Lilley and Comcare and Repatriation Commission

[2003] AATA 738

CATCHWORDS – VETERANS’ AFFAIRS

– whether motor peripheral neuropathy defence caused – exposure to pesticides - whether applicant’s condition arose out of or attributable to defence service – whether claim should be assessed by reference to Statement of Principles made after Repatriation Commission’s decision but before decision reviewed by the Veterans’ Review Board – decision affirmed.

CATCHWORDS – COMPENSATION – exposure to pesticides - whether motor peripheral neuropathy arose out of or in the course of his employment –– decision affirmed.

Safety Rehabilitation and Compensation Act 1988 s. 124
Compensation (Commonwealth Government Employees’) Act 1930 ss. 4 and 9
Compensation (Commonwealth Government Employees’) Act 1971 ss. 5, 27 and 29
Veterans’ Entitlements Act 1986 ss. 5AB, 5Q, 9, 43, 68, 70, 120, 120A, 120B, 196, 196B, 196C, 196D, 196E, 196F, 196G, 196W, 196Y and 196Z
Acts Interpretation Act 1901 ss. 8, 46A, 48, 48A, 48B, 49 and 50
Commonwealth Workmen’s Compensation Act 1912

Workers’ Compensation Act 1926

Smith v Repatriation Commission (1987) 74 ALR 537
Behan v Australian Telecommunications Corporation (1990) 22 ALD 545
Repatriation Commission v Thompson [2001] FCA 341, (2001) 32 AAR 514
Repatriation Commission v Gorton (2001) 33 AAR 370
Repatriation Commission v Keeley (2000) 98 FCR 108
Greenough and Repatriation Commission [2002] AATA 774 and (2002) 70 ALD 470
Re Costello and Secretary, Department of Transport (1979) 2 ALD 934
Repatriation Commission v Keenan (1989) 19 ALD 509
Doolette v Repatriation Commission (1990) 21 ALD 489
Lees v Repatriation Commission [2002] FCAFC 398; (2002) 36 AAR 484
Kavanagh v The Commonwealth (1959-1960) 103 CLR 547

State of New South Wales trading as New South Wales Department of Agriculture v Allen [2000] NSWCA 141

Seltsam Pty Limited v McGuiness [2000] NSWCA 29
Federal Broom Co Pty Ltd v Semlitch (1964) 110 CLR 626
O’Neill v Commonwealth Banking Corporation (1987) 75 ALR 154
Re Welsford and Commonwealth Banking Corporation (1984) 1 AAR 42
Australian Telecommunications Commission v Treloar (1989) 90 ALR 202

Johnston v Commonwealth of Australia (1982) 43 ALR 559

DECISION AND REASONS FOR DECISION [2003] AATA 738

ADMINISTRATIVE APPEALS TRIBUNAL     )          
  )          V2000/103
GENERAL ADMINISTRATIVE DIVISION     )          

Re  WALTER JIM LILLEY

Applicant

And                  COMCARE

Respondent

V2001/434

Re  WALTER JIM LILLEY

Applicant

And                  REPATRIATION COMMISSION

Respondent

DECISION

Tribunal:  Deputy President S A Forgie
  Dr P D Fricker (Member)

Associate Professor J H Maynard (Member)

Date:  1 August, 2003

Place:  Melbourne

Decision:  The Tribunal affirms:

1.a decision of a delegate of the respondent, Comcare, dated 23 October, 1999 to affirm an earlier determination dated 29 January, 1999; and

2.a decision of the respondent, the Repatriation Commission, dated 15 June, 1998 and affirmed by a decision of the Veterans’ Review Board dated 27 March, 2001.

S A FORGIE
  Deputy President

REASONS FOR DECISION

On 28 January, 2000, the applicant, Mr Walter Jim Lilley, applied for review of a decision of a delegate of the respondent, Comcare, dated 23 October, 1999 to affirm an earlier determination dated 29 January, 1999.  In that determination, Comcare disallowed Mr Lilley’s claim for motor peripheral neuropathy.  On 23 April, 2001, Mr Lilley lodged a further application.  His application sought review of a decision of the Repatriation Commission (“the Commission”) dated 15 June, 1998 and affirmed by a decision of the Veterans’ Review Board (“VRB”) dated 27 March, 2001.  Both applications were heard together.

1. At the hearing, Mr Lilley was represented by Mr Croyle of counsel, Comcare by Mr Lenczner of counsel and the Commission by its advocate, Mr Rudge. The documents lodged by both Comcare and the Commission pursuant to s. 37 of the Administrative Appeals Tribunal Act 1975 (“CT documents” and “RT documents”) were admitted in evidence together with material to which we have had regard to some of which we will refer in the course of these reasons. Oral evidence was given by Mr Lilley in support of his case together with Dr Robert Bruce Allen, a Fellow of the Australasian College of Nutritional and Environmental Medicine. Professor Malcolm Ross Sim, an occupational physician and epidemiologist, Dr Robert Hjorth, a neurologist, and Professor Hedley George Peach, a specialist in environmental health and an epidemiologist, gave evidence in support of Comcare’s case. No evidence was called upon behalf of the Commission.

THE ISSUES

1. There are four issues in this case.  The first two arise under the Safety Rehabilitation and Compensation Act 1988 (“1988 Act”) and, more particularly, under the Compensation (Commonwealth Government Employees’) Act 1930 (“1930 Act”) and the Compensation (Commonwealth Government Employees’) Act 1971 (“1971 Act”).  They are whether, at the time to which the 1930 Act applies, Mr Lilley’s condition arose out of, or in the course of his employment or whether, at the time to which the 1971 Act applies, it was contributed to by his employment.  The third of the issues arise under the Veterans’ Entitlements Act 1986 (“VE Act”). One is whether Statements of Principles determined after the Commission had determined Mr Lilley’s claim and after the VRB had reviewed the decision but of which notice had been given after the Commission had made its decision but before the VRB review is relevant in the Tribunal’s review. The other is whether Mr Lilley’s condition is a defence-caused condition and that requires a consideration of whether it arose out of, or was attributable to, his defence service.

BACKGROUND

1. There was no dispute between the parties regarding certain matters forming the background to the issues to be decided in these cases.  In view of that and on the basis of the evidence, we have made the findings of fact set out in the following paragraphs.

1. Mr Lilley was born on 18 December, 1936 and was aged 67 years at the time of the hearing.  After leaving school at 15 years of age in 1951, Mr Lilley joined the railways as a junior clerk in Bunbury where he had been born.  After a year, he moved to Bridgetown in Western Australia and stayed there for the next four years.  He moved back to Bunbury, where he became the station officer for another two years.  He transferred to another station as the station officer for a further two years before resigning.  In the main, his work was clerical and he was not exposed to chemicals or other hazardous substances. 

1. Mr Lilley enlisted in the Royal Australian Air Force (“RAAF”) on 27 April, 1961.  His recruit training lasted for four months and he then spent the next two years at the Basic Pilot Training School in East Sale performing clerical duties.  Again, he was not exposed to any chemicals or hazardous substances.  This continued to be the case when he was transferred to Victoria Barracks in 1963 and later to the storage depot in Kingswood.  1963 was also the year in which Mr Lilley married. He and his wife had two children.  On 11 January, 1971 he was transferred to Port Moresby where he served until 8 January, 1973.  In that time, he undertook clerical duties for the first twelve months at Konedobu and then at Murray Barracks, which were located near Port Moresby.  On 8 January, 1973, Mr Lilley was posted to Point Cook.  He remained there until 14 December, 1976 undertaking clerical duties.  A twelve month posting to Canberra followed and then a further twelve month posting to Laverton.  He was then posted for three years to the Victoria Barracks and finally for four years to Laverton.  Mr Lilley was discharged from the RAAF on 7 November, 1986 with the rank of Warrant Officer. 

1. Mr Lilley suffers from the condition of spondylolisthesis, which has been accepted as a war caused injury within the meaning of s. 9 of the VE Act. He also suffers from the conditions of insomnia and psoriasis and a further condition that has been variously described as peripheral neuropathy due to axonal degeneration, chronic idiopathic axonal neuropathy and sensory motor polyneuropathy.

1. By a notice published in the Commonwealth of Australia Gazette (“Gazette”), the Repatriation Medical Authority (“RMA”) gave notice under s. 196G of the VE Act that it intended to carry out an investigation in respect of neuropathy. That notice was published on 3 November, 1999. On 12 September, 2001, the RMA issued a Statement of Principles (“SoP”) concerning Peripheral Neuropathy in matters to be determined on the balance of probabilities (Instrument No. 80 of 2001) (“SoP 80”). SoP 80 was amended by Instrument No. 14 of 2003 on 7 April, 2003.

THE EVIDENCE

Mr Lilley

1. In his oral evidence, Mr Lilley said that his health had been very good until his transfer to New Guinea.  He had never known of any spraying in his time with the railways.  In cross-examination, Mr Lilley said that he had suffered from nose bleeds as early as the 1960s.  Sometimes they occurred when the weather was hot.  He had never handled insecticides and had never used mosquito repellents.

1. Mr Lilley said that his medical problems started on his return from Port Moresby in 1973 when he started to suffer from nosebleeds, nausea and headaches. 
   In giving his evidence, he said that it was very hot in New Guinea and he wore a shirt and shorts to work.  There were plenty of mosquitos and Mr Lilley said that there was regular spraying every three to four weeks of his workplace and the village in which he lived in an attempt to reduce their numbers.  Spraying was carried out by labourers with knapsack sprays directed to the shrubbery around buildings.  The doors and windows of the buildings were always open at the time because of the heat.  Mr Lilley, who worked on the second floor, said that he was not directly sprayed himself but that spray was always in the air.  He worked some ten to twelve feet from the louvre window and there was no screen between his desk and the window.  Sometimes, if he knew that the sprayers were approaching, he would go outside until they had finished but, for the most part, he had no warning of their approach.  He knew nothing about the dangers associated with spraying, Mr Lilley said. 

1. In cross-examination, Mr Lilley said that he recalled the married quarters’ being sprayed for cockroaches in the last month before he left New Guinea.  Spraying occurred each six months and was carried out by Flick for Jim, who cared for the houses.  He and his family were not asked to leave when the spraying occurred. 

1. Mrs Lilley said that her husband’s skin used to be very clear.  While in New Guinea, Mr Lilley said, he developed a rash or two but it was mainly heat rash, he thought.  He still has a rash on his left hip and he developed that while in New Guinea.  While still in New Guinea, he consulted an Army doctor as there was no RAAF doctor based there.  Generally, though, Mr Lilley thought that he enjoyed good health while he was in New Guinea.  He did not suffer from any nose bleeds while there.

1. While based at Point Cook, Mr Lilley said that his health was all right in the beginning.  He and his wife lived off the base.  Then he began to experience dizziness, nausea and the occasional blood nose.  He experienced his first blood nose towards the end of 1973 or the beginning of 1974.  They could occur anytime and he would get nausea and a headache.  If they did, he would lie down and try to stop it.  There was spraying at Point Cook but it mainly took place in the summer months.  The only difference between spraying in Point Cook and spraying in New Guinea was that a fogging machine was used at Point Cook.  The fogging machine produced a visible spray or fog in the air.  It was used at least once a month and possibly more often.  Mr Lilley said that his duties required him to work inside but that he would always have his window open.  He was not given a mask and the spray would blow inside to his ground floor office.  Shutting the window was not an option.

