Forbes v Selleys Pty Limited

Supreme Court of NSW|2002-07-03|Before: Cripps AJ

CITATION : Forbes v Selleys Pty Limited [2002] NSWSC 547 FILE NUMBER(S) : SC 20241/00; 20233/00 HEARING DATE(S) : 23/04/02, 24/04/02, 26/04/02, 29/04/02, 16/05/02, 17/05/02, 20/05/02 - 24/05/02, 17/06/02, 19/06/02 JUDGMENT DATE : 3 July 2002

First Plaintiff: Charles Barstow Wright Forbes PARTIES : Second Plaintiff: Tara-Jane Forbes Defendant: Selleys Pty Limited (also known as Selleys Chemical Company Pty Ltd) JUDGMENT OF : Cripps AJ at 1

Plaintiff: COUNSEL : PR Hennessy SC & A Capelin M McCulloch & D Villa SOLICITORS : Plaintiff: Abbott Tout Solicitors Defendant: Phillips Fox CATCHWORDS : Product Liability - Legal Causation LEGISLATION CITED : Trade Practices Act 1974 (Cth) Glendale Chemical Products Pty Ltd v Australian Competition & Consumer Commission (1998) 90 FCR 40 CASES CITED : Adelaide Stevedoring Co Ltd v Forst (1940) 64 CLR 538 Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262 DECISION : Verdict and Judgment for the defendant in both actions.

IN THE SUPREME COURT OF NEW SOUTH WALES COMMON LAW DIVISION

20241/00 Charles Barstow Wright Forbes v Selleys Pty Ltd

JUDGMENT 1 His Honour: Mr Forbes and Mrs Forbes (the plaintiffs) have sued Selleys Pty Ltd (the defendants) claiming damages arising out of a seizure suffered by Mr Forbes on Monday 17 February 1997. It is alleged that Mr Forbes suffered toxic encephalopathy as a consequence of using a product known as "Selleys Space Invader" (SSI) on 15 February 1997.

2 As originally framed, it was alleged that the male plaintiff had become sensitised to SSI by reason of its use by him in January 1997, which had the consequence that his use on 15 February 1997 caused his seizure on 17 February 1997. (Because the female plaintiffs case is in nervous shock and her entitlement depends upon a finding of liability by Selleys to the male plaintiff, I will, when discussing the question of liability, refer to the plaintiff in the singular).

3 In the statement of claim, the plaintiff alleges an entitlement pursuant to: (a) Part VA of the Trade Practices Act 1974 (Cth) -75AD

4 No claim was pursued with respect to s52 of the Trade Practices Act 1974 (Cth) ("the Act"), and the breaches alleged under (75AD) of the Act and the common law count were essentially the same viz that Selleys failed to warn the plaintiff of the risk of toxic encephalopathy caused by the inhalation of SSI.

5 After the evidence had concluded I announced that, notwithstanding the actual pleadings, the case should be determined according to the way it was presented at trial. At trial, the case on behalf of the plaintiff was not that he had become sensitised (in the medical sense) to the defendant product by reason of his use of it in January, as it had been earlier. The case was that, more probably than not, the use of SSI on February 15 caused or contributed to toxic encephalopathy suffered by the plaintiff. If that question is determined in the affirmative, a further question may arise concerning foreseeability.

6 The evidence in the case extended over many days. A large number of scientific experts presented written reports. A number of experts were called and some extensively cross-examined. I do not propose to set out in detail the contents of all reports and the examination in chief and cross-examination of the witnesses. The parties are aware of the evidence and in this judgment it is my hope that I can make clear to the parties my reasons for the conclusions I have reached.

7 At about 9.00am on 17 February 1997 the plaintiff was admitted to St Vincent's Hospital in an unconscious condition having suffered a seizure at work. He remained in a deep coma for at least two days, during which period he was intubated. The provisional diagnosis was encephalitis and it was thought that he might not live. Subsequently, he made a rapid recovery and was discharged from hospital on 28 February 1997. He now has significant physical, psychosocial and cognitive loss. He remains able to work but is unable to undertake the type of work he was doing prior to his collapse.

8 On his admission to hospital he came under the care of Dr Paul Darveniza, a specialist neurologist at St Vincent's hospital, who provisionally diagnosed encephalitis but later opined the plaintiff had suffered a severe toxic encephalopathy.

