Aiberti and Military Rehabilitation and Compensation Commission (Compensation) - [2019] AATA 4238

Aiberti and Military Rehabilitation and Compensation Commission (Compensation) [2019] AATA 4238 (14 October 2019)
Division:VETERANS’ APPEALS TRIBUNAL
File Number: 2016/2882
2016/6960

Re:Estate of the Late Stephenson Aiberti
FIRST APPLICANT
and
Joan Aiberti
SECOND APPLICANT

AndMilitary Rehabilitation and Compensation Commission
RESPONDENT

DECISION
Tribunal:Deputy President Boyle

Date:14 October 2019
Place:Perth

The Tribunal affirms:
Application 2016/2882
(i)the reviewable decision of the Respondent dated 24 May 2016 which affirmed a determination which found that liability did not exist pursuant to section 14 of the DRC Act for the claimed mesothelioma condition; and

Application 2016/6960
(ii)the reviewable decision of the Respondent dated 1 November 2016 which affirmed a determination which denied the Second Applicant’s claim for compensation pursuant to section 17 of the DRC Act in relation to the death of Mr Aiberti.

............................[sgd]............................................
Deputy President Boyle
CATCHWORDS
COMPENSATION – Safety, Rehabilitation and Compensation (Defence-related Claims) Act 1988 (Cth) – mesothelioma condition – defence service – presumption under s 7(1) – onus on Respondent to establish that the claimed mesothelioma was not significantly contributed to by defence service –exposure to asbestos in Wittenoom – use of epidemiological evidence – decisions under review affirmed
LEGISLATION
Safety, Rehabilitation and Compensation Act 1988 (Cth) – ss 5B, 7(1), 7(4), 14, 16, 17, 18, 48
Safety, Rehabilitation and Compensation Legislation Amendment (Defence-Force) Act 2017 (Cth) – s 64
Safety, Rehabilitation and Compensation (Defence-related Claims) Act 1988 (Cth) – ss 5A, 5B, 7(1), 14(1), 17, 48
CASES
Amaca Pty Ltd v Booth [2011] HCA 53; (2011) 246 CLR 36
Amaca Pty Ltd v Ellis (2010) 40 CLR 111; [2010] HCA 5
Burns and Military Rehabilitation and Compensation Commission [2018] AATA 35
Comcare v Power (2015) 238 FCR 187; [2015] FCA 1502
Fazio v Fazio [2012] WASCA 72
Freeman and Military Rehabilitation and Compensation Commission [2016] AATA 741
Pryde and Telstra Corporation Limited [2016] AATA 811
Repatriation Commission v Gorton (2001) 110 FCR 321; [2001] FCA 1194
Seltsam Pty Ltd v McGuinness (2000) 49 NSWLR 262; [2000] NSWCA 29
Sydney South West Area Health Service v Stamoulis [2009] NSWCA 153
Tabet v Gett (2010) 240 CLR 537; [2010] HCA 12
The Estate of the Late Mr Vaughan White and Military Rehabilitation and Compensation Commission [2018] AATA 3882
White and Military Rehabilitation and Compensation Commission [2017] AATA 1555
Wiegand v Comcare Australia [2002] FCA 1464
SECONDARY MATERIALS
Safety, Rehabilitation and Compensation and other Legislation Amendment Bill 2006 (Cth)
REASONS FOR DECISION
Deputy President Boyle
14 October 2019
THE APPLICATIONS

There are two applications before the Tribunal.
Estate of the Late Stephenson Aiberti: application 2016/2882
The First Applicant seeks review of a reviewable decision of the Respondent dated
24 May 2016 which affirmed a determination which found that liability did not exist pursuant to the Safety, Rehabilitation and Compensation Act 1988 (Cth) (SRC Act) for the claimed mesothelioma condition on the basis that the First Applicant had previously been paid common law compensation for the disease and was therefore precluded by s 48 of the SRC Act from receiving compensation for the condition under the SRC Act.
Mr Stephenson Aiberti lodged an Application for Review of Decision with the Administrative Appeals Tribunal (the Tribunal) on 1 June 2016 seeking review of the reviewable decision dated 24 May 2016. Mr Aiberti passed away on 10 June 2016 and his claim has since been pursued by the First Applicant.
Joan Aiberti: application 2016/6960
The Second Applicant is the widow of Mr Aiberti. She seeks review of a reviewable decision of the Respondent dated 1 November 2016 which affirmed a determination which denied the Second Applicant’s claim for compensation pursuant to s 17 of the SRC Act in relation to the death of Mr Aiberti.
The Second Applicant lodged the Application for Review of Decision with the Tribunal on 21 December 2016.
BACKGOUND
The facts are largely not in dispute.
Mr Aiberti was born in 1940.
In 1950, at the age of 10 years, Mr Aiberti moved with his family to the town of Wittenoom. His father worked in the Wittenoom asbestos mine initially as an underground miner and then later as a shift boss.
At age 14, Mr Aiberti left school and commenced work on the mine for Australian Blue Asbestos (ABA) as an apprentice electrical fitter. He worked for ABA from April 1954 to March 1956. Most of his work was in the old asbestos mill and the powerhouse.
After completing his apprenticeship, Mr Aiberti left Wittenoom in March 1956 but returned to Wittenoom in July 1956 at which time he worked for ABA as a mineral sampler until June 1957.
It is uncontroversial that in the course of Mr Aiberti’s employment in Wittenoom he was exposed to crocidolite, which is more commonly known as blue asbestos. It is also uncontroversial that, despite the relatively short period of time Mr Aiberti worked on the mine in Wittenoom, this exposure was a significant contributing factor to his mesothelioma.[1]
[1] Applicants’ SFIC para. 11.
Mr Aiberti enlisted in the Royal Australian Navy (RAN) on 26 July 1957 and was discharged on 21 April 1964.
From 26 July 1957 to 23 November 1958, Mr Aiberti was posted at HMAS Cerberus, which was a shore base, where he undertook training as an ordinary radio communications officer. Mr Aiberti’s recollection, as recounted in his statement dated
[2] R1, T12 at 45.
9 November 2015, was that “many of the buildings on the base were constructed utilising asbestos cement sheeting”.[2]
From 3 January 1959 to 18 April 1960 Mr Aiberti was posted on the HMAS Swan.
The HMAS Swan was used as a training frigate. Mr Aiberti’s statement of 9 November 2015 says that the bulkheads and piping on the HMAS Swan were sprayed with lagging which he assumed contained asbestos.[3] I do not understand the Respondent to dispute that the HMAS Swan contained lagging as identified by Mr Aiberti or, as assumed by
[3] R1, T12 at 45.
Mr Aiberti, that the lagging contained asbestos of some sort.
From 12 April to 12 September 1960 Mr Aiberti was posted to the HMAS Harman in Canberra. HMAS Harman was a shore facility where the building ceilings were fireproofed with what Mr Aiberti presumed was asbestos.[4]
[4] R1, T12 at 46.
Between 13 September 1960 and 8 November 1961 Mr Aiberti was posted to HMAS Melville (Coonawarra) in Darwin. This was also a shore facility. Mr Aiberti’s recollection is the building that he worked out of was of asbestos cement construction (R1, T12 at 46).
Mr Aiberti was re-posted to the HMAS Harman from 9 November 1961 to 5 August 1963 except for a period at HMAS Cerberus from 22 February 1962 to 2 April 1962 when he undertook a training course.
From 6 August 1963 to 4 October 1963 Mr Aiberti was posted to HMAS Kimbla which was a small steam powered boom defence vessel which, according to Mr Aiberti’s statement, was “extensively lagged”.[5]
[5] R1, T12 at 46.
Mr Aiberti was then posted to HMAS Diamantina from 17 January 1964 to 23 March 1964. This was an older frigate which had extensive lagging on bulkheads and piping. Hammocks in which the crew slept were slung from lagged piping.[6]
[6] R1, T12 at 46.
From 24 March 1964 to 21 April 1964 Mr Aiberti was based at the land base HMAS Leeuwin in Western Australia before being discharged from the RAN.
From April 1964 to April 1992 Mr Aiberti worked as a flight services officer with the Department of Civil Aviation
In or about 1992 Mr Aiberti ceased work due to the effects of asbestosis.
In 1987, by writ of summons, Mr Aiberti initiated proceedings in the Supreme Court of Western Australia against CSR Limited and Midalco Pty Ltd. The indorsement of claim on the writ of summons stated the claim to be as follows:
The plaintiff’s claim is for damages for personal injuries, loss and damage suffered by the plaintiff as a result of contracting the diseases of asbestosis, pleural thickening, respiratory degeneration, pain, shock and psychological reaction as a consequence of his exposure to asbestos dust and fibres whilst living in and around Wittenoom between 1951 and 1957. The said diseases are a consequence of the negligence and/or breach of statutory duty of the first known defendant, its servants or agents and/or the second known defendant or its servants or agents.
Those proceedings, which had been remitted to the District Court of Western Australia, concluded with a consent judgment on 14 August 1996 with Mr Aiberti receiving a payment of $477,500.00. The minutes of the consent judgment filed with the court also noted, inter alia, as follows:
…..such settlement being in the sum of $477,500…is intended to be, and is, in full and final settlement of all causes of action which I now have and, but for the said settlement, might have had in the future in respect of all injuries, diseases, and conditions, whether patent or latent or which may hereafter develop caused by and/or contributed to by the inhalation or ingestion of asbestos dust and/or fibres including but without limiting the generality thereof, pleural disease, pleural thickening, asbestosis, lung cancer and mesothelioma and any direct or indirect consequences of one, some or all of them.” (Emphasis added.)
On 15 April 2002 Mr Aiberti submitted a claim for compensation under the SRC Act in respect of a then diagnosed condition of asbestosis solely in respect of one aspect of his service being that on HMAS Swan in the period from 3 January 1959 until 18 April 1960. That claim for compensation did not proceed any further once the Respondent sought details from Mr Aiberti of a “court award of $477,500.00”.
In 2015 Mr Aiberti began to lose weight and noticed the onset of pain just under his ribs.[7] Radiological investigations were carried out on 2 September 2015 which revealed findings consistent with peritoneal mesothelioma.[8] In October 2015 a biopsy confirmed a diagnosis of peritoneal mesothelioma.[9]
[7] R1, T12 at 46.
[8] R1, T12 at 51.
[9] R1, T12 at 57.
Mr Aiberti lodged a claim for compensation on 9 November 2015 in respect of mesothelioma. That claim was denied pursuant to s 48 of the SRC Act and the decision was affirmed on reconsideration. Mr Aiberti sought review of that reviewable decision on

1 June 2016 in the Tribunal. He passed away shortly after on 10 June 2016 and the First Applicant continues with the application before the Tribunal in matter 2016/2882.
The Second Applicant lodged a dependency claim in respect of the death of her husband, Mr Aiberti, on 26 July 2016. By determination dated 12 September 2016 and reviewable decision dated 1 November 2016, the Second Applicant’s claim for compensation was denied. The Second Applicant sought review of that decision by the Tribunal on

21 December 2016. That is matter 2016/6960.
ISSUES
In relation to the First Applicant:
(a)Does Mr Aiberti’s estate have an entitlement pursuant to ss 14, 16, 18 and 24 of the SRC Act? Determination of that issue turns on the following questions:
(i)Did Mr Aiberti suffer an injury, being a disease as defined in the SRC Act?
(ii)Does subsection 7(1) of the SRC Act apply to the claimed mesothelioma condition such that the “reverse onus” test applies?
(A)If so, does the evidence establish that the claimed mesothelioma condition was not significantly contributed to by Mr Aiberti’s former defence employment?
(B)If not, was the mesothelioma condition significantly contributed to by Mr Aiberti’s former defence employment pursuant to s 5B of the SRC Act?
(iii)If Mr Aiberti suffered an injury, being a disease, what was the date that the injury was sustained having regard to s 7(4) of the SRC Act?
(iv)If Mr Aiberti suffered an injury (being a disease), did the injury result in his death?
(b)Is the First Applicant precluded from receiving compensation by virtue of the bar in s 48 of the SRC Act?
In relation to the Second Applicant:
(a)Is the Respondent liable to pay compensation to the Second Applicant pursuant to section 17 of the SRC Act in respect of Mr Aiberti’s death? This requires consideration of the following issues:
(i)The issues identified in relation to the First Applicant with the exception of (b); and
(ii)Was the Second Applicant wholly or partly dependent on Mr Aiberti at the date of his death?
THE HEARING
Both applications were heard on 27 and 28 May 2019. The Applicants were represented by Mr McCabe instructed by Slater and Gordon and the Respondent was represented by Mr Clark instructed by Sparke Helmore Lawyers.
Evidence was given at the hearing by:
·Michael Kottek, occupational and environmental health consultant;
·Professor Dr Arthur William Musk, respiratory physician;
·Professor Richard Fox, consultant oncologist; and
·Dr James Leigh, consultant occupational physician.
The following documents were admitted into evidence at the hearing:
·
Report of Michael Kottek dated 17 May 2017 and briefing letter dated

27 April 2017 (Exhibit A1);
·
Report of Michael Kottek dated 7 December 2018 and briefing letter dated

5 November 2018 (Exhibit A2);
·Report of Professor Arthur William Musk dated 9 April 1990 (Exhibit A3);
·Report of Professor Arthur William Musk dated 8 June 2016 and briefing letter dated 8 June 2016 (Exhibit A4);
·Report of Professor Arthur William Musk dated 12 February 2018 and briefing letter dated 2 February 2018 (Exhibit A5);
·Report of Professor Arthur William Musk dated 7 November 2018 (Exhibit A6);
·Curriculum Vitae of Professor Arthur William Musk (Exhibit A7);
·
Medical Report of Dr J Leigh dated 14 November 2018 and briefing letter dated

