Muller v Qld Electricity Com
[1999] QSC 123
•8 June 1999
IN THE SUPREME COURT
OF QUEENSLANDBrisbane No.755 of 1990
Before the Hon. Mr Justice Shepherdson
[Muller v Qld Electricity Com.]
BETWEEN:
ROY ARTHUR MULLER
Plaintiff
AND:
QUEENSLAND ELECTRICITY COMMISSION
DefendantREASONS FOR JUDGMENT - SHEPHERDSON J.
Judgment delivered 8 June 1999
CATCHWORDS: NEGLIGENCE - Master and Servant - Toxic Tort - plaintiff worked as a surface coating inspector for the defendant - now has severe irreversible asthma - claim that exposure to isocyanates at work caused his present condition - pre-May 1987 plaintiff was asthmatic - whether plaintiff has proven a causal relationship between the deterioration in his asthma and exposure to isocyanates - damages.
Holtman v Sampson (1985) 2 Qd R 472
Watts v Rake (1960) 108 CLR 158
Purkess v Crittenden (1965) 114 CLR 164
Skelton v Collins (1966) 115 CLR 94
Malec v JC Hutton Pty Ltd (1990) 169 CLR 638
Counsel:Mr Curran for the plaintiff
Mr Griffin QC with Mr Allan for the defendant
Solicitors: Hillhouse, Burrough, McKeown for the plaintiff
Crown Law for the defendant
Hearing dates: 22 March 1999 - 30 March 1999
IN THE SUPREME COURT
OF QUEENSLANDBrisbane No.755 of 1990
Before the Hon. Mr Justice Shepherdson
[Muller v Qld Electricity Com.]
BETWEEN:
ROY ARTHUR MULLER
Plaintiff
AND:
QUEENSLAND ELECTRICITY COMMISSION
DefendantREASONS FOR JUDGMENT - SHEPHERDSON J.
Judgment delivered 8 June 1999
The plaintiff has sued his former employer for damages for personal injuries allegedly suffered while performing work for the employer.
The claim is based on alleged negligence and alleged breach of contract of employment. His claim essentially is that in the course of performing for the defendant his duties as a surface coating inspector, he was exposed to a toxic chemical named isocyanate, and as a consequence of that, his pre-existing asthma condition was severely aggravated causing him to suffer irreversible lung disease involving fixed airway obstruction.
The main issue litigated at the trial was whether the plaintiff has proved that the irreversible lung disease was caused by his being exposed to isocyanate at certain places named in the pleadings.
There was no dispute that at the time the writ of summons in this action issued - 22 May 1990, - the plaintiff did suffer asthma.
The plaintiff was born on 9 July 1942. He was employed by the defendant since 1973 and from early 1982 worked at Brisbane as a surface coating inspector. I find that on 11 December 1989, he ceased work as a surface coating inspector and that he has not worked since.
Although in evidence he said that the surfaces he was required to inspect included galvanising, rubber lining, basalt, concrete, industrial paints and commercial paints (T38), Exhibit 32 dated 2 February 1982 sets out the position statement for the surface coating inspector of which plaintiff was the then incumbent. I shall later mention Exhibit 32 again and also Exhibit 33 which was an internal memorandum dealing with the plaintiff's reclassification from "civil construction inspector" to "surface coating inspector". (see paras 34 - 37 post)
The parties agreed on a number of issues which were not in dispute and the issues which were in dispute. This agreement appears in Exhibit 4 and the issues not in dispute were:
1.That in the course of his employment the plaintiff worked at the places referred to in paragraphs 6B and 6D of the amended statement of claim;
2.That the defendant knew that isocyanate was a toxic chemical which was harmful to health and could cause lung disease and reduced lung capacity;
3.That polyurethane substances used upon the plant for the defendant's Callide power station would have contained isocyanates; and that the rubber lining solution at Beltreco in 1987, 1988 and 1989 would have contained isocyanates.
The places in paras 6B and 6D of the amended statement of clam were:
·IMP Blast Cleaning and Painting Works at Evans Road, Salisbury, Brisbane
·G&J Dowrie Cranes at Marsden
·Beltreco Rubber Lining Factory at 93 Colebard Street, West Archerfield, Brisbane.
The issues which were in dispute are:
1.The nature and extent of the work done by the plaintiff which might have involved exposure to isocyanate;
2.Whether the plaintiff suffered injury in consequence of the inhalation of isocyanate at any of the places referred to in paras 6B and 6D of the amended statement of claim;
3.Whether the plaintiff's pre-existing asthma condition was aggravated by exposure to isocyanate at any of the places referred to in paras 6B and 6D of the amended statement of claim.
The plaintiff himself gave lengthy evidence both in-chief and in cross-examination. He was as I find reluctant to concede that in 1984 Dr Maurice Heiner, a thoracic physician, then diagnosed plaintiff as having asthma. In February 1987 he underwent a histamine challenge test and then accepted that he had asthma. On 14 February 1986 Dr Black performed surgery on plaintiff's nose to improve his breathing. On the evidence, I find it more likely than not that as a child the plaintiff suffered asthma.
The plaintiff impressed me as a man who had, perhaps not unnaturally, thought long and hard about this case against his former employer. I found him to be a person who denied outright or down played matters or events earlier in his life which he appears to have thought might damage his case. The events with which I am concerned on the issue of liability occurred many years ago; the main focus was on events in the three year period before 22 May 1990, the date of issue of plaintiff's writ. I find the plaintiff was, from about mid 1987 conscious of the statute of limitations and any effect it might have on his claim - I shall later refer to this particular aspect and its effect on plaintiff's credibility.
A number of times the plaintiff flatly rejected as incorrect words and actions attributed to him many years ago. I was surprised at the confident manner in which he made these denials considering the time elapsed since the words and actions. For example, in a report dated 30 July 1984, which Dr Heiner made to Dr G Crichton of Annerley (plaintiff's then general practitioner) after Dr Heiner had first consulted with the plaintiff, Dr Heiner said a number of things each of which the plaintiff denied. For instance, Dr Heiner in that letter recorded plaintiff as having told him that he was "an ex-smoker who quit twenty years ago after smoking up to 100 cigarettes a day for 5 years". The plaintiff denied having told Dr Heiner that he had smoked a 100 cigarettes a day for 5 years saying "No-way that's an impossibility. You have to have a cigarette in your mouth 24 hours a day" (T159). When directed to the substance of the question he said he could not have told Dr Heiner that and added "I never smoked 100 cigarettes a day". In cross-examination he agreed he had smoked for about 5 years, saying "from about 16 on to about 20" He said in evidence he had about 40 to 50 cigarettes a week having built up from 30 a week.
In the same report Dr Heiner recorded "4 years ago he was diagnosed as having asthma and treated in Mackay with nuelin". The plaintiff denied this. Dr Heiner said in evidence that this is what plaintiff would have told him (T437). Plaintiff, while denying before me that he told Dr Heiner that he had been treated in Mackay with nuelin in about 1979, said that it was in 1979 he went on one course of nuelin - put on by Dr Simon Hooton "because I had a chest infection" (T160).
Dr Heiner also recorded "usually an active tennis player, he has been forced to give this up over the last 3 months because of his airway disease". The plaintiff denied having said this saying that he played tennis until March 1986. In contrast to plaintiff's denials, I prefer the accuracy of Dr Heiner's report in the above three matters.
I mention these matters because they and other matters indicated what to me was a determined approach by this plaintiff to deny strenuously any matter which he believed (whether correctly or incorrectly) might damage his case against the defendant and they indicated the plaintiff's determined approach to pin the blame for his condition on isocyanates. I shall later refer to some of these other matters and when I discuss Exhibits 57 and 39. He was as I have said concerned about the statute of limitations. Dr Heiner's report of 1 September 1994 made to Carberry's, plaintiff's then solicitors shows disagreement between plaintiff and Dr Heiner as to when plaintiff first mentioned isocyanates to Dr Heiner. I shall return to this aspect later.
I mention now that Dr Heiner has treated the plaintiff since he first saw him in mid-1984. Dr Heiner gave oral evidence as well as a number of written reports and I shall later come to his evidence. Plaintiff's hospital records in which Dr Heiner made entries are also part of the evidence.
The defendant challenged seriously the plaintiff's credit. Although there were occasions when the plaintiff appeared to be candid and frank in the witness-box, there were many occasions when his evidence contained mis-statements and non-disclosure. Overall, I found the plaintiff was not credible in many respects such that when it came to a number of important matters I have been unable to accept his evidence or accept it entirely.
I mention now one matter which adversely affected his credit. On 19 July 1988 plaintiff signed a statement for the Workers' Compensation Board (Exhibit 21). In that statement he said:
"I did not start to develop respiratory problems until 1984 when I spent a week in hospital (QEII) with industrial asthma."
This statement was, I find, consistent with other statements made by him to the effect that he was affected by solvents - see Exhibit 5 part C p 41 et seq for his application for Workers' Compensation dated 11 July 1988 in which the injury stated was "inhallation (sic) of solvents" and the reference by the plaintiff in a description given at p 45 of the same exhibit where he said:
"Surface coatings of rubber lining adhesives are heavily saturated with toxic petroleum solvents."
It thus appears that in mid-1988 plaintiff believed that his respiratory problems were due to inhalation of solvents. As Exhibit 57, a document prepared by plaintiff and dated 22 October 1997 shows it was about 19 July 1988 that he "began blaming isocyanate for sensitising me to solvents". I shall later return to Exhibit 57. Plaintiff was the surface coatings inspector at the time of his claim - a position in which he was, I find, a specialist. He based his compensation claim against the Board dated 11 July 1988 on inhalation of solvents and when, as he claimed he later found out that the SC2000 hardener used at Beltreco's premises contained isocyanate he thereafter has pursued this claim on the basis that it was exposure to isocyanate in the three year period from 22 May 1987 which aggravated his pre-existing asthma and led to irreversible lung disease involving fixed airway obstruction. In short, he has changed horses mid stream in order to avoid problems with the statute of limitations - a matter to which I find he directed his attention in 1987. (see para 153 post)
Although plaintiff worked for the defendant for many years, and as I find knew certainly from about 1984 that he had been diagnosed as having asthma, it was not until about 17 March 1988 that plaintiff told the defendant that he suffered asthma (T77). In Exhibit 5 part C at pp 39 - 40, is a photocopy of a sickness report and claim form signed by the plaintiff in respect of absence through illness on 16 and 17 March 1988. In that form, when it came to the heading "Nature of Illness" he wrote "breathing difficulties and congested chest" "ASTMA". (sic)
In evidence-in-chief he explained why he had not told the defendant that he had asthma saying (T77, T78):
"I felt it was none of his business it wasn't work related it was my own personal business."
He added that he did not believe that his asthma could be "affected detrimentally" by his work environment.
Although as I said the plaintiff was to some extent apparently candid in parts of his evidence-in-chief - he could hardly deny the contents of the report on pp 39 and 40 as he had signed it - I thought his excuse for not telling his employer of his asthma was unconvincing. Here was a man who was a surface coating inspector, who had been told in 1984 that he suffered asthma and who on his evidence had for a number of years suffered symptoms and respiratory problems after being in the presence of solvents. I thought plaintiff was an intelligent man, and it is clear that he, as a surface coating inspector, did relate his respiratory problems to the solvent fumes he smelt - see his 11 July 1988 Workers' Compensation claim.
It is the essence of the plaintiff's case:
(a)that from about July 1987 to October 1987 at the premises of IMP Blast Cleaning and Painting and thereafter until November 1987 at the premises of G&J Dowrie Cranes, polyurethane paint was used to paint structural steel components which were to be transported to the Callide B Power Station at Callide for erection (para 6B amended statement of claim);
(b)that the polyurethane paint contained isocyanate;
(c)that from about mid-November 1987 through to July 1988 at Beltreco Rubber Lining Factory, within the interior of tanks, vessels and other metal components a rubber lining curing solution which included material manufactured under the trade name RF - SC Hardener (also SC 2000), was used to bond rubber to metal (para 6D amended statement of claim);
(d)that the hardener in the curing solution contained a 10 per cent isocyanate component (para 6E of the amended statement of claim);
(e)that the plaintiff as part of his duties was required to carry out inspections of the work referred to in paras 6B and 6D, and that in respect of Beltreco his inspections concluded about July 1988 but he still had to attend those premises for other inspections until November 1989, and that during this period the curing solution referred to in para 6D was being used for other work.
