Hill and Ors and Comcare and Ors
[2005] AATA 408
•6 May 2005
Administrative
Appeals
Tribunal
DECISION AND REASONS FOR DECISION [2005] AATA 408
ADMINISTRATIVE APPEALS TRIBUNAL )
) № W2000/422
GENERAL ADMINISTRATIVE DIVISION ) Re FRANK HILL
Applicant
And
COMCARE
Respondent
And AUDREY MAUDE HILL
Joined Party
ADMINISTRATIVE APPEALS TRIBUNAL )
) № W2001/12
GENERAL ADMINISTRATIVE DIVISION ) Re FRANK HILL
Applicant
And
TELSTRA CORPORATION LIMITED
Respondent
And AUDREY MAUDE HILL
Joined Party
ADMINISTRATIVE APPEALS TRIBUNAL )
) № W2001/199
GENERAL ADMINISTRATIVE DIVISION ) Re AUDREY MAUDE HILL
Applicant
And
COMCARE
Respondent
ADMINISTRATIVE APPEALS TRIBUNAL )
) № W2001/348
GENERAL ADMINISTRATIVE DIVISION ) Re AUDREY MAUDE HILL
Applicant
And
TELSTRA CORPORATION LIMITED
Respondent
ADMINISTRATIVE APPEALS TRIBUNAL )
) № W2001/429
VETERANS’ APPEALS DIVISION ) Re FRANK HILL
Applicant
And
MILITARY REHABILITATION AND COMPENSATION COMMISSION
Respondent
And AUDREY MAUDE HILL
Joined Party
ADMINISTRATIVE APPEALS TRIBUNAL )
) № W2001/16
GENERAL ADMINISTRATIVE DIVISION ) Re INGEBORG ETHERIDGE
Applicant
And
TELSTRA CORPORATION LIMITED
Respondent
ADMINISTRATIVE APPEALS TRIBUNAL )
) № W2001/118
GENERAL ADMINISTRATIVE DIVISION ) Re INGEBORG ETHERIDGE
Applicant
And
COMCARE
Respondent
ADMINISTRATIVE APPEALS TRIBUNAL )
) № W2001/350
GENERAL ADMINISTRATIVE DIVISION ) Re THE PUBLIC TRUSTEE
Applicant
And
TELSTRA CORPORATION LIMITED
Respondent
ADMINISTRATIVE APPEALS TRIBUNAL )
) № W2001/430
GENERAL ADMINISTRATIVE DIVISION ) Re CEDRIC ETHERIDGE
Applicant
And
COMCARE
Respondent
And THE PUBLIC TRUSTEE
Joined Party
ADMINISTRATIVE APPEALS TRIBUNAL )
) № W2001/431
VETERANS’ APPEALS DIVISION ) Re CEDRIC ETHERIDGE
Applicant
And
MILITARY REHABILITATION AND COMPENSATION COMMISSION
Respondent
And THE PUBLIC TRUSTEE
Joined Party
DECISION
Tribunal
Associate Professor S D Hotop, Deputy President
Dr D Weerasooriya, Member
Date6 May 2005
Place Perth
Decision
The decisions of the Tribunal in respect of the Applications for Review are as follows:
· Application № W2000/422
The Tribunal sets aside the decision under review and, in substitution therefor, decides that Comcare is liable, under s 14 of the Safety, Rehabilitation and Compensation Act 1988 (“the SRC Act”), to pay compensation in accordance with that Act in respect of an “injury” (as defined in s 4(1)), being a “disease” (as defined in s 4(1)), namely, mesothelioma, which resulted in the death of Frank Hill (“Mr Hill”).
· Application № W2001/12
The Tribunal affirms the decision under review
· Application № W2001/199
The Tribunal sets aside the decision under review and, in substitution therefor, decides that Comcare is liable to pay compensation pursuant to s 17 and s 18 of the SRC Act in respect of an “injury” (as defined in s 4(1)), being a “disease” (as defined in s 4(1)), namely, mesothelioma, which resulted in the death of Mr Hill.
· Application № W2001/348
The Tribunal affirms the decision under review.
· Application № W2001/429
The Tribunal sets aside the decision under review and, in substitution therefor, decides that the Military Rehabilitation and Compensation Commission (“MRCC”) is liable, under s 14 of the SRC Act, to pay compensation in accordance with that Act in respect of an “injury” (as defined in s 4(1)), being a “disease” (as defined in s 4(1)), namely, mesothelioma, which resulted in the death of Mr Hill.
· Application № W2001/16
The Tribunal affirms the decision under review.
· Application № W2001/118
The Tribunal sets aside the decision under review and, in substitution therefor, decides that Comcare is liable to pay compensation pursuant to s 17 and s18 of the SRC Act in respect of an “injury” (as defined in s 4(1)), being a “disease” (as defined in s 4(1)), namely, mesothelioma, which resulted in the death of Cedric Etheridge (“Mr Etheridge”).
· Application № W2001/350
The Tribunal affirms the decision under review.
· Application № W2001/430
The Tribunal sets aside the decision under review and, in substitution therefor, decides that Comcare is liable, under s 14 of the SRC Act, to pay compensation in accordance with that Act in respect of an “injury” (as defined in s 4(1)), being a “disease” (as defined in s 4(1)), namely, mesothelioma, which resulted in the death of Mr Etheridge.
· Application № W2001/431
The Tribunal sets aside the decision under review and, in substitution therefor, decides that the MRCC is liable, under s14 of the SRC Act, to pay compensation in accordance with that Act in respect of an “injury” (as defined in s 4(1)), being a “disease” (as defined in s 4(1)), namely, mesothelioma, which resulted in the death of Mr Etheridge.
The Tribunal orders, pursuant to s67(8) of the SRC Act, that Comcare pay the applicants’ costs in respect of Applications № W2000/422, W2001/199, W2001/118 and W2001/430, and that the MRCC pay the applicants’ costs in respect of Applications № W2001/429 and W2001/431, in accordance with the Tribunal’s General Practice Direction.
.... …….(sgd SD Hotop) …….
Deputy President
CATCHWORDS
COMPENSATION – Commonwealth employees – employees employed by Defence Force, Postmaster-General’s Department (“PMG”) and Australian Telecommunications Commission (“ATC”) between 1939 and 1977 – employees exposed to asbestos during Commonwealth employment – employees diagnosed with mesothelioma in 2000 and subsequently died from mesothelioma in 2000 – employees’ mesothelioma caused by asbestos – inhalation of asbestos fibre not an injury simpliciter – mesothelioma a disease, not an injury simpliciter – employees contracted mesothelioma in 1999 – employees’ disease of mesothelioma first resulted in impairment in 1999 – no actual or accrued statutory liability to pay compensation in respect of employees’ injury or disease prior to 1988 – Comcare/Military Rehabilitation and Compensation Commission liable to pay compensation in respect of disease of mesothelioma resulting in deaths of employees – Telstra not liable to pay compensation.
Commonwealth Employees’ Rehabilitation and Compensation Act 1988 (Cth) s 101(2)
Safety, Rehabilitation and Compensation Act 1988 (Cth) ss 4(1), 5, 7, 14(1), 17 and 18
Australian Blue Asbestos Ltd v Rees (unreported, Supreme Court of WA (Full Court), Appeal No 126 of 1981, 9 October 1981)
Australian Postal Corporation v Oudyn (2003) 77 ALD 659
The Commonwealth of Australia v TransAdelaide [2001] NSWCA 52
Connair Pty Ltd v Frederiksen (1979) 142 CLR 485
Crimmins v Stevedoring Industry Finance Committee (1999) 200 CLR 1
Department of Defence v West (1998) 85 FCR 491
Favelle Mort Ltd v Murray (1976) 133 CLR 580
Fisher v Hebburn Ltd (1960) 105 CLR 188
Frank Manford Pty Ltd v QBE Insurance Ltd (unreported, Supreme Court of WA (Full Court), Appeal No 51 of 1992, 23 June 1993, BC 9301328)
GRE Insurance Ltd v Bristile Ltd (1991) 5 WAR 440
Re Halliday and Comcare (1994) 19 AAR 431
Lees v Comcare (1999) 29 AAR 350
Martindale v Burrows [1997] 1 Qd R 243
Orica Ltd v CGU Insurance Ltd [2003] NSWCA 331
Rosillo v Telstra Corporation Ltd (2003) 38 AAR 243
Slattery v Comcare (1996) 70 FCR 131
REASONS FOR DECISION
6 May 2005
Associate Professor S D Hotop, Deputy President
Dr D Weerasooriya, Member
Introduction
1. Applications have been made to the Tribunal for review of the following 2 groups of reviewable decisions made under the Safety, Rehabilitation and Compensation Act 1988 (Cth) (“the SRC Act”):
(a) The Hill Reviewable Decisions
·a reviewable decision of Comcare, dated 13 November 2000, that compensation is not payable under the SRC Act pursuant to a claim for compensation, dated 18 August 2000, made by Frank Hill (“Mr Hill”) in respect of a medical condition described as “mesothelioma” (Application № W2000/422);
·a reviewable decision of Telstra Corporation Limited (“Telstra”), dated 9 January 2001, affirming a determination of 18 December 2000 that Telstra is not liable to pay compensation under the SRC Act pursuant to a claim for compensation, dated 18 August 2000, made by Mr Hill in respect of a medical condition described as “mesothelioma” (Application № W2001/12);
·a reviewable decision of Comcare, dated 6 April 2001, affirming a determination of 16 February 2001 that Comcare is not liable to pay compensation pursuant to s 17 or s 18 of the SRC Act to Audrey Maude Hill (“Mrs Hill”), the widow of Mr Hill, in respect of the medical condition of mesothelioma which resulted in Mr Hill’s death (Application № W2001/199);
·a reviewable decision of Telstra, dated 18 September 2001, affirming a determination of 10 September 2001 that Telstra is not liable to pay compensation pursuant to s 17 or s 18 of the SRC Act to Mrs Hill in respect of the medical condition of mesothelioma which resulted in Mr Hill’s death (Application № W2001/348);
·a reviewable decision of the Military Compensation and Rehabilitation Service (“MCRS”), dated 16 November 2001, affirming a determination of 24 October 2001 that compensation is not payable under the SRC Act pursuant to a claim for compensation, dated 18 August 2000, made by Mr Hill in respect of a medical condition described as “mesothelioma” (Application № W2001/429);
(b) The Etheridge Reviewable Decisions
·a reviewable decision of Telstra, dated 27 December 2000, affirming a determination of 26 October 2000 that Telstra is not liable to pay compensation pursuant to s 17 or s 18 of the SRC Act to Ingeborg Etheridge (“Mrs Etheridge”), the widow of Cedric Etheridge (“Mr Etheridge”), in respect of the medical condition of mesothelioma which resulted in Mr Etheridge’s death (Application № W2001/16);
·a reviewable decision of Comcare, dated 2 April 2001, affirming a determination of 27 February 2001 that Comcare is not liable to pay compensation pursuant to s 17 or s 18 of the SRC Act to Mrs Etheridge in respect of the medical condition of mesothelioma which resulted in Mr Etheridge’s death (Application № W2001/118);
·a reviewable decision of Telstra, dated 18 September 2001, affirming a determination of 7 September 2001 that Telstra is not liable to pay compensation under the SRC Act to The Public Trustee, the legal personal representative of the late Mr Etheridge, pursuant to a claim for compensation made on behalf of Mr Etheridge in May 2000 in respect of a medical condition described as “mesothelioma” (Application № W2001/350);
·a reviewable decision of Comcare, dated 16 November 2001, affirming a determination of 26 September 2001 that Comcare is not liable to pay compensation under the SRC Act pursuant to a claim for compensation lodged on behalf of Mr Etheridge’s estate on 24 January 2001 in respect of a medical condition described as “mesothelioma” (Application № W2001/430);
·a reviewable decision of the MCRS, dated 16 November 2001, affirming a determination of 24 October 2001 that compensation is not payable under the SRC Act pursuant to a claim for compensation lodged on behalf of Mr Etheridge’s estate on 24 January 2001 in respect of a medical condition described as “mesothelioma” (Application № W2001/431).
