Culhane and Repatriation Commission - [2001] AATA 569

DECISION AND REASONS FOR DECISION [2001] AATA 569

ADMINISTRATIVE APPEALS TRIBUNAL )

) No N1997/1389

VETERANS' APPEALS DIVISION       )
           Re      Terence William CULHANE
  Applicant
           And    REPATRIATION COMMISSION
  Respondent

DECISION

Tribunal Mrs M T Lewis, Senior Member Dr J Campbell, Member

Date21 June 2001
PlaceSydney

Decision The Tribunal – (a) sets aside that part of the decision of a delegate of the Repatriation Commission ("the Respondent") dated 3 April 1995 that determined that the condition of osteoarthritis left knee suffered by Terence William Culhane ("the Applicant") was not defence-caused; and (b) substitutes for that part of the decision so set aside, its decision that the Applicant's condition of osteoarthritis left knee is defence-caused, pursuant to s70 of the Veterans' Entitlements Act 1986, with effect on and from 14 April 1994; and (c) remits the matter to the Respondent to determine the rate of pension payable to the Applicant; and (d) varies that part of the Respondent's decision in relation to rheumatoid arthritis by amending that diagnosis to read "adult Still's disease", and (e) affirms that part of the decision under review, as varied.

..............................................
M T Lewis
Presiding Member
CATCHWORDS
VETERANS' AFFAIRS – entitlement -– applicant exposed to chemicals during defence service – applicant suffers from disease of auto-immune system - whether correct diagnosis of Applicant's condition was "rheumatoid arthritis", "adult Still's disease" or "chronic fatigue syndrome" - whether causal link between chemical exposure and Applicant's condition - whether medication used to treat condition had adverse effect on auto-immune system

Veterans' Entitlements Act 1986: ss70, 70(5)(a), 120(4), 120B

Repatriation Commission v Thompson [2001] FCA 341

REASONS FOR DECISION

Mrs M T Lewis, Senior Member Dr J Campbell, Member

This is a review of that part of a decision of a delegate of the Repatriation Commission ("the Respondent") dated 3 April 1995 that refused a claim by Terence Culhane ("the Applicant") that osteoarthritis of the left knee and rheumatoid arthritis were defence-caused. The Veterans' Review Board ("the VRB") on 22 April 1996 affirmed those parts of the decision under review. The Applicant lodged an application for review by this Tribunal on 17 July 1996. During the hearing the Respondent conceded that the Applicant's condition of osteoarthritis of the left knee was defence caused. The Tribunal considers that this was a concession properly made, and so finds. The Tribunal will remit the matter to the Respondent for assessment of the rate of pension payable to the Applicant for this condition.
The Tribunal had before it the documents provided by the Respondent pursuant to s37 of the Administrative Appeals Tribunal Act 1975. The Applicant gave oral evidence at the hearing. Dr Fluhrer and Dr Donohoe gave oral evidence, called by the Applicant. The following documents were tendered as evidence on behalf of the Applicant:

Reports of Dr M Donohoe dated 6 November 1998 and 27 January 1999 (exhibit A) and 27 April 2000 (exhibit P), and Curriculum Vitae (exhibit K)
Report of Dr J Fluhrer dated 28 March 1996 (exhibit B)
Three diagrams of various aspects of Mirage aircraft (exhibit C)
A history of face rash prepared by the Applicant (exhibit D)
List of occurrences of chest pain prepared by the Applicant together with ECG reports dated 19 February 1982, 11 March 1987, 10 November 1985 and 8 February 1986 (exhibit E)
4 photographs assembled by Applicant (exhibit F)
4 photographs of pillow and toilet bowl assembled by Applicant (exhibit G)
Report of Dr W. Knox , consultant psychiatrist, dated 17 May 1999 (exhibit H)
Sundry documents extracted from s137 documents (exhibit J)
Data sheets on Turco Fluro-Chek (exhibit L)
Selected summaries of articles from Medline check provided by Dr Donohoe regarding references listed by Professor J A Bisby (exhibit M)
Copy of Internet home page for Centre of Inherited Disorders of Energy Metabolism (exhibit N)
Notes provided by Dr M. Donohoe commenting on reports of Professor J. A Bisby (undated) (exhibit O).

The Respondent called Professor Bisby and Professor Sambrook to give oral evidence and tendered the following documentary evidence:

Report of Dr G. Duggin, toxicologist, dated 10 April 1995 and blood chemical analysis report dated 11 April 1995 (exhibit 1)
Reports of Professor J A Bisby, occupational physician and toxicologist, dated 28 April 1999 and 29 September 1999 (exhibit 2) and 19 January 2000 (exhibit 4)
Reports of Professor P N Sambrook, rheumatologist, dated 11 May 1999 and 1 June 1999 (exhibit 3).

