DAVID RANDELL and MILITARY REHABILITATION AND COMPENSATION COMMISSION
[2009] AATA 839
•30 October 2009
Administrative Appeals Tribunal
DECISION AND REASONS FOR DECISION [2009] AATA 839
ADMINISTRATIVE APPEALS TRIBUNAL )
) No 2007/5624
VETERANS’ APPEALS DIVISION ) Re DAVID RANDELL Applicant
And
MILITARY REHABILITATION AND COMPENSATION COMMISSION
Respondent
DECISION
Tribunal Senior Member Bernard J McCabe; and
Assoc Prof J B Morley RFD, MemberDate30 October 2009
PlaceBrisbane
Decision The Tribunal affirms the decision under review. ......................[Sgd]........................
Senior Member
CATCHWORDS
WORKERS’ COMPENSATION – claims – disease – chronic myeloid leukaemia – whether disease contributed to in material degree by employment – whether liable to pay compensation – possible causal connection between high level benzene and claimed disease – minimal exposure to benzene – decision affirmed
REASONS FOR DECISION
30 October 2009 Senior Member Bernard J McCabe; and
Assoc Prof J B Morley RFD, Member1.
David Randell, the applicant, is a soldier. He joined the Army in 1988. He has spent most of his career in the Army working in transport and logistics in Australia and overseas. He has been diagnosed with chronic myeloid leukaemia (“CML”). He says the condition arose out of his exposure to benzene in diesel fumes in the course of his work. He has applied for compensation under s 14 of the
Safety, Rehabilitation and Compensation Act 1988(“the Act”). The Military Rehabilitation and Compensation Commission, the respondent, denied liability for the condition. The respondent’s reviewable decision is dated 30 January 2007.
2. There is no dispute over Mr Randell’s diagnosis. There is also no doubt he was exposed to diesel exhaust from trucks and other activities involving the combustion of diesel fumes in the course of his employment. There is an issue over the extent of that exposure. There is some evidence that benzene is carcinogenic, although there is a dispute over whether benzene exposure causes CML as opposed to other forms of leukaemia.
3. The outcome of the case turns on the medical evidence, although it has been necessary for us to make findings of fact in relation to the level of the applicant’s exposure to diesel exhaust (which we take to include the smoke that issued from fires lit using diesel fuel in the garbage tips in East Timor).
4. We are not persuaded that Mr Randell’s CML is caused or aggravated by his exposure to diesel exhaust during the course of his employment. It follows that we have decided to affirm the decision under review. We explain our reasons below.
The factual background
5.
Mr Randell joined the Army on 30 March 1988. He was initially a driver but subsequently assumed supervisory duties in relation to a transport unit. Mr Randell described his work in detail during the course of his oral evidence before the Tribunal. We were provided with pictures and descriptions of the various vehicles that he operated (Exhibits 2 and 3). Some of those vehicles are old and belch exhaust fumes; others have exhaust funnels that might direct exhaust fumes at the driver or someone in close proximity to the vehicles. We were also told about the daily operations of the unit. The vehicles were started and ran for a period in an outdoor parking area every day to ensure they were in working order. When the unit was being deployed, the vehicles would be arranged in “packets” in an outdoor martialling area or on the roadside or at other locations with their motors running.
Mr Randell was required to walk around the vehicles as they generated exhaust.
6. We were also told about Mr Randell’s experience in East Timor between October 2003 and June 2004. His unit was responsible for the management of a garbage dump used by the INTERFET forces in the area. Soldiers from the unit would go to the dump on most days and set fires to the rubbish using diesel. At least once a month, the soldiers would conduct a major burn that involved spraying thousands of litres of diesel around the dump and setting fire to anything that would burn. We saw photographs of one of these burns. The exercise generated a lot of black smoke. We understand Mr Randell did not wear protective clothing or breathing apparatus. We also heard some evidence describing Mr Randell’s exposure to a variety of chemicals in a storage container at the INTERFET base.
The evidence given by the medical experts
7. We heard telephone evidence from two occupational physicians at the hearing, both of whom also provided detailed reports. The applicant called Dr David Douglas, who has expertise and experience in Australia and overseas, in occupational and environmental toxicology, risk assessment and related research. He has written a chapter in an edited monograph, The Physiopathology of Cancer, published in 1976. The respondent's expert witness, Dr Richie Gun, is a Visiting Research Fellow at the Department of Public Health in the University of Adelaide. He was the principal author of an Australasian Faculty of Occupational Medicine (“AFOM”) publication in 2003, entitled Occupational Cancer: A Guide to Prevention, Assessment and Investigation.
