From: Majia Nadesan
RE: Draft Document: Radiological Protection of People and the Environment in the Event of a Large Nuclear Accident
Dear ICRP Committee
This strongly letter opposes the 100 millisievert exposure proposed in the wake of radiological emergencies. We should be reducing exposure levels and preventing radiological accidents rather than enabling them.
The proposed 100 millisievert exposure level violates the principle of “as low as reasonably achievable” and while it may be formally assessed as relatively low risk for adult men in peak health, this level of exposure could be catastrophic for pregnant women and children.
Research on children living in close proximity to nuclear power plants supports the ‘no safe dose’ argument for susceptible populations. A study by the Institut National de la Sante et de la Recherche Medicale (French Institute of Health and Medical Research, or INSERM) documented a leukemia rate twice as high among children under the age of 15, living within a five kilometer radius of France's 19 nuclear power plants, when compared to those living 20 kilometers or more away from a plant.[i] The French study reinforced previous findings on excess risk for leukemia in young children living in close proximity to German nuclear power plants.[ii] In a commentary, ‘Childhood Cancer near Nuclear Power Stations,’ published in Environmental Health Perspectives, Ian Fairlie observed: ‘Doses from environmental emissions from nuclear reactors to embryos and fetuses in pregnant women near nuclear power stations may be larger than suspected. Hematopoietic tissues appear to be considerably more radiosensitive in embryos/fetuses than in newborn babies.’[iii]
RADIATION RISK: UNCERTAINTIES AND CATASTOPHIC HAZARDS
The processes for assessing the biological risks of radiation exposure have historically homogenized effects across distinct populations and underestimated consequences of exposure[iv] by failing to incorporate special vulnerabilities, long-term bioaccumulation and biomagnification, and range of potential effects, especially developmental and transgenerational effects.
For example, radioiodine bioaccumulates in the human thyroid and thereby impacts the entire endocrine system, which helps govern the complex biological cues of growth and development, thereby engendering special hazards for the young. In 1962, Harold Knapp described how radioiodine from a single deposition in pasture-land bioaccumulates and biomagnifies, producing substantial and injurious radiation doses for children consuming milk.[v]
Research on Strontium-90 published in the 1950s and 1960s documented how this particularly dangerous radio-isotope can, in relatively low doses, bioaccumulate and biomagnify in the human body as an analog of calcium, leading to its substitution in bones and the brain and its concentration in milk. Both strontium and cesium (an analog of potassium) can pass the blood-brain barrier by entering the brain’s calcium channels.[vi] Uranium is also particularly chemically toxic and is capable of binding with DNA, whereupon it produces mutations through chemical action alone, as research on Navajo uranium workers and their families has found.[vii]
Decades of findings of radiation ecology demonstrated that radionuclides dispersed by nuclear testing, routine nuclear operations and disposal, and accidents could concentrate within biological bodies at high enough levels to produce heritable genetic damage.
The August 6, 1953 “World Wide Effects of Atomic Weapons: Project Sunshine” report (R-251-AEC Amended) addresses health effects of internal radionuclides, particularly Strontium-90:
The main concern of SUNSHINE is to examine the hazards of radioactive debris, that by one means or another, finds a way into a human being and thereby becomes a source of internal radiation damage; this latter hazard may be present in relatively local areas of earth or may be spread more extensively by natural means or through the commerce of man. (2)
The report indicates that PROJECT GABRIEL had identified Strontium-90 as among the most dangerous radioactive products because of its abundant formulation as a fission product and because “body ingestion is high,” with its “bone-seeking” properties constituting a special health risk:
the bone-retentive and radioactive properties of Sr90 endow it with a high carcinogenic capability; a given amount about threshold (which may be zero) fixed in the bone will cause a certain average percentage of the population to die of bone cancer comparable with that observed in victims of radium poisoning.
