Suthern v Unilever Australia Ltd [2007] ACTSC 81 (28 September 2007)

Last Updated: 30 September 2008

JOHN WILLIAM SUTHERN v UNILEVER AUSTRALIA LTD [2007]
ACTSC 81 (28 September 2007)

NEGLIGENCE – personal injury claim – plaintiff allegedly suffered poisoning due to ingestion of mercury in ice cream – whether mercury introduced into the ice cream during manufacturing process – evidence of mercury levels in subsequent urine samples suggestive of further ingestions – whether continuing symptoms attributable to initial ingestion – no issue of principle.

Trade Practices Act 1974 (Cth), ss 53(a), 74B

Anchor Products Ltd v Hedges 26 [1966] HCA 70; (1966) 115 CLR 493
Schellenberg v Tunnell Holdings Pty Ltd [2000] HCA 18; (2000) 200 CLR 121
Jones v Dunkel [1959] HCA 8; (1958) 101 CLR 298

Wyong Shire Council v Shirt [1980] HCA 12; (1980) 146 CLR 40
Modbury Triangle Shopping Centre Pty Ltd v Anzil [2000] HCA 61; (2000) 205 CLR 254.

Cooper & Ors v Westpac General Insurance Limited [2007] ACTCA 20 (14 September 2007)

Martindale – The Extra Pharamacopoeia, 26th Edition (pg 1053) published in 1972

No SC 178 of 1999

Judge: Crispin J
Supreme Court of the ACT
Date: 28 September 2007

IN THE SUPREME COURT OF THE )
) No SC 178 of 1999
AUSTRALIAN CAPITAL TERRITORY )

BETWEEN: JOHN WILLIAM SUTHERN

Plaintiff

AND: UNILEVER AUSTRALIA LIMITED

Defendant

ORDER

Judge: Crispin J
Date: 28 September 2007
Place: Canberra

THE COURT ORDERS THAT:

1. Judgment be entered for the plaintiff in the sum of $10,000.

1. The plaintiff claims damages for personal injuries allegedly sustained as a result of the ingestion of mercury contained in ice cream that he ate on 13 and 14 June 1996.
2. He gave evidence that his former wife, Mrs Pilar Gee, had bought a tub of Streets Blue Ribbon ice cream from the Cannon’s Superbarn store at Erindale in the ACT on 12 June 1996. He opened it on the following evening and served some onto plates for himself and his two children but did not at that time notice anything unusual about the ice cream. On the evening of 14 June, the plaintiff again served ice cream for himself and his children. In the course of doing so, he ate two spoonfuls of ice cream taken directly from the tub. He then noticed a silver ball in the bottom of the tub and, when he attempted to remove it, noticed it break into two smaller balls. He then examined the ice cream and saw that there were grey streaks in the side from which he had been taking the scoops. He also noticed tiny dots of what appeared to be mercury.
3. He spoke to his wife about what he had seen, telephoned the Poisons Information Service and then had a further conversation with a friend who was a police officer and whom he knew had undertaken a course in occupational health and safety. In response to his advice, the plaintiff and his wife went to the Canberra Hospital where the ice cream was taken from him and x-rayed. The police were called and the attending officers also inspected the ice cream.
4. Subsequent tests confirmed that it contained mercury. The plaintiff was also x-rayed and the images revealed small quantities of a substance presumed to be mercury in his abdomen. He was given laxatives and invited to return to the hospital later.
5. He did not immediately experience any adverse symptoms other than cramping and this may have been attributable to the laxatives. However, as time passed he began to develop a range of unpleasant symptoms that became progressively more disabling. He claims that these were caused by the ingestion of the mercury.
Liability
6. The plaintiff alleges that his injuries and disabilities are attributable to a breach of the duty of care that the defendant owed to him at common law and/or breaches of s 53(a) and 74B of the Trade Practices Act 1974 (Cth).
The claim in negligence
7. The plaintiff’s case on negligence is relatively straightforward. Mrs Gee noticed nothing unusual about the tub of ice cream when she purchased it, and the plaintiff saw nothing unusual about the appearance of the ice cream itself when he removed the lid. The defendant did not receive any communication suggestive of extortion and there is no other reason to suppose that anyone may have tampered with the container or its contents after it had left the factory. Hence, it is a reasonable inference that the mercury was inserted into the ice cream at some stage during the processes of manufacture or packaging. The insertion was unexplained, it occurred whilst all of the relevant circumstances were within the defendant’s control and it was an occurrence of a kind that would not ordinarily occur without negligence. Accordingly, he maintains, negligence on the part of the defendant could be inferred by the application of the principle, res ipsa loquitur.
8. This principle is not a distinct rule of law but an application of an inferential reasoning process from which negligence may be inferred. As the High Court of Australia observed in Anchor Products Ltd v Hedges 26 (1966) [1966] HCA 70; 115 CLR 493 at 500, and the more recent case of Schellenberg v Tunnell Holdings Pty Ltd [2000] HCA 18; (2000) 200 CLR 121 at 133, the burden of proof remains upon the plaintiff. Hence, even if grounds for the application of the principle are established, it remains necessary for the Court to determine whether the burden of proof has been discharged. As Windeyer J determined in Anchor Products v Hedges at 500:

To say that an act speaks for itself does not mean that if no evidence is given for the defendant the plaintiff is entitled in law to a verdict in his favour. The occurrence speaks of negligence, but how clearly and convincingly it speaks depends upon its circumstances. It is evidence from which an inference of negligence may be drawn: it does not mean that this inference must necessarily be drawn, although in some cases it may be evidence so cogent and compelling that any other conclusion would be perverse as Du Parcq L.J. pointed out in Easson v London and North Eastern Railway Co [1944] 1 KB 421 at 425. But always the question whether the plaintiff has discharged the burden of proving his case depends upon the effect of the whole of the evidence given in the case, including such inference as may be drawn from the happening of the accident, if its cause remains unexplained.