5 November 2018 (Exhibit A8);
·Curriculum Vitae of Dr J Leigh (Exhibit A9);
·Specifications of Materials for Marine Engineering (1938 – 1941) (Exhibit A10);
·
Journal article by A Reid, N de Lerk, G Ambrosini, N Olsen, S C Pang and

A W Musk titled “The additional risk of malignant mesothelioma in former workers and residents of Wittenoom with benign pleural disease or asbestosis” dated

10 April 2005 (Exhibit A11);
·
Journal article by A W Musk, N H de Klerk, A Reid, G L Ambrosini, L Fritschi,

N J Olsen, E Merler, M S T Hobbs and G Berry titled “Mortality of former crocidolite (blue asbestos) miners and millers at Wittenoom” dated 28 November 2007 (Exhibit A12);
·Journal article by A Reid, P Franklin, N Olsen, J Sleith, L Samuel, P Aboagye-Sarfo, N de Klerk and A W Musk titled “All-Cause Mortality and Cancer Incidence Among Adults Exposed to Blue Asbetos During Childhood” dated 9 August 2012 (Exhibit A13);
·Victor L Roggli and Anupama Sharma. “Analysis of Tissue Mineral Fiber Content” in Tim D Oury, Thomas A Sport and Victor L Roggli (eds), Pathology of Asbestos-Associated Diseases (Springer, 3^rd ed, 2004) (Exhibit A14);
·Journal article by M Kanarek and M Mandich titled “Peritoneal Mesothelioma and Asbestos: Clarifying the Relationship by Epidemiology” dated 29 March 2016 (Exhibit A15);
·Statement of Mrs Joan Aiberti dated 5 December 2018 (Exhibit A16);
·T-documents in application 2016/2882 (Exhibit R1);
·T-documents in application 2016/6960 (Exhibit R2);
·
Report of Professor Fox dated 6 August 2018 and briefing letter dated

23 July 2018 (Exhibit R3);
·Supplementary report of Professor Fox dated 14 April 2019 and briefing letter dated 26 March 2019 (Exhibit R4);
·Extract in Bruce WS Robinson and A Philippe Chahinian (eds), Mesothelioma (Martin Dunitz, 2002) (Exhibit R5);
·Journal article by J Leigh and Tim Driscoll titled “Malignant Mesothelioma in Australia, 1945-2002” (2003) (Exhibit R6);
·
Journal article by L Strand, J Martinsen, V Koefoed, J Sommerfelt-Pettersen and

T Grimsrud titled “Asbestos-Related Cancers Among 28,300 Military Servicemen in the Royal Norwegian Navy” dated 10 September 2009 (Exhibit R7); and
·Journal article by A Burdorf, M Dahhan and P Swuste titled “Occupational Characteristics of Cases with Asbestos-related Diseases in the Netherlands” dated 22 April 2003 (Exhibit R8).
LEGISLATIVE FRAMEWORK
The applications for review were made on 1 June 2016 and 21 December 2016. Neither application has been completed. By operation of s 64 in Sch 1 of the Safety, Rehabilitation and Compensation Legislation Amendment (Defence Force) Act 2017 (Cth)
(the Amending Act) a process, including the claims for compensation and these applications, are taken to have been begun under the Safety, Rehabilitation and Compensation (Defence-related Claims) Act 1988 (Cth) (the DRC Act).
Pursuant to s 64 of the DRC Act the Tribunal has the power to review the reviewable decision.
The parties’ respective SFICs, the Applicants’ closing submissions and the Applicants’ Submissions in Reply refer to the SRC Act. The Respondent’s closing submissions refer to the Amending Act and to the DRC Act and submit at paragraph 13 that “… the DRC Act now covers defence related claims which were not completed prior to the 12th October 2017. Therefore, for the purposes of these Applications, the relevant sections of the DRC Act are to be applied…” The Respondent then notes that the provisions of the DRC Act are “…identical in wording and numbering to those which appear in the corresponding sections in the [SRC] Act”.
While the Applicants do make the same observation, I am satisfied that the legislation to be applied in the present case is the DRC Act and I have treated the parties’ references to the SRC Act in their respective SFICs and submissions as references to the corresponding sections of the DRC Act.[10]
[10] See Repatriation Commission v Gorton (2001) 110 FCR 321; [2001] FCA 1194 and Burns and Military Rehabilitation and Compensation Commission [2018] AATA 35 at [27].
Section 5A of the DRC Act relevantly provides:
“injury” means:
(a)a disease suffered by an employee; or
(b)an injury (other than a disease) suffered by an employee, that is a physical or mental injury arising out of, or in the course of, the employee’s employment; or
(c)an aggravation of a physical or mental injury (other than a disease) suffered by an employee (whether or not that injury arose out of, or in the course of, the employee’s employment), that is an aggravation that arose out of, or in the course of, that employment;…
Section 5B of the DRC Act relevantly provides:
“disease” means:
(a)an ailment suffered by an employee; or
(b)an aggravation of such an ailment;
that was contributed to, to a significant degree, by the employee’s employment by the Commonwealth.
(2)In determining whether an ailment or aggravation was contributed to, to a significant degree, by an employee’s employment by the Commonwealth, the following matters may be taken into account:
(a)the duration of the employment;
(b)the nature of, and particular tasks involved in, the employment;
(c)any predisposition of the employee to the ailment or aggravation;
(d)any activities of the employee not related to the employment;
(e)any other matters affecting the employee’s health.
This subsection does not limit the matters that may be taken into account.
Section 7(1) of the DRC Act provides:
(1)Where:
(a)an employee has suffered, or is suffering, from a disease or the death of an employee results from a disease;
(b)the disease is of a kind specified by the Minister, by legislative instrument, as a disease related to employment of a kind specified in the instrument; and
(c)the employee was, at any time before symptoms of the disease first became apparent, engaged by the Commonwealth in employment of that kind;
the employment in which the employee was so engaged shall, for the purposes of this Act, be taken to have contributed, to a significant degree, to the contraction of the disease, unless the contrary is established.

By various notices made under s 7(1) of the SRC Act, which apply to the DRC Act,

the Minister has specified mesothelioma as a disease related to employment involving exposure to asbestos.
The Respondent concedes that s 7(1) of the DRC Act creates a presumption that

Mr Aiberti’s RAN service did contribute to a significant degree to his mesothelioma;

a presumption which is amenable to rebuttal if the contrary can be established.[11]
[11] Respondent’s closing submissions para. 17.
Section 14(1) of the DRC Act provides:
Compensation for injuries
(1) Subject to this Part, the Commonwealth is liable to pay compensation in accordance with this Act in respect of an injury suffered by an employee if the injury results in death, incapacity for work, or impairment.
Section 17 of the DRC Act relevantly provides:
Compensation for injuries resulting in death
…
(3)Subject to this section and to sections 16 and 18, if the employee dies leaving dependants some or all of whom were, at the date of the employee’s death, wholly dependent on the employee, the Commonwealth is liable to pay compensation in respect of the injury of $400,000 and that compensation is payable to, or in accordance with the directions of, the MRCC for the benefit of all of those dependants.
MEDICAL EVIDENCE
Professor Arthur William Musk
The earliest medical report relating to Mr Aiberti’s condition before the Tribunal is a report dated 9 April 1990 (A3) prepared by Professor Musk (then Dr Musk) who was at that time the head of the Department of Respiratory Medicine at Sir Charles Gairdner Hospital.
In that report Professor Musk outlines Mr Aiberti’s relevant history, including his time in Wittenoom and his having “worked as an apprentice electrical fitter for 18 months, spending equal amounts of time in the mine, old mill and power house” and his seven years of service in the RAN as a radio operator.
Professor Musk recorded that:
Bronchoalveolar lavage was performed on 3 May 1988. This showed numerous asbestos bodies but normal differential cell count.
…
Mr. Aiberti has a history of exposure to asbestos, crackles on asucultation of his chest, radiological evidence of pleural and mild parenchymal disease,

and impaired lung function. These changes are consistent with asbestosis resulting in mild impairment of lung function and mild disability. There has been no significant deterioration in lung function over the period of observation. Nevertheless it is likely that there will be further progression of disease and increasing disability with time. As a result of his crocidolite exposure he is at increased risk of the development of malignant pleural mesothelioma and bronchogenic carcinoma.
Dr Stephen Goode
By letter dated 14 April 2016 the Department of Veterans’ Affairs (DVA) requested
Dr Stephen Goode, described as a specialist physician in occupational medicine,
to prepare a report on Mr Aiberti in relation to his claim for compensation for peritoneal mesothelioma.[12] In his report dated 30 April 2016 Dr Goode:[13]
[12] R1, T22.
[13] R1, T23.
·Having noted Mr Aiberti’s history including his service in the RAN noted that in the early to mid-1980’s Mr Aiberti “started to develop respiratory symptoms” and that “[b]y 1987, he had further respiratory disability, such that he initiated legal action against CSR/Midalco.”[14]
·Recorded that in June 2015 Mr Aiberti started to lose weight and later developed abdominal pains and saw Dr Greg Deleuil. Following further investigation and pelvic CT scans on 2 September 2015 identified possible peritoneal mesothelioma. Following a biopsy on 5 October 2015 Mr Aiberti was diagnosed as having “peritoneal mesothelioma (of epithelioid-type) with omental and peritoneal deposits”.[15]
·Advised that on the material available (provided by Department of Defence) it was impossible to determine the extent of Mr Aiberti’s exposure to asbestos during his service in the RAN. His advice from the Department of defence was that given the age of the ships and the shore establishments that Mr Aiberti served in “it is possible that Mr Aiberti was exposed to asbestos fibres”.[16]
·Opined that “Wittenoom mine was notorious for having poor working conditions with significant dust levels and poor ventilation, and significant, largely unprotected exposure to high levels of crocidolite” referring to a 1990 report by Dr Musk et al. He also expressed the view that “[i]n the course of his RAN military service, the claimant also likely incurred some further exposure to asbestos…”[17]
·In response to the question “Do you consider that Mr Aiberti’s military service contributed in a material degree to the causation of the asbestosis and the mesothelioma conditions? If so, please specify what employment factors you consider contributed in a material degree”,[18] Dr Goode responded:
Because the claimant’s cumulative asbestos exposure – and particularly to crocidolite – was relatively very much greater at Wittenoom in the 1951 to 1957 period, this particular exposure would be considered a material contributing factor in the genesis of his pulmonary asbestosis/interstitial fibrosis. His likely very much lighter cumulative asbestos exposure – and not necessarily to crocidolite – in the course of his service in the RAN from 1957 to 1964 might only possibly have also been another material contributing factor in the genesis of his asbestosis/interstitial fibrosis.
[14] R1, T23 at 111.
[15] R1, T23 at 111.
[16] R1, T23 at 112.
[17] R1, T23 at 112.
[18] R1, T23 at 115.
In a supplementary report dated 24 May 2016,[19] Dr Goode said:
[19] R1, T24.
As stated in my previous report, the apportionment of liability between this claimant’s past non-service related and service-related asbestos exposures is difficult. The evidence of greatest value in addressing your questions regarding liability would be epidemiological evidence concerning the incidence of asbestos-related diseases in RAN Veterans exposed to the same levels of asbestos as was this claimant i.e. in the cohort of Radio Operators in the same time period. I’m not aware of any such evidence in the literature, nor has this evidence been supplied to me.
However, on the basis of the evidence supplied to date, to paraphrase my previously stated opinion, and for the reasons outlined in my previous report

