Obst v Adelaide Brighton Cement Pty Ltd - [2010] SADC 112

DISTRICT COURT OF SOUTH AUSTRALIA
(Civil)
OBST v ADELAIDE BRIGHTON CEMENT PTY LTD
[2010] SADC 112
Judgment of His Honour Judge Barrett
23 August 2010
DAMAGES - MEASURE AND REMOTENESS OF DAMAGES IN ACTIONS FOR TORT - MEASURE OF DAMAGES
Dust Diseases. Assessment of damages. Plaintiff suffered asymptomatic pleural plaques arising from exposure to asbestos dust during 38 years of employment with the defendant. He had been a smoker for many years but had ceased smoking for about 20 years before experiencing breathlessness. Dispute about whether he suffers from asbestosis, and if he does, how much of his injury was caused by asbestosis and how much by emphysema.
Held: Plaintiff does suffer from asbestosis. It contributes equally with emphysema to the breathlessness but it has a "threshold" effect exacerbating the other injury and perpetuating the symptoms. Awarded $60,000 general damages, Griffiths v Kerkemeyer Damages.
Dust Diseases Act 2005 s 9(3), s 8(1), referred to.
Ewins v BHP Billiton Ltd and Ano (2005) 91 SASR 303; Trevor John Reynolds v Comcare [2006] SADC 136; Raneberg v BHP [1993] SASC (371/92); Mosely v The Broken Hill Proprietary Co Ltd [1998] SASC 6522; Peter Michael Callinan v Comcare [2006] NSWDDT 25 (4 August 2006); John Downes v Amaca Pty Ltd [2008] NSWDDT 25 (1 October 2008); Adrianus Gregoris Marie Bakker v Workcover Queensland and Ors [2008] NSWDDT 37, considered.

OBST v ADELAIDE BRIGHTON CEMENT PTY LTD
[2010] SADC 112
Introduction

The plaintiff is a 76 year old man (born 23 April 1934) who is seeking damages for dust diseases he contracted when employed for some 35 years by the defendant as a fitter and rigger. He retired aged 61 in about 1995. He was asymptomatic until 2002 when he experienced breathlessness. He says his breathlessness is caused by asbestosis.
The defendant does not dispute liability. It accepts that, as a result of the plaintiff’s exposure to asbestos during his employment, he has developed pleural plaques. The defendant says however that the plaintiff’s exposure to asbestos was minor. It denies he suffers from asbestosis. The pleural plaques have nothing to do with his breathlessness. The defendant says that the plaintiff’s breathlessness is caused by emphysema and asthma. The emphysema is caused by years of smoking. If, contrary to its case, the plaintiff does suffer from asbestosis, that disease is a very minor contributor to his breathlessness.
Issues
1.What is the extent of the plaintiff’s exposure to asbestos?
2.Does the plaintiff suffer from asbestosis?
3.If the plaintiff does suffer from asbestosis, does he suffer from any other dust disease which may be contributing to his respiratory disability?
4.If the plaintiff does suffer from asbestosis, to what extent is his respiratory disability caused by that particular condition and any other dust disease?
5.What, if any, loss or injury is caused by a dust disease?
6.What damages should be awarded for any loss or injury caused by a dust disease?

1. The Plaintiff’s Exposure to Asbestos
The defendant operated a quarry and cement factory at Angaston in the Barossa Valley. The plaintiff was employed by the defendant at Angaston from 1957 when he was 23, until he was 61, a period of about 38 years. He was not exposed to asbestos other than during his employment by the defendant.
For the first 10 years of his employment the plaintiff was a fitter’s mate. For the rest of his employment he was a rigger, retiring as a senior rigger. The plaintiff was not very forthcoming about his exposure to asbestos. He did not appear to exaggerate his exposure. On the contrary, he had to be questioned carefully in examination-in-chief before he articulated the aspects of his work which brought him into contact with asbestos and asbestos dust. He did not clearly separate his exposure as a fitter and his later exposure as a rigger.
The plaintiff said that during his employment he used asbestos rope. Asbestos rope was used as an insulator and a sealant but the plaintiff never spelt out how he came to use it.