9. In the present case, the plaintiff contends that the occurrence is one that provides compelling evidence of negligence on the part of the defendant.
10. At an early stage in the proceedings, counsel for the defendant appeared to suggest that the plaintiff may have put mercury into the ice cream himself and knowingly ingested it with a view to providing an apparent basis for a fraudulent claim. This suggestion was not pressed by Mr Watson SC, who later appeared for the defendant with Ms Williams, and I would in any event have rejected it.
11. Mr Watson did, however, submit that the mercury may have got into the ice cream after it had left the factory. He maintained that it could have been attributable to an act of sabotage within the supermarket or that it could have been inserted deliberately or accidentally whilst the ice cream was in the plaintiff’s home. Neither Mrs Gee nor the plaintiff relied or could reasonably have relied upon the skill or judgment of the defendant to prevent the subsequent contamination of the ice cream in any such manner.
12. The defendant provided evidence, in sworn answers to the plaintiff’s interrogatories, that the relevant tub of ice cream had been one of 21,420 produced in a production run between 8.30 pm on 3 May 1996 and 6.50 am on 4 May 1996. Neither the defendant nor the Australian Federal Police received any other complaint of mercury in stock produced in that production run. The defendant tested samples from production runs before and after that run but found no similar problem. The defendant also dismantled and inspected the pasteuriser for signs of mercury but found none. An analysis of burn-on material removed from the pasteuriser showed that there was less than 0.01mg/kg mercury present. The defendant then proceeded to interview 29 staff members who had worked on the relevant production run. They were unable to identify any event that may have been responsible for the introduction of mercury into any of the ice cream. The defendant recalled the product in the ACT, recovering 4,321 containers of ice cream, none of which were found to contain mercury. It also withdrew ice cream produced in that production run from points of sale in other states. It maintained that thermometers were not used in the production of the ice cream but only in its research laboratory.
13. Staff members were asked to complete a questionnaire which included the question “Given that there were small beads of mercury in two distinct spots in the 2L tub of Blue Ribbon, how do you think that the mercury could have got there”? Most of the responses were largely speculative. Some expressed the opinion that it would not have entered the ice cream in the factory whilst others clearly thought that it had. One employee attributed it to the packaging process and added “dirt, plastic, hair, dead and alive spiders have been found in the packaging before”.
14. The defendant also relied on evidence from Professor Hambley who had examined and tested the contents of the remaining ice cream and the relevant tub on 23 October 2000. He also examined x-rays of the tub. He said that the particles of mercury appeared to be distributed only across the irregular surface of the ice cream and were not in the body of it. It was suggested that this demonstrated that the mercury had been added to the ice cream after it had already become frozen.
15. On the other hand, the evidence of the plaintiff and Mrs Gee of their observations of the ice cream received some support from the hospital notes taken on 14 June 1996 which recorded that “mercury . . . was speckled throughout the tub of ice cream”. The plaintiff said that the doctors who looked at it had been “picking pieces out of it” and had expressed the opinion that it was mercury.
16. More than four years had obviously elapsed before Professor Hambley examined the ice cream and it is impossible to know what might have happened to it during those years. There is no reliable evidence as to the time that elapsed between the initial removal from the freezer and the x-ray of the ice cream at the hospital but there is no reason to suppose that it may not have begun to thaw during that period. The evidence does not reveal whether it may have partially melted to the point where it retained its essential shape but became sufficiently soft for droplets to move towards one or other surface depending upon how the tub was held.
17. I will address the issues raised as to the plaintiff’s credibility later in these reasons for judgment. For present purposes it is, I think, sufficient to say that I accept his evidence and that of Mrs Gee as to what they saw in the ice cream on the evening of 14 June 1996.
18. Moreover, even if I were to assume that the mercury had been added after the ice cream had become frozen, that would not demonstrate that it was attributable to the action of someone other than a servant or agent of the defendant. In the absence of any evidence of an extortion demand or of any similar act of sabotage with mercury at any time, there is no reason to suppose that it was inserted deliberately and, if accidental, it presumably occurred in the factory before the lid was placed on the tub. As I have mentioned, there was some evidence that mercury thermometers were used in the defendant’s research laboratory and the defendant did not adduce any evidence with a view to establishing that the tub of ice cream in question could not have been the subject of some examination by a research officer. Nor did it seek to establish that no such thermometers had been broken. Furthermore, it is apparent from the responses to the questionaries submitted to staff involved in the manufacturing process that some, at least, had apparently thought that the mercury might well have got into the ice cream whilst it was still in the factory.
19. Counsel for the defendant stressed that there was little real evidence to explain the presence of mercury in the ice cream and cited the observation of Dixon CJ in Jones v Dunkel [1959] HCA 8; (1958) 101 CLR 298 at 305 that:

... the law ...does not authorise a court to choose between guesses, where the possibilities are not unlimited, on the ground that one guess seems more likely than another or others. The facts proved must form a reasonable basis for a definite conclusion affirmatively drawn of the truth of which the tribunal of fact may reasonably be satisfied.

20. I am mindful of this admonition and of the relative paucity of evidence relevant to this issue. However, I have concluded that there is a sufficient basis for an inference that the mercury got into the ice cream whilst it was still in the factory, and I am satisfied, on the balance of probabilities, that it did.
21. Counsel for the defendant argued that, in any event, there was simply no evidence of any deficiency in the manufacture, storage or distribution of the ice cream that would support a finding of negligence. Nor was there any evidence of the availability of remedial measures or their utility, cost or potential inconvenience. Hence, the balancing exercise discussed in Wyong Shire Council v Shirt [1980] HCA 12; (1980) 146 CLR 40 cannot be undertaken, and there is no basis for a finding of a breach of duty. It was also argued that the defendant could not be held liable for the intervening criminal conduct of a third party: see Modbury Triangle Shopping Centre Pty Ltd v Anzil [2000] HCA 61; (2000) 205 CLR 254.
22. Had the plaintiff not been able to rely upon the principle of res ipsa loquitur, I would have accepted these submissions without hesitation. However, this seems to be a classic case for the application of that principle. As the Court of Appeal recently affirmed in Cooper & Ors v Westpac General Insurance Limited [2007] ACTCA 20 (14 September 2007), the principle may be invoked when three elements are established:

(1) there is an “absence of explanation” of the occurrence that caused the injury;

(2) the occurrence was of the kind that does not ordinarily occur without negligence; and

(3) the instrument or agency that caused the occurrence was under the control of the defendant.
23. There is clearly a relevant absence of explanation, mercury does not ordinarily get into tubs of ice cream without negligence and, if it did so whilst the tub was still in the factory, as I have found, then the instrument or agency responsible was obviously under the control of the defendant.
24. Having considered the whole of the evidence in the case, including that adduced by the defendant in the form of answers to interrogatories, I am satisfied that the plaintiff has discharged the burden of proving his claim in negligence on the balance of probabilities.
The claim under s 53(a) of the Trade Practices Act
25. The first of the claims under the Trade Practices Act is based upon the provisions of s 53, the relevant portions of which are in the following terms:

A corporation shall not, in trade or commerce, in connexion with the supply or possible supply of goods or services or in connexion with the promotion by any means of the supply or use of goods or services:
(a) falsely represent that goods are of a particular standard, quality, value, grade, composition, style or model or have had a particular history or particular previous use. . .

