Farley-Smith and Repatriation Commission
[2005] AATA 968
•4 October 2005
Administrative
Appeals
Tribunal
DECISION AND REASONS FOR DECISION [2005] AATA 968
ADMINISTRATIVE APPEALS TRIBUNAL )
) No V03/673
VETERANS' APPEALS DIVISION ) Re GWENDA FARLEY-SMITH Applicant
And
REPATRIATION COMMISSION
Respondent
DECISION
Tribunal Mr J Handley, Senior Member Date4 October 2005
PlaceMelbourne
Decision The decision under review is set aside and in substitution it is decided that the death of William David Farley-Smith is war-caused. ..............................................
Senior Member
VETERANS’ ENTITLEMENTS – widow’s application – competing hypothesis – exposure to benzene conceded – finding of death by myelofibrosis – SOP not issued – whether a reasonable hypothesis – decision set aside
Veterans’ Entitlements Act 1986 (Cth) s 120
Bushell v Repatriation Commission (1992) 109 ALR 30
Byrnes v Repatriation Commission (1993) 116 ALR 210
Commissioner for Government Transport v Adamcik (1961) 106 CLR 292
Prestegar v Repatriation Commission [1997] 762 FCA
Re Whitworth and Repatriation Commission [2002] AATA 861
East v Repatriation Commission (1987) 74 ALR 518
REASONS FOR DECISION
4 October 2005 Mr J Handley, Senior Member 1. The applicant applies to review a decision made by the Veterans’ Review Board (“VRB”) made on 5 May 2003. The VRB then decided to affirm a decision previously made by the respondent on 7 March 2002 rejecting an application for widows pension.
2. Mrs Farley-Smith applies as the widow of the late William David Farley-Smith who died on 14 November 2001. The deceased was then 78 years of age having been born on 29 March 1923. The certified cause of death was “myelofibrosis/4 years; oesophageal varice/2 years” (T4).
3. The late Mr Farley-Smith served as a member of the Australian Army between 6 April 1942 and 8 August 1946. Part of his service was in the Northern Territory and by reason of the location, the whole of his service is deemed to have been operational.
4. The hypothesis advanced by the applicant’s representative prior to the commencement of the hearing was that service exposed the deceased to petroleum and benzene in the cleaning of guns, engines and machinery which precipitated myelofibrosis. Another hypothesis was that the deceased smoked tobacco which produced benzene which he inhaled. It was submitted that the deceased acquired a smoking habit by service.
5. At the commencement of the hearing, Mr De Marchi who appeared on behalf of Mrs Farley-Smith, notified the Tribunal that another hypothesis was being pursued, namely, that the exposure to benzene in service precipitated a myelodysplastic disorder precipitating chronic myeloid leukaemia, which in turn precipitated myeloid fibrosis.
6. It became evident after much discussion with Mr De Marchi and Mr Nyhof, who appeared on behalf of the respondent, that the Doctors engaged to provide medico-legal opinion had not been acquainted with the additional hypotheses. It also became clear that the hearing would not conclude on 30 August 2004. Accordingly it was decided to hear lay evidence only and adjourn the matter to date to be fixed. In the meantime the three medico-legal witnesses would have the opportunity to consider the additional hypotheses.
7. A number of documents were received into evidence and will be referred to in these reasons.
gwenda farley-smith
8. Mrs Farley-Smith is the widow of the late veteran. She said that she met Mr Farley-Smith in 1950 and married him thereafter. She recalled that he was a very hard worker who had been engaged in full time occupation as a farmer. In his life time he had not suffered serious illnesses, but preceding the diagnosis of myeloid fibrosis in the late 1990’s, her husband suffered a number of “dizzy spells”. A CT scan of his brain did not reveal any abnormality but he was eventually referred to surgeons when his health deteriorated. Surgery was undertaken to arrest internal haemorrhaging and Mr Farley-Smith lost weight rapidly. He was found to have an enlarged spleen and a bone marrow biopsy revealed the presence of myeloid fibrosis.
9. Mrs Farley-Smith said that she had consulted with Dr Thomson the family general practitioner in Bendigo who had told her that it was “a pity” that blood tests had not been taken years earlier than the occasion of diagnosis of myeloid fibrosis, because it may then have revealed the presence of chronic myeloid leukaemia. She said that Dr Thomson had also advised that the presence of myeloid fibrosis with rapid weight loss might have been secondary to an earlier disease process.
10. Mrs Farley-Smith has conducted enquiries by the Internet of the disease of myeloid fibrosis and said that there appeared to be a relationship between benzene exposure and persons who have suffered from that illness. She said that her husband did not speak much about his war service but said that there were occasions where he had cleaned guns and had reassembled them. She understood that he had been engaged extensively in the manoeuvre, cleaning and assembling of guns, particularly because he had accepted disabilities of a fractured right foot and a fractured right finger which was associated with manoeuvring of bofar guns.
11. The applicant said that she had contacted a number of persons in the 112th Light Anti Aircraft Regiment Association and had located Mr Robert Wiseby, Mr Kevan Salter and Mrs Dorothy Prestegar who had all agreed to give evidence on her behalf. She said that she had also spoken with Mr Bannister who was unavailable on the first day of hearing, but who confirmed that he had served with her husband and advised that benzene and petrol were used as cleaning agents. He had told her that kerosene was not ever available for that purpose. She also said that Mr Wiseby, who was also unavailable on the first day of hearing, had indicated to her that petrol and aviation fuel were used as cleaning agents. In fact, he and others “used whatever they could get” to wash down the machinery, engines and gun parts.
12. Mrs Farley-Smith said that it was her belief – having spoken to these persons and from reading information obtained from the Internet – that her husband had previously suffered an undiagnosed chronic myeloid leukaemia which had precipitated myeloid fibrosis. She said that she had read from the literature obtained, that 30 to 40% of persons who suffer chronic myeloid leukaemia eventually suffer myeloid fibrosis.
13. With respect to the “smoking hypothesis” Mrs Farley-Smith said that her husband smoked a pipe on a regular basis until 1990 when he ceased. She was sure that he ceased in 1990 because in that year she was ill and her husband then promised her that he would cease smoking. She said that he eventually reduced his smoking habit and by the end of 1990 or early 1991 he had ceased smoking completely. She said that Mr Farley-Smith commenced smoking in service and continued to smoke at a quantity of approximately 4 ounces of tobacco per week. This estimate was given when Mrs Farley-Smith was acquainted with the average size of pouches of tobacco and the respective weights. She was referred to her answer to a smoking questionnaire, found within the T-documents, which was completed in preparation for her initial claim for pension. That questionnaire was completed with the assistance of a Legacy advocate from Bendigo, who recorded on the applicant’s behalf, that the deceased initially smoked 1 ounce of tobacco during service and between 2 and 3 ounces of tobacco after discharge.
