Rosanne Cleary as the Legal Personal Representative of the Estate of the late Fortunato (aka Frank) Gatt v Amaca Pty Ltd

[2021] NSWDDT 5

Dust Diseases Tribunal

New South Wales

• Amendment notes

Medium Neutral Citation:

Rosanne Cleary as the Legal Personal Representative of the Estate of the late Fortunato (aka Frank) Gatt v Amaca Pty Ltd [2021] NSWDDT 5

Hearing dates:

6 July 2019; 17 July 2020; 29 July 2020; 3 and 4 August 2020; 21 September 2020; 27 October 2020; 9, 10, 11, 12, 13 November 2020; 15 February 2021

Date of orders:

6 September 2021

Decision date:

06 September 2021

Before:

Strathdee, J

Decision:

1.   Judgment for the plaintiff against the defendant in the sum of $540,000.00.

2.   Defendant to pay the plaintiff’s costs as agreed or assessed.

3.   If any alternate costs order is sought, parties must notify my associate within 14 days.

Catchwords:

DUST DISEASES TRIBUNAL – causation – balance of probabilities – negligence – deceased was a smoker – lung cancer – contributory negligence – use of epidemiological evidence – effect of smoking and exposure to asbestos fibres – impossible to determine the cause through medical examination – whether epidemiological evidence established a cause on the balance of probabilities

ADMINISTRATIVE LAW – rules of evidence – examination and cross-examination – rule in Browne v Dunn – whether Tribunal erred in failing to have regard to the circumstances that evidence not accepted by Tribunal went unchallenged by cross-examination

Legislation Cited:

Civil Procedure Act 2005 (NSW)

Uniform Civil Procedure Rules 2005 (NSW)

Workers Compensation (Dust Diseases) Act

Cases Cited:

Ali v Nationwide News Pty Ltd [2008] NSWCA 183

Allianz Australia Ltd v Sim (2012) 10 DDCR 325

Allianz Australia v Sim (2012) 10 DDCR 325

Amaca Pty Ltd v Booth (2011) 246 CLR 36

Amaca Pty Ltd v Ellis (2010) CLR 111; [2010] HCA 5

Amaca v Ellis (2010) 240 CLR 111

Browne v Dunn (1983) 6 R 67

Dasreef v Hawchar (2011) 243 CLR 588

Ellis v Wallsend District Hospital (1989) 17 NSWLR 553

Evans v Queanbeyan City Council (2010) 9 DDCR 541

Ghosh v Medical Council of New South Wales (2020) 102 NSWLR 303

Hull v Thompson [2001] NSWCA 359

Jones v Dunkel (1959) 101 CLR 298

Judd v Amaca Pty Ltd [2003] NSWDDT 12

Scalise v Bezzina & Ors [2003] NSWCA 362

State Rail Authority of New South Wales v Brown (2006) 66 NSWLR 540

Category:

Principal judgment

Parties:

Rosanne Cleary as the legal personal representative of the estate of the late Fortunato (aka Frank) Gatt (Plaintiff)
Amaca Pty Limited (First Defendant)

Representation:

Counsel:
Mr G Parker SC and Mr J Sharpe appeared for the Plaintiff
Mr D Hooke SC and Mr D Klineberg appeared for the Defendant

Solicitors:
Mr Ivan Simic, Taylor & Scott (Plaintiff)
Mr Nick Prentice, Rankin Ellison (Defendant)

File Number(s):

256/2018 2020/00163145

Judgment

INTRODUCTION

1. By a Third Amended Statement of Claim filed 4 August 2020 the plaintiff seeks damages, interest and costs as the legal representative of the estate of the late Fortunato (aka Frank) Gatt (‘Mr Gatt’).

2. The original Statement of Claim sought damages and asserted that as a consequence of his employment with the defendant between 1962 and 1964 at its Camellia factory and plant, Mr Gatt suffered the following injuries:

1. Injury to both lungs;

2. Asbestos related pleural disease;

3. Bilateral calcified pleural plaques;

4. Lung cancer;

5. Loss of expectation of life;

6. Nervous shock, anxiety, depression and other psychological sequelae;

7. Pulmonary Fibrosis;

8. Asbestosis; and

9. Diffuse pleural thickening.

3. The defendant concedes that Mr Gatt developed asbestos related pleural plaques, but the plaintiff’s claim for compensation for lung cancer and asbestosis injuries are disputed.

4. I took the evidence of Mr Gatt at his home on 6 March 2019 as his health was rapidly declining. Mr Gatt sadly passed away on 20 March 2019. His wife, Mary Gatt, was subsequently substituted as the legal representative of Mr Gatt’s estate and a first Amended Statement of Claim was filed reflecting that position. Unfortunately, Mary Gatt also passed away and a second Amended Statement of Claim was filed on 27 November 2019 substituting Roseanne Cleary as plaintiff of the legal representative of Mr Gatt’s estate.

5. The proceedings went to mediation on 23 October 2018 and that was unsuccessful. In compliance with the Regulation, the mediator issued a certificate stating that the mediation failed and the parties put the following issues in dispute:

1. Extent of exposure;

2. Causation;

3. Damages, including but not limited to, s 15B damages; and

4. Contributory Negligence.

6. The defendant filed an Amended Defence on 27 March 2019 and pleaded the following particulars of Contributory Negligence:

1. Smoking cigarettes when he knew such activity carried a risk of injury;

2. Failing to heed warnings as to the dangers of smoking cigarettes;

3. Excessive cigarette smoking;

4. Failing to cease smoking when he knew of the dangers;

5. Failing to act on advice to cease smoking; and

6. Failing to take proper care for his own health.

7. The defendant has admitted breach of duty of care. The defendant does not take issue with the fact that Mr Gatt was exposed to and inhaled asbestos dust and fibre during the course of his employment, but in issue is the level of exposure to respirable asbestos fibre in the course of his employment.

8. Further, with the exception of the development of asbestos-related pleural plaques, the defendant contests the claim that Mr Gatt suffered any injuries which were caused by reason of Mr Gatt’s exposure to asbestos while employed by the defendant. Specifically, the injuries claimed that are disputed include lung cancer and asbestosis.

9. I note that quantum is agreed in the sum of $540,000.00 and the issue of contributory negligence is also agreed.

ISSUES IN DISPUTE

10. The parties summarised the dispute as follows:

1. On the balance of probabilities, did Mr Gatt suffer from asbestosis;

2. What was the cumulative airborne asbestos concentration to which Mr Gatt was, on the balance of probabilities, exposed to during the period of his work at James Hardie; and

3. Examination of the epidemiology of lung cancer and the causal nexis between asbestos exposure, cigarette smoke and the occurrence of lung cancer.

BACKGROUND

11. The late Mr Gatt was born on 17 February 1943. He tragically died on 20 March 2019.

12. Mr Gatt was employed by the defendant between 5 June 1962 and 15 July 1964 as a labourer at its Camellia factory, and during the course of that employment he was exposed to and inhaled asbestos dust and fibre.

13. The defendant does not take issue with the fact that Mr Gatt was exposed to and inhaled asbestos dust and fibre during the course of his employment at its Camellia factory. The defendant does however dispute the level of exposure to respirable asbestos fibres.

14. The plaintiff submits that the issue to be determined by the Tribunal is whether the admitted exposure of Mr Gatt to asbestos dust and fibre in the James Hardie mixing room during his employment caused or materially contributed to the injuries the subject of the proceedings. They submit that the important evidence in the case as to the issue of Mr Gatt’s cumulative exposure to asbestos dust and fibre is:

1. Mr Gatt’s affidavit sworn 19 October 2018, which became Exhibit A, and his evidence as given to Dr Johnson when he examined him;

2. The contemporaneous documentary material expressing the concern of the defendant’s managers at the time of Mr Gatt’s exposure;

3. The evidence of his fellow employees as contained in the Dust Diseases Board (‘DDB’) records; and

4. The clinical assessment and professional judgment of the cumulative exposure by Dr Johnson, an experienced thoracic respiratory physician.

MR GATT’S EVIDENCE

Nature of Mr Gatt’s work

15. Mr Gatt described his exposure in the course of his employment in his affidavit (Exhibit A), in the following terms:

‘15.   During my time at James Hardie I only had one (1) job and that was operating a mixer machine mixing raw asbestos with other materials in the mixer.

1. I and other workers called this part of the factory where we worked the ‘mixing area’. It was a level above the factory floor under the factory building roof. The ‘mixing area’ where I worked was enclosed and very dusty and I breathed in the dust on a daily basis.

2. The mixing area where I worked had four (4) mixers and the mixer I operated was called the number five (5) mixer. Each mixer had one man working on it. There was also a storeroom near the mixers, which held the raw asbestos that was brought over to the mixers by wheelbarrows from the storeroom to the mixer. There were usually two (2) men working on the wheelbarrows just filling them up with raw asbestos from the storeroom then bringing them over to the mixer operators.

3. Every week I worked five (5) normal shifts either day, afternoon, night plus (2) other shifts either on a weekend or a double shift during the weekdays. I worked a minimum of 56 hours a week every week. I was a single man and trying to save as much money as I could to buy a house and get married.

4. In the mixing area every working day, I breathed in vast amounts of asbestos dust and fibre. I could see asbestos dust and fibre in the light constantly. I could not avoid breathing the asbestos dust and fibre as the workers on the other three mixers in the area I worked, did exactly the same dusty work as I did and as the two men in the nearby storeroom holding asbestos brought wheelbarrows of it to the mixing machines.

5. About every twenty minutes, one of the two men pushing the wheelbarrows brought over a big wheelbarrow full of loose asbestos for me to tip into the mixer. I hooked up each large wheelbarrow full of asbestos to the mixing machine, which had a winding mechanism that upended and tipped the wheelbarrow so that the asbestos fell into a large mixing vessel below. Each time this happened a huge cloud of asbestos dust came up that I could not avoid breathing in. I then added other materials that were like wet mixture to the raw dry asbestos in the mixing vessel and switched on the mixer to combine the raw materials with the wet mixture.

6. Once the mixing was done I undid the plug to the mixing vessel and the mixture was poured down onto the factory floor below where it was used to make asbestos cement products.

7. I was not provided with any mask or protective gear.

8. I was never told that asbestos could be harmful for my health.

9. I have never worked or been in a place that was as dusty as the mixing area in the James Hardie factory in my whole life. I was covered in asbestos dust from head to toe all of the time operating the mixer. At times the mixing area looked like a place in a snowstorm especially when the mixing machine operators happened to upend and tip wheelbarrows at the same time with the asbestos dust rising up from each mixer.

10. I estimate that the mixers were about four to five metres apart and the storeroom where the raw asbestos was wheelbarrowed from was about fifteen to fifty metres away from me.

11. I do not know where James Hardie got their raw asbestos from but it looked like raw cotton to me and was like a grey dirty white colour crumbled easily in your hand. Each time a wheelbarrow was hooked up and upended to the mixer a huge cloud of asbestos dust would come as clumps of it turned to powder as it fell into the mixing vessel below which was like a large bowl. This process happened every working day I was there. There was a layer of asbestos dust on every surface in the mixing room, on the floor, on the mixers and it was impossible to avoid breathing in the dust.

12. Each day when I finished a shift or double shift my clothes were covered in asbestos dust and fibre. At the time I was still single and did my own laundry and simply shook out the clothes when I got home. The dust got into my hair, my mouth, my nose, my ears and any exposed part of my body was covered in it after a shift or double shift.’

    16. Mr Gatt’s evidence is not contradicted.

    17. I note at this point that the defendant does not dispute Mr Gatt’s evidence that during his time working for James Hardie, he operated a mixer machine located in the ‘mixer area’ which mixed raw asbestos with other materials, nor does Amaca dispute the nature of the mixing work that Mr Gatt undertook.