26. This aspect of the plaintiff’s claim was not pressed with any real vigour. There were competing arguments about whether, in enacting s 53, the legislature had intended to confer a right to damages or other civil remedy upon any person claiming to have suffered loss as a consequence of a breach of the section. This argument may be of considerable academic interest, but I have found it unnecessary to address it in the present case. It was not suggested that the defendant had falsely made any express representation of this kind and the plaintiff was essentially dependent upon the contention that the presentation and sale of the ice cream gave rise to an implied representation that it was fit for human consumption. Whilst that is a potentially viable claim, it seems to me to be one that is more securely founded upon s 74B of the Trade Practices Act and, even if I were to accept that a breach of s 53(a) can give rise to a cause of action sounding in damages, the plaintiff’s case would not be materially enhanced.
The claim under s 74B of the Trade Practices Act
27. The claim under s 74B is based upon the following provisions of the section:

(1) Where:

(a) a corporation, in trade or commerce, supplies goods manufactured by the corporation to another person who acquires the goods for re-supply;
(b) a person (whether or not the person who acquired the goods from the corporation) supplies the goods (otherwise than by way of sale by auction) to a consumer;
(c) the goods are acquired by the consumer for a particular purpose that was, expressly or by implication, made known to the corporation, either directly, or through the person from whom the consumer acquired the goods or a person by whom any antecedent negotiations in connexion with the acquisition of the goods were conducted;
(d) the goods are not reasonably fit for that purpose, whether or not that is a purpose for which such goods are commonly supplied; and
(e) the consumer or a person who acquires the goods from, or derives title to the goods through or under, the consumer suffers loss or damage by reason that the goods are not reasonably fit for that purpose;

the corporation is liable to compensate the consumer or that other person for the loss or damage and the consumer or that other person may recover the amount of the compensation by action against the corporation in a court of competent jurisdiction.
(2) Subsection (1) does not apply:
(a) if the goods are not reasonably fit for the purpose referred to in that subsection by reason of:
(i) an act or default of any person (not being the corporation or a servant or agent of the corporation); or
(ii) a cause independent of human control;
occurring after the goods have left the control of the corporation; or
(b) where the circumstances show that the consumer did not rely, or that it was unreasonable for the consumer to rely, on the skill or judgment of the corporation.

28. It was not disputed that the defendant was a corporation, in trade or commerce, that it supplied the ice cream manufactured by it to the retailer or that the retailer acquired it for re-supply to a consumer. It was not disputed that, if the ice cream contained mercury when initially supplied by the defendant, then it was not reasonably fit for consumption. It was not disputed that Mrs Gee purchased the ice cream as a consumer, that she did so for the purpose of consuming it and making it available to the plaintiff and their children for consumption, and that this was an obvious purpose made known, by implication, to the defendant. Nor was it disputed that the plaintiff had acquired the ice cream from his wife. Hence, the real issues that arise for determination in relation to this cause of action are whether the plaintiff suffered loss or damage by reason of the goods not being reasonably fit for the purpose of consumption and, if so, whether the defendant can nonetheless elude liability by reason of subs 74B(2).
29. The defendant vigorously resists any finding that the plaintiff suffered any substantial injury as a consequence of ingesting mercury in the ice cream. This aspect of the case is discussed later. For present purposes, it is sufficient to note that he clearly suffered at least some minor loss and/or damage by reason of the ice cream not being fit for consumption. For example, he presumably incurred some expense, even if only for petrol, in travelling to and from the hospital and he also suffered cramping, either as a direct result of the mercury or as a result of the laxatives prescribed to enable him to excrete the mercury more quickly.
30. It should be noted that it is the defendant which bears the onus of proof in relation to the exceptions specified in subs 74B(2). The evidence does not establish that the ice cream was unfit for consumption by reason of an act or default by someone other than a servant or agent of the defendant or a cause independent of human control that occurred after the ice cream had left the control of the defendant. Its case on this issue is really dependant upon supposition that the mercury was put into the ice cream as an act of sabotage, a further assumption that this happened after the ice cream had left its control and a series of answers that it provided to the plaintiff’s interrogatories said to show that it was unlikely that this had occurred in the manufacturing process. In my opinion, that is clearly insufficient to discharge the onus of proof borne by the defendant on this issue. In the context of alternative causes of action with the onus of proof resting on the plaintiff in one and the defendant on the other, reliance upon the admonition of Dixon J not to choose “between guesses” was inevitably a two edged sword and, in my opinion, it effectively precludes any finding for the defendant on this issue.
31. It was argued that s 74B would not apply if the mercury had entered the ice cream after it had already been delivered to the supermarket. That is true, but the premise has not been established. It was also submitted that, if the mercury had been inserted into the ice cream as an act of sabotage by some person unrelated to the defendant, then the defendant would be relieved of liability because the evidence suggested that Mrs Gee had not relied on the skill or judgment of the defendant to prevent such an occurrence, and it would have been unreasonable for her to have done so. Again, this argument is valid but the premise has not been established.
32. I find that the defendant has failed to establish any of the grounds specified in s 74B(2) and that it is therefore liable to compensate the plaintiff for any loss or damage occasioned by reason of the ice cream not being fit for consumption.
Causation
33. The defendant has raised a number of points in relation to the issue of causation. I have taken the view that it is not necessary to address every issue of this kind, but will refer to a number that I found significant. The arguments may best be appreciated in the context of at least a brief account of the relevant history, including such matters as the development of the plaintiff’s symptoms, his courses of treatment, and the mercury levels in his blood and urine at various times.
Relevant history
34. The x-ray taken during the course of the plaintiff’s first visit to the hospital on 14 June 1996 was said to have shown that:

There are multiple specks of radio-opacity which are of metallic density. There is a group in the left upper quadrant close to the mid line presumably in the stomach. There is another group scattered in the right lower quadrant and true pelvis presumably in the caecum and sigmoid colon respectively. There is also one speck seen in the descending colon.

