Beckwith and Military Rehabilitation and Compensation Commission
[2007] AATA 1444
•20 June 2007
Administrative Appeals Tribunal
DECISION AND REASONS FOR DECISION [2007] AATA 1444
ADMINISTRATIVE APPEALS TRIBUNAL )
) No N2004/1229
GENERAL ADMINISTRATIVE DIVISION ) Re PETER BECKWITH Applicant
And
MILITARY REHABILITATION & COMPENSATION COMMISSION
Respondent
DECISION
Tribunal Senior Member, Mrs Josephine Kelly and Member, Dr Max Thorpe Date20 June 2007
PlaceSydney
Decision The decision under review is affirmed
........................[sgd]......................
Presiding Member
Senior Member, Mrs Josephine Kelly
CATCHWORDS
WORKER’S COMPENSATION – applicant diagnosed with brain tumour – diffuse astrocytoma – whether materially contributed to by exposure to radar at work – whether evidence to support connection between radar and brain tumour – whether there is a gene-environment causal relationship – held not sufficient evidence to conclude causative relationship exists on balance of probabilities – decision under review affirmed.
LEGISLATION
Safety, Rehabilitation and Compensation Act 1988
REASONS FOR DECISION
Senior Member, Mrs Josephine Kelly and Member, Dr Max Thorpe Summary
1. Mr Peter Beckwith served in the Australian Navy from July 1996 until June 2003. In April 1997 he joined HMAS Newcastle, and he continued to serve on that ship until about February 2000 when he transferred to a shore base. In November 2001 he was diagnosed with a diffuse astrocytoma (Grade II), which is a tumour in the brain (the tumour). Mr Beckwith’s symptoms were epileptic fits for the previous six weeks. Professor Rosenfeld, neurosurgeon, operated and removed most, but not all, of the tumour. Mr Beckwith then underwent radiotherapy. Post-treatment he suffered depression which resolved over 12 to 18 months. He was discharged from the Navy in June 2003 and resumed work as of October 2005. He told us that he has recently been told that the tumour has returned and his prospects are not good. He is 28 years old and is married. He continues to take medication for depression and epilepsy, however, he is suffering an increasing number of fits.
The Issues
2. Mr Beckwith claimed compensation for the tumour, and consequential epilepsy, psychological stress and short term memory loss, which was refused. The key issue for us to determine is did Mr Beckwith’s exposure to radar while serving on HMAS Newcastle contribute to in a material degree, or aggravate in a material degree, the tumour? The relevant legislation is the Safety, Rehabilitation and Compensation Act 1988.
3.The subsidiary issues are:
(a) Does medical opinion consider that there is a causal relationship between exposure to radar and brain tumours, and in particular to diffuse astrocytoma?
(b) Does medical opinion consider that there is a gene-environment causal relationship with astrocytoma?
(c) If there is a recognised causal relationship between radar and astrocytoma, was Mr Beckwith’s exposure to radar sufficient, relevantly, to cause the tumour?
(d) Although not really addressed by either party, there was then a question of whether the other conditions were a consequence of the brain tumour. On the evidence, it seems that there was no real dispute that they are.
4. The Tribunal’s task is to make the correct or preferable decision on the evidence put before it. The medical evidence before us, on the balance of probabilities, does not support a causative relationship between exposure to radar and astrocytoma, including in terms of a gene-environment interaction. We are therefore unable to find that Mr Beckwith’s exposure to radar on HMAS Newcastle contributed to in a material degree to his tumour. The reviewable decision to refuse Mr Beckwith’s application for compensation is affirmed.
Background
5. Radiofrequency radiation (“RFR”) is the transmission of energy on an electromagnetic wave. RFR is non-ionising radiation. RADAR (an abbreviation of radio direction and ranging) sends out a pulse of RFR in a specific direction and listens for a low level echo signal that is reflected back from the remote object. The distance to that object can be calculated because two factors are known: that the pulse travels at the speed of light, and the time delay between transmission and echo pulse reception. Wavelengths for radars are typically 3 cm to 30 cm (frequencies of 1GHz to 10GHz). Frequency has a significant bearing on human absorption of radiofrequency energy. Frequencies lower than those used by radar coincide with maximum absorption in the human body.