    18. From the evidence with regard to Mr Gatt’s employment, I make the following findings of fact:

    1. Mr Gatt worked in an area he called the mixing area;

    2. He operated a mixer machine mixing raw asbestos with other wet materials;

    3. There were four mixers in the room and he operated the number 5 mixer;

    4. Raw asbestos was brought over to the mixers in wheelbarrows;

    5. When the wheelbarrows were tipped, asbestos dust could be seen rising into the air;

    6. Mr Gatt worked a minimum of 56 hours each week;

    7. There were vast amounts of asbestos dust and fibre in the air which he could see constantly;

    8. The other workers on the mixers performed exactly the same dusty work;

    9. Every 20 minutes or so, one of the two men pushing the wheelbarrow brought over a big wheelbarrow full of loose asbestos for Mr Gatt to tip into the mixer. Each time he did there was a huge cloud of asbestos dust;

    10. The mixing area looked like a place in a snowstorm, and Mr Gatt was covered in asbestos dust from head to toe regularly; and

    11. There was a layer of dust on every surface in the mixing room, on the floor and on the mixers.

Mr Gatt’s smoking history

19. It is not in dispute that Mr Gatt was a smoker, and had been so for many years. In his affidavit, Mr Gatt indicated that he started smoking when he was about 17 and smoked his own hand-rolled tobacco cigarettes, generally without a filter, smoking up to 25 cigarettes per day with an average of 15–20 per day: Exhibit A [48], [49] and [51].

20. In his affidavit at [51], Mr Gatt said that he stopped smoking when he was 62 which was ‘when I became aware of my heart condition’. His oral evidence (T6.16–34) indicted that he continued to smoke until his heart attack in 2007, after which he never smoked again.

21. Dr Johnson, in his report of 20 June 2018, (Exhibit H) records taking a history of Mr Gatt smoking about 25 cigarettes a day.

22. Further, in a letter dated 9 November 2015 from Dr David Michail (Exhibit 16), who had been treating Mr Gatt for some time, to Dr Roland Alvandi, Dr Michail stated that Mr Gatt had smoked from 16 until he was 65 years of age–i.e. about 2007. Dr Alvandi’s report in response (Exhibit 17) states that Mr Gatt ceased smoking in 2007 and had a 70-pack year history.

23. The defendant asserts that this suggests Mr Gatt smoked about 29 cigarettes per day, and that in his oral evidence Mr Gatt agreed that whatever he told Dr Alvandi was an accurate recollection (T7.36–41).

24. An additional conflict arises as to the time at which Mr Gatt stopped smoking. The plaintiff maintains that Mr Gatt stopped smoking in 2005.

25. The defendant submits that Mr Gatt stopped smoking in 2007 after his heart attack. The evidence that supports this is Mr Gatt’s oral evidence (T6.16–34; T7.42–49) and reports by Dr Johnson dated 20 June 2018, Dr David Michail dated 9 November 2015 (Exhibit 16), Dr Alvandi dated 12 November 2015 (Exhibit 17) and notes of Dr Nagrial dated 5 September 2017 (Exhibit 18). On the basis of that evidence the defendant submits that it should be found that Mr Gatt smoked until his heart attack in 2007 and that he smoked on average 20 cigarettes a day from 1960 until 2007, giving a cumulative smoking history in the range of at least 47 pack years to 70 pack years.

26. Given the evidence the defendant can point to, and Mr Gatt’s own account that the history he gave to Dr Alvandi is accurate, and the plaintiff submitting no evidence in support of their assertion Mr Gatt stopped smoking in 2005, it is more probable than not Mr Gatt stopped smoking in 2007, after his heart attack.

27. Further evidence is contained in the notes of Dr Adnan Nagrial (Exhibit 18) and the Clinical History Sheets from the DDB (Exhibit 19) which can be viewed as demonstrating a heavy smoking history of most likely at least 20 cigarettes per day from about 1960 until about 2007. I accept that this can calculate a cumulative smoking history on the range of 47–70 pack years.

DOCUMENTARY EVIDENCE OF ASBESTOS AT CAMELLIA

28. The plaintiff tendered documents that she relies upon to demonstrate the high levels of asbestos dust at the Camellia factory, and the knowledge that the management of James Hardie must have had at the relevant times (Exhibits UU, RR, WW, FF).

29. In Exhibit UU the estimated dust counts for workers relevant to the areas in which Mr Gatt worked ranged between 4–15 million particles per cubic foot (‘mppcf’).

30. The assertion made is that such documentary material demonstrates the defendant’s management’s knowledge that at least some of the workforce at Camellia were exposed to high levels of asbestos dust at the factory, and as such were at high risk of contracting an asbestos related disease. Exhibit FF, a report from about 1957 entitled ‘A Report concerning (a) the incidence of asbestosis and (b) the nature of present-day dust exposures at the Camellia factory of J Hardie & Co Limited’, was prepared by the NSW Department of Health apparently at the request of Dr Hughes of Manufacturers Mutual Insurance Co due to a concern that at least 3 employees were known to have either clinical or radiological evidence of asbestosis.

31. Various testing was done around and about in different locations at the factory where dust levels were measured. The tables in Exhibit FF show dust in some places in the defendant’s factory was in excess of 5 mppcf. In the asbestos cement factory a total of 33 dust counts were performed, with more than 40% of them showing dust counts above a safe level. There were additional tests performed showing that in the AC factory, blower room and number 3 and 5 tide mills, the readings exhibited dust counts of 5 mppcf.

32. The defendant submits that none of this evidence is relevant, as the defendant has admitted duty and breach. They say that it is not relevant to the question that I must determine, which is, did Mr Gatt suffer from asbestosis and were his injuries caused by his exposure to asbestos and the level of cumulative exposure.

33. That is a submission I have difficulty in accepting. In circumstances where these events happened decades ago, surely the testing that was conducted at the exact premises, at a relevant time must be something that assists in the determination that I must make. I am strongly of the view that in determining the cumulative respirable asbestos to which Mr Gatt was exposed, records of testing that was conducted are relevant, and I have had regard to them.

Evidence of other workers at Camellia

34. The plaintiff tendered records of the Dust Diseases Authority (‘DDA’) for workers that worked at the Camellia plant at about the same time as Mr Gatt.

35. Mr Said commenced employment with James Hardie & Co on 20 January 1960 and ended 8 September 1963. For the period 20 January 1960 to 15 July 1962 he worked as a tide mill hand. He died on 16 June 2014. He had asbestos related pleural disease (Exhibit ZZ). His industrial history to the DDB is very similar to Mr Gatt’s, in that he described the process inside the tide mill that ingredients were tipped and mixed with water to make 20–30 batches a day across the two mills. He said that asbestos dust was constantly all over the floor and in the air because there were no fans or dust control equipment.

36. Mr Ronald James died on 12 August 2011 having been certified by the DDB as having asbestosis. He worked for James Hardie at Camellia as a tide mill hand between May 1963 and May 1964. He gave the following industrial history to the DDB which is very similar to the circumstances described by Mr Gatt (Exhibit AAA):

‘Mr James stated that his job was to load the mixers with asbestos. He said that he filled the skips with asbestos by gathering armfuls of the raw powder from the bins where it was sorted. He said that he handled grey and blue asbestos powder. He said that when the skip was full, he tipped the asbestos into the mixer, which created a lot of dust. He said the atmosphere in the tide mill was also full of asbestos dust, regardless of his activities. Mr James stated that he filled the skips at the rate of 4 per hour. He said the process of adding cement and water to the mix took several minutes.’

37. Mr Desmond McMullen died of asbestosis on 29 August 2008. He was employed by James Hardie as a lab assistant and his function was to experiment with materials and manufacturing processes and develop improved asbestos products (Exhibit CCC). Mr McMullen estimated that about 30% of the asbestos he handled was blue asbestos and he collected samples of asbestos from the blow room. He said the conditions were extremely bad, where workers would become covered in dust in a very short period of time, that in the storage shed at James Hardie bags of raw asbestos were delivered as bagged asbestos, likening his work environment to a snow storm.

38. Mr Leonello was employed at Camellia for a period of 3 months in 1963 and died of mesothelioma. He was employed as a labourer at James Hardie in the factory that manufactured asbestos cement products and was using raw asbestos (Exhibit BBB).

39. The defendant submits that these records may be relevant only to the question of duty and breach, both of which are admitted. For a number of reasons articulated at paragraphs 23–25 of the defendants second written submissions in reply, they submit that they are irrelevant and should be given no weight.

40. I disagree with that submission. These are industrial histories taken by a representative of the DDB to assess entitlement, if any, to DDB benefits. The accuracy of the histories is important, and I am entitled to assume that the enquiries made for and on behalf of the DDB, are independent. The individuals identified worked quite contemporaneously at Camellia, in the areas that Mr Gatt worked. The evidence of their working conditions is relevant to the question that I must determine as to the cumulative respirable exposure to which Mr Gatt was exposed.

41. I find that the inferences available from the evidence of fellow workers are:

1. The workers at the Camellia factory performing duties similar to those described by Mr Gatt at about the same time were exposed to very high dust levels;

2. The exposure to these very high levels of asbestos fibre led some workers to develop asbestosis and other asbestos related medical conditions;

3. Substantial amounts of amphibole asbestos was likely to have been used;

4. There was no dust control equipment or ventilation; and

5. The process of transferring raw asbestos from the place of storage to the mixing area and incorporating it into the mix was extremely dusty.

DIAGNOSIS OF ASBESTOSIS

42. The diagnosis of asbestosis is a significant issue in the proceedings.

43. There is no dispute on the radiological evidence that Mr Gatt had;

1. Thick bilateral plaques affecting a significant amount of the pleura; and

2. Diffuse pleural thickening.

44. A/Prof McKenzie (Exhibit 14) states that asbestosis is diagnosed on the following basis:

1. A history of heavy exposure to airborne asbestos fibre;

2. Documentation of heavy asbestos exposure either through histopathology showing asbestos bodies or fibre counts compatible with the diagnosis or radiology documenting significant asbestos exposure such as pleural plaques, diffuse pleural thickening, parenchymal bands and/or rounded atelectasis; and

3. Documentation of pulmonary fibrosis with clinical and radiographic features consistent with asbestosis and exclusion of alternative diagnoses.

45. Further, Dr Leigh, in his report of 31 December 2018, at page 3 (Exhibit B), states as follows:

‘The extensive bilateral calcified pleural plaques are objective evidence of significant cumulative asbestos exposure.’

46. The plaintiff, in support of the allegation of asbestosis, relies upon the evidence of Dr Anthony Johnson. They submit that Dr Johnson is qualified by training, experience and research activities to express an opinion as to whether the cumulative fibre burden as described by Mr Gatt should be regarded as sufficient to support his diagnosis of asbestosis. Dr Johnson’s CV was tendered and marked Exhibit L. During cross-examination (T104.29–42) it was established that Dr Johnson had researched and published with respect to occupational asbestos exposure. At (T104.36) he stated:

‘I do have experience in assessing asbestos exposure based on history.’

47. Dr Johnson explained that his research for the DDB had been designed specifically to provide ‘a reliable measurement for the exposure of a particular worker in a particular job at a particular time’ (T105.18–36). His daily practice for many years, I accept, means that he would assess a patient’s narrative of exposure against diagnostic criteria.

48. Dr Johnson described Mr Gatt’s exposure as ‘likely to be heavy’ (T102.12) and ‘likely to be high’ (T103.7). He concluded the cumulative exposure was ‘appropriate’, ‘heavy and significant’ enough to cause asbestosis (T106.27).

49. In Dr Johnson’s report (Exhibit J) he states as follows:

‘In my opinion it is more likely than not Mr Gatt contracted asbestosis and ARPD due to his asbestosis exposure whilst employed by James Hardie. This is based on the radiological features consistent with a diagnosis of asbestosis related pleural disease and interstitial pulmonary fibrosis. There was no other obvious cause for his interstitial pulmonary fibrosis apart from his asbestos exposure. His asbestos exposure was sufficiently heavy to have caused asbestosis. Therefore, my diagnoses are asbestosis and asbestos related pleural disease i.e. pleural plaques and diffuse pleural thickening.’

50. He then opined:

‘Assuming Mr Gatt was exposed to 25 f/mL.yr in my opinion it is more likely than not his exposure to asbestos dust at James Hardie was a material contributing cause of his lung cancer. As outlined above, even if he was not exposed to 25 f/mL.yr in view of the fact I consider he had asbestosis I consider his exposure to asbestos dust at James Hardie was a material contributing cause of his lung cancer.'

