Ghaleb v Seltsam Pty Limited

[2004] NSWDDT 21

Dust Diseases Tribunal

of New South Wales

CITATION:	Ghaleb v Seltsam Pty Limited & Anor [2004] NSWDDT 21
PARTIES:	Ibrahim Ghaleb Seltsam Pty Limited Amaca Pty Limited
MATTER NUMBER(S):	107 of 2003
JUDGMENT OF:	Walker J at 1
CATCHWORDS:	:-
LEGISLATION CITED:
CASES CITED:
DATES OF HEARING:	24,25 & 31/05/04 & 05/07/04
DATE OF JUDGMENT:	07/14/2004
LEGAL REPRESENTATIVES:	FOR PLAINTIFF: Mr M Cahill instructed by Slater & Gordon Solicitors FOR DEFENDANT: Mr A Ventura instructed by Windeyer Dibbs Solicitors

JUDGMENT:

By further amended statement of claim dated 24 May 2000 the plaintiff sues alleging negligence and breach of statutory duty on the part of the first defendant in that the plaintiff was exposed to and inhaled asbestos dust and fibre in the course of his employment as a factory worker at the first defendants Rosehill premises where it manufactured asbestos cement product.

The plaintiff also sued the second defendant, making the same allegations of negligence but on the basis that the second defendant purchased the first defendant's asbestos cement business, including the Rosehill factory and became the plaintiff's employer on 1 August 1977.

On 24 May 2004 terms of settlement were filed as between the plaintiff and the second defendant for a verdict of $50,000 plus costs. The plaintiff now proceeds against the first defendant alleging that as a consequence of inhaling the asbestos dust and fibre he suffered injury in the form of asbestos related pleural disease and asbestos related pleural effusions. He also seeks an order pursuant to s 11A of the Dust Diseases Tribunal Act 1987 to protect his rights should he subsequently contract asbestosis, mesothelioma or asbestos related cancer. It is common ground between the parties that the injuries of which the plaintiff complains are divisible injuries or conditions.

The Defence

The first defendant does not deny duty of care to the plaintiff, the breach of that duty or the foreseeability of the plaintiff's injury and disability. What is squarely in issue is injury itself as well as damage and the role played by a raft of alleged non asbestos related confounders in the plaintiff's breathlessness. Finally the first defendant alleges that it was a concurrent tort feasor with the second defendant and the verdict already paid to the plaintiff fully discharges any liability to the first defendant.

The first defendant accordingly submits that should the Court find injury and damage as a consequence of asbestos exposure it will then be necessary to determine;

(a) whether the plaintiff has suffered a diminution of respiratory function;

(b) whether any such diminution has resulted in disability;

(c) the extent to which any such disability was caused by an asbestos related condition as opposed to any other unrelated conditions suffered by the plaintiff;

(d) the proportion of any asbestos related condition caused by the first defendant and/or the second defendant;

(e) whether there has already been a full and final satisfaction of any entitlement to damages as a result of the settlement with the second defendant.

The Interlocutory Ruling

At about 4 pm on the first day of the trial Mr Ventura for the defendant managed to extract during cross-examination of the plaintiff's thoracic physician, Dr Johnson, films in his possession of a CT scan of the plaintiff's chest dated 24 July 2003. He then moved the Court that the next witness, Dr Gardiner, the defendant's chest physician, be given possession of that scan prior to his giving evidence. That motion precipitated an interlocutory contest that raged over 46 pages of the transcript and lengthened the trial by a day. At p 110 of the transcript I made an interlocutory ruling in favour of the plaintiff denying Dr Gardiner access to the films and undertook to provide detailed reasons in this judgment.

When the smoke eventually cleared in this contentious application it became apparent that the issues were:

(1) The first defendant having put both injury and causation in issue relied to prove its case on the evidence of its medical witness, Dr Gardiner.

(2) Dr Gardiner had in his report of 24 July 2003 expressed the view from reading x-rays in 1998 and 2000 and 2002 that what the plaintiff's experts diagnosed as pleural thickening down the plaintiff's left lateral chest wall could be due to "fatty deposition that is so called companion shadows." The point of this distinction is that pleural thickening could be asbestos related and fatty deposits could not. The plaintiff's case that he was suffering from restrictive lung disability caused by ARPD rested on the existence of pleural thickening. The first defendant's forensic problem was that Dr Gardiner qualified his opinion about the fatty deposits by saying "A CT scan would be needed to differentiate those possibilities," and he was about to give evidence without having seen such a scan.

Dr Gardiner also expressed the opinion in his reports that even if pleural changes were causing some reduction in lung volume he did not believe that they were sufficient to be restricting pulmonary activity. His reasons for this conclusion are not evident from his written reports but at p 57.20 in his oral evidence Dr Gardiner explains that the x-rays before him suggested the chest walls were invaded but others suggested the costophrenic angle seemed to be clear, which would imply that the zone of apposition was not affected. In that case, in his opinion, the plaintiff's exercise capacity and expansion of the lung should not be affected very much. Thus the twin purposes of Dr Gardiner making his own reading of the film of the CT scan of 24 July 2003 was to ascertain firstly whether he disagreed with the radiologist, Dr Kossoff's opinion that it showed:

Changes consistent with asbestos related pleural disease with areas of bilateral pleural thickening and calcified pleural plaques on the right.

And secondly, with Dr Johnson's report of 10 May 2003 that:

There is blunting of the right costophrenic angle and pleural thickening laterally on the right lung.

As Mr Ventura conceded at p 94.19 his client's forensic purpose was to allow Dr Gardiner, who had not had the benefit of the more reliable CT scan to strengthen his theory that there was no pleural thickening and no blunting of the right costophrenic angle.

Having listened to the arguments and considered the case law, Supreme Court Rules and provisions of the Evidence Act 1995, to which I was referred, I eventually exercised my discretion against allowing Dr Gardiner access to the CT scan. My reasons are as follows:

1. Pt 36 r 13A of the Supreme Court Rules, which I might add is a provision designed to prevent trial by ambush in medical cases, relevantly provides: 13A(2) and (5) apply -

(a) To proceedings in the Court in which damages are claimed in respect of the death of a person or in respect of personal injuries; and.

(a) the oral expert evidence in chief of any expert is not admissible unless that evidence is covered by the experts report served in accordance with this rule;

(b) Neither an expert's report nor a hospital report is admissible when tendered under s 63 or s 64 ors 64 or s 69 of the Evidence Act unless it has been served in accordance with this rule.

2. The defendant has been aware of the existence of Dr Kossoff's report of the CT scan since August 2003 and it was served in September 2003. In the past 10 months the defendant took no action to subpoena the CT scan or require its production. Moreover the defendant took no action to put the issue of Dr Kossoff's misinterpreting the CT scan before the Court either by a subpoena to Dr Kossoff to give oral evidence or by cross-examination of Dr Johnson.

3. R 13A requires that the medical evidence be served well before the trial and subject to discretion renders late reports inadmissible. To allow Dr Gardiner to seek to discredit both Dr Kossoff and Dr Johnson's readings of the scan halfway through the trial after the plaintiff's expert evidence had been taken would have been grossly unfair to the plaintiff.

4. The only course that the Court could have taken that would have provided procedural fairness to the plaintiff would have been to adjourn the proceedings and to allow the plaintiff to recall Dr Johnson and Dr Kossoff and perhaps a further radiologist expert in special investigations of diseases of the lung. That would have involved considerable expense and delay perhaps to no purpose if Dr Gardiner, having studied the films, ended up agreeing with Dr Kossoff.

5. Little would be achieved by such an adjournment because Dr Gardiner basing his opinion on the x-ray evidence had already reached his conclusion that the plaintiff's experts had misread the x-rays and there was no pleural thickening or restriction of the right lung related to asbestos. In other words I took the view that the opening up of the question of the CT scan would be a waste of the Court's time as well as being procedurally unfair. In reaching that conclusion I also had in mind the provisions of s 135 of the Evidence Act 1996 which relevantly states:

135 General Discretion to Exclude Evidence

The Court may refuse to admit evidence if its probative value is substantially outweighed by the danger that the evidence might

(a) be unfairly prejudicial to a party or

(b) cause or result in undue waste of time.

For the reasons previously expressed I formed the opinion on the evidence before me that there was in fact a danger that the evidence might be unfairly prejudicial to the plaintiff and that it would result in an undue waste of time.

The Issues as to Injury, Causation and Disability

The first defendant constructs its lines of defence in this case as follows:

1. The plaintiff does not suffer from an asbestos related condition, because what the plaintiff alleges to be pleural thickening is simply pleural fat.