14. In cross-examination Mrs Farley-Smith said that her husband used petrol to wash his hands whilst he was engaged as a farmer as he found it to be an effective cleaning agent. She knew little of his service in the Northern Territory but was aware that he had suffered a foot, finger and hernia injuries which he associated with the manoeuvring of bofar guns. She said her husband was otherwise a person who would not complain and was reluctant to talk about his service.
kevan ross salter
15. Mr Salter was engaged in service in the Australian Army in Darwin between 1940 and 1942. He was a gunner with heavy artillery. He recalled that tobacco was readily available and “smokos” were taken every hour. He recalled that service in the Army was “a pretty good introduction to smoking for a lot of young guys” and smoking was taken up to relieve boredom and to relieve the stress from the “excitement” of being strafed by Japanese air planes.
16. Mr Salter was a dispatch rider who used petrol, creosote, oil and kerosene to wash and clean engines, machinery and gun parts. He said it was common practice to use petroleum products and whilst he could not recall the ready availability of kerosene he said “we always had plenty of petrol but I don’t know what type”. He could not recall whether aviation fuel was used as a cleaning agent. He remembered that petrol was in plentiful supply because after the bombing raids of Darwin, fuel was decantered into 44 gallon drums and “scattered through the scrub” to avoid the risk of it exploding upon further bombing. He also recalled that petrol was used to wash hands and sometimes clothing.
17. In a proof of evidence completed by him on 26 January 2004 Mr Salter relevantly recorded the following:
It was common practise to use petroleum products such as petrol and phenol to clean parts and machinery and wash your hands in or whatever was at hand. Of course gun oil was used on firing equipment such as guns rifles and Bren or Owen guns (when we finally eventually acquired the last two).
In the case of ordinary mechanical equipment after cleaning with whatever was available whether petrol or kero it would have a bit of engine oil whacked on and as I say then wash your hands in petrol.
18. In cross-examination Mr Salter said that he could not recall if tobacco was available at Coomalie Creek where the deceased had been stationed. He said however, that all Units that he had visited throughout the Territory had a plentiful supply of tobacco.
19. With respect to the use of petrol products as a cleaning agent he said that there were never any warnings against the use of petrol for that purpose. Nor was there any recommendation given to use kerosene or paraffin in preference.
dorothy prestegar
20. Mrs Prestegar is the Honorary Secretary of the 112th Light Anti Aircraft Regiment. Her husband served in the same battalion as the late Mr Farley-Smith. Her husband died from multiple myeloma which she said was accepted by the Repatriation Commission as war-caused, based on the hypothesis advanced, of a prior exposure to benzene in service. She recalled that her husband had told her that petrol containing benzene was readily available as a cleaning agent. Additionally she said that no other cleaning agent was available. She was aware that the United States service personnel also used petrol and petrol products to wash guns, machinery and engines.
21. In cross-examination Mrs Prestegar said that all members of the 112th Light Anti Aircraft Regiment who had used petrol as a cleaning agent had told her that it contained benzene. She said she did not know this by first hand experience. Additionally, she said she could not recall any members of her association speaking of the use of kerosene as a cleaning agent.
resumption of hearing
22. At the conclusion of the first day of evidence I directed the applicant’s representative to identify the hypotheses upon which the applicant intended to rely. There was considerable uncertainty during the first day of hearing and the application could not satisfactorily proceed until the hypotheses were known.
23. On 6 September 2004, the solicitors for Mrs Farley-Smith provided a statement recording the three hypotheses in the following terms:
Following the opening of this case the Tribunal has requested that the applicant spell out with some precision the 3 hypotheses that they are relying upon.
These are:
1.That the veteran’s death from Myelofibrosis was connected to his exposure to tobacco products containing benzene.
That he was further exposed to benzene through the components of the petroleum products that he used to clean machine parts and to wash his hands.
Both Dr Des Parkin and Dr Byron Collins support this hypothesis.
2.That Myelofibrosis is a disease associated with myeloid dysplastic disorder [sic] Instrument No. 15 of 2000 supported by the connection of exposure to benzene as per paragraph 1 above.
3.As the GP has left open the possibility of chronic myeloid leukemia [sic] being the precursor to myelofibrosis there is also a predisposing link between chronic myeloid leukemia [sic] Instrument No. 7 of 1997 and 15 pack years of tobacco consumption.
24. When the hearing resumed on 29 November 2004, the complexion of the application had changed significantly with the respondent conceding in the interim that the late Mr Farley-Smith had been exposed to benzene during service. The respondent’s representative had given this indication in a letter to the Registrar on 22 November 2004. The concession was based upon a report that had been received by Petroch Services Pty Ltd of 16 November 2004. However the respondent had requested a further opinion from Professor Peach having regard to the hypotheses that were identified by the applicant’s representative. The report of Professor Peach was not received by the applicant until one or two days before the resumption of the hearing and in those circumstances – and by reason of the content of the report – Mr De Marchi applied to have the hearing adjourned so that he might obtain a further opinion from Dr Byron Collins.
25. After much discussion and concern expressed as to the way the application had been prepared and was proceeding, the matter was adjourned. I indicated to the parties that having regard to the identified hypotheses, and to the evidence heard and the reports lodged, there seemed to be some merit in narrowing the issues in dispute. Both parties indicated that they were prepared to consider my views on the application as it then stood and also acknowledged that any views that I expressed were not concluded and were upon the evidence heard and read to that point (refer Transcript pages 67 to 72).
26. I indicated to the parties that by reason of the concession made by Mr Nyhoff with respect to benzene, that the hypothesis with respect to myelofibrosis could proceed upon the reasonable hypothesis standard that existed prior to 1994 when SOPs were introduced. I indicated that I understood that the hypothesis with respect to that condition was associated with the deceased’s exposure to benzene in petrol, and benzene being a by-product or a consequence of tobacco smoking. I indicated that my interpretation of the medical evidence then received was that there was little, if any, support for an association between myelofibrosis and myelodysplastic disorder. I noted that there was a SOP with respect to myelodysplastic disorder which contained exposure benzene as one of its factors. In that regard Mr Nyhof clarified his concession to it extending only to an exposure to benzene, but without any concession as to exposure in terms of quantities or duration or frequency. I also indicated on the material then lodged, and the evidence heard, I could not locate any support for the hypothesis of chronic myeloid leukaemia being a pre-cursor to myelofibrosis. However it was noted that chronic myeloid leukaemia was the subject of a SOP where a relevant factor was the smoking of tobacco.
27. I did not seek any response from either practitioner to the observations then made but asked them to consider those observations in the context of any further medical evidence that may be forthcoming prior to the resumption of the hearing.
