D'Argenio v VWA
[2016] VCC 1955
•20 December 2016
| IN THE COUNTY COURT OF VICTORIA AT MELBOURNE WORKCOVER DIVISION | Revised Not Restricted Suitable for Publication |
Case No. CI-16-03704
| GERARDO D'ARGENIO | Plaintiff |
| v | |
| VICTORIAN WORKCOVER AUTHORITY | Defendant |
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JUDGE: | HIS HONOUR JUDGE BOWMAN | |
WHERE HELD: | Melbourne | |
DATE OF HEARING: | 14, 17, 28, 29 & 30 November and 1 December 2016 | |
DATE OF JUDGMENT: | 20 December 2016 | |
CASE MAY BE CITED AS: | D'Argenio v VWA | |
MEDIUM NEUTRAL CITATION: | [2016] VCC 1955 | |
REASONS FOR JUDGMENT
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Catchwords: Accident Compensation Act 1985 – ss82(6) and 86 – plaintiff suffering from adenocarcinoma of the lung – terminally ill – lengthy history of work as a plasterer – plaintiff self-employed for a period, but by family company for last 20 years of employment – plaintiff also a smoker – whether exposure to asbestos and silica in last 20 years of employment – degree of such exposure – whether lung cancer due to nature of employment – whether nature of employment a significant contributing factor – meaning and operation of relevant sections of the Act – conflicting expert evidence – factors to be considered.
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APPEARANCES: | Counsel | Solicitors |
| For the Plaintiff | Mr J Moore QC with Mr A Dimsey | Maurice Blackburn |
| For the Defendant | Ms R Annesley QC with Mr M Clarke | Lander & Rogers |
HIS HONOUR:
General Background
1 This matter comes before me by way of an action brought by the plaintiff pursuant to the provisions of the Accident Compensation Act 1985, hereinafter referred to as “the Act”, and in particular pursuant to ss82(6) and 86 of the Act. The plaintiff is terminally ill and his life expectancy is anything between a number of days or weeks and approximately six months. The opinion expressed by the plaintiff’s treating medical oncologist, Associate Professor Paul Mitchell, in evidence on 30 November last, and having seen the plaintiff on the morning of that day for the purpose of treatment, was that the plaintiff will not survive until Christmas. I would refer to Transcript (hereinafter referred to as “T”) 288.
2 I would also point out that, in accordance with an order of the Supreme Court made by J Forrest J pursuant to s4 of the Evidence (Miscellaneous Provisions) Act 1958 on 14 November last, evidence was taken from the plaintiff at his home on that day. I attended at the plaintiff’s home on that day and for that purpose. The plaintiff was able to give evidence. Apart from evidence-in-chief, he was cross-examined and re-examined. What occurred was fully transcribed. Unfortunately, the numbering of the pages commenced again. As this duplicated some of the page numbers relating to evidence and discussion in the courtroom, henceforth, and in order to avoid confusion, when referring to page numbers of the transcript of evidence taken pursuant to s4 of the Act just mentioned, I shall preface the number with the letters “TACT”. The plaintiff was not bedridden and his evidence was obtained with minimal assistance, when required, from an Italian interpreter. Whilst there were some minor difficulties at times, these essentially being due to misunderstandings, I am quite satisfied that the plaintiff was quite competent to give evidence. Indeed, given the precarious state of his health, he was not as frail as might have been anticipated. That is not to say that he was robust, but, save for the occasional misunderstanding when a question had to be explained further, he was able to give comprehensible, responsive answers throughout. I shall turn to the substance of his evidence and the impression that he made as a witness subsequently. However, I say at the outset that he was a competent witness who gave satisfactory answers to the questions put to him.
3 Another aspect of the urgency of the situation is this. The dire condition of the plaintiff’s health was fully appreciated by all involved. Counsel and their instructors are to be thanked and congratulated for the efficient and co-operative manner in which they dealt with this urgent case. The demands of a tight timetable were met in an exemplary fashion. Juggling of the evidence of expert witnesses, two of whom flew in from Sydney, was also required and, whilst this was a hard-fought case, this aspect of the matter was also carried out in an admirably co-operative manner. The witnesses themselves are also to be thanked. All contributed to the evidence and addresses being able to be concluded in an extremely timely and efficient manner.
4 I apologise in advance for any typographical errors that may be present in these Reasons for Judgment. Given the urgency of this Judgment, as well as its length and the complexity of the case, some errors may have gone undetected. If so, I must take full responsibility for them, because the County Court secretarial staff has done a job at which I can only marvel to get numerous drafts of this Judgment typed and completed in such a short time and in the midst of the predictable and unavoidable December rush.
5 Mr J Moore QC with Mr A Dimsey of counsel appeared on behalf of the plaintiff. Ms R Annesley QC with Mr M Clarke of counsel appeared on behalf of the defendant. In addition to the plaintiff, the following witnesses gave oral evidence:
For the plaintiff – Mr Michael Kottek, occupational and environmental health consultant; Mr Alexander Rosalion, cardiothoracic surgeon; Dr James Leigh, consultant occupational physician; and Associate Professor Paul Mitchell, the plaintiff’s treating medical oncologist.
For the defendant – Mr Alan Rogers, consultant occupational hygienist; Ms Yanel Lara, occupational hygienist; and Professor Richard Fox, specialist in medical oncology and clinical haematology.
6 As shall be discussed, each of the experts had far more qualifications and indications of their expertise than the short descriptions which I have just given.
7 The balance of the evidence was documentary in nature and was tendered either by consent or without objection.
The pleadings
(a)The Amended Statement of Claim
8 The contents of the Amended Statement of Claim could be summarised as follows.
9 The plaintiff was employed as a plasterer by D’Argenio Nominees Pty Ltd between approximately 1981 and 2001 and was acting within the course of that employment. Henceforth, I shall refer to that period of employment as being with “the family company”. The plaintiff is suffering from a disease within the meaning of the Act due to the nature of that employment. Throughout the course of that employment with the family company, the plaintiff worked on renovation and construction sites and was exposed to and/or inhaled asbestos dust and silica dust.
10 The nature of the employment gave rise to a significantly greater risk of contracting the disease. The injury in question is metastatic adenocarcinoma of the lung. Whilst stress, anxiety and depression are also alleged, these effectively received no attention during the conduct of the case.
11 The plaintiff has claimed medical and like expenses and a permanent impairment benefit. That claim has been rejected. The claim for compensation was made pursuant to ss91, 98C, 98E, 99 and 104B of the Act.
12 In the Prayer for Relief, the plaintiff has claimed the following:
“An entitlement to compensation pursuant to the Accident Compensation Act 1985 and:
A. a determination that the Plaintiff is entitled to compensation in relation to the injury;
B. payment of reasonable medical and like expenses;
C. a declaration that the Plaintiff is entitled to compensation for non-economic loss in respect of permanent impairment;
D. interest;
E. such further or other orders as the Court deems appropriate;
F. costs.”
(b) The defence
13 It is to be noted that the named defendant is in fact the Victorian WorkCover Authority, hereinafter referred to as “the VWA”. There is no significance to this distinction and it did not impact upon the running of the case in any way.
14 In any event, the defence admits that the VWA was at all material times a body corporate capable of being sued pursuant to the Act. Employment by the family company is not admitted as such, but at no time during the conduct of the case was this raised as an issue. The defendant admits that the plaintiff has been diagnosed with adenocarcinoma of the lung, but otherwise denies other matters to do with the employment, including assertions of exposure to asbestos and silica dusts. It also denies the causation, aggravation, acceleration or recurrence of the injury in question or that the employment gave rise to a significantly greater risk of the plaintiff contracting the disease.
15 The defendant further denies that the plaintiff has suffered any injury arising out of or in the course of or due to the nature of the relevant employment. It denies that the plaintiff has any entitlement to compensation as alleged under the Act.
(c) An amendment during the conduct of the case
16 There is one further matter that should be mentioned. Initially, the plaintiff was also asserting that he suffered injury arising out of or in the course of his employment. Effectively, the deletion of this, which occurred on 28 November last, was the only point of difference between the Amended Statement of Claim and the original Statement of Claim. In other words, the plaintiff now asserts that his entitlement to compensation is to be found solely in the “disease provisions” (ss82(6) and 86) of the Act. That this is so was stated clearly by Mr Moore when, by consent, he introduced the Amended Statement of Claim – see T35. I should add that, at no time during the conduct of the case was it suggested that the admitted condition of adenocarcinoma of the lung does not fall within the definition of “disease” found in s5 of the Act.
17 Thus, when all is said and done, the contest is one that centres upon the disease provisions and whether the plaintiff has discharged the burden of proof in relation to satisfying them.
The relevant provisions of the Act
18 There was no argument between the parties but that the version of the Act which is applicable is that which was operating as at the date of the plaintiff last working for the family company – that is, the Act as it was in 2001. I shall now set out the provisions which are at the centre of this dispute.
19 Section 82(6) of the Act reads as follows:
“Where a worker suffers an injury which occurs by way of gradual process and which is due to the nature of employment in which the worker was employed and if employment of that nature was a significant contributing factor at any time before notice of the injury was given, the worker or the worker’s dependants shall be entitled to compensation under this Act as if the injury were an injury arising out of or in the course of employment.”
20 Section 86 of the Act reads as follows:
“If –
(a) a worker is suffering from a disease within the meaning of section 5 which incapacitates the worker from earning full wages at the work at which the worker was employed;
or
(b) the death of a worker is caused or was materially contributed to by any disease –
and the disease is due to the nature of any employment in which the worker was employed and if employment of that nature was a significant contributing factor at any time prior to the date of incapacity, the worker or the worker’s dependants shall be entitled to compensation in accordance with this Act as if the disease were an injury.”
21 The meaning of the words “significant contributing factor” is something that also has the potential to be relevant. It is found in s5(1B) of the Act. That definition reads as follows:
“In determining for the purposes of this Act whether a worker’s employment was a ‘significant contributing factor’ to any injury –
(a) the duration of the worker’s current employment; and
(b) the nature of the work performed; and
(c) the particular tasks of the employment; and
(d)the probable development of the injury occurring if that employment had not taken place; and
(e)the existence of any hereditary risks; and
(f)the life-style of the worker; and
(g)the activities of the worker outside the workplace –
must be taken into account.”
22 A further point should be made as to the provisions set out above. The words “and if employment of that nature was a significant contributing factor” were not present in either provision prior to 1992. It is to be remembered that the period of employment upon which the plaintiff relies is from 1981 to 2001. However, as stated, it is not contended that anything other than the provisions set out above apply and that seems to me to be the correct statutory situation.
Findings of fact
23 I make the following findings of fact. Many of these are not contentious. As shall be discussed, others were the subject of considerable debate. However, what follows are my ultimate findings of fact. As the plaintiff was the only lay witness, necessarily there was considerable concentration upon the content of his evidence.
