High Court Of Justice - Queens Bench Division
Benjamin Browne QC and Catherine Foster & Mark James (instructed by Rosenblatt Solicitors) for the Claimants
Charles Gibson QC and Leigh-Ann Mulcahy QC, David Evans & Adam Heppinstall (instructed by Treasury Solicitors) for the Defendants
Full details of the Judgment.
Case No: TLQ/08/0023
Royal Courts of Justice
Strand, London, WC2A 2LL
Continuing on from part one, we pick up the report discussing chromosomes.
Professor Brenner said in his report of 6 November 2008:
“There is independent evidence from large-scale epidemiological studies (in particular Japanese Atomic Bomb survivors, but also nuclear workers (Cardis et al. 2007)) that individuals exposed to radiation doses in this dose range have an increased lifetime risk of both cancer incidence and cancer mortality. For example, atomic bomb survivors exposed in 1945 in the dose range from 5 to 150 mSv (and followed up for many decades) show statistically-significant increased risks of both cancer incidence and cancer mortality (Preston et al. 2003, 2004, 2007). Atomic bomb survivors who received higher
doses have proportionately higher lifetime cancer risks (Preston et al. 2003, 2004, 2007).
In addition to the relevance of chromosome aberrations as biomarkers of past exposure to radiation, there is a well established mechanistic link between chromosome aberrations and cancer. In particular, the majority of all human cancers contain one or more of the same chromosomal aberrations in virtually all the tumour cells, implying that this/these chromosome aberrations must have been present in the original damaged cell(s) from which the tumour originated. This link between chromosome aberrations and cancer has been extensively catalogued, for example by Mitelman et al (1997, 2008).
Finally, I will comment on the issue of the latency period between radiation exposure and the appearance of an associated cancer. A great deal is known about this issue, largely from the detailed follow-up studies of the Japanese atomic bomb survivors, whose cancer risk have been carefully monitored for more than half a century (Preston et al. 2003, 2007). What is well established from these studies is that, for solid tumours (as opposed to haematological cancers), the latency period is long, ranging from about 10 to at least 50 years.
More precisely, the increased relative risk of cancer produced by radiation exposure is generally maintained throughout the lifetime of the exposed individual. Whilst a complete mechanistic understanding of radiation-induced cancer is not yet established, the reasons for this prolonged period of increased radiation-associated risk are qualitatively understood: radiation-induced cancers originate with radiation-induced damage to stem cells, which can be passed on to progeny stem cells when they divide. Thus the radiation-induced damage can remain latent in stem cells for many years until the damaged stem cell or one of its progeny starts to divide inappropriately as a result of the damage.”
Dr Lindahl broadly accepts this mechanism of injury in relation to cancers. In his report of 23 July 2008 he said this:
“Cancer usually results from inactivation of tumour suppressor genes. There are probably 20-50 major such genes. Cancer can also occur by activation of smaller numbers of specific oncogenes. In both the cases of tumour suppressor genes and oncogenes, the critical alteration is malfunction in the cellular signal transduction processes that results in uncontrolled cellular proliferation.
Single site mutations with alteration of a single residue is one cause of a specific rare transformation of a normal cell to a malignant cell. Alternatively, this can occur by chain breaks in DNA with perturbations or rearrangements locally of the DNA sequence. This is triggered by chain breaks in DNA…. Because ionising radiation can generate a track of reactive hydroxyl radicals, such radiation can damage DNA locally at multiple sites, including damage to both strands of DNA with a short region, and this may well result in a double strand break.”
The essential question is whether the Rowland Report has so changed the scientific evidential landscape that it is an inescapable conclusion that the “knowledge threshold” within the Limitation Act has never (and could never) have been crossed until its promulgation or, if it has (or could have) been crossed at any earlier stage, whether the emergence of the report is a factor to which weight should be given in this exercise.
It would be convenient to refer at this stage to the views of Professor Mothersill to which I have made oblique reference thus far. The Defendant has characterised her views which support the proposition “that virtually any illness can be caused by any dose of radiation” as “highly controversial”. She is described by the Defendant as merely a “radiobiologist” who is “not medically qualified”, nor “an immunologist”, whose theories on the “biological mechanisms by which injury might be caused (genomic instability/bystander effects and immune system compromise)” are not supported by current scientific understanding.
The suggestion is, in effect, that her views are so far off received wisdom that they should be discarded. The principal source of this scepticism is undoubtedly Dr Lindahl who is very dismissive of her views. (Dr Tomas Lindahl FRS is a Swedish radiobiologist who joined in 1981 what was then the Imperial Cancer Research Fund, now Cancer Research UK, and is renowned for matters relating to DNA repair.
Professor Mothersill, BSc, PhD, is a Professor of Radiobiology in the Department of Medical Physics and Applied Radiation Sciences, McMaster University, Hamilton, Ontario, who for 20 years prior to 2003 had been, firstly, a lecturer in medical physics and radiation biology at the Dublin Institute of Technology and thereafter Scientific Director of the Radiation and Environmental Science Centre there.
From 2003 onwards she has been based at McMaster University.
