed out, standards of this type are relevant but not determinative.

359 The steps taken by the appellant, apart from labelling its products, such as literature at points of sale and road shows were clearly targeted at those members of the class who purchased the product and not those who occasionally worked with the product after it had been installed.

360 As to the labels, the trial Judge found they were inadequate. He said (at [172]):

"The first labels placed on the [appellant's] asbestos cement products were inadequate. Those labels cautioned the reader only that breathing asbestos dust can damage health. That caution fails to bring to the reader's attention the seriousness of the injury that might result from breathing asbestos dust. The subsequent labels did inform the reader that breathing asbestos dust may cause serious damage to health including cancer but still failed to inform the reader that cancer, or mesothelioma, might result from inhaling a small amount of asbestos dust and that there is no known threshold dose below which no risk of mesothelioma exists."

361 In a similar vein, the trial Judge found that there should have been mass media advertising and that the language had to be "reasonably calculated to impress upon users the gravity of the risk". We take that to be similar to the required warning on the labels.

362 We agree that a reasonable response to the foreseeable risk was to place warning labels on the asbestos cement products and that the first labels were inadequate for the reasons given by the trial Judge. However, the warning suggested by the trial Judge is a communication to the effect that the product is of such a danger as to suggest it should not be permitted to remain in situ and certainly ought not to be worked on at all. A warning of that nature is not justified by the evidence. The content of the second label was adequate for the class of which the respondent was a member. However, for the reasons given by the Chief Justice, we agree that warning labels on building products would not be an effective means of communicating the information to all members in the relevant class and any breach in this case would not have caused the respondent's injury.

363 The remaining issue is whether the appellant should have advertised in the mass media. There are two points about that: one goes to the effectiveness of warnings in the mass media as a tool for modifying behaviour and the second to the practicality of that course of action. The evidence establishes that there was very extensive news and current affairs coverage in the print and electronic mass media in the second half of the 1970s and the first half of the 1980s concerning the dangers of asbestos, the need for product labels warning of the risk of asbestos and the need to handle the products with care. There was also coverage of the risk to handymen. Based on that evidence, it would be reasonable to expect that a person who was an adult in Western Australia in that period would have a general understanding of the risks of asbestos and asbestos cement products. The respondent arrived in Australia from the UK in 1981. He gave evidence, accepted by the trial Judge, that he did not know that exposure to asbestos could cause cancer. That is an illustration of the limitations of mass communication of news and current affairs.

364 Another important factor is whether it is reasonably practicable to warn persons in the class of which the respondent was a member. An impression of the nature and extent of the advertising required for the information to come to the respondent's attention is revealed in the trial Judge's finding on causation. The trial Judge found (at [327]):

"It may be inferred, and I do infer, that if in or before 1983 the [appellant] had made public announcements or placed advertisements in a Perth daily or weekly newspaper monthly or more frequently saying that a handyman or casual user of asbestos cement building products ran a risk of contracting mesothelioma and that the risk could be minimised by the taking of certain steps then that information is likely to have come to the attention of a person such as the plaintiff who watched the news, listened to the radio and regularly read a newspaper, even if only weekly."

365 When assessing reasonableness, a hindsight analysis is to be avoided. Further, what is reasonable has to be assessed by reference to all members in the class, present and future. The advertising would have to apply to all geographic areas in which the products were distributed for a period commencing in 1979 and ending at some unspecified time in the distant future as new generations of adults purchased homes containing asbestos fences and other asbestos cement products.

366 The frequency and scope of the advertisements that would be necessary to reach the majority of the members of the class (membership of which class would continuously change) would itself communicate a warning of a kind that is disproportionate to the very low risk of harm involved. That would be so regardless of the actual content of the communication which would be in line with the message on the second product label. Further, it would be impossible to reach all members of the class, such as for example, new arrivals, non-English speakers and those who avoid commercial media outlets. Mass media advertising of a very low risk of serious harm, particularly having regard to the myriad of sources of such risks to which people are exposed on a daily basis, is not a reasonable or practicable response to the risk. This assessment is consistent with and reflected in the standards and regulations in the period. Accordingly, we would uphold the appeal on this basis.

367 We will address the issue of causation on the assumption that, contrary to our view, the appellant breached its duty of care in failing to warn of the risks of asbestos and the steps necessary to minimise the risk. It was not in dispute that the respondent's mesothelioma was caused by asbestos fibres. There were two sources of exposure to asbestos. First was background exposure, that is, exposure from the environment at large. It was common ground between the parties that the background rate of mesothelioma was calculated from persons who had no recollection of specific exposure to asbestos but who may have been so exposed. It was not suggested that the appellant was tortiously liable for the background exposure. The second source of exposure was from the specific incidents in 1983, 1985 and 1990 ("the specific exposures").

368 The appellant relied on epidemiological evidence on the issue of causation. Epidemiological evidence of this nature is purely statistical, probabilistic evidence that says nothing about the cause of a disease in a specific case. The mathematical expression of increased risk from specific exposures is reflected in the relative risk ("RR"). The background risk for mesothelioma in Western Australia is two to three persons per million per annum which translates to a lifetime risk of 140 to 210 persons per million per lifetime. To calculate the relative risk it is necessary to calculate the increase in the risk of contracting mesothelioma created by any specific exposure. For that purpose it is necessary to calculate the approximate dose of asbestos likely to have been inhaled by the respondent from the specific exposures. Two occupational hygienists, Mr Rogers (called by the appellant) and Dr Francis (called by the respondent) made that assessment.

