Hornibrook and Repatriation Commission
[2001] AATA 160
•2 March 2001
DECISION AND REASONS FOR DECISION [2001] AATA 160
ADMINISTRATIVE APPEALS TRIBUNAL )
) No V99/35
VETERANS' APPEALS DIVISION )
Re BETTY MAY HORNIBROOK
Applicant
And REPATRIATION COMMISSION
Respondent
DECISION
Tribunal Mrs Joan Dwyer, Senior Member Mr A Argent, Member Mr C Ermert, Member
Date2 March 2001
PlaceMelbourne
Decision The Tribunal affirms the decision under review
(Sgd) Joan Dwyer
Senior Member
VETERANS' AFFAIRS - death - whether war-caused - whether reasonable hypothesis raised - hypothesis that exposure to volcanic fumes may have caused asthma which contributed to death - conflicting medical evidence as to whether chronic asthma could develop as a result of exposure to volcanic fumes - whether that part of hypothesis contrary to scientific facts - whether lack of oxygen due to respiratory problems contributed to death from cardiogenic shock - no factual foundation to that hypothesis - clinical records show that low oxygen levels did not contribute to death - decision affirmed
PRACTICE AND PROCEDURE –whether s 120(4) of Veterans' Entitlements Act 1986 requires review and possible amendment
Veterans' Entitlements Act 1986 ss 120(1), (3) and (4)
McKenna v Repatriation Commission (1999) 29 AAR 70
Keeley v Repatriation Commission (1999) 56 ALD 455
Repatriation Commission v Webb, Full Federal Court, 5 November 1998, 981411/1998
Bushell v Repatriation Commission (1992) 109 ALR 30
Byrnes v Repatriation Commission (1993) 116 ALR 210, 30 ALD 1
East v Repatriation Commission (1987) 74 ALR 518
Statement of Principles Instrument No. 59 of 1996
Statement of Principles Instrument No. 75 of 1997
REASONS FOR DECISION
2 March 2001 Mrs Joan Dwyer, Senior Member Mr A Argent, Member Mr C Ermert, Member
background
This is an application for review of a decision of the Repatriation Commission made 1 February 1996 which refused Mrs Hornibrook's claim for war widow's pension under the Veterans' Entitlements Act 1986 ("the Act") on the ground that the death of her husband, Roy Hornibrook, was not a war-caused death within the meaning of that term in s 8 of the Act. The decision of the Repatriation Commission was affirmed by the Veterans' Review Board ("the VRB") on 7 October 1998.
Mr M Croyle of Counsel appeared for Mrs Hornibrook. Mr E Nyhof, an advocate with the Department of Veterans' Affairs, appeared for the Repatriation Commission. Mrs Hornibrook gave evidence. Evidence on her behalf was also given by her son, Mr Brian Hornibrook, and Dr Collins, a forensic pathologist. The respondent called Dr Hart, a respiratory physician and Professor Cade who is the Director of Intensive Care at the Royal Melbourne Hospital. The respondent's witnesses gave evidence by telephone. The Tribunal had before it the documents, ("the T documents") lodged pursuant to s 37 of the Administrative Appeals Tribunal Act 1975 ("the AAT ACT") and also the exhibits tendered during the hearing.
The death certificate (T5 p29) shows the cause of Mr Hornibrook's death on 24 April 1990 and duration of last illness as follows:
Cardiogenic shock – 24 hours
Myocardial infarction – 14 days
Coronary artery disease
Pulmonary embolism – 24 hoursMr Hornibrook served in the Australian Army from 10 March 1942 to 5 August 1946. He served at Rabaul and at Bougainville. Thus the whole of his service constitutes operational service as that term is defined in s 6 of the Act.
Accordingly the relevant standard of proof is that in s 120(1) and (3) of the Act. Those provisions read as follows:
120 Standard of proof
(1)Where a claim under Part II for a pension in respect of the incapacity from injury or disease of a veteran, or of the death of a veteran, relates to the operational service rendered by the veteran, the Commission shall determine that the injury was a war-caused injury, that the disease was a war-caused disease or that the death of the veteran was war-caused, as the case may be, unless it is satisfied, beyond reasonable doubt, that there is no sufficient ground for making that determination.
Note: This subsection is affected by section 120A.
…(3)In applying subsection (1) or (2) in respect of the incapacity of a person from injury or disease, or in respect of the death of a person, related to service rendered by the person, the Commission shall be satisfied, beyond reasonable doubt, that there is no sufficient ground for determining:
(a)that the injury was a war-caused injury or a defence-caused injury;
(b)that the disease was a war-caused disease or a defence-caused disease; or
(c)that the death was war-caused or defence-caused;
as the case may be, if the Commission, after consideration of the whole of the material before it, is of the opinion that the material before it does not raise a reasonable hypothesis connecting the injury, disease or death with the circumstances of the particular service rendered by the person.
Note:This subsection is affected by section 120A.
As the claim was lodged after 1 June 1994 s 120A applies. Section 120A(3) provides that a hypothesis connecting the death of a person with the circumstances of any particular service rendered by the person is reasonable only if there is in force a Statement of Principles ("SoP") that upholds the hypothesis. Section 120A(4) provides that s 120A(3) does not apply if there is no relevant SoP. In fact it seems that there may be some error of drafting in s 120A(4). It reads as follows:
(4)Subsection (3) does not apply in relation to a claim in respect of the incapacity from injury or disease, or the death, of a person if the Authority has neither determined a Statement of Principles under subsection 196B(2), 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)the kind of death met by the person;
as the case may be.
We have some difficulty with the drafting of s 120A(4). It seems to us that the clause beginning with the word, "nor" may have one more negative than is intended. If s 120A(3) does not apply where the Authority has not declared that it does not propose to make a Statement of Principles, the legislation does not explain what is the appropriate means of determining the reasonableness of a hypothesis where such a declaration has been made. We suggest that s 120A(4) of the Act may require review and possible amendment. We see that the Full Court of the Federal Court in McKenna v Repatriation Commission (1999) 29 AAR 70 at p78 did similarly point to some difficulty with the drafting of s 120A(3) and (4).