It appears the plaintiff came into contact with asbestos used as cladding on large fans. He would be involved in doing maintenance work on the fans “a couple of times a year”. Dust containing asbestos was disturbed when that work was undertaken. Asbestos was somehow used to cover the new fans. How that came to be was never explained.
Asbestos was used to lag pipes around a kiln. That kiln was dismantled when it changed from being coal fired to being oil fired. It appears the plaintiff was involved in the dismantling of the kiln on only one occasion. The job took a couple of months but not continuously. It appears that if the job had been done continuously it might have taken a few days.
The plaintiff said that at times he was working closely beside others who were removing or replacing asbestos. He said sometimes he was doing “it” himself, but he did not make clear what that work was. He said he did not really notice dust coming from that operation. He never wore protective clothing and was never told to do so.
It is not possible to accurately describe or quantify the extent of the plaintiff’s exposure to asbestos or asbestos dust. It has been described by Dr Antic as “probably at the mild end of the spectrum”[1]. Associate Professor Holmes said “he would be exposed to asbestos on a regular basis” and he had “ongoing asbestos exposure through much of his [38 years employment]”[2].
[1] Dr Antic’s Report 5 January 2008 Exhibit P8 p 2.
[2] Associate Professor Holmes’ Report 16 March 2007 Exhibit P2.
Mr Hanus for the defendant, described Dr Antic’s account as accurately reflective of the plaintiff’s evidence. He submitted that the inference by Associate Professor Holmes of greater exposure is inaccurate. Associate Professor Holmes thought that an industrial hygienist might be the person best qualified to assess the extent of exposure. Dr Antic agreed.
All I can do is observe that the plaintiff was working for some 38 years in an environment where asbestos was present. No-one adverted to the need to protect workers such as him from exposure to asbestos or asbestos dust. He himself was exposed about twice a year to dust containing asbestos when he undertook maintenance on fans. He had some unspecified connection with asbestos rope. On one occasion he was exposed to asbestos dust when a kiln was dismantled. That was an exposure of several days length although spread over some months.
The twice yearly exposure to asbestos dust could fairly be described both as “regular” and “ongoing”, although neither expression described the frequency of the exposure. Those are the expressions used by Associate Professor Holmes. I do not describe those expressions as inaccurate. Dr Antic says that the plaintiff’s exposure is at the mild end of the spectrum but I have no evidence of the spectrum to which he refers. I cannot describe his evidence as inaccurate.
The finding I make is that the plaintiff had exposure to asbestos dust at least twice a year for 38 years. Further, he had exposure on one other occasion for a period amounting to a few days when he helped dismantle a kiln which was lagged with asbestos.
I have the impression the plaintiff had a greater exposure to asbestos than he has been able to articulate but I cannot quantify this greater exposure.
2. Does the Plaintiff Suffer from Asbestosis?
It is common ground between the two medical witnesses that the plaintiff has pleural plaques. They do not agree that he suffers asbestosis. Associate Professor Holmes says he does. Dr Antic says he does not. The principal symptom from which the plaintiff suffers is breathlessness. Associate Professor Holmes says that on balance asbestosis is the cause of that breathlessness. Dr Antic says that if, contrary to his opinion, the plaintiff does have asbestosis, it is a very minor contributor to his condition. Both doctors agree that pleural plaques do not cause breathlessness. I will deal first with the issue of whether the plaintiff suffers from asbestosis.
No provision of the Dust Diseases Act 2005 (“the Act”) bears on proof of the existence of a dust disease. Section 8(1) provides that once it is established that a person suffers from a dust disease, and that person was exposed to asbestos dust where the exposure might have caused or contributed to the disease, it will be presumed that the exposure caused or contributed to the disease. The presumption is rebuttable. However the onus of proving the disease in the first place rests upon the plaintiff.
Before discussing the disputed medical opinions about the existence of asbestosis, I refer to the plaintiff’s medical history. He suffers from asthma, emphysema, pleural plaques, hypertension, oesophageal reflux, hyper-cholesterolemia, gout and diabetes. He is taking medications for these conditions. He also suffers backache.
