The Estate of the Late Mr Vaughan White and Military Rehabilitation and Compensation Commission (Compensation) - [2018] AATA 3882

The Estate of the Late Mr Vaughan White and Military Rehabilitation and Compensation Commission (Compensation) [2018] AATA 3882 (16 October 2018)
Division:VETERANS' APPEALS DIVISION
File Number: 2016/2016
Re:The Estate of the Late Mr Vaughan White
APPLICANT

Military Rehabilitation and Compensation CommissionAnd
RESPONDENT

DECISION
Tribunal:Deputy President J Sosso and
Member Dr G Maynard
Date:16 October 2018
Place:Brisbane

The Tribunal affirms the decision under review.
...........................[sgd].......................................
Deputy President J Sosso
CATCHWORDS
COMPENSATION – compensation claim by wife of former member of the Australian Army – veteran deceased – smoking – motor neuron disease – was smoking habit contributed, to a significant degree, by his defence service – link between smoking and onset of motor neuron disease – epidemiology – link between smoking and onset of veteran’s motor neurone disease – decision under review affirmed
LEGISLATION
Safety, Rehabilitation and Compensation Act 1988
Safety, Rehabilitation and Compensation (Defence-Related Claims) Act 1988
CASES
Cooper and Military Rehabilitation and Compensation Commission [2017] AATA 429; 158 ALD 64
Military Compensation and Rehabilitation Commission v Wall [2004] FCA 1711
Military Rehabilitation and Compensation Commission v Wall [2005] FCAFC 127; 88 ALD 1.
Repatriation Commission v Tuite (1993) 39 FCR 540
Seltsam Pty Ltd v McGuiness[2000] NSWCA 29; 49 NSWLR 262
SECONDARY MATERIALS
Sir Owen Dixon, “Science and Judicial Proceedings” in Jesting Pilate (1965)
Alonso A et al. 2010, ‘Smoking and the risk of amyotrophic lateral sclerosis: a systematic review and meta-analysis’, Journal of Neurology, Neurosurgery and Psychiatry, vol. 81, issue 11, pp. 1249 – 1252
American Academy of Neurology, Clinical Practice Guideline Process Manual (2017 edition)
Armon C 2003, ‘An evidence-based medicine approach to the evaluation of the role of exogenous risk factors in sporadic amyotrophic lateral sclerosis’, Neuroepidemiology, vol. 22, issue 4, pp. 217 – 228
Armon C 2005, ‘Acquired nucleic acid changes may trigger sporadic amyotrophic lateral sclerosis’, Muscle and Nerve, vol. 32, issue 3, pp. 373 -377
Armon C 2009, ‘Smoking may be considered an established risk factor for sporadic ALS’, Neurology, vol. 73, no. 20, pp. 1693 -1698
Armon C 2016, ‘Accrued somatic mutations (nucleic acid changes) trigger ALS: 2005-2015 update, Muscle and Nerve, vol. 53, issue 6, pp. 842 – 849
Brown H et al. 2017, ‘Amyotrophic lateral sclerosis’, New England Journal of Medicine, vol. 77, no. 2, pp. 162 – 172
Institute of Medicine. 2011. Finding What Works in Health Care: Standards for Systematic Reviews. Washington, DC: National Academies Press
Wang H et al. 2011, ‘Smoking and risk of amyotrophic lateral sclerosis: a partial analysis of 5 prospective cohorts’, Archives of Neurology, vol. 68, no. 2, pp. 207 – 213
Wang M et al. 2017, ‘Identification of risk factors associated with onset and progression of amyotrophic lateral sclerosis using systematic review and meta-analysis’ Neurotoxicology, vol. 61, pp. 101 – 130
REASONS FOR DECISION
Deputy President J Sosso and
Member Dr G Maynard
16 October 2018
INTRODUCTON

