Plaintiff v Defendant

2 After the jury's verdict was announced, the plaintiff applied for judgment in accordance with the verdict. The defendant applied for an order that the jury's verdict be set aside and that judgment be entered in its favour notwithstanding the jury's verdict.[1]

3 The defendant's application was made pursuant to leave that I reserved on 25 August 2011, at the conclusion of the evidence. The application relied on the following grounds:

(a) there was no evidence that an injury of the kind suffered by the plaintiff was reasonably foreseeable in 1972; and

(b) causation was not established between any negligence of the defendant and the plaintiff's mesothelioma.

4 After hearing the parties' submissions, I ruled against the defendant's application and informed the parties that I would deliver reasons for my ruling on 31 August 2011. These are my reasons.

5 The plaintiff claimed that his mesothelioma was caused by his exposure to asbestos dust and fibres in 1972 when he visited one of the defendant's factories in Perth to repair a machine.[2]

6 It was common ground at the trial that the plaintiff's exposure to asbestos dust and fibres at the factory was for a total of six hours, comprising visits of two hours' duration over three separate days ('factory exposure'). The preponderance of the evidence was that the plaintiff was not exposed to asbestos in any other job and that, apart from living in Subiaco and South Perth in the early years of his life, he has lived in non-urban environments.

7 In order for a defendant's application for judgment notwithstanding the jury's verdict to succeed, the defendant must establish that there was no evidence upon which a reasonable jury, properly directed, could return a verdict for the plaintiff.[3]

8 Where there is evidence to support the jury's verdict, the verdict cannot be disregarded even if the trial judge were strongly against the jury's conclusion.[4]

9 A trial judge hearing an application for judgment notwithstanding the jury's verdict should determine the application on the evidence most favourable to the party that carries the onus of proof.[5]

10 A trial judge should proceed with great caution and only exercise the power to give judgment in disregard of the jury's verdict in the clearest of cases.[6]

11 In this case, judgment for the defendant, notwithstanding the jury's verdict, can only be entered if there was no evidence upon which the jury, properly instructed and acting reasonably, could find that:

(a) it was reasonably foreseeable in 1972 that there was a risk of the plaintiff contracting a lung disease such as mesothelioma from the factory exposure; or

(b) the factory exposure was a cause of or materially contributed to the plaintiff's mesothelioma.

12 The plaintiff relied primarily on documentary evidence on the question of whether the risk of his contracting mesothelioma from the factory exposure was reasonably foreseeable by the defendant in 1972. In particular, the plaintiff relied on the first two documents in Exhibit 'P1' which were created by the defendant in 1966. The evidence included comments by the defendant's former chief medical officer, Dr McCullagh, that:

(a) recent literature has reported fairly conclusive evidence that asbestos dust when inhaled can cause cancer of the chest cavity lining;

(b) there is no safe upper limit for asbestos dust;

(d) heaviest exposures cause asbestosis, lighter exposures cause cancer; and

(e) it is almost inevitable that any lung cancer that develops in employees who have had even minimal exposure to asbestos will be classified by courts as compensation cases.

13 The plaintiff also relied on the evidence of the defendant's expert respiratory physician, Dr Gardiner, who said that in the late 1960s, people with minimum exposure to asbestos, like carpenters, were deemed to be at risk of contracting mesothelioma.

14 The defendant relied on the publications and standards of the National Health and Medical Research Council ('NHMRC') that were current in 1972 (Exhibit 'D1'). The NHMRC was then of the view that nearly all workers may be repeatedly exposed day after day to four asbestos fibres per cubic centimetre of air without adverse effect. In 1978, the NHMRC was of the view that limited usage of asbestos might be considered insufficient to cause harm to the health of those exposed. The NHMRC defined limited usage by reference to small users such as construction firms and insulation contractors who use less than five tonnes of raw asbestos per annum or who regularly use products such as asbestos cement building materials.

15 The defendant also relied on the evidence of its expert occupational hygienist, Mr Pickford, who said that neither he nor the industry knew that, by 1972, it was accepted that mesothelioma could be caused by a short-term and low exposure to asbestos.