2. At the hearing the applicants were represented by Mr M Carey of counsel, Comcare and the Military Rehabilitation and Compensation Commission (“MRCC”) (the successor of the MCRS) were represented by Mr T Howe of counsel, and Telstra was represented by Mr P Elliott of Queen’s Counsel and Mr J Wallace of counsel. The Tribunal had before it the documents (“T documents”) lodged by each of the respondents in respect of each relevant Application for Review in accordance with s 37 of the Administrative Appeals Tribunal Act 1975 (Cth), and the following exhibits tendered in evidence by the parties:
·bundle of documents comprising Royal Australian RAN (“RAN”) service records of Frank Hill (Exhibit A1);
·bundle of documents comprising Postmaster-General’s Department and Australian Telecommunications Commission employment records of Frank Hill (Exhibit A2);
·bundle of documents comprising occupational health surveys regarding various telephone exchanges (Exhibit A3);
·report of Professor Bruce Robinson, Consultant Chest Physician, regarding Cedric Etheridge, dated 25 May 2000 (Exhibit A4);
·bundle of documents comprising Australian Army and Australian Military Forces service records of Cedric Etheridge (Exhibit A5);
·Curriculum Vitae of Michael Kottek (Exhibit A6);
·report of Michael Kottek, Occupational and Environmental Health Consultant, regarding Frank Hill, dated 29 August 2003, and statement of Frank Hill, dated 30 August 2000 (Exhibit A7);
·report of Michael Kottek regarding Cedric Etheridge, dated 29 August 2003 (Exhibit A8);
·Curriculum Vitae of Dr James Leigh (Exhibit A9);
·report of Dr James Leigh, Consultant Occupational Physician, regarding Frank Hill, dated 10 August 2003 (Exhibit A10);
·report of Dr James Leigh regarding Cedric Etheridge, dated 10 August 2003 (Exhibit A11);
·report of Michael Kottek regarding Frank Hill and Cedric Etheridge, dated 29 August 2003 (Exhibit R1);
·Curriculum Vitae of Clinical Associate Professor A B X Breslin (Exhibit R2);
·report of Clinical Associate Professor A B X Breslin, Consultant Thoracic Physician, dated 31 March 2003 (Exhibit R3);
·letter from Dibbs Barker Gosling to Sparke Helmore, dated 6 October 2003 (Exhibit R4);
·letter from Sparke Helmore to Professor Breslin, dated 24 October 2003 (Exhibit R5);
·report of Clinical Associate Professor A B X Breslin regarding Frank Hill, dated 28 October 2003 (Exhibit R6);
·report of Clinical Associate Professor A B X Breslin regaring Cedric Etheridge, dated 19 November 2003 (Exhibit R7);
·report of Dr Julian Lee, Thoracic Physician, regarding Cedric Etheridge, dated 10 June 2002 (Exhibit R8);
·report of Dr Julian Lee regarding Frank Hill and Cedric Etheridge, dated 28 February 2003 (Exhibit R9);
·bundle of documents comprising extracts of records of Frank Hill’s treatment at Repatriation General Hospital, Hollywood (Exhibit R10); and
·documents containing data and historical information regarding HMAS Dubbo (Exhibit R 11).
[Exhibit R 1 and R11 were tendered by Comcare/MRCC, and Exhibits R2-R10 were tendered by Telstra.]
Oral evidence was given by Michael Kottek and Dr James Leigh (who were called by the applicants), and by Clinical Associate Professor A B X Breslin (who was called by Telstra).
The Factual Background
3. A “Statement of Agreed Facts” in respect of each of Mr Hill and Mr Etheridge was filed with the Tribunal on 2 July 2002. The Tribunal accepts the account of the factual background as set out in each of those statements.
Mr Hill
4. Mr Hill was born on 4 January 1926. He was raised in Perth and attended school until the age of 13 years.
5. In or about 1940 Mr Hill commenced work as a messenger boy with an unknown employer.
6. In or about 1941 Mr Hill was employed as a storeman with Attwood Motors.
7. Mr Hill commenced service with the Royal Australian Navy (“RAN”) on 7 July 1943. During the period of service he was designated a Stoker and based at the following depots: Cerberus (9 July 1943 to 12 November 1943), Leeuwin (13 November 1943 to 1 February 1944, 12 to 22 February 1944, 25 February to 3 March 1944, 6 March 1944 to 11 July 1944, 21 February 1946 to 29 March 1946, 18 August 1946 to 17 September 1946), Ceylon (2 to 11 February 1944), Lonsdale (12 to 20 February 1946, 30 March to 1 April 1946) and Torrens (2 to 6 April 1946).
8. During the period of service with the RAN Mr Hill served on HMAS Sussex (2 days from 23 to 24 February 1944), HMAS Gambia (2 days from 4 to 5 March 1944) and for a substantial period on HMAS Dubbo (a corvette) between 12 July 1944 and 11 February 1946, and again between 7 April 1946 and 17 August 1946.
9. HMAS Dubbo was engaged in exercises between 17 March and 9 September 1944 before sailing between Onslow, Fremantle, Geraldton, Onslow, Broome and Darwin by 4 April 1945. HMAS Dubbo arrived in Port Moresby on 8 April 1945 and then sailed on to various ports in the South-West Pacific theatre before returning to Brisbane on 15 July 1945. HMAS Dubbo again sailed for ports in the South-West Pacific area on and from 9 August 1945, returning to Brisbane at some point before 19 December 1945 after which it sailed between Australian ports. During the period of service on HMAS Dubbo Mr Hill saw service outside Australian territorial waters.
10. Mr Hill performed stoker duties in the engine and boiler rooms while serving on HMAS Dubbo. The ship was powered by steam engines, and extensive areas of the engine, boiler and pipes were lagged with asbestos.
11. Mr Hill was discharged from the RAN on 17 September 1946.
12. Mr Hill was exposed to asbestos in the course of his period of service with the RAN.
13. In or about late 1946 Mr Hill resumed employment with Attwood Motors as a storeman and continued in those duties for a further 6 to 8 months.
14. In early-to-mid-1947 Mr Hill commenced employment with Lamson’s Engineering as a technician for a period of approximately 6 months.
15. Mr Hill commenced employment with the Postmaster-General’s Department (“PMG”) in or about 1948 as a telephone technician. In the course of his employment with the PMG he was involved in installing automatic telephone exchange equipment requiring him at times to drill through concrete and brick walls. At times he worked on temporary exchanges some of which were constructed from asbestos cement sheets. Mr Hill is likely to have at times cut and drilled those sheets in order to feed cable through the sheet. Mr Hill used a handsaw or rasp to perform this work which raised dust which may at times have contained some asbestos.
16. Mr Hill worked on a variety of exchanges including Tuart Hill, Mount Yokine, Kalamunda, Mundaring, Mount Hawthorn, Subiaco, Wattle Grove, Midland, Bassendean, Maylands, and Scarborough. He continued in PMG employment until he was formally retired from the PMG on the grounds of invalidity on 10 May 1955.
17. In or about March 1954 Mr Hill was admitted to hospital with pulmonary tuberculosis for which he was granted a Veterans pension at 100% of the “general rate”, with effect on and from 4 March 1954.
18. Mr Hill underwent treatment for the pulmonary tuberculosis by way of plombage, triple antituberculosis chemotherapy, and in 1961 he underwent left thoracoplasty, having developed massive haemoptysis.
19. In or about 1958 Mr Hill commenced employment with Jackson’s at Midland and in Hay Street, Perth as a furniture salesman.
20. In or about 1959 Mr Hill was employed by Foy & Gibson as a furniture salesman and ceased at about the time his left lung condition required surgery.
21. In or about 1962 Mr Hill commenced employment with John Allen’s as a furniture salesman for a brief period.
22. Mr Hill recommenced employment with the PMG on 27 July 1962 as a technical and clerical assistant at the Pier Street Exchange. The Pier Street Exchange contained asbestos. Mr Hill was promoted to the position of Technical Assistant Grade II on 4 July 1974. In this position he assisted the Works Specification Officer in the maintenance of records, ordering, preparation and dispatch of modification kits for installation.
23. Mr Hill remained employed with the PMG until 30 June 1975. By operation of section 16 of the Postal and Telecommunications Commissions (Transitional Provisions) Act 1975 he continued in service with the Australian Telecommunications Commission Service created by section 38 of the Telecommunications Act 1975.
24. On 4 February 1977 Mr Hill formally retired from employment with the Australian Telecommunications Commission (“ATC”) due to ill health. Mr Hill last attended work on 26 August 1976. During the period 1 July 1975 to 4 February 1977, Mr Hill had taken recreation leave and extensive sick leave.
25. In late 1999 Mr Hill consulted his general practitioner, Dr Y C Low, concerning symptoms related to mesothelioma. After a period of investigation and treatment Mr Hill was referred to Dr David Bucens and then to Dr J Alvarez and was admitted to The Royal Perth Hospital in August 2000.
26. On or about 3 August 2000 Mr Hill was diagnosed with malignant mesothelioma.
27. On 16 December 2000, Mr Hill died. The cause of death was mesothelioma, with ischaemic heart disease being a contributory cause.
Mr Etheridge
28. Mr Etheridge was born on 15 December 1919. He was raised in Kalgoorlie until about 1935 when he moved to Perth with his family. He completed High School in Kalgoorlie and then commenced at the School of Mines in Kalgoorlie. He transferred to Perth Technical College in 1936 and studied assaying until 1937.
29. From 1935, and while continuing his studies, Mr Etheridge commenced work with Wreath and Lapsley, a firm of assayists and metallurgists, in St George’s Terrace in Perth. He was employed in a junior capacity.
30. He continued in employment on the termination of the employer’s partnership with Mr Lapsley as a part-time employee in an assay laboratory in West Perth.
31. Mr Etheridge worked for approximately 12 months between 1937 and 1938 as a laboratory assistant with Felton, Grimwade and Bickford in Charles Street in North Perth. The employer manufactured and tested products such as “Aeroplane Jelly” and cough medicine. It is unlikely that Mr Etheridge was exposed to any respirable asbestos in this employment.
32. Mr Etheridge sat the Public Service entrance examination for the PMG in 1938.
33. On 6 March 1939, Mr Etheridge commenced Commonwealth employment with the PMG. He was engaged as an apprentice linesman in training and was required to perform cable-jointing duties.
34. In about January 1939 Mr Etheridge enlisted with the 35th Australian Engineers while continuing employment with the PMG.
35. In the course of his PMG employment prior to September 1939 Mr Etheridge had contact with asbestos cement pits while undertaking cable-jointing duties. In the course of this work Mr Etheridge may have been exposed to asbestos.
36. Mr Etheridge began full-time war service on 5 September 1939. On 5 June 1940 he enlisted in the Australian Army (35th Fortress Company) and was classified as an Electrician. He continued in service until 29 October 1945. He was not required for operational service, nor did he engage in actual combat with the enemy, during the period 10 June 1940 to 29 October 1945. He was posted to Fremantle, Claremont, and Rottnest Island in Western Australia, as well as Middle Head in Sydney, New South Wales. Most of his time in the Army during this period was at Rottnest Island.
37. While in the Army Mr Etheridge continued to perform the duties of pit installation, cable jointing and repair in the fortress areas of Garden Island and Rottnest Island. In the course of his service he handled hundreds of pits containing asbestos and was exposed to asbestos.
38. During the course of his Army service Mr Etheridge was exposed to asbestos when staffing the engine rooms where there was dust from asbestos lagging on manifolds and pipes and related attachments.
39. During the course of his Army service Mr Etheridge was exposed to asbestos from drilling and sawing through asbestos cement sheeting used in building construction, when coming into contact with asbestos lagging on hot water and other piping, and handling fire blankets at all fire points in tunnels leading to magazines, and at the barracks which gave off asbestos dust. He also drilled into asbestos sheets used as a firewall backing on switchboards when fitting wiring and related attachments which gave rise to further asbestos exposure.
40. On discharge from the Army on 29 October 1945 Mr Etheridge returned to civilian employment with the PMG and attended the Engineers Branch Training School in Sydney, New South Wales. That course was a rehabilitation course which ran for a period of 12 months. During that period Mr Etheridge performed cable-jointing work, including laying asbestos cement pits and working in those pits in the Sydney metropolitan area. In the course of that work Mr Etheridge may have been exposed to asbestos.
41. In or about 1946 Mr Etheridge was engaged in work laying cables and installing asbestos cement pits between Sydney and Parramatta for approximately two to three years. In the course of those duties he may have been exposed to asbestos. During that period he studied and passed examinations to qualify as a PMG technician.
42. While in Sydney, Mr Etheridge changed jobs within the PMG to perform technician duties in exchanges. He worked in various substations including Randwick, Hornsby, Burwood, City South, and City North.