35. Professor Watling, an analytical forensic chemist, made an assessment that the specks of mercury visible in this x-ray would have amounted to 1.56 grams.
36. A 24 hour urine collection study apparently undertaken on 15 June 1996 revealed a mercury level within normal limits.
37. The plaintiff duly returned to the hospital on 17 June 1996 reporting that he had been well, apart from occasional mild abdominal cramps and occasional mild headaches. As previously mentioned, the cramping may have been caused by the laxatives, though Mr Bartley SC, who appeared for the plaintiff with Mr Tuscano, suggested that it could equally have been a symptom of incipient mercury toxicity. A urine sample was taken but his urinary mercury level proved to be normal. A further abdominal x-ray was also taken and this showed that there were then “many more metallic radio-opacities scattered in a large bowel distribution”.
38. The plaintiff received a letter from the defendant dated 17 June 1996 expressing concern about the “unfortunate incident” that had occurred, and advising him that the relevant batch of ice cream had been recalled. He also received a copy of a media statement in which the defendant announced the withdrawal of the batch of ice cream following the discovery of traces of liquid mercury in one tub sold in Canberra.
39. He returned to the hospital for a further examination on 21 June 1996. He was then found to be asymptomatic. A further abdominal x-ray was taken and the radiological report later revealed that a comparison of that x-ray with the x-ray film taken on 17 June 1996 had demonstrated that there were “now less radio-opaque foreign bodies within the large bowel loops, suggesting clearance of some foreign bodies”.
40. The plaintiff subsequently began to experience various symptoms. By August 1996 he noticed that he was becoming angry and sought medical advice. On 30 August 1996 his general practitioner, Dr Brown, issued him with a medical certificate for a “stress disorder” and advised him to see a counsellor. The plaintiff disagreed with this diagnosis and consulted another general practitioner, Dr Tsintsof. He gave him a history of ingesting mercury in the ice cream and complained of reduced short-term memory, lethargy, headaches, irritability and diminished concentration. Dr Tsintsof noticed that he had a high frequency hand tremor. He subsequently referred the plaintiff to a specialist in occupational medicine, Dr Le Leu.
41. At a time that he thought was “around September” that year, the plaintiff’s face began to become swollen and he experienced associated pain in his neck and the sides of his face under the ears. This condition was subsequently diagnosed as parotitis.
42. The radiological report of a further x-ray taken on 11 October 1996 at Dr Tsintsof’s request stated that:

A single 1 mm diameter focus is noted in the descending colon (as marked) as evidence of any residual mercury within the colon. No other foci were identified, with extensive clearing of the previously noted opacities from the examinations of 14, 17 and 21/6/96.

