Ridgway v Amaca Pty Ltd - [2004] NSWDDT 42

Dust Diseases Tribunal

of New South Wales

CITATION: Ridgway v Amaca Pty Ltd [2004] NSWDDT 42

PARTIES: Richard Wakefield Ridgway
Amaca Pty Limited

MATTER NUMBER(S): 375 of 2002

JUDGMENT OF: Walker J at 1

CATCHWORDS: :-

LEGISLATION CITED:

CASES CITED:

DATES OF HEARING: 23/02/04, 17/03/04, 23/06/04 & 14/09/04

DATE OF JUDGMENT:
11/02/2004

LEGAL REPRESENTATIVES:
FOR PLAINTIFF: Mr G F Little, SC instructed by Watkins Tapsell
FOR DEFENDANT: Mr G Watson, SC instructed by Phillips Fox Lawyers

JUDGMENT:

THE CLAIM.

1. This is an action in negligence by Richard Wakefield Ridgway against Amaca Pty Limited. The plaintiff alleges that the action arises in consequence of his exposure to and inhaling of asbestos dust and fibre in the following circumstances:

1. As an assistant and bystander to the construction of his home on his sheep property over a period of 10 weeks in 1970. The plaintiff alleges that 254 sheets of asbestos manufactured by the defendant were used by the builders in the construction of the home. It is the plaintiff’s allegation that the handling, sawing cutting and fixing of those sheets produced asbestos dust and fibre to which he was exposed. He further alleges that he unloaded semitrailers containing that asbestos sheeting. He also alleges that he carried the off cuts from the sheets to a dump on his property to dispose of them and cleaned up after the builders including sweeping up asbestos dust.

2. In July 1982 he personally constructed an extension to the home using asbestos sheeting manufactured by the defendant. That work involved unloading sheets from a truck, shaping and cutting them with a high-speed angle grinder, fixing the sheets onto the frames and cleaning up afterwards.

3. Between 1980 and 1990 he purchased asbestos water pipes manufactured by the defendant for use as sheep troughs. He used an angle grinder to cut those pipes into lengths producing dust, which he inhaled.

4. He also changed asbestos brake linings he alleges were manufactured by the defendant.

5. The plaintiff claims that the various activities described above exposed him to the inhalation of asbestos dust and fibre causing the development of, pleural thickening and pleural plaques which have reduced his total lung function by 15 per cent.
6. It is the plaintiff's submission that his injuries were suffered as a result of the defendant's negligence arising out of its breach of a general duty of care as the manufacture and supplier of asbestos products to take reasonable precautions to avoid foreseeable risk of injury.

THE DEFENCES.

2. The defendant admits that in 1970 and 1982 it manufactured various cement building materials containing asbestos. It also admits that the plaintiff suffers from pleural thickening and pleural plaques. However the defendant asks the court for a verdict in its favour on the following grounds:

3. Watson SC puts the basis for this defence is as follows:

· This is a South Australian tort to which the limitation laws of that state apply. Pursuant to section 36 of the Limitations of Actions Act 1936 claims for damages in respect of personal injuries must be commenced within three years of the cause of action accruing.

· The statement of claim was issued on 9 September 2002.This means that the cause of action could accrue no earlier than 9 September 1999. Yet a CT scan in 1992 revealed that the applicant had asbestos on his lungs. Clearly the plaintiff needs an extension of time.

· Extensions of time are not granted as a matter of course.S 48 (4) of the South Australian Act provides that where an extension of time is sought, the action may become commenced in the normal manner, but the statement of claim must be endorsed with a statement to the effect that the plaintiff seeks an extension of time. This was not done and the omission is fatal to the plaintiff's case. Moreover, Mr Ridgeway does not qualify for an extension of time because:

(a) although s 48 (1) grants the power to the court speaking in the language of general discretion, this is heavily modified by the requirements of s 48 (3) (b) (i);

(b) s 48 (3) (b) (i) requires an applicant for an extension of time to prove firstly that the applicant has not ascertained some material fact and secondly that the proceedings were commenced within 12 months after ascertaining that material fact;
(c) for the purposes of s 48 a fact is not regarded as material unless it forms an essential element of the cause of action or would have had major significance on the assessment of the plaintiff's loss. There is no evidence that the plaintiff later became aware of a material fact to warrant an extension of time.

· An extension of time always carries an onus of showing that the justice of the case requires an extension to be granted, and that this cannot be done in circumstances where there would be prejudice to the defendant. Here there is prejudice because records have gone missing and there is continuing confusion surrounding diagnosis of the plaintiff's condition.

2. Exposure.

4. The plaintiff's exposure to asbestos is extremely low. On the scientific evidence adduced, the cumulative dose is likely to be less than 0.02 Fibre/mL/years. Further, all of this dose cannot be attributed to asbestos containing products for which the defendant can be legally responsible.

3. Injury.

5. Only part of the plaintiff's current serious health complaints can be attributed to asbestos. The better evidence does not even support that proposition. The only fully informed medical opinion namely that of Dr Antic does not attribute symptoms as a consequence of asbestos inhalation.

4. Liability.

6. No compensable injury is attributable to asbestos inhalation.

5. Damages.

7. An element of the damages claimed by the plaintiff is based on the probability that he is going to run into trouble with his asbestos related condition which will likely deteriorate leading to a reduction of life expectancy. Watson SC narrowly interprets this part of the claim as a request for damages reflecting the risk of contracting mesothelioma or lung cancer. He submits that damages for such risks are unavailable at law and that there is no evidence to support such a claim in any event.

8. With regard to the claim for economic loss the defendant firstly suggests that it should be substantially reduced by taking into account other conditions from which the plaintiff suffers which have a considerable potential to interfere with his capacity to work. It is suggested that the claim is exaggerated by as much as 50%.

9. In regard to the Griffiths v Kirkemeyer damages the defendant suggests that an appropriate allowance for the asbestos related component of the requirement for future care would be 30% of the amount claimed taking into account the degree of likelihood of the plaintiff's condition deteriorating to the stage that such care becomes necessary.

A. IS THE CLAIM STATUE BARRED?

10. Little SC makes the preliminary point that the defendant’s case is based on two irreconcilable propositions namely:

1. Watson SC’s submission that the better view of the evidence ( that is acceptance of the opinion of Dr Antic) is that the plaintiff has no symptoms attributable to the consequences of asbestos inhalation.

2. S 36 of the South Australian Limitation of Action Act 1936 applies because the facts are clear from the CT scan of 9 September 1992 and the plaintiffs evidence that he “ran out of puff” in March 1999 that he suffered asbestos related damage and his cause of action occurred more than 3 years before he commenced these proceedings on 9 September 2002.

11. Mr Little notes that s 36 of the South Australian Limitations Act provides that an action for damages for personal injuries shall be commenced within 3 years after the cause of action accurred. He submits that because a cause of action for negligence cannot accrue until the plaintiff has suffered compensable damage arising out of the defendant’s tort the first question this Tribunal should be addressing is whether or not the plaintiff has been damaged by the defendant’s tort. If the answer to that question is in the affirmative then the Tribunal can then move on to identify the point in time that the plaintiffs claim accrued and then make a decision as to whether a s 48 extension of time is required. I agree and propose to defer the issue of the applicability of the Statue of Limitations.

B. WAS THE PLAINTIFF INJURED BY THE DEFENDANTS TORT?

12. The plaintiff’s case is that he suffers from the medical conditions pleural thickening and pleural plaques caused by inhaling asbestos dust and fibre from the use of the defendants products in the construction of his home its extension and water troughs. In addition to his own evidence he relies upon the expert medical evidence of Dr Porter and Professor Alpers.

13. The defendant relies upon the expert medical evidence of Dr Antic which Watson SC asserts, as a matter of law, this Tribunal should find is the only fully informed medical opinion. Dr Antics ultimate opinion does not attribute Mr Ridgeways symptoms as a consequence of asbestos inhalation.

14. It is appropriate therefore that before entering into a detailed analysis of the medical experts differences of opinion that I should determine Watson SC’s preliminary point that the only admissible evidence is that of Dr Antic because a finding to that effect must result in a verdict for the defendant.

Was Dr Antic the only fully informed medical witness?

15. Underlying this courageous submission is the defendant’s contention that the plaintiff’s symptoms of breathlessness are readily explicable on the basis of long standing constitution health problems unrelated to asbestos. Those alleged confounders are obesity spinal pain, osteoarthritic chest pain, abdominal adhesions and pneumonia.

16. The defendants submission is that with all these possibilities present is was vital that Mr Ridgeway gave a complete and accurate history to his medical experts but he failed to do so.

17. Watson SC alleges that the plaintiff’s histories were incomplete and inaccurate in the following respects:

· The plaintiffs told Professor Alpers on 9 January 2003 that “he had no chest pain on a chronic basis” ( T 73.1)

· He said “his general health is good” ( T 73.7)

· He gave no history of chronic abdominal pain due to abdominal adhesions

· The plaintiff gave Dr Alpers and Dr Antic insufficient information about other possible causes of his pleural effusion such as pneumonia or infections causing them to wrongly assume that the cause of his pleural effusion was asbestos inhalation.

18. Having considered all the evidence I have formed the view of the evidence that this preliminary point of law is misconceived and without merit. My reasons are as follows:

1. Watson SC builds his case for a verdict for the defendant on the ground that both Dr Porters and Professor Alpers evidence is either inadmissible or having been admitted should be given no weight on what he describes as “ a Makita v Sprowles question of the admissibility and acceptability of evidence which is given in the light of an incorrect history”. Although he did not take the Court in his submissions to the relevant part of Justice Heydons judgment in Makita v Sprowles (2001) 25 NSWCCR 218 he did give me a hint (at T 105.48) by suggesting that there was also a Ramsay v Watson (1961) 108 CLR 642 question about the validity of the evidence given in the absence of a proper history.

Bugg v Day (1949) 79 CLR 442 at 462

19. At [66] Justice Dixon referred to Ramsay v Watson where the circumstance was that the assumed facts upon which the expert wanted to base his opinion had been ruled inadmissible. In other words there was no probative evidence before the court upon which the opinion could be based.

20. Justice Heydon concluded that underlying Justice Dixons conclusion “must be the proposition that so massive a disconformity between the facts to be assumed on the basis of the 21 histories and the total failure to seek to prove them justified total rejection of the evidence”

21. However Justice Heydon then went on to discuss in [67} Justice Dixons famous remarks at page 645 namely:-

“That some medical witness should go into the box and say only that in his opinion something is more probable than not does not conclude the case. A qualified medical practitioner may, as an expert express his opinion as to the nature and cause, or probable cause, of an ailment.
But it is for the jury to weigh and determine the probabilities. In doing so they may be assisted by the medical evidence. But they are not simply to transfer the task to the witnesses. They must ask themselves “Are we on the whole of the evidence satisfied on a balance of probabilities of the fact?”

22. I believe Watson SC’s case to be misconceived firstly because the case law does not require every plaintiff to give a complete and accurate history to each and every one of the medical experts before those experts reports are admissible. Plaintiffs are usually lay persons with little medical knowledge and a complete medical history is seldom obtained unless the medical practitioner goes to extraordinary lengths in questioning the patient. Few, if any medical reports would be admitted of Watson SC’s test were rigidly applied. Justice Heydons test on the other hand speaks of a “massive disconformity”.