The US Academy of Sciences issued one, if not the first, independent and public reports on radiation effects: the 1956 “Biological Effects of Atomic Radiation: A Report to the Public from a Study by The National Academies of Science (BEAR).” The New York Times published an introduction to the report and excerpt from the Genetics Subcommittee findings June 13, 1956 (18).[viii] The report begins by diplomatically acknowledging the medical and energy benefits of nuclear. It then turns to examine the health risks, particularly from “fall-out” asking:
Are we harming ourselves and are there genetic effects which will harm our children and their descendants, through this radioactive dust that has been settling down on all of us? Are things going to be still worse when presently we have a lot of atomic power plants, more laboratories experimenting with atomic fission and fusion, and perhaps more and bigger weapons testing? Are there similar risks, due to other sources of radiation, but brought to our attention by these atomic risks? . . . even very small amounts of radiation unquestionably have the power to injure hereditary materials.
The report’s answer to this question is definitely yes if harm is not restricted to acute exposure effects. The report notes that significant long-term risks to the human population are posed by genetic mutations, particularly “mildly deleterious” genes that may persist longer and harm more people. The article details the intergeneration transmission and bio-accumulation of largely recessive mutations, implying that the inheritance of too many mutated genes can lead to sudden genetic instabilities and widespread reproductive failures.
These concerns were countered more recently by claims that the human genome is more resilient than originally theorized because of the capacity for genetic repair. However, although genetic repair mechanisms exist, their capacities are limited and changes to the code governing gene expression, the epigenetic code, persist and can produce lasting adverse impacts, destabilizing genomic integrity.
B.P. Engelward, at the Dept. of Biological Engineering at MIT, has documented indirect and delayed mechanisms for the creation of mutations deriving from changes in cellular behavior caused by exposure to genotoxic insults. Engelward’s study "Methyltransferases Mediate Cell Memory of a Genotoxic Insult" published in Oncogene focuses on how cells retain and transmit “memory” of an insult, resulting in genomic instability that can be transmitted across generations through epigenetic mechanisms of heredity, including DNA methylation, histone modification and the functions of certain non-coding RNAs.[ix] The study looks at how exposure to a genotoxin causes epigenetic methylation of mammalian DNA, producing delayed and persistent changes to the phenotype. The study suggests that memory of genotoxic insults may be “stored structurally in DNA in the form of DNA methylation patterns that are created and maintained by DNA MTases (for example, Dnmt1 and Dnmt3a)” (p. 755). In sum, the study stresses the role of indirect and temporally delayed genomic instabilities stemming from exposure to ionizing radiation and chemical mutagens.
Research on real-world effects of bioaccumulation and biomagnification in eco-systems reveals that the biological effects of living in a radiation contaminated zone cannot be predicted using the paradigm of radiation protection, which lacks ecological validity. Anders Møller and Timothy Mousseau and his colleagues have conclusively demonstrated through their field work in Chernobyl and Fukushima that “Contrary to governmental reports, there is now an abundance of information demonstrating consequences (i.e., injury) to individuals, populations, species, and the ecosystem function stemming from the low dose radiation due to the Chernobyl and Fukushima disasters,” with effects including reduced viability of sperm and smaller brains.[x]
WHAT COUNTS AS ADEQUATE PROTECTION FOR OUR KIDS AND THEIR KIDS?
We must return to the question of what counts as adequately protective exposure to radionuclides? Research by Aaron Datesman of NASA has found that basic assumptions about radiation health physics are flawed because they underestimate time-averaged dissipated power from beta decay.[xi] His finding suggest that we are grossly under-estimating the biological effects of exposure to beta-emitters. The health implications for such ubiquitous radioactive contaminants as tritium are therefore far more severe than previously acknowledged.
Moreover, even the most stringent regulatory standards are often based on risk coefficient tables that presume risk (usually thought only in relation to cancer) can be predicted on the basis of exposure to a single radioactive isotope.[xii] These risk coefficient tables often ignore risks beyond cancer and leukemia, although prolonged exposure to low-dose radiation is increasingly linked to other diseases and conditions, such as diabetes and hyper-tension.[xiii]
Indeed, in the wake of the Fukushima Daiichi disaster researchers found that the number of operations of complex congenital heart disease in neonates and infants increased by ≈14% in 2011.[xiv] Yet, few Fukushima residents were exposed to radiation doses in excess of 50 millisieverts according to the WHO 2012 preliminary dose estimate report that stated the total effective dose received by “characteristic individuals” in two locations of “relatively high exposure” over the first year was estimated between 10 to 50 mSv, primarily from external exposure.