On 26 May 2014, Mr Vaughan White (the veteran), made a claim for liability to be accepted under s 14 of the Safety, Rehabilitation and Compensation Act 1988 (the Act) in respect of Motor Neurone Disease (MND), which disease ultimately led to his death on 2 March 2018 – Exhibit 1 T4 pp. 21 – 29.
During the course of these proceedings, the legal representatives for both parties made submissions by reference to various provisions in the Act. However, in 2017 the defence related provisions of the Act were extracted and separately enacted in the Safety, Rehabilitation and Compensation (Defence-Related Claims) Act 1988 (the SRC (D-R C) Act). The SRC (D-R C) Act removes cover for members of the Defence Force and their dependants from the Act and creates a “military specific” compensation and rehabilitation scheme.
The SRC (D-R C) Act effects no substantive changes to compensation and rehabilitation law, rather, it aims to bring the various strands of veterans’ compensation law into closer alignment and to bring about administrative efficiencies.
For all intents and purposes, then, both the Act and the SRC (D-R C) Act are mirror images of each other, and the position of members of the Defence Force, veterans, or their dependants are not materially changed by this legislative reform.
For ease of reference we will refer to the provisions in the Act in the body of this decision. However, such references can be taken to also refer to the equivalent provision in the SRC (D-R C) Act.
Subsection 55(2) of the Act provides that a claim is not affected by the death of the claimant after the claim was served.
Following the death of the veteran, his wife, Mrs Gladys White (the Applicant) as executor of his estate, took over the proceedings. Nothing of substance for the disposition of this matter turns on this state of affairs – see Transcript (Tr.) 9 April 2018 pp. 2 – 3.
The veteran enlisted in the Royal Australian Army (RAA) on 7 April 1970 when he was 17 years of age, and voluntarily discharged on 15 April 1996, having rendered 26 years of service – Exhibit 3 p. 5. From November 1974, the veteran served as a member of the Military Police and rose to the rank of Warrant Officer Class 1 – Exhibit 3 pp. 5, 8, 16.
The Applicant first met the veteran in August 1978 when they were both living at the Karrakatta Army Barracks in Perth. The Applicant was then a member of the Women’s Royal Australian Air Force and they married in November 1979. Subsequently, the Applicant had two children, a daughter born in 1981 and a son born in 1983 – Exhibit 2 paras 2, 4 and 5; Exhibit 3 p. 6.
From the start of their relationship, the Applicant observed that the veteran was a heavy smoker, consuming up to 2.5 packets daily – Exhibit 2 para 6. The veteran continued smoking until the birth of his son, when he stopped smoking for a few months. He claimed that he ceased smoking completely in 1985 – Exhibit 1 T8 p. 40. Military medical records disclose that by September 1988, the veteran was noted to be a non-smoker – Exhibit 3 p. 44.
The Applicant contends that the veteran’s service in the RAA contributed, to a significant degree, to the development and maintenance of a smoking habit which in turn contributed, to a significant degree, to the development of his MND – Applicant’s Outline of Submissions (AOS) para 8.
Both in her written statement of 16 September 2016, and during her oral testimony, the Applicant primarily attributed this habit to the stress the veteran experienced in carrying out his duties as a Military Police officer – Exhibit 2 para 6; Tr. 9 April 2018 pp. 19 – 20. The Applicant did not refer in her statement to a 1972 live grenade incident which resulted in the veteran being injured. When questioned during the Hearing why this incident was omitted from her statement, the Applicant could provide no reason – Tr. 9 April 2018 p. 21.
Following his discharge from the RAA, the veteran worked with Australia Post as a Senior Postal Delivery Officer – Tr. 9 April 2018 p. 23.
In January 2014, while still working with Australia Post, the veteran suffered a fall at work and he subsequently became aware of a gradually increasing weakness in his legs with a tendency to trip and he experienced difficulty getting up. He then began suffering from leg cramping and twitching of the muscles in his upper and lower limbs. In June 2014, the veteran was examined by Dr John Cameron, Neurologist, and following tests a diagnosis of MND was made – Exhibit 1 T7 pp. 32 – 33.
It is not disputed that the veteran suffered from MND, and that a diagnosis of this condition was made as early as January 2014 – AOS para 8.
When making his claim for compensation, the veteran stated that he was injured while participating in a live grenade practice in the Wide Bay area and received shrapnel wounds to his back and suffered temporary deafness. The veteran claimed that he began smoking as a result of the injuries he received and the stress and anxiety that followed. The veteran further claimed that smoking relieved these symptoms of the incident and helped him control his feelings – Exhibit 1 T4 p. 27.
The veteran’s compensation claim was ultimately rejected by the reviewable decision of 11 April 2016 – Exhibit 1 T19 p. 64.
The central issue before the Tribunal is whether the veteran’s MND was contributed to, to a significant degree, by his service with the RAA. In resolving this issue, two matters need to be addressed:
a. was the veteran’s smoking habit contributed to, to a significant degree, by his service with the RAA?; and
b. if an affirmative response is provided to (a), did the veteran’s smoking habit contribute, to a significant degree, to the development of his MND?
The Hearing presented a number of logistical difficulties. It was conducted over three separate days: 9 April, 3 May and 14 June 2018. The Applicant was represented by Mr Harding of Counsel and the Military Rehabilitation and Compensation Commission (the Respondent) by Mr Clark of Counsel. On the first day of the Hearing the Applicant gave evidence, on the first and second days Dr Carmel Armon gave evidence via telephone from Israel and on the final day of the Hearing Dr John Cameron and Professor Timothy Driscoll gave evidence.
LEGAL PRINCIPLES
Subsection 14(1) of the Act provides that, subject to Part II, Comcare is liable to pay compensation in accordance with the Act in respect of an injury suffered by an employee if the injury results in death, incapacity for work, or impairment.
It is not contested that the veteran, whilst enlisted, was an “employee” for the purposes of the Act.
The historical development of the Commonwealth’s liability to pay compensation to members of the Defence Force are helpfully explained by Hely J in Military Compensation and Rehabilitation Commission v Wall [2004] FCA 1711 at [7] – [13].
Section 17 deals with compensation for injuries that result in death. In this context, s 17 provides that compensation is payable where a deceased has left dependants who were either wholly or partially dependent on the employee at the date of the employee’s death.
The term “injury” is defined by s 5A to include, inter alia, a “disease” suffered by an employee. “Disease” is, in turn, defined by s 5B(1) to mean:
“(a) an ailment suffered by an employee; or
(b) an aggravation of such an ailment;
that was contributed to, to a significant degree, by the employee’s employment by the Commonwealth or a licensee.”
It will be noted that that the test is contributed “to a significant degree” by the employment. Section 5B(3) provides that a significant degree means “a degree that is substantially more than material.”
Further, in determining whether an ailment was contributed to, to a significant degree, by an employee’s employment, the following matters may be taken into account:
1.the duration of the employment;
2.the nature of, and particular tasks involved in, the employment;
3.any predisposition of the employee to the ailment;
4.any activities of the employee not related to the employment;
5.any other matters affecting the employee’s health.
Mr Harding drew our attention to the decision of the Full Federal Court in Military Rehabilitation and Compensation Commission v Wall [2005] FCAFC 127; 88 ALD 1(Wall).
Their Honours Wilcox and Downes JJ made the following observations:
“[31] The Tribunal correctly described its legal function when it said that [t]he ‘real question…is whether the Applicant’s smoking habit can be said to have arisen out of or in the course of his employment…or whether his employment was a contributing factor.’ The Tribunal also said: ‘it must be proved that the disease was caused by the employment and not merely contracted during the said employment’. It concluded that: ‘In this case…to adopt a smoking habit is a risk of that employment’.
[32] We emphasise the Tribunal’s words ‘In this case’. Unlike a civilian employee, the respondent did not have the option of coming and going from his place of employment or the option of living away from the job. The form of national service training which the respondent was required to undertake involved him becoming, for 3 months, a full-time member of the Defence Force. During that time, the respondent was required to live in Army barracks in the company of other trainees. No doubt an important object of the training program was to accustom young men to the experience of living and working together, including under stressful circumstances…
[35] It should not be assumed, from the result of this case, that compensation will be available to every former member of the Defence Force who can establish that he or she took up smoking during military service and subsequently suffered a smoking-related accident or illness. In any particular case, it will be a question of fact whether there is a causal relationship between the person’s smoking during the period of military service and the onset of the accident or illness. In a case where it is concluded that the accident or illness was caused by smoking after the period of military service, it will be necessary for the person to show that he or she became so habituated to smoking, during his or her period of military service, that this habit was the effective cause of the later smoking which resulted in the disease. That is likely always to be a difficult case for an applicant to make good.”
There is a long line of authority which requires a causal connection between a person’s employment (or a veteran’s defence service) and the onset of a smoking habit. A distinction must be drawn between the ascertainment of the operative cause of the development of a smoking habit and merely a temporal connection, or to put it another way, the provision of a setting in which an employee chooses to commence a smoking habit – see Repatriation Commission v Tuite (1993) 39 FCR 540 at 541.
As Wilcox and Downes JJ highlighted, the mere fact that a member of the Defence Force commences smoking whilst enlisted, does not provide the causal connection required. There must be something intrinsic in the nature of a veteran’s particular employment that is the operative cause of the onset of the smoking habit.
Mr Harding also referred to the Tribunal decision of Cooper and Military Rehabilitation and Compensation Commission [2017] AATA 429; 158 ALD 64 (Cooper). In finding in favour of the deceased veteran in that matter, the Tribunal considered the following factors ([79]/74 – 75):
“In reaching a conclusion on whether there is a causal link between the performance of the Deceased’s duties as a member of the RAN and his smoking habit, and, in particular, whether the performance of those duties contributed to a significant degree to his smoking, I have taken into account the following factors:
1.the Deceased was only 15 years of age when he first enlisted;
2.he was separated from his parents and moved from Melbourne to Perth, which in 1977 would have meant he had minimal contact with them;
3.he was placed in a ‘milieu totally different to that which had experienced before his’ enlistment – see Repatriation Commission v Tuite (1993) 29 ALD 609 at 614;
4.he was exposed to a high degree of smoking and passive smoking from the outset and throughout his years of service;
5.he was subject to peer pressure as a young teenager and wanted to be ‘one of the men’;
6.smoking was tolerated and even tacitly encouraged by the RAN during his years of service. It was only after 1 January 2013 that the favourable excise provisions for cigarette sales on board ocean going ships was changed, a policy that had been in force since the 1930s;
7.the Deceased served in the Navy for approximately 23 years; his extended period of service had a marked impression on his character formation and smoking and drinking habits;
8.he did not smoke before enlisting, but commenced smoking after only a month thereafter when he was only 15 years of age;
9.there is no material before the Tribunal that any attempt was made to prevent or inhibit the Deceased from smoking before he reached 18 years of age; and
10.his smoking habit did not increase after he left the RAN, on the contrary, he ceased smoking five years thereafter.”
It will be noted that the evidence presented in this matter is quite different from the factual matrix before the Tribunal in Cooper. This is discussed in detail below.
WAS THE VETERAN’S SMOKING HABIT CONTRIBUTRED TO, TO A SIGNIFICANT DEGREE, BY HIS MILITARY SERVICE?
On 21 August 1972, the veteran sustained shrapnel injuries to his body caused by a training accident with a grenade on the Wide Bay Range. The circumstances of the incident were set out in a letter prepared by the veteran which is dated 1 June 2015 – Exhibit 1 T8 p. 40:
“Whilst participating in a live fire grenade practice in the Wide Bay Training Area, Queensland on the 21 August 1972, I received shrapnel wounds to my back and suffered temporary deafness. I also suffered from anxiety and stress in the months that followed and was very apprehensive around fire arms and especially grenades and this caused me significant stress in my normal operating life as a soldier. This was caused by directly experiencing this traumatic event which I have suffered from for the rest of my life. I got great relief from smoking and drinking and self medicated daily for many years to try to forget the memories of the grenade accident and how close I was to losing my life from such a life threatening event. The exposure to such a threatening situation which almost resulted in my death, but did end in serious injury to myself with shrapnel wounds to my back caused me to commence smoking. I have suffered involuntary distressing memories of the incident and still causes me psychological reactions to the current day and I avoid places that bring me distressing memories thoughts and feelings of the incident and which cause me clinically significant stress in social functioning on a daily basis. The smoking arose out of my service and I have always attributed the smoking habit to the after stresses of the event. I suffered intense fear as a result of this accident which was a life threatening event to me receiving shrapnel wounds to my back and suffered long term hearing problems as well.”.
The RAA medical records confirm that this event occurred and that the veteran was injured. In a Report dated 22 August 1972, the veteran stated:
“I was called out of the Bay to go find a Blind M 26 grenade. We found it and without warning it blew up. I suffered shrapnel wounds in the area of my back.”
The treating doctor recorded: “Superficial penetrating wounds of back.” – Exhibit

3 p. 57. A drawing made by the treating doctor illustrates that the veteran was wounded in five separate locations, with four wounds to his back and one to his right arm – Exhibit

3 p. 65. The veteran was admitted to hospital on 21 August 1972 and discharged on

25 August 1972 – Exhibit 3 p. 63.
With the exception of contemporaneous Army Medical Board examinations in the period 1973 – 1996, there is scant evidence of the state of the Applicant’s physical or mental health from the time of his enlistment until his discharge. Further, due to his tragic demise, the only other evidence before us is that of the Applicant.
First, we note that in the period 1973 – 1996, there are 14 Army Medical Board Reports in the Exhibit 3 documents - Exhibit 3 pp. 93, 56, 54, 53, 51, 49, 47, 44, 42, 39, 37, 36, 34 and 94. In none of those Reports is the veteran observed to have any mental health issues. Further, the veteran was psychologically assessed on 21 May 1974 for the purpose of ascertaining his suitability for a career in the Military Police. His personality was then described as “suitable” and no psychological issues or problems were noted – Exhibit 3 pp. 106 – 107.