23. The critical factual dispute on the medical evidence in this case is the true nature of the pleural effusion that occurred in 1999. Dr Antic suggests it was caused by pneumonia or other infection, Dr Alpers suggests it was asbestos and pneumonia and Dr Porter says it was asbestos related. With respect, Watson SC’s characterisation of Dr Alpers and Dr Porters histories on this point as incomplete and inaccurate cannot be correct. I say that because:

· Dr Porters report of the 30.5.02 takes a history of “pneumonia as a child and possibly 6 episodes of pneumonia in total throughout his life” and “the chest x-ray (i.e. July 1999) suggested pneumonia and a four week course of antibiotics (Augmentin) was given following which there was a gradual resolution of symptoms and reduction in sputum production”. There was no mention of the clinical notes of Dr Shanahan or Dr Quigley but demonstrably Dr Porter had a history of the bout of pneumonia about the time of the effusion and of the sputum. He had ample evidence to consider the possibility that the pneumonia may have caused the effusion. There can be no suggestion here that there was no evidence upon which to base the decision that the effusion was asbestos related.

24. Similarly Dr Alpers in his report of 9.1.03 at page 2 said, “He has had pleurisy and pneumonia 3 years ago and was hospitalised at the Cummins Hospital”. If that was insufficient evidence to base an opinion then Watson SC cured that problem when he cross-examined Dr Alpers on 23 June 2004 (at T 75 to T 78.) Dr Alpers made it clear that he was well aware of the pneumonia and considered then rejected the possibility that the effusion in 1999 was solely related to the infection.

25. Watson SC also put to Dr Alpers the other possible confounders upon which his client relies namely chronic osteoarthritic pain, chronic chest pain and chronic abdominal pain. His opinions do not assist the defendant’s case but they are based on his clinical examination, the plaintiff’s medical history and his reading of the radiology and lung function testing. The court is entitled to take them into consideration along with those opinions expressed in his written reports. Dr Porter in his report of 30.5.02 took a history of the cholecystectomy (which related to the abdominal pain) and the sternum pains thought to be osteoarthritic. He didn’t mention the low back pain but even Dr Antic qualifies his view that musculoskeletal pain can cause restrictive lung deficit with the words “under the right circumstances” and does not allege such circumstances existed in Mr Ridgways Case.

26. In summary I take the view that the plaintiff’s doctors had adequate histories upon which to form the opinions they expressed on the question of the causal relationship between the plaintiffs injury and asbestos. Accordingly I do not propose to reject their evidence and order a verdict for the defendant as requested by Watson SC.

26. The plaintiff presses his claim that as a result of his exposure to asbestos dust and fibre from asbestos products manufactured and supplied by the defendant he has suffered injury in the form of pleural plaques over 10-20 per cent of his lungs and pleural thickening caused by an asbestos related pleural effusion. He further asserts that these medical conditions have produced his breathing problem, which is the result of a restrictive lung deficit. The plaintiff makes the concession that his asbestos related injuries are not the only cause of that restrictive deficit conceding that his obesity is also making a relevant contribution to the breathlessness.

27. The defendant presents a complex defence viz:

1. The better view of medical evidence is that asbestos inhalation was not a causal factor in the development of the plaintiff’s breathlessness.

2. There are multiple possible causes of the plaintiffs breathlessness namely: -

· Pleural thickening caused by an effusion which was the result pneumonia

or some other bacterial or viral infection in 1999-2000.

· Obesity

· Chronic chest pain caused by osteoarthritis

· Chronic low back pain

· Chronic stomach pain.

3. On any view of the evidence the plaintiff’s exposure to asbestos was extremely low. The only scientific evidence before the court puts the cumulative dose at much less than 0.02 fibre \ ml\ years

THE PLAINTIFFS MEDICAL CASE

1. Dr Porter.

28. The plaintiff relies firstly on the evidence of the Adelaide respiratory physician Dr Porter who in his report of 30.5.02 after clinical examination, consideration of the plaintiffs medical history and studying the radiology and lung function testing made the diagnosis that the plaintiff has asbestos related pleural plaques and left lobe fibrotic changes consistent with restrictive lung deficit and asbestosis. He also expressed the opinion that obesity was making a contribution to the plaintiff’s restrictive deficit but said the asbestos related component was greater than 50 per cent. In a further report-dated 6.8.02 Dr Porter said the plaintiffs pulmonary function tests revealed moderate restriction. The CT scans reveal pleural plaque, particularly at the left base and scarring in the left lower lobe not necessarily consistent with asbestos as a cause.

2. Professor Alpers

29. The plaintiff also relied upon the evidence of Professor Alpers, which comes in form of written reports dated 9.1.03; 20.2.03; 26.6.03; 21.8.03;11.3.04 and oral evidence given on 23.2.04.

30. In his report of 9.1.03 after clinical examination, taking a medical history studying the radiography and lung function testing Professor Alpers expressed the opinion that the plaintiff suffered from:

· Benign asbestos pleural disease

· Asbestos related pleurisy

· Obesity

31. He estimated a 30 per cent loss in lung function of which 15 per cent related to the plaintiffs asbestos related pleural disease. He expressed the view that of the coexisting diseases suffered by the plaintiff only the mild obesity was a significant contributor to his restrictive deficit.

32. In his report of 20.2.03 Dr Alpers commented that a TLC reduction to 74 per cent does suggest a moderate restrictive deficit. Considering the radiology and the previous pleural effusion, some band shadows in the left lung with volume loss in the left lobe he maintained his 15 per cent asbestos related disability assessment.

33. In his evidence in chief on 23.6.04 (at T 70.03) he described the plaintiff’s exposure to asbestos as mild to moderate. At T 70.38 he explained that the “asbestos rind” suffered by the plaintiff was a thickening of the skin surrounding the lungs and is a condition which is quite generalised throughout the lungs. The effect of the rind on the pleural cavity is that the lungs are hard to expand particularly during exercise and that accounts for some of his symptoms. Dr Alpers said he described the exposure to asbestos as moderate because the history was the plaintiff “did a lot of sweeping and cleaning up which stirs up a large amount of fibres together with increases in ventilation multiplying significantly the load of fibre. The plaintiff also used angle grinders, which are notorious for producing large amounts of dust close to the face.

34. With regard to the plaintiff problems with pneumonia Professor Alpers said (at T 72.9) that pneumonia is one of his major risks, Because of the abnormalities of his pleural cavity he has a problem clearing mucous. If he was to get bronchitis it would be likely to progress to pneumonia.

35. In cross examination Professor Alpers:

· At T 73.28 agreed that obesity can cause restrictive illness.

· At T 73.29 agreed that neural pain will interfere with lung function tests and said testing is normally deferred if the patient is in pain. At T 73.37 he characterised Watson SC’s assertion that spinal pain can cause restrictive deficit as “really stretching things a little bit” He said you would need to be suffering a very advanced condition such as ankylosing spondylitis, thoracic spine fusion or an abnormality interfering with the phrenic nerve before the diaphragm would be affected. He agreed that if the osteoarthritic condition was being treated with large doses of narcotics that would also affect ventilatory function.

· At T 74.20 Professor Alpers rejected Watson SC’s proposition that osteoarthritis of the sternum or ribs could cause a restrictive deficit. He had not heard of such a condition in 42 years of practice. Osteoarthritis of the sternum which is a fixed structure would not produce such a restrictive condition. If the rib cages became completely rigid with osteoarthritis then a restrictive deficit could be produced but he had never seen such a condition.

· At T 75.2 Professor Alpers said that chronic abdominal pain on a semi permanent basis requiring 4 hourly administration of narcotics would cause a restrictive deficit

· At T 75.42 Dr Alpers agreed that pneumonia can cause pleural effusion. He also agreed that coloured sputum was associated with bacterial infections. At T 76.19 Dr Alpers agreed that infection could cause lower lobe consolidation. However at T 76.22 he disagreed with the word consolidation in Mr Ridgways case. He said Mr Ridgway has a lot of band shadows which are atelectasis ( collapse of the lung). He also has some volume loss in the lower lobe showing it is smaller than it should be and has lost some ability to expand. He felt that condition was “in keeping with an associated pleuro parenchymal disorder which is very common in patients who have been exposed to asbestos. Dr Alpers said that “consolidation” is associated with low bar pneumonia where the whole lung or lobe of the lung is completely filled with blood fluid or something else. He emphasised that there was nothing like that in Mr Ridgway.

· At T 77.23 Professor Alpers agreed that post inflammatory disease of any nature can produce pleural thickening. He also agreed ( at T 77.37) that with true pleural thickening he would expect some shadowing to remain on a permanent basis if it was related to asbestos disease. However he emphasised that asbestos related pleural disease was a dynamic process with small amounts of fluid developing over time. At T 77.45 Dr Alpers said the answer to Watson SC’s question entirely depended on what was causing the shadowing. If it was due to micro atelectasis then the lung can return to normal. If it is a reflection of pleural and parenchymal fibrosis of the lung that is permanent change. Dr Alpers said that band shadows come and go sometimes within hours “you are at risk of recurrent areas of atelectasis if you have basal pleural abnormality”

· At T 78.20 Professor Alpers said that it was “pretty unusual” for pneumonia to leave permanent scars.

· At T 78.33 Dr Alpers disagreed that he had made an assumption that the pleural effusion in 1999 was related to asbestos as opposed to infection. He said that for a man with asbestos exposure with calcified pleural plaques who then develops a left sided pleural effusion with associated parenchymal changes in lung a pleural effusion is a common condition. He could not be sure whether the infection also contributed to his pleural effusion.

· At T 78.33 Professor Alpers said that there aren’t any absolutes about doses of asbestos inhaled. Factors such as individual responses and cigarette smoking cause enormous variation as to what diseases individuals will get and the severity of those diseases. Mr Ridgway has not had a trivial exposure. He has certainly has enough to cause the pleural changes which you don’t get with trivial exposure to asbestos.

· At T 79.13 Dr Alpers said he was familiar with literature that deals with relevant doses necessary to induce asbestos diseases. He agreed that with amphiboles that some literature suggests that a dose of 25 fibre ml years is the lowest level at which asbestosis would emerge. He went on to say that those were very broad guidelines but in an individual case it is impossible to tell and even if you could tell there are huge variation in individuals responses to any infectious inhalation agent. In any event there was no point in calculating fibre ML years for asbestosis because Mr Ridgeway did not have asbestosis.

· At T 81.22 Dr Alpers commented upon the lung function testing carried out by Dr Antic on 18.11.02. He expressed the opinion that the plaintiff suffered from calcified pleural plaques with a minor degree of pleural thickening. He said the only cause of those condition was asbestos related. He also expressed the view that the pleural effusion in 2000 was asbestos related. He maintained his view that the plaintiff had a 15 per cent respiratory impairment.