It is subsequently alleged (in para 6G of the amended statement of claim) that the plaintiff thereby became exposed to and came into contact with and inhaled isocyanate, and that:
"6H As a consequence the plaintiff's pre-existing asthma condition was severely aggravated causing the plaintiff to suffer irreversible lung disease involving fixed airway obstruction."
The plaintiff in this case has nailed his colours to the isocyanate mast, although the evidence makes it abundantly clear that during the period of almost 8 years from about January 1982 when he became a surface coatings inspector, and during which time he worked for the defendant he came in contact with a number of solvents which did not contain isocyanate and that within several hours of such contact he experienced symptoms such as wheeziness, running nose, watery eyes.
His evidence was, and I accept that as at April 1987 the defendant was not using polyurethane paint (T184). I accept that at the premises of G&J Dowrie and IMP, polyurethane paint was used on items destined for the Callide Power Station.
There is no doubt that polyurethane paint, at the times material to the plaintiff's case, did contain isocyanate.
On 27 April 1987, plaintiff during one of his regular visits to see Dr Heiner, had handed to Dr Heiner a list which he himself had written. This list (Exhibit 36) contained the names of a number of solvents to which plaintiff believed he had been exposed in his work. Isocyanate does not appear on the list. I find the 20 or so chemicals on Exhibit 36 are the names which plaintiff had obtained from manuals which he had obtained from the manufacturers of the paints etc. which were being used by the defendant.
The preparation of Exhibit 36 and the handing of it to Dr Heiner resulted from matters discussed by Dr Heiner with the plaintiff, when Dr Heiner saw the plaintiff during plaintiff's visit to Dr Heiner at QEII Jubilee Hospital on 7 February 1987. In Exhibit 5, part A, on the back of p 115, (part of the hospital records) Dr Heiner has recorded "occupation - in & out of factories - chemicals ?". In cross-examination the plaintiff agreed that on 7 February 1987 there had been discussion with Dr Heiner to the effect that he, the plaintiff was in and out of factories and discussion about the fact that the plaintiff might have been exposed to chemicals.
Mr Griffin QC for the defendant then asked the plaintiff:
"I thought you told us that it wasn't till 88 that it even went through your mind that there might be some association between your problems and your work."
and the plaintiff answered:
"That wasn't on my mind. That was Dr Heiner's questions to me."
Mr Griffin said:
"So although you had those discussions it never went through your mind that there was any connection."
and the plaintiff replied:
"Because when I gave Dr Heiner that list he said none of the solvents or the chemicals on the list could cause asthma. That was his exact words. None of the chemicals listed caused asthma and he just said 'that's it'."
The plaintiff's answer to the last question quoted was unresponsive and I find that in February 1987 the plaintiff was aware that there might be some association between his work and the symptoms of which he told me e.g. watery and sore eyes, wheezing, cough and headache.
For the record, I add that on p 116 of Exhibit 5 part A, Dr Heiner has listed in the hospital records the items in Exhibit 36.
I pause to say that although Dr Heiner had been treating the plaintiff since mid-1984 - seeing him every two or three months - it was not until early 1987 that Dr Heiner apparently first heard from the plaintiff of the manner in which he performed his work (T178). I note that in his first report on the plaintiff (dated 30 July 1984 and written to Dr Crichton) Dr Heiner described plaintiff as an inspector for the Queensland Electricity Authority and noted "there is no fibro genic dust exposure". This suggests and I infer that at the time of consultation before the report was written there must have been some discussion between Dr Heiner and the plaintiff as to his working conditions.
I find that the plaintiff regarded his position of surface coating inspector as a specialist one and the defendant took the same view. Exhibit 32 which I have already mentioned is a position statement from the defendant in respect of "surface coating inspector". It was signed by the plaintiff as incumbent; it is dated 2 February 1982. Exhibit 32 shows the area of the defendant's operation in which the position was "inspector of protective surface coatings for the Board State wide"; the exhibit shows the purpose of the position was to "ensure that the quality of finished product workmanship surface preparation and quality of materials employed on equipment and plant required for service within the Board are in accordance with the relevant specifications and codes".
Under the heading "Organisation and Environment" the position statement notes:
"This position is the only specialist surface coating inspection position within the Board and as such provides a service throughout the Board. The incumbent as well as having extensive knowledge of the theory and practice of surface coatings would normally have been a skilled operator and have held supervisory positions in the industry."
A lengthy statement of duties is attached to Exhibit 32.
Exhibit 33 is an internal memorandum dated 2 February 1982, recommending plaintiff's reclassification to "surface coating inspector" in accordance with the position statement which is Exhibit 32.
I find that as the specialist surface coating inspector, plaintiff had in his office about 20 manuals from manufacturers of paints used by the defendant for coating purposes.
I find that to complete the list Exhibit 36 plaintiff had recourse to those manuals. I do not find that before February 1987 the plaintiff did not know the names of the solvents on that list. I find indeed that it is more likely than not that before Dr Heiner in February 1987 raised the question of chemicals in his work, the plaintiff knew the names of these chemicals. I make this latter finding given other evidence before me as to the conscientious manner in which plaintiff performed his duties as surface coating inspector. For example such evidence came from Mr Green of Beltreco.
The extent of the Plaintiff's exposure to Isocyanate
As mentioned already the plaintiff claimed to have been exposed to isocyanates during inspections at the premises of IMP Blast Cleaning and G&J Dowrie Cranes (in both of which places polyurethane paint was used in the final coating) and at Beltreco where the hardener used - SC2000 contained about 10 per cent isocyanate.
The plaintiff said he made inspections at IMP Blast Cleaning between late July/August 1987 and October 1987 (T49). I am satisfied these inspections were randomly made and unannounced. I accept plaintiff's evidence that for the first month he inspected about three times a week. On each occasion he was present for about 1 to 2 hours but all this time was not spent on inspecting the coatings - as plaintiff said the time was spent "going through things, paperwork QA [Quality Assurance] paper work and the items being processed" (T49). He claimed that after the first month he inspected at IMP about four or five days a week (T50).
The work he inspected at IMP and G&J Dowrie Cranes was for the defendant's Callide B project (T585/25).
I am satisfied that whenever the plaintiff attended IMP premises there was no spraying of polyurethane paint there. I am satisfied that in respect of items which plaintiff inspected, the final coating of paint which was the polyurethane paint, was applied by brush or roller. I find that at IMP, plaintiff inspected large pieces of structural steel which were in an enclosed building - plaintiff described the building as about five times larger than the courtroom in which the trial before me was heard. This evidence meant the building had a substantial floor area. I find the building had an entrance sufficiently large to enable trucks to enter.
The items inspected at the premises of G&J Dowrie Cranes were sited in a semi-open area - as I understood the plaintiff, the items to which polyurethane was applied were under a roof, the roof being supported by four posts and there was one wall only between two of the posts - the plaintiff described this area as "semi open" - I infer that on three sides the area under the roof was open to the elements.
The plaintiff estimated he had made inspections at G&J Dowrie Cranes twice a week. He did not say for what length of time he was at these premises but as the polyurethane was applied in the semi open any fumes or vapours from it must, in light of Mr Haig's evidence have been rapidly absorbed by the air (see Exhibit 9 at p 12), and I find it was extremely unlikely indeed that plaintiff was exposed to polyurethane fumes or vapour at G&J Dowrie Cranes.
Exhibit 8 contains photocopies of seven inspection advice notes completed by the plaintiff following three visits to IMP during September 1987, one visit to the Callide B site on an indecipherable date in September 1987, and three visits to G&J Dowrie Cranes in November 1987. These inspection advice notes (IAN's) did not purport to cover all visits plaintiff made to IMP and G&J Dowrie Cranes.
Mr Haig, the senior materials scientist employed by the defendant in addition to giving oral evidence, has provided a report "Investigation into Technical Issued Associated with Litigation: Roy Arthur Muller v QEC" (Exhibit 9). He did not visit the IMP site because by the time he came to prepare his report the IMP site had been closed for several years. It appears also that his report dated 9 February 1999, was probably made before the plaintiff further amended his statement of claim on 24 March 1999 to allege specific inspections at IMP, G&J Dowrie Cranes and Beltreco.
I find that plaintiff was a well experienced and conscientious even fussy surface coatings inspector. I find on the evidence he always approached a spray painter from behind and never from the front (T58). He denied ever having been exposed to over spray of paint at IMP (T58). I find also that when plaintiff saw Dr Robert Edwards, a thoracic physician, who gave a written report and oral evidence, Dr Edwards was left with the impression that plaintiff was not present when spray painting took place (T301/25).
I find also that at IMP's premises, solvent fumes were present in the air for about half an hour after a solvent was applied (T59), that application of polyurethane at IMP was not done in a fully enclosed building, and that at the IMP building the opening which permitted entry and exit of trucks was as the plaintiff said "one big door" (T59).
In respect of the work at the G&J Dowrie site, I accept plaintiff's evidence that application of polyurethane paint occurred "a lot less than 50 per cent" of the times when the plaintiff attended (T65).
I find on the evidence that when the plaintiff made inspections at the premises of IMP and G&J Dowrie, the coatings he inspected were dry and hard and these coatings were the final coatings which consisted of polyurethane paint which had been applied by brush or roller.
The evidence of Mr Haig was not contradicted. He impressed me as a competent and reliable witness. He is the Senior Medical Scientist of the defendant. He had earlier been the analytical chemist of the defendant.
In investigating plaintiff's claim he did not inspect the IMP premises. He did inspect the G&J Dowrie premises.
I accept Mr Haig's opinion that in respect of plaintiff's visits to IMP premises and G&J Dowrie's premises no effective assessment of plaintiff's exposure to airborne isocyanate during inspections of coatings is possible because conditions and activities at each inspection visit in 1987 are unknown.
I accept Mr Haig's further opinions and the reasons he gives for them that:
(a)plaintiff's exposure to airborne isocyanates during those inspections of coatings is possible but of low probability;
(b)that this aspect of the plaintiff's duties was that most subject to ad hoc conditions;
(c)that the potential for exposure to high levels of isocyanate mist, dust and vapour did exist, however normal inspection practices and active avoidance of spray drift would tend to eliminate or minimise exposure.
I find the risk of plaintiff having inhaled fumes from polyurethane paint at the IMP site and at the G&J Dowrie Cranes site was very low indeed and so low as to be negligible. On Mr Haig's evidence, I find also that the isocyanate in the polyurethane paint was of low volatility.
The only witness speaking of conditions at the IMP and G&J Dowrie premises at the time he made the inspections is the plaintiff himself. For reasons I have already stated concerning his credibility I am unable to accept entirely his evidence concerning his inspections at IMP and G&J Dowrie Cranes.
The plaintiff did not at any stage say that when he smelt fumes he immediately suffered symptoms or reactions to those smells other than occasional watery eyes - he spoke of symptoms appearing later.
The next alleged source of the plaintiff's contamination by isocyanate was the Beltreco premises. The items he inspected there were being fabricated for the New South Wales Electricity Commission Munmorah Power Station. On the evidence Beltreco were acting on the instructions of WE Smith Engineering Pty Ltd in performing the work and the plaintiff inspected on behalf of the NSW Electricity Commission. The cold curing process of applying rubber sheeting to a metal surface involved the use of a hardening solution known as SC2000. According to the plaintiff he found out in August or September 1989 (T107) that the hardening solution contained 10 per cent isocyanate. He said he learned this from a document Mr Green of Beltreco had handed to him (see Exhibit 5 - part C at pp 99 - 100 for photocopies of that document). By this time the inspections for New South Wales Electricity Commission at Beltreco had ended (in July 1988) but the plaintiff has alleged that he still had to attend those premises for other inspections until November 1989. I find that although plaintiff learned on about 12 September 1989 that the hardening solution contained isocyanate it was not until 20 November 1989 when he next saw Dr Heiner, that he mentioned to the doctor that he had been given the document to which I have referred. The hospital records (see Exhibit 5 - part A clinical notes - reverse of p 122) show the plaintiff saw Dr Heiner on 20 November 1989. The plaintiff gave evidence that he subsequently received from Dr Heiner in the mail a certificate entitling him to be absent from work for three months and that he ceased work on 11 December 1989 (T108).