369 The background exposure is treated as having a RR of one. Any increased risk attributable to a specific exposure to asbestos is shown by an increase in the RR. If the risk doubled, the RR would be two. Based on Mr Rogers' assessment of the dose of asbestos likely to have been inhaled from the specific exposures (approximately 0.001 fibres per ml years), Professor Berry, a biostatistician and epidemiologist, calculated the RR at 1.14 (an increase in mortality rate of one person per hundred thousand). Based on Dr Francis' assessment (cumulative exposure of 0.2 fibres per ml years), Professor Berry calculated the RR at between 1.3 and 1.4 (an increase in mortality rate of six persons per hundred thousand).

370 Based on his estimate of the respondent's cumulative asbestos exposure from the specific exposures, Mr Rogers concluded that there was a 99.999 per cent probability that the respondent's mesothelioma was caused by the background exposure and the respondent would have experienced it regardless of the specific exposures. The trial Judge gave no weight to Mr Rogers' evidence. He rejected his estimate of cumulative exposure on the basis that there was no proper evidential foundation on which to base the calculation and because it contained too many assumptions, estimates and variables. The trial Judge also rejected Dr Francis' assessment of the cumulative exposure on the same grounds. He also rejected Mr Rogers' opinion as to the cause of the respondent's mesothelioma on the basis that the background rate of mesothelioma used by Mr Rogers included people who may have had specific asbestos exposure that they could not recall. The trial Judge had found (at [223]) that the only specific asbestos exposures to which the respondent was exposed were the three incidents referred to and that therefore his background risk was not the same as that measured in the studies on which Mr Rogers relied.

371 The appellant's other experts, Professor Berry and Professor Breslin (a thoracic physician), based their opinions on Mr Rogers' assessment of the cumulative asbestos exposure resulting from the specific exposures and a background rate that included people who may have had unrecalled specific exposure to asbestos. As a result, the trial Judge also rejected their evidence. Neither party had challenged the evidence of the occupational hygienists on the basis of no proper evidential foundation or had claimed that the background rate of mesothelioma did not apply.

372 The appellant contended the trial Judge erred in applying an incorrect test for determining causation:

1. (a) by incorrectly determining when an evidential burden has shifted or may be shifted;

(b) by blurring the different concepts of the evidential and legal burden of proof;

(c) by, in effect, reversing the onus of proof;

(d) by failing to apply the leading Australian authorities on causation; and

(e) by applying (at least implicitly) inapplicable English authorities on causation.

373 The appellant also contended the trial Judge erred in the treatment of and in the findings consequent upon the evidence on causation:

1. (a) in the findings as were made or by failing to make findings in relation to the dose of asbestos inhaled by the respondent (this relates to the rejection of the evidence of Mr Rogers and Dr Francis);

(b) by failing to make findings in relation to the background risk of contracting mesothelioma;

(c) in finding that the respondent was not otherwise exposed to asbestos (with the result that the background risk used in the epidemiological evidence was held not to apply); and

(d) by denying the appellant procedural fairness in relation to 2(a) and (b).

374 The underlying basis of grounds 2(a) and (b) is the proposition that without epidemiological evidence the Court could not infer any causal link between the specific exposures and the contraction, many years later, of mesothelioma. The appellant claimed the trial Judge made the errors because he failed to consider and apply what it described as the leading Australian authorities on causation in asbestos cases and mesothelioma cases, in particular, Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; (2000) 49 NSWLR 262 and Bendix Mintex v Barnes, to which no reference is made in the reasons. The English authority to which ground 1(e) refers is Fairchild v Glenhaven Funeral Services Ltd [2002] UKHL 22; [2003] 1 AC 32.

The trial Judge's findings on and approach to causation

375 The trial Judge found on the expert evidence that (1) mesotheliomas are by definition tumours that arise from mesothelial cells; (2) the development of mesothelioma tumours is preceded by the inhalation of asbestos fibres; (3) the inhalation of asbestos fibres does not necessarily lead to the development of mesothelioma. Everyone living in urban areas will inhale asbestos fibres in their lifetime but few develop mesothelioma; (4) the precise process by which the inhalation of asbestos fibres leads to mesothelioma is unknown but it involves damage to the DNA. Not all DNA damage causes mesothelioma. Some cancer cell mutations occur in genes that trigger the mesothelioma. The mesothelioma then grows relentlessly; (5) it is not known whether, after asbestos fibres have caused initial DNA damage, further asbestos fibres are required to cause the subsequent development of the mesothelioma tumour, but they may increase the risk of the development of the mesothelioma tumour.

376 All expert witnesses agreed that there is a positive dose-response relationship between asbestos exposure and mesothelioma: the greater the exposure to asbestos, the greater the risk of developing mesothelioma. The trial Judge also found that there is no established threshold below which asbestos fibres cannot cause mesothelioma and that even very low exposure can cause mesothelioma, even if the risk is very low. The trial Judge noted (at [227]):

"The causation issue in this case arises from a situation of scientific uncertainty. Asbestos may have caused the [respondent's] mesothelioma through either a single fibre or through multiple fibres, but there is no way of identifying the source of the fibre or fibres which initiated or promoted the genetic process or processes which culminated in the malignant tumour."

377 It appears from this passage that the trial Judge accepted the "one fibre" theory of causation. Senior counsel for the appellant submitted that none of the medical and other scientists who gave evidence on the subject supported the one fibre theory. That accords with our assessment of the expert evidence.

