Pryde and Telstra Corporation Limited (Compensation)

[2016] AATA 811

Pryde and Telstra Corporation Limited (Compensation) [2016] AATA 811 (14 October 2016)

Division

GENERAL DIVISION

File Number(s)

2011/5617

2013/4437

Re

Barbara Pryde

APPLICANT

And

Telstra Corporation Limited

FIRST RESPONDENT

And

Comcare

SECOND RESPONDENT

DECISION

Tribunal	Egon Fice, Senior Member E A Shanahan, Member
Date	14 October 2016
Place	Melbourne

The Tribunal affirms the decisions under review.

[sgd]........................................................................

Egon Fice, Senior Member

WORKERS’ COMPENSATION - employee of Commonwealth telecommunications agencies - death resulting from lung cancer - where claimant exposed to asbestos fibres in course of work - where claimant a significant smoking over extended period of time - specified disease - whether presumption that specified disease caused by exposure to asbestos fibres rebuttable - conflicting evidence of exposure - insufficient biological evidence to conclude as to causation - epidemiological analysis applied - where epidemiological analysis indicates cancer caused more likely than not by smoking alone - presumption of causation rebutted - decision affirmed.

Legislation

Asbestos-related Claims (Management of Commonwealth Liabilities) Act 2005 (Cth) s. 5

Australian and Overseas Telecommunications Corporation Act 1991 (Cth)

Australian Telecommunications Corporation Act 1999 (Cth)

Commonwealth Employees’ Compensation Act 1930 (Cth)

Compensation (Commonwealth Government Employees) Act 1971 (Cth)

Industrial Relations Legislation Amendment Act (No 3) 1991(Cth)

Safety, Rehabilitation and Compensation Act 1988 (Cth) ss. 4(1), 5A, 5B, 7(1), 17, 18, 69

Safety, Rehabilitation and Compensation (Specified Diseases) Notice 2007 (1) (Cth)

Safety,Rehabilitation and Compensation and Other Legislation Amendment Act 2001 (Cth)

Telecommunications Act 1975 (Cth)

Cases

Bird v Commonwealth of Australia (1988) 165 CLR 1

Comcare v Canute (2005) 148 FCR 232

Comcare v Power [2015] FCA 1502

Comcare v Sahu-Khan (2007) 156 FCR 536

Connair Pty Ltd v Fredricksen (1979) 142 CLR 485

Seltsam Pty Ltd v McGuinness (2000) 49 NSWLR 262

Telstra Corporation Ltd v Worthing (1997) 42 NSWLR 655

Treloar v Australian Telecommunications Commission (1990) 26 FCR 316

Secondary Materials

FD Liddell and BG Armstrong, ‘The Combination of Effects on Lung Cancer of Cigarette Smoking and Exposure in Québec Chrysotile Miners and Millers’ (2002) 46(1) Annals of Occupational Hygiene 5.

Finnish Institute of Occupational Health, ‘Asbestos, Asbestosis and Cancer - Helsinki Criteria for Diagnosis and Attribution 2014’ (Finnish Institute of Occupational Health, 2014).

H Nelson, D Christiani, J Wiencke, E Mark, J Wain and K Kelsey ‘K-ras mutation and occupational asbestos exposure in lung adenocarcinoma: asbestos-related cancer without asbestosis.’ (1999) 59(18) Cancer Research 4570.

H Wolff, T Vehmas, P Oksa, J Rantanen and H Vainio, ‘Asbestos, asbestosis, and cancer, the Helsinki Criteria for diagnosis and attribution 2014: recommendations’ (2015) 41(1) Scandinavian Journal of Work, Environment & Health 5.

International Agency for Research on Cancer Working Group, ‘Asbestos (Chrysotile, Amosite, Crocidolite, Tremolite, Actinolite, and Anthophyllite’ [2012] 100C International Agency for Research on Cancer Monographs, 219.

JT Hodgson and A Darnton ‘The Quantitative Risks of Mesothelioma and Lung Cancer in Relation to Asbestos Exposure’ (2000) 44(8) Annals of Occupational Hygiene 565.

K Husgafvel-Pursiainen, A Karjalainen, A Kannio, S Anttila, T Partanen, A Ojajärvi and H Vainio, ‘Lung cancer and past occupational exposure to asbestos. Role of p53 and K-ras mutations.’ (1999) 20 American Journal of Respiratory Cell and Molecular Biology 667.

L Nielsen, J Baelum, J Rasmussen, S Dahl, K Olsen, M Albin, N Hansen and D Sherson, ‘Occupational Asbestos Exposure and Lung Cancer - A Systematics Review of the Literature’ (2014) 69(4) Archives of Environmental & Occupational Health 191.

N De Klerk, D Henderson, M Jones, J Leigh, AW Musk, K Shilkin and V Williams, ‘The Diagnosis and Attribution of Asbestos-related Diseases in an Australian Context’ (2002) 18(5) Journal of Occupational Health and Safety - Australia and New Zealand 443.

P Sutherland and J O Ballard, Annotated Safety, Rehabilitation and Compensation Act 1988 (The Federation Press, 10^th ed, 2014).

Sir R Doll and R Peto, ‘Mortality in Relation to Smoking – 40 Years Observation on Male British Doctors’ [1994] 309 British Medical Journal 901.

V Roggli, ‘Asbestos content of lung tissue and carcinoma of the lung: a clinicopathologic correlation and mineral fibers analysis of 234 cases’ (2000) 44(2) Annals of Occupational Hygiene 109.

V Roggli, ‘Carcinoma of the Lung’ in T Oury, T Sporn (eds) ‘Pathology of Asbestos-Associated Diseases’ (Springer-Verlag, 3^rd ed, 2014).

Y Ngamwong, W Tangamornsukan, O Lohitnavy, N Chaiyakunapruk, N Scholfield, B Reisfeld and M Lohitnavy, ‘Additive Synergism between Asbestos and Smoking in Lung Cancer Risk: A Systematic Review and Meta-Analysis’ (2015) 10(8) PLoS (Public Library of Science) One Journal 1.

REASONS FOR DECISION

Egon Fice, Senior Member
E A Shanahan, Member

1. Mr Noel Pryde died at the Benalla & District Memorial Hospital on 2 March 2010.  His death certificate states the cause of death as:

   Lung abscess – two months

   Non small cell lung carcinoma – 1 year

   Asbestosis – 20 years

   smoking – 50 years

2. The claims are brought by Mrs Barbara Pryde under ss. 17 and 18 of the Safety, Rehabilitation and Compensation Act 1988 (SRC Act).  Relevantly, those sections provide:

   17       Compensation for injuries resulting in death

   (1)  This section applies where an injury to an employee results in death.

   …

   (3)  Subject to this section and to sections 16 and 18, if the employee dies leaving dependants some or all of whom were, at the date of the employee's death, wholly dependent on the employee, Comcare is liable to pay compensation in respect of the injury of $400,000 and that compensation is payable to, or in accordance with the directions of, Comcare for the benefit of all of those dependants.

   …

   18       Compensation in respect of funeral expenses

   (1)Where an injury to an employee results in death, Comcare is liable to pay compensation in respect of the cost of the employee's funeral to the person who paid the cost of the funeral or, if that cost has not been paid, to the person who carried out the funeral.

   …

3. A person is a dependant if that person satisfies the description set out in s. 4(1) of the SRC Act. It provides:

   “dependant”, in relation to a deceased employee, means:

   (a) the spouse, parent, step-parent, father-in-law, mother-in-law, grandparent, child, stepchild, grandchild, sibling or half-sibling of the employee; or

   (b) a person in relation to whom the employee stood in the position of a parent or who stood in the position of the parent of the employee;

   being a person who was wholly or partly dependent on the employee at the date of the employee’s death.

4. There was no issue about the fact that Mrs Pryde was wholly or partly dependent on Mr Pryde at the date of his death.

5. There was no dispute between the parties regarding Mr Pryde’s employment history.  Between 1954 and 1957 he was employed by the then State Electricity Commission of Victoria (SECV) at Yallourn power station.  In July 1961 Mr Pryde commenced employment with what was then the Post Master General’s Department (PMG).  

6. Mr Pryde’s work history in the four year period between 1957 and 1961 is not entirely clear.  It appears he worked for Olympic Tyres for two short periods where he may have had some bystander exposure to asbestos.  It is likely that his exposure to asbestos over this short period was extremely small.

   History of Telstra Corporation Ltd and Comcare

7. Peter Sutherland and John Oman Ballard, authors of the Annotated Safety Rehabilitation and Compensation Act 1988 (10^th ed, 2014), set out the subsequent history of the PMG as described by Cole JA in Telstra Corporation Ltd v Worthing (1997) 42 NSWLR 655, at 659. His Honour explained:

   Prior to 1 September 1971 there existed a Department of government of the Commonwealth of Australia known as the Postmaster General’s Department. However, by s. 4 of the Telecommunications Act 1975 (Cth) the Australian Telecommunications Commission was created.

