Geyer v RESI Corporation - [2013] SADC 122

DISTRICT COURT OF SOUTH AUSTRALIA
(Civil)
GEYER v RESI CORPORATION
[2013] SADC 122
Judgment of His Honour Judge Jennings
30 August 2013
TORTS - NEGLIGENCE
ASBESTOS - DUTY OF CARE - ASSESSMENT OF DAMAGES
The plaintiff was employed by the defendant from 14/7/57 to 14/9/98 as a boilermaker/welder, leading hand boilermaker, assistant foreman and mechanical foreman at its Playford Power Stations. The defendant conceded that if there is a finding that the plaintiff has mesothelioma it was caused by his employment at the Playford Power Stations. The issue before the Court is whether the plaintiff has mesothelioma. Ruling made pursuant to section 45A of the Evidence Act 1929 (SA) re admissibility of documents.
Held: The plaintiff had extensive exposure to asbestos over a long period. It is more probable than not that the plaintiff has mesothelioma. Assessment of damages: General Damages $175,000; Loss of life expectancy $65,000; Griffiths v Kerkemeyer $50,000; Exemplary damages $20,000; Interest $2,000; making a total of $327,474.
Dust Diseases Act 2005 (SA) s 9(2); Evidence Act 1929 (SA) s 45A, referred to.
Davie v The Lord Provost, Magistrates and Councillors of the City of Edinburgh (1953) SC 34; Geste v Pereira [1991] SASC 3018; Hillier and Carney v Lucas [2000] SASC 331; Amaba Pty Ltd v Booth [2010] NSWCA 344; Dingley v The Chief Constable, Strathclyde Police (1998) SC 548; Sienkiewicz v Greif (UK) Ltd; Knowsley Metropolitan Borough Council v Willmore [2011] UKSC 10; BHP Billiton v Hamilton and Another [2013] SASFC 75; BHP Billiton Limited v Parker (2012) 113 SASR 306; Van Soest v BHP Billiton (No 2) [2013] SADC 95; Southern Equities Corporation Ltd (in liq) and Others v Bond and Others (No 2) [2001] SASC 70; Ryan and Others v ETSA and Others (No 2) (1987) 47 SASR 239; Carr v Baker (1936) 36 SR (NSW) 301; Jones v Dunkel (1959) 101 CLR 298, considered.

GEYER v RESI CORPORATION
[2013] SADC 122
Introduction

This is a claim for damages for personal injury.
The plaintiff was born on 21 August 1928.
Between about 14 July 1957 and 14 September 1988 he was employed by the Electricity Trust of South Australia (ETSA) (the liabilities of ETSA have been assigned to RESI Corporation) (the defendant) as a boilermaker/welder, leading hand boilermaker, assistant foreman and mechanical foreman at its Playford Power Stations. During this employment up until September 1986 he asserts that he was exposed to asbestos dust and fibre whilst installing, mixing, removing and generally handling insulation materials containing asbestos and while working in and about area contaminated by asbestos dust and fibre. He also asserts that he was required to work in the vicinity of others installing, removing and generally working with insulation materials containing asbestos.
As a consequence thereof he asserts that he was exposed to and inhaled asbestos dust and fibre and that he has contracted asbestos related conditions including pleural effusion, asbestos related pleural plaques with calcification, pleural thickening, asbestosis and pleural malignant mesothelioma. He claims that as a result thereof he has suffered injury, loss and damage.
Part of the defendant’s defence was, that whilst it admitted that the plaintiff has pleural plaques, it claimed that they are symptomless and do not cause the plaintiff to suffer any impairment or disability. It denied that pleural plaques were caused as a consequence of exposure to asbestos whilst the plaintiff was employed by it. It asserted that the plaintiff suffers from mycobacterium avium intracellulare complex (MAC), arthritis, hearing loss, knee and shoulder surgeries, peripheral vascular disease, polymyalgia rheumatica, hyperlipidaemia, hypertension, gord, rheumatic heart disease, bronchiolitis, hypercholesterolaemian, coronary artery calcification, palpatations, and chest pain and a malignant tumour and that any of the physical disabilities that he might suffer from could be attributable to these conditions.
The issues initially before the Court included whether any asbestos caused dust disease or diseases resulted from the plaintiff’s exposure to asbestos whilst employed by ETSA.
Following the completion of the plaintiff’s evidence and the evidence of Ms Mareeta Dolling (an Occupational Therapist) and the plaintiff’s daughter Ms Patricia Footner, and prior to the calling of the plaintiff’s medical expert witnesses, the plaintiff’s lawyers Turner Freeman, served on the defendant’s solicitors a further report of Professor Henderson dated 2 May 2012 on the issue of causation. An application by the defendant that the plaintiff not be allowed to rely on that report was resolved by consent:
The resolution is on the basis that the plaintiff is not seeking to rely on the report of Professor Henderson of 2 May 2012. If there is a finding that the plaintiff has mesothelioma the defendant will concede that it was caused by his employment at Playford Power Station.
The issues before the Court are now limited to the diagnosis of the plaintiff’s condition, ie whether or not he has mesothelioma, as well as the quantum of damages and exemplary damages. Mesothelioma is the most common and most frequently referenced primary pleural neoplasm.
The Evidence
The Plaintiff’s Case
The plaintiff’s evidence as to his exposure to asbestos
The plaintiff’s evidence was that prior to his commencing work with ETSA at the Playford A Station he had not been exposed to asbestos in any of the following: the family home in Mildura; in his prior employment for eight years with the First Mildura Irrigation Trust; during the period when he was self-employed; or in his employment with the North Broken Hill Company.
He commenced working with ETSA in 1958 initially as a boilermaker/welder in the Playford A Power Station in Port Augusta.
In 1959 he was promoted to be a leading hand boilermaker. In that role he supervised other people who worked in the boiler shop. When he started his employment the last of six boilers were still being completed. He was later promoted to the position of assistant mechanical foreman which involved work in both the boiler shop and the coal conveyor system. He was promoted to mechanical foreman in 1963. Shortly prior to his retirement he was promoted to the position of acting mechanical workshops engineer. When he was promoted from time to time he continued to work in the boiler shop.
In his first role at ETSA (in Playford A Station) which he occupied for nearly two years he spent eight hours a day at the station on boiler repairs and some manufacturing of steel works. Some of that time when he was working in the boiler room he was in the vicinity of other people who were cutting insulation material. This work created a “light bluish” dust. The dust landed and was visible on his overalls which were dusty at the end of the day. He worked on various metal items that were brought into the workshop for repair work. He had a trades assistant who would brush those items and clean them. He would sometimes be standing next to, or within three to four yards, of the tradesperson. He saw dust going up into the air. He breathed it in.
Underneath the boiler walls were asbestos blocks. Bradford Insulation installed, cut and removed the asbestos blocks so that other workers could work on the tubes below. Bradford Insulation employees were working whilst the plaintiff and others were in the same area. The workers from Bradfords stood on the same platform (which was about 1½ metres wide) with the plaintiff and worked in the same proximity. The plaintiff spent 2 out of every 8 hours of his work on boilers in the vicinity of other people cutting insulation.
His trades assistants cleaned the boiler shop every morning. Because dust was created with the sweeping he got them to put wet sawdust over the floor before they started sweeping. They also cleaned benches, all of the welding machines and the tool boxes, once a month “to reduce the dust” which he thought was residue from the walls. The workers described this as “He’s having a blue moon trip and he’s going to clean the place up”. Bradford Insulation would come in on a few occasions to vacuum some of the areas.
When he was welding he had two sets of gloves, one set was leather and the second type he understood to be made of asbestos. The gloves were dusty. That dust also went up into the air.
ETSA used “blankets” for heat protection. They were 25-30 millimetres in thickness. They came from the stores department. He understood that they were “asbestos blankets”. He noticed light dust in connection with the blankets, some of which fell on the floor. Quite often the blankets were damaged or “holed”. When the trades assistants cleaned the blankets they would shake them and “there’d be dust on the floor”. The blankets were also used in the power station on gratings to protect people working below. Dust was created by them.
He understood that in 1967 as part of a soundproofing exercise, asbestos was sprayed on the full length of both sides of the walls of the boiler shop and on the northern end of it. He was not present when these walls were sprayed. He said that its appearance was “a grey matted material” when it was sprayed on. Once it was installed it was “quite flimsy” and if it was damaged “it would flake off”. Dust was created when the walls were installed. Whilst he was not present when the walls were sprayed he inspected them on a daily basis thereafter to ascertain if there was any damage.
Every now and again the walls were damaged and when this occurred it was reported immediately to him. This created dust. He was present on occasions when that happened. When the walls were damaged he would arrange for Bradford Insulation to fix them. When effecting the repairs Bradford personnel would pour a dry substance or material out of a bag onto a drum and mix it with water. That exercise created a certain amount of dust which he breathed in. He does not recall any “caution” signs being put up when Bradford Insulation removed the insulation. The same substance that was sprayed on the walls was sprayed underneath the benches to reduce noise. When the trade assistants swept up every day they also swept underneath the benches. That created dust.
At some date in late 1979 an acrylic paint was sprayed over the top of the asbestos walls. For 12 years from the insulation of the sprayed asbestos wall up until 1979 the plaintiff worked in the boiler shop. After the wall was painted and when it was damaged a certain amount of dust, depending on the extent of the damage, was created. When a wall was damaged they attached wire mesh to the wall with studs. The asbestos wall was removed in about October 1987 about a year before he retired.
When the machinery was repaired in Playford B Station, dust was created by the welders “brushing off the area that had to be welded”. He was beside the welders “most times” while they undertook the brushing exercise.
Part of his duties included crawling through a manhole to get into the drums in the boiler. There was what he understood to be an asbestos rope attached to the drum to seal it. Inside the manhole was a tight fit and whilst inside he would rub against the sides of the manhole. When he emerged he had dust on his overalls.
At some stage an air conditioning system was put into the boiler shop. They were special industrial air conditioners. The purpose was to provide heating and cooling and to dissipate fumes and dust out of the boiler shop. The dust went out through the doors and the windows. There was no extraction system.
The only time he used a mask or protector for his mouth was when the walls were being sprayed. So for some 12 years when he was working in the boiler room, masks were not used and ETSA did not require their use. No warnings were given by ETSA about the dangers of asbestos.
I will deal with the balance of the plaintiff’s evidence later in these reasons for decision.
Ms Patricia Footner is one of three children of the plaintiff. She grew up in the family home in Port Augusta and left there in 1981.
Her evidence was that the plaintiff came to Adelaide from time to time for doctors’ appointments and hospital admissions. The first hospital admission was at the Queen Elizabeth Hospital for drainage of fluid from his right lung between 23 and 30 April 2010. She said he was very unwell, grey, sweaty and quite exhausted.
When he was released from hospital he stayed at her place for about ten days. He was very tired, in some pain and slept most of the day for the first few days. He spent the first couple of days in bed mostly and she kept an eye on him pretty well all day, going in and out of the room during the course of the whole day, making sure he was okay. He was unable to shower himself. Her husband helped him dress for the first couple of days after he showered. The showering took about half an hour by the time her husband undressed him. Then there were meals that she provided, not that he ate that much for the first couple of days. She did not leave the house and leave him on his own for the first few days.