378 The appellant contended that although the trial Judge stated the principles of causation correctly he applied them incorrectly to in effect impose a legal burden of proof on the appellant. The basis for this submission is to be found in the trial Judge's treatment of the evidence of Professor Berry.

"The [respondent's] asbestos exposure resulting from his handyman activities materially contributed to the risk of the [respondent] contracting mesothelioma and the risk eventuated, that is the [respondent] did contract mesothelioma. Accordingly, it will be taken that the [appellant's] breach of its duty of care caused or materially contributed to the [respondent] contracting mesothelioma unless the [appellant] discharges the evidential onus that its breach had no effect or that the [respondent] would have contracted mesothelioma even if its breach of duty had not occurred."

380 Professor Berry had calculated that the lifetime risk of mesothelioma due to the respondent's handyman exposure was about 3 per cent of the background risk based on the estimates of exposure in Mr Rogers' report. Based on Dr Francis' figures he calculated the RR to be in the range of 1.3 to 1.4. The trial Judge said (at [296]):

"Professor Berry's evidence, if accepted, is not sufficient to discharge the evidential burden on the [appellant] of adducing evidence that the [respondent's] handyman exposure had no effect or that the [respondent] would have suffered mesothelioma even if he had not experienced the handyman exposure. Professor Berry is not able to say that the asbestos fibre or fibres that caused the [respondent's] mesothelioma were not inhaled by the [respondent] in the course of his handyman activities. Professor Berry's evidence, if accepted, is that on a population basis the risk of contracting mesothelioma as a result of 'background exposure' is greater, or many times greater, than the risk of contracting mesothelioma from asbestos exposure in the order of the [respondent's] handyman exposure. Professor Berry does not go so far, and his calculations do not permit him to go so far, as to say that the [respondent's] handyman exposure did not materially increase the risk of contracting mesothelioma."

381 The trial Judge also approached causation on an alternative basis, assuming that the appellant had no evidential onus or that it had discharged that onus. He preferred the evidence of the medical experts (Professor Musk, Professor Robinson, Professor Henderson, Mr Alvarez and Dr Leigh) to that of the industrial hygienists (Mr Rogers and Dr Francis). Based on the medical evidence he drew the inference that the respondent's handyman exposures caused or materially contributed to the respondent's mesothelioma.

382 We agree with the Chief Justice for the reasons he gives that the primary Judge erred in rejecting the evidence of Mr Rogers, Dr Francis, and Professors Berry and Breslin on the stated grounds. However, for reasons to be developed, we do not accept the appellant's contention that epidemiological evidence is the only, or indeed an appropriate basis in this case for establishing that the specific exposures caused or materially contributed to the respondent's mesothelioma.

383 In Bendix Mintex v Barnes, the plaintiff had been exposed to crocidolite asbestos fibres during his service in the Royal Navy from 1947 to 1962. Leave to proceed against the UK Ministry of Defence was refused at an interlocutory stage. The plaintiff had also been exposed to chrysotile asbestos fibre, at least some of which was contaminated by an amphibole, tremolite, during his employment at a service station between 1962 and 1985. His claim in negligence against an employer and a manufacturer and a supplier of brake and clutch componentry failed. Mason P and Beazley JA (Stein JA dissenting) concluded that the plaintiff had not established causation. The majority approached the causation question on the basis that the medical evidence established that there were multiple alternative potential causes of the disease. It was accepted that there was a substantially greater risk associated with crocidolite. The President concluded that the evidence established that it was probable the plaintiff's exposure to asbestos during his Royal Navy service was the sole cause of his mesothelioma. Although the President said that the law does not equate a material increase in the risk of injury with material contribution to the injury, he also said that if the Royal Navy exposure had not occurred, the trier of fact would have found it probable that the defendants were liable.

384 In Seltsam v McGuiness the plaintiff was awarded damages for renal cell carcinoma which was found by the Dust Diseases Tribunal to have been caused by the defendant's negligence in exposing him to asbestos. The question before the Court of Appeal was whether the evidence was capable of establishing causation. The Court (Spigelman CJ, Davies A-JA, Stein JA dissenting) held that causation had not been proved. The Court, relying on High Court authority, said the test of balance of probabilities is not satisfied by evidence which fails to do more than establish a possibility and that the epidemiological evidence was expressed in terms of an increased risk that never rose above the level of a possibility. The plaintiff had relied on an observation by McHugh J in Chappel v Hart (1998) 195 CLR 232 at [27] that:

"If a wrongful act or omission results in an increased risk of injury to the plaintiff and that risk eventuates, the defendant's conduct has materially contributed to the injury that the plaintiff suffers whether or not other factors also contributed to that injury occurring."

"There is a tension between the suggestion that any increased risk is sufficient to constitute a 'material contribution', and the clear line of authority that a mere possibility is not sufficient to establish causation for legal purposes. The latter is too well-established to be qualified by the former. The reconciliation between the two kinds of references is to be found in the fact that, as in Chappel v Hart and in the cases that suggest the former, the actual risk had materialised. The 'possibility' or 'risk' that X might cause Y had in fact eventuated, not in the sense that X happened and Y had also happened, but that it was undisputed that Y had happened because of X."

386 In Chappel v Hart a medical practitioner had breached his duty of care by failing to inform a patient of the risk of perforating her oesophagus during an operation and that risk eventuated. The issue in Seltsam was whether asbestos exposure caused the plaintiff's renal cell carcinoma. There was no direct or established relationship between the breach (asbestos exposure) and harm of the particular type suffered, namely renal cell carcinoma.