51. Dr Johnson gave oral evidence as follows (T115.48):

‘Q.   Can I suggest to you that as a matter of probability, if cumulative exposure was less than 25 fibres per millilitre years, the appropriate diagnosis would not be one of asbestosis.

A.   I wouldn’t agree with that statement.’

52. The defendant disputes the diagnosis of asbestosis. The defendant relies upon the evidence of Dr Graeme Goldin, Dr Andrew Baldey, Dr Michael Jones, Dr Peter Carr, all specialist radiologists, and A/Prof David McKenzie, a respiratory physician.

53. Dr Goldin is one of Mr Gatt’s treating doctors. He reported on the October 2015 CT (Exhibit 23) in a treating capacity. He did not refer to asbestosis or to interstitial lung disease being present nor did Dr Baldey, who, in his report of 26 February 2016 (Exhibit 24), reviewed subsequent CT imaging by reference to the October 2015 CT as a comparison.

54. Dr Michael Jones, an expert radiologist qualified by the defendant, says in his report (Exhibit 9) dated 11 October 2020 as follows:

‘Careful review of the scans dated 15 October 2015 show that the subpleural changes referred to by Dr Anthony Johnson only lie beneath the asbestos pleural plaques and asbestos related diffuse pleural thickening. This has two mechanisms. Firstly, sub pleural fibrosis occurs beneath asbestos pleural plaques and diffuse pleural thickening but it is not interstitial lung disease or asbestosis.

The American Thoracic Society states in relation to diffuse pleural thickening that “the lesion may show a gradient with immature granulation tissue and fibrin at the surface, progressing to mature collagen adjacent to the lung. The fibrosis may extend for a few millimetres into the lung parenchyma and into the lobular septa. That later features do not constitute asbestosis”.

Secondly, Mr Gatt’s pleural plaques and diffuse pleural thickening up to 10mm in thickness. This causes compressive atelectasis in the sub pleural lung, which similarly produces sub pleural lines septal thickening and groundglass opacity. The same phenomenon is observed beneath degenerative discophytes arising from the thoracic spine and impinging into the right lower lobe. This is illustrated below.

Had similar sub pleural lung abnormality been present beneath normal pleura, then interstitial lung disease or asbestosis could be considered. However, since the sub pleural abnormality is only visible beneath the thick pleural plaques and asbestosis-related diffuse pleural thickening and not visible beneath normal pleura, interstitial lung disease and asbestosis are excluded.’

55. The key radiological scan examined by the experts was the high-resolution CT scan of Mr Gatt’s chest taken on 15 October 2015. The defendant asserts, and I agree, that was the last such CT taken prior to the progression of Mr Gatt’s lung cancer and treatment related changes.

56. Dr Jones, in his report of 16 October 2018 (Exhibit 9) having reviewed the radiology, including the Whole Body FDG Pet Scan dated 14 November 2015 states (at p 1–2) as follows:

‘There are very extensive thick fibrous and densely calcified asbestos pleural plaques throughout both pleural cavities, covering around 75% or more of the total pleural surface area. There are large thick plaques over both sides of the diaphragm. These are tending to be confluent. There is however no evidence of asbestos-related diffuse pleural thickening, or any blunting of the costophrenic recesses.’

57. Dr Jones, in his report dated 27 August 2020 (part of Exhibit 9), explains (p 29) that the October 2015 CT:

1. Demonstrates the lung bases in clear detail;

2. Shows none of the changes of early asbestosis;

3. Shows some ‘compressive atelectasis in the lung lying beneath pleural plaques’ which, although it is producing ‘some increased lung density and septal thickening’, does not show any ‘sub-pleural dots corresponding with … early lesions of asbestosis’;

4. Does not evidence that Mr Gatt had any interstitial lung disease; and

5. That ‘careful comparison’ of supine standard and high-resolution scans of the lung base of that scan with the seminal papers on high-resolution CT diagnosis of Asbestos by Akira “Asbestosis: High Resolution CT-Pathologic Correlation” Akira Metal, Radiology 1990 176: 389-394, clearly demonstrates the absence of any findings of early asbestosis in Mr Gatt’s scan.

58. Dr Jones concludes (p 30) that:

1. The October 2015 CT ‘does not confirm asbestosis or any other interstitial lung disease’;

2. There is no evidence of septal thickening bilaterally peripherally or small honeycomb cysts in the lower lobes;

3. The sub-pleural changes are due to ‘compressive atelectasis of the lung beneath the thick pleural plaques’ and ‘are not due to lung disease’ but, rather, ‘commonly occur in the right lower lobe caused by large osteophytes from the thoracic discs impinging on the lung’; and

4. A diagnosis of asbestosis cannot be made based on the October 2015 CT since the ‘fundamental lesion of asbestosis namely sub-pleural dots is not present’.

59. Dr Jones also notes (p 31) that, due to the progressive nature of asbestosis, findings of asbestosis ‘do not come and go’, the consequence being that the lack of any presence of asbestosis on the high resolution scan undertaken on 15 October 2015 means that it was also not present earlier.

60. The defendant submits that Dr Jones’ further report of 11 October 2020 (part of Exhibit 9) is in similar effect when responding to Dr Johnson’s report of 25 September 2020. In particular, Dr Jones explains (pp 66–67) that:

1. ‘careful review’ of the October 2015 CT ‘shows that the sub-pleural changes referred to by Dr Anthony Johnson only lie beneath the asbestos pleural plaques and asbestos-related diffuse pleural thickening’;

2. those changes are ‘not interstitial lung disease or asbestosis’;

3. Mr Gatt’s pleural plaques and diffuse pleural thickening ‘causes compressive atelectasis in the sub-pleural lung, which similarly produces sub-pleural lines, septal thickening and groundglass opacity’;

4. since the sub-pleural abnormality ‘is only visible beneath the thick pleural plaques and asbestos-related diffuse pleural thickening and not visible beneath normal pleura, interstitial lung disease and asbestosis are excluded; and

5. the ‘lung beneath normal pleura appears normal’ and, if Mr Gatt had asbestosis, ‘it would be abnormal’.

61. Dr Jones concludes in that report that (p 67):

1. ‘the late Mr Gatt did not have asbestosis; and

2. the ‘sub-pleural changes’ referred to in Dr Johnson’s report of 25 September 2020 ‘are the direct effects of the asbestos pleural plaques and asbestos-related diffuse pleural thickening on the sub-pleural lung, and ‘do not represent asbestosis’.

62. Dr Carr, in his report of 3 November 2020 (Exhibit 10), having reviewed all the relevant radiology including the October 2015 CT, concludes (p 101) that:

1. there is ‘clear evidence’ that Mr Gatt had asbestos-related pleural plaques with calcification;

2. there are some ‘nonspecific bibasal lung’ parenchymal changes of fibrosis which appear specifically related to the pleural plaques rather than representing the diffuse parenchymal fibrosis of asbestosis; and

3. therefore, ‘there are lung parenchymal changes associated with the pleural plaques but these are not the diffuse changes of typical asbestosis’.

63. A/Prof McKenzie also reviewed Mr Gatt’s radiology including the October 2015 CT. In his report dated 18 December 2018 (Exhibit 14) he says, in relation to the October 2015 CT that there was ‘no significant pulmonary emphysema and there was no interstitial lung disease or asbestosis’ (p 123).

64. The defendant asserts that the sheer weight of the evidence from Dr Goldin, Dr Jones, Dr Carr and A/Prof McKenzie is compelling and notes their various experience and expertise.

65. In particular, they address the relative qualifications and experience of Dr Jones and Dr Johnson as follows (defendant’s first written submissions [37]):

‘[37] Thus, Dr Jones’ CV (DCB, Tab 2, pp26-27) discloses that he has been a specialist radiologist for almost 40 years, having been appointed a Fellow of the Royal Australian and New Zealand College of Radiologists in 1981. He has a special interest in dust diseases and chest radiology and has been providing expert opinions in the radiology of dust diseases, especially asbestos exposure, since 1996. Further, he has had a strong interest in chest radiology, especially high-resolution CT, since 1994 and has seen thousands of cases in that time. The depth of his experience cannot be doubted.’

…

‘[40] In contrast, Dr Johnson is a respiratory and sleep physician, and not a radiologist. Although he is an eminent physician in respiratory medicine with clinical experience in reviewing radiology (T105.50-T106.3), his CV (PCB, Tab 14) discloses that he has not undertaken any specific training in radiology. This includes during his Master of Occupational Health and Safety and during his period as a Research Fellow in Respiratory Medicine. His stated research experience refers to epidemiology, occupational lung diseases and biostatistics but not radiology. He does not appear to have any particular training in high-resolution CT. While he is a member of the Royal Australian College of Physicians, he is not a member of the Royal Australian and New Zealand College of Radiologists.’

…

‘[45] A/Prof McKenzie is also a respiratory and sleep physician, His experience (DCB, Tab12, pp210-211) includes extensive training and experience in occupational lung disease and he has provided pulmonary function and exercise testing services to the Dust Diseases Board for many years. He has also participated in screening of lung function and chest radiographs in various industries including asbestos mining, quarrying, power stations and glass fibre insulation. A/Prof McKenzie’ experience in asbestos-related injuries is, therefore, at least equivalent to that of Dr Johnson who has also worked with the Dust Diseases Board (PCB, Tab 14, p293).’

66. The defendant further submits that as the plaintiff did not cross-examine Dr Jones, Dr Carr or A/Prof McKenzie, noting that their reports were admitted into evidence without challenge, the plaintiff thus cannot advance a case which contradicts their evidence. The basis of this submission starts with an analysis of the rule in Browne v Dunn (1983) 6 R 67.

67. As indicated by the defendant, this was recently explained by Brereton JA in Ghosh v Medical Council of New South Wales (2020) 102 NSWLR 303 at [69]:

‘The rule in Browne v Dunn has two aspects. The first is a rule of procedural fairness, that unless notice has already clearly been given of a party’s intention to rely upon such matters, it is necessary first to put an opponent’s witnesses in cross-examination the nature of the case upon which it is proposed to rely in contradiction of their evidence, and, absent such cross-examination, the party which ought to have cross-examined is precluded from contradicting their evidence. The second is concerned with the weight to be afforded to evidence which has not been the subject of cross-examination, and is to the effect that evidence upon which there has been no relevant cross-examination should not usually be rejected by the Tribunal of fact.’

68. My attention was also directed to Ellis v Wallsend District Hospital (1989) 17 NSWLR 553 at 586–588 (Samuels JA, Meagher JA agreeing) and Ali v Nationwide News Pty Ltd [2008] NSWCA 183 at [188] (Basten JA).

69. As Rolfe AJA (Sheller JA and Davies AJA agreeing) said in Hull v Thompson [2001] NSWCA 359 at [21]–[22]:

‘This court has on a number of occasions, remarked on the difficulties a Court confronts when asked to decide matters involving various types of expertise without the benefit of at least the principal expert witnesses being cross-examined.’

‘Prima facie if there is no cross-examination of an expert, (and indeed most witnesses), there is no basis for a Judge not to accept the unchallenged evidence. I say “prima facie” because there are circumstances in which evidence in a report may be rejected or subject to criticism or doubt. This may occur where, for example, the report is ex facie illogical or inherently inconsistent; or where it is based on an incorrect or incomplete history; or where the assumptions on which it is founded are not established. However, in the absence of such matters, there is no rational reason to not accept unchallenged evidence.’

70. The defendant submits that as in Hull v Thompson, the reports of Amaca’s two experts did not suffer from any of these deficiencies nor the reports of Dr Jones, Dr Carr and A/Prof McKenzie, as they are not reports which are ‘illogical or inherently inconsistent’ or ‘based on an incorrect or incomplete history’ or are based on ‘assumptions … which … are not established’.

71. On that basis, the defendant suggests that the plaintiff is not permitted to advance a case which contradicts the evidence of Dr Jones, Dr Carr and A/Prof McKenzie and that I must accept their evidence to the effect that Mr Gatt was not suffering from asbestosis or interstitial lung disease. Furthermore, they submit that the evidence of Dr Johnson cannot be accepted as it conflicts with the evidence of Dr Jones, Dr Carr and A/Prof McKenzie.