The plaintiff smoked from when he was about 14 until 1983. (He told Associate Professor Holmes 1985). He smoked about a packet of cigarettes a day. His evidence would suggest a smoking history of about 35 years. He had been abstinent for about 24 years when first seen by Associate Professor Holmes in March 2007. The plaintiff first noticed breathing problems in 2002, some seven years after he retired from work.
Associate Professor Holmes first saw the plaintiff on 15 March 2007. His first report[3] is dated 16 March 2007. The plaintiff told Associate Professor Holmes that over the preceding five years he had been gradually getting more short of breath. During the medical examination Associate Professor Holmes heard “basal crackles”. He conducted a lung function test on the day of the consultation. It revealed a “moderate obstructive ventilatory defect with a significant improvement in FEVI with bronchilator”. Associate Professor Holmes found that there was still some abnormality after the bronchilator. He noted “lung volumes revealed a normal total lung capacity and gas trapping”.
[3] Exhibit 2.
The plaintiff brought with him to the consultation a CT scan of his chest taken on 23 March 2006, about a year earlier. Associate Professor Holmes observed calcified pleural plaque in the right posterior lower zone. There was some plaque in the left diaphragm as well. Associate Professor Holmes noted that there were also “interstitial changes of a mild nature in the lung bases with some honeycombing”.
Associate Professor Holmes’ diagnosis was that the plaintiff had mild interstitial lung disease which he believed was asbestosis. He reported that the lung function test revealed the plaintiff had asthma. He said that the plaintiff’s fixed obstructive ventilatory defect was likely to be related to his earlier smoking (Associate Professor Holmes provided a later report dated 3 December 2007[4], but this related to anticipated medical costs and there was no further consultation before that report).
[4] Exhibit P3.
Dr Antic saw the plaintiff on 26 November 2007, about eight months after Associate Professor Holmes. His report is dated 5 January 2008 and is Exhibit P8.
The first difference between the observations of the two doctors is that Associate Professor Holmes detected crackles in the chest examination whereas Dr Antic did not. I will return to that topic.
Dr Antic read the same CT scan taken in 2006 which Associate Professor Holmes had read. He conducted his own lung function tests during his consultation with the plaintiff in November 2007. He had read Dr Holmes’ report of 16 March 2007.
Dr Antic’s observations about the CT scan were somewhat different from Associate Professor Holmes’. Like Associate Professor Holmes he noted the right pleural plaques. He described what he saw in the left diaphragm differently from Associate Professor Holmes who had said that there was some plaque there. Dr Antic described what he saw as “sub-pleural lines of uncertain significance”. He said that there was “no definite evidence of interstitial lung disease and there were a few small apical cysts suggestive of some emphysema”.
Dr Antic regarded the CT scan as being of suboptimal quality for the purposes of identifying interstitial lung disease. He said the scan should be repeated. The scan was repeated on 9 December 2008. I will return to discuss that scan in due course.
Referring to his own lung function tests, Dr Antic said that there was “marked airway narrowing and a significant improvement after bronchodilator therapy indicating that, at least in part, the narrowing is from asthma”. He went on “the diffusing capacity measurement is reduced. This points to a disorder of the lung substance or pulmonary vessels”. He said again that a better quality scan would assist in considering the existence or otherwise of interstitial lung disease.[5]
[5] Exhibit P8 p 1.
Dr Antic suggested that there were three reasons for the plaintiff’s reduced mobility and breathlessness. They were: 1) he has a back problem, 2) he is moderately overweight (height 178cm/weight 97kg), 3) obstructive airway caused by a combination of smoking and asthma, not past asbestos exposure.
The trial began on 18 June 2008. The only CT scan available to both doctors at that stage was the one carried out in March 2006. The doctors gave their evidence in June. The matter was adjourned for addresses. For reasons that are not relevant there were delays in addresses being delivered. On 24 October 2008 the plaintiff applied to recall Associate Professor Holmes. I later granted the application over the defendant’s objection. I need not canvas the reasons for the application or the ruling. There were further delays in Associate Professor Holmes being called. He did not give his evidence until 24 April 2009.
