Amaca Pty Limited (Under NSW Administered Winding Up) v Roseanne Cleary as the Legal Personal Representative of the Estate of the Late Fortunato (aka Frank) Gatt

1. [1]

   BRERETON JA: I have had the benefit of reading in draft the judgment to be delivered by Beech-Jones JA, with which I agree. In particular, the primary judge’s conclusion that Mr Gatt had asbestosis was a finding of fact for which there was some evidence, namely, to some extent, that of Dr Leigh and, more especially, that of Dr Johnson. Although there was also evidence to the contrary – in particular, though not only, that of Dr Jones – which was not the subject of cross-examination, no rule of law requires that uncross-examined evidence be accepted, so long as regard is had to the absence of cross-examination and its significance. In this case, in distinction to Ghosh v Medical Council of New South Wales,1 the primary judge adverted to the absence of cross-examination of the respondents’ expert witnesses and its potential significance, and expressly took it into account in weighing the balance of probabilities. [1] In those circumstances, it cannot be said that her Honour erred in point of law in preferring the evidence of Dr Johnson to the (uncross-examined) evidence of Dr Jones, even if this Court, had the appeal been by way of rehearing (which it is not), might have come to a different conclusion. I agree with the orders proposed by Beech-Jones JA.

2. [2]

   BEECH-JONES JA: This is an appeal from a judgment of the Dust Diseases Tribunal (the “Tribunal”) upholding a claim for damages by the legal estate of a worker, Mr Fortunato Gatto, who died of lung cancer.

3. [3]

   The Appellant, Amaca Pty Limited (under NSW Administered Winding Up) (“Amaca”), employed the late Mr Gatt at its Camellia plant for approximately two years in the early 1960s. During that time, Mr Gatt was exposed to asbestos in circumstances that involved a breach of a duty of care owed to him by Amaca. From about two years before the time he commenced work until around 2007, Mr Gatt was a regular to heavy smoker.

4. [4]

   In 2015 Mr Gatt was diagnosed with carcinoma of the lung and bilateral calcified pleural plaques. In 2018, he commenced proceedings in the Tribunal against Amaca for damages for personal injury. He passed away on 20 March 2019. His widow, the late Mary Gatt, was substituted as the legal representative of Mr Gatt’s estate. However, Mrs Gatt passed away soon after. The Respondent, Ms Roseanne Cleary, was then substituted as the legal representative of the estate.

5. [5]

   On 6 September 2021, the Tribunal upheld the Respondent’s claim against Amaca and entered judgment in her favour for $540,000.00 and costs (Rosanne Cleary as the Legal Personal Representative of the Estate of the late Fortunato (aka Frank) Gatt v Amaca Pty Ltd [2021] NSWDDT 5 (sic)).

6. [6]

   As explained below, the only substantive issue in the proceedings before the Tribunal was causation. The Respondent’s case on causation was that Mr Gatt either developed asbestosis or lung cancer (or both) from his exposure to asbestos fibres during his employment by Amaca. The primary judge found that both were established. Amaca contends that her Honour erred in law in making both findings. While I accept that her Honour erred in law in finding that Mr Gatt’s lung cancer was caused by his exposure to asbestos while employed by Amaca, I do not accept that her Honour so erred in finding that Mr Gatt developed asbestosis. As it was accepted that either basis was sufficient for the Respondent to succeed, I would dismiss the appeal.

Background

1. [7]

   Mr Gatt was born on 17 February 1943. Between 5 June 1962 and 15 July 1964, he was employed by Amaca as a labourer at its factory in Camellia. During his employment, Mr Gatt was exposed to, and inhaled, asbestos dust and fibre. The primary judge found that Mr Gatt operated a “mixer machine mixing raw asbestos with other wet materials”, he worked a minimum of 56 hours per week, that there were vast amounts of asbestos dust and fibre in the air, and he was regularly covered in asbestos dust from “head to toe”. [2] The primary judge found that other employees who had worked at the Camellia plant at around the same time were exposed to very high levels of asbestos fibre which led to some of them developing asbestosis and other asbestos related medical conditions. Her Honour also found that “[s]ubstantial amounts of amphibole asbestos was likely to have been used”. [3]

2. [8]

   Mr Gatt commenced smoking in 1960 at age 17. He smoked up to 25 cigarettes a day at an average of 15 to 20 cigarettes per day. [4] He continued smoking until 2007 when he had a heart attack. [5] The primary judge found that he smoked at least 20 cigarettes a day from “about 1960 until about 2007” which constituted a “cumulative smoking history [in] the range of 47-70 pack years” where one “pack year” constitutes the consumption of 1 packet of 20 cigarettes each day of a year. [6]

The Issues and the Primary Judge’s Findings

1. [9]

   On 4 August 2020, the Respondent filed a Third Amended Statement of Claim. It was pleaded that the injuries suffered by Mr Gatt as a result of Amaca’s negligence included lung cancer, asbestosis, and diffuse pleural thickening. In its defence, Amaca admitted that it owed and breached a duty of care to Mr Gatt. It admitted that Mr Gatt developed asbestos related pleural plaques but did not admit that he suffered the other pleaded injuries. Amaca also pleaded that Mr Gatt was contributorily negligent essentially because of his smoking.

2. [10]

   Ultimately, the parties agreed on an amount for damages of $540,000 which included a discount for contributory negligence of 10%. [7] The primary judge identified the “issues” in dispute as: [8]

3. [11]

   The parties accepted that this statement of the issues was meant to reflect the two alternative bases upon which the Respondent put her case on causation, namely, that (i) Mr Gatt had asbestosis which, if established, resulted from his exposure to asbestos at Amaca’s factory; and that (ii) Mr Gatt’s exposure to asbestos at Amaca’s factory caused him to contract lung cancer without him having necessarily developed asbestosis. If either were established then it was accepted that the Respondent could recover the agreed damages. With the second limb there were two sub-issues, namely, what level of cumulative airborne asbestos concentration was Mr Gatt exposed to during his employment by Amaca and, depending on that level of exposure, whether it was established that that exposure was a cause of his lung cancer. Amaca denied both limbs of the Respondent’s case and pointed to Mr Gatt’s heavy smoking history as the cause of his lung cancer.