Professor Mothersill’s summary of what “genomic instability” means in this context is as follows:
“…Any disease could be caused by an exposure [to a low dose of ionising radiation] as ultimately our genes determine which proteins are expressed in ourselves and thus control our responses to disease situations. Genomic instability is turned on by extremely low doses of radiation and can be triggered in bystander cells as well. Bystander cells received signals from irradiated cells but do not experience the ionising tract. A further important fact is that genomic instability is a delayed effect of radiation which may not be immediately apparent.
The LNT [Linear Non Threshold] model which is used by all radiation protection authorities predicts that any dose no matter how small has a finite probability of causing a cancer due to the ability of radiation to cause DNA damage. The finding of excess chromosome translocation frequencies in the veterans is consistent with this and also with the presence of genomic instability in these individuals. What genomic instability theory does is that it widens the spectrum of diseases inducible by radiation and the time over which these might appear.”
Professor Mothersill goes on to say this:
“It was well established (long before Dr Rowland’s report) that ionising radiation can cause certain illnesses, including (but not limited to) cancers. It follows that, if, as Dr Rowland found, the veterans were exposed to ionising radiation, then this materially increased the risk of the veterans suffering the illnesses from which they have actually suffered.”
Against that background, Professor Mothersill has lent her support to the causal link between their exposure to ionising radiation and certain conditions from which they have suffered on the part of some, but not all, of the Lead Claimants in this case. Her support is expressed on the basis that their exposure to ionising radiation materially increased the risk of their developing the conditions specified.
It follows from all this that, as things stand and without the evidence being fully tested, there is expert support for an explicable link between exposure to ionising radiation and most, if not all, of the conditions sought to be relied upon by the Claimants, either by virtue of (i) the direct effect upon DNA and potential cancerous growth as a result or (ii) the indirect effects by way of bystander effects and consequent genomic instability. Whether that support would translate into a finding that causation had been established in any case would, of course, depend upon the view taken about such evidence at the trial of the substantive cases if such a trial takes place. But, on the evidence as it stands, the necessary link is established for most, if not all, of the conditions relied upon.
The MoD Response
What is the basis for the Defendant’s contention that causation is unarguable in each of the Lead Cases?
In essence what is said is that the claims fall to be assessed by reference to the approach in Wilsher v Essex Area Health Authority  AC 1074 and that the exception to the general rule articulated in Fairchild v Glenhaven Funeral Services Ltd and others  1 AC 32 cannot apply in these cases.
The reason for so submitting is based upon a concession made on behalf of the Claimants in the Opening in the following terms:
“All of these illnesses also occur when there is no known history of exposure to ionising radiation and in all cases there are known to be other identifiable risk factors, such as smoking. In the event that it is possible to identify more than one risk factor medical science is not able to say which of those risk factors as a matter of probability caused the development of the condition. All that can be said is that the condition has developed and that there are a number of risk factors each of which is likely to have played a material part in the causation of the ill-health.”
Significant Areas of Evidence and Argument
(i) What was in the public domain about the effects of ionising radiation?
(ii) The role of the British Nuclear Test Veterans Association (BNTVA).
(iii) The Pearce case.
(iv) The funding issues.
(v) The National Radiological Protection Board (NRPB) reports.
(vii) The essential position taken by successive Governments over the years.
(viii) The Australian Royal Commission.
(ix) The Rowland Report.
(i) What was in the public domain about the effects of radiation?
The Defendant has asserted that there has been a welter of publicity over the years that should have put those who were present near the nuclear tests, or who played a part in their aftermath, on notice of a possible link to any illness, particularly cancerous, which they developed. The Treasury Solicitor commissioned a search of the available archives for newspaper articles relevant to the issues in this case (for example, radiation-linked injuries, veterans’ claims, scientific reports and media coverage) since the tests. The result was to discover about 600 articles in all which fill 6 lever arch files in the material before the Court. That ‘headline’ statistic is, of course, not to be ignored, but as with every headline the subtext needs consideration to reach an informed view.
The Guardian on 13 June 1956 carried a front-page article entitled “Warning on H-Bomb Tests – Long-Term Risks if Rate of Firing Continues – THE STRONTIUM DANGER”. It was reporting the result of an inquiry carried out by the Medical Research Council entitled “The hazards to man of nuclear and allied radiation” (Cmnd. 9780) said in the article to have been commissioned the previous year by Sir Winston Churchill because of “public unrest about the genetic effects of the nuclear explosions carried out by the Americans in the Pacific.” This plainly referred to the Bikini Atoll test referred to in paragraphs 26 and 27 above.
The Defendant draws attention to the following paragraph in the article:
“There are certain constituents of fall-out, of which strontium 90 is the most important, which retain their radio-activity for long periods, and which are deposited on the ground over a very wide area where they may contaminate drinking water and crops. If strontium 90 enters the body it concentrates in bone and may cause cancer.”
(ii) The British Nuclear Test Veterans’ Association (BNTVA)
Because of its involvement in the process of bringing into public awareness the concerns of test veterans and raising general awareness of issues concerning the tests and the alleged health consequences the BNTVA must be mentioned in this report.