. 60 I should at this stage say that it was not the plaintiff's case that during the currency of Beltreco's work for the New South Wales Electricity Commission, he attended Beltreco regularly and frequently for the whole of the period from November 1987 to July 1988. In cross-examination (T139) when he was asked:
"So when we come to 88 what proportion of your working week if you look at it over the year would you have spent in inspections."
he answered:
"Very little because I was under instructions in those days to do quality assurance based [work] and that was to view paper work if paper work only and that was at the completion of the job. I was not given the okay to go into contractors works and inspect in stages I had to only inspect work when it was offered to the QEC to come and inspect."
He agreed the same comment would apply to 1989 and 1987.
In Exhibit 23 which was a handwritten statement made by the plaintiff dated 12 December 1989, he said:
"I am now doing more office work and only go on inspections occasionally. My symptoms usually start up about an hour after exposure to chemicals."
As to particulars of plaintiff's visits to Beltreco, I shall refer first to the evidence of Terence William Green, whom the plaintiff called as a witness.
Mr Green was a rubber liner and the workshop foreman at Beltreco at times when the plaintiff attended Beltreco's premises (T348). He knew the plaintiff as the QEC Inspector and described him as very good at his job saying "He never told us he was coming. He would come in unannounced and watch the guys work and hang around and make sure they were doing it to procedures" (T349). He said:
"He followed the whole process from blasting right through to the inspection of the end of the rubber lining ... there was the blasting and priming then there is the actual rubber application then after the rubber application once it was all dressed up he would come and do the final inspection spark testing and hardness testing."
He said plaintiff watched the whole process including applying the glue (T349).
Mr Green said the hardener used in the cold curing process was SC2000 - at Beltreco it was mixed with the glue in a pot and then applied by brush or roller (T351). I find that after the glue was applied the rubber was applied. Mr Green said plaintiff called at Beltreco at least twice a week, and that towards the end of the job for WE Smith he recalled plaintiff wearing a cartridge mask which he kept on until he came into Mr Green's office to sign paper work. Mr Green's office was enclosed. Mr Green said he asked the plaintiff why he was wearing the mask and the plaintiff replied "that the chemicals and solvents that Beltreco was using were affecting his lungs".
Mr Green described the vessels on which the rubber was applied in the cold curing process as being pipes up to six metres in length with a diameter of about 1.8 metres and open at both ends. He described plaintiff as inspecting the work being performed and being about three metres away from where the work was being done. On occasions plaintiff would come within about a metre of the work (T352). The building at Beltreco had swinging doors which according to Mr Green (and I accept his evidence) were completely open and were as tall as the whole height of the building, the height of the swinging doors being about five and a half metres. I accept Mr Green's evidence that apart from ventilation through the swinging doors there were louvres which would generally be open (save that on very windy and dusty days they were slightly less open) and also two pedestal fans which could be moved from place to place. These fans were sited at least three metres away from a particular job (T357).
Mr Green recalled that during the time when Beltreco were doing the work for the New South Wales Electricity Commission (via WE Smith) the plaintiff asked him for a technical data sheet and when this was supplied the plaintiff brought to Mr Green's attention that isocyanates were in the hardener (T358).
Mr Green told me that the rubber applied to the vessels probably took 5 to 20 minutes to dry - the time depended upon the size area to which the rubber had been applied - the greater the area the longer the time - and that after the rubber was dry the fumes or vapours would have gone (T363).
I should add that in respect of the ventilation of the factory, Mr Green, after having visited a doctor in early 1987, personally took steps to ensure that the louvres in the factory were open save that they were not fully open when there was too much breeze and dirt or dust was being blown into the factory.
I accept Mr Green's evidence as I have set out above.
Exhibit 7 contains photocopies of 19 inspection advice notes signed by the plaintiff in respect of inspections he made at Beltreco between 25 November 1987 and 8 November 1989 (both dates inclusive). The first six inspections were between 25 November 1987 and 3 December 1987 (both dates inclusive) the next 11 inspections were between 5 January 1988 and 24 March 1988 (both dates inclusive), one note was dated 10 June 1988 and the last was dated 8 November 1989.
Exhibit 18 is a photocopy of an inspection advice note signed by plaintiff following an inspection at Beltreco on 14 April 1988 and Exhibits 19 and 20 are photocopies of further such notes for inspections on 27 April 1988 and 18 May 1988 respectively.
The pattern of plaintiff's visits to Beltreco as disclosed in Exhibits 7, 18, 19 and 20 accords with plaintiff's evidence and I find that after April 1988 plaintiff made very few inspections at Beltreco's premises at times when isocyanate was being used in the hardener. I am unable to assign a number to the "very few".
The plaintiff gave evidence that there was a strong smell of solvents of Beltreco (T75). He said that he had no problems breathing while at Beltreco but he had problems later in the day or at night time - sweating and sometimes watery eyes - he "found the solvents offensive" (T79). He did not tell me of any acute reactions at Beltreco and the absence of acute reactions is of some importance.
He estimated the length of time he spent at Beltreco on each visit was "anything from one to two hours". He said that he made probably three visits each week in late June early July 1988 and the frequency probably increased to four visits a week (T75). I do not accept entirely the frequency of plaintiff's visits. I do not accept the frequency increased as he claimed. The IAN's (Exhibit 7) point to most inspections between November 1987 and March 1988 - although I accept the IAN's in evidence do not represent all inspections he made.
I find that plaintiff's inspections at Beltreco were carried out in the crane bay of the building which was well ventilated.
I note also that it was during this Beltreco period that plaintiff first informed the defendant (on about 17 March 1988) that he suffered asthma.
I now return to the report of Mr Haig (Exhibit 9). I find that, for reasons advanced by Mr Haig in that report and in the witness-box, that plaintiff's exposure to airborne isocyanate during inspections of rubber lining operations at Beltreco was highly unlikely and that isocyanate vapour levels during the rubber lining work were negligible. As Mr Haig has pointed out in his report, that view is supported by Worksafe Australia opinions that brush or roller application of isocyanate - cross linked products does not give rise to a hazardous vapour. I find that the hardener used was an isocyanate - cross linked product.
Mr Haig in the course of his oral evidence said in cross-examination that the occupational hygiene literature indicated that trichloroethylene and dichloromethane were both respiratory irritants and in the case of persons working in the Beltreco operation inhalation of the former was probably the major hygiene aspect. I accept Mr Haig's evidence that trichloroethylene is an extremely volatile material (T628).
I accept this evidence as in my view there is a high degree of probability that the symptoms suffered by the plaintiff some hours after his visits to Beltreco were caused by trichloroethylene and not by the isocyanates in the hardener.
I accept evidence that:
(a)the vapour pressure of the isocyanate used in the hardener was extremely low and that there was no way that it could be classed as hazardous;
(b)that the isocyanate used in the hardener at Beltreco was particularly involatile (T629);
(c)isocyanates molecules in the air will react extremely readily with water vapour in the air and on moist or humid days would be "very quickly scrubbed out ... by the humidity of the day" (T599);
I accept Mr Haig's report Exhibit 9 and the opinions stated in it.
Dr Coralie Mary Bishop
On 5 July 1988 Dr Bishop was first consulted by the plaintiff relative to matters in this action (T371). Dr Bishop practised as a general practitioner at 25 Mary Street, Brisbane City - next door to plaintiff's work place. The plaintiff who had been her patient from 14 April 1987, first consulted her on 5 July 1988 in relation to a respiratory or asthma related condition. Although Dr Bishop did not remember the consultation she referred to her notes; these showed he complained his asthma was playing up, that he was experiencing more chest tightness and wheezing, and that he had been having temperatures and sweating on and off over the recent days. She found plaintiff to be in some respiratory distress and sent him for an X-ray.
On 7 July 1988 he returned to see her taking the X-ray with him. This showed a basal collapse consolidation in his left lung. Plaintiff called it a collapsed lung. Dr Bishop referred plaintiff to the QEII Hospital and gave him a letter dated 7 July 1988 for the admitting doctor (see Exhibit 5 part B medical records pp 71 -72).
On 22 July 1988, Dr Bishop sent to the Workers' Compensation Board a typed medical report on the plaintiff (Exhibit 5 part B pp 73 -75). In the history portion of that report she records plaintiff as having said that four years previously he was diagnosed as having asthma, that his work as a construction inspector for the Queensland Electricity Commission required him to enter areas where industry solvents were being used and he claimed that these made him unwell with a facial irritation and wheezing, that he had been under the care of Dr Maurice Heiner, a respiratory physician at the QEII Hospital, and that he was taking certain medications (named in her report). In the prognosis portion Dr Bishop said this:
"Mr Muller has severe asthma. I expect him to recover fully from this chest infection. However, I feel that if the industrial solvents are indeed the trigger for his asthma then he will continue to have problems while exposed to these solvents."
In her oral evidence before me, Dr Bishop said (p 375) that on 5 July he had told her that his asthma was playing up and he attributed the asthma to the new solvents, but she had no recollection of the plaintiff having told her of any particular solvent. Her contemporaneous notes (Exhibit 46) confirmed this recollection and point to the plaintiff having told her of solvents generally. On that date plaintiff was blaming his problems on solvents.
I find that plaintiff did not tell Dr Bishop he was exposed to isocyanates.
I find also that Dr Bishop knew from 12 July 1988 that plaintiff had been treated by Dr Heiner for asthma for three to four years. She noted in Exhibit 46 "industrial asthma" and that plaintiff's employer had bought a respirator for him but it was no use.
I find also that on 23 January 1989, the plaintiff attended Dr Bishop after having been working out at a gymnasium when he felt light headed, nauseated and fainted, being unconscious for about a minute.
Overall Dr Bishop's evidence (and she was called in the plaintiff's case) discloses that in 1988 the plaintiff believed his asthma was affected by inhalation of solvents while at work, but she provides no evidence of his having pointed to any particular solvent as affecting his asthma.
In her letter to the Workers' Compensation Board of 22 July 1988, Dr Bishop remained to be convinced that industrial solvents were "a trigger for his asthma". Obviously, if any solvent was such a trigger it needed to be identified so that again, fairly obviously, the plaintiff could avoid working in conditions where he might come into contact with such solvent or fumes therefrom.
The plaintiff's case against the defendant is based on exposure to isocyanates having been the cause of his present pitiable state and consequently the question whether the evidence has identified isocyanate as the agent which caused his state has been central in this case. I turn then to medical evidence dealing with that aspect.
Dr Robert Leslie Edwards
Dr Edwards is a thoracic physician, who has twice examined the plaintiff. The first occasion was on 7 December 1989 when Dr Heiner referred the plaintiff to Dr Edwards for a second opinion. The second occasion was on 25 August 1997 after a request by the Crown Solicitor, who acted and acts for the defendant.
Dr Edwards has given several written reports and at trial gave oral evidence (by telephone). His first report is dated 28 December 1989. A photocopy appears in Exhibit 5 part B medical reports pp 35 - 36.
From that report it is clear that Dr Edwards was aware that plaintiff was a coatings inspector and that he was required to enter factories to inspect works. In the history portion of the report he says "He moved to Brisbane in 1981 and was then required to inspect proceedings in closed buildings".
In this report he went on to say:
"When he inspects the protective coatings the substances that he is exposed to include polyurethane and epoxy paints in organic zinc and other materials containing isocyanates. With respect to the rubber linings he is also exposed to isocyanates and also tolueline which is used to dissolve the rubber linings. He first developed symptoms in 1984 when he developed a severe cough producing copious brown to yellow sputum and this was associated with wheeze, chest tightness and sleep disturbance.
When he first became ill he was having daily exposure to the fumes whilst visiting factories over a four year period. Symptoms were initially worse at work but tended to improve whilst he was away from work at week-ends and on holidays. Despite having symptoms he has continued to work in the same occupation but he now wears a cartridge filter mask. However, after visiting factories he develops wheeze and chest tightness within an hour of entering the factory. His symptoms are frequently worse the nights that he works in the factories."
It is apparent that Dr Edwards in the above passages was reciting what he recorded the plaintiff having told him.
I point out at this stage that when cross-examined Dr Edwards conceded that the subsequent exposure to solvents and isocyanates of which he spoke was (as he believed) in closed buildings.
