Amaca Pty Ltd v Hannell
[2007] WASCA 158
•2 August 2007
JURISDICTION : SUPREME COURT OF WESTERN AUSTRALIA
TITLE OF COURT : THE COURT OF APPEAL (WA)
CITATION: AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) -v- HANNELL [2007] WASCA 158
CORAM: MARTIN CJ
STEYTLER P
McLURE JA
HEARD: 28 FEBRUARY 2007 & 1 MARCH 2007
DELIVERED : 2 AUGUST 2007
FILE NO/S: CACV 15 of 2007
BETWEEN: AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) (ACN 000 035 512)
Appellant
DAVID RICHARD HANNELL
Respondent
ON APPEAL FROM:
Jurisdiction : SUPREME COURT OF WESTERN AUSTRALIA
Coram :LE MIERE J
Citation :HANNELL -v- AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) [2006] WASC 310
File No :CIV 2412 of 2005
Catchwords:
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
Legislation:
Nil
Result:
Appeal allowed
Judgment set aside
Judgment entered in favour of the appellant
Respondent's claim for damages dismissed
Category: A
Representation:
Counsel:
Appellant: Mr G M Watson SC & Mr A J Power
Respondent: Mr D R Williams QC & Mr J R C Gordon
Solicitors:
Appellant: Minter Ellison
Respondent: Slater & Gordon
Case(s) referred to in judgment(s):
Aerospace Engineering Services Pty Ltd v Ibrahim [2007] WASCA 33
Beale v Government Insurance Office (NSW) (1997) 48 NSWLR 430
Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307
Bennett v Minister of Community Welfare (1992) 176 CLR 408
Bonnington Castings Ltd v Wardlaw [1956] AC 613
Chappel v Hart (1998) 195 CLR 232
City of Stirling v Tremeer (2006) 32 WAR 155
Cole v South Tweed Heads Rugby League Football Club Ltd (2004) 217 CLR 469
Davie v Magistrates of Edinburgh [1953] SC 34
Donoghue v Stevenson [1932] AC 562
Dovuro Pty Ltd v Wilkins (2003) 215 CLR 317
E M Baldwin & Son Pty Ltd v Plane [1999] A Tort Rep 81‑499
Fairchild v Glenhaven Funeral Services Ltd [2003] 1 AC 32
Graham Barclay Oysters Pty Ltd v Ryan (2002) 211 CLR 540
Hannell v Amaca Pty Ltd (Formerly James Hardie & Co Pty Ltd) [2006] WASC 310
Hughes v National Trustees, Executors & Agency Co of Australasia Ltd (1979) 143 CLR 134
Jones v Sutherland Shire Council [1979] 2 NSWLR 206
Makita (Australia) Pty Ltd v Sprowles (2001) 52 NSWLR 705
March v E & M H Stramare Pty Ltd (1991) 171 CLR 506
McGhee v National Coal Board [1973] 1 WLR 1
Modbury Triangle Shopping Centre Pty Ltd v Anzil (2000) 205 CLR 254
Mount Isa Mines Ltd v Pusey (1970) 125 CLR 383
Mount Lawley Pty Ltd v Western Australian Planning Commission (2004) 29 WAR 273
Mulligan v Coffs Harbour City Council (2005) 223 CLR 486
Naxakis v Western General Hospital (1999) 197 CLR 269
Purkess v Crittenden (1965) 114 CLR 164
Roman Catholic Church Trustees for the Diocese of Canberra and Goulburn v Hadba (2005) 221 CLR 161
Rosenberg v Percival (2001) 205 CLR 434
Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262
Seltsam Pty Ltd v McNeill [2006] NSWCA 158
Sibley v Kais (1967) 118 CLR 424
Soulemezis v Dudley (Holdings) Pty Ltd (1987) 10 NSWLR 247
Tame v New South Wales (2002) 211 CLR 317
Thompson v Johnson and Johnson Pty Ltd [1991] 2 VR 449
Vairy v Wyong Shire Council (2005) 223 CLR 422
Wilsher v Essex Area Health Authority [1988] AC 1074
Wyong Shire Council v Shirt (1980) 146 CLR 40
MARTIN CJ:
Introduction
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.
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:
(a)such exposure caused his mesothelioma;
(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.
Mesothelioma
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."
Mr Hannell's exposure to asbestos
The identified incidents of exposure
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.
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.
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.
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.
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.
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.
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.
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.
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.
Background exposure
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).
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.
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.
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.
Mr Hannell's background risk
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.
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."
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."
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.
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.
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.
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".
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.
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.
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.
Causation – legal issues
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 [1973] 1 WLR 1, Wilsher v Essex Area Health Authority [1988] AC 1074 and Fairchild v Glenhaven Funeral Services Ltd [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.
235Another 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."