36. On the 20.2.03 Dr Alpers confirmed his diagnosis. On this occasion he noted Dr Antics views that the plaintiff suffered from excess weight. He also noted that the plaintiff suffered from a number of other medical conditions. He expressed the view that considering the radiology and the previous plural effusion the broad bands shadows in the left lung with volume loss in the left lower lobe half the reduction in TLC was related to asbestos pleural disease.

The Defendants Medical Case

1. Dr Antic

37. Dr Antic, a respiratory physician, tendered reports dated 18.11.02, 30.12.03 and gave oral evidence on 24 June 2004.

38. In his evidence in chief on 24 June 2004, Dr Antic having been furnished by Watson SC with the plaintiff’s evidence, Dr Shanahans notes and Dr Quigleys reports completely changed his diagnosis:-

· At T 87.43 he said that pneumonia can cause pleural effusions.

· At T 87.47 he said that the episode in 1999\2000 “raises the possibility that this was an infective episode relating to lung infection rather than primarily a pleural effusion by itself”. He relied on the high temperature and brown muck to assist him in this conclusion.

· He went on to say at T 88.19” Well it suggests that the incident around 1999/2000 adds a differential diagnosis to the causation of the pleural effusion that I didn’t have previously”. At T 89.30 Dr Antic said that the accumulation of information from Dr Shanahan notes and Dr Quigley letters caused him to review the probable cause of the pleural effusion in late 1999 going on to say ( at T 89.34) “it makes me seriously consider the possibility that the incident in the lung substance to pneumonia and the development of pleural effusion and the subsequent clearance of both”.

· At T 89.48 Dr Antic agreed that pneumonia related pleural effusion can cause pleural thickening.

· At T 90.9 Dr Antic said “I think it more likely than not that the probably cause of the pleural effusion was the result of an infection.”

· At T 90.17 Dr Antic said that “under the right circumstances”, “abdominal pain and musculoskeletal chest pain can cause respiratory deficit.

· At T 90.18 he agreed that obesity can cause respiratory deficit.

· Cross examined by Little SC Dr Antic said at T 91.27 that the pleural effusion in 1999 “would have been an independent event and the presence of pleural effusion as a result of pneumonia would not have been influenced by any past asbestos exposure”.

· At T91.7 Little SC asked Dr Antic what sort of infective process occurred in 1999. He responded “Well I can only speculate in the most general terms whether it was a viral or bacterial event.”

· At T91.8 Dr Antic denied that a person who has their lungs or pleural compromised by past exposure is more prone to infection in the lungs.

· At T91.42 Dr Antic agreed that Mr Ridgways pleural plaques were in January 2000 in the left lower zone area. He said they were scattered around the left lower lobe area as well as other places.

· At T92.21 Dr Antic agreed that atelectasis would normally be asbestos related.

· At T92.44 Dr Antic agreed that Mr Ridgeway has been exposed to sufficient asbestos fibre to cause the formation of pleural plaques over 10-20 per cent of his pleura and those matters are common to asbestos exposure.

· At T93.5 Dr Antic said that it was conceivable that the pneumonia may have caused a pleural effusion and there may have been a pre-existing diffuse pleural thickening but did not agree with the scenario that asbestos lung disease leads to pleural effusion followed by infection. He said “In general terms the presence of pleural plaques or diffuse pleural thickening is not a risk factor for the development of infection.”

· At T93.43 Dr Antic in response to a question from Little SC about whether the onset of pneumonia was likely to be more serious in a person suffering Mr Ridgeways radiological changes said the other factors such as obesity, diabetes, hypertension, cardiac disease could also influence the likelihood of pneumonia.

· At T94.11 Dr Antic expressed the view that even if 20 per cent of a person’s pleural surface is rendered non-elastic from scar tissue caused by plaques that should have no effect on the way the pleura works.

2. Dr Carr

39. Dr Carr, a radiologist, was qualified by the defendant to express an opinion on the 5 high resolution CT scans taken between 15-12-99 and 27-3-02. His report of 29.8.03 stated:

· All scans demonstrate multiple pleural plaques scattered throughout both hemi thoraces, many of which contain linear calcification, typical of asbestos related pleural plaques. He estimated 10-20% of the pleural surfaces are involved.

· The scan on 15.12.99 meets the criteria for pleural thickening in the left lower lobe and there is evidence of a small associated left pleural effusion.

· The scan on 4.1.00 shows underlying linear trans-pulmonary bands in the left lower lobe but no suggestion of parenchymal fibrosis (asbestosis). There is an area of wedge shaped consolidation in the left lower lobe medially. The differential diagnosis rests between round atelectasis and an area of consolidation.

· The scan of 2.5.00 shows some resolution of parenchymal shadowing in the medial base segment of the left lower lobe and this is substantial evidence that this is an area of inflammatory change since round atelectasis should not resolve.

· Dr Carr summarised his findings as:

1. Multiple asbestos related pleural plaques

2. Diffuse pleural thickening in relation to the posterior aspect of the left lower lobe with underlying trans pulmonary bands in the left lower lobe.

3. No evidence of malignancy or asbestosis.

4. The area of consolidation in the left lower lobe, which resolved must have been inflammatory in nature rather than atelectasis.

40. Extracts from the clinical notes of the Locke Community Centre between 2.8.99 and 20.8.99 were tendered. Features of interest are:

· Dr Shanahans notes on 2-8-99 chest pain and a productive cough

· Dr Shanahan on 9.8.99 notes “chest clear” and “much improved”.

· Dr Shanahan notes plaintiff returns after admission to Cummins hospital.

41. Two reports from Dr Quigley dated 22.12.99 and 22.12.99 were tendered.

· The report of 22.12.89 was to the respiratory physician Dr Porter. Dr Quigley diagnosed an episode of left lower lobe pneumonia in August 1999 followed by intermittent episodes of a feeling of bubbling in the left side of his chest wall with occasional pleuritic pain. Plain chest x rays showed areas of asbestosis in the pleura and a bit of fibrosis in the left mid zone.

· The report of 9.1.02 was to a Dr Baker and concerned intermittent pain on the right side of the plaintiff’s head and face and ear. It gave the past medical history as:-

1.11.99 lower respiratory tract infection

10.12.99 low respiratory tract infection (left)

27.3.01 temporomandibular joint dysfunction

3.7.01 insomnia

3.7.01 sinusitis

42. The medical experts being in disagreement on the question of injury and causation I propose to resolve the issues on a commonsense basis giving due regard to the chain of causation. Before I do that however I should first resolve the exposure issue which is a matter that will need to be weighed in determining causation.

EXPOSURE

43. It is the defendant’s submission that, on any view, Mr Ridgeways potential exposure to asbestos is extremely low. On the only scientific evidence adduced (ie the evidence of the occupational hygienist Geoffrey Pickford) the cumulative dose is likely to be much less than 0.02 fibre/ml/years.

44. The plaintiff relies upon the expert evidence of Professors Alpers who opines that the plaintiff’s exposure to asbestos was moderate and the cause of his pleural disease and breathlessness.

45. It is the defendants submission that the plaintiff has failed to prove that either the asbestos in the pipes sawn to make the sheep troughs or the brake linings were of its manufacture.

46. The expert evidence before the court on the question of the manufacture of the asbestos products comes from Warwick Gazzard, a former Product Development and Marketing Manager of the defendant company. He confirmed in his report of 7 April 2004 that he had 7 photographs of the water troughs in his possession when he attended the plaintiffs property on 30 March 2004. However his report remains silent on whether the asbestos cement pressure pipes were manufactured by the defendant. He did not comment upon the brake linings.

47. The only evidence that would associate the manufacture of the pipes which Mr Ridgway sawed longitudinally to form the troughs is to be found in paragraph 28 of the plaintiff’s affidavit of 1 September 2003. There he recounts that between 1980 and 1990 he secured some water main pipes which were “imperfect seconds”. He then identified the pipes he purchased from a James Hardie brochure annexed to the affidavit. The Plaintiffs reliability on identification of the manufacture of the asbestos products purchased for his home was rigorously tested by the defendant and ultimately found to be correct. Taking all the evidence into consideration on the balance of probabilities I find that the asbestos cement pipes were manufactured by the defendant.

48. There is no evidence that goes to the identity of the manufacturer of the brake linings and I find that the plaintiff has failed to prove his case on this issue.

49. I should next refer to the relevant case law on exposure. The question is did the exposure found make a material contribution to the development of his restrictive lung condition?

50. In Brear v Commonwealth (1999) 18 NSWCCR 637 President O’Meally noted with approval (at Page 645) the opinion of the eminent thoracic physician Dr Julian Lee that:-

“ it is a general principle that the risk for development of an asbestos related disorder is directly related to the dose durability and duration of exposure to the fibre…..In an analysis of the relative fibre loads reported by Davis in<Thorax> several years ago, a gradation was evident from pleural plaques, through diffuse pleural thickening to asbestosis which of course, reflects general experience.”

51. At [39] President O’Meally went on to say from his long experience as President of this Tribunal :

”In respect of asbestos related pleural disease evidence has been given repeatedly not only that total exposure is the effective aetiological factor but that all asbestos exposure is causative of the disease. It seems to me therefore that the plaintiff having establishes that he does have asbestos related pleural disease, all exposure was causative of that disease”.

52. In McDonald v State Rail Authority (NSW (1998) 16 NSWCCR 695 President O’Meally held that the plaintiff in an action involving competing scientific views must be able to discharge his or her onus of proof by persuading the trial judge that the hypothesis for which the plaintiff relies in the action has been accepted in the scientific community and by establishing to the judges satisfaction that the hypothesis is probable.

53. At [90] President O’Meally commented:

“It is generally agreed that an industrial hygienist is the person best placed to measure the level of asbestos exposure, but in this field, as in the medical scientific field, certainty is impossible to achieve. Indeed, it would have been folly to conduct tests designed to measure the culmulative asbestos exposure of persons performing the tasks said to have been performed by Mr McDonald. The defendant submits that rough and undetailed estimates based on self assessment, job classification or assumptions cannot substitute for real evidence. That does not, in my view, mean that it is not open to me if the evidence permits of the conclusion, to determine the level of exposure by estimation or by inference. The question is, however whether the evidence allows me to make an estimate or draw an inference”.

54. In this case the competing evidence comes from a respiratory physician (Professor Alpers) and an occupational hygienist (Mr Pickford.) In E.M. Baldwin & Son Pty Ltd v Plane (1998) 17 NSWCCR 434 the Court of Appeal held that :-

“so far as possible, expert evidence must be evaluated by rational assessment of the witness’s respective fields of expertise, qualifications and standing and the apparent plausibility of their different theories, methodologies and conclusions”.

55. In Judd v Amaca Ltd (No2) (2003) 25 NSWCCR 488 my learned colleague His Honour Judge Curtis applied Seltsam Pty Ltd v McGuiness (2000) 49 NSWCCR 262 holding that a case for contribution to a disease may be based on epidemiological evidence establishing that not only was there increased risk of contracting the disease because of toxic exposure but that, on the probabilities that risk came home. Causation in law does not equate to scientific proof. However where a plaintiff can establish no causal circumstances beyond exposure to a toxic substance – and the injury mechanism is unknown – the Tribunal has no basis other than statistical probability on which to rely.