1. Mr Lilley said that his health was not very good by the end of 1976.  He had thought initially that it was due to lack of fitness on his part.  Consequently, he took up jogging but seemed to lack energy either for that or for running.  On a couple of occasions, he consulted a medical practitioner at Point Cook about his blood noses.  Mr Lilley thought that the medical practitioner cauterised his nasal vessels.  He did not tell him about his feelings of weakness, he said, as he tended to keep things to himself.  In cross-examination, Mr Lilley said that he suffered less from headaches and nausea while at Point Cook but the nose bleeds stayed with him.  The nausea now accompanied the nose bleeds.  A particularly bad nose bleed lasted three to four hours.  He would not suffer from a nose bleed all the time.  In summer, they could occur daily but, in winter, they could be weekly.

1. In Canberra, Mr Lilley said in giving evidence, he did not suffer so much from blood noses but did suffer from dizziness at times.  He said he played a fair amount of darts and started to have trouble with his hand/eye coordination and a little difficulty with his balance.  That worried him but he did not do much about it, he said.  On the fitness side of things, he started to take multi vitamins but was not sure if he had seen a medical practitioner while in Canberra. 

1. In cross-examination, Mr Lilley said that he suffered from nose bleeds, headaches and nausea at Canberra, Laverton and Victoria Barracks with the same frequency as he had at Point Cook.  It was when he was at Laverton for the second time that he started to feel unfit and exhausted.  He could not connect his feelings of exhaustion with any particular activity.  He did not take anything for the nose bleeds.

1. At Laverton, Mr Lilley said that he felt much the same as he had in Canberra.  He did notice, though, that his left elbow was starting to waste and that concerned him.  He also noticed a loss of power or strength and the loss was particularly noticeable when he tried to cut wood and the like.  Mr Lilley did not tell his wife of his difficulties at this stage.  He tried exercising and bought a chest expander but was unable to use it as he did not have enough strength in one of his arms.

1. Mr Lilley said that he did not like seeing doctors but if he saw one, he saw a service doctor as that was the rule.  While at Victoria Barracks, he saw a doctor who told him that, as he was right handed, it was only natural that the left arm would waste as he got older.  At this stage, he was not suffering so much from dizziness but was more concerned about the wasting of his arm.  At the same time, he was suffering from a lack of hand/eye coordination.  He used to stumble and he fell quite a few times. 

1. Mr Lilley consulted his wife’s doctor, Dr Rao, privately while he was based at Laverton on three or four occasions.  She was concerned and referred him to a specialist, whom he saw three or four times.  He did not tell the RAAF of this as he was concerned that he would be discharged on medical grounds.  It was very important to Mr Lilley that he complete 20 years of service and he had consulted Dr Rao before its completion.  Mr Lilley started seeing Dr Merory at the Repatriation Hospital in 1981 and Dr Merory told him that he did not know what was wrong with him.  Mr Lilley suspected that the doctor, whom he consulted for three years, thought that it was motor neurone disease.  In 1995, Mr Lilley started to suffer from respiratory failure and he consulted another general practitioner, Dr Fraser.

Medical records

1. In 1981, a nerve biopsy and a muscle biopsy were performed.  Dr Ross Anderson of the University of Melbourne reported that there was axonal neuropathy especially involving large fibres and that the muscle showed neurogenic atrophy plus mild myopathy (Exhibit R1, pages 15-16).

1. Clinical notes from Dr Matkovic were made available to Professor Peach although not formally admitted in evidence.  In his letter of 23 June, 1998 to Dr Fraser, Dr Matkovic summarised the results of investigations:

“… Testing his genatype (sic) showed no size abnormality in exon A of the androgen receptro (sic) gene.  So, on the basis of the genetic analysis he is unlikely to have Kennedy’s disease.

Furthermore his creatine kinase was normal as was serum cholesterol, vitamin E and urinary porphyrins.  His serum immune electrophoresis was abnormal and there was an IgM lamda paraprotein band at 15g/L.  This is a very significant abnormality.  Whether or not it is a cause for his probable peripheral neuropathy I am uncertain about, but certainly it warrants consideration.  Furthermore, I am not sure whether a paraprotein band at a level of 15g/L warrants treatment on its own merits.  Clearly, this is a complex issue and will need to be addressed through further investigation through a brief admission to the Royal Melbourne Hospital.  He will need nerve conduction studies, a skeletal survey, and the opinion of our Haematology/Oncology Unit. …”

1. In a further letter to Dr Fraser dated 28 August, 1998, Dr Matkovic reported:

“… You will know that blood tests carried out during his visits to my Werribee Mercy Hospital Consulting Rooms detected the presence of a IgM lamda paraprotein band at a level of about 8g/L.  He underwent investigations including a skeletal survey, serum calcium, and a bone marrow biopsy.  On the basis of results of investigations he has a benign monoclonal gammopathy of uncertain significance..  Certainly, there is no evidence that he has multiple myeloma.  This is very good news.  However, his serum immune electrophoresis will need to be repeated at regular intervals for the rest of his life, and I would suggest that the tests be carried out at six-monthly intervals.

He underwent nerve conduction studies by Dr Lynnette Kiers, Consultant Neurophysiologist, and she found changes of an end stage neuropathy, most compatible with axonal degeneration. …”

Dr Allen

1. Dr Allen, who had graduated with an MBBS in 1964, said that he had held his qualifications in nutritional and environmental medicine for approximately 30 years.  He has been a senior lecturer in “integrative medicine” at the Swinburne University for the last three years.  At the time of the hearing, he had three papers accepted for publication and had published a paper in 1993 on epilepsy.  None of the papers is related to the subject concerning this case.

1. In his oral evidence, Dr Allen said that DDT is a member of the organochlorine group of pesticides.  Organochlorines were taken off the market nearly 30 years ago because of their toxicity.  In his report dated 30 May, 2000, Dr Allen said that Mr Lilley had been exposed to both Malathion and DDT, which were used to spray mosquitoes in New Guinea.  He had conducted tests for DDE, which he said was a “breakdown product of DDT, and this is how this is usually stored in the body.”  The test showed 1.6ug/l. of DDE in Mr Lilley’s blood.  Dr Allen regarded this as a moderately significant level as no DDE should be found in a person’s blood.  It is found in older people but not in younger ones.  He has seen levels of about one to five ug/l and the highest he ever saw was 13ug/l but that was in a person who had a reasonable amount of exposure.  The figure of 500 is indicative of acute exposure.  People who have more than 1ug/l potentially have a problem.  Dr Allen wrote in his report that the level was indicative of some significant exposure in the past and that Mr Lilley’s level of DDE nearly 30 years ago could have been extremely high.  Generally speaking, it can be expected that he is unlikely to have had any exposure to organochlorines in the last 20 or 30 years.  Dr Allen said that all organochlorines are lipophilic and tend to deposit in fatty tissues such as the brain and the central nervous system.  They last for a long time in those tissues and are significantly neurotoxic. 

1. Dr Allen had also conducted a liver detoxification profile and set out the results and his conclusions:

“       Low Phase I Detox (Cytochrome P450 Enzymes)

Lowish Glucuronidation (UDP Glucuronisyl Transferase)

The activity of these enzymes is to a large extent genetically determined, and Activity will vary widely across a population.

In Walter’s case Phase I (caffeine clearance) was 0.2ml/min/kg – normal range is 0.5 – 1.6ml/min/kg.

This indicates that Walter’s ability to eliminate toxins (especially fat-soluble Ones) such as organochlorines is significantly impaired.

This is would mean that he is genetially much more sensitive to toxic
Exposure than the average person.

These 2 facts considered together, would indicate that Walter’s exposure to DDT (even at supposedly safe levels) would have led to much greater build up of the same in his body, especially in CNS with attendant increased risk to neurotoxicity of same.

It is my opinion that his current problem was undoubtedly caused by his exposure to neurotoxins – to whit DDT, and as a result occurred directly as a result of his RAAF service.” (Exhibit R1, page 76)

1. A document entitled “Detoxification Profile (Standard)” was prepared by Great Smokies Diagnostic Laboratory on 30 March, 2000.  That document stated that the detoxification pathways in the body can be measured by measuring the activity of enzymes in the system.  There are 200 cytochrome enzymes in the body, the most active and the one we measure is cytochrome P450. It is tested with caffeine clearance and the result is a Bell curve of activity.  Its activity can be measured by ingesting a known amount of caffeine and then measuring caffeine levels after three hours and then after eight hours.  The activity of enzymes is genetically predetermined, Dr Allen said, and no two people have the same level of activity.   Two standard deviations either side of the mean cover 95% of the population.  Those at the lower end of the scale react fairly significantly to a minor level of exposure and for those at the top end of the scale the reverse is true.

1. The results in Mr Lilley’s case were interpreted by the laboratory:

“       A reduced (slow) caffeine clearance is indicative of depressed Phase I (cytochrome P450) activity.  This can result in difficulty in processing and removing toxins from the body.  Reduced clearance may be a consequence of gut dysbiosis, nutritional insufficiency, certain inhibitory substances, or a very low xenobiotic exposure.
        All Phase II detoxification pathways appear to be functioning adequately. 
‘Note: Phase I/Phase II ratios which lie below the reference range will not be discussed within the commentary text, even though they may appear in the red boxes labelled ‘abnormal’..  At this time we have not found sufficient information to consider them clinically significant.’

The Phase I/Phase II ratios for glycination and glucuronidation are both below the reference range.  This is not considered to be clinically significant.” (Exhibit D)

In his oral evidence, Dr Allen said that Mr Lilley was outside two standard deviations on the lower end of the scale.  Consequently, Dr Allen continued, Mr Lilley is in the bottom 5% of the population or, to put it another way, 95% of the population will deal with any toxic chemical more adequately than Mr Lilley.  Consequently, Mr Lilley has significant impairment of his detoxification pathway.  The drugs that Mr Lilley takes may have had a little impact upon the test results but it was impractical and expensive to undertake multiple tests.  In cross-examination, Dr Allen agreed that it could not be assumed that Mr Lilley’s results would have been the same in 1970 as they were 30 years later but, equally, it could not be assumed that they would not have been.  At the same time, he agreed that the general pattern is that the rate of the elimination of toxins decreases as a person’s ages.

1. In his second report dated 1 August, 2000, Dr Allen summarised his views:

“… it is highly probable that even that relatively short term exposure could have caused his problems because:-

1.It is probable that his low detox ability is genetically pre-determined, and thus would have made him much more susceptible than the average person.

2.The time frame for development of significant disease is compatible.

3.He would have had little other exposure to account for the elevated levels of DDE.” (Exhibit R1, page 90)

1. In cross-examination, Dr Allen referred to a passage from a publication by the Environmental Protection Agency in the United States of America (“EPA”) entitled Recognition and Management of Pesticide Poisonings (JR Reigart, MD and JR Roberts MD, MPH, 5^th edition, 1999):

“      OPIDN [organophosphate-induced delayed neuropathy]: Rarely, certain organophosphates have caused a different kind of neurotoxicity consisting of damage to the afferent fibres of peripheral and central nerves and associated with inhibition of “neuropathy target esterase” (NTE).  This delayed syndrome has been termed organophosphate-induced delayed neuropathy (OPIDN), and is manifested chiefly by weakness or paralysis and paresthesia of the extremities.  OPIDN predominantly affects the legs and may persist for weeks to years. These rare occurrences have been found shortly after an acute and often massive exposure, but in some cases, symptoms have persisted for months to years. Only a few of the many organophosphates used as pesticides have been implicated as causes of delayed neuropathy in humans. EPA guidelines require that organophosphate and carbamate compounds which are candidate pesticides be tested in susceptible animal species for this neurotoxic property.