The declassified NRC transcripts of conference calls that occurred on 17 March 2011 reveal that the agency had projections of a 40 millisievert dose to the thyroid from radioactive iodine alone for a one-year old child in California from Daiichi fallout: ‘The DITTRA result was four rem [40,000 microsieverts or 40 millisieverts] to the thyroid of a one year-old child based on one year integration of uptake.’[xv]
Researchers studying the effects of fallout in the American west after Daiichi found an increased rate of five congenital anomalies of 13.00% in five western states, a rate that was significantly greater than the 3.77% decrease for all other U.S. states combined (CI 0.030 - 0.205, p < 0.008).[xvi]
Increased radiation exposure in CA after the Fukushima Daiichi disaster correlated with a spike in autism diagnoses, as this article from the Sacramento Bee documents:
Reese, Phillip. July 18 2016. Autism rates in California public schools jumped 7 percent in 2016. Sacramento Bee, http://www.sacbee.com/site-services/databases/article90300877.html#storylink=cpy
The increase was especially sharp among kindergartners, where autism cases grew by 17 percent last year . More than one of every 65 kindergartners in California public schools is classified as autistic
To reiterate, the article is reporting that autism cases grew 17% in kindergartners in 2015. Those kids would have been in their first year of life when exposed to Fukushima fallout. Although no causal connections can be imputed without empirical investigation, this suspicious correlation warrants investigation of the range of biological effects for vulnerable populations from exposure to “low-dose” radiation, especially when internalized.
Measuring exposure and predicting radiation health effects are a slippery business in the real world as a consequence of special vulnerabilities, the bioaccumulation of radionuclides in biological bodies, and cumulative genetic and epigenetic damage transmitted across generations.
Yet, failures to incorporation scientific findings about radionuclide flows, individual and developmental vulnerabilities, and hereditary effects constitute a politics of disregard with potentially catastrophic consequences for the eco-system and the human genome.
It is my personal belief based on extensive review of interdisciplinary knowledge pertaining to human health and development that we should be REDUCING exposures levels rather than raising them.
Yes, that means that more needs to be done to secure against nuclear accidents and to plan for their inevitability given statistical projections that disasters such as Fukushima and Chernobyl are likely to occur every 10-25 years.
OUR COLLECTIVE FUTURE HINGES ON SAFER ENERGY
When the true costs of nuclear are calculated across the uranium supply, utilization and nuclear decommissioning cycle we see that nuclear is not simply inefficient and non-economical, it poses uncertain yet catastrophic risks for us all.
Findings in environmental toxicology, environmental genomics, epigenetics, and proteomics should cause wide-spread discussion about the social-environmental causes of spiking rates of cancer, neurological and immunological diseases coinciding with a dramatic decline in sperm viability.
The viability of human sperm is plummeting in developed economies. Increased exposure to ionizing radiation may play a critical role. “People in the former Soviet republic of Kazakhstan who were exposed to fallout from nuclear-weapon tests have more genetic mutations in their eggs and sperm than normal, researchers have found.”[xvii]
Cancer rates continue to edge upwards globally, as do significant neurological disorders in children and adults. In a review of changing patterns of neurological mortality in the 10 major developed countries (1979-2010), Pritchard, Mayers, and Baldwin (2013)[xviii] conclude that brain diseases are affecting more people and are affecting individuals at earlier ages than previously. The increasing incidents cannot be explained alone by endogenous factors, but must derive from a shift in environmental factors that shape human materialities.
My research on autism has reviewed interesting similarities between UNSCEAR’s description of radiation-induced developmental syndromes[xix] and autism spectrum disorders given that both are distinguishable by increased do novo mutations. Could increased exposure to ionizing radiation play a role in autism? People with autism are especially likely to have micro-deletions[xx] in mitochondrial DNA[xxi] and in DNA regulating brain synaptic development and oxytocin than family members. Mitochondrial DNA is inherited from the mother and mutations are transmitted across generations, with potential adverse health consequences increasing with the accumulation of mutations. Mitochondrial DNA is particularly vulnerable to damage, especially from ionizing radiation.
