Lola Merle Evans v Queanbeyan City Council and Anor

High Court of Australia|2010-03-25|Before: Curtis J, Mr J

CITATION : Lola Merle Evans v Queanbeyan City Council and Anor [2010] NSWDDT 7

Lola Merle Evans PARTIES : Queanbeyan City Council Amaca Pty Limited

CATCHWORDS: DUST DISEASES TRIBUNAL - Negligence :- Causation - Asbestos - Smoking - Lung Cancer

Browne v Dunn (1893) 6 R 67 Amaca Pty Ltd v Ellis [2010] HCA 5 CASES CITED: Workers Compensation (Dust Diseases) Board of NSW v Smith, Munro and Seymour [2010] NSWCA 19 Seltsam Pty Ltd v McGuinness (2000) 49 NSWLR 262 Makita (Australia) Pty Ltd v Sprowles (2001) 52 NSWLR 705

DATES OF HEARING: 25 March 2010 - 26 March 2010, 29 March 2010 - 1 April 2010, 6 April 2010 - 7 April 2010.

Mr G F Little SC with Mr R J M Foord instructed by Denniston and Day appeared for the plaintiff

LEGAL REPRESENTATIVES: Mr J L Sharpe instructed by Thompson Cooper Lawyers appeared for the first defendant

Mr G M Watson SC instructed by DLA Phillips Fox appeared for the second defendant

Dust Diseases Tribunal of New South Wales Matter Number 199 of 2009 Lola Merle Evans v Queanbeyan City Council and Amaca Pty Limited 20 April 2010 JUDGMENT CURTIS J Introduction

The plaintiff is the widow of Mr Henry Evans who contracted lung cancer in 2007. Mr Evans, who died on 5 January 2010, was for many years a heavy smoker of cigarettes and he also worked as a carpenter extensively with asbestos cement building materials. Mrs Evans contends that asbestos fibre liberated from building products manufactured by Amaca Pty Limited, formerly James Hardie and Coy Pty Ltd, materially contributed to her husband's lung cancer.
Mrs Evans sues Amaca, and Queanbeyan City Council, which for a time employed Mr Evans to work with Amaca's products, in negligence.
I have concluded that, on the balance of probabilities, Amaca's products did not materially contribute to the development of Mr Evans' cancer. The Reliability of Mr Evans' Evidence
When Mr Evans gave evidence in his home on 8 August 2009, it was apparent that he was not mentally acute. He was then one week short of his 83rd birthday, five months short of his death, and in extremely poor health. I believe his evidence, although honestly given, was, in respect to his smoking history and his exposure to asbestos, unreliable.
Dr Anthony John Nicholls, a thoracic physician who initially saw Mr Evans on 3 November 2006, and who supervised his treatment from that time until his death on 5 January 2010, said that in the course of this period it became increasingly evident that Mr Evans suffered from dementia.
Mrs Evans said that from 2008, and in particular in the last six months of his life, Mr Evans "just went downhill" and that "he wasn't good with his memory or he just couldn't remember a lot of things". Mr Evans' Smoking History
Mr Evans was born on 13 August 1926. He said in evidence that he commenced smoking at the age of 14 or 15, (about 1941) and smoked three packets of cigarettes (20 to a packet) each fortnight until March 1984. He nevertheless agreed in cross-examination that it was probably true that when he was a smoker, "years ago" he smoked at least a pack a day. He did not deny that he smoked until 1990, but said "the wife would know more about it than me".
It is necessary to reconstruct the balance of Mr Evans' smoking history from contemporaneous records.
On 5 May 1992 Mr Evans attended the Woden Valley Hospital for surgical decompression of a right carpal tunnel syndrome. He was seen by a Dr Chanda, who, under the heading Personal History, recorded: "Non smoker for last 2 1/2 years. Used to 30-35 cigarettes/day".
On 14 November 2003 Dr Corbett, a gastroenterologist consulted by Mr Evans, recorded that "He is an ex-smoker stopping 13 years ago". On 18 November 2003 Dr Ross Hendry, Mr Evans' general practitioner, wrote in his notes: Smoker: Ex-Smoker. Quit date: 18/11/1990. I disregard a later entry in the notes of Dr Hendry made on 5 August 2009 where he records; "After discussion with lawyer's letter" … "Smoked until 1984, up to 20 daily".
On 16 December 2003, Mr Evans told Dr Burke, a consultant physician, that: "He has not smoked now for 13 years". On 13 February 2004 he told Dr David Coles, a cardiologist, that he had smoked quite heavily for many years, stopping 13 years ago. A clinical record of the Queanbeyan Hospital dated 7 July 2004 noted that Mr Evans had ceased smoking 14 years previously.
The Canberra Hospital Respiratory Laboratory, which Mr Evans attended for lung function tests on 1 November 2006, recorded a smoking history of 48 pack years over 40 years.
On 3 November 2006 Dr A J Nicholls examined Mr Evans for the Dust Diseases Board of New South Wales and completed a pro- forma smoking history. He was told by Mr Evans that he had smoked 25 cigarettes a day for 40 years, ceasing in 1990.
On 4 April 2007 Mr Evans attended upon Dr A J Nicholls, a consultant thoracic physician, who in a report to Dr Hendry said of Mr Evans that "He has a 40 pack year smoking history." In a subsequent report of 29 January 2008 Dr Nicholls wrote "He stopped smoking in early 1990".
On 17 December 2008 Mr Evans attended the Emergency Department of the Queanbeyan Hospital. Clinical notes taken at the time record: "No cigarettes in 19 years. 30/day till then. Started aged 14".
I believe that the earliest recorded history, given on 5 May 1992 and most proximate to the cessation of smoking, is probably correct; it has been consistently repeated by Mr Evans over the ensuing years. It is probably true that at the age of 14 or 15 Mr Evans smoked much less. It is also probably true that for a time he smoked three packets of cigarettes (20 to a packet) each fortnight. Nevertheless 50 years have elapsed between the time when Mr Evans commenced smoking and the time when he quit. It is probable that for 40 of those years Mr Evans smoked between 20 and 35 cigarettes each day. Mr Evans's Exposure to Asbestos Fibre The Evidence of Mr Evans
Two affidavits of Mr Evans have been tendered and he gave evidence in his home on 28 August 2009.
In his first affidavit Mr Evans said that between 1942 and 1962 he worked at the Lake George mine at Captains Flat. He was 16 years of age when he commenced. After working for some period of time as a labourer, he trained as a carpenter and worked constructing sheds and accommodation for the mineworkers.
Mr Evans said that he worked with asbestos cement sheets on approximately three occasions each week, cutting between 12 and 20 sheets on each occasion. A sheet took approximately 10 minutes to cut, sometimes half an hour. Initially he used fibro cutters and when these were used "there was hardly any dust".
He said that "in later years" he used an electrically powered cutting wheel to cut the sheeting. This activity created a lot of dust that formed a cloud around the worksite and by the end of the day's work he was "covered in dust".
Mr Evans' solicitors, in a letter of instruction dated 10 July 2009 to Dr Leigh, stated that he cut materials with power saws for a period of 30 years. Mr Evans retired in 1990, and it seems probable that the use of power saws commenced in about 1960, shortly before Mr Evans left Captains Flat.
Between 1964 and 1968 Mr Evans was employed as a carpenter by Mr Edward Malone, whose business was dismantling the houses at Captains Flat for relocation at Queanbeyan after the closure of the mine. Mr Evans said that a lot of dust was created when cutting the cement sheeting with an angle grinder when the houses were broken into compartments for transportation, and that he was "covered in dust in a similar fashion to when I worked at the mine".
Between 1968 and 1975 Mr Evans worked for various building companies in the Queanbeyan area. Most of the construction work was building Housing Commission homes clad in asbestos cement that was cut with an angle grinder. When working on these homes Mr Evans says he was exposed to a similar amount of dust as he was at Captains Flat. Not all of the work required cutting and fixing asbestos cement. That work followed the erection of the timber frame.
Between 1975 and 1990, Mr Evans was employed by Queanbeyan Council as a maintenance carpenter. He said in his affidavit that "a lot of the work" involved repairing older fibro buildings, which involved cutting fibro with an angle grinder.
Mr Evans recalled one particular job at Queanbeyan Council, rebuilding the dog pound with thick sheets of asbestos cement. The job took two weeks. He said that he would "often" get covered in dust when doing this work.
In cross-examination Mr Evans rejected the suggestion that there was not much work with asbestos at the Council. He said: "there was actually quite a bit".
Mr Evans was not cross-examined by counsel for Amaca in relation to his evidence of asbestos exposure at Captains Flat. When Mr Evans' evidence was taken, Amaca appeared solely in response to a cross-claim by Queanbeyan City Council. The Captains Flat exposure was not relevant to any claim pleaded by Mr Evans against the Council or by the Council against Amaca. No Browne v Dunn submission is available.
Mr Anthony James Wynd worked as Mr Evans' offsider at the Queanbeyan Council from 1975 to 1990. His affidavit was tendered by Queanbeyan Council. Mr Wynd says that work repairing damaged asbestos cement sheeting on council buildings took place only once every couple of years, occupying a couple of days on each occasion. The work on the dog pound occurred on three or four occasions over the years, occupying a few days each time.
Where Mr Evans' recollection of the work at Queanbeyan Council differs from the recollection of his younger workmate Mr Wynd, I generally prefer the evidence of Mr Wynd. Quantitative Estimation of Asbestos Exposure Mr Alan Rogers
Mr Rogers has 24 years of experience as an occupational hygienist. He is the coordinator of the Occupational Hygiene Panel for the New South Wales Dust Diseases Board.
Mr Rogers says that in his experience carpenters spent only 10 per cent of their time working with asbestos cement products. He further says that, based on his review of the available data, the daily time weighted average exposure of workers cutting, handling and fixing asbestos cement products in the building industry is around 1.25 fibres/ml or less. He concludes that Mr Evans' cumulative exposure to asbestos dust for around 10 per cent of his working time over 27 years amounts to 3.24 fibre/ml/years or less.
I do not find this evidence persuasive. No other witness with relevant experience estimates that carpenters spent only 10 per cent of the time working with asbestos cement products. If Mr Rogers were correct, a carpenter working with asbestos cement products from the age of 15 to retirement at the age of 60 would accumulate an asbestos dose of no more than 6.25 fibre/ml/years. Such a calculation cannot stand with the circumstance that some carpenters contract asbestosis. The lowest threshold for that disease is 25 fibre/ml/years. Mr Geoffrey Pickford
Mr Pickford is an occupational hygienist with 37 years experience retained by Amaca. He has purported to reconstruct Mr Evans' work experience in terms of a typical carpenter working with a mixture of asbestos and non-asbestos tasks as part of his day-to-day duties.
Pursuant to this reconstruction Mr Pickford estimates Mr Evans' cumulative fibre burden as between 3 and 13 fibre/ml/years.
Mr Pickford proceeded by assigning a particular concentration of airborne asbestos fibres to the various tasks involved in asbestos cement construction, and multiplying those concentrations by the time spent on each task.
He says that, on the basis of his experience of typical jobs in the field, the percentage times for each phase of construction, and the resultant fibre exposures, are as follows; Task % Exposure (fibres/mL) Carrying and handling asbestos-cement 20% 0.60 Measuring and other planning activities (asbestos-cement) 26% 0.05 Using hand cutting methods 30% 0.40 Nailing or screwing asbestos-cement 20% 0.10 Using power saws and grinders 4% 20.00 Total time working with asbestos cement 100%