8. The Australian Telecommunications Commission was established as a body corporate by s. 21 of the Telecommunications Act 1975 (Cth). The Australian Telecommunications Commission was transformed into the Australian Telecommunications Corporation by the Telecommunications Amendment Act 1988 (Cth) which commenced on 14 December 1988. The Australian Telecommunications Corporation continued as a body corporate under the name Telecom under the Australian Telecommunications Corporation Act 1989 (Cth), which commenced on 1 July 1989.

9. Telecom’s functions were taken over by the Australian and Overseas Telecommunications Corporation in 1991. The Australian and Overseas Telecommunications Corporation Act 1991 (Cth), which commenced on 1 July 1991, defined AOTC (Australian and Overseas Telecommunications Corporation) to mean the company incorporated, or to be incorporated, under the Corporations Law of the Australian Capital Territory by the name Australian and Overseas Telecommunications Corporation Limited. The AOTC was registered as an unlisted public company limited by shares on 6 November 1991.  On 13 April 1993 the AOTC was renamed Telstra Corporation Limited (Telstra).

10. When Mr Pryde first commenced working with the PMG, compensation for work injuries was provided to Commonwealth employees under the Commonwealth Employees’ Compensation Act 1930 (Cth). This was subsequently replaced by the Compensation (Commonwealth Government Employees) Act 1971 (Cth). On its introduction the 1988 Act was called the Commonwealth Employees’ Rehabilitation and Compensation Act 1988 (Cth), later being renamed the SRC Act.

11. The AOTC became a licensed authority under Part VIIIA of the SRC Act with effect from 30 June 1992.  Part VIIIA was replaced by part VIII on 1 April 2002 by the Safety, Rehabilitation and Compensation and Other Legislation Amendment Act 2001 (Cth). Under the transitional provisions set out in Schedule 2 to that Act, a Commonwealth authority which held a licence under Part VIIIA continued to be licensed under Part VIII. As such, Telstra’s transitional licence was subsequently converted to a licence under Part VIII. The grant of that licence was dependent upon acceptance by an authority or an eligible corporation of liability under the SRC Act for payments in respect of injury, loss or damage suffered by, or the death of, some or all of its employees.

12. The Industrial Relations Legislation Amendment Act (No 3) 1991, which commenced on 22 June 1992, established a body called Comcare to manage new compensation claims. The functions of Comcare are set out in s. 69 at the SRC Act.

13. Liabilities for asbestos-related claims made against the Commonwealth or a Commonwealth authority were transferred to Comcare under s. 5 of the Asbestos-related Claims (Management of Commonwealth Liabilities) Act 2005 (Cth). This meant that Asbestos-related claims made after the commencement of Part 2 of the Asbestos-related Claims (Management of Commonwealth Liabilities) Act 2005 (Cth) on 26 October 2005 could be made against Comcare.

14. The above somewhat complicated history is set out so as to explain the two respondents named in this proceeding, that is, Telstra Corporation Ltd and Comcare.  References to Telstra in these reasons should be understood to be a reference to Telstra and/or its predecessors.

    Background to the Proceedings

15. Mrs Pryde’s claim for compensation for the work-related death of her husband was said to arise from his exposure to asbestos in the course of his employment with Telstra.  Mrs Pryde lodged an application for compensation against Telstra and Comcare on 16 February 2011.  She claimed her husband died on 2 March 2010 as a result of asbestosis caused by exposure to asbestos among other conditions.

16. In a letter dated 10 August 2011 Telstra notified Mrs Pryde that it had determined she was not entitled to compensation as a result of her husband’s death.  In a letter dated 28 May 2013 Comcare notified Mrs Pryde’s solicitors, Slater & Gordon, that her claim was disallowed.  In both cases, Mrs Pryde sought reconsideration of the determination.

17. In a letter dated 3 October 2011 Telstra notified Mrs Pryde that it had decided to affirm the determination dated 10 August 2011.  In a letter dated 16 August 2013 Comcare also decided to affirm the determination under review.  Mrs Pryde sought review of both of those decisions by this Tribunal, the claim against Telstra being lodged on 23 December 2011 and against Comcare on 3 September 2013.  The claim against Telstra was allocated matter No. 2011/5617 and the claim against Comcare matter No. 2013/4437.  The matters were heard concurrently.

18. There was no dispute between the parties that Mr Pryde’s death was caused by carcinoma of the lung.  Although the death certificate also refers to asbestosis, as will become apparent presently, subsequent pathology neither confirmed nor negated the presence of asbestosis, however the presence of calcified pleural plaques confirmed asbestos exposure.  There was no doubt that Mr Pryde had been exposed to asbestos in the course of his working life.  To complicate matters, Mr Pryde was a heavy smoker for a period of some 50 years.  The issues which confront us on this application are:

    (a)whether the lung cancer which caused Mr Pryde’s death was a disease specified by the Minister for the purposes of s. 7(1) of the SRC Act;

    (b)whether Mr Pryde suffered an injury resulting in death as the word injury is defined in s. 5A of the SRC Act which includes a disease as defined in s. 5B;

    (c)if Mr Pryde suffered an ailment, whether that was contributed to, in a significant degree, by his employment, as defined in ss. 4 and 5B of the SRC Act;

    (d)the degree to which Mr Pryde was exposed to asbestos throughout his employment by the Commonwealth or a licensee;

    (e)whether the degree of exposure to asbestos was such that Mr Pryde’s relative risk of contracting lung cancer was sufficiently high to establish, on the balance of probabilities, a causal connection between that exposure and his lung cancer and;

    (f)the significance and contribution to the risk of developing lung cancer from his extensive period of tobacco smoking, this being an accepted risk epidemiologically.

    SECTION 7 OF THE SRC ACT – PROVISIONS RELATING TO DISEASES

19. In his opening statement, Mr A Dimsey of counsel, who appeared on behalf Mrs Pryde, explained it was alleged that Mr Pryde worked for the SECV between 1954 and 1958 as a trades assistant.  That work was conducted at Yallourn power station operated by the SECV, where Mr Pryde had exposure to asbestos.  He also had exposure to asbestos in the course of his employment between 1961 and 1990 with Telstra.  Given what was claimed to be an extensive period of exposure to asbestos in the course of his employment, Mr Dimsey sought to rely on s. 7 of the SRC Act which, relevantly, provides:

    7         Provisions relating to diseases

    (1)  Where:

    (a)  an employee has suffered, or is suffering, from a disease or the death of an employee results from the disease;

    (b)  the disease is of a kind specified by the Minister, by legislative instrument, as a disease related to employment of a kind specified in the instrument; and

    (c)  the employee was, at any time before symptoms of the disease first became apparent, engaged by the Commonwealth or a licensed corporation in employment at that kind;

    the employment in which the employee was so engaged shall, for the purposes of this Act, be taken to have contributed, to a significant degree, to the contraction of the disease, unless the contrary is established.

    …

    (2)  The death of an employee shall be taken, for the purposes of this Act, to have resulted from a disease or an aggravation of the disease, if, but for that disease or aggravation, as the case may be, the death of the employee would have occurred at a significantly later time.

20. Plainly, the provisions set out in s. 7(1) of the SRC Act place a burden on a respondent to rebut a presumption of causation if an applicant satisfies (a), (b) and (c).

21. The relevant instrument for the purposes of s. 7(1) is the Safety, Rehabilitation and Compensation (Specified Diseases) Notice 2007 (1) (Cth).  The Schedule to the instrument, which is divided into three columns, sets out the specified diseases and the specified employment relating to those diseases.  Insofar as it is relevant to this matter, Item 27 of the Schedule provides:

    Column 2  Column 3

    Specified DiseasesSpecified Employment

    Lung cancer or mesotheliomas  Employment involving exposure to

    caused by asbestos.  asbestos.

22. Mr Dimsey agreed that there was a dispute regarding the cause of Mr Pryde’s lung cancer.  He also agreed that Mrs Pryde did not contend that the disease was mesothelioma caused by asbestos.  There was no evidence that Mr Pryde developed mesothelioma.  Mr Dimsey made it clear that he was referring to asbestos exposure in its totality, which included the exposure Mr Pryde experienced while working at the Yallourn power station despite that employment not being Commonwealth employment.

23. In response to Mr Dimsey’s submissions regarding the application of s. 7(1) of the SRC Act, Mr J Lenczner of counsel, who appeared on behalf of Comcare, referred us to the High Court of Australia (Mason CJ, Brennan, Dean, Toohey and Gaudron JJ) decision in Bird v Commonwealth of Australia (1988) 165 CLR 1. That case involved a member of the Royal Australian Air Force (RAAF) who had been exposed to radioactive air and dust samples after a nuclear test and he subsequently developed cancer of the tongue with right cervical node metastasis.

