Bennett v Workers Compensation Nominal Insurer and Ors

Consideration

1. I will deal with each of the matters to be considered in s 25B(2) in turn.

New evidence

1. It was common ground that new evidence is not the same as fresh evidence. "New evidence" as it is referred to in s 25B(2) is evidence that has not previously been given in the Tribunal: Apostolopoulos v Hatzisarantinos & Others trading as Omonia Constructions (No 3) (2009) 7 DDCR 39.
2. I am satisfied that all of the medical evidence sought to be relied on by the defendants for the purpose of this application is new evidence.
3. The effect of the new evidence can be reduced to the following propositions: 1. silicosis is not a single disease but incorporates simple silicosis (nodular silicosis), acute silicosis (silicoproteinosis), PMF (also called conglomerate silicosis or complicated silicosis, which is a progression of simple silicosis) and accelerated silicosis (a rapidly progressive form of simple silicosis); 2. simple silicosis is the most common form. It takes the form of multiple small nodules of fibrous tissue concentrated in the upper zones of the lungs. The nodules are thought to develop as a result of the ingestion of silica particles by scavenger cells in the lung known as macrophages. The crystalline structure of silica particles causes the death of the macrophage releasing factors that favour the deposition of fibrous tissue and the release of the silica particle to be re-ingested by other macrophages, leading to a repetition of the cycle. The mechanisms that underlie the development of silicosis are complex and elusive, but it is a benign reactive inflammatory-fibrotic (scarring) process. When more silica particles are inhaled the inflammation/fibrotic stimulus is increased and the fibrosis worsens; 3. large quantities of silica interacting with macrophages can also impact the immune system, causing auto-immune disorders such as rheumatoid arthritis or collagen-vascular disorders such as scleroderma; 4. PMF represents a further progression of simple silicosis, where the nodules coalesce and form conglomerate areas of scarring, so that the lesions of PMF are qualitatively the same as simple nodular silicosis, but quantitatively different because they are bigger. The rate at which this progress advances is defined by a complex interaction between the type of silica, the intensity of exposure, the duration of exposure, the genetic responsiveness of the host, and many other factors; and 5. each additional exposure to silica worsens the disease by aggravating the underlying pathological process that causes silicosis, leading to further fibrosis. This makes it a divisible condition.
4. There are a number of recent sources cited by Associate Professor McKenzie and Associate Professor Klebe as supportive of their evidence. These include extensive literature reviews, authoritative pathology texts, animal studies, metabolic studies of macrophages and the inflammatory process, cohort studies including studies of silicosis in engineered stone workers, autopsy studies and comparative studies between the progression of silicosis in natural stone workers versus engineered stone workers.
5. The new evidence, to which I have been referred, is suggestive of there being a scientific consensus on the aetiology of silicosis and PMF for at least the past 10 years.
6. I have also considered the evidence of the late Professor Henderson and Associate Professor Breslin, who has retired from practice, as supportive of the other evidence relied on by the defendants. Whilst I am satisfied that it is appropriate to do so on the question of the existence of new evidence, the admission of that evidence at any later trial, where it cannot be tested in cross-examination, will be a matter for the trial judge.
7. Overall, I am satisfied that there is a wealth of new, scientifically supported evidence suggesting that PMF is a divisible condition, and this favours a grant of leave.