43. In approximately 1952 Mr Etheridge was promoted to the position of Senior Technician and was transferred to Western Australia. He worked at various substations including Mount Hawthorn, City Central, Tuart Hill, Wanneroo, and in the Perth area based at the William Street depot.
44. As a Senior Technician Mr Etheridge’s duties included the instruction of junior employees and the supervision of technical work which at times would have included “hands-on” instruction and assistance. He continued in those duties until 1977.
45. Mr Etheridge remained employed with the PMG until 30 June 1975. By operation of section 16 of the Postal and Telecommunications Commissions (Transitional Provisions) Act 1975 he continued in service with the Australian Telecommunications Commission Service created by section 38 of the Telecommunications Act 1975.
46. Mr Etheridge was deemed unfit to continue his employment with the ATC from 1 October 1975, and was formally retired in 1977.
47. Mr Etheridge visited Wittenoom two or three times from in or about 1959 to 1965. He visited the processing plant in Wittenoom on several occasions. That plant processed asbestos.
48. After the conclusion of the Second World War Mr Etheridge was involved in building a house and renovations in which the construction materials included asbestos cement sheeting and asbestos wool insulation. He cut asbestos sheets using hand tools including a power drill and hand saw.
49. In or about August 1999 Mr Etheridge consulted his general practitioner, Dr Wright, concerning a persistent cough. After a period of investigation and treatment Mr Etheridge was referred to Dr Alan James and admitted to Hollywood Hospital in March 2000.
50. On or about 10 March 2000 Mr Etheridge was diagnosed with malignant mesothelioma.
51. On 21 July 2000 Mr Etheridge died. The cause of death was mesothelioma.
The Evidence
Statutory Declaration of Frank Hill
52. Mr Hill made a statutory declaration on 3 December 2000 setting out his employment history and indicating those employments in which he was not exposed to asbestos and those employments in which he was exposed to asbestos. He stated that he was not exposed to asbestos in the following employments:
·as a messenger boy in 1940-1941;
·as a storeman with Attwood Motors in 1941-1943 and 1946-1947;
·as a technician with Lawson’s Engineering 1947-1948;
·as a furniture salesman with Jackson’s in 1958-1959;
·as a furniture salesman with Foy & Gibson in 1959-1961;
·as a furniture salesman with John Allen’s in 1962.
As regards his employment with the RAN and the PMG, Mr Hill stated:
“1943-1946
3.2I was employed by the Royal Australian RAN as a stoker aboard the HMAS Dubbo. I served in the South Pacific. My work was in the engine and boiler room. The ship had steam engines, which were lagged with asbestos, also lagged were the pipes and the boiler.”
“1948-1953
3.4I was employed by the PMG as a telephone technician. I installed automatic exchange equipment, drilling through concrete and brick walls and taking out old exchanges. I also worked on temporary exchanges where we placed old exchanges equipment from main exchanges. These temporary exchanges were built from asbestos cement sheets. My work included cutting or drilling these sheets to put cables through. I used a handsaw and rasp to do this work. This process raised asbestos dust which was visible, it would also settle on my clothes and in my hair. I believe these exchanges were in Tuart Hill/Mount Yokine, Kalamunda, Mundaring, Mount Hawthorn, Subiaco, Wattle Grove, Midland, Bassendean, Maylands and Scarborough. There were other exchanges however I cannot recall them all. I am unsure which exchanges contained asbestos. As time went by these temporary exchanges were replaced by main exchanges in those suburbs.”
“1962
3.8I was employed by PMG (later Telecom) at the Pier Street Exchange as a technical/clerical assistant. My work was in the stores where I handled equipment. I believe I may have worked with some products which contained asbestos such as cable pits however I am unable to recall each and every item which may have contained asbestos after all that time.
3.9In 1976 I retired on the basis of ill health because of my breathing and troubles with stress. I moved to Mandurah.
3.10My only recollection of exposure to asbestos dust is that outlined above.”
(W2001/429, T36)
Statement of Cedric Etheridge
53. In a signed statement dated 1 June 2000, Mr Etheridge set out his employment history and indicated those employments in which he did not recall being exposed to asbestos and those employments in which he believed that he was exposed to asbestos. He stated that he did not recall being exposed to asbestos in the following employments:
·as a junior worker with Wreath and Laspsley in 1935-1937;
·as a laboratory assistant with Felton, Grimwade and Bickford in 1937-1938.
As regards his employment with the PMG (1939, 1945-1977) and the Australian Army (1939-1945), Mr Etheridge stated:
“From commencement with the PMG in 1939, I essentially continued working with them until my retirement in 1977. The only breaks in this employment occurred during the time that I was in the army from 1939 to 1945. My time in the army was as a result of secondment from the PMG to the Commonwealth Department of Defence doing same undertakings.
I believe that I sustained exposure to asbestos both in my work with the PMG and in my period in the army.
From the time that I commenced with the PMG in 1939, for about the first 7 months, my work was in laying pits and cable jointing. The pits were asbestos pits, soft moulded pits which had a high percentage of asbestos in their composition. I can remember a lot of the edges of the pits had fibres sticking out which easily brushed off.
Entry apertures for cabling and drainage holes were cut into the pits by sawing, drilling and rasping.
The use of asbestos pits of all sizes was extensive. Exposure to asbestos occurred not only on handling and cutting on first installation in those years but also when accessing pits already installed to replace, upgrade or simply add to cabling. In the fortress areas of Rottnest and Garden Islands in WA alone, hundreds of these units were used.
I can remember dust being generated from sawing, drilling and rasping of the pits.
After about 7 months with the PMG being a member of the RAE, AMF (Militia), in about July 1939, I was seconded from the PMG to the army. I spent about the first 6 months as a lance corporal then about 1 year as a corporal followed by about 6 months as a sergeant and thereafter the balance of my time to 1945 as a staff sergeant, T/WO (1A). I then returned to the PMG Engineers Branch Sydney, NSW Training School.
In my army duties I came into contact with asbestos, not just with cable jointing which entailed the use of asbestos cement pits but also as a result of other duties, for example, in workshops and at night it would be the responsibility of the engineers to man the search lights or man the engine rooms. If manning the engine rooms there would be asbestos dust from lagging on manifolds and pipes, etc.
Also a lot of the buildings that we were running cables through were of asbestos cement construction that we were drilling and sawing through these. Also in ceilings we were regularly coming across lagged pipework, eg hot water pipes.
We also handled fire blankets which were at all fire points in tunnels going to the magazines and at the barracks. Every time you would handle a fire blanket the asbestos tended to come away and there was dust from the blanket's fibres.
Apart from my time in Western Australia with the army I also went over east and to the Southwest Pacific with the army. I worked on cable jointing installations on fortresses and magazines and underground tunnels. We were still using asbestos pits. Fire protection was also in common use for switchboards and areas that were fire risks. My recollection is that the switchboards were backed with asbestos and that these were drilled through for wirings and fittings.
Generally the break up of my duties in the army was that day time was cable jointing work and night time was other duties, both with exposure to asbestos.
Induction to Army Services Units entailed same ‘trade’ in cable jointing and usage of same materials and applications. Particularly within the permanent installations of Defence Establishments as engine-rooms, gun emplacements, tunnels, magazines, Defence Department buildings, barracks, etc where cabling for communications was required. This included all types of situations within buildings where dust from asbestos fire-retardant and insulating fibres was constantly encountered and necessarily disturbed.
Duties of fortress engineers included installation and maintenance of ‘hot water boiler’ and services equipment which was insulated with asbestos wool ‘plastering’ and lagging to the many shower, cooking, messing workshops and ablution facilities.
Sheeting asbestos was widely used and cut by hand saws and rasp files in multiple situations for signal equipment installations. Particularly in sand drift situations where fortress installations required rivetting by sheets and remnants being cut to requirements. Also used as walling to ‘manholes’ where ‘pit’ sizes were too small or shallow.
‘Signal Posts’ were also areas where wool asbestos was extensively used as noise insulation as well as fire retardant materials where constant maintenance and installations caused disturbance and contact.
Fire protection asbestos woven blankets were also present and at times handled in many locations abovementioned and at ‘Fire Station’ Points. Throughout my 7 years army service as a foreman of signals, (seconded from the RAE), it would have been almost daily contact with some form in my duties to have made contact with such commonly accepted equipment as asbestos. Also in ceilings where it was also used for insulation and fire retardant, where cabling was so very necessary for multiple signal equipment access. Roofing cover above in very many defence establishments was itself corrugated asbestos, with the underside ‘rough’ where direct contact in confined space was unavoidable and arduous in the placement of telecommunication cables, wiring and equipment.
Within the scope of duties of the Royal Australian Engineers and of Fortress Signal Companies direct contact with hot water pipes asbestos ‘soft rope lagging’ was constantly encountered. Again in very confined and dusty situations I personally experienced.
After the war I went back to the PMG and did so by returning to training school. I attended a 12 month rehabilitation course which was run In Sydney. In this period I again did cable jointing work including laying asbestos cement pits and working in these pits. This was in the Sydney/Parramatta area.
I then transferred to the exchange area as a technician. On this change in duties my asbestos exposure would have occurred from contact with fire protection devices on power boards, etc.
I was employed on substation maintenance working in Sydney until 1952 or 1953 when I transferred back to Western Australia.
On transfer back to Western Australia I continued working in substation maintenance. This brought me into contact with asbestos which was used in various buildings in Perth, for example the ceiling and walling lining at Royal Perth Hospital was asbestos cement sheeting in the older parts of the building on Murray Street.
By this stage I was a senior technician and was training younger employees. Notwithstanding that I was a senior technician I was still in contact with asbestos as I showed younger employees what they needed to do, asbestos cement was used widely, not just for partitioning but also for switchboard equipment and there was also other fireproofing or lagging around us, eg lagged pipework, etc.
3.11"- --
I worked as a senior technician until 1977 when I retired.”
Mr Etheridge also stated:
“Apart from my time in the PMG and in the army I also visited Wittenoom 2-3 times with the St John Ambulance Brigade and on holidays. The visits were in about 1959, 1961 and 1965. I recall visiting the metallurgist in Wittenoom, a Mr McMahon. I recall going and visiting him in the processing plant in Wittenoom several times. Otherwise when I stayed at Wittenoom I stayed in the township camping at the showgrounds.
Apart from my exposure to asbestos in the army and with the PMG I’ve also been involved in building a couple of houses which have used asbestos cement sheeting. That was in the period after the war.
I secured war service finance to build a house, the house had concrete external walls but was lined with asbestos cement sheeting. I cut any sheeting that needed cutting using hand tools. In 1977 when I retired I moved to a brick home near Trigg which I extended with a builder's licence from the City of Stirling. The second storey of the house was constructed of asbestos cement sheeting. I used flat sheeting and Shadowline I had a power drill but otherwise used a handsaw.
Another possible exposure to asbestos occurred as a result of using some asbestos wool from Bells Asbestos. One of the sergeants, a Frank Code, that had been in the Royal Australian Engineers Fortress section of the army as I had been, became the manager at Bells Asbestos when he was discharged. At the time Bells was situated in Murray Street. Through him I arranged to buy 3 potato sacks full of asbestos wool which I used for insulation in the first home that I built to insulate a hot water service. I also used same when I built the Trigg house extensions insulating the hot water storage heater tanks.”
(W2001/431, T41)
Medical reports regarding Mr Hill and Mr Etheridge prepared shortly before death
Dr David Bucens
54. A report of Dr David Bucens, Respiratory Physician, dated 2 September 2000, regarding Mr Hill states as follows:
“…
HISTORY
I first saw Mr Hill on 15.01.00 with a large, recurrent, blood-stained, right sided pleural effusion. His presenting symptoms were gradually increasing breathlessness since the beginning of October 1999, mild wheeziness in the recumbent position and weight loss of approximately 5kg. Systematic inquiry revealed angina pectoris on exertion and symptoms of prostatic enlargement. Past medical history included left sided pulmonary tuberculosis in 1953 which was initially treated with plombage and subsequently triple antituberculosis chemotherapy. Massive haemoptysis occurred in 1961 which led to left thoracoplasty. Other problems included coronary artery disease and glaucoma. He was a light cigarette smoker until stopping at 28 years of age. Mr Hill claimed exposure to asbestos dust while working as a stoker in the Royal Australian RAN from 1943 to 1947 and thereafter while working for PMG/Telecom from 1948 to 1975.