The "time weighted average" of these exposures calculates out to approximately 1.1 fibres/ml. 37. Introducing the concept that Scenario A and Scenario B represent "worst case" and "typical conditions" respectively, Mr Pickford said that it is reasonable to assume that the actual exposures may have been between 1.5 and 0.9 fibres/ml. 38. Mr Evans gave no evidence which assists the estimation, however, on the face of it, the 20 per cent carrying and handling asbestos cement seems very low. The 26 per cent allowance for measuring and planning, with no actual work being done, seems high. 39. There is however within Mr Pickford's own material sufficient evidence to cast doubt upon his conclusions. 40. Mr Pickford assumed that the exposure when using power saws or grinders was 20 fibres/ml. He does however refer to a study by Kumagai who reported 60 fibres/ml, and a table to a British Regulation which listed 60-63 fibres/ml for this work. A German study by Rodelsperger, who took dust measurement at 40 building sites during the cutting and fixing of asbestos cement sheets in roofing and siding work, found that the airborne asbestos fibre measurements in the breathing zone of the operators during the cutting period were as high as 41 fibres/ml. 41. Mr Pickford prepared a further table upon the assumption that power saws were not used as follows: Task % Exposure (fibres/mL) Carrying and handling asbestos-cement 20% 0.60 Measuring and other planning activities (asbestos-cement) 26% 0.05 Using hand cutting methods 30% 0.40 Nailing or screwing asbestos-cement 24% 0.10 Total time working with asbestos cement 100%