387 In this case the respondent had to prove that the failure to warn caused his mesothelioma. That involves two distinct inquiries. The first is whether the breach (failure to warn) caused the respondent to either undertake the work which in the absence of breach he would not have undertaken or, alternatively, undertake it without taking precautions to minimise the release of dust and fibres. The second is whether the resulting exposure to asbestos caused the mesothelioma in a physical sense. The focus of the appeal is on the second inquiry. However, unlike in Seltsam v McGuiness, there was in this case a direct and admitted relationship between the risk of harm giving rise to the breach and the particular injury suffered, the only question being whether one or other or both sources of asbestos caused or materially contributed to the injury.

388 The appellant contended the trial Judge had in effect applied the House of Lords decision in Fairchild v Glenhaven Funeral Services. First, some necessary background which, for convenience, we base on the reasons for judgment of McLure JA in City of Stirling v Tremeer [2006] WASCA 73; (2006) 32 WAR 155.

389 A defendant is liable in negligence only if the damage suffered by the plaintiff was caused or materially contributed to by the defendant's negligent act or omission. The issue of causation is divided into two questions: the question of causation in fact which is ordinarily determined by the application of the "but for" test and the further question of whether the defendant is in law causally responsible for the damage: Bennett v Minister of Community Welfare [1992] HCA 27; (1992) 176 CLR 408 at 412 - 413.

390 Generally, a plaintiff will fail if he or she cannot satisfy the "but for" test. In the United Kingdom, the failure to satisfy the "but for" test of causation is not determinative where there is an evidential gap. That will occur where, for example, there is positive evidence that on the current state of medical knowledge, experts are unable to say whether or not the damage would have been suffered but for the negligent act or omission. McGhee v National Coal Board [1972] UKHL 7; [1973] 1 WLR 1 is such a case. After a short period of working in brick kilns, the plaintiff worker suffered dermatitis. The Court found that the employer had breached its duty of care by failing to provide adequate washing facilities at the workplace. The question before the House of Lords was whether the worker had proved that the breach caused the dermatitis. The evidence established that the provision (and use) of washing facilities would have materially reduced the risk of dermatitis. If the evidence was left there (and provided the Court found that the worker would have used the facilities) the Court could have drawn an inference that the breach caused the dermatitis. However, the evidence did not stop there. None of the medical experts called at the trial would go so far as to say that washing after work would have made it more probable than not that the worker would not have contracted dermatitis. The state of medical knowledge at the time did not allow the medical experts to reach a conclusion on the question. Thus, the worker had not proven on the balance of probabilities that the damage would not have occurred but for the negligent omission. Different members of the Court provided different reasons for concluding that the worker had established causation. The judgment of Lord Wilberforce in McGhee has been referred to with approval by the High Court. Lord Wilberforce said (at 6):

"I agree with the judge below to the extent that merely to show that a breach of duty increases the risk of harm is not, in abstracto, enough to enable the pursuer to succeed. He might, on this basis, still be met by successful defences ...

But the question remains whether a pursuer must necessarily fail if, after he has shown a breach of duty, involving an increase of risk of disease, he cannot possibly prove that this increase of risk caused or materially contributed to the disease while his employers cannot positively prove the contrary. In this intermediate case there is an appearance of logic in the view that the pursuer, on whom the onus lies, should fail ... The question is whether we should be satisfied, in factual situations like the present, with this logical approach. In my opinion, there are further considerations of importance. First, it is a sound principle that where a person has, by breach of a duty of care, created a risk, and injury occurs within the area of that risk, the loss should be borne by him unless he shows that it had some other cause. Secondly, from the evidential point of view, one may ask, why should a man who is able to show that his employer should have taken certain precautions, because without them there is a risk, or an added risk, of injury or disease, and who in fact sustains exactly that injury or disease, have to assume the burden of proving more: namely, that it was the addition to the risk, caused by the breach of duty, which caused or materially contributed to the injury? In many cases, of which the present is typical, this is impossible to prove, just because honest medical opinion cannot segregate the causes of an illness between compound causes."

391 In the subsequent case of Fairchild v Glenhaven Funeral Services the House of Lords concluded that in limited circumstances, of which McGhee was an example, there were exceptions to the ordinary rule requiring proof on the balance of probabilities of causation in fact. In Fairchild, the appellant employees had developed mesothelioma as a result of exposure to asbestos dust during periods of employment with more than one employer. The workers could not establish on the balance of probabilities which of the employers had exposed the employees to the asbestos dust that caused the disease. On the evidence, the mechanism initiating the disease process was unknown; the trigger might equally probably be a single, a few or many fibres; once caused the condition was not aggravated by further exposure; and the greater the quantity of fibres inhaled, the greater the risk of developing the disease. The workers had not proven that, but for the exposure in the course of employment by each individual employer, they would not have contracted the disease. The House of Lords held that the evidential gap justified, on policy grounds, a modified approach to proof of causation. In such a case, proof that each defendant's wrongdoing had materially increased the risk of contracting the disease was sufficient to satisfy the causal requirement for liability.