43. He subsequently he saw Dr Le Leu who also noted that the plaintiff had a fine tremor in the hands. On 12 November 1996 Dr Le Leu reported that he had seen the plaintiff again a few days earlier and that he had complained of emotional problems, headaches, difficulty reading, disorientation, loss of concentration and swelling of the salivary glands “for sixteen days”. He had said that some headaches had started “virtually from the time he ate the ice cream”. Dr Le Leu referred him to a number of other specialists including Dr Gavin Carney, a nephrologist, who later assumed responsibility for the plaintiff’s treatment.
44. When the plaintiff was asked in evidence about matters such as his mood, concentration and memory between August and November 1996, he said that it was a “foggy” period and that he had only a vague recollection of it, though he did recall having trouble concentrating and thinking things through properly. He also recalled that on occasions he had become lost whilst driving to various sites and that he had suffered pain in the face and headaches. Whilst he was dissatisfied with Dr Brown’s diagnosis of post-traumatic stress syndrome, he acknowledged that over time he did begin to experience emotional problems.
45. He saw Dr Tuck, a consultant neurologist on 28 November 1996 and gave him a history of headaches, that he said had developed a few days after ingesting the ice cream, and continuing stabbing pains in the head. He explained that his cognitive symptoms began a little later. He had developed swollen parotid glands and had noticed that some foods have a peculiar taste. During the month or so prior to the consultation he had also noticed pins and needles in his extremities when lying or sitting in the one position. He was referred for a neuropsychological assessment.
46. A renal biopsy carried out in November 1996 revealed no abnormalities.
47. He was given chelation treatment in the Canberra Hospital between 16 and 24 December 1996 with a view to removing mercury from his system. Samples taken immediately prior to the first course of chelation on 18 December 1996 revealed a base serum mercury level of 55 nmols/L and a base urinary mercury level of 442 nmols/d. After treatment with 1,000 mg of penicillamine per day, his peak urinary mercury level was found to be 1019 nmols/d.
48. Samples taken prior to the second course of chelation which commenced on 30 January 1997 revealed a base serum mercury level of 17 nmols/L and a base urinary mercury level of 175 nmols/d. On this occasion the dosage of pencillamine was increased to 1500 mg per day but his peak urinary mercury level reached only 368 nmols/d. Dr Carney subsequently recorded that this response had been very good, though “much blunted compared to the first response”.
49. An abdominal x-ray taken on 5 February 1997 after the conclusion of this course of therapy revealed “two tiny flecks of metallic density in the left hypochondrium which could be within the descending colon”.
50. By that time he had been experiencing severe facial swelling, headaches and other pain. He had exhausted his sick leave and his employment was terminated on 17 February 1997.
51. Towards the end of that month he became short of breath. He was again admitted to the Canberra Hospital on 28 February 1997 and examined not only by Dr Carney but by Dr Hurwitz, a thoracic physician. His breathlessness was thought to have been a reaction to the penicillamine but other symptoms persisted. His facial swelling was diagnosed as parotitis and it was noted that he had been suffering from migraine.
52. On 12 March 1997 the plaintiff’s serum mercury level was found to exceed 2,873 nmols/L.
53. The third course of chelation therapy did not commence until 28 April 1997 and by then this level had fallen to 841 nmols/L. His base urinary mercury level was then found to be 8,964 nmols/d. On this occasion the pencillamine dosage was only 250 mg per day. Yet after this course, his peak urinary mercury level was found to be 76,137 nmols/d. Dr Carney subsequently described this as “an extraordinary figure”. A further abdominal x-ray taken on the second day of this course revealed “multiple pinpoint metallic densities in both sides of the abdomen and in the pelvis”.
54. Dr Carney clearly found the plaintiff’s case very interesting and on 3 September 1997 he made a presentation to medical colleagues at what was described as the “Grand Rounds”. He later recorded that during the course of the ensuing discussion it had been suggested that, because the plaintiff had developed symptoms within a short period of ingesting what had appeared to have been elemental mercury, “he must have been given something else”. Some of the medical practitioners present questioned whether he may have been re-exposed to mercury on several occasions and one suggested poisoning.
55. He had further courses of chelation therapy in December 1997, February, March and July 1998, March, May and December 1999 and March and May of 2000. On these occasions he was treated with varying dosages of Dimercaptosuccinic Acid (“DMSA”) which is apparently a more effective chelating agent for mercury than penicillamine.
56. Dr Carney’s clinical examinations of the plaintiff did not reveal anything significant during this period. From about July 1998 he generally found that the plaintiff was well, apart from side effects of the chelation therapy, some occasional parotitis, headaches and skin lesions. Indeed, on 4 November 1999 he reported that the plaintiff felt “wonderful” and that he had got a job as a commentator in archery at the Sydney Olympics. He added that the plaintiff had been thinking of competing at the Commonwealth Games at some stage and said that he “certainly looks well”.
57. On 28 June 2000 he made a note to the effect that the plaintiff’s archery was still successful and that he had won a bronze medal at the national championships.
58. In March 2001 the plaintiff’s serum and urinary mercury levels were both found to be within the normal range but his urinary mercury levels were again found to be elevated in November 2001 and March 2002. In July 2002 his serum mercury level was again found to be within the normal range and his urinary mercury level only slightly elevated.
59. In April 2003 his urinary mercury level was found to be 6,840 nmols/d. Dr Carney was clearly at a loss to understand how the level could have increased to such an extent and speculated about whether the plaintiff might have been “mobilising further elemental mercury which has been metabolised”. In July 2003 the urinary mercury level had fallen to 388 nmols/d and by July 2004 it had returned to the normal range.
60. The plaintiff’s arsenic levels were also found to be significantly elevated from time to time, though it was suggested that this may have been attributable to his fondness for seafood.
61. His level of disability fluctuated but when he gave evidence on 21 May 2007 he said that he still felt unable to work more than 30 hours per week.
The issue of metallic mercury toxicity
62. The prevailing scientific view is that, at least in the absence of certain gastrointestinal problems, the ingestion of liquid metallic mercury is not toxic to humans. As Dr Karalliedde, an expert toxicologist, explained, less than 0.01% can be expected to be absorbed during the passage of mercury through the body and this is insufficient to cause any toxicity. There was a formidable body of scientific evidence to support this view and it was not seriously challenged.
63. Elemental mercury may, however, be oxidised or converted to a toxic form of mercury in the medium of water and chloride ions, by reactions with enzymes and/or amino acids, and/or reaction with bacteria and other micro organisms. Mr Bartley argued that the conditions capable of causing conversion or oxidisation in this manner could exist in the gastrointestinal tract. He conceded that this would take some time and that liquid mercury usually passed through the gastrointestinal tract quickly. He pointed out, however, that the evidence did not reveal, with any clarity, the minimum period for which the metallic mercury would need to have remained in the gastrointestinal tract for such a process to have occurred. Dr Carney said that the period between 14 and 17 June 1996 would have been sufficient. Professor Spence conceded that the period between 14 and 21 June 1996 would have been “an ample period according to the literature” for conversion into mercuric salt. On the other hand, Professor Watling, who is an expert analytical forensic chemist, said that the chance of metallic mercury being so absorbed was “vanishingly small”.
64. The preponderance of evidence on this issue was to the effect that such absorption would not occur in a normal gastrointestinal tract. Whilst it could possibly occur due to the presence of inflammation, malignancy, infection, disease or some other pathology or malfunction of the intestinal mucosa, no instances of toxicity occurring due to such occurrences had been documented, though there had been a recorded case of absorption after retention of mercury due to a fistula. Furthermore, there was no evidence to suggest that the plaintiff had suffered from any gastrointestinal disease or abnormality, though the evidence does not exclude the possibility that he may have had such a condition. The difficulty with this aspect of the plaintiff’s case is that it is reliant upon an hypothesis that he may have had an undetected illness that apparently did not produce sufficient symptoms to warrant subsequent complaint or medical investigation but which sufficiently affected the mucosa to permit the absorption of elemental mercury.
65. Mr Bartley also relied upon the opinion expressed by both Dr Crank and Dr Allender that elemental mercury might be absorbed if finely divided. This opinion was founded upon a theory that the fine division of the mercury would result in a greater surface area relative to the volume of mercury involved and that this would increase the likelihood of absorption. As Mr Watson established, there is a considerable body of literature about the consequences of ingesting liquid metallic mercury which was apparently widely used for the relief of bowel obstruction in the 17th and 18th centuries. Yet, Dr Crank did not attempt to support this theory by reference to any of the articles or case studies contained in the literature, and Dr Allender was able to point to only a single sentence in the 26th edition of Martindale – The Extra Pharamacopoeia, 26th Edition (pg 1053) published in 1972, and that sentence had been removed from all of the subsequent editions. As Mr Watson pointed out, a discussion of this theory would have been a striking omission from the more recent literature had it been arguable because, as Dr Allender himself conceded, biological mechanisms within the gastrointestinal tract may themselves cause fine division. Furthermore, as Dr Karalliedde observed, the presentation of a larger surface area by fine division would not change the characteristics of the liquid metallic mercury. Whilst Dr Allender maintained that the presentation of a larger surface area would make the mercury more reactive, Professor Hambley explained that it would do so only in the sense of increasing the exposure to any oxidising agent that may be present. Dr Karalliedde said that mercury is not easily oxidised unless exposed to large amounts of oxygen and that a normal gastrointestinal tract does not provide conditions where oxidisation can take place. I found Dr Karalliedde an impressive expert witness and accept this evidence.