24 The plaintiff is aged 75 years, he having been born in Italy on 22 October 1941. He is a married man with an adult family. He received very little education, leaving school at age 11 or 12. His father was a tobacco farmer. The relevance of this is that the age at which the plaintiff commenced smoking was a topic which received some attention. He gave evidence of rolling up some tobacco with newspaper and “stuff like that”, but did not “smoke as smoke” – see TACT30. He denied smoking cigarettes by the age of 12. I accept that. However, there is no doubt but that the plaintiff has a long history of cigarette smoking. He gave evidence that he smoked 30 cigarettes a day, sometimes less and occasionally more, commencing from when he came to Australia in 1960. Indeed, it would seem that he had smoked for a couple of years prior to that, although perhaps not at the same rate. He did not stop smoking completely until 2012. However it is viewed, there is a long history of smoking something in the order of 30 cigarettes per day.
25 The plaintiff came to Australia in 1960. Thereafter, for a period he worked in the country as a labourer and concreter. Between 1965 and 1968 he worked as a labourer and plasterer for the Housing Commission at sites in Carlton, Flemington and Broadmeadows. I accept that there was exposure to asbestos cement sheeting in some of the work that was done during those years. The performance of plastering work for the Housing Commission seems to have involved the taking of asbestos sheeting from walls and the like, using shovels, crowbars and other tools. The impression given is that the exposure to asbestos, when doing this work, may have been quite regular. During that time, he was also mixing cement and sand in his mixer every day and there was sand in the air.
26 In approximately 1968 or 1969, the plaintiff commenced self-employment as a plasterer, trading under his own name. In November 1981, on financial advice, he incorporated and thereafter continued to work as an employee of the family company – see TACT8.
27 This leads me to one of the principal areas of contention, namely the extent to which the plaintiff was exposed to asbestos and silica and his evidence in this regard. There is also scope for legal argument as to the extent to which evidence concerning actual exposure is relevant, given that the plaintiff is relying upon ss82(6) and 86 of the Act. Arguably, these sections are focussed upon the nature of the employment and the risks associated with such nature as opposed to the actual exposure in the individual case, although, as shall be discussed, there may be some scope for looking at individual circumstances.
28 Further, in the provisions as they were from 1992 onwards, the words “and if employment of that nature was a significant contributing factor” are present. It is contended that these words require that attention be given to the plaintiff’s actual exposure and to other actual contributing factors, such as smoking. Furthermore, another possible consideration is whether the exposure to the individual plaintiff in his actual employment in fact caused his condition and, if so, how this is to be viewed.
29 These are matters to which I shall return, but hopefully they assist in understanding why evidence was permitted as to the plaintiff’s particular circumstances or employment and as to his smoking habit, and as to why I am making findings of fact in these regards. It was the subject of some attention.
30 Another matter which should be explained in relation to the history of the plaintiff’s exposure to asbestos is that he has previously brought a common law action based upon his exposure to asbestos between 1965 and 1983. (There may have been some misunderstanding as to the date when the plaintiff commenced work for the family company, as, in the relevant pleadings, it is asserted that he was self-employed until 1983. The evidence in the present case would suggest that such self-employment ended in 1981.) That action was against various manufacturers of asbestos products.
31 I turn now to a discussion of the plaintiff’s actual exposure to asbestos and silica during the period upon which he relies in this action, namely 1981-2001. His evidence was at times a little confusing and internally contradictory, but perhaps that is hardly surprising for a man who is very seriously ill, extremely poorly educated and for whom English is not his native tongue. Whilst he has been in this country for many years, he has a quite pronounced accent and occasionally needed the assistance of an interpreter. It may well be that tiredness and his state of health contributed to that.
32 In any event, ultimately I am satisfied that I am in a position to make findings of fact in relation to his history of exposure. When, in re-examination, he was given a clear event, namely the incorporation of the family company, as a marker or guide, rather than a year or years, the plaintiff was able to answer in a more confident manner. The evidence of the plaintiff was the only lay evidence received. I am satisfied that, on the basis of it, findings of fact on the balance of probabilities can be made.
33 As stated, I am satisfied that there was considerable exposure to asbestos and silica when the plaintiff was performing the work for the Housing Commission. Such exposure would have continued when the plaintiff was self-employed and prior to incorporation of the family company in 1981. The plaintiff then nominated a number of large corporations or entities for which he did sub-contracting work and also described some well-known sites at which he performed such work. Such entities included Kane Constructions and Lend Lease, as well as, to a lesser extent, Grollo. In evidence-in-chief, he was quite definite that such work was performed from 1980 onwards – see TACT8.
34 Mr Moore made a number of references to or reminders of the fact that the 20 year period after incorporation of the family company was what was being discussed – see, for example, TACT7-9, 17, 24 and 28.
35 When directed to this period, the plaintiff described jobs which involved exposure to asbestos in particular and silica at certain sites. These included St Vincent’s Private Hospital, the Melbourne Town Hall, the Freemasons Hospital, Ivanhoe Grammar School, Xavier College and the Banksia Street School in Heidelberg. This project involved demolition or reconstruction of part of the 1956 Olympic Village and its conversion into a college. Several of these jobs seem to have been performed by way of sub-contracting to Kane Constructions. In each instance, the plaintiff was either working directly with asbestos product or in the vicinity of other workers, not plasterers, who were removing it, demolishing it and the like.
36 During this 20 year period, the plaintiff was also doing work on private houses. This included the removal of asbestos products, particularly in relation to eaves. The plaintiff would “…cut it with a saw, it falls on you, of course” – see TACT28. In addition to what he described as his commercial work, the plaintiff used to work on one or two private houses per week.
37 The end result of this is that, as at the end of evidence-in-chief, I had a reasonably clear picture of the plaintiff’s work history and exposure to both asbestos and silica, and particularly in the 20 year period from 1981 to 2001.
38 This picture became more confused during cross-examination. That was in part because a portion of the cross-examination focussed upon the plaintiff’s common law action and what may have been alleged in it, and also quite possibly because the plaintiff seemed to me to tire visibly. Indeed, a rest period was held at the end of evidence-in-chief.
39 The plaintiff’s confusion in relation to questions concerning his common law action is well-demonstrated by the fact that, when asked in cross-examination to identify his signature on the answers to interrogatories, he denied that it was his. It eventuated that the signature at which he was looking was that of the person witnessing his signature.
40 When cross-examined concerning Court documents relating to the common law action, and a statement that he had made, the plaintiff at first agreed that the work that he had done at the Royal Melbourne Hospital, the Melbourne Town Hall and the Freemasons Hospital was between 1969 and 1981. He was uncertain in relation to St Vincent’s Private Hospital and stated that the work which he had done for Lend Lease was in the 1990s.
41 When cross-examined concerning these matters and dates, it was evident to me that the plaintiff was becoming somewhat confused and I requested that questions be put at a slightly slower pace. Following this, the plaintiff said that he did not know when particular jobs had been done. He also said that most of the work which he had performed taking away asbestos lining was “in the eighties” – see TACT52.
42 In re-examination, rather than talking about dates or years, Mr Moore asked questions based on events happening before or after incorporation of the family company, which took place in 1981. The plaintiff was comparatively quite clear in his answers that what he described as the commercial work was mostly after incorporation. By the commercial work, he meant “All the big jobs” – see TACT62. He stated that, after incorporation, he started the commercial jobs, although he may have done one or two before. He specifically identified the work at the Melbourne Town Hall, Ivanhoe Grammar School, the Freemasons Hospital and Xavier College as being after incorporation. I do not doubt the honesty of his answers and, when a particular event such as incorporation was able to be used by him as a starting date or signpost, his answers were quite definite.
43 The bottom line is this. I am satisfied that, during the period relied upon, the plaintiff’s commercial work and work on private houses brought him into regular contact with asbestos, some of which may have been direct contact with it. In many instances, he was working in the vicinity of others who were removing or otherwise dealing with asbestos sheeting and products. I also accept that, in the course of his work, he was regularly exposed to silica.
The expert evidence
44 As stated, the plaintiff gave the only lay evidence that was put before me. I turn now to the expert evidence, medical, occupational and epidemiological.
(a) The expert evidence on behalf of the plaintiff
45 The expert evidence on behalf of the plaintiff could be summarised as follows.
(i) Associate Professor Paul Mitchell
46 Associate Professor Mitchell is the plaintiff’s treating medical oncologist. His speciality is thoracic malignancy, which includes lung cancer and mesothelioma. He is based at Austin Health, which has one of the largest lung cancer and mesothelioma services in Australia. He is active in research in those areas. He has many other qualifications, which I shall not list here, but his practice and expertise basically relate to the area just described.
47 Associate Professor Mitchell has been treating the plaintiff since 26 February 2016, this being on referral from Mr Simon Knight, the plaintiff’s treating thoracic surgeon. In his report of 15 March 2016, Associate Professor Mitchell described the various surgical procedures which have been carried out on the plaintiff. It is also apparent that he had available to him various pathology reports and those of PET scans and radiological investigations. Associate Professor Mitchell organised a further CT scan and PET scan. These revealed multiple bilateral lung metastases and a new abnormality of the fifth thoracic vertebra, which was highly likely to be malignant.
48 In his report, Associate Professor Mitchell took what could be described as a broad history of the plaintiff’s cigarette smoking, which he ultimately calculated as giving a smoking intensity of 106 pack years. He explained that 20 cigarettes per day for a year is 1 pack year. His calculation was effectively based upon an estimate of 40 cigarettes per day from the age of 14 to the age of 67. He had seen the plaintiff for treatment purposes on the morning of the day upon which he gave evidence, that is, 30 November 2016. He said that he had not told the plaintiff that he was coming to Court to give evidence on this very day prior to the plaintiff giving him further information. I would refer to T268.
49 In any event, the further information provided to Associate Professor Mitchell by the plaintiff was that, between the ages of 14 and 35 years, he smoked 10-15 cigarettes per day, and from the age of 35 to 67, he smoked 25 cigarettes per day. This would convert into a total of 53 pack years. Whilst not being precisely the same, it is also closer to the estimate of smoking given by the plaintiff in his evidence – I would refer, for example, to TACT30, 31 and 34. This includes the simple observation that, for example, at the age of 12 he did not have the money to buy cigarettes. That does not seem surprising.
50 In any event, I am of the view that the calculations finally made by Associate Professor Mitchell on 30 November last are more likely to be closer to the mark. A calculation in the range of 50 or a little more pack years still represents a very substantial amount of cigarette smoking.
51 Returning to the reports and oral evidence of Associate Professor Mitchell, in his report of 15 March 2016 he also recorded that the plaintiff worked as a plasterer throughout his working life and was aware of extensive exposure to asbestos during the course of this employment. Professor Mitchell diagnosed adenocarcinoma of the lung, which is metastatic. Based upon the history provided to him, he noted that the plaintiff was regularly exposed to asbestos dust in the course of his work as a plasterer using asbestos cement products between 1965 and the 1980s. He also regularly worked in the vicinity of carpenters cutting and handling asbestos cement sheets. He did some of this work himself. He also used some type of asbestos powder at times. Thus, Associate Professor Mitchell concluded that the plaintiff had had extensive exposure to asbestos.
