Cornish and Repatriation Commission - [2001] AATA 138

DECISION AND REASONS FOR DECISION [2001] AATA 138

ADMINISTRATIVE APPEALS TRIBUNAL )

) No N1998/1548

VETERANS' APPEALS DIVISION       )
           Re      ROBYN CORNISH
  Applicant
           And    REPATRIATION COMMISSION
  Respondent

DECISION

Tribunal Dr D. Chappell, Deputy President Dr J. Vallentine, Member

Date23 February 2001
PlaceSydney

Decision The decision under review is set aside and in substitution the Tribunal finds that the Veteran's death being war-caused the Applicant is entitled to pension under s 13(1) of the Veteran's Entitlement Act 1986. The date of effect is 14 May 1990.

(signed Duncan Chappell)
..............................................
Deputy President
CATCHWORDS
VETERANS' AFFAIRS – Veterans' Entitlements – widow's pension – whether death of Veteran war caused – operational service in Vietnam – reasonable hypothesis test – cause of death carcinoma of the caecum – exposure to pesticides and herbicides throughout service in Vietnam – pesticides and herbicides cause colon cancer – Veteran ingested dapsone throughout service in Vietnam – dapsone causes immuno-suppression that augments the risk of contracting cancers – Tribunal not convinced beyond reasonable doubt that the death of the Veteran was not war caused.

Administrative Appeals Tribunal Act 1975 – s 37
Veterans' Entitlements Act 1986 – ss 8(1), 13(1), 120(1), 120(3)

Re Repatriation Commission & Smith (1990) 19 ALD 464
Repatriation Commission v Schar (1991) 25 ALD 503
Re Peter Edwards & Repatriation Commission (AAT, unreported, 21 December 1992)
Re Humffray & Repatriation Commission (AAT, unreported, 2 July 1991)
Re Kenneth Kain & Repatriation Commission (AAT, unreported, 21 December 1992)
Bushell v Repatriation Commission (1992) 175 CLR 408
Byrnes v Repatriation Commission (1993) 177 CLR 564
Lowerson v Repatriation Commission (1994) 50 FCR 252
Government Transport, Commissioner for v Adamcik (1961) 106 CLR 292
East v Repatriation Commission (1987) 16 FCR 517

REASONS FOR DECISION

23 February 2001 Dr D. Chappell, Deputy President Dr J. Vallentine, Member

BACKGROUND
Application

This is a claim for pension by Robyn Kathleen Cornish ("the Applicant"), who is the widow of the late Captain Robert J Cornish ("the Veteran"). By consent the case has been remitted from the Federal Court for re-hearing by the Administrative Appeals Tribunal of an application for review of a decision of a delegate of the Respondent on 16 August 1990 [T13] that the death of the Veteran was not war-caused.
Mr Vincent of counsel appeared for the Applicant and Mr Butcher for the Respondent. In addition to material lodged pursuant to s 37 of the Administrative Appeals Tribunal Act 1975 the Tribunal received in evidence a number of medical monographs and reports:

Federal Court Appeal Book (Exhibits A-E);
Report authored by Dr Peter McCullagh dated 7 July 1999 (Exhibits A-F)
Report by Dr Stewart dated 21 June 1999 (Exhibits R-iii)
Article written by Kirsten Wiklund et al "Risk of cancer in pesticide applicators in Swedish Agriculture" Accepted 19 December 1988; Article written by Rodolfo Saracci et al Cancer mortality in workers exposed to chlorophenoxy herbicides and chlorophenols" 26 October 1991 (Exhibit R-iv)
Article written by A Sheil "Cancer in Immune-Suppressed Organ Transplant Recipients Aetiology and Evolution" dated 1998 (Exhibit A-G)
Curriculum Vitae, Bernard W Stewart (Exhibit R-v)
Article written by Jorge Rodriquez-Larrain et al "Incidence of Adenomatous Colorectal Polyps in Cardiac Transplant recipients" accepted 29 April 1997 (Exhibit R-vi)
Article written by Pheng Soon Lee and Edwin Lau "Risk of acute non-specific upper respiratory tract infections in healthy men . . ." dated 26 March 1988 (Exhibit R-vii)
Article by William Wolfe et al "Health Status of Air Force Veterans Occupationally Exposed to Herbicides in Vietnam" dated 10 October 1990 (Exhibit R-viii)
International Agency for Research on Cancer, "IARC Monographs on the Evaluation of Carcinogenic Risks to Humans" vol 69, 1997 (Exhibit A-H)
Bundles of articles including A Sheil et al 1997; A Sheil 1996; A Sheil et al 1993; K Yokota et al 1994; U Frei et al 1993 (Exhibit A-I)

The Tribunal also had the benefit of lengthy, detailed expert evidence from two witnesses, Dr Peter McCullagh and Professor Bernard Stewart.
Circumstances
The Veteran died on 26 November 1989. It is not in dispute between the parties that the cause of death was disseminated carcinoma of the colon, which had been diagnosed a few months earlier at an emergency laparotomy in July of that year.
The Veteran had a strong family history of bowel neoplasia - his father died of bowel cancer and one brother had colonic polyps [see Lind T28, and Stewart T33, p270].
There has been some confusion as to the precise anatomical origin of the tumor - the death certificate [at T6] records "carcinoma of the caecum", whereas the operating surgeon Dr D Smart described an "obstructing carcinoma of the hepatic flexure" [T27]. Dr Smart's description finds some support in the anatomical pathology report [T29]. No evidence was led nor submission made at the hearing that the difference is relevant. For the purpose of this case the Tribunal proposed that the generic term "carcinoma of the colon" be used, as it encompasses both anatomical possibilities. The parties accepted the Tribunal's proposition.
The circumstances of the Veteran's military service are not in dispute. He joined the Australian army in March 1967. He rendered operational service in Vietnam from 21 May 1969 until 21 May 1970 and defence service from 7 December 1972 until 6 August 1978. During his operational service in Vietnam, he served with the Royal Australian Army Educational Corps, Public Relations. He was based at Nui Dat for almost all of this time.
Contentions
The Applicant contends that the cocktail of herbicides to which the Veteran was exposed causes carcinoma of the colon and the risk of contracting cancer is augmented by dapsone-induced immunosuppression. The Veteran contracted and died from carcinoma of the colon because of his exposure to the herbicides and his ingestion of dapsone.
The Respondent does not dispute the facts stated by the Applicant. It contends however, that the hypothesis put forward by the Applicant is not reasonable. There is a complete lack of objective evidence to support the critical pillars of the hypothesis relied upon. The various suggested "connections" advanced on behalf of the Veteran by Dr McCullagh are merely speculations, lacking any scientific echo in the literature. Professor Stewart's evidence disproves beyond reasonable doubt the facts supporting the Applicant's hypothesis.
RELEVANT LEGISLATION
Applicant's entitlement to pension
Section 13(1) of the Veterans' Entitlements Act 1986 ("the Act") provides:
13 Eligibility for pension
(1)       Where:
          (a)       the death of a veteran was war-caused; or
          (b)       a veteran has become incapacitated from a war-caused injury or a war-caused disease;
the Commonwealth is, subject to this Act, liable to pay:
          (c)       in the case of the death of the veteran—pensions by way of compensation to the dependants of the veteran; or
          (d)       in the case of the incapacity of the veteran—pension by way of compensation to the veteran;
in accordance with this Act.