9 The plaintiff's case is that the defendant was in breach of its common law duty in failing to take reasonable care to guard against foreseeable risk of injury, in that it failed to warn the plaintiff that with normal use by him of SSI he was exposed to a dangerous or hazardous amount of chemical being diphenyl methane di-isocyanate (MDI). It is also alleged that the defendant was in breach of its obligation, as I have said, under 75AD of the Act in that it sold goods having a defect namely that the label on the goods did not adequately or properly warn users of the extremely dangerous risks of inhalation to which they may become subject (see Glendale Chemical Products Pty Ltd v Australian Competition & Consumer Commission (1998) 90 FCR 40).

10 Putting to one side the foreseeability issue, I must first determine whether it has been established that more probably than not, the plaintiff's encephalopathy was caused or contributed to by the inhalation of SSI.

11 Prior to 15 February 1997, the plaintiff purchased two 500g cans of SSI for the purpose of sealing part of a fireplace. He used the material for between fifteen and thirty minutes. His last memory is washing his hands after that use. His next is waking up some days later in hospital. What happened to the plaintiff during the period following when he washed his hands and when he was admitted to hospital two days later is to be found in the hospital notes, which were compiled as a result of information given to the hospital by the plaintiff's wife.

12 I accept the evidence of the plaintiff that prior to using SSI he was careful to ensure that the area was well ventilated. He opened the windows and the doors, and placed two fans in appropriate positions. There was a breeze passing through the house. The plaintiff followed the instructions on the can. From time to time his face was close to the area to which SSI was directed.

13 I accept that the hospital notes reflect accurately the history given by Mrs Forbes and that that history was correct. The plaintiff developed a headache in the afternoon of 15 February, which worsened on 16 February. He appeared unable to attend to domestic chores and there was a slight slurring of speech at lunchtime on 16 February. The plaintiff went to the movies in the afternoon but could not drive. In the evening his condition progressively worsened and he spoke with "rambling incoherent words" and had difficulty with comprehension. He had a very restless night and on 17 February he presented as ready for work dishevelled and incompletely dressed with his shirt out, trousers undone and without socks or shoes. He would not go to the doctor. He was driven to work, where shortly after arrival, he collapsed and was taken to St Vincent's hospital.

14 The hospital notes also record two matters relied on by the defendant. The first was a note to the effect that on 14 February the plaintiff "donated blood as usual but complained of feeling unusually tired". The second was that he forgot, to his wife's distress, St Valentines Day (which was on 14 February.) There is in my opinion, some significance to the statement that he "donated blood as usual but complained of feeling unusually tired" in view of the fact that this history was not contradicted by Mrs Forbes and it is not inconsistent with a cause of his condition being other than exposure to SSI. The plaintiff does not entirely agree with the statement in the hospital notes, but bearing in mind what happened to him on the following day and that his memory of any events at all completely stopped on 15 February, I think it likely that the history given was as recorded and that it accurately recorded the plaintiff's condition on Friday 14 February. I record that I do not attach any significance to the plaintiff forgetting St Valentines Day.

15 Upon his admission to hospital, the plaintiff was subjected to a number of tests. The purpose of the tests was to determine whether or not he was suffering from some sort of viral or bacterial encephalitis. Dr Darveniza believed he had eliminated what he understood to be the known causes of encephalitis.

16 He took a history from Mrs Forbes, who told him about the plaintiff using SSI the previous Saturday and what had happened to him afterwards. Dr Darveniza thereupon contacted Selleys, which immediately made available to him its Material Safety Data Sheet (MSDS).

17 Of relevance to the present issue is the description in the MSDS concerning the chemical makeup of SSI. This was as follows: " CHEMICAL ENTITY PROPORTION Isocyanate terminated polymer V High 4,4' - Diphenylmethane di-isocyanate Low 1,1,1,2 - Tetrafluoroethane Low Dimethylether Low Proportion (% weight per weight): V High >60%, High 30 -60%, Medium 10 - 30%, Low <10%." Note: 4,4' - Diphenylmethane di-isocyanate is later referred to as MDI 1,1,1,2 - Tetrafluoroethane is later referred to as HFC134a

18 Under the heading "Health Hazard Information" there is a further subheading entitled "Inhaled". Under that was written the following "Vapour and spray mist is irritant to mucous membranes and respiratory tract. Inhalation of vapour or spray mist can result in headaches, dizziness, nausea and possible breathing difficulties due to respiratory sensitisation which may be delayed. Inhalation of high concentrations can produce central nervous depression, which can lead to loss of co-ordination, impaired judgment, and if exposure is prolonged, unconsciousness"

19 There was a warning on the SSI cans to the following effect: " Intentional misuse by deliberately concentrating and inhaling contents can be harmful or fatal."