56. At [9] of the judgment Judge Curtis said in case involving the disease lung cancer “Unless a plaintiff can rely upon other circumstances that operate to weigh the probabilities in his favour, proof of causation which relies upon epidemiological evidence generally requires proof that his relative risk was greater than 2.0”. However Judge Curtis added this important rider at [13]

“Even where the relative risk does not reach 2.0 a court may infer causation as a matter of commonsense; for instance, if one or more of the postulates or criteria in which epidemiologists assess the strength of epidemiological data appeals more strongly to the judge than the expert. Such considerations as strength of association, dose response effect, time sequence, consistency and biological plausibility are referred to in the judgment of Spigelman CJ in Seltsam Pty Ltd v McGuiness. It is for the court to assess the weight of any such criteria in drawing conclusions and in this regard it may infer causation even where an epidemiologist may not”.

57. Before I go into the evidence in detail I should make some preliminary points of distinction:

1. This is a case where the diagnosis is pleural disease in the form of plaques and pleural thickening not asbestosis and not mesothelioma. I make this point because medical science remains mystified as to the precise injury mechanism that causes asbestos damage to the pleura to result in the development of cancer elsewhere in the respiratory tract. The precise pathogenesis of other disorders of the pleura is also not scientifically certain. What is certain however is that asbestos related pleural disease is caused by inhaled asbestos. Moreover as Dr Alpers points at T73 that once pathology such as calcified pleural plaques and pleural thickening are found by the radiology to be present there is no medical mystery as to how those conditions cause a restrictive deficit by impinging upon the bellows function of the lungs.

2. In paragraphs [4] to [9] in Judds case, Judge Curtis explains the rationale for use of epidemiological studies as a tool to establish that a plaintiff falls into a class of persons who are more likely to have contracted a disease because of the designated risk rather than from any other cause – ie not only that there was an additional risk, but upon the probabilities it was that risk which came home.

58. My point here is that there is no evidence of epidemiological studies relevant to asbestos related pleural disease before the court. If the defendant wishes to rely upon epidemiological studies to show that the risk has not come home then the onus is on the defendant to prove those studies and in particular prove that they relate to the class to which the plaintiff belongs namely sufferers of pleural disease in the form of pleural plaques and pleural thickening. The only evidence is from a hygienist who makes estimates from the plaintiffs evidence of the total airborne asbestos fibre dose he received as a bystander, building his extension, sheep troughs and fixing the brake linings. Mr Pickford in making these estimates relies upon experiments that are not epidemiological in nature but involve testing of dust emissions from various operations involving the manipulation of asbestos.

59. Watson SC seeks to bridge this evidentiary gap by relying on Dr Alpers concession at T79.18 that there is medical literature which suggests than in the instance of amphiboles, that is amosite or crocidolite that a dose of 25 fibre/ml/years is the lowest level at which cases of asbestosis would emerge. Watson SC then, unsuccessfully, tried to cut off Dr Alpers attempt to continue his answer. Dr Alpers was eventually able to finish his answer in the following terms

“ I believe in a court of this nature, it is now down to fibre/ml/years – these are absolutely very broad guidelines in the extreme but in an individual case it is impossible to tell, and even if you could tell there are huge variations in individuals responses to any infectious agent, inhalation agent, it is the natural history of our biological variation. We do not behave in the same way. So if in fact there aren’t enough fibres to cause asbestosis according to published literature I would still put some doubt as to whether in his case it was relevant or not”.

60. At T81.1 Dr Alpers rejected the logic of The defendant’s mathematical approach to establishing causation saying “this man does not have asbestosis. Even if he did I’ve seen individuals with asbestosis who have had figures well below the published limits and that is what you would expect. Everybody does not fit the same mould….it’s a totally specious view I believe….lets be realistic here. This man has on his own history of his occupational work and the fact that he does have pleural plaques means he has not had trivial exposure to asbestos”

In Cavanough v Workers Compensation Dust Diseases Board (1998) 16 NSWCCR 626 at [9] I considered an application by the defendant to reject the plaintiffs approach of assessing the balance of probabilities based on epidemiological models of relative risk and deal with the evidence on the balance of probabilities that applied to the plaintiff as an individual. In that context I relied upon the judgment of Justice McHugh in Bennett v Minister for Community Welfare (1992) 176 CLR 408 and 428 where he applied March v Stramare Pty Ltd (1991) 171 CLR 506 and 515 stating:-

“The existence of the causal connexion is to be determined in accordance with common sense notions of causation and not in accordance with any philosophical or scientific theory of causation or any modification or adaption of such a theory for legal purposes. “

62. I also relied upon the decision of Chief Justice King in SGIO v Laube (1984) 37 SASR 37 where he said:

“ the statistical fact based on the epidemiology of populations that a particular proposition is true of the majority of persons cannot of itself amount to legal proof on the balance of probabilities that the proposition is there for any individual”.

63. I should also make the point that a vague reference in cross examination to unnamed and unproved “literature” about unidentified studies that relates to a disease not in issue in this case is not proof of facts that can be relied upon to draw inferences that go to causation of Mr Ridgways breathlessness.

64. To be fair to Watson SC, although he does not say to directly, I gather he is suggesting when from the bar table, he asserts that Mr Ridgeways potential exposure was extremely low that I should be considering his submission in the light of the corporate knowledge of this expert Tribunal which is aware of a great deal of scientific literature concerning the relative risks involved in exposure to asbestos products of varying virulence. That literature is summarised in detail by Judge Curtis in Judds Case. The literature takes the form of various epidemiological studies from countries other than Australia as well as some conferences of international medical experts seeking to find some consensus for purposes not related to determining causation at common law on relative risk of exposure to asbestos. It is fair to say that the outcome of the Helsinki and Adelaide conferences referred to by Judge Curtis was:

a. Agreement that the likelihood that asbestos exposure makes a substantial contribution to lung cancer increases when the exposure increases.

b. Cumulative exposure on a probability basis should be considered the main criterion for the attribution of a substantial contribution to lung cancer risk.

c. The relative risk is roughly doubled for cohorts exposed to asbestos fibres at a cumulative exposure of 25 fibre years but exposures below that level were also associated with an increased risk of lung cancer albeit to a lesser extent.

d. These criteria need to be modified to take into account the relative carcinogenicity of different asbestos fibre types.

65. Judge Curtis placed the caveat on the material issuing from these “accords” of scientists that their opinion did not comply with the requirements of the law of evidence expressed in Makita v Sprowles (2001) 52 NSWCR 705 and could not be regarded as anything more that a position statement from an expert group, not based on identified scientific facts but mere on the basis “because I say so”. The bottom line is that because the literature referred to by Watson SC is not admissible to prove causation and because, so far as I’m aware, makes no reference to the risk of developing pleural plaques or pleural thickening that it is of no assistance to the court in this particular case.

66. I have taken Mr Pickfords report into evidence and propose to weigh it along with all the evidence in reaching my conclusions on causation.

67. There is no dispute here that the plaintiff was exposed to and inhaled asbestos dust and fibre while working with asbestos products manufactured by the defendant. The issue is whether that exposure was sufficient to bring the risk of contracting asbestos related pleural disease home and more specifically whether there is sufficient evidence to support the Tribunal making an estimate or drawing an inference as to the level of the exposure.

68. The plaintiff’s case rests on the expert opinion of the eminent respiratory physician Professor Alpers. The plaintiff submits that when Professor Alpers opinion that dust and fibre from the defendants products have caused his undoubted benign asbestos pleural disease is weighed in balance with the other evidence the Tribunal will be able to reach a level of actual persuasion as opposed to mere conjecture and draw the permissible inference that the risk has come home.

69. The defendants case based on the expert opinion of the occupational hygienist Mr Pickford is that the total dose of asbestos fibre inhaled by the plaintiff ( based on his own evidence) is between 0.008 and 0.037 fibre\ml\years. This evidence could only assist the court if it were given in conjunction with expert epidemiological evidence such as that available in Judds and McDonalds cases which could make sense of his statistics.

70. I must say that even if epidemiological studies of relative risks of developing pleural plaques and pleural thickening were available I would still have difficultly in giving much weight to Mr Pickfords evidence. I say this for the same reasons Professor Alpers rejects Watson SC’s proposition that plaintiffs exposure to asbestos was extremely low. Mr Pickford estimates the plaintiffs exposure from his evidence on 23.2.04 some 34 years after the event. He gives details of handling sweeping, sawing, cutting and carrying asbestos over a period of time of about 2 months. Having, on his own admission, no detailed exposure information Mr Pickford makes his own assumptions as to the extent of that exposure inventing scenarios the basis for which are not explained to the Court. He then relies on various studies only one of which was conducted under Australian conditions and which could hardly be described as independent given it was conducted at the James Hardie Research Centre Camellia. That study was limited to cutting and sawing and drilling. The second study by a Canadian Royal Commissioner in 1954 relied upon data on drilling and sawing from the USA and UK. The third study came from Germany in 1980 and dealt with exposure to asbestos dist on 40 building sites mostly conducted during roofing operations. There were no studies involving the sweeping of dust or carrying of asbestos products.

71. Professor Alpers evidence is that there are no absolutes about doses of asbestos inhaled. Factors such as individual responses and cigarette smoking will cause enormous variation in what diseases individuals will get.

72. The remaining evidence before the Tribunal going to exposure is:

1. The evidence of Professor Alpers that:

· The plaintiff suffers from benign asbestos related pleural disease and asbestos related pleurisy.

· The asbestos related pleural changes namely pleural plaques and generalised pleural thickening are significant not trivial substantially affecting the bellows operation of the plaintiffs lungs and representing a 15 per cent lung and representing a 15 per cent lung function impairment.

· The plaintiffs exposure to asbestos fibre was greatly increased by his sweeping up after the builders and angle grinding.

· In Dr Alpers opinion that while there aren’t any absolutes about dosages of asbestos fibre because individuals responses vary enormously. Mr Ridgeway has not had a trivial exposure. He has had a significant exposure certainly enough to cause the pleural changes .That exposure can be described as “mild to moderate” a realistic view of the evidence concerning the plaintiffs history of exposure and his pleural plaques means that exposure was mild to moderate.

2. The evidence of former manager of the defendant Warwick Gazzard who inspected the plaintiffs home confirming all external wall were clad with “Hardiflex” sheets and walls contained Hardies “Coverline” panels and Hardies “Tilux” Bamboo weave compressed asbestos sheets and Hardies “striated” asbestos cement sheets. The water troughs were also fabricated from asbestos cement pressure pipes spilt longitudinally

3. The evidence of the plaintiff, a farmer who has lived all his life in an isolated area of the South Australian outback far from environments in which significant quantities of asbestos are present in the air that :-

· The only asbestos to which he was exposed was in the construction of his home, the extension to it, making water troughs and changing brake linings.

· He unloaded by hand 254 sheets of the defendants asbestos sheet products.

· He loaded and unloaded off cuts from the builders and his own work when disposing of them at the dump.

· During the construction of his home he was present on site daily while they were cutting and sawing the sheets. He inhaled the dust from that process as he did when he was sawing rasping and cutting the sheets for the extension and cutting the asbestos concrete pipes for the troughs. He was also sweeping and cleaning up after the work was done (this evidence was given to Dr Alpers).