72. The defendant makes the following submission (defendant’s first written submissions):

‘[54] The Court of Appeal has noted that “the deficiency in the assistance given to the court [by failure to cross examine] can redound to a plaintiff’s detriment if the plaintiff fails to satisfy the onus of establishing, on the balance of probabilities, that a particular medical condition exists and that there is some causal connection between that medical condition and the circumstances alleged to give rise to a liability on the part of a defendant”: Fitzsimmons v Coles Supermarkets Australia Pty Ltd [2013] NSWCA 273 at [136] per Emmett JA (and, to a similar effect, Basten JA at [23] and McDougall J at [165] and see also Caruana v Darouti [2014] Aust Torts Reports 82-163; [2014] NSWCA 85 at [123]-[124] per McDougall J (Leeming JA agreeing].’

73. In this instance, the defendant submits that as there was cross-examination by the defendant of Dr Johnson, but no cross-examination by the plaintiff of the defendant’s witnesses, the risk to the plaintiff is even more pronounced similarly.

73. A/Prof McKenzie’s opinion must prevail, as dealt with in paragraphs [56]–[60] of their first written submissions, all of which I have had regard to.

74. However, a later paragraph of the judgment in Ghosh, not referred to by the defendant, to my mind is important. At [71] Brereton JA said:

‘I accept that the first aspect of the rule was not offended, because Dr Ghosh was plainly on notice that the Council took issue with the opinions of the doctors upon whom she relied. However, the second aspect of the rule still had work to do. I nonetheless also accept that the second aspect of the rule did not mean that the Tribunal was legally bound to accept the uncross-examined evidence of the doctors relied upon by Dr Ghosh. However, the fact that they were not cross-examined, and their opinions thus stood unchallenged, though not uncontradicted, should at least have weighed in their favour—rather than, as the Tribunal appears to have thought, against them.’

76. The plaintiff submits that rule does not require the plaintiff to cross-examine Dr Jones where notice has been previously and clearly given of the plaintiff’s intention to rely upon Dr Johnson’s evidence. The plaintiff further submits that there is no issue as to the credit of Dr Jones and Dr Johnson, and that I am not required to form a view as to the specialists’ integrity, nor am I at an advantage or disadvantage by the presence of one witness in the witness box and the other views being expressed entirely in written form. I accept that must be correct.

77. Dr Jones and Dr Johnson were plainly aware of the challenges to each other’s opinions. The doctors engaged in an extensive discourse as to the reason for their differing views as to what the images disclosed.

78. At page 28 of the Defendant’s Tender Bundle, Dr Jones, in his report dated 27 August 2020, says:

‘In your letter of instructions dated 5^th August 2020 you have asked me to review the additional material provided and have asked my opinion as to whether the late Mr Gatt suffered from asbestosis, pulmonary fibrosis or diffuse pleural thickening. In the event my opinion is inconsistent with that of Dr Johnson you have asked me to explain my reasoning.’

79. Dr Jones then provides his views, his views about Dr Johnson’s report, his disagreement and his reasons.

80. In Scalise v Bezzina & Ors [2003] NSWCA 362 at [98], Mason P (Santow JA and Brownie AJA agreeing) said:

‘The rule does not undermine the adversary nature of proceedings or make one party the other’s keeper. Thus, a party who proves fact sufficient to establish a cause of action or a defence upon which that party bears the onus does not have to confront the other side’s witnesses with the issue if they do not address it in their own evidence. To require this would invert that aspect of the rule grounded in what I have described as judicial economy. There is no unfairness in letting sleeping dogs lie and also invoking Jones v Dunkel so long as the moving party has by pleadings or otherwise signalled the matter sought to be proved and led necessary evidence on the topic. There is no need to confront an opponent’s witnesses by cross-examination if they fail to contradict evidence earlier called by the moving party in support of an issue raised in the pleadings or otherwise.’ (citations omitted)

81. On that point, I note that Dr Johnson’s views and the contradiction with Dr Jones’ evidence was plain.

82. In State Rail Authority of New South Wales v Brown (2006) 66 NSWLR 540 at [60]–[66], Basten JA said:

‘[66] As it turned out there was a gap in the defendants’ medical evidence. It was not the obligation of the plaintiff to fill it. He was entitled to say that Dr Millons’ opinion ... was based on incomplete material and should be discounted accordingly.’

83. I accept that the second part of the rule does not require me to accept the uncross-examined evidence. So far as the second limb is concerned, all that the rule requires me to do is to weigh in the balance of probabilities the absence of cross-examination, which I have done. Dr Jones (Exhibit 9) says:

‘Careful review of the scans dated 15^th October 2015 show that the sub-pleural changes referred to by Dr Anthony Johnston only lie beneath the asbestos pleural plaques and asbestos related diffuse pleural thickening. This has two mechanisms. Firstly, sub-pleural fibrosis occurs beneath asbestos pleural plaques and diffuse pleural thickening but it is not interstitial lung disease or asbestosis.’

84. However, Dr Johnson (Exhibit J) said:

‘In my opinion it is more likely than not Mr Gatt contracted asbestosis and ARPD due to his asbestos exposure whilst employed by James Hardie. This is based on the radiological features consistent with a diagnosis of asbestos related pleural disease and interstitial pulmonary fibrosis apart from his asbestos exposure. His asbestos exposure was sufficiently heavy to have caused asbestosis. Therefore, my diagnoses are asbestosis and asbestos related pleural disease i.e. pleural plaques and diffuse pleural thickening.’

85. In cross-examination with regard to radiology, Dr Johnson gave the following evidence: (T105.41–T106.3)

‘Q.   Is a discipline of interpretation of images?

A.    Yes. It's a discipline of collecting images in the best possible way, and then providing a report for referring clinicians, such as myself, with their interpretation of what they see. Yes.

Q.   As a general proposition, you would defer, would you not, to the specialist radiologists in the interpretation of their images.        

A.   As a general proposition, no. Because the radiology is a tool, and the radiologist only has those pictures. When I'm assisting a patient's diagnosis, I'm looking at the person, the history, their exposures, their course of their illness, plus what the findings say. And also with asbestos radiology, and also interstitial lung disease radiology, it's very specified, and there's not that many radiologists who have an expertise in that, who has seen that all the time. Whereas someone like myself is seeing interstitial lung disease and radiology all the time, and often I would disagree with a radiologist's report in what the CT scans find. So I don't just refer to them. I take that as a tool, and what they think, but in making a diagnosis, I would use my interpretation, plus the history.’

86. Further, Dr Johnson gave this evidence: (T110–T111)

‘Q.   You say, "This was visible on a CT scan in 2003." Do you see that on page 5.        

A.   Yes.

Q.   Is that your own opinion, or was that in reliance on what you understood to be Dr Snodgrass' opinion.        

A.No. It's based on my own opinion. On page 4 of my report, I've reviewed the CT in the top paragraph.

Q.   You also then ‑ I'm sorry, Doctor, have you finished.        

A. I concluded that there were increased interstitial markings and small honeycomb cysts seen.

Q.   You say, "It was also visible on a CT scan prior to him commencing treatment for his lung cancer." Is that the scan of 15 October 2015 reported by Dr Golden.        

A.That's correct, yes.

Q.   You describe extensive pleural plaques and diffuse pleural thickening.        

A.   Yes.

Q.   Those are related findings, are they not.        

A.   Well, they're both caused by asbestos exposure, but they're different conditions.

Q.   You say then that there are no other obvious causes for interstitial lung disease, apart from asbestos exposure.        

A.   Yes, I do.

Q.   And you then make a point of saying that his asbestos exposure was sufficient to have caused asbestosis.        

A.That's correct, yes.

Q.   "Given these facts, I would diagnose your client with asbestosis."

A.   That's correct.

Q.   Now, those facts include your view in relation to his cumulative asbestos exposure.        

A.To make a diagnosis of asbestosis in ‑ clinically, I would necessarily use 25 fibre/ml years as a threshold. As we've discussed, there's a dose response relationship, and at that stage I hadn't calculated in fibre/ml years. I considered he had heavy exposure, and he had changes of interstitial lung disease. So at that point, and also in practice, I wouldn't necessarily say if someone doesn't have 25 fibre/ml years they don't have asbestosis. If they have had exposure, and as you said, there's a huge variability in how you assess that, but if I judge it to be heavy, it's an appropriate time period, there's a time period between his exposure and his developing disease and his CT changes for consistent with asbestosis, and there's no other likely cause, he didn't get exposed to drugs or use drugs, or been on drugs that might have caused fibrosis, then I would have diagnosed him with asbestosis.’

87. An unfortunate issue arose with regard to the evidence from Dr Snodgrass, a radiologist. The plaintiff indicated to the Tribunal that they intended to rely on his evidence, and that he had been served with a subpoena to give evidence.

88. It became clear to me, by statements from the Bar table that Dr Snodgrass was a reluctant witness, despite my offer to sit outside court hours at his convenience, and also to take his evidence by AVL or telephone.

89. Thus, the plaintiff was unable to call Dr Snodgrass to give evidence, and his report was removed from the plaintiff’s tender bundle.

90. The defendant submits that as no explanation was offered, that I should infer that Dr Snodgrass’ evidence would not have assisted the plaintiff’s case: Jones v Dunkel (1959) 101 CLR 298, and that as a consequence I would more readily resolve the question in favour of the defendant.

91. I do not accept that the failure to call Dr Snodgrass to give evidence should cause me to infer that his evidence would not have assisted the plaintiff’s case. It is clear to me that the plaintiff tried to get him to attend, but he refused to do so. I cannot see that there was anything else the plaintiff could have done and as such I have had no regard to Dr Snodgrass’ opinion.

CUMULATIVE AIRBORNE EXPOSURE

Evidence

92. The issue to be determined is the cumulative airborne asbestos concentration to which Mr Gatt was, on the balance of probabilities, exposed during the period of his work at James Hardie. This is a necessary step in assessing whether the plaintiff has proved that Mr Gatt’s lung cancer was caused by his exposure to asbestos, as opposed to his smoking, or any other cause.

93. Prior to the commencement of the trial, the plaintiff had obtained two reports from Dr Michael Kottek dated 29 July 2020 (Exhibit BB) and 29 October 2020 (Exhibit CC). The defendant had obtained a report of Mr Geoffrey Pickford dated 1 October 2020 (Exhibit 1) which replaced his initial report of 14 October 2019 (on which the defendant no longer relies).

94. The defendant submits that these reports cease to have significance in light of two matters, as follows:

1. The first is, that following a conclave between Mr Kottek and Mr Pickford on 2 November 2020, which was facilitated by Mr James McIntyre SC, Mr Kottek and Mr Pickford prepared a joint expert report (‘JER’) dated 5 November 2020 (Exhibit DD). That report set out the opinions of Mr Kottek and Mr Pickford as at 5 November 2020, on the questions the subject of the conclave. Of significance, the two experts agreed as to all material matters relevant to assessing the asbestos concentration to which Mr Gatt was exposed as well as the cumulative level of exposure.

2. Secondly, by letter dated 9 November 2020 (‘9 November letter’) to the plaintiff’s solicitor (Exhibit PP), Mr Kottek stated that having been provided with additional documents after the JER was prepared, that he withdrew his opinions as contained in the JER and, by an appendix to the 9 November letter, provided revised answers to questions the subject of the conclave. The additional documents with which Mr Kottek said that he had been supplied were titled ‘Dust Control Notes on Discussion 17.1.1963’ (‘January 1963 notes’) and ‘Notes on Exposure Indices’ (‘Exposure Indices’) (Exhibit UU) (page 1 of the 9 November letter).

95. Mr Pickford maintains his opinions expressed in the JER, save for one matter concerning conversion factors, to which I will refer to later. Thus, the opinions of Mr Kottek and Mr Pickford are now partially reflected respectively in the JER—subject to the matter concerning conversion factors, and the 9 November letter.

The 9 November letter

96. I admitted the letter into evidence over objection of the defendant (Exhibit PP). The defendant’s consequent submission is that the letter should be given no weight.