8.
We were also provided with reports from another occupational physician,
Dr Steven Goode (Exhibit 1 at 265-340). Those reports had several attachments including summaries of online search results for leukaemia and benzene exposure. There were also six brief reports from the applicant’s treating clinical haematologist, Dr Stephen Fanning (Exhibit 1 at 252-256 and 258-264). These doctors were not required for examination by either party.
9. The applicant’s CML was diagnosed by Dr Fanning, on bone marrow biopsy, BCR-abl FISH (“fluorescence in situ hybridization”) studies, and PCR (“polymerase chain reaction”) studies. These studies established his diagnosis by showing that his CML was caused by a single abnormal (“fusion”) gene (Exhibit 1 at 253 and 256), conforming to that which, in the section on Haemopoietic Disorders in Harrison’s Internal Medicine, is designated as the “cytogenetic hallmark” of CML (Exhibit 1 at 279). It is described as a “reciprocal translocation” of chromosomes 22 and 9, located at the breakpoint cluster region (“BCR”) on chromosome 22 (22q11) with the ABL (“abelson murine leukaemia virus”) gene on chromosome 9 (9q34) (Exhibit 1 at 277 and 279). This translocation has the effect of shortening the length of chromosome 22; and it was by this shortened chromosome 22, which has come to be known as the “Philadelphia chromosome”, that this diagnostic translocation was originally recognised (Exhibit 1 at 279).
Dr douglas’ evidence
10. The report of Dr Douglas (Exhibit 4) notes the importance of the discovery of the Philadelphia chromosome “in understanding the pathogenesis, biology and later the molecular biology of CML.” He went on: “It also assisted the [haematological] morphologist in distinguishing from CML other types of marrow disorder.”
11. Dr Douglas then quoted from an article published by Smith in 1996 in the journal Environmental Health Perspectives on the Mechanism of Benzene Induced Leukaemia, saying “Benzene in the majority of its metabolites ... produce[s] chromosomal damage both in vitro and in vivo”.
12.
After referring to the applicant’s diesel fume exposure in East Timor,
Dr Douglas opined that “[Mr Randell’s] diesel and smoke exposures ... would have contained significant amounts of benzene.” Dr Douglas noted that diesel exhaust particulate matter contained comparable amounts of benzene to carcinogenic PAH (“polycyclic aromatic hydrocarbons”) and nitro-PAH, and that these, including benzene, are genotoxicants.
13. Dr Douglas went on to quote from a review article concerning benzene and leukaemia by Vigliani in volume two of the Annals of the New York Academy of Sciences in 1976. Vigliani said:
From the vast literature accumulating over the last 40 years, the conclusion can be drawn that clinical as well as epidemiological data are indicative of a strong leukaemogenic action of benzene in man, the leukaemia being mostly acute and myeloblastic in type, ... and that the probability exists that benzene might also induce chronic types of leukaemia.
14. Dr Douglas added that this had been demonstrated for myeloid leukaemia more than other types. He referred to a very large cohort study of nearly 80,000 Chinese benzene workers that was supported by the US National Cancer Institute, and reviewed by Corbett in 2003. It appears that this study did not distinguish between acute myeloid leukaemia (“AML”) and CML.
15. Dr Douglas then quoted the full text of a review paper by Mehlman published in 2006 in volume 1076 of the Annals of the New York Academy of Science. After alluding to the proposed mechanism by which the Philadelphia chromosome induces CML, Mehlman reviewed the literature on the possible role of benzene exposure. Mehlman cited 18 reports since 1967 of leukaemia associated with benzene exposure. He stated that CML occurred in all but one study, albeit less frequently than AML. Several of these studies purported to show that this was a statistically significant increased incidence. Mehlman was quoted as concluding: “Based on the scientific evidence available, it is reasonable and prudent to conclude that benzene is causally related to CML.”
16. From this material, Dr Douglas opined that “it is more probable than not that Mr Randell’s [CML] was caused by the benzene exposure that he experienced during his years to date in the Royal Australian Army.”
17.
