Leighton and Repatriation Commission
[2000] AATA 144
•28 February 2000
DECISION AND REASONS FOR DECISION [2000] AATA 144
ADMINISTRATIVE APPEALS TRIBUNAL )
) No V98/883
VETERANS' APPEALS DIVISION )
Re Ruth Leslie LEIGHTON
Applicant
And REPATRIATION COMMISSION
Respondent
DECISION
Tribunal Mrs Joan Dwyer, Senior Member Mr W McLean, Member Miss A Shanahan, Member
Date28 February 2000
PlaceMelbourne
Decision The Tribunal sets aside the decision under review and in substitution decides that the death of Dr Leighton was a war-caused death within the meaning of that term in s 8 of the Veterans' Entitlements Act 1986.
(Sgnd) Joan Dwyer
Senior Member
VETERANS' AFFAIRS - whether death of veteran was war-caused within the meaning of s 8 of the Act - whether material raises a reasonable hypothesis connecting death from myelofibrosis with operational service - exposure to benzene during war service - whether inhalation of benzene from petrol and exhaust fumes a factor in the development of myelofibrosis – whether a reasonable hypothesis requires significant or substantial occupational exposure to benzene – whether material raises a reasonable hypothesis connecting cigarette smoking and myelofibrosis – whether Tribunal satisfied beyond reasonable doubt that no sufficient ground for determining death was war-caused - decision set aside
Veterans' Entitlements Act 1986 ss 120(1) and (3)
Bushell v Repatriation Commission (1992) 109 ALR 30
Byrnes v Repatriation Commission (1993) 116 ALR 210
Repatriation Commission and Bey (1998) 47 ALD 481
Repatriation Commission v Cooke (1998) 52 ALD 1
Repatriation Commission v Owens (1996) 70 ALJR 904
Deledio v Repatriation Commission (1997) 47 ALD 261
Repatriation Commission v Deledio (1998) 49 ALR 193
REASONS FOR DECISION
28 February 2000 Mrs Joan Dwyer, Senior Member
Mr W McLean, Member
This is an application for review of a decision of the Repatriation Commission, made 22 May 1997 and affirmed by the Veterans' Review Board ("VRB") on 28 May 1998, which determined that the death of the applicant's husband, Dr Peter Leighton, was not war-caused.
Mr G Moore of Counsel appeared on behalf of Mrs Leighton. Mr R Douglass, an advocate with the Department of Veterans' Affairs, appeared for the Repatriation Commission. 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. Mrs Leighton gave evidence over the telephone. Evidence for the applicant was also given by Dr Parkin and Dr Bisby. The respondent called Professor Fox, Professor Peach, Mr Schey and Mr Piper. After the hearing had concluded, the Tribunal received a letter dated 4 August 1999 from Mr Douglass, enclosing a letter dated 8 July 1999 from Mr Piper, together with a report from Mr Piper enclosing a document received from Petroch Services. The letter from the respondent contained a concession that the exhaust fumes, to which the veteran may have been exposed, contained benzene as set out in paragraph 23. The Tribunal has taken the letter of Mr Piper and the attachment into evidence as exhibit R7. The applicant was offered the opportunity to make submissions in respect of that new material but did not do so.
Dr Leighton died on 21 February 1997 at the age of 74 years. The death certificate (T12 p63) shows the cause of death and duration of last illness as follows:
Myelofibrosis – 7 years;
Parkinson's Disease – 20 years
The issue is whether death caused by myelofibrosis was a war-caused death within the meaning of that term in s 8 of the Veterans' Entitlements Act 1986 ("the Act"). The only relevant paragraph of s 8 is paragraph (b). Thus the issue is whether the death of Dr Leighton "arose out of, or was attributable to, any eligible war service rendered by" him.
Dr Leighton served with the Australian Army from 8 April 1942 to 11 September 1946. He rendered operational service in New Guinea and the South West Pacific between 24 February 1945 and 31 December 1945. Accordingly the relevant standard of proof is that in ss 120(1) and (3) of the Act. As there is no Statement of Principles ("SoPs") issued by the Repatriation Medical Authority ("RMA") with respect to myelofibrosis, this matter is to be determined solely by reference to ss 120(1) and (3) of the Act which provide :
120. (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.
(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.
The hypothesis relied on by Mr Moore was that during his war service Dr Leighton was exposed to inhalation of benzene which was a causal factor in the development of his myelofibrosis. Mr Moore explained that it was claimed that benzene inhalation resulted from cigarette smoking, and also from inhalation of petrol and exhaust fumes while Dr Leighton was serving as a medical orderly on an ambulance boat from 9 January 1945 to 31 December 1945.
The reasons for judgment of the High Court in Bushell v Repatriation Commission (1992) 109 ALR 30, and in Byrnes v Repatriation Commission (1993) 116 ALR 210, establish that the first issue is whether a hypothesis relied on by an applicant is reasonable (s 120(3)).
In deciding whether or not a hypothesis is reasonable, the Tribunal is assisted by the majority judgment of Mason CJ, Deane and McHugh JJ in Bushell. Their Honours said 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. 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.
In Repatriation Commission and Bey (1998) 47 ALD 481, a Full Bench of the Federal Court explained that it is significant that the legislation uses the term "reasonable hypothesis" rather than simply "hypothesis". The reasons of the majority state, at p489, "While a hypothesis may be no more than a possibility or supposition, in order for a hypothesis to be reasonable it must . . . be pointed to or supported, and not merely left open as a possibility, by the material before the decision-maker." Their Honours reiterated what was said by Mason CJ, Deane and McHugh JJ in Bushell at ALR 34, as set out in the previous paragraph.
In determining whether or not the material before the Tribunal raises a reasonable hypothesis, it is necessary to consider the lay evidence as to the raised facts relevant to the service of the veteran, and also whether the medical evidence points to or supports a link between those facts and myelofibrosis, rather than simply leaving it open as a possibility.
Although Mr Moore in his opening (at trans. p6) described the hypothesis as covering inhalation of benzene both from cigarette smoking and from petrol and exhaust fumes, the expert medical evidence separated out the effects of those two possible sources of benzene exposure. The evidence as to a link between smoking and myelofibrosis is quite different from the evidence as to the effects of benzene exposure from the inhalation of petrol and exhaust fumes and myelofibrosis. We therefore propose to consider the evidence as to each factor separately.
lay evidence
Cigarette Smoking
Evidence as to the veteran's smoking habit was given by Mrs Leighton. She said that she met her husband in 1949 and at that stage he was a smoking at least 20 a day. She said that he had told her that he had not smoked prior to joining the Army, and that he started smoking in the Army because of peer pressure and people offering him cigarettes. She said (trans p9 at 25) "he would have been thought a wimp if he hadn't smoked." Mrs Leighton said that she understood that her husband had a cigarette allowance during service, and that he and his fellow soldiers also traded other items with US soldiers for cigarettes. Mrs Leighton said that she understood from her husband that the crew of the ambulance boat would relax with a cigarette, lying in the sun.
Mr Schey was the Captain of the ambulance boat on which Dr Leighton served (R6). The Tribunal had before it a statement from him and he gave evidence. Mr Schey said that he could not recollect any of his medical orderlies smoking. He added that he believed he would remember if they had done so. He told the Tribunal that all the ambulance boat trips were done in the same vessel, Ambulance Boat AH 1569. He said that there were seven people in the crew, an engineer and two deck hands as well as the three medical orderlies and himself. He explained that the boat was based at Torokina on Bougainville, where there was quite a big military hospital. He said that the boat ran a regular schedule. Every second day, in the afternoon, they would go down to Motupina Point and stay overnight. Next day they would come back with walking wounded and stretcher cases. He said the trip would take four and a half hours going down in the afternoon as the seas would be rough. On that trip they would take passengers and parcels. Next morning they would load up with the wounded and the seas would always be very calm on the trip back.
Mr Schey said that he did not remember any of the crew smoking, even when the boat was down at Motupina Point, and the crew would be at a loose end away from their home port (trans. p17). He said the boat would remain tied up at the jetty, and the men would go swimming occasionally to fill in the time, but he did not remember any of them smoking. He said he did not smoke and there was no peer group pressure to smoke. He said some of the wounded would smoke on the boat.
(ii)Inhalation of fumes
Mrs Leighton said that her husband had said there were a lot of fumes on the ambulance boat. He had told her that the cabin where the wounded were tended was right near the engine. Mrs Leighton said that he had also mentioned cooking for the crew on a little stove. She understood that it was an unhealthy environment mainly due to fumes from the engine. Mrs Leighton said that her husband had implied that he was continuously affected by fumes from the boat.
Mr James who served on a similar ambulance boat had provided a statement for the VRB hearing (T4 p26) which read.
H.J.(Jack).James
TO WHOM IT MAY CONCERN:
I, the above mentioned, served in W.W.II from 28.10.1944 to 12.10.1945, overseas in New Guinea as VX119491 W.O.1 Regimental Sergeant-Major H.Q 3 Group Australian Water Transport R.A.E.A.I.F. Among the units under command of this group was 1 Water Ambulance Convoy RAE AIF which was split into 3 detachments and 7 sections and served in all areas of the South West Pacific. The vessels of this unit comprised 40 ft. (wooden) work boats, 62 ft. Halvorsren designed fast supply launches, and a 91 ft. Sea Ambulance ketch.