97. The defendant submits that the oral evidence given by Mr Kottek with regard to the letter in its written submissions at [75]–[79] demonstrates the following, and I accept that it does:

1. The first communication Mr Kottek had after the signing of the JER was a telephone call from Mr Simic, the plaintiff’s solicitor, on the afternoon of Friday, 6 November 2020 (T206.27–43);

2. The next email between Mr Kottek and Mr Pickford on 6 November 2020, which was forwarded by Mr Kottek to Mr Simic at 3.36 pm on 6 November 2020 (Exhibit 2), was in response to Mr Simic’s request to Mr Kottek to obtain all emails passing between Mr Kottek and Mr Pickford in the conclave and leading to the preparation of the JER (T207.2–24);

3. There followed another telephone call between Mr Kottek and Mr Simic on 6 November 2020 in which Mr Kottek and Mr Simic discussed the content of the conclave (T211.5–23);

4. Mr Kottek then sent certain documents to Mr Simic by email at 4.59pm on 6 November 2020 (Exhibit 3), including Notes for Discussion on Dust Control on 28 February 1963 (Exhibit MM, February 1963 notes) (T211.32–42). In this email Mr Kottek states that he had seen the ‘Notes on Discussion 17.1.63’ (presumably a reference to the January 1963 Notes) but ‘not the attached notes on Exposure Indices’ (presumably a reference to the Exposure Indices). Notwithstanding the inference which might have been drawn from this statement to the effect that the Exposure Indices must have been provided to Mr Kottek by this time, Mr Kottek said that he had not yet received the document: see [99(g)] below;

5. There was then a telephone conversation between Mr Kottek and Mr Simic on Saturday 7 November 2020 at 2.50pm during which Mr Kottek and Mr Simic discussed the content of the then draft of the 9 November letter whilst Mr Kottek was drafting it (T212.16–42);

6. Mr Kottek discussed with Mr Simic ‘that the dust indices as a matter of 5 is probably the more—would be a more reliable basis to proceed upon’ (T215.31–33). This was even though he had not received the ‘dust indicies’—i.e. the Exposure Indicies—until after this telephone call: see [99(g)] below (T222.5–9 and T213.14–37);

7. Mr Simic then sent an email to Mr Kottek at 3.47pm on 7 November 2020 to which he attached the January 1963 notes and the Exposure Indices (Exhibit 4), which was the first time that Mr Kottek had received the document (T221.7–11);

8. There then followed another telephone call between Mr Kottek and Mr Simic later on 7 November 2020 (T222.12–24);

9. At about 3.36pm on Sunday, 8 November 2020, Mr Kottek and Mr Simic had two telephone calls totalling about 18 minutes (T222.27–46); and

10. On 9 November 2020 at 1.38am, Mr Kottek and Mr Simic had another telephone conversation (T222.49–T223.2).

98. Each of the telephone conversations between Mr Kottek and Mr Simic referred to in the previous paragraph were to discuss the content of what became the 9 November letter which Mr Kottek sent by email (Exhibit 5) to Mr Simic at 10.12am on 9 November 2020 (T223.5–13).

99. The experts commenced to give their evidence jointly on 9 November 2020 and the Tribunal was provided with the 9 November letter, which went into evidence.

100. During cross-examination, Mr Kottek was asked the following questions (from T254.11):

‘Q But for the communications from Mr Simic last Friday and over the weekend, you would have rested with the position that you took in the joint report, would not you?

A Yes. Whether that would have been ‑ you know, I don't ‑ it's ‑ there was ‑ there's two aspects, but I think following the discussions with Mr Simic, I realised ‑ and, again, it's very hard for me to respond to this. I ‑ I realise ‑ well, yeah, I do believe that in ‑ during the conclave, I took over due regard to ‑ to things that I shouldn't have, and having had that pointed out to me, I thought it was appropriate to ‑ to revise my opinions. Again, it's very hard for me ‑ I am obviously not in a position to go beyond that.’

…

‘Q It was only after Mr Simic's telephone conversations with you in which he said whatever he may have said, and you said whatever you may have said, that you set about a course of seeking to depart from the position that you had honestly and earnestly have reach agreement with Mr Pickford upon over the four days of the conclave and resulting in the joint report on Thursday last; is not that right?

A I, having spoken with Mr Simic, I formed the view that in ‑ in reaching agreement with Mr Pickford, I ‑ I had fallen into error in some of the material that I had considered. In ‑ yeah, some of the material I considered was relevant, and ‑ and that was why I thought ‑ and having reflected on that, and considered the relevance of that ‑ of some of the material I considered, and the appropriateness of that, in fact, that is why ‑ that is how the letter on 9 November came to pass, and –.’

Q Were you asked by Mr Simic to look for a way to get around the agreement contained in the joint report?

A No.

Q Well, what did Mr Simic ask you to do?

A He asked me to reflect on some of the – some of the discussions and considerations – some of the – some of the content of discussions during the conclave that we – that influenced my opinions, as expressed in the transcript. That is what he – that was a – a way of summing it up.’

101. Then further (T256.19–26), there was the following exchange:

‘Q Mr Kottek, the reality is, I suggest to you, that in acceding to depart from the joint report of last week, you have simply endeavoured to formulate a different expression of opinion that it is thought will assist the plaintiff's case, and that that is the purpose for which you have done it.

A No. I don't accept that. It was on ‑ on reflection of the way that the conclave had ‑ had proceeded, and the agreement there that I ‑ that I revised and altered my opinions.’

102. The defendant submits that the above summary of Mr Kottek’s evidence discloses that, at the least, there was considerable influence by Mr Simic on Mr Kottek subsequent to Mr Kottek’s signing of the JER. They submit that Mr Kottek would have rested with what he had agreed in the JER absent the intervention of Mr Simic. Instead, Mr Simic provided the Exposure Indices to Mr Kottek. Mr Simic and Mr Kottek had numerous telephone conversations on 6–9 November 2020 concerning the content of the conclave and the content of the then draft of the 9 November letter. Those conversations included lengthy calls on Sunday 8 November 2020 and a call at 1.38am on 9 November 2020.

103. The defendant further submits that the conduct that occurred between Mr Simic and Mr Kottek following the settling of the JER, is the antithesis of the principles underpinning s 56 of the Civil Procedure Act 2005 (NSW) and the purpose of expert conclaves and joint reports. On that basis the defendant asserts that the JER should be given no weight in my decision.

‘CIVIL PROCEDURE ACT 2005

56   Overriding purpose

(cf SCR Part 1, rule 3)

The overriding purpose of this Act and of rules of court, in their application to civil proceedings, is to facilitate the just, quick and cheap resolution of the real issues in the proceedings.

The court must seek to give effect to the overriding purpose when it exercises any power given to it by this Act or by rules of court and when it interprets any provision of this Act or of any such rule.

A party to civil proceedings is under a duty to assist the court to further the overriding purpose and, to that effect, to participate in the processes of the court and to comply with directions and orders of the court.

(3A)    (Repealed)

Each of the following persons must not, by their conduct, cause a party to civil proceedings to be put in breach of a duty identified in subsection (3)—

(a)  any solicitor or barrister representing the party in the proceedings,

(b)  any person with a relevant interest in the proceedings commenced by the party.

The court may take into account any failure to comply with subsection (3) or (4) in exercising a discretion with respect to costs.

For the purposes of this section, a person has a relevant interest in civil proceedings if the person—

(a)  provides financial assistance or other assistance to any party to the proceedings, and

(b)  exercises any direct or indirect control, or any influence, over the conduct of the proceedings or the conduct of a party in respect of the proceedings.

Note—

Examples of persons who may have a relevant interest are insurers and persons who fund litigation.

(7)    (Repealed)’

104. The Uniform Civil Procedure Rules 2005 (NSW) ss 31.26(3) and (4) apply, and for matters where there is no agreement, the JER must comply with the rules of evidence:

‘Uniform Civil Procedure Rules 2005

31.26   Joint report arising from conference between expert witnesses

(cf SCR Part 36, rule 13CA; DCR Part 28, rule 9D; LCR Part 23, rule 1E)

This rule applies if expert witnesses prepare a joint report as referred to in rule 31.24(1)(c).

The joint report must specify matters agreed and matters not agreed and the reasons for any disagreement.

The joint report may be tendered at the trial as evidence of any matters agreed.

In relation to any matters not agreed, the joint report may be used or tendered at the trial only in accordance with the rules of evidence and the practices of the court.

Except by leave of the Court, a party affected may not adduce evidence from any other expert witness on the issues dealt with in the joint report.’

105. The plaintiff wished to question the witnesses as to what occurred in the meeting with Mr McIntyre SC, that formed the basis of the JER. The defendant objected, and after argument, I upheld the objection, and no further evidence was given as to what occurred during the preparation of the JER.

106. The plaintiff submits that the defendant’s objection to Mr Kottek and Mr Pickford giving evidence by way of explanation of what occurred in the Joint Evidence Conclave leading to creation of the JER means that the Tribunal does not have before it a full explanation of Mr Kottek’s altered position with respect to the JER, and what matters may or may not have influenced Mr Kottek’s initial agreement. However, the plaintiff submits what is significant, is that the Tribunal is aware that there is no agreement between the experts on the conversion factor or the cumulative fibre burden.

107. The plaintiff further submits that the defendant is entitled for forensic reasons to withhold consent to the participants in the Joint Experts Conference from disclosing to the Court the matters discussed in the conference, however:

1. the assertion by the defendant that it adopts a position of principle is, with respect, not consistent with the rules (UCPR 31.24(6)) or the Practice Note (SC Gen 11 [5]–[27]);

2. the Rules and the Practice Note make it clear that an expert may well depart from the JER and become subject to cross-examination; and

3. the court is entitled to have regard to that matter when assessing the evidence of Mr Kottek and Mr Pickford.

108. The plaintiff submits what motivated the JER cannot be assessed because the defendant, who admits breach, is not prepared to consent to Mr Kottek (or for that matter, Mr Pickford) explaining how the JER was produced. What is known from the email trail is that Mr Pickford when asked by Mr Kottek to release the email trail, declined to do so upon instructions from the defendant, as the defendant was entitled to do.

109. The Uniform Civil Procedure Rules s 31.24(6) provides:

‘(6)    Unless the parties agree, the content of the conference between the

expert witnesses must not be referred to at any hearing’.

110. Practice Note SC gen 11 provides relevantly:

‘5.   The objectives of such directions for joint conference of experts

include the following:

…

binding the experts to their position on issues, thereby enhancing certainty as to how the expert evidence will come out at trial. (The joint report may, if necessary be used in cross-examination of a participating expert called at the trial who seeks to depart from what was agreed);

…   

1. Prior to signing of a joint report, the participating experts should not

seek advice or guidance from the parties or the legal representatives except as provided for in this Practice Note. Thereafter, the experts may provide a copy of a report to a party or his or her legal representatives and may communicate what transpired at the meeting in detail if they wish.’

111. Mr Kottek provided a letter and report (Exhibit PP) disavowing his agreement in the JER with respect to the cumulative fibre burden and the conversion factor of 2.2. He sought to explain his initial agreement and subsequent disagreement in his letter of 9 November and otherwise in his oral evidence. He was prevented from doing so by the defendant (T 227.45, 241.16, 241.24, 244.25, 254.17).   

112. It is most unfortunate that there were exchanges between Mr Kottek and Mr Simic after the JER was agreed and signed by both experts. This letter has created a significant issue as to the credibility and credit of not just Mr Kottek, but of the JER itself. It was completely inappropriate for Mr Simic to attempt to assert any influence over Mr Kottek at any time, but most crucially after the JER had been signed. It was completely inappropriate for Mr Simic to forward additional material to Mr Kottek after the JER had been sent to him. I find it very difficult to understand why the material that was clearly in Mr Simic’s possession was not provided to Mr Kottek before the joint conference and before the JER. This would have allowed the conclave to examine the additional material and, possibly, produce a joint report.