Three epidemiologic studies with an exposed group and a control group also suggest that a proportion of patients acutely poisoned from any organophosphate can experience some long-term neuropsychiatric sequelae. The findings show significantly worse performance on a battery of neurobehavioral tests, including memory, concentration, and mood, and compound-specific peripheral neuropathy in some cases. These findings are subtle and may sometimes be picked up only on neuropsychologic testing rather than on a neurologic exam.  Follow-ups of case series have occasionally found some individuals reporting persistent headaches, blurred vision, muscle weakness, depression, memory and concentration problems, irritability, and/or development of intolerance to selected chemical odors.

Intermediate Syndrome: In addition to acute poisoning episodes and

OPIDN, an intermediate syndrome has been described. This syndrome occurs
after resolution of the acute cholinergic crisis, generally 24-96 hours after exposure.  It is characterized by acute respiratory paresis and muscular weakness, primarily in the facial, neck, and proximal limb muscles. In addition, it is often accompanied by cranial nerve palsies and depressed tendon reflexes. Like OPIDN, this syndrome lacks muscarinic symptomatology, and appears to result from a combined pre- and post-synaptic dysfunction of neuromuscular transmission.  Symptoms do not respond well to atropine and oximes; therefore treatment is mainly supportive.  The most common compounds involved in this syndrome
are methyl parathion, fenthion, and dimethoate, although one case with
ethyl parathion was also observed.

Other specific properties of individual organophosphates may render them more hazardous than basic toxicity data suggest. By-products can develop in long stored malathion which strongly inhibit the hepatic enzymes operative in malathion degradation, thus enhancing its toxicity. Certain organophosphates are exceptionally prone to storage in fat tissue, prolonging the need for antidote for several days as stored pesticide is released back into the circulation. Animal studies have demonstrated potentiation of effect when two or more organophosphates are absorbed simultaneously; enzymes critical to the degradation of one are inhibited by the other. Animal studies have also demonstrated a protective effect from phenobarbital which induces hepatic degradation of the pesticide.  Degradation of some compounds to a trimethyl phosphate can cause restrictive lung disease.” (pages 36-37)

1. Dr Allen agreed that this discussion appeared to focus on the acute reaction to exposure rather than on the reaction to long term exposure and that the emphasis appeared to be on organophosphates, of which Malathion is one.  As for delayed onset in cases of exposure to DDT, Dr Allen was not aware that the comments regarding delayed onset were applicable.  DDT is an organochlorine and the section of the EPA publication quoted above had discussed organophosphates:

“       Early manifestations of poisoning by some organochlorine pesticides, particularly DDT, are often sensory disturbances: hyperesthesia and paresthesia of the face and extremities. Headache, dizziness, nausea, vomiting, incoordination, tremor, and mental confusion are also reported. More severe poisoning causes myoclonic jerking movements, then generalized tonic-clonic convulsions. Coma and respiratory depression may follow the seizures.

Poisoning by the cyclodienes and toxaphene is more likely to begin with

the sudden onset of convulsions, and is often not preceded by the premonitory

manifestations mentioned above. Seizures caused by cyclodienes may appear as long as 48 hours after exposure, and then may recur periodically over several days following the initial episode. Because lindane and toxaphene are more rapidly biotransformed in the body and excreted, they are less likely than dieldrin, aldrin, and chlordane to cause delayed or recurrent seizures.” (page 57)

1. Dr Allen said that some of the symptoms of which Mr Lilley complained when he had his initial exposure, such as dizziness, headaches and nausea, fitted the description given in this passage.  Those symptoms had been discussed in Professor Sim’s report, Dr Allen said.  A rash called chloracne is a response to organochlorine exposure.  It looks more like acne but could be described as a heat rash by someone who doesn’t know what they are looking at. Mr Lilley suffered from a rash and, although Dr Allen had not seen it, he said the rash could have been related to organochlorine exposure. 

1. Dr Allen also referred to a text book by NA Ashford and CS Miller entitled Chemical Exposures Low Levels and High Stakes (2^nd edition, 1998, Van Nostrand Reinhold).  That considered organophosphates and their chronic effects:

“         Thus there is accumulating evidence dating back over several decades linking organophosphate-type compounds with chronic illness and new-onset intolerances in a subset of exposed persons.  This unusual complaint of new-onset chemical, food and drug intolerances is a sentinel symptom of MCS [Multiple Chemical Sensitivities], one that should alert practitioners to explore possible chemical initiators in their patients.  It would be difficult to imagine that so many people with prior identifiable chemical exposures would invent such bizarre and inconvenient intolerances: many now avoid fragrances they formerly enjoyed, no longer drive because traffic exhaust makes them fell ill, and have given up favourite foods such as pizza or chocolate because they, feel sick when they eat them.” (page 237)

1. In his oral evidence, Dr Allen said that there may be some suggestion that the immune system has some part to play in the disease process.  Mr Lilley also suffers from psoriasis and that has its basis in the immune system.  In cross-examination, Dr Allen said that he was not a neurologist or a neuropathologist but understood that peripheral neuropathy is due to the degeneration of the axon in the nerve fibre and so to the death of cells centrally.  It is relevant to know what part of the nervous system is damaged as different damage is caused by different causes.  For example mercury and B12 deficiency damage the neuronal sheath.  There is also a difference between how DDT and Malathion operate.  Organophosphates basically act as a neuro toxin while DDT, as an organochlorine, acts as a straight toxin to the nerve cells and affects the central nervous system, including the spine and the brain.  Organophosphates overstimulate the nerves and cause twitching and excessive nervous activity including spasticity, salivation and urination by blocking cholinesterase.  When asked, “Which is completely different from what DDT does?” he replied, “Yes”.

1. Dr Allen agreed with Mr Lenczner that Mr Lilley had initially suffered from dizziness and nausea and that his lack of coordination came later.  He said that he was unaware of Mr Lilley’s nose bleeds.  He said that the nose bleeds could not explain the headaches and the nausea.  A nose bleed usually results from an artery in the nose.  It may result in a headache and nausea but it need not.  Dr Allen said that he would not be satisfied that Mr Lilley related his nose bleeds to his nausea and headaches because it was unusual for them to be associated.  They could do if a person lost enough blood.  Dr Allen said that there was a “significant probability” that they were linked to Mr Lilley’s exposure to spray. 

1. Symptoms could be delayed, he said, as was apparent from the EPA publication.  There is literature that talks of nerve damage from exposure.  That is often ongoing once degeneration starts and the initial damage has been caused.  Dr Allen could not give references to the literature.  He rejected the suggestion that there need be some very quick consequence of exposure, such as twitching or urination, and at least within days of exposure.  He referred to the EPA publication and said that it discussed delays of weeks, months and years for one group of people.

1. Dr Allen said that he neither agreed nor disagreed with Dr Hjorth’s opinion that a genetic component in Mr Lilley’s condition could not be excluded.  There was no family history to suggest a genetic predisposition.  He did agree with Dr Hjorth that the amount of 1.6ug/l of DDE in Mr Lilley’s blood was an amount that was only just measurable.  At the same time, he pointed out that this was the amount that was present in Mr Lilley’s blood 30 years after his exposure.  Dr Allen agreed with Mr Lenczner that DDT was used in Australia prior to World War II and that it would, to some extent, be present in the soil.  He did not, however, agree with him that 95% of Australians of Mr Lilley’s age would have a similar amount of DDE in his or her bloodstream.  To his mind, their readings would be significantly less 30 years later.  He could not provide a publication to support this.

1. Dr Allen agreed with Mr Lenczner that his hypothesis was that organochlorines are stored in the body’s fats, such as the brain, until they are excreted.  The damage is done to the brain’s nervous system at some time in the past and the nervous system does not regenerate terribly well.  Dr Allen agreed with the further proposition that he called Mr Lilley’s condition an immune response because there was no mechanism which could explain how exposure 30 years ago could cause his condition and could cause a condition that is becoming progressively worse.

1. Dr Allen said that he adopted a similar position in relation to the organophosphate, Malathion.  There are reports of delayed reactions in the literature regarding organophosphates even though the literature in this case refers only to a delay of days or weeks.  An immune response of this sort is not impossible.

Professor Sim

1. Professor Sim interviewed Mr Lilley in preparing his report and also had regard to material sent by Mr Lilley’s solicitors and to toxicological data about DDT and other pesticide exposure on his own files.  He observed that he is not a clinical specialist but had ascertained from the material that Mr Lilley is suffering from severe, chronic and progressive motor polyneuropathy of uncertain aetiology.  Professor Sim said that it is difficult to reach any firm conclusions about the cause of Mr Lilley’s condition.  His condition is idiopathic and no specific cause can be identified.  There are several factors that are relevant in deciding whether or not his service in the RAAF was likely to have caused, or materially contributed to, his condition.  One was that chronic conditions usually require a latent period of several years from the first contact until the development of the condition.  Another was that his overseas’ service was in a tropical country where he was likely to have come in contact with a mix of vector-borne microbiological hazards, possibly contaminated food and water, hot and humid conditions, chemical exposures and malarial prophylaxis.  The effects of these mixed exposures in tropical countries has not been well researched.  Professor Sim said that he could not find any possible causative factors outside Mr Lilley’s service in the RAAF.

1. Assuming that DDT and Malathion were the two chemicals to which he was exposed, Professor Sim said that it is known that both have toxic effects on the neurological system and particularly so after high level acute exposure.  In his oral evidence, Professor Sim said that a person’s levels of DDE are not particularly useful in trying to ascertain the level to which a person has been exposed to DDT in the past.  Professor Sim considered that Mr Lilley’s DDE readings were not as high as Dr Allen considered them to be.  The tests, though, were conducted some 13 years after the onset of his condition and so do not assist greatly in assessing what might have been the level of Mr Lilley’s exposure to DDT during his RAAF service.  In his second report, Professor Sim commented upon the long half-life of DDE which means that it takes several years to be eliminated from the body.  That means that internal exposure continues after external exposure.

1. While DDT is highly potent in the body, the rate at which it is broken down in the body differs from person to person and so it is difficult to take a reading and extrapolate it back over time.  Problems can be caused by the absorption of a substantial amount of DDT over a fairly short period of time.  The problems can arise in hours, days or weeks, perhaps.  They are fairly well documented.  The chronic effects of DDT are less well known but it primarily affects the central nervous system.  Although he is not a neurologist, Professor Sim said, it is his understanding that DDT usually affects the myelin sheath, which protects the nerve fibres.  As the myelin sheath is broken down, the transmission along the nerve fibres is affected and the nerve cell itself is gradually broken down. 

1. In his report, Professor Sim said that organophosphates such as Malathion have a well documented delayed neuropathy although the time from cessation of exposure to the development of symptoms is longer in Mr Lilley’s case than in others.  There is some degree of plausibility for this longer time frame, Professor Sim considered, on the basis that both DDT and Malathion are known to affect the nervous system.  Biological persistence and the lipophilic nature of DDT makes it easy for it to permeate the myelin sheath around peripheral nerves.  In his oral evidence Professor Sim said that the published papers documented a delayed reaction in relation to Malathion but none was documented in relation to DDT.  This is consistent with the views expressed by Professor Sim in his report of 2 September, 2002 in which he added that he was not aware of any reports of neurological effects several years after exposure. 