The Applicant rendered eligible defence service under the Veterans' Entitlements Act 1986 ("the Act") from 7 December 1972 to 9 July 1989 in the Royal Australian Air Force and therefore the claim comes for consideration pursuant to s70 of the Act. The standard of proof is that specified in s120(4) of the Act, that being to the Tribunal's reasonable satisfaction.
applicant's evidence
The Applicant was born on 3 September 1945. When he left school he worked as a ceiling plasterer for approximately 12 months. He then worked at an engineering firm until 1964 when he joined the RAAF. After recruitment training the Applicant graduated as an aircraft engine fitter. He was discharged from the Air Force on 9 July 1989. From 1977 to 1989 he was also employed part-time as a waiter at the Wagga Wagga Leagues Club. The Applicant said that prior to his service he was a fairly "athletic" person. He played representative and competitive sport prior to and during his service. After discharge from the RAAF the Applicant started his own business, TWC Automotive Repairs, and continued that business until 1995 when he ceased because of ill health.
The Applicant served in Malaya from 1971 to 1975. During that period he obtained a certificate in non-destructive crack detection ("NDI"). The NDI process involved the examination of engines to determine whether there were cracks or other defects in the engine.
From 1971 the Applicant undertook crack detection work on Mirage aircraft. He was involved in the NDI process for about 6 hours a day, three days a week. The work involved going inside the aircraft, checking for cracks in the engine/after burner. This involved a visual inspection of the area. He would clean the area with penetrant and then identify any cracks or defects by using the penetrant chemical to highlight the crack. The cleaning process took approximately one minute per crack, the pentrant process about 5 minutes per crack. He then applied an emulsifier using a spray can that would react only with the penetrant. This step took about three minutes. He then sprayed a developer onto the emulsifier so that when a black light was shone on the area, the crack would appear as an iridescent line. This took about one minute. He then used the black light for about one minute to "bring the crack out".
The Applicant said he did not wear any protective equipment other than overalls during the crack checking process. He said when he used the emulsifier it would leave a misty atmosphere within the cabin. He recounted on one occasion in 1971 developing a face rash while doing NDI work. The rash lasted about 8 hours. He said he reported the rash but did not receive any treatment for it at the time. He said the rash recurred the next time he carried out the NDI process and regularly thereafter. He said he was treated for the rash by a specialist in Newcastle in 1971.
The Applicant said that he was based in Butterworth in 1974. At that stage he had been posted to full-time NDI inspection - eight hours a day, five days a week.
The Applicant recounted an incident on 16 April 1974 when he lost all movement in his hand and his wrist was very painful. Two days later the skin on his face peeled. He considered this to be the same condition he had suffered in 1971. It lasted for about eight hours. He said he has experienced this since 1971, and it now occurs about three times a month. He said the face rash is accompanied by a lack of strength to a point where he has to lie in bed and "can't even lift the blankets". The duration of these "turns" varies - the last continued for two days.
The Applicant said he continued undertaking the NDI process until his discharge from the RAAF in 1989. In the latter part of his RAAF career he undertook a training/administrative role. He continued to have "hands on" involvement in the NDI process until 1977. After 1977, when demonstrating the NDI process as part of his teaching duties, he no longer had to climb into the engine, but the work continued by the use of tubs. These "tubs" were three containers, filled respectively with penetrant, emulsifier and a developer (a white powder). The Applicant said he dipped the engine parts by hand in the three bins. He did not use a face mask or gloves. He continued this process about five days a week in the earlier stages and once a week in the latter stages until his discharge in 1989. He conceded, however, that he was not demonstrating the NDI process for the entire duration of the course.
The Applicant said he has not received any treatment for the face rash since 1974. In 1974 he sought medical treatment. An x-ray of his left wrist was taken at that time and did not indicate any abnormality. He said after the X-ray he noticed that the veins in his left arm were pronounced and crimson. His arm felt sore and he had no strength for about three days. He was on sick leave for two days and then returned to work although his arm was still weak. He recovered after three days. He said he did not have any other signs or symptoms arising from that episode.
The Applicant said that when he sought further medical attention on 17 April 1974 he complained about his vein. He noted that this episode followed his use of the NDI process. He said the doctor noted "penetrant" on the medical record in his presence. Blood tests were performed and the doctor telephoned Turko Fluro-chek to inquire what was in the penetrant. However, the doctor was not given this information because of "company privacy". The Applicant said he used Turko Fluro-chek emulsifier in a spray can. He then made his own inquiry of the Dangerous Goods Section at the RAAF Base at Wagga Wagga. He said the register disclosed that Turko Fluro-chek included bromide pentaflouride, bromide chloride, synergen bromide and bromide cyanide.
The Applicant said he had a recurrence of loss of strength in his left arm in 1991. He then lost strength in both arms. The loss of strength in his left arm lasted about a week. At the time he was performing his normal work as a motor mechanic. He said he has recurrence of loss of strength in the left arm only when he has "turns".
The Applicant said that he had a loss of strength in his right shoulder prior to 1991 but he was unsure when this was. He recalled that he was doing normal work while on RAAF service when it occurred. It lasted for about four days.
The Applicant said he experienced sharp chest pains in 1974 when he was doing NDI processing. This occurred about two months after the 1974 episode involving the rash. He consulted a doctor and an ECG was normal. He has often experienced chest pains that now occur about twice a month. He prepared a chronology documenting the dates he experienced chest pain (exhibit E).
The Applicant said that after his discharge from the RAAF in 1989 he continued to experience chest pain, face rash and right shoulder weakness. He said the only testing done, apart from the blood test in 1974, was for the face rash. He was referred to a specialist and prescribed medication for a while but he could not recall the medication. He did not recall being treated with steroids during service.
In cross-examination the Applicant agreed that he did not suffer from any face rash between 1974 and 1995 (exhibit D), nor did he suffer from chest pain between 1987 and 1995 (exhibit E). He did not access his RAAF medical file until 1993 but in 1991 he started keeping a history of his symptoms.
The Applicant said his weight had reduced from 70 kilograms to 49 kilograms when he saw Dr Donohoe in 1998. He said his weight loss took place over 12 months in 1998. His present complaints include night sweats, which he described as globules of sweat running down the body from the waist up. He said his head becomes "completely wet" and his pyjamas become saturated. This has occurred every night for about three years. He provided a photograph of stains on his pillow from perspiration (exhibit G). He said he had observed that on the waterline of the toilet pan there is a black mark, which he photographed (exhibit G). He said the brown stain took about four days to accumulate. It has occurred since about February 1999. The Applicant said he now experiences extreme weakness in the muscles throughout his body. He said he has had muscle wasting since he first consulted Dr Carroll, and this has deteriorated significantly in the last two years. He also noted memory and concentration loss and he becomes very irritated.
The Applicant said he has had tests undertaken by an iridologist and Bromide was identified. He said he did not have any tests for bromide or any other chemical while on service.
In cross-examination the Applicant was unable to explain the inconsistency in the history he gave to Dr Knox and Professor Bisby. Dr Knox recorded that the Applicant had a rash and chest pains between 1977 and 1988, and Professor Bisby recorded that his ill health started around 1986. In cross-examination the Applicant said he was coaching football between 1977 and 1989 and he did not have muscle pain during that period. He said the muscle pain first developed in 1991. He said he has muscle pain and muscle weakness, but he does not have pain in the joints. He said his feet swell but this resolves when he goes to bed. He also said his finger joints become numb.
The Applicant described a recent episode when he "went into a coma". An EEG was performed at that time. Although he thought he was conscious during that episode his wife informed him that he was "out cold" for about 5 minutes. He said that he has suffered from similar episodes on three occasions. The main symptom he had for the four months prior to the Tribunal hearing was muscle cramps.
Dr J. Fluhrer
Dr Fluhrer, a medical practitioner who has qualifications in nutritional and environmental medicine and as a naturopath, gave oral evidence to the Tribunal and provided reports dated 8 March 1995 (T25) and 28 March 1996 (exhibit B). He saw the Applicant on about four occasions in 1995. Dr Fluhrer diagnosed chronic bromide toxicity coupled with long-term side effects from solvent exposure. He also considered the Applicant had "a degree of auto-immune disease" because of his chronic toxicity. When questioned by the Tribunal about this statement Dr Fluhrer said that knowledge in this area was developing quickly, and while it had not been proven it had gone beyond "possibility". When advised of Professor Sambrook's opinion that the trigger factors for rheumatoid disease are still unknown Dr Fluhrer in part agreed with this. However he also said there was chronic inflammation and the trigger for this is toxins that could be entoxins and exotoxins.
Dr Fluhrer noted that psychometric testing identified damage to the Applicant's central nervous system, which Dr Fluhrer said was typically caused by xenobiotics. The initial program of treatment by Dr Fluhrer was "protection with antioxidants and bone minerals to 'lock' some of his bromide".
Dr Fluhrer understood that the Applicant suffered from rheumatoid arthritis, a diagnosis that he thought had been made by Professor Sambrook prior to his consultations and one that he had accepted. However, he said the Applicant did not have the typical rheumatoid arthritis but "he's got an auto-immune disease with positive rheumatoid factors…". In addition, he opined that the Applicant suffered from chronic bromide toxicity following significant exposure during his employment. He considered the Applicant had some symptoms that could not be explained by a diagnosis of rheumatoid arthritis.
When Dr Fluhrer examined the Applicant he noted other signs and symptoms which Dr Fluhrer described as "generalised unwellness". These included –
chronic headaches, recurrent rashes, decreased mental ability and memory and recall, weaknesses of many areas in his body… lethargy, chest pains … mental confusion

He considered these signs and symptoms to be very uncommon and rarely seen in people with auto-immune disease. He considered these to be toxicity symptoms.