War-caused death

According to s 8 of the Act:
(1) Subject to this section, for the purposes of this Act, the death of a veteran shall be taken to have been war-caused if:
(a)the death of the veteran resulted from an occurrence that happened while the veteran was rendering operational service;
(b)the death of the veteran arose out of, or was attributable to, any eligible war service rendered by the veteran;
(c)the death of the veteran resulted from an accident that occurred while the veteran was travelling, while rendering eligible was service but otherwise than in the course of duty, on a journey to a place for the purpose of performing duty or away from a place of duty upon having ceased to perform duty;
(d)in the opinion of the Commission, the death of the veteran was due to an accident that would not have occurred, or to a disease that would not have been contracted, but for his or her having rendered eligible war service or but for changes in the veteran's environment consequent upon his or her having rendered eligible war service; or
(e)the injury or disease from which the veteran died:
(i)was suffered or contracted while the veteran was rendering eligible war service, but did not arise out of that service; or
(ii)was suffered or contracted before the commencement of the period, or last period, of eligible war service rendered by the veteran, but not while the veteran was rendering eligible war service;
and, in the opinion of the Commission, the injury or disease was contributed to in a material degree by, or was aggravated by, any eligible war service rendered by the veteran, being service rendered after the veteran suffered that injury or contracted that disease; or
(f)the injury or disease from which the veteran died is an injury or disease that has been determined in accordance with section 9 to have been a war-caused injury or a war-caused disease, as the case may be;
but not otherwise.

The test for "war-caused death"

It is common ground that the Applicant's eligibility for pension is to be determined according to what is known as the "reasonable hypothesis test" - the standard of proof as set down in s120(3) of the Act.
The Tribunal is required to find that the Veteran's death was war-caused, unless it is satisfied beyond reasonable doubt that there is no sufficient ground for making that determination.
The Tribunal shall be so satisfied if the material before it does not raise a reasonable hypothesis connecting the Veteran's death with the circumstances of his war service: s 120(1) and (3).
"120 (1) Where a claim under Part II for a pension in respect... of the death of a Veteran, relates to the operational service rendered by the Veteran, the Commission shall determine that the... death of the Veteran was war-caused, ... unless it is satisfied beyond reasonable doubt, that there is no sufficient ground for making that determination."
120 (2) ...
120. (3) In applying subsection (1)... the Commission shall be satisfied, beyond reasonable doubt, that there is no sufficient ground for determining:
(a) ...
(b) ...
(c)that the death was war-caused or defence-caused; as the case may be, if the Commission, after consideration of the whole of the material before it, is of the opinion that the material before it does not raise a reasonable hypothesis connecting the injury, disease or death with the circumstances of the particular service rendered by the person."