In his evidence-in-chief at the hearing, Dr Douglas stated that, when caused by benzene, there is “no good reason” to distinguish AML from CML. He considered that there was “no safe level of benzene.” When taken to the appendix in Dr Gun’s report (Exhibit 5 at 14-15), in which Dr Gun explained the equation for statistically calculating the probability of the applicant’s benzene exposure causing his CML,
Dr Douglas referred to the equation as “questionable”. Dr Douglas considered that the applicant had “an exceptionally rare leukaemia” for his youthful age, which suggested to him that an environmental factor, such as benzene exposure, was active in his case.
18. On cross-examination, he agreed that in an affected individual, CML might not change to AML, or vice versa. He also agreed that diesel fuel produces benzene only after its combustion, but said that, although it would be present in amounts of only “a few parts per million”, this was “not small”.
Dr gun’s evidence
19. Dr Gun’s report (Exhibit 5) referred early on to a paper published by Boffetta in 2004 in the Journal of Occupational and Environmental Medicine. Boffetta reviewed the epidemiological data on diesel exhaust exposure and leukaemia risk. Although this principally examined AML, Boffetta concluded that diesel exhaust exposure appears not to be associated with increased leukaemia risk.
20. Dr Gun went on to affirm that the International Agency for Research on Cancer (“IARC”) accepts that benzene is carcinogenic. The IARC’s acceptance is based on human studies relating to leukaemia in general, with evidence supporting its causal association with AML. However, Dr Gun pointed out that IARC “is silent on whether benzene specifically causes CML.”
21.
In the course of considering whether benzene exposure can cause CML,
Dr Gun addressed two recent review articles which had surveyed the reports in the literature of studies of the incidence of CML in individuals exposed to benzene:
·
Schnatter et al published in Chemical-Biological Interactions in 2005, finding that “data for CML are sparse and inconclusive”. However,
Dr Gun had reservations about Schnatter’s objectivity, as he is a consultant to Exxon Mobil.
·The other was the Mehlman article quoted by Dr Douglas which concluded there is a significant association between benzene exposure and CML. However, Dr Gun pointed out that Mehlman had been selective in his study, having omitted studies not supporting his conclusions.
22. Dr Gun performed his own independent assessment of the individual studies reviewed in these two papers for the purposes of giving evidence in these proceedings. His review proceeded as follows:
·He included all of the studies in the review by Schnatter et al, because they had been confined to peer-reviewed cohort and case-control studies, in which the leukaemia subtypes and benzene exposure estimates had been identified.
·He included all cohort study publications cited by Mehlman, but not the simple case reports, which had no comparative “control populations” essential for statistical analysis for any benzene causal association (Exhibit 5 at 7). He also excluded two other papers cited by Mehlman that referred only to AML (see generally Exhibit 5 at 5). He made a point of including the only study in Mehlman’s review appearing to show benzene exposure causing more cases of CML than AML (Goguel et al in volume 7 of the 1967 edition of the Nouvelle Revue Francaise d’Hematolgie).
23. All of the reports reviewed by Dr Gun were summarised in a Table (Exhibit 5 at 7). This lists a total of eleven cohort studies and five case-control studies, published between 1967 and 2003. Six of the cohort studies reported no CML cases or deaths; and one case-control study (Glass et al in 2003 in the journal Epidemiology) showed no benzene causal link with CML (Exhibit 5 at 8).
24. These studies encompassed a total of more than 50 CML cases associated with varying degrees of benzene exposure. Dr Gun analysed the data recorded in each for any demonstrable link between benzene exposure and the occurrence of CML. From this analysis, he concluded the reports did not show a consistent association of statistical significance between benzene exposure and CML incidence or mortality.
25. Dr Gun pointed out that four of the five case-control studies showed a mildly increased risk for CML, but not to a statistically significant degree; he conjectured that if the findings in these five case-control studies could be combined in a statistical meta-analysis, “it is possible that they would add up to a significant excess of CML cases” (Exhibit 5 at 8). On the other hand, he added that the remaining one of these which actually showed a statistically significant increase in the CML risk (Adegoke et al in Annals of Epidemiology in 2003) entailed high cumulative benzene exposures (Exhibit 5 at 4). Conducted in Shanghai, Adegoke examined benzene workers, comparing 486 with leukaemia against 502 unaffected controls; they found 15 benzene-exposed CML cases, the risk increasing with the greater exposure.