28. The hearing of the application resumed on 28 February 2005. It was then learnt that further medical opinions were not being lodged by the applicant’s solicitors from Dr Byron Collins. Further opinions had been prepared by Professor Peach which had been exchanged well in advance of the resumed date.
29. On the resumed date I consented to the hearing commencing at 11.00 a.m. to permit the applicant’s representative to appear before the Family Court. However, at 12.00 when the applicant’s representative had not appeared at the Tribunal and with the respondent’s witness waiting to give evidence, contact was made by telephone with Mr De Marchi. It was then learnt that he continued to be detained at the Family Court and it was not known when he would be appearing in this application. I indicated that I intended to hear the evidence from Professor Fox who was the witness called by the respondent and Mr De Marchi consented to his colleague Mrs Black (who attended the Tribunal during the currency of the conversation) to appear and to cross-examine Professor Fox (refer Transcript pages 83 to 87). During that conversation it was learnt that the applicant intended to continue to proceed upon the three hypotheses recorded in the statement of 6 September 2004.
statements of principles
30. Before the evidence in these proceedings is recorded, the SOPs applicable to the hypotheses being advanced should be recited.
31. As recorded above a SOP has not been issued with respect to myelofibrosis.
32. With respect to the remaining two conditions being the subject of the hypotheses advanced by Mr De Marchi, it is noted that the claim for pension was lodged with the respondent on 11 February 2002. That date is the commencement date of the assessment period.
33. Within the assessment period only one SOP has been issued with respect to myelodysplastic disorder being Instrument No. 15 of 2000. The factor upon which reliance was made by Mr De Marchi was 5(b), namely:
(b)being exposed to benzene on more days than not over a period or periods totalling two years before the clinical onset of a myelodysplastic disorder; or
34. For the purposes of the above definition the phrase “being exposed to benzene” is defined at paragraph 8 of the Instrument in the following terms:
“being exposed to benzene” means:
(i)inhaling benzene vapour where such exposure occurs at measured or estimated ambient benzene concentrations exceeding one part per million; or
(ii) having skin contact with liquids containing benzene;
35. The above Instrument also records (paragraph 2) that myelodysplastic disorder attracts ICD Code D46 (refer evidence of Professor Peach later in these reasons).
36. Within the assessment period there were two SOPs with respect to chronic myeloid leukaemia being Instruments No. 7 of 1997 and No. 15 of 2003. Mr De Marchi relied on a factor which was identical in both Instruments. That factor being 5(d) of the former Instrument and 5(a) of the latter Instrument which reads as follows:
smoking at least 15 pack-years of cigarettes, or the equivalent thereof in other tobacco products, before the clinical onset of chronic myeloid leukaemia, and, where smoking has ceased, the clinical onset occurred within ten years of cessation; or
37. The former Instrument defines the expression “pack- years” whereas the latter Instrument defines the expression “pack years of cigarettes or the equivalent thereof in other tobacco products”. Whilst there are differences in the expressions defined and the content of each definition, essentially the terms are intended to mean either 7,300 cigarettes per annum or 7.3 kilos of pipe tobacco or 1,460 cigars.
38. There is a difference also between both Instruments with respect to chronic myeloid leukaemia as to the identification by ICD Code. The former Instrument refers to the attraction of ICD Code 205.1, 206.1 or 208.1, whereas the latter Instrument refers to ICD Code C92.1, C93.1 or C95.1. There is also a difference in the definition of “chronic myeloid leukaemia” under each Instrument. The distinction may be explained by a difference in the identity of the “ICD Code” as found at paragraphs 7 and 8 respectively of each of the Instruments. The former Instrument refers to an ICD Code under the “Ninth revision” whereas the ICD Code under the latter Instrument refers to the “Tenth revision”.
medical evidence
39. During the evidence of Professor Fox and Professor Peach (and in a reference also to reports by Dr Byron Collins) a pathology report completed by Dr Mills on 10 September 1997 (Exhibit 3) assumed considerable importance and significance. That report is reproduced below (Dr Mills was not called to give evidence):
BONE MARROW EXAMINATION
ASPIRATE AND IMPRINT
CELLULARITY: Largely a “dry tap” with a few scattered small hypercellular particles and normocellular trails.
ERYTHROPOEISIS: Hypocellular with micronormoblastic maturation.
GRANULOPOEISIS: Hypocellular with progressiv maturation.
MYELOID: ERYTHROID RATIO: Relatively normal at about 4 to 1.
MEGAKARYOPOEISIS: Hypocellular. However, in view of “dry tap”, cell trails are probably not representative.
LYMPHOCYTES: Sparse.
PLASMA CELLS: Sparse.
RETICULUM CELLS: Sparse.
ATYPICAL CELLS: Not seen.
IRON STAIN: Not performed in view of scanty particles due to relatively dry tap, recluding adequate assessment.
TREPHINE BIOPSY
MICROSCOPY: Overall relatively normocellular for age being about 70% fat and 30% cellular. Haemopoeitic elements are present as scattered islands with focal megakaryocytic hyperplasia with clusters and clumps or irregular, large megakaryocytes. Myeloid and erythroid precursors are relatively well preserved. There is an increase in fine and course reticulin fibres. There is a patchy increase in randomly oriented fine reticulin fibres with streaming bundles of coarse fibres present in some areas in the intertrabecular space. Bone trabeculae appear to show some patchy thickening with associated early collagen formation.
COMMENT: The overall appearances are those of a chronic myeloproliferative disorder consistent with primary, idiopathic myelofibrosis or so called agnogenic myeloid metaplasia. The disease appears to be in an early fibrotic phase, but marrow reserve still appears to be adequate.
CONCLUSION: Chronic primary myelofibrosis.
professor fox
40. Professor Fox holds a Bachelor of Medicine and a Bachelor of Surgery, a Doctorate of Philosophy in Medicine from the University of Sydney and is a Fellow of the Royal Australian College of Physicians. He is also the Professor and Director of the Department of Clinical Haematology and Medical Oncology at the Royal Melbourne Hospital.
41. Professor Fox provided two reports dated 3 March 2004 and 10 August 2004 both received into evidence as Exhibits 1 and 2.
42. In his first report Professor Fox recorded that the aetiology of myelofibrosis is generally unknown and is sometimes referred to idiopathic. He regarded it as being a rare condition but was aware of case reports of individuals having been exposed to benzene developing the condition but he did not know of any “firm epidemiological data”. Whilst he was aware that a hypothesis was being advanced of chronic myeloid leukaemia precipitating myelofibrosis, Professor Fox reported that such a phenomenon does not occur and he knew of no evidence that the deceased had ever suffered from chronic myeloid leukaemia. Professor Fox reported that the pathology report of June 1997 and the contents of other reports led him to conclude that he had “no doubt” that the deceased suffered from myelofibrosis. Professor Fox disagreed with a hypothesis advanced by Dr Byron Collins which he understood to associate myelofibrosis with benzene exposure.