They were used to transport stretcher cases and walking wounded from the shore out to the fast supply launches which were fitted out to carry 17 stretchers; and were then transported out to open roadsteads where the hospital ships were anchored in deep water.
These launches were powered by a variety of engines – 108 HP Chrysler royal marine diesels, V8 114 HP Cadillac conversion petrol engines, and 2/500 HP diesel engines. All these were installed below decks in confined spaces and personnel servicing or fuelling them would be exposed to vapours and fumes, sometimes for long periods of time.
Fuel was hand pumped from a 44 gallon drum into the engine, although later models of launches were fuelled at a landing jetty. When a drum was opened in the "tropics" the vapo[u]r issuing from the hole was a shimmering haze, exposure from this was inevitably detrimental to the health.The Tribunal had before it three different versions of Mr Schey's recollection of the extent of fumes on the ambulance boat. First, there was the record of the evidence Mr Schey gave to the VRB, as set out in its decision (T2). Then there was a summary of a telephone interview Mr Piper conducted with Mr Schey, set out in Mr Piper's report of 13 February 1999 (R5). Thirdly, Mr Schey gave evidence to the Tribunal. There were significant variations in the three versions, and even inconsistencies in Mr Schey's evidence at the hearing.
The VRB decision of 28 May 1998 records Mr Schey's evidence as follows (T2 p12):
Mr. Schey said the others in the crew, apart from himself, took turns sitting at the stern of the boat where they were exposed to the exhaust fumes. He said that even when it was windy the fumes would eddy around the stern of the boat. He said there was nowhere else on the boat where they would have been exposed to exhaust fumes because there was no exhaust leakage within the boat. He said when the seas were rough, the crew went undercover rather than stay out the back of the boat. Mr. Schey said he never had any complaints from any of the crew as to the effects of the exhaust fumes.
Mr Piper's report stated (R5);
Mr Schey was interviewed by phone on the evening of 11 February 1999. He advised that the engine on AH 1569 was a "straight eight" (Chrysler Royal RM8 petrol) with low compression and twin updraught carburettors.
. . .
Both he and other crew members used to tune the engine by adjusting the timing with the distributor as well as richening and leaning the mixture on the carburettors. This was to obtain maximum performance. . . .
The exhaust system on the boat, at the back, was not underwater. The vessel was very well designed and built. There were no fumes and considerable breezes and winds when underway. They departed every afternoon about 1 p.m., usually in breezy conditions, as is consistent with weather patterns on the sea in the Pacific.At the hearing before this Tribunal Mr Schey said that since seeing a diagram of the boat sent to him by Mr Piper he had realised there could not have been any exhaust fumes at the stern of the boat. He said that the doors of the cabin were kept closed and it was impossible that any fumes coming from the engine could enter the cabin. In cross-examination Mr Schey agreed that because it was warm weather the doors at the rear of the cabin would probably be open in the mornings when the sea was calm, and the front door of the cabin would also be open. He said that he did not think there would be fumes in the cabin, because the air would naturally pass through the cabin and out the rear doors.
Further Mr Schey said that the exhaust fumes would not get into the cabin, even if the doors were open, because the exhaust was at the very stern of the boat and the exhaust fumes were well away from the boat. When the Tribunal asked Mr Schey about the smell of fumes on boats generally, he said, "on any boat there is the smell of oil, which people confuse with the smell of exhaust." He said boats "if they are designed at all properly have the exhaust out the stern of the boat." He said that his memory was that "you just could not smell any exhaust" (trans. p27).The Tribunal asked Mr Schey whether it was possible that the exhaust which ran from the engine, approximately mid-ships, could be corroded through exposure to salt water. He said that was not possible because it was a new boat. He said he did not think there would have been a loose seal or joint, because if there had been the crew would have smelt the fumes, and it would have made it very unpleasant.
When Mr Moore asked Mr Schey to explain the difference between his evidence to the Tribunal, and that recorded by the VRB, Mr Schey said that he thought the evidence he gave to the VRB was true when he gave it, but that since then he had spoken to Mr Piper and had seen a diagram of the boat. He said:
"I'm satisfied it didn't happen."
He explained: (trans p19).
I didn't have the benefit of these diagrams at the time. Since then Bob Piper has been in touch with me, he has sent me these diagrams, and now I am much wiser. I've had a time to look at these diagrams and realise that I was just trying to be just too generous.
Mr Schey said the refuelling of the vessel took place at Puruarata Island (trans p22). He said he usually took charge of the refuelling, and the crew might be around, or they might wander off. He said he did not remember a lot of fumes during the refuelling process. Mr Schey said he refuelled every second day and the process took half an hour to three-quarters of an hour.
medical evidence
It was conceded by the respondent by letter dated 4 August 1999, (attachment to R7), that the exhaust fumes to which the veteran may have been exposed would have contained benzene. However, the respondent submitted that the exposure would have been far too small to be of any aetiological significance in the causation of Dr Leighton's myelofibrosis. There is medical evidence raising a hypothesis linking benzene exposure with the development of myelofibrosis. The question for the Tribunal is whether such a hypothesis is reasonable regardless of the extent of benzene exposure, or whether it only becomes reasonable if the exposure is substantial or significant or of some particular quantity or duration. The evidence is that epidemiologists commonly look to exposure expressed in terms of "parts per million years".
Terminology
One complication in this matter is the number of different terms which can be used to refer to myelofibrosis. Witnesses at the hearing agreed that other names given to that same condition include "anogenic myeloid metaplasia", "myelosclerosis" and "myeloproliferative disorder". We find that those terms all describe the same condition.
A difficulty as to terminology arose from Dr Bisby's evidence. He is a physician specialising in occupational medicine. Dr Bisby had provided three reports which were received into evidence as exhibits A1, A2 and A3. In his first report of 23 February 1999 (A1), Dr Bisby wrote of myelofibrosis:
Alternative names for this condition are myeloproliferative disorder, myelodysplastic syndrome or myelodysplasia.
In his second report (A2), Dr Bisby summarised a number of articles on myelofibrosis and some articles highlighting relative risks for various diseases from exposure to benzene including exposure from cigarette smoking. The articles on smoking suggested it may be linked with "myelodysplastic syndrome". That report prompted a suggestion made by a representative of the respondent that Dr Bisby had referred to "the wrong disease".
In his third report (A3), Dr Bisby responded to the suggestion that he had referred to "the wrong disease":
My report does not "refer to the wrong disease" as stated in this letter. The overall conclusions stated in Ms McCulloch's letter are incorrect, as are some of the factual matters. The death certificate states that Dr Leighton died of "Myelofibrosis". Myelofibrosis, as I stated, is synonymous with myelodysplastic syndrome (see Mosby Medical dictionary) and other names are commonly used to mean the same disorder. The primary form of this may be referred to as agnogenic myeloid metaplasia. In Dr Leighton's case the term myelodysplastic syndrome was used in the report from his treating specialist Dr John Zalcberg in his letter to Dr Leighton's general practitioner dated 14 October 1994.
While it is true that Dr Zalcberg in his letter of 14 October 1994 (T7 p55), did use the term "myelodysplastic syndrome" to describe Dr Leighton's disorder, his earlier letter (T6 pp53-54) had stated that Dr Leighton almost certainly had myeloproliferative syndrome. All the medical witnesses, other than Dr Bisby, agreed that "myelodysplasia" and "myelodysplastic syndrome" are terms used to describe a disorder which is not the same as myelofibrosis.
Dr Parkin was asked about Dr Bisby's reference to Mosby's Medical Dictionary as authority for his view. He replied (trans. p45):
The editor of the Dictionary was confused too, I would think.
Professor Fox said (trans. p89):
I don't think anyone would consider myelofibrosis and myelodysplasia to be related diseases. They are entirely different disease processes.
He suggested that he would like to look at Mosby himself (trans. p90).
Professor Peach agreed with Dr Parkin and Professor Fox. In his second report of 20 May 1999 (R4) he contrasted "myelofibrosis" with "myelodysplastic disorders". He wrote that the terms "myelofibrosis" and "myelosclerosis" describe progressive replacement of the bone marrow with fibrous tissue. He wrote of "myelodysplastic syndrome":
(b)Myelodysplastic syndrome
The myelodysplastic disorders are those disorders in which usually all or nearly all haematopoietic cell lines are affected but unlike the myeloproliferative diseases it is characterised by hypoproliferation.
After the hearing the Tribunal looked at the current, 5th, edition of Mosby's Medical Nursing and Allied Health Dictionary (1998). It does not say that myelofibrosis is synonymous with myelodysplastic syndrome. The entry for "myelofibrosis" is as follows:
myelofibrosis the replacement of bone marrow with fibrous tissue. The condition may be associated with anaemia, thrombocytopenia, myeloid metaplasia, new bone formation, polycythemia vera, and other abnormalities. Also called myelosclerosis. See also myeloid metaplasia
That entry follows the entry for "myelodysplasia" which makes no reference to "myelofibrosis". The confusion seems to have been on the part of Dr Bisby, rather than Mosby's Medical dictionary. The Tribunal forwarded the relevant extracts to the parties and invited further submissions on the issue. No further submissions were made.