2. The plaintiff has not proved that asbestos related restrictive abnormality of the lungs is restricting his breathing.

This last submission is developed by introducing a plethora of arguments as to other possible causes proferred to arrive reductio ad impossibile at the ultimate conclusion that if there is any asbestos related disease it is de minimis. Those arguments proceed:

1. The parties are agreed that the plaintiff suffers from a mixed obstructive and restrictive abnormality of his lung function. They are also agreed that the obstructive component is not asbestos related. The lung function tests in evidence demonstrate that not only is the obstructive component more disabling but that since the last pleural effusion it is the only deteriorating factor.
2. The restrictive abnormality itself is not solely caused by pleural thickening. Rather there are a range of other non asbestos related and more serious contributing factors, namely,
· obesity,
· myocardial ischaemia,
· high blood pressure,
· epigastric discomfort,
· a crowded oropharynx and a bull neck,
· tracheomalacia,
· age related decrease in skeletal and myocardial mass.

The Law

This issue requires the application of the law relevant to cases involving multiple possible causes. It has given rise to a preliminary dispute between counsel as to the proper legal approach to the resolution of these issues particularly concerning the onus of proof. Before I address the merits of these issues I should first summarise the basic principles of tort law I propose to apply.

1. It is a basic principle of the law governing the recovery of damages that a claimant does not have to prove that an impugned event was "the" cause in the sense of the one and only cause, it is enough that the claimant shows that the event is "a" cause of the condition for which damages are claimed. (See March v Stramare Pty Ltd 1991 171 CLR 506, Medlin v State Government Insurance Commission 1995 ATR 81-322 at 61-138, Henville v Walker 2001 206 CLR 459 at 480).

2. The plaintiff bears the onus of proving on the balance of probabilities that the first defendant's tort caused or materially contributed to his injury loss and damage. (See Bonnington Castings Ltd v Wardlaw 1956 AC 613, March v Stramare Pty Ltd supra).

3. A negligent defendant must take its victim as it finds him and must pay damages accordingly. (See Watts v Rake 1960 108 CLR 158 at 160). If the injury proves more serious in its incidents and consequences because of the plaintiff's condition that does nothing more than increase the damages the defendant must pay. (See Dixon CJ in Watts v Rake supra at p 160).

4. If the contributing factors to the plaintiff's pulmonary dysfunction need to be disentangled and one or more traced to causes other than the first defendant's tort it is the defendant who should be required to do the disentangling and to exclude the operation of the accident as the contributory clause. There must be substantive evidence from the defendant which, if accepted, would establish with some reasonable measure of precision the nature and extent of the alleged confounding condition. (See Watts v Rake supra, Purkess v Crittenden 1965 114 CLR 164 at 168 and Shorey v P T Pty Ltd 2003 ATR 81-701 at par 46). It should be noted here that the onus being imposed upon the defendant relates to the evidentiary burden.

5. An inference of causation can be drawn from the circumstances of a case even where the medical opinion merely admits of a possibility. (See Australian Iron and Steel Pty Ltd v O'Connell 1959 102 CLR 522, Ramsay v Watson 1961 108 CLR 642 at 645.

6. The trier of factor is entitled to take a robust pragmatic approach to proof of causation. The inability to call lay or expert evidence that shows the precise way in which something happened is not fatal. (See Adelaide Steamship Company v Forst 1940 64 CLR 538).

7. If medical science says a causal connection is possible a judge may decide it is probable on the basis of the lay evidence but may not rely upon intuitive reasoning when the scientific evidence denies there is any such connection. (See EMI (Australia) Pty Ltd v Bes 1970 2 NSWLR 238).

Resolving the Causation Issues

(A) Does the Plaintiff Suffer ARPD?

The first defendant squarely puts in issue the question of damage. The first defendant submits

(a) the plaintiff does not suffer from ARPD.

(b) If the plaintiff has ARPD then it is not causing the requisite disability because it is not making a material contribution to his restrictive abnormality of lung function.

In Brear v The Commonwealth 1999 18 NSWCCR 637 President O'Meally at par 2 described the disease in the following terms:

ARPD is a generic description which covers a number of disorders of the pleurae Such description can refer to pleural thickening, diffuse pleural plaques or pleural effusion that is an accumulation of fluid between the visceral and parietal pleurae and includes the fusion of the pleurae occasioned by the formation of pleural plaques. As the disorders name plainly suggests it is caused by exposure to asbestos, though I think it generally to be accepted, as with some other asbestos related diseases, the precise pathogenesis or aetiology of ARPD is not scientifically certain. What is certain is that asbestos related pleural disease is caused by inhaled asbestos.

It is common ground that between 27 April 1971 and 15 August 1975 and again between 18 November 1975 and 31 July 1977 the plaintiff worked for the first defendant and was in a working environment where he inhaled asbestos dust and fibres. In Brear v The Commonwealth (supra) President O'Meally at par 39 held that all exposure is relevant to the causation of ARPD.

The first defendant does not raise the defence that the plaintiff's exposure was insufficient to cause ARPD, indeed the only issue about exposure relates to the relative exposure with the first and second defendants.

The Medical Evidence

The plaintiff's medical evidence is as follows:

· Dr Johnson in his medical reports and oral evidence opined that the plaintiff suffers from ARPD which he ascribes to diffuse pleural thickening due to Mr Ghalebs occupational asbestos exposure with both defendants. He goes on to say that he has ARPD and that condition is causing him disability in the form of a restrictive abnormality of lung function.

· Dr Saxton, a radiologist, in his x-ray report of 31 July 1979 noted, "Bilateral pleural plaques (evident since 1987) and extensive pleural thickening with opacities in the left upper lobe." On 21 August 1979 he carried out further x-rays concluding, "The left basal effusion is clearing and may well be due to asbestos pleural effusion."

· Dr Davis, a chest physician, in his report of 27 August 1979 opined it was likely that the plaintiff had an asbestos pleural effusion because it cleared without treatment. He said the plaques indicated exposure to asbestos.

· Dr Field, a chest physician, reported on lung function studies on 6 March 1980 stating, "It seems probable that this patient does in fact have pulmonary asbestosis although a relatively minor degree."

· Dr Saxton conducted further x-rays on 12 March 1981 concluding, "There is little more pleural thickening obliterating the right costophrenic angle than was evident in 1979."

· Dr Brook, an occupational physician retained by the second defendant, reported on 25 July 1985 opining, "His past history is suggestive of asbestos related pleural effusion which has resolved with resultant pleural thickening."

· A series of 11 certificates of disablement issued by the medical authority of the Dust Diseases Board dated between 29 May 1980 and 23 May 2002 variously declare that the plaintiff was suffering from, "Pleural asbestos" or "asbestosis". Those certificates assess a 10 per cent disablement and later a 20 per cent disablement.

· Dr Kossoff, a radiologist, reports on 24 July 2003 on a high resolution CT scan of the plaintiff's chest. She noted, "Changing consistent with asbestos related pleural disease with areas of bilateral pleural thickening and calcified plaques on the right."

· Dr Johnson in his report of 10 August 2003 diagnosed ARPD and assessed the disability arising from it as 25 per cent. He ascribed the plaintiff's diffuse pleural thickening to his occupational asbestos exposure. In his report of 17 May 2004 he assessed the plaintiff's impairment and disability arising from his restrictive lung disease at 25 per cent which was a component for pleural thickening.

The first defendant tenders the following medical evidence relevant to this issue.
· Reports of Dr Despas, a respiratory physician retained by the second defendant but who also treated the plaintiff. They are dated 26 July 1985, 20 August 1985, 20 October 1988, 31 October 1988, 17 November 1988, 2 April 1990, 24 December 1993, 7 January 1994, 25 February 1994, 15 December 1994, 18 August 2003. In his report of 7 January 1994 Dr Despas diagnosed, "Pleural plaques and some asbestos related pleural disease, meaning pleural thickening, which is probably contributing to some of his lung function impairment." In his report of 15 December 1994 he found changes in the x-rays due to asbestos exposure but said he told the plaintiff, "He just had bronchitis and asthma."
· Dr Carr, a radiologist, reported on a dynamic CT scan of 24 December 1993. He found changes consistent with asbestos related calcified pleural plaque.
· Dr Crawford, a respiratory physician with the Parramatta Chest Clinic, reported on 16 October noting, "A substantial symptomatic and functional deterioration in this man's respiratory condition." He had nothing to say about the relationship of asbestos to the respiratory condition.
· Dr Preda, a radiologist, reported on x-rays for 1 July 1997 and 21 June 1999. She found, "Pleural thickening along the lateral chest walls though Delta 1 here is optimal due to the superimposition of soft tissue the appearances raise the possibility of past asbestos exposure."
· Dr Gardiner, a chest physician, reported 24 July 2003, 5 December 2003, 18 February 2004 and gave oral evidence on 24 and 25 May 2004. In his report of 24 July 2003 he expressed the view after reading x-rays, in 1989, 1990, 1991, 1998 and 2000 that there was, "Mediastinal broadening which I believe is due to mediastinal fat deposition." He qualified this opinion by saying, "I don't have any CT scans to confirm that." He then considered the x-rays of 2 May 2002, which he said showed, "Broadened mediastinum bronchial wall thickening consistent with airways disease, bilateral pleural base shadows which could be due to pleural thickening or fatty deposition." He then said, "A CT scan would be needed to differentiate those possibilities." He concluded, the plaintiff did not have a significant asbestos related problem but added, "I would, however, like to view a high resolution CT scan of the thorax and a more up to date lung function test before I make a final decision on that."

