Burgess v Accident Compensation Corporation

IN THE DISTRICT COURT HELD AT WELLINGTON Decision No. 2 88 /2008 UNDER The Injury Prevention, Rehabilitation, and Compensation Act 2001 IN THE MATTER of an appeal pursuant to Section 149 of the Act BETWEEN MATTHEW BURGESS of Wellington Appellant (Appeal No. AI 176/04) AND ACCIDENT COMPENSATION CORPORATION a body corporate duly constituted under the provisions of the said Act Respondent DECISION OF JUDGE CADENHEAD ON THE PAPERS THE COURSE OF THESE PROCEEDINGS [1] I part-heard this appeal on 3 October 2007. I made the following directions order: I part-heard this matter on 3 October 2007. It became apparent at the hearing that to fairly dispose of this appeal I required further information. Accordingly, I make the following directions: [i] Written submissions should be filed and served by the appellant within four weeks (28 days). [ii] The respondent will file its written submissions within three weeks 21 days) of receipt of the appellant's submissions. Time limits will be strictly adhered to. If the appellant has not filed its written submissions or obtained a further extension from a Judge within this timeframe, this may provide grounds for striking the appeal out for want of prosecution. [ifi] The Registry, upon receipt of the written submissions of both parties will allocate a date of hearing. 2] Since that date I have received an affidavit sworn by Mrs Burgess and a letter from Mr Whinham, who supervised Mr Burgess at Trentham Army Camp. I also have received two medical reports from Dr Dean Kilfoyle, dated 4 April 2008, and 7 August 2008, along with information provided by Brake & Parts Cleaner. [3] On 26 August I received an email from the Registry that both parties agreed that I should determine this appeal on the papers. THE ISSUE [4] At issue is ACC's decision of 15 November 2002 declining the appellant's claim for cover for peripheral neuropathy on the basis that his injury was not caused by his employment. NARRATIVE OF FACTS [5] The appellant lodged a claim for cover on 12 October 2001 for peripheral neuropathy said to be caused by exposure to solvents, while he was refurbishing tanks for the Army. The date of accident was stated to be "1993 to 1996". [6] ACC sought further information from the Army. In a letter dated 28 August 2002 the Army advised that the appellant had been employed with them permanently between 11 February 1993 and mid 1996 as a vehicle mechanic. He had also been engaged with them on "several short-term contracts" before that period. 7] The Army advised that for a six-year period, staff from the appellant's unit were involved in the refurbishment of the Army's American M113 tanks. The appellant was involved in that process for at least three years. Approximately six tanks were refurbished each year, and so the appellant was involved in about eighteen refurbishments. [8] Among the duties involved in the refurbishment of the American M1 13 tanks was a relining process. This involved exposure to solvents. In particular, the Army advised: "The relining process consisted of two operations separated by different stages of the refurbishments: Rubber removal. This involves applying ADOS Solvent N to the old rubber lining by brush or cloth to release the old glue, scrapping the rubber off and then cleaning up the excess with the solvent. The shell of the vehicle was N then removed for water blasting, sand blasting and painting. Approximately 3 litres of Ados Solvent N were used for each refurbishment. Gluing and fixing. The vehicle rebuild took place when the shell was returned to the workshop. This included the cutting of rubber sheets applying and spreading Ados F2 contact adhesive over the panels of the vehicle and over the cut rubber sheets. The sheets were then fitted to the panels. Approximately 6 litres of Ados F2 contact adhesive were used for each refurbishment." [9] The Army report referred to the material safety data sheet for Ados F2 contact adhesive (used for the gluing and fixing), which showed it included a substance called "n-hexane" which could cause peripheral neuropathy [10] The Army report advised that for each vehicle, the rubber removal process took 2-3 days, and the gluing and refitting one day. The report stated that the appellant was not exposed to the solvents on a continual basis, but he was exposed for "days at a time". The Army report indicated that although disposable half masks were available, they were not effective protective against organic solvent vapours in the confined vehicle shell. [11] ACC then sought advice from Dr Abernethy, neurologist, who had been treating the appellant. Dr Abernethy stated in a report dated 22 October 2002 that the appellant had first presented at the neurology department on 17 October 1995 and reported a number of symptoms including: an 18-month history of burning sharp pains in his feet, calf and thigh muscles as well as the muscles in his shoulder girdle; a tingling sensation under the feet which