73. Finally I note that Dr Antic was initially convinced that the plaintiff had experienced sufficient exposure to asbestos to declare in reports of 18.11.02 and 30.12.03 that he had an asbestos related disease. Whilst it is true that he changed his mind in his oral evidence the basis for that change had little to do with the level of exposure and much to do with his view that the pleural effusion in 1999 was infection not asbestos related.

74. Taking all the evidence into consideration, keeping in mind the strictures of the Court of Appeal to which I have previously referred and taking a robust pragmatic approach to that evidence on the balance of probabilities I determine that the plaintiffs exposure to the defendants products was moderate and sufficient to bring the risk home.

75. The law does not regard the fact of an increase in risk as satisfying the requirements of causing or materially contributing to an injury. Before I can make a determination on that issue I will first have to consider the preliminary question of whether the pleural effusion in 1999 was asbestos related, an infection or both.

The 1999 Pleural Effusion

76. Until the 3rd day of this trial the medical experts were in agreement that the pleural effusion suffered by the plaintiff in 1999 was the result of his exposure to asbestos. However when Dr Antic gave oral evidence it became evident that Watson SC had supplied him with 5 sets of documents namely:

· His cross examination of the plaintiff at T36, T44 and T45.

· Progress notes from the Locke Community Health Centre notably noted by Dr Shanahan between 2.8.99 and 20.8.99.

· Radiology from Perrett Medical Imaging between 3.12.99 and 2.5.00.

· A opinion from the radiologist Dr Carr dated 29.8.03 concerning 5 high resolution CT scans between 5.12.99 and 27.3.02

77. Briefly put, Watson SC by referring to those documents persuaded Dr Antic to recant his previous opinion that the effusion and the pleural thickening it produced was asbestos related and to ultimately express the view at T89 that in this opinion there was a causal link between the pneumonia and the development of the pleural effusion and subsequent clearance of both.

78. Watson SC did not put to Professor Alpers the 5 documents used to change Dr Antics opinion. Instead he was content to secure the general admission from Professor Alpers that post inflammatory disease of any nature can produce pleural thickening. However at T 78.21 Dr Alpers qualified that general statement by saying infection following pneumonia can sometimes resolve completely and it is pretty unusual for it to leave permanent scars.

79. Dr Alpers also agreed that coloured sputum and asbestos related pleural abnormality are not related saying coloured sputum is bronchitis. He then made the point at T 78.29 “having bronchitis with associated pleural disease you’re much more likely to get retention of sputum material in the lung and you’re much more prone to develop more serious complications of bronchial infection particularly pneumonia. So asbestos pleural disease is a real risk factor for more serious infection of the lung”.

80. At T 78.36 Watson SC put to Dr Alpers:

Q. You have made an assumption that the pleural effusion in 1999 was related to asbestos as opposed to induced by an infection?
A. I am not sure whether infection also contributed to his pleural effusion at the time but someone who has asbestos exposure with calcified pleural plaques, pleuro pericardium calcification, which virtually unheard of in any other condition- apart from hemothorax, which he didn’t have, and the situation of recurrent pleural effusion is very common in asbestos related disease. So I was putting the logical context of someone with established exposure and pleural abnormalities who then develops a left sided pleural effusion with associated parenchymal changes in the lung that this was related to his asbestos condition because it’s a very common problem.

81. The question is whether the pleural effusion in 1999 was an asbestos related infection related a viral bacterial infection or both. Taking all the evidence into consideration on the balance of probabilities I determine that the chain of causation was:

a. Prior to August 1999 the plaintiff had well establish asbestos related damage to his lungs manifesting in calcified pleural plaques which limited the ability of his lungs to expand.

b. On the 2.8.99 he had chest pain with a cough which subsequently developed into pneumonia situated in the left lobe. The chest X-ray of 3.12.99 show a small left pleural effusion, calcified bilateral pleural plaques and some pleuro-pericardial calcification.

c. High resolution CT scans shows some resolution of the left sided pleural fluid but remaining pleural thickening with persisting band shadows in the left lower lobe.

d. Lung function tests between 14.1.00 and 14.11.02 reveal reduced total lung capacity and a moderate restrictive deficit.

82. The question here is to determine whether or not ( as Dr Antic hypothesises) the pleural thickening is the result of an infection caused by the pneumonia or ( as Dr Alpers hypothesises) it is the result of a chain of events whereby the asbestos related disease first incapacitated the plaintiff causing his chest pain and pleural inflammation which then left him vulnerable to the development of a severe pneumonia which exacerbated the inflammation.

83. Taking all the evidence into consideration on the balance of probabilities I determine that Dr Alpers hypothesy is the correct one. My reasons are as follows:

a. Both parties agree that in 1992 X-rays revealed that the plaintiff suffered from asbestos related pleural disease – a condition that commonly causes inflammations of the lungs.

b. The plaintiff was able to carry out the very physically demanding work as a farmer between 1992 and August 1999 although from the mid 1990’s he had found the task increasingly demanding and tiring.

c. About August 1999 the plaintiff was laid low with sinusitis then chest pain and a cough. The records of the Locke Community Health Centre do not suggest that he had an infective condition when he presented on 2.8.99. However both Dr Shanahan at the Centre and the plaintiffs GP Dr Quigley agree that by his admission to the Cummins hospital on 2.8.99 he had pneumonia in the lower in lobe of his left lung.

d. The X-rays on 3.12.99 revealed:

i. Atelectasis in the left costophrenic angle with possible fluid about that base.

ii. Appearances of infection

iii. Pleural calcification of the left hemidiaphragm and lateral walls of the hemi thoraces.

e. X-rays on 15.9.99 revealed:

· Calcified pleural plaques

· Suggestions of fibrosis from a previous inflammatory episode in the left mid zone.

f. A HRCT scan on 4.1.00 revealed:

· Underlying linear transpulmonary bands in the left lower lobe.

· A wedge shaped consolidation in the left lower lobe

· Minor architectural distortion which could either be areas of consolidation or enfolded lung round atelectasis.

g. Dr Carr a radiologist retained by the defendant to review the radiology between 15.12.99 and 27.3.02 concludes:

· Multiple asbestos related pleural plaques

· Diffuse pleural thickening in relation to the posterior aspect of the lower lobe with underlying transpulmonary band in the left lower asbestosis.

· A transient area of consolidation in the left lower lobe which has resolved and therefore must be inflammatory in nature rather than enfolded lung\round atelectasis.

h. A HRCT scan of 2.5.00 showed some resolution of the parenchymal shadowing in left lower lobe strongly suggestive of an area of inflammatory change.

i. Dr Antic takes the view that the fact there was an infective episode in 1999 opens the door to a differential diagnosis to the causation of the pleural effusion.

j. Dr Alpers agrees that pneumonia can cause pleural effusion but rejects a differential diagnosis in the particular circumstances of this case. He maintains that it is very unusual for pneumonia to leave permanent scars. What he believes has occurred is that the plaintiff developed bronchitis with associated pleural disease. That meant retention of sputum in the lung and an increased likelihood of the development of more serious complication such as pneumonia. Asbestos pleural disease is real risk factor for more serious lung infections. Dr Alpers maintains that although infection could possible have contributed to the pleural effusion when one looks at all the circumstances of a man with established exposure and pleural- pericardium calcification who subsequently develops a left sided pleural effusion with associated parenchymal changes in the lung the likelihood is that it was caused by asbestos.

k. Dr Porter, who had a history of the pneumonia and bubbling in 1999 diagnosed left lower lobe fibrotic changes consistent with exposure to asbestos.

84. Commonsense suggests to me that a man with well developed asbestos damage which involves fibres sticking out through the visceral surface of the lining of his lung permanently irritating the lung was likely to be involved as Dr Alpers opines in a dynamic ongoing process of minor inflammations leading to pleural thickening. Commonsense further suggests that a man with a damaged lung would be vulnerable to bronchial infection and to more serious infections such as pneumonia. Finally commonsense suggests that a man with widespread permanent damage to his lungs of a sort commonly caused by asbestos is more likely to have developed his pleural thickening from his asbestos related disease than a discrete episode of an unrelated infection which the radiology shows has resolved. To my mind, in the unlikely event that infection from the permanent pneumonia has played a role at all the in the development of the pleural thickening it did so in conjunction with the asbestos related disease in a way that does no break the chain of causation from inhalation of asbestos fibres to pleural thickening.

85. Taking all the evidence into consideration on the balance of probabilities I find that the plaintiffs pleural effusion in 1999 was asbestos related.

AT WHAT POINT IN TIME DID THE PLAINTIFFS CAUSE OF ACTION ARISE?

86. It is trite law that at common law a cause of action accrues when compensable damage occurs. The plaintiffs evidence is that he first became incapacitated for work in 1999. His particulars indicate that he retired as a sole farmer when he “ran out of puff” on 19 March 1999 and began sharing farming with his nephew Jason. His claim for economic loss initially relates to increase profits he alleges would have been made share farming in the agricultural some golden years between 1999 and 2001. In this sense part of his claim for economic loss can be said to arise prior to September 1999 and outside the limitation period.

87. However at that time the evidence is clear the plaintiff did not have medical evidence that would have substantiated a case that it was asbestos related disease that was causing his disability. It was not until the x-rays and CT scans and lung function testing of December 1999 and subsequently that the true picture of the plaintiffs medical condition became apparent. Even if some material fact such as the x-ray in 1992 had inspired Mr Ridgway to rush off for legal advice prior to December 1999 his lawyer would have had to advise him on the facts available at that time that he could not prove injury, damage or liability on the part of the defendant.

88. Taking all the evidence into consideration on the balance of probabilities I determine that the plaintiffs cause of action did not accrue before December 1999 when he came into possession of material facts that established he had an asbestos related lung disability that was causing him compensable damage. Accordingly the claim was brought within the limitation period imposed by s 36 of the South Australians Limitations Act 1936.

1. Obesity

89. The parties are agreed that obesity is a confounder that has made a material contribution to the plaintiff’s lung dysfunction. The next issue is to apportion between the asbestos related component and the obesity.

90. Only two medical opinions are available to assist the Court make that apportionment. Dr Porter opines that “ a smaller component of his impairment chest expansion will relate to his obesity”.

91. Dr Alpers in his report of 9.1.03 finds a 30 % overall reduction in TLC “some of which is related to his obesity”. In his oral evidence he states “ I’d put the two as 50 per cent equal abnormalities “

92. Dr Antic initially expressed the view that obesity was not a contributing factor to the loss of lung function. He was not asked and did not provide an apportionment between the obesity and the asbestos related component because he eventually came to the view that there was no asbestos related component to the plaintiff’s loss of lung function.

93. Taking all the evidence into consideration I apportion the plaintiffs current loss of lung function 50:50 between the asbestos related component and obesity. I will need to deal with his future loss of lung function later.

Musculosketal Pain

94. While Watson SC was able to extract from both Dr Antic and Dr Alpers evidence that pain from spinal injury and osteoarthritis of other parts of the body could conceivably affect lung function testing he did not manage to secure an opinion that the low back pain and arthralgia experienced by the plaintiff in his sternum, spine, rib joints and jaw was actually making a material contribution to his lung function impairment.