113. The conduct of Mr Simic in this regard has occasioned a significant increase in the Tribunal’s time to hear the evidence of these experts, which delayed the proceedings and no doubt occasioned significant costs to the parties. There can be no criticism of the defendant’s conduct, and in particular the opposition of further evidence being attempted to be adduced. The rules provide that what occurred in the conclave are matters that should be contained within the parameters of the conclave. Rule 31.24(6) provides that ‘the content of the conference between the expert witnesses must not be referred to at any hearing’ unless the parties agree. It was open to the defendant to object to questions to the expert witnesses as not allowable on the basis of the legislation. The inappropriate conduct of Mr Simic does not mean that the sanctity of the conclave, and the matters discussed therein ought be violated and ventilated.

114. The effect of the JER, the intrusive conduct of Mr Simic, Mr Kottek’s letter of 9 November 2020 and the further evidence from the experts is such that there is no agreement as to the cumulative fibre burden, nor the conversion factor that ought be applied. The task that I now face is made more complicated and difficult due to the JER in fact not being a ‘joint’ report.

115. The differences of the experts opinion’s before the conclave were set out in their earlier reports (Exhibits BBB and CCC for Mr Kottek, and Exhibit 1 for Mr Pickford).

116. The plaintiff submits that I should reject the JER conversion factor of 2.2 and adopt a conversion factor of 1 mppfc = 6 fibre/ml or, in the alternative, Mr Kottek’s preferred conversion factor of 3–4. They submit that this is the appropriate approach because:

• Mr Pickford applies the conversion factor of 6 in his two reports (Exhibit 2);

• The ACGIH and BOHS adopt a conversion factor of 6;

• The only reading in Exhibit 7 that corresponds approximately to Mr Gatt’s exposure is that at station 25. That produces a conversion factor of 10;

• Dr Leigh in his report of 31 December 2018 (Exhibit B) states that the conversion factor from mppcf to fibres per millilitre is 1 mppcf = 6 fibres/ml; and

• The conversion factor adopted in the JER is arbitrary and not agreed to by Mr Kottek.

117. The plaintiff makes further submissions as to the use of the Lynch and Walton opinion and the Hammad report to support the figure of 2.2. Mr Kottek says the JER conversion factor has not been used in any epidemiological studies and was lower that most conventionally used conversion factors.

118. Mr Pickford rejected Walton, and the Hammad report which involved parallel measurements in 1979 in America using Chrysotile and JER on its terms increased the estimate by 50% (Exhibit DD) however the Lynch report is not in evidence.

119. The plaintiff submits that the opinion of the experts on this point is without reasoning and fails to demonstrate how the opinion is based on the application of the expert’s specialist knowledge, contrary to the requirements of Dasreef v Hawchar (2011) 243 CLR 588 at 602–603. She submits that the factor applied by Mr Kottek in his report of 29 July 2020 (Exhibit BB) applies a very conservative conversion factor of 3 f/ml per mppcf.

120. The plaintiff also submits that a higher conversion factor is appropriate where the content of the atmospheric dust is derived from raw asbestos, and contains a high proportion of amphibole (T315.2, 29–35).

121. In contrast, the defendant submits that the ultimate opinions of Mr Pickford and Mr Kottek are reflected in the JER, subject to the 9 November 2020 letter. Thus, Mr Pickford and Mr Kottek’s earlier reports are of background relevance only. In support of that submission, the defendant draws my attention to the following:

1. The plaintiff’s reliance of the earlier reports of Mr Kottek and Mr Pickford is misplaced as where an expert witness who has provided a report changes his or her opinion, the expert is obliged to provide a supplementary report which sets out the revised opinion: r 31.27(4) of the UCPR and clause 4 of the Expert Witness Code of Conduct;

2. Accordingly, to the extent that the plaintiff seeks to draw some conclusion from the earlier reports of Mr Kottek and Mr Pickford that is not contained in or consistent with, respectively, the 9 November letter or the JER, the plaintiff’s submissions should be rejected, particularly as the plaintiff’s reliance on Mr Pickford’s initial report of 14 October 2019 which was superseded by his report of 1 October 2020, was only tendered by the defendant at the plaintiff’s request. At [31] of the defendant’s closing submission in reply, they submit as follows:

‘[31] … Amaca did not seek to rely on Mr Pickford’s first report, which no longer reflected Mr Pickford’s opinion in the light of additional material, conformably with the obligations on Mr Pickford referred to in the previous paragraph.’

3. With regard to the Peter Russell data containing 20 entries relevant to Mr Gatt’s employment ought be rejected, on the basis that the Peter Russell data disclosed only the single entry which related to the dry mix area where Mr Gatt worked, being 2.5 mppcf, and which area was not the tide mill area, which was the subject of separate entries.

EXHIBITS 7 and 8

122. Exhibits 7 and 8 were provided to the Tribunal by Mr Pickford whilst he was giving evidence.

123. Exhibit 7 is a report on the Hygiene Survey of Camellia – August-September 1969. It shows the conversion factors for the Camellia factory in 1969. Mr Pickford said that Exhibit 7 contained readings that attempted to provide parallel measurements to guide the conversion of dust counts taken in particles per cubic foot to fibres/ml. Exhibit 8 is a spreadsheet prepared by Mr Pickford based on the parallel testing results (Exhibit 7).

124. Mr Pickford explained the relevance of Exhibit 7 was that it contains data from parallel testing of the midget impinge and membrane filter method at Camellia shortly after Mr Gatt worked there, and as such was directly relevant to determining the appropriate conversion factor applicable to Mr Gatt’s work (T282.32–37). The defendant submits that it may then be contrasted with the BOHS and Roberts & Whaite papers on which Mr Kottek relies.

125. Mr Kottek’s reliance on the Exposure Indicies is based upon his surmising that ‘the authors of that document had made some attempt to estimate a long term, average exposure of various operators or work stations using the midget impinge as a particle count, millions of particles per cubic foot’ (T 198.39–41, p 2 of the 9 November letter).

126. Further, Mr Kottek relies on the dust index figure of 5, being a long-term average exposure of 5 mppcf, at the number 6 mixing plant as being ‘not materially different’ in terms of relative risk of exposure from the position at the number 5 mix plant, being where Mr Kottek says Mr Gatt worked (T 198.44–T199.19, p 2 of 9 November letter).

127. The defendant asserts that I should not accept either of those propositions for a number of reasons, detailed as follows:

1. During cross-examination, Mr Kottek agreed that:

• The dust indicies were derived from the Peter Russell data (Exhibit GG) and that it was unclear what level of statistical analysis was used in 1963 when the Exposure Indicies were calculated;

• It was not known what the data out of the 20 pages of Peter Russell data was used to derive the Exposure Indicies;

• In comparison, the actual Peter Russell data ‘tells with specificity what aspect of the work data relates to’ including the specific job, for how long the test sampling was done, how many samples were taken and the prevailing conditions (T216.26–T217.47, T226.34–39);

2. Mr Kottek’s denial that the Peter Russell data was more reliable than the Exposure Indicies (T217.5–T218.5) is something that I should reject on the basis that no scientist would come to the same conclusion, and as such should cast considerable doubt about the nature of the evidence given by Mr Kottek in the 9 November letter;

3. Mr Kottek agreed that the limitation in the Peter Russell data stated in (a)(ii) of the answer to Question 2 of the JER was overcome by the application of the (then agreed) conversion factor (T226.25–31);

4. Despite the 9 November letter, Mr Kottek remained of the view that the Peter Russell data disclosed only the single entry which related to the dry mix area where Mr Gatt worked being 2.5mppcf. Nonetheless, he did not agree with the subsequent proposition that if the data reading of 2.5mppcf was ‘the only data set that bears on the dry mix area in the Peter Russell data, then your inference that an index of 5 equates to 5 million particles per cubic foot is simply unsustainable’ (T229.47–230.2);

5. That refusal, to agree to the obvious, the defendant asserts, was not reasonable in light of the objective circumstances referred to in the previous paragraph, and that at the least, it also casts considerable doubt about the nature of the evidence given by Mr Kottek in the 9 November letter;

6. In relation to the Hammad data, JER page 5, Mr Kottek agreed that he had not identified any different data in relation to the Hammad paper which would cause him to change his opinion expressed in the JER; and

7. As to the Roberts and Whaite data referenced at page 5 of the JER, Mr Kottek agreed that although there was no specific measurement related to the dry mix area, it was relevant to include the data for the tide mill area because ‘the tide mill was likely to be more dusty than the dry mix area’. Mr Kottek not only said he had agreed with that, but that ‘I can’t expand on that further’ (T244.6–25).

128. Mr Pickford disputes the relevance of the reading at workstation 25 on 2 bases:

1. He says that it does not correspond to Mr Gatt’s workstation; and

2. The reading is so high, that it ought be excluded as an ‘outlier’.

129. Mr Pickford says that none of the measurements in Exhibit 7 correspond to Mr Gatt’s workstation (T316.14–23). His evidence at (T317.42) is that the reading is from another part of the factory apparently in an enclosed room with raw asbestos. Mr Gatt’s evidence is that the mixing area where he worked was ‘enclosed and very dusty’: Exhibit 1, p 52 [16].

130. Mr Pickford (Exhibit 8) excludes the reading at station 25 as an ‘outlier’ (T316.31, 282). He agreed that an ‘outlier’ is a deviation from a statistical mean from readings taken in a common area (T315.46–50). He gave the following evidence with respect to the measurements in Exhibit 7 (T316.8):

‘Q   I will come to specific measurements in a moment. The measurements in relation to document Exhibit 7 are from all over the factory are they not.

A   That’s true, yes.

Q   So they are not measurements from a common area are they.

A   No they are not.’

131. Mr Pickford then gives the following evidence (T316.33):

‘Q   But it is not an outlier is it because it’s not common with the other measurements.

A   Well the other measurements are so consistent that the only conclusion you could reach is that it’s an outlier, but again, I recalculated including the outlier.’

132. An informal outlier is described by Mr Pickford as a result 10 times higher than a group of results that are otherwise relatively low and consistent (T315.43). The plaintiff submits that the reading cannot be excluded as an informal outlier only because the measurement is high. I can see some force to that submission.

133. If Mr Pickford excludes station 25 (the outlier) (in Exhibit 8) the average conversion factor would be 0.75. If it is included, the average conversion factor is 1.38. On either calculation, the appropriate conversation factor, is considerably lower than the conversion factor of 2.2 contained in the JER.

134. The defendant is critical of Mr Kottek’s reasoning as set out in the 9 November letter as to why he adopted a conversion factor of 3 as being appropriate, as rather scant. He refers to the BOHS study and the Roberts & Whaite paper, which were used in the formulation of the JER, and which was also adopted in a NSW Department of Health survey at Camellia in 1957. He said that the two studies had ‘broadly equivalent end points’ and that a conversion factor of 4 ‘can be said to be comparable with the epidemiological literature’, although which literature is not identified. That suggests, according to Mr Kottek, that the appropriate conversation factor was 3, which he had adopted in his report of 29 July 2020.

135. The defendant asserts that the problem with the BOHS and Roberts & Whaite paper is that the BOHS is unrelated to Camellia, and is based on a textile factory. The Roberts & Whaite paper is dated 1953, before Mr Gatt worked at James Hardie. Further, the NSW Department of Health paper is dated 1957 and was based on the Roberts & Whaite paper.

136. Importantly, Mr Kottek and Mr Pickford both agree conversion factors can vary from different types of fibres and different types of processes: (Kottek 29 July 2020, Exhibit BB, T270.28–30, T282.38–43). Thus, Exhibits 7 and 8 are of particular significance.

137. Finally, the defendant asserts that I should accept the conversion factor as either 0.75 or 1.38 based on Exhibit 7 as it is the most reliable data applicable to Mr Gatt’s work because it covers the very factory and very asbestos fibre with which Mr Gatt was working, or alternatively, I could find that the appropriate conversion factor is 2.2 as contained in the JER.

138. The plaintiff submits that there is no justification for averaging out the parallel measurements in Exhibit 7, when Mr Pickford asserts (T316.14–23) that none of the measurements correspond with the area in which Mr Gatt worked.