I would, perhaps, add also that it is self-evident from the numbers who have, over the years, been recorded as members of the BNTVA, that not all nuclear test veterans have been members of the Association.
To that extent it cannot be said (nor has it ever been claimed, so far as I understand it) that the BNTVA represents the interests of all 20,000 or so who attended, or had some dealings with the aftermath of, the tests.
By 1997 Dr Sue Rabbitt Roff (Ms Susanne Roff, PhD, of the Centre for Medical Education at Dundee University Medical School) had become Research Adviser to the BNTVA. She was the Cookson Senior Research Fellow at Dundee University, a position, as I understand it, funded by the late Dame Catherine Cookson following an approach by Mrs Sheila Gray, the Secretary of the BNTVA.
Dr Rabbitt Roff, who grew up in Australia, has described herself as having “represented human rights organisations at the United Nations in New York throughout the 1980s, with particular reference to peace and security issues in small states and territories.” From 1991 she had taught Social Sciences and Medical Sociology at Dundee University Medical School, one of the courses dealing with the health hazards of ionising radiation. She had published a number of books including, in 1995, “Hotspots: The Legacy of Hiroshima and Nagasaki”.
From about 1995 she had been assisting veterans (presumably through the BNTVA) with applications to The War Pensions Agency. As a result of that collaboration the BNTVA commissioned a health study of BNTVA members and their families to be undertaken by Dr Rabbitt Roff. A detailed questionnaire was prepared by Dr Rabbitt Roff and sent to all members of the Association in December 1997.
A little earlier in the year, in July, with the assistance of information provided to her by the Association, Dr Rabbitt Roff began a study of the causes of death of the members of the Association of whose death notification had been received by the Association between 1983 and July 1997. Although the results of these two separate surveys became public earlier, they were published in “Medicine, Conflict and Survival” (Vol. 15, Supplement 1, July-September 1999) and entitled “Mortality and Morbidity of
Members of the British Nuclear Tests Veterans Association and the New Zealand Nuclear Tests Veterans Association and their Families”.
The results of Dr Rabbitt Roff’s work did receive some publicity. On 13 December 1998 The Mail on Sunday, under the headline “End A-test injustice”, carried a report of the survey. On 12 January 1999 The Daily Record, under the headline “A-bomb test veterans in case breakthrough”, reported that Dr Rabbitt Roff “who has studied 2,500 cases during the past 18 months, found 45 nuclear veterans had died or had been diagnosed with multiple myeloma - cancer known to be caused by radioactivity.” In January both The Guardian and The Lancet carried reports that the Australian and UK Governments had announced separate inquiries into the results of her work. I deal with that at paragraphs 310-315 and
Before moving on in time, it is also to be noted that in the period 1996-1997 the BNTVA had contact with the NRPB in relation to what became known as the ‘Phelps-Brown study’, an NRPB-funded study (in which, amongst others, Mr N.A. Phelps-Brown, Consultant Opthalmologist, and Dr Darroudi were involved) looking at whether elevated levels of chromosome translocations could be responsible for cataracts in UK Veterans. I deal with the study in paragraphs 304-305 and 371, but it is convenient to record here the exchange of correspondence between the NRPB and the BNTVA in late 1996 and early 1997 because the Defendant places some reliance upon it.
In a letter to the Vice Chairman of the BNTVA, Mr Peter Fletcher, dated 17 December 1996, the Head of the NRPB’s Biomedical Effects Department, Mr Roger Cox, explained the nature of the study in these terms:
“... NRPB have been funding and co-ordinating a study on the possible relationship between the presence of eye cataracts in UK Test Veteran volunteers and the frequency of stable chromosomal aberrations (translocations) in their blood cells. The principal aim was to determine whether volunteers with posterior-subcapsular cataract (PSC), which is known to be inducible by radiation, had levels of chromosome translocations that were elevated sufficiently to suggest that unrecorded high doses of radiation were responsible for their specific eye disorder. ”
This prompted a request by Mrs Sheila Gray, communicated to Mr Cox in a letter of 30 December 1996, for more information about the study. It appears that the study was initiated in 1994 with the blood sampling of volunteers who were recruited with the BNTVA and the BAVA (the British Atomic Veterans Association, an association set up by Mr Tom Armstrong, one of those featured in the first Nationwide programmes. The aim of the study was described in these terms:
“The hypothesis to be tested in the study was whether the presence of posterior-subcapsular cataract in test veterans might be associated with unrecorded high doses (greater than around 1.3 Gy) of radiation. A chromosomal technique believed to be capable of assessing, in blood cells, historical radiation doses of this magnitude was employed in the methodology.”
Tthe Defendant relies upon this exchange of correspondence (plus the knowledge that would have been gained by those actively involved in the BNTVA) to show that in 1996/1997 the BNTVA and the veterans associated with it were aware of the possible association between translocations and disabilities arising from exposure to ionising radiation and the existence of technology designed to reveal the existence of the such translocations.
(iii) The Pearce case
Mr Melvyn Pearce was a former Lance-Corporal in the Royal Engineers who was pres