52 Nevertheless, and even allowing for the fact that he was at the time working on the basis of an estimate of approximately twice the number of smoking pack years that was double the figure at which he finally arrived, Associate Professor Mitchell expressed the opinion that the plaintiff’s asbestos exposure would have played a very significant role in the cause of his lung cancer.
53 Subsequent brief letters of Associate Professor Mitchell to the solicitor for the plaintiff reported on the progression of the cancer and the grim prognosis. On 22 November 2016, he reported again. This was in order to answer three specific questions. He expressed the view that asbestos was recognised as being an important cause of adenocarcinoma of the lung. Exposure to silica dust is also recognised as a cause. The third question and answer was as follows:
“Did the nature of Mr D’Argenio’s employment as a plasterer, involving as it did exposure to asbestos, dust and silica dust, give rise to a greater risk of the contraction of adenocarcinoma of the lung than if he had not been employed as a plasterer?
It was clear that Mr D’Argenio was exposed to asbestos dust and silica dust. It is also clear that this exposure to asbestos and silica dust increased the risk of lung cancer in this man. There are data available from many studies indicating that plasterers have an increased risk of lung cancer, over and above any risk due to cigarette smoking. This risk is generally in the range of a 50% to 100% increased risk of lung cancer.
The report of Dr James Leigh dated 6th of September 2016 details a number of relevant references from literature regarding asbestos and silica dust as a causative agent for lung cancer and the risks associated with employment as a plasterer.”
54 Turning to the oral evidence of Associate Professor Mitchell, I would point out that the defendant specifically raised no issue concerning his expertise – see T258. However, there were some challenges on the question of what was within that expertise. It is also apparent that, apart from the fact that the plaintiff is a patient of Associate Professor Mitchell and that they had some discussions, Associate Professor Mitchell was provided with the transcript of the plaintiff’s evidence, along with material such as the report of Dr Leigh.
55 In any event, Associate Professor Mitchell was of the view that, between 1981 and 2001, the plaintiff was working on a number of large construction projects and that there was exposure in the form of asbestos sheeting, particularly the demolition of same. The exposure appeared to be at least as intense, if not more intense, than that in the period prior to 1981. He also stated that he was able to get a satisfactory picture of the degree of exposure.
56 Associate Professor Mitchell went on to point out that the plaintiff had a significant smoking history. Smoking and asbestos are the two most important causes of lung cancer and are synergistic, not additive. Further, a man working with relatively low exposure to asbestos is some eightfold more likely to get lung cancer, whatever his smoking history background might be, than would otherwise be the case – see T262. In the present case, Associate Professor Mitchell was of the view that the asbestos exposure would be at least as significant as the smoking history.
57 In relation to his expertise, Associate Professor Mitchell said that he has a strong scientific background and a strong understanding as to statistical and epidemiological methodology. He was aware of the International Agency for Research on Cancer (hereinafter referred to as “the IARC”) and aware of the fact that both asbestos and silica are recognised as high-level carcinogens. He was also aware of the comments made by Dr Leigh. He was aware of the data that indicated an increased risk of lung cancer in plasterers and that it varies from 17-19 per cent up to 170 per cent. He reiterated that:
“…certainly that occupation (a plasterer) is associated with an increased risk of contracting adenocarcinoma of the lung. Most studies would be in the range of 50 to 100 per cent increase in risk” – see T265.
58 The literature referred to by Dr Leigh supports the views of Associate Professor Mitchell.
59 In cross-examination, Associate Professor Mitchell said that his specific expertise for the last 15 years has been in the area of thoracic cancers, and particularly lung cancer. He has also been heavily involved in research of lung cancer, which touches upon causation. He agreed that the bulk of his research was in relation to treatment. Whilst he had no formal qualifications in epidemiology, the work that he does and the papers that he writes closely touch upon it. He does not have specific expertise as an occupational hygienist.
60 Associate Professor Mitchell also stated that the median smoking intensity for males who get lung cancer is 52 pack years and his current calculations in relation to the plaintiff were around about that figure. He also stated that he always takes an abbreviated occupational history for lung cancer and mesothelioma patients.
61 Associate Professor Mitchell was not able to say what percentage of the plaintiff’s work was with or in the vicinity or carpenters or whether the plaintiff performed more of that work before or after 1981. Given that the plaintiff was a plasterer, Associate Professor Mitchell would expect that he had exposure to silica. However, he took no particular history in relation to silica exposure. In relation to a threshold for asbestos exposure, his understanding of the international position was that there is no safe level that has been identified for asbestos.
62 He also pointed out that, because a particular pathology report does not mention asbestos fibres, it does not mean that they are absent from that tumour. The absence of pleural plaques was also not determinative of there being no exposure. The presence of such plaques might be a marker of higher exposure, but they may or may not be present in cases of lung cancer or mesothelioma. In any event, the occupational history is of greater weight in terms of assessing exposure. Associate Professor Mitchell expressed the view that exposure to asbestos throughout the plaintiff’s working life would have been part of the cause of the lung cancer.
63 Associate Professor Mitchell stated that he disagreed with the opinion of Professor Fox that the plaintiff’s smoking was the overwhelming cause of his lung cancer. He further said that, given the synergistic relationship between smoking and asbestos exposure, even if the asbestos exposure was very small, it would still be “really important” – see T281. He also disagreed with the opinion of Mr Simon Knight that a causal linkage between lung cancer and asbestos exposure was by no means as clear as the link between the development of mesothelioma and exposure to asbestos. He stated that his figures concerning the increased risk to plasterers effectively came from studies mentioned by Dr Leigh.
64 Associate Professor Mitchell agreed that he saw Dr Leigh as an expert in the area. He had not been provided with reports of Mr Rogers and, whilst recognising his name, was not aware of his level of expertise. He only understood the standards in the Helsinki Criteria in a general sense.
65 In re-examination, Associate Professor Mitchell stated that the plaintiff’s transcript evidence in relation to work activity between 1981 and 2001 gave him no reason to change the views expressed in his reports. Further, his opinion would be exactly the same if the period between 1981 to 2001 was the only one under consideration.
(ii) Mr Alexander Rosalion
66 Mr Rosalion is also a medical practitioner. He is a Fellow of the Royal Australian College of Surgeons, both in general surgery and subsequently in cardiothoracic surgery. He has had extensive experience in that field, having first trained in it in 1983. He has held posts at the Austin Hospital, the Repatriation General Hospital, the Western General Hospital, the Peter McCallum Cancer Institute and Preston and Northcote Community Hospital. Mr Rosalion has been a clinical instructor at the University of Melbourne. In more recent times, he has practised at Knox Private Hospital. He has presented numerous papers concerning his area of speciality and written an extensive list of publications. Mr Rosalion saw the plaintiff at the request of his solicitors.
67 He first reported on 12 June 2016. In that report, Mr Rosalion recorded the plaintiff’s smoking history, which was roughly in line with the history given by the plaintiff in his evidence. Mr Rosalion made his calculations on the basis of the upper end of the plaintiff’s figures and arrived at a 69 pack year history.
68 In relation to the plaintiff’s work history, Dr Rosalion took a long history of exposure to asbestos, both in the plaintiff’s own work and work which he performed in the vicinity of others using asbestos materials. Dr Rosalion noted the extensive use of AC sheeting. He concluded that the plaintiff would have had heavy asbestos exposure for most of his working life. He made specific mention of a job for Lend Lease in the 1990s. The conclusion of Mr Rosalion was that the plaintiff had heavy, unprotected asbestos exposure for more than three decades in his work as a plasterer.
69 Mr Rosalion expressed the opinion that the type of lung cancer which the plaintiff had, being adenocarcinoma, is the type least associated with smoking. Nevertheless, he implicated it as a possible aetiological factor, either as a carcinogenic agent in its own right or in its synergistic effect with asbestos. He considered the asbestos exposure to be a likely aetiological agent in the development of the plaintiff’s condition, both as a primary carcinogen and because of its synergistic effect with smoking. He considered the lack of information concerning pleural plaques to be not relevant and made much the same remark concerning interstitial pulmonary fibrosis. He considered that asbestos exposure has been instrumental in the development of the plaintiff’s condition.
70 Mr Rosalion reported again on 7 November 2016. He had not seen the plaintiff again, but had been provided with the report of Dr Leigh. He expressed the opinion that asbestos is a known carcinogenic agent in the development of all forms of lung cancer and in particular of adenocarcinoma. The IARC has positioned asbestos as a Group 1 carcinogen, which is the highest grouping given by that organisation. Dr Rosalion made a similar observation concerning silica dust. His conclusion was that the plaintiff’s exposure both to asbestos and silica over a prolonged period of time would have markedly increased his risk of developing lung cancer and in particular of the adenocarcinoma variety. His risk of developing this would have been considerably less had he not been employed as a plasterer.
71 Subsequently, the transcript of the plaintiff’s evidence was forwarded to Mr Rosalion, who reported again on 20 November 2016 (an earlier report was based on only part of the transcript). Mr Rosalion saw no need to change the view that he had previously expressed. This report also contains the following opinion:
“The various discussions regarding time-frame and particular employer, although I am sure are important from the medico legal point of view, do not make any medical difference.”
72 Mr Rosalion also gave oral evidence. He gave some additional evidence concerning the synergistic effect of smoking and asbestos in relation to lung cancer. Synergism effectively means that the two agents are acting together, whereas multiplication is looking at the end result. However, it is part of the process and Mr Rosalion does not differentiate between the two. He repeated that people can have asbestos exposure without developing pleural plaques, also stating that the best determinant of whether somebody has or has not been exposed to asbestos is the history taken from that person, along with information concerning the work environment and the like – see T132. Pleural plaques are simply a marker of exposure. The absence of pleural plaques does not mean that there has not been the exposure.
73 Mr Rosalion also disagreed strongly with the view of Professor Fox that the presence of asbestosis is a necessary precursor to the development of asbestos-related cancer. Lung cancer or other forms of cancer can be contracted with relatively low asbestos exposure doses. Further, additional testing in relation to histological changes is not always done, because it is of no medical relevance. The presence or absence of asbestos bodies does not change the medical treatment. Because the plaintiff was exposed to known carcinogens, his risk of developing lung cancer was clearly increased.
74 Mr Rosalion also said that plastering is only one of a number of occupations that increase the likelihood of developing lung cancer. Occupations where there was no asbestos or silica exposure would be less likely to lead to the development of lung cancer. Exposures in the period between 1981 and 2001 are relevant. They have increased the risk of the plaintiff developing lung cancer. In cases of lung cancer and mesothelioma, a high level of exposure to agents such as asbestos and silica is not needed. Mr Rosalion has had a lot of patients who developed their malignancies on the basis of relatively light exposure to such agents. These are lung cancer cases, as opposed to people with silicosis or asbestosis. The lung cancer cases can occur with relatively modest exposures.