24. The relevant statutory provision at that time was s. 30 of the Compensation (Commonwealth Government Employees) Act 1971 (Cth) (the 1971 Act). Other than the disease being specified in Regulations rather than in a legislative instrument, and the final words of that section deeming the exposure to have been a contributing factor to the contraction of the disease, the words are identical to those now found in s. 7(1) of the SRC Act.

25. The relevant provisions in the Regulation referred to the disease as:

    4.  Pathological condition caused by –

    radium or another radioactive substance; or

    x-rays

26. The relevant employment was described as:

    Employment involving exposure to or contact with radium, other radioactive substances or x-rays

27. The plurality in Bird (Mason CJ, Brennan and Toohey JJ) described the purpose of s. 30 of the 1971 Act in terms of what was said in the case Connair Pty Ltd v Fredricksen (1979) 142 CLR 485 where the Court said, at 502:

    … [it is] to enable an employee to recover if he could show that the employment in which he was engaged involved a particular liability to, or a special risk of, contracting the disease from which he suffered, although he could not prove that he contracted the disease in the employment of the defendant employer.

28. The expression disease of a kind in s. 30(b) (also in s. 7(b)) was explained by the plurality at 6 where they said:

    The words “disease of a kind” in par. (b) of s. 30 allow a description in terms more general than those which would identify a particular disease. The kind of disease specified in item 4 is not a discrete pathological condition. It is any pathological condition which is in fact caused by one or other of the nominated substances; but it does not comprehend all pathological conditions which could be caused by the nominated substances. Unless it is found that the pathological condition was in fact caused by one or other of the nominated substances, condition (b) is not satisfied and s. 30 does not operate upon the facts of the particular case.

1. As to the causal link between the condition and the exposure to the relevant substances, the plurality said at 6:

   Items 6 to 23 of the First Schedule and s. 30 together are thus clearly intended to provide the causal link between exposure to or contact with the substance and poisoning which has in fact been caused by the substance. Similarly, item 4 of the Schedule and s. 30 provide the causal link between exposure to or contact with radium or other radioactive substances or x-rays and a pathological condition which has in fact been caused by those substances. The Schedule does not require that the substances to which an employee was in fact exposed or in contact with during his employment be proved to be the actual cause of the poisoning or pathological condition from which a claimant is suffering. The Schedule and s. 30 avoid that necessity. But they do require that the poisoning or pathological condition from which a claimant is suffering be caused by substances of the same description as those to which the employee was in fact exposed or in contact with during his employment.

2. The dissentients (Dean and Gaudron JJ) went a little further and linked s. 30 of the 1971 Act and Regulation 12 of the Schedule with the definition of disease which required the employment to be a contributing factor, not dissimilar to the current s. 5B of the SRC Act which requires a contribution, to a significant degree, by the employee’s employment by the Commonwealth or a licensee. They said, at 9:

   Under that scheme, the relevant question (in a case where an employee or former employee of the Commonwealth has contracted a “disease”) is not whether the employee's condition was actually “caused” by his employment by the Commonwealth. It is whether that employment was “a contributing factor” to the contraction of the disease. The operation of s. 30 of the Act is merely to create a rebuttable presumption that certain kinds of employment by the Commonwealth constitute “a contributing factor” to the contraction of certain kinds of disease. The effect of the construction which we would give to the words of reg. 12 and the Schedule is that there is a presumption that if a person is suffering from the kind of pathological condition caused by exposure to radiation and his earlier employment by the Commonwealth involved his exposure to radiation, there is a rebuttable presumption that his employment was “a contributing factor” to his pathological condition.

3. In our opinion, while there is a slight difference between the plurality and the dissentients, the explanation offered by the dissentients is probably more accurate because it takes into account the definition of disease. In the context of the case before us, perhaps the most controversial aspect of the application of s. 7(1) of the SRC Act was the contribution, if any, of Mr Pryde’s exposure to asbestos when employed by SECV at Yallourn power station. Clearly, to the extent that he was exposed to asbestos while employed by the SECV, that was not a contribution made by Mr Pryde’s employment by the Commonwealth or licensee. We note that s. 7 of the SRC Act refers to the death of an employee, that term being defined in s. 5 (1) which provides:

   employee means:

   (a)  a person who is employed by the Commonwealth or by a Commonwealth authority, whether the person is so employed under a law of the Commonwealth or of a Territory or under a contract of service or apprenticeship; or

   (b)  a person who is employed by licensed corporation.

4. The extent of that exposure and the part it may have played in Mr Pryde developing lung cancer was explored by some of the experts in their evidence to which we will refer shortly.  Essentially, Telstra and Comcare contended that Mr Pryde’s exposure to asbestos while an employee of Telstra did not contribute, to a significant degree, to his lung cancer.  They contend that the cause of his lung cancer was smoking.  If Telstra and Comcare are successful in proving, on the balance of probabilities, that Mr Pryde’s exposure to asbestos, wherever that occurred, did not contribute to a significant degree to his lung cancer, then the presumption set out in s. 7 of the SRC Act will be rebutted.

   COMPENSATION FOR INJURY OR DEATH

5. Section 14 of the SRC Act establishes a liability to pay compensation in accordance with that Act.  Relevantly, it provides:

   14       Compensation for injuries

   (1)Subject to this Part, Comcare is liable to pay compensation accordance with this Act in respect of an injury suffered by an employee if the injury results in death, incapacity for work, or impairment.

6. The word injury is relevantly defined in s. 5A of the SRC Act as follows:

   5A      Definition of injury

   (1)  In this Act:

   injury means:

   (a)  a disease suffered by an employee; or

   (b)  an injury (other than a disease) suffered by an employee, that is a physical or mental injury arising out of, or in the course of, the employee’s employment; or

   (c)  an aggravation of the physical or mental injury (other than a disease) suffered by an employee (whether or not that injury arose out of, or in the course of, the employee’s employment), that is an aggravation that arose out of, or in the course of, that employment; …

7. The word disease is defined in s. 5B of the SRC Act as follows:

   5B      Definition of Disease

   (1)  In this Act:

   disease means:

   (a)  an ailment suffered by an employee; or

   (b)  an aggravation of such ailment;

   that was contributed to, to a significant degree, by the employee’s employment by the Commonwealth or a licensee.

   (2)  In determining whether an ailment or aggravation was contributed to, to a significant degree, by an employee’s employment by the Commonwealth or a licensee, the following matters may be taken into account:

   (a)  the duration of the employment;

   (b)  the nature of, and particular tasks involved in, the employment;

   (c)  any predisposition of the employee to the ailment or aggravation;

   (d)  any activities of the employee not related to the employment;

   (e)  any other matters affecting the employee’s health.

   (3)  In this Act:

   significant degree means a degree that is substantially more than material.

   EXPOSURE TO ASBESTOS IN THE COURSE OF EMPLOYMENT

8. All of the experts who gave evidence in this proceeding agreed that the risk of acquiring lung cancer from exposure to asbestos or tobacco smoke was dependent upon the dosage level.  Risk also varied depending on the type of asbestos to which a person was exposed.  Nevertheless, it is the degree of exposure to carcinogens which appears to play a very significant role in the calculation of the risk of developing lung cancer.  It was this element which was also said in many reports to be the most unreliable element of the risk assessment.  Mr Pryde’s case is no exception.

9. The only medical expert witness before us who had taken an occupational history from Mr Pryde before he died was Professor Fox, a medical oncologist.  That was in August 2009 and Professor Fox said it was difficult to get exact dates from Mr Pryde as his memory was poor and he was confused. 

10. Putting aside his early work history before he went to work with the SECV at Yallourn in about 1954, Mr Pryde told Professor Fox that he commenced that work when he was 18 years old and it continued until he was aged about 26, that is, a period of eight years.  That history does not accord with the Applicant’s Statement of Facts, Issues and Contentions lodged with the Tribunal.  In that document, it is said that Mr Pryde worked for the SECV at Yallourn power station from 1954 to 1957, at most, a period of four years.  As for the intervening period between 1957 and 1961, we had no information about his degree of exposure to asbestos. 

11. In his report dated 8 May 2009 Dr Kilpatrick, an occupational hygienist, stated he interviewed Mr Pryde on 6 May 2009.  In that report, Dr Kilpatrick said Mr Pryde worked at the Yallourn power station as a trade assistant to boilermakers, fitters and welders between 1954 and 1957.  In fact Dr Kilpatrick reported that for the last 12 months while working at the Yallourn power station, Mr Pryde worked on the No.  6 dredge in the open cut.  That evidence suggests that Mr Pryde may have been exposed to airborne asbestos for a period of only three years while at Yallourn power station.