The absence of any recording of psychological issues is not determinative. However, if the veteran was suffering the level of mental distress post August 1972 that he claimed, there is no contemporary medical evidence that supports this alleged state of affairs. It may have been the case that the veteran was loathe to disclose to the examining medical doctors his mental state. Certainly, if he had done so, this may have had a deleterious impact on his desire to join and remain in the Military Police, or, indeed, service in the RAA.
We have no independent evidence to determine whether the veteran was smoking before August 1972. The Applicant, in both her statement (Exhibit 2) and her oral evidence, confirmed that the veteran was a heavy smoker when they met in August 1978 and remained a heavy smoker until the birth of their son. In her statement, the Applicant said that her husband’s heavy smoking was a consequence of the stress he experienced in carrying out his duties as a Military Police officer. In paragraph 7 of her statement, the Applicant describes the stresses experienced by members of the Military Police Platoon. She also describes the physical and psychological isolation of Military Police from other RAA units. She gave evidence of her husband’s mental state while in the RAA, which she described as one of constant alertness for possible offenders and the isolation of military police in the RAA as a whole.
Mr Clark, on behalf of the Respondent, submitted that there were problems with both the Applicant’s written statement and her oral evidence. In the Outline of Submissions on behalf of the Respondent (OSR), the following submission was made:
“24. The written material from the deceased solely focuses upon the consequences of the grenade incident. If that incident had been as pervasive as the deceased seeks to assert, then surely it would have been raised in the Applicant’s statement and for that matter, in her evidence-in-chief. In this regard, the Applicant’s evidence when these matters were put to her finally in cross-examination was simply not indicative of this factor being such a pervasive factor as the deceased seeks to claim.
25. The converse submission can also be made if the psychological consequences of undertaking police work had been as solely important as the Applicant conveyed in her statement, then surely some reference to these factors would have featured in the deceased’s written material.”
There is some force in Mr Clark’s submissions. It was somewhat troubling that the veteran raised the grenade incident as the reason he commenced smoking, yet this was not referred to by the Applicant in her statement. Moreover, when giving evidence she again omitted any reference to this incident until questioned by Mr Clark. Even then, her responses to the questions posed lacked any semblance that the 1972 grenade incident played a significant role in the veteran’s mental health. The following exchange between Mr Clark and the Applicant highlights this – Tr. 9 April 2018 pp. 21 – 22:
“Okay. You don’t mention any of those matters in your statement though, do you?---No.
All right. Well, did he ever confide in you regarding the incident with the hand grenade in 1972?----I knew about it, yes.
Okay. All right----?---He still had shrapnel in his body.
Sorry?---He still had shrapnel in his body, so.
Well, two pieces of shrapnel, weren’t there?---Yes, but it was still there. Yes.
He goes on to say – this is the second large paragraph,
“This is caused by directly experiencing this traumatic event which I have suffered from for the rest of my life”.
Did he ever tell you about that?---What, the suffering from it?
Yes, the psychological stress?---Yes.
Is there any reason why you didn’t set that out in your statement?---No….
Okay, but what about what he says here about the ‘great relief’ that he got from smoking? Did he ever tell you about that?---He never actually stated that he got relief from smoking, it just eased the tension.
Okay. All right. He goes on to say that he suffered ‘involuntary distressing memories of the incident’?---Yes.
Did you ever see that yourself?---I did see a couple, yes.
A couple?---Yes
What, in the whole of your married life?---I probably saw more, but I can only remember a couple.
I see. Is there any reason why you didn’t put that in your statement?---I didn’t think of it.
I see. All right. He goes on to say, ‘It still causes me psychological reactions to the current day.’ Did you ever see any evidence of what he calls ‘psychological reactions’?---Yes. Tension and jumping with loud noises.
I see, all right. Is there any reason why you didn’t put that in your statement?---I didn’t think about that, yes.
I see. He goes on to say,
I’d avoid places that bring me distressing memories, thoughts and feelings of the incident.
Did he ever tell you about that?---No…
All right. So, do I understand you to be saying, you have got a recollection of there being some sort of fallout from the grenade incident?---There was definitely some fallout from it, yes.
Okay, but you haven’t mentioned that in your statement?---No.”
It will be recalled that the veteran did not raise any issue about his Military Police service contributing to his smoking habit. The Applicant, however, stated that it was this service that was a prime issue in contributing to the veteran’s smoking. Yet when she was cross-examined by Mr Clark, the Applicant gave this description of how the veteran viewed his Military Police service – Tr. 9 April 2018 p. 23:
“Okay, all right. From what you saw of his career as a Military Policeman, did it appear to you as if he enjoyed that career?---Yes.
He did?---Yes…
Okay. He was regarded as competent?---Yes.
All right, and he knew that himself?---Yes.”
We agree with the submission of Mr Clark (OSR para 26) that the Applicant’s evidence during cross-examination is at odds with the contention that the veteran was adversely affected by stress emanating from his employment in the Military Police.
The next issue that undercuts the Applicant’s case is that she testified that the veteran actually ceased smoking in July 1983, and not 1985 as the veteran stated – Tr. 9 April 2018 p. 23. We accept the veracity of her testimony, which means that from July 1983 until April 1996 the veteran served in the RAA and in a Military Police role, yet did not smoke. In other words, for almost 13 years whilst allegedly performing “stressful” duties, he voluntarily stopped smoking. This could suggest that the veteran was a person of strong will power and realised the deleterious consequences of tobacco consumption. It could also mean that he was not suffering from the degree of stress claimed, and was able to get on with his life without being dependent on smoking cigarettes.
In making a finding on the first issue before the Tribunal we have had regard to the following matters:
1.the Tribunal has been presented with no independent evidence as to when the veteran commenced smoking;
2.the veteran did not meet the Applicant until 1978, or approximately six years after the grenade incident and the suggested onset of smoking;
3.the grenade incident did require the hospitalisation of the veteran, but contemporary medical reports disclose that the veteran only suffered superficial and non-life-threatening injuries;
4.the Applicant did not mention the grenade incident in her statement, and only referred to it during oral evidence when questioned by Mr Clark;
5.when answering questions posed by Mr Clark, the Applicant did not state that the grenade incident had the traumatic consequences that the veteran claimed;
6.the veteran did not mention his service in the Military Police as a contributing factor to the commencement or maintenance of his smoking habit;
7.the Applicant testified that the veteran actually enjoyed his career in the Military Police;
8.there is no supporting contemporary medical evidence that the veteran was suffering any psychological ailments during his defence service. On the contrary, all of the many contemporary medical reports disclose no evidence of any psychological problems. It is improbable that a member of the RAA who was rising through the ranks, and being continually assessed, and who was suffering from the distress claimed, would not have shown signs of such stress;
9.the veteran voluntarily ceased smoking in either 1983 or 1985, but continued to serve in the Military Police for another decade. In short, the suggestion that the veteran was traumatised by the grenade incident and relied on cigarettes to relieve his tension, or that he was stressed by his Military Police duties, is undercut by the fact that he did not smoke for the last decade of his service.
Unlike Cooper, the veteran was not immediately moved away from his family and the veteran also did not immediately commence smoking. There is no evidence that the veteran was subject to peer pressure to smoke nor is there any evidence that he was placed in stressful situations or was unhappy with his service in the RAA.
The difficulty we face, is that the evidentiary base presented to support the Applicant’s case is scant, and, to a degree, inconsistent.
Wilcox and Downes JJ pointed out in Wall, that the mere fact that a person has enlisted does not automatically default to a finding that there is a causal link between rendering the relevant defence service and the onset of smoking. Clearly in this matter there was a temporal connection between the onset of smoking and service in the RAA, but, the evidence does not disclose that the operative cause of the smoking habit was as a result of the veteran’s defence employment.
Wilcox and Downes JJ also highlighted the evidentiary difficulties faced by an applicant when prosecuting a matter such as this. This difficulty is further compounded when the veteran has passed away and the tribunal of fact is unable to listen to the testimony of the veteran and assess the evidence given.
We are sympathetic to the situation faced by the Applicant, and note that her legal representatives have marshalled from the extant evidence the best possible case for her. However, we regretfully have come to the conclusion that the evidence is not sufficient for us to make a finding in favour of the Applicant.
We find, accordingly, that the veteran’s smoking habit was not contributed to, to a significant degree, by his employment with the RAA.
While our finding that the requisite causal connection between the veteran’s smoking habit and defence employment has not been established is sufficient to dispose of the Application, in the event that we are in error, we will now deal with the second issue.
DID THE VETERAN’S SMOKING HABIT CONTRIBUTE TO, TO A SIGNIFCANT DEGREE, TO THE DEVELOPMENT OF MND?
Mr Harding submitted (AOS para 26) that the Applicant’s case relies upon medical opinion, including epidemiological evidence (i.e. evidence concerning the distribution and determinants of disease in human populations), concerning the possibility, or probability, of a causal link between smoking and MND.
This matter has presented us with some difficulties. A great deal of time was spent hearing expert and very technical epidemiological evidence. It is not open to the tribunal of fact to shy away from dealing with, and assessing, such evidence if it is relevant to the disposition of the matter. To do otherwise would unduly narrow the task required and lead the tribunal of fact into error. We refer to the following exposition of the law given by Sir Owen Dixon in his address of “Science and Judicial Proceedings” in Jesting Pilate (1965) at 16:
“When a judge is confronted with some question which depends upon a scientific inquiry however ill equipped he may be for the task, he is expected to acquire from the evidence of experts a sufficient knowledge of the subject to make him appreciate and even form a judgment upon the scientific facts, inferences and deductions which contribute to a correct solution to the question…”
Both Mr Harding and Mr Clark referred to the well-known decision of the New South Wales Court of Appeal Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; 49 NSWLR 262 (Seltsam). That case concerned the question whether renal cell carcinoma, more probably than not, could be and is caused by the inhalation of asbestos. In answering that question, the strength and quality of epidemiological studies were considered.
Spigelman CJ explained the use of epidemiological studies as follows [59] – [62]/271:
“59 Epidemiology is the study of the distribution and determinants of disease in human populations. It is based on the assumption that a disease is not distributed randomly in a group of individuals. Accordingly, subgroups may be identified which are at increased risk of contracting particular diseases.
60 Epidemiological evidence identifies associations between specific forms of exposure and the risk of disease in groups of individuals. Epidemiologists do make judgments about whether a statistical association represents a cause-effect relationship. However, those judgments focus on what is sometimes called in the epidemiological literature ‘general causation’. Whether or not the particular factor is capable of causing the disease. Epidemiologists are not concerned with ‘specific causation’: Did the particular factor cause the disease in an individual case?...
62 Epidemiology provides two types of material: first, the statistical measurement of an association between exposure and disease and, secondly, interpretation of the data to determine general causation. The second function may be performed by an epidemiologist who had no association with the study or studies which provide the raw data.”
His Honour later outlined at length the proper use of epidemiological evidence:
“78 Epidemiology is, as I have noted above, concerned with the study of disease in human populations. It is not, of itself, directed to the circumstances of an individual case. For the purpose of determining whether exposure to a particular substance is the legal cause of a particular disease, epidemiology only provides evidence of possibility.
79 Evidence of possibility, including expert evidence of possibility expressed in opinion form and evidence of possibility from epidemiological research or other statistical indicators, is admissible and must be weighed in the balance with other factors, when determining whether or not, on the balance of probabilities, an inference of causation in a specific case could or should be drawn. Where, however, the whole of the evidence does not rise above the level of possibility, either alone or cumulatively, such an inference is not open to be drawn.
80 The common law test of balance of probabilities is not satisfied by evidence which fails to do more than establish a possibility….
89 In my opinion, evidence of possibility, including epidemiological studies, should be regarded as circumstantial evidence which may, alone or in combination with other evidence, establish causation in a specific case.
90 Proof on the balance of probabilities, indeed on the beyond reasonable doubt standard, may be established on the basis of circumstantial evidence…
93 With respect to many diseases, medical science is able to give clear and direct evidence of a causal relationship between a particular act or omission and a specific injury or disease. There are, however, fields of inquiry where medical science is not able to give evidence of that character. There are cases in which medical science cannot identify the biological or pathological mechanisms by which disease develops. In some cases medical science cannot determine the existence of a causal relationship. Such a state of affairs is not necessarily determinative of the existence or non-existence of a causal relationship for purposes of attributing legal responsibility. Epidemiological evidence may be able to fill the gap. It is of particular potential utility in the field of what is often referred to as ‘toxic torts’, especially in cases of diseases with long latency periods…
98 The Courts must determine the existence of a causal relationship on the balance of probabilities. However, as is the case with all the circumstantial evidence, an inference as to the probabilities may be drawn from a number of pieces of particular evidence, each piece of which does not itself rise above the level of possibility. Epidemiological studies and expert opinions based on such studies are able to form ‘strands in a cable’ of a circumstantial case.”
His Honour reviewed United States case law, and then made the following observations:
“136 The predominant position in Australian case law is that a balance of probabilities test requires a court to reach a level of actual persuasion. This process does not involve a mechanical application of probabilities…
142 When assessing expert evidence on causation, the legal concept of causation requires the court to approach the matter in a distinctively different manner from that which may be appropriate in either philosophy or science, including the science of epidemiology…
153 As I have also noted above, a circumstantial case can involve drawing a conclusion on the balance of probabilities, or indeed beyond reasonable doubt, on the basis of facts which are expressed only in terms of possibility. Whether or not the inference is open or should be drawn, depends on the quality of the underlying facts, particularly in terms of the degree of ‘possibility’ which is involved.”
One important point that was elucidated by Spigelman CJ is that while epidemiological studies concern the distribution and determinants of disease in human populations, they are not studies that can assist a tribunal of fact in determining individual questions of causation. As Spigelman CJ said (at [150]/287):
“I have no difficulty with a medical practitioner drawing on and assessing epidemiological studies. I have greater difficulty with an epidemiologist expressing an opinion about causation in the individual case…As I understand the position, epidemiology is concerned with populations, not individual cases.”
As previously noted, the veteran was referred to Dr Cameron by Dr Richard Williams, an orthopaedic surgeon, in June 2014. At that time the veteran was employed by Australia Post and had fallen at work. A neurological condition was suspected to be the cause. After several consultations, the veteran was diagnosed as suffering from MND.
MND is a group of progressive neurological disorders that destroy motor neurones, the cells that control essential voluntary muscle activity such as speaking, walking, swallowing and breathing. It may attack different parts of the neurological system, which leads to a number of descriptive diagnoses. In the literature it may be described as Amyotrophic Lateral Sclerosis (AML), Progressive Bulbar Palsy (PBP) or Primary Lateral Sclerosis (PLS).
MND occurs in adults and children. In adults MND occurs more commonly in men than women. with the symptoms usually appearing after the age of forty years. Some MND is inherited but most causes are unknown, with toxic, viral, or genetic factors implicated.
Although MND can occur in anyone, symptoms usually appear in the 40 to 70 age group, with a mean age of about 65 years. Progress in the disease is generally rapid after the onset of symptoms, with an average life expectancy between 2 and 5 years.
The incidence of MND in the community is measured by the number of new cases in a defined period, usually a year. The prevalence is measured by the number of cases present at any point in time. This distinction is important in epidemiological research. The incidence of MND is about 2 per 100,000 of population, while the prevalence is around 6 per 100,000 of population. Research indicates that the incidence is higher in people aged over 50 years. Ten percent of cases are inherited.
MND is classified as a rare disease, with variable symptoms and no routine test available for it. MND may be difficult to diagnose in early stages and it progresses invariably to death as there is no curative treatment presently available.