75 In answer to a question of mine, Mr Rosalion said lung cancers can be created with one asbestos fibre. He went on to say that he had seen patients who had developed lung cancer from asbestos exposure of a very low level. This has occurred “not infrequently” – see T142.
76 In cross-examination, Mr Rosalion agreed that he had no expertise in relation to assessment of exposure levels. However, he has seen industrial hygienist reports and has talked to patients concerning how heavy or light their exposure is. He often takes an extensive occupational history. He has a moderate knowledge of the epidemiology of lung cancer. He had looked at no particular epidemiological studies for the purposes of this case. He agreed that he took little or no history from the plaintiff in relation to exposure to silica.
77 A high level exposure to asbestos is not required in the formation of pleural plaques. The absence of pleural plaques does not exclude asbestos exposure. He is not aware of evidence that shows a direct relationship between the amount of pleural plaques and the exposure.
78 Mr Rosalion said that he found the plaintiff to be an “average” historian, as a result of which there was some difficulty with dates and the like. At the time that he saw the plaintiff, Mr Rosalion did not push him into differentiating between periods.
79 Mr Rosalion said that smoking has to be considered and agreed that the plaintiff had a very heavy extensive smoking history. He believed that the plaintiff’s lung cancer had been caused by a combination of factors, including smoking and the industrial exposure. He would not agree that the evidence suggested that smoking was the overwhelming exposure or risk. Adenocarcinoma is the least common form of lung cancer as far as smoking is concerned, but remains relevant. He referred again to the synergistic effect of the combination of smoking and asbestos exposure – see T153. There is no scientific way of balancing the various risks. He also pointed out that the length of exposure to asbestos is very important. The threshold is not known. Even a transient exposure could increase the risk of developing lung cancer.
80 Mr Rosalion also expressed the view that silicosis is not required in order to establish a link between lung cancer and exposure to silica. Whilst his opinion was that silicosis is not required, he did not have as much evidence for that as compared with the asbestos situation. On the testing of tissue cultures, it is when the carcinogenic agents are introduced that the cancer develops. What is known is that the risk is increased in a person who has had asbestos exposure.
81 When the report of Mr Knight was put to him, Mr Rosalion stated that the testing that had been done indicates that asbestos can be carcinogenic in its own right. This is also consistent with the World Health Organisation listing it as a carcinogenic agent. He again stated that each of the agents (smoking and asbestos exposure) increases the risks, but apportioning them cannot be done.
82 Mr Rosalion again indicated that, when he first consulted with the plaintiff, he did not specifically ask him about any given period of exposure. However, the plaintiff indicated that during the whole of his working period, which included the specific date range, he had the exposures that have been mentioned. As it was for a longer period, probably the period before 1981 represented greater exposure, but Mr Rosalion was not positive as to this. He also referred to the hazards associated with demolition work. Whether old material was being removed and replaced with new material is something to be considered.
83 In re-examination, Mr Rosalion stated that the receipt of the transcript did not affect the opinions which he had previously given. The plaintiff had indicated that he had significant exposure after 1981. He repeated that there is no safe level of exposure to asbestos and silica in relation to lung cancer. The degree and duration of exposure are both important.
(iii) Mr Michael Kottek
84 Mr Kottek is an occupational and environmental health consultant. He has numerous qualifications, including a Bachelor of Science (Honours) Degree from the University of Melbourne and is also a Master of Science. He also has a Graduate Diploma of Occupational and Environmental Health from Monash University. He has advised the Minister for Health and other government departments and agencies in relation to the public health impact of chemical exposures. He has performed workplace surveys, risk assessments, air testing for asbestos and other hazardous materials. He has membership in a number of societies and has frequently given expert evidence concerning asbestos and the like. He has conducted a number of experiments in this regard. That is but part of his curriculum vitae.
85 His report also contains reference to many publications and articles over the years, including output from the World Health Organisation and many other bodies.
86 Mr Kottek provided a report to the solicitors for the plaintiff on 15 April 2016. He had previously interviewed the plaintiff at his home. He took a very detailed history. The conclusion of Mr Kottek was that the plaintiff had experienced significant exposure to asbestos from using asbestos-containing plaster jointing materials, as well as from personally installing and removing asbestos cement materials. He had also experienced significant bystander exposure to asbestos from the spraying of it and the installation of asbestos lagging. He is also likely to have experienced bystander exposure from carpenters handling asbestos cement.
87 In Mr Kottek’s opinion, the plaintiff’s exposure to asbestos could be said to meet the Helsinki Criteria narrative test of 5-10 years of moderate exposure to asbestos. In his more detailed history, he made such observations as that, given the extent of the plaintiff’s onsite work, it was likely that, on many occasions, he would have been on sites installing plaster at the same time that carpenters were handling asbestos cement.
88 On 22 November 2016, Mr Kottek provided a supplementary report, this following receipt of the transcript of the plaintiff’s evidence. In this report, Mr Kottek observed that the transcript indicated that the plaintiff’s work in the 1981-2001 years involved periods when he carried out uncontrolled demolition of internal wall linings or tile underlays, such as at St Vincent’s Private Hospital. Given the timing of this, Mr Kottek considered it most likely that most of the wall linings or tile underlays were asbestos cement. Asbestos-free fibro-cementing first entered the market in the early 1980s, so it is considered unlikely that the plaintiff was removing asbestos-free fibro-cementing until later in that 20 year period. His removal of asbestos cement or fibro-cementing took place in wet areas, such as bathrooms, where ventilation was often poor.
89 In his earlier report, Mr Kottek had also stated that the plaintiff had experienced significant bystander exposure to respirable silica, as well as personal exposure from using silica which contained rendering compounds. In his supplementary report, he referred to the fact that even the mixing of concrete by brickmasons has been reported to involve exposure to silica which could exceed occupational exposure standards. His ultimate conclusion was that over the 1981-2001 period the plaintiff frequently experienced sustained periods of exposure to significantly elevated levels of airborne asbestos and respirable crystalline silica.
90 Mr Kottek also gave quite lengthy oral evidence. At the commencement of his evidence-in-chief, his qualifications, experience and the like were explored at some length. Suffice to say that they are impressive.
91 Mr Kottek stated there has not been identified any level of asbestos exposure which did not create a risk of lung cancer. It is possible that such a level exists, but it has not been identified. He also stated that both asbestos and silica are in Category 1 of the levels of carcinogenicity classified by the IARC. He noted that the plaintiff had described visible dust from his work, in addition to the nature of the work that he carried out.
92 Mr Kottek also stated that the plaintiff’s work involved exposure to asbestos and silica, something unfortunately not uncommon for people in the construction industry. Construction is a recognised risk for exposure to those substances. The plaintiff would have had more exposure compared to other trades outside the construction industry – see T55. He also stated that, in the period 1981-2001, the plaintiff certainly had ongoing exposure to asbestos and silica.
93 In cross-examination, Mr Kottek confirmed that he was a certified industrial hygienist, having been so certified by the American Board of Industrial Hygiene. He also stated that there was a heavy epidemiology component associated with his Graduate Diploma in Occupational and Environmental Health. He conceded that both Mr Rogers and Ms Lara have some qualifications that he does not have. He accepted that, for the purposes of his opinions, he was heavily reliant upon what the plaintiff had told him in relation to his employment history – see T64.
94 He also agreed that some of the studies to which he had had regard were concerned with workers who remained in the same place for a long time or were involved in the same process for such a time. He agreed that there was less variability in such situations than was the case with the plaintiff. He also agreed that there was a dose responsive relationship for asbestosis and lung cancer.
95 Mr Kottek agreed that, given the presence of substances like silica and asbestos in the environment, there is probably a level at which there is no appreciable risk. However, he had not attempted to quantify this. He also stated that the plaintiff’s smoking would be a relevant consideration, but he had not attempted to quantify that risk. He believed that the purpose of his evidence related to the magnitude of exposure to asbestos and silica.
96 From 1975 onwards there has been a reduction in the use of asbestos and some control measures were starting to become more widely implemented. He did not agree with the proposition that there was no scientific or epidemiological evidence to suggest that a small or single exposure of asbestos will cause asbestos-related diseases. He further agreed that bystander dust exposure is very difficult to measure, but visible dust would be an indication. In some circumstances, the assumption that the dust would include asbestos is a given – see T73.
97 He also referred to an asbestos cement product called “Villaboard”, which came onto the market in a big way in the early 1970s, but Mr Kottek guessed that it became asbestos-free in the early 1980s. Mr Kottek also emphasised that he interviewed the plaintiff prior to preparing his first report and took a full occupational history. However, he had not specified particular dates, but thought that, when the plaintiff was working for himself in mainly commercial construction, that may well have included periods when he was employed by the family company. Whilst he had not specified precise dates, he had assumed that the plaintiff was doing this work from the 1980s, given the companies that he was subcontracting to and some of the jobs which he nominated.
98 In relation to his interview with the plaintiff, Mr Kottek stated that the plaintiff was not “great with dates” but “answered the questions I gave him well enough” – see T82. Mr Kottek also stated that there were still a lot of materials which contained asbestos “out in the field”.
99 Mr Kottek had taken a history of the plaintiff demolishing asbestos cement that had been rendered over, this often being in wet areas where there was pipe ducting behind a rendered wall.
100 Mr Kottek had also referred to files concerning people other than the plaintiff, but this seems to have been largely to assist in regard to work done at premises operated by the Housing Commission. The plaintiff’s involvement with the Housing Commission, whilst part of his work history, was well before 1981.
101 Mr Kottek stated that, in relation to silica, there will be a variety of particle sizes within sand. He also stated that, when the plaintiff was working on commercial constructions, some of that would have been patch-up work – for example, at St Vincent’s Private Hospital and the Alfred Hospital – as opposed to new work. By the mid-1980s, there would be very little likelihood of there being any asbestos in materials used in new work in the sense of new high rise buildings and the like. Mr Kottek was not able to give any exact assessment as to the proportion of the plaintiff’s activity which involved new work as opposed to repair work.
102 Mr Kottek referred to a product called “Macrender” used by plasterers. He had one sample analysed, and it had a very high silica content. He conceded that, only one sample having been analysed, this could be an oddity. He also referred to some testing which he had done in 1996 and 1997 in relation to the amount of asbestos contained in visible dust. He did not concede that the fact that the experiments were carried out in a test chamber made a great deal of difference to the outcome. Whilst aware of the criticism of these experiments by Mr Rogers, Mr Kottek did not accept the suggestion that they were flawed. The conclusion reached had been consistent with the previous rule of thumb that, if you could see dust in the air, the content is likely to be above 5m particles per cubic foot. I would refer to the cross-examination at pages T107 and following.