12. There was no dispute that Mr Pryde commenced working for Telstra in 1961.  We had in evidence a written statement from Mr Pryde which, in part, details the nature of some of the work he conducted while with the Telstra.  We also had in evidence a number of reports prepared by various Telstra engineers regarding Mr Pryde’s qualifications, experience and work roles.  As those are essentially contemporaneous documents, we accept their accuracy.

13. As best we are able to determine, Mr Pryde’s employment history with Telstra was as follows:

    ·July 1961 – April 1962 – digging party 14 months (compressor operator 4 months)

    ·April 1962 – cable jointing school (Fisherman’s Bend) 14 weeks

    ·August 1962 – cable jointer – faults on and off for about 7 years, cable and aerial new work

    ·completed the following courses – 1965 moisture barrier enclosure, 1966 lines supervisor safety, 1968 cable rearrangement and 1969 installation plan 1-5     

    ·January 1971 – linesman in training school – appointed Linesman Grade 2 and qualified cable jointer

    ·December 1978 – line supervisor ground (penman duties)

    ·January 1981 cable assignor and relieved lines officer estimating for short periods, up to one month duration

14. In addition to the two occupational hygienists, Dr Kilpatrick and Mr Pickford, who provided their opinions regarding the degree of exposure to asbestos experienced by Mr Pryde in the course of his employment with the SEC and Telstra, we had in evidence statements from a number of lay witnesses who gave their accounts of the nature of the work involved, particularly in the Telstra setting.  We will refer only to two of those statements as it appears the parties relied primarily on those two witnesses.  Mrs Pryde relied on a statement prepared by Mr Noel Angus Kinniburgh while Telstra relied on a statement made by Mr Imre Boroczky.   We should say at the outset that the difference between the evidence of these two lay witnesses is not readily reconcilable.

15. Mr Kinniburgh said he commenced employment with Telstra as a linesman and a pit and pipe worker in 1963.  This was his role until about 1978 after which he became a supervisor and managed teams of linesman.  Mr Kinniburgh said that in his position as a linesman he was involved primarily in the installation of cables, asbestos cement pipes and asbestos cement pits.  He was required to handle those pipes, to cut and rasp cement pipes, make holes in the walls of asbestos cement pits and rasp them, work with asbestos cement pits including inside them and pull cables through asbestos cement pipes and work near others doing the same or similar tasks. 

16. Mr Kinniburgh met Mr Pryde in either 1963 or 1964 when Mr Pryde was working in the same team as Mr Kinniburgh’s brother.  Mr Kinniburgh said he did not know Mr Pryde well but knew that he completed the same duties as did Mr Pryde.  Mr Kinniburgh said that all linesmen were required to complete the same duties and therefore would have been exposed to asbestos during their day to day duties.

17. Mr Kinniburgh explained that to install piping, one would need to cut the asbestos cement pipes to length with a handsaw.  He believed that most if not all of the pipes used at that time contained asbestos.  He also said that the pits themselves had to be cut to size so that they would slip over pipes.  He explained that breaking holes through the wall of asbestos cement pits was a common occurrence due to the fact that the pits were solid on all sides excluding the roof, and in order to feed a pipe through the wall of the pit you would have to hammer a hole through the wall and then rasp the hole (presumably to make its smooth).  He also explained it was not unusual to have to break up a pit because it was damaged or otherwise needed replacing. 

18. Mr Kinniburgh said that when working on site, asbestos dust could be seen going up into the air when a pipe or pit was cut.  He said it was not unusual to see a plume of white smoke above a team member who was cutting the pipe or pit.  It was not unusual to have asbestos dust all over one’s clothes at the end of the day.

19. Mr Kinniburgh also gave evidence and was cross-examined by video link.  In his examination-in-chief Mr Kinniburgh was asked about his best recollection of Mr Pryde’s job.  He said that at the time he met Mr Pryde, Mr Pryde was working in Newport in a pipe and pit party.  He described the work as digging trenches and laying pipe.  The problem with that statement is Mr Pryde’s evidence regarding the work he was doing in 1963.  Mr Pryde was no longer in the pit and pipe (digging) party but was a cable jointer, doing cable and aerial work. 

20. Mr Dimsey then asked Mr Kinniburgh to explain what Mr Pryde was in fact doing at the time his job was described as a compressor operator.  The problem with that question is that it appears to be based on an incorrect assumption.  At that time, Mr Pryde was no longer a compressor operator or with the digging party.  Mr Kinniburgh then described the offloading of asbestos cement pipes off trucks and that they would have to be cut to length at times using a hand saw.  He said there was no person designated to cut the pipes, but it would be the person putting the pits in, being a team leader or sometimes the linesman.  Mr Kinniburgh also described using a hammer to break a hole into a pit to allow pipes to be inserted.  A rasp was used to smooth the edges of the hole.  He said that to do one hole using the rasp would take probably two to three minutes.

21. Mr Dimsey subsequently put to Mr Kinniburgh that Mr Pryde was a compressor operator in April 1962 and asked whether that would have altered the work that he was doing.  Mr Kinniburgh said that it did not and that while Mr Pryde would be using a jackhammer, he would also be laying pipes and pits.

22. Where pits required replacement, as they did in older established suburbs, Mr Kinniburgh said that they would have to be broken up so that they could be taken out without damaging the cable.  A hammer was used to do that task.  He said that a pit and pipe gang would be able to install about three or four pits in a day.  The cabling was pulled through the pipes with the aid of a fibreglass rod.  Mr Kinniburgh said that when the rod and cable came into contact with the edges of the pipe, it produced dust.  He also described the designations of workers working in the pit and pipe gangs as lines assistants.

23. When asked if the fact that Mr Pryde was qualified as a cable jointer would have resulted in any different work he might be doing, Mr Kinniburgh said it did not.  He also described what was required when dealing with fault rectification.  He said that sometimes it required replacement of a pit if it had been damaged.  When asked about the reference to cable and aerial, Mr Kinniburgh said it was simply an aerial cable running between poles.  When it was suggested to him that did not involve contact with pipes and pits, he nevertheless persisted and said sometimes it did.  His explanation was simply that the line had to come down the pole go into a pit at some point.  When asked about penman duties, Mr Kinniburgh explained that was office work.  He also agreed that a cable assigner did not visit the worksite.

24. In cross-examination Mr Lenczner asked Mr Kinniburgh whether he had any recollection of any job site where he worked with Mr Pryde.  Mr Kinniburgh said he did not.  That was despite the fact that he maintained he had worked with Mr Pryde on six or seven jobs.  Mr Kinniburgh agreed that the task of the pit and pipe team was to put pits in the ground and cut the pipes and connect those pipes to the pits.  When it was put to Mr Kinniburgh that the man whose job it was to operate the compressor (jackhammer) would be doing more work on that machine and less work putting pipes in the ground and connecting the pits, he said it could.

25. Mr Lenczner then asked Mr Kinniburgh to describe the role of the jointer.  Essentially, Mr Kinniburgh explained that cables had to be sorted and cut into so they could be joined.  He agreed that the cable jointer came in behind the pit and pipe gang except if dealing with faults when he might have to replace a pit.  Mr Kinniburgh stated that the jointer would come into contact with the asbestos cement pit every day.

26. We had in evidence Mr Boroczky’s statement made on 13 July 2012.  He was employed by Telstra as a linesman in training in January 1971 and then worked as a linesman from 1972.  He completed a cable jointing course in 1973.  In 1981 he was moved to an office position working as a cable assignor, a lines records officer, an estimator and an acting depot manager.  He retired from his employment with Telstra in 1989. 

27. There are parallels regarding the nature of the work and the years Mr Boroczky performed that work with that of Mr Pryde, including his qualification as a linesman and having completed a cable jointing course.  Mr Boroczky said he did his linesman-in-training course at the same time as Mr Pryde in 1971.  He also said cable jointing work included aerial work, that is, cables contained within a box located on telegraph poles.  He said that work did not involve the use of or working near asbestos products.  Likewise, Mr Boroczky said that cable jointing work did not involve the use of or working around asbestos products.

28. Mr Boroczky said he did not perform digging work very often.  He said there was some minor digging for pits and pipes but most of the digging work was done by the Works Department which included the Digging Party which was responsible for digging manholes, installing conduits and pipes and sometimes pits.  A group referred to as the Hauling Hand Group put in larger size cables between manholes.  Mr Boroczky said that as a cable jointer, he was only responsible for joining cables.  When he arrived at a job the cables, pits, pipes and manholes were already in place.  He did not disturb any of those materials when doing his work. 

29. During the period 1971 to 1981 Mr Boroczky said he may have occasionally been asked to replace a smaller pit with a larger pit or to repair or move a pit from where it was located.  He said it was not major work and that he had never in his 20 years of service come across anyone who was required to break up pits.  He said that perhaps half a dozen times during his entire employment was he required to do work on broken pits where those pits, located on footpaths or nature strips, had been damaged by road works or contractors.  He said the same thing about the pipes connecting pits.