In Repatriation Commission v Cooke (1998) 52 ALD 1 the Full Court of the Federal Court held that the issue whether a veteran suffers or suffered from a disease or injury was to be decided to the reasonable satisfaction of the Repatriation Commission. We are satisfied that Dr Leighton suffered from myelofibrosis (which may also be described as "anogenic myeloid metaplasia", "myelosclerosis" and a "myeloproliferative disorder") and did not suffer from myelodysplasia or myelodysplastic syndrome.
Smoking
That issue as to terminology is relevant to the question of whether the material raises a reasonable hypothesis connecting smoking with myelofibrosis. Mr Moore relied on smoking only as part of the hypothesis relating myelofibrosis to benzene exposure. Dr Bisby on the other hand referred to smoking as creating a risk because of exposure to products other than benzene. He wrote in his first report of 23 February 1999 (A1):
Dr Leighton was a smoker for many years, and smoking is considered to increase the risk of later development of myelofibrosis and related disorders. It is therefore a reasonable hypothesis that his years of cigarette smoking did increase his risk of later development of myelofibrosis. It is not possible to quantitatively estimate the additional risk due to smoking, but the most relevant information suggests that the risk in a smoker of many years is increased by 50% to 100% over the risk to an otherwise comparable non-smoker. (emphasis added)
Although Dr Bisby referred to cigarette smoking being considered to increase the risk of later development of "myelofibrosis and related disorders", Professor Fox and Professor Peach said there is no such finding reported in studies. The studies extracted by Dr Bisby as showing a link between smoking and "the disease" in his report (A2), relate to myelodysplastic syndrome and not to myelofibrosis. As explained in paragraph 32 of these reasons, we are satisfied that myelodysplastic syndrome is not the same disease as myelofibrosis.
Mr Moore read to Dr Bisby an extract from an article by Sir Richard Doll entitled "Cancers weakly related to Smoking" published in the British Medical Bulletin on Tobacco and Health, Volume 52 No 1 January 1996 (A8). In that article Sir Richard Doll suggested that smoking 20 to 40 cigarettes a day exposes a smoker to between 1 and 3mg of benzene which might over a 40 year period increase the risk of leukaemia by about 10%. When Dr Bisby was asked to comment on that, he agreed that smoking increases the risk of cancers, but he said he would not personally focus just on two of the carcinogens contained in cigarette smoke, namely benzene and radioactive isotopes of polonium and lead, as in the Doll article. He said that cigarette smoke is a potent carcinogen in itself. He said he did not consider it logical to isolate individual compounds in cigarette smoke. He mentioned that there are other carcinogens not mentioned in the article such as nitrosamines and betanaphthylamine (trans. p60) which are much stronger carcinogens than the benzene in cigarette smoke. In fact that same point is made by Sir Richard Doll in the article to which Mr Moore referred. Dr Bisby said, "[when] rats or humans inhale cigarette smoke they will get cancer including, in the case of humans, leukaemias and myelofibrosis." (trans. p60). However he gave no reference to any article or study linking smoking and myelofibrosis.
In his second report of 14 April 1999 (R2), Professor Fox referred to Dr Bisby's report (A1) raising the issue that smoking is considered to increase the risk of later development of myelofibrosis and related disorders. Professor Fox wrote that there was certainly information that smoking can increase the risk of acute myeloid leukaemia, but he said he was not aware of any information to suggest that smoking increases the risk of myelofibrosis. He said that a computer based search of the Medline data base from 1999 back to 1965 did not reveal any link between myelofibrosis and smoking. He suggested that Dr Bisby should be asked for references to support his statement that the most relevant information suggests that the risk [of myelofibrosis] in a smoker in many years is increased by 50 to 100% over the risks for an otherwise comparable non-smoker. None of the references set out by Dr Bisby in his report (A2) do link myelofibrosis and smoking. Those dealing with smoking refer to myelodysplastic syndrome or myelodysplasia.
Professor Peach said that there was no scientific study which suggested a connection between smoking and myelofibrosis. He said that the most basic fact about myelofibrosis is that it has an equal incidence in men and women. He said that he did not know of any smoking related cancer which did not have a greater incidence in men than in women. He said that was because there was a higher level of smoking among men than among women.
Professor Peach said that there are a number of studies looking at the link between smoking and myelodysplastic syndrome, but that is not the same disease as myelofibrosis. Professor Peach concluded in his report (R4 p7):
4.I am not aware of any epidemiological studies which have found a causal association between smoking and myelofibrosis and myeloid metaplasia. A study which sought an association between smoking and a group of myeloproliferative diseases which included idiopathic myelofibrosis failed to find such an association.
5.I am not aware of any epidemiological studies which point to smoking being associated with the transformation of myelofibrosis into acute myeloid leukaemia.
6.The fact that gender has been found not to be of any prognostic value in myelofibrosis points to smoking not being associated with the transformation of myelofibrosis into acute myeloid leukaemia.
7.Cases of AML with myelofibrosis make up such a small number of all AML cases that associations between smoking and AML cannot be used to point to smoking causing transformation of myelofibrosis into AML.
Mr Moore asked Professor Peach to comment on the Doll article (A8) p42, which suggested that there may be an increased risk of myeloid leukaemia for cigarette smokers. Professor Peach said that he agreed that there is a nexus between smoking and acute leukaemia. He pointed out that he had acknowledged that in his second report (R4). But he said he would "Absolutely not", extrapolate from that fact to a hypothesis of a nexus between cigarette smoke and myelofibrosis. He said (trans. p126):
Absolutely not because as I said back at the very beginning, acute myeloleukaemia is more common in men than women, but myelofibrosis is – has an equal incidence in men as in women and how you explain cigarette smoking causing myelofibrosis without the male excess is beyond me, and also when people looked at the cases of myelofibrosis which transformed into acute myeloleukaemia and looked to see what were the predictive factors, you know, which were the patients with myelofibrosis who were going to get acute myeloleukaemia, they looked to see whether there was a sex difference and there was not. So myelofibrosis occurs with an equal incidence in men and women and the transformation from myelofibrosis to acute myeloleukaemia occurs equally in men as it does in women and that to me is contrary to the hypothesis that smoking causes myelofibrosis and Richard Doll to my mind – I've read all his stuff – has never ever suggested smoking causes myelofibrosis.
We are satisfied that Dr Bisby's evidence as to smoking does not raise or point to a reasonable hypothesis because it stems from Dr Bisby's mistaken view that myelofibrosis is the same condition as myelodysplastic syndrome and thus that studies showing a connection with myelodysplastic syndrome and smoking apply also to myelofibrosis. We agree with Mr Douglass's submission that there was no material before us of any epidemiological studies linking smoking with myelofibrosis.
Inhalation of benzene from petrol and fumes as an aetiological factor in development of myelofibrosis
Dr Parkin was Dr Leighton's treating haematologist. He is the Director of the Division of Laboratory Medicine at the Austin and Repatriation Medical Centre. On 15 September 1997 Dr Parkin replied to Dr Bray Lewis who had asked him whether a link could be made to associate war service and the subsequent development of myelofibrosis. Dr Parkin wrote (T docs p32):
Further to your enquiry as to whether a link could be made to associate war service and the subsequent development of myelofibrosis. Myelofibrosis is as you know an unusual disorder with an average age at onset of about 60 years. The disease is characterised by progressive marrow fibrosis, splenomegaly and increasing pancytopenia.
In most cases myelofibrosis is apparently a primary condition. However it has been associated with atomic radiation, the contrast medium thorotrast and industrial solvents including benzene and toluene.If military service led to a substantial exposure to petroleum or benzene then perhaps a case could be made to support a link between myelofibrosis and military service. The delay in onset to many years after military service should not be an impediment. It is clear that the genetic path to cancer often requires the accumulation of a variety of specific genetic abnormalities which only occur with time. (emphasis added)
On 12 December 1997 Dr Parkin wrote a much fuller report (T docs pp28–31) in which he described the disease of myelofibrosis, and considered its association with benzene exposure. He wrote that idiopathic myelofibrosis, the form Dr Leighton was considered to have, is a cancer of a primitive blood stem cell, and marrow fibrosis is a reaction to that malignant process. Dr Parkin continued:
The question which requires to be answered is whether a relation exists between war service and myelofibrosis. I believe this relationship can be sustained by two observations. Firstly a literature which describes a causal association between myelofibrosis and benzene. Secondly a clear history of exposure to benzene during war service through benzene contamination of exhaust fumes in the ex-member's naval work environment.
In his 12 December 1997 report Dr Parkin had, in his formulation of a hypothesis linking war service and myelofibrosis, dropped his earlier requirement that exposure to benzene must be "substantial".
