[the] efficacy or consequences of a practice” I hereby request a review of the Secretary of State’s Decision:
“Regulatory Justification of the Class or Type of Practice being: “The generation of electricity from nuclear energy using oxide fuel of low enrichment in fissile content in a light water cooled, light water moderated thermal reactor currently known as the EPR designed by AREVA NP.”” hereinafter “the Decision”.
The evidence I submit bears particularly on the consequences of the practice defined in Paragraph1.7 of the Decision in terms of detriment to health, safety and the environment.
The evidence contradicts the Secretary of State’s assertions in para 1.7
that the potential detriment is small [and] well understood;
that the established regulatory regime … actively and effectively works to keep detriments within acceptable limits;
that the risk of health detriment from the building and operation of EPRs in the UK is very low.
The evidence contradicts an implicit assumption made by the Secretary of State in the following passage from para 1.7:
As a proportion of the overall radiation to which members of the public are exposed from all sources, including natural sources, the evidence he has reviewed suggests that the contribution from any EPR would be very small
the implicit assumption being that that the risk of health detriment is necessarily proportional in a linear fashion to the overall radiation to which members of the public are exposed from all sources, including natural sources.
Similarly, the evidence contradicts the assumption that
the radiation dose which members of the public would receive from the normal operation of an EPR on an annual basis would be below detectable risk levels in the context of overall radiation exposure.
New and important evidence on the safety of the radiation risk model upon which EU Directives and domestic regulation depend.
The issue of the genotoxic hazard from internal radionuclides was considered sufficiently important for Environment Minister Michael Meacher and Health Ministers Yvette Cooper to set up the Committee Examining Radiation Risks of Internal Emitters CERRIE in 2001. Mr Meacher was removed from office before CERRIE completed its deliberations and two agreed joint studies which would have assisted the process were cancelled. The final report was not agreed by all the members. Since CERRIE new and important evidence which informs this issue has been published in the peer-review literature.
1. Evidence for the failure of the Hiroshima Studies.
Directives in the European Union and Regulations in the UK depend upon cancer risk factors published by the International Commission on Radiological Protection, an independent NGO. These risk factors are based primarily on the doses and cancer yield of the Japanese Lifespan Study (LSS). This epidemiological study was set up to depend upon comparison of exposed and unexposed individuals and the cancer yield in those exposed compared with unexposed controls. Forensic examination of the methodology and decisions made over the period of the study reveals that significant errors were introduced which resulted in incorrect conclusions being drawn. In particular it appears that the original control group, those who were not in the city at the time of the bombing, was discarded in 1973 when it appeared that their inclusion was suggesting a high level of cancer in the exposed groups. Furthermore, evidence presented in the Royal Courts of Justice in the Pensions Appeals Tribunal (Abdale and Others vs. Secretary of State for Defence; June 13th 2016) showed that all the epidemiological groups were exposed to rainout and subsequent contamination of the city by Uranium nanoparticles. The LSS study did not address internal contamination resulting from inhalation of the nanoparticles. New evidence which has emerged since CERRIE reported in 2004 demonstrates that exposure to Uranium particulates carries levels of genetic hazard which are not incorporated into the ICRP risk model. The matter is outlined in a letter which has been published by a leading peer-review journal in December 2016. The paper which was reviewed by three referees is attached as Appendix A.
2. Evidence of genetic damage leading to heritable effects in those exposed to Chernobyl fallout in Europe.
A review of evidence relating to the genetic effects of chronic internal exposure to contamination from the Chernobyl accident was published in a leading peer-review journal in January 2016 [Schmitz-Feuerhake et al., 2016]. It examined the considerable evidence relating to increases in congenital defects and other heritable conditions in Chernobyl-exposed individuals but also discussed other situations where significant excess risk was shown to exist in offspring of exposed parents. The current ICRP radiation risk factor for such effects is obtained from mice because the LSS study (above) was unable to find any heritable effects in children of the exposed groups. However we now see that the chosen comparison groups were unsafe for the purposes of obtaining evidence of harm (see 1 above). The aggregated evidence presented in Schmitz-Feuerhake et al 2016 demonstrates unequivocally an error in the current risk factor for heritable defects of approximately 1000-fold. It shows that heritable defects occur in offspring of those exposed to internal doses of less than 10mSv and furthermore that the dose response is not linear, as assumed by the ICRP and current legislation.