30. After 1981 Mr Boroczky took on an office role as a cable assignor, a lines record officer and an estimator.  He no longer worked outside of the office and was not present when people were doing any form of physical work.  He did not believe he suffered any exposure to asbestos dust and fibre during this period.

31. Mr Boroczky was of the opinion that between 1971 and 1990, Mr Pryde would have performed the same duties that he did in the course of his employment.  Although he was at a different depot to Mr Pryde, he believed their duties were the same.  He accepted that he was not aware of the duties Mr Pryde performed in his work period prior to 1971 nor could he say whether Mr Pryde had worked with asbestos cement pits or pipes during that time.  Nevertheless, Mr Boroczky said he doubted that the pipes were made of asbestos.  He said the only fibro cement pipes that he was aware were used were 100 mm pipes which were handled by those employed in the Works Department.  He also said that the only people who worked with pits and pipes were allocated to the pit and pipe group.  It was their job to install and replace pits and pipes.  He said that if Mr Pryde was not part of that group then he did not believe that he would have been required to work with pits and pipes. 

1. Mr Boroczky said that if Mr Pryde worked with pipes after 1971, he believed it would only have been on a few occasions and would not have involved breaking pits or being present when pits were being broken.  Although Mr Boroczky understood Mr Pryde’s evidence to be that he spent about 25% of his time out of the office and had intermittent exposure to asbestos while inspecting linesmen and others doing work with asbestos cement pits and pipes, he did not believe Mr Pryde would have suffered exposure to asbestos in this manner.  He said fieldwork accounted for about 10% of the duties and when one went into the field, all work had already been completed and that was no chance of being exposed to any asbestos.

2. Given the above significantly different accounts of the work performed in the employment of Telstra, it comes as no surprise that Dr Kilpatrick and Mr Pickford arrived at significantly different levels of exposure to asbestos attributed to Mr Pryde’s employment. 

3. The first report we had in evidence dated 8 May 2009 was provided by Dr Kilpatrick.  Mr Pickford responded to that report in his first report dated 25 July 2012 and followed up with a further report dated 12 August 2014.  That follow-up report incorporated the material in Mr Pickford’s first report and added further material including Mr Pickford’s tables set out in an Excel spreadsheet. 

4. This was followed by supplementary report from Dr Kilpatrick dated 21 November 2014 and a further supplementary report dated 9 February 2015 which Dr Kilpatrick described as a revised supplementary report.  In that report Dr Kilpatrick stated that he had revised his assumptions and refined his calculations.  He apologised for providing what he described as an inadequately prepared and inaccurate report, which was a reference to his 21 November 2014 report which he said was prepared under considerable private stress. 

5. In the course of his cross-examination by Mr Lenczner, when Mr Lenczner suggested to Dr Kilpatrick that the data produced by his experiments or simulations suggested that either he or his staff were not properly trained, or that he didn’t take particular care, Dr Kilpatrick responded that if some 200 boxes of archive documents had not been destroyed, the detailed records would be available.

6. Mr Pickford provided a further report dated 17 June 2015 in response to Dr Kilpatrick’s further supplementary report.  Given the way in which these reports were made, one occupational hygienist responding to another, they are best understood if examined chronologically.

   Dr Kilpatrick – 8 May 2009

7. This report has scant detail.  Dr Kilpatrick offered a very brief summary in which he stated that between 1954 in 1957 Mr Pryde worked at the Yallourn power station as a trades assistant to boilermakers, fitters and welders and was constantly exposed to airborne asbestos dust, delagging as part of his job on a frequent basis, and working alongside laggers also on a frequent basis.  He opined Mr Pryde was also exposed when welders used asbestos blankets and various other materials such as asbestos rope and asbestos gaskets.  While this information was said to have been obtained from an interview with Mr Pryde in May 2009, we note that Professor Fox did not obtain this information from Mr Pryde when he interviewed him on 7 August 2009. 

8. According to Professor Fox, Mr Pryde told him he did not handle any asbestos but that there was a considerable amount of asbestos powder in the areas where he worked.  In his examination-in-chief Dr Kilpatrick said that generally speaking, trades assistants, boilermakers and welders did not do lagging.  He said the SECV employed laggers.  Dr Kilpatrick also said that the last 12 months of Mr Pryde’s employment with the SECV was spent working on a dredge in the open cut mine.  That seems to indicate that Mr Pryde’s exposure to asbestos in the power station was for a period of approximately 3 years.

9. As for his work with the Telstra, Dr Kilpatrick said that Mr Pryde worked in the pit and pipe gang for 12 years.  This information was not obtained from Mr Pryde by Professor Fox.  Although Mr Pryde apparently told Professor Fox he started in the field in the pits where he would do electrical cable joins, and he did that work on and off while he was at Telstra for 25 years, the remainder of his work was largely office work in cable assigning.  As we have already set out above, the contemporaneous documents regarding Mr Pryde’s work duties indicate that he was with the pit and pipe gang for about 14 months, some four months of that time being spent as a compressor (jackhammer) operator. 

10. Dr Kilpatrick said that for many years Mr Pryde was working as a cable joiner in the pits with some further exposure to asbestos, particularly when pulling cables through the conduit which Mr Pryde apparently said would bring dust out which he would not only breath but would contaminate his clothing.  This information does not appear to have been given to Professor Fox.

11. While Dr Kilpatrick referred to a number of reports dealing with the foreseeability of risk from asbestos exposure, there was nothing in his report to explain how he arrived at the conclusion Mr Pryde had at least 25 fibre/mL years of exposure to airborne asbestos dust during his working life.  The only information provided by Dr Kilpatrick regarding Mr Pryde’s likely levels of asbestos exposure was this statement:

    From the description of the dustiness of his working environment at the SEC and with the PMG I am of the opinion that he was most likely exposed to airborne dust levels in excess of 25mppcf as a time weighted average, from time to time in his work.

12. Dr Kilpatrick’s report drew strong criticism from Mr Pickford.

    Mr Pickford – 25 July 2012

13. Mr Pickford was provided with Dr Kilpatrick’s report of 8 May 2009.  In his opening summary, Mr Pickford said:

    … David Kilpatrick’s estimate of ‘… at least 25 fibre/mL. years’ for Mr Pryde’s total asbestos work is not supported by David Kilpatrick in any way, and should not be used.  Further, his report does not provide any means of estimating Mr Pryde’s cumulative exposure while working at Telstra.

14. Mr Pickford also said that he was provided with a statement made by Mr Boroczky and Mr Pryde’s document.  He said those documents appear to support Telstra’s assertions and place considerable doubt on the applicant’s assertions.  Given the lack of detail, Mr Pickford said he had to rely on his knowledge of asbestos-cement pit and pipe work to draw meaningful conclusions. 

15. Mr Pickford observed that asbestos-cement pipe and pits contain both chrysotile asbestos and amphibole asbestos.  He was of the opinion that they would have contained crocidolite asbestos up to approximately 1966 and amosite after 1966.  Mr Pickford was also the opinion that the asbestos insulation for steam pipes at a power station would have contained a mixture of chrysotile and amosite asbestos.  Asbestos blankets for welding are likely to have contained only chrysotile asbestos. 

16. Mr Pickford concluded by stating that, based on his and his colleagues experience in measurement over many years, it is likely that airborne fibres from insulation products would be mainly amphibole and airborne fibres from asbestos-cement products approximately equal parts of chrysotile and amphibole asbestos.  It is understood that amphiboles, in particular crocidolite, are more dangerous than chrysotile.

17. Mr Pickford was provided with the assumptions of Mr Pryde’s asbestos exposure given to him by Telstra’s solicitors based on Mrs Pryde’s assertions and Telstra’s assertions.  Mrs Pryde’s assumptions were that between July 1961 and 1967, Mr Pryde was engaged in pit and pipe work; between 1967 and 1978 he worked as a jointer, compressor operator and jackhammer operator when working with asbestos-cement pits and pipes; between 1978 and 1990 he worked as a cable assignor, cable estimator and relief worker; and between 1954 and 1957 for the State Electricity Commission as a trades assistant.

18. Telstra’s assumptions were that between April 1961 and July 1962, Mr Pryde was engaged as a linesman and compressor operator and would not have worked with asbestos-cement pits or pipes. From May 1962 to 1971 he worked as a linesman and cable jointer with exposure limited to 6 to 12 times involving replacing or moving smaller and larger asbestos-cement pits, not involving breaking pits or asbestos-cement pipes. In 1971 he completed the linesman-in-training course and was not exposed to asbestos. From 1972 to 1978 worked as a cable jointer and phone installer, with similar levels of exposure to the May 1962 to 1971 period. From 1978 worked as a lines supervisor, performing clerical duties in the office with less than 10% of his work being field work, involving no exposure to asbestos.