The applicant's Statement of Facts and Contentions lodged on 6 September 1999 raised the hypothesis that Mr Hornibrook's death was contributed to by asthma which was war-caused. That hypothesis relied on the opinion of Dr Collins who, in his report of 21 May 1999 (A6), accepted as reasonable the hypothesis that exposure to volcanic fumes, in the South West Pacific area during service, as described by statements from Mrs Hornibrook and by Mr Brian Hornibrook, could have produced Mr Hornibrook's asthma.
Dr Collins wrote in his report of 21 May 1999 (A6):
It is well recognised that various gaseous compounds of sulphur and [sic] which are likely to be present in the fumes/smoke belching forth from an erupting volcano, are highly irritant to the respiratory tree.
In my view, it would be entirely reasonable to argue on sound pathological grounds, that the late Mr Hornibrook's exposure to volcanic fumes whilst on active service would have the very real potential of sensitising his respiratory tree and producing an asthmatic diathesis.
He went on to state:
. . . the presence of any respiratory condition which would restrict the lungs' capacity to properly and efficiently oxygenate blood, such as chronic obstructive airways disease/asthma, would be likely to increase the severity of any episode of myocardial infarction (because of tissue hypoxia) and for the development of serious/lethal complications of a pulmonary embolism via the similar mechanism of reduced tissue oxygenation.
I am of the opinion that, if it is agreed the veteran's exposure to the products of volcanic eruptions were a factor in the generation of his asthma, such exposure could be argued as a contributory factor in his death.
When the matter first came on for hearing on 18 October 1999 there was an issue as to whether Mr Hornibrook had in fact been exposed to sulphur fumes from volcanoes during his service. The Tribunal granted an adjournment to enable the parties to investigate this matter. Unfortunately that took much longer than anticipated. The matter was not ready to resume until shortly before 15 November 2000. After the further investigations undertaken by both parties, the respondent advised the solicitors for Mrs Hornibrook that it conceded that Mr Hornibrook was exposed to sulphur dioxide fumes from volcanoes during his service.
The Tribunal much appreciated the assistance given by the Repatriation Commission to Mrs Hornibrook and to the Tribunal, in investigating whether Mr Hornibrook was exposed to sulphur dioxide fumes from volcanoes. It was on the basis of a report obtained by the respondent from Ima Itikarai, the Assistant Director of the Department of Mining, Papua New Guinea, that the concession was made. Occasionally the Tribunal has found itself in the position of commenting on circumstances where the Commonwealth has not conducted itself in accordance with the Commonwealth as Model Litigant policy. That is not the situation in matters in the Veterans' Appeals Division.
Mr Nyhof advised the Tribunal and the applicant's solicitors by letter dated 25 September 2000, that the respondent accepted that there was a reasonable hypothesis that Mr Hornibrook was exposed to sulphur dioxide during his service in Rabaul, but that the respondent did not accept that this was the cause of his asthma, nor that the asthma contributed to his death.
Mr Croyle and Mr Nyhof agreed in the Statements of Facts and Contentions and throughout the hearing on 15 November 2000 that the relevant SoP was Instrument No. 59 of 1996 which deals with asthma.
When the Tribunal came to write its reasons for decision on 16 November 2000 it noticed that SoP No 59 of 1996 was dated 18 April 1996 and thus was not in operation when the Repatriation Commission determined Mrs Hornibrook's claim on 1 February 1996. The Tribunal therefore arranged for the Senior Member's Associate to send a letter to the parties asking why the parties had agreed that SoP No. 59 of 1996 was applicable. The Tribunal in that letter referred to Keeley v Repatriation Commission (1999) 56 ALD 455 where Heerey J said at p463 that the legal consequences of acts should as a general principle be governed by the law in force when the acts occur. The Tribunal also referred to Repatriation Commission v Keeley [2000] FCA 532, where the Full Court approved the decision of Heerey J and explained:
44 The terms of s 120A(2) show a clear intention by Parliament that such a Statement is to "affect" the accrued right obtained by the lodgement of a claim under the Act to have the claim decided by the Commission. It is plain that by postponing a right to have a claim decided until a Statement has been determined, Parliament intended that the decision, and therefore the right to have a decision made, may be affected by a Statement determined under s 196B and that a pending claim is to be decided by application of the Statement when determined.
45 However, that circumstance does not apply after a claim has been determined and the right that has accrued under the Act is a right to have the determination reviewed. …
46 Unless a contrary intention is clearly disclosed, it is to be presumed that accrued rights are determined under the law as it stood when the right accrued.
The Tribunal concluded its letter:
The Tribunal is wondering why neither party submitted that the matter should be decided in accordance with the principles in Byrnes v Repatriation Commission (1993) 177 CLR 564, and Bushell v Repatriation Commission (1992) 175 CLR 408. It is prepared to receive submissions on this issue. Could you please respond within 7 days.
On 17 November 2000 the applicant's solicitors responded. Their letter so far as relevant read as follows:
We accept that there is no relevant Statement of Principles and we apologise for making an assumption about the applicability about the Statement of Principle discussed at the hearing.
Given that there is no relevant Statement of Principles it will be submitted that the Administrative Appeals Tribunal is bound by s.120 (1) and (3) of the Act as interpreted by the High Court of Australia in Bushell V Repatriation Commission (1992) 175 CLR 408 and Byrnes V Repatriation Commission (1993) 177 CLR 564. We submit that the Tribunal has credible and qualified medical opinion before it supporting each of the parts of the hypothesis propounded on behalf of the applicant. It is therefore submitted that the hypothesis is "reasonable". It is submitted that the dispute between the doctors concerning the relationship between the asthma condition and death should be resolved by reference to the opinions of the High Court in the aforementioned decisions.
It is submitted that the respondent has not discharged the onus under s.120 (1).On 22 November Mr Nyhof replied to the Tribunal. He agreed that SoP 59 of 1996 was not applicable. As to the way in which the Tribunal should decide the matter he submitted.
The respondent notes what Messrs. Williams, Winter & Higgs have to say in their letter dated 17 November 2000. The respondent takes issue with the submission contained in paragraph 3 of their letter and submits that the Tribunal has no "credible" evidence upon which it can conclude that the hypothesis proffered by the applicant is reasonable. Indeed, the evidence of Professor Cade is that the hypothesis is "a colourful and imaginative hypothesis but it is not plausible…" Dr. David Hart's evidence was that he would not have used those words but that he nevertheless supported Professor Cade insofar as the hypothesis was not reasonable
Mr Nyhof went on to discuss the evidence in some detail.