20 Relying in the information in the MSDS, Dr Darveniza opined that, having eliminated as many causes as he was capable of identifying as possibilities, the plaintiff suffered toxic encephalopathy as a result of the inhalation of SSI while it was being sprayed. It is common ground in the proceedings that if a constituent part of SSI were capable of causing the problems experienced by the plaintiff that part would be MDI. Initially, it was part of the plaintiffs case that significance should be attached to the absence of any explanation concerning what the health hazard information sheet was referring to and entitling court to infer that it was referring to a toxic substance and, in particular, MDI. However, in view of the evidence of Dr Drew to the effect that the health hazard information referred to tetrafluoroethane (otherwise referred to as HFC134a), that submission was withdrawn. I record that I accept the evidence of Dr Drew concerning this aspect of the case.

21 Dr Darveniza did not know the chemical makeup of SSI and, as he has said, he is not a toxicologist. His opinion concerning the relationship between the inhalation of MDI and the plaintiff's encephalopathy was the statement in the MSDS together with the history given to him by Mrs Forbes.

22 Dr Spira, another eminent neurologist presented a report to the defendant, initially agreeing with Dr Darveniza's opinion. Later, however, he concluded that, on further reflection, and having regard to other material then available to him he would not support a relevant connection between the two events.

23 In support of their competing claims, the plaintiff and the defendant called expert witnesses having chemical and toxicological knowledge. Dr Crank, called on behalf of the plaintiff, is a chemist. He referred to studies that had been undertaken (to which I will later refer) supporting a view that exposure to toluene di-isocyanate (TDI) could lead to neurological damage. These were referred to as the "firemen studies" and related to approximately 35 firemen in the United Kingdom who in 1967 became exposed to TDI in large quantities. 23 developed neurological symptoms after first developing respiratory problems. SSI did not contain TDI, but both were isocyanates and Dr Crank was of the opinion that their toxicity was the same, allowing him to infer that if TDI was capable of causing neurological damage, so was MDI.

24 The defendant called Dr Drew, a toxicologist. He was of the opinion that the studies relied on by the plaintiff (or at least Dr Crank) did not establish a connection between the inhalation of MDI (and certainly not the amount inhaled by the plaintiff) and encephalopathy. Both Dr Crank and Dr Drew were subjected to extensive cross-examination.

25 I should mention at this point that the studies referred to by Dr Drew and Dr Crank were not presented the way epidemiological studies are presented today. That is, there were not, for example, expressions of opinion concerning relative risk and the like.

26 I record that I accept the opinion expressed by Dr Darveniza to be one that was honestly held. Nonetheless, and bearing in mind that had Dr Darveniza not been aware of the MSDS or, being aware of it he knew that the hazard information did not relate to a toxic substance in the SSI, he would have expressed the opinion that the plaintiff suffered an encephalopathy as a result of an unknown cause.

27 In the course of giving evidence, Dr Darveniza expressed the opinion that the plaintiff's depth of coma and speed of recovery suggested that the cause was not viral. However, to my understanding of his evidence, he could not totally exclude a viral cause but thought that a virus was less likely than any other.

28 There is an absence of any evidence concerning what precisely happens when MDI actually comes in contact with brain tissue, other than that in the opinion of some it is capable of causing encephalopathy because it is a toxic substance. On behalf of the plaintiff it is submitted that one cannot discount the possibility that MDI caused the encephalopathy and, in my opinion, that must be correct. However the real question is whether there is sufficient evidence to persuade me that the encephalopathy was more probably than not the result of exposure to MDI in the circumstances presented in this case.

29 Mr Hennessy QC has relied upon Adelaide Stevedoring Co Ltd v Forst (1940) 64 CLR 538, which, he submits, raises in his favour a presumption of causation by reason of the sequence of events. He does not, of course, submit that it is conclusive of the matter. With due respect, I do not think in the light of all the evidence in this case, that the decision in Forst (supra) assists me one way or the other.

30 In Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262, Spigelman CJ observed that the common sense approach to causation at common law is different from a scientists approach to causation and referred to a number of authorities establishing that proposition.

31 His Honour also referred to the fact that an inference of causation for the purpose of the tort of negligence may be drawn when a scientist, including an epidemiologist, would not draw that inference. However, he pointed to the circumstances that at the end of the day courts were not entitled to choose between guesses. Accordingly, I must consider whether the studies referred to by the plaintiff persuade me that that opinion of Dr Darveniza is, more probably than not, correct.