Dr Fluhrer was not aware of any medication taken by the Applicant that would increase bromide in his body. He did not consider that the Applicant had suffered from bromide poisoning at any time. By toxicity he meant the presence of bromide in a blood test. In his view, both the presence of bromide in a blood test and the symptoms of toxicity would indicate toxicity clinically. .
Dr Fluhrer admitted that he had never treated a person who was suffering from bromine poisoning or acute exposure to bromine. He conceded that he was not aware of any research that showed that bromine remained in the body for 20, 30 or 40 years after exposure, but he added "but one can find 'these compounds' in persons being exposed after 20, 30, 40 years …".
Dr Fluhrer had not considered the diagnosis of adult Still's disease nor has he ever diagnosed that condition. He preferred the view that the Applicant suffered from an auto-immune disease.
Dr Donohoe
Dr Mark Donohoe is a general medical practitioner and a Fellow of the Australian Society of Environmental Medicine with ten years' experience in that area. He examined the Applicant for the purpose of these proceedings at the request of the Applicant's solicitor, and reported on 6 November 1998 (exhibit A). He also gave oral evidence at the hearing.
Dr Donohoe obtained a history that the Applicant's health remained good until 1971 when he developed chest pain and facial rashes. He noted the main deterioration in the Applicant's health occurred after 1974, but in cross-examination he said it was "not immediately after" 1974. Dr Donohoe said –
On 17/4/1974, Mr Culhane was poisoned with high dose exposure to liquid penetrant. Despite the exposure, he continued through his shift, increasing exposure. He developed weakness, numbness and loss of function of his left wrist and hand, and swelling of his left arm, with marked venous engorgement. The cause of this was not clear to me.
Following this exposure incident, he developed skin rashes and acute muscle pain and joint swelling which then persisted. He developed a facial rash in July 1974 for the first time in his life, and this followed prolonged and poorly protected exposure to his workplace chemicals in what I understand was a poorly ventilated work environment. This facial rash has persisted since that time.
He was also diagnosed as suffering from rheumatoid disease around this time, although the medical practitioners appear to have considered the effect of his workplace chemicals in the initiation of this disorder.
He was given aggressive medical therapy for his rheumatoid disease, including methotrexate, gold injections, cyclophosphamide and steroids, despite the fact that joint pain was not prominent at this time. Each treatment seems to have worsened rather than improved his symptoms and underlying disease.
He left work in 1989 because of deteriorating health. He became self employed, installing LPG systems in cars around that time, but was forced to leave this work in 1993-1994 when the progression of his illness, his weakness, weight loss and fatigue, made it impossible for him to work.

In cross-examination Dr Donohoe said he had no record in his notes of the state of the Applicant's health in 1989. He understood the Applicant began to experience serious symptoms of auto-immune disease after 1989.

On the basis of tests undertaken by Dr Donohoe he said –
There appears to be only two likely causes for Mr Culhane's disorder of energy metabolism, with damage to mitochondria caused by the known exposure to brominated compounds in his workplace between 1971 and 1989, or by direct cytotoxic damage from gold, methotrexate or cyclophosphamide.
As I am unable to find medical references to support the view that the medical therapy could cause such damage, I am inclined to the view that the known workplace toxic exposure was the cause of the mitochondrial damage and loss of cellular energy metabolism. I believe it is likely, based on the history, that this damage had commenced prior to the administration of the medications, and was most likely the reason for the unexpected toxicity of the medical treatment program, with the tissues unable to eliminate the hazardous drugs at the rate normally expected.
This secondary biochemical "overdose effect" may well have exacerbated the mitochondrial damage, and led to the rapid progression of his clinical state.
Dr Donohoe considered that the Applicant suffers from rheumatoid disease that is currently in relative remission, and is not the major cause of his present problems. He conceded that he was not an expert in the diagnosis of rheumatoid disease, but he considered the important thing was the process of triggering an auto-immune predisposition in the subsequent development of the Applicant's symptoms, and the exposure to chemicals that he had in the 1970s and 1980s. He diagnosed chronic fatigue syndrome according to the CDC 1994 criteria, but he added that his criteria excluded people who have suffered high dose toxic damage. He said–
It is my view that Mr Culhane has suffered such damage in his poorly protected use of halogenated organic compounds between 1971 and 1989 in his work for the RAAF. He has suffered effects of acute poisoning on at least one occasion, and has evidence of severe mitochondrial damage known to be associated with such compounds on current testing. The damage to his cellular pathways of energy production is severe, and it is my opinion that this has been progressing in the past decade, based on his clinical history.
It is also my view that the mitochondrial damage led to the adverse effects of the medical treatments for his rheumatoid disease, and that he has suffered severe tissue damage as a result of this sequence and combination of insults.
Had he not been exposed to workplace chemicals, it is likely that he would not have demonstrated the clinical manifestations of rheumatoid disease. The occupational trigger for the rheumatoid disease was most likely the exposure to hazardous workplace chemicals, and reduced mitochondrial function leading to alterations of immunological response. The occupational damage to mitochondria would certainly have increased the toxicity and adverse effects of his medical drugs aimed at controlling the rheumatoid disease, leading to a biochemical overload effect intracellularly, due to reduction of oxygen dependent detoxication responses and oxygen dependent antioxidant systems. The result was excessive harm and little benefit from those medications, and more rapid progression of his illness and disease.
In his oral evidence Dr Donohoe said the Applicant was exposed to a broad range of chemicals in a number of different compound solutions over a period of time. He was unable to identify a particular compound solution, including bromide, to be a singular factor that would have adversely affected his health..

Dr Donohoe made the distinction between causation and triggering. He noted that if a person has no predisposition to rheumatoid disease then exposure to chemicals may be irrelevant. They will not develop rheumatoid disease. For those with a potential to develop rheumatoid disease, whether they develop it may depend on exposure and environmental factors. He noted that this has become an important area of toxicology and provided a list of research references he considered reflected developments in the area of energy metabolism (exhibit M).

In cross-examination Dr Donohoe was unable to identify any specific symptoms reported by the Applicant during the incident in 1974 that he could identify as typical of bromide exposure, and he has never treated anyone suffering from poisoning by bromide. He also said that while bromine and bromide compounds are one part of the complex of exposures experienced by the Applicant they are not the major ones. He was unable to identify any chemicals to which the Applicant was exposed that he would not have been able to excrete readily, nor did he think the issue of retention was important. He agreed that silicone may have a part to play in the Applicant's condition because of its known association with rheumatoid disease.
Dr Duggin
The Applicant was examined by Dr Duggin, head of the Toxicology Unit at Royal Prince Alfred Hospital at the request of his local doctor. Dr Duggin provided a report to Dr Carroll dated 10 April 1995 that was tendered by the Respondent (exhibit 1). Dr Duggin reviewed the results of pathology tests that showed the Applicant had a bromide level of 0.07 mmol/L on one occasion and 0.12 mmol/L on another occasion. He considered there was no evidence that the Applicant had bromide poisoning. He said the interval from the time of exposure to bromine to the time of his examination in 1995 would mean that he has eliminated all the bromide. He also said that the upper limit of normal for bromide levels was 0.15.
Associate Professor John Bisby
Associate Professor Bisby is the Associate Professor of Occupational Medicine and Environmental Health at University of Melbourne. He examined the Applicant on 8 April 1998 and provided a report to the Respondent for the purpose of these proceedings (exhibit 2). He said that chronic industrial poisoning from use of products with brominated compounds such as those used by the Applicant in the Air Force is unknown. He said the toxic effects of bromides are well-known, viz.
Acute exposure and poisoning results in nausea, vomiting, slurred speech, memory loss, hallucinations, mania and psychoses. Industrial poisoning is virtually unknown and poisonings have resulted from taking medicines (overdoses). In chronic overdosing, and in susceptible patients, skin rashes are a known toxic effect.