1. In his oral evidence, Professor Sim referred to a passage from Casarett and Doull’s Toxicology The Basic Science of Poisons (5^th edition, 1996, McGraw-Hill) to explain what he meant by a delayed reaction:

“The degeneration of axons does not commence immediately after acute organophosphorus ester exposure but is delayed for 7 to 10 days between the acute high-dose exposure and the clinical signs of axonopathy.  The axonal lesion in the PNS appears to be readily repaired, and the peripheral nerves become refractory to degeneration after repeated doses.  By contrast, axonal degeneration in the long tracks of the spinal cord is progressive, resulting in a clinical picture that may resemble multiple sclerosis.” (page 551)

1. The passage suggests that the dose be acute.  There is an acute phase and then a delayed phase whose onset may be weeks or months but not years.  An acute dose can lead to a substantial inhibition of enzymes but without there being any clinical signs and that is often the case.  It is those who have dramatic symptoms who are written up and he referred to an extract from an article by Argiles, Lison, Lauqwerys, Mahieu, Burcher and Van Den Bergh entitled Acute polyneuropathy after malathion poisoning (1990):

“       A 65 year old white female was admitted 3-4 hours after deliberate ingestion of 100 ml or an aged insecticide preparation, originally containing malathion in isopropanol.  The estimated theoretical dose of malation ingested was 235 mg/kg.

On admission, consciousness was markedly reduced.  Clinical manifestations included miosis, sialorrhea, hyperhidrosis, bradycardia, hypotension, respiratory distress, fasciculations and generalized weakness.  Treatment with artificial ventilation, gastric lavage, atropine and the AChE reactivator, pralidoxime, was initiated immediately.  Depression of serum cholinesterase was total and persisted during seven days; complete normalization had occurred on day 12.

A few days later, the patient had regained consciousness and her muscle strength was improving.  However, various complications were observed following this actue cholinergic crisis.  First, cardiac arrhythmias, consisting of sinus bradycardia, A-V conduction disturbances and runs of ventricular tachycardia were prominent for two weeks.  They were treated with a pace-maker and xylocaine infusion.  Secondly, the patient presented two episodes of pneumopathy: (a) on day 8, a S. aureus bacterial pneumonia, which resolved rapidly with antibiotic treatment, and (b) from day 13 on, an acute respiratory distress syndrome, necessitating ventilatory support for more than 30 days and steroids.  Lung biopsy revealed a non-specific parenchymatous fibrosis.

From day 10 on, muscle strength began to deteriorate again and deep tendon reflexes were diminished.  Weakness predominated in lower extremity muscles, distal muscles being more involved than proximal ones.  Six weeks after admission, muscle strength began to recover and had virtually normalized after three months.” (Exhibit C10, page 191)

Professor Sim said that this picture was not one presented by Mr Lilley.  His is a fairly unusual situation and his clinical findings do not fit with those in the example in the article.  There is no paper that indicates exposure to organophosphates leads to a delayed reaction of the sort suffered by Mr Lilley.

1. The essence of Professor Sim’s opinion expressed in his first report is in the following passage:

“On a balance of probabilities, there is no obvious cause of Mr Lilley’s neuropathy.  I can find nothing in his genetic, non-RAAF occupational, smoking, drinking, dietary or hobbies history which would suggest a possible cause.  If we don’t accept that this condition is truly idiopathic, ie there is an underlying cause, then given that he had a long history of RAAF service including an overseas posting for two years in a tropical country with several episodes of what sounds like sloppy insecticide application, with little regard for protecting residents or office workers from exposure, this is probably the most likely option.  There is scientific evidence of these insecticides causing neurological effects, but the evidence is less convincing of effects occurring quite this long after exposure ceases.  There is some biological plausibility, given the physical and chemical properties of the two insecticides ad that the nervous system is a known target organ for both compounds.” (Exhibit C2, paragraph 6)

1. In his second report dated 2 September, 2002, Professor Sim elaborated upon his thinking:

“It is always difficult to quantify on a percentage basis this type of probability.  I could find no other potential risk factors for a chronic neurological condition in Mr Lilley’s history during my interview with him.  Therefore, in relation to any other possible causes apart from the insecticide exposure he had, I would rate the probability less than 10%.  In relation to the insecticide exposure he had during this time in the RAAF, I would rate the probability considerably higher than this, probably above 50%.  My rationale for this is that the Historian’s report has now confirmed the types of insecticides used, the known long term neurological effects of organophosphates, the long half life of DDE in the body, and Mr Lilley’s demonstrated impaired ability to metabolise these chemicals following exposure.” (Exhibit C3, paragraph 5)

1. In his second report, Professor Sim said that he was unaware of any scientific reports linking DDT or malathion exposure specifically to chronic axonal polyneuropathy.  He was aware only of delayed neuropathy in relation to organophosphate exposure.  As chronic axonal polyneuropathy is an uncommon disease, he would have thought it very unlikely if there had ever been sufficient statistical data to establish a convincing scientific link. 

1. Professor Sim said that he did not know enough about genetics to be able to comment on whether there are any genetic factors in the onset of peripheral neuropathy.  In relation to the depressed cytochrome P450 activity found by Dr Allen, Professor Sim said that it was his understanding that this is an inherent aspect of Mr Lilley’s physiology and the result would have been the same thirty years before.

Dr Hjorth

1. Dr Hjorth, who did not see Mr Lilley, wrote three reports dated 25 July, 2002, 2 September, 2002 and 7 March, 2003 respectively.  In his oral evidence, he said that neuropathies may be divided into two: axonal and demyelinating.  Axonal is the most common and its causes include diabetes, alcohol, renal failure and poisons and drugs.  Dr Hjorth said that he sees several cases of axonal neuropathy each year.  If they are very mild, he explains the condition.  If they are less mild, he follows them for two to three years.  He would have followed 30 to 40 in this way in the last two to three years.  Dr Hjorth estimated that there were a thousand cases of axonal neuropathy in the western world.  Its prevalence in the whole population would be 1% to 2%.

1. In his first report, Dr Hjorth said that idiopathic axonal polyneuropathy is not unusual.  His third report notes that detailed investigations have not revealed its cause other than to identify the presence of an IgM gammopathy.  IgM gammopathy is an asymptomatic disease of the blood that commonly causes polyneuropathy.  It is not an uncommon disease and 1 to 2% of the population aged over 60 years suffers from it.  The neuropathy of IgM gammopathy is normally a demyelinating neuropathy rather than an axonal neuropathy and it was Dr Hjorth’s impression that a person can sometimes get an axonal neuropathy from IgM gammopathy.  He would, however, need to do some research before he drew any further conclusion. 

1. Whether Mr Lilley’s peripheral neuropathy was hereditary was explored in Dr Hjorth’s first report and also in his evidence.  He said that there was no DNA test available to test whether it was or not.  A family history could be used to explore whether there was a history of a slight difficulty with running and jumping and whether there was a mild deformity of the feet called pes cavus and hammer toes.  Although most cases of hereditary neuropathy do give a family history consistent with its diagnosis, a significant number of cases are thought to be due to mutation and occur “out of the blue” (Exhibit C4, paragraph 5).  In his third report, Dr Hjorth said that he could not exclude the possibility that Mr Lilley’s polyneuropathy was due to IgM gammopathy.  He does not understand the origins of such gammopathies but they seem to be due to the overgrowth of a specialised form of white cells.  The great majority of them seem constant over the years but some change into multiple myeloma or lymphoma or some other malignant process.  He did not know whether service in the tropics predisposed them to do this.

1. In relation to exposure to toxins, Dr Hjorth said in his first report:

“6.     When we come to the issue of toxic neuropathy I can make some general comments.  Firstly toxic neuropathy is not common and yet there are several drugs and chemicals that have been reported to cause neuropathy so it’s always important to consider it.  Secondly the great majority of cases of neuropathy are obvious while the patient is still exposed to the toxins and then rapidly improve once the patient stops.  One exception to this is the organophosphates which include Malathione (sic)..  My understanding is that you can get somebody very sick from organophosphate poisoning and then as they are getting better in terms of their general sickness, over the next few months, the neuropathy can actually get worse.  I am not sure if this applies here but Malathione is one of the organophosphates so it is at least possible.

7.The body of evidence suggests that the symptoms of his polyneuropathy first became apparent around 1979.  If this is the case, then, it would be several yeas from his exposure in New Guinea to the Malathione to his development of the polyneuropathy.  I am not aware of any examples of toxic neuropathy where the symptoms first come on after a latent period of several years.  This in itself makes it unlikely that we are dealing with a toxic neuropathy related to his New Guinea service.

8.One of the issues here is the question of DDT toxicity.  My understanding is that DDT has sometimes been claimed to cause Peripheral Neuropathy but the evidence for it is that it’s not watertight.  The fact is that DDT was very widely used for the control of insects for a matter of some decades.  It is my understanding that the use of DDT was stopped not because there was concern that people were suffering but because there was concern that birds were suffering.

9.In general terms with toxicity one knows that the drug agent is toxic because one gets a small outbreak or epidemic of cases. This is true of the majority of cases of toxic neuropathy too.  There is nothing to suggest that this has happened with either DDT or Malathione in TPNG.

10.Of course one cannot exclude the possibility that the individual person might have an idiosyncratic response to a drug or chemical.  It is both impossible to exclude and impossible to prove.” (Exhibit C4)

1. He later conducted a survey of the literature regarding DDT:

   “(b)   I cannot find a reference to DDT causing Polyneuropathy.

   (c)The only example I can find of a toxic neuropathy which has a delayed onset following the exposure to the toxin is the organophosphate induced Polyneuropathy.  The situation here is that the patient initially gets a lot of symptoms from excess accumulation of Acetylcholine and so there are marked cholinergic symptoms include diarrhoea, vomiting, fasciculation, behavioural changes, etc.  These come within hours of the exposure to the toxin.  The Polyneuropathy can be delayed but Dyck’s two volume monograph ‘Peripheral Neuropathy’ says the symptoms of the Axonal Neuropathy occur after a latent period of 7 to 21 days.  I have been unable to find a reference to a toxic agent which causes the onset of a polyneuropathy after months or years.

   (d)I have not been able to find reference to DDT as a cause of Peripheral Neuropathy.  It is not mentioned under ‘Toxic Neuropathies’ in Dyck’s monograph and I could not find it in data bases that I used to search through neurological literature.  There is no reference in Medlink or in Pestronk’s Encyclopaedic web site dealing with neuromuscular disease.  A computer search of the last ten years of neurological literature failed to show an article that had both DDT and Polyneuropathy present.

   (e)My conclusions from this is that DDT is a doubtful cause of Polyneuropathy.  The two qualifications I have about this are firstly that I do know that some years back it was considered as a possible cause of Polyneuropathy and secondly I do not have access to the toxicology data base.” (Exhibit C5)

2. Dr Hjorth’s conclusion was expressed in his final report:

“The central problem here, then, is that we have a very unusual or atypical form of polyneuropathy for which we do not have a clear cause.  Because the case is so unusual, I think it must be said that in the absence of any other cause, the possibility exists that it was in some way related to Mr Lilley’s Service in New Guinea.  I am afraid that I cannot put it any stronger than that.” (Exhibit C6)

In cross-examination, Dr Hjorth said that it is possible with a number of diseases that multiple environmental factors play a part but there is a big difference between keeping open a possibility and suggesting that it is a probability.