43. In his report of 10 August 2004, Professor Fox reaffirmed his opinion that the deceased suffered from myelofibrosis which he regarded as a myeloproliferative disease involving bone marrow which in his opinion was an illness “quite distinct” from myelodysplastic syndrome. Additionally Professor Fox reported that there was no evidence available to him suggesting that the deceased had ever suffered from myelodysplastic disorder.
44. In evidence Professor Fox said that he was aware of medical reporting of petrol station attendants suffering from myelofibrosis but said that reporting concerned “single case” observations only. To his knowledge, there had not been any epidemiological studies associating exposure to benzene, or other solvents, with myelofibrosis. He said the only illness to his knowledge that had been associated with exposure to benzene was acute myeloid leukaemia. He regarded single case studies as being unreliable as opposed to “blind study cases”, which involved an analysis of persons who suffer from myelofibrosis, some of whom had been exposed to benzene and some of whom had not.
45. The witness was aware of conclusions reached by Professor Peach in a report of 26 July 2004, where he concluded that a combination of the deceased’s symptoms, his blood count and bone marrow examination, was definitive of myelofibrosis and not myelodysplastic disorder. Save that the deceased was found to have an enlarged spleen, which in the opinion of Professor Fox is not a feature of myelodysplastic syndrome, he was satisfied that the bone marrow analysis and the chromosome studies of the deceased suggested that myelofibrosis was the correct diagnosis. Professor Fox also said that it was notable from the report of the pathologist that the biopsy revealed a “dry tap” procedure, which he described as the phenomena of the fibrosis prohibiting extraction of bone marrow. In those circumstances the bone marrow is extracted after a drilling procedure (Trephine).
46. The report of Professor Peach of 26 July 2004 also contained a table charting chromosomal changes following exposure to benzene. Professor Fox said that he was aware of the table and was aware also of chromosome changes. He agreed that “chromosomal aberrations” occur following benzene exposure which can be distinguished from other chromosomal changes which would point to a different diagnosis. Whilst he was not prepared to regard the chromosomal features as causing any other diagnosis to be impossible, he said it was “biologically very unlikely” that there could be any diagnosis other than myelofibrosis, by reference to the chromosomes as identified.
47. With respect to the association between myelofibrosis and smoking, Professor Fox said that there was no known medical link between cigarette smoking and myelofibrosis, but there was an association between benzene and cigarette smoking and acute myeloid leukaemia. He also said that “some forms” of myelodysplastic syndrome have an association with benzene.
professor peach
48. Professor Peach is formerly the Professor of Public Health from Melbourne University. He holds the normal medical qualifications, but also has a degree in bio-chemistry, a Phd in Epidemiology and is a Fellow of the Faculty of Public Health of the Royal College of Physicians in the United Kingdom. He is presently a visiting consultant from Melbourne University to the Ballarat Base Hospital.
49. Professor Peach has provided seven reports in this application dated 26 March 2004, 14 July 2004, 26 July 2004, 29 August 2004, 29 October 2004, 30 November 2004 and 5 January 2005 which were all received into evidence as Exhibits 7 to 13 respectively.
50. When giving his evidence, Professor Peach relied on his report of 5 January 2005 which incorporated the material and opinions expressed from the earlier reports.
51. In his report of 5 January 2005, Professor Peach referred to the three hypotheses relied upon by the applicant. He regarded the hypothesis connecting myelofibrosis with benzene by exposure to petrol and cigarettes as being “unreasonable”. He reported that he could find nothing in “world medical literature” suggesting or pointing to smoking being the cause of myelofibrosis. He referred to a paper written by Tondel, Persson and Carstensen (“Tondel”). The article is entitled “Myelofibrosis and Benzene Exposure and is reported in the Journal of Occupational Medicine in 1996 – (refer report of Professor Peach of 26 March 2004). He said the report related to a single case exposure of myelofibrosis, but said that the authors of the report themselves expressed “considerable doubt as whether there was a causal connection or not”. He reported that single case enquiries were not a substitute for epidemiological evidence, and subsequent epidemiological studies into the association (if any) between benzene and myelofibrosis “left open”, but did not “point to” such a hypothesis. Professor Peach referred to a number of other case studies and reports and concluded that there was no epidemiological evidence supporting the hypothesis as being reasonable, upon an analysis of the medical information contained within the T-documents and from other reports. Professor Peach was satisfied that the cause of death was myelofibrosis, noting that this was the cause of death as certified upon the Death Certificate. He noted differences in the history of smoking given by the veteran in his lifetime (where in 1999 he recorded that he had not smoked for 30 years), whereas the widow in her claim said that he had smoked a pipe until 1990. In any event it was the opinion of Professor Peach that if the late veteran’s evidence were accepted, he would have ceased smoking 26 years before the first onset of myelofibrosis symptoms in 1995. It was also noted that the deceased had been exposed to petrol containing benzene more than 50 years prior to the first onset of symptoms and his exposure then would more likely have been intermittent. Referring to other epidemiological studies, he noted that despite increased use of motor vehicles in Sweden in the last 20 years, there had been no change in the incidence of myelofibrosis. On balance, it was Professor Peach’s opinion that no reasonable hypothesis could be found associating benzene with myelofibrosis, having regard also to chromosomal aberrations which have unique characteristics and can distinguish myelofibrosis from myelodysplastic disorder and from chronic myeloid leukaemia.
52. With respect to the second hypothesis, Professor Peach reported that myelofibrosis and myelodysplastic disorder are separate and distinct diseases. He noted that the ICD Codes were different as to both conditions, and they did not incorporate or refer to each other as defined in the SOPs. He acknowledged that myelodysplastic disorder and myelofibrosis are regarded as being neoplasms, but they are distinguished according to morphology and behaviour and not cause.
53. As to the third hypothesis, Professor Peach dismissed the deceased as ever having suffered chronic myeloid leukaemia. He noted that the treating general practitioner did not refer to it in his clinical notes and the same practitioner certified the death as myelofibrosis. Professor Peach was aware that Mrs Farley-Smith had a document in the handwriting of Dr Thompson (the general practitioner) who referred to chronic myeloid leukaemia, but in his view that document leaves open, but does not point to, the presence of chronic myeloid leukaemia. Professor Peach also referred to the opinion of a departmental medical officer (Dr Fitzgibbon) and the pathologist’s report of June 1997 that concluded that the deceased was suffering from primary idiopathic myelofibrosis. Professor Peach said that neither pointed to the presence of chronic myeloid leukaemia.