139. I accept that the description of workstation 25 corresponds with the description given by Mr Gatt as the ‘mixing plant’ (Exhibit A paragraph 26) as it says ‘No 2 Mixing Plant’. Further, it is submitted by the plaintiff that Mr Pickford deals with the data in Exhibits 7 and 8 in a manner likely to achieve an unrepresentative conversion factor and thereby providing a very low cumulative fibre burden. Again, there is to my mind, some significant force to those submissions.

1. X-ray studies, CT scanning and clinical examination of Mr McDonald revealed no evidence of asbestosis. No biopsy was carried out nor post-mortem examination of the lungs undertaken. There was accordingly no radiographic, clinical or histological evidence that he had asbestosis.’

   202. The defendant relies on numerous expert reports which consider the epidemiology of lung cancer and the nexus between asbestos exposure, cigarette smoking and the occurrence of lung cancer.

   203. The defendant served a 25B Notice which was tendered and became Exhibit 20. It contained the following issue of a general nature determined previously in proceedings before the Tribunal:

‘1.   ISSUE

The issue of a general nature is the level of cumulative exposure at which the relative risk of contracting lung cancer doubles in consequence of working with asbestos cement building materials in Australia between 1955 and 1980.

1. DETERMINATION

Judd v Amaca Pty Ltd [2003] NSWDDT 12 at [42] (Judge Curtis):

'The relative risk of contracting lung cancer in consequence of working with asbestos cement building materials in Australia between 1955 and 1980 doubled at 50 fibre ml years of cumulative exposure.'

1. PARTICULARS: the following are matters relevant to the Determination:

a.   The Determination was made in the absence of consideration of the effect of the effluxion of time between an individual's last exposure to asbestos and the individual's diagnosis of carcinoma of the lung.

b.   The Determination was made in the absence of consideration of the effect of the individual's cigarette smoking habit in the circumstances of the period during which the individual was exposed to asbestos and the timing of the individual's diagnosis of carcinoma of the lung.'

204. The defendant also relies on the upper end range of the JER finding, that is a reading of 24.4 f/mL.yr as lower than the level of 25 f/mL.yr identified in the Helsinki Criteria to be the minimum level at which lung cancer could be deemed to have been caused by asbestos exposure. However, the defendant submits that the Helsinki Criteria is not helpful in assisting the determination of the causation of lung cancer where smoking and asbestos exposure are both present, nonetheless the defendant highlights the top end of the JER range.

205. The defendant relies on reports of Prof Moolgavkar, A/Prof Chirieac, A/Prof McKenzie; Dr Gal; and Prof Fox–—all of whom the defendant claims conclude that Mr Gatt’s lung cancer was caused by his cigarette smoking with none or only very minor attribution due to his asbestos exposure.

206. Prof Moolgavkar is a cancer epidemiologist and research scientist. In his report of 10 October 2019 (Exhibit 11), he concludes that Mr Gatt’s lung cancer can be attributed greater than 96% to his cigarette smoking.

207. Prof Moolgavkar submits, inter alia:

1. ‘It is widely accepted that the vast majority of lung cancers is caused by cigarette smoking’;

2. ‘Very high levels of exposure to asbestos are required to increase, even modestly, the risk of lung cancer’. Cigarette smoking is ‘a far stronger lung carcinogen than is asbestos, whether amphibole or chrysotile’. Exposure of at least 15 f/mL.year will increase risk of asbestos-associated disease, anything less lacks epidemiologic data to demonstrate there is an increased risk;

3. Age increases risk of lung cancer;

4. Asbestos exposure made no contribution to the development of Mr Gatt’s lung cancer; and

5. It’s important to note exposure to asbestos ceased 51 years before the diagnosis of lung cancer.

208. Dr Leigh and Prof Moolgavkar are in agreement that the Helsinki Criteria (Exhibit R) cannot reliably assist in determining causation when a person has been exposed to both cigarette smoke and asbestos.

209. Prof Moolgavkar in his report of 10 October 2019 (Exhibit 11) stated that the document ‘made little effort to critically review the epidemiological literature,’ and is an ‘unreliable source for the attribution of cancer.’

210. Dr Leigh referred to the Helsinki Criteria in his report of 31 December 2018 (Exhibit B) and gave evidence before me that by his thesis, ‘in a way I’m throwing out Helsinki by talking the biological, that’s post Helsinki’ (T177.34–35).

211. Further, Dr Leigh co-authored a 2004 paper with Prof Hendersen which selected a range of cumulative exposure of 25 to 100 fibre/mL.years, by adopting a range of relative risk of lung cancer of 4%, equating to 25 fibre/mL.years, was at the bottom of the range.

212. The defendant relies on the evidence of Prof Hendersen in McDonald v State Rail Authority (NSW) (1998) 16 NSWCCR 695 (Exhibit 22). His evidence was summarised by Curtis DCJ in Judd v Amaca Pty Ltd [2003] NSWDDT 12 as follows:

‘20.   Having previously observed that "the relative risk of lung cancer is estimated to increase 0.5 to 4 per cent for each fibre per cubic centimetre per year (fibre-years) of cumulative exposure", (this range may not even have included the totality of the studies considered by the participants (T 188.1)), the authors of the document adopt without explanation the upper boundary of this range (4 per cent) and conclude that a cumulative exposure of 25 fibre years increases the risk of lung cancer twofold. Had the lower boundary been selected a cumulative exposure of 200 years would be required.

1. Professor Henderson has acknowledged that good science may justify the selection of the middle of the range (T 184, McDonald 225) and conceded that he does not know why the figure of 25 fibre ml years was adopted (McDonald page 252). He did not know the cohort upon which the figure was based (McDonald 249) and does not profess great epidemiological expertise (McDonald 223, 258, 223, 258, T184). He says that the figure of 25 fibre ml years was "thrown up by one of the discussants" (T 188) in a "broad ranging discussion" (T189) and a "broad multidisciplinary assessment based on different methodologies" (T190) following "multivariable analysis of prevailing scientific literature" (McDonald 253). The figure was "arrived at by a multivariable crutch taking into account different pieces of information" (McDonald 253) as "a result of a variety of opinions from a variety of studies using a variety of methodologies" (McDonald 255).

2. These observations do not satisfy the requirement that an expert's "assumed" or "accepted" facts be identified. (Makita (Australia) Pty Ltd v Sprowles [2001] 52 NSWLR 705). As Heydon JA observed at 744, "an attempt to make the basis of the opinion explicit may reveal that it is not based on specialised expert knowledge, but, to use Gleeson CJ's characterisation of the evidence in HG v The Queen (at 428), on "a combination of speculation, inference, personal and second-hand views as to the credibility of the complainant, and a process of reasoning which went well beyond the field of expertise".

3. The Helsinki report should be seen for what it is: "A position statement from an expert group" (Prof Henderson T 188.47), not a document which reveals and draws together pursuant to any scientific protocol, identified sources upon which it relies. In consequence, as a persuasive authority upon the discrete question of when, upon the most reliable epidemiological evidence, the relative risk doubles, the figure advanced by the Helsinki group becomes no more than the bare "Because I say so" of a group of like-minded scientists. It cannot be tested or appraised independently as logically flowing from identified sources.

4. One reason suggested by Professor Henderson as possibly leading to the adoption of the figure of 25 fibre ml years as a threshold for the attribution of asbestos related lung cancer was that a British researcher, Kevin Brown, suggested many years ago that asbestosis was required for the attribution of lung cancer to asbestos, (McDonald 253). There is thought to be a threshold below which asbestos does not cause asbestosis (PX13 450, McDonald 253), and this threshold has for some years been seen as 25 fibre ml years, at which cumulative exposure cases of asbestosis begin to appear clinically (McDonald 253, 255.5). However, the Helsinki document conceded that "it is not possible to prove in precise deterministic terms that asbestos is the causative factor for an individual patient even when asbestosis is present" and Professor Henderson thought it merely coincidental that the Helsinki group fixed upon that threshold figure for asbestosis (T 168) as the figure at which the relative risk of lung cancer doubled.’

   213. The plaintiff draws attention to Moolgavkar’s concession that asbestos can cause lung cancer but also that the report frames the wrong question by not questioning whether a ‘material contribution’ was made, rather asking whether it was a ‘substantial contributing factor’. They suggest it is not a question of comparing possible contributors.

   214. At p 16 of that report, Prof Moolgavkar discusses over three paragraphs the risks attributable to asbestos exposure. He states as follows:

‘…What is clear, moreover, is that the fraction of risk attributable to asbestos depends not only on asbestos exposure but also on exposure to other carcinogens, such as cigarette smoking, a fact that is ignored in the Helsinki document.

… From what we know about the lung cancer risks associated with these two carcinogens, I can state the following with reasonable degree of scientific and medical certainty

… In other words, asbestos exposure made no contribution to the development of Mr Gatt’s lung cancer.’

215. The conclusion that the asbestos made no contribution to Mr Gatt’s cancer is not explained to the extent that I would accept that proposition. The vast majority of the opinions expressed in the report relate to ‘risk’. To then opine as to the ‘cause’ of the disease, is not explained and not consistent with the balance of the report. Prof Moolgavkar concedes that 96% of the cancer is attributable to cigarette smoking. In my view, it is therefore reasonable to accept that the remaining 4% on Prof Moolgavkar’s assessment, was caused by his asbestos exposure, given the defendant concedes that Mr Gatt was in fact exposed to asbestos dust and fibre at Camellia.

216. A/Prof Chirieac is a pathologist. In his report dated 16 June 2020 (Exhibit 12) he submits that in the absence of evidence of asbestosis, and in the presence of a long history of smoking, it is ‘highly likely’ that Mr Gatt’s lung cancer was related to a substantial tobacco use, and not caused by asbestos exposure.

217. The difficulty in accepting this opinion is that A/Prof Chirieac has proceeded on an incorrect history regarding exposure to ‘asbestos cement sheeting’ which is not Mr Gatt’s evidence as to what he was exposed to at Camellia.

Dr Andrew Gal

218. Dr Gal has been a specialist pathologist since 1989 and has provided over 1,500 reports on pathology related to illness claimed to be due to exposure to inhaled asbestos. In his report of 2 October 2008 (Exhibit 13), Dr Gal says that over 90% of lung cancers result from cigarette smoking, although exposure to inhaled asbestos dust can also contribute to the causation of lung cancer. In the ‘absence of radiologically detected pulmonary fibrosis tends to exclude the clinical diagnosis of asbestosis’, smoking was the ‘likely cause’ of Mr Gatt’s lung cancer.

Assoc Prof McKenzie

219. A/Prof McKenzie is a respiratory and sleep physician and his experience includes extensive training and experience in occupational lung disease and he has provided pulmonary function and exercise testing to the DDB for many years.

220. In his report dated 18 December 2018 (Exhibit 14) A/Prof McKenzie concludes that Mr Gatt’s asbestos risk is about 1% of the smoking risk, that the smoking increased the risk by 2000% compared to only 20% by asbestos exposure.

221. A/Prof McKenzie notes squamous cell and small cell carcinomas of the lung are the ‘histological forms of lung cancer which have the strongest association with cigarette smoking’. It is not in dispute that Mr Gatt had squamous cell carcinoma of the lung.

222. The plaintiff contests A/Prof McKenzie’s evidence on the basis that he calculates Mr Gatt’s cumulative exposure over a 2 year period, instead of the agreed 2.72 years – therefore his conclusion of a range between 10 f/mL.yr to 20 f/mL.yr is inaccurate. They submit that if the correct time period of the plaintiff’s exposure was inserted, the figure would increase approaching at least the 25 pmLyr level.

Professor Fox

223. Professor Fox is an oncologist and concludes in his report of 23 October 2019 (Exhibit 15), ‘given the passage of time following last asbestos exposure and Mr Gatt’s lung cancer, the past asbestos history had a de minimus effect on causation of lung cancer compared with his smoking history’. He also notes that squamous cell carcinoma has the ‘strongest association with smoking, compared to other carcinomas’.

Dr Carr

224. In his report of 3 November 2020 (DCB, Tab 5), Dr Carr concludes Mr Gatt had asbestos-related pleural plaques with calcification; there are some non-specific bibasal lung parenchymal changes of fibrosis which appear specifically related to the pleural plaques rather than representing the diffuse parenchymal fibrosis of asbestosis; and therefore, there are lung parenchymal changes associated with the pleural plaques but these are not the diffuse changes of typical asbestosis.