He also conceded that when he said "When he inspects the protective coatings the substances that he is exposed to include polyurethane and epoxy paint inorganic zinc and other materials containing isocyanates," he assumed the plaintiff was exposed to epoxy and isocyanates when he made those inspections.
I asked Dr Edwards whether he had any reason for assuming that and he answered:
"Only that I either - he either obviously referred to that or it was my assumption that those materials contained isocyanate."
A little later in his report of 28 December 1989, Dr Edwards said:
"On the basis of his history Mr Muller has developed occupational asthma probably related to isocyanate and epoxy resin exposure. When lungs are sensitised to these substances even minute quantities may produce an exacerbation in airway obstruction. Although he is wearing a cartridge filter mask when he visits the factories he is probably still suffering significant exposure to the fumes. I consider that this is probably contributing to his continuing unstable asthma. My suggestion to his future management was (1) to avoid exposure completely and (2) to use a volumatic to deliver becloforte. If he continues to work in the current environment it is likely that the asthma will deteriorate. I believe that it is very important that he stops work in the current environment and that he works in another area. Provided he has no further exposure it is possible that the asthma will improve somewhat although given the nature of his symptoms and the length of time to which he has been exposed in conjunction with the continuing exposure after he has developed isocyanate sensitivity I do not think symptoms will ever subside completely and that he will continue to require intense regular medication for treatment of the asthma."
On 23 January 1991, Dr Edwards wrote to Quinlan Miller and Treston, plaintiff's then solicitors a report which largely repeated the contents of the report of 28 December 1989, but slightly altered the opinions which he expressed.
That report appears in Exhibit 5, part B, pp 37 - 38. In that report he then said:
"ASSESSMENT
On the basis of his history Mr Muller has developed occupational asthma related to isocyanate and epoxy resin exposure. Having developed asthma in response to exposure of these substances these patients frequently develop exacerbation in asthma when they are exposed to even minute quantities of such substances. Although he is wearing a cartridge filter mask when he visits the factories he is probably still being exposed to small quantities of fumes which is enough to trigger asthma in this situation.
I believed that at that stage I advised Mr Muller that the most important aspect in his management was to avoid any future exposure to these fumes. By doing this it is likely that the asthma will become more readily controlled with his current medication. However as he has continued to work in the same environment in which he developed asthma, it is most unlikely that he will lose the asthma completely at this stage. Once these patients have developed asthma in response to such exposure it is likely that they will continue to suffer from continuing asthma in the future particularly where there has been prolonged exposure after the sensitisation has developed.
Provided he has no further exposure it is possible that his asthma may improve slightly however I think this is unlikely in view of the long term nature of his exposure following the development of asthma."
It is obvious that in that report written in 1991, Dr Edwards was quite unaware that plaintiff had not worked since about mid December 1989.
I note that on 3 October 1994, Dr Edwards wrote a short note to Carberry's the plaintiff's then solicitors in which he said:
"Epoxy resins may cause sensitisation to the respiratory tract to produce asthma. They have a similar effect to isocyanates."
This comment is consistent with Mr Haig's statement in Exhibit 9 that "amine based hardeners for epoxy resins" are a proven occupational asthma agent.
I should say now that after hearing Dr Edwards ' oral evidence, I find that when in his report dated 28 December 1989, he said "When he first became ill he was having daily exposure to the fumes while visiting factories over a four year period", that statement related to the period commencing in 1984 and he, Dr Edwards related the illness to daily exposure (T299-20).
In my opinion, Dr Edwards in his two reports of 1989 and 1991 has made assumptions that in the four years from 1984, plaintiff was daily exposed to substances including polyurethanes and epoxy paints and that these contributed to the production of the symptoms which he developed.
On the evidence led in this case there was no evidence suggesting exposure of the plaintiff to any substance containing isocyanates before July 1987. Thus, any symptoms developed prior to that time could not have been attributable (if they were indeed attributable) to plaintiff having inhaled or been exposed to fumes or vapours emanating from a substance containing isocyanates. Indeed, to be specific, the symptoms which plaintiff told Dr Edwards he developed in 1984 namely a severe cough producing copious brown to yellow sputum associated with wheeze, chest tightness and sleep disturbance could not have been caused by isocyanates.
I should say now that in fairness to Dr Edwards, when he prepared the two reports to which I am about to turn, he said, after having seen and spoken to plaintiff on 25 August 1997, that it was not correct to say that plaintiff in effect was exposed to fumes containing isocyanate when he first came to work in Brisbane in 1981 and that the asthma he developed in 1984 was due to isocyanate exposure. In his report of 25 August 1997, he recorded that the plaintiff was adamant that he had no isocyanate exposure until 1987.
This report is in Exhibit 5 part B pp 40 - 43.
He recorded that since he last saw plaintiff, plaintiff had developed a number of complications including a myocardial infarction on 22 June 1994, but that he currently had no angina symptoms, had developed diabetes mellitus in January 1993 and osteoporosis also diagnosed January 1993. He recorded that plaintiff had had two admissions to hospital because of a severe exacerbation of asthma, one in 1991, and one in 1992, that he had been advised to have several admissions previously but had refused to go in and that he was then on very intense medication for asthma. He recorded also that plaintiff had a depressive illness for which he was being treated, symptoms of allergy for which he took tablets and that he took certain tablets for his cardiac condition.
On p 3 of this report Dr Edwards discussed isocyanates saying:
"Isocyanates are one of the substances that are known to induce asthma in previously non-asthmatic people. The normal history is one of a period of exposure without any symptoms and then developing asthma whilst at work and particularly in the evenings after being at work. The longer one is exposed to isocyanate fumes the more severe the asthma and the more likely it is to be a progressive disease and not respond after withdrawal from isocyanate. If a pre-existing asthmatic is working in conditions where they are exposed to isocyanate those isocyanate fumes can aggravate the asthma considerably and make the situation more severe. A person [who] had pre-existing asthma should never be exposed to isocyanates."
A little later in the same report Dr Edwards said this:
"Mr Muller has developed severe asthma which has been quite rapidly progressive. This sort of asthma is most unusual in development and I do not think he would have developed such severe asthma if he was not exposed to isocyanate fumes."
What is clear from Dr Edwards' report of 25 August 1997 is that by that date the plaintiff had severe chronic irreversible airway obstruction - an end stage of progressive asthma.
Dr Edwards said towards the end of this report:
"With respect to the aggravation of his pre-asthmatic condition it means that he now has severe fixed airway obstruction which is an end stage of progressive asthma. This end stage may be arrived at in some individuals from just severe continuing asthma or people who have had asthma, aggravated by industrial exposure or in people who have asthma which is entirely due to industrial exposure."
In Dr Edward's view there are thus three routes by which a person with a pre-asthmatic condition can arrive at the plaintiff's present state. Dr Edwards then went on:
"Mr Muller admits to having asthma before he was exposed to isocyanates so that it is likely that he would have continued to have asthma during this time. However, his asthma was initially relatively mild and would have been unlikely to have progressed to the extent of disability that he has arrived at now."
I shall later return to the opinions of Dr Edwards which I have just quoted.
In his report of 25 August 1997, Dr Edwards expressed the need to have access to certain hospital records to see if there was any reference to occupation and occupational exacerbation of asthma at the time of the plaintiff's discharge from the QEII Hospital in August 1984. Dr Edwards was then furnished with quite a large amount of material and on 27 July 1998 wrote a further report to Crown Law. He noted that "It would appear that plaintiff started to be exposed to a new substance called SC2000 in November 1987" and that in November 1989 plaintiff apparently discovered that isocyanate was part of the new substance. Dr Edwards noted plaintiff's claim that he was exposed to SC2000 at Beltreco and some exposure to polyurethane paint at IMP Blast and Cleaning Works and G&J Dowrie Cranes.
He prepared and attached to his report of 27 July 1998, a graph showing the plaintiff's spirometry values since February 1990. I find this graph was based on spirometer readings recorded in the plaintiff's hospital records on the occasion of each consultation he had with Dr Heiner. The hospital records from which this graph was plotted are in evidence before me. I shall later refer in some detail to this graph which I find is a document of great importance in this case. I shall particularly refer to it when discussing the evidence of Dr Young.
In his report of 27 July 1998, Dr Edwards said:
"Therefore on the basis of his history and the review of the file provided it would appear that he did have asthma since at least 1984 which may have been aggravated intermittently by substances in the work environment. However, between 1984 and 1987 his lung function was reasonably stable and reversible with his lung function being able to be maintained close to predicted normal values. However, after 1987 the severity of his asthma appeared to increase with him being more unstable and his asthmatic symptoms being more difficult to control. Following cessation of work his lung function has continued to deteriorate over the last nine years with a progressive deterioration until July 1992 with relative stability since then but on large doses of therapy. Therefore after reviewing all the information it would appear that his exposure to isocyanates between 1987 and 1989 has contributed to the deterioration in his lung function leaving him with severe asthma with a severe degree of fixed airway obstruction. There does not appear to be any evidence of isocyanate exposure prior to August 1987."
During his cross-examination Dr Edwards said he understood that the questions whether there was the exposure to isocyanate and the degree of exposure to isocyanate were, he assumed, questions in debate before this Court, and then conceded that he had proceeded on the basis of the degree of exposure of which he had been informed by the plaintiff.
I note also that in respect of his graph Dr Edwards conceded (T300) that the graph showed that it was in August 1991 that the major persistent downturn in the graph occurred.
Dr Edwards, in reaching his opinion, appears to have accepted unreservedly what plaintiff told him concerning exposure to isocyanates. As I have already noted in these reasons the plaintiff's statements as to his exposures cover both solvents and isocyanates - initially he spoke only of solvents and it was not until 1989 that he said he first learned that he may have been exposed to isocyanates. It seems to me that Dr Edwards did not look beyond what plaintiff had told him and did not look for evidence or details of the claimed exposure to isocyanate; did not look for evidence identifying isocyanate as a chemical to which plaintiff had been exposed; accepted unreservedly plaintiff's adamant claim that he had no isocyanate exposure until 1987 (para 110 ante); in short it seems to me that Dr Edward's has not diagnosed in a fashion acceptable to this Court that plaintiff has industrial asthma being aggravation of plaintiff's pre-existing asthma such aggravation being caused by exposure to isocyanate (see para 129 post (para e) for what a diagnosis of industrial asthma requires).
Dr Iven Hunter Young
Dr Iven Hunter Young, is a Consultant Respiratory Physician and Clinical Associate Professor of Medicine at University of Sydney. He is head of the Department of Respiratory Medicine, Royal Prince Alfred Hospital, Camperdown, Sydney and has held that position since 1991. He has been a respiratory physician at the same hospital since 1978.
Dr Young was called as a witness by the defence and by agreement he was interposed as a witness during the presentation of the plaintiff's case. He gave evidence prior to Dr Heiner, who was the principal medical witness for the plaintiff. Dr Young gave evidence in person and later, because of certain evidence given by Dr Heiner, gave further oral evidence (by telephone).
Dr Young wrote a number of reports all of which are in evidence. They are dated 7 December 1998, 16 February 1999, 7 March 1999 (see Exhibit 5, part B pp 27 - 34 inclusive) and 21 March 1999 (incorporated in Exhibit 5, part B to follow p 34).
Dr Young has not seen, examined or spoken with the plaintiff (T310). His curriculum vitae is Exhibit 45. Among his many publications and presentations is "Asthma - diagnosis and management. Practical pulmonary function testing - an invited presentation to the Royal Australian College of General Practitioners June 1986". I find that he currently teaches both undergraduate students in the University of Sydney and the graduate medical programmes there, and does a lot of postgraduate teaching to candidates for the physicians' examinations for the FRACP and for general postgraduate seminars to general practitioners. These are his three major areas of teaching (T309).