3. The ethical basis of the ICRP and regulations which depend on it.
EU Directives and UK Regulations which control radiation exposures encapsulate a decision to tolerate low levels of risk of cancer and genetic damage. The current 1mSv annual dose limit for members of the public enshrined in EU Council Directive 96/29/euratom and its successor 2013/59/euratom is based on a permitted level of absolute cancer risk of 1 in 1 million. The current relative cancer risk factor of the ICRP is about 0.5 per Sievert. Thus an exposure of 1 mSv carries with it an excess risk of 0.5/1000 or 1 in 2000. This is considered acceptable to Society. Regarding heritable damage, the current doubling dose published by the ICRP and agreed also by the United Nations Scientific Committee on the Effects of Atomic Radiation UNSCEAR is 1Sv. Thus an annual dose of 1mSv, the limit for effective dose for public exposures under Directive 2013/59euratom, carries an excess risk of 1 in 500 of heritable effects in the offspring of parents exposed. This is considered to be acceptable as a side effect of the agreed development of nuclear technology. The new and important evidence referred to above shows that this factor is in error by approximately 1000-fold when applied to internal chronic exposures. This issue is relevant to releases of radioactivity from nuclear plant and other sources, to contamination of the sea and watercourses, and other releases which are currently controlled on the basis of the 1mSv level. The issue may be less relevant to external exposures from X-rays or other external sources.
The disagreements which were documented in the CERRIE majority and minority reports and evidence which was brought forward by the various members of the committee can reasonably be revisited in the light of new evidence which has emerged since then; this evidence includes but is not restricted to the above.
5. Here if you wish you can add your own concerns about your local reactor or DU or test veterans or whatever you like.
Schmitz-Feuerhake, Busby C, Pflugbeil P Genetic Radiation Risks-A Neglected Topic in the Low Dose Debate. Environmental Health and Toxicology. 2016. 31Article ID e2016001.http://dx.doi.org/10.5620/eht.e2016001.
Below is a letter by Dr Busby which was published by a leading peer reviewed scientific journal, Genetics.
BUT I couldn’t afford to pay for open access, some 2000 dollars.
Letter to the Editor on “The Hiroshima/ Nagasaki Survivor Studies: Discrepancies between Results and General Perception” by Bertrand R Jordan.
Environmental Research SIA, 1117 Latvian Academy of Sciences, Riga, Latvia
In his recent article  Jordan addresses the public’s “unreasonable” fears of radiation. He claims that the Lifespan Study (LSS) of the Japanese A-Bomb survivors in Hiroshima and Nagasaki has given definitive information on the relation between exposure and genetic damage, expressed as cancer and heritable effects in offspring of those exposed. He presents the LSS as the gold standard in radiation epidemiology, and he is not alone in this . The LSS results are the basis of legal limits for exposure and are employed to dismiss evidence showing that health effects from Chernobyl , Fukushima thyroid cancers  and child leukemias near nuclear sites  etc. somehow cannot be causal because the “dose is too low”. How can the public not accept that the Science on this issue is clear? Jordan observes that according to the LSS study you have to get a dose of 1Sv (1000mSv, 500 times natural background) to have a 42% excess chance of cancer, and as for the offspring, there have been no increased frequencies of abnormalities or genetic effects detected. Unfortunately there are some worrying problems with the epidemiological methods employed, specifically with the key issue of the choice and later abandonment of the control group.
The common understanding of the LSS study is that groups of individuals with known doses are compared over their lifespan with zero dose control groups who were not there. Jordan explains:
The ABCC and later RERF assembled a lifespan study LSS cohort of 120,000 individuals (100,000 exposed at various known levels and 20,000 controls Not in the City (NIC) at the time of the bombing).
But what is not generally known is that the NIC controls were discarded in 1973 because they were apparently “too healthy”. The 1973 ABCC report wrote:
In order to ascertain the effects of radiation exposure it is necessary to compare the mortality experience of the population exposed to ionizing radiation with a comparison control population. For this purpose a group of people who were not present in the cities was included in the sample. . . .
The mortality experience of the NIC comparison group has been very favourable. . . [and] would have the effect of exaggerating the difference in mortality between the heavily exposed population and the control group. . .
[  pp 6-7, ABCC LSS Report 7, 1973]
At that point, in 1973, the original control was discarded in favour of shifting to the lowest dose group as the control, something which should never be done in the middle of an epidemiological study. The substitution with a new lowest-dose control group was followed by the use of mathematical regression methodology. This approach was questionable because of inbuilt assumptions which I list below. Many of these are now known to be wrong.
The concept of “absorbed dose” employed by the study was a legitimate measure of biological damage from internal exposures i.e internal exposures can be translated into “dose” and this carries the same biological hazard as the identical external exposure dose.