4. [12]

   As noted, ultimately, her Honour made findings favourable to the Respondent in respect of both limbs of her case. [9] In relation to the level of cumulative airborne asbestos concentration, the primary judge found that Mr Gatt was exposed to at least 24.4 fibres/ml.years; that is, he was exposed to the equivalent of 1 asbestos fibre per cubic centimetre, per day, for 24.4 years. [10]

5. [13]

   On appeal, Amaca accepted that to succeed it had to demonstrate error in relation to the primary judge’s findings on both limbs of the Respondents’ case, although they did not challenge her Honour’s findings concerning Mr Gatt’s level of cumulative airborne asbestos exposure. The respective parties’ case and her Honour’s reasons are best explained in the context of Amaca’s challenge to each of those findings.

Finding of Asbestosis: Appeal Grounds 1(a) and 2

1. [14]

   Grounds 1(a) and 2 of Amaca’s Amended Notice of Appeal challenge her Honour’s finding that the late Mr Gatt developed asbestosis. Those grounds contend:

2. [15]

   The Respondent called evidence from Dr James Leigh, a consultant occupational physician, who has undertaken extensive research into asbestos related diseases over many years, and Dr Anthony Johnson, a respiratory and sleep physician. Dr Leigh’s evidence was principally directed to the epidemiology of asbestos exposure, smoking and lung cancer. However, in his report dated 31 December 2018, he noted that the “extensive bilateral calcified pleural plaques [observed on Mr Gatt’s lungs] are objective evidence of significant cumulative asbestos exposure.” A report of a CT (computed tomography) scan of Mr Gatt’s chest, undertaken on or around 15 October 2015 (the “October 2015 Scan”), when Mr Gatt was diagnosed with lung cancer, showed “[l]arge calcified pleural plaques” on his lungs. The primary judge found that that scan was significant because it was taken “prior to the progression of Mr Gatt’s lung cancer and treatment related changes.” [11]

3. [16]

   In one of his reports, Dr Johnson referred to the October 2015 Scan and to high resolution CT scans of Mr Gatt’s chest in September 2003 (the “September 2003 Scan”) which showed “bilateral calcified pleural plaques” and “increased interstitial markings sub pleurally in both lower lobes.” Dr Johnson concluded as follows:

4. [17]

   On the issue of whether Mr Gatt had contracted asbestosis, Amaca adduced evidence from four specialist radiologists, Dr Michael Jones, Dr Graeme Goldin, Dr Andrew Baldey and Dr Peter Carr, and a respiratory physician, Associate Professor McKenzie.

5. [18]

   The primary judge summarised Dr Jones’ evidence in some detail. [12] The effect of all three of his reports was that the October 2015 Scan did “not confirm asbestosis or any other interstitial lung disease” [13] and that a finding of asbestosis could not be made based on that scan. [14] Dr Jones’ final report dated 11 October 2020 was responsive to Dr Johnson’s final report. In that report, Dr Jones concluded that “the late Mr Gatt did not have asbestosis”. To similar effect, Dr Goldin reviewed various scans and concluded that “there are lung parenchymal changes associated with the pleural plaques but these are not the diffuse changes of typical asbestosis.”

6. [19]

   The primary judge correctly noted that Dr Goldin was one of Mr Gatt’s treating doctors and his report on the October 2015 Scan did not refer to asbestosis or to interstitial lung disease being present. [15] The same applies to the report of Dr Baldey who reviewed subsequent CT imaging by reference to the October 2015 Scan as a comparison.

7. [20]

   As explained below, the bulk of Associate Professor McKenzie’s evidence was mainly directed to the epidemiological evidence concerning the second limb of the Respondent’s case. Nevertheless, he opined that a diagnosis of asbestosis requires a history of heavy exposure to airborne asbestos fibre, particular forms of documentation of heavy asbestos exposure and documentation of pulmonary fibrosis. He estimated Mr Gatt’s exposure at 1-20 fibres/ml.years which was well below that required to develop asbestosis. His report contains a review of the radiological reports concerning Mr Gatt. In relation to the October 2015 Scan, Associate Professor McKenzie concluded that “[t]here was no significant pulmonary emphysema and there was no interstitial lung disease or asbestosis.” Later he observed that the “radiology … shows pleural plaques but not asbestosis.”

8. [21]

   Of significance to the first ground of appeal is that both Dr Johnson and Dr Leigh were cross-examined but none of the specialists whose reports were tendered by Amaca were cross‑examined on behalf of the Respondent. One part of the hearing concerning the possibility of Amaca calling Dr Jones to give additional oral evidence is addressed below.

9. [22]

   Under the heading “diagnosis of asbestosis”, the primary judge summarised the evidence of the expert witnesses just noted. [16] Her Honour then noted a submission by Amaca that “as the [Respondent] did not cross-examine Dr Jones, Dr Carr or A/Prof McKenzie … the plaintiff thus cannot advance a case which contradicts their evidence” citing the “rule” in Browne v Dunn (1893) 6 R 67 (“Browne v Dunn”) as discussed in Ghosh v Medical Council of New South Wales (2020) 102 NSWLR 303; [2020] NSWCA 122 (“Ghosh”). [17]

10. [23]

    Her Honour accepted the Respondent’s submission that in this case her Honour was “not required to form a view as to the specialists’ integrity” and was not “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.” [18] Her Honour referred to the second “aspect” of the “rule” identified by Brereton JA in Ghosh which is concerned with the weight to be afforded to such evidence that is not the subject of cross‑examination. Her Honour observed: [19]

11. [24]

    Her Honour then referred (again) to the evidence of Dr Jones and Dr Johnson before noting that an issue had arisen with the Respondent’s proposal to call evidence from Dr Snodgrass, a radiologist who had either supervised or at least seen the September 2003 Scan. Her Honour noted that Dr Snodgrass had been served with a subpoena to give evidence although: [20]

12. [25]

    Her Honour then surveyed the evidence concerning the second limb of the Respondent’s case on causation, [21] although in doing so her Honour referred to some of the evidence and submissions concerning the first limb, including the evidence of Dr Goldin, Dr Baldey, Dr Jones and Dr Johnson. [22] Her Honour then returned to the issue of whether Mr Gatt had asbestosis. Her Honour reasoned that its resolution “predominantly revolves around the competition between the evidence of Dr Johnson and Dr Jones” and that the “conflict between their views boil down to the interpretation of images” in the September 2003 Scan and the October 2015 Scan. [23] Ultimately, the primary judge concluded: [24]

13. [26]

    Ground 1(a) is set out above. Amaca’s submissions in support of this ground focussed on the so-called “rule” in Browne v Dunn and Brereton JA’s discussion of that rule in Ghosh. The principal complaint made in writing was that the primary judge did not disclose what impact the failure to cross‑examine had on the weight that was attached to the evidence of the experts relied on by the Respondent. Hence, it was contended that the finding of the primary judge as set out at [25] above does not specify why, notwithstanding the lack of cross-examination of Dr Jones, his evidence was flawed and should not be accepted. It was submitted that her Honour appears to have treated the lack of cross‑examination of Dr Jones and the other experts relied on by Amaca as telling against an acceptance of those witnesses when Ghosh suggests that the position should be to the contrary.

