Sheila Mier and Comcare
[2014] AATA 650
•5 September 2014
[2014] AATA 650
Division GENERAL ADMINISTRATIVE DIVISION File Number
2010/4911
Re
Sheila Mier
APPLICANT
And
Comcare
RESPONDENT
DECISION
Tribunal Miss E A Shanahan, Member
Date 5 September 2014 Place Melbourne The Tribunal affirms the decision under review.
........................[sgd]................................................
Miss E A Shanahan, Member
COMPENSATION – widow’s claim – deceased worker exposed to asbestos leading to the development of pleural plaques – death following cardiac surgery – deceased a plumber with asbestos exposure in non-Commonwealth employment – contribution by Commonwealth employment to death conceded – contribution not significant – decision affirmed
Legislation
Safety, Rehabilitation and Compensation Act 1988
Cases
Amaca Pty Ltd v Ellis HCA (2010) 5 (3 March 2010), (2010) 262 ALR 576
Other Material
Harrison’s Principles of Internal Medicine (4th ed., 1962) and (18th ed., 2011)
The Third Wave of Asbestos Disease, Annals of the New York Academy of Sciences, Volume 643, December 31st 1991REASONS FOR DECISION
Miss E A Shanahan, Member
5 September 2014
Mrs Sheila Mier is the widow of Brian William Mier who died on 12 September 2009. On 5 June 2009 Mr Mier had cardiac surgery; specifically, aortic valve replacement for aortic stenosis and right coronary artery grafting. During the intervening 99 days, Mr Mier was treated in the intensive care unit for 94 days and had been ventilator dependent. He suffered from multiple systems failure and other complications.
Mrs Mier lodged a claim for compensation on 25 June 2010. The cause of Mr Mier’s death was stated in both the claim form and the Death Certificate as asbestosis. In the compensation claim, the asbestosis was said to have been caused by exposure to asbestos during Mr Mier’s employment with the Department of Defence at the Williamstown Dockyard. He was employed there for 17 weeks between 4 October 1962 and 5 February 1963.
The Death Certificate had been completed by Dr Nath, an intensive care registrar at Knox Private Hospital. Dr Nath had attributed Mr Mier’s death to asbestosis; that is, pulmonary fibrosis due to the inhalation of asbestos fibres; also termed interstitial lung disease due to asbestos fibre inhalation.
Mr Mier commenced an action in the Victorian Supreme Court shortly before his death. The respondents were A E Atherton and Son Pty Ltd, Comcare and James Hardie; and the condition resulting in death was said to be asbestosis. This proceeding was settled prior to hearing.
On 29 September 2010 a delegate of Comcare disallowed Mrs Mier’s claim. A review officer affirmed this decision on 27 October 2010. The disallowance was based on the finding that Mr Mier’s asbestosis had not been contributed to, to a significant degree by his employment with the Commonwealth. Mrs Mier lodged an undated application for review by the Administrative Appeals Tribunal in late 2010.
The hearing of this matter was to have commenced in February 2013. The applicant sought an adjournment to obtain information on summons, regarding asbestos use at the Dockyard in 1962 and 1963. The Tribunal considered it extremely doubtful that such data would have been available in an era where the hazards of asbestos exposure, particularly the oncogenic effect, had only just been reported and were not widely circulated. Nevertheless, it granted the adjournment.
Further delays and adjournments were necessitated by the misinterpretation of or failure to photocopy all of Mr Mier’s records at the Knox Private Hospital. These records were then provided to various experts for their opinion. The matter eventually came to hearing on 18 November 2013 and 21 November 2013 and was completed on 21 August 2014. The applicant, Mrs Mier, was represented by Mr Mark Carey of counsel, instructed by Ms C Bolger, a solicitor from Maurice Blackburn. The respondent was represented by Mr John Wallace of counsel, instructed by Mr D Decleva of Sparke Helmore.
The Tribunal was provided with the documents pursuant to s 37 of the Administrative Appeals Tribunal Act 1975 (the T-documents), which were labelled Exhibit R1. Both parties tendered further documents, a list of which is appended to this decision. Mrs Mier, Mr Kottek, Mr Lubicz, Dr Trembath and Mr Kisler gave evidence before the Tribunal in November 2013. It had been intended to call several expert witnesses not available in November 2013, to give evidence at the resumed hearing in August 2014. This was to include Dr Michael Jones, a radiologist, and Stephen Bernard and Dr Orlando Monteiro, both of whom are intensivists. Associate Professor Bernard and Dr Monteiro had been primarily responsible for Mr Mier’s post-operative care during the 99 days between his operation and his death.
At the commencement of the hearing on 21 August 2014, Mr Wallace conceded that the presence of asbestos-related pleural plaques or to use the terminology of the Safety, Rehabilitation and Compensation Act 1988 (the Act) pleural plaque formation, contributed to Mr Mier’s death.
BACKGROUND TO THE APPLICATION
The late Mr Brian Mier commenced an apprenticeship in plumbing in 1950, at the age of 15. Throughout his apprenticeship he worked for AE Atherton and Son Pty Ltd. He completed his apprenticeship, as far as we can tell, in 1955. During this period Mr Mier was involved in the installation of heating and cooling systems which required insulation; which at that time was done with asbestos.
Between 1954 and 1956 Mr Mier did National Service. But after three months of basic training he was allotted to a reservist unit. He then worked for Bellaire Pty. Ltd. an air-conditioning company, for 12 months and it is likely that he was exposed to asbestos in this role. His employment with the Department of Defence in the Naval Dockyard at Williamstown was for a short period of 17 weeks, which included the Christmas break. He apparently left the Department of Defence to take a job with a higher salary. Although it is not absolutely clear, it seems likely that he was subsequently employed by a company known as Fluor Utah, a company in Altona which was involved in the construction of petrochemical plants in the Geelong area.
In 1964 Mr Mier became an organiser for the Australian Plumbers and Gasfitters Employees Union on a full time basis. From 1975 to 1982 he was an organiser for the Victorian branch of the Australian Labour Party, achieving the position of Secretary of the Australian Labour Party in Victoria. From 1982 to 1986 he was a Member of the Legislative Council of the Victorian Parliament.