THE ISSUES

In this case the central issue for the Tribunal is whether a hypothesis attributing the Veteran's death from carcinoma of the colon to his exposure during operational service to carcinogenic chemicals alone, or in conjunction with his ingestion of dapsone, is a reasonable hypothesis within the meaning of the Act.
EVIDENCE
Scientific Papers
A number of scientific papers were reviewed during the course of the hearing. Prominent among them are the following, listed according to date of publication with their eponymous titles:
(a)The Singapore paper - "Risk of Acute Non-Specific Upper Respiratory Tract Infections in Healthy Men Taking dapsone-Pyrimethamine for Prophylaxis against Malaria" Lee and Lau, BMJ vol 296: 893-5 (1988) Among 8337 recruits the mean risk of URTI was 64% higher in the study group than the controls. The cause is postulated to be immunosuppression, perhaps with physical stress having a synergistic effect. [Exhibit R-vii]
(b)The Alavanja Paper - "Mortality Among Forest and Soil Conservationists" Alavanja et al, Archives of Environmental Health, Mar/Apr 1989 vol 44 (No 2), 94-101. In this study carcinoma of the colon demonstrated a statistically significant linear trend with duration of employment as either a forest or a soil conservationist, which suggested to the authors an occupational aetiology for the disease. [T32, p 193]
(c)The Wiklund Paper - "Risk of cancer in pesticide applicators in Swedish agriculture" Wiklund et al, British Journal of Industrial Medicine, 1989;46:809-814. This is an analysis of cancer risk in 20,245 licensed pesticide applicators followed up for a mean period of 12.5 years. No statistically significant risks or time trends were observed. [Exhibit R-iv]
(d)The Brownson Paper – "Cancer Risk among Missouri Farmers" Cancer 64:2381-2386 1989. This reports cancer registry mortality studies which found higher age-adjusted incidence of lymphoma and lip cancer, among other tumors. Unlike most other studies this paper reported a slightly elevated risk of carcinoma of the rectum (age adjusted ratio of 1.21). Carcinoma of the colon however, was less common (age adjusted odds ratio of 0.86).   [T docs p201]
(e)The Ranch Hand Study - "Health Status of Air Force Veterans Occupationally Exposed to Herbicides in Vietnam" Wolfe et al, JAMA October 10 1990 - Vol 264, No 14, 1824-1831. This examined cumulative mortality to 1987 of approximately 1000 of the most heavily herbicide-exposed US service personnel from the Vietnam War. No evidence in the study suggested Ranch Hands were experiencing significantly increased systemic cancer at any particular site.       [Exhibit R -viii]
(f)The Saracci Paper - "Cancer Mortality in workers exposed to chlorphenoxy herbicides and chlorophenols" Saracci et al, Lancet 1991; 338: 1027-32.   This is an historical cohort study of mortality in 18,910 production workers or sprayers from ten countries. It found a non-statistically significant increase in soft tissue sarcoma and also apparent increases in the incidence of endocrine and nasal cancers, compatible with a causal relationship to herbicides but not TCDD (dioxin).   [part of exhibit R-iv]
(g)1993 Sheil Paper - "De Novo Malignancy..." Sheil, Disney, Mathew and Amiss, Transpl Proc Vol 25, No 1 (February) 1993: pp1383-4.   In this series, 90 among 6596 renal transplant recipients were found to have developed alimentary tract cancers. The risk ratio was 2.5. Half of these were large bowel cancers (specific risk ratio unstated).   [part of exhibit A-I]
(h)1996 Sheil Paper – "Malignancy in Organ Transplant Recipients" AGR Sheil, Transplantation Proceedings, Vol 28, No 3 (June) 1996, p1162. In this paper 7% of 6993 renal transplant recipients were reported to have developed non-skin cancers over a mean period of 6.8 years. Of these 20% (104) were "digestive organ" cancers.    [part of exhibit A-I]
(i)1997 Sheil Paper - "Lymphoma Incidence, Cyclosporine, and the Evolution and Major Impact of Malignancy Following Organ Transplantation" Sheil et al, (1997). This paper analyses cancers which occurred in 8% of 7909 renal transplant recipients. 20% of these cancers were "digestive tract" cancers (unfortunately not further categorised), of mean onset 10 years post-transplant. The risk ratio was 2.4.          [exhibit A-I]
(j)The 1997 IARC Paper - extract from WHO Monograph - "Evaluation of Carcinogenic Risks to Humans: polychlorinated dibenzo-para-dioxins and polychlorinated dibenzofurans..." IARC Monographs Vol 69, 4-11 February 1997, Preamble pp 22-27, and Monograph pp 336-343. The working group found that 2,3,7,8-TCDD (dioxin) causes cancer in humans and it is a multi-site carcinogen in animals. The strongest evidence is for all cancers combined, rather than for any specific cancer site, although lymphoma and sarcoma are singled out for special mention. The relative risk for all cancers combined in the most highly exposed and longer-latency sub-groups is 1.4. The authors comment:
"While this relative risk does not appear likely to be explained by confounding, this possibility cannot be excluded. There are few examples of agents which cause an increase in cancers at many sites; examples are smoking and ionising radiation in the atomic bombing survivors… This lack of precedent of a multi-site carcinogen without particular sites predominating means that epidemiological findings must be treated with caution; on the other hand, the lack of precedent cannot preclude the possibility that in fact 2,3,7,8-TCDD, at high doses, does act as a multi-site carcinogen. It should be borne in mind that the general population is exposed to levels far lower than those experienced by the industrial populations."    [Exhibit A-H]
(k)The Renlund Paper – "Incidence of Adenomatous Polyps in Cardiac Transplant Recipients" Renlund et al, Transplantation Vol 64, No 3, 1997, pp528-30.   93 heart transplant recipients were examined for evidence of colonic polyps, considered to be the initial lesions from which colon carcinoma arises. The authors conclude that long term immunosuppression does not increase the risk for adenomatous polyps.                [Exhibit R-vi]
(l)1998 Sheil Paper - "Cancer in Immune-suppressed Organ Transplant Recipients: Aetiology and Evolution" Sheil, Transplantation Proceedings, 30, 2055-2057 (1998). The author concludes that up to 30% of transplant recipients will develop cancer when follow-up analysis is for as long as 30 years after the transplant. It is likely that immunosuppressive agents promote cancer development indirectly through immune inhibition. [exhibit A-G]

Expert Evidence – Dr Bellett

Dr Bellett is a retired senior fellow and former leader of the Cell Transformation Group of the Division of Cell Biology at the John Curtin School of Medical Research. He did not give oral evidence at the hearing. In 1993 he gave a detailed report on the relationship between the deceased's colonic carcinoma and his exposure to chemicals during his military service [T16, pp49-66]. In Dr Bellett's view, the 20-year latent period between exposure and diagnosis of the cancer is not inconsistent with a causal association between the two. There is scientific evidence that the Veteran's risk of developing cancer of the colon would have been increased by his exposure to a number of chemicals in Vietnam. The high incidence of colon cancer in Australia makes it difficult to maintain that this exposure was the sole cause. Nevertheless it is reasonable to hypothesise contribution.
He cited in support the Alavanja paper and the Brownson paper (vide supra), and also papers by Clapp and Commoner (1990), Hoar (1985), Jenkins (1991) and Pratt (1987).
Dr Bellett refers to what he called the "two stage model of carcinogenesis", in which exposure to two or more carcinogens may further increase the risk of cancer by additive effect. In support he refers to evidence (Kikendall, 1989) of an additive effect of tobacco smoke and alcohol on the risk of colonic adenomas.
Finally, Dr Bellett considers the "safe dose" concept - the proposition that even though there is a known relationship between a risk and an undesirable outcome, at some sufficiently low dose of the risk factor the probability of the undesirable outcome is so low that it can be neglected, and assumed to be zero. He rejects this as scientifically invalid because (a) every non-zero dose of chemical must have a non-zero probability of causing cancer, (b) even if an arbitrarily acceptable threshold of risk were set, there is no way of knowing the exact exposure suffered by the deceased, hence whether he is above or below that threshold, and (c) the possibility of synergism between various of the chemicals to which the Veteran was exposed makes an arbitrarily acceptable risk threshold for the combination impossible to define [T16, p59].
Dr Bellett's report is predicated on the absence of an inherited predisposition to colrectal cancer in the Veteran's family tree [T16, p57]. This is incorrect (see below).
Expert Evidence – Dr McCullagh