A study of the mitochondrial DNA of people who live in an area of Iran with high background radiation found that higher rates of mitochondrial DNA mutations correlated with higher background exposure and that point mutations were transmitted across generations. The researchers suggested that the observed mitochondrial mutability might be explained by genetic hot spots that are particularly prone to mutation by radiation.[xxii]
Our antiquated-Mendelian models of heritable genetic disease and strong commitments to autonomous individualism, proclivities reinforced institutionally, may in fact dis-able us from recognizing our material vulnerability to our built environments. Our limited perspective blinds us to the implications of rising disease incidents.
We need to be LOWERING our body burdens of genotoxins, NOT RAISING THEM to please a dying, inefficient, and non-competitive energy industry.
I leave you with this excerpt of findings on wild monkeys exposed to “low dose” Fukushima fallout:
Momoko Suda Nov 25 2018 Effects of suspected radiation exposure seen in Fukushima wild monkeys: researchers
TOKYO -- Researchers found fewer cells that become blood in the bone marrow of wild Japanese macaques living in northeastern Japan's Fukushima Prefecture along with the delayed growth of fetuses after the 2011 nuclear crisis, possibly due to radiation exposure.
Findings of abnormalities in these monkeys have been continuously reported in British scientific journals. Researchers assume that the monkeys ingested items like tree bark contaminated with radioactive cesium emanating from the Fukushima Daiichi Nuclear Power Station. Tohoku University's Department of Pathology professor emeritus Manabu Fukumoto and his research team performed hematological analysis of adult monkeys captured after the nuclear disaster. They inspected blood cell counts in the bone marrow of 18 monkeys caught in locations within 40 kilometers from the plant, including the city of Minamisoma and the town of Namie. Fukumoto's team then compared the data to that of monkeys from other areas. The results revealed various substances destined to mature into blood, like cells that develop into platelets, had decreased in Fukushima monkeys.
Furthermore, the team observed some blood components had greatly decreased in monkeys with higher internal radiation exposure per day. They estimated the radiation dose from the concentration of radioactive cesium in the monkeys' muscles. Fukumoto explained, "We need to conduct long-term research to see if it (the abnormalities) has an effect on the monkeys' health."
Can we save ourselves by coming to grips with our biological vulnerabilities to the catastrophic risks engineered into our energy systems? I can only hope.
Dr. Majia Nadesan
[i] C. Sermage-Faure, D. Laurier, S. Goujon-Bellec, M. Chartier, A. Guyot-Goubin, J. Rudant, D. Hemon and J. Clavel (2012) ‘Childhood Leukemia around French Nuclear Power Plants-The Geocap Study, 2002-2007’, International Journal of Cancer, 131, 5, p. 769-780, http://onlinelibrary.wiley.com/doi/10.1002/ijc.27425/pdf, date accessed 7 September 2012.
[ii] M. Blettner, P. Kaatsch, S, Schmiedel, R. Schulze-Rath, and C. Spix (2008) ‘Leukaemia in Young Children Living in the Vicinity of German Nuclear Power Plant’, International Journal of Cancer, 122, 721–726.
[iii] I. Fairlie (2009) ‘Commentary: Childhood Cancer near Nuclear Power Stations’, Environmental Health Perspectives, 8.43, http://www.ehjournal.net/content/8/1/43, date accessed 24 August 2012.
[iv] A. Makhijani (April 2009) ‘The Use of Reference Man in Radiation Protection Standards and Guidance with Recommendations for Change’, Institute for Energy and Environmental Research, http://ieer.org/downloads/53.
[v] S. Kirsch (2004) ‘Harold Knapp and the Geography of Normal Controversy: Radioiodine in the Historical Environment’, Osiris, 19, 167-181.
[vi] Xu-Friedman, M. A., & Regehr, W G. (1999, April). Presynaptic strontium dynamics and synaptic transmission. Biophys J., 76(4), 2029–2042.
[vii] Carrie Arnold (2014, February). Once upon a mine: The legacy of uranium on the Navajo Nation’ Environmental Health Perspectives, 122(2), A44-A49, http://ehp.niehs.nih.gov/122-a44/
[viii] Text of Genetics Committee Report Concerning Effects of Radioactivity on Heredity” (13 July 1956), The New York Times, 18.