95. Dr Alpers views ( which I have previously recited at length) was that Watson SC was “really stretching things”, when he suggested spinal pain could affect lung function asserting that would only occur in extreme cases such as advanced ankylosing spondylitis particular if treated by large doses of narcotics. Dr Alpers rejected the proposition that an arthritic sternum could produce a restrictive condition. He said that osteoarthritis of the ribs would only do so if the rib cages became completely rigid which was not the case here.

96. Dr Antic would go no further than say “under the right circumstances” musculoskeletal pain can cause respiratory deficit.

97. Taking all the evidence into consideration I determine on the balance of probabilities that the intermittent musculosketal pain the plaintiff has endured over the years has not made a material contribution to his restrictive lung deficit.

3. Abdominal Pains

98. The Plaintiff had a series of operations relating to a gall bladder problem. The last operation was in 1992 but he concedes he endures intermittent pain from scar tissue in his abdomen. Again Dr Antic says that in the right circumstances abdominal pain could cause respiratory deficit. He does not say this was so in the plaintiffs case.

99. Dr Alpers takes the view that for abdominal pain to be causing a restrictive deficit it would need to be “on a semi permanent basis requiring 4 hourly administration of narcotics”. The plaintiffs occasional episodes of pain would not meet that criteria.

100. Taking all the evidence into consideration on the balance of probabilities I determine that the plaintiffs abdominal pain is not making a material contribution to his restrictive lung incapacity.

DAMAGES

101. Having disposed of the only issues raised on the issue of liability in the plaintiff’s favour I find that the plaintiff has proved his case on liability and move on to the issues relating to damages.

Discussion

102. Watson SC characterises the claim for damages in this case as “strange”. He points out that on his own admission the plaintiff currently suffers from a range of non asbestos related conditions namely:

· Abdominal pain

· Gastro-intestinal problems

· Recurrent bouts of pneumonia

· Low back pain with sciatica

· Widespread skeletal pain in the neck, jaw and knee

· Diabetes

· Hypertension

· Obesity

· Hearing loss

· Recurrent headaches

· Insomnia

103. Watson SC suggests these problems have required continuous treatment including narcotic based painkillers. Further between 1997 and 1999 before the plaintiff retired he regularly consulted medical practitioners but never complained about breathlessness except in the context of influenza. Finally the defendant alleges that no medical expert supports the contention that Mr Ridgeways problems are substantially connected with asbestos inhalation.

104. Watson SC does not advance his clients case by indulging in hyperbole. I say that because when the evidence is analysed the defendants portrayal of the extent of the plaintiffs non asbestos related disabilities is exaggerated in the following respects:

a. Whilst it is true that the plaintiff suffers from a number of chronic medical conditions nearly all of them only cause him intermittent discomfort and most are well controlled by medication.

b. The hypertension and diabetes are such an example of medication controlling the condition to the point that the disability is not significant.

c. The abdominal pain mostly occurred between the 1960’s and 1992 when 3 operations resolved the severe pain that necessitated narcotic medication. Subsequently the plaintiff has suffered only occasional pain related to scar tissue from the operation which is effectively managed by analgesics.

d. It is true that the plaintiff has since the 1970s suffered low back pain and in later years widespread musculosketal pain affecting most of his joints. The low back pain became bad in the 1990’s and was effectively treated with conservative measures. More recently the plaintiff has suffered widespread arthritic symptoms particularly in his jaw.

e. Over 30 years his doctors have given him a range of analgesic medications some of which are narcotic based. It is not unusual for men working in very heavy physical labour such as farming to develop widespread arthritis. The true nature of that arthritic condition is not in evidence before the court. What is in evidence is the extent of the disability caused by the arthritis and in particular the plaintiffs evidence that he was able to successfully work a huge sheep and wheat farm by himself up to March 1999. That feat could not have been achieved by a man with severe musculoskeletal pain continuously treated by narcotics. The plaintiff’s evidence was that it was his breathing problems and tiredness that caused him to give up farming alone and become a share farmer in March 1999. Even then he was still able to continue to perform half the work he was previously engaged in as a farmer.

f. The plaintiff did suffer recurrent bouts of pneumonia prior to August 1999. Six of those bouts occurred while he was a child. The only other recorded bout was in August 1999. One bout of pneumonia in 40 years hardly constitutes “recurrent bouts of pneumonia”.

g. The plaintiff agreed in cross-examination that from time to time over the past 40 years when he suffered severe abdominal or back pain he was treated with narcotic based medication. That admission cannot fairly be equated to “continuous treatment including narcotic based painkillers”.

h. What the court is concerned with is a claim for damages commencing late in 1999 and the state of plaintiff health leading up to that point in time. The defendant has put in evidence the plaintiffs medical records from the Locke Community Health Centre which are more likely to give a balanced picture of the nature extent and incidence of those disabilities. The records from the centre in the 28 years up to February 2000 reveals the following facts:-

· Between 1972 and 1978 the plaintiff presented on occasions with abdominal pain or bladder problems. He presented with low back pain on only 2 occasions. He did not present with any of the other problems raised by the defendant

· Between July 1992 and February 2000 the plaintiff presented on 6 occasions with back pain 5 of which were in 1972. He was treated for coccyx pain in 1995 with Naprosyn. He presented with wrist pain on only one occasion and chest pain on one occasion after crutching sheep. He’s blood pressure was regularly taken and he was diagnosed with diabetes in 2000.

· The fact is that Mr Ridgeway did not go to the doctor very often for any complaint most of his visits being for minor injuries related to his heavy work.

(i) Professor Alpers expresses the opinion that the plaintiff suffers from a 30 per cent reduction in his total lung capacity 15 per cent of which is related to his asbestos related restrictive lung disease. This Tribunal regularly awards damages for the breathlessness associated with a 15 per cent impairment of lung function and no fair-minded person could accept the defendant’s characterisation of the plaintiff’s significant disability as “not substantial.”

(J) Contrary to the defendant’s contention both Professor Alpers and Dr Porter strongly support the view that Mr Ridgeways problems are substantially connected with asbestos inhalation. Indeed Dr Antic expressed the same opinion until he was persuaded to take the view that the pleural thickening was related to an infection not associated with asbestos. Putting the pleural thickening aside, the defendant’s radiologist. Dr Carrs opinion is that 10 to 20 per cent of the plaintiffs pleural surfaces are covered with multiple calcified pleural plaques- hardly an insignificant asbestos related condition!

105. The plaintiff claims damages under the following heads:

a. General Damages

b. Loss of expectation of Life

c. Future Medical expenses

d. Griffith v Kirkemeyer damages

e. Economic Loss

106. The defendant’s submissions is that the Tribunal should view this as an ambit claim characterised by unwarranted escalation (especially in the areas of economic loss and Griffith v Kirkmeyer damages). At best the plaintiffs claim is modest and the plaintiff’s claims for damages is not recoverable as a matter of law. I will commence my determination with the defendant’s last point.

Malec v Hutton Damages

107. Watson SC submits that damages based on the risk of injury occurring are not recoverable as a matter of law because different processes trigger mesothelioma and lung cancer and as a matter of legal principle damages are not allowed for different injuries.

108. Little SC submits that this is a question of the assessment of damages and the principle in Malec v J.C Hutton Pty Ltd (1990) 169 CLR 638 allows this Tribunal in personal injury actions to take into account future or hypothetical events in assessing damages. The plaintiff’s case goes much further than the risk of malignancies relying on risks of recurrent pleural effusions, pain syndrome, hypoxaemia and catastrophic infections.

109. In Malec, Deane Gaudron and McHugh JJ explained the approach that should be taken by the Courts at page 642:-

“When liability has been establish and a common law court has to assess damages, its approach to events that allegedly would have occurred, but cannot now occur, or that allegedly might occur, is different from its approach to events which allegedly have occurred… If the probability of the event having occurred is greater than it not having occurred, the occurrence of the event is treated as certain; if the probability of it having occurred is less than it not having occurred it is treated as not having occurred. Hence in respect of events which have or have not occurred damages are assessed on an all or nothing approach. But in the case of an event which it is alleged would or would not have occurred or might not yet occur the approach of the court is different. The future may be predicted and the hypothetical may be conjectured. But questions as to the future or hypothetical effect of physical injury or degeneration are not commonly susceptible of scientific demonstration or proof. If the law is to take account of future or hypothetical events in assessing damages it can only do so in terms of the degree of probability of those events occurring. The probability may be very high-99.9 per cent or very low-0.1 per cent. But unless the chance is so low as to be regarded as speculative-say less than 1 per cent- or so high as to be practically certain-say over 99 per cent- the court will take that chance into account in assessing the damages. Where proof is necessarily unattainable it would be unfair to treat as certain a prediction, which has a 49 per cent probability of occurring. Thus, the court assesses the degree of probability that an event would have occurred or might occur and adjusts its award of damages to reflect the degree of probability”.

110. Watson SC asserts that the development of mesothelioma or lung cancer is the result of different processes and consequently different injuries. There is no doubt they are different conditions but this expert Tribunal is aware that whilst medical science is mystified as to the processes that cause asbestos related tumours there is no doubt that like asbestos related pleural disease they are caused by inhaled asbestos fibre. It begs the question to suggest that because the biological processes involved in inhaled asbestos fibre causing pleural plaques as opposed to pleural thickening or the development of a tumour differ that the injury is not the same. Mr Malec for example suffered from quite different conditions namely brucellosis and two consequential conditions - a disease of the spine and depressive mental illness. The future damages issue was whether his deteriorating back condition would have precluded him from gainful employment had he not contracted brucellosis as a result of the defendant’s negligence. The issue in this case is whether Mr Ridgways deteriorating asbestos related lung condition will so incapacitated him as to entitle him to the heads of damages claimed had he not contracted asbestos related lung disease as a result of the defendants negligence.

111. The relevant medical evidence comes from Dr Antic Dr Alpers and Dr Porter. Dr Antic in his report of 30.12.03 agrees that “there is a small possibility of the development of new catastrophic illnesses such as mesothelioma, this probability is small. There is no reason to believe that his current medical state that is causally related to past asbestos exposure will deteriorate with time, although there is a small possibility that it might”.

112. Dr Alpers prognosis at page 2 of his report 9.5.03 was:

3. stage II will prevail between 2 November 2012 and 2 November 2015.

4. stage III will prevail between 2 November 2015 and 2 November 2017.

5. stage IV will prevail between 2 November 2017 and 2 November 2018.

6. stage will occur between 2 November 2018 and 2 September 2019.

7. stage V1 will occur between 3 September 2019 and 2 November 2019.

149. Further because we are dealing with risks I propose to assess the cost of the care estimated by M\s Morgan and endorsed by Professor Alpers at the very bottom of the range.