103 Mr Kottek said that regulations in relation to asbestos were enacted in Victoria in 1978 and after 1981 there was more substantial knowledge in relation to the substance and its dangers. However, stringent precautions were not taken until the late 1980s or early 1990s. In 1988, the National Occupational Health and Safety Commission introduced a code of practice for the safe removal of asbestos cement, also dealing with friable asbestos. Mr Kottek had supervised the safe removal of asbestos in the first half of the 1990s. Mr Kottek also stated that, in the early 1990s, there was still a lot of uncontrolled asbestos cement removal occurring. He said that the normal method of removing asbestos sheeting from wet areas and the like would be by the use of hammers, wrecking bars, shovel and a wheelbarrow. He agreed that the plaintiff had probably had more exposure before 1981, as opposed to after that year. He also agreed that some construction workers, such as a lagger or boilermaker, would be expected to have more exposure than a plasterer. Carpenters were also expected to have greater exposure than plasterers. Mr Kottek said that activities such as the mixing of mortar lead to elevated levels of silica exposure. That was of some relevance to the plaintiff’s situation.
104 In re-examination, Mr Kottek said there was nothing in the reports of Mr Rogers or Ms Lara that caused him to alter the opinions that he had expressed. The same could be said of matters raised in cross-examination. In relation to his interview with the plaintiff, which went for approximately one and a half hours, Mr Kottek said that the plaintiff did the best that he could. None of the differences that could be detected in the transcript evidence were materially relevant when compared with the interview. He also stated that, in a sample of sand, there would usually be a mixture of large non-respirable particles and some smaller particles that would be respirable if they became airborne.
105 In relation to the plaintiff’s work with asbestos materials, Mr Kottek stated that “knocking the old stuff out in an uncontrolled manner would have led to some exposure” – see T123. He also explained that, if there was visible dust, that is an indication “that a five million particle base standard has possibly been breached” – see T124.
(iv) Dr James Leigh
106 Dr Leigh, who is based in Sydney, is a consultant occupational physician. In addition to his medical degree, he has a lengthy list of qualifications, fellowships, lectureships, published papers and the like. In short, he has been carrying out research and tertiary teaching in occupational respiratory medicine for 51 years and in asbestos-related disease for 29 years. Amongst other qualifications, he is the Honorary Senior Research Consultant to the NSW Asbestos Diseases Research Institute at the University of Sydney. He is a member of the National Health and Medical Research Council Asbestos Working Group.
107 Various materials were sent to him to assist him in the formulating of his report of 6 September 2016 to the plaintiff’s solicitors. He summarised the exposure to asbestos and silica which had occurred to the plaintiff as a plasterer over the 36 year period between 1965 and 2001. This included exposure to asbestos from demolition of structures containing asbestos jointing compound and exposure to asbestos from demolition operations on existing asbestos cement materials, both directly and as a bystander.
108 Further, he referred to exposure to asbestos from 1965 to the mid-1980s from operations on new asbestos cement materials, directly and as a bystander. He also referred to exposure to crystalline silica from cement rendering materials between 1965 and 2001. He considered it very probable that exposure to Chrysotile, Chrysotile/Tremolite and Amphobile asbestos occurred during the exposures.
109 In his initial report of 15 April 2016, Dr Leigh referred to the fact that IARC, being part of the World Health Organisation, has evaluated all the very extensive published literature, both epidemiological and experimental, as at 2009 in relation to the risks of lung cancer with asbestos exposure. It concluded that there is sufficient evidence that asbestos of all types causes cancer of the lung. For that reason, IARC classified all forms of asbestos as Category 1 human carcinogens. He also stated that there is no threshold exposure for asbestos-related lung cancer risk. This means that any level of asbestos exposure increases lung cancer risk.
110 In his report, Dr Leigh went on to state that smoking is only weakly associated with adenocarcinoma.
111 In relation to silica, IARC has evaluated the extensive published literature and has concluded that there is sufficient epidemiological evidence that quartz causes cancer of the lung. Accordingly, quartz is also a Category 1 human carcinogen. There is probably a threshold for the lung cancer risk in relation to quartz, but such threshold level is not known. It was found that all main lung cancer histological cell types had an increased dose-related risk with quartz exposure.
112 In relation to the risk of lung adenocarcinoma in plasterers, Dr Leigh stated in his report of 9 September 2016 that there are epidemiological studies which show increased lung cancer and lung adenocarcinoma risk in the occupational group of plasterers, which grouping includes some related occupations. He referred to some six studies in this regard. The increase in risk in two of these reports (Brueske-Holfeld and Zahm) varied from 43 per cent to 170 per cent. A report in Britain (the UK HSE report) also showed increases in lung cancer risk for male plasterers, which, as far as I can make out, seems to range from 15 per cent to 27 per cent based on data covering the period 1981-1987 and 19 per cent for the period 1991-2000.
113 Needless to say, when Dr Leigh gave oral evidence, there was considerable cross-examination concerning these studies. In any event, in his report, Dr Leigh concluded that epidemiological studies support the proposition that plasterers face an increased risk of adenocarcinoma of the lung.
114 Dr Leigh was subsequently sent the transcript of the plaintiff’s evidence. Having read it, he made no material alterations to his earlier opinions.
115 I turn now to the oral evidence of Dr Leigh. At the outset, the full curriculum vitae of Dr Leigh, which goes for some 43 pages, was tendered.
116 Dr Leigh confirmed that, for the purposes of his report, he had been asked by the solicitors for the plaintiff not to take into account the plaintiff’s smoking history. He also confirmed that asbestos had been categorised by IARC as a Category 1 carcinogen, being the highest level. He described how IARC, which is part of the World Health Organisation, is constituted. It is an expert group of some 100 scientists regarded as the most authoritative in the world. He also stated that the studies show that adenocarcinoma does tend to have a steeper dose response in its relationship with asbestos than other cell types – see T173. He confirmed that silica was also a Category 1 carcinogen.
117 However, Dr Leigh also said that the actual magnitude of the risk in silica is a lot less than asbestos. He confirmed that the studies showed that there was an increased risk of lung cancer in plasterers or, in some cases, plasterers combined with some other categories of workers.
118 Dr Leigh was asked further questions about the increased risk faced by the plaintiff when working between 1981 and 2001 in relation to his exposure to asbestos and silica, as compared with other trades not associated with the construction industry. Dr Leigh said that the proportional mortality studies give increases in risks in the range of 40-100 per cent. I would refer to the discussion at T176.
119 During cross-examination, it was put to Dr Leigh that he had no qualifications in epidemiological studies. His response was that he regarded himself as being one of the founders of modern epidemiology. Qualifications were not introduced until the mid-1980s. However, he had effectively been taught epidemiology when dealing with public health. He had also undertaken degrees in pure applied mathematics, including mathematical statistics and primary computer science. He expanded further upon these qualifications, including that he had effectively developed teaching programs in epidemiology in England. He was probably the first specialist epidemiologist appointment in Melbourne, giving teaching courses here and subsequently in Sydney, in addition to elsewhere in the world. He also undertook a considerable amount of epidemiological and other research when working for the Coal Board. He had been Head of the Epidemiology Unit with the National Occupational Health and Safety Commission.
120 Dr Leigh agreed that he had been provided with particular studies which assisted him to come to a conclusion in relation to the risks associated with plasterers as opposed to other occupations. He was taken to some of the studies. He was questioned firstly about the Brueske-Holfeld report. He agreed it was noted in that study that the main determinant of lung cancer was smoking, a proposition with which he agreed. Within this report, there were two distinct studies, one of which dealt with people whose working life had been largely between 1945 and 1990. Hence, approximately half of their working life would have been before the introduction of controls in relation to asbestos. Plasterers seem to have been put in the same category as insulators and Dr Leigh agreed that insulators would have had a significantly greater exposure to asbestos than plasterers. Grouping plasterers with insulators would not necessarily give an accurate reading in relation to plasterers. Dr Leigh said that he was not relying “terribly heavily” on that study – see T186.
121 Dr Leigh was then taken to the Zahm study, which seems to have been based on extraction of details from medical registry records. This meant that the complete occupational histories were not necessarily taken. In this particular study, plasterers were put in the same category as painters and paper hangers. Dr Leigh was uncertain as to whether painters were exposed to significantly greater risk than plasterers. He agreed with the proposition that current employment may not be relevant for lung cancer, it being a disease of long average latency. He agreed that the studies’ results should be interpreted cautiously.
122 Dr Leigh stated the following:
“…the odds ratios are quite high, so they’re probably immune to a degree of error. The overall conclusions are not likely to be completely vitiated by design weaknesses.” (See T190)
123 Dr Leigh was also taken to the Pearson and Melhem NIOSH Report. This seems to have been based on death certificates. Whilst the report could also be criticised, it showed that, among all deaths in plasterers, there was a higher than expected proportion due to lung cancer than the average of all the other occupations. Lung cancer deaths, adjusted for age, were over-represented in the plasterer group. This particular report produced a result based on proportional mortality – an increased likelihood of death related to occupation.
124 This study grouped plasterers with lathers. Dr Leigh was not precisely sure of the nature of the work of a lather, but, as a lath is a thin strip of wood, he presumed that it is to do with the use of thin wooden strips in association with plastering. (According to the Australian Concise Oxford Dictionary, a lath is a thin flat strip of wood, especially one of a series forming a framework or support for plaster.)
125 In the opinion of Dr Leigh, the study demonstrated that lung cancer, proportionate to other causes of death, showed an increase compared to the average of all other occupations in America. He agreed that it was a study done in a different time and in a different country, where work practices would have differed. He agreed that there were other occupational categories that also carried increased risk. Proportional mortality would also be put up by reason of smoking.
126 In relation to the British report (the UK HSE report), Dr Leigh agreed that the overwhelming determinant of the occurrence of lung cancer was cigarette smoking, either independently or via synergistic association with other risk factors. Dr Leigh also stated that, in relation to plasterers, according to that report, the number of lung cancer deaths was 27 per cent more than expected in the general population – see T200.
127 In further cross-examination, Dr Leigh stated that the mortality rate for plasterers was above that expected of the normal population, this being due to exposure. Dr Leigh agreed that plasterers were not specifically identified as being exposed to an increased risk from silica. However, he believed that there was an increased risk of lung cancer in silica-exposed workers.
128 Dr Leigh also stated that both silica and asbestos are now well-known to cause cancer by a genotoxic mechanism – the slightest dose will cause DNA damage and potentially cause a cell to become malignant, quite irrespective of the development of asbestos or silicosis. His conclusion was that there was no safe level for either.
129 Dr Leigh also agreed with the proposition that, the greater the exposure, the greater the risk. He agreed that a cumulative exposure on a probability basis should be considered as the main criterion for the attribution of a substantial contribution by asbestos to the risk of lung cancer. I might say that this particular line of cross-examination was objected to on the basis that it dealt with causation, as opposed to the “due to the nature of” provisions of the Act.