14. [27]

    Amaca contended that her Honour did not explain how Dr Johnson’s examination of Mr Gatt in 2018 “made him better placed to” interpret the October 2015 Scan than the experts relied on by Amaca. While it was accepted that it was not expressly put to Dr Johnson that the films did not demonstrate “interstitial fibrosis”, Amaca contended that the issue was raised with him and the reliance on the absence of something being put to Dr Johnson only highlighted the flawed approach that was taken to Amaca’s witnesses. It was also submitted that error was somehow demonstrated by the failure of the primary judge to refer to the evidence of Dr Goldin, Dr Baldey and Dr Carr in the discussion section of her Honour’s reasons.

15. [28]

    The Respondent’s written submissions contended that, given the manner in which Dr Johnson was cross‑examined on behalf of Amaca, it was not necessary for her to cross‑examine Dr Jones or Dr Carr. The submissions also contended that the reports of Dr Goldin and Dr Baldey did not state whether or not Mr Gatt had asbestosis or interstitial fibrosis, so that presumably no obligation arose on the Respondent to cross‑examine them on that issue. It was submitted that, to the extent that the “rule” in Browne v Dunn might require the acceptance of evidence, it was only if that evidence was “uncontradicted” whereas the evidence the subject of this ground of appeal was contradicted. During the hearing of the appeal, Senior Counsel for the Respondent, Mr Walker, contended that all of Amaca’s complaints in relation to this limb of the Respondent’s case only raised questions of fact and not points of law for the purposes of s 32(1) of the Dust Diseases Tribunal Act 1989 (NSW) (the “DDT Act”). For the reasons stated next, that submission should be accepted.

16. [29]

    As noted, these appeals are governed by s 32(1) of the DDT Act which relevantly provides that “[a] party who is dissatisfied with a decision of the Tribunal in point of law or on a question as to the admission or rejection of evidence may appeal to the Supreme Court”. This right of appeal is not confined to a case where the Tribunal has made a decision on a point of law. Instead, an appeal lies where a party is dissatisfied in point of law with a decision of the Tribunal; i.e. the scope of the appeal is synonymous with the existence of an error of law (see Seltsam Pty Ltd v Ghaleb [2005] NSWCA 208 at [149]; Amaca Pty Ltd (under NSW administered winding up) v Raines; Seltsam Pty Ltd v Raines [2018] NSWCA 216 at [12] to [17]).

17. [30]

    Long‑standing authority in this Court, namely Azzopardi v Tasman UEB Industries Ltd (1985) 4 NSWLR 139 (“Azzopardi”), demonstrates the significant limitations on the review by this Court of findings of primary fact by an inferior court where the appeal is restricted to demonstrating an error of law. Hence, in Azzopardi (at 155 to 156) Glass JA observed that:

18. [31]

    Azzopardi was an appeal to this Court from the Compensation Court, with such appeals restricted to a “point of law”. The above passage has been held to be applicable to appeals under s 32(1) of the DDT Act (see for example Wallaby Grip Limited & Anor v Peirce & Ors; James Hardie & Coy Pty Limited v Peirce [2000] NSWCA 299; Dionisatos (for the Estate of the late George Dionysatos) v Acrow Formwork & Scaffolding Pty Ltd (2015) 91 NSWLR 34; [2015] NSWCA 281).

19. [32]

    In this case, the relevant finding the subject of challenge is the finding that the late Mr Gatt had asbestosis. That finding was not an “ultimate finding of fact” in the sense used in the above passage from Azzopardi but only a primary finding of fact analogous to whether a worker “suffered injury on a particular date.” There was undoubtedly some evidence capable of supporting that finding, namely Dr Johnson’s evidence. It follows that any complaints about illogicality, perverseness or ignoring contrary evidence in relation to that finding do not raise any complaint about an error of law.

20. [33]

    However, as noted, relying on Ghosh, Amaca contends that the primary judge’s treatment of the evidence from the experts it relied on, and who were not cross‑examined, reveals an error of law. In the relevant part of Ghosh, Brereton JA identified two aspects of the “rule” in Browne v Dunn (at [69]). The first is described as a “rule of procedural fairness, [namely] that unless notice has already clearly been given of a party’s intention to rely upon such matters, it is necessary first to put to an opponent’s witnesses in cross-examination the nature of the case upon which it is proposed to rely in contradiction of their evidence” (id). Save for the matter addressed below, it was not suggested that there was any denial of procedural fairness in this case. Both the parties and the relevant experts were apprised of the competing contentions. The second aspect of the “rule” referred to by Brereton JA in Ghosh has already been described, namely, “that evidence which has not been the subject of cross-examination and upon which there has been no relevant cross-examination should not usually be rejected by the tribunal of fact” (id). It is this aspect of the “rule” which Amaca seeks to engage.

21. [34]

    After describing these two aspects of the “rule”, Brereton JA in Ghosh cited a passage from the judgment of Hunt J, as his Honour then was, in Allied Pastoral Holdings Pty Ltd v Commissioner of Taxation [1983] 1 NSWLR 1 at 18. Brereton JA then stated:

22. [35]

    In Ghosh, Simpson AJA agreed with this passage (at [137]).

23. [36]

    Nothing in Ghosh purports to lay down a rule of law that in all cases, or even “ordinarily”, evidence which is not the subject of cross‑examination must be accepted. Such a proposition was expressly rejected by Brereton JA in Ghosh at [71]. Further, the passage from the judgment of Gibbs J, as his Honour then was, in Precision Plastics Pty Ltd v Demir (1975) 132 CLR 362; [1975] HCA 27 (“Precision Plastics”) set out in Ghosh at [70] does not support that proposition either. In Precision Plastics Gibbs J upheld a finding of this Court that a damages award by a jury was unreasonably low. In the quoted passage, his Honour was comparing the undisputed evidence of the injured plaintiff as to her future intention to work with the amount that was awarded. His Honour did not purport to state that the jury would have erred in law had they rejected the plaintiff’s evidence on that topic. In any event, the above passage from Azzopardi illustrates the differences between the basis for reviewing a jury verdict and an appeal which is restricted to an error, question or point of law.