Conclusion in relation to reasonable foreseeability

16 In my opinion, the jury was entitled to conclude that the defendant's own internal documents that were created on or before 1972 were the best evidence of what the defendant knew in 1972. That evidence, and the evidence of Dr Gardiner, was more than sufficient to enable the jury to conclude that in 1972, the defendant knew or should have reasonably foreseen that there was a risk that persons such as the plaintiff that visited the factory would be exposed to asbestos dust and fibres as a result of attending the factory over a short period to work on a machine, and that there was a risk of contracting a lung disease such as mesothelioma from such exposure.

17 There was broad consensus among the parties' experts on the following matters:

(a) Mesothelioma is usually associated with exposure to asbestos dust and fibres.

(b) In relation to the plaintiff's circumstances, exposure to asbestos was the only possible cause of his mesothelioma.

(c) Asbestos fibres are present in the environment. The quantity of the fibres is higher in urban areas due to the presence of buildings containing asbestos products and motor vehicles with asbestos in the brake linings, compared to rural areas. It is possible to contract mesothelioma from asbestos fibres in the background environment. The risk of doing so, which is known as the 'background risk', is very low.

(d) The precise mechanism by which asbestos fibres cause mesothelioma is not known. In particular, it is not known whether mesothelioma is caused by a single fibre interacting with a single mesothelial cell, or numerous fibres interacting with numerous cells. It is accepted, however, that it is possible that a single fibre can cause mesothelioma and that, for this reason, there is no minimum level of exposure below which there is no risk of contracting mesothelioma. It is also accepted that where there are discrete exposures to asbestos, it is possible that the cause of mesothelioma is either one or the other exposure or a combination of both.

(e) It was not possible to prove scientifically that the plaintiff's mesothelioma was caused by an asbestos fibre that he inhaled at the factory as distinct from a fibre that he inhaled elsewhere.

(f) Inhaling asbestos increases the risk of contracting mesothelioma.

(g) There is a dose-response relationship between exposure to asbestos dust and fibres and the contracting of mesothelioma. The higher the amount and the longer the duration of the dosage, the greater the risk. The risk is cumulative in the sense that each additional exposure increases the risk.

(h) The latency period for mesothelioma is between 15 and 70 years after exposure. The average is 40 years after exposure. The plaintiff's latency period of 38 years in respect of his factory exposure was statistically very close to the period of maximum risk of contracting mesothelioma from that exposure.

(i) There is a distinction between a risk of contracting mesothelioma and a cause of mesothelioma.

(j) There are genetic differences between people. Some people that are exposed to asbestos contract mesothelioma while others do not.

18 Mr Pickford, to whom I have already referred, gave evidence that, between 1977 and 1988, he worked for the defendant as an occupational hygienist and became the chief industrial hygiene engineer. Since 1988, he has worked continuously as an occupational hygienist in private practice. In recent years, he has given advice to, or has been called as a witness by, the defendant towards 10 times per year.

19 Mr Pickford said that, by using dust sample readings taken at the factory between 1971 and 1977 and by applying statistical techniques to those readings, he was able to calculate the cumulative dose of asbestos that the plaintiff was likely to have inhaled at the factory as 0.00036 fibres per millilitre years.

20 The defendant also called Professor Berry, an epidemiologist and biostatistician, who used Mr Pickford's calculation to estimate that the plaintiff's total lifetime risk of contracting mesothelioma from his exposure at the factory ('factory risk') as 0.4 per 100,000 or, on a worst case scenario, 0.9 per 100,000. Professor Berry calculated the background risk as 10 per 100,000. This is a statistical average that does not take into account individual circumstances such as rural living as distinct from urban living. Taking the whole of the risk, Professor Berry calculated the factory risk as four per cent or, on a worst case scenario, eight per cent, and the background risk as 96 per cent or, on a worst case scenario, 92 per cent. Professor Berry acknowledged that his calculations were totally dependent on Mr Pickford's calculation.

