[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.
4.4. 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.
Reference Section 4:
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.
Section 5: Some of the concerns that should be noted are with suspect Fukushima, Romanian, Ukrainian etc food and drinks being transported freely within the EU area. Also, Sellafield Sea Monitoring (which seems only to be sparse testing at 2 locations). I was unable to find the testing regime for fish, seaweed and shell fish products but they are of concern as well. In particular, the current restrictions on sale of fish and shellfish in Ireland are based on the ICRP radiation risk model which is now seen to be unsafe.
Also, the Irish Times highlighted the possible scenario of an accident damaging the Irish mainland based on the same existing and flawed dose model that does not take into account particulates of different isotopes. Air pollution is also a concern and there needs to be some transparent discussion on this area but the new Secrets Act of 2014 April means that all data is “Official Sensitive” and not open to the public (note that nuclear related data was made “Official Sensitive” retroactively cover all data related to nuclear sites to support privatisation secrecy).
The UK has been trying in recent attempts at increasing the allowable dose to some 100 mSv/y from the existing 1mSv/y to the public (ref Richard Wakeford and Wade Allison etc) at the Moscow UNSCEAR meeting 2014 and indeed since then . Also, another UK radiation expert (Geraldine Thomas) gave some shocking advice to the victims of the Fukushima disaster and this was recognised by the BBC and wider international nuclear groups and eventually they had to remove the public advice they had been given but with no public retraction! Here is a link to the debate that helped remove the offending advice from the BBC website; https://www.youtube.com/watch?v=qrgdAA5oiIA
Also, you will have heard that the Sellafield Managers had colluded to lie to the UK Government committee and were in contempt of parliament as a result of a recent Panorama program investigation into unreported contamination incidents that broke the EPSOO Finish cross border contamination agreement and Norway have made representations to the UK on this issue.
The issue of re-Justification involves historic practices. For new practices, new Justification is required by Member State and European law. Both require full, accurate and scientifically plausible assessments on the basis of the new and important evidence which I refer to above.
I look forward to your response.
Appendix A to Section 4
Because this not open access I have been sent a copy by Professor Busby.
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.
1. Jordan, Bertrand R. 2016.The Hiroshima/Nagasaki Survivor Studies: Discrepancies between Results and General Perception. Genetics 203 1505-1512
2. Kamiya K, Ozasa K, Akiba S, Niwa O, Kodama K, Takamura N, Zaharieva EK, Kimura Y and Wakeford R, 2015 Long term effects of radiation exposure on health. The Lancet 386 (9992): 469-478
3. Yablokov A V, Nesterenko V B, Nesterenko A V., 2009 Chernobyl: Consequences of
the Catastrophe for people and the environment. Annals of the New York Academy
of Sciences; 1181 Massachusetts USA: Blackwell
4. Tsuda T, Tokinobu A, Yamamoto E, Suzuki E., 2016 Thyroid Cancer Detection by Ultrasound among residents ages 18 years and younger in Fukushima Japan: 2011 to 2014. Epidemiology; 27(3): 316-322
5. Kaatsch P, Spix C, Schulze-Rath R, Schmiedel S, Blettner M, 2008 Leukaemias in
young children living in the vicinity of German nuclear power plants. Int J Cancer
6. Moriyama I M, Kato H., 1973. Mortality experience of A-Bomb survivors 1970-72, 1950-72. JNIH-ABCC Life Span Study Report 7 (Technical Report 15-73); pp 6-7. Hiroshima Japan: ABCC
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
8. Busby C, Yablolov AV, Schmitz Feuerhake I, Bertell R and Scott Cato M. 2010 ECRR2010 The 2010 Recommendations of the European Committee on Radiation Risk. The Health Effects of Ionizing Radiation at Low Doses and Low Dose Rates. Brussels: ECRR Aberystwyth Green Audit
9. Richardson DB, Cardis E, Daniels RD, Gillies M, O’Hagan JA et al. 2015. Risk of cancer from occupational exposure to ionising radiation: retrospective cohort study of workers in France, the United Kingdom and the United States (INWORKS). British Medical Journal: 351: h5359
10. Muirhead CR, Goodill AA, Haylock RGE et al. 1999. Second analysis of the National Registry of Radiation Workers. Occupational exposure to ionising radiation and mortality. NRPB R-307. Table 6.2 Chilton UK: National Radiological Protection Board.
11. Abdale and Ors. Vs The Secretary of State for Defence. Pensions Appeals Tribunal; Royal Courts of Justice, London June 13th -July 4th 2016
12. Takada J, Hoshi M, Sawada S and Sakanoue M., 1983 Uranium isotopes in black rain soil. J. Radiat.Res: 24(3) 229-36
13. CERRIE, 2004 Report of the Committee Examining Radiation Risk from Internal Emitters. Chilton, UK: National Radiological Protection Board
14. Busby Christopher, 2015 Editorial: Uranium Epidemiology. Jacobs Journal of Epidemiology and Preventive Medicine: 1(2)- 009; http://jacobspublishers.com/index.php/journal-of-epidemiology-articles-in-press
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.