The "time weighted average" of these exposures calculates out to approximately 0.3 fibres/ml. Mr Pickford states that it is reasonable to assume that the above estimate may be 0.4 and 0.2 fibres/ml for Scenarios A and B respectively.
He then goes on to say that if a mixture of hand and power tools were used, and the proportion of each is unknown, it is reasonable to assume that the exposure may be the average of the figures produced on each table, giving 1.0 fibres/ml for Scenario A and 0.6 fibres/ml for Scenario B. He then applied those figures to calculate Mr Evans' cumulative fibre burden.
This approach is unreasonable. The first table proceeded upon the basis that 30 per cent of Mr Evans' time was spent cutting with hand tools, in addition to the 4 per cent cutting with power tools. By mathematical artifice Mr Pickford effectively reduces the percentage time cutting with power tools to 2 per cent. The study by Rodelsperger found that the cutting time to working time varied from 3 per cent to 13 per cent, with a mean value of 5.7 per cent. A "worst-case" scenario should adopt the upper limit of 13 per cent.
I am not persuaded that Mr Pickford's tables and calculations fairly reflect the accumulated fibre burden of Mr Evans.
If Mr Pickford's time weighted average exposures are varied so as to substitute 40 fibres/ml concentration in lieu of 20 fibres/ml, and 13 per cent time using power saws or grinders in lieu of 4 per cent, (the time assigned to measuring and planning activities being reduced by 9 per cent accordingly), the time weighted average when working with power tools is 5.46 fibres/ml. Determination of Mr Evans' Cumulative Asbestos Exposure
It is quite apparent that the estimation of cumulative exposure is fraught with uncertainty. Mr Rogers worked on the basis of a time weighted average of 1.2 fibres/ml or less. Mr Pickford calculated that the time weighted average of men working with power tools was 1.1 fibres/ml but suggested an appropriate range was between 0.9 and 1.5 fibres/ml. (Nevertheless calculating Mr Evans' cumulative burden upon a highest figure of 1.0 fibres/ml).
In a report of 24 February 2010 tendered by Amaca, the epidemiologist Professor Berry refers to a Dust Diseases Board estimate that Mr Evans worked with an average level of exposure of 5.2 fibres/ml. Mr Rogers is the coordinator of the Occupational Hygiene Panel of the Board and I assume that that calculation was made in accordance with protocols with which Mr Rogers concurred.
Because of the inherent uncertainty in the exercise, I propose to accept this figure and calculate Mr Evans' cumulative exposure upon assumptions that I believe reflect the upper limit of his probable exposure. Working with Hand Tools at Captains Flat 1942-1960
I adopt Mr Pickford's estimate of 0.4 fibres/ml as the time weighted exposure of Mr Evans when working at Captains Flat with hand tools on asbestos cement sheets. It accords with the time weighted average of construction workers who did not operate power saws in a James Hardie field study conducted in 1980.
Because it is inconsistent with other evidence of a general nature, I do not accept Mr Evans' statement that he worked with asbestos cement three days each week, that is, 60 per cent of his working time, at Captains Flat as accurate. The work fixing the cladding to a new house is a relatively small task compared to building the frame and the roof, and fitting out the windows and interior joinery.
Mr Alan Rogers said that in his experience carpenters generally only worked with asbestos cement sheeting for 10 per cent of their working time. Mr Pickford said 20 per cent to 40 per cent of the time. Professor Breslin, who has treated many carpenters with lung diseases, says that they generally spend 15 to 30 per cent of the time working on asbestos cement.
I will assume that, because of something unusual about the conditions, Mr Evans worked 40 per cent of his time with asbestos cement at Captains Flat, that is two days each week.
The standard fibre/ml year contains 48 weeks each of 40 hours, that is, a total of 1920 hrs. The cumulative fibre burden acquired by Mr Evans in the 18 years of working with hand tools at Captains Flat may be calculated as follows: 8 hours 2 days = 16 hours. 16 hours 48 weeks = 768 hours. 768 hours 0.4 fibre/ml = 307.2 fibre/ml/hours. 307.2 fibre/ml/hours 1920 hours = 0.16 fibre/ml/years. 0.16 fibre/ml/years 18 years = 2.88 fibre/ml/years. Working with Power Tools at Captains Flat 1960-1962
16 hours x 48 weeks = 768 hours 68 hours 5.2 fibres/ml = 3993.6 fibre/ml/hours. 3993.6 fibre/ml/hours 1920 hrs = 2.08 fibre/ml/years. 2.08 fibre/ml/years 2 years = 4.16 fibre/ml/years. Working with Mr Malone Relocating Houses 1964 - 1968
Mr Evans did not estimate the time spent working with asbestos cement in this employment. He did say that, in order to break the house into compartments; "you might take the laundry off and the rest of the house would fit on the low loader and be transported into town". I think it reasonable to assume that the work with fibro occupied no more than 15 per cent of the working time and that, because power tools were used, the fibre concentration during the work averaged 5.2 fibres/ml. The calculation is as follows: 6 hours each week 48 weeks = 288 hours. 288 hours 5.2 fibres/ml = 1497.6 fibre/ml/hours 1497.6 fibre/ml/hours 1920 hrs = 0.78 fibre/ml/years. 0.78 fibre/ml/years 4 years = 3.12 fibre/ml/years. Work with Various Builders 1968 - 1975
Mr Evans did not say how much of his time was occupied in working with asbestos cement during these years, however he did say that some of the houses were brick veneer, and some were fully brick buildings. I will assume that he worked with asbestos cement sheeting for 30 per cent of his time. 30 per cent of 40 hours is 12 hours 12 hours each week 48 weeks = 576 hours. 576 hours 5.2 fibres/ml = 2995.2 fibre/ml/hours 2995.2 fibre/ml/hours 1920 hrs = 1.56 fibre/ml/years. 1.56 fibre/ml/years 7 years = 10.92 fibre/ml/years. Work with Queanbeyan Council 1975-1990
Although Mr Wynd does not recall any work constructing the dog pound, it may have been that he was absent on vacation when this work was done. I will assume that the work took place over two weeks as Mr Evans states, that, because of the thickness of the compressed asbestos sheets, the average fibre count was double the 5.2 fibres/ml assumed in earlier calculations for work on thin sheets, and that 50 per cent of the building time was occupied in working with asbestos cement. The calculation is as follows: 40 hours 10.4 fibres/ml = 416 fibre/ml/hours. 416 fibre/ml/hours 1920 hrs = 0.2 fibre/ml/years.
Mr Wynd recalls working on the dog pound on three or four occasions for a few days each time. I think it reasonable to allow a further equivalent figure of 0.2 fibre/ml/years in respect of this work.
I discount somewhat the evidence of Mr Wynd in relation to building repairs, because of his recollection of multiple purchases of asbestos cement sheeting. I will assume that on average Mr Evans spent two days each month effecting repairs with asbestos cement. I do accept the evidence of Mr Wynd that fibro cutters were used when doing this work, because the use of such tools for small jobs seems more convenient than arranging for the connection of electricity.
Hardies ceased asbestos cement manufacture in 1986. The calculation is as follows: 16 hours 11 (months) = 176 hours. 176 hours 0.4 = 70.4 fibre/ml/hours. 70.4 fibre/ml/hours 1920 = 0.037 fibre/ml/years. 0.037 fibre/ml/years 11 years = 0.4 fibre/ml/years.
The cumulative fibre burden is then; Working with Hand Tools at Captains Flat 2.88 fibre/ml/years Working with Power Tools at Captains Flat 4.16 fibre/ml/years Working with Mr Malone 3.12 fibre/ml/years Work with Various Builders 10.92 fibre/ml/years Work on dog pound at Queanbeyan Council 0.4 fibre/ml/years Work on Repairs at Queanbeyan Council 0.4 fibre/ml/years Total 21.9 fibre/ml/years. Expert Evidence Dr James Leigh
Dr Leigh was qualified by Mr Evans' solicitors to give evidence in this matter. In the letter of instruction he was asked to assume that Mr Evans had extensive regular exposure to asbestos when working as a carpenter with asbestos cement materials from 1942 to 1990, except for the period 1962-1964.
Dr Leigh is firmly of the opinion that, in every case where a person who has contracted lung cancer has inhaled asbestos fibres, those fibres have contributed to the development of the cancer. Dr Leigh concedes that in a particular case the contribution may be very small but nevertheless the asbestos "must have done something" (T100.46).
His belief is based upon the following circumstances: (a) Epidemiological studies demonstrate that inhalation of asbestos fibres increases the risk of contracting lung cancer and no threshold, below which there is no risk, has been demonstrated. (b) Carpenters are an occupational group well recognised to be at high risk of asbestos related malignancy. (c) Laboratory and animal studies confirm the primary carcinogenic properties of asbestos and: "If a certain chemical reaction takes place in a test-tube -science would assume that the same chemical reaction is going to take place in the body". (T 85.9) (d) Epidemiological studies have established that tobacco smoke and asbestos exposures interact synergistically in increasing the risk of contracting lung cancer. (e) The hypothesis that in all cases asbestos inhalation contributes to the development of lung cancer is medically plausible. Recently published studies suggest that; "If both agents are present then both are acting biologically in producing either tumours, or, in the early stages of carcinogenesis, mutations. They actually demonstrate a more than additive interaction between the tobacco agent and the asbestos, in fact, in a biological sense as opposed to an epidemiological sense." (T 91.29)
The opinion of Dr Leigh is summarised at page 6 of his report of 22 July 2009 (PX 3(A)) where he says: While the precise mechanism of interaction between asbestos and tobacco smoke in causing lung cancer is not known, it is not possible in my view to separate their effects on the individual case when both have acted, as they must do to some extent from a purely physico-chemical point of view , and it is thus more probable than not, that in this situation, the lung cancer was the singular result of the two factors acting together. (Emphasis added)
A similar opinion of Dr Leigh, considered by the High Court in Amaca Pty Ltd v Ellis [2010] HCA 5, was expressed in almost, but not quite, identical language. In his report to the plaintiff's solicitors in that case (Amaca 22) Dr Leigh wrote: While the precise mechanism of interaction between asbestos and tobacco smoke in causing lung cancer is not known, it is not possible in my view to separate the effects on the individual case when both have acted and it is thus more probable than not, that in this situation, the lung cancer was the singular result of the two factors acting together. It is however true that exposure to either factor alone is capable of causing lung cancer.
The words to which I have added emphasis in the Evans report do not appear in the Ellis report. In relation to the Ellis report the High Court said: Reading his opinion as a whole, it is evident that Dr Leigh did not express the view that, if a smoker has been exposed to asbestos and develops lung cancer, the asbestos exposure is, or is probably, a cause of that cancer.