gradually moved up to the mid calf; numbness in the feet and toes and hands; and problems gripping things. He had also reported feeling tired and lethargic for 18 months, and that he had been having headaches, which occurred once a week. [12] Dr Abernethy examined the ingredients of the solvents the appellant had been exposed to (Ados F2 and Ados Solvent N), and reported that hexane in the Ados F2 could cause neuropathy. Dr Abernethy did not however consider that the appellant's condition was due to exposure to solvents in the Army.: [13] Dr Abernethy noted that toxic neuropathy was "typically motor in type", whereas the appellant's neuropathy was "predominantly sensory". [14] The appellant had symptoms attributable to neuropathy before he had started with the Army (pain in the toes reported to Dr Hatfield on 12 February 1992) 3 [15] The appellant's neuropathy had progressed and continued to progress, whereas toxic neuropathies usually related to the period of exposure and then over time either remained static or more typically gradually improved. [16] Axonal neuropathy without a clear cause was a common clinical problem in older persons. [17] On 15 November 2002 ACC declined the appellant's claim for cover on the basis that his condition had not been caused by solvent exposure in his employment. [18] On 19 November 2002 the appellant wrote to ACC regarding ACC's decision. He stated that he had first worked for the Army in 1991, initially on short-term contracts, before later being employed permanently. He stated that when he commenced employment he was working on English Scorpion tanks and he had had no problems with these. It was only after he later began working on the American M1 13 tanks that he noted a deterioration of symptoms. MEDICAL REPORTS [19] ACC referred the matter to Dr Snyman, ACC Director Workwise Wellington. Dr Snyman carried out a thorough review of the clinical records. Dr Snyman noted that peripheral neuropathy is a common condition that was not only caused by hexane or related solvents, and in some cases it was not possible to identify a cause. He concluded that the appellant's condition was not caused by his employment with the Army. [20] The appellant's lawyer obtained a neuropsychological assessment from Dr Kay Farrar. In her report dated 30 September 2003 Dr Farrar documented memory and attention problems from which the appellant had been suffering. She noted that the appellant reported that these problems had started, when he had retired from the Army, and had become worse over the last three years. She stated that although such impairment had been associated with exposure to solvents, it was usual for the exposure to occur for at least ten years unless the exposure was very intense. Further, she reported that the occurrence of these impairments from when the appellant was medically retired, and their increase and severity over the last eight years, was' unusual given that exposure to solvents had ceased in early 1996. She concluded that this was: 4 'not totally in keeping with the association of impairment due to neurotoxicity. I suggested other conditions which underlie a deteriorating attention and memory need to be excluded". 21] The appellant's lawyer then obtained a report dated 22 October 2003 from . . . . . . . Dr Glass, occupational medicine specialist.. Dr Glass reported that the appellant had worked for the Army between 1991 and 1996. For the first eighteen months (1991 to 1992) he had assessed English Scorpion tanks, and in order to do this he used a degreaser and a brake cleaner to strip the tanks. From February 1992 he was involved in refurbishing the American M1 13 tanks. [22] Dr Glass stated that although it was not known what solvents were used in the initial period with the English Scorpion tanks, because this work was similar to his later Army work "it is reasonable to assume the solvents were also similar". He stated: "...there is evidence of exposure to degreasing solvents from 1991 (most likely trichloroethylene), glues from 1991 (probably containing MEK and possibly n-hexane) and, from February 1993, to Ados F2 contact adhesive and Ados solvent N." [23] Dr Glass also reported that Dr Abernethy's view that the symptoms of foot pain in 1992 were due to neuropathy, was "supposition"; the exposure to solvents in the Army pre-dated reported symptoms of peripheral neuropathy; [a] Exposure would have lasted for up to two weeks at a time; [b] Peripheral visual symptoms which the appellant had reported had also been reported by other workers exposed to n-hexane; [c] The appellant was suffering symptoms of both motor and sensory neuropathy, although the sensory symptoms were more marked; [24] The appellant reported using cans of CRC brake clean in his garage at home, and this would account for his continued symptoms beyond 1996. 