(i.e. relative magnitude of exposure and fibre type), I’d opine that the claimant’s exposure to asbestos specifically in the course of his military service as a Radio Communications Officer in the RAN from 1957 to 1964 only possibly additionally contributed in a minor (rather than a material) degree to the subsequent development of his pleural plaques, asbestosis/interstitial fibrosis and malignant peritoneal mesothelioma conditions. In contrast, the claimant’s exposure to asbestos in the course of working and living in Wittenoom from 1951 to 1957 was a definite material contributing factor in the genesis of these asbestos-related conditions (as had in fact already been acknowledged in August 1996).
2.On the balance of probabilities as opposed to possibilities, and having regard to the duration, type of fibres and state of fibres associated with each exposure, what do you consider the likely extent of contribution of the employee’s service exposure to his condition(s)?
The claimant’s pleural plaques, asbestosis/interstitial fibrosis and peritoneal mesothelioma conditions were probably caused by his past exposure to asbestos in the course of working and living in Wittenoom from 1951 to 1957, with only possibly an additional (minor rather than material) contribution from his service-related asbestos exposure from 1957 to 1964.
3.In particular, do you consider the relative contribution of the employee’s exposure to asbestos during his military service was likely to be of minimal impact compared to the pre-service exposure, such that any contribution from service exposure at most could be considered de-minimus [sic]?
Yes.
Professor Musk
Relevantly Professor Musk’s career summary (A7) is as follows:
Prof AW (Bill) Musk has been a respiratory physician at Sir Charles Gairdner Hospital since 1978, Clinical Professor of Medicine at the University of Western Australia since 1992 and, Clinical Professor in the School of Population Health at the University of Western Australia since 1998. Until September 2013 Professor Musk worked as a full-time general respiratory physician with special interest in occupational lung diseases and for the final 5 years of this time spent 3 sessions funded through an NHMRC Practitioner Fellowship Grant which allowed him time to take part in research projects. He has since continued in part-time (3/10) clinical medicine which allows increased time for his research activities.
He is a graduate of the University of Western Australia and postgraduate qualifications in medicine, respiratory disease, occupational lung diseases, and epidemiology from University of New South Wales and Harvard university) and has been a respiratory physician at the Sir Charles Gairdner Hospital as well as a Clinical Professor in the Schools of Medicine and Pharmacology and of Population Health at the University of Western Australia. He has been a Chief Investigator or Associate Investigator on multiple NHMRC grants and Cancer Council grants for asbestos diseases research.
In WA Dr Musk has concentrated his research on the epidemiology of respiratory diseases and cancer particularly related to the Wittenoom blue asbestos industry, Kalgoorlie goldmining and in the Busselton population. He is responsible for the organisation of an annual mesothelioma conference in Western Australia and presents papers to local, national and international Thoracic Society conferences. He has also provided chapters on pleural diseases to authoritative textbooks.
By letter dated 8 June 2016 (A4) Mr Aiberti’s lawyers wrote to Professor Musk asking for his opinion and responses to questions. Those questions, in part, asked Professor Musk to comment on Dr Goode’s reports of 30 April 2016 and 24 May 2016.
In his response, Professor Musk referred to his report of 9 April 1990, which had not been referred to in Mr Aiberti’s lawyer’s letter of 8 June 2016. As well as Dr Goode’s reports, Professor Musk had been provided with a copy of a statement of the Second Applicant dated 9 November 2015.
In his report dated 8 June 2016 Professor Musk made the following observations in response to questions posed in the letter of instruction of 8 June 2016:
3.There is no level of exposure to asbestos below which there is no risk of developing mesothelioma: that is to say that there is no threshold level of asbestos exposure before one can attribute mesothelioma to asbestos. Amphibole varieties of asbestos, especially crocidolite (blue asbestos) are much more potent causes of mesothelioma than chrysotile (white asbestos). It is not possible to identify which specific asbestos exposures caused or materially contributed to any mesothelioma: there is nothing identifiable in the mesothelioma to guide which exposure may have been responsible.
4.Peritoneal mesothelioma can occur from exposure to all types of asbestos, crocidolite being the most potent cause.
5.Having regard to the information available as to Mr. Aiberti’s asbestos exposure and his period of service in the RAN (with reference to his signed statement of 9th November 2015) and/or the exerpt [sic] from the email of Taylor McKinna of Defence to DVA dated 5th February 2016 (referred to in Dr. Goode’s report of 30^th April 2016), it is not possible to accurately estimate the level of asbestos exposure that was sustained during Mr. Aiberti’s Royal Australian Navy Service although the opinion of an expert industrial hygienist may provide some guide.
…
7.Peritoneal mesothelioma can occur in circumstances of asbestos exposure of the nature and extent of that likely to have been sustained by Mr. Aiberti in the course of his RAN service as there is no level of exposure below which there is no risk of developing malignant mesothelioma of the pleura or peritoneum.
8.Mr. Aiberti’s RAN service is certainly within the latency period for peritoneal mesothelioma as it occurred over 50 years ago. Therefore in my opinion it can be said that on the balance of probabilities Mr. Aiberti’s RAN asbestos exposure materially contributed to his risk of developing peritoneal mesothelioma even though the magnitude of this risk would have been much less than that resulting from his Wittenoom exposures.
9.In my opinion Mr Aiberti’s RAN service contributed to his risk of developing peritoneal mesothelioma
10.In the context of Mr. Aiberti’s Wittenoom asbestos exposure it is my opinion that it is still not possible to assert that the RAN service did not materially contribute to his peritoneal mesothelioma even though the risk would have been much less.
11.ln my opinion it is not possible to assert that Mr. Aiberti’s RAN exposure did not materially contribute to his peritoneal mesothelioma even though its contribution to his risk would have been much less than the risk of mesothelioma from his Wittenoom exposures.
Professor Musk provided a further report dated 12 February 2018 (A5). At that time Professor Musk had been provided with a copy of reports of Mr Michael Kottek dated

17 May 2017 (see [63] below) and a copy of the Specifications of Material for Marine Engineering, Engineer in Chief Department, Admiralty (clauses 472-4 only). In that report of 12 February 2018 Professor Musk said:
1.Mr. Kottek’s opinion does not change the opinions expressed in my letter of 8^th June 2016. I note that Mr. Aiberti’s exposure to asbestos (amosite and chrysotile) in the RAN would have been considerably greater than that experienced by the general population and orders of magnitude above general environmental levels but its contribution to his risk of developing mesothelioma would have been less than his risk from crocidolite exposure at Wittenoom.
2.It remains my opinion that Mr. Aiberti’s exposure to asbestos during his RAN service contributed to his risk of developing peritoneal mesothelioma but this risk contribution would have been much less than the Wittenoom crocidolite exposure which was earlier and likely to have been much greater because the risk of mesothelioma is greatest from crocidolite exposure, related to the degree of exposure and increases with time since exposure. Had the RAN exposure been his only asbestos exposure then it could be considered to have made a material contribution to his peritoneal mesothelioma, however even though it may have contributed to his risk of mesothelioma, the relative contribution would have been less.
Professor Musk provided a further report dated 7 November 2018 (A6). That report was a response to the Applicants’ lawyer’s request to comment on certain matters, in particular Professor Fox’s report of 6 August 2018 (see [59]-[60] below]).
In his report of 7 November 2018 Professor Musk makes the observation that Professor Fox’s review of published information in his report was not inconsistent with Professor Musk’s reports. He then observes:
The important issue, I understand, as per my report, is which exposure of

Mr. Aiberti can be held responsible for the development of mesothelioma and I again advise that it is not possible to say which exposure was entirely responsible. I can only repeat my previous opinion that had the RAN exposure been his only asbestos exposure then it could be considered to have made a material contribution to his peritoneal mesothelioma. However, even though it may have contributed to his risk of mesothelioma, its relative contribution would have been much less than that of the Wittenoom exposures and there is no way of separating the contributions except on a probability basis.
Professor Fox’s references are not useful and simply support my previous assessment. l do not consider that it is possible to exclude any documented asbestos exposure as a contributor to his risk and therefore to the development of his disease. Professor Fox also appears to have misinterpreted my report which does not say that “his prior exposure in the naval service would have been the primary cause of his mesothelioma”. The fundamental issue is that there is no demonstrated safe level of exposure so that I believe that the RAN exposure cannot be entirely discounted.
Professor Richard Fox AM
Professor Fox’s evidence at the hearing as to his qualifications was:[20]
·Standard medical qualifications, MBBS with First Class Honours from the University of Sydney.
·BSc (Med) in Medical Science from the University of Sydney.
·PhD in Medicine from the University of Sydney.
·Fellowship of the Royal Australian College of Physicians.
[20] Transcript at 90-91.
Professor Fox’s evidence as to his relevant experience was:[21]
…as part of my general medical training to become a physician, I spent several months in a Thoracic Medicine ward, so we would see all sorts of pulmonary diseases and then, as a medical oncologist for some 30 years, I saw considerable numbers of patients with mesothelioma. In the last several years since retirement from active practice at Royal Melbourne Hospital I have been involved in a lot of medicolegal work-related work consultation and have seen a large number of patients with mesothelioma at the order of over 50 a year.
[21] Transcript at 91.
Professor Fox’s evidence was that he has previously given evidence before the Administrative Appeals Tribunal although he thought not on mesothelioma but in other malignancies and had given evidence on mesothelioma in other jurisdictions.
In a report dated 6 August 2018 Professor Fox, having summarised Mr Aiberti’s history of working in Wittenoom and serving in the RAN, makes the following comments:
3. MESOTHELIOMA AT WITTENOOM
I note a paper by Dr A W Musk et al entitled “Mortality of former crocidolite

(blue asbestos) miners and millers at Wittenoom”. This was published in the Journal of Occupational and Environmental Medicine in 2016.
It notes that nearly 7,000 male workers who worked at the Wittenoom mine and mill had been followed up using death and cancer registries throughout Australia and Italy to the end of 2000.
Person years at risk were derived using two sensory dates in order to produce minimum and maximum estimates of asbestos effect. It notes that there have been 190 cases of pleural and 32 cases of peritoneal mesothelioma in this cohort of former workers at Wittenoom.
I note this is a ratio of 1 case of peritoneal to 5.5 cases of pleural mesothelioma.

I note this is double to triple the ratio of peritoneal to pleural compared to other exposures.
This I would assume is a sequel of the intensity of exposure and also exposure to crocidolite.
This equates with the papers by Hodgson and Darnton “Quantitative risks of mesothelioma and lung cancer in relation to asbestos exposure”. This was published in the Annals of Occupational Hygiene in the year 2000.
This notes the ratio of exposure specific risk of mesothelioma as 1 to 1, in 100 to 1, in 1 to 500 for chrysotile, amosite and crocidolite respectively ie crocidolite is 500 times more potent is [sic] causing mesothelioma than chrysotile.
lt is important to note the paper by Reid, A including Musk and colleagues entitled “All cause mortality in cancer incidence among adults exposed to blue asbestos during childhood”. This is published in the American Journal of Industrial Medicine in 2013.
It notes the standardised incident rates among males who first arrived at Wittenoom under the age of 15 compared with the male West Australian population.
This notes the standardised incidence ratios of 44.5 to 77.5 (depending on exact methods of calculation).
These are extraordinarily high.
4. MESOTHELIOMA IN NAVAL PERSONNEL
There are a few publications regarding mesothelioma in naval personnel (both military and merchant marine). In these publications there is no distinction between pleural and peritoneal.
I have not seen a peritoneal mesothelioma in naval personnel.
a)The Burdorf, A paper et al. This is entitled “Occupational characteristics of cases with asbestos related diseases in the Netherlands”. This was published in the Annals of Occupational Hygiene in 2003.
This is from the Erasmus University Medical Centre in Rotterdam,

The Netherlands.
It notes that in the insulation industry the overall risk of mesothelioma was

5 out of 100 workers and in the ship building industry 1 out of 100 workers.
This is a considerably smaller ratio compared to the outcome in Wittenoom.
b)“Asbestos related cancer among 28,300 military servicemen in the Royal Norwegian Navy”. This was published in the American Journal of Industrial Medicine in 2009.
There were some 22 cases of mesothelioma reported in 28345 naval staff ie an incidence of 1 in 1417.
c)There is a paper entitled “Asbestos related cancers in seamen”. The original is in Italian but there is an abstract in English. This was published in the Italian literature. It is from University Clinic in Trieste, Italy.
It notes a significant excess of mesothelioma in seamen and marine engineers with a standardised incidence ratio between 1.83 and 4.8 as a function of years of exposure.
d)The UK paper entitled “Mortality among United Kingdom servicemen who served abroad in the 1950s and 1960s”. This is by Darby, SC from the Cancer Epidemiology Unity at the University of Oxford. This paper was published in the British Journal of Medicine in 1990.
This is a study of mortality among a group of 30,619 United Kingdom servicemen who served abroad in tropical or desert areas in the 1950s and 1960s and who remained in the services for a total of at least five years.

Of these 12,939 were in the Royal Navy.
Mortality from all causes of death or neoplasms etc was documented.
(It notes examination and mortality in each of the 3 services separately identified. There were 7 deaths from mesothelioma in Navy staff ie a risk of 1 in 1848, not dissimilar, from that seen in the Norwegian navy.
I note this is dramatically less than that seen in Wittenoom particularly those arriving before the age of 15 where the risk factors were in the 40s and seventyfold.
In terms of asbestosis there does not appear to be documented figures of the risk in naval military personnel. This is despite health surveys. I presume this reflects the lack of intense exposure in naval personnel.