He considered that the variation in the Applicant's blood analyses of bromine compounds were within the normal expected variations, and the levels themselves were normal.

Counsel for the Applicant suggested to Professor Bisby that he had also been affected by aluminium that he used on service. Professor Bisby said that aluminium, either as metal or as compounds, does not cause poisoning and is widely used in medicine and is essentially non-toxic. Similarly, he opined that solvents and fuels, specifically benzene, do not cause rheumatoid arthritis.
Professor Bisby considered that there is no literature or theory that would reasonably support the contention that the Applicant's rheumatoid arthritis or rheumatoid syndrome was related to exposure to bromine, bromide compounds or aluminium. Professor Bisby considered that the opinion of Dr Bluhrer that the Applicant was suffering from "chronic Bromide toxicity coupled with long-term side effects from solvent exposure" was "an extraordinary opinion … completely at variance with the facts of this case and with opinions given in the literature …". Professor Bisby opined that the Applicant's exposure to bromine during his service was low, and he used well-known industrial products in a manner consistent with them being non-toxic to users, that is, he followed the instructions for use. Professor Bisby considered none of the symptoms described by the Applicant during his service could be attributable to bromide or bromine intoxication or to chronic bromism.
Professor Bisby considered that the symptoms described by Dr Donohoe were consistent with ongoing rheumatoid arthritis. He also said that he used the term rheumatoid arthritis to include adult Still's disease. In effect, he considered that the issue of differential diagnosis was for a rheumatologist.
Professor Bisby considered that the clinical report regarding the problem the Applicant had with his arm in 1974 was not at all consistent with any toxic exposure. Professor Bisby noted that Dr Donohoe's notation that the Applicant was diagnosed with rheumatoid disease about 1974 is not in accord with the records. He also considered that Dr Donohoe had not provided results of any pathology tests of any significant abnormality that was not associated with rheumatoid disease. Indeed, Professor Bisby identified a number of statements made by Dr Donohoe that were either not consistent with the history or with medical knowledge.
Professor Bisby disagreed with Dr Donohoe's diagnosis of chronic fatigue syndrome. He considered that as the Applicant is suffering from rheumatoid disease this is an obvious and demonstrable reason for his persistent fatigue. A diagnosis of chronic fatigue syndrome cannot be made, by definition, where such other probable cause is already known. Professor Bisby considered that the statements and claim made by Dr Donohoe and Dr Fluhrer are not supported by the known facts.
Professor Bisby considered the extracts of the research publications identified by Dr Donohoe (exhibit M). He said that none of these support a reliable conclusion that rheumatoid arthritis is related to exposure to the types of materials to which the Applicant was exposed during his service.
The Tribunal notes that Professor Bisby's evidence was tested very carefully in cross-examination. While there was some problem with his understanding of the physical environment in which the Applicant performed his crack testing work inside the wing of the aircraft, having considered his responses in cross-examination, the Tribunal is satisfied that this has not materially altered the opinion he expressed in his report.
Professor Sambrook
Professor Sambrook, rheumatologist, diagnosed adult Still's disease. He did not consider the Applicant suffered from classical rheumatoid arthritis. Adult Still's disease is a multi-system disease involving inflammatory synovitis, muscle atrophy and bone refraction. It is an auto-immune disease of unknown aetiology. He also clarified that it is not included in the ICD code for rheumatoid arthritis, but for practical purposes it can be considered a form of rheumatoid arthritis (see exhibit 3, p5).
Professor Sambrook said in his oral evidence that the Applicant's face rash could be consistent with the diagnosis of adult Still's disease although a rash involving the trunk would be more typical. He said that such a rash would occur intermittently and is typical of adult Still's disease. However, it would be unusual, but not impossible, to have adult Still's disease presenting with only a facial rash in 1991 and then the "full blown symptomatology" involving the other manifestations of it later. Later in his evidence he realised that in 1971 the Applicant gave a history of several attacks of widespread urticarial rash involving his face and trunk, that Professor Sambrook said was certainly consistent with a palindromic manifestation of adult Still's disease. He also said that the Applicant's fever and sweats could be part of adult Still's disease. The Applicant had swelling in the joints of his hands and restriction of movement of the wrists that is often present after swelling, leaving a residual restriction of movement. Hence he has had swelling in some joints and signs of previous swelling in other joints. His joint damage is consistent with adult Still's disease. He expected that the Applicant's current treatment with prednisolone would control some features of the condition. Professor Sambrook considered that the recent episodes of "coma" and the discolouration in the Applicant's urine were not related to adult Still's disease.
In respect of the Applicant's wrist episode in 1974, Professor Sambrook considered that a history of pain and swelling in the wrist, rather than loss of strength in the wrist, was consistent with adult Still's disease. However, if one experienced pain one might experience some loss of strength as well. Professor Sambrook considered that the condition would present fairly comprehensively at one time. It would be rare, but not impossible, for there to be a palindromic onset, that is, intermittent episodes over a period before the full blown disease occurs.
Professor Sambrook noted that the various symptoms seen in the Applicant were consistent with the diagnosis of adult Still's disease and rheumatoid arthritis. For example, he said the "general unwellness" noted by Dr Fluhrer was consistent with rheumatoid arthritis. Symptoms of rash, sweats and headaches noted by Dr Fluhrer were also consistent with a diagnosis of rheumatoid arthritis. Weakness in many areas of the body, lethargy and fatigue were consistent with rheumatoid arthritis and adult Still's disease. However decreased memory recall and mental confusion were not typical features of rheumatoid arthritis or adult Still's disease. Professor Sambrook considered that it was difficult for people to distinguish between pain in the joints and muscle pain. The fact that the Applicant did not report joint pain would not necessarily go against the diagnosis of rheumatoid arthritis. He noted that there is evidence that the Applicant has joint damage. Professor Sambrook also noted that chest pain was consistent with a diagnosis of both adult Still's disease and rheumatoid arthritis. The chest pain is usually sharp pain due to inflammation of the pleura. Headaches could be associated with rheumatoid arthritis, but they could be constitutional. Professor Sambrook was not aware of any research showing a relationship between rheumatoid arthritis and chemical causes. He said that rheumatoid arthritis is thought to have a viral trigger, but the exact virus has not been identified.
Professor Sambrook was referred to clinical records dated 15 July 1971 (exhibit J) that described the rash suffered by the Applicant at that time. Professor Sambrook considered that this was consistent with a palindromic manifestation of adult Still's disease. He considered that treatment with steroids and cylcophosomide and methotrexate were appropriate for the Applicant's condition.
Professor Sambrook said that as he was not a toxicologist he was not qualified to comment on that part of Dr Fluhrer's report of 8 March 1995 (T25) regarding the effect of prednisone on the release of bromide from the tissues. He conceded that adult onset rheumatoid arthritis could be classified as an auto-immune disease. He considered that treatment described as "protection with antioxidants and bone minerals to 'lock' some of his bromide" "did not sound like a particularly scientific comment". Professor Sambrook said he was not qualified to recognise the effects of bromide poisoning. However, as a rheumatologist he was not aware of any association between the onset of adult Still's disease and bromide exposure.
Professor Sambrook was provided with summaries of research literature to which Dr Donohoe referred in his evidence (exhibit M), regarding some auto-immune diseases that may have chemicals as a triggering factor. He noted "the strongest link", relatively, was between scleroderma and lupus-like conditions. However these conditions are quite different from rheumatoid arthritis. Professor Sambrook also noted two sets of chemicals that have been linked to scleroderma – silica exposure and a toxic cooking oil that was consumed in Spain. He was not aware from the literature to which reference was made in exhibit M of the involvement of any other chemical. He acknowledged, however, that the clinical significance in rheumatology of some environmental chemicals is raised as a possibility. He also accepted that the Applicant suffered from an auto-immune disease and he accepted that the trigger that caused the alteration to his auto-immune system is as yet unidentified. He accepted that the Applicant has features consistent with adult Still's disease. However, based on the literature he considered the involvement of a chemical to be not more than a remote possibility.
Professor Sambrook recalled that the Applicant was "quite definite or indeed adamant" that the onset of his rheumatoid arthritis was 1991. That was also consistent with the history provided to Dr Carroll (T6). Professor Sambrook also noted the Applicant's history that his weight loss, migratory polyarthralgia, chest pains and skin rashes started primarily in 1991. The history that the Applicant's face rash had been intermittent since 1971 did not change his conclusion about the diagnosis of adult Still's disease.
Professor Sambrook noted that when the Applicant attended for interview he was taking Panadeine Forte, and he concluded therefore that the Applicant was suffering from pain in his joints. He noted that some patients complain of weakness or loss of strength that is usually a result of pain.
Professor Sambrook considered that the "locking up" of the Applicant's shoulders is consistent with adult Still's disease or rheumatoid arthritis. Although he had not recorded whether the Applicant's chest pain was pleuritic he noted an entry on 12 November 1980 of pain increasing with respiration (T3, p16). Although it was not clear whether that reference was to inspiration or expiration, it is possible that it was of a pleuritic nature. However, Professor Sambrook noted the complete absence of any reference to pleurisy anywhere in the medical documents that was suggestive that the Applicant had not suffered from pleurisy.
If indeed the Applicant suffered from rheumatoid arthritis, that manifested itself intermittently in 1971, Professor Sambrook considered that there was no treatment that could have been provided then that would have altered the course of the condition that occurred subsequently in 1991.
Professor Sambrook disagreed in cross-examination that the prednisolone administered to the Applicant is "highly toxic", although he considered it has potential for side effects in a few people, particularly if not administered correctly. He also disagreed with Dr Donohoe's reference to the Applicant suffering from rheumatoid arthritis when the diagnosis is adult Still's disease, and to a degenerative disease whereas in fact it is an inflammatory disease.
Professor Sambrook noted that the Applicant has been treated with a variety of drugs, including salazopryrin, prednisolone and methotrexate. He considered that the reason for moving from one to the other was that the Applicant was not responding very well to the treatment. This is quite typical of adult Still's disease as it can be a difficult condition to treat. He did not consider that the Applicant's treatment was changed because of side effects of treatment, or that the treatment hastened the disease. He considered the evidence for that proposition was "entirely speculative". Professor Sambrook accepted that Dr Donohoe's proposition was "a possibility", but based on his own knowledge of the literature, he did not consider it to be "likely".
Professor Sambrook said that the use of gold injections in treating rheumatoid arthritis was common and it does not have frequent side effects, although he agreed "it can have serious side effects" and it needs to be administered properly.
He also said that methotrexate is commonly used in the treatment of rheumatoid arthritis. In high doses it is highly toxic, but when given in the correct dosage it is the most commonly prescribed drug for rheumatoid arthritis. Professor Sambrook considered that cyclophosphemide has a higher side effect profile, and that it is used in treating rheumatoid arthritis that is unresponsive to other therapy. Again, used correctly, side effects are relatively uncommon but use of the drug should be monitored and stopped if side effects develop. Professor Sambrook also said that salzopryrin is also a commonly used drug in the treatment of rheumatoid arthritis, next to methotrexate, and side effects are relatively uncommon. He noted, however, that prednisone was a corticosteroid that does cause some side effects, including osteoporosis and a change in the fat distribution. He accepted that the Applicant showed some features of the latter. He said that he would prescribe all these drugs, but if the patient was not responsive he would discontinue. He also noted that adult Still's disease was known to be less likely to respond to those drugs than conventional rheumatoid arthritis.