In May 2009 Mr Mier presented to the Knox Private Hospital with syncope (loss of consciousness) associated with episodes of complete heart block. He gave a past history of ischaemic heart disease treated by coronary angioplasty in 2000, rheumatic heart disease, aortic stenosis, late onset diabetes mellitus Type 2 and, according to the cardiologist Dr Christopher Goods, asbestosis. His episodes of syncope required the insertion of a permanent pacemaker. Investigation revealed severe aortic stenosis which had caused progressive shortness of breath over a period of three to four years. Further investigation, in the form of coronary angiography, revealed severe atherosclerosis of the right coronary artery with sparing of the left coronary artery. Cardiac function was assessed as within normal limits. Plain chest x-ray revealed numerous pleural plaques and Mr Mier subsequently underwent CT scanning of his chest. The CT confirmed the presence of pleural plaque formation involving predominantly the diaphragmatic parietal pleura and the pleura in the paraspinal areas. It did not show any evidence of pulmonary (that is lung) fibrosis consistent with a diagnosis of asbestosis.
Mr Mier was referred to Mr Serge Lubicz for aortic valve replacement surgery. Mr Lubicz considered Mr Mier’s aortic stenosis to be critical. While aware of the presence of pleural plaque formation, Mr Lubicz did not think it necessary to perform lung function tests given the severity of the aortic stenosis.
Mr Mier underwent aortic valve replacement and grafting of the right coronary artery using the right radial artery, as a semi-urgent procedure, on 5 June 2009. The operation was conducted as planned. However, it is noted that the time on cardiopulmonary bypass was 182 minutes and that the heart was without oxygen supply, that is cross-clamp time was 159 minutes.
Within two days of surgery Mr Mier developed poor cardiac output with a degree of cardiac failure and ventilator dependence. Chest x-rays revealed what is termed a white out, which was associated with poor gas exchange. These changes persisted for months. Mr Mier suffered several bouts of pulmonary infection and a number of pleural effusions which had to be drained. Eventually further surgery was performed to control the recurrent right pleural effusion. The latter provided the opportunity to perform pleural biopsies which showed acute inflammatory changes only.
For approximately five days Mr Mier managed to breathe spontaneously, although via a tracheostomy tube, and was shifted to a ward. However, he again developed respiratory compromise and required ventilation from 13 August 2009. As Mr Mier did not improve, it was determined after consultation with his family that active treatment would cease.
Whilst the Death Certificate states that the cause of death was asbestosis, the treating surgeon, Mr Lubicz, states that there is no evidence of asbestosis. There is evidence of pleural plaque formation involving predominantly the diaphragmatic surface of Mr Mier’s hemithoraces.
Mrs Mier’s application was based on the claim that Mr Mier’s cause of death was asbestosis. Specifically, that he had been exposed to respirable asbestos fibres during de-lagging and re‑lagging of steampipes on naval vessels during 17 weeks at the Naval Dockyard from October 1962 to early February 1963.
EVIDENCE BEFORE THE TRIBUNAL
Mrs Sheila Mier
Mrs Mier provided two statements. In her first statement dated 26 September 2012 (Exhibit A1), Mrs Mier advised that she and Mr Mier had married in February 1958. She outlined the recent medical history leading to Mr Mier’s death and confirmed that he had worked at the Williamstown Naval Dockyard. However, she was not certain whether this was from her own recollection or had been told to her by Mr Mier in later conversations. Certainly, she seemed clear in her statement that when she and her husband met he was working as a plumber. In later years he had told her that he had used asbestos in the course of his career and that while working at the dockyards he had eaten his lunch while sitting on bags of asbestos.
The second statement, which is undated (Exhibit A2), states that Mr Mier worked at the Williamstown Naval Dockyard from October 1962 to February 1963. It outlines their places of residence, and recalls that they were living in Seddon in 1962 and 1963; her husband would return from the Williamstown Naval Dockyard with his blue bib and brace overalls covered in pieces of hemp or rope, the colour of string (presumed to be beige). She washed these overalls. Mrs Mier said that Mr Mier had told her at the time that he was working on a ship and lagging pipes.
In her evidence before the Tribunal, Mrs Mier adopted her statements but did exhibit some uncertainty as to the dates and the actual nature of the information she was given. She was able to date some events in relation to the birth of her first child David, who was born on 21 February 1963. She did recall that at that time Mr Mier had left the dockyards and was working somewhere else as a plumber. Under cross-examination she admitted she could not remember what Mr Mier’s duties were while he was working at the Williamstown Naval Dockyard. She thought that the string-like substance sticking to his working clothes resembled hemp as she was aware that he kept what she called the hemp stuff in his toolbox. This was used to seal flanges.
Mrs Mier was not certain of the dates when Mr Mier worked full time as a union official but did confirm that he had entered politics in 1982.
Mr Michael Kottek, Occupational and Environmental Health Consultant
Mr Kottek provided a report on 23 November 2010 opining that:
... it is far more likely than not that a plumber working at the Williamstown Naval Dockyard in 1963-1964 would have experienced some degree of exposure to asbestos.
This he said was the case even if the plumber did not go on board a vessel as, to his knowledge, asbestos was used widely in workshops in that period. However, the likely level of a plumber’s exposure was difficult to determine, as it could range from high to very low. In preparing his report, Mr Kottek reviewed the records of Dr David Kilpatrick, with whom he had worked between 1991 and 1996. Mr Kottek had no personal experience of conditions at the Williamstown Naval Dockyard in 1962-63.
In his evidence before the Tribunal, Mr Kottek confirmed the content of his report and in particular that the levels of exposure in terms of fibre counts could be extremely variable depending on the individual’s duties. He regarded a high range as being 55 fibres per ml, with 100 being very high and 200 extreme. In examination-in-chief, Mr Kottek estimated that if the plumber was required to remove lagging from a joint and the lagging came off the pipe cleanly, the fibre count would be quite low. However, if it had to be forcibly removed or if pieces of asbestos lagging were trodden on underfoot, the level of exposure would rise. If the plumbers were working alongside laggers they would have been exposed to high levels of respirable asbestos fibres.