By then the scan carried out on 9 December 2008[6] had been produced and made available to both sides. There was also a lung function testing conducted on the same day at the Northern Respiratory Function Unit[7].
[6] Exhibit P12.
[7] Exhibit P13.
The defendant elected not to seek to call any further evidence after being granted an adjournment to enable it to consider its position. Addresses were completed on 2 July 2009.
The doctors differ in their interpretation of the March 2006 scan. I watched the scan while each doctor made his observations. I cannot make a finding based on my own observations of the scan despite watching each doctor point out features on it. I must evaluate their evidence by reference to their oral evidence and its persuasiveness. There are, as it happens, other factors which assist in coming to a conclusion. I bear in mind that the plaintiff bears the onus of proving the existence of asbestosis.
The first step in the analysis of the scan is to determine whether there is interstitial lung disease. Dr Antic had access to Associate Professor Holmes’ first report when he examined the plaintiff in November 2007. He was invited by Mr Hanus in examination-in-chief to explain the agreements and disagreements he had with Associate Professor Holmes. That was a helpful way of approaching the evidence.
The first observation I make is that Dr Antic thought that while the scan was a reasonable quality it was not of optimal quality and a further scan should be obtained. Associate Professor Holmes thought that the scan was sufficient for the purposes of his diagnosis.
Dr Antic agreed with Associate Professor Holmes that there was “calcified pleural plaque in the right posterior zone” and “some plaque in the left diaphragm”.
Whereas Associate Professor Holmes took the view that “there were interstitial changes of a mild nature in the lung bases with some honeycombing” Dr Antic was less certain. I do not take Dr Antic to be categorically in disagreement with Associate Professor Holmes, but he said in his report, and reaffirmed in his evidence, that “there is no definite evidence of interstitial lung disease”.
Dr Antic said in relation to the part of the scan of the left diaphragm that there were “sub-pleural lines of uncertain significance”.
In cross-examination it was put to Dr Antic that he was wrong in not finding signs of asbestosis on the scans. He reiterated the suboptimal quality of the scan.
There was another difference of view between the doctors. Each interpreted differently cysts which were seen on the scans. Cysts can be caused by interstitial lung disease but they can also be caused by emphysema. Associate Professor Holmes said that emphysemous cysts are thin-walled, unlike the thick-walled honeycombing that he saw. Associate Professor Holmes described them as honeycombing being more consistent with interstitial lung disease. Dr Antic thought they were caused by emphysema. Dr Antic did not report seeing honeycombing. He offered to re-examine the scan and further investigate but that offer was not pursued.
Associate Professor Holmes agreed that the scans themselves would not identify the cause of interstitial lung disease. The causes include asbestosis but they may also be idiopathic or unknown.
So the first question is whether the evidence establishes that there was interstitial lung disease. Limiting for a moment that enquiry to the evidence arising from the scans, I think the second scan conducted in December 2008, tips the balance in favour of Associate Professor Holmes’ opinion. That scan, P12, was read and reported on by Dr Frank Voyvodic of Benson Radiology. Inter alia, Dr Voyvodic reported “there is minor basal interlobular septal thickening in keeping with early pulmonary asbestosis”. When Associate Professor Holmes was recalled, he reiterated his finding and referred to this report. The defendant was given an opportunity to recall Dr Antic. It elected not to do so. I have therefore no evidence suggesting that the second scan was suboptimal. I have no evidence of Dr Antic’s views about what the later scan discloses. I infer that the scan was optimal. I am left with Dr Antic’s views based on what he regarded as a suboptimal scan.
I prefer the evidence of Associate Professor Holmes on this topic. I find that the plaintiff has interstitial lung disease.
The interpretation of the scan does not dispose of the question of whether the plaintiff suffers from asbestosis. While I am satisfied that the plaintiff does suffer interstitial lung disease its cause may or may not be asbestosis.