Professor Sambrook accepted that the Applicant had been chronically exposed to workplace chemicals and insofar as there was chronic exposure there was a "possible" temporal relationship with the development of his health problems. However, he did not consider it "likely" that there was a causal relationship, and in particular he was concerned that there was no ongoing chemical exposure at the time the condition manifested itself about 1991. He noted that Dr Donohue referred to the "chronicity of exposure" and if that was a causal factor Professor Sambrook considered the fact that it took a year or two to develop made it less likely. However he agreed there have been no tests conducted on the Applicant to discredit the chemical exposure hypothesis.
Professor Sambrook said that many features of chronic fatigue syndrome overlap substantially with features of rheumatoid arthritis, and it is "messy" to discern whether indeed there is a separate chronic fatigue syndrome or whether the symptoms are due to rheumatoid arthritis or adult Still's disease.
submissions
Counsel for the Applicant noted that there are three diagnoses proposed in the evidence – the earliest diagnosis was rheumatoid arthritis, the subsequent opinion advanced by Professor Sambrook was adult Still's disease and finally the diagnosis raised by Dr Donohoe was toxic workplace exposure resulting in severe mitochondrial damage. It was submitted for the Respondent that the Applicant's condition was correctly diagnosed by Professor Sambrook as adult Still's disease. He is an expert who is appropriately qualified to make that diagnosis.
Rheumatoid arthritis
It was submitted for the Applicant that the diagnosis of rheumatoid arthritis followed a number of treatments and opinions. Dr Carroll, in his report dated 23 November 1991 (T6), referred to the Applicant having migratory polyarthralgia and arthritis, the cause of which was not clear. By 28 January 1992 Dr Carroll was unable to label the Applicant's condition more specifically than an "inflammatory arthropathy" although he was also concerned that "he might have a system vasculitis or some other nasty underlying cause". Dr Carroll referred to "aggressive rheumatoid" in his report of 25 November 1993 and to "rheumatoid arthritis" in his report of 29 January 1994. Dr McCorkindale in his report dated 7 December 1994 (T5) diagnosed "difficult to control rheumatoid arthritis". Professor Brooks, in his report dated 14 January 1994 (T7, p57), referred to "a fascinating but difficult to control disease".
In his report dated 15 November 1994 (T6) Dr Carrol noted that the Applicant, having been diagnosed with rheumatoid arthritis was treated with medications including Imuran, Salazopurin, parenteral Gold, Methotrexate and Cyclophosphamide. All of these medical treatments failed.
The Applicant's Counsel noted several medical reports that identified the atypical signs and symptoms presented by the Applicant during his treatment for rheumatoid arthritis.
Firstly, in his report dated 7 December 1994 (T5) Dr McCorkindale referred to odd rashes and atypical chest pains reported from RAAF medical consultations from 1974 to 1988. He said "I feel some of his presentations to doctors in his airforce days were prodormal to the illness we now describe as rheumatoid arthritis".
Secondly, in his report dated 29 January 1994 (T6) Dr Carroll stated "exceeding difficulty controlling this man's rheumatoid arthritis. Perhaps the hardest part of it is the migratory tendonitis symptoms rather than actually arthropathy". In his report dated 13 April 1994 (T6) Dr Carroll also observed "atypical chest pain several days ago… thought that his pain was non-cardiac, and probably pleuritic, although there were some atypical features for either diagnosis". In his report dated 15 November 1994 (T6) Dr Carroll observed that the Applicant's "diffuse and rather protean symptoms persist… His cataract is getting worse as is his visual acuity. I wonder if any of his eye problems related directly to his active systemic rheumatoid, apart from the cataract which is obviously steroid induced".
Adult Still's Disease
It was submitted for the Applicant that he accepts Professor Sambrook's diagnosis of adult Still's disease in his 6 May 1999 report (exhibit 3), as being more consistent with the Applicant's signs and symptoms than the earlier diagnosis of rheumatoid arthritis. However this diagnosis does not account for all of the Applicant's complaints.
Counsel for the Applicant noted that in reaching his diagnosis, Professor Sambrook pointed to the consistency of a number of signs and symptoms with his diagnosis of adult Still's disease. These signs and symptoms were an intermittent rash, typically involving the trunk; pain and swelling in wrist; generalised unwellness; headaches; weakness in many areas of the body; joint pains (patient may have problems distinguishing between muscle and joint); lethargy; chest pain, period, sharp pain due to pleurisy; weight loss; migratory polyarthralgia; restriction of shoulder movement; facial rash; fever and sweats and joint damage.
However, Counsel for the Applicant noted that Professor Sambrook also observed atypical, if not inconsistent signs and symptoms such as intermittent rash typically involving the abdomen, but could involve the face; loss of strength in wrist, although if one has pain one may experience loss of strength; decreased memory recall; muscle pain without joint pain; mental confusion; coma episodes; unknown sediment in toilet bowl.
Counsel submitted that these atypical signs and symptoms may be explained either because adult Still's disease is not the correct diagnosis, or because while the signs and symptoms are substantially consistent, it is not a comprehensive diagnosis of the Applicant's condition. It was submitted that if Professor Sambrook's assertion in his oral evidence, that he was 99.9% certain of his diagnosis, is accepted then the alternative of an uncomprehensive diagnosis remains open.
Toxic workplace exposure resulting in severe mitochondrial damage
It was submitted for the Applicant that Dr Donohoe's diagnosis is not inconsistent (in effect, as opposed to causally) with the diagnosis of Professor Sambrook. Dr Donohoe states in his report dated 6 November 1998 (exhibit A) that the Applicant "suffers from rheumatoid disease, which is currently in relative remission… [but] the rheumatoid disease is not the major cause of his problems".
Dr Donohoe opines that the Applicant's exposure to toxic workplace chemicals was the occupational trigger for the rheumatoid disease. The exposure resulted in severe mitochondrial damage. The mitochondrial damage increased the toxicity and adverse effect of the medication aimed at controlling his rheumatoid disease, leading to a biochemical overload with the consequence that the Applicant received little benefit from the medications and was excessively harmed by a rapid progression of his illness and disease (exhibit A, p6). It was submitted that Dr Donohoe's opinion is supported by Professor Sambrook's evidence of palindromic manifestations of adult Still's disease during service and should be considered in the context of the evidence given by the Applicant as to his workplace and medical history.
Causation
It was submitted for the Applicant that he suffered toxic workplace damage as a result of exposure to toxic chemicals while serving in the RAAF throughout the period from 1971 (and including the time of commencement of his eligible defence service, 7 December 1972) until 9 July 1989 (being the date of cessation of eligible defence service).
It was submitted for the Applicant that to the extent that the Tribunal accepts that the Applicant has adult Still's disease and that the trigger was exposure to toxic chemicals then the disease arose out of and was attributable to his service, in which event the appeal should be allowed.
Counsel for the Applicant noted that in his oral evidence and as set out in the medical evidence tendered, the Applicant detailed a number of complaints concerning his health and well-being. These complaints included a history of facial rashes, a reddening of the veins in the left arm accompanied by soreness and loss of strength, loss of strength in both arms, chest pains, night sweats, extreme fatigue and weakness and muscle wasting.