Mr Harding contended that there are two questions that require resolution by the Tribunal, namely:
a. can smoking cause MND – which has been described as the “general causation” question; and, if so
b. did the veteran’s smoking habit result in him developing MND – which is described as the “specific causation” question.
We accept that this is the proper basis for us to resolve the issues in contention, and we will address each question in turn.
Can smoking cause the onset of Motor Neuron Disease?
The main witness for the Applicant was Dr Carmel Armon, a neurologist with epidemiological training. He gave evidence by telephone from Israel on two occasions.
In his evidence, Dr Armon made reference to two papers he authored:
12003, “An Evidence-Based Medicine Approach to the Evaluation of Exogenous Risk Factors in Sporadic Amyotrophic Lateral Sclerosis”, Neuroepidemiology vol. 22, issue 4, pp. 217 - 228 (Exhibit 7); and
22009, “Smoking may be considered an established Risk Factor for Sporadic ALS”, Neurology vol. 73, no. 20, pp. 1693 - 1698 (Exhibit 8).
These are “review papers”, whereby the author identifies all titles relating to a particular subject and then evaluates the results of the combined data. Usually this takes the form of “meta-analysis” which is a common method of academic investigation and assists in eliminating or significantly reducing random biases in data collection and statistical analysis. It usually accepts all titles relating to the subject being reviewed irrespective of the “quality” of a title, but cannot totally eliminate systemic bias.
Dr Armon chose a different method of reviewing the published articles on the role of exogenous risk factors in sporadic MND. His 2003 paper was an exploratory paper, designed to stimulate discussion on the topic by using an Evidence Based Medicine (EBM) approach to review articles, rather than using meta-analysis. Dr Armon explained the different methodologies as follows (Exhibit 7 p. 218):
“In addition, there have been advances in the methodology of analysing the published literature. Readers of epidemiological reviews and chapters 15 and 20 years ago may have encountered what today might be considered relatively uncritical summaries of the published literature. Between 15 and 10 years ago, the idea of a critical review of literature began to impact the way data were summarized and presented: not all reports were accorded equal weight. Approximately 10 years ago, meta-analysis was considered for its utility to summarize and condense the results of many studies, which individually might be ambiguous or conflicting. However, limitations of this method when the component studies were less than perfect or comparable have not permitted its proper application to the epidemiology of ALS.
The past 10 years have seen the emergence of a group of core concepts known as ‘evidence-based medicine’ (EBM) and its incorporation into the way we think about drawing conclusions from the published literature. The application of these concepts has not been done in a uniform fashion. It varies among professional organizations and has undergone changes and refinements over time within individual organizations, including, for example, the American Academy of Neurology. There are advantages to applying this method to the analytic epidemiology of ALS. EBM makes explicit the expectation that review of data in the literature is done for the purpose of drawing conclusions and how that may be done. Where that is not possible, the purpose of the review is to determine what additional data would need to be generated in order to be able to draw conclusions in the future (‘directions for further research’)…EBM determines that all data are not equal as far as the ability to draw conclusions from them and shows why. EBM concerns itself with the extent to which data, derived from subsets or samples of the general population, may be used to draw inferences that may apply to the general population….”
Dr Armon went on to note that there are limitations in the utilisation of EBM methodology. He notes, for example – p. 218:
“There is more than one way to apply EBM, and the choice of the way it is applied is based on opinion, rather than on evidence. Conclusions may depend on which data are allowed to impact on them. Further, the choice of how EBM is to be applied is made with some knowledge of the data that is to be evaluated.”
Having set out at some length the drawbacks associated with using an EBM methodology, Dr Armon opined that it is necessary to have a ratings system to classify the quality of the published literature and translate the published literature into conclusions. Dr Armon outlined his own methodology for this task which was “drawn freely on the approaches of rating systems for the classification of evidence developed over the past few years by professional organizations…”. Dr Armon went to state that the purpose of the 2003 paper was to “generate scientific discussion” and that although it had been peer-reviewed there had been “no attempt to build a consensus around, or seek organizational endorsement for this particular approach to the application of EBM”.
The “Abstract” for the 2003 article contains, inter alia, the following information (Exhibit 7, p. 217):
“An evidence-based medicine approach was applied to evaluate analytic studies of exogenous risk factors for amyotrophic lateral sclerosis (ALS) published since 1991. Classification systems for evaluating the literature and for drawing conclusions based on the class of available evidence were developed, modeled on those used by national societies. Considerations regarding the impact on the general public of confirming a role for putative risk factors were made explicit. There was evidence in support of smoking being a probable (‘more likely than not’) risk factor for ALS. Smoking has broad public health impact, no redeeming features, and is a modifiable risk factor. Evidence supported the conclusion that the following were probably not risk factors for ALS: trauma, physical activity, residence in rural areas and alcohol consumption.”
Twenty-eight articles published since 1991 were identified, and of those, 20 were excluded, either because they did not have comparison groups (2) or were considered to provide only class IV – V evidence. The remainder of Dr Armon’s paper dealt with his analysis of the non-excluded articles.
The purpose of the 2009 article was to ascertain if the conclusions reached in the 2003 article needed to be modified based on studies published in the interim. The same methodology was adopted. Dr Armon conducted a medicine literature search for articles and reviews published between 2003 and April 2009. A total of 28 titles were identified, but only 7 articles met the inclusion criteria. Dr Armon concluded as follows (Exhibit 8 p. 1697):
“Evidence-based analysis of epidemiologic data shows concordance among results of better-designed studies linking smoking to ALS, and lets those results drive the conclusions. An earlier article also demonstrated how higher class studies provided concordant findings at variance with those obtained in lower class studies. It showed how an apparent association of physical activity with ALS in lower class studies was not supported by the findings in studies providing a higher class of evidence, showing no such association. Less vigorous approaches to the evaluation of the epidemiologic literature are likely to lead to erroneous conclusions.”
(References omitted)
We note that the methodology adopted by Dr Armon appears to be in accordance with the standards set by the American Academy of Neurology in the Clinical Practice Guideline Process Manual (2017 edition) – Exhibit 14, and the Institute of Medicine Standards – Exhibits 15 – 17.
The Tribunal was also presented with other published reports that support the proposition that there is a link between smoking and the onset of MND:
1.Wang H et al 2011, ‘Smoking and Risk of Amyotrophic Lateral Sclerosis: A Pooled Analysis of 5 Prospective Cohorts’, Archives of Neurology, vol. 68, no.2 pp. 207 – 213; Exhibit 11; and
2.Brown H et al. 2017, ‘Amyotrophic Lateral Sclerosis’, New England Journal of Medicine vol. 77, no. 2 pp. 162 – 172; Exhibit 13.
The conclusion reached by the authors of the Hao Wang et al article was as follows – Exhibit 11 p. 212:
“Our results are consistent with recent epidemiologic evidence that links cigarette smoking with an increased risk of ALS…
In summary, in this large longitudinal investigation based on 5 cohorts of US men and women, the risk of ALS was higher for cigarette smokers compared with never smokers. Among smokers, the risk of ALS increased with decreasing age at smoking initiation but was unrelated to smoking duration or intensity. Better understanding of the relation between smoking and ALS may further the discovery of other risk factors and help elucidate the nature of the disease.”
Conversely, we were also provided with examples of published articles by medical experts where the learned authors discount a strong association between cigarette smoking and the onset of MND, namely:
1.Alonso A et al. 2010, ‘Smoking and the risk of amyotrophic lateral sclerosis’, , Journal of Neurology, Neurosurgery and Psychiatry vol. 81, issue 11, pp. 1249 – 1252; Exhibit 9; and
2.Wang M et al. 2017, ‘Identification of risk factors associated with onset and progression of ALS using systematic review and meta-analysis’, Neurotoxicology vol. 61 pp. 101 - 130 – Exhibit 12.
The article by Alonso et al did not rule out a link between smoking and the onset of MND, it simply discounted that there was a strong association between men smoking and the development of the disease. The authors made the following observations (Exhibit 9 p. 1252):
“This meta-analysis does not support an overall strong association of smoking and ALS risk but suggests that smoking might be associated with a higher risk of ALS in women.