The hypothesis proposed by Dr Collins as set out in paragraph 8 above, has two aspects. The first is that exposure to volcanic fumes while on service could have produced or caused Mr Hornibrook's asthma. The second is that asthma would restrict the lungs' capacity to oxygenate blood and this could have increased the severity of the myocardial infarction (because of tissue hypoxia) and led to the development of a pulmonary embolism via the similar mechanism of reduced tissue oxygenation.
The respondent claimed both aspects of that hypothesis were not reasonable. Professor Cade in his report of 11 August 1999 (R2) gave his opinion on the issue as follows: (R2 p4)
[A] suggestion has been made by Williams, Winter & Higgs, solicitors for the widow, that exposure to volcanic eruptions during service in the South West Pacific could have caused his asthma and that asthma contributed to death. This is a colourful and imaginative hypothesis but it is not plausible for the following reasons.
1. The mechanism of death was clearly circulatory and not respiratory.
2. No abnormal respiratory features were recorded during the two weeks of his terminal hospital admission, so that his asthma must be considered to have been controlled.
3. Asthma treatment was not an indirect cause of the circulatory impairment, because if so this would have been via serious tachyarrhythmias and in fact the impairment was one of hypotension.
4. Asthma was not noted by the patient or the army medical staff to have been present during service or on discharge.
5. Environmental pollutants such as sulphur dioxide (spewed by volcanoes but better known as urban emissions) are recognized causes of exacerbation of respiratory disease rather than causes of continuing respiratory disease.
6. Volcanoes have been shown not to cause continuing new respiratory disease such as asthma (except in the rare circumstance of heavy exposure to ash which can sometimes cause pulmonary fibrosis). This lack of respiratory damage has been extensively documented, particularly after the eruption of Mt St Helens in the USA in 1980, and subsequently following eruptions in Mexico, Indonesia and Papua New Guinea (see references below). Indeed, in animal experiments, volcanic ash decreases bronchial reactivity (i.e. the opposite of asthma).
Dr Hart in his report of 24 October 2000 (R4 p4) stated:
In this matter I concur entirely with Professor John Cade's opinion that the suggestion that exposure to oxides of sulphur from volcanic eruptions sensitized the veteran creating an asthmatic state which contributed to his death is entirely implausible. I concur with each of the six reasons which he provides.
In Repatriation Commission v Webb, Full Federal Court, 5 November 1998, 981411/1998 the Full Court of the Federal Court discussed the way in which the Tribunal should deal with a hypothesis which contains a number of parts. The Full Court said at part 5 of its reasons:
The proper approach is to ask, in relation to each sequential part of the hypothesis, whether the facts point to that part of the hypothesis being reasonable. Once it is established that a relevant part of the overall hypothesis is reasonable, then any doubts as to the reasonableness of that part of the hypothesis must, for the purposes of s 120(3), be put aside, and the next part of the hypothesis considered. It is not appropriate to carry over or accumulate doubts in relation to the reasonableness of one part of the hypothesis and apply these doubts to a consideration of other parts of the hypothesis or to the hypothesis as a whole. In the present case, each sequence in the overall hypothesis raises a discrete question. What must be answered is the question whether the hypothesis pointed to by each sequential part which makes up the overall hypothesis is reasonable. If this is so then the overall hypothesis may be considered reasonable. The AAT did not do this.
We, therefore, conclude that the AAT adopted an incorrect approach when considering the reasonableness of the overall hypothesis.
We must therefore consider the reasonableness of each part of the hypothesis separately.
the evidence at the hearing
1.the first part of the hypothesis – that exposure to volcanic fumes may have caused asthma
(i) the evidence of family members and friends
Mrs Hornibrook said her husband already had asthma when she met him in 1949, but it was just starting and was not as bad as later although he was already taking medication for his asthma and was short of breath. Mrs Hornibrook said that Mr Hornibrook had never been a smoker.
Mr Brian Hornibrook gave evidence that his father had told him about the effect of breathing sulphur fumes when near volcanoes during his operational service. He said that his father had told him that exposure to sulphur fumes caused a burning sensation towards the back of his nostrils and that the fumes affected his breathing. He understood that it was a constant problem while his father was around volcanoes. He said:
[I]t felt like his breath had been taken away, and he was short of wind, and short of breath, and found it difficult to breathe
He added:
[W]henever he could really smell the fumes coming out of the volcanoes was when it occurred
Mr Brian Hornibrook said he only had one conversation with his father on the topic. He gave more detail of that conversation in his statement dated 11 January 1999 (A2):
I am a member of the CFA. I recall that on one occasion I fought a sulphur fire in Geelong and related the experience to my father. In this conversation my father told me that on a number of occasions he had been exposed to sulphur fumes from volcanoes in the South West Pacific area during his war service years. My father recalled that he had suffered a burning sensation towards the back of his nostrils when exposed to the sulphur fumes and that they had affected his breathing.
Mr Hornibrook's older brother Alfred also made a statement (A3). He stated that he and Mr Hornibrook were less than a year apart in age and lived on a property six miles out of town. He said they were relatively isolated and had a close relationship. Mr Alfred Hornibrook enlisted in the RAAF in 1941 and was not discharged until 1976. Mr Alfred Hornibrook said he did not recall his brother suffering from any respiratory complaint, prior to his own enlistment in 1941, but that in the late 1950's or early 1960's he learned that his brother had asthma.
The Tribunal also received a statement (A4) from Pauline Harvey, Mr Hornibrook's younger sister. She stated:
I was not aware of Roy having any breathing problem or any illness at all prior to his enlistment in the Australian Army during the Second World War. I recall that he had one job which lasted about twelve months which required him to ride his push bike about thirty miles to work. During that period he would ride to work on a Sunday and return home on the Friday evening and the bike ride did not seem to bother him.
I became aware that Roy was suffering asthma when he first returned from his war service. He did return to the family home after discharge (up until his marriage). Whilst I can remember that he was suffering asthma on his return from service, I cannot now recall whether he was taking medication prior to his marriage.