The Applicant associated the face rash occurring in 1971 with his undertaking the non-destructive crack penetration process. The face rash recurred regularly thereafter and was again associated by the Applicant with the non-destructive crack penetration process.
It was submitted for the Applicant, and indeed the Applicant associated himself, that the onset of his condition both temporally and causally was associated with his exposure to chemicals used in the NDI process. In 1974 the Applicant was based at Butterworth and was posted to a position of full time NDI. He described the process of NDI as multi-staged, involving his climbing into the after-burner of a Mirage jet engine, dressed only in overalls, and spraying penetrant and emulsifier within the after-burner as part of the inspection process. The Applicant's exposure to these products continued until his retirement from the Service. Following his discharge, his condition worsened and he received treatment and medication.
It was submitted that the exposure to the products used in the NDI process [the ingredients listed in the Material Safety Data Sheets (exhibit L)] represented an opportunity for exposure to highly toxic bromide compounds. Blood analysis reported by Robert Gayer of Workcover Authority disclosed the presence of bromide in the Applicant's blood as late as 11 April 1995. Other than his exposure to bromide while with the RAAF, the Applicant is unaware of any circumstance, prior to or post service, in which he was exposed to bromide.
On 8 March 1995 Dr Fluhrer reported that the Applicant suffered from chronic bromide toxicity coupled with long term side effects from solvent exposure, superimposed on an established diagnosis of rheumatoid arthritis – an auto-immune disease. Dr Fluhrer considered that the Applicant's condition was consistent with auto-immune disease resulting from his chronic toxicity. While acknowledging that he could not state, as a matter of certainty, that chronic toxicity was the trigger for the diagnosis of rheumatoid arthritis, Dr Fluhrer considered that auto-immune disease was triggered by a process of chronic toxicity, that there is chronic inflammation, and that the trigger for chronic inflammations are toxins which could be endotoxins or exotoxins. Moreover, he considered that such opinion had gone beyond the level of possibility.
Dr Donohoe stated in his report dated 27 April 2000 (exhibit P) that "on the basis of the available evidence, Mr Culhane's rheumatoid disease and degenerative diseases were most likely caused by his workplace exposure to chemicals shown to cause such harm".
It was submitted for the Applicant that Professor Bisby, in his oral evidence, accepted that exposure to chemicals can result in severe mitochondrial damage but was unable to comment upon whether occupational damage to mitochondria would have increased the toxicity and effect of steroids prescribed and used by the Applicant in treatment of his then diagnosed rheumatoid arthritis, although Professor Bisby did acknowledge that steroids were highly toxic.
In relation to chemical exposure, Professor Bisby could not provide an opinion on the cause of the Applicant's signs and symptoms. He acknowledged that no tests had been undertaken while the Applicant served in the RAAF to determine whether there had been exposure to toxic chemicals. He relied on there being no record of any "poisoning" of the Applicant.
It was submitted for the Applicant that if the Tribunal accepts that Professor Sambrook's diagnosis of adult Still's disease is comprehensive and correct, it is open to the Tribunal to accept that the onset of the disease was during the period of the Applicant's eligible service. The Applicant submitted that this is supported by the evidence of Professor Sambrook who, in his oral evidence, raised the prospect of palindromic onset in the context of facial rash and conceded that the urticarial rash involving the face and trunk were certainly consistent with palindromic manifestation of adult Still's disease.
Professor Sambrook notes that chest pain of pleuritic nature was one of the features that led to his diagnosis of adult Still's disease on the assumption that the rheumatoid arthritis first started in 1991 and that around that time he had chest pains. However, Dr McCorkindale in his report dated 7 December 1994 (T5), noted odd rashes and atypical chest pains reported to airforce doctors from 1974 to 1988 and considered that some of the Applicant's presentations to doctors on service were prodormal to the illness now described as rheumatoid arthritis.
As to the cause of adult Still's disease, Counsel for the Applicant noted that Professor Sambrook considered it to be of unknown aetiology. However an altered immune response is one of the features of the condition and the most favoured hypothesis is that of an abnormal immune reaction to a prior viral infection in the presence of a genetically disposed individual. Professor Sambrook made the same observations in relation to adult Still's disease. He also noted that the triggering factors were often not found.
Counsel for the Applicant submitted that to the extent the Tribunal accepts that the palindromic episodes constituted an earlier onset of the adult Still's disease, the contraction of the disease, whether viral or otherwise, either arose out of or was attributable to the Applicant's defence service. It was submitted, in the alternative, that if the disease did not arise out of service, it was contributed to in a material way by, or was aggravated by the defence service that was continuously rendered thereafter by the Applicant. It was noted that the circumstances of the Applicant's resignation from the RAAF was the deterioration in his health, such deterioration manifesting in the full blown systems of the disease.
Counsel for the Applicant submitted there was inconsistency in Professor Sambrook's evidence about the question of chemical exposure. Professor Sambrook accepted that the role of chemicals as a triggering factor for auto-immune disease was "still a matter of active research and yet to be established" and that there was literature raising the possibility of a connection between rheumatoid arthritis to environmental materials. However, when discounting the role of chemical exposure in this case he said that "taking the scientific evidence, I don't think it's raised as a strong possibility". Furthermore, it was submitted that Professor Sambrook does not, and cannot, exclude exposure as a matter of medical certainty. Professor Sambrook acknowledged that no tests had been undertaken in this case to assist him in discrediting chemical exposure
It was submitted for the Respondent that throughout his Professor Sambrook's evidence, and in particular in cross-examination about scientific studies which allegedly showed or suggested a causal link between chemical exposure and adult Still's disease or rheumatoid arthritis, he consistently characterised the possibility of an association between those diseases and chemical exposure as "remote". Professor Sambrook clearly understood the need to address the "balance of probabilities" and not scientific proof in giving his evidence.
It was submitted for the Applicant in reply that when cross-examined on the issue of balance of probabilities as opposed to medical certainty in relation to the causal link between chemical exposure and adult Still's disease, Professor Sambrook responded that he had "trouble with this – with the two levels of evidence from the scientific background applying it to the legal situation". He said that rheumatologists would say:
… it is a remote possibility. Quantifying all the evidence, not trying to say it is proven beyond belief, as a possibility they would regard it as a remote possibility as being a factor in an individual patient and so I believe that my opinion's sort of based upon the fact that although it's a possibility and it's not proven unequivocally, as a possibility it's regarded as still one that is relatively remotely based on our current understanding.