The High Court came to this conclusion because Dr Leigh also said that, for "legal or administrative" reasons, it was possible to apportion causal connection between the two carcinogens, asbestos and tobacco, in accordance with a mathematical model.
In giving evidence before me Dr Leigh sought to explain the reasons for applying this mathematical model. He said that the High Court misunderstood his evidence, and that in Ellis he intended to express the opinion that the causal contributions of asbestos and tobacco could not be apportioned on a biological or mechanistic basis (Transcript 87.14).
He also said: The model I used was chosen from a number of models and it's a model that is the so-called Chase model which was a model written, created or designed in 1985 on behalf of John Mandel Corporation, the big asbestos American company, for equitable apportionment of liability in these very sorts of cases. The model actually includes a multiplicative term and a term for each of the individual items. It's a totally artificial model that bears no relationship to the biological reality and that's admitted in the preamble to the paper and the whole discussion, the whole thing. (Transcript 95.7)
It is appropriate to here interpolate the evidence of Dr Geoffrey Berry, the eminent biostatistician and epidemiologist, concerning the Chase model. He said: It may or may not have a relationship to what's happening biologically, but it is a mathematical construct and the basis of it was that if there were two parties involved in a case like this, if there was a tobacco company involved, then it would be a fair way of subdividing any damages that might be awarded between those parties. (Transcript 207.2)
Specifically in relation to Mr Evans, Dr Leigh said: I say he is dying from the combined cause of smoking and asbestos, but I say the Courts of Justice [are] entitled to make some sort of apportionment on the basis of the relative exposures. (Transcript 102.7)
In an earlier exchange Dr Leigh had said this: A Well, there are two areas here, there is the mechanistic side where I maintain that both are present, both are doing something towards ultimate carcinogen just by a matter of physics and chemistry and what we know from animal cellular level studies. On the other hand you have the epidemiological effect and you have the-almost the public policy issue it's almost impossible to say in these cases, you can't partition out the relative effects by any biological means, put it that way, but if you want to for public policy or some sort of justice and equitability of compensation and overriding the principle of solidarity liability, there are ways of doing it. That's as far as I can take it but I think the High Court got it wrong when I said, you know, you can separate them on a biological basis, I think they got that wrong, they misread the evidence.
It is plain that Dr Leigh, who has a Bachelor of Legal Studies from Macquarie University, is very much aware of the debate surrounding merits of the common law doctrine of solidary damages pursuant to which multiple tortfeasors are each liable for the whole of the plaintiff's damages rather than proportionately in accordance with their responsibility for the loss suffered. (See for example Swanton, J and McDonald, B Reforms to the Law of Joint and Several Liability (1997) 5 TLJ 109 at 114-115.)
Dr Leigh does not hold with the solidary principle. In his report of 22 July 2009 Dr Leigh wrote: My personal opinion is that since asbestos and smoking are inseparable agents in the individual case, there will always be some contribution to causation by the asbestos, even at exposures much less than 25 fibre/ml/years and this should be proportionally compensated, taking the smoking history and any possible genetic susceptibility into account. In evidence Dr Leigh said; A I'm actually saying it's up to the courts to look at it this way, and for them to make the apportionment. I'll say this-even though the apportion model is artificial, I believe it's the way the court should deal with this type of case Q As a matter of policy? A It's a matter of policy.
Despite his reservations as to the utility of the exercise in assessing material contribution, Dr Leigh in accordance with the mathematical construct, and upon assumptions that Mr Evans had a relative risk from smoking of RR 2.5 and from asbestos of RR 2, apportioned the risk factors in these proportions: Asbestos alone = 20 per cent Smoking alone = 30 per cent Interactive effect of smoking and asbestos = 30 per cent Background = 20 per cent
The Chase model to which Dr Leigh refers was adopted by the defendant's experts in Workers Compensation (Dust Diseases) Board of NSW v Smith, Munro and Seymour [2010] NSWCA 19 in an attempt to demonstrate that, in proportion to the causal agent of tobacco smoking, the contribution of asbestos inhalation was minimal.
Basten JA, with whom Allsop P and Handley AJA agreed, observed at [69] that where smoking and asbestos worked interactively, the mechanism of interaction was not known, and the empirical basis upon which the exercise was undertaken was not explained in evidence, the modelling was not helpful in resolving the issue of causation. The question for determination was not whether the inhalation of asbestos dust was a major or predominant cause, but whether it made "a material contribution" to the contraction of the lung cancer.
At [72] His Honour said: One factor can materially contribute to an outcome even though, relative to another factor it has a minor effect. All that is required is that the effect be "material". That required an evaluative judgment on the part of the court.
Notwithstanding his opinion that both smoking and asbestos contributed to the development of Mr Evans' lung cancer, Dr Leigh was unable to say that, more probably than not, Mr Evans would not have contracted the cancer in the absence of the asbestos exposure. (Transcript 84.29, 86.41).
When asked to assume the accuracy of a report by Dr Michael Jones, a radiologist, that Mr Evans suffered from extensive diffuse pleural thickening and multiple calcified plaques, Dr Leigh said this: "From the description of the extent of the pleural thickening it strengthens my confidence in making the statement that there was considerable asbestos exposure. I'm more confident in making that statement". (Transcript 90.1)
The statement, which is strengthened by the radiology, is not that diffuse pleural thickening, of itself, increases the risk of contracting lung cancer, but that it is a marker of exposure.
Dr Leigh also said that because of a rate of clearance from the lungs after exposure ceases, the asbestos fibre levels in Mr Evans' lung at the time he ceased working with asbestos would have been considerably higher than when those levels were counted by the pathologist Professor F D Pooley after Mr Evans contracted lung cancer. (Transcript 92.45, 97.48)
Dr Leigh said that in his opinion, the lifetime exposure of Mr Evans to asbestos amounted to 40 fibre/ml/years. He said that this was because of a long history of exposure, the presence of extensive pleural plaques and diffuse pleural thickening, and his experience in similar cases in which he has seen hygienist reports on lifelong carpenters (Transcript 94.30).
One difficulty in accepting the opinion of Dr Leigh is that the employment history of Mr Evans did not reflect that of the average lifelong carpenter working on asbestos cement products with power tools. His work at Captains Flat between 1942 and 1960 involved no power tools but rather the use of fibro cutters which generated minimal dust. The last 15 years of his working life, at Queanbeyan Council, involved very little contact with asbestos cement products. Dr A J Nicholls
Dr Nicholls examined Mr Evans on 3 November 2006 at the request of the Dust Diseases Board of New South Wales for the purpose of assessing occupational lung diseases.
He was told that Mr Evans had worked for a considerable time with asbestos with a building company, and with the Queanbeyan Council. Dr Nicholls diagnosed pleural plaques secondary to asbestos exposure.
Mr Evans continued under the care of Dr Nicholls who diagnosed the lung cancer, referring Mr Evans to Dr John Tharion who performed a left thoracotomy and lobectomy on 21 February 2008.
In his report of 29 April 2009 to Mr Evans' solicitors, Dr Nicholls noted that Mr Evans had a 40 pack years smoking history plus a significant occupational lung history. He expressed the opinion that Mr Evans' lung cancer was caused by smoking and "significant exposure to asbestos". He relied not only on the history but also upon "objective evidence of very significant asbestos exposure based on the finding of extensive calcified pleural plaques".
Dr Nicholls made no quantitative assessment of the extent to which Mr Evans' smoking history or asbestos exposure increased his risk of contracting lung cancer.
In a further report of 18 December 2009, Dr Nicholls reported that he had received an amended smoking history from Mrs Evans. He stated that his opinion that the asbestos had made a significant contribution to the development of Mr Evans' lung cancer was now "based on his prolonged exposure to asbestos and the fact that Mr Evans had only a minor smoking history (nine pack years) and his cessation of smoking 24 years prior to the diagnosis of cancer".
Dr Nicholls also relied upon a study by Kjuus et al which reported an increased risk of lung cancer of 4.1 "if heavy asbestos exposure was added to light smoking".
I do not find the opinion of Dr Nicholls persuasive in circumstances in which the contributing factors are reversed. During 18 of the 20 years that Mr Evans spent working at Captains Flat he cut the asbestos cement with fibro cutters which produced "hardly any dust". During his 15 years with Queanbeyan Council Mr Evans was exposed to a relatively small asbestos fibre burden. His smoking history was not "light smoking" but "heavy smoking". Dr John Tharion
Dr Tharion saw Dr Evans at the request of Dr Nicholls and performed surgery on 21 February 2008. His operation findings were as follows: There was a tumour situated on the left lower lobe. There were large pleural plaques all through the pleural surface with areas of calcification. The mass had not extended to the pleural surface. The lungs were grossly emphysematous and there was evidence of carbon deposition and it was easily friable. There were also some adhesions between the lung and the chest wall as well as to the aorta, which was more due to inflammation rather than a neoplastic process. There were only a few firm lymph nodes palpable.
In a report of 11 January 2010 to Mr Evans' solicitors, Dr Tharion said that it was more than probable that Mr Evans' lung cancer had been materially contributed to by his exposure to asbestos because; "It is well-known that people who have exposure to asbestos and also smoke have got a much higher incidence than people who smoke". Dr Tharion was not required for cross-examination. I do not think that this expression of opinion carries much weight in the resolution of the issue because Dr Tharion's reasoning process does not address either the mechanism of the process or the relative extent of any contribution. Dr Michael Jones