Dr Young's evidence both oral and written dealt with many aspects relevant to this case. I make the following findings:
(a)I accept his identification of the issue as being "what has made the plaintiff so much worse so that now he has very, very severe irreversible asthma" (T314);
(emphasis is mine)
(b)in the present case there is an absence of evidence from which a finding can be made that the inhalation of isocyanate fumes or vapours was the agent which on the balance of probabilities has brought plaintiff to his present state;
(c)I accept that Dr Edwards' graph is important and I accept Dr Young's conclusions drawn from it; more particularly the fact that in the period from February 1990 (when the graph began) until about August 1991, the spirometry readings taken by Dr Heiner and recorded in the hospital records and plotted on the graph by Dr Edwards showed that the plaintiff's airways were capable of improving to a level compatible with good function and compatible with the level at which he had been before;
(d)I accept Dr Young's opinion that the graph, up until August 1991 showed the plaintiff's asthma was not irreversible and that in or about August 1991, something dramatic happened to the plaintiff which required another explanation, given that August 1991 was so remote from the time when, on the plaintiff's case he was last exposed to isocyanate (T346);
(e)I accept Dr Young's evidence as contained in the following passage from the transcript concerning the diagnosis of industrial asthma:
"The diagnosis of occupational industrial asthma requires the demonstration that the patient develops asthma symptoms and/or objective deterioration in lung function, preferably the latter is included in this, because relying on symptoms alone is clearly not objectively as good. It requires the demonstration of a change in lung function within eight hours of exposure to the suspected agent. The reaction to the agent is often biphasic so the patient can have an immediate reaction within an hour and that can be demonstrated by symptoms, a fall in peak flow or a fall in the FEV1, then recover and have a further reaction 8 to 12 hours later. It usually begins within eight hours and then may persist for another four hours or so before slowly abating. Now that must be demonstrated on exposure to the agent. That can be done in a laboratory setting where you bring the patient in, suspect they are getting sick in the work place so you bring them into a laboratory, expose them to the agent, measure within an hour or two send them home with a peak flow meter or bring them back if you can and measure about eight hours later. If you can demonstrate that you have clear evidence the patient has an asthmatic reaction to the agent. More commonly however, that is done in the workplace because you are not sure what agent they are responding to. You don't know what to pick up and take to the laboratory. There you give the patient a peak flow meter and ask them to take recordings at times they think they are being exposed and again that evening when they get home and try and establish a pattern of exposure and reaction. If you can't demonstrate that then you really can't demonstrate industrial or occupational asthma to the degree of probability that I believe the court requires. Much has been made of the latent period stating that one may be exposed to an agent for some time and yet not have asthma symptoms nor a change in lung function. That is certainly true. But you can't make the diagnosis of occupational asthma unless at some time the patient has been shown to react to that agent. So the latent period refers to the patient developing asthma whilst still being exposed. Then you look back in the history and you say 'this man was exposed to isocyanates for the last three years, why is he reacting now?' That is the latent period. He was exposed earlier, became sensitised over time but there is no way that I would be satisfied that isocyanate was a factor unless he was actually demonstrated to respond to the isocyanate."
(the emphasis is mine)
(f)I accept Dr Young's opinion that it is improbable that isocyanate exposure in the plaintiff caused or triggered a long term increase in bronchial reactivity and particularly the following factors which in Dr Young's opinion make it improbable:
"The major factor that makes it improbable is that there is no pattern of deterioration in spirometry or symptoms in the material I have had to examine that can be related to his exposure either immediately or within eight hours of that exposure. Secondly, his major deterioration and persistent deterioration in both symptoms and in his lung function has occurred probably two years down the track from his last said exposure. That to me is not consistent with isocyanate being the cause of his persistent deterioration which I believe is the clinical problem in this gentleman his persistent irreversible deterioration of asthma. From all the evidence and the lung function evidence in particular this occurred a good two years after his last exposure." (T316)
I accept Dr Young's opinion - and this is not challenged by other medical witnesses - that since 1984, the plaintiff has had unstable asthma.
I accept Dr Young's evidence given in his cross-examination that it was his practice as treating doctor in managing and identifying the cause of a patient's problem to give the patient a peak flow meter and a diary and ask them to carefully document their exposures, and to take peak flow readings at the time of any symptoms, and indeed, at other times as well so at set times during the day in the workplace and keep a diary about their exposures and to continue those peak flow readings when they get home (T324). I find that if such a practice were followed it would enable Dr Young and any other thoracic physician to identify whether environmental factors were in fact either a trigger for an asthma attack, or perhaps the cause of something more serious, something that was causing an underlying worsening of an already not so bad condition. He said (in cross-examination):
"What I would expect in the case of a simple trigger is that the patient would show a reaction at the time maybe a later reaction when they got home but that they would then again recover their lung function to their previous values. If I suspected the agent was an initiator or an agent that exacerbated the underlying bronchial reactivity then I would expect to see a continuing downward trend in their lung function both measured in my office and as measured by the patient in the home." (T324)
I accept that if that practice were followed the doctor would have the diary showing the environment in which the patient was working at the time of each recorded reading.
I accept Dr Young's evidence that as long as the patient recovered following the exposure he would regard it as a trigger factor and not a factor either initiating or permanently worsening the patient's asthma, and that once he had established that the patient was reacting to a workplace chemical, he would be particularly interested in examining those chemicals for the known sensitisers for worsening bronchial reactivity because it is most important that the patient be removed from those (T325).
I accept Dr Young's evidence that anyone with underlying asthma will respond to a large variety of different trigger factors. As he said:
"The concept to have is of an underlying airway inflammation which is briefly exacerbated by various trigger factors which either act through an allergic mechanism such as house dust mites, cat dander, pollens or a simple irritating factor such as cold dry air. Once you remove the patient from those trigger factors the patient recovers quite quickly. On the other hand you have exposure to agents which can cause further serious inflammation and that causes more bronchial reactivity. It makes the airways more sensitive to further assault. The number of industrial agents that are recognised to actually induce that bronchial reactivity or make existing bronchial reactivity worse are relatively few in number. They are isocyanate, epoxy resins to a lesser degree, components of epoxy resins and components from western red cedar timber, plicatic acid. There are rather more unusual ones such as bakers flour which affects a small number of people and probably by a different mechanism that can all induce a degree of bronchial reactivity. They are the agents that can actually produce asthma in some one that has never had it before. I know that doesn't apply to Mr Muller's case but in people that do have asthma those agents can certainly make the underlying bronchial reactivity worse, and I believe that is the issue with this gentleman what has made him so much worse down the track so that now he has very very severe irreversible asthma." (T314)
(underlining is mine)
I also accept Dr Young's opinions "That occupational asthma requires a period for sensitisation which is very variable, and that implies that the patient's first attack is not their first exposure to the agent" (T343) and that once a patient reacts to the exposure to a particular agent the doctor knows the patient is sensitised to that agent and the process of being sensitised of which the patient may not know is the latent period (T343).
I further accept Dr Young's opinion that once a person has become sensitised to a particular agent i.e. by that time he has begun to react to exposure to the particular agent, he will not have any further latent period.
I should at this stage explain the following terms which appear in the spirometry readings and in these reasons - FEV1 and FVC. I adopt Dr Young's definitions. FEV1 stands for the forced expiratory volume in the first second during which the patient blows into the spirometer. The actual test manoeuvre involves the patient being asked to take as big a breath as they possibly can then to apply their mouth tightly to the mouth piece of the spirometer and blow as hard as they can for as long as they can, one single breath. From that you get the total amount of air the patient can blow out which is called the forced vital capacity (FVC) and the FEV1 which is the amount they get out in the first second.
I accept Dr Young's opinion that these two measurements have both been found to be useful in asthma but that the FEV1 has stood the test of time as the single best measure and single most reproducible measure of a patient's lung function from time to time (T311).
In light of Dr Young's opinion that the plaintiff has on the balance of probabilities failed to prove any causal connection between inhalation of isocyanate and his present irreversible lung function, what then is the cause of the plaintiff's present pitiable state? Dr Young has opined that for the vast minority of asthma patients who deteriorate long term, one cannot identify the mechanisms and they are just not known (T335).
He agreed with Mr Curran's suggestion that he was saying it was a progressive deterioration of the asthma which plaintiff already had, and he added "Asthma will go through exacerbations and remissions for unknown causes and at some stage it may well go into an exacerbation which just never remits even with maximum treatment unfortunately" (T335). He further agreed with plaintiff's counsel that assuming plaintiff did not have exposure to isocyanate in 1987, 1988 and even 1989 he would have had the same course to his asthma as has occurred. He denied such an opinion was improbable saying "I don't believe so because in order to implicate the isocyanate I really require those pieces of evidence which are not available". He explained this by saying of the plaintiff's case:
"It is such a dramatic deterioration in his condition around 1991, such a dramatic one, that I would require an exposure at that time to the isocyanate in order to imply that was the cause of that irreversible deterioration. If there were clear evidence of isocyanate induced asthma prior to that in that he had a challenge test which showed his reaction to it or had taken a peak flow meter to work that shows that he definitely reacted to the isocyanate then he had a two year break no exposure to isocyanate and his asthma had remained the same then I would still find it very difficult to imply the isocyanate was the cause of his very serious further decline two years down the track without a subsequent exposure?" (T335)
There was no evidence of any exposure of plaintiff to isocyanate shortly before August 1991 or of any such exposure or possible exposure for some 21 months to 2 years before August 1991.
I should add that while in the witness-box Dr Young had, in addition to Dr Edward's graph, the hospital records from which the graph had been plotted. He told plaintiff's counsel that the graph showed that until about mid 1991, plaintiff was still capable of returning his airways to a reasonable level of function (T337).
Before leaving Dr Young's evidence, I must refer to evidence of a blood test performed in January 1993, in which a sample of the plaintiff's blood was subjected to a test of the major allergenic antibody which is IgE. At the request of Dr Solley, an allergist, the plaintiff's blood was tested for components of epoxy coatings and isocyanate. The tests were negative and Dr Young said the negative results offered no support for sensitisation of the plaintiff to epoxy or isocyanate compounds. Dr Young said (and I accept this statement):
"You can get the asthmatic response without detectable IgE that is important here. If he had the IgE that would be a point in favour of his sensitisation but you can certainly get occupational asthma without detectible IgE. What is more it has been quite a few years down the track and those responses fade away." (T319)
Another matter mentioned by Dr Young which I thought important - he pointed out that the clinical history of the plaintiff showed that he had been having asthma therapy, including taking oral prednisone from 1984 onwards. Dr Young had examined correspondence from Dr Heiner and the chronology of the plaintiff's treatment, and he noted that Dr Heiner commenced treatment with oral prednisone. Dr Young said the use of oral prednisone "must be regarded as an indicator of the severity of his asthma because we only reserve oral prednisone for severe asthma because of its side effects and he started treatment in 1984".
It appears from the evidence that the prednisone treatment finished in about October 1984, and the next reference to prednisone in the chronology was in April 1987. Dr Young on the strength of this evidence said in a passage which I accept:
"Well he appeared to require the prednisone therapy from April 1987 onwards which was prior to his stated exposure and I believe this fits in well with a pattern of asthma which is variable but not related to isocyanate exposure in other words there is evidence he deteriorated prior to his exposure." (T314)
Thus I find that in April 1987 plaintiff's asthma was severe and at that stage he had not been exposed to any isocyanate or compound containing isocyanate.
Further, I find on the evidence that plaintiff has never been sensitised to isocyanates. Had he been so sensitised I find he would, if exposed to isocyanate or compound containing isocyanate, have reacted acutely and there is no evidence that he ever had such acute reaction. I accept Dr Young's opinion that on the evidence in this case the plaintiff's severe fixed airway obstruction is the end result of severe continuing asthma - this is one of the three routes by which a person can reach that state as opined by Dr Edwards (see para 116 ante and para 152 post).
Dr Maurice Heiner
Dr Maurice Heiner is a thoracic physician, who has been treating the plaintiff's asthma for some 15 years. Over that time he wrote a large number of reports and letters concerning the plaintiff beginning with the letter dated 30 July 1984 written to Dr G Crichton. His reports appear in Exhibit 5, part B medical records pp 1 to 26 and in addition there is Exhibit 43, which is his letter dated 22 March 1999 which he wrote to the plaintiff's solicitors. Other letters by him appear in Exhibit 5 part A - "clinical notes" which are part of hospital records. Dr Heiner's evidence is relied on to prove the causal link between the plaintiff's alleged exposure to isocyanates and his irreversible severe airway obstruction.
Mr Curran, counsel for the plaintiff, submitted that I should prefer Dr Heiner's evidence to that of Dr Young on the basis that Dr Heiner was plaintiff's treating thoracic physician, whereas Dr Young had never seen or consulted with the plaintiff. I reject that submission as it seems to me to be an incorrect and invalid ground for distinguishing between two experts testimony. Each comes to court as an expert whose duty is to assist the court by giving impartial and objective evidence and in my view, it is not a pre-requisite to a medical expert giving an acceptable opinion that the expert should first have seen or examined the plaintiff.