19. While the work history provided by Telstra also appears to be inaccurate, it is less inaccurate when compared with the assumptions Dr Kilpatrick used for his calculation.  It nevertheless likely results in an overstatement of Mr Pryde’s exposure to asbestos.

20. In answer to the questions posed by Telstra’s solicitors, Mr Pickford provided his answers based on four discrete scenarios:

    Scenario 1 – (a) Estimate cumulative exposure and type and composition of asbestos, whilst at Telstra, employing David Kilpatrick’s assumptions, and (b) provide an opinion as to whether the assumptions are reasonable.

    Scenario 2 – Estimate cumulative exposure of asbestos, whilst at Telstra, employing the applicant’s assertions.

    Scenario 3 – Estimate cumulative exposure of asbestos, whilst at Telstra, employing Telstra’s assertions.

    Scenario 4 – Estimate cumulative exposure of asbestos, whilst at SEC.

21. Mr Pickford then set out in an Excel spreadsheet all of the assumptions upon which he relied in coming to his conclusions about the degree of asbestos exposure experienced by Mr Pryde when working for Telstra and the SECV.  Those assumptions included the time taken for each task and the distance from pits and pipes. 

22. Mr Pickford calculated a time weighted average exposure based on a working day of eight hours calculated by multiplying the exposure and duration for each of the components, adding those up, and then dividing the sum by the component durations.  He provided two scenarios (A and B) for estimated airborne asbestos concentrations, being the worst case and the typical case possibilities respectively.  Mr Pickford also explained how he calculated a reduction in concentration depending upon distance from the source of dust generation.  Effectively, the concentration was reduced by 10% for each 5 m from the dust source.

23. The degree of asbestos dust exposure calculated by Mr Pickford in the three scenarios set out above was used by Professor Berry in his report which we will deal with presently. 

    Dr Kilpatrick – 21 November 2014

24. In this report, Dr Kilpatrick referred to measurements taken by himself and his colleagues in work simulation trials which were experiments he and his colleagues conducted.  Dr Kilpatrick said those experiments were carried out over a period of about 20 years where asbestos dust levels were measured during simulated use of various asbestos‑containing products, most tests involving asbestos-cement products.  These tests were apparently carried out in chambers varying from the small, as a Telstra tent, up to one which was about 7m x 4 m.  The experiments included holes chipped into asbestos-cement and the hole being rasped, dust and debris being cleaned up with a brush and pan and asbestos cement cut with a hacksaw.

25. Dr Kilpatrick also outlined the history of what Mr Pryde and Mr Pryde’s solicitors had told him regarding the nature of the work that Mr Pryde performed.  Mr Pryde’s history was that he worked for Telstra for 29 years, with about 12 years in the pit and pipe gangs, then as cable jointer, fault rectification and other jobs.  Dr Kilpatrick noted that Mr Pryde’s instructing solicitors told him Mr Pryde worked for about six years in the pit and pipe gangs and then for 11 years as a cable jointer.  Dr Kilpatrick said he based his calculations on the information provided by the solicitors.

26. Dr Kilpatrick also said that he interviewed a number of Telstra linesman and pit and pipe gang members and they uniformly described very similar work.  He said that normally the digging of holes and trenches was done by labourers using shovels and trenching machines such as backhoes, and the pit and pipe men would spend the whole day installing pits.  The number of pits installed per day by an operator varied with pit size and complexity but he was of the view that between 5 and 10 pits per day seemed to be the best estimate.  The hole in a pit would be created by progressively chipping away with the small chipping hammer, finishing off with a half round rasp to get a circular hole.  This process would be repeated on the opposite side of the pit and a third hole made for the branch pipe.

27. Dr Kilpatrick said PVC pipe replaced asbestos-cement pipe in the mid to late 1970s.  Asbestos-cement pits were phased out by Telstra in the late 1970s.  Pit and pipe work was normally carried out in the open air but in inclement weather a canvas-covered tent would be erected over the pit.  Cable joining was invariably carried out under a tent.  When a cable joiner found a pit to be damaged, he would have to remove the pit, break it up and put it on the back of the truck and install the new pit.

28. In arriving at his calculations regarding the degree of exposure to asbestos fibres in conducting the work described above, Dr Kilpatrick said he made assumptions of the timing of the different parts of the job and the likely dust levels at different stages.  Those dust levels were based on the so-called experiments or simulations conducted by Dr Kilpatrick and on published data.  He considered variables such as how close the person’s head was to the point of dust generation, ventilation and air flow considerations.

29. Dr Kilpatrick based his assumption on an average of 7 pits per day being installed.  He then made a number of calculations for each individual task using assumptions about the time taken to perform the task, the fibre/mL exposure and dividing the resultant by 60 (to convert to fibre/mL hours exposure).  The following is an example of his calculation:

    Cutting AC pipes with a hacksaw or handsaw… say 5 minutes X 1f/mL X 7 pits ÷60 = 0.58 f/mL.hrs

30. Dr Kilpatrick then arrived at the total cumulative exposure from six years of pit and pipe work (not under a tent) by the following calculation:

    33.78f/mL.hrs (the addition of all tasks involved in installing 7 pits)/8hr day ÷ 8 = 4.2f/mL average X 6 years = 25 f/mL.yrs

31. As for cable joining work, Dr Kilpatrick said that while that work had the potential for significant asbestos exposure, it would be much less than the pit and pipe work.  Dr Kilpatrick accepted that the pulling of cables through the asbestos-cement pipe created dust, and it was probable that this was mainly asbestos-cement dust, although it had not been proven.  Dr Kilpatrick did not have any figures regarding the frequency with which pits were replaced.

32. Dr Kilpatrick concluded by stating that in interpreting his calculations, they should be treated as guides to cumulative exposures and not as precise measurements.

    Dr Kilpatrick – 9 February 2015

33. In response to a letter from Mrs Pryde’s solicitors dated 6 February 2015, Dr Kilpatrick provided a further report which is dated 9 February 2015.  It seems its purpose was to add a section calculating Mr Pryde’s likely cumulative asbestos exposure with the SECV in an Excel spreadsheet from 1954 to 1957.

34. Dr Kilpatrick referred to his two earlier reports and said he had revised his assumptions and refined his calculations.  He apologised for issuing and inadequately prepared and inaccurate supplementary report on 21 November 2014 for reasons which we have already explained.  Although put into evidence, we understood that we should not rely on that report for the purposes of determining this application.

35. The assumptions forming the basis for Dr Kilpatrick’s further supplementary report are identical to those in his supplementary report.  However Dr Kilpatrick added that his dust level measurements in what he described as experiments on chipping and rasping asbestos cement sheet, hack sawing asbestos cement sheet and the brush and pan clean-up of asbestos dust and debris conducted by him assisted by his colleagues were, in his opinion, the best guide that he had to the fibre/mL years calculations.  He explained the fibre level figures from his simulation tests were significantly adjusted downward in order to avoid or minimise positive bias created by factors differing between the experiments (although he did not say how that adjustment was performed) and Mr Pryde’s actual day to day work. These factors included the environment, which he said was mostly conducted in the open air, the head position in some tasks, air movement, and degree of tent flap opening, work rates and techniques and relative ages of the asbestos-cement sheets used in the experiments.

36. Dr Kilpatrick’s revised calculations included pit and pipe work both in a tent and in the open air.  The total cumulative exposure from six years of pit and pipe work without tents was calculated at 16.2 fibre/mL years.  Where a tent was used, his calculation provided an exposure of 32.3 fibre/mL years.  As for the cable joining work which he assumed was conducted between 1967 and 1978, Dr Kilpatrick said that although statements taken from persons who had conducted this work indicated dust was created when cables were pulled through the asbestos cement pipes, to his knowledge, the quantum of exposure had not been determined.  He had no data upon which to base any competent calculations.  Similarly, for the work conducted between 1978 and 1990, Dr Kilpatrick said he had no data upon which to base any competent calculations for this period.

37. Dr Kilpatrick also made an assessment of Mr Pryde’s exposure to asbestos dust during his period of employment at the Yallourn power station.  He assumed that the work was conducted over a three-year period.  Dr Kilpatrick relied on the assumptions he had made regarding the nature of Mr Pryde’s work in his supplementary report.  He also explained that in 1983 he was engaged by the SEC as an independent consultant hygienist for the project of stripping and demolition of three Newport power stations which he said were of a similar size to two of the Yallourn power stations.  He carried out asbestos sampling at Loy Yang A power station in the mid-1980s shortly after it was commissioned. 

38. Dr Kilpatrick said that he had observed operations at the Spencer Street Power Station in March 1978, which he said were not dissimilar to those described by men who worked at Yallourn. Dr Kilpatrick said that he had observed the power station in operation and was able to verify the levels of dust although he had no air monitoring equipment in 1978 when that occurred. In his opinion, Mr Pryde’s combination of personal exposure, bystander exposure and general background exposure to dispersed asbestos dust would have given him an average asbestos exposure level in excess of 10 fibre/mL and a cumulative exposure in excess of 30 fibre/mL years at the SECV.