· In his report of 5 December 2003 Dr Gardiner complained again to the first defendant's solicitors that he still had not seen the CT scan. In his evidence-in-chief on 24 May 2004 he agreed that Mr Ghaleb had both a restrictive and obstructive component to his lung problems saying he thought the obstructive component was due to asthma. He told the Court, "You could have degrees of pleural thickening which do not impact on lung function."
· At p 55.16 of the transcript Mr Ventura asked Dr Gardiner whether there was an objective way of delineating the percentage contribution made to the plaintiff's restrictive lung disability by obesity and pleural thickening. He replied at p 56.5, "It's difficult but I think the fact that this man's total lung capacity has been relatively the same going from 81 per cent of predicted in 1980 to 73 per cent of predicted in March 2003, that sort of reduction would be consistent with the rise in his weight from 98 kilos to 111 kilos." Dr Gardiner said at p 57.16, "So I am not able to say whether this means lung restrictions are more likely to be due to obesity or pleural disease or perhaps I might say equally but if the zone of apposition were not involved I would be reluctant to say that the asbestos related disease was a major contributing factor."
· Dr Gardiner told Mr Cahill that he did not use the ILO criteria for the definition of ARPD, indeed he was unsure whether they existed. He said the old definitions were, "Fraught with error" and people have moved, "to CT definitions where you measure the area 8 by 5 by .3 centimetres." At p 113.21 he agreed that if that measurement was met with pleural thickening of the right base of Mr Ghaleb's hemithorax then a diagnosis of ARPD would be justified, but only if, "It obliterated the zone of apposition and the costophrenic angle." Dr Gardiner told the Court that he gave no consideration to Dr Johnson's report in making his diagnosis. He also agreed at p 115.2 that he had never been provided with a CT scan, which was the best mechanism to enable a proper diagnosis.
· Mr Cahill showed Dr Gardiner the certificate of the medical authority dated 7 April 1994. He agreed he was a member of that panel and had certified that Mr Ghaleb was suffering a condition compensable under the Act. He then sought my leave to explain and at p 120.3 said, "The Board has a policy of where an award has been made a medical authority subsequently disagrees with it we wear that and we don't say to the patient we're going to take it back because we now think that the other doctors were wrong, so we have kept the award as it was determined by doctors in earlier years and it is put into inverted commas to signify to data gatherers that it is not a diagnosis that we agree with." Mr Cahill then showed Dr Gardiner the certificate of 23 May 1996. He agreed that he was a signatory to that certificate and had diagnosed pleural asbestosis. He asserted that the lack of inverted commas around that diagnosis was a clerical error. He also agreed at p 120.40 that he had certified that Mr Ghaleb had a 20 per cent disability but responded, "Yes, for a condition which I don't believe is a true condition."
· At P 121.27 he told the Court that there was no official record of the Dust Diseases Board's direction to the Medical Authority to sign certificates when they knew them to be untrue.
· At p 121.42 Dr Gardiner agreed that obstructive and restrictive lung defects operated together and a restrictive defect may act synergistically with a more significant obstructive defect. He also agreed it was possible that the overall level of disability that results as a consequence of the two defects combining may be increased one over the other or indeed by more than the sum of both. He further agreed at p 122.7 that a simple obstructive defect by itself would not be as disabling as for a person who has had the same level of obstructive defect with a restrictive defect superimposed. He also agreed that the restrictive defect could in some cases be the stick that breaks the camel's back.

Reliability of Dr Gardiner's Evidence

Mr Cahill submits that only to the extent that Dr Gardiner makes concessions favourable to the plaintiff should I accept his evidence because he has been proved to be a partisan witness. I regret to have to say that having listened to Dr Gardiner's evidence I must agree with Mr Cahill's assessment of him. The evidence reveals that Dr Gardiner has been a senior member of the Medical Authority of the Dust Diseases Board of New South Wales for many years. He was appointed to that learned body as a representative of employees and continues to sit in that capacity. On two occasions, namely, April 1994 and May 1996 he was a member of the Medical Authority when it solemnly certified that Mr Ghaleb not only had an asbestos related disease but that he suffered from a 20 per cent disability as a result of that condition.

It was disquietening for the Court to learn that notwithstanding the fact that Dr Gardiner was paid by the taxpayer's of New South Wales to represent employee interests, and on two occasions represented Mr Ghaleb's interests, he appears in this case retained by the first defendant as its only medical expert. Indeed, the only medical expert prepared to tell the Court that not only does the plaintiff not suffer from ARPD but that he has no disability that can be related to asbestos exposure. It was discomforting to hear Dr Gardiner tell the Court that the certificates he and his colleagues executed in April 1994 and May 1996 were false and known by them to be false at the time of signature. He explained to the Court that there was an unwritten policy of the Dust Diseases Board requiring the authority to execute such false certificates where it disagreed with the opinion of an early authority. He told the Court that these false certificates could be identified by the use of inverted commas around the diagnosis. Dr Gardiner agreed that the 1996 certificate had no inverted commas around its diagnosis but put that down to clerical error. I note from the tendered certificates that inverted commas were not used before 28 February 1994.

Mr Cahill characterises Dr Gardiner's explanation about the inverted commas as an unbelievable effort to explain the stark contradiction in the medical opinions he was expressing as the employees' representative and the opinion he is now expressing as the first defendant's retained expert. Mr Cahill also points out that Dr Gardiner has in his sworn evidence changed his story as to the purpose of the inverted commas. Dr Gardiner's first explanation of the use of commas comes in his written report of 5 December 2003 where he explains that the word "asbestos" was placed in inverted commas because at that point in time ARPD was not a disease recognised under the Act. He said that such workers did not really have asbestosis but ARPD. Then during cross-examination when confronted with his two certificates one using the word "asbestos" and the other not he changed his story to explain that inverted commas were put in to signify that it was not a diagnosis with which the authority agreed. That account does not explain why both certificates also certify that the worker has a 20 per cent asbestos related disability. There are no inverted commas around that part of the certificate which strongly suggests to me that the original account in the medical report is the most likely.

The Supreme Court Rules which bind the deliberations of this Tribunal require a written declaration from experts that they have read and agreed to be bound by the Code of Conduct set out in the schedule to the Rules. Sch K (2) and (3) state:

2. An expert witness has an overriding duty to assist the Court impartially on matters relevant to the expert's area of expertise.

3. An expert witness' paramount duty is to the Court and not to the person retaining the expert.

My impression of the evidence of Dr Gardiner is that he sees his paramount duty is to the person retaining him. I appreciate that the medical and legal professions approach ethical issues from very different perspectives. Conflicts caused by professionals serving the interests of opposing parties in the same legal case naturally have low priority in the ethics of a profession who daily confronts questions of life and death. A doctor's perspective is keenly focused on issues concerning the physical health of his or her patient. It is unusual, but not rare, in compensation and personal injury litigation to find the same doctor has given reports on the same patient for both sides of the case. What is rare is that those opinions are, firstly, contradictory, and secondly, follow the interests of the party retaining the doctor. No doubt the public of New South Wales would be concerned to hear Dr Gardiner's evidence that medical experts retained by the Dust Diseases Board are prepared to give false diagnoses and false assessments of disability to meet policy directives of the Board. I find it incredible that such a direction would be given or that a body of such eminent medical practitioners would comply with it. My conclusion is that Dr Gardiner is partisan and I do not accept his evidence insofar as it conflicts with the medical certificates he has signed in April 1994 and May 1996. I should add that I would not have accepted Dr Gardiner's evidence on causation and disability in any event because -

· It was not based on the more accurate CT scans.