54. In evidence Professor Peach adopted the contents of his report of 5 January 2005. With respect to his many references to Journal articles and other medical literature, he explained that he had made searches via the Internet and from International medical data bases. He said he could not find any epidemiological studies pointing to an association between myelofibrosis and benzene. To the extent that such medical data bases contained Journal articles, he said that the International protocol for publication of Journal reports involved submission to the Editor of a reputable Journal of a paper. It is then being assigned anonymously to four appropriately qualified referees or experts, who are then required to report to the Journal Editor whether the submitted paper has merit and is worthy of publication.
55. Professor Peach said that the study completed by Tondel was a single case study only and was not a reliable source of information. Indeed he said that Tondel qualified his article by reporting that “when observing a single case in relation to a particular exposure there is considerable doubt as to whether there is a causal connection or not”. Professor Peach said that this was an acknowledgement by Tondel himself that a finding from a single case study was inappropriate. Indeed Professor Peach said that he was aware of papers subsequently published by persons who previously worked in Tondel’s department, contradicting the opinion contained in the single case study that an association existed between benzene and myelofibrosis. On balance it was the opinion of Professor Peach that the article of Tondel did no more than raise the possibility of the association between benzene and myelofibrosis.
56. Professor Peach then referred to a number of other studies of persons in industry who developed myelofibrosis and who had been exposed to benzene. He said that those studies were unreliable because the exposure to benzene was not measured, and the potential of exposure to other chemicals had not been investigated or discounted. He noted that in another study involving petrol refinery workers who had died, where myelofibrosis had been certified as the cause of death, there was an imbalance in the numbers of deaths between the refineries where he would have expected uniformity of deaths. In each case there had not been a measure of the benzene exposure.
57. Professor Peach said that he could not find any reports of any connection between benzene from tobacco smoke and myelofibrosis.
58. With respect to the difference in the documented evidence between the cessation of smoking as recorded by the deceased and the cessation of smoking by his wife, Professor Peach said there would be no difference in the conclusion that he would reach with respect to the tobacco exposure. He said that any mutation in bone marrow over the lifetime of a person must have resulted from an exposure to 120 parts per million to benzene. He said that consumption of three ounces of tobacco per week for 50 years would give a net exposure of 55 parts per million. On the estimate given by the deceased as to when he ceased smoking, the exposure would have amounted to 27 parts per million of benzene. It therefore followed he said, that on his calculations and accepting both smoking histories, the exposure would have been far less than the exposure required to cause a mutation in bone marrow cells. Professor Peach said that the estimate of 120 parts per million of benzene was a conservative standard used by public health agencies in setting safety standards.
59. Referring to the Tondel report, Professor Peach said that exposure to benzene by petrol station attendants did not permit any conclusion that the benzene in the petrol was responsible for myelofibrosis. He said that an examination of the cancer register in Sweden found that there was no greater incidence of myelofibrosis amongst petrol attendants compared to the general population. Professor Peach regarded the data base as being accurate, because an examination of persons with acute myeloid leukaemia or myelodysplastic disorder who had been exposed to benzene, had a far greater incidence of exposure than the general population who had not been exposed to benzene and who had suffered from the same diseases.
60. With respect to the period of the 1980’s and 1990’s, Professor Peach noted that there had been an increase in the density of motor vehicles but in that period there was again no resultant difference in the incidence of myelofibrosis, despite persons being exposed to increased exhaust emissions. In the same period of time, the incidence of lung cancer associated with cigarette smoking increased, but the incidence of myelofibrosis did not. It followed therefore – on his analysis – that if there was an association between benzene from petrol or benzene from smoking, there would have been an increase in the incidence of myelofibrosis reported in the Swedish Cancer Register.
61. With respect to the contents of the reports of Professor Peach discussing chromosomal aberrations, he said that in persons who have suffered myelofibrosis the chromosomes which have changed are numbered 1, 13 and 20. However in diseases caused by benzene exposure for example, acute myeloid leukaemia, the altered chromosomes are numbered 5, 7, 8 and 11. In studies which have been conducted in China, the chromosome changes in persons exposed to benzene have found to have chromosomes numbered 5, 7, 8, 11 and 21. In some laboratory studies where bone marrow has been exposed to benzene, the chromosome changes had been at numbers 5, 7 and 8. It therefore followed on this analysis according to Professor Peach, that the chromosome changes in persons exposed to benzene are different to the chromosome changes to persons who have not been exposed to benzene and who have suffered myelofibrosis. It followed therefore that benzene, on his analysis, did not cause myelofibrosis.
62. With respect to the conditions of myelofibrosis and myelodysplastic disorder, Professor Peach said that they were separate distinct conditions. He said the ICD Codes were different. He noted the distinction between the code numbers as appearing in the SOPs. Additionally he said that myelodysplastic syndrome was contained in an ICD Code group identified as D46 whereas myelofibrosis was recorded in the ICD Code group at D47. He said that the diseases grouped within D46 have an association with benzene, whereas myelodysplastic disorder (D47) refers to diseases which do not have an association with benzene thereby supporting his earlier argument that both conditions are distinct and separate.
63. With respect to the third hypothesis of a connection between chronic myeloid leukaemia and myelofibrosis, Professor Peach said that he knew of no connection between those conditions and said that he could find no support for such a connection. Additionally he said that there was no information available to him to suggest that the deceased had ever suffered from chronic myeloid leukaemia. He also noted that a report of Dr Byron Collins appeared to conclude that there was no association between myelofibrosis and chronic myeloid leukaemia – at least in the present application – based on the biopsy report of June 1997. That is to say, it appeared that Dr Byron Collins was satisfied that the myelofibrosis suffered by the deceased was “primary”, being a disease that was not a consequence of another disease.
64. In cross-examination Professor Peach said that he understood the study conducted by Tondel involved an enquiry directly into whether there was an association between benzene exposure and myelofibrosis. The witness said that Tondel would not have been enquiring into an association between benzene and idiopathic myelofibrosis, because idiopathic, by its description, is of unknown cause. He said that the Tondel study concluded that there was insufficient numbers of cases of myelofibrosis in petrol industry employees and when compared against the Swedish cancer register, an association between benzene and myelofibrosis could not be found. He said those conclusions were supported also by a separate study in Gothenburg which concluded that there was no association between motor vehicle usage and myelofibrosis. Professor Peach acknowledged that the study concluded that there was an association between benzene exposure and acute myeloid leukaemia and whilst there is also a known association between benzene and myelodysplastic disorder that association was not the subject of the Gothenburg study.