Associate Professor Holmes agreed that, in the absence of pleural plaques, he would not be able to determine that asbestosis was the cause. Both doctors agree that the presence of pleural plaques establishes exposure to the inhalation of asbestos dust.
Associate Professor Holmes agreed that the plaintiff suffers obstructive lung disease caused by asthma and emphysema. Emphysema is likely to have been brought about by the plaintiff’s history of smoking.
There is another difference in the evidence of the two doctors but, unlike the CT scan, it does not necessarily arise from the doctors both interpreting the same data. It is the topic of crackles. When Associate Professor Holmes examined the plaintiff’s chest in March 2007, he heard crackles. The doctors agree that crackles are a characteristic sign of asbestosis but they may also be caused by other conditions such as emphysema and asthma. The crackles would be consistent with asbestosis but not determinative of its presence. Both doctors agree that if asbestosis was the cause of crackles it would normally be heard consistently. Unlike causes such as emphysema and asthma which may see crackles appear intermittently, asbestosis would be expected to produce crackles consistently. When Dr Antic examined the plaintiff in November 2007 he did not hear crackles. There is no basis upon which I would be able to find either doctor mistaken or unreliable on this topic. The only further piece of information relevant to this topic is that Associate Professor Holmes said that crackles are usually only caused by emphysema when that condition is severe. Neither doctor suggested that the scans showed severe emphysema. Dr Antic did however think that the lung function tests demonstrated that the plaintiff has severe obstructive disorder. Associate Professor Holmes thought it was moderate.

I am unable on the evidence to make any finding on the topic of crackles.
Finally, there is the evidence of the lung function tests. They were relevant to the question of whether asbestos is present.
Both doctors agree that the lung function test, do not, of themselves, demonstrate that the plaintiff suffers from asbestosis. The plaintiff suffers from obstructive airways disease. That condition is caused by a combination of asthma and emphysema. The emphysema is likely to have been caused by the plaintiff smoking, albeit that he stopped smoking over 20 years before the lung function tests were conducted in 2007. The later lung function test conducted in 2008 shows that the emphysema contribution to the plaintiff’s lung problems was reduced by better treatment of asthma. Associate Professor Holmes concluded that asbestosis was contributing to the plaintiff’s breathlessness. He so concluded by looking at the overall picture. He saw as significant that the plaintiff’s symptoms of breathlessness occurred quite dramatically around 2002. Before that the plaintiff had been able to undertake quite strenuous exercise but within quite a short period of time he was very much reduced in the activities he could undertake. Associate Professor Holmes thought that an opportunistic condition such as asthma might have been the trigger for the breathlessness but the symptoms remain notwithstanding that the asthma component is now being better treated.
Dr Antic did not see the relatively sudden onset of breathlessness as being helpful in isolating the cause. He thought emphysema was the likely explanation.
Associate Professor Holmes conceded that, in the absence of the plaintiff’s exposure to asbestos and the absence of the diagnostically significant pleural plaques, he would not have been able to attribute the lung function disability to asbestosis. The lung function results, in the absence of the wider history, would not point to asbestosis.
I accept that evidence is persuasive. The lung function tests are consistent with the presence of asbestosis but not determinative of its presence. Given the presence of pleural plaques and relying on the CT scan evidence, I find that, on balance, the plaintiff does suffer from asbestosis.
3. If the plaintiff does suffer from asbestosis, does he suffer from any other dust disease which may be contributing to his respiratory disability?
There is no evidence of any other dust disease which may be contributing to his respiratory disability. The pleural plaques do not contribute to any disability. There are however other contributors to his respiratory disability which are not related to asbestos exposure.
4. If the plaintiff does suffer from asbestosis, to what extent is his respiratory disability caused by that particular condition?
In his report of 5 January 2008[8] Dr Antic identified three reasons for the plaintiff’s “reduced mobility and breathlessness”. He said they were: 1) the skeletal disorder causing backache, 2) the plaintiff being moderately overweight, and 3) the airway obstruction. Dr Antic did not suggest that the back problem would contribute to the plaintiff’s breathlessness. Associate Professor Holmes said it would not. Dr Antic did not elaborate on the causal link between the plaintiff being overweight and his breathlessness. Associate Professor Holmes agreed that being overweight can increase breathlessness but he was not asked to comment on the degree of contribution being made by the plaintiff being overweight. Dr Antic was not asked about the contribution made by the plaintiff’s weight. In 2007 the plaintiff was described as moderately overweight. It is not clear how long he had been overweight.