Mr Carey informed Mr Kottek that all lagging in new ships was performed at night by employees of Bells Asbestos. The plumbers’ actual exposure was greatest in the workshop.
Mr Kottek was asked to comment on the document entitled Insulation Materials at Williamstown Dockyard provided by the Department of Defence (Exhibit A4). The document relates to redundant high temperature insulation to be found in Royal Australian Navy ships. Four of these insulation materials contained asbestos. They were calcium silicate plastic, calcium silicate pipe sections, calcium silicate high temperature blocks and re-wettable asbestos cloth. Of these materials, Mr Kottek was familiar with asbestos rope (used to seal flanges and joins), which was kept in position by metal wire but more commonly by asbestos slurry. Of the list provided, Mr Kottek thought it most likely that the wettable asbestos cloth was not commonly used by plumbers but he was uncertain.
Under cross-examination, Mr Kottek agreed that he had no way of knowing the levels of exposure in the naval dockyard’s machine shop, on any particular ship and in the blacksmith shop. He admitted he did not have any knowledge of what plumbers in 1962-63 used as insulation on low temperature flanges and pipe fittings. It was his understanding that the lagging contractors did all new lagging but what he termed the rip out was done in-house but he was not absolutely certain that was correct. Mr Kottek was able to confirm that asbestos slurry was not string coloured but of a dirty white or whitish grey colour. Mr Kottek was not able to assist in the identification of the pieces of string-like material that Mrs Mier said were glued to her husband’s work overalls as to his knowledge, no glue was used.
Mr Kottek had some knowledge of other sites where Mr Mier was said to have worked, namely his employment with Bellaire and Fluor Utah at Altona. He knew that asbestos was constantly in use at both of these companies. While much of the work done by Fluor Utah was in construction of petrochemical complexes they did cut into existing plants as well. De-lagging and re-lagging took place as new plants were connected to the existing plant.
In answer to questions posed by the Tribunal, Mr Kottek said it was his understanding that delagging and re-lagging processes were staged rather than simultaneous processes. While work in ships might involve large numbers of workers, Mr Kottek did not believe that laggers and de-laggers would be in the same compartment at the same time.
Mr Leroy Kisler
Mr Kisler provided an undated statement, which he formally adopted in the giving of his evidence. Mr Kisler had been a member of the Royal Australian Navy working at the Williamstown Naval Dockyard from January 1953 to February 1988; the dockyards having been privatised in late 1987. For the first five years, Mr Kisler was an apprentice shipwright. He went on to become a draftsman, a senior planner and the Chief of the drawing office. Finally, he was employed as a trouble-shooter dealing with project problems in the dockyard.
Mr Kisler advised that plumbers working in the dockyard were primarily responsible for making large diameter pipes out of steel and copper and removing old pipes identified for repair or replacement. Plumbers also worked on these old pipes in the workshop. The insulation to be replaced consisted of asbestos slurry covered with asbestos cloth. Plumbers had no involvement in applying the insulation or in its removal aboard the ship. External contractors undertook these processes. However, dust was generated by other tradesmen working in the workshop and specialist coppersmiths and plumber welders working in this site used woven asbestos blankets to protect themselves while welding.
According to Mr Kisler, it was not until the mid-1970s that asbestos was phased out of use in the dockyard. Safety devices and safety warnings were not introduced until the late 1970s. Extractor fans were present inside the ships being worked on, having been installed at the insistence of the Painters’ and Dockers’ Union, whose members were responsible for removing any debris throughout the day.
In his oral evidence Mr Kisler expanded on his statement. It was clear that he had a great deal of experience and knowledge of the functioning of the dockyard. While he had been employed at the site from 1953 until 1988, he had spent six months on secondment to Garden Island in Sydney. He was in the United Kingdom from1978 to 1980 performing similar work; and in the United States of America from 1981 to 1983. He would have been working at the Williamstown Naval Dockyard at the same time as Mr Mier from October 1962 until early February 1963. Mr Kisler could not recall meeting Mr Mier.
While Mr Kisler could not be 100 per cent certain, he believed that at that time there were three ships at the dockyard. There was one ship being refitted, a Destroyer Escort (which he thought was the HMAS Derwent) under construction at the pier, and a third ship on the slipway in an early structural stage for launch. There would have been very little plumbing work on the third vessel. During the period under consideration there was a very strict demarcation of the duties of tradesmen in the dockyards. Plumbers were provided with plumbers’ assistants and worked primarily in the workshop, which was also used by coppersmiths and sheet metal workers (who also did major pipework).
Mr Kisler said that when a ship came in for repairs, the plumber would remove the faulty pipework after the bulk of the insulation had been removed by the contractor, Bells Asbestos. However, small amounts of lagging would be left around flanges in particular. This was removed by the plumber in the workshop using a scraper and occasionally a wire brush, which would produce dust on the workbench. Mr Kisler considered that the general atmosphere in the workshop was comparatively clean. Following the repair of old pipes or the construction of new pipes, plumbers would return the pipe to the ship and install it to the extent that they loosely inserted two bolts. It was the responsibility of a fitter and turner to do up the bolts and flanges. Similarly, in the removal of pipes, the fitters undid the flanges, the plumbers removed the last two bolts and the plumber and his assistant carried the pipe from the ship to the workshop. Once the pipe was reconstructed and replaced, Bells Asbestos employees undertook lagging in eight hour shifts, from approximately 11.00 pm until 7.20 am the following morning. No plumbers were onsite at that time. Similarly, when Bells Asbestos employees removed lagging, the pipes were left up to 48 hours before the final two bolts were removed by the plumber and the pipe transferred to the workshop.
According to Mr Kisler, there was no observable cloud located around the workbenches of the plumbers. However, there were small lumps of what was described as residual material, which Mr Kisler believed to be small pieces of lagging lying around on the workbenches or on the floor. Mr Kisler believed that any dust that was generated on board the ship would be a mixture of asbestos, swarth (skin or rind) from steelworks grinding, and smoke from welding procedures. It was in these compartmentalised areas of the ship that the extraction fans were used.