65. The witness was then taken to part of his report of March 2004 where he referred to a study in the United Kingdom of 24,500 male employees in three petroleum refineries. He said that having regard to the incidence of myelofibrosis in the United Kingdom, it was expected that there would be three deaths (having regard to the numbers involved in the survey), but in fact there were five deaths. Despite the greater number of deaths than would have been expected, Professor Peach said that it could not be concluded that the myelofibrosis was associated with exposure to benzene in those refineries because the measure of benzene exposure had not been conducted and there was not an equal number of deaths among the refineries. That is to say, there was an imbalance of deaths in one refinery as opposed to the others. In terms of epidemiological methodology, Professor Peach acknowledged that the statistically greater number of deaths than expected would not have been a “chance finding”, but the study did not conclude an association between myelofibrosis and benzene because of the absence of any measure of exposure to benzene and the absence of any enquiry into whether there had been exposure by the deceased persons to other chemicals. Professor Peach said that there had been studies conducted within the Australian petroleum industry which had concluded that there was no association between myelofibrosis and benzene and where there had been a measure of the extent of benzene exposure.
66. Professor Peach acknowledged that the occupational health and safety association in Australia had recommended that the permissible exposure limit for benzene is 1 part per million. He acknowledged that his earlier evidence had referred to 120 parts per million but said that was in the context of determining whether there was any chromosomal aberrations. He said that if there was inquiry into whether benzene had affected bone marrow causing anaemia, the exposure limit would have been set at 50 parts per million. If there was inquiry into the toxic effects generally upon the immune system, the exposure limit would have been set at 3 parts per million. Professor Peach then discussed different exposure limits in the context of different diseases and inquiry into diseases affecting children or adults. For example, the exposure limit when researching childhood leukaemia in the United Kingdom has been set at 0.5 and the exposure limit with respect to acute myeloid leukaemia had been set at 0.01. Despite the differing thresholds of exposure limits, Professor Peach reaffirmed that the deceased did not, in his opinion, develop myelofibrosis by an association with benzene, and despite what appeared to be a direct association with benzene in service, the deceased did not suffer from acute myeloid leukaemia.
67. It was acknowledged that the deceased did probably wash engine and gun parts with petrol containing benzene so that there would have been direct exposure to his skin. It was understood that benzene can be absorbed through the skin and whilst it is understood to evaporate rapidly, it is also absorbed through the lungs when breathing. Professor Peach said that there were studies which had concluded that petrol station attendants who had washed their hands with benzene had a high incidence of acute myeloid leukaemia, but there was no evidence, in his opinion, associating myelofibrosis with benzene by absorption through skin.
68. Professor Peach acknowledged that there was a known association between smoking and chronic myeloid leukaemia. He acknowledged that whilst the deceased had been smoking he had probably also been exposed to benzene. Nonetheless Professor Peach said that it was known that the deceased did not have chronic myeloid leukaemia. Upon an examination of the clinical notes of Dr Thompson, he said there was no possibility nor was there anything which pointed to the deceased having suffered from chronic myeloid leukaemia. He acknowledged that the late Mr Farley-Smith had made notes based on his interpretation of attendances upon doctors and his understanding of the discussions with those doctors. He acknowledged that in some of those notes (found within the T-documents) the words “chronic myeloid leukaemia” appear in the deceased’s handwriting. There are notes which also appear in the handwriting of the deceased’s general practitioner where the words “chronic myeloid leukaemia” appear. However, Professor Peach said that an examination of the practitioner’s notes and an examination of the pathology reports, clearly indicate that chronic myeloid leukaemia did not ever exist. Professor Peach pointed to the use of the expression “dry tap”, which was, in his opinion, a characteristic of treatment procedures for myelofibrosis. Additionally the language used to describe the appearance and production of red and white blood cells are all suggestive of myelofibrosis and positively point against a diagnosis of chronic myeloid leukaemia (refer Transcript page 141 to 142).
dr byron collins
69. Dr Byron Collins provided two reports at the request of the applicant’s solicitors dated 31 December 2003 and 15 June 2004. He was not called to give evidence.
70. In the first report (Exhibit G), having observed the pathologist’s report of June 1997, Dr Bryon Collins reported that he had no reason to doubt the certified cause of death of myelofibrosis, although, he did query the terminal event. Dr Bryon Collins concluded this report in the following terms:
2.The hypothesis that the late Mr Farley-Smith’s myelofibrotic condition was “as a complication of pre-existing chronic myeloid leukemia,” as proposed to the Hearing by the Veterans’ Review Board, cannot be substantiated, in my view, having regard to the information contained in the trephine biopsy/bone marrow examination report. It is highly likely that the late veteran did suffer from primary, idiojpathic myelofibrosis or agnogenic myeloid metaplasia, as indicated by Dr Mills.
3.Myelofibrosis is a descriptive term which refers to the deposition of excessive amounts of collagen in the bone marrow. This condition has been classified as primary or secondary, with primary myelofibrosis being as a consequence of a clonal disorder of a multipotent haematopoietic progenitor (stem) cell, generally of unknown aetiology, whilst secondary myelofibrosis develops in association with a well-defined, pre-existing primary disease process such as infection or malignancy.
4.It has been generally accepted that in primary myelofibrosis, there is no definitively known cause and hence the use of various terminologies for this condition, such as “idiopathic” or “agnogenic,” although with recent research these descriptive terms would appear somewhat inappropriate. The development of this form of the disease has been linked to exposure to petroleum derivatives, particularly toluene and benezene, [sic] or to ionizing radiation (see accompanying example article by Tondel).
5.It has been suggested that, as a Bofors gunner during the war, the late Mr Farley-Smith may have been exposed to petrol/benzene. If such a suggestion can be appropriately substantiated then, in my opinion, there is a real possibility his death was war associated through the link between benzene exposure causing toxic effects on the bone marrow which then resulted in myelofibrosis.
71. In his second report of 15 June 2004 (Exhibit H), Dr Byron Collins acknowledged that he had read reports of Professor Peach of 26 March 2004 and of Professor Fox of 3 March 2004. He concluded his report in the following terms:
1.Whilst I agree with Prof. Peach’s view that the proposed relationship between benzene exposure and the subsequent development of myelofibrosis is based on epidemiological studies and individual case reports, such a correlation does not necessarily exclude a definitive causal connection.
2.I do not believe it is appropriate for Prof. Peach to indicate, as he has done on page 3 of his report, that the case reported by Tondel et al, 1995 “….was misleading.” In reality, it may or may not be, but either alternative is possible. A copy of the article by Tondel is enclosed for your assessment which shows, inter alia, that whilst a search in the Swedish Cancer Environment Register in relation to myelofibrosis indicated there was no increased risk found for petrol station attendants (noted by Prof. Peach), but that myelofibrosis was increased among motor vehicle drivers and in the transport industry.