32 Dr Darveniza agreed that if SSI was implicated that would not have affected his treatment. That statement does not mean, as submitted by the defendant, that unlike Dr Spira, Dr Darveniza was not concerned with the issue of cause. Dr Darveniza made it clear he was concerned with knowing the cause because that knowledge might have effected the treatment. However, in answer to the following question, " So to be clear about it, in the case of the diagnosis relating to Mr Forbes, you did not attribute the toxic event to any particular component individually; is that correct?" He said, "No, because it was beyond my expertise at the time".

33 As I have said, had Dr Darveniza understood that the hazard information in the MSDS was directed to a non-toxic substance, his diagnosis would have been encephalopathy of unknown cause.

34 The plaintiff relies very much on the evidence of Dr Crank, who, as I have said, in turn relied principally on the firemen studies. The firemen studies were undertaken in 1976. They were concerned with the effects on thirty-five firemen involved in fire fighting and cleanup operations at a polyurethane foam factory in 1967. The firemen were exposed to very large doses (approximately 4500 Litres) of TDI. Under the heading "Discussion" the authors referred to the fact that the neurological symptoms complained of were the first that the authors were aware of where it was said that exposure to TDI could cause neurological complications. The authors then queried whether the claimed association was the result of mass hysteria or compensation neurosis or possibly some other toxic factor. It was said, "There have been some difficulties in establishing whether the disorder has an organic basis. Abnormal physical signs on neurological examination have been few, although some of the most severely effected men did have mild ataxia for a few weeks after the fire. Encephalograms were normal in the men on whom this examination was performed. This however does not exclude the diagnosis of mild encephalopathy". As I have said, Dr Crank extrapolated from this study the conclusion that MDI was capable of causing neurological damage, because it was an isocyanate and, in his opinion, was of equal toxicity with TDI.

35 In support of his opinion, Dr Crank referred to certain workplace studies, including that of the National Occupational Health and Safety Committee (NOHSC) and Work Safe as establishing that it was viewed as unsafe for there to be exposure to isocyanates in excess of .02mg/ m3, being the time weighted average concentration of the work atmosphere for a normal eight hour day and a 40 hour work week, to which nearly all workers may be repeatedly exposed day after day. In excess of this could, it was said, lead to adverse effects. It was also said that .07mg/m3 should not be exceeded for short term exposure limit, being the average airborne concentration over a 15 minute period over a normal 8 hour working day.

36 The MSDS, referred to the circumstances that SSI can cause specific immune response - ie sensitisation, in some people with the consequence that that person might subsequently react to exposure to minute levels of the substance. As I have said the sensitisation case was abandoned.

37 Dr Crank's assumption that MDI was as toxic as TDI does not appear to be supported on the material before me. It was disputed by Dr Drew, whose evidence I accept, that TDI was more toxic than MDI. Dr Crank subsequently admitted that was so, but was of the opinion that the increase in toxicity was not relevant. I note also that the NOHSC classifies TDI as "toxic" and MDI as "harmful" and both are directed to respiratory problems and/or sensitisation.

38 The plaintiff has asked me to accept estimates made by Dr Crank concerning the dose to which the plaintiff may have been exposed in the course of applying SSI. It is to be recalled that the firemen in the "firemen study" were subjected to massive doses of TDI. Dr Crank made a number of assumptions, which I think are questionable at best. He posed a theoretical model about the amount of MDI that could be released in an enclosed space at a particular equilibrium point. He had regard to the fact that there was, probably, ten grams of MDI in the two cans and that the plaintiff may have been exposed to it. I have already referred to the fact that the plaintiff gave evidence that the area was well ventilated, a breeze was blowing and indeed he had turned on fans. The product was not used in an enclosed space. It would seem to me that it is unrealistic for me to assume that all the MDI would have been in the atmosphere at any one time bearing in mind that large quantities of it were hardening in the material that had been applied. Moreover, I gain little assistance by the inference said, by Dr Crank, to arise from the odour referred to by Mrs Forbes. It is argued that if exposure had risen to a level where it could be detected by smell, then a dangerous amount of MDI had escaped. So much may be accepted, but the danger is the risk of sensitisation (not claimed) or respiratory problems. It does not assist in determining whether it causes brain damage. Moreover, the smell test is unhelpful bearing in mind that the evidence appears to be that an odour threshold (if it is met and even if people are capable of recording the odour of MDI) generally cannot be reached unless the substance is heated (and this substance was not).