3. Will the ratio obesity: asbestos related disease remain at 50:50 in the future?

150. My determination that the plaintiff’s restrictive lung deficit caused by asbestos will progress until his ultimate death from it in 2019 raises the question of whether the relative proportion of the restrictive lung deficit attributed to obesity will remain as his condition worsens in the future. Little SC also raises in his oral submissions whether the Court should accept that the obesity present during the lung function testing is itself likely to deteriorate given the not so overweight appearance of the plaintiff in the witness box and Dr Antics opinion that it was not a contributing factor at the time of his lung function testing in November 2002. The plaintiff’s evidence ( at T24) was that he has in recent years lost 15 kilograms in weight but was still about 104 kg.

151. The plaintiff’s forensic problem is that his medical experts have not taken all that weight loss into account in assessing his loss of lung capacity due to obesity. The best the court can do is assume that the 15 per cent contribution being made by the obesity to the restrictive lung deficit will remain constant. However accepting Professor Alpers evidence that the chances are that the plaintiff will be enduring a series of minor asbestos related effusions as well as serious infections and hypoxaemia which will eventually end his life, logic suggests that over the next 15 years his restrictive lung deficit attributable to asbestos will substantially increase as a proportion to the deficit from obesity.

4. The need to Discount for Vicissitudes

152. I have previously expressed my views about the alleged confounders and have already substantially discounted the claim by truncating its time frame and limiting the costs. However it must be said that the plaintiff is getting on and conditions such as hypertension and diabetes though effectively treated and unlikely to prematurely bring the plaintiffs life to end still represent a risk of causing disability to the plaintiff. Accordingly I propose to take that risk into account and discount this head of damages by the usual 15 per cent.

5. Lolomanaia’s Case

153. In Van Gervan v Fenton [1991-1992] 175 CLR 327, the High Court considered an appeal from the Full Court of the Supreme Court of Tasmania on the question of whether in respect of a Griffiths v Kirkemeyer claim, compensation for the value of the services provided for the appellant by his wife was property assessed by reference to what she would have earned if she had continued in paid employment.

154. Mason CJ, Toohey and McHugh JJ applied the principle that wages foregone by a care provider are not an appropriate criterion for determining the value of services provided gratuitously to an injured person. As a general rule the market cost or value of those services is the fair and reasonable measure of the injured persons loss.

155. The learned judges took the view that it was necessary to determine two questions:

1. What are the services required to satisfy the plaintiffs need resulting from the defendants wrong? and

2. What is the value of those services?

At page 338 their Honours said:

“ In this case, the appellants need is essentially for constant care and attention. No doubt some of the services which are now needed by the appellant were provided for him by his wife before the accident. But with great respect to those judges who have taken the contrary view no allowance in favour of the respondent can be made in respect of such matters. A defendant is no more entitled to have the pre-accident voluntary contribution of a spouse taken into account than a defendant would be entitled to have the pre-accident work of a paid housekeeper taken into account. If the defendant has created the need for the services that person is not entitled to have the damages reduced because, before the accident, the plaintiff elected to pay for similar services or had the benefit of having them performed gratuitously. By the tort, the defendant has transformed the choice of the plaintiff to pay for such services or to have them done voluntarily into the need for the plaintiff to have those services performed for him or her.”

156. Brennan J agreed with Mason CJ, Toohey and McHugh JJ. However he took the view at page 341,

“ it is appropriate to omit from the list of services to be paid by the defendant some of the time spent or some of the minor services rendered by the care provider to the plaintiff where those services would have been provided in any event as an incident of an antecedent personal relationship between them, provided the plaintiff is able to offer services to the care provider in return. If the plaintiff is unable to offer services to the care provider in return, but some pecuniary allowance would be fair compensation to the care provider for the plaintiffs failure to do so, the plaintiff should recover as damages a capital sum representing that allowance”.

157. It seems clear that Brennan J is saying that minor services incidental to a personal relationship such as spending time together need not be compensated by defendants unless the victim of the tort is no longer able to reciprocate.

158. Gaudron J at page 347 adopted the reasoning of Mason CJ, Toohey and McHugh JJ that

“the true basis [for compensation] is the need of the plaintiff for those services provided for him and …..the plaintiff does not have to show … that the need is or may be productive of financial loss. What follows from this is that compensation for that need must be calculated by reference to the value of the services concerned .

159. As I read Justice Gaudrons judgment it appears that the reason to she delivered it separately was to provide the opportunity to lambast the male chauvinist porcinity of the defendant’s arguments. I say that because at page 350 she said:

“There are only two bases on which it can be argued that some reduction should be made by reason that Mrs Van Gervan provided domestic services before her husband became ill. The first is that, to the extent of the services previously provided, there was a pre-existing need and, thus, no need resulted from the accident. That assumes that the services were provided because they were needed and not as a give-and take usually involved in domestic arrangements. There is no justification for an assumption of that kind, involving, as it does incompetence and selfishness of a very high order. The second basis on which the argument can be put is that the accident would have given rise to a need for the services of a wife, but to the extent that Mr Van Gervan already had the services of a wife, no need actually resulted. At best this equates a wife to an indentured domestic servant-which she certainly is not. The argument must fail.”

160. In rejecting those two bases in such strong language Justice Gaudron is clearly rejecting the minority judgment.

161. Deane and Dawson JJ dissented on the question of row domestic cooking washing and cleaning services provided by Mrs Van Gervan should be treated taking the view that in assessing compensatory damages the ordinary incidents of a particular relationship such as joint activities and companionship cannot legitimately be seen as transformed by the injury to one spouse into services which would otherwise exist. They qualified that view by stating such services will be taken out of the area of the ordinary give and take of marriage to the extent the spouses injuries prelude him or her from providing countervailing services.

162. As I read the judgments a clear majority of four judges namely Mason CJ, Toohey McHugh and Gaudron JJ support the view that no allowance can be made for a defendant in assessing Griffith v Kirkemeyer damages for domestic services already provided by a plaintiffs wife before he became ill. Further Justice Brennan only qualifies that proposition slightly by raising the issue of whether some “minor” services such as spending time together might not be compensable and then only if the plaintiff was able to reciprocate those services after his injury.

163. Watson SC submits this court is bound to follow the decision of the Court of Appeal in Roads & Traffic Authority in Roads & Traffic Authority of NSW v Lolomanaia ( Unreported 27 August 2001 Hodgson JA and Fitzgerald and Davies AJA CA 40628\00).

164. In that case Justice Hodgson at paragraphs [45] to [50], (although the point was not raised before the primary judge nor made a ground of the appeal) took the opportunity discuss the decision of the High Court in Van Gervan expressing personal views that were contrary to the majority judgments. As these views were clearly obiter dicta I do not regard myself as bound by them and propose to apply the principles enunciated by the majority of the High Court.

The Calculations

165. Having determined the services required to satisfying the plaintiffs future needs and determined the timing of their requirement and having determined the value of those services I should now proceed to calculate their quantum.

Stage I :- 2 November 2009 to 2 November 2012
156 weeks care at $20 per week or :- $ 3120

Stage II:- 2 November 2012 to 2 November 2015.
156 weeks care at $126 per week or:- $19,656

Stage III:- 2 November 2015 to 2 November 2017
104 weeks care at $287 per week or: $29,848

Stage IV 2 November 2017 to 2 November 2018
52 weeks care at $1620 per week or $84,240

Stage V 2 November 2018 to 2 September 2019
48 weeks care at $2126 per week or:- $102,048

Stage VI 2 September 2019 to 2 November 2019
8 weeks care at $3599 per week:- $28,792

Total :- $ 267,704

Equipment Needs

166. At page 11 of her report M\s Morgan provides an estimate of the rental or purchase costs of necessary equipment such as wheel chairs, beds, walking frames, shower chairs etc. I prefer to base these calculations on a rental basis and propose to limit their use to the final two stages i.e. between 2 November 2018 to 2 November 2019.

167. By my calculations the rental of that equipment over 52 weeks would cost $214 per week or $11,128 making at total for Griffith v Kirkemeyer damages of $ 278,832. I have previously decided to discount that sum by 15 per cent for vicissitudes leaving $ 237,007. That sum will finally have to be reduced by a further 15 per cent to take into account the obesity confounder leaving $ 201,456.

Damages For Economic Loss

168. The plaintiff claims damages for economic loss on the general basis that the defendants tort caused him to cease working for himself as a farmer on the 11 March 1999 and his earnings have been cut short by this premature retirement.

Allegation that Plaintiff ceased work for non asbestos related health reasons.

169. Watson SC raises a preliminary issue which I should determine at this point. The defendant’s position is that no damages for economic loss should be awarded. This submission is based on the following testimony ( at T 60.41 to 44):

Q. “You see the point is you did not retire because of shortness of breath, you retired because you had become generally unhealthy. Is that no right?
A. Yes.

170. I do not believe Mr Ridgway could see the point Watson SC was trying to make. His” yes” to multiple questions is a rather shaky foundation to build a case for an verdict for his client particularly given the rest of the plaintiff’s evidence and my previous findings on the alleged confounders upon which the defendant sought to rely. It also suffers from a lack of explanation about what “generally unhealthy” meant.

171. The plaintiff is a farmer who left school aged 15 and worked on the land all his life. He obviously did not divine the deeper contextual meaning of Watson SC’s framing of the complex second of 3 questions. I do not read into the plaintiff’s evidence the admission the defendant asks of me. Rather I note his own evidence on the subject of why he stopped farming by himself in March 1999, viz:

· At [35] of his affidavit he says:

“ I stopped farming full time as I basically ran out of puff. I found that I struggled to do the heavy work on the farm due to shortness of breath. I found working with sheep and heavy lifting particularly difficult. I found that I simply did not have the strength to do this. I used to run the farm basically single-handed. I used to keep 1400 sheep. I used to grow grain on 1500 acres which would produce a crop of anywhere between 800 and 1400 tonnes. Less in drought years.”

· At [37] of his affidavit he said:

“It was always my intention to work on the farm until at least the age of 70. Effectively I finished work 12 years prematurely. Farming is something that you keep doing until you die. It is you life not simply a job”.

· At T 23.49 to T 24 the plaintiff described how he was feeling while carrying out his work as farmer from 1990 to1999. He said:

“ it was getting harder. I’d come home buggered-lay down and sleep when I come home. I used to be really worn out-used to lay up over the weekends…. I was puffing more”.

172. At T 24.36 he was asked:

Q. “What were you like by 1999? ”
A. “Worn out, I took the year off”

173. I have already dealt at length with the nature and extent of the plaintiff’s constitutional health problems and found they are not contributing to his breathlessness. There is no doubt however that his obesity is playing a significant role in his breathlessness and tiredness. Over a long period of time he had periods of ill health with severe musculosketal pain severe abdominal pain, hypertension diabetes and most of those problems are still with him. However they have been controlled by medical treatment and are not causing the breathlessness and fatigue that caused him to stop work in 1999. Taking all the evidence into consideration on the balance of probabilities I find the sole cause of the plaintiff ceasing work on 19 March was his restrictive lung deficit.

174. The plaintiff has proved that he was injured by the plaintiffs tort. I have found that he has suffered damage as a result of that tort and that damage will exacerbate over the next 15 years. The plaintiff is entitled to damages for any economic loss he may have sustained as a result of his injuries. Before I address the complex accounting issues raised in respect of the calculation of that loss I should first explain the background to the claim and refer to some legal principles I am required to apply.