Dr Parkin in his report of 12 December 1997, referred to a study and three case reports which showed an association between myelofibrosis and benzene exposure. Dr Parkin also quoted passages linking toxic exposure to benzene with myelofibrosis in two standard haematology text books. Dr Parkin wrote that vehicle exhaust fumes contain benzene. On the basis that the exhaust fumes of an ambulance boat would also contain benzene, he suggested that a reasonable hypothesis could be made linking Dr Leighton's war service and his idiopathic myelofibrosis. Dr Parkin summarised that hypothesis as follows (T docs p31):
(i)Agnogenic myeloid metaplasia or idopathic myelofibrosis has been attributed to benzene.
(ii)Benzene is a significant component of gasoline derived exhaust gases.
(iii)The ex-member had significant exposure to exhaust gases in his work on a water ambulance.
(iv)Agnogenic myeloid metaplasia is a clonal malignant disorder. The delay between exposure and the disease is entirely consistent with the known latent period between environmental exposure and subsequent malignancy in a variety of circumstances where environmental factors are involved in the causation of cancer.
In evidence, Dr Parkin confirmed the opinions advanced in his report of 12 December 1997 (T docs p31). Mr Moore asked him about the development of leukaemia in patients with myelofibrosis, as the connection between benzene exposure and acute myeloid leukaemia is well recognised. Dr Parkin explained that the estimates are that from about 5% to 25% of people with myelofibrosis develop acute myeloid leukaemia. The other medical witnesses were in general agreement with that estimate.
Dr Parkin explained that the diagnosis of acute leukaemia is made where there is an excess of 30% of marrow nucleated cells which are described as blast cells. He said that when a patient has myelofibrosis you can not actually aspirate bone marrow, so the diagnosis becomes more difficult (trans. pp33-34). He said that the result of full blood examinations (ex A6) showed that Dr Leighton consistently had a very small number of blast cells in the peripheral blood. He said that blast cells are a necessary requirement for the diagnosis of leukaemia. In this case the finding of a very small number of blast cells in the peripheral blood does not indicate that Dr Leighton had acute leukaemia.
Even though there was no evidence suggesting, raising or pointing to the fact that Dr Leighton had acute leukaemia, Mr Moore asked Dr Parkin to explain the link between exposure to benzene and leukaemia. Dr Parkin then varied the hypothesis, as set out in his letter dated 12 December 1997 (T docs pp28-31), to include the fact that leukaemia risk can be related to the degree and length of exposure to benzene. He produced extracts from an EPA report Carcinogenic Affects of Benzene: An Update, National Center for Environmental Assessment–Washington Office, Office of Research and Development, U.S. Environmental Protection Agency Washington, DC (A7). He said that report substantially reduced the actual concentration of benzene which "clearly gave rise to added risk of leukaemia genesis". He said that over the last 20 or 30 years as more information has become available, "the safe level of benzene has been consistently reduced". Dr Parkin said at trans. pp37–38:
And this very substantial document really has just two major conclusions in the abstract. And they are, firstly, that a linear dose response curve – it actually says:
There is insufficient evidence to deviate from using an assumption of a linear dose response curve for benzene.
Now, I'm not an epidemiologist, but I take that simply to mean that in a linear way any increment in the concentration of benzene is associated with an increment in the risk of developing leukaemia.
. . .
The second conclusion from this document is in relation to an absolute risk. Now, although I think the EPA recommendation, and I think there were Commonwealth recommendations which talk about 42 parts per million years and such like. The EPA actually states here that there is at one part per million of benzene an absolute risk which ranges from 7.1 per thousand to 2.5 per hundred. So what they're saying is that at that very low exposure to benzene of one part per million there still is an identifiably increased risk of leukaemia. I mean, one may, I guess, spend weeks going through the literature and the epidemiology and statistics of these associations, I'm certainly neither a statistician nor an epidemiologist, and certainly not fitted to make any comments in that area, but that information has all been digested by experts, a panel of experts, and presented in this document. So, I mean, that's I think the best expert statement that we have about the situation at the moment. (emphasis added)Dr Parkin then proposed a reasonable hypothesis as follows (trans. pp38–39):
(i)benzene exposure was first associated with acute leukaemia in case reports;
(ii)a dose relationship was established with acute leukaemia and benzene in cohort studies;
(iii)the relationship between benzene and acute leukaemia was reproduced in animal models;
(iv)leukaemia is a disease of the haematological stem cell, it is a stem cell disorder;
(v)benzene can be shown to induce dose dependent changes in these haematological stem cells in animals.
Then turning to "follow the same steps through with myelofibrosis", Dr Parkin added (trans. p40–41):
(i)myelofibrosis has been associated with benzene exposure in case reports;
(ii)myelofibrosis has also been associated with benzene exposure but not in all cohort studies;
(iii)myelofibrosis is clearly a disorder of the haematological stem cell, as is leukaemia;
(iv)myelofibrosis also exhibits non-random cytogenetic changes, and those cytogenetic changes are exactly similar to the ones that are most often seen in myelodysplasia and acute leukaemia. So those critical points of damage to DNA, which the best information tells us is what makes the cell behave as a cancerous cell, are very similar in myelofibrosis and myeloproliferative diseases, which is the bigger group that it comes from, as it is in acute leukaemia and myelodysplasia;
(v)there is a close clinical association between myelofibrosis and acute leukaemia. . . . somewhere between five and 25 per cent of cases of idiopathic myelofibrosis terminate as acute leukaemia;
(vi)other mutagenic agents, for example, ionising radiation, can also produce leukaemia and myelofibrosis. What I am saying is that benzene, which presumably acts by a fairly common mechanism of damage of DNA, is like other mutagenic agents;
(vii)myelofibrosis, idiopathic myelofibrosis and acute myeloid leukaemia have a very, very close relationship.
There is no dispute about it being a reasonable hypothesis that the development of myelofibrosis may in some circumstances be linked with exposure to benzene. Professor Fox and Professor Peach, as well as Dr Bisby agreed with that suggestion if the exposure is significant or substantial. Dr Parkin, who had himself in his letter of 15 September 1997 (T docs p32) qualified the hypothesis so as to require "a substantial exposure to . . . benzene", recognised that difficulty. He said at trans. p41:
And the third thing that I would like to do is to try and produce a hypothesis to deal with very low dose benzene exposure, because I think that's going to be the major problem for the court [sic]. And as I said before, public health data in this area generally lags behind the known facts in benzene/leukaemia genesis, and for that reason the trend over some decades has been to reduce the permissible levels of benzene, not to increase them.
Dr Parkin acknowledged that the extract from the EPA report, (A7), talks of a linear dose effect. However he did not refer to the fact that the abstract makes the point that "Occupational Studies continue to provide the bulk of evidence of benzene's carcinogenecity. Workers are exposed at much higher levels than the general public." Although the major issue in the study involved, "the nature and magnitude of the inhalation risk of cancer to humans exposed to low levels of benzene" its findings related only to "highly exposed occupational cohorts". The authors commented:
Currently, there is insufficient evidence to deviate from using an assumption of a linear dose-response curve for benzene, hence, the Agency's past approach of using a model with low-dose linearity is still recommended.
Dr Parkin advanced an argument as to the danger of even low levels of benzene exposure based on the article by Sir Richard Doll "Cancers weakly related to Smoking" referred to in paragraph 35 of these reasons (A8). He claimed that it was Sir Richard Doll's view that benzene is the factor causing the leukaemogenic effect from cigarette smoking (trans. p42). He suggested that, if that is so, a very small amount of benzene exposure must be creating those leukaemogenic effects. Dr Parkin said at trans. p42:
So if, as Professor Doll says, it's the benzene in cigarette smoke that causes the leukaemia, then, in fact, the leukaemia is caused by exposure to .005 parts per million, which is very small and certainly of a different order of magnitude altogether to the one part per million identified by the EPA.
Then if, in fact, there is a linear relationship between exposure and leukaemia one would have to say that any exposure to benzene is additive, that is, the benzene that we're exposed to normally in the environment plus what the ex member might have smoked plus any molecules of benzene which [Dr Leighton] may have inhaled from the exhaust. . . .
He proposed a reasonable hypothesis at trans. pp42-43:
The combination of what [Dr Leighton] would inhale from the environment plus his smoking plus what comes from the exhaust would be additive according to this model, and therefore certainly in terms of providing a reasonable hypothesis, not scientific proof but a reasonable hypothesis, I think therefore a reasonable hypothesis can be sustained. I mean, to deny that hypothesis would have to be to deny that smoking caused leukaemia and that it was due to benzene, which is, in fact, the opinion of Sir Richard Doll, who is the major international epidemiologist of the 20th century.
There seem to be a number of inaccuracies in Dr Parkin's evidence. First, Professor Doll, (A8 at p42), did not say it is the benzene in cigarette smoke that causes the leukaemia. He wrote that the benzene in cigarettes is likely to be more important than radioactive isotopes of plonium and lead, as they are present in cigarettes in only minimal amounts. But he added "other chemicals in smoke may prove to be equally or more important". Secondly, he did not, in the extract received in evidence, give the estimate of benzene exposure from smoking as 0.005 parts per million. He wrote:
According to Hoffman and Hoffman the consumption of 20–40 cigarettes a day exposes a smoker to between 1–3 mg of benzene which, according to calculations made for the US National Institute for Occupational Safety and Health might, over a 40-year period, increase the risk of leukaemia by about 10%.