Smoking could increase the risk of ALS through several mechanisms. Cigarette smoke contains a large amount of oxidant compounds which target certain molecules such as fatty acids in cell membranes and reduces the antioxidant capacity of the organism…Also, numerous chemicals, some of them with potential neurotoxic effects, abound in cigarette smoke. Lead and formaldehyde, both present in cigarette smoke, have been associated with the risk of ALS in some studies.
The stronger association between smoking and ALS in women could be explained by differences in the metabolism of chemicals present in cigarette smoke…
The present meta-analysis has some limitations. The methodological quality of the included studies was not uniform. Some studies had an unclear definition of the outcome, potentially biased selection of controls, greater opportunities for measurement error in smoking assessment and insufficient control for confounding. However, methodological quality is unlikely to explain our findings as the results did not differ between cohort and case control studies even though cohort studies were of better methodological quality overall. As in any meta-analysis, publication bias could be present but there is no clear evidence of it.”
(References omitted)
Likewise the 2017 Ming-Dong Wang article did not discount a link between smoking and the onset and progression of MND in some people, but opined that smoking was not a “strong factor” and was a greater risk for women than men. The learned authors said – Exhibit 12 p. 122:
“Early studies produced controversial results about the association between smoking and ALS…In the present analysis, we found that the association between smoking and ALS was significant in females, not in males. Since a high proportion of bulbar onset ALS cases have occurred in females, smoking may be a risk factor for bulbar ALS, or may promote early onset in females…A meta-analysis of evidence from cohort studies suggested that smoking was a causal risk factor for ALS in females, with former smokers found to be at higher risk of ALS (Wang et al., 2011 a,b). Since males tend to be more frequently exposed to other potential ALS risk factors, such as pesticides or organic solvents during their working life, the lack of associations in males might have been confounded by occupation. More population-based studies designed to study ALS aetiology are required, as most of the studies quoted in this project were not designed specifically for that (Wang et al., 2011 a,b; Gallo et al., 2009)…..”
The reliability of this study was questioned by Dr Armon, and Mr Harding spent most of his time cross-examining Professor Driscoll on 14 June 2018, focusing on suggested inaccuracies in the study.
It is the case, as Mr Harding was able to demonstrate, that the reference to the 2011 Wang article in the above quote, was most probably a reference to the 2010 Alonso et al article.
However, Professor Driscoll explained that the missing supplemental material in the printed article was able to be located by means of a “hotlink” in the article itself, and that he had read the material – Tr. 14 June 2018 pp. 110 – 111.
Professor Driscoll dealt in detail with this article in his Comments dated 11 June 2018 – Exhibit 23 pp.3 - 4. Each of Dr Armon’s criticisms of this article were dealt with and, in our respectful opinion, convincingly refuted.
As for the quality of the Ming-Dong Wang et al article, Professor Driscoll testified – Tr. 14 June 2018 p. 112:
“Yes, I think it’s of reasonable quality. It’s not perfect, but I certainly think it is of good quality”
We note that the Ming-Dong Wang et al article is almost 30 pages in length and deals with a multitude of risk factors associated with the onset and progression of ALS. Smoking was just one of a number of risk factors assessed, and the smoking commentary comprised less than half of one page of the article. Further, although a number of articles were cited by the learned authors, the analysis of the relationship between smoking and the onset of ALS was somewhat limited compared to the analyses of Dr Armon.
We deal further with this article below, and we agree with Professor Driscoll’s analysis of it, subject to our above caveat.
The principal witness for the Respondent was Professor Driscoll. Professor Driscoll’s qualifications are: MBBS BSc(Med) MOHS PhD FAFOEM FAFPHM. He is a Professor of Epidemiology and Occupational Medicine in the School of Public Health at the University of Sydney. He is a Medical Officer at Canterbury Hospital and the Institute of Rheumatology and Orthopaedics at Royal Prince Alfred Hospital. He has written approximately 170 book chapters and original papers in referred journals. Most of the journal articles and book chapters address issues of epidemiology and occupational health and safety.
Professor Driscoll submitted a report (Exhibit 6) at the request of the Respondent, which addresses the epidemiological aspects of this matter. He has tendered comments (Exhibit 23) on the transcript of Dr Armon’s evidence.
In the Executive Summary of Professor Driscoll’s report, the following conclusions were set out – Exhibit 6 p. iii:
·The available epidemiological evidence is not sufficient to conclude that cigarette smoking increases the risk of developing MND. I do not discount the possibility of a causal connection, but the published evidence is equivocal and the most comprehensive and valid systematic review available did not provide convincing evidence of a causal relationship.
·If previous cigarette smoking does increase the risk of developing MND, it is likely that Mr White would have smoked enough to consider that his smoking could have caused his MND.
·Dr Armon’s report contains many reasonable statements but a number of statements that are either not supported by evidence or that are not correct. Dr Armon’s conclusion that Mr White’s smoking should be considered to be entirely (“100%”) responsible for him having developed MND is based on the presumption that smoking does indeed increase the risk of developing MND. I do not consider that Dr Armon establishes that causal relationship in his report, either entirely within the report or in his published papers to which he refers in his report.
·Dr Cameron does not believe there is convincing evidence that smoking increases the risk of developing MND. This conclusion is based on his reading of papers on individual studies and his suspicion of the methodological quality of meta-analyses.
·Dr Todman believes that smoking does increase the risk of developing MND. This conclusion on the two review papers by Dr Armon, which Dr Todman believed were of good quality and provided the best quality relevant evidence available.”
It will be noted that the Executive Summary deals with both the epidemiological findings of Dr Armon, as well as specific findings made by Dr Armon on the probable cause of the veteran developing MND. The latter matter is discussed below.
Professor Driscoll, helpfully, sets out in Chapter 2 of his report, background information on relevant epidemiological principles, and, in particular explains key terms such as “systematic review”, “cohort study”, “case control study”, “confidence interval” and “Attributable Fraction” – Exhibit 6 pp. 3 – 4.
Professor Driscoll critiqued, firstly, Dr Armon’s 2003 article. He pointed out that Dr Armon classified each article he reviewed into five classes, with Class 1 being of the highest quality and Class 5 of the lowest. Within each class there were multiple criteria against which the study was measured – Exhibit 6 p. 6 para 26.
Professor Driscoll opined that there “was nothing inherently wrong with this sort of approach.” However, he went on to contend that:
“…there is increasing evidence that giving a single score for an article or study is not helpful and that the assessment should focus on the resultant potential for and implications of a range of possible biases arising from any methodological shortcoming, rather than simply excluding a study because the overall score (or Class) was too poor.” – Exhibit 6 p. 7 para 27
After closely analysing the methodology used by Professor Armon, Professor Driscoll noted that the 2003 article was a form of “systematic review” in that it identified relevant studies, assessed the methodological strengths and weaknesses of each and then considered the weight of evidence that arose from these studies. Professor Driscoll argued – Exhibit 6 p. 7 paras 31 and 32:
“However, there are a number of concerning aspects of the paper that arise from the fact that Dr Armon did not use a standard approach to conducting the systematic review. No meta-analysis was conducted.
There are several published guidelines regarding how a systematic review (and a meta-analysis, if conducted) should be undertaken and reported). The approach used by Dr Carmel (sic), meets some, but does not meet many, of the important aspects of these criteria.”
Of some concern is the observation by Professor Driscoll that, to his knowledge, there is no empirical basis for Dr Armon’s approach used to grade and classify individual papers, or to synthesise the evidence, as was undertaken. Professor Driscoll opined – Exhibit 6 p. 8 paras 34 – 35:
“Concerns about this type of approach are heightened when the grading, classification and synthesis are undertaken by a single person, as individual bias and opinion may influence (unconsciously or consciously) decisions made. This is one of the reasons systematic review and meta-analysis guidelines typically require more than one person to be involved in identifying and assessing studies.
The usual approach in terms of grading the methodological quality of studies is to consider the potential for bias to arise from any of a number of different areas. Each of these would be rated. Some authors do develop an overall quality score for each paper, akin to the grading system used by Dr Carmel (sic), but in general this is not seen as the most suitable approach.”