21 The plaintiff did not call expert evidence in support of an alternative calculation of the plaintiff's factory risk. The plaintiff did, however, adduce extensive evidence about the unreliability of the dust sample readings upon which Mr Pickford based his calculations. The plaintiff also called Mr Kottek, an occupational and environmental health consultant, who criticised Mr Pickford's data inputs and methodology.

22 The plaintiff called Dr Leigh, a consultant occupational physician who has had extensive experience in researching the causes of asbestos-related diseases, including mesothelioma. On the question of whether the plaintiff's factory exposure was a cause of or materially contributed to his mesothelioma, Dr Leigh's evidence which was most favourable to the plaintiff may be summarised as follows:

(a) In determining whether there is a causal relationship between exposure to asbestos and the contracting of mesothelioma, there are a number of factors to consider. These are: the precise diagnosis of the disease and whether it truly is mesothelioma; the history of exposure to asbestos as recalled and estimated by the scientists; and the latency from that history and whether it is consistent with what is known about the typical latency of mesothelioma. If a person has mesothelioma and an asbestos exposure history, then, taking into account the latency and the fact that the consensus of authoritative scientific opinion is that there is no minimum level below which mesothelioma cannot be contracted, the mesothelioma was caused by the exposure. Even if the amount of specific asbestos exposure is small, it would have at least added to the background, and would have increased the total risk, and would have played some small part in contracting mesothelioma.

(b) It is more likely than not that the plaintiff's factory exposure made a significant contribution to the causation of his mesothelioma. This was because, as mesothelioma is only caused by asbestos and the plaintiff had asbestos exposure, it is most likely that his mesothelioma was caused by his asbestos exposure, which was not a trivial asbestos exposure. The factory exposure was qualitatively heavy, although for a quite short time in comparison with other cases. The plaintiff's latency period is almost spot on the average latency of 40 years and is totally consistent with his exposure causing mesothelioma.

(c) All asbestos fibres of all types have something to do with the progress or development of mesothelioma where it has occurred. This view is based on the best current synthesis of the scientific knowledge. Fibres can act at the very early stage of the development when the cancer is initiated into becoming a cell with potentially damaged DNA that will start to divide into altered cells which ultimately become cancer. The fibres can also act at later stages where several of these chains of mutations have already happened some years after the initial exposure, for example, when they can affect the chemical factors which cause these altered cells to multiply. They can affect the chemical factors which cause these altered cells to be themselves clear because they are a further defence mechanism apart from the fibres being removed in the first place. Sometimes the body detects this is an altered cell and says it has to be removed because it may ultimately become a cancer cell. The cell can be removed by a process of apoptosis. This happens down the track. Asbestos fibres have been shown to affect this process, and to affect the production of chemicals which attract other cells to the cancer. Fibres have also been shown to affect genes that produce suppression of the ligament process - the further dividing of the damaged cell. As fibres can act at all stages of the process, all the fibres in the lung must be doing something to the overall causation of mesothelioma. That is the cumulative effect.

(d) In the plaintiff's case, if he has had actual asbestos exposure on top of background exposure, the additional exposure has added significantly to the causal process and has had a significant effect in the causal process.

23 The plaintiff also called Professor Musk, a specialist in respiratory and occupational medicine. He is involved in research into occupational lung diseases, particularly asbestos-related diseases, and treats patients with such diseases, including mesothelioma. On the question of whether the plaintiff's factory exposure was a cause of or materially contributed to his mesothelioma, Professor Musk's evidence which was most favourable to the plaintiff may be summarised as follows:

(a) The evidence indicates that, when a person has had discrete episodes of exposure to, and inhalation of, asbestos dust over and above any background exposures, the cumulative exposure, including the background exposures, contributes to the risk of developing mesothelioma and therefore contributes to the mesothelioma development. All exposures more than 10 to 15 years before the occurrence of mesothelioma contribute.

(b) Apart from the plaintiff's factory exposure and the background exposure, Professor Musk did not think that there was any other realistic or reasonable explanation for the plaintiff's mesothelioma. The latency period between the plaintiff's factory exposure and the diagnosis of mesothelioma is very consistent with a causal relationship between the two events.