Dr Jones is a radiologist qualified by the defendant's solicitors whose report of 2 September 2009 was tendered in Mr Evans' case.
Dr Jones reviewed CT scans taken on 8 March 2002 and 19 January 2007. In relation to the scan of 8 March 2002 he reported that there were multiple fibrous and calcified typical asbestos pleural plaques bilaterally, which were predominantly fibrous but with early calcification. He also reported diffuse pleural thickening in both posterior mid and lower zones about 10 x 8 cm in extent on each side.
In relation to the scan of 19 January 2007, Dr Jones reported that the asbestos pleural plaques and diffuse pleural thickening had become a little more prominent, increasing in thickness and the extent of calcification indicating plaque ageing.
Dr Jones wrote; "In summary this imaging shows typical asbestos pleural plaques and diffuse pleural thickening indicating asbestos exposure has occurred."
Dr Jones was not required for cross-examination. Professor A B X Breslin
Professor Breslin is a highly eminent consultant thoracic physician qualified by Mr Evans' solicitors. He was instructed that Mr Evans had very significant asbestos exposure, working as a carpenter between 1942 and 1990.
Professor Breslin attended upon Mr Evans at the latter's home. Mr Evans told him that from the age of 14 to the age of 58, he smoked three packets (20 per pack) of cigarettes every two weeks.
In a report of 11 January 2010 Professor Breslin said that, based on the history, he believed that Mr Evans had significant asbestos exposure over his working life and that it reached 25-55 fibre/ml/years. He said that there was both x-ray and surgical evidence of pleural plaque formation confirming asbestos exposure.
Professor Breslin also said that, although Mr Evans had been a reasonably light smoker, his smoking was sufficient to cause emphysema and definitely sufficient to raise the likelihood of his developing lung cancer, because some individuals are more sensitive to cigarette smoke than others.
Professor Breslin wrote that he believed that Mr Evans' lung cancer was due to a combination of his cigarette smoking and his asbestos exposure for these reasons:
1. There was a significant smoking history of 9 pack years which increased the risk of developing lung cancer.
2. Lung cancer developing as a consequence of cigarette smoking may occur many years after cessation of smoking.
Mr Evans fulfilled the "Helsinki Criteria for Attribution of lung Cancer to Asbestos Exposure."
The Helsinki criteria formerly fixed 25 fibre/ml/years as the cumulative dose at which the risk of contracting lung cancer from asbestos is doubled. Those criteria have been modified by their proponents so as to now reflect a doubling of the risk of contracting lung cancer from the mixed asbestos fibres found in asbestos cement at 50/ml/years. Mr Evans exposure of 21.9 fibre/ml/years fulfils neither criteria.
In evidence Professor Breslin said that the presence of pleural thickening in the CT scan of 8 March 2002 was a matter that he took into account when expressing his opinion, because such abnormality may occur with asbestos exposure. He added that although the pleural thickening resulted as a consequence of resolving pleural effusions, those pleural effusions may occur at relatively low levels of asbestos exposure.
In cross-examination Professor Breslin agreed that pleural plaques may also occur at relatively low doses of asbestos, and that persons suffering from pleural plaques had no increased risk of lung cancer in the absence of asbestosis.
Professor Breslin conceded that if the cumulative dose of asbestos was not greater than 25 fibre/ml years, (which he took to be the Helsinki Criteria) but rather 3.4 to 13 fibre/ml/years, and if the lung fibre burden measured by the pathologist Professor Pooley was only 13 per cent of the Helsinki criterion for that value, then Mr Evans' lung cancer was "not a lung cancer associated with inhaling asbestos".
In re-examination Professor Breslin said that he had seen the CT scans, and did not share the opinion of Dr Michael Jones that the pleural thickening was diffuse. He also said that the degree of plaques and pleural thickening observed by him was not inconsistent with exposure in the range of 3.4 to 13 fibre/ml/years. It follows that it is not inconsistent with the greater exposure of 21.9 fibre/ml/years, at which concentration the risk of contracting lung cancer from asbestos exposure still does not fulfil the Helsinki criteria. Professor Martin Tattersall
Professor Tattersall, also an eminent physician, examined Mr Evans on 14 August 2009 at the request of the solicitors for Queanbeyan Council. Mr Evans related his history of asbestos exposure between 1942 and 1990 and told Professor Tattersall that his heaviest exposure was during 1942-1964 at Lake George Mines, and that his exposure with the Queanbeyan Council was minor.
Mr Evans told Professor Tattersall that he smoked three packets of 20 cigarettes each two weeks until the age of 58 (1984). Mrs Evans, who was present, said that she met Mr Evans in 1950, and that he was never a heavy smoker. I do not accept that this was the correct history.
In his report of 20 August 2009 Professor Tattersall expressed the opinion that: for some asbestos exposed people without asbestosis and notably those with pleural plaques as the only tissue marker of post asbestos exposure, the increase in the risk of lung cancer, if it exists, may be small after allowance for other factors such as tobacco smoke.
Professor Tattersall went on to state his belief that, on the balance of probabilities, occupational exposure to asbestos dust and fibre (and particularly during his employment by Queanbeyan City Council between 1975-1990) did not cause or make a material contribution to the development of Mr Evans' lung cancer.
Professor Tattersall said that he would not change his opinion upon the assumption that Mr Evans had a cumulative asbestos exposure of between 3 and 14 fibre/ml/years because, on his reading of the literature, 25 fibre/ml/years was the absolute bottom end of any risk calculation for lung cancer.
In cross-examination Professor Tattersall said that pleural thickening has many causes. He did not accept that the presence of diffuse pleural thickening indicated a much more extensive exposure to asbestos than mere pleural plaques because, as he said, "I don't know if it's true".
Professor Tattersall did accept that there was an interaction in lung tissue between the effects of cigarette exposure and asbestos fibre exposure, but that "the extent to which they interact has been a subject of considerable controversy over recent years".
Professor Tattersall agreed that Dr Leigh's explanation of the interaction between tobacco and asbestos was a plausible hypothesis, although the evidence is incomplete. He added that the epidemiological evidence did not support any correlation between asbestos exposure and increased risk of lung cancer in non-smokers.
When asked specifically whether it would be reasonable to attribute Mr Evans' lung cancer to the work at Lake George Mines Professor Tattersall replied: "Certainly not". Professor F D Pooley
Professor Pooley is a Research Professor in the Cardiff University School of Medicine attached to the Department of Pathology Medical Microscopy Sciences Group. He examined a lung tissue sample taken from Mr Evans and estimated the lung fibre burden, reporting that; "The levels of amphibole asbestos fibres detected are well in excess of those considered to be related to an environmental asbestos exposure but are equivalent to a low level occupational exposure".
Professor Pooley's findings represent 13 per cent of the fibre burden required by the Helsinki criterion for attribution of lung cancer to asbestos exposure. However, because the lung continually clears asbestos fibres, and because of the usually long time between Mr Evans' last exposure, this fibre count may not reflect the true fibre counts in Mr Evans' lungs at the time his exposure ceased. Professor Geoffrey Berry
Professor Berry has been for many years an internationally renowned epidemiologist. His expertise is beyond question. He prepared two reports concerning the relative risks of smoking and asbestos that confronted Mr Evans.
Professor Berry describes the epidemiological tools by which the relative risks from asbestos and smoking are measured.
Risk is usually expressed in terms of the measure relative risk (RR). This is defined as the ratio of the risk of disease or death among the exposed to the risk among the unexposed. Thus if no greater number of persons in the exposed population contract the disease or die than do in the unexposed population, the ratio is 1:1 and the relative risk is RR 1. If double the number of persons in the exposed population contract the disease or die, compared to the unexposed population the ratio is 1:2 and the relative risk is RR 2.
Another measure of risk is attributable fraction among the exposed. This is defined as (RR-1)/RR, so that a relative risk of RR 9 for smoking gives an attributable fraction of 8/9 = 89%. An interpretation of this figure is that 89 per cent of lung cancers in persons who smoke to that degree are attributable to smoking and 11 per cent are background cases.
Professor Berry was asked to assume that Mr Evans was a cigarette smoker from 1940 to 1990 and that he smoked an average of 20 cigarettes a day. Upon this history epidemiological tables included in Professor Berry's report assign to Mr Evans a relative risk of RR 9 after taking into account the reduction in risk over the years since 1990 when he ceased smoking.
Professor Berry was also asked to assume that Mr Pickford's assessments of Mr Evans cumulative fibre burden at 3.4-13 fibre/ml/years were correct.
The relative risk of exposure to asbestos fibres varies in accordance with their toxicity, amphibole fibres being far more toxic than chrysotile fibres. The mix of fibres in asbestos cement products is usually in the proportion 40 per cent of amphibole to 60 per cent chrysotile. Dr Berry says that, according to epidemiological studies, the risk of contracting lung cancer from exposure to such a mix is doubled at a cumulative dose of 50 fibre/ml/years.
The relative risk of contracting lung cancer from exposure to asbestos cement products is then 1+ (estimated fibre/ml/years)/50. Mr Pickford's estimates result in relative risks of RR 1.07 and 1.26.
There is a synergistic effect between asbestos and smoking in the causation of lung cancer so that the combined effect of asbestos exposure and smoking on the risk is approximately multiplicative. The effect of the synergy can be given mathematical form by multiplying together the relative risks of smoking and asbestos and deducting the sum of those risks.
Professor Berry prepared the following table based on this multiplicative model, subdividing Mr Evans' risk of lung cancer into components representing the percentage contributions of the different risks where his relative risk from asbestos was RR 1.26 and his relative risk from smoking was RR 9. RR due to asbestos = 1.26 RR due to smoking = 9 a) Due to asbestos alone 2% b) Due to smoking alone 71% c) Addition due to asbestos-smoking combination 18% d) Background risk 9%