24. [37]

    Ghosh was an appeal from the NSW Civil and Administrative Tribunal and, as such, was restricted to a question of law (at [12]). The error of law identified in Ghosh was the failure of the Tribunal in that case to give “any significance to the circumstance that the witnesses favourable to [the appellant] were not cross‑examined” and instead “regarded … the circumstance that they were not called as adverse to their acceptance” (at [72]). The primary judge made neither error in this case. In the passage set out at [23] above, her Honour expressly acknowledged the potential significance of the witnesses having not been cross-examined. Her Honour did not regard the failure to call them as adverse to Amaca’s case. Amaca also complains about her Honour’s failure to further state how the fact that the witnesses were not cross‑examined was considered. To an extent, her Honour did that by noting that the evidentiary dispute did not concern their credit or integrity and accepting that no advantage was derived, nor disadvantage suffered, in comparing evidence given in the witness box with evidence given in written form. Nothing in Ghosh imposed any further obligation on her Honour. The primary judge’s reasoning beyond that point was purely a matter of fact.

25. [38]

    During oral argument, Senior Counsel for Amaca, Mr Hooke, embraced the proposition that, in the absence of cross‑examination, the primary judge was obliged to accept the expert medical opinion unless there was some “glaring or obvious” defect. However, there is no support in the authorities for the proposition that any such obligation was imposed on the primary judge as a matter of law. In the end result, all the complaints made by Amaca only amount to complaints about the basis for the finding of fact that Mr Gatt had asbestosis or the content of the reasons for that finding. In relation to the former, those complaints are foreclosed by Azzopardi. In relation to the latter, this being an appeal restricted to an error or point of law, it is sufficient that the reasons “[reveal] the ground for, although not the detailed reasoning in support of, [the] finding of fact” (Soulemezis v Dudley (Holdings) Pty Ltd (1987) 10 NSWLR 247 at 282 per McHugh JA; “Soulemezis”). Her Honour complied with that obligation.

26. [39]

    I would reject ground 1(a).

27. [40]

    Amaca’s written submissions in support of ground 1(a) noted that, during the hearing before the primary judge, it sought to call Dr Jones “with the intention of assisting the Court by asking Dr Jones to explain the images reproduced in his reports.” The submissions contended that, following objection by the Respondent, “the primary judge advised that she did not need such assistance and declined to allow Dr Jones to be called”. Amaca contends that this was an “indication” by the primary judge that her Honour “fully understood and accepted the evidence of Dr Jones”. This is said to be a “circumstance relevant to whether the primary judge erred in law, and denied the appellant procedural fairness, in accepting the evidence of Dr Johnson over that of Dr Jones and the rest of the body of evidence to the same effect.”

28. [41]

    The complaint of a denial of procedural fairness was not raised as a ground of appeal. In any event, it has no substance. During the hearing before the primary judge, Senior Counsel for Amaca sought to lead oral evidence from Dr Jones about the images to show “why Dr Johnson is wrong”. He added that if “there is simply no challenge to Dr Jones, his evidence is taken to be accepted, then I do not need to call him”. Senior Counsel for the Respondent opposed the application on the basis that he was “content with what Dr Jones says in his report”. He said he had not “secured radiological evidence to contradict Dr Jones” and had determined not to cross‑examine him. He added that if “Dr Jones is now going to lead some additional evidence, there should be a report and I will have to determine whether or not in light of that whether I have to find additional radiological evidence”. Her Honour stated that she agreed.

29. [42]

    After further submissions the following exchange occurred:

30. [43]

    I do not consider that these exchanges constitute any “indication” by her Honour that she “fully understood and accepted” Dr Jones’ evidence. Her Honour’s statement that she did not need assistance was directed to whether her Honour needed assistance in understanding Dr Jones’ report. It did not constitute any statement that his evidence would be accepted. Nothing that occurred in this exchange means that the findings her Honour made in relation to Dr Jones involved any denial of procedural fairness.

31. [44]

    Ground 2 of the Amended Notice of Appeal contends that her Honour erred in law in failing to draw an inference that Dr Snodgrass would not have assisted the Respondent’s case on the issue of whether Mr Gatt suffered asbestosis. Dr Snodgrass had viewed the September 2003 Scan. During the hearing of the appeal, the suggested inference that it is submitted her Honour should have drawn was refined to an inference that Dr Snodgrass “would not have given evidence that supported the plaintiff’s case in terms of the presence on the imaging of signs of early asbestosis”.

32. [45]

    The reasons of the primary judge in relation to this issue are set out above. Amaca’s submissions in this Court contend that there was no evidence to support her Honour’s assessment that Dr Snodgrass had “refused to attend” and that her Honour’s refusal to draw the inference sought was erroneous in law.

33. [46]

    This ground is misconceived. Jones v Dunkel (1959) 101 CLR 298; [1989] HCA 8 (“Jones v Dunkel”) is authority for the proposition that two possible consequences may follow from a party’s failure to call a witness whom they might be expected to call. The first is that the Court may infer that the evidence of the witness who was not called would not have assisted that party’s case (a “Jones v Dunkel inference”). The other consequence is that the Court may have greater confidence in drawing an inference unfavourable to that party (Jones v Dunkel at 308 per Kitto J; Kuhl v Zurich Financial Services Australia Ltd (2011) 243 CLR 361; [2011] HCA 11 at [63] to [64]; ASIC v Hellicar (2012) 247 CLR 345; [2012] HCA 17 at [232] per Heydon J; “Hellicar”). This latter consequence can be put aside as no inference unfavourable to the Respondent was contended for by Amaca in this case.

34. [47]

    A Jones v Dunkel inference has relatively weak evidentiary value. It does not enable the trier of fact to infer that the absent evidence would have been positively adverse to the party (Hellicar at [168] per French CJ, Gummow, Hayne, Crennan, Kiefel and Bell JJ and at [232] per Heydon J), and it does not enable a court to discount or diminish the value of the evidence that a party adduced (Hellicar at [164] to [170] and [233]). In this case, a Jones v Dunkel inference was irrelevant to both the Respondent’s case and her Honour’s reasoning, because both relied on Dr Johnson’s evidence and that evidence could not be diminished by any failure to call Dr Snodgrass (Hellicar supra). Otherwise, the inference is only available where the party could be expected to call a witness who was in their “camp” (Hellicar at [265]). It is doubtful that a specialist such as a doctor who viewed a scan in September 2003 could be properly described as being in the Respondent’s camp.