Professor Fox responds to specific questions as follows:
3.You ask me to describe the relevant pre-existing or non-work related history and the significance of the history to the peritoneal mesothelioma? You ask when answering this question, could I please give consideration to Mr S Aiberti’s employment history prior to his service in the RAN and the fact that Mr S Aiberti lived in the town of Wittenoom?
I have described above the studies by Musk and Reid regarding growing up in Wittenoom, working in Wittenoom and the significantly high risk of development of mesothelioma. There are suggestions that the rate of mesothelioma at Wittenoom may approach 1 in 10 of the workers. This is- less than 1 % of the rates in naval personal noted above.
In particular, the paper by Musk noting the high ration of peritoneal to pleural ie., 1 to 5.5 as distinct to the much lower ratio in non-Wittenoom areas, is evidence of the intensity of exposure at Wittenoom both at a residential and occupational level.
4.You ask, would Mr S Aiberti have developed the peritoneal mesothelioma as a natural progression irrespective of his service in the RAN?
My answer to this is yes given the known high incidence of mesothelioma in general and in particular peritoneal mesothelioma in those that lived and worked in Wittenoom.
5.You ask me to consider Mr S Aiberti’s service in the RAN and any contribution from his RAN service to the peritoneal mesothelioma condition having regard to a) duration of employment, b) nature of particular tasks involved in his employment, c) any predisposition of the employee to the ailment or aggravation, d) any activities of the employee not related to the employment and e) other factors effecting the employee’s health?
I note the various reports that you have received from Dr Musk, Mr Kotteck [sic] and Dr Goode who have noted that his prior exposure to naval service would have been the primary cause of his mesothelioma.
They have not addressed what might be the differences in specific risk, living and working at Wittenoom compared to the Royal Australian Navy.
There are few specific documentations of the incidence of mesothelioma in naval personnel. It is clearly significantly dramatically less than that at Wittenoom.
The British & Norwegian navy reports document the low rates of mesotheliomas c/f Wittenoom, by orders of magnitude.
This would suggest/ prove there was not a significant contribution to the development of Mr Aiberti’s mesothelioma while working in the Royal Australian Navy.
My comments accord with those of Dr Goode that his naval service was

de minimus [sic].
6.You ask, having regard to the factors outlined above you ask;
a)Is it as probable as distinct from possible that his service in the RAN contributed to the development of the peritoneal mesothelioma condition?
On the balance of probabilities, any contribution would have been de minimus [sic].
b)You ask if so what specific service factors contributed to the peritoneal mesothelioma condition?
Obviously there is a level of asbestos exposure in naval service but it is low (de minimus) [sic] – 2 orders of magnitude compared to Wittenoom.
The other factor apart from intensity of exposure is that the Wittenoom exposure was purely crocidolite with its much higher risk of mesothelioma.
c)You ask, was the contribution proportion significant, material or de minimus [sic]?
I have described this as de minimus [sic] based on a comparison between what appears to be the incidence in naval personnel versus those that lived and worked in Wittenoom.
Professor Fox provided a further report dated 14 April 2019 (R4) in which he noted that he had been provided with further reports from Professor Musk, Dr J Leigh and Mr Kottek. Professor Fox observes:
I note the following regarding Prof Musk’s report. This is dated 7th November 2018.
He states in regard to the Wittenoom exposure and the naval exposure “It is not possible to say which exposure was entirely responsible”.
He said he could “only repeat his previous opinion that the RAN exposure had made a material contribution.
He noted, “Even though it may have contributed to his risk of mesothelioma,

its relatively contribution would have been much less than that of Wittenoom exposures and there is no way of separating the contributions except on a probability basis”.
He does not attempt to express this probability basis. I considered, in my earlier report that the probabilities could be determined by the relative risks of the two exposures, based on known epidemiology studies.
I note Prof Musk’s extensive publications in the risks of mesothelioma at Wittenoom. There are papers expressing an SIR of 44.5 fold to 77.5 fold. As well data suggested that the risk for those who worked and lived in Wittenoom was a mesothelioma rate of the order of 1 in 10.
The Wittenoom experience is often stated as the greatest occupational disaster in Australia. This reflects both intensity of exposure, but as well the exposure was to crocidolite, the most potent of the asbestos types re mesothelioma causation.
I noted in my prior report regarding the Norwegian Navy that the risk of mesothelioma was approximately 1 in 1417 and a similar rate in the British Navy of approximately a risk of 1 in 1848. This was based on data in the papers I had mentioned in my report.
This would allow an assessment that the risk of mesothelioma in naval work

(I have assumed it is similar in the Australian Navy), of between 140 and 180 fold less than that of the Wittenoom exposure.
This alone allows an assessment of the relative contribution of Wittenoom exposure versus the RAN exposure.
This would indicate a de minimis or risk less than material ie non significant.
…
I note he mentions a paper by Rafnsson, V entitled, “Cancer incidence among marine engineers, a population-based study in Iceland”. This was published in Cancer Causes & Control in 2003.
…
There did not appear to be any increased risk of mesothelioma among deck officers. They obviously would have lived and slept etc. inside the ship and would have been exposed to such lagging there.’
…
Mr Aiberti was not a marine engineer.
…
a) Is it probable as distinct from probable [sic] that his service in the RAN contributed to the development of his peritoneal mesothelioma condition?
My opinion is there would have been a contribution but de minimis, ie., less than material.
…
There was the potential for asbestos exposure in RAN ships but this would have been much lower than in Wittenoom, based on data re the relative risks.
…
Based on my analysis above, I would suggest his contribution was less than material. That is, it was a mere contributing factor.
Mr Michael Kottek
Mr Kottek describes himself (A1) as an occupational and environmental health consultant. His curriculum vitae (A1, pages 3 of 6 to 6 of 6) relevantly reveals that Mr Kottek:
·has:
oBSc (Hons): University of Melbourne 1984-1987 major in botany
oMSc: University of Melbourne 1991-1993 major in history and philosophy of science
oGraduate Diploma of Occupational and Environmental Health: Monash University 1996-1997
oLLB Hons: University of Melbourne 1996-2003;
·has held various research positions for government and in the private sector and has published and presented at conferences widely on public health issues including exposure to asbestos, lead and other environmental hazards;
·has been in private consulting from 1999 and has given evidence in the Supreme Courts of Victoria and Western Australia, the County Court of Victoria, the Dust Diseases Tribunal of NSW, the District Court of South Australia and the Administrative Appeals Tribunal; and
·is a member of:
oAmerican Board of Industrial Hygiene – Certified Industrial Hygienist;
oAmerican Conference of Governmental Industrial Hygienists – Associate Member;
oAustralian Institute of Occupational Hygienists – Full Member, Certified Occupational Hygienist; and
oBritish Occupational Hygiene Society – Member.
In his report dated 17 May 2017 Mr Kottek made the following observations:
While on the Swan, Mr Aiberti was required to spend a considerable time in the boiler room burning paper records. The vessel also had sprayed insulation on the bulkheads; I am unaware of any asbestos free sprayed insulation being used on naval vessels in the period in which Mr Aiberti served. Mr Aiberti was on the Swan when it was undergoing a refit at Garden Island; he refers to carrying out chipping during the refit…
The Swan was also subject to vibration during regular gunnery practice which would release dust from lagged surfaces. Mr Aiberti’s exposure in the RAN is consistent with exposure that has been described in other matters I have been involved in.
Relying on Mr Aiberti’s statement and documents from other matters involving exposure aboard RAN vessels, in my opinion Mr Aiberti would have been exposed to asbestos during his RAN service… It is unclear if the sprayed insulation on the Swan would have contained brown or blue asbestos. The pipe and boiler lagging on naval vessels was often friable sectional lagging with a very high amosite content, such as Caposite…
ln my opinion, all the vessels Mr Aiberti served on would have contained asbestos insulation materials for pipes and plant, and some contained sprayed asbestos insulation on bulkheads. These materials release airborne asbestos fibres when subject to disturbance, and these materials would have been disturbed from programmed maintenance and breakdown repairs as well as incidental disturbance such as from vibration during manoeuvres and gunnery practice. Given the extent of Mr Aiberti’s presence in the boiler room of the Swan, in my opinion, it is likely that there would have been instances when programmed maintenance or breakdown repairs occurred in the engine room while he was present.
Is it possible to estimate the level of asbestos exposure he is likely to have sustained during his RAN service and/or to categorise it in terms of light, heavy or medium?
In my opinion there is insufficient information to attempt a meaningful quantification of the levels of airborne asbestos Mr Aiberti’s experienced over his RAN service. However, in my opinion, he is likely to have experienced ongoing low level exposure when working onboard ship, interspersed with periods of moderate and/or heavy exposure when he was in the vicinity of lagging and/or spray which was subject to physical disturbance.
…
What type of asbestos was Mr Aiberti likely to have been exposed to during his RAN service?
Even with with the the [sic] limited information available, in my opinion there is little reason to doubt that Mr Aiberti was exposed to amosite and chrysotile asbestos during his service with the RAN. It is less clear if he would have experienced exposure to crocidolite, which may have been present in sprayed asbestos coatings on bulkheads/deckheads…
Any comments or observations on the opinions expressed in the reports of

Dr Goode dated 30 April 2016 and 24 May 2016 and Professor Bill Musk dated

8 June 2016?
I partially disagree with Dr Musk’s opinion that crocidolite is the most potent cause of peritoneal mesothelioma. In their seminal meta-analysis, Hodgson & Darnton, proceeded on the basis that the exposure response relationship for pleural and peritoneal mesothelioma differed, such that as exposure increased,

‘each additional unit of exposure will add – progressively – less risk for pleural tumours, and more for peritoneal tumours.’ They estimated that the risk of peritoneal mesothelioma became higher than the risk of pleural mesothelioma for exposures exceeding around 90 f/ml·yr of crocidolite exposure and 55 f/ml·yr of amosite exposure. While the absolute risk of mesothelioma is higher for crocidolite exposure, given the different exposure response relationships; there may be situations where at high levels of cumulative exposure, amosite exposure is a more potent cause of peritoneal mesothelioma than crocidolite.
Given the somewhat peculiar nature of Mr Aiberti’s exposure to both crocidolite and amosite, there is considerable difficulty in extrapolating the Hodgson & Darnton meta-analysis to his particular circumstances. In any event, the attribution of disease in an individual is beyond my expertise and a matter for medical evidence.
Mr Kottek provided a further report dated 7 December 2018 (A2) largely commenting on Professor Fox’s report dated 6 August 2018 and Professor Musk’s report dated

12 February 2018 (see [53] and [59]-[60]). Mr Kottek refers to a number of the studies of the incidence of mesothelioma in naval personnel cited in Professor Fox’s report and concludes:
In my opinion the above papers clearly indicate that naval personnel are at increased risk of mesothelioma.[22]
[22] A2 at 2.
Mr Kottek goes on to comment as follows:[23]
[23] A2 at 4.
Considering the epidemiological evidence above, if Mr Aiberti’s RAN exposure was considered in isolation: in my opinion his exposure in the RAN would have placed him at a significantly increased risk of mesothelioma.
In contrast, Professor Fox expresses the view that:
The British & Norwegian navy reports document the low rates of mesothelioma c/f Wittenoom by orders of magnitude.
I cannot see where in his report Professor Fox makes an explicit comparison of reported rates of mesothelioma, particularly any comparison which demonstrates that the rate of mesothelioma in naval personnel is orders of magnitude

(at least 100 times) less than Wittenoom residents/workers. Given the limited information available, I do not agree with Professor Fox that Mr Aiberti’s RAN exposure is necessarily de minimus.
I note again that the attribution of disease in an individual is beyond my expertise and a matter for medical evidence, and that circumstances of Mr Aiberti’s exposure to asbestos are quite peculiar. However, considering the available information in my opinion there seems little reason to doubt that Mr Aiberti’s residence and work at Wittenoom would have created a considerably greater risk of mesothelioma than his service in the RAN. Given the limited information available on the exact magnitude and composition of Mr Aiberti’s exposure to asbestos and the limited epidemiological evidence; in my opinion any attempt to quantitatively apportion his risk of mesothelioma would be quite speculative.
Dr James Leigh
Dr Leigh provided a report dated 14 November 2018 (A8). Dr Leigh’s relevant experience and qualifications, as set out in his report and curriculum vitae, are:
·MB BS (Sydney) 1967 (Prosector in anatomy in 1963);
·PhD (Sydney) 1972 (Medicine) (Thesis);
·MD (Sydney) 1992 (Published work);
·BSc (Hons) [MSc (Prelim)] (Monash) 1974 (Applied Mathematics);
·MSc (Sydney) 1980 (Applied Mathematics) (Thesis);
·MA (Sydney) 1981 (Pre Mathematics) (Pass with merit);
·Post-graduate Diploma in Numerical Analysis and Automatic Computing (Sydney) 1969 (Diploma in Computer Science);
·BLegS (Macquarie) 1989;
·Barrister Supreme Court NSW 1993;
·
Carrying out research and teaching in occupational respiratory medicine for

53 years and in asbestos related diseases for 31 years;
·Member of the National Health and Medical Research Council (NHMRC) Asbestos Working Group;
·Honorary Senior Research Consultant to NSW Asbestos Diseases Research Institute (University of Sydney);
·
1988-2001: Co-ordinator of the Australian Mesothelioma Register