In some areas Dr Heiner differed in his opinions from those held by Dr Edwards and Dr Young. For example, Dr Edwards said (T302) that as far as testing for asthma was concerned the FEV1 and forced vital capacity tests are the most recognised and reliable tests for asthma (T302). Dr Heiner disagreed with this proposition saying "no, not anymore". (T463) He went on to say:
"What I am saying to you is that I have always believed that the most significant test is the small airway function which is called the MMEFR, but up until recently its been the state of the practice for general practitioners and others to accept the FEV1 and the FVC as very significant, and I accept that that is still important, but if you ask me what is the most significant its the small airway function and that's the teaching nowadays."
Dr Heiner conceded he was speaking of the present, but agreed that when he wrote his letter or report of 1 September 1994, (Exhibit 5 part B p 19) he also knew that the small airways test was most important but that the FEV1 and forced vital capacity tests were "good enough for the purposes of the letter".
On referral to the end stage of progressive asthma demonstrated in Dr Edward's graph, Dr Edwards had agreed (T301-302) that there were three possibilities for someone to get to the end stage of progressive asthma. The first was that the end stage may be arrived at in some individuals from just severe continuing asthma; the second was - people who have had asthma aggravated by industrial exposure and the third was people who have asthma entirely due to industrial exposure.
Dr Heiner did not entirely agree with this proposition; he said (p 467):
"I agree with that statement provided a patient isn't being treated correctly and properly. I think it can happen with sensitisers such as isocyanate. I do not believe it can happen with irritants because irritants by definition usually cause symptoms immediately and if you remove the irritant and the patient is being treated I've not ever seen that " - and - "I have not seen ever an asthmatic who has deteriorated inexorably to the end stage whose got pure asthma and who is being treated properly." (T467)
Rather unfortunately I thought that on occasions Dr Heiner failed to display the objectivity which an expert witness is expected to bring when giving evidence to a court. He was referred to a document prepared by the plaintiff (see Exhibit 5, part A p 30). This document had been given to Dr Heiner by the plaintiff and placed on the hospital file. The document was a chart prepared by the plaintiff and the chart started shortly before August 1984. The chart or graph shows a level base line. Slightly above that base line is a second line running parallel to the base line until reaching the words "August 1984", written on the chart and then gradually diverging upwards from the baseline. On that diverging line the plaintiff has written "1987" and above that "due to the statute of limitations I cannot claim for any damage before May 1987". A little further on on the same line he has marked "1988" which indicates (as he wrote) "exposure to isocyanate in large amounts from Nov 1987 onwards". Beginning from "1988" a third line appears branching upwards from the second line at "1988" and gradually curving upwards and diverging from the second line. Above this curved line plaintiff has written "present curve on deterioration". In between the top curved line and the second line the plaintiff has written "I can claim this portion minus an amount if they find me on 'contributory negligence'." (sic) The middle or second line was described by plaintiff on the document as "natural deterioration curve resulting from pre May 1987 asthma" In between the baseline and the second line the plaintiff has written "this portion is deducted (sic) from the present state of my lungs".
When Dr Heiner was cross-examined on this document he agreed the purpose of the document appears to be to determine or to indicate what part of plaintiff's claim is within the statute of limitations and what isn't. He was asked whether he recalled discussing the document with the plaintiff and he replied:
"He has told me that but I also recall him saying to me on a number of occasions in the last few months when he's come to see me that the statute of limitations was no longer going to be brought up in court. He told me the Crown had dropped their pleading of that."
Cross-examining counsel asked Dr Heiner to think about what he had discussed with plaintiff in the past and he said "In relation to that document your understanding was it was telling you he couldn't claim for any damage before May 87". The doctor answered:
"That's what this document says but let me just say something to the court. In the first few years that I looked after Mr Muller compensation was not ever discussed. What was only discussed was Roy Muller getting well so that he could go back to leading his normal life style and let me say to the court that if Roy Muller had told me in 1987 that he had been exposed to isocyanate my actions - if he told me definitely that he was exposed to isocyanate then my actions would have been to take Roy Muller away from the workforce at that time. Isocyanate is a very bad chemical." (T7457)
Counsel then reminded the doctor that he was not answering the question. Dr Heiner ultimately conceded that the plaintiff had told him on a number of occasions there was a statute of limitations.
In his report of 7 February 1994 made to Carberry's the doctor said, "In November of 1989 he reported for the first time that he was exposed to isocyanates" and he confirmed in the witness-box that it was his recollection that plaintiff never mentioned isocyanates to him before November 1989. He said that on that particular occasion the plaintiff said "I have been exposed to isocyanates". Dr Heiner said he did not realise that it was also part of the plaintiff's case that he had been unwittingly exposed to isocyanates (T462/15).
I found these statements by Dr Heiner rather difficult to understand particularly in the light of letters he had written earlier. For instance, on 9 November 1988, he wrote to the secretary of the Association of Architects, Engineers, Surveyors and Draftsmen of Australia, concerning the plaintiff (Exhibit 5 part B pp 8 - 9). In it he confirmed his first consultation with the plaintiff of 30 July 1984 and his findings. In this letter he said this:
"Since 1984 Mr Muller has been on aggressive, conventional therapy including chronic steroid therapy. Attempts have been made to alter his diet and remove various additives and aspirin containing drugs in an effort to stabilise his disease. When this failed further enquiries were made as to whether or not this gentleman was exposed to volatile chemicals in his place of employment. In fact he stated that in his job he was often exposed to isocyanates and other volatile chemicals. When specifically asked and when he recorded values with a peak flow meter it was shown in fact that his symptoms were worse when he was exposed to these chemicals, namely when he was in sub-stations he noted an increase in his respiratory symptoms. Since that time he has been trying to limit his exposure and believes that his condition has improved."
That passage in a letter written on 9 November 1988 contradicts Dr Heiner's sworn evidence before me, namely that it was in November 1989 that plaintiff first told him he had been exposed to isocyanates.
That particular report which is in Exhibit 5, part B pp 8 and 9 concluded:
"In conclusion this man is an asthmatic. There is probable history of childhood asthma. The disease was exacerbated almost certainly by a viral infection in 1984. However at this time he also moved to Brisbane and his occupation led him to be exposed to various chemicals including isocyanates. His disease has not stabilised, he has had aggressive conservative therapy and I think that there is strong circumstantial evidence that his disease is exacerbated by his ongoing chemical exposure."
Exhibit 57 is a six page document dated 22 October 1997 headed "re: The Crowns opinion that I had Industrial Asthma since 1984" and signed by the plaintiff.
I do not propose to go through this statement in great detail but I do note that the statement shows plaintiff's concern to prove that his exposure to isocyanates could not have occurred before 22 May 1987 and that the claim against the defendant could not be defeated by a plea of the statute of limitations. In Exhibit 57 plaintiff has referred to his application for workers' compensation dated 11 July 1988 (Exhibit 5 part C pp 41 to 44) that application being based on inhalation of solvents injuring his lungs.
The application stated "Inhallation (sic) of solvents used to fix rubber linings and paints" was how the injury occurred and the injury was sustained "Inspecting the application of rubber linings inspecting the internal surface of painted vessels".
The application further said that the injury occurred "In various blast cleaning and paint and rubber lining works" and "over a period of time from 1984 to 1988".
In Exhibit 57 plaintiff said:
"IT MUST BE REMEMBERED THAT IN EARLY JULY OF 1988, WHEN I MADE THOSE STATEMENTS ABOUT HAVING INDUSTRIAL ASTHMA SINCE 1984, I WAS NOT WELL (partly collapsed lung) AND MY INCREASED ASTHMA SYMPTOMS WAS WORRYING ME, NO DOUBT I WAS NOT THINKING CLEARLY AND WAS LOOKING FOR SOMETHING TO BLAME MY SUDDEN INCREASED ASTHMA SYMPTOMS AND PARTLY COLLAPSED LUNG ON.
At that point in time I only had problems when exposed to solvents at Beltreco's, I never had problems with solvents or chemicals at any other works before the year 1988.
I THEN WRONGLY BLAMED SOLVENTS FOR MY ASTHMA (only having a reaction to solvents at Beltreco's) AND FOR FURTHER LOSS OF HEALTH SINCE EARLY 1988, (contrary to what Dr. Heiner said in November 1987, about the solvents and chemicals I was being exposed to did not cause asthma, but some could exacerbate it).
As I was blaming the solvents at Beltreco's, I also at that point in time, wrongly blamed my exposure to solvents since 1984 for my asthma.
(I couldn't just say only solvents since late 1987 was the cause of my asthma, I would have been laughed at if solvents since late 1987 was the cause, why not before? not knowing that my exposure to isocyanate at Beltreco's was the cause).
Even on the 5th july 1988, when I first saw Dr. bishop, (sic) I did not refer to my asthma as industrial asthma. It was not until the 11th july 1988, did I began to do so (sic). (See attached copy of Dr. Bishops medical certificate dated 5th July 1988).
It was sometime between filling out both the WCBQ and the QEC forms on the 11th July 1988 and my interview with an Officer of the WCBQ on the 19th July 1988, when I began to think that it could not be the solvents that was the cause of my asthma, as others (spray painters) have been exposed to far greater quantities then I have ever been and it did not harm them, therefor it had to be something else, that is when I gave thought to my isocyanate exposure in that polyurethane paint at IMP in later half of 1987, I then began blaming isocyanate for sensitising me to solvents.
(Remember I was not aware at this point in time of my continued exposure to isocyanate at Beltreco's that was the cause of my problems, and not the solvents).
Dr Bishop referred me to the physiotherapy section of the QE11 Hospital, I saw the Physiotherapist on the 14th July 1988. In their report it is (wrongly) recorded that I have had industrial asthma at that point in time for two years.
It was during my first interview with the WCBQ Officer on the 19th July 1988, when I first mentioned the word Isocyanate and from then on I continued to blame it for my then continuing severe asthma condition and my reaction when exposed to solvents. During this interview I again said Industrial Asthma since 1984, I could not now say since late 1987, as I have already said since 1984 on both the WCBQ and QEC forms.
At the time it didn't matter to me whether my industrial asthma began in 1984 or late 1987, all I knew at the time was that I was having problems when exposed to solvents since 1988.
It must be remembered that it was either late June, or at the very beginning of July 1988, when I began to suffer severe lung problems, it was not until it developed into lung pain when I took a breath, which was happening while I was at work on the 5th July 1988, that is when I first saw Dr. Bishop (who's surgery is next door to the QEC, in Mary Street) who examined me and sent me for x-rays which revealed a partly collapsed lung.
No doubt that during this time I was not thinking clearly and began to blame my lung condition on exposure to solvents, which was noticeable from early 1988 onwards, it was then that my exposure to solvents began to give me problems (never before).
(not knowing it was the isocyanate fumes and not the solvent fumes at Beltreco's that was giving me the problems) since the beginning of 1988."
I have not set out the whole of the Exhibit 57 but I point out the emphases in the above extract are those made by the plaintiff himself.
In my view Exhibit 57 reflects badly on plaintiff's credibility. In the above quoted extract he has said he was not well in July 1988 and "not thinking clearly" when he made statements about having industrial asthma since 1984". These excuses were in my view attempts by plaintiff to ensure that the plaintiff's claim against the defendant - aggravation by exposure to isocyanates - fell wholly within the period beginning 22 May 1987 and to down play the effect on him of solvents in the period prior to 22 May 1987. He conceded in cross-examination (T513) that when he made the statements in Exhibit 57 he was fully conscious of the effect of the statute of limitations and in Exhibit 57 alleged he made misstatements in the documents at Exhibit 5 part C pp 41 et seq and 45 et seq (his workers' compensation claim of 11 July 1988 and his portion of report of injury to employee).
In his statement dated 19 July 1988 (Exhibit 21) he had said (inter alia) "I did not start to develop respiratory problems until 1984 when I spent a week in hospital (QEII) with industrial asthma".