Mr Douglass, in cross-examination, started to ask Dr Parkin about the published studies, and suggested that they only found a causal association between myelofibrosis and benzene where there was a "high level industrial exposure to benzene", Dr Parkin replied at trans. p45:
I am not an expert in industrial medicine, and it would probably not be helpful to take me through the epidemiology of these cases. The point I was trying to make was that both in individual case studies and in cohorts an increase in the observed cases of meylofibrosis is recorded. Now, if you wish to discuss the kind of statistical validity of these studies you're taking me outside my competence.
Dr Bisby, who was also called on behalf of the applicant, did not agree with Dr Parkin's opinions about low level exposure to benzene being a risk factor for myelofibrosis. He wrote in his first report of 23 February 1999 (A1 p3):
As far as is known, there is no risk of leukaemia, or myelofibrosis or other lympho-haematopoietic disorder to workers where exposure is less than about 1ppm time-weighted average exposure over a working lifetime (usually taken as 40 hours per week, for 40 years).
He maintained that view in his evidence saying, at trans. p57:
In my view his exposure to benzene did not put him in a category where on the evidence one could say that he was at higher risk of this disease from exposure to benzene, . . .
Dr Bisby in his report of 23 February 1999 (A1), quoted passages from the review by Infante, of the Office of Standards and Review, Occupational Safety and Health Administration, United States Government – Benzene and Leukaemia, Cell types latency and amount of exposure associated with Leukaemia in Advances in Occupational Medicine and Rehabilitation Vol 1 No 2 1995 FSME Pavia. The passage quoted deals mainly with the link between occupational exposure to benzene and leukaemia but in the conclusion states: "as well . . . myelofibrosis [has] been reported in association with benzene exposure."
Dr Bisby made it clear in his report of 23 February 1999 that he considered Dr Leighton would have had only low levels of exposure to benzene during service. He wrote:
Dr Leighton's exposure to benzene during war service
I have carefully reviewed the information about Dr Leighton's potential exposure to benzene during his war service.
He had some exposure from exhaust fumes when on board ambulance boats, whether petrol or diesel driven. Given the times involved and other factors, this exposure was low.
He would have had some exposure to benzene in petrol fuel, on petrol driven boats, but again this exposure was probably low, perhaps minimal, as he was not involved with refuelling or maintenance. His exposure therefore could not be characterised as "occupational exposure" and was "background" exposure only.
. . .
Summary and opinion.
Dr Leighton died of myelofibrosis at the age of 74 years. The causes of almost all cases of myelofibrosis in the Australian population are unknown.
. . .
His exposure to other sources of benzene [ie not due to smoking] even during war service was not high, and not in a category where he could be characterised as being "occupationally exposed" to benzene. Therefore, his exposure to benzene from the sources identified in relation to his wartime duties cannot be said to have increased the risk of developing myelofibrosis, or related disorders, later in life.Both the respondent's witnesses, Professor Fox and Professor Peach, agreed that there is a reasonable hypothesis of an association between myelofibrosis and occupational benzene exposure, where such exposure is significant occupational exposure. Neither Dr Bisby nor Professor Fox or Professor Peach considered that exposure to benzene from fumes on the deck or in the cabin of an ambulance boat, for 12 months in 1945, could have been sufficient exposure to raise a reasonable hypothesis of an association with myelofibrosis in this matter.
The difference between Dr Parkin on the one hand and Dr Bisby, Professor Fox and Professor Peach on the other hand, depended on their reading of epidemiological articles in the medical literature. Mr Douglass asked Dr Parkin whether he would contest Professor Peach's assertion that the concentration of benzene to which one would need to be exposed over a short period of say 1.3 years, (in fact the relevant period on the ambulance boat was 1 year) before developing a significant increased risk of developing leukaemia (not myelofibrosis), was 130 micrograms per cubic metre. Dr Parkin said he would disagree with Professor Peach's assertion as it was not consistent with "this China study" which, he said, showed that exposure to less than 10 parts per million conferred a significant increased risk of leukaemia (trans. p50). He described that as "significantly lower than the Pliofilm cohort" which is one of the relevant cohort studies.
Dr Parkin did not produce a copy of the study to which he referred as "this China study". Nor was it referred to in his report of 12 December 1997 (T docs pp28–31). Dr Parkin may have been referring to a paper by Hayes RB et al "Benzene and the Dose-Related Incidence Of Haematologic Neoplasms in China" Journal of the National Cancer Institute 1997; 89: 1065-1071. That paper was referred to by Professor Fox (R1) and Professor Peach (R3) in their reports.
Both Professor Fox and Professor Peach in their summaries of the Hayes paper, acknowledged that it showed an increased risk of developing haematological neoplasms with historical exposure at average levels of less than 10 parts per million. But one significant matter about that study, to which Dr Parkin did not refer, was that although it dealt with a cohort of 75,000 benzene exposed workers and almost 36,000 unexposed workers, Professor Fox stated, "There was no evidence of myelofibrotic syndrome as a sequel of benzene exposure".
In his first report of 8 February 1999 (R1), Professor Fox summarised a number of papers in the medical and scientific literature on the relationship between exposure to benzene and haematopoietic malignancies, as well as benzene exposure and myelofibrosis. He commented that none of the large epidemiological studies have shown a relationship with benzene exposure and myelofibrosis, even though there are fairly numerous individual case reports of individuals exposed to benzene who have developed myelofibrosis.
Professor Fox agreed that a hypothesis suggesting an association between obviously significant benzene exposure and the development of myelofibrosis was not fanciful. However he, like Dr Bisby, was of the opinion that Dr Leighton's exposure to benzene from exhaust fumes on an ambulance boat for 12 months would not be significant. He commented that the time in the Pacific Islands would have exposed Dr Leighton to a lesser degree of benzene exhaust fumes than would have been an everyday experience in Melbourne during the war-time. He made the further point that most of the studies relating benzene exposure to the development of haematopoietic malignancies reflect lifetime benzene exposure.
Professor Peach is Professor of Public Health at the University of Melbourne. He accepted that a number of case reports and a descriptive study have led to the hypothesis that exposure to benzene, in some occupational settings, can lead to myelofibrosis or myelosclerosis. Professor Peach in his report set out summaries of a number of epidemiological studies and case reports and concluded that the case reports "generated an hypothesis that exposure to benzene . . ., in some occupations for between 4 and 26 years may lead to myeloid metaplasia", which is one of the alternative names for myelofibrosis.
Professor Peach wrote that one case report also generated the hypothesis that the course of myelofibrosis may depend partly on the continuation of exposure. Three of the cohort studies, he said, had found a significantly greater mortality from myelofibrosis among workers at oil distribution centres, a petroleum manufacturing plant and Chinese factories and a fourth found a non-significantly elevated mortality from myelofibrosis among petroleum refinery workers. Those studies did not contain information about the concentration of benzene, but one study found the risk of acute non-lymphocytic leukaemia and myelodysplastic syndrome, was increased among workers with a cumulative exposure of 40-99 parts per million years, but only among workers exposed within 10 years of diagnosis.
Professor Peach, in his report, referred to three cohort studies which have calculated the cumulative exposure of workers to benzene and then reported the occurrence of leukaemia among workers in various categories of exposure. Those studies are cohorts of workers employed by Pliofilm, Dow and CMA Industries. After referring in some detail to the findings of those studies, Professor Peach, in his report, concluded that in all three studies no adverse effect for acute myelocytic and monocytic leukaemia was shown at levels below 400 parts per million (Pliofilm Cohort), 83 parts per million (Dow Cohort), and 60 parts per million (CMA Cohort). Professor Peach then referred to a recent re-analysis of the Pliofilm Cohort and commented (R4 p10):
A critical concentration of benzene exposure had to be reached in order for the risk of leukaemia to be expressed and this depended on the exposure estimates used in the analyses. For acute myelocytic and monocytic leukaemia the minimum concentration was 20 parts per million. The duration of exposure had to be several years, the average being 13 years for acute myelocytic and monocytic leukaemia.
Professor Peach explained that the standard method of measuring exposure is to multiply the number of years of exposure by the "parts per million" to obtain "parts per million years".
In his evidence Professor Peach, like Professor Fox, explained that everyone is exposed to benzene as it occurs naturally in the environment. He said at trans. pp112–113:
[B]enzene occurs naturally in the environment. I mean the coal in the strata of the earth leaks benzene into the soil and into the water. The world's volcanos emit benzene into the atmosphere and the world's forests and vegetation emit benzene. And in fact if you take myself, for example, living in Melbourne, every day I could be exposed to 400 micrograms of benzene from exhaust in motor vehicles. I could be exposed to up to 250 micrograms of benzene every day for food, and up to 5 micrograms per day from water. Now, everybody is exposed to benzene, but myelofibrosis only occurs in one per 100,000 of the population, it is a very rare disease. So not everybody who is exposed to benzene gets myelofibrosis. And it was suggested . . . –if benzene does cause myelofibrosis it is only if high concentrations. And the significance of these [epidemiological cohort] studies is that they give us, at least in the case of acute myeloid leukaemia, an idea of the sort of exposure which is necessary to cause acute myeloid leukaemia. And the unique thing about these studies is that the workers were exposed to benzene and very few other chemicals.