[8] Exhibit P8.
I make this observation. There is no evidence of the plaintiff being overweight before he became breathless in 2002. His breathlessness has considerably curtailed his physical exercise, which before 2002, was quite vigorous (see details later). I conclude that to the extent that the plaintiff being overweight contributes to his present breathlessness, it, in turn, has been caused partly at least by his reduced physical exercise. I cannot separate or quantify the contribution of weight to the plaintiff’s present breathlessness.
Dr Antic said that if asbestosis was present it would aggravate the plaintiff’s impairment caused by other means. He said that its contribution would be “a small contributory factor to the overall event”. His estimate is that that contribution is hard to categorise “but it may be of the order of 5 or 10 per cent of the overall respiratory impairment”. He explained that these were “very rough, broad figures”. He explained that he tried to fix the estimate by reference “to the volume of lung that was involved rather than what ever its cause was”. He estimated that the volume of lung was probably no more than 10 per cent, probably less. I do not know how valid an exercise that is, ie estimating impairment by reference to affected volume of lung.
I think another factor must be taken into account. Associate Professor Holmes referred to the “threshold” factor. He explained that consideration in these terms. He said if the plaintiff suffered from only emphysema and asthma, he may not have suffered a loss of respiratory function at all. It is possible that the asbestosis did not cause the breathlessness that first became apparent in 2002. Both doctors think that the trigger for that breathlessness was asthma or a viral infection. Nevertheless Associate Professor Holmes said that the asbestosis adds to the other injuries. Despite later better treatment for asthma, with a consequent reduction of the contribution of asthma to the respiratory difficulties, the breathlessness remains. In his opinion there is no evidence that either emphysema or asbestosis is the predominant cause of the 35 to 40 per cent loss of lung capacity as measured by the gas transfer to both these diseases.
In the end I find that approach is persuasive. I find that asbestosis is the cause of 50 per cent of the respiratory disability.
5. What, if any, loss or injury is caused by a dust disease?
The principal injury suffered by the plaintiff is breathlessness arising from emphysema and asbestosis. He has pleural plaques but they are asymptomatic. The emphysema is caused by the plaintiff smoking.
Leaving aside the question of causal apportionment, the plaintiff suffers a loss of respiratory function of 30 to 40 per cent. The doctors disagree about the causes of the loss but not the degree of loss.
The breathlessness became apparent in 2002. The plaintiff was 68. He had been retired from the defendant’s employment for about seven years. He had given up smoking a little under 20 years before that. He had been divorced and living alone for many years. He lives in his own house.
The plaintiff’s breathlessness has restricted the extent to which he can: 1) look after himself and his house, 2) enjoy recreation and 3) exercise. Ms O’Connor opened for the plaintiff saying that he retired from work with a back problem on a disability pension. In cross-examination the plaintiff denied that he left work because of the back problem. He said he left because there was a “golden handshake” offered to him and some other employees. I accept his evidence about the reason for retiring. He said that his back is a problem at times. He receives physiotherapy for backache and “a sciatic nerve”. The plaintiff agreed that most days he feels some pain in his back which he attributes to arthritis. At times he gets pain when he bends down to put on his shoes. He agreed that he does not do house maintenance jobs that require him to climb ladders because he does not like ladders. He has fallen off a few times. He agreed that his back problem was “a bit of a problem” with some of the heavier gardening work such as lawn mowing and digging, although he said that he could “dig a fair bit” before the breathlessness became apparent.
Bearing in mind what I might describe as mobility problems caused by his backache, I turn to describe the plaintiff’s evidence about the effects of his breathlessness.