After the plaintiff’s wife died on 25 October 2002, Mrs Footner and her sister started to provide some assistance to their father with meals and cooking. They would put meals in containers and put them in the freezer for when the plaintiff came down for his appointments. She would make up pots of soup so that there would be food for him in the house when he was not well. She said that since the plaintiff had become unwell in recent years with his chest problems, she and her sister continued to send the meals back with him. This has increased since the earlier days because he was coming down more often.
She was aware that since her mother’s death the plaintiff had someone come and do the heavy cleaning in the house.
She said she goes to Port Augusta on occasions, the last time being when the plaintiff had an assessment with the occupational therapist around March 2012. She was aware that the plaintiff did his own washing and ironing.
She telephones the plaintiff on average once a week. Since he was diagnosed with the health problems, and more so in the latter years, he has sounded like he was emotionally upset and in tears.
She was aware that the plaintiff saw Professor Ruffin some years before his diagnosis of asbestosis. The plaintiff was flat, depressed and upset from time to time even before the diagnosis.
Ms Mareeta Dolling has been an Occupational Therapist since graduating in 1982. She has been undertaking medico-legal assessments of clients with personal injury including mesothelioma since 2007.
Ms Dolling provided a written medico-legal assessment report dated 1 December 2011 after she saw the plaintiff in his home in Port August on 21 November 2011. In preparing the report she had been asked to assume that the plaintiff had the disease of mesothelioma and she was asked to make an assumption about his life expectancy and in that regard, to assume the life expectancy put forward by Professor Ruffin in his report.
Attached to Ms Dolling’s report was an appendix which set out the care dollar rates for South Australian country regions. In August 2011 inquiries were made and three agencies supplied a range of services in Port Augusta. She rang the agencies and confirmed that they each provided services in Port August and they confirmed that they supplied a range of services for domestic assistance and health professional care.
Her evidence was that since 2007 she has seen about 30 patients with mesothelioma and in each case has followed the formula she did in the plaintiff’s case which is to firstly go out to the patient’s home. She said that an average visit to a mesothelioma patient’s home was three to four hours. As part of the visit she looks at the patient’s home and the physical layout and any changes that are needed. She spends a lot of time talking to the patient and also the family members who may be present. One of the topics she speaks about is what care they have been receiving up to that point.
Ms Dolling has visited people who were in the early, the intermediate stage and at the very end stage of the disease who are close to death.
Her report contained estimates of care based upon what are described as stages one, two, three and four. A colleague of Ms Dolling, a Ms Anne Morgan who is also an occupational therapist and who has had extensive experience in this area, was responsible for the description of the various stages.
Ms Dolling said the part of the report that was prepared by Ms Morgan was the agencies’ costs set out in the appendix. The last two pages of her report were prepared by Ms Morgan. The tables of care were also prepared by Ms Morgan. The template of the stages was produced by Ms Morgan but all of the details for each client were completed by Ms Dolling.
She spent three hours interviewing the plaintiff for an assessment. She based the plaintiff’s life expectancy on what she had read in the report of Professor Ruffin.
She did not know whether all the people she had seen suffering from mesothelioma had always been suffering from pleural mesothelioma.
Generally speaking she understood that pleural mesothelioma was a tumour growing in the pleural cavity.
She had a sense from reading the reports that in this case there was a dispute about whether the tumour mesothelioma which she had been asked to assume in this case was not your typical diffuse pleural mesothelioma, but rather a localised mesothelioma.
She was asked whether she was suggesting that in one of the reports that she had read in preparation for her report there was mention of the type of mesothelioma the plaintiff was suffering from, that is that he was suffering from not the normal diffuse pleural mesothelioma but localised mesothelioma: she could not recall. She guessed that it would be important for her to know that. She said it was possible that someone who was suffering from a localised pleural mesothelioma as opposed to a diffuse pleural mesothelioma might suffer from different symptoms. She said she did not have the medical information to comment on whether their prognosis in terms of the progress of the disease was different.
Ms Dolling prepared her report on the basis that the plaintiff had mesothelioma that she had dealt with on previous occasions. She said that she did not have all the medical information or knowledge as to how a localised mesothelioma might give rise to different prognosis in terms of symptomology, treatment and life expectancy.
Ms Dolling documented the observations and the conversation that she had with the plaintiff in November 2011 and that in the report on her conclusions she said that because of his medical conditions, other medical conditions, she had to make the assumption that any changes were as a result of mesothelioma and that would need medical comment because of the other presentations.
For the purposes of her report she attributed all of his symptoms from March or April 2010 to the mesothelioma and she attributed all of his symptoms to mesothelioma in terms of calculating what care he had required and what care he would require in the future.
She was asked to do this assessment based on that he had mesothelioma and that is what she based the future care on.
She said the progress of the disease was unpredictable.
Medical Experts
All of the medical experts who appeared in this case were highly credentialed and very experienced in their respective areas of expertise. All provided extensive CVs which are annexed to or form part of their reports, and whilst I have had regard to the content of same as well as to the extensive material which formed attachments to the reports, I do not propose setting all of them out in these reasons for decision, nor do I propose setting out all of the various reports and medical materials referred to in those reports, nor all of the qualifications or positions held by those witnesses.

Most of the medical experts prepared more than one and some prepared multiple reports for the purposes of these proceedings.
To do justice to this matter, I propose to set out in some detail the content of the various medical reports and to interpose therein elaboration of various aspects of the reports elucidated from the witnesses’ oral evidence.
The Plaintiff’s Medical Experts
Professor Douglas Henderson is a Professor of Anatomical Pathology and was in receipt of a number of letters of instruction from the solicitors acting for the plaintiff.
A letter from Turner Freeman dated 22 November 2011 requested a report from Professor Henderson to address the following issues:
·An opinion ‘on the balance of probabilities’ as to whether or not the plaintiff suffers from mesothelioma.
·An opinion ‘on the balance of probabilities’ as to whether or not the plaintiff suffers from any other asbestos-related condition.
·An opinion/comments in relation to the report from Dr Andrew Gal dated 16 November 2011.
Professor Henderson’s report dated 20 December 2011 contains the following consultation report for the pleural core biopsy taken from the plaintiff.
Report text
CLINICAL SUMMARY
83 year old man with a past history of asbestos exposure (previous occupation included boiler making). He reportedly has asbestos-related pleural disease and this year developed what appears to be a right sided pleura-based mass. It appears to be a broad-based lesion on the parietal pleural aspect of the chest cavity.
I was asked to attend a fine needle aspirate of this mass (our lab ref: 11-851801) and it was during this procedure that I requested a core biopsy be obtained. My initial thought was that this was either biphasic malignant mesothelioma or epithelioid haemangioendothelioma. My immunopanel so far has been directed towards these possibilities with other thoughts being metastatic carcinoma, solitary fibrous tumour and synovial sarcoma … John Miliauskas and John Cooper have kindly reviewed aspects of this case and thus far we have not been able to reach a definite diagnosis. My feeling is that this is probably malignant mesothelioma but I am not sure if I can entirely exclude a vascular tumour although my understanding is that epithelioid haemangioendothelioma should only show patchy cytokeratin reactivity and there is only very little CD31 reaction in this case.
…
MICROSCOPIC
Dr Yung Tran
Department of Surgical Pathology
SA Pathology
The Queen Elizabeth Hospital
Woodville Road
WOODVILLE SA 5011
Fax: 8222 6425
Dear Yung
Thank you very much for sending the pleural core biopsy material for this very difficult and challenging case in terms of diagnosis. I think that the diagnostic problems are in part related to the small amount of tissue represented in the core biopsies (and in this context I have long had serious reservations about the usefulness of fine-needle cytology material from pleural mass lesions for which mesothelioma and other unusual pleural tumours enter into the differential diagnosis).
However, after looking at the sections and carrying out some additional immunohistochemical studies, I think that this is best regarded as a pleural malignant mesothelioma of biphasic type, but with some very unusual histological appearances. In this regard, I have mainly reached a favoured diagnosis of mesothelioma by a process of exclusion – on the basis of the Sherlock Holmesian principle that when all other possibilities have been excluded, what remains, no matter how implausible, is the truth.
In the sections, the appearances are those of a rather bland-appearing yet malignant biphasic tumour with both epithelioid and sarcomatoid components. The epithelioid cells are disposed mainly as small sheets and nets, whereas the sarcomatoid component comprises areas of collagen-rich tissue and some more cellular areas where there is a whirling or targetoid distribution of the tumour cells around blood vessels (a pattern that I cannot remember having seen before in malignant mesothelioma).
Therefore, I have considered a variety of alternative diagnoses, including synovial sarcoma (yet it is unlike any pleuropulmonary synovial sarcomas that I have seen), or even a malignant peripheral nerve sheath cell tumour (MPNST) arising from an intercostal nerve. (I think that an MPNST can be excluded taking into account the apparent pleura-based localisation of the tumour, and the fact that our S100 preparation is entirely negative.)
Your immunohistochemical studies reveal some patchy positive labelling for pan-cytokeratins (AE1/AE3) localised to the sarcomatoid component rather than the epithelioid, and there is some CK8 [CK8/18] positively affecting both components. At most, there is only focal equivocal labelling for calretinin, and the pattern of labelling in the WT1 preparation is non-specific. The CD34 stain demonstrates labelling of blood vessels only.
As mentioned, we have carried out some additional immunohistochemical studies. There is focal weak positivity for CK8/18 (CAM5.2) in the epithelial and sarcomatoid tissue. Our calretinin preparation is negative. There is some minimal focal labelling of the epithelioid component with D2-40 and there is also positive [labelling] of both components for EMA. Our CD99 preparation is positive, but the lesion clearly is not a malignant solitary fibrous tumour of the pleura. The desmin preparation is negative.
Therefore, I think that the histological appearances and immunohistochemical findings essentially exclude an MPNST and an epithelioid haemangioendothelioma, and the histological appearances are not characteristic of a synovial sarcoma. (Having stated this, molecular studies for the T (X;18) translocation are underway and if they show anything, I shall send a supplementary report.)
I have shown the slides to Phil Allen and the whirling perivascular pattern and overall appearances do not correspond to any readily identifiable sarcoma or biphasic tumour of soft tissues that he can think of. Like myself, he gravitated towards a diagnosis of pleural malignant mesothelioma, largely by a process of exclusion.
Any follow-up information that becomes available on this case would be very greatly appreciated.
OPINION
Core biopsy of pleura-based mass lesion: Malignant biphasic neoplasm, with appearances not characteristic of mesothelioma, but a pleural malignant mesothelioma is my favoured diagnosis for the reasons discussed above and by a process of exclusion of alternative diagnoses and also taking into account the fact that the lesion appears to be pleura-based.
He divided the various documentation/reports provided to him into three broad groups: (i) clinical-medicolegal reports; (ii) radiology-imaging reports and (iii) Dr Gal’s report dated 16 November 2011.