Dr Peter McCullagh is Senior Fellow at the John Curtin School of Medical Research. He is not an epidemiologist or an immunologist but an experimental pathologist with an interest in immunosuppression spanning several decades. His reports - dated 10 September 1996, 31 July 1997 and 7 July 1999 - were before the Tribunal and he also gave oral evidence.
In his view, both the Veteran's exposure to dioxin and his ingestion of dapsone each served to increase his inherited risk of developing carcinoma of the colon. In effect, they were additive risk factors. Of the two compounds, dioxin had the greater effect. [See eg transcript 15 May 2000 p31, line 39 et seq]. He does not believe that the 20-year latency period between the chemical exposure and the clinical onset of the Veteran's bowel cancer militates against a causal association.
In his first report [10 January 1996, Exhibit B] Dr McCullagh says he does not think Professor Stewart's 1994 report gave adequate consideration either to the literature associating colon cancer with pesticides or to the role of dapsone in the Veteran's case.
He states that there are scientifically sound and published reports indicating that conservationists (a distinctive feature of whose occupation entails use and/or exposure to herbicides) have a significantly increased risk of colon cancer. Further, he states that animals exposed to herbicides have an increased incidence of bowel cancer. Two reports describe an increased incidence of small bowel carcinoma in sheep which had grazed in herbicide-treated pastures, evidence that hypotheses associating intestinal cancer with herbicide exposure are neither new nor unsupported the scientific literature [Exhibit B, p4, para 4].
In relation to dapsone, Dr McCullagh mentions animal and tissue culture studies and the Singapore paper (Lee et al, vide supra) in support of the proposition that dapsone has immunosuppressive activity. He observes that the heavy immunosuppression initiated in transplant recipients can lead to the development of cancer within as little as 2 years. While dapsone, in comparison, has only a mild effect not significant enough to outweigh its value as an antimalarial drug, extended immunosuppression increases the risk that any cells which have undergone malignant change will develop into clinically evident cancer.
He says that "… in relation to any disease condition, the existence in an individual of a number of discrete risk factors would usually be expected to confer a risk in excess of that attaching to any one of the factors in isolation". He concludes his first report discerning the hypothesis that the Veteran's familial risk of developing colon cancer is likely to have been augmented by his exposure to pesticides and their residues over the course of a year during which his immune system (and its capacity for immune surveillance) was partially but persistently compromised by the use of dapsone.
In a second report [31 January 1997, Exhibit C], Dr McCullagh takes issue with a number of Professor Stewart's conclusions about dapsone and immunosuppression, and the significance of the Alavanja paper.
In his third report [7 July 1999, Exhibit A-F] he reviews the IARC paper (vide supra) and concludes from it that the possibility that 2,3,7,8-TCDD is a multi-site carcinogen in humans cannot be ignored. He cites findings of the 1998 Sheil paper (vide supra) in arguing that the long latency of colonic carcinoma compared with lymphoma may help explain an apparent difference in the incidence of each, when statistics are gathered too early in immunosuppressed patients. But in any case, Dr McCullagh argues, the Sheil publications on tumor incidence establish unequivocally that the incidence of all cancers, including those of the digestive tract, is significantly increased post-transplant. He makes reference to a number of other papers dealing with the incidence of tumors post-transplantation and dismisses as "arrant nonsense" the claim that immunosuppression does not lead to an increased risk of common epithelial cancers.
In cross-examination, Dr McCullagh was asked whether he could name a single instance where he would not believe that Vietnam service was causally relevant to the cancer. He replied:
"Yes, if this man had a family history of polyposis coli and he had developed carcinoma one could say, well, he would have inevitably developed colo-rectal cancer whether he had been in Vietnam or not. Now, whether the Vietnam period might have accelerated that development, I couldn't say but basically, what you are saying is if I'm told that we have a group of people, everyone of whom has been exposed to a category 1, a class 1 carcinogen, can I with confidence exclude a participation or a participatory role by that carcinogen in the developing of any tumor in them, just looking at it generally without taking into account of any other specific information you have about the case, you couldn't as a general proposition exclude that. Now, you may be able to in individual cases, say for example that you find out that the exposure of the individual was very different from that assumed legal fiction." [Transcript: 15 May 2000 p84, 15-28]