35. [48]

    In any event, the mode of reasoning suggested by Jones v Dunkel is directed to fact finding. There is no obligation on a jury or a judge to draw any such inference (Manly Council v Byrne and Anor [2004] NSWCA 123 at [52]). It follows that a failure to draw such an inference is not erroneous in law and does not raise any question or point of law.

36. [49]

    I would reject this ground.

Epidemiology of Lung Cancer: Appeal Grounds 1(b) and 3 to 5

1. [50]

   As noted, one part of the Respondent’s case sought to establish a causal link between Mr Gatt’s exposure to asbestos and his development of lung cancer (without finding that he contracted asbestosis). The primary judge ultimately upheld that part of the Respondent’s case. [25] Grounds 1(b) and 3 to 5 of the appeal attack that aspect of her Honour’s reasons. They contend:

2. [51]

   To address these grounds, it is first necessary to describe the epidemiological evidence that was adduced by the parties and her Honour’s reasoning.

3. [52]

   The Respondent also relied on evidence from Dr Leigh and Dr Johnson on this limb of her causation case. The essence of Dr Leigh’s evidence was that it is not possible to separate the causal effects of asbestos exposure and cigarette smoking “when both have acted, as they must do to some extent, from a purely physio-chemical point of view, and it is thus more probable than not, that in this situation, the lung cancer was the singular result of the two factors acting together”. [26]

4. [53]

   There was a significant debate amongst the parties, which was reflected in the primary judge’s reasons, as to whether Dr Leigh’s evidence in this case was the same as that described in Amaca Pty Ltd v Ellis (2010) 240 CLR 111; [2010] HCA 5 (“Ellis”) (at [33]) and which was held not to have supported a finding of causation in that case (at [65]). It is not necessary to consider this further as the primary judge did not base her finding on this limb of the Respondent’s causation case on Dr Leigh’s evidence. However, it will be necessary to return to Ellis in addressing how the primary judge addressed evidence called by Amaca from Professor Moolgavkar which was responsive to Dr Leigh’s evidence.

5. [54]

   As noted, Dr Johnson diagnosed Mr Gatt with asbestosis. In addition, he concluded:

6. [55]

   Five of the experts relied on by Amaca addressed whether there was a causal connection between Mr Gatt’s exposure to asbestos and his contracting lung cancer in the absence of any diagnosis of asbestosis, being Associate Professor Chirieac, Dr Gal, Professor Fox, Professor Moolgavkar and Associate Professor McKenzie. None of these experts were cross‑examined.

7. [56]

   Lucian Chirieac is an Associate Professor of Pathology at Harvard Medical School. He opined that “to attribute a substantial contributing role for asbestos in the causation of lung cancer, asbestosis must be present clinically or histologically, or there should be a tissue asbestos burden within the range of values observed in patients with asbestosis”. He concluded that “[i]n the absence of clinical, physiologic, pathologic, or radiographic evidence of asbestosis, and in the presence of a long history of smoking, it is highly likely that Mr. Gatt’s lung squamous cell carcinoma was related to a substantial tobacco use, and not caused by asbestos exposure.”

8. [57]

   Dr Gal is a specialist pathologist. In his report he referred to a debate as to whether or not “inhaled asbestos can only be considered to have caused an individual’s lung cancer if asbestosis is also present in that individual”. Dr Gal noted a recent paper that expressed the view that it was unlikely that “epidemiology alone can put either the strict scientific or practical medicolegal questions beyond doubt”. He concluded “that the carcinoma can be shown to be primary to the lung by the clinical exclusion of other possible primary sites, then any history of significant tobacco smoking, would make that smoking the likely cause of Mr Gatt’s pulmonary squamous cell carcinoma”.

9. [58]

   Professor Richard Fox is an Honorary Consultant to the Department of Clinical Haematology and Medical Oncology at the Royal Melbourne Hospital. In his report, Professor Fox referred to a series of research papers indicating that the “the risk of developing lung cancer following asbestos exposure diminishes with time after cessation of asbestos exposure”. He noted that the information in those studies “has never been included in updates of the so called “Helsinki Criteria” which were developed in the 1990s based on data from the 1960s through to the 1980s”. He concluded that the information derived from those studies was “significant” and that “given the passage of time following last asbestos exposure and Mr Gatt’s lung cancer, [his] past asbestos exposure had a de [minimis] effect on causation of lung cancer compared with his smoking history.”

10. [59]

    In light of the primary judge’s reasons, it is necessary to describe the reports of Professor Moolgavkar that Amaca tendered in some detail.

11. [60]

    Professor Moolgavkar is a physician with a PhD in mathematics and post-doctoral training in pharmacology, biophysics, epidemiology and biostatistics. In his first report dated 10 October 2019, he recounts that he was asked to provide a report addressing, inter alia, the “risk of contracting a squamous cell carcinoma of the lung associated with the smoking history identified for Mr. Gatt” and the “cumulative exposure to the relevant asbestos [fibre] type necessary to double the risk of contracting carcinoma of the lung.” His report addressed the epidemiology of lung cancer. He noted that: age is a strong factor for the development of lung cancer; the vast majority of lung cancers are caused by cigarette smoking; and that a recent study “confirms that very high levels of exposure to asbestos are required to increase, even modestly, the risk of lung cancer”. Based on various studies, he observed that “compared to cigarette smoking, asbestos is a weak lung carcinogen, with exposure to several hundred [fibre millions/cubic centimetre years] being required to double the risk”, that “amphibole asbestos is considerably more potent as a lung carcinogen than chrysotile asbestos” and that “[t]here is strong evidence that the risk of lung cancer following asbestos exposure is strongly modified by age”.

12. [61]

    In relation to the interaction between cigarette smoking and asbestos in lung carcinogenesis, Professor Moolgavkar noted that “[t]he Relative Risk [(“RR”)] for joint exposure to asbestos and smoking is generally taken to be multiplicative … although there is some evidence to suggest that it may be less than multiplicative but greater than additive”. RR is the ratio of the probability of an outcome in an exposed group to the probability of an outcome in an unexposed group. Professor Moolgavkar said that it followed that “the assumption of a multiplicative RR puts an upper bound on the risk of lung cancer among smokers who are exposed to asbestos” and for “joint exposure to cigarette smoking and asbestos, an upper bound on the RR is given by a model that is an additive function of cumulative asbestos exposure and multiplies the RR for cigarette smoking.”