· It was at times equivocal.

· It is contrary to the overwhelming weight of the other medical evidence in the case.

Taking all the evidence into consideration, on the balance of probabilities I determine that as a result of his exposure to asbestos fibre and dust during his employment with the first defendant the plaintiff sustained the following damage:

(1) Asbestos related pleural disease.

(2) A restrictive abnormality of his lung function resulting in diminution of respiratory function and disability.

B. Extent to which Disability was caused by the Asbestos Related Condition

There is a contentious legal dispute that goes to the proper manner in which the Court should deal with alleged non asbestos related confounders such as airways obstructive disease, obesity, hypertension, a bull neck, sleep apnoea and aging. It was Mr Ventura's submission that once this Tribunal puts a figure on the extent of the plaintiff's pulmonary dysfunction then it is obliged to assess and then deduct all the other non asbestos related confounders that go to the plaintiff's breathing problems. His ultimate submission is that when this process is carried out then the Tribunal will find that what is left from the asbestos related condition is de minimis and consequently non compensable.

Mr Cahill's response is that once the plaintiff establishes that the first defendant's tort caused the plaintiff's restrictive lung disability then the evidentiary onus falls upon the first defendant to bring evidence which will permit the Court to legally disentangle other contributing factors which the first defendant alleges are not caused by its tort and so exclude them from the assessment of damages.

The most expeditious manner in which to deal with these questions is to determine, firstly, the question of whether the confounders in contention have been successfully disentangled by the first defendant and so excluded as asbestos related contributory causes to the plaintiff's restrictive lung condition. As I read the authorities the defendants evidentiary onus cannot be simply discharged by bringing medical evidence that asserts that medical science does not recognise that exposure to asbestos can be causative of the confounding condition. Disentanglement in the tort of negligence also involves proof to a reasonable measure of precision that the confounder has made a relevant contribution to the disability and identifying to the satisfaction of the Court the nature and extent of that contribution.

1. Obesity

I have extracted from expert evidence the following statements that go to the issue of whether or not the plaintiff's obesity is making a material contribution to his restrictive lung disability.

· Dr Field in his report of 10 June 1980 says, "It is possible that his marked breathlessness on exertion is due at least to his marked obesity."

· Dr Johnson in his oral evidence 24 May 2004 at p 41.29 said, the two processes causing the restrictive impairment were the diffuse pleural thickening and obesity. At p 41.46 he agreed that in general an increase in weight of 11 kilograms over five years could have a deleterious effect in terms of lung function. However, when asked for an apportionment at p 42.2 he described any attempt to determine that relative contribution of the obesity and the pleural thickening as "complete guesswork" and then "I don't know what the proportions are." At p 43.16 Dr Johnson was asked if the patient had put on 11 kilograms over 15 years and his abnormality increased was that circumstance consistent with the weight having an effect on the restriction. He responded, "I don't know if it tells much about the contribution of the two, the other thing is that when they lose weight whether their restrictive abnormality improves." At p 43.25 I pointed out to Dr Johnson that between December 1990 and December 1994 there had been a weight reduction of 7 kilograms. He commented that although the plaintiff's weight increased by 9 kilograms between 1991 and 1994 his FVC remained basically the same.

· Dr Despas expressed the view in July 1985, "He does smoke and I think we're looking at a combination of airflow obstruction and lung restriction relating to his obesity." Mr Ghaleb, of course, did not smoke. In October 1988 Dr Despas said, "Probably his weight and a few other factors have contributed to this." In November 1988 Dr Despas noted the plaintiff was more symptomatic diagnosing the problem of a combination of obstructive lung disease and some restrictive lung disease and his weight "which had been stable since 1985." It was not until December 1993 that Dr Despas belatedly learned that the plaintiff was not a smoker.

· Dr Gardiner in his report of 5 December 2003, "I agree that the obstructive component is attributable to asthma and the restrictive abnormality would be consistent with ARPD and his obesity."

The medical experts are in agreement that it is possible that the plaintiff's obesity is a factor contributing to his restrictive lung problems. The authorities, however, require the first defendant to do much more than just point the finger at obesity as a likely contributor; they require that it be disentangled from the ARPD. To my mind that involves firstly concluding that the obesity is not related to asbestos exposure, secondly determining that obesity has in fact contributed to the plaintiffs restrictive condition and thirdly assessing the extent of that contribution.

There was no evidence of the plaintiff's weight prior to the pleural effusions in 1978 and 1979. Dr Brook, the second defendant's chest specialist, in her letter of 8 August 1979 does not mention obesity, nor does Dr Davis on 27 August 1979 or Dr Farag on 27 February 1980 or Dr Field on 6 March 1980. Indeed, the first mention of the word is in the report of Dr Field, which is dated 10 June 1980. The lung function test of 1 February 1980 provides a weight of some 98 kilograms, which was 13 kilograms lighter than he is now. There is no evidence as to the point when a man of Mr Ghaleb's weight and age becomes so obese that his breathing is affected. Dr Johnson agreed in his evidence that a man who becomes breathless on exertion and consequently unable to exercise will find it very hard to keep the weight off. He suggested stapling Mr Ghaleb's stomach as a solution. The point Mr Cahill makes here is there may well be a causal connection between the cycle of loss of lung function, increase in weight and consequent further loss of lung function. He describes this as a vicious circle.

Notwithstanding that the first defendant's evidence is very light on when it comes to ruling out the possible connection between the ARPD and weight increase the plaintiff has not sought to rely upon that point. The evidentiary issue upon which Mr Cahill relies to assert that the Court cannot be satisfied that disentanglement has been proved is the admission by the medical experts that it is impossible to put a figure on the contribution if any that obesity has made to the restrictive condition revealed in the lung function testing.

When pressed to say what contribution obesity was making the experts ducked for cover. Dr Johnson declared the question to "complete guesswork" and Dr Gardiner said it is difficult to come to a percentage contribution (page 56.5). Dr Despas, who never seemed to be able to understand the plaintiff, began with the thesis that his problems were asthma and obesity related but as the tests came home retreated from both those suggestions.

If the medical experts say it is possible that obesity was a factor making material contribution to the restrictive condition then the Court may, if there is support from the lay evidence, find it to be probable. Mr Ventura turns to the lung function testing in PX.3 and suggests the Court can draw conclusions from those statistics. He submits there is ample evidence to discharge his client's evidentiary onus to be found there, namely:

(1) There is evidence that the plaintiff's weight has increased in recent years.

(2) Dr Crawford told him to see a dietician and lose weight in December 1996.

(3) The evidence of Dr Johnson is that the plaintiff's asbestos related condition has been stable since 1985 so his dramatic increase in disability since 2000, particularly over the last 18 months, cannot be attributed to the ARPD. The only factor that has increased in his weight which has risen to 111 kilograms.

The Lung Function Testing Table PX3

To understand this table one needs to refer to the explanation of its terms and symbols provided by Dr Johnson at p 33 onwards.

FVC equals forced vital capacity and is the amount of air the plaintiff could breath out from a full inspiration.

FEV(1) equals forced expiratory volume and is the amount of air the plaintiff blows out in one second.

FEV(1):FVC ratio is the percentage comparison between two expirations. In a normal person of the plaintiff's age the norm should be 80 per cent, a ratio below 50 per cent is evidence of obstructive airways disease.

TLC equals total lung capacity and is the total amount of air the plaintiff has in his lungs when he takes a deep breath. It is greater than FVC because there is always some air left in the lungs when you breath out.

VC equals vital capacity and is tested by asking the patient not to blow out hard but to take his time.

RV

equals residual volume and is the amount of air left in the plaintiff's lung when he breathes right out. The best way to identify the restrictive element according to Dr Johnson is to study the TLC. Dr Johnson referred to the tests at p 36 making the following points.

· The best test of the obstructive component is the FEV(1):FVC ratio. Mr Ghaleb's readings were constantly below the norm of 80, having low points in 1989 at 58.4 and 2002 at 55 per cent.

· The restrictive element is determined by reference to the TLC but there is a 20 per cent allowable range above and below norm. The TLC has been gradually dropping as the following readings reveal.

Year	TLC
1980	81.8 per cent
1985	81 per cent
1988	77 per cent
1994	75 per cent
2003	73 per cent

Dr Johnson said the first reading outside normal range was in 1988 about 10 years after the pleural effusions. It is also interesting to compare the plaintiff's weight over the same period with the TLC.