392 A number of members of the High Court, relying on the judgment of Lord Wilberforce in McGhee, support a rule that on its face applies to proof of causation generally, it not being confined to evidential gaps that cannot be filled by either side. The approach is reflected in the oft-cited statement of Gaudron J in Bennett v Minister of Community Welfare (at 420 - 421):

"[G]enerally speaking, if an injury occurs within an area of foreseeable risk, then, in the absence of evidence that the breach had no effect, or that the injury would have occurred even if the duty had been performed, it will be taken that the breach of the common law duty caused or materially contributed to the injury." (footnotes omitted)

393 Gaudron J links breach and causation. She said in Bennett (at 422) that there is usually no reason to separate or distinguish the question of breach of a common law duty from that of causation because the duty relates to precautions a reasonable person in the position of the person sued would have taken to prevent a foreseeable risk of harm of the kind suffered and a precaution would not be classified as reasonable unless its performance would, in the ordinary course of events, avert the risk that called it into existence.

394 Gaudron J's statement in Bennett has been cited with approval in Chappel v Hart at 239 per Gaudron J; 257 per Gummow J; 273 per Kirby J; Rosenberg v Percival at 461 per Gummow J; Naxakis v Western General Hospital [1999] HCA 22; (1999) 197 CLR 269 at 279 per Gaudron J. It is consistent with March v E & M H Stramare Pty Ltd [1991] HCA 12; (1991) 171 CLR 506 at 518 - 519 per Mason CJ. In Naxakis, Gaudron and Callinan JJ cited with approval the statement of McHugh J in Chappel v Hart discussed in Seltsam v McGuiness.

395 Any suggestion that Gaudron J's statement contemplates the legal burden shifting to the defendant is rejected by McHugh and Kirby JJ in Chappel v Hart at [34] and [93]. As we understand the law in Australia, once a plaintiff demonstrates that a breach of duty has occurred followed by injury within the area of foreseeable risk, a prima facie causal connection will be established and the defendant has an evidential burden to adduce evidence that the breach had no effect or that the injury would have occurred even if the duty had been performed. If there is evidence sufficient to displace the prima facie case, it remains for the plaintiff upon the whole of the evidence to satisfy the tribunal of fact that the injury was caused by the defendant's negligence: Purkess v Crittenden [1965] HCA 34; (1965) 114 CLR 164 at 168.

396 In Tremeer, the parties accepted that the plaintiff had to establish causation in fact. The evidential burden was satisfied in Tremeer by the defendant adducing evidence which, if accepted, was capable of establishing on the balance of probabilities that the injury would have occurred even if the duty had been performed. The question whether causation in fact could be established by the respondent or rebutted by the appellant in this case was not directly addressed by the parties or the trial Judge. However, it is relevant to an understanding of the causation issues.

397 On the evidence the background exposure and the specific exposures are each independent sufficient causes of mesothelioma. Another question not directly addressed by the parties or the trial Judge is whether they are alternative causes (that is, it must be one or the other but cannot be both) or cumulative causes. If the asbestos exposures are sufficient cumulative causes, then both sources will materially contribute to the respondent's disease: E M Baldwin & Son Pty Ltd v Plane [1999] A Tort Rep 81-499. Moreover, an exposure to asbestos that made a cumulative contribution to the contraction of the disease can be a material contributing factor even if it was not itself a sufficient cause: Bonnington Castings Ltd v Wardlaw [1956] UKHL 1; [1956] AC 613. The appellant's case on causation is based on the unstated assumption that the two sources of exposure are alternative causes.

398 It is necessary to refer to the expert evidence on causation before returning to the application of the legal principles.

399 The appellant challenged the trial Judge's finding that there is no known threshold or minimum lower limit below which asbestos fibres cannot cause mesothelioma. That is in accordance with the evidence. Professors Berry, Robinson, and Musk and Mr Alvarez gave evidence that there was no minimum threshold below which was a safe level of asbestos exposure. The other experts said it was not scientifically known whether or not there was a minimum threshold level because it would be so low as to make measurement impractical. No expert stated that there was a threshold below which asbestos was safe.

400 Every relevant expert agreed that there was a close relationship between asbestos fibres and the contraction of mesothelioma and that increased exposure increased the risk of the disease. They also all agreed that every exposure increased the risk of contracting mesothelioma. The evidence also established that mesothelioma is an indivisible disease and that, once triggered, is not aggravated or otherwise affected by subsequent asbestos exposure.

401 Dr Leigh and Professors Robinson, Breslin and Henderson gave evidence about the aetiology of the disease. The trial Judge quoted at length from the evidence of Dr Leigh concerning the development of mesothelioma. We propose to refer to it, not for the accuracy of its detail, but to demonstrate in broad outline the reconciliation of the propositions that there is no known safe threshold of asbestos exposure and the acknowledged dose/risk relationship.

402 In his report of 12 March 2006 Dr Leigh referred to recent literature that concluded that asbestos fibres can have effects at both the initiation and promotion/proliferation phases of tumour development and said that the concept of asbestos as an initiator and promoter for mesothelioma is accepted in recent standard textbooks. In his oral evidence Dr Leigh explained the concept of asbestos as an initiator and promoter of mesothelioma:

"The current accepted theories of carcinogenesis in general, not just with asbestos but with many other agents, is that cancer is initially a genetic change in the cell. In other words, the genetic material that normally regulates cell division so that ... when one mesothelioma cell divides it becomes two more normal mesothelioma cells and that's regulated by the genes on the chromosomes in the cell. All cancer is thought to be due to a disordered cell division. A cancerous cell is an abnormal cell, that when a cell divides into two, one or both of them is not a normal cell and then that abnormal cell will divide again and again and again and will become a tumour, as long as other things happen as well. That's what is [meant] by initiation initial genetic damage to the cell and asbestos can do that to cells ... Once this abnormal cell has been produced by a genetic alteration and some of these abnormal cells are starting to grow that does not necessarily mean that that little clone of abnormal cells will become a clinical tumour because the body will have defence mechanisms to mop up these funny-looking cells. There will be immune mechanisms and there will be tumours, oppressor genes will come into action, and not all genetically initiated cell damage will turn into a tumour, however other factors then act on the promotion of growth of these abnormal cells. What makes the abnormal cell that has been initiated become yet more abnormal cells. This is due to the action of promoters. They promote the proliferation of abnormal cells and asbestos can act in that way as well, so it can act both on the initial genetic damage and it can act to promote the growth of already initiated cells."