It is appropriate to note of that in his report of 24 February 2010, Professor Berry referred to the Dust Diseases Board estimating Mr Evans' cumulative exposure at 54.6 fibre/ml/years based upon an average level of exposure of 5.2 fibres/ml. If the Dust Diseases Board worked upon the assumption that Mr Evans was exposed to an average concentration of 5.2 fibres/ml during 30 per cent of his working time, then the further assumption must have been that this work continued for 35 years. That further assumption is not warranted on the evidence. Discussion of the Epidemiological Evidence
Professor Berry's table of smoking risks lists the relative risk of smoking 20-29 cigarettes per day over 40+ years at RR 44.9. I have found that to be Mr Evans smoking history.
By 2008 when Mr Evans was diagnosed with lung cancer he was an ex-smoker of 18 years. Professor Berry in this circumstance reduces his relative risk to 24 per cent of the previous figure, that is 10.7. The attributable fraction of lung cancers in persons who smoke to that degree is 90 per cent.
I have found that Mr Evans' cumulative fibre burden was 21.9 fibre/ml/years. In accordance with Professor Berry's method this reflects a relative risk of 1 + 21.9/50 = RR 1.43. The attributable fraction of lung cancers in persons who are exposed to asbestos in that degree is 30 per cent.
If the risk created by exposure to both smoking and asbestos was merely additive, the combined risk would be RR 1 + RR 9.7 + RR 0.43 = RR 11.13. Epidemiologically the actual risk corresponds to RR 15.3 because of the multiplicative affect.
Upon these figures the table prepared by Professor Berry subdividing the various risks would read as follows: RR due to asbestos = 1.43 RR due to smoking = 10.7 a) Due to asbestos alone 3% b) Due to smoking alone 63% c) Addition due to asbestos-smoking combination 27% d) Background risk 7%