EXAMINATION
On examination he was a centrally obese elderly man with a left postero-lateral thoracotomy scar and signs of a moderate size right sided pleural effusion. Expansion of the left upper chest was severely reduced. Digital clubbing, peripheral lymphadenopathy and hepatomegaly were absent. There were no signs of cardiac failure.
INVESTIGATION
A chest radiograph (06.01.00) showed a moderate to large right sided pleural effusion, left first and second rib thoracoplasty and cardiac size at the upper limit of normal. The pleural effusion was absent on a film dated 29.10.99. The results of various blood tests were either normal or non-specific. His family doctor, Dr Y C Low, had performed pleural aspiration which yielded over a litre of sterile blood-stained pleural fluid with no malignant cells. Spirometry revealed a severely reduced forced vital capacity without airflow limitation.
MANAGEMENT
I performed pleural aspiration twice in late January 2000 and obtained 800ml and 1000ml of blood-stained serous fluid. The fluid had the characteristics of an exudate which contained no malignant cells or tuberculosis bacteria. A pleural biopsy was not performed. A CT Scan of thorax showed normal pleura, a right sided pleural effusion and passive collapse of the right lower and middle lobes. The lung parenchyma and mediastinum were otherwise normal.
Because the pleural effusion was reaccumulating rapidly and a definite diagnosis had not been made, I referred him to Dr J Alvarez (cardiothoracic surgeon) at Sir Charles Gairdner Hospital with a view to thoracoscopy, pleural biopsy and pleurodesis. The anaesthetist considered Mr Hill to be unfit for general anaesthesia and, therefore, an intercostal tube was inserted and talc pleurodesis performed.
The talc pleurodesis achieved pleural symphysis (i.e. obliteration of the pleural space) which prevented further accumulation of fluid. Although the pleural effusion did not recur, his condition has gradually deteriorated and reached the point where domiciliary oxygen is required. A repeat CT scan of the thorax (17.07.00) showed severe right sided pleural thickening with resultant ‘encasement lung’ and a small residual loculated basal pleural effusion. This appearance represents marked deterioration since the initial CT scan in January 2000.
A cutting needle biopsy of a right sided anterior mediastinal pleural mass was performed on 03.08.00 at Royal Perth Hospital. Histology of the tissue core revealed a mixed epithelial and sarcomatous (biphasic) malignant mesothelioma.
OPINION
Mr Hill is suffering from right sided pleural malignant mesothelioma which has a mixed epithelial and sarcomatous histology. His prognosis is very poor with a life expectancy of 3-6 months. Poor prognostic indicators include age, poor performance status and the sarcomatous histological component.
Although malignant mesothelioma has been described in individuals without known exposure to asbestos, it is accepted that exposure to asbestos is the most important causative factor. Mr Hill has a clear history of exposure while in the Royal Australian RAN as a stoker. Probably less intense exposure occurred while working for PMG/Telecom. However, both occupations had the potential for sufficient exposure to asbestos dust to be implicated in the subsequent development of malignant mesothelioma. There are no features of asbestosis which indicates that the exposure was not heavy…”
(W2001/429, T6)
Professor Bruce Robinson
55. A report of Professor Bruce Robinson, Consultant Chest Physician, dated 25 May 2000, regarding Mr Etheridge states as follows:
“History
Mr Etheridge describes cough and weight loss present for approximately eight months. He quit smoking about 30 years ago.
He was exposed to asbestos whilst working in the army, working with lagging (he was a fortress engineer), the lagging mostly being present on manifolds. He was required to work with cables, asbestos pits and fire protection and was exposed to asbestos at all times. This occurred during his work with the PMG and also in the army. He did not work at Wittenoom although he visited relatives there briefly between about 1958 and 1960. He also had some incidental exposure whilst cutting sheets building two homes after the war. Post-war he has worked as a telecom technician and has had no significant asbestos exposure during that time. He has a past history of cystitis and hernias.
Examination
Trachea was slightly deviated to the right and heart sounds were soft. He was dull at the right lower zone with reduced percussion notes.
Investigations
Biopsy of the right lung plaque showed malignant cells with the characteristics of probable desmoplastic mesothelioma …. ESR elevated at 59. Platelet count 281. Urea and electrolytes normal. Chest x-ray on 3.4.00 showed pleural thickening on the right with a small effusion on the right and reduction of lung volumes on the left and depression of the horizontal fissure.
Follow-up CT scan is awaited.
Diagnosis
Desmoplastic mesothelioma.
Treatment
Patient is being considered for chemotherapy. He will also require pain relief.
Life expectancy
Median survival is 9 months from diagnosis. Desmoplastic mesothelioma can have a more varied course, some patients having aggressive disease.
Aetiology
I consider the mesothelioma to be due to the patient's exposure to asbestos as described above.
…”
(Exhibit A4)
The evidence of the expert witnesses
Michael Kottek
56. Michael Kottek confirmed that he is a qualified Occupational and Environmental Health Consultant. His curriculum vitae, which was tendered in evidence (Exhibit A6), states that he is, inter alia, a member of the Australian Institute of Occupational Hygienists and is a Certified Industrial Hygienist, American Board of Industrial Hygiene, and has worked as a consultant in the area of occupational health/hygiene since 1991. He said that he has conducted many asbestos surveys of all types of buildings and facilities and has prepared many reports assessing the exposure of persons to asbestos. He estimated that 80%-90% of his work relates to exposure to asbestos and asbestos dust.
57. Mr Kottek confirmed that he had, at the request of the applicants’ solicitors, prepared a report dated 29 August 2003 in respect of each of Mr Hill and Mr Etheridge. Mr Kottek’s report regarding Mr Hill states as follows:
“Thank you for your Ietter dated 5 August 2003 regarding Mr Hill’s occupational history and the causation of his mesothelioma … Based on the information provided in your letter and the associated enclosures it is clear that Mr Hill has experienced some exposure to amphibole asbestos during his time with the RAN [in the period 1943-46] and the PMG in the period 1948-53. It is my opinion that Mr Hill's exposure to asbestos in these positions would have resulted in an exposure exceeding the background environmental exposure experienced by the general population. Consequently, these two sources of exposure are likely to have significantly increased Mr Hill's risk of contracting mesothelioma. This opinion relies on your letter and enclosures, my own experimental work on airborne dust levels generated by the handling of asbestos containing materials, and my own inspection of the Castlemaine (a Bathurst class minesweeper) which has been restored and moored at Williamstown, Victoria. I note that the Castlemaine and Dubbo are both Bathurst class minesweepers and I have assumed that the use of asbestos insulation on Dubbo was not materially different from its use on the Castlemaine.
I note that it is your desire for a report my (sic) opinion as to whether any of Mr Hill's occupational exposures can be excluded as a cause of his mesothelioma. This question is best addressed by comparing any possible risk of mesothelioma from Mr Hill’s other employment to the increased risk caused by the PMG and RAN exposures. This can only be done in a qualitative manner, as the history provided makes it impossible to quantitatively estimate Mr Hill’s exposure with the RAN and PMG. In the circumstances, I believe that Mr Hill’s other employment can be excluded as likely cause of his mesothelioma unless there was sustained but low intensity exposure to asbestos, or sporadic but intense exposure to asbestos.
In this context I offer the following observations on Mr Hill’s employment excluding his time with the PMG and RAN.
There is nothing to suggest that Mr Hill’s employment as a messenger boy in 1940 - 41 would have involved anything exceeding the environmental exposure to asbestos experienced by the general population.
Mr Hill’s employment as a salesman in 1941-43 could possibly have involved some minor exposure to asbestos if Attwood Motors had a workshop, and Mr Hill visited it when asbestos friction linings and the like were being worked on. This exposure is speculative, and any such exposure would have been to chrysotile only. Compared to Mr Hill’s verified exposure to amphibole asbestos, and given the low potency of chrysotile to induce mesothelioma, in my opinion this employment can be neglected as a plausible cause of Mr Hill’s mesothelioma.
It is unlikely that Mr Hill’s work installing dictaphone systems for Lamson Engineering in 1946-7 [involved significant exposure to asbestos]. As Mr Hill was unable to recall any asbestos exposure, sustained exposure to asbestos is unlikely. Given the period and location (Western Australia) there is practically no likelihood that Mr Hill’s work would have involved disturbance to sprayed asbestos. Overall, it is my opinion that it is far more likely than not this work is not a plausible cause of Mr Hill’s mesothelioma, when compared to his exposure in the RAN and PMG.
There is nothing to suggest that Mr Hill would have experienced sustained exposure to asbestos while working as a furniture salesman for Jacksons (in the period 1958-59), Foy Gibson (in the period 1959-61) or John Allens (in 1962). It is speculative, but possible, that the furniture showroom(s) contained friable asbestos material. However, there is nothing to suggest that any putative asbestos containing materials in the showrooms were disturbed while Mr Hill was working there. As such, it is my opinion that it is far more likely than not this work is not a plausible cause of Mr Hill’s mesothelioma, when compared to his established exposure in the RAN and PMG.
On the information provided it is unclear as to whether Mr Hill experienced asbestos exposure with the PMG in the period 1962-75. As Mr Hill suggests it is possible that he directly handled asbestos cement products, I am reluctant to fully exclude this work as a cause of his mesothelioma. The degree to which this work increased Mr Hill’s risk of mesothelioma (if at all) is dependant on the frequency and intensity with which he was exposed to airborne asbestos dust from the handling of such products.
On the information provided it is unclear as to whether Mr HilI experienced asbestos exposure beyond 1975 with the TCS (sic). As Mr Hill suggests it is possible that he directly handled asbestos cement products in this period, I am reluctant to fully exclude this work as a cause of his mesothelioma. The degree to which this work increased Mr Hill’s risk of mesothelioma (if at all) is dependant on the frequency and intensity with which he was exposed to airborne asbestos dust from the handling of such products.
…” (original emphasis)
(Exhibit A7). Mr Kottek’s report regarding Mr Etheridge states as follows:
“Thank you for your letter dated 5 August 2003 regarding Mr Etheridge’s occupational history and the causation of his mesothelioma… Based on the information provided in your letter and the associated enclosures it is clear that Mr Etheridge had experienced some exposure to amphibole asbestos during his time with the Army and PMG. It is my opinion that Mr Etheridge’s exposure to asbestos in these positions would have resulted in an exposure exceeding the background environmental exposure experienced by the general population. Consequently, these two sources of exposure are likely to have significantly increased Mr Etheridge’s risk of contracting mesothelioma. This opinion relies on your letter and enclosures, my own experimental work on airborne dust levels generated by the handling of asbestos containing materials.
I note that it is your desire for a report my (sic) opinion as to whether any of Mr Etheridge’s occupational exposures can be excluded as a cause of his mesothelioma. This question is best addressed by comparing any possible risk of mesothelioma from Mr Etheridge’s other employment to the increased risk caused by his exposure with the PMG and Army. This can only be done in a qualitative manner, as the history provided makes it impossible to quantitatively estimate Mr Etheridge’s exposure with the Army and PMG. In the circumstances, I believe that Mr Etheridge’s other employment can be excluded as likely cause of his mesothelioma unless there was sustained but low intensity exposure to asbestos, or sporadic but intense exposure to asbestos.
In this context I offer the following observations on Mr Etheridge's employment excluding his time with the PMG and Army.
It seems unlikely that any of the work Mr Etheridge carried out at Wreath & Lapsley in the period 1935-7 would have involved the direct handling of asbestos by Mr Etheridge. I base this opinion on my examination of a 1921 text entitled A Text Book of Assaying: For the Use of Those Connected with Mines. While I have not read the entire text from cover to cover, my perusal of the text clearly suggests that assaying in this period did not use asbestos as a reagent in assaying processes. The book does suggest possible asbestos exposure if asbestos gloves were used, and it is certainly possible that internal asbestos insulation was present on the furnaces and other apparatus used in an assaying laboratory. However, as Mr Etheridge was unable to recall the use of asbestos gloves, and the text makes no specific reference to them, it seems more likely than not that if gloves were used they would have been leather. The situation regarding internal asbestos in the furnaces is less clear. However, there is nothing to suggest that the routine use of furnaces in an assaying laboratory would have involved significant disturbance to any internal asbestos insulation that may have been present. Furthermore, it is likely that any putative exposure in this period would have been to chrysotile only. When compared to Mr Etheridge’s verified exposure to amphibole asbestos, exposure in this employment is speculative. Given the low potency of chrysotile to induce mesothelioma, in my opinion this employment can be neglected as a plausible cause of his mesothelioma.