Mr Kisler also advised that steampipes on board ships were always covered with asbestos woven cloth called cotton scrim. Cotton scrim was loosely woven, coarser than hessian and frayed when cut. This cotton scrim was apparently applied not by a plumber but by the external lagging company employees. Early in Mr Kisler’s employment it was his role to liaise with contractors and in particular Bells Asbestos. He would visit the ship in the morning and evening to measure what Bells Asbestos had achieved during the day. It had also been Mr Kisler’s responsibility to archive the data regarding employment, which included the workers’ timesheets and document the ships being built and repaired. The archival records he constructed were held in Laverton and were said to be in existence in 1988. According to Mr Wallace, these archival records had been sought but could not be found.
Mr Kisler confirmed that the lagging removed from pipes was similar in weight and consistency to the lightweight plaster of paris used to reduce fractures, and that it was a dirty white colour.
Mr Kisler said that when he was serving his apprenticeship there had been a major strike at the dockyard in 1955. The strike had lasted for four months and during it the only people working in the dockyard were the foreman, apprentices and contractors. During this period there were dried lumps of asbestos fibre insulation hanging around and the apprentices were in the habit of picking up these fragments and throwing them at each other, resulting in the dried fibre bursting and scattering.
Mr Kisler was aware that following the repair of a vessel or construction of a new vessel trials were undertaken. In the Destroyer-class ships built at the dockyard, the accommodation spaces for the crew were insulated with sprayed limpet asbestos (so-called blue asbestos or crocidolite) and then painted. This crew accommodation was immediately underneath the gun turrets and it became obvious on trial runs that when the guns were fired, the limpet asbestos flaked from the accommodation walls. This did not result in any exposure to plumbers.
Medical evidence provided to the Tribunal
The Tribunal was provided with a considerable amount of documentary evidence, particularly the voluminous records from Knox Private Hospital relating to Mr Mier’s 99-day admission ending in his death. It was originally intended to call the following doctors to give evidence at the hearing: Mr Alexander Rosalion, cardiothoracic surgeon, Dr Michael Jones specialist radiologist, Mr Serge Lubicz cardiothoracic surgeon and Dr Peter Trembath respiratory physician. After considerable discussion between the Tribunal Member and counsel to identify any inadequacies in the medical evidence, it was determined to obtain reports from at least one intensivist who had been primarily responsible for Mr Mier’s care from 5 June until 12 September 2009.
In the course of the hearing on 18 and 21 November 2013, and in directions hearings that took place thereafter, it became evident that the Tribunal possessed a far more complete copy of Mr Mier’s clinical records from Knox Private Hospital than the parties did. Since the expert witnesses had been provided with copies of the documents held by the parties, the experts too lacked the complete records. The Tribunal resolved this problem by inviting the parties to attend the Tribunal and photocopy its copy of the documents.
When the hearing resumed on 21 August 2014, the Respondent conceded that Mr Mier’s death had resulted from pleural plaques possibly resulting from asbestos exposure. Therefore, it became unnecessary to consider the medical reports in detail. However, the Tribunal will summarise them.
Mr Serge Lubicz
Mr Lubicz was the treating surgeon who performed Mr Mier’s aortic valve replacement (using a porcine bioprosthesis) and coronary artery bypass grafting of the right coronary artery (using the left radial artery). In addition, the heavily calcified mitral valve annulus was debrided. This operation was performed on 5 June 2009.
Mr Lubicz performed a second operation on 23 July 2009, a video-assisted right thoracotomy, drainage of pleural effusion, pleural biopsy and pleurodesis (pleurodesis is a mechanical irritation of the pleura lining of the chest wall in order to promote adhesions between the two layers of pleura and obliterate the pleural space). The biopsies of the pleura showed acute inflammatory changes, with no evidence of fibrosis; although Mr Lubicz gave evidence of seeing extensive calcified pleural plaques. The operative findings report does not mention pleural plaques but describes the pleura in the right hemithorax as being inflamed and covered in fibrin and blood in association with a 700 ml pleural effusion. A hand-written Addendum dated 13 August 2009 states:
The right hemidiaphragm was totally covered with calcific plaque and was hard and rigid.
This was not signed and it is not certain who made the entry.
In his evidence before the Tribunal, Mr Lubicz considered Mr Mier’s death was attributable to extensive calcific pleural plaque formation affecting Mr Mier’s chest expansion and respiration, resulting in him becoming ventilator dependent. In his tendered reports and the operative report of 23 July 2009, and in several letters written to referring doctors, Mr Lubicz had stated that Mr Mier suffered from asbestosis. He corrected this in his oral evidence, stating that there was no evidence to support a diagnosis of asbestosis.
Dr Peter Trembath
Dr Trembath, a consultant respiratory physician, provided a written opinion dated 26 May 2011 (Exhibit R2) based on documentation provided to him. Dr Trembath analysed all the data and concluded that the most probable diagnosis explaining Mr Mier’s respiratory complications was the development of acute respiratory distress syndrome (ARDS), a recognised complication of cardiopulmonary bypass surgery, and pulmonary sepsis. Dr Trembath did not believe the presence of bilateral calcific pleural plaques, likely to be due to past asbestos exposure, contributed materially to the respiratory failure. Dr Trembath was unable to comment on the relevance of Mr Mier’s work at the Williamstown Naval Dockyard. He had not been provided with information regarding the precise nature of the work Mr Mier did there. Nor had he been provided with information about the level of exposure to asbestos at any time other than the 17 week period in 1962-63.
Dr Trembath recommended that a report be obtained from the treating intensive care specialists responsible for Mr Mier’s care.
In his evidence before the Tribunal, Dr Trembath confirmed his original diagnosis and opinion. He also provided a provisional alternative diagnosis of persistent pulmonary oedema, secondary to left ventricular failure.
Immediately prior to Dr Trembath giving his evidence, the Tribunal Member expressed her concern that none of the reporting specialists had listed the documentation that they had been provided with. The Member, having read the Knox Private Hospital file in its entirety, had gleaned a different picture to that which had been described in evidence to that date.
Dr Trembath described the documentation he had received as being (a bundle) two inches (five centimetres) thick. The documentation the Tribunal received from Knox Private Hospital is approximately three times that thickness.