(Federal Government);
·1988-1997: Head of Epidemiology Unit at the National Occupational Health and Safety Commission;
·Published 138 peer reviewed papers and 167 other publications; and
·Fellow of the Faculties of Occupational Medicine and Public Health Medicine of the Royal Australasian College of Physicians.
In his report Dr Leigh summarises Mr Aiberti’s exposure to asbestos at Wittenoom and in the RAN. He then provides an extensive summary of relevant scientific studies. In the case of Mr Aiberti he says:
All exposure, recalled and unrecalled or unrecognized, would have contributed cumulatively to the risk and cause of the mesothelioma. The detail provided is insufficient to make any reliable quantitative estimate of exposure. It is impossible to know with any accuracy what the exposure intensities were, what the fibre types were, and what the durations of exposure were…
Workers at Wittenoom are well recognized to be at high risk of mesothelioma. Estimated lifetime mesothelioma risk for workers at the mine or mill is 16.6 % and for working or living in Wittenoom Town 3.1% (Leigh and Driscoll Int J 0cc Env Health 2003;9:206-217).
ln the Australian Mesothelioma Register cases 1/1/86-31/10/2001,162/3956 gave as their only exposure navy/merchant navy, 66 more had such exposures plus additional exposures. Of the 162 navy/merchant navy only exposed cases, 5 were peritoneal mesothelioma… There have been many further cases of this type since 2001. In WA alone there have been 27 cases in armed forces and 11 cases in ship building from 2000-2009 (Musk et al MJA 2015;203:251-252)…
Workers in ships are well recognized to be at high risk of mesothelioma. Estimated lifetime mesothelioma risk for workers in navy/merchant navy is 5.1 % (Leigh and Driscoll Int J 0cc Env Health 2003;9:206-217).
…
There is a dose response relationship between cumulative asbestos exposure and mesothelioma risk, with no known threshold.
…
My opinion, based on my understanding of current scientific literature is that, in view of the capacity of asbestos fibres to be involved at all stages of tumour development, all cumulative exposure to asbestos in an individual case must be playing some contributory part in causation...
There is nothing about Mr Aiberti’s exposure having caused or contributed to causation of his peritoneal mesothelioma that is contrary to medical knowledge. Whilst it is true that peritoneal mesothelioma is proportionally more common (compared to pleural) in heavier exposed cohorts, peritoneal cases can occur at quite low exposures ,with no threshold (Leigh et al Cancer 1991;68:135-141;...
…
Chrysotile is generally considered to be a cause of mesothelioma but less potent in causing mesothelioma than crocidolite or amosite. Quantitative estimates of the relative dose related risk of the two fibre types vary widely (crocidolite 2-500 times more potent per unit fibre inhaled than chrysotile, amosite intermediate)… Hodgson and Darnton in a review of selected epidemiological cohort studies gave a very approximate summary ranking of relative potency crocidolite: amosite:chrysotile of 100:10:1 at low exposure levels and 500:100:1 at high exposure levels … More recent analyses of relative potency using a similar selection of cohorts (but with some significant exclusions) by Berman and Crump (Crit Rev Tox 2008;38(S1) 1-47, 49-73) give similar results…
There was no evidence of erionite or nuoro-edenite exposure in the present case. There was a history of significant asbestos exposure at Wittenoom 1950-1957 (mainly crocidolite) and in the RAN 1957-1964 (chrysotile, crocidolite and amosite). In my opinion it was more probable than not that each of these exposure: episodes would have added to the “background” exposure and increased the risk of mesothelioma. This risk has now been expressed and in my opinion it was more probable than not that each exposure would have made a material contribution to causation. As stated above there is no level of asbestos exposure below which there is no risk of mesothelioma, and the evidence for other factors causing mesothelioma is in my opinion, no more than anecdotal. The Wittenoom exposure would have made the greater contribution and could alone have caused the mesothelioma, but the RAN exposure in my opinion would have made a material contribution to causation and certainly not a “de minimus” [sic] contribution. ln the hypothetical situation of no Wittenoom exposure, the RAN exposure would very probably have been the cause.
To quantify the relative contributions requires data on the timing, duration, intensity and fibre types of the RAN and Wittenoom exposures. Obtaining or estimating such data is not my field of expertise.
While all exposures contribute incrementally to the overall risk, earlier exposures can probably be given more weight. The Peto model where risk is related to exposure level multiplied by time since exposure…
THE PARTIES’ SUBMISSIONS

The facts are largely not in dispute. The differences between the parties are as to which of the medical evidence should be preferred and what that evidence establishes relevant to the requirements of the DRC Act. A further issue, relating only to the First Applicant,

is whether s 48 of the DRC Act applies because of the payment received by Mr Aiberti from CSR Limited and Midalco Pty Ltd (see [23]-[24] above).
The parties, in effect agree, or do not dispute, the following matters:
(a)Mr Aiberti was exposed to asbestos at Wittenoom and during his RAN service.
(b)
Whilst all asbestos causes mesothelioma, crocidolite (blue asbestos) is accepted to be the most potent in causing mesothelioma, followed by amosite

(brown asbestos), and then chrysotile (white asbestos).[24]
(c)Mr Aiberti’s exposure to asbestos in Wittenoom was more significant than in the RAN.[25]
(d)The type of asbestos that Mr Aiberti would have been exposed to in the course of his service in the RAN is not clear.[26]
(e)Peritoneal mesothelioma, subject to satisfaction of the requirements of s 5B(1) of the DRC Act, is to be regarded as a disease.[27]
(f)Because Mr Aiberti’s condition was not diagnosed until 2015 the claims are to be determined under the DRC Act.[28]
(g)Section 7(1) of the DRC Act applies and creates a presumption that Mr Aiberti's RAN service did contribute, to a significant degree, to his mesothelioma which presumption is amenable to rebuttal if the contrary can be established.
[24] Applicants’ closing submissions para. 31.
[25] Applicants’ closing submissions paras. 11 and 32.
[26] Applicants’ closing submissions para. 35.
[27] Respondent’s closing submissions para. 13.
[28] Respondent’s closing submissions para. 13.
The Applicants’ Submissions – Significant contribution
In relation to the issue of whether Mr Aiberti’s RAN service contributed to his development of mesothelioma, to a significant degree for the purposes of s 5B of the DRC Act,
the Applicants submit:[29]
[29] Applicant’s closing submissions at 5-20.
·
The purpose of amending the word “material” to “significant” in s 5B of the DRC Act, as explained in the Explanatory Memorandum of the Safety, Rehabilitation and Compensation and Other Legislation Amendment Bill 2006, was to strengthen the connection necessary between the employment and the contraction

(or aggravation) of the disease, citing Comcare v Power (2015) 238 FCR 187; [2015] FCA 1502 (Comcare v Power) at [93].
·
It is insufficient if the contribution of the employment is more than trivial

(being material), it must be substantially more than trivial to be significant, again citing Comcare v Power at [93].
·The determination as to whether the necessary threshold has been established, is an evaluative exercise that includes consideration of a non-exhaustive list of factors, some of which are set out in s 5B(2) of the DRC Act citing Comcare v Power at [94].
·It is beside the point that one factor contributes greater than another. Nor does it matter that factors outside the employment also contribute to a significant degree. The DRC Act does not require the employment to be the sole, proximate or dominant cause of the injury; rather, the Tribunal must be satisfied, on the balance of probabilities, that the contribution was a significant contributing factor, which is a question of fact to be determined by the Tribunal in each case, citing Comcare v Power at [94].
·To rebut the presumption under s 7(1) of the DRC Act the Tribunal must be satisfied, on the balance of probabilities, that Mr Aiberti’s exposure to asbestos in the RAN did not contribute, to a significant degree, to his mesothelioma citing Freeman and Military Rehabilitation and Compensation Commission (Compensation) [2016] AATA 741 (Freeman and MRCC) at [98].
·To be satisfied on the balance of probabilities, the Tribunal is not required to be satisfied with certainty or precision (Tabet v Gett [2010] HCA 12 at [145] – [149]; White and Military Rehabilitation and Compensation Commission [2017] AATA 1555 [80]). An assessment on the balance of probabilities is not a mathematical calculation but simply a matter of an assessment of what is human experience (Sydney South West Area Health Service v Stamoulis [2009] NSWCA 153 at [139] (Stamoulis); Fazio v Fazio [2012] WASCA 72 at [46]), and the question of what is probable is where the person judging the probability of that thing has the appropriate degree of confidence in its existence or correctness based on or judged according to reason (Stamoulis at [140]-[141]).
·
Epidemiological evidence may be utilised, particularly in cases like the present (Seltsam Pty Ltd v McGuinness (2000) 49 NSWLR 262; [2000] NSWCA at

[93]-[94]).
·Where an expert witness expresses an opinion on the ultimate issue in the case it is important that the decision-maker recognises that this has occurred and ensures that the expert, in reaching that opinion, has correctly applied the relevant legal test upon which the ultimate issue turns (Wiegand v Comcare Australia [2002] FCA 1464 (Wiegand) at [30] per von Doussa J).
·
All asbestos exposure has a cumulative effect in causal contribution to the ultimate development of a mesothelioma, based upon the understanding of physiological mechanisms and not epidemiology (Amaca Pty Ltd v Booth [2011] HCA 53;

(2011) 246 CLR 36 (Amaca v Booth) at [51]).
·There are authoritative studies that put the position beyond any doubt that both workers in Wittenoom and RAN personnel are in a category of occupations that carry significant risks for developing mesothelioma due to occupational exposure to asbestos.
·Mr Aiberti’s exposure to asbestos during his service in the RAN and how asbestos causes mesothelioma establishes that his service in the RAN was a significant contributing factor to the development of his peritoneal mesothelioma because:
oHe was likely exposed to low to high quantities of crocidolite, amosite and chrysotile during his seven years in the RAN, which was significantly higher than background environmental exposure. Considering the duration of his service with the RAN and, the occasions his service would have resulted in him being exposed to asbestos (as is detailed in Mr Aiberti’s statements and Mr Kottek’s reports), his level of exposure to asbestos during his RAN service alone placed him at a significant risk of suffering mesothelioma given:
(i)there is no level of exposure to asbestos that does not result in an increased risk in developing mesothelioma;
(ii)RAN personnel in Australia, as in other international studies examining the incidence of mesothelioma in naval and merchant shipping occupations, are at a significantly increased risk of suffering mesothelioma even if the exposure was of a short duration; and
(iii)in the hypothetical situation that Mr Aiberti’s only exposure to asbestos was during his service in the RAN, it was sufficient to have caused his peritoneal mesothelioma.
·The Respondent relies primarily on Professor Fox. The evidence of Mr Kottek, Professor Musk and Dr Leigh should be preferred over that of Professor Fox as they have greater expertise in epidemiology and biological research in asbestos related disease. Professor Fox has had no training in epidemiology, and has conducted no epidemiological or biological research into asbestos related diseases whereas:
oMr Kottek has postgraduate training in epidemiology at Monash University and expertise in epidemiology.
oProfessor Musk holds postgraduate qualifications in epidemiology from Harvard University and has authored or co-authored hundreds of research articles specifically related to asbestos related disease.
oDr Leigh was the head of the Epidemiology Unit at the National Occupational Health and Safety Commission for almost 10 years and has authored 141 peer reviewed research articles, of which half are specifically related to asbestos related lung disease, and which included research in lung pathology.
·The differences in expertise between Professor Fox and the other experts is stark and offers a starting point to explain their differences in opinion. In particular, epidemiology is concerned with an evaluation of risk to which an inference of causation may be drawn; it is not direct evidence of causation in an individual case. The limit to which epidemiology assists in determining causation in this case was demonstrated in the following evidence:
oMr Kottek explained that, in relative terms, Mr Aiberti’s exposure in Wittenoom is more important as to risk; however, he could not express an opinion as to causation in an individual case. He otherwise expressed the opinion that the risk posed by the RAN exposure was, in and of itself, significant.
oProfessor Musk, in his evidence, demonstrated the difference between risk and causation. In his report dated 8 June 2016, he explained that it is not possible to identify which specific asbestos exposures caused or materially contributed to any mesothelioma. He explained that whilst the Wittenoom exposure was more significant, based on statistical evidence, it does not “tell us what actually happened”.
oProfessor Musk explained that the RAN exposure on its own was significant in increasing Mr Aiberti’s risk of suffering mesothelioma.
oDr Leigh explained that risk is a different concept to causation in an individual case and is not the same as comparing occupational groups and measuring the risk of developing mesothelioma based on incidence rates, because in this case the probability of Mr Aiberti getting mesothelioma was now one. In other words, Mr Aiberti’s risk of developing mesothelioma posed by the two occupations in which Mr Aiberti was exposed to asbestos, has come home.
oDr Leigh and Professor Musk explained that it not a matter of competing risks when comparing the risk from each of the two exposures.
oDr Leigh explained that the exposures are not divided; rather, they are cumulative and any exposure 10 years before the occurrence of the tumour is relevant.
oProfessor Fox concluded, contrary to the other experts, that because the epidemiology evidence confirmed that Mr Aiberti’s risk of developing mesothelioma was greater because of his exposure to asbestos at Wittenoom when compared to the RAN exposure, it meant that the RAN’s contribution was de minimis.
·Both occupations significantly increased Mr Aiberti’s risk of developing mesothelioma, with the Wittenoom exposure being greater than the RAN exposure. However, there is no evidence to say that means the RAN exposure was de minimis.
·Mr Aiberti’s exposure to asbestos in Wittenoom and in the RAN cumulatively contributed to the risk of him developing mesothelioma. The RAN exposure to asbestos was, in and of itself a significant risk factor and there is no evidence the Wittenoom exposure diminished or lessened the contribution the RAN exposure made to Mr Aiberti’s risk of developing mesothelioma. Professor Fox agreed the more fibres an individual is exposed to the greater the risk.
·Continued exposure to asbestos in the RAN, if it did not initiate, would have proliferated the genetic change that ultimately caused Mr Aiberti’s mesothelioma (Dr Leigh).
The Respondent’s submissions – Significant contribution
The Respondent disagrees with the Applicants’ submission that the “new test” under s 5B of the DRC Act, that is the change in the wording from “material” to “significant” has created consternation and submits that the position is clearly set out in Comcare v Power. The Respondent points to Katzmann J’s judgment wherein her Honour:
(a)Highlighted from the Minister’s second reading speech the statement (at [84]) that:
It is intended the test will require an employee to demonstrate that his or her employment was more than a mere contributing factor to the contraction of the disease. Accordingly, it will be necessary for an employee to show there is a close connection between the disease and the employment in which he or she was engaged.
(b)Observed:
90. The first of the principal amendments identified in the EM was the amendment to the definition of ‘disease’. Its purpose, it was said, was

‘to strengthen the connection between the disease and the employee’s employment’. One of the examples of the ‘court interpretations of the legislation’ which was implicitly criticised was the interpretation given by the Full Court in Treloar. The Regulation Impact Statement included in the EM referred under ‘[d]efinition of “disease”’ to the italicised passage in the Second Reading Speech extracted in the joint judgment in Canute

(see above at [84]) and said:
‘It was the original intention of the SRC Act that an employee’s eligibility for compensation payments for a disease suffered by the employee should require a close causal connection between the employee’s work and the contraction or aggravation of the disease. The causality test requires an employee’s employment to have contributed in a “material degree” to the contraction or aggravation of the disease.’
91. The Statement acknowledged what had been said in Canute but added that the comments made there might ‘reduce the erosion in the meaning’ but were ‘yet to be tested at law’.
92. Several options were canvassed and their potential impacts assessed. The option of requiring employment to make a ‘significant contribution’ to the contraction of a disease was recommended, amongst other reasons, because it was ‘considered to provide a stronger causal connection between an employee’s employment and the contraction or aggravation of a disease’ than the existing test, even if ‘material degree’ were defined. Concern was expressed that there was ‘a risk that this test would still allow for worker’s compensation eligibility in cases where employment has made only a minor contribution to the illness’.
93. There is no room for doubt that the purpose of the 2007 amendments was to strengthen the connection necessary between the employment and the contraction or aggravation of a disease. Including a definition of ‘significant’ as ‘substantially more than material’ makes this abundantly clear. In other words, it is insufficient that the contribution of the employment be ‘more than trivial’; it had to be substantially more than trivial. The Tribunal did not recognise this, despite its reference to the definition. The error the Tribunal made is similar to the one made by the Tribunal in Sahu-Khan. In a valiant attempt to save the decision Mr Robinson drew attention to the fact that Dr Lewin had said ‘certainly more than trivial’, but this was no more than an emphatic way of saying ‘more than trivial’. It did not satisfy the statutory test and the Tribunal was mistaken in thinking otherwise.
The consequence of the above is that it is easier to rebut the presumption under s 7(1) of the DRC Act because “if it be shown that the naval exposure only made a material contribution then the statutory presumption will be necessarily rebutted”.[30]
[30] Respondent’s closing submissions para. 19.
At the conclusion of the hearing, I had raised with the parties the apparent difficulty in translating epidemiological evidence, which deals with risks, into the language of the legislation, which talks in terms of contribution to the disease. The Respondent cited the High Court decision in Amaca v Booth as providing guidance on that issue.