I recall observing that Roy would become breathless on exertion on his return from service. If, for instance, we had a game of tennis then he would become breathless – and this was not the case before his enlistment.
Roy never smoked to my knowledge. I have no idea as to what caused his asthma other than to say that my conclusion is that it commenced during his war service years.
. . .The applicant had also lodged an unsigned Statement from Mr Goodear, a friend of Mr Hornibrook, who served with him in Bougainville and Rabaul from September 1944 to March 1946. Mr Goodear stated: (A5)
We served together at Bougainville from about September 1944 to March 1946. Roy's tent was situated approximately 5 metres from mine during that period. We were camped close to Mount Bagana at Bougainville. Mount Bagana was a very steep mountain which was constantly belching smoke whilst we were there. Some days the smoke was worse than on others. On bad days the sulphuric stench was quite strong.
We used to complain amongst ourselves about the fumes belching from Mount Bagana. When the wind was blowing in our direction the amount of smoke and ash blown over us was significant. Some days the ash was quite noticeable and on those days the sulphur was quite pungent. We would often say "old Smokey Joe is bad today".
I often saw elderly natives wearing muslin type masks at Bougainville. I asked the reason for this and was told they were to filter the fumes. Inhaling the fumes in Bougainville did cause some discomfort and burning sensation on occasions.
When we were transferred to Rabaul we were based 1 1/2 to 2 miles from the volcano on the harbour of Rabaul. It was a potent volcano. I cannot remember the name of the volcano but we simply referred to it as the Rabaul volcano. I was at Rabaul for about 4 months. Because Roy and I were at different units at that time I cannot vouch for the length of his service at Rabaul although I did see him on occasions throughout my stay.
The exposure to sulphuric fumes was worse at Bougainville because Mount Bagana was constantly blowing ash, lava and fumes whilst we were there. At Rabaul the exposure to fumes was intermittent. The volcano at Rabaul seemed more violent and less stable than the one at Bougainville. The fumes from the volcano at Rabaul were quite strong when they blew. I regarded Rabaul as more dangerous but I classed Bougainville as more uncomfortable from a respiratory point of view because it was constant.
I do have two photographs of Mount Bagana which were taken from the air by a friend of mine whilst we were based there. The photographs show smoke coming from that volcano.Mr Goodear was present at the hearing but neither party required him to give evidence. The Tribunal inspected Mr Goodear's photographs which did indeed show smoke coming from Mount Bagana during the time Mr Goodear and Mr Hornibrook were stationed nearby. Copies of the photographs were received in evidence and have been marked as exhibit A9. Mr Hornibrook's service records do not seem to show him being in Bouganville throughout the period mentioned by Mr Goodear but we accept that he did serve in Bouganville and at Rabaul with Mr Goodear. The records seem to indicate three periods at Bougainville between September 1944 and February 1946 totalling approximately 9 months, and 3 months at Rabaul.
Mr Hornibrook's exposure to sulphur dioxide fumes, during his service at Bougainville and Rabaul, was conceded by the respondent. The evidence of Mrs Hornibrook and statements from Mrs Pauline Harvey and Mr Alfred Hornibrook, a sister and brother of Mr Hornibrook, point to Mr Hornibrook having developed asthma during service as he did not have asthma before service and he did have asthma from the time he returned from service. The evidence of family members and Mr Goodear does raise a hypothesis that Mr Hornibrook contracted asthma during service as a result of exposure to volcano fumes while serving in Bougainville and at Rabaul.
(ii) the medical evidence
Dr Collins proposed the hypothesis that Mr Hornibrook developed asthma due to exposure to volcano fumes. Professor Cade and Dr Hart said that there is no evidence in the medical literature of chronic asthma developing as a result of exposure to volcano fumes.
Dr Collins in his report of 21 May 1999, as set out in paragraph 8 above, had stated, "it would be entirely reasonable to argue on sound pathological grounds that . . . exposure to volcanic fumes . . . would have the very real potential of sensitising his respiratory tree and producing an asthmatic diathesis."
Dr Collins said that exposure to volcanic eruption material can cause lung disease and irritation of the airways. He said volcanic ash irritates the airways and that can produce sensitivity. He added that because it alters the respiratory architecture it may precipitate an attack of asthma. Dr Collins said that exposure to ash can cause the development of non-specific bronchial activity and there can be a significant individual reaction.
Professor Cade as explained in paragraph 18 above, in his report dated 11 August 1999 (R2) described Dr Collins' suggestion that exposure to volcanic eruptions could have caused Mr Hornibrook's asthma as "colourful, imaginative and not plausible." As to the first part of the hypothesis, that is the connection between exposure to volcanic gases and asthma he wrote:
5. Environmental pollutants such as sulphur dioxide (spewed by volcanoes but better known as urban emissions) are recognized causes of exacerbation of respiratory disease rather than causes of continuing respiratory disease.
6. Volcanoes have been shown not to cause continuing new respiratory disease such as asthma (except in the rare circumstance of heavy exposure to ash which can sometimes cause pulmonary fibrosis). This lack of respiratory damage has been extensively documented, particularly after the eruption of Mt St Helens in the USA in 1980, and subsequently following eruptions in Mexico, Indonesia and Papua New Guinea (see references below). Indeed, in animal experiments, volcanic ash decreases bronchial reactivity (i.e. the opposite of asthma).
Dr Hart said that from reviewing medical notes concerning Mr Hornibrook he saw that he had been taking Ventolin and Beclaforte which are used for asthma. Therefore Dr Hart was prepared to assume that Mr Hornibrook had asthma, although he saw nothing which confirmed that diagnosis in the notes.
Dr Hart said that there is no problem with the proposition that exposure to sulphur dioxide fumes can aggravate asthma temporarily. But he disagreed that it behaves like an occupational antigen which can sensitise a person for life so that in the future very small amounts of that substance can produce asthma. He said that for many sensitising agents such as wood dust and isocyanides there can remain life long asthma, but he distinguished sulphur dioxide from those sensitising agents. He said, at trans. pp55–56:
I would assert that sulphur dioxide like cold and emotional stress and exercise fall into the category of agents which are non-antigenic, non-sensitising and produce transient aggravations of asthma and . . . although I could see no evidence that this was the case – if you were to tell me that there was evidence that he had asthma episodes in Rabaul or Bougainville breathing that smoke it wouldn't surprise me and I would accept that. What I have trouble accepting is that that has led to the development of lifelong asthma. And I maintain that for the reasons that are outlined in Dr Cade's opinion that there simply is no precedent for that belief . . . . in the medical literature. The evidence in terms of exposure to volcanic ashes is negative, and it's listed in the references that Dr Cade – Professor Cade provided in his report.