The Applicant's Counsel submitted that the problem confronting Professor Sambrook is that he is being asked to establish his opinion that chemical exposure is, on balance, a trigger for adult Still's disease in circumstances where the current state of medical knowledge is that there is no known cause for the disease. In these circumstances he is left with only two options: either to exclude chemical exposure as causative, which would have been fatal to the Applicant's claim, if adult Still's disease diagnosis is accepted; or alternatively to accept it as a possibility, which he did. Counsel for the Applicant concluded that Professor Sambrook's qualification of the "possibility" as remote should be understood as "based on our current understanding", that is to say, we do not currently understand the cause, therefore the possibility can only be remote.
It was submitted for the Applicant the Respondent's position is that as the Applicant cannot prove that which current medical opinion cannot understand (but cannot exclude) then the Applicant must fail. The Applicant submitted that that proposition is untenable.
It was submitted for the Applicant that Professor Bisby's opinion, when tested in cross examination, manifested a noticeable lack of impartiality and open mindedness, when compared with the candour of Professor Sambrook, such that the Tribunal should approach his evidence with care.
It was submitted for the Applicant that Professor Bisby claimed a speciality in occupational medicine, and within that speciality, an interest in the causation of chemically induced poisoning of chemically induced toxicity; yet when questioned as to the toxicity of gold, he acknowledged that he had reported the contents of a textbook and that he had no practical experience. The Applicant submitted that in the absence of any relevant testing of the Applicant whilst on service and as testing procedures were available to the RAAF at that time, Professor Bisby's opinion that the Applicant experienced no episode of poisoning, acute or chronic, is without foundation.
It was submitted for the Respondent that Professor Bisby deferred to Professor Sambrook's diagnosis of adult Still's disease and, like Professor Sambrook, he stated confidently that chemical exposure has not been associated with the causation of rheumatoid diseases, including adult Still's disease. Professor Bisby pointed out that this is an area of enormous interest and diligent research.
It was submitted for the Applicant that in the absence of any reliable opinion in the alternative to Dr Fluhrer and Dr Donohoe, their opinion as to the chemical exposure of the Applicant is uncontested and should, on balance, prevail.
In reply, it was submitted for the Respondent that Dr Fluhrer and Dr Donohoe are general practitioners. Neither laid claim to specialist qualifications. Dr Fluhrer described the Applicant as suffering "a type of auto-immune arthritis", a "degree of auto-immune disease" which he attributed to chronic toxicity and chronic bromide toxicity coupled with long term side effects from solvent exposure. Dr Donohoe said that the Applicant was suffering a "gross disorder of energy metabolism" and identified the likely cause as "damage to mitochondria caused by the known exposure to brominated compounds in his workplace between 1971 and 1989". The diagnoses which Dr Donohoe favoured were rheumatoid disease and chronic fatigue syndrome. The second of these diagnoses has not been mentioned in the course of the Applicant's case before the Tribunal and the Tribunal can assume that no reliance is placed on it.