"In view of the capacity of asbestos fibres to be involved at several stages of tumour development, all cumulative exposure to asbestos in an individual case must be considered to play some part in causation."

"That's because the later exposures may be involved in promotion rather than initiation. They may also be involved in and get more initiation than new cells because none of these things are happening simultaneously. They are all happening at different times and, as I say, different processes are occurring at cells. You have got a dose of carcinogen, a number of fibres if you like, acting on a number of cells in a probabilistic way. Not every fibre acts on every cell and at different points in time some cells are suffering genetic damage, some cells that have already suffered genetic damage are being promoted into clones of abnormal cells and becoming tumours. At the same time you've got repair processes going on with suppressor genes being activated and you've got pathological defence mechanisms like antibodies to the cells that are recognised as abnormal and destroying them. Some cells are just dying anyway, necrosis, and some are dying by so called program cell deaths, or apoptosis, where the genetic mechanism in the cell actually programs it to die. At the same time you've got fibres are being cleared, some of the fibres are being cleared at different rates, depending on the type of fibre, and if further exposure is occurring more fibres are being deposited and these are potentially acting either in an initiating or a promoting fashion, so you've got all these processes going on simultaneously so that, as I say in the report ... "

"All these processes at cellular level are stochastic in that probabilities of fibre/cell interaction depend on the number of fibres and number of cells present at any point in time. Hence, simplistically, the more fibres, the more free radicals and greater probability of initiated, promoted or proliferated cells at any given time point."

406 In his oral evidence Dr Leigh further explained:

"[I]t's the free radical that ultimately does the chemical damage to the DNA, which produces the genetic change ... [I]t's like sperm and ova. I mean, only one sperm actually fertilises the ova but there's millions sent out to do the deed, so the more there are the more chance of one being hit ... Ultimately one fibre does initiate the change in the cell, but it's because it's been given a big chance by being one of a huge force."

407 Although Professor Robinson does not find the terms "initiator" and "promoter" useful, his description of how the disease develops is in broad terms consistent. Professor Robinson said that asbestos fibres damage the pleura and repeated cycles of damage and repair and the associated production of molecules like oxidants allow pleura mesothelial cells to accumulate DNA damage. It takes a very long time to accumulate sufficient DNA damage to cause the dangerous mutations to genes in the cell that cause cancer. The initiation of damage to the DNA does not by itself cause cancer. There must be subsequent molecular events that result in disordered growth. Professor Robinson was unable to say whether, after asbestos fibres had caused sufficient DNA damage, further asbestos fibres were necessary for the subsequent development of the tumour. However, he said that asbestos causes chronic inflammation which was thought to promote cancer but that no one knows whether it was the ongoing damage from DNA or the inflammation that was associated with it over that period or both.

408 Professors Breslin and Henderson supported the initiation and promotion theory. Professor Breslin described a process whereby the body's attempts to destroy asbestos fibres produce free radicals and free radicals damage DNA and damaged cells multiply. Some of the damaged cells are neutralised by the body's defences (such as macrophages) but eventually the system is overwhelmed and the first mesothelioma cell survives and multiplies causing a tumour.

409 According to Processor Henderson, asbestos fibres directly and indirectly produce free radicals which damage mesothelial cells and the mutation caused by that damage is transmitted to daughter mesothelial cells which then interact further with asbestos fibres. The inflammatory stimulus eventually built up by this process produces a number of other factors which are thought to produce proliferation of mesothelial cells. The greater number of asbestos fibres and the greater number of cells, the greater number of interactions between the fibres and cells which will lead to all of the complex steps which eventually lead to mesothelioma.

410 On our understanding of the expert evidence, it is generally agreed that all asbestos fibres which penetrate to the sac in which the lung sits, known as the pleura, operate in combination directly and indirectly over a very extended period to cause and accumulate DNA damage in the pleura mesothelial cells. Some damaged cells are destroyed by the body's defence system but eventually there may be sufficient DNA damage that some gene mutations will be dangerous and cause cancer. Whether or not further asbestos exposure is involved in the subsequent molecular events that result in a disorder of growth resulting in a tumour is not significant.

411 Professors Robinson and Henderson and Dr Leigh refer to the lottery ticket analogy but on our reading of their evidence on the aetiology of the disease, only for the purpose of making the point that increased exposure to asbestos results in increased risk of the disease.

412 This case has similarities with Bonnington Castings v Wardlaw. In that case an employee contracted pneumoconiosis in the course of his employment where he was exposed to silica dust from a pneumatic hammer and from swing grinders. The employer was not tortiously liable for the dust from the pneumatic hammer but was liable in relation to dust from the swing grinders. The House of Lords held that the onus was not on the employer to show that the breach was not the cause of the injury. The medical evidence was that the source of the disease was the dust from both sources and the correct question was whether the dust from the swing grinders materially contributed to the disease not which was the most probable source of the employee's disease. What is a material contribution is a question of degree and any contribution which is not de minimis is material (at 621 per Lord Reid). Although much greater amounts of dust came from the hammer, the proportion which came from the swing grinders was not negligible. The disease was held to have been caused by the whole of the material inhaled.