130 As with several other objections, I permitted the cross-examination to continue, given the circumstances of the case. In any event, whilst I could understand the objection, it seemed to me that the question was probably permissible. Dr Leigh pointed out that, where there is both smoking and asbestos exposure, interaction between them is somewhere between additive, or more than additive, and multiplicative or more than that.
131 In re-examination, Dr Leigh stated that he had applied the contents of the various articles or studies referred to in order to give an answer to the question as to whether there was an increased risk. His conclusion was that there is such an increase.
(b) The expert evidence on behalf of the defendant
132 The expert evidence on behalf of the defendant could be summarised as follows.
(i) Mr Alan Rogers
133 Mr Rogers is an occupational hygiene consultant. He is also based in Sydney. He has provided to the solicitors for the defendant two reports. The earlier of these is dated 11 November 2016. It is a very lengthy report.
134 Mr Rogers also has numerous and impressive qualifications. Amongst other things, he is a Master of Science in Occupational Hygiene from the University of London and a Master of Science in Environmental Chemistry from the University of NSW. He is also a Certified Industrial Hygienist with the American Board of Industrial Hygiene and a Certified Occupational Hygienist and Fellow of the Australian Institute of Occupational Hygienists. He has completed extensive post-graduate training in relation to toxicology, statistics, epidemiology and respiratory physiology. He has provided occupational health advice and risk assessment when employed by the Australian Government. Since 1978, he has actively researched the association between dusts such as asbestos and silica and the development of diseases such as lung cancer, mesothelioma and the like. During the 44 years of his career, he has been extensively involved with the mining and manufacturing industries and the design and supervision of small and large scale asbestos removal projects in buildings. He has also published numerous articles. In short, as with the other expert witnesses, he has an impressive list of credentials.
135 The report of Mr Rogers is of such length that it is perhaps preferable that I simply summarise his conclusions. Firstly, he observed that the plaintiff’s clinical findings indicate that his lifetime cumulative asbestos exposure would have been very low and his cumulative crystalline silica exposure extremely low. Based upon Mr Rogers’ interpretation of the alleged claim of exposure, 99.7 per cent of that exposure was experienced in the period 1965-81 and 0.3 per cent of the exposure may have arisen in the 1981-2001 period.
136 The issue of exposure translates into a relative risk of around 1.06 compared to that of the normal Australian population, which is 1.0. In relation to the silica, the plaintiff’s exposure was extremely low and the lifetime lung cancer risk would amount to approximately 1 in 35 million or more. His tobacco smoking alone resulted in exposure to a lung cancer risk of up to 31.2 times higher than that of a non-smoker. Even after allowing for the synergistic effect, 0.2 per cent of the plaintiff’s lung cancer risk arose from asbestos exposure and only 0.3 per cent of that from exposure after 1981. Ninety-seven per cent of the risk arose from long-term cigarette smoking. The effect of that long-term smoking effectively swamps the minor effect from the asbestos exposure, regardless of the value of any reasonable estimated asbestos exposure or the method of synergism applied in the risk calculation.
137 Mr Rogers supplied a second report dated 25 November 2016. This was in response to information contained in the transcript of the plaintiff’s evidence and in supplementary reports prepared by others. The conclusions of this report were that the clinical findings indicated that the plaintiff’s lifetime cumulative asbestos exposure would have been extremely or very low and that his cumulative crystalline silica exposure was extremely low.
138 Based upon the transcript and the interview of Professor Fox with the plaintiff, the alleged cumulative asbestos and crystalline exposure was now much less than previously insinuated. Without going through the mathematics, Mr Rogers reduced the likely relative risk assessment to 1.01, presumably as against the norm of 1.00. He assessed the effects in relation to silica as being approximately 1 in 500,000, a value immeasurable in a working population. He again repeated the importance of the smoking history and repeated his opinion that the plaintiff’s heavy, long-term smoking imposed such an overwhelming risk of lung cancer that it effectively swamped the minor effect from asbestos exposure.
139 It is of interest that Mr Rogers noted that the plaintiff denied that it was his signature on a Court document and hence Mr Rogers disregarded assertions of exposure, duration of exposure and the like contained in such statement, unless otherwise consistent with his evidence. If he is there referring to the Answers to Interrogatories, as has been stated, the plaintiff clearly directed his attention to the signature of the person witnessing the document, rather than his own signature. Mr Rogers made some criticism of the basis of at least one expert report and, in general terms, the opinion expressed in his earlier report remained unaltered.
140 Mr Rogers gave oral evidence. In evidence-in-chief, he was taken through his reports and qualifications. He stated that the nature of employment as a plasterer has become more specialised, with more narrow areas of speciality since the 1970s and with the introduction of high rise buildings and large scale construction. Between 1981 and 2001, there was a move to ready-mix type materials and the use of smoothing and lubrication agents. In relation to the use of plasterboard and the like, there was no asbestos in such products after 1981 or that era. He referred to the fact that smoking was a large, overriding and confounding factor in any analysis of lung cancer risk – see T218. He stated that there was an increased risk of lung cancer in people exposed to quite high levels of silica, but the level of exposure needs to be well in excess of the norm.
141 In arriving at his conclusions, Mr Rogers made some assumptions based upon his observations of trades in the construction industry and inferences made in the plaintiff’s evidence as to what appeared to Mr Rogers to be the highest of the upper limits of his contact with the relevant materials. He clearly regarded the Helsinki Criteria as having real limitations. However, the updating of the Criteria in 2014 strengthened the requirement of getting correct occupational histories and assessing the cumulative exposure. The best way of assessing the risk of asbestos exposure in relation to lung cancer is to take a proper and detailed occupational history, in order to assess the duration of the exposure and then to apply specific dose, response and risk estimates to the different products in the industry – see T223. Detailed information is not available in relation to silica.
142 Tobacco smoking, asbestos and silica are all dose-related risks of lung cancer. Accordingly, these have to be sorted in terms of the level of risk associated with each of the agents.
143 In relation to asbestos, the higher the dose, the higher the risk. It is more difficult at the lower end of the dose response relationship. With asbestos, it is difficult to determine whether there is or is not a threshold. With silica, there appears to be a clear threshold.
144 Mr Rogers stated that the level of risk related to asbestos and lung cancer before and after 1981 is roughly equal. The same applies to silica. In the case of the plaintiff and asbestos, the risk is so small that it would not be able to be measured in the normal population. The risk in relation to silica is immeasurably low. Because of his smoking, the risk to the plaintiff of lung cancer was in the order of 31 times higher than that of a non-smoker. There is also a background risk of something in the order of 3 per cent, which relates to genetic predisposition, environmental factors and the like.
145 Unless smoking histories are matched to the particular industry in which people are engaged, one cannot make much difference out of lung cancer risks – see T228. Nothing much can be made of the epidemiological studies which rely upon work done before 1981 in terms of assisting and understanding exposure after 1981.
146 Turning to the cross-examination of Mr Rogers, he agreed that asbestos was a proven human carcinogen and a recognised cause of adenocarcinoma. He further stated that asbestos and tobacco smoke act together to give a near multiplicative effect. He also agreed that workers who are regularly exposed to asbestos dust have an increased risk of lung cancer, provided that they get to a set level of exposure.
147 Interestingly, Mr Rogers stated that “you can massage any data any way you like. That’s the modern epidemiology” – see T232. He agreed that, with the work such as that performed by the plaintiff performed at various sites over a period of time and with work that was varied in nature, difficulties were created.
148 Mr Rogers stated that there had been a difficulty in the present case because a proper occupational history had not been taken. He asserted that the experience of the individual occupational hygienist as to tasks and the time taken to perform them was important. In relation to problems with the history, Mr Rogers stated that he had given an upper estimate and a more probable estimate.
149 In relation to someone who is doing a number of tasks, Mr Rogers takes the average of such tasks. Mr Rogers agreed that the use of a shovel, crowbar or hammer for the purpose of removing asbestos cement sheets and the shovelling of material into a wheelbarrow was the sort of process that he would have expected, based on his experience. However, he did not read the plaintiff’s description of work that he performed as “smashing up materials” – see T244.
150 He also stated that corrugated sheets had more asbestos in them than flat sheets. He was critical of some observations of Mr Kottek in relation to the removal of asbestos sheeting, in that an exaggerated amount of exposure had been created. Mr Rogers was also critical of the Helsinki Criteria. He was critical of the calculation done in relation to one year of heavy exposure.
In relation to the meaning and operation of the words “due to the nature of”, I agree that very considerable assistance can be obtained from a long line of cases, including some English decisions. As was stated by Lord Sumner in Blatchford, if the disease is incidental to that class of employment so that it can be attributed to service therein, the injured worker is to be compensated. “Nature” is, as was said by Dixon CJ in Bourne, a vague word the application of which should not be narrowed or reduced to too much precision. As was said by Marks J in Botezatu:
“…it is sufficient that a connection exists between the nature of the employment and the disease which the worker actually contracted. It is not necessary to establish that the employment had actually caused it.”
His Honour went on to refer to the “tendencies, incidents or characteristics” of the employment and the risks involved.
(ii) I turn now to the somewhat vexed question of how the plaintiff’s employment should be categorised. What label should be attached to it for the purposes of ascertaining whether the disease suffered by him is due to the nature of such employment? The plaintiff could be described as a plasterer. He could be described as a plasterer in the construction industry. He could be described as a plasterer working with or in the vicinity of products containing asbestos and/or silica. Potentially, issues may arise as to features of the industrial environment in which the plaintiff actually worked as opposed to the environment existing or operating generally in relation to that occupation, however it may be described. This type of consideration is not made any simpler by the fact that, whilst the plaintiff had the one employer throughout the relevant period, he worked at a considerable number of sites.
In Botezatu, Ashley J referred to the flexibility of application of the word “employment” in s86. In the same case, Marks J stated the following:
“The judge (at first instance) was not compelled to treat the employment as merely that of a bias cutter or machine operator. He was entitled in the present case to consider that the employment was in the one establishment, to determine what the worker did there and the existence or otherwise of any relevant risk to which he was exposed. It means that the judge was entitled, as he appears to have done, to find that the worker was exposed to the risk of adenocarcinoma (or its aggravation or acceleration), the very disease from which he died, by virtue of the nature of his employment with Dunlop Australia Ltd (the employer).”
His Honour subsequently stated the following:
“It is important, I think, to distinguish clearly between the fact-finding task of the tribunal and its task of applying the correct legal principles. The way in which the former is performed depends on the circumstances of the case. It was contended, as though it was a matter of law, that the tribunal was required to determine what was the risk to which bias cutters were exposed generally in the tyre manufacturing or rubber industry. I do not accept that this is so, although evidence of such risk was no doubt admissible. It may be thought to be particularly so where the proof of the claim by a worker is dependent on showing that his disease is due to the nature of his employment and that he was employed by different employers over a period during which he was exposed to the risk which, according to the evidence, existed.