39 On behalf of the defendant, Dr Drew did not dispute that the firemen's studies referred to above supported an hypothesis of association between exposure to TDI and the onset of neurological symptoms, but argued that it went no further and that is a view that I accept. He also is of the opinion, which Dr Crank later agreed with, that TDI is more toxic than MDI. Some reliance was placed by the plaintiff on what has been referred to as the Reidy & Bolter study. This study is the only one purporting to investigate whether exposure to MDI results in neurological problems. The study was undertaken in 1994 and concerned five men who were exposed to MDI and who claimed to be suffering from respiratory distress, reduced concentration, and forgetfulness amongst other neurological symptoms. That study was referred to in the "Concise International Chemical Assessment Document 27" (CICAD 27), a publication of WHO at Geneva in 2001. The authors concluded "Despite these data (the subjective symptoms of respiratory distress, headaches, depression, irritability) the small sample size, possible selection bias for workers involved in litigation, possible confounding factors, lack of pertinent matched control, lack of objective exposure data, and lack of knowledge on mechanism preclude the credibility of the finding (ie an association between MDI and neurological damage) " Moreover, the CICAD 27, although finding an association between exposure to MDI and respiratory problems and sensitisation, could find no connection between exposure to MDI and neurological problems.

40 It is also worth noting that CICAD 27, being a report on the consequence of exposure of humans to MDI made no mention of the "firemen's studies" referred to above. Dr Drew knew of no occasion where it was suggested that there might be some connection between isocyanates and neurological damage when brain damage had not been preceded by respiratory problems (of which there is no evidence in the present case).

41 I accept Dr Darveniza's opinion that it would not necessarily follow that toxic encephalopathy must be preceded by respiratory problems. Nonetheless, none of the experts could point to an occasion where neurological damage caused by exposure to isocyanates did not involve respiratory problems. Dr Spira could find no evidence in the literature and Dr Crank could not find a case of anyone having suffered from neurological problems from exposure to isocyanates that had not suffered respiratory problems. It would seem to me therefore, that even if one could extrapolate from TDI to MDI (and one were able to make allowances for the massive doses of TDI to which people were exposed in the firemen's study and exposure to a number of other chemicals to which those firemen were exposed) there were differences between the neurological symptoms exhibited by Mr Forbes and those exhibited by the firemen. In the study it was reported that one fireman became unconscious at the site of the fire but none was reported to have lapsed into a coma. All these taken together, it would seem to me, make the firemen's study unreliable for the purpose of establishing a relevant connection between the inhalation of MDI and neurological brain damage.

42 It would seem to me with respect to Mr Hennessy's argument it is not correct to conclude, as he asks me to do, that Dr Darveniza's evidence was conclusive unless it was established that it was impossible for neurological damage to be caused by exposure to MDI. As I have said, Dr Darveniza eliminated as many known possible causes as he was able. He did not conclude that the only cause left would necessarily have to be toxic in origin, and he had no occasion to follow that up after his patient survived. He eliminated a number of viral and bacterial causes. But that still left a number of possible other causes in existence. As I have said, had he not seen a reference to the "central nervous depression" (which, with respect to Dr Darveniza he misinterpreted) he would have simply recorded "encephalopathy cause unknown". Conclusion

43 I am not persuaded, on the balance of probabilities, that exposure to MDI (which I find to have been in the substance used by Mr Forbes on 15 February) caused or materially contributed to the encephalopathy he suffered. In law, I am required to be satisfied on the balance of probabilities that the plaintiff suffered toxic encephalopathy by reason of the use of SSI. At first blush it might be thought that the proximity between the use of SSI and the symptoms which ultimately lead to the plaintiffs coma establish a probable cause. But that finding depends on the capacity of MDI to have that consequence. Of course, none of the studies can prove conclusively that there could be no possible connection. But to my mind, the studies demonstrate that a relevant connection is rarely raised above a mere possibility. Thus it is possible, of course, that the plaintiff did suffer a toxic encephalopathy from the inhalation of MDI. However, I am not satisfied on the balance of probabilities that this was so. It is possible that he did not, notwithstanding that bacterial and viral causes (to the extent that they were capable of being identified) were eliminated. As I have said, Dr Darveniza said that had he understood the reference to "central nervous depression" as being a reference to the anaesthetic component (and not to a toxic component), he would have diagnosed the plaintiff's condition as an encephalopathy of unknown origin.

44 It is unnecessary for me to consider the submissions made on the question of foreseeability or to pursue further the plaintiff's submission that it was not necessary for the defendant to foresee the actual injury suffered by the plaintiff - ie, it was sufficient that it could foresee the possibility of a respiratory consequence. Accepting that as correct in law, the plaintiff still must establish a causal nexus between the encephalopathy suffered by him and the exposure to SSI.

45 Accordingly there must be a verdict for the defendant in both actions.

46 Plaintiff to pay the defendant's costs. **********

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Trade Practices Act 1974(Cth)

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