[ix] R. E. Rugo, J. T. Mutamba, K. N. Mohan, T. Yee, J. R. Chaillet, J. S. Greenberger, and B. P. Engelward (2011) "Methyltransferases Mediate Cell Memory of a Genotoxic Insult." Oncogene (2011) 30, 751-756.
[x] Timothy A. Mousseau: (2014, August 22) [Press Conference] "Fukushima Catastrophe and its Effects on Wildlife" FCCJchannel https://www.youtube.com/watch?v=8IcTGUMwVtU
Møller, A. P., Bonisoli-Alquati, A., Rudolfsen, G., & Mousseau, T. A. (2011). Chernobyl birds have smaller brains. PlOS One, 6(2), e16862.
Møller, A. P. & Mousseau, T. A. (2006). Biological consequences of Chernobyl. Trends in Ecology and Evolution, 21. https://doi.org/10.1016/j.tree.2006.01.008
[xi] Datesman, A. (2019). Shot noise explains the Petkau Na result for rupture of a model phospholipid membrane. Health Physics. https://www.ncbi.nlm.nih.gov/pubmed/31211753
[xii] Environmental Protection Agency (1999) Cancer Risk Coefficients for Environmental Exposure to Radionuclides Federal Guidance Report No.13, http://www.epa gov/radiation/docs/federal/402-r-99-001.pdf, date accessed 25 November 2012
[xiii] American Heart Association (May 3, 2019). Prolonged exposure to low-dose radiation may increase the risk of hypertension, a known cause of heart disease and stroke Science Daily, https://www.sciencedaily.com/releases/2019/05/190503080554.htm
[xiv] Murase, K, Murase, J and Mishima, A, (2019). Nationwide Increase in Complex Congenital Heart Diseases After the Fukushima Nuclear Accident, Journal of the American Heart Association 8(6). https://www.ahajournals.org/doi/10.1161/JAHA.118.009486.
[xv] U.S Nuclear Regulatory Commission (17 March 2011) ‘Official Transcript of Proceedings of Japan’s Fukushima Daiichi ET Audio File’, http://pbadupws.nrc.gov/docs/ML1205/ML12052A109.pdf, p. 187, date accessed November 5, 2012.
[xvi] Mangano, J. and Sherman, J. (2015) Changes in Congenital Anomaly Incidence in West Coast and Pacific States (USA) after Arrival of Fukushima Fallout. Open Journal of Pediatrics, 5, 76-89. doi: 10.4236/ojped.2015.51013.
[xvii] Sperm and eggs fall foul of fallout (2002, February 8). Nature. doi:10.1038/news020204-10 http://www.nature.com.ezproxy1.lib.asu.edu/news/2002/020208/full/news020204-10.html AND Dubrova,Y.E. (2002) Nuclear weapons tests and human germline mutation rate. Science 295, 1037 AND Dubrova, Y.E. et al. (1996) Human minisatellite mutation rate after the Chernobyl accident. Nature 380, 683 - 686(996).
[xviii] Pritchard C., Mayers, A., & Baldwin, D. (2013). Changing patterns of neurological mortality in the 10 major developed countries 1979-2010. Public Health 127(4), 357-68. DOI: 10.1016/j.puhe.2012.12.018.
[xix] United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) (2001). ANNEX: Hereditary Effects of Radiation. Available, http://www.unscear.org/docs/reports/2001/2001Annex_pages%208-160.pdf
[xx] Sebat J., Lakshmi, B., Malhotra, D., et al. (2007l). Strong association of de novo copy number mutations with autism. Science 316, 445–449.
[xxi] Goh, S., Dong, Z., Zhang, Y., DiMauro, S., & Peterson, B. (2014). Mitochondrial dysfunction as a neurobiological subtype of autism spectrum disorder. JAMA Psychiatry 71(6), 665-671. DOI: 10.1001/jamapsychiatry.2014.179
[xxii] Lutz-Bonengel, S., Brinkmann, B., Forster, L., Forster, P., & Willkomm, H. (2002). Natural radioactivity and human mitochondrial DNA mutations. Proceedings of the National Academy of Sciences of the United States of America, 99.21. Available, http://www.pnas.org/content/99/21/13950.long, date accessed 22 October 2012.