In the present case, I am of the view that the tribunal of fact was entitled to reach the conclusion it did on evidence as to the tendencies, characteristics and incidents of the employment of the worker with Dunlop Australia Ltd. The exercise depended less on a classification of the kind for which Mr Gorton contended than on a finding of correspondence between the environment in which the worker actually worked (his employment) and the environment attributed by the witnesses to the tyre building industry in which the relevant risk was said to exist.”
Certainly it may be that, whilst the plaintiff in the present case had only one employer, the fact that he worked at different sites makes evidence of exposure generally in the appropriate industry “particularly” admissible. However, it is also clear that Marks J, with whom Smith J agreed, considered that the environment in which the worker actually worked was of relevance and that a judge determining the matter is entitled to find that the worker was exposed to the risk of contracting the relevant disease by virtue of the nature of his employment with the particular employer.
In other words, whilst statistical evidence in relation to plasterers generally may well be “particularly” admissible in the present case, I am not confined to determine the matter on the basis of the assessment of risk to which plasterers are generally exposed. If the evidence warrants it, I am entitled to find that the plaintiff was exposed to the risk of adenocarcinoma by virtue of the nature of his particular employment.
If that be so, the “labelling” process can be comparatively specific. I am entitled to consider the plaintiff not just as a plasterer, but as a plasterer who worked at numerous sites where, during the relevant period, products containing asbestos were being handled and removed. He was also in regular contact with silica. It is a short step, and one that I am prepared to take, from that proposition to the proposition that the plaintiff was in fact exposed to asbestos and silica due to the nature of his employment.
(iii) Even if this more specific description of the plaintiff’s employment is not adopted and he is placed in the simple and generic category of “plasterers”, in my opinion there is little or no difference to the outcome of this particular line of enquiry. It seems to me that the only specific epidemiological evidence that was placed before me supports the proposition that plasterers generally have an increased risk of suffering from adenocarcinoma.
I would refer to the reports of Dr Leigh and to the epidemiological studies annexed to his report of 6 September 2016. I would agree that the Brueske-Holfeld study, which showed a risk increase of 43 per cent of contracting lung cancer, grouped plasterers with upholsterers and insulators. It was not disputed but that insulators may well have a greater exposure to asbestos than plasterers, and that the estimate of a 43 per cent increase in risk may be skewed as a result.
However, the Zahm study calculated the risk for plasterers, paperhangers and painters. Even allowing for the fact that this may not be an ideal grouping, the end result was a 100 per cent increase in lung cancer risk and a 170 per cent increase in lung adenocarcinoma risk. These are very substantial increases. The Petersen and Milham study grouped plasterers with lathers. Whilst the precise work performed by lathers is not entirely clear, it does seem clear that laths are thin flat strips of wood which form a support or framework for plaster. I would refer to what was previously stated when I was summarising the evidence of Dr Leigh.
In short, the grouping of lathers with plasterers seems quite appropriate. The end result of the study was that, statistically, there was a significantly elevated age standardised lung cancer proportional mortality ratio for this group and this finding apparently was consistent with three other studies. Another study by Milham found an elevated lung cancer risk for the group of plasterers and lathers.
Various figures compiled in the UK HSE report in relation to occupational cancer in Great Britain, this study being focussed on male plasterers, showed an increase in lung cancer risk ranging from 15 per cent to 27 per cent. The data involved appears to have covered the period 1981-2000. These seem to be the only studies specifically involving plasterers to which any detailed reference has been made or which have been put before me.
Leaving to one side the Brueske-Holfeld study, which grouped plasterers with insulators, the increased risk to plasterers in relation to adenocarcinoma seems to range from 15 per cent to 170 per cent. Even if the Zahm study, which included painters, is left to one side, the risk to plasterers (and the grouping of lathers with them seems to me to be fair) is described in the studies as being significant or in the range of 15 per cent to 27 per cent.
Accordingly, even if the plaintiff is described simply as a plasterer and the test applied is that applicable to plasterers generally, rather than taking into account the exposure relating to the specific employment, the plaintiff has established to my satisfaction that there was a significantly increased risk of developing adenocarcinoma relating to his work as a plasterer.
Further, I would refer to certain aspects of the evidence given by Ms Lara, called on behalf of the defendant. At T305 into 306, she was asked the following:
“You’d agree, wouldn’t you that the level between 3 and 6 fibre/ml years is significantly above the cumulative exposure level you’d see in the general community? --- Yes, it would be, for a person who does not work with asbestos.”
It should be said that the estimate to which she was referred in the questioning was her best estimate of the plaintiff’s total cumulative exposure to asbestos dust. When she was asked as to whether that was significantly above the cumulative exposure levels she had seen in other industries, her effective response was “only in the area of removing and cementing sheeting”. She also stated that, by the 1980s, the only other levels that would have been higher would have been during the removal of asbestos and friable asbestos-containing materials. She added that, by the mid-1980s, those sort of removal jobs were done in a controlled environment. She went on to refer to people who wore appropriate respiratory protection, qualifying that by saying:
“…that would’ve been high if they couldn’t do a job wet, you know, in a wet manner but in terms of other occupations other than removal, I think cement sheeting removal would’ve been the only one…” – see T306.
Ultimately, she was asked whether “…this level represents a higher level as against all occupations, doesn’t it?” Her answer was “It is a moderate level, yes. I wouldn’t call it a high level, a moderate level”.
I would also refer to the following questions and answers found at T307:
“But the only other occupation you can identify where you’d expect higher levels and you’ve suggested that they would involve a great degree of control, the only other industry that you’ve identified is the removal of friable asbestos, isn’t it? --- That’s one of them, yes.
Well, it’s the only one that you’ve provided us with? --- Yes, well, that’s the one that I can think of at this stage.”
In short, there were aspects of the evidence of Ms Lara, called as an expert occupational hygienist by the defendant, which seem to me to be supportive of the proposition that the exposure to asbestos alleged on behalf of the plaintiff by reason of the nature of his employment as a plasterer would be sufficient to satisfy the statutory test.
(iv) The second limb of the test contained in ss82(6) and 86 relates to the wording “and if employment of that nature was a significant contributing factor”. It has been argued that this represents another requirement which must be met. These words were added by Act No 67 of 1992. As previously mentioned, how they are intended to operate is a vexed question. During the course of submissions, I referred to the amended provision as being “somewhat clumsy” and not a provision that I liked. I was told that there was “heated agreement” from the Bar table – see T365 and 366.
It is somewhat reassuring to find that at least one eminent judge further up the judicial tree has not been impressed with the 1992 amendments. In Hegedis v Carlton & United Breweries Ltd & Anor [2000] VSC 380, Ashley J, whilst only having to deal with these provisions in a peripheral manner, stated the following:
“So, ss.82(6) and 86 do not deal with injuries arising out of or in the course of employment. There the criterion of compensability is that injury or disease be due to the nature of employment. It may be said that the 1992 amendments to those sections were apparently intended to reinforce that particular criterion of compensability - although it is clear, regrettably, that the particular amendments were thoroughly confused.”
His Honour went on to say that the amendments were not “presently relevant” to the issue then being determined. This was a far more eloquent description of the amendments than my attempt, but the bottom line is that the words inserted by way of amendment did render the provisions “thoroughly confused” and it is perhaps little surprise that they were later removed.
However, it is the “thoroughly confused” amendment with which those involved in this case have had to deal. Frankly, I find it difficult to understand what the added words “and if employment of that nature was a significant contributing factor” add to the pre-existing requirements. What has to be the “significant contributing factor” is not the specific employment in which a plaintiff was engaged prior to the date of incapacity. What is required is that employment of that nature was a significant contributing factor.
Simply, I fail to see how, if a disease is due to the nature of any employment in which a worker was employed, employment of that nature can fail to be a significant contributing factor. Logically, if a disease is due to the nature of the employment, how can such nature of employment not be a significant contributing factor? To use a very basic example, if I have a head cold due to the nature of the weather, how can weather of that nature not be a significant contributing factor to my head cold?
According to the Australian Concise Oxford Dictionary, the phrase “due to” means “because of”, a definition with which it would be very hard to argue. If a condition from which a person is suffering is “because of” some particular circumstance, how, as a matter of logic, could it be said that such circumstance is not a “significant contributing factor” to the condition? Does not such a proposition defy logic? It is hardly surprising that Ashley J described the amendments under consideration as “thoroughly confused”.
The temptation is to simply dismiss the words inserted by the amending act as being “thoroughly confused” and being nothing more than mere verbiage.
However, I will deal with them.
Even if an attempt is made to give to the words under consideration some useful meaning in the context in which they appear, it seems to me that the plaintiff has discharged the burden in relation to their operation. If the insertion of the words “significant contributing factor” in the Act generally represents an attempt to “tighten up” the entitlement to compensation and the words bear the meaning identified in Popovski (in a different statutory context) of “considerable amount or effect”, the plaintiff has nevertheless satisfied such a requirement.
In Tran, his Honour Judge Dyer stated that the plaintiff bears the burden of proving on the balance of probabilities that the nature of the particular employment is more likely to expose the worker to the contraction of such a disease than would be the case in other employment or other non-employment related activities and that such proof must be sufficient so that, as a question of fact, it satisfies the requirements of the definition of significant contributing factor set out in s5(1B) of the Act.
In Tran, his Honour found that what was required was a qualitative evaluation of the nature of the increased risk of contraction of adenocarcinoma by virtue of the plaintiff’s employment as a welder generally. He was satisfied that the evidence established that the increased risk of the development of adenocarcinoma faced by welders, as against non-welders, was in the order of a 23 per cent increase in risk. At paragraph 83, he then stated as follows:
“The fact that other and perhaps more obvious risks, such as cigarette smoking, provide a more likely risk, does not, in my view, submerge the fact that there is an increased risk and that increased risk is of such an order as to satisfy the test that it is a significant contributing factor.”
He went on to say that the finding of “significant contributing factor” is a question of fact and that the provisions of s5(1B) appear to provide “…no more than supplemental guidance on the primary question posed by s86”. He referred to the fact that s86 did not mandate an evaluation of the actual levels of exposure or the actual tasks performed by a worker in coming to a conclusion. He referred to the decision in Botezatu in this regard.
As has been stated, in the present case there have been various estimates of the increased risk of the development of adenocarcinoma faced by plasterers, as against non-plasterers. If one took the UK HSE report, which covers the period which almost coincides with the period under consideration in the present case, the increased lung cancer risk for male plasterers was in the range of 15-27 per cent, with the figure for the period 1991-2000 being an increased risk of 19 per cent. Of course, other studies have produced figures as high as an increase of 170 per cent in relation to lung adenocarcinoma risk.
However, the UK HSE figures are specifically based upon a relevant period. Further, Dr Leigh has stated that the proportional mortality and proportional rate ratios, such as those used in that British study, are based upon a large set of cases and generally provide valid estimates of increased risks in specific occupations. I accept Dr Leigh’s evidence in this regard.