(c) On the balance of probabilities, the plaintiff's factory exposure contributed to him contracting mesothelioma. The plaintiff's exposure contributed to his risk of developing mesothelioma and, as the risk has materialised and the plaintiff has contracted mesothelioma, the exposure contributed to the development of the mesothelioma.

(d) The background risk is of the order of one or two cases per million people per year in Western Australia. As risk is related to exposure, the risk is lower for a person who lives in a rural-type environment with less asbestos. Mesothelioma from background exposure to asbestos is uncommon.

(e) If one adds to the plaintiff's background exposure to asbestos the factory exposure, whatever the latter level of exposure was, it increased the risk of contracting mesothelioma because any exposure increases the risk of contracting mesothelioma. In the plaintiff's case, as the risk has been realised because he has contracted mesothelioma, one cannot avoid the conclusion that the factory exposure at whatever level was a cause of the mesothelioma. One cannot say which fibre or its source was actually the cause if it was just one fibre, but one can say that as both the background exposure and the factory exposure posed a risk, then they both contributed to the development of the plaintiff's mesothelioma.

24 In the course of cross-examination and re-examination, Professor Berry gave evidence that was favourable to the plaintiff. Professor Berry's evidence may be summarised as follows:

(a) His calculations were concerned with risk rather than cause. Realistically, there were two possible causes of the plaintiff's mesothelioma, the first being the background exposure and the second being the factory exposure. A cause of the mesothelioma could be a combination of both the background exposure and the factory exposure. There could be two causes acting together. It could be that one exposure causes stage one and another exposure causes stage four, however, this was not known.

(b) The risk of contracting mesothelioma from exposure to asbestos is maximum at 40 years after the exposure. The latency period of 38 years between the plaintiff's factory exposure and the diagnosis of his mesothelioma is well within the range that one would see in known high-risk situations. The latency period of 38 years strengthened any evidence that the plaintiff's mesothelioma was caused by the factory exposure.

(c) If one is looking at the risk in trying to implicate the plaintiff's factory exposure as being a cause of his mesothelioma, a latency period of 38 years is 'spot on' in terms of the risk being at its highest at that stage.

(d) His calculation of the plaintiff's factory risk did not take into account the plaintiff's latency period of 38 years.

25 The defendant called Dr Gardiner who treats mesothelioma patients and has experience in assessing claims for compensation by some sufferers of mesothelioma. Unlike Dr Leigh and Professors Musk and Berry, Dr Gardiner had conducted very little research and had not written any papers on the issue of asbestos-related diseases. Dr Gardiner gave evidence that it is unlikely that the plaintiff's factory exposure caused his mesothelioma.

26 In my opinion, applying the commonsense test of causation,[7] there was sufficient evidence to enable the jury to conclude, on the balance of probabilities, that the factory exposure was a cause of, or materially contributed to, the plaintiff's mesothelioma.

27 The jury was entitled to reject Mr Pickford's calculation because of the extensive evidence that the underlying data was unreliable. Although Mr Kottek was younger and less experienced than Mr Pickford, the jury was entitled to accept his criticisms of Mr Pickford's data and methodology, because Mr Pickford himself acknowledged the correctness of some of Mr Kottek's criticisms. Mr Pickford also acknowledged that all of the errors that he had made in his calculation favoured the defendant.

28 The jury was also entitled to form the view, as I did, that Mr Pickford was not a neutral witness. He came across as an apologist for the defendant. In particular, his answer in re-examination - that the documents that indicated that dust samples were unreliable did not cause him to doubt the accuracy of his assessment of the plaintiff's factory exposure, but, in fact, caused him to believe that his estimate was probably too high - was devoid of any credibility.

29 The jury was entitled to reject Professor Berry's calculations because, as he acknowledged, they were based entirely on Mr Pickford's calculation. The jury was also entitled to reject Professor Berry's calculations because they did not take into account the plaintiff's latency period which, as Professor Berry acknowledged, was 'spot on' in terms of the factory risk being at its highest at that stage. In addition, his calculations did not take into account the plaintiff's predominantly rural lifestyle.