Similar considerations apply to Mr Etheridge’s employment at Felton, Grimwade & Bickford in the period 1937-38. While some asbestos containing materials may have been present in the laboratory, there is nothing to suggest that they would have been significantly disturbed by routine operations. Furthermore, given the period, any asbestos containing materials would most likely have contained only chrysotile. Once again, when compared to Mr Etheridge’s verified exposure to amphibole asbestos, exposure in this employment is speculative. Given the low potency of chrysotile to induce mesothelioma, in my opinion this employment can be neglected as a plausible cause of his mesothelioma.
It is unclear how long Mr Etheridge was employed by TCS (sic). Paragraph 25 of the agreed statement of facts indicates that Mr Etheridge was deemed unfit to continue from 1 October 1975 (ie three months after commencing to be employed by TCS (sic)). If this is correct, given the nature of his duties and short duration of employment, it seems unlikely that any asbestos exposure in this period could significantly contribute to Mr Etheridge’s risk of mesothelioma. If Mr Etheridge was actively employed by TCS (sic) until formal retirement in 1977, I would be reluctant to fully exclude this work as a cause of his mesothelioma. The degree to which work with TCS (sic) increased Mr Etheridge's risk of mesothelioma (if at all) is dependant on the frequency and intensity with which he was exposed to airborne asbestos dust from the handling/disturbance of asbestos containing products.
…” (footnote omitted)
(Exhibit A8).
58. A further report of Mr Kottek, dated 29 August 2003, was tendered in evidence by Comcare. That report states as follows:
“Thank you for your letters dated 5 August 2003 regarding Messrs Hill & Etheridge. Both these letters had annexed a report dated 31 March 2003 by Associate Professor Breslin regarding the classification of mesothelioma as a disease or injury. I take this opportunity to provide some observations and some comments on the Breslin report.
The first observation to make is that as far as l am aware neither term (disease and injury) has a specific universally accepted medical meaning. The second observation to make is that Breslin has assumed (erroneously in my opinion) that the two terms are mutually exclusive. I offer a number of points in support of both these observations.
The first point is that injuries are but one subcategory of ‘Disease’ included in the two most recent editions of the International Classification of Diseases (ICD9 and ICD 10). This classification is overseen by the World Health Organisation and is widely used in research and the gathering of national and international statistics. However, I do also need to point out that earlier editions of the ICD carried the full title Manual of International Statistical Classification of Diseases, Injuries and Causes of Death. Nevertheless, I suggest that this provides some evidence that injury and disease are not mutually exclusive and that the classification of mesothelioma as a disease does not entail that it is not the result of an injury. I also need to point out that in ICD9 and ICD10, mesothelioma is classified as a disease, and not under the injury and poisoning category. However, ICD9 includes the condition ‘Toxic effects of asbestos’ (code 989.81) under the category of ‘Injury and Poisoning’. It appears that this category has not been included in ICD 10, although further research would be needed to clarify this point.
In terms of distinctions between injury and disease I believe the most relevant differences are that injuries are always caused by external agents and/or forces, whereas a disease may have only endogenous causes, although clearly external agents and forces can also be the cause of diseases. The other area where a distinction may be made between disease and injury is in the temporal relationship between outcome and the external agent or force causing the outcome. An injury is typically caused over a short period of exposure, whereas a disease results from long term or repeated exposure.
This distinction is made in the Type of Occurrence Classification System (TOOCS) used in Australia to classify workers compensation cases. I have extracted the relevant section from TOOCS below:
‘An injury is the result of a single traumatic event where the harm or hurt is immediately apparent, for example, a cut resulting from an accident with a knife or burns resulting from an acid splash. A disease, on the other hand, results from repeated or long term exposure to an agent or event, for example, loss of hearing as a result of long term exposure to noise.
Since the classification identifies the harm that occurred to the worker rather than the way it came about, the allocation of the correct nature of injury/disease code should not normally require a decision on whether an occurrence is an injury or disease.’
On the face of it TOOCS mesothelioma would be classified as a disease. However, I offer the example of a worker intensely exposed to asbestos for one shift (at say 1000 f/ml) who later develops mesothelioma and has no other asbestos exposure beyond background exposure. In this situation, the person’s mesothelioma is the result of a single event, and it would not be classifiable into either category using the extracts from TOOCS. This is because according to TOOCS it is not an injury as it is not a traumatic event, and nor is the harm immediately apparent. However nor is the mesothelioma a disease, as it is not the result of repeated or long term exposure.
In my opinion there is no doubt that mesothelioma is a disease, however whether it is the result of an injury depends not on the definition of disease but rather what definition of injury that (sic) is adhered to. Clearly any acceptable definition would require injuries to be the result of external agents or forces. On this broad definition the inhalation of asbestos fibres per se could be considered to be an injury (as the existence of the category ‘toxic effects of asbestos’ in ICD9 suggests). However, if a more restricted definition is adopted, the results of the inhalation of asbestos fibres may not constitute an injury. This occurs if injuries are defined such that there is a requirement that an injury is restricted to harm from an exposure/force that is immediately apparent.
Finally, I offer the following specific comments on Professor Breslin’s report. I refer to the final paragraph on page four of Breslin’s report. In my opinion no insight is to be gained from his analogy between individual human immune cells engulfing asbestos fibres through phagocytosis, and humans eating food. The two processes are so radically different that I have trouble understanding what point Breslin is trying to make with his statement that ‘Simplistically one can think of this as a human eating food where the food is is not causing the injury, but the individual is consuming the food’.
The first paragraph on page five of Breslin’s report suggests that in diseases (tuberculosis and mesothelioma), much of the damage is caused by the response of the human body to the external agent and is not caused by the external agent (tubercle bacilli, asbestos fibres) directly. He contrasts this to an injury (a knife wound) where the external agent causes the harm directly. I would offer the additional example of another type of injury such (sic) (say an ankle sprain). In this type of injury, much of the damage is caused not directly by the external agent/force, but by the endogenous inflammatory (and other) responses to the external agent/force.
In closing it is my opinion that mesothelioma is a disease. However it is also my opinion that in individuals with occupational exposure to asbestos, it may also be considered the ultimate result of an injury.
…” (footnote omitted)
(Exhibit R1). [The Tribunal notes that the report of Associate Professor Breslin dated 31 March 2003, referred to in Mr Kottek’s report, is set out in paragraph 68 below.]
59. Mr Kottek also gave oral evidence but it is unnecessary to set out the substance of that evidence in these reasons.
Dr James Leigh
60. Dr James Leigh confirmed that he is a Consultant Occupational Physician, holds a Fellowship of the Australasian Faculty of Occupational Medicine, and has been interested in occupational lung diseases since 1965, with a particular interest in asbestos-related diseases since 1987. A comprehensive curriculum vitae of Dr Leigh, which includes a very extensive list of his published work relating to his abovementioned areas of interest, was tendered in evidence (Exhibit A9).
61. Dr Leigh confirmed that he had, at the request of the applicants’ solicitors, prepared a report dated 10 August 2003 in respect of each of Mr Hill and Mr Etheridge. Dr Leigh’s report regarding Mr Hill states as follows:
“Thank you for your letter of 5 August 2003 and the attached reports (proposed statement of agreed facts 25/3/2002; Bucens 2/9/2000: Hill statement 18/8/2000; Breslin 31/3/2003).
From the above, the late Frank Hill died of mesothelioma of the right pleura (diagnosed in 2000) on 16/12/2000.
From the above, he had a clear history of significant asbestos exposure with the PMG 1948-53; 1962-1975, later Telstra 1975-1977, and during his war service 1943-1946 in the RAN. The exposure came from a variety of well known sources (RAN engine room lagging, operations on asbestos cement products) and probably included significant amphibole exposure. Exposures of this type are well known to be able to cause mesothelioma … The above exposures were the only reported recalled exposure. It is possible that there was other unrecalled or unrecognized exposure. He had plombage treatment on his left lung in 1953 and left thoracoplasty in 1961.
The latency of 23-57 years is appropriate. All exposure, recalled and unrecalled or unrecognized, would have contributed cumulatively to the risk of mesothelioma.
Causation
Background risk, cumulative risk and thresholds for asbestos related mesothelioma
Although there is generally a dose response relationship between asbestos exposure and mesothelioma risk, the threshold, if any, is not known, although recent quantitative studies have shown it to be less than 0.15 fiber yr/ml …
While there are still many outstanding research questions in the pathogenesis of fibre induced mesothelioma, the current consensus view is that asbestos is involved in both the initiation phase and the promotion/proliferation phase of mesothelioma tumour development. A recent monograph on Mechanisms of Fibre Carcinogenesis (IARC Sci Pub 140 1996) reviews the evidence and the Consensus Report states that:
‘Carcinogenesis by fibres appears to be a multistage process and may arise by the ability of fibres to cause (i) altered expression or function of key genes arising from genetic or epigenetic alterations; (ii) altered cell proliferation; (iii) altered regulation of apoptosis; or (iv) chronic, persistent inflammation.’
(IARC above p3)
Another comprehensive recent review entitled ‘Cell Biology Effects and the Mechanisms of Pathogenicity of Asbestos’ reviews the evidence and concludes that asbestos is a complete carcinogen, ie initiator and promoter, for mesothelioma. … Other recent reviews … detail the molecular biology of genotoxicity and other mechanisms in fibre induced mesothelioma, concluding the asbestos fibres can have effects at both the initiation and promotion/ proliferation phases of tumour development. The biology is very complex and involves phagocytic cells, cytokines and free radicals. Fibres can produce free radicals with or without the interaction with cells. The concept of asbestos as an initiator and promoter for mesothelioma is accepted in the most recent standard textbook used at The University of Sydney (Harber Schenker and Balmes, Occupational and Environmental Respiratory Disease, 1995, p 318) and in the latest (2nd) edition of the textbook Churg and Green, Pathology of Occupational Lung Disease, 1998, p 344.
In view of the capacity of asbestos fibres to be involved at several stages of tumour development, all cumulative exposure to asbestos in an individual case must be considered to play some part in causation. In an individual case current understanding suggests that cells are being initiated, initiated cells promoted and altered cells proliferating at different times. DNA repair processes are occurring, and oncogenes and suppressor genes being activated and inactivated. Altered cells are being removed by apoptosis, necrosis and immunological means. Fibres are being cleared at differing rates and, if exposure is continuing, being deposited in the lung. All these processes at cellular level are stochastic in that probabilities of fibre/cell interaction depend on the number of fibres and number of cells present at any point in time. Hence, simplistically, the more fibres, the more free radicals and greater probability of initiated, promoted or proliferated cells at any given time point.
…
It is well recognized that mesothelioma can be caused by very brief intense occupational, para occupational or hobby exposures. Mesothelioma can also be caused by lower level environmental exposures.
Mesothelioma has been recorded after exposures as short as one day... In the Australian Mesothelioma Program and Register cases, exposures of one week, and others certainly less than that in the present case, have been recorded… In the Australian Mesothelioma Program cases, 6/726 had exposure of < 1 month … In 1976, an authoritative review appeared in American Review of Respiratory Diseases… The review showed that mesothelioma could be caused by low level exposures. Scattered case reports have appeared in the literature since the mid 70s illustrating mesothelioma apparently caused by very slight exposures …
…
Chrysolite 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)… A common figure accepted is crocidolite 30 times more mesotheliomagenic than chrysotile, with amosite intermediate. Hodgson and Darnton in a recent review 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…
…
Except for the case of fibrous erionite, the evidence for other factors (eg ionising radiation, SV40 virus, TB treatments, such as undergone by Mr Hill) which have been proposed as possible causal or adjunct causal agents for human mesothelioma is in my opinion no more than anecdotal.
…
In my opinion it is very unlikely that the TB treatment on Mr Hill’s left lung in 1953 and 1961 was a significant contributory factor to his mesothelioma.
…
Given sufficient sensitivity of analysis, fibres can be found in the lungs of almost everybody in the population … Even failure to find fibres in the lung at death does not negate asbestos causation as they may have been cleared after tumour initiation. Recent cellular level studies show that asbestos is mutagenic and a complete carcinogen (initiator and promoter). Thus a no threshold relationship is consistent with the genetic toxicology…
Australian studies of dose response between lung fibre content and mesothelioma risk are consistent with a no threshold model…
Thus, it is possible to attribute almost all cases of human mesothelioma to asbestos or erionite exposure, ie ‘background’ or ‘spontaneous’ cases are due to low level asbestos or erionite exposure … All exposures, including the ‘background’ asbestos exposure, add cumulatively to the risk of mesothelioma.