1. In his oral evidence, Dr Hjorth said that organophosphates block one of the enzymes that break down acetylcholine at the nerve endings and this leads to a consequential increase in the body’s acetylcholine.  Symptoms include a minor flicker of the muscle.  When asked about the differences between the symptoms displayed by Mr Lilley and those to whom he referred in his reports, Dr Hjorth said that a person becomes acutely sick from organophosphates.  Peripheral neuropathy following exposure to organophosphates comes on and it progresses over weeks or months.  In Mr Lilley’s case, he did not suffer an acute illness.  Instead, he had a latent period of some years and then suffered the onset of peripheral neuropathy.  He knew of no other case in which the symptoms had manifested themselves in that way.  Symptoms from exposure to organophosphates have the most delayed onset but the delayed onset is weeks or months but not years.

1. When asked in cross-examination whether treatment can assist, Dr Hjorth said that it all depends upon the underlying cause.  If the cause can be identified the cause is treated but, if it cannot, the symptoms are treated.  Dr Hjorth said that he could not see blood noses as a relevant symptom.  Dizziness can be due to anaemia and that could be linked.  Clumsiness or lack of coordination could be caused by polyneuropathy even though it was an unusual first presentation.  For all that, it was still possible.  The other symptoms suffered by Mr Lilley were non specific and could not be linked with polyneuropathy.  Dr Hjorth said that it was possible to have exposure to pesticide without a person’s suffering from clinical symptoms.  Presentation with dizziness, exhaustion and blood noses are not particularly suggestive of polyneuropathy.  Tingling and numbness are the most common symptoms.  It is possible that a person could have reduced coordination of the sort that would show itself in a game of darts. 

1. In Dr Hjorth’s opinion, Mr Lilley first started to show symptoms of polyneuropathy in 1978 or marginally later when there were signs of wasting.  He agreed that a history is important as it can be difficult to determine onset and particularly so when the onset is insidious.  He held this view when he was told that the doctors’ notes in the Commission’s T documents (Exhibit R1) showed a 12 month history of weakness and wasting of muscles in July, 1981, a two year history of the same in March, 1982 and a reference to deterioration over the previous two to three years in 1983.

1. Had he seen Mr Lilley in the mid 1970s, he would have tested for causes of the disease such as diabetes or renal failure.  If there had been such a cause, it might have been possible to change the course of the disease.  If there had been no such cause, Dr Hjorth said that he would have told Mr Lilley to avoid exposure to toxins had Mr Lilley mentioned that he had been exposed.  Had he thought that there had been such exposure, he would have ordered a Red Cell Cholinesterase as the exposure would have then been fairly recent.  The only other advice that he could have given would have been related to physical aids.

Professor Peach

1. Professor Peach had reviewed Mr Lilley’s history extensively as well as the medical evidence and the scientific literature.  He prepared three reports dated 17 June, 2002, 13 August, 2002 and 29 November, 2002 respectively and each explored the possible causes of Mr Lilley’s condition and reached similar conclusions. 

1. In his oral evidence, Dr Peach said that polyneuropathy usually begins in the finger tips and then develops.  That is its pattern.  It begins outside the central nervous system but can involve tracts in the spinal cord.  Professor Peach said that he is not aware of any treatment for peripheral neuropathy as suffered by Mr Lilley.  If it arises from IgM gammopathy, there have been attempts to treat it with electrical impulses and immunological drugs.  There has been some success but there is no suggestion that IgM gammopathy is the cause of Mr Lilley’s condition.  In cross-examination, Professor Peach explained that IgM gammopathy appears to attack the myelin sheath but there is no link between it and the axon.  IgM gammopathy is not so rare in the community as about 1% of the population over 50 years of age and 3% of those over 70 years suffer from it.

1. In his first report, Professor Peach noted that Dr Matkovic’s letter dated 21 April, 1998 to Dr Fraser stated that Mr Lilley first noticed wasting of muscles in his left arm.  That would have warranted a diagnosis at the time that he first noticed it.  Although peripheral neuropathy was not diagnosed until 1981, its clinical onset occurred in 1978.  In cross-examination, he explained that, by “clinical onset”, he meant the time at which there were clinical signs to enable a diagnosis to be made. 

1. Professor Peach said that the hypothesis that Mr Lilley’s peripheral neuropathy was caused by exposure to DDT during his service in New Guinea is no more than a theoretical possibility.  While DDT is toxic, it acts chiefly on the cerebellum and motor cortex, rather than on the peripheral nervous system.  While it is true that DDT concentrates in fat, this does not point to its being the cause of Mr Lilley’s condition.  Storage of DDT in fat is considered to be protective because it decreases the amount of chemical at its site of toxic action i.e. the brain.  In any event, this is not relevant in Mr Lilley’s case as he is suffering from a disorder of his peripheral, rather than his central, nervous system.

1. Professor Peach did not accept the suggestion that Mr Lilley’s polyneuropathy was due to an unusually high build up of DDT in his central nervous system based on a single low reading for his caffeine clearance in 2000 when he was 64 years of age.  He said that caffeine clearance varies from person to person and within the same person from time to time.  For that reason, he said, several measurements should be performed.  Caffeine clearance decreases with age so that a low clearance at the age of 64 does not mean that he had a low clearance when he was stationed in New Guinea in his mid thirties.  Moreover, Professor Peach continued, relatively low doses of DDT as occur within residential spraying causes chemical changes in the body that lead to an increase in its metabolism and excretion.

1. He also considered as no more than a theoretical possibility a hypothesis that Mr Lilley’s condition was caused by his exposure to Malathion without his ever having been poisoned.  There is nothing pointing to Malathion’s being able to cause a polyneuropathy in the absence of poisoning and certainly not polyneuropathy starting one to two years after the cessation of exposure and progresses slowly over the next 20 years.  Professor Peach said that he had reviewed the literature and that there is only one reported case of a delayed onset and that occurred after a delay of only ten days after a deliberate poisoning.  The neuropathy was attributed to an impurity in the Malathion.  The only reported cases of death after the use of Malathion have occurred when used by workers in third world countries who have not been trained in its use.  Malathion, Professor Peach said in his oral evidence, is a particularly safe pesticide.  It has been used extensively in aerial spraying for mosquitoes in the United States when those mosquitoes bore encephalitis.  Hospitals and doctors were monitored for patients reporting with symptoms but there was not a single patient who reported with symptoms of polyneuropathy. 

1. In cross-examination, Professor Peach said that organophosphates block an enzyme.  The nerves in the body are connected by chemical agents with the most common being acetylcholine.  If the message is carried down, acetylcholine is released so that the next nerve carries the message.  Once it has done its job, it is removed by the acetylcholinesterase enzyme.  If, therefore, the enzyme that removes the acetylcholine has been removed, a person suffers such symptoms as blurred vision.  If a person absorbed quantities of Malathion, he or she would suffer from blurred vision and respiratory problems followed by a slow heart beat and probably a drop in blood pressure and a tremor.  There would be a whole lot of symptoms, Professor Peach said, and a person would require medical treatment.  Professor Peach said that a person can be treated if he or she is acutely poisoned with an organophosphate.  If he or she does not seek medical treatment, it would set him or her back in dealing with the disease. 

1. Professor Peach said that a cocktail of DDT and Malathion would not have been used.  DDT was phased out of use in Australia in the early 1970s whereas most of the rest of the western world had phased it out in 1960s.  Malathion was sprayed because there was concern about an outbreak of encephalitis in New South Wales. 

1. In cross-examination, Professor Peach said that he did not consider dizziness, exhaustion and nausea as indicative of early symptoms of polyneuropathy.  DDT acts on the central nervous system and he did not know of a single paper suggesting that it could cause polyneuropathy.  Nor did he think that Malathion caused it.  When he is looking for a cause, he said, he asks five questions:

What clinical features are exhibited and are they a known neurological toxic effect of DDT or Malathion?  The answer is that a progressive disease leading to Mr Lilley’s symptoms is not known.  Malathion is widely used in the world and has been for the past 20 years.  If there were a relationship, it would have been found by now.

Do the symptoms match the degree of exposure?  Professor Peach said that he could find nothing to suggest that Mr Lilley’s exposure was anything other than normal.  He did not complain of blurred vision or of respiratory problems.  Malathion is absorbed so rapidly that symptoms occur rapidly.  If Mr Lilley’s exposure has been normal, his symptoms are out of all proportion.

Are there signs of having been intoxicated?  There are none in Mr Lilley’s case.  He never complained of acute symptoms associated with Malathion poisoning. 

Did the symptoms improve or stabilise after he was removed from exposure?  They did not and in fact took two years to appear and then worsened.

Did other people with whom Mr Lilley was associated suffer similar symptoms?  The answer is that they did not.

1. Professor Peach considered whether drugs that Mr Lilley took while he was in New Guinea as a prophylaxis against malaria could have caused his condition.  He considered the possibility that he was given chloroquine or proguanil.  There is evidence that patients given at least 500mg of chloroquine each day for a year for the treatment of malaria (as opposed to preventing the contraction of malaria) or 250mg for the treatment of a disease other than malaria may develop a combination of sensorimotor peripheral neuropathy and myopathy.  There have been no reports of polyneuropathy in patients taking proguanil.

1. The only micro-organisms known to cause polyneuropathy are Mycobacterium leprae, human immuno deficiency virus, Borrelia burgdorferi, Crynebacterium diphtheriae and varicella zoster virus but there is nothing that points to Mr Lilley’s having been infected with any of these micro-organisms whilst in New Guinea.

1. Professor Peach considered whether hot and humid conditions in New Guinea could have played a role.  He said that unacclimatised visitors to hot climates can suffer heat stroke and altered consciousness.  Although permanent neurological abnormalities may persist after satisfactory cooling in a few patients but those abnormalities do not include a slowly progressive polyneuropathy five years later.

1. Professor Peach said that Professor Sim would have interest in measuring red blood cell cholinesterase in persons exposed to pesticide because he is concerned with people in the workforce.  The red cells remain impaired for a longer time and, if a person’s red cells drop below 30 to 25% of the norm, he or she is removed from exposure until the red cell count increases.  A person only shows symptoms when the level is below 25%.  It is very rare for a person to drop below 30%, Professor Peach said. 

1. With regard to Mr Lilley’s blood noses, Professor Peach said that he understood Mr Lilley to have suffered his first blood nose in 1961.  Blood noses can be hereditary and there is a need to look at what happens over the next 10 to 15 years.  They have been gradually dropping.  It is not surprising that he has since been treated with iron for anaemia.  Tiredness and dizziness are compatible with frequent nose bleeds and it is a distressing condition.  Mr Lilley’s condition now, though, has nothing to do with his nose bleeds, Professor Peach said. 

Dr Chambers

1. Professor Brian Chambers is a neurologist, who was not called to give evidence but who prepared three reports dated 14 June, 2002, 10 July, 2002 and 27 February, 2003 respectively..  In his first report, Professor Chambers said, in part:

“1.      …

There is unlikely to be a genetic cause.  There is no family history of neurological disease and genetic testing for Charcot-Marie-Tooth disease and Kennedy’s syndrome was negative. 