Finally, it is helpful to set out what Professor Driscoll testified about Dr Armon’s studies and conclusions – Tr. 14 June 2018 p. 119:
“Okay, thank you?---But bear in mind, I’m not trying to undermine the credibility of or significantly criticise Dr Armon’s reviews. I think that there are some shortcomings with them, but there are some strengths as well.
Thank you?---In the same way the Wang paper, it’s not perfect, but even if we accepted that they were equally good, let’s say.
Yes?---You’re ending up with one systematic review that’s saying there’s evidence for, and you’ve got one systematic review saying there’s evidence against or not supportive of the evidence for.
Can I just get you to stop there? It’s not that it says there’s evidence against, is it---?---…Yes that’s why I corrected myself.”
As Professor Driscoll explained, there is no body of medical research which disproves a link between smoking and MND. However, one can go further and note that in almost all of the material presented to us, there seems to be a tacit acceptance of a link between smoking and MND in at least some people, or classes of people. In the 2017 Wang et al article, there seemed to be an acceptance of a link between smoking in women and the onset and progress of ALS, but not in men. In other words, even in that article the learned authors did not propound a theory of no linkage per se between smoking and MND.
Professor Driscoll also, helpfully, reviewed the reports provided by Drs Cameron and Todman. We note, in particular, Professor Driscoll’s critique of Dr Cameron’s report of 9 September 2016 and agree with the conclusions reached therein: Exhibit 6 pp. 20 – 21 paras 97 – 101.
The first task of the tribunal of fact is to ascertain if there is an acceptable medical basis for inferring that there could be a link between tobacco consumption and MND, or to put it another way, does the evidence support the proposition that smoking increases the risk of the onset of MND in some people. This is the threshold, but not the determinative, question. Clearly, the determinative question focuses on the facts of the individual case and whether the evidence before the tribunal of fact discloses, in each case, on the balance of probabilities, that there is such a causal connection.
We have been presented with a number of learned papers by experts in the field of epidemiology. There appears to be, at this stage of medical knowledge, no consensus on whether tobacco consumption and the onset of MND are causally linked. Conversely, there is no suggestion from the material we have been presented with that such a link can be discounted or rejected. Indeed, even some of those papers that hold that such a link cannot be demonstrated, “at this time”, nonetheless concede that some people are at higher risk than others of contracting MND as a result of tobacco consumption (e.g. women in the Alonso study). The various articles we have been referred to raise the link above the category of a mere possibility and we are tolerably satisfied that the conclusions drawn by Dr Armon rise above mere advocacy and can be more accurately described as being founded on a reasonably secure epidemiological foundation.
Although we deal with the biological mechanism for the onset of MND below, it is important to note that Dr Armon dealt with this issue in his writings, specifically in two articles:
1.2005, “Acquired Nucleic Acid Changes May Trigger Sporadic Amyotrophic Lateral Sclerosis”, Muscle and Nerve 2005, vol. 32, issue 3, pp. 217 – 228 – Exhibit 18; and
2.2016, “Accrued Somatic Mutations (Nucleic Acid Changes) Trigger ALS: 2005 – 2015 Update”, Muscle and Nerve, vol 53, issue 6,pp. 1 – 8 – Exhibit 19.
Dr Armon’s thesis is that tobacco smoking causes nucleic acid changes, which trigger the onset of MND. The above articles suggest that the onset of MND is a multistep process evolving over the years and that smoking hastens these changes. In his 2016 article, Dr Armon made the following observations – Exhibit 19 pp. 5 – 6:
“The risk of current smoking on developing ALS is at or above the upper range of the risk it confers on developing solid nonlung cancers…
It may be asked why there is not an increased risk of ALS in patients with other known inducers of somatic DNA mutations, such as ionizing radiation exposure. Bradley et al showed that there was a DNA repair defect in skin fibroblasts from patients with ALS and with Alzheimer disease in response to damage caused by the alkylating agent methyl methane sulfonate, but there was normal repair of the damage produced by ionizing radiation, ultraviolet radiation, and mitomycin C. Different carcinogens produce different forms of DNA damage, and there are different repair pathways for the different forms of DNA damage. Furthermore, exposure to smoking is chronic, whereas exposure to other carcinogens under consideration is acute or episodic, possibly providing opportunity to repair the DNA damage caused by the other carcinogens…
The conclusion is that there are is strong indirect evidence that cumulative acquired somatic mutations or nucleic acid changes lead to disease onset in ALS..”
(References omitted)
It is important to note that Professor Driscoll did not, either in oral testimony or in the written evidence presented, reject Dr Armon’s conclusions. He, quite appropriately, highlighted from his perspective, the methodological imperfections and limitations with Dr Armon’s approach. However, he specifically rejected the suggestion that Dr Armon’s opinion about the possibilities of a causal linkage between tobacco consumption and the onset of MND was an “outlier” opinion. Indeed, our reading and understanding of the medical research to date, is that Dr Armon’s findings are respectable and supported by a broad body of research. We do not conclude that they are the predominant view, but they are the view of many experts in this field of endeavour. We also do not need to form a settled view on the merits of the methodology adopted by Dr Armon. There are, from the views previously outlined, issues with aspects of his methodology. This flows, necessarily, from the self-evident fact that Dr Armon was engaging in innovative research. Dr Armon explicitly stated this in his 2003 article. The fact that a methodological approach is innovative is not, of itself, fatal to a conclusion about its worth or probative value. Moreover, the fact that Dr Armon agreed that his findings or hypothesis was in the nature of a “theory” is not fatal to a tribunal of fact accepting that his theory is soundly based and provides a secure platform for concluding that there may be a link between smoking and the onset of MND.
It is not the role of this Tribunal to engage as a referee between duelling experts, or competing medical theories. Our task is more limited and more focused. At this stage of our inquiry, the question to be resolved is whether there is sufficient evidence before us that would support the proposition that, on the balance of probabilities, there is a link between tobacco consumption and an increased risk of the onset of MND. The fact that we have to answer that question at all necessarily means that the issue is not medically settled.
The evidence presented discloses that there is a body of reputable expert opinion which posits that there is a biologically plausible mechanism linking tobacco consumption and the onset of MND in at least some people. The research presented rises above the level of speculation or mere possibility. It has not reached the level of certitude or settled acceptance. The views of Dr Armon are not those of an outlier in this field. There is a respectable body of literature, which is increasing with the progression of time, that supports his thesis on the relationship between tobacco consumption and the onset of MND.
We accordingly affirm the proposition that there can be a link between tobacco consumption and the onset and progression of MND, but that in any individual case, whether there is such a causal link must be resolved having regard to the specific evidence presented to the tribunal of fact.
Did the veteran’s smoking habit cause him to develop MND?
The Applicant relies on the report of Dr Armon dated 20 September 2017 – Exhibit 5. In that document, Dr Armon discussed a measure which is called “relative risk” (RR). RR is the ratio of the incidence of disease in exposed individuals compared to the incidence in unexposed individuals. A RR rating of 1.0 means that the risk in exposed individuals is the same as the risk posed to unexposed individuals.
In Seltsam Spigelman CJ quoted the following extract from the Federal Judicial Centre’s Reference Manual on Scientific Evidence ([121]/280 – 281):
“The civil burden of proof is described most often as requiring the fact finder to ‘believe what is sought to be proved…is more likely true than not true’…The relative risk from an epidemiological study can be adapted to this 50 per cent plus standard to yield a probability or likelihood that an agent caused an individual’s disease… The threshold for concluding that an agent was more likely the cause of a disease than not is a relative risk greater than 2.0. Recall that a relative risk of 1.0 means that the agent has no effect on the incidence of disease. When the relative risk reaches 2.0, the agent is responsible for an equal number of cases of disease as all other background causes. Thus, a relative risk of 2.0 implies a 50 per cent likelihood than an exposed individual’s disease was caused by the agent. A relative risk greater than 2.0 would permit an inference than an individual plaintiff’s disease was more likely than not caused by the implicated agent. A substantial number of courts in a variety of toxic substance cases have accepted this reasoning.”
After extensively considering the American jurisprudence, Spigelman CJ concluded ([137]/285):