Those documents and reports included:
Group 1: Clinical Medicolegal Reports:
Reports of Professor Richard Ruffin dated 21 November 2008, 17 September 2009, 19 January 2010 and 14 April 2011; reports of Dr Ral Antic dated 1 April 2009, 4 August 2009 and 6 December 2011; clinical correspondence from Dr Craig Jurisevic addressed to Professor Ruffin dated 14 October 2011; and medical record for the plaintiff from The Queen Elizabeth Hospital. Appended to this medical record was a copy of a clinical-medicolegal report on the plaintiff from Professor Ruffin dated 12 April 2011.
Group 2: Radiology-Imaging Reports
Chest x-ray on the plaintiff dated 12 April 1997; report from Perrett Medical Imaging (PMI) for a chest x-ray dated 24 October 2005; report from PMI for a chest x-ray dated 18 February 2008; report from PMI for a CT scan of the chest dated 4 March 2008; report from Dr Jones & Partners/PMI for a chest x-ray dated 29 September 2009; report from Dr Jones & Partners/PMI for a CT scan of the chest dated 21 October 2009; report for a CT scan from the Carlton Medical Centre in Port Augusta dated 29 September 2009; report for a chest x-ray from the CMC in Port Augusta dated 22 April 2010; radiology report for a CT scan of the chest from The Queen Elizabeth Hospital dated 29 April 2010; report from Dr Jones & Partners/PMI for a chest x-ray dated 28 July 2010; report from Radiology at Calvary Hospital for an HRCT scan of the chest dated 28 July 2010; radiology-medicolegal reports from Dr Richard Slaughter at the Prince Charles Hospital in Brisbane dated 13 October 2009 and 8 January 2010; radiology-medicolegal reports from Dr Michael Jones dated 9 September 2009 and 7 March 2010; and radiology report from The Queen Elizabeth Hospital for a CT scan dated 8/9 December 2011.
Group 3: Pathology-Medicolegal Report from Dr Andrew Gal
Pathology/medicolegal report from Dr Gal dated 16 November 2011.
Professor Henderson said in the context of those reports and Dr Gal’s report that he found this case to be very difficult and challenging largely due to the very small amount of tumour tissue sampled by the core biopsy. However he considered a pleural malignant mesothelioma to be the most likely diagnosis (ie more likely than any of the alternative diagnoses he considered).
In his oral evidence he said that pleural mesothelioma is not a diagnosis that one comes to lightly and that it is a diagnosis that can be in some cases fairly straightforward but in others, difficult.
He then undertook a discussion of his consultation report and that of Dr Gal’s.
He concluded this report by saying:
I do not resile from the discussion and opinion on diagnosis as set forth in my consultation report for the core biopsy taken from Mr Geyer’s right pleura (SA Pathology Surgical Pathology at Flinders Medical Centre accession number 11/S10956). Despite the diagnostic problems associated with this case and for the reasons discussed in that report and in this present report, pleural malignant mesothelioma remains my favoured diagnosis (ie malignant mesothelioma of the pleura ‘more likely than not’). In relation to the whorling-targetoid appearance of the tumour cells around blood vessels, I indicate that fortuitously I have seen a more recent case of undoubted pleural malignant mesothelioma that showed a similar whorling-targetoid pattern.
Professor Henderson provided a supplementary report dated 18 April 2012. This followed a further letter of instructions from Turner Freeman dated 17 April 2012 requesting his comments for diagnosis on the plaintiff in the context of:
·The results of the test for SYT-SSX translocation for synovial sarcoma dated 18 October 2011.
·The report on the plaintiff from Dr Michael Jones and Associate Professor David McKenzie dated 10 April 2012 [any such comments to necessarily address the issue of whether the right hemithoracic tumour in the plaintiff represents a pleura-based neoplasm or whether it is located in the peripheral zone of the lung].
In this context the further documentation/reports provided to Professor Henderson were: Report of Associate Professor Ken Pittman, oncologist, dated 29 March 2012; Report of Professor Richard Ruffin dated 29 March 2012; Reports of Dr Michael Jones dated 18 December 2011 and 28 March 2012; Reports of Associate Professor David McKenzie dated 6 December 2011 and 10 April 2012; Reports of Dr Richard Slaughter dated 16 December 2009 and 28 January 2012; Report of Dr Chiron Bartholomeusz dated 17 August 2011; CT chest scan report dated 8 March 2012.
As noted in his initial report of 20 December 2011 Professor Henderson said that he had seen a recent case of unquestionable malignant mesothelioma that showed an unusual targetoid pattern of tumour cells around blood vessels.
He noted that if Professor Pittman’s observations in his report dated 29 March 2012 were correct they would appear to favour a pleural localisation for the tumour, with evidence of chest wall invasion. In this context, he opined that chest wall invasion is highly characteristic (but not entirely diagnostic) of pleural malignant mesothelioma so that the chest wall invasion, if validated, would constitute additional strong (albeit not 100% definite) evidence for a diagnosis of mesothelioma.
In relation to the mass lesion he said that he had seen numerous CT images from patients with mesothelioma that depicted similar features to that in the plaintiff. The correlation of the radiological and histological findings is frequently an imperative for a diagnosis of mesothelioma when the tissue sample (biopsy) is small, as it is in this case.
His comments on the Clinical/Medicolegal report from Associate Professor David McKenzie dated 10 April were:
Professor McKenzie commented that the radiological appearance of the tumour in the plaintiff “… is quite typical for localised fibrous tumour of the pleura”, and he concluded that the tumour was not a malignant mesothelioma: “it may be a malignant localised fibrous tumour of the pleura [!] or some other very unusual tumour”.
Professor Henderson’s comment in response was that the lesion in the plaintiff was not a solitary fibrous tumour.
He confirmed that he remained of the opinion that pleural malignant mesothelioma is the most likely diagnosis for the plaintiff’s right thoracic tumour, taking into account the observations set out in his original report and in his report of 20 December 2011, as well as the negative SYT-SSX result, and the evidence that the lesion is not a solitary fibrous tumour. Mesothelioma was more likely than not his diagnosis. This conclusion he said was with a slightly higher order of confidence than in his report of 20 December. He re-emphasised that the diagnostic problems for this case largely related to the very small amount of tumour in the core biopsy.
After the hearing of this matter had commenced, Professor Henderson provided two further reports both dated 13 May 2012. The late filing of these reports led to Turner Freeman issuing an interlocutory application seeking orders from the Court that the plaintiff could rely on them. That application was opposed by the defendant. That led to a hearing and my reasons for decision dated 17 May 2012[1] where I granted the plaintiff leave to refer to those two reports.
[1] [2012] SADC 71
One of those reports was in response to a request that he comment on a report of Dr Andrew Gal dated 4 May 2012 in which he opined that the plaintiff’s tumour might be as a result of the MAC infection (ie that it is a microbacterial abscess). Professor Henderson disagreed with Dr Gal’s opinion and said:
Apart from Dr Gal’s invocation of this diagnosis, all other reports appear to be in agreement that Mr Geyer has a progressive malignant tumour affecting the right hemithorax, the only argument being the character of the neoplastic process. I consider that a ‘mycobacterial abscess/granuloma’ can be excluded by the simple observation that there is no evidence of granulomatous inflammation in the biopsy, and I am not aware of any granulomas that show cytokeratin 5/6 staining as seen in the tumour from Mr Geyer. In his previous report of 16 November last Dr Gal expressed his opinion that the lesion is a malignant tumour.
He then commented on the other possible diagnoses proffered by Dr Gal, viz Mycobacterial Abscess/Granuloma; solitary fibrous tumour; synovial sarcoma; sarcomatoid localised malignant mesothelioma; or other intrapulmonary tumours; and he said:
In the first paragraph on page 8 of his report, Dr Gal comments that it is his belief ‘… that a reasonably definite histological diagnosis is not possible on the available core biopsy material’. He considers solitary fibrous tumour and synovial sarcoma to be unlikely but not impossible diagnoses and he comments in similar fashion concerning malignant mesothelioma. Taking into account the histological findings and progression of the hemithoracic lesion, I do not agree with his comment that a mycobacterial abscess/granuloma should be seriously considered in this case (eg, no granulomas are evident in the biopsy and no other reports – including Dr Gal’s first report of 16 November last – have invoked such a non-neoplastic diagnosis).
On reading the final section of his report, Dr Gal does not set forth an opinion on his preferred diagnosis on a ‘more likely than no’ basis (that is, a diagnosis ‘on the balance of probabilities’), as opposed to a ‘…reasonably definite histological diagnosis …’.
In his other report of 13 May 2012 Professor Henderson in reviewing the matter noted:
The early clinical and radiological reports on Mr Geyer concentrated on his asbestos-related pleural disease (ARPD), and on the question of whether a diagnosis of asbestosis is sustainable or not. It appears that his right hemithoracic mass lesion was detected in about July 2011. The weight of information supplied to me when I prepared my first report of 20 December 2011 indicated that the right hemithoracic tumour is pleura-based. The documents recording this anatomical location include the following:
The letter of referral of the case to me by way of professional consultation (Dr Yung Tran). The slides represent sections of core biopsy tissue taken in about August 2011 – when the thoracic tumour in Mr Geyer was much less advanced than now.
Dr Antic’s report of 6 December 2011 where he referred to the finding on a CT scan of the chest which showed ‘… a new right pleural opacity, well-circumscribed, oval in shape with a base showing attachment to the pleura. There was no longer a right-sided pleural effusion [as] shown in 2010’.
The report for a CT scan of Mr Geyer’s chest dated 8/9 December 2011 (from the Queen Elizabeth Hospital: TQEH). As mentioned on page 11 of my first report, the CT scan report referred to: ‘… interval development of an irregular pleurally-based soft tissue mass in the postero-lateral upper right hemithorax … the entire pleurally-based tumour measures approximately 7x3 cm. This has shown interval increase in size when compared with the more recent (limited) examination from August 2011 …’.
In his report of 16 November last, Dr Gal describes a
… malignant tumour formed by a fairly uniform population of spindle-shaped cells which focally present a somewhat plumper, epithelioid appearance. Despite the presence of these plump cells, a truly biphasic mixed sarcomatoid and epithelioid pattern is not readily discernible.
He sets forth his findings on his review of the IHC preparations from TQEH and he lists the differential diagnoses considered by Dr Tran and myself. He comments further:
There is a clinically malignant tumour located in the right chest wall, which involves the pleura. There is only a small amount of tissue available for microscopic examination and it shows a histological pattern and immuno profile which is typical [sic: I think that he means not typical] of any particular neoplasm which is shown to occur at that anatomical site. Therefore affirm diagnosis cannot be made.
At the time when I prepared my first report, Dr Michael Jones’ medicolegal report of 18 December 2011 was unavailable to me.
In my first report, I addressed the issue of diagnosis, with comments on Dr Gal’s pathology-medicolegal report of 16 November 2011. TQEH slides for the core biopsy had been sent to Dr Gal well before his report of 16 November.