The dose response relation was linear or at least monotonic, a necessity for regression.
There was no fallout which would have contaminated all the exposed groups equally
Internal exposure from fallout was therefore considered to be negligible and was ignored.
Acute exposures carry the same proportional hazard as chronic exposures.
The Japanese survivor population was representative of the general (western) public
These arguments have been reviewed elsewhere [7,8]. The use of the lowest dose group as control is now also standard in all the nuclear worker studies  which (like the LSS) employ linear regression to establish risk factors. Why? Because if the national population is employed as a control, the nuclear workers show a “healthy worker effect” (HWE) and their relative risks for cancer are lower than the general public. But this does not permit the lowest dose group to be valid as a control unless it is also known that there is a linear or monotonic dose response. Also the true value of the HWE is unknown. Let me unpack this. The risk factor for cancer obtained from regression is the gradient of the best straight line that can be fitted to the excess cancer risk in groups aggregated according to their external dose as measured by a film badge. The bigger the dose, the bigger the effect, is the assumption, though the data do not show this. The other problem is that nuclear workers are from a different Social Class than the National Population. They are fundamentally healthier, as are e.g. physicians, optometrists, soldiers, university lecturers etc. So their Relative Risk for cancer should be lower. But how much lower? The epidemiological method used now is to assume (and this is an unfounded assumption) that the effects of radiation on the lowest dose group can be set at zero. It is the point (0,0) for the regression line. But two observations are relevant here. First, the lowest dose group (usually with the most individuals in it) is still a group of workers who mostly work on the contaminated sites (rather like the Hiroshima survivors did) perhaps inhaling radioactive particles. So strictly they should be compared with similar workers who are from a completely different industry where there is no radioactive contamination (or with the national population, adjusting for the healthy worker effect). There is some evidence about the real HWE value from data published by the UK National Radiological Protection Board of the relative risk of cancer in UK nuclear workers stratified by length of time working in the nuclear industry . The level of healthiness (HWE) shifted from about 64% of the National rate at start of employment to nearer 90% after 10 years i.e. the healthy worker effect rapidly disappeared. This could be seen as an effect of exposure. Use of 64% for the HWE results in significant 30-40% excess risk in the lowest dose group for nuclear workers.
To return to the linear dose response regression point, all the published data stratified by dose group define a dose response which is biphasic: it goes up at the lowest dose, then comes down, then goes gently up again at the high doses. There are plausible biological reasons for this (especially in the case of congenital effects where the end point is seen only after birth and at some dose level pre-birth viability stops). Drawing a straight line though these data points results in the wrong answer to the question of risk: there are different risk factors at low dose, medium dose and high dose and plausible biological reasons for this.
Thus it is not epidemiologically valid to employ regression methods for nuclear workers, any more than it is for the Hiroshima survivors which I now turn to.
The LSS dose group populations, like the nuclear workers, whatever their assumed doses, all lived on the contaminated sites of the bombed towns for many years after the bomb. Contamination was a consequence of the black rain. My description is based on Expert and Disclosed evidence presented recently by Prof. Sawada and others in the Royal Courts of Justice in London in the 3 week hearing of the British Nuclear Test Veterans vs. the UK Secretary of State for Defence . The up-draught from the rising fireball at Hiroshima and Nagasaki sucked in moist maritime air which cooled with altitude and condensed on the 95% un-fissioned Uranium nano-particles created in the plasma. This produced black rain over an area which included all of the dose groups used for the LSS study where dose was calculated by distance from the hypocentre. Uranium was measured later in the contaminated areas . The existence of any fallout was denied and external acute doses were calculated based on distance using experiments carried out in the Nevada desert. The last twenty years has seen massive changes in the understanding of the biological effects of radiation. This includes realisation that for internal exposures to elements which have chemical affinity for DNA, and to nanoparticles, the concept of absorbed dose is worthless . Uranium has a high affinity for DNA and a large number of studies have now shown effects which define large errors in the “dose” based approach [8, 14]. The European Union has recently funded research on this issue .