In looking at possible exposure during Dr Leighton's 12 months service on an ambulance boat, in the South Pacific, Professor Peach referred to figures as to exposure from car exhausts and while refuelling at a petrol station. He said that even the highest of those figures, that for refuelling at a petrol station, would not give Dr Leighton anywhere near the threshold figures that have been found to be related to acute myeloid leukaemia, which the studies suggest, has a higher correlation to benzene exposure than does myelofibrosis.
Professor Peach was asked about Dr Parkin's evidence that the safe threshold level for exposure to benzene is constantly being lowered. He agreed that for safety reasons thresholds are constantly lowered below what the scientific evidence really suggests. He said that is called "prudent avoidance". But he added that no scientific paper has suggested that there is no threshold for benzene exposure. He repeated what Professor Fox had said, namely that as we are all exposed to benzene, and yet there is a very low incidence of myelofibrosis, there must be a threshold.
In cross-examination Mr Moore asked Professor Peach whether, as some studies had found a suggestion of a relationship between industrial exposure to benzene and myelofibrosis, epidemiologists had progressed to further studies which found whether lower levels of exposure to benzene might also have a causal association with myelofibrosis. Professor Peach said no such studies had been done because the industrial cohort studies did not provide sufficient epidemiological evidence of a link between benzene exposure and myelofibrosis to justify an application for funding for a study of people without occupational exposure.
Mr Moore asked Professor Peach whether a causal nexus between non-occupational exposure and myelofibrosis had been ruled out. Professor Peach said such a nexus is unlikely. He explained that as there has not been a consistent significant nexus of myelofibrosis among people working in the oil industry, and other industries with a high occupational exposure to benzene, there is no justification for further research among people with less significant benzene exposure. Professor Peach said that one of the problems with science is that you can have great difficulty proving a negative.
Professor Peach said that whatever model of exposure he used, he could not generate a reasonable hypothesis that Dr Leighton's benzene exposure from exhaust fumes of the ambulance boat, from 9 January 1945 to 31 December 1945, could have been of any significance in relation to his development of myelofibrosis.
There is no dispute about the fact that Dr Leighton's exposure to benzene from exhaust fumes would have been low. Dr Parkin was quite correct when he said (see paragraph 51 of these reasons) that the major problem for the Tribunal would be whether "very low dose benzene exposure" raised a reasonable hypothesis connecting the myelofibrosis which caused Dr Leighton's death with the circumstances of his service.
The High Court in Bushell, dealt with the issue of whether a reasonable hypothesis is raised in circumstances where there is conflict between competing medical opinions.Mason CJ, Deane and McHugh JJ at p35 said:
[A] hypothesis cannot be reasonable if it is "contrary to proved scientific facts or to the known phenomena of nature". Nor can it be reasonable if it is "obviously fanciful, impossible, incredible or not tenable or too remote or too tenuous".
But leaving aside cases of those kinds, the case must be rare where it can be said that a hypothesis, based on the raised facts, is unreasonable when it is put forward by a medical practitioner who is eminent in the relevant field of knowledge. Conflict with other medical opinions is not sufficient to reject a hypothesis as unreasonable. As we have earlier pointed out, it is not the function of s 120(3) to require the Commission to choose between competing hypotheses or to determine whether one medical or scientific opinion is to be preferred to another.
This does not mean, however, that in performing its functions under s 120(3) the Commission cannot have regard to the medical or scientific material which is opposed to the material which supports the veteran's claim. Indeed, the Commission is bound to have regard to the opposing material for the purpose of examining the validity of the reasoning which supports the claim that there is a connection between the incapacity or death and the service of a veteran. But it is vital that the Commission keep in mind that that hypothesis may still be reasonable although it is unproved and opposed to the weight of informed opinion. (emphasis added)
In that passage their Honours have stated:
(i)conflict with other medical opinions is not sufficient to reject a hypothesis as unreasonable;
(ii)it is not the function of s 120(3) to require this Tribunal to determine whether one medical opinion is to be preferred to another;
(iii)we are bound to have regard to the medical and scientific material;
(iv)we must use that material for the purpose of examining the validity of the reasoning which supports the claim that there is a connection between Dr Leighton's death from myelofibrosis and his possible exposure to benzene from the inhalation of exhaust fumes and/or from smoking,
(v)we must bear in mind that a hypothesis may still be reasonable although unproved and opposed to the weight of informed opinion.
We have considered the expert evidence and the medical and scientific material to which we have been referred. We are satisfied that the material does not raise a reasonable hypothesis of a connection between smoking and myelofibrosis. We are satisfied that Dr Bisby's opinion on that issue was not "valid" because he had confused myelofibrosis and myelodysplasia or myelodysplastic syndrome. The studies on which he based his opinion did not relate to myelofibrosis. Further we are satisfied that the fact that the incidence of myelofibrosis does not show any gender difference is inconsistent with it being smoking related.
As to the issue of inhalation of benzene from petrol and exhaust fumes, the question is whether for a hypothesis of that connection to be reasonable it requires a level of exposure greater than low or very low exposure. Three of the expert witnesses were of the opinion that what is required to raise a reasonable hypothesis of a connection between benzene and myelofibrosis is "significant" or "substantial" exposure. All the expert witnesses agreed that Dr Leighton's possible exposure to exhaust fumes at the stern of an ambulance boat would have to be characterised as "low" or "very low" exposure to benzene.
Only Dr Parkin advanced the opinion that "very low dose exposure to benzene" could be significant. That evidence from Dr Parkin conflicted with the view he had advanced in his letter of 15 September 1997 to Dr Lewis (T docs p32) where he wrote that it was only if military service led to "a substantial exposure to petroleum or benzene", that perhaps a case could be made to support a link between myelofibrosis and military service. We were not referred to any studies or other medical or scientific material supporting Dr Parkin's attempt to raise a hypothesis linking "very low dose exposure to benzene" with myelofibrosis. The only material supporting the view that such exposure raises a reasonable hypothesis was the evidence of Dr Parkin.
When Mr Douglass attempted to engage Dr Parkin in a discussion of the basis of his changed opinion, he asserted a number of times that he was not an epidemiologist (see paragraph 48 of these reasons). He relied on the proposition that if benzene exposure may be linked with myelofibrosis, then any benzene exposure at all may increase the risk of developing that condition.
In the words of the High Court we must consider "the validity" of Dr Parkin's reasoning. The Full Bench of the Full Court in Bey said at p489:
While a hypothesis may be no more than a possibility or supposition, in order for a hypothesis to be reasonable, it must, as East states, be pointed to or supported, and not merely left open as a possibility, by the material before the decision-maker.
Dr Parkin in evidence, although not in his first report, advanced the hypothesis that any benzene exposure may increase a person's chance of developing myelofibrosis. The other experts thought that to be very unlikely. Mr Moore relied on the fact that they could not prove that it was impossible. As Professor Peach said, it is very difficult to prove a negative. But as the High Court explained in Repatriation Commission v Owens (1996) 70 ALJR 904, the Tribunal must form its opinion as to whether the material raises a reasonable hypothesis on "the whole of the material before it". When we do so it is clear that all the material points to a reasonable hypothesis linking substantial or significant occupational exposure with myelofibrosis, but that there is no material, other than the evidence of Dr Parkin, to support the hypothesis that any level of increased benzene exposure can be associated with a risk of developing myelofibrosis.
However the High Court in Bushell said that conflict with other medical opinions is not sufficient to reject a hypothesis as unreasonable and that it is not our task to determine whether one medical opinion is to be preferred to another. Their Honours said that the Commission and the Tribunal must keep in mind that a hypothesis "may still be reasonable although it is unproved and opposed to the weight of informed opinion." The High Court did not explain in what circumstances that would be the case, although it did say that it would be rare that a hypothesis based on raised facts would be unreasonable if put forward by a medical practitioner eminent in the relevant field of knowledge.
We find ourselves in almost exactly the situation chosen by Heerey J, in Deledio v Repatriation Commission (1997) 47 ALD 261, to explain the role of SoPs. His Honour said at p274:
The concept of "sound medical-scientific evidence" introduced by the 1994 amendments is a standard not unlike the Frye test. In this respect at least, the Parliament has accepted the Baume Committee's criticism of "doctor shopping". If an SoP applies to the particular kind of injury, disease or death in question, a hypothesis will no longer satisfy the test of reasonableness merely by having some expert evidence to support the medical-scientific aspects of the hypothesis. To illustrate by a variation on the facts of the present case, let it be assumed that it could only be established that the veteran increased his animal fat consumption by 20% 50 gm/day for 10 years. Dr X, an appropriately qualified specialist, is called to say that in his opinion that level of consumption could be sufficient to cause malignant neoplasm of the prostate. The commission calls three of the country's leading specialists who vehemently disagree. They say that an increase by at least 40% to at least 70 gm/day for at least 20 years is the minimum required before fat intake can play any part in the development of this cancer. Under Bushell, the hypothesis is nevertheless reasonable. Under the SoP regime it is not.