30 The jury was also entitled to prefer the evidence of Dr Leigh and Professor Musk to the evidence of Dr Gardiner because Dr Gardiner did not engage in research on the causes of asbestos-related diseases, including mesothelioma.

31 Once the jury rejected Mr Pickford's and Dr Gardiner's evidence and Professor Berry's risk calculations, the jury was left with the evidence of Dr Leigh and Professors Musk and Berry in relation to causation. Professor Berry said that there were only two possible causes of the plaintiff's mesothelioma, namely the factory exposure and the background exposure, and that it was possible that the cause was a combination of both exposures. Although this evidence, on its own, was insufficient to establish a causal relationship between the factory exposure and the plaintiff's mesothelioma, it reinforced the evidence of Dr Leigh and Professor Musk in relation to causation.

32 While it is true that both Dr Leigh and Professor Musk focused on the risk associated with the factory exposure and acknowledged that medical science did not enable a definitive statement that the asbestos fibres inhaled at the factory caused the plaintiff's mesothelioma, the jury was entitled to rely on their evidence about the probable cause based on the witnesses' knowledge of the scientific studies. In particular, the jury was entitled to accept Dr Leigh's evidence about the best current synthesis of the scientific knowledge, which is summarised at [22](c) above.

33 On the issue of whether the defendant's failure to provide a protective mask to the plaintiff was a cause of, or materially contributed to, his mesothelioma, the jury was entitled to find causation on the basis of the defendant's own documents in Exhibit 'D1'. These documents demonstrated that the defendant was well aware in 1972 that inhaling asbestos could cause mesothelioma and that the wearing of a protective mask was an essential precaution to minimise or avoid asbestos inhalation and, in turn, to minimise or avoid the contraction of mesothelioma.

34 The jury could not have been confused about the difference between a risk and a cause or between a possible cause and a probable cause because I repeatedly emphasised the differences between these concepts. My directions to the jury included the following:

Now, you will have noticed that I have repeatedly referred to the need for Mr King to satisfy you on the balance of probabilities that the breach of duty that you find was committed by Amaca was a cause of or materially contributed to his mesothelioma. I have been talking about a causal link and not about risk or an increase in risk. There is a difference between risk and cause. It is not enough for you to find that Amaca's breach created a risk of Mr King contracting mesothelioma or increased his risk of contracting mesothelioma even if the risk or the increase in the risk is large. Mr King must satisfy you that it is more probable than not that the breach was a cause of or materially contributed to his mesothelioma. If on the basis of all the evidence, including the expert evidence, you are satisfied that the breach was a possible rather than a probable cause, Mr King must fail. [8]

35 It follows from the above discussion that the defendant has not established either of the two grounds upon which it applied for judgment notwithstanding the jury's verdict.

[1] In this ruling, I will use the expression 'notwithstanding the jury's verdict' instead of the Latin expression 'non obstante veredicto'.

[2] As the preponderance of the evidence was that the plaintiff attended the factory at Welshpool rather than the factory at Rivervale, I will assume that the jury found that the exposure occurred at the Welshpool factory.

[3] Herald & Weekly Times Ltd v Popovic [2003] VSCA 161; (2003) 9 VR 1, 31 [127] ('Popovic'); Naxakis v Western General Hospital [1999] HCA 22; (1999) 197 CLR 269, 274-5 [16].

[4] Phillips v Ellinson Brothers Pty Ltd [1941] HCA 35; (1941) 65 CLR 221, 230, cited in Hayward v Georges Ltd [1966] VicRp 28; [1966] VR 202, 205.

[5] Popovic [2003] VSCA 161; (2003) 9 VR 1, 31 [126].

[6] Popovic [2003] VSCA 161; (2003) 9 VR 1, 32 [134].

[7] March v E&MH Stramare Pty Ltd [1991] HCA 12; (1991) 171 CLR 506, 515, 522, 530_; Bennett v Minister of Community Welfare_ [1992] HCA 27; (1992) 176 CLR 408, 412-13, 418-19, 428.

[8] The quoted passage is from my notes as the transcript is not yet available.