The black rain contamination of Hiroshima and Nagasaki resulted in continuous chronic internal exposure of all the dose groups and controls by inhalation and ingestion of Uranium particles. Thus the only accurate way to establish the real effects is to employ a truly unexposed group and abandon regression methods. In 2009 Wanatabe et al, employed the adjacent Okayama prefecture as control  and compared age and sex specific cancer rates between 1971 and 1990. This period was chosen according to the authors because apparently there were insufficiently accurate cancer data prior to 1971. It was found that there were significantly greater levels of cancer in all the exposed groups, including the LSS lowest dose controls compared with the Okayama control group but also (to a lesser extent) compared with an all Hiroshima control group. When compared with Okayama, the highest cancer effect per unit dose was seen in the 0-5mSv group, the lowest dose LSS group, where there was a 33% excess risk of all cancer in men at external doses estimated at 0-5mSv. The authors write: the contribution of residual radiation, ignored in LSS is suggested to be fairly high. This immediately falsifies all the LSS epidemiology. Similar criticisms were made by Sawada [11, 17] who examined immediate deterministic effects of radiation (epilation, diarrhea) which were reported from areas more than 5km from the hypocentre where black rain fell but where the prompt gamma doses were effectively zero.
Since this journal focuses on genetics, and Jordan also discusses this issue, I mention that similar control group errors in the LSS genetic studies were addressed long ago by de Bellefeuillle  who criticised the sex-ratio results. The LSS researchers focused on sex-ratio, the number of boys born to the number of girls, which is a well-accepted measure of genetic damage . The direction of the effect depends on whether the mother (egg) or father (sperm) are irradiated. But the LSS geneticists analysed results from families where both parents were irradiated and thus effects cancelled: they also employed the wrong controls. That is why they reported that there was no apparent genetic damage seen. Use of the NIC controls gives a sex-ratio effect in the correct direction . This issue is discussed in a recent review by Schmitz-Feuerhake et al (2016) of heritable effects reported at very low doses of internal exposure. Results from Chernobyl in many countries clearly demonstrate that the current genetic risk factor is in error by about 1000-fold and that the dose response is not linear. There are significant increases in major congenital malformations in offspring of those exposed to internal doses less than 1mSv .
I suggest that this adherence to the LSS as a definitive answer to the public’s fears is a result of a scientific culture of acceptance that goes back over a long period, and that few researchers have had the time or funding to forensically examine the many (often obscure) reports needed to open up the methodological black boxes. However, I submit that Jordan’s (and the legislators’) belief in the validity of the Japanese A-Bomb studies, I am sure innocently held, is unsafe, and that the health effects of low level internal exposures to radioactivity should be re-evaluated.
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7. Busby Christopher. 2013 Aspects of DNA Damage from Internal Radionuclides, New Research Directions in DNA Repair, Prof. Clark Chen (Ed.), ISBN: 978-953-51-1114-6, InTech, DOI: 10.5772/53942. Available from: http://www.intechopen.com/books/new-research-directions-in-dna-repair/aspects-of-dna-damage-from-internal-radionuclides
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11. Abdale and Ors. Vs The Secretary of State for Defence. Pensions Appeals Tribunal; Royal Courts of Justice, London June 13th -July 4th 2016
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15. Laurent O, Gomolka M, Haylock R et al 2016 Concerted Uranium Research in Europe (CURE): toward a collaborative project integrating dosimetry, epidemiology and radiobiology to study the effects of occupational uranium exposure. J.Radiol.Prot: 36(2):319-45
16. Wanatabe T, Miyao M, Honda R and Yamada Y., 2008 Hiroshima survivors exposed to very low doses of A-Bomb primary radiation showed a high risk of cancers. Env. Health. Prev. Med. 13: 264-270
17 Sawada S., 2007 Cover up of the effects of internal exposure by residual radiation from the atomic bombing of Hiroshima and Nagasaki. Med. Confl. Surviv. 23: 58-74
18. De Bellefeuille Paul., 1961 Genetic hazards of radiation to man Part I. Acta Radiologica: 56: 65-80
19. Scherb H, Voigt K 2011. The human sex odds at birth after the atmospheric atomic bomb tests, after Chernobyl, and in the vicinity of nuclear facilities. Environ Sci Pollut Res. 18:697-707
20. Padmanabhan VT 2012. Sex Ratio in A-Bomb survivors. Evidence of radiation induced X-linked lethal mutations. In Busby C, Busby J, Rietuma D and de Messieres M Eds. Fukushima: What to Expect. Proceedings of the 3rd International Conference of the European Committee on Radiation Risk May 5/6th Lesvos Greece. Brussels: ECRR; Aberystwyth UK: Green Audit, 2012
21. Schmitz-Feuerhake, Busby C, Pflugbeil P, 2016 Genetic Radiation Risks-A Neglected Topic in the Low Dose Debate. Environmental Health and Toxicology: 31Article ID e2016001. http://dx.doi.org/10.5620/eht.e2016001.