In summary, the hypothesis involving the causal link between benzene and myelofibrosis is based on epidemiological and single case data which appears to be sound, although it should be appreciated no direct pathological association has yet been established. Epidemiology may or may not be a sufficient test of proof for the Tribunal to accept as a reasonable hypothesis.
the tondel study
72. This study was the subject of extensive analysis in the reports and evidence of Professor Peach. A copy of the study was also annexed to both reports of Dr Byron Collins. It is described as a case report only and is not the conclusions of an epidemiological survey. The basis of the study is single case only and is described in the following terms:
In October 1992, myelofibrosis was diagnosed in a 46-year-old previously healthy man. He had had symptoms of increasing muscle pain for one year and a three-week history of fatigue, nightly sweating and weight loss. The patient was referred to the Department of Hematology, University Hospital, Linkoping, where a bone marrow biopsy showed myelofibrosis. In 1962-1979, the man had worked as a petrol station attendant and his work was to refuel cars with petrol or diesel. He was also exposed to petrol fumes when he regularly inspected the petrol level in the arriving tanker lorries.
73. The report then recorded relevant statistics from the United States and Europe and noted that there were different levels of benzene within petrol. It was also noted that the exposure to benzene by breathing could be affected by temperature, wind direction and car model.
74. The report then discussed the incidence of myelofibrosis by regard to the Swedish Cancer Environment Register and reported:
When observing a single case in relation to a particular exposure, there is considerable doubt as to whether there is a causal connection or not. Epidemiological studies would be desirable but sufficient numbers of cases are not easily attainable for this relatively rare disease. In this respect, the Swedish Cancer Environment Register provides the possibility of searching for cancer cases in relation to occupation groups and branches of industry. This nationwide register includes all cancer cases from 1971 to 1984 and employment data from the 1980 census. A search in this register showed that, for men, myelofibrosis was increased among motor vehicle drivers . . . No increased risk was found for petrol station attendants . . . However, myelofibrosis was increased in the transport industry . . .
75. The report concluded:
The fact that petrol station attendants are exposed to benzene, our case report, the earlier reports on the issue, and the findings from the Swedish Cancer Environment Register strongly suggest benzene exposure as a risk factor for myelofibrosis. With regard to the pathogenesis, myelofibrosis, as well as leukaemias, may derive from a multipotent stem cell in the bone marrow. This suggestion would explain why benzene causes various blood malignancies, including myelofibrosis. A multi-centre study on this rare disease and benzene exposure seems warranted.
conclusion and reasons for decision
76. This application involved the potential of three hypotheses each containing a different description of the illness or injury giving rise to the cause of death. A finding must be made on the probabilities of the cause of death in order to determine which SOP is applicable.
77. The cause of death, as certified by the Death Certificate, was myelofibrosis. That was certified by Dr Thomson, the treating general practitioner, who was the same doctor alleged in these proceedings as having had a discussion with the late Mr Farley-Smith about the potential for pre-existing chronic myeloid leukaemia. A bone marrow biopsy was the subject of a report by Dr Mills on 10 September 1997, which concluded that the pathology pointed to myelofibrosis. I note the correlation between the report, completed approximately four years prior to the date of death, and the Death Certificate which recorded that myelofibrosis had been present for four years. Professor Fox said that he was “in no doubt” that myelofibrosis was the cause of death and he agreed with the conclusions reached by Dr Mills. Professor Peach was of the same opinion. Additionally, Professor Fox said that there was no evidence of chronic myeloid leukaemia or of myeloid dysplastic syndrome. Dr Byron Collins was also of the opinion that myelofibrosis was the cause of death.
78. I am satisfied on the balance of probabilities that the cause of death was myelofibrosis. For the purposes of s 120A (4) of the Veterans’ Entitlements Act 1986 (“the Act”), upon the basis that a SOP does not exist with respect to myeloid fibrosis, I am also satisfied and find as a fact, that the “kind of death” for the purposes of this application was myelofibrosis.
79. There is no evidence of the presence previously, or at death, of chronic myeloid leukaemia other than the understanding by Mrs Farley-Smith – based on a conversation she had with her husband – that Dr Thomson had expressed regret that blood tests had not been conducted prior to 1997. It was her belief – based on that conversation with her husband – that Dr Thomson had been of the belief that, had blood tests been undertaken, chronic myeloid leukaemia may have been diagnosed. There was nothing in the clinical notes of Dr Thomson which would suggest that chronic myeloid leukaemia was ever diagnosed. The late Mr Farley‑Smith had apparently made some handwritten notes following a consultation with Dr Thomson, where the words “myeloid leukaemia” were recorded. The relevance and context of those notes is unclear. There is nothing which points to chronic myeloid leukaemia having any relevance to the circumstances of the death of the late Mr Farley‑Smith. Equally it may be said that myeloid dysplastic disorder has no relevance. Professor Fox dismissed it as having any relevance and found no support in any of the clinical data, for it as contributing to, or being the cause of death.
80. Accordingly, the remainder of these reasons will be concerned only with the hypothesis that service exposed the deceased to the use of petroleum products and the consumption of tobacco products, which caused exposure to benzene which precipitated, or was responsible for myelofibrosis, which in turn caused death. A SOP with respect to myelofibrosis has not been published by the Repatriation Medical Authority. Accordingly, the liability of the respondent will be determined by the provisions of s 120 of the Act. The decisions of the High Court in Bushell v Repatriation Commission (1992) 109 ALR 30 (“Bushell”) and Byrnes v Repatriation Commission (1993) 116 ALR 210 (“Byrnes”) continue to remain the predominant authorities concerning the application of s 120.
81. In Bushell the Court decided (page 34) that for the purposes of deciding whether a hypothesis is reasonable under s 120 (3) of the Act ‑
. . .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.
82. In Bushell the Court considered an earlier authority of Commissioner for Government Transport v Adamcik (1961) 106 CLR 292. In that case a connection between emotional disturbance having its origin in trauma, resulting in acute lymphatic leukemia was supported by only one doctor, whilst the opposing opinion of many other doctors and twenty years of medical literature discarded the connection. Windeyer J decided that although the opinion of that one doctor was unproven and not accepted by others, it could not be scientifically established as being false. As an extension of this proposition, the Court decided, at page 35, that the Commission
is bound to have regard to the opposing medical or scientific material for the purpose of examining the validity of the reasoning which supports the claim . . 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.
83. The Court then discussed the operation and interrelationship between s 120 (3) and (1) of the Act and discussed the circumstances where there would be no sufficient ground to make a determination (in favour of the Commission) under subsection (1). The Court discussed whether the raised facts could not be accepted because they were unreliable, or by reason of the superior reliability of other parts of the material, or where inferences could not be drawn. In those circumstances the Court decided that the Commission could be satisfied that there was no sufficient ground to make a determination under subsection (1). The Court, at page 36, then decided that unless the Commission could be 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.