Consideration
Does medical opinion consider that there is a causal relationship between exposure to radar and brain tumours, and in particular to diffuse astrocytoma?
6. What do epidemiological studies of the relationship between exposure to RFR and brain tumours, and in particular astrocytomas, show? We were assisted by reports and oral evidence from Professor Graham Giles, cancer epidemiologist, and Professor Robert Cumming, who is Professor of Epidemiology and Geriatric Medicine at the University of Sydney.
7. Professor Cumming’s first report of 12 March 2007 concerned a computerized literature search for relevant articles in the peer-reviewed scientific literature that he had carried out. He found five articles reporting the results of three separate epidemiological studies that have investigated the relationship between exposure to radar and development of brain tumours. All involved military personnel.
8. Professor Giles identified seven potentially relevant papers. Professor Giles and Professor Cumming agreed that there were really only two papers that should be considered, they were that by Grayson 1996, and the other by Groves et al 2002, which was a follow up to a 1980 paper by Robinette et al.
9. The Grayson paper reported a case-control study of brain tumours and exposure to radiation among US air force personnel. There were 230 men who were diagnosed with a brain tumour between 1970 and 1989 (the “cases”), and 920 “controls” who did not have a brain tumour. Exposure to RFR (mainly radar) was based on review of occupational histories obtained from air force personnel records. This study found a risk of 1.39, or 39% increased risk of developing brain tumours for men ever exposed to RFR. The study concluded that although it had limitations, particularly in exposure estimation, it did suggest that there was a small association between potential exposure to RFR and brain tumours in the US air force population.
10. Professor Cumming and Professor Giles disagreed about the importance of this small association of risk. Professor Cumming considered the risk statistically significant, whereas Professor Giles considered that it was only just statistically significant and made a number of criticisms of the study.
11. Professor Cumming considered that the way that exposure to RFR was assessed meant that the quality of exposure information in the study was relatively good. He noted that there was no clear pattern of increasing risk with increasing level of exposure, that is, there was no dose response, and that the paper did not make clear whether recall bias had been avoided by reviewing occupational histories without knowledge of the subjects’ medical histories. Recall bias is where “cases” give a more accurate history of radar exposure than “controls”. In his report he said that recall bias could have led to an over-estimate of the size of the relationship between radar and brain tumours.
12. He considered that whilst allowing for some uncontrolled recall bias, he would not reject 1.4 as causal, but he also said that 1.39 was not a strong association.
13. Professor Giles reported that the principal criterion for establishing causality in epidemiological studies is the strength of association:
Estimates of ratios less than 4.0 can be a product of poor design and bias
Estimates of above 4.0 need to be considered seriously
Estimates of 10.0 and above are likely to be causal
Estimates of less than 2.0 (in this case 1.39) need to be considered very seriously for alternative explanations to the posited hypothesis.
14. Professor Giles was concerned about the limitations concerning exposure that the authors expressed. The absence of a dose response in the face of a modest estimate argues against a causal association. He considered that the exclusion of controls that were found to have a prior history of diseases that had been associated with RFR exposure could have biased the analysis towards finding a positive association. The study did not differentiate between different forms of brain tumour. Putting them together as one group was not very meaningful.
15. The Groves paper reported on over 40 years of mortality follow-up of 40,581 Navy veterans of the Korean War with potential exposure to radar. There was no evidence of increased brain cancer in the entire cohort or in high-exposure occupations.
16. All the subjects of the Groves study were trained to work with radar. Assessment of exposure was based on the type of work the men did. The low exposure group comprised mainly radio and radar operators who tend to work below deck, and the high exposure group comprised mainly electronics technicians, who repair radar equipment. Each group comprised approximately 20,000 subjects. There was a 35% reduction in risk of death from a brain tumour in the in the high exposure versus the low exposure group.