He was found to have an IgM Iamda monoclonal gammopathy.  The concentration of this paraprotein was 8 g/L on one occasion and 15 g/L on another, both regarded in the clinically significant range.  Usually the peripheral neuropathy associated with monoclonal gammopathy is of demyelinating type and in some cases anti-myelin associated with glycoprotein (MAG) can be identified.  In other cases, the IgM paraprotein shows activity against GM1 and these cases can be expressed as chronic progressive muscular atrophy or multifocal motor neuropathy with conduction block.  There has also been a report of IgM axonal neuropathy with M protein showing antibody activity against chondroitin sulphate A.  It does not appear as though Mr Lilley’s IgM lamda paraproteinaemia has been fully investigated.  I notice that IgM monoclonal gammopathy is listed in the specified list of haematological or lympho-proliferative disorders in the Statement of Principles for peripheral neuropathy.  I do not know the cause of IgM monoclonal gammopathy and a haematological opinion should be considered.

The chronic progressive axonal peripheral neuropathy Mr Lilley suffers from is of the dying back variety and sometimes due to toxic exposure.  There appears to be good evidence that Mr Lilley was exposed to dichlorodiphenyltrichloroethane (DDT), an organochlorine insecticide as well as malathion, an organophosphate insecticide as a consequence of regular spraying during his period of service in Papua, New Guinea and also while stationed at Point Cook.  Fifteen years after this exposure there was measurable organochlorine residues.  In addition metabolic testing has revealed depression of the cytochrome P450 pathway which would increase the clinical effects of exposure to DDT.  Associate Professor Malcolm Sim has indicated that delayed chronic progressive neuropathy is certainly possible with DDT and has been described with malathion (organophosphate-induced delayed neuropathy.

2.The clinical onset of the condition appears to have been around 1978 when weakness and muscle wasting in the left arm were noted.  The diagnosis of peripheral neuropathy was made around 1981 when he was investigated by the Neurology Department at Heidelberg Repatriation Hospital.

3.As indicated above, IgM monoclonal gammopathy is on the specified list of haematological or lympho-proliferative disorders referred to in Clause 5 of the Statement of Principles concerning peripheral neuropathy.  Neither DDT nor malathion are included in the specified list of chemical agents.  Organo-phosphorous pesticide poisoning is only relevant if exposure occurred within 30 days before clinical onset of peripheral neuropathy.

4.I believe there is a ‘reasonable hypothesis’ linking the development of his chronic progressive axonal sensory motor peripheral neuropathy to DDT and/or malathion exposure.” (Exhibit R4)

1. In his second report, Professor Chambers said that he considered that Mr Lilley’s condition had been caused or aggravated by his service on the basis that his type of peripheral neuropathy could have been caused by toxic exposure.  He has been exposed to DDT and Malathion over an extended period and he has an inherited metabolic abnormality which would make him abnormally susceptible to the effects of these chemicals.  His IgM gammopathy is the only other potential cause of his peripheral neuropathy and that is normally associated with a peripheral neuropathy quite different from that from which Mr Lilley suffers.

1. When he wrote his third report, Professor Chambers had considered reports from Professor Peach and Dr Hjorth.  He wrote:

“Whilst I do not disagree with any of the factual material presented in these reports, and I acknowledge that the accepted view of toxin-related axonal peripheral neuropathy calls for a fairly tight temporal association between exposure and development of symptoms, there are still lingering doubts in my mind concerning the possibility of past toxic exposure and delayed development of neurological symptoms.

The majority of cases of chronic axonal peripheral neuropathy are idiopathic.  It is easy to relate a peripheral neuropathy to toxic exposure when neurological symptoms occur very soon after exposure to the toxin.  It is more difficult to prove an association when there is a long latency between exposure and onset of symptoms and the progression of symptoms occurs at a much slower rate.  However, absence of proof of an association does not prove absence of an association.  There are other neurological degenerative conditions where exposure to a toxin (s) is suspected but unproven.

Notwithstanding the above comments, I am happy to modify my opinion in line with the opinions of Drs Peach and Hjorth concerning the ‘balance of probabilities’ standard of proof.  I consider that although it is possible that the applicant’s condition of peripheral neuropathy was caused or aggravated by his service, it is more likely not to have been caused or aggravated by his service.” (Exhibit R8)

THE LEGISLATIVE FRAMEWORK – THE VE ACT

1. Pursuant to sub-section 70(1), the Commonwealth is liable to pay a pension by way of compensation to a member of the Forces if he or she has become incapacitated from a defence-caused injury or defence-caused disease.  Provision is made for that compensation in Part IV of the Act.  A veteran’s injury or disease is taken to have been “defence-caused” if it meets one of the criteria specified in ss. 70(4) or (5).  In so far this case is concerned, only ss. 70(5)(a) is relevant.  In so far as they are relevant to the circumstances of this case, they provide that:

“For the purposes of this Act, … an injury suffered by … a member shall be taken to be a defence-caused injury or a disease contracted by such a member shall be taken to be a defence-caused disease if:

(a)  the … injury or disease, as the case may be, arose out of, or was attributable to, any defence service, or peacekeeping service, as the case may be, of the member;

…”

1. The expression “defence service” is defined in ss. 68(1) and 5Q(1A).  As Mr Lilley has continuous full-time service rendered on or after 7 December, 1972 and before 7 April, 1994, he meets the requirements of s. 68(1)(a) of the definition and so has defence service from 7 December, 1972 until 7 November, 1986. 

1. The VE Act provides for the level of proof that the Tribunal must find before it may decide that an injury or disease is defence-caused. It is found in s. 120(4), which provides:

“Except in making a determination to which subsection (1) or (2) applies, the Commission shall, in making any determination or decision in respect of a matter arising under this Act or the regulations, including the assessment or re-assessment of the rate of a pension granted under Part II or Part IV, decide the matter to its reasonable satisfaction.”

1. The meaning of the expression “reasonably satisfied” has been considered by the Federal Court in Smith v Repatriation Commission (1987) 74 ALR 537. After considering the authorities, Beaumont J concluded that the Tribunal:

“… should have asked itself whether on the facts of the case, it was persuaded on the civil standard. There is, in this connection, a distinction of substance to be drawn between the probabilities on the one hand and mere possibilities, even if they are real as distinct from fanciful, on the other (see Re Repatriation Commission and Delkou (1986) 9 ALD 354; Re Easton and Repatriation Commission (1987) 12 ALD 777; Re Repatriation Commission and Falkner 12 ALD 87. ” (page 547)

1. Section 120(4) must be read with s. 120B, which provides, again in so far as it is relevant to this case, that:

(1)“This section applies to any of the following claims made on or after 1 June 1994:

(a)…

(b)a claim under Part IV that relates to the defence service (other than hazardous service) rendered by a member of the Forces.

…

(3)In applying subsection 120(4) to determine a claim, the Commission is to be reasonably satisfied that an injury suffered by a person, a disease contracted by a person … was war-caused or defence-caused only if:

(a)the material before the Commission raises a connection between the injury, disease … of the person and some particular service rendered by the person; and

(b)there is in force:

(i)a Statement of Principles determined under subsection 196B(3) or (12); or

(ii)a determination of the Commission under subsection 180A(3);

that upholds the contention that the injury, disease … of the person is, on the balance of probabilities, connected with that service.

(4)Subsection (3) does not apply in relation to a claim in respect of the incapacity from injury or disease … of a person if the Authority has neither determined a Statement of Principles under subsection 196B(3), nor declared that it does not propose to make such a Statement of Principles, in respect of:

(a)the kind of injury suffered by the person; or

(b)the kind of disease contracted by the person; or

(c)…;

as the case may be.”

1. The Authority to which reference is made in s. 120B(4) is the RMA.  The RMA must determine a SoP in relation to claims to be assessed according to ss. 120(1) and (3), and so by reference to a reasonable hypothesis, on the one hand and s. 120(4), and so by reference to reasonable satisfaction, on the other (s. 196B).   We are concerned only with those relating to assessment by reference to reasonable satisfaction:

“If the Authority is of the view that on the sound medical-scientific evidence available it is more probable than not that a particular kind of injury, disease or death can be related to:

(a)…

(b)defence service (other than hazardous service) rendered by members of the Forces;

the Authority must determine a Statement of Principles in respect of that kind of injury, disease or death setting out:

(d)the factors that must exist; and

(e)which of those factors must be related to service rendered by a person;

before it can be said that, on the balance of probabilities, an injury, disease or death of that kind is connected with the circumstances of that service.” (s. 196B(3))

1. The opening words of the provision refer to a particular injury or disease’s “being related to” the veteran’s service.  Section 196B(14) defines the concept of “related to service” in terms consistent with those used in s. 70(5)(a) and (d) in relation to “defence-caused injury” and “defence‑caused disease”.  In so far as it is relevant, s. 196B(14) provides that:

“A factor causing, or contributing to, an injury, disease or death is related to service rendered by a person if:

(a)…

(b)it arose out of, or was attributable to, that service; …

(c)…

(d)it was contributed to in a material degree by, or was aggravated by, that service; …

(e)…

(f)…

(g)…”

“Sound medical scientific evidence” has the meaning given in s. 5AB(2)
(s. 5AB(1)):

“Information about a particular kind of injury, disease or death is taken to be sound medical-scientific evidence if:

(a)the information:

(i)is consistent with material relating to medical science that has been published in a medical or scientific publication and has been, in the opinion of the Repatriation Medical Authority, subjected to a peer review process; or

(ii)in accordance with generally accepted medical practice, would serve as the basis for the diagnosis and management of a medical condition; and

(b)in the case of information about how that kind of injury, disease or death may be caused - meets the applicable criteria for assessing causation currently applied in the field of epidemiology.” (s. 5AB(2))

1. How does the RMA decide whether it should come to a view about a particular kind of injury, disease or death and determine a SoP?  This question may be answered by reference to ss. 196E and 196B(4).  If the RMA receives a request from a person or body specified in s. 196E(1) to carry out an investigation in respect of a particular kind of injury, disease or death, it must do so (s. 196B(4)(a) and s. 196E(1)(d)).  Its investigation is conducted in order to obtain information that would enable the Authority to establish how the injury may be suffered, the disease may be contracted or the death may occur and the extent, if any, to which the injury, disease or death may, in the circumstances of this case, be war-caused (s. 196B(4)(c) and (d)).  Those persons or bodies entitled to make a request under s. 196E are the Commission, a person eligible to make claim for a pension under Part II or IV or any organisation representing, in the circumstances of this case, veterans or their dependants (s. 196E(1)(a), (b) and (c)).  The RMA may also decide of its own initiative that a particular kind of injury, disease or death ought to be investigated to find out whether a SoP may be determined in respect of it (s. 196B(4)(b)).

1. Whether the investigation arises as a result of a request or on its own initiative, the RMA must publish a notice in the Government Gazette that it is carrying out that investigation and inviting interested persons or organisations authorised to make written submissions under s. 196F(1) to do so (s. 196G(1)).  The Authority must determine a SoP in respect of an injury, disease or death as soon as possible after carrying out the investigation if it is of the view that there is sound medical-scientific evidence on which it can rely to determine a SoP under ss. 196B(2) or (3) (s. 196B(5)) or if that evidence is insufficient to allow it to do so, the RMA must state in writing that it does not propose to make a SoP and give reasons for its decision (s. 196B(6)).