84. In the present application, the hypothesis of an association between service, exposure to benzene and death was put on the basis that the deceased had used petroleum containing benzene and smoked piped tobacco which produced benzene. The respondent conceded that the petroleum, to which the deceased was exposed, did contain benzene. No other concession was made. There was material pointing to the deceased using petroleum (containing benzene) to wash machinery and gun parts but little else is known. The duration and extent of the usage of petrol, together with the quantities of petrol used, were not known. But by reference to other decisions of this Tribunal it would appear that access to petroleum was readily available and its usage was probably without protective clothing or breathing apparatus (refer Re Whitworth and Repatriation Commission [2002] AATA 861; Prestegar v Repatriation Commission [1997] 762 FCA). Additionally, there was the evidence heard in these proceedings from Mr Salter and from Mrs Prestegar.
85. I am therefore satisfied that there was material which pointed to the deceased using and therefore having been exposed to petrol and petroleum products containing benzene during service.
86. Professor Fox and Professor Peach regarded myelofibrosis as being idiopathic and not having a relationship to benzene exposure. In my view, Professor Fox was far less rigid than Professor Peach in expressing his opinions.
87. Professor Fox said that he was not aware of any “firm epidemiological data” connecting benzene exposure with myelofibrosis. He acknowledged that there was a single case study purporting to support the connection, but he thought that research was unreliable. Further, it was his opinion that chromosome changes by benzene would produce a different outcome to the chromosome changes to Mr Farley-Smith. He said the connection between benzene and myelofibrosis was “not impossible” but did regard it as being tenuous and fanciful. He was not prepared to “rule it out completely” but said on all of the evidence that he knew, no connection existed.
88. Professor Peach said that there was nothing in the “world of medical literature” supporting the connection. Whilst he acknowledged the presence of the Tondel research paper, he said it had been discounted by Tondel himself, and it was a paper which had no value in epidemiological research. He said this was because it involved a single case study which “left open” but did not “point to” the association between benzene and myelofibrosis. He also said the chromosomal alterations were inconsistent with myelofibrosis.
89. Dr Byron Collins also referred to the Tondel study and described the connection between benzene and myelofibrosis “as a real possibility”. He acknowledged the absence of epidemiological studies supporting the connection, but said of those studies which did exist, a “definitive causal connection” could not be excluded. He differed from Professor Peach in the weight to be placed on the study by Tondel.
90. I am not satisfied that the hypothesis raised by these proceedings is “contrary to proved scientific facts or to the known phenomena of nature”. There is no proof that benzene does not cause myelofibrosis and no proof that the connection is false. I cannot be satisfied that the hypothesis is “obviously fanciful, impossible, incredible or not tenable or too remote or too tenuous (Bushell page 35).
91. On the evidence of Professors Fox and Peach alone, it might be thought that medical and/or scientific opinion would not support the hypothesis, and that there was an absence of support within the medical profession and other scientists for the connection between benzene and myelofibrosis. But more is known.
92. Tondel did acknowledge that his survey involved a single case only, and that it would be desirable to have greater numbers within his survey so that he had a sound basis upon which to express scientific opinion. However, he did conclude that there was a strong suggestion that benzene exposure was a risk factor for myelofibrosis. He expressed the view that the pathogenesis might establish that myelofibrosis derives from a multi potent stem cells in bone marrow. It followed that benzene may be the explanation for malignancies of the blood including myelofibrosis. He recommended that further study be undertaken. He also noted that a survey of the Swedish Cancer Register showed that myelofibrosis in male persons increased in the case of motor vehicle drivers. Whilst acknowledging that no increased risk was found for petrol station attendants, myelofibrosis had increased (in number) for persons in the transport industry.
93. Professor Peach referred to the greater incidence of myelofibrosis in petroleum refinery employees in the United Kingdom than expected, but discounted the findings by reason of the epidemiological methodology. He also acknowledged that the Tondel article raised the possibility of an association between benzene and myelofibrosis, but said it should be discounted as demonstrating a “causal connection” as it was a single case study.
94. This appeal has again seen the law and medicine intersect. The differing standards of proof expected by each profession would hardly permit a parallel journey and a collision often occurs. The standard of proof required by epidemiology or medical science is at a far greater level than that required in the finding as to whether a hypothesis is reasonable.
95. As may be seen from the foregoing, a hypothesis may be reasonable despite the fact that it might be unproved, may have little support within the medical profession and may be dependent upon assumption. I cannot find on the material read and heard in these proceedings, that the raised facts are unreliable. Nor can I find that the evidence of Professors Fox and Peach is of such a superior reliability that there is no sufficient ground to determine that death in the present application was war-caused. At the conclusion of the evidence but before the conclusion of the hearing, Mr De Marchi produced a bundle of extracts from internet web sites, without specific attention or submission being directed to any of them. An analysis of those sites indicates that there is some support within the profession for an association between benzene and myelofibrosis – refer and Additionally, one of the documents forming part of the “web” exhibits – the copy of which is so poor that the web address cannot be identified refers to an increased incidence of myelofibrosis in the case of firemen who have been exposed to benzene. Regard for this material may appear unorthodox however it does highlight that contrary to the opinion of Professor Peach, in ‘world medical literature’ there does exist a body of literature raising a connection between benzene and myelofibrosis.
96. I readily acknowledge that those documents were not the subject of examination by the respondent, nor were they put to Professors Fox or Peach. However, the opinions expressed in those documents found at web sites of reputable medical organisations, do indicate that the hypothesis is reasonable because the connection between benzene and myelofibrosis is more than a possibility. Veterans and their widows need not establish a hypothesis as reasonable by a “causal connection” (refer Professor Peach) or a “definitive causal connection” (refer evidence of Dr Byron Collins). The finding of the reasonableness of the hypothesis does not depend on a resolution of or choice between competing medical theories. The contents of the report of Dr Byron Collins, the survey material from Sweden referred to in the report of Tondel (including his own survey), the United Kingdom survey referred to by Professor Peach and the information found from the internet sources as tendered does point to material raising a reasonable hypothesis connecting the operational service of the deceased, his exposure to benzene by petroleum products and myelofibrosis. The hypothesis is not “obviously fanciful, impossible, incredible, or not tenable or too remote or too tenuous” (refer East v Repatriation Commission (1987) 74 ALR 518 at 533.
97. I can find nothing in the material pointing to an association between smoking tobacco and myelofibrosis. Accordingly this decision has regard only the hypothesis involving benzene exposure only by petroleum products.
98. For the purposes of s 120 (1) of the Act, I am satisfied that the respondent must determine that the death of the late Mr Farley-Smith was war‑caused because it cannot be satisfied beyond reasonable doubt that there is no sufficient ground to determine otherwise.
I certify that the 98 preceding paragraphs are a true copy of the reasons for the decision herein of:
Mr John Handley, Senior MemberSigned: .....................................................................................
AssociateDates of Hearing 30 August 2004, 29 November 2004 and 28 February 2005
Date of Decision 4 October 2005
Solicitor for the Applicant Mr D De Marchi
Departmental Advocate Mr E Nyhof
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