17. Professor Cumming said that the reduced risk was not statistically significant. He considered that there were some weaknesses in the study. They were that there was no group of subjects that had no exposure to RFR, rather the study compared those with high and low levels of exposure, and the quality of information on radar exposure was not high, being based on the subjects’ job titles. Consequently, it would tend to lead to an under-estimate of the effect of the exposure to radar on brain tumours in the study.
18. At the end of the day, there is one study that found a small association between RFR and brain cancer, and another that did not find an association.
19. Professor Cumming accepted that exposure to RFR is not a known carcinogen. At highest he said that it was possible that exposure to RFR caused brain tumours. Professor Giles’ opinion was that it was highly improbable.
20. A further area which was addressed by Professors Giles and Cumming was gene-environment interaction. Professor Cumming wrote that gene-environment interaction implies that people with both a particular gene mutation and a particular environmental exposure are at much greater risk of developing a particular disease than people with only one of those characteristics. Mr Beckwith’s uncle died of a brain tumour. The precise classification of that tumour is unknown. Professor Cumming said that it may be that the combination of exposure to radar and an inherited gene mutation put him at particularly high risk of developing a brain tumour. Professor Cumming was unable to find any epidemiological studies of gene-radar interaction in the aetiology of brain tumours.
21. In his further report dated 29 March 2007, Professor Cumming provided examples of papers looking at gene-environment interactions. Of most relevance is a December 2006 paper by Rajaraman et al that found that the risk of meningioma (a kind of brain tumour but not astrocytoma) was increased 13-fold among those with a particular gene and high levels of lead exposure. He concluded that “[t]his study confirms that it is biologically plausible that a gene-environment interaction could have caused Mr Beckwith’s brain tumour”.
22. Professor Giles considered that the finding in the Rajaraman study was not statistically significant. He noted that there was no association with glioma risk (which astrocytoma is) in the study for which the number of cases was much higher than for the meningioma cases (173). He noted that the authors stressed the need for caution in interpreting the results because of the small number of cases upon which they were based. Professor Giles concluded that there are no established risk factors with respect to astrocytoma/glioma and no established genetic factors “so the gene-environment interaction is academic”. He acknowledged that “This is not to say that such a phenomenon is impossible, there is simply no available evidence to support it”.
23. In our opinion, there was really not any disagreement between Professors Giles and Cumming on this subject. In any event, we consider that Professor Giles’ conclusions summarise the present situation.
24. Upon the request of the Respondent’s solicitor, Professor Giles had also addressed in one of his reports, papers by Oneida Kincaid (Can non-ionizing radiation induce cancer?) and by Dr Neil Cherry (Cell phone radiation poses a serious biological and health risk) which were in the T-documents. They were not epidemiological studies. We accept Professor Giles’ assessment of both papers. In particular, the Kincaid paper is silent with respect to the risk of astrocytoma and measured exposure to RFR, and Dr Cherry was an environmental activist whose material was selective and whose interpretation lacks objectivity. That neither paper was referred to by the expert epidemiologists, Professors Giles and Cumming, when addressing the question the subject of these proceedings also reinforces the conclusion that they do not assist us.
25. We had reports from Professor Levi, oncologist, and Dr Teo, neurosurgeon and heard oral evidence from Professor Levi, but not from Dr Teo, who unfortunately for the second time was unable to give evidence because he had to perform a lengthy emergency operation.
26. Dr Teo undertook a survey of various papers about electromagnetic radiation and cancer. He acknowledged that “the only known agent that is clearly associated with astrocytomas is ionising radiation”. Based on his review his conclusion was “that there is certainly enough scientific evidence to suggest that Mr Beckwith’s exposure to EMR may have caused his brain tumour” (emphasis added).
27. We found compelling Professor Giles’ critique of Dr Teo’s report and the papers to which he had referred. While Dr Teo is a neurosurgeon, he is not an expert in the critical appraisal of epidemiological studies. We note that Professor Cumming did not comment on Dr Teo’s report.