Subsequently, I received a request in early March 2012 to refer the additional slides that had been prepared at FMC (accession number 11/S10956) – together with the report for the RT-PCR molecular genetic studies for the t(X;18) translocation characteristic of synovial sarcoma (SYT-SSX) – and the slides and report were despatched to Dr Gal on 9 March 2012. Only after despatch of those slides to Dr Gal did I receive the further reports from Dr Michael Jones (18 December 2011 and 28 March 2012) as well as the reports from Assoc. Prof. David McKenzie (6 December 2011 and 10 April 2012), as well as Dr Antic’s further report of 17 April 2012 – which argue that Mr Geyer’s hemithoracic tumour is not pleura-based, but rather a peripheral tumour located within the lung itself.
In my supplementary report of 28 March 2012 – reiterating his conclusions concerning the localisation of the right hemithoracic tumour as set forth in his earlier report of 18 December 2011 – Dr Jones comments:
The features are now unequivocally those of the mass arising in the periphery of the lung and not the pleural cavity. The tumour lies on the pleural surface but there is no evidence of invasion of the pleural cavity and in some images the extrapleural fat stripe remains visible … this is the typical appearance of intra-pulmonary nodules … there is no evidence of infiltration of the pleura beyond or behind the mass.
In the Opinion section, Dr Jones states that Mr Geyer’s tumour ‘… is unquestionably a tumour arising in the lung and not the pleural cavity’.
In his report of 6 December 2011, Prof. McKenzie comments on page 4:
… new finding of an ovoid mass in the right upper lobe postero-laterally … this had relatively smooth margins with the outer edge of the ovoid mass touching the pleural surface but not obviously invading the pleura or the chest wall.
On page 5, Prof. McKenzie comments further that in his view the radiological appearance was suggestive ‘… of a solitary pulmonary lesion abutting the pleural surface rather than a pleural tumour invading the lung’. In his later report dated 10 April 2012 he comments on page 2 that the tumour did not appear to show ‘… any spread along the pleural surface or into the chest wall’.
In other words, Dr Jones and Prof. McKenzie suggest that not only is the tumour located at the periphery of the lung, within the lung itself, but it does not show any evidence of invasion of the pleura or chest wall.
As requested, all of the core biopsy slides for Mr Geyer – including TQEH and the FMC additional slides – were returned by Dr Gal at my request and they arrived via Australia Post on Tuesday 8 May 2012, so that the earliest opportunity I had to review the slides was on Wednesday 9 May. The point of requesting return of the slides was two-fold:
1. To review and to refresh my memory of the histological and immunohistochemical findings in the slides; and
2. To ascertain whether there any (sic) findings in the slides that would clarify the anatomical distribution of the tumour (as stated above, Dr Gal in his report of 16 November last had referred to the right hemithoracic tumour as ‘… a clinically malignant tumour located in the right chest wall, which involves the pleura’ [italicised emphasis added]).

Professor Henderson reviewed The Queen Elizabeth Hospital and Flinders Medical Centre slides for the core biopsy of the plaintiff and opined:
Upon my further review of the microscope slides to assess the anatomical distribution of the tumour – and which became possible only after the latest reports from Drs Jones and Antic and Professor McKenzie – after the slides were eventually returned on 8 May, it is my assessment that the H&E-stained section prepared at FMC shows clear evidence that the tumour impinges upon and invades into subpleural adipose tissue with associated skeletal muscle fibres, some of which appear to have been artefactually displaced by the biopsy procedure. The combination of the adipose tissue and the skeletal muscle fibres represents clear evidence of involvement of the parietal layer of the pleura by the tumour (ie, invasion of the parietal pleura). Of course, it is not possible from that limited core biopsy to assess the maximum depth of any invasion as mentioned, for example, in Professor Pittman’s report. It is my firm opinion that this histological finding invalidates any claim that Mr Geyer’s tumour does not involve the pleura/chest wall. (Please see also Dr Gal’s report of 16 November last, page 3.)
He then further reviewed the Immunohistochemical studies on the plaintiff’s right hemithoracic tumour with emphasis on solitary fibrous tumour and synovial sarcoma. As to the issue of synovial sarcoma he concluded:
Consideration of the diagnosis in this case has proven to be unexpectedly protracted and complex. To try and reduce the complexity and to summarise, I would offer a series of short simple observations and opinions:
Although the biopsy tissue from Mr Geyer is quite limited in amount, it is my assessment from my recent review of the relevant biopsy slides that the tumour shows clear evidence of a pleural component, in the form of invasion of parietal pleura and into subpleural fat.
Therefore, from consideration of the evidence, especially the histological findings and immunohistochemical profile, it is my assessment that the evidence against a diagnosis of malignant solitary fibrous tumour is much stronger than any evidence in favour of SFT, and might be considered by some to be exclusionary, even taking into account the limited biopsy tissue available (eg, the histological appearances plus the CK5/6 expression).
It is also my assessment that the evidence against a diagnosis of a pleuropulmonary synovial sarcoma is far stronger than any evidence in favour of that diagnosis, and some authorities would assess the negative RT-PRC result for the SYT-SSX fusion gene as persuasive evidence against that diagnosis.
For the reasons discussed above and in my previous reports for Mr Geyer, it remains my opinion that his right hemithoracic invasive (ie, malignant) tumour represents a pleural malignant mesothelioma (possibly localised), on a ‘more likely than not basis’ (ie, mesothelioma on ‘the balance of probabilities’). I have reached and I reaffirm this probabilistic diagnosis on the basis of the cumulative positive and negative (ie, exclusionary) evidence – consolidated by the histological findings in the core biopsy tissue as found in my further review of the biopsy, on 9 May 2012.
In his oral evidence Professor Henderson did not resile from the opinions he expressed in his written reports. He confirmed that he does not arrive at a diagnosis of mesothelioma lightly because “mesothelioma, whether one is dealing with usual diffuse type of mesothelioma which involved the whole pleural cavity, or a localised one, is a progressive and in general and ultimately lethal tumour”.
He was asked that as time has gone by and as further material was produced to him had he altered or modified his original opinion. His response was:
It’s been modified only slightly in that I’ve now had the opportunity to re-review the slides on two further occasions, as has Dr Gal, and on looking at all of the biopsy evidence, including what I interpret as invasion of subpleural fat, and considering all of the other differential diagnoses, it’s now my opinion that this case, no matter how unusual it is, there is only one diagnosis which really fits the evidence and that is that of a localised pleural malignant mesothelioma. I believe that the evidence is strongly against an exclusionary or alternative diagnoses such as a solitary fibrous tumour or a pleural synovial sarcoma. [2]
[2] Tr 229
In cross-examination Professor Henderson conceded that he did not claim to “be the only pathologist who can diagnose it [mesothelioma]. I would say that by way of professional or medico-legal referral, I see a substantial proportion of all of the cases of mesothelioma diagnosed in Australia, but there are other pathologists who can make the diagnosis. But, equally there are other pathologists who, when they encounter cases with which they have difficulty, they refer the case to me”. He said, “I don’t claim 100% infallibility. I do claim that I have seen several thousand cases of mesothelioma and other pleural tumours and that I have worked through and given my professional opinion to the best of my ability, taking into account the positive and the non-characteristic evidence for and against the diagnosis …”.[3]
[3] Tr 237
When asked about his evidence whether malignant mesothelioma was diffuse or localised, and whether it was a lethal tumour, his response was, “Well, yes, because the evidence is that localised malignant mesotheliomas are – in my experience in the literature, have either the capacity to spread through the pleura which I have seen or they have the capacity to metastasise to distant sites”[4]. He rejected the suggestion that the literature showed the opposite.
[4] Tr 240
In relation to the serious reservations that he had expressed about the usefulness of using core biopsy samples from pleural mass lesions for diagnosing mesotheliomas and other pleural tumours, and that in this case too little tissue was obtained which made it difficult to undertake a proper analysis of that tissue, he agreed and said:
These biopsies tend to be small and sometimes one encounters discordant immunohistochemical chemical study results because of the small amount of tissue which may be explicable in some cases, but the expression, or the immunohistochemical staining is often patchy in distribution and the small biopsy may fail to sample a positive area of the tumour, and as a matter of principle the larger a biopsy is, the better the diagnostic work-up that one can carry out and the more confident the diagnosis. But at the same time, we have to deal with what we're given and increasingly clinicians adopt limited core biopsies because they are less invasive than a larger surgical biopsy or a back-sided biopsy.[5]
[5] Tr 243
When it was put to him that Dr Gal’s opinion was based on the pathology alone, that one could not say the plaintiff had a malignant mesothelioma of the pleura, Professor Henderson rejected that and said: “I think that one can say that at a reasonably high order of probability, Mr Geyer’s tumour is a localised pleural malignant mesothelioma, despite the limitations on some of the immunohistochemical studies”. [6]
[6] Tr 247
He rejected the notion that the diagnosis of malignant mesothelioma of the pleura could be ruled out if the neoplasm was lung based as opposed to originating in the pleura. He said, “Well no, I don’t quite agree with that. Firstly, I don’t believe that it is lung based; secondly, even if it were lung based, it does not entirely exclude a mesothelioma, because as I have mentioned, 20 years ago I described a localised mesothelioma which involved – grew into the periphery of the lung. We have illustrated exactly the same in the Dail Hammar book: so that that distribution does not by itself exclude the mesothelioma.”[7] They were excluded by him because they lacked specific required features or exhibited certain features that were incomparable with a definite diagnosis.
[7] Tr 248
He confirmed that he had rejected all the possible alternative diagnoses “because one or more features required for diagnosis were absent for those tumours. That simply didn’t look like them, really, but I did consider them.”[8]
[8] Tr 250
He rejected the diagnosis of a malignant solitary fibrous tumour, mainly because the tumour was cytokeratin positive[9] and the fact that it did not “remotely resemble a solitary fibrous tumour, with which I have now seen about 40 cases at least, including about a quarter of them malignant”.[10]
[9] Tr 251
[10] Tr 252
When it was put to him that there was not one mesothelioma marker that allowed him to say “oh, this is mesothelioma”, his evidence was “well, as I say, there wasn’t one which would allow you to say at 100% confidence ‘this is a mesothelioma’. It’s a no brainer: the simple fact is that there is an absence of detectable staining for some of the mesothelial markers – not all, and therefore one needs to take into account what labelling one does have plus the morphology of the tumour”.[11] He added “well, it was not classical or typical of a mesothelioma. Again, the immunohistochemical profile was not inconsistent but it was not classical of a mesothelioma, and therefore I need to take other factors into consideration to reach a diagnosis and also to exclude any other tumours which enter into the differential diagnosis”. [12]
[11] Tr 253
[12] Tr 253-254
His evidence was that the tumour did not look like a carcinoma of the lung and said that he had seen “many thousands of cases of carcinoma of the lung of various types and has been involved in the WHO Histological Classification of lung cancers, and in the recent revisions of the adenocarcinoma category. As far as I am aware there is no convincing anatomical evidence that this is a characteristic lung cancer in terms of either the imaging studies or the histopathology”[13] and “the histological appearances of the tumour simply do not resemble those of any lung cancer of which I am aware”[14].