25] Dr Glass found that Mr Burgess's work exposures caused or contributed to his peripheral neuropathy, that there was no non-employment exposure, and that the risk of suffering peripheral neuropathy was significantly greater for those exposed to the chemicals he had identified. [26] ACC obtained a report from a Dr Dryson, occupational specialist. Dr Dryson reported that n-hexane was a known cause of peripheral neuropathy. He noted that n- hexane was only in the Ados F2 glue and not the removing solution (Ados Solvent N). He also noted research which suggested that toluene, which was present in the Ados . . . ... F2 glue, "reduced or attenuated" the peripheral neuropathy caused by n-hexane. Dr Dryson stated that based on the GP case notes there appeared to be no reference to symptoms suggesting neuropathy before commencing work at the Army. Dr Dryson considered that while there were arguments both in favour and against the appellant's condition being due to solvent exposure at work, on balance he did not consider it probable that it was due to work exposure. [27] Dr Dryson's report was referred to Dr Glass. In a brief report of 12 February 2004 Dr Glass confirmed his original view regarding the cause of the appellant's neuropathy. He disagreed with Dr Dryson's reliance on research regarding toluene reducing or attenuateng peripheral neuropathy. [28] ACC obtained a further report from Dr Abernethy. In his report of 4 February 2004 he reported: [a] It was not known what solvents the appellant had been exposed to prior to 1993 apart from trichloroethylene. The use of n-hexane began in 1993. [b]. The symptoms complained of in February 1992 of pain in the feet were due to neuropathy. [c] Peripheral visual loss in hexane-induced neuropathy has never been clearly established. In the appellant's case his visual loss had no medical basis. [d] The appellant was not reliable in the manner in which he reported symptoms. [e] Dr Abernethy confirmed his original report that the appellant's condition was not due to work exposure to solvents. 6 THE REVIEW HEARING [29] The matter proceeded to review. The application for review was dismissed. The reviewer adjourned the hearing initially to obtain further evidence. The reviewer noted the differences between Dr Abernethy and Professor Glass as to their conclusions. He noted the evidence of Dr Abernethy, who was the neurologist for the appellant and had had an involvement with him over several years. The reviewer said that to have a claim accepted for neurotoxicity, a positive assertion must be made, rather than one elimination by other causes. Like Dr Dryson, he came to a view that the claim had not been made out. MEDICAL EVIDENCE [30] After a Notice of Appeal was filed, the appellant's lawyer obtained clarification from the Army regarding the period of the appellant's employment, including the fixed term contracts which preceded his permanent employment. In a letter of 1 April 2005 the Army stated: "Mr Burgess commenced his employment at Ist Base Workshop, Trentham Camp on a fixed term contract of employment as a Vehicle Mechanic. The purpose of this position was to complete an overhaul project. The tenure of this fixed term contract was 17 February 1992 to 5 June 1992. Mr Burgess' employment with NZDF was continuous with effect from 17 February 1992 until he left NZDF." [31] ACC then sought clarification from the Army regarding the period the appellant worked with them, the nature of his duties, and the period of exposure to solvents. [32] In a letter dated 13 February 2006 the Army confirmed the 1992 start date. The Army also clarified: [a] The earlier work on the English Scorpion tanks was not a refurbishment process; [b] The refurbishment of the American M113 tanks involved a number of processes, and the relining process involving exposure to solvents was just one such process involved. The Army confirmed that exposure to fumes would have lasted three to four days on each vehicle, and not two weeks as had been suggested by the appellant. 7 [33] ACC then obtained a further brief report from Dr Dryson dated 30 March 2006. He confirmed his original opinion that on a probability basis the appellant's neuropathy was not due to exposure to solvents in employment. SUMMARY OF MEDICAL EVIDENCE Dr Peter Hatfield, Renal Physician, 19 February 1992: [34] In addition to commenting on the appellant's renal health Dr Hatfield reported: "He probably does suffer from gout with acute arthritic pain he complains of in the toes of both feet." Hospital Notes, Capital Coast Health, 15 March 1999; [35] The notes include the following reference: "Bilateral leg & feet pain - 8 yrs" Patient Rehabilitation Plan, Capital Coast Health, 19 March 1999: 36] This plan states that the patient reported: "pain in both lower and upper limbs for eight years". Dr Abernethy, Neurologist, 28 October 2002 [37] Dr Abernethy stated that the appellant had first been seen in the neurology department on 17 October 1995 by Dr Vania Sinovich. He stated that he discussed the appellant's symptoms with him on 30 October 1995. Dr Abernethy stated (at page 3, para 4): "I concluded in February 1996 (from the pain in