He says he is less able to do housework. Before he became “ill”, by which I take him to mean around 2002, he did most of his own housework. His wife used to visit him about twice a month and helped to some extent with the housework. Now she spends a day doing housework each month. She cleans and vacuums and makes the bed. She cleans the bathroom. He has local children clean the windows.
He used to be a keen and active gardener. I treat that as an activity he enjoyed and I include it among his recreational activities. He used to have an extensive vegetable garden. He was virtually self sufficient in vegetables, excluding some root vegetables that are cheaper to buy. He had several fruit tress. He did all the gardening himself. He says that he gradually became puffed out doing the gardening and gave it up altogether two or three years ago (2006‑7). His son-in-law now mows the lawn. A friend does the cleaning up around the garden.
Another recreational activity enjoyed by the plaintiff was fishing. He gave up rod fishing on the River Murray because he lost the inclination but he gave up crabbing at Port Wakefield because the effort of walking long distances and hauling the crabs became too exhausting. Although not specific I infer that that activity was given up two or three years ago.
The plaintiff used to exercise regularly. He had an exercise machine at home which he used twice a day. He would do 200 push-ups twice a day. He used to walk for about an hour in the mornings. He gave up this exercise because he could not manage it any longer because of breathlessness. He was not very precise when he gave up this exercise. He described the time as being a “couple” or a “few” years ago and “three years ago at least … could be longer than that”.
The plaintiff said that when walking from the railway station to his solicitor’s office in Waymouth Street he had to stop three times. I take judicial notice of the fact that there is an uphill rise for most of that distance but I accept that anyone who could do 400 push-ups a day would be unlikely to need a rest on such a journey. Nowadays he still walks for exercise but only around the block.
When the plaintiff first saw his doctor about the breathlessness he was given the scans which were taken and he understood from the commentary to them that he might be suffering from an asbestos related disease. He was frightened. He thought he would probably die. He thinks his breathing has got worse since he first became aware of the problem. He concluded his examination-in-chief by saying that he feels anxious about his symptoms. No psychiatric evidence was called but I accept that someone who experiences breathlessness and who believes it may be related to exposure to asbestos would feel anxious. I have not overlooked the other causative factor in the plaintiff’s case but anxiety about asbestos related illness is, I accept, a very real one.
I found the plaintiff an honest and reliable witness although imprecise about dates. I do not think he exaggerated his conditions or his symptoms. If anything he appeared unable to articulate them clearly.
Associate Professor Holmes said that asbestosis is likely in the plaintiff’s case to be a slow progressive disease although it is not inevitably so. He said it is unlikely to cause the plaintiff pain. The condition is presently in a mild form. Age and emphysema will contribute to the deterioration in lung function caused by asbestosis. Associate Professor Holmes thought that the emphysema would be less likely to contribute to the progress of the disease than asbestosis.
The plaintiff’s life expectation will not be affected. In accordance with life tables his life expectancy would be of the order of 10 years. According to Associate Professor Holmes the plaintiff is at a low risk of contracting mesothelioma. Associate Professor Holmes said 10 per cent, Dr Antic said 5 per cent. Associate Professor Holmes thought that the plaintiff had a 5 per cent chance of contracting lung cancer. He said that while the risk of lung cancer is low, it is increased in patients exposed to asbestos, and more particularly in respect of patients who have previously smoked. He said the added effect of the exposure to asbestos on former smokers is multiplicative rather than additive.
Associate Professor Holmes did not think that the plaintiff’s risk of suffering cor pulmonale and respiratory failure was high. He thought it was in the vicinity of 5 per cent due to asbestosis.
In the next 10 years the lung function deficit due to asbestos is likely to increase from 15 to 20 per cent to 20 to 25 per cent. The consequence of that increased deficit would be to disable the plaintiff from doing heavy housework such as vacuuming and gardening tasks such as lawn mowing. He should still be able to attend to his personal maintenance such as washing, laundering clothes and preparing meals. I accept these prognoses by Associate Professor Holmes.
6. What damages should be awarded for the loss and injury caused by the dust diseases.
The parties have agreed past and future Griffiths v Kerkemeyer damages and Past Replacement Damages[9]. I will confirm the quantum under these heads with counsel before making the final order.