[13] Tr 254
[14] Tr 256
As to the atypical nature of the tumour he said:
It’s not classical of a mesothelioma, but I would say that mesotheliomas are one of the most variable of all human tumours in terms of their range of histological appearances, and this just does not look to me like a conventional lung cancer. For a start, the tumour has sarcomatoid component with collagen deposition, and the cells are very bland, and that is reasonably characteristic of mesothelioma, and not lung cancer, when it gets into the pleura.[15]
[15] Tr 257
When asked about his reference to the Sherlock Holmesian principle[16] (in his letter to Dr Tran) he said: “well, I was just quoting Sherlock Holmes on that: that there were unusual features in this tumour, but I had considered a range of alternative diagnoses, and as I have mentioned, for one or other reasons, I consider those diagnoses not be sustainable. And therefore by the process of exclusion of those alternatives and the positive evidence that I did have in terms of the histological appearances and the immunohistochemical profile, I thought then, and I still think, that a localised malignant mesothelioma is the most likely diagnosis. I cannot think of an alternative one”.[17]
[16] He explained that “…this was not addressed as a finely worded medico legal report, but this was a consultation professional report to a colleague, and I may have been less precise than I usually am in my quotation of that source” (tr 292).
[17] Tr 259
He confirmed that he disagreed with Dr Gal’s opinion that it was not possible to diagnose mesothelioma on the basis of the histological appearance of the immune characteristics in this case[18]. He regarded as “extremely speculative” Dr Gal’s opinion that “this tumour may yet be an undescribed entity”[19]. He said, “we sometimes see mesotheliomas which have unusual histological characteristics. And as I have mentioned, mesothelioma is one of the most protean of all human tumours. To argue that a pleura based biphasic tumour which expressed cytokeratins is a completely undescribed entity, I think is to indulge in speculation for which there is no evidence: but the evidence which suggests that if this is an unusual pattern of tumour that is an unusual variety of mesothelioma in terms of its histology. But I see plenty of mesotheliomas where the histology is not entirely clear” [20].
[18] Tr 259
[19] Tr 259
[20] Tr 260
Professor Richard Ruffin is a Respiratory Physician and a Consultant Physician at The Queen Elizabeth Hospital and a Professor of Medicine.
He first saw the plaintiff on 20 November 2008.
In his report dated 21 November 2008 he noted that the plaintiff had no past history of asthma or hay fever. He noted the history given to him of the plaintiff’s exposure to asbestos and asbestos dust whilst working at Playford A and B power stations.
He carried out formal lung function tests which showed “a pattern of normal flow volume loops with no acute bronchodilator response”.
The plaintiff told him that “he smoked between the ages of 15 to 36, possibly up to 60, cigarettes per day at some of that time”. His diagnosis was that the plaintiff “has pleural plaques, some of which are calcified, significant pleural thickening (exceeding 8cm x 5cm > 3mm thick), and that he has a mild degree of asbestosis”. His reason for that diagnosis was the finding of basal inspiratory crackles, the history of the plaintiff’s exposure to asbestos dust, the CT appearance (from a CT scan dated 4 March 2008) with sub pleural fibrosis and the reduction in the plaintiff’s diffusing capacity compared to predicted values.
He believed that the plaintiff’s exposure to asbestos was directly related to his pleural plaques with calcification, pleural thickening and the mild degree of asbestosis.
He thought that the disability that the plaintiff had as a result of his asbestos related condition was in the vicinity of 10% - 15%.
It was possible that the plaintiff’s disability would increase in the future; he had risk factors for the development of lung cancer because he was also a smoker and there was interaction between smoking and asbestos exposure with lung cancer. He was also at risk of developing mesothelioma.
His prognosis for the plaintiff was good providing he did not develop lung cancer or mesothelioma, and that his life expectancy had not been affected by his asbestos related condition.
In his report dated 17 September 2009 he opined that the plaintiff’s chance of developing mesothelioma and lung cancer could be up to a 10% chance over a lifetime.
In his report dated 19 January 2010, having read Dr Jones’ report dated 9 September 2009 regarding the radiology of the plaintiff, he said that the presence of subpleural dots in the presence of pleural disease attributed to asbestos exposure would support the diagnosis of asbestosis.
In his report dated 14 April 2011 he noted that on 22 April 2010 he received a phone call from the plaintiff’s local doctor advising that the plaintiff had a large right pleural effusion. Arrangements were made for him to be admitted to the QEH and to Dr Polasek as the Consultant Physician. The plaintiff was admitted on 23 April 2010. On 24 April Dr Polasek performed a pleural tap which obtained clear fluid and this fluid was sent for a range of investigations. The fluid was found to be an exudate with a predominance of lymphocytes. Several days later it was arranged to have a larger volume of fluid aspirated to improve the plaintiff’s symptoms of shortness of breath. He noted that the plaintiff became sweaty and felt faint and the procedure was as a consequence thereof discontinued. The plaintiff had had “a vasovagal episode”. The procedure was repeated on 29 April and approximately 2 litres of fluid was removed. A chest x-ray showed improvement with a reduced volume of fluid.
The plaintiff was discharged from hospital on 30 April 2010. He reviewed him on 6 May 2010 when three of the sputum cultures out of 3 were positive for mycobacterium avium intracellulare (MAC) or atypical mycobacterium. He discussed the management options with an RAH Chest Clinic Physician who confirmed that it would be very unusual for MAC lung infection to be causing a pleural effusion. The chest x-ray at this time showed a right pleural effusion, of reduced size compared to 23 April, was still present with some areas of atelectasis in the right lung. The best management option was considered to be further investigation of the pleural disease by a video assisted thoracoscopy (VAT) so that a pleural biopsy could be undertaken. He referred the plaintiff to Mr Craig Jurisevic with a view to doing a VAT with pleural biopsies and possibly also a lung biopsy.
Since he had seen the plaintiff on 25 February 2011, he had had significant side effects with the antibiotic treatment for the MAC infection. Because of this there was cessation of the antibiotics and then a slow sequence of reintroduction of his antibiotic therapy so that the side effects were minimised. He noted that the plaintiff had significant weight loss resulting from his feeling nauseated and anorexic.
He also noted that the plaintiff has been diagnosed with polymyalgia rheumatica. He had been seen by a vascular surgeon with regard to claudication in his legs and had been found to have a significant reduction of arterial blood flow in his right leg.
His diagnosis was the plaintiff “has the asbestos related diseases of pleural plaques, pleural thickening and mild asbestosis”. He suspected that the asbestosis had not progressed, or if it had, it was only to a very small extent.
The plaintiff, he noted, suffered from other conditions which included polymyalgia rheumatica, mycobacterium avium intracellulare infection of the lung and the right sided pleural effusion in 2010, significant peripheral vascular disease and general medical problems.
He opined that the plaintiff’s “previous exposure to asbestos had caused beyond reasonable doubt his pleural plaques, pleural thickening and asbestosis” and that on balance “his pleural effusion in 2010 was also related to an asbestos exposure”. The MAC infection, he said, would be an unusual cause of pleural effusions in Australia.
The other possibility he considered was whether the asbestos related disease had contributed to the plaintiff developing the MAC lung infection: but he could not find literature to support that.
He believed that the plaintiff’s disability as a result of his asbestos related conditions had probably progressed a little further based on the more rapid change in his lung function tests. However he noted that he needed to be guarded in this conclusion given that the plaintiff had had the MAC infection which might be a contributing factor.
He did not think that there was a major impact of the plaintiff’s asbestos related conditions on his condition of MAC and the treatment of it with antibiotic therapy.
In his report dated 22 November 2011 he noted that the plaintiff had a HRCT scan which was ordered by Dr Antic. This showed “asbestos related pleural disease with a pleural mass in the posterolateral lower right upper lobe”. He then arranged with the plaintiff’s doctor for a CT guided biopsy of the right upper lobe lesion. This was performed at the Queen Elizabeth Hospital on 24 August 2011 when “three fine needle aspiration samples and three core biopsies were taken. The pathologist was Dr Y Tran. The sample was sent to Professor Henderson for his opinion of the diagnosis. Having reviewed the matter Professor Henderson’s opinion was that “a pleural malignant mesothelioma was the favoured diagnosis”.
On 14 October 2011 the plaintiff saw Mr Jurisevic who said it was not appropriate to consider further surgery to obtain further tissue.
Professor Ruffin’s diagnosis was that the plaintiff “is suffering from mesothelioma, pleural thickening and pleural plaques, mild asbestosis, mycobacterium avian intracellulare infection of the lung, polymyalgia rheumatica, peripheral vascular disease, and general medical problems”.

He opined that the plaintiff’s previous exposure to asbestos “has caused beyond reasonable doubt, his mesothelioma, pleural plaques, pleural thickening and asbestosis”.
The usual estimates for survival of mesothelioma, he said, range from 4-13 months untreated and 6-18 months when treated.
In his report dated 29 March 2012 he noted that he saw the plaintiff on 8 December 2011 and 8 March 2012. He said that “with the likely diagnosis of mesothelioma, the prognosis for the plaintiff was limited and with the progression in the size of the tumour the prognosis for survival was about a year”.
The likely course of the plaintiff’s condition from mesothelioma “is progressive deterioration”. It was likely that he would “develop pain related to the mesothelioma locally invading structures as well as increasing dyspnoea because of compression of the right lung”. The plaintiff might suffer from weight loss and the combination of pain and weight loss might result in significant depression. It was not clear as to whether the plaintiff would be offered chemotherapy or even if he was, whether he would accept it.
In his oral evidence he said that he spent some time talking to the plaintiff about the possibilities he had a malignant mesothelioma and the possible treatment with chemotherapy or radiotherapy. The plaintiff was uncomfortable about the thought of chemotherapy. He indicated to the plaintiff and his daughter that it should be their decision but he thought it was worthwhile getting Dr Pittman’s view.
In this report he said that the plaintiff was likely to be unable to care for himself into the future and be unable to drive and that he would require substantial home support.
He had read the reports of Dr Antic dated 6 December 2011, Associate Professor McKenzie dated 6 December 2011 and Dr Slaughter dated 28 January 2012. He believed that the publication provided by Dr Slaughter showed that a range of CT scan presentations could occur for mesothelioma. Radiology, he said, was not a good indicator of underlying pathology. Pathological examination was required for the diagnosis. He believed that Dr Slaughter’s conclusion was correct, that the CT scan was definitely not diagnostic, and that the pathological evidence was the best diagnostic tool for mesothelioma.
In cross-examination[21] he agreed that the plaintiff had a number of co morbid medical conditions including: peripheral vascular disease (hardening of the arteries), that he believed that he had had surgery on both legs; that he had claudication (“pain in the legs”); hypertension (high blood pressure) for a number of years; some chest pain for a number of years, and to balance that, he had seen a cardiologist; that he had had a number of tests related to possible heart condition; that he had been treated for atherosclerosis (hardening of the arteries); he understood that the plaintiff had stents in the arteries supplying both legs; that he has been suffering from persistent MAC infection from approximately mid 2010, and polymyalgia rheumatica since late 2010; that he is being treated for gastro-oesophageal reflux diseases (or gord); and that he has had bilateral shoulder surgeries and a knee replacement.