the toes reported to Dr Peter Hatfield 12.02.92) that the neuropathy was of at least four years' standing". [38] With regard to causation Dr Abernethy reported (at page 6): "On the subject on the cause of his neuropathy, there is no question that a toxic neuropathy can develop from exposure to hexacarbon solvents and it is typically motor in type. Mr Burgess's neuropathy is predominantly sensory. More importantly there is evidence from the notes that Mr Burgess had symptoms attributable to neuropathy before the NZ Army ever employed 8 him and this really is the crucial observation. Secondly, the neuropathy gradually progressed and continues to progress even now ... Toxic neuropathies usually relate to the exposure and often continue or coast for some time after the exposure ceases, presumably while the metabolic derangement continues. The neuropathy then, either remains static or more typically gradually improves. ... recovery may be partial or complete but there would be expected to be some degree of recovery. For this ground too, I don't consider it likely that this neuropathy is occupationally based. I think it is unfortunate that he is being encouraged to make a claim under these circumstances.' [39] Dr Abernethy further stated that while hexane exposure can cause neuropathy, neuropathy without a clear cause "is a common clinical problem in older persons" (page 6, under "Conclusion"). Kay Farrar, Neuropsychologist, 30 September 2003 [40] Kay Farrar stated (at page 3): "Mr Burgess described memory and attention problems that had started at the time he was medically retired from the Army and over the last three years had been more marked, causing him to make notes to avoid forgetting. At the present time he has frequent difficulties with attention, where he often lost the track of a topic when talking or listening, found it hard to concentrate with background noise or in crowded situations and was easily distracted. He described severe memory problems where he forgets what he has been told or read, finds it difficult to learn something new and makes errors on routine tasks, forgets to finish a task he started or to do something he intended, and repeats himself often. He often mislays or loses his belongings and has considerable difficulty recalling names of people and words. He said he had some difficulty remembering a route that he should know well and does not always recognise the face of someone he knows. He describes problems with muddling or jumbling words when speaking, and that his spelling was worse and he was much slower at reading. He said he had marked problems with slow thinking, and being less capable at problem solving, planning and organising.' [41] Ms Farrar carried out a series of tests which showed impaired results from memory and attention tests. With regard to causation she stated (at page 6): "...there was no support for the view that solvent toxic encephalopathy was a progressive disease such as Alzheimer's. Therefore, although attention and memory difficulties have been associated with chronic solvent organic neurotoxicity, the occurrence of these impairments at the time Mr Burgess was medically retired, and their increase in severity over the last eight years, is not totally in keeping with the association of impairment due to neurotoxicity. I suggest that other conditions which underlie a deteriorating attention and memory need to be excluded." Dr Bill Glass, Occupational specialist, 22 October 2003 [42] With regard to the level of exposure to solvents in the Army Dr Glass stated (at page 2): "I would estimate from what Mr Burgess told me that out of the approximately 2 months (8 weeks) it took to refurbish an M113 some 2 weeks were involved working in the confined space of the tank, while the air was contaminated by the solvent vapours already referred to. Over the 34 years Mr Burgess worked at this task some 44 weeks would have been spent in this contaminated confined space environment." [43] With regard to the chemicals that the appellant was exposed to Dr Glass stated (at page 6): "Mr Burgess was so exposed, in this case at least to Ados F2 containing N- hexane and probably to other solvents such as MNBK as well as MEK which can potentiate the effects of n-hexane or MNBK and is a common solvent in glues." [44] Dr Glass went on to report (at page 7): I note Mr Burgess's employment began with contract work in 1991 at which time he was exposed to degreasing solvents - possibly trichloroethylene as well as other solvents..." (45] With regard to the report of pain in the feet by Dr Hatfield in 1992, Dr Glass stated: "In fact, in reference to the ACC file, 17.02.1992, Dr Hadfield [sic] notes, 'Mr Burgess has complained of pain in the toes of both feet possibly gout with acute arthritic pain'. Dr Abernethy reinterprets this as 'probably neuropathic complaints of pain to Dr Peter Hadfield' [sic]. However, this is supposition and contradicts Dr Hadfield's [sic] review." [46] With regard to why the appellant's