    Mr Pickford – 17 June 2015

39. Mr Pickford was requested to provide this report in response to Dr Kilpatrick’s further supplementary report.  By way of summary, Mr Pickford said nothing had altered his opinion as a result of Dr Kilpatrick’s report of 9 February 2015.  He also said he strongly disagreed with Dr Kilpatrick’s cumulative exposure estimates of 16 and 32 fibre/mL years for work outside of tents and inside tents respectively.  He said the entire report was based on the results of Dr Kilpatrick’s “experiments” which he said were fatally flawed for the following reasons:

    ·all aspects of the experiments were undocumented thus not permitting a critical review;

    ·there was no evidence that test methodologies and results were peer reviewed;

    ·the entire data comprised of two tests for ‘chip and rasp; one test for ‘brush and pan work; and around six tests for hack-sawing;

    ·the results for ‘chip and rasp’ and ‘brush and pan’ are uncharacteristically high when compared to peer reviewed publications;

    ·comparison with published data show that these results are invalid;

    ·it is possible that the results were caused by contamination, poor work practices or incorrect sampling;

    ·it is likely that a non-skilled operator was used to conduct asbestos cement work;

    ·it is likely that unrealistic work rates we used thus exaggerating dust generation;

    ·airborne sampling was not conducted according to NHMRC requirements;

    ·airborne asbestos analysis was not conducted by NATA accredited analysts;

    ·there was no evidence that analysts were properly trained; and

    ·there was no evidence that analysts participated in internal or external quality control programs.

1. His Honour also explained that epidemiological studies identified the strength of an association by a measure called relative risk (RR) (at 272):

   RR is defined as the ratio of the incidence of disease in exposed individuals compared to the incidence in unexposed individuals. If the relative risk equals 1.0, the risk in exposed individuals is the same as the risk in unexposed individuals. If the relative risk is greater than 1.0 the risk in exposed individuals is greater than the risk in unexposed individuals.

2. Spigelman CJ also explained the meaning of the expression confidence interval.  Results from epidemiological studies are frequently expressed at a 95% confidence interval meaning that the range of, for example relative risk, between 1.1 and 1.8, means the authors have a 95% confidence that an increased RR is within that range even though the best estimate of increased risk may be at say 1.4.  His Honour also mentioned that an RR of 2.0 is used as a point of reference.

3. While Spigelman CJ did not explain why that is the case, it was explained by Dr Leigh.  In his report dated 4 April 2012, Dr Leigh said:

   A relative risk of 2 has some significance in that it has been equated by some with a “probability of causation” of 0.5 in the individual.  Thus if relative risk (RR) (incidence rate exposed/incident rate non-exposed) = Ie/Io = 2, then (Ie – Io)/Ie = (Ie/Io –Io/Io)/(Ie/Io) =(RR –1)/RR =(2 –1)/2 = ½ = 0.5.

4. Dr Leigh explained that the resultant (0.5) is referred to as the attributable fraction, that is, the proportion of disease cases in the exposed group in which the disease is caused by the exposure.  Referred to as a level of probability in the individual, that equates to 50%.  Dr Leigh suggested that can be conveniently mechanically equated with the civil standard of proof.

   The epidemiological case

5. We had epidemiological evidence from Professor Musk, Dr Leigh, Professor Fox and Professor Berry.  Of those experts, Professor Musk described himself as a respiratory physician and epidemiologist; Dr Leigh as an occupational physician and epidemiologist; and Professor Berry as a biostatistician and epidemiologist.  Professor Berry does not hold a medical qualification.

6. We are mindful of the fact that epidemiological studies simply establish a level of risk of developing a particular disease in a particular population.  They do not establish cause in an individual.  Nevertheless, where the relative risk of an individual reaches the level of 2, from a legal perspective, it is possible to find that cause may be established on the balance of probabilities.

7. Arguably, Professor Berry provided the most detailed epidemiological analysis of exposure to tobacco smoke and asbestos fibres.  He referred to research which considered exposure to various types of asbestos and the difference in the relative risk ratios associated with those different types.  The fibre/mL years of exposure were significantly different for example between amphibole asbestos and chrysotile asbestos required to give a doubling of the relative risk ratios.  Therefore, the commonly used figure of 25 fibre/mL years to establish a RR of 2 could be significantly underestimated depending upon the type of asbestos to which the person was exposed.  Unsurprisingly, Professor Berry was critical of the Helsinki Criteria.  Not only did it not account for different types of asbestos, but also because that study used the upper boundary of the range of fibre/mL years cumulative exposure in calculating a relative risk of 2.

8. Professor Berry applied established epidemiological data regarding cigarette smoking to Mr Pryde’s case.  He assumed Mr Pryde smoked 20 cigarettes per day from about the age of 13 years.  That assumption slightly understates the figure which was given to Professor Fox.  Nevertheless, Professor Berry calculated that Mr Pryde’s relative risk of lung cancer was about 37 relative to a lifelong non-smoker.  It could have been higher.

9. Professor Berry was also highly critical of Dr Kilpatrick’s estimates of Mr Pryde’s exposure to asbestos fibres.  He provided calculations for three scenarios, using assumptions made by Dr Kilpatrick, Mrs Pryde and Telstra.  He also assumed Mr Pryde’s exposure at Telstra to be evenly distributed between chrysotile and amphibole asbestos.  In his calculations, Professor Berry used Mr Pickford’s estimate of Mr Pryde’s exposure to asbestos while working at the Yallourn power station.  None of the scenarios which he envisaged produced a relative risk of lung cancer from exposure to asbestos as high as 2.

10. As for the combined risk of smoking tobacco and inhaling asbestos fibres, Professor Berry accepted that the effect on lung cancer risk was more than additive but not as much as multiplicative.  In the three scenarios he established, Professor Berry determined that Mr Pryde’s risk that his lung cancer developed due to smoking alone was 79%, 87% or 92%.  The corresponding risks due to asbestos alone were 0.5%, 0.3% and 0.2%.  He calculated the combined effect of smoking and asbestos exposure risks to be 18%, 10% and 6%.  Therefore, according to Professor Berry, although from a biological viewpoint it is not possible to distinguish which carcinogen was the cause of Mr Pryde’s cancer, what can be said from an epidemiological viewpoint is that if there were 100 people like Mr Pryde with lung cancer, then it can be said that 87% were due to smoking and 0.3% due to asbestos exposure.  While it cannot be said which carcinogen was the cause of his lung cancer, he is more likely to be in the 87% group than in the group of 0.3%.

11. Professor Musk’s assumptions regarding Mr Pryde’s degree of exposure to asbestos were based on the broad work history he was given, presumably by solicitors acting for Mrs Pryde.  He also relied on the degree of exposure provided by Dr Kilpatrick, that is, 25 fibre/mL years.  For the reasons we have explained above, it is our opinion that Mr Pryde’s exposure to asbestos fibres was probably significantly less than that estimated by Dr Kilpatrick.

12. Professor Musk also held the view that there was no threshold exposure to smoking or asbestos fibres below which lung cancer could not be caused.  Although Professor Musk agreed that the Helsinki Criteria regarding exposure to 25 fibre/mL years was a crude estimate of the level of exposure to asbestos which would double the risk of developing lung cancer, he accepted it as an estimate.  Nevertheless, Professor Musk was of the opinion that regardless of the dose of exposure to asbestos fibres, its contribution remained significant.  While he agreed that Mr Pryde’s tobacco smoking posed a greater risk to his developing lung cancer, he remained of the view that his exposure to asbestos was significant.  Professor Musk maintained this view because he said the fundamental process of carcinogenesis was not understood and therefore it was not possible to separate out the asbestos effect from the smoking effect in causing cancer.  As for the increase in risk resulting from smoking and exposure to asbestos, Professor Musk was of the view that more recent studies indicated that it was not quite multiplicative although it was more than additive.

13. Dr Leigh also relied on Dr Kilpatrick’s calculation of Mr Pryde’s exposure to asbestos although he acknowledged that quantitative exposure estimates can be very imprecise.  He also assumed that Mr Pryde smoked an average of 25 cigarettes per day between 1951 and 2004, that is, 66 pack years.  Dr Leigh agreed that the 25 fibre/mL year level or equivalent was reasonable level for attributing lung cancer to asbestos exposure regardless of smoking history.  In any event, Dr Leigh was of the opinion that there would always be some contribution to causation by asbestos even at exposures much less than 25 fibre/mL years.  On that basis, he was of the view that it was possible to apportion the degree of risk to each carcinogen although he cautioned that apportionment was an artificial mathematical construct which did not reflect biological reality. 