An increased risk in the range of 15-27 per cent is an increased risk of such magnitude as to satisfy the test that it is a “significant contributing factor”, assuming that such words add any sensible meaning to the test to be applied.
(v) The next issue to which I turn is that of the relevance and impact of the plaintiff’s smoking habit. I have already stated that there is scarcely any dispute but that he has a long history of smoking something in the order of 30 cigarettes per day. I accept that this represents a heavy smoking habit.
There are then two aspects of this to be considered. Firstly, it may well be that smoking represents a more likely risk or a risk of greater magnitude than does exposure to asbestos. However, that does not alter the fact that, as I have found, there is an increased risk associated with asbestos exposure due to the nature of the employment. If that be so, and given what is said in the authorities, the smoking habits of an individual plasterer or worker become largely irrelevant. Even if the words “if employment of that nature was a significant contributing factor” are given some meaning and are seen as adding a second or additional requirement that must be satisfied, so that smoking has the potential to be of considerable relevance, that does not submerge the fact that the increased risk associated with exposure is of such a magnitude as to satisfy the test of “significant contributing factor”.
Secondly, there is the vexed question of the synergistic or multiplicative effect of the combination of cigarette smoking and asbestos exposure. Are these simply concurrent causes of differing magnitude or is the almost unanimous opinion that the two act in synergy or multiply risk to be taken into account?
Apart from the fact that the plaintiff’s smoking habit may well be largely irrelevant and that I have found that, should it be relevant, asbestos exposure remains a significant contributing factor, it seems to me that the synergistic or multiplicative effect is something to be taken into account.
Associate Professor Mitchell has expressed the opinion that a man working in relatively low exposure to asbestos is some eightfold more likely to get lung cancer, given a smoking background, than would otherwise be the case. He has also stated that the asbestos contribution would be at least as significant as the smoking history and that, even if the asbestos exposure was very small, it would still be very important. I accept these propositions.
However, even leaving such propositions to one side, I am inclined to the view that the synergistic or multiplicative factor is something that can be taken into account. I appreciate that such an approach is close to saying that the defendant must take the plaintiff as he finds him, but it seems to me to make sense. This assumes that the smoking habit of the individual is relevant. If there are two workers engaged in an employment the nature of which is productive of the disease of adenocarcinoma and one worker is a heavy smoker, whilst the other is a non-smoker, and if it is accepted that smoking combined with the nature of the employment has a synergistic effect, why should that not be taken into account in relation to the smoker? Why should the fact that such an effect takes place not be borne in mind if “significant contributing factor” is part of the test? It seems to me that, logically, it should. The plaintiff in the present case had been smoking for something in the order of 25 years before the commencement of the relevant period of exposure in 1981. Thus, at the commencement of that period, he was a long-standing smoker with a vulnerability to asbestos exposure. It seems to me to be quite arguable and logical that the additional impact upon him of asbestos exposure should be taken into account.
I have digressed into the area of synergy and the like because quite considerable attention was paid to it during the conduct of the case. Because of my other findings, I make no specific ruling in relation to it but, given the careful attention paid to it in submissions, I thought that some comment was warranted.
(vi) Another reason why I found that the plaintiff has discharged the burden of proof relates to witnesses. I have already expressed the opinion that, although the plaintiff became confused at times in difficult circumstances, I do not doubt the honesty of his answers. I accept him as a witness of truth.
Further, I prefer the expert evidence called on behalf of the plaintiff to that called by the defendant. That is not to say that Mr Rogers and Ms Lara were not witnesses with extensive qualifications. They were. However, for a number of reasons, I prefer the plaintiff’s witnesses. These reasons include the following:
(a) Associate Professor Mitchell was a particularly impressive witness. He is the plaintiff’s treating medical oncologist. He has wide experience and knowledge of the relevant areas of medicine and of the causation of diseases such as adenocarcinoma of the lung. He did not strike me as “having a barrow to push” or falling into a particular “camp”, as can sometimes be the case with some medico-legal examiners. He is a particularly well-qualified oncologist who happens to be the plaintiff’s treating doctor and who gave clear and persuasive evidence.
(b) Dr Leigh was, effectively, the principal witness who produced epidemiological studies focussed upon the essential question “of the nature of the employment”. He put before the Court the results of studies done in relation to plasterers and lung cancer. These studies may not have been perfect and were the subject of criticism. However, the fact remains that he was able to put before the court highly relevant articles which produced a reasonably consistent picture of the increased risk of lung cancer faced by plasterers. I have discussed them at some length previously. In general, I accept Dr Leigh’s evidence and opinions.
(c) Of the two medico-legal examiners, I prefer the evidence of Mr Rosalion, who was another impressive and very well-qualified witness. His evidence seemed to me to be logical and sensible.
Aspects of the evidence of Professor Fox caused me some concern. I have discussed this previously, but will summarise it again. How, in his report of 25 November 2016, he could say that Mr Rosalion, in his report of 16 November 2016, had been quite clear that there had been no handling of asbestos materials post-corporation of the company in 1981 mystifies me. In his report of 16 November 2016, Mr Rosalion said no such thing, much less being “quite clear”. Such a mis-quoting raises questions of whether Professor Fox had read Mr Rosalion’s report thoroughly or whether he had read into it something that is simply not there.
Secondly, and as previously stated, Professor Fox was, in essence, critical of the reports of Dr Leigh on the basis that Dr Leigh had not considered the period from 1981 onwards. The report of Dr Leigh of 6 September 2016 (which particular report is referred to in the report of Professor Fox) makes three clear references to exposure up to 2001 and a further reference to exposure until the mid-1980s. Thus, the criticism of his reporting seems to me to be unfounded and again raises a question mark as to how carefully the reports of Dr Leigh had been read.
Thirdly, I found the almost dismissive attitude taken by Professor Fox in his oral evidence towards the plaintiff’s transcript evidence to be not particularly fair. Professor Fox described that evidence as a “jumble” and appeared to pay no particular heed to it. True it is, as discussed, that at times the plaintiff’s evidence was confusing but, as I have described, some clarification occurred. He was a very sick man and doing his best in a trying situation. I am of the view that his transcript evidence deserved at least a little more attention and analysis.
Overall, I am of the view that there were some disappointing aspects of the evidence of Professor Fox and I prefer that of Mr Rosalion.
(d) Whilst called by the defendant, in cross-examination Ms Lara agreed that the estimate of the total exposure of the plaintiff to asbestos during the relevant period would be significantly above the cumulative exposure level seen in the general community and for a person who did not work with asbestos. She stated that the only other occupation where she would expect a higher level would be one involved with the removal of asbestos. These concessions were quite properly made and this is no criticism of Ms Lara. She is also particularly well-qualified.
(e) Both Mr Kottek and Mr Rogers gave detailed evidence supporting their respective positions. As earlier stated, Mr Rogers disregarded certain assertions of the plaintiff because of his (mistaken) denial of his signature on a document. This may not have had a great deal of influence upon the thinking of Mr Rogers, but it is unfortunate that the plaintiff’s error may have reduced the assessment of Mr Rogers of the worth of part of the plaintiff’s evidence.
On balance, I prefer the evidence of Mr Kottek, which seems to me to have been directed more towards the central issue to be determined. Mr Rogers placed considerable emphasis on the plaintiff’s smoking and upon the significance of the history taken from the individual worker – an emphasis that gave the impression of being directed much more towards cause than to the nature of the employment.
In summary, I prefer the evidence that was given by and on behalf of the plaintiff.
(vii) In Botezatu, Ashley J made a number of references to a “process” in relation to the nature of the employment. In the case of a worker performing duties at various sites, the task of assessing whether the disease is due to the nature of the employment might be more difficult. However, that is not to say that it is impossible. Indeed, a number of the old English cases which could be described as demonstrating the reasoning and operation of the “disease provisions” involved work at a number of sites and for various employers.
In Blatchford, the plaintiff, who was a painter and claiming benefits in respect of disablement due to lead poisoning, had worked for the navy and for another two firms before being employed by the defendant. In each occupation, he had engaged in painting duties, but obviously at different locations. It could well be argued that the whole rationale for the “disease provisions” is that it enabled a worker injured by reason of a disease contracted over time at different sites to rely upon the nature of the task in which that worker was engaged. The locations and employers may have changed, but there was a “process” which, essentially, was being followed throughout.
In the present case, the plaintiff always had the same employer. Based upon his evidence, I am satisfied that the type of work which he performed and the process in which he engaged in order to perform it remained much the same throughout. I am of the view that, if the concept of “process” is adopted, the fact that the plaintiff worked at different locations is of no great weight when considering that concept. The level of exposure to which he was subject may have varied quite considerably from place to place. However, there is no evidence to suggest that the general process in which he was engaged varied to any great extent, although the level of exposure may have differed from location to location.
(viii) Much of the above is directed towards exposure to asbestos. Given that I have found that the plaintiff has discharged the burden of proof in relation to asbestos exposure and his subsequent contracting of adenocarcinoma of the lung, there would seem to me to be no need for any detailed discussion concerning silica, particularly in the circumstances which are prevailing. Whilst I accept that the nature of the plaintiff’s employment brought him into regular contact with silica, which is a Grade 1 carcinogen, little or no evidence concerning epidemiological studies were placed before me. The expert evidence concerning silica could be described as being less definite. Logic would suggest that a plasterer constantly using sand would have a very substantial exposure to silica. It could be argued that the studies referred to by Dr Leigh are equally applicable to asbestos and silica. However, in the circumstances, there is no necessity for me to rule on the issue of silica exposure and I do not do so.
(ix) Whilst it can be important to distinguish between the “nature of employment” and “causation” concepts, it seems to me that, in any event, there is quite a strong case that the plaintiff’s exposure to asbestos was a substantial cause of his lung cancer. I have already expressed my favourable view of the evidence of Associate Professor Mitchell. He has expressed the opinion that he considers that asbestos exposure would have played a very significant role in the cause of the lung cancer. Leaving to one side the problems of the phrase “significant contributing factor” as it appears in the relevant legislation, it would be difficult to argue that something which has caused a condition was not a “significant contributing factor”. Further, what was said in Botezatu would indicate that consideration can be given to the environment and circumstances in which a plaintiff actually worked.
(x) In bringing this action, the plaintiff relies on both ss82(6) and 86 of the Act. Whilst the former relates to injury by way of gradual process and the latter to a disease, each could be seen to be applicable to the present case. The test contained in each is, for all intents and purposes, identical. Whilst perhaps more attention is being paid to s86, there seems to be little doubt but that the plaintiff has also satisfied the requirements of s82(6).
Conclusion
255 The plaintiff is successful. He has discharged the burden of proof. He is entitled to the relief sought, which is as follows:
· a determination that he is entitled to compensation in relation to the injury;
· payment of reasonable medical and like expenses;
· a declaration that he is entitled to compensation for non-economic loss in respect of permanent impairment.
256 I shall hear from the parties as to the precise wording of the orders and as to any ancillary orders that are required.
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