The risk of Mr Evans contracting lung cancer from the combined effects of smoking and asbestos was 30 per cent, less than half the 70 per cent risk that he would contract the disease because of his exposure to smoking and background risks.
This information is perhaps more easily grasped when reduced to a further table. If the background incidence of lung cancers is 100 in a given population, then the odds ratios relevant to Mr Evans' circumstance predict that over time the following lung cancers will occur: Cause of Cancer No. % Background (RR 1) 100 7% Additional cancers attributable to smoking alone (RR 10.7) 970 63% Additional cancers attributable to asbestos alone (RR 1.43) 43 3% Additional cancers attributable to the synergistic effect of smoking and asbestos exposure 417 27% Total 1,530 100%

Of the total number of 1530 persons who will contract lung cancer, epidemiology predicts that 1070, or 70 per cent, will contract the disease because of smoking or background risk. Only 460 additional persons, or 30 per cent, will contract the disease because of either asbestos exposure alone or the increased risk generated by the combination of smoking and asbestos.
Only in those 460 additional cases was asbestos exposure a necessary condition to the contraction of the disease.
Epidemiology is concerned with populations, not individuals. Mr Evans may be one of those 460 additional cases, however from a statistical point of view, the probability is that he is one of the 1070 cases where the lung cancer occurred independently of asbestos exposure. The plaintiff's submissions
Mr Little SC argues that: (a) In all cases where lung cancer is contracted following exposure to the carcinogens cigarette smoke and asbestos, each agent materially contributes to to the development of the disease. (b) In the alternative, the fibre burden of Mr Evans was probably sufficient to materially contribute to his lung cancer in any event. The "In the All Cases" Argument
The case for the proposition that both tobacco smoke and asbestos contribute to the development of lung cancer in all cases is theoretically sound. Dr Leigh discusses the theory at page 5 of his report where he writes: Tobacco smoke can act at early stages, inducing genetic alterations, DNA adducts, and mutations in genes critical to cancer formation. It is likely that the chemical basis of tobacco induced mutations is oxidisation of DNA groups by free radicals. Epidemiological evidence suggests that tobacco may also act at later stages of the cancer process. Tobacco smoke has both gaseous and particulate components. The latter can stimulate macrophages to release cytokines and free radicals. Asbestos can be cytotoxic (killing cells) and genotoxic (damaging genes) and may cause proliferative lesions in the lungs. Asbestos fibres can generate free radicals either directly or after attempted phagocytosis by macrophages…. asbestos is genotoxic to bronchial epithelial cells. Asbestos may cause chronic inflammatory changes which release cytokines (including growth factors), providing a selective advantage for cells which have undergone cancerous mutation due to carcinogens in the tobacco smoke or due to asbestos in itself. Recent animal studies have directly shown interaction between known long carcinogens of the type found in tobacco smoke and asbestos in causing lung cancer. While the precise mechanism of interaction between asbestos and tobacco smoke in causing lung cancer is not known, it is not possible in my view to separate the effects on the individual case where both have acted, as they must do to some extent, from a purely physico-chemical point of view, and it is thus more probable than not, that in this situation, the lung cancer was the singular result of the two factors acting together.
Two scientific papers tendered in evidence by the plaintiff indicate that a particular tobacco smoke carcinogen strongly enhances the mutagenic effect of amosite when both substances are injected into laboratory rats (PX 4, PX 5). A further paper suggests that the best mechanistic explanation for the multiplicative effects of tobacco and cigarette smoke involves a model where asbestos fibres serve as a vehicle to deliver concentrated doses of tobacco carcinogens to the nucleus of the target cell (PX 6).
Yet another paper suggests that "some smokers" may be genetically predisposed to lung cancer as a result of mutations in DNA repair pathways, or, alternatively, acquired mutations or deletions in key genes involved in DNA repair may facilitate accumulation of additional genetic mutations induced by tobacco smoke carcinogens during the early stages of development of lung cancer.
All experts agree that the precise mechanism of interaction between asbestos and tobacco smoke in causing lung cancer is not known.
I am persuaded that asbestos and cigarette smoking may act in combination in contributing to the development of lung cancer.
I am not persuaded that in all cases, and in particular in this case of Mr Evans, that the contribution of asbestos must have occurred, or if it did, that the contribution was material.
First, because both Professor Breslin and Professor Tattersall, while accepting the theory, dismissed the contribution of asbestos in Mr Evans' case because of its relative insignificance. I accept that a contribution may be material although it is minor but I believe that, in context, the opinions of both medical experts are to the effect that the contribution was not minor but insignificant, that is to say, immaterial.
Secondly, because Dr Leigh concedes that in a particular case the contribution of asbestos may play a very small part, and that he could not say that, more probably than not, Mr Evans would not have contracted his cancer in the absence of the asbestos exposure.
Thirdly, because epidemiological studies predict that among the class of persons who share Mr Evans' smoking history, the greatest number of those who contract lung cancer after exposure to an equivalent asbestos fibre burden are persons who would have contracted the disease in any event.
Fourthly, because, even if asbestos and smoking combined causally in the development of lung cancers in all cases, the contribution of asbestos to the development of lung cancer in smokers may take the form of hastening the development of the cancer. That would reconcile the certainty of epidemiological prediction that a certain number of lung cancers will develop in smokers in any event, with the plausible biological theory that the additional risk factor of asbestos exposure will contribute to that inevitable development by way of acceleration.
That acceleration may be minimal or substantial and yet not change the inevitability of the tumour's appearance. If a motor car without brakes travels at a certain speed toward a collision there comes a time when any additional impetus by way of acceleration will not affect the inevitability of disaster.
The presence of lung cancer is an all or nothing event. There is no evidence in this case that, once contracted, Mr Evans cancer was more serious because of any effect of asbestos.
The contribution of asbestos to the genesis of the cancer may also be so slight as to make no material contribution to the inevitability of its appearance.
The evidence of Dr Leigh illustrates this point. At page 84 of the transcript, theoretical assumptions were put to the doctor concerning the additional risk posed by asbestos, when in a cohort of 1000, epidemiology predicted 10 deaths from smoking alone, and an additional 2 deaths if the cohort was also exposed to the further risk of asbestos.
The transcription which precedes the relevant evidence appears incomplete, however the following questions and answers are accurately recorded: HIS HONOUR Q Now, let us assume that that same thousand who were exposed to smoking were exposed also to asbestos. A---Yes. Q. And 12 die. A---Twelve die, yes. Q. It is your opinion that in relation to each one of those 12, you cannot disentangle the contributory effect of smoking and asbestos. A---Yes. Q. But if 10 were going to die in any event, we do not know which of those 12 were going to die anyway. A---Well, it's a sort of hypothetical, but I suppose, yes. Q. That is the problem, is it not, so that we may end up compensating 10 persons who are going to die from smoking in any event, in order to secure compensation for the two who are the additional cases. A---If they were exposed to smoking, they also had the asbestos, you can't say that they would've died from smoking in any event. You have to say rather that additional exposure of asbestos made some effect. (Emphasis added).
What is the weight of some effect?
In the present state of medical knowledge it is impossible to know, in any individual case, the nature or extent of any contribution by asbestos to the development of lung cancer in a heavy smoker.
Guidance may be found in epidemiological studies, or inductive reasoning from other evidence described by Spigelman CJ in Seltsam Pty Ltd v McGuinness (2000) 49 NSWLR 262 as "Strands in a cable". The " Strands in a Cable" Argument
Mr Little SC submits that the following strands lead to the inference that asbestos made a material contribution to Mr Evans' lung cancer: (a) It is wholly impossible to meaningfully form any numerical estimate of his cumulative asbestos exposure, however Mr Evans' working history is consistent with the generation of a significantly elevated risk of contracting lung cancer. (b) The presence of numerous pleural plaques and diffuse pleural thickening indicate high asbestos exposure. (c) A relatively high residual asbestos fibre count in Mr Evans' lung tissue, after many years of clearance, also indicates high asbestos exposure. (d) Carpenters as a class suffer from an increased incidence of asbestos related diseases indicating Mr Evans' occupational risk of asbestos induced lung diseases was high. (e) Biological theory, and the multiplicative effect demonstrated by epidemiology suggest that Mr Evans as a smoker had a particularly high risk which probably came home. The Impossibility of Numerical Assessment
Were it not for numerical assessment, the relationship between asbestos exposure and lung cancer would not have been demonstrated in the first place. Epidemiology not only drew the correlation but found it to be dose related. Although lung cancer certainly develops in some individuals at relative risks less than RR 2, those persons are a minority.
Whatever links there may be in the chain of reasoning leading to a finding of causation in a case of asbestos exposure, the central fact remains that the risk is related to the dose. A genetically susceptible person may contract lung cancer because of exposure to asbestos at a concentration that reflected minimal risk, however that is not the case advanced for Mr Evans.
The closer the numerical estimation of the level of exposure approaches RR 2 the less compelling the other strands in the reasoning process need be. Conversely, the closer the numerical estimation approaches RR 1, the stronger those strands must be in order to be persuasive.
In forming conclusions as to Mr Evans' probable cumulative fibre dose, I have recognised the difficulty of reconstruction and attempted to make generous assumptions as to his exposure. No occupational hygienists are called in Mr Evans' case.
My finding of 21.9 fibre/ml/years is approximately six times greater than Mr Roger's estimate of 3.24 fibre/ml/years and Mr Pickford's "probable" scenario of 3.4 fibre/ml/years. It is nearly double Mr Pickford's "worst case" scenario. This finding is compatible with the description "significant asbestos exposure". It is also consistent with the circumstance that the cumulative dose of asbestos fibre required to double the risk of contracting lung cancer requires a significant exposure for a prolonged period of time.