14. Dr Leigh shared Professor Musk’s opinion that combined exposure to smoking and asbestos indicated more than an additive effect but less than multiplicative.  This opinion was also shared by Professor Fox.  While Dr Leigh accepted that, mathematically, it was possible to determine an attributable fraction of overall risk to one particular carcinogen, he explained there had been persistent strong criticism of this approach.  In fact, he was of the view that the attributable fraction in the exposed often underestimated the probability of causation.  Dr Leigh concluded that all cumulative asbestos exposure would have made a material contribution to causation of Mr Pryde’s lung cancer in synergistic interaction with tobacco smoking.  That, of course, does not equate to a contribution of significant degree.

15. Professor Fox had a significantly different opinion to that of Professor Musk and Dr Leigh.  While he accepted that the presence of pleural plaques was an indicator that Mr Pryde had been exposed to asbestos fibres, the lack of evidence of interstitial fibrosis and his extensive cigarette smoking led Professor Fox to conclude that Mr Pryde’s lung cancer was due to his cigarette smoking alone.  He estimated that the relative risk of death from lung cancer in cigarette smokers who smoke between 20 and 39 cigarettes per day was 25.1.  In other words, it resulted in a high relative risk of developing lung cancer.  Professor Fox pointed out that Professor Roggli had demonstrated that those with interstitial fibrosis disclosed an increase in asbestos fibre load in the order of 30 times those persons with pleural plaques and 300 times those without plaques.  That led Professor Fox to conclude that while a relatively small level of exposure to asbestos can cause pleural plaques, significantly higher exposure was required to cause asbestosis.  Because Mr Pryde did not have evidence of interstitial fibrosis (asbestosis), Professor Fox believed his inhalation of asbestos fibre load was insufficient to cause lung cancer.

16. Professor Fox also referred to a recent journal article (PLoS One) published on 14 August 2015 which dealt with the relationship between asbestos and smoking in lung cancer risk.  It described the results as pointing to an additive synergism for lung cancer with co‑exposure of asbestos and cigarette smoking.  According to the article, that was because associations may result from independent and unrelated mechanisms.  That is, the common localised inflammatory actions of tobacco smoke and asbestos readily explained the additive effects, while each individual insult could account for the additive synergistic interaction.  Our understanding of that is as follows. 

17. Persons exposed to significant tobacco smoking or inhalation of asbestos fibres have an elevated risk of developing lung cancer.  However, many of those persons exposed to tobacco smoking alone will not develop lung cancer.  The same can be said of those persons who have inhaled significant asbestos fibres.  Furthermore, many persons who are lifelong smokers of tobacco and have been exposed to significant asbestos fibres also will not develop lung cancer.  Because tobacco smoke and asbestos fibres are both carcinogens, a person exposed to both, logically, will have a higher risk of developing lung cancer.  That is not necessarily due to the interaction of those carcinogens, but rather, because exposure to multiple carcinogens necessarily increases the risk of acquiring lung cancer due to any single carcinogen.  Hence the expression, additive synergism.

18. In our opinion, resolution of the relationship of relative risk between exposure to tobacco smoke and asbestos fibres will only be achieved by further research at a biological level.

19. Professor Fox also commented on two studies dealing with the impact of asbestos exposure and tobacco smoke at a molecular level and in particular mutations of the K-ras and p53 genes.  He described the K-ras molecule as acting as a gatekeeper in terms of cell proliferation which may become mutated in certain cancers.  He said that was generally seen in adenocarcinoma of the lung and while it was not clear as to the nature of the carcinoma in Mr Pryde’s case, it was described as moderately to poorly differentiated squamous cell carcinoma.  Professor Fox also referred to the p53 gene as being associated with cancer drive.

20. Because there seems to be no dispute about the fact that the risk of developing lung cancer from either smoking or the inhalation of asbestos fibres is dose-dependent, and we do not accept Dr Kilpatrick’s estimates of Mr Pryde’s cumulative exposure to asbestos, we find, on the epidemiological evidence, that the primary cause of Mr Pryde’s lung cancer was his tobacco exposure.  That is because the relative risk of Mr Pryde having developed his lung cancer through the inhalation of asbestos fibres does not reach anywhere near the level required to make a significant contribution finding on the balance of probabilities.

    The biological case

21. The biological case was, in the main, propounded by Associate Professor Breslin.  He said he supported the Helsinki criteria but believed that they needed to be applied to each individual patient on the patient’s merits.  Such things as genetic susceptibility and the nature of the asbestos to which the individuals are exposed are important.  Exposure to crocidolite or amosite was significant.  It was not known in an individual if there was a safe dose.

22. Associate Professor Breslin shared the view that if an individual smokes tobacco and is exposed to asbestos, their risk of developing lung cancer is markedly increased.  He described the effect is being somewhere between additive and multiplicative.

23. Despite there being no evidence that Mr Pryde had asbestosis, Associate Professor Breslin nevertheless expressed the opinion that on the balance of probabilities, there had been a material contribution to the development of his lung cancer from asbestos exposure.  That was based essentially on Mr Pryde’s exposure to asbestos fibres being in excess of 25 fibre/mL years.  Given our findings from the best evidence about Mr Pryde’s exposure to asbestos, because his exposure dose is unlikely to have been even close to 25 fibre/mL years, we can place little weight on Associate Professor Breslin’s conclusions.

    CONCLUSIONS

24. We have found that the most difficult aspect in this case was determining the degree of exposure to asbestos experienced by Mr Pryde in the course of his working life.  While we have found that the degree of exposure determined by Dr Kilpatrick was excessive taking into account the objective evidence regarding the nature of his work with SECV and Telstra, and that we also have some concerns with Mr Pickford’s estimation, we nevertheless accept that Mr Pickford‘s calculations should be preferred to those of Dr Kilpatrick.

25. While mindful of the fact that epidemiological evidence only establishes the relative risk of causation, where the relative risk exceeds 2, in a legal sense, it can be inferred, on the balance of probabilities, that causation may be attributed to carcinogenic exposure with that relative risk level. In Mr Pryde’s case, his exposure to tobacco smoke is significantly disproportionate to his exposure to asbestos fibres. Furthermore, we have found that the relative risk of Mr Pryde having developed his lung cancer through the inhalation of asbestos fibres is insufficient to find, on the balance of probabilities, that it was also a contributing cause. Because we are unable to make such a finding, it follows we cannot attribute a degree of contribution, let alone a significant degree as required by s. 5B(1)(b) of the SRC Act, by asbestos exposure to Mr Pryde’s lung cancer.

26. The biological case for establishing contribution to Mr Pryde acquiring lung cancer is insufficiently strong on the evidence before us to make such a finding.  Associate Professor Breslin’s assessment of an 11% contribution to the total risk of Mr Pryde developing lung cancer from exposure to asbestos fibres was made on the assumption that he was exposed to 25 fibre/mL years of asbestos.  Given we have found that to be an overstatement of his most likely exposure to asbestos, and that irrespective of the absence of asbestosis, because Associate Professor Breslin agreed that the risk of developing lung cancer by inhaling asbestos fibres was dose dependent, we cannot find on the balance of probabilities that Mr Pryde’s exposure to asbestos contributed to him developing lung cancer.

27. Given our findings regarding the cause of Mr Pryde’s lung cancer, we find that Telstra and Comcare have discharged the onus of rebutting the presumption of contribution to Mr Pryde developing lung cancer from exposure to asbestos fibres set out in s. 7 of the SRC Act.

28. In our opinion, the decision made by Telstra on 3 October 2011 affirming the determination dated 10 August 2011 and the decision made by Comcare on 16 August 2013 were correct.  We affirm those decisions.

29. We should also mention that following conclusion of the hearing of this matter, Mr J Wallace of counsel, who appeared on behalf Telstra, provided written submissions regarding liability of the relevant authority.  In particular, those submissions related to the operation of s. 11 of the SRC Act.  Mr Lenczner provided written submissions on behalf of Comcare in response to those submissions.  However, given the findings we have made regarding the cause of Mr Pryde’s lung cancer, it is unnecessary for us to determine that question.

I certify that the preceding 261 (two hundred and sixty-one) paragraphs are a true copy of the reasons for the written reasons herein of Egon Fice, Senior Member and E A Shanahan, Member

[sgd]......................................................

Associate

Dated   14 October 2016

Dates of hearing	24 August 2015 - 27 August 2015 23 November 2015 - 25 November 2015 17 December 2015 19 February 2016
Counsel for the Applicant	Mr A Dimsey
Solicitors for the Applicant	Slater & Gordon Lawyers
Counsel for the First Respondent	Mr J Wallace
Solicitors for the First Respondent	Sparke Helmore Lawyers
Counsel for the Second Respondent	Mr J Lenczner
Solicitors for the Second Respondent	Australian Government Solicitor