Dr Hart said that in general non-antigenic stimuli do not have a lasting effect once the stimulus is withdrawn, but he volunteered that some doctors believe that beta blockers are an exception to that rule in that they provoke a lasting worsening even after the drug is withdrawn. He explained at trans. p58:
I have seen a butcher who had to mix sulphur dioxide into sausage meat as part of his job for six months and had continuous six months of asthma, but the moment he had it pointed out to him that this was the sensitising – or the irritating agent his asthma went away. So it's not been my experience that these agents such as cold, emotional stress and exercise, respiratory infection and sulphur dioxide produce a permanent decline in organ functions unless the exposure is continuous.
The Tribunal asked Dr Hart whether, because the susceptibility of different people varies, a different individual might react differently to ongoing exposure to sulphur dioxide. He replied, at trans. p61:
I think that's true. But the problem – the rationale is that with the antigenic stimuli you – the stimulus that triggers the development of an immune response which remains permanently – immune memory remains in the system and the body remains then capable of producing antibodies to that irritant whenever it is encountered up to the remainder of their lifetime. And it's not thought that the sulphur dioxide works by the development of a permanent lasting immune response, but that it's an immediate irritant response, technically mediated, so that there is not left behind a memory of this exposure which is called sensitisation with the previous position to occur again on minimal exposure later in life.
Dr Hart said that from his experience and reading he did not think exposure to sulphur dioxide produced permanent airway damage. He said that to believe that was possible he would have to see someone becoming much worse after sulphur dioxide exposure and remaining worse from that time on.
Professor Cade, at trans. p75, repeated the opinion expressed in his report:
Sulphur dioxide is able to exacerbate asthma but it doesn't cause it, as such. It doesn't cause a non-asthmatic person to become asthmatic, and it doesn't cause somebody with an asthmatic tendency then to develop asthma as a long term problem. It is a respiratory irritant which I think, as you know, it is most common in the urban setting as a motor car emission and people with asthma often fare fairly poorly on days of urban pollution. It hasn't caused their asthma in the first place.
But it can worsen their asthma?---For the time that it is present, it doesn't have a long term effect, it is exacerbated, the asthma, at the time that it is present.The Tribunal had before it two attachments to a report from Professor Cas of the Department of Earth Sciences, Monash University. One attachment was entitled "Hazards of Volcanic Gases" by Drs. G Williams-Jones and H. Rymer, of the Open University, Great Britain, from the recently released "Encyclopedia of Volcanology", edited by H. Sigurdsson (2000, Academic Press, p. 997-1004). Table 1 to that article under the heading "Sulpfur dioxide (SO2)" reads as follows:
Effects of overexposure
Short-termInflammation and irritation of the eyes and respiratory tract resulting in burning of the eyes, coughing, and difficulty in breathing. Approximately 90% of inhaled SO2 is absorbed in the upper respiratory tract where it forms sulfurous acid, which then oxidizes to form sulfuric acid. Concentrations of 6–12 ppm cause immediate irritation of nose and throat. Exposure to > 20 ppm causes irritation of the eyes, while concentrations of 10,000 ppm irritate moist skin within minutes.
Long-termProlonged exposure to low concentrations may be dangerous for persons with preexisting cardiopulmonary diseases.
The second attachment to Professor Cas' report of 5 February 2000 was a copy of an article by Dr. P.J. Baxter, University of Cambridge Clinical School and Addenbrooke's Hospital, Great Britain, entitled "Impacts of Eruptions on Human Health" (in Sigurdsson, H. [editor], op cit., p. 1035-1041). On page 1041 Dr Baxter points out "Sulphur dioxide is the main gas of interest as it can provoke asthma attacks in asthma patients at the low concentrations that can be found at long distances from the source of the emission".
The evidence establishes that the weight of scientific evidence is that sulphur dioxide is a non-antigenic stimulus and that exposure may bring on an attack of asthma. But the weight of the evidence suggests that the asthma response will cease when exposure ceases, and that exposure does not bring about permanent change. Dr Collins expressed the opinion that this is not necessarily always correct because of the significance of different individual reactions and because prolonged exposure or any exposure which precipitates an onset of asthma "has altered the respiratory architecture such that it is not normal".
As there is no applicable SoP the matter is to be determined by reference to s 120(1) and (3) of the Act as explained by the High Court in Bushell v Repatriation Commission (1992) 109 ALR 30 and Byrnes v Repatriation Commission (1993) 116 ALR 210, 30 ALD 1. In Bushell Mason CJ, Deane and McHugh JJ said at pp34:
Clearly enough, a relevant consideration in forming an opinion whether a particular hypothesis is reasonable is whether, as a matter of common or medical experience, the occurrence of an injury etc. of the kind sustained by the veteran is commonly accompanied by or associated with the occurrence of raised facts of the kind which constitute the relevant incidents of the service of the veteran. However, a hypothesis may still be reasonable even though such an accompaniment or association is not demonstrated or even if it is shown to be uncommon. So, in determining whether a hypothesis is reasonable for the purpose of s 120(3), it is not decisive that a connection has not been proved between the kind of injury which occurred and circumstances of the kind which constitute the relevant incidents of the veteran's service. Nor is it decisive that the medical or scientific opinion which supports the hypothesis has little support in the medical profession or among scientists. (emphasis added)
Professor Cade in his report described Dr Collins' opinion as to a connection between exposure to sulphur dioxide and the onset of an asthma condition as "colourful and imaginative but not plausible", and thus as not raising a reasonable hypothesis. Dr Hart also described it as implausible. However Dr Hart acknowledged that some doctors believe beta blockers, which are non-antigens, may have a lasting effect after they are withdrawn. He also said that before he could accept that sulphur dioxide could have a lasting effect, he would need to see someone becoming much worse after exposure to sulphur dioxide; that is to say the airways being damaged in a non-reversible way. Thus he did not rule out the possibility that a person's airways may be damaged in a non-reversible way by exposure to sulphur dioxide even though this has not been documented. The suggestion that beta blockers may have a lasting effect even though they are non-antigins may also be applicable to sulphur dioxide. Sulphur dioxide exposure does not seem to be similar in nature to "cold and emotional stress and exercise" as referred to by Dr Hart in paragraph 34 of these reasons.