26. From this analysis Dr Gun concluded (Exhibit 5 at 8, emphasis in original):
I would conclude that there is a possible causal association between CML and benzene exposure ... but if such an association exists, it is only manifest at high exposure levels.
This evaluation is not given with a high degree of confidence, since relevant data are sparse and several of the cohort studies found no CML excess. Moreover in two studies where exposure was sufficient to have caused benzene toxicity no cases of CML were found (Aksoy et al in Blood, 1974; and Rothman et al in Cancer Research in 1997).
27. Dr Gun concluded his report with the observations about the applicant’s claim, according to the guidelines in the AFOM publication Occupational Cancer: A Guide to Prevention, Assessment and Investigation, of which he had been the principal author. We summarise these below:
·Is the agent carcinogenic to humans? Benzene exposure can cause AML; the sparse data on benzene exposure and CML are “open to interpretation of such a causal link”, but only at “relatively high exposures.”
·Is the particular agent associated with cancer at this site and of the same histological type? The site of the applicant’s cancer (CML) is consistent with the route of uptake of the agent (benzene).
·Is the site of the cancer consistent with the route of uptake of the agent? Yes.
·Could the exposure have led to uptake of the agent? Exposure to diesel liquid or vapour does not cause benzene exposure, but benzene can be formed from diesel fuel combustion.
·What was the intensity and duration of exposure? To estimate the applicant’s intensity and duration of benzene exposure, Dr Gun referred to two studies published in 1998 and 2002 which measured airborne benzene levels for workers in large confined work building environments exposed to diesel exhaust (Exhibit 5 at 9-10). The highest concentrations found were, respectively, 0.2 parts per million (“ppm”) and 0.001-0.015 ppm, ie significantly less than the current threshold limit value of 0.5 ppm. He concluded that diesel fuel combustion generates “very little benzene”.
·Was the time from exposure to disease onset consistent with the induction latency period of the agent? Including his service before deployment to East Timor, yes.
·Were there other factors that might have contributed to the risk of cancer in this person? No other disease risk factors, such as smoking, ionising radiation, or specific viral infections, have been identified in the applicant’s case; this does not exclude his CML having occurred randomly.
28. Dr Gun affirmed that benzene exposure studies have shown that airborne benzene levels from diesel fuel combustion, even indoors, are low. He added that these levels would be greatly reduced with outdoors exposure.
29. At the Tribunal hearing, Dr Gun disagreed with Dr Douglas that CML and AML are variants of the same disease. Dr Gun insisted that acute exacerbations of CML are not properly characterised as AML. He said the International Classification of Diseases of the World Health Organisation recognises the conditions as separate diseases. Only CML is linked specifically to the Philadelphia chromosome. Indeed, CML and AML may even coexist, but one does not metamorphose into the other.
30.
Dr Gun agreed with Dr Douglas that there is “no safe level” of benzene, but
Dr Gun says low-level exposure entails only a low-level risk of AML. However, although an individual with “a non-zero exposure” to benzene had a “non-zero risk”, the lower is the level of the exposure, the less distinguishable is the risk from “general environmental risk.”
31. Dr Gun disagreed with Dr Douglas that the probability of causation equation which Dr Gun had used in the appendix to his report was “questionable.” He confirmed that it is widely used in epidemiological studies, its only qualification being that it depends on whether the dose of benzene exposure is sufficient to double an individual’s observed risk of developing CML.
32. During cross-examination, Dr Gun concluded following his review of the literature that, apart from the Shanghai study in which benzene exposures were higher (Adegoke et al), the benzene exposure risk for CML cannot be distinguished from that of the general population. He was asked why he thought the paper by Glass et al was the only case-control study in which no CML benzene causal link was found, even though it showed an increased risk of AML at lower exposure levels than shown in other studies. Dr Gun answered that this study’s low CML numbers meant that, as an epidemiological study, it was not powerful enough to provide results which are statistically significant.
Assessment of the medical evidence
33. The two medical witnesses differed in their opinions on each of the three questions to be addressed by the Tribunal. Each of these questions now is examined in turn.
(i) To what extent was the applicant exposed to benzene during his period of service?
34. Dr Douglas referred to the applicant’s many years of exposure to diesel exhaust, but particularly during his several months service in East Timor, and the “significant amounts of benzene” in diesel exhaust. He did not provide an estimate of the benzene concentrations to which the applicant was exposed.