I turn to Exhibit 39 which is a seven page typed document which plaintiff said he prepared in about 1993 (T210) and described by plaintiff as a draft for his solicitor. At page 4 he said:
"Unbeknown to me at the time, from November 1987 onwards I began being exposed to isocyanate in a chemical used to chemically cure rubber linings ... ."
(the emphasis is the plaintiff's)
He agreed in cross-examination that passage related to the work at Beltreco and agreed that as at September, October and November of 1987 he knew that the polyurethane paint he was inspecting at IMP and G&J Dowrie contained isocyanate (T210).
Mr Griffin QC then asked him:
"Well then, why did you not tell Dr Heiner that you were being exposed to isocyanate in consequence of your work at IMP and G&J Dowrie?" (T210)
Plaintiff replied:
"I told him that I was exposed to - he asked me was I exposed to isocyanate in November of 1987. I replied to him that I was being exposed to polyurethane paint over the previous few months and I thought there was isocyanate in that. That was it."
Mr Griffin then asked:
"I understood that you have said that you never told him that you were exposed to isocyanate until November 1989?"
He replied:
"No. I told him in November 1987 during a conversation at the QEII Hospital that I thought - I know the exact words - that I thought it was in polyurethane paint that I'd been exposed to over the past few months."
Mr Griffin then asked plaintiff to look at page 5 of Exhibit 39 and read out:
"On the 19th July 1988 I was interviewed by an Officer from the WBCQ where I added the chemical "Isocyanate" to the previous statement of 'Inhalation of solvents' as I knew that the solvents I was being exposed did not cause of (sic) asthma, so I included Isocyanate which I at the time wrongly believed was in the Polyurethane paint I was inspecting in October/November 1987."
Plaintiff said:
"mmm. I at that particular time of filling that document out and - when I say talking to the Workers' Compensation Board I believed it was correct and then when I spoke to the British paints man a couple of months later I learnt that was incorrect."
Plaintiff said that it was somewhere about September, October 1988 that the British Paints man had told him that isocyanate had been taken out of the polyurethane paint and agreed that up until September, October 1988 he believed polyurethane paint did contain isocyanate.
I formed the firm view that Exhibit 39 and the cross-examination of plaintiff on that exhibit showed that plaintiff was well aware in 1987 that polyurethane paint contained isocyanates. I thought Exhibit 39 and cross-examination of plaintiff on it harmed plaintiff's credit.
On all the evidence before me, I find that plaintiff has failed to show that the irreversible lung disease involving fixed airway obstruction has been caused by severe or any aggravation of pre-existing asthma, such aggravation being caused by exposure to isocyanates while in the defendant's employ.
The result will be that the plaintiff's claim fails.
Before I turn to the issue of damages, I shall mention two articles published by Edward Christie, Associate Professor in Ecology, Faculty of Environmental Sciences, Griffith University; Barrister at Law. They are:
1."Toxic Tort Disputes: Distinctive Characteristics Require Special Preparation for Trial." (1992) 22 QLSJ 279.
2."Toxic Tort Disputes: Proof of Causation and the Courts" (1992) 9 E.P.L.J. 302
In the first of these articles, the author said (at p 281 QLSJ):
"There are a number of distinctive characteristics which distinguish a toxic tort from traumatically induced injury - the latter representing the type of injury associated with the law's traditional experience in the field of torts:
(a)In a toxic tort case, the nature of the injury is different. In particular, the injury is not always as direct as is the case with a traumatically induced injury such as personal injury arising from an automobile collision, where a well defined, direct traumatic interaction between the injurer and the victim exists.
In contrast, a toxic tort involves injury resulting from genetic or biochemical disruption, but where the injury may develop without identifiable prior traumatic events.
(b)A long lag time (or latency period) between exposure to the toxic chemical and expression of the injury usually occurs, sometimes up to twenty years or more. The injury manifests itself after the latency period. Consequently, exposure to the toxic chemical increases the risk of contracting the disease but does not produce an immediately observable response.
It is this specific characteristic of the harm remaining latent for many years following exposure, often occurring at background levels of exposure without even causing an apparent cause, which leads to the "central problem" for a prospective toxic tort plaintiff. In particular, the difficulty - even impossibility, of tracing the etiology of the disease to exposure to a specific toxic chemical."
At p 287 QLSJ under the heading "Preparing For Toxic Tort Litigation: Evidentiary Needs" - the author said:
"On the basis that an individual has been exposed to a toxic chemical, the following issues are the foundations for preparation - not only in formulating an opinion for the claimant, but also for determining the nature and course of future litigation.
(a)The claimant must become aware that exposure to a toxic chemical may have caused the condition at issue - a requirement which may be limiting where a very long latency period is involved;
(b)The claimant must characterise the nature of exposure to the toxic chemical. This is a further problem exacerbated, not only by the long latency period, but also by the possibility that exposure occurred in association with other toxic chemicals; or that exposure occurred in a diffuse manner;
(c)The claimant must establish that the toxic chemical can cause the condition at issue. Recourse can be made to scientific research even though the plaintiff was not a subject in such research.
(d)The toxic chemical to which the claimant was exposed must be the same as that in the research study. Also, the exposure history in relation to concentration and duration of the claimant, must approximate that of the subjects in any published research study relied upon.
(e)The claimant must then establish that exposure to this toxic chemical has caused the injury for which compensation is now sought. It is vital that evidence relied upon distinguishes between injuries allegedly caused by exposure to the toxic chemical from those induced by the general environment. The disease should be specific for exposure to that particular toxic chemical."
Not all the above five issues are relevant to the plaintiff's claim but issue (e) is very relevant.
In the second article, Professor Christie has said at p 302:
"... the injury in a toxic tort may develop without prior identifiable traumatic events, as it results from biochemical or genetic change. Furthermore, a very long lead time or latency period occurs from the time of initial exposure to the toxic chemical to the time the disease manifests itself into an observable response. It is this specific characteristic of the harm remaining latent for many years following exposure, often occurring at background levels of exposure without even having an apparent cause, which leads to the central problem of proof in toxic tort litigation [S. Gold, "Causation in Toxic Torts: Burdens of Proof, Standards of Persuasion, and Statistical Evidence" (1986) 96 Yale L.J. 376-402.] Because of the passage of time following exposure, doubts relating to the question of exposure could arise, as the chain of events would not be immediate. Moreover, the plaintiff in toxic tort litigation must be able to establish the characteristics of exposure to the particular chemical at the relevant time."
(underlining is mine)
and at p 303:
"To establish scientific proof of causation in toxic tort litigation the plaintiff is required to adduce evidence which demonstrates that the chemical to which the plaintiff was exposed caused the plaintiff's condition at issue; that is, a causal relationship must be established. It represents a fundamental pre-condition for recovery of damages."
I have mentioned these articles so that any readers of these reasons for judgment who has a Toxic Tort case may consult them and become aware of the difficulties which may face a plaintiff in toxic tort litigation.
Damages
In case I should be wrong and the view is taken elsewhere that the plaintiff has proven negligence in the defendant it is necessary for me now to assess damages. The plaintiff is now 56 years old - almost 57. It is first necessary for me to make a finding concerning plaintiff's life expectancy, and I do this because various doctors have expressed opinions on that topic and the finding bears on some of the components of the damages assessment which concern future loss either wholly or partly.
In his report dated 28 January 1993 written to plaintiff's then solicitors Carberry's (Exhibit 5 part B - medical reports at pp 78 - 79) Dr Myers a physician said this:
"At present therefore your client is a respiratory cripple due to chronic obstructive airways disease and asthma which had been [at] least precipitated and exacerbated as a result of occupational exposure to volatile chemicals. He has numerous other problems including obesity, diabetes and potential osteoporosis due to the drugs which he takes for his asthma and since there is no prospect of his being able to cease these drugs their side effects will continue to trouble him indefinitely. He will therefore endure a life of chronic invalidity, the significant contributory factors to which in my opinion are his previous occupational exposure to chemicals and the treatment which has been necessary for his asthma consequent upon this exposure.
You client has numerous health problems including coronary artery disease, chronic obstructive airways disease, asthma and iatrogenic Cushing's Disease (the side effects of his high dosage of cortisone therapy). He will also be particularly prone to infections particularly respiratory ones over the years to come. As a consequence of his illnesses his potential life span is likely to be limited so that a prognosis of a further ten years of life is relatively optimistic."
Since Dr Myers offered that prognosis the plaintiff has developed osteoporosis and in 1994 suffered a heart attack.
If Dr Myers' prognosis be accepted then plaintiff has about four years more life.
Dr Heiner has also written on the topic of plaintiff's life expectancy. In a letter dated 30 May 1997 (Exhibit 5 part B - p 25) he said:
"I find it impossible to calculate Mr Muller's life span. ... there is no doubt that Mr Muller has a marked increase in mortality over the next two years when compared to a normal member of society or indeed a normal asthmatic."
In his letter of 20 June 1997 (Exhibit 5 part B p 26) he said:
"I do not have a formula to accurately predict Mr Muller's life span but I feel confident in stating that an acute infection or deterioration in his asthma which could occur at any time would be life threatening. The stress and anxieties surrounding his litigation also has (sic) led to a marked deterioration in his asthma and continues to contribute to his airway instability. Mr Muller's risk of dying is high if his asthma deteriorates further."
That letter was obviously written, as the text in fact said, to support plaintiff's application to obtain a speedy trial.
Nevertheless, although Dr Heiner cannot accurately predict plaintiff's life span - no one can do this - it is my task to make some such prediction. On the evidence and particularly bearing in mind the opinion of Dr Myers, I find that on the balance of probabilities the plaintiff has approximately four years more life and I propose to assess on this basis.
Pain, suffering and loss of amenities
The plaintiff is a divorced man who lives alone. I find he was a regular tennis player until about 1989 and that he has since then been forced to give up playing tennis. He has therefore lost the ability to participate in a pastime which I am satisfied he enjoyed. He has also lost the ability to participate in and enjoy dancing. He has trouble sleeping and his tongue is frequently cracked and painful so that eating is a painful exercise. There is no dispute that the plaintiff had pre-existing asthma and on the assumption that he has proven negligence in the defendant, it may be said that his damages on this head are to be assessed from December 1989 to 2003 in respect of his pain, suffering and loss of amenities beyond pain suffering and loss of amenities attributable to the pre-existing asthma alone. As Dr Myers has said many of plaintiff's problems are consequent on the treatment of his asthma e.g. the high dose cortico-steroid drugs have induced moderate maturity onset diabetes and osteoporosis. No attempt has been made to decide whether all or what part of those problems is due to the basic asthma such that without any aggravation by exposure to isocyanates he would have been in the same state. I consider I should attribute all the medical problems (apart from heart problems) to the aggravation in the absence of any disentangling (Watts v Rake (1960) 108 CLR 158; Purkess v Crittenden (1965) 114 CLR 164). Plaintiff also has some depression which I find is not serious but he is to be compensated for it. He requires some treatment for it. The chronic fixed airway obstruction disease which plaintiff has had since about August 1991, has obviously been debilitating for the plaintiff, although in court he appeared to walk normally and spoke firmly and well. He has regular medication. For this component which is a period of some 14 years including 4 years in the future I allow $40,000 of which $28,000 is for past pain, suffering and loss of amenities.
For interest purposes I have taken account of a lump sum disability settlement of $33,510 paid to the plaintiff by the Workers' Compensation Board. The date of payment is uncertain but I infer from the document in Exhibit 5 Part C at p 75 that this sum was paid on or about 30 June 1990 - the plaintiff's claim closed on 12 June 1990. There will be no interest as the $33,510 exceeds $28,000.
Impairment of Earning Capacity
The plaintiff has not worked since December 1989. His counsel relies on the pay records of a man named Grahame Clayworth, a former employee of the defendant for the period from 1 January 1990 to 30 June 1996 to show the plaintiff's loss of earnings (after tax) in that same period.
Thereafter and until 30 March 1999 the plaintiff's lawyers have calculated the loss of earnings on the basis of a CPI increase of 1.5 per cent per annum in the net weekly wage existing at 30 June 1996.
Mr Griffin QC agrees that the Clayworth figures indicate the amounts plaintiff could have earned if he had continued to work full time for the defendant up to 30 March 1996. Exhibit 67 is a document prepared by the plaintiff's lawyers described as "past economic loss and past loss of superannuation benefits". This document shows that to 30 March 1999 the plaintiff's claim for loss of earnings from December 1989 to 30 March 1999, is $287,285.64. It shows that in the same period he has lost superannuation of $20,942.76.