Dr Collins (at trans. p34) disagreed with the opinions of Professor Cade and Dr Hart and said he considered the suggestion that exposure to volcanic eruptions caused asthma, and that the asthma contributed to death, "an entirely reasonable possibility, given the clinical science and symptoms that this man apparently complained of during the time at war."
Although scientific literature has not documented cases of permanent airways damage from sulphur dioxide exposure that does not in, our opinion mean that Dr Collins' hypothesis is contrary to proved facts. The connection between sulphur dioxide exposure and temporary airways damage has been demonstrated. It does not seem "fanciful, impossible, incredible or not tenable or too remote or too tenuous", to suggest that in some individuals there may be a permanent effect similar to that being postulated in regard to beta blockers. Attachment 1 to Professor Cas' report does recognize long term effects of exposure to sulphur dioxide for persons with pre-existing cardio pulmonary disease. The material before the Tribunal points to Mr Hornibrook having developed his asthma during service. The respondent has conceded that he was exposed to a substance which can provoke temporary attacks of asthma. It does not seem to us fanciful to accept, as suggested by Dr Collins that Mr Hornibrook's long term asthma may be due to the exposure, although long term effects of such exposure have not been demonstrated in the literature.
None of the medical witnesses stated that sulphur dioxide only affected people who already had asthma. Attachment 1 to Professor Cas' report seems to say that long term effects, as distinct from short term effects, are restricted to persons with pre-existing cardio pulmonary disease. However there is no discussion of the effects of repeated exposure over nine months or a year and whether that results in aggravation of the "alterations [to] the respiratory architecture" referred to by Dr Collins (see paragraph 31 of these reasons) as resulting from the early exposure. That possibility is not in our opinion ruled out, even though such an association is not demonstrated. Dr Hart did not rule out the possibility that exposure to sulphur dioxide may produce permanent damage, but he said that to believe it was possible he would need to see one such person.
We find that the first part of the hypothesis proposed by Dr Collins is raised on the material before the Tribunal, especially the evidence of family members, as well as by the evidence of Dr Collins. We find that the hypothesis raised by Dr Collins as to development of asthma due to exposure to fumes is reasonable.
2.the second part of the hypothesis – that asthma contributed to death
(i) the evidence of family members
Mrs Hornibrook said that her husband took asthma medication every day in the period before his death. She said that for five years he had been using the Ventolin machine with a mask about four times a day, and he also used the Ventolin puffer. She said Mr Hornibrook was very short of breath and had a constant wheeze. He was too out of breath to use a lawn mower at home so Mrs Hornibrook had done the lawns for the last 12 months.
(ii) the medical evidence
Dr Collins suggested that the evidence pointed to a man suffering from fairly significant obstructive airways disease or asthma, which would cause reduced air supply or oxygen supply to his blood. He also said that one possible cause or mechanism of death could have been a pulmonary embolus or clot within the blood vessels of the lungs. Such a clot would block the vessels to a certain extent and thus decrease the oxygen supply to the heart and brain. Dr Collins suggested that if the lack of oxygen is exacerbated by pre-existing airways disease the end result will be a greater lack of oxygen to the vital organs than in somebody who did not have obstructive airways disease.
Dr Collins noted that Mr Hornibrook died in cardiogenic shock which means that his heart failed, and he claimed that one reason for the failure was lack of oxygen supply to the heart.
When Mr Nyhof put to Dr Collins Professor Cade's opinion that the mechanism of death was clearly circulatory rather than respiratory, Dr Collins agreed. He said that part of the reason for the heart failure was that the heart muscle was deprived of adequate oxygen. He added at trans. p32:
And part of that deprivation, in my view, was due – or could be argued to be due – to the abnormality in this man's respiratory tree compromising the oxygenation of blood.
Yes?--- - - - in association with his pulmonary embolus or without his pulmonary embolus.Dr Collins was asked to comment on Professor Cade's statement that there were no abnormal respiratory features recorded during the two weeks of the terminal hospital admission and thus that the asthma must be considered to have been controlled. Dr Collins replied that there must have been some respiratory symptoms for Mr Hornibrook to have been on drugs for asthma (trans p33).
Dr Collins at trans. p34 conceded that there was no material in the hospital notes (ex. R1) pointing to the hypothesis he proposed. But he claimed that there was also a lack of evidence to support the hypothesis proposed by Professor Cade and Dr Hart.
Dr Collins explained that what he was talking about would not be documented in the progress notes of a terminally ill patient, especially when he was not in a "treating clinical hospital in Melbourne" (trans. p35), where there would be vastly different data available. Dr Collins agreed that there was no note of increased medication to control breathing difficulties.
Dr Collins agreed that the oxygen levels recorded were close to the mid range but he said (trans. p37):
Well, one single blood gas reading means nothing. That is a … single blood gas reading, and that is all it is.
The Tribunal also had the benefit of Dr Hart and Professor Cade's interpretation of the clinical notes. Dr Hart said there was no material in the clinical notes to point to or support the contention or hypothesis that a chronic lung condition reducing oxygen levels might have increased the severity of Mr Hornibrook's heart attack, and might have aggravated the tendency of the pulmonary embolism to be fatal. He said that in fact the evidence refutes the contention.
Dr Hart pointed to the records of a chest examination having been clear at Casterton Hospital on 17 April 1990 (R1 p19) and on transfer to Hamilton Hospital (R1 page after p46). He said that if asthma had been sufficiently active to make Mr Hornibrook low in oxygen there would have been wheeze and respiratory symptoms present.
Dr Hart also referred to the arterial oxygen reading of 87 noted at the time of transfer to Hamilton Hospital and said, as Dr Collins conceded, that it was not low. Dr Hart also noted an earlier entry at the time of hernia surgery recording a chest examination as "perfectly clear" with a report of breathlessness only on "extreme exertion".