condition had continued to progress after leaving the Army Dr Glass stated: "Mr Burgess told me that he uses CRC brake clean in a spray can form for cleaning things at home. He has a work bench in his garage and told me he would use on average one spray can every week and only stopped in 2003. ..It is not surprising, given these circumstances, that his symptoms as investigated by Dr Farrar continued and even worsened over this period." Dr Dryson, Occupational Specialist, 18 December 2003 [47] Dr Dryson considered there were arguments both for and against a causal relationship between the appellant's employment with the Army and his peripheral neuropathy: "Arguments for: 1. Matthew was exposed to what would appear to be a significant amount of solvents, with poor respiratory protection, for 3 years while employed with the New Zealand Army. 2. Symptoms of peripheral neuropathy are most likely to have started after commencement of work with the New Zealand Army. 3. Matthew has a clinically confirmed peripheral poly-neuropathy. 4. Solvents, and in particular n-hexane are a known cause of peripheral poly-neuropathy. 5. Matthew has peripheral visual defects maybe related to a peripheral neuropathy 6. Matthew has neuropsychological impairments, which are also associated with exposure to solvents, among other things. Arguments against: 1. Peripheral neuropathy has many causes, and Matthew's neurologist, Dr Abernethy believes that the type he has is not consistent with exposure to solvents. 2. There is research evidence showing that the neurotoxicity of n-hexane is reduced by concurrent exposure to toluene, rather than increased. 3. The total time of exposure at 3 years is somewhat short, and there is a difference of opinion in the file between the total time spent using solvents as indicated by the New Zealand Army report, and as given by Matthew himself 4. The changes seen on the neuropsychological tests could be equally as well explained by Matthew's sleep apnea, as to any solvent exposure. 5. N-Hexane is a contaminant of the hexane component of the Ados glue. It is likely to be fairly small, perhaps 10% of the hexane component and therefore 1-3% of the mixture as a whole. This does not suggest high exposure." [48] Dr Dryson concluded on balance that the likelihood of a workplace cause for the appellant's peripheral neuropathy did not reach the 50% threshold of probability. 11 Dr Abernethy, 4 February 2004 [49] With regard to the symptoms of foot pain reported to Dr Hatfield in February 1992, Dr Abernethy confirmed his original opinion that these were signs of neuropathy: "Dr Glass comments that my contention that the symptoms MB had in his feet that Dr Hatfield thought at the time might possibly be due to gout, were in fact due to peripheral neuropathy as "speculation". I have the advantage of hindsight, and of extensive professional experience and post graduate training in the diagnosis of peripheral neuropathy... Pain in the feet defying immediate explanation is common early in neuropathy. When unequivocal neuropathy did develop the cause of these early symptoms then become apparent. Gout on the other hand causes typically acute severe monoarthritis and associated pain or sometimes a polyarthritis neither of which MB had or subsequently developed." [50] With regard to the progression of the appellant's condition, Dr Abernethy stated: "Neuropathy can continue to worsen for a brief period of a few months after exposure stops but then improves (see reference in previous report). His neuropathy continues to progress, documented by repeated examinations up to April 2003. This is not consistent with solvent induced neuropathy." [51] With regard to the appellant's visual symptoms, Dr Abernethy stated: "Peripheral visual loss in hexane induced neuropathy has never been clearly established. (See my previous report for reference) In MB's case this visual field loss was at first suspected by Mr Halliwell and then demonstrated by myself on 4.5.02 to have no medical basis." [52] With regard to the type of neuropathy he stated: 'Other aspects of his neuropathy are also not consistent with the neuropathy ascribed to solvents in the published literature. He has a painful sensory neuropathy with very little motor involvement, the literature reports that hexane causes a predominantly motor neuropathy (see previous report for reference). Neuropathy proven to arise from occupational exposure is very rare to non-existent in NZ in my personal experience. " Dr Bill Glass, 12 February 2004 [53] In responding to Dr Dryson's report Dr Glass stated: "In my experience peripheral neuropathy can occur rapidly after relatively modest amounts of exposure to N-hexane, It is, therefore my opinion that Mr Burgess' exposure was more than sufficient to account for his symptoms of peripheral neuropathy. 