Dust Diseases Authority

225. Mr Gatt made an application to the DDB, as it then was, and on 15 September 2016 the DDB found that Mr Gatt had “Lung Cancer in Association with Asbestos Exposure” with a level of disablement due to this disease of 100% (Exhibit XX).

226. A further certificate issued by the DDB on 9 May 2019 (part of Exhibit XX) confirms that diagnosis and states that Mr Gatt’s death is reasonably attributable to his exposure to and the inhalation of dust. The Chairperson of the Board on that certificate was Dr Ian Gardiner.

227. The plaintiff relies on Dr Gardiner’s certificate for the purpose of the DDA to the effect that the lung cancer was associated with the asbestos exposure (Exhibit XX).

228. Although Dr Gardiner’s assessment is referrable to the Workers Compensation (Dust Diseases) Act, there is no difference in terms of causation.

229. The Panel certified that the claimant is suffering from a dust disease, defined as ‘any disease specified in Sch 1 and includes any pathological condition of the lungs, pleura or peritoneum that is caused by dust that may also cause a disease so specified’. The plaintiff argues asbestos is a dust and the certification by Dr Gardiner is that the lung cancer was caused by asbestos exposure.

Dr Goldin And Dr Baldey

230. Dr Goldin and Dr Baldey were both treating radiologists of Mr Gatt and did not refer to asbestosis or to interstitial lung disease in their reports of the CT scans of 2015.

Dr Jones

231. The plaintiff argues Dr Jones’ evidence is based on limited material that does not include the key radiological evidence, being the CT scans of 2003 and 2015. In Exhibit 9, Dr Jones submits that the CT scan of 2003 shows ‘early sub-pleural interstitial thickening and honeycomb cysts suggesting early fibrosis/asbestosis’ (Plaintiff submission [135]).

232. The defendant submits any critiques of Dr Jones’ evidence is unable to be advanced given he was not cross-examined by the plaintiff.

233. However, in his report of 27 August 2020 (DCB, Tab 3) relating to the October 2015 CT, Dr Jones says there are no changes of early asbestosis in the lung bases; while there are some ‘compressive atelectasis in the lung lying beneath pleural plaques’ which is producing ‘some increased lung density and septal thickening’, does not show any ‘sub-pleural dots corresponding with early lesions of asbestosis’; no findings similar to CT diagnosis of Asbestosis by Akira; no evidence of septal thickening bilaterally peripherally or small honeycomb cysts in the lower lobes; and a diagnose of asbestosis cannot be made based on the October 2015 CT since ‘fundamental lesion of asbestosis namely sub-pleural dots is not present’.

234. In addition, Dr Jones submits that a diagnosis of asbestosis does not ‘come and go’, a lack of any presence of asbestosis in 2015 means that it was also not present earlier.

235. In his further report of 11 October 2020 (DCB, Tab 4), which responded to Dr Johnson’s report, Dr Jones maintains there is no interstitial lung disease or asbestosis changes. That the sub-pleural changes that Dr Johnson points out, lie beneath the asbestos pleural plaques and asbestos-related diffuse pleural thickening, based on the positions of the plaques, and that the lung beneath normal pleura appears normal, Dr Jones considers it would be ‘abnormal’ if Mr Gatt had asbestosis.

236. Dr Jones concludes Mr Gatt did not have asbestosis and that the sub-pleural changes are the direct effects of the asbestos pleural plaques and asbestos-related diffuse pleural thickening on the sub-pleural lung causing compressive atelectasis, and do not represent asbestosis.

Dr Johnson

237. Dr Johnson’s report of 31 July 2020 submits that the October 2015 CT scans shows ‘septal thickening bilaterally peripherally and small honeycomb cysts in the lower lobes’ in which some changes ‘are related to overlying pleural plaques but some are not’, concluding that the changes are consistent with pulmonary fibrosis/asbestosis.

238. He concludes Mr Gatt had interstitial lung disease, as there are no other obvious causes other than asbestos exposure, and diagnoses Mr Gatt with asbestosis. He maintains this position in his second report dated 25 September 2020, even after Dr Jones’ report, mentioned above.

239. The defendant submits that the Tribunal should favour the evidence of their experts over the evidence of Dr Johnson because of the ‘sheer weight’ which makes it compelling. They separate Dr Goldin, Dr Baldey, Dr Jones and Dr Carr as medical practitioners who are specialist radiologists compared to Dr Johnson (and A/Prof McKenzie) who are not radiologists but physicians.

240. Dr Johnson disagreed that he would defer to specialist radiologist in the interpretation of images because he considered that there were not many radiologists who have expertise with asbestos radiology, but agreed Dr Jones was highly experienced and extremely confident in the interpretation of chest radiology.

241. It appears the defendant’s argument is that because there are more reports in their favour, the ‘sheer weight’ of that evidence could not, on the balance of probabilities establish Dr Johnson’s evidence as enough to make a finding of asbestosis.

242. That being the case, the defendant’s also submit that A/Prof McKenzie and Dr Johnson have similar qualifications, and there is ‘no basis’ for the Tribunal to prefer the evidence of Dr Johnson over A/Prof McKenzie.

DISCUSSION

243. As previously indicated, the issues that I must determine are:

On the balance of probabilities, did Mr Gatt suffer from asbestosis;

What was the cumulative airborne asbestos concentration to which Mr Gatt was, on the balance of probabilities, exposed to during the period of his work at James Hardie; and

Examination of the epidemiology of lung cancer and the causal nexus between asbestos exposure, cigarette smoke and the occurrence of lung cancer.

244. The question of diagnosis of asbestosis predominantly revolves around the competition between the evidence of Dr Johnson and Dr Jones. Dr Johnson is an experienced respiratory physician and Dr Jones is an experienced radiologist. Their respective qualifications are not in dispute. What is in dispute is whether the opinions of a radiologist should be preferred over that of a respiratory physician.

245. The conflict between their views boil down to the interpretation of images, in particular the CT Scan of September 2003 and the HRCT scan of 15 October 2015.

246. It is not in dispute that Mr Gatt had lung cancer, but the question is, did he also have asbestosis. Dr Johnson says Mr Gatt did have asbestosis and Dr Jones says Mr Gatt did not.

247. Drs Johnson and Jones were both well aware of the conflict between their views and they had engaged in extensive discourse about this issue in their various reports (Dr Johnson’s reports:  Exhibit H, J, K and L; and Dr Jones: Exhibit 9).

244. Issue was taken by the defendant that as Dr Jones was not cross-examined, his opinions cannot be disputed by the plaintiff. The legal basis for that argument has been addressed previously.

245. However, the plaintiff submits that while the defendant did cross-examine Dr Johnson, he was not questioned about the specific images contained in the CT and the HRCT.

246. I note that there were reports being provided by both experts, which were then referred to the other for commentary. There was academic discourse between the doctors with reference to articles referred to, and both provided opinions as to how the scans should be interpreted.

247. Dr Johnson describes the radiology as a tool, and his interpretation of the scans is considered in the context of his clinical findings. Dr Johnson is the only doctor who examined Mr Gatt. Having done so, he opines that Mr Gatt was exposed daily to heavy exposure mixing raw asbestos into an asbestos cement mixture. He considered it likely that Mr Gatt’s asbestos exposure was above 25 fibre/mL years and that such exposure had contributed significantly to his lung cancer.

248. Dr Jones in his report of 11 October 2020, having carefully reviewed the scans of 15 October 2015 concedes that there is fibrosis. He refers to pleural plaques and diffuse pleural thickening, compressive atelectasis and ground glass opacity, which are to my mind, indicative of asbestosis. Dr Jones then says that because the fibrosis is underneath the plaques, it cannot be asbestosis.

249. It is referenced that 75% of Mr Gatt’s pleura was covered with plaques. One wonders then, with so much pleural thickening and plaques covering the pleura, and given the other indicators, whether this was in fact masking the asbestosis.

250. Prof McKenzie also commented on the 15 October 2015 scans, but did not in fact see the actual scans, only the reports thereon.

251. I prefer the opinions of Dr Johnson, who has examined the scans, and placed his interpretation of them in the context of his clinical examinations. It was never put to Dr Johnson that the films did not demonstrate interstitial fibrosis. I accept that Mr Gatt had asbestosis.

252. Next, I must examine the causal potency, and the estimates of the fibre loads to which Mr Gatt was exposed. The defendant does not dispute that Mr Gatt was exposed to asbestos dust and fibre in the course of his employment with James Hardie at Camellia. The defendant admits breach of duty of care, and the diagnosis of ARPD.

253. It is accepted by the parties that asbestos can cause lung cancer. This is further borne out by the s 25B Notice upon which the plaintiff relies. I must then decide if it is more probable than not that the negligence of the defendant was a cause of Mr Gatt’s cancer. The question is not why did he develop lung cancer, but what caused it. To observe only that the exposure to asbestos may have been a cause does not answer that question affirmatively.

254. The difficulties that arose with the JER and the 9 November letter are significant. However, looking at the range that was agreed to by the experts in the JER, it was their opinion that Mr Gatt’s cumulative airborne asbestos exposure lies in the range of 12.2 fibres/mL.years and 24.4 fibres/mL.years. If Mr Kottek’s figures form the 9 November letter are accepted, the figure becomes much higher to 41 fibres/mL.years.

255. Professor McKenzie in his report of 18 December 2018 accepted that Mr Gatt would have worked in a dusty environment, and the cumulative exposure to asbestos over two years would have been between 10 and 20 fibres/mL.years. It is agreed by the parties that given the lengthy shifts and overtime that Mr Gatt worked, the appropriate period during which he worked for the defendant is 2.72 years. If Prof McKenzie’s calculations were amended to allow for this additional period, I find it more likely that his figure would be closer to 25 fibre/mL.years.

256. The Helsinki Criteria of 25 fibre/mL.years has also been referred to by the experts. As this was a figure at which there was for sometime a consensus as to the bottom limit of cumulative exposure, it strengthens my view that the JER upper figure of 24.4, Prof McKenzie’s figures of 10–20 fibres/mL.years and Dr Johnson’s assessment of more than 25 fibres/mL.years, that Mr Gatt was more probably than not exposed to an airborne concentration of at least 24.4 fibres/mL.years.

257. Thus, I find that it is more probable than not that Mr Gatt’s exposure to asbestos dust and fibre was a cause of Mr Gatt’s lung cancer. I find that one substance (asbestos dust) which has been accepted by the parties as capable of causing lung cancer, did cause the injury and that Mr Gatt’s cancer was intimately connected with, and contributed to by his exposure to asbestos. Having found that there is a connection between Mr Gatt inhaling asbestos and his development of lung cancer, I find that the inhalation of the asbestos dust and fibre made a material contribution to his development of lung cancer on the scientific evidence as I find that the fibre burden was sufficient to cause asbestosis.

258. I accept Prof Moolgavkar’s view that lung cancer can be attributed to his cigarette smoking. Prof Moolgavkar apportions >96% to it. However, implicit in that statement, must be that there is some other carcinogen present to account for the other 4%, and I find on the balance of probabilities, that that was Mr Gatt’s inhalation of asbestos dust which materially contributed to his lung cancer.

259. I find that the evidence establishes that the asbestos exposure did contribute to the cancer in the sense that it was a necessary precondition to it, and that contribution was material.

260. I find that the plaintiff has established on the balance of probabilities that Mr Gatt was exposed to sufficient asbestos dust and fibre in his employment with the defendant and as such dust and fibre materially contributed to his lung cancer.

ORDERS

265. I make the following orders:

1. Judgment for the plaintiff against the defendant in the sum of $540,000.00.

2. Defendant to pay the plaintiff’s costs as agreed or assessed.

3. If any alternate costs order is sought, parties must notify my associate within 14 days.

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Amendments

07 September 2021 - Paragraph 243: Replace the word "casual" with the word "causal".

Paragraph 246: Replace the words "lung cancer" with the word "asbestosis".

Paragraph 256: Replace the word "casual" with the word "causal".

Decision last updated: 07 September 2021