In his oral evidence, Dr Trembath confirmed his opinion that the mostly likely diagnosis was ARDS. An alternative differential diagnosis would be acute, bordering on chronic, pulmonary oedema with recurrent pulmonary infection. Dr Trembath bemoaned the absence of opinions from the intensive care consultant physicians as the notes provided were essentially a description of progress without an opinion as to underlying diagnosis. The Tribunal Member provided Dr Trembath with further information from the more complete Knox Private Hospital records. He considered that the additional information reinforced his opinion, that while the pleural plaques contributed to Mr Mier’s death, the contribution was not material.
Dr Trembath disagreed with Mr Lubicz’s evidence that in the first three post-operative days Mr Mier made steady, uneventful progress because he had had to be re-intubated and ventilated within 24 hours of removal of his endotracheal tube. The records showed that while Mr Lubicz did make short visits to the unit, he was not directly involved in Mr Mier’s day-to-day care while he was in Intensive Care and had been on leave for a period of two to three weeks during Mr Mier’s hospitalisation.
Dr Michael Jones, Radiologist
Dr Jones is an interventional radiologist of many years of experience, particularly in relation to occupational lung disease. He works at several major public hospitals in Sydney. He had been provided with all of the radiological investigations, that is the chest x-rays and CT scans, that Mr Mier underwent. There were almost daily post-operative chest x-rays performed, one CT scan performed pre-operatively and two in the post-operative phase. The extent of the clinical notes provided to Dr Jones is not known.
From his examination of the radiography, Dr Jones concluded that the pleural effusions present pre-operatively were most likely due to heart failure. The CT scan performed three weeks prior to surgery, confirmed calcified extensive typical asbestos-related pleural plaques bilaterally over the diaphragm, in both mid-zones and along the paraspinal recess. He noted dense coronary artery calcification involving both the right and left coronary arteries. He also noted extensive calcification of the aortic valve, left ventricular hypertrophy and dense calcification of the mitral valve annulus. In Dr Jones’ opinion, the CT scan showed no evidence of emphysema or chronic obstructive pulmonary disease and no evidence of any interstitial lung disease, that is, pulmonary fibrosis. (Tribunal note: these opinions and interpretation of CT scans agree with the report of the radiologist who performed the scan.)
In the post-operative phase, the daily chest x-rays and the CT scans performed on 17 July 2009 and 22 July 2009 were, in Dr Jones’ opinion, consistent with cardiogenic pulmonary oedema. Dr Jones concluded that Mr Mier had extensive calcified pleural plaques, confirming exposure to asbestos in the past; that there was no evidence of asbestosis or other lung disease; and that Mr Mier had undergone aortic valve replacement following which persistent heart failure had occurred producing pulmonary oedema and pleural effusions which never resolved radiologically.
Mr Alexander Rosalion
Mr Rosalion is a cardiothoracic surgeon who works in the same hospitals as Mr Lubicz. He had provided locum cover (by telephone) while Mr Lubicz was on leave in June 2009. Mr Rosalion stated that Mr Mier’s care was provided by the intensive care doctors. Mr Rosalion had no specific memory of Mr Mier’s post-operative course or management.
Mr Rosalion had been provided with the reports of Mr Lubicz, Dr Trembath, Dr Jones and Dr Kottek. While noting Mr Mier’s employment at the Williamstown Naval Dockyard for a four-month period, Mr Rosalion did not believe there was any clear evidence of his exposure to asbestos in his subsequent employment as a plumber. Mr Rosalion addressed Mr Mier’s presentation with left ventricular failure secondary to aortic stenosis and his surgical treatment. In his report, Mr Rosalion stated that he had not seen any of the x-rays or CT scans conducted on Mr Mier, nor had he consulted the intensive care notes.
In Mr Rosalion’s opinion, Mr Mier had suffered multiple respiratory complications, pulmonary infections, possible aspiration of gastric contents into his lung and could not be weaned from ventilatory support. Mr Rosalion did not think that in the absence of a lung biopsy, pulmonary asbestosis had been entirely excluded, despite there being no radiological evidence of pulmonary fibrosis.
Mr Rosalion concluded that Mr Mier suffered a significant restrictive lung process due to severe pleural thickening. Based on the information he had been given, he concluded that asbestos exposure while working at the Williamstown Naval Dockyard would have been the major cause of these pleural plaques. Given that he had no knowledge of Mr Meir’s exposure to asbestos other than at the Williamstown Naval Dockyard, Mr Rosalion stated he was unable to comment as to whether other employment had been a contributing factor. He was of the opinion that the pleural plaques resulted in a restriction of pulmonary function contributing to Mr Mier’s post-operative pulmonary complications and his eventual demise.
In a second report dated 8 April 2013, Mr Rosalion confirmed his opinion that Mr Mier had significant exposure to asbestos over a four-month period working at the Williamstown Naval Dockyard. Any further exposure while subsequently working as a plumber would have had an additive effect. Mr Rosalion makes no reference to Mr Mier’s prolonged employment in plumbing and the installation of heating and air‑conditioning prior to his employment at the Naval Dockyard.
At the request of Mrs Mier’s solicitors, Mr Rosalion opined that Mr Mier would have had the maximum 85 per cent of predicted lung function for someone of his age, height and weight; and that after surgery, Mr Mier had 100 per cent impairment as he was completely ventilator dependant.
The applicant had intended to call Mr Rosalion to give evidence before the Tribunal. However, he was unable to attend as he had to undertake a semi-urgent cardiac procedure. Similarly, Dr Michael Jones was unavailable as he was in Canada.
The intensive care physicians’ reports
Following consultation between the Tribunal Member and counsel for both parties (at their request), it was determined that the opinions of two intensive care physicians, Associate Professor Stephen Bernard and Dr Orlando Monteiro, should be obtained. Dr Trembath had recommended such opinions and the Tribunal agreed, given that the intensivists had almost the sole care of Mr Mier post-operatively until his death.