[21] Tr 316-320
In his report dated 14 April 2011 he said “Mr Geyer’s previous exposure to asbestos has caused beyond reasonable doubt his pleural plaques, pleural thickening and asbestosis”. He was asked in cross-examination, “You’re not there saying, are you, that the plaintiff has mesothelioma beyond reasonable doubt. What you’re saying is that on the assumption that he does have mesothelioma – in other words on the assumption that Professor Henderson is correct that it was caused by exposure to asbestos”. His response was, “Yes”.[22]
[22] Tr 376
His evidence was that if the plaintiff has asbestosis that it has not progressed since he first saw him in 2008.
He agreed that asbestosis is one form of pulmonary fibrosis and that there are many causes or medical conditions that can give rise to pulmonary fibrosis.
He agreed that lung crackles are not specific to pulmonary fibrosis, and that if crackles are caused by pulmonary fibrosis one would expect them to be present on each examination and that if respiratory crackles were present at one examination but not the next it might suggest that they are related to something other than pulmonary fibrosis.
He would not diagnose the plaintiff as having pulmonary fibrosis solely from the CT image of 4 March 2008. He agreed that the improvement in diffusing capacity in 2011 was an indicator against the plaintiff having asbestosis and whatever had caused the reduction in diffusing capacity in 2008, it was not asbestosis.
Associate Professor Ken Pittman is a Medical Oncologist with a particular interest in malignancies involving the respiratory system. He is currently the Director of Medical Oncology at the Queen Elizabeth Hospital.
He first saw the plaintiff at the Queen Elizabeth Hospital on 31 January 2012, and then on 9 March 2012.
In his report dated 29 March 2012 he said that on the balance of probabilities it was “highly likely” that the plaintiff has malignant mesothelioma. He based that on the fact that the plaintiff “has a malignant tumour involving the pleura” which had been reviewed by Professor Henderson who, he said, was a world expert in the field of pathology of the pleura. In his practice as a Medical Oncologist in Adelaide, any unusual pleural tumours were usually finally reviewed by Professor Henderson for a definite opinion. He had read the counterview of Dr Andrew Gal and noted that Dr Gal’s view was that the plaintiff was suffering from a malignant tumour but that he did not believe that a more specific diagnosis was possible. However, on the review of possible differential diagnoses that Dr Gal had raised, the alternate diagnoses appeared to have already been excluded by means of various immunohistochemical tests. He noted that Dr Gal did not have the clinical and radiological information to aid in any overriding diagnosis. The plaintiff’s extensive past exposure to asbestos with radiological changes was suggestive of asbestosis and with radiological evidence particularly with the most recent CT scan showing a progressive pleurally based tumour, the diagnosis of malignant mesothelioma appeared to be sound.
The natural history of mesothelioma was usually one of relentless progression of the tumour involving the pleura. The majority of patients with malignant mesothelioma eventually died of complications of local disease due to increasing tumour bulk that resulted in progressive respiratory failure, pneumonia or eventual myocardial dysfunction with arrhythmias due to local tumour bulk.
He reviewed the correspondence from Dr Jones dated 28 March 2012 in which he concluded:
·Mr Geyer’s tumour is unquestionably a tumour arising in the lung and not the pleural cavity;
·Mr Geyer’s tumour has progressed since the previous scans;
·Mr Geyer’s supine 3 mm lung images do not show any changes on which a diagnosis of asbestosis could be made.
He agreed with Dr Jones’ second conclusion, ie that the tumour had progressed, but disagreed with his conclusions 1 and 3.
He further saw and reviewed the plaintiff on 14 June 2012. On that occasion the plaintiff reported a slight increase in non-productive cough and in intermittent sensation of pressure over the right side of his chest which symptoms Dr Pittman said he believed were consistent with progressive mesothelioma. The plaintiff’s MAC disease seemed quite stable when compared with it in October 2011. The most recent CT scan showed a slowing progression of the pleurally based tumour. This was consistent with slowly progressive mesothelioma. The plaintiff told him he was keen to minimise any treatment that would negatively impact on his quality of life.
He noted that in Professor Henderson’s most recent report he had confirmed there is a pleural invasion which he noted, is entirely in keeping with a diagnosis of malignant pleural mesothelioma.
In his final report of 11 October 2012 he noted that on that examination the plaintiff had a frequent dry cough and that the latest CT scan showed “a slow progression of the mesothelioma”. He discussed with the plaintiff the possibility of chemotherapy but said that might be complicated by the plaintiff’s treatment for MAC.
He disagreed with Dr Jones’ evidence on the radiology that there was no evidence of chest wall invasion. He said “I don’t think anyone can say with certainty that there is chest wall invasion … the appearances are consistent with chest wall invasion but I don’t think you can make that diagnosis from a CT scan”.
Mr Craig Jurisevic is a Thoracic Surgeon.
In a report dated 14 October 2011 he reported on the question of performing surgery to obtain further tissue from the plaintiff. He said that he did not feel that that was appropriate in this case because: “As his pleural space is now obliterated, he would require a thoracotomy to obtain further tissue. We know he has a malignant pleural neoplasm and it is almost certainly mesothelioma. To subject him to a major operation to obtain further tissue to clarify what is a legal situation does not sit well with me at this point in time. I have made the recommendation that he does not have further surgery to obtain further tissue and that any other legal matters should be sorted out by the lawyers”.
In cross-examination he agreed that pleural effusions are the most common presentations of mesothelioma and in 100 hypothetical cases 90 would present with a pleural effusion.
The primary reason he believed surgery was not an option for the plaintiff was that there is no real evidence of any cure from surgical resection to remove widespread diffuse mesothelioma and his interpretation that Dr Ruffin’s request to obtain a further tissue sample was that it may be for “a legal issue”.
Dr R E Slaughter is a specialist radiologist practising in Queensland. He is at present the Deputy Director of Radiology and Chairman of the Division of Medical Imaging at the Prince Charles Hospital.
He prepared reports dated 13 October 2009, 16 December 2009, 8 January 2010, 28 January 2010 and 16 April 2012.
In his report of 13 October 2009 having reviewed the CT scan of the plaintiff’s chest dated 4 March 2008 and chest radiographs performed on 24 October 2005 and 18 February 2008 and the report of Dr Jones dated 9 September 2009, he said that he disagreed with Dr Jones’ opinion. However he said that he believed that a diagnosis of interstitial lung disease due to asbestosis was unlikely.
In his report dated 16 December 2009 having reviewed a further series of CT scans performed on the plaintiff dated 21 October 2009 and reviewed a report from Dr Antic, he said that the recent CT scans showed evidence of bilateral pleural plaques which were similar to those demonstrated on the previous study and that “this appearance is typical of asbestos related pleural disease”.
In his report of 28 January 2010 he again disagreed with Dr Jones’ opinion and said as he stated previously in his report of 13 October 2009 that he believed that definite pleural plaques were demonstrated anteriorly on the plain chest radiographs and that these were confirmed on the CT scan.
In his report dated 28 January 2012 Dr Slaughter noted, having reviewed the various CT scans, that he believed that the mass lesion in the plaintiff’s chest was on radiological grounds most likely a malignant pleural based tumour. He believed that the appearance was “certainly consistent with a diagnosis of mesothelioma although it was definitely not diagnostic of that cause and could have other causes”. He noted, “In a patient who is asbestos exposed and has pleural plaques however particularly in the presence of the histological evidence reported by Dr Douglas Henderson, I believe the most likely diagnosis of this lesion is malignant mesothelioma”.
In his report of 16 April 2012 Dr Slaughter said he had reviewed the CT scan of the chest performed on the plaintiff and dated 8 March 2012. He had also read reports of Dr Jones dated 28 March 2012 and a report of Associate Professor Ken Pittman dated 29 March 2012.
After reviewing the recent CT scan and reading the further reports he said that he had no reason to change his opinion given in his report of 28 January 2012.
In cross-examination he agreed with Dr Jones that the CT imaging showed the existence of pleural plaques. Dr Jones’ opinion was that the pleural plaques and thickening is only first observable from the CT imaging of 4/3/2008 whereas his opinion was that a pleural plaque was able to be seen on the earlier x-ray from 2005. He also differs from Dr Jones in relation to the interpretation of the CT scans in relation to the right side of the pleural mass or lung lesion: he disagreed with Dr Jones that the tumour’s appearance suggests that it arises in the lung.
In his report of 13/10/2009 he considered the diagnosis of asbestosis as unlikely. In subsequent reports whilst suggesting such a diagnosis was possible, in cross-examination he said “I cannot make a diagnosis of asbestosis and I have not”.
Defendant’s Medical Experts
Dr R Antic is a Respiratory and Sleep Physician, a Director of Thoracic Medicine.
In his report dated 1 April 2009 he noted that he saw the plaintiff on 16 February 2009. He organised for lung function studies to be done on the same day. The plaintiff told him that he was generally well; that he had had shoulder and knee operations; and that he had smoked between 1945 and 1960, less than 10 cigarettes per day. His main current symptoms were a dry cough when sleeping and pains across the top of his chest; that occasionally he produced yellow phlegm but there was no wheezing and no breathlessness.
The clinical examination was within normal limits. There were no lung crackles and there was no finger clubbing.
In his oral evidence Dr Antic said that there are many conditions that cause lung crackles. Importantly he said if pulmonary fibrosis caused the interstitial lung disease he would expect the lung crackle on each and every occasion he examined the patient.
He saw the chest x-rays dated 24 October 2005 which showed a few pleural plaques. The CT scan of 4 March 2008 showed some basal paravertebral pleural thickening with calcification and occasional plaques elsewhere. There was some bronchial wall thickening. There was no evidence of interstitial lung disease.
The lung function studies were within normal limits.
His diagnosis of the plaintiff was pleural plaques and localised pleural thickening caused from past asbestos exposure; bronchitis probably from past smoking; and that the asbestos exposure caused the pleural disease.
He noted that there were some differences between his findings and those of Professor Ruffin. The first was that the plaintiff reported to Professor Ruffin that he smoked up to 60 cigarettes per day whereas the plaintiff told him that he smoked up to 10 cigarettes per day. The second was that Professor Ruffin heard lung crackles on examination of the chest and he did not. Professor Ruffin explained that this and the exposure to asbestos as well as subpleural fibrosis lead him to conclude that there was mild pulmonary asbestosis. Dr Antic’s interpretation of the lung function studies of 16 February 2009 was that they were within normal limits and in the absence of lung crackles he did not find evidence for pulmonary asbestosis.
In Dr Antic’s report dated 4 August 2009, he said that he had seen a copy of the chest x-ray reports dated 24 October 2005 and 18 February 2008, and a CT scan of the plaintiff’s chest dated 4 March 2008 and the x-ray reports. The CT scan of the chest did not, he said, show any evidence of asbestos related lung disease.
His diagnosis was pleural plaques and localised pleural thickening caused by past asbestos exposure; and bronchitis, possibly bronchiectasis and bronchiolitis, not caused by past asbestos exposure.