66. Mr Bartley argued that the decisive question was whether the mercury ingested by the plaintiff on 13 and/or 14 June 1996 may have been delayed in its passage through the gastrointestinal tract for a sufficient period to enable such conversion and/or oxidisation to occur. The x-rays subsequently taken on 17 and 21 June 1996 both revealed the presence of mercury well after it should have passed through the plaintiff’s body in the ordinary course of events. Whilst the evidence did not demonstrate that he had been suffering from any particular gastrointestinal problem sufficient to account for this delay, Mr Bartley pointed out that it did not exclude such a possibility. In any event, he argued, the x-rays demonstrated that a substantial delay had in fact occurred. Hence, it was possible that some of the elemental mercury had been converted or oxidised into a form capable of being absorbed through the mucosa. Such a process was, he submitted, the only rational explanation for the elevated levels of mercury subsequently found in the plaintiff’s body.
67. Dr Karalliedde bluntly rejected this hypothesis, explaining that the conditions for oxidation were simply not present in a normal gastrointestinal tract. Mr Watson also argued that the metallic densities observed in the x-rays taken on 17 and 21 June 1996 were not the residue of mercury ingested on 13 and 14 June 1996 but were attributable to subsequent ingestions.
68. Mr Watson submitted that it was most unlikely that the plaintiff could have had a gastrointestinal problem of sufficient severity to delay the passage of metallic mercury through his body for such an extended period without producing significant symptoms. Yet on 17 June 1996 the plaintiff had complained only of mild discomfort and cramping, that may have been attributable to the laxatives, and on 21 June 1996 he had apparently been asymptomatic.
69. The plaintiff had been invited to undertake specialist medical examination to determine whether he might have suffered from an oesophageal or pharyngeal abnormality that might have provided some conceivable explanation for the absorption of metallic mercury. He declined on medical advice and it would clearly be inappropriate to draw any adverse inference against him by reason of this decision.
Was further mercury ingested?
70. Mr Watson pointed out that the x-ray taken on 17 June 1996 had revealed many more metallic radio densities than had been present three days earlier. This suggested a further ingestion of mercury rather than the retention of mercury that would otherwise have been expected to have quickly passed through the body.
71. I note that Dr Korber, a radiologist, confirmed that there was “clearly more” mercury evident in the x-ray taken on 17 June than had been seen in the x-ray taken three days earlier. He agreed that an accurate volume-metric comparison of absolute volume between the mercury visible and the x-ray of 14 June 1996 and that visible in the x-ray of 17 June 1996 could not be made and that it was possible, but extremely unlikely, that there could have been mercury in part of the stomach not captured on the earlier x-ray. The x-ray taken on 11 October 1996 revealed only one density and Dr Korber thought that this had not been metallic in nature.
72. Both Professor Watling and Dr Karalliedde said that the x-ray taken on 17 June 1996 appeared to reveal mercury globules higher in the gastrointestinal tract than any visible in the x-ray taken three days earlier.
73. Professor Watling, whom I found to be an impressive witness, was also asked to examine the x-rays taken of 14 and 17 June 1996 and those subsequently taken on 5 February and 29 April 1997. He expressed the opinion that the number and distribution of radio opaque particles could not have been from a single ingestion.
74. Dr Carney suggested that the mercury apparently revealed by the x-ray on 29 April 1997 may have actually been present since the plaintiff ingested the ice cream on 13 and 14 June 1996 but that it had not been evident on the earlier x-rays because it had divided into fine particles which had subsequently “coalesced” and “reformed larger globules”. Mr Watson submitted that this suggestion should be rejected. Dr Carney had not explained how such re-coalescence could have occurred in the gut and the hypothesis had received no support from other expert witnesses. Indeed, Dr Allender dismissed it as “preposterous”. Dr Korber also gave evidence that the resolution of plain x-rays was sufficiently high to capture images of microscopic size and said that even fine particles of mercury should have been visible in those taken on 11 October 1996 and 5 February 1997.
75. Mr Watson argued that the excretion of larger amounts of mercury due to later courses of chelation therapy also provided strong evidence of further exposures to mercury. Dr Karalliedde and Professor Spence both said that the maximal excretion of mercury would be expected to occur during the initial chelation and that, whilst the mercury levels following the first and second courses of chelation may have been understandable, the extraordinary level found in the plaintiff’s urine after the third course of chelation using much lower doses of Pencillamine provided strong evidence of a more recent ingestion of mercury. This was, of course, consistent with the x-rays taken at that time. When asked whether the blood and urinary mercury levels found in the samples taken from the plaintiff over several years could be explained by a single exposure to metallic mercury on 13 and 14 June 1996, Professor Watling said that nothing was impossible but that it was “beyond the realm of probability”.
76. Mr Watson submitted that the plaintiff’s elevated arsenic levels and at least some elevation in his mercury levels could be explained by reference to his high consumption of seafood. That is possible, though it seems unlikely that this could account for the high level of mercury in the plaintiff’s urine in April 1997 and it could not, of course, explain what was revealed by the x-rays at that time. Nonetheless, Dr Allender, who gave evidence on the plaintiff’s behalf, conceded in cross-examination that the inclusion of substantial amounts of shellfish in the plaintiff’s diet would provide a much better explanation for the long term elevation in his serum and urinary mercury levels than the ingestion of metallic mercury in June 1996.
77. A further impediment to acceptance of Dr Carney’s theory arises from the apparent implausibility of a single ingestion of mercury in June 1996 accounting for the subsequent fluctuation of mercury readings throughout the ensuing years. It also seems unlikely that it could explain the presence of a substantial quantity of mercury in the plaintiff’s urine as late as April 2003, nearly seven years after the initial ingestion. Professor Watling gave evidence that 90 days was the longest period ever recorded in which metallic mercury had remained in the human gut. He also explained that mercury would normally be wholly eliminated from the body in about five “half lives”, even in the absence of chelation. The literature provides estimate for the half life of mercury ranging from 18 to 90 days and Professor Watling carried out experiments which revealed a half life of up to 120 days. Even on this basis, one would have expected the mercury to have been eliminated in less than two years. Hence, it is difficult to see how the initial ingestion could account for the elevated mercury levels in 2001, 2002 and 2003.
78. Mr Bartley sought to answer this objection by reference to evidence that the concept of a half life relates to the period during which mercury is excreted from the blood rather than from organs of the body. As Professor Watling explained, different organs have different accumulation and depuration rates. Mr Bartley argued, in essence, that mercury may have been absorbed into the plaintiff’s organs, including his brain, and subsequently drawn back into his blood and urine by chelation. There are, however, a number of impediments to acceptance of this hypothesis as an adequate explanation for the apparently incongruous mercury levels in the plaintiff’s blood and urine at various times. There was evidence that when mercury compounds cross the blood/brain barrier they cannot return. The plaintiff was examined by Dr Tuck, a neurologist, on several occasions between 1996 and 2005 and no clinical evidence of any neurological injury was detected. The hypothesis would presumably have required a substantial absorption of mercury immediately after the initial ingestions and, as previously mentioned, there does not appear to have been any unequivocal symptoms of mercury toxicity at that time. Furthermore, this hypothesis could obviously not explain the presence of radio opaque densities on subsequent occasions.
79. As previously mentioned, Professor Watling calculated that approximately 1.56 grams of mercury would have been present in the plaintiff’s gut at the time of the x-ray on 14 June 1996. On the other hand, when Professor Hambley examined the remaining ice cream in October 2000, he found that it contained only 0.127 grams. Mr Watson submitted that it was highly improbable that the plaintiff could have consumed ninety per cent of the mercury in the small percentage of ice cream he had consumed prior to noticing the presence of mercury in the remainder. I did not find this argument particularly compelling. There is obviously no evidence as to how one would expect mercury to have been distributed in or upon ice cream when derived in an unknown manner from an unknown source.
80. Viewed overall, however, the evidence does suggest that the plaintiff has not only been further exposed to mercury after 14 June 1996, but that he has on some occasions orally ingested further liquid metallic mercury.