Dr Hart also stated that the notes clearly show that Mr Hornibrook died from low blood pressure and not from hypoxia or lack of oxygen. He said after referring to the arterial oxygen reading of 87, at trans. p51:
And if that reading had been particularly low, there might be some force to the argument that hypoxia was aggravating the situation, but neither was the oxygen low nor was the chest wheezy, and the mechanism of death was gradual progressive shock, due either to septicaemia, heart failure or a pulmonary embolis. And I don't think any of those – I don't think in any of those cases that hypoxia was making a contribution.
Mr Croyle, at trans. p59, asked Dr Hart whether he would agree that it was at least a possibility that the thesis advanced by Dr Collins had "some basis to it". Dr Hart did not agree. He said that the death "was clearly, as Dr Cade outlined, a hypo-tensive death due to shock not a death due to oxygen problem".
Dr Hart said, at trans 59, from reading the hospital notes, he concluded that the asthma medication given to Mr Hornibrook while he was in hospital was not administered for respiratory symptoms, but was simply continued on from before admission. He said (trans. p60):
I can find no mention of asthma occurring during the admission and I can find, I think, on two occasions a record of chest examination which was clear.
Dr Hart explained that at the end Mr Hornibrook's heart just was not pumping enough blood around his body to maintain life. He said the problem was not getting oxygen into the blood, but was rather a problem of getting enough blood around the body to supply the vital organs.
Professor Cade said that the cardiogenic shock, which was the mechanism of death, was due to pump failure. He, like Dr Hart, said that it was clear from the blood oxygen level of 87 recorded in the hospital notes, that Mr Hornibrook was well oxygenated at the time of his admission to Hamilton Hospital, after his final collapse.
Professor Cade said the death was purely circulatory failure rather than reflecting a lack of oxygen. He said that Mr Hornibrook in the terminal event suffered cardiogenic shock which means that very little blood flow gets to the vital organs. He explained that is the result of the very low blood pressure as shown in the hospital notes. Professor Cade also pointed out, as did Dr Hart, that the hospital notes, on two occasions, record that the chest was clear (R1 p19 and the page following p46). Professor Cade said that in order for asthma to lower the oxygen in the blood it needs to be clinically very dramatic. He said low oxygen does not result unless the asthma is causing an obvious clinical problem. He said, at trans. p72, "it is a manifestation only of very advanced, very obvious asthma, with marked wheeze, marked shortness of breath, can't be missed."
Professor Cade was quite clear that in the absence of noticeable effects of asthma, asthma cannot be a cause of hypoxia. He said, as did Dr Hart, that the hospital notes showed that Mr Hornibrook's asthma was well controlled with the medication which he was taking, and thus it was not a cause of hypoxia.
Professor Cade said that the disagreement between him and Dr Collins on the issue of the consequences of the asthma reducing the oxygenation of the blood was "more than just a normal professional disagreement". He said of the hypothesis put forward by Dr Collins (trans. p75):
I don't believe that it is at all possible to be correct.
discussion of the reasonableness of the second part of the hypothesis
Dr Collins did raise a hypothesis as to how asthma could have resulted in low oxygen levels and could thereby have contributed to Mr Hornibrook's death. But that alone is not sufficient for the Tribunal to conclude that the second part of the hypothesis is reasonable. In Bushell, the High Court stated at p34:
The material will raise a reasonable hypothesis within the meaning of s 120(3) if the material points to some fact or facts ("the raised facts") which support the hypothesis and if the hypothesis can be regarded as reasonable if the raised facts are true.
In this matter the hypothesis is contribution to death of low blood oxygen (hypoxia) resulting from asthma. Obviously that need not be proven for a reasonable hypothesis to be raised. But there must be something in the material which points to or raises that hypothesis. Not only do the clinical records not support the hypothesis, they in fact contradict it. They show the only oxygen level recorded was not low, two chest examinations were recorded as clear, and there is no record of chest wheeze or other sign of chest problems. There was no breathing difficulty or arrythmia recorded. The asthma medication administered was simply the maintenance of the medication taken before admission. There is no fact or material which raises or points to the hypothesis.
In East v Repatriation Commission (1987) 74 ALR 518 at p533 the Full Court considered the concept of the raising of a reasonable hypothesis saying:
The adoption of Brennan J's notion of a reasonable hypothesis meant that Parliament was requiring something by way of causal link, but which fell short of proof of the link even prima facie as a fact. The meaning of the phrase "reasonable hypothesis" was felicitously explained by a Veterans' Review Board in Stacey (Nos V83/0396, V84/0821 and V28/072); words quoted by the Administrative Appeals Tribunal in Re Dell and Repatriation Commission (1986) 9 ALD 596 at 615:
"A hypothesis may be conveniently defined as: 'proposition made as basis for reasoning, without assumption of its truth; supposition made as starting point for further investigation from known facts; groundless assumption': The Concise Oxford Dictionary...
The addition of the word 'reasonable' would however seem to imply that what is required is more than a mere hypothesis. In the opinion of the Board, to be reasonable, a hypothesis must possess some degree of acceptability or credibility it must not be obviously fanciful, impossible, incredible or not tenable or too remote or too tenuous. For a reasonable hypothesis to be 'raised' by material before the Board, we think it must find some support in that material that is, the material must point to, and not merely leave open, a hypothesis as a reasonable hypothesis. At the same time, however, a hypothesis may be reasonable without having been proved (either on the balance of probability or beyond reasonable doubt) to be correct as a matter of fact. Were it otherwise, it would no longer be a hypothesis but would have been elevated to some higher status. Accordingly a connection asserted by a hypothesis to exist between death or incapacity and service may still be reasonable, even though theoretical, and it may be theoretical in either or both of at least two senses: by postulating a known medical fact but in circumstances not known to have definitely existed in the instant case; or by postulating a medical principle which science is not yet able to definitely prove but is unable to describe as unreasonable."We agree with this analysis. A reasonable hypothesis requires more than a possibility, not fanciful or unreal, consistent with the known facts. It is an hypothesis pointed to by the facts, even though not proved upon the balance of probabilities. (emphasis added)
That passage was considered in Bushell and Byrnes. It was not criticised or corrected, but in Byrnes the High Court explained at p214:
The statement in Bushell that the material must point to some fact or facts which support the hypothesis means no more than that the material before the Commission must raise some fact or facts which give rise to the hypothesis. When that fact or those facts have been identified, the question for determination is whether the hypothesis is reasonable. In Bushell ((4)ibid, at p.414.), Mason CJ, Deane and McHugh JJ said:
"(A) hypothesis cannot be reasonable if it is 'contrary to proved scientific facts or to the known phenomena of nature ((5) Commissioner for Government Transport v. Adamcik (1961) 106 CLR 292, at p 306.)'. Nor can it be reasonable if it is 'obviously fanciful, impossible, incredible or not tenable or too remote or too tenuous' ((6) East v. Repatriation Commission (1987) 16 FCR 517, at p 532.)."