1. A SoP may be reviewed by the RMA in certain circumstances as may a decision that it does not propose to make a SoP.  A person or body specified in s. 196E may ask it to do so or the RMA may do so if it thinks that there are grounds for such a review.  It may also be directed by the Specialist Medical Review Council (“Review Council”) under s. 196W(7) to do so (s. 196B(7)).  If it decides of its own accord or receives a request or direction, the Authority must, subject to certain provisos set out in s. 196C(4) in relation to a request from a person or body specified in s. 196E, carry out an investigation to find out if there is new information.  That new information must, in the circumstances of this case, relate to how the injury may be suffered, the disease may be contracted or the death may occur, or the extent to which the disease, injury or death may be war-caused (s. 196B(7)(d) and (e)).

16.    However this approach overlooks the clear words of the applicable Statements of Principles and the function they perform in the legislative scheme.  In relation to SoP1, the definition of ‘generalised anxiety disorder’ does not suggest that the disease exists if only some but not all of the symptoms (or features) are manifest.  The exception to this statement is par C which provides that only three of the six specified symptoms are necessary for the disease to exist, though in the frequency and for the period identified.  The purpose of the definition is to identify those symptoms (or features) which, if observed by a clinician, would warrant a conclusion that the patient suffered from generalised anxiety disorder.  While it is true that Statements of Principles are directed to causation, the means of establishing the necessary link in SoP1 between disease and war service is to require that the symptoms (or features) of the disease are, in a case such as the present, revealed within two years of the veteran experiencing a severe psychosocial stressor (relevantly, during operational service).  This is intended to establish sufficient proximity between the experiences during operational service and the manifestation of the disease to point to a causal link to sustain the hypothesis.  In our view, the Tribunal did not err in its approach to the meaning of the expression ‘clinical onset’. (paragraphs 13-16) (pages 488-490)

1. Dr Hjorth and Professor Peach both considered that the first appearance of symptoms enabling a diagnosis of polyneuropathy to be made occurred in 1978 when Mr Lilly exhibited signs of wasting in his left arm although the diagnosis was not actually made until some time later.  Mr Lilley suffered from blood noses, exhaustion and dizziness.  The evidence as to when he first did so is inconsistent for Mr Lilley said that he suffered from his first in 1973 when he was based in Canberra but Professor Peach, who had examined the medical records, dated them from 1961.  Whether or not this is significant depends upon whether or not they are relevant symptoms in Mr Lilley’s condition.  Dr Allen said that they were relevant although he acknowledged that they could have another cause such as a weakened artery.  He only associated headaches and nausea with blood noses if there was a sufficient loss of blood.  Dr Hjorth and Professor Peach took a different view.  Both considered that they were not relevant.  The weight of medical evidence persuades us on the balance of probabilities that blood noses are not a symptom relevant to polyneuropathy and so there is no need to consider further the date of their onset.

1. Dr Hjorth considered that a lack of hand eye coordination could possibly be a symptom of polyneuropathy.  That was something that Mr Lilley said that he noticed in Canberra where he was based from the end of 1976 and remained for a year.  He did not go so far as to say that the appearance of that symptom would have enabled a diagnosis of polyneuropathy to have been made at that stage and, in view of the evidence of Dr Hjorth and Professor Peach, we find that the clinical onset occurred in 1978.

1. That is not an end of the matter, though for it is not enough that the clinical onset of polyneuropathy occur during Mr Lilley’s service.  It must be consistent with SoP 80 as amended.  On its face, the most likely factor is that in clause 5(k)(iv) for it relates to organophosphates.  We have no evidence that Malathion is a pesticide specified in the list in clause 8 of SoP 80.  We have evidence on which we are satisfied that it is an organophosphate pesticide.  While the pesticides listed must also be presumed to be organophosphates we cannot, without evidence, make the leap that Malathion is one of the listed pesticides.  That would be enough to end the matter but, should we be incorrect in that conclusion, we considered SoP 80 on the basis that Malathion is a listed pesticide.

1. That requires us to consider whether Mr Lilley suffered from any cholinergic health effects immediately after exposure to organophosphorous pesticides within 30 days before the clinical onset of peripheral neuropathy.  The word “cholinergic” means “Pertaining to or designating the type of chemical activity characteristic of acetylcholine or of agents which mimic the actions of acetylcholine …” (Blakiston’s Gould Medical Dictionary, 4^th edition, 1979).  Consequently, “cholinergic health effects” means effects on a person’s health that are consistent with the effects of the chemical activity of acetylcholine in the body. 

1. Assuming that Malathion, which is an organophosphorous pesticide, was sprayed in Point Cook, there is no definitive evidence of what was sprayed and nor is there evidence when the last spraying took place in Point Cook.  Furthermore, even if Mr Lilley’s lack of hand eye coordination can be said to be cholinergic health effects, there is no evidence that he suffered from it within 30 days of the last spraying.  He left Point Cook on 14 December, 1976 and did not suffer from the lack of hand eye coordination until he was in Canberra.  He did not say whether he identified it in Canberra in his first two weeks in that city at the end of 1976 or in 1977.  Taking the lack of evidence as to the time of spraying and the time at which Mr Lilley first suffered from lack of hand and eye coordination, we are not satisfied on the balance of probabilities that he suffered organophosphorous pesticide poisoning from one of the specified pesticides within 30 days before the clinical onset of peripheral neuropathy.

1. On the balance of probabilities, we are satisfied that Mr Lilley does not satisfy any of the other factors.  There is no reference to DDT or to climatic factors.  If, therefore, the SoP regime is relevant, we are not satisfied that Mr Lilley’s polyneuropathy arose out of or was attributable to either his eligible war service or his defence service as we are not satisfied that any of the factors in SoP 80 as amended by SoP 14, or indeed, SoP 80 before its amendment, has been established.

1. That brings us to consider the Commission’s decision without reference to the SoP regime for that was the situation when the Commission made it.  We are now not confined to the factors that are set out in the SoP but may consider the factors raised by Mr Lilley.  They seem to be the effects of Malathion and/or DDT poisoning, environmental factors including heat and humidity in New Guinea and a mixture of all of the above.  Our finding in relation to the clinical onset of Mr Lilley’s condition in 1978 remains relevant.

1. Only Dr Allen supports a finding, on the balance of probabilities, that Mr Lilley’s polyneuropathy has the necessary connection with his eligible war service or defence service.  He considered there was the connection on all three bases.  His evidence was inconsistent with that given by Dr Hjorth, Professor Sim and Professor Peach and it was not supported by the literature to which he referred.  The literature does not support a polyneuropathy that develops without an incident of poisoning or acute exposure as opposed to episodic exposure of the sort experienced by Mr Lilley.  Furthermore, it does not support the onset of polyneuropathy after a delay between exposure and the onset of clinical symptoms of a period beyond a matter of weeks or months in the case of Malathion.  It does not support its onset after a considerable amount of time and up to at least two years after his last exposure to Malathion.

1. In relation to exposure to DDT, Dr Allen has based his opinion on Mr Lilley’s DDE levels and to his decreased rate of caffeine clearance but their relevance is contradicted by Professor Sim, Dr Hjorth and Professor Peach.  Having considered the scientific basis of their evidence, we prefer it.  The DDE levels are not indicative of the level of DDT exposure some 30 years ago.  We find that caffeine clearance is not relevant as it varies from person to person, from time to time and decreases as a person ages.  As Dr Hjorth said, Mr Lilley’s level of DDE is only just measurable and we are satisfied that it does not lead us to any conclusion as to the degree of Mr Lilley’s exposure.  We are also satisfied on the basis of the evidence of Professor Sim, Professor Peach and even of Dr Allen that DDT is more likely to affect the central nervous system rather than the peripheral nervous system, which has been affected in Mr Lilley’s case.   Having regard to all of the evidence, we are not satisfied that Mr Lilley’s condition arose out of or was attributable to spraying of DDT during any part of his service.

1. We have considered the other factors explored by the medical witnesses during their evidence and touched upon by Mr Lilley.  The most that any of the medical experts other than Dr Allen will go is to say that Mr Lilley’s condition might possibly have arisen out of or been attributable to them.  They have searched for a connection with great care and with reference to scientific papers and reports and we prefer their considered approach to that of Dr Allen who is most sincere in his opinions but cannot point to any material to support them.

1. For these reasons, we are not satisfied that Mr Lilley’s condition, which has variously described as peripheral neuropathy due to axonal degeneration, chronic idiopathic axonal neuropathy and sensory motor polyneuropathy, arose out of or was attributable to either his eligible war service or to his defence service and so is not war-caused or defence caused.  Therefore, we affirm the decision of the Commission dated 15 June, 1998 and affirmed by a decision of the VRB dated 27 March, 2001.

The 1930 Act

1. In the case of Mr Lilley, the personal injury that is said to have happened is the peripheral neuropathy, however described, from which he suffered.  The question is whether it was “by accident arising out of or in the course of his employment by the Commonwealth”. The words as they are used in s. 9 of the 1930 Act were considered in a number of cases including Kavanagh v The Commonwealth (1959-1960) 103 CLR 547, Dixon CJ, Fullagar and Menzies JJ, Taylor and Windeyer JJ dissenting). Having traced the history of provisions such as that in s. 9 and noting that they had originally provided that the injury must both “arise out of” and “be in the course of” employment rather than being expressed in the alternative as in s. 9, Dixon CJ said:

“Few, if any, expressions had received so much judicial consideration and in so many jurisdictions as had the words ‘personal injury by accident arising out of and in the course of the employment’.  Repeatedly the contrast had been made between the effect of the words ‘out of’ and the effect of the words ‘in the course of’.. Whatever language was chosen to institute the contrast the first expression was treated as requiring a causal connexion between the employment or its incidents and the second as requiring that the pursuit of the employment should be an accompanying condition. I have seen nothing to suggest that within the expression ‘in the course of the employment’ there had been discovered any element of causal relation with the employment and its incidents. To prescribe that element was considered to be the work of the words ‘arising out of’.. It was thus natural for this Court to say after the word ‘or’ had been substituted for ‘and’ in the Western Australian provision that the result of English authority was ‘to show that the words “arising in the course of the employment” describe a condition which is satisfied if the accident happens while the workman is doing something in the exercise of his functions although it is no more than an adjunct to or an incident of his service’.  That was said in Pearson v Fremantle Harbour Trust ((1929) 42 CLR 320 at pp. 329, 330)…” (page 556)

1. For the reasons we have already given in relation to our consideration under the VE Act in the absence of the SoP regime, we are not satisfied that there is the necessary causal relationship between Mr Lilley’s condition and his service. Only Dr Allen supports such a relationship and, for the reasons that we have already given, we prefer the evidence of the other medical experts, who support a conclusion that there is a possibility that it arose out of, or in the course of, his employment but not of a probability that it did so. That is so whether the possible cause of Mr Lilley’s condition is said to be from Malathion, DDT, heat effects or a cocktail of events associated with his service.