The medical opinions

81. Dr Carney clearly commenced treating the plaintiff in the belief that his symptoms of emotional lability and occipital headaches had commenced within three days of 14 June 1996, and that there had been a “recrudescence” of symptoms a month later. This history was not supported by the plaintiff’s evidence as to the onset of symptoms and it appears that Dr Carney laboured under a potentially significant misconception until the plaintiff’s account was put to him in cross-examination.
82. Dr Carney did not then change his opinion and it was suggested, in essence, he had become committed to a view about the causation of the plaintiff’s symptoms that he was either unable or unwilling to relinquish. He had plainly become very interested in the case, having earlier raised it at the “Grand Rounds”, and mentioned in evidence that he intended to write a paper about it. Mr Watson suggested that it was evident from his responses to questions put to him in cross-examination that he had substantially lost objectivity about this issue.
83. It is true that Dr Carney responded to some questions in an emphatic manner, but his robust defence of his opinion must be considered in context. He had treated the plaintiff for a long period of time and the presence of mercury in his body had been confirmed not only by successive x-rays but by samples of blood and urine taken before and after sessions of chelation therapy on no less than ten occasions between 1996 and 2000, and further samples taken between 2001 and 2004. Whilst it was suggested that he should not have accepted the history given to him by the plaintiff, there was no obvious reason for Dr Carney to have doubted its reliability. Furthermore, he is not an expert in mercury toxicity but a nephrologist who seems to have done the best he could to respond to a most unusual case. His theory that mercury initially ingested on 13 and 14 June 1996 may have divided into fine particles that were absorbed or otherwise eluded detection by x-ray, and subsequently coalesced and reformed into larger globules was, I think, the most plausible hypothesis he could formulate to explain what he regarded as a clear inference from the medical evidence available to him. There is no suggestion that he was ever given any hint that the plaintiff might have been exposed to mercury on subsequent occasions and he did not have the benefit of the other expert evidence now available to me. Even without the subtle influence of a long-term doctor/patient relationship, it would have been understandable for him to have assumed that mercury from the initial ingestions of ice cream had remained in the plaintiff’s body for extended periods and to have attempted to postulate some possible explanation for its retention.
84. Nonetheless, Dr Carney’s hypothesis is not supported by the preponderance of medical and scientific evidence and I am unable to accept it.
85. Dr Carney’s opinion that the plaintiff’s symptoms were causally related to the ingestion of metallic mercury on 13 and 14 June 1996 is dependent substantially upon the fact that they commenced within a few months of those ingestions and are otherwise unexplained. However, the temporal connection has not been shown to have been sufficiently close to support an inference of any real strength. I accept the evidence of Professor Watling that symptoms of mercury toxicity generally commence almost immediately after exposure. As I have mentioned, the plaintiff experienced some abdominal discomfort and cramping prior to his return to hospital on 17 June 1996 that may have been attributable to the laxatives given to him on the earlier occasion and by 21 June 1996 he was apparently asymptomatic. The symptoms of which he now complains did not emerge for some time. He agreed that “by August” he had noticed that he was having difficulty in coping with problems at work and he was becoming frustrated and angry with sub-contractors. He also said that he was having difficulty with headaches. When asked when he first started to have the facial swelling later diagnosed as parotitis, he said that he did not know the date but he thought it was around September of that year. As mentioned above the plaintiff described his memory of that period as “pretty foggy” but the evidence does not establish that these symptoms occurred so soon after the ingestion of the mercury in the ice cream as to raise an inference that they were attributable to mercury toxicity.
86. Furthermore, whilst some of the plaintiff’s symptoms could have been attributable to mercury toxicity, there were none that could be explained only by reference to such a cause. Emotional responses, such as frustration and anger with subcontractors, are not necessarily indicative of any physiological problem, and neither migraine headaches nor parotitis are recognised symptoms of mercury toxicity. Indeed, as counsel for the defendant pointed out, at the time the plaintiff’s current wife, Mrs Janine Suthern, filmed the plaintiff apparently suffering from severe parotitis his serum and urinary mercury levels were within the normal range. The plaintiff himself says that he continues to suffer from parotitis and that it is bought on by “overdoing it” physically. Parotic swelling can also be induced by insufflation. It was suggested to the plaintiff in cross-examination that he had deliberately induced this condition, which is referred to as pneumoparotitis. During the course of subsequent argument, counsel for the defendant pointed out that there had been no evidence that the parotic swelling had been accompanied by other symptoms indicative of inflammation, as might have been expected if there had been a disease of the parotic gland. Furthermore, the swelling of the plaintiff’s parotic gland had on occasion appeared and diminished within a short period and this could not reasonably be explained by inflammatory parotitis. The plaintiff also explained that on most occasions he had migraine headaches and parotic swelling simultaneously. It is, I suppose, possible that the plaintiff unwittingly produces pneumoparotitis by his bodily responses to exertion and/or the pain of migraine headaches, though there is no evidence to this effect. Dr Kariallidde also said that chelating agents may cause inflammation of the parotic gland, though chelation therapy was last administered in May 2000 and this obviously could not explain his more recent episodes.
87. His claim to have suffered cognitive impairment due to mercury toxicity is not supported by the preponderance of evidence. I note, in particular, that he was subjected to neuropsychological testing by Professor Mattick in 1997, 2003, 2004 and 2005 and on each occasion Dr Mattick found no impairment of cognitive functioning, though on the last of these occasions he noted a significant deterioration in the plaintiff’s performance on a number of tests which, he said, “makes no sense”. He went on to explain that this suggested a variation in motivation, effort, fatigue or “some ongoing sinister process affecting his neurological status” that required further neurological diagnosis. He also explained that following an exposure to a neurotoxin such as mercury one would expect “an acute effect” and the return of function over a long period of time rather than the reverse pattern. I found Professor Mattick a most impressive witness and accept his evidence.
The credibility of the plaintiff’s complaints
88. I must say that I have found this matter quite perplexing. The defendant has mounted a formidable scientific case to the effect that the plaintiff has repeatedly been exposed to mercury since 13 and 14 June 1996. This and other aspects of the evidence have raised substantial questions about the credibility of the plaintiff’s evidence.
89. However, I had the benefit of seeing him in the witness box for long periods and observed him respond to rigorous cross-examination extending, subject to some interruption, over a period of seven days. I had ample opportunity to assess his demeanour throughout this period and, despite the sustained assault upon his credibility by Mr Shore QC, the experienced senior counsel who then appeared for the defendant, I formed the impression that he was transparently honest. He seemed to me to be a straightforward and somewhat stolid man doing his best to accurately recount the relevant events. At times he appeared to be struggling to recall exactly what had occurred or to determine how to properly respond to certain questions. During the course of the cross-examination he was shown section of a videotape that had been recorded by his second wife, Mrs Suthern, in order to demonstrate the extent to which his face had become swollen and his evident suffering. It was put to him that he had deliberately inflated his cheeks and that he had pretended to be in pain. Whilst this aspect of the cross-examination was forcefully maintained, I must say that I was unable to see the suggested signs of fabrication. In my opinion, the DVD recording does not reveal any sign of an attempt to create pressure in the mouth for the purpose of inducing or aggravating parotitis and I accept his evidence that he had never made any such attempt. I also accept his evidence that he had not attempted to simulate signs of pain and distress and that the apparent symptoms had been genuine. It is true that there were some inconsistencies in his evidence but I think that they may well have been attributable to confusion and/or difficulties of memory. He certainly betrayed no hint of deviousness in the manner in which he gave evidence. The apparent lapses in his memory did leave me in some doubt as to the extent to which I could rely upon his account of the earlier events, some of which had occurred more than a decade before he was asked to describe them in evidence, but I am satisfied that he had conscientiously tried to tell the truth.
90. I note, in passing, that whilst Professor Mattick said that one of the tests he had administered suggested that the plaintiff had been “faking bad” and perhaps overstating his problems, he did not believe that the plaintiff had been lying.
91. I am satisfied that the plaintiff’s first wife, Mrs Gee, was an honest witness who did her best to describe the manner in which the plaintiff changed following the incident in question. She said that he became angry and withdrawn, that they were always fighting and that he was constantly unwell. They separated in May 2000 and she seemed to attribute the breakdown in their relationship to these symptoms. Sadly, however, it is not unusual for people to look back at the behaviour and attitudes of a former spouse and wonder why he or she had seemed to change. The deterioration of a relationship is itself a stressful experience and may lead people to become angry, withdrawn or even argumentative.
92. I accept that Mrs Gee looked back on four years between June 1996 and May 2000 as a time in which the plaintiff was “always sick” and accept that he suffered from the symptoms she described but I am inclined to doubt that they were as constant as this phrase may have suggested.
93. I also note the plaintiff met his present wife, Mrs  Suthern in June 2000 and she found him to be a charming man with a good sense of humour. She said that she developed a romantic attachment to him within two or three weeks of their first meeting and that he had been able to develop a good rapport with her two young sons. The very formation of this relationship may, of course, have had a positive impact upon the plaintiff’s emotional state. Accordingly, whilst I do not see the contrast in their evidence concerning the plaintiff’s condition mid 2000 as casting substantial doubt upon the credibility of either woman, it is, I think necessary to bear in mind the likelihood that both the plaintiff’s condition and the impressions which these women formed of him may have been influenced by the state of the respective relationships at the times they were describing.
94. I see no reason to doubt Mrs Suthern’s evidence as to the nature and severity of the symptoms he had been experiencing during the period immediately prior to her evidence. Furthermore, the videotape which she took of him whilst he was apparently suffering from parotitis and headache revealed, in my opinion, a man who was genuinely suffering pain.