The trial Judge then referred to a number of decisions of the High Court, including Bennett v Minister of Community Welfare (1992) 176 CLR 408; Chappel v Hart (1998) 195 CLR 232; Naxakis v Western General Hospital (1999) 197 CLR 269 and Rosenberg v Percival (2001) 205 CLR 434. He also referred to the decision of this Court in City of Stirling v Tremeer (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."
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.
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.
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257The 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] 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.' "
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.
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,
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) 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?
21His 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.
22The 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. "
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:
"78Epidemiology 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.
79Evidence 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.
80The 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] 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.'
81In 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] 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. ...'
82See 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.
83The 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.'
84It 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.
…
88The test is whether, on the basis of the primary facts, it is reasonable to draw the inference: see, eg, Luxton v Vines (1952) 85 CLR 352 at 358.
89In 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."
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):
"102Some 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.
103Mason 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.
104In 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.
105The 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.'
106Although 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]; 162 ALR 540 at 547 [31], per Gaudron J and (at 806 [127]; 574 [127]), per Callinan J.
107The 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'.
108This 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?"
After referring to a number of other cases, Spigelman CJ went on:
"118The issue in the present case is whether an increased risk did cause or materially contribute to the injury actually suffered.
119There 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.
120The 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."
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:
"67Most 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."
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."
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.
He described the situation in Australian law in the following paragraphs:
"136The 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) 60 CLR 336 at 361-362; Jones v Dunkel (1959) 101 CLR 298 at 304-305; West v Government Insurance Office (NSW) (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) 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.
137In 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."
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.
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:
"175The 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.
176One 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."
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.
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.
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".
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.
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.
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:
"312I 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."
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.
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.
The evidence led by Amaca
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.
The evidence of Mr Rogers
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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) 52 NSWLR 705) support a strong inference that he was, in effect, ruling the opinions inadmissible.
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) 143 CLR 134, 153; Jones v Sutherland Shire Council [1979] 2 NSWLR 206, 219; Cross on Evidence (7th Aust ed, [1645], et seq)).
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.
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."
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.
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.
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.
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.
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.
Dr Francis
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.
Dr Francis produced two reports containing her opinions on issues relevant to Mr Hannell's case. They were each tendered without objection.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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."
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.
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 Bennettv 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)
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.
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) 197 CLR 269 at 279 per Gaudron J. It is consistent with March v E & M H Stramare Pty Ltd (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.
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) 114 CLR 164 at 168.
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.
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] AC 613. The appellant's case on causation is based on the unstated assumption that the two sources of exposure are alternative causes.
It is necessary to refer to the expert evidence on causation before returning to the application of the legal principles.
Expert evidence and analysis
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.
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.
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.
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 his report Dr Leigh said that:
"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 his oral evidence Dr Leigh elaborated:
"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 … "
In his report Dr Leigh had said:
"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."
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."
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.
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.
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.
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.
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.
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.
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 [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.
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.
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.
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.
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.
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.
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.
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).
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
TITLE OF COURT : THE COURT OF APPEAL (WA)
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)
CORAM: MARTIN CJ
STEYTLER P
McLURE JA
HEARD: 28 FEBRUARY & 1 MARCH 2007
DELIVERED : 2 AUGUST 2007
SUPPLEMENTARY
DECISION :22 FEBRUARY 2008
FILE NO/S: CACV 15 of 2007
BETWEEN: AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) (ACN 000 035 512)
Appellant
PATRICIA MARGARET HANNELL as Executor of the Estate of DAVID RICHARD HANNELL (Dec)
Respondent
ON APPEAL FROM:
Jurisdiction : SUPREME COURT OF WESTERN AUSTRALIA
Coram :LE MIERE J
Citation :HANNELL -v- AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) [2006] WASC 310
File No :CIV 2412 of 2005
Catchwords:
Costs - Whether the issues on appeal justify departure from the general rule that the successful party should recover its costs - Turns on own facts
Legislation:
Rules of the Supreme Court 1971 (WA), O 66 r 1
Result:
Respondent pay 50% of appellant's costs of the appeal, to be taxed
Respondent pay appellant's costs of the trial, to be taxed
Category: B
Representation:
Counsel:
Appellant: No appearance
Respondent: No appearance
Solicitors:
Appellant: Minter Ellison
Respondent: Slater & Gordon
Case(s) referred to in judgment(s):
J‑Corp Pty Ltd v Australian Builders Labourers Federated Union of Workers (Western Australian Branch) (No 2) (1993) 46 IR 301
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.
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.
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.
The respondent submits that the issues that arose at trial, and on appeal, can be segregated into four substantive and discrete areas, namely:
(a)foreseeability;
(b)duty of care;
(c)breach;
(d)causation.
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.
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) 46 IR 301.
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.
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.
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.
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.
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.
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