“In Australian law, the test of actual persuasion does not require epidemiological studies to reach the level of Relative Risk of 2.0, even where that is the only evidence available to a court. Nevertheless, the closer the ratio approaches 2.0, the greater the significance that can be attached to the studies for the purposes of drawing an inference of causation in an individual case. The ‘strands in the cable’ must be capable of bearing the weight of the ultimate inference.”
Dr Armon made the following conclusions about the relative risk of the veteran developing MND as a result of his smoking habit – Exhibit 5 pp. 9 – 10:
“F. Mr. White’s specific smoking history and ALS onset:
1.    Mr. White, was born in 1952, smoked heavily between 1972-1983 (ages 20-31), stopping completely by age 33, and developed ALS in 2013-2014 (ages 61-62 at clinical onset).
2.    Mr. White reported he smoked 2.5 ppd (25 cigarettes per pack), which translates into 3.125 ppd of 20 cigarette packs.
3. This translates to 31.25 pack years if we allow for some ramp-up (and assume only 10 years of heavy smoking), but may be as high as 35 pack years or more if we consider 11 years of continuous smoking at this level (34.375 pack years), and allow also for the intermittent smoking between ages 31-33.
G. Estimating the effect of smoking on Mr. White’s developing ALS:
Mr. White’s 32.5 or more pack-years of smoking are in the highest ranges of smoking reported by the referenced studies, all of which showed a dose-response effect.
Mr. White starting smoking at an early age (applying the concept of increasing risk with earlier age of starting smoking -- Wang et al).
Hence – the point estimates for his increased risk should be adjusted upward, to reflect that his risk is higher than the average.
It needs to be recognized that all the estimates are more likely than not underestimates, biased towards unity by the inability to account for passive smoking among non-smokers and former smokers.
With reference to the standard applied by the RMA -- ‘a small but measurable increase in risk:’
1.    Mr. White’s risk was definitely increased by his former smoking.
2.    The unadjusted magnitude of increased risk ranges from 1.4 – 1.9, reflecting a 40 – 90% increase in risk. All these numbers are point estimates, and ‘more likely than not’ reflect the true increase in risk.
3.    Mr. White’s risk was greater than these average, unadjusted numbers because (a) he began smoking at a young age, (b) the quantity of his smoking was in the highest range, and (c) the estimates are shifted downward by the inability to control for passive smoking….
In addition, considering that there is a fairly good understanding of the presumptive mechanism by which smoking causes ALS...- my opinion, expressed in terms of medical probabilities (‘more likely than not’) is that 100% of Mr. White’s ALS occurrence can be attributed to his smoking. Had he not smoked to the degree that he did, it is unlikely, in my opinion, that he would have developed ALS at the age he did.”
We have a number of problems with the reasoning and conclusions reached by Dr Armon.
First, it will be recalled that Spigelman CJ in Seltsam observed ([153]/287):
“Whether or not the inference is open or should be drawn, depends on the quality of the underlying facts...”
Dr Armon’s estimate of the relative risk of the veteran contracting MND from his smoking habit is predicated entirely on the quantity of cigarettes that were smoked in the period 1972 – 1983. In short, the totality of Dr Armon’s analysis is based on what could only be described as a very fragile factual matrix.
The primary evidence of the veteran’s smoking habit comes from his letter of 1 June 2015, wherein he estimated that he smoked 2.5 packets of cigarettes each day from 1972 until 1985, with a gap for a few months after the birth of his son in July 1983 – Exhibit 1 T8 p. 40.
The only other evidence is that of the Applicant, who deposed in her statement of 16 September 2016, that the veteran ceased smoking completely in 1983 and smoked “up to” 2.5 packets each day.
The veteran’s RAA records contain scant information on his smoking habits, with the exception of two records post 1983, which note he had ceased smoking.
As previously noted, the contemporary RAA records disclose:
1.the grenade incident only caused the veteran superficial injuries;
2.the veteran thereafter rose through the ranks of the Military Police;
3.the veteran was able to immediately cease smoking, according to the Applicant, in 1983 and not resume smoking; and
4.the veteran served in the Military Police for more than a decade after he ceased smoking.
In short, the undisputed evidence does not disclose that the veteran was suffering great stress during his defence-service, nor does it disclose that he was heavily dependent on smoking to relieve such stress.
Apart from the veteran claiming more than 30 years after he ceased smoking that he was smoking at such a high level in the 1972 – 1983 periods there is simply no other independent and objective evidence that would support that proposition. Even the Applicant’s statement tends to undercut the proposition that the veteran was smoking at a uniformly high level of two and a half cigarettes packets each day. She refers that the veteran smoked “up to” that level; and it must be recalled that of the 11 years that the veteran smoked, the Applicant only knew him for the final five years of his smoking habit. The Applicant did not know the veteran for the first six years of his smoking habit and cannot provide the Tribunal with any objective evidence of the level of his smoking during that period; or indeed even if he was smoking during all of that period.
To return to Spigelman CJ’s observation, the “quality of the underlying facts” in this matter so far as the period of time the veteran smoked and the amount of tobacco consumed, is weak and sparse. It provides, with due respect to Dr Armon, a potentially insecure basis, for reaching a conclusion on the balance of probabilities.
Second, the body of epidemiological research which is supportive of a link between smoking and MND, does not provide a consistent body of accepted factors for that linkage. Of relevance to this matter is the finding of Hao Wang et al in the article admitted as Exhibit 11. The learned authors of that article, referred to Dr Armon’s 2009 review article in the context of an analysis using five large ongoing cohort studies involving 832 participants suffering from ALS. Although finding that cigarette smoking increased the risk of contracting ALS, the authors found that such contraction was “unrelated to smoking duration or intensity” – Exhibit 11 p. 212.
This finding is at odds with Dr Armon and in turn undercuts the validity of his relative risk calculation.
Third, Dr Armon’s analysis is focused solely on the veteran’s (presumed) smoking habit as the sole cause of the development of MND. In short it would appear that Dr Armon’s relative risk calculation is predicated implicitly on the assumption that the veteran did not have any other exogenous risk factors for MND.
A perusal of the copious literature on the development of MND illustrates that a range of factors are potentially related to the onset and progression of the disease. The most recent research which we were referred to is the article by Ming-Dong Wang et al previously referred to.
The “Abstract” for the article helpful sets out its main findings – Exhibit 12 p 101:
“Although amyotrophic lateral sclerosis (ALS) was identified as a neurological condition 150 years ago, risk factors related to the onset and progression of ALS remain largely unknown. Monogenic mutations in over 30 genes are associated with about 10% of ALS cases. The age at onset of ALS and disease types has been found to influence ALS progression. The present study was designed to identify additional putative risk factors associated with the onset and progression of ALS using systematic review and meta-analysis of observational studies. Risk factors that may be associated with ALS include: 1) genetic mutations, including the intermediate CAG repeat expansion in ATXN2; 2) previous exposure to heavy metals such as lead and mercury; 3) previous exposure to organic chemicals, such as pesticides and solvents; 4) history of electric shock; 5) history of physical trauma/injury (including head trauma/injury); 6) smoking (a weak risk factor for ALS in women); and 6) other risk factors, such as participating in professional sports, lower body mass index, lower educational attainment, or occupations requiring repetitive/strenuous work, military service, exposure to Beta-N- methylamino-L-alanin and viral infections. Risk factors that may be associated with ALS progression rate include: 1) nutritional status, including vitamin D deficiency; 2) comorbidities; 3) ethnicity and genetic factors; 4) lack of supportive care; and 4) smoking…”
As is illustrated from the Abstract quoted, there are a multitude of potential risk factors for the development and progression of MND, and it would be fair to observe that this is not a settled area of medical research. Although much more is now known about the causes and progress of MND, perhaps much more still remains unknown or only partially known.
Further, we agree that there is some force in the submission of Mr Clark (OSR para 46) that the Applicant’s case solely focuses on the veteran’s smoking habit, and, by implication, has not sought to exclude other potential causative factors. Mr Clark refers to an article which we are unable to ascertain, however he states that aside from genetic factors, five environmental factors are nominated as having a “strong association” with the onset of MND. Such a conclusion is not inconsistent with the thesis propounded by Ming- Dong Wang et al in the 2017 article.
Mr Clark goes on to contend (OSR para 46), that in seeking to meet the “significant contribution” threshold, it would have been incumbent on the Applicant through her legal advisors to exclude those genetic and nominated environmental factors.