Adopting His Honour's illustration to fit the material before the Tribunal the relevant passage would read:
[L]et it be assumed that it could only be established that the veteran had a very low benzene exposure during service. Dr Parkin, an appropriately qualified specialist, is called to say that in his opinion that level of exposure could be sufficient to cause myelofibrosis. The commission calls two of the country's leading specialists who vehemently disagree as does the other witness for the applicant. They say that a substantial occupational exposure is the minimum required before benzene exposure can play any part in the development of myelofibrosis. Under Bushell, the hypothesis is nevertheless reasonable. Under the SoP regime it is not.
The Full Court in Repatriation Commission v Deledio (1998) 49 ALR 193 dismissed an appeal from the decision of Heerey J. Their Honours did not specifically refer to the passage quoted in para 82 of these reasons, but they stated, at p204, of their joint judgement that they agreed with Heerey J's explanation "of the early legislation, O'Brien's case, the "reasonable hypothesis" and its operation in Bushell and Byrnes and the role of the SoP."
Heerey J's comments, at p274 were obiter dicta, as in Deledio there was a SoP. However his Honour gave lengthy and full reasons explaining the operation of the reasonable hypothesis standard of proof as well as the role of the SoPs.
We regard Bushell and the two Deledio decisions as establishing that unless we are satisfied that Dr Parkin is not "an appropriately qualified specialist", the hypothesis he advanced must be held to be "a reasonable hypothesis" connecting Dr Leighton's death from myelofibrosis with the circumstances of the service rendered by Dr Leighton.
As set out in paragraph 41 of these reasons, Dr Parkin is the Director of the Division of Laboratory Medicine at the Austin and Repatriation Medical Centre. As he readily acknowledged, he is not an epidemiologist. The hypothesis relied on as to benzene exposure does depend on epidemiological studies. Not only did Dr Parkin decline to answer some questions as to those studies on the ground that he is not an epidemiologist, there were also some inaccuracies in his evidence as to some studies. Those matters give rise to some concern but we cannot find that he is not an appropriately qualified specialist.
According to Professor Fox and Professor Peach, occupational exposure, over a significant period, and at levels significantly above normal everyday exposure of city living is required to increase the risk of developing myelofibrosis. The reason why they suggested that exposure above normal everyday exposure of city living is required, is because myelofibrosis remains a rare disease even among those exposed to benzene in daily city living. Dr Parkin did not address that significant issue. Without doing so the hypothesis which he advanced in our opinion lacks credibility, but it is not our task to determine whether one medical opinion is to be preferred to another.
We have considered Bey, where a Full Bench of the Federal Court allowed an appeal and affirmed a decision of the Tribunal, which had held that the evidence raised a hypothesis of a connection with the relevant disease, but that the hypothesis was not reasonable. In doing so the Tribunal said that the evidence of the specialist who supported the hypothesis "lacked the hallmarks of a properly considered opinion". The Tribunal in Bey commented that the specialists "demeanour was more that of an advocate than of a professional witness."
In this matter Dr Parkin said that he would like "to try and produce a hypothesis to deal with very low dose benzene exposure, because he saw that as a problem. In fact in his first report (T docs p32) he had expressed the opinion that it was only "if military service led to a substantial exposure to petroleum or benzene then perhaps a case could be made to support a link between myelofibrosis and military service" (emphasis added). In the process of changing from that opinion to advance a hypothesis designed to deal with "very low dose benzene exposure", Dr Parkin in our opinion adopted a role akin to that of an advocate rather than that of an expert in the relevant field of knowledge.
We have considered the whole of the material before us. We have reservations about some aspects of Dr Parkin's evidence, but we cannot find that he is not an "appropriately qualified specialist" and eminent in his field. We consider that as explained by Heerey J, in Deledio we must find that in the absence of a SoP dealing with myelofibrosis, "[U]nder Bushell, the hypothesis is nevertheless reasonable."
Having found that the material before us does raise a reasonable hypothesis as required by s 120(3) of the Act connecting Dr Leighton's death with the circumstances of his service we must turn to s 120(1) of the Act.
The High Court in Bushell said at p36:
The Commission will be satisfied beyond reasonable doubt "that there is no sufficient ground for making [the] determination" if it is satisfied beyond reasonable doubt that it cannot accept the raised facts or so many of them as are necessary to support the hypothesis. Thus, if the Commission is satisfied beyond reasonable doubt that it cannot accept the raised facts because of the unreliability of the material which is claimed to support them or because of the superior reliability of other parts of the material before the Commission or because the raised facts depend on inferences which the Commission is satisfied cannot be drawn, the Commission will be satisfied that there is no sufficient ground for making the determination. But unless the Commission is satisfied beyond reasonable doubt that there is no sufficient ground for the factual foundation of the hypothesis, the claim must succeed; we cannot conceive of a case where, for the purpose of s 120(3), the hypothesis is reasonable having regard to the raised facts, yet the Commission could be satisfied, "beyond reasonable doubt, that there is no sufficient ground for making the determination" even though the raised facts are not disproved. Indeed, once there is sufficient factual material to point to a reasonable hypothesis connecting the injury etc with the operational service, it seems convenient simply to treat the case as governed by the application of s 120(1). If that is done, the claim will succeed unless the Commission is satisfied beyond reasonable doubt that the factual foundation upon which the hypothesis can operate does not exist. 7 (emphasis added)
We cannot be satisfied under s 120(1) of the Act that the necessary factual foundation for the hypothesis connecting myelofibrosis with low dose exposure to benzene does not exist. The respondent has conceded that the exhaust fumes to which the veteran may have been exposed contained benzene. It is true that the evidence of Mr Schey was unreliable in that he changed his views between the VRB hearing and the hearing before this Tribunal. He even gave inconsistent evidence as to whether or not the doors of the cabin of the ambulance boat were kept closed during voyages. But the applicant's case did not rest only on the evidence of Mr Schey. There was also the statement of Mr James (T4 p26), which was unchallenged, and the evidence of Mrs Leighton as to the fact that her husband had told her that there were a lot of fumes on the ambulance boat. We are not able to be satisfied beyond reasonable doubt that we cannot accept the raised fact of low dose benzene exposure. Thus in our view the claim must succeed.
We consider that the decision under review should be set aside. In substitution it should be decided that the death of Dr Leighton was a war-caused death within the meaning of that term in s 8 of the Act.
I certify that the 95 preceding paragraphs are a true copy of the reasons for the decision herein of Mrs Joan Dwyer, Senior Member, and Mr W McLean, Member.
Signed: Anne O'Rourke
Associate
Date/s of Hearing 24 June 1999
Date of Decision 28 February 2000
Counsel for the Applicant Mr G Moore
Solicitor for the Applicant Williams Winter & Higgs
Counsel for the Respondent Nil
Solicitor for the Respondent Nil
Departmental Advocate Mr R Douglass
ADMINISTRATIVE APPEALS TRIBUNAL )
) No V98/883
VETERANS' APPEALS DIVISION )
Re Ruth Leslie LEIGHTON
Applicant
And REPATRIATION COMMISSION
Respondent
REASONS FOR DECISION
28 February 2000 Miss E A Shanahan, Member
I accept the detailing of the facts before the Tribunal by Senior Member Dwyer and Mr McLean, Member, and their explanation of the application of the law to these facts. The hypothesis raised by the applicant (the widow of the veteran Dr Peter Leighton) is that his exposure to benzene in both cigarette smoke and during the period of 24 February 1945 to 31 December 1945 when he served as a medical orderly on an ambulance boat in New Guinea and the South West Pacific, had led to the development of myelofibrosis first diagnosed in 1990.
Whilst it was acknowledged by all expert witnesses that cigarette smoke contains benzene in very small amounts, they all agreed that there was no scientific evidence to support a causal relationship between cigarette smoking and the development of myelofibrosis. This is therefore not an issue for the Tribunal to decide.
The applicant's hypothesis rested primarily with exposure to benzene whilst serving as an ambulance – medical orderly in New Guinea between 24 February 1945 and 31 December 1945.
The evidence before the Tribunal has been presented and considered in detail in the majority decision. I will confine my consideration of the evidence to those areas that have led me to conclude that the hypothesis raised is not reasonable on the grounds that the "raised facts" which are argued to support the hypothesis are too remote and too tenuous. There is no evidence to suggest the late veteran's exposure to benzene on board an ambulance launch in Papua New Guinea was any higher than the exposure to which the general population of this city is exposed in the streets of Melbourne.