13. [62]

    One part of Professor Moolgavkar’s first report is entitled “framework for attribution of risk of cancer to specific exposures”. In this section, he described the concept of an “attributable fraction” (AF) in epidemiology, which he said has “often been interpreted as the probability that the disease in a diseased individual was caused by the exposure, and an attributable fraction of 0.5 or above, which corresponds to a RR of 2 or more, has been interpreted to mean that it was more likely than not that the exposure caused the disease.” All of these passages are directed to an assessment of the risk or probability that a particular factor was causative.

14. [63]

    The last part of Professor Moolgavkar’s first report set out his opinions in relation to the probabilities that Mr Gatt’s contraction of lung cancer was attributable to smoking and his exposure to asbestos. Based on the assumptions that he was given about Mr Gatt’s asbestos exposure and tobacco consumption, Professor Moolgavkar states that the “very worst-case assumption” is a RR associated with Mr Gatt’s asbestos exposure of 2 and a “better assumption” is 1.03 (with his RR for smoking being 30). Professor Moolgavkar then describes how one derives an upper bound of probability of causation in which cigarette smoking and asbestos exposure have a multiplicative effect and a lower bound in which they have an additive effect. He obtained the following results:

15. [64]

    The figure of 96% in the last observation refers to the attributable fraction for smoking derived using a RR for asbestos of 1.03. Professor Moolgavkar opined that that figure of around 96% was “rather insensitive to the choice of model”; i.e., additive or multiplicative.

16. [65]

    In his second report dated 20 November 2019, Professor Moolgavkar responded to the reports of Dr Leigh and Dr Mossman. In relation to Dr Leigh’s report, Professor Moolgavkar disputed the RR rates attributed by Dr Leigh to smoking and asbestos for Mr Gatt. Professor Moolgavkar described Dr Leigh’s figures as “unrealistic and extreme”. Nevertheless, Professor Moolgavkar undertook the above calculations using Dr Leigh’s figures. He concluded that “even with the extreme assumptions made by Dr. Leigh, the impact of cigarette smoking on the development of Mr. Gatt’s lung cancer was far greater (~82-85%) than the impact of asbestos exposure (~11-12%).”

17. [66]

    As noted, Associate Professor McKenzie did not accept that Mr Gatt had asbestosis. However, he accepted that ‘[a]sbetos exposure has been reported to increase the risk of developing lung carcinoma” and described the Helsinki Criteria as “recognis[ing] epidemiological literature which indicated that individuals with a history of heavy exposure to asbestos had an increased risk of developing lung carcinoma, even if they did not have asbestosis.” He noted that “[t]he Helsinki Criteria determined the level of exposure to amphibole asbestos which would be sufficient to double the risk of developing carcinoma of the lung, ie, would equate to a probability of causation of 50%.”

18. [67]

    Associate Professor McKenzie’s report records that he undertook a similar process of assessing the risk attributable to smoking and asbestos to that undertaken by Professor Moolgavkar. Associate Professor McKenzie assumed a RR for cigarette exposure of 20, a RR for asbestos exposure of 1.2 and a “background risk” of 4.5%. He divided the “combined asbestos-smoking component of the risk” between the two causes with the contribution of smoking being 94.5% and asbestos being 1.0%. Based on those calculations he concluded “on the balance of probabilities, that the carcinoma in Mr Gatt’s case was on the basis of cigarette smoking”.

19. [68]

    The primary judge’s reasons in relation to this limb of Mr Gatt’s causation case addressed in detail the evidence and submissions concerning the cumulative level of asbestos exposure. [27] Her Honour then addressed the authorities in relation to causation and the epidemiology of lung cancer, including Ellis and Amaca v Booth (2011) 246 CLR 36; [2011] HCA 53 (“Booth”). Her Honour placed particular emphasis on the proposition accepted in Strong v Woolworths (2012) 246 CLR 182; [2012] HCA 5 at [26] that “[n]egligent conduct that materially contributes to the plaintiff’s harm but which cannot be shown to have been a necessary condition of its occurrence may, in accordance with established principles, be accepted as establishing factual causation”. [28] Her Honour then described aspects of Dr Leigh’s evidence and the debate about whether his reasoning on causation was precluded by Ellis. [29] Her Honour then summarised some aspects of the other experts’ reports, including that of Professor Moolgavkar. Her Honour noted Professor Moolgavkar’s conclusion that “asbestos exposure made no contribution to the development of Mr Gatt’s lung cancer” and observed: [30]

20. [69]

    Her Honour then returned to the first limb of the Respondent’s causation case before reaching the conclusion above that Mr Gatt had asbestosis. Her Honour then returned to the second limb, reasoning as follows:

21. [70]

    This reasoning is further analysed below. However, at this point it suffices to state that I understand that the finding of causation in the first sentence of [261] is explained by what follows, that is, her Honour relied on Professor Moolgavkar’s evidence to base a conclusion that Mr Gatt’s exposure to asbestos made a “material contribution” to his development of lung cancer and that was sufficient to amount to causation in law.

22. [71]

    Ground 1(b) makes the same point as ground 1(a) except that it is directed to the epidemiological experts whose reports were relied on by Amaca. This ground fails for the reasons noted above in relation to ground 1(a).

23. [72]

    Ground 3 of the further Amended Notice of Appeal is set out above. The ground cross references various paragraphs of the primary judgment. Of those paragraphs, [215] and [262] of her Honour’s reasons are set out above. Paragraph [214] of the primary judgment set out extracts from Professor Moolgavkar’s reports that confirm that he was opining on the “risk” of asbestos exposure and smoking causing lung cancer. Paragraphs [198] to [199] contain a description and analysis of Professor Moolgavkar’s evidence that is not materially different to that set out by her Honour in [215] and [263].

24. [73]

    With respect to her Honour, these passages of the primary judgment misapprehend Professor Moolgavkar’s evidence and the concept of “material contribution” as used in causation in the law of negligence.