The epidemiological evidence points to the conclusion that the risk of Mr Evans' contracting lung cancer from his degree of exposure was less than 50-50. The significant exposure of Mr Evans to asbestos fibre took place over the nine years he worked with power tools building asbestos cement houses. Had he performed this work for 25 years the probability that his lung cancer was caused by the work would rise to greater than 50-50. The presence of pleural plaques and pleural thickening
A CT scan of Mr Evans' lungs was taken on 8 March 2002. The radiologist Dr Michael Jones reported that this CT scan showed multiple fibrous and calcified typical asbestos pleural plaques bilaterally, that the plaques were predominantly fibrous but there was early calcification, and that there was diffuse pleural thickening in both posterior mid and lower zones about 10 x 8 centimetres in extent on each side.
The plaintiff has tendered a paper by Miles Sandrini et al entitled Clinical Consequences of Asbestos Related Diffuse Pleural Thickening: a Review published in J Occup Med Toxicol 2008.
The authors report that although pleural disorders may also occur after household or environmental exposure, the prevalence of both diffuse pleural thickening and pleural plaques increases significantly with past occupational exposure to asbestos. The development of diffuse pleural thickening is thought to be dose related. Workers who have worked in occupations with heavy exposures are more likely to have pleural disease than those with moderate or minimal exposures.
Analysis of British naval dockyard workers suggested that patients with bilateral diffuse pleural thickening had significantly more exposure than those with unilateral disease.
Professor Breslin was asked to comment upon this article and agreed that pleural thickening was a matter which he took into account in forming his opinion because pleural abnormality may occur with asbestos exposure. Professor Breslin said that the fact that the pleural thickening in Mr Evans was bilateral was not conclusive as to the degree of exposure, because pleural thickening results as a consequence of resolving pleural effusions, and pleural effusions can occur at relatively low levels of asbestos exposure.
Professor Breslin viewed the scans upon which Dr Jones had reported. In his opinion the pleural thickening in evidence was localised rather than diffuse. In this respect he disagreed with Dr Jones. Significantly Professor Breslin said that the degree of plaques and pleural thickening shown in the scan was not inconsistent with an exposure as limited as 3.4- 13 fibre/ml/years.
A review of the literature by Dr William Weiss published in Chest, the official publication of the American College of Chest Physicians, in 1993 reported that the weight of evidence was against the hypothesis that persons with asbestos related pleural plaques are at increased risk of lung cancer compared with unexposed persons or the general population.
The presence of diffuse pleural thickening does indicate significant asbestos exposure, but I have no evidence that correlates the presence of diffuse pleural thickening with an increased risk of contracting lung cancer. Professor Breslin says he took into account the presence of the pleural thickening. The Residual Fibre Count
The pathologist Professor Pooley examined a lung tissue sample taken from Mr Evans. His analysis disclosed that: In respect of fibres greater than 1 m length the sample contained: Chrysotile 0.054 million fibres per gram of dry tissue Crocidolite 0.217 million fibres per gram of dry tissue Amosite 0.433 million fibres per gram of dry tissue Professor Pooley said that in total 13 asbestos fibres were detected and analysed. In his report Professor Pooley said that; "The levels of amphibole asbestos fibres detected by well in excess of those considered to be related to an environmental asbestos exposure but are equivalent to a low level occupational exposure"
As Mr Rogers pointed out in a report critical of this analysis, if the report is based on a total of 13 fibres, then the examination revealed 1 fibre of chrysotile, 4 fibres of crocidolite and 8 fibres of amosite.
The Helsinki Criteria assert a doubling of the risk of lung cancer is related to retained fibre levels of 2 million amphibole fibres greater than 5 m in length, or 5 million fibres greater than 1 m in length, per gram of dry lung tissue.
Although Mr Rogers rejects the Helsinki criteria, he points out that the combined total of 0.650 of amphibole fibres in Mr Evans' lung greater than one m in length, is only 13 per cent of the value used by that criteria to indicate a doubling of the risk.
Professor Pooley does not specify the level that he considers to be consistent with mere environmental exposure. Mr Rogers has compared the results with reference values prepared by Dr Pooley in another study comparing lung fibre content in mesothelioma cases and controls. The comparison indicates that the concentration of asbestos fibres found in the lung tissue of Mr Evans is slightly above the median value, but well within the range of values found in the normal UK population.
This is not surprising, nor is it helpful. Professor Berry gave evidence that amphibole fibres remained in the lungs for many years, and but there is clearance rate of about 10 per cent a year. When the tissue sample was taken from Mr Evans he had not been exposed to asbestos for at least 18 years. His heaviest exposure occurred before 1975, over 30 years before the sample was taken. It is reasonable to assume that at one time Mr Evans lungs may have contained a higher fibre count.
Mr Rogers criticises the authors of the research which purports to show a clearance rate from the lungs of 9 per cent per year on the basis that the data does not permit such a conclusion with any statistical confidence. It is impossible to know how much higher the fibre burden was when Mr Evans stopped work, and no estimate has been proffered in his case.
The Helsinki Criteria have been the subject of much criticism, and are not universally accepted as useful guides to conclusions as to causation. Mr Rogers, a long-time critic, points out in his report that in relation to the fibre burden criteria, one German study relied upon by the Helsinki proponents found that a lung burden of 1million fibres per gram of dry tissue could be associated with cumulative exposures somewhere in the range of 0.05 to 20 fibre/ml/years and a lung burden of 5 million fibres could be associated with a cumulative exposure in the range of 0.1 to 35 fibre/ml/years.
Because the original fibre burden in Mr Evans' lungs is unknown, and because the validity of the Helsinki Fibre Burden Criteria have not been established upon Makita v Sprowles principles, this strand of the plaintiff's argument is without weight. Occupational risks of Carpenters as a Class
Dr Leigh, who has practised for many years as an Occupational Physician, says in his report that carpenters are an occupational group well recognised to be at high risk of asbestos related malignancy. It may be accepted that carpenters working with asbestos cement products had an increased risk of asbestos related malignancies. Whether the risk was low, moderate or high depended on the individual circumstances.
It is reasonable to assume that at a time when asbestos fibre was included in fibrous cement sheeting, many carpenters worked exclusively with wood in joinery work. Some may have worked predominantly on brick or brick veneer construction and others exclusively with asbestos cement materials. Some may have left the industry after a few years, and others may have continued for 50 or 60 years.
Workers engaged in the manufacture of asbestos cement products are all exposed to the same risk of contracting asbestos related diseases. Similarly coalminers, welders and workers in chemical plants may be exposed to generic risks. This is not the case with carpenters. It is impossible to consider the risk faced by any carpenter without taking into account his personal circumstance.
Further, this is not a case where an occupational disease has been contracted in which there is no competing cause. The competing cause in the case of Mr Evans, smoking, is, because of the magnitude of the risk, compelling.
The trade of carpentry, of itself, is not a risk factor relevant to the development of Mr Evans' lung cancer. Biological Theory, and the Multiplicative Effect
Both Dr Nicholls and Dr Tharion, relying upon biological theory and the multiplicative affect, addressed causation in this case upon the basis that in every case where a smoker has been substantially exposed to asbestos and a cancer develops, the asbestos has made a material contribution to that cancer.
This reasoning cannot stand with the epidemiological data that demonstrate that even in the case of a former heavy smoker such as Mr Evans, the chances of contracting lung cancer from an exposure to asbestos that is substantial, but less than a cumulative dose of 50 fibre/ml/years, is less than 50-50.
Professor Berry said of biological modelling that if it did not agree with the epidemiological data it must be incorrect. A Contrary Strand
Mr Evans' lungs were found to be grossly emphysematous when Dr Tharion performed the left thoracotomy on 21 February 2008. There is strong evidence that cigarette smokers who develop chronic obstructive airways disease are at much greater risk for the development of lung cancer than cigarette smokers with an equivalent smoking history without obstructive airways disease. (Exhibit Amaca 27).
This circumstance indicates that the causative effects of smoking in the development of Mr Evans' lung cancer are greater than those suggested by the epidemiological tables of Professor Berry which have been used to apportion the relative causal effects of smoking and asbestos. A Suggested Paradox
Mr Little echoes the submission to the High Court in Ellis to the effect that if Mrs Evans cannot succeed in this claim, no smoker contracting lung cancer after an exposure to asbestos insufficient to double the risk can succeed, although epidemiological studies show that asbestos must have been a cause of cancer in some cases. This, he suggests, is unfair.
As the High Court pointed out, any unfairness results from the nature of legal proof, and the limits of knowledge about what causes cancer.
The law imposes a corresponding unfairness upon defendants, who must compensate every plaintiff whose risk was greater than 50 per cent, although asbestos may not have been a cause of the cancer in an individual case.
The solution proposed by Dr Leigh, that liability be proportional to risk, although attractive, is not compatible with legal principle. Conclusion
I am not persuaded that it is more probable than not that any contribution of asbestos to the cause or progression of Mr Evans' lung cancer was, in the light of his smoking history, material.
It is unnecessary to address the defendants' further arguments in defence of this claim. Orders
Judgment for the defendants. Plaintiff to pay the defendants' costs.

Mr G F Little SC with Mr R J M Foord instructed by Denniston and Day appeared for the plaintiff Mr J L Sharpe instructed by Thompson Cooper Lawyers appeared for the first defendant Mr G M Watson SC instructed by DLA Phillips Fox appeared for the second defendant

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