The Respondent submitted that the attempts by Dr Fulher and Dr Donohoe to postulate a causal connection between the applicant's adults Still's disease and chemical exposure were unpersuasive, when viewed in the light of the authoritative evidence of Professor Sambrook and Professor Bisby. The research literature which Dr Donohoe cited in support of his opinion was found to be either irrelevant or speculative when it was subjected to scrutiny by these two experts.
In reply, Counsel for the Applicant submitted that to the extent Dr Donohoe's opinion is accepted in lieu of the opinion of Professor Sambrook, his opinion could support the allowance of the appeal, although Dr Dohonoe certainly advocates the carrying out of further tests. In his report dated 6 November 1998 (exhibit A) Dr Donohoe notes the Applicant's gross disorder of energy metabolism and markedly raised lactate levels which are strongly suggestive of severe mitochondrial damage. Dr Donohoe postulates two possible causes for the disorder being either the known exposure to brominated compounds in the workplace between 1971 and 1989, or by direct cytotoxic damage from his medical therapy, but favours the latter, opining that the mitochondrial damage had occurred prior to the administration of the medications and was the most likely reason for the unexpected toxicity of the medical treatment.
The Applicant submitted that Dr Donohoe received support from both Professor Sambrook and Professor Bisby. Professor Bisby accepted that chemical exposure could result in severe mitochondrial damage. Professor Sambrook considered that adult Still's disease is a condition less likely to respond to some of the drugs taken by the Applicant (in respect of the rheumatoid arthritis diagnosis) than perhaps conventional drugs. Professor Bisby considered that if mitochondrial damage were sufficient clinical illness that "it might well have interactions with other toxic materials" such as the medication he was taking.
It was submitted for the Respondent that the additional "diagnoses" of chronic toxicity, chronic bromide toxicity, gross disorder of energy metabolism and damage to mitochondria proffered by Dr Fluhrer and Dr Donohoe were not diagnoses of diseases at all. Professor Bisby explained that toxicity simply means, in medical terminology, poisoning. There is no evidence before the Tribunal that the Applicant was poisoned in the course of his eligible defence service by any substance. Professor Bisby, in his oral evidence, described the signs and symptoms of poisoning by bromine or other solvents and it is clear that these would readily have been recognised. Professor Sambrook said "damage to mitochondria" was not a diagnosis but a mechanism of what might become a clinical syndrome. In reply, it was submitted for the Applicant that Professor Sambrook is not a toxicologist.
In relation to the "damage to mitochondria" counsel for the Respondent also noted the observation of Professor Bisby. When he was asked whether proper management of mitochondrial defects would include a full assessment of the Applicant's pathways of energy metabolism, he replied that mitochondrial damage is not a diagnosis upon which one could rest an investigation or treatment regime. It is a laboratory finding that may or may not be relevant.
Given all the above, it was submitted for the Respondent that the Tribunal would be satisfied, on the balance of probabilities, that the disability originally described by the Applicant as "muscular problems" and later described by him as "chemical poisoning" is answered by Professor Sambrook's diagnosis of adult Still's disease. The Respondent also submitted that the evidence before the Tribunal would not satisfy it, on the balance of probabilities, that there exists a connection between that disease and the Applicant's eligible defence service.
Finally, Counsel for the Applicant submitted that the evidence of the Applicant himself, about exposure, effects and onset of symptoms, and his physical deterioration, have a probative value which supports the opinion of Dr Donohoe, and should on balance satisfy the Tribunal that there exists a connection between the Applicant's condition and his eligible defence service.
consideration of evidence and findings of fact
The Tribunal finds that the Applicant is suffering from a very debilitating chronic condition and that during the years since about 1991 he has paid increasing attention to his concern that his present condition was associated with the chemicals he used during his service in the RAAF. Over the years he has invested considerable effort in pursuing that hypothesis. In the course of those investigations and particularly since he lodged his claim with the Respondent in respect of the condition, the proper diagnosis of the condition has also been at issue. The Applicant is now of the view that he does not suffer from rheumatoid arthritis but from some condition that has arisen from a form of chemical poisoning that occurred during his service. The Tribunal must come to a decision, on the balance of probabilities, with regard to diagnosis, before the issue of causation can be addressed. Indeed, the diagnosis will also affect whether the Tribunal is required to apply a Statement of Principles pursuant to s120B in making its determination.
The diagnoses to be considered are rheumatoid arthritis, chronic fatigue syndrome, and adult Still's disease. The Tribunal finds, on the evidence, that a diagnosis of rheumatoid arthritis or adult Still's disease precludes a diagnosis of chronic fatigue syndrome. The Tribunal considers the expertise of Professor Sambrook to be clearly superior in providing a diagnosis in this case. Not only is this an area of particular relevance to rheumatology, but also Professor Sambrook is an eminent rheumatologist. Moreover, the Tribunal has considered carefully his reasoned responses to and rebuttal of the opinions of Dr Donohoe and Dr Fluhrer. These doctors were not qualified in rheumatology.
The Tribunal is reasonably satisfied that the Applicant suffers from adult Still's disease, a form of rheumatoid disease, but one which carries a different ICD code that is not included in the Statement of Principles for Rheumatoid Arthritis Instrument No. 127 of 1996. As that Statement of Principles was gazetted in 1996, after the primary decision was made, the Statement of Principles does not need to be applied in determining the matter: Repatriation Commission v Thompson [2001] FCA 314. In any event, nothing turns on this issue, as the Tribunal notes that there is no Statement of Principles for Adult Still's Disease.
The Tribunal finds that the onset of the adult Still's disease occurred about 1991, but even if it occurred during his eligible service (and we are not reasonably satisfied that it did) the mere occurrence of the condition on service is not sufficient to meet the requirements of s70 of the Act. It needs to have "arisen out of, or was attributable to, any defence service…": ss70(5)(a).
The next issue is whether the Applicant's adult Still's disease, which is an auto-immune disease, was related to the circumstances of his defence service. The Applicant's case is either that his auto-immune system was affected by his exposure to chemicals on service, or that the medication used to treat his condition has a toxic effect such that it negatively affects the auto-immune system.
The Tribunal notes that the history recorded by Dr Donohoe is not consistent with the history the Applicant has given to the Tribunal and to other doctors and thus finds that Dr Donohoe's record was not correct. This has obviously been used as a basis for providing his opinion. Indeed, on the evidence of Professor Bisby, which the Tribunal accepts, the Tribunal finds there is a considerable amount of Dr Donohoe's report that is not correct, either by way of fact about the Applicant or in relation to medical knowledge. Having carefully analysed Dr Donohoe's evidence the Tribunal finds that it is based on conjecture rather than on sound medical or scientific knowledge. It raises no more than a possibility. Professor Sambrook has countered Dr Donohoe's evidence very carefully, to a point where the Tribunal prefers the evidence of Professor Sambrook.
The Tribunal is not reasonably satisfied that the Applicant suffered from bromide toxicity while on service. The Tribunal is also not reasonably satisfied that the Applicant's exposure to chemicals on his service acted as a trigger for him later to develop adult Still's disease.
The Tribunal is satisfied, to the requisite standard, that there is no causal relationship between the Applicant's adult Still's disease and his defence service. Therefore, even if the toxic effects of the medication he has had for that condition has contributed in some way (and the Tribunal makes no finding to that effect) it still does not establish a causal link with his service.
The Tribunal will vary the diagnosis to read "adult Still's disease". That part of the decision under review in respect of rheumatoid arthritis, now varied to read "adult Still's disease" is affirmed.

I certify that the 112 preceding paragraphs are a true copy of the reasons for the decision herein of Mrs M T Lewis, Senior Member and Dr J Campbell, Member
Signed:         .....................................................................................
  Associate
Date/s of Hearing  12-13 October 1999, 15 August 2000
Date of Decision  21 June 2001
Counsel for the Applicant         Mr J Darvall
Solicitor for the Applicant          Denniston & Day
Counsel for the Respondent    Ms R Henderson
Solicitor for the Respondent    Australian Government Solicitor