Background to the Claim

1. The plaintiff ceased work as a sole farmer on the 19 March 1999. Since that time he has participated in a share farming arrangement with his nephew Jason Ridgway. The water and fertilizer expenses are shared by the plaintiff and his nephew whilst the proceeds from the farm are divided between the plaintiff and the nephew on a 50\50 basis.

2. The plaintiffs evidence is that farming is a lifetime occupation but he only claims for 12 years ( ie to his 70th birthday). His evidence is that but for his injury he would have continued to operate his farm single handed and so retained all its profits to himself.

3. The plaintiff, as is his right, has chosen to maximise his profits and minimise his taxation by operating his farming activities through a family company known as J W Ridgway & Co Pty Limited (JWR) which pays the plaintiff and his wife an equal wage depending on the farms success in a given year.

4. Notwithstanding the equal wage the evidence is that the business was comprised primarily of the personal exertions of the plaintiff and the distribution was for tax minimisation purposes and was not a true reflection of Mrs Ridgways role in the business which only involved clerical work for a few hours each work.

5. The plaintiff’s accountants Furzer Crestiani Services constructed the following table from the company’s account showing the remuneration from the plaintiffs operation of the farm to be as follows.

Financial Year Directors Fees Salary Sale of Shares Net Profit Total

1994 $ 15,000 Unknown Nil ($167) $14,833

1995 Nil Nil Nil ($20,030) $ 20,030

1996 Nil $29,000 Nil ($19,925) $ 48,925

1997 Nil $32 500 Nil ($ 445) $ 32,055

1998 Nil $10,000 Nil ($10,498) $498

1999 Nil $20,000 Nil ($350) $ 19,650

2000 Nil $20,000 $ 8733 ($16 771) $5,544

2001 Nil $25,000 $ 32083 (22,146) $ 29,229

2002 Nil $12,000 Nil $36,123 $ 48,133

6. The accountant’s note the following matters revealed by these figures:

1. Clearing sale proceeds of $35,727 were earned in 1999 when the plaintiff ceased farming.

2. Results fluctuated year to year due to climate, commodity prices etc.

3. The plaintiffs farming activities were based on those seasonal factors.

7. Jason Ridgways results when compared with the plaintiffs were as follows:

Farm Profit 2000 2001 2002

JWR $3229 $2854 $48,123

Jason Ridway $20,663 $25,374 $117,382

Profit from Farm $17,434 $28,228 $165,505

8. The nephews efforts have been added back in order to derive the total profit from the plaintiffs farm but for his condition.

9. Furzer Crestani then prepared estimated income of the plaintiff but for injury on the alternative bases of either including or excluding the $35725 obtained from the sale in 1999 obtaining outcomes of either $25,598 gross per annum or $21,628 gross per annum.

10. Those calculations involved the following assumptions:

(a) In the financial years 2000 to 2002 the plaintiff would have derived additional income has he been uninjured based on his nephews results.

(b) From 1 July 2000 would have derived either $25,598 or $ 21628 from his farming activity and

(c) Assumed that as result of his condition the plaintiff would continue share farming deriving approximately 50% of his estimated income.

(d) That both injured or uninjured plaintiff and his wife would have organised their wages in a way that would best minimise tax by taking advantage of accumulated losses being carried forward.

175. Furzer Crestiani eventually arrived at a total loss of income of $242,154:

176. They made no allowance for vicissitudes of life taking the view that if that was appropriate for the court make that calculation.

177. Horwarths, the defendants forensic accountants eventually took the view that it was not possible to calculate the plaintiffs economic loss on the information they held, Nevertheless they gave it a go.

178. Their approach was as follows:

1. They too divided the economic loss into past and future components.

2. They decided to estimate the earning capacity of the plaintiff but for his illness and deduct from that figure his estimated residual earning capacity.

3. In making these calculations that made the following assumptions:

1. Future values should be discounted at 3% per annum compound, No allowance was made for inflation, interest or taxation on interest.

2. No allowance was made for disability support.

4. Economic loss was calculated on the basis:

(a) the plaintiffs income but for injury would be taxed.

(b) Any verdict would not be taxed

5. The plaintiff would retire aged 65 years.

6. The plaintiff has a residual net income injured of 50% of his income uninjured.

7. The present value date is 1 July 2003.

8. 15% should be deducted for vicissitudes.

9. Horwarths conclusion was that the total economic loss was $204,314 Little SC identifies the only financially significant differences in the accountants approach to the calculation as follows:

(i) Offset for wife’s contribution.

(ii) Difference in Retirement date.

(iii) Deduction for vicissitudes.

THE LAW

179. My understanding of the law is that the plaintiff must be compensated for his loss of earning capacity. The financial loss occasioned by his loss of earning capacity is the loss of what income the injured plaintiff would have expected to have under his control and at his disposal by exercising that capacity. The Court must therefore inquire as to what the plaintiff could have done as a farmer but for his injury and what sum of money he would therefore have had at his disposal. His lost earning capacity is the loss of his ability to control and dispose of income he would have earned if he had not been a victim of the defendants tort.

180. In Husher v Husher (1999) 197 CLR 138 ,the High Court held:

1. There is no principle of law that a plaintiff, who at the time of the accident was a partner in a business, can never recover more for the loss of future earning capacity than a sum calculated by reference to the plaintiffs past share of partnership profits.

2. The financial loss occasioned by impairment of earning capacity is the loss of what (if there had been no accident) the injured plaintiff would (as opposed to could) have expected to have under his control and at his disposal by exercising that capacity.

3. What the plaintiff would have had under his control and at his disposal, but for the accident, was the whole fruits of his skill and labour.

181. The High Court at [23] cautioned that in deciding what value is to be ascribed to the loss of future earning capacity of an injured plaintiff Courts are required to pay close attention to the facts of each case. The task is not one to be undertaken by seeking to classify cases as concerning “sole traders” or “partnerships” or “wage earners” or “trading trusts” and then attempting to adduce some rule of general application to all cases falling within the classification thus devised. Rather the enquiry is about what could the plaintiff have done in the workforce but for the accident and what sum of money would the plaintiff have had at his disposal.

182. Only when those enquiries are pursued can a judgment be made about what capital sum to allow for damages for the impairment of the plaintiffs earning capacity. In doing so regard must be had, of course, to all those contingencies of life that might reasonably be expected to affect the course of events in the future.

183. On the question of what account should be taken of the taxation consequences of income splitting arrangements the High Court said at [25] :-

“The assessment of damages for loss of future economic capacity involves questions

of judgment and estimation. Being an attempt to predict what would have happened, the process can never be exact. The fact that calculations are made by multiplying present values of net income by the expected duration of remaining working life should not obscure that the process is necessarily inexact. Even so, the assessment of lost earning capacity require some care in identifying (as best one can) what net income the plaintiff would have had at his or her disposal. That may require some consideration of the taxation consequences of different arrangements.”

183. The High Court then at [26] noted the reasons of the Full Court of the Supreme Court of South Australia in Spargo v Haden Engineering (1993) 60 SASR 39 where the plaintiff was a trustee of a discretionary family trust and while he alone generated the income it was also distributed to members of his family to minimise tax. The Full Court decided that the allowance for income tax should approximate the amount which he might have paid on the gross earnings if they had been brought to account by him rather than the family trust. The High Court commented that adjustment was not inappropriate in those circumstances.

The Date of Retirement

184. The Plaintiff claims damages to age 70 while the defendant submits that the normal retiring age of 65 is more appropriate. We are talking about farmers here and the plaintiff’s evidence is that he sees farming as a lifetime activity rather than a job. His elderly father is actually running a larger farm by himself. I accept the plaintiff’s evidence and find on the balance of probabilities that he intended to work as a sole farmer until the age of 70 years.

Offset of Mrs Ridgways Contribution

185. Howarths allege that the Crestinani Report overstates the plaintiff’s loss by making no allowance for the value of Mrs Ridgway’s clerical services which amounted to 4.5 per week.

186. I take the view that the few hours per week of book keeping were genuine labour and should be taken into account.

Taxation

187. There are two issue here:

1. How tax minimisation should be treated

2. Carrying forward of tax losses.

188. I have already agreed that some allowance should be made for the fact that Mrs Ridgway was performing some genuine book keeping services and it is not appropriate to treat all the income as the Plaintiffs.

189. There does not seem to be a great sum of money involved in this debate which revolves around Howarths view that only tax losses which have accumulated prior to 30 June 1999 and any arising “but for the illness” should be allowed. Adopting the principles in Husher concerning what the appellant would have under his control and disposal but for the accident I take the view that the Furzer Crestiani approach is the better one.

190. The Court is left therefore with two sets of figures for both past and future damage. In summary the bottom lines are:

Furzer Crestiani: $ 242, 154
Howarths: $ 204, 314
Difference: $ 37,840

191. The authorities point out that such assessments are a very inexact science and the parties are not very far apart. Little SC indicates that this client would see a sum of $220,000 as fair and reasonable.

192. Given my previous determinations I agree that such a sum would be appropriate subject to a deduction of 15 per cent for vicissitudes. I therefore award the plaintiff $ 187,000 damages for his future economic loss.

Summary of Damages Awarded.

1. General Damages:- $75,000

2. Loss of Expectation of Life:- $ 5,000

3. Future Medical Expenses:- $51,700

4. Griffiths v Kirkemeyer Expenses:- $201,456

5. Future Economic Loss:- $187,000

Total Damages:- $520,156

ORDERS

1. The Plaintiff is entitled to a verdict for $520,156

2. The defendant pay the plaintiffs costs.

CITATION:	Ridgway v Amaca Pty Ltd [2004] NSWDDT 42
PARTIES:	Richard Wakefield Ridgway Amaca Pty Limited
MATTER NUMBER(S):	375 of 2002
JUDGMENT OF:	Walker J at 1
CATCHWORDS:	:-
LEGISLATION CITED:
CASES CITED:
DATES OF HEARING:	23/02/04, 17/03/04, 23/06/04 & 14/09/04
DATE OF JUDGMENT:	11/02/2004
LEGAL REPRESENTATIVES:	FOR PLAINTIFF: Mr G F Little, SC instructed by Watkins Tapsell FOR DEFENDANT: Mr G Watson, SC instructed by Phillips Fox Lawyers

Financial Year	Directors Fees	Salary	Sale of Shares	Net Profit	Total
1994	$ 15,000	Unknown	Nil	($167)	$14,833
1995	Nil	Nil	Nil	($20,030)	$ 20,030
1996	Nil	$29,000	Nil	($19,925)	$ 48,925
1997	Nil	$32 500	Nil	($ 445)	$ 32,055
1998	Nil	$10,000	Nil	($10,498)	$498
1999	Nil	$20,000	Nil	($350)	$ 19,650
2000	Nil	$20,000	$ 8733	($16 771)	$5,544
2001	Nil	$25,000	$ 32083	(22,146)	$ 29,229
2002	Nil	$12,000	Nil	$36,123	$ 48,133

Farm Profit	2000	2001	2002
JWR	$3229	$2854	$48,123
Jason Ridway	$20,663	$25,374	$117,382
Profit from Farm	$17,434	$28,228	$165,505