Expert Evidence – Professor Stewart

This witness' bona fides are impressive. His curriculum vitae is summarised at page 251 in the T-documents and also in the transcript of his evidence (16 May 2000 at p 4). He has made a study of the carcinogenicity of chemicals in humans over 30 years and on this subject is clearly an expert of international renown. His reports (dated 20 February 1994, 19 November 1996, 24 June 1997 and 21 June 1999) in total run to more than 40 pages.
A central platform of Professor Stewart's evidence is that there is little if any significant statistical support in the scientific literature for the proposition that either the herbicides to which the deceased was exposed or the dapsone which he ingested is associated with a measurable increase in the incidence of carcinoma of the colon.
In his first report [T33, pp249-271] written in February 1994, Professor Stewart reviews in detail the evidence for carcinogenicity of the so-called "Vietnam" chemicals including dapsone, the chlorphenoxy herbicides (including dioxin or 2,3,7,8-TCDD), the cyclodienes (Chlordane and Dieldrin) and DDT. Apart from arsenic and arsenical compounds (which in high dose are associated with skin and lung cancer) none of the drugs, pesticides or herbicides to which Australian service personnel may have been exposed in Vietnam attracted an IARC Group 1 classification at the time of writing (1994). Of course this has now changed.
He made the following points:
"There is...significant evidence that chlorphenoxy herbicides (including the dioxin contaminant where relevant) may cause cancer in humans...[but]...all known chemical carcinogens exhibit a target organ or small number of target organs.
[None]...is known which increases the incidence of cancer generally..."
"None of the chemicals used in Vietnam may be characterised as causing, or probably causing, or possibly causing bowel cancer in humans. Confidence in this generalisation is increased by the generalisation that no occupational chemical...has been shown to cause bowel cancer in humans. Causation of bowel cancer is a rare response in experimental animals." [T33 p261]
Professor Stewart rejects as advocacy statements three published reports which Dr Bellett says find an association between colo-rectal cancer and exposure to phenoxy herbicides, dioxins and arsenic. He believes that of all the studies cited by Dr Bellett, the only one which cannot be dismissed out of hand is the Alavanja paper (vide supra). This records colon cancer risk but does not, in the view of its authors (or subsequent reviewers) establish or clearly implicate chlorphenoxy herbicides as causing colon cancer. Professor Stewart says that of the various studies which have recorded an increased cancer risk among farm workers, colon cancer is almost conspicuous by its absence.
On the "no safe dose" theory, Professor Stewart agreed in cross examination that there are no studies which demonstrate thresholds in respect of carcinogens, and that it is prudent public health practice to presume that there is no level of exposure to a known carcinogen which does not increase the risk of cancer [transcript 16 May 2000, p50 line 18].
Of dapsone, Prof Stewart says there is no evidence of carcinogenicity [T33, p264] commenting:
"…it is extremely difficult to sustain the hypothesis that massive immunosuppression (as achieved in transplant patients) leads to an increased risk of colon cancer. The notion that mild immunosuppression, as may occur following use of dapsone, places individuals at risk to develop colon cancer, is unworthy of serious consideration." [Exhibit R-iii]
He rejects Dr McCullagh's argument that immunosuppression and herbicide exposure have a cumulative impact on bowel cancer risk [Exhibit R-i]. This is because epithelial cancers are not more common in immunosuppressed persons, immunosuppression in humans is not known to increase the risk consequent upon exposure to environmental carcinogens, and because in animal experiments dapsone has not further increased the cancer risk in mice exposed to known carcinogens.
"The remarkable feature of Dr McCullagh's discussion is that he sets aside data concerning actual cancer causation in favour of primary concern with the mechanism. If dapsone did actually cause cancer in humans - at any anatomical site - discussion of immunosuppressive activity might be relevant. To…say that because dapsone is immunosuppressive it may reasonably be suspected of causing cancer, might be valid if there were no information, one way or the other, concerning actual cancer causation by dapsone. But there is, and dapsone doesn't cause cancer in humans."
Tumors in immunosuppressed patients have been overwhelmingly lymphomas, skin cancers and one kind of sarcoma (Kaposi's sarcoma). While single instances of colon cancer have been recorded, these cases go nowhere towards confirming the general theory that cancer arises from a failure of immune surveillance. The possibility cannot be excluded that these few colon cancers were detected only because immunosuppressed patients were scrutinised more closely than the population at large.
At page 3 of his 1994 report Professor Stewart states bluntly that immunosuppression does not cause increased risk of the most common cancer types, cancers arising from 'epithelial' tissue. But at the conclusion of the same report he softens his previous outright rejection of a possible causal relationship between the Vietnam chemicals and colon cancer when he observes that:
"… there are no data directly implicating herbicides, pesticides, etc as causing colon cancer. The possibility that Vietnam service contributed to disease cannot be excluded. However this supposition cannot be deemed a reasonable hypothesis. " [T33, p 271]
The most likely 'cause' of the deceased's cancer was his familial predisposition to the disease. The hypothesis that family history was the cause of disease development can be assessed at the level of more probable than not.
Dapsone, Immunosuppression and Carcinogenesis
The Applicant tendered a paper by Lee and Lau (the Singapore Paper) which reported an increased incidence of acute non-specific upper respiratory tract infections in healthy young Singaporean men taking dapsone for antimalarial prophylaxis.
Dr McCullagh postulates that mild immunosuppression caused by long term dapsone ingestion makes clinical cancer more likely to develop in someone otherwise already predisposed to the condition. In support of this proposition he cited the Sheil papers (vide supra) and other evidence of significantly increased cancer rates in renal and heart transplant patients treated with immunosuppressive drugs. He referred to the theory of immune surveillance in postulating a mechanism by which this may occur. He agreed that dapsone is a much milder immunosuppressant than the drugs used after transplantation procedures. In cross-examination he said he was not aware of any epidemiological evidence that dapsone was itself associated with an increased incidence of cancer. Nevertheless, in conjunction with other risk factors for cancer in this case (dioxin, family predisposition), dapsone was a small but contributing factor.
Professor Stewart argues that immunosuppression is not known to increase the risk consequent upon exposure to environmental carcinogens and disagrees that immune compromise is relevant when one is considering dapsone and colonic carcinoma. In his view immunosuppressed patients have no significant increase in bowel cancer [Exhibit R-i p3, para 4]. He did not comment on the results set out in the 1993 Sheil paper, in which 90 of 6596 renal transplant recipients were reported to have developed alimentary tract cancers. The risk ratio was 2.5. While the specific risk ratio for colon cancer (as opposed to "alimentary cancer") is not stated by the authors, they do report that half of the alimentary cancers in the series were large bowel cancers. Prima facie this causes the Tribunal to question Professor Stewart's assertion that immunosuppression does not cause epithelial cancers.
The cumulative effect of a number of risk factors
Dr McCullagh argued that mild dapsone-induced immunosuppression, combined with a genetic predisposition to colonic cancer and exposure to carcinogenic herbicides, together caused the Veteran's cancer.
Professor Stewart does not accept that there is any cumulative effect, at least between dapsone and chemical carcinogens. He gave 3 reasons - firstly, epithelial cancers are not more common in immunosuppressed persons; secondly, immunosuppression in humans is not known to increase the risk consequent upon exposure to environmental carcinogens, and thirdly, because in animal experiments dapsone has not further increased the cancer risk in mice exposed to known carcinogens. As has been suggested, the first of these reasons appears erroneous.
In answer to questions from the Tribunal about cumulative risk from genetic and environmental factors to the development of cancer however, Prof Stewart was less dogmatic. He said that the literature on the susceptibility of individuals to external carcinogens, based on their genetic make-up, is relatively scant [transcript: 16 May 2000 p55, line 19]. He agreed that his doubts about the hypothesis linking herbicides and colon cancer arose from a paucity of evidence [transcript: 16 May 2000 p56 line 5, p57 line 36]. The Tribunal found his answers to the following questions significant:
"Okay. Can I ask you then what you think of the suggestion that this man, the deceased, would be in a smaller sub-group of people with a family history, where the hypothesis…[is]…that a herbicide which did not seem from the literature to cause measurable colonic cancer in the population as a whole may well act synergistically or cumulatively? --- I can't exclude that. To the best of my knowledge that hasn't been put to me in exactly those words but if it were my answer would be I can't exclude that.
Do you think it is a ridiculous hypothesis? --- Oh no, it's only - it's only ridiculous in one sort of sad sense, that is, with present technology it's extremely difficult to study…there is not a lot, there is very little information generally about the susceptibility of genetically determined subgroups to environmental carcinogens. It is tremendously important…"