In his report of 6 December 2011, he noted the further medical reports and records that had been sent to him and said that the plaintiff’s clinical state had changed significantly between 16 February 2009 and 28 July 2011. When Dr Antic saw him on 16 February 2009 he was not breathless. When he saw him on 28 July 2011 he was very breathless. He had a dry cough and a pain on deep breathing across his chest. The plaintiff told him that he was no longer able to play golf for more than two holes and at a very slow pace. He had to sit down while mowing the lawn which was 15 metres in length, or when hanging clothes on the line. When making his bed he felt breathless and had to sit down in the middle of this.
He noted from the medical records at the Queen Elizabeth Hospital and the x-ray imaging that in April 2010 the plaintiff was investigated at the QEH for a large right pleural effusion. No specific diagnosis was made despite extensive investigations. In April 2010, sputum cultures grew mycobacterium avium organisms and he was treated for this at the Chest Clinic by Dr S Cameron. Subsequently he was diagnosed with having polymyalgia rheumatica and treated with Prednisolone. At that time he was also having difficulty with claudication in his legs and was found to have narrowing of the arteries to his legs.
When Dr Antic saw the plaintiff on 28 July 2011 his clinical examination showed a blood pressure of 1490/90 mmHg with a regular pulse of 105 bpm. There was no finger clubbing. The heart sounds were normal. He was unsure whether there were lung crackles in the right axilla. The lung function studies showed that the overall lung size was reduced compared to that of 16 February 2009 but the other measurements of lung size, including vital capacity, were within the normal range.
The CT scan of the plaintiff’s chest showed a new right pleural opacity, well circumscribed, oval in shape with a base showing attachment to the pleura. There was no longer a right sided pleural effusion shown in 2010. The cause of the right pleural effusion had not been found. Dr Antic noted the pleural mass histopathology reports with expert opinions from Dr Gal on 16 November 2011 and Professor Henderson from 29 August 2011. They confirmed the presence of a malignant tumour, the type of which had not been established. He noted the difference in opinion between the two pathologists, with Professor Henderson favouring a pleural malignant mesothelioma, whereas Dr Gal indicated that he was not able to categorise it.
He said that the CT scan findings on 28 July 2011 showed a new right pleural opacity well circumscribed, oval in shape with a base showing attachment to the pleura. This scan “which showed a well circumscribed tumour was not characteristic for malignant mesothelioma”. Normally mesothelioma tended to spread along the pleural surfaces to cover the chest cage and lung and constrain its normal movement. This atypical x-ray appearance further questioned in his mind the diagnosis of mesothelioma and made it unlikely.
The plaintiff’s current treatment plan was not available to him. He noted that Professor Ruffin had not seen the plaintiff recently. He also noted that Dr Jurisevic had declined to perform a surgical biopsy of the plaintiff’s right lung mass and that his letter infers that he was asked to do this for medico-legal reasons. This, he said, was reasonable but it was not clear whether there was scope for this to be surgically resected as therapy. This, he said, would depend on the further assessment of the plaintiff’s overall health and in particular, his cardiac state.
When he saw the plaintiff on 28 July 2011 he sought another CT scan of the plaintiff’s chest to seek an explanation for his breathlessness.
This, he said, showed a new right pleural malignant tumour whose type had not been established. It was not typical of mesothelioma both on imaging and histopathological grounds. The cause of the right pleural effusion which occurred in 2010 had not been established and it had not recurred. The abnormalities documented in 2009 had not changed significantly except that the total lung capacity was smaller than previously. Whilst there may be minor patches of lung fibrosis, that did not, he said, amount to pulmonary asbestosis and would not be expected to cause significant respiratory impairment.

It would not have taken these measures unless it knew that asbestos dust could result in a dust disease. In light of my finding that as the plaintiff’s career continued with ETSA in his various supervisory roles, he continued to work in the boiler shop in a hands-on role and the clear evidence that the boiler shop contained asbestos dust it must follow that the defendant knew that whilst the plaintiff was working in the boiler shop, at least from 1973 onwards, that he was exposed to asbestos dust and that as a result he was at risk of contracting a dust disease.
Whilst the defendant is to be given some credit for taking measures to attempt to ameliorate the potential dangers to the plaintiff it plainly did not go far enough. They were certainly not enough to militate against an award of exemplary damages. Consistent with the approach taken by this court in Van Soest v BHP Billiton Ltd (No 2) [2013] SADC 95 I think an award of $20,000 under this head of damage is appropriate.
Interest
Taking a broad axe I allow $2,000 for interest.
In summary I award as follows:
General damages   $175,000
Loss of life expectancy                   $     5,000
Past medical expenses  $   10,474
Future medical expenses                $   65,000
Griffiths v Kerkemeyer$   50,000
Exemplary damages  $   20,000
Interest  $     2,000
Total  $327,474

ANNEXURE
Ruling on documents (EDD) on the issue of exemplary damages
1.The plaintiff sought to tender two volumes of paginated documents (EDD) on the issue of exemplary damages and the plaintiff’s exposure to asbestos. The defendant has taken objection to some of those documents. Set out hereunder is my ruling in relation to those objections.
2.The plaintiff asserts that each of the documents, which were discovered by the defendant, are admissible pursuant to section 45A of the Evidence Act 1929 (SA) which provides as follows:
Admission of business records in evidence
(1) An apparently genuine document purporting to be a business record—
(a)shall be admissible in evidence without further proof; and
(b)shall be evidence of any fact stated in the record, or any fact that may be inferred from the record (whether the inference arises wholly from the matter contained in the record, or from that matter in conjunction with other evidence).
(2) A document shall not be admitted in evidence under this section if the court is of the opinion—
(a)that the person by whom, or at whose direction, the document was prepared can and should be called by the party tendering the document to give evidence of the matters contained in the document; or
(b) that the evidentiary weight of the document is slight and is outweighed by the prejudice that might result to any of the parties from the admission of the document in evidence; or
(c) that it would be otherwise contrary to the interests of justice to admit the document in evidence.
(3) For the purpose of determining the evidentiary weight, if any, of a document admitted in evidence under this section, consideration shall be given to the source from which the document is produced, the safeguards (if any) that have been taken to ensure its accuracy, and any other relevant matters.
(4) In this section—
"business" means business, occupation, trade or calling and includes the business of any governmental or local governmental body or instrumentality;
"business record" means—
(a) any book of account or other document prepared or used in the ordinary course of a business for the purpose of recording any matter relating to the business; or
(b)any reproduction of any such record by photographic, photostatic, lithographic or other like process.
3.The plaintiff then contends that the documents should be tendered and relied upon because it can be inferred that they were in the possession of the defendant at or around the date of the particular document and that it can be inferred that the defendant knew of the contents of each document at or about that time.
4.Justice Lander in Southern Equities Corporation Ltd (in liq) and Others v Bond and Others (No 2) [2001] SASC 70 set out a three step process that is required to be established before the tender of a document pursuant to this provision can be considered.
5.First, the document must be an apparently genuine document.
6.Secondly, it must purport to be a business record, being a document which is prepared or used in the ordinary course of business.
7.Thirdly, if it is an apparently genuine document which has been prepared or used in the ordinary course of business, it must have been prepared or used “for the purpose of recording any matter relating to the business”. See also: Ryan and Others v ETSA and Others (No 2) (1987) 47 SASR 239 at 246.
8.Once these matters have been established the issues raised by s 45A (2) and (3) need to be considered.
9.The defendant objects to the tender of many of the documents for various reasons.
10.In some instances it contends that particular documents are not business records for the purpose of s 45A. It submits that some were not in the possession of the defendant during the relevant period of exposure, viz 14/7/57 up until September 1986 and therefore cannot be relevant to the issue of the defendant’s knowledge at the relevant time. It submits that without more the mere fact that documents bear a certain date and were discovered by it does not prove when the defendant came into the possession of the document or more particularly when it became aware of the contents of the document.
11.The defendant submitted that a number of documents did not relate to the Playford Power Station and were therefore not relevant. Finally it submitted some of the documents were not relevant as they did not touch upon a fact in issue.
12.In developing these submissions the defendant took me to the judgment of Jordan CJ in Carr v Baker (1936) 36 SR (NSW) 301. It submitted that an inference may only reasonably be drawn upon the basis of facts, which have been established by the plaintiff in evidence, such that “it is more probable that it exists than it does not”. It submitted that if the evidence goes no further than establishing a possibility, that is not enough.
13.The defendant also took me to Jones v Dunkel (1959) 101 CLR 298 where Kitto J stated at [305]:
One does not pass from the realm of conjecture into the realm of inference until some fact is found which positively suggests, that is to say provides a reason, special to the particular case under consideration, for thinking it likely that in that actual case a specific event happened or a specific state of affairs existed.
14.The defendant submitted that the plaintiff has not proven any facts in respect of which an inference of the kind suggested could be said to arise. In particular, there is no factual basis to assert why the Court should accept that the defendant would have received a document shortly after it was produced by the relevant entity. He had not established any relationship with the particular entity and the defendant to enable that inference to be drawn. He had not identified any correspondence or other communication between the two, in respect of which the inference sought to be drawn, might reasonably arise. It was said that the plaintiff’s submission is based on nothing more than unsubstantiated conjecture.
15.I agree with these submissions. Moreover, no adverse inference can be drawn against the defendant for not adducing evidence to suggest otherwise. Given the time lag involved it is highly unlikely that there would be any witnesses available or alive that the defendant would have called to give evidence as to whether or not it had received those documents at or about the date of publication.
16.With that in mind I now turn to the documents that were the subject of objection by the defendant.
Document [5] to [21]
17.This is a document of the Australian Fibre Glass Pty Ltd of Frankston Road Dandenong dated 6 April 1970. The plaintiff asserts in the top right corner a notation appears “PSE” and that stands for Power Station Engineer. It asserts that it is a business record and is directly relevant to the assessment of the quantum of exemplary damages because it tends to prove that there was an alternative to asbestos insulation namely fibre glass insulation. Whilst it concedes it is not apparent when ETSA received it, there is an available inference that the document was received shortly after the date of the document.
18.The defendant does not agree that the notation “PSE” appears on the top right corner of the document. That notation is not clear on the Court’s copy of the document. As beforementioned, for a document to be classed as a business record for the purposes of s 45A of the Evidence Act 1929 (SA) it must be a document which is “prepared or used in the ordinary course of business” and must have been “prepared or used for the purpose of recording any matter relating to the business”. The plaintiff has not established in this case either of those criteria.
19.Furthermore the plaintiff has conceded that it is not apparent from the document the date that it was received by ETSA. As beforementioned, I am not prepared to accept the plaintiff’s submission that it can be inferred that it was received shortly after publication.
20.That document is not admitted into evidence.
Document [22] – [41]
21.This is a document produced by the National Health and Medical Research Council and was published in 1971. The plaintiff submits that it is a business record because it has been discovered by the defendant and that there is an inference that the defendant received it at or about the time of its publication. The mere fact that the document has been discovered by the defendant does not make it a business record of the defendant. On the basis of my finding on the inference submission I am not prepared to accept that this document was received by the defendant at or about the time of its publication.