Mr Max Schey the Captain of the ambulance launch upon which the veteran served (Launch AH1569 listed with the name of Hulda) gave evidence before this Tribunal which conflicted with previous evidence given at the Veterans' Review Board. This is addressed in detail in the majority decision. Mr Schey stated his evidence before this Tribunal differed as a result of him having had the opportunity to examine the engineering drawings of the ambulance launches (Drg No MGO (WC) 59). Having studied these drawings he was now of the opinion that it would be impossible for exhaust fumes containing benzene to enter the cabin and ambulance bay of the launch. The launch was a relatively new boat commissioned within the year of its service in 1945 and Mr Schey was adamant that there could not have been a leak from any of the exhaust pipes. He gave evidence that the journey to Motrapina Point from Toraquina which transported the wounded back to the military hospital, was always undertaken in the morning when seas were calm, the average speed was 8 to 9 knots and frequently the front sliding window of the ambulance bay structure and the back doors of the structure were left open and there would be a moderate breeze passing through this cabin. The journey from Toraquina to Motrapina Point was always conducted in the afternoon when seas were rough. Mr Schey described this journey to pick up casualties as being quite rough and stated the boat movements was "it was like a cork in a washing machine" (trans. p14 line 22). Refuelling of the vessel was conducted every second day at Kuriata Island. The process of refuelling was performed by Mr Schey (trans. p22 line 20). This refuelling was undertaken in still weather.
The fuel used on the vessel was petroleum and Mr Schey agreed that he had since been told that it was a 72 octane grading. The fuel was imported from the United States of America. Journeys from Toraquina to Motrapina Point averaged four and a half hours and the return trip carrying the causalities would average four or slightly less hours. Outside these times the crew of the ambulance launch were mainly on land, although, some members of the crew would stay with the boat whilst it was at anchorage. Mr Schey agreed that members of the crew did from time to time sunbathe whilst the vessel was underway. However he disagreed that they would do so toward the stern of the vessel and that any sunbathing would have taken place on the top of the cabin roof (trans. p24 line 12). The Tribunal had available to it the drawings of the ambulance launch and data regarding type of fuel used, the engine and the maximum speed and range of these vessels.
Mr Robert Piper, Military Historian and Author, gave evidence as to the design and performance of ambulance launches such as AH 1569 and the requirement that such vessels use low octane fuel. He stated that the fuel used by this vessel was known to have been red in colour and this would indicate about an 80 octane level. High octane fuels were reserved for the use of the aviation squadrons. Mr Piper was of the opinion that benzene would not have been added to the original fuel imported from the United States of America. No benzene was available in Australia or New Guinea at that time as all benzene produced in Australia was exported to the United States of America. Mr Piper was of the opinion that the red coloured fuel used was that then known as super with an octane rating of 83 achieved by the addition of a small percentage (1 in 821) of tetraethyl lead to the fuel. He was not able, as a result of his research, to find any evidence that benzene was added to the fuel although there would be some benzene content in so called straight run petroleum. It was subsequently conceded by the respondent in the letter dated 4 August 1999, that the exhaust fumes, to which the veteran may have been exposed, would have contained benzene. However it was submitted that exposure would have been far too small to be of any etiological significance in the causation of Dr Leighton's myelofibrosis.
Mr Moore, Counsel for the applicant, developed the hypothesis as previously stated by analogy with the accepted causal relationship of benzene exposure and the development of acute myeloid leukaemia (trans. p38 line 5). This line of argument was based on the observed 5 to 25% incidence of acute myeloid leukaemia reported in the agonal stages of patients with long standing myelofibrosis. There was no evidence presented that Dr Leighton had developed acute myeloid leukaemia. In fact blast cell counts were at the most 6%. (Blast cell count at 30% is required for diagnosis for acute myeloid leukaemia). While neither party referred to it, there is in force a Statement of Principle for acute myeloid leukaemia and benzene exposure. Instrument 169 of 1996 provides as follows:
Factors
5. The factors that must as a minimum exist before it can be said that a reasonable hypothesis has been raised connecting acute myeloid leukaemia or death from acute myeloid leukaemia with the circumstances of a person's relevant service are:
. . .
(c)being heavily occupationally exposed to benzene for a period or periods of time totalling at least two years, where the first exposure occurred more than five years before the clinical onset of acute myeloid leukaemia; or
(d)being occupationally involved in the handling of AVGAS or petroleum products containing benzene greater than 5% by volume for one month or more, where the first exposure occurred more than five years before the clinical onset of acute myeloid leukaemia; or
(e)being occupationally involved in the handling of AVGAS or petroleum products containing benzene greater than 1% by volume for one year or more, where the first exposure occurred more than five years before the clinical onset of acute myeloid leukaemia; or
There is no existing Statement of Principle for myelofibrosis and benzene exposure. I have however taken note of the Statement of Principle of acute myeloid leukaemia and benzene exposure as this determination of the Repatriation Medical Authority provides some guideline as to the levels of benzene exposure considered by the authority to be causally related to the development of acute myeloid leukaemia.
As previously stated neither party referred to the Statement of Principle but given the experience of both the applicant's and respondent's representatives, they would be aware of the existence of this Statement of Principle.
Dr Des Parkin, the Director of Division of Laboratory of Medicine at the Austin Hospital, gave expert evidence for the applicant. Dr Parkin described a 5–25% transformation rate of myelofibrosis to acute myeloid leukaemia. Dr Parkin stated that Dr Leighton had a small percentage of blast cells but there was no overt evidence, nor laboratory evidence, for transition to acute myeloid leukaemia. Dr Parkin referred to numerous studies which have linked exposure to benzene to the development of acute myeloid leukaemia. He agreed there was probably a linear response curve for benzene exposure. He also addressed the evidence showing that over many years the recommended levels of benzene exposure from a safety point of view have reduced and that the current United States Environmental Protection Authority recommendation is that a concentration of 1 part per million of benzene is associated with an absolute risk which ranges from 7.1 per thousand to 2.5 per hundred. Most of the cohort studies he had examined had involved high levels of occupational exposure. He noted that the cohort studies varied in the incidence of individuals with myelofibrosis, there being increased numbers in some cohorts, and no increase in others. Dr Parkin was of the opinion that there was no known lower limit of benzene exposure that could be confidently termed safe.
In his initial report of 15 September 1997 Dr Parkin had used the terminology "substantial exposure to petroleum or benzene" as being a possible causative factor in the development of myelofibrosis. In oral evidence he stated that whilst he was not an epidemiologist, he could not state that there existed a lower limit of safe exposure to benzene. When asked by Mr Douglass for the respondent as to whether there are any studies that compared the exposure of an urban population to benzene and the incidence of acute myeloid leukaemia Dr Parkin answered that he "could not answer that and it might be a difficult study to do" (trans. p50 line 24). Dr Parkin agreed that the studies relating to myelofibrosis were all in groups of workers industrially exposed to benzene. He agreed there were no studies examining dose response relationship between benzene and myelofibrosis at non-occupational levels of exposure. Dr Parkin was unable to comment on the levels of benzene exposure in various occupational and urban living environments and stated that he was not very knowledgeable in that area. Dr Parkin agreed that the benzene exposure from a cigarette would be less than that associated with pollution in an urban area. He was of the opinion that exposure to benzene would be additive or incremental. However he stated this in relation to cases of acute leukaemia not myelofibrosis.
Professors Fox and Peach who gave evidence for the respondent summarised the most current scientific literature on benzene exposure and the development of myelofibrosis. They found no supportive evidence of a causal link. They agreed that benzene exposure was linked causally with the development of acute myeloid leukaemia. Professor Fox was of the opinion that on the facts before the Tribunal the late veteran's exposure to benzene during his service as an ambulance officer in 1945 for a period of 10 months would not have been greater than ordinary urban pollution levels.
Given the design of the ambulance launch, in particular the exhaust disposal, the constant weather patterns experienced on a day-to-day basis on the journeys between Toraquina and Motrapina Point, the use of low octane petroleum required by the engine dimensions of the launch and that all refuelling operations were carried out by the Captain of the vessel, Mr Max Schey, I find it highly probable that the levels of benzene exposure to which the veteran, Dr Peter Leighton, may have been subject, would have been of the order of or less than benzene levels in urban pollution. Dr Parkin, in evidence, stated that at the Austin Hospital he would see one new case of myelofibrosis per annum compared to 30 or 40 new cases of acute myeloid leukaemia. This does not indicate that urban pollution benzene levels are a factor in the development of myelofibrosis. None of the scientific reports have linked urban exposure to the development of myelofibrosis. For this reason I find the hypothesis proposed unreasonable on the grounds that it is too remote and too tenuous.
I consider that the decision under review that the death of Dr Leighton was not war-caused within the meaning of that term in s 8 of the Act should be affirmed.
I certify that the 14 preceding paragraphs are a true copy of the reasons for the decision herein of Miss E A Shanahan, Member.
Signed: Anne O'Rourke
AssociateDate/s of Hearing 24 June 1999
Date of Decision 28 February 2000
Counsel for the Applicant Mr G Moore
Solicitor for the Applicant Williams Winter & Higgs
Counsel for the Respondent Nil
Solicitor for the Respondent Nil
Departmental Advocate Mr R Douglass
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