The Respondent referred to the judgment of French CJ in which, according to the Respondent,[31] his Honour:
…noted that a number of the expert witnesses – Drs Musk, Heiner and Leigh – had utilised the word “risk” in the course of their evidence. Later in his judgment, French CJ considered at some length the concept of “risk of harm” and “factual causation”. These passages from the judgment belie easy summation. Eventually though, at page 57, paragraph 49, French CJ noted as follows:
“In summary, a finding that a defendant’s conduct has increased the risk of injury to the plaintiff must rest upon more than a mere statistical correlation between that kind of conduct and that kind of injury. It requires the existence of a causal connection between the conduct and the injury, albeit other causative factors may be in play. As demonstrated by medical evidence in this case and in particular by Professor Henderson’s evidence, a causal connection may be inferred by somebody expert in the relevant field considering the nature and incidence of the correlation.”
[31] Respondent’s closing submissions para. 21
Evidence of increased risk, epidemiological evidence, alongside other evidence, can be used to resolve the issue as to whether a particular exposure in the workplace contributed to a significant degree to the contraction of the particular disease.
In relation to the way that epidemiological evidence should be used, the Respondent points to the often cited decision of the New South Wales Court of Appeal in Seltsam Pty Ltd v McGuinness (2000) NSWCA 29 (Seltsam) which was applied by the Tribunal in

The Estate of the Late Mr Vaughan White and Military Rehabilitation and Compensation Commission
[2018] AATA 3882 (White and MRCC). The Respondent submits that the relevant passages in the Seltsam decision are extracted in [56] to [59] of the Tribunal’s decision in White and MRCC with the focal point being at [57] which describes how epidemiological evidence is to be treated with the conclusion being set out in [89] of the Seltsam judgment as:
89. In my opinion, evidence of possibility, including epidemiological studies, should be regarded as circumstantial evidence which may alone or in combination with other evidence establish causation in a specific case.
The Respondent also refers to Amaca v Ellis (2010) 40 CLR 111; [2010] HCA 5 (Amaca v Ellis) a case in which a smoker exposed to respirable asbestos fibres in the course of his employment with two employers sought to establish liability for an asbestos related condition. Both tobacco smoke and asbestos inhalation fibres were capable of causing the lung cancer condition and no medical evidence could stipulate why the late Mr Ellis developed the cancer. A number of experts (including Dr Musk, Dr Leigh and Professor Fox) gave epidemiological evidence which drew conclusions from studies of large groups. In that case, the evidence of a very limited exposure to asbestos, coupled with limited epidemiological evidence, was found not to support an inference that asbestos exposure was a factual cause for Mr Ellis’s fatal lung cancer.
In relation to Dr Musk’s evidence, the Respondent contends that the term “competing risks” was used by Dr Musk in the course of his evidence. The Respondent submits that in hindsight perhaps a better term might have been “competing potential causes”. Whilst it may be open to consider what Mr Aiberti’s level of risk to the development of mesothelioma was in respect of both employment settings, the real issue here is to whether or not which of those potential competing causes falls within the category of having satisfied the statutory test of “contributing to a significant – substantially more than material degree”. [Tribunal note: In relation to this statement of the issue, I think that the appropriate test is not which of the competing causes falls within the category of “contributing to a substantial degree”, it is whether Mr Aiberti’s exposure to asbestos during his RAN service so contributed].
In relation to the factual evidence, the Respondent submits:[32]
[32] Respondent’s closing submissions at 15-16.
·
Exhibit R5 at pages 81 and 82 (Paper by Professor Bruce Robinson and Professor Philippe Chahinian on Mesothelioma which dealt with levels of exposure to asbestos fibres in Wittenoom) accurately sets out the level of exposure to which

Mr Aiberti would have been exposed. The portions of that chapter, co-authored by Dr Leigh, were put to Mr Kottek and Dr Leigh and neither demurred to the accuracy of the statements made in those parts of the paper. Relevantly, they had been taken to the part of that paper which said as follows:
Whilst the underground work in the mine was difficult with the low stope, heat and dirt, clearly the most appalling working conditions were to be found in the mill. Dust levels were so high that workers would often have difficulty seeing the other side of the mill. More sinister, however, was the fact that whereas the underground dust included a lot of silica and unmilled asbestos, the dust in the mill contained a substantial amount of fine, lethal crocidolite fibres. It is therefore no surprise to note that the mortality amongst mill workers is extremely high.
…
Equally sadly, the partners and children of workers were exposed to large amounts of crocidolite in what, at the time, seemed like innocuous circumstances. To deal with the problem of the dry red dust at Wittenoom, which was capable of penetrating any door or window, asbestos-containing tailings were transported from the mine site to the township 7 kilometres away and used to cover the school playground, the airport, driveways of houses and other areas in which children played. Many of these children have since died of mesothelioma in their 20s, 30s and 40s. Many of their mothers have also died of mesothelioma.
·Those paragraphs record Mr Aiberti being exposed to “one of the worst industrial disasters in human history” for not only workers at the mill and mine site but also for the workers’ families in the township.
·In cross-examination Dr Leigh accepted the existence of a third avenue of exposure of Mr Aiberti as a child by way of transference of asbestos fibres from his father’s clothes when the father returned to the family home after work at the mine.[33]
·The factual details of the alleged navy exposure were set out in Mr Aiberti’s statement.[34] That statement revealed that Mr Aiberti’s naval career of approximately seven years only took in 18 months approximately on naval shipping. Of that time, the real focus of the Applicant’s case has been on the boiler room visits when Mr Aiberti served on HMAS Swan, for approximately 14 months. In his evidence during cross-examination, Mr Kottek conceded that much of the asbestos insulation in such shipping was installed with “fixing agents” to keep it in place.[35] Further, Mr Kottek conceded that he did not know if the more potent crocidolite asbestos was utilised in the installation on HMAS Swan.
·All of the witnesses agreed that there was no evidence just what the levels of asbestos fibres would have been in the air on naval vessels.
·The specific type of asbestos being mined at Wittenoom was crocidolite, or blue asbestos. The peculiar potency of this type of asbestos is well documented. In his report, Professor Fox noted a study done by Hodgson and Darnton which found that crocidolite is 500 times more potent in causing mesothelioma than any other form of asbestos.[36] In cross-examination, Mr Kottek did not challenge this assessment and agreed that the article was from a credible source and reflected the “best estimate that’s available”.[37]
·All of the evidence was entirely speculative as to what type of asbestos was utilised in navy insulation. It could never be safely contended that Mr Aiberti was exposed to crocidolite in the course of his navy career, as he was so undeniably exposed whilst living and working in Wittenoom.
·The Respondent submits that on this factual evidence, the following conclusions can be fairly made. The potency and magnitude of the Wittenoom exposure is self-evident and undeniable. In contrast, the navy exposure is substantially less and speculative as to the duration of the exposure and the type of asbestos involved. Further, as noted earlier, if the navy exposure was as crucial as the Applicants now assert, it would have been mentioned in Dr Musk’s reporting in 1990, which it was not.
[33] Transcript at 76.
[34] R1, T12 at 45-47.
[35] Transcript at 25-26.
[36] R3 at page 3.
[37] Transcript at 31-32.

Having noted that, the evidence in the present matter largely proceeded on the basis that all exposure to asbestos is relevant in considering the risk of the development of mesothelioma. The basis of the Respondent’s argument is that while Mr Aiberti was exposed to asbestos in the RAN, the level and type of asbestos to which Mr Aiberti was exposed in Wittenoom was of such a magnitude greater than that in the RAN, the RAN exposure could not be considered to have contributed, to a significant degree, to his mesothelioma.
In looking at the use of epidemiological evidence, Deputy President Sosso and Member Maynard in White and MRCC cited (at [56]-[57]), amongst others, the following passages from Spigelman CJ’s decision in Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262; [2000] NSWCA 29 (Seltsam):
59Epidemiology is the study of the distribution and determinants of disease in human populations. It is based on the assumption that a disease is not distributed randomly in a group of individuals. Accordingly, subgroups may be identified which are at increased risk of contracting particular diseases.
60Epidemiological evidence identifies associations between specific forms of exposure and the risk of disease in groups of individuals. Epidemiologists do make judgments about whether a statistical association represents a cause-effect relationship. However, those judgments focus on what is sometimes called in the epidemiological literature ‘general causation’. Whether or not the particular factor is capable of causing the disease. Epidemiologists are not concerned with ‘specific causation’: Did the particular factor cause the disease in an individual case?...
62Epidemiology provides two types of material: first, the statistical measurement of an association between exposure and disease and, secondly, interpretation of the data to determine general causation.

The second function may be performed by an epidemiologist who had no association with the study or studies which provide the raw data.
…
79Evidence of possibility, including expert evidence of possibility expressed in opinion form and evidence of possibility from epidemiological research or other statistical indicators, is admissible and must be weighed in the balance with other factors, when determining whether or not, on the balance of probabilities, an inference of causation in a specific case could or should be drawn. Where, however, the whole of the evidence does not rise above the level of possibility, either alone or cumulatively, such an inference is not open to be drawn.
80The common law test of balance of probabilities is not satisfied by evidence which fails to do more than establish a possibility....
89In my opinion, evidence of possibility, including epidemiological studies, should be regarded as circumstantial evidence which may, alone or in combination with other evidence, establish causation in a specific case.
90Proof on the balance of probabilities, indeed on the beyond reasonable doubt standard, may be established on the basis of circumstantial evidence...
…
93With respect to many diseases, medical science is able to give clear and direct evidence of a causal relationship between a particular act or omission and a specific injury or disease. There are, however, fields of inquiry where medical science is not able to give evidence of that character. There are cases in which medical science cannot identify the biological or pathological mechanisms by which disease develops. In some cases medical science cannot determine the existence of a causal relationship. Such a state of affairs is not necessarily determinative of the existence or non-existence of a causal relationship for purposes of attributing legal responsibility. Epidemiological evidence may be able to fill the gap. It is of particular potential utility in the field of what is often referred to as ‘toxic torts’, especially in cases of diseases with long latency periods...
…
98The Courts must determine the existence of a causal relationship on the balance of probabilities. However, as is the case with all the circumstantial evidence, an inference as to the probabilities may be drawn from a number of pieces of particular evidence, each piece of which does not itself rise above the level of possibility. Epidemiological studies and expert opinions based on such studies are able to form ‘strands in a cable’ of a circumstantial case.
Having cited the above passages from the judgment of Spigelman CJ, the Tribunal in White and MRCC noted at [59]:
59. One important point that was elucidated by Spigelman CJ is that while epidemiological studies concern the distribution and determinants of disease in human populations, they are not studies that can assist a tribunal of fact in determining individual questions of causation. As Spigelman CJ said