Again, if we refer to the masterly exposition of the law by Spigelman CJ in Seltsam, we note that in reaching a conclusion the various “strands in the cable” of establishing causation must be considered and duly weighted.
In this matter we have proceeded on the following assumptions:
1.the veteran was correctly diagnosed with MND;
2.the veteran had a smoking habit;
3.cigarette smoking increases the risk of either the onset of MND or its rapid progression (or both); and
4.the veteran died as a result of MND.
However, the evidence presented leaves open two key strands in the causative chain, namely:
1.the period the veteran smoked and the amount of cigarettes smoked during that period; and
2.whether, apart from smoking, there were other factors, either environmental or genetic, that may have played a role (whether in whole or part) in the veteran being afflicted by MND.
When Dr Armon concluded “that 100% of Mr White’s ALS occurrence can be attributed to his smoking.” (Exhibit 5 p. 10) he proceeded on a basis that was prone to error on two counts. First, as previously noted, he proceeded on the basis that the amount of cigarettes smoked, on which he based his calculations, was proven and secondly he did not, as Mr Clark contends, seek to explicitly discount the consequences of other factors.
Professor Driscoll concluded by suggesting that the methods used by Dr Armon call into question the validity of his conclusion – Exhibit 6 p. 8 para 38.
Accordingly, while we are prepared to accept that Dr Armon’s hypothesis that, on the balance of probabilities, there is a link between smoking and the onset and progression of MND in some persons, we are not satisfied, on the balance of probabilities, that the evidence adduced supports such a linkage in the case of the veteran.
DECISION
The decision under review is affirmed.

I certify that the preceding 138 (one hundred and thirty-eight) paragraphs are a true copy of the reasons for the decision herein of Deputy President J Sosso and, Member Dr G Maynard

.............................[sgd]......................................
Associate
Dated: 16 October 2018

Dates of hearing: 9 April 2018, 3 May 2018 and 14 June 2018

Counsel for the Applicant: Mr Anthony Harding

Advocate for the Applicant: Mr Terrence O'Connor

Solicitors for the Applicant: Terrence O'Connor Solicitors

Counsel for the Respondent: Mr Charles Clark

Advocate for the Respondent: Ms Lisa Palmer

Solicitors for the Respondent: Moray & Agnew Lawyers

Dates of hearing:	9 April 2018, 3 May 2018 and 14 June 2018
Counsel for the Applicant:	Mr Anthony Harding
Advocate for the Applicant:	Mr Terrence O'Connor
Solicitors for the Applicant:	Terrence O'Connor Solicitors
Counsel for the Respondent:	Mr Charles Clark
Advocate for the Respondent:	Ms Lisa Palmer
Solicitors for the Respondent:	Moray & Agnew Lawyers