Associate Professor Stephen Bernard
Professor Bernard is the Director of Intensive Care at Knox Private Hospital. His opinion was based on the material supplied to him by the applicant’s solicitor rather than the (complete) original records at Knox Private Hospital. The Tribunal has previously noted the deficiencies in the photocopies of these records. Professor Bernard detailed Mr Mier’s progress in the intensive care unit and in answer to specific questions stated that Mr Mier had extensive pleural plaque formation which on the balance of probabilities, in his opinion compromised Mr Mier’s recovery. He concluded that Mr Mier’s death was the result of acute lung injury, possibly secondary to cardiopulmonary bypass, pulmonary basal atelectasis, pleural effusions and possibly pulmonary infection.
Professor Bernard listed the conditions Mr Mier suffered from following his surgery on 5 June 2009 as:
·Pulmonary atelectesis [sic]
·Acute lung injury (Adult Respiratory Distress Syndrome)
·Pleural effusions
·Ventilator acquired pneumonia
·Acute renal failure
·Neuro-muscular weakness syndrome
·Vocal cord palsy
Professor Bernard considered it was likely that Mr Mier suffered from ARDS after cardiac surgery as a result of cardiopulmonary bypass; with an element of pulmonary oedema being less likely as the pulmonary opacities did not resolve with diuretic therapy. Professor Bernard was asked to comment on the significance of Mr Mier’s pulmonary artery wedge pressure levels post-operatively. He was unable to find any record of these being performed. He did state an echocardiogram of 9 June 2014 showed a normal ejection fraction, which was not consistent with the diagnosis of left ventricular failure.
Dr Orlando Monteiro
Dr Monteiro is a Consultant Intensivist at Knox Private Hospital. He provided an extremely lengthy report. The report was based on the documentary material provided to him by the applicant’s solicitors, rather than the (complete) original records at Knox Private Hospital. In response to the question as to the cause of Mr Mier’s death, Dr Monteiro was of the opinion that his death was caused by severe Respiratory Failure from restrictive lung disease, but contributed to by the complications of aspiration of gastric contents into the lungs, infection, sputum retention and mucus plugging, recurrent pleural effusions and nutritional issues. Mr Mier had also suffered from acute renal failure requiring dialysis, anaemia requiring multiple transfusions, hypernatremia (elevated sodium content of the serum) and mild dehydration as well as polyneuromyopathy of the critically ill.
Dr Monteiro was only able to find one pulmonary artery wedge pressure reading, which he said was measured at 24 mm of mercury. He opined that this elevated reading reflected fluid overload in the presence of renal failure and reduced myocardial contractility. He did note that the echocardiography performed in the early post-operative days revealed normal left ventricular function.
Report of Dr Peter Trembath, dated 8 May 2014 (Exhibit R5)
Dr Trembath was provided with a further copy of the Knox Private Hospital clinical record relating to Mr Mier, given that the original provided to him was incomplete. As a result of his examination of these records, Dr Trembath concluded that the diagnosis leading to Mr Mier’s death could not definitely be determined but the possibilities remained ARDS, pulmonary oedema secondary to heart failure with a further input from aspiration of gastric contents and a neuromyopathy.
Dr Trembath did not believe that the pleural thickening and plaque formation would have reduced lung compliance significantly. Thus, he did not consider that pleural fibrosis and plaque formation was a material factor leading to Mr Mier’s death.
Dr Trembath was later provided with the reports of Associate Professor Bernard and Dr Monteiro, following which he provided a further report dated 16 July 2014 (Exhibit R6). Following consideration of these reports Dr Trembath concluded that:
... it would be appropriate to consider that the contribution of the diffuse pleural plaques affecting the lung surfaces and the diaphragms were of a material significance in compromising the capacity for the deceased to recover from his cardiac surgery.
... I have some difficulty in accepting that in the absence of pleural plaques, and the presence of all those complications, the outcome would not have been different. ... I am obliged, though still with some hesitation, to alter the earlier opinions that I have provided.
FURTHER DOCUMENTARY EVIDENCE
Statement of Claim in the matter of Sheila Ann Mier and Atherton & Sons Pty Ltd and Others – Supreme Court of Victoria
The Tribunal was provided with a copy of this Statement of Claim. Comcare was named the second defendant. In this claim, the injuries suffered by Mr Mier were said to be asbestosis causing death and asbestos related pleural disease. The other particulars were merely a listing of symptoms.
Clinical Records of Knox Private Hospital relating to Mr Brian Mier
Despite all efforts by the parties, and the assistance of the staff of the Tribunal, it would appear that the documentation provided to various expert witnesses and the treating doctors was incomplete. For example, Dr Monteiro was only able to find one pulmonary artery wedge pressure reading while Dr Barnard was unable to find any record of these being performed, whereas the records in the Tribunal’s possession reveal that measurements were recorded for several days in early June 2009 following Mr Mier’s cardiac surgery, and that the levels were abnormally elevated. However, given that the respondent has conceded that the pleural plaque formation, probably due to past asbestos exposure, has contributed to or resulted in Mr Mier’s death, these shortcomings in terms of the evidence are not significant.
RELEVANT LEGISLATION
Section 5 of the Safety, Rehabilitation and Compensation Act 1988 (the Act) provides definition of an injury and a disease. Section 5A defines an injury as:
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 a physical or mental injury (other than a disease) suffered by an employee (whether or not that injury arose out of, or in the course of, the employee’s employment), that is an aggravation that arose out of, or in the course of, that employment;
but does not include a disease, injury or aggravation suffered as a result of reasonable administrative action taken in a reasonable manner in respect of the employee’s employment.
and the definition of a disease in s 5B as:
5B Definition of disease
(1)In this Act:
disease means:
(a)an ailment suffered by an employee; or
(b)an aggravation of such an ailment;
that was contributed to, to a significant degree, by the employee’s employment by the Commonwealth 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;
...
(d)any activities of the employee not related to the employment;
(e)any other matters affecting the employee’s health.
This subsection does not limit the matters that may be taken into account.
(2)In this Act:
significant degree means a degree that is substantially more than material.
Compensation for such injuries is provided by s 14 which states:
14 Compensation for injuries
(1)Subject to this Part, Comcare is liable to pay compensation in accordance with this Act in respect of an injury suffered by an employee if the injury results in death, incapacity for work, or impairment.
...
Section 17 of the Act deals with compensation for injuries resulting in death and provides:
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.