In some cases, the hypothesis may assume the occurrence or existence of a "fact". That itself does not make the hypothesis unreasonable. So, in the present case, the appellant's hypothesis is not unreasonable simply because it assumes that the appellant sustained a severe injury when he dived into a swimming pool in Townsville, notwithstanding that the materials before the Commission did not reveal the extent of the injury which he then suffered.
In Bushell there was evidence of injury to the neck caused by diving into a swimming pool. The hypothesis was that the injury was a severe injury such as to later result in cervical spondylosis. The High Court said that did raise a reasonable hypothesis. Here there is no material pointing to symptoms or consequences of the asthma being present while Mr Hornibrook was hospitalised after his heart attack, let alone to such consequences contributing to death as hypothesised by Dr Collins. In Byrnes the High Court, at p215, said:
The position may be summarised as follows: (1) First, sub-s.(3) of s.120 is applied: do all or some of the facts raised by the material before the Commission give rise to a reasonable hypothesis connecting the veteran's injury with war service? The hypothesis will not be reasonable if it is contrary to known scientific facts or is obviously fanciful or untenable. If the hypothesis is not reasonable, the claim fails. Proof of facts is not in issue at this point. (2) If a reasonable hypothesis is established, sub-s.(1) of s.120 is applied. The claim will succeed unless: (a) one or more of the facts necessary to support the hypothesis are disproved beyond reasonable doubt; or (b) the truth of another fact in the material, which is inconsistent with the hypothesis, is proved beyond reasonable doubt, thus disproving, beyond reasonable doubt, the hypothesis.
Contrary to the submission of Mr Emmett, the appellant's claim was not dependent on proof that he had sustained a severe injury. The sustaining of a severe injury was part of the hypothesis upon which the appellant relied to support his case. He testified that he had dived into a pool and injured his neck, causing him to be hospitalised. This was the factual foundation for the hypothesis that the dive had caused a severe ligamentous injury to his neck and perhaps to a disc. (emphasis added)Dr Collins, at trans. p34, conceded that there is no factual foundation for the hypothesis of asthma contributing to death. It is purely speculative. As the High Court explained in Bushell, at p34, and in Byrnes, at p214, the material before the Tribunal must point to some fact or facts which raise the hypothesis, or to some material which gives rise to the hypothesis. Here there are simply no facts or material pointing to or raising the second part of the hypothesis advanced by Dr Collins, namely the contribution to death of low blood oxygen resulting from asthma.
When Dr Collins conceded, at trans. p34, that there was no material in the clinical notes supporting his hypothesis, he claimed there was nothing supporting the other opinion either. That is not accurate. But what is more relevant is that there must be material or facts raised which is or are capable of supporting the hypothesis. The material need not be proven or accepted facts, but there must be some material capable of providing the factual foundation for the hypothesis. In this matter the suggestion of Dr Collins that low oxygen levels may have contributed to death is no more than an idea. It lacks any underlying support or factual foundation in the material.
We therefore conclude, after considering the whole of the material before the Tribunal, that the material does not raise a reasonable hypothesis connecting the death of Mr Hornibrook with the circumstances of his service. The hypothesis proposed by Dr Collins is not reasonable because there is no fact or material which points to or supports the hypothesis so as to provide its factual foundation, in the sense in which that term was used by the High Court in Byrnes, as set out in paragraph 71 of these reasons.
In case contrary to our conclusion the material could be found to raise a reasonable hypothesis, we will also consider the application of s 120(1) of the Act, on the basis that Dr Collins' evidence does raise a reasonable hypothesis linking Mr Hornibrook's death with the circumstances of his service.
Section 120(1) of the Act requires us to consider whether we are satisfied beyond reasonable doubt there is no sufficient ground for determining that Mr Hornibrook's death was war-caused as hypothesised by Dr Collins. The evidence of Professor Cade that there must be an obvious manifestation of asthma for it to result in low oxygen levels, and the material in the hospital notes showing no record of obvious manifestation of asthma, and two clear chest examinations and a blood oxygen level in the normal range on transfer to Hamilton Hospital satisfies us that Mr Hornibrook's death was not contributed to by asthma reducing the oxygenation of the blood. We are satisfied beyond reasonable doubt by the evidence of Professor Cade and Dr Hart that the notes show that death was due to circulatory or pump failure and not to lack of oxygenation. We note that Dr Collins did not disagree with their conclusions from the notes. What he did was say that hypoxia could also have played a part. We are satisfied beyond reasonable doubt for the reasons given by Professor Cade and Dr Hart, that the death was "a hypotensive death due to shock not a death due to oxygen problem" (see paragraph 60 of these reasons). We are satisfied beyond reasonable doubt that there is no sufficient ground for determining that Mr Hornibrook's death was a war-caused death.
The decision under review will be affirmed.
I certify that the 77 preceding paragraphs are a true copy of the reasons for the decision herein of Mrs Joan Dwyer, Senior Member, Mr A Argent, Member and Mr C Ermert, Member.
Signed: Anne O'Rourke
AssociateDate/s of Hearing 18 October 1999, 23 October and
15 November 2000
Date of Decision 2 March 2001
Counsel for the Applicant Mr M Croyle
Solicitor for the Applicant Williams Winter & Higgs
Counsel for the Respondent Nil
Solicitor for the Respondent Nil
Departmental Advocate Mr E Nyhof, Department of Veterans' Affairs
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