25. [74]

    To establish a cause of action in negligence, a plaintiff must prove on the balance of probabilities that the defendant’s wrong caused or materially contributed to his or her loss. It is not sufficient for the plaintiff to show that the wrong only materially increased the risk of harm where medical science does not permit any further proof (Evans v Queanbeyan City Council [2011] NSWCA 230 at [20]-[23] per Allsop P, as his Honour then was, at [56] per Hodgson JA, and [93] and [103] per Basten JA, citing Ellis and Tabet v Gett (2010) 240 CLR 537; [2010] HCA 12). The concept and context of a material contribution were explained by Gummow, Hayne and Crennan JJ in Booth at [70] as follows:

26. [75]

    Their Honours then referred to the discussion of Bonnington Castings Ltd v Wardlaw [1956] AC 613 (“Bonnington Castings”) in Ellis. That discussion is of particular significance at this point. Like this case, Ellis concerned a smoker who had been exposed to asbestos and who later developed lung cancer. In Ellis, the Court described the effect of epidemiological evidence that was very similar to that set out above. This evidence utilised attributable fractions which “expressed the probability that the cancer in question was caused by exposure to the carcinogen or carcinogens in question” (at [24]). Although, in Ellis, various figures were attributed to the percentage likelihood that lung cancer was caused by asbestos, that figure was not greater than 23% and was always much less than that assigned to smoking being not less than 67% (at [30]). Of these figures, their Honours observed (at [64] to [65]):

27. [76]

    In Ellis, the High Court then addressed the concept of a material contribution noting Lord Reid’s observation in Bonnington Castings (at 621) that any contribution which is not de minimis must be material (Ellis at [66]). The Court in Ellis observed that that statement had to be understood in the context of the facts in Bonnington Castings. An employee who developed pneumoconiosis was exposed to silica dust at his workplace, some of which was released from a negligent source, being poorly maintained equipment, and some of which was produced by other activities that did not involve negligence. The medical evidence was that pneumoconiosis was caused by a gradual accumulation of silica particulars inhaled over a number of years. Thus, Bonnington Castings did not involve any consideration of what the most probable source of the employee’s disease was. Instead, it concerned whether the negligent source of silica dust materially contributed to the gradual accumulation of dust that resulted in disease (Ellis at [67]).

28. [77]

    In this case, the epidemiological evidence from Professor Moolgavkar (and Associate Professor Mackenzie) was no different in substance from the epidemiological evidence surveyed in Ellis. Their evidence concerned the probability that Mr Gatt’s lung cancer was caused by smoking or exposure to asbestos. With respect to her Honour’s statement in [215] of the primary judgment, Professor Moolgavkar’s conclusion that Mr Gatt’s asbestos exposure made no contribution to the development of his lung cancer was explained very clearly. Professor Moolgavkar’s percentage figures were a calculation of the respective likelihoods that Mr Gatt’s lung cancer was caused by either smoking, exposure to asbestos or a background cause. They were not, and did not, purport to be an assessment of the respective contributions of those factors to Mr Gatt’s lung cancer like some apportionment of the two different sources of silica dust in Bonnington Castings.

29. [78]

    Like the evidence in Ellis described above, the conclusions of Professor Moolgavkar and Associate Professor Mackenize about the balance of probabilities were simply based on a quantitative comparison of the probability that the lung cancer was caused by smoking compared to the probability that it was caused by exposure to asbestos. In Booth at [49], French CJ observed that a “causal connection may be inferred by somebody expert in the relevant field considering the nature and incidents of the correlation” between the relevant disease and the relevant exposure. Both Professor Moolgavkar and Associate Professor MacKenzie’s evidence was of that kind, although they expressed an opinion about the causal connection with smoking (and a negative opinion about a causal connection with asbestos).

30. [79]

    It is evident that the primary judge misconceived the effect of Professor Moolgavkar’s evidence in concluding that it supported the conclusion that the “remaining 4%” of Mr Gatt’s cancer was caused by asbestos exposure (at [215]), and that implicit in his evidence is “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” (at [262]). Leaving aside the fact that Professor Moolgavkar’s figures addressed the residual 4%, this treats his evidence concerning attributable fractions as though it were directed to the percentage contribution to a state of affairs that caused the lung cancer in the same way that there might have been a (rough) apportionment of the sources of silica dust in Bonnington Castings. However, Professor Moolgavkar’s evidence was only that there was a (greater than) 96% chance that Mr Gatt’s lung cancer was caused by his smoking. It was not a statement that 96% of whatever active agent caused his lung cancer was sourced from smoking, much less that the other 4% was sourced from asbestos exposure (or elsewhere).

31. [80]

    This approach of the primary judge appears to be more than a mere misunderstanding of the effect of Professor Moolgavkar’s evidence as was contended by Mr Walker on this appeal. Instead, it reveals that the primary judge misunderstood (and misapplied) the legal concept of “material contribution” in causation. In [261] to [264] of the primary judgment, her Honour moved from the proposition that asbestos exposure was “sufficient” to cause lung cancer, that is, that it can cause lung cancer, to concluding that it did cause Mr Gatt’s lung cancer (cf Ellis at [68]). The only basis that her Honour identified for taking that logical step was that her Honour relied on Professor Moolgavkar’s evidence to conclude that asbestos exposure made a material contribution to Mr Gatt’s lung cancer. In taking that step, her Honour equated evidence which might have been capable of suggesting that there was a material chance of asbestos exposure causing Mr Gatt’s lung cancer with evidence that it in fact made a material contribution to the causation of his lung cancer. For the reasons explained above, that involved a misunderstanding and misapplication of the concept of material contribution as explained in Ellis. It was erroneous in law.

32. [81]

    I would uphold ground 3.

33. [82]

    Section 25B of the DDT Act provides:

34. [83]

    In the proceedings before the primary judge, each of the parties served a notice identifying an issue of a general nature that they contended had been determined in previous proceedings by the Tribunal. The Respondent referred to McDonald v State Rail Authority (1998) 16 NSWCCR 695; [1998] NSWDDT 4 at [72] (“McDonald”) as demonstrating that “carcinoma of the lung may be attributed to asbestos exposure in the absence of asbestosis where the exposure was sufficient to have caused asbestosis”. Amaca’s notice referred to Judd v Amaca Pty Ltd (2003) 25 NSWCCR 125; [2003] NSWDDT 12 (“Judd”) at [44] where Curtis DCJ concluded that “that 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.”

35. [84]

    On appeal, Amaca submitted that the primary judge erred in finding that, on the balance of probabilities, Mr Gatt’s asbestos exposure caused his lung cancer “because, having found that Mr Gatt was exposed to an airborne concentration of at least 24.4 fibres/ml.years, her Honour then failed to apply that finding to the issue of a general nature determined in Judd”. It was contended that the consequence of the primary judge’s finding about Mr Gatt’s level of cumulative exposure meant “that her Honour could not have been satisfied that it had been established, on the balance of probabilities, that Mr Gatt was exposed to a cumulative airborne asbestos concentration of greater than 50 fibres/ml.years”.