28. Professor Levi referred to studies in the relevant area and addressed the Kincaid and Cherry papers in his report. In summary, his opinion is that a linkage between non-ionising radiation and brain cancer is speculative. He said that the evidence of a biological effect of non-ionising radiation is inconclusive. On the available evidence about non-ionising radiation, he is not persuaded that there will ever be a positive link established with brain cancer. He considered that Dr Teo’s report did not provide adequate evidence of the likely association between exposure to radar waves and the development of brain cancer.
29. Professor Levi also gave evidence about the development of Mr Beckwith’s tumour. He estimated that the 3 centimetre tumour had been present for 18 months to 2 years before the MRI scan was done in November 2001.Astrocytoma Grade II is fairly slow growing. He also talked about the latency period, that is, the time from exposure to a carcinogen until the appearance of the cancer. There is a lengthy duration of time before cells are altered sufficiently to become cancerous. The latency period is usually many years. If radar exposure had been a causative influence, it was associated with an apparently short latency period, the three years immediately before diagnosis. Further, Mr Beckwith’s statements indicated that he may have had pre-existing symptoms up to nine months before diagnosis. Clinical symptoms only arise when the tumour has reached a certain size. Mr Beckwith told Professor Levi that Professor Rosenfeld had indicated a period of clinical development of up to two years before actual diagnosis. In Professor Levi’s opinion, the latency is extremely short and he feels that represents a major impediment to any consideration of radar exposure being a possible causative factor.
30. In relation to the significance of a family history of brain tumour, Professor Levi said that we do not know what kind of tumour Mr Beckwith’s uncle had, that everyone who develops cancer has an underlying genetic susceptibility, and that little work had been done on the familial history of brain cancers.
31. Professor Giles said that the familial risk for brain cancer is about 3-fold the population risk, that is, the risk for a man with a family history would increase from around 0.7% to 2.1% or from 1 in 150 to 1 in 50. The history that was given was that Mr Beckwith’s uncle died of a brain tumour at age 30. In Professor Giles’ opinion, Mr Beckwith’s family history may have contributed significantly to the development of his tumour. The relatively early age at diagnosis, 23 years, supports the likelihood of an inherited susceptibility.
32. He stated that low-grade astrocytomas are slow-growing and Mr Beckwith’s tumour could have been present prior to his exposure to radar. Professor Giles agreed with Professor Levi’s reservations in regard to the very short latency period that would have to be accepted were RFR exposure to be considered the culpable agent. In his opinion, it is improbable that Mr Beckwith’s tumour was contributed to by his military service.
33. In response to a specific question, in his report dated 3 June 2002 Professor Rosenfeld commented that that exposure to communication signals may contribute to the development of a neoplastic condition. There was no basis given for that opinion.
Conclusion
34. We consider that the evidence before us suggests at highest, that is, based on the evidence of Professor Cumming and Dr Teo, that there may be a causative relationship between RFR and brain cancer. That it is possible that such a relationship exists is not sufficient to persuade us on the balance of probabilities that Mr Beckwith’s brain tumour was contributed to in a material degree by his exposure to radar, assuming we were satisfied about the extent of his exposure.
35. In any event, we prefer the evidence of Professor Giles and Dr Levi who specialise in oncology in their respective areas of expertise. Their evidence also admits of the possibility of a causative relationship, but they both consider it is unlikely.
36. As noted above Professor Rosenfeld is a neurosurgeon and did not provide a basis for his opinion about the causative connection. In that circumstance we give little weight to his opinion.
37. We consider the gene-environment interaction theory to be quite speculative and not of assistance in this case.
38. Given our finding, it is unnecessary to consider the other issues.
Decision
39. For the reasons set out above, we affirm the decision under review to disallow Mr Beckwith’s claim for compensation.
I certify that the 39 preceding paragraphs are a true copy of the reasons for the decision herein of Senior Member,
Mrs Josephine Kelly.Signed: Ms P Nimmagadda
Associate
Date of Hearing 12 and 13 April, and 10 May 2007
Date of Decision 20 June 2007
Solicitors for Applicant Winship Lawyers
Counsel for Applicant Mr C. JacksonSolicitors for Respondent Sparke Helmore Lawyers
Counsel for Respondent Mr B. Dube
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