DISCUSSION AND FINDINGS OF FACT

In this case the Tribunal must deal with a number of vexing questions: was the Veteran exposed to chemical defoliants and/or pesticides during his operational service? If so, what was the nature and the level of exposure? Are any of those chemicals carcinogenic either singly, or in combination either with one another or with the antimalarial drug dapsone? More particularly, can they cause cancer of the colon? Is it reasonable to hypothesise a causal nexus between those chemicals and carcinoma of the colon in the Veteran's particular case?
Chemical Exposure
Central to the case is the proposition that the deceased was exposed to a variety of chemicals during his service in Vietnam. There is no argument between the parties as to the fact of general herbicide use in the vicinity of Nui Dat during the Vietnam War. The subject has been examined by the Evatt Royal Commission; Repatriation Commission & Smith (1990) 19 ALD 464 [T17 at pp72-4]; Repatriation Commission & Schar (1991) 25 ALD 503 [see T19], and also in various unreported AAT decisions: re Peter Edwards (21 December 1992) [T20], re Humffray (2 July 1991) [T18] and re Kenneth Kain (21 December 1992) [T21]. The issue was also considered by Dr AJD Bellett in his report of 11 March 1993 [T16 p 49 et seq]. Except for the Evatt Royal Commission Report all of these were before the Tribunal.
No oral evidence was led about the Veteran's specific exposure. In the T documents reference is made by LtCol DJ Roylance (ret'd) to the Veteran having spoken about patrolling through defoliated areas while at Nui Dat [T22, p141], but there is no other documented evidence as to the Veteran's herbicide contact during his service in Vietnam. There has been no suggestion that the Veteran did not ingest dapsone in appropriate dose during his entire time in Vietnam.
Dr Bellett, Dr McCullagh and Professor Stewart all considered it reasonable to presume the Veteran's exposure to the chemicals sprayed by the American forces - specifically including the chlorphenoxy agents 2,4-D and 2,4,5-T with the contaminant TCDD (dioxin) - and that this exposure was that common to other members of the Australian forces in Vietnam at that time [T33, p262; Exhibit B p1].
When asked whether the Tribunal may assume that the Veteran's exposure to chemicals at Nui Dat was as that generally adumbrated in the Evatt Royal Commission, counsel for the Respondent did "...not dispute that there was exposure to the same cocktail of herbicides about which the deeming has been referred to."
Accordingly, the propositions (a) that the Veteran was exposed to a cocktail of herbicides of the kinds specified in Smith etc, to a material degree and (b) that he regularly ingested the antimalarial dapsone during his service in Vietnam are accepted by the Tribunal.
Potential carcinogenicity of chemicals to which the Veteran was exposed
In 1994 Professor Stewart reviewed the evidence and IARC conclusions in relation to the possible carcinogenicity of chemicals to which the Veteran is presumed to have been exposed during his operational service [T33, p254 et seq]. These chemicals include:

(a)the antimalarial drug dapsone
(b) the chlorphenoxy herbicides (2,4-D and 2,4,5-T) - Agent Orange

(c) the Agent Orange contaminant "dioxin" (2,3,7,8-TCDD)
(d) the cyclodiene pesticides (chlordane and heptachlor, and Dieldrin)
(e) DDT
(f) Cacodylic compounds (arsenicals contained in Agent Blue)

At the time of writing (1994), only arsenic and arsenic compounds were categorised as a Group 1 carcinogen - definitively known to cause cancer in humans - by the IARC. It seems however, that malignancy after arsenical exposure is largely limited to skin cancer and lung cancer. While cacodylic compounds may have been part of the "cocktail" of chemicals to which the Veteran was exposed, they were not at any stage during the hearing put forward specifically as a cause of carcinoma of the colon.
Three years later, in 1997, the IARC revised its assessment of the carcinogenicity of dioxin, upgrading it to a Group 1 carcinogen in humans and a multi-site carcinogen in animals. It is not surprising that as these proceedings have progressed the attention of the Tribunal has been directed by the parties largely towards the carcinogenicity of the chlorphenoxy herbicides and their production contaminant dioxin, as modified by simultaneous ingestion of dapsone.