(at [150]/287):
“I have no difficulty with a medical practitioner drawing on and assessing epidemiological studies. I have greater difficulty with an epidemiologist expressing an opinion about causation in the individual case... As I understand the position, epidemiology is concerned with populations, not individual cases.”
While Spigelman CJ’s comment cited in the preceding paragraph might be seen as an impediment in using epidemiological evidence in determining the cause of a disease in any particular case, the courts and the Tribunal have in fact taken into account epidemiological evidence, coupled with other evidence, to do just that. By necessity the vast majority, if not all, cases of this type that come before courts and tribunals relate to an individual contracting a disease. In fact in Seltsam Spigelman CJ was considering extensive epidemiological evidence that had been led before the judge. Spigelman CJ found at [155]:
155However, the trial judge did not simply fail to give reasons. He said he would not consider the detailed submissions made to him about the epidemiological studies. In this, as I have said above, in my opinion he erred. This justifies the intervention of the court and, indeed, may well have done so even if the new s32 of the Act were applicable to the case.
In other words, the judge not only could have, but should have, considered the epidemiological evidence that had been presented and his refusal to do so, at least without reason to do so, was an error of law. Spigelman CJ’s judgment then analysed the epidemiological evidence that was before the judge at first instance and observed:
173 It must be borne in mind that references to increased risk in the studies and the epidemiological literature are references to increases in human populations. The application of that information to the case of a specific individual requires a separate and distinct step by way of inference.
174In my opinion, the extent of increased risk indicated by all but one,

or perhaps two, of the epidemiological studies is too small to justify an inference of causation, either alone or in combination with other factors including biological plausibility, the laboratory experiments and the expressions of professional opinion which were, in large measure, based on the epidemiological evidence.
…
183Epidemiological studies and expert epidemiological opinion evidence on general causation go no further than establishing a possibility. Applying a common sense test of causation to the evidence of possibility in the present case does not, in my opinion, justify an inference of causation on the balance of probabilities in the individual case.
Most of the cases to which both parties have referred in relation to how epidemiological evidence is to be treated are looking at the establishment of a causal link between an event or an exposure and the development of a disease. As Spigelman CJ put it, “Epidemiologists do make judgments about whether a statistical association represents a cause-effect relationship” (see [89] above). In the present case, however, the causal link between exposure to asbestos and development of mesothelioma is not in dispute

(see [69] above). Further, s 7(1) of the DRC Act and the gazetting of exposure to asbestos and the subsequent development of mesothelioma and the Respondent’s concessions in that regard, make the causal link between exposure to asbestos and the subsequent development of mesothelioma a legal reality (see [40]- [42] above).
The contest in the present case is not whether, based on epidemiological and other evidence, Mr Aiberti’s exposure to asbestos in the RAN caused his mesothelioma, but rather whether such exposure contributed, to a significant degree, to his development of mesothelioma given that he was also exposed to asbestos to a much greater extent in Wittenoom.
The Applicants postulate the cumulative effect theory, that all exposure to asbestos increases the risk of developing mesothelioma. Professor Fox was cross-examined on this as follows:[51]
[51] Transcript at 119.
COUNSEL: Yes. Then Dr Leigh says at page 8,
Hence simplistically, the more fibres, the more free radicals and the greater probability of genetically damaged and proliferated damaged cells at any given point in time.
Would you agree with that?
PROFESSOR FOX: I would think that is the whole key issue in what we are discussing – total number of fibres.
COUNSEL: Yes, and so then we – - -?
PROFESSOR FOX: You’ve hit the jackpot.
COUNSEL: And so then if we then go to Dr Leigh’s opinion at page 8 where he says,
In view of the capacity of asbestos fibres to be involved at all stages of tumour development, all cumulative exposure to asbestos in an individual case must be playing some contributory part in causation.
COUNSEL: Do you agree with that?
PROFESSOR FOX: Not completely because you’d have to put it into a proportional basis and it’s the key – comes back to the numbers that he said and I will also add there is a key factor in that later exposure is of less significance if you take the pico hypothesis which relates to the incident of mesothelioma to increase with time post first exposure to the degree of time cubed, so it’s the first exposure that is more significant than the second – or third – or fourth. So it’s the total number of fibres that is a key issue and there’s a formula that is quite complex which introduces number of fibres, potency of the different fibres, chrysotile versus crocidolite, the number of fibres and the time and the time relationship is cubed, which puts a lot more emphasis on early exposure.
COUNSEL: So your answer is you don’t agree with that statement?
PROFESSOR FOX: Well, you have to put it into context. You can’t – it would have to put all those factors into that statement, so alone I can’t agree with that statement, it needs modification.
COUNSEL: Well, would you agree that the additional exposure that Mr Aiberti’s service in the RAN would have added to his risk?
PROFESSOR FOX: At what level? Perhaps at – based on some of the figures that I have quoted out at Roggli – one per cent – two per cent – possibly three per cent, something like that – which fits in, I think, with the epidemiology as well as the fibre analysis in lungs of patients with asbestosis and mesothelioma versus pleural versus peritoneal and you have to then put the factor of crocidolite in.
COUNSEL: It doesn’t reduce his risk though, does it?
PROFESSOR FOX: No. But as I said, it’s a comparative analysis and just based on that data of fibre level that I spoke about, asbestosis versus no asbestosis,

the most you can pull out of that is a 50 mol difference.
The above exchange encapsulates the difference between the parties and the difference between the approaches of Professor Musk, Dr Leigh and Mr Kottek on the one hand, and Professor Fox on the other.
In cross-examination of Dr Leigh the following exchange took place which, in my view,

is also illustrative of the difference between the parties’ respective expert evidence but also identifies a further point of difference, namely, on what it is that the experts are to opine:[52]
[52] Transcript at 85.
COUNSEL: Now, under our legislative scheme, to draw – you know, to establish liability as between his navy employment and his mesothelioma, it has to be shown that the navy exposure contributed in what’s called to a significant degree.

And the words “to a significant degree” are further defined to mean something more substantially than material. Okay?
DR LEIGH: M’mm.
COUNSEL: The proposition I’m putting to you is that the navy exposure, when looked at compared to the Wittenoom exposure, does not fit the descriptor that I’ve just described to you. What do you say to that?
DR LEIGH: Well, again, I admit that it’s a lot less, but that decision of what’s significant and what’s not significant, I believe, is an administrative decision or legal administrative decision.
In the cross-examination of Mr Kottek the following exchange took place:[53]
[53] Transcript at 32-33.
COUNSEL FOR THE RESPONDENT: Let’s come back to the section. Can I put the proposition to you that the naval exposure, in the presence of the undoubted Wittenoom exposure, falls well short of that yardstick of contributing to a significant degree to his illness?
COUNSEL FOR THE APPLICANTS: Sir, I just have to raise an objection. In

Mr Kottek’s reports, on, I think, both of them, he identifies that he is not an expert – sorry, I should rephrase that; opinions about medical causation are beyond his area of expertise. He can comment on epidemiology, but in individual cases, it’s beyond his area of expertise. So I think it’s important that – his qualification in that respect is important to the proposition that’s being put by my learned friend.
DEPUTY PRESIDENT: But doesn’t he opine – isn’t the purpose of his evidence really going to that issue?
COUNSEL FOR THE APPLICANTS: The purpose of his evidence is to explain asbestos exposure. The next step is the asbestos exposure that then results in the condition. It’s an important qualification, sir.
DEPUTY PRESIDENT: But he does, doesn’t he, in his reports – I think he talks about material contribution.
COUNSEL FOR THE APPLICANTS: Well, he talks about risk, but it’s got an important qualification. So perhaps if I can just take – for example, if you look at 17 May, page 2 makes reference to the Hodgson and Darnton – - -
…
Considerable difficulty in particular circumstances. And in any event,

the attribution of disease in an individual is beyond my expertise, and is a matter for medical evidence.
So the question needs to be phrased in the context of that qualification. He says that again, I think, in 7 December 2018. So there can be discussion of risk in that respect, but it’s just an important qualification that needs to be noted, with respect to the question that’s being asked.
…
COUNSEL FOR THE APPLICANTS: The questions related to how much, or by what degree of asbestos exposure Mr Aiberti had. I think the comment perhaps is when he’s talking about Dr Goode and Professor Musk. But where he discusses the Hodgson and Darnton study in terms of what the results and how the results are interpreted with respect to amosite and crocidolite exposure, but it’s all in the context that the attribution of disease in an individual is beyond his area of expertise.
Following some further exchanges between both counsel and me, the following question was put by the Respondent’s counsel to Mr Kottek:[54]
[54] Transcript at 34-35.
COUNSEL FOR THE RESPONDENT: Okay. Let’s take you to page 4 of your report, the second report?
MR KOTTEK: Yes.
COUNSEL FOR THE RESEPONDENT: You make the point at the top of the page that in the absence of the Wittenoom exposure, you consider his exposure in the RAN would have placed him at a significantly increased risk of mesothelioma, all right?
MR KOTTEK: Yes
COUNSEL FOR THE RESPONDENT: But the reality is we have to look at both, and the proposition I put to you was that when you look at what’s called “contributing in a significant degree”, the preponderance of the epidemiological evidence would point to the Wittenoom experience, do you agree with that?
MR KOTTEK: It would be the more important of the two exposures, definitely.
COUNSEL FOR THE APPLICANTS: Well, more important in the sense that the Navy exposure could not be fairly seen, as exposed to the Wittenoom,

as contributing in the significant degree to any onset of his mesothelioma?
MR KOTTEK: Look, I mean, as I and – yes, we were discussing before, as an occupational hygienist, I don’t see that I have the expertise to give an opinion on individual causation.
COUNSEL FOR THE RESPONDENT: I don’t want to interrupt you, but I’m asking this question clearly on the field that you profess to have some expertise in respect of epidemiology. What do you say on that score?
MR KOTTEK: Well, the risk is much, much greater from the Wittenoom exposure, and the risk would be attributable if you were to add the – assuming they could be – even assuming they could be calculated on an individual basis, and with the limited information available, it’s clear that Mr Aiberti’s risk of mesothelioma would primarily have arisen out of his residence and work in Wittenoom. Yes, that would have been made much – would have been the biggest contribution to his risk of mesothelioma.
Professor Musk was similarly cross-examined. The following exchanges occurred:[55]
[55] Transcript at 50-51, 58-60.
COUNSEL: Can I just go back to your second report, please. That’s the one of

12 February 2018…. At the bottom of page 1 you say this:
It remains my opinion that Mr Aiberti’s exposure to asbestos during his RAN service contributed to his risk of developing peritoneal mesothelioma, but this risk contribution would have been much less than the Wittenoom crocidolite exposure which was earlier and likely to have been much greater because the risk of mesothelioma is greatest from crocidolite exposure.
…
COUNSEL: You go on to say at the top of page 2:
Related to the degree of exposure and increases with time since exposure.
You posit this there:
Had the RAN exposure been his only asbestos exposure then it could be considered to have made a material contribution to his peritoneal mesothelioma. However even though it would have been contributed to his risk its relative contribution would have been less.
COUNSEL: I am not trying to play with words, Dr Musk, please accept that assurance, I am just trying to get a sense of what you have to say in respect of the competing risks and to put my case to you, you understand. As high as you’re prepared to put it for argument sake in looking at the RAN exposure you say at its best that’s what you would call a material contribution?
PROFESSOR MUSK: Yes, because he could have got it without any other exposure, and we know that those cases we’ve seen.
…
COUNSEL: Sorry. From the anecdotal history – I appreciate what you say that you can’t discount the barest possibility of the navy experience, but for want of a better term, Dr Musk, the exposure that this man had Wittenoom compared to what we have been able to glean by way of evidence in respect of the navy, for want of a better term like cheese and chalk, weren’t they?
PROFESSOR MUSK: The exposure at Wittenoom would have been far and away beyond the exposure in the navy.
COUNSEL: And indeed in fairness to you in the second last paragraph in your report of 9 April 1990 you say this – this is five lines up from the bottom of that paragraph. I will go a little bit further. You say:
These changes are consistent with asbestosis resulting in mild impairment of lung function and mild disability. There has been no significant deterioration in lung function over the period of observation. Nevertheless it is likely that there will be further progression of the disease and increasing disability with time. As a result of his crocidolite exposure he is at increased risk of the development of a malignant pleural mesothelioma and bronchogenic carcinoma.
By bronchogenic carcinoma you’re referring to lung cancer, aren’t you?
PROFESSOR MUSK: Yes.
COUNSEL: But nevertheless inasmuch as you’re referring to the crocidolite exposure you’re making the point there about the Wittenoom exposure, aren’t you?
PROFESSOR MUSK: Yes.
COUNSEL: And at that time there was never any history given to you of any navy exposure, was there?
PROFESSOR MUSK: No, I don’t know – I usually take a full occupational history and I don’t know why it didn’t end up in this report, but – - -
DEPUTY PRESIDENT: You do refer to him as being in the navy in the first paragraph, but there’s no reference to exposure?
PROFESSOR MUSK: Yes.
…
COUNSEL: …You have been asked some questions and you gave the answer “significant”, yet you said you believed the navy exposure was significant.

Can I ask you to look at the question from the point of view of competing risks.

I am not here to give you a law lecture, but the words in our section which guides us sets out for a disease like mesothelioma or a disease process it has to be shown that the employment has contributed to a significant degree. I appreciate that you as a medico-legal reporter may have been used to that word “material”, and I suspect that may be why you used it, I don’t make any point about that. Then it goes on to mean “a significant degree means a degree that is substantially more than material”. Can I put this proposition to you; the Wittenoom exposure from what you have said to us certainly fits those descriptors, doesn’t it?
PROFESSOR MUSK: There’s no question that the Wittenoom exposure would have contributed vastly more to his risk of developing mesothelioma than the naval exposure, but the only point – - -
COUNSEL: The proposition – sorry, I don’t want to cut you short – the proposition I am putting to you, what I have just read out to you, the Wittenoom exposure would more than fit in within those descriptors that I’ve described?
PROFESSOR MUSK: Yes.
COUNSEL: A further proposition I put to you is on those words you have said there’s a bare possibility, there’s a possibility that there was some risk from the navy, but the navy exposure falls a long way short of fitting those descriptors, doesn’t it, compared to the Wittenoom exposure?
PROFESSOR MUSK: Yes.