DATE WEIGHT TLC

09.11.88 100 kilograms 77 per cent

04.12.89 102 kilograms nil

02.12.91 95 kilograms nil

04.01.94 104 kilograms 75 per cent

28.02.94 104 kilograms nil

10.04.96 103 kilograms nil

27.04.98 106 kilograms nil

02.05.98 106 kilograms nil

11.03.03 111 kilograms 73 per cent

The plaintiff increased his weight over five years between 1988 and 1994 by 4 kilograms and his TLC dropped a mere two percentage points. In the seven years between 1996 and 2003 his weight increase was double that yet the drop in TLC was again only two percentage points, strongly suggesting to me that there may not be a link between the weight increase and the change in TLC.

Dr Johnson was not persuaded by Mr Ventura's theory that a large weight increase with a corresponding large TLC increase meant the weight was causing restrictive disability. (See p 43.20 and p 43.3). He took the view that the only change that would impress him as definitive would be a large reduction in weight followed by the restriction going away completely.

The forensic reality here is that while the medical experts accept that it is possible that obesity can restrict a patient's lung function they have no idea whether that is actually the case with Mr Ghaleb and are not prepared to say that it is probable or put a figure on it . The lung function test tables are very inconclusive on this point and Dr Johnson says they cannot be relied upon in this way.

Taking all the evidence into consideration on the balance of probabilities I determine that the first defendant has failed to discharge its evidentiary onus to disentangle the obesity confounder and to prove either that it is making a material contribution to the plaintiff's restrictive lung condition or with any precision prove the extent of that contribution.

Myocardial Ischaemia and Hypertension

Dr Patel, the cardiologist, assessed the plaintiff on 2 February 1994. He had no history of hypertension, diabetes or rheumatic fever and said Mr Ghaleb did not smoke and his alcohol consumption was modest. Dr Patel was not sure of a diagnosis of myocardial ischaemia because the EEC was inconclusive but thought there might be a small area of ischaemia, (which I understand to be an obstruction of flow of arterial blood.)

On 5 May 2001 the plaintiff saw another cardiologist, Dr Mardini, after a sestambi scan. The scan revealed no evidence of ischaemia. Dr Mardini could find no abnormality. On 8 December 2001 Dr Mardini performed an Echocardiogram which showed "Mild left ventricular hypertrophy." He felt this finding was “reassuring”. Another echocardiogram was taken on 12 July 2003 again finding, "Left ventricular hypertrophy." At p 51.19 to 22 of the transcript Mr Ventura questioned Dr Gardiner about these findings, asking him whether they had any significance so far as breathlessness was concerned. Dr Gardiner said at p 51.19:

When I examined his blood pressure it was, I think, 160 on 90, which is high. There is also evidence from Dr Patel that the high blood pressure had led to thickening and enlargement of the left ventricle and as a consequence that ventricle has become stiff, what we call diastolic non compliance. The consequence is that blood flowing into the heart gets banked up in the lung and causes breathlessness.

Cross-examined by Mr Cahill at p 123.34 Dr Gardiner conceded that the sestambi scan did not reveal any significant evidence of myocardial ischaemia. Dr Gardiner also agreed that Dr Mardini said that the plaintiff's main problems in exertion was dyspnoea. He also agreed the plaintiff had no palpitations, prescyncopl episodes or arrhythmia. He also agreed that the only treatment offered to the plaintiff by Dr Mardini was referral for a CT scan of his chest to explore lung function further and a sleep study. He finally agreed that hypertension can be controlled by medication.

It is clear from this evidence that the plaintiff's heart problems are minor and easily controlled by medication. Taking all the evidence into consideration on the balance of probabilities I find that the first defendant has not discharged its evidentiary onus to prove that myocardial ischaemia, left ventricular hypertrophy and hypertension are factors making a material contribution to the plaintiff's breathlessness.

Epigastric Discomfort

Dr Patel on 18 August 2003 reported the plaintiff was suffering epigastric discomfort but states, "I cannot give you an explanation. I do not believe it is due to any lung disease." Again the first defendant has failed to discharge its evidentiary onus.

Obstructive Sleep Apnoea

In his report of 21 July 2003 Dr Gardiner notes the plaintiff wakes at night unable to breath and snores very loudly. The plaintiff's evidence is that he underwent a sleep study at Camperdown Sleep Disorder Centre in 1996 under the care of Dr Crawford, who confirmed he had sleep apnoea.

An nasophayngoscopy performed by Dr Collett revealed a marked and generalised narrowing of both the naso- and hypopharynx typical of obstructive sleep apnoea. Dr Crawford reported on 11 December 1998 that the plaintiff was able to walk for 10 minutes on the flat without significant dyspnoea and was no longer experiencing choking episodes or apnoea at night.

Taking all the evidence into consideration on the balance of probabilities I determine that the first defendant has failed to discharge its evidentiary onus to prove that the plaintiff's apnoea has made a material contribution to either the plaintiff's obstructive or restrictive lung conditions.

Bull Neck and Tracheomalacia

Dr Gardiner raises the relevance of the plaintiff's alleged bull neck and crowded oropharynx in his report of 10 December 2002. Dr Crawford in his report of 16 October 1995 describes the oropharynx as, "Grossly narrowed." However, in his report of 11 December 1996 he states, "This man's airflow obstruction has come under good control." Dr Crawford in his report of 3 April 1996 also raises the possibility of, "A degree of tracheomalacia" (which I understand to be damage to the tracheal wall.) He thought that might be causing airflow obstruction problems. I take this to refer to the obstructive not restrictive problem. Dr Johnson in his evidence did not agree that Mr Ghaleb had a bull neck. Dr Gardiner does not assert that the alleged bull neck is a discrete factor contributing to the breathlessness.

Mr Cahill submits that this is a very minor matter in the scheme of confounders and should be put aside. I agree. Taking all the evidence into consideration on the balance of probabilities I determine that the first defendant has not discharged its evidentiary burden to prove that the bull neck or the tracheomalacia are making a material contribution to the plaintiff's obstructive or restrictive breathing problems.

Orthopaedic Problems

The plaintiff's evidence is that he has arthritic problems in his arms and legs and takes analgesics to relieve the pain. Whilst in extreme cases spinal pain can effect breathing Mr Ventura does not seriously raise this issue in submissions as a factor contributing to Mr Ghaleb's breathing problems.

Relative Contribution of Obstructive Disease and Restrictive Condition to Plaintiff's Disability

The plaintiff concedes that the obstructive airways disease, which seems primarily to be asthma and perhaps bronchitis is a factor which has made a contribution to the plaintiff's mixed obstructive and restrictive lung defect. The plaintiff does not concede that the first defendant has discharged its onus of proving disentanglement.

Dr Johnson at p 45.3 said he had not used the AMA guidelines but assesses that the plaintiff has lost 60 per cent of his lung function from the combination of the obstructive and restrictive defects. His best guess was that obstructive component represented 35 per cent and the restrictive component 25 per cent. Dr Gardiner on the other hand had signed a certificate in 1996 that the plaintiff's asbestos related condition represented a 20 per cent loss. Dr Gardiner was encouraged by Mr Ventura to put a figure for the Court and at p 54.27 he replied, "Well, I think in most cases the severity of the airways obstruction would far outweigh the restriction element unless it was gross, and I don't think it's gross in this case." At p 55.8 he went on to explain that it was very difficult to determine the likely percentage contribution of each component, there is no perfect test.

In his submissions Mr Cahill makes the task of the Court even more difficult because he challenges the assumption in Dr Johnson's figures that each condition could be simply untangled by giving a value which added up to the total loss of pulmonary function. Mr Cahill laid the ground for his submission in his cross-examination of Dr Gardiner and his examination in chief of Dr Johnson.

At p 48.44 Dr Johnson agreed that the relationship between the obstructive and restrictive defects was not a simple one, that can be easily separated out. Indeed, he agreed the defects were acting together and could have a synergistic effect of the two working together to produce an overall greater restriction than the sum of the two acting alone. He also agreed that it was not possible to rule out one from the other in the function of breathlessness.

At p 121.49 Dr Gardiner also agreed with the proposition that obstructive and restrictive disabilities act synergistically. He did not necessarily agree that the outcome of the two acting together always would be greater than the sum of both but he did agree such an outcome was a possibility. He also agreed that the obstructive defect by itself would not be as disabling as when it has the restrictive defect superimposed upon it and that the restrictive defect could be regarded as the straw that breaks the camel's back.