413 The approach to causation in Bonnington Castings is conventional and has been approved by the High Court in March v Stramare at 514, 532; Bennett at 419, 428; Chappel v Hart at [27]. Further, it demonstrates the limitations of epidemiological evidence on causation. That evidence can have a role where the range of potential causes are alternative in the sense that they are incapable of operating jointly to produce the same indivisible injury (as in Wilsher v Essex Area Health Authority [1987] UKHL 11; [1988] AC 1074) or where there is no direct or proven connection between the breach and the particular injury (as in Seltsam v McGuiness). But it is of no assistance in answering the question whether or not as a matter of fact a negligent act or omission contributed to the injury although it may be of assistance in determining whether a contribution was material.

414 Unlike Bendix Mintex v Barnes, the evidence in this case does not establish on the balance of probabilities that a prior exposure to asbestos was the sole cause of the mesothelioma. Moreover, the background exposure operated concurrently with the specific exposure from 1983 rather than sequentially, as in Bendix Mintex v Barnes and Seltsam v McGuiness.

415 As previously noted, the expert evidence is to the effect that asbestos fibres directly and indirectly produce DNA damage in mesothelial cells some of which cells survive the body's defence mechanisms and, over a very lengthy period, the damage in turn produces gene mutations some of which are dangerous and, in combination with other processes, cause disordered growth resulting in the contraction of mesothelioma. Inhaled asbestos from exposures within the long latency period each contribute to sufficient accumulated DNA damage which is a precondition to the contraction of the disease. Thus, asbestos fibres from all sources make a cumulative contribution to the contraction of the disease. The next question is whether the contribution is material. That can be assessed by reference to the quantitative assessment of the respective levels of asbestos fibre contribution. Based on Dr Francis' assessment of the dose of asbestos likely to have been inhaled by the respondent from the specific exposures and Professor Berry's calculation of the RR at between 1.3 and 1.4, that would on any view be a material contribution to the contraction of the disease. A RR at 1.14 which involves a mortality increase of one person per hundred thousand from a background level of six per hundred thousand would also qualify as a material contribution to the contraction of the disease.

416 Professors Musk and Henderson and Dr Leigh acknowledged that they were unable to say that, but for the specific exposures, the respondent would not have contracted mesothelioma. Professor Breslin accepted that the fibres from the specific exposures could not as a matter of science be excluded as a cause of the respondent's mesothelioma. That concession reflects the limitations in the epidemiological evidence to which we referred.

417 Thus, the respondent could not establish on the balance of probabilities that he would not have contracted mesothelioma but for the specific exposures. That is always the case where there are multiple sufficient causes of an indivisible disease. However, as Hayne J in Chappel v Hart acknowledged, the "but for" test is neither a comprehensive nor exclusive test of causation, in particular, it does not readily resolve the case where there are two causes at work and each is a sufficient independent cause or if both alone are insufficient (at [116]). However, the application of Gaudron J's approach in Bennett ("the Bennett test") results in a prima facie case that the specific exposures caused the respondent's mesothelioma. This application of the Bennett test is not controversial where multiple sufficient causes operate together to contribute to, or produce, the injury. However, it is controversial if the multiple sufficient causes are alternative (or if it cannot be proven that the two causes operated together to contribute to the injury). The application of the Bennett test in those circumstances produces the same result as in Fairchild.

418 When the Bennett test is applied to evidence that is required to satisfy the "but for" test of causation, the resulting prima facie factual inference of causation can be rebutted by adducing evidence that is capable of supporting a finding, on the balance of probabilities, that the act or omission did not cause the injury. If the Bennett test is intended to endorse Lord Wilberforce's statement in McGhee so that it also applies to multiple sufficient alternate causes, then that test will produce results that are inconsistent with a purely statistical, probabilistic conclusion about causation. In particular, such a statistical conclusion could not be a proper basis for preventing (or rebutting) a prima facie case under the Bennett test. Indeed, the application of the Bennett test to multiple sufficient alternative causes has the practical effect of depriving a defendant of the ability to satisfy the evidential burden at all. It only assists the plaintiff to jump the evidential gap.

419 The trial Judge went further than permitted by the Bennett test by placing an onus on the appellant to exclude any possibility that asbestos fibres from the specific exposures caused or contributed to the disease. That is to place a legal onus on the appellant to discharge a standard of proof that equals or exceeds the criminal standard. However, it produces no error if, as the trial Judge in effect found, the two sources of exposure are multiple alternative causes because in that situation a prima facie case based on the Bennett test cannot be rebutted in any event.

420 If we are wrong in characterising the sources of exposure in this case as multiple sufficient cumulative causes rather than alternative causes, it is necessary to decide whether the statements of Gaudron J in Bennett and McHugh J in Naxakis are intended to apply where there is an evidential gap of the kind discussed by Lord Wilberforce in McGhee, at least where the same causative agent is involved (as in McGhee and Fairchild). In our view that is the intention. Lord Wilberforce's judgment in McGhee was approved by Gaudron J in Bennett at 420 - 421 and Kirby J in Chappel v Hart at 273 and Gaudron J's statement was itself approved in Chappel v Hart, Rosenberg v Percival and Naxakis (as indicated above).