SUBMISSIONS
In his opening address to the Tribunal on 18 November 2013, Mr Carey informed the Tribunal that Mrs Mier was making no claim in relation to her late husband having suffered from asbestosis. Despite the content of the Death Certificate, there was no evidence Mr Mier had asbestosis and throughout the proceedings, which commenced in 2010, this term had been misused. The condition claimed to be work related was that of calcified pleural plaques which the applicant contended resulted from asbestos exposure.
At the commencement of the resumed hearing on 21 August 2014, Mr Wallace informed the Tribunal that the respondent conceded that Mr Mier’s documented pleural plaque formation had contributed to his death, or in the terms of the Act, his death had resulted from pleural plaque formation.
Mr Carey identified the major issue as whether Mr Mier’s employment with the Department of Defence was a relevant contribution to Mr Mier’s pleural plaque formation. The applicant relied on the evidence of Mr Kisler, Mr Kottek and, in particular, of Mrs Mier. In her statement, Mrs Mier stated that her late husband had told her that he was involved in lagging work in the holds of ships and that he would eat his lunch sitting on bags of asbestos fibre. Mr Carey contended that Mrs Mier’s identification of pieces of string on her late husband’s overalls indicated a high probability that this string was part of asbestos cloth.
Mr Carey contended that Mrs Mier’s evidence was supported by that of Mr Kisler, who as a member of the Australian Navy had worked at the dockyards from 1953 until 1988. He had given evidence of the dusty atmosphere in the workshop when plumbers cleaned the pipes. Mr Kisler had also identified the structure of what was called cotton scrim, cloth containing asbestos, which could be correlated with Mrs Mier’s evidence of the string on her husband’s overalls.
Mr Kottek estimated Mr Mier’s exposure to be in the high range. He supported the applicant’s contention that Mr Mier’s four months at the Williamstown Dockyard was a significant exposure to asbestos, leading to a significant contribution to the development of pleural plaques.
Mr Carey submitted that there was no evidence of likely exposure to asbestos in Mr Mier’s employment as a plumber for 15 years, before he worked at and after he had left the Naval Dockyard.
Mr Wallace identified two issues:
(i)whether Mr Mier’s employment at the Williamstown Dockyard by the Department of Defence led to asbestos exposure which significantly contributed to the development of pleural plaques; and
(ii)had the applicant fulfilled the requirement regarding the standard of proof necessary to satisfy s 5B of the Act, that being the usual civil standard enunciated in Briginshaw v Briginshaw (1938) 60 CLR 336 and referred to as a requirement of reasonable satisfaction or a balance of probability test to be met in order to support a claim for compensation before a court or tribunal.
Mr Wallace contended that the required standard of the Tribunal’s reasonable satisfaction or on the balance of probabilities could not be satisfied when there was a lack of evidence, such as existed in Mrs Mier’s claim.
Mr Wallace contended that Mrs Mier’s two statements were unreliable. Her second statement included information not provided in the initial statement regarding Mr Mier working in the ships hold and performing lagging. He submitted that this change in content suggested recent invention with respect to the description of Mr Mier’s work.
The respondent relied on Mr Kisler’s evidence, that while there were high levels of dust on board ships in the Dockyard, plumbers were not involved in the lagging. This was done by external contractors at night; and the plumbers only removed the pipes they had to work on up to 48 hours after de-lagging had been completed. Mr Kisler had given evidence that the external contractor, Bells Asbestos, performed the lagging at night and left by 7.20 am, bringing with them the bags of asbestos which were removed when they left.
Mr Wallace pointed out that Mr Kisler could not quantify what exposure Mr Mier was likely to have experienced, as he did not know Mr Mier’s duties other than the fact that like all plumbers, Mr Mier’s work was performed in the workshop. Mr Kisler had described the strict demarcation of duties that existed at the dockyards at that time following industrial action in 1955.
Cleaning up of all sites was performed by members of the Painters’ and Dockers’ Union and continued throughout the day. Mr Kisler’s evidence had also been that it was during the strike in 1955 that apprentices entertained themselves by throwing balls of asbestos fibre at each other. There was no evidence that this had occurred at any other time.
As Mr Kisler had raised the possibility that in October 1962 and in the months thereafter Mr Mier was actually working on the construction of a new ship, HMAS Derwent, which would involve minimal if any exposure to asbestos, Mr Wallace raised the contention that Mr Mier may not have been exposed to any significant quantities of asbestos. In reality his exposure was unknown.
Mr Wallace submitted that Mr Kottek had conceded that he did not know what Mr Mier’s duties involved; and that his estimation of the likely exposure was only a possibility, given this lack of knowledge. Mr Kottek had been aware that asbestos was present on every site that Fluor Utah, a petrochemical construction company, was involved in. In relation to Mr Kottek’s evidence, Mr Wallace referred to the general comments of the High Court in Amaca Pty Ltd v Ellis as to evidentiary limits of epidemiological data and their Honours reference to the trial judge’s finding that the estimates of asbestos exposure (as provided by Mr Kottek in this case) were rather superficial and approximate.
Mr Wallace contended that the decision should be affirmed as the applicant had not made out a case as to the cause of Mr Mier’s pleural plaques. He submitted that some of the expert evidence, in particular that of Mr Rosalion, should be ignored as Mr Rosalion was unaware of, or did not consider, the late Mr Mier’s potential asbestos exposure throughout his employment over 15 years as a plumber. Mr Rosalion had confined himself to only considering Mr Mier’s employment at the Williamstown Dockyard.
TRIBUNAL’S DELIBERATIONS
Mrs Mier’s claim for compensation lodged on 25 June 2010 was based on Mr Mier’s death on 12 September 2009 due to pulmonary asbestosis. The claim was disallowed on the basis that there was no evidence before the Comcare delegate that Mr Mier was exposed to asbestos during the course of his four-month employment at the Naval Dockyard. The Department of Defence had been unable to identify Mr Mier’s duties during this term of employment which might have exposed him to asbestos. The Department did confirm Mr Mier’s employment as being from 4 October 1962 to 5 February 1963.