This Tribunal is of course familiar with the synergistic interaction between tobacco smoke and asbestos fibres in asbestos related cancer cases. The point of this submission is that if the two factors are working together to produce an enhanced result then the relative contributions are irrelevant because the combination is indivisible. Mr Cahill, relying on the evidence of Dr Gardiner and Dr Johnson puts the legal proposition that if the medical evidence says it is possible that the plaintiff's asbestos related restrictive condition and his obstructive airways disease are acting synergistically to cause his pulmonary dysfunction then in all the circumstances the Court can find that it is probable. Having done so it should then find that the first defendant has failed to discharge its evidentiary onus to disentangle the dual confounders. The question for the Tribunal therefore is whether the obstructive airways disease and the restrictive conditions are working together to produce the loss in function. The medical evidence says that it is a possibility and I propose to apply commonsense to the chain of causation to determine whether it is a probability. The chain of causation as I read the evidence is as follows:

1. Prior to 1977 the plaintiff had the occasional respiratory problem such as colds but did not suffer breathlessness or chronic obstructive airways disease such as asthma or bronchitis.

2. Between 1978 and 1979 the plaintiff suffered two asbestos related pleural effusions affecting both lungs and leaving him with pleural thickening, rind and pleural plaques in both lungs. Those pleural effusions had cleared by the end of 1979 but they left a legacy of pleural thickening and pleural plaques in both lungs.

3. Dr Farag and Dr Field early in 1980 said the plaintiff had been suffering bronchitis and a wheezing chest ever since early 1979.

4. The evidence suggests the plaintiff was treated for chronic bronchitis by his GP and later Dr Despas between 1980 and January 1994 when his condition no longer responded to the bronchodilators and he began to be treated for chronic asthma.

5. For reasons I will express later in this judgment I do not accept the evidence of Dr Brook as proving a pleural effusion on the right side about 1985.

It is evident from this chain of causation that the plaintiff's symptoms are suggestive of the obstructive airways disease commencing shortly after the radiology opines the pleural effusions were clearing or about the time the pleural plaques and pleural thickening was identified. It beggars belief that chronic obstructive airways disease would coincidentally appear in the lungs of a man who had suffered no such previous disorder at the very time he experiences restrictions in his lungs. Commonsense suggests to me that there must be some relationship between the two. Medical science does not accept that asbestos fibres cause obstructive airways disease but the medical evidence before this Court acknowledges that it is possible that a synergistic relationship could nevertheless exist between the two conditions. Commonsense also suggests that the fact that the chronic airways disease has not resolved and continues to deteriorate despite years of treatment could be related to the influence of the continuing restrictive condition.

Taking all the evidence into consideration on the balance of probabilities I determine that the plaintiff's asbestos related restrictive lung condition is working synergistically with his obstructive airways disease.

Having reached that conclusion I am left with synergistically acting conditions that cannot logically be disentangled using Dr Johnson's approach of separately assessing each condition and adding them together to attain the 60 per cent loss of pulmonary function revealed by the lung function tests. There is no other evidence as to how this entanglement might be achieved. Mr Cahill submits that if the first defendant is unable to separate the compensable from the non compensable then the presumptio hominus has not been discharged and in the absence of evidence that reasonably and fairly enables the Tribunal to make the necessary distinction then the first defendant must pay for the lot.

Mr Ventura relies on the plaintiff's admission that the obstructive airways disease is not asbestos related and it has made a relevant contribution to the total loss of pulmonary function. In his general submission Mr Ventura pointed out the principle of the law of damages that the victim's of tort should not be over compensated. I take it that what he is suggesting here is that the Court, absent any satisfactory medical evidence to facilitate the disentangling should nevertheless should do justice by giving it a go. That is an approach that would normally appeal to me, even though on the state of the evidence the assessment of the relative contribution of the two elements is very much a stab in the dark. However, the High Court in Purkess v Crittenden and in Shorey v PT Pty Ltd makes it clear that the task required is one of disentanglement with some reasonable measure of precision not just a conclusion that one of the factors might not be related to the first defendant's tort. Such a process of necessity involves the Court prescribing a percentage contribution that the obstructive element is making to the total loss of pulmonary function as it works together with the restrictive element to produce the total loss. The problem with synergistic relationships, as this Tribunal has found in the interaction between tobacco smoke and asbestos fibre is that it is the combination of the two elements that produces the total loss not the relative contributions they individually make to pulmonary dysfunction. It may well be as Dr Gardiner suggests that they cannot be disentangled scientifically. The point is that absent evidence as to how disentanglement might properly occur I am unable to carry out that task.

According, taking all the evidence into consideration I take the view that the requisite disentanglement has not been proved by the first defendant and I must find on the state of the evidence that the plaintiff is entitled to the full loss.

Age Related Restrictions

Mr Cahill conceded that the vicissitudes of time on Mr Ghaleb's body, particularly as he reaches old age involves a deterioration of both his skeletal and myocardial mass contributing to his loss of pulmonary function and breathlessness. He also agreed that loss is not asbestos related. However, Mr Cahill does not concede that the first defendant has discharged its onus of proof, rather he points out two factors that need to be considered by the Tribunal before it makes its decision as to whether or not a deduction should be made for past age related loss of pulmonary function.

1. The loss of pulmonary function has been calculated in this case by reference to the lung function tests, (PX.3.) When one studies the basis upon which those tests were made in the lung function comparison chart it is clear that in calculating the norm the plaintiff's age has been already taken into account. This is evident from the changes in prediction levels which allow for deterioration over time in the background levels of human performance. Mr Cahill has considerable experience in interpreting lung function tests and Mr Ventura does not seek to deny the truth of his submission. I note that the predictors in the test put in evidence change as Mr Cahill asserts.

2. The principle in Watts v Rake needs to be applied because Mr Ghaleb was about 50 years of age when he had his effusions and 56 when his restrictive disability became evident and would already be somewhat decayed when it comes to his skeletal and myocardial masses.

Given that the calculation of Mr Ghaleb's dysfunction is being made on the basis of tests that already take into account his age related breathlessness by comparing his lung function test results to a man of his own age I agree that it would be double dipping for the first defendant to receive an allowance for the aging effect in respect of past disabilities. The plaintiff's advancing age when he was injured by the first defendant's tort only reinforces that point.

Accordingly I propose to make no deduction for the plaintiff's age related restrictive disability in respect of the claims for past damages.

The Second Defendant's Tort

It is Mr Ventura's submission that I should find the first and second defendants are concurrent tortfeasors. He refers the Court to learned articles by Mr Andrew Broadfoot, solicitor, on multiple defendant litigation and the rule against double recovery (See 2002 10 Torts Law Journal) and Mr Peter Kane on multiple torts contribution and the dynamics of the settlement process (1999, 7 Torts Law Journal).

The common law draws a distinction in cases involving multiple torts between joint tortfeasors and concurrent tortfeasors. Joint tortfeasors are liable for the same tort and the same damage while concurrent tortfeasors are liable for the same damage but different torts. Mr Ventura asserts that because the torts are concurrent and the damage is the same the rule against double recovery applies and the plaintiff's verdict against the second defendant should be deducted from any verdict the plaintiff secures against his client.

Mr Cahill rejects Mr Ventura's submission that the defendants are concurrent tortfeasors, submitting that this is a case of successive torts where the damage is not the same and no deduction should be made. He refers to the decision of President O'Meally in Brear v The Commonwealth (supra). There Mr Brear, who worked for Halvorsens on naval vessels owned and used by the Commonwealth of Australia sued the Commonwealth and the asbestos producers James Hardie & Co Pty Ltd and Seltsam Pty Ltd after he developed ARPD. The Tribunal's approach to the claim against the Commonwealth was to assess its damages separately from the other defendants.

I agree with Mr Cahill's submission. Mr Ghaleb worked for discrete employers at different times, albeit at the same place. The damage he sustained was caused by the exposure to different asbestos dust and fibre at different times. It cannot be said to be the same damage. The rule against double recovery only applies when damage is the same. The Court is therefore not able to entertain in this claim arguments about the verdict obtained by the plaintiff against the second defendant. The Court is concerned here with the award of damages for damage sustained by the plaintiff solely as a result of the first defendant's tort.

Having said that I must say that the assessment of necessity involves consideration of the causation of the plaintiff's asbestos related damage to ensure that that damages are not sheeted home to the first defendant for damage caused by the second defendant's tort. In making this determination the Court is concerned, firstly, with the issue of latency periods and secondly with the issue of exposure to asbestos including arguments about the relative times of exposure and the nature of the asbestos to which the plaintiff was exposed in each employment.