421 For these reasons we would allow the appeal, set aside the orders made by the trial Judge and order that the action be dismissed. We would hear from the parties as to costs.

JURISDICTION : SUPREME COURT OF WESTERN AUSTRALIA

CITATION : AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) -v- PATRICIA MARGARET HANNELL as Executor of the Estate of DAVID RICHARD HANNELL (Dec) [2007] WASCA 158 (S)

BETWEEN : AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) (ACN 000 035 512)

PATRICIA MARGARET HANNELL as Executor of the Estate of DAVID RICHARD HANNELL (Dec)

Jurisdiction : SUPREME COURT OF WESTERN AUSTRALIA

Citation : HANNELL -v- AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) [2006] WASC 310

Costs - Whether the issues on appeal justify departure from the general rule that the successful party should recover its costs - Turns on own facts

Respondent pay 50% of appellant's costs of the appeal, to be taxed

Respondent pay appellant's costs of the trial, to be taxed

1 JUDGMENT OF THE COURT: By orders made on 7 September 2007, the Court allowed this appeal, set aside the judgment of the trial judge and instead ordered that the respondent's action against the appellant be dismissed. Directions were made for the exchange of written submissions in relation to the costs of the trial and the appeal. These reasons are concerned only with those costs issues.

2 The appellant submits that the general rule, reflected in O 66 r 1(1) of the Rules of the Supreme Court 1971 (WA) is that 'the Court will generally order that the successful party to an action or matter recover his costs' (O 66 r 1). It submits that in this case, there is no basis for departing from that general rule.

3 The respondent acknowledges the existence of the general rule, but relies upon the modification to that general rule established by practice and authority, and expressly recognised in O 66 r 1(3), which provides:

Where a party though generally successful in an action has, by the introduction of some issue or issues on which he has failed, increased the costs the Court may order such party to pay the costs of such issue or issues.

4 The respondent submits that the issues that arose at trial, and on appeal, can be segregated into four substantive and discrete areas, namely:

5 The respondent points out that on the decision of the majority in this Court, it was successful in all of those issues other than breach. The respondent submits that, as a result of its success on three out of the four issues identified, the appropriate orders to be made in respect of costs are:

(a) that each party bear their own costs of the trial and the appeal; or in the alternative

(b) that the respondent pay 25% of the appellant's costs of the trial and the appeal.

6 The power to depart from the general rule to the effect that costs follows the event and to instead adjust the costs order to be made by reference to the failure of the generally successful party on specific and particular issues within the litigation, is recognised by practice, authority and the express provisions of O 66 r 1(3). However, its application depends upon the identification of discrete and severable issues, the litigation of which has increased the costs of conducting the proceedings. Established practice in this State, and the authorities, suggest that the exercise of this power should be approached broadly, and as a matter of impression, and without an attempt at 'mathematical precision' which is likely to prove illusory - see, for example J-Corp Pty Ltd v Australian Builders Labourers Federated Union of Workers (Western Australian Branch) (No 2) [1993] FCA 42; (1993) 46 IR 301.

7 Accordingly, the power to adjust an order for costs by reference to particular issues upon which the generally successful party has failed, is properly exercised only where there are discrete and severable issues upon which the generally successful party has failed, and which have added to the cost of the proceedings in a significant and readily discernible way. In a case in which the generally successful party has failed on only a minor issue, which did not add materially to the cost of the conduct of the proceedings, it would not ordinarily be appropriate to depart from the general rule, unless the conduct of the generally successful party in relation to that issue had been unreasonable. In the event of unreasonableness, different considerations may apply.

8 Applying those principles to the circumstances of this case, it is undoubtedly the case that the four issues identified by the respondents arose for determination both at trial and on appeal. However, the factual and evidentiary substratum to each of those issues was substantially common to all issues, and was largely addressed by each of the experts who were called by each of the parties. At the heart of each of the issues was the question of the extent to which the inhalation of respirable asbestos fibre in the course of what were characterised as 'home handyman activities' performed infrequently on materials containing asbestos fibre, caused or contributed to the risk of each of the respondents contracting mesothelioma. That issue, and particularly the state of knowledge in relation to that issue, bore directly upon the issues of foreseeability, and duty of care, and also upon the question of whether the appellant was in breach of the duty of care which the majority found it owed to each respondent. The issue was central to the issue of causation. So, although this is a case in which the legal consequences of the basic factual and evidentiary substratum had to be enunciated in the resolution of different questions, it was also one in which there was some overlap between the basic factual and evidentiary substratum in respect of each of those questions.

9 Applying those considerations to the issue of the costs of the trial, because the major part of the time spent at trial was concerned with evidence which spanned all four identified issues, and because it seems to us that it was reasonable for the appellant to put the respondent to the proof of all of the issues necessary to establish their cause of action, there should be no departure from the general rule, and the respondent should be ordered to pay the appellant's costs of the trial to be taxed.

10 So far as the appeal is concerned, a significant and discrete portion of the argument on appeal was directed to the issue of causation upon which the appellant failed (by a majority). Accordingly, in respect of those costs, it is appropriate to adjust the order to be made to reflect the appellant's failure on that issue. Approaching the issue of apportionment at the level of impression, and without attempting to achieve mathematical precision, the respondent should be ordered to pay 50% of the appellant's costs of the appeal, to be taxed.

11 So the orders of the Court will be that the respondent pay the appellant's costs of the trial, and 50% of the appellant's costs of the appeal, to be taxed.