35. Dr Gun has cited two studies reported in the literature in which airborne benzene levels were measured to which workers in large confined workspace buildings were exposed. Although the magnitudes of the two results differed considerably (0.2 ppm, and 0.001-0.015 ppm, respectively), both concentrations were very low in these indoor environments, and he concluded to this effect (Exhibit 5 at 11). He added that, because the applicant’s East Timor exposure was outdoors, this had the effect of “greatly reducing the inspired concentration of benzene compared with indoor concentrations.”
36. The estimates provided by Dr Gun are not precisely applicable to the applicant’s case. However, there is force in Dr Gun’s point that confined workspace conditions will provide higher estimates than the outdoors exposure experienced by the applicant. In the absence of more specific measurements, we accept the estimates referred to by Dr Gun can be used as guides. In those circumstances, we accept Mr Randell’s benzene exposure was “minimal” notwithstanding it occurred over more than 16 years.
(ii) Might exposure to benzene cause cml?
37. Dr Douglas has cited three reviews. The first two, by Vigliani and Corbett, were of benzene causing leukaemia, of acute myeloid type, but without findings on CML. At the Tribunal hearing, Dr Douglas stated his view that, when caused by benzene, there is “no good reason” to distinguish AML from CML. This is despite his observation early in his report that the discovery of the Philadelphia chromosome enables the distinction of CML from other types of bone marrow disorders, which presumably includes leukaemias other than CML. In particular, we note the observation in the Haemopoietic Disorders section in Harrison’s Internal Medicine that this genetic abnormality is known as the “cytogenetic hallmark” for CML. This diagnostic chromosome abnormality was found in the applicant’s case.
38. Dr Douglas’ other citation, of the review by Mehlman published in 2006, does address CML. Mehlman concludes benzene exposure is causally related. However, Dr Gun has criticised the study on the basis that Mehlman did not include any studies that did not support his conclusions. We understand that is why Dr Gun decided to conduct his own analysis of the cases referred to in the Mehlman study. He also referred to a similar review reported one year earlier by Schnatter et al, these authors finding that the CML data were inconclusive. Although Dr Gun also had some reservations about the objectivity of Schnatter’s paper, this review had the merits of being confined to peer-reviewed cohort and case-control studies.
39. We prefer Dr Gun’s views. We are impressed by the scientific rationality and objectivity of his study of 16 reports in the literature between 1967 and 2003. By applying the standard epidemiological criteria, he has found that only one of the published reports, by Adegoke et al in 2003, had a sufficient number of excess CML cases pointing to a statistically significant increase in the CML risk. However, he has pointed out that the benzene workers studied in this report had high cumulative exposures. Accordingly, Dr Gun has worded his conclusion from his analysis carefully, to allow “a possible causal association between CML and benzene exposure” (Dr Gun’s emphasis); but he further qualified this by adding that, if this exists, it is only manifest at high benzene exposure levels. He explained his lack of greater confidence as being due to sparse relevant data, and because the other cohort studies that he examined “found no CML excess.”
40. We are satisfied that:
·CML is a separate disease entity to AML. Observations regarding causal effects of benzene exposure and AML cannot be assumed to apply to CML.
·Dr Gun’s rigorously comprehensive scientific approach to the applicant’s case has been appropriate to the requirements for our determination.
41. It suggests we cannot be satisfied on the balance of probabilities that Mr Randell’s exposure to benzene is causally connected to the onset of his CML condition.
(iii) Did the applicant’s exposure to benzene cause him to develop cml?
42. From the foregoing, we find:
·notwithstanding his more than 16 years of exposure, the level of the applicant’s benzene exposure from diesel exhaust fumes was minimal; and
·there is only a possible (ie not probable) causal association between CML, which, if it exists, is only at high levels of benzene exposure.
43. Accordingly the Tribunal determines that his exposure to benzene did not cause the applicant to develop CML.
Conclusion
44. The decision under review must be affirmed.
I certify that the 44 preceding paragraphs are a true copy of the reasons for the decision herein of Senior Member Bernard J McCabe and Assoc Prof J B Morley RFD, Member.
Signed:..........................[Sgd]....................................................
Michael Buckingham, AssociateDates of Hearing 27-28 May 2009
Date of Decision 30 October 2009
Counsel for the Applicant Mr A Harding
Solicitor for the Applicant Woods Prince Lawyers
Counsel for the Respondent Miss E Ford
Solicitor for the Respondent DibbsBarker Lawyers
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