Findings

95. I am satisfied that the ice cream purchased by the plaintiff’s former wife, Mrs Gee, contained a quantity of metallic mercury and was accordingly unfit for human consumption. I am satisfied that the plaintiff ate some of the ice cream and some of the mercury contained in it on 13 and 14 June 1996. I accept his account of discovering mercury in the ice cream on the second evening and of attending at the hospital in response to that discovery. I am satisfied that the multiple specks of radiopacity of metallic density seen in the x-rays taken on 14 June 1996 consisted of metallic mercury that he had ingested with the ice cream that he ate that evening.
96. I do not accept that he knowingly ingested further mercury between 14 and 17 June 1996. Since he had apparently been told when he attended the hospital on the first occasion that metallic mercury was non-toxic, it is difficult to imagine that he would have swallowed more of it in the hope of providing support for a spurious claim. In any event, I accept his sworn evidence that he did not do so. He may have accidentally ingested further metallic mercury from another unknown source, someone else may have deliberately or inadvertently administered it to him without his knowledge or, as Mr Bartley suggested, he may have had some undiagnosed physical condition that delayed the entry of some of the mercury into the area of the gastro-intestinal tract covered by the abdominal x-ray. Perhaps fortunately, I am not required to solve every mystery, only to determine whether the relevant onus of proof has been discharged in relation to the decisive issues.
97. Despite my belief that his complaints are genuine, I am unable to be satisfied that he suffered any substantial injury due to mercury toxicity arising from the ingestion of mercury in the ice cream on 13 or 14 June 1996. That finding is not wholly fatal to his case because he did suffer at least some consequential loss and damage. The discovery of the mercury in the ice cream and the realisation that he had swallowed some of it caused him to go to hospital and seek medical advice. He was obviously worried and suffered some abdominal discomfort and cramping. I am unable to determine whether the cramping was attributable to the toxicity arising from some conversion of mercury into a form capable of passing through the mucosa and being absorbed into the body or whether it was merely a reaction to the laxatives, though I suspect it was the latter. In either event, I am satisfied that these symptoms were directly or indirectly attributable to the plaintiff’s ingestion of mercury in the ice cream and that this was in turn attributable to the defendant’s negligence and/or breach of s 74B of the Trade Practices Act.

Damages

98. I think that the plaintiff is entitled to damages for the symptoms he then suffered and for the inconvenience and any expense associated with returning to the hospital on 17 and 21 June 1996 for follow up examinations.
99. Mr Bartley submitted that he was at least entitled to damages in respect of the inconvenience and discomfort associated with the courses of chelation undertaken between December 1996 and May 2000. This submission could be sustained only if it had been established that this treatment was causally related to the mercury he ingested on the nights in question. However, by 21 June 1996 he had been asymptomatic. It was the development of further symptoms in August and September 1996 that caused him to seek further medical advice and, in due course, treatment from Dr Carney. I accept that he remained concerned about the possible effect of the mercury he had earlier consumed, notwithstanding the advice given to him at the hospital that it was not toxic. I also accept that this may have been a contributory factor in his decision to seek further medical advice and even, perhaps, to undergo chelation treatment. Nonetheless, the subsequent symptoms, raised serum and mercury levels and presence of further metallic densities in the gut all seem to be indicative of further exposures to mercury that must in my opinion be regarded as novus actus interveniens.
100. There will be judgment for the plaintiff in the sum of $10,000.
101. I will hear counsel as to costs.

I certify that the preceding one hundred (100) numbered paragraphs are a true copy of the Reasons for Judgment herein of his Honour, Justice Crispin.

Associate:

Date: 28 September 2007

Counsel for the plaintiff: Mr A J Bartley SC with Mr F Tuscano

Solicitor for the plaintiff: Porters Lawyers

Counsel for the defendant: Mr H Shore SC and Mr G Watson SC with Ms K Williams

Solicitor for the defendant: Astridge & Murray

Dates of hearing: 14-24 November 2005, 17-28 July 2006, 4-7 September 2006, 21-31 May 2007, 4-8 June 2007

Date of judgment: 28 September 2007