Mr Griffin has conceded the arithmetical accuracy of Exhibit 67, although he submits that there should be some discounting of the figures for the vicissitudes of life.
Although plaintiff told me that there were occasions when he was ill and entitled to take sick leave but did not do so, I nevertheless find that had he continued working for the defendant from December 1989 up to today it is more likely than not that he would have taken some days off work. Of course he would have been entitled to sick leave and thus it may be said the figures in Exhibit 67 are reasonably accurate indicators of his loss of earnings from the defendant in the period covered by Exhibit 67. I do not overlook that in 1994 he had several weeks in hospital following a heart attack. This event gives some justifiable reason for discounting the figures in Exhibit 67 notwithstanding such leave. The plaintiff has survived until now and had he been working until now there was some risk that what are called the vicissitudes of life may have interfered with his earning capacity and deprived him of income.
In my view any discount of the figures will not be great. I also have to notionally amend Exhibit 67 to bring the calculation shown in it to the date of judgment. I shall assess the loss for impairment of earning capacity from December 1989 to today at $285,000 and for loss of superannuation in the same period at $21,000. For interest purposes, I have taken account of weekly workers compensation payments totalling $17,107.39 paid to plaintiff to 12 June 1990 (see Exhibit 5 part C page 75).
Future Impairment of Earning Capacity
Plaintiff has sought $232,989.70 on this head and also $16,174.08 for "future superannuation loss" (see Exhibit 67).
The net weekly loss of earnings as at 30 March 1999 and shown in Exhibit 67 is $674.16. I shall adopt this figure.
The plaintiff said he had hoped to work for the defendant until he was aged 65 and thereafter to become self-employed doing inspection work and quality assurance work privately (T127). For earnings after 65 he relies on evidence of earnings of a Mr James John Kemp, a former employee of the defendant who at the age of 55 was retrenched from his employment as mechanical inspector and thereafter set up his own business. I am satisfied that from about 1989 to early 1999 Mr Kemp was the main spring of a company named Niad Holdings Pty Ltd trading as Quality Assurance Representative Services - he and his wife were equal shareholders.
At date of trial he was aged 65 and had retired. He gave evidence that in February 1999 his company "ceased". He spoke of charging an hourly rate of $35 which could vary and be as high $60 per hour which was a charge he made for business planning and quality assurance to Gippsland Water.
I find the work he did was in the mechanical field and apart from quality assurance quite different from the work plaintiff hoped to perform when he began his new venture on reaching 65 years of age. While each of Mr Kemp and plaintiff might have held quality assurance auditing certificates, it seemed to me each was experienced in different areas of work.
Mr Kemp's evidence was given from memory - no books were produced. I find he conducted the business personally. The business in effect was a partnership with his wife - intended to split income and reduce the incidence of income tax.
Mr Kemp described himself as fortunate in having his business at its commencement obtain a job at Ipswich which kept him going for about six months. He spoke of his business gradually building up with 1997 - 1998 year being his best year with gross earnings of his company of $90,000. He said that for the year ended 30 June 1996 the gross earnings would have been close to $70,000. It appears the Gippsland Water job was particularly remunerative because the client paid accommodation and airfares and thereby reduced the company's overheads.
I do not regard Mr Kemp's company's earnings in 1997-98 as being representative of his usual earnings in his business. I find the earnings in that year, given particularly that the client paid for his accommodation and airfares to and from Gippsland were exceptional and of no real help to me in considering the quantum of the probable loss to the plaintiff of the business he hoped to set up after age 65.
As for the aspect of future impairment of earning capacity, I find the present value of a weekly loss of $674.16 for four years on the 5 per cent tables is $128,690. After the end of four years the plaintiff's damages on this head will be in the realm of "the lost years". In 2003 he will be 61 years old, and if still alive and able to work would be entitled to work for the defendant for another four years unless retrenched.
Assuming he worked to age 65 i.e. to 2007, then on the 5 per cent tables the present value of a weekly loss of $674.16 for eight years from today is $233,259.
From the difference between $233,259 and $128,690 which is $104,569 there must be set off the saving of expenditure on plaintiff's maintenance during this period of "the lost years" from 2003 to 2007 (Skelton v Collins (1966) 115 CLR 94).
I have no evidence of that expenditure. Nevertheless, I must make some estimate - assuming that expenditure on his maintenance were $200 per week the present value of $200 per week for four years on the 5 per cent tables is $36,000. That figure must be discounted back to the present - the loss will not begin until 2003. I estimate $25,000 for the value today of his maintenance and that sum must he deducted from the $104,569.
I propose to allow $207,000 for impairment of earning capacity to age 65.
As for the plaintiff's business after the age of 65, I find that the evidence of Mr Kemp as to his earnings is of little assistance.
I bear in mind that plaintiff would have to start his own business from scratch. How successful he would have been and how long he would have continued in that business is difficult to estimate. I am required to make a forecast (Malec v JC Hutton Pty Ltd (1990) 169 CLR 638). I find there was a reasonable chance that plaintiff would have begun working as a specialist surface coatings inspector, but I also find it very unlikely that he would have continued beyond about 3 years i.e. to about age 68. I find he probably would have worked from home and been required to travel at his own expense and that all expenses in association with the business would more likely than not have had to be borne by him from any gross income earned.
I find his earnings as inspector and auditor would have been modest to begin with and that there may well have been an entire period of up to six months when he would be looking for clients and obtaining clients and in this time have little or no work. In this six months period, I find that his expenses would probably have exceeded income. Of course, given that this projected business would have been attempted in his "lost years" his maintenance costs must be set off against any nett profits.
The best I can do is make a global assessment of a present figure for a loss to commence in eight years time after taking into account the Skelton v Collins principle. I allow $10,000 on this head.
As for future loss of superannuation, plaintiff claims $16,174.08 to 2007 being the present value on the 5 per cent tables of a weekly loss of $46.80 for eight years. I allow $16,000.
Although I have found that he will probably die by 2003, it seems to me that as this loss includes four "lost years" it should be allowed with no deduction being made for plaintiff's maintenance during the four lost years - that maintenance has already been deducted in the future loss of earning capacity claim.
Griffiths v Kerkemeyer - Past
The plaintiff claims one hour per week at $10 per week from 1 January 1990 to date. I find this a reasonable claim and I allow $4,940.
Griffiths v Kerkemeyer - Future
I allow claims for the following items:
·Lawn mowing - 18 times per year at $30 per month = $540 per annum - $10.40 per week
·Garden maintenance - 3 hours per month at $18 per hour = $648 per annum - $12.50 per week
·Washing exterior of house and gutters at $155 which cost will be incurred
twice each year - $5.95 per week
$28.85
I disallow the claim for painting the interior of the house and the exterior of the house. I am not satisfied on the balance of probabilities this is a reasonable expense for which plaintiff is to be compensated and it is my view that given this plaintiff's age irrespective of whether he had asthma then it is almost certain that he would have paid a tradesman to do this painting and not have done it himself.
The total per week is therefore $28.85 which I round out to $30. The present value of that weekly cost on the 5 per cent tables for four years is $5,700. I therefore allow that sum on this head of claim.
Special Damages
I allow these as follows:
(a)moneys paid by Workers' Compensation Board on behalf of the plaintiff
(as per letter in Exhibit 5 part C p 75) - $1,346.52
(b)moneys paid by Workers' Compensation Board - Fox v Wood Principle $4,638.26
In respect of the claims made in Exhibit 29 to which exhibit I have been referred by plaintiff's counsel in his written submissions, I allow $18,370.44. Exhibit 29 contains in considerable detail out of pocket expenses of the plaintiff from 1989 up to and including 1999. These expenses are divided into pharmaceutical expenses, travel expenses, medical expenses and parking. According to the summary in Exhibit 29 these expenses total $22,370.79. However, some are claimed in respect of the plaintiff's heart attack in 1994 and ensuing visits to his cardiologist Dr Singh. The moneys paid to Dr Singh including the travel costs identified in respect of visiting Dr Singh, are not related to the plaintiff's asthma or aggravation of it. On my calculations the amounts claimed in respect of Dr Singh and visits to him total $4,000.35. This sum is made up of $985.85 claimed in 1994, $1,219.65 and $96 (travel) for 1995, $254.60 for 1996, $1,118.30 for 1997 and $325.95 for 1998.
I have deducted the $4,000.35 from the total claimed in Exhibit 29. I have allowed the balance claimed viz $18,370.44. I find the claims for diabetes result from medication for plaintiff's asthma. There has been no disentangling of expenses for asthma alone and the aggravation of it. In my view the plaintiff is therefore entitled to the $18,370.44.
In summary then I allow $24,355.22 for special damages. For many of the items in Exhibit 29 plaintiff has been substantially reimbursed by Medicare. He has paid out of his own pocket some $13,100. I allow interest on this sum only.
Future out of pocket expenses
I allow these as follows:
·ten visits per annum to Dr Heiner at $20 per visit - $200 $4.00 per week
·four visits per annum to Dr Strakosch - an endocrinologist - $0.75 per week
at $10 per visit - $40
·one bone density scan per annum at $80 $1.50 per week
·Dr Rodney psychiatrist - 6 visits per annum at $44.50 per visit $5.15 per week
·pharmaceutical expenses - $267 $30.00 per week
·micro-neb (nebuliser) $500 every 3 years $3.20 per week
Total $44.60 per week
I round out this sum to $45
On the 5 per cent tables the present value of a weekly cost of $45 payable over the next four years is $8,550.
To that sum I am prepared to add a sum of $6,000 for air-conditioning of the plaintiff's home. I find that that sum (which is the amount claimed) is a fair and reasonable expense.
I decline to allow the plaintiff a claim for private health fund membership cost as I do not consider this to be a reasonably necessary expense for which plaintiff is to be compensated.
In summary then I assess damages as follows:
1.Pain, suffering and loss of amenities past $28,000.00
2.Pain, suffering and loss of amenities - future $12,000.00
3.Loss of earning capacity - past $285,000.00
4.Interest on $267,893 @ 6 per cent p.a. for 9 years $144,662.00
5.Loss of superannuation - past $21,000.00
6.Interest thereon @ 6 per cent p.a. for 9.5 years $11,970.00
7.Loss of earning capacity - future $217,000.00
8.Loss of superannuation - future $16,000.00
9.Griffiths v Kerkemeyer - past $4,940.00
10.Interest thereon @ 2 per cent p.a. for 9.5 years $958.00
11.Griffiths v Kerkemeyer - future $5,700.00
12.Special damages $24,355.22
13.Interest on $13,100 for 10 years @5 per cent per annum $6,550.00
(I have chosen 5 per cent because Exhibit 29 shows the
bulk of the plaintiff's payments have occurred in the past 5 -6 years)
14.For future out of pocket expenses $14,550.00
Total $792,685.22
From these damages I would deduct the Workers' Compensation Board charge of $51,963.91 (see Exhibit 5 part C p 76).
Orders
I dismiss the plaintiff's claim and in the action give judgment for the defendant against the plaintiff.
I shall hear from the parties on costs.
IN THE SUPREME COURT
OF QUEENSLANDBrisbane No.755 of 1990
Before the Hon. Mr Justice Shepherdson
[Muller v Qld Electricity Com.]
BETWEEN:
ROY ARTHUR MULLER
Plaintiff
AND:
QUEENSLAND ELECTRICITY COMMISSION
DefendantINDEX
Page
Issues and general matters (paras 1 - 39) 1-10
Extent of plaintiff's exposure to isocyanates (paras 40 - 82) 11-19
Evidence of Mr Haig (paras 52 - 56) 13-14
(paras 78 - 82) 18-19
(para 106) 24
Dr Coralie Mary Bishop (paras 83 - 92) 19-21
Dr Robert Leslie Edwards (paras 93 - 124) 21-28
Dr Iven Young (paras 125 - 147) 28-35
IgE test (para 143) 34
Dr Maurice Heiner (paras 148 - 174) 35-45
Dr Graham Solley (para 177) 46
Exhibits 57 and 39 (paras 182 - 194) 47-51
Conclusion on liability (paras 195 - 196) 51
Damages (paras 201 - 249) 53-63
Orders (para 250) 63
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