22.That document will not be admitted into evidence.
Document [159] – [165]
23.This document is entitled “Asbestos” and appears to be a publication in a journal “National Safety News” published in August 1973. It deals with “recognised hazard to health when asbestos dust is inhaled excessively, causing asbestosis, bronchiogenic (lung) cancer and mesothelioma”. The plaintiff again submits that the document was discovered by the defendant and there is an available inference that it came into the defendant’s possession at or about the time of publication.
24.The plaintiff has not established that this is a business record for the purposes of s 45A and I again reject its inference submission.
25.This document will not be admitted into evidence.
Document [187] – [189]
26.This is a copy of a letter dated 18 December 1974 and two handwritten schedules. The letter contains the notation “PSE”. It is titled “Asbestos Dust Sampling - Torrens A” and refers to dust sampling being conducted on 6 December 1974. The handwritten schedules identifies where the sampling was undertaken.
27.This document is in my view a business record of the defendant. The defendant however submits that it is not relevant because it does not deal with the dangers of exposure to asbestos dust and does not relate to its Playford Power Station.
28.I find that the document is relevant for the following reasons (which formed the basis of the plaintiff’s submission):
·It shows that the defendant was conducting dust sampling on 6 December 1974 to determine the concentration of asbestos dust in air thereby proving that it had the capability of conducting such tests in the plaintiff’s working environment.
·The defendant was aware that fans could be used to remove the dust from the immediate work areas including in the plaintiff’s work environment.
29.That document is admitted.
Document [199] – [200]
30.This document is an address by Professor Irvine Selikoff to a Canadian Labour Congress on the health risks of asbestos in industry.
31.Again the plaintiff relies on the fact that the defendant has discovered this document and it contends that it is inconceivable that the AMWSU would not have forwarded it to the defendant at the time that it received it. It calls for the Court to draw inference that the defendant was in receipt of that document in or about 1975.
32.I reject this submission for the reasons explained in connection with Document [22] – [41].
33.This document is not admitted into evidence.
Document [256] – [263]
34.The plaintiff repeated its submissions in relation to document [22] – [41]. The defendant repeats its objection re same. On the basis of my finding in relation to that document this document is not accepted into evidence.
Document [288] – [304]
35.This document is entitled “Asbestos Strip-Off” “Code of Practice” “Removal of Insulation Materials containing Asbestos” “First Edition – August 1978”.
36.It is not apparent on the face of the document who produced it. The plaintiff asserts that it is clearly a business record of the defendant and that the defendant had discovered it. The plaintiff asserted that it related to a process of stripping asbestos insulation, a practice which was carried out by the defendant in all of its power stations. Again it asked the Court to draw an inference that the defendant became aware of it at or about the time of its publication.
37.There was no reference in the document to any power stations and I agree with the defendant’s submission that it cannot be inferred that it was a relevant document within the business of operating the defendant’s power stations.
38.It is not a business record for the purposes of s 45A and again I am not prepared to infer that document came into the possession or knowledge of the defendant at or about the time of its publication.
39.The document is not admitted.
Document [382]
40.This document relates to medical examinations of the defendant’s employees at Torrens, Playford and Osborne Power Stations and is on ETSA letterhead dated 23 February 1979. The plaintiff asserts that its relevance is that the defendant had actual knowledge that some of its workers showed signs that they had asbestosis and that this is clearly relevant to the quantum of exemplary damages.
41.The defendant concedes that this is a business record potentially admissible under s 45A. However, it asserts that the document (together with [383]) does not relate to the plaintiff and that both documents show that only one worker had signs of asbestosis. The defendant further asserts that the circumstances of that worker’s exposure are not explained and that one could not draw inferences absent properly established evidence.
42.Whilst the document may not carry much weight as far as the plaintiff’s claim is concerned I am prepared to accept that it is relevant and it is admitted into evidence.
Document [390]
43.This is a memorandum of interview the subject being a chest x-ray for a person “E Cilento” dated 7 March 12979. It is on the defendant’s letterhead. The plaintiff asserts that it is relevant as it proves that the defendant was aware that pleural thickening may be related to asbestos. Again the defendant asserts that the document relates to other employees.
44.Whilst it is not directly relevant to the plaintiff I am prepared to accept it into evidence though afford it little weight.
Document [393]
45.That document is headed “Extract from ABC News Morning Bulletin, Thursday 8 March 1979”. It refers to a union campaigning for the removal of asbestos from the defendant’s power stations. The document contains a handwritten notation, the meaning of which is not clear.
46.I find this is not a business record for the purpose of s 45A and again I accept the defendant’s submission in relation to the impermissible inference submission. The document is not admitted into evidence.
Document [394]
47.This document is a copy of an article published in the Advertiser newspaper on 9 March 1979. It reports the union reporting three cases of asbestosis being diagnosed by ETSA employees and of this being denied by ETSA’s General Manager.
48.The plaintiff asserts that a notation on the top right corner “PSE” stands for power standards engineer and that it is clearly a business record.
49.The defendant asserts and I agree that there is no such notation that is identifiable on the Court’s copy nor has the plaintiff established that it is a business record of the defendant.
50.The document is not accepted into evidence.
Document [432] – [441]
51.This document is entitled “National Health and Medical Research Council” “The Medical Aspects of the Effects of the Inhalation of Asbestos” “Adopted at the 88^th Session of Council, October 1979”.
52.The plaintiff asserts that the document was discovered by the defendant and is clearly a business record of the defendant.
53.I do not accept that the plaintiff has established that it is a business record for the purposes of s 45A. Again I accept the defendant’s submission in relation to the impermissible inference.
54.The document is not accepted into evidence.
Document [454]
55.This document is a departmental letter of the defendant dated 15 February 1980 and is titled “Airborne Asbestos Dust Determinations” “Waikerie Depot”.
56.It contains asbestos fibre concentration counts taken by the defendant in its Waikerie depot. The plaintiff’s solicitors concede that the plaintiff did not work at that depot. It asserts that the document is relevant also because it establishes that the defendant knew and was in receipt of NH&MRC publications.
57.The defendant concedes that this is a business record potentially admissible under s 45A. However, it asserts that the document is not relevant because it concerns a different workplace from that at which the plaintiff worked and in any event, it does not concern a powerhouse.
58.I reject the defendant’s submissions. This document does establish that in 1980, which was within the relevant period, the defendant was aware of issues concerning safety and the presence of asbestos in the workplace.
59.The document is admitted into evidence.
Document [496] – [510]
60.This document is titled “Code for the safe removal of asbestos – based thermal/acoustic insulating materials”. It is a document of the National Health and Medical Research Council and “Adopted by the 88^th Session of the Council, October 1979 and amended by the 91^st Session of the Council, June 1981”.
61.The plaintiff submits the document was discovered by the defendant and is clearly a business record of the defendant.
62.I do not accept that the plaintiff has established that this is a business record for the purposes of s 45A.
63.Again I accept the defendant’s submission in relation to the drawing of an inference.
64.The document is not accepted into evidence.
Document [516] – [533]
65.This document is titled “Torrens Island Power Station” “Guidelines for Working with Asbestos”. It is undated but refers to a date being 4 December 1981 as the date upon which a working party was formed to formulate a policy to ensure the safety of persons working at the Torrens Island Power Station working with or in the vicinity of asbestos products. Included in the document is a statement “The breathing of asbestos dust can cause serious lung disease”. It then makes reference to asbestosis, lung cancer, mesothelioma and other cancers and that the way to prevent them is to avoid breathing asbestos dust.
66.Again the plaintiff submits the document was discovered by the defendant and is clearly a business record.
67.The defendant concedes that this is a business record for the purposes of s 45A of the Evidence Act. It however submits that as it relates to the Torrens Island Power Station it is not of any relevance to the facts in issue in the plaintiff’s claim.
68.I reject the defendant’s submissions. This document does establish that in about 1981, which was within the relevant period, the defendant was aware of issues concerning safety and the presence of asbestos in the workplace and of appropriate measures to deal with risk.
69.This document is admitted into evidence.
Document [534] – [598]
70.This document has an Electricity Trust stamp on it and is headed “National Health and Medical Research Council” “Report on the Health Hazards of Asbestos”.
71.Again the plaintiff asserts that the document was discovered by the defendant and that it is inconceivable that the defendant did not receive it on or about the date of its publication in 1982.
72.Again I find that the plaintiff has not established this as a business record for the purposes of s 45A and I accept the defendant’s submission in relation to the drawing of an inference. The document is not accepted into evidence.
Document [663] – [681]
73.This is a document of the defendant’s titled “Torrens Island Power Station” “Guidelines for Working with Asbestos”.
74.This is an updated version of the document at page 516. For the same reasons this document is admitted into evidence.
Document [719]
75.This is a departmental letter of the defendant’s with some handwritten notations and headed “Playford Power Station” “Boiler Shop Asbestos Removal” and is dated 2 March 1987. It contains the following statement:
This is a very sensitive issue and it is essential that no officer visits site to do any costing work – at this stage. Hence the photos and drawings to enable ‘remote’ costing of the work. No discussions with any Trust Section or outside body should be initiated at this stage.
76.The plaintiff submits that this tends to show that the defendant took measures to conceal the fact that there was a problem with asbestos at the Playford Power Station.
77.Without more I do not think that inference can be drawn. I therefore reject the tender of this document.
Document [720] - [723]
78.This is a departmental letter of the defendant’s dated 13 March 1987 and is titled “Playford Boiler Shop Acoustic Wall Treatment”.
79.I find that this is a business record and it is accepted into evidence.
Document [726] – [728]
80.This document is headed “Playford Boiler Shop Acoustic Wall Treatment”.
81.It relates to the operation and maintenance of the Playford Boiler Shop. It refers to events that occurred in 1979 when the Union brought to the attention of the defendant the fact that sprayed asbestos on the boiler shop wall needed to be removed.
82.I find this is a business record of the defendant that is relevant and it is admitted into evidence.
Document [804] – [805]
83.This document sets out dust sampling results in a workshop where the plaintiff worked between 1979 and 1987.
84.I find it is a business record of the defendant and it is admitted into evidence.
Document [825]
85.This is a departmental letter of the defendant dated 27 June 1988 and is titled “Asbestos Removal Turbine Hall Playford Power Station Turbo-Alternators No 1 and 2”. The letter seeks approval to obtain process for the removal of asbestos at the Playford Power Station outside of the public tender process. Amongst the reasons put forward was “The asbestos issue is of a delicate nature and advertising its presence is considered unwise.”
86.This document is plainly a business record of the defendant.
87.The plaintiff contends that this indicates an attitude of ETSA concealing the presence of asbestos from its employees and should be admitted for that purpose.
88.The defendant submits that it is irrelevant because it does not give rise to that inference and it said: “ETSA employees were well aware by 1988 of the risks associated with asbestos”. It then contends that dust suppression and minimisation was something the plaintiff and other employees of ETSA had been practising for years.
89.The letter does demonstrate some desire to conceal the presence of asbestos. But it cannot necessarily be inferred that it was intended to conceal this from employees of ETSA. I therefore reject the tender of this document.