The proceedings in Harris

1. I have had regard to the decision of Johns J in Harris, which was his second judgment on the question of the damages to be awarded to the plaintiff.
2. In his first judgment, following the hearing of the evidence including the medical evidence, Johns J entered a single judgment for $502,272 against the three defendants and ordered that the limitation period for the commencement of the proceedings be extended on the basis that the plaintiff did not know the nature and extent of his injury.
3. The defendants appealed: Commercial Minerals Pty Ltd v Hollins; Aqual Pty Ltd v Hollins [1993] NSWCA 74. The Court of Appeal decided that: 1. the plaintiff knew of the nature and extent of his injury at an earlier date and set aside the orders extending the limitation periods; 2. future compensation benefits under the Workers' Compensation (Dust Diseases) Act 1942 (the 1942 Act) should have been deducted in computing future economic loss; and 3. a single judgment against all of the defendants could not have stood on principle because they were consecutive tortfeasors whose separate acts and omissions caused some separate damage, following Thompson v Smith's Shiprepairers Ltd [1984] QB 405.
4. The plaintiff's administrator appealed to the High Court following the plaintiff's death: Harris v Commercial Minerals Ltd (1996) 186 CLR 1. The High Court upheld the appeal as to the extension of the limitation periods and dismissed the appeal in relation to the accounting for compensation received under the 1942 Act. The High Court remitted the matter to the Tribunal to assess the damages to be awarded against the second and third defendants on the basis of the findings and the evidence before Johns J.
5. In his second judgment, Johns J decided on the basis of the evidence given prior to the first judgment that: 1. silicosis and PMF were separate conditions; and 2. the evidence did not prove which damage was caused by the different periods of exposure and that as a matter of law, that made PMF an indivisible condition.
6. The Court of Appeal rejected an appeal from Johns J's decision: Commercial Minerals Ltd v Harris (1999) 18 NSWCCR 11. The Court of Appeal decided that Johns J was entitled to find that PMF was a separate injury because there was medical evidence to support that finding. The appeal was limited to a question of law: s 32 Dust Diseases Tribunal Act 1989. I am bound to accept that the second judgment was correct in law.
7. The plaintiff submitted that the conceptual understanding of PMF that underlies the new evidence was the subject of evidence from the medical experts in Harris, considered by Johns J and rejected. In support of that submission, the plaintiff took me to extracts of the medical evidence before Johns J in Harris, and to Associate Professor Klebe's report of 20 October 2023, where she accepted the evidence of those experts was still supported by more recent scientific evidence. I do not accept that submission for the reasons that follow.
8. I was not taken to any report of any of the medical experts in Harris where any of them expressed an opinion on whether the damage caused by PMF was indivisible;
9. I was not taken to any questioning in the oral evidence of the medical experts in Harris, where any of them were asked to express an opinion on whether the damage caused by PMF was indivisible.
10. There was no evidence from a pathologist in Harris.
11. From the extracts of the medical experts in Harris, the following salient points can be taken: 1. continued exposure to silica in someone with established silicosis will worsen the problem because, "he is asking his lung to take on extra burden of silica and deal with it. Clearly his lung cannot deal with it, and it's going to be deposited within his lung, and it's going to set up a fibrotic reaction which will worsen what is already there and established;" 2. reactions to exposure to silica are idiosyncratic. Small exposures to silica in a small number of cases have produced acute reactions; 3. PMF is an uncommon manifestation of the process, where there is coalescence of the rounded deposits (silicotic nodules); 4. once silicosis is established, ongoing exposure to silica may act in a catalytic manner to keep the process going. The rate at which it keeps going is dependent on the degree of exposure but all exposure would keep it going; 5. the reason why the condition progresses with time is that the fibrosis continues to develop, restricting the elasticity of the lungs; 6. Mr Hollins' continued exposure to silica after being diagnosed with silicosis accentuated and accelerated the problem; 7. in most cases, the development of silicosis is dose-related; 8. symptoms are exacerbated by further exposure post diagnosis with silicosis because the additional dust will get into areas of the lung that were previously unaffected; 9. silicosis is usually required for the development of PMF; 10. PMF is more likely to develop in more serious cases of silicosis, where there has been a previous infection, like tuberculosis and where the person has a rheumatoid condition that predisposes them to PMF; and 11. the total dose of silica is important to the development of PMF.
12. Judge Johns could not be satisfied as to the cause of PMF, notwithstanding the medical evidence which I infer he accepted. Whilst the evidence in Harris referred to the fibrotic process, it was silent on how the fibrotic process operated and was repeated by the inability of the macrophages to clear silica from the lung tissue leading to fibrosis.
13. The new evidence calls into question the first of Johns J's conclusions that silicosis and PMF are separate conditions, by alleging in effect that PMF is an acceleration or aggravation of the fibrotic process involved in silicosis. If it is established, on the balance of probabilities, that PMF is caused by the same inflammatory/fibrotic process responsible for causing silicosis, then it will be open to find that PMF is an acceleration or aggravation of silicosis and therefore a divisible condition, because each exposure to silica causes separate damage to the lung and surrounding tissues of the same kind, namely fibrosis.
14. The references provided by Associate Professor Klebe and Associate Professor McKenzie that support their opinions, did not exist at the time when Harris was decided.
15. I am satisfied that there were far fewer studies and far less authoritative commentary available in the medical and scientific community about the aetiology of silicosis, PMF and fibrotic processes at the time that Harris was decided. Accordingly, the opinions of the medical experts called in Harris are likely to be less reliable than if they had been able to consider that material.
16. I have doubts that the question, whether the damage caused by PMF was indivisible, was squarely raised in Harris, at the time when the medical experts gave evidence.
17. On balance, I am satisfied that this factor also supports a grant of leave.

Other relevant matters

1. The plaintiff's case is not urgent by reason of his medical condition and that permits this issue to be resolved in an orderly way.
2. There has been a recent influx of cases filed in the Tribunal involving the contraction of silicosis and PMF, particularly arising from working with engineered stone products which have a high silica content. Accordingly, the issues sought to be re-litigated in these proceedings will be of importance to a number of litigants in the Tribunal and will affect how future proceedings are conducted. This is a further factor that warrants a grant of leave.
3. As to the matters sought to be relied on pursuant to s 25B, the issue in [1] of the s 25B notice is supported by the medical evidence in Harris and the new evidence. Nevertheless, it is appropriate to grant leave to re-litigate that issue because it is likely to be the subject of evidence in the hearing and it would be artificial to exclude evidence relevant to progression of PMF when that is inexorably linked to the determination of the other issues.
4. The proceedings were at an advanced stage of preparation before the application to re-litigate the issues was brought. The plaintiff has thrown away costs by reason of the adjournment of the hearing. I have reserved the question of costs of the adjournment. It is likely that he will incur further additional costs in preparing a case that involves re-litigating a long-settled proposition. The defendants' conduct in not seeking leave earlier in the proceedings permitted the plaintiff to run his case on the understanding that part of his damage was indivisible.
5. The plaintiff submitted that he should be paid his costs of the re-litigated issue and any costs arising from the re-litigated issue on the indemnity basis. It was submitted that this should extend to the costs of joining other defendants to the proceedings to protect his position on the recoverability of all of his damages.
6. I am satisfied that this is an appropriate case to make it a condition of granting leave that the defendants pay the plaintiff's costs of arguing the re-litigated issues, irrespective of the outcome, because the case has become a "test case" on those issues. I do not accept that the costs order should extend to any costs arising from the re-litigated issues as contended for by the plaintiff. For example, if the plaintiff chooses to join other defendants and succeeds against them, he will be entitled to a costs order against the new defendants. The order should extend to qualifying additional medical evidence, preparation for and conduct in the argument of the re-litigated issues before the Tribunal.

Orders

1. The orders I make are as follows: 1. I grant leave to the defendants to re-litigate the matters set out in [1] to [5] of the plaintiff's s 25B notice. 2. The defendants are to pay the plaintiff's costs of re-litigating the issues, the subject of order 1, irrespective of the outcome of the proceedings and including the costs of the Notice of Motion, on the indemnity basis. 3. I will list the matter for directions before me in the DDT List on Monday 5 February 2024.

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