1. In reaching that conclusion, we are mindful of the distinction drawn by the New South Wales Court of Appeal in State of New South Wales trading as New South Wales Department of Agriculture v Allen [2000] NSWCA 141 (Priestley, Powell and Heydon JJA) between proof of a fact to the satisfaction of a tribunal on the balance of probabilities and proof of a fact for scientific purposes to the satisfaction of those expert in the particular field of science. This has not been a case of perusing the evidence to find the necessary causal connections to a scientific level but to find evidence that supports it at any level. Only the evidence of Dr Allen does so but the basis upon which he founds his opinion does not, in our view, provide the necessary causal relationship at anything above the level of a possibility. It finds no support in the studies that have been undertaken and both DDT and Malathion are pesticides that have been in the public domain for a sufficient period and under sufficient scrutiny to have some confidence that there would be at least reports of clinical signs similar to those suffered by Mr Lilley were there a causal connection between his condition and his exposure. The caffeine tests do not assist and nor do the tests relating to IgM gammopathy for there is no evidence suggesting a link between that and Mr Lilley’s condition. Dr Hjorth raised it as a possibility but only on the basis that he did not know of its relevance and Professor Peach clearly rejected it on the basis that it attacked the myelin sheath and not the axon as in Mr Lilley’s case. That is short of satisfying us on the balance of probabilities and we have had no regard to the far higher standard of proof that would apply were we seeking to establish the link in scientific terms.

1. We have also considered a further case considered by the New South Wales Court of Appeal.  That is the case of Seltsam Pty Limited v McGuiness [2000] NSWCA 29 (Spigelman CJ and Davies AJA, Stein JA dissenting) in which the majority held, as is expressed in a summary at the outset:

“1.     Epidemiological evidence that exposure to a substance is a possible cause of an injury may be used to establish that the exposure is a legal cause of the injury. 

2.       The balance of probabilities test is not satisfied by evidence which fails to do more than establish a possibility: St George Club Ltd v Hines (1961-62) 35 ALRJ 106; Tubemakers v Fernandez (1976) 50 ALJR 720; Fernandez v Tubemakers of Australia Ltd (1975) 2 NSWLR 190.

3.      …

4.       Causation in an individual case can be established by a process of inference from circumstantial evidence which combines primary facts like ‘strands in a cable’..  Epidemiological evidence of the effects on populations of exposure to a substance is circumstantial evidence which may form part of this process inference.”

1. Spigelman CJ, with whom Davies AJA agreed, explained the fourth aspect in a little more detail in his judgement:

“       As I have also noted above, a circumstantial case can involve drawing a conclusion on the balance of probabilities, or indeed beyond reasonable doubt, on the basis of facts which are expressed only in terms of possibility.  Whether or not the inference is open or should be drawn, depends on the quality of the underlying facts, particularly in terms of the degree of ‘possibility’ which is involved.” (paragraph 153)

1. This is a case in which, sadly, we do not think that the strands of possibility can be woven to form a cable supporting our finding the necessary causal connection on the balance of probabilities.  On the basis of our analysis of the evidence, we consider that the strands are no more than conjecture and do not satisfy us on the balance of probabilities.

The 1971 Act

1. What is meant by the expression “a contributing factor” as it is used in s. 29(1)?   The leading case in this area is Federal Broom Co Pty Ltd v Semlitch (1964) 110 CLR 626 (McTiernan, Kitto, Taylor, Windeyer and Owen JJ) in which the High Court considered the provisions of the New South Wales Workers’ Compensation Act 1926.  In considering whether or not an employee’s employment was a contributing factor to the aggravation or acceleration of her disease, Windeyer J said at pages 641-642:

“I pass then to the next, and I think more difficult, question, was this aggravation or deterioration contributed to by her employment?  This requirement of the Act is not satisfied by showing only that a worker suffering from some disease would or might have suffered less severely if he had not been employed at all.  When the Act speaks of ‘the employment’ as a contributing factor it refers not to the fact of being employed, but to what the worker in fact does in his employment.  The contributing factor must in my opinion be either some event or occurrence in the course of the employment or some characteristic of the work performed or the conditions in which it was performed.  In this case it was said that the employment was a contributing factor in the worsening of the disease, because the applicant focussed her delusions of pain and discomfort upon her right side which she believed she had hurt when lifting a tea chest in the course of her work.  A minor physical strain she magnified in her irrational imagination into a serious and continuing derangement of her internal organs.  The incident directed, or re-directed, her hypochondriacal attention to her abdominal muscles.  But said the appellant, all that it did was to focus her existing delusional tendencies in a particular way: it was a cause of her condition only in the sense that it acted as a precipitant.  That may be true: nevertheless, Doctor Ellard agreed that ‘something obviously happened in December to her to cause a change in her way of life’.

The question involved is difficult.  Can the event to which a disordered mind irrationally attributes physical suffering, that is real to the patient but delusional, be properly called a contributing factor?  Ordinary concepts of cause and consequence are perhaps not applicable.  Yet it seems to me that the incident which precipitated or stimulated, however irrationally, the worsening of her condition could be regarded as a factor contributing to it.  It was said that in any event she might have broken down sooner or later: that some other incident might have provided a focus for her delusions.  But it was this event at work that in fact did so.”

1. Provided that it is a person’s employment, or some aspect of it, that has aggravated or accelerated his or her disease, there is no need to establish that the employment or any aspect of it was in any way out of the ordinary.  That is to say, the person does not need to establish that the employer was at fault in some way.  As Pincus J said in O’Neill v Commonwealth Banking Corporation (1987) 75 ALR 154 (Pincus J):

“It is, of course, not the law that mental conditions caused by employment are compensable only if there is unusual stress or extra stimulus, although no doubt the absence of such stress would make it more difficult to show a causal connection between a mental condition and the employment. Nor is it the law that only neurotic conditions arising in circumstances in which an ordinary man of normal personality would become neurotic (if there are such circumstances) are compensable.” (page 159)

1. Whether employment contributes to the contraction, aggravation, acceleration or recurrence of the disease is a question of fact. In Re Welsford and Commonwealth Banking Corporation (1984) 1 AAR 42, Davies J said at 43:

   “It is sufficient that the employment contributes to the contraction, aggravation, acceleration or recurrence of the disease. The contributing factor need do no more than contribute in a material way. The factor is not required to be the real, proximate or effective cause of the disease or of its development. In a case where a number of separate factors contribute to the contraction of a disease or its acceleration, aggravation or recurrence, all that is required is that one such factor exhibits the necessary connection with the worker's employment. See Federal Broom Co Pty Ltd v Semlitch (1964) 110 CLR 626 at 641-643 per Windeyer J and Favelle Mort Ltd v Murray (1976) 133 CLR 580 at 598 per Mason J. Moreover, as Barwick CJ said in Favelle's case at 585:

   ‘..the idea that the employment must have been of a nature to carry a special risk of suffering injury of some particular kind has been exploded and is no longer valid.’

   Similarly, in Thom or Simpson v Sinclair [1917] AC 127 at 145, Lord Parmoor said:

   ‘The fact that the risk may be common to all mankind does not disentitle a workman to compensation if in the particular case it arises out of the employment.’

His Lordship was there considering a case of injury ‘arising out of’ employment but the principle which he expounded is equally applicable with respect to a disease in respect of which the worker’s employment is a contributing factor.” (pages 43-44)

1. This is consistent with the views expressed by Davies in Australian Telecommunications Commission v Treloar (1989) 90 ALR 202 (Davies J), to which Mr Croyle referred. His Honour said:

“… The test propounded by the 1971 Act, like the test propounded by the 1988 Act, requires that there be a contribution of a causal nature and therefore that the contribution be causally significant or, to use another term, material.  …” (page 204)

and later:

“In discussing, in Bendy’s case [Repatriation Commission v Bendy (1989) 18 ALD 144] this particular issue, the point that melanoma is brought about by exposure to sunlight, I said, inter alia:

‘If a veteran develops a disease as a result of his war service or if some event involved in the disease, it is not necessary to show that the factor was of a special character or involved any special risk. …” (page 206)

1. For the reasons we have previously given, we are not satisfied that any aspect of Mr Lilley’s service was, on the balance of probabilities, a contributing factor in his contracting his condition or in its aggravation or acceleration in any way.  We will not repeat those reasons. 

1. We have also considered the case of Johnston v Commonwealth of Australia (1982) 43 ALR 559 (Gibbs CJ, Mason, Murphy and Wilson JJ) to which Mr Croyle referred. In that case, Mr Johnston’s son had served in the Royal Australian Navy. In 1970, he reported to a military hospital in Vietnam complaining of a pain in the region of the bowel. He was told that he was suffering from haemorrhoids and was given medication for that condition. He continued to suffer pain and took the medication but did not seek further treatment until 1974 when he was diagnosed as suffering from bowel cancer. He died in 1975. The essence of the judgements is found in the headnote to the case and it reads, in part:

“(i)    The failure to diagnose and treat the cancer resulted in a worsening or aggravation of the condition when compared with the course which, given timely treatment, it should have taken.  This should properly be seen as an aggravation of the disease within the meaning of the Act.

Lee v Minister of Pensions (No 2) (1948) 3 War Pensions Reports 1901, applied.

Ogeden Industries Pty Ltd v Lucas (1967) 116 CLR 537, distinguished.

(ii)     The course taken by the disease between 1970 and 1974 was a direct consequence of the failure in 1970 to diagnose its presence and thereafter to provide appropriate treatment.  That failure occurred in the course of the employment of the appellant’s son and was related directly to it.  The employment was therefore a contributing factor to the aggravation of the disease.” (page 559)

1. In our view, the principles in this case are not applicable in the circumstances we must consider.  On the evidence, we are not satisfied that any failure to diagnose Mr Lilley’s condition contributed in any way to its course.  Professor Peach and Dr Hjorth both said that the only form of treatment would have been to give him physical aids to cope.  In other words, there is no known treatment that could have altered the course of the disease.  We have considered whether removal of Mr Lilley from his workplace would have made a difference to the course of his condition.  On the findings that we have made, the earliest that this course could have been considered would have been 1978 with the disease’s clinical onset.  By that time, removal would have been irrelevant for Mr Lilley was no longer exposed to any of the factors to which he attributes responsibility for his condition.  Even if it could have been diagnosed at an earlier stage, we are satisfied that there would have been no difference in outcome.  That follows from our being satisfied that none of the factors in Mr Lilley’s service contributed to his condition.

1. It follows that we are not satisfied on the balance of probabilities that Mr Lilley’s employment was a contributing factor to his contraction of polyneuropathy, however described, or to its aggravation or acceleration in the context of the 1971 Act.

1. For the reasons we have given, we affirm:

1.a decision of a delegate of the respondent, Comcare, dated 23 October, 1999 to affirm an earlier determination dated 29 January, 1999; and

2.a decision of the respondent, the Repatriation Commission, dated 15 June, 1998 and affirmed by a decision of the Veterans’ Review Board dated 27 March, 2001.

I certify that the one hundred and thirty-nine preceding paragraphs are a true copy of the reasons for the decision herein of Deputy President S A Forgie,

Dr P D Fricker (Member) and

Associate Professor J H Maynard (Member)

Signed:           ................................................................
  P. Paczkowski  Associate

Date/s of Hearing  9 September, 2002;
  12 and 13 March, 2003
Date of Decision  1 August, 2003
Counsel for the Applicant             Mr M. Croyle
Solicitor for the Applicant            Williams Winter
Counsel for Comcare  Mr J. Lenczner
Solicitor for Comcare                   Sparke Helmore

Solicitor for the Commission       Mr K. Rudge, departmental advocate