12 Dr Dryson ignores Mr Burgess' ongoing exposure to solvents in his home as a likely explanation for Dr Farrar's concern Dr Dryson refers to a 1992 research paper on rats which in his words "suggests" that toluene actually reduces or attenuates the peripheral neuropathy caused by N-hexane. He translates that reference and its uncertainty into an argument against causation in this "human" case. This in itself, in my view, brings into question the credibility of his final conclusion as stated in his last paragraph." Dr Dryson, 30 March 2006 [54] In a report to ACC Dr Dryson stated: "Dr Abernethy also makes the point that hexane polyneuropathy generally tends to be a motor neuropathy, and that it generally tends to clear up after cessation of exposure. I would agree that N-hexane neuropathy is mostly a motor one and that recovery is usually expected to occur within a year of cessation of exposure." STATUTE AND LEGAL PRINCIPLES 55] Section 30 of the Injury Prevention, Rehabilitation, and Compensation Act 2001 states: "30 Personal injury caused by work-related gradual process, disease, or infection- (1) Personal injury caused by a work-related gradual process, disease, or infection means personal injury (a) suffered by a person; and (b) caused by a gradual process, disease, or infection; and (c) caused in the circumstances described in subsection (2). (2) The circumstances are- (a) the person- i) performs an employment task that has a particular property or characteristic; or (ii) is employed in an environment that has a particular property or characteristic; and (b) the particular property or characteristic- (i) causes, or contributes to the cause of, the personal injury; and 13 (ii) is not found to any material extent in the non-employment activities or environment of the person; and ifi) may or may not be present throughout the whole of the person's employment; and (c) the risk of suffering the personal injury i) is significantly greater for persons who perform the employment task than for persons who do not perform it; or (ii) is significantly greater for persons who are employed in that type of environment than for persons who are not. (3) Personal injury caused by a work-related gradual process, disease, or infection includes personal injury that is of a type described in Schedule 2 that is suffered by a person who is or has been in employment involving exposure to agents, dusts, compounds, substances, radiation, or things (as the case may be) described in that schedule in relation to that type of personal injury." [56] In ACC v Ambros [2007] NZCA 304 the Court of Appeal confirmed its decision in Atkinson v ARCIC [2002] 1 NZLR 374 (CA) which had found that the claimant was required to prove causation in claiming cover for personal injury caused by medical misadventure. [57] In Ambros the Court of Appeal went on to find that in considering causation, in some situations there may be a "tactical burden" which shifts to ACC such that ACC is required to obtain further medical evidence (paras 55-64). The Court also found that the Court may be able to draw "robust inferences" on the medical evidence in determining causation (paras 65-70). The Court emphasised (at para 70): "It must, however, always be borne in mind that there must be sufficient material pointing to proof of causation on the balance of probabilities for a Court to draw even a robust inference on causation. Risk of causation does not suffice." CONCLUSION [58] At issue in this appeal is whether the appellant's employment had a particular property or characteristic which caused his peripheral neuropathy (section 30(2)(a), and 30(2)(b) (i)). [59] More particularly in this case, the main issues are: [a] Whether the appellant was exposed in his employment to a substance that could potentially have caused his condition. 14 [b] Whether the identified substance did in fact cause his condition. [60] If these are established, the appellant must then establish the other criteria of section 30 i.e. that the causative property or characteristic was not found to any material extent in his non-work activities (section 30(2)(b)(ii)), and that the risk of suffering the injury was "significantly greater" for persons employed in his environment than for persons not so employed (section 30(2)(c)). [61] I have concentrated on the first issue of whether the identified substance did in fact cause or contribute to the condition of the appellant. That issue to a large extent is a medical issue and that is why I called for a further medical report from another neurologist. This neurologist is Dr Kilfoyle. He notes: "In summary Mr Burgess has a severe painful sensorimotor peripheral neuropathy. The clinical and electrophysiologic pattern is of a slowly progressive length-dependent axonal neuropathy. This common pattern of neuropathy has many potential causes. Despite extensive investigation however a definite cause can not be found in up to 50% of such cases, so-called idiopathic neuropathy. 