The Latency Period

The only medical expert to give evidence about the latency period in this case was Dr Johnson, who at p 4.13 said:

In general pleural effusion has been described five or six years after exposure up to about twenty to twenty-five years.

In Brear's case Dr Lee, whose views were adopted by President O'Meally, said that benign pleural effusion occurs sometimes within ten years but a latency of less than twenty years is rare. President O'Meally also took the view that it is more likely that early exposure would be the cause of the condition. The evidence in this case is that the plaintiff commenced work for the first defendant on 27 April 1971 and worked for the second defendant between 1997 and November 1986. On the basis of Dr Johnson's evidence concerning latency periods the earliest work for the defendant could have caused pleural damage would be about mid 1978 and the earliest pleural damage could have resulted from the second defendant's employment was late 1982 or early 1983.

Both Mr Ventura and Mr Cahill, for their own forensic reasons, suggested that the damage occurred consequent to two pleural effusions in about 1979 and 1985. What the tendered medical evidence shows is as follows:

· Dr Brooks records that Mr Ghaleb's personal files reveal a normal x-ray in 1971.

· Dr Saxton's chest x-ray of 7 July 1979 shows, "dense left pleural fluid or thickening has developed in the past 12 months." There was also evidence of right pleural plaques.

· Dr Saxton's chest x-ray report of 31 July 1979 notes bilateral pleural plaques were evident in films taken in 1978. Since then pleural thickening has developed with opacities in the left upper lobe.

· Dr Saxton's chest x-ray of 21 August 1979 notes the left basal pleural effusion is clearing and may well be due to asbestos pleural effusion. Dr Davis confirmed this view in his report of 27 August 1979.

· Dr Saxton's x-ray of 3 December 1979 concluded there was no evidence of further resolution of the left lateral pleural thickening but saw bilateral persisting pleural plaques.

· Dr Farag on 17 February 1980 noted the plaintiff was suffering acute bronchitis with a wheezing chest.

· Dr Field in a report of 6 March 1980 reads checks chest x-rays to confirm diffuse pleural changes and diagnose pulmonary asbestosis. On 10 June 1980 he noted respiratory symptoms over the past twelve months.

· On 5 June 1980 the Medical Authority of the Dust Diseases Board diagnosed pleural asbestosis and a 10 per cent disability.

· Dr Saxton's report on the chest x-ray of 12 March 1981 concluded there was a little more pleural thickening on right side obliterating the costophrenic angle.

· Lung function studies on 1 February 1980 and 26 February 1980 found lung volume reduced.

· An exercise test by Dr Warner on 26 February 1980 revealed chest tightness after 5 minutes.

· The Medical Authority issued further certificates on 11 March 1982 and 8 November 1984 for asbestosis with a 10 per cent disability.

Dr Brook in a report of 25 July 1985, which has led counsel to conclude that pleural effusion occurred about then, states:

His past history is suggestive of high line pleuritis complicate (asbestos related pleural effusion with resultant pleural thickening). The present history is suggestive of a similar process occurring on the contralateral side alternatively some or all of the changes could be due to some other pathology or pleural fat.

When one fully analyses Dr Brook's report it can be seen that she takes the following history;

1. Mr Ghaleb was extensively investigated between 1978 and 1980 for a presumed left pleural effusion.

2. The plaintiff had no specific chest symptoms when examined on 25 July 1985.

3. The 1985 spirometry tests were poor due in part to obesity and poor English comprehension.

4. The poor FVC results were "Due to presumed pleural changes which are occurring."

5. The radiography was difficult to interpret.

6. Clearly there are no signs of effusion and crepitation were not heard.

It appears from reading Dr Brook's report of 26 July 1985 with the chronology handed to me by the plaintiff that a Dr Gandevia x-rayed the plaintiff's chest on 23 May 1985. Unfortunately that report is not in evidence. Presumably it is the basis of Dr Brook's speculation as to whether it shows right pleural thickening or mere pleural fat. Dr Brooks immediately raised this issue with Dr Despas who on 26 July 1985 responded to her saying:

There haven't been any changes in the x-ray appearances since around 1981 and if anything at all is present it's simply some pleural thickening perhaps on the left and also perhaps on the right side.

Dr Johnson in his report of 17 May 2004 after reviewing the same material states at p 3:

Mr Ghaleb appears to have had two episodes of pleural effusion one on the left and on the right. They have left him with pleural thickening.

What he does not say is when they occurred. What is clear from a more careful reading of Dr Saxton's radiological reports is that pleural plaques have been evident on the right since 1978, moreover, his report of 21 August 1979 refers to, "A little right upper zone scarring with pleural thickening in the horizontal fissure" which he thought had been present since 1978.

Dr Davis records in his report of 27 August 1979 that the film in July 1979 showed pleural effusion on the right but had almost completely resolved by August 1979.

Dr Saxton's reports of 23 March 1981 noted pleural thickening obliterating the right costophrenic angle was evident in December 1979.

Dr Brook's assessment on 25 July 1985 is based on "The present history" not a review of the radiology.

Taking all this evidence into consideration on the balance of probabilities I find that pleural effusion of both the plaintiff's lungs occurred between 1978 and December 1979 with consequential pleural thickening developing in both lungs.

Dr Kossoff's CT scan of 24 July 2003 found changes consistent with pleural thickening and calcified on the right but not the left.

The conclusion I draw from the available evidence is the only pleural effusions occurring in this case fell within the latency period of the first defendant not the second defendant. Dr Despas in his report of 26 July agreed with that view of the radiology. The point is that the Court is concerned with damage and the consensus of the medical evidence is that the only damage which could be causing the restrictive condition is pleural thickening, rind and plaques. All of that damage was evident in late 1979 and as Mr Ventura was heard to point out on many occasions, that damage appears to have been radiologically stable ever since, even if the disability has increased.

There being no pleural effusions at a time after the second defendant's latency period commenced to run, (about 1983) then it is highly unlikely on the balance of probabilities that exposure to asbestos with the second defendant could be held responsible for the damage, notwithstanding the principle in Brear's case that all exposure is relevant to the causation of ARPD. This finding is consistent with the evidence of the plaintiff's early exposure to large quantities of raw asbestos in the first year of employment with the first defendant.

Accordingly I do not propose to make any deduction in this case to take into account damage allegedly sustained by any tort of the second defendant.

Assessment of Restrictive Loss

The only evidence before the Court assessing the plaintiff's loss of lung function as a result of the first defendant's tort is that of Dr Johnson, who assesses:

1. A total loss of lung function of 60 per cent.

2. He then divides that total into obstructive airways disease 35 per cent and restrictive impairment 25 per cent.

3. He would then further divide the 25 per cent restrictive element between obesity and pleural thickening but could not put a figure on that apportionment.

I found that the first defendant has failed to discharge its evidentiary onus to disentangle the non asbestos related confounders, notably the obstructive airways disease, obesity and age related deterioration but also the other possibilities such as sleep apnoea, bull neck, neural pain, tracheoomalacia, hypertension, et cetera.

The outcome is that the plaintiff, having discharged his onus and proved the first defendant's tort caused his ARPD and consequently his restrictive lung condition manifesting as breathlessness is entitled to damages from the first defendant for his total loss of pulmonary function. The only evidence that I accept that assesses that loss is that of Dr Johnson who says it represents a 60 per cent impairment of the plaintiff's lung function.

Taking all the evidence into consideration on the balance of probabilities I find the plaintiff has proved that the first defendant's tort has left him with a 60 per cent lung impairment.

DAMAGES

Comparative Verdicts

Notwithstanding the decision of the High Court in Planet Fisheries Ltd v La Rosa 1968 119 CLR 118 Mr Ventura urges the Court to bring in a verdict for general damages commensurate with that awarded in the tendered cases of Nasr and Russell. In the case of Mr Nasr the verdict was $41,320 and Mr Russell $25,000. I appreciate that Court of Appeal in Wallaby Grip v Pierce 2000 NSWCA 299 held that it was not a breach of the principles enunciated in Planet Fisheries if a trial judge utilises the knowledge of this specialist Tribunal as well as his own general experience about verdicts. That corporate knowledge and experience would include, for example, decisions such as Gyptopoulos v Corporate Ventures Pty Ltd & Ors 1 November 2002 unreported Johns J DDT446 of 2001 where general damages of $160,000 were awarded and Isaac v Hastings Co-operative Ltd 18 October 2001 unreported Duck J DDT87 of 94 where general damages of $100,000 were awarded. With respect I do not propose to take Mr Ventura up on his offer to indulge in the exercise of comparing and contrasting the sufferings of individuals. What the law requires is that the amount of damages I assess be fair and reasonable for the plaintiff's injuries and disabilities. My verdict must be proportionate to the particular circumstances of Mr Ghaleb's case and not to the situations of other litigants, notwithstanding the similarities counsel might derive from reviewing other awards of damages.