There was no evidence of erionite exposure in the present case. There was a clear history of asbestos exposure in the period 1943-1977, including probable amphibole exposure, and this was, on the evidence available to me, the only reported exposure. In my opinion it was sufficient to cause mesothelioma and to add significantly and materially to the risk due to ‘background’ environmental exposure.
From the above, in answer to your specific question, I am not able to positively exclude the PMG/Telstra and Navy exposures as possible causes or contributing factors to the development of the late Mr Hill’s mesothelioma.” (references omitted)
(Exhibit A10). Dr Leigh’s report regarding Mr Etheridge states as follows:
“Thank you for your letter of 5 August 2003 and the attached reports (proposed statement of agreed facts 25/3/2002; Robinson 25/5/2000; Etheridge statement 6/4/2000; Burn fax 30/6/2000; Breslin 31/3/2003).
From the above, the late Cedric James Etheridge died of mesothelioma (diagnosed in 2000) on 21/7/2000.
From the above, he had a clear history of significant asbestos exposure with the PMG 1939-1975, later Telstra 1975-1977, and during his war service 1939-1945. The exposure came from a variety of well known sources (proximity to deteriorating lagging and insulation, operations on asbestos cement products) and probably included significant amphibole exposure. Exposures of this type are well known to be able to cause mesothelioma … He had further exposure when visiting Wittenoom in about 1959, 1961 and 1965 and when building two houses using asbestos cement sheet after 1945. The above exposures were the only reported recalled exposure. It is possible that there was other unrecalled or unrecognized exposure.
The latency of 23-61 years is appropriate. All exposure, recalled and unrecalled or unrecognized, would have contributed cumulatively to the risk of mesothelioma.
Causation
Background risk, cumulative risk and thresholds for asbestos related mesothelioma
[The report then sets out the same research information and opinions as set out in the abovementioned report regarding Mr Hill, and concludes:]
…
There was no evidence of erionite exposure in the present case. There was a clear history of asbestos exposure in the period 1939-1977, including probable amphibole exposure, and this was, on the evidence available to me, the only reported exposure. In my opinion it was sufficient to cause mesothelioma and to add significantly and materially to the risk due to ‘background’ environmental exposure.
From the above, in answer to your specific question, I am not able to positively exclude the PMG/Telstra and Army exposures as possible causes or contributing factors to the development of the late Mr Etheridge’s mesothelioma.” (references omitted)
(Exhibit A11).
62. In his oral evidence-in-chief, Dr Leigh was questioned about the process of development of mesothelioma. His evidence was as follows:
“The process of the production of mesothelioma, it is a tumour, isn’t it? --- It is a tumour, yes.
And it grows until such times as it becomes clinically significant and comes to the attention of the medical profession? --- Yes.
Now, how long before the typical diagnosis is the tumour forming? How long does it take to form? --- Well, as I understand it from my reading and personal experimental work in other tumour formation, I believe that the asbestos fibres in the lung are constantly causing chemical and genetic level changes and physiological repair mechanisms that are constantly in operation for basically the whole of the – they’re very close to the whole of the so-called latency period. I believe the point where the tumour starts to proliferate in uncontrolled fashion, in other words the cells are multiplying very quickly and they’ve sort of overwhelmed the defensive mechanisms, they’re abnormal cells. My understanding is that the late phase is quite short, a matter of months. But preparatory to that a lot of things going on, the actual – actual time from start of actual proliferation to what is definitely going to become a tumour and clinical detection is some months.
So if I understand it correctly, while the changes in the body may be an ongoing process over up to 60-odd years, the tumour itself doesn’t develop until the last few months. Is that what you say? --- Yes.
And what are typically the first signs of this in a clinical sense? --- In a clinical sense typically a pleural effusion, that is fluid accumulating in the pleural space, possibly breathlessness and/or pain.
And we’ve been provided with one of the papers, that is the British Thoracic Society paper, which you mentioned in your report? --- Yes.
And there is a copy with all the parties. That talks about a fairly short period, in general, from diagnosis to death? --- Yes.
A matter of months? --- A matter of months.
And that is indicative, is it, of the degree of aggressiveness of the tumour? --- Yes.
Now, because one of the issues here deals with some hypothetical issues I want to put a hypothetical situation to you, Doctor. In a case where you have mesothelioma, this aggressive tumour developing in about 1999 or 2000 in a patient, if you went back over 10 years to 1988 and hypothetically examined in some way or other tissues of the lung where this disease typically forms would you be able to examine the tissues in any way and say whether there is mesothelioma present in the lung tissues? --- No.
And if you examined such a patient and saw whatever pathology was available to you could you say with any degree of certainty that it was likely that that patient was going to develop mesothelioma? --- No.
So do we understand it then, that this is a disease which while it has a long latency period and a long development period it is still uncertain at any particular stage as to whether mesothelioma will develop in any one case or other? --- You can’t say it definitely or not, no.
Thank you, Doctor. Now, I just want to follow up one other issue. The fibres enter the body and we’ve discussed this dose response relationship and it is the heaviness of the exposure, so it is more than one fibre that causes this disease. Is that right? --- Yes.
And you have put in your paper that there is a process of initiation, promotion and proliferation involved? --- Yes.
So that fibres come into the body, and as I understand it, the body also clears these fibres? --- Yes.
And the clearance of these fibres is a natural body reaction to this substance? --- It’s a general body reaction to any inhaled article or fibre.
Is it fair to say that that is the response of any healthy body? --- Yes.
Yes. I gather from your reports that it is also possible to have these cases of mesothelioma where there are no asbestos fibres found in the lung at the time of the disease. Is that right? --- Yes.
Is that because the body can still clear the whole lot of fibres? --- Well, the body can clear the fibres to the point below which they can be detected by. The analytical methods used, I mean, theoretically if you examine a large amount of lung – a large enough amount of lung tissue and look at enough infections the more you look for them the more likely you are to find them but, basically, yes, the fibres can have – cause a tumour, initiated – cause its initiation, promotion and proliferation and then by the time the tumour is actually clinically detected or a sample of lung is obtained – or at a post-mortem fibres can be very difficult to detect.
So that the process is not merely just the entry of the fibre into the lung or even its clearance, it is a whole series of processes in the meantime? --- Yes.
And somewhat removed from that entry of the fibre? --- A whole lot of things are going on simultaneously, as I stated in my report.
Yes? --- Like fibres are coming in, fibres are staying there, fibres are being cleared, the body is reacting to the fibres in various ways, the molecular and cellular level, genetic and other changes are happening and, you know, all these things are happening in a … or probabilistic way, as I say on page 3 of the report, you know, the more fibres the more free radicals the greater probability of initiated promoted or proliferated cells at any time point.”
(Transcript, pp 86 – 89)
63. In cross-examination by Mr Elliott (for Telstra), Dr Leigh confirmed that he regarded mesothelioma as a disease and that he agreed with the contents of Associate Professor Breslin’s report of 31 March 2003 (see paragraph 68 below). His evidence continued:
“Now, you’ve said that the development of the tumour takes a relatively short period of time, it – from when it is diagnosed. It is a short period of time for that to develop? --- It’s a short period of time from the point at which it’s diagnosed to the point at which it grows to kill you.
Yes? --- And it’s also a short period of time, I believe, from where the sort of final phase of unregulated multiplication of cells up to the point at which it is clinically detectable, that’s also relatively short. In other words, once they start to grow big time, they grow quickly.
And so it would be ---? --- So that last phase is an accelerated phase, if you like.
It would be at that time, when they are growing quickly, that – there is the first sign of an interference with the usefulness of the body? --- Yes.
And from that time on, I think as you’ve said, Doctor, there is a relatively short time from when it starts and leads to the existence of the tumour, that is a short period of time taking into account the whole of the process, and then from the existence of the tumour to death is only a matter of months, in most cases? --- Yes, yes.
So if you look at disease as being something that inherently has the nature of interfering with the normal functioning of the body and the usefulness of the body itself, could it not be said that the disease process starts at that relatively late period leading up to the development of the tumour and then death? That in itself is the disease process? – If you – if you define that to be the disease process, yes.
(2)Subject to this section, Part VIIIA of the Principal Act [the CERC Act] as amended by Division 2 of this Part applies to a notional licence and so applies as if the licence had been granted under that Part.
(3)Any conditions determined under subsection (1) are taken to have been determined under section 107G of the Principal Act [CERC Act] as amended by Division 2 of this Part.
(4)A notional licence comes into force on the date of commencement of this Division and continues in force for the period 1 year beginning on that date.
44. … section 29 of the 1992 Act provided:
Any liability of an administering authority to pay compensation, or make any other payment, under the Principal Act [CERC Act] in respect of an injury, loss or damage suffered by, or in respect of the death of, an employee of the authority, being a liability that existed immediately before the commencement of this Division but had not been discharged before that commencement, continues after that commencement. (emphasis added)”
The Submissions
88. It is common ground that the applicants are entitled to compensation under the SRC Act in respect of the condition of mesothelioma which resulted in the death of Mr Hill and of Mr Etheridge. The ultimate question for the Tribunal’s determination is: which of the respondents – Comcare/MRCC or Telstra – is liable to pay such compensation to the applicants?
89. Extensive oral and written submissions were made by each of the parties. It is convenient first to set out the contentions of Comcare/MRCC as summarised in paragraphs 4 and 5 of Mr Howe’s written submissions:
“…Comcare contends that the ‘relevant authority’ or the liable respondent for the purposes of the applicants’ claims is Telstra.
4.1Upon the commencement of the Commonwealth Employees’ Rehabilitation and Compensation Act 1988 (the CERC Act) on 1 December 1988 all liability (actual or contingent) was transferred under s 101 from the Commission for the Safety, Rehabilitation and Compensation of Commonwealth Employees (the Commission) to the predecessor of Telstra as an ‘administering authority’. Therefore Telstra is liable for the applicants’ claims.
4.2In the alternative, even if contingent liability was not transferred to Telstra on 1 December 1988, actual liability existed at that date and was transferred because:
4.2.1the inhalation of asbestos fibres is characterised as an injury other than a disease, an injury simpliciter. The inhalation of the asbestos fibres by Mr Hill and Mr Etheridge occurred well before 1 December 1988;
4.2.2mesothelioma is the final stage of a slow developing disease process. Section 7(4) of the SRC Act defines, for present purposes, the date of the disease as being the date the ‘disease’ (defined to mean a morbid condition of gradual onset) first resulted in ‘impairment’ (as defined). ‘Impairment’ is defined to include ‘damage or malfunction of any part of the body or of any bodily system or function or part of any such system or function’. The medical evidence establishes that this damage /manifestation commenced well before 1 December 1988. The morbid condition which resulted from the inhalation of asbestos fibres, and which ultimately expressed itself at the discernible end stage known as mesothelioma, occurred prior to the commencement of section 101 of the CERC Act. Upon commencement of section 101 an accrued liability was transferred to Telstra’s predecessor.
5.In respect of the applicants’ claims against MRCC, it is contended that Mr Hill and Mr Etheridge were not ‘employees’ for the purposes of the Commonwealth Employees’ Compensation Act 1930 (the 1930 Act) during their military service between 1939 and 1946 and therefore are not entitled to compensation under the SRC Act.”
Each of the contentions summarised in subparagraphs 4.1 and 4.2 was elaborated in detail in both oral and written submissions. The contention summarised in paragraph 5 was elaborated in oral submissions which in turn relied upon an amended Statement of Facts and Contentions dated 6 July 2004 which had previously been filed.
90. The contentions of the applicants, as summarised in paragraph 1 of Mr Carey’s written submissions, are as follows:
“1.In response to the submissions of the respondents, principally Comcare and MRCC, in so far as they deal with the issues of how to determine the question of liability to pay compensation, the applicants contend:
(a)Section 7(1) of the Safety Rehabilitation and Compensation Act 1988 (‘the SRC Act’) provides a special scheme to determine the liability to pay compensation in specific cases.
(b)The correct method of determining the liability to pay compensation in all cases is to firstly determine the issue of injury prior [to] determining whether it arose from employment. After dealing with those issues in the proper order the question of who bears liability to pay compensation is determined by the terms of the statute.