What then are we to make of the supposedly competing expert evidence? The Applicants say that the evidence of Professor Musk, Dr Leigh and Mr Kottek should be preferred over that of Professor Fox and, presumably, Dr Goode. The Applicants submit that the evidence of Professor Musk, Dr Leigh and Mr Kottek should be preferred over that of Professor Fox because they are more relevantly qualified to express the opinions that they express than Professor Fox. I do not accept that proposition. Professor Fox is, in my view, as qualified to give expert evidence on the matters relevant to the matters in issue as the witnesses produced by the Applicants. In that regard I note that in a number of the cases cited by the parties (Freeman and Military Rehabilitation and Compensation Commission [2016] AATA 741; Pryde and Telstra Corporation Limited [2016] AATA 811; Amaca v Ellis) Professor Fox gave evidence. In a lot of those cases Professor Musk also gave evidence as did Dr Leigh and Mr Kottek. The courts and tribunals in those cases did not question Professor Fox’s expertise or qualification to give the sort of evidence that he did in this matter. I accept that he is as qualified as Professor Musk, Dr Leigh and

Mr Kottek to give the evidence that he gave. This matter is not to be decided on one set of expert evidence being preferred over the other on the basis of one set of experts being more suitably qualified than the other.
What is important is to analyse the evidence of each of the witnesses in light of what this Tribunal must decide. I must decide whether the evidence shows that Mr Aiberti’s exposure to asbestos during his RAN service did not contribute, to a significant degree, to his mesothelioma. What was the evidence of each of the relevant expert witnesses on that issue?
Professor Musk expressed the view in his reports of 8 June 2016 (A4) that:[56]
[56] A4 at page 4 [10].
In the context of Mr Aiberti’s Wittenoom asbestos exposure it is my opinion that it is still not possible to assert that the RAN service did not materially contribute to his peritoneal mesothelioma even though the risk would have been much less.
and in his 12 February 2018 (A5) report that:
2.It remains my opinion that Mr. Aiberti’s exposure to asbestos during his RAN service contributed to his risk of developing peritoneal mesothelioma but this risk contribution would have been much less than the Wittenoom crocidolite exposure which was earlier and likely to have been much greater because the risk of mesothelioma is greatest from crocidolite exposure, related to the degree of exposure and increases with time since exposure. Had the RAN exposure been his only asbestos exposure then it could be considered to have made a material contribution to his peritoneal mesothelioma, however even though it may have contributed to his risk of mesothelioma, the relative contribution would have been less.
and in his 7 November 2018 report that:
… I can only repeat my previous opinion that had the RAN exposure been his only asbestos exposure then it could be considered to have made a material contribution to his peritoneal mesothelioma. However, even though it may have contributed to his risk of mesothelioma, its relative contribution would be much less than that of the Wittenoom exposures and there is no way of separating the contributions except on a probability basis.
(Emphasis added.)
At the hearing Professor Musk’s evidence-in-chief was:[57]
COUNSEL: The tribunal needs to determine whether or not Mr Aiberti’s exposure in the RAN is a significant contributor, and there’s been some descriptors as to what all of that means. You have seen references in the reports from Professor Fox of the word “de minimis” or trivial and the word “material” has been described to mean more than trivial, and the word “significant” has been described to mean substantially more than trivial. In relation to Mr Aiberti’s exposure to asbestos in the navy how would you characterise the navy’s contribution to Mr Aiberti’s mesothelioma?
PROFESSOR MUSK: This is a sort of legal idea, but I mean to me he had significant exposure in the navy. So therefore it made a significant contribution.
and in cross-examination his evidence was as set out in [100] above.
[57] Transcript at 50.
Dr Leigh’s report of 14 November 2018 (A8) relevantly opined:
In my opinion it was more probable than not that each of these exposure: episodes would have added to the “background” exposure and increased the risk of mesothelioma. This risk has now been expressed and in my opinion it was more probable than not that each exposure would have made a material contribution to causation. As stated above there is no level of asbestos exposure below which there is no risk of mesothelioma, and the evidence for other factors causing mesothelioma is in my opinion, no more than anecdotal. The Wittenoom exposure would have made the greater contribution and could alone have caused the mesothelioma, but the RAN exposure in my opinion would have made a material contribution to causation and certainly not a “de minimus” [sic] contribution. ln the hypothetical situation of no Wittenoom exposure, the RAN exposure would very probably have been the cause.
At the hearing Dr Leigh’s evidence was as set out at [97] above.
Mr Kottek’s report of 17 May 2017 (A1) spoke to the relative exposures to asbestos that Mr Aiberti would have had in his RAN service and while living and working in Wittenoom. In the end he conceded that “…attribution of disease in an individual is beyond my expertise and a matter for medical evidence”.
Mr Kottek’s report of 7 December 2018 (A2) was as set out in [65] above. In that report he opined that Mr Aiberti’s exposure to asbestos in the RAN would have been greater than that of the general population and that the level of exposure in Wittenoom “would have created as considerably greater risk of mesothelioma than his RAN service” but that “…any attempt to quantitatively apportion his risk of mesothelioma would be quite speculative”.
At the hearing Mr Kottek’s evidence was as set out in [99] above.
In effect Mr Kottek was not able to express any view as to the level of contribution that

Mr Aiberti’s RAN service would have had on his mesothelioma.
It is important to look at the evidence of the experts in light of the issue that must be determined by the Tribunal. As the Applicants submit at paragraph 24.4 of their closing submissions, citing Wiegand v Comcare Australia [2002] FCA 1464 at [30] per

von Doussa J:
24.4.Where an expert witness expresses an opinion on the ultimate issue in the case it is important that the decision-maker recognises that this has occurred and ensures that the expert, in reaching that opinion, has correctly applied the relevant legal test upon which the ultimate issue turns.
The primary question for me to determine in this matter is whether Mr Aiberti’s exposure to asbestos while serving in the RAN contributed, to a significant degree, to his developing mesothelioma. As Dr Leigh rightly noted in cross-examination, the answer to that question, the ultimate issue, is a legal decision to be made based on the medical evidence (see [97] above). A useful discussion of how a decision maker is to treat specialist or expert evidence in determining the ultimate issue appears in Deputy President Forgie’s decision in Freeman and MRCC wherein, in discussing whether the presumption under

s 7(1) of the DRC Act had been rebutted, the Deputy President said as follows:
99.Turning to the evidence, I will first consider Ms Spencer’s submission to the effect that I should disregard Professor Fox’s evidence as not being addressed to the correct legal test. In the case of Wiegand, von Doussa J considered a situation in which an expert witness, Professor Goldney, had been asked to express his view on whether Mr Wiegand was suffering an ailment, or an aggravation of an ailment, that was contributed to in a material degree by his employment. His Honour said that:
“... Professor Goldney was not to be criticised for having complied with that request. However, where an expert witness expresses an opinion on the ultimate issue in this case, it is important that the decision-maker recognise that this has occurred, and ensures that the expert, in reaching that opinion, has correctly applied the relevant legal test upon which the ultimate issue turns. ...”
100.This is not the case here. As is apparent from the questions that Professor Fox was answering and that I have set out at [23]-[27] above, he was not asked to express an opinion on the ultimate issue. There is nothing in Wiegand that suggests that he needed to be asked in those terms. All that von Doussa J stressed was that, if an expert were asked in those terms, he or she had to take especial care to apply the relevant legal test upon which that ultimate issue turned. Professor Fox has been asked to express an opinion on the level of contribution, if any, that service related sun exposure would have had on the onset of Ms Freeman’s melanoma. That is not the ultimate issue that I must decide but is no less relevant as a piece of the evidence to which I must have regard in deciding the ultimate issue.
…
106.Professor Fox was first asked to report after Ms Freeman had completed the SSD Questionnaire and it was made available to him together with surgical and specialist reports. The material on which he based his opinion is consistent with the findings I have made. His expertise was not questioned although his expression of his opinion was. Ms Spencer questioned Professor Fox’s expression of his opinion when he used expressions such as “likely to influence”, “in a significant way” or “responsible for” in relation to the development of the melanoma. To express his opinions in that way is to attach an additional requirement to the statutory test of material contribution. I do not agree. Professor Fox has expressed his opinion in medical terms as he understands them to be and in light of the questions that he was asked. The questions and his answers have to be read together and his report has to be understood as a whole. Had he expressed his opinion in terms of “material contribution” or otherwise, it would have been open to Ms Spencer to submit that he was expressing an opinion on the ultimate issue and to question whether he understood what resolution of that ultimate issue entailed. Professor Fox has written his report and answered the questions as asked drawing on his medical expertise in the relevant field.
(Footnotes omitted.)
It is coincidental that the passages that I cite above relate to evidence given by Professor Fox. In the present case, the principle expressed by Deputy President Forgie in the above passages is probably more applicable to the evidence of Professor Musk, Dr Leigh and

Mr Kottek than it is to the evidence of Professor Fox. Professor Fox’s evidence more directly addressed the specific adjectival question of significant contribution, in the context of multiple or parallel potential contributors, while the evidence of Professor Musk,

Dr Leigh and Mr Kottek was couched in less direct terms, terms reflecting their respective disciplines and terms reflecting the evidence being based largely on epidemiological principles. As Deputy President Forgie notes, the task is to assess the substance and purport of the expert evidence taking care to apply the relevant legal test upon which the ultimate issue turns.
Has the presumption raised by s 7(1) been rebutted?
Deputy President Forgie in Freeman and MRCC made the following observation at [98]:
98. Section 7(1) does not prescribe any standard of proof by which the “contrary is established” if its deeming provisions are not to apply. In ordinary usage, the meanings of the word “establish” include “... 3 to find, show or prove something. ...” That is a meaning that is consistent with the place of s 7(1) in the SRC Act. Section 7(1) is concerned with the existence or otherwise of a causal relationship between employment and ailment. The meaning of the word “establish” is shaped by that context. Having regard to that context and its ordinary meaning, it follows that the word is intended to relate to matters of proof and evidence. Given that decisions made under the SRC Act are administrative decisions, they are made according to the civil standard or balance of probabilities. It would follow that this is the standard of proof that would apply in determining whether the contrary has been established within the meaning of s 7(1).
(Footnotes omitted.)
I accept the above to be a correct statement of the effect of the presumption under s 7(1) of the DRC Act.
I am satisfied that the evidence, on the balance of probabilities, establishes that

Mr Aiberti’s exposure to asbestos in the RAN did not contribute, to a significant degree, to his mesothelioma. At best the evidence of Professor Musk, Dr Leigh and Mr Kottek, established that Mr Aiberti’s exposure to asbestos in the RAN, which could not be quantified, increased Mr Aiberti’s risk of developing mesothelioma. In particular Professor Musk’s evidence in the highlighted passage set out in [103] above falls short of establishing that Mr Aiberti’s exposure to asbestos in the RAN contributed significantly to his developing mesothelioma.
I am mindful of the need to “translate” the epidemiological evidence, which by its nature looks at risk rather than directly at causation, into evidence of contribution, the appropriate legal test for the purposes of s 5B of the DRC Act. I am satisfied, on the balance of probabilities, that the evidence shows that Mr Aiberti’s risk associated with his exposure to asbestos during his time living and working in Wittenoom so significantly outweighed the increase in risk caused by his RAN service, that the latter could not be considered to have contributed, to a significant degree, to his mesothelioma.
The approach taken by Professor Fox was, in my view, the correct one when considering contribution for the purposes of s 5B of the DRC Act. While it is likely, and I accept it to be the case, that Mr Aiberti’s exposure to asbestos during his time in the RAN increased his risk of developing mesothelioma, the overwhelming risk factor was his exposure to asbestos fibre, particularly crocidolite, in Wittenoom. As much was conceded,

quite correctly, by each of Professor Musk, Dr Leigh and Mr Kottek (see [97]-[100] above).
This approach is also consistent with the provisions of s 5B(2), in particular subsections (d) and (e). Mr Aiberti’s exposure to asbestos in the navy cannot be viewed in isolation, ignoring the accepted, much greater, risk factor not related to his RAN employment, namely his exposure to asbestos in Wittenoom.
Given the above findings, I find that the presumption under s 7(1) of the DRC Act is rebutted. Further, given the above findings, both applications must fail.
DECISIONS
For the reasons set out above, I affirm:
Application 2016/2882
(i)the reviewable decision of the Respondent dated 24 May 2016 which affirmed a determination which found that liability did not exist pursuant to section 14 of the DRC Act for the claimed mesothelioma condition; and
Application 2016/6960
(ii)the reviewable decision of the Respondent dated 1 November 2016 which affirmed a determination which denied the Second Applicant’s claim for compensation pursuant to section 17 of the DRC Act in relation to the death of Mr Aiberti.

I certify that the preceding 121 (one hundred and twenty-one) paragraphs are a true copy of the reasons for the decision herein of Deputy President Boyle

..........................[sgd]..............................................
Associate
Dated: 14 October 2019

Date(s) of hearing: 27 and 28 May 2019

Counsel for the Applicant: Mr R McCabe

Solicitors for the Applicant: Slater and Gordon

Counsel for the Respondent: Mr J Clarke

Solicitors for the Respondent: Sparke Helmore

Date(s) of hearing:	27 and 28 May 2019
Counsel for the Applicant:	Mr R McCabe
Solicitors for the Applicant:	Slater and Gordon
Counsel for the Respondent:	Mr J Clarke
Solicitors for the Respondent:	Sparke Helmore