It is common ground that at least some of the chemicals to which the Veteran is presumed to have been exposed are carcinogenic. In particular, the IARC working group's review of the world scientific literature has found that 2,3,7,8-TCDD ("dioxin") causes cancer in humans and is a multi-site carcinogen in animals. It is a Group 1 carcinogen.
The Tribunal finds that the cocktail of chemicals to which the Veteran was exposed included known carcinogens. For the purposes of these proceedings, the most important of them is 2,3,7,8-TCDD ("dioxin").
Evidence for the hypothesis linking the carcinogens specifically with colon cancer
This leads to a pivotal issue - the question not of general carcinogenicity of the chemicals to which the Veteran was exposed but of their anatomical site specificity. Can the herbicide cocktail cause cancer specifically of the colon?
There is a paucity of evidence specifically linking colonic carcinoma with herbicide exposure, but the parties agree that the Alavanja paper (vide supra) raises the possibility of a positive correlation. While that paper found an increased incidence of colon cancer in one occupational group with probable herbicide exposure, its authors advised cautious interpretation of their data because information was not available of occupational exposure to specific individuals, nor was information available on potential exposures to confounders such as diet, phenacetin use, family history of lymphomas and other cancers, and exposure to immunosuppressive drugs.
In the documents before the Tribunal there has been passing reference also to the veterinary study of New Zealand sheep reporting an increased incidence of small bowel carcinoma in sheep which had grazed in herbicide-treated pastures (Newell et al, "Herbicides and Small Intestinal Carcinoma in Sheep", Lancet 1984:2:1301-5). Alavanja himself refers to this paper, and Dr McCullagh cited it and another similar report as evidence that hypotheses associating intestinal cancer with herbicide exposure are neither new nor unsupported by the scientific literature [Exhibit B, p4].
Professor Stewart did not accept Dr McCullagh's proposition that dapsone had a contributory role, and as a scientist he relied heavily on the absence of positive evidence of an association between drugs and chemicals to which the veteran was exposed and his colonic cancer in concluding that any causal association is at best a possibility.
When asked about a hypothesis that herbicides may increase the risk of developing carcinoma of the colon specifically in a person with an underlying genetic predisposition to the condition, Professor Stewart said that there were no data on the subject, and it would be very difficult to study. However, he said he did not think it was a ridiculous hypothesis.
In the Tribunal's view, the question of whether the chemicals to which the Veteran was exposed caused or contributed materially to the development of his colonic cancer remains unanswered.
APPLICATION OF THE LAW
In this case the Tribunal is required to make a finding that the Veteran's death was war-caused if it is satisfied under s 120(3) that the material before the Tribunal raises a reasonable hypothesis connecting the death with the circumstances of his war service, unless under the terms of s 120(1) one or more of the facts which underpin that hypothesis are considered to have been disproved beyond reasonable doubt.
The most authoritative consideration of what constitutes a reasonable hypothesis is to be found in the High Court judgements in Bushell v Repatriation Commission (1992) 175 CLR 408. At 414 Mason CJ, Deane and McHugh JJ said:
"The material will raise a reasonable hypothesis within the meaning of s 120(3) if the material points to some fact or facts ("the raised facts") which support the hypothesis and if the hypothesis can be regarded as reasonable if the raised facts are true.
In Byrnes v Repatriation Commission (1993) 177 CLR 564 at 571 the High Court said:
"The position may be summarised as follows: (1) First, sub-s. (3) of s.120 is applied: do all or some of the facts raised by the material before the Commission give rise to a reasonable hypothesis connecting the Veteran's injury with war service? The hypothesis will not be reasonable if it is contrary to known scientific facts, or is obviously fanciful or untenable. If the hypothesis is unreasonable the claim fails. Proof of facts is not in issue at this point. (2) If a reasonable hypothesis is established, sub-s (1) of s.120 is applied.
In coming to its decision in this matter the Tribunal carefully considered the many reports and research papers before it, the written and oral evidence of each of the experts and the very helpful submissions of Counsel.
Application of s 120(3)
The Applicant's contention that the chemical cocktail to which the Veteran was exposed causes carcinoma of the colon is one of the facts raised to establish the hypothesis. The Respondent asserts that the hypothesis put forward by the Applicant is not reasonable - there is a complete lack of objective evidence to support the critical pillars of the hypothesis relied upon and the various suggested "connections" advanced by Dr McCullagh are merely speculations, lacking any scientific echo in the literature.
For the purpose of determining whether the hypothesis is reasonable however, the Tribunal is required by subsection (3) to assume that the raised facts are true (see Lowerson v Repatriation Commission (1994) 50 FCR 252 at p260). In other words, at this stage proof of the colon-specific carcinogenicity of the chemical cocktail is not necessary. Under sub-s (3), the Tribunal need only decide whether all or some of the facts raised by the material before the Commission give rise to a reasonable hypothesis connecting the Veteran's injury with war service.
The question for the Tribunal is not whether there is a convincing body of scientific evidence that herbicide exposure with or without dapsone increases the risk of colon cancer in general. If it were, the Tribunal could only agree that at present the evidence is only meagre. As Professor Stewart himself said,
"The tribunal's task would be a happier one…if it were assessing a whole group of people which at least is something which epidemiology can contend with… The distinguishing between the inability of epidemiology to resolve certain issues on the one hand and the effect just not being there on the other is the bane of all these studies. It's the bane of low dose exposures, it's a huge problem." [Transcript: 16 May 2000 p54, line 38]
While the general issue of causation may provide a route to a final determination, what is important is the Veteran's specific case and the question of causation as it relates to that individual. But even then it is not for the Tribunal to determine whether as a matter of scientific probability his carcinoma was caused by exposure to the herbicide cocktail. Rather, the Tribunal must assess the reasonableness of the hypothesis that there is a causal association between the two.
The members of this Tribunal are not epidemiologists and it would be inappropriate for them to embark on detailed scientific analysis of the methodology and verisimilitude of the many research papers and other primary source documents cited in this case. That is the responsibility of the expert witnesses, whose evidence the Tribunal must assess. But even then, the Tribunal must do more than simply choose between their competing views. If it were simply a matter of preferring one expert to another in determining whether there is reliable scientific evidence that herbicides and their contaminants (with or without dapsone potentiation) cause cancer of the colon, the Tribunal's task would be much easier.
As we have noted, Dr Bellett's 1993 report was prepared on the assumption that in the Veteran's case there was no inherited predisposition to colo-rectal cancer [T16, p57]. Clearly he was not aware of the Veteran's family history when he prepared his report. Furthermore, the IARC re-assignment of 2,3,7,8-TCDD as a Group 1 carcinogen in 1997 post-dated his report. As he did not give oral evidence in the present proceedings the Tribunal has no way of knowing what effect this potentially significant information may have had on Dr Bellett's earlier conclusions. Accordingly, the Tribunal gives appropriately less weight to Dr Bellett's evidence
For the Applicant, Dr McCullagh believes that herbicide exposure and dapsone ingestion each magnified the Veteran's familial risk of developing carcinoma of the colon. On the other hand Professor Stewart says there is almost no evidence that bowel cancer is caused by the cocktail of chemicals to which the Veteran was exposed.