(c)The deceased employees died as a result of mesothelioma that is a disease of gradual onset.
(d)The characterisation of the diseases as injuries simpliciter is not appropriate in the circumstances.
(e)There was no disease in existence in either case until a period of months prior to the onset of symptoms and hence there was no actual liability to transfer to the ATC on the commencement date of the SRC Act.
(f)Employees suffering from diseases of gradual onset have been provided for in workers’ compensation statutes, the Commonwealth legislation included, by a separate scheme by reference to the nature of the disease and the nature of the employment which is different to the ordinary scheme of liability.
(g)It is a rule of statutory construction that where a statute contains a provision of a general nature as well as those relating to a particular subject matter, the general provisions should give way to the provisions that deal with the same subject matter specifically.
(h)The issue of whether the disease arose out of or in the course of employment is determined by reference to the applicable provisions in section 7 of the SRC Act, particularly subsection 7(4) as to the date of injury, and section 5 of the Act in respect of the definition of employment.
(i)The final issue, once the existence of liability is determined, is the question of which is the relevant authority, and the SRC Act provides a simple scheme that leaves no ‘lacunae’.”
Each of those contentions was elaborated in detail in oral and written submissions.
91. Mr Elliott (for Telstra) supported the applicants’ contention that the question of liability to pay compensation in this case falls to be determined solely under the SRC Act – in particular, ss 7 and 14 – and not by reference to the provisions of earlier legislation – in particular, the 1930 Act and the 1971 Act. He submitted that the condition of mesothelioma suffered by Mr Hill and Mr Etheridge was a disease contracted by each of them after 1 December 1988 (the date of commencement of the SRC Act). He further submitted that the earlier inhalation of asbestos fibres by Mr Hill and Mr Etheridge, which ultimately resulted in their contracting mesothelioma, did not constitute an injury simpliciter which thereby involved a simultaneous liability to pay compensation. Nor, he submitted, did Mr Hill’s and Mr Etheridge’s disease of mesothelioma arise before 1 December 1988 because, as at that date, neither Mr Hill nor Mr Etheridge had suffered any “impairment” (as defined in s 4(1) of the SRC Act) by reason of the inhalation of asbestos fibres or by reason of any ongoing disease process; rather, neither of them suffered relevant “impairment” until well after 1 December 1988 and shortly before death. Finally, Mr Elliott submitted that the transfer of liability provisions in the CERC Act and the SRC Act relate only to existing actual liability to pay compensation, and do not include inchoate or contingent liability, and in the present case there was, as at 1 December 1988, no existing actual liability to pay compensation to the applicants which might be transferred to Telstra.
Consideration And Findings
The Contentions of Comcare and the MRCC
92. For the purposes of considering the various issues raised in this case, and making the necessary findings, the Tribunal will proceed by first addressing the contentions advanced on behalf of Comcare and the MRCC.
Did the phrase “any liability…” in s 101(2)(a) of the CERC Act include an inchoate or contingent liability, as well as an existing actual or accrued liability?
93. Section 101(2) (a) of the CERC Act provided as follows:
“(2) Where the Minister declares a Commonwealth authority to be an administering authority:
(a)any liability of the Commission to pay compensation or make any other payment under this Act in respect of an injury, loss or damage suffered by an employee of the authority, or in respect of the death of such an employee, being a liability that had not been discharged before the day on which the declaration takes effect, shall, by force of this subsection, vest in the authority on that day;”.
In contending that the phrase “any liability …” included an inchoate or contingent liability, as well as an existing actual or accrued liability, Mr Howe submitted that a purposive, rather than a literal, approach to the construction of that provision should be adopted in order to avoid lacunae, ambiguities and inconsistencies in the legislation, together with absurd, inconsistent and unintended consequences, which were elaborated in his submissions. He relied chiefly on Crimmins v Stevedoring Industry Finance Committee (1999) 200 CLR 1 and The Commonwealth of Australia v TransAdelaide [2001] NSWCA 52 in support of the construction of s 101(2)(a) of the CERC Act for which he contended.
94. In Crimmins, a former registered waterside worker died in July 1998, the cause of death being mesothelioma caused by the inhalation of asbestos fibres. He was diagnosed as suffering from mesothelioma in May 1997 when he began to experience the symptoms of mesothelioma. According to the evidence, he was employed as a waterside worker for the period 1961-1965 during which his employment duties involved the unloading and handling of bagged asbestos fibre thereby exposing him to asbestos dust and fibres. At that time stevedoring operations in Australia were regulated by the Australian Stevedoring Industry Authority which was subsequently abolished and replaced by the Stevedoring Industry Finance Committee with effect from 26 February 1978. Section 14(b) of the Stevedoring Industry Acts (Termination) Act 1977 (Cth) provided that the Committee was “liable … to discharge all the liabilities and obligations of the Authority that existed immediately before” 26 February 1978. The High Court held that the Authority owed a common law duty of care to the waterside worker during the period 1961-1965, and that s 14(b) of the Act vested in the Committee on 26 February 1978 liability for a breach of that duty of care by the Authority, notwithstanding that the injury resulting from that breach of duty, and a cause of action in negligence, did not arise until May 1997. In reaching the latter conclusion, the Court construed the phrase “all the liabilities … that existed” in s 14(b) of the Act to include “contingent” or “potential” liabilities, as well as actual liabilities.
95. In TransAdelaide, a similar approach was taken, and a similar conclusion was reached, by the New South Wales Court of Appeal in respect of factual circumstances and statutory provisions analogous to those in Crimmins.
96. In the present case the relevant phrase in s 101(2)(a) of the CERC Act is:
“any liability of the Commission to pay compensation … under this Act in respect of an injury …”
That phrase is narrower and more specific than the relevant statutory phrase in Crimmins, namely, “all the liabilities … of the Authority that existed immediately before” a specified date. Whereas the latter statutory phrase was held in Crimmins to be sufficiently broad to include contingent or potential common law liabilities, the above-quoted phrase in s 101(2)(a) of the CERC Act is literally and unambiguously confined to a particular kind of liability, namely a liability (relevantly) to pay compensation under that Act in respect of an “injury” (as defined).
97. The above-quoted phrase in s 101(2)(a) of the CERC Act, in the Tribunal’s opinion, unambiguously refers only to an actual or existing liability to pay compensation which has been established under, and in accordance with, the CERC Act. As the Full Court of the Federal Court in Lees v Comcare (1999) 29 AAR 350 made clear, the liability to pay compensation under the SRC Act (previously named the CERC Act) means the liability to pay compensation in accordance with the provisions of that Act (s 14) and comprises the following 5 elements:
“First, that an appropriate notice of injury has been given to the relevant authority as required by s 53 of the Act; secondly, that a claim for compensation has been made as required by s 54 of the Act; thirdly, that the person who made the claim or on whose behalf the claim was made was an ‘employee’ at the time of the alleged injury (ss 4 and 5); fourthly, that the employee suffered an injury (s 4); and finally, that the injury has resulted in death, incapacity for work or impairment.” (at 359)
In Australian Postal Corporation v Oudyn (2003) 77 ALD 659 the Federal Court (Cooper J) referred to the abovementioned elements of liability as stated in Lees and added (at 667):
“A determination … that one or more of the elements did not exist is a determination that there was at no time a liability under s 14 of the Act to pay compensation for the particular injury.”
See also Rosillo v Telstra Corporation Ltd (2003) 38 AAR 243 at 246-247.
98. Accordingly, in the Tribunal’s opinion, the phrase “any liability of the Commission to pay compensation … under this Act in respect of an injury …” in s 101(2)(a) of the CERC Act referred only to an existing actual or accrued liability – it did not include an inchoate or contingent liability. Section 101(2)(a) of the CERC Act did not, therefore, vest in the ATC (a predecessor of Telstra) on 1 December 1988 any inchoate, potential or contingent liability to pay compensation to Mr Hill or to Mr Etheridge which might subsequently be transferred to Telstra.
Did the inhalation of asbestos fibres by Mr Hill and by Mr Etheridge constitute an “injury simpliciter”, such that actual liability to pay compensation in respect of that injury existed as at 1 December 1988 and was subsequently transferred to Telstra?
99. Mr Howe cited dicta in various authorities in support of the proposition that the very inhalation of an asbestos fibre constitutes an injury simpliciter. Those authorities included: Fisher v Hebburn Ltd (1960) 105 CLR 188; Slattery v Comcare (1996) 70 FCR 131; Favelle Mort Ltd v Murray (1976) 133 CLR 580; Connair Pty Ltd v Frederiksen (1979) 142 CLR 485; Australian Blue Asbestos Ltd v Rees (unreported, Supreme Court of WA (Full Court), Appeal No 126 of 1981, 9 October 1981); GRE Insurance Ltd v Bristile Ltd (1991) 5 WAR 440; Frank Manford Pty Ltd v QBE Insurance Ltd (unreported, Supreme Court of WA (Full Court), Appeal No 51 of 1992, 23 June 1993, BC 9301328); Martindale v Burrows [1997] 1 Qd R 243; and Orica Ltd v CGU Insurance Ltd [2003] NSWCA 331.
100. The Tribunal notes that, with the exception of Slattery, none of the abovementioned authorities involved a claim for compensation under Commonwealth employees’ compensation legislation. Furthermore, only in Australian Blue Asbestos, GRE Insurance, Martindale, Frank Manford and Orica do the relevant dicta refer specifically to the inhalation of asbestos fibres, and, with the exception of Martindale, those dicta, to the effect that the inhalation of asbestos fibres constitutes an injury, were uttered in the context of State workers’ compensation legislation ultimately for the purpose of determining the matter of liability to indemnify under the provisions of an insurance policy. In Martindale the relevant dicta were uttered in the context of determining the time at which a common law cause of action in negligence arose. Those dicta, furthermore, did not go so far as to express the view that the initial inhalation of asbestos fibre constituted an injury, and that the cause of action in negligence arose at that time. Likewise, in Crimmins (paragraph 94 above) the High Court accepted that, notwithstanding that the deceased person had inhaled asbestos fibres in the period 1961-1965, no relevant injury was sustained by him, and no cause of action arose, until 1997 when he first developed mesothelioma symptoms.
101. In the present case, the expert medical evidence before the Tribunal does not support the proposition that the mere inhalation of asbestos fibres by Mr Hill and by Mr Etheridge itself constituted an injury simpliciter: see the oral evidence of Dr Leigh (especially at paragraph 65 above), and the report of Professor Breslin dated 31 March 2003 (set out in paragraph 68 above) and his oral evidence (especially at paragraphs 73, 74 and 79 above).
102. The Tribunal, on the basis of the expert medical evidence before it, finds that the inhalation of an asbestos fibre does not itself constitute an injury simpliciter, and that the inhalation of asbestos fibre by Mr Hill and by Mr Etheridge prior to 1988 did not itself constitute an injury simpliciter to either of them such as might give rise to an actual or accrued liability to pay compensation as at 1 December 1988.
103. Furthermore, for the reasons explained by the Federal Court in Lees and Oudyn (see paragraph 97 above), even if the inhalation of asbestos fibre by Mr Hill and by Mr Etheridge prior to 1988 constituted an injury simpliciter to each of them, there was no accrued liability to pay compensation in respect of such “injury” as at 1 December 1988 because no notice of such “injury” had been given, and no claim for compensation in respect of such “injury” had been made, by Mr Hill or by Mr Etheridge in accordance with the 1930 Act (s 16) or the 1971 Act (ss 53,54).
104. Accordingly, the Tribunal finds that, as at 1 December 1988, there was no existing actual or accrued liability to pay compensation under the CERC Act to Mr Hill or to Mr Etheridge by reason of their inhalation of asbestos fibre prior to that date, and that, therefore, no such liability was vested in the ATC by s 101(2)(a) of the CERC Act and subsequently transferred to Telstra.
Did the disease of mesothelioma first result in the “impairment” of Mr Hill and of Mr Etheridge prior to 1 December 1988, such that actual liability to pay compensation in respect of that disease existed as at 1 December 1988 and was subsequently transferred to Telstra?
105. Mr Howe submitted that Mr Hill and Mr Etheridge had each suffered “impairment” (as defined in s 4(1) of the SRC Act) by reason of their inhalation of asbestos fibres prior to 1 December 1988 and that, accordingly, by s 7(4) of the SRC Act, Mr Hill and Mr Etheridge are each to be taken to have sustained an injury, being a disease, prior to 1 December 1988. He submitted that actual liability to pay compensation in respect of that disease existed as at 1 December 1988 and that liability was vested in the ATC by s 101(2)(a) of the CERC Act and was subsequently transferred to Telstra.