'The question here is whether Mr Burgess's neuropathy is due to occupational exposure to n-hexane containing substances. The neuropathy reported in patients exposed to n-hexane is typically a length-dependent sensory predominant symmetrical neuropathy with no specific clinical features. The only specific feature of n- hexane neuropathy are giant axonal swellings which are seen on sensory nerve biopsies of approximately 25-50% of patients in series of industrial n-hexane exposure. Mr Burgess's biopsy did not show these features. Thus while the clinical features of Mr Burgess's neuropathy are potentially compatible with that described in n-hexane neuropathy it is also nonspecific with many other potential causes In order to establish a probable causal relationship between occupational n-hexane exposure and Mr Burgess's neuropathy all of the following criteria would need to be met: 1) The symptoms should begin after the onset of exposure, 2) there should be a sufficient concentration and duration of exposure, 3) symptoms should not continue to progress for more than 6 months after the cessation of exposure, 4) no other explanation can be found despite appropriate investigations. There seems little doubt that Mr Burgess had a significant exposure to n-hexane containing compounds. This exposure was over a prolonged period of time and likely involved both significant skin and respiratory contact in an enclosed space. This level of exposure is at least similar to that described in established cases of n-hexane neuropathy. The onset of neuropathic symptoms has been a contentious issue. Mr Burgess is adamant his neuropathic symptoms began in 1993, at least 12 and possibly 24 months after beginning his work with the army. He believes the symptoms reported to Dr Hatfield in 1992 were different in nature. The description he provided to me which admittedly is based on a recollection now more than 15 years old was of focal pain, redness, swelling and tenderness. Or Hatfields letter does not sufficiently describe the clinical findings to draw any independent conclusion. I must therefore accept Mr Burgess personal recollection which would favour an arthritic condition rather than a neuropathic pain. This appears to have been Dr Hatfields position. I note that Mr Burgess's serum urate was elevated, a risk factor for gout. Dr Abernethy has performed extensive and appropriate evaluation of Mr Burgess's neuropathy and no other identifiable cause of neuropathy has been found. The final barrier to establishing causality is thus the temporal association of neurotoxic exposure to symptom progression. I devoted a significant amount of time during our consultation to examining this issue. It is clear from both Mr Burgess's own account of his symptoms and Dr Abernethy's carefully documented serial examinations that Mr Burgess' 15 neuropathy continued to progress both symptomatically and with respect to objective neurological deficits for at least a further 6 years after leaving the army. It is well recognised that n-hexane neuropathy can continue to progress for up to 4-6 months after removal from exposure but a continuous progression of 6 years is not consistent with the basic principles of neurotoxicology. Mr Burgess did report repeated intermittent exposure to areosolized brake leaner during this period. I have reviewed the manufacturer's information on this agent. It contains heptane but does not contain n-hexanes. Experimental studies on laboratory rats exposed to heptane have not shown evidence of central or peripheral neurotoxicity. From my . review of the literature current consensus opinion is that heptanes do not cause neuropathy. It is my opinion that the continued progression of Mr Burgess's neuropathy after leaving the army cannot be explained by the exposure to brake cleaner and that furthermore this progression, a point of agreement for both Mr Burgess and Dr Abernethy, raises serious doubt over a causal relationship between the original exposure while working for the army and Mr Burgess's neuropathy. Conclusion My final diagnosis is idiopathic sensorimotor neuropathy. This is severe and has caused considerable disability and impairment in quality of life but the timecourse of the neuropathy is not compatible with a causal relationship to occupational n-hexane exposure. I was asked o comment on several issues of Mr Burgess's case for the purposes of his claim with ACC. My answers to these are: 1) Whether Mr Burgess' peripheral neuropathy is motor or sensory in type and whether this is significant in terms of the causation: My answer to this is Mr Burgess' neuropathy is both sensory and motor in type which is a non-specific pattern that does not distinguish causality either for or against. 2) The relevance if any of the pain reported to Dr Hatfield in February 1992: As discussed above, in the absence of detailed documentation I have accepted Dr Hatfield's and Mr Burgess's description that this was arthritic rather than neuropathic pain. I would like to highlight however the difficulty of accurately interpreting a historical subjective complaint over 15 years past. 3) Whether the fact that Mr Burgess's symptoms continued after leaving employment with the Army is relevant to an assessment of causation: As discussed above this continued progression is of critical importance and in my opinion is incompatible with a diagnosis of N-hexane neuropathy. 