[9] Exhibit P10.
General damages.
The plaintiff is a 76 year old man who retired from work about 15 years ago when he was 61. He has been divorced for many years. He lives alone. He has had for some years a variety of conditions which have nothing to do with asbestos exposure. They include asthma, emphysema, hypertension, oesophageal reflux, hypercholesterolemia, gout, diabetes and backache. As numerous as these conditions are, with three exceptions, they have all been managed by medication. The exceptions are asthma, emphysema and backache. The asthma was undertreated from about 2002 until 2007. Since then a ventolin puffer has largely removed the symptom. Emphysema is a continuing contributor to the plaintiff’s major complaint of breathlessness. The plaintiff was a smoker for over 30 years but he gave it up over 25 years ago. The plaintiff’s mobility has been restricted by his backache. He has had backache for many years. He had it when he retired from work. Nevertheless the backache did not stop him from undertaking most of his housework. He was able to do most of his house maintenance except for jobs requiring climbing ladders. He was able to do all of his extensive gardening. He was a keen gardener and maintained a productive fruit and vegetable garden. He was a recreational fisherman. He has given up crabbing because of the breathlessness. He undertook vigorous physical exercise but, apart from limited walking, he has stopped doing so.
The plaintiff’s breathlessness is presently caused equally by his emphysema and asbestosis. I nevertheless accept the evidence of Associate Professor Holmes that the asbestosis may have what he described as a threshold effect. The plaintiff probably suffered from emphysema before 2002 but it was a symptomatic. He had given up smoking many years before and did not suffer breathlessness. Both doctors think that an attack of asthma or possibly a viral infection triggered the symptoms in 2002. In the absence of asbestosis the plaintiff may have recovered from the triggering illness and remained free of breathlessness. But the presence of asbestosis, in combination with the emphysema, has left the plaintiff with the symptoms which will continue to get worse. It is the asbestosis which will contribute more to the deterioration than the emphysema. I accept Associate Professor Holmes’ opinions in these respects.
In these circumstances I agree with the submission of Ms O’Connor for the plaintiff, that I should not simply halve the general damages which would otherwise be appropriate for the total pain and suffering of the plaintiff.
I have had regard to the South Australian cases dealing with awards for asbestos related illnesses[10] and also some of the cases decided by the New South Wales Dust Diseases Tribunal.[11]
[10] Trevor John Reynolds v Comcare [2006] SADC 136.
Raneberg v BHP [1993] SASC (371/92).
Mosely v The Broken Hill Proprietary Co Ltd [1998] SASC 6522.
[11] Peter Michael Callaghan v Comcare [2006] NSWDDT 25 (4 August 2006).
John Downes v Amaca Pty Ltd [2008] NSWDDT 25 (1 October 2008).
Adrianus Gregoris Marie Bakker v Workcover QLD & Ors [2008] NSWDDT 37.
I bear in mind the remarks of Doyle CJ in Ewings v BHP Billiton Ltd[12] in which His Honour held that damages awarded in this State should reflect the approach taken by courts in this State rather than the approach taken by the New South Wales Dust Diseases Tribunal. In that jurisdiction damages appear somewhat higher.
[12] (2005) 91 SASR 303.
Having said that, none of the cases referred to me is exactly the same as this case. I must make an award that reflects as best I can, the unique circumstances of the plaintiff.
I approach the fixing of damages by first treating the whole of the plaintiff’s loss and injury as due to asbestosis. Then I will make a deduction reflecting what I regard as the contribution made by emphysema in particular, but also having regard to the limitations on the plaintiff’s mobility brought about by his back problem. I also bear in mind that he suffers from asthma. Were it not for the non asbestos contributions I would have awarded the plaintiff $90,000 by way of general damages. For the pain and suffering caused by asbestosis alone I reduce the general damages to $60,000. I allocate $30,000 for past loss and $30,000 for future loss.
I will hear from the parties on the other heads of damages including past out-of-pocket expenses, future out-of-pocket expenses, Griffiths v Kerkemeyer damages, s 9(3) damages of the Act, interest and costs.