106. The Tribunal accepts (as submitted by Mr Howe) that the word “impairment” is defined in s 4(1) of the SRC Act in very broad terms in that it includes “the damage or malfunction of any part of the body or of any bodily system or function or part of such system or function”. In Re Halliday and Comcare (1994) 19 AAR 431 the Tribunal, for the purpose of construing the definition of “impairment” in s 4(1) of the SRC Act, referred to dictionary definitions of the words “damage” and “malfunction” and continued (at 441):
“… In the context of the definition of ‘impairment’ in which those words are used and in the context of the whole Act, there seems to be no reason why we should not adopt the ordinary meaning of those words. Consequently, there will be an impairment of a part of the body or a bodily system or function if it has been damaged in the sense that its usefulness or value has been diminished or if it malfunctions in the sense that it fails to perform normally or properly …”
In Department of Defence v West (1998) 85 FCR 491 Merkel J (with whom O’Connor J agreed) referred (at 506, 513) to impairment (as defined in the SRC Act) resulting from a change in the “underlying patho-physiological condition”. See also Comcare v Maida (2002) 36 AAR 69 at 82-83.
107. Having regard to the expert medical evidence before it, the Tribunal is satisfied, and finds, that neither Mr Hill nor Mr Etheridge suffered “impairment” (as defined in s 4(1) of the SRC Act) by reason of their inhalation of asbestos fibres prior to 1 December 1988. According to the evidence and reports of Dr Leigh and Professor Breslin (which were substantially in agreement), although the inhalation of asbestos fibre immediately produces biological and biochemical changes in the body together with cell activity whereby “scavenger” cells (macrophages) engulf the fibre and try to digest it thereby generating oxygen free radicals which may cause damage to cells and DNA, and those changes are ongoing throughout the long latency period (which is usually between 15 and 60 years), those changes are undetectable for most of that latency period and only become apparent when the symptoms of mesothelioma first appear (usually within 2 years, and commonly within 9-12 months, of the death of the person). The Tribunal is satisfied that, prior to the onset of such symptoms, there is no relevant “damage or malfunction of any part of the body or of any bodily system or function or part of such system or function” and, therefore, no “impairment” within the meaning, and for the purposes, of the SRC Act.
108. In the present case, it is common ground that the symptoms of mesothelioma were first experienced by Mr Hill in late 1999 and by Mr Etheridge in or about August 1999. Accordingly, the Tribunal finds that the disease of mesothelioma first resulted in “impairment” (as defined in s 4(1) of the SRC Act), in the case of Mr Hill, in late 1999, and in the case of Mr Etheridge, in or about August 1999, and that, by s 7(4) of the SRC Act, Mr Hill and Mr Etheridge are to be taken to have sustained an injury, being a disease, in late 1999, and in or about August 1999, respectively. There was, therefore, no actual liability to pay compensation to Mr Hill or to Mr Etheridge existing as at 1 December 1988 which might be vested in the ATC by s 101(2)(a) of the CERC Act and which might subsequently be transferred to Telstra.
109. Furthermore, for the reasons explained by the Federal Court in Lees and Oudyn (see paragraph 97 above), even if Mr Hill and Mr Etheridge had each suffered relevant impairment, and were to be taken to have sustained an injury, being a disease, prior to 1 December 1988, there was no accrued liability to pay compensation in respect of such disease as at 1 December 1988 because no notice of such disease had been given, and no claim for compensation in respect of such disease had been made, by Mr Hill or by Mr Etheridge in accordance with either the 1930 Act (s 16) or the 1971 Act (ss 53,54).
110. Accordingly, the Tribunal finds that, as at 1 December 1988, there was no existing actual or accrued liability to pay compensation under the CERC Act to Mr Hill or to Mr Etheridge in respect of an injury, being a disease, sustained prior to that date, and that, therefore, no such liability was vested in the ATC by s 101(2)(a) of the CERC Act and subsequently transferred to Telstra.
Was either Mr Hill or Mr Etheridge, during the period of his RAN or Army (respectively) service between 1939 and 1946, an “employee” of the Commonwealth within the meaning, and for the purposes, of the 1930 Act (as in force at that time)?
111. Having regard to the Tribunal’s view that no issue of liability to pay compensation under the 1930 Act arises in this case, it is unnecessary for the Tribunal to answer the above question.
The liability to pay compensation is to be determined in accordance with ss 7 and 14 of the SRC Act
112. The Tribunal accepts the submissions of the applicants and of Telstra that the issue of the liability to pay compensation to the applicants falls to be determined in accordance with ss 7 and 14 of the SRC Act. The relevant provisions of ss 7 and 14 of the SRC Act, and of a Ministerial Notice under s 7(1) of the SRC Act, were set out in paragraphs 84 and 86 above.
113. For the purposes of s7 of the SRC Act, the Tribunal finds, on the material before it, that:
·Mr Hill and Mr Etheridge were “employees” (as defined in s 5 of the SRC Act);
·the death of each of Mr Hill and Mr Etheridge resulted from mesothelioma, which is a “disease” within the meaning of s 7;
·the disease of mesothelioma, which resulted in the death of Mr Hill and of Mr Etheridge, was caused by asbestos;
·Mr Hill’s employment with the RAN (1943-1946), the PMG (1948-1955, 1962-June 1975), and the ATC (July 1975-August 1976) involved exposure to asbestos;
·Mr Etheridge’s employment with the PMG (March-August 1939, November 1945-June 1975), the Australian Army (September 1939-October 1945), and the ATC (July-September 1975) involved exposure to asbestos;
·Mr Hill first experienced, and sought medical treatment for, symptoms of his disease of mesothelioma in or about October 1999;
·Mr Etheridge first experienced, and sought medical treatment for, symptoms of his disease of mesothelioma in or about August 1999.
114. As regards the employment of Mr Hill and of Mr Etheridge with the Defence Force and with the PMG, the Tribunal finds that there is no evidence which establishes that either of those employments did not contribute in a material degree to the contraction of the disease of mesothelioma by Mr Hill and by Mr Etheridge. On the contrary, the evidence before the Tribunal clearly establishes, to the Tribunal’s satisfaction, that each of those employments did contribute in a material degree to the contraction of the disease of mesothelioma by Mr Hill and by Mr Etheridge. In any event, by s 7(1) of the SRC Act, each of those employments is, for the purposes of the SRC Act, to be taken to have contributed in a material degree to the contraction of the disease of mesothelioma by Mr Hill and by Mr Etheridge.
115. As regards the employment of Mr Hill and of Mr Etheridge with the ATC, the position is much more problematic. Dr Leigh described the exposure to asbestos, and its probable contribution to the contraction of mesothelioma, in the case of each of Mr Hill and Mr Etheridge as “very, very minor”, but not nil. Professor Breslin, on the other hand, consistently expressed the opinion that the effect of any asbestos exposure, in the case of Mr Hill’s and Mr Etheridge’s employment with the ATC, would have been “negligible” – by which he meant (as he explained) that that exposure would have had “no measurable effect on the development of the mesothelioma”. He subsequently confirmed that it was his opinion that Mr Hill’s and Mr Etheridge’s employment with the ATC made no material contribution to their subsequently contracting mesothelioma. To the extent that there is a difference of opinion between Dr Leigh and Professor Breslin on this issue, the Tribunal prefers the opinion of Professor Breslin – a very eminent Consultant Thoracic Physician with over 30 years’ experience, and Clinical Associate Professor in Medicine at The University of Sydney since 1991 – that Mr Hill’s and Mr Etheridge’s employment with the ATC from July 1975 made no material contribution to their subsequently contracting mesothelioma. It may be, however, that there is no significant difference between the views of Dr Leigh and Professor Breslin because Dr Leigh’s description of the relevant asbestos exposure, and its probable contribution to the contraction of mesothelioma by Mr Hill and by Mr Etheridge, as “very, very minor” may be understood as representing the opinion that such contribution was merely de minimis.
116. The Tribunal is reasonably satisfied, and finds, on the whole of the evidence before it, that, in the case of each of Mr Hill and Mr Etheridge, his employment with the ATC during the relevant short periods – from 1 July 1975 to 26 August 1976, in the case of Mr Hill, and 1 July 1975 to 30 September 1975, in the case of Mr Etheridge – did not contribute in a material degree to the contraction of the disease of mesothelioma.
Conclusion
117. On the basis of the abovementioned findings, the Tribunal concludes that Comcare/MRCC is liable, under s14(1) of the SRC Act, to pay compensation to the applicants in accordance with that Act in respect of an “injury” (as defined in s 4(1)), being a “disease” (as defined in s 4(1)), namely, mesothelioma, which resulted in the deaths of Mr Hill and Mr Etheridge.
Decision
118. For the above reasons the Tribunal decides as follows:
(a) The Hill Applications for Review
·Application № W2000/422
The Tribunal sets aside the decision under review and, in substitution therefor, decides that Comcare is liable, under s 14 of the SRC Act, to pay compensation in accordance with that Act in respect of an “injury” (as defined in s 4(1)), being a “disease” (as defined in s 4(1)), namely, mesothelioma, which resulted in the death of Mr Hill.
·Application № W2001/12
The Tribunal affirms the decision under review
·Application № W2001/199
The Tribunal sets aside the decision under review and, in substitution therefor, decides that Comcare is liable to pay compensation pursuant to s 17 and s 18 of the SRC Act in respect of an “injury” (as defined in s 4(1)), being a “disease” (as defined in s 4(1)), namely, mesothelioma, which resulted in the death of Mr Hill.
·Application № W2001/348
·The Tribunal affirms the decision under review.
·Application № W2001/429
The Tribunal sets aside the decision under review and, in substitution therefor, decides that the MRCC is liable, under s 14 of the SRC Act, to pay compensation in accordance with that Act in respect of an “injury” (as defined in s 4(1)), being a “disease” (as defined in s 4(1)), namely, mesothelioma, which resulted in the death of Mr Hill.
(b) The Etheridge Applications for Review
·Application № W2001/16
The Tribunal affirms the decision under review.
·Application № W2001/118
The Tribunal sets aside the decision under review and, in substitution therefor, decides that Comcare is liable to pay compensation pursuant to s 17 and s18 of the SRC Act in respect of an “injury” (as defined in s 4(1)), being a “disease” (as defined in s 4(1)), namely, mesothelioma, which resulted in the death of Mr Etheridge.
·Application № W2001/350
The Tribunal affirms the decision under review.
·Application № W2001/430
The Tribunal sets aside the decision under review and, in substitution therefor, decides that Comcare is liable, under s 14 of the SRC Act, to pay compensation in accordance with that Act in respect of an “injury” (as defined in s 4(1)), being a “disease” (as defined in s 4(1)), namely, mesothelioma, which resulted in the death of Mr Etheridge.
·Application № W2001/431
The Tribunal sets aside the decision under review and, in substitution therefor, decides that the MRCC is liable, under s14 of the SRC Act, to pay compensation in accordance with that Act in respect of an “injury” (as defined in s 4(1)), being a “disease” (as defined in s 4(1)), namely, mesothelioma, which resulted in the death of Mr Etheridge.
119. The Tribunal orders, pursuant to s 67(8) of the SRC Act, that Comcare pay the applicants’ costs in respect of Applications Nos W2000/422, W2001/199, W2001/118 and W2001/430, and that the MRCC pay the applicants’ costs in respect of Applications Nos W2001/429 and W2001/431, in accordance with the Tribunal’s General Practice Direction.
I certify that the 119 preceding paragraphs are a true copy of the reasons for the decision herein of Associate Professor S D Hotop, Deputy President and Dr D Weerasooriya, Member.
Signed: ………....(sgd J Rainey) ……
Associate
Date/s of Hearing 12-16 July 2004
Date of last Submissions 25 October 2004
Date of Decision 6 May 2005
Counsel for the Applicants Mr M Carey
Solicitor for the Applicants Slater & Gordon
Counsel for Comcare/MRCC Mr T Howe
Solicitor for Comcare Australian Government Solicitor
Solicitor for the MRCC Dibbs Barker Gosling
Counsel for Telstra Mr P Elliott QC and Mr J Wallace
Solicitor for Telstra Sparke Helmore
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