4) Whether your view of causation would differ depending on the start date of Mr Burgess's employment with the Army, i.e., whether your view differs if he began with the Army (i) in February 1991; or (ii) on 17 February 1992. Mr Burgess tells me the onset of his neuropathic symptoms was in 1993 (ie after both of these dates) and there are no documented neurological examinations prior to 1993 to contradict this. The discrepancy of the employment onset dates is therefore not relevant to my diagnosis." [62] After this report was received counsel for the appellant forwarded further information to him concerning further clarification of the aerosolised brake cleaner. I set out his reply as follows. "Thank you for your recent letter dated 24/7/08 requesting further clarification of the aerosolised brake cleaner that Mr Burgess reported exposure to. The product that he identified to me as being most frequently used in his home garage between 1996 and 2004 was 16 CRC Brakleen. The Chemwatch number for this product is 5066-10. I have attached the printout of the Chemwatch report. You will note in Section 3 composition/information on ingredients that N-hexane is not an ingredient. Section 3 states that "manufacturers supplied full ingredient information to allow Chemwatch assessment". Mr Burgess did not recall the exact name of the Wynns product that he used less frequently. I was unable to find any reference to brake cleaners on the New Zealand Wynns website product catalog list. A Wynns brake cleaner available in Australia contains no N-hexane (see attached product sheet)." [63] In my view, this report and that of Dr Abernethy conclude this appeal in favour of the respondent. As Dr Kilfoyle writes, in order to establish a probable causal relationship between occupational n-hexane exposure and Mr Burgess's neuropathy all of the following criteria would need to be met: 1) The symptoms should begin after the onset of exposure; 2) there should be a sufficient concentration and duration of exposure; 3) symptoms should not continue to progress for more than 6 months after the cessation of exposure; and 4) no other explanation can be found despite appropriate investigations [64] As Dr Kilfoyle notes there seems little doubt that Mr Burgess had a significant exposure to n-hexane containing compounds. This level of exposure is at least similar to that described in established cases of n-hexane neuropathy. The onset of neuropathic symptoms has been a contentious issue. [65] Mr Burgess is adamant his neuropathic symptoms began in 1993, at least 12 and possibly 24 months after beginning his work with the army. He believes the symptoms reported to Dr Hatfield in 1992 were different in nature. The description he provided to Dr Kilfoyle which admittedly is based on a recollection now more than 15 years old was of focal pain, redness, swelling and tenderness. The doctor writes that he must therefore accept Mr Burgess personal recollection which would favour an arthritic condition rather than a neuropathic pain. This appears to have been Dr Hatfield's position. [66] Dr Abernethy has performed extensive and appropriate evaluation of Mr Burgess's neuropathy and no other identifiable cause of neuropathy has been found. The final barrier to establishing causality is thus the temporal association of neurotoxic exposure to symptom progression. Dr Kilfoyle devoted a significant amount of time during his consultation to examining this issue. It is clear from both Mr Burgess's own account of his symptoms and Dr Abernethy's carefully documented serial examinations that Mr Burgess's neuropathy continued to progress both symptomatically and with respect to objective neurological deficits for at least a further 6 years after leaving the army. It is well recognised that n-hexane neuropathy can continue to progress for up to 4-6 months after removal from exposure, but a 17 continuous progression of 6 years is not consistent with the basic principles of neurotoxicology. From the doctor's review of the literature current consensus opinion is that heptanes do not cause neuropathy. [67] The opinion of Dr Kilfoyle was that the continued progression of Mr Burgess's neuropathy after leaving the army cannot be explained by the exposure to brake cleaner and that furthermore this progression, a point of agreement for both Mr Burgess and Dr Abernethy, raises serious doubt over a causal relationship between the original exposure while working for the army and Mr Burgess's neuropathy. [68] Having regard to this opinion and the opinion of Dr Abernethy I am of the view that this appeal must be dismissed. I, accordingly, dismiss the appeal. There is no order as to costs. DATED this ...?......day of....Center......2008 J Cadenhead District Court Judge 18