For the three years following the lodgement of this claim, the basis of the claim has been that Mr Mier died as a result of asbestosis. On the first day of the Tribunal hearing the basis of the claim altered. Mr Mier’s treating surgeon, Mr Lubicz, who had repeatedly used the term asbestosis in correspondence with medical practitioners, operative surgical reports and his initial correspondence with the applicant’s instructing solicitors, Maurice Blackburn, gave evidence that there was no medical evidence to support a diagnosis of asbestosis. He stated that while he did not know the cause of Mr Mier’s calcified pleural plaques, they could be due to occupational exposure to asbestos.
The respondent’s expert medical witnesses Dr M Jones and Dr P Trembath had opined that there was no evidence of asbestosis, only calcified pleural plaque formation.
The Tribunal is aware that the medical profession, despite being taught otherwise, continues to misuse the term asbestosis. Asbestosis is pulmonary fibrosis caused by inhaled asbestos fibres. This definition has been provided in Harrison’s Principles of Internal Medicine from the 4th Edition in 1962 to the current 18th Edition. The fibrosis (scaring) occurs in the loose connective tissue (termed interstitium), between the alveoli (air sacs), thereby affecting the exchange of oxygen and carbon-dioxide between the alveoli and the bloodstream. Asbestosis is one of many fibrotic processes referred to as interstitial pulmonary disease.
It is agreed by the parties, and accepted by the Tribunal, that Mr Mier had bilateral calcified pleural plaques which may have been secondary to inhalation of asbestos fibres. The medical literature to which the Tribunal referred during the hearing, considers numerous causes of such fibrosis, and this was referred to by Dr Jones and Dr Trembath. Inhalation of asbestos fibres is a known cause of both pleural plaques and diffuse pleural fibrosis. Diffuse pleural fibrosis affects both the visceral and the parietal layers of the pleura. It is frequently associated with asbestosis but may, of itself, give rise to a restrictive pulmonary defect. Discrete plaques, as in Mr Mier’s case, are said to reduce lung volumes but not to statistically significant degree (The Third Wave of Asbestos Disease. Annals of the New York Academy of Sciences, Volume 643, December 31st 1991).
Current medical literature describes discrete pleural plaques, calcified or not, as being an indicator of past asbestos exposure, not pulmonary impairment of any clinical significance (Harrison’s Principles of Internal Medicine, 18th Edition).
Given the above state of medical knowledge, the Tribunal was surprised by the respondent’s concession that Mr Mier’s death was contributed to or resulted from radiologically demonstrated calcified pleural plaques. However, the Tribunal accepts the concession.
The medical condition of calcified pleural plaques is an ailment attracting s 5B definition of disease. Thus, the requirement that the employee’s employment by the Commonwealth or a licensee contributed to a significant degree must be satisfied.
Mr Lubicz stated that he does not know the cause of Mr Mier’s pleural plaques. Others postulated that they were due to or contributed to by Commonwealth employment in the form of exposure to asbestos.
However, no definitive evidence has been produced regarding Mr Mier’s work duties during the four months of his employment by the Commonwealth, let alone whether there was any exposure to asbestos. Mr Kisler’s evidence is likely to be the most reliable, as he was present at the Williamstown Dockyard at the time of Mr Mier’s employment. Mr Kisler’s evidence is inconsistent with the evidence of Mrs Mier (who had stated that her late husband was involved in the application of lagging to pipes performed in the holds of the ships and that he ate his lunch while sitting on bags of asbestos). Mr Kisler provided evidence that there was a strict demarcation of duties of the various union members at the time. Plumbers repairing pipes did so in the workshop, not in holds of ships; all lagging was done by outside contractors (namely Bells Asbestos) and took place at night; and that bags of asbestos provided by Bells arrived on the wharf at night and were removed by 7.20 am the following morning. On Mr Kisler’s evidence, new ship building did not involve any high risk of exposure to asbestos.
The Tribunal is not reasonably satisfied on the evidence before it that the requirement of s 5B (as to a significant contribution) is met. The information provided to the Tribunal is that Mr Mier had a 14 to 15 year possible but undocumented exposure to asbestos in the course of his work as a plumber. There were periods of employment, other than when he was at the Naval Dockyard, where it was possible that he was exposed to excessive amounts of asbestos.
It has been scientifically shown that there is a dose response relationship between asbestos fibre exposure and inhalation and pleural plaque formation. As such, a potential but unproven period of four months exposure to asbestos in a total of 14 years potential exposure to asbestos cannot be considered a significant contribution.
The Tribunal affirms the decision under review.
I certify that the preceding 105 (one hundred and five) paragraphs are a true copy of the reasons for the decision herein of Miss E A Shanahan, Member .......................[sgd].................................................
Associate
Dated 5 September 2014
Date(s) of hearing 18 & 21 November 2013 and 21 August 2014 Counsel for the Applicant Mr M Carey Advocate for the Applicant Ms C Bolger Solicitors for the Applicant Maurice Blackburn Counsel for the Respondent Mr J Wallace Advocate for the Respondent Mr D Decleva Solicitors for the Respondent Sparke Helmore APPENDIX
EXHIBITS
APPLICANT
A1 Statement of Mrs Mier dated 26 September 2012
A2 Unsigned but adopted statement headed “Further Statement of the Applicant”
A3 Statement of Mr Michael Kottek dated 23 November 2010
A4 List 2 of insulation materials used by the DOD “the redundancy list” dated June 1976
A5 Mr Rosalion’s report dated 10 February 2013
A6 Dr Rosalion’s supplementary report dated 8 April 2013
A7 Mr Lee Kisler’s unsigned statement adopted 21 November 2013
A8 Medical report of Professor Bernard dated 6 April 2014
A9 Medical report of Dr Orlando Monteiro dated 12 June 2014
RESPONDENT
R1 T-Documents
R2 Report of Dr P Trembath, respiratory physician, dated 26 May 2011
R3 Knox Private Hospital medical reports for Brian Mier
R4 Report of Dr Michael Jones dated 10 June 2011
R5 Medical report of Dr P Trembath dated 8 May 2014
R6 Medical Report from Dr P Trembath dated 16 July 2014
R7 Supreme Court Writ – Statement of Claim dated 8 December 2010
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