Vicissitudes

Mr Ventura submits that the plaintiff is 72 years old and otherwise troubled by a variety of medical problems and that an appropriate discount for their effect on his age and general health would be 25 per cent rather than the usual 15 per cent. Discounting is commonly used in assessment of damages for economic loss resulting from personal injury to take into account contingencies. Mr Ventura submits that this Tribunal should be making a large discount to take into account the lengthy list of confounders I have previously determined. Unfortunately for the first defendant with the exception of the age related deterioration my findings are that the first defendant has either failed to prove them to be causing disability or failed to exclude them by disentanglement. In the circumstances I will only be applying the usual discount in this case.

Loss of Expectancy of Life

The plaintiff is 72 years of age and has a normal life expectancy of a further 12 years. There is no suggestion in the medical evidence that his life will be prematurely cut short either by the ARPD or by his other medical conditions. There is, of course, a risk he will develop mesothelioma but Dr Gardiner estimates that is only 0.3 per cent.

General Damages

I have determined that the plaintiff suffers from a 60 per cent permanent impairment of his lungs. The lung function studies reveal the impairment is gradually worsening. The loss is very substantial and approaching the point where the plaintiff becomes an invalid. It is easy for judicial officers to appreciate the exquisite pain as a mesothelioma invades a plaintiff's chest wall assaulting the nervous system. However, as my learned colleague his Honour Judge Armitage pointed out in Russell v Cockatoo Dockyard Pty Ltd for those who struggle with breathlessness even mild symptoms are a significant burden unappreciated by those of us lucky enough to be able to breath without conscious thought. For sufferers with a 60 per cent loss of lung function the burden is frightening, painful and discomforting. Mr Ghaleb's symptoms have been with him since 1978 although they did not became severe until 1988. He also suffered two painful effusions and their sequelae, which he has chosen to have assessed separately to his breathing disability. Unlike most sufferers of ARPD he has had a very short latency period which has lengthened the period of breathlessness he has had to endure. He has already suffered for 25 years and has a further expectancy of 12 years.

The parties are well apart on the issue of assessment of damages. So far as the effusions are concerned Mr Cahill suggested $15,000 for the first and $5,000 for the second while Mr Ventura opted for $5,000 each. I agree with Mr Ventura on this assessment.

So far as general damages to compensate the plaintiff for his breathlessness and disability is concerned Mr Cahill submits $100,000 while Mr Ventura points to judgments where the outcome was only $40,000. Over 37 years those outcomes would represent damages of $1,081 per year for Mr Ventura and $2,702 per year from Mr Cahill. It should be noted that the plaintiff's more serious breathlessness manifested about 1988. The picture is one of deterioration which has become much more serious in recent years and very serious indeed if we look to the prognosis of the future.

Taking all the evidence into consideration I think that the appropriate award for general damages for breathlessness should be $100,000.

Interest

I propose to divide past and future damages equally because it is obvious from the pattern of the plaintiff's developing restrictive problems that the loss of lung function was mild in the early years, but has become more severe in later years and no doubt will become much more serious in the future.

Griffiths v Kerkemeyer Damages

The plaintiff's loss entitles him to past and future damages for services that need to be provided for him. The first defendant submits that there is no evidence of the need for care that would justify the plaintiff's claim. Mr Cahill points to the following evidence:
· The plaintiff's evidence is that he struggled with his disability until 1 July 2000 at which point his family intervened and arranged a carer to come to the family home to attend to the personal care of both himself and his wife. For three years that carer came twice a week and thereafter has attended four times a week for a total of 5 hours a week. In addition the plaintiff's daughter-in-law does the heavier cleaning such as washing windows, mopping floors and cleaning bathrooms for one and a half hours per week. Finally his sons help with the shopping, that is the heavy shopping and travel to medical appointments, churches, social events, et cetera. The plaintiff's evidence is that he had to abandon his former role as a handyman and as a gardener. The plaintiff has tendered evidence from an occupational therapist who provides a 39 page report dated 27 August 2003. That report sets out the needs of the plaintiff both past and future.
· Mr Ventura again relying on the multiple confounders he has referred to submits that there should be a large discount for those conditions as well as a large discount for the vicissitudes that will confront a man of Mr Ghaleb's age in the next 12 years. The first defendant has been unable to disentangle the major confounders, namely, obstructive airways disease and obesity and has failed to prove that the minor ones other than aging has made a significant contribution to the breathlessness. There will have to be a small deduction in the future for the age related condition and I have determined to discount any awards for economic loss by the usual 15 per cent for vicissitudes.

Past Needs

Taking all the evidence into consideration I assess the plaintiff's past needs as follows:

(a)Domestic Care

Competing reports from occupational therapists are in evidence but Mr Ventura does not submit that the plaintiff's claims insofar as they relate to the nature of care, hours required or rates for service are unreasonable. The calculations therefore are as follows:

Period 1 1 July 2000 to 1 July 2003.

Domestic Assistance

The claim is 156 weeks or 2.5 hours per week at $25 per hour plus GST or $10,725.

Maintenance Assistance

The claim is 156 weeks for .75 hours per week at $25 per hour plus GST or $3,218.

The total care for this period is $13,943,

Period 2 . 1 July 2003 to 1 July 2004.

Domestic Assistance

The claim is 52 weeks for 4 hours per week at $26.50 per hour plus GST or $6,063.

Maintenance Assistance

The claim is 52 weeks for .75 hours per week at $26.50 per hour plus GST or $1,137.

The total care for the period is $7,200

The combined past care therefore is $21,143.

Future care

Domestic assistance

The claim is for 624 weeks for an average 5 hours per week at $26.50 per hour plus GST or $90,948.

Maintenance assistance

The claim is for 624 weeks for 1.5 hours per week at $26.50 per hour plus GST or $27,284.

Total future care is therefore $118,232.

As indicated I propose to discount this amount, firstly, by 5 per cent for the age related disability, and secondly by a further 15 per cent to take into consideration vicissitudes. The discounted figure is $94,586.

Sullivan V Gordon Damages

The plaintiff who because of the first defendant's tort has lost the capacity to care for his invalid wife who suffers from Parkinson's disease is entitled to be compensated for the cost of that care. The medical evidence of Dr Brimmage as well as the plaintiff's evidence reveals that since July 2000 the plaintiff has not been able to attend to his invalid wife's personal hygiene, toileting and dressing. Further, since 2003 it has been necessary for the plaintiff to employ professional carers 4 hours per week. The evidence suggests that Mr Ghaleb would not, had he been uninjured by the first defendant's tort, have been unable to personally care for his wife beyond July 2009. The calculations are therefore:

Past Care

The claim is 4 hours per week at $25 per hour for 156 weeks plus GST or $15,756.

Future Care

The claim is 5 hours per week at $25 per hour for 260 weeks plus GST or $35,750.

The total care is therefore $51,506. Again I propose to discount future by 20 per cent making a finding of $41,205.

The Table of Damages.

General damages .
· First effusion $5,000
· Interest at 4 per cent for 25 years $5,000.
· Second effusion $5,000
· Interest at 4 per cent for 25 years $5,000.
· Breathlessness et cetera $100,000.
· Interest at 2 per cent on half the sum for 16 years $ 16,000.
· Total general damages $136,000.

Griffiths v Kerkemeyer Damages

Past care - $ 21,143

Future care - $ 94,586

Total- $115,729.

Interest at 4 per cent for four years- $ 3,383.

Total Griffiths v Kerkemeyer damages- $119,112.

Sullivan v Gordon Damages

· Past care $15,756.

· Future care $41,205.

· Total $56,961,

· Interest at 4 per cent for four years $2,521.

Total Sullivan v Gordon damages $59,482.

The total sum of all damages $314,594.

Orders

1.The plaintiff is entitled to a verdict for $314,594 provisional damages plus costs.

2.Pursuant to s 11A of the Dust Diseases Tribunal Act 1989 I order that the plaintiff is entitled to claim further damages at a future date if he should develop any of the following asbestos related diseases;

· Asbestosis

· Mesothelioma

· Asbestos related cancer

Mr M Cahill instructed by Slater & Gordon Solicitors appeared for the plaintiff

Mr A Ventura instructed by Windeyer Dibbs Solicitors appeared for the defendant