36. [85]

    In Judd, a worker contracted lung cancer. He was a heavy smoker who also worked for Amaca during a period around the early 1960s. Curtis DCJ reviewed the origins of the Helsinki Criteria noted above (at [18] to [30]) and various expert commentaries on its conclusions (at [31] to [43]) before finding (at [44]):

37. [86]

    His Honour then addressed the operation of s 25B of the DDT Act in the context of considering (and doubting) the weight to be attached to the proposition sought to be extracted from McDonald by the Respondent in this case. His Honour queried whether it was based on a misapprehension of the effect of the Helsinki Criteria (at [45] to [53]). His Honour then observed (at [54] to [56]):

38. [87]

    As I understand, the significance of the RR of contracting lung cancer doubling in consequence of exposure to asbestos, as referred to in [44] and [56] of Judd, is that a RR of 2 will correspond to an attributable fraction of 50%, yielding a probability of acquiring lung cancer that can be used to reason to a finding of causation on the balance of probabilities in the manner described above (at [62] and [78]). Although not expressly stated, Amaca’s contentions in relation to this ground assume that the effect of the determination of a “general issue” by Curtis DCJ in Judd was that, unless there was a cumulative exposure of 50 fibres/ml.years, then no such finding could be made. That is not what Judd at [44] expressly states, and any doubt about that is resolved by Judd at [55] and [56]. In Judd at [55], Curtis DCJ left open the possibility that a RR of less than 2 could nevertheless lead to an attribution of lung cancer to asbestos exposure in a particular case, as well as permitting evidence to be led to prove that the doubling of the risk occurs at a cumulative exposure lower than 50 fibres/ml.years. In Judd at [56], Curtis DCJ confirmed the latter point by noting that his Honour’s finding was confined to the “present state of medical knowledge”.

39. [88]

    The end result is that Judd did not mandate that once the primary judge found that Mr Gatt’s cumulative exposure was less than 50 fibres/ml.years the Respondent’s case that his lung cancer was attributable to that exposure had to fail.

40. [89]

    I would reject ground 4

41. [90]

    Ground 5 of the Amended Notice of Appeal contends that the primary judge erred in law in failing to “address a substantial and clearly articulated case” that the causal potency of Mr Gatt’s exposure to asbestos diminished over time such that the “relative risk from asbestos exposure was little, if any, greater than 1.”

42. [91]

    The use of the phrase “substantial and clearly articulated” in the formulation of this ground suggests that Amaca seeks to rely upon the statement in Dranichnikov v Minister for Immigration and Multicultural Affairs (2003) 77 ALJR 1088; [2003] HCA 26 (“Dranichnikov”) at [24] that “[t]o fail to respond to a substantial, clearly articulated argument relying upon established facts was at least to fail to accord ... natural justice”. However, nothing in Amaca’s written submissions sought to invoke Dranichnikov or the cases that have followed it.

43. [92]

    In any event, this ground can be disposed of shortly. The proposition that the causal potency of exposure to asbestos diminishes over time vis a vis lung cancer was “clearly articulated” by Professor Moolgavkar. It was incorporated into his estimates of the RR for asbestos that he used in the calculations set out above. However, the primary judge utilised Professor Moolgavkar’s figure of 96% which was derived using a RR for asbestos of 1.03. This figure reflected Professor Moolgavkar’s opinion that the causal potency of the exposure reduced over time. Hence, the foundation for this ground of appeal is not made out. The fact that her Honour misunderstood and misapplied Professor Moolgavkar’s calculation using that figure is a different point and the basis for ground 3 which I have upheld.

44. [93]

    I would reject ground 5.

45. [94]

    Some aspects of Amaca’s submissions do not match its grounds of appeal. For example, Amaca contended that the “primary judge further erred in relying on the Helsinki Criteria” in [260] of the judgment because her Honour disregarded the evidence from the Respondent’s witnesses that was critical of its use. The Helsinki Criteria and some of the expert’s evidence about it are referred to above. Similarly, the submissions complain that the primary judge did not refer to the evidence of Dr Gal and Professor Fox in the “discussion” section of her Honour’s reasons (although it was summarised elsewhere).

46. [95]

    Consistent with the discussion of Azzopardi (and Soulemezis) noted above, these complaints do not raise any error, point or question of law.

Ground 6: Failure to Find a Fact

1. [96]

   Ground 6 of the Amended Notice of Appeal provides:

2. [97]

   As I understand it, in the event the Court were to find error on the part of the primary judge, this ground of appeal invites this Court to make findings of fact favourable to Amaca on the disputed issue(s). Amaca sought to rely on s 32(2) of the DDT Act which confers on this Court power, on the hearing of an appeal under sub-s (1), to remit the matter “for determination by the Tribunal in accordance with any decision of the Supreme Court and may make such other order in relation to the appeal as the Supreme Court sees fit.”

3. [98]

   However, in circumstances where this ground of appeal is confined to errors or “points” of law, neither s 32(2) of the DDT Act, nor any other provision, confers on this Court the power to make findings of fact (Patrick Operations Pty Ltd v Comcare (2006) 68 NSWLR 131; [2006] NSWCA 142; see also Thaina Town (On Goulburn) Pty Ltd v City of Sydney Council (2007) 71 NSWLR 230; [2007] NSWCA 300 at [83] to [87]). If the outcome of the appeal had been that the primary judge’s findings on both limbs of the Respondent’s case were affected by an error of law, then the appropriate order would have been to remit the matter to the Tribunal.

4. [99]

   I would reject this ground.

Additional Challenge: Special Costs Order

1. [100]

   At the hearing of the appeal, Amaca was granted leave to add an additional ground of appeal challenging a special costs order made by the primary judge on 1 December 2021 (Roseanne Cleary as the legal personal representative of the estate of the late Fortunato (aka Frank) Gatt v Amaca Pty Limited [2021] NSWDDT 7). No separate submission was directed to this costs order. As I understand it, this challenge was dependent on the success or otherwise of Amaca’s challenge to her Honour’s principal judgment. As that has failed, this aspect of the appeal falls away.

Proposed Orders

1. [101]

   As Amaca has failed to demonstrate an error of law in relation to both of the primary judge’s critical findings it follows that I consider that the appeal must be dismissed.

2. [102]

   I propose the following orders:

3. [103]

   MITCHELMORE JA: I agree with Beech-Jones JA.