Professor Stewart's practical expertise and international standing in the relevant specialist field are indeed impressive. There is no doubting his bona fides. His evidence was lucid and to the point, whereas in oral evidence Dr McCullagh at times was prolix, lacking in precision and occasionally confusing. Dr McCullagh has not published in the fields of cancer causation; carcinogenesis in relation to herbicides or dioxin; the relationship between dapsone and immunosuppression, or dapsone carcinogencity. While he has no scientific publications of significance in relation to the matters in issue before this Tribunal however, he is nevertheless a senior research pathologist with a long interest in immune compromise. In this context the Tribunal paid close and particular attention to his evidence generally, and especially in relation to dapsone-induced immunosuppression.
On the question of the need to choose between the competing views of experts, the Tribunal has regard to the opinion of Brennan CJ in Bushell v Repatriation Commission (1992) 175 CLR 408, who cited with approval the comment of Davies J when the matter was with the full Federal Court:
"A reasonable hypothesis will ordinarily be established if a responsible medical practitioner, speaking within the ambit of his expertise, and after considering the particular facts of the Veteran's case, puts forward a theory of a likely, in the sense of a realistically possible, not fanciful, causal connection between war service and the Veteran's disability…"
Professor Stewart openly concedes the possibility of a causal association between the Veteran's herbicide exposure and his cancer of the colon but does not accept that the association amounted to a probability. The Respondent contends that the establishment of a mere possibility of association is not enough and Professor Stewart's evidence disproves beyond reasonable doubt essential facts supporting the hypothesis. Is this the case? Is the absence of good scientific evidence of a positive correlation itself proof of an absence of causal association in this case?
In answering these questions the Tribunal has considered the relationship between possible and probable association. To succeed, the hypothesis must be more than possible - it must be realistically possible. The facts of the case must point to it. Otherwise, it does not satisfy the requisite test as adumbrated by the High Court in Byrnes (vide supra). The hypothesis will not be reasonable if it is contrary to known scientific facts, or if it is obviously fanciful or untenable. And if the hypothesis is unreasonable the claim fails.
It is significant that the Veteran belonged to a subset of herbicide-exposed patients, those with a family history of colonic cancer. It is common ground that this subset has not been studied separately. The research papers which failed to find correlation between herbicides and colonic cancer were not examining this group of high-risk patients. As noted earlier Professor Stewart's answers to questions from the Tribunal on the point are pertinent.
The Tribunal accepts that a hypothesis cannot be reasonable if it is "contrary to proved scientific facts or to the known phenomena of nature": Government Transport, Commissioner for v Adamcik (1961) 106 CLR 292 at 306. Nor can it be reasonable if it is "obviously fanciful, impossible, incredible or not tenable or too remote or too tenuous": East v Repatriation Commission (1987) 16 FCR 517 at 532.
The Tribunal notes the paucity of evidence linking herbicide exposure to colonic carcinoma. Of itself however, that lack of evidence does not mean inevitably that an hypothesis linking the two is "contrary to proved scientific facts". To use the philosopher's analogy, the counting of any number of white swans does of itself disprove the existence of black swans. The fact that white swans abound is not a proved scientific fact of the kind which would make the hypothetical existence of a black swan untenable. In the case of chemical carcinogenesis there are a number of reasons why the scientific literature may fail to confirm a causal association which does in fact exist. The latency between exposure and clinical presentation of tumor is one obvious example - the statistics may have been gathered before the complication has declared itself.
In Bushell (at CLR 414), Mason CJ, Deane and McHugh JJ said of s 120(3):
"… in determining whether a hypothesis is reasonable for the purpose of s. 120 (3), it is not decisive that a connexion 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…"
Is the absence of evidence of a positive statistical correlation between chemical exposure and colonic carcinoma decisive in this case? Does it render untenable the hypothesis linking the Veteran's operational service with his death?   The Tribunal answers each of these questions in the negative. Its reasoning is as follows:
(a)      A distinction must be drawn between the general proposition and the particular circumstances of the Veteran's case.
(b)      There is good evidence that components of one or more of the chlorphenoxy herbicides are multi-site carcinogens causing lymphoma, soft tissue sarcoma and, in experimental animals, liver tumors and cancers of the oro-pharynx, lung and endocrine system.
(c)       At least one scientific paper (the Alavanja paper) raises the possibility specifically of a positive causal association between herbicides and colon cancer. Its authors and Professor Stewart both stress that this is no more than inferential - there are other explanations of the association which may not be causal. Nevertheless, the findings cannot be dismissed and must be judged alongside those studies which do not find any association.
(d)      Dr McCullagh, one of the two experts who gave oral evidence in this case, is of the view that the Veteran's exposure to dioxin and his ingestion of dapsone were both significant risk factors for bowel cancer.
(e)      The Veteran belonged to a sub-group of the general population with a familial predisposition to carcinoma of the colon. While chlorphenoxy herbicides have been widely studied, their carcinogenic effects for this sub-group has not specifically been studied. Such a study would be very difficult to undertake.
(f)       On all of the expert evidence in this case, it is at the very least possible that dioxin causes bowel cancer. The dispute between the experts goes largely to the order of likelihood of that being the case.
(g)      The hypothesis that chlorphenoxy herbicides increase the risk of carcinoma of the colon specifically in people with a familial predisposition to the disease is proposed by one expert and is not rejected by the other.
In this case the Tribunal concludes that the absence of evidence of a positive statistical correlation between chemical exposure and colonic carcinoma does not render the hypothesis untenable. The Tribunal finds that the hypothesis put forward by the Applicant in this case is a reasonable hypothesis in the terms of s 120(3) of the Act.
Application of s 120(1)
Having considered the whole of the material before it and determined the reasonableness of the hypothesis raised under the indicia of s 120(3) of the Act, the Tribunal now turns to s 120(1) to determine whether any of the facts necessary to support the hypothesis have been disproved beyond reasonable doubt, or the truth of a fact inconsistent with the hypothesis has been proved beyond reasonable doubt.
It is the Respondent's contention that Professor Stewart's evidence disproves beyond reasonable doubt one or more of the facts supporting the Applicant's hypothesis. The evidence of a causal association between dioxin and the Veteran's colon carcinoma is meagre but not determinative. It remains inconclusive. The experts for both parties acknowledge the possibility of an association but differ stridently as to the probability.
The Tribunal is satisfied that the not insignificant accumulation of research evidence against a causal association between dioxin and colon carcinoma in the exposed population generally does not disprove to the requisite standard the fact of a causal association in the Veteran's specific case. The question is left open by a notable and, in the circumstances, understandable paucity of research into the effects of dioxin in persons who, like the Veteran, have a genetic predisposition to carcinoma of the colon.
Accordingly, in applying s 120(1) the Tribunal cannot be convinced beyond reasonable doubt that the Veteran's death was not war-caused.
The Tribunal sets aside the decision of the Respondent Repatriation Commission dated 16 August 1990 as affirmed by the Veteran's Review Board on 19 February 1996. In substitution the Tribunal finds that the Veteran's death being war-caused the Applicant is entitled to pension under s 13(1) of the Act.
The date of effect is 14 May 1990.

I certify that the 91 preceding paragraphs are a true copy of the reasons for the decision herein of Dr D. Chappell, Deputy President and Dr J. Vallentine, Member.
Signed:         .....................................................................................
  Dominika Rajewski, Associate
Dates of Hearing  5-16 May 2000, 12 December 2000
Date of Decision  23 February 2001
Counsel for the Applicant        Mr Mark Vincent
Solicitor for the Applicant         Whyburn & Associates
Counsel for the Respondent    Mr Ian Butcher
Solicitor for the Respondent    Australian Government Solicitor